Lung Structure & Function Flashcards

1
Q

What do alpha-1 (α-1) adrenoceptors concern?

A

Vascular (veins/artery etc.) smooth muscle contraction

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2
Q

What do alpha-2 (α-2) adrenoceptors concern?

A

Vascular (veins/artery etc.) smooth muscle contraction

Pre-junctional regulation of noradrenaline release

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3
Q

What do beta-1 adrenoceptors concern?

A

Heart rate
Force of contraction
(via the SA node/ventricles)

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4
Q

What do beta-2 adrenoceptors concern?

A

Airway smooth muscle - relaxation

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5
Q

What do beta-3 adrenoceptors concern?

A
Skeletal muscle
Adipose tissue (fat)
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6
Q

What muscarinic subtypes exist and what do they affect?

A

M-1; CNS, salivary glands, gastric glands
M-2; Heart rate, GI smooth muscle contraction, CNS
M-3; Salivary glands, GI smooth muscle, AIRWAY smooth muscle
M-4; CNS
M-5; CNS

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7
Q

How are the airways sympathetically innervated and what are the effects?

A

Via circulating adrenaline.

  • Act on beta-2 adrenoceptors on the bronchial smooth muscle (bronchodilation)
  • Inhibits release of inflammatory mediators from mast cells
  • Also act on beta-2 adrenoceptors present on mucus glands inhibiting secretion
  • Increases clearance of mucus.
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8
Q

How are the airways parasympathetically innervated and what are the effects?

A
Via acetylcholine (ACh).
- Activates muscarinic M-3 receptors, resulting in bronchoconstrictoin and increased mucus secretion.
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9
Q

How do sensory nerves innervate the airways?

A

Local reflexes; response to irritants.
- Causes coughing/bronchoconstriction/increased mucus secretion; protective responses to try and rid of foreign particles

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10
Q

What is the role of sensory nerves in exercise-induced asthma?

A

Water loss from airways during exercise stimulates release of mediators (inflammatory cytokines) which activate sensory nerves; sensory nerves hypersensitive in asthmatics (upregulation; greater response to stimulus)

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11
Q

What can cause breathlessness in general?

A
  • Congenital (from birth) conditions e.g. cystic fibrosis
  • Infection e.g. chest infection/TB
  • Inflammation e.g. asthma/anaphylaxis
  • Cancer
  • Psychological e.g. panic attack
  • Degeneration of lung e.g. COPD
  • Cardiac e.g. heart failure
  • Pulmonary embolism (blood clot in lung)
  • Pregnancy/obesity/altitude
  • Side effect of drugs e.g. beta-blockers, NSAIDs
  • Seeing Eve Duke
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12
Q

What is rhythm of normal breathing known as?

A

Eupnoea.

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13
Q

How is breathing in/inspiration coordinated?

A
  • Diaphragm contracts and expands the thoracic cavity
  • Decreasing pressure causing air to flow into airways
  • External intercostal muscles contract and pull rib cage upwards and outwards (with deep and heavy breathing)
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14
Q

How is breathing out/expiration coordinated?

A
  • During rest, expiration is passive; diaphragm relaxes and rib cage falls
  • During forced expiration (e.g. exercise); internal intercostal muscles contract and pull rib cage inwards
  • Abdominal muscles also contract reducing thoracic volume
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15
Q

What is airway resistance, give two examples.

A
  • The opposition to airflow in the respiratory tree (depends on friction/airway cross section)

E.g.:

  • Contraction of airway smooth muscle leading to bronchoconstriction
  • Increased growth of smooth muscle (remodelling) reducing the size of lumen (e.g. asthma/COPD)
  • Excess mucous production e.g. chronic bronchitis
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16
Q

What is compliance (in relation to the airways)?

A

Indication of ability of lungs to stretch

17
Q

What is elastance?

A

Ability of lung to recoil

18
Q

What is fibrosis’ compliance/elastance?

A

In fibrosis the lungs are stiff:

  • low compliance (difficult to stretch)
  • high elastic recoil (returns to resting position quick)
19
Q

What is FVC?

A

Forced Vital Capacity; difference between deep inward and deep outward breath

20
Q

What is VT?

A

Tidal volume; difference between normal inhalation and exhalation

21
Q

What is TLC and why cannot it be measured accurately?

A

Total lung capacity; lung cannot be emptied fully though.

22
Q

What is the difference in FVC (forced vital capacity) for obstructive disease and restrictive?

A

Obstructive (COPD/asthma):
- Decreased or normal (may be normal if all air can be expelled but bronchoconstriction)

Restrictive (fibrosis):
- Decreased (cannot fill lungs with air)

23
Q

What is the difference in FEV1 (forced expiratory volume in 1 second) for obstructive disease and restrictive?

A

Obstructive (COPD/asthma):
- Decreased (lower as air comes out slower due to narrower lumen)

Restrictive (fibrosis):
- Decreased or normal

24
Q

What is the difference in FEV1/FVC ratio for obstructive disease and restrictive?

A

Obstructive (COPD/asthma):
- Decreased (FEV1 is decreased but FVC is normal)

Restrictive (fibrosis):
- Normal (both FEV1 and FVC are decreased thus normal)

25
What is the difference in TLC for obstructive disease and restrictive?
Obstructive: Normal Restrictive: Decreased
26
What influences Peak Expiratory Flow (PEF) readings?
Constriction of the airways reduces peak flow.
27
What is respiratory acidosis?
An increase in H+ in the blood due to a build of CO2 via impaired expiration (from reduction in lung function); CO2 reacts with H2O to give H2CO3 which yields H+ and HCO3-.
28
How does the body compensate for respiratory acidosis?
Hb in RBCs buffer the intermediate H2CO3 (carbonic acid) so that it doesn't dissociate to H+ (and HCO3-), instead yielding increased HCO3- (thus increasing pH back to norm). Hyperventilation occurs to limit hypoxia and rid of CO2, leads to alkalosis (like hyperexcitation).
29
How does the body limit hyperventilation?
Body detects drop in PCO2 (partial pressure CO2) thus limits/inhibits ventilation to limit hyperventilation
30
What response do the lungs have with diabetes?
Metabolic acidosis occurs w/diabetes where the drop in pH is revered via stimulation of ventilation (to lower blood PCO2)
31
How does vomiting affect breathing?
Metabolic alkalosis occurs, thus ventilation is depressed.