Hyperlipidemia (Exam 1) Flashcards
Cholesterol
-In all cell membranes and is essentail part of phospholipid bilayer
-Important building block for: Estrogen and test, Vit D, Cortisol, and Bile acids
-Highly insoluble and is in our skin. It has to be transported into cells by binding with receptors
Cholesterol Make-up
-Exogenous 25% (Comes from out diet) Has some effect on the cholesterol level but it is not that concerning
-Endogenous 75% (Comes from what our body makes) (Liver)
What pathway produces endogenous cholesterol?
Hydroxymethylglutaryl coenxyme A reductase
(HMG-CoA Reductase)
-Uses SATURATED fat
LDL
Liver has LDL receptors on it in which LDL from the blood attaches to.
HMG CoA reductase turns LDL into cholesterol.
If you have excessive cholesterol the pathway is blocked. The liver recognizes it is not producing cholesterol and think it needs more LDL receptors
Negative feedback loop
6 different kinds of lipoproteins
-Combination of lipids (Cholesterol, trigylcerides) and proteins.
HDL-C (Good)
50% Protein
20% cholesterol
5% triglycerides
LDL-C (Bad)
-20-25% protein
-45-55% cholesterol
-5-10% triglycerides
Because they are made up of less protein and higher level of cholesterol
Increase risk for atherosclerosis
VLDL
-55-65% triglycerides
-Cant measure these.
-Increase risk of heart disease
Hypercholesterolemia
-Too much cholesterol
-Hyperlipemia (HL) (Most common term)
-Dyslipdiemia
How do we test for Hyperlididemia?
Draw blood to look for HDL and LDL cholesterol. Someone with high lipids will have a pink tent serum
Hypercholesterolemia: Check
-Check while fasting overnight
-High level of cholesterol also doesnt have symptoms
Total Cholesterol Score
HDL + LDL + Trigcerides/5
Hypercholesterolemia: Cholesterol levels (Do not memorize)
Range 100-200
HDL: Female > 55 mg/dl. Male > 45 mg/dL
LDL: <130 mg/dL
Triglycerides: <160 mg/dL. Range 40-160
Familial Hypercholesterolemia
-One way people develop high cholesterol and it genetically linked.
-Defect in LDL receptors in the liver cells. Liver cannot remove LDL from blood stream so LDL remains elevated in the blood
-It is hard to treat and reduced no matter the intervention because we are up against genetics and things we cannot change
When do we look for familial pattern of having high cholesterol?
When young adults and children present with hypercholesterolemia
Hypercholestrolemia: General Risks
-Age
-Fam History
-Tobacco use
-HTN
-DM
-Poor diet
-Inactive
Atherosclerosis
-Elevated LDL and Cholesterol (Increase risk)
-It is a build of cholerstol in vessels.
Arteriosclerosis
A form of atherosclerosis where our arterial wall starts to thicken and harden.
Formation of atherosclerotic plaque
-Starts with an injury to the endothelium. (Inside layer of our vessels)
-Coronary and Peripheral arterial walls.
-Cigarette smoking injures endothelium in our vessels.
-Chronic HTN can cause injury
-Hyperglycemia can also cause damage
Atherosclerosis: Steps
First we see INJURY and after the injury we see INCREASED PERMEABILITY.
When that happens molecules more easily get through the endothelial layer.
LDL molecules get into and under the wall which cause an inflammatory process to occur.
Macrophages arrive to engulf lipids which produce FOAM cells.
These FOAM cells appear as fatty streaks in the vessel walls and this LEADS to the development of plaque
Controlling Cholesterol levels in trying to prevent what from occuring
Atherosclerosis (which narrows the vessel)
The release of inflammatory mediators encourage excess lipids and debris to accumulate in the vessel wall creating….
a lipid core
plaque with large lipid core prone to rupture. This can block the vessel off entirely
Atherosclerosis: How do we look for it?
-C-reactive protein (CRP)
-Marker of systemic inflammation
-Drawn from blood and we can tell if there is increase inflammation in the body. (Just because it is elevated does not meant there is atherosclerosis)
Atherosclerosis: Why is it risky?
The ruptured plague can lead to platelet aggregation which can cause a thrombus formation
What plaques are more stable?
Older plaques are more stable because they have collegen
Effects of atherosclerosis on the heart
-Myocardial infraction
Coronary Heart Disease
-Atherosclerosis and the formation of plaque in the artery walls.
-Insufficient delivery of O2 to the heart. (Ischemic heart Disease)
-Atherosclerotic Cardiovascular Disease (ASCVD)
How do we lower the risk of atherosclerosis?
Decrease our LDL
Increase our HDL
Treat with medication
Improve diet
Exercise
STOP SMOKING
Risk factors we can help clients change
-Diet
-Weight control
-Regular Exercise
-Avoid tobacco
