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MBBS I CPRS > L67 – Diffuse Interstitial Lung Diseases > Flashcards

L67 – Diffuse Interstitial Lung Diseases Flashcards

1
Q

Describe Diffuse Intersitital Lung Disease?

A

group of heterogeneous diseases

caused by a number of etiology (known or unknown)

causes Diffuse damage to pulmonary interstitium

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2
Q

What are the 3 components of pulmonary interstitium?

PAP

A

tissues of gas-exchange unit

 Peribronchiolar tissue
 Alveolar septa
 Perivascular tissue

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3
Q

Name the MILD Acute interstitial lung disease and give an example of its cause?

A

Interstitial pneumonitis

e.g. caused by mild viral infectiuon

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4
Q

In acute interstitial lung disease, describe the interstitial tissue?

A

Interstitial tissue infiltrated by lymphocytes, macrophages, plasma cells

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5
Q

Name the SEVERE Acute ILD ?

A

diffuse alveolar damage (DAD)

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6
Q

Name some COMMON causes of LUNG injuries in DAD (Severe Acute ILD)?

A

Common:
- Gastric aspiration (vomit, acid enters lungs)

  • Infections from inhaling infectious agents (e.g. Virus, bacteria)
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7
Q

Name some UNCOMMON causes of LUNG injuries in DAD?

A

Toxic fume inhalation,

drowning,

post-lung transplant immune reaction

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8
Q

Name some COMMON causes of GENERAL injuries in DAD (Severe Acute ILD)?

A

Sepsis
Shock
Severe trauma (caused by hypoxic blood, low BP)

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9
Q

Name some UNCOMMON causes of GENERAL injuries in DAD (Severe Acute ILD)?

A

Acute pancreatitis

Drug overdose

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10
Q

What is the pathogenesis of DAD?

A

Severe injury to epithelium and/or endothelium

> Release inflammatory cytokines for WBC

> Causes necrosis of alveolar wall (damage endothelium and pneumocytes)

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11
Q

What are the consequences of necrosis of alveolar wall in DAD?

A

Alveolar wall necrosis:

  1. Damage endothelium, interstitial cells&raquo_space;> capillary leak
  2. Lose alveolar pneumocytes&raquo_space;> lose alveolar surfactant
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12
Q

What are the physiological effects of DAD?

A

Lose alveolar surfactant&raquo_space; decrease lung compliance due to increase surface tension&raquo_space; alveolar airspace collapse

> > not ventilated but perfused

> > ventilation/perfusion (VQ) mismatch

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13
Q

What replaces the necrotic alveolar wall? What is the result?

A

Type II pneumocytes try to regenerate and
differentiate into type I

> > result in cuboidal, hyperplasia of type II pneumocytes

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14
Q

Explain the formation of Hyaline membrane in DAD?

A

Alveolar wall necrosis > damaged endohelium and pneumocytes

> > Escaped RBC, serum protein + fibrinous exudate, cell debris accumulation

INSPIRATION pushes exudates to outer airspace

> > Hyaline membrane form

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15
Q

What is the effect of hyaline membrane?

A

Lower diffusion capacity

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16
Q

Summarize all the structural changes to alveolar wall in DAD?

A

Congested and dilated capillaries

Form Hyaline membrane

Type II pneumocyte hyperplasia

Interstitial edema + mononuclear exudate

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17
Q

What is the effect of V/Q mismatch in DAD?

A

Severely impaired gas exchange

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18
Q

What is the clinical term for Severe acute Interstitial lung disease/ DAD?

A

Acute Respiratory Distress Syndrome (ARDS)

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19
Q

What is the mortality of acute respiratory distress syndrome (ARDS)?

A

30-40% (surviving patients may develop lung fibrosis due to repair)

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20
Q

DAD, interstitial pneumonitis belong to Acute ILD. Descibe Chronic ILD?

A

Group of heterogenous diseases that causes diffuse injury to lung interstitium

** caused by chronic inflammation and lung fibrosis

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21
Q

What causes Chronic ILD? think what type of injury

A

Recurrent/ continuous/ severe lung damage

Initial injury may be asymptomatic

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22
Q

Could a viral infection lead to Chronic ILD?

A

If the infection is mild/ transient, then no

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23
Q

What are the 4 major causes of Chronic ILD?

TAMO

A

Toxic damages

Autoimmune diseases

Mineral dust deposition

Others (allergy, sarcoidosis…etc)

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24
Q

List some Toxic damages that can lead to Chronic ILD?

A

 Toxic fume
 Irradiation (e.g. radiotherapy)
 Cytotoxic drugs
 Prolonged treatment with hyperbaric O2

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25
What is the name of the condition caused by mineral dust deposition in lungs?
pneumoconiosis
26
What autoimmune diseases can lead to chronic ILD?
Systemic sclerosis (aka scleroderma) Systemic lupus erythematosus (SLE)
27
What type of hypersensitivity reaction is Sarcoidosis?
type IV: delayed-type hypersensitivity (DTH)
28
What type of allergic condition can lead to chronic ILD?
extrinsic allergic alveolitis
29
Give 2 examples of Chronic ILD
1) Idiopathic pulmonary fibrosis** 2) Pneumoconiosis (** No longer called cryptogenic fibrosing alveolitis**)
30
What is the progression of Idiopathic pulmonary fibrosis (chronic ILD) dependent on?
Disease progression = slow, insidious depends on individuals, severity of injury
31
What gender is more affected by Idiopathic pulmonary fibrosis ?
Female
32
What is the signature histological feature of advanced stage Idiopathic pulmonary fibrosis ?
Honeycomb lung
33
What is the initial injury for Idiopathic pulmonary fibrosis ? What type of injury is caused?
Unknown agent, hence idiopathic persistent, chronic, diffuse lung injury on tissue** **not in airspace or airway
34
What is the pathology of Idiopathic pulmonary fibrosis?
Unknown agent cause persistent, chronic, diffuse lung tissue injury/ damage >> B and T lymphocyte activation > Production of cytokines and Antibodies >> Activate macrophage >> recruit neutrophils, induce fibroblast proliferaton + release oxidants and proteases >> Damage to type I pneumocytes
35
What is the pathological result of idiopathic pulmonary fibrosis at distal airways?
Fibroblast proliferation causes fibrosis** + Bronchiolar epithelium grows in / extends to line airspaces Overall: distal airway is “amputated", reduce SA
36
Explain the end stage manifestation of idiopathic pulmonary fibrosis?
Distal airways become "amputated" >> Acini "simplified" to become cystic spaces >> Bronchiolar epithelium grows into cystic spaces >> Honeycomb lung
37
Summarize the pathological features of Idiopathic pulmonary fibrosis?
Interstitial fibrosis >> "amputated" distal airways and honeycomb lungs Obliteration or Cystic dilatation of air spaces May associate with chronic inflammatory cells
38
Summarize the macroscopic appearance of Restrictive pattern lung damage in Acute ILD?
Thickened alveolar wall Rigid, shrunken lungs Pin-like airspaces >>Type I respiratory failure
39
Summarize the macroscopic appearance of End-stage lung damage in Chronic ILD?
Dense interstitial fibrosis Amputated airways and honeycomb lungs Oliterated or cystic air spaces
40
What are the affected lung functions due to interstitial fibrosis?
Decrease compliance / increase elastic recoil
41
What are the gross results of interstitial fibrosis?
Stiff, rigid lungs Restictive lung function
42
What are the affected lung functions due to congested/ damaged alveolar capillaries?
Imparied perfusion, ths gas exchange
43
What are the affected lung functions due to Alveolar wall fibrosis?
Increase wall thickness and decreased surface area >> Decrease diffusion capacity and gas exchange >> Lower ventilation = V/Q mismatch
44
What are some clinical examination features of end-stage diffuse ILD?
Dry cough Shortness of Breathe without wheezing Cyanosis *due to V/Q mismatch)
45
What is observed in CXR for end-stage diffuse ILD?
Corase lines and cystic nodules observed
46
End-stage diffuse ILD increases the risk of ___?
Lung cancer
47
How does chronic hypoxia caused by end-stage diffuse ILD manifest? (think early and late progressions)
Chronic hypoxia > Pulmonary vasoconstriction > Obliterate vessel lumen Early = reversible vasoconstriction Late = irreversible structural changes
48
What are some irreversible structural changes in End-stage diffuse ILD?
Increase in fibroblast proliferation and SM cells Thickening of tunica intima and media
49
How to diagnose ILD? *clin- radi- patho*
Based on a combination of features: Clinical,Radiological,Pathological + Identify etiology from history, relevant tests
50
What drug has no effects on honeycomb lungs?
NSAIDs
51
Why is tissue examination important in diagnosing ILD?
 Assess disease activity (active inflammation vs. fibrosis)  Find the cause (e.g. exposure to asbestos bodies > asbestosis)
52
Describe Pneumoconiosis?
lung fibrosis resulting from inhalation of inorganic dusts
53
What are some determinants of chronic inflammation in pneumoconiosis?
Chemical nature, physical state, particle size of dust Duration, concentration of exposure
54
What is the agent and exposure period causing Silicosis?
exposure to silica = silicon dioxide (SiO2) Prolonged, chronic exposure (>10-20 years) or Massive exposure
55
What are some high risk occupations for silicosis?
quartz-mining, rock-cutting, glassmaking, pottery, sand-blasting
56
Describe the pathogenesis of silicosis.
Silica deposit in alveolar wall > macrophage release FIBROGENIC FACTORS > Fibroblast proliferation and collagen deposition > SILICOTIC NODULES FORM
57
Compare the extent of silicotic nodules in simple and advanced silicosis?
Simple: sporadic, white nodules spread throughout lung Advanced: Massive areas of fibrosis with concentrically deposited collagen
58
Advanced silicosis can lead to what conditions?
Cor pulmonale Respiratory failure Honeycomb lung
59
What is the agent and duration of exposure of Asbestos?
Fibrous magnesium silicate (Long/thin, curved or straight) prolonged / heavy exposure
60
Sources of asbestos?
acoustic / thermal insulator, | industries, old buildings
61
What is the hallmark of Asbestosis?
Asbestos bodies asbestos fibers covered by a film of protein impregnated with haemosiderin*** (RBC breakdown products)
62
Appearance and location of asbestos bodies?
Long, beaded, brown In bronchial fluids, sputum
63
Describe the pathology of asbestosis?
asbestos deposit in airspace Macrophage fails to ingest asbestos, fibroblast proliferation > Interstitial fibrosis Puncture of endothelium, bleeding >> RBC broken down by asbestos and deposits haemosiderin >> Asbestos bodies
64
What are some asbestos related conditions?
Lung cancer > Malignant mesothelioma cancer derived from lining (mesothelium) of pleura, pericardium, peritonium
65
Chronic hypoxia increases risk of developing which diseases?
Cor pulmonale (RHF) Pulmonary Hypertension Polycythaemia

MBBS I CPRS (78 decks)

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