Lipid Testing Flashcards
Lipoproteins
(define, list 4 types)
Def: lipids bound to proteins that are closely inter-related but differ in terms of physiochemical properties (electrophoretic mobility, density)
List:
- Chylomicrons (primarily triglycerides)
- LDLs (primarily cholesterol)
- VLDLs (primarily triglycerides)
- HDLs (pro c small amt cholesterol)
High Density Lipoproteins (HDLs)
(% total cholesterol, production, function)
% Total Cholesterol: 20
Production: Liver and small intestine, increased c exercise
Function:
- Remove cholesterold from pheripheral tissues and endothelium (“vacuum”)
- Transport cholesetrol to liver for excretion
- Reverse cholesetrol transport - protective mechanism for heart disease
Low Density Lipoproteins (LDLs)
(Structure, Function, Result)
Structure:
- 45% cholesterol - core
- 25% protein - amphilic casing
- 10% triglyceride - nonpolar capsule
- 20% phospholipid
Function: Carry cholesterol for deposition in peripheral tissues
- Extra info - ampolipopro B receptors in liver stimulate collection of this molecule
Result: Increased risk of atherosclerotic heart and perhipheral vascular diease
Very Low Density Lipoprotein (VLDL)
(% cholesterol, function, clinical use)
% Cholesterol: 70% triglycerides
Function:
- Transport triglycerides to peripheral tissue
- Convert to LDL by lipoprotein lipase in skeletal muscle
Clinical Use:
- Useful predictor of coronary outcomes
- Second target of hypercholesteremia tx
Lipoprotein Sizes
Chylomicron > VLDL > IDL > LDL > HDL
Chylomicron
(structure, function, physiology)
Structure: 90% triglycerides
Function: Transport exogenous lipids to liver, adipose, cardiac, and skeletal muscle tissue - triglycerdies are then broken down by lipase
“Lipid carriers of the body”
Physiology:
- Carry absorbed lipids from intestinal tract to bloodstream
- Cisterna Chyli receive fat from small intestine
- Dump fat into circulation
Lipoprotein Function
(general)
Transport cholesterol, triglyceride, and other insoluble fats to its location of utilization
- Adrenal glands + gonads = steroid hormone synthesis
- Cell membrane prdctn
- Bile prodctn
Lipid Profile
(6 tests, general fctn)
Tests: Pannel may vary between labs
- Total cholesterol
- Triglycerides
- HDL
- LDL
- VLDL
- Cardiovascular risk ratio
Functions: Screen/monitor arthlerosclerosis
Total Cholesterold Indication
Identify pts at risk for artherosclerotic heart disease
Usually done as part of lipid profile testing, alone it is not useful
Clinical Signficance, Cholesterol
(2 points)
- Main lipid asst c vascular disease
- Required for synthesis of
- Steroids
- Sex hormones
- Bile acids
- Cellular membranes
Physiology, Cholesterol
(origin, metabolism, transport)
- Origin - animal fat and endogenous
- The human body produces enough cholesterol for normal function
- Metabolism - liver
- Transport - via lipoproteins
- 25% - bound to HDL
- 75% - bound to LDL
- LDL is most directly asst c inc CHD risk
Clinical Significance, Triglycerides
(Production, Function, Increase)
Production: In the liver from the following building blocks
- Glycerol
- Other fatty acids
Function: Storage source of energy
Increased: Deposition in fatty tissues
Indications, Triglyceride Testing
(3)
- ID risk of developing CAD
- Suspected fat metabolism disorders
- Diabetes (overeating food that cannot be metabolized so more triglyceride formation)
Differentials, Increased Triglycerides
(7)
- Famlial hypertriglyceridemia
- Hyperlipidemia (primary or secondary) - as lipids exist, so do trigs
- Hypothyroidism - decreased triglyceride catabolism
- High carb, low exercise diet - excess carb conversion to trigs
- Poorly controlled DM - *inc synthesis of trigs carrying VLDL and dec catabolism simultaneously *
- Nephrotic syndrome - loss of PRO dec plasma oncotic pressure, stimulating VLDL and LDL synthesis and decreasing stores
- Chronic renal failure - *no insulin excretion → high insulin levels → insulin desensitivity → inc lipogenesis and inc trigs *
Differentials, Decreased Triglycerides
(3)
- Malabsorption syndrome - cannot absorb fat
- Malnutrition - loss of fat
- Hyperthyroidism - *VLDL catabolism *
Note - not as concerning as high triglycerides
Indications, Lipoprotein Analysis
(2)
- ID pts at risk for developing heart disease
- Monitor lipid therapy
Differentials, Increased HDL
(2)
Not a bad thing!
- “Excessive” exercise
- Familial HDL lipoproteinemia
Differentials, Decreased HDL
(4)
- Metabolic syndrome
- Low HDL
- High triglycerides
- Inc. FBS
- HTN
- Inc waist circumference
- Familial low HDL
- Hepatocellular disease
- HDL synthesized in liver
-
Hypoproteinemia
- Nephrotic syndrome
- Malnutrition
- *Overall, cannot make HDL s protein *
Differentials, Increased LDL and VLDL
(6)
- Familial LDL lipoproteinemia
- Familial hypercholeserolemia type IIa
- Nephrotic syndrome - protein loss decreases plasma oncotic pressure and stimulates LDL synthesis
- Hypothyroidism - * decreased catabolism, common cause of lipid abnormalities*
- Alcohol consumption - EtOH is hepatotoxic
- Chronic liver disease - liver cannot catabolize LDL
Differentials, Decreased LDL and VLDL
(3)
- Familial hypolipoproteinemia
- Hypoproteinemia
- Malabsorption
- Severe burns
- Malnutrition
-
Hyperthryoidism
- *LDL and VLDL catabolism increases *
Cardiovascular Risk Ratio
(Components, Ideal value)
Components - Total cholesetrol/HDL
Ideal - < 4:1 (broken by gender and age)
