MU NURS 611 Adv Patho - Exam 4 Review - GI System Questions and Answers

MU NURS 611 Adv Patho - Exam 4 Review - GI System Questions and Answers obesity BMI 30 kg/m2; caloric intake caloric expenditure leading causes of death associated with obesity cardiovascular disease; type 2 DM; cancer visceral obesity aka intra-abdominal, central, or masculine obesity; distribution of body fat is localized around abdomen and upper body, resulting in apple shape Image: visceral obesity visceral obesity is associated with accelerated lipolysis; increased risk for inflammation, metabolic syndrome, type 2 DM, CV complications, and CA metabolic syndrome hypertriglyceridemia, low HDL, high LDL, HTN, insulin resistance peripheral obesity aka gluteal-femoral, feminine, SQ obesity; distribution of body fat is extraperitoneal; distributed around thighs and buttocks, through the muscle, resulting in pear shape; more common in women Image: peripheral obesity GERD reflux of acid and pepsin from the stomach to the esophagus; causes esophagitis risk factors of GERD obesity, hiatal hernia, drugs/chemicals that relax the LES; triggers asthma/chronic cough clinical manifestations of reflux esophagitis heartburn from acid regurgitation, chronic cough, asthma attacks, laryngitis; upper abdominal pain within 1 hour of eating; worsens if intra-abdominal pressure increases; may also be experienced as chest pain - r/o cardiac ischemia bowel obstruction most common occurring small intestinal obstruction - related to adhesions adhesion obstructions accounts for 50-70% of small bowel obstruction Image: adhesion obstructions clinical manifestations of SBO presents early with abdominal distention obstruction at pylorus or high in the small intestine metabolic alkalosis develops INITIALLY d/t excessive loss of H+ ions that normally would be reabsorbed from the gastric juice prolonged intestinal obstruction lack of circulation produces lactic acid (decreased tissue perfusion) thus metabolic acidosis intussusception telescoping of part of intestine into another, causing strangulation of blood supply Image: intussusception peptic ulcer disease (PUD) break/ulceration in protective mucosal lining of lower esophagus, stomach, or duodenum risk factors of PUD genetics, H pylori infection, habitual use of NSAIDs; smoking, alcohol, acute pancreatitis, COPD, obesity, cirrhosis, age 65 years, psychologic stress; exact cause unknown chronic use of NSAIDs suppresses mucosal prostaglandin synthesis = decreased bicarbonate secretion and mucin production, inc secretion of HCl pathogenesis of peptic ulcer NSAIDs + H pylori disruption of mucosa exposes submucosal areas to gastric secretions and autodigestion causing erosion and ulceration dumping syndrome occurs about 20 minutes after eating; increase pulse, hypotension, weakness, pallor, sweating, dizziness; follows partial gastroectomy/pyloroplasty Image: dumping syndrome dumping syndrome - rapid gastric emptying, creating of high osmotic gradient in small intestine causes sudden shift of fluid from vascular compartment to intestinal lumen dumping syndrome - rapid distention of intestine produces feeling of epigastric fullness, cramping, NVD dumping syndrome management diet - frequent small meals; no fluids during meals; high protein, low carbs Crohn's occurs at any age (10-30 yo); FMH more common; "skip" lesions found all over GI tract; entire intestinal wall involved; fistulae/abscesses/strictures/obstruction common; abd pain, D, small intestinal malabsorption, steatorrhea Image: Crohn's ulcerative colitis (UC) occurs at any age (10-40 yo); FMH less common; found in colon and rectum; no "skip" lesions; mucosal layer found; no fistulae/abscesses/strictures/obstructions; occasional abd pain, D, bloody stools, rare small intestinal malabsorption/steatorrhea Image: ulcerative colitis (UC) liver - main function deamination of amino acids hepatocyte dysfunction hypoalbuminemia hepatitis pathologic lesions similar to those caused by viral infection; hepatic cell necrosis, scarring, Kupffer cell hyperplasia, infiltration by mononuclear phagocytes occurs with varying severity damage tends to be most severe in cases of hepatitis B and C acute fulminating hepatitis associated with Hep B; rare form of hepatitis characterized by massive hepatic necrosis prodromal (preicteric) phase phase 1 - begins 2 weeks after exposure, ends with appearance of jaundice; fatigue, anorexia, malaise, NV, HA, hyperalgia, cough, low-grade fever icteric phase phase 2 - begins 1-2 weeks after prodromal phase, lasts 2-6 weeks; urine dark, stools clay-colored; GI and respiratory symptoms subside; abd pain and fatigue may persist or worsen; mild transient itching posticteric phase phase 3 - recovery phase; resolution of jaundice, 6-8 weeks after exposure; liver may still be enlarged and tender; symptoms are diminished; LFTs return to normal within 2-12 weeks after onset of jaundice cirrhosis irreversible inflammatory, fibrotic liver disease; 12th leading cause of death; common causes alcohol abuse, viral hepatitis patho of cirrhosis chaotic fibrosis laters/obstructs billiary channels and blood flow, producing jaundice and portal HTN; new vascular channels form shunts, blood from portal vein bypasses liver, contributing to portal HTN, metabolic alterations, toxin accumulation portal HTN esophageal varices - most common clinical manifestation Image: portal HTN congestive splenomegaly thrombocytopenia most common; can contribute to increased bleeding tendency hepatic encephalopathy combination of biochemical alterations that affect neurotransmission; liver dysfunction and collateral vessels that shunt blood around liver permit neurotoxins and other harmful substances absorbed from GI tract to accumulate and circulate freely to brain; most hazardous substances are end-products of intestinal protein digestion (ammonia) which cannot be converted to urea by diseased liver acute pancreatitis - clinical manifestations epigastric/midabdominal pain; pain radiates to back d/t retroperitoneal location of pancreas; fever, leukocytosis; hypocalcemia; hypotension, shock occur with hypovolemia and SIRS