Pharm Final Hyperlipidemia

Front 1

what are the 4 classes of drugs that are used to decrease cholesterol

Back 1

1. Bile Acid Binders: Cholestyramine. Inhibit reabs of bile salts from gut

2. Impaired Synthesis of lipoproteins
-Nicotinic Acid
- HMG CoA Reductase Inhibitors; Lovastatin. blocks RLE of cholestero synthesis

3. Fibric acids: gemfibrozil. STim LPL to increase hydrolysis of VLDL

4. Inhibit Absorption: Ezetimibe. inhibit abs of dietary and biliary cholesterol from the Gut

Front 2

ok so we eat some cholesterol...what happens

Back 2

1. enters liver and combines with TG to form VLDL

2. VLDL exported in blood. LPL takes out TG and puts them in adipose. IDL remains

3. IDL becomes LDL

4. LDL causes havoc and it taken up into the liver via LDL receptor

Front 3

where are the 2 places we get cholesterol

Back 3

1. Food

2. We make it in the liver:
AcetlyCoA + HMG CoA -------> Cholesterol (HMG CoA reductase)

Front 4

whats the mech

1. Ezetimibe
2. HMG CoA reductase Inhibitors
3. Bile Acid Resins
4. Niacin
5. Fibrates

Back 4

1. Ezetimibe: inhibits abs of cholesterol from the intestine

2. HMG CoA Reducatase Inhibitor (statins): inhibits production of Cholesterol by blocking rate limiting step

3. Bile Acid Resins (cholestyramine): inhibit reabs of bile acids from the gut

4. Niacin (Vitamin B3, Nicotinic Acid) : inhibits secretion of VLDL from liver

5. Fibrates (gemfibrozil): stimulate LPL to increase hydrolysis of VLDL

Front 5

what are the bile binding resins

Back 5

1. Cholestyramine
2. Colestipol
3. Colesevelam


**prevent reabs of bile acids from the gut

Front 6

what are the 2 main types of drugs that inhibit synthesis of lipoproteins

Back 6

1. HMG CoA Reductase inhibitors (the statins): inhibit the RLE of cholesterol synthesis. Lovastatin, pravastatin, simvastatin, fluvastatin, atorvastatin, rosuvastatin

2. Nicotinic Acid (B3, niacin): ihibits secretion of VLDL from the liver

Front 7

what are the fibric acid derivatives

Back 7

1. Gemfibrozil
2. Fenofibrate
3. Clofibrate

**stim LPL so that VLDL is hydrolyzed

Front 8

what inhibits cholesterol abs in the gut

Back 8

ezetimibe

Front 9

Niacin

1. Effect
2. Pharmacokinetics
3. Uses
4. Toxicity

Back 9

1. inhibit release of VLDL from liver. increase HDL

2. oral abs, renal excretion. take note that it is an acid so its filtered and then there is an active transporter to secrete organic acids in the PCT- interactions with other acids. Can lead to gout

3. used to tx heterozygous familial hypercholesterolemia & combined hyperlipoproteinemia

4. Impair glucose tolerance, causes skin vasodilation--> pt is red and hot!

Front 10

what drug is the BEST at increasing HDL

Back 10

BEST: niacin, B3, nicotinic acid

Front 11

what drug causes impaired glucose tolerance and makes you red and hot!

Back 11

niacin, its the one that blocks release of VLDL and is used to tx heterozygous familial chpercholesterolemia and combined hyperlipoproteinemia. Also the best at increasing HDL. intereferes with other acids

Front 12

what inhibits VLDL release, causes hot flashes and impaired glucose tolerance, and interacts with other acids. what is it used for

Back 12

Niacin, Nicotinic Acid, B3

used to treat heterozygous hypercholesterolemia and familial combines hyperlipoprotenemia

**GREAT at increasing HDL

Front 13

Fibric Acids

1. Drugs
2. Mech
3. Pharmacokinetics
4. Uses
5. Adverse Effects

Back 13

1. Gemfibrozil, Clofibrate, Fenofibrate

2. increase LPL to hydrolyze lots of VLDL. Done by activating PPARa

3. oral abs, renal excretion. its also an acid (as was niacin, inhibit VLDL secretion) so will interefere with other acids

4. familial dysbetalipoproteinemia, hypertryglyceridemia (not good for primary chylomicronemia/familial hypercholesteremia- this one treated with niacin)

5. Gall stones, esp in women who have had some kids.

Front 14

how do you treat...

1. heterozygous famililal hypercholesterolemia

2. famillial dysbetalipoproteinemia

3. hypertriglyceridemia

4. familial combined hyperlipoproteinemia

Back 14

1. fibric acid
2. niacin
3. niacin
3. fibric acid

Front 15

Gemfibrozil
Clofibrate
Fenofibrate

Back 15

these are fibric acid derivatives

**the activate PPARa to increase LPL activity
**abs orally, excreted renally, intereferent with other acids

**used in fa, dysbetalipoprotenemia and hypertriglyceridemia

**increases gallstones, can also increase LDL R

Front 16

what are colestipol cholestyramine nad colesevelam

Back 16

bile acid binding resins. they inhibit reabs of bile acid resins so that more cholesterol is used to replace them. Increase LDL receptors to take up more cholesterol

**not abs, take with meals.

**effective in most except familial hypercholesterolemia bc they dont make functional LDL R

**can cause constipation/bloating, gallstones (but less so that fibric acids), vit K malabs, interferes with abs of acidic drugs like: digitalis, thiazides, tetracycline, thyroxine, asprin

Front 17

in what hyperlipidemia are there no functional LDL R genes, so what class of drugs wont work

Back 17

homozygous familial hypercholesterolemia

**bile acids wont work. colestipol, cholestyramine, colesevelam

Front 18

what drug causes vit K malabsorption

Back 18

bile acid binding resins

**can also impair abs of acidic drugs like: digitalis, thiazides, tetracycline, and thyroxine, adn asprin

**constipation and bloating

Front 19

what is the drug that isnt abs and should be taken with meals

Back 19

bile acid binding resin

colestipol
cholestyramine
colevasevelam

**binds bile acids so they arent reabs, this means that we need to use more cholesterol to make more bile acids. increased LDL R on liver. decreased LDL levels will decrease cholesterol in the plasma

good for heterozygous familial hypercholesterolemia, and combines hyperliporotenemia

NOT good for familial hypercholesterolemia or hypertriglycceridemia

**K malabs, interferes with acidic drugs, constipation, bloating

Front 20

what are statins

Back 20

HMG CoA reductase inhibitors

**HMG CoA reductase is the RLE for cholesterol synthesis

**lovestatin and simvastatin are given as prodrugs --> more biologically available

**increased LDL R, decreases LDL plasma
**decrease plasma TG, increase HDL (still better increase in HDL with niacin)

Front 21

so the drug given at meal times is...
the one given at night is

Back 21

bile resins
statins (HMG CoA reductase inhibitor)

Front 22

what statins are prodrugs

Back 22

levostatin
simvastatin

**tehse are prodrugs so will be more biologically available

**HMG CoA reductase inhibitor: increased LDL R --> decreased plasma LDL. decreased plasma TG, increased HDL (more increased HDL with niacin)

Front 23

how do HMG CoA reductase Inhibitors Act

Back 23

**inhibit RLE for cholesterol synthesis

reduce plasma LDL by increasing LDL R

decrease plasma TG and increase HDL

**also beneficial:
-decrease CRP
- make NO
- increase plaque stability, decrease platelet aggregation and decrease lipoprotein oxidation

Front 24

what class of drugs is really beneficial bc is makes plaques more stable, inhibits platelet aggregation and decrease lipoprotein oxidation (decrease plaque formation(

Back 24

statins, HMG CoA reductase inhibitors

Front 25

wht are the pharmacokinetics of statins

Back 25

HMG CoA reductase inhibitors

**given at night, this is when we make most of our endogenous cholesterol (not eating cholesterol)

**high first pass metabolism, excreted by GI

Front 26

what are statins used for

Back 26

HMG CoA reductase inhibitors

*good in cases where LDL in plasma is high:
-heterozygous famlilal hypersholesterolemia
-combined hyperlipoproteinemia

**CI in preggos and alcoholics (hepatotoxic) and renal disease (can cause rhabdomylosis which plugs kidney)

Front 27

what drug shouldne be used in preg, etoh or kidney

what shouldnt be used in DM II

Back 27

Statins (hepatotoxic, need cholerstoel to make a baby, rhabdomylosis will plug kidney- if you give mannitol its ok)

niacin

Front 28

rhabdomylosis is associated with renal shut down after what class of drugs is used

Back 28

statins, HMG CoA reductase inhibitors
**if you give mannitol can be ok


**also dont use in preg

Front 29

ok so statins when given with inhibitors will do what do drug availability, what are some examples of inhibitors

Back 29

increase plasma conc of statins, increased effects

**macrolides, cyclosporine, ketoconazole, verapamil, ritonavir, grapefruit juice, gemfibrozil

Front 30

what happens to statins

macrolides, cyclosporine, ketoconazole, verapamil, ritonavir, grapefruit juice

Back 30

INCREASE effects

*these things are inhibitors of their metabolism

Front 31

ok so statins when given with indicers will do what to the effects, what are some examples of inducers

Back 31

induced metabolism will DECREASE effects

**phenytoin, griseofulcin, barbituates, rifampin,

Front 32

how does the fibric acid drug gemfibrozol interact with statins

Back 32

gemfibrolozol will inhibits the metabolism of statins, increased bioavailabille

Front 33

what will these thngs do to statins

phenytoin, griseofluvin, barbituates, rifampin

Back 33

decrease plasma conc bc they induce their metabolism

Front 34

what are hte drugs that are sensitive to grapefruit juice

Back 34

the juice will inhance availability of drug bc it inhibits its metabolism

**calcium channel blocker
**statins

Front 35

what is teh drug that will decrease cholesterol but doesnt really have a lot of side effects

Back 35

ezetimibe

**blocks abs of Cholesterol, BUT MI and stroke still high :/

Front 36

what is orlistat

Back 36

weight loss
inhibit pancreatic lipase, decrease TG breakdown so less abs. get fatty stools and decrease abs of fat soluble vitamins

Front 37

what are the ways to treat hyperlipidemia

Back 37

stop eating so much fat!!!

if you use drugs they are used for the lifetime of the pt

Front 38

what is the tx when labs find high ...

1. Cholesterol
2. TG
3. Cholesterol _ TG

Back 38

1. cholestyramine, colestipol, (bile acid binding resin) ezetimibe (inhibit abs of cholesterol)

2. gemfibrozil (fibric acid, increase LPL)

3. statins (HMG CoA reductase inhibitor) niacin (inhibit VLDL secretion) exetimibe