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UGI bleeding, hepatitis, pancreatitis, liver failure
Question | Answer |
---|---|
UGI bleeding causes | PUD, stress ulcer, mallory-weiss tear, stomach cancer, tumors, esophageal varices, esophagitis, aspirin, corticosteroids |
UGI bleeding assessment | BP/ HR, rate and character of pulse, neuro status, urine output --> place foley, hyperactive bowel sounds, apply oxygen |
lab studies for UGI bleeding | CBC, BUN, serum electrolytes (decreased Na, K+), prothrombin time, liver enzyme measurements, typing/cross |
priority treatment of UGI bleeding | hemodynamic stabilization --> large bore IV, fluid administration LR, administration of blood, hct may not reflect actual blood loss |
medication treatment for UGI bleeding | PPIs, antacids, H2 receptor blockers, mucosal barrier enhancers, antibiotics (H. Pylori) |
endoscopic treatment | sclerotherapy (injection of solution into vein to collapse and blood to clot) thermal probe (heat applied directly to bleeding site) |
hypovolemic shock | decreased BP, increased HR, decreased LOC |
priority for hypovolemic shock | establish airway, restore hemodynamics --> get to endoscopy ASAP |
variceal bleeding treatment | stop bleeding, prevent hemorrhage, |
octreotide (Sandostatin) | decreases splanchnic blood flow, reduces portal pressure |
vasopressin drip | vasoconstriction of splanchnic bed, EKG and BP monitoring continuous, risk of fluid and electrolyte imbalances |
hepatitis | acute inflammation of liver cells |
hepatitis A | fecal contamination (contaminated food, milk, water, crowded conditions |
hepatitis B | blood-borne, sexual transmission, (contaminated needles) |
hep C | blood borne - most common cause of cirrhosis, blood |
hep D | combined with hep B |
hep E | fecal oral (contaminated water, poor sanitation) |
acute hepatitis clinical manifestations | anorexia, diarrhea, lethargy, jaundice, low-grade fever, N/V |
chronic hepatitis clinical manifestations | elevated ALT, AST, anemia, ascites, lower extremity edema, malaise, hepatic encephalopathy |
Heptatitis Management | no definitive treatment well balanced diet, vitamins, rest, avoid alcohol and drugs detoxified by liver, notify contacts (pharmacist, nutritionist, mental health specialist) |
cirrhosis | end stage liver disease, extensive degeneration and destruction of liver cells, results in replacement of liver tissue by fibrous and regenerative nodules |
types of cirrhosis | Lannec's (alcoholic), biliary, cardiac (long-standing right HF), postnecrotic |
assessment of cirrhosis | liver enlarges (early sign), inflammation and necrosis of cells, yellow, orange, fatty and scarred liver --> shrinks and portal HTN occurs |
early cirrhosis clinical manifestations | anorexia, flatulence, N/V, change in bowel pattern, fatigue, enlarged liver, normal liver fxn |
late cirrhosis clinical manifestations | jaundice, skin lesions, leukopenia, anemia, endocrine issues, peripheral neuropathy, encephalopathy, ascites, shrinking liver |
neurologic complications of cirrhosis | hepatic encephalopathy, asterixis (flapping tremors) |
GI complications of cirrhosis | dyspepsia, N/V, fetor hepaticus, varices |
diagnostics of cirrhosis | elevated liver enzymes - ALT, AST, ALP elevated bilirubin and ammonia, prolonged PT time |
supportive treatment of cirrhosis | fluids, rest, avoid alcohol, increase calories, increase carbs, decrease fat, treat hypoglycemia, minimize use of NSAIDs, |
ascites | low albumin plus obstruction to flow --> portal HTN fluid in the peritoneal cavity increased aldosterone |
management of ascites | bedrest, sodium and fluid restriction, diuretics (Spironolactone- Aldactone) paracentesis, TIPS |
hepatic encephalopathy | neuropsych manifestation of liver disease, cerebral toxicity from elevated ammonia |
management of hepatic encephalopathy | treat the cause -> constipation, dehydration, hypokalemia limit protein, antibiotics (Rifaximin), lactulose, restrict toxic medications, sedation |
acute liver failure | rapid onset of severe liver dysfunction in someone with no history of liver disease |
most common cause of acute liver failure | acetaminophen, sulfa drugs, anti-convulsants |
clinical manifestations of acute liver failure | jaundice, changes in cognitive function (FIRST SIGN), coagulation abnormalities, encephalopathy, increased AST and ALT |
hepatic failure nursing management | improve nutrition status, protect renal function, maintain fluid and electrolytes, promote comfort, educate patient, avoid NSAIDs, and monitor glucose, |
acute pancreatitis | inflammation of pancreas |
causes of pancreatitis | alcoholism, meds, trauma, pancreatic cancer, biliary tract disease |
patho of pancreatitis | autodigestion of the pancreas, causative factors injure pancreatic cells, releases histamine and bradykines which cause inflammation |
clinical manifestations of pancreatitis | abdominal pain (LUQ and mid-epigastrum) abdominal distention, ascites, N/V, turner's sign (discoloration of flank), Cullen's sign (discoloration of umbilicus) fever, HTN, tachycardia, low urine output, cyanosis, hypocalcemia |
pseudocyst | accumulation of fluid, pancreatic enzymes, tissue debris, inflammatory exudates surrounded by wall next to pancreas |
clinical manifestations of pseudocyst | abdominal pain, anorexia, palpable epigastric mass, N/V |
abscess | when pseudocysts get infected, may rupture or perforate into adjacent organs |
clinical manifestations of abscess | upper abdominal pain, abdominal mass, high fever, leukocytosis surgical drainage required |
labs for pancreatitis | elevated - serum amylase, serum lipase, WBCs, glucose decreased - calcium, albumin, protein, potassium |
treatment of pancreatitis | volume replacement, monitor volume status, vasopressors, electrolyte replacement decrease secretions - NPO, NG suction manage pain with morphine pharmacologic therapy- antibiotics and antacids |
complications of pancreatitis | hypovolemic shock, DIC, pseudocyst and abscess, pulmonary complications, renal failure, high glucose - low calcium |