17. Small Group: Interstitial Lung Disease Flashcards

1
Q

COPD: obstructive or restrictive disease?

A

obstructive

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2
Q

COPD: will we see clubbing?

A

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

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3
Q

what is IPF?

A

idiopathic pulmonary fibrosis – a clinical-pathologic-radiologic sx

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4
Q

what is UIP?

A

usual interstitial pneumonitis. pathologic findings characteristic of IPF.

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5
Q

what measurement will confirm the presence of restriction?

A

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

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6
Q

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

A

red nodules on the shins. indicate sarcoidosis.

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7
Q

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

A

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

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8
Q

what is the problem with rapid shallow breathing?

A

more of your effort goes to the anatomic dead space.

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9
Q

what does honeycombed lung refer to? is it reparable?

A

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

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10
Q

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

A

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.

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11
Q

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

A

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

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12
Q

why is TLC diminisned with restrictive process?

A

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.

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13
Q

Honeycombing: what disease process does it suggest?

A

end stage ILD. basically permanent lung fibrosis.

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14
Q

why does the DLCO decrease with ILD?

A

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

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15
Q

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

A

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

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16
Q

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

A

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

17
Q

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

A

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)

18
Q

what is the role of morphine in dyspnea?

A

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

19
Q

how does morphine relieve dyspnea?

A

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

20
Q

what is the median survival for IPF?

A

3-5 yrs.