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2nd Year 2nd Term > MT6314 SULFONA/TRIMETH/QUINO/ANTIMYCOBACTERIALS > Flashcards

MT6314 SULFONA/TRIMETH/QUINO/ANTIMYCOBACTERIALS Flashcards

1
Q

Antifolate Drugs include?

A

*Sulfonamides
*Trimethoprim and Trimethoprim Sulfamethoxazole Mixtures

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2
Q

DNA Gyrase Inhibitors include?

A

Fluoroquinolones

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3
Q

What are the different antimetabolites?

A

SULFONAMIDES
TRIMETHOPRIM
TRIMETHOPRIM-SULFAMETHOXAZOLE

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4
Q

What are the different quinolones?

A

NARROW SPECTRUM - 1st Gen
WIDE SPECTRUM - 2nd-4th Gen

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5
Q

One of the earliest and successful antibiotics ever developed

A

Sulfonamides

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6
Q

When were Sulfonamides introduced and by who?

A

1935 by Gerhard Domagk

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7
Q

Sulfonamides were marketed as?

A

Prontosil

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8
Q

Sulfonamides are similar to what substance?

A

p-aminobenzoic acid (PABA)

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9
Q

Sulfonamides physical, chemical and pharmacologic properties are produced by?

A

attaching substituents to the amido group (-SO2, -NH, -R) or the amino group (-NH2 group) of the sulfanilamide nucleus

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10
Q

One of the most inexpensive antibiotics today

A

Sulfonamides

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11
Q

Examples of Sulfonamides and PABAs?

A

Sulfanilamide
PABA
Sulfadiazine
Sulfamethoxazole

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12
Q

Sulfonamides inhibit what?

A

Dihydropteroate synthase and folate production

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13
Q

Sulfonamides are bacteriostatic or bactericidal?

A

Static

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14
Q

Sulfonamides are usually given in combination with?

A

Trimetophrim or Pyrimethamine

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15
Q

Action of Sulfonamides and Trimethoprim?

A

PABA and sulfonamides compete in dihydropteroate synthase to form dihydrofolate reductase

Dihydrofolate reductase through Trimethoprim will become tetrahydrofolic acid

Tetrahydrofolic acid -> Purine

Purines -> DNA

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16
Q

Sulfonamide is anti-_____

A

folate

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17
Q

Sulfonamide is bacteriostatic inhibitor of?

A

folic acid synthesis

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18
Q

SULFONAMIDES are antimetabolites of?

A

PABA

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19
Q

SULFONAMIDES are competitive inhibitors of?

A

dihydropteroate synthase

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20
Q

Sulfonamides act as substrates for enzyme synthesis of?

A

nonfunctional forms of folic acid

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21
Q

Inability of mammalian cells to synthesize folic acid is due to what characteristic of Sulfonamide?

A

Selective toxicity and preformed folic acid in diet

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22
Q

TRIMETHOPRIM is a selective inhibitor of?

A

bacterial dihydrofolate reductase

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23
Q

TRIMETHOPRIM prevents the formation of?

A

active tetrahydro form of folic acid

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24
Q

TRIMETHOPRIM and SULFAMETHOSAXOLE combination results to?

A

sequential blockade of folate synthesis

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25
Q

TRIMETHOPRIM and SULFAMETHOSAXOLE are bactericidal or bacteriostatic?

A

Bactericidal

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26
Q

Synergistic action against a wide spectrum of microorganisms

A

SULFONAMIDES and TRIMETHOPRIM

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27
Q

T or F: Resistance occurs but development is slow in sulfonamides only

A

F, in combination SULFONAMIDES and TRIMETHOPRIM

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28
Q

What kind of drugs are not affected by the anti folate drugs?

A

bacteria that depends on exogenous sources of folate

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29
Q

Resistance is also caused by mutations in?

A
  • Overproduction of PABA
  • Production of a folic acid synthesizing enzyme that has low affinity for sulfonamides
  • Impaired permeability to the sulfonamides
  • Antibiotic efflux
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30
Q

Resistance to antifolaxe drugs is common in?

A

sulfonamides

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31
Q

Why is resistance to antifolaxe drugs is common in sulfonamides?

A
  • Plasmid mediated
  • Decreased accumulation of the drug
  • Increase production of PABA by bacteria
  • Decrease in the sensitivity of
    dihydropteroate synthase
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32
Q

Resistance is trimethoprims are due to the production of?

A

dihydrofolate reductase that has reduced affinity for the drug AND an altered reductase with reduced drug binding

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33
Q

Resistance in trimethoprim is also due to [increased/decreased] cell permeability

A

decreased

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34
Q

Resistance is trimethoprims are due to the OVERproduction of?

A

dihydrofolate reductase

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35
Q

3 major groups of sulfonamides based on ROA?

A
  • Oral, absorbable
  • Oral, non-absorbable
  • Topical
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36
Q

What major group of sulfonamides based on ROA are absorbed from the stomach and small intestine, distributed widely including
CNS, placenta and fetus?

A

Oral absorbable

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37
Q

Oral absorbable sulfonamides are absorbed from what part of the body and distributing where?

A

stomach and small intestine, distributed widely including CNS, placenta and fetus

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38
Q

Sulfonamide protein binding ranges from?

A

20% to 90%

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39
Q

Sulfonamides are metabolized in?

A

Liver

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40
Q

Sulfonamides are excreted in?

A

Urine, adjusted in renal failure

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41
Q

SULFONAMIDES have [weak/strong] acidic compounds

A

Weak

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42
Q

Sulfonamides have [modest/major] tissue absorption

A

Modest

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43
Q

SULFONAMIDES undergo what type of metabolism?

A

Hepatic

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44
Q

What form of SULFONAMIDES are seen in the urine excretion?

A

Both intact drug and acetylated metabolites

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45
Q

_____ may decrease in acid urine for sulfonamide excretion

A

Solubility

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46
Q

Solubility may decrease in acid urine for sulfonamide excretion due to the?

A

Precipitation of the drug/metabolites

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47
Q

SULFONAMIDES bind where?

A

to plasma proteins at sites shared by bilirubin and other drugs

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48
Q

Combination of 3 separate sulfonamides is called?

A

Triple sulfa

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49
Q

Triple sulfa is used to?

A

reduce the likelihood to precipitate

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50
Q

SULFONAMIDES based on duration of action is classified into?

A
  • Short-acting (sulfisozaxole)
  • Intermediate-acting (sulfamethosaxole)
  • Long-acting (sulfadoxine)
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51
Q

Short acting sulfonamide

A

sulfisozaxole

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52
Q

Intermediate-acting sulfonamide

A

sulfamethosaxole

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53
Q

Long-acting sulfonamide

A

sulfadoxine

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54
Q

TRIMETHOPRIM is structurally similar to?

A

folic acid

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55
Q

TRIMETHOPRIM is a [weak/strong] base

A

Weak

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56
Q

TRIMETHOPRIM is usually trapped in [acidic/basic] environments

A

ACIDIC

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57
Q

TRIMETHOPRIM is high in concentration in what body fluids?

A

prostatic and vaginal fluids

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58
Q

TRIMETHOPRIM excretion is mainly in?

A

excreted unchanged in urine

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59
Q

t1/2 of TRIMETHOPRIM

A

10-12hrs

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60
Q

CLINICAL USES of SULFONAMIDES include?

A
  • Gram (+)
  • Gram (-) organisms
  • Chlamydia
  • Nocardia
  • Simple urinary tract infection
  • Ocular infection
  • Burn infections
  • Ulcerative colitis, rheumatoid arthritis
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61
Q

Sulfonamide used for simple urinary tract infection

A

Oral (triple sulfa, sulfisoxazole)

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62
Q

Sulfonamide used for Ocular infection

A

Topical (sulfacetamide)

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63
Q

Sulfonamide used for Burn infections

A

Topical (mafenide, silver sulfadiazine)

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64
Q

Sulfonamide used for Ulcerative colitis, rheumatoid arthritis

A

Oral (sulfasalazine)

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65
Q

Clinical Uses of Non-absorbable Agents

A

Ulcerative colitis, Enteritis and other Inflammatory Bowel Diseases (IBDs)

burn wounds

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66
Q

What Non-absorbable Agents is used for Ulcerative colitis, Enteritis and other Inflammatory Bowel Diseases (IBDs)?

A

Sulfasalazine (Salicylazosulfapyrine)

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67
Q

What Non-absorbable Agents is used for burn wounds for prevention of infection?

A

Silver sulfadiazine

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68
Q

What Non-absorbable Agents is used for burn wounds but can cause metabolic acidosis?

A

Mafenide acetate

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69
Q

Mafenide acetate can cause what condition?

A

metabolic acidosis

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70
Q

Oral Absorbable Agents Clinical Uses

A

Acute Toxoplasmosis (1st line) and second line antimalarial agent

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71
Q

first line for Acute Toxoplasmosis

A

Sulfadiazine + Pyrimethimine

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72
Q

second line antimalarial agent

A

Sulfadoxine + Pyrimethamine (Fansinadir)

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73
Q

CLINICAL USES of TRIMETHOPRIM SULFAMETHOSAXOLE (TMP-SMX)

A
  • Urinary tract
  • Respiratory
  • Ear
  • Sinus infections caused by H. influenzae
    and M. catarrhalis
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74
Q

TMP-SMX is the DOC for?

A
  • Pneumocystis pneumonia
  • Toxoplasma
  • Nocardiosis
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75
Q

TMP-SMX is the back-up drug for?

A
  • Cholera
  • Typhoid fever
  • Shigellosis
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76
Q

TMP-SMX is used for the treatment of infections caused by?

A
  • MR staphylococci
  • L. monocytogenes
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77
Q

TOXICITY OF SULFONAMIDES includes?

A

Hypersensitivity
Gastrointestinal
Hematoxicity
Nephrotoxicity
Drug interactions

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78
Q

What is COMMON in the hypersensitivity toxicity of sulfonamides?

A

Skin rash and fever

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79
Q

What is RARE in the hypersensitivity toxicity of sulfonamides?

A

Exfoliative dermatitis, polyarteritis nodosa
and Stevens-Johnson syndrome

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80
Q

In sulfonamide hypersensitivity, there is cross-allergenicity between?

A

individual sulfonamides and chemically related drugs

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81
Q

In sulfonamide hypersensitivity, there is _______________ between individual sulfonamides and with chemically related
drugs

A

cross-allergenicity

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82
Q

In sulfonamide GI toxicity, what is common?

A

Nausea, vomiting, and diarrhea

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83
Q

In sulfonamide GI toxicity, what is UNcommon?

A

Mild hepatic dysfunction, hepatitis

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84
Q

What is the rare kind of toxicity in sulfonamides?

A

Hematoxicity

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85
Q

Hematoxicity in sulfonamides includes?

A

Granulocytopenia, thrombocytopenia, and
aplastic anemia

Acute hemolysis in G-6PD

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86
Q

In nephrotoxicity, Sulfonamide may precipitate in ____ causing _______ and _________

A

acid urine
Crystalluria and hematuria

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87
Q

SULFONAMIDES have competitive drug interactions with?

A

warfarin and methotrexate for plasma binding

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88
Q

SULFONAMIDES also displaces ____ from plasma proteins causing _______

A

Displace bilirubin from plasma protein
Kernicterus (3rd trimester of pregnancy)

89
Q

TOXICITY OF TRIMETHOPRIM

A
  • Megaloblastic anemia, leukopenia, and
    granulocytopenia
  • HIV patients given TMP-SMX experience Fever, Rashes, Leukopenia, Diarrhea
  • Mild elevation of blood creatinine
90
Q

Megaloblastic anemia, leukopenia, and
granulocytopenia in trimethoprim toxicity is due to?

A

Supplementary folinic acid

91
Q

What causes the mild elevation of
blood creatinine in trimethoprim?

A

inhibition in the secretion of creatinine at the distal renal tubule

92
Q

Earliest Fluoroquinolone is?

A

Nalidixic Acid

93
Q

Synthetic fluorinated derivatives include?

A

Ciprofloxacin,
Levofloxacin

94
Q

Fluoroquinolones are bactericidal or bacteriostatic?

A

Bactericidal

95
Q

Examples of Fluoroquinolones

A

Nalidixic Acid
Ciprofloxacin
Moxifloxacin
Gemifloxacin
Norfloxacin
Levofloxacin

96
Q

1st generation FLUOROQUINOLONE

A

Norfloxacin

97
Q

Norfloxacin is derived from?

A

nalidixic acid

98
Q

Norfloxacin is used for?

A

Common pathogens that cause UTI

99
Q

2nd generation FLUOROQUINOLONE

A

Ciprofloxacin

100
Q

Ciprofloxacin is used for?

A
  • Gonococcus
  • Gram (+) cocci
  • Mycobacteria
  • Atypical organisms (M. pneumoniae)
101
Q

Ciprofloxacin has a greater activity against G(-) or G(+)?

102
Q

3rd generation FLUOROQUINOLONES

A

Levofloxacin, gatifloxacin, sparfloxacin

103
Q

Levofloxacin, gatifloxacin, sparfloxacin have more activity against G[-/+] and less activity against G[-/+]

A

More activity for +
Less activity for -

104
Q

Levofloxacin, gatifloxacin, sparfloxacin mainly acts of what bacteria?

A
  • Streptococci
  • S. pneumoniae
  • Staphylococci
  • MRSA
  • Some strains of enterococci
105
Q

4th generation FLUOROQUINOLONES

A

Moxifloxacin, trovafloxacin

106
Q

Moxifloxacin, trovafloxacin have enhanced activity against?

107
Q

Fluoroquinolones are well absorbed through what ROA?

108
Q

Degree of distribution of Fluoroquinolones?

109
Q

Long half-lives of what Fluoroquinolones permits 1x daily dosing?

A

Levofloxacin, Gemifloxacin and Moxifloxacin

110
Q

Levofloxacin, Gemifloxacin and Moxifloxacin are dosed how often in a day?

111
Q

Fluoroquinolones have impaired absorption when combined with?

A

antacids, divalent and trivalent cations

112
Q

Fluoroquinolones should be taken how many hours before and after the antacids, divalent and trivalent cations?

A

2 hours before or 4 hours after

113
Q

Fluoroquinolones mode of excretion is mainly through?

A

Most are renally excreted (requiring renal dose adjustment) except for Moxifloxacin (liver)

114
Q

Fluoroquinolone with the highest oral F

115
Q

Oral F of Ciprofloxacin and Gemifloxacin

116
Q

Fluoroquinolones with the longest half-life

A

Moxifloxacin

117
Q

Does not achieve adequate plasma levels
for use in systemic infections

A

Norfloxacin

118
Q

Moxifloxacin, sparfloxacin, travofloxacin are eliminated partly by?

A

hepatic metabolism and biliary excretion

119
Q

FLUOROQUINOLONES interfere with?

A

Bacterial DNA synthesis and inhibits topoisomerase II (DNA gyrase)

120
Q

FLUOROQUINOLONES block the relaxation of?

A

supercoiled DNA catalyzed by DNA gyrase

121
Q

FLUOROQUINOLONES are bactericidal or bacteriostatic?

A

Bactericidal

122
Q

FLUOROQUINOLONES also exhibit what effects?

A

postantibiotic effects

123
Q

Fluoroquinolone-resistant organisms appears in every?

A

10^7-10^9 especially notable among Staphylococci, P. aeruginosa and S. marcesens

124
Q

Fluoroquinolone resistance can also be brought about by the mutation in?

A

in the quinolone binding region of the target enzyme or to a change in permeability

125
Q

FLUOROQUINOLONES resistance emerged rapidly from what generation?

126
Q

FLUOROQUINOLONES resistance emerged rapidly from 2nd generation, causing resistance in what bacteria?

A
  • C. jejuni and gonococci
  • Gram (+) cocci (MRSA)
  • Pseudomonas and Serratia
127
Q

FLUOROQUINOLONES resistance mechanisms include?

A
  • Production of efflux pumps
  • Changes in porin structure
  • Changes in sensitivity of the enzyme via
    point mutations in the antibiotic binding
    regions
128
Q

FLUOROQUINOLONES CLINICAL USE

A
  • Urogenital and gastrointestinal tract
    infection
  • Gram (-) organisms
  • Gonococci, E. coli
  • K. pneumoniae, C. jejuni
  • Enterobacter, P. aeruginosa
  • Salmonella, Shigella
129
Q

FLUOROQUINOLONES effectiveness is variable due to?

A

resistance in respiratory tract skin and soft tissue infection

130
Q

FLUOROQUINOLONE alternative to 3rd generation cephalosporin

A

Ciprofloxacin and ofloxacin

131
Q

Ciprofloxacin and ofloxacin are used for?

A
  • N. gonorrhea (single oral doses)
  • Ofloxacin will eradicate accompanying
    organisms like Chlamydia (7 day course)
132
Q

FLUOROQUINOLONES used for CAP and Atypical pneumonia (M. pneumoniae)

A

Levofloxacin

133
Q

FLUOROQUINOLONES for Gram (+) organisms Penicillin-resistant pneumococci

A

Sparfloxacin

134
Q

Moxifloxacin and trovafloxacin clinical uses

A
  • Gram (+)
  • Gram (-) organisms
  • Anaerobic bacteria
  • Used in meningococcal carrier state
  • Tuberculosis
  • Prophylactic management of neutropenic
    patients
135
Q

Fluoroquinolones most common adverse effect?

A

Nausea, vomiting and diarrhea

136
Q

Fluoroquinolones most occasional adverse effect?

A

headache, dizziness, insomnia, skin rash or
abnormal LFTs

137
Q

Lomefloxacin, Pefloxacin have what adverse effects?

A

Photosensitivity

138
Q

Gatifloxacin, Levofloxacin, Gemifloxacin
and Moxifloxacin have what adverse effects?

A

QT Prolongation

139
Q

Gatifloxacin has what adverse effects?

A

Hyperglycemia when given alone or Hypoglycemia when given with oral hypoglycemic agents

140
Q

Fluoroquinolones may damage growing cartilage and cause?

A

arthropathy, Tendinitis and tendon rupture

141
Q

Fluoroquinolones must be avoided in?

142
Q

Fluoroquinolones are temporary to?

A

Permanent Peripheral Neuropathy

143
Q

FLUOROQUINOLONES cause superinfection caused by?

A

C. albicans and streptococci

144
Q

FLUOROQUINOLONES also have increased levels of what in toxicity?

A

theophylline and other methylxanthines

145
Q

FLUOROQUINOLONE that causes risk for cardiac arrhythmia and Photosensitivity

A

Sparfloxacin

146
Q

FLUOROQUINOLONE with Hepatotoxic potential

A

Trovafloxacin

147
Q

Mycobacteria appearance?

A

Rod-shaped, aerobic bacteria and a cell wall with peptidoglycolipids, fatty acids, waxes,
and mycolic acid

148
Q

Growth, acid staining and reactance of mycobacteria

A

Slow growth, acid fast, resistant to detergents / antibiotics

149
Q

Mycobacteria infecting humans and their causes

A

M. tuberculosis - Pulmonary tuberculosis,
extrapulmonary TB
M. leprae - Leprosy
M. bovis - Tuberculosis-like illness
Mycobacterium avium complex - Disseminated infection, pulmonary infections, common in immunocompromised states/HIV

150
Q

DRUG COMBINATIONS are used in ANTIMYCOBACTERIAL DRUGS for?

A

*To delay emergence of resistance
*To enhance antimycobacterial efficacy

151
Q

COMPLICATIONS OF CHEMOTHERAPY in the use of ANTIMYCOBACTERIAL DRUGS

A
  • Limited information about the MOA
  • Development of resistance
  • Intracellular location of mycobacteria
  • Chronic nature of the disease (protracted therapy and drug toxicities)
  • Patient compliance
152
Q

What other organs besides the lungs can TB affect?

A

Liver, CNS, Bone, GI, Kidneys

153
Q

First line drugs against TB?

A

Isoniazid (H)
Rifampicin (R)
Pyrazinamide (Z)
Ethambutol (E)

154
Q

Second line drugs against TB?

A

Levofloxacin
Moxifloxacin
Bedaquiline
Linezolid
Clofazimine
Cycloserine
Ethambutol
Delamanid
Pyrazinamide
Imipenem – Cilastatin
Meropenem
Amikacin
Streptomycin
Prothionamide
P-amino salicyclic acid

155
Q

Isoniazid is a structural congener of?

A

pyridoxine

156
Q

In Isoniazid, the inhibition of enzymes required for?

A

the synthesis of mycolic acid

157
Q

Is isoniazid bactericidal or bacteriostatic?

A

Bactericidal

158
Q

T or F: Resistance can emerge rapidly in Isoniazid if used alone

159
Q

Isoniazid resistance involves which substances?

A

katG gene -catalase peroxidase bioactivation of INH

inhA gene – enzyme acyl carrier reductase

160
Q

Isoniazid is well absorbed in what ROA?

161
Q

Isoniazid is metabolized by what process in which organ?

A

acetylation in the liver

162
Q

Metabolism of Isoniazid in the liver is affected by?

A

genetic control of acetylation which can be fast or slow

163
Q

Clinical use of Isoniazid

A

Single most important drug used for TB, making it a component of drug combination regimen

Latent tuberculosis infection (LTBI); close contacts (sole drug)

164
Q

Toxicity with the use of Isoniazid

A
  • Peripheral neuritis, restlessness, muscle
    twitches, insomnia
    ̶ Pyridoxine (25-50mg/d)
  • Hepatotoxic
  • CYP 450 enzyme inhibitor
  • Hemolysis in G6PD deficient patients
165
Q

Rifampin / Rifampicin is bacteriostatic or bactericidal?

A

Bactericidal

166
Q

Rifampin / Rifampicin inhibits _______.

A

DNA-dependent RNA polymerase

167
Q

Resistance to Rifampin / Rifampicin results from?

A

changes in drug sensitivity of polymerase

168
Q

Clinical Uses of Rifampin / Rifampicin

A
  • Used in combination with drugs
  • Can be used as sole drug in LTBI or close contacts with INH-resistant strains
  • In leprosy – it delays resistance to dapsone
  • Used for MRSA, PRSP
169
Q

Toxicities and Interactions observed in Rifampin

A
  • Can impair antibody responses
  • Skin rashes, thrombocytopenia, nephritis, liver dysfunction
  • Flu-like symptoms, anemia
  • Induces liver drug-metabolizing enzymes
170
Q

What other rifamycin is equally effective as anti mycobacterial agent; less drug interactions?

171
Q

What other rifamycin is preferred over rifampin in AIDS patients taking some antiretrovirals?

172
Q

What other rifamycin is not absorbed from GI tract, used in traveler’s diarrhea?

173
Q

Ethambutol inhibits what substance needed for what process?

A

arabinosyltransferase enzyme needed for cell wall synthesis

174
Q

Ethambutol resistance is due to?

A

mutation in emb gene if drug is used alone

175
Q

Ethambutol is well absorbed in what ROA?

176
Q

Ethambutol is [limitedly/widely] distributed in most tissues including CNS

177
Q

Ethambutol is mainly excreted through?

A

unchanged in urine with dose reduction in renal impairment

178
Q

Ethambutol clinical use

A

Mainly for TB, in combination with other drugs

179
Q

Ethambutol Toxicities include?

A
  • Dose-dependent visual disturbances
    ̶ Decrease in acuity, color blindness, optic neuritis, retinal damage
  • Headache, confusion, hyperuricemia, peripheral neuritis
180
Q

Pyrazinamide is bactericidal or bacteriostatic?

A

Bacteriostatic action – through pyrazinamidases

181
Q

Pyrazinamide has a [well-known/unknown] MOA

182
Q

Pyrazinamide resistance is due to?

A

mutations in genes that encode enzymes; drug-efflux systems esp. when used alone

183
Q

Pyrazinamide is well absorbed through what ROA?

184
Q

T or F: Pyrazinamide penetrates most body tissues, including CNS

185
Q

Pyrazinamide is partly metabolized by?

A

Pyrazinoic acid

186
Q

Pyrazinamide t1/2 is [prolonged/shortened] with liver or kidney failure

187
Q

Pyrazinamide t1/2 is prolonged due to?

A

liver or kidney failure

188
Q

Pyrazinamide clinical use is in combination with?

A

other drugs for MTB

189
Q

Pyrazinamide toxicities include?

A
  • Joint pains
  • Asymptomatic hyperuricemia
  • Myalgia, GI irritation, rash, hepatic dysfunction
  • Should be avoided in pregnancy
190
Q

Used in combination for life-threatening TB (meningitis, miliary TB, other EPTB)

A

Streptomycin

191
Q

For TB caused by streptomycin- resistant or MDR-TB

192
Q

Active against strains of MTB resistant to first-line agents; used in combination

A

Ciprofloxacin and ofloxacin

193
Q

Congener of INH; major effect – severe GI irritation & neurologic toxicity

A

Ethionamide

194
Q

The intensive phase of TB treatment lasts for how long?

195
Q

Continuation or maintenance phase of TB treatment lasts for?

A

≥4 months

196
Q

Refers to MTB strains in which resistance to both isoniazid and rifampicin has been confirmed in vitro

A

Multidrug-resistant TB (MDR-TB)

197
Q

Multidrug-resistant TB (MDR-TB) refers to MTB strains which are resistant to?

A

both isoniazid and rifampicin

198
Q

Fixed-dose combination is composed of?

A

anti TB pills containing 2 or more drugs

199
Q

Diagnostic and therapeutic unit that caters patients diagnosed with TB or suspected of having TB

200
Q

DOTS stands for?

A

The Directly Observed Treatment Strategy

201
Q

Drugs for Leprosy include?

A

DAPSONE (Diaminodiphenylsulfone)
Sulfones - ACEDAPSONE
Clofazimine

202
Q

DAPSONE is the most active drug against?

203
Q

DAPSONE MOA includes the inhibition of?

A

folic acid synthesis

204
Q

Dapsone resistance can develop if [low/high] doses are given, usually in combination with __________.

A

Low
Rifampin and / or Cloafazimine

205
Q

Dapsone ROA and excretion

A

Orally
Urine

206
Q

Dapsone toxicity?

A
  • GI irritation
  • Fever
  • Skin rashes
  • Methemoglobinemia
  • Hemolysis in patients with G-6PD
207
Q

Repository form of dapsone

A

ACEDAPSONE

208
Q

ACEDAPSONE provides what for several months?

A

inhibitory plasma concentrations

209
Q

ACEDAPSONE is an alternative drug for?

A

P. carinii pneumonia in HIV patients

210
Q

Phenazine dye for used for multibacillary leprosy

A

Clofazimine

211
Q

T or F: Clofazimine MOA is well-known

A

F, not clearly defined

212
Q

t1/2 of Clofazimine can last as long as?

213
Q

Most prominent adverse effect of Clofazimine?

A

discoloration of skin and conjunctivae

214
Q

What kind of drugs are less susceptible to anti-TB drugs?

A

Nontuberculous Mycobacteria (NTM) Drugs

215
Q

What drugs are active for NTM?

A

Tetracyclines, macrolides, sulfonamides

216
Q

What bacterium are common among AIDS patients?

A

M avium complex: M avium and M intracellulare

217
Q

M avium complex infections are treated with?

A

Azithromycin/Clarithromycin + Ethambutol, or Rifabutin

218
Q

Prophylaxis against M avian includes?

A

Azithro/Clarithromycin

2nd Year 2nd Term (38 decks)

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