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BMS 615 Cardiovascular > Test 3: Wk11: 5 Anti- Tuberculosis Drugs - Allman > Flashcards

Test 3: Wk11: 5 Anti- Tuberculosis Drugs - Allman Flashcards

1
Q

can pts with latent TB spread TB to others

A

no

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2
Q

MDR TB

A

resistant to at least INH and RIF

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3
Q

pts with resistance to Rifampin alone

A

better prognosis than MDR strains however at increased risk of tx failure/ addition resistance

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4
Q

XDR TB

A

extensive drug resistance

Resistant to INF and RIF plus FQN and at least one of the three injectable drugs

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5
Q

Life cycle of TB

A
  1. Active M tuberculosis
  2. Macrophage
  3. Walled off by macrophage
  4. Leukocytes
  5. Granuloma
  6. Active M tuberculosis
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6
Q

Prolonged treatment is required for successful eradication

A

Typically 6 months for routine Pulmonary TB Tx

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7
Q

TB Pericarditis and Meningitis

A

Initial adjunctive corticosteroid therapy with dexamethasone should be given for 6 weeks for ptns with TB Meningitis

Initial adjunctive corticosteroid therapy should not be routinely used; reserved for only selected ptns

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8
Q

ART CD4 <50/mm3

A

Start ART within first 2 weeks of TB treatment

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9
Q

CD4 >50/mm3

A

Start ART by 8-12 weeks of TB treatment

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10
Q

TB meningitis tx

A

TB meningitis = Do NOT start before 8 10 weeks of TB treatment

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11
Q

pts w/ HIV and TB have increased risk of

A

developing paradoxical worsening of sx and clinical manifestations of TB

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12
Q

Immune Reconstitution Inflammatory Syndrome IRIS

A

in HIV pts rxns develop as a consequence of reconstitution of immune responsiveness brought on by ART

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13
Q

Signs of IRIS may include (7)

A

High fevers

Worsening respiratory symptoms

Increase in size and inflammation of involved lymph nodes, new lymphadenopathy,

Expanding central nervous system (CNS) lesions,

Worsening of pulmonary parenchymal infiltrations

New or increasing pleural effusions

Development of intra abdominal or retroperitoneal abscesses

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14
Q

Starting ART within 2 weeks after starting tuberculosis therapy have higher
rates of — than those who start between 8 12 weeks

A

IRIS

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15
Q

does development of IRIS worsen treatment outcomes for either TB or HIV infection

A

no

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16
Q

IRIS may cause

A

severe or fatal neurological complications

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17
Q

Intensive Phase of TB tx

A

2 months (knocking down the volume)

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18
Q

Continuation Phase of TB tx

A

4 months (de escalate)

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19
Q

Dosing Guidelines

A

Daily dosing

Twice or Thrice weekly dosing

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20
Q

TB therapy requires

A

Requires Directly Observed Therapy (DOT)

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21
Q

4 first line agents for TB

A

isoniazid

Ethambutol

Pyrazinamide

Rifampin

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22
Q

Isoniazid function

A

inhibits cell wall synthesis

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23
Q

Ethambutol function

A

inhibits cell wall synthesis

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24
Q

Pyrazinamide function

A

direct target unclear
disrupts plasma membrane
disrupts energy metabolism

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25
Q

Rifampin function

A

inhibits RNA synthesis

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26
Q

3 Major Rifamycins

A

Rifampin

Rifabutin

Rifapentine

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27
Q

Rifampin

Mechanism of Action

A

inhibits DNA dependent RNA pol - suppression of initiation of chain formation in RNA Synthesis

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28
Q

Rifampin bactericidal function

A

Bactericidal: kills slow growing mycobacteria present within

macrophages and in caseating granulomas

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29
Q

Rifampin is active against

A

Active against some gram positive and gram negative bacteria.
(Reserved for TB, except in very rare

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30
Q

Rifampin Combination therapy with

A

INH

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31
Q

Rifampin Distribution

A

Widely distributed; excellent tissue distribution

CNS, tuberculosis abscesses, and intracellular sites

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32
Q

Rifampin Metabolism

A

Primarily metabolized by deacetylation

Autoinduction of metabolism occurs

Maximal induction at ~ 6 doses, whether given daily or twice weekly

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33
Q

Rifampin

Adverse Effects

A

Transient elevation in serum transaminases

Hepatotoxicity (rare)

GI upset (frequent)

Hypersensitivity (rare)

Discoloration of bodily fluids

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34
Q

what drug causes orange discoloration of sweat tears and urine

A

Rifampin

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35
Q

Rifampin Hepatotoxicity

A

Risk factors: alcoholics with preexisting liver disease.

Augmented when combined with INH

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36
Q

Rifampin

Hypersensitivity (rare)

A

Flushing, fever, pruritus

Systemic flu like syndrome

Thrombocytopenia

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37
Q

Rifampin

Drug Interactions

A

Proliferation of the smooth endoplasmic reticulum in
hepatocytes

Results in an increase in cytochrome p 450 (CP450) activity.

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38
Q

Rifampin increases metabolism of

A

P450

Warfarin

Theophylline

Narcotics

Oral Hypoglycemics

Steroids (oral contraceptives)

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39
Q

Rifampin

Place in Therapy

A

Treatment of active TB

2nd line agent for preventative therapy

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40
Q

Rifamycin derivative.

A

Rifabutin (Mycobutin)

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41
Q

when is rifabutin used

A

when pts are receiving meds with unacceptable interactions with Rifampin or had intolerance to rifampin

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42
Q

More active than rifampin against Mycobacterium avium

complex

A

Rifabutin (Mycobutin)

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43
Q

Rifabutin is used in the tx of

A

More active than rifampin against Mycobacterium avium

complex (MAC)

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44
Q

Rifabutin ADRs (7)

A 
Rash
GI
Arthralgias 
Myalgias
Discoloration of urine/sweat/ and tears
neutropenia
hepatoxicity
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45
Q

Used once weekly with INH in the continuation phase of

SPECIFIED treatment of TB

A

Rifapentine (Priftin)

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46
Q

Ptn must be HIV negative to use

A

Rifapentine (Priftin®)

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47
Q

pt must have — to take Rifapentine

A

Non cavitary , drug susceptible pulmonary tuberculosis who have
negative sputum smears at completion of the initial phase of treatment

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48
Q

advantage of Rifapentine

A

Once weekly

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49
Q

Rifapentine ADRs

A

similar to RIfampin

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50
Q

Isoniazid (INH)

Mechanism of Action

A

Inhibits synthesis of mycolic acid

Important constituent of mycobacterial cell walls

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51
Q

— Actively transported into bacterium

A

INH

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52
Q

INH kills actively growing organisms in

A

the extracellular environment

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53
Q

INH inhibits

A

growth of formant organisms within macrophages preventing granulomas

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54
Q

INH metabolism

A

Primarily acetylation

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55
Q

INH important metabolite

A

Monoacetyl hydrazine

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56
Q

Monoacetyl hydrazine excreted

A

in urine or further acetylated to diacyl form or hydroxylated to electrophile intermediated

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57
Q

— is responsible for hepatotoxic effects with INH

A

electrophile intermediated

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58
Q

Rates of acetylation of INH & mono acetyl hydrazine dependent on

A

Dependent on an individual’s phenotypic classification

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59
Q

IMH classifications

A

slow or rapid acetylator

60
Q

Slow acetylators of INH may lead to

A

higher blood concentrations

61
Q

Caucasians acylation of INH

A

equally divided fast and slow

62
Q

Eskimos and Japanese acylation of INH

A

rapid

63
Q

Egyptians acylation of INH

A

slow

64
Q

INH half life in rapid acetylators

A

1-2 hrs

65
Q

INH half life in slow acetylators

A

2-5 hrs

66
Q

INH serum transaminase

A

transient elevation ~15% within first 8-12 wks of therapy

67
Q

INH hepatotoxicity risk factors

A

age, liver dz,

4-8 wks of tx use rifampin

68
Q

INH neurotoxicity

A

alcoholics, children, malnourished, slow acetylators

69
Q

prevent neurotoxicity if INH

A

Pyridoxine (Vitamin B6)

70
Q

hypersensitivity in INH

A

rare

71
Q

Isoniazid

Place in Therapy

A

Treatment of active TB

72
Q

Preventative therapy for patients with (+) PPD

A

INH

73
Q

Pyrazinamide (PZA)

Mechanism of Action

A

not well documented

74
Q

PZA bactericidal toward

A

dormant organisms residing in the acidic

environment within macrophages

75
Q

PZA metabolism

A

Hydrolyzed in liver to active pyrazinoic acid

76
Q

PZA elimination

A

5 hydroxypyrazinoic acid ( hydroxylated pyrazinoic acid) is excreted by the kidneys.

77
Q

PZA t 1/2

A

9-10hrs

78
Q

PZA ADEs

A

Hepatotoxicity
hyperuricemia
GI
Hypersensitivity

79
Q

hepatotoxicity PZA

A

more frequent with high dose
baseline hepatic function should be obtained
monitor for hepatitis

80
Q

PZA hyperuricemia

A

decreased renal excretion of uric acid

Pyrazinoc acid competes with uric acid for elimination

81
Q

PZA hypersensitivity

A

photosensitivity and rash

82
Q

Ethambutol (ETH, EMB, Myambutol) MOA

A

not documents

Bacteriostatic

83
Q

ETH pharmacokinetics

A

60-80% of parent compound + inactive metabolite excreted in urine

84
Q

Ethambutol

Adverse Effects

A

Optic neuritis (Retrobulbar neuritis)

85
Q

Optic neuritis ( Retrobulbar neuritis)

A

Decreased visual acuity and red green color blindness.

86
Q

Optic neuritis ( Retrobulbar neuritis) reversibility

A

usually reversible , tim dependent with degree of impairment

87
Q

Drug that causes eye damage

A

Ethambutol

88
Q

Streptomycin MOA

A

aminoglycoside antibiotic

89
Q

Streptomycin bactericidal through

A

inhibition of protein synthesis

90
Q

Streptomycin inactive against

A

intracellular organisms; limiting activity to suppression

91
Q

Streptomycin is used as an alternative for

A

Ethambutol

92
Q

Streptomycin absorption

A

poor in GI

administer IM or IV

93
Q

Streptomycin ADEs

A

nephrotoxicity
impairment of 8th cranial nerve
pain at injection site/ abscess formation

94
Q

TB drug combo Rifamate

A

Rifampin and Isoniazid

95
Q

TB drug Combo Rifater

A

Rifampin, Isoniazid, Pyrazinamide

96
Q

Bedaquiline MOA

A

inhibits mycobacterial ATP synthetase

97
Q

Bedaquiline safety concerns

A

QT prolongation

increased death potential

98
Q

— used for MDR only

A

Bedaquiline

99
Q

6 2nd line agents

A
  1. Para-Aminosalicylate
  2. Ethionamide
  3. Cycloserine
  4. Capreomycin
  5. Kanamycin
  6. Amikacin
100
Q

— most widely used as anti-leprosy agent

A

Clofazimine (Lamprene)

101
Q

Clofazimine ADRs

A

GI
Severe life threatening abdominal pain and organ damage
discoloration of skin and eyes

102
Q

what causes organ damage with Clofazimine

A

crystal deposition

103
Q

2 Macrolides

A

Clarithromycin and Azithromycin

104
Q

Macrolides effectivity against TB

A

unlikely

105
Q

Macrolides should be used in combination with other agents for — tx

A

MAC - Mycobacterium Avium Complex

106
Q

BCG Vaccine

A

attenuated hybridized strain of M bovis

107
Q

BCG Vaccine against TB

A

does not appear to be effective

108
Q

BCG Vaccine should be avoided in

A

Pregnant and HIV

109
Q

BCG Vaccine side effects

A

prolonged ulceration at vaccine site

lymphadenitis and lupus vulgaris

110
Q

WHO recommendations of BCG Vaccine

A

High risk TB and HIV+ infants with no sx

111
Q

TB Regimens

A

RIPE or RIPS

112
Q

RIPE

A

Rifampin
Isoniazid
Pyrazinamide
Ethambutol

113
Q

RIPS

A

Rifampin
Isoniazid
Pyrazinamide
Streptomycin

114
Q

RIPE / RIPS tx

A

6mos for general TB tx

115
Q

Osteo/miliary/meningitis regimen

A

12-24 mos

116
Q

Concomitant Illnesses (HIV, Hepatitis) Regimen

A

Treat concomitant disease states

117
Q

Renal failure TB regimen

A

Avoid Streptomycin, Kanamycin, and Capreomycin

118
Q

Children TB regimen

A

Avoid Ethambutol if proper assessment is not feasible

119
Q

TB Suspected Treatment Failure

A

Lack of clinical progression 6 8 weeks into therapy
Add 2 new TB agents when failure suspected
Evaluate for non adherence or drug resistance

120
Q

Leprosy Causative agent

A

Mycobacterium leprae (Leprosy)

121
Q

2 major groups of Leprosy

A

Lepromatous widespread

Tuberculoid localized

122
Q

can leprosy be cultured in vitro

A

no

123
Q

Lepromatous Leprosy

A

disseminated , multibacillary , with loss of specific cell mediated immunity

124
Q

Tuberculoid Leprosy

A

localized, paucibacillary , with strong cell mediated immunity)
Paucibacillary = having or made up of few

125
Q

Leprosy transmission requires

A

prolonged contact and occurs directly through intact

skin, mucous membranes, or penetrating wounds.

126
Q

Leprosy infection leads to

A

Lesions

Hypopigmentation

Loss of sensation (anesthesia)

127
Q

Leprosy dx

A

Based on acid fast stain and cytologic examination of affected skin and response to the lepromin skin test

128
Q

Leprosy multidrug therapy (3 drugs)

A

Dapsone / Rifampin/ Clofazimine

129
Q

how long does leprosy tx last

A

3-5 years

130
Q

Dapsone MOA

A

competitive inhibitor of folic acid synthesis
Competitive inhibition of dihydropteroate synthase which prevents
bacterial utilization of para aminobenzoic acid

131
Q

Dapsone is a

A

bacteriostatic

132
Q

Dapsone is absorbed

A

rapidly and completely from the GI tract

133
Q

Dapsone ADRs

A

Hypersensitivity reaction

Fever, Malaise, Dermatitis, Jaundice

134
Q

Dapsone hypersensitivity

A

sulfone syndrome

135
Q

Dapsone Sulfone Syndrome sx occur

A

1-4 wks into therapy

136
Q

Mycobacterium Avium Complex (MAC) sx

A

fever, night sweats, wt loss, anemia

137
Q

MAC stands for

A

Mycobacterium Avium Complex

138
Q

MAC usually occurs in

A

Advanced HIV pts

139
Q

MAC tx

A

combination therapy

140
Q

MAC preferred tx

A

Clarithromycin

Ethambutol

141
Q

Rifampin

A

GI Upset, Drug Drug Interactions, Orange discoloration, Hepatotoxicity

142
Q

Isoniazid

A

Neurotoxicity, Peripheral Neuropathy, Hepatotoxicity

143
Q

PZA

A

GI Upset, Hyperuricemia , Hepatotoxicity

144
Q

Ethambutol

A

Optic Neuritis, Children

145
Q

Streptomycin

A

Neurotoxicity (8 th cranial nerve Vertigo ), Nephrotoxicity potential

BMS 615 Cardiovascular (49 decks)

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