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Pathology Term 1 > Week 5 - RESP > Flashcards

Week 5 - RESP Flashcards

Asthma, Pneumoconioses, Acute Lung Injury

1
Q

What is the pathogenesis of acute lung injury?

A
  • noxious/irritant stimulus
  • necrosis of type I pneumocytes
  • epithelial/endothelial injury and inflammation
  • neutrophils –> inflamm. mediators and proteases
  • breakdown of tissue, vasodilation and plasma protein leakage (EXUDATION)
  • leaked plasma proteins deposited as protein layers which line alveolus and inhibit oxygenation (HYALINE MEMBRANE) –> diffuse alveolar damage (DAD)
  • severe hypoxia, atelectasis, wet heavy lungs filled with exudate
  • healing –> type II pneumocyte proliferation
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2
Q

What is goodpasture syndrome?

A
  • autoimmune disorder of both kidneys and lungs –> anticollagen Ab!
  • diffuse alveolar hemorrhage + rapidly progressive glomerulonephritis
  • rapidly progressive pulmonary and renal failure
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3
Q

What are 2 important complications in newborns with respiratory distress syndrome?

A
  1. Retrolental Fibroplasia

2. Bronchopulmonary Dysplasia

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4
Q

What is the definition of acute lung injury?

A
  • rapid onset hypoxemia and alveolar damage in the absence of heart failure
  • non-cardiogenic pulmonary oedema
  • more severe form = Adult Respiratory Distress Syndrome (ARDS)
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5
Q

What are to common etiologies of acute lung injury?

A
  • pneumonia/sepsis
  • shock
  • gastric aspiration
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6
Q

True or False?

There is clubbing in asbestosis

A

True

-there is clubbing in 50% of patients

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7
Q

What do asbestos bodies cause?

A
  • very severe extensive fibrosis
  • they are very small fibres which are carried to the lung periphery to small bronchioles –> pleural surface –> form PLEURAL PLAQUES
  • Asbestosis
  • diffuse fibrosis, honeycombing, pleural thickening, pleural effusions, dyspnoea, cough
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8
Q

What is sarcoidosis?

A
  • granulomatous multisystem inflammation in response to an UNKNOWN antigen
  • 90% pts show lung involvement (diffuse interstitial fibrosis)
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9
Q

What are the clinical features of sarcoidosis?

A
  • fever
  • fatigue
  • weight loss
  • anorexia
  • night sweats
  • lymphadenopathy
  • SOB from diffuse interstitial fibrosis
  • erythema nodosum
  • hypercalcemia
  • nephrocalcinosis
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10
Q

What is the most characteristic finding in sarcoidosis?

A

Granuloma formation

  • non-caseating
  • contain ASTEROID bodies in giant cells!

*asteroid bodies = star-like shaped inclusions within the giant cells of the non-caseating granulomas

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11
Q

What are the 2 types of asbestos bodies?

A
  1. Flexible serpentine
  2. Stiff straight amphibole

*both cause severe damage and fibrosis

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12
Q

What is the commonest type of pneumoconioses?

A

silicosis

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13
Q

What are the morphologic types of pneumoconioses?

A

Inert - coal workers pneumonia
Fibrous - asbestosis, silicosis
Allergic - bird watchers lung
Neoplastic - mesothelioma -> cancer of pleural laye - common in asbestosis

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14
Q

What are the 5 various grades of coal miners lung?

A
  1. Asymptomatic anthracosis (carbon only)
  2. Simple coal workers pneumonia
  3. Complicated coal workers pneumonia (fibrosis)
  4. Progressive massive fibrosis (PMF) - severely decreased pulmonary function
  5. Honeycomb lung –> end-stage lung (total destruction)
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15
Q

What is the etiology of silicosis?

A
  • inorganic sand & stone dust
  • lung injury
  • activated lymphocytes/macrophages
  • proteases/oxidants also from neutrophils
  • destruction of type I pneumocytes
  • increased type II pneumocytes
  • increased FGFs/fibroblasts –> FIBROSIS!
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16
Q

What is the morphology of silicosis?

A
  • multiple focal fibrotic nodules (with silica particles in the centre of nodules)
  • carbon pigment
  • surrounding irregular emphysema
  • diffuse fibrosis –> honeycomb
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17
Q

What are the microscopic features of idiopathic pulmonary fibrosis?

A
  • irregularly thickened alveolar septum with marked fibrosis and lymphocytes/macrophages within
  • marked hypertrophy of type II pneumocytes (forming clusters)
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18
Q

What is heard on auscultation of idiopathic pulmonary fibrosis?

A

dry “velcro-like” inspiratory crackles

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19
Q

What is the pathogenesis of restrictive lung diseases?

A
  1. Lung injury (inhaled agents, dusts, toxins)
  2. Activated lymphocytes + macrophages/neutrophils –> oxidants/proteases damage type I pneumocytes –> increased replication of type II pneumocytes
  3. Interstitial inflammation and fibrosis –> type II pneumocytes secrete FGFs –> fibroblasts –> FIBROSIS
  4. Stiff Lung!
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20
Q

What are the 2 key features in sputum microscopy of asthma?

A
  1. Charcot-Leyden Crystals
    - eosinophil basic protein
    - part of eosinophil granules –> form big crystals in sputum
  2. Curschmann Spirals
    - long mucous threads with eosinophils inside
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21
Q

What are the microscopic features of asbestosis?

A
  • pulmonary oedema

- emphysema with asbestos bodies

22
Q

True or False?

Asbestosis typically causes pulmonary oedema

A

True

23
Q

Progressive Massive Fibrosis (PMF) is typically seen in?

A

Coal Miner’s Lung

24
Q

Fibrotic nodules on microscopy are typically seen in?

A

Silicosis

25
Q

What are gross and microscopic features of respiratory distress syndrome? (infants)

A

Gross:
-purple, congested, wet, heavy, airless lungs (airless due to lack of surfactant)

Micro:

  • collapsed, inflamed alveoli
  • hyaline membrane of plasma proteins lining alveoli with necrotic cells

*total dysfunction –> severe hypoxemia

26
Q

What is the etiology of respiratory distress syndrome?

A
  • prematurity (<28wks) = MOST COMMON

- maternal diabetes, maternal sedation, trauma

27
Q

What is the pathogenesis of respiratory distress syndrome?

A
  • immature lung
  • decreased surfactant (as type II pneumocytes have not fully developed)
  • when child takes first breath, there is no surfactant to increase compliance/decrease surface tension –> atelectasis as alveoli cannot stay open
  • inflammation results –> exudation

*similar to ARDS but this is in a newborn (HMD)

28
Q

What is respiratory distress syndrome?

A

Hyaline Membrane Disease of new born (HMD)

29
Q

What is DAD/Acute Lung injury referred to as when it is severe? and how does healing occur?

A

ARDS –> Adult Respiratory Distress Syndrome

*Healing by type II pneuomocyte proliferation

30
Q

True or False?

normal/near normal FEV1/FVC ratio is a typical feature of obstructive pulmonary disease COPD

A

False

-restrictive (but decreased TLC)

31
Q

True or False?

sarcoidosis is more common in smokers

A

False

-smoking may give protection

32
Q

True or False?

Carbon alone does not cause damage in coal miner’s lung

A

True

  • acanthrosis + silicosis = coal workers pneumonia
  • associated SILICA causes fibrosis
  • carbon alone causes blackening of lung tissue but is usually asymptomatic –> “asymptomatic acanthrocis”
33
Q

What is the etiology of pneumoconioses?

A 
Due to inhaled dusts
-inorganic (mineral) or organic
Reaction may be:
-inert
-fibrous
-allergic
-neoplastic
*depending on type of dust
34
Q

What is idiopathic pulmonary fibrosis also referred to as?

A

Usual Interstitial Pneumonia (UIP)

35
Q

What size particles cause most damage to alveoli?

A

1-5microns

  • <1 micron = easily removed
  • > 5 microns = too large to reach/deposited in terminal alveoli

*carbon, SILICA, asbestos –> commonest particles

36
Q

Compare type I and type II pneumocytes

A

Type I:

  • larger, squamous cells –> make up most of alveolar wall
  • involved in gas exchange
  • susceptible to toxic insults and CANNOT replace itself

Type II:

  • cuboidal type cells occur more diffusely
  • secrete surfactant and FGFs –> fibrosis
  • CAN replicate itself and will replace damaged type I pneumocytes
37
Q

What is an example of an extrinsic disorder causing restrictive lung disease?

A
  • kyphosis
  • scoliosis
  • gross obesity
38
Q

True or False?

Expiration on a respiratory flow curve occurs over a longer duration in restrictive lung disorders

A

False
-restrictive lung disorders = lung cannot expand –> therefore decreased compliance –> expiration occurs over a SHORTER duration

*whereas obstructive disorders –> expiration occurs over a longer duration

39
Q

What is the definition of restrictive lung disorders?

A
  • decreased expansion of lung due to diffuse fibrosis (“stiff lung” –> decreased lung compliance)
  • decreased FEV1/FVC –> therefore FEV1:FVC ratio is roughly normal (but TLC id decreased)
40
Q

What is status asthmaticus?

A
  • persisting, severe exacerbation of an asthmatic attack with NO response to therapy –> excess mucous plugging major bronchi
  • severe hypoxia, hypercapnia, and acidosis –> may be FATAL
  • hyperinflation of lungs –> bronchi constricted so air retained in alveoli
41
Q

What is the only difference in microscopy between asthma and chronic bronchitis?

A

Very similar microscopy

-except, plenty of eosinophils in asthma and in chronic bronchitis = increase neutrophils

42
Q

What are gross and microscopic features of asthma?

A

Gross:

  • inflamed, thick bronchi
  • mucous plugs

Micro:

  • excess mucous (with eosinophils in mucous)
  • goblet cell hyperplasia
  • inflammation with eosinophilia
  • smooth muscle cell hyperplasia
  • mucous gland hyperplasia
  • increased capillaries/vasodilation
43
Q

What is the hygiene hypothesis?

A
  • proposes that childhood exposure to germs and certain infections helps immune system to develop
  • teaches body to differentiate harmless substances from harmful substances that trigger asthma
  • exposure to certain germs ‘teaches’ immune system NOT to overreact (hypersensitivity)
44
Q

What is the pathogenesis of asthma?

A
  • Th2 lymphocyte stimulation via dendritic cell with allergen attached
  • IL-4 release –> B cells for IgE secretion –> attach to mast cells
  • IL-5 release recruits eosinophils which release chemical mediators and granules
  • IL-13 causes mucous production
  • mast cells –> histamine release, etc
  • inflammation + episodic bronchospasm –> from exposure to irritants (caused by mast cell secretions)
45
Q

What do allergens stimulate in acute vs. chronic allergic reactions?

A 
Acute = Mast cells
Chronic = Dendritic cells --> Th2 cells
46
Q

Which inflammatory cells are predominantly present in asthma?

A

eosinophils

47
Q

What are asthma triggers and in which types of asthma do they occur?

A
  • infections
  • smoke
  • fumes
  • stress
  • exercise

*ALL types

48
Q

What are the types of asthma?

A

Atopic *COMMONEST
-allergen, early age, FHx.

Non-atopic
-no allergen, adult, no FHX., usually due to reaction to pollutants/viral infection

Other

  • drug-induced (aspirin)
  • occupational
49
Q

What is the commonest type of asthma?

A

Atopic

  • allergen (hypersensitivity to environmental allergen)
  • early age (childhood)
  • FHX. (either autoimmune or hypersensitivity disorders)
50
Q

What is the key difference between asthma and COPD?

A 
COPD = permanent/irreversible due to scarring
Asthma = intermittent bronchospasm + reversible (no scarring)

Pathology Term 1 (6 decks)

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