N212: Health Differences Across the Life Span 2

Health Differences Across the Lifespan 2 Study Guide icterus; petecchiae; propensity for bleeding; nausea and vomiting; anorexia; weight loss; clay colored stools; constipation; flatulence; pain or tenderness in RUQ; positive fluid wave; disorientation; decreased level of consciousness; encephalopathy; asterixis (flapping tremorof hand from increased ammonia level); decreased deep tendon reflexes; crackles; gynecomastia; testicular atrophy; erectile dysfunction; anemia; dark urine Laboratory studies: AST, Alt, LDH, PT, amylase, lipase, Hgb, HCT, bilirubin, albumin, and WBCs; measure and record patients abdominal girth daily; use only small gauge needle for injection, and provide prolonged pressure at veni-puncture site; avoid IM injectables; have patients avoid straining with defecation and vigorously blowing nose or coughing; use soft tooth brush; if patient is at risk for bleeding, give vitamin K to increase prothrombin time Treatment: nutritional support; transfusion of platelets; packed RBC and fresh frozen plasma; diuretics; stool softener; abdominal paracentesis for only severe ascites (this is an invasive procedure that drains fluid from the abdomen via needle and insertion of a LeVeen shunt); fluid restrictions; measure abdominal girth, daily weight, and I&O each day; diet should be high calorie, high carbohydrate, low fat, and low sodium; restrict alcohol Medications: diuretics to promote excretion of excess fluid to decrease ascites; the most commonly used is spironolactone (Aldactone), a potassium sparing diuretic, furosemide (Lasix), and a loop diuretic; lactulose (Cephulac), which pulls water into the bowel and helps decrease absorption of ammonia; vitamin K to treat prolonged PT; antihistamines and antiemetics Hepatic Coma or Hepatic Encephalopathy Hepatic coma or hepatic encephalopathy (also known as portosystemic encephalopathy) is the occurrence of confusion, altered level of consciousness, and coma as a result of liver failure. In the advanced stages, it is called hepatic coma or coma hepaticum. It may ultimately lead to death. It is caused by accumulation in the bloodstream of toxic substances that are normally removed by the liver. The diagnosis of hepatic encephalopathy requires the presence of impaired liver function and the exclusion of an alternative explanation for the symptoms. Blood tests (ammonia levels) may assist in the diagnosis. Attacks are often precipitated by an intercurrent problem, such as infection or constipation. Hepatic encephalopathy is reversible with treatment. This relies on suppressing the production of the toxic substances in the intestine and is most commonly done with the laxative lactulose or with non-absorbable antibiotics. In addition, the treatment of any underlying condition may improve the symptoms. In particular settings, such as acute liver failure, the onset of encephalopathy may indicate the need for a liver transplant. The mildest form of hepatic encephalopathy is difficult to detect clinically, but may be demonstrated on neuropsychological testing. It is experienced as forgetfulness, mild confusion, and irritability. More severe encephalopathy is characterized by an inverted sleep-wake pattern (sleeping by day, being awake at night), marked irritability, tremor, difficulties with coordination, and trouble writing. ©2017 Achieve Test Prep Page 92 of 140