Pharm Exam 3
Antilipemic Agents
Triglycerides and Cholesterol
We need some form of fats and cholesterol in order to maintain hemostasis
• Two primary forms of lipids in the blood- is trigylcerides and cholesterol
• Water-insoluble fats that must be bound to apolipoproteins, specialized
lipid-carrying proteins
• Lipoprotein is the combination of triglyceride or cholesterol with
apolipoprotein
• Elevated cholestrol especially LDL/ trriglycerides can increase the risk for
cardiovascular disease and stroke
▫ 1st nursing intervention before providing a pt with medication is to
try lifestyle modifications for 3-6 months first educate pt to remove
trans fat from the diet
▫ (trans fats aren’t natural fats so the body stores it as
unhealthy fats)
▫ Limit fats and meats (saturated fat- solid at room temp), encourage
fiber it binds to cholestrol and it gets eliminted and so you would
also encourge fluids along with the fiber to prevent constipation,
encourage polysaturated fats seen in (cooking oils, and nuts)
• Lipoproteins
• Very-low-density lipoprotein (VLDL)- when circulated it loses its
triglyceride component and becomes LDL
▫ Produced by the liver
▫ Transports endogenous lipids to the cells
• Low-density lipoprotein (LDL)- (lousy ones- bad) contributes to vascular
diseases the formation of the fatty streaks (ldl oxidized and gets engulfed
by a marchophage it becomes a foam cell which contributes to fat
development
▫ Want LDL below 100 ideally
▫ TOTAL CHOLESTROL- LESS THAN 200
▫ Trigylceride- less than 150 ideally
• High-density lipoprotein (HDL)- (GOOD ONES- want it above 40)
▫ Responsible for “recycling” of cholesterol
▫ Also known as “good cholesterol”- BENEFICIAL Cholestrol
▫ Cholestrol screening requires fasting beforehand done once a year
is a fasting screening
, Pharm Exam 3
Cholesterol and Coronary Heart Disease (CHD)
• The risk of CHD in patients with cholesterol levels of 300 mg/dL is three to
four times greater than that in patients with levels less than 200 mg/dL.
▫ As cholesterol increases there is an increased risk for coronary
artery disease and stroke
• We really need healthy diets and exercise (move more eat less) cholestrol
drugs are secondary after dietary modifications have not worked
Hyperlipidemias Treatment and Guidelines
• Antilipemic drugs
▫ Drugs used to lower lipid levels
▫ Used as an adjunct to diet therapy & lifestyle changes
• Identification of high-risk groups to be treated with “statins” (Box 27.1)
• Use of hyperlipidemics:
▫ Primary prevention – reduce risk of cardiac events in those with risk
factors
▫ Secondary prevention – reduce risk of subsequent cardiac events
in those who have experienced one
• Statins the mainstay tx for high cholestrol some statins work more
rigioursly then other statins
Antilipemics
• HMG-CoA reductase inhibitors (HMGs, or statins)-most commonly used
and very effective drugs (statins)
• Bile acid sequestrants
• B Vitamin Niacin (vitamin B3, nicotinic acid)
• Fibric acid derivatives (fibrates)
, Pharm Exam 3
• Cholesterol absorption inhibitor (Zetia)
• Combination drugs (Vytorin)
HMG-CoA Reductase Inhibitors (HMGs or statins)- (hint: END IN STATIN)
• Most potent LDL reducers
▫ pravastatin
▫ simvastatin- can be increased in dose higher if pt needs more
cholesterol lowering effects
▫ atorvastatin
▫ fluvastatin
▫ rosuvastatin
▫ Pitavastatin
• Used in pts with hx of coronary vascular disease and stroke, for pts with
high LDL levels, used in pts with DM (tx their cholestrol levels rigioursly
cause DM increases the risk for inflammation and coronary vascular
events)
HMG-CoA Reductase Inhibitors
• Mechanism of Action
▫ Inhibit HMG-CoA reductase, which is used by the liver to produce
cholesterol
▫ Lower the rate of cholesterol production by inhibiting the enzyme
makes less LDL receptors on the liver (making less for LDL to bind
to)
▫ Extra fat and cholestrol goes to the liver which is why fatty
cirrhosis is becoming more prevalent
• Clinical Indications
▫ First-line drug therapy for hypercholesterolemia reduce LDL, raise
HDLs, lower trigylcerides (takes 6-8 weeks for max tx)- given at
night with an evening meal because that’s when cholestrol is made
▫ Limit Grapefruit juice with statins (inhibts their CYP450-
creating more of the drug and increased risk for drug toxicity)
▫ Treatment of types IIa and IIb hyperlipidemias
▫ Reduces LDL levels by up to 50%
▫ Increases HDL levels by 2% to 15%
▫ Reduces triglycerides by 10% to 30%
, Pharm Exam 3
HMG-CoA Reductase Inhibitors:
Adverse Effects
▫ Mild, transient GI disturbances (take with meals or glass of water to
lower GI upset)
▫ Rash
▫ Headache
▫ Myopathy (muscle pain), possibly leading to the serious condition
rhabdomyolysis- when muscle is broken down and can progress to
muscle proteins being excerted through the kidneys leading to
renal failure
▫ ***A sign of rhabdmyolsis is muscle pain the muscle starts to
break down***(SIGNIFICANT ADVERSE EFFECT)
▫ Elevations in liver enzymes or liver disease- Statins increase liver
enzymes (MOINTER)
▫ 6-8 weeks later mointer AST and ALT
▫ If the pt has a PREexsiting liver disease these drugs should
be avoided in
▫ Muscle pain, and urine changes (sign of protein spilling in
the urine) call HCP IMMEDIATELY seen a few days after
drug initaition
Antilipemic Agents
Triglycerides and Cholesterol
We need some form of fats and cholesterol in order to maintain hemostasis
• Two primary forms of lipids in the blood- is trigylcerides and cholesterol
• Water-insoluble fats that must be bound to apolipoproteins, specialized
lipid-carrying proteins
• Lipoprotein is the combination of triglyceride or cholesterol with
apolipoprotein
• Elevated cholestrol especially LDL/ trriglycerides can increase the risk for
cardiovascular disease and stroke
▫ 1st nursing intervention before providing a pt with medication is to
try lifestyle modifications for 3-6 months first educate pt to remove
trans fat from the diet
▫ (trans fats aren’t natural fats so the body stores it as
unhealthy fats)
▫ Limit fats and meats (saturated fat- solid at room temp), encourage
fiber it binds to cholestrol and it gets eliminted and so you would
also encourge fluids along with the fiber to prevent constipation,
encourage polysaturated fats seen in (cooking oils, and nuts)
• Lipoproteins
• Very-low-density lipoprotein (VLDL)- when circulated it loses its
triglyceride component and becomes LDL
▫ Produced by the liver
▫ Transports endogenous lipids to the cells
• Low-density lipoprotein (LDL)- (lousy ones- bad) contributes to vascular
diseases the formation of the fatty streaks (ldl oxidized and gets engulfed
by a marchophage it becomes a foam cell which contributes to fat
development
▫ Want LDL below 100 ideally
▫ TOTAL CHOLESTROL- LESS THAN 200
▫ Trigylceride- less than 150 ideally
• High-density lipoprotein (HDL)- (GOOD ONES- want it above 40)
▫ Responsible for “recycling” of cholesterol
▫ Also known as “good cholesterol”- BENEFICIAL Cholestrol
▫ Cholestrol screening requires fasting beforehand done once a year
is a fasting screening
, Pharm Exam 3
Cholesterol and Coronary Heart Disease (CHD)
• The risk of CHD in patients with cholesterol levels of 300 mg/dL is three to
four times greater than that in patients with levels less than 200 mg/dL.
▫ As cholesterol increases there is an increased risk for coronary
artery disease and stroke
• We really need healthy diets and exercise (move more eat less) cholestrol
drugs are secondary after dietary modifications have not worked
Hyperlipidemias Treatment and Guidelines
• Antilipemic drugs
▫ Drugs used to lower lipid levels
▫ Used as an adjunct to diet therapy & lifestyle changes
• Identification of high-risk groups to be treated with “statins” (Box 27.1)
• Use of hyperlipidemics:
▫ Primary prevention – reduce risk of cardiac events in those with risk
factors
▫ Secondary prevention – reduce risk of subsequent cardiac events
in those who have experienced one
• Statins the mainstay tx for high cholestrol some statins work more
rigioursly then other statins
Antilipemics
• HMG-CoA reductase inhibitors (HMGs, or statins)-most commonly used
and very effective drugs (statins)
• Bile acid sequestrants
• B Vitamin Niacin (vitamin B3, nicotinic acid)
• Fibric acid derivatives (fibrates)
, Pharm Exam 3
• Cholesterol absorption inhibitor (Zetia)
• Combination drugs (Vytorin)
HMG-CoA Reductase Inhibitors (HMGs or statins)- (hint: END IN STATIN)
• Most potent LDL reducers
▫ pravastatin
▫ simvastatin- can be increased in dose higher if pt needs more
cholesterol lowering effects
▫ atorvastatin
▫ fluvastatin
▫ rosuvastatin
▫ Pitavastatin
• Used in pts with hx of coronary vascular disease and stroke, for pts with
high LDL levels, used in pts with DM (tx their cholestrol levels rigioursly
cause DM increases the risk for inflammation and coronary vascular
events)
HMG-CoA Reductase Inhibitors
• Mechanism of Action
▫ Inhibit HMG-CoA reductase, which is used by the liver to produce
cholesterol
▫ Lower the rate of cholesterol production by inhibiting the enzyme
makes less LDL receptors on the liver (making less for LDL to bind
to)
▫ Extra fat and cholestrol goes to the liver which is why fatty
cirrhosis is becoming more prevalent
• Clinical Indications
▫ First-line drug therapy for hypercholesterolemia reduce LDL, raise
HDLs, lower trigylcerides (takes 6-8 weeks for max tx)- given at
night with an evening meal because that’s when cholestrol is made
▫ Limit Grapefruit juice with statins (inhibts their CYP450-
creating more of the drug and increased risk for drug toxicity)
▫ Treatment of types IIa and IIb hyperlipidemias
▫ Reduces LDL levels by up to 50%
▫ Increases HDL levels by 2% to 15%
▫ Reduces triglycerides by 10% to 30%
, Pharm Exam 3
HMG-CoA Reductase Inhibitors:
Adverse Effects
▫ Mild, transient GI disturbances (take with meals or glass of water to
lower GI upset)
▫ Rash
▫ Headache
▫ Myopathy (muscle pain), possibly leading to the serious condition
rhabdomyolysis- when muscle is broken down and can progress to
muscle proteins being excerted through the kidneys leading to
renal failure
▫ ***A sign of rhabdmyolsis is muscle pain the muscle starts to
break down***(SIGNIFICANT ADVERSE EFFECT)
▫ Elevations in liver enzymes or liver disease- Statins increase liver
enzymes (MOINTER)
▫ 6-8 weeks later mointer AST and ALT
▫ If the pt has a PREexsiting liver disease these drugs should
be avoided in
▫ Muscle pain, and urine changes (sign of protein spilling in
the urine) call HCP IMMEDIATELY seen a few days after
drug initaition
