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Endocrinology semester 1 > autocoids > Flashcards

autocoids Flashcards

1
Q

give examples of 3 major autacoids?

A
  • Histamine
  • Prostanoids
  • Leukotrienes
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2
Q

what are the main sites of storage of histamine?

A
  • mast cells

- some neurones in CNS and GI tract

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3
Q

when is histamine released from mast cells?

A

Most commonly released from mast cells during inflammatory and allergic reaction

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4
Q

how is histamine released from mast cells?

A
  • by the interaction of antigen with cell-fixed IgE antibodies
  • interaction of C3a and C5a with their receptors
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5
Q

how else can histamine be released (without antibody interaction)?

A

can be released by many basic drugs such as morphine, radiocontrast media, tubocurarine, vancomycin etc.

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6
Q

what is histamine secretion associated with?

A

rise in cytosolic Ca2+ conc.

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7
Q

what inhibits histamine secretion?

A

Agents that increase cAMP formation (β-adrenoceptor agonists)

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8
Q

how does histamine work?

A

Produces its action by acting on three main types of histamine receptors

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9
Q

what are the 3 types of histamine receptors?

A

H1
H2
H3

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10
Q

where are H1 receptors found?

A

Located mainly on smooth muscles of GI tract, lungs, uterus, blood vessels, sensory nerve endings and in CNS.

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11
Q

where are H2 receptors found?

A

Parietal cells of gastric mucosa, heart etc.

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12
Q

where are H3 receptors found?

A

Presynaptic terminals of histaminergic neurones in CNS and GI tract that regulate release of histamine and other transmitters

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13
Q

what are H1 receptors responsible for?

A
  • vasodilation
  • increased capillary permeability
  • contraction of ileal smooth muscles
  • contraction of bronchial smooth muscles
  • itch and pain
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14
Q

what are H2 receptors responsible for?

A
  • gastric acid secretion

- increases heart rate and output

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15
Q

what causes the triple response to histamine?

A

Intradermal injection of histamine elicits the characteristic “triple response”

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16
Q

what does the triple response to histamine include?

A
  • a red spot
  • flare/brighter red flush
  • a wheal
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17
Q

what causes the red spot in the triple response to histamine?

A

the direct vasodilator effect of histamine

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18
Q

what causes the flare in the triple response to histamine?

A

results from histamine-induced stimulations of axon reflexes that cause vasodilation indirectly

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19
Q

what causes the wheal in the triple response to histamine?

A

results from the histamines capacity to increase capillary permeability.

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20
Q

what are the pathophysiological roles of histamine?

A
  • a mediator of type 1 hypersensitivity reactions

- a stimulant of gastric acid secretion

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21
Q

how can gastro-oesophageal reflux disease and similar conditions be treated?

A

treated with H2 receptor antagonists.

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22
Q

why are antihistamines only effective in some types of allergies?

A

because there are many other mediators released which can produce the same effects as histamines.

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23
Q

what are examples of older antihistamines?

A

Chlorpheneramine, Promethazine, Diphenhydramine

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24
Q

what was the problem with older antihistamines?

A

can cause sedation

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25
Q

what are examples of non-sedating antihistamines?

A

Terfenadine, fexofenadine, loratadine, desloratadine, acrivastine, cetirizine, levocetirizine

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26
Q

what are H1 receptor antagonists (antihistamines) used to treat?

A
  • hay fever (seasonal rhinoconjunctivitis)

- urticaria

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27
Q

what are examples of H2 receptor antagonists?

A

Cimetidine, ranitidine, famotidine, nazatidine.

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28
Q

what are H2 receptor antagonists used for?

A

to decrease gastric acid secretion which
Helps heal peptic and duodenal ulcers
Gastro-oesophageal reflux disease

29
Q

which are more effective H2 receptor antagonists or proton pump inhibitors in treating excess gastric secretion?

A

H2 receptor antagonists are lLess effective than Proton Pump Inhibitors (e.g. omeprazole) but have prominent effects on basal acid secretion and are particularly effective in suppressing nocturnal acid secretion.

30
Q

what are eicosanoids?

A

Lipid autacoids derived from membrane phospholipids

31
Q

what are the main physiologically active eicosanoids?

A

prostanoids

leukotrienes

32
Q

where are eicosanoids stored?

A

Eicosanoids, unlike histamine, are not stored preformed in the tissues; they are generated as required from membrane phospholipids

33
Q

biosynthesis of eicosanoids and PAF?

A

slide 15-19

34
Q

what are the 2 forms of cyclooxyrgenase in the body?

A

COX-1

COX-2

35
Q

where is COX-1 found?

A

occurs in most cells as a constitutive enzyme

36
Q

where is COX-2 found?

A

is induced mainly in inflammatory cells by an inflammatory stimulus

37
Q

where are the main prostanoids produced in the platelets?

A

Thromboxane A2

38
Q

what is the main prostanoid produced in the vascular endothelium?

A

PGI2

39
Q

where else are prostanoids synthesised?

A

lungs and spleen

40
Q

how do non-steroidal anti-inflammatory agents (NSAIDs) produce their anti-inflammatory effect?

A

inhibiting both COX-1 and COX-2

41
Q

what are examples of COX-2 selective inhibitors?

A

Celecoxib

Etoricoxib

42
Q

what are the actions of prostanoids?

A

Affect most tissues and produce diverse effects.

43
Q

what are the actions of PGD2?

A

causes vasodilatation, relaxation of GI and uterine smooth muscles

44
Q

what receptors do PGD2 work on?

A

DP receptors

45
Q

what are the actions of PGI2?

A

causes vasodilatation, inhibition of platelet aggregation, renin release and natriuresis

46
Q

what receptors do PGI2 work on?

A

IP receptors

47
Q

what are the actions of thromboxane A2?

A

causes vasoconstriction and platelet aggregation

48
Q

what receptors do thromboxane A2 work on?

A

TP receptors

49
Q

what are the actions of PGF2a?

A

causes myometrial contraction

50
Q

what receptors do PGF2a work on?

A

FP receptors

51
Q

what are the actions of PGE2?

A

contraction of bronchial and GI smooth muscles (EP1 receptors)
bronchodilation, vasodilatation, relaxation of GI smooth muscles (EP2 receptors)
Increased gastric mucus secretion and decrease acid secretion, contraction of GI smooth muscles, contraction of pregnant human uterus etc (EP3 receptors)

52
Q

how does PGE2 cause fever?

A

The synthesis of mainly PGE2 in hypothalamus in response to pyrogens causes fever

53
Q

what role do prostanoids play in inflammation?

A

inflammation is always accompanied by the release of prostanoids and other mediators

54
Q

what are examples of agonist prostanoid clinical applications?

A

Medical abortion (gemeprost, misoprostol PGE analogue)
Gastric cytoprotection (misoprostol)
Impotence (alprostadil PGE1)
Inhibit platelet aggregation during haemodialysis (epoprostenol PGI2)
Glaucoma (latanoprost)

55
Q

what are examples of antagonist prostanoid clinical applications?

A

COX inhibitors (NSAIDs and Coxibs) are most commonly used anti-inflammatory drugs
Aspirin act as an irreversible COX inhibitor
A low dose aspirin a day keeps the infarcts at bay!
Other NSAIDS cause reversible inhibition of COXs
Glucocorticoids also inhibit COX but they have additional effects which include inhibition of Phospholipase A2
Coxibs are claimed to selectively inhibit COX-2 but not COX-1

56
Q

what are the main uses of non-steroidal anti-inflammatory drugs?

A

Anti-inflammation
Analgesic
Antipyretic
Low dose aspirin for prophylaxis of myocardial infarction

57
Q

what are side effects of non-steroidal anti-inflammatory drugs?

A
  • Gastrointestinal ulceration and intolerance
  • Blockage of platelet aggregation
  • Inhibition of prostaglandin-mediated renal function
  • Inhibition of uterine motility
  • Hypersensitivity reactions
58
Q

what are leukotrienes?

A

Leukotrienes are the products of lipooxygenase pathways

59
Q

what is the main enzyme that results in synthesis of leukotrienes?

A

5-lipoxygenase

60
Q

what are the leukotrienes synthesised by 5-lipoxygenase?

A

LTB4
LTC4
LTD4
LTE4

61
Q

which is the leukotriene mainly produced by neutrophils?

A

LTB4

62
Q

what are cysteinyl-leukotrienes?

A

Slow-reacting substance of anaphylaxix

63
Q

what are examples of cysteinyl-leukotrienes?

A

LTC4
LTD4
LTE4

64
Q

what produces cysteinyl-leukotrienes?

A

mainly produced by eosinophils, mast cells and macrophages

65
Q

what are some other lipoxygenases?

A

Two other lipoxygenases (12- & 15-) are known which produce
12-HETE (by 12-lipooxygenase)
- Modulation of renal function
Lipoxins A & B (by 15-lipoxygenase + 5-
- Oppose the action of LTB4

66
Q

biosynthesis of leukotrienes and LT receptors?

A

Slide 30

67
Q

what are the actions of LTB4?

A

a powerful chemotactic agent for neutrophils, eosinophils and monocytes.
increases degranulation of neutrophils and release of toxic oxygen products

68
Q

what are the actions of the cysteinyl-leukotrienes?

A 
potent bronchoconstrictors (LTC4 and LTD4 are 1000 times more potent than histamine; LTE4 less potent but the effect is longer lasting). Cause bronchoconstriction in healthy individuals and asthmatics.
Increase vascular permeability
69
Q

what are the clinical applications of leukotrienes?

A

Two groups of medicines are available which modify the leukotrienes action
5-lipoxygenase inhibitor: zileuton
Not been very useful due to its 4 times daily dose and potential liver toxicity (Discontinued in UK and EU)
Antagonists of Cys-LT receptors: montelukast, zafirlukast
New drugs that supplement current medicines (beta2 agonists and corticosteroids) used in management of asthma
May be more effective in exercise-induced asthma and in “aspirin sensitive” asthmatics

Endocrinology semester 1 (10 decks)

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