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Skin & MSK > Pharmacologic inhibition of prostaglandin synthesis > Flashcards

Pharmacologic inhibition of prostaglandin synthesis Flashcards

1
Q

Prostaglandins modulate this, the detection of stimuli associated to perception of pain

A

Nociception

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2
Q

Prostaglandins are ligands to this

A

GPCR

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3
Q

Prostaglandins are derived from this

A

Membrane lipids

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4
Q

Prostaglandin that maintains a patent ductus arteriosus during pregnancy

A

PGE2

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5
Q

2 prostaglandins that stimulate mucus secretion and decrease acid production in the GI

A

PGE2 and PGI2

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6
Q

Enzyme that converts membrane phospholipids to arachidonic acid

A

Phospholipase A2

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7
Q

Enzyme that converts arachidonic acid to leukotrienes

A

5-lipoxygenase

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8
Q

Enzyme that converts arachidonic acid to prostaglandin G

A

COX1/2

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9
Q

Enzyme that converts prostaglandin G to prostaglandin H2

A

Peroxidase

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10
Q

In the prostaglandin synthesis pathway, what reaction does phospholipase A2 catalyze?

A

Membrane phospholipids to arachidonic acid

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11
Q

In the prostaglandin synthesis pathway, what reaction does 5-lipoxygenase catalyze?

A

Arachidonic acid to leukotrienes

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12
Q

In the prostaglandin synthesis pathway, what reaction does COX1/2 catalyze?

A

Arachidonic acid to Prostaglandin G

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13
Q

In the prostaglandin synthesis pathway, what reaction does peroxidase catalyze?

A

Prostaglandin G to Prostaglandin H2

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14
Q

NSAIDs inhibit this enzyme

A

Cyclooxygenase enzymes involved in prostaglandin and thromoxane synthesis

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15
Q

Cyclooxygenase enzyme that is mostly constitutive expressed

A

COX-1

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16
Q

Cyclooxygenase enzyme that has inducible expression

A

COX-2

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17
Q

Does COX-1 have inducible or constitutive expression?

A

Mostly constitutive

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18
Q

Does COX-2 have inducible or constitutive expression?

A

Inducible

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19
Q

Therapeutic prostaglandin inhibition has this effect on hypothalamus set point temperature

A

Decreases, lowers fever

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20
Q

Therapeutic prostaglandin inhibition has this effect on peripheral pain receptor activation

A

Blocks it, induces analgesia

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21
Q

Therapeutic prostaglandin inhibition has this effect on inflammation

A

Blocks inflammatory vasodilation, decreasing inflammation

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22
Q

Therapeutic prostaglandin inhibition blocks production of this molecule, thus decreasing platelet aggregation

A

Thromboxane A2

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23
Q

Prostaglandin that promotes platelet adhesion and clot formation

A

Thromboxane A2

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24
Q

What is the MOA for non-aspirin (traditional) NSAIDs

A

Reversible inhibitors of COX-1 and COX-2

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25
Q

All NSAIDs except this are associated with increased risk of cardiovascular effects

A

Naproxen

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26
Q

Naproxen is this exception to NSAIDs

A

Is not associated with increased risk of cardiovascular effects

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27
Q

Naproxen is the only NSAID that is not associated with increased risk of this

A

cardiovascular effects

28
Q

These are reversible inhibitors of COX-1 and COX-2

A

Non-aspirin (traditional) NSAIDs

29
Q

Inhibition of constitutive prostaglandins reduces these in the GI

A

Cyto-protective prostaglandins

30
Q

Inhibition of constitutive prostaglandins reduces prostaglandins that control this blood flow

31
Q

This irreversibly inhibits COX-1 and COX-2 prostaglandin H2 synthesis and function

A

Aspirin (acetylsalicyclic acid)

32
Q

What is the MOA of aspirin (acetylsalicylic acid)?

A

Irreversibly inhibits COX-1 and COX-2 prostaglandin H2 synthesis and function
(acetylates serine in COX, blocks substrate processing)

33
Q

Acetylsalicylic acid is another name for this drug

34
Q

Aspirin irreversibly inhibits COX-1 and COX-2 synthesis and function of this

A

Prostaglandin H2

35
Q

Aspirin acetylates this in COX, blocking substrate processing

36
Q

This acetylates serine in COX, blocking substrate processing

A

Aspirin (acetylsalicyclic acid)

37
Q

Samter’s triad is another name for this

A

Aspirin-exacerbated respiratory disease (AERD)

38
Q

Aspirin-exacerbated respiratory disease (AERD) is associated with this triad of conditions

A

Asthma, nasal polyposis, and rhinitis

39
Q

Samter’s triad of asthma, nasal polyposis and rhinitis are associated with increased sensitivity to this

40
Q

Toxicity to this drug can cause signs of intoxication (nausea, vomiting, dizziness) and tinnitus/decreased hearing

41
Q

Tinnitus and decreased hearing can occur with use of this drug

42
Q

What is salicylism?

A

Nausea, vomiting, dizziness, tinnitus/decreased hearing that are toxicities to aspirin

43
Q

All NSAIDs have block box warning of increased risk of these adverse effects

A

Cardiovascular and GI

44
Q

This type of drug can induce premature closure of ductus arteriosus

45
Q

NSAIDs can induce premature closure of this

A

Ductus arteriosus

46
Q

COX-2 inhibitor that is used in patients at high risk for GI ulceration

A

Celecoxib (Celebrex)

47
Q

What is Celecoxib (Celebrex)?

A

COX-2 inhibitor that is limited to use in patients at high risk for GI ulceration

48
Q

Celecoxib (Celebrex) inhibits this

49
Q

Celecoxib (Celebrex) is limited to NSAID indication in patients at high risk for this

A

GI ulceration

50
Q

Drug whose use is limited to NSAID indication in patients at high risk for GI ulceration

A

Celecoxib (Celebrex)

51
Q

Drug that is a COX-2 inhibitor

A

Celecoxib (Celebrex)

52
Q

Proposed MOA of this is central inhibition of COX1/2

A

Acetaminophen

53
Q

Acetaminophen limited effect on this explains lack of anti-inflammatory action

A

Peripheral COX enzyme

54
Q

Does Acetaminophen have anti-inflammatory action?

A

No
Has limited effect on peripheral COX enzyme

55
Q

Does Acetaminophen have an effect on platelet aggregation?

56
Q

What is the proposed MOA of Acetaminophen?

A

Central inhibition of COX1/2

57
Q

Overdose of this can deplete glutathione, resulting in free NAPQI that damages the liver

A

Acetaminophen

58
Q

Acetaminophen overdose can deplete this, resulting in free NAPQI that damages the liver

A

Glutathione

59
Q

Acetaminophen overdose can deplete glutathione, resulting in this that damages the liver

60
Q

Glutathione precursor that is an antidote to Acetaminophen overdose

A

N-acetylcysteine (NAC)

61
Q

N-acetylcysteine (NAC) is a precursor to this

A

Glutathione

62
Q

N-acetylcysteine (NAC) is an antidote used in overdose of this

A

Acetaminophen

63
Q

N-acetylcysteine (NAC) antidote is most effective when used in this timeframe of acetaminophen overdose

A

within 10 hours

64
Q

What is the cumulative daily dosing limit of Acetaminophen?

A

4g/day
Lowered with existing liver disease or with alcohol use

65
Q

Only prostaglandin synthesis inhibitor that is used to reduce fever and pain only, not inflammation

A

Acetaminophen

66
Q

Prostaglandin synthesis inhibitor that is very toxic to children, and triggers leukotriene-triggered asthma in some patients

Skin & MSK (32 decks)

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