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Respiratory > Respiratory Drugs > Flashcards

Respiratory Drugs Flashcards

1
Q

What are the signs of infectious exacerbations of COPD?

A

Increasing dyspnoea
Increased sputum purulence
Increased sputum volume/viscosity

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2
Q

How is type 2 respiratory failure characterised?

A

Hypercapnic respiratory failure - PaCO2 higher than 50mmHg

- hypoxaemia is common

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3
Q

What are the groups of treatments which someone with infective COPD exacerbation, Type 2 respiratory failure and a right sided chest infection need?

A 
Oxygen 
Nebulisers
Antibiotics 
Steroids
Bronchodilators - if needed
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4
Q

How asthma managed during an acute attack?

A 
High flow oxygen 
Nebulised bronchodilators 
IV magnesium 
IV salbutamol/aminophylline
Steroids 
Consider ventilation - if PaCO2 is normal or increased
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5
Q

How is an acute exacerbation of COPD managed?

A 
Tailored oxygen after ABG results - be careful because oxygen can kill COPD patients 
Nebulised bronchodilators 
IV salbutamol/aminophylline 
Steroids
Consider ventilation (non-invasive)
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6
Q

What antibiotics should be given to an infective COPD exacerbation and a right sides lung infection?

A

IV Amoxicillin - 500mg every 8 hours for 5 days
Oral Clarithromycin - 500mg every 12 hours for 5 days
- inhibits CYP450, so has many drug interactions
Oral Doxycycline - 200mg daily for 5 days
Co-trimoxazole (trimethoprim and sulphamethoxazole)

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7
Q

What drug interactions can occur with Clarithromycin?

A

This inhibits the CYP450 pathway in the liver, meaning the following drugs are inhibited

  • Theophylline warfarin
  • Carbamazepine
  • Digoxin
  • Phenytoin
  • Simvastatin
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8
Q

What methods of action and excretion of doxycycline mean you have to be careful of drug interactions and dosage?

A

Renal and hepatic elimination - can cause hypersensitivity to this drug
Can take when someone has renal impairment - just adjust interval between doses
Chelates iron and calcium, which means there is decreased absorption by antacids

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9
Q

What are the common side effects of co-trimoxazole?

A

Rash, SJS, fever, cough, aching, toxic epidermal necrolysis and blood dyscrasias

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10
Q

Which steroids are used when treating infectious COPD exacerbations?

A

Oral prednisolone - 30-50mg daily for 7 days
OR
IV hydrocortisone - 50-100mg every 8 hours until the patient can swallow

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11
Q

What is the mechanism of action, and the associated effects of prednisolone?

A

Interact with glucocorticoid receptor and nuclear DNA
- alters gene transcription so there is decreased synthesis and activation of prostaglandins, cytokines, leukotrines, T-lymphocytes, macrophages, eosinophils and airway epithelial cells
Reducation in mucosal oedema
Improved responsiveness to beta2-agonists by upregulating adrenoceptors

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12
Q

What are the classes of bronchodilators?

A

Beta-2 agonists
Anti-muscarinics
Theophylline

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13
Q

Describe the mechanism of action of salbutamol.

A

Mimics adrenaline, but with low affinity for cardiac beta-1 receptors
G proteins stimulate adenyl cyclase to increase intracellular cAMP - relaxation of the bronchial smooth muscle

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14
Q

What are the side effects of beta-2 agonist administration?

A

Tremor - stimulates skeletal muscle beta-2 receptors
Vasodilation - flushing, reflex tachycardia
High doses
- beta-2 hypokalaemia, hyperglycaemia, hypomagnesaemia
- beta-1 tachycardia, arrhythmias

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15
Q

How are anti-muscarinics administered?

A

Ipratropium bromide 500mg four times daily via an air driven nebuliser
- use a mouthpiece, not a mask, as this reduces risk of acute angle glaucoma

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16
Q

What is the difference between the anti-muscarinic agents ipratropium bromide be given over trotropium?

A

Inhaled ipratropium bromide reduces the risk of anti-cholinergic side-effects
Ipratropium bromide is short acting (3-6 hours)
Triotropium bromide is long acting (over 24 hours)

17
Q

When would the bronchodilator theophylline be used?

A

If the patient has no response to nebulised salbutamol and ipratropium

18
Q

What is the mechanism of action of theophylline?

A

Inhibits phosphodiesterase type 4 enzyme (PDE4)

- increases mucociliary clearance

19
Q

What are the adverse effects of theophylline?

A 
Over 15-20mg/l
- GI irritation 
- Tachycardia 
- CNS stimulation 
Serious toxicity (over 30-40mg/l)
- hypokalaemia 
- VT
- VF
- seizures
20
Q

Why is theophylline difficult to use?

A

Dose varies with age, weight, height, hepatic disease, smoking, enzyme inducers (Rifampicin) and inhibitors (clarithromycin, ciprofloxacin)
Beware of drug interactions - CYP 1A2

21
Q

What is the definition of type 1 respiratory failure?

A

Ventilation/perfusion inequality

  • low PaO2 (less than 8kPa)
  • normal or low PaCO2 - respiratory failure occurs because having a high PaCO2 normally drives respiratory rate
22
Q

What is the definition of type 2 respiratory failure?

A

Ventilation failure caused by lung damage (emphysema)
- low PaO2 (less than 8kPa)
- raised PaCO2 (greater than 6kPa)
Because the PaCO2 is raised all the time, the patient relies on the low PaO2 to drive respiration
- so giving pink puffers too much oxygen is dangerous as the patient stops breathing

23
Q

When someone has respiratory failure, what PaO2 and saturation that is being aimed for?

A

7.5-10kPa

94-98% (unless the person retains CO2 -> 88-92%)

24
Q

If the person can no longer breathe by themselves though a mask, what can be done?

A

Never use a nasal cannula

Consider nasal intermittent positive pressure ventilation (NIPPV) or intubation and mechanical ventilation

25
Q

What is the mechanism of action of inhaled anti-muscarinics?

A

Blockage of the parasympathetic nervous system (stimulation of cholinergic M2, M3 muscarinic receptors, intracellular calcium release and bronchoconstriction)

26
Q

What are the side effects of ipratropium bromide?

A

Blurred vision
Dry mouth
Decrease gut motility

27
Q

When would the anti-muscarinic agent tiotropium bromide be used?

A 
Chronic conditions (not an acute bronchospasm) 
- long action due to dissociate half life from the M3 receptor
28
Q

What are the side effects of tiotropium bromide?

A

Dry mouth

Difficulty in micturition

29
Q

Why are anti-muscarinics used in COPD?

A

Evidence of increased resting cholinergic tone in COPD - so anti-muscarinic agents are logical
Clinical evidence suggests long acting beta-agonists are as effective or more effective
- effect is enhanced when combined with a beta-agonist

30
Q

When someone is admitted with an acute COPD exacerbation, what drugs need to be stopped/changed?

A

Tiotropium - stop only if they are being put on ipratropium
Salbutamol - stop while on the nebuliser
Secretive - stop while on the nebuliser
Simvastatin - stop while on Clarithromycin
Clarithromycin 250mg - increase to 500mg

31
Q

Name and describe two long-acting beta agonists.

A

Salmetrol
- partial agonist, almost irreversibly binding to the beta-2 receptor
- lasts for over 12 hours
Formoterol
- full agonist, lipophilic
- quick onset and long duration of action

32
Q

Why are long acting beta agonist used?

A

Gives continuous bronchodilators and improves symptoms if inhaled steroids and short acting beta-2 agonist are inadequate

33
Q

What drug must long acting beta agonist be combined with?

A

Steroids

  • combination inhalers aid compliance
    • seretide (fluticasone and salmeterol)
    • symbicort (budesonide and formoterol)
34
Q

What is the mechanism of action of Leukotriene receptor inhibitors (used in asthma)?

A

Block cysteinyl leukotriene receptor in smooth muscle and macrophages
This inhibits eicosanoids LTC4, LTD4 and LTE4 (released from mast cells) and eosinophils
Used for prophylaxis of exercise induced asthma

35
Q

Name some Leukotriene receptor inhibitors.

A

Montelukast

Zafirlukast

36
Q

Name a mucolytic and its mechanism of action.

A

Carbocysteine

  • may facilitate expectoration by reducing the viscosity of the sputum
  • may reduce COPD exacerbations

Respiratory (12 decks)

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