Curriculum for Specialty Certificate Examination in Gastroenterology

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Sunday 21 April 2013

Coeliac disease

10 comments:

  1. Which of the following statements regarding the genetic and immunological basis of coeliac disease is correct?

    1-50% of patients are HLA-DQ 2 or HLA-DQ 8 positive
    2-Alpha-gliadin specific CD8 cells can be identified in the intestinal wall of untreated patients with coeliac disease
    3-Cow's milk proteins may precipitate an immune-related enteropathy indistinguishable from coeliac disease
    4-Tissue transglutaminase generates the antigenic epitopes present in alpha-gliadin
    5-TNF-alpha plays a critical role in the inflammatory response in the intestinal wall of patients with untreated celiac disease

    The prevalence of coeliac disease is 1% in western societies and is thus one of the commonest immune-mediated diseases.

    It arises as a result of genetic predisposition (at least 95% of patients are HLA-DQ2 or HLA-DQ8 positive) and also from the specific immune response to the alpha-gliadin component of gluten.

    Cow's milk can produce an immunologically mediated enteropathy but the condition is rare and transient.

    The action of tissue transglutaminase on alpha-gliadin generates epitopes to CD4+ T-lymphocytes, which provoke an inflammatory response in the intestinal wall.

    In untreated individuals, alpha-gliadin specific CD4+ T cells can be found producing interferon-gamma in the intestinal wall.

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  2. What the approx prevalnce of CD in the general population:
    1-1:3000
    2-1:1000
    3-1:100
    4-1:10

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    Replies
    1. Celiac disease (CD) is one of the most common diseases, resulting from both environmental (gluten) and genetic factors [human leukocyte antigen (HLA) and non-HLA genes]. The prevalence of CD has been estimated to approximate 0.5%-1% in different parts of the world.

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    2. Celiac disease (CD) is one of the most common diseases, resulting from both environmental (gluten) and genetic factors [human leukocyte antigen (HLA) and non-HLA genes]. The prevalence of CD has been estimated to approximate 0.5%-1% in different parts of the world.

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  3. Celiac disease affects the mucosa of the small intestine; the submucosa, muscularis propria, and serosa usually are not involved. The mucosal involvement of the small intestine in celiac disease may vary considerably in both severity and extent. This spectrum of pathologic involvement helps explain the striking variability of the clinical manifestations of the disease. Examination, by hand lens or dissecting microscope, of the mucosal surface of biopsy specimens from untreated celiac disease patients with severe involvement reveals a flat mucosal surface with complete absence of normal intestinal villi. Histologic examination of tissue sections confirms this loss of normal villous structure (see figure). Sparing of the proximal intestine with involvement of the distal small intestine does not occur.

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  4. what are the investigations?

    The laboratory findings in celiac disease, like the symptoms and signs, vary with the extent and severity of the intestinal involvement. Serum IgA endomesial antibodies, tissue transglutaminase antibodies, and small bowel biopsy are the most accurate diagnostic tests for celiac disease. It is also important to document IgA deficiency, as this can lead to falsely negative serology results. Although the diagnosis of celiac disease may be suspected on clinical grounds or as a result of abnormal serologic test results, the current recommendation for confirmation of the diagnosis remains a biopsy of the small intestine. Several biopsy specimens should be obtained from the distal duodenum (second or third parts) to avoid the mucosal architectural distortion produced by Brunner’s glands and changes caused by peptic duodenitis, both of which can cause difficulty in histopathologic diagnosis. Thus, shortening of the villi, crypt hyperplasia, cytologically abnormal surface cells, and increased lamina propria cellularity must be present to firmly make a diagnosis of celiac disease.

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  5. Prevalence of coeliac disease is estimated to be as high as 1 in 200 in the Western world. About 35% of patients present in the childhood, but it can occur in any age. Mode of presentation is variable with very subtle (growth retardation or anaemia) or more obvious with fatty diarrhoea and feature of malabsorption. Coeliac disease is due to gluten (cereal protein) allergy and gluten is present in all foods made from wheat, barley or rye and probably oats. IgA antibodies to gliadin are commonly positive in the serum of patients. Serum anti-endomyseal antibody and anti-tissue transglutaminase antibodies are more specific. Diagnosis is made by demonstration of duodenal or jejunal villous atrophy plus resolution of these changes with gluten withdrawal.
    Splenic atrophy is not uncommon and results in the presence of Howell-Jolly bodies and abnormal shaped red cells in the serum.
    There is a strong association with HLA DR3 antigen. Treatment is gluten-free diet for life.
    There is increased risk of malignancy and T cell lymphoma of the small intestine usually complicates coeliac disease. Risk of oesophageal carcinoma also increases with the condition.
    There is a close link with dermatitis herpetiformis, which is characterised by itchy vesicles over the extensor surfaces of the forearm and other pressure areas. IgA deposits are found at dermo-epidermal junction.
    Ulcerative jejuno-ileitis is a very serious form of coeliac disease with very poor prognosis and some patients respond to corticosteroids and gluten withdrawal.

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  6. The prevalence of coeliac disease is 1% in western societies and is thus one of the commonest immune-mediated diseases.
    It arises as a result of genetic predisposition (at least 95% of patients are HLA-DQ2 or HLA-DQ8 positive) and also from the specific immune response to the alpha-gliadin component of gluten.
    The action of tissue transglutaminase on alpha-gliadin generates epitopes to CD4+ T-lymphocytes, which provoke an inflammatory response in the intestinal wall.

    In untreated individuals, alpha-gliadin specific CD4+ T cells can be found producing interferon-gamma in the intestinal wall.

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  7. I am bold enough among many others to state that there is now a potent cure to this sickness but many are unaware of it. I discovered that I was infected with the virus 3 months ago, after a medical check-up. My doctor told me and I was shocked, confused and felt like my world has crumbled. I was dying slowly due to the announcement of my medical practitioner but he assured me that I could leave a normal life if I took my medications (as there was no medically known cure to Herpes). I went from churches to churches but soon found that my case needed urgent attention as I was growing lean due to fear of dying anytime soon. In a bid to look for a lasting solution to my predicament, I sought for solutions from the herbal world. I went online and searched for every powerful trado-medical practitioner that I could severe, cos I heard that the African Herbs had a cure to the Herpes syndrome. It was after a little time searching the web that I came across one Dr Itua(A powerful African Herbal Doctor), who offered to help me at a monetary fee. I had to comply as this was my final bus-stop to receiving a perfect healing. My last resolve was to take my life by myself, should this plan fail. At last it worked out well. He gave me some steps to follow and I meticulously carried out all his instructions. Last month, to be precise, I went back to the hospital to conduct another test and to my amazement, the results showed that negative,Dr Itua Can As Well Cure The Following Desease…Cancer,Hiv,Herpes,Shingles, Hepatitis B,Liver Inflammatory,Diabetis,Fribroid,Parkinson's,Alzheimer’s disease,Bechet’s disease,Crohn’s disease
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  8. I had my TL a little more than a year ago when my third child was born via c-section. I was not told ANYTHING about the possible side effects of having this procedure. Since then I have experienced heavy bleeding lasting sometimes 3 weeks out of the month, weight gain, severe mood swings. Severe cramping, changes to my libido, severe depression accompanied by suicidal thoughts, headaches, migraines, many new symptoms & older issues are now exacerbated. The father of two of my children doesn't want me anymore. I've become too much of a pain in the ass I guess. We don't talk. We don't sleep in the same bed. I think he might really think I am crazy... & maybe I am. I feel crazy a lot of the time.
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