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MD3001 - Respiratory Pharmacology and Treatment > COPD and Asthma > Flashcards

COPD and Asthma Flashcards

1
Q

What are the 3 main features of asthma?

A
  • airway narrowing (reversible)
  • Airway hyper-responsiveness
  • Airway inflammation
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2
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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3
Q

What are the main approaches to treatment with asthma?

A
  • start at an appropraite level
  • achieve early control
  • maintain control by stepping up when needed and down when control is good

AND

  • Check concordance/compliance/adherence
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4
Q

Main routes of administration of asthma

A
  • inhaled
  • oral/injectable
  • nebulised
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5
Q

What are the main benefits of inhaled medication?

A
  • direct delivery to site of action
  • rapid response with rescue medication
  • smaller doses than systemic route
  • reduced side effects
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6
Q

What are the different types of inhaler devices?

A
  • MDI = metered dose inhaler
  • breath-actuated
  • Accuhaler - dry powder
  • via spacer/aerochamber
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7
Q

Explain how the nebulised route works

A
  • use O2 compressed asir or ultrasonic power to break up drug solutions into fine mist
  • facemask/mouth piece
  • give high doses quickly of ‘reliver’ medications in acute asthma to get a fast response
  • risk of side effects is higher
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8
Q

What are the 5 steps in pharmacological management of asthma?

A
  1. Intermittent reliver therapy
  2. Regular preventer therapy
  3. initial add-on therapy
  4. additional controller therapy
  5. specialist therapies
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9
Q

What are the 5 main drugs used to treat asthma?

A
  1. Beta2 adrenoreceptor agonists
  2. Gluco-corticosteroids
  3. Cysteinyl leukotriene antagonists
  4. Methylxanthines
  5. Monoclonal antibodies
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10
Q

What is step 1 of the asthma treatment therapy?

A

Intermittent Reliver - short acting beta2 agonists (short and long-acting)

e.g. Salbutamol, Terbutaline

Fast acting - lasts up to 5 hrs

“as required for breathlessness” - rescue remedy/reliver

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11
Q

What is the mechanism of beta2 agonists in asthma treatment?

A
  • stimulate bronchial smooth muscle beta2 receptors, relax muscles, dilate airways, 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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12
Q

What is step 3 of the asthma treatment therapy?

A

Long acting beta2 agonist (LABA)

E.g. Salmeterol, Formoterol (never for reliver therapy)

Given regularly (combined with inhaled steroid)

Lasts longer than SABA - up to 12 hrs

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13
Q

Why is a LABA prescribed?

A
  • given to prevent bronchospasm (at night or during exercise) in patients requiring long term therapy
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14
Q

What should not be prescribed for as a sole tehrapy for asthma?

A

Long-acting Beta2 agonist

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15
Q

What is slower to act between salmeterol and formoterol?

A

salmeterol

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16
Q

What are the side effects of beta2 agonists if given orally/IV or high dose inhaled?

A
  • sympathomimetic effects; tachycardia, tremor, headache
  • muscle pain/cramps
  • electrolyte disturbances (hypokalaemia)
  • hyperglycaemia
  • paradoxical bronchospasm (very rare)
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17
Q

What is step 2 in the treatment of asthma?

A

Inhaled corticosteroid (ICS) - regular preventer therapy

  • anti-inflammatory and immunosuppressive
  • Add if they have symptoms that require the use of a SABA more than 3 times per week
  • If waking at night with wheeze
  • if they have had an asthma attack in the last 2 years
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18
Q

What is the mechanism of action of inhaled corticosteroids?

A
  • bind to glucocorticoid receptor, modify ummune response
  • inhibit formation of cytokines (includes interleukins)
  • Inhibit activation and recruitment to airways of inflammatory cells
  • Inhibit generation of inflammatory prostaglandins and leukotrienes, thus reducing mucosal oedema
  • decrease mucosal inflammation, widens airways and reduces mucus secretion
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19
Q

How do inhaled gluco-corticosteroids differ from beta2 agonists?

A
  • Adherance = VITAL
  • slower onset of action
  • longer term effects over months - reduction in airway responsiveness to allergens and irritants (including exercise)
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20
Q

What are examples of inhaled corticosteroids?

A

beclomethasone, budesonide, fluticasone

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21
Q

What is used in acute severe asthma attacks from the corticosteroids?

A
  • Oral = prednisolone
  • IV = hydrocortisone
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22
Q

What are the side effects of corticosteroids?

A
  • oropharyngeal candidiasis (oral thrush)
  • Dysphonia (hoarseness)
  • Systemic:
    • Osteoporsis
    • Adrenal insufficiency
    • Growth retardation
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23
Q

What is Step 4 of the asthma treatment schedule?

A

Additional controller therapy

  • increase dose of ICS
  • add a leukotriene receptor antagonist
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24
Q

Examples of leukotriene receptor antagonists

A

montelukast and Zafirlukast (tablet form)

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25
Q

What is the mechanism of action of the LTRAs

A
  • block effects of bronchoconstriciting cysteinyl leukotrienes (specifically CysLT1) in the airways, resulting in bronchodilation
  • reduce eosinophil recruitment to airways, reducing inflammation, epithelial damage and airway hyperreactivity
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26
Q

In what instances is it good to use LTRAs?

A
  • exercise induced asthma
  • reduce both early and later phase bronchoconstrictor responses to allergens
27
Q

What are the side effects of the LTRAs

A
  • abdominal pain
  • headache
  • hyperkinesia in children (hyperactivity and inability to concentrate)
28
Q

What is step 5 in the treatment of asthma?

A

Specialist therapies

E.g. Methylxanthines and monoclonal antibodies

29
Q

When are methylxanthines used?

A

used in chronic persistent asthma (non-selective)

30
Q

What are the actions of methylxanthines at specific doses

A
  • modulatory and anti-inflammatory action (lower doses)
  • Bronchodilator (higher doses)
31
Q

Examples of methylxanthines

A

Theophylline

Aminophylline

32
Q

What is the mechanism of action of methylxanthines?

A
  • Phosphodiesterase (PDE) inhibitors
  • PDE implicated in inflammatory cells - inhibition reduces inflammation
  • PDE inhibition increases intracellular cAMP in bronchial smooth muscle, causing relaxation (bronchodilation)
  • blocks adenosine receptors (bronchodilation)
  • actiavtes histone deacetylase - immunomodulatory
33
Q

Describe the theraputic index of methylxanthines

A

narrow theraputic index drug group

34
Q

What are the side effects of methylxanthines

A
  • GI upset
  • Arrythmias
  • CNS stimulation
  • hypotension
35
Q

When are monoclonal antibodies used?

A

severe persustent allergic asthma

36
Q

What is the mechanism of action of monoclonal antibodies in asthma treatment?

A

Anitbody to IgE, inhibits mediatory release from basophils and mast cells

37
Q

Example of monoclonal antibodies

A

Omalizumab (Xoalir)

38
Q

What type of therapy are monoclonal antibodies

A

preventer

39
Q

How are monoclonal antibodies administered and how long do they take to work?

A

Injectable

slow to work - peaks at 3 to 4 months

redcuces exacerbations and is steroid sparing

40
Q

What are the possible side effects of monoclonal antibodies

A

can cause anaphylaxis and increased risk of strokes/heartg disease

41
Q

What is part of the monitoring plan for asthma?

A
  • peak expiratpry flow rate
  • if <50% predicted - severe asthma
  • Noctural dip often present
42
Q

What are the characteristics of modertate acute asthma?

A
  • Increasing symptoms
  • PEF >50–75% best or predicted No features of acute severe asthma
43
Q

What are the characteristics of acute severe asthma?

A
  • Any one of:
    • PEF 33–50% best or predicted
    • respiratory rate ≥25/min
    • heart rate ≥110/min
    • inability to complete sentences in one breath
44
Q

What are the characteristics of life-threatening asthma?

A
  • Any one of the following in a patient with severe asthma:
    • Altered consciousness
    • Exhaustion
    • Arrythmia
    • Hypertension
    • Cyanosis
    • Silent chest
    • Poor respiratory effort
    • PEF < 33% best/predicted
    • SpO2 < 92%
    • PaO2 < 8 kPa
    • “Normal” PaCO2 (4.6-6.0kPa)
45
Q

What are the characteristics of near fatal asthma?

A

Raised PaCO2 &/Or requires ventilation/NIV

46
Q

What is the immediate treatment of asthma attacks in adults?

A
  • oxygen (to maintain a SpO2 @ 94-98%)
  • SABA (salbutamol or terbutaline) via nebuliser
  • IV Steroid = hydrocortisone
    • switch to ORAL steroid = prednisolone
    • or – antibiotics
    • or – muscarinic antagonist inhaled
47
Q

How to treat a patient with an asthma attack if not improving following initial therapy?

A
  • IV magnesium sulphate (bronchodilates, anti- inflammatory)
  • switch from nebulised to IV salbutamol or IV methylxanthine (aminophylline)
  • monitor blood gases and patient exhaustion/alertness
48
Q

What are the main features of asthma and its patients?

A
  • Non-smoking related
  • Allergic
  • Tends to be in younger patients
  • intermittent
  • non-progressive
  • eosinophil infiltration
  • diurnal variation
  • good corticosteroid response
  • good bronchodilator response
  • preserved FVC and TLCO
  • normal gas exhcnage
49
Q

What are the main features of COPD and its patients?

A
  • smokers
  • non-allergic
  • over 50s
  • chronic
  • progressive decline
  • neutrophils
  • no diurinal variation
  • poor corticosteroid response
  • poor bronchodilator response
  • reduced FVC and TLCO
  • impaired gas exchange
50
Q

What is recommended for all COPD patients?

A
  • smoking cessation
  • early use if ling acting bronchodilators (LABA)
  • ICS - depend of FEV1.0 and response
  • immunise - pneumovax and flu
  • pulmonary rehab
  • self-management plan
  • optimsie treatment for co-morbidities
51
Q

What is the mechanism of action of muscarinic receptor antagonists?

A
  • Cause bronchodilation, decrease mucous secretion and may increase mucociliary clearance
52
Q

How do LAMAs affect COPD and how do they differ from beta2 agonists?

A
  • improves outcomes and reduces exacerbations
  • slower onset of action
53
Q

What are muscarinic receptor antgonists not effective against?

A

allergen challenger

54
Q

Example of a SAMA

A

ipatropium (acute-nebuilsed route); non-selective

55
Q

Examples of LAMAs

A

Tiotropium, aclindinium, umecelidinum

more selective for M3 receptor

56
Q

what are the side effects of muscarinic receptor antagonists?

A
  • constipation
  • dry mouth
  • nausea
  • headache
  • cough
  • urinary retnetion
57
Q

Treatment steps in COPD patient with no indication of asthma or corticosteroid responsiveness?

A
  1. SABA or SAMA if required
  2. LABA and LAMA
  3. LABA, LAMA and ICS trial
58
Q

Treatment steps in COPD patient with indication of asthma or corticosteroid responsiveness?

A
  1. SABA or SAMA if required
  2. LABA and ICS combination
  3. LABA, LAMA and ICS therapy
59
Q

What are the effects of ICS used in COPD?

A
  • Limited benefit
  • inflammatory cells responsible for COPD have less response than lymphocytes and eosinophils to the actions of corticosteroids
  • Use 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 osteoporosis
60
Q

What does SOS stand for?

A

S = SABA

O = Oxygen

S = Steroid

61
Q

Other treatments for COPD

A
  • Methylxanthines – theophylline, aminophylline
  • Mucolytics – if chronic productive cough, reduce sputum viscosity, Carbocysteine
  • phosphodiesterase type-4 inhibitor – Roflumilast – if severe COPD, repeated exacerbations
  • Longterm antibiotics – azithromycin
  • Anti-IgE monoclonal antibody
  • Long term oxygen
62
Q

Assessment of COPD

A
  • Primarily based on patient symptoms, ADL, exercise capacity, speed of symptom relief with SABA
  • Changes in lung function – Spirometry
  • Risk of exacerbations
  • Two exacerbations or more within the past year or FEV1 < 50 % predicted are indicators of high risk
63
Q

Asthma - COPD overall syndrome

A
  • Difficult to distinguish from asthmatic smokers who have airway remodelling (ie reduced FVC)
  • Higher eosinophil count
  • FEV1 swings
  • Diurnal variation in PEFR
  • Respond better to steroids (reducing exacerbation rate)
  • More reversible to b2 agonists
64
Q

Acute, severe COPD exacerbations treatment

A
  • Nebulise SABA/SAMA (on air) • + oral prednisolone
    • antibiotic if infected
  • Physio
  • 24-28% Oxygen (with care! – watch PaO2/PaCO2)
  • Extreme – NIV, Intubation

MD3001 - Respiratory Pharmacology and Treatment (6 decks)

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