COPD Emphysema Flashcards

(14 cards)

1
Q

What is emphysema?

A

Irreversible damage to the airways and destruction of the alveolar walls due to long term inhalation of irritants

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2
Q

Explain the inflammatory response in emphysema

A

Inflammatory cells like neutrophils and macrophages release a number of inflammatory mediators such as proteases (specifically elastase - breaks down elastin and collagen in aleveolar walls) and leukotrienes (amplify inflammation). Proteases activity overwhelms anti proteases defense in lungs e.g. A1 antitrypsin and leads to overall destruction of alveolar walls and loss of recoil activity.

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3
Q

Why is there compromised surface area in the lungs due to emphysema?

A

The alveolar walls are destroyed, hence there is less surface area for efficient gas-exchange processes. There is also a loss of recoil in the alveoli and surrounding airways, so the lungs cannot effectively contract during exhalation, CO2 not completely exhaled, gas exchange impaired.

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4
Q

Why does the lungs hyper inflate?

A

Because the alveoli cannot effectively contract during normal exhalation, CO2 remains trapped within. Due to the natural anatomy of the pulmonary system, air is trapped distally, and the alveoli hyper inflates.

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5
Q

Is the capillary beds also destructed? Why?

A

The alveolar capillary is destructed along with the structural walls, meaning that pulmonary perfusion is now compromised and contributes to a ventilation-perfusion mismatch. This can lead to chronic hypoxaemia and possibly hypercapnia. Hypoxia can also occur.

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6
Q

Signs and symptoms of Emphysema

A

Chronic cough
Recurrent COPD exacerbations ; dyspnoea, sputum for 14+ days.
Bacterial resistance
Hypoxia
Barrel chest
Pursed-lip breathing
Fatigue
Cyanosis
Weight loss

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7
Q

What is salbutamol? (Ventolin, respigen)

A

A short acting B2 adrenergic agonist used to relieve bronchospasms in COPD

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8
Q

How does salbutamol work?

A

Salbutamol binds to B2 receptors in the smooth muscle of the bronchi. It activates an enzyme which increases cAMP, and relaxes the muscle. It reduces airway resistance for better exhalation as well as hyperinflation. It can improve gas-exchange

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9
Q

What are the common side effects of salbutamol?

A

Dry mouth - reduce saliva production (irritates mucus membrane)
Tachycardia - can stimulate B1 receptors in myocardium (more pumping)
Headache - vasodilation in cerebral blood vessels or shift of BP in brain
Anxiety - stimulation of parasympathetic nervous system
Hypokalaemia - stimulation promotes movement of potassium from bloodstream into cells (weakness, cramps)

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10
Q

What is the goal of giving O2 therapy to COPD patients?

A

Goal is to correct hypoxaemia - not underlying problem. Should not be given if SpO2 more than 92% on room air. Target 88-92% due to altered respiratory drive known as hypoxic drive

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11
Q

What is the hypoxic drive of a healthy respiratory system?

A

In healthy individuals, breathing is controlled by the central chemoreceptors in the medulla oblongata. The receptors detect the ph of CSF which changes in response to CO2 levels in blood. Increased CO2 = decreased pH. The brain then increases respiratory rate to exhale CO2 and restore pH

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12
Q

What is the hypoxic drive in COPD?

A

Due to impaired CO2 removal = hypercapnia. Chemoreceptors in medulla oblongata become desensitized to increased CO2 levels. Body then relies on peripheral chemoreceptors in carotid and aortic bodies to restore ph by responding to low PaO2 rather than PaCO2. When PaO2 below 60mmHg - receptors stimulate ventilation to increase O2 intake.

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13
Q

What will happen if you give too much O2 therapy?

A

As COPD patients rely on the hypoxic drive, giving too much O2 will reduce their overall ventilation. Decreased respiratory rate

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14
Q

Explain the pathological rationale of high Fowlers position;

A
  1. Improves diaphragmatic expansion - reduces abdominal pressure, diaphragm to descend more fully during inspiration increasing tidal volume and ventilation.
  2. Enhance lung expansion - gravity pulls lungs downwards. Lower lobes open, promoting better exhalation of CO2
  3. Promotes better V/Q matching - blood flow is better matched to ventilated areas of the lung improving arterial oxygenation (increasing PaO2)
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