NBME CBSE Comprehensive Actual Test
Bank 2026/2027 Edition Complete Practice
Questions with Verified Solutions
BLOCK 1: GENERAL PRINCIPLES & SYSTEMS 1-25
Q1. A 45-year-old woman presents with fatigue and joint pain. Physical exam reveals
hyperpigmented skin creases and arthralgias. Laboratory studies show elevated serum
iron, decreased total iron-binding capacity, and increased transferrin saturation. Which
of the following genes is most likely mutated in this patient?
A. HFE
B. ATP7B
C. CFTR
D. BRCA1
E. FBN1
Correct Answer: A
High-Yield Concept: Hereditary hemochromatosis genetics
Why Correct (Step-by-Step):
, 1. Classic triad: fatigue (often from diabetes/cardiomyopathy), arthralgias (hands
especially), bronze skin hyperpigmentation
2. Labs confirm iron overload: ↑serum Fe, ↓TIBC (transferrin is saturated),
↑transferrin saturation (>45% diagnostic, >62% strongly suggestive)
3. HFE gene on chromosome 6 (C282Y > H63D mutations) = autosomal recessive
hereditary hemochromatosis, most common in Caucasians
Why Each Distractor is Wrong:
● B: ATP7B mutations cause Wilson disease (copper overload, Kayser-Fleischer
rings, basal ganglia degeneration)
● C: CFTR mutations cause cystic fibrosis (Cl⁻ channel defect, pancreatic
insufficiency, chronic lung disease)
● D: BRCA1 mutations cause hereditary breast/ovarian cancer syndrome (DNA
repair defect)
● E: FBN1 mutations cause Marfan syndrome (fibrillin-1 defect, aortic root dilation,
lens dislocation)
Memory Aid: "HFE = Hemochromatosis = Fe Excess. C282Y: Cysteine to Tyrosine at
position 282—think 'Caucasian' (most common population)"
Related Concepts Frequently Tested with This:
● Complications: "Bronze diabetes" (pancreatic hemosiderosis), restrictive
cardiomyopathy, cirrhosis (risk of hepatocellular carcinoma), hypogonadotropic
hypogonadism
● Hemochromatosis is one of the MCCs of micronodular cirrhosis
vs. Secondary iron overload (transfusion-dependent thalassemias, ineffective
erythropoiesis)
● Clinical Pearl:
● Phlebotomy is first-line (goal ferritin 50-100 ng/mL)
● Screen first-degree relatives with HFE genetic testing + fasting iron studies
● Ferritin >1000 ng/mL predicts cirrhosis risk
Q2. A researcher studying enzyme kinetics adds a competitive inhibitor to a solution
containing enzyme and substrate. Which of the following best describes the expected
changes?
,A. Decreased Vmax, unchanged Km
B. Unchanged Vmax, increased Km
C. Decreased Vmax, decreased Km
D. Increased Vmax, unchanged Km
E. Unchanged Vmax, decreased Km
Correct Answer: B
High-Yield Concept: Competitive inhibition enzyme kinetics
Why Correct (Step-by-Step):
1. Competitive inhibitors bind reversibly to the enzyme's active site, competing
directly with substrate for binding
2. Vmax unchanged: At infinite substrate concentration, substrate outcompetes
inhibitor; maximal velocity achievable with enough substrate
3. Km increased: The apparent affinity for substrate decreases because inhibitor
occupies active sites; more substrate required to reach ½ Vmax (Km is substrate
concentration at ½ Vmax)
4. Lineweaver-Burk plot: Same y-intercept (1/Vmax), different x-intercept (-1/Km
shifts toward origin)
Why Each Distractor is Wrong:
● A: Describes noncompetitive inhibition (inhibitor binds allosteric site, decreases
Vmax, Km unchanged)
● C: Describes uncompetitive inhibition (inhibitor binds enzyme-substrate complex
only, decreases both Vmax and Km)
● D: No common inhibitor increases Vmax (activators/allosteric activators may
increase Vmax)
● E: Describes the effect of allosteric activators or certain non-classical inhibitions
, Memory Aid: "Compete for the site? Km changes (Keeps going up), Vmax stays the
same (can overcome with more substrate). Noncompetitive = Neither changes Km
(stays same), Vmax drops."
Related Concepts Frequently Tested with This:
● Statins: HMG-CoA reductase competitive inhibitors
● Sulfa drugs: Competitive inhibitors of folate synthesis (PABA analogs)
● Methotrexate: Competitive inhibitor of dihydrofolate reductase
Cyanide poisoning: Noncompetitive inhibitor of cytochrome oxidase
● Clinical Pearl:
● Competitive inhibition can be overcome by increasing substrate concentration
(therapeutic implications for drug dosing)
● Km reflects affinity (lower Km = higher affinity); competitive inhibitors make the
enzyme appear to have lower affinity for substrate
Q3. A 32-year-old man is brought to the ED after a high-speed MVC. He is unconscious
with dilated pupils that are non-reactive to light. CT head shows a large, lens-shaped
(biconvex), hyperdense extra-axial collection overlying the right temporoparietal region.
Which vessel is most likely injured?
A. Middle meningeal artery
B. Bridging veins
C. Middle cerebral artery
D. Cerebral cortex veins
E. Superior sagittal sinus
Correct Answer: A
High-Yield Concept: Epidural hematoma vascular source
Bank 2026/2027 Edition Complete Practice
Questions with Verified Solutions
BLOCK 1: GENERAL PRINCIPLES & SYSTEMS 1-25
Q1. A 45-year-old woman presents with fatigue and joint pain. Physical exam reveals
hyperpigmented skin creases and arthralgias. Laboratory studies show elevated serum
iron, decreased total iron-binding capacity, and increased transferrin saturation. Which
of the following genes is most likely mutated in this patient?
A. HFE
B. ATP7B
C. CFTR
D. BRCA1
E. FBN1
Correct Answer: A
High-Yield Concept: Hereditary hemochromatosis genetics
Why Correct (Step-by-Step):
, 1. Classic triad: fatigue (often from diabetes/cardiomyopathy), arthralgias (hands
especially), bronze skin hyperpigmentation
2. Labs confirm iron overload: ↑serum Fe, ↓TIBC (transferrin is saturated),
↑transferrin saturation (>45% diagnostic, >62% strongly suggestive)
3. HFE gene on chromosome 6 (C282Y > H63D mutations) = autosomal recessive
hereditary hemochromatosis, most common in Caucasians
Why Each Distractor is Wrong:
● B: ATP7B mutations cause Wilson disease (copper overload, Kayser-Fleischer
rings, basal ganglia degeneration)
● C: CFTR mutations cause cystic fibrosis (Cl⁻ channel defect, pancreatic
insufficiency, chronic lung disease)
● D: BRCA1 mutations cause hereditary breast/ovarian cancer syndrome (DNA
repair defect)
● E: FBN1 mutations cause Marfan syndrome (fibrillin-1 defect, aortic root dilation,
lens dislocation)
Memory Aid: "HFE = Hemochromatosis = Fe Excess. C282Y: Cysteine to Tyrosine at
position 282—think 'Caucasian' (most common population)"
Related Concepts Frequently Tested with This:
● Complications: "Bronze diabetes" (pancreatic hemosiderosis), restrictive
cardiomyopathy, cirrhosis (risk of hepatocellular carcinoma), hypogonadotropic
hypogonadism
● Hemochromatosis is one of the MCCs of micronodular cirrhosis
vs. Secondary iron overload (transfusion-dependent thalassemias, ineffective
erythropoiesis)
● Clinical Pearl:
● Phlebotomy is first-line (goal ferritin 50-100 ng/mL)
● Screen first-degree relatives with HFE genetic testing + fasting iron studies
● Ferritin >1000 ng/mL predicts cirrhosis risk
Q2. A researcher studying enzyme kinetics adds a competitive inhibitor to a solution
containing enzyme and substrate. Which of the following best describes the expected
changes?
,A. Decreased Vmax, unchanged Km
B. Unchanged Vmax, increased Km
C. Decreased Vmax, decreased Km
D. Increased Vmax, unchanged Km
E. Unchanged Vmax, decreased Km
Correct Answer: B
High-Yield Concept: Competitive inhibition enzyme kinetics
Why Correct (Step-by-Step):
1. Competitive inhibitors bind reversibly to the enzyme's active site, competing
directly with substrate for binding
2. Vmax unchanged: At infinite substrate concentration, substrate outcompetes
inhibitor; maximal velocity achievable with enough substrate
3. Km increased: The apparent affinity for substrate decreases because inhibitor
occupies active sites; more substrate required to reach ½ Vmax (Km is substrate
concentration at ½ Vmax)
4. Lineweaver-Burk plot: Same y-intercept (1/Vmax), different x-intercept (-1/Km
shifts toward origin)
Why Each Distractor is Wrong:
● A: Describes noncompetitive inhibition (inhibitor binds allosteric site, decreases
Vmax, Km unchanged)
● C: Describes uncompetitive inhibition (inhibitor binds enzyme-substrate complex
only, decreases both Vmax and Km)
● D: No common inhibitor increases Vmax (activators/allosteric activators may
increase Vmax)
● E: Describes the effect of allosteric activators or certain non-classical inhibitions
, Memory Aid: "Compete for the site? Km changes (Keeps going up), Vmax stays the
same (can overcome with more substrate). Noncompetitive = Neither changes Km
(stays same), Vmax drops."
Related Concepts Frequently Tested with This:
● Statins: HMG-CoA reductase competitive inhibitors
● Sulfa drugs: Competitive inhibitors of folate synthesis (PABA analogs)
● Methotrexate: Competitive inhibitor of dihydrofolate reductase
Cyanide poisoning: Noncompetitive inhibitor of cytochrome oxidase
● Clinical Pearl:
● Competitive inhibition can be overcome by increasing substrate concentration
(therapeutic implications for drug dosing)
● Km reflects affinity (lower Km = higher affinity); competitive inhibitors make the
enzyme appear to have lower affinity for substrate
Q3. A 32-year-old man is brought to the ED after a high-speed MVC. He is unconscious
with dilated pupils that are non-reactive to light. CT head shows a large, lens-shaped
(biconvex), hyperdense extra-axial collection overlying the right temporoparietal region.
Which vessel is most likely injured?
A. Middle meningeal artery
B. Bridging veins
C. Middle cerebral artery
D. Cerebral cortex veins
E. Superior sagittal sinus
Correct Answer: A
High-Yield Concept: Epidural hematoma vascular source
