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Module 2 > Tuberculosis Chemotherapy > Flashcards

Tuberculosis Chemotherapy Flashcards

1
Q

What is the current 1st line treatment for TB?

A

RIPE for 6 months DOTS

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2
Q

What is the intensive phase of TB treatment?

A

2 months of RIPE

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3
Q

What is the continuation phase of TB?

A

4 months rifampicin and isoniazid

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4
Q

How long is the treatment for drug-resistant TB?

A

1-2 years

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5
Q

What is 1st line for drug resistant TB?

A

fluoroquinolones

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6
Q

What is 2nd line for drug-resistant TB?

A

aminoglycosides; thiamines

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7
Q

Why is such a long course of treatment for TB needed?

A

cells are able to enter into a dormant state as persisters - drugs target active processes

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8
Q

What is resistance?

A

ability of bacteria to survive the presence of a drug at a conc. that normally kills or inhibits growth

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9
Q

What is natural resistance?

A

non-susceptibility due to bacterial cell characteristics

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10
Q

Give an exmaple of natural resistance?

A

Mtb expresses a beta-lactamase so is naturally resistant to penicillin

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11
Q

What is acquired resistance?

A

non-susceptibility due to genotypic change

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12
Q

What are the mechanisms of resistance?

A

target modification; target over-expression; drug-inactivating mechanisms; barrier mechanisms (influx and effflux); plasmid-mediated resistance

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13
Q

Why does drug resistance occur?

A

non-compliance; incomplete drug regimen; sub-optimal dosage; poor drug absorption

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14
Q

What is the target for RIF?

A

RNA polymerase enzyme

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15
Q

What is the MOA of RIF?

A

inhibits DNA transcription by binding to the RNA polymerase enzyme, blocking exit channel preventing the production/exit of mRNA from DNA

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16
Q

What is the most common mutation resulting in RIF resistance?

A

RNA polymerase beta sub-unit rpoB gene- prevents binding of drug to enzyme

17
Q

What does INH require activation by?

A

catalase peroxidase

18
Q

What encodes catalase peroxidase?

A

katG gene

19
Q

What is the action of active INH?

A

generates a range of radicals which target mycolic acid syntehsis; NAD metabolism; oxidative stress response

20
Q

Give an example of INH mutation causing resistance?

A

katG preventing binding and activation of INH

21
Q

When is PZA active?

A

after activation by pyrazinamidase enzyme and at acidic pH

22
Q

What is the active form of PZA?

A

pyrazinoic acid

23
Q

What is the general mechanism of PZA?

A

destabilises the TB membrane using proton motive force3

24
Q

What is the major cause of PZA resistance?

A

mutations in the pro-drug activating PZase pncA gene

25
Q

What is the MOA of EMB?

A

inhibits cell wall arabinogalactan synthesis by blocking arabinosyl transferase

26
Q

What is arabinogalactan?

A

major polysaccharide in cell wall

27
Q

What is the main mechanism of resistance to EMB?

A

mutations in embB- arabinosyl transferase

28
Q

What si hte MOA of fluoroquinolones?

A

inhibits DNA synthesis

29
Q

What causes resistance to fluoroquinolones?

A

mutations in DNA gyrase (gyrA and gyrB)

30
Q

What is the MOA of streptomycin?

A

inhibits mRNA translation in protein synthesis

31
Q

What causes resistance to streptomycin?

A

mutations in sequences encoding the ribosomal subunits

32
Q

Why do bedaquiline get a fast-track approval?

A

based on faster sputum conversion not clinical outcome

33
Q

When is bedaquiline used?

A

in MDR and XDR TB

34
Q

What is a problem with bedaquiline?

A

issues with QTc

35
Q

What is needed in terms of new drugs?

A

active in both MDR - TB and non-dividing cells(to shorten treatment times)

36
Q

What are the environmental conditions in a granuloma?

A

low carbon and oxygen concentrations

37
Q

Who should not receive fluoroquinolones?

A

pregnant women and young children

38
Q

What are the features of ideal TB drug targets?

A

should be required for bacterial growth and persistence; should be possible to inhibt their activty using small molecules and should be accessible to these modulatory compounds

39
Q

Waht is the structure of the mycobacterial cell wall?

A

layer of peptidoglycan then layer of arabinogalactan then mycolic acids with glyoclipids attached

Module 2 (38 decks)

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