HIGH-YIELD CONCEPTS FOR NBME
CBSE EXAM PREPARATION 2026
WITH 600 QUESTIONS AND CORRECT
ANSWERS RATED A+[NEWEST!!!]
Tumor suppressors
Cyclins/CDKs
Regulate progression of the cell cycle
Rb phosphorylation
Promotes cell cycle progression
Bioavailability (F)
Fraction of drug reaching systemic circulation
Cell Cycle Phases
G1 → S → G2 → M
G1/S Checkpoint
Controlled by Rb protein
G2/M Checkpoint
Controlled by p53 protein
p53/p21
Half-life (t½)
t½ = 0.693 × Vd / CL
Volume of Distribution (Vd)
Increases for lipophilic drugs
Clearance (CL)
CL = Rate of elimination / [Drug]
Loading Dose (LD)
LD = Cp × Vd / F
Maintenance Dose (MD)
MD = Cp × CL × τ / F
Agonists
Bind and activate receptors
Antagonists
Block receptors
Competitive Antagonists
Cause a right shift in the dose-response curve, same maximum effect
Noncompetitive Antagonists
, Decrease maximum effect of the agonist
Efficacy
Maximum response of a drug, higher is better
Potency
Dose needed for a drug to achieve its effect, higher means lower dose
required
Michaelis-Menten Curve
Describes the rate of enzymatic reactions
Km
Concentration of substrate at half of Vmax
Competitive Inhibitors
Increase Km, do not affect Vmax
Noncompetitive Inhibitors
Decrease Vmax, do not affect Km
cAMP (Gs)
Involved in signaling pathways for β1/2, H2, D1, TSH, PTH, ACTH, FSH,
LH
IP3 (Gq)
Involved in signaling pathways for α1, M1/3, H1, GnRH, TRH
Tyrosine Kinase (RTK)
Signaling pathway for Insulin, IGF-1, FGF
JAK-STAT Pathway
Signaling pathway for GH, Prolactin, EPO, G-CSF
CD4⁺ T Cells
Subtypes include TH1, TH2, TH17, and Treg, each with specific functions
in immune response.
TH1
Activates macrophages through IL-12 leading to IFN-γ production.
TH2
Activates eosinophils and promotes IgE production via IL-4, IL-5, and IL-13.
TH17
Recruits neutrophils through IL-17.
Treg
Suppresses immune responses using IL-10 and TGF-β.
CD8⁺ T Cells
Responsible for cytotoxic killing via perforin/granzymes or FasL.
B Cell Activation
Requires CD40-CD40L interaction and IL-4/IL-5 from CD4⁺ T cells.
Class Switching
CBSE EXAM PREPARATION 2026
WITH 600 QUESTIONS AND CORRECT
ANSWERS RATED A+[NEWEST!!!]
Tumor suppressors
Cyclins/CDKs
Regulate progression of the cell cycle
Rb phosphorylation
Promotes cell cycle progression
Bioavailability (F)
Fraction of drug reaching systemic circulation
Cell Cycle Phases
G1 → S → G2 → M
G1/S Checkpoint
Controlled by Rb protein
G2/M Checkpoint
Controlled by p53 protein
p53/p21
Half-life (t½)
t½ = 0.693 × Vd / CL
Volume of Distribution (Vd)
Increases for lipophilic drugs
Clearance (CL)
CL = Rate of elimination / [Drug]
Loading Dose (LD)
LD = Cp × Vd / F
Maintenance Dose (MD)
MD = Cp × CL × τ / F
Agonists
Bind and activate receptors
Antagonists
Block receptors
Competitive Antagonists
Cause a right shift in the dose-response curve, same maximum effect
Noncompetitive Antagonists
, Decrease maximum effect of the agonist
Efficacy
Maximum response of a drug, higher is better
Potency
Dose needed for a drug to achieve its effect, higher means lower dose
required
Michaelis-Menten Curve
Describes the rate of enzymatic reactions
Km
Concentration of substrate at half of Vmax
Competitive Inhibitors
Increase Km, do not affect Vmax
Noncompetitive Inhibitors
Decrease Vmax, do not affect Km
cAMP (Gs)
Involved in signaling pathways for β1/2, H2, D1, TSH, PTH, ACTH, FSH,
LH
IP3 (Gq)
Involved in signaling pathways for α1, M1/3, H1, GnRH, TRH
Tyrosine Kinase (RTK)
Signaling pathway for Insulin, IGF-1, FGF
JAK-STAT Pathway
Signaling pathway for GH, Prolactin, EPO, G-CSF
CD4⁺ T Cells
Subtypes include TH1, TH2, TH17, and Treg, each with specific functions
in immune response.
TH1
Activates macrophages through IL-12 leading to IFN-γ production.
TH2
Activates eosinophils and promotes IgE production via IL-4, IL-5, and IL-13.
TH17
Recruits neutrophils through IL-17.
Treg
Suppresses immune responses using IL-10 and TGF-β.
CD8⁺ T Cells
Responsible for cytotoxic killing via perforin/granzymes or FasL.
B Cell Activation
Requires CD40-CD40L interaction and IL-4/IL-5 from CD4⁺ T cells.
Class Switching
