medical_disease.id,medical_disease.ts,medical_disease.title,medical_disease.content
1,"2018-04-20 02:27:11","What is Babesiosis?","By Dr Tomislav Meštrović, MD, PhD Notwithstanding notable progress in medicine and biomedical science, parasitic diseases still represent a burden and a threat to human health. Among a myriad of parasitic diseases, those transmitted by vectors (mainly arthropods) play a significant role. Furthermore, such diseases are very prevalent in the poorest countries of the world, affecting an extensive portion of the human population, as well as posing a health hazard in developed countries. One of these parasitoses is Babesiosis, an infectious diseases caused by the protozoan parasites of the genus Babesia. Already recognized for some time as pathogens that impose a substantial health burden on domesticated animals, Babesia parasites have been progressively ascertained over the last fifty years to be a cause of human morbidity around the globe. In short, Babesia parasites infect vertebrate animals and humans, causing the lysis of red blood cells of the host. The disease is generally considered a zoonosis, since it is acquired by a tick bite when individuals unintentionally interact with the natural life cycle of the parasite. Nonetheless, Babesiosis transmitted via blood-transfusion represents a significant problem in highly endemic areas. The Hallmarks of Babesiosis Infection with Babesia parasites in a human host occurs when the vector (i.e. an infected tick) takes the blood meal from an infected rodent. The parasite can enter the human’s body together with the tick’s saliva as it feeds on the human host. Once in the body, Babesias penetrate the erythrocytes or red blood cells, proliferate and then cause their lysis – resulting in a hemolytic anemia. Even though the first case was characterized by a fatal outcome, Babesia infections range in clinical presentation from asymptomatic to severe forms of the disease. In any case, the severity of infection largely depends on the Babesia species and the underlying immune status of the affected host. Therefore many (otherwise healthy) people infected with Babesia parasites remain asymptomatic and do not exhibit any symptoms. On the other hand, some individuals develop non-specific flu-like symptoms (such as fever, sweats, chills, body aches, headache, nausea, loss of appetite or unexplained fatigue). A life-threatening disease may emerge in people who do not have a spleen, have a weak immune system, have other serious health conditions, or in the elderly. Most human cases of Babesiosis are due to Babesia microti species complex or to Babesia divergens, although other species (some of them newly described) are now emerging. The joint occurrence of Babesiosis and Lyme disease results in a more severe and protracted illness when compared with either of those infections alone. In the diagnosis of Babesiosis, standard diagnostic techniques (investigation of Giemsa-stained thin blood smears and serologic tests) have been supplemented with modern molecular techniques, such as polymerase chain reaction (PCR). Current treatment recommendations for Babesiosis are focused on clindamycin and quinine as the drugs of choice, but certain novel drugs have shown some promise. Epidemiology of the Disease The constantly changing ecology has contributed significantly to the expansion of human Babesiosis in the United States (US), and also around the world. It is often considered an increasing problem due to the spread of tick habitats and the intensified mobility of animals, promoting in turn the dissemination of parasites to new geographical regions. Since 1957, approximately forty cases of human infection with bovine Babesias (usually Babesia divergens) have been identified. A total of 84% of those European cases were patients that previously underwent splenectomy. Nevertheless, infection with Babesia divergens confirmed with PCR was also found in an immunocompetent adult patient from France, emphasizing the fact that this parasite may also cause illness in previously healthy people. The highest number of human Babesiosis cases is found in the US, with Babesia microti being the predominant species (endemic in the Northeast and upper Midwest). In Washington State and California there were cases caused by Babesia duncani, and infections with parasites considered to be Babesia divergens were reported from Kentucky, Missouri and Washington State. Human Babesiosis has also been found in Australia, Taiwan, Japan, Korea and India, and there were reports from Africa and South America. The disease also appears to be endemic on the China-Myanmar border. Serosurveys were also introduced as a useful technique to survey a population for babesial infection, which may result in finding this infection in other parts of the world as well. Reviewed by Liji Thomas, MD Sources https://www.cdc.gov/parasites/Babesiosis/ http://cmr.asm.org/content/13/3/451.long https://www.ncbi.nlm.nih.gov/pubmed/26568987 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3998201/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4458703/ parasitesandvectors.biomedcentral.com/.../s13071-014-0509-3 Chiodini PL. Babesiois. In: Farrar J, Hotez P, Junghanss T, Kang G, Lalloo D, White NJ, editors. Manson's Tropical Diseases, 23rd Edition. Elsevier Health Sciences, 2014; pp. 601-605. // Last Updated: Feb 26, 2017"
2,"2018-04-20 02:27:14","What Causes Babesiosis?","By Dr Tomislav Meštrović, MD, PhD Babesiosis is a parasitic enzootic disease that is triggered by the infection of vertebrate erythrocytes with the protozoan Babesia species. Babesiosis is considered one of the most significant tick-borne infectious diseases in both domestic and wild mammals, and when it infects humans, it still poses substantial diagnostic and therapeutic challenges. This condition shares a plethora of clinical features with malaria (one of the most important parasitic diseases) and can be fatal – especially in the immunocompromised and the elderly. The characteristic causative organism now identified as Babesia was discovered in 1888, by the researcher Babes, who was trying to find the pathogen that caused hemoglobinuria in cattle. Only five years after that, Kilbourne and Smith identified that ticks served as the arthropod vector for the species Babesia bigemina that was recognized to cause Texas cattle fever. This event is significant in that it established the first arthropod vector known to transmit an infectious microbe. In humans, babesiosis was initially found in a splenectomized patient from Europe. However, most cases have been reported from the United States (especially in the northeastern states, as well as the upper midwestern parts). Most affected individuals have an intact spleen and are not known to have any immune deficiencies. Today sporadic cases are reported in Asia, Australia, South America and Europe. Characteristics and Life Cycle of the Pathogen Species of the genus Babesia are from the phylum Sporozoa that contains several important human pathogens, such as Plasmodium, Cryptosporidium and Toxoplasma. They also belong in the order Piroplasmida in the family Babesiidae (the other family is Theileriidae that lacks transovarial transmission which is a characteristic of Babesia). The Babesia species infecting humans belong to four distinct clades: Babesia microti (a small Babesia) that itself exists as a species complex, other small Babesias (like Babesia duncani), small Babesia (including Babesia divergens) which are related to large Babesia, and finally, large Babesias infecting ungulates (including the KO1 strain). As phylogenetic analysis based on stringent molecular criteria develops further, new Babesia species will likely emerge with further revision of the taxonomy of this genus. Apicomplexans (which includes the genus Babesia, as already mentioned) generally show at least three distinct stages of reproduction. These are gamogony (characterized by the formation and coalescence of gametes in the tick gut), sporogony (asexual reproduction that takes place in the salivary glands of the tick), and merogony (which is a term for asexual reproduction in the host). Transmission Patterns A majority of human cases of babesiosis are the result of infection with Babesia microti species complex, but may also be caused by Babesia divergens (which infects cattle) or by Babesia odocoilei (which infect cervids). The primary tick vector of Babesia microti is Ixodes scapularis (commonly known as deer or blacklegged ticks), and its primary reservoir is the white-footed mouse (which may also harbor Borrela burgdorferi, a causative agent of Lyme disease). During the life cycle of Ixodes scapularis, the three known active stages (i.e. larva, nymph and adult) require a meal of vertebrate blood to develop further to the next stage. The life cycle in the tick starts in the latter part of summer, with new larvae. These feed on blood from an infected mouse, which contains Babesia. The larvae then molt to become nymphs, while the parasites remain dormant. Nymphs then transmit the parasite to the vertebrate hosts in the next season, which is usually in in late spring and early summer. Although all three developmental stages do feed on humans, the nymph is the most important vector, because of its minute size (akin to the size of a poppy seed) and summer activity. Therefore infected individuals may not recall a tick bite. Once the parasite is in the human host, Babesias enter erythrocytes (red blood cells) where they undergo asexual replication (also known as budding). The multiplication of blood-stage parasites results in the clinical manifestations that arise after infections. It must be emphasized that humans are usually dead-end hosts. Other potential ways of acquiring infection with Babesia parasites include receiving contaminated blood transfusion (as at the moment there are no tests licensed for donor screening), as well as transplacental/perinatal transmission from an infected mother to her baby. Babesia microti is responsible for most transfusion-mediated infections. About one in five of such cases end in fatality. Reviewed by Liji Thomas, MD Sources https://www.cdc.gov/parasites/babesiosis/ http://cmr.asm.org/content/13/3/451.long https://www.ncbi.nlm.nih.gov/pubmed/17691604 https://www.ncbi.nlm.nih.gov/pubmed/11113258 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3998201/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4458703/ Chiodini PL. Babesiois. In: Farrar J, Hotez P, Junghanss T, Kang G, Lalloo D, White NJ, editors. Manson's Tropical Diseases, 23rd Edition. Elsevier Health Sciences, 2014; pp. 601-605. // Last Updated: Feb 26, 2017"
3,"2018-04-20 02:27:16","Diagnosis of Babesiosis","By Dr Tomislav Meštrović, MD, PhD Babesiosis is an emerging, zoonotic, tick-borne disease caused by intraerythrocytic protozoan parasites of the genus Babesia, which are transmitted by hard-bodied (Ixodes) ticks. Several different species are known to cause disease in humans, most notably Babesia microti, Babesia divergens and Babesia duncani. Babesia infection may be completely asymptomatic or may present with illness. The severity of that illness may range from mild to fulminant and sometimes even results in death. Diagnosis should therefore involve a complete descriptive history that includes any clinical manifestations, travel history to endemic areas, tick bite exposure, splenectomy and recent blood transfusion. Since symptoms and signs of the disease can be relatively non-specific, laboratory testing is essential to establishing a correct diagnosis. The primary diagnostic method is microscopic detection of parasites on blood film examination, although the use of polymerase chain reaction (PCR) is increasing and serodiagnosis can be useful. Microscopy Detection Methods The examination of thin blood smears to detect parasites within erythrocytes is the most commonly used technique for diagnosing infections with Babesia microti in the United States (US) and Babesia divergens in Europe. After adequate staining of peripheral blood smears with Giemsa or Wright’s stain, the Babesia parasites can be seen within erythrocytes as darkly-stained ring shapes with pale blue cytoplasm. It is necessary to examine multiple smears, since, during the early stage of disease (when people tend to seek medical advice,) only a few red blood cells may be infected. Among individuals with healthy immune systems, the extent of parasitemia is rarely more than 5%, but can be up to 85% in asplenic people. Furthermore, the duration of parasitemia that is detectable on blood smears varies form person to person, ranging from three weeks to twelve weeks. There are certain points to consider regarding such blood smear analyses. The ring forms seen within red blood cells can vary significantly and may be mistaken for Plasmodium falciparum (a parasite that causes malaria), although absence of the hemozoin pigment should point to Babesia parasites. Indeed, cases have been described in scientific literature where patients have been misdiagnosed with malaria, which may result in misguided treatment choices and pose a serious risk to the patient. Generally, blood smear analysis is a rather subjective process, which inevitably depends on the observer’s experience and the time dedicated to smear examination. The need to differentiate babesial morphology and the likelihood of low-level parasitemia may lead to inaccurate diagnoses, which is why diagnostic approaches are constantly being refined. Serologic Methods The indirect immunofluorescence assay (IFA) is a commonly used, sensitive and specific serologic test used to diagnose human babesiosis. The cut-off titer for a positive test result varies between laboratories, although higher titers (1:128 to 1:256) are linked to improved diagnostic specificity. In the case of Babesia microti infection, antibodies are generally detectable when patients are initially diagnosed, whereas serological diagnosis in the case of Babesia divergens infection is not usually possible due to the infection being too serious or severe, since the antibodies are only identifiable 7 to 10 days following the onset of hemoglobinuria. A potential drawback to serologic testing is the possibility of cross-reactivity due to the presence of other protozoal parasites. This would generate false-positive results. The presence of connective tissue disorders such as rheumatoid arthritis, for example, may also result in a false-positive, whereas a false-negative result may be generated in the case of an immunosuppressed patient. Molecular Methods Adequate detection of mild babesiosis infection often entails more sensitive methods than those so far discussed. The development of more sensitive techniques based on PCR, has made it possible to diagnose and monitor even mild cases of infection. In the case of Babesia microti infection and Babesia divergens infection, PCR-based detection assays usually involve the amplification of DNA sequences that are highly conserved and comparison of the resulting fragments with known sequences stored in a database. This enables accurate identification of the infecting parasite. Sources https://www.ncbi.nlm.nih.gov/pubmed/11113258 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC88943/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3355466/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3998201/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4557163/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2734943/ Chiodini PL. Babesiois. In: Farrar J, Hotez P, Junghanss T, Kang G, Lalloo D, White NJ, editors. Manson's Tropical Diseases, 23rd Edition. Elsevier Health Sciences, 2014; pp. 601-605. Further ReadingWhat is Babesiosis?What Causes Babesiosis?Treatment and Prevention of BabesiosisPathogenesis and Clinical Presentation of Babesiosis // Last Updated: Feb 20, 2017"
4,"2018-04-20 02:27:19","Treatment and Prevention of Babesiosis","By Dr Tomislav Meštrović, MD, PhD Human babesiosis is an emerging tick-transmitted infection caused by protozoal hematotropic parasites that belong to the genus Babesia. Although this condition is rare, fatal outcomes have been described. For this reason, timely detection, adequate treatment, and prevention efforts are essential tools to control babesiosis. The selection of treatment strategies largely depends on the species responsible for the infection, severity of the disease, as well as the underlying immune status of the affected individual. Individuals without any symptoms usually do not necessitate any treatment. Although there is no vaccine available to prevent human babesiosis, several other preventive measures are successfully used. The Babesia microti life cycle involves - image and information courtesy of DPDx / CDC Therapeutic Modalities After the diagnosis of babesiosis is confirmed by the examination of thin blood smears under the microscope or by polymerase chain reaction (PCR), patients who exhibit symptomatic babesiosis are candidates for a course of antimicrobial treatment. Two commonly employed antimicrobial regimens show high effectiveness: the combination of atovaquone with azithromycin, and the combination of clindamycin with quinine. Atovaquone and azithromycin are used for the treatment of immunocompetent patients facing mild to moderate babesiosis, while clindamycin and quinine are reserved for more severe infections. Significantly fewer adverse effects are seen in those treated with the combination of atovaquone and azithromycin when compared to those treated with clindamycin and quinine. Adverse drug reactions can be seen in three-fourths of patients on clindamycin-quinine combination, with a third of them forced to decrease the dose or to end the treatment prematurely. Some adverse effects that are seen include decreased hearing, tinnitus, gastrointestinal symptoms, visual disturbances, headache, vertigo, and rash. On the other hand, only fifteen percent of patients treated with atovaquone and azithromycin experienced symptoms that were congruous with an adverse drug reaction. Individuals with babesiosis should be strictly monitored during therapy. In a majority of cases, improvement occurs within a day or two after the treatment is instituted. Still, it must be noted that certain patients may have persistent low-grade parasitemia for several months after infection, and if the symptoms do not improve, the possibility of co-infection with Lyme disease or human granulocytic anaplasmosis should be suspected. Whole blood or red cell exchange transfusion can produce a swift and a notable fall in parasitemia, thus its use as an adjunct treatment to chemotherapy should be considered in gravely ill patients with high parasitemia counts. Exchange transfusion can also rapidly correct anemia and remove toxic byproducts of babesia parasites. Prevention Efforts Preventive measures for tackling babesiosis vary, from avoiding exposure to ticks to the modification of habitat. Simple measures involve using tick-repellent chemicals on the skin before visiting a region known to be infested by ticks; minimization or complete avoidance of such areas; and meticulous skin examination after exposure. Diverse public health policies have come into use to reduce the density of tick population in infested areas. This includes the spraying of acaricidal formulations, which is the most commonly employed method. It has been shown that applying such pesticides on the fur of animal reservoir hosts helps to break the cycle of transmission of Babesia parasites successfully. In conclusion, the recognition of human infection with Babesia parasites will probably improve, as physicians (as well as the public) become more cognizant of this condition. The number of known cases is likely to go up as people recreate and live in rural tick-infested regions, and as the number of immunocompromised patients continues to increase. Reviewed by Liji Thomas, MD Sources https://www.ncbi.nlm.nih.gov/pubmed/12804380 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC88943/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3355466/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2734943/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4557163/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3998201/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4458703/ Chiodini PL. Babesiois. In: Farrar J, Hotez P, Junghanss T, Kang G, Lalloo D, White NJ, editors. Manson's Tropical Diseases, 23rd Edition. Elsevier Health Sciences, 2014; pp. 601-605. Further ReadingWhat is Babesiosis?What Causes Babesiosis?Diagnosis of BabesiosisPathogenesis and Clinical Presentation of Babesiosis Last Updated: Feb 27, 2017"
5,"2018-04-20 02:27:22","Pathogenesis and Clinical Presentation of Babesiosis","By Dr Tomislav Meštrović, MD, PhD Babesiosis is an illness similar to malaria, that is caused by the intraerythrocytic parasitic species from the genus Babesia, transmitted by ticks. In the last fifty years the epidemiology of babesiosis in humans has shifted from a handful of isolated cases to the established endemic disease in Europe and northeastern and midwestern United States. The first human case of babesiosis was described in 1957 near Zagreb, a capital of Croatia. The affected individual was a young farmer without a spleen who had been taking care of cattle on tick-infested pastures. He subsequently presented with anemia, hemoglobinuria and fever, and succumbed to renal insufficiency in the second week of the illness. Although the causative agent was initially reported as Babesia bovis, it was most likely Babesia divergens (also a pathogen of cattle). Pathogenesis of Babesiosis As the parasite infects red blood cells in the human body, erythrocyte lysis occurs, which is associated with most of the clinical manifestations and complications of babesiosis – including hemolytic anemia, jaundice as a result of unconjugated hyperbilirubinemia, hemoglobinemia, hemoglobinuria, as well as renal failure due to acute tubular necrosis. Proinflammatory cytokine release may be instigated when immune cells come into contact with the glycosylphosphatidylinositol anchors of babesial proteins, expressed either at the surface of the pathogen or the surface of infected erythrocytes. These cytokines thereupon prompt the production of downstream mediators (such as nitric oxide) which may destroy parasites, but can also be responsible for cellular damage when excessively produced. The development of immunity to Babesia parasites in humans depends upon cellular and humoral factors, although the bulk of the evidence shows that the latter is of limited significance. The role of antibodies is restricted to a period when the parasites have found their way into the bloodstream, but not have yet become intracellular. Therefore T cells are considered pivotal in the development of resistance to Babesia parasites, with CD4+ T helper cell subpopulation as the main player. Moreover, non-specific responses via macrophages and natural killer cells are also noteworthy in resistance to babesial infection. Clinical Features of the Disease In Europe, a majority of cases of human babesiosis are a result of infection by Babesia divergens, whereas in the US the main pathogenic species is Babesia microti. The severity of infection can be highly variable, and is primarily determined by the immune status of the infected host. Various clinical syndromes have been described – from completely asymptomatic infections, through mild or moderate viral-like illnesses, to severe presentations with a fulminant course that may result in death. Most human infections with Babesia microti are subclinical. When clinical illness arises, the incubation period is between one and three weeks, although it can be up to six months (but typically one to nine weeks) when acquired through blood transfusions. The disease usually appears gradually, with fatigue and anorexia as dominant signs, as well as fever and generalized myalgia. In cases of Babesia divergens infection the incubation period varies from one to four weeks. Initially the patient may feel slightly unwell, but at the time of the diagnosis the condition is more severe and characterized by fever, anemia, jaundice, prostration, nausea, vomiting and myalgia. Furthermore, hepatomegaly, pulmonary edema and oliguric renal failure may also occur. Although animal studies suggest that Babeisa duncani, a rare species responsible for only several human infections recorded thus far, is more pathogenic than Babesia microti, its sparse occurrence does not allow any firm conclusions at this moment. Of the nine reported human cases there was one fatal account, one renal insufficiency and pulmonary edema, and the remainder had a somewhat mild clinical course or were without any symptoms. Reviewed by Liji Thomas, MD Sources https://www.cdc.gov/parasites/babesiosis/ http://cmr.asm.org/content/13/3/451.long https://www.ncbi.nlm.nih.gov/pmc/articles/PMC88943/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2734943/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4458703/ Chiodini PL. Babesiois. In: Farrar J, Hotez P, Junghanss T, Kang G, Lalloo D, White NJ, editors. Manson's Tropical Diseases, 23rd Edition. Elsevier Health Sciences, 2014; pp. 601-605. Further ReadingMiddle East Respiratory Syndrome Coronavirus (MERS-CoV) OverviewMiddle East Respiratory Syndrome Coronavirus (MERS-CoV) SymptomsMiddle East Respiratory Syndrome Coronavirus (MERS-CoV) DiagnosisMiddle East Respiratory Syndrome Coronavirus (MERS-CoV) EpidemiologyMiddle East Respiratory Syndrome Coronavirus (MERS-CoV) Treatment and PreventionMore... // Last Updated: Feb 28, 2017"
6,"2018-04-20 02:27:25","Malrotation of the Gastrointestinal Tract","By Jonas Wilson, Ing. Med. Gastrointestinal (GI) malrotation, sometimes referred to as incomplete rotation or intestinal nonrotation, is any deviation from the physiological rotation and/or fixation of the GI tract during embryonic development. During the development of the GI tract, the 3 parts of the tract, namely the fore-, mid- and hindgut, normally bulge out of the abdominal cavity and undergo a counterclockwise rotation of 270 degrees. This rotation occurs around the superior mesenteric blood vessels. Following its physiological rotation, the gut then returns the cavity within the abdomen where it is fixated at the duodenojejunal junction and cecum. Clinical presentation Patients presenting with GI malrotation may have a distended abdomen with tenderness accompanied by guarding (tensing of the abdominal muscles) on physical examination. Abnormal rotation of the GI tract can lead to comprised vascular supply to the affected portions of the intestines and this in turn can cause intraluminal hemorrhage, which manifests as hematemesis (vomiting blood) and/or melena (blood in stools). In addition to hemorrhage, patients may develop shock with signs such as a decrease in urine output, low blood pressure, and poor perfusion. Other signs of compromised vascular supply include inflammation of the peritoneum and skin discoloration. Pathophysiology GI malrotation, has been recently suggested to result from genetic mutations. The gene implicated is the fork head transcription factor (FOXF1) gene. In addition to abnormal rotation, it has been cited that these patients may also have congenital short bowel. FOXF1 is believed to play a crucial role in mediating the physiological rotation of the intestines and the forming of the dorsal mesentery. Inactivating mutations of this gene may result in GI malrotation. In addition to a mutation in FOXF1, mutations in genes that control left-right (L-R) patterning in the embryo and other genes not yet identified may also be associated with GI malrotation. Related StoriesRoutine screenings and early detection can help protect from colorectal cancerMany Australians not using free bowel cancer testing kitsResearchers develop wearable system to monitor electrical activity in the stomach over 24 hoursThere are four suggested etiological groups for GI malrotation: (i) abnormal L-R patterning, (ii) dorsal mesentery, (FOXF1) anomalies, (iii) irregularities of the intestine itself, and (iv) abnormalities of other abdominal contents. Irregularities of the intestine itself include atresias (closed or missing orifices/passages) and congenital short bowel. The fourth category has been postulated on the basis of incorrectly placed intestines and/ or abdominal organs within the abdominal cavity during organogenesis, which subsequently leads to GI malrotation. Epidemiology In the United States, for example, asymptomatic GI malrotation occurs with an incidence somewhere between 1 in 200 to 1 in 500. Symptomatic GI malrotation, on the other hand, has a much lower incidence, being somewhere around 1 in 6000 live births. Nearly 80% of patients will present with malrotation within their first year of life. Moreover, the incidence in males is double that of females in those patients younger than 1 year. Up to 6 out of every 10 children with GI malrotation may have an accompanying congenital anomaly. By default, all children with hernia of the diaphragm, omphalocele (protrusion of abdominal organs into umbilical cord), and gastroschisis (intestines protruding through the abdominal wall) have malrotation. Management Diagnosis of GI malrotation may be confirmed with abdominal radiographs, ultrasound, CT, and fluoroscopy. Emergency surgical treatment is required in cases where volvulus (twisting) and/ or obstruction accompanies GI malrotation. Patients should not be fed orally to avoid exacerbating the situation. Instead, a feeding tube through the nose or mouth is used, while electrolyte and fluid balances are maintained. Shock, if present, is treated with vasopressive agents to correct low blood pressure, appropriate fluid resuscitation and blood products, if applicable. Surgery is done by means of the Ladd procedure. This procedure entails an appendectomy, dividing Ladd’s bands (tissue connecting the cecum to the abdominal wall), proper placement of the small of the large intestines within the abdominal cavity and, if necessary, the treatment of volvulus. Reviewed by Susha Cheriyedath, MSc Sources http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2908440/ http://radiopaedia.org/articles/intestinal-malrotation my.clevelandclinic.org/.../hic-Malrotation http://pubs.rsna.org/doi/full/10.1148/rg.265055167 Further ReadingSymptoms and Diagnosis of Intestinal MalrotationSymptoms and Diagnosis of Intestinal MalrotationTreatment and Prognosis for Intestinal Malrotation // Last Updated: Jan 17, 2017"
7,"2018-04-20 02:27:29",Fontanelle,"By Cashmere Lashkari What is a fontanelle? The soft parts of the newborn baby’s skull are known as fontanelles. While there are six fontanelles found in the skull of a newborn, only two are commonly known. The one in the middle of the head, on the top portion is known as the Anterior fontanelle. It is shaped like a diamond and takes about a year to close. The one in the rear portion of the head is called the posterior fontanelle. It is triangular in shape and closes within a couple of months after birth. How is a fontanelle formed? The newborn human baby has a skull that consists of six different bones. These are also called cranial bones and include a frontal bone, an occipital bone, two parietal bones and two temporal bones. The six cranial bones are held in place by strong and flexible tissues known as sutures. Over a period of time these tissues tend to solidify, knitting the different bones of the cranium together to form the skull. The six different fontanelles are formed along the lines of these six bones. Besides the anterior and posterior fontanelles, there are also two mastoid and two sphenoid fontanelles formed at birth. However these four fontanelles quickly seal up to form the skull leaving just the anterior and posterior fontanelles open for a few months longer. Why do the fontanelles exist? The primary reason for the existence of fontanelles is for child birth. The flexible and elastic sutures let the cranial bones overlap into a smaller and more compact form to allow it safe passage through the birth canal. The brain is protected from any pressure during the birth process and is not damaged due to the protection of the bones. As the infant begins to hold his head up, rolls onto his stomach and even tries to sit up, the neck muscles are not developed enough to support the weight of the head. This results in a fair number of minor impacts to the head. Fontanelles are essential for the proper development of the baby’s brain as they are held together by the flexible sutures which protect the brain from the head impacts. Also the skull bones or cranium grows along with the brain. This happens as the suture lines increase. By the age of two the baby’s skull would have achieved two third of its adult size. The bones continue to reposition themselves as growth adds new layers to the edge of the suture tissue. Finally by the second decade of the child’s life the brain reaches maximum size and the sutures get fused to the bone growth forming a whole skull structure. How fontanelles help doctors Doctors can actually trace the growth and development of the baby by feeling the cranial sutures. The fontanelle must feel firm and be flat when touched. Should there be a bulging of the fontanelle it may be indicative of an increase in pressure inside the brain. The swelling of the fontanelle could be due to an infection of the membrane covering the brain. This condition is also known as meningitis and can be harmful to the normal development of the child. The bulge may be caused by a fluid build up inside the skull. The condition is called hydrocephalus. It is also possible that the fontanelle is sunken or shrunk inside. This could be an indication that the baby is dehydrated and needs more fluids. It can also be an indication of malnutrition in a newborn. Thus, the fontanelle can tell the health care provider a lot about the internal health of the baby. Caring for the fontanelle The shape of the baby’s skull is constantly changing for the first couple of months. This is due to the shifting of the cranial bones as the flexible sutures hold them in position. The two primary soft spots on the skull are located on top of the skull and behind the head. Since the bone there is yet to knit into a solid skull, these are vulnerable regions where the baby may get hurt. The baby’s head should be handledcarefully at all times. When lifting the head of the baby the adult’s hand should support the neck and cover the posterior fontanelle. Also since the soft spots may not be enough to keep out the chill, it is advisable to cover the head of the baby with a soft cap when the temperature drops. That way both anterior and posterior fontanelles are afforded protection from the cold. The skin of the skull should be kept clean to prevent infection. The cranial bones of most babies are sealed by the time they reach about 18 months of age. After that, the sutures will remain somewhat flexible to accommodate the continued growth of the brain and expansion of the skull. Reviewed by Catherine Shaffer, M.Sc. References Medline Plus, Cranial Sutures, https://medlineplus.gov/ency/article/002320.htm Babycentre, Soft Spots, http://www.babycentre.co.uk/x552709/what-are-the-soft-spots-on-my-newborns-head American Family Physician, The Abnormal Fontanelle, http://www.aafp.org/afp/2003/0615/p2547.html Further ReadingMalrotation of the Gastrointestinal TractHeat Rash in BabiesWhy Do Babies Cry?How to Stop a Baby Crying?How to Understand your Baby’s Crying?More... Last Updated: Aug 3, 2017"
8,"2018-04-20 02:27:36","Heat Rash in Babies","By Cashmere Lashkari Rashes occur easily in the summer on the delicate skin of a baby. There are many kinds of rashes that the baby could suffer from. One of the most common skin conditions, not just for babies but also for adults, is developing a heat rash in summer. The baby may also develop a heat rash if he has fever and his temperature does not come down quickly. What causes heat rash? A heat rash normally occurs in hot and humid weather. The humidity along with the heat makes the body sweat profusely in order to regulate the body temperature. When the sweat increases so much that the evaporation from the skin is delayed, a heat rash will begin to develop. The skin is irritated when the sweat ducts get blocked and trap the sweat under the skin. Heat rash is also known as prickly heat and miliaria. They are very common and most people will suffer from a mild case of this skin condition in the summers. It is especially prevalent in babies because of the many skin folds making it difficult for the sweat to dry up and not clog the sweat ducts. Essentially a heat rash forms on the skin when the sweat is collected under the skin due to blocked sweat ducts. What does heat rash look like? The skin will be clustered with small pimple-like blisters which may be red compared to the surrounding skin. Heat rash is most often seen in the folds of the skin of the neck, the groin area and in elbow and knee creases. A heat rash may also come up on areas where clothing hugs the skin tightly, such as the back, stomach and bottom. The scalp and forehead may also be affected if the baby wears a hat. Symptoms of heat rash The prickly heat rash is easy to identify. There are raised pimple like bumps on the skin and the area is red. There may be mild swelling anditching. The skin maybe tender when touched. The red bumpy skin can also cause an intense prickling or stinging sensation. . The baby may be irritable if the skin rash is repeatedly rubbed by cloth touching. The rash can become worse if the baby is wearing synthetic clothing . Treating heat rash in babies Mild cases of heat rash may clear up without treatment. However if the rash is troubling the baby, it may be advisable to get a doctor’s opinion. A hydrocortisone cream of low strength canrelieve the itch. If the rash is severe, the doctor maydecide to add an antihistamine syrup. Skin soothing treatment options include: Calamine lotion Aloe-based lotion or gel Powder to dry the skin Use only products recommended by your doctor. Avoid using over- the- counter medicated ointments as they may be harmful. Remember that a baby’s skin is sensitive and may not handle over the counter products well. The primary requirement is to keep the baby cool so that excessive sweat is not generated. Spend time in a cool room indoors. If you need be outdoors ensure that the baby is in the shade. A small fan can be used to ensure circulation of cool air if you are planning on sitting outdoors for an extended period of time with the baby. Keep baby comfortable when she has a rash: Ensure that the baby has plenty of cool fluids and is dressed comfortably in loose cotton clothing Avoidsynthetic material. Ittraps more heat next to the skin Avoid synthetic clothing Give the baby regular baths to keep the body temperature down. Make sure that the water is not hot as that will make a heat rash worse Use a cold compress on the heat rash area. Wet a clean cotton cloth in ice water and wring it dry, then apply to skin for a few minutes at a time Reviewed by Catherine Shaffer, M.Sc. References CDC, Frequently Asked Questions (FAQ) About Extreme Heat, https://www.cdc.gov/disasters/extremeheat/faq.html Babycenter, Heat Rash, https://www.babycenter.com/0_heat-rash_10881.bc NHS, Prickly Heat, http://www.nhs.uk/conditions/prickly-heat/Pages/Introduction.aspx Further ReadingMalrotation of the Gastrointestinal TractFontanelleWhy Do Babies Cry?How to Stop a Baby Crying?How to Understand your Baby’s Crying?More... Last Updated: Aug 3, 2017"
9,"2018-04-20 02:27:39","Why Do Babies Cry?","By Jonas Wilson, Ing. Med. Babies cry and a lot. It’s just something they all do. Arguably, some are less fussy than others, but the fact remains that it’s impossible to find a baby who will not cry at some point. Crying is a sign that a baby is alive when he or she is born. This process allows for air to enter their lungs for the first time in their lives. From birth onwards, babies quickly learn to use their cry as a primary communication tool in the outside world. This may be particularly demanding for parents, especially those who may have had unrealistic expectations about their infant. Newborns, for quite some time, will not be able to have a real conversation and this makes it easy for people to overlook the reality that babies too have needs. They are just unable to communicate those needs in a way that their caretakers could understand. As we can well imagine, they need to eat, be comfortable and, above all, kept as healthy as possible and free of any morbidity. Babies, like all humans, require attention and affection and they also can experience emotions, like fear, pain, and anger. When their needs are not met, most of them will cry, because that’s their greatest weapon from a communication standpoint. The first cry in the moments after birth For anyone in a delivery room, the absence of crying when the baby arrives is particularly worrying especially as time elapses. It is a signal that something may be gravely wrong. Before a child is born, the blood is oxygenated via the placenta. During intrauterine life, our blood circulates differently. There are several bypasses or unique features, namely, the ductus venosus (i.e. shunt for oxygenated placental blood to bypass the liver), ductus arteriosus (i.e. shunt for oxygenated blood to bypass non-functioning amniotic fluid-filled lungs), and foramen ovale (i.e. passage for oxygenated blood to go from right atrium to the left atrium). In addition to the shunts, the pulmonary vessels are constricted in utero. At birth, all of the shunts are closed and the intense pulmonary vasoconstriction is reversed. This reversal and closing of shunts happens within minutes and are triggered by reflexes. The cold extra-utero environment and being born wet causes great discomfort to the newborn and he or she attempts to cry. To cry, the neonate must breathe and this results in the first inspiratory gasp. Air is sucked into the lungs with the help of the respiratory muscles. This begins the process of transforming fetal into newborn circulation. Common reasons for crying One of the main and most common reasons babies cry is to tell the caregiver that they are hungry. If truth be told, the younger an infant is, the more likely the cause of his or her cry is hunger. If food is not the problem, then a baby may protest if the diaper is soiled or wet or even if clothes are not comfortable enough. So it’s always wise for parents to take a peak and make sure the diapers are dry and clean. Babies, like all of us, can also feel hot or cold. They are even more vulnerable to changes in the environment, because their little bodies are still learning to adapt to the outside world. If a baby is well fed, clean, and comfortable, then may be he or she just wants some attention. After all, who doesn’t like to be cuddled? Physical contact gives children that sense of reassurance that they are well protected by their guardians. Parental concerns about ‘spoiling’ babies by holding them too much can cause parents to neglect giving their babies enough attention. Sometimes babies may cry for no reason at all and it is important for parents to remember that it is ok to let them cry it out. It is imperative that caregivers learn to recognize different tones in their babies’ cries. These vary depending on the reason. Children who are sick may cry differently compared to children who are hungry or just sleepy and need rest. This is a very useful skill that parents develop along the way. If attention is paid close enough, then a parent will be able to decode exactly what their child wants or needs. Reviewed by Susha Cheriyedath, MSc References https://www.nct.org.uk/parenting/coping-crying-baby https://www.helpguide.org/articles/secure-attachment/when-your-baby-wont-stop-crying.htm http://whale.to/a/morley4.html http://www.nhs.uk/conditions/pregnancy-and-baby/pages/soothing-crying-baby.aspx Further ReadingMalrotation of the Gastrointestinal TractFontanelleHeat Rash in BabiesHow to Stop a Baby Crying?How to Understand your Baby’s Crying?More... Last Updated: Aug 3, 2017"
10,"2018-04-20 02:27:42","How to Stop a Baby Crying?","By Jonas Wilson, Ing. Med. Babies cry, because that is their primary means of communicating to their caregivers. While some babies are fussier than others, all babies cry. For the reason that babies cannot talk, it is easy for people to overlook their needs and wants. Understanding why the child is crying in the first instance may be particularly demanding for parents, especially those who are first timers. At birth, crying is a sign that a baby is alive and is at least able to breathe. In the hours, weeks, months, and years thereafter, crying may be for a number of reasons. Reasons why infants cry The first thing a parent or caregiver should try to identify when confronted with a crying baby is the reason for the child’s crying. This becomes easier the more time that is spent with the child or with experience nurturing infants. The reasons why infants cry may be many, but there are some common ones. Heading the top of the list is hunger. The younger an infant is, the greater the chances are that the reason for his or her crying is food. In other circumstances, it may be separation anxiety, illness, sleepiness, overstimulation, colic, or illness. Soothing a crying infant Although all babies are individuals and unique in their own respects, some tips and tricks, with regards to soothing them when crying, do seem to be universal. The first and most important thing a parent or caregiver should remember is to never ever shake a baby. Shaking an infant can cause what is called Shaken Baby Syndrome (SBS). Its hallmarks are retinal and subdural hemorrhages. These babies may die as a consequence or suffer long-term neurological deficits, such as hearing loss, blindness, paralysis, seizures, and mental retardation. SBS is completely preventable by simply refraining from shaking an infant. If a parent can identify the reason why an infant is crying, then the problem is solved immediately. A hungry child will stop crying when given a breast or bottle to suckle on. An uncomfortable baby will be happy if the cause for his or her discomfort is taken care of, such as the removal of a wet or soiled diaper or the adjustment of the temperature in the baby’s room. A baby who is well-fed and comfortable without any signs of illness may just actually want some attention. Some tips to soothe a baby who appears to be crying for no reason include wrapping the child in a blanket or swaddling to create a sense of security. In addition to this, rhythmically swinging the baby, sucking on a pacifier, or positioning the child on the stomach or side may create a soothing effect. Singing to a child may also help to calm him or her. Warm baths may prove effective in some babies, but in others it may agitate them more. Colic Although poorly understood with a yet to be identified clear cause, colic is the term used for crying in babies that lasts longer than 3 hours in a day for more than 3 days in a week over the course of 3 or more weeks in a child who is otherwise healthy. Some studies indicate that the cause may be linked to intestinal problems, such as food allergies or reflux. These babies have a higher pitched crying and often look like they are in pain with rigid tummies and bodies as well as flexed limbs. Colic tends to go away on its own after some time and parents are often asked to wait it out, but gripe water may be used to help alleviate symptoms. Coping with a crying infant It is very normal that many parents, especially those who are new to parenthood, may become worried by not being able to understand all of their baby’s cries. Furthermore, it may even be frustrating at times. It is imperative to remember that crying is a part of the baby package. Parents should take time out to understanding their babies more and always seek support from family and close friends when they feel overwhelmed. If they sense something is wrong with the baby, then consultation with a pediatrician is recommended. Reviewed by Susha Cheriyedath, MSc References http://www.nhs.uk/conditions/pregnancy-and-baby/pages/soothing-crying-baby.aspx https://www.nct.org.uk/parenting/coping-crying-baby https://www.helpguide.org/articles/secure-attachment/when-your-baby-wont-stop-crying.htm https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3183958/ Further ReadingMalrotation of the Gastrointestinal TractFontanelleHeat Rash in BabiesWhy Do Babies Cry?How to Understand your Baby’s Crying?More... Last Updated: Aug 3, 2017"
11,"2018-04-20 02:29:25","How to Understand your Baby’s Crying?","By Jonas Wilson, Ing. Med. Babies, like all of us, have needs and wants. However, they are unable to communicate these in manner that older children and adults do. Thus, they use their most basic, yet effective, means of communicating their wishes – crying. Infants need to eat, sleep, be kept comfortable and healthy. In addition to these, they require attention as well as affection and have emotions like anyone else. In order to understand an infant’s crying, parents and caregivers must first know the reasons why these precious beings cry and the differences in crying for different purposes. Decoding the signals Babies are individuals. Something that upsets one child may not bother another, but all at some point will cry for one reason or the other. It’s crucial that parents take time to pay attention to their babies, because in doing so they’ll be quicker able to identify and understand why their infants cry. Changes in a baby’s mood, although difficult to detect at times, can be used to preemptively avoid crying spells. For instance, an infant may be like clockwork with his or her daily nap and feeding routine, allowing parents to ‘prepare’ in advance. Children who follow biological routines may become easily upset if there is a sudden change to their schedule or environment. While at first, to the untrained ear, all cries may sound the same, parents soon begin to notice subtle differences in their children’s cries. A hungry child may cry differently compared to a child who is sleepy or in pain. Differences in cry may be noted based on pitch, level, intensity, and duration of the cry. It is rather difficult to decode the cries of very young infants, because these cries may overlap. However, those infants who are older may show subtle, yet distinct differences. A hungry child may have a cry that is low-pitched and rather short, which oscillates up and down. Infants who want to be left alone, perhaps due to overstimulation, may also have a similar cry to the hunger cry. In contrast, babies who are in distress, pain, or are ill, may have a high-pitch and long cry that contains a pause and flattening wail at the end. Turbulent cries, on the other hand, may denote anger. Responding to a crying baby It goes without saying that the reason for causing the child’s crying must be dealt with in order for that child to stop crying. A hungry child should be fed, while one with a soiled or wet diaper should have it changed. Taking care of an infant’s needs will no doubt soothe him or her. By paying attention and trying to pinpoint differences in their babies’ cries, parents will be able to quicker address their infants’ needs. It’s normal that parents may feel helpless when they are unable to decipher what is wrong with their children. In cases where babies are fed, comfortable, and healthy, it’s ok to let them cry, as it is well known that this may help them to fall asleep. Reviewed by Susha Cheriyedath, MSc References https://www.helpguide.org/articles/secure-attachment/when-your-baby-wont-stop-crying.htm https://www.nct.org.uk/parenting/coping-crying-baby http://www.peps.org/ParentResources/by-topic/baby-care/infant-crying Further ReadingMalrotation of the Gastrointestinal TractFontanelleHeat Rash in BabiesWhy Do Babies Cry?How to Stop a Baby Crying?More... Last Updated: Aug 3, 2017"
12,"2018-04-20 02:29:31","Baby Holding Techniques: The Hold","By Jonas Wilson, Ing. Med. ‘The Hold’ is a baby calming technique that is the brainchild of Dr. Robert Hamilton, who is an American pediatrician. Dr. Hamilton’s technique can be found brilliantly explained on YouTube, and was seen and liked millions of times in a very short period. This was a clear indication that there are, without doubt, many parents and caregivers out there who are eager to find a means of calming their babies. With more than 3 decades of working with children under his belt, as well as having 6 children of his own, it is safe to assume that Dr. Hamilton anticipated parents would be eager to dip their hands on such information. The hold – procedure Dr. Hamilton’s holding technique consists of some 4 very simple steps. In the first step, the baby’s arms are folded across the baby’s chest. Next, the arms are gently secured. Following this, the baby’s diaper area is grasped before the fourth and final step, which is rocking the infant at an angle of 45 degrees. The parent or caregiver holds the infant with one hand around the infant’s chest, while the other hand is positioned under the bottom while gently rocking the infant back and forth. ‘The Hold’ appears to have an immediate effect, as Dr. Hamilton points out in his YouTube video. Does it work? In a media interview, Dr. Hamilton said that his technique is optimal on children between the first 2 and 3 months of life. The objective of the technique is to attempt recreating an intrauterine feeling. This gives the baby a sense of security and calms him or her. While there is no further evidence to prove or disprove that Dr. Hamilton’s technique is foolproof, one thing that’s for certain is his technique is quite popular. Dr. Hamilton himself has expressed awe about the popularity ‘The Hold’ has received and stated that he never would have expected this to happen in his wildest dreams, but he is humbled by it. Other baby calming techniques Soothing babies can be tricky, especially if they are well-fed, comfortable, and not ill. It’s important to take care of the baby’s most pressing need, as doing this will immediately solve the crying problem. Some means of calming a baby include singing or talking to the baby in a tranquil voice, while gently stroking or rubbing his or her back. Rattle toys and pacifiers are clever ways of distracting a baby. Sometimes all a baby needs is a little walk or a ride in the stroller, or perhaps some music. All babies are unique; thus, what may work for one may not work for another. The trick is for parents or caregivers to pay close attention to the little details that work best for them. One important thing to remember is that sometimes it’s totally ok to let the baby cry, if it is certain that all the baby’s needs have been adequately met. Babies cry. It’s just what they do and is their primary means of communication. Parents just need to have patience and strong support from a family member or close friend for those times when they feel overwhelmed. Reviewed by Susha Cheriyedath, MSc References http://www.today.com/parents/pediatrician-shows-how-calm-your-baby-seconds-hold-t59466 https://www.youtube.com/watch?v=j2C8MkY7Co8 https://www.childrenscolorado.org/conditions-and-advice/calm-a-crying-baby/calming-techniques/ Further ReadingMalrotation of the Gastrointestinal TractFontanelleHeat Rash in BabiesWhy Do Babies Cry?How to Stop a Baby Crying?More... // Last Updated: Jan 25, 2017"
14,"2018-04-20 02:29:34","What Causes Back Pain?","By Dr Ananya Mandal, MD The back is a complex structure made up of: Bones of the vertebrae Muscles Nerves Joints Because of this complex structure it is difficult to pinpoint the exact cause of the pain. In most cases the pain is not caused by serious damage or disease but by sprains, minor strains, minor injuries or an irritated nerve ending. These may be triggered by an awkward position, everyday activities at home and at work, lifting or standing awkwardly or as a result of longstanding bad posture. Common causes of back pain Common causes include: Lifting, carrying, pushing or pulling incorrectly Twisting the back Sprains and injuries Bending awkwardly Sleeping or getting up from the bed awkwardly Overreaching or stretching Slouching while sitting Driving in a hunched position Bending or standing for long periods of time Driving for long hours without breaks Sitting at the desk for long hours without change in posture Repetitive strain injury Unaccustomed exercise Bad or uneven heeled shoes Ankylosing spondylosis Whiplash injury Frozen shoulder Slipped or bulging disc (this disc lies like a cushion between two vertebrae) Sciatica Arthritis Osteoporosis and vertebral fractures Skeletal irregularities (e.g., scoliosis, kyphosis, lordosis, back extension, back flexion) and conditions such as fibromyalgia, kidney stones or infections, endometriosis etc. More serious causes include cauda equine syndrome, bone cancers, spine infections Risk factors for back pain Some persons are typically more prone to getting back pain. Most persons however get back pain at some point in their lifetime. The following are risk factors for back pain: Age – Back pain typically occurs between the ages of 30 and 40. It becomes more common with age Level of fitness - Back pain is more common among people who are not physically fit. these individuals have weak back muscles. Pregnancy – Pregnancy may put a great strain on the back especially at later stages and there may be a dull back pain. Occupation – Persons who need to lift, push or pull and twist their backs at work, they may be at risk of back pain. Those working for long hours at their desks are also at risk of back pain. Stress – this leads to strain of the back muscles and stiffness that may give rise to back pain. Being overweight or obese – These individuals have too much stress on their spine that may lead to pain. Inherited - Some causes of back pain, such as disc disease may be inherited. Ethnicity and race - African American women are found to be two to three times more likely than white women to develop spondylolisthesis. Caucasian women of northern European heritage, on the other hand, are at the highest risk of developing osteoporosis. Smoking - Smoking reduces blood flow to the lower spine and causes the spinal discs to degenerate. Long term use of medications like corticosteroids. These weaken the bones and make them prone to fractures and injury. Depressive illness – those with depression are also prone to getting back pain. Other diseases – Those with arthritis and cancers with spread to bones may also experience back pain. The muscles in your shoulder are connected to your arm by tendons. Between the tendons and bones are small sacs of fluid called bursa. They lubricate the shoulder so it moves easily. Continual stress on your shoulder can cause the bursa to get squeezed, swollen, stiff, and inflamed (bursitis). Bursitis can make it painful, or even impossible, to raise your arm. Image Credit: CDC If you bend forward over and over for months or years, the discs are weakened, which may lead to disc rupture (or ""herniation""). Image Credit: CDC Reviewed by April Cashin-Garbutt, BA Hons (Cantab) Sources http://www.nhs.uk/Conditions/Back-pain/Pages/Introduction.aspx www.patient.co.uk/.../Assessment-and-Management-of-Low-Back-Pain.htm www.bbc.co.uk/.../index.shtml http://fcs.tamu.edu/health/healthhints/2009/jul/back-pain.pdf http://www.who.int/bulletin/volumes/81/9/Ehrlich.pdf http://www.sportspinerehab.com/Back%20Pain.pdf http://www.niams.nih.gov/health_info/back_pain/back_pain_ff.pdf Further Reading What is Back Pain? Back Pain in Pregnancy Back Pain Research Back Pain Treatment Last Updated: Dec 3, 2012"
15,"2018-04-20 02:29:38","What is Back Pain?","By Dr Ananya Mandal, MD Back pain is a common symptom and affects most people at some point in their life. An estimated 75 to 85 percent of all Americans will experience some form of back pain during their lifetime. Most countries take a major blow to their productivity due to back pain through loss of workers on sick leave. Some national governments, notably Australia and the United Kingdom, have launched campaigns of public health awareness to help combat the problem. One of these is the Health and Safety Executive's Better Backs campaign. What does back pain feel like? In most cases rather than an acute stabbing pain, it is a dull stiffness or tension in the back. The pain can be triggered by an awkward posture, bending or sitting awkwardly, or lifting incorrectly. Usually back pain is not a serious disease and usually gets better by 12 weeks. Exercises and pain relievers and advice of good posture maintenance is the treatment of choice. Types of back pain Back pain may occur at any part of the back but commonly affects the lower back. The pain may also be felt along the spine, neck or hips. Common types of back pain include: Neck pain Ankylosing spondylosis Whiplash injury Sprains and injuries Frozen shoulder Slipped or bulging disc (this lies like a cushion between two vertebrae) Sciatica Arthritis Osteoporosis and vertebral fractures Skeletal irregularities (e.g., scoliosis, kyphosis, lordosis, back extension, back flexion) Other conditions include fibromyalgia, stress, pregnancy, kidney stones or infections, endometriosis etc. More serious causes include cauda equine syndrome, bone cancers, spine infections Causes of back pain Risk factors for back pain: Age – Back pain typically occurs between the ages of 30 and 40. It becomes more common with age. Being overweight or obese – These individuals have too much stress on their spine that may lead to pain. Level of fitness - Back pain is more common among people who are not physically fit, these individuals have weak back muscles. Occupation – Persons who need to lift, push or pull and twist their backs at work, they may be at risk of back pain. Those working for long hours at their desks are also at risk of back pain. Inherited - Some causes of back pain, such as disc disease may be inherited. Ethnicity - African American women are found to be two to three times more likely than white women to develop spondylolisthesis. Caucasian women of northern European heritage, on the other hand, are at the highest risk of developing osteoporosis. Smoking - Smoking reduces blood flow to the lower spine and causes the spinal discs to degenerate. Other diseases – Those with arthritis and cancers with spread to bones may also experience back pain. Warning signs of back pain Related StoriesStudy suggests there are health benefits for the ‘tummy tuck’Back pain being mismanaged globallyNew essential oil inhaler facilitates pain management In most cases a few days of rest and adequate mobility may help in recovery from back pain. However, some symptoms may indicate a deeper problem and mandates a visit to the doctor. These symptoms include: Weight loss that is unexplained Swelling and immobility of the back Fever Pain in the limbs Numbness of the lower limbs or other parts of the body including genitals Loss of bladder or bowel control Worsening pain at night Treatment of back pain The primary modality of treatment is by remaining mobile and active. Earlier bed rest was advised for back pain. These days it is known that being inactive for long periods is actually bad for the back. Patient is advised moderate activities such as walking and doing their own daily tasks. Pain relievers like Acetaminophen (Paracetamol) is commonly advised. Hot or cold compression packs may also help reduce the pain. There are other manual therapies including physiotherapy and osteopathy. These may also help relieve pain. For back pain lasting for more than six weeks exercise classes or manual therapy along with pain relievers are advised. Acupuncture may provide relief in some individuals. Spinal surgery is usually only considered when all else has failed. Prevention of back pain Maintenance of good posture while sitting, standing, lifting, lying down. Getting up from sitting or lying position is another important factor that needs to be improved to prevent strain to the back. Individuals are advised not to place too much pressure on the back and ensure their back is strong and supple. Regular exercise, such as walking and swimming, is an excellent way of preventing back pain. Yoga and pilates also improve the flexibility and strength of the back muscles. Reviewed by April Cashin-Garbutt, BA Hons (Cantab) Sources http://www.nhs.uk/Conditions/Back-pain/Pages/Introduction.aspx www.patient.co.uk/.../Assessment-and-Management-of-Low-Back-Pain.htm www.bbc.co.uk/.../index.shtml http://fcs.tamu.edu/health/healthhints/2009/jul/back-pain.pdf http://www.who.int/bulletin/volumes/81/9/Ehrlich.pdf http://www.sportspinerehab.com/Back%20Pain.pdf http://www.niams.nih.gov/health_info/back_pain/back_pain_ff.pdf Further Reading What Causes Back Pain? Back Pain in Pregnancy Back Pain Research Back Pain Treatment Last Updated: Jan 1, 2014"
16,"2018-04-20 02:29:43","Back Pain in Pregnancy","By Dr Ananya Mandal, MD Back pain may affect pregnant women especially during later stages of their pregnancy. The prevalence of back pain during pregnancy is 48 - 56%. In fact it is so common that in most cases this symptom is looked upon as a normal part of pregnancy. Around a third of all pregnant women may get severe back pain that compromises their ability to work in gainful employment during pregnancy and also interferes with their activities of daily living. Furthermore, back pain occurs at night in over one-third of pregnant women, contributing significantly to insomnia. Pregnancy related back pain and risk factors Pregnancy-related back pain is commonly seen in women who have a history of previous episodes of back pain. The pain is usually most intense from the 12th week of pregnancy till 28th week and usually declines in intensity after that. Women with twin pregnancies or in later pregnancies (after the first pregnancy) may be more at risk of back pain. Pregnancy related back pain may also be related to long hours of work and bad posture. Even bad shoes and heels and long hours of standing can contribute to back pain in a pregnant women. Furthermore Hispanic women have a proportionally lower instance of back pain in pregnancy than Caucasian women. Younger age is also a risk factor, possibly due to higher sensitivity to hormonal changes induced by relaxin and estrogens, or to more pronounced collagen laxity Higher weight (obesity and overweight mothers) and those with a short stature are at higher risk of back pain Women who have had pain during pregnancy are also more likely to suffer from back pain after childbirth. Mechanism of back pain during pregnancy Related StoriesBack pain being mismanaged globallyStudy identifies two genes associated with extreme nausea and vomiting during pregnancyPainkiller use during pregnancy could affect unborn child's fertility in later life A normal pregnancy brings about several physiological changes in the body. These include mechanical and structural changes to the spine and hips to facilitate pregnancy and childbirth. Changes also include posture, gait (the nature of walk) and total body water content. There are hormonal changes and engorgement of blood vessels around the spine (epidural blood vessels). The main change in posture is increased forward convexity of the spine (called lumbar lordosis). Most of the weight is thus concentrated low in the pelvis with a protruding abdomen. This leads to low back pain. This also causes a tendency to fall forwards. Increased total body water means there is collection of fluids in the connective tissues around the vertebral column and pelvis. This increases the laxity around these joints. This fluid retention is also aggravated by hormonal changes of pregnancy. There is a hormone relaxin released during pregnancy. It softens the ligaments around the pelvic joints and cervix, possibly by enhancing fluid retention in these tissues and this helps in easy childbirth. Treatment and prevention of back pain during pregnancy Patient education – This is vital. Maintenance of good posture, good methods of rising from sitting or lying position, prevention of awkward lifting etc. should be emphasized. Patient is advised to stop smoking as this aggravates back pain. Physiotherapy – Physiotherapy in the third trimester may help ease back pain. Other physical treatments include mechanical support for the back for example a wedge shaped pillow for support (Ozzlo pillow), a belt or pelvic girdle etc. Labor pain can be managed appropriately to prevent back pain after childbirth. Reviewed by April Cashin-Garbutt, BA Hons (Cantab) Sources www.uws.edu.au/.../...ated_Pelvic_Girdle_Pain_how_can_we_help_0809.pdf http://members.multimania.co.uk/shiryu01/Pdf/MacEvilly%201996.pdf http://www.bioline.org.br/pdf?md06026 http://www.biomedcentral.com/content/pdf/1471-2393-12-30.pdf http://www.nct.org.uk/pregnancy/back-pain-pregnancy Further Reading What is Back Pain? What Causes Back Pain? Back Pain Research Back Pain Treatment Last Updated: Dec 3, 2012"
17,"2018-04-20 02:29:48","Back Pain Research","By Dr Ananya Mandal, MD Back pain affects a significant population worldwide and has a severe impact on a nation’s productivity. Workers worldwide lose a large number of work-days to back pain. Despite this wide prevalence, there are very few sure-fire cures for back pain. Research is constantly taking place worldwide to understand the aetiologies and find therapies to ease back pain. The National Institute of Neurological Disorders and Stroke (NINDS) and the National Institutes of Health (NIH) The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes of the National Institutes of Health (NIH) have several pain research studies in their laboratories. The researchers are looking at use of different drugs to effectively treat back pain, in particular, chronic pain that has lasted at least 6 months. There are yet other studies that compare the different approaches to acute back pain and attempt to find the best approach. These studies in addition compare standard care with pain relievers and hot or cold compresses and physiotherapy with complementary therapies like chiropractic, acupuncture, or massage therapy. There are studies that compare various surgical approaches to back pain as well. Related StoriesJury’s in: Opioids are not better than other medicines for chronic painYoung athletes commonly have bone marrow edema in lower spine, study showsChronic opioid users at increased risk of complications after spinal fusion surgery The studies on back pain look at various factors like symptom relief, restoration of function, and patient satisfaction. Arthritis Research UK Primary Care Centre at Keele University Arthritis Research UK Primary Care Centre at Keele University is also conducting research on back pain. They have found that a new model of primary care management called stratified primary care management can have significant benefits for patients seeking help from their GP for back pain. For their approach they group patients into different levels of treatment depending on their level of risk (low, medium or high) for persistent or chronic back pain problems. This stratification helps in more effective treatment of patients. This also reduced healthcare costs because fewer patients ended up coming back through the healthcare system at a later date after being managed effectively at first contact. Vertebroplasty Vertebroplasty is a new approach that has been studied extensively. It involves injection of surgical cement into vertebral bodies that have collapsed due to compression fractures to immobilize the spine. Severe biological response modifier drugs Like for treatment of arthritis, severe biological response modifier drugs are being tried in chronic back pain. These may provide rapid pain relief and prevent disease progression in back pain. Reviewed by April Cashin-Garbutt, BA Hons (Cantab) Sources http://www.ninds.nih.gov/disorders/backpain/backpain.htm www.arthritisresearchuk.org/.../research-and-new-developments.aspx www.spineuniverse.com/.../back-pain-research-treatment-updates www.pottsmerc.com/.../why-does-low-back-pain-recur-new-research-findings-and-treatment-considerations Further Reading What is Back Pain? What Causes Back Pain? Back Pain in Pregnancy Back Pain Treatment Last Updated: Dec 3, 2012"
18,"2018-04-20 02:29:53","Back Pain Treatment","By Dr Ananya Mandal, MD Back pain treatment varies with the severity, cause and associated factors. Some of the treatments and therapies that may be tried for back pain may be outlined as follows. Management of acute or short term back pain This is commonly seen in most individuals with back pain. The pain lasts no longer than six weeks and can be treated with pain relievers that are available over-the-counter or without prescription at a pharmacy and home treatments. Of the pain relievers Paracetamol (Acetaminophen) is commonly used successfully. Some people find anti-inflammatory drugs such as ibuprofen more effective. Stronger pain killers like codeine may be taken for more severe pain along with paracetamol. Those with muscle spasms may be prescribed a muscle relaxant like diazepam along with a pain reliever. Pain relievers may also be applied as creams, ointments or sprays over the affected area. Hot and cold compresses Heat with the use of a hot bath, hot water bottle or heated pad may provide relief from back pain in some individuals. In yet others application of ice packs or a bag of frozen vegetables over the pain may ease the pain. Ice packs, however, should not be applied directly over the back as this may cause cold burns. Some persons also benefit by alternating hot and cold using ice packs and hot compression packs. Lifestyle changes Sleeping posture – Sleeping posture and mattress may be contributing to the back pain. By changing the sleeping position and/or mattress the pain may be eased or prevented. Patient is advised to sleep on their side and draw their legs up slightly towards their chest and pillow is put between their legs. For those who sleep on their backs, a pillow may be placed under the knees to maintain the normal curve of the lower back. Relaxing muscle tensions – this can be achieved by deep breathing and conscious relaxation of back muscles before retiring to bed each day. Maintaining regular physical activity – Long periods of inactivity is bad for the back. People who remain active are likely to recover more quickly. Earlier those with back pain were advised bed rest. These days they are advised to walk or perform their daily activities to prevent immobility of the back. Weight loss – Being overweight and obese is a risk factor for back pain. Having a healthy and balanced diet along with regular exercise helps in keeping excess weight in check. Reduction of stress Regular exercise and being active and physically fit – This may be achieved by walking, swimming, yoga and pilates. These help in maintaining the flexibility and strength of the back muscles and prevent recurrence of back pain Management of long term or chronic back pain Related StoriesBack pain being mismanaged globallyBack pain affects nearly half of well-functioning, highly active older adultsModifying Oncolytic Adenoviruses to Target Pancreatic Cancer Back pain lasting over six weeks is called chronic back pain A more intensive exercise programme is prescribed. This is usually up to eight sessions over a period of up to 12 weeks. It will usually be a group class supervised by a qualified instructor. These exercises help to strengthen the muscles and improve posture. There are aerobic and stretching exercises as well. Manual therapy is prescribed and this includes manipulation, mobilisation and massage. This is performed by chiropractors, osteopaths or physiotherapists. These are usually for up to nine sessions over a period of up to 12 weeks. Acupuncture may be tried as a treatment modality as well. These may include up to 10 sessions over a period of up to 12 weeks. Some patients may suffer from concurrent depression due to their back pain. These patients require antidepressant medications, counselling and cognitive behavioral therapy as well. Surgery is usually only recommended as a treatment option when all else has failed. A common procedure is spinal fusion surgery. This involves fusion or joining up of the joint that is causing pain to prevent it moving. Other therapies include low level laser therapy. In this low energy lasers are focused on the back to reduce the inflammation. Ultrasound waves may also be used to accelerate healing and encourage tissue repair Interferential therapy (IFT) is performed by a device that passes an electrical current through the back to improve healing. Transcutaneous electrical nerve stimulation (TENS) – This is delivered by a machine that provides small electrical pulses to the back through electrodes that are placed on the skin. This helps to reduce the pain signals from the back. Mechanical measures – This includes lumbar supports like cushions, pillows and braces, traction devices for the spine. Drugs – Pain killers and steroids may be directly injected into the affected joints to reduce inflammation and pain. Warning signs of back pain and when to see the physician In most cases a few days of rest and adequate mobility may help in recovery from back pain. However, some symptoms may indicate a deeper problem and mandates a visit to the doctor. These symptoms include: Weight loss that is unexplained Fever Swelling and immobility of the back Pain in the limbs Worsening pain at night Numbness of the lower limbs or other parts of the body including genitals Loss of bladder or bowel control Unsteadiness when standing Reviewed by April Cashin-Garbutt, BA Hons (Cantab) Sources http://www.nhs.uk/Conditions/Back-pain/Pages/Treatment.aspx http://www.knowyourback.org/documents/back_pain_basics_web.pdf www.patient.co.uk/.../Assessment-and-Management-of-Low-Back-Pain.htm www.bupa.co.uk/individuals/health-information/directory/b/backpain www.bbc.co.uk/.../prevention_back_pain.shtml Further Reading What is Back Pain? What Causes Back Pain? Back Pain in Pregnancy Back Pain Research Last Updated: Dec 3, 2012"
19,"2018-04-20 02:29:55","Lower Back Pain Management","By Yolanda Smith, BPharm The management of lower back pain typically depends on the nature and cause of the pain. In most cases, management involves a combination of physical therapy and drug treatments. Surgical procedures are reserved for refractory cases, or when there is significant and worsening nerve damage. Physical therapy Hot or cold packs are often recommended for the relief of pain and to reduce inflammation, particularly for individuals who have suffered an injury to the lower back. There is currently no research-backed evidence to prove that this is effective. However, many individuals find it helpful, and it does not appear to have adverse effects. People with lower back pain should be encouraged to continue with their normal daily activities, as long as it is not heavy manual labor, and resist the urge to stay in bed for more than the acute phase. Inactivity can worsen the pain and increase the risk of depression and blood clots. Instead, physical therapy with light stretching exercises can help to enable the area to heal more efficiently. Strengthening exercises are also recommended for people with chronic (but not acute) low back pain, and is particularly important for pain caused by irregularities of the spine. Medications There are many different medications that may be used in the management and relief of lower back pain. These include: Simple analgesics: acetaminophen and aspirin Opioids: codeine, oxycodone, hydrocodone, morphine Non-steroidal anti-inflammatory drugs (NSAIDS): ibuprofen, ketoprofen, naproxen Anticonvulsants Tricyclic antidepressants: amitriptyline Selective serotonin-receptor inhibitors (SSRIs) or serotonin–norepinephrine reuptake inhibitors (SNRIs) Each of these medications has its own specific risks and benefits, and the best treatment will depend on the individual factors of the patient. Points to consider may include: The cause of pain Duration of treatment Safety in pregnancy Side effects Availability Cost Other non-pharmacological treatments There are also various other non-pharmacological treatments that may be used in the management of lower back pain. These include: Spinal manipulation or mobilization: Chiropractors are practitioners who practice spinal mobilization, adjustment, massage, or stimulation, to improve the alignment and strength of the spine and connective tissues in the lower back. Traction: Weights or pulleys are used to gradually reposition the spine and improve alignment so as to relieve pressure on the spinal cord and nerves. Acupuncture: This technique involves the insertion of needles into so-called pressure points of the body. It is not known precisely how this works but it appears to be effective in some patients at least. Acupuncturists explain the effect as being linked to clearing blockages in Qi or stimulating neurotransmitters. Related StoriesCorin introduces new Unity Knee with EquiBalance at AAOS 2018 Annual MeetingEnvironmental pollutants found to worsen rheumatoid arthritisHottest pepper gives man “thunderclap” Biofeedback: This involves the attachment of electrodes to the skin and the use of electromyography to increase awareness of breathing, heart rate, temperature and muscle tension. Nerve block therapies: This treatment involves the inhibition of nerve conduction in specific areas with the use of local anesthetics, botulinum toxin or steroid injections. Transcutaneous electrical nerve stimulation (TENS): Placement of an electrode on the skin of the affected area to create electrical impulses and block pain signals from nerves. Surgery Surgical techniques are usually reserved as a last-line option when other techniques have failed to provide adequate relief of lower back pain. This is because it is associated with a risk of nerve compression and worsening pain. Surgery is most often needed in cases with musculoskeletal injuries or compression of the nerves that causes neuropathic pain. Procedures that may be used include: Vertebroplasty Kyphoplasty Spinal laminectomy Discectomy Microdiscectomy Foraminotomy Intradiscal electrothermal therapy (IDET) Nucleoplasty (plasma disc decompression, PDD) Radiofrequency denervation Spinal fusion Artificial disc replacement The treatment decision about whether to use surgery for low back pain, and, if so, which procedure to use, will vary from case to case of lower back pain. Each procedure has unique risks and benefits that promote its use over others in certain situations. Reviewed by Liji Thomas, MD References http://www.ninds.nih.gov/disorders/backpain/detail_backpain.htm#3102_3 http://patient.info/health/nonspecific-lower-back-pain-in-adults http://emedicine.medscape.com/article/310353-treatment#showall http://orthoinfo.aaos.org/topic.cfm?topic=a00311 Further ReadingWhat Causes Back Pain?What is Back Pain?Back Pain in PregnancyBack Pain ResearchBack Pain TreatmentMore... // Last Updated: Aug 3, 2017"
20,"2018-04-20 02:29:57","What is Degenerative Disc Disease?","By Joseph Constance BA, MA Degenerative disc disease and the soreness in the back that it causes are a significant socioeconomic burden on the health care system. Studies have shown that back pain racks up costs greater than $100 billion annually in the U.S., including lost wages and reduced productivity. More than 75 percent of those costs are generated by fewer than five percent of patients. As they age, almost everyone will experience some wear on their spinal discs. But not everyone will have the symptoms of what is known as degenerative disc disease. The pain caused by degenerative disc disease arises when a disc loses its integrity. Most people older than 60 years of age have some disc degeneration, but they do not all experience discomfort. When a disc fails, the vertebral facet joints grind against each other, and cause pain. If there is no other cause found for the pain, the patient is diagnosed with degenerative disc disease. Spinal discs The vertebral discs in the spine act as shock absorbers for the bones. The discs enable the spine to remain elastic, flexible, and strong. A disc is composed of: The anulus fibrosus, which is a strong outer wrapping, on the outside of which are nerves. If this area is damaged, the pain can become extensive. The nucleus pulposus, the soft inner core of the spinal disc. It holds proteins that can cause swelling, tenderness, and an extensive amount of pain, if they leak into the outer layers of the disc. Causes of degenerative disc disease Loss of fluid due to aging can cause the intervertebral discs to compress. . When this occurs, the discs do not handle shocks to the system well. Daily activities cantear the disc components, resulting in swollen and sore tissues. A disc receives little blood flow. Unable to repair itself, it begins to deteriorate. Symptoms of degenerative disc disease Related StoriesStudy identifies exercises to help prevent chronic back pain in runnersBack pain affects nearly half of well-functioning, highly active older adultsThe Importance of Fetal Fibronectin Testing for Women with Symptomatic Preterm LaborThere are a variety of symptoms of degenerative disc disease: Pain exacerbated by movement or standing Muscle spasms Sciatic nerve pain Leg muscle weakness Numbness of the leg or foot Reduced reflexes in the ankle or knee Problems with bowel or bladder function Diagnosing and treating degenerative disc disease Diagnostic imaging, such as an MRI scan, can reveal damage to discs, but alone it cannot confirm degenerative disc disease. To make a diagnosis, a physician will review a patient’s history and carry out a physicalexam. The patient’s symptoms will be reviewed, a diagnosis made, and treatment plan determined. Controlling back pain, and degenerative disc disease, requires exercise that will improve the flexibility and strength of the muscles of the spine.. Exercise boosts the amount of blood circulation, . bringingnutrients to the area while reducing inflammation. In addition to physical activity, additional treatment may be necessary. Physical therapy Massage Pain relievers Non-steroidal anti-inflammatory drugs Disc replacement or spinal fusion surgery Applying heat or cold to the affected area. . Mobilization of the spinal joint Degenerative disc disease can also be managed by nutrition, weight loss, and healthy lifestyle. Reviewed by Catherine Shaffer, M.Sc. Sources: http://www.ncbi.nlm.nih.gov/pubmed/16595438 www.cedars-sinai.edu/.../Degenerative-Disc-Disease.aspx www.arthritis.org/about-arthritis/types/degenerative-disc-disease/ www.beaumont.edu/.../ www.cedars-sinai.edu/.../index.aspx Further ReadingWhat Causes Back Pain?What is Back Pain?Back Pain in PregnancyBack Pain ResearchBack Pain TreatmentMore... // Last Updated: Jan 11, 2017"
21,"2018-04-20 02:30:00","Bacterial Vaginosis","Bacterial vaginosis, also called BV is the most common vaginal infection in women of childbearing age. It happens when the normal balance of bacteria in the vagina is disrupted and replaced by an overgrowth of certain bacteria. The vagina normally contains mostly ""good"" bacteria, and fewer ""harmful"" bacteria. BV develops when there is an increase in ""harmful"" bacteria and fewer ""good"" bacteria. What causes Bacterial vaginosis? The cause of BV is not understood. It can develop when something, like sexual contact, disrupts the balance between the good bacteria that protect the vagina from infection and the harmful bacteria that don't. It is not clear what role sexual activity plays in the development of BV, but BV is more common among women who have had vaginal sex. But BV is not always from sexual contact. We do know that certain things can upset the normal balance of bacteria in the vagina and put you more at risk for BV: Having a new sex partner or multiple sex partners Douching Using an intrauterine device (IUD) for birth control Not using a condom We also know that you do not get BV from toilet seats, bedding, swimming pools, or from touching objects around you. What are the signs of Bacterial vaginosis? Women with BV may have an abnormal vaginal discharge with an unpleasant odor. Some women report a strong fish-like odor, especially after sexual intercourse. The discharge can be white (milky) or gray and thin. Other symptoms may include burning when urinating, itching around the outside of the vagina, and irritation. However, these could be symptoms of another infection too. Some women with BV have no symptoms at all. How can I find out if I have Bacterial vaginosis? There is a test to find out if you have BV. Your doctor takes a sample of fluid from your vagina and has it tested. Your doctor may also be able to see signs of BV, like a grayish-white discharge, during an examination of the vagina. How is Bacterial vaginosis treated? BV is treated with antibiotics, which are medicines prescribed by your doctor. Your doctor may give you either metronidazole or clindamycin. Generally, male sex partners of women with BV do not need to be treated. You can get BV again even after being treated. Is it safe to treat pregnant women who have Bacterial vaginosis? All pregnant women with symptoms of BV or who have had a premature delivery or low birth weight baby in the past should be tested for BV and treated if they have it. The same antibiotics that are used to treat non-pregnant women can be used safely during pregnancy. However, the amount of antibiotic a woman takes during pregnancy may be different from the amount taken if not pregnant. Can Bacterial vaginosis cause medical problems? In most cases, BV doesn't cause any problems. But some problems can happen if BV is untreated. Pregnancy problems. BV can cause premature delivery and low birth weight babies (less than five pounds). PID. Pelvic inflammatory disease or PID is an infection that can affect a woman's uterus, ovaries, and fallopian tubes, which carry eggs from the ovaries to the uterus. Having BV increases the risk of getting PID after a surgical procedure, such as a hysterectomy or an abortion. Higher risk of getting other STDs. Having BV can increase the chances of getting other STDs, such as chlamydia, gonorrhea, and HIV. Women with HIV who get BV increase the chances of passing HIV to a sexual partner. How can I prevent Bacterial vaginosis? BV is not well understood by scientists, and the best ways to prevent it are unknown. What is known is that BV is associated with having a new sex partner or having multiple sex partners. Follow these tips to lower your risk for getting BV: Don't have sex. The best way to prevent any STD is to practice abstinence, or not having vaginal, oral, or anal sex. Be faithful. Have a sexual relationship with one partner is another way to reduce your chances of getting infected. Be faithful to each other, meaning that you only have sex with each other and no one else. Use condoms. Protect yourself with a condom EVERY time you have vaginal, anal, or oral sex. Condoms should be used for any type of sex with every partner. For vaginal sex, use a latex male condom or a female polyurethane condom. For anal sex, use a latex male condom. For oral sex, use a dental dam. A dental dam is a rubbery material that can be placed over the anus or the vagina before sexual contact. Don't douche. Douching removes some of the normal bacteria in the vagina that protects you from infection. This may increase your chances of getting BV. It may also increase the chances of BV coming back after treatment. Talk with your sex partner(s) about STDs and using condoms. It's up to you to make sure you are protected. Talk frankly with your doctor or nurse and your sex partner(s) about any STDs you or your partner have or had. Talk about any discharge in the genital area. Try not to be embarrassed. Have regular pelvic exams. Talk with your doctor about how often you need them. Many tests for STDs can be done during an exam. If you are pregnant and have symptoms of BV or had a premature delivery or low birth weight baby in the past, get tested for BV. Get tested as soon as you think you may be pregnant. Finish your medicine. If you have BV, finish all the medicine that you are given to treat it. Even if the symptoms go away, you still need to finish all of the medicine. Last Updated: Sep 14, 2013"
22,"2018-04-20 02:30:06","Vaginal Microbiome Variation and Bacterial Vaginosis","By Dr Tomislav Meštrović, MD, PhD By forming a mutual relationship with the host, the vaginal microbiome (i.e. various kinds of vaginal microbial communities present in healthy women) has a significant impact on women’s health and disease. In the recent years our knowledge of those vaginal bacteria communities has expanded rapidly as a consequence of using modern molecular (cultivation-independent) methods for species identification. Bacterial vaginosis represents the most prevalent type of vaginal infection that occurs among reproductive-age women, and also the most common condition that prompts women to seek medical care. This condition, which is highly dependent on resident microbial flora, is linked to some severe sequelae such as pelvic inflammatory disease, preterm labor, as well as increased sensitivity to infection with various sexually-transmitted agents. A Shift in Vaginal Microbial Communities Although the term ‘bacterial vaginosis’ was coined more than half a century ago, its etiology and natural history remains elusive. Generally, this condition is characterized by a shift in microbial composition from an abundance of lactobacilli in healthy women, to an increase of commensal anaerobic bacteria (such as Gardnerella, Atopobium, Prevotella and a panoply of other species). As the aforementioned loss of lactobacilli results in reduced lactic acid production, the pH in the vaginal lumen increases. Furthermore, amine and salidase production increases, while the production of hydrogen peroxide and lactocin is diminished, leading to signs and symptoms of bacterial vaginosis. Women with this condition are characterized by heterogeneous communities of bacteria that exhibit increased richness and diversity of existent bacterial species. Such species heterogeneity in bacterial vaginosis is thought to arise from functional redundancy between them, which is in turn associated with improved community reliability when faced with environmental changes. Moreover, a thorough analysis of the vaginal microbiome may predict the recurrence of bacterial vaginosis if changes in the resident microflora are compared. Such recurrences in sexually-active women are not rare, and may even appear three times or more during the year. Microbial Associations with Clinical Criteria for Bacterial Vaginosis Related StoriesCertain bacterial species may increase HIV risk in women, finds new studyNew study finds certain bacterial species may increase HIV risk in womenIn a majority of clinical settings, women are diagnosed with bacterial vaginosis by using the Amsel criteria when three or more signs are present, such as a vaginal pH higher than 4.5, thin vaginal discharge, amine odor if potassium hydroxide is added to vaginal fluid, as well as the presence of vaginal epithelial cells overlaid with bacteria (also known as “clue cells”). Nugent scores that are based on weighted tallies of various cellular morphotypes (most notably lactobacilli, Gardnerella vaginalis, Bacteroides, as well as curved Gram-variable rod-shaped bacteria) are also widely used in the diagnosis of bacterial vaginosis. This scoring system ranges from 0-10, and scores higher than 7 are indicative of bacterial vaginosis. The advantage of these clinical criteria is that the diagnosis can be achieved by using light microscopy; however, that way it is impossible to get deep insights into the composition of present bacterial communities. On the other hand, deep sequencing analysis is quite expensive and still not pervasive in clinical practice, even though it can provide a clear picture of vaginal microbiota and allow the detection of recurrences and treatment failures. Reviewed by Afsaneh Khetrapal BSc (Hons) Sources http://cmr.asm.org/content/29/2/223.full https://www.nature.com/articles/srep26674 https://www.ncbi.nlm.nih.gov/pubmed/26385347 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3780402/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3249696/ http://www.pnas.org/content/108/Supplement_1/4680.full journals.plos.org/plosone/article?id=10.1371/journal.pone.0037818 journals.plos.org/plosone/article?id=10.1371/journal.pone.0082599 Further ReadingBacterial VaginosisWhat is Vaginal Microbiome?Vaginal Microbiome During PregnancyVaginal Microbiome and Sexually Transmitted InfectionsVaginal Microbiome and Gynecological Cancer // Last Updated: Aug 8, 2017"
23,"2018-04-20 02:30:10","Balance Disorder - What are Balance Disorders?","By Dr Ananya Mandal, MD Balance disorders are disturbances in co-ordination that makes a person feel unsteady, dizzy or have a sensation of movement or spinning. The problem more often than not lies within the ears. Within the ear is a part called the inner ear. This has organs that are responsible for normal balance mechanisms. Normal mechanism of balance The inner ear contains an organ called the labyrinth. The inner ear co-ordinates with the eyes (what they see), as well as the feeling of the bones and joints, to maintain normal balance. The inner ear sends signals to the brain that also receives signals from these peripheral organs to given an idea of the position of the body. This helps in maintenance of balance. The labyrinth has a structure called the semicircular canals. These allow a person to feel and experience rotary (circular) motion. There are three semicircular canals called the superior, posterior, and horizontal canals. The canals converge at a point and this is close to the cochlea that is responsible for hearing. These are filled with a fluid. As the body moves, this fluid also moves. The ends of the semicircular canals have a bulb like formation that contains hair-like tiny cells. Rotation of the head causes a movement of the fluid leading to movement of the top portion of the hair cells that are embedded in the jelly-like cupula. There are two other organs called the utricle and saccule that are called otoliths. These detect linear acceleration, or movement in a straight line. Symptoms of balance disorders The symptoms of balance disorders include difficulty in maintaining orientation. One of the commonest complaints is feeling dizzy or experiencing vertigo. The room appears to be spinning. There may be light headedness or a feeling of floating. Sometimes there may be blurring of vision as well. Along with vertigo there is commonly nausea and vomiting, diarrhea, faintness, palpitations, drop in blood pressure, fear, anxiety, or panic. Causes of balance disorders There are several causes of balance disorders. Diseases and disorders affecting the brain or the inner ears are commonly responsible for balance disorders. Some common causes include infections of brain or inner ear, head injury, disorders of blood circulation affecting the inner ear or brain, certain medications, as part of aging etc. Some of the types of balance disorders include Benign Paroxysmal Positional Vertigo (BPPV), labrynthitis, Ménière's disease, vestibular neuronitis etc. Diagnosis of balance disorders Diagnosis of a balance disorder involves several laboratory as well as imaging studies. There are several associated conditions that may lead to balance disorders including ear infections, blood pressure changes, problems in vision etc. Diagnosis is usually made by an ENT specialist (Ear, nose and throat disease specialist) also known as an otolaryngologist. Treatment of balance disorders Treatment of balance disorders depends on the cause underlying the condition. Problems of balance are symptoms of an underlying disease rather than a disease in itself. One of the options is to treat the underlying disease such as ear infection, stroke, or multiple sclerosis. The second option is to treat the symptoms of the condition. This can be achieved by balance retraining exercises (vestibular rehabilitation) etc. Reviewed by April Cashin-Garbutt, BA Hons (Cantab) Sources www.royalberkshire.nhs.uk/.../balance_disorders.aspx?theme=Patient www.nidcd.nih.gov/.../balance.pdf familymed.uthscsa.edu/.../Gait%26Balance10.pdf www.medoto.unimelb.edu.au/files/doto/DizzinessandBalanceDisorders.pdf http://iapmr.org/ijpmr/ijpmr01/200105.pdf Further Reading Balance Disorder Symptoms What Causes Balance Disorders? Balance Disorder Pathophysiology Balance Disorder Diagnosis Balance Disorder Treatments Balance Disorder Research Last Updated: Oct 7, 2014"
24,"2018-04-20 02:30:12","What Causes Balance Disorders?","By Dr Ananya Mandal, MD Several diseases and disorders affecting the inner ear or brain or certain medications may cause balance disorders. The causes may vary from infections (viral or bacterial), head injury, disorders of blood circulation etc. Those who have injuries or illnesses of the eyes or have problems with the skeletal system (e.g. arthritis) may also experience balance difficulties. These disorders may lead to a conflict of signals to the brain about the sensation of movement and can lead to balance problems. If there is a conflict of signals between the eyes and the brain, for example, if a person tries to read while riding in a car, there is motion sickness. Some symptoms of motion sickness include dizziness, sweating, nausea, vomiting, and generalized discomfort. Main causes of balance disorders Broadly classifying balance disorders may occur due to problems in any of the four areas:- Disturbances of the labyrinth in the inner ear – Peripheral vestibular disorder Disturbances in the brain or its connecting nerves - Central vestibular disorder Problems of the body other than the head and brain – Systemic disorder Blood flow problems or Vascular disorder Types of balance disorder Some of the different types of balance disorder leading to impaired sense and maintenance of balance include:- Benign Paroxysmal Positional Vertigo (BPPV) This condition is characterized by brief but severe episodes of vertigo brought about by specific positional change of the head. The movement could be trivial for example rolling within the bed or trying rise up to a sitting position from lying position or even looking up at an object. It is found that movement of chalk crystals (otoconia) within the inner ear from one part of the balance system (utricle and saccule) to another part of the balance system (semi-circular canals) due to movement of the head gives rise to the symptoms. Although the exact cause of the condition is unknown, it is thought to be caused as a part of normal aging, infection or head injury. Ménière's disease This is caused by an imbalance between the pressures of the fluids within the inner ear. The exact cause is unknown. There are episodes of vertigo, hearing loss and sensation of fullness in the ear along with tinnitus (a ringing or roaring in the ears). Labrynthitis This is caused by infection and/or inflammation of the inner ear causing dizziness and loss of balance. Vestibular neuronitis This is caused by an infection of the vestibular nerve caused by a virus. There is generally rotatory vertigo (horizontal or vertical spinning) that may last for up to 48 hours, exacerbated by movement. Perilymph fistula In this condition there is leakage of inner ear fluid to the middle ear. This occurs due to head injury. Other causes of balance disorders Certain medications that depress the central nervous system may also increase the rate of falls by increasing the lack of coordination. Arthritis, joint pain, stroke, visual impairment, back or neck pain, myelopathy due to cervival spondylosis, normal-pressure hydrocephalus, parkinsonism and fall of blood pressure on standing (orthostatic hypotension) are other causes of balance problems and risk of falls among the elderly. Problems in the cerebellum of the brain also contribute to balance disorders. Reviewed by April Cashin-Garbutt, BA Hons (Cantab) Sources www.royalberkshire.nhs.uk/.../balance_disorders.aspx?theme=Patient www.nidcd.nih.gov/.../balance.pdf familymed.uthscsa.edu/.../Gait%26Balance10.pdf www.medoto.unimelb.edu.au/files/doto/DizzinessandBalanceDisorders.pdf http://iapmr.org/ijpmr/ijpmr01/200105.pdf Further Reading Balance Disorder - What are Balance Disorders? Balance Disorder Symptoms Balance Disorder Pathophysiology Balance Disorder Diagnosis Balance Disorder Treatments Balance Disorder Research Last Updated: Feb 6, 2014"
25,"2018-04-20 02:30:13","Balance Disorder Symptoms","By Dr Ananya Mandal, MD Balance disorders are diseases that give rise to symptoms of impaired balance and co-ordination. The balance problems are thus symptoms rather than a disease it itself. Some of the symptoms associated with balance disorders include:- Dizziness or vertigo with the room appearing to be spinning. There may be disorientation. There is marked change and deterioration of independent walking and mobility. The gait is typically staggering as the sufferer struggles to maintain balance. Some persons may have difficulty in rising from a lying or sitting position. There may be an increased risk of falls or actual falls. The sufferer may also complain of a feeling of falling. There is a sensation of light headedness or feeling woozy. Sometimes there may be double vision or blurring of vision. Nausea and vomiting, diarrhea and faintness may be seen as associated symptoms. The heart rate may accelerate leading to palpitations. In addition there may be fall in blood pressure accompanied by increased sweating. There may be exaggerated fear, anxiety or panic in response to disorientation. Sometimes there may be symptoms of depression, fatigue and reduced concentration as well. In specific balance disorders like Benign Paroxysmal Positional Vertigo (BPPV) there are characteristic symptoms. These include severe and intense short episodes of dizziness associated with moving the head or even turning over in bed or sitting up from lying position. In acute vestibular neuronitis, or labyrinthitis there is inflammation of the inner ear. This leads to sudden, intense vertigo persisting along with nausea and vomiting for several days. This condition leads to severe disability and mandates bed rest. Meniere's disease leads to repeated sudden episodes of vertigo lasting 30 minutes or longer. This is accompanied by fluctuating hearing loss and a feeling of fullness in the ear. In addition to these symptoms there are symptoms of buzzing or ringing in the ear (tinnitus). Vestibular Migraine may present with or without severe headaches. The dizziness may last for several minutes to days. The episodes of dizziness may be brought about by quick head turns, driving or riding in a vehicle or when watching TV. In addition there may be hearing loss, and ringing in the ears (tinnitus). Reviewed by April Cashin-Garbutt, BA Hons (Cantab) Sources www.royalberkshire.nhs.uk/.../balance_disorders.aspx?theme=Patient www.nidcd.nih.gov/.../balance.pdf familymed.uthscsa.edu/.../Gait%26Balance10.pdf www.medoto.unimelb.edu.au/files/doto/DizzinessandBalanceDisorders.pdf http://iapmr.org/ijpmr/ijpmr01/200105.pdf Further Reading Balance Disorder - What are Balance Disorders? What Causes Balance Disorders? Balance Disorder Pathophysiology Balance Disorder Diagnosis Balance Disorder Treatments Balance Disorder Research Last Updated: May 26, 2013"
26,"2018-04-20 02:30:17","Balance Disorder Pathophysiology","By Dr Ananya Mandal, MD Balance disorders are caused by several incidents that may be episodes of infection, injury or blood flow problems to the inner ear or to the brain. Normal functioning of the balance organs within the ear The ears are divided into three discernible parts – the outer, middle and the inner ear. The outer ear is composed of the pinna that brings in sound waves onto the ear drum. The middle ear amplifies the sound wave and transmits it into the inner ear. The inner ear contains an organ called the labyrinth. There two major organs in the inner ear – the cochlea or the shell shaped hearing organ and the semicircular canals or the balance organs. The semicircular canals work to co-ordinate with the eyes (what they see) as well as the feeling of the bones and joints to maintain normal balance. When the inner ear coordinates with the signals from the eyes, it is called the vestibulo-ocular reflex (VOR). The inner ear sends signals to the brain that also receives signals from these peripheral organs to given an idea of the position of the body. This helps in maintenance of balance. The semicircular canals are three tubes set in three different right angles. They have a bulb at their ends. These are called superior, posterior, and horizontal canals. The canals converge at a point and this is close to the cochlea. These are filled with a fluid. As the body or the head moves, this fluid also moves. The bulbs at the ends of the canals contain tiny hair like structures. Rotation of the head causes a movement of the fluid leading to movement of the top portion of the hair cells that are embedded in the jelly-like cupula. There are two other organs called the utricle and saccule that are called otoliths. These detect linear acceleration, or movement in a straight line. When the hair is displaced, it sends signals to the brain via nerves and the body corrects itself or balances accordingly. Pathophysiology of balance disorders An acute loss of balance sensation can be either partial or total. It may be caused by viral infections or due to injury to the vital structures of the brain or inner ear. In the case of benign paroxysmal positional vertigo (BPPV), calcium carbonate crystals get dislodged from their usual position and move to one of the semicircular canals of the inner ear when the head is moved. There is an incorrect registration of movements with changes in body position and this may trigger an episode of intense vertigo. Injuries to the central nervous system may be caused by head injury or by disturbances of the blood circulation. This leads to dizziness, vertigo, and disequilibrium. With age there is a deterioration of the balance system leading to balance problems. Physical disabilities such as arthritis and joint pain also contribute to the problem. Reviewed by April Cashin-Garbutt, BA Hons (Cantab) Sources www.royalberkshire.nhs.uk/.../balance_disorders.aspx?theme=Patient www.nidcd.nih.gov/.../balance.pdf familymed.uthscsa.edu/.../Gait%26Balance10.pdf www.medoto.unimelb.edu.au/files/doto/DizzinessandBalanceDisorders.pdf http://iapmr.org/ijpmr/ijpmr01/200105.pdf http://www.nidcd.nih.gov/health/balance/pages/balance_disorders.aspx fyss.se/.../27.-Dizziness-and-balance-disorders.pdf Further Reading Balance Disorder - What are Balance Disorders? Balance Disorder Symptoms What Causes Balance Disorders? Balance Disorder Diagnosis Balance Disorder Treatments Balance Disorder Research Last Updated: May 26, 2013"
27,"2018-04-20 02:30:21","Balance Disorder Diagnosis","By Dr Ananya Mandal, MD There are several disorders that may lead to balance problems. Diagnosis aims at detecting the cause of balance problems. Balance problems thus are symptoms of an underlying condition rather than a disease in itself. The cause of balance problems may vary between ear infections, blood pressure changes, vision problems or even medications that may cause balance problems. Steps in diagnosis of the conditions include:- Complete evaluation of the problem with history of onset, duration of the balance disorders and family history. A precipitating ear infection, vision problem or head injury or a history of intake of a balance problem causing medication is often found upon enquiring the history from the patient. This may provide valuable clues in diagnosing balance problems. Evaluation and diagnosis may be made by a primary physician who may then request the opinion or refer to an otolaryngologist to help evaluate a balance problem. An otolaryngologist or ENT surgeon is a physician/surgeon who specializes in diseases and disorders of the ear, nose, throat, head, and neck. Physical examination – the next step is to obtain a detailed physical examination. The general health is examined that includes blood pressure and blood sugar evaluations, fluctuations of which may lead to balance problems or dizziness and falls. The ears are examined for abnormalities, hearing difficulties and infections if any. An electronystagmogram (ENG) is often advised. This test checks for abnormalities of the vestibular system. The caloric test may be performed as part of the ENG. For this test each ear is flushed with warm and then cold water one at a time. When water is flushed, the eyes move rapidly from side to side. This is called nystagmus. The amount of nystagmus resulting from the test is measured. Weak nystagmus or the absence of nystagmus may indicate an inner ear disorder. Another test for vestibular health is called posturography. The patient is asked to stand on a special platform capable of movement within a controlled visual environment. The sway of the body in response to movement and visual environment is recorded. Blood tests for detection of abnormalities like anemia, high or low blood sugar are advised. Usually a complete blood count, thyroid function test, liver and kidney function tests, electrolytes, blood urea nitrogen, creatinine, glucose, and vitamin B12 levels are tested. Imaging studies of the head including CT scan (Computed Tomography scan) or MRI scan (Magnetic resonance imaging scan) are performed to check for injuries and abnormalities in the brain and cerebellum part of the brain that controls balance and coordination. Reviewed by April Cashin-Garbutt, BA Hons (Cantab) Sources www.royalberkshire.nhs.uk/.../balance_disorders.aspx?theme=Patient www.nidcd.nih.gov/.../balance.pdf familymed.uthscsa.edu/.../Gait%26Balance10.pdf www.medoto.unimelb.edu.au/files/doto/DizzinessandBalanceDisorders.pdf http://iapmr.org/ijpmr/ijpmr01/200105.pdf Further Reading Balance Disorder - What are Balance Disorders? Balance Disorder Symptoms What Causes Balance Disorders? Balance Disorder Pathophysiology Balance Disorder Treatments Balance Disorder Research Last Updated: May 26, 2013"
28,"2018-04-20 02:30:24","Balance Disorder Treatments","By Dr Ananya Mandal, MD Balance problems are symptoms of an underlying condition rather than disease in itself. There are several different causes and varieties of disorders that may lead to balance problems. Thus treatment of balance disorders is also wide ranging and varied. For example, balance problems caused by ear infections are treated using antibiotics and anti-inflammatory agents while those due to side effects of medications are treated with stopping the suspected drug or medication. Some of the treatment options include:- Treatment for a disease or disorder that is leading to balance problems. This could be an ear infection, stroke, or multiple sclerosis. Other causes such as head injuries and disorders of the joints, high or low blood pressure and blood sugar are also treated specifically. Diet and lifestyle changes – in patients of Ménière's disease, dietary changes such as reducing intake of sodium or salt may help in reducing the symptoms of dizziness. In most patients avoidance of alcohol, caffeine and nicotine is advised. Treatment of inflammation within the inner ear. This includes labyrinthitis or vestibular neuroninitis. These are treated using anti-inflammatory agents including corticosteroids. Some aminoglycoside antibiotics, such as gentamicin and streptomycin may be used in treatment of balance problems caused by Ménière's disease. Streptomycin injections and application of gentamicin directly into the inner ear are useful for their ability to affect the hair cells of the balance system. Gentamicin also can affect the hair cells of the cochlea leading to hearing loss. Certain drugs may be used in some balance disorders. For example, in Ménière's disease Beta-histine can ease symptoms. Diuretics like hydrochlorthiazide may also be used. Other drugs include sedatives for dizziness including lorazepam that does not ease symptoms but helps patients cope with the sensation. Some drugs that work on motion sickness may be used. This includes drugs belonging to the classes antihistaminics and anticholinergics. Some calcium channel blockers like Verapamil and Nimodipine and GABA modulators like gabapentin and Baclofen may also help. Neurotransmitter reuptake inhibitors such as antidepressants SSRIs (Selective Serotonin Reuptake Inhibitors) including Fluoxetine, Escitalopram and trycyclic antidepressants including imipramine etc. may be useful in some patients. Balance retraining exercises (vestibular rehabilitation) – these exercises involve specific movements of the head and body. This helps in promotion of the compensation for the disorder. These are usually performed under the guidance of professionals with knowledge and understanding of the vestibular system and its association with other organs of the body. Those with Benign Paroxysmal Positional Vertigo (BPPV) suffer from dizziness due to misplaced crystals within the ear. Treatment involves moving these crystals out of areas that may trigger dizziness. This is achieved by head and neck positional exercises. In addition there may be counselling and cognitive behavioral therapy that is useful in persons with anxiety and depression. Surgery is necessitated in some severe causes of balance disorders. For example, in severe cases of Ménière's disease, surgery is the last resort. Surgical methods for Ménière's disease include Vestibular neuronectomy and Labyrinthectomy. Reviewed by April Cashin-Garbutt, BA Hons (Cantab) Sources www.royalberkshire.nhs.uk/.../balance_disorders.aspx?theme=Patient www.nidcd.nih.gov/.../balance.pdf familymed.uthscsa.edu/.../Gait%26Balance10.pdf www.medoto.unimelb.edu.au/files/doto/DizzinessandBalanceDisorders.pdf http://iapmr.org/ijpmr/ijpmr01/200105.pdf Further Reading Balance Disorder - What are Balance Disorders? Balance Disorder Symptoms What Causes Balance Disorders? Balance Disorder Pathophysiology Balance Disorder Diagnosis Balance Disorder Research Last Updated: May 26, 2013"
29,"2018-04-20 02:30:29","Balance Disorder Research","By Dr Ananya Mandal, MD Balance disorders are a variety of diseases and disorders that affect the inner ear or the brain. These conditions may also be caused as a side effect of several chemicals and medications. Scientists are researching the various underlying pathologies that may give rise to balance problems. The areas of research include the complex interactions between the balance-sensing organs, vision, labyrinth and the brain. Age and balance Researchers are looking at how advanced age is affecting normal balance. With the increase in the elderly population due to longer life expectancies these areas of research are gaining importance. More elderly are suffering from an impaired quality of life due to impaired mobility, lack of motor co-ordination and inability to lead an independent life. Vision and balance disorders The correlation between vision and balance disorders is also an important area of research. Researchers are looking at disease and injuries of the eyes and the nerves that connect the balance organs, eyes and the brain. Researchers are looking at eye movement and posture changes that may affect balance. Pathological diseases of the inner ear and balance disorders Pathological diseases of the inner ear and long term consequences of ear infections and brain infections like meningitis and encephalitis are also an area of research. Genetic causation of ear problems and subsequent balance problems in some diseases and disorders are being studied widely all over the world. Treatments of balance disorders The other part of research focuses on treatments of balance disorders. In addition, there are studies supported by the National Institute on Deafness and Other Communication Disorders (NIDCD) that also show that the vestibular system plays an important role in modulating blood pressure. This could help in management of posture related fall of blood pressure called orthostatic hypotension. Orthostatic hypotension refers to sudden fall of blood pressure when an individual changes his or her position from sitting to standing or lying to sitting. This leads to severe dizziness and balance problems. Studies on otolithic organs There are studies that explore otolithic organs within the inner ears that detect linear movement. It is being studied how these organs differentiate between downward (gravitational) motion from linear (forward-backward or side-to side) motion. Exercises as a treatment Several researchers are working on the effectiveness of certain exercises as a treatment option. Strategies for new physical rehabilitation are also under investigation in clinical and research settings. Further research NIDCD, along with other Institutes at the National Institutes of Health, joined the National Aeronautics and Space Administration (NASA) for Neurolab are studying exposure to the weightlessness of space and balance changes associated with the condition. Reviewed by April Cashin-Garbutt, BA Hons (Cantab) Sources www.royalberkshire.nhs.uk/.../balance_disorders.aspx?theme=Patient www.nidcd.nih.gov/.../balance.pdf familymed.uthscsa.edu/.../Gait%26Balance10.pdf www.medoto.unimelb.edu.au/files/doto/DizzinessandBalanceDisorders.pdf http://iapmr.org/ijpmr/ijpmr01/200105.pdf Further Reading Balance Disorder - What are Balance Disorders? Balance Disorder Symptoms What Causes Balance Disorders? Balance Disorder Pathophysiology Balance Disorder Diagnosis Balance Disorder Treatments Last Updated: May 26, 2013"
30,"2018-04-20 02:30:35","Health Benefits of Bananas","By Liji Thomas, MD Bananas have been around for centuries, and the largest production is in India which, however, consumes most of what it produces itself. This is not surprising, given the unique blend of taste and health that makes up a banana, complete with its own individual wrapper (biodegradable to boot), and inbuilt marker of expiry dates (as the skin turns black). Credit: Hanna_photo/ Shutterstock.com Bananas are often classified as sweet bananas, which are eaten as a dessert or snack, and cooking bananas, which are usually called plantains. Votaries swear by them either raw or cooked or processed in various forms. Nutrient composition Bananas contain several bioactive compounds including: Phenolic compounds Carotenoids Biogenic amines Phytosterols They are also rich in a number of beneficial nutritional components. These include (per medium banana, about 118 g): 27g carbohydrates of which 14g is in the form of sugars (5.9 g glucose, 5.7 g fructose, and 2.8 g sucrose Dietary fiber of 3.1 g, of which 2.1g is soluble and 1g insoluble. Fibers are a form of insoluble starch composed of multiple sugars bonded by chemical linkages, which are resistant to chemical hydrolysis within the gut. Thus, they reach the colon intact and are subjected to microbial fermentation by gut bacteria. This not only produces better stool volume by binding water but results in the formation of some essential short-chain fatty acids (SCFAs) which are absorbed and used as energy sources. Fiber thus comprises not only dietary fiber which is mainly mechanical in effect but functional fiber which has a positive effect upon health. The sources of fiber which yield 5 g per serving are called excellent, and good if they give 2.5 g per serving. Under this classification, bananas are good sources of fiber. Resistant starch is slow to be digested by alpha-amylase and thus prevents a spike in the blood glucose. Potassium content of 422 mg which is positively related to cardiovascular health Vitamins: 33% of the RDI of B6, 11% for vitamin C Minerals: 8% of the RDI for magnesium and copper, 14% for manganese Protein content is 1.3 g and fat is only 0.4 g per medium banana. Health effects Related StoriesQUT researchers develop golden-orange bananas rich in pro-vitamin AResearch shows probiotics can reduce incidence of sepsis in infantsRestaurant placemats can encourage children to choose healthier food optionsBanana consumption has been studied in a number of ways, and some of the health impacts include: Energy food for athletes One medium banana contains about 105 calories, compared to 144 calories for a serving of potato. Bananas are thus cost-effective as a source of energy. They are used as quick nutrient-dense boosts of energy for endurance workouts and sports, with a glycemic index of 51. Antioxidant actions The bioactives in bananas include several strong antioxidants (banana has over 1000 mmol of TE in ORAC units, comparable to kiwi fruit), and are thus useful in protecting the body against inflammatory and oxidative stresses. They may protect against age-related or other chronic degenerative conditions. Lowering of blood pressure and cardioprotective effect The high potassium content is probably responsible for its ability to reduce the blood pressure, along with its low sodium content. Potassium deficiency is thought to be the underlying factor in hypertension, especially because it helps to push down sodium concentration in the blood. Some studies found that eating a couple of bananas a day led to a 10% fall in blood pressure over one week, and that 5 bananas a day was half as effective as the use of antihypertensive medication. Control of blood sugar levels and metabolic syndrome Diabetics would benefit from consuming under-ripe rather than overripe bananas, which have a glycemic index of 43 and 74 respectively and cause the blood glucose to rise to an average of 62 and 106 respectively. This is due to the increased starch content as compared to sugar content in under-ripe bananas. Control of body weight The high fiber content of banana makes it ideal as a low-calorie nutrient-dense food for overweight people. The resistant starch in under-ripe bananas and plantains can substitute for many calorie-rich starchy foods, and its benefits go beyond diabetes control to dyslipidemia correction and weight control. It also promotes satiety and reduces total energy intake. Prevention of kidney tumors While having 75 or more servings of fruits or vegetables per month is known to be protective against renal cell carcinoma by about 40%, this effect was most marked in the case of banana consumption. Protection against colon cancer Resistant starch may also help reduce or dilute the concentrations of toxic substances such as fecal ammonia and N-nitroso compounds in the colonic lumen, but this is still under study. If confirmed, bananas would play a part in preventing colon cancer by reason of the lente carbohydrate (slowly digested carbohydrate). Reviewed by Afsaneh Khetrapal Bsc (Hons) Sources https://www.ncbi.nlm.nih.gov/pubmed/27041291 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3649719/ https://www.ncbi.nlm.nih.gov/pubmed/1395467 https://www.ncbi.nlm.nih.gov/pubmed/20968236 https://www.ncbi.nlm.nih.gov/pubmed/15287678 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3355124/ http://www.news.appstate.edu/2012/05/28/bananas-are-beneficial/ https://www.ncbi.nlm.nih.gov/pubmed/15455348 Last Updated: Feb 27, 2018"
31,"2018-04-20 02:30:39","Barbiturates - What are Barbiturates?","By Sally Robertson, BSc Barbiturates are synthetic drugs used in medicine to depress the central nervous system. The effects range from mild sedation to coma and they may be used a sedatives, hypnotics or as part of anesthesia. Some barbiturates are used to relieve tension or anxiety prior to surgery. Barbiturates used to be regularly prescribed to treat insomnia, depression and anxiety, but the small difference between a normal dose and an overdose led to a number of accidental deaths, as well as people using them to commit suicide. Therefore, the use of barbiturates as sedatives or hypnotics to relieve insomnia or daytime restlessness caused by everyday stresses is no longer advised and has been replaced with safer medicines. Today, they are generally only used to treat extreme and serious cases of insomnia. They are also used to help control seizures in epilepsy and some are used as an adjunct to anesthesia. Pharmacological barbiturates are based on the parent compound barbituric acid. The type of barbituate depends on the substituent used at position 5 of this basic skeleton. Around 2500 different types of barbiturates have been synthesized since 1881, when barbital, the first pharmacologically active form, was synthesized. However only around 50 of these agents have ever been used in medicine. Availability and Legal Status Under the Medicines Act, barbiturates are only available as prescription doctors, meaning they can only be bought at a pharmacy with a doctor’s prescription. They are available in the following forms. Tablet Capsule Elixir Solution Suspension Enema Suppository The Misuse of Drugs Act classes barbiturates as class B drugs, which means they can be bought in accordance with a doctor’s prescription, but any other form of possession or supply counts as an offence. The maximum penalty a person can receive for any unauthorised possession is 5 years in prison and a fine for possession. For supply, the maximum penalty is 14 years in prison and a fine. If barbiturates are prepared as injection drugs, they are then classified as class A drugs and the penalties for possession and supply are more severe. Effects of Barbiturates Barbiturates slow down the CNS in a similar way to alcohol and depending on how rapidly they produce effects and the duration of those effects, they may be classed as ultra-short-, short-, intermediate- or long-acting. In the case of the long-acting phenobarbital and barbital, effects may last for up to 24 hours and these are used in combination with other drugs to prevent convulsion in epilepsy. The effects of Intermediate-acting barbiturates such as butabarbital sodium last for between 6 and 12 hours and these are used to treat insomnia. Pentobarbital is an example of a short-acting barbituate used to help patients fall asleep. The ultra-short acting thiamylal is administered as an injection to induce unconsciousness patients about to undergo surgery. Gaseous anesthetics are then used to maintain the unconsciousness throughout the surgical procedure. Small does of barbiturates make people feel relaxed, uninhibited, mildly euphoric, free of anxiety and sleepy. Larger doses can cause hostility, anxiety, body ataxia, slurred speech, paranoia and suicidal thoughts. The risk of falling over or having an accident is also increased. With prolonged use, tolerance can quickly develop, meaning larger does than the original dose are then required to produce the same effects. This can increase the risk of overdose, signs of which include shallow breathing, rapid and weak pulse, dilated pupils, clammy skin, coma and even death as a result of the central nervous system and respiratory system become severely depressed. Withdrawal Since tolerance and physical dependence can develop with p prolonged use of barbiturates, withdrawal from regular use can lead to various problems including the following: Irritability Faintness Anxiety Nausea Insomnia Sometimes convulsions In cases where a person withdraws from regular use of very high doses, symptoms can be more severe and include the following: Low blood pressure Hallucinations Delirium Seizures Sudden withdrawal from the regular use of high doses can be fatal and for individuals who have become addicted to barbiturates it is essential that they seek the care of trained rehabilitation professionals to help them withdraw safely and effectively. Sources www.mayoclinic.org/.../drg-20069290 https://www.dea.gov/druginfo/drug_data_sheets/Barbiturates.pdf http://www.britannica.com/science/barbiturate http://www.emcdda.europa.eu/publications/drug-profiles/barbiturates Further ReadingBarbiturate HistoryBarbiturate AbuseBarbiturate MechanismBarbiturate Risks Last Updated: Jun 19, 2016"
32,"2018-04-20 02:30:41","Barbiturate History","By Dr Ananya Mandal, MD Sleep disorders have been managed using several means throughout the history of mankind. It all began with alcohol and alkaloids of opium and other narcotic plants (hemp, belladonna, henbane, etc). It was in the late 19th and early 20th centuries that drugs such as paraldehyde, chloral hydrate, and bromides were developed for induction and maintenance of sleep. In 1864 Adolf von Bayer developed malonylurea from which in the early 20th century came the barbiturates. These agents were first brought to the market in 1904 by Farbwerke Fr Bayer and Co. Barbiturates are basically a closed-chain ureic compound, whose nucleus is malonylurea. Malonyurea is a combination of urea and malonic acid, an acid derivative taken from apples. Barbiturates were synthesized in 1864 by Adolf von Baeyer. The process was then perfected by the French chemist Edouard Grimaux in 1879. Origin of the term barbiturates There are several speculations about the origin of the term barbiturates. Some suggest it was a name given by Baeyer in honor of his friend Barbara. Yet others suggest that Baeyer celebrated his discovery of these compounds in a tavern near his home that was frequented by artillery officers. These officers were celebrating the day of their patron, St Barbara. The name could have come from there. Another possibility of the name was that the name came from the “barbed” appearance of the molecule due to the appearance of the crystals of these ureic compounds. Revolution in psychiatric and neurological disorders The first agent of this class was diethyl-barbituric acid. This spelled a revolution in psychiatric and neurological disorders of the time. It was successfully used in many patients with serious neuroses and psychoses. They were one of the first agents to be used in controlling seizures and in inducing sleep in insomniacs. With time barbiturates started the era of intravenous anesthetic agents. Before thiopentone, general anesthesia meant induction using the gases like nitrous oxide. Barbiturates in the 20th century Over the initial years of the 20th century more than 2,500 barbiturates were synthesized. Of these 50 were eventually employed clinically. Their use spread wide before physicians became aware of their risk of dependence and abuse liability. It was in 1912 that the first cases of dependence on barbiturates were reported from Germany. After initial reports, more physicians reported delirium and withdrawal symptoms on abrupt discontinuation or dose reduction of barbiturates. It was in 1950 that researchers published a paper that finally established that physical dependence on barbiturates is a possibility that can be induced in the laboratory as well in experimental conditions. What was surprising was that despite use of barbiturates for over five decades, it was only in the 1950’s that barbiturates were accepted as drugs that could cause dependence. It took another two decades for the physicians to be aware that these agents could cause dependence and abuse and should be prescribed only sparingly in select cases. Today 5 or 6 derivates of barbiturates are still being used as inducers of general anesthesia and serious forms of insomnia and in some types of epilepsy. Reviewed by April Cashin-Garbutt, BA Hons (Cantab) Sources http://www.duc.auburn.edu/~deruija/GABA_Barbiturates2002.pdf http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2424120/ http://www.tropiart.com/i_home/drugs/Barbiturates.pdf www.md.rcm.upr.edu/publications/sidney_kaye/Barbiturate_Poisoning.pdf www.homehealth-uk.com/medical/professional_drugtests_barbiturates.htm Further Reading Barbiturates - What are Barbiturates? Barbiturate Mechanism Barbiturate Risks Barbiturate Abuse Last Updated: May 26, 2013"
33,"2018-04-20 02:30:47","Barbiturate Abuse","By Dr Ananya Mandal, MD Barbiturates were first used in 1903. They are derivatives of the chemical molecule barbituric acid. There are over 2000 derivatives of barbituric acid that have been used in medicine. Dependence and abuse liability It was in 1912 that the first cases of dependence on barbiturates were reported from Germany. Dependence or physical dependence is defined as a condition when long term use of a drug results in the phenomenon of tolerance and discontinuation or dose reduction of the drug leads to onset of negative symptoms called withdrawal symptoms. Tolerance means that increasingly high doses of the drug are needed to achieve the same efficacy. After initial reports, more followed on the same lines. These reported delirium and withdrawal symptoms on abrupt discontinuation or dose reduction of barbiturates. It was in 1950 that researchers published a paper that finally established that physical dependence on barbiturates is a possibility that can be induced in the laboratory as well in experimental conditions. What was surprising was that despite use of barbiturates for over five decades, it was only in the 1950’s that barbiturates were accepted as drugs that could cause dependence. It took another two decades for the physicians to be aware that these agents could cause dependence and abuse and should be prescribed only sparingly in select cases. Drug abuse Drug abuse has been defined by the World Health Organization (WHO, I969) as the “persistent or sporadic excessive use of a drug inconsistent with or unrelated to acceptable medical practice”. Both dependence and abuse are closely related and are parts of the same spectrum of conditions with abuse being at the lower end of the spectrum and dependence being at the higher end. Abuse of barbiturates may vary between occasional use of a barbiturate hypnotic at night to intermittent use during the day leading to intoxication. Severe cases include intravenous use of the agent and finally physical dependence and addiction. Barbiturate abuse Regular consumption of 450 mg of a barbiturate that is traditionally used for sedation or sleep induction for a period of eight weeks is likely to lead to a psychological and/or physical dependence. There are around 60 different barbiturate compounds that are in use:- The ones that have a short duration of action have a low abuse potential and their use in limited to the hospitals in general anesthesia. The ones that have a longer duration of action include phenobarbitone and are used as anti-seizure drugs. Dependence of these agents are also rare but not impossible. Barbiturates that are rapidly acting and useful for sleep induction are the ones that lead to a high or a mood change and intoxication. These have the highest abuse potential and may cause dependence. Common agents abused include amylobarbitone, quinalbarbitone, pentobarbitone etc. Unlike the social profiles of other drug abusers barbiturate abuse is seen among socially stable, middle-aged persons who may be stably employed or housewives. These persons however do not abuse injectable barbiturates. Reviewed by April Cashin-Garbutt, BA Hons (Cantab) Sources pubmedcentralcanada.ca/picrender.cgi?artid=926509&blobtype=pdf http://www.duc.auburn.edu/~deruija/GABA_Barbiturates2002.pdf http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2424120/ http://www.tropiart.com/i_home/drugs/Barbiturates.pdf www.md.rcm.upr.edu/publications/sidney_kaye/Barbiturate_Poisoning.pdf www.homehealth-uk.com/medical/professional_drugtests_barbiturates.htm Further Reading Barbiturates - What are Barbiturates? Barbiturate History Barbiturate Mechanism Barbiturate Risks Last Updated: May 26, 2013"
34,"2018-04-20 02:30:50","Barbiturate Mechanism","By Dr Ananya Mandal, MD Barbiturates may have been abandoned as sedatives and tranquillizers due to their high abuse and dependence potential and risk of side effects, but they continue to hold an important place in neurology practice today. There are several uses of these agents and at present there are two major uses – as an agent that induces general anesthesia and as an agent that may control seizures. Mechanism of action The primary mechanism of action of barbiturates is inhibition of the central nervous system. It causes central nervous system depression. This is brought about by stimulating the inhibitory neurotransmitter system in the brain called the [gamma]-aminobutyric acid (GABA) system. The GABA channel is a Chloride channel that has five cells at its gate. When barbiturates bind to the GABA channel they lead to prolonged opening of the channel letting in Chloride ions into the cells in the brain. This leads to increased negative charge and alters the voltage in the brain cells. This change in voltage makes the brain cells resistant to nerve impulses and thus depresses them. Barbiturates used in anesthesia including Thiopentone sodium (also known as pentothal) also act by decreasing Calcium flow between the membranes. Barbiturates for controlling seizures and maintaining sleep Barbiturates that are used in controlling seizures include phenobarbitone. These are found to be effective in partial, complex partial and secondarily generalised seizures. There are other first line and more effective agents useful for these conditions, but phenobarbitone remains one of the effective agents that may be used when all others fail. Barbiturates are also used for inducing and maintaining sleep. Due to the narrow therapeutic dose range that leads to an increased risk of over dosage these agents are not routinely prescribed in sleep disorders. Another use of these agents is in the evaluation of patients with medically intractable seizure disorders for possible surgical therapy. Uses of barbiturates Sedation – these agents have largely been replaced by more modern and safer agents like benzodiazepines in this area. Sleep induction or hypnosis – in short term insomnia, barbiturates may be effective. This is because they tend to lose their effectiveness in sleep induction and maintenance after 2 weeks of use. Before surgery as a preanesthetic agent – sedation is given prior to surgery to allay anxiety and to ease the process of induction of general anesthesia. This is also an area where benzodiazepines have replaced barbiturates. Induction of general anesthesia – Thiopentone or pentothal is routinely used as an injectable induction agent in general anesthesia. Treatment of seizures - treatment of partial and generalized tonic-clonic and cortical focal seizures could still utilize barbiturates including mephobarbital, Phenobarbital. Acute convulsions – acute onset convulsions including status epilepticus, eclapmsia during pregnancy, meningitis, tetanus and toxic reactions to strychnine or local anesthetics, convulsions during cholera etc. are indications for use of barbiturates. Onset and duration of action Long-Acting Barbiturates – these are generally used in seizures. The action starts slow (30-60 minutes) and lasts longer (10-16 hrs). Intermediate-Acting Barbiturates – these are generally used in inducing and maintaining sleep. The action starts slow (45-60 minutes) and lasts for an intermediate duration (6-8 hrs). Short-Acting Barbiturates – these are also used as sedatives. Relatively rapid onset (10-15 minutes) and relatively short duration of action is seen (3-4 hrs). Ultra-Short-Acting Barbiturates – these are used in induction of anesthesia. These have an immediate onset of action that lasts for a very short duration. Reviewed by April Cashin-Garbutt, BA Hons (Cantab) Sources adisonline.com/.../...nical_Use_of_Barbiturates_in_Neurological.3.aspx http://www.duc.auburn.edu/~deruija/GABA_Barbiturates2002.pdf http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2424120/ http://www.tropiart.com/i_home/drugs/Barbiturates.pdf www.md.rcm.upr.edu/publications/sidney_kaye/Barbiturate_Poisoning.pdf www.homehealth-uk.com/medical/professional_drugtests_barbiturates.htm Further Reading Barbiturates - What are Barbiturates? Barbiturate History Barbiturate Risks Barbiturate Abuse Last Updated: May 26, 2013"
35,"2018-04-20 02:30:55","Barbiturate Risks","By Dr Ananya Mandal, MD Barbiturates once enjoyed vast popularity as sedatives and sleep inducing agents. Over time their side effects led to more caution and at present these agents are seldom prescribed for insomnia and sleep disorders. Some of the risks associated with barbiturates use include:- Drowsiness Barbiturates are primarily sedatives and they induce sleep. Since this is their primary pharmacological effect, some amount of excessive drowsiness is commonly seen especially in case of overdose. This sleepiness may persist over the next day as well. This may manifest as a hangover sleepiness that makes driving and operating heavy machinery on the next day morning a hazard. There is impaired psychomotor function and increased pain perception that may persist over the next day. Dependence and tolerance to barbiturates Over long term use dependence develops to barbiturates. This means that patients are unable to sleep without taking barbiturates. Tolerance is an associated phenomenon. This means over long term use sleep is difficult without increasing the dose. Finally the highest dose range of the drugs fails to produce sleep but may lead to other side effects. Depression of respiration Barbiturates have a narrow therapeutic range. This means these agents lead to side effects when they cross the normal dose range. Since this range is a narrow one there is a risk of over dose. Barbiturates in high doses cause depression of the respiratory centre of the brain leading to decreased drive for respiration. In severe cases of over dosage there is a complete suppression of respiration leading to respiratory failure. Peripheral Nervous System depression The peripheral nervous system is also depressed with over dosage of barbiturates. There is a decreased excitation of neuronal receptors that is enhanced by several other concomitant agents and drugs. Cardiovascular depression There is decreased cardiac contractility and cardiac output. This means the heart pumps blood with less power of contraction. There is also a decrease in blood flow to the brain. Action on enzymes of the liver There are several enzymes present in the liver that function in metabolizing various drugs. Barbiturates enhance the action of these enzymes. This is called enzyme induction. Enzyme induction leads to increased metabolism of certain medications concomitantly taken along with barbiturates. This means the duration of action of these drugs is markedly reduced when taken alongside barbiturates. Some of the drugs whose metabolism and effectiveness is affected by barbiturate use include anti-seizure drugs like phenytoin and carbamazepine, antibiotics like rifampicin etc. Action on the renal function There is decreased flow rate (glomerular flow rate) into the kidneys and decreased blood flow to the kidneys due to use of barbiturates. This results in lowered blood pressure and decreased urine volume Barbiturate risks in older patients and pregnant women The risk of side effects of barbiturates is higher in older patients and among pregnant women. This is because with age the ability to excrete and eliminate the drugs from the system decreases. Elderly over the age of 65 are at higher risk of experiencing adverse effects of barbiturates and also are at risk of drug dependence and accidental overdose. If taken during pregnancy these agents pass through the mother’s blood into the fetus via the placenta. The baby may be born with congenital abnormalities. Reviewed by April Cashin-Garbutt, BA Hons (Cantab) Sources http://www.duc.auburn.edu/~deruija/GABA_Barbiturates2002.pdf http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2424120/ http://www.tropiart.com/i_home/drugs/Barbiturates.pdf www.md.rcm.upr.edu/publications/sidney_kaye/Barbiturate_Poisoning.pdf www.homehealth-uk.com/medical/professional_drugtests_barbiturates.htm Further Reading Barbiturates - What are Barbiturates? Barbiturate History Barbiturate Mechanism Barbiturate Abuse Last Updated: May 26, 2013"
36,"2018-04-20 02:30:56","Bardet-Biedl Syndrome - What is Bardet-Biedl Syndrome?","By Dr Ananya Mandal, MD Bardet-Biedl syndrome is a condition that affects several parts of the body. It runs in families and may severely impair the sufferer. Symptoms and features of the condition One of the major features of Bardet-Biedl syndrome is loss of vision. Loss of vision occurs as the retina, that is the light sensing tissue or layer at the back of the eye, fails gradually. The problems appear initially as difficulty in seeing in the dark. This is seen in childhood as a slow onset condition. This is followed by development of blind spots in vision that leads to falls and knocks initially. Over time, these blind spots enlarge and turn into a tunnel where only the center is visible. With time the central clear area also clouds. By the time the child reaches adolescence or early adulthood, he may become legally blind. Another characteristic feature is obesity. There is typical abdominal obesity that begin in early childhood and continues throughout life. This may give rise to other complications like type 2 diabetes, high blood pressure and abnormally high levels of cholesterol. Typically there may also be presence of extra fingers and/or toes along with mental retardation, learning problems, and abnormalities of the genital organs. Bardet-Biedl syndrome epidemiology This is a rare condition and is seen in 1 in 140,000 to 1 in 160,000 newborns in most of North America and Europe. The prevalence is slightly higher on the island of Newfoundland (off the east coast of Canada), where it affects an estimated 1 in 17,000 newborns. Further Bedouin population of Kuwait and Arabs are also more commonly affected with prevalence there being about 1 in 13,500 newborns. Causes of Bardet-Biedl syndrome Bardet-Biedl syndrome is a genetically inherited condition. It results from mutations in at least 14 different genes in the body. These are commonly called BBS genes. It is found that these genes help make the hair like cellular structures called cilia. These cilia are involved in cell movement, different chemical signalling pathways perception of sensory input (such as sight, hearing, and smell) etc. The BBS genes code for proteins that maintain the functions of the cilia. Defects in these genes lead to defective cilia. The inheritance of Bardet-Biedl syndrome is autosomal recessive. This means parents of an individual with an autosomal recessive condition each carry one copy of the mutated gene but have no symptoms of the condition (carriers of the gene). Reviewed by April Cashin-Garbutt, BA Hons (Cantab) Sources http://ghr.nlm.nih.gov/condition/bardet-biedl-syndrome http://www.jnma.com.np/issue/172/235-237.pdf http://mun-h-center.se/upload/MunhDoc/Diagnoser/Eng/Fr%C3%A5/eLAUf.pdf http://www.cags.org.ae/pdf/209900.pdf http://www.japi.org/september2005/PC-781.pdf Further Reading Bardet-Biedl Syndrome Symptoms Bardet-Biedl Syndrome Pathophysiology // Last Updated: Oct 7, 2014"
37,"2018-04-20 02:31:00","Bardet-Biedl Syndrome Symptoms","By Dr Ananya Mandal, MD Bardet-Biedl syndrome affects more than one system in the body and symptoms may vary between individuals even in the same family. Common symptoms that may be seen in this condition include:- Vision loss One of the major features of Bardet-Biedl syndrome is loss of vision. Loss of vision occurs as the retina, that is the light sensing tissue or layer at the back of the eye, fails gradually. The problems appear initially as difficulty in seeing in the dark. This is seen in childhood as a slow onset condition. This is followed by development of blind spots in vision that leads to falls and knocks initially. Over time, these blind spots enlarge and turn into a tunnel where only the center is visible. With time the central clear area also clouds. By the time the child reaches adolescence or early adulthood, he may become legally blind. Obesity Another characteristic feature is obesity. There is typical abdominal obesity that begins in early childhood and continues throughout life. Obesity related conditions Obesity may give rise to other complications like type 2 diabetes, high blood pressure and abnormally high levels of cholesterol. Abnormalities of the fingers and/or toes Typically there may also be presence of extra fingers and/or toes. In addition the fingers and/or toes may be short and fused together. Learning difficulties There may be mental retardation, learning problems, intellectual disability and impaired speech. There may be delayed development of motor skills such as standing and walking. Behavioral problems There are associated behavioral problems including emotional immaturity and inappropriate outbursts, and clumsiness or poor coordination. Underdeveloped genitals The genital organs may also be underdeveloped. The amount of sex hormones produced by males with this condition is typically low and this makes them infertile. Kidney and other organ problems There may be mild to severe life threatening kidney problems and kidney formation abnormalities in these patients. The heart, liver, and digestive system may also be affected. In the heart there may be enlargement of the ventricles and cardiomyopathy. In the digestive system there may be presence of fibrosis. Facial abnormalities There are distinctive facial abnormalities in most patients. There are jaw and tooth deformities. There may be extra teeth or small and thin teeth roots. Due to these deformities snoring is common. In addition there may be feeding difficulties and drooling as well. Anosmia There may be a partial or complete loss of the sense of smell (anosmia). Reviewed by April Cashin-Garbutt, BA Hons (Cantab) Sources http://ghr.nlm.nih.gov/condition/bardet-biedl-syndrome http://www.jnma.com.np/issue/172/235-237.pdf http://mun-h-center.se/upload/MunhDoc/Diagnoser/Eng/Fr%C3%A5/eLAUf.pdf http://www.cags.org.ae/pdf/209900.pdf http://www.japi.org/september2005/PC-781.pdf Further Reading Bardet-Biedl Syndrome - What is Bardet-Biedl Syndrome? Bardet-Biedl Syndrome Pathophysiology Last Updated: Jul 22, 2013"
38,"2018-04-20 02:31:06","Bardet-Biedl Syndrome Pathophysiology","By Dr Ananya Mandal, MD Bardet-Biedl Syndrome is a genetically inherited condition. It is the result of inheriting mutations or alterations in the genes. At least 14 different genes have been identified that may be mutated or altered in individuals with this syndrome. Genetics of Bardet-Biedl syndrome There are 14 different genes that may be altered or mutated in individuals with Bardet-Biedl syndrome. These are commonly termed BBS genes. These genes code for proteins that are involved in the maintenance and function of cilia of the cells. What are cilia? Cilia are finger-like or hair-like structures that are present on the surfaces of many types of cells. These are involved in movement of the cells and different chemical signalling pathways. Cilia are also vital in perception of sensory input including sight, smell and hearing. Deformed cilia Mutations in BBS genes may lead to deformed cilia. Due to these defects there may be disruptions in important chemical signalling pathways. This leads to impaired sensory perceptions. These defective cilia are the basic pathology of Bardet-Biedl syndrome. BBS1 and BBS10 gene Around 25% of all cases of this syndrome result from mutations in the BBS1 gene. Another 20 percent of cases are caused by mutations in the BBS10 gene. The other BBS genes each account for only a small percentage of all cases of this condition. In a quarter of patients no specific gene or cause is known. Genetic changes in a specific BBS gene may exist alone or in combination with mutations in other genes that may modify the course of the disease. These additional changes of genes along with the original changes in the genes are responsible for the variations of signs and symptoms of Bardet-Biedl syndrome. Inheritance of Bardet-Biedl syndrome Bardet-Biedl syndrome is inherited in an autosomal recessive pattern. This means for a child to inherit the condition both parents have to have a single copy of the mutated gene. These parents do not manifest the symptoms of the condition and typically do not show signs and symptoms of the condition. Associations with other genetic disorders There are several genetic disorders that may be associated with Bardet-Biedl syndrome. Commonly other cilia related disorders may be associated with this syndrome. This includes Meckel–Gruber syndrome, Alstrom syndrome, nephronophthisis, polycystic kidney, primary ciliary dyskinesia, retinitis pigmentosa and some forms of retinal degeneration. Reviewed by April Cashin-Garbutt, BA Hons (Cantab) Sources http://ghr.nlm.nih.gov/condition/bardet-biedl-syndrome http://www.jnma.com.np/issue/172/235-237.pdf http://mun-h-center.se/upload/MunhDoc/Diagnoser/Eng/Fr%C3%A5/eLAUf.pdf http://www.cags.org.ae/pdf/209900.pdf http://www.japi.org/september2005/PC-781.pdf Further Reading Bardet-Biedl Syndrome - What is Bardet-Biedl Syndrome? Bardet-Biedl Syndrome Symptoms Last Updated: Jul 22, 2013"
39,"2018-04-20 02:31:08","Bariatric Embolization","By Dr Liji Thomas, MD Obesity affects almost half a billion people worldwide. It is fast becoming the major killer, overtaking even long-term predators such as tobacco. Its consequences range from diabetes and cardiovascular disease, which are metabolic in origin, to cancers of the endometrium, breast, and colon. Secondary complications of obesity include diabetes-linked blindness, renal failure, and psychological disturbances. Conventional Treatments for Obesity Obesity treatment has long focused on dietary regulation, exercise, and behavioral modification techniques. Some drugs have also been used in the treatment of obesity but are linked with unacceptable adverse effects. Bariatric surgery is advised in patients with morbid obesity, where the body mass index is 40 or above, or even 35 with other medical conditions. These include techniques which reduce gastric volume, or those which prevent proper digestion. These are considered to be of high efficacy in selected patient groups, both in reducing obesity and its linked complications. However, with unaltered eating habits, even bariatric surgery may be followed by a gradual return to weight gain. In this context, gastric artery embolization or bariatric arterial embolization (BAE) is emerging as a powerful tool. Bariatric Arterial Embolization The stomach is supplied by left and right gastric arteries, as well as the right gastroepiploic artery, and the short gastric arteries. Embolization of some vessels in the upper gastrointestinal (GI) tract has been a well-rehearsed practice in the treatment of GI bleeding as in portal cirrhosis with resulting portal hypertension. This technique rarely produces gut ischemia due to numerous collateral vessels in the foregut. Bariatric arterial embolization refers to percutaneous catheter-directed left gastric artery embolization in order to induce relatively poor blood supply to the fundus, the area of the stomach that produces ghrelin. At least two branches are occluded, introducing transarterially a sclerosant agent such as morrhuate or polyvinyl alcohol (PVA) beads of varying diameter. While the efficacy of embolization in reducing ghrelin secretion is unchallenged, the effect in terms of weight loss has not been proved as conclusively. The Importance of Ghrelin in Obesity The stomach is not merely a storehouse of ingested food, nor a digestive organ. It is also a neurohormonal system. The fundus carries numerous pathways for the nervous regulation of appetite and satiety. Ghrelin is a peptide hormone released mainly from the fundus of the stomach, which regulates long-term appetite and energy maintenance. It is released under conditions of hunger or starvation and stimulates the brain to initiate food intake. The next major site of ghrelin production is the duodenum, which releases the peptide at up to 20 times lower concentrations than the fundus. In response to ghrelin secretion, the following actions occur: a rise in growth hormone release a rise in gastric acid secretion Increased gastric motility faster gastric emptying reduced insulin secretion Increased ghrelin levels lead to increased adipose tissue deposition and obesity. Safety Profile of BAE Complications of the procedure have included: Pulmonary embolism Perforated gastric ulcers Gastritis Distal esophageal stricture Non-target embolization with unintended tissue damage Greater safety for the procedure involves various measures such as doing it under CT guidance, using radio-opaque alginate beams which are visualized under fluoroscopic guidance, and a special microcatheter which prevents reflux of the injected material. Trials are still underway to establish optimum procedural guidelines for patient safety. Reviewed by Susha Cheriyedath, MSc References http://evtoday.com/2014/04/gastric-embolization-to-treat-obesity/ http://www.hindawi.com/journals/jobe/2014/185349/ http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4414740/ // Last Updated: Aug 17, 2016"
40,"2018-04-20 02:31:12","Bariatric Surgery - What is Bariatric Surgery?","By Dr Ananya Mandal, MD Exercise and diet alone often fails to effectively treat people with extreme and excessive obesity. Bariatric surgery is an operation that is performed in order to help such individuals lose weight. Evidence suggests that bariatric surgery may lower death rates for patients with severe obesity, especially when coupled with healthy eating and lifestyle changes after surgery. Principles of bariatric surgery The basic principle of bariatric surgery is to restrict food intake and decrease the absorption of food in the stomach and intestines. The digestion process begins in the mouth where food is chewed and mixed with saliva and other enzyme-containing secretions. The food then reaches the stomach where it is mixed with digestive juices and broken down so that nutrients and calories can be absorbed. Digestion then becomes faster as food moves into the duodenum (first part of the small intestine) where it is mixed with bile and pancreatic juice. Bariatric surgery is designed to alter or interrupt this digestion process so that food is not broken down and absorbed in the usual way. A reduction in the amount of nutrients and calories absorbed enables patients to lose weight and decrease their risk for obesity-related health risks or disorders. Body mass index (BMI) Body mass index (BMI), a measure of height in relation to weight, is used to define levels of obesity and help determine whether bariatric intervention is required. Clinically severe obesity describes a BMI of over 40 kg/m2 or a BMI of over 35 kg/m2 in combination with severe health problems. Health problems associated with obesity include type 2 diabetes, arthritis, heart disease, and severe obstructive sleep apnea. The Food and Drug Administration (FDA) approves the use of adjustable gastric banding for patients with a BMI of 30 kg/m2 or more who also have at least one of these conditions. Types of Bariatric Surgery There are various types of bariatric surgeries that can be performed. Surgery may be performed using an “open” approach, which involves cutting open the abdomen or by means of laparoscopy, during which surgical instruments are guided into the abdomen through small half-inch incisions. Today, most bariatric surgery is laparoscopic because compared with open surgery, it requires less extensive cuts, causes relatively minimal tissue damage, leads to fewer post-operative complications and allows for earlier hospital discharge. There are four types of operations that are offered: Adjustable gastric banding (AGB) Roux-en-Y gastric bypass (RYGB) Biliopancreatic diversion with a duodenal switch (BPD-DS) Vertical sleeve gastrectomy (VSG) Diagram of Surgical Options. Image credit: Walter Pories, M.D. FACS. Related StoriesObesity surgery reduces the risk of death by half finds new studyEach of the surgery types has advantages and disadvantages and various patient factors affect which procedure is chosen including BMI, eating habits, health problems related to obesity, and number of previous stomach surgeries. The patient and provider should discuss the most suitable option by considering the benefits and risks of each type of surgery. Surgical and post-operative risks People who have had bariatric surgery need to adhere to a rigorous and lifelong diet and exercise plan to prevent complications and to avoid putting on weight after surgery. In addition, patients may develop excess loose and folded skin that requires further surgery to remove and tighten. As with all types of surgery, bariatric surgery is associated with risks including internal bleeding, deep vein thrombosis, infections, and pulmonary embolism (blood clot in the lungs). It is estimated that the risk of dying shortly after bariatric surgery is around 1 in 200. Reviewed by Sally Robertson, BSc References http://www.nhs.uk/conditions/weight-loss-surgery/Pages/Introduction.aspx http://win.niddk.nih.gov/publications/PDFs/Bariatric_Surgery_508.pdf http://www.medicine.virginia.edu/clinical/departments/medicine/divisions/digestive-health/patients/clinics/bariatric/bariatric/BARIATRIC-SURGERY.pdf http://www.siumed.edu/surgery/bariatric/files/Gastric%20bypass%20surgery%20guide.pdf http://www.lapsf.com/bariatricsurgery.pdf https://louisville.edu/medschool/gimedicine/division-lecture-files/marsano-lectures/bariatric%20surgery.pdf Further ReadingBariatric Surgery Side EffectsBariatric Surgery TypesDiet After Bariatric SurgeryWeight Loss After Bariatric SurgeryTaste Changes Following Bariatric SurgeryMore... Last Updated: Oct 7, 2014"
41,"2018-04-20 02:31:15","Bariatric Surgery Side Effects","By Dr Ananya Mandal, MD Bariatric surgery is a procedure performed on obese individuals in order to help them achieve rapid weight loss. The risks associated with bariatric surgery fall into two main categories: those related to restricted food intake and rapid weight loss and those associated with the surgical procedure itself. Accordingly, side effects can be categorized as: Immediate post-operative complications Infection of the wound and of the operative site (affects around 1 in 20 patients) Internal bleeding (occurs in around 1 in 100 patients) Development of blood clots (occurs in around 1 in 100 patients). Clots may develop in leg veins (deep vein thrombosis) or travel up to the lungs causing a pulmonary embolism, which can be life threatening. Death The immediate complications of bariatric surgery can result in a patient’s death. Pulmonary embolism, severe bleeding, major infection, stroke, or heart attack are all conditions that put the patient’s life at serious risk. The estimated risk of death after gastric band insertion is around 1 in 200 and after gastric bypass surgery, the risk is around 1 in 100. Factors that raise the risk of dying due to post-operative complications include age, male gender, high blood pressure, increased risk for pulmonary embolism and a body mass index of 50 or above. Risks for pulmonary embolism include a history of pulmonary hypertension, deep vein thrombosis, and blood clots. Development of gallstones Gall bladder stones are a common outcome of bariatric surgery, with stones developing in around 1 in 12 individuals. Gallstones are aggregates of chemicals and cholesterol that eventually clog up the gall bladder. The stones may be symptomless or may cause intense pain in the abdomen as well as nausea, vomiting and jaundice. Stoma blockage Stoma blockage is a common complication of gastric bypass surgery that occurs when the opening (stoma) that connects the stomach pouch to the small intestine becomes blocked by a piece of food, resulting in persistent vomiting. The condition occurs in around one-fifth of patients and is treated by directing a small flexible tube called an endoscope into the stoma where a balloon attached to the endoscope is inflated to remove the obstruction. To avoid stoma blockage, food must always be taken in small bites and chewed thoroughly. Excess skin Related StoriesObesity surgery reduces the risk of death by half finds new study Rapid weight loss among obese individuals results in skin becoming excessively loose and folded. Folds of skin are most typically acquired around the breasts, back, abdomen, limbs, and hips and are normally most apparent 12 to 18 months after surgery. The folds can be unsightly and may harbour moisture leading to infections and rashes. These excess skin flaps can be removed and the skin tightened using cosmetic surgery. Effects on mental health Rapid weight loss may have a detrimental effect on mental health, with many patients suffering from depression and anxiety after surgery. Patients may also develop relationship problems with their partner. Additionally, social occasions orientated around meals may make the patient feel isolated and anxious due to their much reduced appetite and restricted diet. Slippage of the gastric band Gastric band slippage is a problem that affects around 1 in 50 patients who have had an adjustable band fitted. The band slips out of position and the stomach pouch becomes bigger than it should be, resulting in nausea, vomiting and heartburn. Further surgery is then required to repair the slippage. Intolerance to foods Food intolerance occurs in around 1 in 35 patients who have had bariatric surgery and may develop years after the procedure. Foods such as red meat may bring on heartburn, nausea and vomiting. Reviewed by Sally Robertson, BSc References http://www.nhs.uk/Conditions/weight-loss-surgery/Pages/risks.aspx http://win.niddk.nih.gov/publications/PDFs/Bariatric_Surgery_508.pdf http://www.medicine.virginia.edu/clinical/departments/medicine/divisions/digestive-health/patients/clinics/bariatric/bariatric/BARIATRIC-SURGERY.pdf http://www.siumed.edu/surgery/bariatric/files/Gastric%20bypass%20surgery%20guide.pdf http://www.lapsf.com/bariatricsurgery.pdf https://louisville.edu/medschool/gimedicine/division-lecture-files/marsano-lectures/bariatric%20surgery.pdf Further ReadingBariatric Surgery - What is Bariatric Surgery?Bariatric Surgery TypesDiet After Bariatric SurgeryWeight Loss After Bariatric SurgeryTaste Changes Following Bariatric SurgeryMore... Last Updated: Aug 27, 2013"
42,"2018-04-20 02:31:19","Bariatric Surgery Types","By Dr Ananya Mandal, MD The type of bariatric surgery that is used to help extremely or morbidly obese individuals lose weight depends on a number of factors, with each type of surgery associated with advantages and disadvantages. Patients and healthcare providers need to discuss the risks and benefits of procedures before deciding on the most suitable type of surgery. Open and laparoscopic surgery An open surgery involves cutting open the abdomen and making modifications to the digestive tract. This involves making a single, large incision across the abdomen that may later take time to heal and may also lead to complications such as hernias. A laparoscopic surgery involves distending the abdomen with an inert gas and making several small half-inch incisions across it to enable insertion of surgical instruments and a small camera that can be used to aid the operating surgeon. Today, most bariatric surgery is laparoscopic because compared to open surgery, it requires smaller incisions that heal faster, are associated with fewer post-operative complications (especially hernias) and allow for early hospital discharge. However, not all patients are suitable for laparoscopy. Extremely obese individuals, those with complex medical problems such as severe heart and lung disease or those who have previously had abdominal surgery may require the open surgery approach. Types of bariatric surgery There are four types of operations that are commonly offered to patients: Adjustable gastric banding Roux-en-Y gastric bypass Biliopancreatic diversion with a duodenal switch Vertical sleeve gastrectomy Factors that are considered when choosing the surgery include: Benefits and risks associated with surgery type Patient preference and willingness to adhere to the post-surgery dietary recommendations Body mass index Eating habits Health conditions related to obesity Previous stomach surgeries Diagram of Surgical Options. Image credit: Walter Pories, M.D. FACS. Related StoriesNeurocognitive deficits worsen outcomes for joint replacement surgery, finds studyThe Human Microbiome – A New Potential Fingerprint in Forensic Evidence?Breast cancers more likely to spread after surgery finds study Adjustable Gastric Banding (AGB) The basic principle of this type of surgery is to decrease food intake with the use of a small bracelet-like band placed around the top of the stomach. The band restricts the size of the opening from the throat to the stomach, limiting the amount of food a patient can ingest. The size of the opening can be modified using a balloon inside the band that can be inflated or deflated with saline solution according to the needs of the patient. Roux-en-Y Gastric Bypass (RYGB) This method is also used to decrease food intake and involves creating a small pouch that is similar in size to the pouch created with AGB. The food bypasses the rest of the stomach and reaches the small intestine, where it is absorbed to a much lesser degree than if it had passed through the stomach, duodenum, and upper intestine. Vertical Sleeve Gastrectomy (VSG) This procedure involves removal of most of the stomach, which not only restricts food intake and absorption, but lowers levels of the hormone ghrelin that is responsible for appetite. Biliopancreatic Diversion with a Duodenal Switch (BPD-DS) Also called the duodenal switch, this three-stage procedure involves the removal of a large part of the stomach which makes the patient feel full after eating only a small meal, followed by re-routing of the small intestines to prevent food absorption. The third step involves changing how bile and other digestive juices affect the process of digesting and absorbing calories. Reviewed by Sally Robertson, BSc Sources www.nhs.uk/conditions/weight-loss-surgery/Pages/Introduction.aspx http://win.niddk.nih.gov/publications/PDFs/Bariatric_Surgery_508.pdf www.medicine.virginia.edu/.../BARIATRIC-SURGERY.pdf www.siumed.edu/.../Gastric%20bypass%20surgery%20guide.pdf http://www.lapsf.com/bariatricsurgery.pdf louisville.edu/.../bariatric%20surgery.pdf Further ReadingBariatric Surgery - What is Bariatric Surgery?Bariatric Surgery Side EffectsDiet After Bariatric SurgeryWeight Loss After Bariatric SurgeryTaste Changes Following Bariatric SurgeryMore... Last Updated: Aug 27, 2013"
43,"2018-04-20 02:31:21","Diet After Bariatric Surgery","By Dr Ananya Mandal, MD Weight loss surgery involves reducing the capacity of the stomach to hold food, and therefore the amount of calories and nutrients that can be absorbed in the intestines. A patient’s diet needs to be modified accordingly after surgery to ensure maximum nutrition while reducing calorie intake. A typical diet plan for a patient who has undergone bariatric surgery involves: The stage 1 diet that is provided at hospital immediately after surgery. This initial diet comprises mainly liquids that the patient can slowly sip until the new stomach or stomach pouch is full. The stage 2 diet is made up of low-sugar, liquid or semi-liquid foods such as warmed cereal with milk. The stage 3 diet is designed for when a patient is discharged from hospital and includes semi-solid, pureed, and finally soft foods. The progress to soft food is slow to allow time for post-operative wounds in the stomach and intestines to heal. Diet progression Initial requirements include enough liquid to prevent dehydration and sufficient protein. Later, the diet needs to be adjusted to accommodate nutritional needs. The size of the stomach pouch is about one ounce and initially, as little as two to three teaspoons of food may make the patient feel full. Over time, the pouch stretches bit-by-bit to allow more food intake. The diet’s composition Related StoriesObesity surgery reduces the risk of death by half finds new study About three quarters of the patient’s calorie intake should come from protein sources such as eggs, fish and meat, while carbohydrates such as potatoes, rice and wheat should provide 10 to 20 % of the calorie intake, and fats between 5 to 15 %. For the first six months, the diet should provide the patient with 800 to 1,000 calories and 75 grams of protein a day. Foods to avoid Foods containing sugars should be avoided, firstly because they may hamper weight loss and, secondly, because eating sugary food may lead to a condition called dumping syndrome, which describes when sugar moves directly from the stomach pouch into the small intestine where it can cause palpitations, nausea, abdominal pain and diarrhea. Liquids should be avoided for a period of 30 minutes before and after eating solid food. When taken together with solids, liquids may cause nausea, as well as pushing food through the stomach pouch at a faster rate, leading to more eating than advised to satisfy appetite. Overeating should be avoided at all costs. Overeating by even an ounce may induce nausea, vomiting or lead to stretching of the pouch. Hydration Patients must maintain good levels of hydration, with 1 ½ to 2 liters of water consumed every 24 hours. This amount is to be increased by 20% if the patient is sweating. Carbonated beverages, soft fizzy drinks, sweetened drinks, and caffeine-containing drinks need to be avoided. Maintaining nutrition Due to the decreased food intake post-surgery, patients are at risk of vitamin and mineral deficiency and diet must be supplemented with multivitamins and minerals for the rest of the patient’s life. Reviewed by Sally Robertson, BSc Sources www.nhs.uk/conditions/weight-loss-surgery/Pages/Introduction.aspx http://win.niddk.nih.gov/publications/PDFs/Bariatric_Surgery_508.pdf www.medicine.virginia.edu/.../BARIATRIC-SURGERY.pdf www.siumed.edu/.../Gastric%20bypass%20surgery%20guide.pdf http://www.lapsf.com/bariatricsurgery.pdf louisville.edu/.../bariatric%20surgery.pdf Further ReadingBariatric Surgery - What is Bariatric Surgery?Bariatric Surgery Side EffectsBariatric Surgery TypesWeight Loss After Bariatric SurgeryTaste Changes Following Bariatric SurgeryMore... Last Updated: Aug 27, 2013"
44,"2018-04-20 02:31:25","Weight Loss After Bariatric Surgery","By Sally Robertson, BSc Also called weight loss surgery, bariatric surgery is an operation performed to reduce the size of the stomach and help people to lose weight if they have become severely or morbidly obese. Bariatric surgery has proved an effective tool for helping such individuals to reduce their food intake, lose weight and improve or cure conditions they have as a result of obesity. The main bariatric surgeries are gastric bypass, a gastric band procedure and sleeve gastrectomy, all of which reduce the amount of food the stomach can hold and decrease the amount a person needs to eat in order to feel full. In order to successfully lose weight after one of these procedures, it is crucial that patients adhere to the dietary recommendations made by their healthcare provider. Diet Following Gastric Band Procedure Immediately after this operation and for the next four weeks, patients are only able to consume liquids and small amounts of pureed foods. Soft foods can usually be consumed between four to six weeks after the procedure. After six weeks, people can gradually start to follow a healthy, long-term diet that includes small, nutritious amounts of food. People should adhere to this diet plan for the rest of their lives. Although weight loss is the aim of this diet plan, nutritional content must not be overlooked. Gastric Band for Weight Loss. Image Credit: bearsky23 / Shutterstock According to the “British Obesity Surgery Patient Association” (BOSPA), there are six main rules people should follow in order to benefit the most from their surgery. These include the following: Not eating any more than three meals a day. Avoiding eating snacks in-between meal times. Consuming solid foods – These make a person feel full more easily than soft foods do. Soft foods also tend to contain more fat and carbohydrate than solid foods. Eating slowly and stopping eating once full – Food should be cut into chunks that are then chewed slowly for as long as possible before being swallowed. People should not continue to eat once they feel full because over-eating can result in pain and sickness. Avoiding drinking while eating – Drinking fluids can push food through the small stomach and leave a person feeling less full. Not consuming calorie-rich drinks – These increase the intake of calories. Water or diet drinks should be consumed instead. Diet Following Gastric Bypass and Other Types of Weight Loss Surgery A person’s progression towards a healthy diet after gastric bypass is similar to that after a gastric band procedure. Patients only consume liquids for the first week following their surgery, moving on to pureed foods between weeks two and four and soft foods between weeks four to six. After six weeks, patients can follow a healthy diet and apply the same six rules recommended by BOSPA. Gastric Bypass for Weight Loss - Image Credit: bearsky23 / Shutterstock Related StoriesObesity surgery reduces the risk of death by half finds new studyHowever, patients need to bear several additional points in mind. Sugar-rich foods should be avoided, since the bypass alters how sugar is digested and sugar consumption will trigger the production of high amounts of insulin. This can lead to what is termed “dumping syndrome,” in which nausea, diarrhea, and abdominal pain occur. The bypass also affects the body’s ability to absorb all the vitamins and nutrients it requires and patients will need to take daily vitamin and mineral supplements. The dietary recommendations following any other type of bariatric surgery are likely to be similar to those described so far, but patients can discuss any particulars with their healthcare specialist. Exercise Weight loss and maintenance of a healthy weight also involve burning calories by exercising. In addition to aiding weight loss, exercise reduces the risk of heart disease and certain cancers, as well as leading to an overall improved sense of well-being. Exercise plans patients are provided with usually recommend engaging in low-to-moderate levels of physical activity and then slowly increasing the amount of exercise over time. The exercise should be sufficient to increase the heart rate and leave the person feeling short of breath. Recommended exercises include brisk walking, cycling, swimming, stair climbing and supervised exercise programs. Of course, people are more likely to maintain their exercise plan if they choose activities they enjoy. Due to this, patients are encouraged to be creative with their plans if wished. Reviewed by Afsaneh Khetrapal BSc (Hons) Sources https://medlineplus.gov/ency/patientinstructions/000173.htm www.nhs.uk/Conditions/weight-loss-surgery/Pages/Recommendations.aspx http://www.chelwest.nhs.uk/services/surgery/weight-loss-surgery Further ReadingBariatric Surgery - What is Bariatric Surgery?Bariatric Surgery Side EffectsBariatric Surgery TypesDiet After Bariatric SurgeryTaste Changes Following Bariatric SurgeryMore... Last Updated: Mar 15, 2017"
45,"2018-04-20 02:31:27","Taste Changes Following Bariatric Surgery","By Sally Robertson, BSc Also known as weight loss surgery, bariatric surgery is a procedure carried out to help people who are severely or morbidly obese, to lose weight. Image Credit: Ursula Ferrara / Shutterstock Types of Bariatric Surgery There are four types of bariatric surgery that may be performed: Gastric band procedure – The size of the stomach is reduced using a band placed around the stomach. This reduces the amount of food a person needs to eating order to feel full. Gastric bypass – This involves dividing the stomach into a smaller upper section and larger lower section. The smaller section is then connected to part of the small intestine. Food only passes into the small stomach and this part of the small intestine, bypassing the remaining stomach and bowel. This reduces the amount of calories absorbed when food is passed through the digestive system, as well as decreasing the amount of food a person needs to eat in order to feel full. Sleeve gastrectomy – Here, a part of the stomach is removed to reduce its size and limit the amount of food intake required for a person to feel full. Sensory Changes Following Surgery Change in the taste, smell or tolerance of food following bariatric surgery is a common phenomenon. One study showed that as many as 97% of patients experience at least one such change following these surgeries. Related StoriesObesity surgery reduces the risk of death by half finds new studyFortunately, the changes often benefit patients, with research showing that they help people to lose more weight than people who do not experience any changes. According to a study conducted by researchers from the University Hospitals of Leicester, which included 103 patients who underwent gastric bypass, 73% reported changes in the taste of food and almost 50% reported changes in smell. The most commonly reported taste changes were heightened sensitivity to sweet food, sour food and fast food. Some patients also developed an oversensitivity to sweetness in protein shakes, which can be a problem should patients need to follow a liquid-only diet after their operation. If this happens, a patient should talk to their doctor to ensure their dietary requirements s are being met. Eating behaviors may also change following bariatric surgery. Patients may be less likely to find emotional eating is a problem and eating cues may have less impact. Evidence also suggests that the mood-altering effect of sweet foods may be reduced, with patients less likely to experience a “sugar high” after a bariatric procedure. The tendency to eat purely as a matter of habit may also fade. Cause The exact cause of these changes following bariatric surgery is not yet clear, but many researchers suspect that fluctuating gut hormones and the effect these have on the nervous system may play a role. The central nervous system relays hunger, craving and satiety messages between the brain and gastrointestinal tract. The nerves that carry these messages are affected when a part of the stomach removed, which impacts a person’s sense of taste, smell and satiety. Ghrelin is a hormone that plays an important role in hunger. A reduced calorie intake and weight loss leads to increased ghrelin production, which makes people feel hungry. In contrast, weight loss as a result of bariatric surgery leads to decreased ghrelin production, therefore reducing hunger and food intake following the procedure. Another important hormone, which is involved in satiety, is leptin. This relays messages between the gut and brain about how full a person is and determines whether calories are burned or stored as fat. Losing weight is thought to increase a person’s sensitivity to these messages, resulting in a person feeling full more easily after eating only small amounts of food. Reviewed by Afsaneh Khetrapal BSc (Hons) Sources bariatrictimes.com/.../ www.njbariatriccenter.com/.../ www.nhs.uk/Conditions/weight-loss-surgery/Pages/Introduction.aspx Further ReadingBariatric Surgery - What is Bariatric Surgery?Bariatric Surgery Side EffectsBariatric Surgery TypesDiet After Bariatric SurgeryWeight Loss After Bariatric SurgeryMore... // Last Updated: Mar 15, 2017"
46,"2018-04-20 02:31:30","Metabolic Syndrome and Bariatric Surgery","By Sally Robertson, BSc Also called weight loss surgery, bariatric surgery is a procedure used to treat people who have become dangerously obese. Life-threatening obesity is defined by the following: A body mass index (BMI) of 40 or more. A BMI of 35 or more and the presence of a serious metabolic risk factor that would benefit from weight loss such as type 2 diabetes or hypertension. Types of Bariatric Surgery The three main types of bariatric surgery include: Gastric band procedure – The size of the stomach is reduced by the use of a band placed around the stomach. By effectively reducing the storage capacity of the stomach, it follows that less ingested food is required to make a person feel full. Gastric bypass – The stomach is divided into a smaller upper portion and a larger lower portion. The smaller section is connected to a part of the small intestine. Food then only passes into the smaller part of the stomach and this section of the intestine, bypassing the remaining stomach and bowel. The new stomach absorbs less calories than before and this reduces the amount of food a person needs to eat to make them feel full. Sleeve gastrectomy – A part of the stomach is removed to reduce its size and make a person feel full after eating only small portions of food. People who are morbidly obese have a 50 - 100% increased risk of dying prematurely, compared with healthy individuals, and bariatric surgery reduces this risk by up to 40%. The procedure does this by quickly and effectively reducing body fat and can help to prevent, improve or even resolve over forty metabolic conditions related to obesity, including the following: Heart disease Type 2 diabetes Certain cancers Gastroesophageal reflux disease Hypertension Joint problems Sleep apnea Metabolic Syndrome “Metabolic syndrome” is the collective term for the health factors that increase the risk of metabolic conditions such as heart disease, stroke, diabetes, non-alcoholic fatty liver disease and coronary artery disease. Metabolic syndrome, signs and symptoms. Image Credit: Designua / Shutterstock Related StoriesRed and processed meat may increase the risk of liver diseaseExercise could extend the life expectancy of breast cancer survivors, study statesObesity surgery reduces the risk of death by half finds new studyIn general, compared to a person who does not have metabolic syndrome, a person who does have it is at twice the risk of developing heart disease and five times the risk of developing diabetes. The risk of developing metabolic syndrome is associated with excessive weight, obesity and inadequate levels of physical activity. Insulin resistance, which is associated with being overweight and obese, is another risk factor. Insulin resistance is a condition in which the body fails to use insulin effectively, and the blood sugar level rises as a direct result. The reasons why bariatric surgery can improve diabetes and other conditions are not yet clear, although the benefits are mainly assumed to result from the weight loss patients achieve, which is usually around a quarter of their overall weight. However, in the 1980s, clinicians observed fast metabolic changes in some patients after they had undergone surgery, which triggered curiosity over other potential factors involved. There has been much research interest in this area, with scientists performing a range of studies to try to identify the potential mechanisms underlying the ability of the digestive system to adapt to its rearrangement. Researchers hope to eventually be able to use such research to establish which patients will show the most positive effects in response to treatment. They also hope it will lead to the possibility of metabolism being altered in patients, without them having to undergo surgery. Reviewed by Afsaneh Khetrapal BSc (Hons) Sources www.nature.com/.../...ht-loss-surgery-a-gut-wrenching-question-1.15560 bariatric.surgery.ucsf.edu/.../metabolic-syndrome.aspx https://asmbs.org/resources/metabolic-and-bariatric-surgery www.nhs.uk/Conditions/weight-loss-surgery/Pages/Introduction.aspx Further ReadingBariatric Surgery - What is Bariatric Surgery?Bariatric Surgery Side EffectsBariatric Surgery TypesDiet After Bariatric SurgeryWeight Loss After Bariatric SurgeryMore... Last Updated: Mar 15, 2017"
47,"2018-04-20 02:31:37","Bariatric Surgery Research","By Sally Robertson, BSc Bariatric surgery is a procedure that makes changes to the digestive system in order to help people with severe or morbid obesity to lose weight. Research has shown that, depending on which form of surgery they have, many individuals who undergo bariatric or weight loss surgery manage to lose around 15% to 30% of the weight they were prior to surgery. However, none of the procedures can guarantee weight loss and some individuals are disappointed with the results. Factors that may influence how much weight is lost post-operatively include how obese the person was in the first place and the surgical method applied. The main procedures in bariatric surgery include Roux-en-Y gastric bypass, gastric band and sleeve gastrectomy. Currently, research is ongoing into the safety, effectiveness, and long-term outcomes of the different procedures, as well as the possibility of alternative, non-surgical treatment options. A study by K Ryan and R Seeley (University of Cincinnati, Ohio, US) investigated how vertical sleeve gastrectomy (VSG) leads to health benefits for obese individuals. VSG involves a reduction in stomach size of around 80% and the creation of a gastric “sleeve” to connect the small intestine to the esophagus. The procedure is known to increase the amount of circulating bile acids, which bind to a receptor that regulates the expression of a gene called farsenoid-X receptor (FXR). To investigate whether the influence VSG has on weight loss is associated with FXR, the team compared knock-out mice that did not have the FXR receptor to mice that did have the receptor. As reported in Nature in 2014, all of the mice were fed a high-fat diet until they became obese and then subjected to VSG. Following the procedure, all mice lost weight and their glucose tolerance improved. The composition of their gut microbes also changed. However, among the mice that did not have the FXR receptor, the improved glucose tolerance and weight loss were significantly less than that among the FXR mice. Related StoriesObesity surgery reduces the risk of death by half finds new studyauthors say the finding suggests that the health benefits resulting from VSG were not just down to the reduced stomach size, but to a higher level of circulating bile acids and altered gut microbes as a result of FXR signaling. Seeley says that manipulation of gut microbes may provide a way of imitating the effects of surgery, “without having to do the cutting and stapling.” In a study published in the International Journal of Obesity in 2016, A McCullough (Cleveland Clinic, Ohio, US) and colleagues investigated the efficacy and safety of bariatric surgery in patients with non-alcoholic fatty liver disease (NAFLD) and advanced fibrosis. Currently, the procedure is safely performed in people with NAFLD who only have minimal fibrosis (stage 1 to 2) and the benefits and safety of the procedure for patients with stage 3 to 4 fibrosis are not clear. The team compared patient outcomes between 99 patients with stage 3 to 4 fibrosis (group 1) and 198 patients with stage 1 to 2 fibrosis (group 2) over a one-year period, following bariatric surgery. Although group 1 patients did require a longer hospital stay than group 2 patients (4 versus 3 days), there was no significant difference in the proportion of people who experienced post-operative complications, at 36.4% versus 32.8%. Group 1 also had significantly higher transaminase levels than group 2, which improved over the one-year follow-up period. The authors say the findings suggest that post-operative complications are no more likely to occur among patients with advanced versus minimal fibrosis, following bariatric surgery. The improved transaminase level also implies that bariatric surgery results in reduced inflammation in the livers of those with advanced fibrosis. Other examples of research include a study by M Svane (Copenhagen University Hospital Hvidovre, Denmark), which concluded that increased postprandial secretion of glucagon-like peptide-1 and peptide YY among patients who have had a gastric bypass, may account for the reduced appetite and weight loss people experience as a result of the procedure. This research was published in Nature in 2016. Another study published in BMJ Open in 2016 looked at the effects that the experiences and expectations of individuals who undergo bariatric surgery may have on post-operative outcomes. C Homer (Sheffield Hallam University, Sheffield, UK) and colleagues found that patients unrealistically expected to see major physical and psychological improvement following the procedure. The expectations stemmed from feelings of stigma and shame and experiences of failed attempts at weight loss in the past. The authors concluded that the expectation could have negative effects on post-operative outcomes and that healthcare providers should address any feelings of shame or stigma, so as to modify expectations following surgery. Reviewed by Susha Cheriyedath, MSc Sources http://www.nature.com/ijo/journal/v41/n3/full/ijo2016212a.html www.nih.gov/.../new-insights-into-bariatric-surgery-obesity www.nhs.uk/conditions/weight-loss-surgery/Pages/Introduction.aspx www.niddk.nih.gov/.../definition-facts.aspx http://www.nature.com/ijo/journal/v40/n11/full/ijo2016121a.html http://bmjopen.bmj.com/content/6/2/e009389 Further ReadingBariatric Surgery - What is Bariatric Surgery?Bariatric Surgery Side EffectsBariatric Surgery TypesDiet After Bariatric SurgeryWeight Loss After Bariatric SurgeryMore... // Last Updated: Aug 3, 2017"
48,"2018-04-20 02:31:40","What is a Barium-Meal?","By Dr Ananya Mandal, MD Principles of Barium meal A barium meal is a diagnostic test used to detect abnormalities of the esophagus, stomach and small bowel using X-ray imaging. X-rays can only highlight bone and other radio-opaque tissues and would not usually enable visualization of soft tissue. However, infusion of the contrast medium barium sulfate, a radioopaque salt, coats the lining of the digestive tract, allowing accurate X-ray imaging of this part of the abdomen. The images produced are fluoroscopic and can be viewed in real-time as well as on plates. Who can perform a Barium meal test? A barium meal can be performed by a radiologist (or radiographer) who has specialist skills in imaging studies and works as a healthcare professional to diagnose and treat illness. Procedure Before a barium meal test is performed, the duodenum needs to be empty to allow clear visualization of structures. A patient may be given a laxative the night before the procedure to ensure the small bowel is empty at the time of the test, which is usually performed on an empty stomach. The patient is first asked to change into a hospital gown and remove all jewellery, dentures, glasses, metal objects and clothing as these items can interfere with imaging. First, some fizzy granules, called carbex granules are given to the patient to create gas and expand the stomach for clearer viewing. Next, the barium contrast liquid is given to the patient to drink. Some initial images are taken to check that the barium has passed through the esophagus, and into the stomach and small bowel. The radiographer then takes a series of X-ray images over time as the barium contrast moves through the digestive system. This may mean images are taken over anywhere between 1 and 4 hours. Once the barium contrast has passed through to the large bowel or the colon, more pictures are taken. The whole test may take around 5 hours. Why is this procedure performed? Barium meal examination is usually performed to help diagnose various diseases or disorders of the digestive system. These include constrictions, hernias, obstructions or masses in the esophagus or stomach, and inflammatory or other diseases of the intestines. Risks Exposure to X-rays carries a similar risk as exposure to ionizing radiation. However, the amount of radiation a person is exposed to during an X-ray is is very low and risks are minimal. There are no risks associated with the barium liquid because it is not absorbed by the body. Some patients, however, are at risk of breathing in or aspirating the barium. X-rays are also harmful to unborn babies and should be avoided by women who are or may be pregnant. Women are asked details of the dates of their last menstruation to ensure the test is performed while the risk of pregnancy is at its lowest. After the test Some patients may feel abdominal bloating after a barium meal test and the test may also lead to constipation. Patients are therefore advised to drink plenty of fluid and eat plenty of fruit and vegetables. Mild laxatives may also help. Stools may be pale or whitish for a few days after the test. Reviewed by Sally Robertson, BSc References http://www.nationalcapitaldiagnosticimaging.com.au/wp-content/uploads/2010/06/NCDI_018_BariumMeal_PIB-web.pdf http://www.ouh.nhs.uk/patient-guide/leaflets/files%5C100204bariummeal.pdf http://www.guysandstthomas.nhs.uk/resources/patient-information/radiology/Havingabariummealandfollowthrough.pdf http://www.scumj.eg.net/pdf/vol11-n1-2008/19.pdf http://prpimaging.com.au/Assets/Downloadablefile/PRP-Barium-Meal-15253.pdf http://www.liv.ac.uk/HumanAnatomy/phd/mbchb/travel/ba2.html Last Updated: Aug 27, 2013"
49,"2018-04-20 02:31:46","What is a Barium-Enema?","By Dr Ananya Mandal, MD A barium enema, in principle, is similar to a barium meal or barium follow-through but is used specifically to obtain X-ray images of the large intestine. Unlike the barium meal and follow through procedures where a patient swallows the barium solution, the barium enema involves insertion of a small tube via the anus into the colon where the liquid is then infused. When is this test performed? A barium enema is performed in cases of suspected bowel polyps or diverticulitis. Patients with abdominal pain or bleeding on defecation may be advised to have this test. Procedure The lower intestine needs to be completely empty before the barium enema is performed, so the patient is usually given a laxative the night before the procedure is due. A patient may also be advised to restrict their diet to soft or liquid food intake for two days prior to the test. The patient is instructed not to eat or drink anything after midnight before the enema, as residual food matter shows up on X-ray and interferes with image interpretation. At the hospital, a patient is asked to remove dentures, jewellery, clothes and all metallic objects from their person and to wear a hospital gown. Metals may compromise image accuracy. Once in the X-ray room, the patient is laid on a tilting table, over which an X-ray tube is suspended and connected to a monitor where images are displayed. The first image taken is checked to ensure the lower abdomen is clear. Next, the enema tube is inserted into the rectum via the anus. The tube is lubricated with a local anesthetic to numb any pain. Liquid barium flows through the enema tip a little at a time, coating the wall of the lower intestine and allowing radiographic visualization of the gastrointestinal tract. After the barium is infused, the patient is asked to turn over to one side as this helps the physician study the colon and obtain a series of X-rays. The patient may feel a pressure or fullness in the bowel and have an urge to defecate, but they are asked to try and hold in the enema until the procedure is complete. Afterwards, the toilet may be used to expel the enema and another image is then taken to check there is no residual barium in the large intestine. In some patients, air may be introduced along with the barium solution. This procedure is commonly called a double-contrast or air-contrast barium enema. The underlying principle is that air expands the walls of the colon, allowing the radiographer to view the barium-coated lining in more detail. Risks Exposure to X-rays carries a similar risk as exposure to ionizing radiation. However, the amount of radiation a person is exposed to during an X-ray is very low and risks are minimal. No risks are associated with the use of barium liquid because it is not absorbed by the body. X-rays are harmful to unborn babies and should be avoided by women who are or may be pregnant. The test is performed on females within ten days of the first day of their last menstruation, when the risk of pregnancy is low. After the test Some patients may feel abdominal bloating or cramping after a barium enema and the procedure may also lead to constipation. Patients are therefore advised to drink plenty of fluids and eat plenty of fruit and vegetables. Mild laxatives may also help. Stools may be pale or whitish for a few days after the test. Reviewed by Sally Robertson, BSc Sources www.ouh.nhs.uk/patient-guide/leaflets/files%5C100204bariumenema.pdf http://www.cw.bc.ca/library/PDF/pamphlets/BCCH1093BariumEnema.pdf http://www.iowaradiology.com/quickguide/Fluoro_Barium_Enema.pdf http://www.asrt.org/docs/PatientPages/BarEnema_PaPg.pdf // Last Updated: Aug 27, 2013"
50,"2018-04-20 02:31:49","Barrett's Esophagus - What is Barrett's Esophagus?","By Dr Ananya Mandal, MD Barrett's esophagus is a condition in which the flat, squamous cells lining the esophagus (food pipe) are replaced by columnar shaped cells resembling those present in the lining of the intestines. This change in the cellular lining is called metaplasia and is not usually associated with any signs or symptoms. The Healthy Esophagus The esophagus contains two sphincters or muscular gates at either end. When a person swallows, the upper sphincter relaxes to allow food or drink to pass from the mouth into the esophagus and the lower sphincter opens to let food into the stomach. The lower esophageal sphincter then rapidly closes to prevent the food or drink from leaking out of the stomach and back into the esophagus and mouth. Risk Factors for Barrett's Esophagus Barrett's esophagus is most commonly found in people with gastroesophageal reflux disease (GERD). Also called acid reflux disease, GERD occurs when the lower esophageal sphincter opens at inappropriate times or does not close properly, allowing the contents of the stomach to seep back into the esophagus. If GERD is left untreated, it can eventually lead to complications such as ulcer, scarring, narrowing of the esophagus or Barrett's esophagus. Although people who do not have GERD can develop Barrett's esophagus, the condition is found about three to five times more often in people who have GERD. Other risk factors include: Age: Barret's esophagus is commonly diagnosed in middle-aged and older adults, with an average age-at-diagnosis of 50 to 55 years. Barrett's esophagus is uncommon in children. Male gender: Men are twice as likely as women to develop Barrett's esophagus. Lifestyle: Smokers are more frequently diagnosed with Barrett's esophagus than nonsmokers. Outcome Barrett's esophagus may occasionally give rise to esophageal cancer. Less than one percent of people with Barrett's esophagus develop cancer but of those who do, Barrett's esophagus may well have been present for several years. Barrett's esophagus affects about one percent of adults in the United States. Diagnosis Detection of the condition is difficult as there may be few or even no symptoms. Physicians recommend that adults older than 40 who have had GERD for a number of years undergo a screening procedure called upper gastrointestinal endoscopy to test for the disease. The procedure involves inserting a thin flexible tube with a light and camera into the esophagus to view the inner lining. Surgical instruments can be slid through the tube to remove a small piece of tissues if a site appears to be affected, a process called biopsy. The tissue is then sliced into thin, microscopic sections, fixed onto a glass slide and stained with appropriate dyes. The slide is then examined under the microscope and checked for any alteration in cellular pattern. Treatment Treatment of Barrett's esophagus may be endoscopic or surgical. The endoscopic therapies available include destroying the altered wall lining using ablation techniques such as laser beam therapy or cryotherapy. The goal of the treatment is to encourage normal esophageal tissue to replace the damaged and destroyed areas. Surgical therapy involves removal of the affected segments of the esophagus. Those with severe cellular changes may require complete removal of the esophagus. Reviewed by Sally Robertson, BSc Sources http://digestive.niddk.nih.gov/ddiseases/pubs/barretts/barretts.pdf http://www.bsg.org.uk/pdf_word_docs/Barretts_Oes.pdf http://gastro.ucsd.edu/fellowship/Documents/BarrettEsophagus.pdf gastroconsa.com/pdfs/patient_education/GCSA_Barretts-Esophagus.pdf http://s3.gi.org/patients/gihealth/pdf/barretts.pdf www.ldh.nhs.uk/.../Barretts_oesophagus_L&D_2011.pdf Last Updated: Oct 7, 2014"
51,"2018-04-20 02:31:53","What Causes Barrett's Esophagus?","Barrett’s esophagus (BE) is an abnormal metaplastic change in the esophageal epithelium (similar to intestinal tissue). BE may progress into esophageal adenocarcinoma, which is a rare cancer type. Even though the risk of converting BE to cancer is low, periodic checkups for precancerous cells or dysplasia must be performed. Usually, BE does not have any symptoms, but when associated with gastroesophageal reflux disease (GERD), it exhibits symptoms that include repeated heartburn, trouble swallowing, bloody vomit, and tarry stools. Causes The specific cause of BE is not exactly known, but one of the major risk factors is gastroesophageal reflux disease (GERD). People with long-term GERD are at higher risk of BE. In GERD, the sphincter valve at the lower end of the esophagus is damaged and allows the back flow of acids from the stomach into the esophagus. Patients with GERD are found to have metaplasia in the cells lining the wall of the esophagus because of the acid. This consequently leads to BE. Ten to twenty percent of patients with GERD present with BE. It is also possible for the people without GERD to develop BE. But the condition with GERD occurrs 3 to 5 times more often in people with GERD than people without GERD. The other risk factor for BE is hiatal hernia in which an acidic sack-like muscle from the stomach protrudes through diaphragm into the esophagus and thereby decreases the peristalsis. This in turn can cause BE. In studies, patients affected with GERD who progressed to BE were diagnosed with hiatal hernia. Other Risk Factors Age, Sex, and Race The risk factors for BE are dependent age, sex, and race, as well as few other factors like tobacco smoking, and heartburn symptoms that last longer than ten years. P eople aged 60 years and above are most often diagnosed with BE. There is often a delay of 10 to 20 years before BE is diagnosed. . When compared with women, men tend to have three to four times the chance of developing BE. In addition, BE is more prevalent among c aucasian people. Obesity A nother risk factor for BE is obesity. A case-control study was conducted by comparing patients affected with and without BE. That study demonstrated that there is a direct relationship between high body mass index (BMI) and BE. A meta-analysis also concluded that people with a BMI higher than 30 kg/m2 are at greater risk of BE than the people with a BMI lower than 30 kg/m2. In another case-control study by Edelstein and colleagues, it was reported that the total risk for BE was greater in people with higher waist and hip ratios. Alcohol Alcohol consumption has also been considered as a risk factor for BE. Studies have shown an association between alcohol consumption and BE. BE occurs more commonly in people consuming alcohol at the highest level than people at a lower level. Diabetes and Metabolic Syndrome Type 2 diabetes increases risk for BE by 49% , while metabolic syndrome carries a 2-fold increase in risk in people with or without the symptoms of acid reflux. S tudies indicate that the increased risk of BE from both of these factors (diabetes and metabolic syndrome) is independent of other risk factors such as BMI, alcohol consumption, and smoking. Absence of Heliobacter pylori Infection Infection by Heliobacter pylori (H. pylori) causes gastritis, stomach ulcers, and gastric cancers. However, it was found that BE and bacterial infection are inversely related when endoscopically comparing people with and without BE. The bacterium has a strong relationship with abnormal change in the cells of the intestine and the stomach. The bacterial infection prevents BE by reducing the secretion of gastric acid. A study on H. pylori found that infection with a cytotoxin-associated gene A (cagA+) strain shields against BE. Another study from Japan also indicates that people with BE have a lower prevalence of Helicobacter infection. Therefore, absence of H. pylori infection can increase the risk of BE. The other risk factors for BE are lower birth weight, obstructive sleep apnea (OSA), and increased adipokine and cytokine levels. People who were born less at than 32 weeks of gestation are more likely to develop BE. OSA associated with a proinflammatory condition may lead to BE. Furthermore, the levels of cytokines and adipokines produced by adipose tissue were high in patients affected with BE. Reviewed by Catherine Shaffer, M.Sc. Sources Mayo Clinic, Barrett’s esophagus, www.mayoclinic.org/.../dxc-20322961 NIH, Symptoms & Causes of Barrett's Esophagus, www.niddk.nih.gov/.../symptoms-causes Barrett’s oesophagus, www.macmillan.org.uk/.../barretts-oesophagus.html NIDDK, Barrett’s esophagus, http://www.ecnb.org/pdf/barretts.pdf Barrett’s esophagus: Incidence, etiology, pathophysiology, prevention and treatment, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2387291/ Pubmed Health, Barrett’s esophagus, https://www.ncbi.nlm.nih.gov/pubmedhealth/PMHT0025308/ The prevalence of Helicobacter pylori infection and the status of gastric acid secretion in patients with gastroesophageal junction adenocarcinoma in Japan, https://link.springer.com/article/10.1007/s10787-006-1549-x Risk factors for Barrett’s esophagus, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5121541/ Further ReadingBarrett's Esophagus - What is Barrett's Esophagus?Barrett's Esophagus SymptomsBarrett's Esophagus PathologyBarrett's Esophagus TreatmentsBarrett's Esophagus GeneticsMore... // Last Updated: Oct 24, 2017"
52,"2018-04-20 02:31:55","Barrett's Esophagus Symptoms","By Dr Ananya Mandal, MD Barrett's esophagus may present with very few or even no symptoms. Some of the risk factors that are associated with Barrett's esophagus, however, may provide clues to the cause and symptoms of this condition. Risk factors and features associated with Barrett's esophagus Gastroesophageal reflux disease: Barrett's esophagus is most commonly found in people with gastroesophageal reflux disease (GERD), a condition that occurs when the lower esophageal sphincter opens at inappropriate times or does not close properly. Although people who do not have GERD can develop Barrett's esophagus, the condition is about three to five times more common in people who also have GERD. Among individuals with Barrett's esophagus, GERD may well have been present for a decade or more. Age: Barrett's esophagus is often diagnosed in middle-aged and older adults with an average age-at-diagnosis of 50 to 55 years. The condition is rarely found in children. Gender: Men are twice as likely as women to develop Barrett's esophagus. Lifestyle: Smokers are more frequently diagnosed with Barrett's esophagus than nonsmokers. Symptoms common to both Barrett's esophagus and GERD Symptoms that are associated with both Barrett's esophagus and GERD include: Heartburn: Heartburn is a feeling of discomfort or a burning sensation that occurs beneath the breast bone and is caused due to irritation of the inner lining of the esophagus by a backflow of acid from the stomach. The pain worsens after eating or when bending over or lying down. The pain may resemble the pain felt during a heart attack or as a result of angina. Regurgitation of reflux: Acid from the stomach may sometimes be regurgitated into the back of the mouth, causing a sour or bitter taste in the mouth or throat. Some patients may experience nausea or even vomit. Regurgitation of reflux may also lead to a persistent dry cough and if acid seeps into the airways, it may trigger asthma symptoms, pneumonia, lung abscesses, or pulmonary fibrosis. Regurgitation of reflux may manifest in the following ways: There may be repeated burping Some patients experience water brash or excessive salivation Seepage of the acid into the wind pipe may lead to inflammation of the larynx or voice box, leading to laryngitis and a hoarse and raspy voice Persistent acid in the mouth may lead to decaying and erosion of the teeth's enamel and therefore tooth decay There may be pain over the abdomen and bloating in some individuals Reviewed by Sally Robertson, BSc Sources http://digestive.niddk.nih.gov/ddiseases/pubs/barretts/barretts.pdf http://www.bsg.org.uk/pdf_word_docs/Barretts_Oes.pdf http://gastro.ucsd.edu/fellowship/Documents/BarrettEsophagus.pdf gastroconsa.com/pdfs/patient_education/GCSA_Barretts-Esophagus.pdf http://s3.gi.org/patients/gihealth/pdf/barretts.pdf www.ldh.nhs.uk/.../Barretts_oesophagus_L&D_2011.pdf Last Updated: Sep 23, 2013"
53,"2018-04-20 02:31:59","Barrett's Esophagus Pathology","By Dr Ananya Mandal, MD Barrett's esophagus is a condition characterized by abnormal alterations in the cells that line the esophagus. A normal esophagus is lined with flat squamous cells, while in the case of Barrett's esophagus, these cells adopt a tall columnar shape that closely resembles that of the cells found in the linings of the intestines. Sometimes called columnar-lined esophagus, the condition is diagnosed when these columnar cells are identified on endoscopy or microscopic analysis. The abnormal cells have an increased likelihood of becoming dysplasic over time and Barrett's esophagus is therefore considered a risk factor for esophageal cancer. Pathology Barrett's esophagus occurs as a result of long-standing and severe gastro-esophageal reflux disease (GERD). When acid regurgitation has occurred over a long-term period, the lower end of the esophagus and its mucosal lining can become inflamed and irritated on exposure to the gastric acids. In a small proportion of people with long term GERD, the cells of the esophageal lining adopt the columnar shape of the intestinal cells. In addition to GERD, a patient may also have had duodeno-gastro-esophageal reflux, which leads to reflux of the contents of the duodenum (first part of the small intestines) into the esophagus. In such cases, the lining of the esophagus is exposed to the corrosive and injurious effects of both the gastric acids and the bile present in the duodenum. With repeated exposure to acids, the lower end of the esophagus becomes inflamed which can eventually induce esophageal stem cells to produce new cells in an attempt to repair the tissue and, over time, the cells lining the esophagus may change into columnar cells. The extent of this cell metaplasia depends on the duration and severity of exposure to the acids as well as on the nature of the cytokine response or inflammatory response to injury. Risk factors Research suggests that there is an association between Barret's esophagus and smoking cigarettes, and alcohol consumption is also thought to be a risk factor. In addition, both smoking and alcohol consumption are in fact risk factors for GERD. By contrast, Helicobacter pylori infection has been shown to be protective against the development of Barret's esophagus, as the infection leads to reduced gastric acidity, thereby reducing the likelihood and extent of GERD. Reviewed by Sally Robertson, BSc Sources http://digestive.niddk.nih.gov/ddiseases/pubs/barretts/barretts.pdf http://www.bsg.org.uk/pdf_word_docs/Barretts_Oes.pdf http://gastro.ucsd.edu/fellowship/Documents/BarrettEsophagus.pdf gastroconsa.com/pdfs/patient_education/GCSA_Barretts-Esophagus.pdf http://s3.gi.org/patients/gihealth/pdf/barretts.pdf Further ReadingBarrett's Esophagus - What is Barrett's Esophagus?What Causes Barrett's Esophagus?Barrett's Esophagus SymptomsBarrett's Esophagus TreatmentsBarrett's Esophagus GeneticsMore... Last Updated: Sep 23, 2013"
54,"2018-04-20 02:32:08","Barrett's Esophagus Treatments","By Dr Ananya Mandal, MD The therapeutic approach to Barrett's esophagus involves treating a patient's symptoms as well as the disease itself. Symptoms of this condition primarily manifest as a result of gastro esophageal reflux disorder (GERD), the most common cause of Barrett's esophagus. Therefore, treatment of GERD is a central focus for relieving symptoms in patients with Barrett's esophagus. Treatment of GERD Treatment is based on lifestyle changes as well as medications. Medications include: Antacids: Available over the counter, these agents neutralize gastric acid and relieve the symptoms of heartburn and acid reflux. These drugs should not be taken along with other medications for GERD, due to the possibility of drug-to-drug interaction that may reduce their efficacy. Proton-pump inhibitors (PPIs): Patients who fail to respond to over-the-counter medications and lifestyle changes are prescribed PPIs such as omeprazole, pantoprazole, rabeprazole and lansoprazole, all of which reduce the acid produced by the stomach. H2-receptor antagonists: These are a variety of drug that may be taken along with or in place of PPIs. These agents include ranitidine, cimetidine and famotidine which all work by blocking the effects of histamine in helping to produce stomach acid. Lifestyle changes include: Weight reduction Cessation of smoking Eating smaller and more frequent meals Avoidance of alcohol, coffee, chocolate, and fatty or spicy foods. Eating a healthy, balanced diet and exercising regularly Sleeping with head propped up Avoidance of tight clothes, especially around the abdomen Treatment stages for Barrett's Esophagus During the early stages of the condition when a patient has low-grade dysplasia, acidsuppressing medication is either initiated or increased. Endoscopic examinations are performed every six months to monitor the esophageal tissue for growth or change in cancer status. During the later stages of dysplasia, treatment options are decided on after taking into consideration factors such as the patient's age, health status and the physician's preference. Surgical options include partial or entire removal of the esophagus (esophagectomy) and the removal of affected mucosa (endoscopic mucosal resection). Affected mucosa may also be destroyed using photodynamic or other ablation therapies. Surgery for Barrett's esophagus People with severe reflux may benefit from surgical procedures. Barrett's esophagus leads to precancerous changes in the lower part of the esophagus, which if left untreated, may progress to advanced changes and eventually cancer that may spread and affect surrounding tissues. There are several surgical options available to patients and these include: Esophagectomy: This is used only in cases of high-grade dysplasia or cancer and involves removing either the whole or part of the esophagus to prevent cancerous invasion of surrounding tissue. Endoscopic mucosal resection (EMR): During this procedure, a large but thin area of esophageal tissue is removed using an endoscope. Endoscopic tissue samples can then be sent for examination to aid treatment decisions. EMR is the preferred alternative to esophagectomy in patients with high-grade dysplasia or early stage esophageal cancer. Photodynamic therapy: This technique employs chemicals called photosensitizers which become toxic to diseased cells on exposure to light. Other ablation techniques: Affected tissue may also be ablated using laser beams, electro cauterization or cryotherapy. Reviewed by Sally Robertson, BSc Sources http://digestive.niddk.nih.gov/ddiseases/pubs/barretts/barretts.pdf http://www.bsg.org.uk/pdf_word_docs/Barretts_Oes.pdf http://gastro.ucsd.edu/fellowship/Documents/BarrettEsophagus.pdf gastroconsa.com/pdfs/patient_education/GCSA_Barretts-Esophagus.pdf http://s3.gi.org/patients/gihealth/pdf/barretts.pdf www.ldh.nhs.uk/.../Barretts_oesophagus_L&D_2011.pdf Further ReadingBarrett's Esophagus - What is Barrett's Esophagus?What Causes Barrett's Esophagus?Barrett's Esophagus SymptomsBarrett's Esophagus PathologyBarrett's Esophagus GeneticsMore... Last Updated: Sep 23, 2013"
55,"2018-04-20 02:32:14","Barrett's Esophagus Genetics","Although epidemiologic studies point to environmental factors, obesity, smoking, esophageal reflux, and diet as the main causes of Barrett’s esophagus (BE), there is growing evidence of a genetic predisposition as well. It is now fairly clear that the role of genetics is greatest in the initial stages of the disease. Intestinal (Barrett's) metaplasia of the esophagus is a response to injury from acid reflux (heartburn). It is associated with dysplasia and adenocarcinoma. Endoscopic biopsy photomicrograph. Image Credit: David Litman / Shutterstock A number of research studies on this subject have concluded that three genes are primarily responsible for this condition. These genes are thought to play a vital role in increasing the risk of Barrett’s esophagus following their transformation or mutation. These are CTHRC1, ASCC1, and MSR1, also called the predisposition genes, as they do not actually cause Barrett’s esophagus unless in mutated form. Genes Responsible for Barrett's Esophagus (BE) The germline mutations in the predisposition genes cause the progress of esophageal disorders. Also, the mutations in the MSR1, CTHRC1, and ASCC1 genes are associated with BE and esophageal adenocarcinoma (p<0.001). BE is typically identified only in the terminal phase, which endangers the patient severely. Esophageal carcinomas arise from the pre-existing condition of BE, which in turn develops as a result of chronic gastroesophageal reflux which produces chronic inflammation. MSR1 gene: The MSR1 gene encodes the A class scavenger macrophage receptors that include Type 1, Type 2, and Type 3. All the aforementioned types are due to random splicing of the MSR1 gene. These isoforms are macrophage-specific integral glycoproteins of the cell membrane and have been associated with several macrophage-associated pathological and physiological processes. These include atherosclerosis, host defenses, and Alzheimer’s disease. Type 1 and Type 2 genotypes are known as the operative receptors, which are capable of intermediating the modified low density lipoproteins (LDLs) in endocytosis. The position of the MSR1 gene is on the short arm (p) of chromosome 8 at position 22 (8p22). ASCC1 gene: The ASCC1 gene encodes a subunit that activates the signal co-integrator 1 (ASC-1). The ASC-1 complex is defined as the transcriptional co-activator that performs a vital role in transactivation of the gene through multiple transcription elements comprising protein 1 called AP-1, serum factor (SRF), and nuclear factor kappa-B. All these encoded proteins carry an N-terminal KH-type RNA-binding motif that is important for AP-1 transactivation through ASC-1 complex. Mutations in this gene are associated with both esophageal adenocarcinoma and Barrett’s esophagus. Spliced transcripts encode multiple isoforms. The ASCC1 gene is located on the long arm (q) of chromosome 10 at position 22.1 (10q22.1). CTHRC1 gene: The CTHRC1 gene is a locus that encodes the protein that plays a vital role in response to arterial cellular injury by vascular remodeling. Mutations of this gene locus are associated with Barrett’s esophagus and esophageal adenocarcinoma. They may act as negative regulators of the collagen matrix homeostasis. This gene is located on the long arm (q) of chromosome 8 at position 22.3 (8q22.3). Differential analytic techniques such as integrative genomic, single-SNP, and haplotype analysis generated 12 potential genes for future identification of gene mutations. The chromosome that contains the MSR1 gene encodes scavenger receptors which may be involved in pathologic inflammation and apoptosis. Apart from the truncating MSR1 c.877C>T mutation that has been identified in patients, another separate MSR1 germline mutation (c.760C>G, p.L254V) has been found in some patients. The ratio of occurrence of these gene mutations is estimated as 0.017 (95% 0.021 to 0.061, P=0.19). Furthermore, there were two other mutations identified, one of which is located on ASCC1 (c.869A>G, p.N290S) and the other on CTHRC1 (c.131A>C, p.Q44P). Genetic Code Involved in Barrett's Esophagus (BE) Inherited BE: First- or second-degree relatives of patients affected with BE, adenocarcinoma on the gastroesophageal junction, or esophageal adenocarcinoma (EAC) have increased risk of developing inherited BE. It has been identified from recent work that the risk of BE may be increased by a rare autosomal dominant susceptibility mutation in affected families. The exact mutation is still unidentified. Sporadic Barrett’s esophagus: The primary risk factors of the Barrett’s esophagus include age, gender (male), the presence of gastroesophageal reflux disorder (GERD), and skin tone (white-skinned people). Obesity and GERD are known to be the most predictive factors for the development of genetic BE. GERD is a primary risk factor for BE. Sporadic cases have been found where patients are found to inherit GERD as well as BE. Many studies have confirmed that families affected by BE might actually have a GERD-related genetic component. The mechanism of obesity in the development of BE is not clearly defined, but it is found to increase the risk of GERD. Obesity-induced increases in signaling through certain insulin-like growth factor pathways which favor proliferation, and through insulin pathways, may be involved as well in the etiology of BE. Patients with obesity, either with or without BE, have been studied to determine the IGF-1R genotype. It was found that obese patients with BE had the pro-proliferative IGF-1R genotype more commonly than those without BE or GERD. Reviewed by Liji Thomas, MD. References https://deepblue.lib.umich.edu/bitstream/handle/2027.42/86844/j.1749-6632.2011.06043.x.pdf https://www.cancer.org/treatment/understanding-your-diagnosis/tests/understanding-your-pathology-report/esophagus-pathology/barrets-esophagus.html http://www.adasp.org/FAQs/02-esoph.html http://www.gastro.org/info_for_patients/barrett-s-esophagus-107-low-grade-dysplasia-in-barrett-s-esophagus http://surgpathcriteria.stanford.edu/gi/barrett-esophagus/dysplasia.html http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2796.2011.02400.x/pdf https://rarediseases.info.nih.gov/diseases/20/barrett-esophagus https://ghr.nlm.nih.gov/gene/ASCC1#location Further ReadingBarrett's Esophagus - What is Barrett's Esophagus?What Causes Barrett's Esophagus?Barrett's Esophagus SymptomsBarrett's Esophagus PathologyBarrett's Esophagus TreatmentsMore... // Last Updated: Sep 13, 2017"
56,"2018-04-20 02:32:17","Barrett's Esophagus with Dysplasia","Barrett’s esophagus is a condition in which the tissue lining the esophagus – the tube that passes the food from the mouth to the stomach – is replaced by tissue similar to that of the intestinal lining. This occurs chiefly in the cells of the epithelial tissue which lines the lower end of the esophagus. About 10% of the patients with gastroesophageal reflux may be expected to develop Barrett’s esophagus, and in about 10% of the patients with Barrett’s esophagus, dysplasia occurs. Dysplasia is a pre-cancerous stage in Barrett’s esophagus, where the cell develops abnormal features. However, these abnormal cells do not have the capability to spread to other parts of the body. Depending upon the grades of dysplasia, treatment options are available. Characteristics of Dysplasia in Barrett’s Esophagus Dysplasia in Barrett’s esophagus is histologically classified into two types: “adenoma” and “non‐adenoma‐like” on the basis of the similarity or otherwise of the dysplastic cells to cells found in sporadic colonic adenomas. Other than these, uncommon and atypical forms of dysplasia are also known to occur in epithelium affected both by Barrett’s esophagus and by inflammatory bowel disease. There are two grades of dysplasia in Barrett’s esophagus: low-grade dysplasia and high-grade dysplasia. These are identified through either endoscopy or biopsy. Low Grade Dysplasia in Barrett’s Esophagus If microscopic examination reveals the presence of a few cells with mildly abnormal features, it is termed “low-grade dysplasia” (LGD). This condition is considered as the earliest precancerous stage of the esophageal epithelium. Cells with LGD have crowded nuclei which are elongated, irregular, and hyperchromatic, show prominent chromatin with or without numerous small nucleoli. Adenomatous LGD is the usual type of dysplasia in Barrett's esophagus. Here the crypts show comparatively preserved glandular architecture or only minimal distortion of nuclear architecture but a normal number of nuclei. Most often, dysplastic nuclei are observed aggregated at the base of the cells. The significance of LGD in Barrett’s esophagus is controversial, but in general, follow-up is recommended. Diagnosis and Treatment In low-grade dysplastic BE, the diagnosis might be difficult as there is little difference seen between “indefinite for dysplasia” and LGD in biopsies. However, there are substantial inter- and intra-observer differences in the diagnosis of both these conditions, which are thus combined into one as regards their clinical management. LGD requires effective treatment of the gastroesophageal reflux with proton pump inhibitors, or PPIs. Maintaining a healthy and balanced diet can also help in reducing the reflux. Regular biopsies are suggested to make sure that the dysplasia will not progress or develop into malignancy. When the dysplasia is no longer seen, endoscopic follow up may be discontinued, but it is wise to continue taking PPIs. In cases where the acid reflux drugs do not produce adequate response and fail to eliminate the dysplasia, endoscopic eradication therapy (EET) is suggested. Endoscopic Resection (ER) Endoscopic resection (ER) utilizes endoscopic techniques to remove dysplastic tissue. For proper dysplasia assessment, endoscopic resection should be performed only in patients with abnormalities that are visible on endoscopy. Generally, most of the suspicious areas of tissue are dissected during endoscopic resection for further analysis. Residual areas of dysplasia are removed through the radiofrequency ablation technique. Radiofrequency Ablation (RFA) In the RFA technique, radiofrequency waves are passed through a catheter to remove the diseased tissue in the esophagus without causing too much damage to the healthy neighboring tissues. Replacement of abnormal Barrett’s tissue by healthy tissue takes about four weeks with the RFA treatment. High Grade Dysplasia in Barrett’s Esophagus High-grade dysplasia (HGD) in Barrett’s esophagus (BE) is a further step on the precancerous continuum of tissue changes before the actual development of an esophageal adenocarcinoma. Barrett’s esophagus that occurs as a complication of gastroesophageal reflux disease (GERD) is an abnormal change that occurs in normal esophageal cells. HGD increases the risk of esophageal adenocarcinoma. Diagnosis and Treatment Esophagectomy: This procedure is the removal of the abnormal tissue of Barrett’s esophagus by surgery, and is also used to treat patients with HGD. in this procedure, the whole esophagus is removed and then an artificial organ reconstructed using parts of other organs (usually the stomach). Endoscopic Mucosal Resection (EMR): This procedure helps to remove abnormal tissue areas in the esophageal mucosa, including HGD. EMR is also frequently used to remove rough HGD areas. Radiofrequency ablation with Barx ablation: To treat HGD due to Barrett’s esophagus, heat energy is applied to the areas of intestinal metaplasia to ablate the abnormal cells in the esophagus. Photodynamic Therapy (PDT): It is a kind of treatment for HGD which uses light energy to remove the diseased cells in esophagus, following their pretreatment with a sensitizing chemical. Cryotherapy: This process involves spraying of liquid nitrogen or carbon dioxide onto the esophageal mucosa, which freezes the BE and HGD. Reviewed by Liji Thomas, MD. References http://www.pathology.washington.edu/about/education/barretts/page2.php https://www.ncbi.nlm.nih.gov/pubmedhealth/PMHT0025308/ https://www.cancer.gov/publications/dictionaries/cancer-terms?cdrid=45675 https://www.cancer.org/treatment/understanding-your-diagnosis/tests/understanding-your-pathology-report/esophagus-pathology/barrets-esophagus.html http://www.gastro.org/info_for_patients/barrett-s-esophagus-107-low-grade-dysplasia-in-barrett-s-esophagus https://www.bmc.org/gastroenterology/high-grade-dysplasia https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1861756/ http://surgpathcriteria.stanford.edu/gi/barrett-esophagus/dysplasia.html http://www.albertahealthservices.ca/assets/info/hp/cancer/if-hp-cancer-guide-gi011-barretts-esophagus.pdf http://apps.pathology.jhu.edu/blogs/barretts/?tag=high-grade-dysplasia Further ReadingBarrett's Esophagus - What is Barrett's Esophagus?What Causes Barrett's Esophagus?Barrett's Esophagus SymptomsBarrett's Esophagus PathologyBarrett's Esophagus TreatmentsMore... // Last Updated: Sep 13, 2017"
57,"2018-04-20 02:32:19","Barrett's Esophagus Research","By Jeyashree Sundaram (MBA) Barrett’s esophagus (BE) which is a condition defined by the unusual growth of esophagus cells, in rare occasions, might grow into a cancer known as esophageal adenocarcinoma. The major cause of BE is GERD and acid reflux. Risk of arising adenocarcinoma is greater by 30-125 times in BE affected humans than in humans who doesn’t have BE. In case of BE, the diagnosis and treatment methods available are efficient enough; and the condition itself is not considered a harmful disease. But, if it converts into cancerous stage, it attains complexity. Therefore, researches in this field targets for preventing the progression of BE, for controlling the symptoms, and for providing better survival to the patient. Intestinal metaplasia of the esophagus, aka Barrett's, is a response to injury due to acid reflux. Image Credit: David Litman / Shutterstock Research on Genes In 2012, a study was conducted to examine the DNA methylation of vimentin gene in the neoplasm of the upper part of the gastrointestinal (GI) tract. Using a real-time quantitative methylation particular polymerase chain reaction (PCR) assay, researchers tested the archival samples of gastric neoplasia and esophagus for the methylation of vimentin. They found that the abnormal DNA methylation of vimentin gene is high in this type of neoplasm. Finally, they proved by cytology brushings test that vimentin DNA methylation noticeable in the case of BE is 100%, but it was beyond control. These results recommend that the biomarker of the upper part of GI tract is vimentin methylation. These findings are expected to be helpful in future studies of BE. Another study was carried out for finding the specific genes that methylate abnormally in BE. For this, a group of researchers conducted a genome-wide approach for DNA methylation during 2016. They analyzed the specimens of BE and stomach and then compared each specimen’s level of methylation at around 485,000CpG sites inside the DNA samples. Pyrosequencing assays are used for the approval of results and develop methylight assays for identifying the alleles of DNA methylated in endoscopic brushings. Thus, the result showed that the gene ZNF793 and B3GAT2 are unusually methylated highly in BE and these genes methylated grade were used to identify BE in sample tissues. Research on Cellular Process A study was carried out in 2015 for identifying the role of autophagy in a BE patient. At present, this research is poorly studied. In this, the level of autophagy in the cell lines of a BE patient, a transgenic BE mouse model, and biopsy of esophageal adenocarcinoma (EAC) are defined. The researchers found that the level of autophagic vesicles (AVs) is high in the non-dysplastic BE person, whereas it is decreased in the usual BE cells of dysplastic and squamous cells, and is not present in EAC. They also found that the level of AVs is highly increased in BE humans than EAC or usual squamous and recommended that functions of autophagy after damage by acid reflux improves the survival of cell. Thus, autophagy can play an important role in the progression and pathogenesis of BE. Research on Treatment Methods In May 2016, an article was published by ten authors on the development of treatment for BE. In this article, they state that BE can develop into cancer due to many reasons; this is identified by new testing methods (pH monitoring and specifically multichannel within lumen impedance) that aid to get better knowledge of the pathophysiology of GERD along with its complications. Such findings are more helpful in predicting the progression of BE neoplasm. Finally, they show a new treatment choice for BE and EAC termed endoscopic elimination, which is more effective for patients. This information gives more knowledge on the mechanical connection between GERD and BE. Research on Hereditary Factors In 2017, research is ongoing for predicting BE within the family; authors have come together to examine a clinical model from 92 multiplex pedigrees of BE and 787 individually ascertained pedigrees of BE, fitting a model to a multivariate logistics that includes medical risk factors and family history. The risk factors included in the model are education level, smoking, age, parental status, sex, regurgitation frequency, heartburn frequency, and using acid suppressant. Using the training dataset and separate validating dataset of the 643 multiplex pedigrees with BE, the exact prediction was determined. Eventually, the result showed that BE risk can be found with the help of family information; the possibility of predicting risk for individuals who are not a member of the family without the suggestion from any family relation was also identified. Research Related to Pathogenesis During 2007, a few authors combined to predict the risk of high-grade dysplasia and esophageal adenocarcinoma from BE. These were prospectively evaluated by the cases of nearly 325 BE patients; they were subjected to endoscopic biopsies. Among them, 269 patients were continuously followed up with one or many endoscopies by a strong platform for the analysis of heterozygosity loss (LOH) with baseline 17p (p53). Finally, it was found that LOH is the predictor of BE progression and the outcome is an increase in esophageal adenocarcinoma and high-grade dysplasia. Reviewed by Afsaneh Khetrapal Bsc (Hons) Sources: www.macmillan.org.uk/.../barretts-oesophagus.html https://www.ncbi.nlm.nih.gov/pubmed/22315367 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4670566/ https://www.ncbi.nlm.nih.gov/pubmed/26373456 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4848241/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4873373/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1808263/ Further ReadingBarrett's Esophagus - What is Barrett's Esophagus?What Causes Barrett's Esophagus?Barrett's Esophagus SymptomsBarrett's Esophagus PathologyBarrett's Esophagus TreatmentsMore... // Last Updated: Sep 21, 2017"
58,"2018-04-20 02:32:21","Barrett’s Esophagus and Cancer Risk","By Jeyashree Sundaram, MBA Barrett’s esophagus (BE) is a condition where the tissues present in the esophagus undergo transformation and become similar to those found in the intestinal lining. It is present mostly in people who have gastroesophageal reflux disease (GERD), especially if it has been present for a very long period. This in turn is related to an increased risk for developing esophageal cancer. Endoscopic biopsy photomicrograph of intestinal (Barrett's) metaplasia of the esophagus. Credit: David Litman/Shutterstock.com Risk of transformation of cells Barrett’s esophagus does not proceed to cancer in all patients; however, it is estimated that around 10–15% of cases of BE may progress to esophageal cancer. There are two kinds of cell transformations that are associated with either squamous cell or adenocarcinoma of the esophagus. Squamous cell cancer of the esophagus is more common in people who drink excessively and/or smoke cigarettes. When there is a prolonged abnormal backward flow of stomach acid into the lower esophagus, it can affect the inner lining of the esophagus. Squamous cell metaplasia is caused by this process; here, the cells that line the esophagus are replaced by gland cells. These gland cells resemble the normal lining cells of the stomach and the small intestine. This, however, is not a frequently occurring cell transformation in Barrett’s esophagus. Adenocarcinoma of the esophagus occurs in people who have GERD. Patients who have a long history of acid reflux may develop Barrett’s esophagus. Most patients with this condition may have symptoms of heartburn, while a few do not exhibit any symptoms at all. The frequency of this type of cancer has rapidly increased over the years. Most adenocarcinomas of the esophagus start in Barrett’s tissue. Risk factors Dysplasia Dysplasia is a condition in which cells show precancerous changes, and it can occur within Barrett’s tissue. The development of dysplasia maybe the only risk factor for cancer in BE. Dysplasia is generally defined as the stage preceding the development of frank cancer. This condition can be diagnosed by endoscopic biopsy in Barrett’s esophagus. If dysplasia is identified by examining a biopsy under the microscope, healthcare providers often advise performing an endoscopy in order to destroy the whole of the metaplastic tissue. Though the risk of dysplasia is low, it is important to have regular checkups for dysplasia, so that it can be treated and prevented from developing into esophageal cancer. Depending upon the level of risk possessed by the dysplasia, it can be classified into different grades: negative to dysplasia, low grade dysplasia, and high grade dysplasia. Without Dysplasia/ negative to dysplasia: Barrett’s esophagus without dysplasia or negative to dysplasia means that no precancerous changes were identified in the cells visualized on microscopy of the biopsy tissue. If the area of dysplasia is very small or negligible, it may be missed when the biopsy is taken. Therefore, a higher number of biopsies may be taken, or more frequent endoscopies may be performed, every 3–5 years regularly. This may help to identify and destroy the abnormal changes in the Barrett’s tissue. The risk of cancer for non-dysplastic Barrett’s esophagus is very low. Low grade dysplasia (LGD): In this type, the cell changes are present but minimal. Out of 100 patients with BE and low-grade dysplasia, 20 are at risk of developing cancer of the esophagus within 5 years. High grade dysplasia (HGD): In this type, there are abnormal changes in the cells. This is mainly linked to a higher risk of esophageal carcinoma. In 30-60% of cases, it may progress to cancer if not treated properly. HGD is a more advanced pre-cancerous condition of the esophagus than low grade dysplasia. Both high as well as low grade dysplasia does not have the capability to spread to other parts of the body. Risk factors for HGD Some of the risk factors associated with the development of high grade dysplasia are: Segment: A recent study from Berlin has determined that segment length is associated with an increased risk of high grade dysplasia. That is, patients with long segment Barrett’s esophagus (LSBE) are at an increased risk of progression to high grade dysplasia than people with short segment Barrett’s esophagus (SSBE). Mucosal abnormalities: In Barrett’s esophagus, some types of mucosal changes are related to an increased risk of high grade dysplasia. Erosive and ulcerative esophagitis are associated with increased risk of progression to esophageal adenocarcinoma or high grade dysplasia. The greatest risk for patients with Barrett’s esophagus is the development of adenocarcinoma. However, only a few patients are at risk. According to epidemiological data, most patients with BE and adenocarcinoma are older white males. Patients who have specialized columnar epithelium cells are also at high risk for developing adenocarcinoma associated with BE. An additional risk factor for metachronous and synchronous adenocarcinoma is the presence of epithelial dysplasia, especially high grade. Many studies have also indicated that the frequency of the occurrence of dysplasia, either close to or distant from Barrett’s esophagus, is also connected with adenocarcinomas. Dysplasia is not only a sign of increased risk of adenocarcinoma but a pre-invasive lesion. Reviewed by Liji Thomas, MD. References https://www.cancer.org/cancer/esophagus-cancer/causes-risks-prevention/risk-factors.html https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1861756/ https://www.asge.org/home/for-patients/patient-information/understanding-gerd-barrett-39-s https://www.bmc.org/gastroenterology/high-grade-dysplasia https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4113043/ http://pathology.uic.edu/understanding-your-report-esophagus-barretts/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4449455/ // Last Updated: Oct 12, 2017"
59,"2018-04-20 02:32:27","Barrett’s Esophagus and GERD","Gastro esophageal reflux disease (GERD) is considered the main cause of Barrett’s esophagus (BE). GERD results in BE, but the exact cause of GERD is still unknown, and the complications of BE and GERD are interrelated. Credit: CHAjAMP/Shutterstock.com Roughly 5%–13% of patients with GERD symptoms are susceptible to develop BE over their lifetime. Several other factors of GERD such asseverity, frequency, and duration of the symptoms have a huge impact on increasing the risk of BE. Gastro esophageal reflux disease The upward regurgitation of the stomach acid to the esophagus is referred to as GERD. GERD can cause specific symptoms of BE and may harm the esophagus. The primary and most common symptom of GERD is identified as heartburn. Heartburn is usually a burning sensation in the chest that frequently arises from the bottom of the breastbone leading towards the upper chest. These indications can be associated with excessive salivation in the mouth, dysphagia (discomfort in swallowing food), and burping. All the above symptoms can be positional and may become severe when lying down. Symptoms of GERD can worsen when consuming alcohol, fatty food, acidic food, peppermint, and juices with citric content. These symptoms have a prolonged association with acid reflux disorder. While these symptoms have a long-term association with reflux disease, there is now a growing concern about other symptoms that can be caused by reflux disease. These symptoms are known as the extra-esophageal symptoms of reflux disease such as sleep disorders, asthma, laryngitis, halitosis, and chronic cough. Complications of GERD and BE BE is a condition in which the tissue in the esophagus appears like the tissue that lines the intestine. It is known as the precancerous intestinal metaplasia (Dysplasia) of the lower esophagus mucosa, which develops in response to chronic exposure to the acidic contents of the stomach. The adenocarcinoma caused by BE is increasing by 30 to 40 times each year. BE is a complication of GERD. Patients affected by GERD symptoms at an early age are more prone to develop esophageal adenocarcinoma. It is uncertain that the risks for BE related with GERD indication depend only upon age. Furthermore, risks of esophageal adenocarcinoma linked with GERD symptoms are greater for people who are obese or a chain smoker. The potential modifiers of BE are still unclear; hence, there might be many other elements that might regulate the reaction of GERD with the risk of BE. Risk of BE in GERD GERD symptoms are more frequently observed in BE patients than in non-BE people. The risk of BE increases with prolonged increase in the frequency of GERD. Studies performed to analyze the association between symptoms related to age and risk of BE found that the huge risk of BE is observed in the people with long-term GERD symptoms at an early age of onset. By comparing patients of different age groups without GERD symptoms, it has been identified that the people aged 30 years or less with frequent symptoms of GERD are at greater risk of BE than those aged between 30 and 49 years and 50 to 79 years. Another analysis which was performed to study the relationship between age of onset of heartburn and risk of BE identified that both GERD and heartburn had a similar pattern of association with BE risk. GERD severity The risk of BE is mainly associated with the severity of the symptoms of the GERD. It has been identified that patients with GERD symptoms had 12-fold greater risk of developing BE when compared to those without GERD symptoms. Age of onset for higher risk of BE was found to be 30 years in patients with severe GERD symptoms, but these results were not statistically reliable as they overlapped with each other. GERD symptoms (cumulative) The powerful linear trend of increasing BE risk is linked with a rising cumulative GERD duration of the indications. In the case of patients with GERD symptoms, the risk of BE is increased to 30% with every ten additional years of the exposure. Patients of less than 20 years of age with prolonged cumulative GERD symptoms and patients of 30 years of age with recurring GERD symptoms had a similar risk of BE when compared with patients who developed later in their lifetime. As the age of onset varies continuously, it has been observed that an early age at onset of GERD symptoms are significantly related to the risk of BE. Esophagus adenocarcinoma is reported as the fatal condition that becomes common in several countries (United States, Industrialized nations, Australia, and Western Europe). Most of all cases of esophageal adenocarcinoma are reported to emerge with Barrett's Esophagus than GERD. The number of BE cases reported has risen drastically during the last few decades. Reviewed by Afsaneh Khetrapal Bsc (Hons) Sources https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3972036/ https://www.ncbi.nlm.nih.gov/pmc/articles/mid/NIHMS611949/ www.asge.org/.../understanding-gerd-barrett-39-s www.spg.pt/.../...sis-and-Management-of-Barrets-Esophagus-nov-2015.pdf www.valleyhealthcancercenter.com/.../barretts_first_brochure.pdf https://www.med.umich.edu/1info/FHP/practiceguides/gerd/gerd.12.pdf http://s3.gi.org/patients/gihealth/pdf/barretts.pdf Last Updated: Oct 12, 2017"
60,"2018-04-20 02:32:30","Non-Dysplastic Barrett's Esophagus","Barrett's esophagus (BE) is a condition in which tissue that is similar to the tissue lining in the intestines changes or replaces the lining of the esophagus (the tube that transports food from the mouth to the stomach). Even though BE has a chance of progressing into low- or high-grade dysplasia (a precancerous condition) and then transform into cancers of the esophagus, in most cases, the dysplasia may not be presented or cannot be identified by biopsy specimens. Such a condition is termed as non-dysplastic BE. All patients with non-dysplastic BE are subjected to endoscopic surveillance every two to three years in order to diagnose any prevalent signs for dysplasia. If discovered with such a risk of progression to dysplasia, patients are provided with rigorous treatment. Clinical Presentation and Risk Factors Non-dysplastic BE manifests as column-like cells including mucin-filled, blue-tinted goblets. The risk factors of progression from non-dysplastic BE to esophageal cancer may include length of the BE greater than or equal to 6 cm and hiatal hernia of length more than 3 cm. However, progression of non-dysplastic BE to esophageal adenocarcinoma and higher grade dysplasia is really uncommon with the risk accounting for less than 1%. This grade of non-dysplastic BE, where the tissue begins to change to resemble the red intestinal tissue linings is also referred as Intestinal Metaplasia (IM). Diagnosis BE (both with and without dysplasia) is diagnosed by a diagnostic endoscopy, which is performed using very high resolution and white light to view the internal lining of the esophagus. The management therapy and surveillance interval for patients with BE is determined by dysplasia grade. For non-dysplastic patients with BE, endoscopic surveillance is suggested every three years along with biopsies, as some patients with additional risk factors such as age less than 30 at the time of BE diagnosis and family history of esophageal cancer may promote non-dysplastic BE to cancer. The non-dysplastic BE suspected patient undergoes endoscopy for 6–12 months and biopsies are done each time to determine the cytological and structural changes to the epithelial cells. New advanced imaging techniques for detecting BE are improved and they include narrowband imaging, chemoendoscopy, optical coherence tomography, and laser confocal microscopy. Management of Non-Dysplastic BE For BE without the presence of dysplasia or cancer, the traditional management techniques are used as the common primary approach of treatment. This includes controlling the symptoms of BE and regular endoscopic surveillance to prevent progressive disease. Healthy changes in the lifestyle may help in clearing acid in the esophagus and lessening the prevalence of reflux events. Avoiding certain food such as citrus foods, beverages, spicy and fatty foods, and tomatoes will benefit in controlling the symptoms. Periodical endoscopies and biopsies must be done to estimate the affected area by Barrett’s disease. Some high-risk patients without dysplasia are recommended with treatment options such as endoscopic mucosal resection and radiofrequency ablation therapy. Endoscopic mucosal resection: Patients of BE without dysplasia may primarily undergo endoscopic mucosal resection as an initial diagnostic or treatment step. In this approach, the affected mucosal linings in the esophagus are therapeutically removed using endoscope. The damaged mucosa is resected and lifted using a saline solution and then eliminated by means of a cap or snare accessory. Adjacent and deep margins are examined by proper handling of the sample. In non-dysplastic BE cases, the patients are not subjected to routine endoscopic ablative therapy due to their lower risk of development of esophageal adenocarcinoma. Radiofrequency ablation: The non-dysplastic BE in patients is managed by radiofrequency ablation (RFA) therapy. The RFA process involves radiofrequency energy to ablate the damage tissue through endoscopy. Depending on cryotherapy, two methods are available. The first approach includes a liquid nitrogen spray that removes the tissue by freezing it, while the second approach involves a cryoballoon, i.e., a balloon filled with nitrous oxide is placed on the tissue to freeze them. The RFA therapy is repeated once or thrice to confirm the eradication of the whole affected tissue by BE. In this technique, the risk for bleeding after the procedure is very less and also does not involve any stricture formation. After RFA, initial surveillance is done to ensure complete elimination of BE and no recurrence. It is usually done every three to five years. The RFA for non-dysplastic BE is cost-effective and has an efficiency upto 90%; however, the periodic surveillance in non-dysplastic BE is quite expensive. Follow-up Patients with non-dysplastic BE after ablation therapy should involve follow-up of 4-quadrant biopsy for every 1 or 2 cm of complete area that was previously affected with BE. Endoscopic surveillance should be done on a routine basis initially once in six months in the first year post ablation therapy. Reviewed by Afsaneh Khetrapal Bsc (Hons) Sources www.albertahealthservices.ca/.../...guide-gi011-barretts-esophagus.pdf www.mja.com.au/system/files/issues/205_07/10.5694mja16.00796.pdf https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5114519/ gi.org/.../ACG-2015-Barretts-Esophagus-Guideline.pdf https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3002583/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1357704/ [Further:Barrett's Esophagus] // Last Updated: Oct 30, 2017"
61,"2018-04-20 02:32:33","Barth Syndrome","By Dr Ananya Mandal, MD Barth syndrome is a rare, genetic disorder that affects males. The condition is caused by mutations in the tafazzin gene, which codes for an enzyme involved in the synthesis of cardiolipin, an important lipid component of the inner mitochondrial membrane. The condition affects energy production in the mitochondria and leads to complications such as cardiomyopathy, muscle weakness and neutropenia. Symptoms Symptoms are not always present but some typical features of Barth syndrome include: Cardiomyopathy - Cardiomyopathy describes a deterioration in the myocardium or heart muscle. The muscle is usually dilated or stretched with a varying degree of hypertrophy (increase in size). Neutropenia - This refers to an abnormally low number of neutrophils (a type of white blood cell) in the blood. Skeletal muscle development may be abnormal and muscle tone weak. Levels of organic acids in the blood and urine may be increased. Levels of 3-methylglutaconic acid, for example, are typically raised by 5 to 20-fold. Delayed growth during pre-teen years with growth often accelerated later on, in adolescence. Cardiolipin abnormality Complications of Barth's syndrome Barth's syndrome may cause a range of complications some of which are listed below: Cardiomyopathy increases the likelihood of a dangerous abnormal heart rhythm or arrhythmia which can be fatal. Neutropenia increases the likelihood of infection, particularly of the mucous membranes such as the skin or inside of the mouth. A fever may also be present. Diarrhea and/or constipation. Weak muscle tone may lead to fatigue and difficulty exercising. Affected individuals may have feeding problems such as difficulty in sucking, swallowing or chewing, an aversion to some foods and be selective or fussy eaters. The risk of thrombosis or blood clots is increased. There is a risk of hypoglycemia or low blood sugar, especially when a child is newborn. Chronic (long-term) headache, abdominal pain, and/or body aches, particularly, during puberty. Mild learning disabilities may develop. The risk for osteoporosis is increased. Phases of Barth syndrome General phases of the disease are often but not always seen in children with the syndrome and these include: Children often become seriously ill before the age of 5 Between ages 5 to 11, symptoms typically improve and patients tend to be free of symptoms Adolescence often marks the return of symptoms Treatment and management There is no cure for Barth's syndrome and treatment is focused on managing the condition. Usually, the treatment approach to Barth's syndrome involves a team of specialists including experts in biochemistry, genetics and neurology as well as nurses, social workers, nutritionists and physical and occupational therapists. Barth syndrome is suspected if a person presents with one of the main characteristics of the disease or if there is a family history of the condition. Diagnosis involves DNA sequencing to detect the tafazzin gene (TAZ, also called G4.5) mutation and analysis of cardiolipin in various cells and tissues. Genetics This is an X-linked inherited genetic disease, so a mother may be a carrier of the mutated gene despite not having any symptoms. There is a 50% chance that a boy born to a carrier mother will have the condition and a 50% chance that any daughters she has will be carriers themselves. All daughters of a male with the condition will be carriers but no sons will be affected. Reviewed by Sally Robertson, BSc Sources www.barthsyndrome.org/.../...re_BSF_June2011_web37PEL-6282011-6122.pdf https://www.orpha.net/data/patho/Pro/en/Barth-FRenPro1059.pdf http://www.childrenshospital.org/az/Site1404/mainpageS1404P1.html www.barthsyndrome.org/.../...eFAQs_FINAL_May200637WDF-5292006-9233.pdf Last Updated: Nov 18, 2013"
62,"2018-04-20 02:32:35","Basal Cell Carcinoma - What is Basal Cell Carcinoma?","By Dr Ananya Mandal, MD Basal cell carcinoma is one of the most common types of skin cancer, affecting over 1 million Americans each year and accounting for 75% of all skin cancers. This type of cancer has a 95% cure rate, but may become life threatening if left untreated. Symptoms and characteristics of basal cell carcinoma Basal cell carcinoma is most commonly seen in the most exposed parts of the body such as the face, ears, neck, scalp, shoulders and back. Initially, basal carcinoma may have a similar appearance to psoriasis or eczema. It may also present as a bleeding or non-healing sore, a shiny bump, pink growth over a scar or a reddish patch. Those with exposure to known risk factors for basal cell carcinoma are carefully monitored for changes in the skin. The appearance of the lesion and any change in size, color, texture, and appearance along with pain, itching or bleeding are noted. Risk factors and causes of basal cell carcinoma Basal cell carcinomas are slow growing cancers. One of the main causative factors is over exposure to sunlight and individuals who spend a lot of time in the sun such as those who work outdoors or like to sunbathe are at particular risk of basal cell carcinoma. The risk is generally higher among those with fair skin, blue, green, or grey eyes and blonde or red hair. These individuals also have a 50% risk of getting another tumour within the five years after basal cell carcinoma is diagnosed. Other factors that may increase the risk of this cancer include exposure of the skin to radiation, scarring, tattoos or burns. Diagnosis and treatment The lesion is first examined and a tissue sample or biopsy taken for analysis. The sample is then sliced into thin slices, fixed on a glass side, stained with special dyes and examined under the microscope by a pathologist. Depending upon the size, location and extent of cancer spread, treatment is determined. Treatment may range from the use of topical or locally applied medications to removal by curettage or surgery. Locally applied medications commonly include imiquimod or fluorouracil. Some small lesions may be removed using a procedure called curettage and electrodessication. Electrically charged needles are used to kill and burn off the cells of the cancer. Cryosurgery, on the other hand, describes the use of extremely cold temperatures to kill off the cancer cells. The tumor then forms a crust and eventually falls off. Laser beams may also be used to achieve the same outcome and is called photodynamic therapy. This is often used to treat the face and scalp when more than one lesion is present. Surgical excision of the lesion may also be performed, which involves the removal of the tumor along with a margin of normal skin as a safety margin, to ensure all of the tumour is captured. Radiation therapy is another alternative, which directs high-energy, pinpointed X-rays at cancer cells in order to destroy them. Reviewed by Sally Robertson, BSc Sources http://www.med.muni.cz/biomedjournal/pdf/2006/05/261_270.pdf www.ashfordstpeters.nhs.uk/.../...%20of%20Basal%20Cell%20Carcinoma.pdf www.cap.org/apps/docs/reference/myBiopsy/SkinBasalCellCarcinoma.pdf www.fbae.org/.../Basal%20Cell%20Carcinoma.pdf http://www.skinpathology.net/pdf/basal-cell-carcinoma.pdf www.ncbi.nlm.nih.gov/.../westjmed00080-0077a.pdf http://www.pjo.com.pk/27/1/Ibrar%20Hussain.pdf Further ReadingBasal Cell Carcinoma DiagnosisBasal Cell Carcinoma PathophysiologyBasal Cell Carcinoma TreatmentsBasal Cell Carcinoma PrognosisBasal Cell Carcinoma Epidemiology Last Updated: Oct 7, 2014"
63,"2018-04-20 02:32:37","Basal Cell Carcinoma Diagnosis","By Dr Ananya Mandal, MD Basal cell carcinoma is the most common skin cancer in the United States and Australia. Incidence is also on the rise in the United Kingdom. The most significant causative factor that has been associated with basal cell carcinoma is excessive and long term exposure to ultraviolet light radiated by the sun. Clinical symptoms of the cancer More often than not, basal cell carcinoma is found in parts of the body that are more prone to sun exposure such as the face, ears, neck, scalp, shoulders, and back. Basal cell carcinoma varies in appearance and lesions may present as an open sore, a growth with a raised border, a scar-like area, a reddish patch or a bump or nodule. People who are exposed to the sun are advised to look out for changes in the skin such as alterations in the appearance of a mole or freckle. A change in the size, color, texture and the presence of pain, itching or bleeding are all treated as suspicious. Basal cell carcinoma is more common among individuals with fair skin, blue, green, or grey eyes and blonde or red hair. These individuals also have a 50% risk of getting another tumour in the five years following the first diagnosis of the cancer. Other factors that may raise the risk of basal cell carcinoma include exposure to arsenic or radiation and the presence of scars, tattoos or burns. Once a person has developed a basal cell carcinoma, they are at an increased risk of developing the same cancer in other regions. Diagnosis Diagnosis is made based on the clinical appearance of a lesion and a biopsy. During biopsy, a tiny tissue sample is taken from the lesion after numbing the area with a local anesthetic agent. Shave biopsy is appropriate in the case of a raised lesion. For flat lesions, a punch biopsy may be performed if the lesion is large while the whole lesion may ne excised for examination if it is small. The sample is then thinly sliced, fixed and stained with special dyes for microscopic viewing on a glass slide. Low and high risk basal carcinoma Basal cell cancers may be divided into low-and high-risk categories by determining certain prognostic factors that affect the outcome of the cancer. These factors include: Size of the tumor Location of the tumor The nature of the tumor's margins (whether they are clear cut or diffuse) Rate and pattern of tumor growth Whether tumors are recurrent Health status of immune system Reviewed by Sally Robertson, BSc Sources http://www.med.muni.cz/biomedjournal/pdf/2006/05/261_270.pdf www.ashfordstpeters.nhs.uk/.../...%20of%20Basal%20Cell%20Carcinoma.pdf www.cap.org/apps/docs/reference/myBiopsy/SkinBasalCellCarcinoma.pdf www.fbae.org/.../Basal%20Cell%20Carcinoma.pdf http://www.skinpathology.net/pdf/basal-cell-carcinoma.pdf www.ncbi.nlm.nih.gov/.../westjmed00080-0077a.pdf http://www.pjo.com.pk/27/1/Ibrar%20Hussain.pdf Further ReadingBasal Cell Carcinoma - What is Basal Cell Carcinoma?Basal Cell Carcinoma PathophysiologyBasal Cell Carcinoma TreatmentsBasal Cell Carcinoma PrognosisBasal Cell Carcinoma Epidemiology Last Updated: Nov 17, 2013"
64,"2018-04-20 02:32:42","Basal Cell Carcinoma Pathophysiology","By Dr Ananya Mandal, MD Basal cell carcinomas are slow-growing cancers. They typically appear as elevated or flat lesions present on the sun-exposed parts of the body such as the face, scalp, chin, neck or back. The lesions are more common in fair-skinned and blond or red-haired individuals and are therefore common among those of European ancestry. Those with albinism are also at a greater risk of developing basal cell carcinomas (albinism refers to genetic absence of all pigment producing melanin in the body). Individuals of African or South Asian descent with dark skin colour are highly resistant to skin cancer, including basal cell cancer. After an organ transplant, the susceptibility to basal cell cancers rises. Among those of European ancestry, the risk for basal cell carcinoma is increased ten-fold compared with individuals with a similar sun exposure who have not had an organ transplant. By contrast, among East Asian patient, incidence of the tumors is extremely low, even after organ transplant. Basal cell carcinoma is slightly more common in men than in women, possibly due to an increased likelihood of outdoor work and therefore greater sun exposure among men. The incidence among women, however, has been on the rise over the past few decades, which could be attributable to an increase in the use of sun beds or due to an increased tendency to seek early medical attention and diagnosis. Basal cell carcinoma is also more common among individuals over the age of 50. However, the number of younger people being diagnosed with the condition is increasing, mainly due to the rising popularity of sun beds for cosmetic tanning. Pathology Basal cell carcinoma is highly localized and does not usually spread. However, as this type of cancer can still invade and destroy surrounding tissue, it is considered a malignant form of cancer. Individuals who develop a single lesion of basal cell carcinoma are at an increased risk of developing additional lesions. According to estimates, the risk of developing additional lesions within 3 years is 44%. Genetics A rare hereditary disorder called basal-cell nevus syndrome (BCNS) raises the risk of developing basal cell carcinoma. Also known of as Gorlin syndrome, BCNS is associated with mutations of genes located at human chromosome 9q22. A tumor suppressor gene PTCH1 has also been identified. If mutations occur in this gene, cell signalling pathways may fail to prevent cancerous growth of the cell. Basal cell carcinoma localization Basal cell cancers are limited in their growth and very rarely spread to other organs. Therefore, their careful excision by surgery results in 100% cure-rates. According to researchers, basal cell cancers are also genetically stable which prevents further DNA mutation leading to metastasis. Reviewed by Sally Robertson, BSc Sources http://www.med.muni.cz/biomedjournal/pdf/2006/05/261_270.pdf www.ashfordstpeters.nhs.uk/.../...%20of%20Basal%20Cell%20Carcinoma.pdf www.cap.org/apps/docs/reference/myBiopsy/SkinBasalCellCarcinoma.pdf www.fbae.org/.../Basal%20Cell%20Carcinoma.pdf http://www.skinpathology.net/pdf/basal-cell-carcinoma.pdf www.ncbi.nlm.nih.gov/.../westjmed00080-0077a.pdf http://www.pjo.com.pk/27/1/Ibrar%20Hussain.pdf Further ReadingBasal Cell Carcinoma - What is Basal Cell Carcinoma?Basal Cell Carcinoma DiagnosisBasal Cell Carcinoma TreatmentsBasal Cell Carcinoma PrognosisBasal Cell Carcinoma Epidemiology Last Updated: Nov 17, 2013"
65,"2018-04-20 02:32:44","Basal Cell Carcinoma Treatments","By Dr Ananya Mandal, MD Basal cell carcinoma is highly localized and very rarely spreads, meaning that treatment can achieve a cure rate of almost a 100%. Some of the methods for treatment include surgical and nonsurgical approaches. Surgery Surgery is the most common approach to treating basal cell carcinoma and surgery can be divided into two types, destructive and excisional surgery. Destructive surgery This type of surgery attempts to destroy and kill the cancer cells. One of the most common methods used is curettage and eletrodessication. An instrument called a curette is used to scrape off any cancer until the dermis is reached. An electrical device is then used to denature a layer of the dermis and the currette used again to remove denatured dermis until the surgeon is happy that reasonable margins have been achieved. Curettage and cautery is best suited for low-risk lesions that are small, well defined and non-aggressive. With this therapy, the 5 year cure rates are around 97%. Another example of destructive surgery is cryosurgery. This is used to treat both solitary and multiple lesions. This method employs the extremely cold tips of instruments to freeze and kill cancer cells. The lesion then forms a crust and falls off. Use of the curette before cryosurgery may improve the results. Another destructive surgery technique is carbon dioxide (CO2) laser surgery. This is not a widely used form of treatment and is recommended for low-risk lesions. Excisional surgery Excisional surgery is used for cases where the tumor is completely removed, as well as some of the surrounding healthy flesh in order to provide a safety margin. Excisional surgery is a highly effective treatment for primary lesions. After removal, the lesion is examined under a microscope. Curettage may be combined with excision. For recurrent or previously treated lesions, the success rates are lower than for primary or untreated lesions. Mohs' micrographic surgery is one of the most accurate surgical methods for the excision of basal cell carcinoma. The technique allows accurate microscopic control which allows healthy tissue to be preserved while cancerous tissue is removed. High cure rates are achieved with this approach, even with lesions that are particularly difficult to treat. Non surgical therapies There are several nonsurgical approaches to treating basal cell carcinoma. Radiotherapy describes the use of high energy beams which are directed at the lesion to destroy cancerous cells. Skin therapy refers to the use of medications such as fluorouracil for treating lesions. Skin therapy is useful for low-risk, superficial lesions such as those found on the legs or trunk. Photodynamic therapy is a treatment approach that involves priming the lesion with medication and then using laser beams to kill the cancer cells. Chemotherapy with anticancer drugs is not usually necessary in the treatment of basal cell cancer. If the cancer is recurrent, multiple, aggressive and has spread to other organs, chemotherapy may be needed. Reviewed by Sally Robertson, BSc Sources http://www.med.muni.cz/biomedjournal/pdf/2006/05/261_270.pdf www.ashfordstpeters.nhs.uk/.../...%20of%20Basal%20Cell%20Carcinoma.pdf www.cap.org/apps/docs/reference/myBiopsy/SkinBasalCellCarcinoma.pdf www.fbae.org/.../Basal%20Cell%20Carcinoma.pdf http://www.skinpathology.net/pdf/basal-cell-carcinoma.pdf www.ncbi.nlm.nih.gov/.../westjmed00080-0077a.pdf http://www.pjo.com.pk/27/1/Ibrar%20Hussain.pdf Further ReadingBasal Cell Carcinoma - What is Basal Cell Carcinoma?Basal Cell Carcinoma DiagnosisBasal Cell Carcinoma PathophysiologyBasal Cell Carcinoma PrognosisBasal Cell Carcinoma Epidemiology Last Updated: Nov 17, 2013"
66,"2018-04-20 02:32:49","Basal Cell Carcinoma Prognosis","By Dr Ananya Mandal, MD Basal cell carcinoma is one of the most common skin cancers in America and Australia and incidence is also on the rise in the UK. This rise is thought to be attributable to an increase in exposure to UV rays from the sun. If basal cell cancer is treated in a timely and appropriate manner, full recovery is likely. Sometimes, carcinomas reoccur after being successfully treated and removed for the first time but this is less likely in the case of smaller lesions. Risk of metastasis Unlike most other cancers, basal cell carcinoma rarely spreads to other parts of the body and remains localized to the site of origin. However, it is considered a malignant cancer as it can still invade and destroy surrounding tissues. The cancerous lesion may invade vital structures such as nerves and result in loss of sensation or loss of function in the affected area. In addition, those with basal cell carcinoma have a 50% likelihood of being diagnosed with another tumor in the five years following the first diagnosis. Low risk and high risk cancers Tumors can be categorized according to certain prognostic factors that influence patient outcomes. These factors include: Tumor size Large and more deep-rooted lesions have a worse prognosis than small and superficial lesions. Tumor margins Tumors with a diffuse margin are usually less responsive to treatment than those with more clear-cut margins. Rate and pattern of growth The presence of more rapidly growing tumors and multiple tumors increases the risk of a poor treatment outcome. Recurrent tumors Recurrent tumors and failure of initial therapy signifies a less positive patient outcome. Immune system Suppressed immunity due to the use of immunosuppressants after organ transplant or to treat HIV for example, can lead to a poorer treatment outcome. Reviewed by Sally Robertson, BSc Sources https://ufandshands.org/basal-cell-carcinoma http://www.med.muni.cz/biomedjournal/pdf/2006/05/261_270.pdf www.ashfordstpeters.nhs.uk/.../...%20of%20Basal%20Cell%20Carcinoma.pdf www.cap.org/apps/docs/reference/myBiopsy/SkinBasalCellCarcinoma.pdf www.fbae.org/.../Basal%20Cell%20Carcinoma.pdf http://www.skinpathology.net/pdf/basal-cell-carcinoma.pdf www.ncbi.nlm.nih.gov/.../westjmed00080-0077a.pdf http://www.pjo.com.pk/27/1/Ibrar%20Hussain.pdf Further ReadingBasal Cell Carcinoma - What is Basal Cell Carcinoma?Basal Cell Carcinoma DiagnosisBasal Cell Carcinoma PathophysiologyBasal Cell Carcinoma TreatmentsBasal Cell Carcinoma Epidemiology Last Updated: Nov 17, 2013"
67,"2018-04-20 02:32:51","Basal Cell Carcinoma Epidemiology","By Dr Ananya Mandal, MD Basal cell carcinoma is the most common type of skin cancer in the United States and Australia and was first described by Arthur Jacob in 1827. The condition was first referred to as a histopathological entity in 1903, by Edmund Krompecher who believed that the cancer arose from basal cells in the epidermis. Also called Jacob's ulcer and ulcus rodens, basal cell cancer is localized and rarely spreads. However, because it can still invade and destroy surrounding tissue, it is termed malignant. Basal cell carcinoma is more common among fair skinned, fair haired individuals. The incidence of basal cell carcinoma is highest in Australia, where there are 726 cases per 100,000 people per year. Both genetics and sun exposure are thought to contribute to this high incidence. In England, the incidence of basal cell carcinoma has increased from 173.5 to 265.4 per 100,000 inhabitants every year over the last 10 years. In Germany, there are 96 new cases per 100,000 men per year and 95 cases per 100,000 women per year. For men an women in Canada, Switzerland, the Netherlands, and Finland the respective annual rates of new cases per 100,000 individuals are 87 and 68, 52 and 38, 53 and 38 and 49 and 45. Geographic variations There is notable variation in the geographic location of basal cell carcinoma incidence. Generally, the incidence of basal cell carcinoma increases as a region's latitude decreases because the closer an area is to the equator, the greater the UV radiation. In Australia, the incidence in regions of lower latitude is as high as 1,600 per 100,000 inhabitants per year while in areas of higher latitude in Northern Europe, for example, incidence is significantly lower, ranging from 40 to 80 per 100,000 inhabitants per year. Rising numbers Over the last few decades, the number of people affected by basal cell carcinoma has been on the increase. Among white individuals, the annual incidence has increased by an average of 3.7% in the U.S., Canada and Australia and in the U.S., the incidence is twice that of 20 years ago. In Brazil, the rate of skin cancer increased by around 113% between 2001 and 2006. Estimates suggest that nearly half of fair-skinned individuals over 60 years old will develop some type of skin cancer. Due to a yearly growth rate of 10% in many countries, basal cell cancer will soon surpass the incidence of all other cancers combined. The rise in the number of newly diagnosed cases may be attributed to a greater awareness and understanding of the condition, with healthcare professionals making greater efforts to diagnose and refer patients. A greater cumulative exposure to UV rays, a rise in the popularity of tanned skin, increased longevity and ozone depletion are among other factors suggested. Previous data has shown that men are more commonly affected by basal cell cancer than women. However, recent studies suggest a rise in the amount of females being diagnosed, possibly due to an increase in the use of sun beds and to an increased tendency to seek dermatological care and early medical attention. Basal cell carcinomas excised in women tend to have smaller diameters than those excised in men, suggesting they do indeed seek early medical attention. Reviewed by Sally Robertson, BSc Sources http://www.scielo.br/pdf/abd/v86n2/en_v86n2a13.pdf www.ashfordstpeters.nhs.uk/.../...%20of%20Basal%20Cell%20Carcinoma.pdf www.cap.org/apps/docs/reference/myBiopsy/SkinBasalCellCarcinoma.pdf http://www.skinpathology.net/pdf/basal-cell-carcinoma.pdf Further ReadingBasal Cell Carcinoma - What is Basal Cell Carcinoma?Basal Cell Carcinoma DiagnosisBasal Cell Carcinoma PathophysiologyBasal Cell Carcinoma TreatmentsBasal Cell Carcinoma Prognosis Last Updated: Nov 17, 2013"
68,"2018-04-20 02:32:55","What is Batten Disease?","By Dr Ananya Mandal, MD Batten disease is an inherited neurological disease that is often fatal. It usually develops during childhood, between the ages of 5 and 10 years. The earliest symptoms range from being fairly obvious, with a child experiencing seizures or vision problems, through to subtle signs such as mild personality changes or clumsiness. Pathology and manifestations of Batten disease Batten disease is also known as Spielmeyer-Vogt-SjögrenBatten disease and is the most common of the diseases collectively known of as neuronal ceroid lipofuscinoses (NCL). Batten disease was originally used to describe the juvenile form of NCL but is now more commonly used to refer to all forms of NCL. The symptoms of Batten disease are caused by a build up of substances called lipopigments, composites of fat and protein, in the tissues of the body. These lipopigment deposits accumulate in the eyes, brain, skin, muscles and other tissues, damaging neurons in the retina and central nervous system. Eventually, children develop mental impairment, seizures, and worsening sight and motor skills until they became blind or bedridden. Batten disease epidemiology and inheritance NCLs are rare disorders, affecting around 2 to 4 of every 100,000 live births in the United States. The disease has a higher prevalence in Finland, Sweden and other parts of northern Europe. Batten disease is inherited in an autosomal recessive fashion, meaning a child needs to inherit two defective genes (one from each parent) for the disorder, if they are to develop the disease. When both parents carry one defective gene, each of the couple's children has a one in four chance of developing NCL. Each child also has a one in two chance of inheriting just one copy of the defective gene, making them a carrier of the gene. This means they can pass the gene onto their children even though they do not develop the illness themselves. Diagnosis Tissue sampling Tissue can be examined using an electron microscope to look for NCL deposits. Skin, muscle, conjunctiva or blood samples may be used. Electroencephalogram (EEG) This instrument is used to measure electrical activity in the brain, to give an indication of whether a patient may be experiencing seizures. Electrical studies of the eye These tests can be used to examine the retina and visual responses for signs of problems that are common in Batten disease. Brain scan A computed tomography scan or magnetic resonance imaging scan may be used to reveal areas of decay in the brains of NCL patients. Treatment Currently, there are no specific treatments to stop or prevent the progression of Batten disease. However, symptoms of the disease such as seizures can be controlled with anticonvulsant drugs or anti-epileptic drugs. Physiotherapy and occupational therapy may also provide some symptom relief and help to retain bodily function for as long as possible. Reviewed by Sally Robertson, BSc Sourceshttp://www.ninds.nih.gov/disorders/batten/batten_pamphlet-pdf.pdf www.bdsra.org/.../Batten-Disease-An-Easy-To-Understand-Guide.pdf http://www.blakespurpose.org/pdfs/BlakesPurposeBrochure.pdf internationalorthoptics.org/.../..._neuronal_ceroid_lipofuscinosis.pdf http://www.ninds.nih.gov/disorders/batten/batten.htmFurther ReadingBatten Disease SymptomsBatten Disease Treatment Last Updated: Feb 13, 2014"
69,"2018-04-20 02:32:59","Batten Disease Symptoms","By Dr Ananya Mandal, MD Batten disease is one of a group of diseases called neuronal ceroid lipofuscinoses, or NCLs. The term Batten disease was previously used to refer to a juvenile form of NCL but it has become increasingly common to refer to all forms of NCL as Batten disease. Inheritance Batten disease is inherited in an autosomal recessive fashion, meaning a child needs to inherit one copy of the defective gene for the condition form each of their parents in order to develop the disease. When both parents carry the defective gene, each of the children has a one in four chance of developing NCL. Each child also has a one in two chance of inheriting just one copy of the defective gene. This would make them a carrier of the gene, which they may pass onto their children even though they never develop the condition themselves. Pathology and symptoms of Batten disease The symptoms of Batten Disease arise due to a build up of substances called lipopigments, composites of fat and protein, in the bodily tissues. The word ""lipo,"" means lipids or fat and ""pigment"" refers to the greenish-yellow colour they exhibit under the ultraviolet light microscope. These lipopigments accumulate in various tissues of the body including the retina, skin, muscles and central nervous system. They form deposits inside cells that can be viewed as distinctive half-moon shapes, fingerprint shapes or sand grain shapes. These NCL deposits damage neurons in the tissues, eventually leading to symptoms of the disease. Symptoms Batten disease usually develops during childhood between the ages of 5 and 10 years. Symptom onset may be obvious, with the child suffering from seizures or vision loss or it may be subtle, only causing mild personality changes or clumsiness. Over time, symptoms progress and the patient begins to suffer form mental impairment, loss of vision, loss of motor skills and worsening seizures. Eventually, the child may become blind, bedridden and unable to communicate. By this stage, individuals are at risk of losing their lives. People who develop childhood forms of NCL do not usually live much beyond the age of 30 years. Types of neuronal ceroid lipofuscinoses There are four main types of NCL. These include: Infantile NCL - Also called Santavuori-Haltia disease, this is a severe form of the disease that starts to develop between 6 months and 2 years of age and is rapidly progressing. Affected children have unusually small heads (micorcephaly), fail to thrive and often suffer from short, sharp contractions or jerks. The condition progresses rapidly and children only live into their mid-childhood years. Late infantile NCL - Also called Jansky-Bielschowsky disease, this form starts to affects children at age 2 to 4 years. Typical early symptoms include loss of muscle control (ataxia), mental deterioration and seizures. Late infantile NCL also progresses rapidly and children usually die between the ages of 8 and 12. Juvenile NCL (Batten disease) - This form of the condition starts to develop between the ages of 5 and 8 years. The first signs of the condition often include clumsiness, vision loss, ataxia or seizures. This form progresses more gradually, with individuals usually dying in their late teens or early twenties, although some sufferers make it into their 30s. Adult NCL - Also called Kufs Disease or Parry Disease, this condition usually affects individuals before the age of 40. This form of NCL is slower to progress and symptoms are milder. Age at death varies somewhat but the condition does shorten lifespan. Reviewed by Sally Robertson, BSc Sourceshttp://www.ninds.nih.gov/disorders/batten/batten_pamphlet-pdf.pdf www.bdsra.org/.../Batten-Disease-An-Easy-To-Understand-Guide.pdf http://www.blakespurpose.org/pdfs/BlakesPurposeBrochure.pdf internationalorthoptics.org/.../..._neuronal_ceroid_lipofuscinosis.pdf http://www.ninds.nih.gov/disorders/batten/batten.htmFurther ReadingWhat is Batten Disease?Batten Disease Treatment Last Updated: Feb 13, 2014"
70,"2018-04-20 02:33:00","Batten Disease Treatment","By Dr Ananya Mandal, MD One of the common early symptoms of Batten disease is loss of vision and the disease may first be suspected during an ophthalmic examination. A loss of cells within the eye can be an indicator of several forms of Batten disease but because cell loss occurs in other forms of eye disease, an eye exam alone is not enough to diagnose the illness. Other steps taken in the diagnosis of Batten disease include: Detailed family history is obtained - Batten disease is inherited in an autosomal recessive fashion and family history can provide an indication of the likelihood that the disease has been inherited. Blood and urine tests - Certain abnormalities in the blood and urine can indicate Batten disease. For example, an elevated level of dolichol in the urine can be an indicator, as can the presence of white blood cells that contain holes or vacuoles. Tissue samples - Tissue analysis using an electron microscope can reveal the presence of the lipopigment deposits seen in Batten disease. These deposits may resemble the shape of half-moons or sand grains. The deposits are often observed in skin cells and cells lining the sweat glands. The deposits are found in many different tissues and skin, muscle, conjunctiva or blood samples may be used. Electroencephalogram (EEG) - An EEG is used to measure electrical activity in the brain to give an indication of whether a patient may be experiencing seizures. Brain scans - The brain is also examined using computed tomography (CT) scans and magnetic resonance (MRI) scans to reveal any areas of decay. Electrical studies of the eye - These tests can be used to examine the retina and visual responses and check for signs of problems that are common in Batten disease. DNA analysis - Each type of Batten disease is caused by a defect in a particular gene and genes for eight of the ten known forms have been identified. These genes can be tested for diagnostic purposes as well as for identifying carrier or prenatal status. Treatment There is currently no specific treatment that can cure or slow progression of this condition and therapy is instead focused on preventing and relieving symptoms. For example, anti-convulsant drugs may be used in cases where patients suffer form seizures and physiotherapy can help individuals retain function of their body for as long as possible. Reviewed by Sally Robertson, BSc Sources http://www.ninds.nih.gov/disorders/batten/batten_pamphlet-pdf.pdf www.bdsra.org/.../Batten-Disease-An-Easy-To-Understand-Guide.pdf http://www.blakespurpose.org/pdfs/BlakesPurposeBrochure.pdf internationalorthoptics.org/.../..._neuronal_ceroid_lipofuscinosis.pdf http://www.ninds.nih.gov/disorders/batten/batten.htmFurther ReadingWhat is Batten Disease?Batten Disease Symptoms Last Updated: Feb 13, 2014"
71,"2018-04-20 02:33:07","Bed Bugs - Parasitic Insects","By Yolanda Smith, BPharm Bedbugs are small insects without wings. They are a type of nocturnal parasites, as they rest during the day and feast at night, although they may also bite during the day occasionally. Bed bugs usually live in bedding or mattresses and feed on the blood of humans. Their mouth has evolved in such a way that allows bed bugs to easily pierce skin without causing pain to humans. They are small insects (about 5 mm long) with six legs and a flat, oval-shaped body. They do not have any legs and are light brown in color, with a reddish tinge after feasting on blood. They have a small head with large antennae and large mandibles in their mouth. Close up cimex hemipterus on corrugated recycled paper, bedbug, blood sucker - Image Copyright: Smith1972 / Shutterstock Life Cycle Bedbugs have a complex lifecycle with several different developmental stages: Egg (approximately 1 mm in size) 1st stage nymph (approximately 1.5 mm in size) 2nd stage nymph (approximately 2.0 mm in size) 3rd stage nymph (approximately 2.5 mm in size) 4th stage nymph (approximately 3.0 mm in size) 5th stage nymph (approximately 4.5 mm in size) Adult bedbug (approximately 5.0 mm in size) Bedbugs mate through a process known as traumatic insemination, which involves piercing of the female’s abdomen and ejaculation by the hypodermic penis of the male. The sperm travels to storage areas in the body and, eventually, fertilization occurs, allowing for the production of eggs in females. Bedbugs can survive for long periods of time, up to several months, without feeding on human blood. However, they are susceptible to very hot or very cold climates and may not survive extreme temperatures. Interaction with Humans Bedbugs are parasites that rely on blood to survive. They can feed on the blood of any mammal, although they appear to prefer the blood of humans. They are attracted to the warmth surrounding mammalian bodies and the carbon dioxide present in breath expiration. It is usually these factors that guide bedbugs to locate a suitable host for feeding. Bedbugs usually bite the shoulders and arms of humans. The proboscis of the bedbug pierces the skin and allows the bedbug to feed on the blood. The saliva of the bedbug is injected into the host, which contains an anticoagulant substance that some people have an allergic reaction to. The feed process takes approximately 5-10 minutes. The bedbug becomes filled with blood, changing in color from light brown to rusty red. Human Reaction to Bites The human reaction to bedbug bites varies from one individual to another. Some people do not react at all, whereas others will experience intense itching and inflamed skin. Symptoms may include: Large welts on skin Itchiness Reddening Inflammation Blister formation Loss of skin Bedbugs have the potential to carry diseases in the body, but it is very unlikely that these diseases would be transmitted to humans when they bite them. As such, this risk is not substantial. The most severe reaction to bedbugs occurs when an individual is allergic to bedbugs. It is recommended that people affected by bedbugs resist the urge to scratch, which may lead to scarring and infection of the skin. Instead, the bites should be washed and medications may be used to decrease symptoms, such as itchiness. Reviewed by Susha Cheriyedath, MSc References http://www.nhs.uk/conditions/bed-bugs/Pages/Introduction.aspx http://www.orkin.com/other/bed-bugs/bedbug-bites/ https://www.aad.org/public/diseases/itchy-skin/bedbugs https://www.betterhealth.vic.gov.au/health/conditionsandtreatments/bedbugs Further ReadingBedbugs - Diagnosis and ManagementBedbugs Life CycleBedbugs Evolution and History Last Updated: Oct 24, 2016"
72,"2018-04-20 02:33:09","Bedbugs - Diagnosis and Management","By Yolanda Smith, BPharm The diagnosis of bedbugs hinges on the symptoms of the bites and evidence of bedbugs living in the environment of the individual. If a diagnosis is made, the bedbugs should be eradicated from the area and the symptoms managed appropriately, as described below. Diagnosis There are two key factors that may indicate that an individual has bed bugs: evidence of bites on the body and of bedbugs in bedding. Bites from bedbugs typically cause itchy welts, which appear in a zigzag pattern on the skin. Some skin conditions can sometimes be confused with bedbug bites, such as skin rashes, hives, measles, or chickenpox, which can make accurate diagnosis more difficult. Bed Bug - Image Copyright: jareynolds / Shutterstock It is unlikely to see the actual bedbugs unless they are present in vast numbers. As the bed bugs are not usually visible, many people assume they have been bitten by other insects such as mosquitos, fleas, or spiders. To confirm that the bites are caused by bedbugs, it is essential to check for signs of the presence of bedbugs. Signs that may indicate the presence of bedbugs include: Musty odor: Bedbugs produce chemicals as a method of communication and these chemicals have a sweet, musty smell. Blood on bedding or upholstered furniture: Specks of blood on the mattress, bedding or soft furniture, particularly near the seams, may be an indication of bedbugs. Evidence of exoskeletons: As bedbugs progress through their complex lifecycle, they shed a series of exoskeletons from their body. These shell-like outer layers may be left behind and seen on bedding or other soft surfaces. Evidence of feces: Tiny, black specks may be visible on bedding due to the excrement of the bedbugs. Evidence of eggs: Tiny white oval eggs may be found in cracks and crevices of the bedding, such as in the seams of the mattress, from when the female bedbug lays eggs. Management Bedbugs are not a serious medical concern, although they can lead to significant anxiety and disturbed sleep in affected individuals. All bedding and soft surfaces in the home environment should be well cleaned and vacuumed. The bites should be washed with soap and water to prevent infection and reduce itchiness. Most bites usually heal within a few weeks without treatment. To manage symptoms of itching, an oral antihistamine medication is often effective. Additionally, corticosteroid cream can be applied topically to reduce itch. Patients with severe symptoms related to bedbug bites should be referred to a dermatologist who is experienced in treating the infection and relieving the symptoms of the bites. In some cases, an antibiotic or antiseptic medication may be required to treat or prevent an associated infection. For patients who have experienced an allergic reaction to the bedbug bites, an injection may be required to abate this. An antihistamine or corticosteroid injection is commonly used for mild reactions, or epinephrine for more severe reactions. Eradicating the bedbugs from the environment is the only way to successfully stop being bitten by bedbugs. The use of bug spray is not recommended as it has poor efficacy on bedbugs; a pest-control agency is usually the best option. Reviewed by Susha Cheriyedath, MSc References https://www.aad.org/public/diseases/itchy-skin/bedbugs#treatment https://www.betterhealth.vic.gov.au/health/conditionsandtreatments/bedbugs http://www.nhs.uk/conditions/bed-bugs/Pages/Introduction.aspx Further ReadingBed Bugs - Parasitic InsectsBedbugs Life CycleBedbugs Evolution and History Last Updated: Oct 24, 2016"
73,"2018-04-20 02:33:13","Bedbugs Life Cycle","By Yolanda Smith, BPharm There are various species of bedbugs with slight differences in the way they reproduce and their lifestyle. This article is an overview of the general lifecycle of most bedbugs, which includes six significant transformations and a unique method of reproduction. Life Stages In addition to the egg, there are six main life stages of a bed bug: five immature nymph life stages followed by a final sexually mature adult stage. These life stages of a bed bug are as follows: Egg (approximately 1 mm in size) 1st stage nymph (approximately 1.5 mm in size) 2nd stage nymph (approximately 2.0 mm in size) 3rd stage nymph (approximately 2.5 mm in size) 4th stage nymph (approximately 3.0 mm in size) 5th stage nymph (approximately 4.5 mm in size) Adult bedbug (approximately 5.0 mm in size) At each stage, the bedbugs discard their outer exoskeleton through a process known as ecdysis. They must feed with at least one blood meal before shedding each exoskeleton and must complete this cycle six times before reaching fertile adulthood. Each life stage typically lasts about a week, depending on environmental factors such as temperature and food availability. Once a bedbug has reached maturation and is classed as an adult, it is possible for the bedbug to mate with another and reproduce. Reproduction of Bedbugs Bedbugs mate through a process known as traumatic insemination. The females have a reproductive tract that functions during oviposition, although this is not used for sperm insemination. Traumatic insemination refers to the piercing of the female’s abdomen by the hypodermic penis of the male, with ejaculation into the mesospermalege of the body. The sperm then travels to sperm storage structures known as seminal conceptacles. Over time, fertilization occurs in the ovaries of the female. In some cases, male bedbugs attempt to mate with other males via traumatic insemination, usually due to sexual attraction related to the size of the bug. Males who are mounted may be severely injured, as they lack the spermalege organ that females have evolved for protection. Instead, males may excrete alarm pheromones to prevent the traumatic insemination. Fertilization leads to the completion of the ovary development and allows for egg production in the corpus allatum. The sperm can be carried in the conceptacle of the female, where the body temperature is optimal for conservation, for an extended period of time. The female then lays fertilized eggs until all the sperm in her conceptacle have been used, possibly generating several hundred eggs in this time. Following the depleted supply of sperm, the female lays several eggs that are sterile. The quantity of sterile eggs depends on the nutritional status of the female and is independent of the sperm. Special Cases Cimexlectularius males have microbes on their genitals that damage their sperm; rendering them incapable of fertilizing female eggs. However, to cope with this, the males have evolved to ejaculate antimicrobial substances to protect the sperm from damage, so that they can still reproduce. Reviewed by Susha Cheriyedath, MSc References http://www.nhs.uk/conditions/bed-bugs/Pages/Introduction.aspx https://www.epa.gov/bedbugs/bed-bugs-appearance-and-life-cycle http://www.orkin.com/other/bed-bugs/bedbug-life-stages/ http://www.cdc.gov/parasites/bedbugs/biology.html Further ReadingBed Bugs - Parasitic InsectsBedbugs - Diagnosis and ManagementBedbugs Evolution and History Last Updated: Oct 24, 2016"
74,"2018-04-20 02:33:17","Bedbugs Evolution and History","By Yolanda Smith, BPharm Bedbugs have a long history, and it has been suggested that they originated in caves occupied by humans and animals, such as bats, in the Middle East region. This report summarizes the known history of bedbugs from the reports available. Ancient History The first known record of bedbugs was in ancient Greece in approximately 400 BC. Aristotle also made reference to the bugs shortly afterwards. Pliny the Younger was a well-known figure in ancient Roman times for publishing the first edition of Natural History in circa 77 AD. This edition cited the medicinal value of bedbugs in the treatment of certain ailments, such as ear infections and snakebites. This belief was largely uncontested for the following centuries, until the 18th century. There was little mention of bedbugs throughout the Middle Ages. They were, however, noted in historical documents in Germany and France in the 11th, and 13th century, respectively. Modern Era There was no mention of bedbugs in England until the 16th century, although they remained to be rarely noticed until the 17th century. In fact, some people of that era believed that bedbugs were introduced to London on the imported supplies used to rebuild the city following the Great Fire of London in 1666. Guettard was a natural doctor in the 18th century who recommended the use of bedbugs in the treatment of hysteria. One method implemented to eradicate bedbugs used in the 19th century was the smoke from peat fires. Dust has commonly been used to repel insects from grain storage sites throughout history and was also trialed for bedbugs. Some types of soil, such as diatomaceous earth, continues to be used by some for managing a bedbug infestation. Contemporary History The prevalence of bedbugs in common households was high in the beginning of the 20th century. In 1933, the UK Ministry of Health published a report indicating that most houses were infested to some degree in many areas of the UK. This was thought to be linked to the significant rise in population at this time and the introduction of electric heating, which allowed the temperature-sensitive bedbugs to survive cold weather. Bedbugs posed a significant problem to military bases during World War II. This was initially managed with fumigation, later with hydrogen cyanide gas, and finally with DDT. Throughout the latter half of 20th century, the prevalence bedbugs declined, which is likely due to the introduction of potent pesticides, public health campaigns, and improved cleanliness in households. In recent decades, there has been a resurgence of bedbug infestations, without a clear cause. This may be due to factors such as resistance, decreased pesticide used, increased travel, and complacency. According to the U.S. National Pest Management Association, there was a 71% increase in calls related to bedbugs from 2000 to 2005. Historical Methods of Extermination Throughout history, various methods have been used to repel or exterminate bedbugs. Some of these include the use of: Actaea racemosa (black cohosh) Pseudarthria hookeri Laggera alata Eucalyptus saligna Lawsonia inermis Melolontha vulgaris Amanita muscaria Mentha arvensis Lepidium ruderale Geranium robertianum Reduvius personatus Reviewed by Susha Cheriyedath, MSc References http://www.bedbugs.org/the-history-of-bed-bugs/ http://www.bbc.com/earth/story/20150130-origin-of-bed-bugs-revealed http://www.bedbuggeneral.com/History_of_Bed_Bugs_s/83.htm http://entsoc.org/PDF/2011/AE-Potter-spring2011.pdf Further ReadingBed Bugs - Parasitic InsectsBedbugs - Diagnosis and ManagementBedbugs Life Cycle Last Updated: Oct 24, 2016"
75,"2018-04-20 02:33:20","What is Bedwetting?","By Dr Ananya Mandal, MD Bedwetting or nocturnal enuresis is a condition that affects millions of children worldwide, as well as some adults and elderly individuals. Although it is common for children younger than five years to wet the bed several times a week, this is a cause for concern in children older than five years. For most children who wet the bed, there is no underlying disease or pathology causing the condition. Parents need to refrain from scolding, berating or frightening a child who bed wets as this will only worsen the condition, which can stem from emotional stress or major life changes such as moving house or starting a new school. Bedwetting may resolve over time as the child develops and grows up. Bedwetting is more common among boys than girls but the cause of this gender difference is not known. Possible triggers of bedwetting include Excess fluid intake before bed time Caffeine intake before bed time Excess urine production due to deficiency of vasopressin, a hormone that regulates urine production Urinary tract infection Type 1 diabetes Abnormality of the urinary tract Abnormality of the nerves that send signals from the bladder to the brain Cause Usually, once the bladder has become full, a signal is sent from the bladder to the brain to wake up and an individual may then get up and visit the loo. However, in young children and deep sleepers this wake up response may not occur, leading to voiding of the bladder in bed. In children, this may happen because the nerves connecting the brain to the bladder are not yet fully developed. Symptoms Symptoms of bedwetting include: Needing to visit the toilet frequently during daytime hours Pain on urination or fever due to possible urinary tract infection Constipation Straining to pass urine Excessive thirst Accidental passing of stools due to nerve abnormality Diagnosis Diagnosing bedwetting involves maintaining a diary recording the symptoms and frequency of incidents as well as the volume of urine passed each day. Any history of symptoms is also obtained and blood and urine analysis performed to check for conditions such as urinary tract infection or diabetes. In addition, an abdominal ultrasound may be recommended to check for stones in the bladder or urinary tract. Treatment Treatment is focused on providing support and advice to the person experiencing bedwetting and this is often enough for the problem to resolve independently in a child as they grow older. Lifestyle modifications that a child may be encouraged to adhere to include: Reducing fluids consumed before bedtime Ensuring regular toilet visits throughout the day and particularly before bedtime Minimising caffeine intake as caffeine is a diuretic and stimulates urine production The adequate amount of daily fluid intake for a 4 to 8 year old child is usually 1,000 to 1,400 ml and a normal voiding frequency is 4 to 7 times per day. Medication Some medications that have been found to be useful in correcting bedwetting include: Desmopressin, the synthetic version of the hormone vasopressin that regulates urine production Oxybutynin which relaxes the muscles in the bladder, reducing its activity Imipramine which blocks certain nerve receptors in the wall of the bladder that would usually stimulate the bladder to empty Reviewed by Sally Robertson, BSc Sources http://www.kidney.org/atoz/pdf/bedwetting.pdf http://kidney.niddk.nih.gov/kudiseases/pubs/pdf/WINTKABedwetting.pdf http://www.nhs.uk/Conditions/Bedwetting/Pages/Introduction.aspx http://cks.nice.org.uk/bedwetting-enuresis http://www.nice.org.uk/nicemedia/live/13246/51367/51367.pdf Further ReadingBedwetting Diagnosis and TreatmentBedwetting CausesBedwetting Impact on Children Last Updated: Sep 24, 2013"
76,"2018-04-20 02:33:22","Bedwetting Diagnosis and Treatment","By Dr Ananya Mandal, MD Nightime bedwetting or nocturnal enuresis is a common phenomenon among children younger than five years of age. However, among children older than five years, night time bed wetting that occurs more than twice a week is a cause for concern. Diagnosing nocturnal enuresis Diagnosis of the condition involves obtaining a detailed history of the child's symptoms and the frequency of their bedwetting. Parents are asked to keep a diary recording the number of times per week the child has wet their bed as well as daily recordings of their fluid intake, toilet visits, and voiding volume. The child is then examined and tests are run to rule out other underlying conditions. Some of these tests include: Blood sugar assessment to check for type 1 diabetes Urine analysis if urinary tract infection is suspected An abdominal ultrasound to test for urinary tract disorder and the presence of stones Treatment In the majority of cases, childhood bedwetting does not require any specific treatment and usually resolves with parental support and lifestyle modifications. Such lifestyle alterations include: Reducing and controlling the child's fluid intake, especially during the evening before bedtime. The amount of fluid a child aged 4 to 8 years requires is around 1.5 litres per day. Eliminating the child's intake of caffeine-containing drinks such as hot chocolate or Coca-Cola, prior to bedtime. Allowing the child to empty their bladder before bedtime. A healthy child passes urine at least 4 to 7 times during the day. Not reprimanding or punishing the child for bedwetting as this raises the child's anxiety level and reduces their self esteem, only increasing the likelihood of bedwetting. Rewarding the child, however, for adhering to agreed lifestyle changes may help reduce bedwetting episodes. Managing bedwetting Petroleum jelly applied to the child's buttocks and inner thighs can help prevent rashes associated with frequent bedwetting. Waterproof bed sheets and disposable diapers can be used to keep the child dry at night. A bedwetting alarm can be used to help parents monitor the frequency of bedwetting as well as to help the the child become adjusted to waking up and going to pass urine during the night. Specific therapies Specific therapies may be used to treat children with underlying causes of bedwetting and these include: Antibiotic treatment for urinary tract infections Glucose lowering treatment for type 1 diabetes The prescription of desmopressin, a synthetic form of the hormone vasopressin which regulates urine production The use of oxybutynin to relax the bladder muscles and increase its capacity to hold urine The use of imipramine to treat mood disorders that may be exacerbating bedwetting, such as panic disorders or depression Reviewed by Sally Robertson, BSc Sources http://www.kidney.org/atoz/pdf/bedwetting.pdf http://kidney.niddk.nih.gov/kudiseases/pubs/pdf/WINTKABedwetting.pdf http://www.nhs.uk/Conditions/Bedwetting/Pages/Introduction.aspx http://cks.nice.org.uk/bedwetting-enuresis http://www.nice.org.uk/nicemedia/live/13246/51367/51367.pdf Further ReadingWhat is Bedwetting?Bedwetting CausesBedwetting Impact on Children Last Updated: Sep 23, 2013"
77,"2018-04-20 02:33:27","Bedwetting Causes","By Dr Ananya Mandal, MD In general, childhood bedwetting does not have an underlying cause and is not the child's fault. Reprimanding or embarrassing the child will only aggravate the problem further. Bedwetting may run in families and is twice as common among boys than among girls. Causes Some of the causes of bedwetting include: Failure to wake up and use the toilet Normally, when the bladder is full, a signal is sent to the brain that causes a person to wake up and go to the toilet. However, children under five years of age may sleep so deeply that they fail to wake up. This is due to underdevelopment of the nerves that carry signals along the spine from the brain to the bladder. Furthermore, even when children do wake up they may be too afraid of the dark to get up and go to the toilet. Excessive fluid intake before bedtime Compared with adults, children have a smaller bladder with less filling capacity and they are therefore more likely to wet the bed if they have had too much fluid during the evening or before bedtime. Caffeine intake before bedtime Drinking caffeine-containing drinks before bedtime can lead to increased bedwetting as caffeine is a diuretic and therefore increases urine output. Caffeine is found in drinks such as tea, coffee, Coca-Cola and hot chocolate, all of which need to be avoided if bedwetting is to be prevented. Vasopressin deficiency Excess urine production may be caused by a deficiency of vasopressin, a hormone that regulates urine production. Overactive bladder syndrome Some children may suffer from overactive bladder syndrome, a condition which causes the bladder muscles to contract more frequently, leading to excessive voiding of the bladder. Medical conditions Medical conditions that may cause bedwetting include type 1 diabetes, severe constipation, urinary tract infection, bladder stones, or abnormalities of the urinary tract or the nerves that connect the bladder to the spine. Emotional experiences Changes in emotion triggered by, for example, going to a new school, the introduction of a new sibling, moving house or parental discord may all lead to the incidence of bedwetting in a child who does not normally wet the bed. This condition is called secondary nocturnal enuresis. Children with clinical depression, attention-deficit hyperactivity disorder or behavioral problems may also develop a problem with bedwetting. Reviewed by Sally Robertson, BSc Sources http://www.kidney.org/atoz/pdf/bedwetting.pdf http://kidney.niddk.nih.gov/kudiseases/pubs/pdf/WINTKABedwetting.pdf http://www.nhs.uk/Conditions/Bedwetting/Pages/Introduction.aspx http://cks.nice.org.uk/bedwetting-enuresis http://www.nice.org.uk/nicemedia/live/13246/51367/51367.pdf Further ReadingWhat is Bedwetting?Bedwetting Diagnosis and TreatmentBedwetting Impact on Children Last Updated: Sep 23, 2013"
78,"2018-04-20 02:33:32","Bedwetting Impact on Children","By Dr Søren Rittig By Keynote ContributorDr. Søren RittigPediatrics Professor, Aarhus University Bedwetting, also known as nocturnal enuresis, is an uncontrollable leakage of urine from the bladder while asleep. 1 For children aged five years and older, bedwetting is abnormal and should not be considered a trivial condition. 2,3,4 Bedwetting is common; with approximately 5–10% of 7 year-olds regularly wetting their beds.5 Bedwetting can and should be treated6, but despite this, nearly half of parents do not seek help, as many believe that their child will eventually outgrow the problem.7 In fact, if left untreated bedwetting will not necessarily go away by itself and can persist for life, with approximately 1 in 100 people continuing to wet the bed into adulthood.8 Bedwetting can have a serious effect on the quality of life of children and their families9 Bedwetting can be very distressing for children, however, the impact is often underestimated and trivialized by parents and doctors.9 Children may suffer from feelings of low self-esteem at an age when image is extremely important for optimal personal development.10,11 Bedwetting is also associated with reduced day time functioning, including school and social performance.2,3,4,10,11 More than half of parents do not allow their children to spend time away from home, so they often miss out on social activities such as sleepovers at friends’ houses and school trips.12 A lack of understanding can also cause parents to be frustrated and this contributes to the child’s sense of failure and shame; reinforcing the social stigma surrounding bedwetting.13,14 Aside from the social and emotional stress, there is also a recognized economic burden on families.15 Bedwetting creates additional work for families in the form of increased household duties and so results in often substantial financial costs.16 Successfully treating bedwetting removes the burden placed on both the child and family. The causes of bedwetting A frequent misconception of bedwetting is that the cause is psychological; however extensive research suggests that this is not the case.2,3,4 Bedwetting is often caused by over-production of urine at night or reduced capacity of the bladder. An inability to wake up to the signals from a full bladder is common for all bedwetting children.2,3,4 There are also likely to be genetic factors, with nearly two thirds of children who wet the bed having one or both parents with a history of the condition.17 World Bedwetting Day raises awareness of the condition so that children and families can get the help they deserve The International Children’s Continence Society (ICCS) and the European Society of Pediatric Urologists (ESPU) have launched World Bedwetting Day to raise awareness among the public and healthcare professionals that bedwetting is a common medical condition that can and should be treated.6 World Bedwetting Day 2015’s slogan is ‘Time to Take Action’, in recognition that much more can be done to diagnose and treat children who suffer from bedwetting. The aim of World Bedwetting Day is to encourage children and their families to discuss the condition with their healthcare professional without embarrassment or guilt. Children who wet the bed tend to feel a sense of shame,18,19 and it is hoped that increased public awareness will urge more families the get the help that they need. World Bedwetting Day is initiated by a working group consisting of the ICCS and ESPU, and from 2016 onwards, will take place every year in May. About Dr Søren Rittig Søren Rittig graduated from Aarhus University Medical School in 1987 and passed the ECFMG (Educational Committee for Foreign Medical Graduates, U.S.A.) exam in 1990. He has completed a Research Fellowship at Aarhus University, Clinical Institute and Northwestern University Medical School, Dept. of Medicine, Chicago, USA. He became a specialist in Pediatrics in 2002 and has been consultant in Pediatric Nephrology at Aarhus University Hospital, Aarhus Denmark since 2004. In 2010 he defended his thesis on circadian regulation of urine output in normal children and children with nocturnal enuresis. He became full Professor in Pediatrics, Aarhus University in 2012. He has since Medical School been heavily involved in research in childhood incontinence, especially nocturnal enuresis. His research has been focusing especially on circadian rhythms and enuresis pathophysiology and treatment; e.g. the description of a deficient circadian rhythm of vasopressin secretion in nocturnal enuresis that was correctable with administration of the vasopressin analogue desmopressin. Since 1992, he has also been involved in molecular genetic research of inherited forms of diabetes insipidus and other renal tubular disorders and his laboratory has contributed with description of many mutations in familial diabetes insipidus. Søren Rittig has published app. 150 peer reviewed papers, 6 book chapters, and co-edited several supplements in International journals. Furthermore, he has supervised 20 PhD programs. Since 1999, he has been director of Center for Child Incontinence in Aarhus and he is the current Scientific Chairman of the International Children’s Continence Society (ICCS). He also currently holds the post as Board member of the European Society for Pediatric Nephrology (ESPN). Supported by Ferring Pharmaceuticals. For more information please visit www.worldbedwettingday.com. References Tryggve Nevéus et al. The Standardization of Terminology of Lower Urinary Tract Function in Children and Adolescents: Report from the Standardization Committee of the International Children’s Continence SocietyJ Urol 2006;176:314-324 Vande Walle J, Rittig S et al. Eur J Pediatr. Jun 2012; 171(6): 971–983 Vande Walle J et al, Erratum to: Practical consensus guidelines for the management of enuresis. Eur J Pediatr 2013;171:971-983 Vande Walle J et al, Erratum to: Practical consensus guidelines for the management of enuresis. Eur J Pediatr 2012;171:971-983 Nevéus T. Nocturnal enuresis—theoretic background and practical guidelines. Pediatr Nephrol. 2011; 26:1207–1214 Hjälmås K et al. Nocturnal Enuresis: An International Evidence Based Management Strategy. The Journal of Urology. 2004; 171:2545–2561 Schlomer, Bruce et al Parental beliefs about nocturnal enuresis causes, treatments, and the need to seek professional medical care, Journal of Pediatric Urology (2013) 9, 1043e1048 NHS Conditions: http://www.nhs.uk/conditions/Bedwetting/pages/introduction.aspx [Last accessed: October 2015] Nathan D, Nocturnal enuresis guidelines. Notthingham Children’s Hospital. 2014. 1-17 Joinson C et al, Pediatrics. 2007 Aug;120(2):e308-16 Theunis M et al. Self-Image and Performance in Children with Nocturnal Enuresis. European Urology. 2002; 41:660-667 ERIC: http://www.eric.org.uk/Campaigns/BedwettingAwarenessWeek [Last accessed: October 2015] Morison M J. Living with a young person who wets the bed; the families’ experience. Br J Nursing 2000; 9 (9): 572-588 Läckgren G et al. Nocturnal enuresis: a suggestion for a European treatment strategy. Acta Paediatr 1999; 88: 679-690 Tryggve Nevéus et al, Enuresis – Background and Treatment Scand J Urol Nephrol Suppl 206: 1–44, 2000 Schulpen TWJ. The burden of nocturnal enuresis. Acta Paediatr 86: 981-4. 1997 Von Gontard A et al. The genetics of enuresis: a review. J Urol 2001; 166: 2438-2443 Hagglof B, Andren O, Bergstrom E, Marklund L, Wendelius M. Self-esteem before and after treatment in children with nocturnal enuresis and urinary incontinence Scand J Urol Nephrol Suppl. 1997;183:79-82 Hjälmås K. Pathophysiology and impact of nocturnal enuresis. Acta Paediatr. 1997 Sep;86(9):919-2 Disclaimer: This article has not been subjected to peer review and is presented as the personal views of a qualified expert in the subject in accordance with the general terms and condition of use of the News-Medical.Net website. Last Updated: Aug 3, 2017"
79,"2018-04-20 02:33:38","What is Behavioral Medicine?","By Liji Thomas, MD Behavioral medicine (BM) is a newly developing field of study which integrates behavioral, psychosocial, and biomedical concepts and practices to prevent, diagnose, and treat patients with psychosomatic disorders. The practice of BM targets the relation between how both thought and behavior can affect mental and physical health. Image Credit: Monkey Business Images / Shutterstock Evolution of Behavioral Medicine BM emerged in the late 19th century as a subordinate of psychosomatic medicine. The psychoanalysis therapists recognized that most medical disorders are caused by behavioral patterns. This finding resulted in the evolution of BM. In 1975, the first research laboratory was created at Stanford to analyze behavioral medicine. The contribution from the Yale conference on Behavioral Medicine led to the official launch of the field in the year 1977. After 1982, greater investments in research began and this led to the advancement of organized study in BM. Therapy Programs of Behavioral Medicine Behavioral therapy It is a response-based therapy that helps an individual to acquire new positive behaviors that either decrease the severity of or eradicate mental conditions such as addiction, anxiety, phobias, and obsessive-compulsive disorder. It has two basic techniques. Classical conditioning: This principle of behavior therapy is normally known as applied behavioral analysis, which employs several methods to attain a change in behavior. Flooding: Flooding is commonly known as extended exposure treatment, and has beem found effective for phobias and anxiety. For example, if an individual is afraid of dogs, he is exposed to dogs for long periods to reduce the intensity of the fear. Desensitization: Individuals are asked to list the particular situations or things that make them extremely sensitive. Based on this list, the therapist teaches relaxation techniques, which when practiced regularly helps to overcome hypersensitivity. Aversion therapy: This method makes use of substances or techniques that produce an antagonistic effect to unwanted behaviors in many ways. For example, some medications produce side effects such as nausea, vomiting, and severe headaches when ingested along with alcohol. These medications are sometimes prescribed for alcohol addicts as a means of helping them to give up the undesirable alcoholism behavior as a result of the adverse reactions caused by the drug-alcohol binding. Operant conditioning: This theory has given rise to the following schemes for the management of behavior: Reinforcement concept: The therapist either rewards an individual as a result of a desired behavior change or imposes a penalty for not altering the undesirable behavior. Modeling: A good behavioral model is fixed as the target to which an individual is to aim in order to get rid of an unwanted behavior. The model might be a therapist or any other person close to the patient. Extinction: This theory suggests that reduction in anxiety results by repeated encounters with anxiety-raising situations without unpleasant results. Related StoriesLack of sleep and arguments with your spouse can cause stress-related inflammation, study revealsCognitive behavioral therapy (CBT) CBT is a type of psychotherapy that is commonly known as talk treatment. It combines the disciplines of psychotherapy and behavioral therapy. This therapy aims to change the motif of thoughts that affects the behavior and feelings of a person. CBT is beneficial for persons with mental disorders such as depression, posttraumatic stress disorder, eating disorder, addiction and insomnia. In a typical CBT session, the following things may happen: the patient and therapist interact about mental problems like anger which are experienced by the patient the therapist teaches new skills that include biofeedback and relaxation techniques for the management of mental symptoms faced by the person the patient has to practice the learned skills at home and apply them in day-to-day life. Dialectical behavior therapy (DBT) Since this is a type of CBT, it pursues the same procedure that helps to transform negative thinking patterns into positive thoughts leading to desirable behaviors. DBT additionally creates a psychosocial environment for individuals, so that they can practice the management of their emotions and change their behavior. It was found effective for individuals with eating disorders, substance dependence and depression. Biofeedback therapy During this type of therapy, the therapist connects electrodes to the patient’s skin to detect the range of mental activities that is associated with irregular body functions. The therapy enables the person to practice the control of involuntary body functions such as the heart rate and muscle tension, through relaxation techniques. It is effective in managing many chronic health problems and stress-related illnesses. Integrative Therapies of Behavioral Medicine The term integrative therapy refers to the combination of supportive therapies with other therapies like CBT and behavioral therapy in order to provide effective rehabilitation for patients with psychosomatic disorders. Relaxation training This training helps to calm a person to achieve a state of reduced stress, pain, and anxiety. It includes progressive muscle relaxation, deep breathing, creative visualization or listening to music. Mindfulness therapy This therapy focuses on the power of meditation to target the reduction of the recurrence of symptoms in those who are vulnerable to repeated episodes. The therapy helps to address difficult situations by creating an increased awareness of one’s surroundings and interior milieu, which helps the individual to act with less emotion. Distress tolerance This skill educates patients to tolerate pain during difficult situations through distraction techniques. Cerebral blood flow training This training increases the performance and functioning of the brain by enabling improved blood flow to specific regions of the brain. References http://www.medicinenet.com/script/main/art.asp?articlekey=31817 http://ecp.acponline.org/marapr02/trask.pdf https://link.springer.com/article/10.1007/s12529-014-9405-7 http://www.counselling-directory.org.uk/behavioural.html https://depts.washington.edu/psyclerk/secure/psychotherapy.pdf http://www.mayoclinic.org/tests-procedures/biofeedback/home/ovc-20169724 https://intermountainhealthcare.org/services/brain-spine/neurosciences-institutes/spine-institute/assessment-and-treatment/treatment/behavioral-medicine/ // Last Updated: Jun 29, 2017"
80,"2018-04-20 02:33:42","Causes of Excessive Belching","Written by Yolanda Smith, BPharm Although belching is a physiological process, there are various conditions that may lead to or cause excessive belching or burping, usually conditions that involve the stomach, duodenum, gallbladder, and esophagus. It may also be caused by lifestyle and dietary factors, such as the type of food eaten and the method of eating. It is important to note that belching is a normal part of human behavior and is needed to rid the stomach of excess gas that is swallowed when eating or produced during the process of digestion. However, excessive belching can become problematic if it occurs on a very frequent basis and is paired with other symptoms, such as abdominal pain. Physiological causes Lifestyle and dietary factors may contribute to some cases of excessive belching. This may include swallowing air when eating or drinking or the consumption of certain food and drink, such as cabbage, cauliflower, broccoli, beans, and carbonated beverages. It is a commonly believed myth that most cases of excessive belching are associated with swallowing air or certain foods and drinks. However, this is not true as most cases of excessive belching are, in fact, related to diseases of the gastrointestinal tract. These are widely grouped together as pathological causes and discussed in more detail in the following sections. Hiatal hernia A hiatal hernia is a condition that involves the extension of a portion of the stomach through the esophageal hiatus into the chest cavity. This alters the passage of food into the stomach and disrupts the mechanisms that are needed to prevent the backflow of stomach acid into the esophagus. In this case, periods of burping tend to come and go, according to the changing position of the stomach. Small intestine bacterial overgrowth Similar to the bacterial infection of the stomach, the small intestine can also sometimes be affected by bacterial overgrowth that may lead to excessive belching. Small intestine bacterial overgrowth (SIBO) usually affects the duodenum, which can lead to the production of gas and burping. Infections of the stomach Bacterial infections of the stomach, such as Helicobacter pylori (H. pylori) can lead to the production and release of gas from the stomach. As such, it may contribute to burping to some extent, although the volume of gas is thought to be slight. However, the bacterial infection also leads to increase the acidity of the stomach, which can also contribute to the accumulation of gas and, hence, burping. Food intolerance Indigestion of or intolerances to certain foods can also contribute to excessive belching. This is because the nutrients remain in the gut for consumption by bacteria, which produces gas as a byproduct. Common intolerances that may be associated with frequent burping include lactose intolerance, gluten intolerance, fructose malabsorption, and sorbitol malabsorption. Insufficiency of the pancreas The pancreas is an important organ for the production of digestive enzymes that are needed for the chemical breakdown of foods in the gastrointestinal tract. Insufficiency of the pancreas, due to bile duct stones, pancreatitis, or pancreatic cancer, can lead to an inability to digest food adequately, leading to food intolerances and malabsorption. As a result of the bacterial consumption of the nutrients, excessive belching may occur. Reviewed by Susha Cheriyedath, MSc References http://patients.gi.org/topics/belching-bloating-and-flatulence/ http://search.medscape.com/search/?q=excessive%20belching&plr=mln&page=1 http://www.phaa.com/excessive-burping-belching.htm https://www.ncbi.nlm.nih.gov/pubmed/20095992 Further ReadingWhat is Digestion?Digestive SystemsVertebrate Digestion Last Updated: Aug 3, 2017"
81,"2018-04-20 02:33:47","Bell's Palsy Pathology","By Dr Tomislav Meštrović, MD, PhD Seventh cranial nerve (facial nerve) passes through a portion of temporal bone known as the facial canal. Inflammation of at the part of the nerve termed geniculate ganglion (a group of fibers and sensory neurons) leads to compression within this bony canal. This can in turn block the transmission of neural signals, result in ischemia and demyelination, and cause facial paralysis or Bell's palsy. Injury is peripheral to the facial nerve's nucleus, and such compression has been proven on MRI scans (magnetic resonance imaging). Bell's palsy is considered an idiopathic condition, which means the cause of the inflammation is not known and the exact pathophysiology remains uncertain. Several viruses are associated with this disease, and herpes simplex virus type 1 (HSV-1) is thought to be the most probable causative factor, as affected individuals have elevated antibody titers for this virus. Other infectious agents may play a role in certain cases, such as Epstein-Barr virus and cytomegalovirus (which both cause infectious mononucleosis), adenovirus, mumps and rubella. Bilateral facial palsy has also been linked to acute HIV-infection. The hypothesis that HSV-1 is the etiologic agent in Bell's palsy was proposed in 1972 by McCormick. After causing primary infection in the form of cold sores (clusters of small fluid-filled blisters on the lips, mouth or nose), the virus travels along the neuron (in a process called retrograde transport) to the geniculate ganglion. There a lifelong silent infection is established, and autopsy studies showed the presence of HSV-1 in the ganglions of affected patients. The virus can be reactivated when the immune defenses are low, causing local damage to the nerve. Other conditions can also produce isolated facial nerve palsy that can be hard to distinguish from Bell's palsy, however their pathophysiological background is different. Pathological structures in the ear or parotid gland, such as cholesteatoma or salivary tumors, can result in facial nerve compression and subsequent paralysis. Ramsay-Hunt syndrome is characterized by an outbreak of herpes zoster in the facial nerve distribution and can present with an indistinguishable clinical picture. Guillain-Barré syndrome, an acute polyneuropathy affecting the peripheral nervous system, can also result in similar facial weakness. Lyme disease, sarcoidosis, otitis media and reaction to influenza vaccine are other causes of peripheral nerve palsies. All of them usually present with additional features that sets them apart from Bell's palsy. In approximately 4% of cases this condition can be linked to a family history. The inheritance in such cases is thought to be autosomal dominant with low penetrance, which means that merely a fraction of those who inherit the mutation actually develop the disease, despite the fact that only one mutated copy of the gene is needed. Still, the specific predisposing factors that are inherited are still unclear. In hereditary cases family history may also be positive for other nerve disorders or neurologic deficits. A rare form of familial Bell's palsy that has a propensity for young women also exists. Sources http://www.nejm.org/doi/full/10.1056/NEJMcp041120 http://www.aafp.org/afp/2007/1001/p997.html http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3907546/ http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2700557/ http://www.ninds.nih.gov/disorders/bells/detail_bells.htm http://emedicine.medscape.com/article/1146903-overview Further ReadingWhat is Bell's Palsy?Bell's Palsy SymptomsBell's Palsy DiagnosisBell's Palsy RecoveryBell's Palsy Complications Last Updated: Oct 31, 2017"
82,"2018-04-20 02:33:51","What is Bell's Palsy?","By Dr Tomislav Meštrović, MD, PhD Bell's palsy is a common neurologic disorder characterized by peripheral paralysis of the seventh cranial nerve (also known as the facial nerve), resulting in muscle weakness on one side of the face. The condition is named after Sir Charles Bell, a young surgeon from London who described a case of facial palsy in 1828, along with the detailed anatomy and function of the seventh cranial nerve. Today it is thought to be the most common cause of facial paralysis, responsible for up to 75% of unilateral mononeuropathies (disorders which involve only one nerve). Epidemiological studies reveal that Bell’s palsy affects 15–30 individuals per 100.000 persons each year, with peak incidence mostly in the range between 20 and 40 years of age. In contrast to other potential causes of facial paralysis such as stroke, tumors or middle ear lesions, this condition is often referred to as idiopathic, which means a specific cause cannot be pinpointed. Still, herpes simplex virus (HSV) has become accepted as the likely cause of Bell's palsy. Reactivation of a dormant virus when body's immune defenses are low leads to swelling and inflammation of the facial nerve, resulting in its damage and subsequent palsy. The classic sign of Bell's palsy is a weakness or complete paralysis of muscles on one side of the face with an abrupt onset, usually within 48 hours. The condition involves the forehead and lower aspect of the face, and patients are often unable to keep an eye closed or to retain food in the affected side of the mouth. Inappropriate reaction to loud noises, taste disturbances and decreased tearing also represent some of the concomitant symptoms of this disease. The most important step in diagnosis is to determine whether facial paralysis occurred due to a problem in the central nervous system (as in stroke) or is it actually Bell's palsy. Only the lower facial muscles are affected in stroke patients, while Bell's palsy is characterized by the paralysis of both the upper and lower parts of the face. Apart from such facial paralysis, symptoms arise within several days and usually subside within 6 weeks. A prolonged and gradual course with persistent relapses and no recovery suggest that a tumor might be an underlying cause. Since Bell's palsy is essentially a diagnosis of exclusion, patients should be referred to a neurologist as soon as possible to rule out more serious conditions. Corticosteroids are often used to treat Bell's palsy, as they proved helpful in reducing inflammation of the nerve and shortening symptom duration; the key is to use them shortly after onset to attain the desired effect. Antiviral medications are sometimes added to the therapy regimen, and surgical nerve decompression is pursued in more challenging cases. Although a majority of affected individuals recover completely and spontaneously over time, some patients can be left with lifelong consequences. Sources http://www.nejm.org/doi/full/10.1056/NEJMcp041120 http://www.aafp.org/afp/2007/1001/p997.html http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3907546/ http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2700557/ http://www.ninds.nih.gov/disorders/bells/detail_bells.htm http://emedicine.medscape.com/article/1146903-overview Further ReadingBell's Palsy PathologyBell's Palsy SymptomsBell's Palsy DiagnosisBell's Palsy RecoveryBell's Palsy Complications // Last Updated: Nov 6, 2017"
83,"2018-04-20 02:33:52","Bell's Palsy Symptoms","By Dr Tomislav Meštrović, MD, PhD Clinically, Bell's palsy is primarily characterized by the dysfunction of peripheral seventh cranial nerve (i.e. facial nerve), leading to a complete or partial facial paralysis. The classic sign of the disease is the involvement of only one side of the face with a sudden onset. Both sides of the face are simultaneously affected in less than 1% of cases. Symptoms usually peak in less than 48 hours and pain behind the ear sometimes occurs as a preceding symptom. The paralysis includes the forehead and lower aspect of the face. The forehead loses the ability to furrow, and the corner of the mouth droops on the affected side. The eyelids will not close and when the patient attempts to close them, the eyeball can roll upward (this is known as Bell's phenomenon). Although tear production decreases, the loss of lid control allows tears to spill freely from the eye, thus creating the appearance of excessive tearing. Loss of sensation along the external auditory canal sometimes also occurs, which is known as a positive Hitselberger sign. Parts of the cranial nerve that supply the ear and the tongue can also be affected, resulting in inappropriate reaction to loud noises (hyperacusis) and a loss of taste on the frontal two-thirds of the tongue. Normal lip movement is usually heavily affected by Bell's palsy, resulting in the inability to purse the lips and show the teeth on the affected side. Facial spasm can rarely occur, more likely as a result of fatigue or stress, and usually in patients in their fifth or sixth decades of life. A large proportion of patients report numbness on the side of the face affected by paralysis. Although this symptom could be attributed to the lack of mobility of the facial muscles, it could also indicate a secondary involvement of the trigeminal nerve. General (albeit mild) contracture of the facial muscles can result in a narrower fissure of the eyelids of the affected side when compared to the opposite part. This manifestation usually occurs after several months. It is of utter most importance to differentiate Bell’s palsy from a stroke. Both of these conditions can cause unilateral paralysis; however, presence of other symptoms can be used to distinguish between them. Bell's palsy affects only the facial nerve; hence the symptoms are limited to facial symptoms (muscle paralysis or weakness, taste problems and decreased tearing). On the other hand, stroke can cause additional problems in active speaking or understanding others, paralyze the arm or leg on the same side and severely impair vision quality. In essence, Bell's palsy affects the peripheral nerve and causes weakness of the eyelid and (most importantly) forehead, while stroke represents a problem with central nervous system and typically affects only muscles of the lower face. Sources http://www.nejm.org/doi/full/10.1056/NEJMcp041120 http://www.aafp.org/afp/2007/1001/p997.html http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3907546/ http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2700557/ http://www.ninds.nih.gov/disorders/bells/detail_bells.htm http://emedicine.medscape.com/article/1146903-overview Further ReadingBell's Palsy PathologyWhat is Bell's Palsy?Bell's Palsy DiagnosisBell's Palsy RecoveryBell's Palsy Complications Last Updated: Oct 31, 2017"
84,"2018-04-20 02:33:55","Bell's Palsy Diagnosis","By Dr Tomislav Meštrović, MD, PhD Bell’s palsy is a clinical diagnosis that can be established based on the patient's history and physical exam findings. It essentially represents a diagnosis of exclusion when all other possibilities are eliminated. The timing of symptoms is extremely important, as Bell’s palsy typically has a sudden onset and progression when compared to other causes of facial palsy such as tumors, which cause a gradual progression of muscle weakness. Although this condition is the most common cause of acute facial paralysis, similar presentation of other conditions can have detrimental effects in the case of a misdiagnosis. Since there are no readily available laboratory tests or imaging methods that can verify the diagnosis of Bell's palsy, the key is to differentiate this condition from other possible etiologies. Laboratory workup which includes CBC (complete blood count), erythrocyte sedimentation rate measurement, thyroid hormones analysis, HIV (human immunodeficiency virus) screening, serum glucose level, blood urea nitrogen, liver enzymes and cerebrospinal fluid analysis can help identify or exclude other disorders. If the paralysis does not improve or becomes even worse, imaging studies like magnetic resonance imaging (MRI) may also help rule out a tumor, especially if the patient has a palpable parotid mass. Herpes zoster infections that involve the facial nerve and Lyme disease are sometimes difficult to exclude in the differential diagnosis. In herpes zoster infection there are usually small blisters and vesicles present in the external ear canal, accompanied by hearing difficulties. Serum titers for herpes simplex virus may be obtained, although this test may not prove helpful due to the ubiquity of this virus. Lyme disease can also produce facial palsy, and may be easily diagnosed by looking for Lyme-specific antibody titer in the blood and finding a circular expanding rash on a physical exam. In endemic areas, Lyme disease often represents the most common cause of facial palsy. Electroneurography, which uses electricity for stimulating facial muscles on both sides of the face, may be used to provide prognostic information in cases of complete facial paralysis. Degree of nerve degeneration can be successfully quantified by mutual comparison of the responses on both sides of the face. The hearing threshold is usually not affected by Bell palsy, thus audiography and auditory evoked potentials should be pursued if hearing loss is suspected. Computer-based analysis of eyelid motion (also known as blepharokymographic analysis) may prove helpful in establishing diagnosis, predicting prognosis and evaluating therapy response. Two different diagnostic scales are used to grade the severity of Bell's palsy. Those are House-Brackmann Facial Nerve Grading System and the Sunnybrook Facial Grading System. House-Brackmann system categorizes the condition into six different categories, with first category representing normal facial function and sixth category a state of complete paralysis. It can also help clinicians monitor disease progression and evaluate recovery of the patient. The Sunnybrook system is a recommended method for subjective assessment of the mimic muscles and facial symmetry using a scale from 0 to 100. Although both scales are useful, several aspects of Bell's palsy such as tearing and facial discomfort may not be adequately assessed. Sources http://www.nejm.org/doi/full/10.1056/NEJMcp041120 http://www.aafp.org/afp/2007/1001/p997.html http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3907546/ http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2700557/ http://www.ninds.nih.gov/disorders/bells/detail_bells.htm http://emedicine.medscape.com/article/1146903-overview Further ReadingBell's Palsy PathologyWhat is Bell's Palsy?Bell's Palsy SymptomsBell's Palsy RecoveryBell's Palsy Complications // Last Updated: Nov 6, 2017"
85,"2018-04-20 02:34:00","Bell's Palsy Recovery","By Dr Tomislav Meštrović, MD, PhD Most patients with Bell's palsy recover completely within 6 weeks, regardless of eventual treatment received. In some cases full recovery ensues after 9 months or even longer, but often with residual damage and development of sequelae. Patients who show signs of recovery within 3 weeks upon onset of symptoms are most likely to undergo a complete recovery. A general rule is as follows: the sooner the recovery begins, the less chance there is that permanent sequelae will develop. The recurrence rate of Bell’s palsy is between 4-14%, with 36% of such patients re-experiencing paralysis on the same side of the face. Severity of the nerve inflammation and the degree of facial paralysis are important prognostic factors, thus full restoration usually occurs in patients with partial facial palsy. Age is also an important prognostic factor, with younger patients recovering more swiftly. Risk factors associated with a bad outcome in affected individuals include age greater than 60 years, complete paralysis, as well as decreased salivary flow or taste on the side of paralysis. Other factors related with less favorable outcomes are decreased lacrimation and pain in the posterior area of the ear. Because the exact cause of Bell's palsy remains elusive, there is no specific prevention or cure available. Attempts of treatment are geared toward improving facial nerve function, reducing neuronal inflammation and preventing complications stemming from corneal exposure. The cornea of affected individuals is particularly at risk of drying due to an improper lid closure and decreased production of tears; therefore prescription of eye ointments and lubricating eye drops is recommended. Adequate psychological support should also be provided in the early stages of the disease. The use of oral corticosteroids to reduce facial nerve inflammation in patients with Bell's palsy is supported by evidence, and prednisone remains the single best treatment for this condition. Antiviral medications (acyclovir, valacyclovir or famciclovir) can be added to the treatment regimen, although studies have been inconclusive whether they provide an additional benefit. Given the safety profile of the aforementioned drugs, patients with no specific contraindications and presenting within three days of the onset of symptoms should be offered a combination therapy. In cases of complete facial nerve paralysis the rate of spontaneous recovery is significantly lower, therefore such patients may be more likely to benefit from this treatment. Surgical facial nerve decompression within three weeks of onset is sometimes recommended for patients with persistent loss of function (i.e. loss greater than 90 percent shown on electroneurography). The most frequent complication of such approach is a postoperative hearing loss, affecting up to 15% of patients. As other risks are also imminent, this specific surgery should be considered only in refractory cases, given the paucity of data and lack of consensus on the topic. Physical therapy may hasten the recovery process and reduce sequelae, but additional randomized controlled trials are needed. Electrical nerve stimulation is a suggested method of accelerating the recovery of patients via invoked muscle stimulation. Sources http://www.nejm.org/doi/full/10.1056/NEJMcp041120 http://www.aafp.org/afp/2007/1001/p997.html http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3907546/ http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2700557/ http://www.ninds.nih.gov/disorders/bells/detail_bells.htm http://emedicine.medscape.com/article/1146903-overview Further ReadingBell's Palsy PathologyWhat is Bell's Palsy?Bell's Palsy SymptomsBell's Palsy DiagnosisBell's Palsy Complications Last Updated: Oct 31, 2017"
86,"2018-04-20 02:34:04","Bell's Palsy Complications","By Dr Tomislav Meštrović, MD, PhD Both major and minor long-term complications can ensue from Bell’s palsy in 30% of the patients, and 5% of them are left with a high degree of sequelae. In case of incomplete or aberrant regeneration of damaged nerve fibers, a phenomenon known as synkinesis can occur. During regrowth, some nerve fibers originating from facial nerve can sidetrack and erroneously connect with the lacrimal ducts instead of the salivary glands. In such instances patients will shed tears while eating, which is in medical literature also known as crocodile tear syndrome, Bogorad's syndrome or gustatolacrimal reflex. Other example of synkinesis is when the nerves controlling the eye muscles misdirect and regrow connections with the muscles of the mouth. Abnormal movement or different facial muscle group occurs afterwards, since movement of one muscle can now affect the other one. For example, the corner of the mouth can involuntarily lift when the affected individual closes the eye. Such synkinesis is often treated with botulinum toxin injections (Botox) and facial reanimation by means of cosmetic surgery. Botulinum injections are sometimes administered to the non-affected side as well, in order to improve facial symmetry. Incomplete motor regeneration is also an important long-term complication. As the largest portion of the facial nerve contains efferent fibers for stimulation of facial muscles and formation of facial expressions, subpar regeneration in this part of the nerve can result in permanent paralysis of all or several muscles on that side of the face. That can in turn manifest as an inadequate function of the mouth, excessive tearing (epiphora) and nasal obstruction. Incomplete sensory regeneration can also occur as a result of Bell's palsy. Deterioration or loss of taste (also known as dysgeusia or ageusia, respectively) can occur after partial regeneration of the chorda tympani (an important branch of the facial nerve that carries taste information from the anterior part of the tongue). If other afferent branches are affected, a change or sensation to normal stimuli can occur. This condition is known as dysesthesia, although it is still a controversial topic as it seems other cranial (glossopharyngeal or trigeminal) nerves are also involved. Recent studies show that Bell’s palsy can increase the risk of non-hemorrhagic stroke. That particular finding can be linked to previous research that has shown an increased risk of stroke in patients with HSV-1. The pathogen in question has also been implicated in inflammation, vasculopathy and atherosclerosis in the cerebral blood vessels. All things considered, a multi-specialist approach is needed when dealing with a myriad of complications arising as a result of Bell's palsy. Sources http://www.nejm.org/doi/full/10.1056/NEJMcp041120 http://www.aafp.org/afp/2007/1001/p997.html http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3907546/ http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2700557/ http://www.ninds.nih.gov/disorders/bells/detail_bells.htm http://emedicine.medscape.com/article/1146903-overview Further ReadingBell's Palsy PathologyWhat is Bell's Palsy?Bell's Palsy SymptomsBell's Palsy DiagnosisBell's Palsy Recovery Last Updated: Oct 31, 2017"
87,"2018-04-20 02:34:08","Beta Blockers - What are Beta Blockers?","By Dr Ananya Mandal, MD Beta-blockers are used to treat several conditions, usually by regulating heart activity. Also called beta-adrenoreceptor blocking agents, these medications bind to beta receptors present on the cells of the heart, arteries, kidneys and other tissues that are stimulated by the stress hormones (e.g. adrenaline and noradrenaline). Beta blockers are often used to treat high blood pressure, angina, heart attack and atrial fibrillation. Less common indications include migraine, tremor and anxiety. Examples of drugs in this class include acebutolol, atenolol, bisoprolol, carvedilol, celiprolol, labetalol, metoprolol, nadolol, nebivolol, oxprenolol, pindolol and timolol. Mechanism of action The sympathetic nervous system is part of the autonomic nervous system that controls various vital functions of the body including heart rate and blood pressure. The two main beta receptors that are targeted by beta blockers are the beta 1 receptor and the beta 2 receptor. A large number of beta 1 receptors are present on the heart and kidney cells, while the beta 2 receptor is the predominant regulator of vascular and nonvascular smooth muscles. Some beta blockers are selective and block the beta 1 receptor more than the beta 2 receptor. These are called cardioselective agents. Nonselective beta blockers are those that bind to both types of receptors. Some of the effects of using beta blockers to block these receptors include: Effects on the kidney - Blocking of the beta 1 receptors on the kidneys prevents the release of renin from juxta-glomerular cells. This suppresses the renin-angiotensin-aldosterone system, helping to regulate blood pressure as well as fluid and electrolyte balance. Effects on the heart - Beta 1 receptors are present on the sino-atrial node, which is responsible for generating the impulses that make the heart beat. Blocking the sino-atrial node therefore reduces heart rate. Uses of beta blockers Some examples of the conditions beta blockers are used to treat include high blood pressure, angina, heart failure, cardiac arrhythmias and atrial fibrillation, anxiety, severely overactive thyroid (thyrotoxicosis), glaucoma and migraine. Pharmacological Properties Beta blockers can be taken in the form of capsules, a solution, eye drops or by injection and are usually eliminated from the body via the liver or kidney. Beta blockers that are soluble in fats such as labetalol, metoprolol, pindolol and propranolol are excreted by the liver, while those that are soluble in water such as atenolol are cleared by the kidney. Fat soluble drugs have a short duration of action, while water soluble drugs have a longer duration of action. Side effects Some of the side effects of beta blockers are more common than others. Some examples of more common side effects are given below: Dizziness Fatigue Cold extremities (hands and feet) Slow heartbeat Blurred vision Diarrhea and nausea Some examples of the less common side effects include: Insomnia Loss of libido Depression Reviewed by Sally Robertson, BSc Sources www.bpac.org.nz/.../bpac_betablocker_options_sept_2007.pdf www.bhsoc.org/.../...-adrenoceptor%20Antagonists%20(Beta-Blockers).pdf www.medicaid.nv.gov/Downloads/provider/NVRx_DCR_Beta_Blockers.pdf xa.yimg.com/.../_AC%20Beta%20blockers.pdf http://www.japi.org/special_issue_2009/article_02.pdf http://www.inaactamedica.org/archives/2007/17297209.pdf http://repub.eur.nl/res/pub/4090/1105.pdf Further ReadingWhat are Beta Blockers Used for?Beta Blocker DrugsBeta Blocker Side Effects Last Updated: Oct 7, 2014"
88,"2018-04-20 02:34:15","What are Beta Blockers Used for?","By Dr Ananya Mandal, MD Beta blockers are medications that are commonly used to treat various types of heart conditions as well as some other illnesses. Some of the uses of beta blockers include: Heart failure Beta blockers are one of the most important drugs used today in heart failure. Studies have shown that the use of beta blockers can reduce the risk of death due to heart failure by 30% and the risk of hospitalization by 40%. Among patients with chronic or long-term heart failure, there is a 38% reduction in the risk of sudden death. Examples of beta blockers that are useful in heart failure include carvedilol, bisoprolol, nebivolol and long-acting metoprolol. After an acute myocardial infarction or heart attack Beta blockers such as carvedilol and netoprolol can reduce the risk of further heart attack and death. These agents are of particular benefit in high risk patients who have ongoing cardiac ischemia or left ventricular dysfunction. Chronic stable angina In patients with this condition, there is a lack of blood supply (ischemia) to the heart muscles which leads to chest pain, especially during exertion. Beta-blockers help by reducing the myocardial oxygen demand and heart rate. A specific form of angina called Prinzmetal's angina should not be treated with nonselective beta-blockers, as these agents can aggravate the condition. Heart rhythm abnormalities or arrhythmias Some beta-blockers can be used to treat arrhythmias and examples include sotalol, esmolol and propranolol. In patients who have had a heart attack, beta blockers are superior to other anti-arrhythmic agents. They are especially useful in cases of arrhythmia that involve the ventricles and can reduce the risk of cardiac death from ventricular arrhythmia. Beta-blockers are also effective in the treatment of an inherited arrhythmia called Long QT syndrome 1 (LQTS 1). Hypertension or high blood pressure Beta blockers are used to treat high blood pressure and are a particularly effective therapy in hypertensive individuals with angina or who have suffered a heart attack. They also reduce the risk of coronary heart disease events and stroke. Hypertrophic obstructive cardiomyopathy Beta blockers are the first drug of choice for patients with this condition. Mitral stenosis Patients with mitral stenosis, a narrowing of the opening between the left atrium and the left ventricle, benefit from beta blocker therapy. Anxiety Propranolol is used to treat symptoms of anxiety such as facial blushing, sweating and palpitations. Overactive thyroid Propranolol is also effective in severely overactive thyroid (thyrotoxicosis). Glaucoma Agents such as timolol, betaxolol, carteolol, levobunolol and metipranolol are used to treat the eye condition glaucoma. Migraine Propranolol is used as a preventive agent in migraine. Bleeding prevention Beta blockers are also used to reduce the risk of bleeding in patients with chronic liver disease and portal hypertension complicated by oesophageal varices. Reviewed by Sally Robertson, BSc Sourceswww.bpac.org.nz/.../bpac_betablocker_options_sept_2007.pdf www.bhsoc.org/.../...-adrenoceptor%20Antagonists%20(Beta-Blockers).pdf www.medicaid.nv.gov/Downloads/provider/NVRx_DCR_Beta_Blockers.pdf xa.yimg.com/.../_AC%20Beta%20blockers.pdf http://www.japi.org/special_issue_2009/article_02.pdf http://www.inaactamedica.org/archives/2007/17297209.pdf http://repub.eur.nl/res/pub/4090/1105.pdfFurther ReadingBeta Blockers - What are Beta Blockers?Beta Blocker DrugsBeta Blocker Side Effects Last Updated: Feb 13, 2014"
89,"2018-04-20 02:34:16","Beta Blocker Drugs","By Dr Ananya Mandal, MD Beta-blockers are medications that are mainly used to treat various heart conditions, usually by decreasing the heart’s activity. These agents are often prescribed for the treatment of angina, heart failure, atrial fibrillation, and heart attack. Beta-blocker therapy can also benefit patients with anxiety, overactive thyroid (thyrotoxicosis), glaucoma and migraine. The two main beta receptors that are targeted by beta blocker therapy are the beta 1 receptor and the beta 2 receptor. A large number of beta 1 receptors are present on the heart and kidney cells, while the beta 2 receptor is the predominant regulator of vascular and nonvascular smooth muscles. Some beta blockers are selective and specifically target the beta 1 receptor. These are called cardioselective agents. Nonselective beta blockers are those that bind to both types of receptors. Examples of the beta blocker drugs that are currently available include: Non selective agents Alprenolol Bucindolol Carvedilol Labetelol Nadolol Penbutolol Carteolol Mepindolol Pindolol Propranolol Timolol Cardioselective agents Acebutolol Celiprolol Atenolol Betaxolol Bisoprolol Esmolol Metoprolol Nebivolol Agents that are highly selective for the beta 2 receptor include butaxamine and several other therapies currently in development. However, there are no known clinical applications for these drugs and they are currently used only for experimental purposes. Beta blockers that are fat soluble are excreted by the liver and include labetalol, metoprolol, pindolol and propranolol. Those that are water soluble such as atenolol, celiprolol, nadolol, sotalol are cleared by the kidney. Specific beta blocker treatments Some examples of the specific conditions certain beta blockers are used for include: Cardiac arrhythmia – Esmolol, landilol, sotalol. Congestive heart failure – metoprolol, bisoprolol, carvedilol, nebivolol. After heart attack – atenolol, metoprolol, propranolol. Glaucoma – betaxolol, carteolol, levobunolol, metipranolol, timolol. Migraine prevention – timolol, propranolol. Reviewed by Sally Robertson, BSc Sourceswww.bpac.org.nz/.../bpac_betablocker_options_sept_2007.pdf www.bhsoc.org/.../...-adrenoceptor%20Antagonists%20(Beta-Blockers).pdf www.medicaid.nv.gov/Downloads/provider/NVRx_DCR_Beta_Blockers.pdf xa.yimg.com/.../_AC%20Beta%20blockers.pdf http://www.japi.org/special_issue_2009/article_02.pdf http://www.inaactamedica.org/archives/2007/17297209.pdf http://repub.eur.nl/res/pub/4090/1105.pdfFurther ReadingBeta Blockers - What are Beta Blockers?What are Beta Blockers Used for?Beta Blocker Side Effects Last Updated: Feb 13, 2014"
90,"2018-04-20 02:34:22","Beta Blocker Side Effects","By Dr Ananya Mandal, MD The various effects of beta blocker therapy on different parts of the body can lead to patients experiencing several side effects. Some examples of these side effects include: Slowed heart rate Beta blockers that target the beta 1 receptor prevent stimulation of the heart activity by stress hormones. Sometimes, the heart rate can become too slow and lead to the patient feeling dizzy and faint. The slowing of heart rate is usually brought about by the effect on the sino-atrial node, which generates the impulses that cause the heart to beat. Cold extremities Beta blockers can cause constriction of the small blood vessels and lead to a reduction in the amount of blood that is circulated to the peripheries such as the hands and feet. Aggravation of asthma Blocking of the beta 2 receptors in the bronchioles can lead to constriction of the airways and patients with asthma or chronic obstructive pulmonary disease (COPD) are advised not to take beta blockers. Sleeping and emotional difficulties Beta blocker therapy can lead to fatigue, depression, vivid dreams, nightmares and impotence in some individuals. Risks in diabetes If blood sugar drops severely (hypoglycaemia) in diabetic individuals, symptoms occur that can act as warning signs such as palpitations, increased heart rate and sweating. However, if a diabetic individual is taking beta blocker therapy, these symptoms are masked, meaning patients may not be alerted to their low blood sugar level. Risk of diabetes Some research suggests that beta blockers raise blood sugar levels and that the therapy can increase the likelihood of diabetes developing. Reviewed by Sally Robertson, BSc Sourceswww.bpac.org.nz/.../bpac_betablocker_options_sept_2007.pdf www.bhsoc.org/.../...-adrenoceptor%20Antagonists%20(Beta-Blockers).pdf www.medicaid.nv.gov/Downloads/provider/NVRx_DCR_Beta_Blockers.pdf xa.yimg.com/.../_AC%20Beta%20blockers.pdf http://www.japi.org/special_issue_2009/article_02.pdf http://www.inaactamedica.org/archives/2007/17297209.pdf http://repub.eur.nl/res/pub/4090/1105.pdfFurther ReadingBeta Blockers - What are Beta Blockers?What are Beta Blockers Used for?Beta Blocker Drugs Last Updated: Feb 13, 2014"
91,"2018-04-20 02:34:28","Beta-Carotene - What is Beta-Carotene?","By Dr Ananya Mandal, MD Chemistry Beta carotene is a member of the carotenoid family belonging to the isoprenoid compounds, which are polyunsaturates with antioxidant properties. The formula for beta carotene is C40H56 and it can exist as cis- or trans-isomers. Most of the naturally-occurring and synthesized forms of beta exists as the all-trans isomer. Where is beta carotene found? Beta carotene is produced by plants and microorganisms, with the main sources being yellow or orange and green-leaved vegetables or fruits such as sweet potato, spinach, carrots, pumpkin, butternut squash and apricots. Beta carotene is also available as supplements, which may be synthetic or derived from palm oil, algae or fungi. When taken as a vitamin or mineral supplement, the dose ranges form 0.4 mg to 20 mg per day. When used as a medicine to treat vitamin A deficiency, a dose of up to 6 mg/day may be given and in cases of erythropoietic protoporphyria (EPP), up to 300 mg/day may be taken. Beta carotene is also widely used as a yellow colouring agent (EC160a) in food and drink. Although beta carotene is not classed as an essential nutrient, it is a precursor to vitamin A and the recommended daily intake is expressed as part of the reference nutrient intake (RNI) for vitamin A as retinol equivalents (RE). Beneficial effects of beta carotene As a provitamin of vitamin A, the importance of beta carotene in an individual depends on their level of pre-formed vitamin A. It is therefore difficult to define a beta- carotene deficiency. Beta carotene also interacts with other carotenoids during absorption and metabolic processes. Studies have shown an association between high dietary intake of beta carotene and a reduced risk of heart disease and cancer. This may be due to the antioxidant properties of the molecule. Properties The absorption of beta carotene is facilitated by dietary fats and bile salts in the small intestine. Around 10% to 90% of the total dietary beta carotene is thought to be absorbed in the gut, with absorption decreasing, the higher the intake is. Low fat diets also reduce the amount of beta carotene absorbed. Smokers have a low blood level of beta carotene, as do individuals with a high alcohol intake and those with HIV infection. People with impaired fat absorption from diet due to conditions such as jaundice, liver cirrhosis and cystic fibrosis also have a low blood level of beta carotene. Beta carotene is excreted in the feces and sweat. Reviewed by Sally Robertson, BSc Sources http://www.crnusa.org/safetypdfs/003CRNSafetybetacarotene.pdf www.sunchlorellausa.com/.../PR_10Facts%20About%20Beta%20Carotene.pdf http://www.food.gov.uk/multimedia/pdfs/evm_bcarotene.pdf http://www.govita.com.au/library/Vitamins/VitaminBetacarotene.pdf www.mccordresearch.com/.../Multi-Vitamin-A.pdf http://www.nal.usda.gov/fnic/DRI/DRI_Vitamin_C/325-382_150.pdf www.usp.org/sites/default/files/usp_pdf/EN/USPNF/beta_carotene.pdf Further ReadingBeta-Carotene Side Effects Last Updated: Oct 7, 2014"
92,"2018-04-20 02:34:33","Beta-Carotene Side Effects","By Dr Ananya Mandal, MD Until recently, beta carotene was not thought to be toxic to humans. High levels of plasma beta carotene (hypercarotenemia) have not been associated with adverse side effects apart form causing a yellowing of the skin (carotenodermia) that eventually resolves. Beta carotene effects on reproductive health Beta carotene is a precursor of Vitamin A, a group of retinoids that includes retinol, retinyl esters and retinoic acid. An excess intake of vitamin A or synthesized retinoids has been associated with birth defects such as eye, lung and heart deformities and pregnant women are advised not to take high doses of supplemental vitamin A. However, the beta carotene precursor for vitamin A has not been associated with reproductive toxicity, even at large doses of 20 to 30 mg per day. Diets high in carotenid-rich foods also have not been associated with toxicity. High levels of beta carotene do not cause vitamin A toxicity because the level of vitamin A in the body regulates the metabolic conversion of beta carotene to vitamin A. If the levels of vitamin A are high, there is a decrease in the conversion of beta carotene to vitamin A and vice versa. Animal studies No side effects of high-dose beta carotene have been observed in standard toxicity studies in experimental animals. Doses for acute toxicity (up to 5000 mg/kg body weight per day) and for chronic toxicity (up to 1000 mg/kg body weight per day for life) showed no ill effects in rats. Doses for reproductive toxicity (up to 1000 mg/kg body weight per day for 3 generations of rats) also showed no toxic effects. Reviewed by Sally Robertson, BSc Sourceshttp://www.crnusa.org/safetypdfs/003CRNSafetybetacarotene.pdf www.sunchlorellausa.com/.../PR_10Facts%20About%20Beta%20Carotene.pdf http://www.food.gov.uk/multimedia/pdfs/evm_bcarotene.pdf http://www.govita.com.au/library/Vitamins/VitaminBetacarotene.pdf www.mccordresearch.com/.../Multi-Vitamin-A.pdf http://www.nal.usda.gov/fnic/DRI/DRI_Vitamin_C/325-382_150.pdf www.usp.org/sites/default/files/usp_pdf/EN/USPNF/beta_carotene.pdfFurther ReadingBeta-Carotene - What is Beta-Carotene? Last Updated: Feb 17, 2014"
93,"2018-04-20 02:34:39","What is Beta-Thalassemia?","By Dr Liji Thomas, MD Beta-thalassemia is one of a group of hereditary blood conditions that result from reduced or absent synthesis of the beta-globin chain of the hemoglobin molecule. It occurs as the result of a point mutation or less commonly, a deletion in the gene that codes for the beta chain, on chromosome 11. It occurs in 1 of 10,000-100,000 people, depending on the ethnicity. It is inherited in an autosomal recessive manner. The symptoms vary from none to severe anemia. Three main forms are clinically distinguished, namely, beta-thalassemia major, beta-thalassemia intermediate, and beta-thalassemia minor, depending on the time of presentation of anemia, and its severity. These forms depend upon the type of inheritance, namely homozygous or heterozygous. Beta-thalassemia may also occur in combination with other hemoglobin defects. Thalassemia major Thalassemia major presents early in life with anemia severe enough to warrant regular blood transfusions. Other symptoms include: poor growth pallor jaundice enlargement of the liver and spleen due to the breakdown of red cells containing the abnormal hemoglobin leg ulcers bone changes secondary to marrow expansion the appearance of other masses due to the formation of blood outside the bone marrow. Complications As a result of repeated transfusions to keep the hemoglobin level between 9 and 10.5 g/dL, iron overload occurs. The excessive iron levels lead to iron toxicity, reflected as: growth failure sexual immaturity diabetes mellitus hypofunctioning of several endocrine glands heart failure due to cardiac muscle weakening liver cirrhosis following fibrosis. Cardiac complications due to hemosiderosis are the most common cause of death. Other secondary complications include the possibility of infection with hepatitis B and C viruses, and HIV infection. Thalassemia intermedia The intermediate forms of thalassemia show the same type of symptoms but at a later age, and with less severity. More distinctive symptoms of this form include thrombosis of the deep veins, presenting as: leg thrombosis portal vein thrombosis stroke or embolism. These are more common in the intermediate form as compared to the major form. Diabetes, hypogonadism and thyroid insufficiency are less common, however. Thalassemia minor Thalassemia minor is often asymptomatic, but sometimes patients have mild to moderate anemia. Diagnosis and treatment Diagnosis is based on the presence of characteristic findings on hematologic testing. Thus the RBC indices show a microcytic hypochromic anemia. Peripheral blood smear examination shows the presence of nucleated red cells, as a result of accelerated but ineffective hemopoiesis. Hemoglobin analysis by electrophoresis and other means shows the type and quantity of abnormal hemoglobin being produced. The diagnosis of thalassemia is confirmed by molecular genetic testing. Genetic counseling is advisable because of the mode of inheritance. Treatment includes regular transfusions of packed red cells, prevention of iron overload by iron chelating agents, and early treatment of complications related to iron accumulation. When there is severe hemolysis which makes it difficult to maintain a normal hemoglobin level, and precipitates secondary complications such as thrombosis and splenic sequestration, splenectomy is often helpful. Definitive management is by bone marrow transplantation. References http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2893117/ http://www.ncbi.nlm.nih.gov/books/NBK1426/ http://www.ncbi.nlm.nih.gov/pubmed/20098328 Further ReadingBeta-Thalassemia TypesBeta-Thalassemia Testing and Complications Last Updated: Feb 25, 2016"
94,"2018-04-20 02:34:46","Beta-Thalassemia Types","By Dr Ananya Mandal, MD Beta-thalassemia is an inherited disorder of the blood that affects the hemoglobin inside red blood cells. The condition is caused by an abnormality in the production of the beta globin chain found in hemoglobin. This results in haemoglobin that has a reduced capacity to transport oxygen around the body, which can lead to symptoms of anemia. Beta thalassemia statistics In the UK, the majority of beta-thalassemia cases occur in individuals of Mediterranean, Middle Eastern and particularly South Asian origin, with 80% of babies with the condition born to parents of Indian, Bangladeshi and Pakistani descent. Globally there are around 80 to 90 million people (1.5% of the total population) that are carriers of beta thalassemia and 60,000 symptomatic children born each year. Types of beta thalassemia There are several sub-categories of beta thalassemia. These include: Beta thalassemia major Beta thalassemia intermedia Beta thalassemia minor Two genes are involved in coding for beta globin, with one gene inherited from each parent. Beta thalassemia is caused by mutations in these genes. If one of the genes inherited is mutated, symptoms are mild and this form of the condition is referred to as beta thalassemia minor. If both of the genes inherited are mutated, moderate-to-severe symptoms will develop. The most severe form of the condition is referred to as thalassemia major. Individuals with this condition will need to have blood transfusions for their entire life. However, the inheritance of two defective genes can also lead to a milder form of the condition and this is referred to as beta thalassemia intermedia. Beta thalassemia major Individuals with beta thalassemia major usually develop symptoms within the first two years of life. The infant may fail to thrive and often has difficulty feeding, tires easily and suffers from severe anemia. The infant may also suffer from diarrhea, irritability, recurrent episodes of fever, and other intestinal problems. These children have trouble gaining weight and growing at the rate expected for their age. Other complications include enlarged spleen, heart and liver and misshapen bones. In many cases, regular blood transfusions are required to replenish the blood with healthy red blood cells. However, these regular transfusions can lead to a build up of iron in the blood that can damage the heart, liver and endocrine system and chelation therapy may be needed to remove this iron from the body. Beta thalassemia intermedia The symptoms of thalassemia intermedia are milder than those of thalassemia major and often manifest later in life. Such individuals may have mild-to-moderate anemia and growth abnormalities. Often patients do not require transfusions when they are younger but may need to start them when they are older. Beta thalassemia minor This form of thalassemia usually gives rise to mild symptoms but patients do not require blood transfusion. Although this condition is not life threatening, quality of life may be affected by mild-to-moderate anemia. This form of the condition is also referred to as beta thalassemia trait. Sickel-beta thalassemia Sometimes, individuals inherit one gene for beta thalassemia from one parent as well as a gene for sickle hemoglobin (hemoglobin S) from the other parent. This is called sickle-beta thalassemia and can present with similar symptoms to sickle cell disease such as pain, fatigue, an enlarged spleen and vulnerability to infections. Reviewed by Sally Robertson, BSc Sourceshttp://www.nhs.uk/conditions/Thalassaemia/Pages/Introduction.aspx http://www.cooleysanemia.org/updates/pdf/Beta_Thalassemia.pdf http://www.biomedcentral.com/content/pdf/1750-1172-5-11.pdf http://www.doh.wa.gov/Portals/1/Documents/5220/BetaThal.pdf www.thalassaemia.org.au/.../vic%20beta_fact%20sheet_2.pdfFurther ReadingWhat is Beta-Thalassemia?Beta-Thalassemia Testing and Complications Last Updated: Feb 17, 2014"
95,"2018-04-20 02:34:50","Beta-Thalassemia Testing and Complications","By Dr Ananya Mandal, MD There are three forms of beta thalassemia that vary in severity and symptom onset and these are described below: Thalassemia major Individuals with thalassemia major usually develop symptoms within the first two years of life. These infants may fail to thrive and often have difficulty feeding, tire easily and suffer from severe anemia. The infants may also suffer from diarrhea, irritability, recurrent episodes of fever, and other intestinal problems. These children have trouble gaining weight and growing at the rate expected for their age. Other complications include enlarged spleen, heart and liver and misshapen bones. In many cases, the symptoms are severe enough to warrant regular blood transfusion to replenish the blood with healthy red blood cells. However, these regular transfusions can lead to a build up of iron in the blood that can damage the heart, liver and endocrine system and chelation therapy may be needed to remove this iron from the body. Beta thalassemia intermedia The symptoms of thalassemia intermedia are milder than those of thalassemia major and often manifest later in life. Such individuals may have mild to moderate anemia and growth abnormalities. Often patients do not require transfusions when they are younger but may need to start them when they are older. Beta thalassemia minor This form of thalassemia usually gives rise to mild symptoms but patients do not require blood transfusion. Although this condition is not life threatening, quality of life may be affected by mild-to-moderate anemia. This form of the condition is also referred to as beta thalassemia trait. Diagnosis Beta thalassemia is diagnosed based on various different tests which include: Blood tests In cases of beta thalassemia, the red blood cells appear small (microcytic) and pale (hypochromic), compared to those seen on normal blood smears. The red blood cells may also be nucleated, an indication that they are immature forms (also known as erythroblasts). In thalassemia major, the hemoglobin (Hb) level is usually less than 7 g/dl; the mean corpuscolar volume (MCV) less than 70 fl and the mean corpuscolar Hb (MCH) is over 20 pg. In thalassemia intermedia, the hemoglobin level is between 7 and 10 g/dl; the MCV between 50 and 80 fl and MCH between 16 and 24 pg. Thalassemia minor is characterized by a reduced MCV and MCH and an increased haemoglobin A2 level. Molecular genetic analysis DNA analysis can be performed to check for mutations in the genes that code for the beta globin chains found in hemoglobin. The test is not usually carried out routinely but may be performed in cases where a physician suspects the condition based on signs and symptoms such as anemia, breathlessness and the results of blood tests. DNA analysis can help diagnose the condition as well as determining carrier status in other members of the family. Complications Some of the complications associated with beta thalassemia (especially thalassemia major) include: Enlargement of the spleen increases the risk of injury and rupture of the organ which can be life threatening. An enlarged spleen also presses against other vital organs, in which case it may need to be removed in a procedure called a splenectomy. Since the spleen plays an important part in fighting infection, a splenectomy can result in an increased risk of infection. Liver complications include hepatitis, enlarged liver or scarring of the liver (cirrhosis). Affected bone marrow and bone deformities increase the risk of joint pain, osteoporosis and susceptibility to fracture. Other complications include pulmonary hypertension (high blood pressure within the blood vessels of the lungs), thromboembolic complications and sepsis after splenectomy. Blood transfusion is also associated with complications. Regular transfusions can increase the risk of iron overload which can lead to complications such as: Hormonal disturbances - Iron overload can disrupt the endocrine system and balance of hormones, which can result in hypogonadism (low functioning of the genital and reproductive organs), infertility, underactive thyroid and diabetes. The secretion of growth hormone may also be impaired and retard growth. Liver damage and fibrosis Heart damage and disease Reviewed by Sally Robertson, BSc Sourceshttp://www.nhs.uk/conditions/Thalassaemia/Pages/Introduction.aspx http://www.cooleysanemia.org/updates/pdf/Beta_Thalassemia.pdf http://www.biomedcentral.com/content/pdf/1750-1172-5-11.pdf http://www.doh.wa.gov/Portals/1/Documents/5220/BetaThal.pdf www.thalassaemia.org.au/.../vic%20beta_fact%20sheet_2.pdfFurther ReadingWhat is Beta-Thalassemia?Beta-Thalassemia Types Last Updated: Feb 17, 2014"
96,"2018-04-20 02:34:52","Avastin (Bevacizumab) - What is Avastin?","By Dr Ananya Mandal, MD Avastin is the brand name for the anti-cancer medication bevacizumab, which belongs to a group of drugs called monoclonal antibodies. An antibody is a molecule produced by the body in response to a foreign invader or antigen. A monoclonal antibody is created in the laboratory to target and inhibit certain proteins. These agents are very specific for the molecules that they are created against and are therefore called targeted therapies. Mechanism of action Bevacizumab (Avastin) is a recombinant humanised monoclonal IgG1 antibody. Monoclonal antibodies recognise and lock on to specific proteins (receptors) that are present on the surface of cancer cells. Once a monoclonal antibody attaches to the target receptor, it triggers the immune system to attack the cancer cells, which then destroy themselves. The antibody can also prevent the receptor from acting on another protein to stimulate tumor growth, proliferation or angiogenesis (blood vessel formation). In the case of bevacizumab, the mechanism of action is inhibition of a cell surface protein called vascular endothelial growth factor (VEGF). This VEGF helps tumors to form new blood vessels and blocking VEGF stops the cancer from developing its own blood supply. This reduces the tumor’s supply of oxygen and nutrients, therefore preventing its growth and survival. Starved of vital nutrients, the tumour stops growing and shrinks. Drugs that prevent the growth of blood vessels are termed angiogenesis inhibitors or anti-angiogenics. Clinical uses The United States Food and Drugs Administration has approved bevacizumab for the first-line treatment of patients with advanced and metastatic (cancer that has spread to vital organs) carcinoma of the colon or rectum. The therapy can also be used to treat advanced non-small cell lung cancer or advanced cancer of the breast, kidney or bowel. Bevacizumab has also been used successfully in the treatment of eye disorders such as age-related macular degeneration and diabetic retinopathy, where abnormal blood vessel growth in the retina leads to leaky vessels that cause retinal damage. Mode of administration Bevacizumab may be given in combination with chemotherapy or when being used to treat kidney cancer, it may be given in combination with interferon. The drug is given as a drip into a vein (infusion) every two or three weeks. Bevacizumab is usually administered over a period of 90 minutes for the first infusion and 60 minutes for the second infusion, with infusions thereafter lasting for about 30 minutes. Pharmacological properties The estimated half life (a measure of drug action duration) of bevacizumab is approximately 20 days and the time taken for the drug to reach a steady-state concentration in the blood is around 100 days. The volume of distribution is 46 mL/kg and the drug is eliminated from the body at a rate of 2.75 to 5 mL/kg/day, depending on factors such as body weight, gender and extent or size of the tumor. Side effects There are several side effects associated with the use of bevacizumab. Side effects may occur either as a reaction to the infusion or as a response to the drug itself. Some examples of infusion-related reactions include flu-like symptoms, skin rash, allergy, angioedema and abdominal pain. The drug itself may cause nausea, vomiting, diarrhea, constipation, loss of appetite, weakness, hypertension and mouth ulcers as well as raising the risk of bleeding disorders. Bevacizumab can also decrease the white blood cell count and make patients more susceptible to infection. Reviewed by Sally Robertson, BSc Sources http://www.ukmi.nhs.uk/NewMaterial/Secure/Bevacizumab051004.pdf www.nhs.uk/.../Avastin(Bevacizumab)(CB4pages).pdf http://www.pmda.go.jp/english/service/pdf/Abastin-Bevacizumab.pdf www.roche-australia.com/.../avastin-pi.pdf faculty.ksu.edu.sa/hisham/Documents/PHCL_510/Students_Work/Avastin.pdf www.betterhealth.vic.gov.au/.../rocavast.pdf Last Updated: Oct 14, 2014"
97,"2018-04-20 02:34:56","Avastin (Bevacizumab) Indications","By Dr Ananya Mandal, MD Bevacizumab (brand name Avastin) is an anti-cancer therapy that belongs to a group of drugs called monoclonal antibodies. A monoclonal antibody is a drug created in the laboratory that is designed to target and inhibit certain proteins. These agents are very specific for the molecules that they are created against. Mechanism of action Bevacizumab binds to and inhibits the activity of a protein present on the surface of cells called vascular endothelial growth factor (VEGF). This VEGF helps cancer cells to form new blood vessels and by blocking the action of VEGF, bevacizumab stops the cancer from developing its own blood supply This reduces the tumor’s supply of oxygen and nutrients, causing it to stop growing and shrink. Drugs that interfere with blood vessel growth are called angiogenesis inhibitors or anti-angiogenics. Clinical uses The United States Food and Drugs Administration has approved bevacizumab as a first-line treatment for patients with advanced and metastatic (cancer that has spread to vital organs) carcinoma of the colon or rectum. The therapy can also be used to treat advanced non-small cell lung cancer or advanced cancer of the breast, kidney or bowel. In addition, bevacizumab has been used successfully in the treatment of eye disorders such as age-related macular degeneration and diabetic retinopathy, where abnormal blood vessel growth in the retina causes the vessels to leak fluid, giving rise to retinal damage. Administration Bevacizumab may be given in combination with chemotherapy or when used to treat kidney cancer, it may be given alongside interferon. The drug is given as a drip into a vein (infusion) once every two or three weeks. Bevacizumab is usually administered over a period of 90 minutes for the first infusion, 60 minutes for the second infusion, with infusions thereafter lasting for about 30 minutes. Reviewed by Sally Robertson, BSc Sources http://www.ukmi.nhs.uk/NewMaterial/Secure/Bevacizumab051004.pdf www.nhs.uk/.../Avastin(Bevacizumab)(CB4pages).pdf http://www.pmda.go.jp/english/service/pdf/Abastin-Bevacizumab.pdf www.roche-australia.com/.../avastin-pi.pdf faculty.ksu.edu.sa/hisham/Documents/PHCL_510/Students_Work/Avastin.pdf www.betterhealth.vic.gov.au/.../rocavast.pdf Further ReadingAvastin (Bevacizumab) - What is Avastin?Avastin (Bevacizumab) Side Effects Last Updated: Apr 2, 2014"
98,"2018-04-20 02:35:02","Avastin (Bevacizumab) Side Effects","By Dr Ananya Mandal, MD Most anti-cancer drugs are associated with moderate to severe side effects and Avastin (bevacizumab) is no exception. The side effects of Avastin occur either as reactions to infusion of the drug or in response to the drug itself. Infusion-related side effects Side effects associated with the intravenous infusion of Avastin may be seen for up to 24 hours after infusion and examples include: Flu-like symptoms such as fever, chills, dizziness and weakness Skin rash that may appear red, warm and itchy Angioedema or allergic reactions leading to swelling in the lips, tongue or back of the throat making it difficult to swallow or breathe Wheezing or coughing Pain in the back or abdomen Tightness and pain in the chest Other side effects Examples of side effects that may occur for up to days or weeks after the infusion include: Nausea and vomiting – Usually anti-emetics or drugs that prevent nausea are prescribed to control these symptoms Loss of appetite – A dietician or a nutritional advisor may help plan a healthy diet that helps prevent malnutrition due to loss of appetite. High blood pressure – Blood pressure is routinely monitored among patients receiving Avastin to check for abnormal changes. Headaches, nose bleeds or dizziness may indicate a change in blood pressure. Mouth ulcers and sores – These may be prevented by drinking plenty of fluids, maintaining good oral hygiene and supplementing nutrients in diet. Increased risk of developing blood clots – This increase in risk is more common among individuals who are already at risk of such clots. Possible signs of blood clotting include chest pain, breathlessness, changes in vision, difficulty speaking, paralysis of the limbs and swelling, pain, or redness in one of the arms or legs. This condition may be life threatening if not treated promptly. Increased vulnerability to infections – Avastin can reduce the number of white blood cells in the body and increase susceptibility to infection. Common symptoms include high fever and chills. Risk to unborn baby – Avastin may be harmful to the fetus or a nursing infant. Reviewed by Sally Robertson, BSc Sources http://www.ukmi.nhs.uk/NewMaterial/Secure/Bevacizumab051004.pdf www.nhs.uk/.../Avastin(Bevacizumab)(CB4pages).pdf http://www.pmda.go.jp/english/service/pdf/Abastin-Bevacizumab.pdf www.roche-australia.com/.../avastin-pi.pdf faculty.ksu.edu.sa/hisham/Documents/PHCL_510/Students_Work/Avastin.pdf www.betterhealth.vic.gov.au/.../rocavast.pdf Further ReadingAvastin (Bevacizumab) - What is Avastin?Avastin (Bevacizumab) Indications Last Updated: Apr 2, 2014"
99,"2018-04-20 02:35:05","Avastin (Bevacizumab) Price","By Dr Ananya Mandal, MD Avastin or bevacizumab is one of the most expensive drugs that is currently marketed. In many countries with national health services, the use of bevacizumab has been restricted based on cost-benefit calculations that suggest the drug is not cost-effective. The National Institute for Health and Care Excellence (NICE) does not approve of the NHS funding the use of bevacizumab because estimates show the cost is £21,000 per patient, with only minimal benefits seen in many cases. One study published in the New England Journal of Medicine reported that bevacizumab extended life by 4.7 months (20.3 months versus 15.6 months) at a cost of $42,800 to $55,000. The cost of Avastin as currently supplied by the manufacturer is £1,848.80 per month for a typical 70 kg patient. The recommended dosage is 5 mg/kg and is to be given once every 14 days as an intravenous infusion until disease progression is slowed. In 2000, the rate of death in England and Wales due to colorectal cancer was around 29 per 100,000 population and it has been estimated that around 15 patients per 100,000 may benefit from chemotherapy that may include bevacizumab treatment. Based on the current cost of supplying bevacizumab (£1,848.80 per month for a 70 kg person) and the median length of time that treatment is required for (approximately 10 months), the cost of bevacizumab would be around £18,500 per patient treated. This would be in addition to the cost of fluoropyrimidine-based chemotherapy. In Canada, the cost is to the tune of $40,000 per year. In the United States, insurance companies have refused to pay for all or part of the costs of Avastin therapy and reimbursement is also restricted in Canada due to the low benefit-to-cost ratio. Reviewed by Sally Robertson, BSc Sources http://www.ukmi.nhs.uk/NewMaterial/Secure/Bevacizumab051004.pdf www.nhs.uk/.../Avastin(Bevacizumab)(CB4pages).pdf http://www.pmda.go.jp/english/service/pdf/Abastin-Bevacizumab.pdf www.roche-australia.com/.../avastin-pi.pdf faculty.ksu.edu.sa/hisham/Documents/PHCL_510/Students_Work/Avastin.pdf www.betterhealth.vic.gov.au/.../rocavast.pdf Further ReadingAvastin (Bevacizumab) - What is Avastin?Avastin (Bevacizumab) IndicationsAvastin (Bevacizumab) Side Effects Last Updated: Apr 2, 2014"
100,"2018-04-20 02:35:15","Test for Bile Duct Cancer","By Afsaneh Khetrapal BSc (Hons) Bile duct cancer is identified, diagnosed, and staged with the help of tests that analyze bile ducts and neighboring organs. It is essential to be aware whether the bile duct can be detached by surgery, when planning for treatment. To find, diagnose, and confirm bile duct cancer; tests and procedures are generally performed at once. Tests for Diagnosing Bile Duct Cancer Physical checkup and medical history: A general check-up of the body is carried out to examine health signs, including the signs of ailment, such as any abnormal condition or formation of lumps. It also includes exploring the lifestyle and medical history of the patient. Laboratory tests: This is a medical procedure for examining specimens of blood, tissue, urine, or additional components present in the body. With the help of these tests, the disease can be diagnosed so as to plan for appropriate treatment and observation over a period of time. CA 19-9 tumor marker test and carcinoembryonic antigen (CEA) test: In this procedure, the volume of certain components produced by tumor cells, tissues, and other organs in the body is measured in a sample of tissue, urine, or blood. The presence of increased levels of certain components in the body can relate to specific cancer types. These certain components are termed as tumor markers. For example, bile duct cancer is indicated by abnormal levels of CA 19-9 and CEA, which is also known as a carcinoembryonic antigen. Ultrasound exam: In this method, high energy sound waves known as ultrasound produce echoes by becoming deflected off interior tissues or organs like the abdomen. A sonogram is the image of body tissues that are generated from the echoes, the images of which can be printed for later use. CT scan or CAT scan: A sequence of accurate images of interior body sections (especially abdomen) is captured at different angles in this procedure. The images are generated by a computer connected to an x-ray machine. For more detailed views of tissues and organs, one may be asked to consume a dye or it may be infused. This method is also termed as computerized axial tomography, computed tomography, or computerized tomography. Magnetic resonance imaging or MRI: In this method, a sequence of images of interior body parts is generated by making use of radio waves, a magnet, and a computer. This method could also be called as NMRI (nuclear magnetic resonance imaging). MRCP (magnetic resonance cholangiopancreatography): In this method, a sequence of images of interior body parts such as bile duct, pancreas, liver, gall bladder, and pancreatic duct are generated by making use of radio waves, a magnet, and a computer. Biopsies for Bile Duct Cancer Related StoriesInvestigating new cancer therapy candidates with live-cell imagingNeedle biopsy: In this method, without making a surgical cut initially, a fine hollow needle is infused into the tumor through the skin. A local anesthesia is initially used to desensitize the skin. Generally, the needle is directed into the spot by using a CT scan or ultrasound. When the picture displays that the needle is pointed towards the tumor, a specimen is drawn into the needle and is observed under a microscope in the lab. A fine-needle aspiration, which is also known as FNA, is the biopsy used in many cases that make use of a very thin needle connected to a syringe for drawing cell samples. It is rare that the FNA does not provide sufficient cells for an accurate diagnosis. If this is the case, however, more samples can be collected by making use of a large needle by performing a core needle biopsy. Laparoscopy: This is a surgical procedure to examine the interior portion of the abdomen such as liver and bile duct to check up for signs and symptoms of cancer. Tiny cuts are made in the abdominal wall and a thin tube fitted with light known as a laparoscope is inserted through one of the cuts (incisions). To check for signs of cancer, samples of tissues are collected by inserting the equipment either through the same or through some other incisions. Endoscopic retrograde cholangiopancreatography (ERCP): Bile is carried from the liver to the gallbladder and then from the gallbladder to the small intestine. This ERCP method is used to x-ray the ducts (also known as tubes). These ducts tend to be confined and the flow of bile is restricted or slowed down, which leads to jaundice. Endoscope reaches the small intestine by passing through the mouth and abdomen. Percutaneous transhepatic cholangiography (PTC): This is a method used to x-ray the bile ducts and the liver, in which a thin needle is infused into the liver through the skin beneath the ribs. X-ray is taken by infusing the dye into the bile ducts or the liver. To check for cancer signs, tissue samples are collected. The stent is a thin soft tube that may remain in the liver to drain out bile into the small intestine or a collection bag exterior to the body when the bile duct is obstructed. This method is used if surgery is not applicable for a patient. Sources https://www.cancer.gov/types/liver/patient/bile-duct-treatment-pdq http://www.genesiscare.co.uk/bile-duct-cancer https://medlineplus.gov/bileductdiseases.html www.cancer.org/.../how-diagnosed.html https://www.cancer.gov/types/liver/patient/bile-duct-treatment-pdq www.urmc.rochester.edu/.../content.aspx www.nhs.uk/Conditions/Cancer-of-the-bile-duct/Pages/Diagnosis.aspx Further ReadingBile Duct Cancer PrognosisCauses of Bile Duct CancerBile Duct Cancer - CholangiocarcinomaBile Duct Cancer ResearchSigns and Symptoms of Bile Duct CancerMore... // Last Updated: Aug 11, 2017"
101,"2018-04-20 02:35:17","Bile Duct Cancer Prognosis","By Jeyashree Sundaram (MBA) Cholangiocarcinoma (bile duct cancer) usually develops in the bile duct system that arises from the liver and bile ducts and ends at the small intestine. Cancer that develops in the section of bile ducts within and outside the liver is called as intrahepatic and hilar cholangiocarcinoma, respectively. Distal cholangiocarcinoma is developed in the bile section that is associated with small intestine. Prognostic factors of cholangiocarcinoma are highly disputable. The prognosis of bile duct cancer is affected by various factors such as the site of cancer, type and grade (extent of cell abnormalities when examined under a microscope) of cholangiocarcinoma, physical health condition, treatment, etc. The risk factors for bile duct cancer include primary sclerosing cholangitis (a gradually developing disorder in which inflammation and scarring block bile ducts), chronic ulcerative colitis, and cysts within the bile ducts (these block bile flow, leading to bile duct enlargement, infection, and inflammation). Post-Segmentectomy Prognostic Factors of Distal Cholangiocarcinoma Distal bile duct cancer is the most common type of bile duct cancer after intrahepatic bile duct cancer. Nevertheless, the prognosis of distal cholangiocarcinoma is better when compared to other two types of bile duct cancer. Initial stage symptoms of distal cholangiocarcinoma include cholangitis, jaundice, etc. These symptoms can help in early identification of the disease. Further development of the tumor can be prevented by segmentectomy. Some of the risk factors that affect the prognosis of distal bile duct cancer are perineural infiltration, tumor markers, tumor cell differentiation, serum bilirubin, lymph node metastasis, amount of transfusion, age, etc. Complications within a Month Post-Surgery Around 44% of patients suffered from complications after a month of surgery. Complications experienced by bile duct cancer patients after they are treated with pancreaticoduodenectomy and whipple procedures for distal bile duct cancer are as follows. The most common postoperative problem faced is collection of intra-abdominal fluid and postoperative bleeding, which was experienced by almost 37% patients post-operation. Few patients suffered with life-threatening consequences such as liver failure, left hepatic artery damage, etc. Minimum number of patients hadn’t survived. Complications in Average Follow-up Period (2 to 177 Months) Around 47% of patients were affected by distal bile duct cancer for the second time, which indicates that 53% of patients do not experience recurrence during follow-up. Related StoriesInvestigating new cancer therapy candidates with live-cell imagingOut of the patients experienced with recurrence bile duct cancer, 47.3% of the patients were affected by local recurrence, 30% were affected with intrahepatic recurrence, and 23.2% were affected with systematic recurrence. Survival Rate The survival rate within first three years after the operation is around 55.3%. After five years, the survival rate was around 48.3%. Finally, after ten years, it was around 33.7%. Post-Segmentectomy Prognostic Factors of Extrahepatic Cholangiocarcinoma After extrahepatic cholangiocarcinoma segmentectomy, various data are subjected to evaluation to find the prognostic factors after segmentectomy of extrahepatic bile duct cancer. Such data include postoperative adjuvant treatment, pathologic factors, patient demographics, and intraoperative factors. Lymph node metastasis, tumor histology, and 5th American Joint Committee on Cancer stage were significant prognostic factors. Lymph node metastasis and tumor histology were identified as the prognostic factors that are independent, during the Cox proportional hazard regression for multivariate analysis. Despite the fact that the patients suffering from lymph node metastasis had experienced mean recurrence than those are not affected by lymph node metastasis, some patients attained cure post-segmentectomy. Survival Rate Around 20% to 30 % of the extrahepatic bile duct cancer patients survive for five years after surgical resection. Some patients survive even after five years even though they are affected with recurrent extrahepatic bile duct cancer. In some cases, recurrent bile duct cancer is identified only after five years post-segmentectomy. But the average survival rate is less when compared to the first five-year survival rate. The average survival rate within first year after the segmentectomy was around 72.9%. After three years, the survival rate was around 41.1%. Finally, after five years, it was around 32.5%. Factors Influencing Prognostic Factors in Advanced Cholangiocarcinoma After Surgery and Chemotherapy The survival rate of patients affected with advanced cholangiocarcinoma in the first year after the therapy, such as segmentectomy, chemotherapy, etc., was around 10.8%. After three years, the survival rate was around 5.4%. Finally, after five years, it was around 4.5%. Average survival rate of advanced bile duct cancer was eight and a half months. Univariate analysis method was used to evaluate the impact of various factors such as tumor-related, treatment, and multiple clinical parameters on advanced cholangiocarcinoma survival. Some of the parameters that do not affect the prognosis of advanced cholangiocarcinoma are perineural invasion, stenting, vascular invasion, age, history of cholelithiasis, resection margin status, diabetes, presence of metastasis, and gender. The prognosis of advanced bile duct cancer is also not influenced by size, location, and stage of the tumor. Survival rate of patients who underwent surgery was less compared to those treated with chemotherapy. Reviewed by Afsaneh Khetrapal Bsc (Hons) Sources https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1356849/ www.mayoclinic.org/.../ovc-20202771 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3834019/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2712857/ http://www.cancerresearchuk.org/about-cancer/bile-duct-cancer/survival www.urmc.rochester.edu/.../content.aspx Further ReadingTest for Bile Duct CancerCauses of Bile Duct CancerBile Duct Cancer - CholangiocarcinomaBile Duct Cancer ResearchSigns and Symptoms of Bile Duct CancerMore... // Last Updated: Sep 18, 2017"