NA-FASI-Antimyco Flashcards by BAI JANNAH ABDULKARIM

What are the Antifolate Drugs?

Sulfonamides
Trimethoprim
Trimethoprim-Sulfamethoxazole mixtures

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What is the mechanism of action of antifolate drugs?

Inhibit dihydropteroate synthase and folate production.
Bacteriostatic when given alone.
Usually given in combination with trimethoprim or pyrimethamine.

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Sulfonamides and Trimethoprim has a _ action against _ spectrum of microorganisms.

synergistic; wide

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The resistance of Sulfonamides and Trimethoprim occurs but the development is _ (fast, slow).

slow

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Sulfonamides are one the _ and most _ antibiotics ever developed.

earliest; successful

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Sulfonamides are introduced in what year?

1935

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Sulfonamides are introduced in 1935 by _?

Gerhard Domagk

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Sulfonamides are introducted in 1935 by Gerhard Domagk and marketed as?

Prontosil

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True of False:

Sulfonamides are one of the most expensive antibiotics today.

False

Should be inexpensive.

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Sulfonamides chemistry:

It is similar to:

p-aminobenzoic acid (PABA)

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Sulfonamides chemistry:

Its physical, chemical, and pharmacologic properties are
produced by attaching substituents to the:

Amido and amino group of sulfanilamide nucleus

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Sulfonamide chemistry:

The amido group of sulfanilamide nucleus includes:

-SO2
-NH
-R

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Sulfonamide chemistry:

The amino group of sulfanilamide nucleus includes:

-NH2

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Antimicrobrial activity:

What are the coverage of Sulfonamides drugs?

Gr(+) : Staphylococcus sp.
Gr(-) organisms: Klebsiella, Salmonella, Shigella, Enterobacter sp, Nocardia sp, Chlamydia trachomatis (KSSENC)

Can also cover protozoa, poor against anaerobes.

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True or False:

Sulfonamides is not active against Rickettsiae and P. aeruginosa.

True

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What is the mechanism of action of Sulfonamides?

Bacteriostatic inhibitors of folic acid synthesis.
Competitive inhibitors of dihydropteroate synthase.
Antimetabolites of PABA.
Act as substrates for this enzyme → synthesis of nonfunctional forms of folic acid.
Selective toxicity - Inability of mammalian cells to synthesize folic acid (Preformed folic acid in the diet)

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True or False:

What is the reason behind Sulfonamides and Trimethoprim providing synergistic activity?

Due to sequential inhibition of folate synthesis

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What are the resistance mechanisms of Sulfonamides?

Some depend on exogenous sources of folate -> not affected by this drug
M: Overproduction of PABA
M: Production of folic acid synthesizing enzyme -> low affinity
Impaired permeability
Antibiotic efflux

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What is the common resistance occuring in Sulfonamides?

Plasmid-mediated
Decreased accumulation of the drug
Increase production of PABA by bacteria
Decrease in the sensitivity of dihydropteroate synthase

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Sulfonamides pkinetics:

It has three major groups:

Oral, absorbable (stomach & SI)
Oral, non-absorbable
Topical

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Sulfonamides pkinetics:

The protein binding varies from:

20% to 90%

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Sulfonamides pkinetics:

Therapeutic blood concentration ranges from:

40-100 mcg/mL of blood

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Sulfonamides pkinetics:

The blood levels peak at _ to _ hours after oral administration

2 to 6 hours

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Sulfonamides pkinetics:

It is metabolized through:

Hepatic metabolism

Portion of the drug is either acetylated or glucuronidated.

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# Sulfonamides pkinetics: It is excreted through:

Urine | both intact drug and acetylated metabolites in urine.

# Sulfonamides pkinetics: It has weakly _ (acidic, basic) compounds.

acidic

# Sulfonamides pkinetics: It is the combination of **3 separate sulfonamides**, used to **reduce** the likelihood to **precipitate.**

Triple Sulfa

What are the Triple Sulfa?

1. Sulfisoxazole 2. Sulfamethoxazole 3. Sulfadoxine

# Triple sulfa: Short-acting

Sulfisoxazole

# Triple sulfa: Intermediate-acting

Sulfamethoxazole

# Triple sulfa: Long-acting

Sulfadoxine

# Sulfonamides clinical uses: Simple UTI: *Oral*

* Triple sulfa * Sulfisoxazole

# Sulfonamides clinical uses: Ocular infection: *Topical*

Sulfacetamide

# Sulfonamides clinical uses: Burn infection: *Topical*

* Mafenide * Silver sulfadiazine

What are the clinical uses of Sulfasalazine (Salicylazosulfapyridine)?

* Ulcerative colitis * Enteritis * Inflammatory bowel disease (IBDs)

What are the Oral Absorbable Agents Sulfonamides?

1. Sulfamethoxazole 2. Sulfadiazine + Pyrimethamine 3. Sulfadoxine + Pyrimethamine (Fansinadir/Fansidar)

# Identify this Oral Absorbable Agents Sulfonamides: * Commonly used absorbable agent * Only available as the fixed dose combination of trimethoprim-sulfamethoxazole in the USA

Sulfamethoxazole

# Identify this Oral Absorbable Agents Sulfonamides: * First line for **acute toxoplasmosis** * Synergistic (block sequential steps in the folate synthesis pathway)

Sulfadiazine + Pyrimethamine

# Identify this Oral Absorbable Agents Sulfonamides: * Marketed in some countries * Second-line **antimalarial** agent

Sulfadoxine + Pyrimethamine (Fansinadir/Fansidar)

What is the Oral Nonabsorbable Agents Sulfonamides?

Sulfasalazine

Sulfasalazine is used in the treatment of:

Inflammatory bowel disease (IBDs)

What are the Topical Agents Sulfonamides?

1. Sodium sulfacetamide 2. Mafenide acetate 3. Silver sulfadiazine

# Identify this Topical Absorbable Agents Sulfonamides: * Ophthalmic solution or ointment * Effective in the treatment of bacterial conjunctivitis * Considered to be second-line due to potential allergic reactions

Sodium sulfacetamide

# Identify this Topical Absorbable Agents Sulfonamides: * Burn wounds for prevention of infection * Inhibit carbonic anhydrase * Can cause metabolic acidosis

Mafenide acetate

# Identify this Topical Absorbable Agents Sulfonamides: * Less toxic topical sulfonamide * May slow wound healing * Prevent infection of burn wounds * Can cause metabolic acidosis

Silver sulfadiazine

What are the toxicities of Sulfonamides?

* Cross-allergic * Hypersensitivity * Hematotoxicity (Hematopoietic Disturbances) * Nephrotoxicity (UT Disturbances)

# Sulfonamides toxicities: Most common for hypersensitivity:

* Fever * Skin rashes * Exfoliative dermatitis * Photosensitivity * Urticaria

# Sulfonamides toxicities: Rare for hypersensitivity:

* Exfoliative dermatitis * Polyarteritis nodosa * Stevens-Johnson syndrome

# Sulfonamides toxicities: Most common for gastrointestinal toxicity:

* Nausea * Vomiting * Diarrhea

# Sulfonamides toxicities: Uncommon for gastrointestinal toxicities:

* Mild hepatic dysfunction * Hepatitis

# Sulfonamides toxicities: Sulfonamides can cause hematopoietic disturbances such as:

* Granulocytopenia * Thrombocytopenia * Aplastic anemia * Leukemoid reactions * Kernicterus

# Sulfonamides toxicities: Nephrotoxicity, or UT disturbances, causes urine precitation, especially acidic or neutral. It causes:

* Crystalluria * Obstruction * Hematuria

# Sulfonamides drug interactions: It has a competition with _ and _ for **plasma binding** by increasing the levels of these drugs.

warfarin and methotrexate

# Sulfonamides drug interactions: Displaces _ for plasma protein.

bilirubin

A trimethoxybenzyl pyrimidine.

Trimethoprim

What is the mechanism of action of Trimethoprim?

1. **Selective inhibitor** of *bacterial dihydrofolate reductase.* 2. **Bacterial dihydrofolate reductase** 3. **Bactericidal** when combined with **sulfamethoxazole**

What is the resistance mechanisms of Trimethoprim?

1. Production of **dihydrofolate reductase** that has **reduced affinity** for the drug. 2. **Reduced cell permeability.** 3. **Overproduction** of dihydrofolate reductase. 4. Production of an **altered reductase** with **reduced drug binding.**

# Trimethoprim pkinetics: It is usually given via:

orally, IV

# Trimethoprim pkinetics: Well absorbed by the _.

gut

# Trimethoprim pkinetics: It is distrubuted widely in body fluids and tissues including CSF and has a __ (larger, smaller) volume of distribution than sulfamethoxazole due to increase lipid solubility.

larger volume of distribution

# Trimethoprim pkinetics: The peak plasma concentration ratio is:

1:20

# Trimethoprim pkinetics: Half-life of Trimethoprime:

10-12 hours

# Trimethoprim pkinetics: It has a high concentration in _ and _ fluids.

prostatic and vaginal fluids

# Trimethoprim pkinetics: It is excreted through:

Urine | large fractions excreted unchanged.

# Trimethoprim pkinetics: It has a weak _ (acid, base) and trapped in (acidic, basic environments).

base; acidic

# Trimethoprim pkinetics: It is structurally similar to:

folic acid

# Trimethoprim clinical uses: Oral Trimethoprim can be given alone (100 mg daily) in _

acute UTIs

# Trimethoprim clinical uses: Oral Trimethoprim-Sulfamethoxazole (TMP-SMZ) is effective in treating wide variety of infections, such as:

* P jirovecii * UTIs * Prostatitis * Shigella * Salmonella * Nontuberculous mycobacteria

# Trimethoprim clinical uses: IV Trimethoprim-Sulfamethoxazole is an agent of choice for moderately severe to severe:

pneumocystis pneumonia

# Trimethoprim clinical uses: What is used in the treatment of toxoplasmosis?

Oral Pyrimethamine with Sulfonamide

# Trimethoprim clinical uses: It is also known as **folinic acid**, should be taken 10 mg orally each day and should be administered to minimize bone marrow suppression seen with pyrimethamine.

Leucovorin

# Trimethoprim toxicities: What are the predictable adverse of Trimethoprim?

* Megaloblastic anemia * Leukopenia * Granulocytopenia

# Trimethoprim toxicities: What are the occasional effects of Trimethoprim-sulfamethoxazole?

* Nausea and vomiting * Drug fever * Vasculitis * Renal damage * CNS disturbances

# Trimethoprim toxicities: It inhibits the secretion of _ at the distal renal tubule, resulting in mild elevation of blood creatinine. The important to distinguish from true nephrotoxicity that may be caused by sulfonamide.

creatinine

What is the mechanism of action of Trimethoprim & Sulphamethoxazole (TMP-SMX)?

1. Combination results in **sequential blockade** of folate synthesis. 2. **Bactericidal** against susceptible organisms.

What is the toxicities of Trimethoprim & Sulphamethoxazole (TMP-SMX)?

* HIV patients * Fever * Rashes * Leukopenia * Diarrhea

What is the clinical uses of Trimethoprim & Sulphamethoxazole (TMP-SMX)?

* Urinary tract * Respiratory * Ear * Sinus infections caused by *H. influenzae* & *M.catarrhalis*

What is the **drug of choice** for the prevention of:

* Pneumocystis pneumonia * Toxoplasma * Nocardiosis

Trimethoprim & Suphamethoxazole (TMP-SMX) is the backup drug for:

* Cholera * Typhoid fever * Shigellosis

Trimethoprim & Suphamethoxazole (TMP-SMX) is the treatment of infections of:

* MR staphylococci * L. monocytogenes

What is the earliest DNA gyrase inhibitors?

Nalidixic acid

What are the synthetic fluorinated derivates DNA gyrase inhibitors?

* Ciprofloxacin * Levofloxacin

What are the coverage of Fluoroquinolones?

* Atypical and intracellular pathogens * Gr (+) bacteria * Gr(-) organisms

What is the 1st generation of Fluoroquinolones?

Norfloxacin

# Fluoroquinolones first gen: Norfloxacin is derived from:

nalidixic acid

# Fluoroquinolones first gen: Norfloxacin is the common pathogens that causes:

UTI

# True or False: Norfloxacin is the least active of the fluoroquinolones against both gram negative and gram positive organisms.

True

What is the 2nd generation of Fluoroquinolones?

Ciprofloxacin

# Fluoroquinolones 2nd gen: What is the coverage of Ciprofloxacin?

● Greater activity against Gr(-) ● Gr(+) cocci ● Gonococcus ● Mycobacteria ● Atypical organisms (M. pneumoniae)

What are the 3rd generation of Fluoroquinolones?

1. Levofloxacin 2. Gatifloxacin 3. Sparfloxacin

What are the coverage of 3rd generation Fluoroquinolones drugs?

* Slightly less active against Gr(-) * Greater activity against Gr(+) cocci * Streptococci (S. pneumoniae) * Staphylococci (MRSA) * Some strains of enterococci

What are the 4th generation Fluoroquinolones drugs?

1. Moxifloxacin 2. Trovafloxacin

What are the coverage of 4th generation Fluoroquinolones?

* Broadest spectrum * Enhanced activity against anaerobes

What is the mechanism of action of Fluoroquinolones?

1. Interfere with **bacterial DNA synthesis** * Topoisomerase II (relaxation) * Topoisomerase IV (separation) 2. **Bactericidal** 3. Exhibit **post-antibiotic** effects

What are the resistance mechanism of Fluoroquinolones?

* **Mutation** in the quinolone binding region of the target enzyme or to a change in permeability * Production of **efflux pumps** * Changes in **porin** structure * Changes in **sensitivity** of the enzyme via point mutations in the antibiotic binding regions

# Fluoroquinolones pkinetics: It is well-absorbed:

orally

# Fluoroquinolones pkinetics: Bioavailability

80-90%

# Fluoroquinolones pkinetics: Serum half-life:

3-10 hours

# Fluoroquinolones pkinetics: Long half-live permit **once-a-day dosing.** DNA gyrase inhibitors such as:

* Levofloxacin * Gemifloxacin * Moxifloxacin

# Fluoroquinolones pkinetics: **Impaired absorption** when combined wth:

* Antacids * Divalent cations * Trivalent cations

# Fluoroquinolones pkinetics: This should be taken _ hours or _ hour safter taking any of the antacids, divalent or trivalent cations.

2 hours before; 4 hours after

What are the clinical uses of Fluoroquinolones?

* Urogenital and GI tract infections (Except for moxifloxacin. * Soft tissues, bones, joints, and intra-abdominal and respiratory tract infections (Except norfloxacin) * Eradication of mingococci from carriers * Prophylaxis of BI with neutropenia due to cancer therapy

This fluoroquinolones is recommended in combination with azithromycin as an alternative to ceftriaxone.

Gemifloxacin

This fluoroquinolones is initially appeared promising in vitro against ciprofloxacin-resistant gonococcal strains but it failed to show activity compared to ceftriaxone.

Delafloxacin

What are the first-line drugs of Antimycobacterials?

* Rifampin/Rifampicin * Isoniazid * Pyrazinamide * Ethambutol

# Identify this first-line anti-TB drug based on its pkinetics * Orally absorbed * Acetylated by the liver * Renally excreted * NO BBB Penetration

Isoniazid

# Identify this first-line anti-TB drug based on its pkinetics * Distributed to most tissues including CNS * Enterohepatic cycling (Liver into bile) * High protein binding * Excreted in feces, urine

Rifampin/Rifampicin

# Identify this first-line anti-TB drug based on its pkinetics: ● Orally absorbed ● Distributed to most tissues including CNS ● Excreted in urine

Ethambutol

# Identify this first-line anti-TB drug based on its pkinetics: * Orally-absorbed * Distributed to most tissues including CNS * Metabolized by the liver * Partly to pyrazinoic acid

Pyrazinamide

# Identify this first-line anti-TB drug based on its MOA: * Bactericidal * Inhibits mycolic acid synthesis * Activated by KatG * Forms a covalent complex with AcpM and KasA * Drug interactions: Phenytoin, carbamazepine, benzodiazepines

Isoniazid

# Identify this first-line anti-TB drug based on its MOA: * Bactericidal * Inhibits DNA-dependent RNA polymerase * Binds to beta-subunit of bacterial DNA-dependent RNA polymerase * Inhibits RNA synthesis * Drug interactions: Methadone, Anticoagulants, Cyclosporine

Rifampin/Rifampicin

# Identify this first-line anti-TB drug based on its MOA: * Bactericidal or Bacteriostatic depending on the bacteria’s reproductive activity * Inhibits arabinosyltransferase enzyme needed for cell wall synthesis (polymerization of arabinoglycan) * Encoded by embCAB operon

Ethambutol

# Identify this first-line anti-TB drug based on its MOA: ● Bacteriostatic ● Inhibits tubercle bacilli Converted to pyrazinoic acid Encoded by pncA ● Disrupts mycobacterial cell membrane metabolism and transport functions

Pyrazinamide

# Identify this first-line anti-TB drug based on its resistance mechanism: 1. Overexpression of **inhA gene** 2. Mutation or deletion of **katG gene** 3. Promoter mutations resulting in overexpression of **ahpC** 4. Mutations in **kasA**

Isoniazid

# Identify this first-line anti-TB drug based on its resistance mechanism: 1. Any one of several possible point mutations in rpoB 2. These mutations result in reduced binding of rifampin to NA polymerase

Rifampin/Rifampicin

# Identify this first-line anti-TB drug based on its resistance mechanism: 1. Mutation in embB gene if drug is used alone. 2. Results in overexpression of emb gene products or within the embB strucutral gene

Ethambutol

# Identify this first-line anti-TB drug based on its resistance mechanism: 1. Impaired uptake of pyrazinamide 2. Mutations in pncA that impair conversion of PZA to its active form 3. Drug-efflux systems, especially when used alone

Pyrazinamide

# Identify this first-line anti-TB drug based on clinical applications: ● **Single most important drug** for TB (PTB [Combination Therapy]) ● **Sole** - LTBI, Close contact, prophylaxis

Isoniazid

# Identify this first-line anti-TB drug based on clinical applications: ● **PTB** (combination therapy) ● (Sole) INH-resistant TB or INH-intolerant LTBI ● Atypical mycobacterial infections ● **Leprosy** - delays resistance to dapsone ● MRSA, PRSP ● **Meningococcal & Staphylococcal** carriage ● Prophylaxis against **H. influenzae type b disease**

Rifampin/Rifampicin

# Identify this first-line anti-TB drug based on clinical applications: ● TB (combination therapy); usually EMB + INH, RIF, or PZA ● Combination with other agents for nontuberculous mycobacterial infections (MAC and M. kansasii)

Ethambutol

# Identify this first-line anti-TB drug based on clinical applications: ● MTB (combination therapy) ● Sterilizing agent with INH or RIF that deals with intracellular mycobacteria

Pyrazinamide

# Identify this first-line anti-TB drug based on toxicities: * **Peripheral neuritis** * Restlessness, Muscle twitches, Insomnia * **CNS toxicity**: Memory loss, Psychosis, Ataxia Seizures * **Hemolysis (G6PD)** * **CYP 450 inhibitor** (↑ conc) * **Hepatitis** (most common) * Fever and skin rashes * Drug-induced lupus erythematosus * Peripheral neuropathy * Miscellaneous: Hematologic abnormalities, Pyridoxine deficiency anemia, Tinnitus, GI discomfort

Isoniazid

# Identify this first-line anti-TB drug based on toxicities: * Orange color * Skin rashes, Thrombocytopenia, Nephritis * Cholestatic jaundice, Light-chain proteinuria, Flu-like syndrome * Acute tubular necrosis (associated)

Rifampicin/Rifampin

# Identify this first-line anti-TB drug based on toxicities: * Dose-dependent visual disturbances * Eyes : **Retrobulbar neuritis**, loss of visual acuity, red-green color-blindness * Headache, confusion, hyperuricemia

Ethambutol

# Identify this first-line anti-TB drug based on toxicities: * Joint pains, **myalgia**, GI irritation, rash * Nausea, vomiting, fever, photosensitivity * **Hyperuricemia** (gout) * Hepatotoxicity * **Contraindicated in pregnant women**

Pyrazinamide

What are the second-line anti-TB drugs?

* Streptomyin * Ethionamide * Capreomycin * Cycloserine * Aminosalicyclic acid (PAS) * Kanamycin & Amikacin * Fluoroquinolones * Linezolid * Rifabutin * Rifapentine * Rifaximin * Bedaquiline | SEC CAK sa FLR RRB

# Identify this second-line anti-TB drug based on its MOA: * Mainly affects extracellular tubercle bacilli * Irreversible inhibition of protein synthesis via the binding to the 30S subunit

Streptomycin

# Identify this second-line anti-TB drug based on its MOA: * INH derivative; also inhibits mycolic acids. * Low-level cross resistance between isoniazid and ethionamide

Ethionamide

# Identify this second-line anti-TB drug based on its MOA: * Binds to 70S ribosomal subunit. * Cross-resistance with amikacin and kanamycin * Resistance occurs due to rrs, eis, tlyA gene mutations

Capreomycin

# Identify this second-line anti-TB drug based on its MOA: Inhibits cell-wall synthesis (peptidoglycans)

Cycloserine

# Identify this second-line anti-TB drug based on its MOA: Inhibits **folic acid synthesis** and **mycobactin synthesis**

Aminosalicyclic acid (PAS)

# Identify this second-line anti-TB drug based on its MOA: * No cross-resistance with streptomycin and amikacin * Binds to 30S subunit * Interferes with mRNA binding and tRNA acceptor sites (to cause misreading of t-RNA; disrupting protein synthesis)

Kanamycin & Amikacin

# Identify this second-line anti-TB drug based on its MOA: * Class-resistance (resistance to one fluoroquinolone indicates resistance to others) * Inhibits DNA gyrase and topoisomerase IV to block bacterial DNA synthesis, inhibiting cell division

Fluoroquinolones

# Identify this second-line anti-TB drug based on its MOA: * Point mutations causes linezolid resistance * Inhibitor of monoamine oxidase enzymes and binds to the 50S subunit to prevent bacterial division

Linezolid

# Identify this second-line anti-TB drug based on its MOA: * Inhibition of DNA-dependent RNA polymerase * Cross-resistance with rifampin

Rifabutin

# Identify this second-line anti-TB drug based on its MOA: Inhibiting of DNA-dependent RNA polymerase

Rifaximin

# Identify this second-line anti-TB drug based on its MOA: Inhibits a bacteria’s generation of energy by interfering with their proton pump of mycobacterial ATP

Bedaquiline

# Identify this second-line anti-TB drug based on clinical applications: * **Life-threatening TB disease** (meningitis, miliary dissemination, severe organ TB) * **Pott’s disease**, extracellular TB

Streptomycin

# Identify this second-line anti-TB drug based on clinical applications: * PTB treatment regimen for **INH-intolerant patients** * Can be used for **leprosy treatment**

Ethionamide

# Identify this second-line anti-TB drug based on clinical applications: Treatment of drug-resistant tuberculosis

Capreomycin

# Identify this second-line anti-TB drug based on clinical applications: Used in combination treatment for **Mycobacterium avium complex and TB**

Cycloserine

# Identify this second-line anti-TB drug based on toxicities: * Ototoxicity & nephrotoxicity * Vertigo and hearing loss

Streptomycin

# Identify this second-line anti-TB drug based on toxicities: Hepatotoxicity, GI irritation, and neurotoxicity

Ethionamide

# Identify this second-line anti-TB drug based on toxicities: * [Ototoxicity] tinnitus, deafness, vestibular disturbances * Nephrotoxicity

Capreomycin

# Identify this second-line anti-TB drug based on toxicities: * Peripheral neuropathy * CNS dysfunction (depression and psychoses)

Cycloserine

# Identify this second-line anti-TB drug based on clinical applications: Anti-mycobacterial agent used in combination to treat active tuberculosis

Aminosalicylic acid (PAS)

# Identify this second-line anti-TB drug based on clinical applications: Used in combination for Treatment of **streptomycin-resistant or MDR-TB**

Kanamycin & Amikacin

# Identify this second-line anti-TB drug based on clinical applications: MTB resistant to **first-line agents**

Fluoroquinolones

# Identify this second-line anti-TB drug based on clinical applications: Used in combination with pyroxidone for treatment of MDR tuberculosis

Linezolid

# Identify this second-line anti-TB drug based on its toxicities: * High concentrations can cause crystalluria * Gastrointestinal symptoms, hypersensitivity, hemorrhage * Hepato-, nephro-, and thyroid toxicities

Aminosalicylic acid (PAS)

# Identify this second-line anti-TB drug based on its toxicities: * Ototoxicity * Nephrotoxicity

Kanamycin & Amikacin

# Identify this second-line anti-TB drug based on its toxicities: * Nausea, vomiting, diarrhea, abnormal liver function, headache, dizziness. * Peripheral neuropathy and central neurotoxicities (agitation, impaired memory etc.)

Fluoroquinolones

# Identify this second-line anti-TB drug based on its toxicities: * Bone marrow suspension, irreversible peripheral and optic neuropathy * **Serotonin syndrome**

Linezolid

# Identify this second-line anti-TB drug based on clinical applications: * Equally effective as anti-mycobacterial agent * For HIV/AIDS patients taking ARVs * MAC, MTB, M. fortuitum

Rifabutin

# Identify this second-line anti-TB drug based on clinical applications: * Active against Mycobacterium avium complex and M tuberculosis * Used in combination with isoniazid to LTBI in PLHIVs

Rifapentine

# Identify this second-line anti-TB drug based on clinical applications: Used for **traveler's diarrhea**

Rifaximin

# Identify this second-line anti-TB drug based on clinical applications: Treats **isoniazid and rifampin resistant tuberculosis**

Bedaquiline

# Identify this second-line anti-TB drug based on its toxicities: * Ototoxicity & nephrotoxicity * Vertigo and hearing loss

Rifabutin

# Identify this second-line anti-TB drug based on its toxicities: * Should NOT be used to treat ACTIVE tuberculosis in HIV patients due to risk of relapse * Can cause subtherapeutic levels of ARVs

Rifapentine

# Identify this second-line anti-TB drug based on its toxicities: Nausea, headache, dizzine, joint pain, muscle tightening

Rifaximin

# Identify this second-line anti-TB drug based on its toxicities: Nausea, arthralgia, headache, hepatotoxicity, cardiac toxicity

Bedaquiline

NA-FASI-Antimyco Flashcards

(162 cards)