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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
What is the mechanism of action of the LTRAs
* 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
26
In what instances is it good to use LTRAs?
* exercise induced asthma * reduce both early and later phase bronchoconstrictor responses to allergens
27
What are the side effects of the LTRAs
* abdominal pain * headache * hyperkinesia in children (hyperactivity and inability to concentrate)
28
What is step 5 in the treatment of asthma?
Specialist therapies E.g. Methylxanthines and monoclonal antibodies
29
When are methylxanthines used?
used in chronic persistent asthma (non-selective)
30
What are the actions of methylxanthines at specific doses
* modulatory and anti-inflammatory action (lower doses) * Bronchodilator (higher doses)
31
Examples of methylxanthines
Theophylline Aminophylline
32
What is the mechanism of action of methylxanthines?
* 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
Describe the theraputic index of methylxanthines
narrow theraputic index drug group
34
What are the side effects of methylxanthines
* GI upset * Arrythmias * CNS stimulation * hypotension
35
When are monoclonal antibodies used?
severe persustent allergic asthma
36
What is the mechanism of action of monoclonal antibodies in asthma treatment?
Anitbody to IgE, inhibits mediatory release from basophils and mast cells
37
Example of monoclonal antibodies
Omalizumab (Xoalir)
38
What type of therapy are monoclonal antibodies
preventer
39
How are monoclonal antibodies administered and how long do they take to work?
Injectable slow to work - peaks at 3 to 4 months redcuces exacerbations and is steroid sparing
40
What are the possible side effects of monoclonal antibodies
can cause anaphylaxis and increased risk of strokes/heartg disease
41
What is part of the monitoring plan for asthma?
* peak expiratpry flow rate * if \<50% predicted - severe asthma * Noctural dip often present
42
What are the characteristics of modertate acute asthma?
* Increasing symptoms * PEF \>50–75% best or predicted No features of acute severe asthma
43
What are the characteristics of acute severe asthma?
* 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
What are the characteristics of life-threatening asthma?
* 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
What are the characteristics of near fatal asthma?
Raised PaCO2 &/Or requires ventilation/NIV
46
What is the immediate treatment of asthma attacks in adults?
* 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
How to treat a patient with an asthma attack if not improving following initial therapy?
* IV magnesium sulphate (bronchodilates, anti- inflammatory) * switch from nebulised to IV salbutamol or IV methylxanthine (aminophylline) * monitor blood gases and patient exhaustion/alertness
48
What are the main features of asthma and its patients?
* 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
What are the main features of COPD and its patients?
* 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
What is recommended for all COPD patients?
* 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
What is the mechanism of action of muscarinic receptor antagonists?
* Cause bronchodilation, decrease mucous secretion and may increase mucociliary clearance
52
How do LAMAs affect COPD and how do they differ from beta2 agonists?
* improves outcomes and reduces exacerbations * slower onset of action
53
What are muscarinic receptor antgonists not effective against?
allergen challenger
54
Example of a SAMA
ipatropium (acute-nebuilsed route); non-selective
55
Examples of LAMAs
Tiotropium, aclindinium, umecelidinum more selective for M3 receptor
56
what are the side effects of muscarinic receptor antagonists?
* constipation * dry mouth * nausea * headache * cough * urinary retnetion
57
Treatment steps in COPD patient with no indication of asthma or corticosteroid responsiveness?
1. SABA or SAMA if required 2. LABA and LAMA 3. LABA, LAMA and ICS trial
58
Treatment steps in COPD patient with indication of asthma or corticosteroid responsiveness?
1. SABA or SAMA if required 2. LABA and ICS combination 3. LABA, LAMA and ICS therapy
59
What are the effects of ICS used in COPD?
* 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
What does SOS stand for?
S = SABA O = Oxygen S = Steroid
61
Other treatments for COPD
* 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
Assessment of COPD
* 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
Asthma - COPD overall syndrome
* 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
Acute, severe COPD exacerbations treatment
* 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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