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NSG 3850 Patho II.pdf, Exams of Nursing

Galen Health Institute - San AntonioNursing

NSG 3850 Patho II.pdf practice exercise

Typology: Exams

2025/2026

Available from 04/18/2026

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NSG 3850 Patho II: Exam 1 Review | New 2026 Update with complete
solutions
Liver Function & Pathophysiology
The liver is a complex metabolic factory responsible for synthesizing essential proteins, processing
waste products, and maintaining hematologic stability. Understanding these four core functions is
critical for identifying clinical manifestations of hepatic failure.
1. Albumin Synthesis
• Oncotic Pressure: Albumin is the primary protein responsible for maintaining osmotic
pressure within the vascular space.
• Hypoalbuminemia: When levels drop, fluid shifts from the blood vessels into the interstitial
tissues, causing systemic edema.
• Ascites: Low oncotic pressure in the portal circulation leads to significant fluid accumulation in
the peritoneal cavity.
• Molecular Transport: Albumin acts as a carrier for various hormones, ions, and medications
throughout the bloodstream.
2. Bilirubin Metabolism
• Conjugation Process: The liver takes unconjugated (indirect) bilirubin and converts it into
water-soluble conjugated (direct) bilirubin.
• Excretion Pathway: Once conjugated, bilirubin is secreted into the bile and eventually
eliminated from the body via stool.
• Jaundice Manifestation: A failure in conjugation or excretion leads to hyperbilirubinemia,
causing yellowing of the skin and sclera.
• Stool & Urine Changes: Obstruction leads to clay-colored stools (lack of bile) and dark, tea-
colored urine (excess bilirubin filtered by kidneys).
3. Clotting Factor Production
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NSG 3850 Patho II: Exam 1 Review | New 2026 Update with complete

solutions

Liver Function & Pathophysiology

The liver is a complex metabolic factory responsible for synthesizing essential proteins, processing waste products, and maintaining hematologic stability. Understanding these four core functions is critical for identifying clinical manifestations of hepatic failure.

1. Albumin Synthesis - Oncotic Pressure: Albumin is the primary protein responsible for maintaining osmotic pressure within the vascular space. - Hypoalbuminemia: When levels drop, fluid shifts from the blood vessels into the interstitial tissues, causing systemic edema. - Ascites: Low oncotic pressure in the portal circulation leads to significant fluid accumulation in the peritoneal cavity. - Molecular Transport: Albumin acts as a carrier for various hormones, ions, and medications throughout the bloodstream. 2. Bilirubin Metabolism - Conjugation Process: The liver takes unconjugated (indirect) bilirubin and converts it into water-soluble conjugated (direct) bilirubin. - Excretion Pathway: Once conjugated, bilirubin is secreted into the bile and eventually eliminated from the body via stool. - Jaundice Manifestation: A failure in conjugation or excretion leads to hyperbilirubinemia, causing yellowing of the skin and sclera. - Stool & Urine Changes: Obstruction leads to clay-colored stools (lack of bile) and dark, tea- colored urine (excess bilirubin filtered by kidneys). 3. Clotting Factor Production

  • Synthesis: The liver is responsible for producing essential Vitamin K-dependent clotting factors, including II, VII, IX, and X.
  • Coagulopathy: Hepatic dysfunction results in a prolonged Prothrombin Time (PT) and elevated INR, indicating slow clotting.
  • Hemorrhage Risk: Patients with liver failure are at high risk for spontaneous bleeding, petechiae, and easy bruising.
  • Fibrinogen & Platelets: The liver also synthesizes fibrinogen and regulates thrombopoietin, which is necessary for platelet production. 4. Ammonia Conversion
  • The Urea Cycle: The liver converts toxic ammonia, a byproduct of protein metabolism, into urea for safe removal.
  • Renal Excretion: Once converted to urea, it is transported to the kidneys and excreted from the body in urine.
  • Hyperammonemia: If the liver cannot process ammonia, levels rise in the blood, leading to systemic toxicity.
  • Hepatic Encephalopathy: High ammonia levels cross the blood-brain barrier, causing neurotoxicity, confusion, and asterixis. Nursing Alert: Lab Correlation When reviewing a patient with suspected liver failure, look for the 'Liver Failure Triad' in lab results: Low Albumin , Elevated Bilirubin , and Prolonged PT/INR. These findings collectively indicate a failure of the liver's synthetic and metabolic capabilities. Critical Thinking: Based on the functions described above, explain why a patient with end-stage cirrhosis might present with both a distended abdomen (ascites) and significant confusion (encephalopathy).

Viral Hepatitis: Pathophysiology & Transmission

  • Prevention: HBV vaccination (prevents HDV by preventing the necessary HBV co-infection). Hepatitis E (HEV)
  • Transmission: Fecal-oral route; most commonly through contaminated water supplies in developing regions.
  • Chronicity: No risk of chronic infection (acute only), except in severely immunocompromised individuals.
  • Prevention: Ensuring a safe water supply and proper sanitation; no widely available vaccine. Nursing Alert: Hepatitis Chronicity Hepatitis B, C, and D are the primary causes of chronic hepatitis, which can progress to cirrhosis and hepatocellular carcinoma. Hepatitis C is the most common reason for liver transplantation in the United States due to its high rate of chronicity.

Biliary Disorders: Cholelithiasis vs. Cholecystitis

Cholelithiasis (Gallstones)

  • Pathophysiology: The formation of calculi (stones) in the gallbladder, typically resulting from the precipitation of cholesterol or bilirubin from supersaturated bile.
  • Risk Factors: Classically described by the "4 F's": Female, Fat (BMI > 30), Forty (Age > 40), and Fertile (Multiparity or estrogen use).
  • Clinical Signs: Often asymptomatic; may present as biliary colic (episodic RUQ pain) that frequently occurs after consuming high-fat meals.
  • Progression: Pain occurs when stones move and temporarily obstruct the cystic or common bile duct. Cholecystitis (Inflammation)
  • Pathophysiology: Acute or chronic inflammation of the gallbladder wall, most commonly caused by a gallstone becoming impacted in the cystic duct.
  • Risk Factors: Secondary to cholelithiasis; also associated with prolonged fasting, total parenteral nutrition (TPN), or major trauma (acalculous cholecystitis).
  • Clinical Signs: Sharp RUQ pain, fever, and leukocytosis; characterized by a positive Murphy's Sign (arrest of inspiration during RUQ palpation).
  • Complications: Potential for gallbladder empyema (pus), gangrene, or perforation leading to life-threatening peritonitis. Clinical Application: Critical Thinking A patient presents with severe RUQ pain radiating to the right shoulder, nausea after eating a cheeseburger, and a positive Murphy's sign. Explain the physiological link between the high-fat meal and the onset of pain in the context of biliary obstruction.

Activity 3: Cirrhosis & Portal Hypertension Pathophysiology

Cirrhosis is the end-stage of chronic liver disease, characterized by the replacement of healthy liver tissue with fibrotic scar tissue. This structural change obstructs blood flow through the liver, leading to Portal Hypertension and a cascade of systemic complications. Review the pathophysiology-to-clinical manifestation flows below. Complication Pathophysiology to Clinical Manifestation Flow Esophageal Varices

  • Portal Hypertension: Increased pressure in the portal vein forces blood into collateral circulation. Vessel Engorgement: Fragile submucosal veins in the lower esophagus become distended and thin- walled. • Rupture Risk: High hydrostatic pressure or mechanical trauma (e.g., coughing, vomiting) leads to life-threatening upper GI bleeding. • Management: Non-selective beta-blockers (Propranol are used to decrease portal pressure and prevent initial hemorrhage.
  1. A nurse is caring for a patient with end-stage cirrhosis. Which laboratory result best explains the presence of 3+ pitting edema and significant ascites? A) Serum Albumin 1.8 g/dL B) Total Bilirubin 4.5 mg/dL C) Ammonia 90 μmol/L D) Platelets 85,000/mm³ Correct Answer: A Rationale: Albumin is responsible for maintaining colloid oncotic pressure. When the liver fails to synthesize albumin (hypoalbuminemia), fluid leaks from the intravascular space into the interstitial space (edema) and peritoneal cavity (ascites). Bilirubin (B) relates to jaundice, Ammonia (C) to encephalopathy, and Platelets (D) to bleeding risk.
  2. Which assessment finding should the nurse prioritize as a sign of worsening Hepatic Encephalopathy? A) Presence of spider angiomas on the chest B) A flapping tremor of the hands when extended (asterixis) C) Clay-colored stools and dark amber urine D) Intense pruritus and yellowing of the sclera Correct Answer: B Rationale: Asterixis is a hallmark sign of hepatic encephalopathy caused by the neurotoxic effects of elevated ammonia. Spider angiomas (A) relate to estrogen metabolism, while clay-colored stools (C) and jaundice (D) relate to biliary obstruction/bilirubin conjugation.
  3. A patient with a history of esophageal varices is admitted. Which medication should the nurse expect to administer to reduce the risk of variceal rupture?

A) Lactulose B) Vitamin K C) Propranolol D) Spironolactone Correct Answer: C Rationale: Non-selective beta-blockers like propranolol are used to reduce portal venous pressure, thereby decreasing the pressure in esophageal varices and reducing rupture risk. Lactulose (A) is for ammonia, Vitamin K (B) for clotting, and Spironolactone (D) for ascites.

  1. A nurse is reviewing the transmission of viral hepatitis. Which type is primarily transmitted via the fecal-oral route through contaminated food or water? A) Hepatitis B B) Hepatitis C C) Hepatitis D D) Hepatitis E Correct Answer: D Rationale: Hepatitis A and E are transmitted via the fecal-oral route ("The vowels come from the bowel"). Hepatitis B, C, and D are transmitted via blood and body fluids (parenteral).
  2. A patient is diagnosed with Cholecystitis. Which physical assessment finding is most consistent with this diagnosis? A) Pain in the left lower quadrant that radiates to the back B) Tenderness at McBurney's point

Correct Answer: A Rationale: Lactulose creates an acidic environment in the bowel that converts ammonia ( 𝑁 𝐻 3 NH 3 ) to ammonium ( 𝑁 𝐻 4

NH 4

), which is trapped in the gut and excreted via its laxative effect.

  1. A patient is suspected of having Hepatitis D. The nurse knows that this virus can only replicate in the presence of which other virus? A) Hepatitis A B) Hepatitis B C) Hepatitis C D) Hepatitis E Correct Answer: B Rationale: Hepatitis D is a defective virus that requires the HBsAg (Hepatitis B surface antigen) to replicate. Therefore, it only occurs as a co-infection or super-infection with Hepatitis B.
  2. Which clinical manifestation is specifically associated with the 'triple threat' of Status Asthmaticus pathophysiology? A) Increased peak flow meter readings B) Respiratory alkalosis on ABG C) Mucus plugging and refractory bronchospasm D) Rapid resolution with a single albuterol treatment Correct Answer: C Rationale: Status asthmaticus involves a "triple threat": intense bronchospasm, mucosal edema, and thick mucus plugs. It is refractory (unresponsive) to standard SABA treatments.
  3. A patient with cirrhosis presents with a distended abdomen and a fluid wave. Which hormonal system activation contributes to this fluid retention? A) Increased Insulin secretion

Correct Answer: C Rationale: Post-hepatic jaundice occurs when bile cannot flow into the duodenum due to an obstruction (like a stone), causing conjugated bilirubin to back up into the blood.

  1. A patient with HIV has a CD4+ count of 150 cells/mm³. The nurse should monitor for which AIDS- defining condition? A) Seasonal Influenza B) Pneumocystis jirovecii pneumonia (PJP) C) Iron deficiency anemia D) Type I Hypersensitivity Correct Answer: B Rationale: A CD4+ count below 200 cells/mm³ defines the transition to AIDS. PJP is a common opportunistic infection that occurs at this level of immunosuppression.
  2. During the 'Uncoating' stage of the viral life cycle, what is released into the host cell? A) Mature virions B) Viral mRNA C) Viral nucleic acid (DNA or RNA) D) Host cell ribosomes Correct Answer: C

Rationale: Uncoating is the enzymatic removal of the viral capsid, which releases the viral genome (nucleic acid) so replication can begin.

  1. A patient is experiencing anaphylaxis. Which physiological change leads to the profound hypotension seen in this Type I hypersensitivity reaction? A) Systemic vasoconstriction B) Massive histamine release causing systemic vasodilation C) Increased cardiac output D) Decreased capillary permeability Correct Answer: B Rationale: Histamine causes widespread vasodilation and increased capillary permeability (leaky vessels), leading to a drop in blood pressure and distributive shock.