Wk 2 HLD Flashcards
Cholesterol
HDL - good (lots of protein)
LDL - bad (lots of cholesterol in it)
- in all cell membranes
- essential part of phospholipid bilayer
Building Blocks
- estrogen and testosterone
- vitamin D
- cortisol
- bile acids
Cholesterol + skin
highly insoluble, which is why it makes a good barrier for skin, blocks transdermal absorption of water molecules
Cholesterol transportation
has to be transported into cells by binding with cell surface receptors, primarily on aterial muscle cells
Cholesterol + diet
exogenous - 25% from our diet
- dietary
- some impact on our cholesterol
- not a nutrient for concern
Endogenous cholesterol
75% - cholesterol our body makes
- manufactured by cells in liver
- Hydroxymethylglutaryl coenzyme A reductase (HMG-CoA reductase)
Saturated fat
increase in intake of saturated fat increases body’s production of cholesterol (because it uses saturated fat to make cholesterol) so then body’s levels rise by 10-15%
- not good
VLDL
high triglycerides, increased risk of heart disease
Hypercholesterolemia
too much cholesterol
- aka hyperlipidemia (HL)
- aka dyslipidemia
Hypercholesterolemia labs
FASTING
cholesterol score = HDL + LDL + triglycerides/5
< 200 best
Familial Hypercholesterolemia
genetically linked, despite diet and lifestyle
- defect in LDL receptors in liver cells
- liver cannot efficiently remove LDL from bloodstream which leads to high levels of LDL in blood
General risks of high cholesterol
- age
- family hx (not familial hypercholesterolemia)
- smoking
- HTN
- DM
- physical inactivity
- poor diet
Atherosclerosis
- build-up of cholesterol in our vessels
- plaques can rupture that become emboli
- particular problem with exercising
Arteriosclerosis
specific form
any thickening or hardening of the arterial wall
- we are most concerned with this because arteries carry oxygenated blood to tissues
Artherosclerotic plaque formation
begins with injury to the endothelium
– coronary arteries
– peripheral arterial walls
- cigarette smoking injures endothelium
- chronic hemodynamic wall stress (HTN)
- hyperglycemia = high levels of blood sugar injures
Injury -> increased permeability
molecules can more easily get through endothelium
- LDL molecules get into vessel wall
- become oxidized and damage the endothelium
- macrophages arrive and engulf lipids and create foam cells and that leads to development of plaque
Lipid core
plaque buildup on side
- plaque with large lipid core prone to rupture, can block vessel off entirely
C-reactive protein (CRP)
non-specific marker of systemic inflammation
- other markers erythrocyte sedimentation rate
- elevated levels indicate increased risk of disease state
Coronary heart disease (CHD) or Coronary artery disease (CAD) or atherosclerotic cardiovascular disease (ASCVD)
almost all is atherosclerosis
- insufficient delivery of oxygen to the heart which leads to ischemic heart disease (IHD)
Lower the risk of atherosclerosis
- decrease LDL and increase HDL
- treat with medication
- heart healthy diet and increase exercise
- stop smoking
- weight control
Prior to therapy
- fasting lipid panel
- ALT
- CK (creatine kinase)
- consider secondary causes
AVOID GRAPEFRUIT WITH STATINS
Secondary causes of HLD
diet
drugs
diseases
disorders/altered metabolism
