NBME CBSE Question and Answer | Latest
Update Complete Exam Prep with Accurate
Solutions | Grade A+
• Cell Cycle Phases -✓✓G1 → S → G2 → M
• G1/S Checkpoint -✓✓Controlled by Rb protein
• G2/M Checkpoint -✓✓Controlled by p53 protein
• p53/p21 -✓✓Tumor suppressors
• Cyclins/CDKs -✓✓Regulate progression of the cell cycle
• Rb phosphorylation -✓✓Promotes cell cycle progression
• Bioavailability (F) -✓✓Fraction of drug reaching systemic circulation
• 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 -✓✓The process where B cells change the class of antibody they
produce, influenced by cytokines.
• IL-4 -✓✓Promotes class switching to IgE and IgG.
• IL-5 -✓✓Promotes class switching to IgA.
• Antibody Types -✓✓Includes IgM, IgG, IgA, IgE, and IgD, each with distinct functions.
• IgM -✓✓The first antibody produced; exists as a pentamer.
,• IgG -✓✓The most abundant antibody in circulation; can cross the placenta.
• IgA -✓✓Provides mucosal immunity.
• IgE -✓✓Involved in allergic reactions and defense against parasites.
• IgD -✓✓Function is unclear.
• Classic Pathway -✓✓Activation of the complement system via IgG or IgM leading to
C1 activation.
• Alternative & Lectin Pathways -✓✓Complement activation triggered directly by
microbial components.
• C3b -✓✓Acts as an opsonin in the complement system.
• C5a -✓✓Functions in neutrophil chemotaxis.
• MAC (C5b-C9) -✓✓Forms a membrane attack complex leading to cell lysis.
• C1 esterase inhibitor deficiency -✓✓Causes hereditary angioedema.
• C5-C9 deficiency -✓✓Leads to recurrent Neisseria infections.
• Hypersensitivity Reactions -✓✓Classified into four types based on mechanism and
examples.
• Type I Hypersensitivity -✓✓IgE-mediated reactions such as anaphylaxis and asthma.
• Type II Hypersensitivity -✓✓Involves IgG/IgM binding to cells, causing cytotoxic
effects.
• Type III Hypersensitivity -✓✓Characterized by immune complex formation, examples
include SLE and serum sickness.
• Type IV Hypersensitivity -✓✓T-cell mediated reactions, delayed response (48-72
hours), examples include TB test.
• X-linked Agammaglobulinemia (Bruton) -✓✓Characterized by no B cells leading to
recurrent bacterial infections.
• Selective IgA Deficiency -✓✓Most common immunodeficiency, leads to recurrent
mucosal infections.
, • DiGeorge Syndrome -✓✓Caused by a 22q11 deletion resulting in no thymus and
recurrent infections.
• IL-12 Receptor Deficiency -✓✓Results in decreased IFN-γ and weak TH1 response,
leading to mycobacterial infections.
• SCID (Severe Combined Immunodeficiency) -✓✓Characterized by decreased B and T
cells, often referred to as 'bubble baby' disease.
• Wiskott-Aldrich Syndrome (WAS) -✓✓X-linked condition with thrombocytopenia,
eczema, and recurrent infections.
• Hyper-IgE Syndrome (Job Syndrome) -✓✓Characterized by coarse facial features,
cold abscesses, and eczema.
• SLE -✓✓Autoimmune disease marked by ANA+, anti-dsDNA, low complement levels,
and photosensitivity.
• RA -✓✓Rheumatoid arthritis characterized by RF+ and anti-CCP antibodies, with
morning stiffness.
• Hashimoto -✓✓Autoimmune thyroiditis indicated by anti-TPO antibodies leading to
hypothyroidism.
• Type 1 DM -✓✓Autoimmune destruction of pancreatic β-cells.
• Live attenuated vaccines -✓✓Examples include MMR, varicella, and yellow fever.
• Killed vaccines -✓✓Examples include Polio (IPV), Hep A, rabies, and influenza (shot).
• Toxoid vaccines -✓✓Examples include tetanus and diphtheria.
• Subunit vaccines -✓✓Examples include HBV and HPV.
• Aortic Dissection -✓✓Characterized by sudden tearing chest pain radiating to the
back.
• Myocardial Infarction (STEMI/NSTEMI) -✓✓Presents with crushing substernal chest
pain not relieved by rest.
• Heart Failure (Left vs Right) -✓✓Left HF presents with pulmonary edema; Right HF
presents with peripheral edema.
Update Complete Exam Prep with Accurate
Solutions | Grade A+
• Cell Cycle Phases -✓✓G1 → S → G2 → M
• G1/S Checkpoint -✓✓Controlled by Rb protein
• G2/M Checkpoint -✓✓Controlled by p53 protein
• p53/p21 -✓✓Tumor suppressors
• Cyclins/CDKs -✓✓Regulate progression of the cell cycle
• Rb phosphorylation -✓✓Promotes cell cycle progression
• Bioavailability (F) -✓✓Fraction of drug reaching systemic circulation
• 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 -✓✓The process where B cells change the class of antibody they
produce, influenced by cytokines.
• IL-4 -✓✓Promotes class switching to IgE and IgG.
• IL-5 -✓✓Promotes class switching to IgA.
• Antibody Types -✓✓Includes IgM, IgG, IgA, IgE, and IgD, each with distinct functions.
• IgM -✓✓The first antibody produced; exists as a pentamer.
,• IgG -✓✓The most abundant antibody in circulation; can cross the placenta.
• IgA -✓✓Provides mucosal immunity.
• IgE -✓✓Involved in allergic reactions and defense against parasites.
• IgD -✓✓Function is unclear.
• Classic Pathway -✓✓Activation of the complement system via IgG or IgM leading to
C1 activation.
• Alternative & Lectin Pathways -✓✓Complement activation triggered directly by
microbial components.
• C3b -✓✓Acts as an opsonin in the complement system.
• C5a -✓✓Functions in neutrophil chemotaxis.
• MAC (C5b-C9) -✓✓Forms a membrane attack complex leading to cell lysis.
• C1 esterase inhibitor deficiency -✓✓Causes hereditary angioedema.
• C5-C9 deficiency -✓✓Leads to recurrent Neisseria infections.
• Hypersensitivity Reactions -✓✓Classified into four types based on mechanism and
examples.
• Type I Hypersensitivity -✓✓IgE-mediated reactions such as anaphylaxis and asthma.
• Type II Hypersensitivity -✓✓Involves IgG/IgM binding to cells, causing cytotoxic
effects.
• Type III Hypersensitivity -✓✓Characterized by immune complex formation, examples
include SLE and serum sickness.
• Type IV Hypersensitivity -✓✓T-cell mediated reactions, delayed response (48-72
hours), examples include TB test.
• X-linked Agammaglobulinemia (Bruton) -✓✓Characterized by no B cells leading to
recurrent bacterial infections.
• Selective IgA Deficiency -✓✓Most common immunodeficiency, leads to recurrent
mucosal infections.
, • DiGeorge Syndrome -✓✓Caused by a 22q11 deletion resulting in no thymus and
recurrent infections.
• IL-12 Receptor Deficiency -✓✓Results in decreased IFN-γ and weak TH1 response,
leading to mycobacterial infections.
• SCID (Severe Combined Immunodeficiency) -✓✓Characterized by decreased B and T
cells, often referred to as 'bubble baby' disease.
• Wiskott-Aldrich Syndrome (WAS) -✓✓X-linked condition with thrombocytopenia,
eczema, and recurrent infections.
• Hyper-IgE Syndrome (Job Syndrome) -✓✓Characterized by coarse facial features,
cold abscesses, and eczema.
• SLE -✓✓Autoimmune disease marked by ANA+, anti-dsDNA, low complement levels,
and photosensitivity.
• RA -✓✓Rheumatoid arthritis characterized by RF+ and anti-CCP antibodies, with
morning stiffness.
• Hashimoto -✓✓Autoimmune thyroiditis indicated by anti-TPO antibodies leading to
hypothyroidism.
• Type 1 DM -✓✓Autoimmune destruction of pancreatic β-cells.
• Live attenuated vaccines -✓✓Examples include MMR, varicella, and yellow fever.
• Killed vaccines -✓✓Examples include Polio (IPV), Hep A, rabies, and influenza (shot).
• Toxoid vaccines -✓✓Examples include tetanus and diphtheria.
• Subunit vaccines -✓✓Examples include HBV and HPV.
• Aortic Dissection -✓✓Characterized by sudden tearing chest pain radiating to the
back.
• Myocardial Infarction (STEMI/NSTEMI) -✓✓Presents with crushing substernal chest
pain not relieved by rest.
• Heart Failure (Left vs Right) -✓✓Left HF presents with pulmonary edema; Right HF
presents with peripheral edema.
