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MED234 Respiratory > Resp Path 2 - OBSTRUCTIVE DZ, Emphysema, Chronic Bronchitis, Asthma, Bronchiectasis, CF - Galbraith > Flashcards

Resp Path 2 - OBSTRUCTIVE DZ, Emphysema, Chronic Bronchitis, Asthma, Bronchiectasis, CF - Galbraith Flashcards

1
Q

What is obstructive lung disease?

A

Resistance to airflow from trachea to alveoli.

Forced expiration: FEV/FVC

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2
Q

Together, emphysema and chronic bronchitis form….

A

COPD

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3
Q

What demographic is most susceptible to COPD?

What environmental factor has a strong association?

A
  • Females and African Americans

- SMOKING

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4
Q

How is asthma distinguishable from emphysema and chronic bronchitis?

A

Presence of reversible bronchospasms.

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5
Q

Emphysema is characterized by __1__ of airspaces __2__ to terminal bronchioles.

A
  • irreversible enlargement

- distal

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6
Q

Location and demographic of centriacinar emphysema.

A
  • Destruction/enlargement of central or proximal parts of respiratory unit - SPARES DISTAL ALVEOLI.
  • UPPER LOBE/APEX involvement.
  • Occurs in HEAVY SMOKERS (with chronic bronchitis)
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7
Q

Location and associated deficiency in Panacinar Emphysema.

A
  • Destruction/enlargement of acinus (ALVEOLI).
  • Lower basal (BASE of LUNGS) zones involvement.
  • Associated with alpha1-antitrypsin deficiency.
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8
Q

Location of distal acinar (paraseptal) emphysema.

What does this often subsequently cause?

A
  • Involves DISTAL ACINUS.
  • Near pleura and adjacent to fibrosis or scars.
  • Causes spontaneous pneumothorax
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9
Q

What is the pathogenesis of alveolar destruction in emphysema?

A

Smoking/pollutant and congential a1-antitrypisin deficiency results in 3 imbalances:

1) Imbalances between pulmonary proteases and antiproteases (elastase release).
2) Inflammatory cells
3) Oxidative stress

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10
Q

Define a1-antitrypsin’s role in emphysema.

A
  • An antiprotease
  • Chromosome 14
  • 80% of homozygotes for Z allele (PiZZ) will develop SYMPTOMATIC PANACINAR EMPHYSEMA
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11
Q

PiZZ

A

alpha1-antitrypsin deficiency, leading to panacinar emphysema

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12
Q

What accelerates and intensifies severity of a person with PiZZ?

A

SMOKER.

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13
Q

Why is emphysema considered an obstructive lung disease?

A

Destruction of elastic alveolar walls surrounding respiratory bronchioles leads to COLLAPSE of those bronchioles during EXPIRATION - normally held open by elastic recoil of lung parenchyma.

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14
Q

how much lung parenchyma must be loss for symptoms of emphysema to show?

A

1/3

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15
Q

What is this?
A patent presents with weight loss, dyspnea, wheezing, cough, barrel chested/overdistension, prolonged expiration due to OVER VENTILATION.

A

Emphysema

“Pink puffer”

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16
Q

What may emphysema progress to?

What 4 things are death usually due to?

A

Pulmonary HTN and right sided HF.

Death: respiratory acidosis/failure, RHF, pneumothorax&raquo_space; lung collapse.

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17
Q

What is this?

A chronic, persistent productive cough without other identifiable cause. Common in smokers/polluted environments.

A

Chronic bronchitis.

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18
Q

What is the pathogenesis of chronic bronchitis?

A
  1. Initiating factor&raquo_space; exposure of bronchi to inhaled irritants.
  2. Mucus hypersecretion
  3. Chronic inflammation&raquo_space; damage and fibrosis of small airways
  4. Diminished ciliary action of respiratory epithelium, leading to STASIS OF MUCUS.
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19
Q

What are three other form of emphysema?

A

1) Compensatory hyperinflation
2) Obstructive overinflation
3) Insterstitial emphysema

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20
Q

What is compensatory hyperinflation

A

Form of emphysema - LOSS OF ALVEOLI but WITHOUT SEPTAL WALL DESTRUCTION
(dt surgical removal of diseased lung with recoil, allowing alveolar expansion)

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21
Q

What is obstructive overinflation?

A

Form of emphysema - expansion of lung because of TRAPPED AIR, but WITHOUT SEPTAL WALL DESTRUCTION

subtotal obstruction of an airway, thereby creating a ball-valve that admits air on inspiration but TRAPS it on expiration.
(dt tumor, FBAO, Asthma)

22
Q

What is interstitial emphysema?

A

Form of emphysema - alveolar tears, resulting of ENTRY OF AIR INTO CONNECTIVE TISSUE of lung/mediastinum/subQ tissues.

23
Q

Morphology in chronic bronchitis (5)

A

1) Edema of lung mucous membranes
2) Mucinous secretions plugging small bronchi and bronchioles (goblet cells)
3) Bronchilar inflammation and fibrosis
4) Mucous gland HYPERPLASIA (*Reid index)
5) bronchial epith SQUAMOUS METAPLASIA and dysplasia.

24
Q

What is the Reid index

A

Ratio of mucous glad layer thickness to distance from epithleium to cartilage.

  • Normally 0.4
  • > 0.4 = increased thickness = hyperplasia of mucous glads
25
Q

What is this?

Persistent, productive cough. Dyspnea on exertion. Classically: Hypercapnic, hypoxia, mild cyanosis.

A

Chronic Bronchitis, “Blue Bloater”

hypoxia=trouble moving air in/out

26
Q

What does long standing chronic bronchitis often progress to?

A

Cor pulmonale with HF.

Death can be secondary to infection.

27
Q

What are two defining characteristics of:

1) Emphysema
2) Chronic bronchitis
3) Asthma

A

Emph/CB due to chornic injury/small airway dz:
1) Alveolar wall destruction, overinflation.
2) Productive cough, airway inflammation
Asthma due to bronchial hyperresponiveness (triggered by allergen, infection)
3) Reversible obstruction

28
Q

What is this?

Recurrent wheezing, SOB/chest tightness, cough. More frequent in early AM/late PM.

A

Asthma

29
Q

What are three characteristics of asthma?

A

1) **RECURRENT BRONCHOCONSTRICTION (unique)
2) Inflammation of bronchial walls
3) Increased mucucs secretion

30
Q

What is atopic asthma?

A
  • Most common
  • Caused by IgE hypersensitivity reaction to environmental allergen (or NSAIDS)
  • Family Hx
31
Q

Pathogenesis of atopic asthma

A

Th2 stimulated production of IgE recruits eosinophils and stimulates mucus production.
- Reexposure links IgE on mast cells&raquo_space;> degranulation and IMMEDIATE hypersens reaction.

32
Q

What characterizes the two phases of atopic asthma?

A

1) Immediate phase - minutes (Ag bind to IgE mast cells = LT and cytokine release)
- Bronchoconstriction, mucus secretion, increased vascular permeability
2) Late phase - hours (recruited leukocytes)
- Persistent bronchospasm and edema, Inflam cell recruitment&raquo_space; DAMAGE TO MUCOSAL TISSUE

33
Q

What triggers nonatopic asthma (4 things)?

A

1) Respiratory viruses
2) Inhalation of irritants
3) Cold air
4) Exercise

34
Q

In asthma, what does repeated allergen exposure induce?

A

AIRWAY REMODELING

  • Bronchial wall smooth m hypertrophy and hyperplasia (and inc goblet/subepith cells).
  • Subepithelial fibrosis
  • Submucosal gland hyperplasia, increased goblet cells
  • Increased airway vascularity
  • Increased thickness of airway wall.
35
Q

Genetics of asthma

A
  • HLA alleles
  • polymorphisms in IL-13
  • CD14
  • ADAM-33
  • B2-R
  • IL-4-R
36
Q

Curschmann spirals, think what?

A

ASTHMA - expelled in sputum/BAL as bronchi and bronchioles occluded by thick mucus plugs

37
Q

Chorcot-Leyden crystals, think what?

A

ATPOIC ATHMA

-Contained (with eosino) in sputum/BAL

38
Q

What is this?
Chronic, RECURRENT NECROTIZING INFECTIONS eventually destroying smooth muscle and elastic tissue.

What does this lead to?

A

Bronchiectasis

- Leads to permanent dilation of bronchi and bronchioles.

39
Q

What does the recurrent necrotizing infection in bronchiectasis result in?

A

Inflammation and destruction and plugging up of small airways. Can obliterate nearby bronchioles&raquo_space; obstructive.
- Lower lobes

40
Q

Predisposing conditions for bronchiectasis

A

Anything that affects mucus clearing - primary ciliary dyskinesia (kartageners), CF, Allergic Bronchopulmonary Aspergillosis
- Immunodeficiency

41
Q

What is this caused by? PERIOBRONCHIAL FIBROSIS&raquo_space; bronchiolitis obliterans

A

Repeated attempts to resolve inflammatory process that causes bronchiectasis

42
Q

Describe the genetics and dysfunction in CF.

A

CFTR, ch7&raquo_space; abnormal function of, or lack of epithelial chloride channel.

43
Q

CTFR function in sweat glands v. other epithelia

A

Sweat glands: Cl from surface INTO CELL

Other: from cell TO THE LUMEN

44
Q

What is CTFR’s normal function?

Dysfunction?

A

Normally inhibits ENaC, found on all non-sweat glad epithelial cell apical surfaces.
Dysfunction results in overactive ENaC, resulting in epithelia taking up Na ions&raquo_space; WATER FOLLOWS

45
Q

What is the result of airway CTFR dysfunction in CF?

A

DEHYDRATED MUCUS because Cl is not transported out of the cel, so lots of Na comes into cell, followed by lots of water.

46
Q

Deficient hydration of airway mucus leads to what in CF?

A

defective ciliary activity&raquo_space; inability to clear mucus&raquo_space; CHRONIC INFECTION&raquo_space; BRONCHIECTASIS

47
Q

What are the 4 primary infectious species in CF?

A

Bacteria - S. aureus, H flu, Burkholderia cepacia.

- Pseudomonas aeruginosa

48
Q

What does Pseudomonas aeruginosa do that makes it more resistant to antibiotics and inflammatory cells in a CF patient?

A

Produces a mucoid capsule that allows it to form a protective biofilm.

49
Q

Classis s/s for:

“persistent cough with productive sputum”

A

Bronchitis

50
Q

Obstructive disease means what change in FEV1/FVC??

A

Decreased

51
Q

Describe the pathogenesis of bronchitis.

A

Smoking = increase proteinase, normal antiproteinase

alpha1-antitrypsin deficiency = normal proteinase, decreased antiproteinase

MED234 Respiratory (15 decks)

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