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Cardiology > Lipids/Triglycerides > Flashcards

Lipids/Triglycerides Flashcards

1
Q

Genetically deficient/defective hepatic LDL receptors
* no receptors produced
* receptors don’t migrate to surface of cell
* defective LDL binding
* internalization defect

Autosomal dominant/co-dominant
* Elevated total & LDL cholesterol levels from birth
* heterozygotes = 325-450mg/dL
* homozygotes= 500-1000mg/dL

A

Familal hypercholesterolemia

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2
Q

what are some physical findings in hypercholesterolemia?

A
  • Tendon Xanthomata
  • xanthelasmas, arcus corneus
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3
Q

In a patient with familial hypercholesterolemia, when would cardiac events (MI, SCD, Aortic Stenosis) be seen?

A

Homozygotes: 1st decade of life
heterozygotes: men- 3rd, women-4th decades of life, especially aggressive with tobacco abuse, low HDL-C, high lipoprotein

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4
Q

What medications mainly lower LDL-C?

A
  • Statins (HMG-CoA reductase inhibitors)
  • Azetidinone (ezetimibe)
  • Resins (bile acid binding resins or sequestrants)
  • PCSK9 inhibitors
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5
Q
  • Best evidence for CVD reduction and safety
  • major effect is reduction in LDL-C: 20-60% (modest lowering of TG, modest increase HDL-C)
  • Seven on the market in U.S (potency and and metabolism vary by agent)
  • MOA: inhibition of HMG-CoA reductase–> reduce intrahepatic cholesterol pool–> upregulation of hepatic LDL receptors and removal of LDL from bloodstream
A

Statins

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6
Q

what are major side effects/contraindications to statin medications?

A

Major side effects:
* myalgia/ myopathy
* abnormal liver function tests

Contraindications
* Liver disease
* pregnancy
* caustion in combination with fibrates

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7
Q

What are high intensity statins?

A
  • atorvastatin 40-80mg
  • rosuvastatin 20-40mg
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8
Q

what is considered moderate intensity statins?

A

Atorvastatin 10-20mg
rosuvastatin 5-10mg

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9
Q
  • reduces CVD risk in combination with statins; safety demonstrated over medium-term use
  • major effect is reduction in LDL-C: 14-20%
  • minimal decrease in TG, minimal increase in HDL-C
  • MOA: Blocks absorption of cholesterol in the small intestine by inhibiting the Niemann-pick C1 like protein—> reduce intrahepatic cholesterol pool–> increases hepatic LDL receptors +LDL removal
  • compensatory increase HMG-CoA–> best with statins
  • well tolerated; avoid w/ severe liver disease
A

Azetidinones (Ezetimibe)

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10
Q
  • MOA: block absorption of bile salts in the terminal ileum–> reduce intrahepatic cholesterol pool–> upregulation of hepatic LDL receptors + removal of LDL from blood
  • major effect is reduction in LDL-C: 15-30% (modest increase in TG and increase HDL-C)
  • woerks best with statins
A

Bile Acid binding resins

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11
Q

what are side effects/contraindications of Bile acid binding resins?

A

side effects:
* Abdominal discomfort and constipation
* decrease absorption of other durgs
* reduce absorption of fat solube vitamins

Contraindications
* Elevated TG (Especially > 200mg/dL)
* multiple, complex medicatin regimens
* bowel or biliary obstruction

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11
Q
  • Reduce CVD risk; short-term safety only
  • two on the market; both injectables
  • MOA: secreted from hepatocytes–> binds LDL–> receptor–>endocytosis–> lysosomal degradation. Prevents LDL receptor degradation + preserves recycling to hepatocyte surface–> increase receptor density–> increase LDL-C clearance
  • Very well tolerated (expensive)
  • makes liver twice as effective at removing LDL
A

Proprotein Convertase Subtilisin/ Kexin Type- 9 (PCSK9) Inhibitors

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12
Q

Nutritious way to lower LDL-C

A
  • Reduce dietary cholesterol to < 200mg/day–> decrease LDL-C by 3-5%, depending on baseline intake
  • reduce saturated fats and trans fat to 5-6% of daily calories –> this reduces LDL-C by 8-10%, depending on baseline intake
  • Dietary soluble fiber is weak bile acid binder (adding psylllium 6-12g/day)–> decrease LDL-C by 5-10%
  • plant sterols block cholesterol absorption- adding plant stanol/sterol margarines (2g/day)–> decrease LDL-C by 7-15%
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13
Q
  • varying patterns of LDL-C and VLDL-C levels in families with high apo-B-100 levels
  • overproduce apo B-100: increase VLDL + LDL
  • 1/3 with LPL abnormality (leads to increased TGs)
  • increased atherogenicity (LDL: small and dense; VLDL: cholesterol-enriched; HDL: low, less anti-oxidant/inflammatory)
  • genetic predisposition, acquired due to overweight
  • Commonly associated with HTN, type II diabetes mellitus, obesity in families
A

Familial combined hyperlipidemia

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14
Q

which medications primarly lower triglycerides and increase HDL-C?

A
  • Fibrates (fibric acid derivatives)
  • omega-3 fatty acids (fish oils)
  • niacin (nicotinic acid; also lowers LDL-C)
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15
Q
  • Modest evidence for CVD reduction as monotx; limited benefit when added to statins + side effects
  • best in TG> 400-500mg/dL to prevent pancreatitis
  • MOA: complex mechanism: main is to activate LPL and reduce apo CIII (LPL inhibitor)
  • 2 on the market, differ in clearance pathways and interactions with statins
  • major effects (used if very high TGs): ( decreased TG by 20-50%, increased HDL 10-20%, increased LDL-C by 5-10% but often increase if high TG)
A

Fibrates

16
Q

What are side effects and contraindications of fibrates?

A

Side Effects
* Abdominal pain
* gall stones
* increased creatinine (secretion, not GFR reduction)
* DVT/ pulmonary embolism (uncommon)
* myalgia/myopathy, especially with statins

Contraindications
* Liver disease
* severe kidney disease (Especially fenofibrate)
* gall stones
* caution with statins (fenofibrate may be safer)
* pregnancy

17
Q
  • decreases triglycerides by 20-50%
  • modest increase in HDL-C, related to TG reduction
  • LDL-C may increase or not change
  • non-lipid effects: platelets, membrane stabilization
  • both low and high dose have weak evidence for CVD risk reduction
A

Omega-3 Fatty Acids (fish Oils)

18
Q

What are complex mechanisms, major side effects and major contraindications of omega-3 fatty acids?

A

Complex Mechanisms
* Decrease VLDL production
* Decrease lypolysis in adipocytes
* Decrease TG synthesis

Major side effects
* eructation
* flatulence
* abdominal pain
* bruising/bleeding
* atrial fibrillation

No major contraindications

19
Q
  • Modest evidence for CVD reduction as monotx, limited benefit when added to statins + side fx
  • increases HDL-C by 15-30%
  • decreases TG by 20-50%
  • decreases LDL-C by 10-30% (at higher doses)
  • Complex mechanisms: Decreases lypolysis from adiopcytes, VLDL syntheses, decrease APO A-1 catabolism, but not increase cholesterol removal from HDL
A

Niacin (Nicotinic Acid, Vitamin B3)

20
Q

what are side effects/contraindications to niacin?

A

Side effects
* flushing and itching- reduced with aspirin
* abdominal pain, ulcers
* insulin resistance/hyperglycemia
* hepatotoxicity
* gout
* myalgia/myopathy- especially with statins

Contraindications
* Liver disease
* Gout
* Uncontrolled type II diabetes mellitus
* pregnancy

21
Q

Nutrition to lower TGs?

A
  • Achieve healthy weight (decrease insulin resistance)
  • avoid alcohol
  • limit simple carbohydrates and sweets
  • fat intake should be 25-30%/day of total calories
  • limit saturated fatty acids
  • emphasize polyunsaturated fats and monounsaturated fats
22
Q
  • TGs> 500-1000mg/dl
  • usually acquired, but can be genetic
  • acquired- obesity, alcohol abuse, high fat diet, uncontrolled diabetes mellitus, non-compliance
  • genetic- LPL deficiency, decrease apo CII, orin increase APO CIII
  • main risk is pancreatitis due to hyperviscosity
  • also get fatigue, impaired cognition and memory, paresthesias, hepatosplenomegaly
  • may have eruptive xanthomata, lipemia retinalis
A

Chylomicronemia syndrome

23
Q

how to treat hyperlipidemia (LDL-D: If TG< 500mg/dL)

A

appropriate dose statin to prevent ASCVD
* Add ezetimibe
* consider adding bile acid binding resin
* add PCSK9 inhibitor

24
Q

how to treat hyperlipidemia if triglycerides are > 400-500mg/dL to prevent pancreatitis?

A
  • Fenofibrate (or gemfibrozil, but limits statin use)
  • optimize glycemic control
  • add fish oils
  • consider: niacin

Cardiology (8 decks)

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