MP323 - CVD DRUGS Flashcards
antihypertensives indicated in heart failure
diuretic
beta blocker
ACE-I
ARB
aldosterone antagonist
antihypertensives indicated post MI
beta blocker
ACE-I
aldosterone antagonist
antihypertensives indicated in coronary artery disease risk
diuretic
beta blocker
ACE-I
CCB
antihypertensives indicated in diabetes
diuretic
beta blocker
ACE-I
ARB
CCB
antihypertensives indicated in chronic kidney disease
ARB
ACE-I
antihypertensives indicated in recurrent stroke prevention
diuretic
ACE-I
loop diuretics
furosemide supplemented with spironolactone or amiloride
- works in PCT and loop of henley
- inhibit Na+/K+/2Cl co transporter
thiazides (diuretics)
bendroflumethiazide
- work in distal convoluted tubule
- inhibit the Na+/Cl- cotransporter
potassium-sparing diuretics
amiloride, eplerenone, spironolactone
- act in collecting duct
- not acting directly on Na+ channels
renin inhibitors
aliskiren
beta-1 antagonists
catalyses the cleavage of angiotensinogen to angiotensin I
ACE inhibitors
ramipril, captopril, lisinopril, enalapril
- ACE is a membrane-bound enzyme
- catalyses the conversion of angiotensin I to angiotensin II
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
ARBs (angiotensin receptor blockers)
losartan, valsartan, candesartan
- block the action of angiotensin II on the AT1 receptor
aldosterone antagonists
spironolactone, eplerenone
- competitively bind to aldosterone receptor
- promote sodium and water excretion in the collecting tubule and duct
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
non-selective beta blockers
propanolol, carvedilol, timolol
- used to prevent recurrent variceal haemorrhage in patients with cirrhosis and portal hypertension (bad liver function)
selective beta-1blockers
atenolol, bisoprolol, metoprolol
- used in heart therapy
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
