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respiratory system year 1 > Tuberculosis > Flashcards

Tuberculosis Flashcards

1
Q

epidemiology of TB - worldwide

A

incidence rate worldwide is falling 2%/yr
number 1 killer of comunicable disease (> HIV and malaria combined)
2/3 of all cases in 8 countries: India, China, Indonesia, Philippenes, Pakistan, Nigeria, Bangladesh, South Africa
30 high TB burden countries account for 87% of all the world’s cases
~2bln people infected worldwide

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2
Q

epidemiology of TB - national

A

major problem in London - immigration from high incidence areas
39% of TB cases in UK are in London
2/3 cases born abroad
clusters in cities

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3
Q

vulnerable groups in the UK

A

those from high prevalence countries
70% are non-UK born, most aged 15-44
HIV +ve, immunosuppressed
elderly, neonates, diabetics

homeless, alcoholics, IDUs, mental health problems, prison - 1/10 of all cases

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4
Q

mycobacteria

A

numerous species, ubiquitous in soil, water

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5
Q

which species of mycobacteria cause human disease

A

Tuberculosis (M. TUBERCULOSIS, M. africanum, M. bovis (bovine TB, BCG strain)

non-tuberculosis mycobacteria, NTM infections/atypical mycobacteria

Leprosy (M. leprae)

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6
Q

why does TB take a long time to treat

A

non-motile bacillus, very slow growing

disease is slow, treatment is long

cultures take a long time to grow to recieve results back

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7
Q

is TB aerobic or anaerobic

A

aerobic - predilection for apices of lungs where there is a higher oxygen conc

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8
Q

describe the cell wall of mycobacteria

A

uniquely has a very thick fatty cell wall - have to treat with many antibiotics for a long period of time
resistant to acids, alkalis and detergents
resistent to neutrophil and macrophage destruction
acid and alcohol fast bacilli - Ziehl Nielson stain

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9
Q

are all AAFBs TB

A

NO

can’t differentiate mycobacteria from TB on initial stain

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10
Q

how is TB spread

A

airbone - pulm and laryngeal TB
someone with TB bacteria in their lungs coughs/sneezes/yells
TB bacteria attached to aerosol droplets which remain suspended in air for many hours esp w/ poor air circulation
someone else breathe in the bacteria
usually requires prolonged closed contact

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11
Q

what is TB NOT spread by

A 
shaking hands
sharing food
touching surfaces
sharing toothbrushes
kissing
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12
Q

what are outdoors mycobacteria eliminated by

A

UV radiation

dilution

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13
Q

what is the exeption to the spread of TB

A

M. bovis

can be spread by the consumption of unpasteurised infected cow milk

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14
Q

why do HIV patients respond worse to TB

A

Their T cell response is impacted

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15
Q

what does the T cell immune response cause

A

tissue destruciton

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16
Q

immunopathology of TB

A

activated macrophages –> epithelioid cells –> Langhan’s giant cells

accumulation of macrophages, epithelioid and Langhan’s cells –> Granuloma

central caseating necrosis which may later calcify

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17
Q

is the Th1 cell mediated response good or bad

A

eliminated/reduces number of invading mycobacteria

tissue destruction is a consequence of activation of macrophages

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18
Q

what affects the outcome of TB infection

A

infection - virulence, number

susceptibility - genetics, nutrition, age, immunosuppression

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19
Q

primary TB infection

A

no preceding exposure or immunity
mycobacteria spread via lymphatics to draining hilar lymph nodes
usually no symptoms
can be fever, malaise, erythema nodosum, rarely chest signs

associated with development of immunity to tuberculoprotein

20
Q

what happens in the majority of 1y TB infections

A

> 85%
initial lesion and local lymph node (1y complex)
heals w/ or w/o scar
may calcify (Ghon focus and complex)

21
Q

what are the 3 different outcomes of 1y TB infections

A

progressive disease
contained latent
cleared cured

22
Q

tuberculous bronchopneumonia

A

small number of 1y infections (1%) progress
1y focus continues to enlarge - cavitation
enlarged hilar lymph compress bronchi, lobar collapse
enlarged lymph node discharges into bronchus
poor prognosis

23
Q

miliary TB

A

occurs in 1-3% of 1y TB infections
hematogenous spread of bacteria to multiple organs
fine mottling on X ray, widespread small granulomata
CNS TB in 10-30%

24
Q

post-1y disease

A

most common outcome
only in humans
typically 1-5yrs after exposure
2 main theories:
1. TB bacteria enter dormant stage with low/no replication over prolonged time period
2. balanced state of replication and destruction by immune mechanisms

25
Q

clinical presentation of TB

A

cough - present with pulmonary TB
fever
sweats (mainly night)
weight loss

all 3 symptoms

26
Q

what % of patients have extra-pulmonary TB

A

50

27
Q

in what % of patients are CRP and ESR normal

A

CRP - 15%

ESR - 21%

28
Q

in what % of pts are symptoms absent

A

fever - 37%
sweats - 39%
weight loss - 38%
all 3 absent in 25%

29
Q

appearance of pulmonary TB on CXR

A

classical: apices, soft ‘fluffy/nodular’ upper zone, cavitation in 10-30%

lymphadenopathy rare

normal CXR in 13% of definitive pulm TB (22% in HIV)

30
Q

when to consider CT

A 
normal CXR but clinical suspicion
miliary TB
cavitation and other differential 
lymphadenopathy, alternative diagnosis
targets for BAL
31
Q

appearance of 1y TB on CXR

A

mediastinal lymphadenopathy (mainly unilateral, 15% bilateral)
pleural effusion
miliary (hematogenous spread, 1-3%)
pnuemonic lesion w/ enlarged hilar nodes - consider 1y TB
(no swollen lymph nodes in pneumonia)

32
Q

how to sample the bacteria

A

sputum: 3 samples, 8-24hrs gap, at least 1 early morning sample
induced sputum if they can’t cough
bronchoscopy with BAL
endobronchial US with biopsy
lumbar puncture (CNS TB)
urine (urogenital TB)
aspirate/biopsy from tissue (lymph node, bone, joint, brain, abscess)
mantous/IGRA are NOT routinely used in diagnosing active TB

33
Q

what are the 4 drugs used to treat TB

A

isoniazid (H)
pyrazinamide (Z)
rifampicin (R)
ethambutol (E)

34
Q

rules of TB treatment

A

multiple drug therapy is essential - single agent treatment leads to drug resistant organisms within 14 days
therapy must continue for at least 6 months
legal requirement to notify all cases
test for HIV, hep B and C (risk of hepatotoxicity)

35
Q

standard TB treatment

A

2 mths R/H/Z/E + 4 R/H

6 mths duration minimum

36
Q

other drugs used in TB treatment

A

pyridoxine (vit b6) with isoniazid to reduce risk of neuropathy
steroids (CNS, miliar, pericardial)
vit D substitute?

37
Q

when is TB treatment >6mths

A

7-9mths - monoresistance
12 mths - CNS TB, h monoresistance extensive disease
9-12-18-20 mths - MDR RR TB

treatment in the brain/drug resistance takes longer

38
Q

how long does it take to kill the MTB

A

90% MTB dead in 2 days when using isoniazid

99% MTB dead in 14days when also using rifampicin

39
Q

side effects of rifampicin

A

orange urine/tears/lenses - indicates tablet is being absorbed
induces liver enzymes, prednisolone, anticonvulsants
all hormonal contraceptive methods ineffective
hepatititis
rash

40
Q

side effects of isoniazid

A

hepatitis
peripheral neuropathy - pyridoxine B6 to prevent this
rash

41
Q

side effects of pyrazinamide

A

hepatitis
gout
rash

42
Q

side effects of ethambutol

A

optic neuropathy

rash

43
Q

BCG vaccination

A

given selectively to risk groups
neonates or unvaccinated children under 5, whose parent/grandparents were born in a country with an annual incidence of TB of 40/100 000 or greater
unimmunised contacts of cases
unimmunised high risk employees

44
Q

latent TB screening

A

screen: contacts of people with active pulmonary/laryngeal TB who are <65 (hepatotoxitity increases with age), new entrants from high endemic areas, pre-biologics (TNF-alpha inhibitors), outbreaks

asymptomatic with normal CXR and norma examination AND +ve mantous/IGRA test

45
Q

treatment of LTBI

A 
always rule out actie TB 
rifampicin and isoniaid for 3 mths 
OR isoniazid only for 6mths 
OR rifampicin only for 6mths 
OR rifapentine and isoniazide once weekly for 12 weeks (underserved population)

respiratory system year 1 (25 decks)

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