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.

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)?

25
What is primarily responsible for the degradation of fibrin clots?
Plasmin
26
What is the lifespan of a platelet?
7-10 days
27
What factor is the convergence point between the extrinsic and intrinsic pathway?
Factor Xa
28
How are platelets activated?
Activate P2Y1/P2Y12 R stimulate COX and GPIIb/IIIa - fibrinogen cross-links COX mediated --> TXA2/PGI2 Thrombin can activate platelets too
29
What leads show the inferior wall?
II, III, aVF (RCA)
30
What leads show the lateral wall?
I, aVL, V5, V6 (CIRC)
31
What leads show the anterior wall
V2-V4 (LAD)