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RW Respiratory > Obstructive Airway Disease > Flashcards

Obstructive Airway Disease Flashcards

1
Q

What area is affected by obstructive disease?

A

Airways

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2
Q

How many times does the airways bifurcate after the trachea bifurcation?

A

23

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3
Q

What is the conducting zone?

A

Conducting zone of the respiratory system is made up of the nose, pharynx, larynx, trachea, bronchi, bronchioles, and terminal bronchioles

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4
Q

What is the function of the conducting zone?

A

Filter, warm, and moisten air and conduct it into the lungs

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5
Q

What makes up the respiratory zone?

A

Respiratory bronchioles and the alveolar ducts

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6
Q

What is the function of the respiratory zone?

A

Exchanging of gases

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7
Q

Respiratory tract =

A

Conducting zone + Respiratory zone

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8
Q

What is happening in obstructive lung disease?

A

People find it hard to exhale of the air in their lungs due to obstruction

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9
Q

What is the main symptom that obstructive and restrictive lung disease share?

A

Shortness of breath with exertion

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10
Q

Obstructive airway syndrome (3 components):

A

1) Chronic bronchitis 2) Emphysema 3) Asthma (umbrella term including COPD and asthma)

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11
Q

3 main events in airway obstruction:

A

1) Mucosal invagination due to inflammation and oedema, which narrows the lumen 2) Increased tonicity in away smooth muscle 3) Alveolar wall breakdown

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12
Q

What is the main cell causing inflammation in COPD?

A

Neutrophil

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13
Q

What is the main cell causing inflammation in asthma?

A

Eosinophil

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14
Q

What is COPD?

A

Progressive disease state characterised by airflow limitation that is not fully reversible, characterised by chronic bronchitis and emphysema

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15
Q

What conditions does COPD encompass?

A

Chronic bronchitis and emphysema (and airway narrowing)

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16
Q

What is chronic bronchitis?

A

Mucous hyper secretion due to mucous gland hypertrophy and increased number of goblet cells resulting from inflammation of bronchi and bronchioles

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17
Q

What is emphysema?

A

Distention and damage of the alveoli with destruction of their walls leading to reduced gas exchange - becomes one large pouch’

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18
Q

What is asthma?

A

Disease characterised by airway inflammation with increased airway responsiveness resulting in airway obstruction

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19
Q

What is the asthma triad (characteristics of asthma)?

A

1) Airway inflammation (due to eosinophils) 2) Reversible airflow obstruction 3) Airway hyper responsiveness (smooth muscle becomes twitchy)

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20
Q

Difference between asthma and COPD in general?

A

Asthma is caused primarily by airway inflammation and hyperreactivity leading bronchial muscle contraction that is reversible, while COPD is structural and histological changes (i.e. narrowing and remodelling) that is only partially reversible.

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21
Q

What is atopic vs non-atopic asthma?

A

Atopic (60%) asthma indicates there is an allergic (IgG) reaction involved, non-atopic does not

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22
Q

What is extrinsic vs intrinsic asthma?

A

Extrinsic means there is an identifiable external trigger involved, while if there is no identifiable factors then it is intrinsic

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23
Q

What is the dynamic evolution of asthma over time?

A

1) Bronchoconstriction (causing brief symptoms) 2) Chronic airway inflammation 3) Airway remodelling (scarring due to persistent inflammation leading to fixed airway obstruction)

24
Q

What are the aims of treatment of asthma, considering the dynamic evolution?

A

Clear brief symptoms, Reverse exacerbations AHR and prevent fixed airway obstruction

25
Q

What are the hallmarks of remodelling in asthma?

A
  • Basement thickening - Collagen deposition in the submucosa - Hypertrophy of the smooth muscle
26
Q

What is the inflammatory cascade in asthma?

A

1) Genetic loading for the cascade (initiates cascade when interact with triggers) 2) Eosinophilic inflammation occurs 3) Release of preformed allergic mediators e.g. histamine, leukotriene D4 and TH2 cytokines 4) Twitchy smooth muscle occurs (hyper-reactivity)

27
Q

What is the treatment for Stage 1) Genetic loading in the inflammatory cascade in asthma?

A

Avoidance of the trigger

28
Q

What is the treatment for Stage 2) Eosinophilic inflammation in the inflammatory cascade in asthma?

A

Anti-inflammatories e.g. corticosteroids

29
Q

What is the treatment for Stage 3) Release of allergic mediators in the inflammatory cascade in asthma?

A

Anti-leukotrienes/histamines and anti-IgE

30
Q

What is the treatment for Stage 4) Twitchy smooth muscle in the inflammatory cascade in asthma?

A

Bronchodilators to relax the bronchial smooth muscles, or muscarine antagonists to block airway constriction

31
Q

Why are inhaled corticosteroids the mainstay of first line treatment for asthma?

A

They are the only class of drugs which will converted the anatomical mess of airway inflammation into organised anatomy

32
Q

What are the diagnostic indicators of asthma?

A

-Reduced forced expiratory ratio (Fev1/FVC

33
Q

What is the inflammatory cascade in the development of COPD?

A

1) Cigarette smoke or other noxious particles 2) activate resident alveolar macrophages and airway epithelial cells 3) These release cytokines 4) Activation of neutrophils, CD8 T cells, increased macrophage numbers 5) Neutrophils and macrophages release proteases that break down connective tissue in the lung parenchyma and also stimulate hyper secretion 6) Result in chronic bronchitis and emphysema

34
Q

Diagnostic factors of COPD:

A
  • Chronic symptoms (not episodic like asthma) - Smoking - Non-atopic - Daily productive cough - Progressive SOB - Frequent infective exacerbations - Expiratory wheeze from chronic bronchitis - Reduced breath sounds from emphysema
35
Q

What is the progression of disease in COPD?

A

1) Progressive fixed airflow obstruction 2) Impaired alveolar gas exchange 3) Respiratory failure (decreased PaO2 and Increases PaCO2) 4) Pulmonary hypertension 5) Right ventricular hypertrophy/failure 6) Death

36
Q

What are the main differences between asthma and COPD?

A

.

37
Q

Asthma vs. COPD: Smoking

A

Asthma = non-smokers COPD = smokers

38
Q

Asthma vs. COPD: Allergic

A

Asthma = allergic COPD = non-allergic

39
Q

Asthma vs. COPD: Onset

A

Asthma = early or late COPD = late

40
Q

Asthma vs. COPD: Symptoms duration

A

Asthma = intermittent COPD = chronic

41
Q

Asthma vs. COPD: Inflammatory cells involved

A

Asthma = Eosinophils COPD = Neutrophils

42
Q

Asthma vs. COPD: Diurnal variation

A

Asthma = Diurnal variaion COPD = None

43
Q

Asthma vs. COPD: Corticosteroid and bronchodilator response

A

Asthma = Good COPD = Poor

44
Q

Asthma vs. COPD: Progression

A

Asthma = none COPD =progressive decline

45
Q

Asthma vs. COPD: FVC and TLCO

A

Asthma = Preserved COPD = Reduced

46
Q

Asthma vs. COPD: Gas exchange

A

Asthma = Normal COPD = Impaired

47
Q

Asthma vs. COPD: Cough

A

Asthma = non-productive cough COPD = productive cough

48
Q

What classes as ‘brittle asthma’?

A

Wide PEF variability or sudden attacks when otherwise well controlled

49
Q

What classes ‘moderate asthma exacerbation’?

A

PEF >50-75% predicted with increasing symptoms but no signs of acute asthma

50
Q

What classes ‘acute severe asthma?’

A

Any one of: - PEF 33-50% predicted - RR>25/min - HR >110/min - Inability to complete sentences in one breath

51
Q

What classes ‘life threatening asthma’?

A

Any one of the following seen in acute severe patients: - Altered conscious level - Exhaustion - Arrhythmia - Hypotension - Cyanosis - Silent chest - Poor respiratory effort - PEF

52
Q

What classes ‘near fatal asthma’?

A

Raised PaCO2 and/or requiring mechanical ventilation with raised inflation pressures

53
Q

How is smoking involved in the pathogenesis of COPD?

A

Smoking-tobacco smoke increases the number of neutrophils and macrophages in the lungs, its slow transit of these cells promotes neutrophil degranulation and inhibits a1-antitrypsin

54
Q

Which 2 coniditons make up COPD?

A

Chronic bronchitis and emphysema

55
Q

Chronic bronchitis

A

Cough productive of sputum on most days for 3 months of at least 2 consecutive years.

Chronic irritation leads to increased mucus production associated with goblet cell metaplasia, macrophage accumulation and fibrosis around bronchioles generate functional obstruction

56
Q

Emphysema

A

Increase beyond normal size in distal airspaces to terminal bronchiole due to loss of alveolar walls (tissue destruction) due to protease activity.

Emphysema impairs respiratory function –diminished alveolar surface area for gas exchange. Loss of elastic recoil and loss of support of small airways leads to tendency to collapse.

57
Q

Asthma

A

Chronic inflammatory disorder (eosinophilic infiltration) characterised by hyper-reactive airways leading to episodic reversible bronchoconstriction

RW Respiratory (17 decks)

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