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Clinical Medicine Endocrine > Hyperlipidemia > Flashcards

Hyperlipidemia Flashcards

1
Q

What is hyperlipidemia?

A

An excess of lipids, including glycolipids, lipoproteins, and phospholipids in the plasma

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2
Q

What are the types of lipoproteins?

A
  • Chylomicrons
  • Very low-density lipoproteins (VLDL)
  • Intermediate density lipoproteins (IDL)
  • Low-density lipoproteins (LDL - “bad cholesterol”)
  • High-density lipoproteins (HDL - “good cholesterol”)
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3
Q

What is measured in the fasting lipid panel?

A
  • HDL
  • Total cholesterol
  • Triglycerides
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4
Q

How is LDL cholesterol calculated?

A

Total cholesterol - (HDL + triglycerides/5)

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5
Q

Which type of Lipoproteins are associated with clot formation?

A
  • LDLs
  • VLDLs
  • IDLs
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6
Q

What is a chylomicron?

A

A type of lipoprotein that transports lipids absorbed in the intestine to the adipose, cardiac, and skeletal muscle tissue

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7
Q

Chylomicrons contain mostly what?

A
  • Mostly triglycerides

- Some cholesterol

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8
Q

Pathway of Chylomicrons

A
  1. Fat & Cholesterol absorbed in the GI tract are assembled to formChylomicrons
  2. The Chylomicrons head into the blood stream
  3. In the peripheral tissues (e.g.adipose) chylomicrons release theirfats when they meet tissues expressing Lipoprotein Lipase, which allows fats to be absorbed in the form of fatty acids & glycerol (it breaks down triglycerides)
  4. The Chylomicrons are nowsmaller& called Chylomicron Remnants
  5. Empty HDL is produced as a bi-product of this process
  6. They then travel to the liver & are removed by the binding of apoE to their Remnant Receptor
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9
Q

Do Chylomicrons participate in an endogenous or exogenous cholesterol pathway?

A

Exogenous

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10
Q

In someone who is “downregulated” (less LDL removal), what might you see?

A
  • Increase dietary cholesterol/saturated fats
  • Increased age
  • Familial hypercholesterolemia
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11
Q

In someone who is “unregulated” (more LDL removal), what might you see?

A
  • Decrease dietary cholesterol/saturated fats
  • Estrogen
  • Thyroid hormones
  • Statins (help to decrease cholesterol synthesis)
  • Bile acide resins (decreased bile acid uptake by GI tract)
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12
Q

What are some secondary causes of hyperlipidemia?

A
  • Diet
  • Obesity, but also anorexia nervosa
  • Pregnancy
  • DM2
  • Cholestatic liver disease
  • Nephrotic syndrome
  • Chronic renal failure
  • Hypothyroidism
  • Smoking
  • Drugs
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13
Q

Clinical Manifestations of Hyperlipidemia

A
  • Arcus corneas (white rim around the iris)
  • Xanthelasma (lipid deposits along the eye)
  • Xanthoma (lipid deposits anywhere on the body)
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14
Q

When should you check a Lipid Panel? (2 Different Recommendations)

A
  1. Beginning at age 20 y/o: fasting (9-12hr) serum lipid profile (repeat testing every 5 years)
  2. Women greater or equal to 45 y/o and men greater or equal to 35 y/o every 5 years
    • Total cholesterol is >200 or HDL < 40
    • Cholesterol screening should begin at 20 y/o in patients with multiple CV risk factors, DM, or family hx
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15
Q

Triglyceride level classification

A 
<150 = normal 
150-199 = mild 
200-999 = moderate
1000-1999 = severe 
> or equal to 2000 = very severe
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16
Q

Monounsaturated and Polyunsaturated effects on cholesterol levels?

A

Lower LDLs and Raise HDLs

17
Q

Saturated (cis) effects on cholesterol levels?

A

Raise both LDL and HDL

18
Q

Trans saturated effects on cholesterol levels?

A

Raise LDL

19
Q

Treatment of Hyperlipidemia?

A
  • Lifestyle modification (diet, exercise)

- Quit smoking

20
Q

Medications for Hyperlipidemia

A
  • HMG CoA reductase inhibitors (Statins)

- Fibric Acids (Fibrates)

21
Q

Effects of Statins in Hyperlipidemia

A
  • Significantly reduce LDL (18-55)
  • Increase HDL (5-15)
  • Decrease TG (7-30)
22
Q

Effects of Fibrates in Hyperlipidemia

A
  • Decrease LDL (5-20)
  • Increase HDL (10-20)
  • Significantly decrease TG (20-50)
23
Q

4 Statin Benefit Groups

A
  1. Individuals with clinical ASCVD
  2. Individuals with LDL greater or equal to 190 mg/dL
  3. Individuals 40-75 y/o with DM or with LDL 70-189 mg/dL
  4. Individuals without clinical ASCVD or DM who are 40-75 y/o with LDL 70-189 mg/dL and an estimated 10-year ASCVD risk of greater or equal to 7.5%
24
Q

High-intensity Statin Therapy medications

A
  • Atorvastatin
  • Rosuvastatin

Daily dose lowers LDLs, on average, by greater or equal to 50%

25
Q

Side effects of Statins

A
  • Myalgia, myopathy, rhabdomyolysis
  • Liver enzyme elevation
  • Higher blood sugars
  • Memory loss (maybe)
26
Q

Primary Causes of Hyperlipidemia?

A
  1. High LDL
    - Familial hypercholesterolemia
    • Mutations of apoB100
    • Mutations of PCSK9
    • Mutations of LDL R adaptor protein
      • Sitosterolemia
      • Cerebrotendinous xanthomas
  2. High TG
    - Familial Chylomicronemia
    - Familial Hypertriglyceridemia
    - Familial combined hyperlipidemia
  3. Low HDL
    - Familial HDL deficiency
    - LCAT deficiency
    - Tangier Disease

Clinical Medicine Endocrine (2 decks)

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