1|Page
BIOD 171 FINAL EXAM 2025–2026 | QUESTIONS 160 WITH
VERIFIED ANSWERS & DETAILED EXPLANATIONS | A+
LATEST VERSION
Q1. A 58-year-old man presents with progressive muscle weakness,
especially in the proximal limb muscles, and difficulty swallowing.
Laboratory testing shows elevated serum creatine kinase and autoantibodies
against the postsynaptic acetylcholine receptor. Which pathophysiological
mechanism best explains the patient’s symptoms?
A. Autoimmune destruction of presynaptic calcium channels resulting in
decreased acetylcholine release
B. Autoimmune blockade of postsynaptic acetylcholine receptors leading to
impaired neuromuscular transmission
C. Degeneration of lower motor neurons causing denervation atrophy of
skeletal muscle
D. Metabolic dysfunction of muscle mitochondria decreasing ATP
availability for contraction
Answer: B
Rationale: Myasthenia gravis is caused by autoantibodies that bind and
block nicotinic acetylcholine receptors at the neuromuscular junction,
preventing effective postsynaptic depolarization and causing fatigable
weakness. Option A describes Lambert–Eaton myasthenic syndrome
(presynaptic calcium channel antibodies), which presents differently and
often improves with activity. Option C refers to motor neuron disease such
as ALS, which causes different signs (fasciculations, mixed UMN/LMN).
Option D is mitochondrial myopathy, which has different lab/biopsy
findings and not specific acetylcholine receptor antibodies.
Q2. A researcher measures the uptake of radiolabeled glucose into cultured
hepatocytes at increasing extracellular glucose concentrations and plots
,2|Page
velocity versus substrate concentration. The curve shows a hyperbolic
relationship that approaches a maximum rate (Vmax). Which enzymatic
model best describes this transport phenomenon, and what does Vmax
represent in this context?
A. Michaelis–Menten kinetics; Vmax equals the maximal transport rate
when all transporter sites are saturated
B. First-order kinetics; Vmax equals the rate constant times substrate
concentration
C. Zero-order kinetics; Vmax equals the basal metabolic rate independent of
substrate
D. Cooperative kinetics; Vmax equals the rate when all binding sites on a
multimeric enzyme have increased affinity
Answer: A
Rationale: Transport mediated by a carrier protein that becomes saturated
with substrate follows Michaelis–Menten kinetics, producing a hyperbolic
curve and a Vmax that reflects the maximal velocity when all transporter
sites are occupied. First-order kinetics (B) imply a linear relationship at low
substrate concentrations, not an asymptotic maximum. Zero-order kinetics
(C) apply when rate is constant irrespective of substrate over a range, but the
description of saturation fits Michaelis–Menten better. Cooperative kinetics
(D) produce a sigmoidal curve (not hyperbolic) and describe multimeric
enzymes like hemoglobin, not typical single-carrier facilitated transport.
Q3. During exercise, skeletal muscle increases oxygen consumption and
shifts metabolism. Which sequence of biochemical changes most directly
supports ATP generation under sustained aerobic exercise?
A. Increased glycolysis → lactate production → reduced ATP yield per
glucose
B. Increased beta-oxidation of fatty acids → increased acetyl-CoA delivery
to TCA cycle → enhanced oxidative phosphorylation
C. Increased proteolysis → gluconeogenesis from amino acids → immediate
ATP from gluconeogenesis
D. Increased pentose phosphate pathway flux → more NADPH → direct
ATP generation
,3|Page
Answer: B
Rationale: During sustained aerobic exercise, muscles utilize fatty acids via
beta-oxidation to produce acetyl-CoA, feeding the TCA cycle and enhancing
NADH/FADH2 production for oxidative phosphorylation, which yields
abundant ATP. Option A describes anaerobic glycolysis that predominates
during intense, short exercise and yields less ATP. Option C (proteolysis →
gluconeogenesis) is a slower process and does not directly supply immediate
ATP for contracting muscle. Option D (PPP) mainly generates NADPH and
ribose-5-phosphate for biosynthesis, not direct ATP for muscle contraction.
Q4. A patient has a mutation causing loss of function in the Na⁺/K⁺ ATPase
in renal tubular cells. Which immediate effect on renal epithelial cell ion
gradients and membrane potential would you predict, and how would that
affect intracellular volume?
A. Intracellular Na⁺ falls, K⁺ rises, hyperpolarization; cellular shrinkage
B. Intracellular Na⁺ rises, K⁺ falls, depolarization; cellular swelling due to
osmotic influx of water
C. No change in Na⁺ or K⁺ but increased Cl⁻ influx; no volume change
D. Increased activity of basolateral H⁺ pumps to compensate; intracellular
acidification with no volume change
Answer: B
Rationale: Na⁺/K⁺ ATPase normally extrudes 3 Na⁺ in exchange for 2 K⁺,
maintaining low intracellular Na⁺ and high K⁺ and contributing to the
negative membrane potential. Loss of function causes intracellular Na⁺ to
rise and K⁺ to fall, depolarizing the cell. Elevated intracellular Na⁺ increases
intracellular osmolarity, driving water influx and cellular swelling. Options
A and C do not reflect the expected ion accumulation. Option D proposes a
compensatory H⁺ pump response that is not the primary immediate effect of
Na⁺/K⁺ ATPase failure.
Q5. A pregnant woman in her second trimester develops asymptomatic
bacteriuria. Which of the following best explains why screening and
treatment are recommended during pregnancy?
, 4|Page
A. Pregnancy decreases urinary stasis, lowering infection risk so treatment is
optional
B. Untreated asymptomatic bacteriuria increases risk of pyelonephritis and
adverse pregnancy outcomes, such as preterm labor
C. Antibiotics are contraindicated in pregnancy, so screening is unnecessary
D. Asymptomatic bacteriuria in pregnancy usually resolves spontaneously
without sequelae
Answer: B
Rationale: Pregnancy predisposes to urinary stasis and vesicoureteral reflux
due to hormonal and mechanical changes; untreated asymptomatic
bacteriuria carries a higher risk of progression to pyelonephritis and is
associated with adverse outcomes, including preterm birth, so screening and
treatment are recommended. Option A incorrectly states decreased urinary
stasis. Option C is false—many antibiotics are safe in pregnancy and
targeted therapy is used when indicated. Option D underestimates risk in
pregnancy where spontaneous resolution is less reliable.
Q6. A 45-year-old with a history of chronic hypertension develops left
ventricular hypertrophy (LVH). Which cellular and molecular adaptations in
cardiomyocytes primarily account for the increased wall thickness in
pressure overload LVH?
A. Cardiomyocyte hyperplasia due to reactivation of mitosis in adult heart
cells
B. Cardiomyocyte hypertrophy mainly via increased synthesis of contractile
proteins and sarcomeres arranged in parallel
C. Apoptosis of cardiomyocytes with fibroblast proliferation leading to
thinning of the wall
D. Accumulation of lipid droplets within cardiomyocytes causing expansion
Answer: B
Rationale: In adult hearts, increased pressure load induces cardiomyocyte
hypertrophy—cells enlarge by synthesizing more contractile proteins and
adding sarcomeres in parallel, resulting in thicker ventricular walls and
increased muscle mass. Option A is incorrect because adult cardiomyocytes
have limited proliferative capacity; hyperplasia is not the mechanism.
BIOD 171 FINAL EXAM 2025–2026 | QUESTIONS 160 WITH
VERIFIED ANSWERS & DETAILED EXPLANATIONS | A+
LATEST VERSION
Q1. A 58-year-old man presents with progressive muscle weakness,
especially in the proximal limb muscles, and difficulty swallowing.
Laboratory testing shows elevated serum creatine kinase and autoantibodies
against the postsynaptic acetylcholine receptor. Which pathophysiological
mechanism best explains the patient’s symptoms?
A. Autoimmune destruction of presynaptic calcium channels resulting in
decreased acetylcholine release
B. Autoimmune blockade of postsynaptic acetylcholine receptors leading to
impaired neuromuscular transmission
C. Degeneration of lower motor neurons causing denervation atrophy of
skeletal muscle
D. Metabolic dysfunction of muscle mitochondria decreasing ATP
availability for contraction
Answer: B
Rationale: Myasthenia gravis is caused by autoantibodies that bind and
block nicotinic acetylcholine receptors at the neuromuscular junction,
preventing effective postsynaptic depolarization and causing fatigable
weakness. Option A describes Lambert–Eaton myasthenic syndrome
(presynaptic calcium channel antibodies), which presents differently and
often improves with activity. Option C refers to motor neuron disease such
as ALS, which causes different signs (fasciculations, mixed UMN/LMN).
Option D is mitochondrial myopathy, which has different lab/biopsy
findings and not specific acetylcholine receptor antibodies.
Q2. A researcher measures the uptake of radiolabeled glucose into cultured
hepatocytes at increasing extracellular glucose concentrations and plots
,2|Page
velocity versus substrate concentration. The curve shows a hyperbolic
relationship that approaches a maximum rate (Vmax). Which enzymatic
model best describes this transport phenomenon, and what does Vmax
represent in this context?
A. Michaelis–Menten kinetics; Vmax equals the maximal transport rate
when all transporter sites are saturated
B. First-order kinetics; Vmax equals the rate constant times substrate
concentration
C. Zero-order kinetics; Vmax equals the basal metabolic rate independent of
substrate
D. Cooperative kinetics; Vmax equals the rate when all binding sites on a
multimeric enzyme have increased affinity
Answer: A
Rationale: Transport mediated by a carrier protein that becomes saturated
with substrate follows Michaelis–Menten kinetics, producing a hyperbolic
curve and a Vmax that reflects the maximal velocity when all transporter
sites are occupied. First-order kinetics (B) imply a linear relationship at low
substrate concentrations, not an asymptotic maximum. Zero-order kinetics
(C) apply when rate is constant irrespective of substrate over a range, but the
description of saturation fits Michaelis–Menten better. Cooperative kinetics
(D) produce a sigmoidal curve (not hyperbolic) and describe multimeric
enzymes like hemoglobin, not typical single-carrier facilitated transport.
Q3. During exercise, skeletal muscle increases oxygen consumption and
shifts metabolism. Which sequence of biochemical changes most directly
supports ATP generation under sustained aerobic exercise?
A. Increased glycolysis → lactate production → reduced ATP yield per
glucose
B. Increased beta-oxidation of fatty acids → increased acetyl-CoA delivery
to TCA cycle → enhanced oxidative phosphorylation
C. Increased proteolysis → gluconeogenesis from amino acids → immediate
ATP from gluconeogenesis
D. Increased pentose phosphate pathway flux → more NADPH → direct
ATP generation
,3|Page
Answer: B
Rationale: During sustained aerobic exercise, muscles utilize fatty acids via
beta-oxidation to produce acetyl-CoA, feeding the TCA cycle and enhancing
NADH/FADH2 production for oxidative phosphorylation, which yields
abundant ATP. Option A describes anaerobic glycolysis that predominates
during intense, short exercise and yields less ATP. Option C (proteolysis →
gluconeogenesis) is a slower process and does not directly supply immediate
ATP for contracting muscle. Option D (PPP) mainly generates NADPH and
ribose-5-phosphate for biosynthesis, not direct ATP for muscle contraction.
Q4. A patient has a mutation causing loss of function in the Na⁺/K⁺ ATPase
in renal tubular cells. Which immediate effect on renal epithelial cell ion
gradients and membrane potential would you predict, and how would that
affect intracellular volume?
A. Intracellular Na⁺ falls, K⁺ rises, hyperpolarization; cellular shrinkage
B. Intracellular Na⁺ rises, K⁺ falls, depolarization; cellular swelling due to
osmotic influx of water
C. No change in Na⁺ or K⁺ but increased Cl⁻ influx; no volume change
D. Increased activity of basolateral H⁺ pumps to compensate; intracellular
acidification with no volume change
Answer: B
Rationale: Na⁺/K⁺ ATPase normally extrudes 3 Na⁺ in exchange for 2 K⁺,
maintaining low intracellular Na⁺ and high K⁺ and contributing to the
negative membrane potential. Loss of function causes intracellular Na⁺ to
rise and K⁺ to fall, depolarizing the cell. Elevated intracellular Na⁺ increases
intracellular osmolarity, driving water influx and cellular swelling. Options
A and C do not reflect the expected ion accumulation. Option D proposes a
compensatory H⁺ pump response that is not the primary immediate effect of
Na⁺/K⁺ ATPase failure.
Q5. A pregnant woman in her second trimester develops asymptomatic
bacteriuria. Which of the following best explains why screening and
treatment are recommended during pregnancy?
, 4|Page
A. Pregnancy decreases urinary stasis, lowering infection risk so treatment is
optional
B. Untreated asymptomatic bacteriuria increases risk of pyelonephritis and
adverse pregnancy outcomes, such as preterm labor
C. Antibiotics are contraindicated in pregnancy, so screening is unnecessary
D. Asymptomatic bacteriuria in pregnancy usually resolves spontaneously
without sequelae
Answer: B
Rationale: Pregnancy predisposes to urinary stasis and vesicoureteral reflux
due to hormonal and mechanical changes; untreated asymptomatic
bacteriuria carries a higher risk of progression to pyelonephritis and is
associated with adverse outcomes, including preterm birth, so screening and
treatment are recommended. Option A incorrectly states decreased urinary
stasis. Option C is false—many antibiotics are safe in pregnancy and
targeted therapy is used when indicated. Option D underestimates risk in
pregnancy where spontaneous resolution is less reliable.
Q6. A 45-year-old with a history of chronic hypertension develops left
ventricular hypertrophy (LVH). Which cellular and molecular adaptations in
cardiomyocytes primarily account for the increased wall thickness in
pressure overload LVH?
A. Cardiomyocyte hyperplasia due to reactivation of mitosis in adult heart
cells
B. Cardiomyocyte hypertrophy mainly via increased synthesis of contractile
proteins and sarcomeres arranged in parallel
C. Apoptosis of cardiomyocytes with fibroblast proliferation leading to
thinning of the wall
D. Accumulation of lipid droplets within cardiomyocytes causing expansion
Answer: B
Rationale: In adult hearts, increased pressure load induces cardiomyocyte
hypertrophy—cells enlarge by synthesizing more contractile proteins and
adding sarcomeres in parallel, resulting in thicker ventricular walls and
increased muscle mass. Option A is incorrect because adult cardiomyocytes
have limited proliferative capacity; hyperplasia is not the mechanism.
