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MSK II Midterm > Fitzy: NSAIDS > Flashcards

Fitzy: NSAIDS Flashcards

1
Q

What cleaves phospholipids to make AA?

A

Phospholipids A2

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2
Q

What turns AA into PGH2?

A

COX

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3
Q

What turns PGH2 into the different PG’s that we know and love?

A

Tissue specific isomerases

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4
Q

Which PG is also know as prostacyclin?

A

PGI2

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5
Q

Where is PGFalpha and E2?

A

Uterus

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6
Q

What is a cox Independent toxicity of salicylate a and aspirin?

A
  • acid base disturbance
  • tinnitus
  • hypersensitivity
  • Reyes syndrome
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7
Q

What do we get if we take too much (20 gym) of aspirin?

A
  • early resp alkalosis
  • later metabolic acidosis, fever, dehydration
  • plus shock and coma
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8
Q

How do salicylate so makeour body think it’s in a hypoxic state?

A
  • salicylate a stop coupling of mitochondrial ox phone…. Lower ATP
  • body thinks it’s hypoxic….hyperventilation happens
  • blows off CO2, resp alkalosis… Kidney depletes bicarb
  • organic acids accumulate because ATP isn’t made in Rebs cycle anymore
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9
Q

Is Reye’s syndrome related to COX?

A

Nah

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10
Q

What drug do we give kids instead of aspirin?

A

Acetaminophen

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11
Q

What do NSAIDS block?

A

COX mediated formation of AA

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12
Q

What kind of inflammation do NSAIDs stop

A

LOCAL inflammation

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13
Q

Which COX has constitutive expression and has role in response to normal physiologic stimuli?

A

COX 1

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14
Q

How is COX2 different from 1?

A

This one gets INDUCED when it’s needed…. Usually pathological stimuli
-IL1,2, TNF

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15
Q

Which organ expresses both COX’s at the same time?

A

The kidney

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16
Q

What induces COX2 in inflammation?

A

Inflammatory cytokines

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17
Q

What do you not use NSAIDs for?

A
  • asthma
  • gut instinct inflammation
  • infectious inflammation fever… Paradox
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18
Q

Which drug inhibits COX 2 more so than COX 1?

A

Celecoxib

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19
Q

Whaich NSAID has the most COX 1 selectivity and is the only one that is parenteral?

A

Ketorolac

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20
Q

What is an important side effect of celecoxib due to its sulfonamide characteristics

A

Stevens-Johnson syndrome

  • if they have a sulfonamide allergy
  • skin looks red and hyperreactive
21
Q

What is more important, half life of cox or half life of aspirin?

A

Half life of cox trumps all

22
Q

Can platelets regenerate cox?

A

No, because they don’t have a nucleus

23
Q

What is a consequence of blocking PGE2?

A
  • inhibit inflammation

- but also inhibit normal gastric mucosa…. ulcers

24
Q

What is aspirin metabolize by?

A
  • liver
  • turns it into salicylate
  • so , high dose ASA is a pro-drug for anti=inflammatory doses of salicylate
25
Q

What was the big underlined thing that he had as a contraindication to salicylates and aspirin?

A

-Reye’s syndrome

26
Q

Describe the progression of aspirin/salivylate toxicity

A
  • they uncouple mitochondrial ox phos in CNS
  • resp venter thinks that means low ATP
  • hyperventilation happens so we can get more O2
  • drop in CO2 causes alkalosis… kidney depletion of bicarb
  • organic acids accumulate because ATP is no longer generated through the krebs cycle
  • Metabolic acidosis becomes life-threatening
27
Q

what is preferred over aspiring in children <19?

A
  • acetaminophen

- don’t want to give them Reye’s syndrome

28
Q

What are the traditional NSAIDs?

A
  • ibuprofen
  • naproxen
  • diclofenac
  • indomethacin
29
Q

What is the one Coxib?

A

-celecoxib

30
Q

What are the salicylates?

A
  • salicylate
  • diflunisal
  • aspirin
31
Q

What is the main step that NSAIDs and co. block?

A

-COX mediatd conversion of AA into PG

32
Q

difference between COX1 and COX2?

A
  • COX1 is constitutive: prominent role responding to physiological stimuli
  • COX2 is the induced kind…. prominent role responding to pathological stimuli
  • both of them are in the Kidney
33
Q

COX1’s role in inflammation?

A
  • inflammation stimulates AA release
  • COX1 converts AA into PGE2
  • PGE2 causes symptoms
34
Q

What will amplify the symptoms of inflammation?

A

-COX2 derived PGE2

35
Q

What does tNSAIDs mean?

A
  • traditional NSAIDS
  • Ibuprofen
  • Naproxen
  • Diclofenac
36
Q

Are salicylates and NSAIDs selective?

A
  • No!

- they inhibit both COX1 and 2

37
Q

When are NSAIDs contraindicated?

A
  • Asthma for sure
  • Gut inflammation
  • Infectious inflammation fever (paradox)
38
Q

Risks and complications of tNSAIDs?

A
  • Ulcer
  • Bleeding
  • Peripheral edema from high BP (b/c kidneys arent getting enough blood
39
Q

What is so great about COXibs?

A
  • selective inhibition of COX2 isoenzyme

- COX1 sparing

40
Q

Coxibs contraindications?

A
  • hypersensitivity to sulfonamides
  • Stevens-Johnson syndrome
  • toxic epidermal necrolysis
41
Q

What contraindication do we still have with Coxibs?

A

-peripheral edema because COX2 is still supposed to be doing things in the renal artery

42
Q

Is low dose aspirin anti inflammatory?

A

-no, but it is good for its anti thrombotic effects

43
Q

What is special about the cox inhibition from ASA?

A
  • it is irreversible!
  • COX inhibition persists days after ASA is metabolized and excreted
  • duration of action depends on cells’ ability/rate of COX regeneration
44
Q

What is more important, the half life of COX protein or half life of aspirin?

A

-t1/2 of COX protein trumps t1/2 of aspirin

45
Q

Why can’t platelets regenerate COX?

A

-because they don’t have a nucleus!

46
Q

MOA for aspirin at anti-inflammatory doses?

A
  • it’s a pro-drug… gets turned into salicylate which is a reversible COX inhibitor
  • but aspirin itself is an IRREVERSIBLE inhibitor because it acetylates COX… so the only way we can get COX function back after that is to make more of it!
47
Q

What does COX1 make that gives us increased risk for CV probs with coxibs?

A

-thromboxane!

48
Q

With the exception of aspirin, what do all NSAIDs have as of 2005?

A

-a black box warning for CV risks

49
Q

When should we avoid use of NSAIDs?

A

-pt’s with existing CV disease or risk factors for CV disease

MSK II Midterm (15 decks)

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