Exam 2 Flashcards

1
Q

What are the LDL lowering meds?

A
  • Statins
  • Ezetimibe
  • Bile Acid Sequestrants
  • PCSK9 Inhibitors
  • Niacin
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2
Q

What are the TG lowering meds?

A
  • Omega 3s
  • Niacin
  • Fibric Acid Derivatives
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3
Q

Statins (HMG-CoA Reductase Inhibitors) – MECHANISM OF ACTION & TARGET

A

Target → LDL

MOA → Competitive inhibitor of HMG-CoA Reductase which stops the endogenous production of LDL

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4
Q

Statins (HMG-CoA Reductase Inhibitors) – ADVERSE EFFECTS

A
  • Pregnancy category X
  • Hepatic Dysfunction (AST/ALT monitoring)
  • Headache
  • Muscle Complication (myalgia, myopathy, rhabdomyolysis)
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5
Q

Statins (HMG-CoA Reductase Inhibitors) – DDI

A

-CYP3A4 Substrates (ALS) → Atorvastatin, Simvastatin, and Lovastatin
→inhibitors increase concentration of statin which
causes muscle complications (grapefruit juice,
protease inhibitors, anti-fungal, warfarin)

  • Binding Statin w/ other meds (bile acid sequestrants and calcium containing products)
  • Simvastatin and Amlodipine (bc Aml causes Sim to break down fast causing muscle problems)
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6
Q

Statins & Pleiotropic Effect

A
  • Increase plaque stability (so parts of plaque doesn’t break off and cause stroke)
  • Decrease platelet activation and aggregation
  • Decrease vascular inflammation
  • Decrease endothelial dysfunction
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7
Q

Statins: Primary Prevention

A

-Moderate intensity
-No cardiac event
→LDL > 190
→Diabetes + age > 40
→Diabetes + age < 40 – with high ASCVD risk

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8
Q

Statins: Secondary Prevention

A
  • Clinically evident cardiac event

- Angina, STEMI, NSTEMI, Stroke, TIA, and Peripheral Artery Disease

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9
Q

Statins – INTENSITY BY DOSE

A

HIGH (>50%) – most LDL clearance
→Atorvastatin
→Rosuvastatin

MODERATE (30-50%)
→Atorvastatin
→Rosuvastatin
→Simvastatin
→Pravastatin
→Lovastatin
LOW (<30%) -- used when have family hx
→Simvastatin
→Pravastatin
→Lovastatin
→Fluvastatin
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10
Q

Statins (HMG-CoA Reductase Inhibitors) – DRUGS

A
→Rosuvastatin -- most potent, least muscle issues &amp; DDIs
→Atorvastatin
→Simvastatin
→Lovastatin
→Pravastatin
→Fluvastatin --least potent

Ending in -STATIN

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11
Q

Chylomicron → HDL Pathyway

A

Chylomicron → VLDL (via liver) → LDL (via adipose) → HDL (via other tissue)

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12
Q

Low Density Lipoproteins (LDL)

A
  • “Bad Cholesterol”
  • Deposit extra cholesterol into vascular tissue → causing atherosclerosis
  • Removed by the liver
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13
Q

High Density Lipoproteins (HDL)

A
  • “Good Cholesterol”
  • Removes excess cholesterol from cells and brings them to liver to be excreted
  • Removes cholesterol directly from artery walls
  • Stops atherogenic lipoproteins from oxidizing
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14
Q

Atherosclerosis

A

-Build up of plaque in arteries

→Ex: CAD, Angina, CKD, PAD

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15
Q

The Lipid Panel

A

Total Cholesterol (<200)

LDL (<130)

HDL (>40)

TGs (<150)

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16
Q

Dyslipidemia

A

-One or more abnormalities of any blood lipids (deficiency of HDL or overproduction of LDL/TGs)

  • Hyperlipidemia → too much LDL
  • Hypertriglyceridemia → too much TGs
  • Familial Hypercholesterolemia → genetically defective LDL clearance
17
Q

Treatment of Dyslipidemias

A
#1 -- Diet
#2 -- Exercise
#3 -- Alcohol Avoidance/ Decreased Intake
#4 -- Smoking Cessation
#5 -- Lipid Lowering Meds
18
Q

Bile Acid Sequestrants – MECHANISM OF ACTION & TARGET

A

Target → LDL
MOA → Bind to bile acid in GI tract to increase secretion (get rid of bile acid) and then cholesterol is utilized to create more bile acids

Last line use from LDL lowering meds

19
Q

Bile Acid Sequestrants – ADVERSE EFFECTS

A
  • Poorly Tolerated (isn’t absorbed by body, floats in the GI tract and causes GI issues)
  • GI Side Effects (bloating, gas, constipation, abdominal pain)
  • Potential increase in TGs
20
Q

Bile Acid Sequestrants – DDI

A

-Bind to many meds → making them ineffective
-Give med 1 HOUR BEFORE or 4 HOURS AFTER
→Warfarin
→Levothyroxine
→Digoxin
→Statins
-Contraindicated if patient has hypertriglycerides

21
Q

Bile Acid Sequestrants – DRUGS

A

→Cholestyramine -powder
→Colestipol -powder
→Colesevelam -tablet

Starting in CHOLE- or COLE-