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FPC2 Exam 8 > Dyslipidemia > Flashcards

Dyslipidemia Flashcards

1
Q

What is the risk of high lipids?

A

Cardiovascular risk

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2
Q

Lipproteins particles include:

A

HDL, IDL, LDL, VLDL, chylomicrons, triglycerides.

Used for ell membranes.

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3
Q

Chylomicrons carry ____

A

dietary lipid

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4
Q

VLDL carry ___ and to a less degree ____

A

endogenous triglycerides

cholesterol

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5
Q

IDL carry ___ and ___

A

cholesterol esters and triglycerides

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6
Q

LDL particles carry ____

A

Cholesterol esters . ApoB100 and C3

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7
Q

HDL particles carry ___

A

cholesterol esters

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8
Q

What is the path from dietary fat to lipoprotein?

A

dietary fat-> chylomicrons-> travel in blood + synthesized in cells-> cholesterol-> lipoprotein packaged with protein, phospholipids, and apolipoprotein

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9
Q

___ is the major transporter of cholesterol (⅔ of all body cholesterol)

A

LDL

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10
Q

___ takes excess cholesterol back to liver for excretion

A

HDL

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11
Q

Cholesterol is involved in the formation of ____

A

VitD, hormones from adrenal glands, bile salts

cell membrane

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12
Q

Pathophysiology of cholesterol affecting CV risk

A

Elevated LDL-> atherosclerotic plaques-> endothelial damage-> LDL permeate-> cholesterol in intima->macrophages -> -> fibrous plaque formed

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13
Q

Apoprotein ___ is associated with increased CVD risk

A

CIII.

Triglycerides + CV is unclear but does increase APO C=III (pancreatitis)

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14
Q

Screening for diagnosis of dyslipidemia

A

FH of lipid disorders, FH of CVD, pancreatitis

50% of people have abnormal lipid

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15
Q

NMR lipid profile is used to ______

A

adjudicate response to treatment + guide adjustment in therapy

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16
Q

Physical exam findings in someone with high cholesterol?

A

tuberoeruptive xanthomata, palmar xanthomata, eruptive xanthomata

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17
Q

LDL > ____ should be treated. HDL < ____ should be treated

A

160

40

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18
Q

Triglyceride level >___ is elevated. Why are high triglycerides bad

A

150

high trigly-> decreased chylomicron clearance-> pancreatitis

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19
Q

LDL goal for someone who has T2DM?

A

<100

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20
Q

_______ is the most common AD genetic disease.

A

Familial hypercholesterolemia.

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21
Q

Clinical syndrome of familial hypercholesterolemia is____

A

extremely elevated LDL-> early onset atherosclerotic CVD

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22
Q

Familial hypercholesterolemia is a mutation in ____

A

one of the genes critical for LDL catabolism (>190mg or first degree relative for clinical dx)

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23
Q

______ are associated with dyslipidemia

A

HIV and antiviral therapy

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24
Q

What are ASCVD? (atherosclerotic coronary vascular disease)

A

Hx of ACS, MI, angina, coronary or arterial revascularization, stroke, TIA, peripheral artery dz

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25
What are the recommendations for screening with lipid panel
adults >20 years old | significant FH- earlier
26
Do you need to fast for a lipid panel?
no
27
What does the pooled cohort equation (PCE) look at?
ASCVD ridk- 10 year risk of non fatal MI, CV death, or stroke (low borderline intermediate high risk)
28
What does SCORE look at for ASCVD
10 year risk of first fatal event of a CVD
29
When should you not use PCE for determine risk for ASCVD
PCE is used to assess primary prevention. If there is already clinical ASCVD or LDL-C>190mg/dL do not use it
30
What does PCE not include?
all races/ethnicities (over/underestimation)
31
First line treatment for ASCVD primary and secondary prevention are
statins!!!!
32
What is the MOA of statins?
acts at HMG-CoA reductase. blocks HMG-CoA -> mevalonic acid (which later turns into cholesterol)
33
What are the statin categories
``` low intensity (30% reduction in LDL-C) Moderate (30-50%) High Intensity (>50%) ```
34
What are the two statins that are offered at high intensity
atorvastatin 40-80mg | rosuvastatin 20-40mg
35
What are the monitoring procedure for statins? what are the baseline labs?
lipid panel 4-12 weeks after initiation then 3-12 months | transaminases + lipi panel
36
What is the point of a low intensity statin?
some patients that is the max dose they can tolerate
37
What are the statin- | associated muscle symptoms
myalgia (muscle weak w/o CK elevation), myopathy (muscle weak with CK elevation), myositis (muscle inflammation), rhabdomyolysis (up CK ULN w myoglobinuria acute renal failure)
38
What are risk factors for statin associated muscle symptoms
higher intensity, older, frequent exerciser, small body, female, CKD, drug drug (EtOH), hypothyroid, VitD deficiency
39
Only __ in ___ patients who qualify for a high intensity statin are actually prescribed one
1 in 5
40
In patients at a very high risk, reduction of LDL-C to ____ with the addition of non statin therapies
<70mg/dL
41
The lower achieved LDL-C, the lower the risk of ____ with no _____
CV events | lower limit for LDL values
42
What is not actually helpful for statin associated muscle symptoms
CoQ10 supplement | routine CK monitoring
43
Who is in the clinical ASCVD bucket and what should they be prescribed
Age <75 = high intensity statin | Age >75: moderate or high intensity
44
Who are "very high risk patients" for ASCVD? What is the treatment goal?
multiple major ascend events or 1 major and multiple high risk conditions. want LDL to be <70mg
45
What are non statin therapies for ASCVD
ezetimibe 1st line | PSCK9 inhibitor if want LDL to be even lower (this is expensive though)
46
What is the MOA of ezetimibe?
inhibit cholesterol absorption from small intestine by inhibiting Niemann-Pick C1-like 1 on intestinal epithelial cells.
47
What are AE of ezetimibe?
GI upset, slight increase risk of hepatic enzyme elevation with statin
48
What are drug drug interactions with ezetimibe?
cyclosporine, decrease effect with cholestyramine
49
What is the MOA of PCSK9 (alirocumab, evolulcumab) inhibitors?
inhibit PSCK9- facilitations degradation of LDL receptors in the liver-> LDL receptor recycling-> increase number of available receptors to remove LDL from blood
50
How much is esetimibe expected to lower cholesterol
LDL 18-20%, TG 5-10%, raise HDL 1-5%
51
How much does PCSK9 inhibitors lower cholesterol
LDL 60% down
52
What are adverse effects of PCSK9 inhibitors
injection site reactions
53
In primary hypercholesterolemia (LDL>190), what is the indicated therapy
maximally tolerated statin (look to add ezetimibe (>20yo) / bile acid sequestrate (>20yo)/ PCSK9 inhibitor (>30yo) with <50% reduction)
54
What are the 3 bile acid sequestrants
cholestyramine, colestipol, colesevelam
55
What is the MOA of bile acid sequestrants
bind to bile acids to disrupt enterohepatic recirculation. this binds to other drugs
56
What is the effect of cholesterol on bile acid sequestrant
LDL down 15-26% TG up to 10% HDL up 3-6%
57
What is the indicated therapy for patients with diabetes with regard to ASCVD
20-39y.o- consider moderate statin 40-75yo- calculate PCE- (if indicated) either high intensity or high intensity with ezetimibe >70yo- should probably just take statin
58
What should be done for primary prevention for statin therapy
low risk- life style borderline risk- moderate intensity stain intermediate risk- moderate intensity. want 30-49% LDL, can add ezetimibe or BA sequestrate to achieve goal high risk- start statin
59
What is moderate hypertriglyceridemia and what is the treatment indication
177-499mg/dL | ASCVD, age >40 with DM-> maximize statin therapy and add icosapent ethyl
60
What is severe hypertriglyceridemia and what is the treatment indication
>500 mg/dL 40-75y.o and ASCVD risk >5%-> up statin therapy, push low fat diet, fibrate, or icosapent ethyl to reduce risk of pancreatitis 20-39 y.o or 40-75yo with ASCVD risk <5% + no DM-> low rate diet, fibrate, icosapent ethyl to reduce risk of pancreatitis
61
What is icosapent ethyl and how does it work
An omega 3 fatty acid. decrease VLDL-TG synthesis in liver and up TG clearance by circulating VLDL particles EPA, lowers TG by 33%
61
What is icosapent ethyl and how does it work
An omega 3 fatty acid. decrease VLDL-TG synthesis in liver and up TG clearance by circulating VLDL particles EPA, lowers TG by 33%
62
Fibrate MOA (fenofibrate, gemfibrozil)
activates lipoprotein lipase and reduces apoprotein C-III-> increased lipolysis. decrease LDL, TG, and raise HDL
63
AEs in fibrates
interact with statins (more myalgias)
64
When do you use fibrates really only
reducing TG
65
Niacin is ______ for LDLC lowering or increasing HDL due to _____
not recommended lack of clinical benefit (also has no benefit for TG)
66
Niacin MOA
inhibit mobilization of free FA from peripheral adipose tissue-> reduce VLDL synthesis
67
Bempedoic acid MOA
inhibit ATP citrate lyase (upstream from HMG-CoA)
68
How much does bempedoic acid decrease LDL when added onto statin
15-25% reduction
69
Is there a definitive effect of bempedoic acid on ASCVD
no
70
Inclisiran MOA
siRNA-> prevents formation of PCSK9 proteins-> promote degradation of LDL
71
What is the effect of Inclisiran on LDL when added to again therapy
50%
72
What is inclisiran approved for
adults with established ASCVD and HeFH
73
Can a women who is trying to become pregnant be on a statin
no, they are contraindicated
74
What is the dyslipidemia drug of choice for someone who is pregnant
bile acid sequestrants

FPC2 Exam 8 (5 decks)

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