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Dyslipidemia Overview & Treatments

Dyslipidemia is defined as elevated levels of total cholesterol, LDL-C, or triglycerides, or decreased levels of HDL-C. It can lead to atherosclerosis and cardiovascular diseases. Primary dyslipidemias are genetic and familial, while secondary dyslipidemias are caused by diseases, diet, or drugs. Treatment involves therapeutic lifestyle changes like diet modification and exercise as well as drug therapy like statins, fibrates, resins, and niacin to lower lipid levels and reduce cardiovascular risk. Statins are the most powerful and commonly used drugs for lowering LDL-C levels. Both statins and fibrates can cause hepatotoxicity and myopathy as side effects.

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Mohamed Abouzaid
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214 views15 pages

Dyslipidemia Overview & Treatments

Dyslipidemia is defined as elevated levels of total cholesterol, LDL-C, or triglycerides, or decreased levels of HDL-C. It can lead to atherosclerosis and cardiovascular diseases. Primary dyslipidemias are genetic and familial, while secondary dyslipidemias are caused by diseases, diet, or drugs. Treatment involves therapeutic lifestyle changes like diet modification and exercise as well as drug therapy like statins, fibrates, resins, and niacin to lower lipid levels and reduce cardiovascular risk. Statins are the most powerful and commonly used drugs for lowering LDL-C levels. Both statins and fibrates can cause hepatotoxicity and myopathy as side effects.

Uploaded by

Mohamed Abouzaid
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Pharmacology

Dyslipidemia (Hyperlipidemia) I
STAFF MEMBERS, DEPARTMENT OF PHARMACOLOGY,
Faculty of MEDICINE, NUB

Code of the module


DEFINITION
• Dyslipidemia is defined as
• elevated TC, LDL-C , or TG
• OR decreased HDL-C
• OR combination of these abnormalities.

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• Dyslipidemia  atherosclerosis 
• coronary disease,
• cerebrovascular disease
• peripheral vascular disease.

• Every 1%  in blood cholesterol  1- 2%  in incidence


of CHD.
• Every 1% in HDL-C  1- 2%  in incidence of CHD.

3
Pathophysiology:
Lipoproteins

TG CE

Apoprotein boat

- Apo A for HDL


- Apo B100 for LDL & VLDL
Pathophysiology:
Lipoproteins

HDL LDL

C C
TG TG

A I, A II B 100

VLDL CM

TG TG
C
B 100 + E +C
B 48+E+C

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Lipid Metabolism
• Lipoproteins are classified to:
Composition Density Size

Chylomicrons TG >> C, CE Low Large


Apo B
VLDL TG > CE
lipoproteins
(Non HDL) IDL CE > TG
LDL CE >> TG
Apo A HDL CE > TG High Small
lipoprotein

6
7
The story of lipids
• Chylomicrons transport fats from the intestinal mucosa to liver &
adipose tissues
• VLDL is formed in the liver from TG & cholesterol then released into
blood, hydrolyzed by LPL to become IDL then LDL (LDL then carries
cholesterol to the body’s cells).
• HDL carry cholesterol back to the liver for excretion (Reversible
cholesterol transport).

• When oxidized LDL-C gets high  atheroma formation in the artery


walls  atherosclerosis.
• HDL-C remove cholesterol from the atheroma.
• Atherogenic cholesterol → LDL, VLDL, IDL

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Types & causes of dyslipidemia

1ry dyslipidemia 2ry dyslipidemia 95%


(Genetic, Familial) 5%

1- Diet
2- Disease
3- Drugs
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1ry dyslipidemia
• polygenic hypercholesterolemia & atherogenic dyslipidemia, are the most
common & the result of interaction between genes & lifestyle.
1. polygenic hypercholesterolemia :
• most prevalent form,
•  LDL-C (130-250 mg/dl)
2. Atherogenic dyslipidemia:
• 25% of patients who have lipid disorder,
• moderate  TG & LDL-C with  HDL-C

3. Familial hypercholesterolemia: marked  LDL-C (250-450 mg/dl)


4. Familial Hypertriglyceridemia (chylomicronemia) (due to LPL deficiency): 
chyomicrons & VLDL
5. Familial combined hyperlipidemia:  VLDL & LDL-C

6. Hypoalphalipoproteinemia: HDL-C
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2ry dyslipidemia

Diseases Drugs

1- Accutane (isotretenoin)
1- Endocrinal: DM & Hypothyroidism 2- BB
2- Renal: CKD & Nephrotic 2- Cortisone
syndrome 3- Cyclosporine
3- Pregnancy 4- Oral Contraceptives
5- Diuretics

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3- Treatment of dyslipidemia

Therapeutic lifestyle change


Drug therapy
(TLC)

- Statin
- Diet modification:
- Fibrates
- Weight reduction:
- Resins
- Smoking cessation
- Niacin
- Physical activity increase:
- Ezetimibe

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1) Statins 2)Fibrates
HMG-Co A reductase
inhibitors
Examples - Atorvastatin - Pravastatin - Etofibrate - Fenofibrate
- Lovastatin - Simvastatin - Gemfibrozil - Bezafibrate
- Rosuvastatin - Clofibrate (should not be used as
it may cause cholangiocarcinoma and
other GIT cancers)
Mechanism  HMG-Co A reductase enz  TG through :
[rate limiting enz] ➔  1.  LPL enz. ➔  LDL
cholesterol synthesis ➔ 2.  Hepatic synthesis of T.G
compensatory  in LDL & VLDL
receptors on hepatocytes ➔ 3  HDL
 LDL & cholesterol
NB.: better take at night (as
cholesterol synthesis is maximum at
night) except atorvastatain &
rosuvastatin (long t ½)
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• The most powerful drugs for lowering LDL-C (30- 63 %) .

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1) Statins 2)Fibrates
HMG-Co A reductase
inhibitor
Side effects 1. Hepatotoxic ➔  serum 1. Hepatotoxic ➔  serum
tansaminases transaminases
2. Myopathy & myositis 2. Myopathy & myositis
➔  serum creatine kinase ➔  serum creatine kinase
3. Contra indicated in 3. Contraindicated in
pregnancy & lactation pregnancy & lactation

4. Cholesterol gall stones &


cholecystitis
5. Displace other drugs
from plasma proteins

15

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