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Flashcard Topics: Antimycobacterial Drugs

1. Mycobacteria - Overview

Q: What are the key characteristics of mycobacteria? A: Rod-shaped, aerobic, acid-fast bacilli that multiply slowly. Their cell walls contain mycolic acids (long-chain β-hydroxylated fatty acids). Infections cause slow-growing granulomatous lesions. M. tuberculosis is the leading infectious cause of death worldwide; a quarter of the world's population is infected.

2. First-Line Anti-TB Drug Regimen

Q: What is the standard short-course TB treatment regimen? A: Intensive phase (2 months): Isoniazid + Rifampin + Ethambutol + Pyrazinamide (RIPE). Continuation phase (4 months): Isoniazid + Rifampin. Total = 6 months for drug-susceptible TB.

3. Isoniazid (INH) - Mechanism of Action

Q: How does Isoniazid work? A: Inhibits acyl carrier protein reductase (InhA) and β-ketoacyl-ACP synthase (KasA) - enzymes essential for mycolic acid synthesis - disrupting the bacterial cell wall.

4. Isoniazid - Pharmacokinetics

Q: What are the key PK features of Isoniazid? A: Orally absorbed (impaired by high-fat meals). Diffuses into all body fluids, cells, and caseous material. CSF levels = serum levels. Undergoes N-acetylation: Fast acetylators t½ ~90 min; Slow acetylators t½ 3-4 hrs. Excreted renally (no dose adjustment needed in renal failure).

5. Isoniazid - Adverse Effects

Q: What are the major adverse effects of Isoniazid? A:

Hepatitis (most serious; fatal if unrecognized) - risk increases with age >35, co-use of rifampin, daily alcohol
Peripheral neuropathy (pyridoxine/B6 deficiency) - prevented by daily pyridoxine supplementation
CNS effects (convulsions in seizure-prone patients)
Hypersensitivity (rash, fever)
Drug interaction: inhibits metabolism of carbamazepine and phenytoin

6. Rifampin - Mechanism of Action

Q: How does Rifampin work? A: Blocks RNA synthesis by binding the β subunit of mycobacterial DNA-dependent RNA polymerase.

7. Rifampin - Pharmacokinetics & Key Features

Q: What are the PK features of Rifampin? A: Orally absorbed, distributes to all body fluids/organs. Undergoes enterohepatic recycling. Eliminated primarily via bile into feces (small % in urine). No dose adjustment needed for renal or hepatic insufficiency. Classic finding: Orange-red discoloration of urine, feces, tears, secretions (warn patients; can stain soft contact lenses).

8. Rifampin - Adverse Effects & Drug Interactions

Q: What are the adverse effects and drug interactions of Rifampin? A: Adverse effects: nausea, vomiting, rash, thrombocytopenia, nephritis, hepatitis (rare). Intermittent/high-dose use causes flu-like syndrome (fever, chills, myalgia, +/- hemolytic anemia, renal failure, shock). Key interaction: Potent inducer of CYP450 enzymes and transporters - causes numerous drug interactions. Use with caution in elderly, alcoholics, and chronic liver disease patients.

9. Rifabutin vs. Rifapentine

Q: How do Rifabutin and Rifapentine differ from Rifampin? A:

Rifabutin: Preferred in TB-HIV co-infected patients on protease inhibitors or NNRTIs. Less potent CYP450 inducer (fewer drug interactions). Unique adverse effects: uveitis, skin hyperpigmentation, neutropenia.
Rifapentine: Longer half-life. Used once weekly (with isoniazid) for latent TB infection and in select HIV-negative patients with minimal pulmonary TB.

10. Pyrazinamide - Key Points

Q: What are the key features of Pyrazinamide? A: Active against TB bacilli in acidic lesions and macrophages. Orally effective; penetrates the CSF. Converted to pyrazinoic acid (active form). Adverse effects: liver toxicity, uric acid retention (rarely causes gout), photosensitivity. Usually discontinued after the first 2 months of the 6-month regimen (clinical benefit mainly in early treatment).

11. Ethambutol - Mechanism, PK & Adverse Effects

Q: What is the mechanism and key adverse effect of Ethambutol? A: Mechanism: Inhibits arabinosyl transferase - an enzyme critical for mycobacterial cell wall synthesis. Bacteriostatic and mycobacteria-specific. PK: distributes well; excreted in urine. Key adverse effect: Optic neuritis - reduced visual acuity and red-green color discrimination loss. Risk increases with higher doses and renal impairment. Baseline and periodic visual acuity/color discrimination testing required. Also decreases uric acid excretion (caution in gout).

12. Second-Line Anti-TB Drugs

Q: What are the second-line anti-TB agents? A:

Aminoglycosides: Streptomycin, Kanamycin, Amikacin
Capreomycin (peptide antibiotic - protein synthesis inhibitor)
Cycloserine (d-alanine analog - inhibits cell wall synthesis)
Aminosalicylic acid (PAS) - folate synthesis antagonist (similar to sulfonamides)
Fluoroquinolones (e.g., Levofloxacin, Moxifloxacin)
Linezolid (oxazolidinone)
Bedaquiline (ATP synthase inhibitor)

13. Bedaquiline - Key Points

Q: What is Bedaquiline used for and what are its adverse effects? A: Approved for MDR-TB. Mechanism: ATP synthase inhibitor. Oral administration; active against many mycobacteria types. Adverse effects: QT prolongation (ECG monitoring required), elevated liver enzymes (monitor LFTs). Metabolized via CYP3A4 - avoid co-administration with strong CYP3A4 inducers like rifampin.

14. MDR-TB and XDR-TB Treatment

Q: How is MDR-TB and XDR-TB treated? A:

MDR-TB (resistant to at least INH + Rifampin): Injectable aminoglycoside (streptomycin/kanamycin/amikacin) or capreomycin + a fluoroquinolone (levofloxacin/moxifloxacin) + any remaining active first-line drugs + cycloserine, ethionamide, or PAS. Lasts ~2 years.
XDR-TB: Empiric use of clofazimine and linezolid.

These 14 flashcards cover every major topic in the presentation - drug mechanisms, pharmacokinetics, adverse effects, drug interactions, TB biology, and treatment regimens. Let me know if you'd like these formatted as printable cards or exported to a file!

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