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Phase 3a Medicine > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Medication for acne

A

Tetracyclines

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2
Q

Acute coronary syndrome

A

ACE inhibitors
Aspirin
Beta blockers
Clopidogrel
Fibrinolytic drugs
Heparins and fondaparinux
Nitrates
Strong opioids
Statins

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3
Q

Addison’s disease

A

Systemic corticosteroids (glucocorticoids)

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4
Q

Adrenal insufficiency

A

Systemic corticosteroids (glucocorticoids)

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5
Q

Psychomotor agitation

A

Phenothiazines antiemetics
First-generation (typical) antipsychotics
Second-generation (atypical) antipsychotics

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6
Q

Alcohol withdrawal

A

Benzodiazepines

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7
Q

Allergy

A

Antihistamines (H1-receptor antagonists)
Systemic corticosteroids (glucocorticoids)

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8
Q

Anaemia

A

Iron
Vitamins

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9
Q

Medications for anaphylaxis

A

Adrenaline (epinephrine)
Antihistamines (H1-receptor antagonists)
Systemic corticosteroids (glucocorticoids)

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10
Q

Angina

A

Beta blockers
Calcium channel blockers
Nicorandil
Nitrates

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11
Q

Anxiety

A

SSRI antidepressants
Venlafaxine and mirtazepine antidepressants
Benzodiazepines
Gabapentin and pregabalin

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12
Q

Ascites

A

Aldosterone antagonists
Loop diuretics
Colloids (plasma substitutes)

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13
Q

Asthma

A

Antimuscarinic bronchodilators
Beta 2 agonists
Compound (beta 2 agonist-corticosteroid) inhalers
Inhaled corticosteroids (glucocorticoids)

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14
Q

AF and atrial flutter

A

Amiodarone
Aspirin
Beta blockers
Calcium channel blockers
Clopidogrel
Digoxin
Warfarin

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15
Q

Autoimmune disease

A

Aminosalicylates
Systemic corticosteroids (glucocorticoids)
Methotrexate

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16
Q

Benign prostatic hyperplasia

A

Alpha blockers
5 alpha-reductase inhibitors

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17
Q

Bipolar disorder

A

First-generation (typical) antipsychotics
Second-generation (atypical) antipsychotics
Carbamazepine
Valproate

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18
Q

Bone metastases

A

Bisphosphonates

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19
Q

Drugs for bowel preparation

A

Osmotic laxatives

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20
Q

Bradycardia

A

Antimuscarinics

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21
Q

Breathlessness

A

Loop diuretics
Strong opioids

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22
Q

Carbon monoxide poisoning

A

Oxygen

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23
Q

Medications for cardiac arrest

A

Adrenaline (epinephrine)
Amiodarone

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24
Q

Chemotherapy

A

Allopurinol
Systemic corticosteroids (glucocorticoids)
Methotrexate
Serotonin 5-HT3-receptor antagonists antiemetics

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25
Q

Childhood immunisations

A

Vaccines

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26
Q

Chronic kidney disease

A

Angiotensin receptor blockers
ACE inhibitors
Calcium and vitamin D

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27
Q

Chronic obstructive pulmonary disease

A

Antimuscarinic bronchodilators
Beta 2 agonists
Compound (beta 2 agonist-corticosteroid) inhalers
Inhaled corticosteroids (glucocorticoids)

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28
Q

Things to prescribe for circulatory compromise

A

Colloids (plasma substitutes)
Compound sodium lactate (Hartmann’s solution)
Sodium chloride

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29
Q

Clostridium difficile colitis

A

Metronidazole
Vancomycin

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30
Q

Constipation

A

Bulk-forming laxatives
Osmotic laxatives
Stimulant laxatives

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31
Q

Contrast nephropathy

A

Acetylcysteine (N-acetylcysteine)

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32
Q

Hormonal contraception

A

Oestrogens and progestogens

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33
Q

Deep vein thrombosis

A

Heparins and fondaparinux
Warfarin

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34
Q

Dental infection

A

Metronidazole

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35
Q

Depression

A

SSRI antidepressants
Tricyclics antidepressants
Venlafaxine and mirtazepine

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36
Q

Diabetes mellitus

A

Insulin
Metformin
Sulphonylureas
Thiazolidinediones

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37
Q

Diabetic ketoacidosis

A

Insulin

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38
Q

Diabetic nephropathy

A

Angiotensin receptor blockers
ACE inhibitors

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39
Q

Drugs for diarrhoea

A

Antimotility drugs
Bulk-forming laxatives

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40
Q

Dry eyes

A

Ocular lubricants (artificial tears)

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41
Q

Dry skin

A

Emollients

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42
Q

Dyspepsia

A

Alginates and antacids
H2 receptor antagonists
Proton pump inhibitors

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43
Q

Eczema

A

Topical corticosteroids (glucocorticoids)
Emollients

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44
Q

Endocarditis

A

Aminoglycosides
Penicillins
Penicillinase-resistant penicillin
Vancomycin

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45
Q

Absence seizures

A

Valproate

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46
Q

Focal seizures

A

Carbamazepine
Gabapentin and pregabalin
Phenytoin
Valproate

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47
Q

Generalised epilepsy

A

Phenytoin
Valproate

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48
Q

Medications for status epilepticus

A

Benzodiazepines
Phenytoin

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49
Q

Erectile dysfunction

A

Phosphodiesterase (type 5) inhibitors

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50
Q

Faecal impaction

A

Bulk-forming laxatives
Osmotic laxatives
Stimulant laxatives

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51
Q

Fever

A

Aspirin
Paracetamol

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52
Q

6 fluid and electrolyte therapy

A

Colloids (plasma substitutes)
Compound sodium lactate (Hartmann’s solution)
Glucose (dextrose)
IV potassium
Oral potassium
Sodium chloride

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53
Q

Medications for gastro-oesophageal reflux disease

A

Alginates and antacids
H2 receptor antagonists
Proton pump inhibitors

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54
Q

Generalised anxiety disorder

A

Venlafaxine and mirtazepine antidepressants
Gabapentin and pregabalin

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55
Q

Open-angle glaucoma

A

Prostaglandin analogue eye drops

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56
Q

Gout

A

Allopurinol
Non-steroidal anti-inflammatory drugs

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57
Q

Hay fever (seasonal allergic rhinitis)

A

Antihistamines (H1-receptor antagonists)

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58
Q

Heart failure

A

Aldosterone antagonists
Angiotensin receptor blockers
ACE inhibitors
Beta blockers
Digoxin
Loop diuretics

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59
Q

Heart valve replacement

A

Warfarin

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60
Q

Helicobacter pylori eradication

A

Macrolide
Broad-spectrum penicillins
Proton pump inhibitors

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61
Q

Hepatic encephalopathy

A

Osmotic laxatives

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62
Q

Hormonal replacement therapy

A

Oestrogens and progestogens

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63
Q

Hyperaldosteronism

A

Aldosterone antagonists

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64
Q

Hypercalcaemia of malignancy

A

Bisphosphonates

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65
Q

Hyperglyaemic hyperosmolar syndrome

A

Insulin

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66
Q

Medications for hyperkalaemia

A

Beta 2 agonists
Calcium and vitamin D
Glucose (dextrose)
Insulin

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67
Q

Hyperlipidaemia

A

Statins

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68
Q

Medications for hypertension

A

Alpha blockers
Angiotensin receptor blockers
ACE inhibitors
Beta blockers
Calcium channel blockers
Thiazide and thiazide-like diuretics

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69
Q

Hyperuricaemia

A

Allopurinol

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70
Q

Hypocalcaemia

A

Calcium and vitamin D

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71
Q

Hypoglycaemia

A

Glucose (dextrose)

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72
Q

Hypokalaemia

A

Potassium-sparing diuretics
IV potassium
Oral potassium

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73
Q

Hypopituitarism

A

Systemic corticosteroids (glucocorticoids)
Thyroid hormones

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74
Q

Hypothyroidism

A

Thyroid hormones

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75
Q

Hypoxaemia

A

Oxygen

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76
Q

Urinary incontinence

A

Antimuscarinics

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77
Q

Complicated infection

A

Cephalosporins and carbapenems
Antipseudomonal penicillins

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78
Q

Fungal infection

A

Antifungal drugs

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79
Q

Protozoal infection

A

Metronidazole

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80
Q

Inflammation

A

Corticosteroids (glucocorticoids) (systemic/inhaled/topical)
NSAIDs

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81
Q

Insomnia

A

Benzodiazepines
Z-drugs

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82
Q

Irritable bowel syndrome

A

Antimuscarinics

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83
Q

Ischaemic heart disease

A

Angiotensin receptor blockers
ACE inhibitors
Aspirin
Beta blockers
Clopidogrel
Fibrinolytic drugs
Statins

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84
Q

Keratoconjunctivitis sicca

A

Ocular lubricants (artificial tears)

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85
Q

Korsakoff’s psychosis

A

Vitamins

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86
Q

Leg cramps

A

Quinine

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87
Q

Local anaesthesia

A

Adrenaline (epinephrine)
Lidocaine

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88
Q

Lyme disease

A

Tetracyclines

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89
Q

Malaria

A

Quinine

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90
Q

Meningitis

A

Cephalosporins and carbapenems
Penicillins

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91
Q

Migraine

A

Gabapentin and pregabalin

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92
Q

Mucosal bleeding

A

Adrenaline (epinephrine)

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93
Q

Myocardial perfusion scan

A

Dipyridamole

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94
Q

Nausea and vomiting

A

Antiemetics
- Dopamine D2-receptor antagonists
- Histamine H1-receptor antagonists
- Phenothiazines
- Serotonin 5-HT3-receptor antagonists
First-generation (typical) antipsychotics

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95
Q

Prevention of neural tube defects

A

Vitamins

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96
Q

Obsessive compulsive disorder

A

SSRI antidepressants

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97
Q

Ocular hypertension

A

Prostaglandin analogue eye drops

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98
Q

Drugs for oedema

A

Loop diuretics

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99
Q

Opioid toxicity

A

Naloxone

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100
Q

Osteomyelitis

A

Penicillinase-resistant penicillins
Vancomycin

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101
Q

Osteoporosis

A

Bisphosphonates
Calcium and vitamin D

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102
Q

Overdose

A

Acetylcysteine (N-acetylcysteine)
Activated charcoal

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103
Q

Paget’s disease

A

Bisphosphonates

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104
Q

Pain

A

Aspirin
NSAIDs
Compound preparations opioids
Strong opioids
Weak opioids
Paracetamol

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105
Q

Neuropathic pain

A

Tricyclics and related drugs antidepressants
Gabapentin and pregabalin

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106
Q

Panic disorders

A

SSRI antidepressants

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107
Q

Paracentesis

A

Colloids (plasma substitutes)

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108
Q

Secondary Parkinsonism

A

Dopaminergic drugs for Parkinson’s disease

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109
Q

Parkinson’s disease

A

Dopaminergic drugs for Parkinson’s disease

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110
Q

Peptic ulcer disease

A

H2-receptor antagonists
Proton pump inhibitors

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111
Q

Peripheral arterial disease

A

Aspirin
Clopidogrel

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112
Q

Pneumonia

A

Cephalosporins and carbapenems
Macrolides
Metronidazole
Penicillins
Antipseudomonal penicillins
Broad-spectrum penicillins
Quinolones
Tetracyclines

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113
Q

Pneumocystis pneumonia

A

Trimethoprim (as co-trimoxazole)

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114
Q

Pneumothorax

A

Oxygen

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115
Q

Poisoning

A

Acetylcysteine (N-acetylcysteine)
Activated charcoal
Benzodiazepines
Naloxone
Oxygen
Vitamins

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116
Q

Pruritis

A

Antihistamines (H1-receptor antagonists)

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117
Q

Psoriasis

A

Emollients
Methotrexate

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118
Q

Pulmonary embolus

A

Fibrinolytic drugs
Heparins and fondaparinux
Warfarin

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119
Q

Pulmonary hypertension

A

Phosphodiesterase (type 5) inhibitors

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120
Q

Pulmonary oedema

A

Loop diuretics
Nitrates
Strong opioids

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121
Q

Pyelonephritis

A

Aminoglycosides

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122
Q

Reconstitution and dilution of drugs

A

Glucose (dextrose)
Sodium chloride

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123
Q

Respiratory secretions

A

Acetylcysteine (N-acetylcysteine)
Cardiovascular and GI uses antimuscarinics

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124
Q

Rheumatoid arthritis

A

Aminosalicylates
Methotrexate

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125
Q

Schizophrenia

A

First-generation (typical) antipsychotics
Second-generation (atypical) antipsychotics

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126
Q

Sedation

A

Benzodiazepines

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127
Q

Sepsis

A

Aminoglycosides
Cephalosporins and carbapenems
Penicillins
Antipseudomonal penicillins
Vancomycin

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128
Q

Intra-abdominal sepsis

A

Aminoglycosides
Metronidazole
Antipseudomonal penicillins
Broad-spectrum penicillins

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129
Q

Septic arthritis

A

Penicillinase-resistant penicillins

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130
Q

Shock

A

Colloids (plasma substitutes)
Compound sodium lactate (Hartmann’s solution)
Sodium chloride

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131
Q

Skin and soft tissue infection

A

Macrolides
Penicillins
Antipseudomonal penicillins
Penicillinase-resistant penicillins

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132
Q

Sjogren’s syndrome

A

Ocular lubricants (artificial tears)

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133
Q

Smoking cessation

A

Nicotine replacement and related drugs

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134
Q

Stroke

A

Aspirin
Clopidogrel
Dipyridamole
Fibrinolytic drugs

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135
Q

Subacute combined degeneration of the cord

A

Vitamins

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136
Q

Supraventricular tachycardia

A

Adenosine
Amiodarone
Beta blockers
Calcium channel blockers

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137
Q

Tetanus

A

Penicillins

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138
Q

Thiamine deficiency

A

Vitamins

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139
Q

Tonsilitis

A

Penicillins

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140
Q

Trigeminal neuralgia

A

Carbamazepine

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141
Q

Tumour lysis syndrome

A

Allopurinol

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142
Q

Ulcerative colitis

A

Aminosalicylates

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143
Q

Urinary catheterisation

A

Lidocaine

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144
Q

UTI

A

Cephalosporins and carbapenems
Nitrofurantoin
Antipseudomonal penicillins
Broad-spectrum penicillins
Quinolones
Trimethoprim

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145
Q

Urticaria

A

Antihistamines (H1-receptor antagonists)

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146
Q

Vaccinations

A

Vaccines

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147
Q

Prophylaxis of venous thromboembolism

A

Heparins and fondaparinux

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148
Q

Treatment of venous thromboembolism

A

Fibrinolytic drugs
Heparins and fondaparinux
Warfarin

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149
Q

Ventricular fibrillation

A

Adrenaline (epinephrine)
Amiodarone
Lidocaine

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150
Q

Ventricular tachycardia

A

Adrenaline (epinephrine)
Amiodarone
Lidocaine

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151
Q

Vitamin D deficiency

A

Calcium and vitamin D

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152
Q

Vitamin K deficiency bleeding

A

Vitamins

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153
Q

Reversal of warfarin

A

Vitamins

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154
Q

Wernicke’s encephalopathy

A

Vitamins

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155
Q

Acetylcysteine (N-acetylcysteine)

A

Antidote for paracetamol poisoning
To prevent renal injury due to radiographic contrast material (contrast nephropathy)
To reduce viscosity of respiratory secretions (acting as a mucolytic)

156
Q

How does acetylcysteine work as an antidote to paracetamol poisoning?

A

Paracetamol is metabolised by conjugation with glucuronic acid and sulfate and a small amount is converted to NAPQI (hepatotoxic). This is detoxified by conjugation with glutathione, which is overwhelmed in paracetamol poisoning. Acetylcysteine replenishes the body’s supply of glutathione.

157
Q

Activated charcoal

A

Reduce absorption of certain poisons (including some drugs in overdose) from the gut
Increase the elimination of certain poisons

158
Q

Adenosine

A

Supraventricular tachycardia

159
Q

What are contraindications for adenosine?

A

Hypotension
Coronary ischaemia
Decompensated heart failure
Asthma
COPD

160
Q

Which drug prolongs and potentiates the effect of adenosine?

A

Dipyridamole

161
Q

Adrenaline (epinephrine)

A

Cardiac arrest
Anaphylaxis
Local vasoconstriction, e.g. during endoscopy to control mucosal bleeding or mixed with local anaesthetic drugs to prolong local anaesthesia

162
Q

How does adrenaline work?

A

Potent agonist of the alpha 1, alpha 2, beta 1 and beta 2 adrenoceptors, and so has many sympathetic effects.
* Vasoconstriction of vessels supplying skin, mucosa and abdominal viscera (mainly alpha 1)
* Increases in heart rate, force of contraction and myocardial excitability (beta 1)
* Vasodilatation of vessels supplying the heart and muscles (beta 2)
* Bronchodilatation (beta 2)
* Suppression of inflammatory mediator release from mast cells (beta 2)

163
Q

Which drug can cause widespread vasoconstriction when being treated with adrenaline?

A

Beta blocker
Alpha 1 mediated vasoconstricting effect is not opposed by beta 2 mediated vasodilatation

164
Q

What is the presciption of adrenaline in cardiac arrest and anaphylaxis?

A

Cardiac arrest: 1mg IV after the third shock (or ASAP if not shockable) and repeated every 3-5 minutes thereafter
Anaphylaxis: 500ug IM, repeated after 5 minutes if necessary

165
Q

Aldosterone antagonists

A

Ascites and oedema due to liver cirrhosis (spironolactone)
Chronic heart failure
Primary hyperaldosteronism

166
Q

How do aldosterone antagonists work?

A

Inhibit the effect of aldosterone by competitively binding to the aldosterone receptor. This increases sodium and water excretion and potassium retention.

167
Q

Important adverse effects of aldosterone antagonists

A

Hyperkalaemia, which can lead to muscle weakness, arrhythmias and cardiac arrest
Spironolactone causes gynaecomastia

168
Q

What are contraindications of aldosterone antagonists?

A

Severe renal impairment
Hyperkalaemia
Addison’s disease (who are aldosterone deficient)

169
Q

Alginates and antacids

A

Gastro-oesophageal reflux disease
Dyspepsia

170
Q

How do alginates and antacids work?

A

Alginates increase the viscosity of the stomach contents, which reduces the reflux of stomach acid into the oesophagus
Antacids buffer stomach acids

171
Q

How can alginates and antacids interact with other drugs?

A

Divalent cations in compound alginates can bind to other drugs, reducing their absorption.
Antacids can reduce serum concentrations of other drugs, so the doses should be taken at different times, e.g. ACE inhibitors, some antibiotics, bisphosphonates, digoxin, levothyroxine and proton pump inhibitors. They can also increase the excretion of aspirin and lithium.

172
Q

When should alginates and antacids be taken?

A

Following meals, before bedtime and/or when symptoms occur

173
Q

Allopurinol

A

Prevent acute attacks of gout
Prevent uric acid and calcium oxalate renal stones
Prevent hyperuricaemia and tumour lysis syndrome associated with chemotherapy

174
Q

How does allopurinol work?

A

Xanthine oxidase inhibitor
Xanthine oxidase metabolises xanthine (produced from purines) to uric acid. Inhibition of xanthine oxidase lowers plasma uric acid concentrations and reduces precipitation of uric acid in the joints or kidneys.

175
Q

What are contraindications to allopurinol?

A

Acute attacks of gout
Recurrent skin rash
Signs of more severe hypersensitivity

176
Q

Alpha blockers

A

Benign prostatic hyperplasia
Resistant hypertension

177
Q

Alpha blockers

A

Most drugs in this class are selective for the alpha 1-adrenoceptor, which is found mainly in smooth muscle, including in blood vessels and the urinary tract (the bladder neck and prostate in particular). Blockage induces relaxation, and so vasodilatation and a fall in BP and reduced resistance to bladder outflow.

178
Q

What are some important adverse effects of alpha blockers?

A

Postural hypotension
Dizziness
Syncope

179
Q

When should alpha blockers be taken?

A

At bedtime (to reduce BP lowering effect)

180
Q

Aminoglycosides

A

Severe infections, particularly those caused by Gram-negative aerobes (including Pseudomonas aeruginosa)
* Severe sepsis, including where the source is unidentified
* Pyelonephritis and complicated UTI
* Biliary and other intra-abdominal sepsis
* Endocarditis

181
Q

How do aminoglycosides work?

A

Bind irreversibly to bacterial ribosomes (30S subunit) and inhibit protein synthesis. They are bactericidal (kill bacteria). Their spectrum of action includes Gram-negative aerobic bacteria, staphylococci and mycobacteria.

182
Q

Why do aminoglycosides only work on certain bacteria?

A

Enter bacterial cells via an oxygen-dependent transport system. Streptococci and anaerobic bacteria don’t have this transport system, so have innate aminoglycoside resistance.
Other bacteria acquire resistance through reduced cell membrane permeability to aminoglycosides or acquisition of enzymes that modify aminoglycosides to prevent them from reaching the ribosomes. As penicillins weaken bacterial cell walls, they may enhance aminoglycoside activity by increasing bacterial uptake.

183
Q

What are the most important adverse effects of aminoglycosides?

A

Nephrotoxicity and ototoxicity
They accumulate in renal tubular epithelial cells and cochlear and vestibular hair cells where they trigger apoptosis andcell death. Nephrotoxicity presents as reduced urine output and rising serum creatinine and urea. Ototoxicity may present with hearing loss, tinnitus (cochlear damage) and/or vertigo (vestibular damage).

184
Q

Which groups of people are most susceptible to renal, cochlear and vestibular damage from aminoglycosides? Those with which condition should not take aminoglycosides unless absolutely necessary?

A

Neonates, elderly and those with renal impairment
Myasthenia gravis

185
Q

Aminosalicylates

A

Ulcerative colitis (mesalazine)
Rheumatoid arthritis (sulfasalazine)

186
Q

How do aminosalicylates work?

A

Release 5-aminosalicylic acid (5-ASA), which has anti-inflammatory and immunosuppressive effects

187
Q

What are adverse effects of aminosalicylates?

A

GI upset and headache
Serious blood abnormalities (e.g. leucopenia, thrombocytopenia)
Renal impairment
Sulfasalazine can cause decrrease in number of sperm

188
Q

What is a contraindication to aminosalicylates?

A

Aspirin hypersensitivity (aspirin is a salicylate, too)

189
Q

2 aldosterone antagonists

A

Spironolactone
Epleronone

190
Q

2 alginates and antacids

A

Gaviscon
Peptac

191
Q

3 alpha blockers

A

Doxazosin
Tamsulosin
Alfuzosin

192
Q

2 aminoglycosides

A

Gentamicin
Amikacin

193
Q

2 aminosalicylates

A

Mesalazine
Sulfasalazine

194
Q

How can mesalazine be given to someone with ulcerative colitis?

A

Enema or suppository
Oral

195
Q

Amiodarone

A

Tachyarrhythmias, including AF, atrial flutter, supraventricular tachycardia, ventricular tachycardia and refractory ventricular fibrillation

196
Q

How does amiodarone work?

A

Many effects on myocardial cells, including blockade of sodium, calcium and potassium channels, and antagonism of alpha- and beta-adrenergic receptors. This reduces spontaneous depolarisation, slows conduction velocity and increases resistace to depolarisation, including in the AV node. By interfering with the AV node conduction, amiodarone reduces the ventricular rate in AF and atrial flutter. It may also increase the chance of conversion to, and maintenanec of, sinus rhythm.

197
Q

What are some adverse effects of taking amiodarone chronically?

A

Pneumonitis
Bradycardia and AV block
Hepatitis
Photosensitivity and grey discolouration
Thyroid abnormalities

198
Q

In patients with which conditions should amiodarone be avoided?

A

Severe hypotension
Heart block
Active thyroid disease

199
Q

For which drugs should the dose be halved if amiodarone is started?

A

Digoxin
Diltiazem
Verapamil

200
Q

When is amiodarone used in cardiac arrest?

A

For VF or pulseless VT immediately after the 3rd shock, 300mg IV followed by 20mL of 0.9% sodium chloride or 5% glucose as a flush

201
Q

Angiotensin-converting enzyme inhibitors

A

Hypertension
Chronic heart failure
Ischaemic heart disease
Diabetic nephropathy and chronic kidney disease with proteinuria

202
Q

How do ACE inhibitors work?

A

Block the action of ACE, to prevent the conversion of angiotensin 1 to angiotensin 2. Angiotensin 2 is a vasoconstrictor and stimulates aldosterone secretion. Blocking its action reduces peripheral vascular resistance, which lowers BP. It particularly dilates the efferent glomerular arteriole, which reduces intraglomerular pressure and slows the progression of CKD. Reducing the aldosterone level promotes water and sodium excretion, which helps to reduce venous return, which is beneficial in heart failure.

203
Q

What are common adverse effects of ACE inhibitors and ARBs?

A

Hypotension
Persistent dry cough (!ACE inhibitors only! increased levels of bradykinin)
Hyperkalaemia (lower aldosterone level promotes K+ retention)
Renal failure

204
Q

What are contraindications to ACE inhibitors?

A

Renal artery stenosis or AKI
Pregnancy or breastfeeding

205
Q

3 ACE inhibitors

A

Ramipril
Lisinopril
Perindopril

206
Q

Angiotensin receptor blockers

A

When ACE inhibitors are not tolerated due to cough (same indications):
* Hypertension
* Chronic heart failure
* Ischaemic heart disease
* Diabetic nephropathy and chronic kidney disease with proteinuria

207
Q

How do ARBs work?

A

Block the action of angiotensin 2 on the AT1 receptor. Angiotensin 2 is a vasoconstrictor and stimulates aldosterone secretion. Blocking its action reduces peripheral vascular resistance, which lowers BP. It particularly dilates the efferent glomerular arteriole, which reduces intraglomerular pressure and slows the progression of CKD. Reducing aldosterone level promotes water and sodium excretion, which helps to reduce venous return, which is beneficial in heart failure.

208
Q

3 ARBs

A

Losartan
Candesartan
Irbesartan

209
Q

Selective serotonin reuptake inhibitors

A

Moderate-to-severe depression and mild depression if psychological treatments fail
Panic disorder
Obsessive compulsive disorder

210
Q

How do SSRIs work?

A

Inhibit neuronal reuptake of serotonin (5-HT) from the synaptic cleft, increasing its availability for neurotransmission

211
Q

Adverse effects of SSRIs

A

GI upset, appetite and weight disturbance
Hypersensitivity reactions, including skin rash
Hyponatraemia (confusion and reduced consciousness)
Suicidal thoughts and behaviour
Lower the seizure threshold, prolong the QT interval and can predispose to arrhythmias
Increase risk of bleeding
Serotonin syndrome - autonomic hyperactivity, altered mental state and neuromuscular excitation

212
Q

People with which conditions should SSRIs be prescribed with caution?

A

Epilepsy
Peptic ulcer disease

213
Q

4 SSRIs

A

Citalopram
Fluoxetine
Sertraline
Escitalopram

214
Q

What does a patient starting on antidepressants need to be told?

A

Symptoms should improve over a few weeks, particularly sleep and appetite
Carry on with drug treatment for at least 6 months after they feel better to stop the depression from coming back
Don’t stop treatment suddenly, as it may cause tummy upset, flu-like symptoms and sleeplessness; instead reduce the dose slowly over 4 weeks

215
Q

Tricyclics and related drugs

A

Moderate-to-severe depression (where SSRIs are ineffective)
Neuropathic pain (not licensed)

216
Q

How do tricyclic antidepressants work?

A

Inhibit neuronal reuptake of serotonin (5-HT) and noradrenaline from the synaptic cleft, increasing their availability for neurotransmission.
Also has extensive adverse effects due to blocking a wide array of receptors, including muscarinic, histamine (H1), alpha-adrenergic and dopamine (D2) receptors.

217
Q

Adverse effects of tricylic antidepressants

A

Antimuscarinic: dry mouth, constipation, urinary retention and blurred vision
H1 and alpha 1 receptors: sedation and hypotension
Arrhythmias and ECG changes (prolongation of QT and QRS durations)
Convulsions, hallucinations and mania
Dopamine receptors: breast changes and sexual dysfunction, and rarely extrapyramidal symptoms (tremor and dyskinesia)

218
Q

Which groups of people are particularly at risk of adverse effects from tricylic antidepressants?

A

Elderly
Cardiovascular disease
Epilepsy
Constipation
Prostatic hypertrophy
Raised intraocular pressure

219
Q

2 tricyclic antidepressants

A

Amitriptyline
Lofepramine

220
Q

Venlafaxine and mirtazapine

A

Major depression where SSRIs are ineffective
Generalised anxiety disorder (venlafaxine)

221
Q

How does venlafaxine work?

A

Serotonin and noradrenaline reuptake inhibitor (SNRI), which interferes with uptake of these neurotransmitters from the synaptic cleft. Increase availability of monoamines for neurotransmission.
Weak antagonist of muscarinic and histamine (H1) receptors.

222
Q

How does mirtazapine work?

A

Antagonist of inhibitory pre-synaptic alpha 2-adrenoceptors. Increase availability of monoamines for neurotransmission.
Potent antagonist of histamine (H1) but not muscarinic receptors.

223
Q

Adverse effects of venlafaxine and mirtazapine

A

GI upset (dry mouth, nausea, change in weight, diarrhoea or constipation)
CNS effects (headache, abnormal dreams, insomnia, confusion, convulsions)
Hyponatraemia
Serotonin syndrome
Suicidal thoughts and behaviour

224
Q

When should mirtazapine be taken?

A

At night (sedative)

225
Q

Dopamine D2-receptor antagonists

A

Prophylaxis and treatment of nausea and vomiting, particulary in the context of reduced gut motility

226
Q

How do dopamine D2-receptor antagonists work?

A

Dopamine, acting via D2 receptors, is:
* The main receptor in the chemoreceptor trigger zone, which is responsible for sensing emetogenic substances in the blood (e.g. drugs)
* An important neurotransmitter in the gut, where it promotes relaxation of the stomach and lower oesophageal sphincter and inhibits gastroduodenal coordination. Blocking D2 receptors has a prokinetic effect, promoting gastric emptying (e.g. opioids, diabetic gastroparesis)

227
Q

What are some adverse effects of dopamine D2-receptor antagonists?

A

Diarrhoea
Extrapyramidal symptoms (metoclopramide) - acute dystonic reaction, e.g. oculogyric crisis

228
Q

What are contraindications to dopamine D2-receptor antagonists?

A

GI obstruction
GI perforation
Antipsychotics (metoclopramide)
Dopaminergic agents for Parkinson’s disease (metoclopramide)

229
Q

2 dopamine D2-receptor antagonists

A

Metoclopramide
Domperidone

230
Q

Histamine H1-receptor antagonists

A

Prophylaxis and treatment of nausea and vomiting, particularly in the context of motion sickness or vertigo

231
Q

How do histamine H1-receptor antagonists work?

A

Histamine (H1) and acetylcholine (muscarinic) receptors predominate in the vomiting centre and in its communication with the vestibular system.

232
Q

Contraindications to histamine H1-receptor antagonists

A

Hepatic encephalopathy
Prostatic hypertrophy

233
Q

3 histamine H1-receptor antagonists

A

Cyclizine
Cinnarizine
Promethazine

234
Q

Phenothiazines

A

Prophylaxis and treatment of nausea and vomiting in a wide range of conditions, particularly when due to vertigo
Psychotic disorders, e.g. schizophrenia

235
Q

How does phenothiazine work?

A

Blockade of various receptors, including dopamine (D2) receptors in the chemoreceptor trigger zone and gut and, to a lesser extent, histamine (H1) and acetylcholine (muscarinic) receptors in the vomiting centre and vestibular system

236
Q

Adverse effects of phenothiazines

A

Drowsiness
Postural hypotension
Extrapyramidal syndromes (D2 receptor blockade) - acute dystonic reaction (e.g. oculogyric crisis), tardive dyskinesia
QT interval prolongation

237
Q

What are contraindications to phenothiazines?

A

Severe liver disease
Prostatic hypertrophy

238
Q

2 phenothiazines

A

Prochlorperazine
Chlorpromazine

239
Q

Serotonin 5-HT3-receptor antagonists

A

Prophylaxis and treatment of nausea and vomiting, particularly in the context of general anaesthesia and chemotherapy

240
Q

How do serotonin 5-HT3-receptor antagonists work?

A

High density of 5-HT3 receptors in chemoreceptor trigger zone
Serotonin is the key neurotransmitter released by the gut in response to emetogenic stimuli. Acting on 5-HT3 receptors, it stimulates the vagus nerve, which activates the vomiting centre via the solitary tract nucleus.

241
Q

2 serotonin 5-HT3-receptor antagonists

A

Ondansetron
Granisetron

242
Q

Antifungal drugs

A

Treatment of local fungal infections, including of the oropharynx, vagina or skin
Systemic treatment of invasive or disseminated fungal infections

243
Q

How do antifungal drugs work?

A

Polyene antifungals (nystatin) bind to ergosterol in fungal cell membranes, creating a polar pore which allows intracellular ions to leak out of the cell, which kills or slows the growth of the fungi.
Imidazole (clotrimazole) and triazole (fluconazole) antifungals inhibit ergosterol synthesis, impairing cell membrane synthesis, cell growth and replication.

244
Q

Adverse effects to fluconazole

A

GI upset (nausea, vomiting, diarrhoea, abdominal pain)
Headache
Hepatitis
Hypersensitivity (skin rash, cutaneous reactions, anaphylaxis)
Severe hepatic toxicity
Prolonged QT interval (arrhythmias)

245
Q

Contraindications to fluconazole

A

Pregnancy

246
Q

Antihistamines (H1-receptor antagonists)

A

Allergies, particularly hay fever
Aid relief of itchiness (pruritis) and hives (urticaria) due, for example, to insect bites, infections (chickenpox) and drug allergies
Adjunctive treatment in anaphylaxis, after administratno of adrenaline and other life-saving measures

247
Q

3 antifungals

A

Nystatin
Clotrimazole
Fluconazole

248
Q

How do H1-receptor antagonists work?

A

Histamine is released from storage granules in mast cells as a result of antigen binding to IgE on the cell surfaces. Mainly via H1 receptors, histamine induces features of immediate type 1 hypersensitivity: increased capillary permeability casing oedema formation, vasodilatation causing erythema and itch due to sensory nerve stimulation. When histamine is released in the nasopharynx, as in hay fever, it causes nasal irritation, sneezing, rhinorrhoea, congestion, conjunctivitis and tich. In the skin, it cause urticaria. Widespread histamine release, as in anaphylaxis, produces generalised vasodilatation and vascular leakage, with consequent hypotension. Antihistamine blocks the H1 receptor.

249
Q

H1-receptor antagonists

A

Cetirizine
Loratadine
Fexofenadine
Chlorphenamine

250
Q

Antimotility drugs

A

Diarrhoea, usually in the context of irritable bowel syndrome or viral gastroenteritis

251
Q

How do opioids work as antimotility drugs?

A

Agonist of opioid u-receptors in the GI tract, which increases non-propulsive contractions of the gut smooth muscle, but reduces propulsive (peristaltic) contractions. As a result, transit of bowel contents is slowed and anal sphincter tone is increased. Slower gut transit allows more time for water absorption, which hardens the stool.

252
Q

Contraindications of loperamide

A

Acute ulcerative colitis (inhibition of peristalsis increases risk of megacolon and perforation)
Clostridium difficile colitis
Acute bloody diarrhoea

253
Q

Antimotility drugs

A

Loperamide
Codeine phosphate

254
Q

Antimuscarinic bronchodilators

A

Chronic obstructive pulmonary disease
Asthma

255
Q

How do antimuscarinic bronchodilators work?

A

Bind to muscarinic receptor, where they act as a competitive inhibitor of acetylcholine. Blocking the receptor reduces smooth muscle tone (including in the respiratoy tract) and reduces secretions from glands in the respiratory and GI tract.

256
Q

Which condition do antimuscarinics need to be used with caution?

A

Angle-closure glaucoma
Arrhythmias

257
Q

3 antimuscarinic bronchodilators

A

Ipratropium
Tiotropium
Glycopyrronium

258
Q

Antimuscarinics for CV and GI uses

A

Severe or symptomatic bradycardia (atropine)
Irritiable bowel syndrome (hyoscine butylbromide)
Reducing copious respiratory secretions (hyoscine butylbromide)

259
Q

How do antimuscarinics work CV and GI?

A

Bind to muscarinic receptors, where they act as competitive inhibitor of acetylcholine. Blocking the receptor results in increased heart rate and conduction, reduced smooth muscle tone and peristaltic contraction (including in the gut and urinary tract) and reduce secretions from glands in the respiratory tract and gut.

260
Q

Adverse effects of antimuscarinics

A

Tachycardia
Dry mouth
Constipation
Urinary retention in those with BPH
Blurred vision

261
Q

Antimuscarinic for GI and CV symptoms

A

Atropine
Hyoscine butylbromide
Glycopyrronium

262
Q

Antimuscarinics for GU use

A

Reduce urinary frequency, urgency and urinary incontinence in overactive bladder

263
Q

How do antimuscarinics work GU?

A

Bind to muscarinic receptors, where they act as competitive inhibitor of acetylcholine. Contraction of the smooth muscle of the bladder is under parasympathetic control. Blocking muscarinic receptors promotes bladder relaxation, increasing bladder capacity.
Relatively selective for the M3 receptor.

264
Q

Contraindication to antimuscarinics GU

A

UTI

265
Q

3 antimuscarinics GU

A

Oxybutynin
Tolterodine
Solifenacin

266
Q

First-generation (typical) antipsychotics

A

Urgent treatment of severe psychomotor agitation that is causing dangerous or violent behaviour, or to calm patient to permit assessment
Schizophrenia
Bipolar disorder, particularly in acute episodes of mania or hypomania
Nause and vomiting, particularly in palliative care setting

267
Q

How do typical antipsychotics (FGA) work?

A

Block the post-synaptic dopamine D2 receptors. D2 blockade of the mesolimbic/mesocortical pathway between the midbrain and limbic system/frontal cortex.
D2 receptors also found in chemoreceptor trigger zone, where blockade accounts for their use in nausea and vomiting.

268
Q

Adverse effects of antipsychotics

A

Extrapyramidal effects (D2 blockade in nigrostriatal pathway) - acute dystonic reactions (involuntary parkinsonian movements or muscle spasms), akathisia (state of internal restlessness) and neuroleptic malinancy syndrome (rigidity, confusion, autonomic dysregulation, pyrexia), tardive dyskinesia
Drowsiness
Hypotension
QT prolongation (arrhythmias)
Erectile dysfunction
Hyperprolactinaemia (tuberohypophyseal D1 blockade) - menstrual disturbance, galactorrhoea, breast pain

269
Q

3 first generation (typical) antipsychotics

A

Haloperidol
Chlorpromazine
Prochlorperazine

270
Q

Ways of administering typical antipsychotics

A

Orally (tablet and liquid)
Slow-release IM (‘depot’) injection
Rapid-acting IM injection (haloperidol)
IV (haloperidol)

271
Q

Who do you need to be careful with when prescribing antipsychotics?

A

Elderly
Dementia
Parkinson’s disease

272
Q

Second-generation (atypical) antipsychotics

A

Urgent treatment of severe psychomotor agitation that is causing dangerous or violent behaviour, or to calm patient to permit assessment
Schizophrenia, particularly when extrapyramidal SEs have complicated the use of typical antipsychotics or negative symptoms are prominent
Bipolar disorder, particularly in acute episodes of mania or hypomania

273
Q

Why can second-generation (atypical) antipsychotics be considered better than typical?

A

Improved efficacy in ‘treatment-resistant’ schizophrenia and against negative symptoms (higher affinity for other receptors, particularly 5-HT2A receptors)
Lower risk of extrapyramidal symptoms (looser binding to the D2 receptors)

274
Q

What is a common problem with second-generation (atypical) antipsychotics?

A

Metabolic disturbance - weight gain, DM, lipid changes

275
Q

What are 2 rare adverse effects of clozapine?

A

Agranulocytosis (severe deficiency of neutrophils)
Myocarditis

276
Q

Who must not be given clozapine?

A

Severe heart disease
History of neutropenia

277
Q

4 second-generation (atypical) antipsychotics

A

Quetiapine
Olanzapine
Risperidone
Clozapine

278
Q

Aspirin

A

Acute coronary syndrome and acute ischaemic stroke
Long-term secondary prevention of thrombotic arterial events in those with cardiovascular, cerebrovascular and peripheral arterial disease
Reduce the risk of intracardiac thrombus and embolic stroke in AF where warfarin and novel oral anticoagulants are contraindicated
Mild-to-moderate pain and fever

279
Q

How does aspirin work?

A

Irreversibly inhibits cyclooxygenase (COX) to reduce production of the pro-aggregatory factor thromboxane from arachidonic acid, reducing platelet aggregation and the risk of arterial occlusion

280
Q

Adverse effects of aspirin

A

GI irritation
GI ulceration and haemorrhage
Hypersensitivity reactions (bronchospasm)

281
Q

Who should not be given aspirin?

A

Children under 16 (Reye’s syndrome)
Aspirin hypersensitivity
Third trimester of pregnancy (premature closure of ductus arteriosus)

282
Q

How does the dose of aspirin change when given for acute coronary syndrome vs acute ischaemic stroke vs long-term prevention of thrombosis?

A

ACS: once-only loading dose of 300mg followed by a regular dose of 75mg daily
Acute ischaemic stroke: aspirin 300mg daily for 2 weeks before switching to 75mg daily
Prevention of thrombosis: low-dose aspirin 75mg daily

283
Q

When taking low-dose aspirin, what additional medication should be considered in those at risk of GI complications?

A

Proton pump inhibitor, e.g. omeprazole 20mg daily

284
Q

When should aspirin be taen?

A

After food

285
Q

Benzodiazepines

A

Seizures and status epilepticus
Alcohol withdrawal reactions
Sedation for interventional procedures
Short-term treatment of severe, disabling or distressing anxiety or insomnia

286
Q

How do benzodiazepines work?

A

Facilitate and enhance binding of GABA to GABAA receptor. Depressant effect on synaptic transmission, resulting in reduced anxiety, sleepiness, sedation and anticonxulsive effects.

287
Q

Who should avoid benzodiazepines?

A

Respiratory impairment
Neuromuscular disease, e.g. myasthenia gravis
Liver failure (hepatic encephalopathy)

288
Q

5 benzodiazepines

A

Diazepam
Temazepam
Lorazepam
Chlordiazepoxide
Midazolam

289
Q

Which benzodiazepine is recommended for seizures and why?

A

Lorazepam (initial dose 4mg IV) or diazepam (10mg IV or rectally)
Long-acting

290
Q

Beta2-agonists

A

Asthma: short-acting to relieve breathlessness and long-acting as step 3 treatment for chronic asthma
COPD: short-acting to relieve breathlessness and long-acting as an option for second-line therapy
Hyperkalaemia (nebulised)

291
Q

How do beta2-agonists work?

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.
Also stimulate Na+/K+-ATPase pumps on cell surface membranes, causing a shift of K+ from extracellular to intracellular compartment.

292
Q

2 short-acting beta2-agonists

A

Salbutamol
Terbutaline

293
Q

2 long-acting beta2-agonists

A

Salmeterol
Formoterol

294
Q

Adverse effects of beta2-agonists

A

Fight or flight
* Tachycardia
* Palpitations
* Anxiety
* Tremor

Promote glycogenolysis > increased serum glucose
Muscle cramps

295
Q

Use of what can help improve airway deposition and treatment efficacy of inhaled medication?

A

Spacer with metered dose inhalers

296
Q

Beta blockers

A

Ischaemic heart disease (angina and acute coronary syndrome)
Chronic heart failure
AF
Supraventricular tachycardia
Hypertension

297
Q

How do beta blockers work?

A

Beta1-adrenoreceptors are located mainly in the heart and beta2-adrenoreceptors are found mainly in smooth muscle of blood vessels and the airways.
Beta blockers reduce force of contraction and speed of conduction in the heart, relieving myocardial ischaemia by reducing cardiac work and oxygen demand and increasing myocardial perfusion.
Slow the ventricular rate in AF by prolonging the refractory period of the AV node.
Lower BP in a variety of ways, including reducing renin secretion from the kidney.

298
Q

Adverse effects of beta blockers

A

Fatigue
Cold extremities
Headache
GI disturbance, e.g. nausea
Sleep disturbance and nightmares
Impotence

299
Q

Who should not have beta blockers?

A

Asthma
Non-dihydropyridine calcium channel blockers, e.g. verapamil, diltiazem
Haemodynamic instability
Heart block

300
Q

4 beta blockers

A

Bisoprolol
Atenolol
Propranolol
Metoprolol

301
Q

Bisphosphonates

A

Osteoporotic fragility fractures (alendronic acid)
Severe hypercalcaemia of malignancy (pamidronate and zoledronic acid)
Myeloma and breast cancer with bone metastases (pamidronate and zoledronic acid)
Metabolically-active Paget’s disease

302
Q

How do bisphosphonates work?

A

Reduce bone turnover by inhibiting the action of osteoclasts, the cells responsible for bone resorption. As bone is resorbed, bisphosphonates accumulate in osteoclasts, where they inhibit activity and promote apoptosis, resulting in reduction in bone loss and improvement in bone mass.

303
Q

Adverse effects of bisphosphonates

A

Oesophagitis (when taken orally)
Hypophosphataemia
Osteonecrosis of the jaw
Atypical femoral fracture

304
Q

Who cannot have bisphosphonates?

A

Severe renal impairment
Hypocalcaemia
Upper GI disorders (oral administration only)

305
Q

3 bisphosphonates

A

Alendronic acid
Disodium pamidronate
Zoledronic acid

306
Q

How should alendronic acid be taken

A

Swallowed whole
At least 30 minutes before breakfast or other medications
With plenty of water
Remain upright for 30 minutes after taking (reduce oesophageal irritation)

307
Q

Calcium and vitamin D

A

Osteoporosis (Ca + vit D)
Chronic kidney disease (secondary hyperparathyroidism and renal osteodystrophy) (Ca + vit D)
Severe hyperkalaemia to prevent life-threatening arrhythmias (Ca)
Hypocalcaemia that is symptomatic (e.g. paraesthesia, tetany, seizures) or severe (Ca)
Vitamin D deficiency, including for rickets and osteomalacia (vit D)

308
Q

4 calcium and vit D

A

Calcium carbonate
Calcium gluconate
Colecalciferol
Alfacalcidol

309
Q

Calcium channel blockers

A

Hypertension (amlodipine, nifedipine)
Stable angina
Supraventricular arrhythmais (diltiazem, verapamil)

310
Q

How do calcium channel blockers work?

A

Decrease Ca entry into vascular and cardiac cells, reducing intracellular calcium concentration. This causes relaxation and vasodilation in arterial smooth muscle, lowering arterial pressure.
Reduce myocardial contractility. Suppress cardiac conduction, particularly across the AV node, slowing ventricular rate.

311
Q

What are the 2 types of calcium channel blockers and how do they differ?

A

Dihydropyridines (amlodipine, nifedipine): relatively selective for vasculature
Non-dihydropyridines: more cardioselective

312
Q

Adverse effects of amlodipine and nifedipine

A

Ankle swelling
Flushing
Headache
Palpitations

313
Q

Adverse effects of verapamil

A

Constipation
Bradycardia
Heart block
Cardiac failure

314
Q

4 calcium channel blockers

A

Amlodipine
Nifedipine
Diltiazem
Verapamil

315
Q

Carbamazepine

A

Epilepsy, for focal seizures and primary generalised seizures
Trigeminal neuralgia
Bipolar disorder, as an option for prophylaxis in those resistant or intolerant of other medication

316
Q

Adverse effects of carbamazepine

A

GI upset (nausea and vomiting)
Neurological effects (dizziness and ataxia)
Oedema
Hyponatraemia
Hypersensitvity (mild maculopapular skin rash)
Antiepileptic hypersensitivity syndrome (severe skin reactions, fever, lymphadenopathy, systemic involvement and 10% mortality)

317
Q

Who should not have carbamazepine?

A

Antiepileptic hypersensitivity syndrome
Pregnancy

318
Q

Cephalosporins and carbapenems

A

Urinary and respiratory tract infections (oral cephalosporins)
Treatment of infections that are very severe or complicated, or caused by antibiotic-resistant organisms (IV cephalosporins and carbapenems)

319
Q

How do cephalosporins and carbapenems work?

A

Beta-lactam ring. During bacterial cell growth, they inhibit enzymes responsible for cross-linking peptidoglycans in bacterial cell walls, which weakens cell walls, preventing them from maintaining an osmotic gradient, resulting in bacterial cell swelling, lysis and death.

320
Q

Which antibiotic is more resistant to beta-lactamases and why?

A

Cephalosporins and carbapenems due to fusion of the beta-lactam ring with a dihydrothiazine ring (cephalosporins) or hydroxyethyl side chain (carbapenems)

321
Q

Adverse effects of cephalosporins and carbapenems

A

GI upset (nausea and diarrhoea)
Antibiotic-associated colitis
Hypersensitivity
CNS toxicity (seizures)

322
Q

2 cephalosporins

A

Cefalexin
Cefotaxime

323
Q

2 carbapenems

A

Meropenem
Ertapenem

324
Q

How can cephalosporins be administered vs carbapenems?

A

Cephalosporins: orally (tablets, capsules, suspension), injection (IV, bolus injection, infusion), IM
Carbapenems: IV injection or infusion

325
Q

Clopidogrel

A

Generally prescribed with aspirin
* Acute coronary syndrome
* Prevent occlusion of coronary artery stents
* Long-term secondary prevention of thrombotic arterial events in those with cardiovascular, cerebrovascular and peripheral arterial disease
* Reduce the risk of intracardiac thrombus and embolic stroke in AF where warfarin and novel oral anticoagulants are contraindicated

326
Q

How does clopidogrel work?

A

Prevents platelet aggregation and reduces the risk of arterial occlusion by binding irreversibly to adenosine diphosphate (ADP) receptors (P2Y12 subtype) on the surface of platelets

327
Q

Adverse effects of clopidogrel

A

Bleeding
GI upset (dyspepsia, abdominal pain, diarrhoea)
Thrombocytopenia

328
Q

Who shouldn’t be prescribed clopidogrel?

A

Active bleeding
7 days before elective surgery and other procedures

329
Q

Compound (beta2-agonist-corticosteroid) inhalers

A

Asthma: control of symptoms and prevention of exacerbations
COPD: control of symptoms and prevention of exacerbations

330
Q

How do compound inhalers work?

A

Inhaled corticosteroid suppresses airway inflammation
Long-acting beta2-agonist (LABA) stimulates bronchodilation

331
Q

2 compound inhalers

A

Seretide
Symbicort

332
Q

What advice can be given to patients taking compound inhalers to avoid sore mouth and hoarse voice?

A

Rinse mouth and gargle after taking inhaler

333
Q

Systemic corticosteroids (glucocorticoids)

A

Allergic or inflammatory disorders, e.g. anaphylaxis and asthma
Suppression of autoimmune disease, e.g. inflammatory bowel disease and inflammatory arthritis
Treatment of some cancers as part of chemotherapy or to reduce tumour-associated swelling
Hormone replacement in adrenal insufficiency or hypopituitarism

334
Q

How do systemic corticosteroids work?

A

Mainly glucocorticoid effects. Bind to cytosolic glucocorticoid receptors, which then translocate to the nucleus and bind to glucocorticoid-response elements, which regulate gene suppression.
Upregulate anti-inflammatory genes and downregulate pro-inflammatory genes (cytokines, tumour necrosis factor alpha).
Direct actions on inflammatory cells: suppression of circulating monocytes and eosinophils.
Metabolic effects: increase gluconeogenesis from increased circulating amino and fatty acids, released by catabolism of muscle and fat.

Mineralocorticoid effects: Na+ and water retention and L+ excretion in the renal tubule.

335
Q

Adverse effects of systemic corticosteroids

A

Infection
DM
Osteoporosis
Proximal muscle weakness
Skin thinning with easy bruising
Gastritis
Mood and behavioural changes: insomnia, confusion, psychosis and suicidal ideas
Addisonian crisis (If withdrawn suddenly)

Mineralocorticoid actions: HTN, hypokalaemia and oedema

336
Q

3 systemic corticosteroids

A

Prednisolone
Hydrocortisone
Dexamethasone

337
Q

Inhaled corticosteroids (glucocorticoids)

A

Asthma
COPD

338
Q

How do inhaled corticosteroids work for asthma and COPD?

A

Pass through the plasma membrane and interact with receptors in the cytopmas. Activated receptor passes into the nucleus to modify the transciption of a large number of genes. Pro-inflammatory interleukins, cytokines and chemokines are downregulated, while anti-inflammatory proteins are upregulated. In the airways, this reduces mucosal inflammation, widens the airways and reduces mucus secretion.

339
Q

Adverse effects of inhaled corticosteroids

A

Oral candidiasis
Hoarse voice

340
Q

3 inhaled corticosteroids

A

Beclometasone
Budesonide
Fluticasone

341
Q

Topical corticosteroids (glucocorticoids)

A

Inflammatory skin conditions, e.g. eczema

342
Q

2 topical corticosteroids

A

Hydrocortisone
Betamethasone

343
Q

Digoxin

A

AF and atrial flutter
Severe heart failure

344
Q

How does digoxin work?

A

Negatively chronotropic (reduces heart rate) and positively inotropic (increases force of contraction).
Indirect pathway increases vagal (parasympathetic) tone, reducing conduction at the AV node, preventing some impulses from being transmitted to the ventricles, thereby reducing the ventricular rate.
Direct effect on myocytes through inhibition of Na+/K+-ATPase pumps, causing Na+ to accumulate in the cell. As cellular extrusion of Ca requires low intracellular Na concentrations, elevation of intracellular Na causes Ca to accumulate in the cell, increasin contractile force.

345
Q

Adverse effects of digoxin

A

Bradycardia
GI disturbance
Rash
Dizziness
Visual disturbance (blurred or yellow vision)

346
Q

What are contraindications to digoxin?

A

Second-degree heart blok and intermittent complete heart block
Ventricular arrhythmias

347
Q

Dipyridamole

A

Cerebrovascular disease (TIA or ischaemic stroke), for secondary prevention of stroke
Induce tachycardia during a myocardial perfusion scan in the diagnosis of ischaemic heart disease

348
Q

How does dipyridamole work?

A

Antiplatelet and vasodilatory effects. Inrease in intra-platelet cyclic adenosine monophosphate (cAMP) that inhibits platelet aggregation, reducing the risk of artieral occlusion. Blocks cellular uptake of adenosine, prolonging its effect on blood vessels to produce vasodilation.

349
Q

Loop diuretics

A

Relief of breathlessness in acute pulmonary oedema
Symptomatic treatment of fluid overload in chronic heart failure
Symptomatic treatment of fluid overload in other oedematous states, e.g. due to renal disease or liver failure

350
Q

How do loop diuretics work?

A

Act principally on the ascending limb of the loop of Henle, where they inhibit the Na/K/2Cl co-transporter, which is responsible for transporting Na, K and Cl ions from the tubular lumen into the epithelial cell, and so water then follows by osmosis. Inhibiting this has a potent diuretic effect.
Direct effect on blood vessels, causing dilatation of capacitance veins.

351
Q

Adverse effects of loop diuretics

A

Dehydration
Hypotension
Low electrolyte state

352
Q

What are contraindications to loop diuretics?

A

Hypovolaemia
Dehydration

353
Q

2 loop diuretics

A

Furosemide
Bumetanide

354
Q

Potassium-sparing diuretics

A

Hypokalaemia arising from loop- or thiazide-diuretic therapy

355
Q

How do potassium-sparing diuretics work?

A

Weak diuretics.
Counteract potassium loss and enhance diuresis when combined with another diuretic.
Acts on distal convoluted tubules in the kidney. Inhibits the reabsorption of Na and therefore water by epithelial sodium channels, leading to sodium and water excretion and retention of potassium.

356
Q

Who should not take potassium-sparing diuretics?

A

Severe renal impairment
Hyperkalaemia
K supplements
Aldosterone antagonists

357
Q

1 potassium-sparing diuretic

A

Amiloride

358
Q

Thiazide and thiazide-like diuretics

A

Hypertension

359
Q

How do thiazide diuretics work?

A

Inhibit the Na/Cl co-transporter in the distal convoluted tubule of the nephron. This prevents reabsorption of sodium and its osmotically associated water. The resulting diuresis causes an initial fall in extracellular fluid volume.
Vasodilatation.

360
Q

Adverse effects of thiazide diuretics

A

Hyponatraemia
Hypokalaemia (arrhythmias)

361
Q

3 thiazide (and thiazide-like) diuretics

A

Bendroflumethiazide
Indapamide
Chlortalidone

362
Q

Dopaminergic drugs

A

Early Parkinson’s disease
Later Parkinson’s disease
Secondary parkinsonism

363
Q

How do dopaminergic drugs work?

A

Precursor of dopamine that can enter the brain via a membrane transporter

364
Q

Adverse effects of dopaminergic drugs

A

Nausea
Drowsiness
Confusion
Hallucinations
Hypotension
Dyskinesia (excessive and involuntary movement)

365
Q

3 dopaminergic drugs

A

Levodopa
Ropinirole
Pramipexol

366
Q

What is important about the administration of Parkinson’s medications?

A

Taken at the right time, to produce the best symptom control

367
Q

Emollients

A

Topical treatment for all dry or scaling skin disorders

368
Q

How do emollients work?

A

Replace water content in dry skin. Contain oils or paraffin-based products that help to soften the skin and can reduce water loss by protecting against evaporation from the skin surface.

369
Q

2 emollients

A

Aqueous cream
Liquid paraffin

370
Q

Fibrinolytic drugs

A

Acute ischaemic stroke (alteplase)
Acute STEMI (alteplase, streptokinase)
Massive PE with haemodynamc instability

371
Q

How do fibrinolytic drugs work?

A

Catalyse the conversion of plasminogen to plasma, which acts to dissolve fibrinous clots and re-canalise occluded vessels. This allows reperfusion of affected tissue, preventing or limiting tissue infarction and cell death.

372
Q

Adverse effects of fibrinolytic drugs

A

Nause and vomiting
Bruising
Hypotension
Serious bleeding
Allergic reaction
Cardiogenic shock
Cardiac arrest
Cerebral oedema (brain infarction)
Arrhythmia (heart infarction)

373
Q

What are contraindications to fibrinolytic drugs?

A

Bleeding: recent haemorrhage, recent trauma or surgery
Bleeding disorders
Severe hypertension
Peptic ulcers
Previous streptokinase treatment

374
Q

2 fibrinolytic drugs

A

Alteplase
Streptokinase

375
Q

Gabapentin and pregabalin

A

Focal epilepsies
Neuropathic pain (pregabalin)
Migraine prophylaxis (gabapentin)
Generalised anxiety disorder (pregabalin)

376
Q

How does gabapentin and pregabalin work?

A

Binds with voltage-sensitive Ca channels, where it prevents the inflow of Ca and inhibits neurotransmitter release. This interferes with synaptic transmission and reduces neuronal excitability.

377
Q

H2-receptor antagonists

A

Peptic ulcer disease
GORD and dyspepsia

378
Q

How do H2-receptor antagonists work?

A

Reduce gastric acid secretion. Histamine is released by local pararine cells and binds to H2-receptors on the gastric parietal cell. Via a second-messenger system, this activates the proton pump. Blocking the H2-receptors therefore reduces acid secretion.

379
Q

1 H2-receptor antagonist

A

Ranitidine

380
Q

Heparins and fondaparinux

A

Venous thromboembolism: DVT and PE
Acute coronary syndrome

381
Q

How do heparins and fondaparinux work?

A

Thrombin and factor Xa are key components of the final common coagulation pathway that leads to formation of a fibrin clot. By inhibiting their function, they prevent the formation and propagation of blood clots.
Unfractionated heparin activates antithrombin, which inactivates clotting factor Xa and thrombin.
LMWH preferentially inhibit factor Xa.
Fondaparinux inhibits factor Xa only.

382
Q

In which patients should anticoagulants be used cautiously?

A

Clotting disorders
Severe uncontrolled hypertension
Recent surgery or trauma
Invasive procedures (lumbar puncture, spinal anaesthesia)

383
Q

3 heparins

A

Enoxaparin
Dalteparin
Unfractionated heparin

384
Q

Insulin

A

Type 1 and 2 DM
Diabetic emergencies (DKA, hyperglycaemia hyperosmolar syndrome) (IV)
Perioperative glycaemic control in selected DM patients
Hyperkalaemia

385
Q
A

Phase 3a Medicine (7 decks)

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