This document summarizes several classes of antilipidemic drugs used to treat elevated blood lipids. It discusses bile-sequestering drugs like cholestyramine which bind to bile acids in the intestines. Fibric acid derivatives like fenofibrozate and gemfibrozil are used to reduce triglycerides and LDL. Statins like HMG-CoA reductase inhibitors block cholesterol production to lower LDL and increase HDL slightly. Ezetimibe inhibits cholesterol absorption from the intestines. Nicotinic acid lowers LDL and triglycerides while raising HDL but causes flushing as a side effect. All work in combination with lifestyle changes to reduce cardiovascular risks from high lipids.

1. ANTILIPEMIC DRUGS
(ANTIHYPERLIPIDEMIC AGENTS)
By: MJJH

2. ANTILIPEMIC DRUGS
(ANTIHYPERLIPIDEMIC AGENTS)
Used for patients/clients with elevated blood
lipids, such as cholesterol, triglycerides, and
phospholipids.
Drugs are used in combination with lifestyle
changes (such as proper diet, weight loss, and
exercise) to decrease the risk of CAD.

3. THE CLASSES OF ANTILIPEMIC
DRUGS INCLUDE:
BILE-SEQUESTERING DRUGS- The bile-
sequestering drugs are cholestyramine,
colestipol, and colesevelam.
Bile Sequestering drug bind with bile acids,
leading to their excretion in the feces.

4. Pharmacokinetics-Bile-sequestering drugs
aren’t absorbed from the GI tract. Instead,
they remain in the intestine, where they
combine with bile acids for about 5 hours.
Eventually, they’re excreted in stool.

5. Pharmacodynamics-The bile-sequestering
drugs lower blood levels of low-density
lipoproteins (LDLs). These drugs combine
with bile acids in the intestines to form an
insoluble compound that’s then excreted in
stool. The decreasing level of bile acid in
the gallbladder triggers the liver to
synthesize more bile acids.

6. Pharmacotherapeutics- Bile-sequestering
drugs are the drugs of choice for treating type
ii hyperlipoproteinemia (familial
hypercholesterolemia) when the patient can’t
lower his LDL levels through diet alone.

7. Drug interactions- They may bind with
acidic drugs in the GI tract, decreasing their
absorption and effectiveness. Bile-sequestering
drugs may reduce absorption of lipid-soluble
vitamins, such as vitamins A, D, E and K.
Poor absorption of vitamin K can affect
prothrombin times significantly, increasing the
risk of bleeding.

8. ADVERSE REACTIONS TO BILESEQUESTERING DRUGS
Short-term adverse reactions to these drugs are
relatively mild.
More severe reactions can result from long-term
use. Adverse GI effects with long-term therapy
include severe fecal impaction, vomiting,
diarrhea, and hemorrhoid irritation.

9. FIBRIC ACID DERIVATIVES
Fibric acid is produced by several fungi. Two
derivatives of this acid are Fenofibrate and
gemfibrozil.
These drugs are used to reduce high
triglyceride levels, and to a lesser extent, high
LDL levels.

10. Pharmacokinetics- Fenofibrate and
gemfibrozil are absorbed readily from the
GI tract and are highly protein-bound.
Fenofibrate is hydrolyzed while
gemfibrozil undergoes extensive
metabolism in the liver. Both drugs are
excreted in the urine.

11. Pharmacodynamics- Although the exact
mechanism of action for these drugs isn’t known,
researchers believe that fibric acid derivatives may:
•Reduce cholesterol production early in its
formation
•Mobilize cholesterol from the tissues
•Increase cholesterol excretion
•Decrease synthesis and secretion of lipoproteins
•Decrease synthesis of triglycerides.

12. Pharmacotherapeutics- Fibric acid drugs
are used primarily to reduce triglyceride
levels, especially very-low-density
triglycerides, and secondarily to reduce blood
cholesterol levels. They’re typically used to
treat patients with types ii, iii, iv, and mild
type v hyperlipoproteinemia.

13. Drug interactions- Fibric acid drugs may
displace acidic drugs, such as barbiturates,
phenytoin, thyroid derivatives, and cardiac
glycosides. The risk of bleeding increases
when fibric acid derivatives are taken with
oral anticoagulants.

14. HMG-COA REDUCTASE (OR 3HYDROXY-3-METHYL-GLUTARYL-COA
REDUCTASE OR HMGCR)
is the rate-controlling enzyme of the
mevalonate pathway, the metabolic pathway that
produces cholesterol and other isoprenoids.
If these enzyme is blocked, serum cholesterol and
LDL levels decrease, because more LDLs are
absorbed by the cells for processing into
cholesterol. HDL levels increase slightly with this
alteration in fat metabolism.

15. Therapeutic Action and Indications- HMGcoA Reductase inhibitors block the formation of
cellular cholesterol, leading to decrease in serum
LDLs, with a slight increase or no change in the
levels of HDLs. Because these drugs undergo a
marked first-pass effect in the liver, most of their
effects on the process that generates atheromas in
vessel walls. That exact mechanism of action is not
understood.

16. These drugs are indicated as adjuncts with
diet and exercise for the treatment of
increased cholesterol and LDL levels that are
unresponsive to dietary restrictions alone; to
slow the progression of CAD in patients
with documented CAD; and to prevent first
MI in patient who are at risk for MI.

17. Pharmacokinetics-the statins are all
absorbed from the GI tract and undergo the
first- pass metabolism in the liver. They are
excreted in the feces and urine. The peak
effect of this drug is usually seen within 2-4
weeks. These drugs cross the placenta and
have been associated with skeletal
malformations of he fetus.

18. Contraindications and action- These
drugs are contraindicated in the presence
of allergy to any of the statins or to fungal
byproducts or compounds. They are also
contraindicated with active liver disease or
a history of alcoholic liver disease, w/c
could exacerbate, leading to severe liver
failure.

19. Adverse Effect- The most common adverse
effects associated with these drugs reflect
their effects on the GI system: flatulence,
abdominal pain, nausea, vomiting, and
constipation. CNS effects can include
headache, dizziness, blurred vision, fatigue,
and cataract development and may effect
changes in the cell membrane and synthesis
of cholesterol.

20. Cholesterol Absorption Inhibitors- are a
class of compounds that prevents the uptake of
cholesterol from the small intestine into the
circulatory system.
Lower the amount of cholesterol that your
body absorbs. So your blood has lower
total cholesterol and lower LDL (bad)
cholesterol

21. Therapeutic action and indicationsEzetimibe works in the brush border of the
small intestine to decrease the absorption of
dietary cholesterol, leading to drop in serum
cholesterol levels. It is indicated as an adjunct to
diet and exercise to lower cholesterol levels as
monotherapy or as part of combination therapy
with an HMG-CoA inhibitors or a bile acid
sequesterant.

22. Pharmacokinetics- Ezetimibe is
absorbed well after oral administration,
reaching peak levels in 4-6 hours. It is
metabolized in the liver and the small
intestine, with a 22 hours half- life.
Excretion in the feces and urine.

23. Contraindications and CautionsEzetimibe is contraindicated with allergy
to any component of the drug. If it is used
in combination with a statin, it should not
be used during pregnancy or lactation or
with severe liver disease because of the
known effects of statins, including
possible liver problems and renal failure.

24. Adverse Effect- The most common adverse
effect associated with ezetimibe are mild
abdominal pain and diarrhea. It is not
associated with the bloating and flatulence
that occurs with the bile acid sequestrants and
fibrates, other adverse effect have been
reported include headache, dizziness, fatigue,
URI, back pain, muscle aches and pain.

25. NICOTINIC ACID- Lowers total cholesterol,
LDL-cholesterol, and triglyceride levels, while
raising HDL-cholesterol levels.
Vitamin B (Niacin) or Nicotinic Acid, inhibits
release of free fatty acids in the adipose tissue,
increases the rate of triglyceride removal form
plasma, and generally reduces LDL and
triglycerides level and increases HDL levels.

26. The initial effect on lipid levels is usually
seen within 5 to 7 days, with the maximum
effect occurring 3 to 5 weeks. Niacin is
associated with intense cutaneous flushing,
nausea, and abdominal pain, making its use
somewhat limited.

27. It also increases serum levels of uric acid
and may predispose patients to the
development of gout. Niacin is often
combined with bile acid sequestrants fro
increased effect. It is given at bedtime to
make maximum use of nighttime cholesterol
synthesis, and it must be given 4 to 6 hours
after bile sequestrant to ensure absorption.