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PHAM02 > TB > Flashcards

TB Flashcards

1
Q

MDR-TB

A

multi drug resistant TB

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2
Q

bacteria that causes TB

A

mycobacterium tuberculosis

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3
Q

What type of bacteria is mycobacterium tuberculosis?

A
  • aerobic (needs O2)
  • G+ve
  • acid fast (stain not removed by acid)
  • bacilli
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4
Q

What does intracellular mean (about mycobacterium tuberculosis)?

A

able to survive inside macrophages

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5
Q

structure of mycobacterium tuberculosis

A
  • layer of mycolic acid surrounds the cell
  • gives it a waxy, waterproof coating
  • difficult to penetrate by ABX - resistance
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6
Q

How is TB transmitted?

A

aerolised droplets from infected patient

inhaled into alveoli of new host

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7
Q

outcomes TB can have

A

– Primary Tuberculosis (first infection)
– Complete clearance
– Post-primary Tuberculosis (re-infection)
– Active Tuberculosis
– Latent Tuberculosis

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8
Q

first infection of TB

A
  • Mostly affects lungs
  • Usually clinically silent in immunocompetent
  • Results in an area of granulomatous inflammation, shadow on an x-ray, called Ghon focus.
  • 90% will never develop active disease due to good immune response
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9
Q

latent TB

A
  • bacillus can stay trapped inside the granuloma in some patients
  • skin prick test to ID latent TB
  • can reactivate any time, from abnormalities in cell mediated immunity
  • long ABX regimens used to get rid of latent TB
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10
Q

What test to detect latent TB?

A

skin prick test - tuberculin test

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11
Q

active/post primary active TB

A
  • small no. develop at 1st aquisiton
  • more commonly reactivation of latent TB infection
  • can occur if become immunocompromised (HIV, cs, chemo)
  • aggressive immune system reaction
  • large granulomas with ‘cheesy’ contents called caseation
  • coughed up (incl live bacteria) leaving large lesions, seen on x-ray
  • lesions become pus filled, can exudate
  • ideal breeding ground for bacillus and large nos. released
  • active = contagious
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12
Q

What is extrapulmonary TB?

A
  • can cause disease at any site of body
  • usually from reactivation of latent infection

common sites:
- lymph nodes
- GIT
- bone
- CNS

  • eg. Miliary TB
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13
Q

What is disseminated disease? (Miliary tuberculosis)

A
  • bacilli transported in blood or lymphatic system
  • can develop as primary infection or post primary reactivation
  • can affect many organs
  • can cause diagnostic delay, esp if lungs not infected
  • more common in children and immunocompromised
  • CXR look like small seeds
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14
Q

presentation of active TB

A

initial Sx vague/non-specific
cough - persistent, productive
weight loss
fever
night sweats
fatigue
dyspnoea
chest pain
haemoptysis

(depends on site of infection, 60% respiratory)

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15
Q

people who are at inc risk of TB

A
  • born in high prevalence area
  • immunocompromised
  • contact with active TB
  • previous TB Tx
  • alcohol/drug misusers
  • settled migrants in UK
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16
Q

diagnosis of TB

A

respiratory
- CXR
- acid fast bacilli test
- sputum cultures
- NAAT (nucleic acid amplification test), often PCR
non respiratory
- biopsy/needle aspiration (culture)
- MRI/CT/ultrasouns
- CXR (confirm/exclude respiratory disease)

17
Q

diagnosis of TB

A

respiratory
- CXR
- acid fast bacilli test
- sputum cultures
- NAAT (nucleic acid amplification test), often PCR

non respiratory
- biopsy/needle aspiration (culture)
- MRI/CT/ultrasouns
- CXR (confirm/exclude respiratory disease)

18
Q

INITIAL management of pulmonary TB

A
  • TB specialist
    hospital
  • isolated
  • PPE
  • -ve pressure room if MDR-TB

community
- advise highly contagious when active
- no work/school/crowded places
- face mask in public during first 2 weeks of Tx

19
Q

phases of TB Tx

A
  1. intensive/initial phase Tx
  2. continuation phase
20
Q

intensive/initial phase Tx

A

lasts 2 months

with 4 drugs

21
Q

continuation phase Tx

A

4-7 months

with 2 drugs

22
Q

drugs in initial Tx

A

rifampicin
isoniazid (with pyridoxine)
pyrazinamide
ethambutol

-> for 2 months

23
Q

drugs in continuation Tx

A

rifampicin
isoniazid (with pyridoxine)

-> for further 4 months

24
Q

Why is combination of drugs used?

A

to reduce risk of resistance

25
Q

MOA of rifampicin

A
  • bactericidal
  • blocks RNA polymerase and prevents protein formation
26
Q

rifampicin and food

A
  • absorbed in the GIT
  • reduced if taken with food
  • take on empty stomach
27
Q

s/e of rifampicin

A
  • red/orange disconoration of body fluid (stains contact lenses)
  • liver damage (inc liver enzymes, 4x ULN STOP Tx)
  • enzyme inducer
27
Q

s/e of rifampicin

A

red/orange disconoration of body fluid
- stains contact lenses

liver damage
- inc liver enzymes
- 4x ULN then STOP Tx

28
Q

isoniazid MOA

A
  • inhibits synthesis of mycolic acids required for cell wall
  • bactericidal
  • acts rapidly to reduce initaial bacterial load
29
Q

metabolism of isoniazid

A

by liver

acetylation
- some people fast metabolisers, some slow
- affects t1/2

30
Q

Who is more likely to have adverse effects with isoniazid?

A

slow acetylates

advanced HIV

31
Q

of isoniazid

A
  • hepatotoxicity
  • N&V
  • hypersensitivity rxn
  • peripheral neuropathy
32
Q

How to avoid PN with isoniazid?

A

supplement with vitamin B6 -> pyridoxine

33
Q

Why does pyrazinamide no longer become effective later in therapy?

A
  • pyrazinamide only works in acidic pH, inside the macrophages in the tubercle (nodules of dead cells filled with TB bacteria)
  • no. of these decrease later in therapy
  • it no longer becomes effective
34
Q

Is pyrazinamide bacteriostatic or bacteriocidal?

A

bacteriostatic

35
Q

adverse effects of pyrazinamide

A

hepatotixicity
rashes
urticaria
gout

36
Q

pyrazinamide and hepatotoxicity

A
  • elevation of LFTs
  • regular LFTs

Sx of liver disease
- N&V
- malaise
- jaundice

PHAM02 (32 decks)

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