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M2 Cardiovascular > Lipoprotein & Lipid Disorders - Gleeson > Flashcards

Lipoprotein & Lipid Disorders - Gleeson Flashcards

1
Q

When testing lipids, what is included in the ‘classic’ lipid profile?

A
  • total cholesterol
  • triglycerides
  • HDL
  • LDL (calculated)
  • non-HDL (calculated)
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2
Q

How is LDL-C calculated?

Non-HDL?

A

Friedwald equation:

  • LDL-C = TC - (HDL-C + VLDL-C)
  • Non-HDL = TC - HDL
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3
Q

A triglyceride level >1000 mg/dL is a significant risk for what?

A

pancreatitis

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4
Q

What LDL-C and HDL levels are considered risks for ASCVD?

A
  • LDL-C > 100
  • HDL < 40
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5
Q

Total cholesterol

What is (mg/dL):

  1. optimal?
  2. normal?
  3. clearly abnormal?
A
  1. < 150
  2. <200
  3. >325
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6
Q

Triglycerides (TG)

What is (mg/dL):

  1. optimal?
  2. normal?
  3. clearly abnormal?
A
  1. < 75
  2. < 150
  3. > 150
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7
Q

HDL

What is (mg/dL):

  1. optimal?
  2. normal?
  3. clearly abnormal?
A
  1. M > 40; F > 50
  2. M > 40; F > 50
  3. < 35
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8
Q

LDL

What is (mg/dL):

  1. optimal?
  2. normal?
  3. clearly abnormal?
A
  1. < 70
  2. < 130
  3. > 260
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9
Q

Non-HDL

What is (mg/dL):

  1. optimal?
  2. normal?
  3. clearly abnormal?
A
  1. << 100
  2. < 160
  3. > 290
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10
Q

What type(s) of genetic lipid disorder(s) are usually dormant until lifestyle and/or other diseases ‘unmask’ them?

A

Types IIB, III, IV, and V

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11
Q

What type(s) of genetic lipid disorder(s) are predominantly genetic, with little-to-no influence from lifestyle or other diseases?

A

Types I and IIA

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12
Q

Type IIa genetic hyperlipidemia is also known as what?

What is the common presentation?

A

Familial hypercholesterolemia

CAD < age 60

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13
Q

Type IIb genetic hyperlipidemia is also known as what?

What is the common presentation?

A

Familial combined hyperlipidemia or with metabolic syndrome

CAD risk 2X normal despite borderline/normal lipid numbers

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14
Q

A child presenting with triglycerides >2000 mg/dL is likely to be diagnosed with what?

A

Severe hypertriglyceridemia (Type I genetic hyperlipidemia)

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15
Q

What is the main abnormal lipid seen in Type I genetic hyperlipidemia?

  1. What is the primary defect?
  2. What is the excess lipoprotein?
A

TG > 2000 mg/dL

  1. LPL or apoC2 or apoC3 defect
  2. chylomicrons
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16
Q

What is the main abnormal lipid seen in Type IIa genetic hyperlipidemia?

  1. What is the primary defect?
  2. What is the excess lipoprotein?
A

TC > 275, LDL-C > 190

  1. LDL-R
  2. LDL
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17
Q

What is the main abnormal lipid seen in Type III genetic hyperlipidemia?

  1. What is the primary defect?
  2. What is the excess lipoprotein?
A

TC and TG both 200-500

  1. apoE2 + overproduction
  2. VLDL, IDL
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18
Q

What is the main abnormal lipid seen in Type V genetic hyperlipidemia?

  1. What is the primary defect?
  2. What is the excess lipoprotein?
A

TG > 1000

  1. LPL or apoC3
  2. VLDL, chylomicrons
19
Q

What is the main abnormal lipid seen in Type IV genetic hyperlipidemia?

  1. What is the primary defect?
  2. What is the excess lipoprotein?
A

TG 500-1000

  1. LPL or apoC3
  2. VLDL
20
Q

What is the main abnormal lipid seen in Type IIb genetic hyperlipidemia?

  1. What is the primary defect?
  2. What is the excess lipoprotein?
A

LDL 100, TG 200-500, HDL < 40

  1. overproduction of apoB100
  2. LDL, VLDL
21
Q

What disease features defective LPL, apoC2, or apoC3 on chylomicrons, resulting in failure to remove TG from chylomicrons

A

Type I Chylomicronemia

22
Q

Describe the defect in Type II familial hypercholesterolemia

A

LDL-R is defective, so LDL accumulates

23
Q

Describe the lipoprotein changes of visceral adiposity and insulin resistance

A
  • insulin resistance increases central adiposity
  • central adiposity exports FFA and TG to the liver
  • The liver releases more VLDL
  • VLDL drives increased CETP activity
  • increased CETP activity drives further LPL/HL activity
24
Q

Describe the defect in type III dysbetalipoproteinemia

A

apoE2/E2 defect and environmental factors

apoE2/E2 on IDL is poorly recognized by LDL-R

25
Q

Describe the defect in type IV hypertriglyceridemia

A

apoC2 or apoC3 on VLDL is defective, so VLDL accumulates

26
Q

Describe the defect in Type V familial hypertriglyceridemia

A

apoC2 or apoC3 on both VLDL and chylomicrons do not work. Both VLDL and chylomicrons accumulate.

27
Q

Name 3 lipid particle types that are predominantly filled with triglycerides (TG):

A
  • Chylomicrons
  • VLDL
  • IDL
28
Q

Name some medical conditions that increase triglycerides

What else might increase triglycerides?

A
  • metabolic syndrome, insulin resistance
  • diabetes
  • hypothyroidism
  • anorexia
  • HIV
  • pregnancy
  • alcohol
  • fructose >50g/day

certain medications will also increase triglycerides (examples: estrogens, birth control, thiazide diuretics, steroids, protease inhbitors, etc)

29
Q

Describe the following triglyceride disorders:

  1. Type I hyper-chylomicronemia
  2. Type IIB familial combined hyperlipidemia
  3. Type IV
  4. Type I
A
  • Type I hyperchylomicronemia
    • children, TG > 2000
    • inherited loss of LPL or defective apoC3 or apoC3
    • chylomicrons fill with TG in the gut (at enterocytes) but cannot offload TG to peripheral cells
  • Type IIB familial combined hypertriglyceridemia
    • TG 200 to 500
    • over-production of VLDL. Inherited, but also seen with insulin resistance, metabolic syndrome, inflammation, and visceral adiposity
  • Type IV
    • TG 500 to 1000
    • dysfunctional LPL, resulting in large VLDL particles
    • combination of genetics and environment
  • Type I
    • TG > 1000
    • results in excessive TG and chylomicrons
30
Q

LDL contains approximately what percentage of circulating cholesterol?

A

90%

31
Q

What two lipid particle types are especially atherogenic?

A

IDL (a.k.a. VLDL remnants) and VLDL

32
Q

Describe some lipid disorders that increase risk of ASCVD

A
  • Elevated total cholesterol or LDL levels
  • Excess apoB lipoproteins
  • Depressed HDL levels
  • Elevated Lp(a)
33
Q

What medical conditions result in increased LDL-C?

What else might contribute to increased LDL-C?

A
  • hypothyroidism
  • renal disease
  • obstructive liver disease
  • anorexia
  • polycystic kidney disease
  • pregnancy

some medications also increase LDL-C (examples: anabolic steroids, cyclosporines

progestins, thiazide diuretics)

34
Q

Name some factors/behavior that increase HDL

Lower HDL

A
  • Raise HDL
    • aerobic exercise
    • alcohol
    • estrogens
  • Lower HDL
    • insulin resistance and metabolic syndrome
    • anabolic steroids
    • progestins
    • trans-fats
    • smoking
35
Q

Why is elevated Lp(a) a risk factor for ASCVD?

A
  • Lp(a) is homolgous between LDL and plasminogen
  • Lp(a) may compete with plasminogen, reducing the fibrinolytic capacity of the blood, increasing the chance of atheroscerotic plaque and thrombus formation
36
Q

If a patient’s 10-year risk of ASCVD is >7.5%, what treatment should be started?

A

statins

37
Q

Familial hypercholesterolemia (type IIa) is particularly prevalent in what 3 populations? Why?

A

Due to the founder effect:

French Canadians

South Afrikaners

Ashkenazi Jews

38
Q

LDL 2-5 times normal since bith is indicative of what?

How is this treated?

A

Familial hypercholesterolemia

Start statin therapy immediately if age >12

39
Q

What is the most common mutation seen in Familial Hypercholesterolemia?

What other mutations might be commonly seen?

A

90%: LDL-R mutation (decreased number or function, over 1600 mutations)

also: apoB mutation or PCSK9 gain-of-function mutation

40
Q

What is result of a PCSK9 gain-of-function mutation?

PCSK9 loss-of-function mutation?

A

Familal hypercholesterolemia, leading to increased catabolism of LDL-R, resulting in fewer available LDL-R to remove LDL from circulation. LDL levels rise.

Loss-of-function decreases LDL-R catabolism, leading to increased LDL-R, lowering circulating LDL (significant drug target!)

41
Q

Describe the underlying conditions seen with type IIb dyslipidemia

A
  • metabolic syndrome
  • insulin resistance (environmental or genetic)
  • visceral adiposity
  • western lifestyle
  • diabetes
42
Q

What is atherogenic dyslipidemia? What causes it?

A

TG:HDL > 4; LDL-P >> LDL-C

Increased LDL-P, increased VLDL remnants (IDL) -> both very atherogenic

metabolic syndrome

43
Q

Name the criteria for metabolic syndrome

A

Require 3:

  • Waist M >=40; F >=35
  • TG > 150
  • HDL M<40; F<50
  • BP > 135/85 or Rx
  • FBG >=100

M2 Cardiovascular (40 decks)

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