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BIOL 252 Human Anatomy & Physiology II w/Lab EXAM with Questions and Answers/Plus a Rationale Updated 2026 A+/Instant Download PDF

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BIOL 252 Human Anatomy & Physiology II w/Lab EXAM with Questions and Answers/Plus a Rationale Updated 2026 A+/Instant Download PDF

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BIOL 252 Human Anatomy & Physiology II w/Lab
EXAM with Questions and Answers/Plus a Rationale
Updated 2026 A+/Instant Download PDF
EXAM COVERAGE


1. Cardiovascular System: Blood, Heart, and Hemodynamics


2. Lymphatic System and Immunity


3. Respiratory System and Gas Exchange


4. Urinary System, Fluid, Electrolyte, and Acid-Base Balance


5. Digestive System, Nutrition, and Metabolism


6. Reproductive Systems and Embryological Development

1. A patient with severe dehydration presents with an elevated hematocrit and increased plasma
osmolarity. Which of the following physiological compensatory mechanisms is primarily
responsible for restoring extracellular fluid volume in this acute phase?

A. Secretion of antidiuretic hormone (ADH) from the posterior pituitary to increase water
reabsorption in the collecting ducts.

B. Release of atrial natriuretic peptide (ANP) from cardiac muscle cells to promote profound
natriuresis and diuresis.

C. Decreased sympathetic nervous system activity leading to vasodilation of afferent renal
arterioles.

D. Direct stimulation of the adrenal cortex by low blood pressure to increase aldosterone-
independent water clearance.

CORRECT ANSWER : A

Rationale: Dehydration increases plasma osmolarity, which is detected by hypothalamic
osmoreceptors, triggering ADH release from the posterior pituitary; ADH inserts aquaporins

, into renal collecting ducts to increase water reabsorption. Option B is incorrect because ANP is
released in response to hypervolemia, not dehydration. Option C decreases blood pressure
rather than restoring it. Option D is incorrect because aldosterone reabsorbs sodium and water,
but ADH is the primary responder to hyperosmolarity.

2. A patient with chronic obstructive pulmonary disease (COPD) develops compensatory metabolic
changes to offset chronic respiratory acidosis. Which of the following arterial blood gas and
renal laboratory profiles best illustrates this compensation?

A. Decreased pH, decreased partial pressure of carbon dioxide, and decreased plasma
bicarbonate.

B. Normal pH, increased partial pressure of carbon dioxide, and decreased plasma bicarbonate.

C. Decreased or near-normal pH, elevated partial pressure of carbon dioxide, and
significantly elevated plasma bicarbonate.

D. Elevated pH, decreased partial pressure of carbon dioxide, and normal plasma bicarbonate.

CORRECT ANSWER : C

Rationale: Chronic respiratory acidosis results from CO2 retention due to alveolar
hypoventilation, which the kidneys compensate for by reabsorbing and generating excess
bicarbonate over days to weeks, bringing the pH back toward normal. Option A describes
metabolic acidosis or uncompensated respiratory conditions. Option B describes acute
uncompensated changes. Option D describes respiratory alkalosis.

3. During the rapid depolarization phase of a ventricular myocardial action potential, which of the
following cellular events occurs?

A. Inward movement of potassium ions through slow delayed rectifier channels.

B. Inward movement of sodium ions through voltage-gated fast sodium channels.

C. Outward movement of calcium ions through transient T-type calcium channels.

D. Closure of all membrane ion channels resulting in a transient resting plateau.

CORRECT ANSWER : B

Rationale: Phase 0 of the ventricular myocardial action potential is characterized by a rapid
influx of sodium ions through voltage-gated fast sodium channels, causing membrane
depolarization. Option A occurs during repolarization. Option C describes calcium movement
during the plateau phase (Phase 2), but calcium enters, not leaves. Option D is incorrect
because the membrane is highly active during this phase.

,4. A biomedical researcher is analyzing an enzyme kinetic curve for a digestive hydrolase in the
small intestine. Under conditions of high substrate concentration, the reaction velocity reaches a
maximum limit ($V_{max}$). Which of the following interventions would successfully increase
this maximal velocity ($V_{max}$)?

A. Adding a competitive inhibitor to the reaction mixture.

B. Decreasing the temperature of the enzymatic assay below physiological norms.

C. Adding more active enzyme molecules to the incubation mixture.

D. Further increasing the concentration of the substrate by a factor of ten.

CORRECT ANSWER : C

Rationale: The maximal velocity ($V_{max}$) of an enzyme-catalyzed reaction is directly
dependent on the total enzyme concentration; adding more active enzyme increases $V_{max}$.
Option A affects the apparent $K_m$ but not $V_{max}$. Option B decreases reaction rates.
Option D does not change $V_{max}$ because the enzyme is already saturated with substrate at
high concentrations.

5. A patient presents with classic signs of left-sided heart failure, including orthopnea and
paroxysmal nocturnal dyspnea. Which of the following hemodynamic shifts directly causes these
respiratory symptoms?

A. Systemic venous congestion leading to increased capillary hydrostatic pressure in the lower
extremities.

B. Elevated pulmonary capillary hydrostatic pressure driving fluid transudation into the
pulmonary interstitium and alveoli.

C. Decreased oncotic pressure within the pulmonary arterial bed secondary to hepatic protein
synthesis failure.

D. Bronchospasm triggered by reflex parasympathetic activation of pulmonary stretch receptors.

CORRECT ANSWER : B

Rationale: Left-sided heart failure causes blood to back up into the pulmonary circulation,
increasing pulmonary capillary hydrostatic pressure beyond the oncotic pressure, which forces
fluid into the alveoli and impairs gas exchange. Option A describes right-sided heart failure.
Option C describes nephrotic syndrome or liver failure mechanisms. Option D describes asthma
pathology.

, 6. In the renal nephron, the macula densa cells located in the distal convoluted tubule play a critical
role in tubuloglomerular feedback. What specific physiological stimulus activates the macula
densa?

A. Elevated systemic blood pressure detected by stretch receptors in the renal artery wall.

B. Changes in the concentration of sodium and chloride ions flowing through the distal
tubule fluid.

C. Decreased partial pressure of oxygen in the renal medullary interstitium.

D. Increased hydrostatic pressure within Bowman's capsule surrounding the glomerulus.

CORRECT ANSWER : B

Rationale: The macula densa cells monitor the concentration of sodium and chloride ions in the
tubular fluid passing through the ascending limb into the distal tubule, adjusting glomerular
filtration rate accordingly. Option A describes baroreceptors in the juxtaglomerular cells.
Option C describes erythropoietin regulation. Option D describes capsular pressure effects.

7. A patient is diagnosed with primary hyperparathyroidism, resulting in chronically elevated
parathyroid hormone (PTH) levels. Which of the following systemic mineral and bone
alterations should the clinician expect to find?

A. Hypocalcemia, hyperphosphatemia, and increased bone mineralization density.

B. Hypercalcemia, hypophosphatemia, and accelerated osteoclastic bone resorption.

C. Normal serum calcium, marked hyperphosphatemia, and decreased renal calcium
reabsorption.

D. Hypocalcemia, hypophosphatemia, and decreased activation of vitamin D in the kidneys.

CORRECT ANSWER : B

Rationale: Parathyroid hormone increases serum calcium by stimulating osteoclast bone
resorption, enhancing renal calcium reabsorption, and promoting renal synthesis of active
vitamin D while increasing urinary phosphate excretion, leading to hypophosphatemia. Options
A, C, and D contradict the well-established endocrine actions of PTH.

8. During the digestion and absorption of dietary lipids in the human small intestine, triglycerides
are emulsified by bile salts and subsequently digested by pancreatic lipase. What is the
immediate fate of the resulting free fatty acids and 2-monoglycerides?

A. They diffuse directly across the basolateral membrane of enterocytes into the portal vein
blood.

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