Term
| what is important for tx of TB pts? |
|
Definition
| nutrition and multi-drug therapy |
|
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Term
| when are pts considered infectious? |
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Definition
| when pts are coughing, undergoing cough-inducing/aerosol-generating procedures, have sputum smears positive for acid-fast bacilli, are not receiving therapy, have just started therapy, or have poor clinical response to therapy |
|
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Term
| what are the first line drugs for TB? (*know these*) |
|
Definition
| isoniazid, rifampicin, pyranzinamide, ethambutol, rifabutin, and rifapentine |
|
|
Term
| what are the second line drugs for TB? |
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Definition
| streptomycin, cycloserine, p-aminosalicylic acid, ethionamide, amikacin, capreomycin, levofloxacin, moxifloxacin, and gatifloaxcin |
|
|
Term
| what is bactericidal vs sterilizing activity? |
|
Definition
| killing TB initially vs killing persistent sub-populations of TB |
|
|
Term
| what is the shortest time range for TB therapy? |
|
Definition
|
|
Term
| what is the MOA for isoniazid? |
|
Definition
| isoniazid is a nicotinic acid hydrazine that *inhibits mycolic acid synthesis (component of mycobacterial cell walls). mycolic acid inhibits the fusion of a phagosome w/a lysosome, thus preventing release of toxic proteases intended to kill intracellular organisms. it is bacteriostatic for resting and cidal for dividing mycobacterial cells. it has good penetration, *acetylation in the liver and excretion by the kidneys |
|
|
Term
| what is the main ADR associated with isonazid? how is this prevented?(*know this*) |
|
Definition
| *hepatotoxicity and peripheral neuropathy. hepatotoxicty is avoided by *monitoring ALT levels, and isonazid should be discontinued if ALT levels are 3x ULN in symptomatic pts (nausea/anorexia/abdominal pain), or 5x ULN in asymptomatic pts. vit B6 can help with neuropathy. |
|
|
Term
| is isoniazid used for any other infections besides TB? |
|
Definition
|
|
Term
| when is rifampicin usually used? |
|
Definition
| in pts who cannot tolerate isonazid to manage latent TB |
|
|
Term
| what is the MOA for rifampicin? |
|
Definition
| inhibition of bacterial DNA dependent RNA polymerase |
|
|
Term
| what are ADRs associated with rifampicin? |
|
Definition
| *rifampicin induces cytochrome P-450, which causes drug interactions with many drugs (incl: protease inhibitors, azoles, digoxin, warfarin, estrogens, phenytoin, steroids, and dilantin). it can also cause an orange-pink discoloration of the bodily secretions/fluids and soft contact lenses (red man syndrome) |
|
|
Term
| can rifampicin be used for neisseria meningitidis? |
|
Definition
|
|
Term
| what drug can be substituted for rifampicin, and why would you switch them out? |
|
Definition
| rifabutin may be substituted for rifampicin and has less interaction with other drugs such as *protease inhibitors - which are commonly prescribed in AIDs pts |
|
|
Term
| what is the main ADR associated with rifbutin? |
|
Definition
| anterior uveitis - ocular pain/blurred vision |
|
|
Term
|
Definition
| a sister drug of rifampicin, it increases the action of protease inhibitors, and therefore is contraindicated for HIV + pts. it is also only administered for pts >12 yrs old |
|
|
Term
| what is pyrazinamide? MOA? |
|
Definition
| a nicotinamide analong that inhibits fatty acid sythestase. hydrolyzed in the liver/excreted by the kidneys. |
|
|
Term
| what are ADRs associated with pyrazinamide? |
|
Definition
| hepatitis, rash, joint aches, hyperuricemia, and gout |
|
|
Term
| what is the only first line TB drug that is bacteriostatic, not cidal? |
|
Definition
| ethambutol, which inhibits cell wall synthesis. it is used as a companion drug to curtail resistance. |
|
|
Term
| what ADRs are associated with ethambutol? |
|
Definition
| optic neuritis - loss of green - *red discrimination and visual acuity, peripheral neuritis |
|
|
Term
| what is the MOA of streptomycin? ADRs? |
|
Definition
| streptomycin inhibits translocation by binding to the 30s ribosomal bacterial subunit (aminogylcoside) - *inhibiting protein synthesis. streptomycin can cause *renal and ototoxicity |
|
|
Term
| what drugs are important in XDR TB? |
|
Definition
| amikacin, kanamycin, and cycloserine |
|
|
Term
| what characterizes isoniazid, rifampicin, pyrazinamide, and ethambutol? |
|
Definition
| these are the standardized first line TB tx drugs. they are administed for 6-9 mos, are safe/effective/inexpensive, cure 95%, cost $20, and are based on extensive evidence |
|
|
Term
| what is the rationale for combining isonazid, pyrazinamide, rifampacin? |
|
Definition
| there are three populations of mycobacterium TB in cavitary TB, which each of these drugs target individually. *isonazid attacks *log phase growth. *pyrazimamide attacks slowly replicating bacilli under acidic conditions and *rifampicin attacks non-replicating bacilli under hypoxic conditions |
|
|
Term
| how should tx for TB be handled if there is an interruption w/out medication? |
|
Definition
| if the interruption is <14 days, continue, if >14 days, start over |
|
|
Term
| when are TB pts no longer considered infectious? |
|
Definition
| if they are on adequate therapy, have ad a significant clinical response to therapy and have had 3 consecutive negative sputum smear results |
|
|
Term
| what is a fundamental tenet for ID? |
|
Definition
| the longer it takes to dx and tx an infection, the more chances those infected have to get sicker and spread the disease. latent, dormant, persistent, nonreplicating, resting, metabolically inactive and quiescent infections need to be "sterilized" by successful drug combinations in all subpopulations to prevent recurrence |
|
|
Term
| how do populations of TB become drug resistant primarily? secondarily? |
|
Definition
| primary: when monotherapy is used, for ex if isonazid/rifampicin/pyrazinamide are used, no TB population will be able to develop resistance to all, but if just isonazid is used, a certain population will likely be able to develop resistance to it. secondary: poor adherence to therapeutic regimen, improper prescribing, drug interactions, and malabsorption |
|
|
Term
| what is there a recent link between TB and ? |
|
Definition
| TB and vit D deficiency (good vitamin D levels enhance TB clearance) |
|
|
Term
| what is the definition of MDR TB? (*know this*) |
|
Definition
| TB isolate that is resistant to both isonazid and rifampicin |
|
|
Term
| what is the definition of XDR TB? (*know this*) |
|
Definition
| MDR + resistance to fluoroquinolone and one of the 2 injectable drugs (amikacin, kanamycin, and capreomycin) |
|
|
Term
| what sign is characteristic of TB upon auscultation? |
|
Definition
| hollow, tubular breathing |
|
|
Term
| what are some of the challenges for TB tx adherence? |
|
Definition
| access to care, interpretation of wellness, financial burdern, attitude/knowledge/beliefs, laws/immigration status, pt characteristics, family/community/household influences |
|
|
Term
|
Definition
| Directly Observed Therapy Short course - hailed as one of the most important public health interventions to control TB worldwide, which addresses the problem of pts feeling better (after eradication of the intensive phase - rapid growth, and before the continuation phase - slow growing persistent bacilli) and stopping therapy before they should. |
|
|
Term
| can pts on immunosuppressives such as TNF alpha blockers develop IRS? |
|
Definition
| yes for the same reason that HIV + pts do |
|
|
Term
| should TB and HIV treatments be combined? |
|
Definition
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