Discussion of Cholesterol lipoproteins Flashcards

1
Q

What are the guidelines for needing to be treated with statins?

A

known heart disease or diabetes
LDL cholesterol >= 190mg/dL

if you’re talking statins, there’s no need to monitor LDL levels or take non-statin drugs

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2
Q

What are the guidelines for needing to be treated with statins?

A

known heart disease or diabetes
LDL cholesterol >= 190mg/dL

if you’re talking statins, there’s no need to monitor LDL levels or take non-statin drugs

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3
Q

What are some clinical manifestation of familial hypercholesterolemia?

A

corneal arcus, thickened achiles tendons, high total cholesterol, normal TAG and HDL, very high LDL

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4
Q

What is optimal LDL levels

A
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5
Q

What are the main causes of hypercholesterolemia?

A

LDL receptor defects, defects in ApoB, gain function mutation of PCSK9

inability to clear plasma LDL

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6
Q

What is the prevalence of heterozygous hyperchoelsteremia?

A

1: 500 (autosomal dominant)

- premature atherosclerosis

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7
Q

What is the prevalence of homozygous hyperchoelsteremia?

A

1:1000000

cardiac disease in childhood

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8
Q

What is the treatment of FH?

A

diet, exercise (not all that effect because its a genetic problem), reduce total fat and cholesterol intake, statin drugs, Ezetimibe (NPC1L1 inhibitor) in combo with statins,

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9
Q

What are some new therapies for homozygous FH patients?

A

lomitapide- MTP inhibitor
Mipomersen- apoB inhibiting
synthetic HDL injections

possible liver transplant- liver has the most LDL receptors but this is extreme

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10
Q

What would a mutation in the large subunit of MTP (abetalipoproteinemia) show as clinically?

A

very low total cholesterol, HDL, LDL, TAG, undetectable apoB, acanthocytes (pointy red cells), lipids in enterocytes after fasting, eye problems

heterozygotes are normal, homozygotes are not- thus, autosomal recessive

due to vitamin E deficiency

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11
Q

Treatment for Abetalipoproteinemia?

A

huge doses of vitamin E (absorbed with chylomicrons, so if you can’t make chylomicrons, you can’t make vitamin E) to reverse neurologic and optic problems and supplements of fatty acids.

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12
Q

What are the symptoms of Metabolic syndrome?

A

hypertensive, abdominal obesity, extremely high TAG, elevated total cholesterol, slightly elevated LDL, elevated ApoB (higher than LDL), and low HDL

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13
Q

Why is abdominal obesity worse than hip

A

most of the fat in the abdomen is visceral adipose tissue which is more metabolically active which makes cytokines that dump into the liver while hip fat is subcutaneous

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14
Q

What are some clinical manifestation of familial hypercholesterolemia?

A

corneal arcus, thickened achiles tendons, high total cholesterol, normal TAG and HDL, very high LDL

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15
Q

What is optimal LDL levels

A
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16
Q

What are the main causes of hypercholesterolemia?

A

LDL receptor defects, defects in ApoB, gain function mutation of PCSK9

inability to clear plasma LDL

17
Q

What is the prevalence of heterozygous hyperchoelsteremia?

A

1: 500 (autosomal dominant)

- premature atherosclerosis

18
Q

What is the prevalence of homozygous hyperchoelsteremia?

A

1:1000000

cardiac disease in childhood

19
Q

What is the treatment of FH?

A

diet, exercise (not all that effect because its a genetic problem), reduce total fat and cholesterol intake, statin drugs, Ezetimibe (NPC1L1 inhibitor) in combo with statins,

20
Q

What are some new therapies for homozygous FH patients?

A

lomitapide- MTP inhibitor
Mipomersen- apoB inhibiting
synthetic HDL injections

possible liver transplant- liver has the most LDL receptors but this is extreme

21
Q

What would a mutation in the large subunit of MTP (abetalipoproteinemia) show as clinically?

A

very low total cholesterol, HDL, LDL, TAG, undetectable apoB, acanthocytes (pointy red cells), lipids in enterocytes after fasting, eye problems

heterozygotes are normal, homozygotes are not- thus, autosomal recessive

due to vitamin E deficiency

22
Q

Treatment for Abetalipoproteinemia?

A

huge doses of vitamin E (absorbed with chylomicrons, so if you can’t make chylomicrons, you can’t make vitamin E) to reverse neurologic and optic problems and supplements of fatty acids.

23
Q

What are the symptoms of Metabolic syndrome?

A

hypertensive, abdominal obesity, extremely high TAG, elevated total cholesterol, slightly elevated LDL, elevated ApoB (higher than LDL), and low HDL, possibly high glycoxyslated hemoglobin, nigricans

24
Q

Why is abdominal obesity worse than hip fat deposition?

A

most of the fat in the abdomen is visceral adipose tissue which is more metabolically active which makes cytokines that dump into the liver while hip fat is subcutaneous

25
Q

What is metabolic syndrome?

A

associated with diabetes, hypertension, hyperinsulinemia, low HDL, inflammatory that can lead to plaque formation