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M2 Cardiovascular > Lipid Pharmacology - Pfister > Flashcards

Lipid Pharmacology - Pfister Flashcards

1
Q

What is the mechanism behind HMG CoA reductase (statins) inhibitors?

A

They block the formation of squalene by competitively inhibiting the active site. This is the rate limiting step in cholesterol synthesis.

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2
Q

Name three statins

A

Atorvastatin
Lovastatin
Simvastatin

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3
Q

What is SREBP? How is it regulated?

A

SREBP is a transcription factor which controls synthesis of cholesterol enzymes.

SREBP is activated by site-1 protease and site-2 protease when cholesterol levels are low.

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4
Q

What is SCAP?

A

SREBP cleavage activating protein. It senses the levels of cholesterol in the cell.

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5
Q

What are the pharmacokinetics of statins?

A 
High first pass
Targets liver
Transported from gut by OATP1B1
High levels of plasma binding 
Variable Half-life
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6
Q

What is the active form for statins? Which statins are administered as active drugs?

A

Hydroxy-acids are the active statin form (compared to lactones).

Atorvastatin is administered as a hydroxy-acid.

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7
Q

How are statins metabolized?

A

CYP3A4

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8
Q

What are major adverse effects of statins? Minor adverse effects?

A

Myopathy, Rhabdomyolysis

GI side effects, Increased liver enzymes

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9
Q

What risk factors are there for myopathy or rhabdomyolysis?

A

High dose of statins
SLCO1B1 SNP
other CYP3A4 metabolized drugs
(also a bazillion other things)

these lead to higher plasma concentrations

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10
Q

What are contraindications for statins?

A

Active liver disease
Hypersensitivity
Pregnancy/Lactation

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11
Q

Why do statins cause myopathy?

A

Isoprenoids, a protective compound in muscles, are synthesized using intermediates in the cholesterol pathway

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12
Q

What happens to triglycerides, HDL, and LDL in a patient on statins?

A

Triglycerides go down (depending on [initial])
LDL goes down
HDL goes up slightly

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13
Q

How is cholesterol excreted?

A

It is used to make bile acids, which are secreted.

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14
Q

What is cholestyramine?

A

A bile-acid binding agent

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15
Q

How does cholestyramine work?

A

It is a positively charged resin that binds to the negatively charged bile acids and is too big to be reabsorbed.

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16
Q

How is SREBP affected by statins and cholestyramine?

A

SREBP upregulates LDL receptors to pull LDL out of the blood when statins and cholestyramine decrease cholesterol availability.

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17
Q

What are the adverse effects of cholestyramine?

A

Constipation/bloating
Gritty consistency
Decreased absorption of oral, negatively charged drugs
Moderate, transient increase in triglycerides

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18
Q

What happens to triglycerides, HDL, and LDL in a patient on cholestyramine?

A

Transient increase in triglycerides
Dose-dependent decrease in LDL
small increase in HDL

19
Q

What is Nicotinic acid?

A

Vitamin B derivative

20
Q

What three effects does Nicotinic acid have?

A

Decreases free fatty acid release
Decreases VLDL synthesis
Decreases HDL breakdown

21
Q

How is Nicotinic acid administered?

A

Orally

Immediate release
Long acting release
Extended release

22
Q

What is the most frequent adverse effect with nicotinic acid? How can it be lessened?

A

Flushing/pruritis

Gradually increasing dose, NSAIDs, bedtime administration

23
Q

What are adverse effects associated with nicotinic acid?

A

GI upset, increased liver enzymes, hyperuricemia, increased resting glucose levels

24
Q

What are contraindications for nicotinic acid?

A

peptic ulcer disease, concurrent statin use, gout, diabetes

25
Q

What happens to triglycerides, HDL, and LDL in a patient on nicotinic acid?

A

decreased triglycerides, LDL
increased HDL

(also decreases lipoprotein A)

26
Q

What is ezetimibe? How does it work?

A

Ezetimibe blocks cholesterol absorption from the bowel by binding to the Niemann Pick C10 like Protein.

27
Q

How is ezetimibe administered?

A

It is given orally and glucuronidated to its active form.

28
Q

What happens to triglycerides, HDL, and LDL in a patient on ezetimibe?

A

small decrease in triglycerides and LDL

small increase in HDL

29
Q

What is PPAR-a?

A

A transcription factor expressed in liver and adipose tissue.

30
Q

How does Retinoid X Receptor interact with PPAR-a?

A

It forms a heterodimer with the activated PPAR-a.

31
Q

How are PPAR-a activators administered?

A

Fenofibrate is administered as a pro-drug

Gemfibrozil is administered as an active drug

32
Q

How is fenofibrate excreted?

A

Fenofibrate is excreted in the urine, in glucoronidated form.

33
Q

What are contraindications for PPAR-a activators?

A

Renal impairment

use caution with statins

34
Q

What happens to triglycerides, HDL, and LDL in a patient on PPAR-a activators?

A

decrease in triglycerides
variable decrease in LDL
increase in HDL

35
Q

What are PPAR-a activators prescribed to treat?

A

High triglycerides associated with metabolic disorders like diabetes

36
Q

Where are omega-3 fatty acids found?

A

Fatty fish like tuna, salmon, mackeral

37
Q

What effect do omega-3 fatty acids have on lipids?

A

inhibit lipogenesis
increase beta-oxidation
increase phospholipid synthesis
increase ApoB degradation

38
Q

What are the pharmacokinetics of omega-3 fatty acids?

A

very slow acting, stop if no benefit has been seen ater two months

39
Q

What are adverse effects of omega-3 fatty acids?

A

Fish allergy
Increased LDL
Increased liver enzymes
Prolongation of bleeding times

40
Q

What is PCSK9?

A

A protein that targets LDLreceptors to lysosomes

41
Q

What is Microsomal Triglyceride Transfer Protein?

A

A protein that takes cholesterol out of the membrane and assembles it into lipoproteins

42
Q

How are MTP inhibitors metabolized?

A

CYP3A4

43
Q

What are adverse effects of MTP inhibitors?

A

GI upset

Hepatotoxicity

44
Q

What are MTP inhibitors used for?

A

Treatment of homozygous familial hypercholesteremia

M2 Cardiovascular (40 decks)

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