Flashcards in TB Deck (15):
what are some risk factors for relapse in non-MDR-TB?
sputum culture that remains positive at 8 weeks
in what situation of TB/HIV coinfection would you avoid starting the anti-retroviral straight away?
if a patient had tuberculous meningitis, then you would risk local Immune Reconstitution Inflammatory Syndrome (IRIS)
do any of the common TB drugs have any impact on HIV therapy?
rifampicin significantly reduces the concentration of protease inhibitors
this means that substitution of rifampicin for rifabutin and increasing PI dose is a good idea (but also a little risky?)
how long should a patient with pulm TB stay resp isolated?
the official answer is 2-3 weeks after treatment started
what is the college recommended management of skin or generalised hypersensitivity reactions?
(note: this is not the same as LFT abmormality)
cease all drugs
restart treatment once a combination of two drugs is found
what is the definition of MDR-TB?
what is meant by primary and secondary MDR-TB infections?
this is a resistance to isoniazid and rifampicin
primary is the infection with an already resistant organism
secondary is drug resistance emerging during chemotherapy
what are the common side effects of the standard short course for TB?
rif- drug interactions, N/V, hepatitis, orange wee, thrombocytopenia
isoniazid - hepatitis, peripheral neuropathy (give drug with pyridoxine), lupus syndrome, optic neuritis
pyrazinamide - hepatotoxicity high uric acid, arthralgia, skin rash
ethambutol - optic neuritis, skin rash
what is the management of MDR-TB?
ideally it is a 2 year treatment
give an injectable (aminoglycoside for e.g.) plus moxiflox plus ethambutol plus pyrazinamide
lots of debate about other additions
which of the standard short course should be avoided if patient has pre-existing liver disease?
ideally avoid all hepatotoxics (isoniazid, rif and pyrazin) BUT
the first one to avoid is pyrazinamide
if severe liver disease, then avoid all three
which of the standard short course for TB should be avoided if there is renal failure?
ethambutol/streptomycin should be avoided, unless you can closely monitor blood levels
dose reduction should be considered for pyrazinamide and isoniazid
how does isoniazid work?
this is a prodrug.
it is activated by the bacterial catylase/peroxidase. Once activated it impairs fatty acid synthesis and downstream cell wall
how does rifampicin work?
it inhibits RNA synthesis by inhibiting RNA polymerase
how does pyrazinamide work?
this is a prodrug that only has effect in mycobacterial infection
it is activated by TB to pyrazinoic acid, then changes the environment. The actual MoA is not clear
How does ethambutol work?
it disrupts the cell wall formation by inhibiting the upstream binding of mycolic acid to the rest of the cell wall
(this may be slightly inaccurate, but it is a cell wall inhibitor)