CPTP 2.18 Respiratory

Question 1

What is extrinsic asthma?

Answer 1

Allergic asthma

Commonly seen in children

Triggered by allergens e.g. pollens, dust mites, animals, peanuts, eggs

Question 2

Describe the pathophysiology of asthma after the first exposure to antigen

Answer 2

First exposure to antigen

• > Production of IgE antibodies
• > Stimulation of mast cells to release chemical mediators e.g. histamine, leukotrienes
• > Triggers asthma attack

Question 3

What are the causes of intrinsic asthma?

Answer 3

exposure to chemical agents/ drugs, exercise, respiratory infections or stress

can be due to beta-blockers prescribe for hypertension/ angina

These agents act by stimulating sensory receptors and nerves in the air passage

Question 4

What are the innervations of bronchial smooth muscle

Answer 4

Sensory receptors (Irritant receptors and C-fibres), bronchoconstriction

Parasympathetic innervation (M3 Ach receptor), bronchoconstriction

No sympathetic innervation (Beta2 adrenoreceptor, relaxation)

Question 5

Describe inflammatory changes in airway

Answer 5

Arachadonic acid is produced from phospholipid plasma membrane by phospholipase A2

COX aids conversion of arachadonic acid into prostaglandins

5-lipoxygase aids conversion of arachadonic acid into leukotrienes

Question 6

function of prostaglandins

Answer 6

bronchoconstrictor

inflammatory mediators released in asthma

Question 7

fucntions of leukotrienes

Answer 7

bronchoconstrictors

promote mucus secretion

recruit immune cells which enhance airway inflammation

Question 8

Describe hyper-responsiveness

Answer 8

Hyper-responsiveness: exaggerated bronchoconstriction at low doses of stimulus

asthmatic response

It consist of hypersensitivity and hyperreactivity

Question 9

Describe hypersensitivity

Answer 9

a normal response at abnormally low doses of stimulus

Question 10

Describe hyper-reactivity

Answer 10

an exaggerated response at normal doses of stimulus

Question 11

Describe immediate phase of asthma attack

Answer 11

release of spasmogens (e.g. histamine, prostaglandins) from mast cells

immediately cause massive vasoconstriction

Question 12

Describe delayed phase of asthma attack

Answer 12

Influx of inflammatory cells delay bronchoconstriction

results in:
airway inflammation
mucus production
bronchospasm -> asthma attack

Question 13

Two types of drugs used to treat asthma?

Answer 13

bronchodilators and corticosteroids

Question 14

five types of bronchodilators

Answer 14

1. B2 adrenergic receptor agonist
2. Muscarinic antagonist
3. Theophylline
4. 5-lipoxygenase inhibitors
5. leukotriene antagonists

Question 15

mechanism of B2 adrenergic receptor agonist?

Answer 15

receptor stimulated

• > g protein binds to adenylyl cyclase
• > cAMP produced
• > PKA activated
• > reduced cytosolic Ca2+
• > SM relaxation

Question 16

clinical uses of salbutamol

Answer 16

• short-acting
• agent of choice for acute exacerbation
• side effects minimised with delivery via inhalation

Question 17

clinical uses of salmeterol

Answer 17

long-acting
; a long lipophilic side chain anchors the drug in the lipid membrane

not used for relief on an acute asthma attack

Question 18

side effect of b2 agonists

Answer 18

`uncommon at normal doses

tachycardia, hyperglycaemia, skeletal muscle tremors

Question 19

mechanism of muscarinic antagonists

Answer 19

e.g. ipratropium, tiotropium

relax bronchial SM and decrease mucus secretion

administered by inhalation as it is highly absorbed across the respiratory epithelium

Question 20

Side effects of muscarinic antagonists

Answer 20

systemic anticholinergic side effects
(This is because M3 receptors are distributed around the body)

dry mouth is the commonest

tachycardia, nausea, constipation

Question 21

clinical uses of muscarinic antagonist

Answer 21

second line drugs

slow acting; so normally used in addition to slabutamol

Question 22

Theophylline

Answer 22

inhibits phophodiesterase to cause an increase in cAMP in SM cells

inhibit acute and delayed phases

administered orally

Question 23

5-lipoxygenase inhibitors

Answer 23

e.g. zileuton

administered orally
undergo biliary excretion
not effective for acute exacerbation

has a 4% risk of hepatic toxicity so periodic liver function testing is required

Question 24

Corticosteroids

Answer 24

e.g. beclomethasone (inhaled), prednisolone and hydrocortisone (IV)

inhibit phospholipase A2 and COX, and so inhibit synthesis of prostaglandins

Question 25

NICE guideline on the uses of asthma drugs

Answer 25

1. salbutamol (inhalation)
2. corticosteroid(inhalation)
3. salmeterol (inhalation)
4. oral corticosteroid
5. leukotriene antagonist

anti-muscarinic drugs not used due to systemic side effects