celiac's disease Flashcards
What are the 4 take-home pts of celiac’s disease?
- common
- significant non-GI disease
- commonly overlooked and under-diagnosed
- diagnostic screening blood test
classic celiac GI presentation
diarrhea, steatorrhea, bloat and flatulence, weight loss, failure to grow, muscle wasting, low serum proteins, ascites. maldigestive wasting disease from severe atrophy of the intestinal mucosal absorptive surface.
common celiac GI presentation
episodic loose stool, bloat, vague abdominal discomfort. often labeled IBS. mean time to diagnosis 7-11 yrs
non-GI presentations of celiac’s disease
aphthous stromatitis and excessive cavities iron deficient anemia, rarely B12 osteopenia neuro secondary hyperparathyroidism, infertility, amenorrhea, impotence dermatitis herptiformis arthralgia abnormal LFTs hyposplenism tetany
most commonly associated conditions with celiac’s (not caused by celiac’s)
DM type I
auto-immune thyroiditis
Down’s
autoimmune hepatits
normal gut immunity
intestine has a difficult job: must decide what is food, what is BAD bacteria that must be killed, and what bacteria shouldn’t be let through but is commensal.
this recognition is done via pattern recognition of key molecular sequences. PAMPS (pathogen associated molecular patterns) on bad bacteria interact with receptors on the surface of immune cells to cause an immune response with activated T cells and antibodies. Immune suppressors dampen these mechanisms when the antigen is just food. This process is complex and poorly understood.
cereals in gut
cereals are hard for primates to digest. proline peptidase is necessary for wheat digestion but is only present at low concentrations.
Celiac pathophysiology
HLA molecules DQ2 and DQ8 have the ability to develop into celiac’s disease. when wheat antigens are presented in celiac’s pts by DQ2 and DQ8, the inflammatory cascade is initiated. T cell derivatives cause cell and tissue injury resulting in shortened intestinal villi and reduced absorptive surface in the proximal intestine. Also results in the production of antibodies against tissue transglutaminase (which plays a role in antigen presentation and can be measured as a serum marker for celiac pathology).
Celiac pts also have some defect, either congenital or acquired, during the development of intestinal immune tolerance.
histologic features of celiac’s disease
proximal intestinal lesion of flattened villi and crypt hyperplasia with an incr. pop of active intra-epithelial lymphocytes.
What part of wheat is inflammatory in celiac’s disease? where else is this found?
gluten, more specifically gliadin. also found in barley and rye
Why are most celiac’s lesions in the proximal gut?
there is lots of gluten antigen in the proximal gut. With time and gut enzymes, the antigent is eliminated in more distal gut tissue. Importantly, this means that most adults with celiac’s disease have enought distal gut to get enough macronutrient digestion (most adults don’t have symptoms from maldigestion of macronutrients). However, there isn’t always enough space for calcium and iron absorption –> osteoporosis and iron deficiency anemia
Dx of celiac’s disease
antibodies to TTG (tissue transglutaminase) have high sensitivity and specifity. Good negative predictive value. if test is positive, do an upper endoscopy with biopsy for confirmation.
Tx for celiac’s
gluten free diet