Gout
It is indicated in a 37-year-old with uric acid 0.42 mmol/L and one attack of gout
Treatment at a glance
- Acute attack: NSAID (naproxen or indomethacin), colchicine or prednisolone
- Allopurinol only after the attack has settled, with prophylaxis
Gout
- Deposition of monosodium urate crystals in and around joints.
- Hyperuricemia (plasma urate 6.8 mg/dL) is necessary but not sufficient
- Uric acid = end product of purine catabolism
- Elevated urate results from overproduction, reduced renal excretion, or both
- Kidney: urate filtered by glomerulus → almost completely reabsorbed by proximal tubule → small amount secreted distally
Read this in Bone & Joint Pathology: Basic Structure, Cells, and Fractures
GOUT
- Transient attacks of acute arthritis initiated by monosodium urate (MSU) crystal deposition within and around joints, driven by hyperuricemia .
Read this in Infectious Arthritis: Bacterial, TB & Viral Joint Infections
What our notes say
- It is indicated in a 37-year-old with uric acid 0.42 mmol/L and one attack of gout (Internal Medicine Rheumatology CAT: 30 MCQs and 5 short answer questions)
- Gout is a disorder in which deposits of uric acid crystals accumulate in the joints because of high blood levels of uric acid. (Junior Clerkship in Internal Medicine (MBIM4100) main exam, Paper One: 31 Januar)
- A patient with gout has recently been started on allopurinol and is undergoing dose titration. (Internal Medicine (MBIM 4100) main exam, Paper One: 3 July 2019)
- Gout is a type of arthritis that occurs due to the accumulation of in the blood that causes needle-like crystals to form around the joints. (Internal Medicine (MBIM 4100) special/supplementary exam, Paper Two: 14 August 2)
- B—false, urinary uric acid excretion falls (this is the basis of its use in gout/urate stones). (bchem EOY 2011 — Past Paper Questions & Answers)
- Gout vs pseudogout — the crystal difference is everything (Bone & Soft Tissue Tumour Pathology: Must-Know Diagnoses)
Study material on Gout
- Infectious Arthritis: Bacterial, TB & Viral Joint Infections
- Internal Medicine (MBIM 4100) special/supplementary exam, Paper Two: 14 August 2019
- Junior Clerkship in Internal Medicine (MBIM4100) main exam, Paper One: 31 January 2024
- Internal Medicine (MBIM 4100) main exam, Paper One: 3 July 2019
- Master Bone & Soft Tissue Pathology: CAT 2 MCQs & Answers
- Pharmacology CRASH Course
- Bone & Joint Pathology: Basic Structure, Cells, and Fractures
- Internal Medicine Rheumatology CAT: 30 MCQs and 5 short answer questions
- Bone & Soft Tissue Tumour Pathology: Must-Know Diagnoses
- Chemical Path Mcqs
Practice questions on Gout
Allopurinol treats gout by inhibiting
- Urate transporter URAT1
- Prostaglandin synthesis
- Xanthine oxidase
- Tubular urate reabsorption
Answer: C. Xanthine oxidase catalyzes the final steps of uric acid synthesis; its inhibition reduces urate production. ---
The drug of choice for acute gout that inhibits microtubule polymerization in neutrophils is
- Allopurinol
- Probenecid
- Colchicine
- Indomethacin
Answer: C. Colchicine inhibits neutrophil microtubule assembly, reducing inflammation in acute gout. ---
Monosodium urate crystals in gout appear under polarized light as
- Rhomboid-shaped, weakly positively birefringent
- Round and non-birefringent
- Needle-shaped and negatively birefringent
- Rectangular and strongly positively birefringent
Answer: C. MSU = needle-shaped, negatively birefringent (yellow when parallel to slow axis). First MTP joint (podagra) is classic. Causes: overproduction or underexcretion of uric acid. ---
In gout, monosodium urate crystal deposition is most commonly seen in the
- Hip joint
- Proximal interphalangeal joints
- First metatarsophalangeal joint (podagra)
- Shoulder joint
Answer: C. Gout = inflammatory arthritis due to monosodium urate crystal deposition. Hyperuricemia is a prerequisite but not diagnostic. Most common site: first MTP joint (podagra). Other sites: knees, ankles, wrists, elbows. Tophi (urate deposits in soft tissues). Diagnosis: needle-shaped, negatively birefringent crystals in synovial fluid. Treatment: acute attack (NSAIDs, colchicine, steroids); prophylaxis (allopurinol, febux
The enzyme deficient in classic gout leading to hyperuricemia is ---
- Adenosine deaminase
- Hypoxanthine-guanine phosphoribosyltransferase (HGPRT)
- Xanthine oxidase
- Purine nucleoside phosphorylase
Answer: B.
Allopurinol treats gout by inhibiting ---
- Urate transporter URAT1
- Prostaglandin synthesis
- Xanthine oxidase
- Tubular urate reabsorption
Answer: C.