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CPT > L13 Respiratory Pharmocology > Flashcards

L13 Respiratory Pharmocology Flashcards

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1
Q

Asthma

A

Chronic, intermittent and reversible airway disease causing obstruction and type 4 hypersensitivity to small airways

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2
Q

Features of asthma

A 
Eosinophilic 
Mucosal oedema and plugging 
Bronchospasm - constriction of small airways 
Wheezing 
Coughing 
Atopy
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3
Q

Considerations before stepping up or down

A

Adherence
Inhaler technique
Eliminate triggers I.e. allergens

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4
Q

Uncontrolled asthma

A

3+ days a week with symptoms
3+ days a week with SABA required
1+ nights a week with awakening due to asthma

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5
Q

Stepwise treatment of asthma

A
  1. SABA throughout - salbutamol
  2. low dose ICS
  3. Regular preventer - low dose ICS
  4. Add LABA - salmeterol
  5. Increased dose of ICS or LTRA
  6. Specialist therapies
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6
Q

Inhaled corticosteroid examples

A

Beclometasone
Budesonide
Fluticasone

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7
Q

ICS mechanism of action

A

Regular preventer when reliever alone is not sufficient

  • passes through the plasma membrane as liopophilic
  • activates cytoplasmic receptors (glucocorticoid receptor in cytosol)
  • forms complex and passes into the nucleus
  • modifies transcription therefore controls gene expression
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8
Q

Effects of ICS

A

Reduces mucosal inflammation - activates genes for anti- inflammatory mediators and represses genes for inflammatory mediators
Widens airways - activates genes for Beta 2 agonists for bronchodilation
Reduces mucus - represses genes for inflammatory mediators

  • Therefore reduces symptoms and exacerbations to prevent death
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9
Q

Side effects of ICS

A

Local immunosuppression - candidiasis (oral thrush) and hoarse voice

Pneumonia risk in COPD patients

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10
Q

Pharmacokinetics of ICS

A
  • Poor oral bioavailability but inhaled
  • large lipophilic side chain for slow dissolution in aqueous bronchial fluid
  • adheres and acts locally
  • high affinity for glucocorticoid receptors in the cytosol
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11
Q

If ICS taken orally

A
  • Transported from stomach to the liver via the hepatic portal system quickly
  • almost complete first pass metabolism - low risk of systemic side effects
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12
Q

Beta 2 agonists

A

SABA - short acting beta 2 agonist used when required - symptom relief via bronchodilation

LABA - add on to ICS used when required

  • bronchodilation
  • increases mucus clearance by cilia action
  • prevents bronchoconstriction prior to exercise
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13
Q

Beta 2 agonists used regularly

A

Reduced tolerance

Quickly fixed in young adults

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14
Q

Beta 2 agonist examples

A

Fast:
SABA - salbutamol and terbutaline
LABA - formoterol (more potent and efficacious than salmeterol)

Slow:
LABA: salmeterol

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15
Q

Beta 2 agonist mechanism

A
  1. Beta 2 agonist bind to GPCR
  2. GDP is replaced by GTP
  3. G alpha S sub unit dissociates from the G beta and gamma sub unit
  4. G alpha S activates adenyl cyclase
  5. Which stimulates ATP to convert into cAMP
  6. cAMP activate protein kinase A
  7. Which causes bronchial smooth muscle relaxation
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16
Q

Beta 2 agonist ADR

A

Increases sympathetic activity - flight or flight effects e.g.

  • tachycardia
  • palpitations
  • anxiety
  • tremor

COPD patients:

  • Supraventricular tachycardia - increased SAN activity, increases HR and decreased refractory period and the AVN
  • increased risk of right sided HF And CVD
Increased glycogenolysis (liver) - increased blood glucose 
Increased renin (kidney) - due to increeas3d HR
17
Q

Why is LABA used with ICS?

A

Increased risk of death when used alone

Masks airway inflammation and near fatal attacks

18
Q

Contraindications of beta agonists

A

Beta blockers as antagonist

19
Q

When is LABA added?

A

Asthma not controlled with ICS

Frequent asthma exacerbations

20
Q

Advantages of combined inhaler

A

Increase adherence
Safer for the patient - as not taking LABA alone
Less prescriptions
Easier to take

21
Q

Leukotriene receptor antagonist example

A

Montelukast

22
Q

Leukotrienes

A
  • Mast cells and eosinophils release LTC4
  • leukotrienes which cause bronchoconstriction, increased mucus production and mucosal oedema as there is increased vascular permeability
  • via CysLT1 - GPCR
23
Q

LTRA mechanism of action

A

Block CysLT1 receptors preventing bronchoconstriction, increased mucous production and mucosal oedema

Only useful in 15% of asthmatic patients

24
Q

ADRs of LTRA

A

Headache
GI disturbances
Dry mouth
Hyperactivity

25
Q

Additional controller therapies

A

LAMA - long acting muscarinic antagonist - tiotropium
SAMA - short a timing muscarinic antagonist- ipratropium
Adenosine receptor antagonist - theophylline

Special maintenance therapy - prednisolone

26
Q

LAMA mechanism of action

A

Use:
- in severe asthma and COPD

Mechanism:

  • selective for M3
  • inhibition of muscarinic receptors - anticholinergic
  • prevents bronchoconstriction
27
Q

Side effects of LAMA

A

Anticholinergic therefore:

  • dry mouth
  • urinary retention
  • dry eyes
28
Q

Adenosine receptor antagonist

A

Type of methylxanthine - found in coffee
Also acts as a phosphodiesterase inhibitor

Theophylline - oral
Aminophylline - IV in acute emergency asthma patients

29
Q

ADRs of adenosine receptor antagonists

A

Narrow therapeutic index
Potentially life threatening arrhythmia

Interactions with CYP450 inhibitors - increases the concentration of theophylline as there is less metabolism

30
Q

Prednisolone

A

Oral steroid for severe uncontrolled asthma
Prescribed by a specialist and given a steroid card (COPD)

Post acute exacerbation - short course for at least 5 days
Post acute COPD - 5-7 days after hospital discharge

31
Q

Self management plan

A

For asthmatic patients

Written instruction of when and how to take inhalers

32
Q

Acute severe asthma presentation

A

Struggling to complete sentences
Resp rate - 25 +
Heart rate - 110+
Peak flow - a third to half of best or predicted

33
Q

Life threatening

A

Peak flow - less than a third of best or predicted
Arterial oxygen saturation - less than 92%
Silent chest
Cyanosis
Exhaustion
Hypotension
Altered conscious level

34
Q

Treatment for acute severe or life threatening asthma

A

Oxygen - aim for 94-98%
High dose nebulised beta 2 agonist
Prednisolone for 7- 14 weeks along with ICS
Nebulised ipratropium bromide with B2 agonist - if beta 2 agonist response is poor

Aminophylline is life threatening with no success with other treatments
- caution if taking theophylline

35
Q

COPD 5 tasks of management

A 
Task 1 - confirm COPD diagnosis 
Task 2 - stop smoking 
Task 3 - record MRC dyspnoea score - pulmonary rehabilitation for score less than 2 
Task 4 - offer vaccinations 
Task 5 - consider medication
36
Q

How to treat COPD

A

Acute exacerbation requiring hospitalisation:

  • nebulised salbutamol or ipratropium driven by air not oxygen if hypercapnic
  • prednisolone (less effective than eosinophilic asthma as COPD is neutrophilic)
  • antibiotics
  • review of chronic treatment and action plan
37
Q

Inhalers

A

Blue - salbutamol reliever SABA
Brown - beclometasone preventer - ICS
Green - Ipratropium - SAMA

38
Q

Inhaler options

A

Pressurised metered dose inhalers - slow breath in and hold
- can be used with spacer

Breath actuated pMDI - when breathing in

Dry powder inhalers (DPI) - fast deep inhalation

39
Q

Particle size

A

1-5 microns - perfect

Too small - inhaled to alveoli and exhaled without being deposited
Too big - deposited in mouth and oropharynx

CPT (23 decks)

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