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LC Respiratory Week 1 > Pharmacology 1 - Neurohumoral control of the airways and asthma > Flashcards

Pharmacology 1 - Neurohumoral control of the airways and asthma Flashcards

1
Q

Where the pre and postganglionic fibres are in relation to parasympathetic stimulation of the airways?

A

Pre = brainstem
(travel in axons in vagus nerve)
Post = embedded in the walls of the bronchi and bronchioles

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2
Q

What two types of postganglionic fibres are there?

A

Cholingeric fibres

Non Cholingeric fibres

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3
Q

What does stimulation of the Cholingeric fibres cause in relation to the parasympathetic stimulation of the airways?

A
  • Bronchial smooth muscle contraction (bronchoconstriction) (Mediated by M3 muscarinic Aah receptors on the airway smooth muscle cells)
  • Increased mucus secretion (Mediated by M3 muscarinic Aah receptors on gland (goblet)cells)
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4
Q

What is bronchial smooth muscle (bronchoconstriction) mediated by in cholingeric stimulation?

A

Mediated by M3 muscarinic Aah receptors on the airway smooth muscle cells

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5
Q

What is increased mucus secretion mediated by in cholingeric stimulation?

A

Mediated by M3 muscarinic Aah receptors on gland (goblet)cells

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6
Q

What does stimulation of non cholingeric fibres cause in relation to the parasympathetic stimulation of the airways?

A
  • Bronchial smooth muscle relaxation (Mediated by Nitric Oxide (NO) and Vasoactive intestinal peptide (VIP))
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7
Q

What is bronchial smooth muscle relaxation mediated by in noncholingeric stimulation?

A

Mediated by Nitric Oxide (NO) and Vasoactive intestinal peptide (VIP)

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8
Q

Where the pre and postganglionic fibres are in relation to sympathetic stimulation of the airways?

A

Pre= Spinal cord

Post = There are no post-ganglionic fibres directly in the airways. Instead the relaxant effect is due to the release of (largely) adrenaline from the adrenal medulla (driven by pre-ganglionic sympathetic fibres). Sympathetic post-ganglionic fibres do innervate vascular smooth muscle and glands within the airways and the relevant pre-ganglionic neurones emerge from the thoraco-lumbar region of the spinal cord (specifically the lateral horn).

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9
Q

Is there sympathetic invitation in airway smooth muscle?

A

No, there is no invervation of bronchial smooth muscles. But post ganglionic fibres supply submucosal glands and smooth muscle of blood vessles

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10
Q

What does stimulation of the sympathetics cause?

A
  • Bronchial smooth muscle relaxation (via B2 adrenoceptors on airways smooth muscle cells activated nay adrenaline released from the adrenal gland)
  • Decreased mucus secretion (mediated by B2 adrenoceptors on gland (goblet) cells)
  • Increased mucociliary clearance (mucociliary elevator) (mediated by B2 adrenoceptors on epithelial cells)
  • Vascular smooth muscle contraction (mediated by A1 adrenoceptors on vascular smooth muscle cells)
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11
Q

What is bronchial smooth muscle relaxation mediated by in sympathetic stimulation?

A

B2 adrenoceptors on airways smooth muscle cells activated nay adrenaline released from the adrenal gland

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12
Q

What is decreased mucus secretion mediated by in sympathetic stimulation?

A

mediated by B2 adrenoceptors on gland (goblet) cells

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13
Q

What is increased mucociliary clearance mediated by in sympathetic stimulation?

A

mediated by B2 adrenoceptors on epithelial cells

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14
Q

What is vascular smooth muscle contraction mediated by in sympathetic stimulation?

A

mediated by A1 adrenoceptors on vascular smooth muscle cells

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15
Q

Briefly describe how the initiation of contraction by Ca2+ in Smooth Muscle takes place?

A

Calcium causes calmodulin –> Ca2+ calmodulin
This causes inactive MLCK to become active
This causes ADP formation (uses ATP)
Which causes the actin and myosin filaments to slide over each other, which causes contraction as they are anchored onto the smooth muscle

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16
Q

What does contraction of smooth muscle result from?

A

Contraction results from phosphorylation of the regulatory myosin light chain (MLC) in the presence of elevated intracellular Ca2+ (and ATP)

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17
Q

What does relaxation of smooth muscle result from?

A

Relaxation results from dephosphorylation of MLC by myosin phosphatase which has constitutive (ongoing) activity

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18
Q

What does myosin light chain kinase cause?

A

MLC phosphorylation = contraction

19
Q

What does myosin phosphatase cause?

A

MLC dephospho rylation = relaxation

20
Q

What happens when there is an increase in intracellular calcium?

A

the rate of phosphorylation exceeds the rate of dephosphorylation

21
Q

What does relaxation require in terms of calcium?

- and how is this achieved?

A

requires return of intracellular Ca2+ concentration to basal level – achieved by primary and secondary active transport

22
Q

What degrades cAMP (cyclic AMP)?

A

PDE - phosphodiesterase

23
Q

What is PKA and what does it do in terms of causing relaxation of bronchial smooth muscle?

A

PKA – protein kinase A
Phosphorylates and stimulates myosin phosphatase (facilitates relaxation)
Phosphorylates and inhibits myosin light chain kinase (inhibits contraction)

24
Q

What is asthma?

A

Is a recurrent and reversible (in the short term) obstruction to the airways in response to substances (or stimuli) that are not necessarily noxious and normally do not affect non-asthmatic people.

25
Q

Give some examples of causes of attacks in asthma?

A

Allergens (in atopic individuals)
Exercise (cold, dry air)
Respiratory infections (viral e.g.)
Smoke, dust, pollutants etc

26
Q

What is acute sever asthma?

A

A medical emergency and can be fatal

27
Q

What does intermittent attacks of bronchoconstriction cause?

A

Tight chest
wheezing (breathing out) §
cough
difficulty in breathing

28
Q

What happens in chronic asthma?

A

Pathological changes to the bronchioles due to long standing inflammation

29
Q

Describe these changes (5)?

A
  1. There is an increase mass of smooth muscle (hyperplasia and hypertrophy)
  2. There is accumulation of interstitial fluid (oedema)
  3. There is increase mucus secretion (from goblet cells)
  4. Theres epithelial damage (which exposes sensory nerve endings)
  5. Sub-epithelial fibrosis (which makes it more difficult for airway smooth muscle to relax)
30
Q

In asthma what happens to the airway resistance, and what happens to the FEV1 and PEFR?

A

Increased airway resistance
Decreased FEV1
Decreased PEFR

31
Q

Describe bronchial hyper-responsiveness in asthma?

A

In asthma there is epithelial damage, exposing the sensory nerve endings, this contributes to increased sensitivity of the airways to bronchoconstrictor influences

32
Q

What are the 2 components of bronchial hyper-responsiveness in asthma?

A
  1. Hypersensitivity

2. Hyper - reactivity

33
Q

Describe the changes in the 2 components in terms of mild and sever asthma?

A

Mild asthma - slightly increase hypersensitivity, slightly increased hyper-reactivity
Severe asthma - Huge increase in hypersensitivity, huge increase in hyper-reactivity

34
Q

What receptors do histamine and methacholine activate?

A 
Histamine = activates ASM H1 receptors 
Methacholine = activates ASM M3 receptors
35
Q

Describe the 2 different phases of an asthma attack?

A

Early phase = type 1 hypersensitivity - bronchospasm + inflammation
Late phase = type 4 hypersensitivity - bronchospasm + delayed inflammation

36
Q

Describe asthma as an immune imbalance in a nonatopic individual?

A

Low-level TH1 response
Cell-mediated immune response involving IgG
and macrophages
Exposure early in life to microbes favouring TH1 response?

37
Q

Describe asthma as an immune imbalance in an atopic individual?

A

Strong TH2 response
Antibody-mediated immune response involving IgE
A hygienic ‘western lifestyle’ - keeping kids away from infections

38
Q

What is one of the major causes of asthma? In terms of Th1 and Th2?

A

That there is an imbalance between Th1 and Th2 lymphocyte mediated responses

39
Q

Describe the development of allergic asthma?

A

Initial presentation of an antigen initiates an adaptive immune response
Antigen presented by antigen presenting cell
Processed allergen onto T CD4+ cells
Th0 cells preferentially mature to th2 cells that produce a cytokine environment
Th2 cells activate B cells by binding to them and by IL-4 production
B cells mature to IgE secreting P (plasma) cells
Eosinophils (differentiate and activate in response to IL-5 released from Th2 cells
Mast cells in airway tissue (express IgE receptors in response IL-4 and Il-13 released from Th2 cells)

40
Q

What does the cross link of IgE receptors and the antigen onto the mast cell stimulate?

A
  • calcium entry into mast cells

- release of Ca2+ from intracellular stores

41
Q

What does release of Ca2+ from intracellular stores evoke?

A
  • release of secretory granules containing preformed histamine and the production and release of other agents (e.g. leukotrienes LTC4 and LTD4(spasmogens)) that cause airway smooth muscle contraction
  • release of substances (e.g. LTB4 and platelet-activating factor (PAF) and prostaglandins (PGD2)) that attract cells causing inflammation (e.g. mononuclear cells and eosinophils) into the area
42
Q

Describe the key events in the intermediate phase of asthma?

A
  • Eliciting agent - allergen or non-specific stimulus
  • Mast cells and mononuclear cells
  • Spasmogens, histamine etc
  • Causes bronchospasm and early inflammation
43
Q

Describe the key events in the late phase of asthma?

A
  • Chemotaxins and chemokine released from the intermediate phase cause infiltration of cytokine releasing - Th2 cells and monocytes, activation of inflammatory cells (particularly eosinophils)
  • Causes eosinophil major, basic and cationic proteins - which cause epithelial damage
  • At the same time mediator, cysLTs etc
  • Causes airway inflammation, airway hyper-responsiveness and bronchospasm, wheezing, mucus over secretion and cough

LC Respiratory Week 1 (1 decks)

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