CPTP 2.18 Respiratory Flashcards
(25 cards)
What is extrinsic asthma?
Allergic asthma
Commonly seen in children
Triggered by allergens e.g. pollens, dust mites, animals, peanuts, eggs
Describe the pathophysiology of asthma after the first exposure to antigen
First exposure to antigen
- > Production of IgE antibodies
- > Stimulation of mast cells to release chemical mediators e.g. histamine, leukotrienes
- > Triggers asthma attack
What are the causes of intrinsic asthma?
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
What are the innervations of bronchial smooth muscle
Sensory receptors (Irritant receptors and C-fibres), bronchoconstriction
Parasympathetic innervation (M3 Ach receptor), bronchoconstriction
No sympathetic innervation (Beta2 adrenoreceptor, relaxation)
Describe inflammatory changes in airway
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
function of prostaglandins
bronchoconstrictor
inflammatory mediators released in asthma
fucntions of leukotrienes
bronchoconstrictors
promote mucus secretion
recruit immune cells which enhance airway inflammation
Describe hyper-responsiveness
Hyper-responsiveness: exaggerated bronchoconstriction at low doses of stimulus
asthmatic response
It consist of hypersensitivity and hyperreactivity
Describe hypersensitivity
a normal response at abnormally low doses of stimulus
Describe hyper-reactivity
an exaggerated response at normal doses of stimulus
Describe immediate phase of asthma attack
release of spasmogens (e.g. histamine, prostaglandins) from mast cells
immediately cause massive vasoconstriction
Describe delayed phase of asthma attack
Influx of inflammatory cells delay bronchoconstriction
results in:
airway inflammation
mucus production
bronchospasm -> asthma attack
Two types of drugs used to treat asthma?
bronchodilators and corticosteroids
five types of bronchodilators
- B2 adrenergic receptor agonist
- Muscarinic antagonist
- Theophylline
- 5-lipoxygenase inhibitors
- leukotriene antagonists
mechanism of B2 adrenergic receptor agonist?
receptor stimulated
- > g protein binds to adenylyl cyclase
- > cAMP produced
- > PKA activated
- > reduced cytosolic Ca2+
- > SM relaxation
clinical uses of salbutamol
- short-acting
- agent of choice for acute exacerbation
- side effects minimised with delivery via inhalation
clinical uses of salmeterol
long-acting
; a long lipophilic side chain anchors the drug in the lipid membrane
not used for relief on an acute asthma attack
side effect of b2 agonists
`uncommon at normal doses
tachycardia, hyperglycaemia, skeletal muscle tremors
mechanism of muscarinic antagonists
e.g. ipratropium, tiotropium
relax bronchial SM and decrease mucus secretion
administered by inhalation as it is highly absorbed across the respiratory epithelium
Side effects of muscarinic antagonists
systemic anticholinergic side effects
(This is because M3 receptors are distributed around the body)
dry mouth is the commonest
tachycardia, nausea, constipation
clinical uses of muscarinic antagonist
second line drugs
slow acting; so normally used in addition to slabutamol
Theophylline
inhibits phophodiesterase to cause an increase in cAMP in SM cells
inhibit acute and delayed phases
administered orally
5-lipoxygenase inhibitors
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
Corticosteroids
e.g. beclomethasone (inhaled), prednisolone and hydrocortisone (IV)
inhibit phospholipase A2 and COX, and so inhibit synthesis of prostaglandins
