CVS drugs Flashcards
what are the 5 classes of CVS drugs to know
- lipid lowering drugs
- anti-hypertensives
- ischaemic heart disease drugs
- heart failure drugs
- anti-arrhythymic drugs
what are the 5 types of lipid lowering drugs?
SENd the FBi
S: statins E: ezetimibe N: niacin F: fibrates B: bile acid sequestrants
what are examples of statins?
simvastatin/lovastatin
what is the MOA of statins?
it is a HMG-CoA reductase inhibitor = prevents production of cholesterol and increases LDL receptor
after statins, what drug is next?
ezetimibe
what is the MOA of ezetimibe?
inhibits intestinal absorption of cholesterol (both from dietary and biliary sources)
after statins and ezetimibe, what drug comes next?
niacins (which are essentially vitamins b3)
what is the MOA of niacins?
inhibits lipolysis in adipose tissue and hence the triacylglyceride is used to make HDL instead of LDL/VLDL
after statins, ezetimibe and niacins, what drug class is next?
fibrates e.g. gemfibrozil
what is the MOA of gemfibrozil?
ligand activator of PPAR-alpha, which is involved in many general pathways; one of which involves activation of lipoprotein lipase
thus more LPL is activated to breakdown TG into free fatty acids which are stored by adipocytes = plasma TG decreases
after statins, ezetimibe, niacins and fibrates, what drug class is next?
bile acid sequestrants e.g. cholestyramine
what is the MOA of cholestyramine?
binds to bile salts in GI and decrease its reabsorption back into the system = hence depletes hepatic cholesterol to make more bile salts
when and how are statins administered?
orally in the evening, as cholesterol synthesis happens are night when the body is in a fasting state and there’s no dietary cholesterol to supplement
how are all these drugs administered?
all orally as you want into to enter GIT
what are the DDI’s of fibrates e.g. gemfibrozil?
recap: gemfibrozil is PPAR-a activator
it also displaces warfarin and potentiates anti-coagulants so risk of bleeding
what are the contraindications/side effects of bile acid sequestrants e.g. cholestyramine?
inhibits absorption of vitamin ADEK too, as well as many other drugs
so need to adjust dose and consider giving vitamin supplements
what is the general contraindication of lipid lowering drugs?
safe bet is to say that almost all are hepatotoxic (note that fibrates have additional renal toxicity)
except for statins (which cannot give at all), the rest are pregnancy cat c which means give with precautions
what is the standard therapy for lipid lowering?
first line is always to change diet and lifestyle
if that doesn’t work, consider giving drugs; in which statins will be first line
moving on from lipid lowering drugs, what are the anti-hypertensive drugs?
A: ace-1 inhibitor or angiotensin-2 type 1 inhibitor B: b blockers C: calcium channel blocker D: diuretics V: vasodilators
what are the drug examples of ace-1 inhibitor and angiotensin-2 type 1 inhibitor?
- -prils = ACE1 inhibitor
2. -sartans = Angiotensin 2 type 1 inhibitor
what is the MOA of ACE 1 inhibitor?
- blocks angiotensin-converting enzyme
- decreases vasoconstriction
- blocks inactivation of bradykinin so it can continue to vasodilate
what is the MOA of angiotensin-2 type 1 inhibitor?
blocks angiotensin 2 type 1 receptor directly
what is important about the effects of ACE-1 inhibitor?
it simultaneously resets pressure sensor sensitivity and hence blocks the baroreceptor reflux to increase BP when the BP drops
what are the drug examples of b blockers?
should be b1 blockers such as atenolol and betaxolol
what is the MOA of b1 blockers?
decrease HR and contractility
what are the drug examples of calcium channel blockers?
- verapamil/diltiazem
- nifedipine
what is the MOA of verapamil/diltiazem?
blocks Ca channel to decrease intracellular Ca = decreased conductivity
what is the MOA of nifedipine?
blocks Ca channel + decrease smooth muscle tone
recap: what is the pathway of depolarisation and repolarisation of cardiac myocytes?
- sodium-potassium pump maintains negative membrane potential
- depolarisation happens when Na+ channels open and enters cell
- repolarisation begins when K channels open again to let K+ out
- repolarisation slows down as Ca2+ channels open and works against the repolarisation
- Ca2+ channels close and K+ continues to go out until repolarisation is complete
what are examples of diuretics?
loop diuretics like furosemide
and thiazides
what is the MOA of loop diuretics like furosemide?
affects ascending limb of Loop of Henle
blocks the Na/K/2Cl so there’s less K in the tubular cells, which means there’s less K available to be exchanged out for Mg and Ca that is taken back in during reabsorption = more Mg and Ca excretion along with water
what are the side effects/contraindications of loop diuretics?
- hypokalaemic metabolic alkalosis
ultimately K is taken from blood in exchange with Na (which is then in the blood), so that this K can be used to exchange with Mg and Ca
- dehydration
- acute renal failure
what is the MOA of thiazides?
affects distal convoluted tubule
blocks NaCl transporter so there’s less NaCl in the tubular cells, thus cell compensates by increasing Ca channel uptake
what are the side effects/contraindications of thiazides?
tbh same as loop diuretics
- hypoK metabolic alkalosis
- dehydration
- acute renal failure
what are the drug examples of vasodilators?
minoxidil
what is the MOA of minoxidil?
it is dilates arterioles only and not veins
it is a K+ channel opener = makes cell hyper polarised and prevents Ca channel from opening = decreased contractility
fun fact: can be used to help male pattern baldness
what are the side effects/contraindications of minoxidil?
it can cause reflex sympathetic stimulation (which ACE-1 inhibitor does not)
hence must be used together with diuretics and is used only for severe to malignant hypertension
drug combinations for angina
you can’t really work with the vessels so you just aim to increase contractility
- b1 blockers
- Ca channel blockers
drug combinations for congestive heart failure
you want to work on reducing volume load so use ACE inhibitors
drug combinations for MI
you want to increase contractility and also hope to decrease preload
- b1 blockers
- ACE inhibitors
what anti-hypertensive is contraindicated in renal patients?
ACE inhibitors
what anti-hypertensives are contraindicated in pregnant?
ACE inhibitors
what anti-hypertensives are contraindicated in asthmatics?
B blockers
moving on from lipid lowering drugs and anti-hypertensives, what is a drug used in ischemic heart disease?
drug class: nitrates
drug example: nitroglycerin
what is the MOA of nitroglycerin?
releases NO in smooth muscles, leading to smooth muscle relaxation of both veins and arteries
(compared to minoxidil which is only arteries)
how does venodilation and arteriole dilation help IHD?
venodilation = decreased preload
arteriole dilation = decreased afterload
together = decreased O2 consumption
therapy for heart failure can be split based on early HF and late HF; name the aims of therapy for each type
early HF: aim to increase contractility
late HF: aim to decrease volume load
what drugs are used in early HF (with the aim to increase contractility)?
positive inotropic drugs:
- cardiac glycosides e.g. digoxin
- beta 1 agonist e.g. dobutamine
- PDE inhibitor (also used for late HF)
what drugs are used in late HF (with the aim to decrease volume load)?
- vasodilators like nitrates e.g. nitroglycerin
- anti-hypertensive drugs (ACE inhibitors and diuretics)
- PDE inhibitor (also used for early HF)
what is the MOA of cardiac glycosides like digoxin?
inhibits NA/K ATPase = increased Na = less Ca efflux = more Ca in the cells = increased contractility
opposite of calcium channel blockers
what is digitoxin?
more toxic version of digoxin that has a longer half-life and a stronger affinity
when do we use digitoxin preferentially over digoxin?
when the patient has renal impairment, use digitoxin instead
what are drug examples of PDE inhibitors?
sildenafil (viagra) and other -afils
what is the MOA of PDE inhibitors?
increase cAMP = increases Ca = increased contractility
finally we move on to the last drug type, which is anti-arrythmics - what are the 4 diff drug classes?
class 1A, 1B, 1C class 2 class 3 class 4
what is the MOA of class 1?
targets Na channel and blocks it = prolongs phase 0 so the cardiac myocytes cannot be depolarised
what are examples of class 1 drugs?
1A: procainamide
1B: lidocaine
1C: flecainide
what is the MOA of class 2?
B blocker = suppresses phase 4
what are the examples of class 2 drugs?
any b blocker e.g. propranolol
what is the MOA of class 3?
targets K channel and blocks it = prolongs phase 3 repolarisation
what are the examples of class 3 drugs?
amiodarone
what is the MOA of class 4?
targets Ca channel and blocks it = delays phase 2 repolarisation = prolongs action potential
