High Cholesterol and Familial Hypercholesterolemia, Animation


Lipid profile, cholesterol regulation, risk factors for high cholesterol, pathology and genetics of familial hypercholesterolemia. This video and other related images / videos (in HD) are available for the instant download license here:
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Cholesterol is an essential component of all animal cells, but TOO MUCH BLOOD cholesterol is a high risk factor for cardiovascular diseases such as heart attacks and strokes.
Cholesterol levels are measured in a blood test known as lipid panel or lipid profile. This test usually reports: total cholesterol; Low density lipoprotein, LDL, also known as "bad" cholesterol; High density lipoprotein, HDL or "good" cholesterol; and triglycerides. A desirable profile includes LESS than 200 mg / dL of TOTAL cholesterol, with LESS than 100 mg / dL of LDL and MORE than 40 mg / dL of HDL.
The body obtains cholesterol in 2 ways: from foods of animal origin, and its own endogenous production. Usually, cholesterol levels are kept under negative feedback control. THE LOW INTRACULULAR cholesterol levels INDUCE your own production, while HIGH cholesterol levels INHIBIT.
It should be noted, however, that this regulation applies to the concentration of cholesterol INSIDE CELLS, NOT in BLOOD. The HIGH prevalence of HIGH-BLOOD cholesterol throughout the world suggests that this control mechanism is NOT sufficient to maintain healthy cholesterol levels when challenged by a number of factors, including poor diet, lack of exercise, smoking, obesity, diabetes and aging.
In addition, some people have a HEREDITARY condition called "familial hypercholesterolemia," FH, which causes very high levels of LDL, the "bad" cholesterol, at a young age. If left untreated, patients are likely to have heart attacks between 40 and 50 years. LDL is basically a vehicle that transports cholesterol from the liver to peripheral cells so that it can be used in the cell membrane. Peripheral cells take LDL by endocytosis, using their LDL receptor, which binds to a protein ligand on the surface of LDL. Most cases of FH are caused by a MUTATION in the LDL receptor gene. A defective LDL receptor REDUCES the absorption of LDL, leaving MORE LDL in the circulation while the cells are DEFICIENT in the cholesterol. LOW intracellular cholesterol levels induce a higher production of endogenous cholesterol in the liver, causing even higher levels of circulating LDL. A copy of the mutated gene is enough to cause high cholesterol. Therefore, the condition is inherited in an autosomal DOMINANT manner. A father with an altered gene has a 50% chance of passing it on to a child. If both parents have HF, each child has a 50% chance of having HF, a 25% chance of NOT having HF and a 25% chance of having TWO copies of the mutated gene, called HOMOCIJA FH. Without treatment, homozygous patients with HF may have heart attacks in their twenties and may not survive after 30 years.
Treatments for high cholesterol should start with changes in lifestyle, such as healthy diets and physical exercise. In addition to that, some people may require medications to lower cholesterol. These medicines inhibit the production of cholesterol, intestinal absorption or reabsorption in the form of bile. Patients homozygous with HF generally require more DRASTIC treatment measures that include a procedure called APLICES LDL. In this procedure, blood is diverted through a FILTRATION device where LDL is removed before the remaining plasma and blood cells return to the body. The procedure is repeated weekly or biweekly.

Video credits to Alila Medical Media YouTube channel





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    High Cholesterol and Familial Hypercholesterolemia, Animation

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