Infections of the lung Flashcards

1
Q

Pneumonitis vs pneumonia

A
  • Pneumonitis: inflammation and consolidation of the lung parenchyma, but not necessarily caused by infection (hypersensitivity)
  • Pneumonia (PNA): inflammation and exudative solidification of the lung (consolidation) due to an infectious agent
  • Possible types of PNA: community acquired acute/atypical, hospital acquired, aspiration, chronic PNA, necrotizing PNA and lung abscesses
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2
Q

Community acquired acute PNA (CAAcP)

A
  • Usually due to bacteria: strep pneumo (most common), H influenza, Moraxella Catarrhalis, S aureus, P aeruginosa, L pneumophila (legionella)
  • Can be either bronchopneumonia or lobar pneumonia pattern
  • Bronchopneumonia: diffuse foci of consolidation affecting multiple lobes
  • Lobar: globally/uniformly affects a single lung
  • Sx: fever, chills, cough, dyspnea, chest pain, coryza
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3
Q

Pathogenesis of CAAcP

A
  • 4 stages of CAAcP
  • First there is congestion of the vasculature
  • Then there is red hepatization, in which there is exudation of inflammatory cells (mostly PNMs into alveolar lumens), along w/ congested capillaries
  • Inflammation will eventually leave behind necrotic inflammatory debris in the alveoli
  • The lung becomes gray and fibrosed (gray hepatization)
  • Micoscopically during gray hepitization there are fibrous plugs resulting in organizing of the necrotic exudate
  • If the organization occurs quickly there can be resolution (final stage) and return to normal lung
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4
Q

Community acquired atypical PNA (CAAtP)

A
  • An infectious interstitial PNA that most commonly affects children and young adults
  • Most common etiology is Mycoplasma pneumonia (also viruses and chlamydia pneumonia can)
  • Organisms attach to the upper respiratory tract and extend distally
  • Once in alveoli there is inflammation, which is predominantly interstitial w/ widened septa and scattered PMNs (patchy or lobar)
  • Atypical b/c of lack of classic PNA presentation (less sputum, no cough, may think they have a cold)
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5
Q

Hospital acquired PNA (HAP)

A
  • Usually in pts who are under ventilators, have IV caths, severe underlying disease, immunosuppression or prolonged antibio Rx
  • Organisms: E Coli, P Aeruginosa, S aureus
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6
Q

Aspiration PNA

A
  • Debilitated pts and unconscious individuals at risk for aspirating gastric or oral contents
  • Possibly produces granulomatous alveolar exudate
  • But more often produces abscesses: aspiration PNA is most common cause of lung abscesses
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7
Q

Chronic PNA

A
  • Usually a localized process that usually causes chronic granulomatous inflammation
  • Most commonly TB, but can also be fungal (histoplasma, blastomycoses, coccidiomycoses)
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8
Q

Mycobacterium tuberculosis complex

A
  • Unpasteurized milk: M bovis
  • Initial 1o Sx characteristically ASx, but indefinitely at risk for reactivation
  • Risk factors: blacks, native american, diabetes, etoh, malnutrition, heart disease, chronic lung disease, ARDS
  • Pathogenesis: host response is type IV delayed hypersensitivity, causes caseous necrosis granulomatous reaction
  • Acid-fast bacillus are resistant to intracellular digestion
  • ASx disease resides in lower lungs, upon activation and Sx showing the disease is seen in upper (apices) lungs
  • Caseous necrosis: Ghon focus
  • Can spread hematogenously to anywhere, especially to meninges in children
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9
Q

TB vs sarcoidosis

A
  • TB has necrotizing granulomas, sarcoid has non-necrotizing

- Sarcoid tends to cluster around lymphatics and airways

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