MP323 - CVD DRUGS Flashcards by olivia rucka

antihypertensives indicated in heart failure

diuretic
beta blocker
ACE-I
ARB
aldosterone antagonist

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antihypertensives indicated post MI

beta blocker
ACE-I
aldosterone antagonist

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antihypertensives indicated in coronary artery disease risk

diuretic
beta blocker
ACE-I
CCB

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antihypertensives indicated in diabetes

diuretic
beta blocker
ACE-I
ARB
CCB

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antihypertensives indicated in chronic kidney disease

ARB
ACE-I

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antihypertensives indicated in recurrent stroke prevention

diuretic
ACE-I

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loop diuretics

furosemide supplemented with spironolactone or amiloride
- works in PCT and loop of henley
- inhibit Na+/K+/2Cl co transporter

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thiazides (diuretics)

bendroflumethiazide
- work in distal convoluted tubule
- inhibit the Na+/Cl- cotransporter

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potassium-sparing diuretics

amiloride, eplerenone, spironolactone
- act in collecting duct
- not acting directly on Na+ channels

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renin inhibitors

aliskiren
beta-1 antagonists
catalyses the cleavage of angiotensinogen to angiotensin I

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ACE inhibitors

ramipril, captopril, lisinopril, enalapril
- ACE is a membrane-bound enzyme
- catalyses the conversion of angiotensin I to angiotensin II

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ACE inhibitors effect on the heart

reduces peripheral vascular resistance which lowers BP
reducing aldosterone levels promotes sodium and water excretion which can help to reduce venous return

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ARBs (angiotensin receptor blockers)

losartan, valsartan, candesartan
- block the action of angiotensin II on the AT1 receptor

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aldosterone antagonists

spironolactone, eplerenone
- competitively bind to aldosterone receptor
- promote sodium and water excretion in the collecting tubule and duct

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beta blockers

block of cardiac beta-1 receptors decreasing HR, contractility and CO

blockage of beta-1 receptors in JG cells in kidney, decreasing renin release

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non-selective beta blockers

propanolol, carvedilol, timolol
- used to prevent recurrent variceal haemorrhage in patients with cirrhosis and portal hypertension (bad liver function)

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selective beta-1blockers

atenolol, bisoprolol, metoprolol
- used in heart therapy

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CCBs (dihydropyridines)

nifedipine, amlodipine
- block Ca channels in arterioles
- do not block cardiac channels at therapeutic doses

CCBs (dihydropyridines) effects on the heart

indirect reflex effect which increases HR and contractility of heart - may not be desirable in someone with heart disease

CCBs (non-dihydropyridines)

verapamil, diltiazem
both cardiac specific

will reduce Ca2+ in cells and cause a reduction in vascular tone (NOT VASODILATORS)
indirect vasodilatory effect
act on heart to slow conduction and decrease contractility (arrhythmia)

alpha-1antagonists (alpha-blockers)

Prazosin, doxazosin, tamsulosin
- inhibit smooth muscle contraction
- used in hypertension and benign prostate hypertrophy

alpha-2 agonists (sympathomimetics)

clonidine
- stimulates alpha-adrenoceptors in the brain stem
- results in reduced sympathetic outflow from CNS
- decreases in peripheral resistance, renal vascular resistance, HR and BP

aspirin MOA

blocks production of thromboxane A2 by inhibiting COX1 which is responsible for its synthesis

action is permanent lasting the lifespan of the platelet (7-10 days)

clopidogrel MOA

ADP is a platelet agonist produced and released by platelets

irreversible inhibitor of ADP receptor on platelets and so prevents ADP from activating platelets

statins MOA

lipid-lowering drugs reduce plasma LDL HMG-CoA reductase inhibitors, and so inhibit the synthesis of cholesterol

alleviation of angina symptoms

BBs FIRST LINE - if intolerant treat with rate-limiting CCB, long-acting nitrates or nicorandil inadequate control of symptoms - add a CCB sublingual GTN tabs or spray for immediate relief

nitrates MOA

- relax coronary arteries and veins decreasing preload, myocardial oxygen consumption and increasing myocardial perfusion - nitrates donate nitric oxide, stimulates cGMP cyclase increasing cGMP to decrease calcium entry and increase calcium removal

nitrates

glyceryl trinitrate (GTN), isosorbide mononitrate, isosorbide dinitrate

K+ channel activators

nicorandil activation of K+ ATP channels on smooth muscle cells hyperpolarises the membrane and decreases calcium entry

ticagrelor

antiplatelet inhibits P2Y12 ADP-receptor preventing platelet activation benefit with dual antiplatelet therapy

secondary prevention (A,B,C,D,E)

A - antiplatelet, ACE-I/ARB B - BB, breathing C - cholesterol, cigarettes D - diuretic, diet, diabetes E - eplerenone, education

penetration enhancers

dimethysulfozide, lecithin, water, oleic acid, azone

use of diuretics in HF

- loop diuretics usually required - aim for lowest possible dose - require monitoring of renal function and electrolytes - symptom control

use of ACE inhibitors in HF

- most evidence for enalapril - aim to reach target dose 20mg - not to lower BP but symptom control - require renal monitoring after initiation and dose change

use of ARBs in HF

- similar effect to ACE-I - candesartan/valsartan - can combine with ACE-I for more benefit - can be used if intolerant to ACE-I

use of beta blockers in HF

- reduce hospitalisation, morbidity and mortality - patient's HF must be stable before initiation - avoid abrupt withdrawl

use of ivabradine in HF

- reduce mortality and hospitalisation - use in beta-blocker intolerant patients or in combo with BB if HR>75bpm - avoid grapefruit

use of aldosterone antagonists in HF

- reduces morbidity and mortality when added to treatment in advanced patients - eplerenone reduced mortality when added to treatment in MI complicated by HF or spironolactone intolerant patients

use of digoxin in HF

- indicated in AF with HF - consider patients who can't tolerate ACE-I/ARB - narrow therapeutic index - careful in patients with hyperkalaemia

use of vasodilators in HF

hydralazine combined with isosorbide dinitrate - inferior to ACE-I - only indicated if patient remains asymptomatic and all other options explored - use in renal impairment

drugs that exacerbate HF

- NSAIDs/COX-2 inhibitors - rate-limiting CCBs - chemotherapy - anti-psychotics - glitazones - corticosteroids and fluid retaining drugs - meds with high Na content

warfarin

- inhibits synthesis of vitamin K dependent clotting factors - delayed onset of action as clotting factors decline - daily monitoring of INR

oral anticoagulants

warfarin, rivaroxaban, apixaban, edoxaban