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a complex disorder with no single factor as the cause
metabolic syndrome
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2 main characteristics of metabolic syndrome
- abdominal obesity
- insulin resistance
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4 metabolic risk factors for metabolic syndrome
- atherogenic dyslipidemia
- hypertension
- high plasma glucose
- a prothrombic and pro-inflammatory state
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major cause of death in the western world
vascular disease dominated by artherosclerotic heart disease
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the obvious indicator for susceptibility to plaque buildup
hyperlipidemia
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5 causes of hyperlipidemia
- diet
- liver disease
- kidney disease
- pancreas disease
- thyroid disease
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degenerative changes in the intima of medium and large vessels
artherosclerosis
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2 characteristics of artherosclerosis
- plaque
- decrease lumen diameter
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what leads to the lipid rich core of plaque
- inflammation
- macrophage activation
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intraplaque thrombus
stable angina
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mural thrombus
unstable angina
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occlusive thrombus
acute myocardial infarction
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macromolecules that consist of triglycerides and cholesterol non-covalently associated with protein and carbohydrates
lipoproteins
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natural molecule of lipid
cis fatty acids
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produced by partial hydrogenation of unsaturated oils, margarines, vegetable shortening, frying oils
trans fatty acids
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what is the implication of trans fat
elevated LDL
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their source is exogenous fat in the diet
90% triglycerides by weight
chylomicrons
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their source is the liver
60% triglycerides
VLDL
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rapidly produced from chylomicrons and VLDL
IDL
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major cholesterol carrying protein
50% cholesterol and 10% triglycerides
major concern in hyperlipidemic states and diseases
LDL
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25% cholesterol and 50% protein and accounts for 17% of serum cholesterol
HDL
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type of hyperlipoproteinemia with abnormal amounts of chylomicrons resulting in plasma with a creamy top
massive elevated triglycerides
I
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no drugs to treat this type of hyperlipoprotein, treat by decreasing dietary fat
I
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cause of this type of hyperlipoproteinemias is decrease in lipoprotein lipase that clears plasma of chylomicrons
I
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type of hyperlipoprotein with elevated beta-lipoproteins and LDL
normal triglycerides
heavily elevated total cholesterol
clear plasma
IIa
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type of hyperlipoproteinemia with elevated pre-beta-lipoproteins and LDL+VLDL
triglycerides slightly elevated
heavily elevated total cholesterol
slightly turbid plasma
IIb
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type of hyperlipoproteinemia that is very common
familial autosomal dominant abnormality often expressed at infanct
II
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type of hyperlipoproteinemias that cause appears to be disturbed catabolism of LDL
II
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type of hyperlipoproteinemia with heavily elevated beta-lipoproteins
abnormal VLDL/LDL compostion
elevated trilycerides and total cholesterol
III
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type of hyperlipoproteinemia that is rare
familial inheritance
III
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type of hyperlipoproteinemia that is treated with dietary restrictions and drugs
all but type I
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type of hyperlipoproteinemia with elevated pre-beta-lipoproteins and VLDL
moderate to heavy elevated triglycerides
normal to elevated total cholesterol
turbid plasma
IV
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type of hyperlipoproteinemia that has an unknown metabolic defect
IV
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type of hyperlipoproteinemia with elevated pre-beta lipoproteins with chylomicrons present
VLDL elevated
massively elevated TG
slightly elevated total cholesterol
turbid plasma with floating layer of chylomicrons
V
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type of hyperlipoproteinemia with a metabolic defect unknow however clearance of dietary fat is impaired
V
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3 general considerations when considering how to approach antihyperlipidemic agents
- identify the type of hyperlipidemia
- estabish baseline cholesterol
- institute revised diet, weight loss, and increased physical activity
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5 drug therapy approaches for hyperlipidemia
- first choice drugs (statins or HMG-CoA reductase inhibitors
- consider ERT
- combination drug therapy
- fibric acid type of drugs
- thyroid hormone - drugs of last resort
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why are fibric acids and HMG-CoA reductase inhibitors not recommended
- myopathy
- rhabdomyolysis
- renal failure
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rate limiting step in the synthesis of cholesterol
HMG-CoA reductase
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generally accepted that lowering of cholesterol levels is best accomplished by
reducing LDL levels
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what 2 means do HMG-CoA reductase inhibitors contribute to lowering of LDL
- decreased cholesterol synthesis by blocking the HMG-CoA reductase active site
- leads to an increase hepatic LDL receptros causing increase processing of plasma LDL
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why are statins contraindicated in pregnancy
you need cholesterol to build little johnny's cells
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side effect of statins
photosensitivity
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can you drink alcohol when on statins
no
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lipophilic statins
- atorvastatin
- lovastatin
- simvastatin
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which statins are more hydorphilic
- pravastatin
- rosuvastatin
- fluvastatin
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what happens when cholesterol levels drop below 100mg/dl
anxiety and clinical depression
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this is used as a starting material for statin class synthesis and is isolated from penicillium citrinum
compactin
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a naturally occuring lipid-soluble, vitamin like substance found in the inner mitochondrial anc cellular membranes and in blood
CoEnzyme Q10
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in what sense can fibrates be used cardiovascularly
reduce the occurence of nonfatal MI but have no significant effects on other adverse CV outcomes
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new mechanism by which fibrates may act
T1Rs inhibition
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gene mutation that can have an affect on statin induced myopathy
SLCO1B1 - a gene that encodes for the protein involved in the transport of statins from the blood into the liver
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