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Gastrointestinal Block - Coggle Diagram
Gastrointestinal Block
Histology
Gallbladder and Pancreas
Lipase. Breaks Down Fats. Protease. Breaks Down Proteins. Alpha-Amylase. Breaks Down Carbs. Bile Breaks Down Fat Into Smaller Particles. Pepsin Breaks Down Protein Into Smaller Particles. The endocrine portion of the pancreas appears lighter and in clusters. The apical portion of acinar cells are filled with eiosinophilic zymogen granules hosting all pro-enzymes. The basal portion is strongly basophilic due to rough endoplasmic reticulum. The acinar cells constitute the majority of the organ and no myoepithelial cells are present. The intralobular ducts are lined by a simple cuboidal epithelium and goes into intercalated ducts which are lined by low cuboidal epithelium. Lighter colored granules in acinar cells are pre-mature while darker colored granules. Proenzymes are synthesized in the basal portion of cytoplasm then packaged in the Golgi complex stored in the apical cytoplasm as zymogen granules. The secretion of zymogens is stimulated by secretin and CCK where the release of secretin happens when gastric acid in the intestinal lumen stimulates secretin release which causes acinar and ductal cells to add water and bicarbonate to fluid in order to neutralize the chyme.
long chain fatty acids, gastric acid, some amino acids -------------- > release of CCK --------> pancreatic secretion of enyzmes
gastric acid in intestinal lumen -----------> secretin stimulates acinar and ductal cells add water and bicarbonate to fluid to neutralize chyme [makes sense that gastric acid stimulate bicarbonate release]
Clinical Correlations
Liver
Hepatic Infarct --- uncommon since the liver has two blood supplies. The liver appears yellow surrounding hyperemia.
Chronic Passive Congestion [Nutmeg Liver] --- Accumulation of RBC's in centrilobular regions creating a nutmeg pattern appearance from passive congestion around central veins
Liver Cirrhosis --- fibrosis and proliferation of fibroblasts and hepatic stellate (Ito) cells occur at areas OTHER THAN portal areas. Key feature is significant disruption of hepatic architecture by the laying down of excessive connective tissue [compensatory adjusting and healing becomes destructive]. This occurs late in chronic liver disease caused by alcoholism and portal hypertension. Caput medusae and ascites as a sequelae of portal hypertension caused by abnormal blood flow pattern.
High Yield
Chronic Passive Congestion [Nutmeg Liver] --- Right-sided heart failure leads to nutmeg pattern from congestion around central veins. Think congestion due to the accumulation of Red Blood Cells in the centrilobular regions. The nutmeg pattern appears around central veins. Since this is due to right sided heart failure [Cor Pulmonale] we see hemosiderin [light brown pigment] surrounding the central veins. A pronounced passage congestion manifests as centrilobular necrosis.
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Liver Cirrhosis --- chronic alcoholism or genetic causes leads to portal hypertension which on a cellular level leads to a proliferation of fibroblasts and Ito cells [a peri-sinusoidal, hepatic stellate cell and precursor fat cell]. This disrupts the hepatic architecture significantly.
Peptic Ulcer Disease --- Overproduction of HCl or pepsinogen as well as decreased secretion of mucus and bicarbonate and colonization of H. pylori leads to chronic, solitary lesions of mucosa that may extend to lower levels caused by exposure to HCl or pepsin. Research: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1117475/ [a unique, acid gated membrane channel of H. pylori allows urea into the cytoplasm of the bacterium and when acid levels are high there is an increase in activation of this channel. H. Pylori activates its own cytoplasmic urease in the stomach that converts urea into carbon dioxide and ammonia. The ammonia neutralizes the gastric acid preventing acidification of the H. pylori membrane.
Barrett's Esophagus --- Chronic GERD leads to stratified squamous tissue in the esophagus to become metaplastic columnar epithelia
Ulcerative Colitis --- Inflammation confined to the mucosa and submucosa within the colon [think colitis and colon] that leads to a sloughing off of mucosa and blood in stool. Ulcerative Colitis increases risk for adenocarcinoma
Crohn's Disease [Regional Enteritis] --- Immune, environmental, and genetic factors led to excessive lymphocytic activity and inflammation in ALL LAYERS of GI Tract wall leading to linear mucosal ulcers, cobblestone appearance in mucosa, and thickened intestinal wall. Think Ulcerative Colitis is Colon but Crohn's Disease is Cobblestone.
Colon
Ulcerative Colitis --- ulcero-inflammatory disease limited to colon mucosal damage. UC is a chronic, continual mucosal disease affecting and confined to primarily mucosa and submucosa and in severe cases extends in continuous manner proximally from rectum. Blood in stool is seen and the sloughing of mucosa, granulomas are absent and risk for adenocarcinoma increases.
Intestinal Polys --- tumorous mass protruding into intestinal lumen either pedunculated with stalk or sessile without stalk and about 90 percent are non-neoplastic.
Crohn's Disease [Regional Enteritis] --- chronic inflammatory bowel disease that occurs commonly in the ileum or colon resulting from poorly understood combination of immune, environmental and genetic factors. Excessive lymphocytic activity and transmural inflammation occur in any or all layers of tract wall [effects any level of the digestive tract]. Grossly one would see a small intestinal stricture, linear mucosal ulcers, perforation and associated serositis, and creeping fat. Histologically you see noncaseating granulomas, enteroenteric [bowel to bowel] fistula formation [fissure extends through mucosa into submucosa toward muscular wall].
Villous Adenoma --- histologically appears cauliflower like with elongated glands and dysplastic epithelium and grossly sessile adenoma
Esophagus
GERD affects lower esophageal sphincter and Barrett's Esophagus is a complication of long-standing GERD [about 11% of GERD patients have Barrett's Esophagus]. With Barrett's Esophagus normal stratified squamous tissue becomes chronically damaged metaplastic esophageal tissue [metaplastic columnar epithelium]. This switching from stratified squamous to metaplastic columnar epithelium is a protective measure. Goblet cells will appear in columnar mucosa. Adenocarcinoma of Esophagus is what Barret's Esophagus can become. The sequence is GERD -----------> Barrett's Esophagus ---------> Adenocarcinoma of Esophagus. The progression has to do with the level of penetration and invasion of metaplastic tissue. In Adenocarcinoma of Esophagus the tissue is moderately glandular [gland starts to appear where they shouldn't think adeno means gland] and the distal esophagus invades into muscular layer or adventitia of cardiac stomach and cells are move from metaplasia to dysplasia and angiogenesis is now seen at this stage. In Squamous Cell Carcinoma (SCCA) of Esophagus you can see fungus-associated and nitrosamine-containing foodstuffs. Dietary deficiencies, alcohol consumption, smoking, HPV exposure are all implicated in development of pathology. You will see irregularly reddish color, growing outward of substance and ulcerations and histologically will see infiltrating nests of neoplastic cells and abundant keratin in the cytoplasm.
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Salivary Glands
There are many head and neck tumors that can develop in the salivary glands alone one of which is Pleomorphic Adenoma arising in three epithelium cell types. In the serous cell you can find the granules located on the apical portion. In the mucous cell you can find the nucleus pushed down and filled with mucus on the apical side causing them to appear light
Stomach
Gastric (Peptic) Ulcer --- this is chronic, solitary lesions of mucosa that may extend to lower levels caused by exposures to HCl or pepsin. Overproduction of HCl or pepsinogen & decreased secretion of mucus and bicarbonate is seen as well as H pylori coupled with intermittent healing and scarring. The Upper GI bleeding is the most common complication here and the surface is disrupted. Gastric Carcinoma includes Intestinal Type Gastric Adenocarcinoma [infiltrates submucosa and lamina propria below the squamous epithelium of esophagus] and Signet Ring Carcinoma Stomach Diffuse Type [nucleus is pushed to one side of gastric cells because mucin vacuoles push the nuclei to one side]
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