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MD3001resp > pharmacological treatment of asthma and COPD > Flashcards

pharmacological treatment of asthma and COPD Flashcards

1
Q

what are the features of asthma?

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

what is the pathogenesis of asthma?

A

acute and chronic inflammatory responses in airway

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3
Q

what are the goals of treatment for asthma?

A
  • no daytime systoms
  • no time time waking
  • no need for rescue medication
  • no asthma attacks
  • no limitations on activity
  • normal lung function FEV1>1%)
  • minimal side effects from medication
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4
Q

what are the routes of administration for treating asthma?

A

primarily inhaled
- directly delivered to the site of action
- rapid response
- allows smaller doses than systemic route
- reduces side effects
- efficacy. of route depends on type and severity of asthma

  • oral and injectable treatment aswel.
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5
Q

what are the different types of inhaler device?

A
  • MDI= metered dose inhaler
  • breathe - acuated
  • accuhaler = dry powder
  • spacer/ aero chamber
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6
Q

what is the purpose of ‘spacers’?

A
  • large particles of aerosol are deposited in the chamber before the patient inhales
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7
Q

what is good about ‘spacers’/ nebulisers?

A

people who take inhalers are more prone to getting a hoarse voice or oral thrush, so by taking their medication through a spacer they are less likely to develop these symptoms.

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8
Q

what are the downsides to nebulisers?

A
  • they are not used as much because they need yearly maintenance
  • people who have them in their house are less likely to call an ambulance when they are having an asthma attack which is bad.
  • higher risk of side effects
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9
Q

describe nebuliser route?

A
  • use O2, ultrasonic power or compressed air to break up the drug in solution into fine mist.
  • uses a face mask/mouth piece
  • gives a high dose of reliever quickly in acute severe asthma.
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10
Q

what are the 5 steps up and down of pharmacological treatment of asthma?

A

1) intermittent receiver therapy
2) regular preventer therapy
3) initial add on therapy
4) additional controller therapy
5) specialist therapies

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11
Q

what are the 5 main drugs used to treat and prevent asthma? (receivers and preventers)

A

1) beta-2 agonist = salbutamol (short acting)
2) glucocorticoids = beclometasone, budesonide
3) beta- 2 agonist = salmeterol (long acting)
4) cysteine leukotriene antagonist (LRTA) = montelukast
5) a) methylxanthines = theophylline
b) monoclonal antibodies = anti-IgE treatment = omalizumab

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12
Q

describe the mechanism of action of B2 agonist
(LABA and SABA)

what steps do these cover?

A

THESE WILL COVER STEPS 1 AND 2!!!!

  • they stimulate bronchial smooth muscle B2 receptors, relax smooth muscle, dilate airways and reduce breathlessness (basically reduce symptoms)
  • inhibit mediator release from mast cells and infiltrating leukocytes
  • increase ciliary action of away epithelial cells, aiding in mucus clearance.
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13
Q

describe the difference ion duration of LABA and SABA?

A

SABA= fast acting last up to 5 hrs, used as required

LABA= given regularly (with inhaled steroid), lasts longer (up to 12 hrs, given to prevent bronchospasm in patients requiring long term therapy

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14
Q

what are the side effects of B2 agonists?

A

(you tend to only get side effects if its a high dose that is given orally or through IV)

  • sympathomimetic effects (increase in heart rate, tremor etc)
  • muscle pain/cramps
  • electrolyte disturbances
  • hyperglycaemia
  • paradoxical bronchospasm
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15
Q

describe step 2?
what drug is given?

A

give INHALED CORTICOSTEROIDS

  • this is regular preventer therapy
  • acts as an anti-inflammatory and immunosuppressive
  • slow onset of action
  • longer term it will effect the airways responsiveness to allergens and irritants
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16
Q

when will you add an inhaled corticosteroid?

A
  • add if has symptoms of or using SABA more than 3 times a week
  • if waking up in the middle of the night with wheeze
  • ## is they have had an asthma attack in the last 2 years
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17
Q

describe the mechanism of action of inhaled corticosteroids?

A
  • bind to glucocorticoid receptor, modify immune response
  • inhibit formation of cytokines
  • inhibit activation and recruitment to airways of inflammatory cells
  • inhibits generation of inflammatory prostaglandins and leukotrienes, reducing coal oedema.
  • DECREASE MUCOSAL INFLAMMATION, WIDENS AIRWAY AND REDUCES MUCUS SECRETION.
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18
Q

WHAT ARE THE SIDE EFFECTS OF CIRTICOSTEROID USE?

A
  • oropharyngeal cadidiasis (oral thrush)
  • dysphonia (hoarseness)
  • systemic effects
  • osteoporosis
  • adrenal insufficiency
  • growth retardation
19
Q

what drugs are given at step 4?

A

LRTA’s (leukotriene receptor antagonist)
BUT
first try increasing dose if the inhaled corticosteroids.

LRTA’s = montelukast
- for prophylaxis treatment (not for an acute attack) therefore it must be taken daily orally

20
Q

mechanism of action of step 4 drugs (LRTA’s)?

A
  • blocks leukotrienes
  • blocks the effect of bronchocontstricitng cysteinyl leukotrienes (specifically CysLT1) in the airways, resulting in bronchodilator.
  • reduces eosinophil recruitment to always, reducing inflammation, epithelial damage and airway hyper- reactivity
21
Q

when are LRTA’s good?

A
  • exercise induced asthma
  • reduce both early and late phase bronchocontriction reposes to allergies
22
Q

what are the side effects to LRTA’s

A
  • abdominal pain
  • headache
  • hyperkinesia in children
23
Q

what is step 5? “specialist therapies”
what drug is given?
EXAMPLE A

A
  • immunomodulatory and anti-inflammatory action at lower doses
  • bronchodilator (at higher dose)

EXAMPLE A (theophylline) = methylxanthines which are used in the chronic chronic persistent asthma

24
Q

describe the mechanism of action of methylxanthines?

A
  • phosphodiesterase inhibitors (PDE)
  • PDE implicate in inflammatory cells (therefore inhibition reduces inflammation)
  • PDE inhibition increases intracellular cAMP in bronchial smooth muscle, causing relaxation
  • blocks adenosine receptor, resulting in bronchodilator
  • activates histone deacetylase (immunomodulatory)
25
Q

what are the side effects of methylxanthine?

A

narrow therapeutic index drug group, measuring serum drug concentrations, be aware of potential for drug interactions.

dose or rate related:
- gi upset
- arrhythmias
- CNS stimulation
- hypotension

26
Q

example B of specialist therapies drug?

when are they used?

A

monoclonal antibodies (the mass) eg- Omalizumab
‘preventer’
- used is severe persistent allergic asthma

27
Q

describe the mechanism of action of monoclonal antibodies (MABS)

A
  • antibody to IgE, inhibits mediate release from basophils and mast cells
    -injectible
  • slow to work (peaks at 3 to 4 months)
  • reduces excererbations and is steroid sparing
28
Q

down sides to MABS?

A
  • can cause anaphylaxis and increase the risk of strokes and heart disease
  • expensive
29
Q

describe a monitoring plan?

A
  • peak Flow meter, 3 times, twice a day.
  • should see a nocturnal dip

<50% then severe asthma

30
Q

manaamnet of acute severe asthma?

A

SOS
- SABA via a nebuliser
- Oxygen (94-98%)
- steroid h(hydrocortisone or prednisolone)

give an antibiotic if triggered by an infection

31
Q

how should the short acting b2- agonist be given?

A

give 2-10 puffs, each to be inhaled separately through a spacer

32
Q

what do you give the patient is still not improving?

A

IV magnesium sulphate (bronchodilators, anti-inflammatory)

switch from neublised to IV salbutamol or IV methylxanthine

33
Q

What is the recommendation for all COPD patients?

A
  • Smoking cessation,
  • Early use of bronchodilators,
  • Inhaled corticosteroids,
  • Immunise against pneumovax and flu
  • Pulmonary rehab
  • Self management,
  • Optimise treatment for co-morbidities
34
Q

What are the features of muscarinic receptor antagonists?

A

They cause bronchodilation, decrease mucus secretion and may increase mucociliary clearance. Long acting muscarinic antagonists can improve outcomes, has a slower onset of action, not effective against allergen challenge.

35
Q

Describe the overview of the NICE COPD guidelines if there is suggestion of asthma/steroid responsiveness

A

Step one - If required SABA or SAMA.

Step two - LABA and ICS combination.

Step three - LAMA and LABA and ICS

36
Q

Describe the overview of the NICE COPD guidelines if there is no suggestion of asthma/steroid responsiveness

A

Step one - If required then SABA or SAMA.

Step two - LABA and LAMA.

Step three - LABA, LAMA and ICS trial

37
Q

what are the different types of Long acting muscarinic antagonist (LAMA)
and SAMA?

A

SAMA = short acting
Ipratropium - non selective, nebulised route

LAMA= long acting
tittropium = more selective for M3 receptor

38
Q

what are the side effects to muscarinic antagonists

A

uncommon
- constipation
- dry mouth
- naesuae
- headache
- cough

39
Q

describe the use of inhaled corticosteroid in COPD?

what may a high dose increase the risk of?

A
  • they have limited benefit
  • inflammatory cells are responsible for COPD (neutrophils and macrophages) , so they are less responsive than lymphocytes and eosinophils to the action of corticosteroids.
  • only use of FEV1<50% and you have 2 or more exacerbations in a year which have required steroids or antibiotics
  • a high dose may increase the risk of pneumnia and osteoporosis
40
Q

What are some other treatments for COPD?

A
  • Methylxanthines,
  • Mucolytics - If chronic productive cough, reduced sputum viscosity.
  • Phosphodiesterase Type-4 inhibitors,
  • Long term antibiotics,
  • Anti-IgE monoclonal antibody.
  • Long term oxygen
41
Q

Describe the assessment of COPD

A
  • Primarily based on patient symptoms,
  • Changes in lung function (spirometry)
  • Risk of exacerbation
42
Q

Describe the treatment of acute severe COPD exacerbations

A
  • Nebulise SABA/SAMA,
  • Add oral prednisolone,
  • Antibiotics if infected
  • Physio
  • 24-28% O2,
  • If extreme then NIV or intubation
42
Q

Describe features of asthma-COPD overlap syndrome

A
  • Higher eosinophil count
  • FEV1 swings,
  • Diurnal variation in PEFR
  • Respond better to steroids
  • More reversible to Beta 2 agonists.

MD3001resp (41 decks)

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