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Physiology 3001 > Pharmacology of Asthma > Flashcards

Pharmacology of Asthma Flashcards

1
Q

What perecentage of asthma deaths are thought to be preventable?

A

2/3

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2
Q

Every day how many people die from asthma?

A

3 people

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3
Q

What are the goals of asthma treatment?

A
  • No daytime symptoms
  • No night-time waking due to asthma
  • No need for rescue medication
  • No asthma attacks
  • No limitations on activity including exercise
  • Normal lung function FEV1 and/or PEF > 80% predicted or best
  • Minimal side-effects from medication
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4
Q

What are the basic inhaler devices?

A
  • MDI = Metered dose inhaler
  • Breath-actuated
  • Accuhaler - dry powder
  • Via spacer/reservoir
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5
Q

What is the 5 step programme (up and down)?

A
  1. Intermittent reliever therapy
  2. Regular preventer therapy
  3. Initial add-on therapy
  4. Additional controller therapy
  5. Specialist therapy
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6
Q

What drugs are involved in step 1 therapy and how long do they work for?

A
  • Salbutamol, terbutaline
  • Short acting Beta2 agonist
  • Fast-acting, lasts up to 5 hrs
  • Used as required for breathlessness - rescue remedy / reliever
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7
Q

What are the side-effects of B2 agonists? (if given orally/I.V or high dose inhaled)

A
  • Sympathomimetic effects (tachycardia, tremor, heaadache)
  • Muscle pain/cramps
  • Electrolyte disturbances (e.g hypokalaemia)
  • Hyperglycaemia
  • Paradoxical bronchospasm (v. rare)
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8
Q

What are the mechanisms of action of B2 agonists?

A
  • Stimulate bronchial smooth muscle B2 receptors, relax muscles, dilate airwyas, reducing breathlessness
  • Inhibit mediator release from mast cells and infiltrating leucocytes
  • Increase ciliary action of airway epithelial cells - aids mucus clearance
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9
Q

What is involved in step 3 “initial add-on therapy”?

A
  • Long acting B2 agonist (LABA)
  • Salmeterol, Forrmoterol
  • Given regularly (combined with inhaled steroid)
  • Lasts longer (up to 12 hrs)
  • Given to prevent bronchospasm (at night or during exercise) in patients requiring long-term therapy
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10
Q

What long acting B2 agonist is slower to act? salmeterol or formoterol

A

Salmeterol (formoterol can be used as a reliever therapy salmeterol cannot be)

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11
Q

When are step 2 drugs (inhaled corticosteroids) added?

A
  • If has symptoms or using SABA more than 3 times per week
  • If walking at night with wheeze
  • If asthma attack in last 2 years
  • Adherence vital
  • Slower onset of action
  • Longer term effects over months - reduction in airways responsiveness to allergens and irritants (including exercise)
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12
Q

Describe the inhaled corticosteroid mechanism of action

A
  • They bind to glucocorticoid receptor, modify immune response
  • Inhibit formation of cytokines (includes interleukins) produced by Th2
  • Inhibit activation and recruitment to airways of inflammatory cells
  • Inhibit generation of inflammatory prostaglandins and leukotrienes, thus reducing mucosal oedema
  • Decrease mucosal inflammation, widen airway and reduces mucus secretion
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13
Q

Give some examples of inhaled corticosteroids which are used in asthma

A
  • Beclometasone
  • Budesonide
  • Fluticasone
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14
Q

Give examples of corticosteroids which would be administered during an acute severe attack

A
  • Oral route: prednisolone

- IV: hydrocortisone

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15
Q

What are the side-effects of corticosteroids?

A
  • Oropharangeal candidiasis
  • Dysphonia (hoarsness)
  • Systemic (chronic high dose, inhaled and oral)
    Osteoporosis
    Adrenal insufficiency
    Growth retardation
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16
Q

What are the drugs used in step 4 “Additional controller therapy”?

A

Leukotriene receptor antagonists (LTRA)

  • Motelukast, Zafirlukast
  • For prophylaxis therefore must be taken daily, no good for acute attacks
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17
Q

Desribe the step 4 additional controller therapy leukotriene receptor antagonists mechanism of action

A
  • Block effects of bronchoconstricting cysteinyl leukotrienes (specifically CysLT1) in the airways, resulting in bronchodilation
  • Reduce eosinophil recruitment to airways, reducing inflammation, epithelial damage and airway hyper-reactivity
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18
Q

What is the mechanism by which Montelukast and Zafirlukast are administered?

A

Orally (tablet form)

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19
Q

When are LTRAs usually indicated?

A
  • Exercise induced asthma

- Reduce both early and late phase bronchoconstrictor responses to allergens

20
Q

What are the side-effects of LTRAs?

A
  • abdo pain
  • Headache
  • Hyperkinesia in children
21
Q

What are the step 5 specialist therapies?

A
  • Methylxanthines
    Theophylline and Aminophylline
  • Monoclonal antibodies: omalizumab or mepolizumab
22
Q

How do Methylxanthines work?

A
  • Immunomodulatory and anti-inflammatory action (lower doses)
  • Bronchodilator (at higher doses)
  • Phosphodiesterase (PDE) inhibitors
  • PDE implicated in inflammatory cells - therefore inhibition reduces inflammation
  • Also PDE inhibition increases intracellular cAMP in bronchial smooth muscle, causing relaxation (bronchodilation)
  • Also blocks adenosine receptors - results in brochodilation
  • Activates histone deacetylase - immunomodulatory
23
Q

What are the side-effects of methylxanthines?

A 
- Narrow therapeutic index 
Side effects dose or rate related:
- GI upset 
- Arrhythmias 
- CNS stimulation e.g seizures
- Hypotension 
- Can possibly interact with antibiotics
24
Q

Describe how an monoclonal antibody such as omalizumab is used to treat asthma

A
  • “Preventer”
  • Inject route (fortnightly/monthly)
  • Slow to work - peaks at 3 to 4 months
  • Reduces exacerbations and is steroid sparing
  • Can cause anaphylaxis and increase risk of strokes/heart disease
  • Expensive
25
Q

How is asthma monitored?

A
  • Peak expiratory flow
  • If >50% predicted - severe asthma
  • Nocturnal dip often present
26
Q

What levels of peak flow indicate what level of asthma?

A
  • Moderate acute asthma PEF >50-75%
  • Acute severe asthma PEF 33-50%
  • Life-threatening asthma < 33%
27
Q

What indicates near-fatal asthma?

A

Raised PaCO2 &/or requires ventilation/NIV

28
Q

What indicates acute severe asthma?

A

Any one of:

  • PEF 33-50% best or predicted
  • RR >= 25/min
  • HR >= 110/min
  • Inability to complete a sentence in one breath
29
Q

What indicates life-threatening asthma?

A

Any one of the following

  • Altered consciousness
  • Exhaustion
  • Arrythmia
  • Hypertension
  • Cyanosis
  • Silent chest
  • poor respiratory effort
  • PEF < 33% best/predicted
  • SpO2 < 92%
  • PaO2 < 8 kPa
  • “Normal” PaCO2 (4.6 - 6 kPa)
30
Q

How is acute severe asthma managed immediately?

A
  • Oxygen (to maintain a SpO2 at 94-98%)
  • SABA (salbutamol or terbutaline) via nebuliser
  • IV steroid = hydrocortisone…SWITCH to ORAL steroid = prednisolone
  • +/- antibiotics
  • +/- muscarinic agonist inhaled
31
Q

If patient does not improve after steps are taken to treat severe asthma what should you consider?

A
  • IV magnesium sulphate (bronchodilates, anti-inflammatory)
  • Switch from nebulised to IV salbutamol or IV methylxanthine (aminophylline)
  • Monitor blood gases and patient exhaustion/alertness
32
Q

What are the first 3 basic treatments for asthma?

A

SOS

  • Salbutamol
  • Oxygen
  • Steroid
33
Q

When would an ICS be used in the treatment of COPD?

A
  • limited benefit
  • If FEV1<50% predicted and have 2 or more exacerbations in a year which require antibiotics or oral steroids
  • High doses may increase risk of pneumonia and osteoperosis
34
Q

What are muscarinic receptor antagonists used to treat?

A

COPD (not asthma)

35
Q

What can muscarinic antagonists cause?

A
  • Increased bronchodilation
  • Decreased mucous secretion
  • Increased mucociliary clearance
36
Q

How long does it take for muscarinic antagonists take affect?

A

30 - 60 minutes

37
Q

What muscarinic receptor is in the airways and is involved in brochoconstriction and mucous secretion?

A

M3

38
Q

Give an example of a SAMA?

A

Ipratropium (acute - nebulised route), non selective

39
Q

Give an example of a LAMA

A

Tiotropium, aclidinium, umeclidinium - more selective for M3 receptor

40
Q

What are the side effects of muscarinic antagonists?

A

Uncommon

  • Constipation
  • Dry mouth
  • Nausea
  • Cough
  • Urinary retention (men)
  • Can worsen angle closure glaucoma
41
Q

What other treatments can be used in the treatment of COPD?

A
  • Methylxanthines
  • Mucolytics - if chronic productive cough, reduce sputum viscosity, Carbocysteine
  • Phosphodiesterase type 4 inhibitor - Roflumilast - if severe COPD, repeated exacerbations
  • Longterm antibiotics - azirthromycin
  • Anti-IgE monoclonal antibody
  • Long term oxygen
42
Q

How is COPD assessed?

A
  • Primarily based on patient symptoms, ADL, exercise capacity, speed of symptom relief with SABA
  • Changes in lung function - spirometry
  • Risk of exacerbations
43
Q

What are indicators of high risk?

A

Two exacerbations or more within the past year or FEV1 < 50% predicted are indicators of high risk

44
Q

What indicates that a patient has ACOS - Asthma COPD Overlap Syndrome?

A
  • Higher eosinophil count
  • FEV1 swings
  • Diurinal variation in PEFR
  • Respond better to steroids (reducing exacerbation rate)
  • More reversible to B2 agonists
45
Q

How are exacerbations of acute, severe COPD treated?

A
  • Nebulise SABA/SAMA (on air)
    • oral prednisolone
    • antibiotic if needed
  • Physio
  • 24-28% Oxygen (PaO2/PaCO2 needs to be monitored)
  • Extreme - NIV - non-invasive ventilation , Intubation

Physiology 3001 (20 decks)

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