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Physiology Exam 4 > Eicosanoids > Flashcards

Eicosanoids Flashcards

1
Q

Eicosanoids are?

A

Agonists

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2
Q

Eicosanoids mediate their effects via?

A
  1. 7-pass transmembrane receptors

2. Heterotrimeric G-proteins

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3
Q

Eicosanoid half-life

A

Very short (seconds to minutes)

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4
Q

Why do eicosanoids have limited range of action?

A

Very short half-life

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5
Q

Eicosanoid signaling

A
  1. Paracrine

2. Autocrine

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6
Q

Eicosanoids are clinically important because they participate in?

A
  1. Platelet aggregation
  2. Inflammation, arthritis, asthma
  3. GI integrity
  4. Kidney and liver homeostasis
  5. Repro (ovulation and parturition)
  6. Development
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7
Q

Eicosanoids are named for being?

A

Derivatives of a 20 (eicos) carbon FA chain

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8
Q

4 major classes of eicosanoids

A
  1. Prostacyclins
  2. Prostaglandins
  3. Thromboxanes
  4. Leukotrienes
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9
Q

Subscript number in eicosanoid name indicates?

A

Number of unsaturated bonds in their chemical structure

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10
Q

Prostaglandins mediate?

A

All 4 cardinal signs of inflammation

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11
Q

4 cardinal signs of inflammation

A
  1. Rubur
  2. Tumor (swelling)
  3. Calor
  4. Dalor
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12
Q

Rubor is caused by?

A

Vasodilation

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13
Q

Tumor

A

Swelling via increased vascular permeability

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14
Q

Dolor

A

Pain by sensitizing nociceptors

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15
Q

Survival factors for GI stem cells are generated by?

A

COX-1

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16
Q

Glucocorticoid function

A

Increase blood glucose levels to support brain function

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17
Q

Signal for glucocorticoid production

A

ACTH

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18
Q

ACTH is released in response to?

A

Stress

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19
Q

ACTH stands for?

A

Adenocorticotropic hormone

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20
Q

ACTH is released from?

A

Pituitary gland

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21
Q

Effect of ACTH on glucose transport and metabolism

A

Inhibits (counteracts insulin)

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22
Q

ACTH action in muscle, CT, skin and bone

A

Protein catabolism

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23
Q

ACTH action in liver

A

Gluconeogenesis from AAs

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24
Q

ACTH suppresses:

A
  1. Immune-response

2. Inflammation

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25
Q

Synthetic glucocorticoids are used to treat?

A
  1. Auto-immune disease

3. Inflammatory disease

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26
Q

COX-1 is involved in?

A
  1. Platelet aggregation

2. Vasoconstriction

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27
Q

COX-2 contributes to?

A

Prevention of unwanted platelet aggregation and vasoconstriction

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28
Q

Toxicity of COX-2 inhibitors are associated with?

A

Inhibition of protective mechanisms

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29
Q

Low doses of aspirin block?

A

COX-1 in platelets without affecting COX-2 in endothelia

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30
Q

Healthy endothelial cells express?

A

COX-2

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31
Q

COX-2 in endothelial cells generates?

A

PGI(2)

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32
Q

PGI(2)

A
  1. Prevents platelet activation and aggregation

2. Promotes vasodilation via PI-R

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33
Q

PI-R stands for?

A

PGI(2) receptors

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34
Q

PI-R signals via?

A
  1. G(s)
  2. Adenylyl cyclase (AC)
  3. cAMP
  4. PKA
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35
Q

PI-R activates?

A

Ca2+-ATPases in ER or CR to keep cytosolic Ca2+ low

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36
Q

Low cytosolic Ca2+ in platelets

A

Prevent shape change and aggregation

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37
Q

Low cytosolic Ca2+ in vascular smooth muscle cells

A

Promotes vasodilation

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38
Q

What stimulates COX-1 in destroyed endothelium?

A

Platelet adhesion to ECM

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39
Q

COX-1 in platelets generates?

A

TXA(2)

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40
Q

TXA(2) causes?

A
  1. Platelet activation and aggregation

2. Vasoconstriction

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41
Q

How does TXA(2) cause platelet activation, aggregation and vasoconstriction?

A

TP-R

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42
Q

TP-R stands for?

A

TXA(2) receptors

43
Q

TP-R signals?

A
  1. G(q)
  2. IP3
  3. PLC
44
Q

PLC stands for?

A

Phospholipase C

45
Q

TP-R signals G(q), PLC and IP3 to?

A

Release Ca2+ from ER → elevates cytosolic Ca2+

46
Q

High cytosolic Ca2+ in platelet initiates?

A

Shape changes and aggregation

47
Q

High cytosolic Ca2+ in smooth muscle cells cause?

A

Vasoconstriction

48
Q

Mast cells in the airway mucosa react to antigen by releasing?

A

Leukotrienes:

  1. LTB(4)
  2. LTC(4)
  3. LTD(4)
  4. LTE(4)
49
Q

LTB(4) does what?

A

Attracts eosinophils to leave bloodstream and enter airway mucosa

50
Q

Eosinophils are an additional source of?

A

Leukotrienes

51
Q

LTC(4), LTD(4) and LTE(4) cause?

A

Asthmatic symptoms

52
Q

Asthmatic symptoms caused by LTC(4), LTD(4) and LTE(4)?

A
  1. Bronchioconstriction
  2. Edema
  3. Secretion of heavy mucus
53
Q

How do LTC(4), LTD(4) and LTE(4) cause edema?

A

Increasing vascular permeability

54
Q

Asthmatic symptoms can be a side-effect of?

A

Cyclooxygenase inhibitors

55
Q

Why can asthmatic symptoms be a side-effect of cyclooxygenase inhibitors?

A

Shuffling o arachidonic acid metabolism toward 5-lipoxygenase pathway

56
Q

Hormones high during follicular phase

A
  1. Estrogen
  2. LH

→ Ovulation

57
Q

Hormones high during luteal phase

A
  1. Progesterone
  2. PGF(2alpha)

→ Regression

58
Q

LH stands for?

A

Luteinizing hormone

59
Q

GnRH stands for?

A

Gonadotropin releasing hormone

60
Q

GnRH is secreted by?

A

Hypothalamus

61
Q

GnRH stimulates release of?

A
  1. FSH
  2. LH

From pituitary

62
Q

FSH and LH are released from?

A

Pituitary

63
Q

LH stimulates?

A

Theca cells of follicle to synthesize androgens

64
Q

2 examples of androgens released by LH stimulus

A
  1. Testosterone

2. Androstendione

65
Q

FSH stimulates?

A
  1. Granulosa cells to synthesize estradiol from androgens

2. Production of inhibin

66
Q

Inhibin

A

Reducses FSH release by negative feedback mechanism

67
Q

Estrogen stimulates?

A
  1. Follicular growth

2. GnRH secretion

68
Q

LH surge leads to?

A
  1. Ovulation

2. Rebuilding of follicle into CL

69
Q

CL synthesizes?

A
  1. Progesterone

2. Oxytocin

70
Q

Progesterone

A

Inhibits secretion of GnRH → inhibits maturation of ovarian follicles

71
Q

PGF(2alpha) causes?

A

Luteolysis

72
Q

PGF(2alpha) is generated by what in non-pregnant uterus?

A
  1. Estradiol from maturing follicles

2. Progesterone and oxytocin from CL

73
Q

Luteolysis does what?

A

Removes inhibitory effect of progesterone on hypothalamus → promotes re-entry into estrus cycle

74
Q

SAID stands for?

A

Synthetic glucocorticoids

75
Q

Most common SAID

A

Prednisolone

76
Q

Phospholipase A(2)

A

Removes arachidonic acid from membrane lipids

77
Q

SAID blocks?

A

Phospholipase A(2)

78
Q

COX stands for?

A

Cyclooxygenase

79
Q

LOX stands for?

A

Lipoxygenase

80
Q

NSAIDs block?

A

COX-1 & 2, 5-LOX

81
Q

PGH(2) is generated by?

A

COX

82
Q

LTA(4) is generated by?

A

5-LOX

83
Q

COX-1 is precursor for?

A
  1. PGE(2)
  2. PGI(2)
  3. Thromboxane TXA(2)
84
Q

PGE(2) and PGI(2) role in gastric mucosa

A
  1. Protection

2. Anti-apoptoic

85
Q

Thromboxane TXA(2) found in?

A

Platelets

86
Q

Role of thromboxane TXA(2) in platelets?

A
  1. Platelet aggregation

2. Vasoconstriction

87
Q

Molecules in gastric mucosa

A

Prostaglandins

88
Q

COX-2 is precursor for?

A
  1. PGE(2)
  2. PGI(2)
  3. PGD(2)
  4. PGF(2alpha)
  5. Prostacyclin PGI(2)
89
Q

Prostaglandins in gastric mucosa

A
  1. PGE(2)

2. PGI(2)

90
Q

Type of molecules in joints and soft tissue

A

Prostaglandins

91
Q

Prostaglandins in joints and soft tissue

A
  1. PGE(2)
  2. PGI(2)
  3. PGD(2)
  4. PGF(2alpha)
92
Q

Role of prostaglandins in joints and soft tissue

A
  1. Inflammation

2. Pain

93
Q

Type of molecule in vascular endothelium

A

Prostacyclin PGI(2)

94
Q

Role of PGI(2) in vascular endothelium

A
  1. Platelet resting

2. Vasodilation

95
Q

Type of molecule in colon cancer

A

Prostaglandin PGE(2)

96
Q

Role of PGE(2) in colon cancer

A
  1. Protection

2. Anti-apoptotic

97
Q

Type of molecule in bovine uterus

A

Prostaglandin PGF(2alpha)

98
Q

Function of PGF(2alpha) in bovine uterus?

A

Luteolysis

99
Q

TXA(2) aka?

A

Thromboxane

100
Q

PGI(2) aka

A

Prostacyclin

101
Q

5-LOX is precursor for?

A

Leucotrienes:

  1. LTB(4)
  2. LTC(4)
  3. LTD(4)
  4. LTE(4)
102
Q

Leucotrienes are found in?

A

Airways

103
Q

Role of leucotrienes in airways

A
  1. Bronchioconstriction

2. Mucus secretion

Physiology Exam 4 (10 decks)

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