It is the pathology of the infiltration
of the alveoli and interstitium
that dictates what ILD the patient has. For
pulmonary fibrosis, there are two main patterns.
One is a largely inflammatory cell infiltrate
into the alveoli and interstitium, and that’s
called non-specific interstitium pneumonitis
Another is where you have large amount of
increased extracellular matrix, collagen,
and fibroblast, a sort of fibroblastic infiltration
of the lungs leading to essentially what looks
like scar tissue forming in the lung and that
is called Usual Interstitial Pneumonitis,
(UIP). It is not entirely clear, but probably,
NSIP may evolve into UIP in some patients.
However, with other interstitial lung disease,
you get a completely different pattern of
lung infiltrations, for example, sarcoidosis
as mentioned already. You get infiltration
of non-caseating granulomas, and hypersensitivity
pneumonitis, and also you get non-caseating
granulomas but much more poorly formed than you
do in sarcoid, and associated with mononuclear
infiltrate and a peribronchial fibrosis leading
to some small airways obstruction.
And then diseases such as pulmonary eosinophilia
and lymphocytic interstitial pneumonitis cause
respectively as the names might suggest an
eosinophinic and a lymphocytic infiltration
of the lung. So the pathology of the ILD is
dictated by the underlying cause.