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My Pharmacology > Autocoids > Flashcards

Autocoids Flashcards

1
Q

Eicosanoids are synthesized in response to which kind of stimuli

A 
IgE reactions
inflmmmatory mediators
trauma
toxins
heat
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2
Q

Eicosanoids act via which method of signal tranduction

A

G-protein coupled receptors

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3
Q

Membrane phospholipds are broken down to arachidonic acids by which enzyme

A

phosphoplipase A2

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4
Q

What is the function of phosphoplipase A2

A

Breaks down membrane phospholipids into arachidonic acid

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5
Q

Which 2 enzymes break down arachidonic acid?

A

Cyclooxygenase

Lipoxygenase

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6
Q

The reaction of Cyclooxygenase and Lipoxygenase produces which 2 molecules

A

Endoperoxides and Hydroperoxides

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7
Q

Cyclooxygenase and Lipoxygenase act on which molecule

A

Arachidonic acid

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8
Q

Which inflammatory mediators are derived from Endoperoxides

A

Prostaglandins and thromboxane A2

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9
Q

Prostaglandins and thromboxane A2 is derived from which molecule directly

A

Endoperoxide

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10
Q

Which inflammatory mediators are derived from Hydroperoxides

A

Leukotrienes

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11
Q

Leukotrienes are derived from which molecule directly

A

Hydroperoxide

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12
Q

Which group of drugs inhibit phospholipase A2

A

glucocorticoids

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13
Q

Which group of drugs inhibit cyclooxygenase

A

NSAIDs

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14
Q

Which drugs is a selective inhibitor of COX 2

A

Celecoxib

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15
Q

Which drug is an inhibitor of lipoxygenase

A

Zileuton

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16
Q

Which drugs inhibits leukotrienes

A

Zafirlukast

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17
Q

What is the mechanism by which the drug Zafirlukast inhibits leukotrienes

A

It antagonizes the receptor for leukotrienes

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18
Q

Zileuton and Zafirlukast inhibits the production of leukotriene in the treatment of which condition

A

Asthma

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19
Q

What is the action of leuktrienes A4, C4 and D5

A

bronchoconstriction

vasodilation

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20
Q

Which product from endoperoxides are needed for platelet aggregation

A

Thromboaxane A2

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21
Q

A product of endoperoxides responsible for pain, swelling, fever and renal vasodilation

A

PGE2

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22
Q

Which prostaglandins are necessary for maintenance of GI mucosa

A

PGE2 and PGI2

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23
Q

Which cyclooxygenase is constitutively expressed

A

COX1

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24
Q

Which COX is necessary for protecting GI mucosa and platelet aggregation

A

COX1

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25
Q

Which COX is necessary for making the inflammatory prostaglandins

A

COX2

26
Q

Which COX is necessary for platelet stabilization

A

COX2

27
Q

COX2 aid in platelet stabilization by allowing the production of which arachidonic acid derivative

A

Prostaglandin I2 (prostacyclin)

28
Q

Another name for prostacyclin

A

Prostaglandin I2

29
Q

Misoprostol is the synthetic version of which arachidonic acid derivative

A

PGE1

30
Q

Which drug is an identical form of the naturally occurring PGE1

A

Alprostadil

31
Q

What is the contraindication of using Alprostadil during pregancy

A

Can cause uterine contraction

32
Q

What is misoprostol used for?

What is the mechanism of its action

A

Treat NSAID induced gastric ulcers

  • it is a synthetic version of PGE1, which maintains the gastric mucosa
33
Q

What are 2 uses of alprostadil?

What is the mechanism of its action

A

Maintains patency of ductus arteriosus
- it is identical to PGE1 which dilates vascular smooth muscle

Aids erectile dysfunction
-vasodilation

34
Q

Which drug is a version of PGE2 and what is it used for

A

DInoprestone

  • cervical ripening and abortifacient
35
Q

Carboprost is a version of which prostaglandin?

- what is its use

A

PGF2 alpha

- abortifacient

36
Q

Latanoprost is a version of which prostaglandin?

- what is its use

A

PGF2 alpha

-glaucoma by reducing intraocular pressure

37
Q

Which drug, that is a synthetic version of PGI2 is used to treat pulmonary hypertension

A

Epoprostenol

38
Q

Which 2 derivatives of endoperoxide have opposing effects on platelets

A

Thromboxane A2

PGI 2

39
Q

Thromboxane A2 works via which signal transduction pathway

A

Gq

40
Q

PGI 2 works via which signal transduction pathway

A

Gs

41
Q

Platelet stabilization is done by which prostaglandin

A

PGI 2

42
Q

Cyclooxygenases are irreversibly inhibited by which drug

A

Aspirin

43
Q

High does of aspirin has what effect on uric acid elimination

A

decreases tubular reabsorption which leads to uricosuria

44
Q

How is the occurrence of gout possible while taking low doses of aspirin

A

low doses of aspirin decreases renal tubular secretion of uric acid, leading to hyperurecemia

45
Q

What kind of respiratory acid/bases condition is seen in high vs. toxic doses of aspirin

why?

A

High does: respiratory alkalosis because it increases resp rate which lower pCO2

Toxic doses: respiratory acidosis because it inhibits the resp. center leading to high pCO2

46
Q

What is the underlying mechanism of gastritis seen in NSAID use

A

Inhibition of PGE2 which is needed to maintain the gastric mucosa

47
Q

What physical symptoms are seen in salicylism

A

tinnitus
vertigo
decreased hearing

48
Q

Why is bleeding time increased why on NSAIDs

A

Inhibition of COX1, leads to inhibition of thromboxane A2 production which is needed for platelet aggregation

49
Q

What is the triad seen in aspirin hypersensitivity

A

asthma
nasal polyps
rhinitis

50
Q

What clinical symptoms is seen when aspirin is taken with alcohol

A

GI bleeding

51
Q

How does aspirin affect the use of warfarin

A

Warfarin’s effect is increased (possible toxicity)

52
Q

How does aspirin affect the use of uricosurics

A

decreases its effect

53
Q

Three treatments for aspirin toxicity

A

Gastric lavage
activated charcoal
Alkalizing the urine (eg. sodium bicarb)

54
Q

What is the use of the drug ketorolac

A

analgesic

55
Q

What is the use of the drug indomethacin

-what is the mechanism of action

A

Closure of ductus arteriosus by inhibiting COX, so PGE2 cannot be made

56
Q

Why would increased serum creatine be seen in someone using an NSAID

A

NSAID inhibit the production of prostaglandins which vasodilate the afferent arteriole of the kidney

57
Q

What kind of drug is celecoxib

A

Selective COX 2 inhibitor

58
Q

Why would less antiplatelet action and less GI toxicity be seen in someone using celecoxib

A

Celecoxib is a COX2 inhibitor. COX1 is necessary for making PGE2 and TXA2 which re needed for GI mucosa and platelet aggregation respectively.

59
Q

Why is there an increased risk for MIs and stroke while on celecoxib

A

celecoxib is a COX2 inhibitor which is need to make PGI2 (prostacyclin) which stabilizes platelets

60
Q

This drug acts on CNS cyclooxygenases only

A

Acetaminophen

61
Q

How can chronic alcohol increase liver toxicity while on acetaminophen

A

Chronic use of ethanol enhances liver
toxicity via induction of P450, which results in formation of a reactive metabolite (N-acetylbenzoquinoneimine), usually inactivated by glutathione
(GSH). In overdose situations, the finite stores of GSH are depleted causing the metabolite to react even more with hepatocytes

62
Q

Which NSAID has the highest antithrombotic effect

A

aspirin

My Pharmacology (2 decks)

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