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Cardio Quiz 2e - PHARM

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

Drugs to Treat Angina and HTN

****OVERVIEW
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
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Nitrates
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)
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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
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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
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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)
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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)
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Lipid Altering Medications

Statins
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
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*****Ezetimibe
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)
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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
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****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)
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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%
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