Drugs Of Hyperlipidemia

2. Hyperlipidemia
• Presented to: Sir Muhammad Riaz
• Presented by: Nayab Ali & Memoona Muqim

3. Hyperlipidemia
• It is an abnormally elevated level of
any or all lipids or lipoproteins in
blood.
• Coronary Heart Disease is leading
cause of death worldwide.
• CHD is correlated with elevated
levels of low density lipoproteins,
cholesterol, TG and low levels of
high density lipoproteins cholesterol
HDL.
• Elevated cholesterol
levels(Hyperlipidemia) may be due
to life style factors e.g Lack of
exercise.
• Diet containing excess saturated fats.

4. .
• HYPERLIPIDEMIA defect can also be inherited in
lipoproteins metabolism or more common form of
combination of genetic and life style factors.
• Appropriate life style changes along with drug therapy
can lead to 30_40% reduction in mortality.
• Normal value of body's cholesterol levels in lumen of
blood stream is less than 200mg/dL.
• NOTE : High level of low density lipids and low level of
high density lipid are risk factors for CHD.

5. .

6. .
• NOTE: Therapeutic life style change such as diet,
exercise and weight loss may help to reduce cholesterol
levels however life style modifications do not replace the
need for drug therapy in patients who fall in one of the
four statin benefit group.

7. DRUGS FOR HYPERLIPIDEMIA
.

8. Drugs for Hyperlipidemia
• Statins
• Niacin
• Fibrates
• Bile Acid sequestrants
• Cholesterol absorption inhibitors
• Omega 3 Fatty acids
• Combination drug therapy.

9. STATINS (HMG CoA reductase inhibitor)
• HMG CoA Reductase inhibitor is
commonly known as STATINs, lower low
density lipids resulting in a substantial
reduction in coronary events and death
from CHD.
• Statins are first line treatment for the
patients with elevated risk of ACSVD
• ( Arteriosclerosis cardio vascular disease)

10. Mechanismofaction
• Drugs :
Atorvastatin, Simvastatin, rosuvastatin, fluvastatin.
• Statins are competitive inhibitors of HMG CoA
reductase, the rate limiting step in cholesterol
synthesis.
• Plasma cholesterol level is reduced by decrease
cholesterol synthesis.
• Rosuvastatins and atorvastatin are most potent
low density lipid lowering statins.

11. • Note:
• Because statin undergo a marked first pass extraction
by liver their dominant effect is on that organ. The HMG
CoA reductase inhibitor also decrease triglycerides level
and may increase high density lipids in some patients.

12. Therapeutic drugs
• These drugs are used to lower the risk of ASCVD for the
patients in four statins benefit groups:
• B.P
• ASCVD
• cholesterol level

13. • Side Effects :
• Increase liver enzymes ALT , AST, ALP increase
therefore LFT should be evaluated
• Note :
• Hepatic insufficiency can cause drug accumulation.
Increase the effect of warfarin.
• PT APTT INR monitoring is necessary.
• Rhabdomyolysis
• Contraindicated : pregnancy , lactation , active liver
disease.

14. 2) NIACIN NICOTINIC ACID
• Also known as nicotinic acid is an organic compound and a
form of vit B3 an essential human nutrient
• Niacin decrease LDL 10 – 20% and is the most effective agent
for increase HDL.
• It also lowers the triglyceride by 20% - 35%, at typical doses
1.5 to 3g / day.
NOTE:
Uses in pellagra deficiency of niacin.

15. Niacin can be used in combination with statins.
Mechanism of action:
• At gram doses niacin strongly inhibits lipolysis in adipose
tissues, thereby decrease production of free fatty acids.
• The liver normally uses circulating free fatty acids as a major
precursor for triglyceride synthesis.
• Low level of TG decrease the production of Hepatic VLDL as
a result LDL-C also decreases.
Adverse effects :
• Uncomfortable feelings
• Pruritus
• Nausea
• Abdominal pain
• Gout

16. .

17. 3) FIBRATES :
Fenofibrate and gemifibrozil are derivatives of fibric acid that
decrease serum triglyceride and increase HDL-C
Mechanism Of Action:
• The peroxisome proliferator, activated receptors(PPARs) are
member of the nuclear receptor family that resilete lipid
metabolism PPAR upon binding to their natural ligands for
antihypertensive drugs, PPARs are activated.
• Then they bind to peroxisome proliferator response elements
• Which ultimately leads to decrease TG concentration through
increase expression of lipoprotein lipase.

18. NOTE:
• Fenofibrate is more effective then gemifibrozil in decreasing
triglyceride level.

19. Side Effects:
• GIT disturbances
• Myositis
• Muscle weakness
• Myopathy and rhabdomyolysis

20. • (Resins) rare significant LDL-C lowering affects, although the
benefits are less than those observed with statins.
Mechanism of Action:
• Anion exchange resins bindwith
• Negatively charges(bile acids + bile salts) in samall intestine.
• Resin + bile acid complex excreted into feces
• They lowering the bile acid concentrations
Bile Acid Sequestrants

21. • Due to which hepatocytes increase conversion of cholesterol to
bile acids, which are essential component of bile
• Cholesterol concentration decrease LDL-C also decrease.
Uses:
Anti Hyperlipidemia
Side Effects :
• GIT disturbing
• Constipation
• Nausea
• Flatulence

22. 5) Cholesterol Absorption Inhibitors.
Drug name:
Ezetimibe.
• Selectively inhibits absorption of dietary and biliary
cholesterol in the small intestine.
• Leading to a low in the delivery of intestinal cholesterol to the
liver.
• This cause a reduction of cholesterol in stores and Increase in
cholesterol clearances from blood.

23. 6) Omega-3 Fatty Acids:
• Omega-3 polyunsaturated fatty acids are essential fatty acids
inhibit VLDL and TG synthesis in the liver.
Side effects:
• Abdominal pain
• Nausea
• Diarhea

24. 7) Combination Drug Therapy
• Is given by two anti hyperlipidemic drugs to arrive treatment
goals.
• Patients with ASCVD (atherosclerotic cardiovascular
disease ) risk or tolerated with statins may be consider
combination therapy.
But risk involves:
• Liver toxicity
• Muscles myopathy