Lipids, lipoproteins and hyperlipidemias Flashcards

1
Q

What are the 3 functions of lipids?

A
  1. Precursors for steroid hormones
  2. Energy source
  3. Structural component in cell membrane
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the different types of lipids?

A
Cholesterol
Fatty acids
Mono, di and triglycerides
Phospholipids
Steroids, prostaglandins and sphingolipids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Describe the structure of a triglyceride.

A

Glycerol backbone and 3 fatty acids

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

What is the major fuel source for lipolysis?

A

Triglycerides

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

What are the 2 functions of phospholipids?

A

Part of the membrane bilayer

Fuel source

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

Describe the structure of a phospholipid.

A

Glycerol backbone with 2 FA tails and a polar (hydrophilic) head group

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

What are the 4 functions of cholesterol that make it important for human life?

A
  1. Cell membrane permeability and fluidity
  2. Precursor for steroid hormone synthesis
  3. Vitamin D synthesis
  4. Manufacture bile salts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How do we get cholesterol in the body?

A

Absorbed through the diet (animal fats) or synthesized in the body

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

How is cholesterol broken down in the body?

A

Humans cannot breakdown cholesterol - can only be excreted in faeces

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

Where does cholesterol synthesis occur?

A

90% of cholesterol synthesis occurs in the liver and intestine

Also occurs in the brain, skin, adrenals, gonads

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

What is the rate limiting enzyme in cholesterol synthesis?

A

HMG-CoA reductase (converts HMG-CoA to mevalonate)

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

What controls cholesterol synthesis?

A

Cholesterol levels - increased cholesterol inhibits synthesis
Insulin - increases cholesterol synthesis
Glucagon - decreases cholesterol synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How are lipids packaged?

A

In structures called lipoproteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the general structure of a lipoprotein?

A

Lipid core - primarily triglycerides and cholesterol esters with small amounts of sphingolipids and fat soluble vitamins

External layer - hydrophilic layer made of phospholipids, unesterified free cholesterol, and apolipoproteins/apoproteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the 4 main types of lipoproteins?

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

What is the function of chylomicrons?

A

Main carrier of dietary triglycerides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the function of VLDL?

A

Main carrier of endogenously produced triglycerides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the function of LDL?

A

Main carrier of cholesterol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the function of HDL?

A

Protective function - carries cholesterol from extrahepatic tissues to liver for excretion

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

Where is VLDL synthesized?

A

In the liver

21
Q

How is LDL synthesized?

A

Generated from VLDL

22
Q

Why should you not see chylomicrons in fasting plasma?

A

Because they are only synthesized by the gut after a meal

23
Q

Structurally what is Lp(a)?

A

Structurally related to LDL but has a carbohydrate rich protein apo(a)

24
Q

What is the function of Lp(a)?

A

Functional role not established but it is known to compete with plasminogen for binding sites = may play a role in thrombogenesis (clotting)

Plays a role in atherogenesis - increase levels are associated with increased risk for CHD

25
Q

What are the 4 roles/functions of apoproteins/apolipoproteins?

A
  1. Facilitate lipid solubilisation
  2. Help maintain structural integrity of lipoproteins
  3. Serve as a ligand for lipoprotein receptors
  4. Regulate activity of lipoprotein metabolic enzymes
26
Q

What are the 4 major lipid transport pathways?

A
  1. Exogenous pathway (chylomicrons)
  2. Endogenous pathway (VLDL)
  3. Intracellular-cholesterol pathway (LDL)
  4. Reverse-cholesterol transport pathway (HDL)
27
Q

What are the 3 types of hyperlipidemias?

A
  1. Hypercholesterolemia
  2. Hypertriglyceridemia
  3. Combined hyperlipidemia
28
Q

What are the causes of hyperlipidemias?

A

Primary cause - genetic defect
Secondary causes - endocrine/metabolic, kidney/liver damage, drugs

Often they are a combination of genetic and environmental factors

29
Q

What causes familial hypercholesterolemia?

A

Defect in LDL receptor - mutations can occur in various parts of the receptor synthesis, transport, binding, clustering and recycling

30
Q

What does familial hypercholesterolemia cause?

A

Xanthomas - deposition of cholesterol rich material (lumps of cholesterol in the skin)

31
Q

What causes familial hypertriglyceridemia and what does it lead to?

A

LPL deficiency - causes high serum triglyceride levels due to accumulation of chylomicrons and VLDLs

32
Q

What are the symptoms of familial hypertriglyceridemia?

A

Manifests in early childhood with repeated episodes of abdominal pain, xanthomas, acute pancreatitis

33
Q

What causes familial combined hyperlipidemia?

A

Elevated TG or cholesterol or both

Causes increased production of ApoB which leads to increased VLDL and LDLs

34
Q

What are some possible causes of secondary hyperlipidemias?

A

Diabetes/obesity - cause LPL deficiency, overproduction of VLDL by the liver, incomplete VLDL metabolism

Hypothyroidism

Nephrotic syndrome (kidney disease)

Drugs

Other eg alcohol, high CHO diet, pregnancy

35
Q

What is polygenic hypercholesterolemia?

A

Most common cause of elevated serum cholesterol - caused by western life style of a high fat diet on a susceptible genotype - causes downregulation of LDLR

36
Q

What is arteriosclerosis?

A

Any disease which leads to thickening and hardening of the artery wall (becomes narrowed or even blocked completely)

37
Q

What is atherosclerosis?

A

Specific type of arteriosclerosis - involves the formation of plaques (fatty tissue accumulation) in the inner (intimal) layer of large and medium sized elastic arteries

38
Q

What is the lipid panel?

A

Total cholesterol
Triglycerides
LDL cholesterol
HDL cholesterol

Results interpreted with medical history to establish risk for developing CHD

39
Q

How do you measure TG and cholesterol?

A

Coupled enzyme assays which involved linked reactions to form a coloured product

40
Q

How do you measure lipoproteins?

A

Measured by ultracentrifugation to seperate lipoproteins based on their physical properties - density, size, charge

41
Q

How do you measure chylomicrons?

A

Standing plasma test - plasma placed in fridge (4c) overnight, chylomicrons accumulate as floating ‘cream’ layer

In fasting plasma chylomicrons are abnormal

42
Q

What are the major risk factors for cardiovascular disease?

A
Hyperlipidemias
Obesity
Smoking
Nutrition
Exercise
Genetics
Hypertension
43
Q

What are the therapeutic interventions to reduce plasma/serum lipids?

A

Dietary changes/exercise - to increse HDL and lower LDL = omega 3 and 6 FA eg fish oils

Drugs eg statins - inhibit HMG-CoA reductase to lower LDL cholesterol

44
Q

Explain the exogenous lipid transport pathway.

A

Check with writing.

45
Q

Explain the endogenous lipid transport pathway.

A

Check with writing.

46
Q

Explain the intracellular-cholesterol transport pathway.

A

Check with writing.

47
Q

Explain the reverse cholesterol transport pathway.

A

Check with writing.

48
Q

Explain the pathophysiology of atherosclerosis.

A

Check with writing.