Pharmacology Block D Lecture 2(B)

Front 1

Atherosclerosis happens though a complicated process of cholesterol plaque formation that involves what

Back 1

Damaged endothelium

Cholesterol invasion

Plaque formation

Front 2

What is hyperlipidemia

Back 2

Classified at familial causes by specific genetic abnormalities or acquired when resulting from another underlying disorder that leads to alterations in plasma lipid and lipoprotein metabolism

Front 3

What are the drugs therapy for hyperlipidemia

Back 3

Statins, bile acid sequestrants, niacin, fibric acid derivatives, ezetimibe and the inhibition of dietary cholesterol

Front 4

Increase in serum cholesterol levels is in positive correlation with what

Back 4

Disease development

Front 5

What do statins inhibit

Back 5

An early and rate limiting step in cholesterol biosynthesis

Hepatic cholesterol sythesis results in increased expression of the LDL receptor gene

It also reduces the degradation of LDL receptors

Front 6

By satins inhibiting hepatic cholesterol synthesis results in increased expression of the LDL receptor gene, what does decreased free cholesterol cause

Back 6

Membrane bound SREBPs to be cleaved and translocated to the nucleus to bind the sterol responsive element of the LDL receptor gene, it enhances transcription and increases synthesis of ldl receptors

Front 7

Form acetyl coA to CHOLESTEROL and whats the rate limiting step1)

Back 7

Acetyl coA to HMG CoA to mevalonate(by HMG-CoA reductase) to farnesyl pyrophosphate to squalene to cholesterol

Rate limiting steonis HMG COA REDUCTASE

Front 8

2) whats the biproduct if farnesyl pyrophosphate

Back 8

Farnesylates proteins

Front 9

3) whats the biproduct of squalene

Back 9

Dolichol

Geranylgeranyl pyrophosphate which goes into geranylgeranylated proteins or ubiquinones

Front 10

What are rho and rac

Back 10

Monomeric proteins

Front 11

What is rho

Back 11

Blocks eNOS (good in cardioprotection)

Front 12

What is rac

Back 12

Produces superoxide nadpH

Front 13

Where to rho and rac come from

Back 13

Geranylgranyl PP

Front 14

What are competative inhibitors of HMG-CoA reductase

Back 14

Statins

Front 15

what are statins documented in reducing

Back 15

Fatal and non fatal CHD events, strokes and total mortality

Front 16

Why do we want a increased expression of LDL receptor gene

Back 16

Greater number of LDL receptors on the surface if hepatocytes results in increased removal of LDL from the blood and therefore lowering LDL-C levels

Front 17

Whats statins effects on triglycerides

Back 17

Decreases triglycerides in hypertriglyceridemic

Increase HDL-C

Decrease LDL-C

Front 18

Statins effect on non-lipid lowering effects

Back 18

Endothelial function (enhances production of nitric oxide

Anti inflammatory

Reduce venous thromboembolic events

Front 19

Adverse effects of statins

Back 19

Hepatotoxicity

Myopathy

Front 20

What are the statin clinical trials and whats the end points

Back 20

Statin vs placebo,Statin vs statin

Disease outcome and surrogate marker( not directly related to statin itself i.e production of blood pressure) cholesterol would be the first marker but surrogate is something else

Front 21

What are the benefits and risks of statins?

Therapeutic effects and adverse effects

Back 21

Therapeutic-cardiovascular protection

Adverse- muscle, liver, drug interactions