Exam 1 Flashcards

1
Q

What enzyme initiates bile acid synthesis from cholesterol?

A

cholesterol 7α-hydroxylase

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2
Q

What 3 things decrease activity HMG-CoA reductase?

A
  1. Glucagon
  2. Epinephrine
  3. AMPK
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3
Q

What upregulates HMG-CoA reductase?

A

Low cellular sterol level - SREBP dissociates from SCAP moves to nucleus (TF)

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4
Q

What are 4 mechanisms for regulating cholesterol synthesis and transport?

A
  1. Covalent modification of HMG-CoA reductase
  2. Transcriptional regulation of HMG-CoA reductase
  3. Activation of ACAT - storage
  4. Transcriptional regulation of LDL-R
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5
Q

SR-B1 expression is _________ with regards to atherosclerosis.

A

Protective

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6
Q

PLTP

A
  1. Catalyzes transfer of phospholipids between lipoprotein classes
  2. Needed for maximal activity of LCAT (HDL)
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7
Q

What tissues express ABCG1 and what is its function?

A
  1. Spleen, thymus, lung, brain, liver, and macrophages

2. Promotes cholesterol efflux to HDL

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8
Q

Absence of ABCA1 (Tangier Disease) results in what?

A
  1. Near-absence of normal HDL particles - no discoidal or spherical HDL
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9
Q

ABCA1 helps release ____________ to apoA1 to make ________.

A
  1. Free cholesterol

2. Discoidal HDL

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10
Q

Lp(a)

A

LDL-like where apoB-100 is covalently bound to apolipoprotein(a) - variable due to Kringle IV repeats in LPA gene

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11
Q

Lp(a) is a _____________ for cardiovascular disease.

A

Risk factor

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12
Q

What is the most effective way to modulate plasma LDL-C levels?

A

Manipulation of hepatic LDL-R gene expression

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13
Q

Thyroxine and ________ enhance LDL-R gene expression.

A

Estrogen

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14
Q

VLDL remnants become IDL and LDL. C apolipoproteins and ______ redistribute to _____.

A
  1. ApoE

2. HDL

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15
Q

ACAT-1 is to ________ as ACAT-2 is to liver and intestine.

A

Macrophages, foam cells, adrenocortical cells and skin

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16
Q

Mutations in ABCG5/G8 cause what disease?

A

Sitosterolemia - absorb unusually large amounts of plant sterols - tendon and subcutaneous xanthomas

17
Q

Where does ezetimibe act?

A

Blocks NPC1L1 to prevent cholesterol absorption in the intestine.

18
Q

ASCVD

A

Heart attacks, strokes, and peripheral artery disease

19
Q

CAD

A

Coronary atherosclerosis disease

20
Q

Lipid disorders that cause ASCVD (4)

A
  1. Elevated TC or LDL
  2. Excess apoB lipoproteins - metabolic syndrome/Familial Hyperchol
  3. Depressed HDL
  4. Elevated Lp(a)
21
Q

Lowering LDL with ______ lowers risk.

A

Statins

22
Q

Reduced action of SLCO1B1 can lead to what?

A

Dec. hepatic uptake and Inc. statin concentration in the blood

23
Q

What is the only mechanism for cholesterol excretion?

A

Conversion to bile salts

24
Q

What converts fibrinogen to fibrin(glue)?

A

Thrombin

25
Q

What is primarily responsible for the degradation of fibrin clots?

A

Plasmin

26
Q

What is the lifespan of a platelet?

A

7-10 days

27
Q

What factor is the convergence point between the extrinsic and intrinsic pathway?

A

Factor Xa

28
Q

How are platelets activated?

A

Activate P2Y1/P2Y12 R stimulate COX and GPIIb/IIIa - fibrinogen cross-links
COX mediated –> TXA2/PGI2

Thrombin can activate platelets too

29
Q

What leads show the inferior wall?

A

II, III, aVF (RCA)

30
Q

What leads show the lateral wall?

A

I, aVL, V5, V6 (CIRC)

31
Q

What leads show the anterior wall

A

V2-V4 (LAD)