Crohn's disease Flashcards
What is Crohn’s disease
inflam bowel disease that normally effects terminal ileum and colon but can be present throughout GI tract.
Causes raised inflam markers, increase calprotectin, anaemia, vit b12 and D defficiency
Pathogenesis of Crohn’s
genetic susceptibility involving polymorphism of CARD15, ATG16L1, IRGM causing problems in recognition and handling intracellular bacteria
what are symptoms and causes of Crohn’s
inflam of all GI wall layers down to serosa therefore prone to strictures, fistulas and adhesions
the chronic inflam mediated by Th1 especially cytotoxic T cells (In UC mediated by Th2) vausing mucosal hyperresponsiveness to GI flora as well as defective mucosal barrier (altered cell adhesion molecule genes) causing barrier dysfunction
cobblestone appearance from nodular swelling, fibrosis and linear mucosal ulceration can develop to deep, linear fissures
obstructive symptoms can occur due to narrowin of lumen from inflam, swelling, fibrosis
What are clinical features of Crohn’s
abdominal pain, haematomesis diarrhoea and mucus, right ower quadrant pain (mimics appendicitis), malabsorption and malnutrition
What is the treatment and management for Crohn’s
Short-term
corticosteroids, sulfasalizine, metronoidazole,asathioprine, 6-mecaptopurine, methotrexate and inflimuab, however these give rise to oppurtunistic infections
Long term
non-greasy foods, stop dairy
suregery- remove inflammed parts of bowel
Dx between Crohn’s and UC
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How does Crohn’s lead to anaemia
Blood-loss anaemia, malabsorbtion of iron, anaemia of inflam (inflam cytokines IL-6 stops iron transport in entarocytes and macrophages), aneamia of chronic disease (folate deficiency inhibits conversion of hoocysteine to methionine causing increase homocysteine in blood (pro-oxidant AA) increasing oxidative stress, which slows down DNA synthesis causing megaloblastic anaemia (underdeveloped erythrocytes)
MOA prednisilone
glutacorticoid, which binds to specific nuclear receptors on nucleus, which alters gene expression and inhibits proinflam cytokine production, so less leukocyte recruitment and stimulating apoptosis in immature leukocytes
MOA ferrous sulphate
iron transported into macrophage via DMT1 and be incorrparated into ferritin and stored in macrophage or carried off macrophage via feroportin. Exported iron then oxidised via ceruloplasmin to Fe3+ and then following sequestration by transferrin taken to bone marrow or liver to combine with porphyrin ring to form haemogloblin
What does a blood test show in Crohn’s
CBC to detect infection or anaemia
ESR and CRP to see inflam markers
LFTs to see liver or bile duct problems
Vit B12 to see if absorbtion issues
Antibody blood test for Dx, pANCA for UC and ASCA for Chron’s
Why is a stool sample done in Crohn’s
to detect protein calprotectin. Inflam causes high levels of neutrophil recruitment, which conatin calprotectin in cytosol therefore high calprotectin indicates inflammation
Differences between Chron’s and UC
UC limited to colon and rectum, however disease of entire colon- pancolitis
In UC mucosa is red an dulcers are broad and granular
Pseudopolyps on either side of GIT can grow and fuse together to form mucosal bridges
UC is not trasmural, so colon wall is not thickened, serosal surface normal and no strictures, no granulomas
