Lung Structure & Function Flashcards

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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
Q

What is the difference in TLC for obstructive disease and restrictive?

A

Obstructive: Normal

Restrictive: Decreased

26
Q

What influences Peak Expiratory Flow (PEF) readings?

A

Constriction of the airways reduces peak flow.

27
Q

What is respiratory acidosis?

A

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
Q

How does the body compensate for respiratory acidosis?

A

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
Q

How does the body limit hyperventilation?

A

Body detects drop in PCO2 (partial pressure CO2) thus limits/inhibits ventilation to limit hyperventilation

30
Q

What response do the lungs have with diabetes?

A

Metabolic acidosis occurs w/diabetes where the drop in pH is revered via stimulation of ventilation (to lower blood PCO2)

31
Q

How does vomiting affect breathing?

A

Metabolic alkalosis occurs, thus ventilation is depressed.