9/26/25, 5:54 PM NBME 29 <span style="color:#000;font-weight:bold;">200+</span> (2025-2026 A+ Graded) Exam-Style Questions | Verified Solutio…
NBME 29 EXAM WITH QUESTIONS AND
ANSWERS
Page 1 of 434
1/434
,9/26/25, 5:54 PM NBME 29 <span style="color:#000;font-weight:bold;">200+</span> (2025-2026 A+ Graded) Exam-Style Questions | Verified Solutio…
Question 1
1
Exam Section 1: Item 1 of 50
National Board of Medical Examiners'
Comprehensive Basic Science Self-Assessment
1. Patients with prolonged starvation or untreated type 1 diabetes mellitus
overproduce ketone bodies. Which of the following is a common factor that is
responsible for ketosis in patients with
these two conditions?
A) Depletion of pentose phosphate pathway intermediates
B) Increased availability of acetyl COA
C) Inhibition of fatty acid oxidation
D) Inhibition of gluconeogenesis
E) Inhibition of glycogenolysis
Correct Answer
B.
Increased availability of acetyl CoA is common to states of starvation and untreated
type 1 diabetes mellitus. In starvation, glycogen stores are gradually depleted. The
body then relies on the
breakdown of fat through oxidation of fatty acids to provide energy. Fatty acid
oxidation occurs in the mitochondria of the cell. In each cycle of oxidation, two-
carbon fragments are cleaved to form
acetyl CoA, which leaves the mitochondria via the carnitine shuttle. In addition to a
molecule of acetyl CoA which then enters the citric acid cycle, a molecule of NADH
is produced in each cycle.
Ketogenesis occurs in starvation via two-carbon fragments, with formation of
ketoacids such as acetoacetyl CoA and B-hydroxybutyrate. The ability to generate
energy from adipose during a
period of starvation is critical to maintaining the function of vital organs, such as the
brain. In untreated type 1 diabetes mellitus, there is an absolute deficiency of
insulin, which renders many
cells incapable of shuttling glucose into the cell for use in cellular respiration. While
there are several glucose transporters that do not require insulin for glucose entry,
GLUT4 is commonly
expressed in many cell types and requires insulin to function. Patients with
untreated type 1 diabetes mellitus will have serum glucose concentrations in the
high-normal to high range as a result
of ongoing gluconeogenesis and glycogenolysis, but insulin deficiency prevents
entry of circulating glucose into cells through glucose transport proteins, effectively
resulting in a state of
starvation. This results in ketogenesis and accounts for the presence of ketone
bodies in the blood and urine of patients with starvation or untreated type 1
diabetes mellitus.
Page 2 of 434
2/434
,9/26/25, 5:54 PM NBME 29 <span style="color:#000;font-weight:bold;">200+</span> (2025-2026 A+ Graded) Exam-Style Questions | Verified Solutio…
Incorrect Answers: A, C, D, and E.
Depletion of pentose phosphate pathway intermediates (Choice A) is not correct.
This pathway is active in many tissues including the liver, adrenal cortex, and in
erythrocytes. It produces
NADPH, ribose-5-phosphate, and erythrose-4-phosphate from glucose. Decreased
activity of this pathway would not lead to generation of ketones.
Inhibition of fatty acid oxidation (Choice C) is not correct. Fatty acid oxidation is
increased during states of starvation or untreated type 1 diabetes mellitus.
Inhibition of gluconeogenesis (Choice D) and inhibition of glycogenolysis (Choice E)
are not features of starvation or untreated type 1 diabetes mellitus. In fact, these
processes are accelerated in
both states, although in starvation, this is caused by a deficiency of glucose. In
untreated type 1 diabetes mellitus, these pathways are upregulated as a result of
insulin deficiency, perceived by
the cell as a hypoglycemic state.
Educational Objective: Both starvation and untreated type 1 diabetes mellitus result
in an increased rate of fatty acid oxidation, which generates acetyl CoA to be used
in the citric acid cycle and
NADH. Concomitant ketogenesis results in the formation of ketone bodies that can
be detected in serum and urine.
%3D
Next
Score Report
Lab Values
Calculator
Help
Pause
Page 3 of 434
3/434
, 9/26/25, 5:54 PM NBME 29 <span style="color:#000;font-weight:bold;">200+</span> (2025-2026 A+ Graded) Exam-Style Questions | Verified Solutio…
Question 2
2
Exam Section 1: Item 2 of 50
National Board of Medical Examiners'
Comprehensive Basic Science Self-Assessment
2. A 65-year-old man comes to the emergency department because of a 1-week
history of blood in his sputum. A mass is found on a radiograph. Bronchoscopy is
planned. In order to pass the
bronchoscope through the oropharynx to the lungs without eliciting a gag reflex, the
pharynx is anesthetized. The afferent limb of the reflex is most likely to be blocked by
anesthesia to which
of the following cranial nerves?
A) Trigeminal
B) Facial
C) Glossopharyngeal
D) Vagus
E) Hypoglossal
Correct Answer
C.
The glossopharyngeal nerve (cranial nerve IX) contains somatic afferent fibers that
control the sensation of the palate and upper pharynx, providing afferent
information for the gag reflex. The
efferent nerve for the gag reflex is the vagus nerve, which innervates the soft palate
and pharyngeal muscles to control gagging and swallowing. In addition to its role in
the gag reflex, the
glossopharyngeal nerve contains other afferent and efferent nerve fibers.
Components of the glossopharyngeal nerve include general visceral afferent fibers
(carotid body and sinus chemo- and
baroreceptors), special sensory fibers (taste from posterior third of the tongue),
general visceral efferent fibers (parasympathetic innervation of the parotid gland),
and special visceral efferent
fibers (stylopharyngeus muscle). Lesions of the glossopharyngeal nerve lead to
impaired sensation and taste in the posterior third of the tongue, impaired
sensation of the palate and pharynx,
parotid gland dysfunction, difficulty swallowing, and an absent gag reflex.
Incorrect Answers: A, B, D, and E.
The trigeminal nerve (Choice A), or cranial nerve V, provides somatic sensory
innervation to the face and scalp. The mandibular nerve (the V3 branch of the
trigeminal nerve) additionally controls
the muscles of mastication and mediates pain and temperature sensation in the
anterior two-thirds of the tongue. The trigeminal nerve does not innervate the
pharynx.
The facial nerve (Choice B), or cranial nerve VII, contains afferent and efferent fibers
Page 4 of 434
4/434
NBME 29 EXAM WITH QUESTIONS AND
ANSWERS
Page 1 of 434
1/434
,9/26/25, 5:54 PM NBME 29 <span style="color:#000;font-weight:bold;">200+</span> (2025-2026 A+ Graded) Exam-Style Questions | Verified Solutio…
Question 1
1
Exam Section 1: Item 1 of 50
National Board of Medical Examiners'
Comprehensive Basic Science Self-Assessment
1. Patients with prolonged starvation or untreated type 1 diabetes mellitus
overproduce ketone bodies. Which of the following is a common factor that is
responsible for ketosis in patients with
these two conditions?
A) Depletion of pentose phosphate pathway intermediates
B) Increased availability of acetyl COA
C) Inhibition of fatty acid oxidation
D) Inhibition of gluconeogenesis
E) Inhibition of glycogenolysis
Correct Answer
B.
Increased availability of acetyl CoA is common to states of starvation and untreated
type 1 diabetes mellitus. In starvation, glycogen stores are gradually depleted. The
body then relies on the
breakdown of fat through oxidation of fatty acids to provide energy. Fatty acid
oxidation occurs in the mitochondria of the cell. In each cycle of oxidation, two-
carbon fragments are cleaved to form
acetyl CoA, which leaves the mitochondria via the carnitine shuttle. In addition to a
molecule of acetyl CoA which then enters the citric acid cycle, a molecule of NADH
is produced in each cycle.
Ketogenesis occurs in starvation via two-carbon fragments, with formation of
ketoacids such as acetoacetyl CoA and B-hydroxybutyrate. The ability to generate
energy from adipose during a
period of starvation is critical to maintaining the function of vital organs, such as the
brain. In untreated type 1 diabetes mellitus, there is an absolute deficiency of
insulin, which renders many
cells incapable of shuttling glucose into the cell for use in cellular respiration. While
there are several glucose transporters that do not require insulin for glucose entry,
GLUT4 is commonly
expressed in many cell types and requires insulin to function. Patients with
untreated type 1 diabetes mellitus will have serum glucose concentrations in the
high-normal to high range as a result
of ongoing gluconeogenesis and glycogenolysis, but insulin deficiency prevents
entry of circulating glucose into cells through glucose transport proteins, effectively
resulting in a state of
starvation. This results in ketogenesis and accounts for the presence of ketone
bodies in the blood and urine of patients with starvation or untreated type 1
diabetes mellitus.
Page 2 of 434
2/434
,9/26/25, 5:54 PM NBME 29 <span style="color:#000;font-weight:bold;">200+</span> (2025-2026 A+ Graded) Exam-Style Questions | Verified Solutio…
Incorrect Answers: A, C, D, and E.
Depletion of pentose phosphate pathway intermediates (Choice A) is not correct.
This pathway is active in many tissues including the liver, adrenal cortex, and in
erythrocytes. It produces
NADPH, ribose-5-phosphate, and erythrose-4-phosphate from glucose. Decreased
activity of this pathway would not lead to generation of ketones.
Inhibition of fatty acid oxidation (Choice C) is not correct. Fatty acid oxidation is
increased during states of starvation or untreated type 1 diabetes mellitus.
Inhibition of gluconeogenesis (Choice D) and inhibition of glycogenolysis (Choice E)
are not features of starvation or untreated type 1 diabetes mellitus. In fact, these
processes are accelerated in
both states, although in starvation, this is caused by a deficiency of glucose. In
untreated type 1 diabetes mellitus, these pathways are upregulated as a result of
insulin deficiency, perceived by
the cell as a hypoglycemic state.
Educational Objective: Both starvation and untreated type 1 diabetes mellitus result
in an increased rate of fatty acid oxidation, which generates acetyl CoA to be used
in the citric acid cycle and
NADH. Concomitant ketogenesis results in the formation of ketone bodies that can
be detected in serum and urine.
%3D
Next
Score Report
Lab Values
Calculator
Help
Pause
Page 3 of 434
3/434
, 9/26/25, 5:54 PM NBME 29 <span style="color:#000;font-weight:bold;">200+</span> (2025-2026 A+ Graded) Exam-Style Questions | Verified Solutio…
Question 2
2
Exam Section 1: Item 2 of 50
National Board of Medical Examiners'
Comprehensive Basic Science Self-Assessment
2. A 65-year-old man comes to the emergency department because of a 1-week
history of blood in his sputum. A mass is found on a radiograph. Bronchoscopy is
planned. In order to pass the
bronchoscope through the oropharynx to the lungs without eliciting a gag reflex, the
pharynx is anesthetized. The afferent limb of the reflex is most likely to be blocked by
anesthesia to which
of the following cranial nerves?
A) Trigeminal
B) Facial
C) Glossopharyngeal
D) Vagus
E) Hypoglossal
Correct Answer
C.
The glossopharyngeal nerve (cranial nerve IX) contains somatic afferent fibers that
control the sensation of the palate and upper pharynx, providing afferent
information for the gag reflex. The
efferent nerve for the gag reflex is the vagus nerve, which innervates the soft palate
and pharyngeal muscles to control gagging and swallowing. In addition to its role in
the gag reflex, the
glossopharyngeal nerve contains other afferent and efferent nerve fibers.
Components of the glossopharyngeal nerve include general visceral afferent fibers
(carotid body and sinus chemo- and
baroreceptors), special sensory fibers (taste from posterior third of the tongue),
general visceral efferent fibers (parasympathetic innervation of the parotid gland),
and special visceral efferent
fibers (stylopharyngeus muscle). Lesions of the glossopharyngeal nerve lead to
impaired sensation and taste in the posterior third of the tongue, impaired
sensation of the palate and pharynx,
parotid gland dysfunction, difficulty swallowing, and an absent gag reflex.
Incorrect Answers: A, B, D, and E.
The trigeminal nerve (Choice A), or cranial nerve V, provides somatic sensory
innervation to the face and scalp. The mandibular nerve (the V3 branch of the
trigeminal nerve) additionally controls
the muscles of mastication and mediates pain and temperature sensation in the
anterior two-thirds of the tongue. The trigeminal nerve does not innervate the
pharynx.
The facial nerve (Choice B), or cranial nerve VII, contains afferent and efferent fibers
Page 4 of 434
4/434