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endocrine term 2 quiz 2 - julia's notes > prostaglandins - notes > Flashcards

prostaglandins - notes Flashcards

1
Q

prostaglandins

A

active principle in human serum that induced rhythmic contraction and relaxation of myometrium
produced in highest concentration in seminal vesicles
metabolic products of unsaturated membrane FA

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2
Q

eicosanoids

A

metabolic products of unsaturated membrane FA (the 20-carbon eicosaenoic acids)
includes prostaglandins, leukotrienes, thromboxanes
produced by virtually all cells
synthesized and released in response to inflammatory, mechanical, neurological, or hormonal stimuli
degraded by dehydrogenase enzymes, most effectively in lung
short half lives so local - autocrine or paracrine

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3
Q

nomeclature of eicosanoids

A

letters designate ring structure

numbers denote number of double bonds - important for receptor binding and function

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4
Q

receptors for eicosanoids

A

usually g-protein coupled

specific for each eicosanoid - each can have multiple

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5
Q

production of eicosanoids

A

produced by virtually all cells
different cells make different ones
precursors = unsaturated membrane FA, primarily arachidonic acid
stimuli activate phospholipase A2 family => release of membrane FA (eicosaenoic acids)
prostaglandins and thromboxanes are formed via cyclooxygenase (COX) pathways
leukotrienes produced via enzyme 5-lipoxygenase
lipoxins products of 5, 12, adn 15- lipoxygenases

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6
Q

cyclooxygenase (COX)

A

makes prostaglandins and thromboxanes

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7
Q

5-lipoxygenase

A

makes leukotrienes and lipoxins

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8
Q

5-, 12- and 15-lipoxygenases

A

make lipoxins

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9
Q

inflammatory signals and eicosanoids

A

inflammatory signals induce expression of COX-2
activate phopholipase A2 in many cell types
=> eicosanoid production at sites of inflammation

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10
Q

eicosanoids and pain

A

hyperalgesic - don’t produce pain directly, but increase tissue sensitivity to other stimuli

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11
Q

e-protaglandins

A

induce hyperalgesia via EP4

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12
Q

eicosanoids and edema

A

enhance the edema caused by bradykinin, histamine, adn teh C5a anaphylaatoxin

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13
Q

cox-2

A

makes prostaglandins

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14
Q

eicosanoids and immune response

A

contribute to leukocyte activation and chemostaxis

e.g.: LTB4 is chemotaxic for both T cells and PMNs

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15
Q

eicosanoids in asthma

A

cysteinyl leukotrienes induce abnormalities in asthma
eg cysLTs; LTC4; D4; E4
1: induce SM contraction and protracted bronchoconstriction
2: promote microvascular permeability, bronchovascular leakage, mucous secretion
3: promote leukocyte infiltration and production of proinflammatory cytokines

therefore 5-lipoxygenase inhibitors and leukotriene receptor anatagonists are effective anti-asthma drugs

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16
Q

inhibitors of eicosanoid production

A

NSAIDs
coxibs (COX2 inhibitors)
glucocorticoids

17
Q

things that counter inflammatory effects of leukotrienes

A

lipoxins, resolvins, protectins

18
Q

eicosanoids in platelet function (summary card)

A

1: thromboxane A2 released by platelets via COX-1 => stimulates platelet aggregation and vasoconstriction
2: prostacyclin produced by vascular endothelial cells via cox1 and cox2 inhibits platelet aggregation and causes vasodilation
3: aspirin inhibits cox1 and cox2 => impaired thromboxane production
4: endothelial cells, via synthesis of new cox 1 and cox2, can produce protacyclin once aspirin levels decline

19
Q

thromboxane A2

A

released by platelets via cox1

stimulates platelet aggregation and vasoconstriction

20
Q

prostacyclin (PGI2)

A

produced by vascular endotehlial cells via cox-1 and cox-2

inhibits platelet aggregation and causes vasodilation

21
Q

aspirin in platelet function

A

unlike other nsaids, aspirin irreversibly inhibits cox1 and cox2
anucleate platelets can’t make new Cox1, so thromboxane production impaired
once aspirin levels decline, endothelial cells can synthesize new cox1 and cox1 and make prostacyclin

22
Q

ductus arteriosus patency

A

maintained in the fetus by locally produced and circulating I and E prostaglandins

23
Q

indomethacin and ibuprofen on eicosanoids

A

can reduce blood flow through ductus arteriosus within 24 hours
eliminate need for surgery in many premature infants

24
Q

E and I protaglandins

A

reduce areterial blood pressure by direct vasodilator action on resistance vessels, modulation of norepi release, modulation of renal hormones

25
Q

atherogenesis

A

5-lipoxygenase gene polymorphisms are linked to coronary occlusion
omega-3 FA rich diet decreases cardiovascular disease = thromboxane B3 is inactive and PGI3 is active

26
Q

aspirin in cardiovascular physiology

A

low dose aspirin can reduce arterial thrombosis

27
Q

coxibs

A

cox-2 inhibitors

can increase thrombosis by selectively inhibiting prostocyclin but not thromboxane

28
Q

eicosanoids in reproductive physiology

A

1: PGE2 and PGF2 essential for follicular rupture
2: also induce cervical softening/dilation and uterine contractions
3: PGE2 induces penile erection
4: NSAIDs can prolong gestation and are sometimes effective in arresting premature labor
5: e-prostaglandins can be used for termination of both early and late pregnancies

29
Q

eicosanoids and renal physiology

A

1: PGI2 and PGE2 are normally low but are increased by angiotensis II, norepi and vasopressin
2: maintain renal blood flow through direct renal vasodilatory action
3: PGs antagonize hydroosmotic and vacular effects of ADH
4: I and E have positive role in baroreceptor induced renin release

30
Q

eicosanoids and the gut

A

PGE»PGA>PGI in decreasing acidity, stimulating bicarbonate and mucous secretion by epi cells, and protecting the gastric mucosa

31
Q

misoprostol

A

e prostaglandin analog
useful for protection against gastric ulcers in high-risk groups s.a. patients receiving NSAID therapy for arthritis and other inflammatory diseases

32
Q

NSAIDs and the gut and eicosanoids

A

inhibit PG ability to decrease acidity, stimulate bicarbonate and mucous secretion, and protect gastric mucosa
decrease frequency of colorectal polyps, but increase frequency of gastric ulcers

33
Q

TXA2 causes:

A

1: platelet aggregation (thrombosis formation)
2: vasoconstriction
3: bronchoconstriction
4: may promote atherosclerosis

34
Q

PGI2 causes:

A

1: antiaggregation (throbolysis)
2: vasodilation
3: coronary blood flow (patent ductus arteriosus)
4: GI protection

35
Q

PGE1, PGE2, PGF2alpha cause:

A

1: GI protection
2: hyperalgesia
3: cervical dilation
4: uterine contraction (high in dysmenorrhea)
5: fever
6: immune regulation
7: may reduce atherosclerosis
8: penile erection
9: vasodilation

36
Q

LTC4, LTD4, LTE4

A

1: increase vascular permeability
2: smooth muscle contraction
3: vasoconstriction
4: bronchoconstriction

37
Q

LTB4 causes

A

1: leukocyte chemotaxis
2: leukocyte adhesion
3: increase vascular permeability

endocrine term 2 quiz 2 - julia's notes (16 decks)

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