Cholessterol 1.7 Flashcards

1
Q

Where is the majority of cell atp made and why

A

Mitochondria

Because Acetyl coA is produced from both sugars and fats (major food molecules) here and so most cellular oxidation occurs there

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2
Q

Where are the primary sources of fats

A

Diet

Lipogenesis (de novo biosynthesis in the liver)

Storage deposits in adipose

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3
Q

What breaks down dietary fats

A

Lipases

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4
Q

What solubilise dietary fatty acids

A

Bile salts

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5
Q

Generation and storage of bile salts

A

Generated in the liver

Stored in gallbladder

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6
Q

Steatorrhea

A

Fatty stool

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7
Q

Fat soluble vitamins

A

ADEK

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8
Q

Where does bile emulsify fats

A

Intestine

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9
Q

Lack of bile salts causes

A

Steatorrhea where fat passes through the gut undirected and unabsorbed

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10
Q

Orlistat

A

Reduces fat absorption - treat obesity

Side effects: abdominal pain, Steatorrhea, increased flatus (gas)

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11
Q

Types of lipoprotein

A

Chylomicrons

VLDL

IDL

LDL

HDL

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12
Q

How are lipids transported

A

Lipoprotein

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13
Q

Source of chylomicrons

A

Intestines

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14
Q

Role of chylomicrons

A

Dietary fat transport

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15
Q

Source of VLDL

A

Liver

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16
Q

Role of VLDL

A

Endogenous fat transport

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17
Q

Source of IDL

A

VLDL

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18
Q

Role of IDL

A

LDL precursor

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19
Q

Source of LDL

A

IDL

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20
Q

Role of LDL

A

Cholesterol transport

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21
Q

Source of HDL

A

Liver

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22
Q

Role of HDL

A

Reverse cholesterol transport

23
Q

Enterocytes

A

Intestinal absorptive (simple columnar) lining intestines

24
Q

anatomy of chylomicron

A

Triglycerides
Apoporotein (from HDL when in bloodstream)
Phospholipid

25
Q

Where do cm travel

A

From lacteals of intestine to thoracic duct and left subclavian vein where they enter blooodstream

26
Q

Here is lipoprotein lipase found

A

Capillary endothelial cells lining tissues (adipose. Skeletal and heart)

27
Q

Life cycle of cm

A

From intestinal villus,

Gain apoproteins,

B oxidation to glycerol and FFA

Transfer apoproteins back

Liver uptakes remnants

Restart

28
Q

What type of molecule is cholesterol

A

Steroid

29
Q

Role of cholesterol

A

Modulates membrane stiffness depending on temp and nature of membrane

30
Q

Cholesterol synthesis pathway

A
  1. Isopentenyl pyrophosphate synthesis (cytoplasm)
  2. Condensation of 6 of these molecules to form squalene (cytoplasm)
  3. Cyclisation and demethylation of squalene by monooxygenases to give cholesterol (er)
31
Q

Synthesis of isopentenyl pyrophosphate

A
  1. Condensation of 2 Acetyl coA molecules to form acetoacetyl coA
  2. Condensation of another Acetyl coA to form HMG+-coa
  3. HMG -coA reduced to mevalonate
  4. Mevalonate phosphorylated at hydroxylase groups (3 and 5) to form 3-isopentenyl pyrophosphate
32
Q

Condensation of 2 Acetyl coA molecules

A

Acetoacyl coA

-coA

B-ketothiolase enzyme

33
Q

Second step of isopentenyl pyrophosphate synthesis

A

Condensation of another Acetyl coA to form HMG coA (from acetoacetyl coA)

-coA

HMG-coA synthase

34
Q

3rd step of isopentenyl pyrophosphate synthesis

A

Reduction of HMG coA to mevalonate

Hmgcoa reductase

Negative feedback from mevalonate, cholesterol and bile salts

35
Q

Isopentenyl pyrophosphate to squalene

A

Isomerisation to dimethylallyl pyrophosphate

Condensed with another ipp to geranyl pp

Third ipp added to Farnesyl pp

2 molecules condense to squalene and 2 pp molecules (squalene synthase)

36
Q

What is cholesterol the precursor of

A

Steroid hormones

Generates pregnenolone by desmolase

37
Q

Vitamin d3 deficiency in children

A

Rickets

38
Q

Vitamin d from cholesterol

A

7-dehydrocholesterol + exposure to uv light from the sun

Provitamin d3

D3 (cholecalciferol)

Hydroxylatio. To calcitriol

39
Q

Bile salts synthesised from

A

Cholesterol

40
Q

Cholesterol converted into the primary bile salts…

A

Glycholate and taurocholate

41
Q

How are lipoproteins categorised

A

Density

42
Q

Anatomy of a lipoprotein

A

Phospholipid mono layer
Cholesterol
Apoproteins

Cholesterol esters and triacylglycerol core

43
Q

Cholesterol ester formation

A

Cholesterol and acyl chain of lecithin (phosphatidykcholine)

Catalysed by LCAT

44
Q

IDL formation

A

Triacylglycerol removal of vldl

45
Q

LDL formation

A

CE transfer from HDL to IDL

46
Q

VLDL formation

A

Synthesised in liver

47
Q

Why are ldl refered to as bad cholesterol

A

Prolonged elevation leads to atherosclerosis
They transport cholesterol to peripheral tissues which are cholesterol rich

48
Q

FH

A

Family hypercholesterolaemia

Mono genie dominant trait

49
Q

Familial hypercholesterolaemia

A

One copy of gene higher than normal levels, susceptible to atherosclerosis middle age

Both copies are severely affected, severe atherosclerosis and coronary infarct in adolescence

50
Q

Controlling hypercholesterolaemia

A

Resins for the intestine

Statins in liver (HMG coA reductase inhibitors)

51
Q

Statins

A

HMG coA reductase inhibitor,

Resembles mevalonate which has a negative feedback

52
Q

Resins in controlling hypercholesterolaemia

A

Cholestyramine

Prevent reabsorption by intestine

Raising HDL and lowering ldl

53
Q

FH results from

A

Malfunctioning ldl receptors