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Pathophys U5
Pathophysiology Unit 5
| Question | Answer |
|---|---|
| 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
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