Hyperlipidemia Flashcards
Hyperlipoproteinemia
Increase in Lipoproteins
What lipids contribute to lactescence
Chylomicrons and VLDLs
Physiologic hyperlipidemia
Increase in chylomicrons
-Ingest TG-> digested to MG and FA-> absorbed by intestine-> TG rich chylomicrons-> enter lymphatic vessel-> enter blood through thoracic duct
When should physiological hyperlipidemia be cleared
6-12hr
Hyperlipidemia in a fasted state causes
Increased synthesis of VLDL
Decreased lipoprotein degradation
Defective lipoprotein removal
Idiopathic hyperlipidemia
Primary or congenital hyperlipidemia
Miniature schnauzers
Leads to defective intravascular processing of lipoproteins
Disorders that result in hyperlipidemia
-Acute pancreatitis
-Cholestasis
-Hypothyroidism
-Nephrotic syndrome and PLE
-Equine hyperlipemia
-Diabetes mellitus
Acute pancreatitis
Increase in TG due to increase in VLDL
Pancreatic damage-> decreases insulin and LPL activity and inflammatory cytokines alter metabolism-> decreased intravascular lipolysis and processing of lipoproteins-> increased VLDL and increased TG and sometimes cholesterol
Cholestasis
Increase in cholesterol usually without TG
Decreased cholesterol excretion into bile and defective hepatocyte uptake of LDL
Diabetes mellitus
Increase in TG.
Decreased insulin-> decreased LPL
Increased VLDL synthesis and increased mobilization of lipids from increased hormone sensitive lipase and then those FA enter the liver and are made into TG, cholesterol and ketones
Hypothyroidism
Increased cholesterol
Decreased thyroid hormone-> decreases intravascular lipolysis or processing because of decreased hepatic lipase and decreased clearance of LDL, decreased thyroxine also decreases LPL activity-> increased cholesterol rich LDL
Nephrotic syndrome and PL nephropathy
Increased cholesterol and TG later on
Early: decreased clearance of LDL from loss of protein needed for expression (LCAT)-> decreased ability to pick up excess cholesterol from tissue
Late: stimulate VLDL synthesis in hepatocytes and defective lipolysis of lipoproteins in plasma-> decreased intravascular processing-> loss of protein needed for LPL binding to endothelial cells
Equine hyperlipemia
Increased TG
Due to negative energy balance-> rapid mobilization of peripheral adipose tissue-> increased TG synthesis-> increased VLDL in plasma
Forms of equine hyperlipemia
-Hyperlipidemia (mild)
-Hyperlipidemic syndrome( fatty liver impaired hepatic function) also known as equine metabolic syndrome
Response to fasting in equines
Lipemia dominates over ketosis unlike other species