L57 – Pathology of Small Airway Obstruction Flashcards Preview

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Flashcards in L57 – Pathology of Small Airway Obstruction Deck (60):
1

Compare the cause and effects between small airway pathologies and large airway pathologies?

Small airway = Functional impairment, Generalized, diffuse

Large airway = Not functional impairment, Regional

2

Airflow obstruction belongs to small or large airway pathologies?

Small

3

Infection, collapse and atelectasis belongs to small or large airway pathologies?

Large

4

When does large airway pathologies become functional impairments?

When pathology affects lobe of lung supplied by a large bronchi

5

What is acinus in lungs?

The ending of a tiny airway in the lung, where the alveoli (air sacs) are located.

6

What structures are included in small airways?

 Terminal bronchioles
 Respiratory bronchioles (gas exchange starts)
 Alveolar duct
 Alveoli

7

What is the definition of asthma?

Proxysmal (episodic) narrowing of airways

reversible spontaneously or with treatment

8

What increase in FEV1/FVC post-bronchodilator is considered effective treatment of asthama?

at least 15% increase

9

What is the reduction of FEV1/FVC in asthma?

less than 70%

but threshold is age dependent

10

Is asthma a small airway disease or a large one?

Small
Due to reduction in airflow from airway narrowing

11

What is extrinsic asthma caused by?

Type I HS triggered by allergen inhalation

12

What is the action of extrinsic asthma? (from allergen to production of mediators)

Inspire foreign Ag (e.g. allergen) > binds to IgE antibodies on submucosal mast cells > mast cells
degranulate > release chemical mediators

13

What 2 conditions can aggrevate asthma?

Air pollution
Upper respiratory tract infection

14

What are the 3 major effects of mast cell degranulation in extrinsic asthma?

1. Mucus hypersecretion

2. Bronchospasm/ bronchoconstriction

3. Vascular dilatation > edema

15

What chemical mediators are released in extrinsic asthma mast cell degranulation?

histamine, leukotrienes, eosinophil chemotactic factor

16

Explain the pathology of Airway inflammation?

Histamine > submucosal vessels dilate > proteins and plasma leak into interstitial space + congestion of RBC > Oedema and swelling

17

Explain the pathology of Mucus plugs?

Histamine + leukotrienes > stimulate goblet cells at respiratory epithelium > mucus hypersecretion > Mucus plug

18

Explain the pathology of bronchospasm/ ' thick muscle coat' ?

Histamine, leukotrienes > stimulate airway smooth muscle contraction > bronchospasm / bronchoconstriction

19

How does asthma affect V Q?

Narrow lumen of airway increases Raw > affect ventilation, not perfusion

20

Does asthma affect exhalation or inhalation?

Exhalation:
expiration = passive process: depends on elastic recoil

Increase Raw means air cannot escape > cause air-trapping in lungs and hyperinflation

21

Why is asthma not affected by inspiration?

active effort: builds up suction pressure by muscles > air can still go into lungs

22

In CXR of asthma patient, what are the changes?

Due to hyperinflation of lungs:
Elongated, narrowed heart / cardiac shadow

Horizontal ribs

Suppressed diaphragm

23

When does asthma attack subside spontaneously?

when allergen is removed

24

What are the functional volume changes in asthma? (tidal, VC, Residual)

Decrease Tidal volume, Vital capacity

Increase residual lung volume

25

What are the clinical features of asthma?

 Shortness of breath, difficulty in breathing

 Long expiration phase + high-pitched wheezing (turbulent airflow hit on narrow airways)

 Episodic attacks with recovery in-between (paroxysmal, reversible)

26

On a volume flow graph, what is the change in the expiratory phase curve in asthma?

Change from concave to convex

27

What are the spirometry changes in asthma? (FEV, FVC, ratio)

Dis-proportionally reduced FEV1

FVC also reduced but not as much as FEV1

FEV1/FVC becomes <70% predicted

28

What are the 2 types of asthma? What are their triggers?

Extrinsic - triggered by allergens in environment

Intrinsic - etiology is unknown/ not always due to antigen

29

Name some causes of intrinsic asthma?

Aspirin
exercise
cold air
viral infection
stress

30

Compare the onset between extrinsic and instrinsic asthma?

Extrinsic = childhood onset, familial, Well-controlled childhood asthma = subside in adolescence

Intrinsic = adult onset, usually not fully reversible

31

Is COPD a small or large airway disease?

Small >> chronic AIRFLOW obstruction

32

What are some alternative terms for COPD?

Alternative terms:
 Chronic obstructive airway disease (COAD)
 Chronic obstructive lung disease (COLD)
 Chronic obstructive respiratory disease (CORD)

33

Name the most important factor in the etiology of COPD and other contributing factors?

Most important inducing factor (80%-95%) = tobacco

Other contributing factors:
 Occupational
 Air pollution = co-factor (increases risk, duration of
hospital stay)
 Genetics = susceptibility factors

34

What are the 2 clinical entities of COPD?

Chronic bronchitis
Emphysema

35

What is the clinical definition of Chronic Bronchitis?

chronic productive cough with mucoid sputum, at least 3 months per year for 2 consecutive years

in absence of other lung diseases that can account for the symptom

36

How does Tobacco cause activation of inflammatory cells?

Tobacco / cigarette smoke / irritant gas >> contain ROS or induce ROS production > Activate NFκB > express inflammatory mediators and chemotaxis > attract inflammatory cells to airway

37

What inflammatory cells are involved in chronic bronchitis?

activated macrophages, neutrophils,
lymphocytes

38

What are the 4 pathological conditions in chronic bronchitis?

Affect airway:
1) Induce mucus thickening
2) Peribronchiolar fibrosis
3) Chronic inflammation

Affect airSPACE
4) Proteolytic enzyme > emphysema

39

What causes increased mucus accumulation in COPD patients? What are the results?

Impaired ciliary clearance

> mucus plugs + cough and mucoid sputum + prone to lung infection

40

What are the long term effects of chronic bronchitis?

Overall: narrow obstruction of small airways due to:

1) non-reversible bronchoconstriction

2) Chronic inflammation causing slowly progressive peribronchial/ peribronchiolar fibrosis

41

What is the definition of emphysema?

permanent destruction of alveolar wall / interstitial septum between alveolar airspace

permanent enlargement of airspaces beyond terminal bronchioles

42

The balance of which enzymes determine the progression of emphysema?

imbalance between protease, anti-protease

43

How does smoking increase the level of proteases whilst decrease level of Anti-proteases?

Toxins in smoke neutralize and decrease level of anti-protease

Smoke causes activation of inflammatory cells and ROS > neutrophils (PMN) and macrophages release proteolytic enzymes > increase protease level

44

What are the results of proteolytic enzymes released in lung tissue?

 Apoptosis of alveolar tissue cells

 Degradation/ uncontrolled proteolysis of elastic tissue in extracellular matrix

45

How does Alpha 1 anti-trypsin deficiency cause an imbalance in proteases?

Congenital deficiency of anti- proteases >> causes emphysema even without smoking ... etc

46

Which parts of lung lobules are involved in centriacinar (centrilobular) emphysema? How about panacinar (panlobular) emphysema?

Centriacinar= happens first, Involve alveoli at centre of lobules

Panacinar = advanced cases involve entire lung lobule

47

Describe how alveolar tissue lose function in emphysema? (2)

1) Loss of surface area for gas exchange

2) Proteases break down connective tissue > loss of lung recoil, respiratory bronchioles not supported by radial traction

> early small airway closure during expiration and air-trapping

48

a-1 antitrypsin deficiency is related to which type of emphysema?

Panacinar (panlobular) emphysema

49

What is the gross morphology of lungs with emphysema?

pale, soft, expanded

pale due to loss of capillaries
Expanded due to air-trapping

50

Compare chronic bronchitis and emphysema. Which one is defined clinically, which on pathologically?

Clinically defines = chronic bronchitis

Pathologically defined = emphysema

51

Compare chronic bronchitis and emphysema. Which one affects airspace, which one airway?

Airway affected = chronic bronchitis

Airspace affected = emphysema

52

What induces Acute exacerbation of emphysema ?

upper respiratory tract / bronchial infections, air pollution, irritant gas, dusts

53

Can COPD symptoms be stopped by smoking cessation?

 Not completely stopped by smoking-cessation > progressive disease
 Deteriorates (does not recover)

54

What are 4 long term complications of COPD?

1) Chronic persistent hypoxia

2) Pulmonary hypertension > irreversible pulmonary artery narrowing due to chronic alveolar hypoxia

3) Cor pulmonale - Right heart failure due to primary lung disease

4) Polycythaemia - Increased RBC production under chronic hypoxia for compensation of low PaO2

55

How is COPD asociated with lung cancer?

Smoking > inflammation > release of ROS/ RNS, inflammatory mediators and growth factors can cause:

1) chronic inflammation leading to COPD
2) DNA damage, mutation and Cancer

56

Compare asthma with COPD:
What is the etiology?

Asthma = allergy
COPD = smoking mostly

57

Compare asthma with COPD:
What is the disease pattern?

Asthma = reversible
COPD = non-reversible

58

What are some acute complications of severe asthma and COPD exacerbations?

Pneumothorax

Superimposed bacterial infection (pneumonia)

Acute respiratory failure (type II ventilation failure)

59

What are some common clinical features of asthma and COPD?

Prolonged expiration

Expiratory wheeze due to turbulent flow in narrow airways

Cough, sputum, shortness of breath

60

The symptoms and sings, pathophysiological effects and acute complications appear common in small airway diseases. What pathology is not common?

Different long term complications

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