GI, Hepatobiliary & Pancreatic Disorders Flashcards
Anorexia
Loss of appetite. Appetite is regulated by the hypothalamus, can be triggered by sense of smell, emotional factors, and certain drugs.
Nausea
Unpleasant subjective sensation that stimulates vomiting center in brainstem. Common causes of nausea include motion sickness, food poisoning, hypoglycemia, and duodenum dissension. The ANS triggers watery salivation, pallor (vasoconstriction), sweating, tachycardia.
Vomiting
Physiologic protective mechanism that limits damage from ingested noxious agents. Deep breaths are important because vomiting ceases respiration from airway closure. Abdominal muscles and diaphragm contract while the gastroesophageal sphincter relaxes.
Accompanied by dizziness, hypotension, and bradycardia. Aspiration pneumonia and metabolic alkalosis are risk factors.
Retching
Without vomitus; involves rhythmic spasmodic movements of the diaphragm, chest wall, and abdominal muscles.
Non-inflammatory acute diarrhea
Self limited course is less/equal to 2 weeks.
Large volume of watery & non-bloody stools. Affects small bowel; disrupts absorption and secretory process. Causes bloating, N/V. Caused by E. coli, C. difficile, S. aureus, Vibrio cholera, and Giardia.
Inflammatory acute diarrhea
Self limited course is less/equal to 2 weeks.
Small volume bloody stool with fever (dysentery), affects colon. LLQ abdominal pain and urgent desire to defecate. Cell invasion pathogens (Salmonella, shigella, yersinia, campylobacter, C. difficile, E. coli).
Chronic diarrhea
Associated with IBS. Symptoms persist over 3-4 weeks for adults or over 4 weeks for infants.
Osmotic diarrhea: Water is pulled into bowel lumen (hyperosmotic); people with lactase deficiency, magnesium ingestion.
Secretory diarrhea: Increased secretory process, occurs in small intestine from overgrowth of pathogens.
Factitious diarrhea: Overuse of laxatives, overconsumption of laxative type foods.
Chronic parasitic infection: Protozoans and immunocompromised patients.
Inflammatory diarrhea
Associated with acute or chronic inflammation. Intrinsic disease of the colon; UC or CD. Frequent and urgency to defecate, colicky abdominal pain and soiled clothes, tenesmus (sensation of inadequate bowel evacuation), painful straining of stool passage.
Constipation
Infrequent of difficult passage of stools. Etiology includes inadequate fiber and fluid intake, bed rest, pregnancy, hemorrhoids, or weak abdominal muscles.
Associated with bowel obstruction (mechanical or paralytic), spinal cord injury, Parkinson’s disease, multiple sclerosis, and hypothyroidism (decreased metabolism).
Clinical manifestations of constipation
Bloating, abdominal pain, normal transit constipation is the perceived difficulty in defecation (usually in response to increased fluid and fiber), slow transit constipation involves infrequent bowel movements; innervation alteration (Hirschsprung disease), defecation disorder involves the dysfunction of the pelvic floor and/or anal sphincter.
Constipation diagnosis, plan, interventions
Diagnosis: Med Hx & assessment, digital rectal examination, change in bowel habits (high index of suspicion for colon cancer).
Plan: Healthy lifestyle (increased fluid, fiber, exercise, and smoking cessation), medication reconciliation (narcotics, anticholinergics, calcium channel blockers, diuretics, antacids, and iron supplements).
Interventions: Remove fecal impaction, client education (respond to defecate urge, set aside time after meals to defecate, increase fiber and fluids, moderate exercise, judicious use of laxatives and enemas, 4Ps.
What are the 4 Ps used for hourly rounding?
Potty (offering toileting)
Positioning of client (utilize bed & chair)
Pain management (assess for pain frequently)
Periphery/placement (personal belonging are readily accessible)
Hiatal hernia
Etiology: Stomach protrusion or herniation through the diaphragm
Risk factors: Smoking, obesity, age
Clinical manifestations: Asymptomatic, abdominal pain, esophagitis, GER, difficulty swallowing, sudden/severe chest pain that radiates and is not relieved by antacid, hematemesis, dark stools
Diagnosis: Med Hx & assessment (bowel sounds in thorax), radiography of bowel above diaphragm
Plan: Monitor client
Interventions: Pain management, surgical repair
Evaluation: Herniation resolved
Sliding hiatal hernia (axial)
Bell shaped protrusion of stomach above diaphragm, common and insignificant for asymptomatic clients. Combined with GERDS; impedes esophageal acid clearance; esophagitis.
Paraesophageal hiatal hernia
Stomach portion of fundus enters thorax and protrudes into thorax and progressively enlarges. Requires surgical repair.
GERD
Etiology: Gastric mucosal damage; reflux of gastric contents into esophagus. Associated with post/meal complications; weak/incompetent esophageal sphincter
CM: Heartburn 30-60 minutes after eating, epigastria pain confused with angina and may radiate to retrosternal and throat or shoulder and back. Hoarseness, wheezing, cough.
Diagnosis: Med Hx & assessment, endoscopy to visualize or biopsy or stomach/esophagus.
Plan: Correct underlying causes
Interventions: Smoking cessation, medications (PPIs), eat meals in sitting position, avoid certain foods (alcohol, chocolate, fatty foods, coffee), surgical treatment
Evaluate: Pain free
Peptic ulcer disease
Etiology: Ulcer may affect stomach and/or duodenum, or may penetrate mucosal surface (perforation). Spontaneous remission and exacerbation, lesions replaced with scar tissue.
Risk factors: H. pylori, aspirin and NSAIDS, O blood type, jalapeños.
CM: Dizziness, thirst, hypotension, epigastrium rhythmic pain (burning) occurs on empty stomach in intervals of weeks or months. Hematemesis (coffee grounds), melena (occult blood in stool).
Diagnosis: Med Hx & assessment, positive H. pylori, biopsy, positive stool occult blood test.
Plan: Correct underlying causes
Interventions: Smoking cessation, eradicate H. pylori, H2 antagonist, PPI, avoid aspirin and NSAIDS.
Evaluate: No pain or H. pylori
Diverticular disease
Etiology: Hollowed out pouch (haustra) within intestinal lumen; distal descending sigmoid colon. Most people remain asymptomatic.
CM: Abdominal pain in LLQ, N/V, fever, increased WBC
Diagnosis: Med Hx & assessment, radiography to confirm, colonoscopy
Plan: Screen for colorectal cancer
Interventions: Increased fiber and fluid, bowel retraining, antibiotics, bowel resection surgery
Evaluation: Daily bowel movements
Appendicitis
Etiology: Intraluminal obstruction, fecalith common in 20-30 age group.
CM: N/V, fever, initially vague abdominal pain, abrupt pain onset in epigastric/periumbilical region; appendix stretches during inflammation. Rebound abdominal tenderness in RLQ, fingertip size area.
Diagnosis: Med Hx & tenderness, rebound tenderness, radiography to confirm, increased WBC,
Plan: Prepare client for laparoscopic surgery
Interventions: Antibiotics (more common now) surgery (increased risk of bowel adhesions)
Evaluation: Pain free
Colorectal cancer
Etiology: Unknown. Most cases occur in 40 y/o adults; family Hx of cancer, CD, UC.
CM: Rectal bleeding is early sign, change in bowel habits, painful defecation is late sign
Diagnosis: Med Hx & assessment (digital fecal), fecal occult blood test, radiography (barium enema/CT), colonoscopy.
Plan: Screen starting at 50 y/o. Colonoscopy every 10 years with annual occult stool test.
Interventions: Aspirin and NSAIDS protect against colorectal cancer, surgical removal, adjuvant chemotherapy, palliative chemotherapy and radiation.
Evaluation: Cancer free and palliative care
What do UC and CD have in common? (4)
Both diseases produce inflammation of bowel
Lack of confirming evidence of a proven causative agent
Have patterns of familial occurrence
Accompanied by systemic manifestation
Crohn’s disease
Etiology: Unknown; affects esophagus to anus; transmural. Slow progressive, women being affected more often than men; genetic proponent.
CM: Remission & exacerbation. Fever, slightly bloody diarrhea, abdominal pain, weight loss, fecal urgency.
Diagnosis: Sigmoidoscopy. stool cultures, radiography (contrast studies show fistulas, CT shows inflammatory mass)
Plan: No cure, decrease inflammatory response
Interventions: Smoking cessation, pain control, avoid fatty diet, total parenteral nutrition
Evaluate: Weight gain
Ulcerative colitis
Etiology: Confined to colon and rectum, affects mucosa, begins in rectum and spreads; proximal affecting. Smoking decreases incidence of ulcerative colitis but increases risk for colon cancer.
CM: Fever, tachycardia, diarrhea w/ Frank blood, abdominal pain, hypovolemia, fecal incontinence
Diagnosis: Occult stool blood test, sigmoidoscopy, colonoscopy, stool cultures for parasites, radiography.
Plan: Cancer screening (increased risk for colon cancer)
Interventions: Smoking is good (decreases incidence of UC), blood transfusion, surgery, avoid caffeine, dairy, and spicy foods. Increase fiber in diet.
Evaluation: Pain free
Comparison of Crohn’s disease and ulcerative colitis
Inflammation type:
CD; Granulomatous (aggregation of macrophages)
UC; Ulcerative and exudative
Involvement level:
CD; Primarily submucosal
UC; Primarily mucosal
Involvement extent:
CD; Skip lesions
UC; Continuous
Involvement areas:
CD; Primarily ileum, secondarily colon.
UC; Primarily rectum & left descending colon
Diarrhea: Common in both
Rectal bleeding:
CD; Rare
UC; Common
Fistulas, strictures, perianal abscesses:
CD; Common
UC; Rare
Development of cancer:
CD; Uncommon
UC; Relatively common
Acute pancreatitis
Etiology: Auto-digestion of pancreatic tissue by inappropriate active pancreatic enzyme; systemic inflammatory response syndrome. ETOH abuse/viral infection. Gallstones account for 70-80% of all cases.
CM: Fever, abdominal pain in epigastric/periumbilical area, Cullen sign, Grey Turner sign, abdominal dissension, dyspnea, tachycardia, hypotension
Diagnosis (2/3): Abdominal pain, increased amylase or lipase, CT for fluid accumulation, increased hematocrit level, C+ reactive protein
Plan: Pain control
Interventions: Withhold oral food and fluid to decrease pancreatic enzyme secretions, NGT to LIS, IV fluids and electrolytes, restore lost plasma volume, meperidine for pain relief (decreases pancreatic duct sphincter spasms), or morphine (increases spasms).
Evaluate: Amylase and lipase within normal ranges
Chronic pancreatitis
Risk factors: Diabetes mellitus, malabsorption syndrome
Etiology: Most common with ETOH abuse, less common with pancreatic duct obstruction
CM: Persistent recurring epigastric pain, N/V, constipation, flatulence, weight loss, fatty stools
Diagnosis: Abdominal pain, increased amylase, lipase, WBC, serum bilirubin, hematocrit, +C reactive protein, ultrasound for presence of gallstones, CT for necrotic tissue and abdominal fluid
Plan: Chronic pain management
Interventions: Diabetes mellitus, pain management, low fat diet, NO ETOH
Evaluation: Patient/family teaching, irreversible, opioid addiction
Cholelithiasis (gallstones)
Etiology: 3 contributing factors; abnormal composition of bile, stasis of bile, inflammation of gallbladder. Precipitation of substances contained in bile (80% cholesterol, 20% composed of mucin glycoproteins and calcium.
Cholecystitis
Etiology: Inflammation of the gallbladder secondary to gallstone obstruction
CM: Asymptomatic, acute onset abdominal pain; URQ or epigastric pain, chronic irritation by gallstones always present, fever, N/V, impaired fat digestion, steatorrhea (fatty stool).
Diagnosis: Increased WBC, liver function test showing increased AST and ALT, increased bilirubin, radiography (ultrasound, cholecintography)
Plan: Client education, removal of gallbladder does not interfere with digestion
Interventions: Laparoscopic cholecystectomy
Evaluation: Pain relief
What do the liver and bilirubin maintain?
Blood glucose, lipid metabolism, protein synthesis, conversion of ammonia to urea, fat soluble vitamins are stored or converted in the liver.
What are the clotting factors of the liver?
Clotting factors II, VII, IX, and X
Unconjugated bilirubin (fat soluble)
Insoluble in plasma and transported (attached to albumin). Passes through liver and absorbed through hepatocytes cell membrane. Released from albumin carrier molecule.
Conjugated bilirubin (water soluble)
Combines with glucuronic acid to create water soluble bilirubin. Secreted as bile into the small intestine. Gives yellow color to feces and urine.
Altered liver function
Etiology: 80-90% hepatic function, fulminant hepatitis, chronic ETOH abuse
CM: Mental status changes (increased ammonia), fector hepaticas (sweet breath from bacteria), asterixis (flapping tremor), telangiectasis, spider angiomas, palmar erythema, clubbing of fingers, jaundice, hepatorenal syndrome
Diagnosis: Med Hx & assessment, liver function test/liver panel showing increased AST & ALT, bilirubin, albumin
Plan: Management of symptoms, infection control, diet with sufficient calories, adequate fluid intake
Interventions: Liver transplant, lactulose to treat hepatic encephalopathy, antibiotics
Evaluation: Infection free, palliative care
Pre-hepatic jaundice
Hemolysis occurs when RBCs are destroyed at a rate in excess of liver’s ability to remove bilirubin for blood. May follow hemolytic blood transfusion reaction or genetic disorder (increased unconjugated bilirubin). Stool are normal color, urine is amber colored.
Intra-hepatic (hepatocellular) jaundice
Caused by hepatitis and cirrhosis, a disorder that directly affects the liver’s ability to remove bilirubin from blood and eliminate conjugated bilirubin in bile (leads to increases ALP, and unconjugated bilirubin), dark urine.
Post-hepatic (obstructive) jaundice
Obstruction/stricture of bile duct between liver and intestines; gallstones, tumors, bile duct occlusion, pancreas. Increases conjugated bilirubin, clay-colored stools from lack of bilirubin in bile, dark urine from increased blood levels of bile acids, pruritus.
Jaundice (Icterus)
High levels (> 2 or 2.5 mg/dL) of bilirubin in the blood (normal range is 0.1-1.2 mg/dL). Yellow discoloration of skin, deep tissue, and sclera.
Causes: Excessive destruction of RBCs, impaired uptake of bilirubin by liver cells (decreases conjugation of bilirubin), obstruction of bile flow, medications that promote jaundice, anesthetic agent halothane, oral contraceptives
A prudent nurse knows that UC involves the following gastrointestinal mucosa?
Rectum, proximal colon
Diet high in broccoli and legumes contributes to which type of diarrhea?
Factitious
What is the best explanation on how esophageal balloon works to stop the bleed?
It is used to tamponade esophageal bleeding
As a nurse, you understand that water soluble bilirubin excreted by kidneys is known as
Conjugated bilirubin
Which hepatitis viruses are concerns for deployed military personnel traveling outside the U.S?
HEV & HAV are contracted by fecal to oral route
Which of the following is the highest composition of gallstones?
Cholelithiasis is mainly composed of cholesterol
Which pancreatic hormone stimulates hunger?
Gherkin is a pancreatic hormone that stimulates hunger
Which bacteria is associated with gastric mucosa injury?
H. pylori is associated with GI mucosal injury
Hepatitis (HAV)
Etiology: Occurs worldwide because of poor sanitation condition. Incubation period is 25-30 days
CM: Fever, nausea, abdominal pain, dark urine, jaundice
Diagnosis: Serum test positive for HAV antibodies (IgM is acute HAV and IgG appears one month after illness)
Plan: Avoid fecal to oral contamination
Interventions: HAV vaccine, hand hygiene
Evaluation: Asymptomatic
Hepatitis (HBV)
Etiology: Virus transmission inoculation of infected blood, oral or genital, unprotected sex, IV drug use
CM: (Abrupt on-set) fever, nausea, abdominal pain, dark urine, jaundice
Diagnosis: Serological markers (HBcAg, HBeAg, HbsAg)
Plan: Follow CDC guidelines
Interventions: Vaccine, universal precautions, safe sex, screen blood
Evaluation: Asymptomatic, vaccinations up-to-date, most common causes are chronic hepatitis, cirrhosis, and hepatic cancer.
Hepatitis (HCV)
Etiology: Flaviviridae family single-stranded RNA virus. Most common cause is chronic hepatitis, cirrhosis, hepatocellular cancer. Incubation period is 2-26 weeks.
CM: Fever, nausea, abdominal pain, dark urine, jaundice is uncommon
Diagnosis: Antibody and viral tests. HCV antibodies are not protective (disease markers)
Plan: Follow CDC guidelines, no vaccine
Interventions: Treat underlying causes, screen blood, drug abuse counseling
Evaluation: Asymptomatic, blood screen
Hepatitis (HDV)
Defective enveloped single strand RNA virus requires concomitant infection with HBV for replication. Increased risk with IV drug use. There is no vaccine but you can vaccinate for HBV.
Hepatitis (HEV)
Fecal-oral transmission route. High mortality rate among pregnant women living in developing countries. There is no vaccine.
HDV & HEV
CM: Fever, nausea, abdominal pain, dark urine, jaundice
Diagnosis: HBsAg for HDV, virus test for HDV and HEV
Plan: Follow CDC guidelines
Interventions: Follow CDC prevention guidelines for HEB. Food and water sanitation for HEV
Evaluation: Asymptomatic
Cirrhosis
End stage of chronic liver disease. Diffuse fibrosis and conversion of normal liver architecture into nodules containing proliferating hepatocytes encircled by fibrosis.
CM: Jaundice, spider angiomas, palmar erythema, ascites, hematemesis, weight loss, abdominal pain, diarrhea, hemorrhoids, testicular atrophy
Diagnosis: Hx/assessment, radiography (for splenomegaly of portal hypertension), serum laboratory test showing increased AST & ALT, albumin <3.4 g/dL, thrombocytopenia, decreased clotting factors
Plan: Hemorrhage control
Interventions: Stop the bleed, palliative care, liver transplant
Evaluation: Adequate pain control, organ transplant eligibility
What conditions are associated with cirrhosis?
Alcoholism, viral hepatitis, biliary disease, hemochromatosis (iron deposits), Wilson disease (copper deposits)
Portal hypertension
Etiology: Increased resistance and pressure in portal venous system
CM: Mental status changes (hepatic encephalopathy), abdominal pain, esophageal bleeding (varices)
Diagnosis: Radiography, endoscopy, serial CBCs
Plan: Monitor for bleeding, decrease portal venous pressure
Interventions: Esophageal balloon (tamponade), lactulose (removes ammonia from blood)
Evaluation: No bleeding, platelets within normal ranges
What are the different types of portal hypertension?
Pre-hepatic: Obstruction thrombosis, narrowing of portal vein, massive splenomegaly
Post-hepatic: Right sided heart failure, hepatic vein outflow obstruction
Intrahepatic obstruction: Portal hypertension from cirrhosis, increased resistance to blood flow
Esophageal Varices
Etiology: Gradual obstruction of venous blood flow in liver; increased portal vein pressure, large collateral channels develop between portal and systemic veins; subject to rupture and hemorrhage (lower rectum, esophagus, umbilical vein)
CM: Hx/assessment of portal venous pressure, anemia, esophageal bleeding, cyanosis
Diagnosis: Medical hx/assessment, radiography for increased portal venous pressure, endoscopy for esophageal varies, decreased serum platelets and WBCs.
Plan: Prevention of initial hemorrhage
Interventions: Lower portal venous pressure (beta-adrenergic blockers; propranolol, nadolol), esophageal balloon tamponade
Evaluation: No bleeding, hemoglobin and hematocrit within normal range
Ascites
Etiology: Unknown; increased amount of fluid in peritoneal cavity, late-stage manifestation of cirrhosis and portal hypertension
CM: Enlarged abdomen (interferes with breathing), daily girth measurements (>=500 ml of fluid accumulated in peritoneal cavity)
Diagnosis: Med Hx & assessment (focused abdominal), paracentesis (fluid serous <=3 grams of protein, decreased colloidal osmotic pressure due to impaired synthesis of albumin (protein) by liver)
Plan: Infection control
Interventions: Albumin, dietary and water restriction, distal nephron and loop diuretics, oral potassium, paracentesis (remove up to 5mL of ascites fluid at the risk of hypovolemic shock and infection), antibiotics
Evaluation: Decreased abdominal girth
Splenomegaly
Eiotlogy: Portal hypertension shunts blood into splenic vein, decreased lifespan and number of formed blood elements.
CM: Enlarged spleen, abdominal pain in LUQ, esophageal varices, hypotension, hemorrhoids
Diagnosis: Med Hx & assessment (focused abdominal), CT scan
Plan: Monitor for bleeding
Interventions: Stop the bleed (esophageal balloon tamponade), decreased portal hypertension, B-adrenergic blocker, surgery for portosystemic shunt
Evaluation: No bleeding and platelets within normal range
