🦠 Antimycobacterial Drugs for the MCAT: RIPE Therapy and Mechanisms Made Visual

Tuberculosis (TB) is more than just a historical disease—it's an MCAT micro high-yield favorite, especially when it comes to understanding the RIPE drug regimen, mechanisms of action, and resistance patterns.

📚 MCAT Relevance: Tuberculosis in Test Questions

MCAT questions related to TB often show up in:

• MCAT Section: Biological and Biochemical Foundations of Living Systems

• AAMC Categories:

  • 3B: Respiratory system structure and function

  • 3C: Immune response, infectious disease

  • 1A/1B: Biochemistry of drug mechanisms

They may include:

• Drug MOA (mechanism of action)

• Resistance profiles

• Acid-fast properties

• Granuloma formation

🔬 Breakdown of TB Drug Mechanisms (RIPE)

Drug	Target	Function
Rifampin / Rifabutin	RNA Polymerase	Inhibits mRNA synthesis (DNA-dependent)
Isoniazid	Mycolic acid synthesis	Disrupts fatty acid synthesis, essential for cell wall
Pyrazinamide	Acidic intracellular environment	Active inside macrophages; unclear precise MOA
Ethambutol	Arabinogalactan synthesis	Inhibits arabinosyl transferase in the cell wall

🧠 MCAT Tip: Match drug to location—e.g., Isoniazid works on the cell wall; Rifampin acts on nucleic acid synthesis.

🩺 Drug Summary Table (from the image)

Bacterium	Prophylaxis	Treatment
M. tuberculosis	Isoniazid	Rifampin, Isoniazid, Pyrazinamide, Ethambutol (“RIPE” mnemonic)

🔥 Mnemonic: RIPE for Treatment

• R = Rifampin

• I = Isoniazid

• P = Pyrazinamide

• E = Ethambutol

📌 Extra MCAT Nugget: Rifampin turns body fluids orange. Ethambutol causes optic neuritis. Isoniazid is linked with vitamin B6 deficiency.

🚨 High-Yield Clinical Correlations

• HIV/TB co-infection: Rifabutin preferred over rifampin to avoid P450 induction

• PPD+ (Latent TB): Ison

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