17. Small Group: Interstitial Lung Disease Flashcards Preview

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Flashcards in 17. Small Group: Interstitial Lung Disease Deck (20):

COPD: obstructive or restrictive disease?



COPD: will we see clubbing?

no, clubbing is not associated with COPD. it is associated with lung cancer, interstitial lung disease, chronic hypoxia....


what is IPF?

idiopathic pulmonary fibrosis -- a clinical-pathologic-radiologic sx


what is UIP?

usual interstitial pneumonitis. pathologic findings characteristic of IPF.


what measurement will confirm the presence of restriction?

TLC. restriction is characterized by a normal or increased FEV1/FVC ratio, and confirmed by TLC REDUCTION.


what are erythema nodosum? what disease process do they indicate?

red nodules on the shins. indicate sarcoidosis.


What breathing pattern would you see in pts with ILD and other interstitial diseases?

rapid shallow breathing, to minimize work of breathing -- because lungs are less compliant, and the more they are stretched, the more difficult it is.


what is the problem with rapid shallow breathing?

more of your effort goes to the anatomic dead space.


what does honeycombed lung refer to? is it reparable?

formation of cystic spaces in lung parenchma. characteristic of advanced interstitial lung disease. not reversible with treatment.


what is another reason that might account for rapid shallow breathing?

there are receptors in the lung parenchyma (C-fibers) that may be stimulated by the interstitial process, and the stimulation of these incr resp rate.


why is there a drop in the resp rate of patients with ILD when they sleep?

because part of their rapid/shallow breathing is due to stimulation of the C-fibers in the interstitium, which is less noticed during sleep.


why is TLC diminisned with restrictive process?

elastic recoil is much increased (ie compliance is decreased) and thus the insp muscles are unable to inflate the system to as great a volume.


Honeycombing: what disease process does it suggest?

end stage ILD. basically permanent lung fibrosis.


why does the DLCO decrease with ILD?

loss of alveolar surface (due to epithelial metaplasia perhaps, or reduced lung volume overall), and thickening of the alveolar-capillary membrane.


why is the resting SaO2 ok, but exercising SaO2 diminishes a lot?

due to decr time in capillary: does not have time to equilibrate. fibrotic lung needs full (resting) timeframe to do gas exchange.


what is the principal mechanism of hypoxia in pts with ILD?

V/Q mismatch and lung heterogeneity. fibrosis will contribute to exercise-induced hypoxia.


why do steroids (anti-inflammatory) not always work in ILD patients?

to the extent that ILD is an inflammatory process, steroids are effective. but we are coming to realize that ILD is more of a pro-fibrotic process (collagen deposition, fibroblast function)


what is the role of morphine in dyspnea?

only drug that has been shown in randomized controlled trials to relieve the sensation of dyspnea.


how does morphine relieve dyspnea?

decr resp drive and thereby decr work/effort of respiration
altering the central processing of information related to breathing. ie, decr intensity to which the dyspnea is perceived


what is the median survival for IPF?

3-5 yrs.