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MCM Eicosanoids and Lipid Mediators > Eicosanoids and Prostaglandins > Flashcards

Eicosanoids and Prostaglandins Flashcards

1
Q

What determines which prostaglandins are made in a cell?

A

The isomerases that are present in the cell.

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2
Q

Where is Arachidonic Acid derived from?

A

Cell Membrane

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3
Q

What liberates Arachidonic Acid from the cell membrane?

A

Phospholipase A2

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4
Q

Converts AA to PGH2 Prostaglandin endoperoxide

A

COX

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5
Q

Phospholipase A2 Substrate and Function

A

Substrate -Cell membrane phospholipds

Role- Liberate Arachidonic Acid from phospholipids

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6
Q

Cyclooxygenase contains what?

A

Iron

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7
Q

Cyclooxygenase substrates/cofactor & role

A

Substrate -Arachidonic Acid(or related PUFA)
Cofactor - O2
Role - converts AA+O2 into PGH2

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8
Q

PGH2 is the pivotal ________ __________

A

biosynthetic intermediate

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9
Q

PG isomerases- substrates and role

A

Substrate- PGH2

Role - converts PGH2 into PGD2, PGE2 PGF2alpha

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10
Q

Tx synthase or PGI synthase- substrate & role

A

Substrate PGH2

Role Converts PGH2 into TxA2 or PGI2

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11
Q

15-OH PG dehydrogenase- substrate & role

A

Substrates - PGD2, PGE2, PGF2alpha

Role - Inactivation

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12
Q

Prostaglandins or Thromboxane- made or stored in cell?

A

Made on demand, when proper stimuli activate phospholipase A2

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13
Q

What are some limiting factors in PG or Tx synthesis?

A
  1. O2 and AA availability
  2. Auto-inactivation of Cox enzyme
  3. Rapid&comprehensive PG enzymatic degradation
  4. Spontaneous hydrolysis of Tx and PGI2
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14
Q

What dictates whether PG or Tx is made?

A

Isomerase enzymes

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15
Q

Eicosanoid and Action in Vasculature Endothelium

A

PGI2

Vasodilation and decreased platelet aggregation

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16
Q

Eicosanoid and Action in Blood Platelets

A

TxA2

Vasoconstriction and Increased platelet aggregation

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17
Q

Eicosanoid and Action in Vasculature

A

PGE2

Permeability

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18
Q

Eicosanoid and Action in GI (Gut)

A

PGE2
Mucosal cytoprotection
Muscle tone
Motility

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19
Q

Eicosanoid and Action in Renal system

A

PGI2, PGE2

Na+ and H2O excretion

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20
Q

Eicosanoid and Action in Uterus

A 
PGF2alpha, PGE2
Muscle contraction (parturition AKA delivery)
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21
Q

Eicosanoid and Action in CNS

A

PGE2

Temperature

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22
Q

Eicosanoid and Action in PNS

A

PGE2

Pain sensitization

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23
Q

Receptors that relax smooth muscles AKA vasodilate blood vessels

A

EP2, EP4, and IP - Relax smooth muscles

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24
Q

Receptors that contract smooth muscles AKA vasoconstriction

A

FP and TP - contract smooth muscles

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25
Phospholipase A2 (PLA2) liberates ______
Arachidonic acid from phospholipids of cell membrane
26
Phospholipase C (PLC) liberates _______
IP3 and DAG from phospholipids
27
What will happen with excess TxA2:TP receptors and deficient PGI2:IP receptors in coronary arteries?
Vasoconstriction
28
The difference between COX-1 & COX-2
COX-1 is expressed all the time AKA constitutive | COX-2 is expressed in response to physiological stimuli to regulate physiological functions of PGs and TXs
29
In the Gut (COX1) - Deficient PGE2 leads to _____
Ulcers
30
In the Gut (COX1) - Excess PGE2 leads to ______
Diarrhea, cramps
31
Reproduction - Deficient PGE2 or PGF2alpha (COX1) results in _____
delayed birth
32
Reproduction (COX1) - Excess PGE2 or PGF2alpha results in _______
Premature labor
33
What can be used to counteract excess PGE2 and PGF2alpha (COX1) and avoid premature labor?
NSAIDs
34
Neonatal development (COX1)- role of PGE2: EP (EP4) receptors in neonatal development?
maintain the ductus arteriosus in the open position
35
Withdrawal of PGE2 (COX1) at birth results in ______
closure of ductus arteriosus
36
Why might a premature baby be treated with NSAIDs?
NSAIDs tend to negate the effects of prostaglandins (COX1), and in this case they would help close the patent ductus arteriosus.
37
COX2 is normally expressed where?
the kidneys
38
COX2 complements COX1 where?
Kidneys and brain
39
COX2 is induced in "all" tissues at "all" times. T or F
F - just "some" tissues at "some" times
40
COX2 has a prominent role in responding to pathological stimuli such as ____ and ______
Inflammation and cancer
41
COX2 and COX1 in the Kidneys - Deficient PGs in Kidney leads to _____ and ______ retention and __________
Na+ and H2O and mild hypertension
42
Inflammation stimulates __ release and COX1 converts it into __ which causes symptoms of _____, _______, and ______.
Arachidonic Acid, PGE2, Erythema, Edema, Pain
43
Inflammation stimulates ____ expression which ultimately results in ______ symptoms of PGE2 expression
COX2, amplified
44
Platelets - Have no nucleus, but make the eicosanoid Thromboxane A2 which _____ blood vessels and amplifies _____ ______
constricts, platelet aggregation
45
Endothelium - allows blood to flow without clotting. Endothelial cells make prostacyclin (PGI2) which ____ blood vessels and ______ platelet aggregation.
relaxes, inhibits
46
If most tissues express COX1 how does the body modulate the ratio of TxA2 and PGI2?
Different cells possess different isomerases and synthase enzyme which produce different eicosanoids in different cells.
47
Platelets- COX1 and Tx synthase produce ___ and __&__ receptors. This leads to
TxA2 TP & IP receptors Vasoconstriction/increased BP/platelet aggregation
48
Endothelial cells- COX1 and PGI2 synthase produce ____ and __&__ receptors. This leads to ______
PGI2 TP&IP Receptors Vasodilation/decreased BP/inhibited platelet aggregation
49
Collagen ____ platelets
stimulates
50
Platelets make which Eicosanoid?
Thromboxane
51
What stops the process of platelet aggregation from spreading throughout the blood stream, and what keeps it local?
Collagen is a local stimulus for Thromboxane synthesis. PGI2 is made by all endothelial cells and PGI2 opposes the action of TxA2 on blood vessels and platelets
52
COX2 induction in endothelial cells can augment ____ synthesis.
PGI2
53
COX2 augmentation of PGI2 can lead to good and bad outcomes. Good: Bad:
Good: Adaptation to protect against thrombosis Bad: part of underlying disease process of atherosclerosis..inflamation
54
COX2 induction in platelets can augment____
NOTHING, COX2 cannot be induced in platelets
55
Deficient PGI2 in endothelial cells leads to _____
TxA2 domination, platelet aggregation, vessel blockage
56
PGI2 causes ____ which results in ______
vasodilation/decreased BP | inhibited platelet aggregation
57
TxA2 causes ____ which results in ______
Vasoconstriction/Increased BP | platelet aggregation
58
Arachidonic acid metabolism can also occur using an enzyme called _____ to produce ______
5-lipoxygenase, leukotrienes
59
``` Leukotriene A4 Leukotriene B4 Leukotriene C4 Leukotriene D4 Leukotriene E4 ```
``` LTA4 LTB4 LTC4 LTD4 LTE4 ```
60
Receptors for LTA4
None
61
Receptors for LTB4
BLT1,2
62
Receptors for LTC4
CysLT1,2
63
Receptors for LTD4
CysLT1
64
Receptors for LTE4
CysLT
65
Why are Leukotrienes called leukotrienes?
They are made by leukocytes and have a conjugated triene in their structure.

MCM Eicosanoids and Lipid Mediators (1 decks)

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