Dyslipidemia Concept Map

Dyslipidemia (Hyperlipidemia) Concept Map: An Overview

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

EXPLANATION VIDEO

DEFINITION

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, the 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:

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 undergoes 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” lipoprotein.

CLINICAL PRESENTATION

Most patients are asymptomatic for many years prior to the appearance of physical findings.  Physical findings can include:

• corneal arcus of the eye and
• tuberous xanthomas in the Achilles tendon, hands, feet, elbows, and/or knees.

And symptoms of dyslipidemia can include paresthesias, dyspnea, and confusion.

CLASSIFICATION

Primary Dyslipidemia; occurs due to genetic mutations; it affects lipoprotein synthesis and metabolism causing the following lipid disorders:        

Isolated hypercholesterolemia (increase in cholesterol only) 

• Familial hypercholesterolemia (FH) 
• Familial defective apoB-100 (FDB) 
• Polygenic hypercholesterolemia         

Isolated hypertriglyceridemia (increase in TGs only)

• Familial hypertriglyceridemia (FHTG)
• Lipoprotein lipase (LPL) deficiency
• Familial apoC-II deficiency         

Mixed or combined hyperlipidemias (increase in both cholesterol and TGs) 

• Familial combined hyperlipidemia (FCHL)
• Familial dysbetalipoproteinemia (FDBL)

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, hypothyroidism, 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.

RISK FACTORS

Dyslipidemia risk factors are classified as: 

• Positive Risk Factors
• Negative Risk Factors
• Emerging Risk Factors

Details are available in the video above.

DIAGNOSIS 

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):

1. CHD and CHD Risk Equivalents.
2. For patients with ≥2 risk factors, perform Framingham 10-year CHD risk assessment.
3. For patients with ≤1 risk factor, 10-year risk assessment is not required.These risk categories are linked to (treatment goals) part in the map.

TREATMENT

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.

Pharmacological treatment of dyslipidemia includes:

Four classes of lipid-lowering drugs:

• the 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (the “statins”), including; atorvastatin, fluvastatin, lovastatin, pravastatin, rosuvastatin, simvastatin, and pitavastatin
• the fibrates (gemfibrozil and fenofibrate),
• niacin/nicotinic acid, and
• the bile acid binding resins (colestipol, colesevelam, and cholestyramine)

In addition to; 

• the cholesterol absorption inhibitor, Ezetimibe, and
• Omega-3 fatty acids (fish oils)

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.

Order the map

You can order the Dyslipidemia concept map in any of the following forms according to your preference. Our maps are comprehensive in a way that can benefit both students and clinicians.

This map is available in two forms;
1. Printable version.
2. Whole map version.

Check them out below to know the difference, so that you can choose what is suitable for you. And please feel free to leave your feedback, comments, or questions in the comments section below.

Dyslipidemia concept map is written by: May Mehanna, BCPS
Reviewed and edited by Maha Atef, B Pharm.
Last updated on: 11 January 2013