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1Principles of Biomedicine - MD1 > 34 - Lipid Mediators > Flashcards

34 - Lipid Mediators Flashcards

1
Q

Arachidonic acid

A

Precursor for many bioactive lipids

Also called C20:4 (20 carbons, 4 double bonds), eicosatetraenoid acid.

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2
Q

How does the body get arachidonic acid?

A

From dietary poly-unsaturated fatty acids
Indirectly as linoleic acid, which is converted to arachidonic acid.
Directly as arachidonic acid

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3
Q

Type of fat that arachidonic acid is

A

Omega-6-polyunsaturated acid

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4
Q

How is arachidonic acid stored?

A

Stored esterified in membrane phospholipids (plasma, nuclear membranes)

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5
Q

How is arachidonic acid released from cell membranes?

A

Phospholipase A2 releases arachidonic acid.

Phospholipase A2 is activated by increased intracellular Ca2+ or ERK (extracellular receptor kinase)

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6
Q

Part of arachidonic acid pathway that is tightly regulated

A

Phospholipase A2 activation. If not controlled, can have excessive bradykinins and leukotrienes produced.

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7
Q

Component of many snake venoms

A

Phospholipase A2

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8
Q

Name for biologically-active metabolites of arachidonic acid

A

Eicosanoids

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9
Q

What determines eicosanoid type?

A

Which type of enzyme metabolises arachidonic acid

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10
Q

Enzymes that can metabolise arachidonic acid
1)
2)
3)

A

1) Cyclo-oxygenase I (COXI) - constitutively expressed
2) COXII - Inducible by inflammatory stimuli (EG: IFN)
3) Lipoxygenase (expressed in inflammatory cells, eosinophils, mast cells)

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11
Q

Effect of arachidonic acid metabolism by COXI

A

Physiological prostaglandin production

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12
Q

Effect of arachidonic acid metabolism by COXII

A

Patho-physiological prostaglandin production

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13
Q

Intermediate stage between arachidonic acid and stable prostaglandins?

A 
Cyclic endoperoxidases (very unstable).
These are quickly converted to stable prostaglandins by peroxidases.
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14
Q

Nomenclature of stable prostaglandins

A

Letter describes ring structure.

Number describes number of double bonds

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15
Q 
PGE2 
1)
2)
3)
4)
A

1) Relaxes vascular smooth muscle
2) Hyperalgesic
3) Pyrogenic
4) Angiogenic (wound healing, tumour growth)

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16
Q

Prostaglandins that are bronchoconstrictors

A

PGD, PGF2alpha

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17
Q

Site of action of prostaglandins

A

Very local.
Degraded by endothelial cells of pulmonary capillaries.
Unstable, don’t last more than a few minutes.

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18
Q

Main indications of NSAIDS
1)
2)
3)

A

1) Analgesic
2) Antipyretic
3) Anti-inflammatory

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19
Q

Effect of PGE2 on blood flow

A

Increases blood flow

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20
Q

Local mediators that increase vascular permeability

A

Histamine, bradykinin

21
Q

Difference in hyperalgesia induced by bradykinins and prostaglandins

A

Bradykinins are directly painful.

Prostaglandins enhance sensitivity to pain, but aren’t painful in and of themselves

22
Q

Long-term interaction between IL-1b and arachidonic acid pathways
1)
2)

A

1) IL-1b induces increase in bradykinin receptors,

2) Increased COXII, phospholipase A2 levels

23
Q

Factor responsible for core temperature rise in fever

A

PGE2

24
Q 
PGE2 effects on the gut
1)
2)
3)
4)
A

1) Promotes blood flow (vasodilation)
2) Promotes angiogenesis
3) Increases mucus secretion
4) Reduces gastric acid secretion

25
Q

How can chronic NSAID use lead to gastric ulcers?

A

PGE2 protects the gut by promoting blood flow (increased healing), increasing mucus secretion and reducing gastric acid secretion in the gut). NSAIDS inhibit PGE2 formation, so there is no more gastric protection by it

26
Q

Characteristic chemical structure in prostaglandins

A

Cyclopentane ring

27
Q

Prostacyclin effects
1)
2)

A

1) Vasodilator

2) Reduces platelet activation

28
Q

Prostacyclin half life

A

Very short.

T1/2 is about 3 minutes

29
Q

Thromboxane A2 effects
1)
2)

A

1) Increases platelet activation

2) Vasoconstrictor

30
Q

Thromboxane A2 half life

A

Very short.

About 30 seconds

31
Q

Two opposing factors controlling platelet aggregation

A

Thromboxane A2 and prostacyclin

32
Q

Cells that produce prostacyclin

A

Endothelial cells

33
Q

Cells that produce thromboxane A2

A

Platelets

34
Q

Thromboxane A2 function in clotting

A

Platelets release thromboxane in a positive feedback loop.
The more platelets near each other, the more thrmoboxane is released, and the more vasoconstriction and platelet activation occur

35
Q

Factor that promotes coronary artery disease

A

Thromboxane A2

36
Q

Factor that protects against coronary artery disease

A

Prostacyclin

37
Q

Another name for prostacyclin

A

PGI2

38
Q

How does aspirin protect against heart disease?
1)
2)
3)

A

1) Aspirin covalently binds COX, inactivates it.
2) Endothelial cells can replenish COX as they are nucleated. Therefore they can continue releasing prostacyclin (takes a few hours to re-synthesise COX).
3) Platelets can’t replenish COX, as they don’t have a nucleus. Therefore can make more thromboxane for the rest of their lifespan (~8 days)

39
Q

Effect of aspirin on lipoxygenase

A

Increases activity of lipoxygenase.
Therefore when aspirin is administered, there is an increase in anti-inflammatory arachidonic acid derivatives (‘aspirin-triggered lipoxins’)

40
Q

Aspirin-triggered lipoxins

A

Analogues of normally-triggered lipoxins.

Generated from aspirin-mediated enhancement of lipoxygenase activity

41
Q

Why are omega-three fatty acids considered beneficial to health?

A

Replace arachidonic acid derivatives with those from omega3 fatty acids.
These derivatives are converted to prostacyclin at the same level, but much less thromboxane A2 is produced.

42
Q

How are leukotrienes formed?
1)
2)
3)

A

1) Arachidonic acid is metabolised by 5-lipoxygenase instead of COX.
2) 5-lipoxygenase converts arachidonic acid to 5-HPETE.
3) 5-HPETE converted to leukotrienes

43
Q

5-lipoxygenase cell distribution

A

Only known to be made by inflammatory cells

44
Q

5-lipoxygenase function

A

Only known function is inflammation

45
Q 
LTA4
1)
2)
3)
4)
A

1) Bronchoconstrictor
2) Vasoactive - leads to tissue oedema.
3) Implicated in asthma
4) Derived from 5-PETE.

46
Q

Leukotriene B4

A

No direct action on smooth muscle

Promotes inflammation by attracting leukocytes

47
Q

How do glucocorticoids work?

A

Induces annexin-1, which inhibits phospholipase A2

48
Q

Leukotriene receptor antagonist

A

Montelukast

1Principles of Biomedicine - MD1 (157 decks)

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