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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
Q

Phospholipase A2 (PLA2) liberates ______

A

Arachidonic acid from phospholipids of cell membrane

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26
Q

Phospholipase C (PLC) liberates _______

A

IP3 and DAG from phospholipids

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27
Q

What will happen with excess TxA2:TP receptors and deficient PGI2:IP receptors in coronary arteries?

A

Vasoconstriction

28
Q

The difference between COX-1 & COX-2

A

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
Q

In the Gut (COX1) - Deficient PGE2 leads to _____

A

Ulcers

30
Q

In the Gut (COX1) - Excess PGE2 leads to ______

A

Diarrhea, cramps

31
Q

Reproduction - Deficient PGE2 or PGF2alpha (COX1) results in _____

A

delayed birth

32
Q

Reproduction (COX1) - Excess PGE2 or PGF2alpha results in _______

A

Premature labor

33
Q

What can be used to counteract excess PGE2 and PGF2alpha (COX1) and avoid premature labor?

A

NSAIDs

34
Q

Neonatal development (COX1)- role of PGE2: EP (EP4) receptors in neonatal development?

A

maintain the ductus arteriosus in the open position

35
Q

Withdrawal of PGE2 (COX1) at birth results in ______

A

closure of ductus arteriosus

36
Q

Why might a premature baby be treated with NSAIDs?

A

NSAIDs tend to negate the effects of prostaglandins (COX1), and in this case they would help close the patent ductus arteriosus.

37
Q

COX2 is normally expressed where?

A

the kidneys

38
Q

COX2 complements COX1 where?

A

Kidneys and brain

39
Q

COX2 is induced in “all” tissues at “all” times. T or F

A

F - just “some” tissues at “some” times

40
Q

COX2 has a prominent role in responding to pathological stimuli such as ____ and ______

A

Inflammation and cancer

41
Q

COX2 and COX1 in the Kidneys - Deficient PGs in Kidney leads to _____ and ______ retention and __________

A

Na+ and H2O and mild hypertension

42
Q

Inflammation stimulates __ release and COX1 converts it into __ which causes symptoms of _____, _______, and ______.

A

Arachidonic Acid, PGE2, Erythema, Edema, Pain

43
Q

Inflammation stimulates ____ expression which ultimately results in ______ symptoms of PGE2 expression

A

COX2, amplified

44
Q

Platelets - Have no nucleus, but make the eicosanoid Thromboxane A2 which _____ blood vessels and amplifies _____ ______

A

constricts, platelet aggregation

45
Q

Endothelium - allows blood to flow without clotting. Endothelial cells make prostacyclin (PGI2) which ____ blood vessels and ______ platelet aggregation.

A

relaxes, inhibits

46
Q

If most tissues express COX1 how does the body modulate the ratio of TxA2 and PGI2?

A

Different cells possess different isomerases and synthase enzyme which produce different eicosanoids in different cells.

47
Q

Platelets- COX1 and Tx synthase produce ___ and __&__ receptors. This leads to

A

TxA2
TP & IP receptors
Vasoconstriction/increased BP/platelet aggregation

48
Q

Endothelial cells- COX1 and PGI2 synthase produce ____ and __&__ receptors. This leads to ______

A

PGI2
TP&IP Receptors
Vasodilation/decreased BP/inhibited platelet aggregation

49
Q

Collagen ____ platelets

A

stimulates

50
Q

Platelets make which Eicosanoid?

A

Thromboxane

51
Q

What stops the process of platelet aggregation from spreading throughout the blood stream, and what keeps it local?

A

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
Q

COX2 induction in endothelial cells can augment ____ synthesis.

A

PGI2

53
Q

COX2 augmentation of PGI2 can lead to good and bad outcomes.
Good:
Bad:

A

Good: Adaptation to protect against thrombosis
Bad: part of underlying disease process of atherosclerosis..inflamation

54
Q

COX2 induction in platelets can augment____

A

NOTHING, COX2 cannot be induced in platelets

55
Q

Deficient PGI2 in endothelial cells leads to _____

A

TxA2 domination, platelet aggregation, vessel blockage

56
Q

PGI2 causes ____ which results in ______

A

vasodilation/decreased BP

inhibited platelet aggregation

57
Q

TxA2 causes ____ which results in ______

A

Vasoconstriction/Increased BP

platelet aggregation

58
Q

Arachidonic acid metabolism can also occur using an enzyme called _____ to produce ______

A

5-lipoxygenase, leukotrienes

59
Q 
Leukotriene A4
Leukotriene B4
Leukotriene C4
Leukotriene D4
Leukotriene E4
A 
LTA4
LTB4
LTC4
LTD4
LTE4
60
Q

Receptors for LTA4

A

None

61
Q

Receptors for LTB4

A

BLT1,2

62
Q

Receptors for LTC4

A

CysLT1,2

63
Q

Receptors for LTD4

A

CysLT1

64
Q

Receptors for LTE4

A

CysLT

65
Q

Why are Leukotrienes called leukotrienes?

A

They are made by leukocytes and have a conjugated triene in their structure.

MCM Eicosanoids and Lipid Mediators (1 decks)

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