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Cardiology > lipid metabolism > Flashcards

lipid metabolism Flashcards

1
Q

What is the solubility of lipids like?

A

insoluble or sparingly soluble in water

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2
Q

What are the uses of lipids?

A
  • Lipids are important for synthesis and maintenance of biological membranes
  • Also good energy sources

-Also important as the precurser of a number of steroid hormone particles.
The commencement of all steroid hormone particles is cholesterol

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3
Q

How are lipids transported in the blood?

A

Via lipoproteins

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4
Q

What is cardiovascular disease strongly associated with?

A

elevated LDL, decreased HDL

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5
Q

What are the causes of elevated LDL and decreased HDL?

A

diet/lifestyle, gentic factors

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6
Q

What do lipoproteins consist of?

A

-hydrophobic core and hydrophilic coat

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7
Q

What is found in the hydrophobic core?

A

estrified cholesterol and trigylicerides

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8
Q

What is found in the hydrophobic core?

A

monolayer of amphipathic cholesterol, phospholipids and one, or more apoproteins

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9
Q

What are the major lipoproteins (in order of size)?

A
  • HDL particles
  • LDL particles
  • VLDL
  • chylomicrons
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10
Q

What are the two roles of lipoproteins?

A

-deliver cholesterol and triglyceride to peripheral tissue
OR
-return cholesterol and triglyceride to liver

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11
Q

What is meant by the exogenous pathway?

A

Absorption and distribution of lipids to the periphery by chylomicrons formed in intestinal cells

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12
Q

What is meant by the endogenous pathway?

A

Lipids are synthesised by the liver (triglycerides especially) They are then delivered from the liver to peripheral tissues via LDL

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13
Q

How is ApoB48 formed?

A

Stop codon in the gene produces a smaller mass ApoB in the intestine than in the liver.

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14
Q

What is the life cycle of ApoB containing liposomes?

A
  • assembly
  • intravascular metabolism
  • receptor mediated clearance
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15
Q

How does triglyceride enter enterocytes?

A
  • we eat foods containing triglycerides
  • triglycerides are split into monoglyceride and fatty acids.
  • these enter the enterocytes via diffusion where they are converted back into triglyceride.
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16
Q

How does cholesterol enter enterocytes?

A

Niemann-Pick C1-like 1 protein
(NPC1L1) binds to cholesterol, moves it into the cell and then releases it. Cholesterol is esterified to form a cholesterol ester.

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17
Q

What are enterocytes?

A

cells that line the intestine

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18
Q

How are chylomicrons assembled?

A
  • As triglyceride droplets form, apoB48 protein is added to them.
  • Lipidation occurs using Microsomal triglyceride transfer protein.
  • ApoB48 lipoprotein then forms a shell.
  • Cholesterol and apoA1 gets added.
  • The end product is a mature chylomicron.
  • Chylomicrons enter into systemic circulation
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19
Q

What are VLDL particles made up of?

A

-triglycerides and free fatty acids

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20
Q

Where are VLDLs assembled?

A

liver hepatocytes

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21
Q

Where do the free fatty acids in VLDLs come from?

A

-de novo synthesis
OR
-adipose tissues

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22
Q

How does activation of chylomicrons and VLDL occur?

A

-apoC2 is liberated from HDL and is incorporated into the shell of VLDL and chylomicrons.

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23
Q

What is the role of ApoCII in intravascular metabolism?

A

ApoCII facilitates the binding of chylomicrons and VLDL particles to Lipoprotein lipase enzyme.

24
Q

What is the role of Lipoprotein lipase in intravascular metabolism?

A

LDL etabolises core triglycerides to release them.

25
Q

What are chylomicron and VLDL remnants?

A

Particles with cholesterol but without triglyceride are termed chylomicron and VLDL remnants

26
Q

How are ApoB containing lipoproteins cleared?

A
  • chylomicrons and VLDL dissociate from LPL
  • ApoCII is transferred to HDL particles in exchange for apoE
  • Particles are now remnants
  • remnants metabolised by hepatic lipase in liver
  • remnants cleared by receptor mediated endocytosis into hepatocytes
  • remaining apo100 remnants become LDL particles lacking apoE and retaining doley apo100
27
Q

What are apoE?

A

a high affinity ligand for receptor mediated clearance.

28
Q

What percentages of apoB48 and apoB100 are cleared by receptor mediated endocytosis into hepatocytes?

A

All apoB48-containing remnants and 50% of apo100 containing-remnants

29
Q

What is clearance of LDL particles dependant on?

A

LDL receptor expressed by liver and other tissues

30
Q

What causes the uptake of LDL particles?

A

receptor mediated endocytosis

31
Q

How is cholesterol released?

A

Within the cell at the lysosome, cholesterol is released from cholesteryl ester by hydrolysis

32
Q

What does the release of cholesterol cause?

A
  • inhibition of de novo cholesterol production via HMG-CoA reductase
  • storage of cholesterol as cholesterol ester
33
Q

How is atherosclerosis initiated?

A

dysfunction and injury of the lining of blood vessels

34
Q

What are the risk factors of atherosclerosis?

A

diabetes, high BP, smoking

35
Q

How does atherosclerosis progress?

A
  • uptake of LDL from blood into intima of artery
  • LDL oxidised to atherogenic oxidised LDL
  • monocytes migrate into intima and become macrophages
  • OXLDL uptake by macrophages which converts them to cholesterol-laden foam cells that form a fatty streak
  • division and proliferation of smooth muscle cells by inflammatory substances. Collagen deposition
  • athermanous plaque formation.
36
Q

What is an athermanous plaque made of?

A

a lipid core (product of dead foam cells) and a fibrous cap (smooth muscle cells and connective tissue)

37
Q

What is the only organ able to eliminate cholesterol from the body?

A

liver

38
Q

What is HDLs role in cholesterol removal?

A

Mature HDL accepts excess cholesterol from the plasma membrane of cells (e.g. macrophages) and delivers cholesterol to the liver, known as reverse cholesterol transport, by several mechanisms

39
Q

Where is HDL formed?

A

liver

40
Q

What is HDL before it matures?

A

ApoA1 in association with a small amount of surface phospholipid and unesterified cholesterol (pre--HDL)

41
Q

What is mature HDL like?

A

Disc-like pre-HDL matures in the plasma to spherical alpha-HDL as surface cholesterol is enzymatically converted to hydrophobic cholesterol ester that migrates to the core of the particle

42
Q

What happens when HDL reaches the liver after collection of cholesterol?

A

HDL reaching the liver interacts with a receptor (scavenger receptor-B1, SR-B1) that allows transfer of cholesterol and cholesteryl esters into hepatocytes

43
Q

What is the role of cholesterol ester transfer protein?

A

mediates transfer of cholesteryl esters from HDL to VLDL and LDL, indirectly returning cholesterol to the liver

44
Q

What is primary dyslipidaemia?

A

Too much cholesterol caused by a combination of diet and genetic factors

45
Q

What is secondary dyslipidaemia?

A

Too much cholesterol a consequence of other diseases (e.g. type II diabetes, hypothyroidism, alcoholism, liver disease)

46
Q

How affective as statins?

A

– very effective in reducing total and LDL cholesterol (up to 60%), decrease triglycerides (up to 40%) and modestly increase HDL (about 10%)

47
Q

What are two examples of statins?

A

simvastatin and atorvastatin

48
Q

How do statins work?

A

They inhibit HMG-CoA reductase which reduces cholesterol synthesis. This causes an increase in LDL receptor expression and enhanced clearance of LDL

49
Q

What are other benefits of statins?

A
  • Decreased inflammation
  • Reversal of endothelial dysfunction
  • Decreased thrombosis
  • Stabilization of atherosclerotic plaques
50
Q

When are statins given?

A

Orally at night

51
Q

What are the adverse effects of statins?

A

Adverse effects are few but include myositis and rarely rhabdomyolosis incidence of which is increased if statin is combined with a fibrate

52
Q

What are fibrins?

A

Lipid lowering drugs

53
Q

How effective are fibrates?

A
  • decrease in triglycerides (up to 50%)
  • decreases (up to 15%) in LDL
  • and increases (up to 20%) in HDL,
54
Q

What are examples of Fibrates?

A

bezafibrate and gemfibrozil

55
Q

What are fibrates first line in treateing?

A

patients with very high triglyceride levels

56
Q

How do fibrates work?

A

Act as agonists of a nuclear receptor (PPAR) to enhance the transcription of several genes, including that encoding LPL

57
Q

What are the adverse effects of fibrins?

A

Have few adverse effects, but like statins may rarely cause myositis – combination with latter is generally inadvisable. Best avoided in alcoholics who are predisposed to hypertriglyceridaemias, but also rhabdomyolosis
-Incidence of other adverse effects (G.I. symptoms, pruritus and rash) greater than for statins

Cardiology (32 decks)

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