Exam 1: Lecture 12, Hyperlipidemia Flashcards

1
Q

what is leading cause of death for most racial/ethic groups in US?

A

Heart disease

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2
Q

Key heart disease risk factors

A

High BP, High LDL cholesterol, and smoking

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3
Q

Lipoproteins

A

complexes of lipids and proteins that transport lipids through the plasma

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4
Q

Hyperlipoproteinemias/hyperlipidemias

A

metabolic disorders that involve elevations in any lipoprotein species

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5
Q

Apolipoproteins

A

The protein constituents of lipoprotein particles that play a key role in transporting cholesterol, triglycerides, phospholipids, and fat-soluble vitamins between the intestine, liver and peripheral tissues

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6
Q

“Good” cholesterol

A

HDL

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7
Q

Statin prototype:

A

Lovastatin

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8
Q

Statin MOA:

A

Competitive inhibitors of HMG-CoA reductase, which catalyzes an early, rate-limitng step in cholesterol biosynthesis

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9
Q

Statins Applications:

A

Hyperlipidemia

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10
Q

Statins Notables:

A

First pass effect

Drug-Drug interactions related to CYP3A4

Liver toxicity, muscle breakdown (myopathy)

Not for pregnant people, baby needs cholesterol

No grapefruit * 6+/day *

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11
Q

Drugs in Statin class?

A
Lovastatin
Pravastatin
Simvastatin
Rosuvastatin
Atorvastatin
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12
Q

High intensity statins?

A

Lower LDL-C by 50% or more

Atorvastatin 40-80mg
Rosuvastatin 20-40 mg

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13
Q

Moderate-intensity statins?

A

Lower LDL-C by 30% - <50%

A bunch

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14
Q

Low-intensity statins?

A

Lower LDL-C, on average by < 30%

A bunch, lower dose than moderate-intensity

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15
Q

MOA Statins detailed

A
  1. Inhibit HMG-CoA reductase, leading to decreased conc of cholesterol within cell
  2. Low intracellular cholesterol stimulates the synthesis of LDL receptors
  3. Increase number of LDL receptors promotes uptake of LDL from blood
  4. Low intracellular cholesterol decreases secretion of VLDL.
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16
Q

Clinical Application statins

A

Intensive statin treatment leads to no change in lumen size but decrease in lipid core.

Will also cause increase in fibrous and calcified tissues

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17
Q

Bile acid-binding resins: Prototype

A

Cholestyramine

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18
Q

Bile acid-binding resins: MOA

A

bind bile acids in GI tract and promote excretion

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19
Q

Bile acid-binding resins: Applications

A

Primary hypercholesterolemia

20
Q

Bile acid-binding resins: Notables

A

in patients who also have hypertriglyceridemia, VLDL levels may be increased during treatment

Bloating, and effect drug absorption (don’t use if on many other drugs)

21
Q

Drugs in Bile acid-binding resins class?

A

Cholestyramine

Colestipol

22
Q

Bile acid-binding resins MOA detailed:

A

Bile acid binding resin will bind to the cholesterol along with bile and cause it to be excreted.

can have GI complications, not 1st line

23
Q

Nicotinic acid: prototype

A

Niacin (Vitamin B3)

24
Q

Nicotinic acid: MOA

A

Inhibits VLDL secretion, decreasing production of LDL

25
Nicotinic acid: Applications
Combo with resin or reductase inhibitor will normalize LDL in most patients with heterozygous familial hypercholesterolemia and other forms of hypercholesterolemia
26
Nicotinic acid: Notables
Hepatotoxicity, platelet deficiency, birth defects w/ high dose, tachycardia, flushing, diarrhea, itchiness, dry skin
27
Fibrates: Prototype
Gemfibrozil
28
Fibrates: MOA
Function primarily as ligands for nuclear transcription receptor PPAR-a up regulate LPL, apo A-I, and apo A-II down regulate apo C-III (inhibitor of lipolysis)
29
Fibrates: Applications
Hypertriglyceridemias in which VLDL predominate
30
Fibrates: Notables
Stomach aches, gas ** Rare **: rashes, GI symptoms, myopathy, arrhythmias
31
Ezetimibe prototype
Its own prototype
32
Ezetimibe MOA
Inhibits NPC1L1 mediated cholesterol reabsorption
33
Ezetimibe Applications:
Hypercholesterolemia, synergistic with reductase inhibitors
34
Ezetimibe Notables:
Reversible impaired hepatic function, myositis (inflamed muscle)
35
PCSK9 inhibitors
Alirocumab Evolocumab
36
PCSK9 inhibitors MOA
Bind to PCSK9, inhibiting it from binding to LDL receptor. This increases the number of LDL receptors available to clear LDL, thereby lowering LDL-c levels. Normally PCSK9 promotes degradation of receptors
37
Dietary Management of Hyperlipoproteinemia
total calories from fat should be <25% Saturated fat <7% Cholesterol <200mg/day
38
What increase VLDL?
Sucrose and fructose
39
Principal factors increasing LDL?
Cholesterol, saturated and trans fats
40
What do Omega 3 fatty acids do?
Activate PPARa = reduce tyiglycerides
41
Lomitapide MOA:
prevents apoB and Triglycerides from coming together and prevents VLDL loading. Inhibits MTTP
42
Mipomersen MOA:
Mipomersen is an antisense strand that binds to ApoB mRNA Prevents the translation and synthesis of ApoB-100, causing decrease VLDL, leading to decrease LDL-C
43
Exogenous pathway
internalization of lipids chlymicron formed, goes into capillaries LPL releases Free Fatty Acids and returns to liver by engaging with LDLR
44
Endogenous
VLDL with ApoB-100 on it released by liver and goes into capillary LPL releases FFA and IDL returns to liver or forms LDL which can bind on peripheral tissues
45
value of HDL?
being able to scavenge a lot and in peripheral tissues