NUR326 Exam 2 Flashcards
Hepatitis A: Cause, Symptoms, Risk Factors, and Prevention
Cause: Unsanitary practice of healthcare workers or food handling workers, transmitted by fecal-oral, parenteral, sexual, or by IV drug use
Symptoms: acute onset with fever, fatigue, nausea, stomach pain, vomiting, no appetite, dark pee, pale poop, diarrhea, and jaundice
RF: sharing contaminated food, touching contaminated objects, unprotected sex, and sharing drug items.
Prevention: vaccine and hand hygiene
Hepatitis B: Cause, Symptoms, Course, and Prevention
Cause: transmitted through parenteral and sexual routes (common with contaminated needles)
Symptoms: insidious onset with long incubation period
Course: may develop into chronic disease (10%)
Prevention: HBV vaccine, safe sex, hand hygiene
Hepatitis C: Cause, Symptoms, Course, Prevention
Cause: parenteral, sexual, some mother to fetus
Symptoms: insidious onset with mild to severe symptoms (many don’t have any)
Course: can lead to hepatocellular carcinoma or liver transplant
Prevention: no vaccine (in the works), hand hygiene, screening blood
Cirrhosis: definition and cause
definition: irreversible, inflammatory, fibrotic liver disease
cause: hepatitis B & C, excess alcohol intake, idiopathic, and nonalcoholic fatty liver disease
Relationship of Alcoholism and Liver Disease
Stages before Cirrhosis
alcoholic cirrhosis is the most common type of liver disease, there are various stages before cirrhosis:
alcoholic fatty liver, alcoholic steatohepatitis, alcoholic cirrhosis
Cirrhosis Pathogenesis
- liver cells destroyed
- cells try to regenerate
- disorganized process
- abnormal growth
- poor blood flow and tissue eschar
- hypoxia
- liver failure
Stages of Liver Damage
- healthy liver
- fatty liver
- liver fibrosis
- cirrhosis
Early vs Late CM of Cirrhosis
Early: GI disturbances (N/V, anorexia, flatulence, change in bowel habits), fever, weight loss, palpable liver
Late: jaundice, peripheral edema, decreased albumin and PT, ascites, skin lesions, hematologic problems, endocrine problems, esophageal and anorectal varices, and encephalopathy
portal hypertension: def, causes, symptoms, and treatment
def: resistant portal blood flow that leads to varices and ascites
causes: systemic hypotension, vascular underfilling, stimulation of vasoactive systems, plasma volume expansion, and increased CO
symptoms: asymptomatic until complications arise (variceal hemorrhage, ascites, peritonitis, hepatorenal syndrome, cardiomyopathy)
treatment: prevent and treat complications (can’t treat portal hypertension without liver transplant)
hepatic encephalopathy: incidence, grading scale, and symptoms
incidence: 30-45% of cirrhosis patients
grading: minimal, Grade I, Grade II, Grade III, Grade IV (based on severity)
symptoms: LOC changes (correlate with liver labs - ammonia is the primary LOC driver)
Acute Liver Failure: Definition, Cause, Patho, Course, and Treatment
Definition: liver failure that is not caused by cirrhosis or other type of liver disease
Cause: most commonly by acetaminophen overdose (acystelene)
Patho: swollen hepatocytes and patchy areas of necrosis and inflammatory cell infiltrates disrupt liver tissue
Course: 6-8 weeks after viral hepatitis or metabolic liver disease, 5-8 days after acetaminophen overdose
Treatment: Liver transplant
lactulose
reduces ammonia absorption for hepatic encephalopathy
MOA: converts ammonia to ammonium
must have S/S of encephalopathy, not just high ammonia
** Make sure patient is not hypokalemic
rifaximin
second line treatment, could be preventative
MOA: blocks bacterial DNA synthesis by binding to bacterial DNA
SE: edema, n, ascites, dizziness, fatigue, pruritis, skin rash, abdominal pain, anemia
** Has been associated with an increased risk of CDiff
cholelithiasis: definition, RF, patho, CM
gallstones
RF: woman, older than 40, high estrogen levels, lifestyle, high cholesterol and fat diet, low fiber diet, family history
Patho: bile stasis, super saturation with cholesterol, precipitation, stones may stay or migrate through ducts
CM: could be asymptomatic, severity depends on movement and size of obstruction, **biliary colic, jaundice, dark urine, clay colored stools, steatorrhea, pruritis, intolerance to fatty foods, bleeding tendencies
cholecystitis: definition, causes, patho, CM
definition: inflammation of GB
cause: obstruction of gallstones or biliary sludge (could also be due to NPO status, bacterial infections, parenteral nutrition, DM)
patho: obstruction causes swelling which causes scarring and decreased functioning
CM: similar to cholelithiasis, could cause systemic symptoms (fever, n/v, restlessness, diaphoresis) causes an increase in bilirubin, LFT, WBC, and amylase
gallbladder pharm:
ketorolac
antiemetics
anticholinergics
bile acids
ketorolac - pain control
antiemetics - control nausea and vomiting
anticholinergics - decrease gallbladder secretions and stop smooth muscle spasms
bile acids - dissolve stones
pancreatitis - RF, etiology, patho, CM, complications
RF: middle age and African American
etiology: biliary tract disease (women), alcohol abuse (men)
patho: cells are injured, enzymes are activated inappropriately, autodigestion
CM: LUQ or epigastric pain (sudden and may radiate to back), tenderness, n/v, distention, hypoactive bowel sounds, fever, hypotension, tachy, jaundice, cyanosis, ecchymoses (grey turner’s sign and cullen’s sign)
increased amylase, lipase, glucose, and WBC
complications: pseudocyst, abscess, pulmonary complications, hypotension, tetany, increased risk for clotting
chronic pancreatitis: definition, patho, CM
definition: inflammation of the pancreas that lasts weeks to months, mainly caused by alcohol abuse
patho: destruction of the tissue, fibrosis, loss of pancreatic enzymes and insulin, may continue after alcohol abuse stops
CM: attacks of acute pancreatitis with progressive signs of dysfunction after the attack stops, **chronic pain, could include DM, malabsorption of fat, and weight loss
pancreatitis pharm:
morphine
dicyclomine
antacids
H-2 receptor antagonist
pancrealipase
insulin
morphine - pain
dicyclomine - decrease secretions and relax smooth muscle
antacids - decrease HCl secretion in the stomach which decreases the secretion of pancreatic enzymes
H-2 receptor antagonist - decrease HCl secretion in the stomach which decreases the secretion of pancreatic enzymes
pancrealipase - replace pancreatic enzymes
insulin - treat DM
jaundice vs bilirubin
jaundice - increased level of bilirubin, could be hemolytic, hepatocellular, or obstructive
bilirubin - by-product of heme breakdown, direct (can’t get bilirubin out of liver) or indirect (bilirubin overproduction/impaired liver function)
CM of jaundice
dark urine
increased LFT
normal or clay colored stools
pruritis
3 important endocrine functions of the kidney
- produces erythropoietin
- activated vitamin D
- produces renin
kidney blood supply
1/4 of CO is delivered to the kidneys
1200mL/min
nephron functions
- filter water soluble substances from the blood
- reabsorb filtered nutrients, water, and electrolytes
- secrete waste and excess
kidney obstructions (name/cause):
renal pelvis
ureter
bladder/urethra
renal pelvis - renal calculi
ureter - renal calculi, pregnancy, tumors
bladder/urethra - bladder cancer, neurogenic bladder, prostatic hyperplasia, prostate cancer, urethral strictures
nephrolithiasis: definition, RF, etiology, patho, CM
definition- renal calculi or kidney stones
RF- male, 20-30s, white, family history, congenital defect, hot weather, obesity
etiology- crystalized solutes in urine
patho- super saturation of urine, crystals form in the nephron, crystal formation enhanced by dehydration and immobility
CM- acute renal colic, N/V, diaphoresis, tachy, increased respirations
risk factors for UTI
CAUTI, female, increased age, pregnancy, sexual activity, urinary obstruction
ascending pattern of UTI
contaminated perineum, urethra, bladder, ureter, kidney
pylonephritis: def, RF, etiology, patho
inflammation of the kidneys
RF- pregnancy
etiology- ascending E coli infection, bloodstream infection
patho- inflammatory response causes kidney tissue damage
urosepsis: definition, high risk, prognosis
definition - severe systemic response to UTI
high risk - elderly, DM, immunosuppressed
prognosis- high mortality
first line antibiotics for UTI
ciprofloxacin and vancomycin
renal cell carcinoma: RF, prognosis, CM, treatment
RF- smoking, obesity, increased age, male, genetics
prognosis- normally found late, 5 year survival rate
CM- normally no early CM, late = CVA tenderness, hematuria, palpable abdominal mass
resistant to chemo
bladder cancer: type, RF, CM, treatment
fourth most common cancer in males (urothelial carcinoma)
RF- smoking, male, exposure to toxins, low fluid intake
early symptoms- hematuria
late symptoms- frequency, urgency, dysuria
treated with instravesical chemo (early), systemic chemo for late stages
normal lab values:
BUN
creatinine
GFR
BUN - 10-20
creatinine - 0.5-1.2
GFR - >90mL/min
chronic kidney disease: causes, RF, patho, CM
causes - **DM, HTN, glomerulonephritis
RF - family history, increased age, male, African American, HTN, DM, smoking, overweight
patho - glomerulosclerosis, interstitial fibrosis, interstitial inflammation
CM - HTN starts in stage 3, manifestations become apparent in stage 4, stage 5 includes uremia
**effects whole body system (high electrolytes, weight loss, anemia)
drugs used to slow the progression of CKD
ACE, ARB, statins
how to treat:
volume overload
hyperkalemia
metabolic acidosis
hyperphos
renal osteodystrophy
anemia
volume overload - loop diuretic
hyperkalemia - combo
metabolic acidosis - sodium bicarb
hyperphos - calcium carbonate
renal osteodystrophy - calcitrol
anemia - erythropoietin
glomerular nephritis: def, location, primary and secondary, symptoms
def - variety of conditions that cause inflammation of glomeruli
location - local or diffuse
primary - isolated to kidney
secondary - caused by systemic disease
symptoms - hematuria, azotemia, retention, proteinuria
treatments for glomerulonephritis
corticosteroids
diuretics
immunosuppressants
antihypertensives
dialysis
diet
diabetic neuropathy
major complication of glomerilopathy caused by gross thickening of GBM
ends in thick urine and more toxins
hypertensive glomerular disease
underlying pathology - decreased renal perfusion, sclerotic glomerular changes
nephrotic syndrome
glomerulus is too permeable to plasma proteins, eliminate >3g per day
patho - increased glomerular permeability, proteinuria, hypoalbuminemia
CM - edema, HTN, HL, hypercoagulation, loss of antithrombin and plasminogen
prerenal AKI
commonly caused by inadequate perfusion
decreased GFR due to low glomerular pressure
failure to restore blood volume, BP, and oxygen delivery
intrarenal AKI
caused by acute tubular necrosis
can come from prerenal
postrenal AKI
rare condition that usually occurs with obstruction
AKI
sudden decline in function
CM - oliguria
pharm - stabilize patient until function returns (lasix, dextrose, binders, sodium bicarb)
