HyperLip pathopharm (325E1) Flashcards by Stef Sis

cholesterol is a building block for what

-estrogen and testosterone
-Vit D
-Cortisol
-Bile salt
-found in skin to help decrease evaportion of H2O & blocks absorption of water sol molecules
essential part of the lipid bilayer

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is cholesterol soluble or insoluble

highly insoluble (does not break down easily)

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exogenous vs endogenous cholesterol

-exo: dietary chol, 25%
-endo: body makes (spec liver cells) in response to dietary chol , 75%

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what is the pathway in which cholesterol is produced

HMG-CoA reductase

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what does liver use saturated fat for

to make more cholesterol so if you have an increased intake of sat fat then your liver will make cholesterol

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what receptor pulls cholesterol out of the blood

LDL receptor (negative feed back loop: LDL attaches to receptors -? HMG CoA concerts into chol -> if excess chol then pathway is blocked & the body recognizes this & thinks it needs more so -> more LDL receptors are made to pull out chol)

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what lipoprotein (cholesterol) is considered good and has a good source of protein

HDL-C (50% pro)

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what lipoproteins (cholesterol) are considered bad

-LDL-C (sticks to artery wall & causes build up)
-VLDL-C (cant measure but high in TAGs & TAGs can be measured)
**correlate with risk of heart disease)

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hyperlipidemia

too much cholesterol in the blood

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when checking cholesterol levels, what do we want to test

fasted levels ; eating can cause large variation compared to baseline levels

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why is screening of hyperlipidemia important

it is a silent disease so people >20y/o should be screened every 5 years, can start younger if at high risk

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cholesterol normal range

100-200 (goal <200)

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what is the best lab to test for hyperlipidemia

total cholesterol = HDL + LDL + (TAGs/5)

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HDL goal values

M: >55 mg/dL
W: >45 mg/dL
optimal >60

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LDL goal values

<100 mg/dL

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triglycerides goal values

40-150 (goal <150)

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LDL to HDL ratio goals

M: <5.0
F: <4.5
if slightly elevated LDL but high HDL, can balance out

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familial hypercholesterolemia

caused by a defect in LDL receptors (so cannot pull LDL from blood) in the liver cells so it does not matter what the person eats, they will still have high cholesterol -> hard to treat & worse if inherited from both parents

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why might you see a child with heart disease or have a MI

familial hypercholesterolemia

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general risks for high cholesterol

-age, family hx (non controllable)
-cigarette smoking, htn, dm, physical inactivity, obesity, poor diet w/ high sat fat (controllable)

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why do we care when cholesterol is high

it causes atherosclerosis

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what increases you risk for atherosclerosis

elevated LDLs and cholesterol

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arteriosclerosis

-a specific type of atherosclerosis
-thickening or hardening of the arterial walls
-most symptomatic
-used interchangeably w/ atherosclerosis

why is arteriosclerosis so concerning

it blocks the arteries which bring oxygenated blood to the tissues

after there is a build up of cholesterol, how does atherosclerotic plaque form

HTN/Hyperglycemia/smoking -> injury from chronic irritation to the endothelium -> plaque begins to form in arteries bc LDL want to pack the damaged areas

what does injury do to permeability

it increases permeability so the cells instead of being tightly packed, they're more open and anything can get into them **LDL vessel into wall**

when LDLs vessel into the damaged tissue walls, what process occurs

the inflammatory process begins so macrophages arrive and they try to engulf the lipids which produces foam cells

foam cells

fatty streaks on the vessel wall and they lead to the development of plaque

lipid core

lipid cells + foam cells **when large, prone to rupture**

what happens when a lipid core rupture

a clot can form and everything beyond that point will not get oxygen or nutrients unless we get that vessel back open

what minimally invasive test can we run to look for atherosclerosis

look at the inflammation mark CRP **it is non specific so we also look at high cholesterol and risk factors to determine likelihood of atherosclerosis** can also use erythrocyte sedimentation rate

what type of plaque are more stable (less likely to rupture)

older plaques because they have more collagen and fibrins in them **older does not mean worse**

how can people have large artery blockages but not have symptoms

-low physical activity so they do not need a lot of increased blood flow -if the obstruction is in a small vessel that doesn't carry much blood so effects go unnoticed **look for fatigue, angina, inability to do activities they used to as main signs**

what is atherosclerosis a big risk factor for

CAD, heart attacks, strokes

CAD

plaque build up in the heart leading to insufficient delivery of oxygen to the heart -> ischemic heart disease **atherosclerosis**

what do we do for atherosclerosis

**lower cholesterol in blood** -decrease LDL -increase HDL **do this by meds, diet, exercise, wt loss, stop smoking**

main drugs for atherosclerosis

HMG-CoA redutase inhibitors "statins"

when to start medications after diet and lifestyle changes do not work

6 months

if we stop HMG CoA reductase, what do we stop

the liver from making endogenous cholesterol

who will not respond to statins

people with familia hypercholesterolemia bc they do not have working LDL receptors

benefits of statins

-prevent nonfatal and fatal cardiac events (stroke & MI) -reduce risk of disability from non fatal stroke (women have a greater of disability post stroke) -put pt who have had an event on for prevention -primary & secondary preventions

who are the four people who benefit from statins

-people who have ASCVD (prior stroke or MI) -people w/ LDL >/190 -people 40-75yo w/ DM who have LDL between 70-189 -estimated 10 year risk of ASCVD 7.5% or higher

MOA of statins

inhibits HMG-CoA reductase so less cholesterol is produced & then liver makes more LDL receptors which also pull cholesterol out of the blood **also stabilizes plaque & decrease inflammation**

can you stop taking statins after your levels normalize

no, it is a life long drug bc it is not a permanent drop in levels

effects of statins

LDLs decrease by 21-63% HDLs increase by 5-22% TG decrease by 6-43%

adverse reactions of statins

myopathy (muscle weakness) -> rhabdomyolysis (breakdown of muscle fibers & leads to AK failure)

what should you monitor in someone taking statins

liver and kidney labs

how long does it take to see effect of statins

2 weeks

what statins need to be taken at night

simvastatin and rosuvastatin bc chol is highest at night and these drugs have short half lives

cholesterol absorption inhibitor MOA

blocks absorption of choleseterol

what is the first line drug for atherosclerosis

statins

why don't cholesterol absorption inhibitors work as well as statins

they affect dietary cholesterol which only makes up 25%

what do we do before we give anyone cholesterol meds

-fasting lipid panel -ALT (liver) -CK (rhabdo) -consider secondary causes

what drugs cause elevated LDLs

diuretics, cyclosporine, glucocorticoids, amiodarone

what are other drugs used to treat hyperlipidemia

-bile acid sequestrants -niacin -fibric acid derivatives (fibrates) -fish oil

what is the gold standard for hyperlipidemia treatment

statins w/ diet & exercise