Drugs Flashcards
(228 cards)
1
Q
What are the common indications for prescribing statins?
A
Primary prevention of cardiovascular disease (CVD) in people over 40 with a 10-year cardiovascular risk >20%.
Secondary prevention of CVD to prevent further cardiovascular events.
Primary hyperlipidaemia (e.g., hypercholesterolaemia, mixed dyslipidaemia, familial hypercholesterolaemia).
2
Q
How do statins work in the body?
A
Statins inhibit HMG CoA reductase, an enzyme involved in cholesterol production. This leads to:
Decreased cholesterol production by the liver.
Increased clearance of LDL-cholesterol from the blood, lowering LDL levels.
Reduced triglycerides and a slight increase in HDL-cholesterol levels, slowing or reversing atherosclerosis.
3
Q
What are the common adverse effects of statins?
A
Headache.
Gastrointestinal disturbances.
Muscle issues (ranging from aches to myopathy or, rarely, rhabdomyolysis).
A rise in liver enzymes (e.g., ALT); rare but serious drug-induced hepatitis.
4
Q
What are important warnings when prescribing statins?
A
Use with caution in patients with hepatic impairment.
Reduce the dose in patients with renal impairment.
Avoid in pregnant or breastfeeding women.
5
Q
What drugs interact with statins and what is the risk?
A
Cytochrome P450 inhibitors (e.g., amiodarone, diltiazem, itraconazole, macrolides, protease inhibitors) may reduce statin metabolism, increasing the risk of adverse effects.
Amlodipine also interacts with simvastatin - causing increased side effects.
Grapefruit juice can increase the risk of side effects when taking simvastatin or atorvastatin, but this is not the case for pravastatin and rosuvastatin.
6
Q
How should statins be prescribed and taken?
A
Statins are typically taken orally once daily.
Simvastatin has a short half life so must be taken in the evening.
7
Q
What monitoring is required when prescribing statins?
A
Primary prevention: No routine lipid checks are required after starting statins, but a lipid profile should be checked before treatment.
Secondary prevention: Check target cholesterol levels and adjust treatment if needed.
Monitor liver enzymes (e.g., ALT) at baseline and after 3 and 12 months.
Creatine kinase does not need to be checked routinely, but muscle symptoms should be reported and investigated.
8
Q
What are the common indications for prescribing ACE inhibitors and ARBs?
A
Hypertension: First- or second-line treatment to reduce the risk of stroke, myocardial infarction, and death from cardiovascular disease.
Chronic Heart Failure: First-line treatment for all grades of heart failure to improve symptoms and prognosis.
Ischaemic Heart Disease: To reduce the risk of subsequent cardiovascular events such as myocardial infarction and stroke.
Diabetic Nephropathy and CKD with Proteinuria: To reduce proteinuria and slow the progression of nephropathy.
9
Q
How do ACE inhibitors work in the body?
A
ACE inhibitors block the enzyme ACE, preventing the conversion of angiotensin I to angiotensin II. This leads to:
Reduced vasoconstriction and lowered peripheral vascular resistance, helping lower blood pressure.
Dilation of the efferent glomerular arteriole, reducing intraglomerular pressure, which helps slow CKD progression.
Increased sodium and water excretion, which lowers preload and benefits heart failure.
10
Q
What are the common side effects of ACE inhibitors?
A
Hypotension (especially after the first dose).
Persistent dry cough (due to increased bradykinin).
Hyperkalaemia (due to reduced aldosterone levels).
Renal dysfunction, particularly in patients with renal artery stenosis.
Rare but serious side effects include angioedema and anaphylactoid reactions.
11
Q
What are the important warnings when prescribing ACE inhibitors?
A
Avoid in patients with renal artery stenosis or acute kidney injury.
Contraindicated in pregnant or breastfeeding women.
Use with caution in patients with chronic kidney disease, and monitor renal function closely.
Use lower doses and monitor renal function carefully in patients with existing renal impairment.
12
Q
What are the important drug interactions with ACE inhibitors?
A
Potassium-elevating drugs (e.g., potassium supplements, potassium-sparing diuretics) should be avoided due to the risk of hyperkalaemia.
ACE inhibitors can cause profound hypotension when used with diuretics, especially with first doses.
NSAIDs (e.g., ibuprofen) combined with ACE inhibitors increase the risk of renal failure.
13
Q
How should ACE inhibitors and ARBs be taken?
A
ACE inhibitors can be taken with or without food.
It’s best to take the first dose before bed to reduce the risk of symptomatic hypotension.
14
Q
What monitoring is required when prescribing ACE inhibitors?
A
Before starting: Check electrolytes and renal function.
1-2 weeks after starting and after dose adjustments: Repeat tests to monitor for changes in creatinine, eGFR, and potassium levels.
Acceptable biochemical changes:
Creatinine rise: ≤30%.
eGFR fall: ≤25%.
Potassium: ≤6.0 mmol/L.
If limits are exceeded, stop the drug and seek expert advice.
15
Q
How do ARBs work in the body?
A
ARBs block the action of angiotensin II on the AT1 receptor, preventing its vasoconstrictive and aldosterone-stimulating effects. This leads to:
Reduced peripheral vascular resistance, helping to lower blood pressure.
Dilation of the efferent glomerular arteriole, reducing intraglomerular pressure and slowing CKD progression.
Decreased aldosterone levels, promoting sodium and water excretion, which helps reduce preload in heart failure.
Work very similar to ACE inhibitors.
16
Q
What are the common side effects of ARBs?
A
Hypotension (particularly after the first dose).
Hyperkalaemia (due to reduced aldosterone).
Renal failure (particularly in patients with renal artery stenosis).
Less likely to cause dry cough or angioedema compared to ACE inhibitors, as ARBs do not affect bradykinin metabolism.
17
Q
What are the important warnings when prescribing ARBs?
A
Avoid in patients with renal artery stenosis or acute kidney injury.
Contraindicated in pregnant or breastfeeding women.
Use lower doses and monitor renal function closely in patients with chronic kidney disease.
18
Q
What are the important drug interactions with ARBs?
A
Avoid ARBs with potassium-elevating drugs (e.g., potassium supplements, potassium-sparing diuretics) unless under specialist advice for advanced heart failure.
NSAIDs (e.g., ibuprofen) combined with ARBs can increase the risk of renal failure.
ARBs may cause profound hypotension when used with other diuretics, especially during the first dose.
19
Q
What monitoring is required when prescribing ARBs?
A
Before starting: Check electrolytes and renal function.
1-2 weeks after starting and after dose increases: Repeat tests to monitor creatinine, eGFR, and potassium levels.
Biochemical changes can be tolerated if:
Creatinine rises ≤30%.
eGFR falls ≤25%.
Potassium does not rise above 6.0 mmol/L.
If any of these limits are exceeded, stop the drug and seek expert advice.
20
Q
What is a clinical tip regarding the use of ARBs in black patients?
A
The incidence of angioedema related to ACE inhibitors is five times higher (around 1%) in black people of African or Caribbean origin. Since ARBs do not affect bradykinin levels, they are less likely to cause angioedema and may be preferable to ACE inhibitors in this group.
21
Q
Name ARBs.
A
Losartan, Candesartan, Irbesartan, Valsartan
22
Q
What is Entresto and what should you check when starting it?
A
Entresto combines sacubitril (neprilysin inhibitor) and valsartan (ARB).
Check patient is not on an ACE/ARB already.
Sacubitril is a neprilysin inhibitor. It works by inhibiting the enzyme neprilysin, which normally breaks down natriuretic peptides (like BNP). By preventing this breakdown, sacubitril increases levels of these peptides, which help to relax blood vessels, reduce fluid retention, and decrease strain on the heart.
23
Q
What is midodrine primarily used to treat?
A
Orthostatic hypotension (low blood pressure when standing).
24
Q
How does midodrine help increase blood pressure?
A
It stimulates alpha-1 adrenergic receptors, causing vasoconstriction, which raises blood pressure.
25
What is the usual starting dose of midodrine for treating orthostatic hypotension?
5 mg three times a day.
26
What are common side effects of midodrine?
Supine hypertension (high blood pressure when lying down), chills, headache, GI discomfort.
Rare - heptatic function adnormal.
27
28
When should midodrine not be used?
In patients with aortic aneurysm, bradycardia, CHF, hypertension, urinary retention, narrow angle glaucoma.
Caution in the elderly.
29
How should midodrine be administered to avoid night time hypertension?
It should be taken during the day and not within 4 hours of bedtime to prevent increased blood pressure while lying down.
30
Which of the following drugs can interact with midodrine?
Other vasoconstrictors, such as certain decongestants.
31
What drug class is midodrine?
Vasoconstrictor - Alpha 1 adrenergic agonist.
32
What is the primary mechanism of action of mineralocorticoid receptor antagonists?
They competitively inhibit aldosterone binding at mineralocorticoid receptors, primarily in the kidneys, reducing sodium reabsorption and promoting potassium retention.
33
Which MRAs are commonly used in clinical practice?
Spironolactone, eplerenone (only licensed in HR), and finerenone are widely used.
34
What are the main clinical indications for MRAs?
Heart failure with reduced ejection fraction (HFrEF), resistant hypertension, primary hyperaldosteronism, chronic kidney disease with proteinuria (especially finerenone) and ascites and oedema due to liver cirrhosis.
35
How does spironolactone differ from eplerenone in terms of receptor selectivity?
Spironolactone is less selective and also antagonizes androgen and progesterone receptors, leading to side effects like gynecomastia. Eplerenone is more selective for mineralocorticoid receptors, reducing such side effects.
36
What is a key advantage of finerenone over other MRAs?
Finerenone is a nonsteroidal MRA with high selectivity and potency, and it has a lower risk of hyperkalemia and hormonal side effects compared to steroidal MRAs.
37
What are common adverse effects associated with MRAs?
Hyperkalemia, hypotension, renal impairment, and hormonal side effects (e.g., gynecomastia (increased breast tissue in men) with spironolactone).
38
What are the common indications for calcium channel blockers?
First- or second-line treatment of hypertension, ischaemic heart disease and supraventricular arrhythmias (diltiazem and verapamil).
39
What is the general mechanism of action of calcium channel blockers?
They inhibit calcium influx into vascular and cardiac cells, causing vasodilation and reduced myocardial contractility.
40
Which CCB is most cardioselective?
Verapamil.
41
What are common side effects of dihydropyridines?
Ankle swelling, flushing, headache, and palpitations.
42
What adverse effect is commonly associated with verapamil?
Constipation, and more seriously, bradycardia and heart block.
43
Why can diltiazem cause a wider range of side effects?
Because it affects both vascular tone and cardiac conduction.
Ankle swelling, flushing, headache, and palpitations.
Constipation, and more seriously, bradycardia and heart block.
44
In which structural heart disease are dihydropyridines contraindicated?
Severe aortic stenosis.
45
Why should verapamil or diltiazem not be combined with β-blockers?
Both decrease heart rate and contractility, increasing the risk of bradycardia or heart block.
46
What is a common angina regimen for diltiazem MR?
90 mg orally twice daily.
47
How is treatment efficacy monitored for different indications?
BP for hypertension, chest pain for angina, pulse/ECG for arrhythmias.
48
Name CCBs.
Amlodipine, felodipine, nifedipine, diltiazem, verapamil, nimodipine, lercanidipine.
49
What can nimodipine be used for?
Subarachnoid haemorrhage - treatment or prevention.
50
What are the 2 types of CCBs and what do they aim to do?
Dihydropyridines - primarily act to vasodilate.
Non dihydropyridines - slows HR (rhythm control): diltiazem, verapamil.
51
What are common indications for loop diuretics?
Acute pulmonary oedema (with oxygen and nitrates).
Chronic heart failure with fluid overload.
Oedematous states due to renal or liver disease.
52
Where do loop diuretics act in the nephron?
The ascending limb of the loop of Henle.
53
What transporter do loop diuretics inhibit?
Na⁺/K⁺/2Cl⁻ co-transporter.
54
What is the effect of inhibiting the Na⁺/K⁺/2Cl⁻ co-transporter?
Reduces sodium, potassium, and chloride reabsorption → water follows → potent diuretic effect.
55
How do loop diuretics improve symptoms in acute heart failure before diuresis begins?
They dilate capacitance veins, reducing preload and improving cardiac function.
56
What electrolyte imbalances can loop diuretics cause?
Hyponatraemia
Hypokalaemia
Hypochloraemia
Hypocalcaemia
Hypomagnesaemia
Metabolic alkalosis
57
What are other key adverse effects of loop diuretics?
Dehydration
Hypotension
Ototoxicity (hearing loss, tinnitus) at high doses
58
In which condition are loop diuretics contraindicated?
Severe hypovolemia or dehydration.
59
What conditions require caution when using loop diuretics?
Hepatic encephalopathy (risk of coma from hypokalaemia)
Severe hypokalaemia
Severe hyponatraemia
Gout (due to reduced uric acid excretion)
60
How do loop diuretics affect lithium levels?
They reduce lithium excretion, increasing the risk of toxicity.
61
How do loop diuretics interact with digoxin?
Hypokalaemia increases the risk of digoxin toxicity.
62
When should oral loop diuretics be taken?
In the morning (and early afternoon if twice daily) to avoid nocturia.
63
When are thiazide diuretics used as first-line treatment in hypertension?
When calcium channel blockers are unsuitable (e.g. due to oedema or heart failure features).
64
How are thiazides used in combination therapy for hypertension?
As an add-on to calcium channel blocker + ACE inhibitor or ARB if BP remains uncontrolled.
65
Where in the nephron do thiazide diuretics act?
Distal convoluted tubule.
66
What transporter do thiazides inhibit?
Na⁺/Cl⁻ co-transporter.
67
What is the initial and long-term mechanism by which thiazides lower BP?
Initial: Diuresis and reduced extracellular volume.
Long-term: Vasodilation (mechanism not fully understood).
68
What are common electrolyte-related side effects of thiazides?
Hyponatraemia
Hypokalaemia (may cause arrhythmias)
69
What metabolic effects can thiazides have?
↑ Plasma glucose (may unmask type 2 diabetes)
↑ LDL-cholesterol and triglycerides
May cause impotence in men
70
Which common OTC drugs may reduce thiazide effectiveness?
NSAIDs (except low-dose aspirin).
71
What are common thiazide-like diuretics and their doses for hypertension?
Indapamide: 2.5 mg daily
Chlortalidone: 12.5–25 mg daily
72
Why is bendroflumethiazide less preferred today?
It lacks supporting clinical trial evidence for cardiovascular benefit.
73
What are the 5 main indications for beta-blockers?
Ischaemic heart disease (e.g. angina, ACS)
Chronic heart failure
Atrial fibrillation (rate control; rhythm control in paroxysmal AF)
Supraventricular tachycardia (SVT)
Hypertension (not first-line)
74
Where are β1 and β2 adrenoreceptors located?
β1: Mainly in the heart
β2: In smooth muscle (vessels, airways)
75
How do beta-blockers help in heart failure?
They protect the heart from chronic sympathetic stimulation.
76
How do beta-blockers help in atrial fibrillation and SVT?
AF: Slow AV conduction by prolonging refractory period
SVT: Disrupt re-entry circuits involving AV node
77
What are common side effects of beta-blockers?
Fatigue
Cold extremities
Headache
Nausea/GI upset
Sleep disturbance, nightmares
Impotence in men
78
Why should beta-blockers be avoided in asthma?
They can cause life-threatening bronchospasm via β2 blockade.
79
Which patients with lung disease may still tolerate beta-blockers?
Those with COPD – use cardioselective β1-blockers like bisoprolol or atenolol.
80
When are beta-blockers contraindicated?
Heart block
Haemodynamic instability
Significant hepatic impairment (dose reduction needed)
81
Which drug class must not be combined with beta-blockers?
Non-dihydropyridine calcium channel blockers (verapamil, diltiazem) – risk of heart failure, bradycardia, asystole.
82
What are key monitoring parameters for beta-blocker therapy?
Symptoms (e.g., angina, breathlessness)
Heart rate (target 55–60 bpm in ischaemic heart disease)
83
Why is short-acting metoprolol preferred acutely (e.g., ACS)?
Easier to titrate, quick onset/offset, and safer if drug needs to be withdrawn rapidly. Transition to long-acting beta-blocker like bisoprolol for maintenance.
84
What are the cardio selective beta blockers - B1?
MANBABE
Metoprolol
Atenolol
Nebivolol
Bisoprolol
Acebutolol
Betaxolol
Esmolol
85
What beta blockers are preferred in migraine?
Propranolol - lipid soluble.
86
Name non-cardioselective beta blockers.
Carvedilol
Labetalol
Propranolol
Timolol
Sotalol.
87
Why is sotalol a drug to be cautious in pharmacy?
May cause dangerous heart rhythm problems called QT prolongation and torsade de pointes.
88
What are the main clinical indications for short-acting nitrates like glyceryl trinitrate (GTN)?
Treatment of acute angina and chest pain in acute coronary syndrome.
89
What are long-acting nitrates like isosorbide mononitrate used for?
Prophylaxis of angina, especially when β-blockers and/or calcium channel blockers are insufficient or not tolerated.
90
What is the role of intravenous nitrates?
Treatment of pulmonary oedema, usually with furosemide and oxygen.
91
How do nitrates work at the molecular level?
Nitrates are converted to nitric oxide (NO), which increases cGMP and reduces intracellular Ca²⁺, causing vascular smooth muscle relaxation.
92
What is the main cardiovascular effect of nitrates?
Venous vasodilation (mainly) reduces preload and myocardial oxygen demand, relieving angina.
93
What are common side effects of nitrates?
Flushing
Headache
Light-headedness
Hypotension
94
What is nitrate tolerance and how is it prevented?
Tolerance (tachyphylaxis) is reduced response with continued use. It’s prevented by a daily nitrate-free period, usually overnight.
95
Why are nitrates contraindicated in aortic stenosis?
Because they may cause cardiovascular collapse due to inability to maintain pressure in dilated vasculature.
96
Which drug interaction makes nitrate use dangerous?
Phosphodiesterase inhibitors (e.g. sildenafil) – can cause severe hypotension.
97
How is glyceryl trinitrate (GTN) prescribed in stable angina?
Sublingually as a spray or tablet for immediate symptom relief.
98
What is the plasma half-life of sublingual GTN?
<5 minutes – very quick onset and offset.
99
How should isosorbide mononitrate (ISMN) be prescribed for prevention of angina?
Immediate-release: 2–3 times daily
Modified-release or patches: once daily (with nitrate-free period)
Example - Take doses in morning and mid-afternoon to ensure a 12+ hour nitrate-free period overnight.
100
Why should modified-release ISMN be prescribed by brand name?
Due to important differences between brands.
101
What monitoring is required during IV GTN infusion?
Frequent blood pressure checks to avoid systolic BP <90 mmHg.
102
What should patients be advised when taking sublingual GTN?
May cause headache
Use before exertion
Sit and rest before and 5 minutes after taking.
103
When should GTN sublingual tablets be discarded?
After 8 weeks once opened – sprays may be better for infrequent use.
104
What is the main indication for ivabradine?
Chronic heart failure with sinus rhythm and a resting heart rate ≥75 bpm, where β-blockers are contraindicated or insufficient.
105
What is the mechanism of action of ivabradine?
It selectively inhibits the funny current (If) in the sinoatrial node, slowing pacemaker activity and heart rate, without affecting contractility or blood pressure.
Ivabradine is in a class of medications called hyperpolarization-activated cyclic nucleotide-gated (HCN) channel blockers.
106
In which type of rhythm is ivabradine effective?
Only in patients with sinus rhythm, since it acts on the sinoatrial node.
107
What are the common side effects of ivabradine?
Bradycardia
Luminous phenomena (phosphenes: transient enhanced brightness in visual field)
Headache
Dizziness
108
What are the contraindications to ivabradine?
Bradycardia (<70 bpm) at rest
Acute decompensated heart failure
Sick sinus syndrome
Atrial fibrillation
Severe hepatic impairment
109
What makes ivabradine different from β-blockers or calcium channel blockers?
It reduces heart rate without affecting myocardial contractility or blood pressure.
110
What is the primary clinical use of nicorandil?
For the prevention and treatment of stable angina when β-blockers or calcium channel blockers are insufficient or not tolerated.
111
What two mechanisms contribute to nicorandil’s vasodilatory effect?
Nitrate-like action (increasing nitric oxide)
Activation of ATP-sensitive potassium (K⁺-ATP) channels
It causes K⁺ efflux, leading to cell membrane hyperpolarisation, which inactivates voltage-gated Ca²⁺ channels, reducing intracellular calcium and causing smooth muscle relaxation.
112
What are common side effects of nicorandil?
Headache
Flushing
Dizziness
Nausea or vomiting
Hypotension
113
In which conditions should nicorandil be avoided?
Hypotension
Poor left ventricular function
Pulmonary oedema
114
Which drug class must not be combined with nicorandil and why?
Phosphodiesterase inhibitors (e.g. sildenafil), because they potentiate hypotension.
115
When should a cardiology referral be considered for patients on nicorandil?
If angina is not controlled with two anti-anginal drugs, including nicorandil.
116
What is the primary clinical indication for ranolazine?
Chronic stable angina in patients not adequately controlled by first-line therapies (e.g., β-blockers, calcium channel blockers).
117
Is ranolazine used for acute angina or as first-line therapy?
No, it is not for acute angina and is not a first-line treatment.
118
What is the main mechanism of action of ranolazine?
It inhibits the late sodium current (INa) in cardiac myocytes, reducing intracellular sodium and calcium overload, which improves myocardial relaxation and reduces oxygen consumption.
Ranolazine does not significantly affect heart rate or blood pressure.
119
What are common side effects of ranolazine?
Dizziness
Constipation
Nausea
Headache
120
What serious adverse effect is associated with ranolazine?
QT interval prolongation, which can increase the risk of arrhythmias.
121
In which patients should ranolazine be used with caution or avoided?
Pre-existing QT prolongation
Hepatic impairment
Severe renal impairment
122
What are important drug interactions with ranolazine?
It interacts with CYP3A4 inhibitors (e.g. ketoconazole, clarithromycin) and inducers, and may increase plasma concentrations of digoxin and simvastatin.
123
What are the primary clinical indications for adrenaline?
Cardiac arrest (as part of ALS protocol)
Anaphylaxis
Local vasoconstriction (e.g. during endoscopy or with local anaesthetics)
124
Why is adrenaline useful in cardiac arrest?
It promotes vasoconstriction and improves coronary perfusion, potentially aiding return of spontaneous circulation.
125
Why is adrenaline used in anaphylaxis?
It reverses hypotension, bronchospasm, and mast cell mediator release.
126
What are common side effects of adrenaline in conscious patients?
Anxiety
Tremor
Headache
Palpitations
Hypertension (especially post-cardiac arrest).
127
When is adrenaline contraindicated?
No contraindications in cardiac arrest or anaphylaxis. Use cautiously in patients with heart disease when used for local vasoconstriction.
Adrenaline–local anaesthetic combinations however should not be used in end-artery areas due to risk of tissue necrosis due to prolonged vasoconstriction (e.g., fingers, toes).
128
What is the adult dose of adrenaline in cardiac arrest?
1 mg IV (1:10,000 solution), every 3–5 minutes.
129
What is the adult dose of adrenaline in anaphylaxis?
500 micrograms (0.5 mL of 1:1000 solution) IM, repeated after 5 minutes if necessary.
130
What are the common indications for low molecular weight heparin (LMWH)?
VTE prophylaxis in hospital inpatients
Initial treatment of DVT and PE
Acute coronary syndrome (ACS)
131
What are the common indications for fondaparinux?
Treatment of ACS
VTE prophylaxis and treatment
132
How do unfractionated heparin (UFH) and LMWH work?
They activate antithrombin, which inhibits factor Xa and thrombin (UFH); LMWH preferentially inhibits factor Xa.
133
How does fondaparinux work?
It is a synthetic factor Xa inhibitor that works via antithrombin, similar to LMWH.
134
Why is LMWH preferred over UFH in many cases?
More predictable effect
No need for routine monitoring
Lower risk of heparin-induced thrombocytopenia (HIT)
135
Why would fondaparinux be given over LMWH?
Fondaparinux might be chosen over low-molecular-weight heparin (LMWH) in certain situations, particularly when a reduced risk of heparin-induced thrombocytopenia (HIT) is desired. While both are effective in preventing venous thromboembolism (VTE), fondaparinux has a lower incidence of HIT compared to LMWH. Additionally, fondaparinux may be preferred for its potential to reduce major bleeding and improve long-term outcomes.
136
What conditions require caution when using heparins or fondaparinux?
Bleeding risk (e.g. recent surgery, trauma, clotting disorders)
Severe uncontrolled hypertension
Renal impairment.
137
What are common doses for VTE prophylaxis with LMWH?
Enoxaparin 40 mg SC daily
Dalteparin 5000 units SC daily
138
How is UFH typically administered?
IV infusion, adjusted based on APTR (activated partial thromboplastin ratio).
139
How is heparin anticoagulation reversed in major bleeding?
Protamine reverses UFH completely
Partially reverses LMWH
Ineffective for fondaparinux
140
What are the main indications for aspirin in cardiovascular care?
Acute coronary syndrome (ACS)
Acute ischaemic stroke
Secondary prevention of thrombotic events in CV, cerebrovascular, and peripheral arterial disease.
141
How does aspirin work as an antiplatelet?
It irreversibly inhibits COX, reducing thromboxane A2 production → decreased platelet aggregation.
142
Why is the effect of aspirin long-lasting?
Platelets lack nuclei and can’t resynthesize COX, so effect lasts for the life of the platelet (~7 days).
143
What are common side effects of aspirin?
GI irritation
GI ulcers and bleeding
Bronchospasm (in sensitive individuals)
144
What is a serious adverse effect of high-dose or chronic aspirin use?
Tinnitus (early sign of toxicity)
Salicylate poisoning (overdose): metabolic acidosis, hyperventilation, confusion, seizures, collapse
145
Why is aspirin contraindicated in children under 16?
Risk of Reye’s syndrome, a rare but serious liver and brain condition.
146
In which patients should aspirin be used with caution?
Peptic ulcer disease
Asthma (if aspirin-sensitive)
Gout
Pregnancy (3rd trimester)
147
What is the initial and maintenance dosing of aspirin in ACS?
300 mg loading dose, then
75 mg daily
148
What is the aspirin dosing strategy for acute ischaemic stroke?
300 mg daily for 2 weeks, then
Switch to 75 mg daily
149
What is the maximum total daily dose of aspirin for pain relief?
4 grams daily, divided into doses
150
When should gastroprotection be considered with aspirin?
Age >65
History of ulcers
Comorbidities (e.g. CVD, diabetes)
Use of NSAIDs or steroids
151
What is the main indication for dipyridamole in clinical use?
Secondary prevention of stroke, especially after TIA or if clopidogrel is not tolerated.
152
What diagnostic use does dipyridamole have?
To induce tachycardia during a myocardial perfusion scan to assess for ischaemic heart disease.
153
What is the mechanism of dipyridamole?
Increases intra-platelet cAMP, which inhibits platelet aggregation.
Blocks adenosine uptake, prolonging adenosine’s vasodilatory effect on blood vessels.
154
What are common side effects of dipyridamole?
Headache
Flushing
Dizziness
GI upset
Increased bleeding risk
(Haematological side effect - Thrombocytopenia).
155
What important interaction exists between dipyridamole and adenosine?
Dipyridamole inhibits adenosine uptake, increasing its effect—reduce adenosine dose.
156
What is the recommended dose for dipyridamole MR in stroke prevention?
200 mg twice daily.
157
What are the main indications for clopidogrel?
Acute coronary syndrome (ACS)
Coronary stent thrombosis prevention
Long-term secondary prevention (CVD, cerebrovascular, PAD)
Atrial fibrillation if warfarin/NOACs contraindicated.
158
What is the most common and serious side effect of clopidogrel?
Bleeding, especially GI, intracranial, or post-op.
159
Other common side effects of clopidogrel?
Dyspepsia
Abdominal pain
Diarrhoea
Rarely: thrombocytopenia
160
When should clopidogrel be stopped before surgery?
7 days before elective surgery
161
Why should omeprazole be avoided with clopidogrel?
Omeprazole inhibits CYP450, reducing clopidogrel activation (prodrug).
162
Which PPIs are preferred with clopidogrel for gastroprotection?
Lansoprazole or pantoprazole
163
How long should dual antiplatelet therapy continue after a drug-eluting stent?
12 months, unless advised otherwise by a cardiologist.
164
What are the main indications for ticagrelor?
Acute coronary syndrome (ACS) (e.g. STEMI, NSTEMI, unstable angina)
Prevention of stent thrombosis after percutaneous coronary intervention (PCI)
Used in dual antiplatelet therapy with aspirin.
165
When is ticagrelor preferred over clopidogrel?
When faster, more potent, and reversible platelet inhibition is desired.
166
Common adverse effects of ticagrelor?
Bleeding (including serious bleeding)
Dyspnoea (SOB) (up to 14–20%)
Bradycardia, ventricular pauses
GI symptoms: nausea, diarrhoea
167
Important drug interactions with ticagrelor?
CYP3A4 inhibitors (↑ ticagrelor levels)
CYP3A4 inducers (↓ effect)
Digoxin and statins (ticagrelor increases their levels)
168
What is the usual dosing regimen for ticagrelor in ACS?
Loading dose: 180 mg orally once (2 × 90 mg)
Then 90 mg twice daily
Typically given for 12 months post-ACS.
169
What are the main indications for prasugrel?
Acute coronary syndrome (ACS), particularly in patients undergoing percutaneous coronary intervention (PCI)
Often used in combination with aspirin as dual antiplatelet therapy (DAPT)
Especially effective for STEMI patients treated with primary PCI.
170
What class of drug is alteplase or tenecteplase (clot busters)?
They are fibrinolytic agents (thrombolytics) that mimic tissue plasminogen activator (tPA), promoting the breakdown of clots.
171
What are the main indications for alteplase/tenecteplase?
Acute ischaemic stroke (alteplase is commonly used) – within 4.5 hours of symptom onset
ST-elevation myocardial infarction (STEMI) – where PCI is unavailable within 2 hours
Tenecteplase often preferred in this setting due to single bolus administration
Massive pulmonary embolism (PE) – with haemodynamic compromise
172
What are the major adverse effects of tPA drugs?
Bleeding, including intracranial haemorrhage, which can be fatal
Hypotension and allergic reactions are less common
Reperfusion arrhythmias after MI (usually self-limiting).
173
What important interactions should be considered with alteplase/tenecteplase?
Anticoagulants (e.g. warfarin, heparin) and antiplatelets (e.g. aspirin, clopidogrel) ↑ bleeding risk
Should not be co-administered unless specifically indicated and carefully timed.
174
What is a clinical tip for alteplase use in stroke?
Only consider alteplase if:
Stroke onset is within 4.5 hours
CT scan excludes haemorrhage
No contraindications
Patient meets local stroke protocol
175
What are the common clinical indications for warfarin (vitamin k antagonist)?
Prevention of clot extension and recurrence in deep vein thrombosis (DVT) and pulmonary embolism (PE), prevention of embolic stroke in atrial fibrillation, and prevention of embolic complications after heart valve replacement.
176
Is warfarin used to prevent arterial thrombosis like myocardial infarction? Why or why not?
No, because arterial thrombosis is mainly caused by platelet aggregation, which is better prevented by antiplatelet drugs like aspirin or clopidogrel.
177
What is the mechanism of action of warfarin?
Warfarin inhibits vitamin K epoxide reductase, preventing reactivation of vitamin K, which is essential for synthesis of vitamin K-dependent clotting factors.
178
What are key warnings when prescribing warfarin?
Avoid in patients at immediate bleeding risk (e.g., after trauma or surgery), use cautiously in liver disease, contraindicated in the first trimester of pregnancy and near term due to fetal malformations and bleeding risks.
179
How do cytochrome P450 inhibitors affect warfarin?
They decrease warfarin metabolism, increasing warfarin levels and bleeding risk.
180
How do cytochrome P450 inducers affect warfarin?
They increase warfarin metabolism, decreasing its anticoagulant effect and increasing the risk of clotting.
181
What effect can many antibiotics have on warfarin therapy?
They may increase anticoagulation by killing gut flora that synthesize vitamin K, thereby increasing bleeding risk.
182
What is the typical target INR range for warfarin in atrial fibrillation and VTE?
Usually between 2.0 and 3.0.
183
How long does it take for warfarin to achieve full anticoagulation?
Several days, so bridging with heparin is often needed for immediate anticoagulation.
184
When is warfarin usually taken during the day and why?
Around 18:00 (early evening) to provide consistent INR results the following morning and help patients remember.
185
What should be considered if a patient on warfarin requires surgery?
Warfarin is usually stopped 5–7 days before surgery to reduce bleeding risk; bridging therapy may be required depending on thrombotic risk.
186
What is the typical induction dose of warfarin?
10 mg daily for 2 days, tailored to the individual.
187
How does lidocaine work as a local anaesthetic?
It blocks voltage-gated sodium channels in neurons, preventing nerve impulse transmission, thus producing local numbness.
188
What does NOAC/DOAC stand for?
NOAC: Non-vitamin K Oral Anticoagulant
DOAC: Direct Oral Anticoagulant
(Both terms refer to the same drug class.)
189
Name the four commonly used NOACs.
Apixaban
Rivaroxaban
Edoxaban
Dabigatran
190
What are the main indications for NOACs/DOACs?
Stroke prevention in non-valvular atrial fibrillation
Treatment and prevention of DVT/PE
Postoperative VTE prophylaxis (e.g. after hip/knee surgery)
191
What is a key advantage of NOACs over warfarin?
Fewer drug and food interactions
Rapid onset and offset
Fixed dosing
192
What are common adverse effects of NOACs?
Bleeding, especially GI bleeding
Dyspepsia (particularly with dabigatran)
Bruising
193
Which NOAC has a specific antidote?
Dabigatran: antidote is idarucizumab
Apixaban and rivaroxaban: reversal agent is andexanet alfa
194
In which condition should NOACs not be used?
Mechanical heart valves
Significant mitral stenosis
(Warfarin is preferred in these cases.)
195
How are NOACs eliminated?
Dabigatran: mainly renal
Apixaban, Rivaroxaban, Edoxaban: renal and hepatic
196
What should be considered before initiating NOAC therapy?
Renal function (eGFR)
Liver function
Bleeding risk
Drug interactions
197
Can NOACs be used in pregnancy or breastfeeding?
No, they are contraindicated due to limited safety data.
198
What are the two main clinical indications for digoxin?
Atrial fibrillation/flutter – to reduce ventricular rate
Severe heart failure – as a third-line agent
199
Why is digoxin not typically a first-line agent in AF?
Because β-blockers or non-dihydropyridine calcium channel blockers are usually more effective for rate control.
200
What are the common side effects of digoxin?
Bradycardia
GI upset (nausea, diarrhoea)
Visual disturbances (blurred/yellow vision)
Rash
Dizziness
Arrhythmias (due to proarrhythmic effect)
201
What electrolyte disturbances increase the risk of digoxin toxicity?
Hypokalaemia
Hypomagnesaemia
Hypercalcaemia
(Most important: hypokalaemia)
202
In which heart conduction conditions is digoxin contraindicated?
Second-degree heart block
Intermittent complete heart block
203
Which common drugs increase digoxin plasma levels?
Amiodarone
Calcium channel blockers
Spironolactone
Quinine
204
Why do loop and thiazide diuretics increase digoxin toxicity risk?
They cause hypokalaemia, which enhances digoxin’s effects on the Na⁺/K⁺ pump.
205
When should digoxin levels be checked?
Only when toxicity is suspected; routine monitoring is not required.
206
What is the most dangerous complication of digoxin toxicity?
Arrhythmias – including bradycardia, ventricular tachycardia, or fibrillation.
207
What visual symptoms are characteristic of digoxin toxicity?
Blurred vision
Yellow vision (xanthopsia)
Visual halos
208
What gastrointestinal and neurological symptoms are seen in digoxin toxicity?
Nausea
Vomiting
Anorexia
Diarrhoea
Dizziness
Confusion
Weakness
Fatigue
Headache
209
What are signs of warfarin overdose?
Prolonged INR
Bleeding gums
Nosebleeds
Unexplained bruising
Black/tarry stools
Haematuria
Intracranial haemorrhage (life-threatening)
210
What dietary factors can enhance warfarin's anticoagulant effect?
Low vitamin K intake, especially from green leafy vegetables.
211
Which drugs increase the risk of warfarin toxicity by inhibiting CYP450 metabolism?
Fluconazole
Macrolides (e.g. erythromycin)
Amiodarone
Protease inhibitors
212
How is warfarin toxicity treated?
Withhold warfarin
Administer vitamin K (oral or IV)
Give prothrombin complex concentrate (PCC) or fresh frozen plasma for major bleeding
213
What is the primary toxic effect of NOACs/DOACs (e.g. apixaban, rivaroxaban, dabigatran)?
Bleeding, especially gastrointestinal and intracranial haemorrhage.
214
What are symptoms of NOAC-related bleeding?
Dark stools or rectal bleeding
Nosebleeds
Heavy menstrual bleeding
Coughing/vomiting blood
Fatigue or dizziness from blood loss
215
What are the common clinical indications for amiodarone?
Atrial fibrillation (AF)
Atrial flutter
Supraventricular tachycardia (SVT)
Ventricular tachycardia (VT)
Refractory ventricular fibrillation (VF)
216
When is amiodarone typically used?
When other antiarrhythmic treatments (e.g. drugs or cardioversion) are ineffective or inappropriate.
217
What is the mechanism of action of amiodarone?
Blocks sodium, potassium, and calcium channels; antagonizes α- and β-receptors.
It reduces automaticity, slows conduction, and increases refractoriness.
218
What are important adverse effects of chronic amiodarone use?
Pulmonary toxicity (pneumonitis)
Bradycardia and AV block
Hepatitis
Thyroid dysfunction (hypo- or hyperthyroidism)
Photosensitivity
Grey skin discoloration
219
Why does amiodarone cause thyroid dysfunction?
Due to its iodine content and structural similarity to thyroid hormone.
220
What are some early symptoms that may indicate serious amiodarone toxicity?
New or worsening breathlessness
Persistent cough
Weight changes
Jaundice
Fatigue or restlessness
221
In which patients is amiodarone contraindicated?
Severe hypotension
Heart block
Active thyroid disease
222
Which medications interact importantly with amiodarone?
Digoxin
Verapamil
Diltiazem
Amiodarone increases their plasma levels, raising the risk of bradycardia, AV block, and heart failure.
223
How should digoxin, diltiazem, or verapamil doses be adjusted if starting amiodarone?
Their doses should be halved.
224
What is the primary clinical use of adenosine?
As a first-line diagnostic and therapeutic agent in supraventricular tachycardia (SVT).
225
What is adenosine’s plasma half-life?
<10 seconds — it is rapidly taken up by cells (e.g., red cells).
226
What are the common adverse effects of adenosine?
Bradycardia or transient asystole
Chest discomfort (sinking feeling)
Breathlessness
Feeling of impending doom (brief but unpleasant)
The unpleasant effects of adenosine are short-lived - half-life (<10 seconds).
227
Which drugs potentiate adenosine’s effect and require a lower dose?
Dipyridamole – it blocks adenosine uptake → dose should be halved.
228
Which drugs antagonize adenosine’s effects?
Theophylline
Aminophylline
Caffeine
(All are adenosine receptor antagonists)
