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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
Total Bilirubin Normal Range
0.3-1.0 U/L
26
At what total bilirubin level does jaundice manifest?
>2.0 mg/dL
27
Liver Function Tests (LFTs)
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)
28
Diagnostic Evaluation
Diagnostic testing may include the following:  CT & ultrasound  Liver biopsy: confirms dx  Analysis of ascitic fluid
29
Radio Isotope Liver Scan
May be performed to assess liver size, blood flow, & obstruction
30
Liver Elastography
Uses ultrasound-based vibration & scanning to identify liver fibrosis & determine its extent
31
Magnetic Resonance Elastography
Uses mechanical shear waves to identify stiff tissue
32
Nursing Role in Liver Biopsy
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
33
Which hepatic dysfunction is more common? Acute or Chronic?
Chronic
34
Hepatic Dysfunction
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)
35
Fatty Liver Disease
Accumulation of lipids in the liver
36
Manifestations of Hepatic Dysfunction
Jaundice Portal hypertension Ascites and varices Hepatic encephalopathy or coma Nutritional deficiencies
37
Jaundice
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
Stool changes w/jaundice
Clay-colored stool
39
Steatorrhea
"Fatty Stool" Bulky, pale foul-smelling stool
40
Hemolytic Jaundice
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
Clinical Manifestations of Hemolytic Jaundice
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
Hepatocellular Jaundice
Mild or severely ill Lack of appetite, N/V, weight loss Malaise, fatigue, weakness Headache, chills, fever, infection
43
Obstructive Jaundice
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
What skin changes occur w/jaundice?
Yellow pigmentation of the skin & pruritus
45
Portal HTN
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
Physical Assessment Findings Associated w/ Portal HTN
Splenomegaly w/hypersplenism
47
Portal HTN results in...
...ascites and esophageal varices
48
Ascites
Accumulation of fluid in the abdominal cavity
49
Pathophysiological Processes of Ascites
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
Clinical Manifestations of Ascites
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
Assessment of Ascites
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
Treatment of Ascites
Low Na+ diet Diuretics Bed rest Paracentesis Admin of albumin infusions: Ensure that BP doesn't bottom out Transjugular Intrahepatic Portosystemic Shunt (TIPS)
53
Advantages of Transjugular Intrahepatic Portosystemic Shunt(TIPS)
Reduces portal HTN Decreases Na+ retention Prevents reoccurrence of fluid accumulation
54
Medical Management of Ascites
Paracentesis IV infusion of albumin Provides only temporary removal of fluid
55
Paracentesis
Removal of large volume (5-6L) ascites from peritoneal cavity
56
Nursing Interventions for Paracentesis
Review labs Monitor vitals Post-procedure: assess puncture site for bleeding Monitor for S&S of infection
57
Nursing Management of Ascites
Strict I&O Measure abdominal girth daily Daily weights Close monitoring of respiratory status Monitoring of labs:  Serum ammonia  Creatinine  Electrolyte values
58
Hepatic Encephalopathy & Coma
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
Hepatic Insufficiency
The inability of the liver to detoxify toxic by-products of metabolism
60
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
61
Hepatic Encephalopathy Clinical Manifestations
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
Assessment & Stages of Hepatic Encephalopathy
Assessment  EEG  Changes in LOC  Potential seizures  Fetor hepaticus  Monitor fluid, electrolyte, and ammonia levels
63
Stage 1 of Hepatic Encephalopathy
Normal LOC
64
Stage 2 of Hepatic Encephalopathy
Increased drowsiness
65
Stage 3 of Hepatic Encephalopathy
Stuporous Difficult to arouse
66
Stage 4 of Hepatic Encephalopathy
Comatose - May not respond to painful stimuli
67
Medical Management of Hepatic Encephalopathy
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
Nursing Management of Hepatic Encephalopathy
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
Esophageal Varices
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
Clinical Manifestations of Esophageal Varices
Hematemesis Melena Mental deterioration Shock -Tachycardia -Hypotension -Cool clammy skin
71
Melena
Black, tarry stool
72
Treatment of Bleeding Varices
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
Procedural Treatment of Bleeding Varices
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
Nursing Management of Esophageal Varices
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
Viral Hepatitis
A systemic viral infection that causes necrosis and inflammation of liver cells with characteristic symptoms and cellular and biochemical changes
76
Hep 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
Clinical Manifestations of Hep A
Mild flu-like symptoms Low-grade fever Anorexia Later jaundice and dark urine, indigestion and epigastric distress, enlargement of liver and spleen
78
Management of Hep 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
Hep B
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
Clinical Manifestations of Hep B
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
Management of Hep B
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
Hep C
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
Management of Hep C
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
Hepatitis D
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
Hepatitis E
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
Pathophysiology of Hepatic Cirrhosis
Episodes of necrosis of hepatic celss Destroyed liver cells replaced by scar tiss Amount of scar tissue exceeds that of func liver tiss
87
Alcoholic Hepatic Cirrhosis
Scar tissue characteristically surrounds the portal areas
88
Postnecrotic Hepatic Cirrhosis
Broad bands of scar tissue from previous acute hepatitis
89
Biliary Hepatic Cirrhosis
Scarring occurs in the liver around the bile ducts
90
Clinical Manifestations of Hepatic Cirrhosis
Liver enlargement Portal obstruction Ascites Infection and peritonitis Varices, GI varices Edema Vitamin deficiency Anemia Mental deterioration
91
What skin changes occur w/jaundice?
Yellow pigmentation of the skin & pruritus

NURS3313 Adult Health (27 decks)

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