final med portion Flashcards
function of the liver
- metabolism (medications, alcohol)
- detoxification
- production of proteins (plasma proteins, coagulation factors, albumin)
- bile production (what aids us in digesting fats so we can absorb vitamins)
what are some causes of liver dysfunction?
- vital infections (hep B & C)
- alcohol abuse
- non alcoholic fatty liver disease –> obesity –> fat accumulation in the liver
- autoimmune conditions
- toxins & medications (tylenol/alcohol OD or misuse)
acute liver failure
rapid deterioration of the liver function resulting in encephalopathy and coagulopathy in persons with no known hx of liver disease
most common cause of acute liver failure
medications in combination with alcohol
clinical manifestations of acute liver failure
jaundice, coagulation abnormalities, encephalopathy, changes in cognitive function
liver cirrhosis
chronic inflammation of the liver which leads to scar tissue development
S/S of cirrhosis
- peripheral edema
- ascites
- anorexia
- dyspepsia
- SOB
- jaundice
- pruritus
- pale “clay” stool
- pain
- splenomegaly
hepatic encephalopathy
neuropsychiatric condition of advanced liver disease
neurotoxic levels of ammonia d/t it crossing the blood-brain barrier which causes an altered LOC, inappropriate behaviour, concentration difficulties
nursing management for encephalopathy
lactulose to reduce ammonia levels and expel ammonia from the colon (ensure a regular bowel regimen)
rifaximin used if lactulose unsuccessful alone
esophageal varices
enlarged and swollen veins at the lower end of the esophagus d/t portal hypertension
at risk of bleeding = EMERGENCY
ascites
accumulation of serous fluid in the peritoneal cavity d/t low albumin levels
management: sodium restriction, diuretics, fluid removal (paracentesis drain)
medications for hepatic dysfunction
- lactulose (to reduce ammonia)
- rifaximin (antibiotic for hepatic encephalopathy)
- diuretics (decrease fluid)
- beta-blockers (decrease portal htn)
what meds should pts with hepatic dysfunction avoid?
ASA, NSAIDS, sedatives, alcohol
what should we be monitoring for pts with hepatic dysfunction?
- labs (albumin, ammonia, urea, clotting factors, LFTs, CBCs, ETOH level)
- ins & outs
- CIWA
- LOC
- nutrition
- daily weights
pancreatitis
inflammation and necrosis of the pancreas –> autodigestion and leakage of enzymes
- severe pain
causes of pancreatitis
- gallstones (middle aged women)
- alcohol use disorder (men)
Others: trauma, viral infection, penetrating duodenal ulcer, cysts, abscesses, cystic fibrosis, medications, metabolic disease
S/S of pancreatitis
- RUQ or LUQ epigastric pain which radiates to back
- tender/distended abdomen
- pale, diaphoretic
- nausea/vomiting
- diarrhea
what are the main systemic complications of acute pancreatitis?
cardiovascular & pulmonary (hypotension, tachycardia, pleural effusion, atelectasis, pneumonia, acute respiratory distress)
pulmonary complications due to passage of exudate containing pancreatic enzymes from peritoneal cavity through lymph channels
primary diagnostic tests for pancreatitis
- serum amylase (3x normal level)
- serum lipase
- increase in liver enzymes, triglycerides, glucose, bilirubin and low calcium levels
nursing interventions for pancreatitis
keep pt NPO to reduce pancreatic secretion
urgent ERCP may be performed
monitor glucs
hepatitis A
transmitted by fecal-oral route
no specific tx, rarely leads to hepatic failure
hepatitis B
transmitted through exposure to contaminated blood or body fluids
vaccine preventable
hepatitis C
transmitted through blood or bodily fluids (primarily percutaneously)
hepatitis D
extremely low prevalence
typically acquired at the same time as HBV
hepatitis E
transmitted through fecal-oral route most commonly through contaminated water
peritonitis
inflammation of the peritoneal cavity
inflammatory bowel disease
autoimmune disease that refers to Crohn’s disease and ulcerative colitis
characterized by idiopathic inflammation and ulceration
3 characteristics of the etiology of inflammatory bowel disease
- genetics
- altered dysregulated immune response
- altered response to gut microorganisms
ulcerative colitis
inflammation and ulceration of the rectum and colon
inflammation is diffuse and involves mucosa and submucosa with alternate periods of exacerbation and remission
disease begins in rectum and spreads proximally along the colon in a CONTINUOUS fashion
clinical manifestations of ulcerative colitis
- bloody diarrhea (multiple BMs/day)
- abdominal pain
- fever, malaise, anorexia (when severe)
how is ulcerative colitis diagnosed?
BW: CBC, serum electrolytes, serum protein
sigmoidoscope, colonoscopy
nursing management for ulcerative colitis
- rest the bowels
- control the inflammation
- manage fluids & nutrition
- manage pt stress
- symptom relief (corticosteroids, sulphasalazine)
Crohn’s disease
chronic inflammation of any part of the GI tract from mouth to anus (most commonly in terminal ileum and colon)
skip lesions
(15-30 yrs, higher in women, Jewish & upper middle class urban populations)
clinical manifestations of Crohn’s disease
insidious onset with nonspecific symptoms
diarrhea (non-bloody), abdominal pain
how is Crohn’s disease diagnosed?
- lab work (electrolyte imbalances)
- barium studies
- endoscopic studies
nursing management for Crohn’s disease
- sulphasalazine (when large intestine is involved)
- corticosteroid therapy
- immunosuppressive agents (when corticosteroids fail)
- metronidazole (used to treat Crohn’s of the perianal area)