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Stack #131712
a MCPHS- Provider I- Ch 39- Assessment & Management of Pts w/Hepatic Disorders
| Question | Answer |
|---|---|
| 75% of liver's blood supply comes from | Portal vein |
| Supplies liver with oxygen | Hepatic artery |
| Most common phagocyte in human body | Kupffer cells |
| Main function r/t Kupffer cells | Engulf particulate matter |
| End product r/t gluconeogenesis | Ammonia |
| Liver converts ammonia to | Urea |
| Examples r/t Protein metabolism of liver | Synthesizes almost all plasma proteins including albumin, alpha & beta globulins, blood clotting factors |
| Required for synthesis of prothrombin | Vitamin K |
| Vitmains stored in large amounts in liver | A, B-complex and D |
| Fraction of an administered medication that actually reaches systemic circulation | Bioavailability |
| Bioavailability is decreased if medication is metabolized to a great extent by liver before it reaches systemic circulation | First-pass effect |
| Enteropathic circulation | Pathway from hepatocytes to bile to intestines and back to hepatocytes |
| Amount of bile salts excreted in feces | Small fraction |
| Route r/t bilirubin elimination | Excreted to bile |
| Most common changes to liver r/t Aging | Decreases in size, weight and total hepatic blood flow |
| Abnormal liver function tests r/t Aging process | Abnormal results indicate abnormal liver function and are not result of aging |
| Alcohol consumption r/t High risk for cirrhosis | Men:60-80 g/day or 4 cocktails, Women: 40-60 g/day |
| Viral hepatitis vs. Alcoholic hepatitis r/t Liver tenderness | VH:tender, AH:nontender |
| Amount of liver damage before liver function tests may become abnormal | 70%+ |
| ALT level increase vs. AST level increase vs. GGT level increase r/t Liver function | ALT:primarily d/t liver disorders, AST:damage/death to organ tissues, GGT:cholestasis or alcoholic liver disease |
| Acute vs. Chronic r/t More common liver dysfunction | Chronic |
| Most common and significant symptoms r/t liver disease | Jaundice, Portal hypertension, Ascites, Varices, Nutritional deficiencies, Hepatic encephalopathy |
| Hemolytic vs. Hepatocellular vs. Obstructive jaundice | Hemo:increased destruction of RBC's, Hepato:inability of damaged liver cells to clear normal amounts of bilirubin, O:extrahepatic obstruction from occulsion of bile duct |
| Extrahepatic vs. Intrahepatic obstruction | I:obstruction involves small bile ducts w/in liver, E:occlusion of bile duct |
| Urine & Stool r/t Obstructive jaundice | U:deep orange and foamy, S:light/clay-colored |
| Pathophysiology r/t Varices | Develop d/t elevated pressure in veins |
| Treatment goal r/t Pt w/ascites | Negative Na balance to reduce fluid retention |
| Commercial salt substitutes r/t Physician approval | May contain ammonia which could cause hepatic coma, May also contain K |
| Second treatment option r/t Ascites | Diuretic therapy |
| Pathophysiology r/t Esophageal varices | Almost always d/t portal hypertension |
| Factors contributing to hemorrhage r/t Esophageal varices | Muscular exertion, Straining at stool, Sneezing, Coughing, Vomiting, Esophagitis, Irritation of vessels d/t poorly chewed food, Reflux of stomach contents |
| Signs r/t Potential hypovolemia | Cold clammy skin, Tachycardia, Drop in BP, Decreased urine output, Weak peripheral pulses |
| Order to removing Balloon tamponade | Esophageal balloon deflated first, Pt monitored for recurrent bleeding, Gastric balloon deflated, Monitor for recurrent bleeding, Remove balloon tamponade |
| Treatment of choice r/t Esophageal varices | Esophageal band ligation |
| Surgical decompression prevents variceal bleeding | Decompression of portal circulation |
| Precipating factors r/t Hepatic encephalopathy | Profound liver failure, Accumulation of ammonia and other toxic metabolites |
| Earliest symptoms r/t Hepatic encephalopathy | Minor mental changes & motor disturbances |
| Medication used to decrease serum ammonia levels | Lactulose |
| Pathophysiology r/t Generalized edema | Hypoalbuminemia d/t decreased hepatic production of albumin |
| Bleeding r/t Hepatic impairment | Production of clotting factors is reduced, Increased bruising and bleeding from wounds |
| Hep A vs. Hep B r/t Transmission route | A:fecal-oral, B:blood |
| Active vs. Passive immunity | Active acquire immunity:develop by own body, Passive acquired immunity:obtained from source outside of body like immune globulin, antiserum, or mother to baby |
| Most frequent side effect r/t Hep C treatment | Hemolytic anemia |
| Only risk factor r/t Hep D | Those w/Hep B |
| Almost always present w/Hep E | Jaundice |
| Common chemicals r/t Nonviral hepatitis | Carbon tet, Phosphorus, Chloroform & gold compounds |
| Common med that leads to hepatitis | Acetaminophen |
| Most common cause of acute liver failure | Drug-induced liver disease |
| Sudden/severe impaired liver function in previously healthy Pt | Fulminant hepatic failure |
| Common causes r/t Fulminant hepatic failure | Viral hepatitis, Toxic meds, Toxic chemicals, Metabolic disturbances, Structural changes |
| Replacement of normal tissue w/diffuse fibrosis that disrupts liver function | Cirrhosis |
| Alcoholic vs. Postnecrotic vs. Biliary cirrhosis | A:scar tissue surrounds portal areas, P:result of acute viral hepatitis, B:scar tissue around bile ducts |
Created by:
rpclothier
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