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Respiratory system > Asthma therapeutics > Flashcards

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
Q

Long B2 agonists

A

Salmeterol, formoterol
Use with regularly inhaled corticosteroid
Long term control of chronic asthma

26
Q

Monoclonal antibodies

A

E.g. omalizumab
Selectively binds to IgE to form complex
Other MABs target inflammatory mediators

27
Q

Well controlled asthma

A
  • 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

Respiratory system (23 decks)

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