NBME CBSE ACTUAL TEST QUESTIONS AND ANSWERS
2024/2025(Quiz bank with all the correct answers)(usmle step
1)Medical examination - 190 Questions and Answers Already
Graded A+ Premium Exam Tested And Verified
Subject Area Basic Sciences & Clinical Foundations
Description This comprehensive exam assesses mastery of foundational medical sciences
including biochemistry, physiology, pharmacology, pathology, microbiology,
immunology, and behavioral science, integrated with clinical reasoning. It mirrors
the rigor and breadth of the USMLE Step 1 and NBME CBSE, emphasizing
application of concepts to novel clinical scenarios.
Expected Grade A+
Total Questions 190
Duration 3 hours
Learning Outcomes 1. Integrate basic science principles to explain disease mechanisms and treatment
rationale.
2. Apply pharmacokinetic and pharmacodynamic concepts to predict drug effects
and interactions.
3. Analyze laboratory and imaging data to differentiate among similar clinical
presentations.
4. Interpret epidemiologic and biostatistical data to guide evidence-based
decisions.
5. Synthesize knowledge across disciplines to solve complex clinical problems.
Accreditation This exam adheres to the standards of the US medical education accreditation
(LCME) and reflects the content blueprint of the NBME CBSE/USMLE Step 1.
Page 1
,1. A researcher investigates a signaling pathway where binding of a ligand to a
receptor tyrosine kinase leads to activation of Ras, followed by a kinase cascade.
Which mutation would most likely result in constitutive activation of this pathway,
independent of ligand binding?
A. Loss-of-function mutation in the GTPase-activating protein (GAP) for Ras
B. Loss-of-function mutation in Ras GTPase-activating protein (GAP) and gain-of-function
mutation in Ras
C. Gain-of-function mutation in the receptor tyrosine kinase that prevents dimerization
D. Loss-of-function mutation in Ras that increases its intrinsic GTPase activity
Answer: B. Loss-of-function mutation in Ras GTPase-activating protein (GAP)
and gain-of-function mutation in Ras
Constitutive activation of Ras occurs when Ras is locked in the active GTP-bound state.
Loss of GAP (which accelerates GTP hydrolysis) prolongs Ras activation, and a
gain-of-function mutation in Ras (e.g., Gly12Val) impairs GTPase activity. Option B
combines both mechanisms, ensuring persistent signaling. Option A alone (loss of GAP)
still allows some inactivation by intrinsic GTPase, though slow. Option C prevents
dimerization, reducing activation. Option D would increase GTP hydrolysis,
inactivating Ras.
2. A patient presents with muscle cramps, fatigue, and hypertension. Laboratory
findings show hypokalemia and metabolic alkalosis. Plasma renin activity is low, and
aldosterone levels are low. Which of the following is the most likely diagnosis?
A. Conn syndrome (primary hyperaldosteronism)
B. Renal artery stenosis
C. Liddle syndrome
D. Bartter syndrome
Answer: C. Liddle syndrome
Liddle syndrome is an autosomal dominant condition causing constitutive activation of
the epithelial sodium channel (ENaC) in the collecting duct, leading to sodium
reabsorption, potassium excretion, and hypertension. Renin and aldosterone are
suppressed due to volume expansion. Conn syndrome would have high aldosterone.
Renal artery stenosis would have high renin. Bartter syndrome typically presents with
normotensive hypokalemic alkalosis and high renin/aldosterone.
Page 2
,3. Which of the following best explains why a drug that is a weak base (pKa 8.4) is
more rapidly absorbed in the small intestine (pH 6) than in the stomach (pH 2)?
A. The drug is more ionized in the small intestine, facilitating paracellular transport
B. The drug is less ionized in the small intestine, increasing its lipid solubility
C. The drug is more ionized in the stomach, promoting active transport
D. The drug is less ionized in the stomach, but the small intestine has a larger surface area
Answer: B. The drug is less ionized in the small intestine, increasing its lipid
solubility
Weak bases are better absorbed in environments where they are predominantly
non-ionized (uncharged), as only the non-ionized form is lipid-soluble and can cross cell
membranes. At pH 6 (small intestine), a weak base with pKa 8.4 is mostly non-ionized
(pH < pKa), whereas at pH 2 (stomach), it is highly ionized. Option B correctly states
the principle. Option A is incorrect because ionized drugs do not readily cross
membranes. Option C is false; active transport is not the primary mechanism for most
weak bases. Option D is true about surface area but does not explain the pH-dependent
absorption difference directly.
4. A 48-year-old individual with a history of recurrent sinopulmonary infections and
autoimmune hemolytic anemia is found to have a deficiency in early complement
components. Which of the following complement proteins is most likely deficient?
A. C3
B. C5
C. C1q
D. Factor B
Answer: C. C1q
Deficiency of early complement components (C1q, C1r, C1s, C4, C2) is associated with
immune complex diseases such as systemic lupus erythematosus (SLE) and recurrent
infections with encapsulated organisms. C1q deficiency is the most common and
strongly linked to SLE and pyogenic infections. C3 deficiency leads to severe infections
but less autoimmune hemolytic anemia. C5 deficiency predisposes to Neisseria
infections. Factor B deficiency is rare and affects the alternative pathway.
Page 3
, 5. In a study of a new chemotherapeutic agent, the drug is found to have a volume of
distribution of 40 L and a half-life of 8 hours. If a loading dose of 400 mg is
administered intravenously, what is the approximate plasma concentration
immediately after administration?
A. 5 mg/L
B. 10 mg/L
C. 20 mg/L
D. 40 mg/L
Answer: B. 10 mg/L
Plasma concentration after IV bolus is dose divided by volume of distribution: C = Dose
/ Vd = 400 mg / 40 L = 10 mg/L. Half-life is not needed for this calculation. Option B is
correct. Option A would be 5 mg/L if Vd were 80 L. Option C would be 20 mg/L if Vd
were 20 L. Option D would be 40 mg/L if Vd were 10 L.
6. A 60-year-old man with chronic alcoholism presents with confusion, ataxia, and
ophthalmoplegia. MRI shows symmetric hyperintensities in the periaqueductal gray,
mammillary bodies, and thalamus. Which vitamin deficiency is most likely
responsible?
A. Vitamin B12 (cobalamin)
B. Vitamin B1 (thiamine)
C. Vitamin B3 (niacin)
D. Vitamin B6 (pyridoxine)
Answer: B. Vitamin B1 (thiamine)
The triad of confusion, ataxia, and ophthalmoplegia (Wernicke encephalopathy) is due
to thiamine (vitamin B1) deficiency, often in alcoholics. MRI findings of symmetric
hyperintensities in periaqueductal gray, mammillary bodies, and thalamus are classic.
Vitamin B12 deficiency causes subacute combined degeneration (dorsal columns and
corticospinal tracts). Niacin deficiency causes pellagra (dermatitis, diarrhea, dementia).
Pyridoxine deficiency causes peripheral neuropathy and sideroblastic anemia.
Page 4
2024/2025(Quiz bank with all the correct answers)(usmle step
1)Medical examination - 190 Questions and Answers Already
Graded A+ Premium Exam Tested And Verified
Subject Area Basic Sciences & Clinical Foundations
Description This comprehensive exam assesses mastery of foundational medical sciences
including biochemistry, physiology, pharmacology, pathology, microbiology,
immunology, and behavioral science, integrated with clinical reasoning. It mirrors
the rigor and breadth of the USMLE Step 1 and NBME CBSE, emphasizing
application of concepts to novel clinical scenarios.
Expected Grade A+
Total Questions 190
Duration 3 hours
Learning Outcomes 1. Integrate basic science principles to explain disease mechanisms and treatment
rationale.
2. Apply pharmacokinetic and pharmacodynamic concepts to predict drug effects
and interactions.
3. Analyze laboratory and imaging data to differentiate among similar clinical
presentations.
4. Interpret epidemiologic and biostatistical data to guide evidence-based
decisions.
5. Synthesize knowledge across disciplines to solve complex clinical problems.
Accreditation This exam adheres to the standards of the US medical education accreditation
(LCME) and reflects the content blueprint of the NBME CBSE/USMLE Step 1.
Page 1
,1. A researcher investigates a signaling pathway where binding of a ligand to a
receptor tyrosine kinase leads to activation of Ras, followed by a kinase cascade.
Which mutation would most likely result in constitutive activation of this pathway,
independent of ligand binding?
A. Loss-of-function mutation in the GTPase-activating protein (GAP) for Ras
B. Loss-of-function mutation in Ras GTPase-activating protein (GAP) and gain-of-function
mutation in Ras
C. Gain-of-function mutation in the receptor tyrosine kinase that prevents dimerization
D. Loss-of-function mutation in Ras that increases its intrinsic GTPase activity
Answer: B. Loss-of-function mutation in Ras GTPase-activating protein (GAP)
and gain-of-function mutation in Ras
Constitutive activation of Ras occurs when Ras is locked in the active GTP-bound state.
Loss of GAP (which accelerates GTP hydrolysis) prolongs Ras activation, and a
gain-of-function mutation in Ras (e.g., Gly12Val) impairs GTPase activity. Option B
combines both mechanisms, ensuring persistent signaling. Option A alone (loss of GAP)
still allows some inactivation by intrinsic GTPase, though slow. Option C prevents
dimerization, reducing activation. Option D would increase GTP hydrolysis,
inactivating Ras.
2. A patient presents with muscle cramps, fatigue, and hypertension. Laboratory
findings show hypokalemia and metabolic alkalosis. Plasma renin activity is low, and
aldosterone levels are low. Which of the following is the most likely diagnosis?
A. Conn syndrome (primary hyperaldosteronism)
B. Renal artery stenosis
C. Liddle syndrome
D. Bartter syndrome
Answer: C. Liddle syndrome
Liddle syndrome is an autosomal dominant condition causing constitutive activation of
the epithelial sodium channel (ENaC) in the collecting duct, leading to sodium
reabsorption, potassium excretion, and hypertension. Renin and aldosterone are
suppressed due to volume expansion. Conn syndrome would have high aldosterone.
Renal artery stenosis would have high renin. Bartter syndrome typically presents with
normotensive hypokalemic alkalosis and high renin/aldosterone.
Page 2
,3. Which of the following best explains why a drug that is a weak base (pKa 8.4) is
more rapidly absorbed in the small intestine (pH 6) than in the stomach (pH 2)?
A. The drug is more ionized in the small intestine, facilitating paracellular transport
B. The drug is less ionized in the small intestine, increasing its lipid solubility
C. The drug is more ionized in the stomach, promoting active transport
D. The drug is less ionized in the stomach, but the small intestine has a larger surface area
Answer: B. The drug is less ionized in the small intestine, increasing its lipid
solubility
Weak bases are better absorbed in environments where they are predominantly
non-ionized (uncharged), as only the non-ionized form is lipid-soluble and can cross cell
membranes. At pH 6 (small intestine), a weak base with pKa 8.4 is mostly non-ionized
(pH < pKa), whereas at pH 2 (stomach), it is highly ionized. Option B correctly states
the principle. Option A is incorrect because ionized drugs do not readily cross
membranes. Option C is false; active transport is not the primary mechanism for most
weak bases. Option D is true about surface area but does not explain the pH-dependent
absorption difference directly.
4. A 48-year-old individual with a history of recurrent sinopulmonary infections and
autoimmune hemolytic anemia is found to have a deficiency in early complement
components. Which of the following complement proteins is most likely deficient?
A. C3
B. C5
C. C1q
D. Factor B
Answer: C. C1q
Deficiency of early complement components (C1q, C1r, C1s, C4, C2) is associated with
immune complex diseases such as systemic lupus erythematosus (SLE) and recurrent
infections with encapsulated organisms. C1q deficiency is the most common and
strongly linked to SLE and pyogenic infections. C3 deficiency leads to severe infections
but less autoimmune hemolytic anemia. C5 deficiency predisposes to Neisseria
infections. Factor B deficiency is rare and affects the alternative pathway.
Page 3
, 5. In a study of a new chemotherapeutic agent, the drug is found to have a volume of
distribution of 40 L and a half-life of 8 hours. If a loading dose of 400 mg is
administered intravenously, what is the approximate plasma concentration
immediately after administration?
A. 5 mg/L
B. 10 mg/L
C. 20 mg/L
D. 40 mg/L
Answer: B. 10 mg/L
Plasma concentration after IV bolus is dose divided by volume of distribution: C = Dose
/ Vd = 400 mg / 40 L = 10 mg/L. Half-life is not needed for this calculation. Option B is
correct. Option A would be 5 mg/L if Vd were 80 L. Option C would be 20 mg/L if Vd
were 20 L. Option D would be 40 mg/L if Vd were 10 L.
6. A 60-year-old man with chronic alcoholism presents with confusion, ataxia, and
ophthalmoplegia. MRI shows symmetric hyperintensities in the periaqueductal gray,
mammillary bodies, and thalamus. Which vitamin deficiency is most likely
responsible?
A. Vitamin B12 (cobalamin)
B. Vitamin B1 (thiamine)
C. Vitamin B3 (niacin)
D. Vitamin B6 (pyridoxine)
Answer: B. Vitamin B1 (thiamine)
The triad of confusion, ataxia, and ophthalmoplegia (Wernicke encephalopathy) is due
to thiamine (vitamin B1) deficiency, often in alcoholics. MRI findings of symmetric
hyperintensities in periaqueductal gray, mammillary bodies, and thalamus are classic.
Vitamin B12 deficiency causes subacute combined degeneration (dorsal columns and
corticospinal tracts). Niacin deficiency causes pellagra (dermatitis, diarrhea, dementia).
Pyridoxine deficiency causes peripheral neuropathy and sideroblastic anemia.
Page 4
