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a path 3 > CHEMPATH: Lipids Lecture > Flashcards

CHEMPATH: Lipids Lecture Flashcards

1
Q

Name some features of atherosclerosis lesions.

A
  • Fibrous cap
  • Foam cells - contents of macrophages exude if squeezed
  • Necrotic core with cholesterol crystals
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2
Q

What are the types of lipoproteins from biggest to smallest?

A
  • Chylomicrons
  • VLDLs - both rich in triglycerides
  • LDLs - main carriers of cholesterol
  • HDLs
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3
Q

How is cholesterol transported?

A
  • <5% in chylomicrons
  • 13% VLDL
  • 70% LDL - major transporter
  • 17% HDL
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4
Q

Summarise cholesterol absorption and metabolism.

A
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5
Q

How is cholesterol transported across the intestinal brush border?

A

Via NPC1L1- goes into lymphatics and then into liver

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6
Q

Which transporters transport cholesterol back into the intestinal lumen?

A

ABC-G5 and ABC-G8.

The balance between NPC1L1 and the above taransporters determined how much cholesterol gets absorbed.

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7
Q

Where are bile acids absorbed?

A

Terminal ileum and transported using BAT

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8
Q

What is the function of HMG CoA reductase in the liver?

A

It converts acetate into mevalonic acid(MVA) which is converted into cholesterol.

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9
Q

What is the relationship between cholesterol absorption of cholesterol and its synthesis in the liver?

A

Those who have high absorption will have low synthesis of it and vice versa

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10
Q

What is the fate of cholesterol after its synthesis in the liver or absorption?

A

It is broken down into bile acids (by 7-alpha hydroxylase)

OR esterified into cholesterol ester (by ACAT) and incorporated into VLDL particles with apoprotein B and triglcerides (using a transfer protein MTB)

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11
Q

What is the precursor of LDL? When does the change occur?

A

VLDL changes into LDL after its circulation in plasma for 3-4 days. LDL is then taken up into the liver by the LDL receptors.

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12
Q

What is the function of HDL? Which transporter is important in this effect?

A

Picks up excess cholesterol from the peripheries. ABC A1 is very important in the process of transfer of cholestrol from the peripheries into HDL.

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13
Q

What is the role of CETP (cholesterol ester transfer protein)?

A

Mediates the movement of:

  • cholestrol ester from HDL to VLDL
  • and movement of triglycerides from VLDL to HDL.
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14
Q

What is the role of SR-B1 receptor on the liver?

A

Transfer of cholesterol ester from HDL into the liver

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15
Q

What are the main compartments/organs involved in cholesterol metabolism?

A
  1. Liver
  2. Intestine
  3. Plasma
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16
Q

How are triglycerides transported in the fasting state?

A

<5% chylomicrons (short half life in plasma)

55% VLDLs (major transporter of TG)

29% LDLs

11% HDLs

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17
Q

Summarise TG transport and metabolism.

A
  1. Main source of TG is small intestine from fatty foods
  2. These are transported by chylomicrons into plasma
  3. Plasma into lipoprotein lipase in capillaries hydrolyses chylomicrons into free fatty acids (FFAs)
  4. FFAs are taken up into (1) the liver and (2) adipose tissue
  5. In the liver, the FFAs are remade into TGs and transported by VLDLs
  6. VLDLs are again hydrolysed by lipoprotein lipase into FFAs (ad IDL remnant) and LDLs
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18
Q

Name 4 types of primary hypercholesteroleaemia. What genes are involved?

A
  1. Familial hypercholesterolaemia (type II): Dominant mutation of the LDL receptor, apoB or PCSK9 genes. 50% expression in the heterozygous state. Rarely it is also inherited in autosomal recessive inheritance (LDLRAP1)
  2. Polygenic hypercholesterolaemia: multiple loci including NPC1L1, HMGCR, CYP7A1 polymorphisms with small effects
  3. Familial hyper-alpha-lipoproteinaemia: sometimes CETP deficiency, causes increases in HDL
  4. Phytosterolaemia: mutations of ABC G5 and G8 (found in small intestine). Plant sterols will move into plasma in this disorder and cause premature atherosclerosis as they may be more atherogenic.
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19
Q

What does this show?

A

LDL binds to “coated pit” on the liver which then invaginates and causes its uptake into the liver

20
Q

How does severity of familial hypercholesterolaemia vary?

A

Mutations causing changes to different parts of the LDL receptor have different effects on severity.

21
Q

How common is homozygous familial hypercholesterolaemia(FH)?

A

About 1 in a million

May present as corneal arcus in a child etc. or cholesterol levels of 30 mmol/L from birth onwards.

22
Q

How common is heterozygous FH?

A

1:500 many undiagnosed

Will have xanthelasma and corneal arcus around age 40 and tendon xanthoma (thick lump on the Achilles’ tendon)

23
Q

What is the function of PCSK9 and its role in primary hypercholesterolaemia?

A

PCSK9 =proprotein convertase subtilisin/kexin type 9

Chaperone protein , binds the LDL receptor and promotes its degradataion.

  • A gain of function mutation in this will cause increased LDLR degradation so LDL will not be bound and taken up at the normal rate.
  • Loss of function mutations are associated with low LDL levels.
24
Q

What are the causes of primary hypertriglyceridaemia?

A
  1. Familial type I - LPL (degrades chylomicrons) or apoC II (its activator) deficiency
  2. Familial type IV - increased synthesis of TG (not decreased clearance), unknown cause
  3. Familial type V - sometimes due to apoA V deficiency (a more sever version of type IV)
25
Q

This is plasma in a primary hyperlipidaemia. Which one?

A

The second tube is after the plasma has been refrigerated overnight and shows a white layer of chylomicrons which confirms type I hyperlipidaemia

26
Q

What skin manifestations can occur in type I hyperlipidaemia?

A

Eruptive xanthomas

27
Q

How would whole blood look after refrigeration overnight in type IV hyperlipidaemia?

A

Separation into layers but this is a VLDL layer (not chylomicron as with type I)

28
Q

Which type of hyperlipidaemia is this?

A

Type V hyperlipidaemia

29
Q

What is an easy way to manage the effects of type I hyperlipidaemia? What about type V?

A

Type I - r educe the amount of fat in the diet as type I is a clearance problem

In type V there is high VLDL which may mean overproduction which can be a result of high carbohydrate so you would reduce this.

30
Q

What are the types of primary mixed hyperlipidaemias?

A
  1. Familial combined hyperlipidaemia - some in the family have high cholesterol and some have high TG, unknown cause
  2. Familial hepatic lipase deficiency
  3. Familial dys-beta-lipoproteinasemia (type III) - uncommon, aberrant form of apoE 2/2.
31
Q

What are the results of these apoE polymorphisms?

A

ApoE 2/2 = diagnostic of type III dys-beta-lipoproteinaemia if detected in homozygous form

ApoE 3/3 = normal

ApoE 4/4 = 10-fold increased risk of Alzheimer’s disease if homozygous

32
Q

What is this sign which is diagnostic of a type of hyperlipidaemia?

A

Yellow palmar striae (should be red) - diagnostic of type III familial dys-beta-lipoproteinaemia.

They also get eruptive tendon xanthomas as shown below.

33
Q

List the major groups of causes of secondary hyperlipidaemia.

34
Q

What are the hormonal causes of secondary hyperlipidaemia?

A
  • Pregnancy - always increase lipoproteins so if they also have a type I deficiency then they can get pancreatitis during pregnancy which may be fatal
  • Exogenous sex hormones e.g. oestradiol increases TG
  • HYPOthyroidism
35
Q

Name 2 renal dysfunction causes of secondary hyperlipidaemia.

A
  1. Nephrotic syndrome switches on the synthesis of LDL and VLDL so can cause high cholesterol (check urine protein)
  2. Chronic renal failure - high TG may be found post renal transplant or in patients on dialysis
36
Q

Which 2 classes of drugs commonly cause secondary hyperlipidaemia?

A
  • Antihypertensives
  • Immunosuppressants
37
Q

Name the types of hypolipidaemia.

A
  1. A-beta-lipoproteinaemia - very rare, MTP deficiency (recessive), low LDL and low VLDL cholesterol
  2. Hypo-beta-lipoproteinaemia - apoB gene affected (dominant), truncated versions of the protein
  3. Tangier’s disease - HDL deficiency from ABC A1 mutations
  4. Hypo-alpha-lipoproteinaemia - due to apoA-I mutations (sometimes)
38
Q

What is the “ideal” ratio between total:HDL cholesterol?

39
Q

What happens to LDL once it crosses the endothelium?

A

Oxidises and is taken up by macrophages. The cholesterol within it gets esterified and you get foam cells etc.

40
Q

Describe the sequelae of plaque fissuring (briefly).

41
Q

Compare the effects of various lipid-regulating drugs?

A
  1. Statins - major (~50%) reduction in LDL, some increase in HDL and reduction in TG
  2. Gemfibrozil - fibrate, best at reducing TG
  3. Ezetimibe - cholesterol absorption blocker (MPC1L1 blocker), reduces LDL
  4. Colestyramine - anion exchange resin which binds bile acids so that they cannot be reabsorbed, so liver senses this and makes more bile acids which are made from cholesterol

Nicotinic acid - no longer used

42
Q

What is the effect of statins on total/coronary mortality and vascular events?

A
  • total/coronary mortality - 12% and 19% reduction
  • vascular events - 25% reduction for every 1mmol/L reduction
43
Q

Name 3 new LDL-lowering drugs

A
  • MTP inhibitor - lomitapide
  • Anti-PCSK9 mAb- REGN727 - 40-60% reduction in LDL in trials
  • Anti-sense apo-B oligonucleotide - not licensed due to SE
44
Q

What are the treatments for obesity?

A
  1. Hypocaloric diet and exercise
  2. Iatrogenic malabsorption - orlistat 120-360mg daily (pancreatic lipase inhibitor)
  3. Bariatric surgery if BMI >40kg/m2
45
Q

What are the forms of bariatric surgery for obesity?

A
  1. Gastric banding
  2. Roux-en-Y bypass
  3. Biliopancreatic diversion
46
Q

What are the risks and benfits of bariatric surgery?

47
Q

What is the effect of gastric bypass/biliopancreatic diversion/medical therapy?

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