Antihypertensive drugs Flashcards
Thiazide diuretics
1) Give an example of this type of drug
2) How do they work?
3) Name a side effect of these drugs
1) Indapamide, chlorothiazide and metolazone
2) Blockade of the Na/Cl channel in the distal convoluted tubule - decreasing the amount of sodium that crosses the luminal surface, therefore decreasing the action of the Na/K pump, which decreases sodium and water passage into the interstitium
3) Hypokalaemia, hypercalcaemia, raised urate which can cause gout, sexual dysfunction
Loop diuretics
1) Give an example of this type of drug
2) How do they work?
3) Name a side effect of these drugs
1) Furosemide, bumetanide
2) Inhibit the Na/K/2CL co-transporter in the thick ascending loop of Henle, reducing the reabsorption of those electrolytes. This increases how much water is drawn from the nephron to increase urine volume
3) Ototoxicity (hearing or balance problems), hypokalaemia, hypocalcemia, hyponatraemia
Potassium sparing diuretics
1) Give an example of this type of drug
2) What are the 2 main differences between these diuretics and the other 2 types?
3) How do they work?
1) Spironolactone, amiloride, eplerenone
2) They aren’t as powerful as the other 2 and they don’t cause the loss of potassium
3) Interfere with the Na/K exchange in the distal convoluted tubule and antagonise aldosterone receptors. As aldosterone promotes the retention of sodium and water, blocking this effect increases diuresis. By not promoting the secretion of potassium during diuresis, they decrease the risk of hypokalemia unlike other diuretics
Beta blockers
1) How do they work?
2) Which receptor - alpha adrenoreceptor or beta receptor is found on the heart (and therefore the target of cardioselective beta blockers)?
3) Name a selective beta blocker
4) Name a non-selective beta blocker
5) Name a side effect of these drugs
6) How is beta blocker overdose managed?
1) Bind to βadrenoreceptors therefore blocking the effect of adrenaline and noradrenaline on these receptors, inhibiting normal sympathetic effects which results in a decrease in: HR, heart contractility, conduction velocity in the heart and the relaxation rate of the heart
2) Beta
3) Atenolol, bisoprolol, metoprolol
4) Labetalol, propranolol, pindolol and timolol
5) lethargy, ED, headache, bradycardia, hypotension
6) Glucagon
ACE inhibitors (1)
1) Give an example of this type of drug
2) How do they work (4)?
3) Name a side effect of these drugs
1) Ramipril, lisinopril, enalapril, captopril
2) ACE inhibitors cause vasodilation by inhibiting the formation of angiotensin II which is a vasoconstrictor. ACE also breaks bradykinin down which is a vasodilator therefore inhibiting the breakdown of bradykinin contributes to the vasodilator effect of ACE inhibitors. ACE inhibitors also downregulate sympathetic adrenergic activity by blocking the facilitating effect angiotensin II has on sympathetic nerve release of adrenaline and noradrenaline. Angiotensin II also promotes the reabsorption of water and sodium through the stimulation of aldosterone release. ACE inhibitors inhibit this effect, which reduces blood volume, venous pressure and arterial pressure
3) Dry cough, hyperkalaemia, angioedema,
ACE inhibitors (2)
1) Name 2 cautions/indications of ACEi
2) A rise in serum potassium and creatinine may be seen with ACE - what increase is acceptable of both?
3) If K+ does increase more than what is acceptable, what is done?
1) Pregnancy, renovascular disease, aortic stenosis. Specialist advice if K+ >5 mmol\L
2) K+ up to 5.5mmol\L. Creatinine <30% increase from baseline.
3) ECG
Angiotensin receptor blockers (ARB’s)
1) Give an example of this type of drug
2) How do they work?
1) Candesartan, losartan, olmesartan and eprosartan
2) Receptor antagonists that block type 1 angiotensin II (AT1) receptors on blood vessels and the heart - inhibiting the effect of angiotensin II on them (vasoconstriction)
Calcium channel blockers (CCB’s)
1) How do they work?
2) What is the most smooth-muscle-selective class of CCBs, and give an example
3) Which class of CCB’s is used in the treatment of hypertension, and which is used in the treatment of angina + arrhythmias?
4) Give an example of non-dihydropyridine CCBs
5) What group of drugs should non-dihydropyridines NOT be given with?
6) Name a contraindication for CCBs
7) NAme a side effect of CCBs
1) Bind to L-type calcium channels that’re located on the vascular smooth muscle, cardiac myocytes and cardiac nodal tissue which results in vascular smooth muscle relaxation (vasodilation), a decreased myocardial contractile force (negative inotropy), a decreased heart rate (negative chronotropy) and a decreased conduction velocity in the heart (negative dromotropy) specifically at the AV node
2) Dihydropyridines - amlodipine and nifedipine
3) Dihydropyridines for hypertension, non-dihydropyridines for angina and arrhythmias
4) Verapamil, diltiazem
5) Beta blockers
6) Heart block
7) Headache, flushes, ankle oedema
Alpha blockers
1) Give an example of these drugs
2) How do they work?
3) What does stimulation of alpha1 adrenoreceptors cause?
4) What does stimulation of alpha2 adrenoreceptors
1) Prazosin, doxazosin
2) Drugs block the effect of sympathetic nerves on blood vessels by binding to α adrenoreceptors located on the vascular smooth muscle by acting as a competitive antagonist
3) Vasodilation
4) Vasodilation + increase the release of NA and adrenaline
Alpha 2 receptor antagonists
1) How do these drugs work?
2) Give an example of these drugs
1) Block sympathetic activity by binding to and activating α2 adrenoreceptors. This has the effect of reducing sympathetic outflow to the heart therefore decreasing cardiac output by decreasing heart rate and contractility. Reduced sympathetic output to the vasculature decreases sympathetic vascular tone, which causes vasodilation and reduced systemic vascular resistance, which decreases arterial pressure
2) Clonidine, guanfacine
