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13 Cards in this Set

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Function of Prostaglandins (PG), Thromboxanes (TX), Leukotrienes(LT)?
control cellular response to injury
PGE2
-major site of action
-biological activities
SITE: kidney, spleen, heart
ACTIVITY: vasodilation, enhances effects of bradykinin & histamine, induces uterine contraction, platelet aggregation
****PGI2

Site:
Activity
Site: Heart, Vascular endothelial cells
Activity: Inhibits platelet aggregation and induces vasodilation
****TXA2

Site:
Activity
Site: Platelets
Activity: Induces platelet aggregation vasoconstriction
LTC4

Site:
Activity:
Site: Monocytes, Alveolar macrophages, basophils, eiosonophils, mast cells, epithelial cells

Activity: component of slow reactive substance of anaphalaxis, induces vasodilation and vasoconstriction
LTD4

Site:
Activity:
Site: Monocytes, Alveolar macrophages, eiosonophils, mast cells, epithelial cells

Activity: Predominant component of slow reactive substance of anaphalaxis, induces vasodilation and vasoconstriction
Linoleate
omega 6 fatty acid
required from diet
Membrane sources of Arachadonic Acid
Phospholipase A2 pathway
-phospholipase A2 cleaves choline phosphoglyceride to form Arachadonic acid or monoacylglycerase which is then cleaved to form arachadonic acid

Phospholipase C pathway
Isotolphosphoglyceride is cleaved by phospholipase C to form 1,2 Diacelglycerol which is then cleaved by Diacelglycerol lipase to form Arachadonic Acid
Arachadonic Acid is the precursor for
1)cyclooxygenases ((prostaglandins)PG,(thromboxanes) TX)
2)Lipooxigenases ((leukotrienes) LT, (lipoxins) LX, (hydroperoxyacids) HPETE)
**IMPORTANT CARD****
Eicosanoids
PGE2, PGI2, TXA2, LTC4, LTD4.
**IMPORTANT CARD****
Sources of Eicosanoids
omega 6 fatty acids -- arachadonic acid via Phospholipase A2 & C pathway
Aspirin
Platelets : COX-1
Anucleate
Irreversible
“Suicide Substrate”
*** inhibits production of TXA-2 from platelets****
Low-Dose Aspirin Therapy for Stroke and MI.
A 52 y/o female executive status post a transient ischemic attack is placed on daily aspirin therapy.
WHY?
aspirin ireversibly binds to COX1 on platelets which are anucleated so it is therefore permanantly inhibiting the effects of platelets to form TXA2, which fxns to promote platelet aggregation & vasoconstrict.
However it does not inhibit the production of prostocyclin (PGI2) by endothelium of vessels. Because these are nucleated cells. PGI2 results in vasodilation and inhibits aggragation of platelets.