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Pathophys U5

Pathophysiology Unit 5

Steatorrhea greasy, loose stools
Melena tarry stools caused by bleeding
Dysphagia difficulty swallowing
Antiemetic drug used to decrease nausea and vomiting
Anorexia loss of appetite
Hematemesis vomit containing blood
Impaction retention of feces
Candidiasis opportunistic oral fungal infection
Gingivitis inflammation of tissue surrounding teeth
Cholelithiasis formation of gallstones
Diverticulum outpouching of mucosa in the colon
Causes of vomiting distention/irritation of GI tract, unpleasant sights or smells, pain or stress, stimulation of vestibular apparatus in inner ear (motion sickness), increased intracranial pressure, stimulation of chemoreceptor trigger zone
Measures used to decrease vomiting treat cause (analgesics for pain, laxitives/enema); antiemetic drugs, sedatives, antacids, ventilation to remove odors
Cause of constipation inadequate dietary fiber
Cause of constipation inadequate fluid intake
Cause of constipation failure to respond to defecation reflex
Cause of constipation muscle weakness, inactivity
Cause of constipation neuro disorders like MS, spinal cord trauma
Cause of constipation drugs i.e. opiates, CNS depressants, anti-cholinergics
Cause of constipation some antacids, iron meds, and bulk laxatives w/ insufficient fluid intake
Cause of constipation obstruction caused by tumors or strictures
Ways to relieve chronic constipation increased fiber and fluid intake
Causes of dysphagia esophageal fibrosis, compression, diverticulum, congenital atresia, tracheoesophageal fistula, neuro damage to cranial nerves V, VII, IX, X, and XII, echolalia
Hiatal hernia part of stomach is elevated and protrudes through opening in diaphragm into thoracic cavity
Hiatal hernia postprandial heartburn or pyrosis, brief substernal burning sensation w/ sour taste, belching, vomiting, dysphagia
Treatment of hiatal hernia eliminating factors that reduce LES pressure like caffeine, fatty foods, alcohol, cigarette smoking, and certain drugs
GERD (gastroesophageal reflux disease) periodic flow of gastric contents into esophagus; caused by hiatal hernia as well as other conditions that lower LE pressure or increase intra-abdominal pressure
Meds that treat GERD Antacids, histamine2 (H2 receptor) antagonists, proton pump inhibitors
Acute gastritis inflammation of the gastric mucosa due to variety of causes including infection, food/drug allergy, ingestion of spicy/irritating food, excessive alcohol intake, aspirin or other acrogenic drugs, toxic substances, radiation, chemotherapy
Acute gastroenteritis inflammation of both the stomach and intestine usually caused by infection but may result from food/drug allergies
Chronic gastritis inflammation of gastric mucosa caused by peptic ulcers, alcohol abuse, aging, pernicious anemia; causes epigastric discomfort and intolerance of spicy foods
Proximal duodenum, antrum of stomach, lower esophagus locations where ulcers occur
Factors contribute to peptic ulcers decreased mucosal resistance, excessive HCl or pepsin secretion, and presence of H. pylori
Pathophysiology of peptic ulcers acid/pepsin penetrates mucosal barrier, expose tissue to continued damage b/c of acid diffusion into gastric wall; may erode more deeply into muscle layers and perforate; inflammation and bleeding surround when blood vessel involved
Complications of peptic ulcers perforation leading to chemical peritonitis and eventually bacterial peritonitis; obstruction of GI tract due to scarring and stricture formation
Symptoms/manifestations of peptic ulcers epigastric burning/pain usually 2 to 4 hours after meals and at night, heartburn, nausea, vomiting, weight loss, iron deficiency anemia or occult blood in stool
Ulcer treatments drug therapy of combo of antimicrobials and acid reducers; coating agents or antacids for symptomatic relief; reducing exacerbating factors; vagotomy, partial gasterctomy or pyloroplasty in pt with perforation/bleeding
Individuals at high risk for gallstones women with high cholesterol in bile; obesity, high cholesterol intake, multiparity; use of birth control or estrogen supplements; indivs with hemolytic anemia, alcoholic cirrhosis, or biliary tract infections
Manifestations of gallstones sudden severe waves of pain in upper right quadrant of abdomen or epigastric area, often radiating to back or right shoulder; nausea and vomiting, increasing and decreasing pain followed by jaundice
Disorders that cause jaundice prehepatic, intrahepatic, and posthepatic disorders
Prehepatic disorders cause of jaundice; results from excessive destruction of RBCs, i.e. physiologic jaundice of some newborns, hemolytic anemias, transfusion reactions
Intrahepatic disorders cause of jaundice; due to liver disease resulting in impaired uptake of bilirubin from blood and decreased bilirubin conjugation; i.e. indivs with liver disease like hep or cirrhosis
Posthepatic disorders cause of jaundice; obstruction of biliary flow due to congenital atresia of bile ducts, cholelithiasis, inflammation/tumors of liver
Causes of nonviral hepatitis infectious mononucleosis or amebiasis
Hepatitis A RNA virus; oral-fecal enteric transmit; ppl in large institutions @ risk, children w/ poor hygiene, lower income grps, travelers to developing countries, oral/anal sex; incubation 2-6 wks, mild symptoms (jaundice); duration manifest 2 months
Hepatitis B HBV double stranded DNA virus; blood/body fluid transmission; drug users, unprotected sex, hemodialysis pts, infants born to infected moms, tattooing/piercing, health profs, blood transfustion prior to 1984; 1-6 mo incubation; symps severe; lasts 4-12 wks
Hepatitis C HCV RNA virus; blood/body fluid transmit; drug users, unprotected sex, hemodialysis, infants born to pos. moms; tattooing/piercing, health prof, blood transfusion before '90; organ recipients, insemination; incubates 2 wk – 6 mo; asymptomatic; 2-12 wks
Hep B, Hep C hepatitis carrier states
Rare hep A complications?
Hep B complications chronicity, hepatocellular carcinoma, cirrhosis and liver failure, fulminant hepatitis
Hep C complications chronicity (more than 50%); hepatocellular cancer, cirrhosis and liver failure
Serological marker for Hep A anti HAV IgM indicates acute infection; anti HAV IgG indicative of past exposure
Serological marker for Hep B HbsAG indicates infection; Anti HBs indicate recovery and noninfection w/ effective protection; HbeAg
Serological marker for Hep C anti HCV shows nonprotective infection; HCV RNA shows active infection
Hep A hepatitis that has no medication treatment
Treatment for Hep B chronic cases with abnormal liver function tests can be treated w/ interferon alpha 2b, lamivudine
Treatment for Hep C with elevated ALT treated with interferon alpha 2b, ribavirin
Fecal oral route route of infection from virus contaminated stool/food/fomites to hands to mouth and fomites by poor hygiene, unsanitary toilet practices
Incomplete RNA virus that requires presence of HBV to replicate why Hep D occurs only in pt who have Hep B
Serological markers how Hep D infection can be detected if pt also has hep B
Fecal-oral route how is hep E contracted?
Stages of hepatitis preicteric stage, icteric stage, posticteric stage
Preicteric stage stage of hepatitis; fatigue and malaise, anorexia and nausea, and general muscle aching; elevated serum levels of liver enzymes (AST, ALT)
Icteric stage stage of hepatitis; jaundice; light-colored stool; dark urine and pruritic skin; tender, enlarged liver, causing mild aching pain; blood clotting times elevated in severe cases
Posticteric stage stage of hepatitis; reduction in signs, may last for several weeks; depending on specific viral etiology
Info needed from pt with hepatitis date of diagnosis, type, ever told not to give blood, carrier status, meds
Cirrhosis progressive destruction of liver tissue eventually leading to liver failure
Causes of cirrhosis alcoholic liver disease, biliary cirrhosis due to immune disorders, stones, cystic fibrosis; chronic hepatitis or long-term exposure to chemicals
Pathophysiology of cirrhosis liver fibrosis, loss of lobular organization; nodules of hepatocytes poss. present & nonworking b/c of distorted vascular and biliary network; fibrosis interferes w/ blood supply, back up bile causes inflammation/damage; liver becomes scarred and shrunken
Liver function lost/impaired with cirrhosis decreased removal and conjugation of bilirubin
Liver function lost/impaired with cirrhosis decreased bile production
Liver function lost/impaired with cirrhosis impaired digestion and absorption of nutrients, esp fat and fat soluble vitamins
Liver function lost/impaired with cirrhosis impaired glucose/glycogen metabolism
Liver function lost/impaired with cirrhosis inadequate storage of iron, vit. B12
Liver function lost/impaired with cirrhosis decreased inactivation of hormones, esp aldosterone and estrogen
Liver function lost/impaired with cirrhosis decreased removal of toxic substances from blood
Manifestations of cirrhosis Fatigue, anorexia; ascites; edema; esophageal varices, hemorrhoids; splenomegaly; anemia; Leukopenia, thrombocytopenia; increased bleeding, purpura; hepatic encephalopathy, tremors, confusion; gynecomastia, impotence, irregular menses; jaundice, pruritis
Portal hypertension blockage of blood flow through liver leading to high pressure in portal veins
Complications of portal hypertension ascites, splenomegaly, esophageal varices; impaired respiration, increased risk of peritonitis, impaired digestion and absorption
Treatments/interventions for cirrhosis supporting/symptomatic trtmt avoiding fatigue & exposure to infections; dietary restrictions on protein/sodium; high carb intake, vit supplements; diuretics; paracentisis; albumin transufions, antimicrobials, transplant
Cause of acute pancreatitis gallstones and alcohol abuse
Pathophysiology of acute pancreatitis premature activation of pancreatic enzymes w/ autodigestion of pancreatic tissue; tissue necrosis w/ severe inflammation of pancreas; enzymes leak into gen circulation and cause shock, intravascular coagulation, respiratory distress syndrome; peritonitis
Manifestations of pancreatitis severe epigastric or abdominal pain radiating to the back; increases when supine; signs of shock
treatment of pancreatitis stopping all oral intake; relieving bowel distention; treating shock and electrolyte imbalances; and prescribing analgesics but NOT morphine
celiac disease Malabsorption syndrome, primarily in childhood; genetic factors resulting in defect in intestinal enzymes need to complete digestion of gliadin, a breakdown product of gluten
pathophysiology of celiac disease combo of digestive block with immunologic response results in a toxic effect on the intestinal villi; villi atrophy resulting in decreased enzyme production and reduced surface area for absorption of nutrients, resulting in malabsorption and malnutrition
characteristics of malabsorption syndromes steatorrhea, muscle wasting, failure to gain weight, irritability, malaise
treatment of celiac disease adopting gluten free diet, avoiding grains like wheat, barley, oats
pathophysiology of appendicitis obstruction of appendiceal lumen by fecalith, gallstone, foreign material, twisting, spasm; fluid buildup, inflammation, swelling, ischemia & necrosis; bacteria & toxins cause bacterial peritonitis; rupture/perforation can release contents into peritoneum
acute appendicitis manifestations periumbilical pain, nausea/vomiting, increasing LRQ pain/tenderness with steady, severe abdomen pain; low grade fever, onset of peritonitis include rigid abdomen, tachycardia, hypotension
chronic inflammatory bowel disease crohn’s disease and ulcerative colitis of unknown etiology
crohn’s disease Ashkenazi Jews, whites @ risk; familial tendency etiology; lesions of TI; transmural skip lesions/granules; malabsorption, steatorrhea, adhesions/strictures, fistulas,fissures, loose/semiformed stool, melena, cramping, weight loss, fatigue, delayed growth
ulcerative colitis whites, Ashkenazi jews, young adults; high familial tendency; lesions in colon and rectum of mucosa with continuous ulcerations; malabsorption, toxic megacolon, obstruction, iron anemia; frequent watery stools, blood, mucus, cramping, fever, weight loss
treatment of inflammatory bowel disease identification and removal of stressors, anti-inflammatory meds, antimotility agents, nutritional substances, antimicrobials, immunotherapeutic agents, and surgical resection of affected areas
diverticulitis inflammation of diverticula
warning signs of colorectal cancer signs depend on location in colon
ascending colon cancer signs liquid stool, occult blood/melena, anemia, fatigue, late palpable mass
transverse colon cancer signs semisolid stool, anemia, occult blood, change in bowel habits
descending colon cancer signs solid stood, constipation, discomfort, abdominal fullness and distention, red or dark blood in stool
rectum cancer signs solid stool, abdominal discomfort and cramps; ribbon or pellet stool, incomplete emptying, red blood on surface of stool
causes of intestinal obstruction mechanical issues due to tumors, adhesions, hernias or functional issues like adynamic obstruction b/c of neuro impairment, paralytic ileus
Created by: michellerogers