1 - Paeds - Resp - Chest infections - TB Flashcards

1
Q

why is incidence rising?
spread by?
3 RFs?

A

due to HIV infection and multi-drug resistant strains

spread - resp route
RFs - lose proximity, infectious load, underlying immdef

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2
Q

how is tb infection different to Tb disease?

A

tb infection (latent TB) is more likely to progress to disease in infants and young kids

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3
Q

however - children vs adults??

A

kids generally not infectious vs adults, kids usually acquire it from an infected adult in the household

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4
Q

Clinical features - primary infection can be one of two things? % of infants + older kids show Sx+signs?

A

aSx and Sx

~50% of infants and 90% of older children will show minimal signs/Sx of infection

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5
Q

what limits Sx progression? disease does what? may do what? what may become +ve ? what then? what does CXR show?

A

local inflam reaction
disease remains latent and may activate later
Mantoux test may become +ve (>10mm or >15mm with BCG) - initiate treatment

CXR can showed marked hilar lymphadenopathy

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6
Q

what happens if local host response fails to contain inhaled tubercle bacilli?

A

it spreads by lymph to regional LNs. Lung lesion + LN = Ghon (primary) complex

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7
Q

how long does host cellular immune response take to respond? what slows and what develops?

A

3-6 weeks

mycobacterial replication slows but Sx develop -> fever, anorexia, weight loss, cough, CXR changes

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8
Q

What happens to primary complex ? inflam reaction may lead to what? what may also be present?

A

usually heals and may calcify

local enlargement of peribronchial LNs > bronchial obstruction > collapse and consolidation of affected lung

pl effusions may also be present

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9
Q

if its not halted by host immune response what happens?

A

local dissemination to other lung regions. primary infection may involve other organs eg gut, skin

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10
Q

2 steps before post primary TB?

A

dormancy + dissemination > reactivation > post primary TB

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11
Q

Miliary TB - sites? whats likely in paeds? causing?

A

bones, joints, kidneys, pericardium, CNS - CNS seeding is likely, causing tuberculous meningitis - sig mort and morb if not treated early

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12
Q

Initial treatment? examples?

what next?

A

triple, quad therapy (rifampicin, Isoniazid, Pyrazinamide, Ethambutol) initially
decreased to rif and ison after 2 months

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13
Q

length of treatment ? when is longer needed?

A

6m usually for uncompx pulm or LN TBif TB meningitis, or disseminated disease

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14
Q

what if pt is post puberty?

A

pyridoxine is given weekly to prevent peripheral neuropathy from isoniazid

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15
Q

what else in TB meningitis?

A

dexamethasone given for 1 month to reduce long term sequelae - ensure adherence

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16
Q

what is aSx kid - but mantoux +ve (latent TB)

A

treated for 3m with rifampicin and isoniazid to reduce risk of reactivation later in life