Resp disease Flashcards

1
Q

What is asthma?

A
  • Intermittent episodes in which airway smooth muscle contracts strongly, markedly increasing airway resistance
  • Chronic inflammation of the airways, cause varies from person to person -includes allergy, viral infections, and sensitivity to environmental factors
  • This underlying inflammation makes the airways smooth muscles hyper responsive and causes them to contract strongly in response to certain stimuli
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2
Q

What stimuli do asthma sufferers have hyper responses to?

A

-exercise (particularly in cold, dry air)
-cigarette smoke
environmental pollutants
-viruses
-allergens
-normally released bronchoconstrictor chemicals
-other potential triggers

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3
Q

Therapy for asthma

A
  1. Anti-inflammatory drugs
    aim to reduce chronic inflammation and airway hyper responsiveness
    particularly leukotriene inhibitors and inhaled glucocorticoids
  2. Bronchodilator drugs
    relax airways to overcome excessive airway contraction
    or block action of broncoconstrictors
    eg, blocking of muscarinic cholinergic receptors which are involved in broncocontrciotn
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4
Q

What is Chronic Obstructive Pulmonary Disease? (COPD)

A

-Emphysema (destruction or enlargement of air spaces), chronic bronchitis (excessive mucus production and thickening of inflamed airways-causes obstruction) or a combination of the two
-Both caused by smoking
(bronchitis can also be acute due to viral infections, 2-3 weeks of excess sputum and phlegm production)

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5
Q

General structural and functional changes of the lung that occur with ageing

A
Decreased chest wall compliance
Decreased respiratory muscle strength
Decrease in elastic recoil
Decreased response to hypoxia and hypercapnia
Impaired gas exchange
Decreased immune system function
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6
Q

Describe the changes to the chest wall with ageing

A

Changes in the shape of the thorax - kyphosis increases with age
Costal cartilage calcification and stiffness

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7
Q

Describe the changes in the respiratory muscles with ageing

A

Skeletal muscles (intercostals)

  • Reduction in type 2A muscle fibres (fast - fatigue resistant)
  • Decrease in muscle mass
  • Denervation of type 2 fibres

Diaphragm

  • More slow fibres than intercostal muscles
  • Affected by poor nutritional status
  • Decreased power due to geometric changes to rib cage
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8
Q

Describe the changes in the lung parenchyma with ageing

A

LOSS OF ELASTIC RECOIL
Changes in the structure and function of collagen and elastin fibres - increased crosslinking
Elastin fibres in alveoli and respiratory bronchiole degenerate and rupture
Homogenous enlargement of the airspaces

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9
Q

Describe impaired gas exchange with ageing

A

Ventilation-perfusion mismatch increases

  • More areas which are ventilated but not perfused
  • More areas which are perfused but not ventilated

Reduction in alveolar surface area

Reduced lung capillaries and blood flow

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10
Q

Describe the impaired immunity that comes with ageing

A

Glandular epithelial cells decrease - less protective mucus
Decreased sputum clearance
Small airways collapse and aetlectasis
Immunoscenescence

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11
Q

Define respiratory failure.

A

Respiratory failure: is a syndrome in which the respiratory system fails in one or both of its gas exchange functions: oxygenation and carbon dioxide elimination. In practice, it may be classified as either hypoxemic, decreased CO2 (type 1) or hypercapnic, increased CO2 (type 2).

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12
Q

Define type 1 respiratory failure

A

Hypoxemic respiratory failure (type I) is characterized by an arterial oxygen tension (PaO2) lower than 60 mm Hg with a normal or low arterial carbon dioxide tension (Pa CO2).

⇒ This is the most common form of respiratory failure, and it can be associated with virtually all acute diseases of the lung, which generally involve fluid filling or collapse of alveolar units.
⇒ Some examples of type I respiratory failure are cardiogenic or noncardiogenic pulmonary edema, pneumonia, and pulmonary hemorrhage.

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13
Q

What can cause type 1 resp failure

A
  • Hypoventilation: breathing at an abnormally slow rate. This is caused by either; a defect anywhere along the respiratory control pathway, by severe thoracic cage abnormalities or by major obstruction of the upper airway.
  • Diffusion impairment: results from thickening of the alveolar membranes or a decrease in their surface area. In turn, it causes blood PO2 and alveolar PCO2 to fail to equilibrate. Often it is apparent only during exercise. e.g. in pneumonia or ARDS
  • A Shunt: an anatomical abnormality of the cardiovascular system that causes mixed venous blood to bypass ventilated alveoli in passing from the right side of the heart to the left side or an intrapulmonary defect in which mixed venous blood perfuses unventilated alveoli.
  • Ventilation-perfusion inequality: the most common cause of hypoxemia. It occurs in chronic obstructive lung diseases and many other lung diseases. This is when parts of the lung receive oxygen but not enough blood to absorb it e.g. in pulmonary embolism.
  • Low ambient oxygen: e.g. at high altitude
  • Diseases that damage lung tissue: pneumonia, pulmonary oedema, pulmonary fibrosis, athsma, pneumothorax, pulmonary embolism, pulmonary hypertension, bronchiectasis, obesity, ARDS (acute respiratory distress syndrome)
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14
Q

Define type II respiratory failure

A

Hypercapnic or type II respiratory failure is characterised by a PaCO2 higher than 50 mmHg or 6kPa.

  • Hypoxemia is also common in patients with type II respiratory failure who are breathing room air.
  • The blood pH depends on the level of bicarbonate, which depends on the duration that type II failure has been happening.
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15
Q

What can cause type II respiratory failure?

A
•	Common causes of type II respiratory failure:
¬	COPD
¬	Severe asthma
¬	Drug overdose, poisoning
¬	Myasthenia gravis
¬	Polyneuropathy
¬	Poliomyelitis
¬	Muscle disorders
¬	Head injuries and neck injuries
¬	Obesity
¬	Pulmonary oedema
¬	Adult respiratory distress syndrome
¬	Hypothyroidism
•	An increased PO2 means that peripheral chemoreceptors don’t respond to PCO2.
•	Hypercapnia causes pulmonary arteriolar constriction as alveolar hypoxaemia occurs.  This increases pulmonary vascular resistance which can increase the afterload for the right side of the heart – may induce right ventricular failure.
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