2.1.1 Hypertension drugs

module 2 cardiovascular drugs

What do ACE inhibitor drugs end in

-pril

What do ACE inhibitors inhibit

the conversion of Angiotensin I to Angiotensin II (hence reducing aldosterone release); by competitively inhibiting ACE conversion enzyme

What is a common side effect of ACE inhibitors that causes most people to switch to an ARAs if they experience it

Dry cough (5-20% of people) - due to inhibiting the breakdown of vasodilator kinins

Name 4 drug interactions that occur with ACE inhibitors

1) Potassium supplements - increased risk of hyperkalaemia

2) Loop diuretics - increased risk of severe hypotension

3) NSAIDs - May reduce antihypertensive effect of ACE I

4) Thiazide diuretics - increased risk of severe hypotension

Angiotensin Receptor Antagonists (ARAs) drugs end with

-sartan

Mechanism of Action of ARAs

Competitively block the binding of ANGII to ANGII(subtype 1) receptors. Hence reduce angiotensin-II-induced vasoconstriction, sodium reabsorption, and aldosterone release

What are common adverse effects of ARAs

Dizziness, hyperkalaemia, headache

Name 4 drug interactions that occur with ARAs

Diuretics: Prior treatment with diuretics and increased risk of excessive hypotension.

K+, K-sparing diuretics, cyclosporin: increased risk of hyperkalaemia.

NSAIDS (including selective COX-2 inhibitors): May decrease antihypertensive response & increase risk of hyperkalaemia or acute renal failure.

Lithium: Decreased excretion of Li+ , increased risk of Li+ toxicity

What are the 8 vasodilator drugs

1. Calcium channel blockers (nifedipine, diltiazem, verapamil)

2. Potassium channel activators (nicorandil, minoxidil, diazoxide) Unknown Mechanism (Hydralazine)

3. Endothelial NO production stimulators (sodium nitroprusside, perhexiline)

4. Organic nitrates (glyceryl trinitrate)

5. Angiotensin converting enzyme inhibitors (enalapril, ramipril, lisinopril, captopril, fosinopril, perindopril, quinapril, trandolapril)

6. Angiotensin II ATI receptor blockers (irbesartan, losartan, candesartan, eprosartan, olmesartan, telmisartan, valsartan)

7. Alpha blockers (prazosin, terazosin)

8. Beta blockers (atenolol, bisoprolol, carvedilol, esmolol)

What are the 3 types of calcium channel blockers and give an example of each

Dihydropyridines - Amlodipine , Felodipine, Lercanidipine, Nifedipine, Nimodipine, Clevidipine

Benzothiazepines - Diltiazem

Phenylalkylamines - Verapamil

Which CCB is used for prophylaxis of angina

Dihydropyridines

Which CCBs are used for prevention and treatment of supraventricular arrhythmias

Non-dihydropyridines; Diltiazem, Verapamil

mechanism of action of calcium channel blockers

Blocking inward current of Ca2+ into cells in vascular smooth muscle, myocardium and the cardiac conducting system. Via binding to the calcium channels, altering the conformation of channel, and preventing entry of calcium. Inhibiting voltage-gated L-type Ca+ channels

NET EFFECT; smooth muscle relaxation, and suppression of cardiac activity

Calcium channel blockers are used because they create the pathophysical effects of;

1)Dilate coronary arteries and peripheral arterioles but NOT veins.

2)Cardiac contractility

3)Automaticity at SA

4)Conduction at AV node

DONT FORGET TO FIND WALLY!

PURRR LISA TEE!

What are diuretics

Drugs that enhance the renal excretion of salt and water

Clinical uses of different diuretics are:

Volume depletion in hypertension (thiazides, potassium sparing diuretics)

Managing fluid overload in heart failure (loop diuretics, aldosterone antagonists)

Hypercalciuria with kidney stone formation (thiazides)

Acute brain injury (mannitol)

Osmotic Diuretics include

Mannitol

Loop or High Ceiling Diuretics include

Frusemide

Thiazides related Diuretics include

Chlorthalidone , Hydrochlorothiazide. Indapamide

Aldosterone Antagonists

Spironolactone, Eplerenone

Where do thiazide diuretics work on in he nephron

Distal convoluted tubule

What are the adverse effects of thiazide diuretics

Loss of electrolytes as with the loop diuretics

Hyperuricaemia-gout uric acid retention (competes for weak acid excretory pathway)

Orthostatic hypotension, dizziness

Suppression of lactation

Hyperglycaemia-diabetics (impaired glucose tolerance)

Hypercalcaemia

What drugs make up the triple whammy

Diuretics (Thiazides, loop diuretics), ACE inhibitors / angiotensin receptor antagonists, NSAIDs

What are two Alpha-1 selective receptor antagonists

Prazosin and Terazosin

Sleective alpha-1 adrenergic antagonists mechanism of action is:

Blocks alpha1 (postsynaptic) receptors

VASODILATION - Dilate arteries and veins

Reduce tone in arteriolar resistance vessels

Dilate venous capacitance vessels which reduce venous return and cardiac output

Very little effect on presynaptic alpha2-adrenoceptors much less likely to cause reflex tachycardia than nonselective alpha-blockers

Prazosin is less likely to cause tachycardia because

Prazosin does not block α2 receptor-mediated inhibition of noradrenaline (NA) release.

Beta blockers drugs end in

-olol

Beta-blockers mechanisms of actions are;

Decrease cardiac contractility and heart rate

Decrease cardiac output without reflex increase in peripheral vascular resistance

Reduce sympathetic outflow from CNS (vasomotor centre) to the peripheral blood vessels

Decrease in renin secretion from the kidney

Decrease peripheral vascular resistance

Precaution should be considered before giving beta-blockers to a person with diabetes because

Beta-blockers may mask signs of hypoglycaemia & delay recovery from hypoglycaemia

Centrally acting hypertensives are selective alpha 2 agonists, example of these drugs included

Methyldopa, Clonidine, and Moxonidine

Mechanism of action of Selective Alpha 2 adrenergic agonists are;

Reduces sympathetic tone

Vasodilation and decrease heart rate and contraction

Methyldopa is often used to treat hypertension in what particular condition

Pregnancy - (CNS and hepatic adverse effects limit its use in non-gestational hypertension)

also has common adverse effect of sedation (which is made worse by dose increases), light-headedness, headache, dizziness, tiredness, and fever

What is the difference between a dihydropyridine CCB and a non-dihydropyridine CCB

Dihydro; Primarily work on arteriolar vascular smooth muscle

Non-dihydro: Have effects on cardiac muscle and arteriolar smooth muscle