Respiratory Path 2 - Galbraith Flashcards

1
Q

Obstructive disease

A

Increased resistance to airflow anywhere in the tract

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2
Q

Restrictive disease

A

Reduced expansion of lung parenchyma with decreased lung capacity

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3
Q

PFTs for obstructive disease

A

Decreased FEV1

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4
Q

4 obstructive diseases

A
  • Emphysema
  • Chronic bronchitis
  • Asthma
  • Bronchiectasis
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5
Q

COPD is a combo of what obstructive diseases? Why is this a common combo?

A

Emphysema + chronic bronchitis

BOTH are caused by SMOKING

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6
Q

Emphysema description

A

Irreversible enlargement of airspaces DISTAL TO terminal bronchioles (ACINUS)

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7
Q

Centriacinar emphysema…

  • Occurs in who?
  • Lung involvement?
  • Seen in which lung part?
A
  • Smokers (COPD)
  • Respiratory bronchioles (more proximal)
  • Upper lobes/apical parts
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8
Q

Panacinar emphysema…

  • Occurs in who?
  • Lung involvement?
  • Seen in which lung part?
A
  • Alpha-1 antitrypsin deficiency
  • Distal alveoli
  • Lung bases
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9
Q

Roles of tobacco smoke in emphysema pathogenesis (4)

A
  • Recruit/activate neut’s and macrophages
  • Induce protease release from neutrophils (elastase)
  • Reducing antioxidants via abundant ROS’s
  • Inactivate antitrypsin-1

ALL cause alveolar wall destruction

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10
Q

PiZZ chromosome 14 homozygote

Most will develop what?

A

Alpha-1 antitrypsin deficiency

–> Panacinar emphysema that’s accelerated by smoking

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11
Q

Why and when is emphysema obstructive?

A

Destruction of elastic alveolar walls around bronchioles –> collapse of bronchioles during EXPIRATION

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12
Q

Dyspnea, cough, wheezing, weight loss, barrel chest, prolonged expiration

A

Emphysema

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13
Q

Progression/complication of emphysema

A

Pulmonary HTN –> R heart failure

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14
Q

4 causes of death in emphysema

A
  • CAD
  • Respiratory failure
  • RHF
  • Pneumothorax/collapse
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15
Q
  • Smoker or inhabitant of polluted environment
  • Chronic, persistent, productive cough
  • Dyspnea on exertion
A

Chronic bronchitis

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16
Q

Changes seen in chronic bronchitis

A
  • Mucus gland hyperplasia and hypersecretion
  • Bronchiolar fibrosis and thickening
  • Mucus stasis
  • Respiratory squamous metaplasia
  • Increased goblet cells
  • Small airway mucous plugging
17
Q

Pink puffer vs. blue bloater

A

PP = over-respiration of normal parenchyma in emphysema

BB = cyanosis in bronchitis

18
Q
  • Recurrent episodic wheezing, shortness of breath, chest tightness, cough
  • Common in morning and night
19
Q

3 changes in asthma

A
  • Recurrent bronchoconstriction
  • Inflammation of bronchial walls
  • Increased mucus secretion
20
Q

Atopic asthma

A
  • Type 1 (IgE) hypersensitivity to allergen(s)
21
Q

Atopic asthma 2-part pathogenesis

A
  1. Th2 cells stimulate IgE production, eosinophil recruitment, and mucus production in response to allergen
  2. IgE binds to mast cells (Fc), then cross linked by allergen re-exposure –> hypersensitivity reaction
22
Q

Immediate phase of asthma attack (3)

A
  • Bronchoconstriction
  • Mucus secretion
  • Vascular permeability
23
Q

Late phase of asthma attack (2)

A
  • Inflammatory recruitment

- Mucosal tissue damage

24
Q

Non-atopic asthma

A

Non-allergen stimulation of bronchoconstriction (viruses, irritants/smoke, cold air, exercise)

25
Morphologic changes over time due to recurrent asthma attacks
- SM hypertrophy/hyperplasia - Subepithelial fibrosis - Mucosal gland hyperplasia - Increased airway vascularity - Increased airway thickness
26
Curschmann spirals
ASTHMA - Mucus plugs from occluded bronchi and bronchioles that are expelled in sputum/lavage
27
Charcot-Leyden crystals
ASTHMA - Eosinophil granule debris deposited in airways and expelled in sputum/lavage
28
Status asthmaticus | - Danger?
- Acute asthma symptoms lasting for days | - Can cause cyanosis and death
29
Bronchiectasis pathogenesis
Airway obstruction -->/or chronic destructive necrotizing infections of airway --> SM and elastic destruction --> permanent dilation of airways
30
Predisposing conditions for bronchiectasis
- Conditions affecting mucus clearing - 1º ciliary diskinesia - Cystic fibrosis - Bronchial obstruction - Immunodeficiency
31
Bronchiolitis obliterans
Bronchiectasis --> repeated attempts to resolve inflammatory process --> fibrosis --> small bronchiolar obliteration
32
Cystic fibrosis - cause
Defect or lack of epithelial chloride channel (CFTR)
33
CFTR functions (3)
- Sweat glands - chloride on surface --> cell (w/ Na+) - Epithelia - chloride in cell --> lumen - Inhibits epithelial ENaC channel
34
A deficient/missing CFTR leads to what? (2)
- Over-active ENaC --> sodium uptake into cells --> water uptake --> thicker respiratory mucus - Under-active sweat gland Na+ channels --> excess Na+ in sweat --> salty sweat
35
Why do CF patients get recurrent infections?
Thick mucus + defective ciliary activity --> can't clear microbes in the mucus --> INFECTIONS
36
Eventually, CF recurrent infections leads to _____
Bronchiectasis
37
4 common infection species in CF
- S. aureus - H. influenzae - Burkholderia cepacia - Pseudomonas aeruginosa
38
Special thing about Pseudomonas in CF?
Produces mucoid capsule --> biofilm --> protection from immune system