antimicrobial drugs

Question 1

What is the mechanism of action of rifampin?

Answer 1

Binds to the β-subunit of bacterial DNA-dependent RNA polymerase → inhibits RNA synthesis.

Question 2

What mutation causes resistance to rifampin?

Answer 2

Point mutations in the rpoB gene (coding for the β-subunit of RNA polymerase).

Question 3

What are the adverse effects of rifampin?

Answer 3

Red-orange body fluids, renal effects, rashes, hepatotoxicity. CYP inducer. Safe in pregnancy.

Question 4

What is the mechanism of action of isoniazid?

Answer 4

Inhibits synthesis of mycolic acids, disrupting the mycobacterial cell wall.

Question 5

What causes high-level resistance to isoniazid?

Answer 5

Deletion of KatG gene.

Question 6

What causes low-level resistance to isoniazid?

Answer 6

Overexpression of inhA and KasA.

Question 7

What are the adverse effects of isoniazid?

Answer 7

Neurotoxicity (prevented by pyridoxine), hemolysis, lupus-like syndrome, hepatotoxicity. CYP inhibitor. Safe in pregnancy.

Question 8

What is the role of pyridoxine in TB treatment?

Answer 8

Prevents isoniazid-induced neurotoxicity.

Question 9

What activates pyrazinamide?

Answer 9

Hydrolyzed by pyrazinamidase (pncA gene) to active pyrazinoic acid.

Question 10

What causes resistance to pyrazinamide?

Answer 10

Impaired uptake or mutations in the pncA gene.

Question 11

What are the adverse effects of pyrazinamide?

Answer 11

Hyperuricemia, non-gouty polyarthralgia, hepatotoxicity, myalgia, porphyria, photosensitivity.

Question 12

What is the mechanism of action of ethambutol?

Answer 12

Inhibits arabinosyltransferases (emb gene), reducing arabinogalactan polymerization in the cell wall.

Question 13

What causes resistance to ethambutol?

Answer 13

Mutations or overexpression in the emb gene.

Question 14

What are the adverse effects of ethambutol?

Answer 14

Visual disturbances (e.g., red-green color blindness, optic neuritis). Not used in very young children.

Question 15

What is Direct Observation Therapy (DOT)?

Answer 15

A strategy to ensure adherence by observing patients take their TB medication, improving outcomes and reducing resistance.

Question 16

What are first-line drugs for tuberculosis?

Answer 16

Rifampin, isoniazid, pyrazinamide, and ethambutol.

Question 17

What are second-line drugs for tuberculosis?

Answer 17

Streptomycin, amikacin, ethionamide, levofloxacin.

Question 18

What is the MOA of streptomycin and amikacin?

Answer 18

Aminoglycosides that inhibit protein synthesis by binding the 30S ribosomal subunit.

Question 19

What are the adverse effects of streptomycin and amikacin?

Answer 19

Ototoxicity, nephrotoxicity. Not safe in pregnancy.

Question 20

What is the MOA of ethionamide?

Answer 20

Blocks mycolic acid synthesis (like isoniazid). Causes GI upset and neurotoxicity.

Question 21

What is the MOA of levofloxacin?

Answer 21

Fluoroquinolone that inhibits DNA gyrase (topoisomerase II), interfering with DNA replication.

Question 22

What are levofloxacin’s adverse effects?

Answer 22

Tendinopathy. Not safe in pregnancy.

Question 23

What is the advantage of rifabutin over rifampin?

Answer 23

Rifabutin has fewer drug interactions due to weaker CYP induction.

Question 24

What drugs are used to treat leprosy?

Answer 24

Dapsone, rifampin, clofazimine.

Question 25

What is the MOA of dapsone?

Answer 25

Inhibits folate synthesis by targeting dihydropteroate synthetase.

Question 26

What are adverse effects of dapsone?

Answer 26

Hemolysis in G6PD deficiency, methemoglobinemia, erythema nodosum leprosum.

Question 27

What is the MOA of clofazimine?

Answer 27

Binds to bacterial DNA, inhibiting replication.

Question 28

What are clofazimine's adverse effects?

Answer 28

Skin and conjunctival discoloration. Does not cause erythema nodosum leprosum.

Question 29

What drugs are used to reverse erythema nodosum leprosum?

Answer 29

Corticosteroids and thalidomide.

Question 30

What is the WHO regimen for leprosy?

Answer 30

Multidrug therapy with rifampin, dapsone, and clofazimine.

Question 31

What are atypical mycobacteria?

Answer 31

Environmental organisms like M. avium and M. kansasii that are not communicable person-to-person.

Question 32

How are atypical mycobacterial infections treated?

Answer 32

With combination drug therapy due to frequent resistance.

Question 33

What is the goal of TB chemotherapy?

Answer 33

Eradicate bacilli, prevent transmission, prevent resistance, and eliminate persistent bacilli to prevent relapse.

Question 34

When is latent TB treated?

Answer 34

If the patient is recently infected or immunocompromised.

Question 35

What is commonly used to treat latent TB?

Answer 35

Isoniazid (monotherapy) or combination with rifapentine.

Question 36

Who is at high risk for developing active TB?

Answer 36

Recently infected individuals, HIV patients, immunosuppressed, young children, and people in congregate settings.

Question 37

What are key risk factors for TB reactivation?

Answer 37

HIV, diabetes, silicosis, low body weight, organ transplants, and immunosuppressive therapy.