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BFCBP Respiratory Pharmacology > The Neurohumoral Control of the Airways > Flashcards

The Neurohumoral Control of the Airways Flashcards

1
Q

Where are cell bodies of the preganglionic fibres which control the airways located?

A

In the brainstem.

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2
Q

Where are cell bodies of postganglionic fibres which control the airways located?

A

In the walls of the bronchi and bronchioles.

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3
Q

What is the effect of stimulation of postganglionic parasympathetic cholinergic fibres on muscle in the airways? What receptors mediate this?

A

This causes bronchial smooth muscle to contract.

Mediated by M3 muscarinic ACh receptors.

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4
Q

What is the effect of stimulation of postganglionic parasympathetic cholinergic fibres on mucus secretion in the airways? What receptors mediate this?

A

This causes increased mucus secretion.

Mediated by M3 muscarinic ACh receptor on ASM cells.

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5
Q

What is the effect of stimulation of noncholinergic (nitrergic) fibres on muscle in the airways? What two substances mediate this?

A

This causes bronchial smooth muscle to relax.

Mediated by nitric oxide (NO) and vasoactive intestinal peptide (VIP).

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6
Q

Is bronchial smooth muscle innervated by sympathetic nerves in humans?

A

No.

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7
Q

What do post-ganglionic sympathetic fibres innervate instead of the bronchial smooth muscle?

A

Submucosal glands and smooth muscle of the blood vessels.

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8
Q

What is the effect of stimulation of the sympathetic division on bronchial smooth muscle? What mechanism causes this?

A

Bronchial smooth muscle relaxation.

Occurs via beta(2)-adrenoceptors on ASM cells activated by adrenaline released from the adrenal gland.

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9
Q

What is the effect of stimulation of the sympathetic division on mucus secretion in the airways? What is this mediated by?

A

Decreased mucus secretion.

Mediated by beta(2)-adrenoceptors on epithelial cells (mucociliary escalator).

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10
Q

What is the effect of stimulation of the sympathetic division on vascular smooth muscle supplying the airways? What is this mediated by?

A

Vascular smooth muscle contraction.

Mediated by alpha(1)-adrenoceptors on vascular smooth muscle cells.

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11
Q

What G protein pathway is stimulated by parasympathetic stimulation of the airway smooth muscle?

A

G(q/11).

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12
Q

What steps follow on from stimulation of the G(q/11) pathway?

A
  1. PLC (phospholipase C) activity increased which converts PIP(2) to IP(3).
  2. IP(3) acts on IP(3) receptors in the SR membrane - this opens a channel allowing calcium efflux.
  3. This calcium efflux results in muscle contraction.
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13
Q

Describe the steps leading up to myosin light chain kinase (MLCK) activation.

A
  1. Calcium bind to calmodulin, to form Ca(2+)-calmodulin.

2. Ca(2+)-calmodulin activates MLCK.

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14
Q

What does active myosin light chain kinase (MLCK) do? What does this require?

A

Phosphorylates the inactive myosin cross bridge such that it can bind actin.

Requires ATP.

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15
Q

What filaments slide across each other to generate the force of muscle contraction?

A

Actin and myosin filaments.

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16
Q

Phosphorylation of what results in muscle contraction?

What intracellular conditions are required for this?

A

The myosin light chain (MLC) (by myosin light chain kinase).

The presence of calcium ions and ATP.

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17
Q

Dephosphorylation of what results in muscle relaxation What enzyme mediates this?

A

The myosin light chain (MLC).

This is mediated by myosin phosphatase.

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18
Q

How do the activities of myosin light chain kinase (MLCK) and myosin phosphatase compare?

A

Their activities oppose each other.

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19
Q

What intracellular conditions results in the rate of MLC phosphorylation exceeding the rate of its dephosphorylation?

A

Elevated intracellular calcium ion concentration.

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20
Q

What change in intracellular conditions is required for relaxation to occur? How is this achieved?

A

Relaxation requires the return of intracellular calcium concentration to basal level.

This is achieved by primary and secondary active transport.

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21
Q

What G protein pathway is stimulate by beta(2)-adrenoceptor activation by adrenaline?

A

The G(s) pathway.

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22
Q

What steps follow on from the stimulation of the G(s) pathway?

A
  1. Stimulation of adenyl cyclase (AC) to convert ATP to cAMP.
  2. cAMP stimulates protein kinase A (PKA).
  3. PKA phosphorylates both myosin light chain kinase and myosin phosphatase, inhibiting the former and stimulating the latter.
  4. This causes relaxation of bronchial smooth muscle.
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23
Q

What does phosphodiesterase (PDE) do?

A

Degrades cAMP to 5’ AMP.

24
Q

What percentage of the population of industrialised countries is affected by asthma?

A

5-10%.

25
Q

What is asthma?

A

A recurrent and reversible (in the short term) obstruction to the airways.

26
Q

Describe two unusual things about the substances/stimuli that can trigger airway obstruction in asthma.

A
  1. They are not necessarily noxious.

2. They normally do not affect non-asthmatic subjects.

27
Q

List some of the many numerous causes (“triggers”) of asthma attacks.

A
  1. Allergens (in atopic individuals).
  2. Exercise (cold, dry air).
  3. Respiratory infection (e.g. viral).
  4. Smoke, dust, environmental pollutants etc.

These are just some of the triggers, which vary from individual to individual.

28
Q

What is the medical term for acute severe asthma (a medical emergency) and how many people die per year in the UK from this?

A

Status asthmaticus.

~2000 deaths per annum in the UK.

29
Q

What are the four main symptoms during intermittent attacks of bronchospasm during asthma?

A
  1. “Tight chest”.
  2. Wheezing.
  3. Difficulty in breathing.
  4. Cough.
30
Q

What are the five pathological changes which can result from long standing airway inflammation?

A
  1. Increased mass of smooth muscle (hyperplasia and hypertrophy).
  2. Accumulation of interstitial fluid (oedema).
  3. Increased secretion of mucus.
  4. Epithelial damage (exposing sensory nerve endings).
  5. Sub-epithelial fibrosis.
31
Q

What is the effect of airway narrowing by inflammation and bronchoconstriction on FEV1 and PEFR?

A

FEV1 and PEFR both decreased.

Makes sense from physiology teaching - smaller radius of conducting airway so flow greatly reduced.

32
Q

What as a result of inflammation in asthma contributes to increased sensitivity of the airways to bronchoconstrictor influences?

A

Epithelial damage which exposes sensory nerve endings (C-fibres, irritant receptors).

33
Q

What two components make up bronchial hyperresponsiveness?

A
  1. Hypersensitivity to bronchoconstrictors.

2. Hyperreactivity to bronchoconstrictors.

34
Q

What are two types of inhaled bronchoconstrictors (spasmogens) used in provocation tests for asthma and what receptors are activated by these?

A
  1. Histamine, by activating ASM H(1) receptors.

2. Methacholine, by activating ASM M(3) receptors.

35
Q

Describe what happens to the curve of fall in FEV1 against the concentration of inhaled bronchoconstrictor in hypersensitivity.

A

Leftward shift in curve.

36
Q

Describe what happens to the curve of fall in FEV1 against the concentration of inhaled bronchoconstrictor in hyperreactivity.

A

Curve much steeper.

i.e. small increase in concentration inhaled results in much larger fall in FEV1 than in a normal subject.

37
Q

What is the difference in the components of hyperresponsiveness in patients with mild asthma versus more severe asthma?

A

In mild asthma, hypersensitivity and hyperreactivity are both present.

However, in severe asthma both of these are to a much greater degree with much more severe hypersensitivity in many cases.

38
Q

What do the immediate and late asthma attack phases consist of?

A

Immediate - mainly bronchospasm, a type I hypersensitivity reaction,.

Late - inflammatory reaction, a type IV hypersensitivity reaction.

39
Q

What does exposure to an allergen and subsequent phagocytosis by an APC (dendritic) cell result in in non-atopic individuals?

A

A low-level TH1 response. This is a cell mediated immune response involving IgG and macrophages.

40
Q

What does exposure to an allergen and subsequent phagocytosis by an APC (dendritic) cell result in in atopic individuals?

A

A strong TH2 response. This is an antibody-mediated immune response involved IgE.

41
Q

What is the hygiene hypothesis?

A

This posits that a hygienic “Western lifestyle” drives TH cells towards differentiation into TH2 cells whereas exposure early in life to microbes favours a TH1 response.

42
Q

What T(H) cell response predominates in mild to moderate asthma? Is severe asthma the same?

A

In mild, to moderate, asthma, a TH2 response predominates.

In severe asthma, a TH1 response also contributes.

43
Q

What type of immune response does initial presentation of an antigen initiate in allergic asthma?

A

An adaptive immune response.

44
Q

How is the immune system initially presented a captured aeroallergen antigen by an APC?

A

It is presented bound to a major histocompatibility complex (MHC) class II protein.

45
Q

What type of immune cell does an APC initially present a captured aeroallergen antigen to? What response does this bring about?

A

A CD4+ T cell.

This brings about maturation of this cell into a TH0 cell.

46
Q

What do TH0 cells preferentially mature into? Why are these preferred?

A

TH2 cells.

As they produce a “cytokine environment”.

47
Q

Via which two methods do TH2 cells activate B cells?

A
  1. Production of IL-4 cytokines.

2. By binding to B cells directly.

48
Q

What happens to B cell upon their activation?

A

They divide to produce memory B cells and effector (plasma) cells.

49
Q

Which three types of interleukin (IL) are secreted from TH2 cells?

A
  1. IL-4.
  2. IL-5.
  3. IL-13.
50
Q

Which type of IL secreted from TH2 cells acts to stimulate eosinophils? What response does this produce?

A

IL-5.

This results in the differentiation and activation of eosinophils.

51
Q

Which types of IL secreted from TH2 cells act to stimulate degranulation of mast cells in airway tissue?

A

Il-4 and IL-13.

52
Q

What do specific IgE antibodies produced by plasma B cells do to bring about an immune response?

A

Bind to Fce (epsilon) receptors of both mast cells and eosinophils such that these receptors can detect the antigen again in the future.

53
Q

What two initial responses does cross-linking of antigen to IgE receptors on mast cells bring about as part of a secondary exposure?

A
  1. Stimulation of calcium entry into mast cells.

2. Stimulation of release of calcium from intracellular stores.

54
Q

What does the rise in intracellular concentration of calcium in mast cells bring about after an antigen cross-links to IgE receptors in terms of bringing about bronchospasm?

A

Release of granules containing preformed histamine + other agents (e.g. leukotrienes, LTC4 and LTD4).

This results in smooth muscle contraction - bronchospasm.

55
Q

What does the rise in intracellular concentration of calcium in mast cells bring about after an antigen cross-links to IgE receptors in terms of recruitment of inflammatory cells?

A

Release of substances [e.g. LTB4, platelet activating factor (PAF), and prostaglandins (PGD2)] that attract inflammatory cells (e.g. mononuclear cells and eosinophils) into the area.

BFCBP Respiratory Pharmacology (1 decks)

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