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This Concept Map, created with IHMC CmapTools, has information related to: LDLR deficiency, HDL which can be degraded by hepatic lipase, excreted leading to further creation of Bile Acids, Bile Salts and reabsorbed, Bile Acids in The Liver, APO B/E receptor leading to accumulation of plasma LDL, Golgi Apparatus where it is cleaved into a Soluble Fragment, excreted leading to LOWERED Cholesterol Levels, APO C-11 and APO E becomes LDL, diagnosis of homozygous familial hypercholesterolemia (FH) which at 3 yrs of age was characterized by normal triglyceride levels, Cholesterol Levels when Low Cholesterol Levels, reabsorbed maintaining Cholesterol Levels, cholesterol can be converted into Bile Acids, parents' total cholesterol levels = 300-400 mg/dL aids with diagnosis of homozygous familial hypercholesterolemia (FH), truncated LDL receptor resulting in "receptor-defective" LDL receptor activity, lipoporteins in to the Nascent VLDL, oxidized LDL which is phagocytosed, macrophage scavenger receptors which at high lipoprotein levels become Foam cells, Myocardial Infarction which is a leading cause of Death, APO B/E receptor at Clathrin coated pit, leads to clearance of lipoproteins from circulation into the Liver