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Pharmacology > NSAIDS > Flashcards

NSAIDS Flashcards

1
Q

NSAIDs Funtion?

A

Treat inflammation, pain & fever

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2
Q

NSAIDS MOA?

A

Inhibition of the enzyme cyclooxygenase (COX).

Cyclooxygenase is required to convert arachidonic acid into thromboxanes, prostaglandins, and prostacyclins.[9] The therapeutic effects of NSAIDs are attributed to the lack of these eicosanoids.

↓ production of prostaglandins → ↓inflammation, relieve pain,
↓fever

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3
Q

Inflammation process?

A
  1. Membrane Phospholipids.
  2. Phospholipase A2
  3. Arachnoic Acid
  4. Cyclooxygenase(COX)
  5. COX 1 & COX 2
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4
Q

COX-1 Function

A
  1. Increase GIT integrity/mucous lining(PGE2)
    2.Promotes pain, inflammation and pain
  2. Thromboxane(TXA2)-promotes clotting aggregation and thus increase in bleeding time
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5
Q

COX-1 Inhibition

A

Peptic Ulcers and GI Bleeding

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6
Q

COX-2 Function?

A
  1. Promote pain, fever and inflammation
  2. Increased in synovial fluid
  3. Reduces platelet aggregation
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7
Q

COX and prostaglandins ?

A

COX-1: Prostaglandins E29(PGE2)
COX-2:Prostacyclin(PGI2)

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8
Q

Classes of NSAIDs?

A
  1. Irreversible COX inhibitors (Aspirin)
  2. Reversible COX inhibitors (non‐aspirin NSAIDs):
    A) Non‐selective COX inhibitors (e.g. Ibuprofen)
    B) Selective COX‐2 inhibitors (e.g. Celecoxib)
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9
Q

Irreversible COX inhibitors drug?

A

Aspirin(acetylsalicylic acid; ASA)

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10
Q

Aspirin MOA?

A

*Irreversible inhibitor of COX‐1 & COX‐2
-Higher afffinity fro COX-1
*Taken orally

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11
Q

Aspirin MOA antiplatlet?

A

MOA (antiplatelet): (‐) COX‐1 in platelets → ↓producƟon of thromboxane
A2 (platelet acƟvator) → (‐) platelet production of new COX‐1; new
platelets → COX‐1 enzymes → ↑bleeding Ɵme (w/o affecting PT)

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12
Q

Aspirin is non-selective fro COX but which Cox does it have a higher affinity for?

A

COX-1

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13
Q

Aspirin MOA anti-inflammatory MOA?

A

MOA (anti‐inflammatory): in liver; metabolised into salicylate (anti‐
inflammatory; no antiplatelet effect); (‐) COX‐2 →↓prostaglandin
producƟon → ↓inflammaƟon, pain, fever.

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14
Q

Aspirin I?

A

I: headaches, musculoskeletal pain; short term Tx of chronic pain (e.g.
osteoarthritis, rheumatoid arthritis)

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15
Q

Aspirin Doses and effects?

A

Dose‐dependent effects

Low doses: antiplatelet effect
High doses: Dose‐dependent effects (<300 mg/day, antiplatelet; 300‐2400 mg/day,
antipyretic & analgesic; >2400 mg/day, anti‐inflammatory) & analgesic; >2400 mg/day, anti‐inflammatory)

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16
Q

Aspirin CI?

A

aspirin‐associated hypersensitivity
bleeding GI ulcers
hemolytic
anemia
hemophilia
hemorrhoids,
Lactation
UC
asthma
chronic diarrhea

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17
Q

Aspirin AE?

A

ASPIRIN

Allergy like reactions
Susceptibility to bleeding
Peptic Ulcer
Idiosyncratic reactions
Reye’s Syndrome
rIing in ear(Tinititus)
Nephtopathy

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18
Q

NSAIDS CI?

A

BARS

Bleeding
Asthma
Renal Disease
Stomach(Peptic Ulcer)

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19
Q

Aspirin Kinetics?

M&E

A

Kinetics: A=80‐100%
D=90‐95% protein‐bound
M=liver
E=urine (80‐100%), sweat, saliva, feces

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20
Q

Effects of Inhibtion of NSAIDS?

A

5A’s

Analgesia
Antipyretic
Anti-inflammatory
Antithrombotic
Arteriosis

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21
Q

Non-selective COX-Inhibitors?

A
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22
Q

Reversible COX inhibitors admin?

A

Orally

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23
Q

Which Reversible COX inhibitors is taken rectaly?

A

indomethacin

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24
Q

Which Reversible COX inhibitors is taken as eye-drops only?

A

ketorolac(eye drops), phenazone(ear drops only)

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25
Q

Non‐selective COX inhibitors:
MOA?

A

Reversibly (‐) COX‐1 (→ ↓producƟon of thromboxane A2 → (‐)
platelet aggregation; transient) & COX‐2 (→↓prostaglandin producƟon →
↓inflammaƟon, pain, fever)

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26
Q

Ibuprofen I?

A

Analgesia, inflammation (high dose required for anti‐inflammatory
action), ductus arteriosus in premature new‐born infants (IV prep.)

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27
Q

Ibuprofen CI?

A

hypersensitivity to aspirin/other NSAIDs active peptic ulceration
pregnancy (3rd trim.)
proctitis/haemorrhoids (suppositories)

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28
Q

Ibuprofen AE?

A

epigastric pain, heartburn, dizziness, nausea, rash, tinnitus

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29
Q

Ibuprofen Kinetics?

A, D, M & E

A

Kinetics:
A=rapid (85%) reduced by food; bioav. 80‐100%; onset30‐60
min; duration4‐6 hr
D=90‐99% protein‐bound
M=rapidly in liver by
CYP2C9; CYP2C19 substrate, E= t 1/22‐4 hr (adults); 1.6 hr (child 0.25‐1 yr)

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30
Q

Naproxen I?

A

Analgesia & inflammation in rheumatic disease, gout, dysmenorrhea

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31
Q

Analgesia?
Antipyretic?
Anti-inflammatory?
Antithrombotic?
Arteriosus?

A

Analgesia: Inability to feel pain
Antipyretic: used to prevent or reduce fever
Anti-inflammatory: used to prevent inflammation
Arteriosus:

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32
Q

Naproxen CI?

A

hypersensitivity to aspirin/other NSAIDs, active peptic ulceration,
pregnancy (3rd trim.), proctitis/haemorrhoids

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33
Q

Naproxen A/E?

A

epigastric pain, peptic ulceration, headache, dizziness, rash, tinnitus,
nephrotoxicity, hepatic dysfunction

34
Q

Naproxen kinetics?

M, D & E

A

A= rapid oral; bioav. 95%; onset30‐60 min; duration<12 hr,
D=99% protein‐bound
M=in liver via conjugation
E= t 1/212‐15 hr; 95% in
urine as metabolites

35
Q

Diclofenac I?

A

pain & inflammation in rheumatic disease, gout

36
Q

Diclofenac CI?

A

hypersensitivity to aspirin/other NSAIDs, active peptic ulceration,
pregnancy (3rd trim.), proctitis/haemorrhoids (suppositories)

37
Q

Diclofenac A/E?

A

epigastric pain, peptic ulceration, headache, dizziness, rash, tinnitus,
nephrotoxicity, hepatic dysfunction

38
Q

Diclofenac Kinetics?

A, D, M & E

A

A=absolute bioav. 55%
D=diffuses into/out of synovial fluid; 99%
protein‐bound
M=in liver via glucuronidation
E= t 1/212‐15 hr; in bile

39
Q

Indomethacin I?

A

pain & inflammation in rheumatological disorders

40
Q

Indomethacin CI?

A

hypersensitivity to aspirin/other NSAIDs, active peptic ulceration,
pregnancy (3rd trim.), proctitis/haemorrhoids (suppositories)

41
Q

Indomethacin A/E?

A

as for diclofenac (more than diclofenac on GI), dizziness, drowsiness,
headaches, retinal disturbances (prolonged use)

42
Q

Indomethacin Kinetics?

A, D, M & E

A

A= bioav. 100%; onset30 min; duration4‐6 hr
D=99% protein‐bound
M=in liver
E= t 1/24.5 hr; 60% in urine; >33% in feces

43
Q

Ketorolac I?

A

short‐term management of moderate postoperative pain

44
Q

Ketorolac CI?

A

duration >5 days, chronic pain, hypersensitivity to NSAIDs, PUD

45
Q

Ketorolac A/E?

A

dizziness, drowsiness, headaches, GI pain, nausea, dyspepsia,
somnolence

46
Q

Ketorolac Kinetics?

A

A= bioav. 80‐100%; onset10 min IM, 30‐60 min PO; duration4‐6 hr
D=99% protein‐bound
M=in liver, E= t 1/22‐6 hr; dialysable; 91% in urine; 6% in feces

47
Q

Lornoxicam I?

A

short‐term treatment of mild to moderate pain, osteoarthritis,
rheumatoid arthritis

48
Q

Lornoxicam CI?

A

GI bleeding, coagulation disorders, children <18 yrs, known
hypersensitivity to NSAIDs, active peptic ulceration

49
Q

Lornoxicam A/E?

A

dizziness, insomnia, migraines, gastritis, N&V, dyspepsia, somnolence,
gastro‐esophageal reflux

50
Q

Lornoxicam Kinetics?

A

E= t 1/23‐4 hr

51
Q

Meloxicam I?

A

painful osteoarthritis, rheumatoid arthritis, ankylosing spondylitis, acute
sciatica

52
Q

Meloxicam CI?

A

GI bleeding/perforation/ulceration, IBD, heart failure, known
hypersensitivity to NSAIDs

53
Q

Meloxicam A/E?

A

light‐headedness, dizziness, insomnia, headache, gastritis,
bronchospasm, rash, renal failure

54
Q

Maloxicam kinetics?

A

E= t 1/220 hr

55
Q

Piroxicam I?

A

rheumatic disorders, acute musculoskeletal disorders, acute gout,
dysmenorrhea

56
Q

Piroxicam CI?

A

GI bleeding/perforation/ulceration, IBD, heart failure, known
hypersensitivity to NSAIDs

57
Q

Piroxicam A/E?

A

light‐headedness, dizziness, insomnia, headache, gastritis,
bronchospasm, rash, renal failure

58
Q

Piroxicam Kinetics?

A

E= t 1/250 hr

59
Q

Mefenamic acid I?

A

post‐traumatic conditions, dysmenorrhea

60
Q

Mefenamic acid CI?

A

GI bleeding/perforation/ulceration, IBD, heart failure, known
hypersensitivity to NSAIDs

61
Q

Mefenamic acid A/E?

A

light‐headedness, dizziness, insomnia, headache, gastritis,
bronchospasm, rash, renal failure

62
Q

Mefanamic Kinetics

A

A= bioav. Extensiveonsetrapid, D=↑protein‐bound
M=in liver via oxidation/conjugation
E= t 1/22 hr; dialysable; 66% urine; 20‐25% feces

63
Q

Reversible COX inhibitors?

A

Selective COX‐2 inhibitors

64
Q

Selective COX‐2 inhibitors?

A

Celecoxib
etoricoxib
parecoxib
meloxicam

65
Q

Selective COX‐2 inhibitors MOA?

A

selectively (‐) COX‐2 → ↓prostaglandins synthesis → ↓pain +
inflammation

66
Q

Selective COX‐2 inhibitors decreases risk of what?

A

↓risk of pepƟc ulceraƟon; ↓risk of renal failure (or other AE of
NSAIDs); ↑risk of heart aƩacks, strokes and thrombosis by a relaƟve ↑
in thromboxane

67
Q

Celecoxib I?

A

symptomatic treatment of inflammation & pain in osteoarthritis and rheumatoid arthritis; pain after dental surgery

68
Q

Celecoxib CI?

A

hypersensitivity to sulphonamides, severe renal/hepatic impairment,
asthma, allergy to NSAIDs, risk to cardiovascular disease, pregnancy

69
Q

Celecoxib A/E?

A

dyspepsia, abd. pain, diarrhea, N&V, flatulence, SJS

70
Q

Celecoxib Kinetics?

A

A= bioav. undetermined
D=97% protein‐bound
M=in liver via CYP2C9
E= t 1/211 hr; inactive metabolites in urine and feces

71
Q

Etoricoxib I?

A

osteoarthritis, rheumatoid arthritis, gouty arthritis, primary
dysmenorrhea

72
Q

Etoricoxib CI?

A

hypersensitivity to sulphonamides, severe renal/hepatic impairment,
asthma, allergy to NSAIDs, risk to cardiovascular disease, pregnancy

73
Q

Etrocicoxib kinetics?

A

A= bioav. undetermined
D=97% protein‐bound
M=in liver via CYP2C9
E= t 1/211 hr; inactive metabolites in urine and feces

74
Q

Etoricoxib I?

A

osteoarthritis, rheumatoid arthritis, gouty arthritis, primary
dysmenorrhea

AE:dizziness, headache, palpitations, bronchospasm, gastritis, SJS, tinnitus

74
Q

Etoricoxib CI?

A

hypersensitivity to sulphonamides, severe renal/hepatic impairment,
asthma, allergy to NSAIDs, risk to cardiovascular disease, pregnancy

75
Q

Etoricoxib A/E?

A

AE:dizziness, headache, palpitations, bronchospasm, gastritis, SJS, tinnitus

76
Q

Parecoxib I?

A

I: preoperative pain

77
Q

COX-1 Inhibits what?

A

Decreases production of thromboxane

78
Q

COX-2 decreases production of PGs

A

COX-2 decreases production of PGs

79
Q

Names of common NSAIDS?

A

CAIN Caused pain lol

Celebrax
Aspirin
Indomethicin/Ibuprofen
Naproxen

80
Q

Names od common NSAIDS?

A

NSAIDS

Naproxen
Salicylate
Advil
Ibuprofen/Indomethicin
Diclofenac
Sulindac

81
Q

Reversible COX-Inhibitions self-separation to distinguish CI?

A

DIN

CI: Hypersensitivity to aspirin, active peptic ulceration, pregnancy, proctitis

LMPM

CI: GI bleeding, perforation, ulceration, IBD, Heart failure, known hypersensitivity to NSAIDS

Ketorolac

CI: Duration >5days, chronic painii, hypersensitivity to NSAIDS, PUD

Pharmacology (44 decks)

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