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Cardiovascular Therapeutics > Cholesterol Tx > Flashcards

Cholesterol Tx Flashcards

1
Q

Statins are a….

A

HMG-CoA reductase inhibitors

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2
Q

Statins main effect is on…..

A

LDL levels in the blood

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3
Q

Statin Examples

A

Atorvastatin
Fluvastatin
Lovastatin
Pravastatin
Rosuvastatin
Simvastatin

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4
Q

Statin MOA

A

Inhibits an enzyme in the pathway for intracellular synthesis of cholesterol

Cellular levels of cholesterol become depleted

Cell upregulates LDL receptor

LDL levels in the blood decrease

Primary site of action appears to be hepatic cells  liver takes up a bunch of LDL

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5
Q

Statins primary Site of ACtion

A

Liver - Hepatocytes

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6
Q

Statin Benfits

A

Clinical benefits of LDL lowering have been demonstrated repeatedly

Similar to HTN control, lipid reduction is NOT a cure for ACVD

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7
Q

The most benefit of statins in….

A

Greatest absolute benefit occurs in patients with a “statin-indicated condition” due to their high global risk

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8
Q

greater benefits are a reesult of

A

Greater LDL reductions

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9
Q

Current Strategy of Statin Usage. Why?

A

Maximize statin dose in everyone who can tolerate it

Trials show that high dose statins are better than low dose statins

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10
Q

Statin effects on other plasma proteins. Are we certain?

A

HDL may ↑ 5-10% (up to 15% or not at all)

TG ↓ up to 30% (higher baseline TG = greater effect)

Benefits of these effects UNCLEAR

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11
Q

What is the most controversial aspect of statin tx?

A

One of the MOST controversial aspects of statin therapy is its role in LOW risk patients

Primary prevention

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12
Q

When is benefit of a drug reduced?

A

If few events are occurring WITHOUT drug, the opportunity for benefit is drastically reduced

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13
Q

NNT in Statin Tx that is acceptable

A

NNT of <50 to prevent 1 CV event over 5 years is generally accepted as reasonable for statins (threshold for where they think statins are of benefit)

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14
Q

Are the benefits of statins the same for everyone?

A

For statins, relative benefits seem to be the same in everyone assuming a fixed LDL reduction.

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15
Q

The NNT is often impcated by….

A

Thus, NNT is generally impacted by the RISK level

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16
Q

The recommended use of statins is based on…

A

RISK

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17
Q

Why can’t diets/lifestyle be used to reduce LDL?

A

Diets are terrible at lowering LDL levels

Healthy Lifestyles –> Start way to late –> If you are 60, this is nieve –> Do not have time to change their life as much as a 20 year old

Critical for global CV risk reduction

Limited benefits for LDL specifically

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18
Q

Risk of early onset of dz is reduced when…

A

Healthy diet/lifestyle throughout life would almost eliminate an individual’s risk (at least for early onset dz)

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19
Q

Is titration needed with statin meds?

A

NO

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20
Q

High Intesnity Statin Lowers LDL by…. Examples

A

> than or equal to 50%

Atorvastatin 40/80 mg
Rousuvastatin 20/40

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21
Q

Moderate Intensity Statins Lower LDL by…. Examples

A

30-49%

Atorvastatin 10mg
Rousuvatstain 10mg
Simvastatin 20-40 mg
Pravastatin 40-80 mg
Lovastatin 40-80 mg
FLuvastatin 40 mg

All rats swim past lakes fast.

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22
Q

Low intensity Stains lower LDL by… Examples

A

<30%

Simvastatin 10mg
Pravustatin 10-20 mg
Lovastatin 20 mg

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23
Q

Why do all pt’s get high-dose statins?

A

More intensive LDL reduction is clearly associated with greater protection against ACVD events

24
Q

Exceptions to high dose strategy?

A

Intolerance
Drug interactions
Patient preference

25
Q

What do we do if we don’t reach targets?

A

Time – wait at least 6-12 weeks to ensure full effect

Adherence - Has Jibby experienced challenges taking it?

Lifestyle – has Jibby implemented lifestyle changes yet?

26
Q

Statin Time to Effect

A

6-12 weeks

27
Q

Chart for Intensifying tx

A

Study

28
Q

PCSK9

A

Evolocumab
Alirocumab

New and expensive

29
Q

PCSk9 MOA

A

PCSK is An enzyme that promotes degradation of the LDL receptor on hepatocytes. (antibodies to the enzyme)

Alirocumab and evolucumab are antibodies to PCSK9

Fully “humanized” monoclonal antibodies

Result is increased expression of LDL receptors on hepatocytes and increased clearance of LDL from blood

30
Q

Are PCSK9 safe to use with statins?

A

Yes –> Different mechanism

31
Q

PCSk9 Criteria

A

40 to 85 years of age

Clinically evident atherosclerotic disease
MI
Ischemic stroke
PAD

LDL 1.8mmol/L or higher (or Non-HDL at least 2.6mmol/L)

Currently taking Atorvastatin equivalent of 20mg/day (why on 20 is b/c most likely could not tolerate the high dose)

32
Q

Ezetimibe MOA

A

Inhibits luminal cholesterol absorption in small intestine

↓ cholesterol absorption = ↓ chylomicron formation

↓ chylomicron remnants to the liver = ↓ hepatocyte chol

↑ LDL receptor expression in liver = greater clearance of LDL

LDL reduces LDL by 15% to 20% as monotherapy (weak)

33
Q

Ezetimibe undergoes….

A

Despite its local effect, the drug undergoes enterohepatic recirculation

34
Q

Is ezetimibe used in monotx?

A

No

35
Q

Ezetimibe is combined with statins when…..

A

Statin escalation impossible – tolerability –> Use Atorvo 20 and add ezetimibe can equal high does statin LDL reduction

Statin dose maxed out – LDL still not at goal

36
Q

Eicosapent Ethyl

A

Eicosapent Ethyl (n-3 fatty acid)  Omega-3 fatty acids
Purified ester of EPA (eicosapentaenoic acid) (fish source)  Now in guidelines  NOT AN LDL DRUG

37
Q

Inclisiran

A

interferes with PCSK9 messenger RNA

38
Q

Bempedoic Acid

A

Inhibitor of ATP citrate lyase – reduced cholesterol synthesis

39
Q

Stain Tolerability Variability

A

Very Variable

40
Q

Statin S/e

A

GI discomfort
Fatigue

Rhabdomyolyisis –> Rare
Muscle effects  Rhabdomyolysis (ultimate neg muscle outcome)  such inflamed muscles, muscles rupturing and letting go of myoglobin

Diabetes (increased detection) –> VERY LOW –> Increase blood glucose

Cognitive Impairemnt - Low

41
Q

Myopathy

A

Muscle Pain

42
Q

Myalgia

A

CK < or eqaul to ULN

43
Q

Myositis

A

CK > ULN

44
Q

Rhabdomyolysis

A

CK > 10 times ULN

45
Q

CK Tests

ULN

A

Creatinine Kinase Tests

Upper Limit of Normal

46
Q

When are CK tests ordered?

A

Ask about muscle diseases, wasting/frailty  may indicate higher risk for statin-myopathy (might consider lowering statin dose)

If the risk for muscle effects is high, consider a baseline CK (i.e., before statin started)

Otherwise, CK levels ONLY ordered if symptoms appear

47
Q

To ensure muscle sx are from statin?

A

Ensure it is from the statin

Symptoms resolve when statin d/c
Symptoms recur when statin restarted
Symptoms recur when another statin tried

48
Q

How to deal with intolerability?

A

D/c statin for short period, re-challenge after resolution of symptoms
Lower doses / every other day dosing
Lower potency statins (e.g., fluvastatin)
Non-statin drugs

49
Q

Most likley origin of DI’s for statins

A

Hepatic Metabolism

50
Q

All statins undergo the

A

First Pass effect

51
Q

All statins are metabolized by…

A

Liver

52
Q

Interactions of Statins

A

3A4 / grapefruit juice

53
Q

C.I. of Statins

A

People with muscle disease
Gemfibrozil (fibrates can increase adverse muscular effects)

54
Q

Dosing of Statins

A

OD

55
Q

Which has fewer drug interactions?

A

Rosuvastatin – fewer drug interactions vs atorva

56
Q

In renal disease, use this statin?

A

Atorvostatin

Reduce dose if CrCl <30m/min for ROSUVA —- Atorva does NOT require dose adjustment in renal dysfx

Cardiovascular Therapeutics (5 decks)

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