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Drug Formulary Y3 > Respiratory Drugs > Flashcards

Respiratory Drugs Flashcards

1
Q

Name 4 beta2-agonists?

A
  1. Salbutamol
  2. Salmeterol
  3. Formoterol
  4. Terbutaline
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2
Q

What are the indications for use of beta2-agonists?

A
  1. Asthma
  2. COPD
  3. Hyperkalaemia
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3
Q

In the treatment of asthma, when are short- and long- acting beta2-agonists used?

A

Short-acting beta2-agonists are used to relieve breathlessness.
Long-acting beta2-agonists are used as ‘step 3’ treatment for chronic asthma, but must always be given in combination with inhaled corticosteroids.

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4
Q

In the treatment of COPD, when are short- and long- acting beta2-agonists used?

A

Short-acting beta2-agonists are used to relieve breathlessness.
Long-acting beta2-agonists are an option for second-line therapy of COPD

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5
Q

In which form is salbutamol given as urgent treatment of a high serum potassium concentration (hyperkalaemia)? and which other drugs are given alongside it?

A

Nebulised salbutamol.

Given alongside insulin, glucose and calcium gluconate.

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6
Q

What is the mechanism of action of beta2-agonists in treating asthma/COPD?

A

Beta2-receptors are found in smooth muscle of the bronchi, GI tract, uterus and blood vessels. Stimulation of this G protein-coupled receptor activates a signalling cascade that leads to smooth muscle relaxation. This improves airflow in constricted airways, reducing the symptoms of breathlessness.

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7
Q

What is the mechanism of action of beta2-agonists in treating hyperkalaemia?

A

Like insulin, beta2-agonists stimulate Na+/K+-ATPase pumps on cell surface membranes, thereby causing a shift of K+ from the extracellular to intracellular compartment. This makes them a useful adjunct in the treatment of hyperkalaemia, particularly when IV access is difficult.

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8
Q

Why are other drugs needed to treat hyperkalaemia, as well as beta2-agonists?

A

The effect of beta2-agonists in treating hyperkalaemia is less reliable than other therapies, so they should not be used in isolation.

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9
Q

Which 2 beta2-agonists are short-acting and which are long-acting?

A 
Short-acting:
1. Salbutamol
2. Terbutaline
Long-acting:
1. Salmeterol
2. Formoterol
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10
Q

What are the possible side effects caused by beta2-agonists? (5)

A

Activation of beta2-receptors in other tissues accounts for the common ‘fight or flight’ adverse effects of:
1. Tachycardia
2. Palpitations
3. Anxiety
4. Tremor
They also promote glycogenolysis, so may increase the serum glucose concentration. At high doses, serum lactate levels may also rise. Long-acting beta2-agonists can cause muscle cramps.

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11
Q

What are the warnings associated with beta2-agonist use? (2)

A
  1. Long-acting beta2-agonists should be used in asthma only if an inhaled corticosteroid is also part of the therapy - this is because without a steroid, long-acting beta2-agonists are associated with increased asthma deaths.
  2. Care should be taken when prescribing them for patients with CVD, in whom tachycardia may provoke angina or arrhythmias.
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12
Q

What are the important interactions to note when prescribing beta2-agonists?

A
  1. Beta-blockers may reduce the effectiveness of beta2-agonists.
  2. Concomitant use of high-dose nebulised beta2-agonists with theophylline and corticosteroids can lead to hypokalaemia, so serum potassium concentrations should be monitored.
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13
Q

What is important to remember when prescribing nebuliser therapy?

A

You should always indicate whether the nebuliser should be driven by oxygen or air. In general, oxygen should be used in asthma, whereas medical air should be used in COPD, due to the risk of CO2 retention.

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14
Q

Name 3 anticholinergics/antimuscarinics/bronchodilators?

A
  1. Ipratropium
  2. Tiotropium
  3. Glycopyrronium
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15
Q

What are the 2 indications for use of antimuscarinics (anticholinergics)?

A
  1. COPD

2. Asthma

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16
Q

When are short- and long- acting antimuscarinics indicated for use in COPD?

A

Short-acting antimuscarinics are used to RELIEVE breathlessness brought on by exercise or during exacerbations.
Long-acting antimuscarinics (LAMAs) are used to PREVENT breathlessness and exacerbations

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17
Q

When are short- and long- acting antimuscarinics indicated for use in asthma?

A

Short-acting antimuscarinics are used in adjuvant treatment for relief of breathlessness during acute exacerbations (added to a short-acting beta2-agonist, e.g. salbutamol).
Long-acting antimuscarinics are added to high-dose inhaled corticosteroids and long-acting beta2-agonists at ‘step 4’ in the treatment of chronic asthma.

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18
Q

What is the mechanism of action of antimuscarinics?

A

Antimuscarinic drugs bind to the muscarinic receptor, where they act as a competitive inhibitor of acetylcholine. Stimulation of the muscarinic receptor brings about a wide range of parasympathetic ‘rest and digest’ effects. In blocking the receptor, antimuscarinics have the opposite effects: they increase heart rate and conduction; reduce smooth muscle tone, including in the respiratory tract; and reduce secretions from glands in the respiratory and GI tracts. In the eye they cause relaxation of the pupillary constrictor and ciliary muscles, causing pupillary dilatation and preventing accommodation, respectively.

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19
Q

What are the side effects caused by antimuscarinics? (1)

A

Other than a dry mouth, side effects are uncommon as when they are taken by inhalation, relatively little is absorbed systemically.

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20
Q

What are the warnings for use of antimuscarinics? (1)

A

Angle-closure glaucoma - they can precipitate a dangerous rise in intraocular pressure

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21
Q

Are there any important drug interactions to consider when prescribing antimuscarinics?

A

No - they are not generally a problem due to the low systemic absorption.

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22
Q

Name 3 systemic corticosteroids (glucocorticoids)?

A
  1. Prednisolone
  2. Hydrocortisone
  3. Dexamethasone
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23
Q

What are the common indications for use of systemic corticosteroids?

A
  1. To treat allergic or inflammatory disorders e.g. anaphylaxis, asthma.
  2. Suppression of autoimmune disease, e.g. IBD, inflammatory arthritis
  3. In the treatment of some cancers as part of chemotherapy or to reduce tumour-associated swelling
  4. Hormone replacement in adrenal insufficiency or hypopituitarism
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24
Q

What is the mechanism of action of systemic corticosteroids (glucocorticoids), and how they modify immune responses?

A

These glucocorticoids bind to cytosolic glucorticoid receptors, which then translocate to the nucleus and bind to glucorticoid-response elements, which regulate gene expression. Corticosteroids are most commonly prescribed to modify the immune response. They upregulate anti-inflammatory genes and downregular pro-inflammatory genes (e.g. cytokines, tumour necrosis factor alpha).
Direct actions on inflammatory cells include suppression of circulating monocytes and eosinophils.

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25
Q

What mineralocorticoid effects do systemic corticosteroids have?

A

They stimulate Na+ and water retention, and K+ excretion in the renal tubule.

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26
Q

What side effects are caused by systemic corticosteroid use? (6 ‘categories’)

A
  1. Immunosuppression increases the risk and severity of infection and alters the host response.
  2. Metabolic effects include diabetes mellitus and osteoporosis.
  3. Increased catabolism causes proximal muscle weakness, skin thinning with easy bruising and gastritis.
  4. Mood and behavioural changes include insomnia, confusion, psychosis and suicidal thoughts.
  5. Mineralocorticoid actions can result in hypertension, hypokalaemia and oedema.
  6. Corticosteroid treatment suppresses ACTH secretion, switching off the stimulus for normal adrenal cortisol production.
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27
Q

What can happen if systemic corticosteroids are withdrawn suddenly?

A

An acute addisonian crisis with cardiovascular collapse may occur. Slow withdrawal is required to allow recovery of adrenal function

28
Q

What side effects occur during withdrawal of systemic corticosteroids/glucocorticoids?

A

Chronic glucocorticoid deficiency occurs during treatment withdrawal and symptoms of this include fatigue, weight loss and arthralgia.

29
Q

In whom should systemic corticosteroids be prescribed with caution? (2)

A
  1. In children (they can suppress growth)

2. In people with infection

30
Q

What important drug interactions are important to be aware of when prescribing systemic corticosteroids? (4)

A
  1. They increase the risk of peptic ulceration and GI bleeding when used with NSAIDS
  2. They enhance hypokalaemia in patients taking B2-agonists, theophylline, loop or thiazide diuretics
  3. Their efficacy may be reduced by cytochrome P450 inducers (e.g. phenytoin, carbamazepine, rifampicin).
  4. Corticosteroids reduce the immune response to vaccines.
31
Q

Name 3 inhaled corticosteroids (glucocorticoids)?

A
  1. Beclometasone
  2. Budesonide
  3. Fluticasone
32
Q

Name the 2 indications for use of inhaled corticosteroids?

A
  1. Asthma - to treat airway inflammation

2. COPD - to help symptoms in patients with severe airflow obstruction on spirometry and/or recurrent exacerbations.

33
Q

At which step in asthma treatment are inhaled corticosteroids recommended for use?

A

Step 2

34
Q

What are inhaled corticosteroids usually prescribed in combination with, to help control and prevent symptoms in COPD?

A

Long-acting beta2-agonist and/or long-acting antimuscarinic bronchodilator

35
Q

What is the mechanism of action of inhaled corticosteroids?

A

Corticosteroids pass through the plasma membrane and interact with receptors in the cytoplasm. The activated receptor then passes into the nucleus to modify the transcription of a large number of genes. Pro-inflammatory interleukins, cytokines and chemokines are down regulated, while anti-inflammatory proteins are unregulated.
In the airways, this reduces mucosal inflammation, widens the airways, and reduces mucus secretion. This improves symptoms and reduces exacerbations in both asthma and COPD.

36
Q

What are the side effects that inhaled corticosteroids can cause? (3)

A
  1. Oral candidiasis (thrush infection) - due to their immunosuppressive effect
  2. Hoarse voice
  3. In COPD - some evidence suggests increased risk of pneumonia
37
Q

When should inhaled corticosteroids be prescribed with caution?

A

High-dose inhaled corticosteroids, particularly fluticasone, should be used with caution in COPD patients with a history of pneumonia and in children.

38
Q

What are the possible drug interactions related to inhaled corticosteroids?

A

There aren’t any :)

39
Q

Name 3 topical corticosteroids (glucocorticoids)?

A
  1. Hydrocortisone
  2. Betamethasone
  3. Mometasone furoate
40
Q

What is the indication for use of topical corticosteroids? (1)

A
  1. Used in inflammatory skin conditions e.g. eczema - to treat disease flares or to control chronic disease where emollients alone are ineffective
41
Q

What is the mechanism of action of topical corticosteroids?

A

They have as previously described about other corticosteroids, multiple effects, including immunosuppression, metabolic and mineralocorticoid. Where they are applied topically, their effects are mostly limited to the site of application, however with potent or prolonged used, systemic absorption and effects can occur.

42
Q

Of the examples give, of topical corticosteroids, which is mild and which is potent?

A

Hydrocortisone is mild
Mometasone furoate - moderately potent - potent
Betamethasone is potent - very potent

43
Q

What side effects can potent topical corticosteroids cause?

A
  1. Skin thinning, striae, telangiectasia and contact dermatitis
  2. If used on face; perioral dermatitis and cause/exacerbate acne
  3. Withdrawal of the topical corticosteroid can cause a rebound worsening of the underlying skin condition
  4. Rarely, adrenal suppression and systemic adverse effects
44
Q

When should topical corticosteroids be used with caution or avoided?

A
  1. Where there is an infection - this can cause the infection to worsen or spread
  2. Where facial lesions are present
45
Q

Are there any drug interactions to be aware of?

A

None

46
Q

What type of drug is carbocisteine?

A

A mucolytic (or expectorant)

47
Q

What is the indication for use of carbocisteine/carbocysteine?

A

Reduction of sputum viscosity - can be used in COPD and bronchiectasis

48
Q

Name another mucolytic indicated for use in cystic fibrosis?

A

Ivacaftor

49
Q

What is the mechanism of action of carbocisteine?

A

Carbocisteine is a mucolytic that reduces the viscosity of sputum and so can be used to help relieve the symptoms of chronic obstructive pulmonary disorder (COPD) and bronchiectasis by allowing the sufferer to bring up sputum more easily.
Carbocisteine is produced by alkylation of cysteine with chloroacetic acid.

50
Q

Which drugs should not be prescribed/used in combination with mucolytics?

A

Antitussives (cough suppressants) or medicines that dry up bronchial secretions.

51
Q

When is the use of carbocisteine contra-indicated?

A

In a patient with active peptic ulcers

52
Q

What is the rare side effect caused by mucolytics?

A

GI bleeding

53
Q

What are the indications for use of theophylline? (3)

A
  1. Asthma
  2. COPD
  3. Bronchospasm
54
Q

What is the mechanism of action of theophylline?

A

Theophylline relaxes the smooth muscle of the bronchial airways and pulmonary blood vessels and reduces airway responsiveness to histamine, methacholine, adenosine, and allergen. Theophylline competitively inhibits type III and type IV phosphodiesterase (PDE), the enzyme responsible for breaking down cyclic AMP in smooth muscle cells, possibly resulting in bronchodilation. Theophylline also binds to the adenosine A2B receptor and blocks adenosine mediated bronchoconstriction. In inflammatory states, theophylline activates histone deacetylase to prevent transcription of inflammatory genes that require the acetylation of histones for transcription to begin.

55
Q

What are the possible side effects theophylline can cause?

A

It can cause:

  1. Nausea
  2. Diarrhoea
  3. Tachycardia
  4. Arrhythmias
  5. CNS excitation (headaches, insomnia, irritability, dizziness and lightheadedness)
56
Q

Theophylline has a narrow therapeutic window, what are the possible complications of this?

A

Toxicity, leading to seizures.

57
Q

What drugs are known to interact with theophylline?

A
  1. Erythromycin
  2. Cimetidine
  3. Fluoroquinolones
  4. There are 522 drug interactions listed on DrugBank …
    …nearly all increase chance of toxicity, as they reduce the metabolism of theophylline.
58
Q

What is the half-life of theophylline and where is it metabolised?

A

8 hours, and in the liver.

59
Q

What is the indication for use of oxygen therapy?

A
  1. To increase tissue oxygen delivery in states of hypoxaemia.
  2. To accelerate reabsorption of pleural gas in pneumothorax
  3. To reduce the half-life of carboxyhemoglobin in carbon monoxide poisoning
60
Q

What are the mechanisms of action of oxygen therapy?

A
  1. Oxygen therapy increases the arterial pressure of oxygen, so improves gas exchange and oxygen delivery to tissues.
  2. Oxygen supplementation acts to restore normal cellular activity at the mitochondrial level and reduce metabolic acidosis.
61
Q

What is the mechanism of action of oxygen therapy specifically in pneumothorax?

A

In pneumothorax, supplemental oxygen therapy has an additional benefit of reducing the fraction of nitrogen in alveolar gas. This accelerates the diffusion of nitrogen out of the body. Since pleural air is composed mostly of nitrogen, this increase its rate of reabsorption.

62
Q

What is the mechanism of action of oxygen therapy in carbon monoxide poisoning?

A

In carbon monoxide (CO) poisoning, oxygen competes with CO to bind with haemoglobin and thereby shortens the half-life of carboxyhemoglobin, returning haemoglobin to a form that can again transport oxygen to tissues.

63
Q

When does oxygen therapy need to be monitored carefully?

A

Oxygen therapy can induce hypercapnic respiratory failure in patients with respiratory diseases and musculoskeletal diseases in upper airways. Sudden cessation of oxygen supplementation in these patients can further lead to rebound hypoxaemia. In patients with mild or moderate strokes, hyperoxaemia may cause absorption atelectasis or myocardial infarction. Oxygen content should be monitored following the administration to verify therapeutic benefit.

64
Q

What is the half life of oxygen therapy? :)

A

122.24 seconds

65
Q

What is the most common adverse effect of oxygen?

A

Adverse effects are related to the delivery of oxygen; the discomfort of the face mask and its lack of water vapour leading to a dry throat.

Drug Formulary Y3 (9 decks)

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