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Kaplan: Drugs for Inflammatory and Related Disorders > Eicosanoid Pharmacology > Flashcards

Eicosanoid Pharmacology Flashcards

1
Q

Be able to draw out the eicosanoid pathway along with drugs blocking each step.

A
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2
Q

Which COX has constitutive action and which is inducible?

A

COX1 constitutive action
COX 2 inducible

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3
Q

LTB4 action?

A

inflammatory mediator > neutrophil and chemoattractant; activates PMNs; inc free radical formation > cell damage

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4
Q

LTA4, LTC4, and LTD4 effects?

A

cause anaphylaxis and bronchoconstriction (role in asthma)

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5
Q

Where is COX 1 primarily found in the body?

A

most tissues, including platelets and stomach where acts to synthesize thromboxane and cytoprotective prostaglandins, respectively

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6
Q

Where is COX 2 primarily found in the body?

A

the brain and kidney and at sites of inlammation

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7
Q

What are some PGE1 drugs?

A

misoprostol, alprostadil

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8
Q

Indication of alprostadil?

A

maintains patency ductus arteriosus

vasodilation; used in male impotence

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9
Q

In what conditions are misoprostol and alprostadil contraindicated in?

A

contraindicated in pregnancy, unless used as abortifacient

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10
Q

Name a PGE2 analog drug that is used for cervical ripening and as an abortifacient?

A

dinoprostone

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11
Q

Name a PGF2a drug/s?

A

carboprost
latanoprost

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12
Q

Carboprost indication?

A

abortifacient

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13
Q

MOA PGF2a drugs?

A

uterine and bronchiolar smooth muscle contraction

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14
Q

PGI2 analog drug name?

A

PGI2 (prostacyclin)

epoprostenol

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15
Q

Indication for epoprostenol?

A

pulmonary HTN

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16
Q

PGE2 and PGF2 stimulation have what effects on the body?

A

both inc. in primary dysmenorrhea

17
Q

What is the function of TXA2?

A

platelet aggregator

18
Q

TXA2 is coupled to what pathway. Explain how this may lead to its effects?

A

IP3 DAG

activation of TxA2 receptors> stimulation of phospholipase C > PIP2 hydrolysis > inc IP3 > mobilization of bound Ca2+ > free Ca2 > plt. aggregation

19
Q

Describe how activation of PGI2 receptors affect platelets and the pathway taken.

A

activation of PGI2 receptors> stimulation of adenylyl cyclase > inc. cAMP > inc. activity of internal Ca2+ “pumps” > dec free Ca2+ > plt stabilization

20
Q

Does aspirin cause irreversible or reversible inhibition of COX?

A

irreversible

21
Q

In low doses what is the main benefit of aspirin use?

A

anti platelet aggregation

22
Q

In moderate doses what is the main benefit of aspirin use?

A

analgesia and antipyresis

23
Q

At high doses what is the major benefit to using aspirin?

A

anti-inflammatory effects

24
Q

List some S/E of aspirin use? (List 5)

A
  • Gi irritation: gastritis, ulcers, bleeding
  • salicylism: tinnitus, vertigo, dec. hearing - often first signs of toxicity
  • bronchoconstriction: exacerbation of asthma
  • hypersensitivity, especially the “triad” of asthma, nasal polyps, rhinitis
  • Reye syndrome: encephalopathy
  • inc. bleeding time (antiplatelet)
  • chronic use: associated with renal dysfunction
25
Q

What are some drug interactions to be aware of when using aspirin?

A

ethanol (inc. GI bleeding,) warfarin (^ effects), and uricosurics (dec effects)

26
Q

What are some reversible inhibitors of COX 1 and COX 2 with analgesic, antipyretic, and anti-inflammatory action?

A

Ibuprofen, Naproxen, Indomethacin, Ketorlac, Sulindac

27
Q

NSAIDs (other than aspirin) are associated with an increased risk of what adverse events?

A

adverse CVS thrombotic events such as MI and stroke

28
Q

Which NSAID has the most analgesic efffect?

A

ketorlac

29
Q

How can NSAIDs affect the renal system?

A

chronic use may cause nephritis, nephritic syndrome, acute failure (via dec. formation of PGE2 and PGI2, which normally maintain GFR and RBF) does not occur with sulindac

30
Q

Sulindac toxicities?

A

SJS, hematotoxicity

31
Q

Indomethacin toxicity?

A

thrombocytopenia, agranulocytosis, and > CNS effects

32
Q

What is the primary difference between Celecoxib and the other antiinflammatory agents?

A

Selective COX 2 inhibitor

less GI toxicity
less antiplatelet action

33
Q

Acetaminophen MOA?

A

inhibition of COX but not in peripheral tissues

34
Q

Describe the properties of acetaminophen compared to ASA?

A

equivalent analgesic and antipyretic activity but lacks significant antiinflammatory effects

no antiplatelet action

not implicated in Reye syndrome

No effect on uric acid

not bronchospastic (safe in NASID hypersensitivity and asthmatics

GI distress is minimal

35
Q

When should you preferable take NAC after toxic doses of Tylenol?

A

within first 12 hours

36
Q

Does indomethacin close or maintain patency of ductus arteriosus?

A

it closes it

Kaplan: Drugs for Inflammatory and Related Disorders (8 decks)

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