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CR - Interstitial Lung Disease (Pul Fibrosis) (iii) (Acute/adult resp…
CR - Interstitial Lung Disease (Pul Fibrosis) (iii)
Hypersensitivity pneumonitis
aka EAA, farmer's lung, pigeon-fancier's lung
organic antigen inhaled
mouldy hay
aspergillus
avian antigens
initially causes type 3 hypersensitivity
acute, 6-8hrs post exposure
circulating Igs react + cause ICD
can progress to chronic (type 4)
pul fibrosis in upper lobes
irreversible
often subtle clinical findings
classic clinical Dx
acute febrile episodes
headache, malaise, cough, dyspnoea
bibasal creps
alveolar walls infiltrated by lymphocytes, plasma cells, macrophages, granulomas
investigations
Hx (timing, repeat episodes, exposures)
find causal antigens via serum precipitins or specific IgE
good prognosis if hasn't progressed to chronic
Tx: antigen avoidance, wear mask, steroids when acute
Acute/adult resp distress syndrome (ARDS)
decreased pul gas exchange caused by acute diffuse injury of alveolar-capill barrier
epithelial, 90% type 1 (flat, easily injured), 10% type 2 (cuboidal, more resistant)
alveoli filled with proteinaceous fluid + marked infiltrates of inflamm cells (neutrophils in early stage, then macrophages + CKs)
causes
direct lung injury (pneumonia, aspiration of gastric contents)
indirect lung injury (sepsis, trauma, shock, multiple transfusions)
noncardiogenic pul oedema
high morbidity + mortality
most die unless given O2 + assisted ventilation
ventilation may contribute to further injury
alv overdistension -> repeated collapse + reopening stims ck release
often in ICU
common, affects both medical + surgical patients (some already have lung pathology)
Dx
arterial hypoxaemia (difficult to Tx)
bilat pul infiltrates on CXR
formation of protein-rich hyaline membranes on basement membranes
if uncomplicated rapid resolution
some progress to fibrotic lung injury