Cardiovascular drugs Flashcards
What are the 3 main groups of anti-cholestrol drugs ?
- Statins (simvastatin, atorvastatin)
- Fibrates
- PCSK 9 Inhibitors (evolocumab, alirocumab)
What are the 4 main groups of anti-hypertensive drugs?
- Thiazide Diuretics
- Beta Blockers
- Vasodilators = Calcium channel blockers (CCB), Alpha Blockers, ACE Inhibitors (ACEI) & Angiotensin Receptor Blockers (ARBs)
- Mineralocorticoid antagonist (spironolactone)
How do you recognise what is a statin ?
Think ‘statin’ at the end of its name e.g. simvastatin or artorvastatin
What is the mechanism of action of statins ?
They inhibit the action of HMG-CoA reductase
Who should recieve a statin ?
- All people with established CVD (stroke, TIA, ischaemic heart disease e.g. angina/MI, PVD)
- Anyone with a 10-year cardiovascular risk >= 10% (using QRISK2)
- Patients with T2DM should be assessed using QRISK2 like other patients are, to determine whether they should be started on statins
- Patients with T1DM who were diagnosed more than 10 years ago OR are aged over 40 OR have established nephropathy
What are the 2 main contraindications to statin use ?
- Macrolides (e.g. erythromycin, clarithromycin)
- Pregnancy
What are the main potential adverse effects of statin use ?
- Myopathy - myalgia, myositis, rhabdomyolysis and asymptomatic raised creatine kinase
- Rhabdomyolysis can lead to renal failure
- Liver impairment
- Avoid in those who have had a stroke due to increased risk of ICH
Give examples of fibrates and state what they are used for
- e.g. Bezafibrate (think ‘fibrate’)
- They are used for hypertriglyceridaemia or low HDL cholesterol
How do PCSK 9 Inhibitors (evolocumab, alirocumab) work and what condition may they be used for (not 1st line tho)
- Work by binding of PCSK9 to LDLR, this increases the number of LDLRs, thereby lowering LDL-C levels
- May be used for Familial Hypercholesterolaemia
Diuretics actions etc are covered in renal flashcards
What are the 2 main groups of beta-blockers and there mechanisms of actions?
- Cardioselective β Blockers - Only block β1 adrenoreceptors
- Non selective β Blockers - Block both β1 and β2 adrenreceptors
How do you recgonise a beta-blocker?
Think ‘olol’
Give examples of cardioselective beta-blockers and there main uses
- e.g. Atenolol, bisoprolol
- Used in angina, ACS, MI, hypertension and heart failure
Give examples of non-selective beta-blockers and there main uses
- e.g. Propranolol, carvedilol (is both alpha & beta-blocker)
- Used in thyrotoxicosis, migraine
What are the main side effects of beta-blockers?
- bronchospasm - contraindicated in ‘severe’ asthma
- cold peripheries
- fatigue
- sleep disturbances, including nightmares
- erectile dysfunction
- Can worsen heart failure in short term (esp cardiogenic shock ==> not used actuley in HF)
What are the 2 main groups of calcium channel blockers(CCB’s) and give examples of them ?
- Dihydropyridines e.g. Amlodipine, nifedipine, felodipine (think ‘ipine’)
- Rate limiting CCB’s e.g. Verapamil & Diltiazem
What is the general mechanism of action of CCB’s?
Voltage-gated calcium channels are present in myocardial cells, cells of the conduction system and those of the vascular smooth muscle.
What is the difference in the action of dihydropyridines compared to rate limiting CCB’s ?
Dihydropyridines affect the peripheral vascular smooth muscle more than the myocardium and therefore do not result in worsening of heart failure
When may dihydropyridines be used?
Used in hypertension and angina
What are the main side effects of dihydropyridines ?
- Flushing
- Headache
- Ankle swelling
When may rate-limting CCB’s be used ?
- Used in hypertension and angina
- Plus Supraventricular Arrhythmias (AF, SVT)
What are the main side effects associated with rate-limiting CCB’s?
- Hypotension
- Bradycardia
- Heart failure
Ankle swelling - dilatiazem
Constipation & flushing - Verapamil
What is the mechanism of action of ACEi’s & give examples of them
- They inhibit the conversion angiotensin I to angiotensin II
- e.g. Lisinopril - think ‘pril’
When are ACEi’s used?
- Used in hypertension and heart failure
- Diabetic nephropathy and have a role in the secondary prevention of IHD
What are the contraindications to ACEi use?
- Pregnancy and breastfeeding - avoid
- Renovascular disease - bilateral renal artery stenosis
- Aortic stenosis - may result in hypotension
- Hereditary of idiopathic angioedema
- specialist advice should be sought before starting ACE inhibitors in patients with a potassium >= 5.0 mmol/L
What are the main side effects of ACEi’s?
- Cough
- Renal dysfunction
- Hyperkalaemia
- Angioedema
What is the mechanism of action of ARB’s & give examples of them
- Block effects of angiotensin II at the AT1 receptor
- e.g. Candesartan & Losartan think ‘sartan’
When are ARB’s used ?
When ACEi is not tolerated usually due to the development of a cough. (i.e. same uses as ACEi’s)
What are the main side effects of ARB’s?
Like ACE inhibitors they should be used with caution in patients with renovascular disease (dont use if renal artery stenosis)
Side-effects include:
- Hypotension
- Renal dysfunction
- Hyperkalaemia.
What is the mechanism of action of alpha blockers & give examples of them?
- Block a adrenoceptors to cause vasodilatation
- e.g. doxazosin (for HTN) and tamsulosin (for BPH)
What are the uses of alpha blockers ?
Use in hypertension and BPH
What are the side effects of alpha blockers?
- Postural hypotension
- Drowsiness
- Dyspnoea
- Cough
When should caution be taken in the use of alpha blockers?
Patients who are having cataract surgery due to the risk of intra-operative floppy iris syndrome
Mineralocorticoid antagonists covered in renal flashcards
What are the 3 main groups of vasodilating drugs ?
- Nitrates
- Nicorandil (K ATP channel opener)
- Calcium Antagonists (Dihydropyridine)
What are the 3 main groups of drugs used to slow heart rate ?
- Beta Blockers
- Calcium Antagonists (Diltiazem, Verapamil)
- Ivabradine
What is the mechanism of action of nitrates & give examples of them
- Mechanism of action = vasodilators by causing the release of NO in smooth muscle, resulting in converting GTP to cGMP, which in turn leads to a fall in intracellular calcium levels
- e.g. Isosorbide mononitrate, GTN & isosorbide dinitrate
When are nitrates used ?
Angina & Acute heart failure
What are the side effects of nitrates ?
- Headaches & flushing
- Hypotension/Collapse
- Tachycardia
What is recommended to help prevent nitrate tolerance developing ?
Leave 8 hr/day nitrate-free
What is the mechanism of action of nicorandil and its use
- It is a potassium-channel activator with vasodilation is through activation of guanylyl cyclase which results in increase cGMP.
- Used to treat angina
What are the side effects of nicoradnil and the one contraindication to its use
- Headache & flushing
- Mouth/GI ulceration
- Contraindicated if LVF
What is the mechanism of action of ivrabradine & its use
- Acts on the If (‘funny’) ion current in the SA node to reduce HR
- Use in angina & HF
What are the side effects of ivrabradine ?
- Altered visual disturbance
- Headache
- Bradycardia, heart block
What is the mechanism of action of Ranolazine & its use ?
- It is a late sodium channel modulator which decreases calcium load on heart
- Effective for refractory angina
What is the mechanism of action of fibrinolytic drugs & give examples of them
- Thrombolytic drugs activate plasminogen to form plasmin. This in turn degrades fibrin and help breaks up thrombi.
- e.g. alteplase, tenecteplase, streptokinase & tissue Plasminogen activator (tPA)
What is the main use of fibrinolytic drugs ?
- Primarily used for STEMI
- But sometimes used for PE’s or strokes (selected cases only)
What is the main side effect of fibrinolytic drugs ?
Haemorrhage serious risk
What are the main contraindications to fibrinolytic drug use ?
- Recent haemorrhage (stokes < 3months), trauma or surgery
- Bleeding tendencies or active bleeding
- Severe diabetic retinopathy
- Peptic ulcer
What is the mechanism of action of digoxin ?
- Blocks atrial-ventricular (AV) conduction which slows HR in AF or atrial flutter (good effect)
- Increases ventricular irritability which produces ventricular arrhythmias (bad effect)
What is the main use of digoxin ?
Rate control in AF
What is the problem with digoxin ?
It has a narrow theraputic window so easy to result in digoxin toxicity
What are the signs of digoxin toxicity ?
- Nausea, vomiting
- Yellow-green vision
- Bradycardia, Heart Block
- Ventricular Arrhythmias
What is the management of digoxin toxicity ?
- Digibind
- correct arrhythmias
- monitor potassium
