Pathology of obstructive lung disease Flashcards

1
Q

What is Chronic Obstructive Pulmonary disease? (COPD)

A

Chronic bronchitis and emphysema occurring together

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2
Q

What is FEV1?

A

FEV1 is the Forced Expiratory Volume of air exiting the lung in the first second of this exercise.
Usually about 70-80% of FVC
Normally about 3.5-4 L

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3
Q

What is FVC?

A

FVC is the Final Total amount or air expired
Normal FVC is 5 L

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4
Q

What is the normal ratio of FEV1:FVC?

A

0.7-0.8

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5
Q

Give the negative characteristics of obstructive lung disease?

A

-there is airflow limitation
- peak expiratory flow rate is reduced
-FEV1 is reduced
-FVC may be reduced
-FEV1 is less than 70% of FVC

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6
Q

What are the two mechanisms of reduction of the luminal cross-sectional area of the airways?

A

type 1 hypersensitivity in lungs- orchestrated by the granulation of mast cells in our airways.
Degranulation of mast cells releases lots and lots of different chemical factors which orchestrates an inflammatory response in the airways.
De granulation of mast cells also releases substances which cause smooth muscle to contract either very quickly or sometimes very slowly.
Cross sectional area of that airway will reduce and that will cause airflow limitation.

The evolution of that inflammatory response with lots of lots of inflammatory cells and perhaps fluid and oedema causes swelling of the bronchial mucosa.
This also reduces the cross sectional luminal area of the airways that are affected.

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7
Q

Why is bronchial asthma considered to be reversible?

A

bronchial smooth muscle contraction and inflammation can both be modified by drugs

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8
Q

What are the factors of COPD?

A
  • common factor is irritation (inhalation of substances that cause irritation to the airway)
    tobacco smoking
    atmospheric pollution
    dust
    -effect of age and susceptibilty
    -more common in men as men tend to smoke more
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9
Q

What is the rare cause of emphysema that is an enzyme deficiency?

A

Alpha-1-antiprotease (antitripsin) deficiency

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10
Q

How is chronic bronchitis defined clinically?

A

Cough productive of sputum most days over a period of three consecutive months for two or more consecutive years

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11
Q

What is chronic bronchitis clinically confused for?

A

chronic bronchial asthma

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12
Q

What is an infective exacerbation of chronic bronchitis?

A

when sputum turns mucopurulent -turns yellow or green (acute infective exacerbation)

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13
Q

What is complicated bronchitis?

A

When FEV1 begins to fall

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14
Q

Describe the morphological changes in the large airways in chronic bronchitis?

A

-mucous gland hyperplasia
-goblet cell hyperplasia
-inflammation and fibrosis is a minor component

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15
Q

Describe the morphological changes in the small airways in chronic bronchitis?

A

-goblet cells appear
-inflammation and fibrosis in long standing disease

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16
Q

How is emphysema defined?

A

Increase beyond the normal in the size of airspaces distal to the terminal bronchiole arising either from dilatation or from destruction of their walls and without obvious fibrosis

17
Q

Describe centriacinar emphysema?

A

the loss of the alveolar tissue occurs in the middle of the acinus

18
Q

Where does centricacinar emphysema predominantly occur?

A

in apical parts of the upper and lower lobes

19
Q

Describe panacinar emphysema?

A

predominantly occurs in the basal parts of the lung and it’s a complete wipe out
-all of the alveolar walls in the affected acinus are wiped out

20
Q

Describe periacinar emphysema?

A

when emphysema develops at the edges of the acini and not in middle
-aini against pleura get spaces underneath the pleura
-associated with smoking and genetics (tall young people)
-if “blebs” pop and leak- get a pneumothorax

21
Q

How do patients with chronic bronchitis and emphysema find it easier to breathe?

A

find it easier to breathe in and out by retaining a lot of air in their lungs and therefore develop hyper inflation

22
Q

Describe the pathogenesis of emphysema?

A
  • smoking
  • protease - antiprotease imbalance
    ageing
    alpha -1 -antitrypsin deficiency
23
Q

What are anti proteases for?

A

to protect our lungs against the effect pf our inflammatory cell proteases
-when balance is maintained the elastin and the other structural proteins in the lung tissue are safe

24
Q

What happens if you have alpha 1 antitrypsin deficiency?

A

don’t have the anti-proteases and may have severe emphysema

25
Q

Why would smoking contribute?

A

various compounds in tobacco smoke which negate the function of the anti proteases. Increase proteases and inflammatory cells - tissue destruction.

26
Q

Do patients with COPD get drugs to make them feel better?

A

the contracting of the small airways muscle and inflammation may be reversed

cant reverse fibrosis or emphysema (likely contributes most to airflow limitation by loss of alveolar tissue that surrounds terminal and respiratory bronchioles)

27
Q

What is hypoxia?

A

a reduction in the concentration of oxygen in the alveoli distal to that obstruction

28
Q

What are the causes of hypoxaemia in COPD?

A

airway obstruction - poor ventilation of alveoli
reduced respiratory drive - IMPORTANT
loss of alveolar surface area
shunt - only during severe acute infection

28
Q

Describe physiological pulmonary arteriolar vasoconstriction?

A

blood vessels carrying blood to areas of lung that are hypoxic constrict and therefore limit the amount of blood that goes to the well less oxygenated area of the lung

29
Q

What is pulmonary hypertension a result of?

A

Pulmonary vasoconstriction
Pulmonary arterioles
-muscle hypertrophy and intimal fibrosis
if lost aveolar tissues -Loss of capillary bed
Secondary polycythaemia – increased blood viscosity- heart trying to pump more viscous blood through fewer blood vessels that are narrower than normal
Bronchopulmonary arterial anastamoses

29
Q

What happens if you’re globally hypoxic and when all of your pulmonary arterials constrict?

A

nowhere for blood to go and more stress put on RHS of heart and RHS suffers badly.
Pulmonary hypertension

30
Q

What is hypoxic cor pulmonale?

A

heart disease because of a lung disease thats causing hypoxia

30
Q

Why is pulmonary artery pressure lower than pressure in aorta?

A

vascular resistance in lungs is very low, much lower than systemic vascular resistance. Therefore pulmonary artery pressure is much lower than the pressure in the aorta because you don’t in normal situation as much pressure to make the blood flow through your lungs.

30
Q

What happens to patients with longstanding hypoxic cor pulmonale?

A

the strain RHS of heart causes muscle bunk in right ventricle to increase and eventually it fails

31
Q
A