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cardiovascular > Lipid Mediators > Flashcards

Lipid Mediators Flashcards

1
Q

What is the structure of arachidonic acid?

A

20 carbon omega 6 fatty acid with 4 double bonds

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2
Q

How is arachidonic acid derived?

A

From dietary polyunsaturated fatty acids - e.g. converted from linoleum acid via desaturation, elongation and then desaturation

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3
Q

How is arachidonic acid stored?

A

esterified in membrane phospholipids

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4
Q

How is arachidonic acid released from membranes?

A

Enzyme phospholipase A2 metabolises membrane and releases arachidonic acid

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5
Q

How is phospholipase A2 activated?

A

By an increase in intracellular calcium

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6
Q

How is arachidonic acid metabolised?

A

by cyclooxygenase (COX) or by lipoxygenase

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7
Q

What is the role of COX-1?

A

homeostasis - doesn’t require post translational modification

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8
Q

What is the role of COX-2?

A

it is inducible - the gene is induced by inflammatory stimuli such as IL-1 or growth stimuli

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9
Q

What are cycloendoperoxides?

A

The product of metabolism of arachidonic acid by COX

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10
Q

Are cycloendoperoxides stable?

A

No - they are rapidly metabolised into stable prostaglandins by isomerases

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11
Q

What does the nomenclature of prostaglandins represent?

A

The letter denotes the ring structure and the subscript number represents the number of double bonds

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12
Q

What are the actions of PGE2?

A

vasodilations, natriuretic, hyperalgesic, pyrogenic, angiogenic

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13
Q

What are the actions of NSAIDs?

A

Blocks COX - anti-inflammatory, analgesia, antipyretic

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14
Q

What are the side effects of NSAIDs?

A

gastric irritation

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15
Q

What is the benefit of the anti-inflammatory action of NSAIDs?

A

Because prostaglandins are only involved in the vascular component of inflammation and not cellular inflammation, NSAIDs wont modify the course of inflammation and will only give palliative care

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16
Q

What is the benefit of using NSAIDs for pain relief?

A

Prostaglandins on their own don’t cause pain, it is involved in synergy with another analgesic substance, therefore if the cause of the pain is unknown, removing prostaglandin will always stop the pain from being amplified

17
Q

How does prostaglandin cause fever?

A

Prostaglandin itself doesn’t reach the brain because it would be metabolised in circulation, instead IL-1 released by macrophage activation travels to the hypothalamus where it acts to activate COX and increase prostaglandin at the site which increases cAMP to cause fever

18
Q

How does PGE2 protect against gastric ulceration?

A

By promoting blood flow, promoting angiogenesis, increasing depth of mucous barrier, reducing gastric acid secretion

19
Q

How do NSAIDs cause gastric ulceration?

A

By removing action of PGE2

20
Q

What are prostacyclin and thromboxane?

A

Other products of COX metabolism of arachidonic acid

21
Q

When and where is prostacyclin produces?

A

All the time by endothelial cells

22
Q

What is the action of prostacyclin?

A

reduces platelet activation and causes vasodilation

23
Q

Why is prostacyclin important?

A

Because it protects against coronary artery disease

24
Q

Where is thromboxane produced?

A

By platelets

25
Q

What are the actions of thromboxane?

A

Increases platelet activation and causes vasoconstriction - opposite of prostacyclin

26
Q

Why is aspirin used in the treatment of coronary artery disease?

A

Because it causes COX activity to be lost in platelets for 8 days, whereas it only causes COX activity to be lost in endothelium for a few hours - this means that it tips the ratio of prostacyclin and thromboxane in favour of prostacyclin enhancing its protective effects against coronary artery disease

27
Q

Why is aspirin different from other NSAIDs?

A

Because it enables increased production of epi-LXA4 and epi-LXB4 which are involved in inflammation resolution

28
Q

What is eicosapentaenoic acid?

A

fish oil - an omega 3 dietary polyunsaturated fatty acids

29
Q

What is the benefit of eicosapentaenoic acid?

A

Metabolism results in more prostacylin than thromboxane - this may explain the low incidence of coronary artery disease in cultures that have a rich marine oil diet

30
Q

What are the products of metabolism of arachidonic acid by lipoxygenase?

A

5-HPETE which makes leukotrienes

31
Q

What is the role of 5-lipoxygenase?

A

No physiological role - only important in inflammation - which means that it is a good target for intervention

32
Q

How is 5-lipoxygenase activated?

A

By increased intracellular calcium (from infection, allergy, inflammation)

33
Q

What are the actions of leukotrienes?

A

bronchoconstriction, leaky vessels

34
Q

What is the action of leukotriene B4?

A

No direct action on smooth muscle, promotes inflammation by attracting leukocytes

35
Q

Are there any therapeutics to target the leukotriene B4 receptor (BLT)?

A

No

cardiovascular (36 decks)

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