Uric acid + Lipids Flashcards

1
Q

Cholesterol is absorbed in the… via which receptor?

A

Jejunum via NPC-1L1 receptor

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2
Q

Bile acids are absorbed in the… via which receptor?

A

Terminal Ileum via BAT receptor

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3
Q

What happens to cholesterol synthesis when cholesterol is transported from the gut into the liver?

A

Cholesterol influx downregulates HMG-CoA-Reductase (main enzyme in liver for cholesterol synthesis)

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4
Q

How does HMG-CoA-Reductase make cholesterol

A

Acetate -> MVA (mevalonic acid) -> Cholesterol

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5
Q

How is bile acid made?

A

7a-hydroxylase converts cholesterol into bile acids

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6
Q

What happens to cholesterol in the liver?

A
  1. Cholesterol -> Cholesterol ester (via ACAT - acylCoA:cholesterol acylTransferase)
  2. Cholesterol ester + TG + apoB -> VLDL (via Microsomal Triglyceride Transfer Protein - MTP)
  3. VLDL -> LDL in plasma, which goes to cells
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7
Q

What is the role of HDL?

A

Picks up EXCESS cholesterol from periphery

ABCA1

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8
Q

How is most of the cholesterol stored in our body?

A

LDL 70%

HDL 17%

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9
Q

How is most of the triglycerides stored in our body?

A

VLDL

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10
Q

Where are TGs absorbed?

A

Small intestine

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11
Q

Which enzyme controls the movement of Cholesterol ester and TGs from HDLs to VLDLs

A

Cholesterol Ester Transfer Protein (CETP)

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12
Q

Which enzyme hydrolyses Chylomicrons into free fatty acids?

A

Lipoprotein Lipase (LPL)

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13
Q

Lomitapide

A

Inhibits MTP (Microsomal Triglyceride Transfer Protein)

40-50% reduction in LDL

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14
Q

Evolocumab

A

Monoclonal Ab against PCSK9

MOST POTENT LDL lowering therapy

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15
Q

Ezetemibe

A

Inhibits NPC-1L1

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16
Q

Statins

A

HMG-CoA-Reductase inhibitor

Most potent after Evolucumab
Atorvastatin is best

17
Q

Colestyramine

A

Inhibits Bile reabsorption

18
Q

Fibrates

A

Most potent reducers of TGs

19
Q

Familial Hypercholesterolaemia Type 2 is associated with mutations of what?

A

LDL receptor
ApoB
PCSK9