Liver Cirrhosis Flashcards

1
Q

?

Is the end-stage of liver dz

Is characterized by extensive degeneration & destruction of liver cells

Results in the replacement of liver tissue by fibrosis (scar tissue) & regenerative nodules that occur from the liver’s attempt to repair itself

A

Cirrhosis

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2
Q
  • Usually happens after decades of chronic liver dz
  • Cirrhosis combined w/chronic liver dz ranks as 8th leading cause of death in the US
A
  • Is twice as common in men compared to women
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3
Q
  • Most common causes in US are chronic hepatitis C & alcohol-induced liver dz
  • Chronic hepatitis combined w/alcohol ingestion has a synergistic effect in accelerating liver damage
  • Approx 20% w/chronic Hep C & 10-20% w/chronic Hep B will develop cirrhosis
A

Other causes
> Extreme dieting, malabsorption, obesity

> Environmental factors

> Genetic predisposition

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4
Q

[Photo] - cirrhosis that developed 2° alcoholism

A

Characteristic diffuse nodularity of the surface is d/t the combo of regeneration & scarring of the liver

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5
Q

___ cirrhosis

Results from long-standing severe right-sided HF

> Causes venous congestion, parenchymal damage, necrosis of liver cells, & fibrosis over time
! Treatment towards managing underlying HF

A

Cardiac (cirrhosis)

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6
Q

___ cirrhosis

Includes primary biliary cirrhosis (PBC) & primary sclerosing cholangitis (PSC)

A

Biliary (cirrhosis)

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7
Q

?

This is a chronic inflammatory condition affecting the liver & bile ducts that’s frequently found in men

A

Primary sclerosing cholangitis (PSC)

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8
Q

Clinical Manifestations

  • Relatively few sx’s in early stage dz
  • Fatigue & enlarged liver may be early sx’s
A
  • Blood tests may be normal - compensated cirrhosis
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9
Q

Late Manifestations

  • Result from liver failure & portal HTN
    > Jaundice, peripheral edema, ascites
A

Other

> Skin lesions, hematologic disorders, endocrine disturbances, & peripheral neuropathies

  • In adv stages, liver becomes small & nodular
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10
Q

?

This condition results from decreased ability to conjugate & excrete bilirubin into the small intestines

A

Jaundice

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11
Q

Jaundice

  • Overgrowth of connective tissue in liver compresses bile ducts
    > Leads to obstruction
    > Inc in bilirubin in vascular system
A
  • May be minimal or severe, depending on ° liver damage
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12
Q
  • Skin lesions

> D/t inc in circulating estrogen caused by inability of liver to metabolize steroid hormones

A

> Spider angiomas (telangiectasia or spider nevi)

> Palmar erythema

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13
Q
  • Hematologic disorders

> Thrombocytopenia
Leukopenia
Anemia
Coagulation disorders

A
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14
Q

Thrombocytopenia, leukopenia, & anemia are thought to be caused by the splenomegaly that results from backup of blood from the portal vein into the spleen (__ __)

A

portal hypertension

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15
Q

Anemia can result from inadequate RBC production & survival, poor diet, poor absorption of folic acid, & bleeding from varices

A

Coagulation problems result from liver’s inability to produce PT & other factors essential for blood clotting

> Bleeding tendencies incl epistaxis, purpura, petechiae, easy bruising, gingival bleeding, & heavy menstrual bleeding

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16
Q

Endocrine disorders

  • 2° to dec metabolism of hormones
  • Gynecomastia, loss of axillary & pubic hair, testicular atrophy, impotence, & loss of libido (men) [d/t inc estrogen lvls]
A
  • Amenorrhea or vaginal bleeding
  • Hyperaldosteronism in both sexes
    > If the liver fails to metabolize aldosterone adequately; subseq sodium & water retention & K loss
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17
Q

___ ___

Is a common finding in alcoholic cirrhosis & is probably d/t a dietary deficiency of thiamine, folic acid, & cobalamin

Usually results in sensory & motor sx’s, but sensory sx’s may predominate

A

Peripheral neuropathy

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18
Q

Patients who are cirrhotic but who have no obvious complications are considered to have ___ cirrhosis

A

compensated (cirrhosis)

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19
Q

Those who have 1 or more complications of their liver dz have ___ cirrhosis

A

decompensated (cirrhosis)

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20
Q

Major complications of cirrhosis

! Portal HTN w/resultant esophageal and/or gastric varices

! Peripheral edema & abd ascites

A

! Hepatic encephalopathy (mental status changes, incl coma)

! Hepatorenal syndrome (a late complication of cirrhosis aff kidneys & manifested by oliguria, elevated BUN & creatinine, & inc urine osmolarity)

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21
Q

___ ___

  • Increased venous pressure in portal circulation
  • Splenomegaly
  • Large collateral veins
  • Ascites
  • Gastric & esophageal varices
A

Portal hypertension

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22
Q

Esophageal varices [80%]
> A complex of tortuous, enlarged veins @ lower end of the esophagus

A

Gastric varices [make up 20% of all varices]
> Located in upper portion of stomach

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23
Q

Both are very fragile, bleed easily
> Ruptured are the most life-threatening complication of cirrhosis & are a med emergency

A
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24
Q

Peripheral edema

↓ colloidal oncotic pressure from impaired liver synthesis of albumin

↑ portacaval pressure from portal HTN

A

Occurs as lower extremities [ankle]/presacral edema

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25
Q

?

Is the accumulation of serous fluid in the peritoneal or abdominal cavity

> Several mechanisms lead to this

A

Ascites

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26
Q

Mechanisms

> Portal hypertension
- causes proteins to shift from blood vessels into lymph space
- when lymphatic system unable to carry off excess proteins & water, they leak into peritoneal cavity
- osmotic pressure of proteins pulls add’l fluid into peritoneal cavity

A

> Hypoalbuminemia
- d/t liver’s dec ability to make albumin
- results in dec colloidal oncotic pressure

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27
Q

> Hyperaldosteronism
- happens when aldosterone is metabolized by damaged hepatocytes

  • inc lvl of aldosterone causes inc Na reabsorption by renal tubules
A
  • retention of Na combined w/an inc in ADH in blood, leads to add’l water retention
  • b/c edema formation, there’s dec intravascular volume & subs dec renal blood flow & glomerular filtration
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28
Q

Mechanisms of Ascites - Pathophysiology Map

A
  • Abd distention; weight gain
  • Eversion of umbilicus
  • Abd striae w/distended abd wall veins
  • Sx’s of dehydration (dry tongue & skin; sunken eyeballs; muscle weakness)
  • Dec u/o
  • Hypokalemia d/t hyperaldosteronism & diuretic therapy
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29
Q

?

Is a bacterial infection of the ascites fluid; occurs in 15-25% of hospitalized pts w/cirrhosis & ascites; particularly common >variceal hemorrhage

> E. coli causative

A

Spontaneous bacterial peritonitis (SBP)

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30
Q

?

Is a neuropsychiatric manifestation of liver dz

  • Neurotoxic effects of ammonia
  • Abn neurotransmission
  • Astrocyte swelling
  • Inflammatory cytokines
A

Hepatic encephalopathy

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31
Q
  • Liver unable to convert inc ammonia
A
  • Ammonia crosses blood-brain barrier
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32
Q
  • Changes in neurologic & mental responsiveness
  • Impaired consciousness and/or inappropriate behavior
A
  • Sleep disturbances, trouble concentrating, coma
  • Grading system of stages 0-4, 4 being most advanced (textbook has stages 1-4, p. 1157)
33
Q

?

Flapping tremors most common in arms & hands

A

Asterixis

34
Q
  • Impairment in writing
    > Difficulty in moving pen left to right

> ___ (difficulty to construct simple figures)

> Hyperventilation, hypothermia, tongue fasciculations, & grimacing/grasping reflexes

A

apraxia

35
Q

?

Is a musty, sweet odor of the pt’s breath

Odor is from the accumulation of digestive byproducts that the liver is unable to degrade

A

Fetor hepaticus

36
Q

?

  • Is a type of renal failure w/azotemia, oliguria, & intractable ascites
  • No structural abnormality of kidneys
  • Portal HTN → vasodilation → renal vasoconstriction
  • Treat w/liver transplantation
A

Hepatorenal syndrome

  • In the pt w/cirrhosis, this typically follows diuretic therapy, GI hemorrhage, or paracentesis
37
Q

Pathophysiology of Cirrhosis

A

Systemic clinical manifestations of liver cirrhosis

38
Q

Diagnostic Studies

  • Liver enzyme tests
    > Alkaline phosphatase, AST, ALT, GGT are initially elevated b/c release from inflamed liver cells
    > In end-stage dz, AST & ALT lvls may be normal d/t death & loss of hepatocytes

↓ serum total protein & albumin levels

↑ serum bilirubin & globulin levels

A
  • Prolonged prothrombin time
  • Dec cholesterol levels
  • US elastography (Fibroscan) [to quantify the ° of liver fibrosis]
  • Liver biopsy
  • Diff analysis of ascitic fluid
39
Q

Interprofessional Care

  • Rest
  • Admin of B-complex vitamins
  • Avoidance of alcohol
  • Minimization or avoidance of asa, acetaminophen, & NSAIDs
A
  • Ascites
  • Sodium restriction (based on ° of ascites)
    > 2 g/day
    > Severe = 250-500 mg/day
  • Albumin (infusion to maintain intravascular volume & adequate u/o by inc plasma colloid oncotic pressure)
  • Diuretics
  • Tolvaptan (Samsca)
40
Q

?

Is an effective diuretic, even in pts w/severe ascites

Is also an antagonist of aldosterone & is K-sparing

A

spironolactone (Aldactone)

41
Q

?

This is a high-potency loop diuretic that’s freq used in combo w/a K-sparing drug

A

furosemide (Lasix)

42
Q

?

A vasopressin-receptor antagonist, often seen in pts w/cirrhosis

Causes an inc in water excretion, resulting in an inc in serum Na conc

A

Tolvaptan (Samsca)

43
Q
  • Paracentesis
  • Transjugular intrahepatic portosystemic shunt (TIPS)
    > Is used to alleviate ascites that doesn’t respond to diuretics
A
  • Peritoneovenous shunt
44
Q

?

This is a surgical procedure that provides continuous reinfusion of ascitic fluid into the venous system

A

Peritoneovenous shunt

Its use has almost been eliminated b/c high rate of complications

45
Q

Esophageal & gastric varices - Prevent bleeding/hemorrhage

  • Avoid alcohol, asa, NSAIDs
  • Screen for presence w/upper endoscopy (EGD)
A
  • Nonselective β-blocker
  • nadolol (Corgard)
  • propranolol (Inderal)
    > Reduces incidence of hemorrhage by dec high portal pressure, which dec risk for rupture
46
Q
  • If bleeding occurs, stabilize pt, manage airway, provide IV therapy, & blood products
A

Drug therapy
> octreotide [Sandostatin] (somatostatin analog)
> Vasopressin [VP]

Endoscopic therapy
> Band ligation
> Sclerotherapy

47
Q
  • IV admin of octreotide or VP produces vasoconstriction of the splanchnic arterial bed, dec portal blood flow, & dec portal HTN
A
  • Now, octreotide is more widely used in this setting b/c of its limited side effect profile when compared w/VP
48
Q

?

Involves injection of a sclerosing solution into the swollen veins through an injection needle that’s placed through the endoscope

A

Sclerotherapy

49
Q

?

Is placement of a small rubber band (elastic O-ring) around the base of the varix (enlarged vein)

A

Endoscopic variceal ligation (EVL or “banding”)

50
Q

Balloon tamponade

> Controls the hemorrhage by mechanical compression of varices
Sengstaken-Blakemore tube

A

> Minnesota tube
Linton-Nachlas tube

51
Q

Sengstaken-Blakemore tube

  • Tube inserted into esophagus & stomach; 3 lumens
A

SAFETY ALERT

  • Label each lumen to avoid confusion
  • Secure the tube to prevent movement of the tube which could result in occlusion of the airway
  • Deflate balloons for 5 min every 8 to 12 hrs per institutional policy to prevent tissue necrosis
52
Q

Supportive measures for acute bleed

  • Fresh frozen plasma & packed RBCs
  • Vitamin K (Aquamephyton [phytonadione])
  • Antibiotics (prevent bacterial infection)
A
  • Proton pump inhibitors (pantoprazole [Protonix])
  • Lactulose (Cephulac) & rifaximin (Xifaxan)
  • Prevent hepatic encephalopathy from breakdown of blood & release of ammonia in intestine
53
Q

Long-term management

  • Nonselective β-adrenergic blockers
  • Repeated band ligation
  • Portosystemic shunts
A
54
Q

Shunting procedures

  • Used more after 2nd major bleeding episode
  • Nonsurgical: TIPS [transjugular intrahepatic portosystemic shunt]
A
  • Surgical: portacaval & distal splenorenal shunt
55
Q

Currently, the surgical shunts most commonly used are the portacaval & distal splenorenal shunt

A
56
Q

Total portal diversion after TIPS

  • A catheter is placed in the jugular vein & then threaded through the superior & inferior vena cava to the hepatic vein
  • Wall of hepatic vein is punctured, & the catheter is directed to the portal vein
A
  • Stents are positioned along the passageway, overlapping in liver tissue & extending into both veins
  • This reduces portal venous pressure & decompresses the varices, thus controlling bleeding
57
Q

! TIPS does not interfere w/a future liver transplantation

A

! Is contraindicated in pts w/severe hepatic encephalopathy, hepatocellular carcinoma, severe hepatorenal syndrome, & portal vein thrombosis

58
Q

Portacaval shunt

Portal vein is anastomosed to the IVC, diverting blood from the portal vein to the systemic circulation

A

Distal splenorenal shunt

Splenic vein is anastomosed to the renal vein

Portal venous flow remains intact, & esophageal varices are selectively decompressed

Spleen conducts blood from the high-pressure esophageal & gastric varices to the low-pressure renal vein

59
Q

Interprofessional Care - Hepatic encephalopathy

  • Reduce ammonia formation
  • Lactulose (Cephulac), which traps ammonia in gut
  • Rifaximin (Xifaxan) antibiotic
  • Prevent constipation
A
  • Treatment of precipitating cause
  • Lowering dietary protein intake
  • Preventing & controlling GI bleeding
  • Remove blood from GI tract
60
Q

Drug therapy

  • Not specific for cirrhosis
  • Used to treat symptoms & complications of advanced liver dz
A

Diet for patients w/o complications

  • High in calories (3000 cal/day)
  • ↑ carbohydrate
  • Moderate to low fat
  • Protein restriction rarely justified

> For many pts, malnutrition is a more serious clinical problem than hepatic encephalopathy

61
Q
  • Protein supplements for protein-calorie malnutrition
  • Low-sodium diet for pt w/ascites & edema
A
  • Seasonings to make food more palatable
  • Collaborate w/a dietician
62
Q

Past Health History
- Hepatitis
- NASH
- Chronic biliary obstruction & infection
- Severe right-sided HF

A

Rx’s
- Adverse rxn’s
- Anticoagulants, asa, NSAIDs, acetaminophen

63
Q

Health perception-health management
- Chronic alcoholism
- Weakness, fatigue

Nutritional-metabolic
- anorexia, wt loss
- Dyspepsia
- N/V
- Gingival bleeding

A

Elimination
- dark urine
- dec u/o
- light-colored or black stools
- flatulence
- change in bowel habits
- dry, yellow skin
- bruising

64
Q

Cognitive-perceptual
- dull, RUQ or epigastric pain
- numbness, tingling of extremities
- pruritus

Sexuality-reproductive
- impotence
- amenorrhea

A

General
- fever, cachexia, wasting of extremities

Integumentary
- icteric sclera, jaundice
- petechiae, ecchymoses
- spider angiomas, palmar erythema
- alopecia, loss of axillary & pubic hair
- peripheral edema

65
Q

Respiratory
- shallow, rapid respirations
- epistaxis

Gastrointestinal
- abd distention, ascites
- distended abd wall veins
- palpable liver & spleen
- foul breath
- hematemesis; black, tarry stools
- hemorrhoids

A

Neurologic
- altered mentation, asterixis

Reproductive
- gynecomastia & testicular atrophy (men)
- impotence (men)
- loss of libido (men/women)
- amenorrhea or heavy menstrual bleeding (women)

66
Q

Possible diagnostic findings
- anemia, thrombocytopenia, leukopenia
- ↓ serum albumin & K levels
- Abn LFT’s
- ↑ INR, ammonia, & bilirubin levels
- Abn find on abd US or MRI

A

Nursing Diagnoses (for the pt w/cirrhosis)

  • Imbalanced nutrition: less than body requirements
  • Impaired skin integrity
  • Excess fluid volume
  • Ineffective health management
  • Dysfunctional family processes
67
Q

Overall Goals (for the pt w/cirrhosis)

  1. Have relief of discomfort
  2. Have minimal to no complications (ascites, esophageal varices, hepatic encephalopathy)
A
  1. Return to as normal a lifestyle as possible
68
Q

Health Promotion

  • Reduce or eliminate risk factors
  • Treat alcoholism
  • Maintain adequate nutrition
  • Identify & treat acute hepatitis
  • Bariatric surgery for morbidly obese (reduces incidence of NAFLD)
A

Acute Care

Rest needs
> Prevent complications
> Modify schedule

Nutritional needs
> Oral hygiene
> Between-meal nourishment
> Food preferences
> Explanation of dietary restrictions

69
Q

Assess for jaundice

Measures to relieve pruritus
- Cholestyramine or hydroxyzine
- Baking soda or Alpha Keri baths
- Lotions, soft or old linen
- Temperature control
- Short nails; rub w/knuckles

Monitor color of urine & stools
- when jaundice is present, the urine is often dark brown & the stool is gray or tan

A
  • Accurate I&O recording
  • Daily wt measurement
  • Extremities measurement
  • Abd girth measurement
70
Q

Acute Care - Paracentesis

  • Pt voids immediately before
  • When done, place in high-Fowler’s position or sitting on side of bed
  • Monitor for hypovolemia & electrolyte imbalances
A
  • Monitor BP & HR
  • Monitor dressing for bleeding/leakage of ascitic fluid
71
Q

Acute Care - Relief of dyspnea
- semi- or high Fowler’s position

Skin care
- special mattress
- turning schedule, @ least q2h

A
  • ROM exercises
  • C&DB exercises
  • Elevate lower extremities/scrotum [edema]
72
Q

! Dyspnea is a freq problem for the pt w/severe ascites & can lead to pleural effusions

A
73
Q

Monitor for F&E disturbances
- Hypokalemia
- Water excess (hyponatremia)

  • Observe for bleeding disorders
A
  • Assess pt’s response to altered body image
    > Supportive listening
74
Q

Acute Care - Bleeding varices

  • Close observation for signs of bleeding
  • Balloon tamponade care
    > Explanation of procedure
    > Check for patency
    > Position of balloon verified by x-ray
A
75
Q

Acute Care - Bleeding varices

  • Close observation for signs of bleeding
  • Balloon tamponade care
    > Explanation of procedure
    > Check for patency
    > Position of balloon verified by x-ray
A

! Monitor for complications (i.e., aspiration, pneumonia)
- Scissors @ bedside
- Semi-Fowler’s position
- Oral/nasal care

76
Q

Acute Care - Hepatic encephalopathy

  • Maintain safe environment
  • Assess carefully; sustain life
    ! Reduce ammonia formation
    ! At risk for falls d/t confusion
A
  1. Level of responsiveness
  2. Sensory & motor abnormalities
  3. F&E imbalances
  4. Acid-base imbalances
  5. Effects of treatment measures
77
Q
  • Perform neurologic assessment every 2 hrs
  • Prevent falls & injuries
  • Minimize constipation (reduce ammonia production)
A
  • Encourage fluids (if not contraindicated)
  • Control factors known to precipitate encephalopathy
    > GI bleeding
    > Constipation (d/t dehydration, opioid rx’s)
78
Q

Supportive measures
* Proper diet
* Rest
* Avoidance of hepatotoxic OTC rx’s [acetaminophen in high doses]
* Abstinence from alcohol

Caring attitude always

A
  • Community support programs (AA)
  • Sx’s of complications
  • When to seek medical attention
  • Written instructions w/adequate explanations for pt/family
  • Referral to community or home health RN
79
Q

Evaluation - Expected Outcomes

✓ Maintain food & fluid intake adequate to meet nutritional needs

✓ Maintain skin integrity w/relief of edema & pruritus

A

✓ Experience normalization of fluid balance as a result of medical & nursing interventions

✓ Acknowledge & get treatment for a substance abuse problem