Cardio Quiz 2e - PHARM

eem8u's version from 2016-12-17 16:16

Drugs to Treat Angina and HTN

Question Answer
angina is caused bycardiac ischemia (in CAD_
main goal of tx of angina**reduce myocardial oxygen requirement**
3 mechanisms to reduce myocardial o2 demand1-decrease wall stress 2- decrease contractility 3- decrease HR
3 factors that INCREASE wall stress1- increase afterload (HTN, aortic stenosis) 2- increased preload (volume UP or venous dilation) 3- ventricular hypertrophy
***4 classes of drugs used to tx anginaNitrate, CC blocker, Beta blocker, late Na+ channel blocker (ranolazine)
drug used in hypertensive emergenciesnitroprusside (nitrate)
nitroglycerin - classnitrate
isosorbide dinitrate- classnitrate
nitroprusside- classnitrate (IV)
drug that causes headachenitrate (Vasodilation of meningeal artery)
drug that can cause cyanide poisoningNitroprusside (only with prolonged use)
drug w/ possible tachyphylaxis(tolerance) nitrates
nifedipine - classCCBlocker, dihydropyridine (DIPINE)
amlodipine - classCCBlocker, dihydropyridine (DIPINE)
diltiazem - classCCBlocker, NONdihydropyridine
verapamil - classCCBlocker, NONdihydropyridine
hydrochlorothiazide - classThiazide Diuretic
Ranolazine(Late NA+ Channel Inhibitor)
hydralazine - classvasodilator (mechanism unknown)
minoxidil - classunspecific vasodilator
***causes peripheral edemaall CCB’s, hydralazine, minoxidil
causes Lupus erythematous syndromehydralazine
causes hypertrichosisminoxidil (hair growth!)
must be taken with beta blocker and diureticminoxidil
action of drug specific to ischemic cellsranalozine


Question Answer
mechanism of action (all)nitrates release NO > stimulates cGMP production > de-phosphorylation of myosin light chain phosphate > smooth muscle relaxation > vasodilation
decreased myocardial O2 demand via1- venodilation (decreased preload) 2- arterial dilation (decreased afterload >> lower SVR) 3-arteriolar dilation (decreased afterload and BP)
secondary action/effectincrease coronary blood flow into ischemic area by DILATION of collateral vessels
clinical indication***angina (and HTN emergency, nitroprusside)
****contraindicationdo not use w/ PDE 5 inhibitor (also increase cGMP) >> extreme hypotension -- e.g. sildenafil
SE’s (3)reflex tachycardia, orthostatic hypotension, headache (dilation of mening. artery)
tx for tachyphylaxisdiscontinue overnight (esp with patch)


calcium channel blockers
Question Answer
site of action (2)smooth muscle and cardiac muscle, L-type Ca Channels (**though calcium channels are pervasive**)
mechanism of action (general)bind voltage gated L-type Ca Channels (Usually channels allow for Ca++ to enter cell >> Ca binds calmodulin >> plates MLCK >> cause contraction)
effect - nondihydropyridines (2)**cardiac ** 1- decrease cardiac contractility 2- decrease HR
****effect - dihydropyridinesvasodilation of arterioles & arteries >> lower SVR >> lower AFTERload
dihydropyridines - decreased myocardial O2 demand vialower afterload (no change in preload)
NONdihydropyridines - decreased myocardial O2 demand viareduce HR & reduce contractility
mechanism of decreased HR (2)(NONdihydropyridines) 1- negative dromotropy (at AV node, which is Ca dependent) 2- negative chronotropy (at SA node)
causes reflex tachycardianifedipine (b/c of vasodilation)
****no effect on HRamlodipine (b/c less reflex tachy)
clinical indications (3)angina, HTN, supra ventricular tachycardia (for nondihydropyridines)
***SE’s, general (3)hypotension, edema, constipation (b/c smooth muscles in gut)
***NONdihydropyridines - contraindicationCHF! causes bradycardia and reduced contractility
mechanism of edemavasodilation >> reduced renal perfusion >> increased renin >> AT II >> aldosterone >> na+ and h20 retention


Ranolazine (Late NA+ Channel Inhibitor)
Question Answer
mechanism of actionInhibits prolonged activation of Late Na+ channel (active at plateau phase 2) > decreased intracellular Na+ >> decreased Ca2+ in cell via Na/Ca exchanger (
site of action**ischemic myocardial cells**
decreased ***myocardial O2 demand viareduced intracellular Ca2+ (which causes impaired relaxation / electrical instability /cell death)
****clinical indication*stable angina
SEprolongs QT (b/c drug also blocks IKr)
why is there no risk of torsades de pointesb/c main action of late Na+ channel block + side action of IKR block balance extent of prolonged QT


Thiazide Diuretic
Question Answer
****mechanism of actionblock Na/CL symporter @ distal convoluted tubule (DCT) > na + h20 wasting
****side effects (3)hypotension, hypokalemia, volume depletion
change in K+ and mechanismHypokalemia >> more Na wasted >> more Na+ delivered to CD >> more Na reabsorbed via ENaC >> lumen more negative >> K+ excreted
clinical indications (2)1- HTN (more common than loop) 2- edema (loop diuretics are better)


Other Vasodilators
Question Answer
hydralazine - mechanism(unknown) dilates arterioles (NOT veins)
hydralazine - clinical indicationsHTN
***hydralazine - side effects (4)hypotension, reflex tachycardia, edema, drug-induced LUPUS erythematous syndrome
***minoxidil - mechanism(think one step before CC blocker )-- dilates arterioles (NOT veins) via OPENING ATP-dependent K+ channels > more K+ out > hyper polarization > inhibits voltage-gated Ca+ channels >> smooth muscle relations >> decrease blood pressure
minoxidil - clinical indicationsHTN (***not first line b/c of side effects)
****minoxidil - SE’s (4)hypotension, reflex tachycardia, edema, hypertrichosis
minoxidil - must be administered w/ (2)B-Blocker (for reflex tacky) and diuretic (for edema)

Lipid Altering Medications

Question Answer
_________% of LDL-C level regulated by hepatocyte receptors70%
mechanism of actionHMG CoA reductase inhibition > less LDL produced in liver >> lower intrac. [LDL] >> SREBP on ER activates more LDL-R expression >> MORE LDL-R on cell membrane *don’t forget role of SREBP**
Lovastatin - able to lower LDL- C by ____ %40%
most potentrosuvastatin (then atorvastatin)
explain rule of 6doubling dose of statin reduces LDL-C only another 6%
LDL-C and CHDlower LDL reduces both PRIMARY and Secondary (i.e. post MI) (effect greater in secondary >> primary)
**** 80 mg ATV (atorvastatin) yield ____ reduction in Mi/CHD death and ____ reduction in stroke22% / 25%
****SE’s (4)(as seen in ATV trial) 1- myalgia (lower extremities), 2- rhabomyalgia (super rare) 3- elevated liver enzymes (rare) 4- myopathy (rare)
grapefruit - metabolic effectinhibits CYP 450 3A4
grapefuit- consumption recommendations4-8 oz, 1/2 fruit per day OK
PCSK9 inhibitor (substilin/kexin) -mechanismmonoclonal antibody that targets protein responsible for LDL-R degradation >> increase LDL-receptor available and LDL uptake


Question Answer
mechanismblocks neiman pick receptor (INTESTINAL brush border) = blocks cholesterol absorption in gut >> decrease intrac [LDL] in hepatocyte >> more LDL-C receptors expressed
why does this work when you are not consuming cholesterolb/c endogenously produced LDL is reverse transported via HDL > Gut > taken up
_________% of LDL-C level reduction20%
***effect on HDL/TGNONE
***clinical use10 mg in combination with ATORVASTATIN (same effect w/ 10 mg ATV as 80 mg ATV alone) — ~50% reduction
SEmyalgia (rare)
FDA approval for (2)LDL-C lowering AND ischemic CV events (in combo with statin)


Bile Acid Binders
Question Answer
mechanismanion binders - take up bile acid >> inhibit cholesterol absortion
cholestyramine vs colesevelamolder generation has much more DRUG interference / newer gen only interferes with thyroid meds
_________% of LDL-C level reduction15-20%
advantage/disadvantagenot absorbed - very safe // difficult to take (big pill or gritty powder)
SE (2)constipation, interference with other drugs (levothyroxine, coumadin, fat soluble vitamins, birth control, phentoin) ***consuption must be staggered by 4 hours***
FDA approval for (2)LDL-C reduction, decrease of CHD events (within 3 years)
4 medications that reduce TG (related to next box)statin, fibrin acid, niacin (B3), fish oils


****Medications for Triglycerides
Question Answer
normal Triglycerides levels< 150 mg/dL
Chylomicrons appear at ____ mg/dL of TGTG > 1000mg/dL
chylomicrons are RF foracute pancreatitis at levels TG > 2000
elevated TG are risk factor forCHD (esp with low HDL)
statins that decrease TG’s (2) and ___ % reductionrosuvastatin & atorvastatin (between 20-28% reduction)
Fibric Acids- FDA approval forlower TG / prevent ischemic heart dx (Gemfibrozil only)
Fenofibrate reduces ischemic CV events in what conditionsSUPER HIGH TG (> 200) and low HDL (<40)
drug that raises statin levelsgemfibrozil
drug that raises creatininegemfibrozil (+statin)
Fibric acids - mechanism for TG (2)1- direct inhibit synthesis 2- increases VLDL clearance (via increase LPLipase, which takes TG into cell, and decrease APO c-III which degrades LPLipase)
*****Fibric acids-effect on LDLreduces NUMBER OF LDL particles (shifting LDL particle size from small >> large) = reduced LDL contact with endothelium
Fatty acids- FDA approval forlower TG (at 3 gm / day)
****Fatty acids-mechanismincrease hepatic proteolysis of VLDL (before secretion)


Medications for HDL
Question Answer
first lineNiacin (Vitamin B3)
statin w/ HDL raising efficacyRovstatin (also decreases TG)
Niacin (B3) - FD approval1- lower TG / 2- reduce CV events
Niacin & statin(mixed data), so NOT added to a statin to reduce CV events
Niacin- increase HDL by up to _____ %up to 25%