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NU318 Exam 5 > cirrhosis > Flashcards

cirrhosis Flashcards

1
Q

cirrhosis

A

chronic progressive disease of the liver characterized by extensive degeneration and destruction of liver cells

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2
Q

disorganized regeneration

A

liver cells attempt to regenerate but the process is not organized and results in abnormal blood vessels and abnormal bile duct architecture

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3
Q

overgrowth of connective tissue

A

distorts liver’s normal lobular structure and results in lobules that are irregular in size and shape (impede blood flow)

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4
Q

etiology and pathophysiology of cirrhosis

A

most common causes are chronic hep C and alcohol-induced liver disease

protein malnutrition
environmental factors and genetic disposition
chronic inflammation and cell necrosis
synergistic factors accelerates damage

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5
Q

risk factors for cirrhosis

A

alcohol abuse
obesity (NAFLD)
chronic viral hep B and C
cardiac cirrhosis - right sided heart failure

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6
Q

neurologic manifestations of cirrhosis

A

hepatic encephalopathy
peripheral neuropathy
asterixis (flapping tremors)

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7
Q

GI manifestations of cirrhosis

A 
anorexia
dyspepsia
N/V
change in bowel habits
dull abdominal pain
fector hepaticus (musty smelling breath)
esophageal and gastric varices
gastritis
hematemesis
hemorrhoidal varices
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8
Q

reproductive manifestations of cirrhosis

A

amenorrhea
testicular atrophy
gynecomastia
impotence

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9
Q

integumentary manifestations of cirrhosis

A 
jaundice
spider angioma
palmar erythema
purpura
petechiae
caput medusae
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10
Q

hematologic manifestations of cirrhosis

A 
anemia
thrombocytopenia
leukopenia
coagulation disorders
splenomegaly
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11
Q

metabolic manifestations of cirrhosis

A

hypokalemia
hyponatremia
hypoalbuminemia

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12
Q

CV manifestations of cirrhosis

A

fluid retention
peripheral edema
ascites

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13
Q

complications of cirrhosis

A 
jaundice
portal HTN
esophageal varices 
hematological problems
peripheral edema and ascites 
hepatic encephalopathy
endocrine alterations
peripheral neuropathy
hepatorenal syndrome
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14
Q

esophageal varices

A

collateral circulation develops in attempt to reduce high pressure and reduce plasma volume
complex veins at lower end of esophagus that are enlarged and swollen
little elastic ability; very fragile
most life threatening complication of cirrhosis

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15
Q

hepatic encephalopathy

A

increase in ammonia levels in the brain
mental and personality changes
abnormal neurotransmission, astrocyte swelling, inflammation
treat with lactulose

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16
Q

portal hypertension

A

structural changes in the liver result in compression and deconstruction of the portal hepatic veins

changes cause obstruction in the normal flow of blood that goes through the portal system

characterized by increased venous pressure, splenomegaly, enlarged collatoral veins, ascites, gastric varices, esophageal varices

at risk for bleeding

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17
Q

portal hypertension can lead to

A

pooling of blood - thrombocytopenia, leukopenia, anemia

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18
Q

peripheral edema and ascites

A

decreased intravascular oncotic pressure secondary to decreased production of plasma proteins (albumin) - causes ascites

increased capillary filtration pressure secondary to portal HTN

altered metabolism of hormones

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19
Q

ascites

A

transfer of fluid from intravascular space to extravascular space

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20
Q

patients with ascites are at risk for _____

A

spontaneous bacterial peritonitis (SBP)

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21
Q

as albumin levels _____, fluid accumulation _______

A

decrease

increase

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22
Q

neuropsychiatric manifestation of end-stage liver disease

A

hepatic encephalopathy

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23
Q

symptoms of hepatic encephalopathy

A 
sleep disturbances
asterxis
confusion
drowsiness to coma
personality changes
irritability
disoriented
slowed speech
forgetfulness, memory loss
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24
Q

endocrine dysfunction in cirrhosis

A 
gynecomastia
loss of body hair
testicular atrophy
vaginal bleeding
impotence and decreased libido
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25
Q

skin lesions in cirrhosis

A

palmar erythema - blanchable

spider angioma - small, dilated blood vessels present on nose, cheeks, upper trunk, neck, shoulders

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26
Q

skin lesions appear due to

A

increase of estrogen circulating in the blood stream

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27
Q

diagnostic studies related to cirrhosis

A 
alkaline phosphatase - initially elevated
AST - may be normal
ALT - may be normal
GGT - initially elevated
total protein - decreased
globulins - increased
cholesterol levels - decreased
prothrombin time - prolonged
liver biopsy - liver cell damage
ascites fluid differential analysis - establish diagnosis
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28
Q

care for cirrhosis

A 
ascites
esophageal and gastric varices
hepatic encephalopathy
conservative therapy with rest
administration of B vitamins
minimize hepatotoxic drugs
avoid alcohol
29
Q

assessment of ascites and edema

A 
fluid volume deficit
hypokalemia
abdominal girth
spontaneous bacterial peritonitis
acute respiratory decompensation (PE)
30
Q

abdominal girth

A

measure every day and mark belly with permanent marker to ensure measurement in the same place

31
Q

care for ascites and edema

A 
sodium restrictions
diuretics (spironolactone and furosemide)
fluid removal (parecentesis)
skin care
respiratory care 
medical management (diuretics/albumin)
peritoneovenous shunt
TIPS
32
Q

peritoneovenous shunt

A

allows continuous redirection of acidic fluid into venous system

33
Q

paracentesis

A

large bore needle stuck into the abdominal cavity to remove a large amount of fluid

34
Q

pre-procedure for paracentesis

A

obtain baseline assessment, instruct patient to void prior, position patient sitting upright or in high fowlers, assess abdominal girth, check VS and breath sounds

35
Q

intraprocedure for paracentesis

A

measure, collect, and describe fluid

monitor VS

36
Q

post-procedure for paracentesis

A

maintain dry sterile dressing, monitor for hematuria, monitor for leakage at site, monitor for fluid volume deficit (hypovolemia and electrolyte imbalances)

37
Q

TIPS

A

standard of care for ascites that is unable to get treated by diuretics

non-surgical

reduces portal venous pressure and decompresses the varices, thus controlling bleeding

does not interfere with liver function or liver transplantation

38
Q

prevention for varices

A

avoid meds that may lead to bleeding (aspirin, NSAIDs)

avoid constipation

avoid activities that increase portal HTN

endoscopy used to diagnose varices

39
Q

patients with varices at risk of bleeding are started on

A

beta blockers

40
Q

acute intervention

A

stabilize patient and protect airway
manage bleed and fluid volume deficit
risk for recurrence for bleeds

41
Q

drug therapy

A

goal is to stop bleeding so treatment can be initiated
beta-blockers
vasopressin
IV octreotide

42
Q

EGD band ligation and sclerotherapy

A

if there’s large bleed seen with endoscopy, a ligation or banding can be done on varices

sclerotherapy - sclerose the bleeding vessel

43
Q

balloon tamponade

A

sits in the esophagus and inflates and puts continuous pressure on the bleed to stop it

used in patients who have acute esophageal or gastric varices that are not controlled with initial endoscopy

2 balloons - esophageal and gastric

3 lumens - gastric balloon, esophageal balloon, gastric aspiration

gastric balloon inflated to 250 cc of air and if pt is still bleeding, the esophageal balloon will be inflated

use sphygmometer to maintain pressure between 20-40mL

check balloon position with XR

44
Q

endoscopy pre-procedure

A

NPO ~ 8 hours
informed consent signed
education

45
Q

endoscopy intraprocedure

A

administer meds

monitor VS and airway

46
Q

endoscopy post-procedure

A

keep NPO until gag returns
position patient in high fowlers or side-lying
monitor for complications

47
Q

nursing considerations for balloon tamponade

A

protect airway

label each lumen

explain to patient the procedure

deflate balloon per hospital policy (usually 5 mins every 8-12 hours)

observe for skin breakdown

monitor for complications

always have a scissor at the bedside in case you need to cut the balloon to open up the airway

oralpharyngeal suction

48
Q

complications of balloon tamponade

A

rupture, erosion of esophagus, regurgitation, aspiration of gastric contents, occlusion of airway

49
Q

assessment for hepatic encephalopathy

A

assess neuro/mental status every 2 hours
medications (narcotics)
safety assessment
asterixis

50
Q

medical management for hepatic encephalopathy

A

rifaximin, lactulose – reduces amount of ammonia formed in the intestines; traps ammonia in the gut; pass out flatulence = pass out ammonia

51
Q

avoid triggers of hepatic encephalopathy

A

dehydration/infection/GI bleed/constipation

controlling GI bleeding and removing blood from GI tract to decrease protein in the intestine

52
Q

diet for patients without complications

A

high in calories (3000/day)
increase in carbs
moderate to low fat
protein restriction rarely justified

53
Q

diet for patients with ascites and edema

A

low sodium

54
Q

nursing care plans for cirrhosis

A 
imbalanced nutrition 
impaired skin integrity 
ineffective self-health management
dysfunctional family processes
altered body image
fluid volume excess 
fluid volume deficit
risk for falls
55
Q

nursing management: implementation

A 
reduce or eliminate risk factors 
treat alcoholism
maintain adequate nutrition
identify and treat acute hepatitis
bariatric surgery for obese pts
56
Q

measures to relieve pruritis

A 
cholestyramine or hydroxyzine
baking soda or alpha keri baths
lotions, soft or old linen
temperature control
rub with knuckles
57
Q

symptoms of hypokalemia

A

dysrhythmias, hypotension, tachycardia, muscle weakness

58
Q

symptoms of fluid volume excess

A

muscle cramping, weakness, lethargy

59
Q

action of spirinolactone (PO)

A

Antagonizes aldosterone in the distal tubules, increasing sodium and water excretion.

60
Q

action of vasopressin (IV)

A

Causes contraction of smooth muscle in the vascular bed and increases systemic vascular resistance and mean arterial BP and decreases HR and cardiac output.

61
Q

action of propranolol (PO, IV)

A

Reduces cardiac oxygen demand by blocking catecholamine-induced increases in HR, BP, and force of myocardial contraction. Drug depresses renin secretion and prevents vasodilation of cerebral arteries.

62
Q

action of lactulose (PO, rectal)

A

Produces an osmotic effect in colon; resulting distention promotes peristalsis. Also decreases ammonia, probably as a result of bacterial degradation, which lowers the pH of colon contents.

63
Q

adverse effects of spironolactone

A

Drowsiness, confusion, rash, nausea, vomiting, dizziness, diarrhea, hyperkalemia.

64
Q

considerations for spironolactone

A

warn patient to avoid excessive ingestion of potassium-rich foods (such as citrus fruits, tomatoes, bananas, dates, and apricots), salt substitutes containing potassium

65
Q

adverse effects of vasopressin

A

Hyponatremia, ventricular arrhythmias, rhabdomyolysis, nonspecific GI symptoms, peripheral, mesenteric, or coronary ischemia.

66
Q

adverse effects of propranolol

A

Bradycardia, cardiac failure, hypotension, bronchospasm.

67
Q

considerations for propranolol

A

Drug masks common signs and symptoms of shock and hypoglycemia.

68
Q

adverse effects of lactulose

A

abdominal cramps, belching, diarrhea, flatulence, gaseous distention, nausea, vomiting.

69
Q

considerations for lactulose

A

Monitor sodium level for hypernatremia, especially when giving in higher doses to treat hepatic encephalopathy

Monitor mental status and potassium levels when giving to patients with hepatic encephalopathy.

NU318 Exam 5 (4 decks)

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