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MT 6314 (3rd Shifting) > NA-FASI-Antimyco > Flashcards

NA-FASI-Antimyco Flashcards

1
Q

What are the Antifolate Drugs?

A
  • Sulfonamides
  • Trimethoprim
  • Trimethoprim-Sulfamethoxazole mixtures
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2
Q

What is the mechanism of action of antifolate drugs?

A
  1. Inhibit dihydropteroate synthase and folate production.
  2. Bacteriostatic when given alone.
  3. Usually given in combination with trimethoprim or pyrimethamine.
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3
Q

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

A

synergistic; wide

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4
Q

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

A

slow

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5
Q

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

A

earliest; successful

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6
Q

Sulfonamides are introduced in what year?

A

1935

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7
Q

Sulfonamides are introduced in 1935 by _?

A

Gerhard Domagk

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8
Q

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

A

Prontosil

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9
Q

True of False:

Sulfonamides are one of the most expensive antibiotics today.

A

False

Should be inexpensive.

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10
Q

Sulfonamides chemistry:

It is similar to:

A

p-aminobenzoic acid (PABA)

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11
Q

Sulfonamides chemistry:

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

A

Amido and amino group of sulfanilamide nucleus

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12
Q

Sulfonamide chemistry:

The amido group of sulfanilamide nucleus includes:

A
  • -SO2
  • -NH
  • -R
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13
Q

Sulfonamide chemistry:

The amino group of sulfanilamide nucleus includes:

A

-NH2

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14
Q

Antimicrobrial activity:

What are the coverage of Sulfonamides drugs?

A
  • 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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15
Q

True or False:

Sulfonamides is not active against Rickettsiae and P. aeruginosa.

A

True

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16
Q

What is the mechanism of action of Sulfonamides?

A
  1. Bacteriostatic inhibitors of folic acid synthesis.
  2. Competitive inhibitors of dihydropteroate synthase.
  3. Antimetabolites of PABA.
  4. Act as substrates for this enzyme → synthesis of nonfunctional forms of folic acid.
  5. Selective toxicity - Inability of mammalian cells to synthesize folic acid (Preformed folic acid in the diet)
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17
Q

True or False:

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

A

Due to sequential inhibition of folate synthesis

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18
Q

What are the resistance mechanisms of Sulfonamides?

A
  1. Some depend on exogenous sources of folate -> not affected by this drug
  2. M: Overproduction of PABA
  3. M: Production of folic acid synthesizing enzyme -> low affinity
  4. Impaired permeability
  5. Antibiotic efflux
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19
Q

What is the common resistance occuring in Sulfonamides?

A
  1. Plasmid-mediated
  2. Decreased accumulation of the drug
  3. Increase production of PABA by bacteria
  4. Decrease in the sensitivity of dihydropteroate synthase
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20
Q

Sulfonamides pkinetics:

It has three major groups:

A
  1. Oral, absorbable (stomach & SI)
  2. Oral, non-absorbable
  3. Topical
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21
Q

Sulfonamides pkinetics:

The protein binding varies from:

A

20% to 90%

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22
Q

Sulfonamides pkinetics:

Therapeutic blood concentration ranges from:

A

40-100 mcg/mL of blood

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23
Q

Sulfonamides pkinetics:

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

A

2 to 6 hours

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24
Q

Sulfonamides pkinetics:

It is metabolized through:

A

Hepatic metabolism

Portion of the drug is either acetylated or glucuronidated.

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25
Q

Sulfonamides pkinetics:

It is excreted through:

A

Urine

both intact drug and acetylated metabolites in urine.

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26
Q

Sulfonamides pkinetics:

It has weakly _ (acidic, basic) compounds.

A

acidic

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27
Q

Sulfonamides pkinetics:

It is the combination of 3 separate sulfonamides, used to reduce the likelihood to precipitate.

A

Triple Sulfa

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28
Q

What are the Triple Sulfa?

A
  1. Sulfisoxazole
  2. Sulfamethoxazole
  3. Sulfadoxine
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29
Q

Triple sulfa:

Short-acting

A

Sulfisoxazole

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30
Q

Triple sulfa:

Intermediate-acting

A

Sulfamethoxazole

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31
Q

Triple sulfa:

Long-acting

A

Sulfadoxine

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32
Q

Sulfonamides clinical uses:

Simple UTI: Oral

A
  • Triple sulfa
  • Sulfisoxazole
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33
Q

Sulfonamides clinical uses:

Ocular infection: Topical

A

Sulfacetamide

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34
Q

Sulfonamides clinical uses:

Burn infection: Topical

A
  • Mafenide
  • Silver sulfadiazine
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35
Q

What are the clinical uses of Sulfasalazine (Salicylazosulfapyridine)?

A
  • Ulcerative colitis
  • Enteritis
  • Inflammatory bowel disease (IBDs)
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36
Q

What are the Oral Absorbable Agents Sulfonamides?

A
  1. Sulfamethoxazole
  2. Sulfadiazine + Pyrimethamine
  3. Sulfadoxine + Pyrimethamine (Fansinadir/Fansidar)
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37
Q

Identify this Oral Absorbable Agents Sulfonamides:

  • Commonly used absorbable agent
  • Only available as the fixed dose combination of trimethoprim-sulfamethoxazole in the USA
A

Sulfamethoxazole

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38
Q

Identify this Oral Absorbable Agents Sulfonamides:

  • First line for acute toxoplasmosis
  • Synergistic (block sequential steps in the folate synthesis pathway)
A

Sulfadiazine + Pyrimethamine

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39
Q

Identify this Oral Absorbable Agents Sulfonamides:

  • Marketed in some countries
  • Second-line antimalarial agent
A

Sulfadoxine + Pyrimethamine
(Fansinadir/Fansidar)

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40
Q

What is the Oral Nonabsorbable Agents Sulfonamides?

A

Sulfasalazine

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41
Q

Sulfasalazine is used in the treatment of:

A

Inflammatory bowel disease (IBDs)

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42
Q

What are the Topical Agents Sulfonamides?

A
  1. Sodium sulfacetamide
  2. Mafenide acetate
  3. Silver sulfadiazine
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43
Q

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
A

Sodium sulfacetamide

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44
Q

Identify this Topical Absorbable Agents Sulfonamides:

  • Burn wounds for prevention of infection
  • Inhibit carbonic anhydrase
  • Can cause metabolic acidosis
A

Mafenide acetate

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45
Q

Identify this Topical Absorbable Agents Sulfonamides:

  • Less toxic topical sulfonamide
  • May slow wound healing
  • Prevent infection of burn wounds
  • Can cause metabolic acidosis
A

Silver sulfadiazine

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46
Q

What are the toxicities of Sulfonamides?

A
  • Cross-allergic
  • Hypersensitivity
  • Hematotoxicity (Hematopoietic Disturbances)
  • Nephrotoxicity (UT Disturbances)
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47
Q

Sulfonamides toxicities:

Most common for hypersensitivity:

A
  • Fever
  • Skin rashes
  • Exfoliative dermatitis
  • Photosensitivity
  • Urticaria
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48
Q

Sulfonamides toxicities:

Rare for hypersensitivity:

A
  • Exfoliative dermatitis
  • Polyarteritis nodosa
  • Stevens-Johnson syndrome
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49
Q

Sulfonamides toxicities:

Most common for gastrointestinal toxicity:

A
  • Nausea
  • Vomiting
  • Diarrhea
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50
Q

Sulfonamides toxicities:

Uncommon for gastrointestinal toxicities:

A
  • Mild hepatic dysfunction
  • Hepatitis
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51
Q

Sulfonamides toxicities:

Sulfonamides can cause hematopoietic disturbances such as:

A
  • Granulocytopenia
  • Thrombocytopenia
  • Aplastic anemia
  • Leukemoid reactions
  • Kernicterus
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52
Q

Sulfonamides toxicities:

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

A
  • Crystalluria
  • Obstruction
  • Hematuria
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53
Q

Sulfonamides drug interactions:

It has a competition with _ and _ for plasma binding by increasing the levels of these drugs.

A

warfarin and methotrexate

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54
Q

Sulfonamides drug interactions:

Displaces _ for plasma protein.

A

bilirubin

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55
Q

A trimethoxybenzyl pyrimidine.

A

Trimethoprim

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56
Q

What is the mechanism of action of Trimethoprim?

A
  1. Selective inhibitor of bacterial dihydrofolate reductase.
  2. Bacterial dihydrofolate reductase
  3. Bactericidal when combined with sulfamethoxazole
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57
Q

What is the resistance mechanisms of Trimethoprim?

A
  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.
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58
Q

Trimethoprim pkinetics:

It is usually given via:

A

orally, IV

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59
Q

Trimethoprim pkinetics:

Well absorbed by the _.

A

gut

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60
Q

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.

A

larger volume of distribution

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61
Q

Trimethoprim pkinetics:

The peak plasma concentration ratio is:

A

1:20

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62
Q

Trimethoprim pkinetics:

Half-life of Trimethoprime:

A

10-12 hours

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63
Q

Trimethoprim pkinetics:

It has a high concentration in _ and _ fluids.

A

prostatic and vaginal fluids

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64
Q

Trimethoprim pkinetics:

It is excreted through:

A

Urine

large fractions excreted unchanged.

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65
Q

Trimethoprim pkinetics:

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

A

base; acidic

66
Q

Trimethoprim pkinetics:

It is structurally similar to:

A

folic acid

67
Q

Trimethoprim clinical uses:

Oral Trimethoprim can be given alone (100 mg daily) in _

A

acute UTIs

68
Q

Trimethoprim clinical uses:

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

A
  • P jirovecii
  • UTIs
  • Prostatitis
  • Shigella
  • Salmonella
  • Nontuberculous mycobacteria
69
Q

Trimethoprim clinical uses:

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

A

pneumocystis pneumonia

70
Q

Trimethoprim clinical uses:

What is used in the treatment of toxoplasmosis?

A

Oral Pyrimethamine with Sulfonamide

71
Q

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.

A

Leucovorin

72
Q

Trimethoprim toxicities:

What are the predictable adverse of Trimethoprim?

A
  • Megaloblastic anemia
  • Leukopenia
  • Granulocytopenia
73
Q

Trimethoprim toxicities:

What are the occasional effects of Trimethoprim-sulfamethoxazole?

A
  • Nausea and vomiting
  • Drug fever
  • Vasculitis
  • Renal damage
  • CNS disturbances
74
Q

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.

A

creatinine

75
Q

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

A
  1. Combination results in sequential blockade of folate synthesis.
  2. Bactericidal against susceptible organisms.
76
Q

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

A
  • HIV patients
  • Fever
  • Rashes
  • Leukopenia
  • Diarrhea
77
Q

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

A
  • Urinary tract
  • Respiratory
  • Ear
  • Sinus infections caused by H. influenzae & M.catarrhalis
78
Q

What is the drug of choice for the prevention of:

A
  • Pneumocystis pneumonia
  • Toxoplasma
  • Nocardiosis
79
Q

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

A
  • Cholera
  • Typhoid fever
  • Shigellosis
80
Q

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

A
  • MR staphylococci
  • L. monocytogenes
81
Q

What is the earliest DNA gyrase inhibitors?

A

Nalidixic acid

82
Q

What are the synthetic fluorinated derivates DNA gyrase inhibitors?

A
  • Ciprofloxacin
  • Levofloxacin
83
Q

What are the coverage of Fluoroquinolones?

A
  • Atypical and intracellular pathogens
  • Gr (+) bacteria
  • Gr(-) organisms
84
Q

What is the 1st generation of Fluoroquinolones?

A

Norfloxacin

85
Q

Fluoroquinolones first gen:

Norfloxacin is derived from:

A

nalidixic acid

86
Q

Fluoroquinolones first gen:

Norfloxacin is the common pathogens that causes:

87
Q

True or False:

Norfloxacin is the least active of the fluoroquinolones against both gram negative and gram positive organisms.

88
Q

What is the 2nd generation of Fluoroquinolones?

A

Ciprofloxacin

89
Q

Fluoroquinolones 2nd gen:

What is the coverage of Ciprofloxacin?

A

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

90
Q

What are the 3rd generation of Fluoroquinolones?

A
  1. Levofloxacin
  2. Gatifloxacin
  3. Sparfloxacin
91
Q

What are the coverage of 3rd generation Fluoroquinolones drugs?

A
  • Slightly less active against Gr(-)
  • Greater activity against Gr(+) cocci
  • Streptococci (S. pneumoniae)
  • Staphylococci (MRSA)
  • Some strains of enterococci
92
Q

What are the 4th generation Fluoroquinolones drugs?

A
  1. Moxifloxacin
  2. Trovafloxacin
93
Q

What are the coverage of 4th generation Fluoroquinolones?

A
  • Broadest spectrum
  • Enhanced activity against anaerobes
94
Q

What is the mechanism of action of Fluoroquinolones?

A
  1. Interfere with bacterial DNA synthesis
    * Topoisomerase II (relaxation)
    * Topoisomerase IV (separation)
  2. Bactericidal
  3. Exhibit post-antibiotic effects
95
Q

What are the resistance mechanism of Fluoroquinolones?

A
  • 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
96
Q

Fluoroquinolones pkinetics:

It is well-absorbed:

97
Q

Fluoroquinolones pkinetics:

Bioavailability

98
Q

Fluoroquinolones pkinetics:

Serum half-life:

A

3-10 hours

99
Q

Fluoroquinolones pkinetics:

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

A
  • Levofloxacin
  • Gemifloxacin
  • Moxifloxacin
100
Q

Fluoroquinolones pkinetics:

Impaired absorption when combined wth:

A
  • Antacids
  • Divalent cations
  • Trivalent cations
101
Q

Fluoroquinolones pkinetics:

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

A

2 hours before; 4 hours after

102
Q

What are the clinical uses of Fluoroquinolones?

A
  • 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
103
Q

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

A

Gemifloxacin

104
Q

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

A

Delafloxacin

105
Q

What are the first-line drugs of Antimycobacterials?

A
  • Rifampin/Rifampicin
  • Isoniazid
  • Pyrazinamide
  • Ethambutol
106
Q

Identify this first-line anti-TB drug based on its pkinetics

  • Orally absorbed
  • Acetylated by the liver
  • Renally excreted
  • NO BBB Penetration
107
Q

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
A

Rifampin/Rifampicin

108
Q

Identify this first-line anti-TB drug based on its pkinetics:

● Orally absorbed
● Distributed to most tissues including CNS
● Excreted in urine

A

Ethambutol

109
Q

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
A

Pyrazinamide

110
Q

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
111
Q

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
A

Rifampin/Rifampicin

112
Q

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
A

Ethambutol

113
Q

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

A

Pyrazinamide

114
Q

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
115
Q

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
A

Rifampin/Rifampicin

116
Q

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
A

Ethambutol

117
Q

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
A

Pyrazinamide

118
Q

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

119
Q

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

A

Rifampin/Rifampicin

120
Q

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)

A

Ethambutol

121
Q

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

A

Pyrazinamide

122
Q

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
123
Q

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)
A

Rifampicin/Rifampin

124
Q

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
A

Ethambutol

125
Q

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
A

Pyrazinamide

126
Q

What are the second-line anti-TB drugs?

A
  • Streptomyin
  • Ethionamide
  • Capreomycin
  • Cycloserine
  • Aminosalicyclic acid (PAS)
  • Kanamycin & Amikacin
  • Fluoroquinolones
  • Linezolid
  • Rifabutin
  • Rifapentine
  • Rifaximin
  • Bedaquiline

SEC CAK sa FLR RRB

127
Q

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
A

Streptomycin

128
Q

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
A

Ethionamide

129
Q

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
A

Capreomycin

130
Q

Identify this second-line anti-TB drug based on its MOA:

Inhibits cell-wall synthesis (peptidoglycans)

A

Cycloserine

131
Q

Identify this second-line anti-TB drug based on its MOA:

Inhibits folic acid synthesis and mycobactin synthesis

A

Aminosalicyclic acid (PAS)

132
Q

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)
A

Kanamycin & Amikacin

133
Q

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
A

Fluoroquinolones

134
Q

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
135
Q

Identify this second-line anti-TB drug based on its MOA:

  • Inhibition of DNA-dependent RNA polymerase
  • Cross-resistance with
    rifampin
136
Q

Identify this second-line anti-TB drug based on its MOA:

Inhibiting of DNA-dependent RNA polymerase

137
Q

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

A

Bedaquiline

138
Q

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
A

Streptomycin

139
Q

Identify this second-line anti-TB drug based on clinical applications:

  • PTB treatment regimen for INH-intolerant patients
  • Can be used for leprosy treatment
A

Ethionamide

140
Q

Identify this second-line anti-TB drug based on clinical applications:

Treatment of drug-resistant tuberculosis

A

Capreomycin

141
Q

Identify this second-line anti-TB drug based on clinical applications:

Used in combination treatment for Mycobacterium avium complex and TB

A

Cycloserine

142
Q

Identify this second-line anti-TB drug based on toxicities:

  • Ototoxicity & nephrotoxicity
  • Vertigo and hearing loss
A

Streptomycin

143
Q

Identify this second-line anti-TB drug based on toxicities:

Hepatotoxicity, GI irritation, and neurotoxicity

A

Ethionamide

144
Q

Identify this second-line anti-TB drug based on toxicities:

  • [Ototoxicity] tinnitus, deafness, vestibular disturbances
  • Nephrotoxicity
A

Capreomycin

145
Q

Identify this second-line anti-TB drug based on toxicities:

  • Peripheral neuropathy
  • CNS dysfunction (depression and psychoses)
A

Cycloserine

146
Q

Identify this second-line anti-TB drug based on clinical applications:

Anti-mycobacterial agent used in combination to treat active tuberculosis

A

Aminosalicylic acid (PAS)

147
Q

Identify this second-line anti-TB drug based on clinical applications:

Used in combination for Treatment of streptomycin-resistant or MDR-TB

A

Kanamycin & Amikacin

148
Q

Identify this second-line anti-TB drug based on clinical applications:

MTB resistant to first-line agents

A

Fluoroquinolones

149
Q

Identify this second-line anti-TB drug based on clinical applications:

Used in combination with pyroxidone for treatment of MDR tuberculosis

150
Q

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
A

Aminosalicylic acid (PAS)

151
Q

Identify this second-line anti-TB drug based on its toxicities:

  • Ototoxicity
  • Nephrotoxicity
A

Kanamycin & Amikacin

152
Q

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.)
A

Fluoroquinolones

153
Q

Identify this second-line anti-TB drug based on its toxicities:

  • Bone marrow suspension, irreversible peripheral and optic neuropathy
  • Serotonin syndrome
154
Q

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
155
Q

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
A

Rifapentine

156
Q

Identify this second-line anti-TB drug based on clinical applications:

Used for traveler’s diarrhea

157
Q

Identify this second-line anti-TB drug based on clinical applications:

Treats isoniazid and rifampin resistant tuberculosis

A

Bedaquiline

158
Q

Identify this second-line anti-TB drug based on its toxicities:

  • Ototoxicity & nephrotoxicity
  • Vertigo and hearing loss
159
Q

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
A

Rifapentine

160
Q

Identify this second-line anti-TB drug based on its toxicities:

Nausea, headache, dizzine, joint pain, muscle tightening

161
Q

Identify this second-line anti-TB drug based on its toxicities:

Nausea, arthralgia, headache, hepatotoxicity, cardiac toxicity

A

Bedaquiline

MT 6314 (3rd Shifting) (7 decks)

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