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Karan - MBBS Year 1: Respiratory Week 2 > Bronchodilators > Flashcards

Bronchodilators Flashcards

1
Q

Describe allergic asthma.

A
  • Commonly seen in children
  • Triggered by allergens which cause IgE production
  • Exposure to antigen causes IgE binding
  • Stimulation of mast cells to release chemical mediators e.g leukotrienes and histamines
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2
Q

Describe non-atopic asthma. PART 1

A
  • Likely to occur in adults
  • Usually caused by irritants - causative agent generally unknown
  • Can be due to viral infection/aspirin sensitivity/sensitisation to specific chemicals
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3
Q

Describe non-atopic asthma. PART 2

A
  • Stimulate sensory receptors and nerves in airways
  • Increased eosinophil count/other inflammatory mediators normal
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4
Q

What are the main inflammatory changes in the airways?

A
  • HYPER-RESPONSIVENESS - exaggerated bronchoconstriction at low doses of stimulus
  • CHARACTERISED BY HYPERSENSITIVITY - normal response at low doses of stimulus
  • CHARACTERISED BY HYPER-REACTIVITY - exaggerated response at normal doses
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5
Q

Describe the immediate and delayed phase of asthma.

A
  • BRONCHOSPASM - caused by spasmogens and chemokines released from mast cells e.g leukotrienes
  • DELAYED - influx and actication of inflammatory cells e.g PAF and leukotrienes causing mucus production and airway inflammation
  • Can be reversed by salbutamol
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6
Q

Describe the arachadonic acid pathway.

A
  • Phospholipase A2 released from plasma membrane and activates arachadonic acid.
  • Cyclooxygenase produces prostaglandins causing bronchoconstriction
  • 5-lipoxygenase produces leukotrienes - causing bronchoconstriction and mucus secretion
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7
Q

Describe the innervation of bronchial smooth muscle.

A
  • Irritant receptors and C-fibres respond to extrinsic and intrinsic agents. Cause bronchoconstriction.
  • PARASYMPATHETIC - M3 receptors - cause constriction
  • NO SYMPATHETIC INNERVATION - circulating adrenaline acts on B2 receptors causing relaxation
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8
Q

Describe the mechanism of action of beta agonists with examples.

A
  • Activates the Gs pathway
  • Reduced release of bronchoconstricting agents from mast cells
  • EXAMPLES - salbutamol, salmeterol and formoterol
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9
Q

Describe SABAs

A
  • EXAMPLE - salbutamol
  • Acute effect - onset of 5-30 min with relief for 4-6h
  • Protects against various stimuli e.g exercise
  • Used for acute exacerbations
  • Preferred delivery - inhalation rather than systemic
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10
Q

Describe LABAs. PART 1

A
  • EXAMPLES - salmeterol and formoterol
  • Chemical analogue of salbutamol
  • Long lipophilic side chain - anchors drug in lipid membrane
  • Allows active portion of molecule to remain at receptor site
  • Used in combination e.g with corticosteroids.
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11
Q

Describe LABAs. PART 2

A
  • Provides bronchodilation for at least 12hrs
  • Slow onset - not used in acute asthma attacks
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12
Q

What are the side effects of beta-2 agonists?

A
  • Uncommon at normal doses
  • At high doses - tachycardia, hyperglycaemia and skeletal muscle tremors
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13
Q

Describe muscarinic antagonists. PART 1

A
  • EXAMPLE - ipratropium and tiotropium
  • Second line drugs - used as an alternative
  • Competitive antagonists for ACh at M3 receptors
  • Relaxes bronchial smooth muscle
  • Reduced mucus secretion
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14
Q

Describe muscarinic antagonists. PART 2

A
  • No effect on delayed phase
  • Not effective in asthma unless COPD also present
  • Useful in patients not able to tolerate adrenergic agonists (eg patients with ischaemic heart disease/tachycardia)
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15
Q

Describe the mechanism of action of respiratory muscarinic receptor antagonists.

A
  • Blocks the Gq pathway
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16
Q

Describes the pharmacokinetics of muscarinic receptor antagonists e.g ipratropium.

A
  • Administered by inhalation
  • Highly absorbed across respiratory epithelium
  • 8% bioavailability (2% when orally) so high potency - less drug required to elicit response
  • Onset following 30-60 minutes, relief for 4-6hrs
17
Q

What are the side effects of muscarinic antagonists?

A
  • Systemic anticholinergic side effects
  • EXAMPLE: Tachycardia, nausea, blurred vision, dried mucuous membranes
18
Q

Describe aminophylline.

A
  • Second line drug
  • 2:1 complex of theophylline and ethylenediamine
  • Causes acute bronchodilation - may inhibit delayed phase
  • Administered orally
  • Narrow therapeutic window - CONSTANT MONITORING by titrate to desired dose
19
Q

What is the mechanism of action of aminophylline?

A
  • Inhibits PDE2
  • Reduced breakdown of cAMP to AMP
  • Smooth muscle relaxation
20
Q

Describe the pharmacokinetics of aminophylline. PART 1

A
  • Effects unpredictable. Not predicted by age, sex, body weight etc.
  • Administered orally and IV
  • 100% bioavailability orally - no first pass effect
  • 3-5 half lives to reach steady state concentration
  • Usually either a very large or very small dose given
21
Q

Describe the pharmacokinetics of aminophylline. PART 2

A
  • 40% bound to albumin
  • Low Vd - 0.5litres per kg
  • Half life is variable
  • Usually loading dose of 10-20 mcg/ml used
  • > 20mcg/ml - will cause high severity and frequency of adverse drug reactions
22
Q

Describe the pharmacokinetics of aminophylline. PART 3

A
  • Theopylline primarily eliminated by hepatic metabolism
  • Hepatic impairment effects clearance by 50% - not used in hepatic failure
  • 90% released as range of acids. 15-20% as 3-methylxanthine - active metabolite
  • 10% of theophylline recovered as unchanged drug.
23
Q

Describe the pharmacokinetics of aminophylline. PART 4

A
  • No change in renal impairment in adults
  • 50% reduction in clearance in neonates
24
Q

What is the mechanism of action of montelukast?

A
  • Leukotriene receptor antagonist
25
Q

What are the side effects of aspirin?

A
  • Ringing in ears
  • Nausea, stomach pain, heartburn, vomiting
  • Bloody vomit
  • Rash
  • Fast heartbeat
  • Labored breathing, wheezing
26
Q

What are the side effects of beta-blockers?

A
  • Beta 1 blockers affect heart
  • Beta 2 blockers affect lungs

Karan - MBBS Year 1: Respiratory Week 2 (10 decks)

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