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?

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
Leukotrienes are directly related to:
Asthma
26
By blocking the COX, due to ________, you open the pathway for _________
Aspirin (NSAIDS), Leukotrienes
27
By blocking the pathway through COX enzymes, leukotrienes are produced, inducing ________ ________
Asthmatic response
28
How does aspirin work?
Irreversibly inactivated COX by acetylation
29
Asprin is a ________ _________ of COX
Suicide inhibitor
30
Platelets have no ______ and cannot synthesize new ___________
Nucleus, COX
31
Aspirin inhibition persists for the life span of the _______, which is how long?
Platelets, 7-10 days
32
With the affect of aspiring, the platelets can no longer produce _________
Thromboxanes, due to no COX activity
33
Vascular endothelial cells have a ________ therefore can synthesize __________ and produce _________
Nucleus, COX, prostacyclin
34
Role of aspirin in those with increased risk of cardiovascular disease
Reduce the risk of unwanted blood clotting
35
End result of aspirin
Inhibits pathway for thromboxane production Creates a mild hemostatic defect Reduces blood coagulation