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Amino acid metabolism
Nitrogen and urea cycle
Citric acid cycle
Electron transport chain and oxidative phosphorylation
Pentose phosphate pathway
Physiological changes during exercise
Fatty acid oxidation
Fatty acid synthesis
Ketone body metabolism
Maple syrup urine disease
Ornithine transcarbamylase deficiency
Glucose-6-phosphate dehydrogenase (G6PD) deficiency
Hereditary fructose intolerance
Pyruvate dehydrogenase deficiency
Glycogen storage disease type I
Glycogen storage disease type II (NORD)
Glycogen storage disease type III
Glycogen storage disease type IV
Glycogen storage disease type V
Mucopolysaccharide storage disease type 1 (Hurler syndrome) (NORD)
Mucopolysaccharide storage disease type 2 (Hunter syndrome) (NORD)
Fabry disease (NORD)
Gaucher disease (NORD)
Metachromatic leukodystrophy (NORD)
Niemann-Pick disease type C
Niemann-Pick disease types A and B (NORD)
Tay-Sachs disease (NORD)
Disorders of amino acid metabolism: Pathology review
Disorders of carbohydrate metabolism: Pathology review
Disorders of fatty acid metabolism: Pathology review
Dyslipidemias: Pathology review
Glycogen storage disorders: Pathology review
Lysosomal storage disorders: Pathology review
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Dysbetalipoproteinemia (Type III Familial Dyslipidemia)
Familial Hypercholesterolemia (Type IIa Familial Dyslipidemia)
Hyperchylomicronemia (Type I Familial Dyslipidemia)
Hypertriglyceridemia (Type IV Familial Dyslipidemia)
Jamie is a 24-year-old male presenting to the emergency department complaining of sudden onset chest pain and shortness of breath when playing soccer.
On further evaluation, his ECG showed ST-segment elevation and laboratory evaluation showed elevated troponin I levels.
After instituting treatment, Jamie and his family inquire about the odd early onset of his disease.
The physical examination of the skin showed numerous xanthomas.
A lipid panel is ordered and shows marked elevation of LDL.
Jamie had a myocardial infarction which was caused by an underlying lipid disorder.
Lipid disorders include both hyper and hypolipidemia.
Hyperlipidemia can manifest as a high level of cholesterol, a high level of triglycerides, or a combination of both.
Hypolipidemia is the opposite where there’s a low level of these lipids.
So let’s do a quick overview of the physiology of lipid metabolism.
After eating a fatty meal, cholesterol and fatty acids enter the intestinal cells.
The fatty acids are assembled into triglycerides, and then they, along with a small amount of cholesterol, are packaged together with lipoproteins to form chylomicrons.
Chylomicrons move into the lymphatic vessels and eventually end up getting emptied into the left and right subclavian veins where they enter into the blood.
Now an enzyme in capillaries called lipoprotein lipase breaks down the chylomicrons to free the triglycerides, and then it also breaks the triglycerides down into fatty acids.
These can be taken up by nearby tissues to generate energy, like in the muscle cells, or for storage, like in adipocytes.
The remains of the chylomicrons will contain lipoproteins and a small amount of triglyceride and cholesterol, so these chylomicron remnants head to the liver to deposit the leftover lipid molecules.
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