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Y1Systems > Pathology of Obstructive Lung Disease > Flashcards

Pathology of Obstructive Lung Disease Flashcards

1
Q

Give examples of localised obstructive diseases (not necessarily obstructive diseases)

A

Lung cancer and other tumours, inhaled foreign bodies and chronic scarring diseases (bronchiecstasis and secondary tuberculosis)

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2
Q

What are the three main obstructive airway diseases?

A

Chronic bronchitis

Emphysema]

Asthma

(Mechanisms for each are different)

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3
Q

What is Chronic Bronchitis and Emphysema also known as?

A

COPD

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4
Q

What are the normal values for FEV1, FVC and the ratio between them?

A

Normal FEV1 is about 3.5 – 4 litres Normal FVC is about 5 litres Normal ratio FEV1 : FVC is 0.7 – 0.8

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5
Q

What is used to predict FVC?

A

Age, sex and height

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6
Q

Besides FEV1/FVC ratio, how else can an obstructive lung disease be demonstrated?

A

Peak expiratory flow rate

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7
Q

What are the normal values for PEFR?

A

Normal 400 – 600 litres/min Normal range is 80-100% of best value

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8
Q

What is a moderate fall in PEFR?

A

50-80% of best

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9
Q

What is a marked fall in PEFR?

A

<50% of best is a marked fall

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10
Q

What is FEV1, FVC, and PEFR in obstructive lung diseases?

A

There is AIRFLOW LIMITATION Peak Expiratory Flow Rate (PEFR) is reduced FEV1 is REDUCED FVC may be reduced FEV1 is less than 70% of FVC

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11
Q

What causes the decrease in diameter size in bronchial asthma?

A

Degranulation of mast cells and smooth muscle contraction (both reversible by use of drugs, or spontaneously)

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12
Q

What type of hypersensitivity is bronchial asthma?

A

Type 1

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13
Q

What physical substances obstruct airways in chronic asthma?

A

Oedema,

mucus,

plasma exudation

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14
Q

What are the aetiologies of chronic bronchitis and emphysema?

A

SMOKING

Atmospheric Pollution

Occupation : dust

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15
Q

What is the effect of smoking on alpha-1-antiprotease (antitrypsin)?

A

Malfuntion of antitrypsin (alpha-1-antiprotease) -= emphysema or COPD

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16
Q

What is the result of antitrypsin deficiency?

A
  • Neutrophil elastase is free to break down elastin, which contributes to the elasticity of the lungs.
  • Antitrypsin would normally protect tissues from enzymes of inflammatory cells, especially neutrophil elastase
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17
Q

How does FEV1 change with age?

A

Reduces

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18
Q

What is chronic bronchitis defined as clinically?

A

Cough productive of sputum most days in at least 3 consecutive months for 2 or more consecutive years

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19
Q

What does chronic bronchitis exclude?

A

TB Bronchiecstasis These may be confused with asthma

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20
Q

What is acute exacerbation of COPD?

A

Sudden worsening of COPD symptoms (shortness of breath, quantity and colour of phlegm) that typically lasts for several days. It may be triggered by an infection with bacteria or viruses or by environmental pollutants. Infection is most common cause (75%)

21
Q

How does the frequency of exacerbations change as the COPD progresses?

A

Exacerbations become more and more frequent

22
Q

What are the morphological changes in large airways in chronic bronchitis?

A

Mucous gland hyperplasia

Goblet cell hyperplasia

Inflammation

fibrosis (minor component)

23
Q

What are the morphological changes in small airways in chronic bronchitis?

A

Goblet cells appear

Inflammation

fibrosis in long standing disease

24
Q

What is the pathological definition of emphysema?

A

Increase beyond the normal in the size of airspaces distal to the terminal bronchiole arising from wither dilation or from destruction of their walls without obvious fibrosis. Loss in alveolar tissue, more space between alveoli.

25
Q

Define acinus

A

A region of the lung supplied with air from one of the terminal bronchioles

26
Q

Define centriacinar emphysema

A

Most common type of pulmonary emphysema mainly localized to the proximal respiratory bronchioles with focal destruction and predominantly found in the upper lung zones. This is because most material inhaled ends up here - max inflammation and destruction occurs here

27
Q

What is a secondary pulmonary lobule?

A

The subsegment of lung supplied by three to five terminal bronchioles and separated from adjacent secondary lobules by intervening connective tissue (interlobular septa)

28
Q

Define panacinar emphysema

A

Emphysema affecting all parts of the secondary pulmonary lobule, typically involving the inferior part of the lung and often asociated with a α1-antitrypsin deficiency.

29
Q

What is a Bulla?

A

Emphysematous space greater than 1 cm

30
Q

What is a bleb?

A

A Bulla just underneath the pleura

31
Q

What is the pathogenesis of Emphysema?

A

Smoking (Protease - Antiprotease imbalance) Ageing Alpha-1-antitrypsin deficiency

32
Q

How does antitrypsin deficiency affect this diagram?

A

Anti-elastase (anti-proteases are reduced)

33
Q

How does smoking affect this diagram?

A

Decrease in anti-elastase

Increase in Elastase and neutrophils and macrophages

Decrease in the activity of Repair mechanisms and Elastin synthesis

34
Q

What portion of COPD is reversible?

A

Smooth muscle tone and inflammation

35
Q

What are the normal reference ranges of PaO2 and PaCO2?

A
36
Q

What are the two types of respiratory failure?

A
37
Q

What are the common causes of Hypoxaemia?

A

Ventilation/perfusion imbalance

Diffusion impairment

Alveolar Hypoventilation

Shunt

38
Q

How does COPD involve V/Q mismatch, aveolar ventilation, diffusion impairment and shunt?

A

Airway obstruction

Reduced Respiratory Drive

Loss of alveolar surface area

Shunt only during acute infective exacerbation

39
Q

Why does pneumonia cause hypoxaemia?

A

Ventilation / perfusion abnormality (mismatch) - some ventilation of abnormal alveoli just not enough

Shunt - No ventilation of abnormal alveoli

40
Q

What is the commonest cause of hypoxaemia clinically?

A

LOW V/Q

41
Q

What is the normal percent of blood that is shunted?

A

2-4%

42
Q

What is meant by Shunt?

A

•Blood passing from Right to Left side of Heart WITHOUT contacting ventilated alveoli

43
Q

Why does shunt respond poorly to increase in FI O2?

A

•Blood leaving normal lung is already 98% saturated

44
Q

What is the effect of hypoventilation on PACO2 and PAO2?

A
  • Hypoventilation increases PACO2, and thus increases PaCO2
  • Increase in PACO2 decreases PAO2, which causes PaO2 to fall
45
Q

How do you correct a fall in PaO2 due to hypoventilation?

A

•Raising FIO2

46
Q

What causes physiological pulmonary vasoconstriction?

A

When alveolar oxygen tension falls

47
Q

How is Physiological pulmonary arteriolar vasoconstriction protective?

A

Do not send blood to alveoli short of oxygen

48
Q

What is cor pulmonale?

A

Hypertrophy of the RV resulting from disease affecting the function and/or structure of the lung

Except where pulmonary alterations are the result of diseases primarily affecting the left side of the heart or congenital heart disease

49
Q

What causes pulmonary hypertension?

A

Pulmonary vasoconstriction

Pulmonary arterioles - muslce hypertrophy and intimal fibrosis

Loss of capillary bed

Secondary polycthaemia

Y1Systems (24 decks)

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