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NURS3313 Adult Health > Chapter 43 Assessment & Management of Patients w/ Hepatic Disorders > Flashcards

Chapter 43 Assessment & Management of Patients w/ Hepatic Disorders Flashcards

1
Q

Liver

A

Largest gland in the body
- Located in patient’s RUQ

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2
Q

Functions of the Liver

A

Glucose Metabolism

Ammonia Conversion

Protein Metabolism

Fat Metabolism

Vitamin and Iron Storage

Bile Formation
- Bilirubin is excreted in bile

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3
Q

The Liver’s Role in Glucose Metabolism

A

Plays a major role in the metabolism of glucose & the regulation of blood glucose concentration

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4
Q

The Liver’s Role in Ammonia Conversion

A

The use of amino acids from protein for glycogenesis results in the formation of ammonia as a by-product

The liver converts this ammonia into urea which is excreted in the urine

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5
Q

The Liver’s Role in Protein Metabolism

A

Synthesis of almost all the plasma proteins such as albumin, and blood clotting factors

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6
Q

The Liver’s Role in Fat Metabolism

A

Can break down fatty acids to produce energy and ketone bodies (can provide a source of energy for muscles).

Primarily happens when glucose is not available for metabolism

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7
Q

The Liver’s Role in Vitamin & Iron Storage

A

Vitamins A, B and D plus several of the B-complex vitamins along with iron and copper are stored in the liver

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8
Q

The Liver’s Role in Bile Formation

A

Bile is continuously formed by the liver and stored in the gallbladder

Empties into the intestine when needed for digestion of fats

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9
Q

Age-Related Considerations

A

Atypical clinical presentation of biliary disease

Decreases in:
- Drug metabolism and clearance capabilities
- Intestinal & portal vein blood flow
- Rate of replacement and repair of liver cells after injury
- Size & weight of the liver, particularly

Increased prevalence of gallstones due to the increase in cholesterol secretion in bile

More rapid progression of Hep C infection & lower response rate to therapy

More severe complications of biliary tract disease

**Changes is drug metabolism and clearance → may need to reduce dosage to prevent toxicity

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10
Q

Risk Factors for Hepatic Disorders

A

Previous exposure to hepatotoxic agents/infectious agents

Any alcohol/IV drug use

Meds that cause hepatic dysfunction

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11
Q

Health History

A

Exposure to:
 Substances toxic to the liver (hepatotoxins)
 Industrial chemical for example
 Infectious diseases

Alcohol Use Risk for Cirrhosis
- Men: 60-80 g/day
- Women: 40-60 g/day

Drug use
- Including IV drugs (exposure to infectious diseases)
- Use of Tylenol
- Acetaminophen
- Ketoconazole
- Valporic acid

Lifestyle behaviors

Sexual practices

Foreign travel

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12
Q

Physical Assessment

A

Early Symptoms are vague & non-specific
- Fatigue
- Vague abdominal symptoms: loss of appetite, n/v, indigestion, gas, RUQ pain

Advanced Liver Disease/ Cirrhosis Symptoms
- Pallor
- Jaundice
- Peripheral edema & ascites
- Skin changes: palmor erythema, spider nevi
- Confusion or disorientation
- Extremities: Muscle atrophy, edema, skin excoriation r/t to itching

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13
Q

Physical Assessment Findings Associated w/ Hepatic Disorders: Integumentary Assessment

A

Pallor (chronic illness)

Assess skin, mucosa, & sclera for jaundice

Assess extremities for muscle atrophy, edema, and skin excoriation from scratching

Assess skin for petechiae, ecchymosis, spider angiomas, and palmar erythema

Male patient considerations: asses for unilateral or bilateral gynecomastia and testicular atrophy

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14
Q

Physical Assessment Findings Associated w/ Hepatic Disorders: Neurological Assessment

A

Recall

Memory

Abstract thinking

General tremor, asterixis, weakness, and slurred speech

Assess for Associated Nervous System Disorders
- Depression
- Mood changes: anger & irritability

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15
Q

Physical Assessment Findings Associated w/ Hepatic Disorders: Percussion & Palpation

A

-Assess for the presence of abdominal fluid

-Assess the liver size and detect tenderness

-When palpable, the liver is in the right upper quadrant with a firm, sharp ridge

Tenderness indicates acute enlargement

Size of liver determined by percussion

Nurse notes and records size, consistency, tenderness, and whether its outline is regular or irregular

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16
Q

Patient Assessment Related to Genetic Hepatic Disorders

A

Assess for physical signs or history of the following:
- Abdominal bloating & constipation
- Changes to skin color or yellow hue to sclera
- Enlarged liver, abdomen, or spleen
- Episodes of n/v
- Hemorrhoids, esophageal varices, or gallstones
- Intolerance to fatty foods or alcohol
- Pale stools
- Presence & frequency of dyspepsia or reflux
- Unexplained weight loss
- Assess for associated blood-sugar problems
- Inquire about & assess for abnormal bleeding/ bruising
- Obtain & review lab values
-> LFTs, ammonia, bilirubin, & fat soluble vitamins

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17
Q

Cirrhosis

A

Chronic liver disorder characterized by fibrotic changes, the formation of dense connective tissue w/in the liver, subsequent degenerative changes, & loss of functional liver tissues

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18
Q

Asterixis

A

Involuntary flapping of the hands

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19
Q

Diagnostic Evaluation: Common Lab
Tests to Assess Liver Function

A

Liver enzymes: (Serum AST, ALT, GGT) are elevated

Total protein and albumin
will be decreased

Increased ammonia level
Elevated LDH

Increased serum bilirubin

Increased PT

Serum alkaline phosphatase

Increased lipids

Refer to Table 43-1 (pg.1370)

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20
Q

AST (SGOT) Range

A

10-40 U/mL

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21
Q

ALT (SPGT) Range

A

8-40 U/mL

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22
Q

Normal Albumin Range

A

3.5-5.2 g/dL

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23
Q

Normal PT & INR Range

A

PT: 11-13 secs

INR: <1.1

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24
Q

Alkaline Phosphate Range

A

52-142 U/L

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25
Q

Total Bilirubin Normal Range

A

0.3-1.0 U/L

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26
Q

At what total bilirubin level does jaundice manifest?

A

> 2.0 mg/dL

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27
Q

Liver Function Tests (LFTs)

A

Serum aminotransferases
* Levels increase primarily in liver disorders
* Used to monitor the course of hepatitis, cirrhosis, the effects of treatments that may be toxic to the liver

Alanine aminotransferase (ALT)
* Not specific to liver diseases
* Levels of AST may be increased in cirrhosis, hepatitis, and
liver cancer

Aspartate aminotransferase (AST)
* Levels are associated with cholestasis; alcoholic liver disease
Gamma-glutamyl transferase (GGT)

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28
Q

Diagnostic Evaluation

A

Diagnostic testing may include the following:
 CT & ultrasound
 Liver biopsy: confirms dx
 Analysis of ascitic fluid

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29
Q

Radio Isotope Liver Scan

A

May be performed to assess liver size, blood flow, & obstruction

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30
Q

Liver Elastography

A

Uses ultrasound-based vibration & scanning to identify liver fibrosis & determine its extent

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31
Q

Magnetic Resonance Elastography

A

Uses mechanical shear waves to identify stiff tissue

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32
Q

Nursing Role in Liver Biopsy

A

Prior to sending a patient for biopsy:
 Assess Vital Signs
 **Make sure coagulation studies completed
 Abnormalities are treated
 Compatible donor blood is available

Post-procedure:
 Assume the right side-lying position with a pillow placed under the right
costal margin.
 VS per orders
 Assess for S&S of bleeding

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33
Q

Which hepatic dysfunction is more common? Acute or Chronic?

A

Chronic

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34
Q

Hepatic Dysfunction

A

Acute or chronic - cirrhosis of the liver
 Liver failure associated with alcohol use
 Infection
 Fatty liver disease
 Nonalcoholic fatty liver disease (NAFLD)
 Nonalcoholic steatohepatitis (NASH)

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35
Q

Fatty Liver Disease

A

Accumulation of lipids in the liver

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36
Q

Manifestations of Hepatic Dysfunction

A

Jaundice

Portal hypertension

Ascites and varices

Hepatic encephalopathy or coma

Nutritional deficiencies

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37
Q

Jaundice

A

Caused by the inability of damaged liver cells to clear normal amounts of bilirubin from the blood

Yellow- or greenish- yellow sclera and skin

Bilirubin level exceeds 2 mg/dL

Hemolytic,
hepatocellular,
obstructive

Hereditary hyperbilirubinemia
- Hepatocellular and
obstructive jaundice are
most associated with
liver disease

38
Q

Stool changes w/jaundice

A

Clay-colored stool

39
Q

Steatorrhea

A

“Fatty Stool”

Bulky, pale foul-smelling stool

40
Q

Hemolytic Jaundice

A

Result of an increased destruction of RBCs
- Effect: Plasma is rapidly flooded w/bilirubin -> liver cannot excrete the bilirubin as quickly as it is formed

Encountered in patients w/ hemolytic blood transfusion reactions & other hemolytic disorders

41
Q

Clinical Manifestations of Hemolytic Jaundice

A

Bilirubin is predominately unconjugated or free

Urine & fecal urobilinogen levels are increased (urine is free of bilirubin)

Unless hyperbilirubinemia is extreme, pts do not experience complications

If prolonged:
- Predisposes to formation of pigments stones in gall bladder
- Severe jaundice (bilirubin exceeds 20-25 g/dL)
- Poses a CNS risk

42
Q

Hepatocellular Jaundice

A

Mild or severely ill
Lack of appetite, N/V, weight loss
Malaise, fatigue, weakness
Headache, chills, fever, infection

43
Q

Obstructive Jaundice

A

Maybe caused by occlusion of the bile duct from a gallstone, inflammatory process, tumor, or pressure from enlarged organ

Dark orange-brown urine, clay-colored
stools

Dyspepsia and intolerance of fats,
impaired digestion

Pruritus

44
Q

What skin changes occur w/jaundice?

A

Yellow pigmentation of the skin & pruritus

45
Q

Portal HTN

A

Obstructed blood flow through the liver results in increased pressure throughout the portal venous system

Cirrhosis is the most common cause

Results in: Ascites & Esophageal varices

46
Q

Physical Assessment Findings Associated w/ Portal HTN

A

Splenomegaly w/hypersplenism

47
Q

Portal HTN results in…

A

…ascites and esophageal varices

48
Q

Ascites

A

Accumulation of fluid in the abdominal cavity

49
Q

Pathophysiological Processes of Ascites

A

1) Portal HTN resulting in increased capillary pressure and obstruction of venous blood flow

2) Vasodilatation of splanchnic circulation (blood flow to the major abdominal organs)

3) Changes in the ability to metabolize aldosterone, increasing fluid retention

4) Decreased synthesis of albumin, decreasing serum osmotic pressure

5) Movement of albumin into the peritoneal cavity

50
Q

Clinical Manifestations of Ascites

A

Increased abdominal girth

Rapid weight gain

SOB due to enlarged abdomen

Distended veins may be visible over abdomen

Umbilical hernia may occur

Fluid and electrolyte imbalances are common

Edema of lower extremities

51
Q

Assessment of Ascites

A

Record abdominal girth and weight daily

Patient may have striae, distended veins, and umbilical hernia

Assess for fluid in abdominal cavity by percussion for shifting dullness or by fluid wave

Monitor for potential fluid and electrolyte imbalances

52
Q

Treatment of Ascites

A

Low Na+ diet

Diuretics

Bed rest

Paracentesis

Admin of albumin infusions: Ensure that BP doesn’t bottom out

Transjugular Intrahepatic Portosystemic Shunt (TIPS)

53
Q

Advantages of Transjugular Intrahepatic Portosystemic Shunt(TIPS)

A

Reduces portal HTN

Decreases Na+ retention

Prevents reoccurrence of fluid accumulation

54
Q

Medical Management of Ascites

A

Paracentesis

IV infusion of albumin

Provides only temporary removal of fluid

55
Q

Paracentesis

A

Removal of large volume (5-6L) ascites from peritoneal cavity

56
Q

Nursing Interventions for Paracentesis

A

Review labs

Monitor vitals

Post-procedure: assess puncture site for bleeding

Monitor for S&S of infection

57
Q

Nursing Management of Ascites

A

Strict I&O

Measure abdominal girth
daily

Daily weights

Close monitoring of respiratory status
Monitoring of labs:
 Serum ammonia
 Creatinine
 Electrolyte values

58
Q

Hepatic Encephalopathy & Coma

A

Life-threatening complication of liver disease seen in profound liver failure.

Accumulation of ammonia and other toxic metabolites in the blood

Survival is 40% after first bout w/ hepatic encephalopathy

Two major alterations underlie its development in acute and chronic liver disease

- Hepatic insufficiency: the inability of the liver to detoxify toxic by-products of metabolism

- Portosystemic shunting: collateral vessels develop allowing elements of the portal blood (laden with potentially toxic substances usually extracted by the liver) to enter the systemic circulation

Early signs: mental changes and motor disturbances

59
Q

Hepatic Insufficiency

A

The inability of the liver to detoxify toxic by-products of metabolism

60
Q

Portosystemic Shunting

A

Collateral vessels develop allowing elements of the portal blood (laden with potentially toxic substances usually extracted by the liver) to enter the systemic circulation

61
Q

Hepatic Encephalopathy Clinical Manifestations

A

Early Signs:
 Mental status changes
 Confusion
 Motor disturbances
 Asterixis- involuntary flapping of the hands
 Handwriting becomes difficult (Apraxia)
 Sleeps during day
 Insomnia at night

Late Signs:
 Becomes difficult to awaken
 Completely disorientated
 Coma
 Seizures

62
Q

Assessment & Stages of Hepatic Encephalopathy

A

Assessment
 EEG
 Changes in LOC
 Potential seizures
 Fetor hepaticus
 Monitor fluid, electrolyte, and ammonia levels

63
Q

Stage 1 of Hepatic Encephalopathy

A

Normal LOC

64
Q

Stage 2 of Hepatic Encephalopathy

A

Increased drowsiness

65
Q

Stage 3 of Hepatic Encephalopathy

A

Stuporous
Difficult to arouse

66
Q

Stage 4 of Hepatic Encephalopathy

A

Comatose
- May not respond to painful stimuli

67
Q

Medical Management of Hepatic Encephalopathy

A

Eliminate precipitating cause

Lactulose to reduce serum ammonia levels
 Oral
 NG tube
 Enema

IV glucose to minimize protein catabolism

Avoid protein restriction

Reduction of ammonia from GI tract by gastric suction, enemas, oral antibiotics

Discontinue sedatives, analgesics, and tranquilizers

Monitor or treat complications and infections

68
Q

Nursing Management of Hepatic Encephalopathy

A

Maintain safe environment, prevent injury: Pad all 4 siderails

Monitor for respiratory compromise due to depressed neurological status

Positions changes every 2 hours

Prevent skin breakdown, atelectasis

Neuro checks every 2-4 hours

Strict I & O

Daily weights

Monitor results of Ammonia testing, electrolytes

Daily handwriting

69
Q

Esophageal Varices

A

Occurs in 30% of patient with compensated cirrhosis and 60% of
patients with decompensated cirrhosis

First bleeding episode has a mortality rate of 10% to 30% depending on
severity

Manifestations include hematemesis, melena, general deterioration, and
shock

Patients with cirrhosis should undergo screening endoscopy every 2 to 3 years

70
Q

Clinical Manifestations of Esophageal Varices

A

Hematemesis

Melena

Mental deterioration

Shock

-Tachycardia

-Hypotension

-Cool clammy skin

71
Q

Melena

A

Black, tarry stool

72
Q

Treatment of Bleeding Varices

A

Treat for shock; administer oxygen

IV fluids, electrolytes, volume expanders, blood and blood products

Vasopressin, somatostatin, octreotide to decrease bleeding

Nitroglycerin in combination with vasopressin to reduce coronary vasoconstriction

Propranolol and nadolol to decrease portal pressure; used in combination with other treatment

Balloon tamponade

73
Q

Procedural Treatment of Bleeding Varices

A

Endoscopic sclerotherapy

Endoscopic variceal ligation (esophageal banding therapy)

Transjugular intrahepatic portosystemic shunt

Additional therapies

Surgical management
 Surgical bypass procedures
 Devascularization and transection
Endoscopic
Sclerotherapy

74
Q

Nursing Management of Esophageal Varices

A

Maintain a safe environment
 Prevent injury
 Bleeding
 Infection

Administer prescribed treatments and monitor for potential complications

Encourage deep breathing and position changes

Education and support of patient and family

75
Q

Viral Hepatitis

A

A systemic viral infection that causes
necrosis and inflammation of liver cells with characteristic symptoms and cellular and biochemical
changes

76
Q

Hep A

A

Spread via poor-hand hygeine; fecal oral route

Incubation: Between 2-6 weeks

Illness may last 4-8 weeks

Mortality rate <40 yrs: 0.5%

77
Q

Clinical Manifestations of Hep A

A

Mild flu-like symptoms

Low-grade fever

Anorexia

Later jaundice and dark urine, indigestion and epigastric distress, enlargement of liver and spleen

78
Q

Management of Hep A

A

Promote Prevention

-Good handwashing, safe H2O, & proper sewage disposal

-Vaccine

-Immunoglobulin injections (if not previously vaccinated) for sexual contacts and household members to provide passive immunity

Encourage bed rest during the acute stage

Provide nutritional support: frequent small feedings & IV fluids w/glucose

79
Q

Hep B

A

Transmitted through blood, saliva, semen, and vaginal secretions; sexually transmitted; transmitted to the infant at the time of birth

A major worldwide cause of cirrhosis and liver cancer Long incubation period: 1 to 6 months

80
Q

Clinical Manifestations of Hep B

A

Insidious and variable; similar to Hepatitis A

Loss of appetite

Dyspepsia

Abdominal pain

Generalized aching

Malaise, and weakness

Jaundice may or may not be evident

81
Q

Management of Hep B

A

Administer medications for chronic hepatitis type B including alpha-interferon and antiviral agents: entecavir (ETV) and tenofovir (TDF)

Promote bed rest and nutritional support-gradual resumption of physical activity

Promote vaccine: for persons at high risk, routine vaccination of infants

Passive immunization for those exposed

Standard precautions and infection control measures

Screening of blood and blood products

82
Q

Hep C

A

Transmitted by blood and sexual contact, including needle sticks and sharing of needles

The most common bloodborne infection

A cause of one-third of cases of liver cancer and the most common reason for liver transplant

Incubation period is variable: ranging from 15 to 160 days

Symptoms are usually mild

Chronic carrier state frequently occurs

83
Q

Management of Hep C

A

Administer antiviral medications

Educate patient on avoiding alcohol and medications that affect the liver

Promote prevention: public health programs to decrease needle sharing among drug users

Screening of blood supply

Use safety needle

84
Q

Hepatitis D

A

Only persons with Hepatitis B are at risk

Blood and sexual contact transmission

Use of IV or injection drugs, patients undergoing hemodialysis, and recipients of multiple blood transfusions

Likely to develop fulminant liver failure or chronic active hepatitis and cirrhosis

Incubation period between 30 and 150 days

Interferon alfa is the only licensed drug available in
the treatment for HDV infection

85
Q

Hepatitis E

A

Transmitted by fecal–oral route, contaminated water

Incubation period: 15 to
65 days

Resembles Hepatitis A; self-limiting, abrupt onset, not chronic

Prevention: good hygiene,
handwashing

86
Q

Pathophysiology of Hepatic Cirrhosis

A

Episodes of necrosis of hepatic celss

Destroyed liver cells replaced by scar tiss

Amount of scar tissue exceeds that of func liver tiss

87
Q

Alcoholic Hepatic Cirrhosis

A

Scar tissue characteristically surrounds the portal areas

88
Q

Postnecrotic Hepatic Cirrhosis

A

Broad bands of scar tissue from previous acute hepatitis

89
Q

Biliary Hepatic Cirrhosis

A

Scarring occurs in the liver around the bile ducts

90
Q

Clinical Manifestations of Hepatic Cirrhosis

A

Liver enlargement

Portal obstruction

Ascites

Infection and peritonitis

Varices, GI varices

Edema

Vitamin deficiency

Anemia

Mental deterioration

91
Q

What skin changes occur w/jaundice?

A

Yellow pigmentation of the skin & pruritus

NURS3313 Adult Health (27 decks)

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