Lipids & Glucose Flashcards
(48 cards)
What is hyperlipidemia? Hypolipidemia?
HYPER = increased circulating lipids, including cholesterol and/or triglycerides (NOT LIPEMIA)
HYPO = decreased circulating lipids, including cholesterol and/or triglycerides
What are the 5 major functions of lipids?
- physical: thermogenesis, thermal insulation, shock absorption
- energy source (triglycerides, fatty acids)
- structural components to cell membranes (phospholipids, cholesterol)
- substrates for hormones and other messengers
- precursors for synthesis of steroid hormones, vitamin D, and bile acids
- immunity
What happens to dietary lipids after they are ingested? What are the 5 major types found in the plasma?
digested by pancreatic lipas and emulsified by bile salts to monoglycerides and fatty acids
- cholesterol
- cholesterol esters
- triglycerides
- phospholipids
- non-esterified fatty acids (NEFAs)
What is the importance of triglycerides and cholesterol?
TRIGLYCERIDES - comprises stored fats and is metabolized for energy (most common and efficient form of energy storage in mammals)
CHOLESTEROL - make up cell membranes, are the building blocks for steroid hormones, and used to synthesize bile acids
What are the 2 major functions of non-esterified fatty acids (NEFAs)? What sources do they come from?
- energy source
- metabolic building blocks - incorporated into triglycerides
diet or mobilized from fat stores from triglycerides metabolism
What happens to non-esterified fatty acids (NEFAs) after the are ingested or mobilized from fat stores?
- forms acetyl-CoA and enters the TCA cycle to produce ATP
- converted into ketone bodies
- reformed back into triglycerides in fat stores
How are lipids transported?
insoluble in water —> attach to apoproteins that stabilize and solubilize them in the aqueous phase of blood
What are lipoproteins?
proteins (apoprotein) + lipids
large spherical particles with a hydrophobic core containing TGs and cholesterol, and a hydrophilic surface composed of phospholipids, free cholesterol, and apoproteins
How is lipemia observed grossly? What does it indicate?
visibly hazy to white/opaque serum or plasma (larger particles = increased blocking of light transmission)
presence of chylomicrons or VLDLs
What is expected on biochemistry panels with lipemia?
increased triglycerides +/- increased cholesterol
(NOT increased cholesterol alone - serum/plasma with increased cholesterol alone appears normal)
What are 2 common artifacts caused by lipemia in vitro?
- falsely elevated Hgb, MCH, and MCHC due to its detergent effec on cell membranes, leading to RBC hemolysis
- falsely elevated plasma protein on refractometer byt causing the formation of and indistinct demarcation line
What chemistry panel artifacts are seen with lipemia
- hyperglycemia
- hypercalcemia
- hyperphosphatemia
- hyperbilirubinemia
- hyponatremia
- hypokalemia
- hypoproteinemia
- hypoalbuminemia
(depends on the methodology and analyzer)
What is a primary cause of hyperlipidemia?
hereditary alterations in lipoprotein metabolism or production
What are some secondary causes of hyperlipidemia?
- postprandial
- DM
- acute necrotizing pancreatitis in dogs
- equine hyperlipidemia in ponies, horses, and donkeys
- hypothyroidism
- hyperadrenocorticism
- anorexia in horses
- obstructive cholestasis in dogs and cats
- nephrotic syndrome and protein-losing enteropathy
- endotoxemia and inflammation
(secondary > primary)
How are lipid values affected by postprandial hyperlipidemia? In what animals is this most common?
- triglycerides are mildly to markedly increased
- mild increases in cholesterol possible
MONOGASTRICS - dogs and cats within 1-2 hr after a meal, peaks at 2-8 hr, and is cleared by 8-16 hours
Why is a 12-hour fast recommended before bloodwork?
increased lipid values typically clear within 8-16 hours after a meal
- if still elevated after 12 hours = persistent hyperlipidemia
How are lipid values affected by diabetes mellitus? What causes the hyperlipidemia? In what animals is this common?
- mild to marked hypertriglyceridemia
- mild hypercholesterolemia
decreased insulin causes defective VLDL processing and LPL inhibition
cats, dogs, and horses with a complex pathogenesis, so lipid profile will be highyl variable
How are lipid values affected by acute pancreatitis? What causes this?
- mild to moderate hypertriglyceridemia
- mild hypercholesterolemia
decreased insulin production and the production of inflammatory cytokines inhibit lipoprotein lipase and LPL activity
(biliary excretion and increased hepatic production increases cholesterol)
How are lipid values affected by equine hyperlipidemia syndrome? In what animals is this most common?
marked hypertriglyceridemia
Shetland ponies, miniature horses, donkey mares
What is the mechanism of equine hyperlipidemia syndrome causing secondary hyperlipidemia? What are the 2 groups?
negative energy balance (decreased feed consumption, anorexia, pregnancy, lactation, obesity, renal failure, endotoexmia) causes the mobilization of fatty acid to the liver, which causes a marked increase in triglycerides and VLDL
- hyperlipidemia (mild disease): [TG] < 500 mg/dL
- hyperlipidemic syndrome (poor prognosis): [TG] > 500 mg/dL —> fatty liver with cholestasis and decreased liver function
How does hypothyroidism cause secondary hyperlipidemia?
lack of thyroid hormones (T3, T4) decreases LPL and hepatic lipase activity
- marked hypercholesterolemia
- +/- concurrent hypertriglyceridemia
How does hyperadrenocorticism cause secondary hyperlipidemia?
increased endogenous or exogenous steroids causes increased VLDL synthesis and insulin resistance
- hypercholesterolemia +/- hypertriglyceridemia
What is obstructive cholestasis most likely secondary to? How does it cause secondary hyperlipidemia? What is characteristic of lipid values?
decreased clearance of bile
obstruction causes an increased cholesterol content in hepatocytes and reduced cholesterol excretion
cholesterolemia without hypertriglyceridemia
How do nephrotic syndrome and protein-losing enteropathy cause secondary hyperlipidemia? How are lipid values affected? What are the 4 most common signs?
increased VLDL production, defective lipolysis, and defective conversion of cholesterol to bile acids
hypercholesterolemia +/- hypertriglyceridemia
