Term
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Definition
Old, versatile drug - impacts all lipid parameters:
REDUCES LDL and TRIGLYCERIDES
INCREASES HDL
Water soluble B complex vitamin (once converted to NAD)
Decreases TG synthesis in liver -> reduced hepatic VLDL (lower LDL); decreased lipolysis in adipose; reduced hepatic clearance of HDL apo A1 (raises HDL)
Side effects: flushing and pruritis of face/trunk (PG-mediated), rashes, acanthosis nigricans, dyspepsia/peptic ulcer reactivation, hepatotoxicity, hyperglycemia, hyperuricemia, toxic amblyopia, tachyarrythmia, a-fib, myopathy
CONTRAINDICATED in pts with diabetes, gout |
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Term
Fibric Acid Derivatives (Fibrates)
Clofibrate, Gemfibrozil, Fenofibrate, Ciprofibrate, Bezafibrate |
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Definition
Synthetic ethyl chlorophenoxyisobutyrates - REDUCES VLDL (TGs), INCREASE (slight) HDL, variable LDL effects
Used in pts with hypertriglyceridemia
Unclear mechanism - interacts with PPARa - stimulate LPL synthesis, enhancing TG clearance, inhibit apoC III to enhance VLDL clearance, stimulation of apoA1 and 2 expression
Side effects: GI, myositis flu-like symptoms, increase gallstone formation, potentiate oral anticoagulants by displacing them from albumin |
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Term
Bile Acid Sequestrants
Cholestyramine, Colestipol, Colesevelam |
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Definition
Anion-exchange resins - hygroscopic powders, insoluble in water - old form, but very safe (only form recommended for children)
Highly positively charged and bind to negative bile acids -> large, so are not absorbed -> excreted in stool -> depletes liver supply of bile acids -> increased hepatic bile acid synthesis -> pulls cholesterol from blood (increased LDL receptors) to lower LDL
REDUCES LDL, INCREASES (SLIGHT) HDL, TG
Side effects: bloating, dyspepsia, unpleasant/gritty taste, constipation, may bind other drugs (cardiac glycosides, coumarin anticoagulants, fat soluble vitamins)
CONTRAINDICATED in hypertriglyceridemia (raises TGs) |
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Term
| HMG-CoA Reductase Inhibitors (Statins) |
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Definition
Isolates from PCN and Aspergillus - most effective and best tolerated for dyslipidemia
Reduce fatal and nonfatal events - REDUCE LDL, TG and INCREASE HDL
HMG CoA reductase catalyzes rate limiting step for cholesterol synthesis - Statins inhibit this (reversible, competitive)
Also inhibit cholesterolgenesis in liver -> reduced free cholesterol -> SREBP cleaved and translocated and enhances synthesis of LDL receptors -> increased removal of LDL from blood (also decreased LDL receptor degradation) -> decreased hepatic VLDL synthesis -> decreased TGs
Concentrations peak in 1-4 hrs
Hepatic cholesterol synthesis maximal between midnight-2am = take in evening
Side effects: few - hepatic dysfunction, myopathy/rhabdomyolysis; side effects enhanced by advanced age, hepatic/renal dysfunction, perioperative, diabetes, hypothyroidism, concomitant fibrate (increased myopathy)
CONTRAINDICATED in pregnancy/nursing women
Cardioprotective, counteract osteoporosis, decreased LDL oxidation |
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Term
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Definition
LOWERS total and LDL cholesterol
Inhibits cholesterol absorption by enterocytes in small intestine (inhibits transport protein) -> reduced cholesterol integration into chylomicrons -> decreased atherogenesis
No effect on luminal TG absorption
Complementary to statins (stains inhibit cholesterol synthesis and increase intestinal cholesterol absorption - zetia increases cholesterol biosynthesis)
Side effects: allergic reactions |
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Term
| COMBINATIONS of LIPID LOWERING DRUGS |
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Definition
Most effective in lowering LDL:
statin + resin + niacin (70-75% reduction), statin + ezetimibe (60%)
NEVER statin + fibrate -> myopathy!
Niacin + statin (lovastatin) and ezetimibe + simvastatin sold as combination pills |
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Term
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Definition
Antihypertensive - reduces BP by increasing Na and water excretion (lowers intravascular volume)
Thiazides vasodilate (decreased PVR) + diuresis -> first line
Once GFR falls below 30, use loop diuretics
Use potassium sparing drugs to reverse hypokalemia induced by loops/thiazides
Also good choices for CHF, kidney disease
Side effects: hypo or hyperkalemia, hypomagnesium, hyperuricemia |
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Term
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Definition
Central sympathetic drug - antihypertensive
alpha2 agonist - older drug used in pregnancy now
toxicity: hemolytic anemia
act by reducing sympathetic activity, decrease PVR and CO |
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Term
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Definition
Antihypertensive (Central Sympathetic Drug)
3rd or 4th line agent; alpha2 agonist
toxicity: dry mouth, drowsiness |
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Term
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Definition
Adrenergic Neuron Blocking Agent - decreases NE release from postganglionic sympathetic neurons
Usually not used clinically
Toxicity: postural hypotension, male sexual dysfunction |
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Term
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Definition
Adrenergic Neuron Blocking Agent
Depletes central amine stores - crosses blood brain barrier and causes depression, sedation, parkinsonism-like symptoms
Antihypertensive
Not used anymore |
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Term
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Definition
Meds end in "olol" (propranolol, metoprolol, atenolol, carvedilol)
Useful for hypertension + CAD or CHF
Induce bradycardia and decrease CO and decrease PVR (agonist for vasodilation), inhibit catecholamine-induced renin release (suppress RAAS)
Side effects: bradycardia, asthma exacerbation, worsening of hypoglycemia (block Epi) |
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Term
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Definition
Antihypertensive - antagonize alpha1-mediated vasoconstriction (decrease PVR) and decrease presynaptic NE release (alpha2)
Also treat BPH
Side effects: reflex tachycardia, increased cardiovascular mortality - use under cover of beta-blockers, orthostatic hypotension (take at night to minimize this) |
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Term
| Direct Vasodilators (General) |
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Definition
Antihypertensive
Relax vascular smooth muscle to decrease PVR and MAP; induce compensatory RAAS activation due to reduced renal blood flow -> beta blockers and diuretics oppose compensatory response to decreased BP
Side effects: tachycardia, edema
Renal effects: constrict efferent arteriole -> increase glomerular pressure, increase albumin excretion rate |
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Term
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Definition
Direct Vasodilator - works by release of NO
Short half life
Side effects: lupus-like syndrome (reverse by discontinuing drug) |
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Term
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Definition
Direct Vasodilator - activates guanylyl cyclase (directly or via NO)
Powerful, parenteral - for hypertensive emergencies
Side effects: cyanide accumulation, renal failure with prolonged use |
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Term
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Definition
Direct Vasodilator - causes hyperpolarization of smooth muscle by opening potassium channels
Used topically for baldness too
Side effects: excessive hair growth (hypertrichosis), pericardial effusion, retention of salt and water
3rd or 4th line antihypertensive drug |
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Term
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Definition
Reduce calcium influx into myocyte
1.Dihydropyridine (affect vascular smooth muscle) - amlodipine, nifedipine, can cause reflex tachycardia
2. Nondihydropyridines (affect myocyte) - verapamil, diltiazem, can cause bradycardia and cardiac depression -> don't use with beta blockers (potentiates bradycardia)
Both: peripheral edema
Renal effects: constrict efferent arteriole -> increase glomerular pressure, increase albumin excretion rate |
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Term
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Definition
Antihypertensives - inhibits peptidyl transferase so ACE I can't be converted to ACE II and bradykinin cannot be inactivated -> decrease potent vasoconstrictor and increase potent vasodilator (decrease PVR)
Side effects: dry cough, angioedema (bradykinin effects), hyperkalemia, renal failure in pts with renal artery stenosis
Good for HTN + diabetes or kidney disease or CHF
Renal effects: dilate efferent arteriole -> decrease glomerular pressure, decrease albumin excretion |
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Term
| Angiotensin Receptor Blockers |
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Definition
Antihypertensive - competes with angiotensin II for receptor -> decreases arterial vasoconstriction (decreased PVR and BP)
Do not impact bradykinin levels
Side effects: renal failure in pts with renal artery stenosis, hyperkalemia
Good for HTN + Diabetes or CHF or Chronic Kidney Disease
Renal effects: dilate efferent arteriole -> decrease glomerular pressure, decrease albumin excretion |
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