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
counselling on pyrazinamide
N&V, jaundice (only used in first 2 months) joint pain and swelling
20
how does ethambutol work
bacteriostatic
21
counselling on ethambutol
eyesight checks as can lead to optic neuritis dose reduction if have renal impairment
22
what are combination products
reduce tablet burden and aid compliance 1. Rifater - isoniazid, rifampicin, pyrazinamide Voractive - isoniazid, rifampicin, pyrazinamide, ethambutol 2. Rifinah - isoniazid, rifampicin
23
what is MDR-TB
resistant to at least isoniazid and rifampicin
24
what is XDR-TB
resistant to isoniazid and rifampicin plus a quinolone (ciprofloxacin) plus at least one 2nd line injectable agent
25
risk factors for resistance
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