Learn / FMK
Every FMK condition
299 diseases, deficiencies, toxicities and drug mechanisms harvested from every FMK deck — the ones sprinkled through a single bullet as much as the ones with their own slide. Pick what you're given and what you have to name, or let it cycle; distractors come from the same category so you have to discriminate (hypoketotic vs. ketotic hypoglycemia, which GSD, which urea-cycle enzyme…). Every answer shows the whole card with the lecture and slide.
Nucleotide · FMK 08.1
Gout Acquired / not inherited
Defect / target: Multifactorial hyperuricemia (uric acid overproduction and/or underexcretion); humans lack urate oxidase so uric acid is the insoluble end product of purine degradation
Mechanism: Hyperuricemia supersaturates joint fluid, monosodium urate (MSU) crystals deposit in and around joints, and the inflammatory response to the crystals drives acute gouty arthritis; recurrent attacks lead to chronic tophaceous gout.
↑ Accumulates: Uric acid / monosodium urate crystals (joints, renal collecting system)
Presentation: Podagra (hot, swollen, exquisitely tender first MTP joint, classically waking the patient at ~2 AM), painful monoarthritis, tophi, urate nephrolithiasis (kidney stones)
Labs: Needle-shaped, negatively birefringent MSU crystals in aspirated synovial fluid under polarized light microscopy (gold standard, distinguishes from pseudogout and septic arthritis); serum uric acid above saturation (~6.5 mg/dL)
Treatment: Acute: colchicine, NSAIDs (indomethacin), or glucocorticoids (prednisolone); chronic under-excretors: uricosurics (probenecid, sulfinpyrazone); chronic over-producers: allopurinol (xanthine oxidase inhibitor); rasburicase for tumor lysis syndrome
Mr. Alvarez, 52: great toe at 2 AM that cannot tolerate a bedsheet = podagra. Purines -> insoluble uric acid -> crystal disease; pyrimidines -> soluble products -> no crystal disease.
Learn the mechanism: Purine degradation & uric acid →
FMK 08.1 Nucleic Acid Metabolism · slide 2, 18, 19, 20, 27, 28