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Cardio > Atherosclerosis Pharmacology > Flashcards

Atherosclerosis Pharmacology Flashcards

1
Q
A
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2
Q

HMG CoA Reductase Inhibitors

A

Atorvastatin Lovastatin Simvastatin

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3
Q

What is the MOA of the statins?

A

Decrease production of cholesterol which also increase transcription of LDL-r on the cell which also helps to decrease LDL in the serum

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4
Q

How are the statins metabolized?

A

CYP3A4

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5
Q

What is the main side effect with the statins?

A

Myopathy: muscle pain without CK elevation (possible d/t depletion of secondary metabolic intermediates) Rhabdomyolysis: muscle symptoms with increased CK d/t the breakdown of muscle fibers

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6
Q

Which polymorphism is associated with statin-induced myopathy?

A

SLCO1B1

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7
Q

In what population are statins contraindicated?

A

Liver disease Women who are pregnant, lactating or likely to become pregnant

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8
Q

Highly positively charged, binds to negatively charged bile acids causing them to be excreted in the stool

A

Cholestyramine

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9
Q

What is the MOA of Cholestyramine?

A

It decreases the pool of bile acids (increasing excretion) which causes more production of bile acids from cholesterol. This decreases hepatic cholesterol and stimulates LDL-r through SREBP TF.

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10
Q

What are some side effects of Cholestyramine?

A

Constipation/bloating Bad compliance – gritty consistency Modest increase in TGs

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11
Q

Water soluble B complex vitamin Main effect to decrease TG but also decreases cholesterol

A

Nicotinic acid (Niacin)

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12
Q

What is Niacin’s MOA?

A

In adipose – inhibits FFA mobilization In liver – decreases synthesis of VLDL by inhibiting DGAT2 and inhibits catabolism of HDL by inhibiting it’s uptake through apoA1

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13
Q

What is a main adverse effect of Niacin?

A

Intense cutaneous flush/pruritus GI, elevated liver enzymes, hyperuricemia, increase fasting glucose

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14
Q

What population is Niacin CI in?

A

Peptic ulcers Gout Hepatic disease Diabetes

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15
Q

What is Niacin used for?

A

Typically not first line for hypercholesterolemia but is used for individuals with hypercholesterolemia and hypertriglyceridemia.

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16
Q

Inhibits Niemann pick C10-like protein decreasing the rate of cholesteryl ester incorporation into CM

A

Ezetimibe

17
Q

What is a side effect of Ezetimibe?

A

Well-tolerated

18
Q

What is the main use of Ezeimibe?

A

Primary hypercholesterolemia; combined with statins to further decrease LDL

19
Q

Ligands for nuclear transcription regulator–PPAR (in adipose and liver). Primarily decrease TG.

A

Gemfibrozil Fenofibrate (2nd gen)

20
Q

How does PPAR gene transcription help with high TG and cholesterol?

A

Increase LDL particle size Increase HDL synthesis Increase reverse cholesterol transport Decrease inflammation Decrease TG

21
Q

What are some adverse affects of Gemfibrozil and Fenofibrate?

A

Generally well tolerated GI symptoms most common CI with renal impairment

22
Q

What patient populations are Gemfibrozil and Fenofibrate use in?

A

Patients with high TG and low HDL with metabolic syndrome or type 2 diabetes Not a primary therapy for hypercholesterolemia w/o increase TG

23
Q

How do omega-3 fatty acids have lipid lowering effects?

A

Decrease TG Decrease rate of secreted VLDL TG Enhance plaque stability and improve EC function

24
Q

What are some adverse effects of omega-3 fatty acids?

A

Fish allergy May increase LDL May increase liver enzymes Prolong bleeding time

25
Q

Decreases expression of LDL-r normally

A

PCSK9 – inhibitors of this as treatment for hypercholesterolemia would increase availability of cell surface LDL-r

26
Q

Transfers neutral lipids between membrane vesicles

A

MTP (microsomal TG transfer protein)

27
Q

Directly binds to and inhibits MTP; prevents assembly of apo-b containing lipoproteins –> decreases production of CMs and VLDL and subsequently decrease LDL-C

A

Lomitapide

28
Q

Essential component of LDL-C and VLDL; ligand that binds to LDL-r and is important for transport and removal of atherogenic lipids

A

Apoprotein B-100

29
Q

Antisense oligonucleotide to inhibit synthesis of apoB-100 in the liver; lipid lowering effects last almost 3 months after subq dose. Treatment for familial hypercholesterolemia

A

Mipomersen

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