NUR326 Exam 2 Flashcards

1
Q

Hepatitis A: Cause, Symptoms, Risk Factors, and Prevention

A

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

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2
Q

Hepatitis B: Cause, Symptoms, Course, and Prevention

A

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

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3
Q

Hepatitis C: Cause, Symptoms, Course, Prevention

A

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

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4
Q

Cirrhosis: definition and cause

A

definition: irreversible, inflammatory, fibrotic liver disease
cause: hepatitis B & C, excess alcohol intake, idiopathic, and nonalcoholic fatty liver disease

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5
Q

Relationship of Alcoholism and Liver Disease
Stages before Cirrhosis

A

alcoholic cirrhosis is the most common type of liver disease, there are various stages before cirrhosis:
alcoholic fatty liver, alcoholic steatohepatitis, alcoholic cirrhosis

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6
Q

Cirrhosis Pathogenesis

A
  1. liver cells destroyed
  2. cells try to regenerate
  3. disorganized process
  4. abnormal growth
  5. poor blood flow and tissue eschar
  6. hypoxia
  7. liver failure
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7
Q

Stages of Liver Damage

A
  1. healthy liver
  2. fatty liver
  3. liver fibrosis
  4. cirrhosis
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8
Q

Early vs Late CM of Cirrhosis

A

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

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9
Q

portal hypertension: def, causes, symptoms, and treatment

A

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)

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10
Q

hepatic encephalopathy: incidence, grading scale, and symptoms

A

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)

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11
Q

Acute Liver Failure: Definition, Cause, Patho, Course, and Treatment

A

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

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12
Q

lactulose

A

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

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13
Q

rifaximin

A

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

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14
Q

cholelithiasis: definition, RF, patho, CM

A

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

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15
Q

cholecystitis: definition, causes, patho, CM

A

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

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16
Q

gallbladder pharm:
ketorolac
antiemetics
anticholinergics
bile acids

A

ketorolac - pain control
antiemetics - control nausea and vomiting
anticholinergics - decrease gallbladder secretions and stop smooth muscle spasms
bile acids - dissolve stones

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17
Q

pancreatitis - RF, etiology, patho, CM, complications

A

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

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18
Q

chronic pancreatitis: definition, patho, CM

A

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

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19
Q

pancreatitis pharm:
morphine
dicyclomine
antacids
H-2 receptor antagonist
pancrealipase
insulin

A

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

20
Q

jaundice vs bilirubin

A

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)

21
Q

CM of jaundice

A

dark urine
increased LFT
normal or clay colored stools
pruritis

22
Q

3 important endocrine functions of the kidney

A
  1. produces erythropoietin
  2. activated vitamin D
  3. produces renin
23
Q

kidney blood supply

A

1/4 of CO is delivered to the kidneys
1200mL/min

24
Q

nephron functions

A
  1. filter water soluble substances from the blood
  2. reabsorb filtered nutrients, water, and electrolytes
  3. secrete waste and excess
25
Q

kidney obstructions (name/cause):
renal pelvis
ureter
bladder/urethra

A

renal pelvis - renal calculi
ureter - renal calculi, pregnancy, tumors
bladder/urethra - bladder cancer, neurogenic bladder, prostatic hyperplasia, prostate cancer, urethral strictures

26
Q

nephrolithiasis: definition, RF, etiology, patho, CM

A

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

27
Q

risk factors for UTI

A

CAUTI, female, increased age, pregnancy, sexual activity, urinary obstruction

28
Q

ascending pattern of UTI

A

contaminated perineum, urethra, bladder, ureter, kidney

29
Q

pylonephritis: def, RF, etiology, patho

A

inflammation of the kidneys
RF- pregnancy
etiology- ascending E coli infection, bloodstream infection
patho- inflammatory response causes kidney tissue damage

30
Q

urosepsis: definition, high risk, prognosis

A

definition - severe systemic response to UTI
high risk - elderly, DM, immunosuppressed
prognosis- high mortality

31
Q

first line antibiotics for UTI

A

ciprofloxacin and vancomycin

32
Q

renal cell carcinoma: RF, prognosis, CM, treatment

A

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

33
Q

bladder cancer: type, RF, CM, treatment

A

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

34
Q

normal lab values:
BUN
creatinine
GFR

A

BUN - 10-20
creatinine - 0.5-1.2
GFR - >90mL/min

35
Q

chronic kidney disease: causes, RF, patho, CM

A

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)

36
Q

drugs used to slow the progression of CKD

A

ACE, ARB, statins

37
Q

how to treat:
volume overload
hyperkalemia
metabolic acidosis
hyperphos
renal osteodystrophy
anemia

A

volume overload - loop diuretic
hyperkalemia - combo
metabolic acidosis - sodium bicarb
hyperphos - calcium carbonate
renal osteodystrophy - calcitrol
anemia - erythropoietin

38
Q

glomerular nephritis: def, location, primary and secondary, symptoms

A

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

39
Q

treatments for glomerulonephritis

A

corticosteroids
diuretics
immunosuppressants
antihypertensives
dialysis
diet

40
Q

diabetic neuropathy

A

major complication of glomerilopathy caused by gross thickening of GBM
ends in thick urine and more toxins

41
Q

hypertensive glomerular disease

A

underlying pathology - decreased renal perfusion, sclerotic glomerular changes

42
Q

nephrotic syndrome

A

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

43
Q

prerenal AKI

A

commonly caused by inadequate perfusion
decreased GFR due to low glomerular pressure
failure to restore blood volume, BP, and oxygen delivery

44
Q

intrarenal AKI

A

caused by acute tubular necrosis
can come from prerenal

45
Q

postrenal AKI

A

rare condition that usually occurs with obstruction

46
Q

AKI

A

sudden decline in function
CM - oliguria
pharm - stabilize patient until function returns (lasix, dextrose, binders, sodium bicarb)