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x M2 Respiration > 12. Interstitial Lung Disease > Flashcards

12. Interstitial Lung Disease Flashcards

1
Q

what are the major categories of Interstitial Lung disease?

A
  • Idiopathic Pulm Fibrosis
  • due to Occupational/Environmental inhalants
  • Drug-related
  • Sarcoidosis
  • Circulatory
  • Assoc’d with connective tissue disorders
  • Radation-based
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2
Q

symptoms of ILD?

A

dyspnea, cough

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3
Q

physical findings with ILD?

A

fine crackles, clubbing, findings related to underlying disease process

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4
Q

Effects of ILD on lung function: compliance?

A

decreased due to inflammation and/or deposition of collagen. altered pressure/volume relationship in lungs in ILD

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5
Q

Effects of ILD on lung function: diffusion?

A

impaired. due to incr thickness of the interface. thickened by interstitial inflammation, and/or deposition of collagen.

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6
Q

Effects of ILD on lung function: V/Q?

A

mismatch. ILD impacts the lungs unequally/heterogeneous.

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7
Q

what happens to the lung areas that are less compliant than others?

A

receive less ventilation than normal areas (remember compliance = dV/dP, so if you apply the same pressure to a less compliant area, it will receive less volume/less ventilation)

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8
Q

most patients with ILD have a restrictive or obstructive pattern?

A

restrictive

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9
Q

Lung volume in ILD: incr or decr?

A

decr.

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10
Q

flow rates in ILD?

A

decr, but increased relative to lung volume. flow rates vary as a function of elastic recoil. since elastic recoil is increased, flow rate is increased.

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11
Q

ILD: DLCO?

A

lower due to diffusion impairment

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12
Q

what is idiopathic pulmonary fibrosis?

A

fibrosing disease of unknown etiology, generally seen in elderly.

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13
Q

what is the pathologic finding in IPF?

A

UIP: usual interstitial pneumonia.

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14
Q

what is the sequence of events in IPF?

A

stimulus (known or unknown) –> alveolitis (accumul of inflam cells in interstitium)–> derangement of alveolar-capillary units (interstitial edema) –> loss of alveolar-capillary units for gas exchange (ie fibrosis)

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15
Q

does IPF require inflammation

A

no, can occur independently of inflammation.

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16
Q

what is the established therapy for IPF?

A

there is none: used to be anti-inflammatories, but those barely worked. (note this is only IPF, not all ILD)

17
Q

what is the mean survival time for IPF?

A

3yrs from dx

18
Q

what are the occupational/environmental inhalants that contribute to ILD?

A
  • dusts (silica/asbestos)
  • moldy hay (Farmer’s Lung)
  • gases/fumes/vapors/aerosols
19
Q

what drugs may cause ILD?

A 
cancer drugs (methotrexate)
antibiotics
20
Q

what is sarcoidosis?

A

multi-system disorder characterized by granulomatous inflammation. thorax is most common site of involvement.

21
Q

why are patients with ILD dyspneic?

A
  • inc work of breathing (lower compliance, more dead space)

- stimulation of vagal fibers

22
Q

why do patients with ILD have cough?

A

Interstitial inflammation may stimulate vagal fibers

23
Q

why is there decr compliance in ILD?

A

deposition of collagen –> decr compliance

24
Q

what are the lung volumes in ILD: TLC, FRC, RV, VC

A

Everything is reduced!

  • TLC reduced: stuff lungs. Makes it harder to inflate, resp muscles have to work harder
  • FRC detd by recoil v. chest wall.
  • Decr RV: because of incr recoil, minimizes air trapping
  • Decr VC
25
Q

why is there an incr FEV1/FVC ratio in ILD?

A

increased recoil. subranormal flow rates for volume

26
Q

in ILD, what is the change to patency of small airways?

A

due to fibrosis, tends to keep more airways patent at smaller volumes/pressures. contrast with emphysema which has collapse.

27
Q

what is the pattern for C02 removal with ILD?

A

pts tend to be hypocapnic.

Increase in ventilation offsets the increase in physiological dead space

28
Q

what PFT patterns might make you think of ILD?

A

low diffusing capacity, high ratio

29
Q

why would an ILD patient take quick shallow breaths?

A

to minimize discomfort.

30
Q

Structure/function relationship summary

A 
Decreased compliance
Restriction of the lung
Decreased diffusing capacity
Hypoxia that worsens with exercise
Increased VD/VT
31
Q

what does IPF look like on radiology?

A

honeycombing

32
Q

ILD: if not inflammation, what is the problem?

A

possibly a genetic predisposition to profibrotic cytokines/growth factors that cause fibrosis.

33
Q

what is erythema nodosum, and in what condition do we see it?

A

sarcoidosis

34
Q

what is adenolathy? when do we see it?

A

lymph node swelling. see in sarcoidosis

35
Q

Drug induced ILD: what are the most common drugs involved?

A 
Large number of agents
Most common:
Cancer chemotherapy (bleomycin, carmustine)
Amiodarone (anti-arrythmic)
Nitrofurantoin (abx)
36
Q

How does Bleomycin factor into ILD?

A 
Occasional cause of ILD
Important model of lung injury
Role of TGF-β, TNF-α
Mechanism: oxidant injury
Occurrence modified by:
Oxygen
Radiation

x M2 Respiration (36 decks)

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