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D&D Infectious Disease FINAL > Pharm - Tuberculosis Part 1 > Flashcards

Pharm - Tuberculosis Part 1 Flashcards

1
Q

true or false

tuberculosis is not caused by bacteria

A

FALSE

caused by mycobacterium tuberculosis bacteria

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2
Q

true or false

tuberculosis is contagious

A

true

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3
Q

true or false

tuberculosis is not a significant public health concern

A

FALSE - it is

global health concern affecting millions worldwide

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4
Q

name 3 types of infections that mycobacterium tuberculosis can cause

A

silent
latent
active

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5
Q

3 risk factors for tuberculosis infection

A

immunocompromised
poverty
crowding living conditions

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6
Q

TB is one of the top ___ causes of death worldwide

A

10

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7
Q

which 2 countries account for majority of tb cases

A

asia and africa

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8
Q

around how many people are infected with the TB bacterium

A

2 billion

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9
Q

does the mycobacterium tuberculosis bacterium go into our cells?

A

YES - it’s an intracellular pathogen. goes into the macrophages specifically

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10
Q

is mycobacterium tb aerobic or anaerobic?
motile or non motile?

A

aerobic non motile

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11
Q

does mycobacterium tb grow fast or slow

A

slowly replicates and lies dormant for a long time

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12
Q

how is mycobacterium tb able to be resistant to many antibiotics

A

it has a very thick hydrophobic (!60% LIPID) cell well that is rich in mycolic acids - hard for drug to get in

also, the antibiotic we design has to go into our body, then into our cells, and then into the bacteria to kill it - lot of steps bc it’s an intracellular pathogen

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13
Q

true or false

mycobacterium tuberculosis has a thicker cell wall than most bacteria

A

TRUE

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14
Q

mycobacterium TB has a ___- cell wall

A

waxy - from mycolic acids

~60% lipids

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15
Q

name the 4 layers of the cell wall of mycobacterium tuberculosis

what is the “mycomembrane?”

A

glycolipids (top)
mycolic acids
arabinogalactan
peptidoglycan (bottom)

4 LAYERS

“mycomembrane” is the glycolipids + mycolic acids

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16
Q

primary TB vs latent TB vs reactivation TB

A

primary TB = initial infection within the lungs

latent TB = ASYMPTOMATIC infection with no active disease

reactivation = return of active disease (often bc of some immunosuppression)

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17
Q

symptoms of pulmonary tb vs extrapulmonary tb

A

pulmonary tb symptoms - cough, chest pain, weight loss, fever

extrapulmonary - infection in other organs like lymph nodes bones and kidneys

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18
Q

true or false

mycobacterium tuberculosis can only infect the respiratory system

A

FALSE

can affect other tissues like lymph nodes, bone, kidneys, and even brain

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19
Q

4 diagnostic ways to test for TB

A

-tuberculin skin test

-IFNY release assay

-chest XRAY

-sputum culture

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20
Q

what does the tuberculin skin test measure

A

how the immune system of the patient will respond to tuberculosis proteins

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21
Q

issue with using chest x ray to diagnose TB

A

may get false positives of TB - just looking at pulmonary abnormalities and not any specific marker

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22
Q

5 first line drugs for tuberculosis

A

isoniazid
rifampin
pyrazinamide
ethambutol
streptomycin

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23
Q

what is DOT

A

directly observed therapy - done to ensure that the patient is being compliant with TB therapy

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24
Q

what is MDR-TB

A

multi-drug resistant TB

challenges to treat - needs specialized treatment

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25
5 SECOND line drugs for TB
capreomycin ethionamide cycloserine kanamycin PAS (para-amino salicylate)
26
what is vDOT
VIDEO directly observed therapy for tb
27
when is the tb bacteria considered to be multi drug resistant in a patient
if it is resistant to 1st line drugs (isoniazid, ethambutol, rifampin, streptomycin, pyrazinamide)
28
what is is XDR-TB
VERY resistant TB that is resistant to at least rifampin and isoniazid PLUS any quinoline PLUS 1 of these 2nd lines: kanamycin, capreomycin, or amikacin
29
explain the profile of patients that are more likely to develop XDR tuberculosis resistance
more likely to be younger 65 and older are actually less likely
30
name 2 1st line TB agents that work by inhibiting cell wall synthesis and the specific layers they block the formation of
isoniazid and ethambutol isoniazid - mycolic acid ethambutol - arabinogalactan
31
which 1st line TB agent inhibits RNA synthesis and how does it accomplish this
rifampin inhibits DNA dependent RNA polymerase if no RNA, can't make protein
32
give 2 MOAs of pyrazinamide
disrupts the plasma membrane disrupts energy (ATP) synthesis
33
what is the general size of isoniazid and what does this say about its function as an anti TB agent
SMALL MOLECULE thus, able to penetrate the macrophages where the tb bacteria is located, and also easily absorbed however, still kinda hard to get into the bacteria itself because of the waxy 4 layer cell wall
34
is isoniazid bacteriostatic or cidal
CIDAL - for tb bacteria that are actively growing
35
isoniazid is actually LESS effective for what kind of TB bacteria
atypical species
36
is isoniazid usually used alone? why or why not
NO usually used as combo therapy to reduce resistance to it
37
true or false isoniazid is a prodrug
TRUE activated by KatG (mycobacterial catalase peroxidase) + coenzyme NADH into it's active form
38
isoniazid inhibits the synthesis of ________
mycolic acids
39
what does isoniazid inhibit and how
inhibits the enzyme ACYL CARRIER PROTEIN REDUCTASE does this by forming a complex with Acp and KasA doing this inhibits the synthesis of the mycolic acid portion of the cell wall
40
4 methods of isoniazid resistance
-bacteria can overexpress the enzyme (acyl carrier protein reductase - inhA) -mutate or delete the katG gene that activates isoniazid into its active form -mutate KasA (complex that forms with isoniazid) -overexpress ahpC mutant (protects cell from oxidative stress)
41
can isoniazid: -be absorbed from GI tract? -widely distribute in the tissues? -penetrate the CNS?
yes to all IT IS A SMALL MOLECULE
42
Since isoniazid is absorbed from the GI tract, can we give it orally?
yes
43
4 adverse effects of isoniazid*
drug-induced systemtic lupus erythematosus hypersensitivity rxns isoniazid-induced hepatitis peripheral neuropathy
44
as mentioned, an adverse effect of isoniazid is peripheral neuropathy can anything be done to reduce the chance of this happening?
give with vitamin b6
45
aside from helping to prevent peripheral neuropathy from isoniazid, why else is vitamin b6 good to administer with isoniazid
it can reduce the chance of SEIZURES (seizures is a potential but rare AE of isoniazid bc it is able to cross BBB)
46
explain the metabolism of isoniazid and is there any concern with it
phase 2 acetylation happens FIRST -- to N-Acetyl INH then it undergoes phase 1 hydrolysis -- to ACETYLHYDRAZINE WHICH IS HEPATO TOXIC!!! acetylhydrazine can acetylate macromolecules -- hepatic proteins
47
if isoniazid is administered alone, around how long is it until resistence emerges what is the mechanism of resistance?
2-3 months the drug can't get into the organism (bacteria)
48
rifampin is a semisynthetic derivative of ______
rifamycin
49
is rifampin static or cidal and what is spectrum
broad spectrum - (+), (-), and enteric bactericidal also obviously active against mycobacterium tuberculosis
50
explain the regimen in which rifampin is given
ALWAYS given with isoniazid for cases of active TB NOT GIVEN ALONE
51
explain the MOA of rifampin
binds beta subunit (ALLOSTERIC SITE) of DNA dependent RNA polymerase to INHIBIT RNA SYNTHESIS (inhibit mRNA synthesis = no proteins and bacteria can't survive)
52
true or false rifampin does not bind human RNA polymerase
TRUE - only bacterial
53
explain the resistance mechanism for rifampin
point mutations occur in the RNA polymerase WHICH DECREASES RIFAMPIN BINDING TO IT
54
what is the name of the enzyme that promotes transcription of DNA to mRNA
DNA-dependent RNA polymerase (this is the enzyme that rifampin inhibits)
55
is rifampin given orally?
yes - well absorbed given as capsules
56
true or false rifampin is not well distributed
FALSE readily distributed in tissues and phagocytic cells (including macrophages where mycobacterium infects!)
57
significance of how rifampin is metabolized
metabolized by liver into bile, where it undergoes enterhepatic recirculation --- this gives it a longer half life
58
differentiate between the excretion of isoniazid vs rifampin
isoniazid - in urine rifampin - mainly in feces as deactlyated metabolite
59
**3 main AE of rifampin
turns urine/sweat/tears orange nephrotoxicity - nephritis, acute tubular necrosis cholestatic hepatitis
60
**MAIN special consideration of rifampin
it is an inducer of CYP450 isoforms!!! therefore, serum levels of many drugs will decrease bc their metabolism is increased ie - oral contraceptives may not work
61
name 6 classes of drugs that are metabolized by CYP system and thus will have a DDI with rifampin and their serum levels will decrease
methadone oral contraceptives anticoagulants anticonvulsants protease inhibitors NNRTIs
62
RIFAMPIN inhibits the synthesis of _____________
mRNA
63
2 mechanisms rifampin resistance
mutations in rpoB gene (encodes B subunit of RNA polymerase) ABC transporters such as Dac C (D-ala-D-ala-carboxypeptidase) can pump the drug out
64
true or false pyrazinamide is a first line agent for tb
true
65
explain the MOA of pyrazinamide
diffuses into granuloma of mycobacterium tuberculosis this is where pyrazinamidase (a tb enzyme) converts pyrazinamide into the ACTIVE FORM -- PYRAZINOIC ACID this pyrazinoic acid BLOCKS THE SYNTHESIS OF COENZYME A ---- thus inhibiting ATP synthesis - less energy -- inhibits trans-translation in acidic conditions, acid gets protonated and disrupts cell membrane function to cause cell death mechanism is not well established -- BUT THOUGHT TO COLLAPSE MEMBRANE POTENTIAL AND AFFECT TRANSPORT FUNCTIONS OF THE MEMBRANE
66
true or false pryazinamide is a prodrug
TRUE converted by pyrazinamidase into the active form - pyrazinoic acid
67
true or false pyrazinamide does not enter macrophages
FALSE it does
68
half life pyrazinamide
6 hours
69

D&D Infectious Disease FINAL (21 decks)

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