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PHRM 844 > Anti-hyperlipidemics > Flashcards

Anti-hyperlipidemics Flashcards

(78 cards)

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1
Q

Structure of cholesterol?

A
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2
Q

What do lipoproteins do?

A

Transport TG and cholesterol in blood

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3
Q

What are lipoprotein’s surface made of?

A

Phospholipids, proteins, and cholesterol

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4
Q

What are lipoprotein’s core made of?

A

Cholesterol esters and TGs

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5
Q

What is the lipoprotein lipase system?

A

Release of free FAs from the lipoprotein

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6
Q

Chylomicron function

A

Involved in transport of dietary lipids from from gut to liver and intestine

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7
Q

What is VLDL

A

It is the main source of TGs that is secreted in the blood from liver

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8
Q

What is IDL

A

TG-free LDL

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9
Q

What is LDL

A

Main source of cholesterol in blood

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10
Q

HDL function

A

Secreted from liver and acquires free cholesterol from peripheral tissues and atheromas

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11
Q

ApoA-1 info

A

Found in HDL and forms its structure
ABCA1 receptor ligand
Mediates reverse cholesterol transport
Produced in liver and intestine

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12
Q

ApoB-100 info

A

Found in VLDL, IDL, LDL and forms their structure
LDL receptor ligand
Produced in liver

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13
Q

ApoB-48 info

A

Forms chylomicron structure
Produced in intestine

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14
Q

ApoE info

A

Found in HDL
LDL remnant receptor ligand
Produced in liver and other tissues

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15
Q

ApoCII info

A

Found in chylomicron, LDL
Binds to LPL and enhances TG hydrolysis

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16
Q

Lipid absorption and transport diagram

A
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17
Q

Liver synthesis of cholesterol pathway

A

De novo synthesis is major source of cholesterol

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18
Q

Lipoprotein disorders ratios

A

> 4.5 is associated with increased risk of CVD
<=3.5 desirable
<3 optimal

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19
Q

cholesterol levels

A

<200 desirable
200-239 borderline high
>240 high

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20
Q

LDL levels

A

<140 desirable
140-159 borderline high
>160 high

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21
Q

TG levels

A

<150 desirable
150-199 borderline high
>200 high

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22
Q

HDL levels

A

> 40 in men desirable
50 in women desirable

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23
Q

Goals of therapy for hyperlipidemia

A

Decrease reabsorption of excreted bile acids
Decrease liver secretion of VLDL
Decrease synthesis of cholesterol
Increase hydrolysis of lipoprotein TGs

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24
Q

Bile acid binding resins MOA

A

Inhibits reabsorption of bile acids by binding bile acids from intestine to form insoluble complex excreted in feces; upregulate LDL receptors in liver

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25
bile acid binding resins drugs
Cholestyramine (Queastran) Colestipol (Cholestipid)
26
bile acid binding resins therapeutic use
tx of primary hypercholesterolemia
27
bile acid binding resins effects
produces 20% decrease in LDL in 2-4 weeks may cause 5% increase in HDL may increase TG
28
bile acid binding resins SEs
constipation bloating
29
bile acid binding resins drug interactions
acetaminophen, thiazides, digoxin, warfarin, fibrates, zetia, oral contraceptives, corticosteroids, thiazolindineiones
30
cholesterol absorption inhibitor MOA
inhibits absorption of cholesterol from dietary lipids and reabsorption of cholesterol excreted in bile AKA inhibits NPC1-L1
31
cholesterol absorption inhibitor drug
Ezetimibe (Zetia)
32
zetia effects
reduction of LDL levels by 17% adjunct with statins (enhances LDL reduction to 20%)
33
zetia AEs
low incidence of myopathy/rhabdomylosis
34
HMG-CoA reductase inhibitor drugs
statins
35
which statins are prodrugs
Lovastatin (Alteprav) Simvastatin (Zocor)
36
what are statins derived from
mevalonic acid
37
which statins do not get metabolized by CYPs
pravastatin (pravachol) - sulfation pitavastatin (livalo) - excreted unchanged
38
which statins get metabolized by CYP3A4
lovastatin (alteprev) simvastatin (zocor) atorvastatin (lipitor)
39
statins MOA
competitively inhibit HMG-coa reductase, the rate limiting step in cholesterol synthesis
40
statins indications
hypercholesteremia
41
statins efficacy
20-60% decrease in LDL 10-33% decrease in TG 5-10% increase in HDL
42
which statins are metabolized by CYP2C9
fluvastatin (lescol) rosuvastatin (crestor)
43
statins AEs
skeletal muscle effects - rhabdomyolysis with renal dynsfunction; monitor serum creatine phosphokinase hepatotoxicity
44
ATP citrate lyase inhibitor drug
bempedoic acid (nexletol)
45
what is bempedoic acid used adjunct to
used as adjunct to statins
46
nexletol indication and effects
reduces serum LDL and cholesterol in pts with HeFH or ASCVD
47
nexletol metabolism
metabolized by glucoronidation via kidneys
48
PCSK9 inhibitor drugs
alirocumab (praluent) evolocumab (repatha) inclisiran (leqvio)
49
PCSK9 inhib effects
increases LDL receptor # and reduce serum LDL levels
50
what are PCSK9 inhibs used as
adjunct to statins for patients with HeFH, HoFH, and ASCVD
51
leqvio moa
a siRNA that inhibits PSCK9 protein translation and directs degradation against hepatacytes
52
ApoB lipoprotein synthesis inhibitor drug
Juxtapid (Lomitapide) Mipomersen (Kynamro)
53
what is juxtapid
small molecule microsomal TG transfer protein inhibitor
54
juxtapid moa
disrupts chylomicron and LDL processes inhibits assembly of apob containing lipoproteins
55
which drugs have high risk of liver damage
juxtapid (lomitapide) Mipomersen (Kynamro)
56
what is kynamro
phosphorothioate anti-sense oligonucleotide inhibitor of apob100
57
kynamro moa
hybridizes apob100 mrna in liver and promotes degradation
58
kynamro indication
as adjunct to other tx for pts with HoFH
59
angiopoietin-like protein 3 inhibitor
evinacumab-dgnb (evkeeza)
60
evkeeza indication
tx of HoFH
61
what does evinacumab do
increases LPL and endothelial lipase activity by preventing ANGPTL3 mediated inhibition lowers LDL cholesterol
62
types of fibrates
63
fibrates moa
fibrates bind to PPAR alpha and regulate gene transcription along with retinoic acid receptor
64
fibrates efficacy
reduce serum LDL by 6-20% reduce serum TGs by 35-52% elevate HDL by 15-30%
65
fibrates indication
hypertriglyceridemia
66
fibrates SEs
gallstones rhabdomyolysis
67
niacin structure
68
niacin effects
reduces serum TGs increases lipase activity to increase clearance of VLDL decreases hepatic VLDL production may significantly reduce serum LDL and TG usually increases HDL levels
69
niacin in adipose tissue effect
inhibits TG lipolysis by hormone sensitive lipase, decreasing FA transport to liver via activation of GPR109A
70
niacin in liver effect
inhibits FA synthesis and esterification reducing TG export via VLDL reduces clearance of ApoA1
71
niacin in macrophages effect
increases expression of CD36 and ABCA1
72
niacin indications
mixed hyperlipidemias hypertriglyceridemia with high risk of pancreatitis
73
niacin AEs
marked vasodilation - flushing, itching, tingling (treat with prostaglandins) hepatotoxicity
74
omega-3 FA drugs
Lovaza Omtryg (EPA + DHA) Vascepa (EPA only)
75
O3FA moa
reduce synthesis of TGs in liver inhibit esterification of other FAs
76
O3FA indications
severe hypertriglyceridemia >500 mg/dl combined with statins to reduce LDL levels
77
what is done before initiating lovaza
start lipid lowering diet
78
O3FA AE
can increase LDL levels; Vascepa cannot alone

PHRM 844 (13 decks)

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