cirrhosis Flashcards
cirrhosis
chronic progressive disease of the liver characterized by extensive degeneration and destruction of liver cells
disorganized regeneration
liver cells attempt to regenerate but the process is not organized and results in abnormal blood vessels and abnormal bile duct architecture
overgrowth of connective tissue
distorts liver’s normal lobular structure and results in lobules that are irregular in size and shape (impede blood flow)
etiology and pathophysiology of cirrhosis
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
risk factors for cirrhosis
alcohol abuse
obesity (NAFLD)
chronic viral hep B and C
cardiac cirrhosis - right sided heart failure
neurologic manifestations of cirrhosis
hepatic encephalopathy
peripheral neuropathy
asterixis (flapping tremors)
GI manifestations of cirrhosis
anorexia dyspepsia N/V change in bowel habits dull abdominal pain fector hepaticus (musty smelling breath) esophageal and gastric varices gastritis hematemesis hemorrhoidal varices
reproductive manifestations of cirrhosis
amenorrhea
testicular atrophy
gynecomastia
impotence
integumentary manifestations of cirrhosis
jaundice spider angioma palmar erythema purpura petechiae caput medusae
hematologic manifestations of cirrhosis
anemia thrombocytopenia leukopenia coagulation disorders splenomegaly
metabolic manifestations of cirrhosis
hypokalemia
hyponatremia
hypoalbuminemia
CV manifestations of cirrhosis
fluid retention
peripheral edema
ascites
complications of cirrhosis
jaundice portal HTN esophageal varices hematological problems peripheral edema and ascites hepatic encephalopathy endocrine alterations peripheral neuropathy hepatorenal syndrome
esophageal varices
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
hepatic encephalopathy
increase in ammonia levels in the brain
mental and personality changes
abnormal neurotransmission, astrocyte swelling, inflammation
treat with lactulose
portal hypertension
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
portal hypertension can lead to
pooling of blood - thrombocytopenia, leukopenia, anemia
peripheral edema and ascites
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
ascites
transfer of fluid from intravascular space to extravascular space
patients with ascites are at risk for _____
spontaneous bacterial peritonitis (SBP)
as albumin levels _____, fluid accumulation _______
decrease
increase
neuropsychiatric manifestation of end-stage liver disease
hepatic encephalopathy
symptoms of hepatic encephalopathy
sleep disturbances asterxis confusion drowsiness to coma personality changes irritability disoriented slowed speech forgetfulness, memory loss
endocrine dysfunction in cirrhosis
gynecomastia loss of body hair testicular atrophy vaginal bleeding impotence and decreased libido
skin lesions in cirrhosis
palmar erythema - blanchable
spider angioma - small, dilated blood vessels present on nose, cheeks, upper trunk, neck, shoulders
skin lesions appear due to
increase of estrogen circulating in the blood stream
diagnostic studies related to cirrhosis
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
care for cirrhosis
ascites esophageal and gastric varices hepatic encephalopathy conservative therapy with rest administration of B vitamins minimize hepatotoxic drugs avoid alcohol
assessment of ascites and edema
fluid volume deficit hypokalemia abdominal girth spontaneous bacterial peritonitis acute respiratory decompensation (PE)
abdominal girth
measure every day and mark belly with permanent marker to ensure measurement in the same place
care for ascites and edema
sodium restrictions diuretics (spironolactone and furosemide) fluid removal (parecentesis) skin care respiratory care medical management (diuretics/albumin) peritoneovenous shunt TIPS
peritoneovenous shunt
allows continuous redirection of acidic fluid into venous system
paracentesis
large bore needle stuck into the abdominal cavity to remove a large amount of fluid
pre-procedure for paracentesis
obtain baseline assessment, instruct patient to void prior, position patient sitting upright or in high fowlers, assess abdominal girth, check VS and breath sounds
intraprocedure for paracentesis
measure, collect, and describe fluid
monitor VS
post-procedure for paracentesis
maintain dry sterile dressing, monitor for hematuria, monitor for leakage at site, monitor for fluid volume deficit (hypovolemia and electrolyte imbalances)
TIPS
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
prevention for varices
avoid meds that may lead to bleeding (aspirin, NSAIDs)
avoid constipation
avoid activities that increase portal HTN
endoscopy used to diagnose varices
patients with varices at risk of bleeding are started on
beta blockers
acute intervention
stabilize patient and protect airway
manage bleed and fluid volume deficit
risk for recurrence for bleeds
drug therapy
goal is to stop bleeding so treatment can be initiated
beta-blockers
vasopressin
IV octreotide
EGD band ligation and sclerotherapy
if there’s large bleed seen with endoscopy, a ligation or banding can be done on varices
sclerotherapy - sclerose the bleeding vessel
balloon tamponade
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
endoscopy pre-procedure
NPO ~ 8 hours
informed consent signed
education
endoscopy intraprocedure
administer meds
monitor VS and airway
endoscopy post-procedure
keep NPO until gag returns
position patient in high fowlers or side-lying
monitor for complications
nursing considerations for balloon tamponade
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
complications of balloon tamponade
rupture, erosion of esophagus, regurgitation, aspiration of gastric contents, occlusion of airway
assessment for hepatic encephalopathy
assess neuro/mental status every 2 hours
medications (narcotics)
safety assessment
asterixis
medical management for hepatic encephalopathy
rifaximin, lactulose – reduces amount of ammonia formed in the intestines; traps ammonia in the gut; pass out flatulence = pass out ammonia
avoid triggers of hepatic encephalopathy
dehydration/infection/GI bleed/constipation
controlling GI bleeding and removing blood from GI tract to decrease protein in the intestine
diet for patients without complications
high in calories (3000/day)
increase in carbs
moderate to low fat
protein restriction rarely justified
diet for patients with ascites and edema
low sodium
nursing care plans for cirrhosis
imbalanced nutrition impaired skin integrity ineffective self-health management dysfunctional family processes altered body image fluid volume excess fluid volume deficit risk for falls
nursing management: implementation
reduce or eliminate risk factors treat alcoholism maintain adequate nutrition identify and treat acute hepatitis bariatric surgery for obese pts
measures to relieve pruritis
cholestyramine or hydroxyzine baking soda or alpha keri baths lotions, soft or old linen temperature control rub with knuckles
symptoms of hypokalemia
dysrhythmias, hypotension, tachycardia, muscle weakness
symptoms of fluid volume excess
muscle cramping, weakness, lethargy
action of spirinolactone (PO)
Antagonizes aldosterone in the distal tubules, increasing sodium and water excretion.
action of vasopressin (IV)
Causes contraction of smooth muscle in the vascular bed and increases systemic vascular resistance and mean arterial BP and decreases HR and cardiac output.
action of propranolol (PO, IV)
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.
action of lactulose (PO, rectal)
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.
adverse effects of spironolactone
Drowsiness, confusion, rash, nausea, vomiting, dizziness, diarrhea, hyperkalemia.
considerations for spironolactone
warn patient to avoid excessive ingestion of potassium-rich foods (such as citrus fruits, tomatoes, bananas, dates, and apricots), salt substitutes containing potassium
adverse effects of vasopressin
Hyponatremia, ventricular arrhythmias, rhabdomyolysis, nonspecific GI symptoms, peripheral, mesenteric, or coronary ischemia.
adverse effects of propranolol
Bradycardia, cardiac failure, hypotension, bronchospasm.
considerations for propranolol
Drug masks common signs and symptoms of shock and hypoglycemia.
adverse effects of lactulose
abdominal cramps, belching, diarrhea, flatulence, gaseous distention, nausea, vomiting.
considerations for lactulose
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.
