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202 Cards in this Set
- Front
- Back
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what is the receptor for cholesterol absorption?
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Niemann-pick C1-like 1 protein (NPC1L1)
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chylomicrons are the _____ plasma lipoproteins as well as the ____, they are ____% lipid
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1. largest
2. least dense 3. 98-99 |
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what tissues synthesize lipoprotein lipase?
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skeletal and cardiac muscle, adipose tissue, breast tissue of lactating women
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what is released from lipoprotein lipase with broken down triglycerides?
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chylomicron remnants
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what are the two receptors for ApoE in the liver?
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LDLR and LRP
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what is rate limiting step of the endogenous pathway of lipid metabolism?
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conversion of HMG-CoA to melvalonate using the enzyme HMG-CoA reductase
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what makes up VLDLs?
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cholesterol, CE, apoB-100, triglycerides, and phospholipids, apoE
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what are VLDL remnants called?
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intermediate-density lipoproteins (IDLs)
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what is produced when IDLs interact with hepatic lipase and apoE is removed?
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low density lipoproteins (LDLs)
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what do HDLs do?
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regulate the blood levels of cholesterol
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what causes LDLs to be taken up in the liver or other tissues
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binding of apoB-100 to LDLR with resultant endocytosis
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what are some ways that cholesterol levels are controlled?
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activity of HMG-CoA reductase and synthesis of LDLR, negative feedback control of the activity of HGM-CoA reductase, downregulation of LDLR synthesis
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what diseases are excessive levels of cholesterol associated with?
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peripheral arterial disease, myocardial infarction, stroke
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what form of cholesterol leads to atherosclerosis?
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LDL
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what is the major problem with high triglycerides?
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pancreatitis
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what is a xanthoma
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tumorous mass of lipids contained in foam cells, associated with plasma cholesterol levels greater than 300 mg/dl
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how do statins work
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competitively inhibit the rate limiting enzyme in cholesterol biosynthesis, HMG-CoA reductase, thereby reducing the synthesis of cholesterol, resulting decrease of plasma LDLs causes an upregulation of LDLR,
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lovastatin
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prototype statin drug
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what are the adverse effects of statins
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myopathy and rhabdomyolysis
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how do bile acid resins work?
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positively charged, bind the negatively charged bile acids, increase excretion of bile acids, this causes synthesis to increase, which reduces cholesterol in the liver, activity of HMG-CoA and synthesis of LDLR both increase
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cholestyramine
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bile acid resin
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how does niacin work
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inhibits the lipolysis of triglycerides in adipose tissue, fewer free fatty acids are delivered to the liver, in the liver, niacin inhibits the synthesis and esterification of fatty acids, both of these effects prevent the liver from synthesizing VLDLs, which reduces LDLs, also increases the activity of lipoprotin lipase, clearance of ApoA-1 is reduced, which increases HDLs
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what is the major adverse effect of niacin
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hepatotoxicity
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how does ezetimibe work
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blocks cholesterol absorption by interfering with the transport protein NPC1L1 - give with a statin
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how do fibrates (PPAR activators) work
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uncertain, activation of peroxisome proliferator activated receptors (PPAR) which regulate gene transcription, fatty acid oxidation and synthesis of LPL are facilitated whne fibrates bind to PPAR, reduce triglycerides in plasma
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what is the first choice for treating severe triglyceridemia
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fibrates
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what is the drug interaction between gemfibrozil and statins?
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myopathy and rhabdomyolysis
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what is the first drug of choice in patients with hyperlipedemia
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statin
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list of thiazide diuretics used for antihypertension
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chlorothiazide
hydrochlorothiazide chlorthalidone |
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list of loop diuretics used for antihypertension
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furosemide
bumetanide ethacrynic acid |
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list of potassium sparing diuretics used for antihypertension
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amiloride
triamterene spironolactone |
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list of centrally acting sympatholytics used for hypertension
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clonidine
methyldopa guanabenz |
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list of adrenergic neuron blocking agents used for hypertension
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guanethidine
reserpine |
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list of beta adrenoceptor anatgonists used for hypertension
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propranolol
metoprolol atenolol betaxolol pindolol |
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list of alpha adrenoceptor antagonists used for hypertension
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prazosin
terazosin doxazosin |
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list of mixed sympathetic antagonists used for hypertension
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labetalol
carvedilol |
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list of arterial vasodilators used for hypertension
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hydralazine
minoxidil diazoxide |
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ganglionic blocker used for hypertension
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trimethaphan
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arterial/venous vasodilators used for hypertension
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sodium nitroprusside
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calcium channel blockers used for hypertension
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verapamil
nifedipine diltiazem |
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ACE inhibitors used for hypertension
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captopril
enalapril lisinopril quinapril ramipril |
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angiotension receptor blockers used for hypertension
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losartan
valsartan |
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direct renin inhibitors used for hypertension
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aliskiren
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mechanism of thiazide diuretics
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deplete body sodium stores and blood volume by acting on the various sites of the renal tubule transport systems
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side effects of thiazide diuretics
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hypokalemia
hyperuricemia hypercalcemia hyperglycemia hyperlipidemia |
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mechanism of loop diuretics
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directly dilate arterioles and decrease TPR by unknown mechanism
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side effects of loop diuretics
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hypokalemia, hypocalcemia
hypomagnesemia renal failure |
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what diuretic is used for treatment of CHF, edema, and hypertensive crisis?
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loop diuretics
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side effects of potassium sparing diuretics
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hyperkalemia
renal failure gynecomastia |
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mechanism of clonidine
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CNS alpha2 adrenoceptor agonist, lowers sympathetic outflow and increases vagal tone thereby decreasing CO and peripheral resistance
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what centrally acting sypatholyic is used for hypertensive crisis
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clonidine
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side effects of clonidine
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compensatory response - water and sodium retention
sedation, drowsiness rebound hypertension of drug withdrawal dry mouth, constipation sexual dysfunction |
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mechanism of methyldopa
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prodrug which can be converted to alpha methyldopamine and alphamethylepinephrine to work as agonist on the central alpha2 receptors
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what is methyldopa used for?
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mild to moderately severe HTN and chronic HTN during pregnancy
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side effects of methyldopa
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sedation, dowsiness, decreased mental acuity
orthostatic hypotension, sodium and water retention positive Coomb's test dry mouth |
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mechanism of guanethidine
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inhibits release of NE from nerve endings, used to treat moderate to severe HTN
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side effects of guanethidine
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sodium and water retention
orthostatic hypotension drowsiness, fatigue, headache diarrhea sexual dysfunction |
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mechanism of reserpine
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blocks the ability of aminergic transmitter vesicles in adrenergic nerve terminals to take up and store biogenic amines, used to treat mild to moderate hypertension
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side effects of reserpine
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depression, sedation, drowsiness, parkinson-like syndrome
bradycardia, edema nasal congestion, stiffness sodium and water retention at high doses |
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mechanism of beta blockers
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decrease CO by blocking B1 adrenoceptor; block B1 adrenoceptor-mediated renin release; may have CNS sympatho-inhibitory actions
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side effects of beta blockers
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fatigue, sedation, sleep disturbance
bradycardia and heart block dry mouth, nausea, vomit, constipation hypoglycemia, hypocalcemia, sexual dysfunction, agranulocytosis |
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contraindications of beta blockers
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never use in patients with asthma
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alpha blocker mechanism
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selectively block alpha1 recepors and cause dilation of both arterioles and veins, may also act in CNS to decrease sympathetic tone
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use of alpha1 adrenoceptor antagonists
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patients with refractory hypertension, prostatic hypertrophy, CHF
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side effects of alpha blockers
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orthostatic hypertension, edema, slight tachycardia, headache, dizziness, fatigue, nervousness, nausea, abdominal pain, sexual dysfunction
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mechanism of mixed blockers
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selective alpha1 and non-selective B antagonist, blood pressure is lowered by reduction of systemic vascular resistance and heart rate
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when do you use mixed sympatholytic blockers?
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patients with both HTN and angina
HTN of pheochromocytoma and HTN emergencies rebound HTN due to withdrawl of clonidine BPH carvediol in patients with CHF |
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side effects of mixed sympatholytic blockers
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blockade of both types of adrenergic receptors
orthostatic hypotension |
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mechanism of trimethaphan
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directly blocks ganglionic transmission, drug is no longer available due to significant adverse effects
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mechanism of minoxidil
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via its metabolie minoxidil sulfate which opens up potassium channel on the plasma membrane of smooth muscle cells and stabilizes membrane resting potential
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when is minoxidil used
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patients refractory to other antihypertensive agents and patients with severe renal disease, used combined with beta blocker to prevent increase in the heart rate and with a diuretic to prevent fluid retention
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side effects of minoxidil
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marked compnesatory response - tachycardia, salt and water retention, pericardial effusion, hypertrichosis (hair growth)
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mechanism of hydralazine
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direct vasodilator
releases NO which acts on teh vascular smooth muscle cells to activate guanylate cyclase and subsequently increase the cyclic GMP production to relax the vascular smooth muscle |
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when is hydralazine used
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in combination with a diuretic or beta blocker to treat patients with refractory hypertension
high first pass effect and low bioavailability |
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side effects of hydralazine
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reflex compensatory response - tachycardia, salt and water retention
tremor, nausea, headache, palpitations, sweating angina attack and ischemic arrhythmias LUPUS LIKE SYNDROME |
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mechansim of diazoxide
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direct vasodilator
acts as a potassium channel opener |
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when is diazoxide used
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management of HTN emergencies by IV route
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side effects of diazoxide
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orthostatic hypotension, reflex tachycardia, dizziness
sodium and water retention edema hyperglycemia |
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mechanism of sodium nitroprusside
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aterial/venous vasodilator
nitrates release NO into smooth muscle tissue --> cGMP --> vasodilation |
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when is sodium nitroprusside used
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powerful parenterally administered vasodilator, main drug of choice in hypertensive emergencies, short duration and has to be prepared freshly
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side effects of nitroprusside
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cyanide released by RBCs and thiocyanate released by liver
toxicity from cyanide - excessive hypotension, metabolic acidosis, arrhythmias, even death toxicity from thiocyanate - weakness, disorientation, psychosis, muscle spasms, and convulsion |
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side effects of calcium channel blcokers
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inhibition of heart function, cardiac depression, bradycardia, and CHF
mild salt and water retention flushing, edema, nausea, constipation |
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which calcium channel blocker has the greatest vasodilation and least cardiodepression effect
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nifedipine and amlodipine
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what calcium channel blocker has the greatest cardiodepression effect and moderate vasodilation effect
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verapamil
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mechanism of ACE inhibitors
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decrease angiotension II production and increase local vasodilator bradykinin production, lower blood pressure principall by decreasing peripheral vascular resistance, do not result in reflex sympathetic activation adn can be used safely in patients with ischemic heart disease
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when are ACE inhibitors used
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more effective in whites than blacks, slowing the progression of renal dysfunction in HTN patients with kidney disease resulting from diabetes, first choice for HTN in CHF, heart attack, and chronic kidney failure patients, may be used to reduce the loss of potassium in patients put on diuretics
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side effects of ACE inhibitors
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dry cough, hyperkalemia, headache, dizziness, fatigue, nervousness, postural hypotension, angioedema, diarrhea, nausea, peptic ulcer reactivation, acute renal failure
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contraindications of ACE inhibitors
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second and third trimesters of pregnancy because of risk of fetal hypotension, anuria, and renal failure, sometimes associated with fetal malformations or death
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mechanism of angiotensin II receptor blockers
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blockade of AT1 receptor decreases vasoconstriction and water and sodium retention
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when are angiotension II receptor antagonists used
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in combination with diuretics, patients with left ventricular hypertrophy, patients with diabetic nephropathy
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advantages of angiotension II receptor angtagonists over ACE inhibitors
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little effect on bradykinin, therefore more specific and causing less cough and angioedema
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what is the mechanism for aliskiren
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direct renin inhibitor
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what are the side effects of aliskiren
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edema in hand, face and or body
diarrhea, abdominal pain, gastroesophageal reflux elevated uric acid, gall and renal stones |
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what is the choice for initial HTN medication
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thiazide diuretics
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what are the backbone therapies of HTN
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diretics, beta blockers, CCBs, ACE inhibitors, and ARBs
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what are the most common combination HTN therapies
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ACE inhibitors and thiazide diuretics
angiotension II receptor blockers, thiazide diuretics, and potassium sparing diuretics beta blockers and thiazide diuretics thiazide diuretics and potassium sparing diuretics clacium channel blockers and ACE inhibitors beta blockers plus alpha blockers for BPH |
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what do you not comibine with beta blockers
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CCBs - suppress heart function
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in which form is iron more easily absorbed
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heme iron - ferrous iron (Fe2+), ferric (Fe3+) must be reduced
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what enhances the reduction of ferric iron to ferrous iron
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vitamin C
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what regulates the body's levels of iron
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absorption
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what is hemochromatosis
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a relatively common genetic disorder that can lead to excessive absorption of iron, toxic levels of iron can accumulate in teh liver and other tissues which is toxic. treatment it phelbotomy
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who is at the greatest risk for iron deficient anemia (microcytic anemia)
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infants (premies especially), adolescents in growth sputs, pregnant women, women during menstruation
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treatments for iron deficieincy
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ferrous sulfate, iron dextran (parenteral)
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who is susceptible to death by iron overdose?
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children between the ages of 12-24 months
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how is vitamin B12 absorbed
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intrinsic factor is secreted by gastric parietal cells, binds to vitamin B12 in the duodenum, complex is absorbed in the ileum when intrinsic factor binds to a receptor, once inside the enterocyte, B12 dissociates from intrinsic factor, and binds to a transporter that transfers it to the portal circulation
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what is one cause of pernicious anemia?
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gastric surgery or gastric atrophy causes a reduction in secretion of intrinsic factor by gastric parietal cells
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what is the major form of folic acid provided to tissues
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N5- methyltetrahydrofolate
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what is the primary result of the lack of DNA synthesis due to vitamin B12 and folic acid deficiency?
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megaloblastic anemia
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what does a lack of vitamin B12 lead to?
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reduces the production fo methionine, which disrupts numerous metabolic reactions. in addition, it reduces the transfer of methyl goups from N-methyltetrahydrofolate. in effect, folic acid gets stuck in its methylated form, which reduces downstream production of dTMP, and thus DNA
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what is pernicious anemia
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a form of megaloblastic anemia that is due to a reduction in secretion of intrinsic factor with resultant vitamin B12 deficiency
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what deficiency can cause neruological defects
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B12, interferes with myelin
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what deficiency can cause neural tube defects
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folic acid deficiency during pregnancy
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treatment for B12 deficiency
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intramuscular or subcutaneous injection of cyanocobalamin
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do folic acid supplements prevent the neurological damage produced by vitamin B12 deficiency
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no
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what does erythropoietin do
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stimulates the production of RBCs in the bone marrow
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what RBC problem happens with chronic renal failure
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can't secrete erythropoietin, these patients are the most responsive to treatment with exogenous erythropoietin
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what is used to treat anemia due to chronic renal failure or anemia as a result of myelosuppresive cancer chemotherapy
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epoetin alpha
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what are the side effects of epoetin alfa
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hypertension and thromboses
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what do myeloid growth factors do
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enhance the production and function of neurtrophils
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filgrastim
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G-CSF
myeloid growth factor available for therapy |
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sargramostim
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GM-CSF
myeloid growth factor available for therapy |
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pegfilgrastim
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filgrastim with longer half life - treatment of myeloid growth factor deficieny
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what are filgrastim, sargramostim, and pegfilgrastim used for
|
treatment of neutropenia associated with cancer chemotherapy, also with autologous stem cell transplantation
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what do megarkaryocyte growth factors do
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increase production of platelets
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oprelevekin
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recomninant form of IL-1 that is used clinically for thrombocytopenia, especially those associated with cancer chemotherapy
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rombiplostim
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acts on receptors stimulated by thrombopoietin, used to treat thrombocytopenia, especially those associated with cancer chemotherapy
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describe the actions of platelets
|
platelets bind to collagen using von Willibrand factor, this binding causes the platelets to release ADP, serotonin, adn thromboxane A2, all of which bind to platelets. these substances activate platelets, producing a conformational change in a receptor termed GP IIb/IIIa that allows this receptor to bind fibrinogen, platelets adhere to each other by binding fibrinogen, this process leads to positive feedback in whcih more platelets aggregate and release their contents, teh result is a platelet plug that represents an attempt to seal the break in the vessel wall
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what does thrombin do
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activates factors V, VIII, and SI, as well as platelets, which ultimately facilitates the production of large amounts of thrombin and thus an adequate clot
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what do thrombomodulin and protein C do
|
thrombomodulin is a receptor on endothelial cells, binding of thrombin to thrombomodulin inactivates the thrombin, in addition, the bound thrombini can now bind to protien C, which activates protein C, activated protein C inactivates factors Va and VIIIa, in this way, clotting is inhibited in locates where endothelium is intact
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what do antithrombin III and heparan do
|
antithrombin III is a plasma protein that inactivates thrombin adn factors IXa and Xa, activity of antithrombin II is enhanced at least 1000X in the presence of heparan, process also helps prevent a clot from spreading beyond the damaged area
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how does heparin work
|
similar to heparan, heparin facilitates the action of antithrombin III, leading to inactivation of thrombin adn factors IXa and Xa
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what is heparin used for
|
treat people with thromboses
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what are the adverse effects of heparin
|
bleeding (can be treated with protamine sulfate), thrombocytopenia
|
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enoxaparin
|
low molecular weight heparin
|
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fondasparinux
|
like heparin
synthetic pentassaccharide that inhibits only factor Xa and is less likely to induce thrombocytopenia |
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how does warfarin work
|
inhibits vitamin K epoxide reductase, thereby preventing the synthesis of the clotting factors factors VII, IV, and C
|
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what can inhibit the action of warfarin
|
vitamin K
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what is the major adverse effect of warfarin
|
bleeding
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how does lepirudin work
|
a recombinant form of hirudin that binds to thrombin, inhibiting thrombin's action
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what is the main adverse reaction of thrombin drugs
|
bleeding
|
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how do fibrinolytic drugs work
|
drugs facillitate the formation of plasmin from plasminogen, which dissolves the fibrin in clots
|
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streptokinase
|
fibrinolytic drug
protein that binds to plasminogen, binding produces a conformational change in plasminogen that allows it to be converted to plasmin, the drug is not used since the development of newer drugs |
|
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alteplase
|
recombinant form of t-PA, and works similarly to endogenous t-PA
fibrinolytic drug |
|
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how do antiplatelet drugs work
|
inhibit the ability of platelets to activate, thus inhibiting the initiation of the clotting cascade
|
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|
aspirin
|
irreversible inhibitor or platelet action
prevents the formation fo thromboxane A2 by irreversibly binding cyclooxygenase which syntehsizes thromboxane A2 |
|
|
clopidogrel
|
antiplatelet drug
blocks the ADP receptor on platelets, which prevents released ADP from activating them |
|
|
abcliximab
|
antiplatelet drug
monoclonal antibody that binds to the GP IIb/IIIa receptor, inactivating it |
|
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eptifibatide
|
antiplatelet drug
binds to the GP IIb/IIIa receptor |
|
|
cilostazol
|
antiplatelet drug
blocks phosphodiesterase III which inhibits platelet aggregation |
|
|
what are antiplatelet drugs used for clinically
|
prevention of myocardial infarction, prevention of TIA and stroke
|
|
|
systolic heart failure
|
heart does not develop adequate force to eject enough blood, contractility of heart is reduced, can be from an MI
|
|
|
diastolic heart failure
|
heart cannot fill, heart loses compliance, stiffens
|
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in the U.S. the primary cause of heart failure is _____ or ____
|
ischemic disease or MI
|
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for the world as a whole, the primary cause of heart failure is ____
|
hypertension
|
|
|
recommended sequence of treatment for heart failure
|
1. loop diuretic
2. ACE inhibitor 3. Beta blocker 4. aldosterone inhibitor 5. angiotensin receptor blocker 6. inotropic agent |
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In CHF, only the diuretics that ____ adequately reduce plasma volume
|
block Na+ reabsorption in the thick ascending limb
|
|
|
furosemide
|
loop diuretic used for CHF
used to reduce plasma volume to achieve a normal volume status, this reduces end-diastolic volume and pressure, thereby reducing the work of the heart increases venous capacitance which reduces preload |
|
|
adverse effects of furosemide
|
excessive excretion of Na, Cl, K, H, MG, and Ca thereby producing volume depletion and acid-base abormalities, renal function must be closely monitored
|
|
|
chlorothiazide
|
thiazide diuretic used for CHF
blocks the Na-Cl symporter in teh distal tubule, used in some patients who do not respond well to loop diuretics |
|
|
how do K sparing diuretics/aldosterone antagonists work in CHF
|
the major influence is thought to be a reduction in remodeling of the heart
|
|
|
spironolactone
|
K sparing diuretics/aldosterone antagonist that is used to treat CHF, has been shown to reduce mortality in heart failure
|
|
|
adverse effect of spronolactone
|
hyperkalemia
|
|
|
what is the primary benefit of ACE inhibitors in CHF
|
block the degradation of bradykinin may be the beneficial effect of these drugs on the peripheral vasculature
|
|
|
Catopril and Enalapril
|
ACE inhibitors used for CHF
|
|
|
adverse effects of ACE inhibitors
|
hypotension and dry cough
|
|
|
carvedilol and metoprolol succinate
|
beta blockers used for CHF
|
|
|
adverse effects of beta blockers
|
exacerbate heart failure if given too much or sudden withdrawl, brochoconstriction
|
|
|
candesartan and valsartan
|
angiotensin receptor blockers used to treat CHF
|
|
|
adverse effects of angiotensin receptor blockers
|
hypotension
|
|
|
digoxin
|
ionotropic agent used to treat CHF, blockade of Na, K-ATPase in sarcolemma, only used in hospitals, CHF crisis
|
|
|
when is digoxin recommended
|
use only in patients who have a high heart rate (such as from afib) or who are not adequately treated for heart failure with the drugs already described
|
|
|
adverse effects of digoxin
|
different types of cardiac arrhythmias which can lead to sudden death
|
|
|
dopamine and dobutamine
|
beta agonist used for CHF
only used to treat severe heart failure |
|
|
isosorbide dinitrate
|
CHF drug
is converted to nitric oxide with resultant vasodilation, major effect is due to increased venous capacitance which reduces ventricular filling |
|
|
hydralazine
|
CHF drug
vasodilator whose mechaism of action is not known reduces afterload by reducing pulmonary and systemic vascular resistance |
|
|
bidil
|
isosorbide dinitrate and hydralazine together
|
|
|
nesiritide
|
recombinant version of brain natriuretic peptide, produce Na and water excretion and acts as a vasodilator
used to treat dyspnea caused by heart failure |
|
|
angina is______
|
discomfort or pain associated with an imbalance between myocardial oxygen supply and demand
|
|
|
how do nitrates relieve angina
|
the primary hemodynamic effect of nitrates that relieves angina is the increase in venous comliance with resultant decrease in myocardial oxygen demand
|
|
|
nitroglycerin
|
nitrate drug used for angina
|
|
|
isosobide dinitrate
|
nitrate drug used for angina
|
|
|
isosorbide mononitrate
|
nitrate drug used for angina
|
|
|
how are nitrate drugs adminstered
|
sublingual
|
|
|
adverse effects of nitrate drugs
|
hypotension/orthostatic hypotension, very quickly developing tolerance
|
|
|
contraindications of nitrate drugs
|
don't give to someone on sildenafil due to the risk of a large decrease in arterial pressure
|
|
|
nifedipine
|
CCB used to treat angina
|
|
|
nicardipine
|
CCB used to treat angina
|
|
|
how do nifedipine and nicardipine work to treat angina
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relax arterial smooth muscle but have little to no effect on the heart or venous smooth muscle
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verapamil and diltiazem
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CCBs used to treat angina
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how do verapamil and diltiazem work to treat angina
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reduce the rate of phase 4 depolarization in the SA nodal cells which slows heart rate, reduces intracellular Ca in cardiac muscle cells which decreases contractility, and slow conduction through the AV node, the net result of the drugs effects and the reflex compensationi are reductions in heart rate, contractility, and afterload, all of which decrase myocardial oxygen demand
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bepridil
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CCB used to treat angina
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all of the CCBs reduce _____
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myocardial oxygen demand
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CCBs are not good for ____ angina
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unstable
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adverse effects of CCBs
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hypotension, headache
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contraindication for verapamil and diltiazem
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should not be administered if a patient is taking beta blockers
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beta blockers are not good for ____ angina
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variant
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propranolol and metoprolol
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beta blockers used to treat angina
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adverse effects of beta blockers
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congestive heart failures if patient already has a weak heart
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contraindications of beta blockers
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asthma and bronchospasms
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slidenafil
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PDE 5 inhibitor, viagra
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contraindications for slidenafil
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nitrate drugs and alpha adrenergic antagonists
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alprostadil
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PGE1 analog that is the most common drug used in men with ED who do not respond to slidenafil
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