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Respiratory system > restrictive (interstitial) lung diseases > Flashcards

restrictive (interstitial) lung diseases Flashcards

1
Q

what is the interstitium of the lung?

A

The connective tissue space

around the airways and vessels and the space between the basement membranes of the alveolar walls

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2
Q

are interstitial lung diseases usually unilateral or bilateral?

A

bilateral

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3
Q

is pulmonary oedema a restrictive lung disease?

A

no, however it does cause restriction

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4
Q

what happens to the interstitium in restrictive lung diseases?

A

it becomes thicker so the capillaries and pneumocytes no longer as close together. This is causes buy a build up of a substance in the interstitium, usually fibrous tissue.

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5
Q

what happens to compliance in restrictive lung disease?

A

it is reduced

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6
Q

what happens to FEV1 in restrictive lung disease?

A

it is reduced

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7
Q

what happens to FVC in restrictive lung disease?

A

it is reduced

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8
Q

what happens to the FEV1/FVC ratio in restrictive lung disease?

A

it remains nomal

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9
Q

what happens to gas transfer in restrictive lung disease?

A

it is decreased

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10
Q

why is gas transfer reduced in restrictive lung diseases?

A

the distance between alveoli and capillaries is increased as there is increases tissue in the interstitium

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11
Q

why is there a V/Q imbalance in restrictive lung diseases?

A

the disease can sometimes cause small airways to be constricted

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12
Q

when can a restrictive lung disease present?

A

when there is an abnormal discovery on a CXR.
dyspnoea that gets worse (SOB exertion –> SOB rest)
type 1 resp. failure
heart failure

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13
Q

why do sufferers of restrictive lung disease experience type 1 respiratory failure?

A

it is much easier for carbon dioxide to diffuse across the thickened alveolar walls than it is for oxygen.

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14
Q

what does an interstitial lung disease look like on a CXR?

A

lung extends <10 ribs

more lung markings because increased tissue

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15
Q

what is diffuse avleolar damage associated with?

A 
Major trauma
Chemical injury / toxic inhalation
Circulatory shock
Drugs 
Infection
Auto(immune) disease
Radiation
idiopathic
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16
Q

what is the evolution of DADS?

A

oedema–> Hyaline membranes –>interstitial inflammation —> interstitial fibrosis

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17
Q

what are the histological features of DADS?

A 
protein rich oedema
fibrin
hyaline membranes
denuded basement membranes
epithelial proliferation
fibroblast proliferation
scarring-interstitium and airspaces
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18
Q

what is sarcoisosis?

A

a multisystem granulomatous disoder of unknown aetiology

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19
Q

what is the histopathology of sarcoidosis?

A

-epitheloid and giant cell ganulomas
-no necrosis
-little lymphoid infiltration
variable associated fibrosis

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20
Q

is DADS an acute of chronic response?

A

acute

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21
Q

what causes the protein rich oedema in DADS?

A

damage to the capillary walls in the lung (probably by neutophils) which causes the massive leakage of fluid and proreins

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22
Q

is DADS a serious condition?

A

yes, sufferers usually end up in ITU

23
Q

what sets DADS apart from pneumonia histologically?

A

the alveoli in DADS are not filled with debris like in pneumonia

24
Q

what sets sarcoidosis apart from infections histologically?

A

the absence of tissue necrosis

25
Q

what are the presentations of sarcoidosis?

A 
1.
-acute arthralgia (joint pain)
-erythema nodosum (red bumps and patches on the skin)
-bilateral hilar lymphadenopathy
2.
incidental abnormal CXR w/ no symptoms
3. 
SOB, cough and abnormal CXR
26
Q

is treatment required for sarcoidosis?

A

most resolve themselves after 2 years but those that don’t should be given corticosteroids

27
Q

what is used to diagnose sarcoidosis?

A
  • clinical findings
  • image findings
  • serum Ca++ and ACE ( angiotensin converting enzyme)
  • biopsy
28
Q

what are the antigens for hypersensitivity pneumonitis?

A

mostly antigens of plant or animal origin:

  • Thermophilic actinomycetes
  • Bird / Animal proteins - faeces, bloom
  • Fungi - Aspergillus spp

some chemicals

29
Q

what is the acute presentation of hypersensitivity pneumonitis?

A

Fever, dry cough, myalgia,
Chills 4-9 hours after Ag exposure
Crackles, tachyopnoea, wheeze
Precipitating antibody

30
Q

what is the chronic presentation of hypersensitivity pneumonitis?

A
  • Insidious
  • Malaise, SOB, cough
  • Low grade illness
  • Crackles and some wheeze
31
Q

what is hypersensitivity pneumonitis mediated by?

A

Type III and Type IV Hypersensitivity reaction

32
Q

what is the main histological presentation of hypersensitivity pneumonitis?

A

soft centriacinar epithelioid granulomata

33
Q

what zone of the lung does hypersensitivity pneumonitis primarly affect?

A

upper zone

34
Q

why is hypersensitivity pneumonitis more likely to occur in central acinar areas?

A

this is the area where airflow changes from laminar to diffusion

35
Q

where may UIP be seen?

A
  • connective tissue diseases
  • in drug reaction
  • in post infection
  • in industrial exposure
36
Q

which connective tissue diseases can cause UIP?

A

scleroderma and rheumatoid disease

37
Q

what is the most common form of UIP?

A

cryptogenic or idiopathic

38
Q

what is another name for idiopathic UIP?

A

idiopathic pulmonary fibrosis

39
Q

what is another name for cryptogenic UIP?

A

cryptogenic fibrosing alveolititis

40
Q

what are the histopathological features of UIP?

A

-patchy interstitial chronic inflammation
-type II pneumocyte hyperplasia
-smooth muscle and vascular proliferation
evidence of old and recent injury as well as a spatial variation in injury
-proliferating fibroblastic foci

41
Q

what is temporal heterogeneity in UIP?

A

injury in the lungs occuring at different times

42
Q

what is spatial heterogeneity in UIP?

A

injury in lungs in different areas

43
Q

who does idiopathic pulmonary fibrosis normally affect?

A

elderly >50 and M>F

44
Q

what are the clinical signs of idiopathic pulmonary fibrosis?

A

dyspnoea, cough, basal crackles, cyanosis, clubbing

45
Q

what is the prognosis of idiopathic pulmonary fibrosis?

A

most die within 5 years

46
Q

what treatments are available for idiopathic pulmonary fibrosis?

A

steroidal therapy,

anti-angiogenesis treatment, (largely uneffective though)

47
Q

what is the appearance of idiopathic pulmonary fibrosis on a chest x-ray?

A

basal/posterior diffuse infiltrates, cysts, appears like ground glass

48
Q

which of the chronic responses is most likely to lead to end-stage honeycomb lung?

A

UIP

49
Q

which of the chronic responses is least likely to lead to end-stage honeycomb lung?

A

granulomatous response

50
Q

what are the three chronic responses to parenchymal (interstitial) lung injury?

A
  • usual interstitial pneumonitis
  • granulomatous response
  • other patterns (non specific interstitial pneumonitis)
51
Q

what are the granulomatous responses to parenchymal lung injury?

A
  • sarcoidosis

- hypersensitivity pneumonitis

52
Q

why do diseases caused by inhaled particulates often start at the respiratory bronchioles?

A

this is where bulk flow airflow becomes diffusion

53
Q

what are the four abnormal states associated hypoxaemia?

A
  • alveolar hypoventilation
  • shunt
  • ventilation/ perfusion imbalance
  • diffusion impairment

Respiratory system (38 decks)

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