50 Drugs Flashcards

1
Q

State the class of drugs to which Aspirin belongs

A

Anti-Platelet

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Describe the MOA of Aspirin

A

Irreversible inactivation of Cyclooxygenase enzyme This reduces production of Platelet Thromboxane (TXA2) and Endothelial Prostaglandin (PGI2) Reduced TXA2 production reduces platelet aggregation and thrombus formation Reduced prostaglandin synthesis decreases nociceptive sensation and inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

State indications for Aspirin

A

Secondary prevention of thrombotic events Pain relief

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

State side effects of Aspirin

A

Bleeding Peptic Ulcer Disease Angiooedema Bronchospasm Reye’s Syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Describe important pharmacokinetic features of Aspirin

A

Half life increases with very large doses (therefore pharmacokinetics may be non-linear in overdose)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

State some important pieces of patient information that should be given alongside Aspirin

A

May be advisable to take PPI with long term aspirin Avoid OTC preparations containing aspirin Not to be take by children under 16

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

State the class of drugs to which Clopidogrel belongs

A

Anti-Platelet

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe the MOA of Clopidogrel

A

Irreversibly blocks the ADP receptor on platelet cell membranes Therefore prevents formation of the GPIIb/IIIa complex, required for platelet aggregation Decreased thrombus formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

State indications for Clopidogrel

A

Secondary prevention of thrombotic events

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

State side effects of Clopidogrel

A

Abdominal Pain Diarrhoea Bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe important pharmacokinetic/pharmacodynamic features of Clopidogrel

A

Should be avoided in patients with liver failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

State some important pieces of patient information that should be given alongside Clopidogrel

A

Patients may be advised to stop clopidogrel before surgical procedures Patients should not stop clopidogrel without consulting their doctor if they have an arterial stent in-situ

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Give examples of Recombinant Tissue Plasminogen Activators

A

Tenecteplase Alteplase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Describe the MOA of Recombinant Tissue Plasminogen Activators

A

Catalyses conversion of plasminogen to plasmin to promote fibrin clot lysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

State indications for the use of Recombinant Tissue Plasminogen Activators

A

Acute Ischaemic Stroke (within 4.5 hours) Myocardial Infarction (within 12 hours) Massive Pulmonary Embolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

State side effects of Recombinant Tissue Plasminogen Activators

A

Bleeding Allergy Angiooedema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Describe important pharmacokinetic/pharmacodynamic features of Recombinant Tissue Plasminogen Activators

A

Alteplase is given as a bolus-infusion regimen Tenecteplase is given as a single bolus Interacts with other blood thinners (anticoagulants/antiplatelets)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

State some important pieces of patient information that should be given alongside Recombinant Tissue Plasminogen Activators

A

Patient should be made aware of the risk benefit ratio which should include reference to bleeding complications

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Describe the MOA of Unfractioned Heparin

A

Unfractioned Heparin enhances the action of Antithrombin III, which inhibits thrombin

It also inhibits multiple other components of the coagulation cascade to have an anticoagulant effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

State the indications for Unfractioned Heparin

A

Treatment and Prophylaxis of Thromboembolic Disease

Renal Dialysis (Haemodialysis)

Treatment of Acute Coronary Syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

State the side effects of Unfractioned Heparin

A

Bleeding

Heparin-Induced Thrombocytopaenia

Osteoporosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

State important pharmacokinetic/pharmacodynamic features of Unfractioned Heparin

A

Administered by continuous IV infusion or subcutaneous injection

Complex kinetics - non-linear relationship between dose/half life and effect

Requires Therapeutic Dose Monitoring (TDM)

Anticoagulant effect can be reversed by Protamine

Shorter duration of action than LMW Heparin

Used in preference to LMW Heparin in selected patients due to shorter duration of action and reversibility (e.g. peri-operatively)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

State some important pieces of patient information that should be given with Unfractioned Heparin

A

Risk of bleeding

Requires regular blood monitoring

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Describe the MOA of LMW Heparin

A

LMW Heparin enhances the action of Antithrombin III, which inhibits thrombin

It also inhibits multiple other components of the coagulation cascade to have an anticoagulant effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
State the indications for LMW Heparin
Treatment and Prophylaxis of Thromboembolic Disease Renal Dialysis (Haemodialysis) Treatment of Acute Coronary Syndrome
26
State the side effects of LMW Heparin
Bleeding Heparin-Induced Thrombocytopaenia Osteoporosis
27
Describe important pharmacokinetic/pharmacodynamic features of LMW Heparin
Administered by subcutaneous injection More predictable dose-response relationship than Unfractionated Heparin 2-4 times longer plasma half life than Unfractionated Heparin Mostly renal clearance, therefore half life may be elevated in patients with renal failure so dose adjustment may be needed Regular TDM not needed Less readily reversed with Protamine than Unfractionated Heparin
28
State some important pieces of patient information that should be given with LMW Heparin
Risk of Bleeding Requires Injection May need regular monitoring in prolonged therapy (FBC to check for thrombocytopaenia)
29
To which class of drugs does Warfarin belong?
Vitamin K Antagonists
30
Describe the MOA of Warfarin
Inhibits Vitamin K epoxide reductase Prevents recycling of Vitamin K to reduced form after carboxylation of coagulation factors II, VII, IX and X Therefore, prevents thrombus formation
31
State indications for Warfarin
Treatment of Venous Thromboembolism Thromboprophylaxis in AF/Metallic Heart Valves/Cardiomyopathy
32
State side effects of Warfarin
Bleeding (risk increases with increasing INR) Warfarin Necrosis Osteoporosis
33
Describe important pharmacokinetic/pharmacodynamic features of Warfarin
Numerous drug/food interactions Reversed by Vitamin K Polymorphisms in key metabolising enzymes (VKORC1 and CYP2C9) Needs therapeutic dose monitoring and monitored loading regimen Monitored with INR and dose adjusted depending on indication
34
State some important pieces of patient information that should be given with Warfarin
Need for compliance and attendance for monitoring Care needed with alcohol Must inform doctor before starting new drugs Should avoid OTC preparations including aspirin
35
To which class of drugs does Dabigatran belong?
Direct Thrombin Inhibitors
36
Describe the MOA of Dabigatran
Direct thrombin inhibitor that prevents conversion of fibrinogen to fibrin Thus prevents thrombus formation
37
State indications for Dabigatran
Prophylaxis of Venous Thromboembolism (especially post-operative) Thromboprophylaxis in Non-Valvular AF
38
State side effects of Dabigatran
Bleeding Dyspepsia
39
Describe important pharmacodynamic/pharmacokinetic features of Dabigatran
Rapid onset of action No food and few drug interactions Not metabolised by CYP450 No need for therapeutic monitoring No available antidote
40
State some important pieces of patient information that should be given with Dabigatran
Risk of bleeding
41
To which class of drugs does Rivaroxaban belong?
Factor Xa Inhibitors
42
Describe the MOA of Rivaroxaban
Inhibits conversion of prothrombin to thrombin, thereby reducing thrombin concentrations in the blood This inhibits formation of fibrin clots
43
State indications for Rivaroxaban
Prophylaxis of Venous Thromboembolism (especially post-operatively) Thromboprophylaxis in Non-Valvular AF Treatment fo Venous Thromboembolism
44
State side effects of Rivaroxaban
Nausea Bleeding
45
Describe important pharmacodynamic/pharmacokinetic features of Rivaroxaban
Predictable drug interactions (metabolised by CYP450 and CYP3A4) No need for therapeutic monitoring Currently no available antidote
46
Describe important pieces of patient information that should be given with Rivaroxaban
Risk of bleeding
47
To which class of drugs does Apixaban belong?
Factor Xa Antagonists
48
Describe the MOA of Apixaban
Inhibits conversion of prothrombin to thrombin, thereby reducing concentration of thrombin in the blood This inhibits formation of fibrin clots
49
State indications for Apixaban
Prophylaxis of Venous Thromboembolism Following Hip or Knee Replacement Surgery Thromboprophylaxis in Non-Valvular AF
50
State side effects of Apixaban
Nausea Bleeding
51
Describe important pharmacodynamic/pharmacokinetic features of Apixaban
Predictable Drug Interactions (metabolised by CYP450 and subtrate for p glycoprotein) 75% is metabolised by the liver, the rest is renally excreted No need for therapeutic monitoring Currently no available antidote
52
Describe important pieces of patient information that should be given with Apixaban
Risk of bleeding
53
Give examples of drugs in the class of 'Cardioselective Beta Blockers'
Atenolol Bisoprolol
54
Describe the MOA of Cardioselective Beta Blockers
e.g. Atenolol and Bisoprolol Preferentially block Beta-1-Adrenoceptors in cardiac and renal tissue Inhibits sympathetic stimulation of heart and renal vasculature Blockage of the sino-atrial node reduces heart rate (negative chronotropic effect) and blockage of receptors in the myocardium depresses cardiac contractility (negative inotropic effect) Additionally, blockade of beta-1 adrenoceptors in renal tissue inhibits the release of renin, depressing the vasoconstrictive effects of the renin-angiotensin-aldosterone system
55
State indications for the use of Cardioselective Beta Blockers such as Atenolol and Bisoprolol
Hypertension Angina Rate Control in AF (Bisoprolol may be used as supportive therapy in mild-moderate Heart Failure)
56
State side effects of Cardioselective Beta Blockers such as Atenolol and Bisoprolol
Bradycardia Hypotension Bronchospasm Fatigue Cold Extremities Sleep Disturbance Loss of Hypoglycaemic Awareness
57
Describe important pharmacodynamic/pharmacokinetic features of Cardioselective Beta Blockers such as Atenolol and Bisoprolol
Avoid higher doses and use with caution in patients with COPD/Asthma due to risk of bronchospasm Avoid in patients with a history of frequent hypoglycaemia Do not combine with Rate Limiting Ca2+ Channel Blockers in anti-hypertensive therapy due to risk of heart block
58
Describe important pieces of patient information that should be given with Cardioselective Beta Blockers such as Atenolol and Bisoprolol
Compliance is important as patients may stop the drug as they don't feel physically better - but should be reminded that HTN is asymptomatic but dangerous and needs to be controlled Fatigue and cold extremities are common side effects
59
Give examples of Non-Cardioselective Beta Blockers
Propranolol Carvedilol
60
Describe the MOA of Non-Cardioselective Beta Blockers such as Propranolol and Carvedilol
Propranolol - Non-Cardioselective Beta-1-Adrenoceptor Agonist Carvedilol - Non-Selective Beta-1, Beta-2 and Alpha-1-Adrenergic Receptor Antagonistic Effects Inhibits sympathetic activity in the heart and vascular smooth muscle
61
State indications for Non-Cardioselective Beta Blockers such as Propranolol and Carvedilol
Hypertension Anxiety Angina Migraine Prophylaxis Post-MI Prophylaxis (Carvedilol may be used as supportive therapy for mild-moderate heart failure)
62
State side effects of Non-Cardioselective Beta Blockers such as Propranolol and Carvedilol
Bradycardia Hypotension Bronchospasm Fatigue Cold Extremities Sleep Disturbances Loss of Hypoglycaemic Awareness
63
Describe important pharmacodynamic/pharmacokinetic features of Non-Cardioselective Beta Blockers such as Propranolol and Carvedilol
Caution in diabetic patients due to risk of deranged carbohydrate metabolism Avoid in patients with Asthma/COPD due to risk of bronchospasm Do not combine with Rate Limiting Ca2+ Channel Blockers (Verapamil/Diltiazem) in anti-hypertensive therapy Propranolol is lipid-soluble and predominantly cleared by the liver, therefore, should be avoided in liver impairment and abrupt withdrawal should be avoided due to risk of liver impairment
64
Describe important pieces of patient information that should be given with Non-Cardioselective Beta Blockers such as Propranolol and Carvedilol
Nightmares and sleep disturbances may occur Compliance is important as patients may stop drugs if they do not feel a physical benefit but should be reminded that HTN is asymptomatic but dangerous and needs to be controlled Fatigue and cold extremities are common side effects
65
Give examples of ACE Inhibitors
Ramipril Enalapril Lisinopril Perindopril
66
Describe the MOA of ACE Inhibitors
Inhibits conversion of AngI to AngII (a potent vasoconstrictor) This subsequently inhibits aldosterone release from the adrenal cortex, depressing renal sodium and fluid retention to decrease blood volume
67
State indications of ACE Inhibitors
Hypertension Heart Failure Nephropathy Prevention of CV Events in High Risk Patients
68
State side effects of ACE Inhibitors
Dry Cough Hypotension Hyperkalaemia Renal Impairment Angiodema
69
Describe important pharmacodynamic/pharmacokinetic features of ACE Inhibitors
Adverse drug reactions are higher in patients with: High Dose Diuretics Hypovolaemia Hyponatraemia Hypotension Unstable Heart Failure Renovascular Disease
70
Describe important pieces of information that should be given with ACE Inhibitors
Blood test require at 1-2 weeks to check electrolyte balance Dry cough is a common (10%) side effect
71
Give examples of Nitrates
Isosorbide Mononitrate Glyceryl Trinitrate (GTN)
72
Describe the MOA of Nitrates
Converted to Nitric Oxide (NO), a potent vasodilator Cardioselective, acting mainly on coronary blood vessels to enhance blood flow to ischaemic areas of the myocardium Also reduces myocardial oxygen demand by reducing cardiac afterload and preload
73
State indications for Nitrates
Treatment of Angina Severe HTN (IV GTN may be used)
74
State side effects of Nitrates
Headaches Postural Hypotension Dizziness Tachycardia
75
Describe important pharmacodynamic/pharmacokinetic features of Nitrates
Tolerance develops with long-term use In order to avoid tolerance, patients should have a daily nitrate-free period Isosorbide Mononitrate: Oral, Longer Duration of Action than GTN GTN: Rapidly inactivated by first pass metabolism, Sublingual Spray/Tablet only or IV
76
Describe important pieces of patient information that should be given with Nitrates
Headache is a common initial side effect but incidence decreases with long term use GTN should be taken before activity that brings on angina
77
Give two examples of Rate Limiting Calcium Channel Blockers
Verapamil Diltiazem
78
Describe the MOA of Rate Limiting Calcium Channel Blockers
Prevent cellular entry of Ca2+ by blocking L-type calcium channels Myocardial and Smooth muscle contractility is depressed Cardiac contractility will be reduced Dilate coronary blood vessels and reduce afterload Antidysrhythmic actions due to prolonged atrioventricular node conduction – depresses heart rate
79
State indications for Rate Limiting Calcium Channel Blockers
Supraventricular Arrhythmias Angina Hypertension
80
State side effects of Rate Limiting Calcium Channel Blockers
Verapamil - Constipation, Flushing, Headache, Dizziness, Hypotension Diltiazem - GI Disturbances, Bradycardia, Peripheral Oedema, Dizziness, Headache, Hypotension
81
Describe important pharmacodynamic/pharmacokinetic features of Rate Limiting Calcium Channel Blockers
Contra-indicated in heart failure and LV dysfunction due to potent negative inotropy Avoid in bradycardia and hypotension Do not use with beta-blockers
82
Describe important pieces of patient information that should be given with Rate Limiting Calcium Channel Blockers
Constipation is a common side effect with **Verapamil** Ankle swelling is a common side effect with **Diltiazem**, hot weather making it worse Compliance is important – Patients may stop Calcium-channel blockers if they do not feel any better Remind them that hypertension is asymptomatic but nonetheless a dangerous risk factor that needs controlled
83
Give examples of Non-Rate Limiting Calcium Channel Blockers
Amlodipine Nifedipine Felodipine
84
Describe the MOA of Non-Rate Limiting Calcium Channel Blockers
Prevent cellular entry of Ca2+ by blocking L-type calcium channels Myocardial and smooth muscle contractility depressed – these drugs mainly affect smooth muscle Dilate coronary blood vessels and reduce afterload These drugs do not lower heart rate (heart rate may increase)
85
State indications for Non-Rate Limiting Calcium Channel Blockers
Hypertension Angina
86
State side effects of Non-Rate Limiting Calcium Channel Blockers
Ankle Oedema Nausea Abdominal Pain Palpitations Headaches Dizziness Flushing
87
Describe important pharmacodynamic/pharmacokinetic features of Non-Rate Limiting Calcium Channel Blockers
Avoid in: Cardiogenic Shock, Unstable Angina, Significant Aortic Stenosis
88
Describe important pieces of patient information that should be given with Non-Rate Limiting Calcium Channel Blockers
Compliance is important – Patients may stop Calcium Channel Blockers if they do not feel any better Remind them that hypertension is asymptomatic but nonetheless a dangerous risk factor that needs controlled Ankle swelling is a common side effect, hot weather making it worse
89
Give examples of HMG CoA-Reductase Inhibitors
Atorvastatin Simvastatin Pravastatin
90
Describe the MOA of HMG CoA-Reductase Inhibitors
Competitively inhibits HMG CoA Reductase; the rate-determining enzyme in the mevalonate pathway synthesis of cholesterol This causes an increase in LDL-receptor expression, on the surface of hepatocytes Increases hepatic uptake of cholesterol, reducing plasma cholesterol levels Reduces development of athersclerotic plaques Statins may have additional pleotropic effects
91
State indications for HMG CoA-Reductase Inhibitors
Familial Hypercholesterolaemia Prevention of CV Events in High-Risk Patients
92
State side effects of HMG CoA-Reductase Inhibitors
Myalgia Myopathy and Rhabdomyolysis GI Disturbances LFT Derangement
93
Describe important pharmacodynamic/pharmacokinetic features of HMG CoA-Reductase Inhibitors
Myalgia and Rhabdomyolysis are dose-related, so begin with a low dose especially in patients with previous side effects Hypothyroidism should be corrected before assessing need for Statin use
94
Describe important pieces of patient information that should be given with HMG CoA-Reductase Inhibitors
Report any unexplained muscle pains to their GP, who will check a creatine kinase blood level Diarrhoea and abdominal pain may be present initially
95
To which class of drug does Digoxin belong?
Cardiac Glycosides
96
Describe the MOA of Digoxin
Increases vagal parasympathetic activity and inhibits the Na+/K+ pump, causing a buildup of Na+ intracellularly In an effort to remove Na+, more Ca2+ is brought into the cell by the action of Na+/Ca2+ exchangers The buildup of Ca2+ is responsible for the increased force of contraction and reduced rate of conduction through the AV node
97
State indications for Digoxin
Heart Failure Rate Control in AF
98
Describe side effects of Digoxin
Nausea Vomiting Diarrhoea Confusion
99
Describe important pharmacodynamic/pharmacokinetic features of Digoxin
Digoxin has a narrow therapeutic index Symptoms of digoxin toxicity are similar to effects of clinical deterioration Additionally, the plasma-concentration is not a reliable indicator of toxicity Digoxin-specific antibody fragments are used for life-threatening digoxin overdose Digoxin has a long half-life and maintenance doses may only be required once-daily Renal function, age and heart disease are major determinants for safe digoxin dosage
100
Describe important pieces of patient information that should be given with Digoxin
Risk of Toxicity
101
State the class of drug to which Amiodarone belongs
Anti-Arrhythmics
102
Describe the MOA of Amiodarone
Amiodarone blocks cardiac K+ channels, prolonging repolarization of the cardiac action potential to restore regular sinus rhythm It also slows atrioventricular nodal conduction
103
State indications for Amiodarone
Supraventricular/Ventricular Arrhythmias
104
State side effects of Amiodarone
Photosensitivity Skin Reactions Hypersensitivity Reactions Hyper/Hypothyroidism Pulmonary Fibrosis Corneal Deposits Neurological Disturbances GI Disturbances/Hepatitis
105
Describe important pharmacodynamic/pharmacokinetic features of Amiodarone
Very long half-life, once daily dosing, can take weeks-months to achieve steady-state amiodarone-plasma concentrations Thyroid function tests should be performed before treatment and every six months, or where symptomatic LFTs should be taken during treatment
106
Describe important pieces of patient information that should be given with Amiodarone
Requires good compliance and attendance for monitoring blood tests Avoid exposure to the sun, wear protective clothing and sunscreen Report presence of rash after use (hypersensitivity risk)
107
Give examples of drugs in the Penicillins class
Flucloxacillin Amoxicillin Benzylpenicillin Penicillin V
108
Describe the MOA of Penicillins
Attaches to penicillin-binding-proteins on forming bacterial cell walls This inhibits the transpeptidase enzyme which cross-links the bacterial cell wall Failure to cross-link induces bacterial cell autolysis Amoxicillin provides some amount of gram-negative cover in addition to gram-positive
109
State indications for Penicillins
Different drugs in the class have different indications due to having different spectrums of cover Flucloxacillin provides *Staph. Aureus* cover whereas Amoxicillin does not Flucloxacillin: Soft Tissue Infection, Staphylococcal Endocarditis, Otitis Externa Amoxicillin: Non-Severe CAP
110
State side effects of Penicillins
Diarrhoea Vomiting Impaired Liver Function Hypersensitivity Reaction
111
Describe important pharmacodynamic/pharmacokinetic features of Penicillins
Good Oral Absorption Flucloxacillin: Beta-Lactamase Stable/Insensitive Amoxicillin: Beta-Lactamase Susceptible (often combined with Claculinic Acid, a beta-lactamase inhibitor)
112
Describe important pieces of patient information that should be given with Penicillins
Return if symptoms persist after the course of antibiotics, may be infected with resistant organism Diarrhoea is a common side effect Report any incidence of a rash after use – risk of hypersensitivity reactions To overcome resistance in bacteria that secrete Beta-lactamase, a Beta-lactamase inhibitor is given with the penicillin. An example is Clavulonic Acid, when combined with amoxicillin, it forms co-amoxiclav.
113
Give two example of Cephalosporin antibiotics
Ceftriaxone Cephalexin
114
Describe the MOA of Cephalosporins
Attaches to penicillin-binding-proteins on forming bacterial cell walls This inhibits the transpeptidase enzyme which cross-links the bacterial cell wall Failure to cross-link induces bacterial cell autolysis Less susceptible to beta-lactamases than penicillins Both Gram +ve and -ve Cover
115
State indications for Cephalosporins
Serious Infection: Septicaemia, Pneumonia, Meningitis
116
State side effects of Cephalosporins
Hypersensitivity Reactions Antibiotics Associated C. Diff Impaired Liver Function
117
Describe important pharmacodynamic/pharmacokinetic features of Cephalosporins
Renal Excretion Longer Half-Life, Needs to be given once daily
118
Describe important pieces of patient information that should be given with Cephalosporins
Diarrhoea is a common side effect Report any incidence of a rash after use – risk of hypersensitivity reactions
119
To which class of drug does Vancomycin belong?
Glycopeptide Antibiotic
120
Describe the MOA of Vancomycin
Bactericidal, inhibiting cell-wall synthesis in Gram +ve bacteria
121
State indications for Vancomycin
Severe Gram +ve Infections MRSA Severe C. Diff
122
State side effects of Vancomycin
Fever Rash Local Phlebitis at Injection Site Nephrotoxicity Ototoxicity Blood Disorders, inc. Neutropenia Anaphylactoid Reaction (Red Many Syndrome is Infusion Rate Too Fast)
123
Describe important pharmacodynamic/pharmacokinetic features of Vancomycin
Can either be given as a continuous intravenous infusion or as a pulsed infusion regimen Long duration of action, can be given every 12 hours Therapeutic drug-monitoring should be undertaken as Vancomycin has a narrow therapeutic range
124
Describe important pieces of patient information that should be given with Vancomycin
Risk of kidney damage Patients should report any changes in hearing Regular blood tests required for monitoring
125
State the class of drug to which Gentamicin belongs
Aminoglycosides
126
Describe the MOA of Gentamicin
Binds to 30s ribosomal subunit, inhibiting protein synthesis, inducing a prolonged post-antibiotic bacteriostatic effect Additionally, bactericidal action on bacterial cell wall results in rapid killing early in dosing interval and is prominent at high doses Also provides a synergistic effect when used alongside other antibiotics (such as flucloxacillin or vancomycin in gram-positive infections)
127
State indications for Gentamicin
Severe Gram -ve Infection (e.g. Biliary Tract Infection, Pyelonephritis, Hospital Acquired Pneumonia) Some Gram +ve Infections (e.g. Soft Tissue Infection and Endocarditis)
128
State side effects of Gentamicin
Nephrotoxicity Ototoxicity
129
Describe important pharmacodynamic/pharmacokinetic features of Gentamicin
Give high initial dose to take advantage of rapid killing Leave long dosing interval to minimise toxicity Measure trough level to ensure gentamicin is not accumulating and only prescribe further doses once this is confirmed Try to limit use to approximately 3 days to minimise risk of side-effects
130
Describe important pieces of patient information that should be given with Gentamicin
Ask patients to report any change to their hearing Risk of kidney damage so monitoring of drug levels and renal function tests are required
131
State the class of drug to which Ciprofloxacin belongs
Quinolone
132
Describe the MOA of Ciprofloxacin
Interferes with bacterial DNA replication and repair Broad spectrum bactericidal antibiotic, provides both Gram +ve and -ve cover
133
State indications for Ciprofloxacin
Gram -ve Bacterial Infection Respiratory Tract Infection Upper UTI Peritoneal Infection Gonorrhoea Prostatitis
134
State side effects of Ciprofloxacin
GI Toxicity QT Segment Prolongation C. Diff Infection Tendonitis
135
Describe important pieces of patient information that should be given with Ciprofloxacin
Risk of diarrhoea after use
136
Give two examples of Macrolide antibiotics
Clarithromycin Erythromycin
137
Describe the MOA of Macrolide antibiotics
Binds to 50s ribosomal subunit Inhibits bacterial protein synthesis
138
State indications for Macrolide antibiotics
Atypical Organisms Causing Pneumonia Severe CAP Severe Campylobacter Infection Mild-Moderate Skin and Soft Tissue Infection Otitis Media Lyme Disease H.Pylori Eradication Therapy
139
State side effects of Macrolide antibiotics
Diarrhoea Vomiting QT Segment Prolongation Ototoxicity
140
Describe important pharmacodynamic/pharmacokinetic features of Macrolide antibiotics
Uses hepatic enzyme Cytochrome P450 pathway Can interact with all drugs using this pathway, especially Simvastatin, Atorvastatin and Warfarin
141
Describe important pieces of patient information that should be given with Macrolide antibiotics
Risk of Diarrhoea Senses of smell and taste may be disturbed during therapy Tooth and tongue discolouration may occur during therapy
142
State the class of drug to which Trimethoprim belongs
Inhibitor of Folate Synthesis
143
Describe the MOA of Trimethoprim
Inhibits folate metabolism pathway and leads to impaired nucleotide synthesis Therefore interferes with bacterial DNA replication
144
State indications for Trimethoprim
1st Line Antibiotic in Uncomplicated UTI Acute/Chronic Bronchitis Pneumocystis Pneumonia Good Range of Gram +ve and -ve Cover Some MRSA Cover
145
State side effects of Trimethoprim
Elevated Serum Creatinine Hyperkalaemia Depressed Haematopoiesis Rash GI Disturbance
146
Describe important pharmacodynamic/pharmacokinetic features of Trimethoprim
Penetrates well into the prostate, suitable for men with uncomplicated UTI Avoid in the first trimester of pregnancy Resistant organisms are a major problem in clinical use Hyperkalaemia is more common in patients with impaired renal function
147
Describe important pieces of patient information that should be given with Trimethoprim
Blood tests required in those at risk of hyperkalaemia Return to the doctor if symptoms do not clear after trimethoprim course, resistance does occur Rash and GI disturbances are common adverse reactions
148
State the class of drug to which Aciclovir belongs
Anti-Virals
149
Describe the MOA of Aciclovir
A guanosine derivative converted to triphosphate by infected host cells Aciclovir triphosphate then inhibits DNA polymerase, terminating the nucleotide chain and inhibiting viral DNA replication
150
State indications for Aciclovir
Herpes SImplex Infection Varicella Zoster Infection
151
State side effects of Aciclovir
Nausea Vomiting Local Inflammation at Infusion Site (IV Only)
152
Describe important pharmacodynamic/pharmacokinetic features of Aciclovir
Can be given orally, intravenously or topically Penetrates well into the CSF with CSF concentrations being 50% concentration of that of plasma Excreted by the kidneys so dose adjustment is needed in renal impairment
153
Describe important pieces of patient information that should be given Aciclovir
Multiple/repeat doses may be required in immunosuppressed patients Type of infection or recurrent infections may prompt HIV infection
154
State the class of drug to which Salbutamol belongs
Beta-Adrenergic Bronchodilators | (Short-Acting)
155
Describe the MOA of Salbutamol
Short-acting Beta-2 adrenoceptor agonists (SABA) Relaxes bronchial smooth muscle, inducing bronchodilation Inhibit pro-inflammatory cytokine release from mast cells and TNF-α release from monocytes, reducing airway inflammation Increase mucus clearance from the airways by stimulating cilia action
156
State indications for Salbutamol
Asthma COPD
157
State side effects of Salbutamol
Tremor Tachycardia Cardiac Dysrhythmia Headache Sleep Disturbance
158
Describe important pharmacodynamic/pharmacokinetic features of Salbutamol
Only a small percentage of inhaled drug reaches target in the airways (a spacer may improve delivery)
159
Describe important pieces of patient information that should be given with Salbutamol
Check inhaler technique, review the need for spacer / nebuliser In exercise-induced-asthma, a dose immediately before exercise can reduce incidence of symptoms If required more than once daily, treatment needs reviewed
160
State the class of drug to which Salmeterol belongs
Beta-Adrenergic Bronchodilators | (Long-Acting)
161
Describe the MOA of Salmeterol
Long-acting Beta-2 adrenoceptor agonist (LABA) Relaxes bronchial smooth muscle, inducing bronchodilation Inhibit pro-inflammatory cytokine release from mast cells and TNF-α release from monocytes, reducing airway inflammation Increase mucus clearance from the airways by stimulating cilia action
162
State indications for Salmeterol
Asthma COPD
163
State side effects of Salmeterol
Tremor Tachycardia Cardiac Dysrhythmia Headache Sleep Disturbance
164
Describe important pharmacodynamic/pharmacokinetic features of features of Salmeterol
Not to be commenced in patients with rapidly deteriorating asthma due to slower onset of action than SABAs
165
Describe important pieces of patient information that should be given with Salmeterol
Report any deterioration in symptoms following initiation of LABA Do not exceed stated dose Seek medical advice when stated dose fails to control symptoms
166
Give two examples of Anti-Muscarinic Bronchodilators
Tiotropium Ipratropium Bromide
167
Describe the MOA of Anti-Muscarinic Bronchodilators
Muscarinic receptor (M3) antagonists producing bronchodilatory effects Reduces mucus secretion and may increase bronchial mucus clearance by stimulating cilia
168
State indications for Anti-Muscarinic Bronchodilators
Asthma COPD Rhinitis
169
State side effects of Anti-Muscarinic Bronchodilators
Dry Mouth Cough Constipation
170
Describe important pharmacodynamic/pharmacokinetic features of Anti-Muscarinic Bronchodilators
Inhaled and poorly absorbed into the circulation – unable to affect systemic muscarinic/cholinergic receptors Nebulised Ipratropium Bromide should always be administered via a mouthpiece to minimize the risk of acute angle closure glaucoma
171
Describe important pieces of patient information that should be given with Anti-Muscarinic Bronchodilators
Good inhaler technique improves efficacy Cough may arise
172
State the class of drug to which Beclomethasone belongs
Inhaled Corticosteroids
173
Describe the MOA of Beclomethasone
Anti-inflammatory effect on the airways Decreases formation of pro-inflammatory cytokines Up-regulates Beta-2 Adrenoceptor in airways
174
State indications for Beclomethasone
Asthma COPD
175
State side effects of Beclomethasone
Oral Candidiasis (Thrush) Adrenal Suppression Osteoporosis
176
Describe important pharmacodynamic/pharmacokinetic features of Beclomethasone
Takes several weeks to months for full effect of therapy Spacer devices can reduce risk of thrush and improve drug delivery
177
Describe important pieces of patient information that should be given with Beclomethasone
If on higher doses, should carry a steroid card Increase dose during periods of illness
178
Give example of Anti-Histamine (H1 Receptor Antagonist) drugs
Chlorpheniramine Desloratidine Fexofenadine Hydroxyzine
179
Describe the MOA of Anti-Histamines
H1 Receptor Antagonists Inhibit histamine-mediated contraction and vasodilation of the bronchial smooth muscle
180
State indications for Anti-Histamines
Anaphylaxis Hay Fever Urticaria Sedation
181
State side effects of Anti-Histamines
Drowsiness Tinnitus
182
Describe important pharmacodynamic/pharmacokinetic features of Anti-Histamines
Renally excreted Sedation arises from CNS H1 antagonism (second generation H1 antagonists do not cross BBB in therapeutic doses)
183
Describe important pieces of patient information that should be given with Anti-Histamines
Do not operate heavy machinery Do not drive
184
Describe the MOA of Levodopa
Pro-drug (dopamine precursor) Crosses the BBB and is converted to dopamine Striatal dopaminergic neurotransmission is increased
185
State the indications for Levodopa
Parkinson's Disease
186
State side effects of Levodopa
Dyskinesia Compulsive Disorders Hallucinations Nausea GI Upset
187
Describe important pharmacodynamic/pharmacokinetic features of Levodopa
Converted to dopamine in the peripheries (which can cause motor side effects) Given with a dopamine decarboxylase inhibitor or COMT inhibitor to reduce these effects Short half-life of 50 to 90 minutes Rapidly absorbed from the proximal small intestine via the large neutral amino acid (LNAA) transport carrier system
188
Describe important pieces of patient information that should be given with Levodopa
Dyskinesia is common Reduced efficacy over time Avoid abrupt withdrawal
189
Give examples of Dopamine Agonists
Apomorphine Pramipexole Bromocriptine Pergolide Rotigotine
190
Describe the MOA of Dopamine Agonists
Stimulate post-synaptic dopamine receptors Apomorphine: Non-Selective D1 and D2 Dopamine subfamily of receptors Pramipexole: Selective D3 Receptor
191
State indications for Dopamine Agonists
Parkinson's Disease
192
State side effects of Dopamine Agonists
Apomorphine: Pain at Injection Site, Nausea and Vomiting Pramipexole: Hallucinations, Nausea, Drowsiness, Involuntary Movements
193
Describe important pharmacodynamic/pharmacokinetic features of Dopamine Agonists
Have reduced efficacy over time Apomorphine: Highly emetic (hence limited use), short half-life (40mins), must be given by injection Pramipexole: Cimetidine increases its toxicity, long half-life (8hrs)
194
Describe important pieces of patient information that should be given with Dopamine Agonists
Apomorphine can only be injected Dopamine Agonists are weaker than L-Dopa so treatment may need to be modified in time
195
State the class of drug to which Entacapone belongs
Catechol-o-methyl Transferase (COMT) Inhibitor
196
Describe the MOA of Entacapone
Prevents peripheral breakdown of levodopa by inhibiting COMT (COMT converts L-Dopa into 3-OMD which does not cross the BBB) Therefore, more levodopa reaches the brain
197
State indications for Entacapone
Parkinson's Disease In conjuncion with L-Dopa and Dopamine Decarboxylase Inhibitors
198
State side effects of Entacapone
Dyskinesia Nausea Abdominal Pain Vomiting Dry Mouth Dizziness
199
Describe important pharmacodynamic/pharmacokinetic features of Entacapone
Rapidly absorbed L-Dopa dose may need to be reduced by 10-30% when given with Entacapone
200
Describe important pieces of patient information that should be given with Entacapone
Urine may turn brown, this is normal Could become lightheaded/dizzy while doing daily activities Avoid abrupt withdrawal
201
State the class of drug to which Carbamazepine belongs
Anti-Epileptic
202
Describe the MOA of Carbamazepine
Voltage-gated Na+ channel blocker on the pre-synaptic membrane Blocks the Na+ influx, reduces neuronal excitability and decreases the action potential
203
State indications for Carbamazepine
Epilepsy Trigeminal Neuralgia Neuropathic Pain
204
State side effects of Carbamazepine
Dizziness Dry Mouth Ataxia Fatigue Headache Diplopia Blurred Vision Hyponatraemia Stevens-Johnson Syndrome (Rare)
205
Describe important pharmacodynamic/pharmacokinetic features of Carbamazepine
Response to the drug can be variable Enzyme inducer of cytochrome P450 (induces metabolism of itself) Interactions with other anti-convulsants A transporter (RALBP1) can confer drug resistance Grapefruit can significantly increase serum levels (bioavailability) of the drug HLA-B 1502 allele raises the risk for SJS, avoid in these patients
206
Describe important pieces of patient information that should be given with Carbamazepine
Avoid alcohol Avoid grapefruit
207
State the class of drug to which Sodium Valproate belongs
Anti-Epileptic
208
Describe the MOA of Sodium Valproate
Weak sodium ion channel blocker Inhibitor of GABA degrading enzymes Increased GABA stops action potential
209
State indications for Sodium Valproate
Epilepsy Bipolar Disorder Depression
210
State side effects of Sodium Valproate
Nausea Diarrhoea Gastric Irritation Weight Gain Hyponatraemia Behavioural Disturbance Confusion Stevens-Johnson Syndrome (Rare)
211
Describe important pharmacodynamic/pharmacokinetic features of Sodium Valproate
Enzyme inhibitor of cytochrome P450 Rapidly absorbed from GI tract - Varies with formulation administered (liquid, solid or powder) and when administered (post-prandial or fasting) Can cause interactions with other anti-epileptic drugs
212
Describe important pieces of patient information that should be given with Sodium Valproate
Avoid alcohol Take with food Do not take with milk LFTs must be monitored before and during the initial 6 months VERY teratogenic, should not be given to women of child-bearing potential unless other options have been exhausted and effective contraception must be used
213
State the class of drug to which Phenytoin belongs
Anti-Epileptics
214
Describe the MOA of Phenytoin
Acts as a voltage-gated Na+ channel blocker on the pre-synaptic neuronal membrane Limits action potential transmission Hence limits spread of seizure activity
215
State indications for Phenytoin
Epilepsy (incl. Status Epilepticus) Trigeminal Neuralgia
216
State side effects of Phenytoin
Insomnia Headache Rash Constipation Vomiting Gingival Hyperplasia Liver Damage Stevens-Johnson Syndrome Leucopenia Thrombocytopenia
217
Describe important pharmacodynamic/pharmacokinetic features of Phenytoin
Enzyme inducer of cytochrome P450 Can cause interactions with other anti-epileptic drugs Narrow therapeutic index Relationship between dose and plasma concentration in non-linear
218
Describe important pieces of patient information that should be given with Phenytoin
Avoid alcohol Do not take calcium, aluminium, magnesium or iron supplements within 2 hours of ingestion Take with food to reduce irritation
219
State the class of drug to which Lamotrigine belongs
Anti-Epileptic
220
Describe the MOA of Lamotrigine
Varied MOA Inhibits voltage-gated Na+ channels and/or Ca2+ channels Acts on pre-synaptic neuronal membrane Reduces action potential and excitatory signals
221
State indications for Lamotrigine
Epilepsy (Focal and Generalised Seizures) Depressive Disorders associated with Bipolar Disorder
222
State side effects of Lamotrigine
Nausea Vomiting Diarrhoea Tremor Insomnia Blurred Vision Aggression Skin Reactions (incl. Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis)
223
Describe important pharmacodynamic/pharmacokinetic features of Lamotrigine
Half-life doubles in chronic renal impairment so dose adjustment is required
224
Describe important pieces of patient information that should be given with Lamotrigine
Take without regard to meals Seeks medical advice if any rash or signs/symptoms of hypersensitivity
225
State the class of drug to which Levetiracetam
Anti-Epileptic
226
Describe the MOA of Levetiracetam
SV2A is a synaptic vesicle protein required for neurotransmitter release Levetiracetam blocks this and reduces neurotransmitter release Induces an anti-epileptic effect
227
State indications for Levetiracetam
Epilepsy
228
State side effects of Levetiracetam
Headache Fatigue Anxiety Irritability Drowsiness Constipation
229
Describe important pharmacodynamic/pharmacokinetic features of Levetiracetam
Rapidly and almost completely absorbed after oral administration (99%) Food does not affect bioavailability Cytochrome P450 is not involved in its metabolism
230
Describe important pieces of patient information that should be given with Levetiracetam
May affect ability to drive or operate machinery Not recommended during pregnancy or breast feeding
231
Give examples of Selective Serotonin Reuptake Inhibitors (SSRIs)
Citalopram Fluoxetine Paroxetine Escitalopram Sertraline
232
Describe the MOA of SSRIs
Inhibition of reuptake of serotonin at the serotonin reuptake pump of the synaptic cleft (in the CNS) Increases serotonin stimulation of somatodendritic 5-HT1A and terminal autoreceptors
233
State indications for SSRIs
Depression Bulimia Obsessive Compulsive Disorder
234
State side effects of SSRIs
Dry Mouth Nausea Insomnia Anxiety Decreased Libido Seizures Dyskinesia
235
Describe important pharmacodynamic/pharmacokinetic features of SSRIs
SSRIs bind with less affinity to histamine, acetylcholine and noradrenaline receptors than TCAs leading to fewer side effects Less dangerous in overdose than TCAs
236
Describe important pieces of patient information that should be given with SSRIs
Be wary with alcohol, toxicity is possible Improvement in depressive symptoms may take several weeks to occur Abrupt discontinuation of SSRIs may cause withdrawal symptoms (fatigue, tremor, sweating)
237
Give examples of Tricyclic Antidepressants (TCAs)
Amitriptyline Imipramine Doxepin
238
Describe the MOA of TCAs
Stops the reuptake of monoamines Binds to monoamine pump at pre-synaptic cleft The reduced reuptake of noradrenaline and/or serotonin combats depression
239
State indications for TCAs
Depression Panic Disorders Neuropathic Pain
240
State side effects of TCAs
Sedation (anti-histaminergic effects) Postural Hypotension, Tachycardia (anti-adrenergic effects) Urinary Retention, Dry Mouth, Blurred Vision, Diplopia (anti-cholinergic effects)
241
Describe important pharmacodynamic/pharmacokinetic features of TCAs
Blocks histamine H1 receptors, alpha1 adrenergic receptors and muscarinic receptors which accounts for their sedative, hypotensive and anti-cholinergic effects Well absorbed orally First pass effect from the liver
242
Describe important pieces of patient information that should be given with TCAs
Reduction in depressive symptoms may take several weeks to appear TCA overdose can be serious and cause seizures and cardiac arrythmias
243
Give examples of Anti-Psychotic drugs
1st Generation (Act non-selectively on D1-like and D2-like receptors): Haloperidol or Chlorpromazine Atypical (Varying effects on dopamine and serotonin receptors): Olanzapine or Clozapine
244
Describe the MOA of Anti-Psychotics
Block dopamine receptors Action on mesolimbic and nigrostriatal parts of brain Also have anti-histaminergic and anti-cholinergic effects These effects reduce positive symptoms of schizophrenia and can cause sedation and provide anti-emetic activity
245
State indications for Anti-Psychotics
Schizophrenia Mania Delusions Hallucinations Behavioural Problems Anti-Emetic (Haloperidol)
246
State side effects of Anti-Psychotics
Sedation (anti-histaminergic effect) Postural Hypotension, Tachycardia (anti-adrenergic effect) Urinary Retention, Dry Mouth, Blurry Vision (anti-cholinergic effect)
247
Describe important pharmacodynamic/pharmacokinetic features of Anti-Psychotics
Has effects on numerous receptor symptoms within the CNS
248
Describe important pieces of patient information that should be given with Anti-Psychotics
Symptoms may not always disappear while on medication Dosage may have to be increased if no improvement is made after a few weeks
249
Give examples of Benzodiazepines
Diazepam Lorazepam Midazolam
250
Describe the MOA of Benzodiazepines
Increases GABA affinity for GABA receptor GABA binding to receptor increases chloride flow through chloride channels Hyperpolarisation occurs - reducing activity of limbic, thalamic and hypothalamic areas of the brain
251
State indications for Benzodiazepines
Anxiety Epilepsy Muscle Spasm Alcohol Withdrawal
252
State side effects of Benzodiazepines
Sedation Ataxia Altered Mental State Insomnia
253
Describe important pharmacodynamic/pharmacokinetic features of Benzodiazepines
**Diazepam** is a long-acting benzo with active metabolites so can accumulate in long-term use and in patients with liver failure. It can be given orally, rectally or parenterally **Lorazepam** accumulates less with long-term use or in patients with liver failure so is preferred in this setting. It cannot be given rectally **Midazolam** is a potent and short-acting benzo typically given parenterally although buccal preparations exist
254
Describe important pieces of patient information that should be given with Benzodiazepines
Monitor breathing and report if severe breathlessness or palpitations Only prescribed for short terms due to risk of addiction
255
Give examples (three each) of oral, topical and parenteral glucocorticoids
Oral - Prednisolone, Hydrocortisone, Dexamethasone Topical - Hydrocortisone, Betamethasone, Clobetasone Parenteral - Methylprednisolone, Hydrocortisone, Triamcinolone
256
Describe the MOA of glucocorticoids
Bind to glucocorticoid receptors Causes up-regulation of a variety of anti-inflammatory mediators and down-regulation of pro-inflammatory mediators Provides immunosuppression Also have metabolic effects including increasing gluconeogenesis and some may have a little mineralocorticoid activity
257
State indications for glucocorticoids
Replacement in Adrenal Insufficiency Post-Transplant Immunosuppression Treatment of Exacerbation of Various Inflammatory Conditions (incl. Eczema, RA, IBD and MS) Treatment of Acute Exacerbation of Asthma
258
State side effects of glucocorticoids
Sleep Disturbance Mood Disturbance/Psychosis Hyperglycaemia Immunodeficiency Easy Bruising Moon-Faced Increased Abdominal Fat Glaucoma Striae Hypertension Gastric Irritation
259
Describe important pharmacodynamic/pharmacokinetic features of glucocorticoids
Variety of different preparations are available Drugs have differing degrees of glucocorticoid and mineralocorticoid activity
260
Describe important pieces of patient information that should be given with glucocorticoids
Avoid Alcohol and Caffeine Take with food to avoid gastric irritation Don't stop abruptly Allway tell doctor if on prednisolone Carry steroid card Take a higher dose when ill
261
State the relative glucocorticoid/mineralocorticoid activity of Prednisolone, Betamethasone, Hydrocortisone, Dexamethasone and Fludrocortisone
Prednisolone: Predominantly G, Low M Betamethasone: Potent G, No M Hydrocortisone: Good G and M Dexamethasone: Potent G, Minimal or No M Fludrocortisone: Mild-Moderate G, Potent M
262
Give three examples of Anti-TNF Agents
Etanercept (Receptor Fusion Protein) Infliximab (Monoclonal Antibody) Adalimumab (Monoclonal Antibody)
263
Describe the MOA of Anti-TNF Agents
Anti-TNF-Alpha and Anti-TNF-Beta Blocks its interactions with TNF cell receptors TNF Alpha and Beta are produced by macrophages and T-Cells TNF stimulates cytokines including IL-1, 6 and 8 Therefore they reduce inflammation
264
State indications for Anti-TNF Agents
Rheumatoid Arthritis Psoriatic Arthritis Ankylosing Spondylitis Juvenile Arthritis
265
State side effects of Anti-TNF Agents
Injection Site Reactions Flu-Like Symptoms (Fever, Headache, Runny Nose) Immune Deficiency (Particular risk of Legionella and Listeria and reactivation of TB)
266
Describe important pharmacodynamic/pharmacokinetic features of Anti-TNF Agents
Given parenterally by subcutaneous injection
267
Describe important pieces of patient information that should be given with Anti-TNF Agents
Maintain good hygiene and report symptoms of infection early
268
Give examples of Immunosuppressant drugs
Methotrexate Azathioprine Mercaptopurine
269
Describe the MOA of immunosuppressants
Disrupt DNA synthesis Azathioprine: Blocks purine synthesis mainly in lymphocytes Methotrexate: Stops the action of the enzyme dihydrofolate needed for production of DNA
270
State indications for immunosuppressant drugs
Post Transplantation Immunosuppression Inflammatory Bowel Disease Renal Vasculitis Paediatric Leukaemia (Methotrexate)
271
State side effects of immunosuppressant drugs
Bone Marrow Suppression (Leucopenia) Risk of Infection Nephrotoxicity Hepatotoxicity Seizures GI Upset Mucosal Ulceration Alopecia
272
Describe important pharmacodynamic/pharmacokinetic features of immunosuppressant drugs
Does not cross the BBB Undergo hepatic metabolism Oral absorption is dose-dependent Patients with low levels of thiopurine methyltransferase activity are more prone to azathioprine and mercaptopurine related marrow suppression
273
Describe important pieces of patient information that should be given with immunosuppressant drugs
Limit caffeine intake Take without regard to meals
274
Give examples of Proton Pump Inhibitors
Omeprazole Lansoprazole Pantoprazole
275
Describe the MOA of PPIs
Bind to H/K ATPase pump on gastric parietal cells Reduces HCl production and hence reduces gastric acidity
276
State indications for PPIs
Peptic Ulcers Gastro-Oesophageal Reflux Disease H. Pylori Infection Prophylaxis in Patiens Receiving Long Term NSAIDs
277
State side effects of PPIs
Nausea Vomiting Insomnia Vertigo Headaches
278
Describe important pharmacodynamic/pharmacokinetic features of PPIs
Omeprazole is an inhibitor of cytochrome P450 enzymes
279
Describe important pieces of patient information that should be given with PPIs
Avoid alcohol Take 30-60 minutes before food
280
Give examples of H2 receptor antagonists
Ranitidine Cimetidine Famotidine Nizatidine
281
Describe the MOA of H2 receptor antagonists
Histamine binds to H2 receptors on gastric parietal cells stimulating gastric acid secretion Drugs antagonise the effect of histamine at these H2 receptors Reduced cAMP and hence reduced activity of H/K ATPase pump
282
State indications for H2 receptor antagonists
Peptic Ulcer Gastro-Oesophagal Reflux Disease Zollinger-Ellison Syndrome
283
State side effects of H2 receptor antagonists
Headache Dizziness Diarrhoea Reduced B12 Absorption Gynaecomastia
284
Describe important pharmacodynamic/pharmacokinetic features of H2 receptor antagonists
Cimetidine is an inhibitor of cytochrome P450 enzymes
285
Describe important pieces of patient information that should be given with H2 receptor antagonists
Avoid a high protein diet Take without regard to meals
286
Give examples of Laxatives
Lactulose Senna
287
Describe the MOA of Laxatives
Bulk Producing Agent (e.g. Lactulose) - Reduces water reabsorption in the intestine, pulling water into the bowel and thus promotes distention and movement Stimulant/Irritant (e.g. Senna) - Acts on intestinal mucosa to alter water and electrolyte secretion Stool Softeners - Add more water and fat into the stool Hydrating Agents (e.g. Milk of Magnesia) - Intestines hold more water
288
State indications for Laxatives
Constipation Pregnancy Prophylaxis in Opiate Analgesic Use
289
State side effects of Laxatives
Dehydration Salt Loss Abdominal Cramps Fatigue
290
Describe important pharmacodynamic/pharmacokinetic features of Laxatives
Lactulose - Consists of the monosaccharides fructose and galactose. Breakdown of this in the intestine by colonic bacteria increases osmotic pressure Senna - Recommended for short-term use only due to risk of organ failure with long term use or abuse
291
Describe important pieces of patient information that should be given with Laxatives
Take liberally without regard to meals
292
To which class of drug does Cyclizine belong?
Anti-Emetic
293
Describe the MOA of Cyclizine
H1 Histamine Receptor Antagonist Acts on vomiting centre in the medullary region Mild anti-cholinergic and anti-muscarinic effects
294
State indications for Cyclizine
Nausea and Vomiting Motion Sickness Vertigo and Dizziness Prophylaxis alongisde chemotherapy and opiate analgesic use
295
State side effects of Cyclizine
Headache Sedation Diarrhoea
296
Describe important pharmacodynamic/pharmacokinetic features of Cyclizine
Can also be a central nervous system depressant
297
Describe important pieces of patient information that should be given with Cyclizine
Avoid alcohol Food may reduce irritation Take without regard to meals
298
To which class of drug does Metoclopramide belong?
Anti-Emetic
299
Describe the MOA of Metoclopramide
Dopamine D2 receptor antagonist Raises activity in the chemoreceptor trigger zone, reducing input from afferent visceral nerves Also increases gastric emptying and intestinal transit Reduces oesophageal reflux
300
State indications for Metoclopramide
Nausea Vomiting To increase gastric emptying
301
State side effects of Metoclopramide
Dystonia (due to dopamine antagonism) Confusion Dizziness Diarrhoea Parkinsonism with long-term use
302
Describe important pharmacodynamic/pharmacokinetic features of Metoclopramide
Can be given orally/parenterally Dystonic reactions and movement disorders are more common at the extremes of age so caution is needed in these groups
303
Describe important pieces of patient information that should be given with Metoclopramide
Avoid alcohol Take 30 minutes before food
304
To which class of drug does Prochlorperazine belong?
Anti-Emetic
305
Describe the MOA of Prochlorperazine
Penothiazine anti-psychotic drug that is also used as an anti-emetic Dopamine D2 receptor antagonist Causes increased dopamine turnover (in mesolimbic and chemoreceptor trigger zone)
306
State indications for Prochlorperazine
Nausea Vomiting Adjunct in some psychotic disorders
307
State side effects of Prochlorperazine
Dry mouth Tachycardia Restlessness Drowsiness
308
Describe important pharmacodynamic/pharmacokinetic features of Prochlorperazine
Anti-cholinergic and alpha-adrenergic receptors antagonism occurs leading to sedation, muscle relaxation and hypotension The dose differs substantially when given parenterally
309
Describe important pieces of patient information that should be given with Prochlorperazine
Avoid alcohol and caffeine Take with food and a full glass of water
310
Give examples of Thiazide Diuretics
Bendroflumethiazide Indapamide Chlortalidone
311
Describe the MOA of Thiazide Diuretics
Inhibit Na/Cl transporter at the distal convoluted tubule and collecting duct Increases Na/Cl and water excretion
312
State indications for Thiazide Diuretics
Hypertension Oedema of Cardiac/Renal/Hepatic/Iatrogenic Origin
313
State side effects of Thiazide Diuretics
Hypokalaemia Hypomagnesaemia Hyponatraemia Hypercalcaemia Hyperuricaemia Reduced Glucose Tolerance Hypersensitivity Reactions - Rashes, Pneumonitis
314
Describe important pharmacodynamic/pharmacokinetic features of Thiazide Diuretics
Produces diuresis quickly within 1-2 hours NSAIDs reduce efficacy of thiazide diuretics Urinary symptoms are less common with the lower dose used for the treatment of hypertension
315
Describe important pieces of patient information that should be given with Thiazide Diuretics
Urinary frequency usually not affected Report if sudden rash Make aware of risk of electrolyte imbalance
316
Give examples of Loop Diuretics
Furosemide Bumetanide Torasemide
317
Describe the MOA of Loop Diuretics
Na/Cl/K Symporter Antagonists Act on the thick ascending loop of henle Increase secretion of Na/K/Cl and water
318
State indications for Loop Diuretics
Hypertension Hyperkalaemia Heart Failure Cirrhosis of the Liver (Fluid Retention) Nephrotic Syndrome
319
State side effects of Loop Diuretics
Hypokalaemia hypovolaemia Hyperuricaemia Metabolic Acidosis Abdominal Pain Ototoxicity
320
Describe important pharmacodynamic/pharmacokinetic features of Loop Diuretics
60% absorbed in patients with normal renal function Renal and hepatic excretion - increased half-life for patients with renal or hepatic disease
321
Describe important pieces of patient information that should be given with Loop Diuretics
Avoid alcohol excess Urinary frequency increases
322
Describe the different insulin preparations available
Rapid Acting (e.g. Novorapid) - Reaches circulation within 15 minutes after injection, peaks 30 to 90 minutes later and lasts for up to 5 hours Short Acting - Reaches circulation 30 minutes after injection, peaks 2 to 4 hours later and lasts up to 4-8 hours Intermediate Acting - Reaches circulation in 2-6 hours and peaks 4-14 hours later and lasts for up to 20 hours Long Acting (e.g. Glargine) - Reaches circulation in 6 to 14 hours with a minimal peak and lasts for up to 24 hours
323
Describe the MOA of Insulin
Increases cellular uptake of glucose Stimulates glycogenesis, encourages DNA synthesis and promotes release of growth hormone
324
State indications for Insulin
Type 1 Diabetes Mellitus Type 2 Diabetes Mellitus Hyperkalemia (in conjunction with Dextrose)
325
State side effects of Insulin
Hypoglycaemia Sweats, Shakes, Tachycardia, Headache, Weakness, Fatigue (typically signs of hypoglycaemia) Oedema Injection Site Reactions
326
Describe important pharmacodynamic/pharmacokinetic features of Insulin
Patients are given varying types of insulin combinations based on their activities and preferences Given subcutaneously and short-acting (actrapid) can be given IV
327
Describe important pieces of patient information that should be given with Insulin
Only in the form of an injection Compliance is very important Never skip a meal when on insulin
328
Give two examples of Sulphonylureas
Gliclazide Glimepiride
329
Describe the MOA of Sulphonylureas
Stimulates beta cells of the pancreas to produce more insulin Increase cellular glucose uptake and glycogenesis while reducing gluconeogenesis
330
State indications for Sulphonylureas
Type 2 Diabetes Mellitus
331
State side effects of Sulphonylureas
Hypoglycaemia Rashes Nausea Vomiting Stomach Pain Indigestion Weight Gain
332
Describe important pharmacodynamic/pharmacokinetic features of Sulphonylureas
Renally excreted so accumulates in renal failure Gliclazide is short-acting (12 hours) Glimepiride is long-acting
333
Describe important pieces of patient information that should be given with Sulphonylureas
Compliance is important Maintain constant diet Avoid alcohol
334
To which class of drug does Metformin belong?
Biguanides
335
Describe the MOA of Metformin
Increases the activity of AMP-Dependent Protein Kinase (AMPK) This inhibits gluconeogenesis and reduces insulin resistance
336
State indications for Metformin
Type 2 Diabetes Mellitus Metabolic/Reproductive Abnormalities Associated with Polycystic Ovarian Syndrome
337
State side effects of Metformin
Diarrhoea Nausea Vomiting Taste Disturbance Lack of Appetite Risk of LActic Acidosis in Patients with Renal Failure
338
Describe important pharmacodynamic/pharmacokinetic features of Metformin
Not recommended in pregnancy Not recommended in renal failure if eGFR\<30 Absorption reduces when taken with food
339
Describe important pieces of patient information that should be given with Metformin
Take them at the same time everyday Avoid alcohol Does not increase weight
340
Give examples of GLP-1 Agonists
Exanatide Liraglutide (Glucagon Like Peptide)
341
Describe the MOA of GLP-1 Agonists
GLP-1 is a hormone that is released after meals to increase insulin secretion Therefore GLP-1 agonists increase insulin secretion while decreasing glucagon secretion and reducing hunger
342
State indications for GLP-1 Agonists
Type 2 Diabetes Mellitus + Excess Weight
343
State side effects of GLP-1 Agonists
Hypoglycaemia Nausea Vomiting Diarrhoea
344
Describe important pharmacodynamic/pharmacokinetic features of GLP-1 Agonists
It can lower glucose alone, but when given in conjunction with metformin, sulphonylureas and/or insulin it can improve glucose control Renally excreted so dos adjustment needed in renal failure
345
Describe important pieces of patient information that should be given with GLP-1 Agonists
Only given as injections Twice a day
346
To which class of drug does Levothyroxine belong?
Synthetic Thyroid Hormone
347
Describe the MOA of Levothyroxine
Thyroxine increases the metabolic rate of all tissues in the body Synthetically prepared levo-isomer of thyroxine Acts like T4 and gets converted to T3 in the liver and kidney Maintains brain function, food metabolism and body temperature among other effects
348
State indications for Levothyroxine
Hypothyroidism Chronic Lymphocytic Thyroiditis
349
State side effects of Levothyroxine
Chest Pain Coma Diarrhoea Tachycardia Itching Muscle Cramps (If dosing is correct, side effects are unusual)
350
Describe important pharmacodynamic/pharmacokinetic features of Levothyroxine
Primarily eliminated by the kidneys IV formulations available Long half-life (6-7 days) so thyroid function should be rechecked 6 weeks after a dose adjustment
351
Describe important pieces of patient information that should be given with Levothyroxine
Take 30-60 minutes before breakfast
352
Give examples of Anti-Thyroid Thionamides
Carbimazole Propylthiouracil
353
Describe the MOA of Anti-Thyroid Thionamides
Reduces activity of peroxidase enzyme (required for the production of thyroid hormones) May also reduce peripheral conversion of T4 to T3 Carbimazole is a pro-drug
354
State indications for Anti-Thyroid Thionamides
Hyperthyroidism Thyrotoxicosis Preparing Patients for Thyroid Surgery
355
State side effects of Anti-Thyroid Thionamides
Rash Agranulocytosis Sore Throat
356
Describe important pharmacodynamic/pharmacokinetic features of Anti-Thyroid Thionamides
Carbimazole is rapidly metabolised to thiamazole, meaning peak plasma concentration occurs after one hour It crosses the placenta and can be found in breast milk The effect of anti-thyroid drugs can take several weeks to occur so are usually prescribed alongside a beta blocker to reduce symptoms of hyperthyroidism
357
Describe important pieces of patient information that should be given with Anti-Thyroid Thionamides
Compliance is important Regular blood checks will be needed to monitor treatment response and renal and hepatic function and full blood counts
358
Give examples of Bisphosphonates
Alendronate (Alendronic Acid) Ibandronate Risedronate Zalendronate (Zalendronic Acid)
359
Describe the MOA of Bisphosphonates
Inhibits osteoclast bone resorption No effect on bone formation Little effect on bone density but large effect on fracture risk
360
State indications for Bisphosphonates
Osteoporosis Paget's Disease of the Bone
361
State side effects of Bisphosphonates
Abdominal Pain Dyspepsia Acid Regurgitation Dysphagia Headache Avascular Necrosis of the Jaw (Rare but important) Atypical Femoral Fracture (Rare but important)
362
Describe important pharmacodynamic/pharmacokinetic features of Bisphosphonates
Bioavailability reduces with breakfast (with coffee or orange juice)
363
Describe important pieces of patient information that should be given with Bisphosphonates
Avoid caffeine Administer 30 minutes before or after food or drink and remain upright for at least 30 minutes afterwards Most are given once weekly, some can be given daily and some by 6-monthly IV infusion
364
Give examples of the Oral Contraceptive Pill (OCP)
Microgynon (Combined) Cerazette (Progestogen Only)
365
Describe the MOA of the OCP
A progestin (synthetic form of progesterone) along with an oestrogen (combined oral contraceptive pill) or a progestin alone (progestogen only pill) Acts on female reproductive tract, the mammary glands, hypothalamus and the pituitary gland Reduces the production of Gonadotrophin Releasing Hormone (GnRH) Blunts the LH surge that stimulates ovulation
366
State indications for the OCP
Contraception Menopausal and Postmenopausal Disorders Polycyctsic Ovarian Syndrome
367
State side effects of the OCP
Mood Swings Headache Breast Tenderness Increased Risk of Breast and Ovarian Cancer Increased Risk of Venous Thromboembolic Disease
368
Describe important pharmacodynamic/pharmacokinetic features of the OCP
Antibiotics and some enzyme inducers (e.g. St John's Wort) can reduce efficacy
369
Describe important pieces of patient information that should be given with the OCP
Take at the same time everyday - compliance is critical for efficacy Take with food Use alternative forms of contraception when taking concurrent antibiotics or enzyme inducers
370
State the class of drug to which Codeine belongs
Opiate
371
Describe the MOA of Codeine
Opioid receptor agonist; acts on mu, kappa and delta receptors on presynaptic neurons This gives numerous effects that increase nociceptive thresholds throughout the central and peripheral nervous system
372
State indications for Codeine
Mild to Moderate Pain Persistent Dry Cough Diarrhoea
373
State side effects of Codeine
Nausea Vomiting Constipation Biliary Spasm Headache on Withdrawal
374
Describe important pharmacodynamic/pharmacokinetic features of Codeine
Metabolised to morphine which is responsible for analgesic effects Predominantly metabolised by the liver Active metabolites are excreted in the urine so can accumulate in renal failure 10% of population resistant to codeine’s analgesic properties as they lack the demethylating enzyme that converts it to morphine
375
Describe important pieces of patient information that should be given with Codeine
Can be taken with paracetamol for greater analgesic effect Constipation is a likely side effect
376
State the class of drug to which Morphine belongs
Opiate
377
Describe the MOA of Morphine
Opioid receptor agonist; acts on mu, kappa and delta on presynaptic neurones This gives numerous effects that increase nociceptive thresholds throughout the central and peripheral nervous system
378
State indications for Morphine
Acute Severe Pain (incl. in setting of MI) Acute Pulmonary Oedema Chronic Pain
379
State side effects of Morphine
Nausea Vomiting Abdominal Pain Constipation Respiratory Depression Sedation
380
Describe important pharmacodynamic/pharmacokinetic features of Morphine
Predominantly metabolised by the liver Metabolites are active and can accumulate in renal failure Accumulation can result in respiratory and central nervous system depression
381
Describe important pieces of patient information that should be given with Morphine
Often given with an anti-emetic to reduce nausea/vomiting
382
State the class of drug to which Oxycodone belongs
Opiate
383
Describe the MOA of Oxycodone
Opioid receptor agonist; acts on mu, kappa and delta on presynaptic neurones This gives numerous effects that increase nociceptive thresholds throughout the central and peripheral nervous system
384
State indications for Oxycodone
Moderate to Severe Pain Relief in Cancer Patients Post-Operative Pain Severe Pain
385
State side effects of Oxycodone
Nausea Vomiting Abdominal Pain Constipation
386
Describe important pharmacodynamic/pharmacokinetic features of Oxycodone
Available as long and short-acting preparations Predominantly metabolised by the liver Often administered via slow IV/SubCut infusion
387
Describe important pieces of patient information that should be given with Oxycodone
Nausea and constipation are common side effects
388
Give two examples of Non-Selective NSAIDs
Ibuprofen Diclofenac
389
Describe the MOA of Non-Selective NSAIDs
Non-selective inhibition of COX 1 and 2 enzymes, thereby decreasing the key inflammatory mediator prostaglandin from being synthesised Thereby reduces pain, inflammation and swelling
390
State indications for Non-Selective NSAIDs
Mild to Moderate Pain Relief Rheumatic Disorders (e.g. RA or OA) Fever (Anti-Pyretic Effect)
391
State side effects of Non-Selective NSAIDs
Gastric and Duodenal Ulceration (risk increases with duration of therapy and dosage) Nausea Diarrhoea Small increased risk of thrombotic events when used short-term, particularly diclofenac and high dose ibuprofen Renal Impairment Hyperkalaemia Avoid in pregnancy, particularly the 3rd trimester (risk of closure of foetal ductus arteriosus in utero and pulmonary hypertension in newborn)
392
Describe important pharmacodynamic/pharmacokinetic features of Non-Selective NSAIDs
Pain relief starts soon after the first dose, full analgesic effects can take up to one week and anti-inflammatory effects can take up to three weeks Avoid in patients with renal impairment – use lowest dose, for shortest time if unavoidable Caution should be used in the elderly – risk of gastrointenstinal bleeds.
393
Describe important pieces of patient information that should be given with Non-Selective NSAIDs
Risk of stomach bleeds if on long-term use Take with food or milk, to reduce abdominal discomfort and to reduce the risk of bleeding Take only when required In elderly patients a proton pump inhibitor is usually given alongside NSAID drugs
394
Give an example of a Selective NSAID
Celecoxib
395
Describe the MOA of Celecoxib
Selective inhibitor of COX-2, decreasing key inflammatory mediator prostaglandin from being synthesised Thereby reduces pain, inflammation and swelling (The gastrointestinal side effects are mediated via COX-1 inhibition)
396
State indications for Celecoxib
Pain and Inflammation in: OA, RA, Ankylosing Spondylitis
397
State side effects of Celecoxib
Gastric and Duodenal Ulceration (risk increases with duration of therapy and dosage) Nausea Diarrhoea Renal Impairment Hyperkalaemia
398
Describe important pharmacodynamic/pharmacokinetic features of Celecoxib
Less incidence of serious gastrointestnal bleeds/ulceration compared to non-selective NSAIDs Presumed higher risk of cardiovascular events, compared to non-selective NSAIDs Avoid in patients with renal impairment – use lowest dose, for shortest time if unavoidable Caution should be used in the elderly – risk of GI bleeds Avoid in pregnancy particularly 3rd trimester (risk of closure of fetal ductus arteriosus in utero and pulmonary hypertension in newborn)
399
Describe important pieces of patient information that should be given with Celecoxib
Risk of stomach bleeds if on long-term use Take with food or milk to reduce abdominal discomfort and to reduce the risk of bleeding Take only when required
400
Describe the MOA of Paracetamol
A weak cyclooxygenase enzyme (COX) inhibitor with selectivity for brain COX It therefore lacks peripheral anti-inflammatory actions but is useful in increasing the threshold for nociceptive activation by inhibiting prostaglandin synthesis and its effects centrally
401
State indications for Paracetamol
Mild to Moderate Pain Relief Fever
402
State side effects of Paracetamol
Rash/Blood Disorders (Rare)
403
Describe important pharmacodynamic/pharmacokinetic features of Paracetamol
Overdose must be avoided – severe liver damage can occur and can be fatal Careful dosing in younger patients and patients with low body weight (reduce dose to 500mg 4-6 hourly, QID in patients \<50kg)
404
Describe important pieces of patient information that should be given with Paracetamol
Take only the prescribed amount and be wary of other over-the-counter medications that may contain paracetamol
405
State the class of drug to which Allopurinol belongs
Xanthine Oxidase Inhibitors
406
Describe the MOA of Allopurinol
Reduces synthesis of uric acid by competitively inhibiting xanthine oxidase Reduces serum uric acid level
407
State indications for Allopurinol
Prophylaxis of Gout Prophylaxis of Calcium Oxalate Renal Stones Hyperuricaemia Associated with Cancer Chemotherapy
408
State side effects of Allopurinol
Rash Hypersensitivity GI Disturbance Neutropenia (Rare)
409
Describe important pharmacodynamic/pharmacokinetic features of Allopurinol
Not used to treat acute attack of gout, can exacerbate the inflammation, so should not be started during acute episodes Cytochrome P450 enzyme inhibitor Azathioprine metabolism affected
410
Describe important pieces of patient information that should be given with Allopurinol
Rash and abdominal disturbances are relatively common Rash should be reported to a doctor Keep taking allopurinol, even when there is no sign of gout In order to prevent an exacerbation of gout, an NSAID or cochicine is often prescribed for the first 3 months of therapy