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Old TB (Examination
Chest (Auscultation (± bronchial breathing, ↓ AE,…
Old TB
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Viva
Past Mx of TB
It was believed that lower PAO2 would inhibit TB
proliferation SO inducing apical collapse was a treatment
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Key Facts
Pathophysiology
Primary TB
Childhood or naïve TB infection
Organism multiplies @ pleural surface → Ghon Focus
Macros take TB to LNs
Nodes + lung lesion = Ghon complex
Mostly asympto: may → fever and effusion
Cell mediated immunity / DTH controls infection in 95%
Fibrosis of Ghon complex → calcified nodule
(Ranke complex)
Rarely may → 1O progressive TB (immunocomp)
Primary Progressive TB
Resembles acute bacterial pneumonia
Mid and lower zone consolidation, effusions, hilar LNs
Lymphohaematogenous spread → extra-pulmonary and milliary TB
Latent TB
Infected but no clinical or x-ray signs of active TB Non-infectious
May persist for years
Weakened host resistance → reactivation
Secondary TB
Usually reactivation of latent TB due to ↓ host immunity
May be due to reinfection
Typically develops in the upper lobes
Hypersensitivity → tissue destruction → cavitation and formation of caseating granulomas.
Dx
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Active TB
If suggestive CXR take ≥3 sputum samples (one AM)
May use BAL if can’t induce sputum
Microscopy for AFB: Ziehl-Neelsen stain
Culture: Lowenstein-Jensen media (Gold stand)
CXR
Consolidation, cavitation, fibrosis, calcification
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Tuberculin Skin Test
Intradermal injection of purified protein derivative
Induration measured @ 48-72h
False +ve: BCG, other mycobacteria, prev exposure
False –ve: HIV, sarcoid, lymphoma
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