The Neurohumoral Control of the Airways and an Introduction to Asthma Flashcards

1
Q

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

A

Brainstem

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2
Q

Where are the cell bodies of the postganglionic fibres in the airways?

A

Bronchi and bronchioles?

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3
Q

(parasympathetic) Stimulation of postganglionic cholinergic fibres causes?

A

Bronchial smooth muscle contraction. Muscus Secretion.

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4
Q

(parasympathetic)stimulation of the postganlionic nonchlinergic fibres causes?

A

Bronchial smooth muscle relaxation.

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5
Q

(parasympathetic)What mediates the causes of Stimulation of postganglionic cholinergic fibres?

A

M3 muscarinic ACh receptors on the cells of which it caused effect.

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6
Q

(parasympathetic)What mediates stimulation of the postganglionic nonchlionergic fibres?

A

Nitric oxide and vasoactivated intestenal peptide.

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7
Q

(sympathetic)What do post-ganglionic fibres supply?

A

Submocosal and smooth muscle of blood vessels

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8
Q

(sympathetic)Stimulation causes?

A

bronchial smooth muscle relaxation. Decreased mucus secretion. Increased mucociliary clearance. vascular smooth muscle contraction.

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9
Q

(sympathetic)What mediates the causes of stimulation?

A

B2-adrenoceptors on the cells of the tissue of the cell affected (they are activated by adrenaline).

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10
Q

What is the first step of the depolarisation in Excitation Contraction Coupling in Smooth Muscle?

A

Depolarisation activated Ca2+ (voltage activated) channel which allows Ca2+ to travel into the cell.

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11
Q

What is the second step of the depolarisation in Excitation Contraction Coupling in Smooth Muscle?

A

The Ca2+ then acts as a ligand and activates ryanodine receptor which allows Ca2+ to pass from the sarcoplasmic reticulum into the cell. (this has stored Ca2+)

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12
Q

What is the third step of the depolarisation in Excitation Contraction Coupling in Smooth Muscle?

A

The Ca2+ in the cell causes contraction.

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13
Q

How does Ca2+ cause contraction in smooth muscle cells? first reaction.

A

Ca2+ binds with calmodulin to form Ca2+-calmodulin.

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14
Q

How does Ca2+ cause contraction in smooth muscle cells? second reaction.

A

Ca2+-calmodulin activates myosin light chain kinase.

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15
Q

How does Ca2+ cause contraction in smooth muscle cells? third reaction.

A

Myosin light chain kinase then phosphorylates myosin cross bridge with breakdown of ATP.

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16
Q

What types of reactions does myosin light chain kinase and myosin phosphatase do and what does that cause?

A

Respectively, phosphorylation - contraction and dephosphorylation - relaxation.

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17
Q

In the presence of elevated Ca2+ the rate of phosphorylation is what compared to the rate of dephosphorylation?

A

Exceeds the rate of dephosphylation

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18
Q

How does relaxation happen after contraction?

A

It uses primary and secondary transport of Ca2+ out of the cell to make the intracellular Ca2+ concentration at basal level

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19
Q

What is the first and second reaction in the regulation of myosin chain kinase and phosphatase.

A

B2-adrenoceptor (GPCR) is activated by adrenaline and then activates Gs which activates AC(adenylyl cyclase).

20
Q

What is the third and fourth reaction in the regulation of myosin chain kinase and phosphatase.

A

AC with ATP forms cAMP. cAMP is then degraded by PDE to form PKA and 5’AMP.

21
Q

What is the two options of the fifth reaction in the regulation of myosin chain kinase and phosphatase.

A

PKA phosphorlates and inhibits myosin light kinase. It also phosphoylates and stimulates phosphatase. These both cause relaxation of bronchial smooth muscle.

22
Q

State the definition of Asthma

A

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

23
Q

What are the causes of asthma attacks?

A

Allergens, exercise, respiratory infection and environmental pollutants (smoke/dust etc)

24
Q

What are the symptoms of asthma?

A

Tight chest, wheezing, difficulty in breathing, cough.

25
Q

Chronic asthma involves what?

A

Pathological changes to the bronchioles that result from long standing inflammation.

26
Q

What are the 5 spesific effects of asthma on the broncholes?

A
  1. increase mass from smooth muscle (hyperplasia and hypertrophy)
  2. accumulation of interstitial fluid (oedema)
  3. increase secretion of mucus.
  4. epithelial damage (exposing sensory nerve endings)
  5. sub-epithelial fibrosis
27
Q

What does the narrowing by inflammation and cronchoconstriction cause?

A

increasing airway resistance which causes a decrease in FEV1 and PEFR.

28
Q

What can epithelial damage do in the bronchial?

A

Expose nerve endings that contributes to increased sensitivity of the airways to bronchoconstrictors.

29
Q

What are bronchoconstrictors?

A

They are drugs that cause the bronchial to contract (histamine or methacholine etc)

30
Q

What is hypersensitivity in asthma?

A

When it takes less of a bronchoconstrictor concentration to initiate a fall in FEV1.

31
Q

What is hyper-reactivity in asthma?

A

When the fall in FEV1 increases dramatically with an increase in concentration of bronchoconstrictor.

32
Q

What is early phase asthma attack?

A

When there is a sudden drop straight after the inhalation of a brochoconstrictor.

33
Q

What is the late phase asthma attack?

A

This is after the patient has recovered from the early phase and then suddenly drops even further again.

34
Q

What happens during an early phase asthma attack?

A

Mainly brochospasm and also acute inflammation.

35
Q

What happens during a late phase asthma attack?

A

Bronchospasm and delayed inflammation

36
Q

What is FEV1?

A

The forced expiratory volume (in litres) in 1 second.

37
Q

What is the cause of a big immune response in asthma?

A

There is more strong Th2 responce. Antibody-mediated immune response involving IgE

38
Q

What happens with the Th1 response in severe asthma

A

It can cause so much Th1 response that this contributes to the big immune response as well

39
Q

What are the two stages called in the development of allergic asthma as a whole and individually?

A

Induction phase

  1. Antigen presentation
  2. Clonal expansion and maturation
40
Q

What happens in the first phase of the development in allergic asthma?

A

Allergen is captured and presented to T CD4+ by an antigen presenting cell. This then activates Th0.

41
Q

What happens in the second phase of the development in allergic asthma?

A

The Th0 then becomes Th1 and preferentially matures to become Th2. Th2 then activates B cells which then mature to IgE secreting plasma cells.

42
Q

What is the two ways Th2 can activate a B cell?

A

It can bind to them and produces IL-4 which also activates them.

43
Q

The Th2 cells do what to eosinophils and mast cells?

A

They activate eosinophils through IL-5 and cause mast cells in the airway tissue to express IgE receptors through IL-13.

44
Q

How does IgE receptors help in the development of allergic asthma?

A

They bind to the surface of a activated mast cell and when the antigen binds to them then they cause the release of granules containing preformed histomine and other egents (leukotriences LTC4 and LTD4) that cause airway construction.

They also release substances and platelet activating factor and prostaglandins that attract cells causing inflammation.

45
Q

What is the events in the immediate phase of asthma?

A

Allergen or non-spesific stimulus causes activates mast cells and mononuclear cells. These then activate spasmogens, CysLTs and Histamine (all of which cause bronchospasms and early inflammation).

46
Q

What connects the intermediate phase to the late phase of asthma?

A

The chemotaxins and chemokines cause the first response of the late phase.

47
Q

What is the events in the late phase of asthma?

A

infiltration of cytokines releasing Th2 cells and monisytes, activation of inflammatory cells (particularly eosinophills)

This activates mediators and CysLTs which cause airway inflammation, airway hyper-responsiveness. This leads to bronchospams and the other symptoms.

The first stage also activates eosinophils major basic and cationic proteins which cause epithelial damage and so airway hyper-responsiveness.