Resp - TB Flashcards

1
Q

suggest risk factors for TB

A
  1. close contact with TB pt
  2. ethnic minority group
  3. homeless pts, alcoholics and other drug abusers
  4. HIV +ve and other immunocompromised pts
  5. elderly pts and children
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2
Q

how is TB usually transmitted?

A

person-to-person by inhalation of infected droplets

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3
Q

describe the process of primary TB infection

A
  1. Mtb inhaled and deposited in alveoli…
  2. organisms phagocytosed by alveolar macrophages and carried to hilar LNs…
  3. Mtb prevents phagolysosome fusion but macrophages initiate cell-mediated immunity…
  4. over 6 wks, Th cell response mounted against Mtb, causing IFNy production and activation of macrophages to become bactericidal and produce TNF…
  5. monocyte recruitment and differentiation into ‘epithelioid histiocytes’…
  6. formation of caseating granulomas, i.e. Ghon’s foci.
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4
Q

describe the microscopic appearance of a TB granuloma

A

Caseous necrosis core surrounded by epithelioid macrophages, Langerhans giant cells and lymphocytes.

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5
Q

describe the possible outcomes of primary TB infection

A
  1. spontaneous healing and bacteria elimination (80%) - may form Ranke complexes (healed Ghon foci that have calcified)
  2. latent infection - some organisms may disseminate via lymphatics or bloodstream to distant sites, and persist in otherwise healthy individual
  3. primary active disease (5%)
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6
Q

name 3 differences between active and latent TB

A

Active

  • active, multiplying bacilli in body
  • symptomatic
  • infectious

Latent

  • inactive contained bacilli in body
  • asymptomatic
  • non-infectious
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7
Q

why can secondary infection occur? how is it different to primary active TB?

A

Re-activation of Mtb usually precipitated by impaired immune function, e.g. malnutrition, steroids, AIDS DM.

  • Usually occurs in apex of lungs (higher alveolar pO2) - can spread locally or to distant sites.
  • Usually more severe as involves activation of secondary immune response (stronger so more tissue damage) and bacteria has time to mutate and adapt.
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8
Q

describe the complications/lung damage that can occur as a result of pulmonary TB

A
  1. cavity formation - softening and liquefaction of caseous material which is discharged into bronchus, resulting in cavity formation which may then fibrose.
  2. haemorrhage - from extension of caesous process into vessels of cavity walls causing haemoptysis
  3. spread to rest of lung - caseous and liquefied material spread infection through bronchial tree to other lung zones
  4. pleural effusion (exudate), lobar collapse, beonchiectasis, pneumonia
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9
Q

what is miliary TB?

A

Haematogenous spread of Mtb causing widespread infection - lungs always involved as well as multiple other organs.

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10
Q

describe examples of how TB can affect extra-pulmonary organs

A
  • CNS (tuberculous meningitis): initially non-specific symptoms (headache, vomiting, altered behaviour) followed by diminishing consciousness +/- focal neurological signs
    2. cervical lymph nodes (scrofula)
    3. pericardial: initially non-specific, may be signs of pericardial effusion (pulsus paradoxus, elevated JVP) or constrictive pericarditis
    4. GI or peritoneal: mainly ileocaecal lesions (abdo. pain, bloating, obstruction and simulating appendicitis) but occasionally peritoneal spread causes ascites
    5. genito-urinary: slow progression to renal disease and subsequent spreading to lowe urinary tract, infertility in females, epididymal swelling in males
    6. bones and joints, esp. spine (Pott’s disease): pain, arthritis, osteomyelitis and absecess formation
    7. skin: erythema nodosum (represents early immunological response to infection), skin sinus formation (scrofuloderma)
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11
Q

describe the symtpoms associated with pulmonary TB

A
  • chronic productive cough
  • purulent +/- bloodstained sputum
  • dyspnoea (if pleural effusion)
  • general symptoms: fever, night sweats, weight loss, anorexia, tiredness and malaise
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12
Q

how would you diagnose active TB?

A

Imaging
- CXR: essential even in non-pulmonary disease as there may have been pulmonary infection

Bedside tests
- sputum culture and microscopy (or BAL if not possible):
~ Ziehl-Neelsen stain and rapid direct microscopy for acid/alcohol-fast bacilli
~ culture on Lowenstein-Jensen slope (gold-standard but slow, 4-8 wks)
~ antibiotic sensitivity cultures (further 3-4 wks)
- TB culture of other samples if relevant, e.g. LN biopsies, urine…

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13
Q

which CXR features suggest TB infection?

A
  • typical TB appearance: patchy or nodular shadows in upper zones, loss of volume, fibrosis +/- cavitations
  • primary TB usually appears as central apical portion with L lower lobe infiltrate or pleural effusion
  • reactivated TB: no pleural effusion and lesions are apical in position
  • miliary TB: millet seed-like pattern indicating severe disease with poor immune response with uniform 1-10 mm shadows throughout the lung
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14
Q

how would you diagnose latent TB?

A
  1. tuberculin skin test (Mantoux): type IV hypersensitivity reaction (induration) if positive
  2. interferon-gamma release assay: results within 24 hrs and no cross-reaction with BCG but cannot distinguish between latent and active TB
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15
Q

which drug regimen would you use to treat active TB?

A
  • RIFAMPICIN (6 mths)
  • ISONIAZID (6 mths) + vit B6
  • PYRAZINAMIDE (2 mths)
  • ETHAMBUTOL (2 mths)
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16
Q

which drug regimen would you use to treat latent TB?

A
  • HIV -ve pts: 6 mths isoniazid OR 3 mths rifampicin + isoniazid
  • HIV -+ve: 6 mths isoniazid