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NURS 5315 GI MODULE 9 EXAM 5 2026
FULL SOLUTION STUDY GUIDE GRADED A+
⩥ upper GI anatomy. Answer: mouth, esophagus, stomach, duodenum ⩥ lower GI anatomy. Answer: small intestine, large intestine, colon ⩥ GI blood flow. Answer: 25% of cardiac output arterial blood supply- celiac and mesenteric artery venous blood supply- blood flows through gut to hepatic circulation via the portal vein, liver blood flow, from liver via hepatic vein to IVC after detoxification ⩥ reticuloendothelial cells. Answer: kupffer cells=macrophages ⩥ kupffer cells. Answer: macrophages in the liver. remove toxins, bacteria and metabolic waste products ⩥ hepatic circulation. Answer: blood flows through liver sinusoids, where kupffer cells remove toxins, bacteria, and metabolic waste products
⩥ non-fat, water soluble nutrients are absorbed by. Answer: gut and enter hepatic circulation ⩥ reticuloendothelial cells and hepatocytes. Answer: absorb and store the nutrients ⩥ intermediate chemical processing of nutrients occurs. Answer: in the liver ⩥ constipation. Answer: difficult or infrequent stooling, individual definition based upon baseline stooling patterns (2-3 day-week) ⩥ primary constipation. Answer: functional: normal motility but difficulty passing stool slow-transit: slow colon transit and accumulation of stool in sigmoid colon pelvic floor dysfunction: failure of pelvic floor or anal sphincter muscle relaxation ⩥ secondary constipation. Answer: opioid-induced, SCI, stroke, Parkinson's, Hirschsprung disease ⩥ constipation manifestations last 3+ months. Answer: straining with stooling, lumpy or hard stools, sensation of incomplete emptying, and/or
⩥ Upper GI bleeding. Answer: esophageal or gastric varicies, mallory- white tear, cancer, peptic ulcers, medications ⩥ lower GI bleeds. Answer: polyps, IBD, diverticular disease, cancer, hemorrhoids ⩥ GI bleed manifestations. Answer: - Hematemesis: bright red or coffee ground appearance
- Melena: black tarry stool
- Hematochezia: fresh, bright red blood via rectum
- Occult blood in stool: unable to be seen with the eye ⩥ peptic ulcer. Answer: break in lining of esophagus, stomach or duodenum ⩥ risks for peptic ulcers. Answer: H pylori, ASA and NSAID use, alcohol, smoking, pancreatitis, COPD, obesity, 65+, SES ⩥ gastric ulcers. Answer: 50-70 y/o. no family hx stress increases risk increases risk for cancer less h.pylori (60-80), increased gastrin, associated with gastritis pain: intermittent, with food, relieved with antacids
⩥ duodenal ulcers. Answer: 20-50 y.o., family history ulcerogenic drug use increase risk h. pylori (95-100%), increased parietal cell mass and acid production, not associated with gastritis pain: intermittent, nocturnal, remission and exacerbation of pain ⩥ IBD. Answer: relapsing, chronic disease prevalent in white and ashkenazi jews causes- genes, environment, alteration in epithelia cells, altered immune response to intestinal microflora (T cell mediated) increases risk for developing colon cancers ⩥ inflammatory bowel disease. Answer: chrons and UC ⩥ ulcerative colotis. Answer: 10-40 y.o., no family history
- continuous lesions common in colon and rectum affects the mucosal layer only sx. diarrhea with bloody stools and presence of antineutrophil cytoplasmic antibodies ⩥ chrons disease. Answer: 10-30 y.o with family history
⩥ bowel obstructions. Answer: anything that blocks normal flow or motility of intestines
- acute or chronic, partial or complete, intrinsic or extrinsic, mechanical or functional causes: herniation, constriction from adhesion, volvulus, intussusception ⩥ small intestine bowel obstruction. Answer: leads to distension and decreased absorption with increased fluid accumulation proximal to obstriction. emesis, dehydration and electrolyte abnormalities. presents as colicky pain associated with peristaltic waves. once ischemia occurs, pain more constant and severe ⩥ large intestine bowel obstruction. Answer: less common, often related to cancer. presents with hypogastric pain and distension, bowel sounds are usually present. vomiting is a late sign. ⩥ perforation. Answer: results from distension and abdominal wall tension that decreases arterial blood flow --> ischemia ⩥ appendicitis. Answer: inflammation of the appendix (projection at apex of cecum)
- most common abdominal surgical emergency, typical in adolescence but can occur at any age
manifestations: epigastric or periumbilical pain, increases in intensity over time. may subside and then RLQ pain with rebound tenderness. N/V/fever. tx. surgical vs non-surgical and antibiotics ⩥ cholelithiasis (gall stones). Answer: cause obstruction and inflammation of the gallbladder. if obstruction in cystic duct=cholecystitis. risks: female, obesity, age (40), oral contraception, white. ⩥ gall stones patho. Answer: stones result from impaired metabolism of cholesterol, unconjugated bilirubin, fatty acids, calcium carbonates and phosphates. hepatocytes secrete bile that is supersaturated in cholesterol ⩥ manifestations of gall stones. Answer: asymptomatic until blocking duct. epigastric pain (30 min-hours after eating), intolerance of fatty foods. vague: heartburn, epigastric discomfort, jaundice. obstruction: jaundice, fever ⩥ pancreatitis. Answer: inflammation of pancreas that is acute or chronic, mild--> severe risks: obstructive billary disease, alcoholism, hyperlipidemia, genetics
⩥ anorexia of aging patho. Answer: decreased energy needs, waning hunger, decreased smell and taste, poor production of saliva, altered satiety control (high levels of ghrelin) decreased food intake--> malnutrition, fragility, mitochondrial dysfunction, increased oxidative stress, hormone imbalance ⩥ acute liver injury. Answer: severe acute hepatocyte necrosis without hepatic encephalopathy without previous liver disease or cirrhosis ⩥ acute liver failure. Answer: acute liver injury+coagulopathy and hepatic encephalopathy
- INR > 2.0, ALT >10x normal, bilirubin > 3.
- elevated ammonia, tylenol level, renal failure ⩥ common causes of acute liver failure. Answer: tylenol overdose, acute or chronic liver failure (hep B and C, metabolic liver disease). manifestations: anorexia, vomiting, abdominal pain, progressive jaundice--> ascites and GI bleeding ⩥ chronic liver failure (cirrhosis). Answer: irreversible inflammatory, fibrotic disease
- kupffer cells activate--> release inflammatory mediators--> ROS--> activate fibrotic hepatic stellate cells.
- fibrosis results in obstruction of biliary channels and blood flow. develops over years. severity and progressiveness depend on the underlying cause. etiology- viral, autoimmune, genetic, alcohol, nonalcoholic fatty liver disease ⩥ liver failure manifestations. Answer: jaundice portal hypertension ascites hepatic encephalopathy ⩥ jaundice. Answer: yellow/green pigmentation cauesd by hyperbilirubinemia ⩥ causes of jaundice. Answer: - extrahepatic obstruction of bile (gall stones)
- intrahepatic obstruction (liver disease-bile canaliculi)
- prehepatic excessive production (RBC hemolysis) ⩥ manifestations of jaundice. Answer: result of excessive bilirubin in systemic circulation
- conjugated bilirubin is water soluble and excreted in urine
- stools light in color due to lack of bile pigment
- extrahepatic- increased risk for bacterial translocation and sepsis
- skin discoloration, sclera first--> skin xanthoma and pruritus
⩥ hepatic encephalopathy. Answer: impaired behavior, cognition, or motor function associated with advanced liver disease
- results from alteration in neurotransmitters and increased neurotoxins in circulation
- ammonia is typically worst offending agent due to mechanism of cerebral metabolism-results in cytotoxic edema, changes to BBB, increased GABA- reduced LOC ⩥ manifestations of hepatic encephalopathy. Answer: change in LOC, hand tremor (asterisks), slow speech, bradykinesia, stupor, seizure, coma ⩥ alcohol liver disease. Answer: related to amount and duration of alcohol ingested and acetaldehyde
- spectrum steatosis--> alcoholic hepatitis--> alcoholic cirrhosis
- malnutrition from alcohol abuse increases severity risk ⩥ patho of alcoholic liver disease. Answer: increased fat deposition in hepatocytes--> oxidative stress with lipid peroxidation and permanent hepatocyte injury. alcoholic cirrhosis: acetaldehyde inhibits liver metabolism+autoantibodies to hepatic cells+ increased bacterial translocation--> infalmmation and cellular injury ⩥ hepatitis A. Answer: fecal/oral 4 - 6 wk. incubation
Anti-HAV IgM antibodies develop within 4 weeks--> IgG antibodies elevated for years - least severe, chronic form ⩥ hepatitis C. Answer: serum+sexual transmission 6 - 8 week incubation
- HCV PCR positive for active infection
- Anti-HCV IgG elevated for chronic infection
- high rates of undiagnosed infection, leads to cirrhosis ⩥ hepatitis B. Answer: serum+sexual transmission 6 - 8 week incubation vaccine preventable ⩥ hepatitis presents with. Answer: elevated ALT and AST ⩥ neonatal jaundice. Answer: transient and begin in first week of life
- determined based upon serum level per hours of age ⩥ risks for neonatal jaundice. Answer: ABO and Rh incompatability , prematurity, breastfeeding, maternal age, male, delayed meconium passage, birth trauma
