Infectious disease

Antitubercular Drugs - RIPE song

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Antitubercular Drugs - RIPE

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Key points in this song10

First-line TB treatment uses the RIPE regimen: Rifampin, Isoniazid, Pyrazinamide, and Ethambutol for 2 months, followed by Rifampin and Isoniazid alone for 4 months (2RIPE/4RI).
Isoniazid inhibits mycolic acid synthesis by blocking InhA (enoyl-ACP reductase); it requires activation by catalase-peroxidase (KatG), and KatG mutations cause the most common INH resistance.
Isoniazid causes peripheral neuropathy due to pyridoxine (B6) deficiency; B6 supplementation is given prophylactically, especially in malnourished patients, pregnant women, and alcoholics.
Rifampin inhibits DNA-dependent RNA polymerase; it is a potent CYP450 inducer, decreasing levels of warfarin, oral contraceptives, methadone, and HIV protease inhibitors.
Rifampin causes harmless orange-red discoloration of urine, tears, and sweat; drug-induced lupus and flu-like syndrome can occur with intermittent dosing.
Pyrazinamide is active only in acidic environments (inside phagolysosomes), making it essential for sterilizing intracellular bacilli; its major adverse effect is hyperuricemia leading to gout.
Ethambutol inhibits arabinosyl transferase, blocking arabinogalactan (mycobacterial cell wall) synthesis; its hallmark toxicity is retrobulbar optic neuritis causing red-green color blindness and decreased visual acuity.
Isoniazid monotherapy (9 months) is used for latent TB infection (LTBI) in tuberculin skin test or IGRA-positive individuals without active disease.
Rifampin resistance is the key marker for multidrug-resistant TB (MDR-TB), defined as resistance to at least Rifampin and Isoniazid; GeneXpert MTB/RIF rapidly detects both.
Isoniazid is metabolized by N-acetyltransferase 2 (NAT2); slow acetylators accumulate INH and are at higher risk for peripheral neuropathy and hepatotoxicity, while fast acetylators may have reduced efficacy.