Asthma and Airway Control Flashcards

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?

A

1st line

23
Q

What are useful for nocturnal asthma?

A

LABAs

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
Q

Is isoprenaline a selective or non selective beta agonist?

A

non selective

26
Q

Are non selective beta agonists recommended in asthma?

A

No

27
Q

What is montekulast an example of?

A

CysLT1 receptor antagonists

28
Q

What are xanthines present in?

A

coffee, tea, chocolate-containing beverages