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Unit 4 > Eicosanoids > Flashcards

Eicosanoids Flashcards

1
Q

How is eicosanoids produced and released? and what do they make?

A

Membrane phospholipids—(phospholipase A2)—>arachidonic acid
—-(lipooxygenase)—>leukotriene
or —(COX)—>prostaglandins or thromboxane A2

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2
Q

What condition does leukotrienes have a major role in?

A

Asthma (drug looking to stop the action or production of leukotrienes to treat asthma)

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3
Q

Which COX is constitutive and inducible? and what drugs inhibit them?

A

COX1—>constitutive
COX2—>inducible during inflammation
NISAIDs block both COX1/2
“-coxib” drug blocks ONLY COX2

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4
Q

What is glucocorticoid’s role in eicosanoids production?

A

It inhibits phospholipase A2 and COX2

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5
Q

How might NISAIDs exacerbate asthma?

A

Blocking COX activity—->increase leukotriene production—>exacerbate asthma

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6
Q

What is PGs role in PDA/renal vasculature/stomach/uterus?

A

PDA—>maintain PDA
Renal vasculature—>vessel dilate afferent arteriole
Stomach—>decrease acid production
Uterus—>contraction

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7
Q

What are the roles of LTA4/C4/D4?

A

Anaphylaxis and bronchoconstriction

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8
Q

What drug inhibit lipooxygenase? and what is it used for?

A

Zileuton/asthma

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9
Q

What drugs block LT receptor? and what are they used for?

A

“-lukasts”—>for asthma

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10
Q

Where is COX1/2 expressed?

A

COX1—>everywhere

COX2—->brain/kidney/site of inflammation

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11
Q

What are the PGE1 analogs?

A

Misoprostol—>NSAIDs inducer ulcer

Alprostadil—>keep PDA open/male impotence (alternative to the”-fils”)

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12
Q

What is dinoprostone/carboprost/latanoprost used for?

A

Dinoprostone—>PGE2 analog—>uterus contraction—>induce labor
Carboprost—>PGF2alpha analog—>uterus contraction—>abortion
Latanoprost—>increase drainage—>glaucoma

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13
Q

What is a PGI2 analog and what is it used for? what other drugs can be used for the same condition?

A

Epoprostenol—>vasodilator/inhibit platelet aggregation–>used for pul HTN
Pul HTN—>bosentan/sildenafil

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14
Q

Why do we use baby aspirin after MI?

A

Aspirin stop TXA2 production—>inhibit platelet aggregation

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15
Q

What are the effects of NSAIDs? and what is the prototype?

A

Analgesic/antipyretic/anti inflammatory/antiplatelet

Aspirin

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16
Q

How is aspirin irreversibly inhibit COX?

A

Covalent bond via acetylation of serine hydroxyl group near active site

17
Q

How is aspirin dose dependent?

A

Low dose—>antiplatelet (81mg)
Moderate dose—>analgesia and antipyresis (650mg)
High dose—>anti inflammatory (up to 4000mg)

18
Q

What is the side effect with low to moderate dose of aspirin and what other drugs have the same effect? what about high dose?

A

Hyperuricemia—>same with loop and thiazide—>gout

High dose side effect—>uricosuria/respiratory alkalosis

19
Q

What do you see with aspirin overdose?

A

Hearing problem—>first sign
Inhibit respiration—>respiratory acidosis—>respiratory failure
Inhibit Krebs cycle—>shut down ATP production—>metabolic acidosis
Hyperthermia and hypokalemia

20
Q

What is Reye syndrome and when do you see it?

A

Kids with viral illness taking aspirin—> vomiting/fever/lethargy

21
Q

What is the drug interaction with aspirin?

A

Ethanol increase risk of GI bleed with aspirin

22
Q

How do we manage aspirin overdose?

A

Right after ingestion—>gastric lavage or activated charcoal
Hours after ingestion—>alkalinize urine/dialysis

23
Q

What are some other NSAIDs besides aspirin? and do they cause acid base imbalance and hyperuricemia like aspirin?

A

Ibuprofen/naproxen/indomethacin/ketorolac (pain management)/sulindac
Nah

24
Q

Which NSAIDs is the strongest and weakest analgesic?

A

Ketorolac

Aspirin

25
Q

Which NSAIDs have side effect of bone marrow suppression? and which with Stevens-Jonhson syndrome?

A

Indomethacin

Sulindac

26
Q

What are the benefits and adverse effects of Celecoxib?

A

Benefit—>no effect on COX1—>less GI side effect

Adverse effect—>pro thrombotic—>MI and stroke

27
Q

All NSAIDs increase risk for MI and stroke, except ?

28
Q

How is acetaminophen difference from aspirin?

A

Acetaminophen has only analgesic and antipyretic effect/work via CNS/no peripheral effect

29
Q

What does acetaminophen overdose cause? and how does it happen?

A

Hepatotoxicity
Acetaminophen is degraded through glucuronidation (major pathway) and P450 (minor)
Acetaminophen—(P450)—>NAPQI (toxic to the liver)

30
Q

How does N-acetylcysteine work as an antidote for acetaminophen? and when do you have to give this drug?

A

It supply SH group to inactivate NAPQI

Within the first 12 hours

31
Q

P450 inducer or inhibitor would worsen the toxicity of acetaminophen?

A

Inducer like alcohol

Unit 4 (28 decks)

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