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Respiratory system SA > Pathology of Restrictive lung disease > Flashcards

Pathology of Restrictive lung disease Flashcards

1
Q

Where does restrictive lung diseases affect the lungs

A

In the Interstitium lying within the alveoli of the lungs

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2
Q

What is the interstinum of the lung

A

potential space between alveolar epithelium and alveolar capillary endothelium, which sit on basement membranes

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3
Q

What is the outcome of restrictive lung disease

A

reduces the lungs compliance - creates a stiff lung
reduced total lung capacity
reduced gas transfer
ventilation/perfusion imbalance

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4
Q

What is the result of restrictive lung disease on the FEV1 FVC and their ratio

A

FEV1 AND FVC are reduced,

but the FEV1/FVC ratio remains the same

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5
Q

What causes the reduction of the total lung capacity in restrictive lung disease

A

altering of lung parenchyma - portion of the lung involved in gas transfer

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6
Q

In normal alveolar wall what is the relationship between e alveolar epithelial and intersitial capillary endothelial cell basement membranes, what does this allow

A

direct contact allowing efficient gas exchange

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7
Q

What is the pathological process of restrictive lung disease and what does it result in

A

interstitial inflammation
alveolar wall thickening due to interstital filtrate
potentially resulting in scaring and fibrosis

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8
Q

What is the clinical presentations of restrictive lung disease

A

Dyspnoea:
shortness of breath during exercise followed by at rest
Respiratory failure type 1 (reduced oxygen in the blood)
Heart failure
Abnormal Chest X-ray

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9
Q

What is the overall aetiology of restrictive lung disease

A

Something damages the lung tissue parenchymal and the lung injury leads to an inflammatory process

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10
Q

What is the two responses to Parenchymal (Interstitial) Lung Injury

A

either chronic or acute

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11
Q

What are the the further responses of the chronic response to parenchymal lung injury

A

interstitial pneumonitis response
granulomatous response
or other patterns

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12
Q

What is the acute response to Parenchymal (Interstitial) Lung Injury

A

Diffuse alveolar damage

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13
Q

What is the potential causes of Diffuse alveolar damage

A 
Major trauma
Chemical injury / toxic inhalation
Circulatory shock
Drugs 
Infection
Auto(immune) disease
Radiation
idiopathic
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14
Q

What is the two stages in the pathology of Diffuse alveolar damage

A

Exudative stage

proliferation stage

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15
Q

What steps occur in the exudative stage of diffuse alveolar damage

A
  1. Damage and destruction to the endothelia cells results in the capillary cells becoming very leak
  2. The leads to a massive pulmonary oedema - much more than acute inflammatory response
  3. alveolar spaces fill with protein rich fluid
  4. The massive outpour of macromolecule and proteins form a layer on the degraded basement membrane
  5. Form hyaline membrane
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16
Q

What does the body want to achieve in proliferation stage of diffuse alveolar damage

A

The body wants to repair the damage to the alveoli

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17
Q

What is the outcome of the proliferation stage of diffuse alveolar damage

A

alveolar proliferation leads to a mixture of fibril and inflammatory cells, these then attempt to repair the damage by laying down rapid fibrosis tissue, thus creating a solid mass in the lungs

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18
Q

What is the outcome of most patients with Diffuse alveolar damage

A

Its a fatal disease as may patients die from respiratory distress ARDS, shocked lung etc, as lung loses all compliance

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19
Q

What is the histological features of DAD

A 
Protein rich oedema
Fibrin
Hyaline membranes - Epithelial proliferation
Fibroblast proliferation
Scarring - interstitium and airspaces
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20
Q

What are the two Granulomatous responses in Parenchymal (Interstitial) Lung Injury

A

sarcoidosis

Hypersensitivity pneumonitis

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21
Q

What is sarcoidosis

A

is a mulit granulomatous disorder

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22
Q

Do sarcoidosis granulomas cause necrosis

A

no

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23
Q

How can you differentiate between sarcoidosis and TB

A

caseations are very unusual in sarcoidosis, but necrosis occur in TB, causing these caseation cheese like appearance

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24
Q

What is the most key feature of sarcoidosis

A

The alveoli around the granulomas are normal

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25
Q

How does scarring occur in sarcoidosis

A

fibrosis of the granuloma

26
Q

sarcoidosis is a multi system disorder but what is the most common sites of infection

A

Skin, Lungs and lymph nodes

eyes - sometimes

27
Q

What is the symptoms of sarcoidosis

A

Tender reddish bumps or patches on the skin (Erythema nodosum)
Red and teary eyes or blurred vision.
Swollen and painful joints (acute arthralgia)

Bilateral hilar lymphadenopathy - enlarged lymph

shortness of breath
cough
abnormal CXR

28
Q

What specific cell types are present in Lymph node

Sarcoidosis

A

Non-caseating Epithelioid Granulomas

29
Q

What are the investigation need for the diagnosis of Sarcoidosis

A 
Clinical findings
Imaging findings - CXR
Serum calcium levels 
angiotensin converting enzyme levels (high levels present in Sarcoidosis)
Biopsy
Pulmonary function test 
Spirometry
30
Q

What is Hypersensitivity Pneumonitis

A

an inflammation of the alveoli within the lung caused by hypersensitivity to inhaled organic microorganism

31
Q

What is examples of organisms that trigger Hypersensitivity Pneumonitis

A

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

32
Q

Examples of Thermophilic actinomycetes are:
- Micropolyspora faeni
- Thermoactinomyces vulgaris
What type of hypersensitivity pneumonitis does this cause

A

Farmers lung

33
Q

Where would you find

  • Micropolyspora faeni
  • Thermoactinomyces vulgaris
A

Mouldy hay

34
Q

What is the pathology of hypersensitivity pneumonitis that leads to disruption of diffusion and then respiratory failure

A

Inhalation of particle, which then deposits in the interstitium, disrupting the diffusion by creating an inflammatory reaction and lowering gas transfer

35
Q

What is the signs and symptoms for acute hypersensitivity pneumonitis

A

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

36
Q

What is the main aetiology of hypersensitivity pneumonitis

A

causative antigens

37
Q

What is the signs and symptoms of chronic hypersensitivity pneumonitis

A

Malaise, SOB, cough

Crackles and some wheeze

38
Q

hypersensitivity pneumonitis is immune complex mediated by what hypersensitivity reactions

A

Type III and Type IV Hypersensitivity reaction

39
Q

What cells are present in hypersensitivity pneumonitis

A 
epithelioid granulomas
Foamy histiocytes (macrophages laden with lipid)
40
Q

Where is hypersensitivity pneumonitis located in the lungs

A

Upper zones - centriacinar

41
Q

what can chronic hypersensitivity pneumonitis lead on to cause

A

Bronchiolitis obliterans - fixed airway obstruction

42
Q

Why is hypersensitivity pneumonitis more likely to be an upper zone disease

A

as corresponds to inhalation of antigens as thats where the are more likely to deposit

43
Q

interstitial pneumonitis UIP is a lung diseases characterised by

A

progressive scarring of both lungs (no granulomas)

44
Q

What is the potential causes of interstitial pneumonitis UIP

A

Connective tissue diseases ; esp scleroderma and rheumatoid disease
Drug reaction
Post infection
Industrial exposure - asbestos

45
Q

What is the morphology of interstitial pneumonitis UIP

A

Patchy interstitial chronic inflammation
proliferating fibroblastic foci
Type 2 pneumocyte enlarge

46
Q

What gives you the evidence if its an old or a recent injury

A

whether interstitial pneumonitis UIP is temporal or spatial

47
Q

What is the general demographic of interstitial pneumonitis

A

Ages 50 above

More likely to be male >female

48
Q

What is the clinical signs of interstitial pneumonitis

A

Dyspnoea, Cough,
Basal Crackles, Cyanosis, Clubbing
Progressive disease

49
Q

What is used to investigate interstitial pneumonitis

A

Chest X ray
Pulmonary function test - reduced gas transfer
spirometry

50
Q

What is the outcome of end stage interstitial pneumonitis

A

The lung tries to repair itself with cystic fibrosis but fails creating the appearance of a honeycomb lung

51
Q

When is V/Q imbalance the lowest

A

In hypoxemia conditions

due to local alveolar hypoventilation due to some focal disease

52
Q

What increases the V/Q ratio imbalance

A

increase even the slightest amount of oxygen breathed in (FIO2)

53
Q

Restrictive disease affects diffusion in what two ways

A

Increase thickness and surface areas of membrane, increasing gas transfer time

increase equilibration time above 0.25 seconds

54
Q

What is the normal equilibration time?

A

0.25 seconds

55
Q

What is the normal capillary transit time

A

0.75seconds

56
Q

If restrictive lung diseases increases equilibration time, how does this create hypoxia

A

as equilibration time increases to the same time or more as capillary transit time, meaning there is not enough time to fully saturate RBC,

57
Q

When can an increased equilibrium time cause problems

A

Its fine at rest,

when excise results in a decrease in PaO2

58
Q

When Pa o2 falls it causes hypoxemia, what corrects hypoxemia and restores diffusion

A

corrected by increasing FIO2, which increase PA O2 again thus increasing the rate of diffusion

59
Q

Why does a large shunt respond badly to increase in FI O2

A

Blood leaving normal lung is already 98% saturated

60
Q

Why does CO2 levels increase in alveolar hypoventilation

A

lack of air moving in and out of the lungs leading to an imbalance in the alveolar CO2 levels – leads to retention of CO2 in arterial blood

Respiratory system SA (37 decks)

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