CARE OF CLIENTS WITH PROBLEM IN

NUTRITION, AND GASTRO-INTESTINAL,

METABOLISM AND ENDOCRINE,
PERCEPTION AND COORDINATION, (ACUTE
STUDENT’S ACTIVITY SHEET AND CHRONIC)
BS NURSING / THIRD YEAR
Session # 8 (2 hours and 30 minutes)

Materials:
Book, pen and notebook, projector
LESSON TITLE: HEPATIC DISORDERS: REVIEW OF
SYSTEM, DIAGNOSTIC EVALUATION, AND HEPATIC
DYSFUNCTION MANIFESTATIONS
LEARNING OUTCOMES:
Upon completion of this lesson, the nursing student can:
1. Review the functions of the liver. References:
2. Identify the common diagnostic tests used to determine liver
Smeltzer, S., Bare, B., Hinkle, J., & Cheever, K.
function
(2008). Brunner &Suddarth’s Textbook of
3. Point out common manifestations of a patient with liver
Medical-Surgical Nursing 12th Edition.
problems.
Lippincott Williams &Wilkins
4. Recognize medical and nursing management related to the
disorder.

LESSON REVIEW / PREVIEW OR HOOK ACTIVITY (1 minute)

The instructor will ask the students to list the 8 functions of the liver.
1. Glucose metabolism
2. Ammonia conversion
3. Protein metabolism
4. Fata metabolism
5. Vitamin and iron storage
6. Bile formation
7. Bilirubin excretion
8. Drug metabolism

MAIN LESSON (2 hours and 9 minutes)

The students will study and read their book about this lesson (Chapter 39 of the book).

DIAGNOSTIC EVALUATION

A. Liver Function Tests

Serum Enzyme Activity: Serum Aminotransferases, Alkaline Phosphatase
Serum Protein Concentrations: Albumin and Globulins
Total serum protein: 7.0–7.5 g/dL (70–75 g/L)
Serum albumin: 4.0–5.5 g/dL (40–55 g/L)
Serum globulin: 1.7–3.3 g/dL (17–33 g/L)
Bilirubin: Serum bilirubin, direct: 0–0.3 mg/dL (0–5.1 umol/L
Serum bilirubin, total: 0–0.9 mg/dL (1.7–20.5 umol/L)
Ammonia: 15–45 ug/dL (11–32 umol/L)
Clotting Factors: Prothrombin time: 100% or 12–16 seconds

Serum Aminotransferases (Transaminases): sensitive indicators of liver cells injury and useful in detecting acute
liver disease
1. Alanine Aminotransferase (ALT): 5–35 units (2.4–17 U/L)

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 - increased primarily in liver disorders and may be used to monitor the course of hepatitis or cirrhosis
2. Aspartate Aminotransferase (AST): 10–40 units (4.8–19 U/L)
- increased if there is damage in the heart, liver, skeletal muscle, and kidney
3. Gamma-glutamyl Transferase (GGT): 10–48 IU/L
- increased with cholestasis caused by alcoholic liver disease

Serum Alkaline Phosphatase: 20-140 IU/L

- elevated levels confirm liver disease of origin

B. Liver Biopsy
Before:
1. Coagulation studies (PT, PTT, Platelet count)
2. Signed consent
3. Vital signs

During:
1. Expose the right side of the patient’s upper abdomen
2. Instruct the patient to inhale and exhale deeply several times, finally to exhale, and to hold breath at the end of
expiration. The physician promptly introduces the biopsy needle by way of the transthoracic (intercostal) or
transabdominal (subcostal) route, penetrates the liver, aspirates, and withdraws.
3. Instruct the patient to resume breathing.

After:
1. Assist the patient to turn onto the right side; place a pillow under the costal margin, and caution
the patient to remain in this position, recumbent and immobile, for several hours.
2. Instruct the patient to avoid coughing or straining.
3. Measure and record the patient’s pulse, respiratory rate, and blood pressure at 10- to 15-minute intervals for the
first hour, then every 30 minutes for the next 1 to 2 hours or until the patient’s condition stabilizes.
4. If the patient is discharged after the procedure, instruct the patient to avoid heavy lifting and strenuous activity
for 1 week.
Complications: Bleeding and Bile Peritonitis

C. Other Tests: Ultrasonography, Computed Tomography (CT), and Magnetic Resonance Imaging

MANIFESTATIONS OF HEPATIC DYSFUNCTION

A. JAUNDICE
When the bilirubin concentration in the blood is abnormally elevated, all the body tissues, including the sclerae
and the skin, become yellow-tinged or greenish-yellow

Hepatocellular Jaundice
Hepatocellular jaundice is caused by the inability of damaged liver cells to clear normal amounts of bilirubin
from the blood. The cellular damage may be caused by hepatitis viruses, other viruses that affect the liver (yellow
fever virus, Epstein-Barr virus), medications or chemical toxins (carbon tetrachloride, chloroform, phosphorus,
arsenicals, certain medications), alcohol, or cirrhosis of the liver.

Obstructive Jaundice
Obstructive jaundice resulting from extrahepatic obstruction may be caused by occlusion of the bile duct
from a gallstone, an inflammatory process, a tumor, or pressure from an enlarged organ (liver, gallbladder). Bile
cannot flow normally into the intestine and becomes backed up into the liver substance. It is then reabsorbed into
the blood and carried throughout the entire body, staining the skin, mucous membranes, and sclerae. It is excreted
in the urine, which becomes deep orange and foamy. Because of the decreased amount of bile in the intestinal
tract, the stools become light or clay-colored.

B. PORTAL HYPERTENSION
Increased blood pressure caused by obstructed blood flow through the damaged liver throughout the portal
venous system. Two major consequences of portal hypertension are ascites and varices.

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C. ASCITES
Accumulation of large amounts of albumin-rich fluid, 15 L or more into the peritoneal cavity. Results from: portal
hypertension; failure of the liver to metabolize aldosterone (sodium and water retention); failure of the liver to metabolize
albumin (hypoalbuminemia).

Pathophysiology
1. Portal hypertension and the resulting increase in capillary pressure and obstruction of venous blood flow
through the damaged liver are contributing factors.
2. The vasodilation that occurs in the splanchnic circulation (the arterial supply and venous drainage of the GI
system from the distal esophagus to the mid-rectum including the liver and spleen) is also a suspected causative
factor.
3. The failure of the liver to metabolize aldosterone increases sodium and water retention by the kidney. Sodium
and water retention, increased intravascular fluid volume, increased lymphatic flow, and decreased synthesis
of albumin by the damaged liver all contribute to the movement of fluid from the vascular system into the
peritoneal space. The process becomes self-perpetuating; loss of fluid into the peritoneal space causes further
sodium and water retention by the kidney in an effort to maintain the vascular fluid volume.
4. As a result of liver damage, large amounts of albumin- rich fluid, 15 L or more, may accumulate in the peritoneal
cavity as ascites. (Ascites may also occur with disorders such as cancer, kidney disease, and heart failure.)
5. With the movement of albumin from the serum to the peritoneal cavity, the osmotic pressure of the serum
decreases. This, combined with increased portal pressure, results in movement of fluid into the peritoneal cavity.

Clinical Manifestations
1. Increased abdominal girth and rapid weight gain - common
2. Shortness of breath
3. Striae and distended veins may be visible over the abdominal wall
4. Fluid and electrolyte imbalances are common

Assessment and Diagnostic Findings

1. By percussing for shifting dullness or by detecting a fluid wave
2. Daily measurement and recording of abdominal girth and body weight are essential

Medical Management
1. Dietary modification
a. Avoid table salt, salty foods, salted butter and margarine, and all ordinary canned and frozen
foods (foods that are not specifically prepared for low-sodium diets). Use salt substitutes such as lemon
juice, oregano, and thyme.
b. Liberal use of powdered, low-sodium milk and milk products
If fluid accumulation is not controlled with this regimen, the daily sodium allowance may be reduced further
to 500 mg, and diuretics may be administered.
At home: 2-g sodium, approximately 10% of patients with ascites respond to these measures alone.

2. Diuretics: Use of diuretics along with sodium restriction is successful in 90% of patients with ascites.
Spironolactone (Aldactone) - is most often the first-line therapy in patients with ascites from cirrhosis.
Furosemide (Lasix) may be added but should be used cautiously
Ammonium chloride and acetazolamide (Diamox) are contraindicated

a. Daily weight loss should not exceed 1 to 2 kg (2.2 to 4.4 lb) in patients with ascites and peripheral edema
or 0.5 to 0.75 kg (1.1 to 1.65 lb) in patients without edema.
b. Fluid restriction is not attempted unless the serum sodium concentration is very low.

3. Bed rest - In patients with ascites, an upright posture is associated with activation of the renin-angiotensin-
aldosterone system and sympathetic nervous system. This results in reduced renal glomerular
filtration and sodium excretion and a decreased response to loop diuretics. Bed rest may be a useful
therapy, especially for patients whose condition is refractory to diuretics.

4. Paracentesis - is the removal of fluid (ascites) from the peritoneal cavity through a small surgical incision or
puncture made through the abdominal wall under sterile conditions. Performed primarily for diagnostic

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 examination of ascitic fluid, for treatment of massive ascites that is resistant to nutritional and diuretic
therapy.

Before:
1. Instruct the patient to void.
2. Place patient in upright position on edge of bed with feet supported on stool, or place in chair. Fowler’s
position should be used for the patient confined to bed.
3. Place sphygmomanometer cuff around patient’s arm to allow monitoring of blood pressure during the
procedure.

During:
1. The physician, using aseptic technique, inserts the trocar through a puncture wound below the umbilicus.
The fluid drains from the abdomen through a drainage tube into a container.
2. Help the patient maintain position throughout procedure.
3. Measure and record blood pressure at frequent intervals from the beginning of the procedure.
4. Monitor the patient closely for signs of vascular collapse: pallor, increased pulse rate, or decreased blood
pressure.

After:
1. Return patient to bed or to a comfortable sitting position.
2. Measure, describe, and record the fluid collected.
3. Label samples of fluid and send to laboratory.
4. Continue to monitor vital signs every 15 minutes for 1 hour, every 30 minutes over 2 hours, then every
hour over 2 hours and then every 4 hours. Monitor temperature after procedure and every 4 hours.
5. Assess for hypovolemia, electrolyte loss, changes in mental status, and encephalopathy.
6. Check puncture site when taking vital signs for bleeding and leakage.
7. Provide patient education (especially if patient is discharged after procedure) regarding monitoring for
bleeding or excess drainage from puncture site, avoiding heavy lifting or straining, changing
position slowly, and monitoring for fever.

Nursing Management
1. Monitor intake and output
2. Measure abdominal girth
3. Weigh daily
4. Monitor serum ammonia and electrolyte levels
5. Teach patient self-care:
a. avoid alcohol intake
b. low-sodium diet
c. take medications as prescribed
d. check with the physician before taking any new medications
e. proper skin care
f. weigh daily
g. watch for and report signs and symptoms of complications

D. ESOPHAGEAL VARICES
Are varicosities that develop from elevated pressures transmitted to all of the veins that drain into the
portal system. They are prone to rupture and often are the source of massive hemorrhages from the upper GI
tract and the rectum.
This condition is almost always caused by portal hypertension, which results from obstruction of the portal
venous circulation within the damaged liver.

Factors that contribute to hemorrhage:

Lifting heavy objects; Straining at stool; Sneezing, coughing, or vomiting; Esophagitis; Irritation of vessels
by poorly chewed foods or irritating fluids; Reflux of stomach contents (especially alcohol); and Salicylates and any
medication that erodes the esophageal mucosa

Pathophysiology
1. Portal hypertension (caused by resistance to portal flow and increased portal venous inflow)

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 2. Development of pressure gradient of 12 mm Hg or greater between portal vein and inferior vena cava (portal
pressure gradient)
3. Venous collaterals develop from high portal system pressure to systemic veins in esophageal plexus,
hemorrhoidal plexus, and retroperitoneal veins
4. Abnormal varicoid vessels form in any of above locations
5. Vessels may rupture causing life-threatening hemorrhage

Clinical Manifestations
1. Bleeding esophageal varices: hematemesis, melena, or general deterioration in mental or physical status and
often has a history of alcohol abuse
2. Signs and symptoms of shock (cool clammy skin, hypotension, tachycardia) may be present

Assessment and Diagnostic Tests

1. Endoscopy – identifies bleeding site; it is recommended that these patients undergo screening endoscopy every
2 years in an effort to identify and treat large varices, which are the ones most likely to bleed
2. Portal Hypertension Measurements
Portal hypertension may be suspected if dilated abdominal veins and hemorrhoids are detected
3. Laboratory Tests
Liver function tests, such as serum aminotransferases, bilirubin, alkaline phosphatase, and serum
proteins

Medical Management
1. Evaluate the extent of bleeding.
2. Monitor vital signs continuously and observe for signs of bleeding (hematemesis and melena).
3. Note for signs of potential hypovolemia, such as cold clammy skin, tachycardia, a drop in blood pressure, de-
creased urine output, restlessness, and weak peripheral pulses.
4. Administer oxygen.
5. Administer IV fluids with electrolytes and volume expanders.
6. Transfusion of blood components also may be required.
7. Insert an indwelling urinary catheter.
8. Pharmacologic Therapy
a. Vasopressin (Pitressin)
Vasopressin constricts distal esophageal and proximal gastric veins, thus reducing the inflow into
the portal system and therefore the portal pressure. Vital signs and the presence or absence of blood in the
gastric aspirate indicate the effectiveness of vasopressin. Monitoring of fluid intake and output and
electrolyte levels is necessary because hyponatremia may develop and vasopressin may have an
antidiuretic effect.
b. Combination of vasopressin with nitroglycerin (administered by the IV, sublingual, or transdermal route)
has been effective in reducing or preventing the side effects (constriction of coronary vessels and angina)
caused by vasopressin alone.
c. Somatostatin and octreotide (Sandostatin)
These medications cause selective splanchnic vasoconstriction and are used mainly in the
management of active hemorrhage.
d. Propranolol (Inderal) and nadolol (Corgard), beta-blocking agents that decrease portal pressure, are the
most common medications used both to prevent a first bleeding episode in patients with known varices and
to prevent rebleeding.
9. Balloon Tamponade
Pressure is exerted on the cardia (upper orifice of the stomach) and against the bleeding varices by a
double-balloon tamponade (Sengstaken-Blakemore tube) to control bleeding. The tube has four openings, each
with a specific purpose: gastric aspiration, esophageal aspiration, gastric balloon inflation, and esophageal
balloon inflation.
10. Endoscopic Therapies
In endoscopic sclerotherapy, also referred to as injection sclerotherapy, a sclerosing agent is injected
through a fiberoptic endoscope into the bleeding esophageal varices to promote thrombosis and eventual
sclerosis. The procedure has been used successfully to treat acute GI hemorrhage but is not recommended for
prevention of first and subsequent variceal bleeding episodes.
11. Esophageal Banding Therapy (Variceal Band Ligation)
In variceal banding, also referred to as esophageal variceal ligation (EVL), a modified endoscope

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 loaded with an elastic rubber band is passed through an overtube directly onto the varix (or varices) to be
banded. After the bleeding varix is suctioned into the tip of the endoscope, the rubber band is slipped over the
tissue, causing necrosis, ulceration, and eventual sloughing of the varix. Variceal banding also significantly
reduces the rebleeding rate, mortality, procedure-related complications, and the number of sessions needed to
eradicate varices. Esophageal band ligation has replaced sclerotherapy as the treatment of choice in the
management of esophageal varices.
12. Transjugular Intrahepatic Portosystemic Shunting (TIPS)
In 10% to 20% of patients for whom urgent band ligation or sclerotherapy and medications are not
successful in eradicating bleeding, a TIPS procedure can effectively control acute variceal hemorrhage by
rapidly lowering portal pressure. TIPS is also indicated for those patients who rebleed after pharmacologic or
endoscopic prophylaxis has failed.

Surgical Management
1. Surgical Bypass Procedures
2. Devascularization and Transection

Nursing Management
1. Monitor the patient’s physical condition and evaluating emotional responses and cognitive status.
2. Monitor and record vital signs and assess the patient’s nutritional and neurologic status.
3. If complete rest of the esophagus is indicated because of bleeding, initiate parenteral nutrition. Gastric suction
usually is initiated to keep the stomach as empty as possible and to prevent straining and vomiting. The patient
often complains of severe thirst, which may be relieved by frequent oral hygiene and moist sponges to the lips.
4. Closely monitor the blood pressure.
5. Administer Vitamin K and multiple blood transfusions for blood loss.

E. HEPATIC ENCEPHALOPATHY AND COMA

Results from the accumulation of ammonia and other toxic metabolites in the blood. Ammonia
accumulates because damaged liver cells fail to detoxify and convert ammonia to urea. The increased ammonia
concentration in the blood causes brain dysfunction and damage, resulting in hepatic encephalopathy.

Pathophysiology
Two major alterations underlie its development in acute and chronic liver disease.
1. First, hepatic insufficiency may result in encephalopathy because of the inability of the liver to detoxify toxic
byproducts of metabolism.
2. Second, portal-systemic shunting, in which collateral vessels develop as a result of portal hypertension, allows
elements of the portal blood (laden with potentially toxic substances usually extracted by the liver) to enter the
systemic circulation.
3. Ammonia is considered the major etiologic factor in the development of encephalopathy. It enters the brain and
excites peripheral benzodiazepine-type receptors on astrocyte cells, thus increasing neurosteroid synthesis;
this then stimulates gamma-aminobutyric acid (GABA) neurotransmission. GABA causes depression of the
central nervous system. Ammonia inhibits neurotransmission and synaptic regulation, producing sleep and
behavior patterns associated with hepatic encephalopathy.
4. Circumstances that increase serum ammonia levels tend to aggravate or precipitate hepatic encephalopathy.
The largest source of ammonia is the enzymatic and bacterial digestion of dietary and blood proteins in the GI
tract. Ammonia from these sources increases as a result of GI bleeding (bleeding esophageal varices, chronic
GI bleeding), a high-protein diet, bacterial infection, or uremia.
5. The ingestion of ammonium salts also increases the blood ammonia level. In the presence of alkalosis or
hypokalemia, increased amounts of ammonia are absorbed from the GI tract and from the renal tubular fluid.
6. Conversely, serum ammonia is decreased by elimination of protein from the diet and by the administration of
antibiotic agents, such as neomycin sulfate (Mycifradin, Neo-fradin), which reduce the number of intestinal
bacteria capable of converting urea to ammonia.
7. Other factors unrelated to increased serum ammonia levels that can cause hepatic encephalopathy in
susceptible patients include excessive diuresis, dehydration, infections, surgery, fever, and some medications
(sedatives, tranquilizers, analgesics, and diuretics that cause potassium loss).
8. Additional causes include elevated levels of serum manganese, as well as changes in the types of circulating
amino acids, mercaptans, and levels of dopamine and other neurotransmitters in the central nervous system .
Mercaptans are toxic metabolites of sulfur-containing compounds that are excreted by the liver under normal
conditions. Mercaptans and these other so- called “false” neurotransmitters may be generated from an intestinal

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Education (Department of Nursing) 6 of 10
 source or from metabolism of protein by the liver and, with defective hepatic clearance, may precipitate
encephalopathy.

Clinical Manifestations
Stages
I Normal level of consciousness with periods of lethargy and euphoria; reversal of day–night sleep patterns
Earliest symptoms: minor mental changes and motor disturbances (slightly confused, has alterations in
mood, becomes unkempt, and has altered sleep patterns: sleep during the day and have restlessness
and insomnia at night); Asterixis (flapping tremor of the hands); Constructional apraxia

II Increased drowsiness; disorientation; inappropriate behavior; mood swings; agitation

Asterixis; fetor hepaticus; abnormal EEG with generalized slowing.

III Stuporous; difficult to rouse; sleeps most of time; marked confusion; incoherent speech
Asterixis; increased deep tendon reflexes; rigidity of extremities; EEG markedly abnormal.

IV Comatose; may not respond to painful stimuli

Absence of asterixis; absence of deep tendon reflexes; flaccidity of extremities; EEG markedly abnormal.

Assessment and Diagnostic Findings

1. Electroencephalogram (EEG) – shows generalized slowing, an increase in the amplitude of brain waves, and
characteristic triphasic waves
2. Fetor Hepaticus – a sweet, slightly fecal odor to the breath (freshly mowed grass, acetone, or old wine odor)

Medical Management
1. Lactulose (Cephulac) to reduce serum ammonia levels. It acts by several mechanisms that promote the
excretion of ammonia in the stool: (1) ammonia is kept in the ionized state, resulting in a decrease in colon pH,
reversing the normal passage of ammonia from the colon to the blood; (2) evacuation of the bowel takes place,
which de- creases the ammonia absorbed from the colon; and (3) the fecal flora are changed to organisms that
do not produce ammonia from urea. Two or three soft stools per day are desirable; this indicates that lactulose
is performing as intended.
The patient receiving lactulose is monitored closely for the development of watery diarrheal stools,
because they indicate a medication overdose.
2. IV administration of glucose to minimize protein breakdown, administration of vitamins to correct deficiencies,
and correction of electrolyte imbalances (especially potassium).
3. Administer antibiotics: Neomycin, metronidazole (Flagyl), and rifaximin (Xifaxan) have been used to reduce
levels of ammonia-forming bacteria in the colon.
4. Dietary
- Keep daily protein intake between 1.0 and 1.5 g/kg (40 to 60 g/day), depending on the degree of
decompensation.
- Moderately restrict protein intake in patients who are comatose or who have encephalopathy that is
refractory to lactulose and antibiotic therapy.
- Avoid long-term restriction of dietary protein to less than 1 g/kg daily.
- Use vegetable or dairy proteins as most patients can tolerate a diet of vegetable protein up to 120 g/day.
- Advise patients and families about foods that are high in protein (meat, eggs), which may need to be
eliminated from the diet for the short term to reduce production of ammonia.
- Provide small, frequent meals and an evening snack of complex carbohydrates to avoid protein loading.
5. Additional principles of management of hepatic encephalopathy:
- Assess neurologic status frequently.
- Monitor mental status by keeping a daily record of handwriting and arithmetic performance.
- Record Fluid intake and output and body weight each day.
- Measure and record vital signs every 4 hours.
- Monitor serum ammonia level daily.
- Monitor electrolyte status.
- Discontinue sedatives, tranquilizers, and analgesic medications.
- Administer Benzodiazepine antagonists such as flumazenil (Romazicon) to improve encephalopathy.

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F. EDEMA AND BLEEDING
Generalized edema may develop from hypoalbuminemia from decreased hepatic production
of albumin. The production of blood clotting factors by the liver is also reduced, leading to an increased incidence
of bruising, epistaxis, bleeding from wounds, and, as described above, GI bleeding.

G. VITAMIN DEFICIENCY
1. Vitamin A deficiency: resulting in night blindness and eye and skin changes
2. Thiamine deficiency: leading to beriberi, polyneuritis, and Wernicke-Korsakoff psychosis
3. Riboflavin deficiency: resulting in characteristic skin and mucous membrane lesions
4. Pyridoxine deficiency: resulting in skin and mucous membrane lesions and neurologic changes
5. Vitamin C deficiency: resulting in the hemorrhagic lesions of scurvy
6. Vitamin K deficiency: resulting in hypoprothrombinemia, characterized by spontaneous bleeding and
ecchymoses
7. Folic acid deficiency: resulting in macrocytic anemia

H. METABOLIC ABNORMALITIES
Blood glucose level may be abnormally high shortly after a meal (a diabetic-type glucose tolerance test
result), but hypoglycemia may occur during fasting because of decrease hepatic glycogen reserves and decreased
gluconeogenesis.
Many endocrine abnormalities also occur with liver dysfunction because the liver cannot properly
metabolize hormones, including androgens and sex hormones. Failure of the damaged liver to inactivate estrogens
normally can cause gynecomastia, amenorrhea, testicular atrophy, loss of pubic hair in the male, menstrual
irregularities in the female, and other disturbances of sexual function and sex characteristics.

I. PRURITUS AND OTHER SKIN CHANGES

Resulting from biliary obstruction commonly develop severe itching (pruritus) due to retention of bile
salts. Vascular (or arterial) spider angiomas (spider’s legs) may develop on the skin, generally above the waistline.
Reddened palms (“liver palms” or palmar erythema) may also develop.

CHECK FOR UNDERSTANDING (15 minutes)

The instructor will prepare 10-15 questions that can enhance critical thinking skills. Students will work by themselves to
answer these questions and write the rationale for each question.
Multiple Choice

(For 1-10 items, please refer to the questions in the Rationalization Activity)

RATIONALIZATION ACTIVITY (DURING THE FACE TO FACE INTERACTION WITH THE STUDENTS)
The instructor will now rationalize the answers to the students and will encourage them to ask questions and to discuss
among their classmates for 20 minutes.

1. A 52-year-old man was referred to the clinic due to increased abdominal girth. He is diagnosed with ascites by the
presence of a fluid thrill and shifting dullness on percussion. After administering diuretic therapy, which nursing action would
be most effective in ensuring safe care?
A. Measuring serum potassium for hyperkalemia
B. Assessing the client for hypervolemia
C. Measuring the client’s weight weekly
D. Documenting precise intake and output
Answer: _____
Rationale:________________________________________________________________________________________
_________________________________________________________________________________________________
_________________________________________________________________________________________________

2. Sharon has cirrhosis of the liver and develops ascites. What intervention is necessary to decrease the excessive
accumulation of serous fluid in her peritoneal cavity?

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Education (Department of Nursing) 8 of 10
A. Restrict fluids
B. Encourage ambulation
C. Increase sodium in the diet
D. Give antacids as prescribed
Answer: _____
Rationale:________________________________________________________________________________________
_________________________________________________________________________________________________
_________________________________________________________________________________________________

3. A client with cirrhosis begins to develop ascites. Spironolactone (Aldactone) is prescribed to treat the ascites. The nurse
should monitor the client closely for which of the following drug-related side effects?
A. Constipation
B. Hyperkalemia
C. Irregular pulse
D. Dysuria
Answer: _____
Rationale:________________________________________________________________________________________
_________________________________________________________________________________________________
_________________________________________________________________________________________________

4. For which of the following positions would be appropriate for a client with severe ascites?
A. Fowler’s
B. Side-lying
C. Reverse Trendelenburg
D. Sims’
Answer: _____
Rationale:________________________________________________________________________________________
_________________________________________________________________________________________________
_________________________________________________________________________________________________

5. You’re caring for Jane, a 57 y.o. patient with liver cirrhosis who developed ascites and requires paracentesis. Before her
paracentesis, you instruct her to:
A. Empty her bladder.
B. Lie supine in bed.
C. Remain NPO for 4 hours.
D. Clean her bowels with an enema.
Answer: _____
Rationale:________________________________________________________________________________________
_________________________________________________________________________________________________
_________________________________________________________________________________________________

6. Nurse Farrah is providing care for Kristoff who has jaundice. Which statement indicates that the nurse understands the
rationale for instituting skin care measures for the client?
A. “Jaundice is associated with pressure ulcer formation.”
B. “Jaundice impairs urea production, which produces pruritus.”
C. “Jaundice produces pruritus due to impaired bile acid excretion.”
D. “Jaundice leads to decreased tissue perfusion and subsequent breakdown.”
Answer: _____
Rationale:________________________________________________________________________________________
_________________________________________________________________________________________________
_________________________________________________________________________________________________

7. Develop a teaching care plan for Angie who is about to undergo a liver biopsy. Which of the following points do you
include?
A. “You’ll need to lie on your stomach during the test.”
B. “You’ll need to lie on your right side after the test.”
C. “During the biopsy you’ll be asked to exhale deeply and hold it.”
D. “The biopsy is performed under general anesthesia.”

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Education (Department of Nursing) 9 of 10
Answer: _____
Rationale:________________________________________________________________________________________
_________________________________________________________________________________________________
_________________________________________________________________________________________________

8. Immediately after a liver biopsy, which of the following complications should the client be closely monitored for?
A. Abdominal cramping
B. Hemorrhage
C. Nausea and vomiting
D. Potential infection
Answer: _____
Rationale:________________________________________________________________________________________
_________________________________________________________________________________________________
_________________________________________________________________________________________________

9. Which of the following tests confirms that the origin of the disorder is in the liver?
A. Alanine Aminotransferase (ALT)
B. Aspartate Aminotransferase (AST)
C. Gamma-glutamyl Transferase (GGT)
D. Serum Alkaline Phosphatase
Answer: _____
Rationale:________________________________________________________________________________________
_________________________________________________________________________________________________
_________________________________________________________________________________________________
10. Mr. Hasakusa is in end-stage liver failure. Which interventions should the nurse implement when addressing hepatic
encephalopathy? Select all that apply.
A. Assessing the client’s neurologic status every 2 hours
B. Monitoring the client’s hemoglobin and hematocrit levels
C. Evaluating the client’s serum ammonia level
D. Monitoring the client’s handwriting daily
E. Preparing to insert an esophageal tamponade tube
F. Making sure the client’s fingernails are short
Answer: _____
Rationale:________________________________________________________________________________________
_________________________________________________________________________________________________
_________________________________________________________________________________________________

LESSON WRAP-UP (5 minutes)

Teacher directs the student to mark (encircle) their place in the work tracker which is simply a visual to help students track
how much work they have accomplished and how much work there is left to do. This tracker will be part of the student
activity sheet.

You are done with the session! Let’s track your progress.

Sell It To Us
The instructor will ask the students to write a jingle that explains the main idea of the lesson (the students
will only choose 1 topic).

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