Advanced Pathology NR 507- final exam Questions & Answers

Angle of His - ANSWERSCreates a flap valve effect to prevent reflux and makes gastro esophageal junction longer which increases the pressure GERD (gastroesophageal reflux disease) - ANSWERSA digestive disease in which stomach acid or bile irritates the food pipe lining. Obesity makes the angle of His a widened angle which decreases the pressure at the gastro esophageal junction big fatty meals and carbonation stretches the stomach out which thins out the muscles around the stomach which decreases the pressure on the flap valve Hypotonic lower esophageal sphincter also allows reflux, as well as hiatal hernia, gastroparesis, and obesity heartburn and regurgitation are typical symptoms chest pain, hoarseness, cough, asthma, and globus (lump in throat) are atypical for classic GERD Associated symptoms are dyspepsia, epigastric pain, bloating, belching, and nausea H.Pylori bacteria is associated with GERD Barrett's esophagus - ANSWERScaused by exposure to enzymes coming from the stomach - stomach acid does not cause this - so can have non-acid reflux Barrett's esophagus diaphram - ANSWERSa muscle that separates the chest from the abdominal cavity also makes up the lower esophageal sphincter The top 1/3 of the esophagus is ______________ muscle. - ANSWERSskeletal muscle the middle of the esophagus muscle is made up of...muscle - ANSWERSskeletal and smooth muscle the bottom 1/3 of the esophagus is made up of....muscle - ANSWERSsmooth muscle simple obstruction of the GI tract - ANSWERSresult from the blockage of the intestine. Causes of simple obstructions include adhesions, hernias, tumors, or even ingestion of inorganic objects that become lodged within the intestine. intussusception, or the telescoping of the intestinal wall onto itself, is more common in children less than 2 years of age, surgical adhesions are more common in adults. Ingestion of objects that result in simple obstructions are more common during the toddler years. Functional obstructions occur because of a lack of gut motility, such as during a paralytic ileus peptic ulcer disease - ANSWERSulcer formation in the GI tract that affects the lining of the stomach (gastric ulcer) or duodenum (duodenal ulcer) or lower part of the esophagus (esophageal ulcer) form due to gastric acid and pepsin and the breakdown of the stomach lining Risk factors for developing PUD include: NSAID use. Age greater than 65 years. Genetic predisposition. Alcohol ingestion. the role of the stomach - ANSWERSto liquify food by churning it and using enzymes and acid to assist in the breakdown pylorus - ANSWERSa muscle like structure that squeezes food down into the duodenum can become scarred and lead to obstruction with gastric ulcers the mucosa layer of the stomach lining - ANSWERSsecrets mucosa rich in bicarbonate - it protects the lining of the stomach from acid has gastric pits that contain parietal cells, chief cells, and G-cells parietal cells - ANSWERSsecrete HCl (hydrochloric acid) and intrinsic factor chief cells - ANSWERSsecrete pepsinogen, which is converted to pepsin via the action of hydrochloric acid G-cells - ANSWERSreleases gastrin submucosa - ANSWERSon top of mucosa contains connective tissue, nerves, and vessels Muscularis Externa - ANSWERSon top of the submucosa three smooth muscle layers: aid in peristalysis serosa - ANSWERSon top of muscularis externa outer layer of connective tissue that connects to organs Good and Bad key players in peptic ulcer disease - ANSWERSGood: "defense system" bicarb = coats and protects cells prostaglandins = regulates perfusion to stomach and mucus to release bicarb, controls acid amount secreted by parietal cells Bad: "toxic system" ulcer (H. Pylori, NSAIDs, etc) = acid penetrates mucosa = histamine released = parietal cells release even more HCL acid = more stomach irritation HCL acid via parietal cells + Pepsinogen via chief cells = pepsin Heliobacter pylori - ANSWERSspiral shaped bacteria that is the cause of most gastric ulcers produces urease which breaks down urea = ammonia & carbon dioxide = neutralizes acid and breaks down mucosa spreads through oral/oral or oral/fecal NSAIDs effect on gastric system - ANSWERSdecreases production of prostaglandins = impacts the health of the stomach Zollinger-Ellison syndrome - ANSWERSGastrin-secreting tumor associated with ulcers = increased stomach acid signs and symptoms of peptic ulcer disease - ANSWERSIndigestion & epigastric pain (burning, gnawing or dull) Gastric = eating food makes it worse (1-2hrs after), pain = dull & aching, weightloss, sever: vomit = coffee grounds or frank red blood Duodenal = eating food makes it better (3-4 hours after), wake in the middle of night with pain, gnawing pain, severe: tarry dark stool diagnosing peptic ulcer disease - ANSWERSscope of the stomach upper GI series: drink barium to coat upper GI tract CT scan of abdomen with contrast H. Pylori = blood test, stool test, Urea breath test Urea breath test - ANSWERSPatient ingests Urea with radio labeled Carbon Measures exhaled radio labeled Carbon Complications of peptic ulcer disease - ANSWERSGI bleeding = erodes a hole in stomach = perforation = peritonitis bowel blockage @ pylorus from chronic ulceration increased risk for GI cancer treatments for peptic ulcer disease - ANSWERSPPIs, H2 receptor blockers, antibiotics, antacids, bismuth subsalicylates severe cases with complications: vagotomy, pyloroplasty, gastric resection vagotomy - ANSWERScutting of certain branches of the vagus nerve, to reduce the amount of HCL produced by the gut pyloroplasty - ANSWERSsurgical repair of the pylorus gastric resection - ANSWERSpartial removal and repair of the stomach -watch for dumping syndrome = cant regulate movement of food effectively = enters too fast into intestines = food acts hypertonically pulling water from blood (early) and (late) rich in carbs & sugar = pancreas releases insulin = hypoglycemia Chrones disease - ANSWERSA form of inflammatory bowel disease, symptoms include Crampy abdominal (right lower quadrant area) pain Fever Fatigue Loss of appetite Pain with passing stool (tenesmus) Persistent, watery diarrhea Unintentional weight loss - can occur throughout the digestive system - from mouth to anus. Non-continuous manner = skip lesion most often found in terminal illium, colon, and other areas of small intestine has a cobblestone appearance when visualized transmural inflammation = goes through all three layers of intestinal wall non-caseating granulomas = sign of chronic infection Fistula formation occurs when worsening inflammation results in tunneling between two structures with the lumen of one section of bowel in communication with a different section of bowel. A fistula location can be anywhere a lesion is adjacent to an area Obstruction, malabsorption of vitamins A, D, B12, can become cancerous Pharmacological management may include the use of aminosalicylic acid (5-ASA), corticosteroids, immunomodulating drugs, biologic therapies, and Janus kinase inhibitors. ulcerative colitis - ANSWERSa chronic condition of unknown cause in which repeated episodes of inflammation in the rectum and large intestine cause ulcers and irritation Bloody diarrhea is the hallmark sign of ulcerative colitis, -abdominal cramping, -fecal urgency and tenesmus (a continual or recurrent inclination to evacuate the bowels). Extra-intestinal symptoms may also be present such as arthralgias, arthritis, iritis or uveitis, aphthous skin lesions, or gallstones. continuous disease - does not skip areas along the intestinal tract. begins in rectum and travels backwards to sigmoid colon - can travel to the entire colon Smooth walls - friable appearance - looks like it will easily bleed inflammation of mucosa & submucosa layers of intestines only non-caseating granulomas = sign of chronic infection Pseudo-polyp formation occurs with worsening inflammation causing thinning of the mucosal and submucosal layers in an uneven pattern. Has the appearance of a polyp protruding out of the intestinal wall, but not an actual growth Pharmacological management may include the use of aminosalicylic acid (5-ASA), corticosteroids, immunomodulating drugs, biologic therapies, and Janus kinase inhibitors.