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32 Cards in this Set

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Niacin: effects?
lower VLDL and LDL conc. in blood

lowered triglycerides and cholesterol

lowers circulating fibrinogen

increases t-PA release

decreases Lp(a)
Niacin: Pharmocokinetics?
good oral availibility

t-1/2= 1 hr
Niacin: mechanism of action?
inhibits lipolysis in adipose tissue

causes deficiency of free fatty acids needed to make triglycerides in liver, that are in turn needed to make VLDL

decreased secretion of VLDL causes decreased LDL and increased HDL
Niacin: adverse effects?
flushing

prurtisis (itching)

vomiting, nausea, peptic ulcers
Niacin: therapeutic uses?
all types of hyperlipidemia, except Type I
Fibric Acids: names of drugs?
Gemfibrozil

Fenofibrate
Fibric Acids: effects?
lower VLDL conc. in blood

lowered triglycerides and cholesterol
Fibric Acids: pharmacokinetics?
oral administration

t-1/2= 1.5 hrs

70% eliminated by kidneys
Fibric Acids: mechanism of action?
ligand for a nuclear transcription regulator

increased clearance of VLDL by LPL

decreases lipolysis in adipose tissue

Only modest effects on LDL
Fibric Acids: adverse effects
mild GI effects

increased risk of gallstones

potentiates warfarin(anticoagulant)

myositis

contraindicated in pts. w/ impaired hepatic or renal function and in pregnant or nursing women
Fibric acids: therapeutic uses?
reduces cholesterol and triglycerides

reduces myocardial infarctions
Bile acid binding resins: names of drugs?
Cholestipol

Cholestyramine

Colesevelam
Bile acid binding resins: effects?
lowers LDL conc. in blood
Bile acid binding resins: pharmacokinetics
not absorbed from GI tract
Bile acid binding resins: mechanism of action?
bind cholesterol in bile in intestine

conversion of cholesterol to bile acids is increased

LDL receptors upregulated

more LDL taken up by liver
Bile acid binding resins: adverse effects?
constipation

nausea

Absorption of vitamins or drugs may be impaired
Bile acid binding resins: therapeutic uses?
Type II hyperlipedemia, except homozygous LDL receptor defect
Ezetimibe (Inhibitor of Intestinal sterol absorption): effects
lowers LDL levels in blood
Ezetimibe: Pharmacokinetics
absorbed in the intestine and conjugated to glucuronide

t-1/2= 22 hrs

peak levels at 12 hrs

80% excreted in feces
Ezetimibe: mechanism of action
Selective inhibitor of intestinal absorption of cholesterol

inhibits reabsorption of bile cholesterol
Ezetimibe: adverse effects?
not metabolized by liver

some impaired liver function
Inhibitors of HMG-CoA reductase: names of drugs?
Lovastatin

Simvastatin

Atorvastatin

Pravastatin

Fluvastatin

Rosuvastatin
Inhibitors of HMG-CoA reductase: effects
lower plasma LDL levels
Inhibitors of HMG-CoA reductase: pharmacokinetics?
absorption in gut varies

high first pass effect, most of drug sequestered in liver

most of absorbed drug excretedin bile
Inhibitors of HMG-CoA reductase: mechanism of action?
hydrolyzed in gut

inhibitor blocks first committed step of cholesterol synthesis

LDL receptor upregulation in liver

decrease in plasma LDL
Inhibitors of HMG-CoA reductase: adverse effects?
liver toxicity (monitor levels of aminotransferase)

Myopathies (monitor creatine kinase)
Inhibitors of HMG-Coa reductase: therapeutic uses?
Type II hyperlipidemia, except homozygous LDL receptor defect

not used in pregnant or nursing women
THIAZIDE DIURETICS
Chlorothiazide
Hydrochlorothiazide
USE
Control BP in Stage 1 HT pts. and Stage 2 HT pts.
Used in combo to control fluid retention and edema caused by other anti-HT drugs
Increase plasma renin

MECHANISM
Increase sodium and H20 excretion by inhibiting reabsorption of Na and Cl in nephron
Decrease plasma vol. and CO; this can activate cardiopulmonary reflexes increasing resistance, HR, and plasma renin levels, however w/ continued therapy the reflex subsides
Decrease systemic vascular resistance

ADVERSE EFX
Muscle weakness
Fatigue
Potassium loss: Cardiac arrythmia and muscle cramp
Hyperglycemia
Increase VLDL and LDL
Impotence
POTASSIUM SPARING DIURETICS
Spironolactone
Triamterene
Amiloride
Use
Combined w/ Thiazide and Loop diuretics to maintain normal potassium levels in plasma
Loop Diuretics
Use
Combined w/ hypertensives to control edema formation and fluid retention
Used in renal insufficiency pts.
Lipid Soluble B-blockers
MECHANISM
Non-selective B-blocker

ADVERSE EFX
Cross the BBB/CSF
Confusion
Memory Loss
Vivid dreams
Inability to concentrate
CA+2 CHANNEL BLOCKERS
Nifedipine
Verapamil
Diltiazem
USE
used alone in Stages 1,2,& 3 HT
Combined w/ thiazide diuretic or an ACE inhibitor for all stages of HT

MECHANISM
Block L-type Ca+2 channels in SA & AV nodes to decrease cardiac automaticity, AV conduction velocity and cardiac contractility
Block L-type Ca+2 channels in vascular SM & myocardium to cause vasodilation and deceased contractility