Asthma therapeutics Flashcards

1
Q

Extrinsic

A

Allergic

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2
Q

Intrinsic

A

Non-allergic

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3
Q

Triggers for asthma

A
Pets
Exercise
Pollen
Bugs
Chemicals
Cold air
Fungus
Dust
Smoke
Odours
Pollution
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4
Q

What antibody mediates asthma?

A

IgE

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5
Q

How does IgE provide longer protection?

A

First formed in response to allergen
First exposure = sensitisation
Re-exposure = allergen binds to IgE on mast cell

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6
Q

What happens when allergen binds to IgE on mast cell?

A

Calcium channels open = degranulation = histamines/prostaglandins

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7
Q

Why is asthma bad?

A

Smooth muscle spasms and narrows airway
Lining of the lung is inflamed
Mucus production increased

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8
Q

Early phase of asthma attack

A

Allergen
Mast cells
Spasmogens (bronchospasm) or chemotaxis and chemokine

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9
Q

Late phase of asthma attack

A

Chemotaxis and chemokines
Infiltration of TH2 cells
Activates inflammatory cells by cysts or EMBP/ECP
cystLTs cause airway inflammation, bronchospasm and wheezing
EMBP causes damage to epithelial cells = hyper-sensitive airways

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10
Q

Symptoms of asthma

A

Coughing, wheezing, shortness of breath, thight chest

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11
Q

Asthma symptoms on spirograph

A

Obstructive disease = increased resistance = air can’t escape lungs
FVC doesn’t change but FEV1 is reduced

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12
Q

Moderate asthma

A

SpO2 >92%
Speech normal
respiration <25/min
Pulse <110

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13
Q

Acute severe asthma

A

SpO2 >92%
Can’t complete sentences
Respiration >25
Pulse >110

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14
Q

Life-threatening asthma

A

SpO2 <92%
Silent chest, cyanosis or poor respiratory effort
Arrythmia or hypotension
Exhaustion, altered conscious

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15
Q

Treatment/monitoring of asthma

A
  • Minimise/eliminate symptoms
  • Maximum lung function
  • Prevent exacerbations
  • Minimise medication
  • Minimise adverse effects
  • Promote adherence
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16
Q

Asthma relievers

A

B2 agonists/ antimuscarinics/ methylxanthines

17
Q

Asthma preventers

A

Corticosteroids, leukotrienes, receptor antagonists, croons

18
Q

B2 agonists

A

Salbutamol/terbutaline
Stimulates B2 receptors on airway smooth muscle
Can cause tremor, tension, headache, tachycardia

19
Q

Action of B2 agonists

A

Vascular tone mediated by parasympathetic action (ACh)
Via G-alpha-q
Salbutamol activates G-protein coupled receptor
G-alpha-S receptor means that AC makes cAMP from ATP
cAMP inhibits MLCK = relaxation
PDE breaks down cAMP

20
Q

Methylxanthines

A

Theophylline
Inhibits phosphodiesterase
- Additive effect when used in conjunction with small doses of B2 agonists
- Given orally or by very slow IV infusion
- Hepatically metabolised (principally CYP1A2)
- Narrow therapeutic range
- Adverse effects: nausea, headaches, insomnia, abdominal discomfort, toxic effects in high amounts

21
Q

Antimuscarinics

A
  • Block muscarinic receptors
  • E.g. ipratropium
  • Administered by inhalation - maximal effect 30-60 mins after use but can act 3-6 hours
  • Adverse effects: dry mouth, constipation, diarrhoea, cough, headache
  • Caution needed in prostatic hyperplasia, bladder outflow obstruction, angle-closure glaucoma
22
Q

Corticosteroids

A
  • Reduce bronchial inflammatory reactions (e.g. oedema and mucous hypersecretion)
  • E.g. beclametasone, budesonide, fluticasone
  • Metered inhalation
  • Must be used regularly for maximum benefit
  • Fewer systemic effects but can cause hoarse voice, reflex cough (use spacer to relieve) and oral candidiasis
  • Oral therapy (prednisolene)for acute/chronic attacks, associated with many serous adverse effects, taken as single dose in morning
  • Hydrocortisone iv injection in emergency treatment of severe acute asthma
23
Q

Leukotriene-receptor antagonists

A
  • E.g. montelukast, zafirlukast
  • Block effects of cysteinyl leukotrienes in airways
  • Effective in reduced late phase response
  • Effective alone or with inhaled corticosteroid
  • Well tolerated
24
Q

Cromones

A
Mechanism unclear
Thought to stabilise mast cells 
Sodium cromoglicate, nedocromil sodium 
Phophylatic drug (no value for acute attacks)
25
Long B2 agonists
Salmeterol, formoterol Use with regularly inhaled corticosteroid Long term control of chronic asthma
26
Monoclonal antibodies
E.g. omalizumab Selectively binds to IgE to form complex Other MABs target inflammatory mediators
27
Well controlled asthma
- No daytime symptoms - No night-time awakening due to asthma - No need for rescue medication - No limitations on activity, including exercise - Normal lung function with minimal side effects