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Examen

NURS 6630 Midterm Exam QUESTIONS WITH COMPLETE SOLUTIONS (100 % CORRECT AND VERIFIED) ALREADY PASSED!!

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Escrito en
2025/2026

Ace your NURS 6630 Midterm Exam with this comprehensive 180-question predictor for 2026–2027. Includes clinically verified multiple-choice questions with detailed rationales, covering all high-yield topics in advanced nursing concepts. Perfect for exam preparation, HESI review, and NCLEX readiness, designed to boost confidence and ensure mastery of course content.

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Subido en
6 de enero de 2026
Número de páginas
51
Escrito en
2025/2026
Tipo
Examen
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Question 1
A patient with long-standing diabetes presents with burning foot pain worse at night. Which
pathophysiologic mechanism is most responsible
A Microvascular ischemia causing Schwann cell apoptosis
B Immune-mediated demyelination
C NMDA receptor hyperactivation in dorsal horn neurons
D Sodium channel mutation in peripheral nerves

Answer A
Diabetic neuropathy is primarily caused by microvascular ischemia leading to Schwann cell
apoptosis and axonal degeneration. Chronic hyperglycemia damages small blood vessels
supplying peripheral nerves. Immune-mediated demyelination or channelopathies are not
typical in diabetic neuropathy.



Question 2
A patient on ACE inhibitors develops persistent cough. What is the underlying mechanism
A Increased prostaglandin synthesis
B Decreased angiotensin II
C Bradykinin accumulation
D Alveolar irritation from metabolites

Answer C
ACE breaks down bradykinin. Inhibition leads to bradykinin accumulation, which irritates
the airway and produces a dry, persistent cough.



Question 3
Which lab best differentiates SIADH from cerebral salt wasting
A Serum sodium
B Urine osmolality
C Serum uric acid
D Plasma ADH

Answer C
SIADH presents with low serum uric acid due to dilutional effects and renal excretion,
whereas cerebral salt wasting typically shows normal or high uric acid because of volume
depletion.



Question 4
An elderly patient on warfarin is started on trimethoprim-sulfamethoxazole. INR rises
dramatically. What is the mechanism
A CYP2C9 inhibition
B Increased vitamin K synthesis
C Increased albumin binding
D Reduced hepatic clearance via CYP3A4

,3|Page


Answer A
TMP-SMX inhibits CYP2C9, the enzyme responsible for warfarin metabolism, causing
accumulation and supratherapeutic INR.



Question 5
Most accurate early indicator of acute kidney injury
A Serum creatinine
B BUN
C Urine output
D GFR

Answer C
Urine output declines before serum creatinine rises because creatinine may lag hours to days
behind the injury. Early oliguria is the most sensitive early indicator.



Question 6
A patient with metabolic acidosis has Kussmaul respirations. What is the purpose
A Increase PaCO₂
B Increase oxygen delivery
C Blow off CO₂ to raise pH
D Compensate for hypokalemia

Answer C
Kussmaul respirations are a respiratory compensatory mechanism to decrease PaCO₂ and
raise blood pH in metabolic acidosis, commonly seen in diabetic ketoacidosis.



Question 7
Which drug class is contraindicated in pregnancy due to fetal renal agenesis
A Beta-blockers
B ACE inhibitors
C Calcium channel blockers
D Thiazides

Answer B
ACE inhibitors block fetal renin-angiotensin system, leading to oligohydramnios and renal
agenesis.



Question 8
Which condition causes widened pulse pressure
A Aortic stenosis
B Cardiac tamponade

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C Aortic regurgitation
D Pulmonary embolism

Answer C
Aortic regurgitation leads to high systolic and low diastolic pressure, producing a wide pulse
pressure.



Question 9
A patient with Graves disease has tachycardia and tremors. Best initial drug
A Methimazole
B Propylthiouracil
C Propranolol
D Radioactive iodine

Answer C
Beta-blockers control adrenergic symptoms immediately. Antithyroid drugs take days to
weeks to reduce hormone levels.



Question 10
Most sensitive test for early diabetic ketoacidosis
A Serum glucose
B Urine ketones
C Serum beta-hydroxybutyrate
D ABG pH

Answer C
Beta-hydroxybutyrate is the predominant ketone in DKA and rises before urine ketones or pH
changes.



Question 11
A patient with chronic hypertension develops concentric left ventricular hypertrophy. Which
molecular mechanism is responsible
A Increased preload causing sarcomere lengthening
B Pressure overload causing parallel sarcomere replication
C RAAS suppression decreasing myocyte size
D Increased intracellular calcium causing eccentric dilation

Answer B
Pressure overload stimulates parallel sarcomere replication, resulting in concentric
hypertrophy. Volume overload causes sarcomeres in series leading to eccentric hypertrophy.
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