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Yr 3 - Pharmacology > Drugs - Respiratory > Flashcards

Drugs - Respiratory Flashcards

1
Q

After ensuring the airway was secured, what observations would you do in ‘B’ in a RRAPID response to an acute severe asthma attack?

A
  • O2 sats
  • RR
  • Check tracheal position
  • Auscultation of lungs
  • Percussion of lungs
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2
Q

What investigations can be done in ‘B’ in an acute severe asthma attack?

A
  • ABG
  • PEFR
  • CXR (shouldn’t delay management)
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3
Q

Typical ABG results in acute asthma attack?

A

Low PaO2 and low PaCO2 in asthma (concerning if normal or raised PaCO2)

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4
Q

Give the stepwise pharmacological management of an acute severe asthma attack

A
  1. Oxygen
  2. High dose inhaled short-acting beta-agonist (SABA) e.g. salbutamol
  3. Inhaled ipratropium bromide (antimuscarinic)
  4. Steroid therapy (oral prednisolone or IV hydrocortisone)
  5. Magnesium sulphate IV
  6. IV aminophylline
  7. Abx if infection suspected
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5
Q

How should O2 be delivered in an acute asthma attack?

A

Non-rebreathe mask at 15L/min & sit patient upright

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6
Q

How should O2 be delivered in an acute asthma attack/COPD exacerbation in COPD patients?

A

give oxygen via Venturi facemask to maintain O2 sats >90%

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7
Q

Why should care be taken when giving O2 to COPD patients?

A

Supplemental O2 can remove a patient’s hypoxic (low level of O2) drive causing hypoventilation, higher CO2 levels, apnoea, and respiratory failure.

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8
Q

How often should nebulised salbutamol be repeated in an acute severe asthma attack?

A

Every 15-30 mins

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9
Q

Why should ipratropium be given in a severe asthma attack?

A

Combining nebulised ipratropium bromide with a nebulised b-2 agonist produces significant bronchodilation than a b-2 agonist alone.

Add for patients with acute severe or life-threatening asthma or to those with a poor initial response to b2 agonist therapy.

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10
Q

Which steroid is indicated in severe asthma?

A

Oral prednisolone 40-50mg OR if oral route unavailable, hydrocortisone can be administered IV as alternative

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11
Q

Which patients should you administer steroids to in a severe asthma attack?

A

Administer steroids to all patients with acute asthma

The earlier steroids are administered, the better the outcome.

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12
Q

Purpose of administering IV magnesium sulphate in a severe asthma attack?

A

Evidence that this has bronchodilatory effects in adults.

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13
Q

Who should you consider administering a single dose of IV magnesium sulphate in during an acute asthma attack?

A
  • Acute severe asthma who have not had a good response to inhaled therapy
  • Life-threatening or near-fatal asthma

Only use after consultation with senior medical staff

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14
Q

Give 3 main indications for prescribing emergency O2

A
  • Increase tissue oxygen delivery in acute hypoxaemia
  • Accelerate reabsorption of pleural gas in pneumothorax
  • Reduce carboxyhemoglobin half-life in carbon monoxide poisoning
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15
Q

Hypoxaemia vs hypoxia?

A

Hypoxemia refers to low oxygen levels in your blood

Hypoxia refers to low levels of oxygen in the tissues of your body.

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16
Q

Mechanism behind supplemental O2 increasing tissue O2 delivery?

A
  • Supplemental O2 therapy increases the PO2 in alveolar gas (PaO2), driving more rapid diffusion of O2 into blood.
  • The result increase in PaO2 increases delivery of oxygen to the tissues, which in effect ‘buys time’ while the underlying disease is corrected.
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17
Q

Why does supplemental O2 have a benefit in pneumothorax?

A
  • Supplemental O2 has benefit of reducing the fraction of nitrogen in alveolar gas
  • Since pleural air is composed mostly of nitrogen, this increases its rate of reabsorption
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18
Q

Why does supplemental O2 have a benefit in CO poisoning?

A

O2 competes with CO to bind with haemoglobin, shortening the half-life of carboxyhemoglobin, returning haemoglobin to a form that can transport O2 to tissues

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19
Q

Potential side effects of supplemental O2?

A
  • Discomfort of face mask (nasal cannulae may be more comfortable)
  • Lack of water vapour causing dry mouth (humidification may improve this)
  • Danger of hyperoxaemia (abnormally high PaO2)
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20
Q

Contraindications to supplemental O2?

A
  • Patients with type 2 respiratory failure (e.g. severe COPD) - caution
  • Smoking – fire risk if exposed to heat source or naked flame
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21
Q

Why should caution be taken in prescribing O2 in patients with type 2 respiratory failure?

A
  • Patients with type 2 respiratory failure (e.g. severe COPD) exhibit several adaptive changes to chronic hypoxaemia and hypercapnia
  • If exposed to high inspired O2 concentration, this may result in a rise in PaCO2 → respiratory acidosis, depressed consciousness, worsened tissue hypoxia
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22
Q

Which mask is used in critical illness (in those with normal target O2 sats)?

A

Non-rebreathe reservoir mask

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23
Q

Which mask is used in critical illness for patients in chronic type 2 respiratory failure?

A

Venturi

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24
Q

Flow rate of reservoir masks?

A

15L/min

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25
Q

O2 concentration of reservoir masks?

A

Contain high O2 concentration (60-80%)

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26
Q

How do venturi masks work?

A

These blend O2 with air in a fixed ration

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27
Q

What 2 investigations are used to monitor patients receiving O2?

A
  • Frequent SpO2 monitoring
  • ABG measurement

These are important in critical illness

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28
Q

PaO2 is only one determinant of the amount of oxygen reaching the tissues. What are the other 2?

A

cardiac output and haemoglobin concentration

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29
Q

What are some indications for beta-2 adrenoceptor agonists?

A
  • Chronic asthma
  • Acute asthma
  • Prophylaxis of allergen or exercise induced bronchospasm
  • COPD exacerbation
  • Hyperkalaemia
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30
Q

Mechanism of b-2 adrenoceptor agonists?

A

Act directly on beta-2 receptors, causing smooth muscle relaxation and dilatation of the airways (bronchodilation)

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31
Q

Contraindications for b2 agonists?

A
  • Hyperthyroidism
  • Diabetes mellitus
  • CVS disease (including hypertension)
  • Hypokalaemia
  • Convulsive disorders
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32
Q

Why are b2 agonists contraindicated in hyperthyroidism?

A

b2 agonists may stimulate thyroid activity

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33
Q

Why are b2 agonists contraindicated in DM?

A

rare risk of ketoacidosis

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34
Q

Why are b2 agonists contraindicated in CVS disease?

A

b2 agonists may cause increased risk of arrhythmias, changes to BP and HR → due to stimulation of b1 receptors in heart

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35
Q

Why are b2 agonists contraindicated in hypokalaemia?

A

Plasma potassium concentration may be reduced by b2-agonists

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36
Q

Side effects of B2 agonists?

A

Activation of B2 receptors in other tissues accounts for the common fight or flight response:

  • Fine tremor – occurs in hands and usually worse in first few days of treatment
  • Palpitations
  • Headache
  • Anxiety
  • Tachycardia

Other side effects:

  • Seizure
  • Anxiety
  • Hypokalaemia
  • Cardiac arrhythmia & paradoxical bronchospasm (rare)
  • Acute angle-closure glaucoma
  • Hyperglycaemia (due to promotion of glycogenolysis)
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37
Q

Can b2 agonists lead to hyper or hypokalaemia?

A

Hypokalaemia

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38
Q

2 main interactions of b2 agonists?

A
  • Beta blockers → can reduce effectiveness of b2-agonists
  • Drugs that may potentiate hypokalaemia – theophylline, corticosteroids, diuretics, hypoxia
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39
Q

Give 2 examples of short acting b2 agonists (SABAs)

A

Salbutamol, Terbutaline

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40
Q

Onset of SABAs?

A

15 mins

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41
Q

Duration of SABAs?

A

Up to 4 hours

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42
Q

Use of SABAs?

A

1-2 puffs when needed to relieve symptoms

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43
Q

Give 2 examples of LABAs

A

Salmeterol, Formoterol

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44
Q

Duration of LABAs?

A

Up to 12 hours

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45
Q

What should LABAs only be given alongside?

A

Should only be used in people who regularly use an inhaled corticosteroid

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46
Q

Give 2 examples of anticholinergic drugs that can be sued in the treatment of asthma

A

Ipratropium bromide

Tiotropium

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47
Q

Indications for ipratropium bromide / Tiotropium?

A

Used to control symptoms related to bronchospasm (i.e. reversible airway obstruction):

  • Acute asthma attack (severe/life-threatening) → if nebulised salbutamol has not eased symptoms
  • COPD exacerbation
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48
Q

Mechanism of ipratropium bromide?

A
  1. ACh antagonist → blocks the muscarinic cholinergic receptors (antimuscarinic)
  2. This inhibits the PNS
  3. This decreases the production of cGMP which decreases the contraction of smooth muscle → bronchodilation
  4. This reduces symptoms e.g. wheeze, SOB, chest tightness
49
Q

Elimination of antimuscarinics?

A

Renal

50
Q

Side effects of antimuscarinics?

A
  • Can’t see (blurred vision)
  • Can’t spit (dry mouth)
  • Can’t pee (urinary retention)
  • Can’t shit (constipation)

Others: arrhythmias, nausea

51
Q

Contraindications of antimuscarinics?

A
  • Hypersensitivity
  • Glaucoma
  • Blockage of urinary bladder
  • Enlarged prostate
52
Q

Give some examples of inhaled corticosteroids used in the management of asthma

A

Beclomethasone, budesonide, fluticasone

53
Q

Indications for inhaled corticosteroids?

A
  • Prophylaxis of asthma (prevention inhalers)
  • Reduce symptoms of acute asthma & COPD exacerbation
54
Q

What are corticosteroids?

A

Corticosteroids areas synthetic analogues of hormones produced by the adrenal cortex (they have mineralocorticoid and glucocorticoid properties).

55
Q

Via which mechanisms do corticosteroids produce a potent anti-inflammatory effect?

A
  • Decrease formation of cytokines
  • Decrease microvascular permeability
  • Inhibit influx of eosinophils into the lung, reducing overall inflammation
  • Reduce bronchial hyper-responsiveness
56
Q

Why are nebulised corticosteroids used over oral?

A

Delivered directly into lungs to reduce systemic absorption and risk of adverse effects compared to oral.

57
Q

Side effects of inhaled corticosteroids?

A
  • Oral candidiasis, sore mouth, dysphonia, and hoarseness (especially in high doses)
  • Paradoxical bronchospasm
  • Systemic side effects are rare
    • Potential growth suppression in children
58
Q

Patient notes for use of preventer inhalers?

A
  • 1x puff twice a day
  • Rinse mouth with water after using inhaler
  • Avoid rapid reduction in corticosteroid dose after prolonged use
  • Use lowest dose of ICS possible
59
Q

What is the main oral corticosteroid used in the treatment of asthma/COPD?

A

Prednisolone

60
Q

Indications for oral prednisolone?

A
  • Chronic asthma
  • Acute asthma
  • Acute exacerbation of COPD
  • Severe croup
  • Suppression of inflammatory and allergic disorders (e.g. rheumatoid arthritis, ophthalmology)
61
Q

What is the most widely used steroid for maintenance therapy in patients with chronic asthma?

A

Prednisolone (oral)

62
Q

What type of receptors are b2 receptors?

A

G protein coupled receptors

63
Q

Mechanism of B2 agonists in the management of hyperkalaemia?

A

B2 agonists also stimulate Na+/K+ ATPase pumps on cell surface membranes → causes a shift of K+ from extracellular to intracellular → lowers serum potassium

64
Q

Why should LABAs only be given in association with an inhaled corticosteroid?

A

As without a steroid, LABAs are associated with increased asthma deaths

65
Q

How can co-administration of LABA and steroid in asthma be ensured?

A

they may be prescribed as part of a combination inhaler (e.g. Symbicort or Seretide)

66
Q

When prescribing nebuliser therapy, you should always indicate whether the nebuliser should be driven by oxygen or air.

Which is used in asthma? COPD?

A

In general, oxygen should be used in asthma, whereas medical** **air should be used in COPD due to the risk of CO2 retention.

67
Q

Is ipratropium bromide long acting or short acting?

A

short acting antimuscarinic (SAMA)

68
Q

Is tiotropium long acting or short acting?

A

long acting antimuscarinic (LAMA)

69
Q

Indications for SAMAs vs LAMAs in COPD

A
  • SAMAs - used to relieve SOB brought on by exercise or during exacerbation
  • LAMAs - used to prevent SOB and exacerbations
70
Q

Indications for SAMAs vs LAMAs in asthma?

A
  • SAMAs → help relieve SOB during acute exacerbations (added to a SABA e.g. salbutamol)
  • LAMAs → can be added to high-dose inhaled corticosteroids and LABAs as maintenance treatment
71
Q

What are the metabolic effects of oral corticosteroids?

A

Increased gluconeogenesis from increased circulating amino and fatty acids – released by catabolism of muscle and mat

72
Q

What are the mineralocorticoid effects of oral corticosteroids?

A

Stimulate Na+ and water retention and K+ excretion in renal tubule

73
Q

Who should oral corticosteroids be used with caution in?

A
  • Infection
  • Children (can suppress growth)
  • Diabetes
  • Glaucoma
  • Hypothyroidism
  • Osteoporosis
  • Hypertension
  • Mood disorders
74
Q

Give some side effects of oral corticosteroids

A
  • Immunosuppression – increases risk and severity of infection
  • Metabolic effects – diabetes mellitus, osteoporosis
  • Proximal muscle weakness
  • Skin thinning and easy bruising
  • Gastritis
  • Mood & behavioural changes – insomnia, confusion, suicidal ideas
  • Mineralocorticoid actions – hypertensin, hypokalaemia, oedema
75
Q

How do corticosteroids affect ACTH secretion?

A
  • Corticosteroids suppress pituitary ACTH secretion
  • This causes adrenal atrophy, preventing endogenous cortisol secretion → Addison’s disease
  • Addisonian crisis can occurs if corticosteroids are withdrawn immediately
76
Q

Corticosteroids can increase the risk of peptic ulceration and GI bleeding when used alongside which drug?

A

NSAIDs (consider concurrent use of PPI)

77
Q

What effect can happen if corticosteroids are taken alongside taking b2-agonists, theophylline, loop or thiazide diuretics?

A

Hypokalaemia can be enhanced

78
Q

How is the efficacy of corticosteroids affected by drugs such as phenytoin, carbamazepine and rifampicin?

A

These are enzyme inducers → reduced efficacy of corticosteroids

79
Q

When should oral corticosteroids be taken during the day? Why?

A

Once daily in morning to mimic natural circadian rhythm and reduce insomnia

80
Q

What class of drug is montelukast and zafirlukast?

A

Leukotriene receptor antagonists

81
Q

How does the indication for montelukast differ between adults and children?

A

Both indicated in chronic asthma:

  • Adults → add-on therapy (only if asthma is incompletely controlled with inhaled corticosteroids and LABAs)
  • Children → alternative to LABAs as an add-on to inhaled corticosteroids
82
Q

How is montelukast taken?

A

Taken orally once a day (important to keep taking it even when you have no symptoms)

83
Q

What is the name of the leukotriene receptor? What type of receptor is it?

A

CystLT 1 (g protein-coupled receptor)

84
Q

Mechanism of montelukast?

A

Blocks action of leukotriene in the lungs at leukotriene receptor CystLT 1 (G protein-coupled receptor), resulting in decreased inflammation (anti-inflammatory) and relaxation of smooth muscle (bronchodilation).

85
Q

Side effects of leukotriene receptor antagonists?

A
  • Arthralgia (body aches and pains)
  • Headaches
  • Abdominal pain
86
Q

What class of drug is theophylline?

A

Xanthine

87
Q

Indication for theophylline?

A

Can be used as an add on therapy in the treatment of asthma

88
Q

What are xanthines?

A

Xanthines are purine bases found in most human body tissues and fluids. Several stimulants are derived from xanthine, including caffeine, theophylline, and theobromine.

89
Q

Which enzyme does theophylline competitively inhibit?

A

Competitively inhibits phosphodiesterase (PDE)

90
Q

What is PDE responsible for?

A

The enzyme responsible for breaking down cyclic AMP in smooth muscle cells to cause:

  • Relaxation of the smooth muscles located in the bronchial airways and pulmonary blood vessels.
  • Reduction of the airway responsiveness to histamine, adenosine, and allergens.
91
Q

What is the antidote to theophylline toxicity?

A

Activated charcoal

92
Q

Theophylline can interact with which other drugs to potentiate hypokalaemia?

A

B2 agonists, corticosteroid & diuretics → check serum potassium regularly

93
Q

How can theophylline affect lithium?

A

excretion of lithium may be potentiated

94
Q

Sodium cromoglicate can be considered an add on treatment for asthma (prophylaxis). What is its mechanism?

A

Inhibits the degranulation of mast cells, preventing the release of histamine.

95
Q

What class of drug is carbocisteine?

A

Mucolytic

96
Q

Purpose of mucolytics?

A

Reduce sputum viscosity and manage mucus hypersecretion

97
Q

Indications for mucolytics?

A

Recurrent infections in patients of:

  • COPD
  • Cystic fibrosis
  • Bronchiectasis
98
Q

Mechanism behind mucolytics?

A

Makes mucus less sticky so it is easier to cough up in conditions where the body produces too much mucus.

99
Q

What class of drug is alteplase and streptokinase?

A

Fibrinolytics

100
Q

3 main indications for fibrinolytics?

A
  1. Acute ischaemic stroke
  2. Acute STEMI
  3. Massive PE
101
Q

How quickly do fibrinolytics have to be given in acute ischaemic stroke?

A

Within 4.5 hours of onset of stroke

102
Q

How quickly do fibrinolytics have to be given in an acute STEMI?

A

within 12 hours of onset of symptoms

103
Q

What treatment is better than fibrinolytics in STEMI?

A

PCI

104
Q

Mechanism of fibrinolytics?

A
  • Catalyse conversion of plasminogen to plasmin which acts to dissolve and re-canalise occluded vessels
  • This allows reperfusion of affected tissue, preventing or limiting tissue infarction and cell death
105
Q

Side effects of fibrinolytics?

A
  • N&V
  • Bruising around injection site
  • Hypotension
  • Serious:
    • Severe bleeding
    • Cardiogenic shock
    • Allergic reaction
    • Cardiac arrest
106
Q

What is the antidote to serious bleeding caused by fibrinolytics?

A

Tranexamic acid (anti-fibrinolytic)

107
Q

Contraindications to fibrinolytics?

A
  • Factors to predispose to bleeding:
    • Recent trauma, haemorrhage, surgery
    • Bleeding disorders
    • Severe hypertension
    • Peptic ulcers
  • Intracranial haemorrhage – rule out with CT scan
  • Previous streptokinase treatment – development of antistreptokinase Abs can block its effect
108
Q

A 12 y/o boy sees his GP following hospital admission for an acute asthma attack. He has made a good recovery and is now asymptomatic. What is the most appropriate treatment to prevent further asthma attacks?

  1. Beclometasone
  2. Formoterol
  3. Chlorphenamine
  4. Ipratropium
  5. Salbutamol
A

Beclomethasone

109
Q

What class of drug is formoterol?

A

long acting b2-agonist

110
Q

What class of drug is chlorphenamine?

A

antihistamine

111
Q

A 72 y/o man with HTN, COPD and IBS sees his GP for a medication review. His medicines are amlodipine, doxazosin, fluticasone, hyoscine butylbromide, ipratropium and salmeterol. What receptors are most likely to have been activated by this treatment?

  1. a1-adrenoceptors
  2. a2-adrenceptors
  3. b1-adrenoceptors
  4. b2-adrenoceptors
  5. Muscarinic receptors
A

b2-adrenoceptors

B2-adrenoceptors are activated by salmeterol, a LABA.

112
Q

A 62 y/o man with COPD complains that one of his medications is causing a dry mouth. He is taking aminophylline, fluticasone, salbutamol, salmeterol and tiotropium. What is the most likely cause of the dry mouth?

A

Tioptropium

Tiotropium is a long-acting antimuscarinic bronchodilator which inhibits parasympathetic stimulation of salivation, causing a dry mouth (can’t spit).

113
Q

A 31 y/o man presents 7 hours after a paracetamol overdose. His only symptoms are nausea and epigastric discomfort. He has no relevant PMH and takes no regular medication. The serum paracetamol concentration is above the treatment line on the paracetamol poisoning treatment graph. What is the most appropriate treatment?

  1. Acetylcysteine
  2. Activated charcoal
  3. Cyclizine
  4. Omeprazole
  5. Naloxone
A

Acetylcysteine

114
Q

A 68 y/o man is brough to A&E as he has become increasingly drowsy over the past 24 hours. He has had diarrhoea for the preceding week. His PMH includes chronic back pain., epilepsy and depression. DH includes diazepam, morphine, fluoxetine, paracetamol and sodium valproate. On examination, he has a GCS of 9 and a RR of 8. His pupils are pinpoint. He appears dehydrated and blood tests reveal an AKI. Drug toxicity as a result of reduced renal eliminated is suspected. What is the most appropriate initial treatment?

  1. Acetylcysteine
  2. Activated charcoal
  3. Flumazenil
  4. Naloxone
  5. Sodium bicarbonate
A

Naloxone

115
Q

A 24 y/o woman is receiving an IV infusion of acetylcysteine for paracetamol poisoning. 30 minutes into the infusion, she develops a rash. On examination, her HR is 95 bpm and her BP is 117/78 mmHg. She has a widespread urticarial rash. What is the most appropriate immediate management?

  1. Continue acetylcysteine and give chlorphenamine
  2. Continue acetylcysteine and give ranitidine
  3. Temporarily stop acetylcysteine and give adrenaline
  4. Temporarily stop acetylcysteine and give chlorphenamine
  5. Temporarily stop acetylcysteine and give ranitidine
A

Temporarily stop acetylcysteine and give chlorphenamine

  • When administered at IV at high doses (such as in paracetamol poisoning), acetylcysteine can cause an anaphylactoid reaction
  • Appropriate to stop acetylcysteine and give IV antihistamine (H1-recetpor antagonist) e.g. chlorphenamine
116
Q

What class of drug is ranitidine?

A

an H2 receptor antagonist used to suppress gastric acid secretion

117
Q

Effect of ACh on smooth muscle?

A

Increases cGMP which causes smooth muscle contraction

118
Q

Effect of nitrous oxide on smooth muscle?

A

Decreases tone

119
Q

What 2 classes of drugs are in Seretide/Symbicort (combination inhalers)?

A

LAMA (e.g. salmeterol) + corticosteroid (e.g. budesonide)

Yr 3 - Pharmacology (18 decks)

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