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Pulmonology > ILD > Flashcards

ILD Flashcards

1
Q

what are the physiologic properties of ILD?

A
  • restriction - decreased compliance - abn gas exchange
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2
Q

in idiopathic pulmonary fibrosis what is issue?

A

the initial inflammation is unknown but TGF-beta is involved by activating fribroblasts leading to deposition of collagen thus fibrosis

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3
Q

what do see in PFTs in ILD?

A

-decreased TLV, FRC and RV - decreased FEV1, FVC and either normal or increased FEV1/FVC - decreased DLCO

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4
Q

what is the course of IPF?

A

it is pretty grim, not high survival rates however there is new tx. that slows down the decline in FEV1 and thus might be able to improve survival rates but thatis unknown

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5
Q

when you one use glucocorticoids in treating certain ILD?

A

if there are inflammatory (eosinophils, lymphocytes or granulomatous) or ground glass/alv infiltrates (sarcoidosis, COP, ceP) are present

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6
Q

what is there is extensive honeycombing?

A

no effective treatment, one should ocnsifer lung transplant

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7
Q

what do both ninetdanib and pirfenidone do?

A

slows down decline in function and increases exercise tolerance

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8
Q

inorganic dusts

A

pneumoconiosis

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9
Q

organic proteins

A

hypersensitivity pneumonitis

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10
Q

hallmark of silicosis

A

ineffective clearance

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11
Q

hallmark of HP

A

exaggerated immune response

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12
Q

amphiboles

A

asbestos fiber

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13
Q

worse asbestosis manifestation in pleura

A

mesothelioma

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14
Q

treatment of HP

A

removal of the causative agent, and steroids in symptomatic patients

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15
Q

silo filler’s lung and metal fume fever

A

are direct tissue injury

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16
Q

byssinosis

A

inhalation of unprocessed cotton dust causing direct airway tissue injury

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17
Q

RADS

A

irritant induced asthma where caustic fumes cause direct airway damage

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18
Q

when do we start to see asthma like symtpoms in RADS?

A

within 12 hr

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19
Q

what should we do about RADS?

A

treat it like asthma. most improve over time but may lead to permanent airway hyperresponsiveness

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20
Q

in immunologic occupational asthma we see ____ and we should expect what are two of the most common cause?

A

we see IgE mediated response and there is latency between exposure and symptoms - western red cedar and baker’s asthma

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21
Q

what can we do to determine if it is occupational asthma?

A

PEFR

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22
Q

treatment of occupational asthma

A

remove exposure, bronchodilators and anti-inflammatory (steroids)

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23
Q

true or false asbestosis can be seen quickly?

A

nope disease seen in many years after exposure but one can see pleural plaques with recent exposure

24
Q

where are the silicosis particles mainly deposited? who are the main instigators? where can nodules be seen in?

A

deposited in upper lobes - macrophages release pro-inflammatory and pro-fibrotic mediators - seen in hilar lymph nodes

25
Q

HP examples

A
  • farmer’s lung - maple bark disease - bird-fancier’s lung -humidifier or air conditioner lung
26
Q

HP hallmark in histology

A

lymphocytes

27
Q

Inflammatory pattern characterized by the presence of collections of epithelioid histiocytes (macrophages), with or without multinucleated giant cells (these are also histiocytes) and necrosis

A

granuloma granulomatous

28
Q

prototypical idipathic granulomatous disorder

A

sarcoidosis

29
Q

sarcoidosis hallmark

A

non-necrotizing granulomas in different organs and increased serum ACE

30
Q

Vasculitis and necrotizing granulomas in upper and lower respiratory tract and necrotizing or crescentic glomerulonephritis

A

GRANULOMATOSIS WITH POLYANGIITIS

31
Q

GRANULOMATOSIS WITH POLYANGIItis has a c-ANCA

A

positive test

32
Q

LANGERHANS CELL HISTIOCYTOSIS

A

proliferation of langerhan cells/APC and strongly associated with smoking

33
Q

Organizing pneumonia histologic pattern without known cause

A

cryptogenic organizing pneumonia

34
Q

dissuse alveolar damage

A

acute interstitial pneumonia

35
Q

alveolar macrophages sfill alveolar spaces leading to mild interstitial fibrosis but there is good response to smoking ceddation and steroids

A

desquamative interstitial pneumonia

36
Q

You are evaluating a patient with dyspnea, non-productive cough, and inspiratory crackles on exam. A chest CT shows diffuse ground glass opacities. Which of the following would NOT be expected? - decreased FEV1, decreasedFVC, nl FEV/FVC, decreasedTLC, decreasedDLCO - decreased compliance -Fibrosis on lung biopsy -Rapid shallow breathing - H/O tobacco smoking

A

-Fibrosis on lung bio-Fibrosis on lung biopsypsy

37
Q

Do we see hypercapnia in ILD?

A

yea, they have a rapid shallow breathing, cystic airspaces and diffusion abnormality at later stages

38
Q
A

asbestos (ferruginous) body

39
Q
A

Birbeck granules are seen ultrastructurally within langerhans

40
Q
A

birefringent silica particles under polarized ligh

41
Q
A

Diffuse airspace filling by macrophages with light brown cytoplasmic pigment; In RB-ILD, the process is less extensive and has bronchiolocentric distribution

42
Q
A

geographic necrosis

43
Q
A

granulomatosis with polyangiitis the lung shows multiple cavitating mass-like lesions

44
Q
A

HP- airway centered lymphocyte predominant inflammation extending into alveolar septa

45
Q
A

interstitium infiltrated by lymphocytes

46
Q
A

interstitium widened by fribrosis

47
Q
A

LHC- Langerhans have a prominent nuclear grooves

48
Q
A

microscopic cysts-honeycombing

49
Q
A

normal interstitium

50
Q
A

normal interstitium with elastic fibers

51
Q
A

pathcy fibrosis- abestosis

52
Q
A

sarcoidosis- notice the little background inflammation

53
Q
A

sarcoidosis- packed histiocytes

54
Q
A

silicotic nodule

55
Q

what is this?and what do they suggest?

A

what is this- diffuse reticular infiltrates and what do they suggest- that fibrosis is presen

56
Q

what is this? and what do they suggest?

A

what is this- ground glass opacities and what do they suggest- infection,blood and inflammation

Pulmonology (13 decks)

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