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CPT > Respiratory Pharmacology > Flashcards

Respiratory Pharmacology Flashcards

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1
Q

Examples of inhaled corticosteroids

A

Beclometasone
Budesonide
Fluticasone

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2
Q

What is the mechanism of action of inhaled corticosteroids for asthma management?

A
  • pass through plasma membrane > activate cytoplasmic receptors > receptors pass into nucleus to modify transcription
  • reduce mucosal inflammation, widens airways + reduces mucous
  • reduces symptoms, exacerbation + prevents death
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3
Q

What are adverse drug reactions of inhaled corticosteroids?

A

Local immunosuppressive action - candidiasis + hoarse voice

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4
Q

What are contraindications of inhaled corticosteroids?

A

Pneumonia risk in possible COPD at high dose

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5
Q

Step wise management of asthma in adults

A
  • low dose ICS
  • inhaled LABA added
  • increase ICS dose or add leukotriene receptor antagonist
  • refer for patient specialist care
    .
  • and SABA as required
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6
Q

Describe the basic mechanism of how steroid work

A
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7
Q

Outline the pharmacokinetics of inhaled corticosteroids

A
  • poor oral bioavailability
    FINISH
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8
Q

Examples of SABA

A

Salbutamol
Terbutaline

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9
Q

Examples of LABA

A

Salmeterol
Formoterol

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10
Q

Compare when SABA and LABA are used?

A
  • SABA: symptoms relief as required
  • LABA: add on therapy to ICS in asthma treatment
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11
Q

What is the mechanism of action of SABA + LABA

A
  • B2 agonists
  • Act on airway smooth muscle > increase cAMP > increase protein kinase A > bronchodilation
  • increase mucous clearance by action of cilia
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12
Q

What are adverse drug reactions of B2 agonists

A
  • tachycardia
  • palpitations
  • anxiety
  • tremors
  • increased glycogenolysis + renin
  • superventicular tachycardia (rare)
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13
Q

Why should LABA only be prescribed alongside ICS?

A

Alone can mask airway inflammation + (near) fatal attacks

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14
Q

What are important drug drug reactions of B2 agonists

A

B blockers

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15
Q

Example of leukotriene receptor antagonist

A

Montelukast

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16
Q

What is the mechanism of action of montelukast?

A

leukotriene receptor antagonists
blocks CysLT1 at CYSLTR1
- decreases action of leukotriene from mast cells/eosinophils
- decreases bronchoconstriction, mucous + oedema

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17
Q

What class of drug is montelukast?

A

Leukotriene receptor antagonist

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18
Q

What are adverse drug reactions of montelukast?

A

Headache
GI disturbance
Dry mouth

19
Q

Examples of long acting Muscarinic antagonist

A

Tiotropium

20
Q

What class of drug is tiotropium?

A

Long acting Muscarinic antagonist

21
Q

What are the uses of tiotropium?

A

Severe asthma
COPD

22
Q

What is the mechanism of action for tiotropium?

A
  • LAMA with selectivity for M3 recpetors
  • Blocks vagally mediated contraction of airway smooth muscle
23
Q

What is the adverse drug reactions of tiotropium?

A

Anticholinergic effects:
- Dry mouth
- Urinary retention + constipation
- Dry eyes

24
Q

What class of drug is theophylline?

A

Adenosine receptor antagonist
Phosphodiesterase inhibitor

25
Q

What are the uses of theophylline?

A

Chronic poorly controlled asthma

26
Q

What are important drug drug reactions of theophylline?

A

CYP450 inhibitors - increase concentrations

27
Q

When should an asthmatic self managment plan be reviewed?

A

Following treatment of exacerbation
On discharge from hospital following acute attack

28
Q

When should life threatening asthma be suspected?

A
  • Unable to complete sentences
  • peak flow 33-50% of their best
  • resp rate >25
  • > 110bpm
  • cyanotic
  • <92% O2 sats
29
Q

Treatment of acute severe + life threatening asthma

A
  • high dose B2 agonist
  • oral steroids for minimum 5 days + continue ICS
30
Q

What is the class of drug of ipratropium?

A

Short acting muscarinic antagonist

31
Q

Examples of steroids given in acute severe asthma

A

Prednisolone
Hydrocortisone

32
Q

Treatment of acute exacerbations of COPD

A
  • Nebulised salbutamol and or ipratropium
  • oral steroids
  • antibitoics (narrow spectrum if less severe, broad in greater severity)
33
Q

What are the inhaler options?
How does the technique differ?

A
  • Pressurised metered dose inhalers: slow breath in + hold
  • dry powder inhalers: own inspiratory flow (faster + deep inhalation)
34
Q

Why do ICS have relatively few systemic side effects?

A
  • low oral bioavailability
  • when absorbed P.O. > transported from stomach to liver
  • almost compete first pass metabolism
35
Q

5 tasks of managment of COPD

A
  • Confirm diagnosis
  • smoking cessation
  • record MRC dyspnea score
  • annual flu + pneumococcal vaccinations
  • medication e.g. inhalers
36
Q

Drug treatment of TB + course length

A
  • rifampicin: 6 months
  • isoniazid: 6 months
  • ethambutol: 2 months
  • pyrazinamide: 2 months
37
Q

What are adverse drug reactions of TB meds?

A
  • hepatitis: rifampicin, isoniazid, pyrazinamide
  • visual disturbances: ethambutol
  • peripheral nerve damage: isoniazid
  • orange secretions: rifampicin
38
Q

What addition management needs to be given for TB alongside the drugs and why?

A

Vitamin B6
Limit peripheral nerve damage from isoniazid

39
Q

Compare the blue vs brown inhaler

A
  • blue: bronchodilator to improve symptoms
  • brown: preventative used everyday - reduces inflammation
40
Q

Difference in NICE + BTS stepwise asthma management

A
  • low dose ICS first for both
  • NICE: add LTRA
  • BTS: add LABA
41
Q

Describe why inhale drug particles that are too small AND too big are ineffective in asthma management

A
  • too small: inhaled in alveoli + exhaled without deposition in lung
  • too big: deposition in mouth and oropharynx
42
Q

what is the mechanism of action of beta agonists?

A
  • bind to B2 adrenergic recpeotr on smooth muscles lining the airway
  • activates adenylate cyclase
  • this converted ATP > cAMP
  • cAMP activates PKA
  • causes smooth muscle relaxation > bronchodilation
43
Q

Example of SAMA + LAMA

A

SAMA: ipratropium
LAMA: tiotropium

CPT (28 decks)

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