Dyslipidemia (Hyperlipidemia) Concept Map: An Overview

The aim of this map is to cover the pharmacotherapy of dyslipidemia in an easy and an interesting way that will help you understand the topic and link it with the other related cardiovascular diseases as atherosclerosis.  Look inside the map and understand it through this video. 

EXPLANATION VIDEO

The concept map of Dyslipidemia (Hyperlipidemia) starts with the definition.  Dyslipidemia is a disorder of elevated or abnormal levels of lipids and/or lipoproteins in the blood, characterized by high cholesterol, triglycerides (TGs), or both, or low High-density lipoprotein (HDL) level. 

From this definition branches out the normal physiology of lipid metabolism including what is meant by lipoproteins, function of lipoproteins, and their classification. Low-density lipoproteins (LDL); carry cholesterol from the liver to cells of the body; it is referred to as the "bad cholesterol" lipoprotein.  LDL has a role in initiating the atherosclerosis process; this is how dyslipidemia is a risk factor for atherosclerosis and consequently cardiovascular diseases (a small map for cardiovascular diseases categories is included).

LIPID METABOLISM (Normal Physiology)

In this map lipid metabolism is explained briefly through the following diagram:

Lipid Metabolism - Normal Physiology Click to enlarge

The intestine absorbs dietary fat and packages it into chylomicrons, which are transported to peripheral tissues through the blood.  The enzyme lipoprotein lipase breaks down chylomicrons; and fatty acids enter muscle and adipose tissues. The chylomicron remnants are subsequently taken up by the liver to start the process of very-low-density lipoproteins (VLDLs) synthesis.  The liver secretes VLDL, which undergo lipolysis by lipoprotein lipase to form LDLs.  LDLs are then taken up by the liver and by the peripheral tissues.  HDL is produced by the liver.  Its function is to transport cholesterol from the body back to the liver.  That is why it is called “good cholesterol” lipoprotien.

Most patients are asymptomatic for many years prior to the appearance of physical findings. 

Physical findings can include:

And symptoms of dyslipidemia can include: paresthesias, dypsnea, and confusion.

Watch the video to know when Primary Dyslipidemia is suspected in a patient.

On the other hand, Secondary Dyslipidemia can be caused by the following:

- Diseases: diabetes, hypothyrodism, obstructive liver disease/ biliary cirrhosis, renal disease, nephrotic syndrome/ chronic renal failure, or obesity.

- Drugs: estrogen, progestins, protease inhibitors, anabolic steroids, corticosteroids, isotretinoin, cyclosporine, atypical antipsychotics, thiazide diuretics, or β-Blockers.

These causes should be considered in the diagnosis and the management of dyslipidemia.

Dyslipidemia risk factors are classified as:

Details are available in the video above.

Diagnosis of dyslipidemia is based on the Fasting Lipid Profile of the patient; accompanied by the assessment of cardiovascular risk factors using Framingham Risk Score for patients with ≥2 risk factors.

Three Categories of Risk that Modify LDL-Cholesterol Goals (details are included in the map/video):

These risk categories are linked to (treatment goals) part in the map.

This part of the map starts with dyslipidemia treatment goals (classified according to the risk category) and targets (primary target for therapy is LDL).

Therapeutic Lifestyle Changes (TLC) and dietary recommendations are stated under the part of non-pharmacological treatment of dyslipidemia.

Four classes of lipid-lowering drugs:

In addition to; 

•  the cholesterol absorption inhibitor, Ezetimibe, and

Each drug / drug class has its own map that covers: the mechanism of action, indications, adverse effects, drug interactions, contraindications, and precautions if any.  The map also shows you how to manage certain adverse effects and drug interactions for these drugs.  See the following example for Bile acid sequestrants.

Bile Acid Sequestrants Click to enlarge

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Reviewed and edited by Maha Atef, B Pharm.
Last updated on: 11 January 2013