NEETPGAI
FeaturesNEET PGFMGEINI-CETBlogPricing
Log inStart Free
NEETPGAI

AI-powered NEET PG preparation platform. Master all 19 subjects with adaptive MCQs, AI tutoring, and spaced repetition.

Product

  • Features
  • Subjects
  • Previous Year Questions
  • NEET PG Preparation
  • FMGE Preparation
  • INI-CET Preparation
  • Compare
  • Pricing
  • Blog

Features

  • Adaptive MCQ Practice
  • AI Tutor
  • Mock Tests
  • Spaced Repetition

Resources

  • Blog
  • Study Guides
  • NEET PG Updates
  • Contact & support

Legal

  • Privacy Policy
  • Terms of Service

Stay updated

© 2026 NEETPGAI. All rights reserved.
    Subjects/Pathology/Amyloidosis
    Amyloidosis
    medium
    microscope Pathology

    A 52-year-old woman with a 10-year history of rheumatoid arthritis presents with nephrotic syndrome and renal biopsy shows AA amyloidosis. What is the drug of choice to prevent further amyloid deposition and slow renal disease progression?

    A. Tafamidis
    B. Bortezomib
    C. Colchicine
    D. Lenalidomide

    Explanation

    Management of Secondary (AA) Amyloidosis

    Key Point
    Colchicine is the first-line agent for secondary AA amyloidosis by suppressing serum amyloid A (SAA) production through inhibition of IL-1β and IL-6 in inflammatory cells.
    Pathophysiology of AA Amyloidosis

    AA amyloidosis develops in chronic inflammatory conditions (rheumatoid arthritis, chronic infections, inflammatory bowel disease). The acute-phase reactant serum amyloid A (SAA) is persistently elevated and misfolds to form amyloid deposits, particularly in kidneys, liver, and spleen.

    Mechanism of Colchicine
    1. 1.
      Inhibits microtubule polymerization in neutrophils and macrophages
    2. 2.
      Reduces production of pro-inflammatory cytokines (IL-1β, IL-6, TNF-α)
    3. 3.
      Decreases serum amyloid A (SAA) levels
    4. 4.
      Prevents further amyloid fibril deposition and halts disease progression
    Treatment Strategy for AA Amyloidosis
    Loading diagram...
    Colchicine Dosing & Monitoring
    • Dose: 0.5–1 mg daily (adjust for renal function)
    • Monitoring: SAA levels, serum creatinine, 24-hour urine protein
    • Goal: Reduce SAA to <10 mg/L to halt amyloid deposition
    • Adverse effects: GI upset, diarrhea; contraindicated in severe renal/hepatic disease
    High-YieldNEET PG
    Colchicine + aggressive control of the underlying inflammatory disease (DMARDs, biologics) is the cornerstone of AA amyloidosis management. Early intervention can stabilize or reverse renal disease.
    Clinical Pearl
    In this patient, optimizing rheumatoid arthritis control (e.g., TNF inhibitors, methotrexate) is equally important as colchicine — the goal is to lower SAA production at the source.
    Comparison: AA vs. AL vs. TTR Amyloidosis
    Table
    TypeCauseFirst-Line DrugMechanism
    AA (Secondary)Chronic inflammation (RA, TB, IBD)ColchicineReduces SAA production
    AL (Primary)Misfolded Ig light chains (plasma cell dyscrasias)Melphalan + ASCTChemotherapy + stem cell transplant
    TTR (Hereditary/Wild-type)Transthyretin mutations or agingTafamidisStabilizes transthyretin tetramer
    Mnemonic
    SAA → Colchicine (Secondary Amyloidosis Amyloid → Colchicine). AA amyloidosis is driven by persistent SAA elevation; colchicine suppresses it.

    Practice similar questions

    Sign up free to access AI-powered MCQ practice with detailed explanations and adaptive learning.

    Start Practicing Free More Pathology Questions

    Join our NEET PG community

    Daily MCQs, study tips, and topper strategies on Telegram.

    Join on Telegram →