Cholesterol Flashcards

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1
Q

What are the three primary sources of fats?

A
  1. The diet
  2. De novo biosynthesis (liver)
  3. Storage depots in adipose
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2
Q

What breaks down dietary fats?

A

Lipases

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3
Q

What are needed to solubilize dietary fats?

A

Bile acids

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4
Q

What does a lack of bile acids result in?

A

Steatorrhea (Fatty stool) - this is because majority of fat passes throuhg the gut undigested and unabsorbed

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5
Q

What produced bile salts?

A

Liver

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6
Q

What do bile salts do in digestion?

A

They emulsify fats in the intestine and aid the digestion of fat soluble vitamins (A, D, E and K)

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7
Q

What is Orlistat?

A

A potent inhibitor of gastric and pancreatic lipases

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8
Q

What is the main side effect of Orlisats?

A

Steatorrhea

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9
Q

what do lipoproteins do?

A

Transport lipids in the plasma

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10
Q

Where are chylomicrons produced and what is their role?

A

Intestine - dietary fat transport

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11
Q

Where are digested dietary products absorbed?

A

By the enterocytes that line the brush border of the small intestine

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12
Q

Where do chylomicrons acquire apoproteins from?

A

From HDL following release into the blood stream

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13
Q

How do chylomicrons enter into the blood stream?

A

Travel from the lacteals of the intestine into the thoracic duct and into the left subclavian vein from which they enter into the blood stream

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14
Q

What is the primary role of cholesterol in the body?

A

Maintenance of cell membrane integrity - can increase or decrease the stiffness depending on the temperature and nature of the membrane

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15
Q

How are all the physiological requirements for cholesterol met?

A

They are supplied by the liver thorugh the de novo synthesis of cholesterol from Acetyl CoA

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16
Q

What is the first step in cholesterol biuosynthesis?

A

Acetyl CoA + Acetyl CoA = Acetoacetyl CoA

Condensation of 2 Acetyl-CoA molecules to form Acetoacetyl CoA.

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17
Q

What is the second step of cholesterol biosynthesis?

A

Condensation of another Acetyl-CoA molecule to form HMG-CoA - using HMG-CoA Synthetase

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18
Q

What is the third step in cholesterol biosynthesis?

A

HMG-Co-A is reduced to generate mevalonate.

19
Q

What enzyme is used to convert HMG-CoA into Mevalonate?

A

HMG-CoA Reductase

20
Q

Describe how HMG CoA is under negative feedback?

A

HMG-CoA reductase is under negative feedback control by the end product cholesterol, as well as intermediates bile salts and mevalonate

21
Q

What is the fourth step in cholesterol biosynthesis?

A

Mevalonate undergoes sequential phosphorylation at the hydroxyl groups at position 3 and 5, followed by decarboxylation to form 3-Isopentenyl pyrophosphate.

22
Q

Why is ubiquinone confined to the inner membrane of the mitochondria?

A

because it has lipophilic properties of the isoprene unit

23
Q

What is cholesterol the precursor of?

A

Pregnenolone

24
Q

Describe the synthesis of Vitamin D from cholesterol?

A

7-Dehydrocholesterol in the skin under UV is converted into Pre Vitamin D. This is then converted into Cholecalciferol.

The cholecalciferol then undergoes hydroxylation using 25-Hydroxylase to form 25-OH Cholecalciferol.

Then, 1-alpha hydroxylase from the kidney produced 1,25(OH)2 Cholecalciferol = CALCITRIOL

25
Q

What are the names of the bile salts which are synthesized from cholesterol?

A

Cholesterol is converted by a series of reactions into the primary bile salt glycocholate and also taurocholate.

26
Q

What is HDL?

A

Cholesterol which functions to take cholesterol away from the peripheral tissue back to the liver for use or disposal - helps to lower total serum choleterol

27
Q

What does prolonged levels of LDL lead to?

A

atherosclerosis

28
Q

What do LDLs do

A

They transport chlesterol which has been made in the liver to the peripheral tissues - more than 40% weight is cholesterol esters

29
Q

What is reverse cholesterol transport?

A

When cholesterol is transported back to the liver by the actions of HDL

30
Q

Describe the pathophysiology of hypercholesterolaemia?

A

patients with severe FH lacked functional LDLRs. .

31
Q

How is hypercholesterolaemia treated?

A

Using Resins and HMG-CoA Reductase Inhibitors

32
Q

What is an example of a HMG-CoA-Reductase inhibitors?

A

Statin

33
Q

How do resins work as a medication to contain hypercholesterolaemia?

A

Resins bind or sequester bile acid-cholesterol complexes preventing their reabsorption by the intestine.

34
Q

What do fats need in order to be made soluble?

A

They need to be emulsified by bile

35
Q

What does the emulsification of large fat droplets result in?

A

The formation of micelles

36
Q

How do emulsified fat droplets form micelles?

A

Pancreatic lipase breaks down the triglycerides which have been emulsified into Free Fatty Acid and Monoglycerides

37
Q

Once pancreatic lipases have digested the emulsified fats, what happens next?

A

The free fatty acids and monoglycerides leave the micelle and enter into the enterocytes of the small intestine

38
Q

What happens to FFAs and MGs in the enterocytes of the mall intestine?

A

They reform Triglycerides

39
Q

what forms inside the golgi of the enterocytes?

A

The fatty triglyceride globules combine with proteins to form chylomicrons

40
Q

Once the chylomicrons are extruded from the enterocyte what happens to them?

A

They enter into a lacteal and lymph in the lacteal transports chylomicrons away from the intestine

41
Q

After the chylomicron has left the enterocyte of the small intestine, what happens to it on the way to the liver?

A

The chylomicron starts making its way to the liver and picks up Apoproteins from HDL

42
Q

What is the benefit of apoproteins binding to the chylomicron after it has left the enterocyte?

A

The chylomicron can bind to lipoprotein lipase which can metabolise the triglyceride component into free fatty acids and the glycerol

43
Q

What are the free fatty acids and glycerol used for?

A

Adipocytes - storage

Skeletal Muscle - Generate energy

44
Q

What happens to the chylomicron remanants?

A

They are sent back to the liver