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pharm II exam 2 > Hyperlipidemia > Flashcards

Hyperlipidemia Flashcards

1
Q

Liver maintains a pool of cholesterol at all times. What are the routes of what happens to that cholesterol

A
  1. broken down into bile acids to be secreted into intestine
  2. packaged into VLDL to go into circulation
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2
Q

Liver maintains a pool of cholesterol at all times. What are the various sources of this cholesterol

A
  1. remnants of chylomicrons
  2. from LDL taken up through LDL receptors on liver
  3. make cholesterol from acetyl CoA using HMG-CoA
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3
Q

Where does HDL come from? what it is function?

A
  • extrahepatic takes up LDL and excretes HDL which is then ready to scavenge any free cholesterol found in the blood stream
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4
Q

What is IDL?

A
  • intermediate density lipoprotein
  • formed from
    • HDL that has picked up cholesterol
    • VLDL after it has given free fatty acid to tissues
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5
Q

what happens to intermediate density lipoprotein

A

They are cleared from the plasma into the liver by receptor-mediated endocytosis, or further degraded to form LDL particles.

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6
Q

cause of familial hypercholesterolemia

A

LDL receptor deficiency -> leads to high LDL

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7
Q

what happens to cholesterol levels during weight loss

A
  • cholesterol levels are low during weight loss
    • check after weight loss has stabilized for one month
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8
Q

in patients with hyperlipidemia, dietary changes should always be instituted first except in patients wtih

A
  • coronary or peripheral vascular disease
  • familial hypercholesteremia
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9
Q

MOA of statins

A
  • blocks de novo synthesis of cholesterol
  • statins are the structural analog of HMG-CoA reductase
  • reduced plasma LDL by inhibiting the reductase to increase high affinity LDL receptors
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10
Q

DOC for decreasing LDL levels

A

statins

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11
Q

which two of the statin drugs are inactive and hydrolyzed to active form

A
  • Lovastatin
  • Simvastatin
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12
Q

why should patients take statins in the evening

A
  • diurnal pattern of cholesterol synthesis; de novo cholesterol synthesis peaks at night
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13
Q

What are the hallmark adverse effects of statins

A
  • increase levels of serum aminotransferase (LFTs)
  • Myopathy and muscle pain
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14
Q

when are statins contraindicated

A
  • pregnancy (category X)
  • active hepatic disease
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15
Q

metabolism of statins

A

liver by P450s

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16
Q

P450 inhibitors have what effect on statins

A
  • will increase the plasma concentrations of statins
  • ex: grapefruit juice, macrolides, ketoconazole
17
Q

list the bile acid-binding resins

A
  • Cholestyramine
  • Colestipol
  • Colesevelam
18
Q

MOA of bile acid-binding resins

A
  • bind to bile acids and prevent their intestinal reabsorption
  • decrease in bile acids -> increased expression of hepatic LDL receptors -> increased uptake of plasma LDL to make more bile acids
    • decreased LDL levels will decrease plasma cholesterol (20%)
19
Q

why does bile acid binding resins have no effect in homozygous familial hypercholesterolemia

A

there are no functional LDL receptors

20
Q

indications to use bile acid binding resins

A
  • whenever LDL is elevated
21
Q

why is bile acid binding resins not effective in hypertiglyceridemia

A

may increase VLDL

22
Q

hallmark adverse effect of bile acid binding resins

A

constipation and bloating

  • only stays in GI, not absorbed
23
Q

List the Niacins

A
  • Nicotinic Acid
  • Vitamin B3
24
Q

MOA of Niacin

A
  • lowers VLDL and LDL by inhibiting VLDL secretion
25
Q

indications to use Niacin

A
  • increases levels of HDL (most effective agent)
26
Q

hallmark adverse effects of Niacin

A
  • cutaneous vasodilation -> warm sensation, pruritus
  • impairs glucose tolerance
27
Q

List the Fibric acid derivatives (Fibrates)

A
  • Gemfibrozil
  • Fenofibrate
  • Fenofibric acid
28
Q

MOA of Fibric acid derivatives (Fibrates)

A
  • PPAR-a ligand (nuclear receptor)
    • upregulates LDL and other genes involved in fatty acid oxidation
29
Q

indications/theraputic use of Fibric acid derivatives (Fibrates)

A
  • decreased triglycerides by lowering VLDL concentration
  • effective in hypertriglyceridemia
30
Q

hallmark adverse effect of Fibric acid derivatives (Fibrates)

A
  • increased incidence of cholelithiasis or gallstones
31
Q

MOA of Ezetimibe

A

selectively blocks intestinal absorption of cholesterol and related phytosterols

32
Q

when is Ezetimibe used

A
  • decreases LDL (18%)
  • combining Ezetimibe with a statin -> synergism
33
Q

List the PCSK9 inhibitors

A
  • Alirocumab
  • Evolocumab
34
Q

MOA of PCSK9 inhibitors

A
  • normally, PCSK9 binds to LDLR and leads to LDL receptor degradation
  • Inhibiting the binding of PCSK9 to LDLR, the number of LDLRs available to clear LDL increases, thereby lowering LDL-C concentrations.
35
Q

how is PCSK9 inhibitors given

A

monthly, subcutaneous injections

pharm II exam 2 (9 decks)

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