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Pharm 2 > Statins > Flashcards

Statins Flashcards

1
Q

Overview of LDL, HDL, VLDL

A
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2
Q

Types of Lipids

A
  1. Cholesterol- plasma lipids-> transported by lipoproteins
  2. Triglycerides- plasma lipids- same
  3. Phospholipids

lipoproteins= cholesterol + triglycerides + 1 apolipoprotein B100 molecule (apoB)

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3
Q

Classification of lipoproteins

A
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4
Q

High density Lipoproteins (HDL)- why are they so good?

A
  1. Retrieve cholesterol from the artery wall and recycle
  2. Inhibit oxidation of atherogenic lipoproteins
  3. Low levels= INCREASED RISK FOR ATHEROSCLEROTIC DISEASE
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5
Q

Why do we treat hyperlipidemia and hypertriglyceridemia?

A

Causes Atherosclerosis and Acute Pancreatitis

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6
Q

Why treat hyperlipidemia?

A

Atherogenic lipoproteins inhibit the release of nitric oxide (which causes dilation)-> reduce changes in acute coronary events-> target LDL

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7
Q

Nonpharmacologic therapy

A
  1. Exercise and smoking cessation
  2. Reduce percent of calories from saturated and trans fats
  3. Increased intake of soluble fibers 25 g
  4. Fish- cold water fish
  5. Red Yeast Rice- OTC not regulated
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8
Q

Treatment of Hyperlipidemia

A
  1. HMG-CoA Reductase Inhibitors
  2. Cholesterol absorption inhibitors
  3. Bile Acid Sequestrants
  4. Proprotein Convertase Subtilisin/Kexin Type 9 (PCSK9) Inhibitors
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9
Q

HMG-CoA Reductase inhibitors

A

MOA: competitively inhibit HMG coA reductase= rate limiting step in cholesterol biosynth
Efficacy: Most powerful drugs for lowering LDL
SE: Adverse muscle events, hepatitis dysfunction, renal dysfunction, Behavior (suicide), DM
NOT FOR PREGNANCY
Drug interactions: CYP3A4, CCB, HIV protease inhibitors, Amiodarone, Grapefruit juice, cyclosporine, HCV antivirals, Fibrates, colchicine, fusidic acid, niacin

ALSO LOWERS TRIGLYCERIDES (1ST LINE) AND LOWER CRP markers

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10
Q

HMG-COA reductase inhibitor choices

A
  1. strongest= Rosuvastatin and Atorvastatin
  2. if renal impaired= Atorvastatin or Fluvastatin
  3. if chronic liver disease= Pravastatin with alcohol abstinence
  4. Fewest drug interactions= Pravastatin, Fluvastatin, rosuvastin, and pitavastatin
  5. muscle related adverse effects? Pravastatin and Fluvastatin = lower risk
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11
Q

Statin therapy high high intensity

A

Lowers LDL by over 50%
Atorvastatin 40-80 mg
Rosuvastatin 20-40 mg

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12
Q

Statin therapy moderate intensity

A

Lowers LDL from 30-50%
FLARS
Fluvastatin 40
Lovastatin
Atorvastatin 10-20
Rosuvastatin 5-10
Simvastatin 20-40

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13
Q

Statin therapy low intensity

A

Lowers by less than 30%
Pravastatin 10-20
Lovastatin 20 mg

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14
Q

Rule of 6

A

double the dose = added 6% reduction

5 mg= 40%
10 mg= 46%

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15
Q

HMG-COA reductase inhibitors muscle-related adverse events

A

Statin Associated Muscle symptoms= SAMS
relatively uncommon= 2% pts
RF: increased age, female, low body weight, kidney disease, high physical activity, hyperthyroid
Clinical features: larger muscle groups
Diagnosis? Clinical and/or Creatinine Kinase= marker for muscle degradation
Management? Discontinuation, switching statins, alternate dosing (MWF dosing- ensure compliance), Coenzyme Q (no benefit)

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16
Q

Rhabdomyolysis

A

DISCONTINUE STATIN IMMEDIATELY
Muscle necrosis
Symptoms: Myalgia, red/brown urine, elevated CK- pain, weakness, swelling
Assoc manifiestations: Fluid/electrolyte imbalance-? Cardiac dysrhythmias, AKI (myoglobin release damaging kidneys), Compartment syndrome, DIC
Management: Prompt recognition, evaluation, management, AGGRESSIVE VOLUME REPLETION

17
Q

Cholesterol Absorption inhibitors

A

Ezetimibe (Zetia)- 2nd MC RX
MOA: impairs dietary and biliary cholesterol absoption @ brush border of intestine-> inhibit cholesterol transporter
efficacy: by 10-14% LDL
QUICK ONSET= 10 HRS
SE: arthralgia, GI, sinusitis/URI, hepatitis

alone or with another statin

18
Q

Bile acid-binding resins

A

Cholestyramine colestipol and Colesevelam
MOA: bind to bile acids in intestine resulting in interruption of reabsorption of bile acids
MOSTLY COMBO WITH STATINS OR NICOTINIC ACIDS
AE: nausea, bloating, cramping, increase liver enzymes
Drug interactions: digoxin, warfarin, fat soluble vitamins, HCTZ, furosemide, NSAIDS, thyroxine
INCREASE TRIGLYCERIDE LEVELS BC TRICKS BODY INTO THINKING ITS LOW AND INCREASE

19
Q

Proprotein convertase subtilisin/Kexin Type 9 (PCSK9) inhibitors

A

Evolocumab (Repatha) and Alirocumab (Praluent)
MOA: binds and inhibits PSCK9 (enzyme in liver that binds to LDL and increases it in the plasma)
REDUCTION IN RATES OF STROKE AND MI
MONO OR COMBO
AE: injection site rxn
EXPENSIVE
Indications: pts on Maximally tolerated doses of statin w/ familial hypercholesterolemia or pts with cvd needing lowering of LDL

20
Q

Bempedoic acid

A

MOA: inhibitor of adenosine triphosphate-citrate lyase-> upstream of HMG reductase inhibit
mono or combo
AE: nasopharyngitis, myalgia, URI, elevated uric acid in gout patients-> worsen wont cause
Indications: heterozygous familial hypercholesterolemia or established atherosclerotic CVSD who require additional lowering of LDL

15-25% reduction in LDL

21
Q

Combo therapies

A

Who requires it?
1. Familial hypercholesterolemia w/ on-tx LDL of >100 mg/dl
2. Existing CVD w/ on-tx LDL >70 mg/dlL (2ndary prevention)
3. High risk w/ TG >150 mg/dL and non HDL > 100 mg/dL

Ezetimibe + statin= no reduction in mortality but MI AND STROKE REDUCED and higher rate of LDL < 70

PCSK9- Antibodies plus statins= REDUCTION IN CARDIOVASCULAR EVENTS

22
Q

Hypertriglyceridemia

A

Why tx? Reduce risk of pancreatitis and ASCVD

Nonpharmacologic measures:
1. Management of HTN
2. Smoking cessation
3. Sedentary lifestyle modification
4. Weight loss
5. diet and alcohol consumption

Classification:
Normal <150 mg/dL
Moderate 150-499 mg/dL
Mod-Severe 500-999 mg/dL
Severe >1000 mg/dL

23
Q

Treatment of Hyperglyceridemia

A
  1. Statins
  2. Fibric Acid derivatives (Fibrates)
  3. Omega- 3 polyunsaturated fatty acids (PUFA)
  4. Niacin
24
Q

Fibric acid derivatives (fibrates)

A

ex: Fenofibrate and gemfibrozil
MOA: Peroxisome proliferation-activated receptor- alpha (PPAR-alpha) agonist-> increases HDL and decreases VLDLs
AE: ASSOC MUSCLE TOXICITY, POSSIBLE RHABDOMYOLYSIS, NEPHROTOXIC, FDA BLACK BOX WARNING FOR SEVERE LIVER INJURY WITH FENOFIBRATE
Drug interactions: Warfarin

Benefits:
Reduce LDL by 10-15%
TG by 40%
increase HDL by 15-20%

25
Q

Omega-3 Fatty acids

A

types:
1. Omega 3 GA (EPA+DHA)= LOWERS TG BY 20-50% AND REDUCES MI
2. Icospaent ethyl (EPA) aka Vascepa-> reduce CVD, nonfatal MI, strokes, UA

AE: Gi symptoms with diarrhea, Atrial fibrillation

OTC= not regulated

26
Q

Niacin

A

LARGE DOSES- 1500-2000 MG PER DAY-> reduce TG by 15-25%, increase HDL by 25-30%, reduce LDL by 15-25%

MOA: inhibits lipolysis in adipose tissues, reduces production of free FA, decreases production of TG in liver
AE: insulin resistance, hyperuricemia, infection risk, myopathy, elevated transaminases and bilirubin, and GI symptoms

Common side effects: FLUSHING, ITCHING, GERD-> Aspirin will counteract

27
Q

Stepwise therapy for hypertriglyceridemia (based on trig levels)

A

Moderate TG- High
ASCVD: marine omega 3 FA
No ASCVD: nonpharmacologic measures

Moderate to severe TG
ASCVD: icosapent ethyl then fibrates
No ASCVD: marine omega-3 FA

Severe TG
ASCVD and No ASCVD= Fibrates

28
Q

Primary prevention of ASCVD

A
29
Q

Secondary Prevention-> Clinical atherosclerotic cardiovascular disease ASCVD

A

Nonfatal myocardial infarction
Coronary heart disease
Stroke
Transient Ischemic Attack TIA
Peripheral Arterial Disease PAD

Pharm 2 (15 decks)

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