Internal Medicine (Theory) · MU Sofia

60. Gout (podagra)

Explains gout as a crystal-induced arthritis driven by monosodium urate deposition in joints, starting with its definition and the classic podagra presentation. It then covers the causes of hyperuricaemia, the inflammatory pathway behind attacks, and acute versus chronic features such as tophi and renal involvement. Diagnosis by joint fluid analysis, X-ray findings, complications, and a short terminology table close the note.

Inside: 9 sections · 4 labelled pictures · 1 table · 15 flashcards · 3 min

Topic 56 of 58 in the MU Sofia syllabus for Internal Medicine (Theory) (Medicine, Year 3). The free AceMed note covers it in 9 sections, about 324 words (3 min of reading), with 15 flashcards.

In this note

  1. Gout (Podagra)
  2. Definition:
  3. Etiology:
  4. Pathogenesis:
  5. Clinical Features:
  6. Diagnosis:
  7. Treatment:
  8. Complications:
  9. Terminology to Remember:

Definition:

Gout is a crystal-induced inflammatory arthritis caused by deposition of monosodium urate crystals in synovial joints due to hyperuricemia (serum uric acid > 6.8 mg/dL). It classically presents as sudden, severe pain, swelling, and redness in joints—most commonly the first metatarsophalangeal joint ("podagra").

Etiology:

Hyperuricemia arises due to either:

  • Decreased excretion of uric acid (most common cause – 90% of primary gout):
  • Chronic kidney disease (↓ GFR)
  • Thiazide or loop diuretics
  • Lead nephropathy
  • Dehydration
  • Alcohol abuse
  • Increased production of uric acid:
  • High purine intake (meat, seafood, alcohol)
  • Increased cell turnover: leukemias, lymphomas, psoriasis
  • Enzyme defects: PRPP synthetase overactivity, HGPRT deficiency (→ Lesch-Nyhan syndrome)

Pathogenesis:

  • Uric acid is the end product of purine metabolism.
  • When uric acid levels exceed solubility threshold, monosodium urate (MSU) crystals precipitate, particularly in:
  • Cooler joints (e.g., great toe, ankle, knee)
  • Crystals are phagocytosed by macrophages, triggering:
  • Activation of NLRP3 inflammasome
  • Release of IL-1β, TNF-α, prostaglandins → strong neutrophilic inflammation
  • This leads to:
  • Pain, swelling, erythema, and warmth
  • Resolution occurs via: crystal coating by proteins, anti-inflammatory cytokines, neutrophil apoptosis, and macrophage clearance.

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