Prostaglandin Flashcards

1
Q

Arachidonic acid can be converted into..

A

Leukotrienes and prostaglandins

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2
Q

Enzyme that catalyzes arachidonic acid into leukotrienes

A

Lipoxygenase

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3
Q

Enzyme that catalyzes arachidonic acid into prostaglandins

A

Cycloxygenase

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4
Q

Can can prostaglandins be converted into that are important for blood-clotting?

A

Thromboxanes and prostaglandins

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5
Q

What inhibits prostaglandins from being formed from arachidonic acids?

A

Aspirin and other NSAIDS

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6
Q

What are eicosanoids?

A

Prostaglandins and other related compounds (leukotrienes and thromboxanes)

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7
Q

How do eicosanoids differ from hormones?

A

Synthesized in cells

Act locally (vs systematically)

Extremely short half lives

Extremely small concentration to elicit a desired effect

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8
Q

Almost every cell can produce _________ and there are nearly thousands that elicit a multitude of physiological effects!

A

Eicosanoids

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9
Q

What type of eicosanoids do platelets produce? What do they do?

A

Thromboxane, they promote platelet aggregations and vasoconstriction.

Procoagulant

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10
Q

what’s an example of a Procoagulant?

A

Thromboxane

Synthesized by platelets

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11
Q

What eicosanoids do vascular epithelial cells synthesize? What do they do?

A

Prostacyclin, inhibit lately aggregation and stimulate vasodilation

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12
Q

What is an example of a anticoagulant?

A

Prostacyclin, synthesized by vascular endothelial cells

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13
Q

_________ produces arachidonic acids

A

Linoleic acid

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14
Q

What is the most common precursor of eicosanoids?

A

Arachidonic acid

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15
Q

What enzyme must be activated for the release of arachidonic acid?

A

Phospholipase A2

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16
Q

Synthesis of prostaglandins requires what two enzymes?

A

Lipoxygenase (for leukotrienes) and cyclooxygenase (for prostacyclin and thromboxanes)

17
Q

What is the enzyme target of steroids?

A

Phospholipases A2, which produces arachidonic acid

18
Q

What is the enzyme target of NSAIDS?

A

Cyclooxygenase, production of thromboxanes and prostacyclin (prostaglandins)

19
Q

What is the most common NSAID?

A

Aspirin

20
Q

What class of drugs are used to minimize inflammatory reactions (asthma attacks), reduce discomfort associated with inflammation, and promote gene level up-regulation of Phospholipases A2 inhibitor?

A

Glucocorticoids

21
Q

All steroids have ______ __________ and therefore act at the level of ______ _________

A

Nuclear receptors, gene expression

22
Q

COX

A

Cyclooxygenase

23
Q

NSAIDS inhbit the ___________ ____ in formation of both _________ and ____________

A

Cyclooxygenase step, prostacyclins and thromboxanes

24
Q

Aspirin inhibits both ________ and _______

A

COX1 and COX2

25
Q

Leukotrienes are directly related to:

A

Asthma

26
Q

By blocking the COX, due to ________, you open the pathway for _________

A

Aspirin (NSAIDS), Leukotrienes

27
Q

By blocking the pathway through COX enzymes, leukotrienes are produced, inducing ________ ________

A

Asthmatic response

28
Q

How does aspirin work?

A

Irreversibly inactivated COX by acetylation

29
Q

Asprin is a ________ _________ of COX

A

Suicide inhibitor

30
Q

Platelets have no ______ and cannot synthesize new ___________

A

Nucleus, COX

31
Q

Aspirin inhibition persists for the life span of the _______, which is how long?

A

Platelets, 7-10 days

32
Q

With the affect of aspiring, the platelets can no longer produce _________

A

Thromboxanes, due to no COX activity

33
Q

Vascular endothelial cells have a ________ therefore can synthesize __________ and produce _________

A

Nucleus, COX, prostacyclin

34
Q

Role of aspirin in those with increased risk of cardiovascular disease

A

Reduce the risk of unwanted blood clotting

35
Q

End result of aspirin

A

Inhibits pathway for thromboxane production

Creates a mild hemostatic defect

Reduces blood coagulation