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Pharmacology > Management of pain and inflammation Part 2 > Flashcards

Management of pain and inflammation Part 2 Flashcards

1
Q

Nonopioid analgesions incluse

A

NSAIDs (nonsteroidal anti-inflammator drugs) and Acetaminophen

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2
Q

NSAIDs: primary effects

A

-analgesic
-anti inflammatory
-antipyretic (reduce fever)
-anticoagulant
-anticancer?
(NSAAAAAIDs)

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3
Q

OTC (over the counter) NSAIDs

A

aspirin, ibuprofen, naproxen, ketoprofen

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4
Q

prescription NSAIDs

A
  • Etodolac
  • Fenoprofen
  • Ketorolac
  • Meclofenamate
  • Piroxicam
  • etc.
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5
Q

OTC vs Rx: therapeutic differences?

A

not really if give same relative dose

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6
Q

OTC vs Rx: safety differences?

A

not really– related to dosage

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7
Q

OTC vs Rx: cost differences

A

OTC much cheaper

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8
Q

NSAIDs inhibit synthesis of

A

prostaglandins

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9
Q

lipid compounds produced in cells (usually when cell is injured)

A

prostaglandins

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10
Q

NSAIDs decrease prostaglandins by inhibiting

A

cyclooxygenase

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11
Q

NASIDs inhibit

A

cyclooxygenase enzyme (COX) (decreaes prostaglandin synthesis)

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12
Q

COX enxyme: 2 primary subtypes

A

1) COX-1

2) COX-2

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13
Q

COX-1 vs COX-2: normal constituent certain cells

A

COX-1

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14
Q

COX-1 vs COX-2:synthesizes PGs to protect cells, maintain function

A

COX-1

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15
Q

COX-1 vs COX-2: induced when cell is injured

A

COX-2

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16
Q

COX-1 vs COX-2:synthesizes PGs that mediate pain, inflammation

A

COX-2

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17
Q

COX-1 vs COX-2: ex= stomach, kidneys, platelets

A

COX-1

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18
Q

COX-1 vs COX-2: ex= RA, other pathologies

A

COX-2

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19
Q

COX-2 selective drugs inhibit …

A

synthesis of PGs in pain, inflammation

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20
Q

COX-2 selective drugs spare production of beneficial PGs in…

A

stomach, kidney, platelets

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21
Q

COX-2 selective drugs may decrease pain and inflammation with…

A

less toxicity

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22
Q

COX-2 selective drugs include

A

celecoxib (Celebrex)

23
Q

Evidence that COX-2 inhibitors promote ( )

A

infarction (heart attack, stroke)

24
Q

some ( ) more selective for COX-2

A

NSAIDs

25
Q

which NSAIDs are 5-50 times more selective for COX-2?

A
  • Diclofenac (voltaren)
  • Etodolac (lodine)
  • Meloxicam (mobic)
26
Q

why does COX-2 inhibition promote infarction:

A

normally there is balance b/w PGs that cause vasodilation/constriction…the drugs allow PGs that increase platelet activity and promote constriction to dominate

27
Q

acetaminophen effects

A

analgesic and antipyretic

28
Q

what effects does acetaminophen not have?

A

gastric irritation, anti-imflammatory, anticoagulant (peripheral effects)

29
Q

high doses of actaminophen lead to

A

liver toxicity

30
Q

actaminophen and opioid combos: tramadol + acetam

A

altraCET

31
Q

actaminophen and opioid combos: hyrocodone + acetam

A

lorTAB, lorCET, vidoden, detc.

32
Q

actaminophen and opioid combos: oxycodone + acetam

A

endoCET, roxiCET, primalev

33
Q

are NSAIDs the same as acetaminophen?

A

NO

34
Q

anti inflammatory: nonsteroidal

A

NSAIDs

35
Q

anti inflammatory: steroids

A

glucocorticoids

36
Q

NSAIDs inflammation: inhibit ( )

A

PG biosynthesis

37
Q

NSAIDs inflammation: anti-inflammatory higher or lower dosage than analgesisc?

A

higher

38
Q

NSAIDs inflammation: T/F: should be used continuously until inflammation is resolved

A

T (ex. dumping water on fire)

39
Q

glucocorticoids inflammation: powerful anti-inflammatory AND ( )

A

immunosuppressive effects

40
Q

common glucocorticoids

A

betamethasone, cortisone, dexamethasone, hydrocortisONE, praramethasONE, predinisolONE

41
Q

anti inflammatory effects: act on ( )

A

inflammatory cells (macrophages, leukocytes)

42
Q

anti inflammatory effects: drug binds to ( ) in cytoplasm

A

glucocorticoid receptor

43
Q

anti inflammatory effects: when drug-receptor travels to nucleus, it decreases…

A

expression of inflammatory proteins (cytokines, enzymes, etc)

44
Q

anti inflammatory effects: when drug-receptor travels to nucleus, increases…

A

expression of antiinflammaotry proteins

45
Q

administration methods: regular maintenance dose, dose packs

A

oral, systemic

46
Q

administration methods: intra-articular, 3-4 per year

A

injections

47
Q

administration methods: other

A

inhalation, topical, nasal, opthalmic, otic

48
Q

why would you use injection?

A

put drug right where you need it

49
Q

primary concern for anti-inflammatory steriods

A

catabolic effect on bone, muscle, ligament, tendon, skin (break down collagen in these tissues)

50
Q

other anti-inflammatory steroid side effects:

A

salt/water retention, increased infection, gastric ulcers, glucose intolerence, glaucoma…adrenal suppression (METABOLIC DYSFUNCTIONS)

51
Q

can we intervene with the primary problem?

A

yes, with resistance exercises and stuff

52
Q

how long is gap where body does not have adrenal hormones?

A

4-5 days

53
Q

glucocorticoids: adrenocortical shock

A

vascular collapse, severe hypotension, organ damage

54
Q

when can adrenocortical shock occur?

A

when GCs are suddenly discontinued

Pharmacology (2 decks)

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