Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

1.1 POM Cells > Cholesterol > Flashcards

Cholesterol Flashcards

1
Q

Which 3 sources are fats derived from?

A
  1. Diet
  2. De novo synthesis
  3. Adipose tisse deposits (storage)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Which enzymes break down dietary fats?

A

Lipases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Where are bile salts made and stored?

A
  1. Liver
  2. Gall bladder
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How do bile salts reach fats?

A

Bile duct to intestine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the function of bile salts?

A

Emulsify fats

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is an essential property of bile salts?

A

Amphipathic
- Hydrophobic 27C skeleton
- Hydrophilic hydroxyl groups

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What does a lack of bile salts result in?

A

Steatorrhea (fatty stool)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What drug can be used to treat obesity and how?

A

Olistat
- Inhibitor of gastric and pancreatic lipases
- Dec fat absorption 30% —> excreted out
- Clinical trials show treat for up to 2 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the side effects of orlistat?

A

Abdominal pain
Urgency to defecate
Inc flatus (farting)
Steatorrhoea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How is orlistat produced?

A

Chemically synthesised derivative of lipstatin (from Streptomyces toxytricini bacteria)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How are lipids transported and why?

A

Lipoproteins
- Lipids hydrophobic but lipoproteins amphipathic —> transportable in plasma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the 5 types of lipoproteins?

A
  1. Chylomicron
  2. Very low density (VLDL)
  3. Intermediate density (IDL)
  4. Low density (LDL)
  5. High density (HDL)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the source and role of chylomicrons?

A
  • Intestines
  • Dietary fat transport
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the source and role of VLDLs?

A
  • Liver
  • Endogenous fat transport (synthesised fat)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the source and role of IDLs?

A
  • VLDL
  • LDL precursor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the source and role of LDLs?

A
  • IDL
  • Cholesterol transport
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the source and role of HDLs?

A
  • Liver
  • Reverse cholesterol transport
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What 3 parts do chylomicrons consist of?

A
  • Triglycerides in core
  • Phospholipid monolayer membrane
  • Apoproteins embedded in membrane
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Which cells absorb digested dietary products and where?

A

Enterocytes lining brush border of small intestine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Which system transports CMs to the bloodstream and what are the 4 steps?

A

Lymphatic
1. Lacteals of intestine
2. Thoracic duct
3. Left subclavian vein
4. Bloodstream

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Where do CMs acquire apoproteins from?

A

HDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How does lipoprotein lipase bind to CMs?

A

Binds to complimentary apoproteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Where is lipoprotein lipase found?

A

Capillary endothelial cells lining tissues (adipose, heart, skeletal muscle)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What happens to the products of digested triglycerides?

A
  • Fatty acids —> B-oxidation
  • Glycerol —> gluconeogenesis in liver
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are the 5 stages of the cycle of a CM?

A
  1. Fat absorbed by enterocytes
  2. Chylomicrons synthesised in enterocytes
  3. Apoproteins added by HDL
  4. Lipoprotein lipase cleave chylomicron —> fatty acids to tissue and glycerol to liver
  5. Remnant chylomicron to liver (HDL adds apoproteins)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the function of cholesterol?

A

Regulate stiffness of cell membranes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Where is cholesterol found?

A

Cell membranes (90%)

28
Q

What type of chemical is cholesterol?

A

Steroid

29
Q

Why is cholesterol amphipathic?

A
  • Hydrophobic C skeleton tail
  • Hydrophilic hydroxyl group head
30
Q

Why is most cholesterol in the body produced via de novo synthesis?

A

Limited intake via diet (0.5g/day)

31
Q

What are the 3 stages of cholesterol synthesis?

A
  1. Synthesis of isopentenyl pyrophosphate (C5)
  2. Condensation of 6 to form squalene (C30)
  3. Cyclisation and demethylation
32
Q

Where does each of the 3 stages of cholesterol synthesis occur?

A
  1. Cytoplasm
  2. Cytoplasm
  3. ER
33
Q

What is the first reaction in the synthesis of isopentenyl pyrophosphate? (acetyl CoA start)

A

2 Acetyl CoA + H2O —> Acetoacetyl CoA + CoA
- B-ketothiolase

34
Q

What are the 2nd and 3rd steps of isopentenyl pyrophosphate? (acetoacetyl CoA start)

A
  1. Acetoacetyl CoA + Acetyl CoA + H2O —> HMG-CoA + CoA
    - HMG-CoA synthase
  2. HMG-CoA —> Mevalonate + CoA
    - HMG-CoA reductase
    - uses 2 NADPH + 2H+ —> 2NAD+
    -RDS
35
Q

How is isopentenyl pyrophosphate synthesis regulated?

A

HMG-CoA reductase inhibited by mevalonate, cholesterol and bile salts (negative feedback)

36
Q

What are the 4th, 5th, 6th and 7th steps of isopentenyl pyrophosphate synthesis? (mevalonate start)

A
  1. Mevalonate —> 5-Phosphomevalonate
    - Mevalonate kinase (use ATP)
    - Phosphorylation
  2. —> 5-Pyrophosphomevalonate
    - Phosphomevalonate kinase (use ATP)
    - Phosphorylation
  3. —> phosphorylated intermediate
    - Kinase (use ATP)
    - Phosphorylation
  4. —> 3-Isopentenyl pyrophosphate
    - Phosphomevalonate decarboxylase
    - Decarboxylation
37
Q

What are the 2 products final isopentenyl pyrophosphate synthesis?

A
  1. Isopentenyl pyrophosphate
  2. Activated isoprene
38
Q

What are the 7 steps in stage 1 of cholesterol synthesis? (isopentenyl pyrophosphate synthesis)

A
  1. 2 Acetyl CoA —> Acetoacetyl CoA
  2. add Acetyl CoA —> HMG-CoA
  3. —> Mevalonate
  4. —> 5-Phosphomevalonate
  5. —> 5-Pyrophosphomevalonate
  6. —> phosphorylated intermediate
  7. —> 3-Isopentenyl pyrophosphate
39
Q

What 3 reactions occur in stage 2 of cholesterol synthesis? (IPP condensation)

A
  1. Isopentenyl PP —> Dimethylallyl PP (C5)
    - Isomerisation
  2. Dimethylallyl PP + Isopentenyl PP —> Geranyl PP (C10)
    - Condensation
  3. Geranyl PP + Isopentenyl PP —> Farnesyl PP (C15)
40
Q

What are the first 4 steps in stage 3 of cholesterol synthesis? (cyclisation and demethylation)

A
  1. 2 Farnesyl PP —> Squalene (C30) + 2Pi
    - Squalene synthetase
    - uses NADPH —> NAD+ + H+
  2. —> Squalene epoxide
    - Squalene monoxygenase
  3. —> Prosterol cation
  4. —> Lanosterol
41
Q

How is lanosterol finally converted to cholesterol?

A
  • More cyclisation
  • 3 Demethylations
  • add HCOOH + 2 CO2
42
Q

What are the 3 main derivatives of cholesterol?

A
  1. Steroid hormones
  2. Vitamin D
  3. Cholesterol esters
43
Q

What is the precursor of all steroid hormones?

A

Pregnenolone

44
Q

What are the 5 classes of steroid hormones?

A
  1. Gluticosteroids
  2. Mineralcorticosteroids
  3. Androgens
  4. Estrogens
  5. Progestagens
45
Q

How is pregnenolone produced?

A

Cholesterol —> Pregnenolone
- Desmolase

46
Q

What is vitamin D synthesised from?

A

Cholesterol

47
Q

What are the 4 steps of calcitriol synthesis?

A
  1. Cholesterol —> 7-Dehydrocholesterol
  2. —> Previtamin D3
    - UV light
  3. —> Vitamin D3 (cholecalciferol)
  4. —> Calcitriol
    - Hydroxylation
48
Q

What is the function of calcitriol?

A

Calcium regulation

49
Q

What does a vitD3 deficiency cause?

A

Rickets (bowed legs)

50
Q

What are the 2 primary bile salts?

A
  1. Glycocholate
  2. Taurocholate
51
Q

How and where are bile salts produced?

A

Liver
- Hydroxylation and carboxylation of cholesterol

52
Q

What are the 5 parts of a lipoprotein?

A
  1. Triglycerols in core
  2. Cholesterol esters in core
  3. Phospholipid monolayer membrane
  4. Apoproteins embedded in membrane
  5. Cholesterol embedded in membrane
53
Q

Where are cholesterol esters synthesised?

A

Plasma

54
Q

What reaction occurs to synthesise cholesterol esters?

A

Cholesterol + acyl chain of Lecithin
- LCAT enzyme (lecithin cholesterol acyl transferase)

just remember enzyme —> tells all about reaction

55
Q

What are the 6 steps in the life cycle of lipoproteins?

A
  1. VLDL synthesised in liver
  2. VLDL into circulation —> broken down —> triglycerides released
  3. Lipid-depleted remnant —> IDL + apoprotein to HDL
  4. IDL + CE from HDL —> LDL
  5. LDL uptake by macrophages or liver
  6. HDLs take lipids and cholesterol from tissue back to liver (reverse transport)
56
Q

What is the function of LDL?

A

Transport cholesterol to peripheral tissues

57
Q

What is the function of HDL?

A

Transport cholesterol back to liver for use/disposal

58
Q

Why is the HDL “good” and LDL “bad”?

A
  • HDL lowers total serum cholesterol
  • Elevated LDL levels can lead to atherosclerosis
59
Q

What is Familial Hypercholesterolaemia?

A
  • Genetically high cholesterol
  • Lack functional LDLRs (receptors) —> cholesterol remains in circulation
  • Inherited monogenic dominant disease
60
Q

What is the difference between inheriting 1 vs 2 FH genes?

A
  1. Cholesterol 2-3x higher —> atherosclerosis in middle age
  2. Cholesterol 5x higher —> severe atherosclerosis and coronary infarcts in adolescence
61
Q

What are the 6 steps of LDL endocytosis?

A
  1. LDL bind to receptor
  2. Endocytosis
  3. Uncoating of vesicle (clathrin)
  4. Vesicle fuse with endosome
  5. Endosome fuse with lysosome —> hydrolyse LDL
    —> cholesterol free
  6. Transporter LDL receptor buds of endosome and returned to membrane
62
Q

How many classes of FH mutations are there?

A

5

63
Q

What are the 5 different mutations that cause FH and how do they do this?

A
  1. Frameshift/deletion/promoter mutation —> no LDLR
  2. Coding region —> LDLR not transported
  3. N-terminus —> LDLR doesn’t bind to LDL
  4. Cytoplasmic domain —> LDL not in via endocytosis
  5. EGFP domain —> LDL not released from receptor + LDLR not back to cell membrane
64
Q

Which 2 drugs can treat hypercholesterolaemia?

A
  1. Resins
  2. HMG-CoA reductase inhibitors (statins)
65
Q

How do statins work to treat hypercholesterolaemia?

A

Competitive inhibitor of HMG-CoA reductase
- Similar shape to mevalonate —> binds to HMG-CoA reductase —> inhibits cholesterol synthesis
- Act in liver
- Lipitor

66
Q

How do resins work to treat hypercholesterolaemia?

A

Bind to bile-acid cholesterol complexes —> prevents reabsorption by intestine
- Act in intestine

1.1 POM Cells (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions