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Pharm Test 2 > NSAIDS > Flashcards

NSAIDS Flashcards

1
Q

Aspirin

A

Aspirin

Salicylate

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2
Q

NSAIDs

A

Ibuprofen
Naproxen
Acetaminophen
Celecoxib

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3
Q

GI protective

A

Misoprostol

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4
Q

NSAIDs treat :

A

SYMPTOMS only

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5
Q

NSAIDS block

A

Cyclooxygenase pathway to make prostaglandins

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6
Q

Eicosanoids

A

*bind to receptors on cell membrane
*From AA (omega6)
Prostaglandins, thromboxanes, leukotrienes
*short half life

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7
Q

COX -1

A
  • constitutive expression
  • housekeeping
  • inhibition - GI side effects
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8
Q

COX- 2

A
  • induced
  • renal problems w/ inhibition - renal perfusion down
  • make prostanoids at inflammation sites (cancer)
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9
Q

What can be liberated during stress?

A

EPA, AA

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10
Q

PGE2 does…

A
  • Up body temp
  • inflammation
  • protective against peptic ulcer
  • less platelet function
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11
Q

TXA2 does

A
  • UP Platelet agregation from COX -1 (in platelets)

* Vasoconstriction/Bronchoconstriction

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12
Q

Arachidonic Acid Pathway

A

Stimulus –> phospholipase A2 –> Phospholipids –> arachidonic acid –> Eicosanoids

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13
Q

Phospholipase A2

Key step in inflammatory pathway

A

Phospholipase A2 –> hydrolyze fatty acids in cell membrane INNER layer

  • Arachidonic Acid (AA)=Omega6
  • Eicosapentaeoic Acid (EPA)=Omega3
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14
Q

Prostanoids

how synthesized?

A

From isomerases/transferases

  • Platelets = TXA2 (from Cox 1)
  • Activated Macrophages = TXA2/PGE2 (from Cox 2)
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15
Q

PGI2

A
  • made from vascular epithelium
  • LOWER platelet aggregation
  • Vasodilation
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16
Q

NSAIDs inhibit Cox 1 + 2

A

Aspirin
Ibuprofen
Naproxen
Piroxicam

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17
Q

NSAIDs inhibit COX-2

A

Celecoxib (CV risk)

*Less GI toxicity

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18
Q

NSAID

Excretion?

A

Renal

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19
Q

NSAID

Type of inhibition

A

*Reversible competitive inhibitor of Cox 1 + 2
(Not like aspirin!-irreversible)
*inhibit prostaglandin synthesis

20
Q

NSAIDs

Tx effects

A

Low dose -

  • Analgesia
  • Antipyretic

High dose -

  • anti-inflammatory
  • close patent ductus arteriosus
21
Q

Anti inflammatory dose

A

Ibuprofen - 400-800mg 6-8hr

Aspirin - 4-5g per day

22
Q

How possibly can Nsaid protect from cancer?

A

Cox-2 inhibition, stopping constant inflammation

23
Q

NSAID

S.E.

A
  • GI - aspirin more
  • renal - less clearance, proteinuria, analgesic nephropathy (w/ UTIs)
  • NO w/ pregnant! (Acetaminophen OK)
24
Q

NSAID drug interactions

A
  • Ibuprofen impairs aspirin’s ability to acetylate COX

* NO w/ ace inhibitor

25
Q

How is aspirin special?

A

IRREVERSIBLE cox 1 + 2 inhibitor

26
Q

Aspirin

Uses

A
  • analgesic
  • antipyretic
  • anti-inflammatory (irreversible inhibition of cox 1 + 2)

*cardio (low dose = less platelet clumping). (TXA2 inhibited!)

27
Q

Aspirin metabolized in liver to

A

Salicylate ! (Reversible competitive COX inhibitor)

*PCT/glomerular filtration excretion

28
Q

Aspirin

S.E.

A 
SAME AS all
*gi 
*renal - analgesic neuropathy, less perfusion
*less urate excretion - low dose
More urate excreation - high doses
*hypersensitivity (all NSAIDs)
29
Q

Aspirin

Toxicity

A

Tinnitus
Respiratory/met acidosis
(Alkalosis at normal levels)

30
Q

Ibuprofen

Half life

A

Short 2h, take frequently

31
Q

Ibuprofen w/ aspirin?

A

Lower cardioprotective effects

32
Q

Naproxen

A

Half life 14 hrs

*rheumatoid arthritis, etc.

33
Q

Celecoxib

A
  • Only Cox 2 inhibitor
  • HTN /thrombosis risk- not in HF/CVA patients
  • sulfa-sensitve
34
Q

Mechanical damage - inflammatory response cascade

A

PHOSPHOLIPASE A2 - activates to hydrolize fatty acids on INNER LAYER of cell membrane to make AA + EA

34
Q

Prostanoids

A

Synthesized due to COX 1 + 2

Certain cells have certain Prostanoids

34
Q

EPA + AA metabolized into what ecosanoids?

A
  • EPA - 3 ecosanoids

* AA - 6 ecosanoids (more potent)

34
Q

Eicosanoid functions

A
  • Vasodilation
  • Bronchoconstriction
  • PGI2-LESS platelet aggregation
  • Thomboxane- MORE platelet aggregation
35
Q

w-3 Fatty acids lessen inflammation by

A

1) less AA to make w-6
2) compete with AA for COX,LipoOX
3) compete with w-6 for receptors

36
Q

NSAIDs inhibit

37
Q

PGI2 does…

A
  • from vascular epithelium

* LESS platelet aggregation

38
Q

Aspirin Allergy

A
  • Often w/ nasal polyp people

* Cross with ALL NSAIDs

39
Q

How does Cox 2 inhibitor UP CV risk?

A

COX-2 inhibit –>up PGI2 –> LESS platelet aggregation. JUST FUCKING REVIEW THIS SLIDE

40
Q

GI protective agent to add to Aspirin/NSAIDS

A

Misoprostol

  • PGE1-like - stop acid secretion, stop peptic ulcer
  • PREGGER! +Mifepristone - terminate early
41
Q

Acetaminophen

A

Oral, iv
NO ANTI-INFLAMMATORY

Large dose - liver toxic, glucorination+sulfation saturated, no excretion

42
Q

Acetaminophen toxicity

A

CYP2E1 induction

43
Q

Acetaminophen OD Tx

A

Mucomyst

N-acetylcystein

Pharm Test 2 (13 decks)

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