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GI

UGI bleeding, hepatitis, pancreatitis, liver failure

QuestionAnswer
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
Created by: ebrewer12
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