Asthma and Airway Control Flashcards

(28 cards)

1
Q

What is the dominant control of bronchial smooth muscle tone?

A

parasympathetic cholinergic innervation of airways

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2
Q

What does stimulation of bronchial smooth muscle and submucosal glands by post ganglionic fibres cause?

A

Bronchial smooth muscle contraction
Increased mucus secretion
Overall increased airway resistance

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3
Q

Which muscarinic ACh receptor mediates bronchial smooth muscle relaxation?

A

M3

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4
Q

What does stimulation of bronchial smooth muscle by B2 adrenoceptors of the sympathetic division cause?

A

bronchial smooth muscle relaxation

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5
Q

What activates B2 adrenoceptors?

A

adrenaline released from adrenal gland

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6
Q

Does the sympathetic division increase or decrease mucociliary clearance?

A

Increase

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7
Q

Give examples of stimuli which may cause airway obstruction in asthma.

A

Allergens, exercise, respiratory infections, smoke, dust, pollutants etc

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8
Q

Which pathological changes occur in asthma to the smooth muscle in bronchioles?

A

Increased mass of smooth muscle by hyperplasia and hypertrophy

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9
Q

What happens to mucus secretion in asthma?

A

increases

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10
Q

What other pathological changes occur in asthma?

A

Epithelial damage, interstitial fluid (oedema)

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11
Q

How does increased sensitivity occur in asthma?

A

Epithelial damage leads to sensory nerve endings being exposed

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12
Q

Test with what will reveal hyper responsiveness in asthma?

A

Inhaled bronchoconstrictors (spasmogens) e.g. histamine or metacholine

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13
Q

Are asthma attacks immediate or delayed?

A

may be both

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14
Q

How does allergic asthma develop?

A
  • Antigen cross links IgE receptors
  • Stimulates calcium entry into mast cells and release of calcium from intracellular stores
  • This releases secretory granules containing histamine
  • Other agents eg leukotrienes ,LTD4 and LTC4 are produced causing smooth airway muscle contraction
  • Substances are released (e.g LTB4 and PAF and PGD2) to attract cells like mononuclear cells and eosinophils intro area
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15
Q

In the late phase of asthma, what causes infiltration of cytokine release Th2 cells and monocytes and activation of inflammatory cells?

A

Chemotoxins and chemokines

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16
Q

What do eosinophils and major basic cationic proteins cause?

A

epithelial damage and airway hyperreactivity

17
Q

In immediate asthma what causes bronchospasm?

A

Spasmogens caused by mast cells and mononuclear cells

18
Q

What kinases are involved in broncodilator action?

A

protein kinase A (PKA) and G protein receptor kinases (GRKs) – specifically B-adrenoceptor kinases

19
Q

What does B-arrestin act as in bronchodilator action?

A

a scaffold protein that links the desensitized B-adrenoceptors to ‘endocytic machinery’ that internalizes the receptor

20
Q

What does persistent activation of B2-adrenoceptors cause?

A

Receptor desentization and endocytosis (resulting in loss of function)

21
Q

Where does the action of B-arrestin occur?

A

clathrin-coated pits and vesicles

22
Q

What line of treatment are SABAs for asthma?

23
Q

What are useful for nocturnal asthma?

24
Q

How are CystLT1 receptor antagonists used in asthma?

A

add on therapy in mild persistent asthma, especially exercise/antigen induced asthma, not for acute/severe cases

25
Is isoprenaline a selective or non selective beta agonist?
non selective
26
Are non selective beta agonists recommended in asthma?
No
27
What is montekulast an example of?
CysLT1 receptor antagonists
28
What are xanthines present in?
coffee, tea, chocolate-containing beverages