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Respiratory-Pharmacology > Pharmacology of asthma > Flashcards

Pharmacology of asthma Flashcards

1
Q

What is the dominant neuronal control innervation of the airways?

A

Parasympathetic cholinergic innervation

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2
Q

Which main nerve carries preganglionic fibres to the airways?

A

Vagus nerve

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3
Q

What effect does stimulation of the parasympathetic division have on the airways? (3)

A
  • Bornchial smooth muscle contraction, by ACh acting on M3 muscarinic ACh receptors
  • Increased mucous secretion, by ACh acting on M3 muscarinic ACh receptors
  • Overall increase in airway resistance
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4
Q

What does stimulation of the sympathetic division have on the airways? (4)

A
  • Bronchial smooth muscle relaxation (via B2-adrenoceptors activated by adrenaline released from the adrenal gland)
  • Decreased mucous secretion by B2 receptors
  • Increased mucociliary clearance mediated by B2 receptors
  • Overall decreased airway resistance
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5
Q

What is asthma?

A

A recurrent and reversible obstruction to the airways in response to a substance or stimuli

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6
Q

Name causes of asthma attacks (8)

A
  • Allergens
  • Exercise
  • Cold air
  • Dry air
  • Respiratory infections (e.g. viral)
  • Smoke
  • Dust
  • Environmental pollutants
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7
Q

What are the symptoms of asthma?

A

Coughing

Wheezing

Difficulty breathing

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8
Q

What is the pathological cause of asthma? (5)

A
  • Increased mass of smooth muscle (Hypertrophy and hyperplasia)
  • Accumulation of interstitial fluid (Oedema)
  • Increased secretion of mucous
  • Epithelial damage (exposing sensory nerve endings)
  • Overall narrowing of airways
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9
Q

What effect does asthma have on the FEV1 and PEFR?

A

Decrease in both

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10
Q

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

A
  • Hypersensitivity

- Hyperreactivity

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11
Q

What is the pathology behind bronchial hyper-responsiveness in asthma?

A

Epithelial damage–> Exposure of sensory nerve endings–> Increased sensitivity of the airways to bronchoconstrictor infulences

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12
Q

What test reveals hyper-responsiveness?

A

Provocation tests with inhaled bronchoconstrictors (e.g. histamine or methacholine)

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13
Q

What are the two classes of drugs that can be used in treatment of asthma?

A
  • Relievers

- Preventers

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14
Q

What action do relievers have on bronchial tissue?

A

-Bronchodilation

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15
Q

What two classes are B2 agonists used in asthma treatment separated into?

A
  • Short acting B2 agonists (SABA)

- Long acting B2 agonists (LABA)

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16
Q

What types of bronchodilators are available in asthma treatment?

A
  • B2 Agonists

- CysLT1 receptor antagonists

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17
Q

What are preventers and what action do they have on the airways?

A

Anti inflammatory agents that reduce airway inflammation

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18
Q

What types of preventers are available in asthma treatment?

A
  • Glucocorticoids
  • Chromoglicate
  • Humanised monoclonal IgE antibodies
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19
Q

What is the function of myosin light chain kinase?

A

Causes contraction of actin and myosin

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20
Q

What is the mechanism of action of B2 agonists? (6)

A
  • Activation of B2 receptors
  • Activation of enzyme adenylyl cyclase
  • Formation of Cyclic adenosine-mono-phosphate (cAMP) from ATP
  • Activation of enzyme protein kinase A (PKA)
  • Phosphorylation of Myosin light chain kinase (MLCK)
  • Airway smooth muscle relaxation
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21
Q

What causes receptor desensitisation and endocytosis resulting in loss of function of receptor?

A

Persistent activation of the receptor

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22
Q

How does PKA affect B2 Adrenoceptors?

A

Phosphorylates receptor, causing reduced G protein coupling, preventing relaxation pathway.

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23
Q

Give an example of a SABA.(1)

A

-Salbutamol (Albuterol)

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24
Q

What drug is the first line treatment for mild intermittent asthma?

A

SABAs

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25
Q

Are SABAs relievers or preventers?

A

Relievers

26
Q

How are SABAs usually administered? Why this route?

A

Metered dose or dry powder devices in order to lessen systemic effetcs.

27
Q

How long do SABAs take to act?

A

Often within 5 minutes

28
Q

How long to SABAs effects persist?

A

4-6 hours

29
Q

How long do SABAs take to reach maximal effect?

A

Around 30 minutes

30
Q

What effect do SABAs have on mucous clearance and release of mediators from mast cells and neutrophils?

A

Increased mucous clearance and decreased mediator release.

31
Q

What are some adverse effects of SABAs (2)

A
  • Fine tremor

- Occasional tachycardia (Due to stimulation of B1 receptors in heart)

32
Q

Name an example of a LABA

A

Salmeterol

33
Q

What kind of asthma are LABAs effective in treating and why?

A

Nocturnal asthma due to their long half life

34
Q

Should LABAs be used as a monotherapy?

A

No- should be used as add-on.

35
Q

What adverse effect does Isoprenaline (Non specific B agonist) have?

A

Harmful stimulation of cardiac B1 adrenoceptors

36
Q

Why are non selective B antagonists such as Propranolol contraindicated in asthmatic patients?

A

Due to their cause of bronchospasm

37
Q

What part do CysLTs play in asthma? (4)

A

Derived from mast cells

Cause smooth muscle contraction

Cause Mucous secretion

Cause oedema

38
Q

Give an example of CysLT1 receptor antagonists. (2)

A

Montelukast

Zafirlukast

39
Q

What type of asthma are CysLT1 antagonists effective in?

A

-Add on therapy in mild persistent asthma and in combination with other treatments in more severe conditions

40
Q

How are CysLT1 antagonists administered?

A

Orally

41
Q

Give an example of a xanthine. (2)

A

Theophylline

Aminophylline

42
Q

How are xanhine drugs administered?

A

Orally

43
Q

What adverse effects do xanthines cause? (4)

A

Nausea

Vomiting

Abdominal discomfort

Headache

44
Q

What is the suspected mechanism of action of xanthines?

A

Inhibition of isoforms of Phosphodiesterase–>inactivate cAMP and cGMP

45
Q

Which drugs should xanthines be combined (added on) to?

A

B2 agonists and glucocorticoids

46
Q

Do xanthines possess bronchodilator or anti inflammatory actions?

A

Some of both

47
Q

Where are the two main classes of steroid hormone (Glucocorticoids and mineralocorticoids) synthesised in the body?

A

The adrenal cortex

48
Q

Where are glucocorticoids synthesised in the adrenal cortex?

A

Zona fasiciculata

49
Q

Where are mineralocorticoids synthesised in the adrenal cortex?

A

Zona glomerulosa

50
Q

What is the main hormone in humans?

A

Cortisol (Hydrocortisone)

51
Q

What are the two most important functions regulated by Cortisol (Hydrocortisone)?

A
  • Inflammatory responses decrease

- Immunological response decrease

52
Q

What are glucocorticoids primary function in asthma treatment?

A

Prophylactic treatment

53
Q

Why are glucocorticoids preferably delivered by the inhalational route?

A

To prevent adverse systemic effects

54
Q

How do glucocorticoids affect transcription of anti-inflammatory and inflammatory?

A
  • Decrease transcription of genes encoding inflammatory proteins
  • Increase in transcription of genes encoding inflammatory proteins
55
Q

What are the function of histone acetyltransferases?

A

Acetylation of histones (Causes DNA to unwind from histone allowing transcription).

56
Q

How do glucocorticoids benefit asthma sufferers?

A
  • Prevent inflammation

- Resolve established inflammation

57
Q

Which inhaled glucocorticoid is often used in mild to moderate asthma/

A
  • Beclometasone
58
Q

What side effects does deposition of glucocorticoids in the oropharynx cause? (2)

A
  • Dysphonia (Hoarse and weak voice)

- Oropharyngeal candidiasis (Thrush)

59
Q

Which oral glucocorticoid is often used in severe or rapidly deteriorating asthma?

A

Prednisolone

60
Q

What are cromolins?

A

Drug infrequently used as prophylactic therapy in allergic asthma (Particularly children)

61
Q

What is Omalizumab?

A

Monoclonal antibody treatment directed against IgE

62
Q

How is omalizumab administered?

A

IV

Respiratory-Pharmacology (1 decks)

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