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Respiratory HQ > Pathology of Restrictive Lung Disease > Flashcards

Pathology of Restrictive Lung Disease Flashcards

1
Q

What is the interstitium of the lung

A
  • connective tissue space around the airways and vessels

- space between the basement membranes of the alveolar walls

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2
Q

In the normal alveolar wall, what parts are in direct contact

A

the pneumocyte and interstitial capillary basement membranes

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3
Q

What us the pathological basis of restrictive lung disease

A
  • space fills with inflammatory response cells
  • space widens
  • elastic fibres unable to stretch
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4
Q

What four physiological processes are reduced in restrictive lung disease

A
  • lung compliance
  • FEV1 and FVC
  • gas transfer
  • V/Q
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5
Q

What is the FEV1/FVC ratio in interstitial lung disease and why

A
  • normal
  • there is no resistance to airflow, meaning you can expire all inhaled air but only small inspiration is possible in the first place
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6
Q

How does interstitial lung disease usually present and progress

A
  • dyspnoea from exertion to at rest

- type 1 respiratory failure leading to heart failure (hypoxic cor pulmonale)

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7
Q

What does an acute response to lung injury lead to

A

diffuse alveolar damage syndrome (DADS)

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8
Q

What two terms are synonymous with DADS

A
  • ARDS

- ‘shock lung’

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9
Q

What may cause DADS

A
  • major trauma
  • circulatory shock
  • infection
  • autoimmune disease
  • radiation
  • idiopathy
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10
Q

Why is there more interstitial inflammatory material in DADS than in normal acute inflammation elsewhere in the body

A

there is damage to capillary cells, meaning the vessels are more leaky than usual

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11
Q

What are the main histological features of DADS

A
  • protein rich oedema
  • fibrin
  • hyaline membranes
  • epithelial and fibroblast proliferation
  • scarring
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12
Q

What is a hyaline membrane

A

membranes that are formed when the proteins in the exudate are precipitated out

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13
Q

Why do some cells proliferate in DADS

A

in an unsuccessful attempt by the body to repair the damage to the lung

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14
Q

How prone is DADS to progress to end-stage/honeycomb lung

A

not very

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15
Q

What is sarcoidosis

A
  • a multisystem granulomatous disorder of unknown cause

- abnormal collections of inflammatory cells into granulomas

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16
Q

What are the main histological components of sarcoidosis

A
  • epitheloid and giant cell granulomas

- little necrosis/lymphoid infiltrate/fibrosis

17
Q

Name the main organs involved in sarcoidosis

A
  • lymph nodes
  • lungs
  • spleen
  • liver
18
Q

How does sarcoidosis usually present

A
  • acute athralgia (joint pain)
  • erythema nodosum (red blotches)
  • bilateral hilar lymphadenopathy
  • SOB
  • cough
19
Q

How prone is sarcoidosis to progress to end-stage/honeycomb lung

A

most patients don’t progress, but sometimes those with SOB do progress

20
Q

What is hypersensitivity pneumonitis

A
  • alveolar inflammation caused by hypersensitivity
21
Q

Where in the lungs is it most likely to find hypersensitivity pneumonitis

A
  • in the centriacinar region, where turbulent air flow becomes gaseous diffusion and material is deposited
  • in the apex where blood flow is lower and there is less clearance of deposited material
22
Q

Give some of the main antigens that can cause hypersensitivity pneumonitis

A
  • thermophilic actinomycete bacteria
  • bird/animal proteins
  • fungi e.g. aspergillus
23
Q

How does hypersensitivity pneumonitis present acutely

A
  • fever
  • dry cough
  • chills post-exposure
  • crackles
  • tachypnoea
  • wheeze
24
Q

How does hypersensitivity pneumonitis present chronically

A
  • malaise
  • SOB
  • cough
  • crackles
  • some wheeze
25
Q

What are the main histological components of hypersensitivity pneumonitis

A
  • soft and ill-defined granulomata
  • interstitial pneumonitis
    immune complex precipitation (type 3/4 hypersensitivity)
26
Q

What is usual interstitial pneumonitis (UIP)

A
  • lung scarring brought on by connective tissue diseases, drug reactions, asbestos, infection…
27
Q

What are the main histological components of UIP

A
  • patches of chronic inflammation

- type 2 pneumocyte/smooth muscle/vascular proliferation

28
Q

What is the name given to the clinical syndrome of UIP

A

idiopathic pulmonary fibrosis

29
Q

What are the main symptoms/signs of pulmonary fibrosis

A
  • dyspnoea
  • cough
  • basal crackles
  • cyanosis
  • clubbing
  • diffuse infiltrates
  • cysts
30
Q

Where in the lung is honeycombing observed in idiopathic pulmonary fibrosis

A
  • base

- posterior

31
Q

How prone is idiopathic pulmonary fibrosis to progress to end-stage/honeycomb lung

A

it is the most common interstitial lung disease to progress to end-stage fibrosis and is mostly fatal

32
Q

How do CO2 levels in the body change in interstitial lung disease

A

they do not; it has high solubility and doesn’t take long to equilibrate across the blood/air barrier

Respiratory HQ (26 decks)

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