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NSG3850/NSG 3850 Exam 4 | Pathophysiology for Nurses II | Galen | 26/27 Guaranteed(PDF)

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INSTANT PDF DOWNLOAD — Verified NSG 3850 Exam 4 | Pathophysiology for Nurses II | Galen College of Nursing | 2026–2027 Updated (PDF) resource featuring actual exam questions, NGN‑style case studies, and complete rationales. Coverage includes advanced cellular injury, inflammatory and immune responses, cardiovascular and respiratory pathophysiology, renal and hepatic disorders, endocrine and metabolic dysfunctions, neurological and musculoskeletal conditions, hematologic/oncologic disease processes, and complex multisystem disorders. Emphasis on clinical reasoning, patient safety, therapeutic communication, and evidence‑based nursing interventions ensures exam readiness. Designed for guaranteed 100% correctness and alignment with Galen College curriculum, this study guide is ideal for students searching NSG 3850 Exam 4 PDF, Pathophysiology for Nurses II Study Guide, NSG 3850 Test Bank, NSG 3850 Verified Answers, NSG 3850 Exam Prep 2026–2027, Advanced Pathophysiology Workbook, and NCLEX‑Style Exam Solution.

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,NSG3850/NSG 3850 Exam 4 | Pathophysiology for
1. A client with heart failure has crackles in all lung fields, jugular venous distention, and 3+ pitting
edema. Which medication should the nurse expect to administer first?

A) Digoxin

B) Furosemide

C) Enalapril

D) Carvedilol

Correct Answer: Furosemide



Rationale: Furosemide is a loop diuretic that rapidly reduces preload by promoting diuresis, directly
relieving the pulmonary congestion and peripheral edema seen in this client. Digoxin, enalapril, and
carvedilol are important chronic therapies but do not address the acute fluid overload as the
immediate priority.



2. A client is prescribed digoxin for heart failure. Which assessment finding is most indicative of
digoxin toxicity?

A) Heart rate of 62 beats per minute

B) Anorexia, nausea, and vomiting

C) A 1-kg weight gain over 2 days

D) An increase in urine output

Correct Answer: Anorexia, nausea, and vomiting



Rationale: Anorexia, nausea, and vomiting are early and common signs of digoxin toxicity. Other signs
include visual disturbances like yellow-green halos and cardiac arrhythmias. A heart rate of 62 is
within normal limits, weight gain suggests fluid retention, and increased urine output is a desired
effect of diuretic therapy.



3. A client with chronic heart failure and a preserved ejection fraction is most likely to have which
underlying condition as the primary cause?

A) Coronary artery disease

B) Hypertension

,C) Valvular heart disease

D) Dilated cardiomyopathy

Correct Answer: Hypertension



Rationale: Hypertension is the most common cause of heart failure with preserved ejection fraction
(HFpEF). Chronic high blood pressure leads to left ventricular hypertrophy and diastolic dysfunction.
Coronary artery disease, valvular disease, and cardiomyopathy can also cause HFpEF but are less
common than hypertension.



4. A client with an acute ST-elevation myocardial infarction (STEMI) is receiving fibrinolytic therapy.
Which finding indicates that reperfusion has been successful?

A) Persistent ST-segment elevation

B) Worsening of chest pain

C) Resolution of ST-segment elevation

D) New onset of bundle branch block

Correct Answer: Resolution of ST-segment elevation



Rationale: Successful reperfusion is indicated by the resolution of ST-segment elevation (at least a
50% reduction) and relief of chest pain. Persistent ST elevation suggests failed reperfusion. New
bundle branch block is a complication, not a sign of successful reperfusion.



5. A client with a history of an anterior wall myocardial infarction develops a harsh holosystolic
murmur at the left sternal border and acute pulmonary edema. Which complication is most likely?

A) Papillary muscle rupture

B) Ventricular septal rupture

C) Left ventricular free wall rupture

D) Pericarditis

Correct Answer: Ventricular septal rupture



Rationale: Ventricular septal rupture is a complication of anterior wall MI, producing a harsh
holosystolic murmur and acute pulmonary edema from a left-to-right shunt. Papillary muscle rupture

, is more common with inferior MIs. Free wall rupture causes tamponade, and pericarditis causes a
friction rub.



6. A client with chronic aortic regurgitation has a widened pulse pressure and a water-hammer pulse.
Which pathophysiological mechanism explains these findings?

A) Decreased stroke volume from reduced forward flow

B) Increased stroke volume from volume overload and rapid diastolic runoff

C) Decreased systemic vascular resistance from vasodilation

D) Increased systemic vascular resistance from vasoconstriction

Correct Answer: Increased stroke volume from volume overload and rapid diastolic runoff



Rationale: Aortic regurgitation causes a volume overload of the left ventricle, increasing stroke
volume. The rapid runoff of blood back into the left ventricle during diastole causes a rapid fall in
diastolic pressure, resulting in a widened pulse pressure and a bounding, water-hammer pulse.



7. A client with severe aortic stenosis experiences syncope during exertion. Which pathophysiological
mechanism is the primary cause of this symptom?

A) Fixed obstruction to left ventricular outflow causing inadequate cerebral perfusion

B) Decreased systemic vascular resistance from vasodilation

C) Increased vagal tone leading to bradycardia

D) Embolization of aortic valve calcifications to the brain

Correct Answer: Fixed obstruction to left ventricular outflow causing inadequate cerebral perfusion



Rationale: In aortic stenosis, the fixed obstruction limits the increase in cardiac output during
exertion, leading to inadequate cerebral perfusion and syncope. Vasodilation is not the primary
mechanism, bradycardia is not characteristic, and embolization is a complication of endocarditis, not
aortic stenosis.



8. A client with infective endocarditis has a history of a prosthetic mitral valve. Which microorganism
is most likely responsible for early prosthetic valve endocarditis (within 1 year of surgery)?

A) Streptococcus viridans

B) Staphylococcus aureus

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