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Laboratory Medicine and Pathobiology
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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 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 H pylori gastritis – where infection and immunology meet Antrum mostly Prevalence increases with age In developing countries, see epidemiology is different – lots of H pylorid infections in children, and young adults Clinical effects Many clinical implications – can be prevented easily – increases risk of peptic ulceration – gastric physiology changed – increases risk of gastric lymphoma – Lamina propria – lots of lymphocytes – gastric glands poited by arrows, inside of them are neutrophils – this is how to decide acute, indicated by neutrophils – chronic has more lymphocytes Chronic infection – increased number of lympohcytes No neutrophils seen Lumen side Chronic h pylori gastritis – do not see lymphoid follicles in stomach – see the darker outline is lymphoid follicle, first clue of infection Yellow is stomach crypt – yellow is pylori Silver stain binds to outer surface of organism Complications of chronic gastritis – Intestinal metaplasia 0 blue cells have mucin in them are NOT Part of normal physiology of stomach – when have them, they have been current destruction and assault to epithielium – intestinal epilasia is very resistant to acid and to destruction – the body adopts to the assult and changes the type of epithelium – intestinal metaplasia can progress to cancer Inflammatory bowel disease Can result due to various etiologies Idiopathic IBD – do not know specific etiology Multi0factorial disease – some genetic links – fifteen percent chance of involvement of Some genetic links, but definitely env factors Smoking – Lymphocytes and epithieal cells – increasd number of lympohcytes Ratio of CD4 and CD8 normal – in IBD, this balance is normal Some genetic links that suggest the NOD1 gene suppressed so immune system is overactivated and doesn’t recognize between own cells and outside antigen – IBD – humoral immunity – more IgG type cells Autoantibodies is goblet cell mucopolysaccaride – epithelial associated protein – pANCA – one of few au
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