Classification Physicians and basic researchers classify<unk> s in two distinct ways. One way is its presentation in the body (including the specific type of lipid that is increased). The other way is due to the underlying cause for the condition (genetic, or secondary to another condition). This classification can be problematic, because most conditions involve the intersection of genetics and lifestyle issues. However, there are a few well-defined genetic conditions that are usually easy to identify. The three main blood levels collected to assess for<unk>  is triglycerides(TG), high density lipoprotein cholesterol (HDL-C), and low density lipoprotein cholesterol (LDL-C). High triglyceride levels (>1.7 mmol/L fasting) can indicate<unk> . Triglycerides are transported through the blood by using very low density lipoproteins (VLDL) as a carrier. One thing to note when measuring triglyceride levels is that fasting for 8-12 hours is required to get an accurate result as non-fasting TG results may be falsely elevated. If TG results are greater than 10 mmol/L, then this needs to be addressed since severe hypertriglceridemia is a risk factor for acute pancreatitis. Another blood level collected to assess<unk>  is HDL-C. HDL cholesterol is made up of very little lipids and a high amount of protein. It is beneficial in the body because it functions by going to the tissues and picking up extra cholestrol and fat. Due to the positive effects of HDL-C, it is named "good cholesterol" since it helps prevent plaque formation. Other functions of HDL-C is promoting cardiovascular health such as antioxidation effects, protection against thrombosis, maintenance of endothelial function, and maintaining low blood viscosity. Due to the positive functions of HDL cholesterol, a low level indicates<unk>  and is a risk factor for complications. Another diagnostic test that is often reviewed is LDL cholesterol. Low density lipoproteins are made up of cholesterol, TG, phospholipids, and apolipoproteins. LDL-C molecules bind to the endothelium of blood vessels and cause plaque formation. Once plaques are formed, LDL-C floating in the bloodstream can attach to the plaques and cause further accumulation. In addition to plaque formation, LDL-C molecules can undergo oxidation. Oxidation can cause further accumulation of cholesterol and the release of inflammatory cytokines, which damages the blood vessels. Due to the damaging effects of LDL-C, high levels increase the risk for cardiovascular disease and indicate<unk> .<unk> s can also be classified based on the underlying cause, whether it is primary, secondary, or a combination of both. Primary<unk> s are caused by genetic disorders that can cause abnormal lipid levels without any other obvious risk factors. Those with primary<unk> s are at higher risk of getting complications of<unk> s, such as atherosclerotic cardiovascular disease, at a younger age. Some common genetic disorders associated with primary<unk> s are homozygous or heterozygous hypercholesterolemia, familial hypertriglyceridemia, combined hyperlipidemia, and HDL-C metabolism disorders. In familial hypercholesterolemia, a mutation in the LDLR, PCSK9, or APOB is usually the reason for this and these mutations result in high LDL cholesterol. In combined hyperlipidemia, there is an overproduction of apoB-100 in the liver. This causes high amounts of LDL and VLDL molecules to form. A unique sign of primary<unk> s is that patients will often present with acute pancreatitis or xanthomas on the skin, eyelids or around the cornea. In contrast to primary<unk> s, secondary<unk> s are based on modifiable environmental or lifestyle factors. Some diseases that are associated with a higher risk of<unk>  are uncontrolled diabetes mellitus, cholestatic liver disease, chronic kidney disease, hypothyroidism, and polycystic ovarian syndrome. What people eat can also have an influence, with excessive alcohol use, too much carbohydrates, and diets high in saturated fats having a higher risk. Some medications that may contribute to<unk>  are thiazide diuretics, beta blockers, oral contraceptives, atypical antipsychotics (clozapine, olanzapine), corticosteroids, tacrolimus, and cyclosporine. Other non-hereditary factors that increase the risk of<unk> s are smoking, pregnancy, and obesity. The Fredrickson Classification seen below classifies<unk> s into categories: Phenotype I IIa IIb III IV V Elevated Lipoprotein Chylomicron LDL LDL and VLDL IDL VLDL VLDL and chylomicrons
Dyslipidemia
Hyperphosphatemia
Hyperlipidemia
Hypertriglyceridemia
Hypolipoproteinemia
Hypercholesterolemia
Hypocholesterolemia
Dysglycemia