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APEA 3P PREDICTOR EXAM , 180 VERIFIED QUESTIONS WITH CORRECT ANSWERS AND DETAILED RATIONALES (PATHO, PHARM & PHYSICAL ASSESSMENT BUNDLE) 100% CORRECT ALREADY GRADED A+

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Escrito en
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Prepare confidently for the APEA 3P Predictor Exam 2026 with this comprehensive 180-question study bundle covering Pathophysiology, Pharmacology, and Physical Assessment. Each question includes the correct answer and detailed rationale to enhance understanding and clinical reasoning. Designed to mirror real APEA and NP board-style exams, this guide helps you master key 3P concepts, improve test performance, and strengthen diagnostic and prescribing skills. Ideal for nurse practitioner students preparing for certification or final semester exams. Updated for 2026 to reflect current guidelines and evidence-based practice.

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Subido en
13 de octubre de 2025
Número de páginas
87
Escrito en
2025/2026
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Examen
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APEA 3P PREDICTOR EXAM 2026-2027 , 180 VERIFIED QUESTIONS
WITH CORRECT ANSWERS AND DETAILED RATIONALES (PATHO,
PHARM & PHYSICAL ASSESSMENT BUNDLE) 100% CORRECT
ALREADY GRADED A+




1. A 58-year-old man with chronic smoking history presents with progressive
dyspnea, chronic productive cough, and barrel chest. Pulmonary function testing
shows a decreased FEV1/FVC ratio and increased total lung capacity. Which of the
following pathophysiologic mechanisms best explains his clinical presentation?
A. Destruction of alveolar walls with loss of elastic recoil and airspace
enlargement.
B. Thickening of bronchial mucosa with increased mucous gland hyperplasia only.
C. Interstitial fibrosis with restrictive ventilatory defect.
D. Autoimmune-mediated alveolar capillary membrane injury.
E. Pulmonary vascular occlusion due to microthrombi.
Correct answer: A.
Rationale: The classic emphysematous COPD picture (barrel chest, decreased
FEV1/FVC, increased TLC) is due to protease–antiprotease imbalance causing
destruction of alveolar walls, loss of elastic recoil, and airspace enlargement —
leading to air trapping. B (mucous gland hyperplasia) is more a feature of chronic
bronchitis and would not explain increased TLC. C (interstitial fibrosis) causes
restrictive pattern (reduced TLC). D (autoimmune alveolar injury) suggests diffuse

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alveolar damage/ARDS, not the chronic obstructive pattern. E (pulmonary
microthrombi) causes pulmonary hypertension features, not the airflow obstruction
pattern.


2. A patient with untreated type 1 diabetes develops severe polyuria, polydipsia,
nausea, and Kussmaul respirations. Labs show blood glucose 650 mg/dL, serum
bicarbonate 10 mEq/L, anion gap metabolic acidosis, and positive serum ketones.
Which intracellular process primarily contributes to ketone production in this
condition?
A. Increased beta-oxidation of free fatty acids in hepatic mitochondria producing
acetyl-CoA.
B. Increased glycolysis producing excess lactate.
C. Increased glycogen synthesis in the liver.
D. Inhibition of lipolysis in adipose tissue.
E. Enhanced citric acid cycle activity using acetyl-CoA.
Correct answer: A.
Rationale: In insulin deficiency, peripheral tissues cannot use glucose efficiently,
so hormone-sensitive lipase activity increases, releasing free fatty acids which
undergo hepatic beta-oxidation producing large amounts of acetyl-CoA. Excess
acetyl-CoA is shunted to ketogenesis, producing acetoacetate and beta-
hydroxybutyrate → ketoacidosis. B (lactate) relates to anaerobic glycolysis, not
ketone formation. C and D are opposite of what occurs. E (enhanced TCA cycle) is
limited because oxaloacetate is diverted to gluconeogenesis, reducing TCA flux
and favoring ketone formation.


3. A middle-aged woman presents with weight gain, easy bruising, purple
abdominal striae, hypertension, and hyperglycemia. Lab testing shows elevated

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cortisol levels that do not suppress with low-dose dexamethasone but suppress with
high-dose dexamethasone. Which of the following is the most likely cause?
A. ACTH-secreting pituitary adenoma (Cushing disease).
B. Ectopic ACTH production from a small cell lung carcinoma.
C. Primary adrenal hyperplasia.
D. Iatrogenic corticosteroid administration.
E. Adrenal carcinoma producing cortisol.
Correct answer: A.
Rationale: Pituitary ACTH-secreting adenomas typically cause elevated ACTH
with cortisol levels that fail to suppress with low-dose dexamethasone but DO
suppress with high-dose dexamethasone (relative suppression). Ectopic ACTH
(B) usually shows no suppression even with high-dose dexamethasone. Primary
adrenal causes (C, E) produce cortisol with low ACTH and would not show
ACTH-driven suppression patterns. Iatrogenic steroids (D) cause low endogenous
ACTH due to feedback suppression.


4. A 70-year-old man presents with progressive difficulty initiating movement and
a shuffling gait. On exam he has masked facies, resting tremor, bradykinesia, and
rigidity. Pathologic examination reveals degeneration of dopaminergic neurons in
which brain region and deposition of which neuronal inclusion?
A. Substantia nigra pars compacta; Lewy bodies (alpha-synuclein).
B. Caudate nucleus; neurofibrillary tangles (tau).
C. Hippocampus; amyloid plaques.
D. Cerebellar Purkinje cells; eosinophilic inclusions of polyglutamine.
E. Motor cortex; TDP-43 inclusions.
Correct answer: A.
Rationale: Parkinson disease features degeneration of dopaminergic neurons in

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the substantia nigra pars compacta with intraneuronal Lewy bodies composed
of alpha-synuclein. B describes Huntington disease (caudate atrophy), C relates to
Alzheimer disease, D references spinocerebellar ataxias, and E relates to some
forms of ALS/FTD.


5. In congestive heart failure due to left ventricular systolic dysfunction, which of
the following compensatory mechanisms initially increases cardiac output but
ultimately contributes to disease progression and remodeling?
A. Activation of the renin–angiotensin–aldosterone system (RAAS) causing
vasoconstriction and sodium retention.
B. Decreased sympathetic outflow.
C. Downregulation of natriuretic peptides.
D. Immediate regeneration of myocardial myocytes.
E. Increased pulmonary capillary oncotic pressure.
Correct answer: A.
Rationale: In heart failure, reduced renal perfusion stimulates RAAS, causing
vasoconstriction, sodium/water retention, and increased afterload/preload — which
initially maintains perfusion but chronically promotes ventricular remodeling,
fibrosis, and worsened heart failure. B is false (sympathetic increases). C is
incorrect — natriuretic peptides increase initially as a compensatory mechanism
(but are insufficient). D is false — adult myocyte regeneration is limited. E is
incorrect — pulmonary capillary hydrostatic pressure increases, causing
pulmonary edema.


6. A patient presents with sudden right-sided hemiparesis and expressive aphasia.
CT confirms an ischemic infarct in the distribution of the left middle cerebral
artery (MCA). Which area is most likely primarily affected to produce expressive
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