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Cardiology > Cholesterol and Lipoprotein Metabolism > Flashcards

Cholesterol and Lipoprotein Metabolism Flashcards

1
Q

Where is ApoB found?

A

VLDL, IDL (chylomicron remnants), LDL

-All considered atherogenic

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2
Q

Where is ApoA-1 and 2 found?

A

HDL

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3
Q

What is ApoE and where is it found?

A

Expressed on chylomicron remnant, IDL, HDL. Binds to LDLR for uptake into liver

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4
Q

What is ApoC-II and where is it found?

A

Found on chylomicrons and VLDL. Required cofactor for LPL (needed to activate it)

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5
Q

What is LPL?

A

Hydrolyzes TGs and frees fatty acids to be taken up by the tissue as fuel. FAs in chylomicron are depleted and eventually you get a chylomicron remnant. In other words, LPL is req for the breakdown of chylomicrons

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6
Q

ApoB-48

A

On chylomicrons

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7
Q

Chylomicron vs VLDL

A

Chylomicron is from the gut (i.e. food source) VLDL is from the liver (i.e. fatty acids in body were broken down, went to liver, packaged in VLDL and transported into systemic circulation). VLDL then drops off FAs at key tissues. Eventually they become IDL (remnants)

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8
Q

IDL

A

VLDL remnants that either allow their ApoE to bind to LDLR and can be taken up to liver for breakdown or that lose their ApoE via conversion to LDLs by hepatic lipase.

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9
Q

LDL

A

LDL is IDL without TG or ApoE. It does, however, still have ApoB-100, allowing it to interact with the LDLR receptor. However, since they don’t have ApoE also, they are less likely to interact than IDL or other particles

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10
Q

Where is ApoB-100 expressed?

A

VLDL, IDL, LDL

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11
Q

What lipoprotein is affected in familial chylomicronemia syndrome (FCS)?

A

Chylomicron

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12
Q

What is the etiology of FCS?

A

Mutation in LPL doesn’t allow it to hydrolyze TGs (i.e. break down chylomicrons in the blood) OR mutations in ApoC-2 doesn’t allow LPL to activate

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13
Q

What is your TG level in FCS?

A

Very elevated

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14
Q

What are the physical exam findings in FCS?

A

Eruptive xanthomas (specific to hyperchylomicronemia)

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15
Q

Clinical consequences of FCS

A

Pancreatitis

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16
Q

What lipoprotein is affected with familial hypercholesterolemia (FH)?

A

LDL

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17
Q

What is the etiology of FH?

A

LDL receptor mutation so that LDL, IDL and CM cannot be taken up by liver
–common disorder

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18
Q

What is your TG level in FH?

A

Normal

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19
Q

Physical exam findings with FH?

A

Heterozygous: tendon xanthoma (specific), corneal arcus and xanthelasma (common but not specific)

Homozygous: Cutaneous xanthomas

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20
Q

Clinical consequences of FH

A
  • CHD

- Homozygotes have early onset heart disease

21
Q

What lipoprotein is affected with familial combined hyperlipidemia (FCHL)?

A

VLDL and LDL

22
Q

What is the etiology of FCHL?

A

Unknown but there is an overproduction of VLDL by the liver with unknown cause (i.e. no insulin resistance etc)

23
Q

What are the physical exam findings with FCHL?

A

None

24
Q

What is the clinical consequences of FCHL?

A

CHD

25
Q

What lipoprotein is affected with familial Dysbetalipoproteinemia (FD)

A

Remnants (IDL and chylomicron)

26
Q

Etiology of FD?

A

mutations in ApoE-II so remnants can’t bind LDLR

27
Q

TG level in FD?

A

Elevated

28
Q

Physical findings in FD?

A

Eruptive palmar tubero xanthomas

29
Q

Clinical consequences of FD?

A

CHD, peripheral arterial disease

30
Q

What lipoprotein is affected with familial hypertriglyceridemia (FHTG)

A

VLDL

31
Q

Etiology of FHTG?

A

Unknown

32
Q

TG level in FHTG?

A

Elevated

33
Q

Clinical consequence of FHTG?

A

None really, but if these people are obese or drink a lot etc, more likely to have problems

34
Q

What lipoprotein is affected with SEVERE FHTG?

A

Chylomicrons and VLDL

35
Q

TG level in severe FHTG?

A

Very elevated

36
Q

Etiology of severe FHTG

A

Unknown (progression?)

37
Q

Physical findings in severe FHTG

A

Eruptive

38
Q

Clinical significance of severe FHTC?

A

Pancreatitis (linked to large elevation in TGs)

39
Q

Apo(a)

A

Lipoprotein with an apo(a) that hangs off of Apo-B and is a major genetic risk factor for CHD and is homologous to plasminogen

40
Q

Epidemiologically, levels of HDL have what relationship to CHD?

A

Inverse

41
Q

Where is HDL made?

A

HDL comes from macrophages which have lots of free cholesterol. ABCA1 allows free cholesterol to add to nascent HDL.

42
Q

LCAT

A

Sits on nascent HDL and esterifies cholesterol allowing HDL to become mature and return to the liver

43
Q

ApoA-1 Mutations

A

Mutation in apoA1 gene (role in biogenesis and formation of HDL) causes nascent HDL to be nonfunctional and be catabolized rapidly

-leads to rapid removal of nascent HDL particle before mature assembly

44
Q

Clinical outcomes of apoA1 mutations

A

Low HDL, no increased risk for CVD

45
Q

Tangier Disease

A

ABCA1 mutation causing faulty transport of free cholesterol from macrophages into HDL. Have a buildup of cholesterol in macrophages and low HDL

46
Q

Clinical outcomes of tangier disease

A

Low HDL, no inc risk for CVD

47
Q

LCAT deficiency

A

Mutation in LCAT gene means that cholesterol cannot be deposited into the center of HDL causing a buildup of free cholesterol

48
Q

Physical findings of LCAT deficiency

A

Cholesterol gets deposited in cornea

49
Q

Clinical consequences of LCAT def

A

Low HDL but do not have higher risk for CVD

Cardiology (16 decks)

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