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ABSN > HyperLip pathopharm (325E1) > Flashcards

HyperLip pathopharm (325E1) Flashcards

1
Q

cholesterol is a building block for what

A

-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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2
Q

is cholesterol soluble or insoluble

A

highly insoluble (does not break down easily)

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3
Q

exogenous vs endogenous cholesterol

A

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

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4
Q

what is the pathway in which cholesterol is produced

A

HMG-CoA reductase

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5
Q

what does liver use saturated fat for

A

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

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6
Q

what receptor pulls cholesterol out of the blood

A

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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7
Q

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

A

HDL-C (50% pro)

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8
Q

what lipoproteins (cholesterol) are considered bad

A

-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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9
Q

hyperlipidemia

A

too much cholesterol in the blood

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10
Q

when checking cholesterol levels, what do we want to test

A

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

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11
Q

why is screening of hyperlipidemia important

A

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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12
Q

cholesterol normal range

A

100-200 (goal <200)

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13
Q

what is the best lab to test for hyperlipidemia

A

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

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14
Q

HDL goal values

A

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

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15
Q

LDL goal values

A

<100 mg/dL

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16
Q

triglycerides goal values

A

40-150 (goal <150)

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17
Q

LDL to HDL ratio goals

A

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

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18
Q

familial hypercholesterolemia

A

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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19
Q

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

A

familial hypercholesterolemia

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20
Q

general risks for high cholesterol

A

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

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21
Q

why do we care when cholesterol is high

A

it causes atherosclerosis

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22
Q

what increases you risk for atherosclerosis

A

elevated LDLs and cholesterol

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23
Q

arteriosclerosis

A

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

24
Q

why is arteriosclerosis so concerning

A

it blocks the arteries which bring oxygenated blood to the tissues

25
Q

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

A

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

26
Q

what does injury do to permeability

A

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

27
Q

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

A

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

28
Q

foam cells

A

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

29
Q

lipid core

A

lipid cells + foam cells
when large, prone to rupture

30
Q

what happens when a lipid core rupture

A

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

31
Q

what minimally invasive test can we run to look for atherosclerosis

A

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

32
Q

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

A

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

33
Q

how can people have large artery blockages but not have symptoms

A

-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

34
Q

what is atherosclerosis a big risk factor for

A

CAD, heart attacks, strokes

35
Q

CAD

A

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

36
Q

what do we do for atherosclerosis

A

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

37
Q

main drugs for atherosclerosis

A

HMG-CoA redutase inhibitors “statins”

38
Q

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

A

6 months

39
Q

if we stop HMG CoA reductase, what do we stop

A

the liver from making endogenous cholesterol

40
Q

who will not respond to statins

A

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

41
Q

benefits of statins

A

-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

42
Q

who are the four people who benefit from statins

A

-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

43
Q

MOA of statins

A

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

44
Q

can you stop taking statins after your levels normalize

A

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

45
Q

effects of statins

A

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

46
Q

adverse reactions of statins

A

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

47
Q

what should you monitor in someone taking statins

A

liver and kidney labs

48
Q

how long does it take to see effect of statins

A

2 weeks

49
Q

what statins need to be taken at night

A

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

50
Q

cholesterol absorption inhibitor MOA

A

blocks absorption of choleseterol

51
Q

what is the first line drug for atherosclerosis

A

statins

52
Q

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

A

they affect dietary cholesterol which only makes up 25%

53
Q

what do we do before we give anyone cholesterol meds

A

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

54
Q

what drugs cause elevated LDLs

A

diuretics, cyclosporine, glucocorticoids, amiodarone

55
Q

what are other drugs used to treat hyperlipidemia

A

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

56
Q

what is the gold standard for hyperlipidemia treatment

A

statins w/ diet & exercise

ABSN (41 decks)

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