SLE - Previous Year Pattern MCQs

NEET PG & Final MBBS | 30 Questions with Explanations

SECTION 1: EPIDEMIOLOGY & BASICS

• A) Men aged 40-60 years
• B) Women of childbearing age
• C) Children under 10 years
• D) Elderly men

• A) Asian/Pacific Islander
• B) White women
• C) Hispanic women
• D) Black women

• A) T-cell mediated cytotoxicity
• B) IgE mediated hypersensitivity
• C) Overactive innate and adaptive immunity causing tissue damage via autoantibodies and immune complexes
• D) NK cell dysfunction

SECTION 2: DIAGNOSIS & CLASSIFICATION CRITERIA

• A) Anti-dsDNA positivity
• B) Malar rash
• C) ANA titer ≥ 1:80
• D) Proteinuria > 0.5 g/24h

• A) 6
• B) 8
• C) 10
• D) 12

• A) Seizure
• B) Acute cutaneous lupus
• C) Renal biopsy showing Class III/IV lupus nephritis
• D) Anti-dsDNA positivity

• A) 4 or more criteria (at least 1 clinical + 1 immunologic) OR biopsy-proven lupus nephritis with positive ANA or anti-dsDNA
• B) 6 or more clinical criteria only
• C) ANA + anti-dsDNA positivity
• D) 4 immunologic criteria

• A) Cheeks
• B) Bridge of nose
• C) Nasolabial folds
• D) Lower eyelids

• A) Acute cutaneous lupus (6 points)
• B) Anti-dsDNA antibody (6 points)
• C) Joint involvement (6 points)
• D) Renal biopsy Class III/IV lupus nephritis (10 points)

SECTION 3: AUTOANTIBODIES (Most Heavily Tested Topic)

• A) Anti-dsDNA
• B) Anti-Smith (Anti-Sm)
• C) Anti-histone
• D) ANA (Antinuclear antibody)

• A) ANA
• B) Anti-dsDNA
• C) Anti-Smith (Anti-Sm)
• D) Anti-histone

• A) Cutaneous vasculitis
• B) Lupus nephritis
• C) Serositis
• D) Seizures

• A) Neonatal thrombocytopenia
• B) Neonatal lupus with congenital heart block
• C) Neonatal renal failure
• D) Neonatal seizures

• A) SLE only
• B) Sjögren's syndrome
• C) Mixed Connective Tissue Disease (MCTD)
• D) Drug-induced lupus

• A) SLE and Lupus nephritis
• B) Drug-induced lupus
• C) Sjögren's syndrome (and neonatal lupus)
• D) Antiphospholipid syndrome

SECTION 4: DRUG-INDUCED LUPUS

• A) Anti-dsDNA
• B) Anti-Smith
• C) Anti-histone
• D) Anti-Ro

• A) Procainamide
• B) Hydralazine
• C) Isoniazid
• D) Hydroxychloroquine

• A) Digoxin
• B) Amiodarone
• C) Procainamide
• D) Verapamil

• A) Renal involvement is more common
• B) Anti-dsDNA is always present
• C) Symptoms resolve after stopping the drug
• D) It primarily affects young women

SECTION 5: LUPUS NEPHRITIS

• A) Class II
• B) Class III
• C) Class IV
• D) Class V

• A) Proteinuria
• B) RBC casts
• C) Hypocomplementemia (low C3, C4)
• D) Elevated CRP (markedly)

• A) Class I
• B) Class II or V lupus nephritis (8 points)
• C) Class III or IV lupus nephritis (10 points)
• D) Mesangial proliferation

SECTION 6: CLINICAL FEATURES

• A) Pulmonary
• B) Cardiovascular
• C) Renal
• D) CNS

• A) Vegetations on the mitral valve on the ventricular surface
• B) Vegetations on BOTH surfaces of the valve leaflets (especially mitral)
• C) Large destructive vegetations like in infective endocarditis
• D) Tricuspid valve involvement only

• A) Rosacea
• B) Dermatomyositis
• C) Systemic Lupus Erythematosus
• D) Erysipelas

SECTION 7: TREATMENT

• A) Methotrexate
• B) Mycophenolate mofetil
• C) Hydroxychloroquine
• D) Cyclophosphamide

• A) Skin disease
• B) Arthritis
• C) Serositis
• D) Severe lupus nephritis (Class IV)

• A) Mild arthralgia
• B) Malar rash
• C) Severe lupus nephritis (Class III/IV)
• D) Drug-induced lupus

• A) Rituximab
• B) Belimumab
• C) Tocilizumab
• D) Abatacept

SECTION 8: ANTIPHOSPHOLIPID SYNDROME & MISCELLANEOUS

• A) Thrombotic thrombocytopenic purpura
• B) Antiphospholipid Antibody Syndrome (APS)
• C) Immune thrombocytopenic purpura
• D) DIC

Quick Revision - High-Yield Points for NEET PG

Pathogenesis of Rheumatoid Arthritis

Easy to Remember & Write in Exams

The Master Diagram (from Robbins & Cellular/Molecular Immunology)

Think of it in 4 Simple Phases

PHASE 1 → PHASE 2 → PHASE 3 → PHASE 4
 TRIGGER   IMMUNE    ENTER     DESTROY
          RESPONSE   JOINT     JOINT

PHASE 1 - The Trigger (What starts it?)

• HLA-DR4 (shared epitope) - most important genetic risk
• Also PTPN22 gene polymorphism (tyrosine phosphatase)
• ~50% of RA risk is genetic

• Smoking - most important environmental trigger
• Infections (especially periodontitis - Porphyromonas gingivalis)
• These cause CITRULLINATION of self proteins

What is citrullination? Enzymatic conversion of arginine → citrulline in self proteins (fibrinogen, collagen type II, alpha-enolase, vinculin). This creates NEW antigens (neoantigens) that the immune system has no tolerance to.

PHASE 2 - The Immune Response (Who attacks?)

Citrullinated proteins (ACPA antigens)
        ↓
Presented by HLA-DR4 to CD4+ T cells
        ↓
    ┌──────────┬──────────┐
  Th1 cells  Th17 cells  B cells
    ↓            ↓          ↓
  IFN-γ       IL-17      ACPA + RF

• Th17 cells - primary driver, secrete IL-17 (recruits neutrophils)
• Th1 cells - secrete IFN-γ (activates macrophages)
• B cells produce two important antibodies:

ACPA can appear years before joint symptoms - earliest ACPAs are IgA type, suggesting disease starts at mucosal sites (lungs, gut)

PHASE 3 - Entering the Joint (The invasion)

PHASE 4 - Joint Destruction (The damage)

Synoviocyte hyperplasia
        +
Dense infiltrate (CD4+ T cells, B cells, plasma cells, macrophages)
        +
Increased vascularity (angiogenesis)
        +
Neutrophils + fibrin deposits
        ↓
      PANNUS forms

What is Pannus? (Most important morphology term)

A mass of edematous synovium + inflammatory cells + granulation tissue + fibroblasts that grows OVER and ERODES articular cartilage

1. Proteases/collagenases (from synoviocytes + macrophages) → cartilage destruction
2. RANKL (expressed on activated T cells) → stimulates osteoclasts → bone resorption → erosions
3. Mechanical invasion of pannus into subchondral bone

End result of untreated disease:

Cartilage erosion → Joint space narrowing
Bone erosion → Periarticular erosions
Fibrous ankylosis → Bony ankylosis (ossification)

Complete Flow Chart (Write this in exam)

GENETICS (HLA-DR4, PTPN22)
        +
ENVIRONMENT (smoking, infection)
        ↓
CITRULLINATION of self proteins
(fibrinogen, collagen II, enolase, vinculin)
        ↓
LOSS OF TOLERANCE
        ↓
T cell activation (Th1 + Th17) + B cell activation
        ↓
ACPA + RF production
        ↓
Lymphocytes + antibodies + macrophages → SYNOVIUM
        ↓
Cytokine storm: TNF-α, IL-1, IL-6, IL-17
        ↓
SYNOVIOCYTE HYPERPLASIA → PANNUS formation
        ↓
Proteases + RANKL → osteoclast activation
        ↓
CARTILAGE + BONE DESTRUCTION
        ↓
Joint deformity: ulnar deviation, swan-neck, boutonnière

Key Morphology Points (Histology of RA Synovium)

1. Synoviocyte hyperplasia and proliferation
2. Dense infiltrate of CD4+ T cells, B cells, plasma cells, macrophages
3. Increased vascularity (angiogenesis)
4. Neutrophils + fibrin deposits on synovial surface
5. Osteoclastic activity → periarticular erosions + subchondral cysts

Rheumatoid Nodules

• Site: subcutaneous tissue over forearm, elbows, occiput, lumbosacral area
• Feel: small, firm, nontender oval masses
• Histology: necrotizing granulomas (resemble them)

Drugs Linked to Each Pathogenesis Step

Quick Memory Pegs for Exam