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Pharm 3 > Statins > Flashcards

Statins Flashcards

1
Q

What are the normal LDL, HDL and TG? Or what do you want them at

A

LDL <160
HDL >35
TG <200

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2
Q

What controls how much LDL cholesterol is circulating in the blood?

A

LDL receptors, through up/down receptor regulation

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3
Q

What are the HMG-CoA reductase inhibitors MOA?

A

Inhibit cholesterol synthesis in the liver, causing the liver to upregulate LDL receptors on the liver, increasing removal of LDL cholesterol in the blood (20-55%), as well as TG

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4
Q

What is the rate limiting step in cholesterol synthesis?

A

Production of melalonate through MHG-CoA reductase

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5
Q

Summed up, what do statins do?

A

Decreased LDL cholesterol through upregulation of hepatic LCL receptors, decreased VLDL, IDL, triglycerides
Increases HDL

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6
Q

What did the WOSCOPS discover?

A

Pravastatin reduced CV events
Independent rate reduction independent of baseline LDL
Event rate reduction did not correlate with pravastatin induced decreases in LDL cholesterol

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7
Q

What are the non lipid effects of statins? Must know

A

Improved Endothelial function- improved ability to release NO
Anti-inflammatory effects- increased plaque stability
Antioxidant effects-reduced susceptibility of LDL to oxidation
Inhibition of platelet aggregation
Inhibition of cardiac hypertrophic growth

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8
Q

What are the “non lipid” effects due to in statins?

A

Inhibition of melvolonate leads to inhibition of Isoprenoids, which are biologically active, causing decrease in downstream cellular processes

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9
Q

What is the absorption like in statins?

A

Poor oral bioavailability due to first pass metabolism

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10
Q

What is the distribution in statins?

A

Most are highly protein bound once reaching the circulation

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11
Q

What is the metabolism of statins?

A

Metabolized in the liver, P450 and 3A4 involved

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12
Q

What are the three statins not involved with the CYP system?

A

Pravastatin, pitavastatin, rosuvastatin

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13
Q

How are most statins eliminated?

A

Hepatically through bile

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14
Q

What is the main adverse effect of statins?

A

Skeletal muscle toxicity
Elevation of Creatine phosphokinase
Possibly leading to rhabdo

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15
Q

What can be added with statins to reduce skeletal muscle toxicity?

A

Gimfibrazil- a fibrate

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16
Q

What is the risk of having lower activity of SLC01B1?

A

Increasesd risk of skeletal muscle toxicity

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17
Q

What are the other adverse effects of statins?

A

elevated AST/ALT

Not for pregnancy

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18
Q

Whats the pneumonic for remembering the specific metabolizations of statins?

A 
Lipid lowering
Statins
Are
First line
Primary
Preventative
Rxs
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19
Q

Which statins are metabolized by CYP3A4?

A

Lovastatin, simvastatin, atorvastatin

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20
Q

What statin is metabolized by CYP2C9?

A

Fluvastatin

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21
Q

What are the three bile acid sequestrants?

A

Cholestryamine, colestipol, and colesevela

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22
Q

What is the MOA of bile acid sequestrants?

A

These meds inhibit reabsorption of bile acid, forcing the liver to upregulate LDL receptors on liver in order to create more bile acid, decreasing plasma levels of LDL

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23
Q

What is also increased in bile acid sequestrants to help produce more bile acid?

A

HMG-CoA reductase

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24
Q

What rebound effect usually occurs after administration of bile acid sequestrants?

A

Hypertriclyeridemia, which is usually transient and returns to baseline with continued treatment

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25
Q

What are the pharmacokinetics for BAS?

A

None. It isn’t absorbed, distributed, metabolized, and gets eliminated in the feces

26
Q

What are the ADE’s for BAS?

A

Very little. Relatively safe and inert because they are not absorbed.

Main ADE’s are related to GI discomfort, like bloating, dyspepsia, constipation, or Borborygmi (Rumbly in his tumbly, just gas movement)

27
Q

What are the drug to drug interactions with BAS?

A

They reduce absorption of many drugs, so BAS should be administered one hour before or 3-4 hours after the resin

28
Q

What are the three fibric acid derivatives?

A

Clofibrate (no longer used), gemfibrozil, and fenofibrate

29
Q

What are fibric acid derivative MOA?

A

Fibrates bind to peroxisome proliferator activated receptor alpha (PPARa). which causes stimulation of fatty acid oxidation, increased expression of lipoproteion lipase, increased expression of apoA-I and apoA-II, reduced ecpression of apoC-III

30
Q

What the main effects fibric acid derivates ultimately cause?

A

Reduced triglycerides, LDL may go up or down

Mainly just effective for hypertriglyceridemia

31
Q

What are the pharmacokinetics to know about fibrates (fibric acid derivatives)? ADME

A

Well absorbed orally, especially on an empty stomach
Highly protein bound, but well distributed
Metabolized by phase II Glucoronidation
Eliminated in the urine

32
Q

What are fibrates ADE’s?

A

N/V, SKELETAL MUSCLE MYOPATHY

33
Q

What medication class should not be administered with fibrates?

A

Statins

34
Q

What are DHA or EPA?

A

Omega-3 fatty acids-fish oil

35
Q

What is fish oil MOA?

A 
Same as fibrate. Activation of PPAR-a
Reduces triglycerides (IN THEORY)
36
Q

What are ADE’s of fish oil?

A

GI-bad taste/regurgitation, GI upset
Allergic reactions
Purity concerns-trace metals like mercury

37
Q

What is the MOA of Niacin?

A

Multiple
Inhibits the lipolysis of triglycerides, reducing the transport of free fatty acids to the liver
In the liver, reduces triglyceride synthesis, as well as LDL levels
Enhances LPL, promoting clearance of chylomicrons and VLDL triglycerides

38
Q

What are the ADE’s of Niacin?

A

Facial flushing on first dose d/t prostoglandin mediated vasodilation, lasts about 1-2 weeks
GI- Dypepsia, n/v, diarrhea
Hepatotoxicity-Elevated LFT’s, fulminate hepatic necrosis
Insulin resistance-hyperglycemia
Increased uric acid levels-gout
Teratogenicity- Birth defects

39
Q

What is the given cholesterol uptake inhibitor?

A

Ezetimibe

40
Q

What is ezetimide MOA?

A

Inhibits the cholesterol transport protein (NPC1L1) in the membrane of jejunal enterocytes, which reduces cholesterol absorption by 54%, inhibits absorption of plant sterols from dietary source

41
Q

What is the bodies compensatory response to ezetimide alone?

A

Liver increasing LDL receptor expression and cholesterol synthesis.
Which stains can inhibit

42
Q

Should ezetimide be used alone?

A

No, used with statins

43
Q

What is important to know about ezetimides ADME?

A

Just that it is restricted to the enterohepatic system, eliminated in the feces mainly

44
Q

What is ezetimides ADE?

A

Very little, not sure if its safe in pregnancy

45
Q

What is PCSK9?

A

Bind to LDL receptors, causing degredation, leading to decreased LDL uptake (more LDL levels in blood)
Genetic mutation

46
Q

What are the PCSK9 inhibitors to know?

A

Alirocumab and evolocumab

47
Q

What is the MOA of PCSK9 inhibitors?

A

Binds to PCSK9 and inactivates it

48
Q

What are the two specific used for PCSK9 inhibitors?

A

Patients with familial hypercholesterolemia

Those who cannot tolerate statins

49
Q

What is the one major downside to PSCK9 inhibitors?

A

Must be injected SQ every two weeks

50
Q

What are the ADE’s of PSCK9 inhibitors?

A

Nasopharyngitis, Upper RTI, injection site reactions, allergic reactions, COGNITIVE IMPAIREMENT (r/t decreased cholesterol)

51
Q

What is the MOA of Antsense Oligonucleotide?

A

Hybridizes with the mRNA, forming a complex, leading to degradation by RNAses

52
Q

What is the antisense oligonucleotide?

A

Mipomersen

53
Q

What is the downside to administration of mipomersen?

A

It is injected sq every week

54
Q

What are the ADE’s for mipomersen?

A

Flu like symptoms
Injection site reactions
HEPATOTOXICITY BBW
Elevated LFTs, hepatic steatosis, contraindicated with drinkers of alcohol

55
Q

What is Lopitamide?

A

MTTP inhibitors

56
Q

What is lopitamides MOA?

A

Inhibits the microsomal triglyceride transfer protein which is used for chylomicron and VLDL assembly and sedcretion, so ultimately decreases LDL

57
Q

What is Lopitamides BBW?

A

Liver toxicity

58
Q

What is bempedoic acid?

A

An ATP Citrate Lyase Inhibitor

59
Q

What is Bempedoic acids MOA?

A

Inhibits ATP citrase Lyase, which is what synthesizes acetyl CoA from citrate, leading to increased LDL receptors and decreased LDL plasma levels

60
Q

What is Bempedoic acids ADEs?

A

Elevated uric acid levels

Pharm 3 (6 decks)

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