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Liver
BC3 - Liver
| Question | Answer |
|---|---|
| Functions of the liver | Bile production & excretion; excretion of bilirubin, cholesterol, hormones & drugs; metabolism of fats, proteins, CHO. Enzyme activation |
| Functions of the liver | Storage of glycogen, vitamins, and minerals; Synthesis of plasma proteins - albumin and clotting factor; Blood detoxification and purification |
| Portal circulatory system - 75% of the blood comes from | Stomach, intestines, spleen, pancreas - to the liver through the portal vein |
| Hepatocytes | secrete bile |
| Bile Flow | Formed in hepatocytes - Through canaliculi - to bile duct - combined to form larger ducts - empty into common bile duct |
| Sinusoids | Surrounded by hepatocytes; Distensible vascular channels - spongy epithelial cells |
| Portal Circulation | Blood flows through sinusoids - Central veins - Hepatic vein - Inferior Vena Cava |
| Kupffer Cells | Phagocytic cells - Remove bacteria & blood toxins |
| Portal Hypertension | r/t anything that causes an increase in pressure |
| Obstruction of the portal circulation | thrombosis, inflammation, fibrosis of the sinusoids |
| Most common cause of portal hypertension | cirrhosis |
| Obstruction of the portal circulation leads to | development of collateral circulation (blood makes its own route) |
| Long term problems of portal hypertension | Varices (increased pressure leads to weakening of vessel walls) |
| Where do varices occur | esophageal, stomach, rectum |
| Why do varices rupture | d/t gastric acid & elevated pressure |
| S/S of varices | vomiting blood, anemia if slow chronic bleed, they will have low Hgb |
| Dx of varices | endoscopy identifes portal HTN |
| Tx of varices | Beta Blockers; Nitrates; |
| Tx of varices (Vassopressors) | Used cocomitantly with NTG to reduce vasopressive action on other organs especially cardiac |
| Sclerotherapy r/t acute bleed of varices | endoscopically delivered medications (injected at site), |
| TIPPS | shunt between hepatic/portal veins; metal stent used to maintain patency; decompresses portal system (used for varices) |
| Splenomegaly | increased pressure in the splenic vein |
| Ascites | fluid accumulates n the peritoneal cavity |
| S/S of ascites | enlarged abd.; visible venous mapping showing collateral circulation; dyspnes because organs displaced; bacterial peritonitis can develoop |
| Tx of ascites | Paracentesis, may spontaneously resolve if functional restoration possible |
| Paracentesis helps to | evaluate fluid, relieve discomfort |
| Hepatic Encephalopathy | CNS disturbance, alterations in consciousness - toxins, ammonia, hormones accumulate in circulation and lead to damage in the brain |
| Hepatic encephalopathy was previously called | hepatic coma |
| What causes hepatic encephalopathy | ammonia freely circulating in the blood: competes with oxygen on Hgb causing hypoxia; it crosses the blood-brain barrier leading to toxic buildup of ammonia/urea in the brain |
| Early stage s/s of hepatic encephalopathy | lethargy, personality changes, irritability, sleep disturbances |
| Late stages s/s of hepatic encephalopathy | confusion, liver flap, stupor, convulsions, coma (liver failure), death |
| Liver flap | hands/arms up and they "flap" when held up |
| Jaundice (other name) | Icterus |
| Three types of jaundice | Hemolytic, Hepatocellular, Obstructive |
| Hemolytic jaundice | excessive breakdown of RBC's; metabolism of the heme component |
| Hepatocellular jaundice | Hepatocytes are damaged; can't conjugate bili; total bilirubin elevated |
| Obstructive jaundice | Extrahepatic - bile duct into duodenum obstructed (gallstones); Intrahepatic - obstruction of bile canaliculi |
| Hyperbilirubinemia | r/t water soluble; excreted by kidneys; transformed/metabolized by liver; cirrhosis; biliary obstruction; infectious hep; pancreatic CA; meds |
| Hepatitis | Inflammation of the liver |
| Hepatorenal syndrome | advanced liver disease with functional renal failure |
| S/S of hepatorenal syndrome | Oliguria, Na & water retention; hypotension; peripheral vasodilation |
| Hepatorenal syndrome is usually associated with | alcoholic cirrhosis & fulminant hepatitis |
| Acute Hepatitis | Viral, most common |
| If you have chronic hepatitis you are a | life long carrier |
| Hepatitis A rout of transmission | Fecal Oral route of transmission; |
| Hep A comes from | crowded living, food handlers, contaminated food/water, sexual contact |
| Hepatitis B routes of transmission | Blood/blood products, sexual contact, perinatal transmission, can produce lifelong carrier |
| Hepatitis C | Same as B, Significant number develop chronic |
| Hepatitis D | Causes infection only in conjunction with B (Very fragile); Superinfection; Same as B - unable to survive independently; infectious during all stages |
| Hepatitis E route of transmission | Fecal-oral |
| Hepatitis E is found in | contaminated water, prevalent in third world countries, unknown period of infectious transmission |
| Prodromal phase (preicteric) | Approximately 2 weeks after exposure; ends with jaundice |
| S/S of hepatitis during the preicteric phase | fatigue, N/V, flu like symptoms |
| Icteric phase | starts when they turn yellow (jaundice); 1-2 weeks after prodromal phase; lasts approx 2-6 wks; enlarged liver (palpable below the ribs and painful); Actual disease phase of hepatitis |
| Recovery phase of hepatitis is called | posticteric |
| Posticteric phase begins | when jaundice resolves; averages 6-8 wks after exposure; symptoms diminish -liver still tender & enlarged; Fnct returns to normal 2-12 wks after onset of jaundice |
| Chronic active hepatitis | Persists after Hep B; Abnl LFT's for more than 6 months; persistent surface antigen; Predisposed to Cirrhosis & primary hepatocellular CA |
| Fulminant Hepatitis | Complication of Hep B/C; Severe impairment or necrosis of liver cells |
| Dx of Cirrhosis | Abd Xrays; Liver US; Nuclear scan of liver & spleen, CT, Percutaneous Liver Bx; Hepatic Angiography |
| Cirrhosis | severe ascites results from cirrhosis as the most common cause |
| Causes of Cirrhosis (diseases) | Alcoholic; Chronic Hep C; Chronic Hep B & D; Autoimmune hepatitis; Inherited disease |
| Causes of Cirrhosis | blocked bile ducts; drugs, toxin & infections; Severe reactions to Rx; Prolonged exposure to environmental toxins; Repeat bouts of heart failure with liver congestion |
| Tx of Cirrhosis | Corticosteroids; Rest; Nutrition management - controlling Na, Diuretics, Paracentesis (for ascites) |
| Cholelithiasis | Gallstones |
| Gallstones are caused by | cholesterol stones & pigmented stones |
| Cholecystitis | Inflamation of the gallbladder; acute or chronic; almost always caused by stone in the cystic duct |
| S/S of cholecystitis | Rebound tenderness, abd muscle guarding, fever, leukocytosis |
| What labs are elevated with cholecystitis | Serum bilirubin & alk phos |
| Dx of Cholecystitis | Cholangiography & ERCP |
| Endoscopic Retrograde Cholangiopancreatography (ERCP) | Used to dx problems in liveer, gallbladder, bile ducts, pancreas |
| Tx of cholecystitis | narcotics to control pain, antibiotics, & cholecystectomy |
| What narcotics are used for cholecystitis | Morphine, Demerol, Dilaudid |
| Pancreatitis | inflammation of the pancreas; generally rare but potentially serious disorder; occurs equally in both sexesw |
| Pancreatitis is associated with | Alcohol, Obstructive biliary tract disease, peptic ulcers, trauma, hyperlipidemia, certain drugs |
| Complications of pancreatitis | Hypovolemia, Hypotension, Myocardial insufficiency |
| Some pts with pancreatitis develop | tachypnea, hypoxemia (secondary to pulm edema), Atelectasis, Pleural effusions from circulating pancreatic enzymes |
| Acute Hemorrhagic Pancreatitis | Usually mild disease; leaking enzymes into the pancreatic tissue from obstruction |
| Tx of Pancreatitis | Pain med, NGT to low intermittent suction, NPO, IVF, Hyperailmentation |
| Chronic pancreatitis | Structural or functional impairment; chronic alcoholic, characterized by intermittent pain (may intensify after eating); Steatorrhea; Malabsorption syndrome |
| Tx of Chronic pancreatitis | Oral enzymes replacement tx; potential loss of islet cells (lead to IDDM); No More Booze; Surgical intervention; at risk for developing pancreatic CA |
| Surgical intervention of chronic pancreatitis | Cyst development, drainage or removal, fibrosis, strictures |
Created by:
okrecota
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