Summary

This document appears to be a test on pathophysiology, focusing on the digestive system. The document covers a range of conditions including swallowing disorders, hernias, ulcers, and syndromes, including dumping syndrome. The document contains practice questions aimed at undergraduates.

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Pathophysiology Test 2 test worth 25% Dysphagia (difficulty swallowing) developmental defect → eg. connection between the esophagus & the trachea via fistula (but it can happen anywhere) contributions to dysphagia a. neurolo...

Pathophysiology Test 2 test worth 25% Dysphagia (difficulty swallowing) developmental defect → eg. connection between the esophagus & the trachea via fistula (but it can happen anywhere) contributions to dysphagia a. neurological damage to cranial nerves can also take part in swallowing difficulty CN V - Trigeminal (chewing nerve) → can't chew your food, can't form a bolus, leads to difficulty swallowing CN X - Vagus (swallowing nerve) → unconscious movements beyond the throat to allow food to go down smoothly b. tumour - from the outside can pressurize the GI tract leading to obstruction c. achalasia - loss of muscle contraction in lower esophagus. (food would get stuck) d. diverticulum - pouch that forms within inner layers of GI tract trapping food in it e. fibrosis: scar tissue can contract & constrict airway Hiatal Hernia (hernia in the upper GI tract) sliding hernia (95%) → sphincter slides upwards, no longer being in line with the diaphragm meaning the part of the stomach that is meant to be below the diaphragm will now POKE it, causing a hernia treatment: can have surgery to suture it in place to prevent it from moving rolling hernia (5%) → loss of rigidity, very mobile. The upper part of the stomach is ABOVE the small opening of the sphincter causing hernias (sphincter is in the right place) Pathophysiology Test 2 1 treatment: small piece will become necrotic that will have to be surgically removed risk factors: being pregnant can result in hiatal hernia manifestations: pyrosis (heart burn), cancerous changes can occur from reoccurring heart burn or herniation → will burn a lot because there is no way to release air Gastric Disorders Gastritis → inflammation of the lining of the stomach caused by alcohol or medications. Endoscopy will look red & inflamed (ordinarily looks yellow & flat) Peptic ulcer → 2 locations (stomach or duodenal) caused by H. pylori or the over use of NSAID drugs affecting the lining of the stomach Pyloric Stenosis → narrow opening between stomach & duodenum thickened pyloric sphincter is same consistency as rubber, can cause projectile vomiting (babies born before their due date with underdeveloped sphincter) or can also happen to adults through unresolved peptic ulcers that can harden over time Pathogenesis of H. Pylori stomach to oral transmission (think of splitting chips & dip with someone infected double dipping) Urease bacterium is an enzyme that H. Pylori makes, allowing them to remain dormant in the environment. Urea molecule turns into NH3, secreting ammonia around itself (alkaline) staying in the stomach because it neutralizes the stomach acid Pathophysiology Test 2 2 associated conditions → cancer of the lining of the stomach or lymphoma, or elongated duration of prescription drugs diagnosed via fast, specific, & noninvasive test (both as equally specific or sensitive) urea breath test: confirmation of uresis in the stomach from breath test after drinking radioactive uresis drink stool sample Medication: triple therapy required → 2 antibiotics & proton pump inhibitor Clarithromycin (starting to see resistance to H. pylori) amoxicillin (metronidazole is given is patient has penicillin allergy) pantoprazole (PPI that reduces uric acid in the stomach) → if someone is immunocompromised they would be given bismuth as QUADRUPLE THERAPY if it may be difficult for pt to pass the bacteria: medication makes a bad reproduction site for toxic cells Dumping Syndrome (condition that may be seen after a gastric bypass) purposed to shrink the stomach to encourage weight loss as you would be full faster. Bypassing a part of the jejunum that reduces the absorption of nutrients patho: accelerated gastric emptying - food leaves stomach too quickly manifestations of dumping syndrome → extreme diarrhea rapid absorption pulls water & electrolytes out of cells, leading to dehydration (sugar is a water magnet) → rapid dehydration as a result of diarrhea → vitamin deficiencies since you are bypassing the jejunum management: never eat sugar on an empty stomach, or eating more frequent or smaller lives can live regularly post gastric bypass (case by case scenario) Inflammatory bowel disease (IBS) Pathophysiology Test 2 3 non inflammatory condition that affects 15% of humans manifestations: abnormal contractions of the large intestinal wall (pinching), changes in bowel habits, typical pain or discomfort in the left quadrant of the abdomen male → diarrhea females → constipation pain for discomfort that is relieved after a bowel movement rules out signs of rectal cancer predisposing factors stress interference with brain to gut axis (Vagus, the controller of peristaltic movement) Stress is a sympathetic response / vagus is a parasympathetic response, meaning they antagonize eachother gut microbiome imbalances broad spectrum antibiotic use food allergies that may cause spastic contractions (IBS) 5-HT imbalance (serotonin) which is a very good promoter for the movement of the bowels kiwi is good to boost serotonin “butterflies in your stomach” is serotonin moving through the gut splenic flexure syndrome: intestine kinks downward when trying to empty the bowel, leading to trapping of material leading to discomfort intestinal obstructions Pathophysiology Test 2 4 inguinal hernia - a twist, more common in males due to heavy lifting volvulus - any twist leading to ischemia or necrosis due to lack of perforation. When tissue dies, cells containing naturally evolving bacteria can explore past the gut, leading to sepsis Inflammatory Bowel Disease (IBD) patho → autoimmune response in the white blood cells from the gut triggered by bacterium in the gut, whether bacteria is present or absent B cell focused (no prevalence between male or females) Crohn's Disease colposcopy will reveal patches of inflammation in GI tract anywhere from mouth to anus. fissures (very deep cracks/lesions) causing porridge looking stool → malabsorption affecting the small intestine, specifically the jejunum complications dependent on form: fissures may cause a fistula combining the small & large intestine (breaking down the wall that separates the two) Ulcerative Colitis inflamed continuous lesions (ulceration of innermost lining only) ulcerating through blood vessels leading to bloody stool from lower GI bleed (blood will be bright red - not digested) leading to anemia from loss of iron complications such as toxic megacolon: fesces filling the large intestine requiring surgical removal. The intestine will be distended or inflamed until potential eruption which can obviously lead to sepsis → rectovaginal fistula (rectum & vagina) = fecal matter coming through the vagina → enterovesicle fistula (between bladder & intestine resulting in fecal matter & potential blockage Pathophysiology Test 2 5 Celiac Disease autoimmune condition with sensitivity to wheat, rye, barley (gluten = protein) → when we eat gluten, it is broken down into gliadin, then bind to tissue transglutaminase creating antibodies in case of celiac Pathophysiology Test 2 6 Acute Appendicitis (inflamed appendix) reservoir of bacteria in case stomach runs out, becomes inflamed if circulation is prohibited through obstruction, most often by fecaliths (hard fecal matter) → if the fecalith cuts the appedix it can result in appendicitis infections: gastro patients can get thus depending on infection mechanism neoplasm: new growth pinching the neck of the tumour ozempic use manifestations: pain in RLQ & belly button, firm upon palpation (eventual distention 1. CHOLELITHIASIS Risk Factors and Pathogenesis (p.359) Cholelithiasis is more common in fair-skinned females and Indigenous populations. List some other risk factors of gallstones. (see paragraph 1) birth control (estrogen & progesterone) estrogen slows down the process of your gallbladder - meaning bile just sits there causing stone formation Biliary sludge often precedes cholelithiasis: what is biliary sludge a result of? → calcium birubinate & cholesterol micro crystals & mucin (glucose proteins) is usually a result of overproduction of cholesterol delayed gallbladder emptying (cholesterol buildup) Contrast the impact of small vs larger calculi → larger: Define: cholecystitis. → infection of the biliary system Manifestations (p.360) List the three types of cholelithiasis Which type is most common? Which type has a strong association with female hormones? Which type is associated with conditions that cause hemolysis? Pathophysiology Test 2 7 Define: biliary colic Locate the abdominal pain caused by cholelithiasis, and where it can radiate. Treatment strategies (p.360-361) Describe the goal of using an NG tube with intermittent suctioning. Describe: lithotripsy Describe: cholecystectomy CHOLESTASIS gall stones in the gall bladder - if stones are loosened they may get stuck in the cystic duct, causing obstruction it may also be stuck in the common bile duct - bile will never be able to make it to the duodenum, backing up into the liver causing lots of problems clay coloured stool because of blockage preventing proper excretion 2. ACUTE PANCREATITIS Pathophysiology Test 2 8 traps digestive enzymes, then we can't absorb proper nutrients so the digestive enzymes will start digesting the pancreas resulting in inflammation then necrosis pancreas becomes irritated from some source (or eat Pathophysiology Test 2 9 #1 trigger for AP is gall stones #2 is alcohol use high triglycerides other: mumps virus, some medications (Ozempic, thiazide diuretics - pancreatic sludge from water depletion) biliary sludge, pregnancy it makes digestive enzymes, so too much fat or oil will irritate the pancreas post-ERCP WHEN IT BENDS (retrograde) curving in other direction to check for an obstruction or irritation CAN ALSO CAUSE PANCREATITIS from irritation of the procedure cause inflammatory response (plasma leaves vessels leading to hypovolemic shock/neurogenic shock) YOU CANNOT VASOCONSTRICT NOW DIC, ARDS septic shock peritonitis (looking for rigid board like tenderness) (rebound) within the inside of the abdominal wall BLOOD TEST lipase & amylase tests ENDOSCOPIC RETROGRADE CHOLANGIOPANCREATOGRAPHY Pathophysiology Test 2 10 3. CHRONIC PANCREATITIS if you have an inflammed pancreas over & over, it can lead to fibrosis, labs will look like low fecal elastase in stool (STOOL TEST) etiology: Pathophysiology Test 2 11 alcohol abuse, smoking, gallstones, manifestations: abdominal pain (nowhere as near as acute) with nausea / vommiting weight loss no appetite due to pain or discomfort digestive enzymes can't absorb steatorrhea (fatty stool) secondary diabetes mellitus - fibrosis of the pancreas will no longer produce insulin 4. CIRRHOSIS infections : hepatitis B, C, D most likely to cause bleeding autoimmune: AIH (autoimmune hepatitis), PBC (primary biliary cholangitis) autoimmune destruction of intrahepatic bile ducts, PSC (primary sclerosis cholangitis) no antibodies involved metabolic NAFLD (non alcoholic fatty liver disease) resistance to blood flow through a scarred liver, or liver does not work anymore hepatocytes can no longer do what they're supposed to do, because of poor blood circulation )(can lead to hepatocytic carcinoma) genetic: HH (hereditary hemochromatosis) iron overload Wilsons disease (copper overload in the liver) A1AT (alpha 1 antitrypsin deficiency) genetic condition causing liver damage Pathophysiology Test 2 12 Primary Biliary Cholangitis (PBC): Autoimmune destruction of intrahepatic bile ducts Primary Sclerosing Cholangitis (PSC): Immune-mediated damage to intra- and extrahepatic bile ducts, often linked to UC. PORTAL CIRCULATION Pathophysiology Test 2 13 how blood flow affects liver step 1: scar tissue obstructs blood flow through liver & go back up to the heart (it can't) so it'll go down (called the back up effect) causing high pressure in oral vein (portal HTN. internal hypertension) follow blue veins to see where blood will be backed up into can lead to hemorrhoids (portal hypertension) back flow of blood or blood congestion, cannot properly absorb nutrients splenomegaly due to blood backup bulging esophageal varices (bulging into the lumen of the esophagus) can lead to GI bleed through vomiting because of forceful regurgitation Pathophysiology Test 2 14

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