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Pharm 5 > Anti-hyperlipidemics > Flashcards

Anti-hyperlipidemics Flashcards

1
Q

Cholesterol absorbed through ______ transporter

A

NPC1L1

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2
Q

Reverse cholesterol transport

A

HDL accepts cholesterol from peripheral tissue - transported to liver
binds SR-B1 through ApoA1 in liver - cholesteryl esters delivered to hepatocytes

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3
Q

Familial Hypercholesterolemia

A

defects in LDL receptors = accumulation of LDL

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4
Q

Familial dysbetalipoproteinemia

A

defects/absence of ApoE = accumulation of VLDL and chylomicrons

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5
Q

Fibric Acid Derivatives

A

“FIBR”
Gemfibrozil
Fenofibrate

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6
Q

MOA Fibrates

A 
PPAR activators
Decreased TG
Increased HDL
Increased reverse cholesterol transport (HDL/SRB1)
Increased FA oxidation
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7
Q

TX Fibrates

A

familial hypertriglyceridemia
familial combined hyperlipoproteinemia
Familial dysbetalipoproteinemia
Secondary hypertriglyceridemia

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8
Q

AE Fibrates

A

Rare
rashes
GI
Myopathy - increased risk w/statin - Gemfibrozil contraindicated

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9
Q

Bile Acid Binding Resins

A

“CHOL”
Cholestyramine
Colesevelam
Colestipol

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10
Q

MOA Resins

A

bind bile acids/salts
Force liver to increase bile acid synthesis - requires uptake of cholesterol
Increased LDL receptors
Lowers LDL but increases TG

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11
Q

TX Resins

A

Familial hypercholesterolemia in pts w/ statin resistance

drug of choice for children/pregnancy

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12
Q

AE Resins

A

increase TG - contraindicated in hypertriglyceridemia
bloating
constipation

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13
Q

MOA Niacin

A

inhibit VLDL synthesis/secretion
lowers VLDL/LDL/FFA
increase HDL

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14
Q

TX Niacin

A

All hypertriglyceridemia

All hypercholesterolemia

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15
Q

AE Niacin

A 
cutaneous flushing/itching - secretion of prostacyclins from skin - pretreat w/NSAID
Hyperuricemia
hepatotoxic
Statin induced myopathy
Safest combo - niacin/fluvastatin
Riskiest combo - niacin/lovastatin
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16
Q

MOA Ezetimibe

A

inhibit NPC1L1 = inhibit cholesterol uptake

Increase LDL receptor = decrease LDL

17
Q

TX Ezetimibe

A

familial combined hyperlipoproteinemia
familial hypercholesterolemia
familial ligand-defective apoB

18
Q

Statins

A

“STATIN”
Most potent - Atorvastatin, Rosuvastatin
Least potent - Fluvastatin

19
Q

MOA statins

A 
inhibit HMG CoA reductase
reduce cholesterol
increase synthesis of LDL receptor
Increase LDL uptake from blood
Decrease secretion of of VLDL
20
Q

Pleotropic effects of statins

A 
decrease coagulation
decrease platelet activation
increase endothelial function/progenitor cells
increase NO
decrease ROS
decrease AT1 receptors
Decrease VSMC proliferation
decrease immune response
decrease endothelin
21
Q

AE Statins

A

Myopathy/myositis
rhabdomyolysis
liver toxicity
High potency statins - elevated ALT/AST - adaptive not toxic
True toxicity = elevated ALT/AST + bilirubin

22
Q

TX Statins

A

Familial combined hyperlipoproteinemia
Familial hypercholesterolemia
Familial ligand-defective apoB
Familial dysbetalipoproteinemia

Pharm 5 (4 decks)

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