Medicine Notes Gastrointestinal (GI) System Notes
These notes helped me achieve a mark of 73% in my GI exam, which is the equivalent of a 1st. The notes are based on a series of lectures on the subject. They are very clearly laid out and easy to follow. They cut out unnecessary information on the topic, making the notes very concise, and fast to get through. Anyone studying medicine, or any other subject requiring knowledge of the GI tract (e.g. physiology or anatomy), would benefit greatly from these notes. There are lecture in the series on th...
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Lecture 24
Crohn’s Disease
What is Crohn’s disease?
Chronic inflammatory disease, effects anywhere from mouth-anus (UC is only colon)
Characterised by patchy inflammation with ulceration (unlike UC, which is confluent)
Symptoms determined by site of disease and severity of inflammation & the complications of inflammation
Symptoms
Pain: Constant or in waves (inflammatory stricture of bowel)
Diarrhoea: Loose/severe, may be bloody
Weight loss: Due to disease, poor absorption & loss of appetite
Fatigue: Partly anaemia, but hard to treat
Who gets it?
Getting more common
Bimodal=young adults & middle aged
1 in 500
Can run in families; Developed nations
More common in smokers (opposite of UC)
Site of disease
Enterocolitis (small & large bowel) 50%
Enteritis (small bowel) 29%
Colitis (large bowel) 19%
Other sites (e.g. cutaneous) 2%
What causes Crohn’s disease?
BACTERIA (abnormal)
Bacterial flora change (is it because of CD or does it cause CD?)
In general, reduced diversity of Firmicutes & Bacterioides
Increased mucosa-associated E. coli in Crohn’s disease
Adherent Invasive E. Coli (AIEC)- able to penetrate gut wall, difficult to kill once there and sit in macs causing inflammation
Abnormalities
Loss of some Firmicutes & Bacterioides
Role of (AIEC)
BUT- Crohn’s disease not transmittable, & what about familial risk?
Mucus (defective)
Too much mucin (opposite of UC)
Mutation of MUC 19 gene in CD
Bowel wall (leaky)
Abnormal permeability
In CD patients and relatives
Tight junction defects
May be secondary to inflammation BUT
MYO9B gene mutation associated with UC
Gene in CD disputed
Abnormal defence
Defective mucus layer and epithelial barrier MAY permit invasion of gut wall by bacteria
Recognition (abnormal); Inflammation (dysregulated); Enhanced recruitment of inflammatory cells
Macrophages
Bug comes along and is engulfed
Become phagocytised
Lots of white cells come along= inflammation and damage
Why do some people’s macs not work? RECOGNITION ABNORMALITIES
Two types
NOD2
1st gene susceptibility locus on genes for Crohn’s
NOD2 involved in recognition of foreign antibodies
Mutation= can’t deal with antigens etc.
Significant increased risk of CD in those homozygous for NOD2 mutation
Autophagy
Another way cell can deal with bacteria
If...
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These notes helped me achieve a mark of 73% in my GI exam, which is the equivalent of a 1st. The notes are based on a series of lectures on the subject. They are very clearly laid out and easy to follow. They cut out unnecessary information on the topic, making the notes very concise, and fast to get through. Anyone studying medicine, or any other subject requiring knowledge of the GI tract (e.g. physiology or anatomy), would benefit greatly from these notes. There are lecture in the series on th...
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