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PT2 Neuro 10-11 and Pain 1-4 > pain pharmacology > Flashcards

pain pharmacology Flashcards

1
Q

three major pathways in arachidonic acid metabolism

A

5-LOX
COX
CYP450
all iron containing

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2
Q

aracadonic acid is metabolized in what part of the COX enzyme

A

cyclooxygenase

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3
Q

parts of COX enzymes

A

peroxidase

cyclooxygenase

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4
Q

features of COX-1

A
  • expressed in most tissues
  • inhibition leads to renal and GI toxicity
  • not induced by cytokines
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5
Q

features of COX-2

A
  • expressed in low levels in most tissues

- highly induced by cytokines

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6
Q

prostacyclin (PGI2) is located where

A

endothelium
kidney
platelets
brain

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7
Q

thromboxane A2 (TxA2) is located where

A
  • platelets
  • vascular smooth muscle
  • macrophages
  • kidney
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8
Q

activation of prostacyclin causes

A
  • vasodilation

- declumping of platelets

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9
Q

activation of thromboxane causes

A
  • vasoconstriction

- platelet aggregation

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10
Q

analgesia effect

A

inhibition of prostanoid production which sensitize pain receptors

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11
Q

antiinflammatory effect

A

inhibit prostanoid synthesis at site of inflammation

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12
Q

antipyresis effect

A

inhibit prostanoid production in CNS

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13
Q

pyresis development process

A
  1. infection/inflammation
  2. leukocytes activated
  3. pyrogenic cytokines are released
  4. PGE2 is produced
  5. set point is elevated
    FEVER
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14
Q

most common AE of pain medications

A

gastric or intestinal ulceration

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15
Q

drugs that promote bleeding

A

aspirin and NSAIDs

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16
Q

renal effects of pain medication

A

-may result in hypertension by decreasing kidney blood flow and increasing water retention

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17
Q

COX2 hypothesis

A

COX-2 selective inhibitors will cause less GI AEs than nonselective COX inhibitors

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18
Q

COX-2 expression in colorectal cancer

A
  • higher expression

- NSAIDs thought to have benefit

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19
Q

COX enzyme with the larger active site

A

COX-2

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20
Q

COX enzyme associated with housekeeping

A

COX-1

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21
Q

prostaglandin G/H synthases also known as

A

cyclooxygenases

22
Q

aspirin MoA

A

unique

-acetylates proteins (a ser residue in COX)

23
Q

aspirin cardiovascular benefit

A

-reduces platelet aggregation via irreversible inhibition of COX-1 in platelets

24
Q

aspirin absorption

A
  • primarily in the small intestine

- peak concentrations 1-2 hrs

25
Q

aspirin distribution

A

highly protein bound

26
Q

aspirin metabolism

A

liver

27
Q

aspirin half life

A

low dose = 3-6 hrs

high dose = 15-30 hrs

28
Q

aspirin uricosuric effects

A
  • low dose = urate retention

- high dose = urate excretion

29
Q

salicylates general MoA

A

inhibit COX gene expression

30
Q

NSAIDs MoA

A

competitive inhibitors of arachidonate binding site

31
Q

diflunisal

A
  • salicylate
  • poor antipyretic because it can’t enter CNS
  • medium half life
32
Q

general NSAID AEs

A

-GI ulceration and bleeding

33
Q

general NSAID MoA

A

reversibly inhibit platelet aggregation

34
Q

NSAID distribution

A

highly protein bound, >90%

35
Q

ibuprofen

A
  • NSAID of choice due to low toxicity
  • CYP2C9 metabolism
  • short half life
36
Q

naproxen

A
  • NSAID of choice due to low toxicity

- long half life

37
Q

indomethacin

A
  • NSAID
  • drug of choice for gout
  • frequent AEs
  • short half life
38
Q

diclofenac

A
  • NSAID
  • available with misoprostol to reduce GI toxicity
  • short half life
39
Q

sulindac

A
  • NSAID
  • used in colorectal cancer
  • medium half life
40
Q

celecoxib

A
  • NSAID
  • COX-2 specific
  • used in colorectal cancer
  • long half life
41
Q

etodolac

A
  • NSAID
  • COX-2 specific
  • medium half life
42
Q

ketorolac

A
  • NSAID
  • as effective as opiates for pain
  • highest GI toxicity
  • medium half life
43
Q

problem with COX-2 specific drugs

A

high cardiovascular risk, MI, thrombosis

44
Q

indications for celecoxib

A
  • rhematoid arthritis

- osteoarthritis

45
Q

therapeutic effect of acetaminophen

A
  • antipyresis

- analgesia

46
Q

acetaminophen toxicity

A

hepatic failure

47
Q

acetaminophen primary site of action

A

CNS

48
Q

acetaminophen MoA

A

thought to be an electron acceptor in peroxidase of COX, which prevents the cyclooxygenase from being active

49
Q

acetaminophen distribution

A

to all fluids

not protein bound

50
Q

acetaminophen half life

A

1-4 hours

51
Q

acetaminophen combination with alochol

A

-alcohol upregulates PG2E1 which increases toxic metabolite production from acetaminophen

52
Q

other name for acetaminophen

A

paracetamol

PT2 Neuro 10-11 and Pain 1-4 (5 decks)

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