Dyslipidemia Flashcards
three components of total cholesterol
LDL, HDL, TAGs
t/f we treat total cholesterol
F, we treat components of tc. high hdl doesnt need to be treated
management of ldl
ldl apharesis for familial hypercholesterolemia - take blood and drain ldl then return blood
lifestyle changes (3 mos.)
medical therapy (statins, ezetimibe, pcsk-9)
source of tags
carbohydrates – make sure to tell patient what not to eat to lower tags (dont eat carbs)
ldl classification for serum tags
normal <150
borderline high 150-199
high 200-499
very high >/=500
when to start tag therapy
very high levels, other levels are diet and lifestyle modifications
causes of elevated tags
modifiable factors, t2dm, chronic renal failure, nephrotic syndrome, drugs, genetic dyslipidemias
drug of choice/treatment for elevated tags
lifestyle changes*, fenofibrate, omega fatty acids
hdl levels
> 50 mg/dl for women
>40 mg/dl for men
t/f larger lipoproteins have higher tendency to go underneath subendothelial lining in blood vessels
f, smaller lipoproteins have higher tendency
signaling molecules on the surface of molecules
APO A-I OR AII - anti atherogenic in hdl (friendly)
APO B100 - pro-atherogenic found in ldl and vldl (can cause atherosclerosis)
APO B-48 - benign found in cms
exogenous lipoprotein pathway
dietary cholesterol and tags enter through intestine
1st byproduct: CMs
2nd byproduct: cm remnants
endogenous lipoprotein pathway
cm remnants enter liver
1st byproduct: vldl
2nd by product: idl
3rd byproduct: ldl (can become atherosclerotic plaques)
low cv risk ldl
score <1%
goal: <116 mg/dl (3.0 mmol/l)
moderate cv risk
score >/=1% and < 5%
young patients with dm duration <10 years without other risk factors
goal: <100 mg/dl (2.6 mmol/l)
high risk
score >/=5% and <10%
tc >8 mmol/l (310 mg/dl) OR ldl >4.9 mmol/l (190 mg/dl) OR BP >/= 180/110
familial hypercholesterolemia without other risk factors
moderate ckd (gfr 30-59)
dm >/= 10 years, no organ damage
goal: <70 or 50 mg/dl (1.8 mmol/l)
very high risk
score >/= 10% ascvd fh with ascvd severe ckd (<30) dm with organ damage >/= 3 major risk factors long duration t1dm
goal; <55 mg/dl
>/=50% reduction from baseline (1.4 mmol/l)
four statin benefit groups
clinical atherosclerotic cvd
t1/t2dm, 40-75 yo, ldl 70-189 mg/dl
nondiabetics, 40-75, ldl 70-189 mg/dl
ldl >/= 190
therapy for clinical atherosclerotic cvd
high intensity statin therapy
therapy for t1/t2dm, 40-75 yo, ldl 70-189 mg/dl
10 yr risk for ascvd
risk <7.5% moderate intensity statin therapy
risk >/= 7.5% high intensity statin therapy
therapy for nondiabetic, 40-75 yo, ldl 70-189 mg/dl
10 yr risk for ascvd
> /=7.5% moderate to high intensity statin therapy
therapy for ldl >/= 190 mg/dl
high intensity statin therapy (may have fh)
____ has emerged as one of the major risk factors for cv events
mixed dyslipidemia or atherogenic dyslipidemia
triad of atherogenic dyslipidemia
elevated tags >/=150 mg/dl
near normal ldlc >/= 120 mg/dl
diminished hdlc men < 40 mg/dl, women <50 mg/dl
atherogenic dyslipidemia in insulin resistance
page 5
t/f diabetics with low ldl actually have low ldl
f, they have smaller denser ldl that can’t be measured
____ can be removed from hdl in diabetics
apo a-I
when apo a-I is removed in hdl it becomes ___
vldl
t/f when diabetics have low hdl, the treatment is not to give hdl cholesterol
t, hdl cholesterol can lose its apo a-I and become vldl, and then become small, dense ldl
eas/esc recommendation for treatment of dyslipidemia in T2DM AT VERY HIGH RISK
ldl-c reduction of >/= 50% from baseline
ldl-c goal of < 1.4 mmol/l (<55 mg/dl)
eas/esc recommendation for treatment of dyslipidemia in T2DM AT HIGH RISK
ldl-c reduction of >/= 50% from baseline
ldl-c goal of < 1.8 mmol/l (<70 mg/dl)
eas/esc recommendation for treatment of dyslipidemia in T1DM who are high/very high risk
statins
if the ldl goal in diabetics is not reached, statin combination with ____ should be considered
ezetimibe
genetics in familial hypercholesterolemia
lof mutation in ldlr
lof in apob
gof in pcsk9
clinical presentation for familial hypercholesterolemia
elevated ldl-c (> 190/mg/dl) and premature cad
in fh, _____ are dysfunctional
ldl receptors
how to compute for cumulative ldl-c burden
circulating ldl-c x years of exposure
ldl levels for hefh/hofh
hefh: ~200 mg/dl
hofh: ~750 mg/dl
age of onset for hefh/hofm
hefh: atherosclerosis 60 yo, mi 30 yo
hofh: 2 yo/10 yo
arcus cornealis
fat deposits in eye
starts as small visible white crescent and can become a corneal ring
more specific in individuals < 45 yo
esc/eas guidelines for management of fh
50% reduction of ldl-c
<1.4 mmol/< 55 mg/dl ldl-c
not achieved: statin + ezetimibe
still not achieved: pcsk9 inhibitor
statin moa
reduces synthesis of cholesterol in liver by competitively inhibiting hmg-coa reductase activity
cholesterol absorption inhibitor (ezetimibe) moa
inhibits npc1l1 protein in intestine so there is not cholesterol absorption –> liver will upregulate ldlr to absorb ldl in blood
pcsk9 inhibitor moa
inhibits the breakdown of ldl-r –> ldl-r can still work and absorb ldl from blood
indication for psck9 inhibitors
when oral therapy is exhausted and patient is still having strokes/heart attacks
primary statins for high intensity therapy
atorvastatin, rosuvastatin
> /= 50% reduction
primary statins for mod intensity therapy
atorvastatin, rosuvastatin, simvastatin
30-49% reduction
primary statins for low intensity therapy
simvastatin
<30% reduction
other drugs for combination therapy
for intolerance to statins
fibrates, omega-3 fatty acids, ezetimibe
drug of choice for diabetic patients with atherogenic dyslipidemia
statins
t/f all dms regardless of their baseline ldl-c should be on statin therapy
t, primary treatment is treating the dm + statin therapy
drug of choice for hdl
lifestyle modification
