INF1 - A. TB-COVERED Flashcards

1
Q

what causes TB and what is it

A

mycobacterium tuberculosis (rod-shaped bacteria)
infection which affects the lungs (can also occur in other organs and joints)

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2
Q

what caused the increase in cases of TB from 1980

A

drug resistance and HIV (more likely to get if have HIV - leading cause of death in those with HIV)

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3
Q

what is latent TB

A
  • the bacteria is present but the person doesn’t have any symptoms
  • the immune system produces inflam that surrounds the TB bacteria and walls off the infection in the lungs
  • can develop TB later if their immune system in weakened
  • screening before drug treatment - ie. infliximab
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4
Q

what is the Mantoux test

A

identifies if someone has TB infection or has had the BCG vaccine

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5
Q

how does the Mantoux test work

A
  • liquid with tuberculin injected intradermally under skin
  • site checked 48-72 hours later
  • +ve result (>15mm) = previous exposure to tuberculin protein, bigger the reaction, more likely they are infected
  • antibodies against TB cause immune response which causes a skin reaction of a raised red bump
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6
Q

how is TB transmitted

A
  • close contact with people with active TB
  • airborne transmission (droplets)
  • only TB of throat/lungs is infectious
  • requires prolonged contact
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7
Q

how does TB cause infection

A
  • bacteria enters the lungs, travels to alveoli and multiples
  • TB develops slowly, can take months for symptoms to show
  • bacteria can enter bloodstream - spread to joints etc
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8
Q

TB risk factors

A

country of birth
travel history - latent TB then travel?
previous TB contact
immunosuppression
living conditions
social risk factors

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9
Q

how does the BCG vaccine work

A
  • contains live attenuated mycobacterium
  • doesn’t offer lifelong protection
  • can protect against development of severe forms of disease ie - TB meningitis
  • limited impact in spread of pulmonary TB
  • small scar left at injection site
  • recommended for children at high risk and healthcare workers
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10
Q

signs and symptoms of pulmonary TB

A

productive cough (possibly with blood in mucus) lasting for more than 3 weeks
very tired
fever
night sweats
loss of appetite
weight loss
enlarged lymph nodes
crackles in lungs

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11
Q

how to diagnose TB

A
  • x-ray = detects lesions in tissue
  • ultrasound = detects peripheral lesions
  • echocardiogram = TB can cause congestive heart failure
  • CT = whole body TB
  • samples of mucus for culture and sensitivity testing (antibiotics)
  • Mycobacteria can take a very long time to grow therefore start treatment
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12
Q

what to do when infection is confirmed

A
  • inform household contacts and those with a cumulative contact of 8> hours in last 3 months
  • Mantoux test for household and non-household contacts >5 yrs
  • IGRAs blood test for TB infection
  • chest x-ray to detect latent/active TB
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13
Q

what is the treatment of latent TB

A

Rifampicin + isoniazid for 3 months OR
Isoniazid for 6 months
(HIV patients - also use HAART to minimise risk of active disease)

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13
Q

how to treat patients who don’t have risk factors for MDR-TB

A

isolated in single room until completed 2 weeks treatment
wear mask if leaving room

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13
Q

what is the standard treatment of active TB

A
  1. 2 months of isoniazid (with pyridoxine), rifampicin, pyrazinamide, ethambutol INITIAL PHASE
  2. 4 months of isoniazid (with pyridine) and rifampicin CONTINUOUS PHASE

(CNS involvement/drug resistance can be up to a year of treatment)

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13
Q

how often is the medication taken

A

daily dosing or 3 times weekly dosing

13
Q

why is the treatment so long

A

mycobacteria grow slowly and dormant bacteria divide only when threatened by antibiotic treatment
so 6 months allows active and dormant bacteria to be eliminated

14
Q

what is DOT

A

improves adherence by using HC workers, community volunteers or family members to observe and record patients taking each dose
(those who don’t adhere to treatment, drug/alcohol misusers, homeless, prisoners, MDR-TB)

14
Q

why are so many drugs taken

A

prevents resistance and eradicates bacteria in different environments
mutated bacteria are unlikely to be resistant to 2 drugs as drugs work in different ways

14
Q

how does isoniazid work

A
  • inhibits mycolic acid synthesis
  • bactericidal against actively dividing mycobacteria
  • metabolised in liver by CP50 enzymes (slow acetylators more susceptible to neuropathy)
  • pyridoxine for prophylaxis of peripheral neuropathy
15
Q

counselling on isoniazid

A

N&V, jaundice (liver)
peripheral neuropathy
take before food

16
Q

how does rifampicin work

A

bactericidal against those that multiply in macrophages or closed caseous lesions
liver enzyme inducer therefore increased metabolism of other drugs (INTERACTIONS)

17
Q

counselling on rifampicin

A

take before food
interactions
colours body fluids orange and contact lenses
N&V, jaundice
rashes
bruise easily

18
Q

how does pyrazinamide work

A

bactericidal
most effective against actively dividing intracellular organisms

19
Q

counselling on pyrazinamide

A

N&V, jaundice (only used in first 2 months)
joint pain and swelling

20
Q

how does ethambutol work

A

bacteriostatic

21
Q

counselling on ethambutol

A

eyesight checks as can lead to optic neuritis
dose reduction if have renal impairment

22
Q

what are combination products

A

reduce tablet burden and aid compliance

  1. Rifater - isoniazid, rifampicin, pyrazinamide
    Voractive - isoniazid, rifampicin, pyrazinamide, ethambutol
  2. Rifinah - isoniazid, rifampicin
23
Q

what is MDR-TB

A

resistant to at least isoniazid and rifampicin

24
Q

what is XDR-TB

A

resistant to isoniazid and rifampicin plus a quinolone (ciprofloxacin) plus at least one 2nd line injectable agent

25
Q

risk factors for resistance

A

history of TB treatment, prior treatment failure
contact with known case of drug resistant TB
patient from a country with high prevalence of resistant TB (due to no access to meds - can’t afford?)
HIV infection
lack of compliance