TB Flashcards
What is the pathogen causing tuberculosis?
Mycobacterium tuberculosis (acid fast staining bacillus)
What are the different types of TB infections?
silent
latent
progressive,active
What groups are most at risk for active disease TB?
children under 2yrs
adults over 65 yrs
What are the 2 most important drugs in the treatment of TB?
isoniazid
rifampin
multidrug resistant TB is resistant to both :o
Why do we use Directly Observed Treatment?
to reduce treatment failures and the selection of drug resistant isolates
What are the diagnostic tests for TB? (2)
Mantoux test (tuberculin unit PPD dose) - read w/in48-72 hrs
Interferon y release assays
**What are the first line agents in the treatment of TB?
(in approx order of preference)
isoniazid
rifampin
pyrazinamide
ethambutol
**Rifampin: MOI
inhibits RNA synthesis (inhibits RNA polymerase –> blocks RNA production)
**Isoniazid: MOI
inhibits cell wall synthesis (inhibits synthesis of mycolic acid)
**Pyrazinamide: MOI
exact target unclear
disrupts plasma membrane
disrupts energy metabolism (ATP synthesis)
**Ethambutol: MOI
inhibits cell wall synthesis (inhibits formation of arabinogalactan)
**What is an appropriate therapeutic plan for latent TB? (drug, duration, dosing)
ISONIAZID: -9mo daily: 270 doses twice/wk: 76 dose -6mo daily: 180 twice/wk: 52
ISONIAZID + RIFAPENTINE
- 3mo
weekly: 12
RIFAMPIN
- 4mo
daily: 120
**What is an appropriate therapeutic plan for active TB? (How many drugs do we use? Which drugs?)
combination chemotherapy is required
use at least 2 drugs to which the isolate is susceptible
outset of tx: all 4 drugs
rifampin
isoniazid
pyrazinamide
ethambutol
“trying to use some synergism putting these 4 drugs together”
**Rifampin: ADEs
turns bodily fluids orange cholestasis (hepatitis) rash flu like syndrome (with intermittent dosing) thrombocytopenia nephritis
cutaneous reactions, GI reactions (nausea, anorexia, abdominal pain), flu-like syndrome, hepatotoxicity, severe immunologic reactions, orange discoloration of bodily fluids (sputum, urine, sweat, tears), drug interactions due to induction of hepatic microsomal enzymes
**Isoniazid: ADEs
hepatic toxicity
peripheral neuropathy: vitamin B6 deficiency
asymptomatic elevation of aminotransferases, clinical hepatitis, fatal hepatitis, peripheral neurotoxicity, CNS effects, lupus-like syndrome, hypersensitivity, monoamine poisoning, diarrhea
**Pyrazinamide: ADEs
hepatotoxicity hyperuricemia rash GI disturbance arthralgias
hepatotoxicity, GI symptoms (nausea, vomiting), nongouty polyarthralgia, asymptomatic hyperuricemia, acute gouty arthritis, transient morbilliform rash, dermatitis
**Ethambutol: ADEs
retrobulbar neuritis (sudden loss of vision) -reversible if drug is stopped
retrobulbar neuritis, peripheral neuritis, cutaneous reactions