Internal Diseases and Therapy · MU Sofia

77. Dyslipidemia

Explains dyslipidaemia as both hyperlipidaemia and hypolipidaemia, beginning with lipoprotein structure and the exogenous and endogenous lipid pathways. Gives reference ranges for a lipid panel, then sets out the primary types I to V with their defects, plus secondary causes. Closes with statin and second-line treatments, including dosing and when statins should be avoided, and then hypolipidaemia causes, investigation and primary disorders.

Inside: 1 section · 2 labelled pictures · 14 flashcards · 5 min

Topic 78 of 139 in the MU Sofia syllabus for Internal Diseases and Therapy (Medicine, Years 4 and 5). The free AceMed note covers it in 1 section, about 713 words (5 min of reading), with 14 flashcards.

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  1. Dislipidemia

Dislipidemia

Dislipidemia can refer to either hyperlipidemia or hypolipidemia. Below we address these two types of lipid disorder.

Overview of lipid metabolism

As lipids are hydrophobic they cannot pass through the bloodstream with ease. They must instead be bound to various lipoproteins, complexes of lipids and proteins. Lipoproteins consist of a lipid core, with TAG and cholesterol esters, and an outer shell made from proteins, phospholipids and nonesterified cholesterol. Lipoproteins can be divided into the following groups:

Image: “Structure of a Lipoprotein” by AntiSense, CC BY-SA 3.0, via Wikimedia Commons.

  • Chylomicrons (mostly TAG, assembled in intestinal mucosal cells)
  • VLDL (50% TAG, delivers TAGs to tissues)
  • LDL (50% cholesterol, delivers cholesterol to tissues)
  • HDL (50% protein, can help to mop up cholesterol)

The formation of lipoproteins can be divided into exogenous and endogenous pathways, depending on if the lipoprotein has come from the diet (exogenous) or synthesis in the liver (endogenous).

Exogenous pathway:

  • Fats consumed and broken down by bile to form chylomicrons
  • Chylomicrons (droplets of fat found in blood or lymph) travel through capillaries, further broken down into free fatty acids by lipoprotein lipase
  • The remnants of this go to the liver and form dietary cholesterol

Endogenous pathway

  • Dietary cholesterol forms VLDLs which travel through the capillaries, again to be broken down to free fatty acids by Lipoprotein lipase.
  • The remnants of this become Intermediate density lipoproteins which either go into the liver to form endogenous cholesterol, or form LDLs
  • These LDLs can then go on to Extrahepatic tissue and form HDLs
  • The HDLs will then go back to form IDLs or go straight back into the liver.

The references ranges for a normal lipid panel are:

  • Total cholesterol - 140-200 mg/dL (3.6-5.2 mmol/L)
  • HDL-C - 40-75 mg/dL (1.0-2.0 mmol/L)
  • LDL-C - 50-130 mg/dL (1.3-3.4 mmol/L)
  • Triglycerides - 60-150 mg/dL (0.7-1.7 mmol/L)

Hyperlipidemias are conditions where there are abnormally elevated levels of lipids or lipoproteins in the blood. Hyperlipidemias are common in the general population and are risk factors for cardiovascular disease due to their influence on atherosclerosis.

Hyperlipidemias are classified as either familial (primary, genetic) or acquired (secondary). The primary types are as follows.

  • Type I
  • Characterised by high numbers of chylomicrons due to deficiencies of lipoprotein lipase enzymes
  • Can lead to acute pancreatitis, lipemia retinas, xanthomas and hepatosplenomegaly.
  • Type II
  • The most common form, sub classified into IIa and IIb

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