Receptors and autonomic regulation of airways Flashcards

1
Q

Where are peripheral chemoreceptors located? In intimate with what?

A

High in the neck at the bifurcation of the common carotid arteries and on the aortic arch= carotid and aortic bodies.
Arterial blood

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2
Q

Peripheral chemoreceptors are composed of specialised receptor cells stimulated by what? What cells are located here and on hypoxia do what? Provide synaptic input to what?

A

Decrease in arterial partial pressure of oxygen and increase in arterial H+ conc.
Released stored neurotransmitters that stimulate the carotid sinus nerve.
Medullary inspiratory neurons

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3
Q

Peripheral chemoreceptors fire when O2 comes close to what value? Haemoglobin what % saturated? Also doesn’t occur when?

A

60mmHg. 90%.

With CO in the blood- does not affect amount of O2 dissolved in blood/ diffusion capacity of the lung.

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4
Q

Where are central chemoreceptors located? Provide excitatory synaptic input to what? Stimulated by what?

A

In the medulla
The medullary inspiratory neurons
Increase in H+ conc of CSF in brain (CO2 diffuses readily and blood partial CO2 pressure can influence CSF pH enabling detection of H+ changes)

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5
Q

Reflex mechanisms controlling ventilation prevent small increases in arterial partial CO2 pressure compared to what? Ventilatory drive extremely sensitive to what?

A

To a much greater degree than they prevent equivalent decrease in arterial partial O2 pressure
Changes in arterial partial CO2 pressure of blood entering brain

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6
Q

Central chemoreceptors account for what % of increased ventilation?

A

70% compared to peripheral chemoreceptors

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7
Q

The nose, nasopharynx and larynx contain what receptor types? Stimulation does what?

A

Chemo and mechanical receptors- some appear to sense and monitor flow.
Inhibit the medullary respiratory centre.

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8
Q

Pharynx has receptors activated by what action? Respiratory activity stops when?

A

Swallowing

During swallowing to protect against risk of aspiration of food/liquid

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9
Q

Where are parasympathetic ganglia located in relation to their targets? What about sympathetic ganglia?

A

Near to with short post-ganglionic nerves.

Near the spinal cord with longer post- ganglionic fibres.

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10
Q

Bronchconstrictor response controlled by what NS?

A

Parasympathetic- vagus nerve neurons terminate in parasympathetic ganglia in airway wall

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11
Q

Neurotransmitter in parasympathetic NS innervating vasculature, glands and airways in lungs? Interacts with what receptors?

A
ACh
Muscarinic (M3) cholinergic receptors on muscle to provide intrinsic muscle tone
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12
Q

Neurotransmitter in sympathetic NS? Innervates lung via what? Innervates what?

A

Noradrenaline
Sympathetic trunk
Vasculature and glands- not the airways

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13
Q

Noradrenaline is released where to? Releases what? Binds to what receptors on muscles of airways? Leads to what process?

A

Adrenal glands– adrenaline released from adrenal medulla– binds to beta-2-adrenareceptors– bronchodilator.

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14
Q

Neurons releasing ACh called what? Degenerate in what disease?

A

Cholinergic receptors

Alzeimer’s disease

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15
Q

Nicotinic receptor responds to what neurotransmitters? Stimulated by what NS? Found where? Has ligand-gated channel permeable to what ions?

A

ACh and nicotine
Para and sympathetic but mainly parasympathetic
In post-ganglionic neurons and neuro-muscular junction
Na+ and K+ ions- opening results in depolarisation

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16
Q

Neurons that released Nad are called what?

A

Adrenergic receptors

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17
Q

Drugs that inhibit bronchoconstriction blocks what receptor? Called what?Used in what conditions?

A

M3 receptor= anti-cholinergic/ anti-muscarinic.

Asthma and COPD

18
Q

Drugs acting as bronchodilators? Pros of LAMAs compared to ipratropium?

A

LAMAs and ipratropium- LAMAs more widely used, long duration, reduce acute attacks and regulates mucus production too.

19
Q

How does activation of beta-2 receptors on airway smooth muscle cause relaxation? Dip in what hormone in morning causes common asthma attacks?

A

Activates adenylate cyclase, raising cyclic AMP.

Cortisol

20
Q

What two drug types are beta-2 agonists and assist in bronchodilator? Given with what in asthma? Not given with steroids in what condition?

A

SABAs and LABAs (short-acting and long-acting beta-2 agonists)
Steroids
COPD

21
Q

What is affinity in relation to receptors? Shown by what 2 things?

A

The degree to which a particular messenger binds to its receptor.
Antagonists and agonists.

22
Q

What is efficacy? High efficacy agonist results in what? Low efficacy agonist results in what? Antagonist results in what?

A

How well a ligand activates a receptor.
Large change in receptor shape when bound
Small change in receptor change when bound
No conformational change to receptor shape when bound

23
Q

Examples of SABAs? Lasts for how long?

Examples of LABAs? Lasts for how long?

A

Salbutamol and terbutaline
4 hours
Salmeterol and formoterol
12 hours

24
Q

Example of short acting muscarinic antagonists?

Long acting?

A

Ipratropium

Tiotropium

25
Q

Where are slowly adapting stretch receptors (SASR’S) found? What do they do?
Activated by what?

A

In airway smooth muscle.
Maintain a persistent/ slowly decaying receptor potential during constant stimulus initiating action potentials in afferent neurons for the duration of the stimulus.
By lung distension

26
Q

What feature do SASR’S have? High activity does what? If initiation is maintained what happens?

A

They are myelinated.
Inhibits further inspiration, thus beginning expiration.
They slowly adapt to low frequency firing.

27
Q

Where are rapidly adapting stretch receptors (RASR’S) found? What do they do? Activated by what?

A

Between airway epithelial cells.
Generate a receptor potential and action potentials at the onset of a stimulus but very quickly cease responding.
Lung distension and irritants.

28
Q

Two types of pulmonary stretch receptors?

A

Slowly adapting and rapidly adapting stretch receptors.

29
Q

Feature of RASR’S? Produce what?

High activity causes what? Might be involved in what?

A

They are myelinated.
Brief burst of activity.
Bronchoconstriction.
The cough reflex

30
Q

Where are C-fibre J receptors found? What are they stimulated by? Can happen when?

A

In the capillary walls or the interstitium of the lungs.
By an increase in lung interstitial pressure caused by collection of fluid in the interstitium.
During vascular congestion caused by pulmonary embolism/ left ventricular heart failure and strenuous activity.

31
Q

Activity of J receptors results in what? Neural input from J receptors gives rise to what?

A
Rapid breathing (tachypena), shallow breathing, bronchoconstriction, cardiovascular depression and a dry cough. 
Sensations of pressure in the chest and dyspnea- laboured/ difficult breathing.
32
Q

Most common form of hypoxia? 4 most common causes?

A

Hypoxemia- arterial partial O2 pressure is reduced.

1) Hypoventilation
2) Diffusion impairment
3) Shunting
4) Ventilation- perfusion mismatch

33
Q

What does hypoventilation result in? Failure to do what adequately? Caused by what?

A

Increased arterial partial CO2 pressure.
Failure to ventilate alveoli.
Muscular weakness, obesity and loss of respiratory drive.

34
Q

Diffusion impairment results from what? Caused by what?

A

Thickening of alveolar membranes or decrease in SA- blood and alveolar partial O2 pressures fail to equilibrate.
Pulmonary oedema, anemia, interstitial fibrosis(between alveolus and capillaries, connective tissue thickened.)

35
Q

What is shunting? Can also occur where?

A

Mixed venous blood to bypass ventilated alveoli in passing from right side of heart to left side e.g. ventricular septal defect (VSD)
In bronchial arteries- venous blood perfuses unventilated alveoli.

36
Q

Most common cause of hypoxemia? Occurs in what? What occurs to arterial partial CO2 pressure? Caused by what?

A

Ventilation- perfusion mismatch. COPD and other lung disease.
May be normal/ increased.
A pulmonary embolus, asthma, pneumonia and pulmonary oedema.

37
Q

What is hypercapnia? Caused by what? Sometimes caused by what?

A

CO2 retention and increased arterial partial CO2 pressure.
Hypoventilation.
Ventilation-perfusion mismatch

38
Q

Partial CO2 and O2 pressures in type 1 respiratory failure? Most common cause of type 1?

A

Low pO2 and low/ normal pCO2.

Pulmonary embolism– hypoxia.

39
Q

Partial CO2 and O2 pressure in type 2 respiratory failure? Cause of type 2?

A

Low pO2 but high pCO2.

Hypoventilation

40
Q

Two circulations in lungs? Pulmonary receives what % of cardiac output? Bronchial receives % of left ventricular output?

A

Pulmonary and bronchial.
100%
2%

41
Q

Vessel wall thickness in pulmonary circulation? Muscularisation and redistribution?

A

Thin. Minor muscularisation and no need for redistribution.

42
Q

Vessel wall thickness in systemic circulation? Muscularisation and redistribution? Pressure difference between systemic and pulmonary?

A

Thick. Significant muscularisation and redistribution is required.
Systemic is much higher.