LMP299Y1 Lecture Notes - Lamina Propria, Muscularis Mucosae, Inflammatory Bowel Disease

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Published on 3 Jun 2013
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March 27, 2013
Multiple organs considered part of GI tract
- Divide into luminal GI liver and pancreas upper tract and lower tract
- Upper tract = stomach and small intestine
- Liver and pancreas are the two solid organs
Lymphoid cells of the GI GALT
Lymphoid immune system called GALT
Amount of T cells in gut >>> number in spleen most abundant
Mostly t cells with gamma delta receptors mostly CD8 positive
Plasma cells secreting IgA2
Stomach/small bowel histology
Small intestine surface epitheium villi considered mucosa; then muscularis mucosa; submucosa;
muscularis externa;
Ileum most prominent lymphoid tissue is peyer’s patch – they are lymphoid follicles in lymphoid
propria important for GI immunity
Colon epithelium
Appendix more lymphoid tissue in appendix than lymphoid tissue most common area to find
lymphoid tissues/follicles
Closer look at the appendix crypts are glands;
Components of the GIT area between villi lamina propria muscularis mucosae
Lamina propria lymphoid cells are cells in between the villin and intraepithelial lymphocytes are
between the epithium in the villi themselves
Special GALT sites
Peyer’s patches
FAE intraepithelial lymphocytes are FAE epithelium on top of lymphoid follicle these are M cells
M cells ultrastructure see infoldings, not vili function has antigen presenting inside can transport
bacteria/viral molecules into the lamina propria and as the number of the luminal bacteria increases,
the number of M cells also increase darker looking under microscope
FAE M cells usually associated with alpha beta memory T cells instead of gamma/delta
IgG and IgA cells rarely found most of Ig secreted by these cells are IgM and IgG
HLA receptors on the basal lateral aspects of these cells HLA involved in immune system as well
Discontin ous different from terminal ilium, lots of peyers’s patches
Special GALT sites
In stomach, get lymphoid tissue but do not get lymphoid follicle lymphoid tissue has mixture of mostly
T cells but lymphoid follicle has certain structure lighter middle, darker outline are lymphoid follicle,
should not be seen in stomach
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When infection in stomach or gastritis, see lymphoid follicles they are acquired! Not there to begin
with
Function of gut epithelium digestion and absorption make tight junctions so works ars barrier of
antigen and bacteria to lumen
Process the antigen and transport to lamina propria express class 2 antigen but do not have
costimulatory molecules
Components of GIT
IEL vs LPC
IEL at tips of villi; LPC between villi
IEL mostly CD3 POSITIVE; majority are CD8 positive, so cytotoxic;
GIT immune response
Will not go through lymphomas and small bowel transplantation
Can get celiac disease other parts of GI tract mostly in lower GI tract (small intestine)
GASTRITIS
Acute alchol induced, NSAIDS incudec, H pylori induced also autoimmune disease
Autoimmune gastritis for the most part present as chronic disease
Eosinophilic increase in number of eosinophils
Collagenous
Graft vs host disease in transplantation when the antibodies invade native organs
H pylorid present as chronic disease as well
Autoimmune gastritis get autoantibodies into cells most for intrinsic factos two types of
antibodies there blocking antibodies and binding antibodies mostly blocking antibodieng how
pernicious anemia results
B12 deficiency pernicious anemia involve din adsorption of B12
Clinical effects of autoimmune gastritis destroys crypts and glands antibodies against these glands,
so get destruction and thus atrophy atrophy of glands can result from other things as well like
prolonged h ylorid infection
Decreased in intrinsic factor does not bind, so B12 not absorbed
Divisions of the stomach
Autoimmune gastritis mostly involved body
Normal gastric folds when there is atrophy, these folds are gone in an advanced stage of gastritis
Autoimmune gastritis with hyperplasia of endocrine cells glands - little dark areas are lymphocytes
increased in numbrs endocrine cells not enough stimulation to proeduce acid, so cells that stimulate
acidsecrection increase to compensate for eduction in acid so get hyperplasia of endocrine cells
IF picture highlights autoantibodies in parietal cells see all the bright areas have antibody against
parietal cells
Gastritis eosinophilic gastritis and lymphocytic gastritis not discussed
H pylorid gastritis
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