NSG 233 Med Surg 3 Exam 3: (Latest 2026/2027 Update) Hepatic, Respiratory,
& Genitourinary Disorders | Q&A | Grade A | 100% Correct (Verified Answers)
– Nursing Program
Subject: NSG 233 – Medical-Surgical Nursing / Advanced Concepts
Source: NSG 233 Med Surg 3 Exam 3 Blueprint 2026/2027
Format: Q&A Guide with Rationale | Verified Grade A
1. What is the pathophysiology of hepatic dysfunction?
Correct Answer: Liver cells become destroyed and replaced with fibrotic tissue (cirrhosis). Blood can
no longer flow easily through the liver back to the right side of the heart.
1. Fibrosis leads to portal hypertension.
2. Impaired synthetic function (albumin, clotting factors).
2. What are some causes of hepatic dysfunction?
Correct Answer: Infectious agents (hepatitis virus), anorexia (inadequate organ perfusion), metabolic
disorders (acidosis), toxins (ETOH), medications (acetaminophen), malnutrition (often ETOH induced).
1. Acetaminophen overdose is leading cause of acute liver failure.
2. Chronic alcohol use causes fatty liver, hepatitis, cirrhosis.
3. Non-alcoholic fatty liver disease (NAFLD) increasing cause.
3. What is cirrhosis and what can cause it?
Correct Answer: Damage to liver cells → inability to clear bilirubin → yellowing of skin and dark
urine. Increase intrahepatic vascular resistance → elevate portal pressure → portal hypertension.
Causes: chronic alcohol, viral hepatitis (B,C), NASH, autoimmune.
1. Leads to complications: ascites, varices, encephalopathy, coagulopathy.
2. Child-Pugh and MELD scores predict prognosis.
3. Irreversible; treatment focuses on slowing progression.
4. How many stages does hepatic encephalopathy have and what should the nurse assess?
Correct Answer: 5 stages (West Haven criteria). Assess mental (neurological) status change and motor
disturbances.
1. Stage 1: normal LOC with lethargy, impaired writing.
2. Stage 2: drowsiness, confusion, asterixis, fetor hepaticus.
3. Stage 3: stuporous, incoherent speech, increased DTR.
4. Stage 4: comatose, no response to pain.
5. Stage 5: deep coma.
, 5. What is asterixis and in what stage do you see it?
Correct Answer: Flapping tremor of the hands. Appears in Stage 2 hepatic encephalopathy.
1. Also called "liver flap."
2. Test: patient extends arms and dorsiflexes wrists → repetitive flapping.
3. Indicates metabolic encephalopathy.
6. What is fetor hepaticus, what does it indicate, and in what stage do you see it?
Correct Answer: Musty, sweet, garlic-like odor of breath caused by inability of liver to filter sulfurous
compounds. Indicates hepatic encephalopathy. Appears in Stage 2.
1. Caused by mercaptans in bloodstream.
2. Distinct from uremic fetor (ammonia, urine breath).
3. Late sign of liver failure.
7. What is constructional apraxia and in what stage do you see it?
Correct Answer: Neurological disorder making it difficult or impossible to build, assemble, or draw
objects, even with physical ability. Stage 2 hepatic encephalopathy.
1. Test: ask patient to draw a clock or star.
2. Inability indicates organic brain dysfunction.
3. Impairment of visuospatial processing.
8. What medications are used for hepatic encephalopathy?
Correct Answer: Lactulose (removes ammonia via stool; goal 2-3 soft stools/day). Antibiotics reduce
ammonia-forming bacteria: metronidazole, rifaximin, neomycin.
1. Lactulose acidifies colon, traps ammonia as ammonium ion.
2. Rifaximin is non-absorbable antibiotic; fewer side effects.
3. Monitor electrolytes with diarrhea.
9. What is lactose and when to use it? (lactulose)
Correct Answer: Lactulose is a laxative used primarily to decrease ammonia levels in patients with
hepatic encephalopathy.
1. Dose adjusted to produce 2-3 soft bowel movements daily.
2. Not absorbed; metabolized by colonic bacteria.
3. Assess for dehydration and electrolyte imbalance.
10. What is the pathophysiology of ascites?
Correct Answer: 1. Increased portal pressure → portal hypertension → vasodilation → fluid leak into
abdominal cavity → decreased blood volume → decreased albumin inhibits fluid return → RAAS
activated → sodium/water retention; liver fails to metabolize aldosterone → increased sodium/water
retention.
1. Two main factors: portal hypertension and hypoalbuminemia.
2. Low albumin reduces oncotic pressure.
3. Sodium retention worsens fluid accumulation.
& Genitourinary Disorders | Q&A | Grade A | 100% Correct (Verified Answers)
– Nursing Program
Subject: NSG 233 – Medical-Surgical Nursing / Advanced Concepts
Source: NSG 233 Med Surg 3 Exam 3 Blueprint 2026/2027
Format: Q&A Guide with Rationale | Verified Grade A
1. What is the pathophysiology of hepatic dysfunction?
Correct Answer: Liver cells become destroyed and replaced with fibrotic tissue (cirrhosis). Blood can
no longer flow easily through the liver back to the right side of the heart.
1. Fibrosis leads to portal hypertension.
2. Impaired synthetic function (albumin, clotting factors).
2. What are some causes of hepatic dysfunction?
Correct Answer: Infectious agents (hepatitis virus), anorexia (inadequate organ perfusion), metabolic
disorders (acidosis), toxins (ETOH), medications (acetaminophen), malnutrition (often ETOH induced).
1. Acetaminophen overdose is leading cause of acute liver failure.
2. Chronic alcohol use causes fatty liver, hepatitis, cirrhosis.
3. Non-alcoholic fatty liver disease (NAFLD) increasing cause.
3. What is cirrhosis and what can cause it?
Correct Answer: Damage to liver cells → inability to clear bilirubin → yellowing of skin and dark
urine. Increase intrahepatic vascular resistance → elevate portal pressure → portal hypertension.
Causes: chronic alcohol, viral hepatitis (B,C), NASH, autoimmune.
1. Leads to complications: ascites, varices, encephalopathy, coagulopathy.
2. Child-Pugh and MELD scores predict prognosis.
3. Irreversible; treatment focuses on slowing progression.
4. How many stages does hepatic encephalopathy have and what should the nurse assess?
Correct Answer: 5 stages (West Haven criteria). Assess mental (neurological) status change and motor
disturbances.
1. Stage 1: normal LOC with lethargy, impaired writing.
2. Stage 2: drowsiness, confusion, asterixis, fetor hepaticus.
3. Stage 3: stuporous, incoherent speech, increased DTR.
4. Stage 4: comatose, no response to pain.
5. Stage 5: deep coma.
, 5. What is asterixis and in what stage do you see it?
Correct Answer: Flapping tremor of the hands. Appears in Stage 2 hepatic encephalopathy.
1. Also called "liver flap."
2. Test: patient extends arms and dorsiflexes wrists → repetitive flapping.
3. Indicates metabolic encephalopathy.
6. What is fetor hepaticus, what does it indicate, and in what stage do you see it?
Correct Answer: Musty, sweet, garlic-like odor of breath caused by inability of liver to filter sulfurous
compounds. Indicates hepatic encephalopathy. Appears in Stage 2.
1. Caused by mercaptans in bloodstream.
2. Distinct from uremic fetor (ammonia, urine breath).
3. Late sign of liver failure.
7. What is constructional apraxia and in what stage do you see it?
Correct Answer: Neurological disorder making it difficult or impossible to build, assemble, or draw
objects, even with physical ability. Stage 2 hepatic encephalopathy.
1. Test: ask patient to draw a clock or star.
2. Inability indicates organic brain dysfunction.
3. Impairment of visuospatial processing.
8. What medications are used for hepatic encephalopathy?
Correct Answer: Lactulose (removes ammonia via stool; goal 2-3 soft stools/day). Antibiotics reduce
ammonia-forming bacteria: metronidazole, rifaximin, neomycin.
1. Lactulose acidifies colon, traps ammonia as ammonium ion.
2. Rifaximin is non-absorbable antibiotic; fewer side effects.
3. Monitor electrolytes with diarrhea.
9. What is lactose and when to use it? (lactulose)
Correct Answer: Lactulose is a laxative used primarily to decrease ammonia levels in patients with
hepatic encephalopathy.
1. Dose adjusted to produce 2-3 soft bowel movements daily.
2. Not absorbed; metabolized by colonic bacteria.
3. Assess for dehydration and electrolyte imbalance.
10. What is the pathophysiology of ascites?
Correct Answer: 1. Increased portal pressure → portal hypertension → vasodilation → fluid leak into
abdominal cavity → decreased blood volume → decreased albumin inhibits fluid return → RAAS
activated → sodium/water retention; liver fails to metabolize aldosterone → increased sodium/water
retention.
1. Two main factors: portal hypertension and hypoalbuminemia.
2. Low albumin reduces oncotic pressure.
3. Sodium retention worsens fluid accumulation.
