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Pharmacology > Hyperlipidemic Drugs > Flashcards

Hyperlipidemic Drugs Flashcards

1
Q

Lipid Membrane

A

Phospholipids

Cholesterol

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2
Q

Hydrophobic core

A

Triglycerides

Cholesterol Esters

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3
Q

Apolipoproteins

A

Structural proteins and ligands for particle uptake

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4
Q

LDL

A

Bad

60% Cholesterol

25% Triglyceride

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5
Q

IDL

A

35% Cholesterol

55% Triglyceride

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6
Q

VLDL

A

20% Cholesterol

55% Triglyceride

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7
Q

Chylomicrons

A

85% Triglyceride

3% Dietary Cholesterol

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8
Q

HDL

A

Good

35% Phospholipid

20% Cholesterol

5% Triglyceride

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9
Q

LDLs and atherosclerosis

A

Endothelial injury allows LDL to enter

Monocytes migrate to activated endothelium

Foam cells (full of cholesterol) secrete proteases and GF to activate SMC proliferation

Increased ECM, increased migration of SMC = growing atherosclerotic plaque

Necrotic foam cells release cholesterol/debris = fatty streak

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10
Q

Protective Role of HDL

A

Inhibit oxidation of LDLs

Inhibit expression of adhesion molecules on endothelium

Inhibit formation of foam cells

Promote REVERSE CHOLESTEROL TRANSPORT (periphery -> liver -> bile)

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11
Q

Very High Lipid Levels

A

LDL-C: >190 mg/dL

Triglyceride: >500 mg/dL

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12
Q

Moderate Hypercholesterolemia with low CV risk

A

Therapeutic lifestyle change

Dietary reduction of cholestrol intake

Exercise/ weight reduction

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13
Q

Severe Hypercholesterolemia and/or a high CV risk

A

LDL > 190 or 70w/diabetes

Clinical evidence of CVD 10 yr

CVD risk

Drug therapy: reduce LDL via STATIN

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14
Q

STATINs

A

Most prescibed drug in US

Significant reduction in LDL

Modest reduction in TG

Modest increase in HDL

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15
Q

STATINs MoA

A

HMG-CoA analog (rate-limiting enzyme in cholesterol biosynthesis) and act as substrate for HMG-CoA reductase

Competetively inhibit HMG-CoA reductase

Decrease endogenous cholesterol synthesis

Triggers signal to activate SREBP transcription factor

SREBP upregulates expression of LDL receptor gene

More LDL receptors

More LDL is taken up from bloodstream

Decreased serum LDL

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16
Q

Other activities of STATINs

A

Inhibits endothelial adhesion molecule expression

Inhibits adhesion of monocytes to endothelium

Inhibits monocyte proliferation and migration

Inhibits oxidation of LDLs (decreases Foam cell formation)

Inhibits SMC proliferation

Inhibits inflammatory responses

Stabilizes endothelium (decreases risk of plaque rupture)

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17
Q

Therapeutic Use of STATINs

A

Drug of choice for increased LDL

Drug of choice for primary and secondary prevention of CVD

STATINS EFFECTIVE IN REDUCING CHD RISK IRRESPECTIVE OF INITIAL BASELINE LDL

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18
Q

Dosing of STATINs

A

Doubling dose minimally improves efficacy while increasing potential for adverse effects

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19
Q

STATIN

Adverse Effects

A

Generally well tolerated

Rare: increase in liver enzymes

Type2 diabetes has small increase in risk

RHABDOMYOLYSIS: Myalgia and myopathy

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20
Q

Rhabdomyolysis

A

Muscle inflammation and disintegration

Rare side effect from statin use

Fever, malaise, myalgia, elevated serum CK, myoglobin, dark urine

High STATIN doses or drug interactions (CYP34A inhibitors)

Polymorphism of STATIN HAT

PRAVASTATIN has fewer adverse muscle effects

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21
Q

STATINs

A

Most potent -> least potent

Rosuvastatin (Crestor)

Atorvastatin (Lipitor)

Simvastatin (Zocor)

Pravastatin (Pravachol)

Lovastatin (Mevacor)

Fluvastatin (Lescol)

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22
Q

STATIN

Pharmacokinetics

A

Absorbed in intestine

Interaction with grapefruit juice DEC bioavailability

Taken up in liver by OATP2

5-30% bioavailability

Metabolized in liver and excreted in bile/feces

Glucoronidated

Variably metabolized by CYP450 system

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23
Q

STATIN Drug Interactions

CYP34A inhibitors

A

INCREASE L,S,A

Cyclosporin, erythromycin, ketaconazole, HIV protease inhibitors, grapefruit juce, Ca-channel blockers, anti-arrhythmia drugs (amiodarone), warfarin

24
Q

STATIN Drug Interactions

CYP2C9 Inhibitors

A

INCREASE F, R

Ketoconazole, itraconazole, metronidazole, sulfinpyrazone

25
Q

STATIN Drug Interactions

Inducers of CYP2A4

A

Reduce L,S,A

Reduce clinical efficacy

Phenytoin

Barbiturates

Rifampin

Thizolidnediones

26
Q

STATIN

Drug Interactions General

A

Pravastain is NOT metabolized by P450, drug of choice when interactions are a concern (transplant patients)

Gemfibrozil: inhibits OATP2 and increases ALL statins, rhabdomyolysis

27
Q

STATIN

Contraindications

A

Pregnancy, nursing mothers (inhibition of cholesterol synthesis may adversely affect the newborn)

Liver disease

28
Q

Bile Acid-Binding Resin

Clinical Effect

A

Modest reduction in LDL

Can cause small increase in TG

29
Q

Bile Acid-Binding Resins

A

Cholestyramine (Questran)

Colestipol (Colestid)

Colesevelam (Welchol)

30
Q

Bile Acid-Binding Resin

MoA

A

Cationic polymers

Bind to (-)bile acids, prevent reaborption in small intenstine

Causes increase bile acid production, decreases hepatic holesterol concentration

Upregulation of LDL-R Increases LDL clearance

31
Q

Therapeutic Use of Bile Acid-Binding Resin

A

Second line agent to reduce CHD events

Used in combination with STATIN (aggressively reuduce)

Used in patient who can’t have STATINs (children, PREGGOS)

32
Q

Bile Acid-Binding Resin

Side Effects

A

Not absorbed or metabolized

Very safe/few side effects GI disturbances

Cholestyramine and Colestipil impair absorption of fat soluble vitamins (ADEK)

33
Q

Bile Acid-Binding Resins

Drug Interactions

A

Cholestyramine and Colestipol, but NOT Colesevelam, interfere with absorption of many drugs.

Should be taken 1-2 hours before or 4-6 hours after Resins

34
Q

Bile Acid-Binding Resins

Contraindications

A

TYPE IIY Dysbetalipoproteinemia

Raised triglycerides

Increased VLDL levels can lead to pancreatitis

35
Q

Inhibitors of Cholesterol Absorption

A

Ezetimibe (Zeita)

36
Q

Inhibitors of Cholesterol Absorption

MoA

A

Inhibits NPC1L1 protein in intestine, cholesterol not absorbed

Reduced cholesterol decreases VLDL and LDL production

LDL-R increased, more cholesterol taken up from serum

37
Q

Inhibitors of Cholesterol Absorption

Therapeutic Uses

A

Reduces LDL in patients

Not dependent on intact LDL-R

Combined with STATIN significantly reduces LDL levels (more efficacy, less STATIN side effects)

38
Q

Inhibitors of Cholesterol Absorption

Adverse Effects

A

Generally well tolerated

GI disturbance: flatulence and diarrhea

39
Q

Inhibitors of PCSK9

A

Alirocumab

Evolocumab

40
Q

Inhibitors of PCSK9

MoA

A

PCSK9 is secreted by liver, binds to LDL-R and prevents LDL-R recycling (instead sends it to lysosome)

Thought to be responsible for tonically controlling the levels in LDL-R expressed on liver cells

Some people with FH have gain of function mutations and have overactive protein

Drugs are human antibodies to the protein, prevents it from binding to the LDL-R

41
Q

Lomitapide

A

New drug for homo FH

Mutation in LDL- R, cannot treat with STATIN

Inhibits microsomal TG transfer protein (MTP)

MTP required for assembly of chlyo/VLDLs

Less chylo/VLDL, less LDL

42
Q

Mipomersen

A

New drug for homo FH

Mutation in LDL-R, cannot treat with STATINs

Antisense oligonucleotide for apoB100

Reduces apoB100, less production of VLDL, less LDL

43
Q

Tx Options for Hyperglyceridemia

A

TG 150-199: Lifestyle modifications

TG > 500: lower TG with drugs, prevent pancreatitis

44
Q

Niacin

Clinical Effect

A

Nicotonic acid with vit B3

30-80% reduction in TG

10-20% reduction in LDL

10-30% increase in HDLs****(most effective drug)

FH, dysbetalipoproteinemia, (cholesterol and TG are elevated)

Often combined with STATINs or Resins

45
Q

Niacin

MoA

A
  1. Agonist for Gi receptor in adipose (inhibits lypolysis, reduces FFA, less TG synthesis/less VLDL
  2. Inhibits DGAT2, RLE in hepatic TG synthesis, reduces hepatic VLDL synthesis
  3. Reduces liver ApoC3, increased LPL activity, VLDL breakdown, increased VLDL clearance
  4. Increase 1/2 life ApoAI, increases [serum HDLs}, reverse cholesterol transport
  5. Inhibits macrophage recruitment to atherosclerotic lesions
46
Q

Niacin

Adverse Effects

A

GI distress, nausea, abdominal pain

Skin flushing/itching (tx with NSAIDs)

Inhibits uric acid secretion -> GOUT

Exacerbate peptic ulcers

Modest hyperglycemia in Type2 diabetes

Rare: Hepatic toxicity

47
Q

Niacin

Contraindications

A

Peptic Ulcer disease

Pts with hx of Gout

Caution in diabetics

Caution in pts with impaired liver function

48
Q

Fibrates

A

Fenofibrate (Tricor/Lofibra)

Gemfibrozil (Lopid)

49
Q

Fibrates

Clinical Effect

A

40-60% reduction in Tg

Mild (10-20%) reduction in LDL

10-30% increase in HDL

Tx of dysbetaliporoteniema and Type III hyperlipoproteinemia

Reduce coronary events, stroke and TIA

50
Q

Fibrates

MoA

A

Ligands for nuclear hormone TF PPARalpha

Activate PPARalpha and express genes involved in FFA oxidation/transport

Increased HDL, decreased TG

51
Q

Fibrates

Adverse Effects

A

Generally well tolerated

Mild GI disturbance

Increased predisposition to galltones (inhibit cholesterol 1alpha-hydroxylase)

Myopathy and Rhabdomyolysis (more common in Gem), increased risk with HIGH DOSE STATIN

Hepatitis

52
Q

Fibrates

Drug INteractions

A

Strong protein binder, displace other drugs (warfaring, sulfonylureas)

Gem can increases serum [STATINs] and cause myopathy and rhabdomyolysis

Fenofibrate is durg of choice for combination therapy

53
Q

Fibrates

Contraindications

A

PREGGOS

Severe hepatic dysfunction/renal disease

Pre-existing gallbladder disease (the increased risk of gallstones)

54
Q

Fish Oils

A

Omega 3 long chain polyunsaturated fatty acids

Eicosapentaenoic acid

Docosahexaenoic acid

55
Q

Fish Oils

Clinical Effect

A

Lowers serum TG

Minor increase in HDL

Increase of LDL in some pts

56
Q

Fish Oils

Therapeutic Uses

A

Only as an adjunct to diet in treatment of hypertriglyceridema in individuals with TG > 500

57
Q

Fish Oils

MoA

A

Unclear, maybe inhibits expression of genes involved in TG synthesis

Anti-inflammatory activity (acts via GPC-R expressed on macrophages)

Pharmacology (44 decks)

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