Obstructive Pulmonary Diseases Flashcards

1
Q

What is the normal FEV1? (In litres)
What is the normal FVC?
What is the normal FEV1/FVC ratio?

A
FEV1 = 3.5-4 litres
FVC = 5 litres
FEV1/FVC = 0.7-0.8 (70%)
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2
Q

When testing peak expiratory flow rate, what sit the normal rate?

A

400-600 litres/min

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3
Q

Describe briefly what chronic bronchitis is.

A

Excessive production of mucous causing a cough.

Cough for most days in at least 3 months for 2 consecutive years.

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4
Q

What is complicated chronic bronchitis?

A

In complicated chronic bronchitis the sputum is mucopurulent - infected

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5
Q

Describe what emphysema is.

A

Emphysema is an increase in the size of the airways distal to the terminal bronchioles due to the destruction of their walls.
There is loss of alveolar wall attachment and elasticity which reduces their tendency to recoil. This causes the airways to collapse on expiration.
There is loss of lung tissue with no obvious fibrosis

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6
Q

Name and describe the different forms of emphysema.

A

Emphysema is named according to where it occurs in the acinar (distal part of the terminal bronchiole)
Centriacinar = center of acinus. Peripheral parts stay in tact. Occurs at the upper zones of the lobes.
Panacinar - whole of acinar structure is lost. Occurs at the lower parts of the lobes. This is found when people get emphysema due to alpha 1 anti trypsin deficiency.
Periacinar - holes in peripheral pats of acinus. Bullae just under the pleura (emphysematopus space) which have tendency to pop which causes pneumothorax.

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7
Q

In emphysema, is the TLC increased or decreased or unchanged and why?

A

Total lung capacity is increased in patients with emphysema.
The loss of elastic recoil results in an increase in total lung capacity in order to prevent airways from collapsing. Premature closure of airways limits expiratory flow. However the loss of alveoli surface area decreases the capacity for gas transfer.

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8
Q

State the mechanisms of airway obstruction in COPD.

A

Smooth muscle contraction
Loss of alveolar wall attachment
Inflammation
Fibrosis

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9
Q

What are the causes of hypoxaemia in patients with COPD?

A

Airway obstruction
Reduced respiratory drive
Loss of alveolar surface area
Only during acute infective exacerbation

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10
Q

Describe how reduced respiratory drive can cause hypoxaemia.

A

In patients with COPD, they may be living with borderline increased CO2 levels and very low 02 levels due to ventilation/perfusion mismatch. However due to the long term C02 levels, they become desensitised to it. Therefore when C02 crosses the BBB and dissociates into HC03 and H+ , the receptors don’t detect the increased H+ levels in the CFS to increase ventilation to counteract the rise in C02. (Which is the main ventilatory drive)
In these patients, they rely on hypoxia as their main ventilatory drive.

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11
Q

What do patients who have COPD and rely on hypoxaemia as their main ventilatory drive present with?

A

They wont be as breathless
Due to renal hypoxia, they will retain fluid and increase in erythrocytes production (leading to polythaemia).
They will appear bloated and blue due to being cyanotic.

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12
Q

Describe type 2 respiratory failure.

A

Type 2 respiratory failure is due to C02 retention
Its due to a problem with the ventilation not the lungs (hypoventillation)
There is a drop in Pa02 and an increase in PaCO2

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13
Q

Describe what cor pulmonale is.

A

May occur in patients with COPD who have hypoxia.
It causes hypertrophy of the right ventricle because it needs to work harder to pump blood through the part of the lung which is damaged / hypoxic.
This is due to:
Hypoxaemia which causes vasoconstriction of the pulmonary arterioles which increases the pulmonary arterial pressure.
Pressure also increases because hypoxia increases RBC formation (erythropoeitin) so blood becomes more viscous. It causes a loss of lung tissue as there are few blood vessels to provide the lung with oxygen to perfuse it.

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14
Q

What are the main pathophysiological finding in patients with COPD?

A

Hyperplasia of mucous secreting goblet cells
Infiltration of inflammatory neutrophils and CD8+ lymphocytes
Thickening of the alveolar walls
Loss of interstitial support (alveolar attachment)

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15
Q

what type of hypersensitivity reaction is asthma?

A

type 1

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16
Q

how does specific triggers cause smooth muscle contraction and chronic inflammation in asthma?

A

specific triggers cause mast cell degranulation

this releases chemotactic factors and spasmogens i.e. histamine

17
Q

what immunoglobulin is a trigger of asthma response ?

A

IgE

18
Q

which component of COPD is without obvious fibrosis?

A

emphysema

19
Q

what is elastase produced from?

A

inflammatory cells

20
Q

what is the function of elastase (protease) ?

A

it causes tissue destruction which destroys the rapid mechanisms of the lungs and stops elastin synthessis.
this results in inelastic lungs

21
Q

what 4 abnormal states are associated with hypoxaemia?

A

V/Q mismatch
shunt
alveolar hypoventillation
diffusion impairement

22
Q

what is the normal V/Q ratio?

A

4/5 or 0.8

cardiac output = 5l/min and breathing = 4l/min

23
Q

what is cor pulmonale?

A

hypertrophy of the right ventricle resulting from disease affecting the function and/or structure of the lung

24
Q

why does cor pulmonalre result in pulmonary hypertension?

A

pulmonary vasoconstriction
pulmonary arterioles smooth muscle hypertrophy and intimal fibrosis
loss of capillary bed
secondary polycythaemia