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► Med - Pathology > Pulmonary Pathology II > Flashcards

Pulmonary Pathology II Flashcards

1
Q

What is the change in the FEV1/FVC in obstructive airway disease?

A

FEV1 decreases while FVC is largely unchanged. Thus, the ratio will DECREASE

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2
Q

What is the change in FEV1/FVC in restrictive airway disease?

A

FEV1 remains normal while the TLC decreases, hence decreasing the FVC. The ratio can be normal or in some cases, increased.

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3
Q

What are some examples of obstructive airway diseases?

A
  • Emphysema
  • Chronic bronchitis
  • Bronchiectasis
  • Asthma
  • Tumor
  • Foreign body
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4
Q

What are some examples of restrictive airway diseases?

A
  • Due to chest wall disorders (polio, obesity, pleural disease, kyphoscoliosis)
  • Interstitial / infiltrative diseases (ARDS, dust diseases, interstitial fibrosis)
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5
Q

Asthma

A

Intermittent and reversible airway obstruction
- Chronic bronchial inflammation with eosinophils
􏰄- Bronchial smooth muscle hypertrophy hyper-reactivity
􏰄- Increased mucus production

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6
Q

What is the pathogenesis of atopic asthma?

A

Immune Mediated. Type I hypersensitivity reaction. Involving Ig E bound to mast cells
• Begins in childhood, triggered by environmental allergens (dust, pollen etc.)

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7
Q

What is the pathogenesis of non-atopic asthma?

A

Non-immune triggering mechanisms (e.g. respiratory viruses, air pollutants like ozone)
• Hyperirritable bronchial tree; virus induced inflammation of the respiratory mucosa lowers the threshold of subepithelial vagal receptors to irritants

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8
Q

What is the main drug that can induce asthma?

A

Aspirin

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9
Q

What is occupational asthma?

A

Asthma develops after repeated exposure to inciding agent - ranges from fumes, to dust to organic agents

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10
Q

What is the cellular mechanism of asthma?

A

Th2 will produce IL-3/5 which is chemotactic for
eosinophils - IL-4 will lead to the promotion of B cells
to produce IgE

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11
Q

What are some susceptibility genes of asthma?

A
  • ADAM 33- 20q

- Chromosome 5q

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12
Q

Status Asthmaticus

A

Persistent hyperinflated lungs

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13
Q

What can be seen in asthma mucus under the microscope?

A

Curschmann Spirals

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14
Q

What can be seen on microscopy of asthma after the degranulation of granulocytes?

A

Charcot Leyden Crystals

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15
Q

What is the difference between bronchi and bronchioles?

A

Bronchi have mucus glands and cartilage while bronchioles will have neither

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16
Q

What is the clinical definition of chronic bronchitis?

A

Persistent productive cough for at least three consecutive months in at least two consecutive years

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17
Q

What are some of the risks for chronic bronchitis?

A

-􏰄 Smokers
􏰄- Urban dwellers, smog-ridden cities
􏰄- Most common in middle aged men

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18
Q

What are the morphological changes with chronic bronchitis?

A
  • Hypertrophy of mucus secreting glands
  • Goblet cell metaplasia
  • Inflammation
  • Fibrosis (bronchiolitis obliterans)
19
Q

What is the Reid Index?

A

The Reid index measures the gland to wall ratio (normally glands are 40% of wall thickness as measured from epithelial basement membrane to cartilage) - this will be higher in chronic bronchitis

20
Q

What are the complications of chronic bronchitis?

A

􏰄Cor pulmonale with cardiac failure 􏰄
Infections
􏰄Bronchogenic carcinoma

21
Q

How does cor pulmonale result from chronic bronchitis?

A

Hypoxia of the lung will lead to vasoconstriction in the

lungs which will increase BP - cor pulmonale

22
Q

How does bronchogenic carcinoma result from chronic bronchitis?

A

Squamous metaplasia can occur to better handle

the wear and tear - possible leading into cancer from the metaplasia

23
Q

Emphysema

A

Destruction of walls of airspaces distal to terminal bronchioles, leading to permanent abnormal
enlargement of air spaces.

24
Q

What does Centriacinar (Centrilobular) emphysema affect and who does it often affect?

A
  • Upper lobes
  • Respiratory bronchioles
  • Male smokers
  • Often associated with chronic bronchitis
  • Coal-workers pneumoconiosis
25
Q

What does Panacinar emphysema affect and what mutation is most often associated with it?

A
  • Lower lobes
  • Whole acinus
  • Alpha1-antitrypsin deficiency
26
Q

What does Distal acinar (Paraseptal) emphysema affect

A
  • Distal acinus - “grocery bag”
  • Along pleura and lobular septa
  • Adjacent to areas of fibrosis, scarring, atelectasis
27
Q

What is a major complication of Distal acinar emphysema?

A

Pneumothorax in young adults

28
Q

What does Irregular emphysema affect?

A
  • Acini irregularly involved

* Associated with scarring/healed inflammatory lesions

29
Q

What is the pathogenesis of emphysema?

A

Mild chronic inflammation, i.e. macrophages, CD8+ T lymphocytes, and neutrophils

30
Q

Why does Alpha1-antitrypsin deficiency cause emphysema?

A

Alpha1-antitrypsin2 inadequacy causes a
functional deficiency which leads to increased elastase activity in the neutrophils which contributes to increased tissue damage

31
Q

Where is Alpha1-antitrypsin encoded?

A

Pi locus of chromosome 14

32
Q

Buzz word for the appearance of chronic bronchitis

A

Blue Bloaters

33
Q

Buzz word for the appearance of emphysema

A

Pink Puffers

34
Q

Bronchiectasis

A

Permanent dilatation of bronchi and bronchioles caused by destruction of the muscle and elastic tissue caused by chronic necrotizing inflammation.

35
Q

What are some of the causes of bronchiectasis?

A
  • Obstruction (tumor, foreign bodies)
  • Infection (TB, Aspergillus)
  • Congenital/Hereditary
    • Cystic fibrosis
    • Kartagener’s syndrome
    • Immunodeficiency states
36
Q

What is the pathogenesis of bronchiectasis?

A

Obstruction of the airways leads to impaired clearing mechanisms which causes the pooling of excretions distal to the obstruction. This culminates with inflammation of the airway with necrosis and fibrosis and finally dilatation

37
Q

Why are cystic fibrosis patients at increased risk of bronchiectasis?

A

Primary defect in Chloride transport causing accumulation of viscous secretions obstructing the airways which causes increased susceptibility to repeated infections, and wide spread damage to the airway walls

38
Q

Kartagener Syndrome

A
  • Caused by primary ciliary dyskinesia
  • Autosomal-recessive with variable penetrance
  • Absence/ shortening of dynein arms
39
Q

What is associated with Kartagener Syndrome?

A
  • Infertility
  • Dextrocardia
  • Bronchiectasis
40
Q

Centriacinar emphysema association

A

Smoking

41
Q

Panacinar emphysema association

A

Alpha 1 antitypsin deficiency

42
Q

What is the general feature of emphysema?

A

Destruction and dilatation of acini

43
Q

What are the general features of chronic bronchitis?

A

􏰄Cough
􏰄Hypersecretion of mucus 􏰄
Smoking, pollutants
􏰄Small airway disease

► Med - Pathology (203 decks)

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