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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
Non‐selective COX inhibitors: MOA?
Reversibly (‐) COX‐1 (→ ↓producƟon of thromboxane A2 → (‐) platelet aggregation; transient) & COX‐2 (→↓prostaglandin producƟon → ↓inflammaƟon, pain, fever)
26
Ibuprofen I?
Analgesia, inflammation (high dose required for anti‐inflammatory action), ductus arteriosus in premature new‐born infants (IV prep.)
27
Ibuprofen CI?
hypersensitivity to aspirin/other NSAIDs active peptic ulceration pregnancy (3rd trim.) proctitis/haemorrhoids (suppositories)
28
Ibuprofen AE?
epigastric pain, heartburn, dizziness, nausea, rash, tinnitus
29
Ibuprofen Kinetics? A, D, M & E
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)
30
Naproxen I?
Analgesia & inflammation in rheumatic disease, gout, dysmenorrhea
31
Analgesia? Antipyretic? Anti-inflammatory? Antithrombotic? Arteriosus?
Analgesia: Inability to feel pain Antipyretic: used to prevent or reduce fever Anti-inflammatory: used to prevent inflammation Arteriosus:
32
Naproxen CI?
hypersensitivity to aspirin/other NSAIDs, active peptic ulceration, pregnancy (3rd trim.), proctitis/haemorrhoids
33
Naproxen A/E?
epigastric pain, peptic ulceration, headache, dizziness, rash, tinnitus, nephrotoxicity, hepatic dysfunction
34
Naproxen kinetics? M, D & E
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
Diclofenac I?
pain & inflammation in rheumatic disease, gout
36
Diclofenac CI?
hypersensitivity to aspirin/other NSAIDs, active peptic ulceration, pregnancy (3rd trim.), proctitis/haemorrhoids (suppositories)
37
Diclofenac A/E?
epigastric pain, peptic ulceration, headache, dizziness, rash, tinnitus, nephrotoxicity, hepatic dysfunction
38
Diclofenac Kinetics? A, D, M & E
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
Indomethacin I?
pain & inflammation in rheumatological disorders
40
Indomethacin CI?
hypersensitivity to aspirin/other NSAIDs, active peptic ulceration, pregnancy (3rd trim.), proctitis/haemorrhoids (suppositories)
41
Indomethacin A/E?
as for diclofenac (more than diclofenac on GI), dizziness, drowsiness, headaches, retinal disturbances (prolonged use)
42
Indomethacin Kinetics? A, D, M & E
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
Ketorolac I?
short‐term management of moderate postoperative pain
44
Ketorolac CI?
duration >5 days, chronic pain, hypersensitivity to NSAIDs, PUD
45
Ketorolac A/E?
dizziness, drowsiness, headaches, GI pain, nausea, dyspepsia, somnolence
46
Ketorolac Kinetics?
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
Lornoxicam I?
short‐term treatment of mild to moderate pain, osteoarthritis, rheumatoid arthritis
48
Lornoxicam CI?
GI bleeding, coagulation disorders, children <18 yrs, known hypersensitivity to NSAIDs, active peptic ulceration
49
Lornoxicam A/E?
dizziness, insomnia, migraines, gastritis, N&V, dyspepsia, somnolence, gastro‐esophageal reflux
50
Lornoxicam Kinetics?
E= t 1/23‐4 hr
51
Meloxicam I?
painful osteoarthritis, rheumatoid arthritis, ankylosing spondylitis, acute sciatica
52
Meloxicam CI?
GI bleeding/perforation/ulceration, IBD, heart failure, known hypersensitivity to NSAIDs
53
Meloxicam A/E?
light‐headedness, dizziness, insomnia, headache, gastritis, bronchospasm, rash, renal failure
54
Maloxicam kinetics?
E= t 1/220 hr
55
Piroxicam I?
rheumatic disorders, acute musculoskeletal disorders, acute gout, dysmenorrhea
56
Piroxicam CI?
GI bleeding/perforation/ulceration, IBD, heart failure, known hypersensitivity to NSAIDs
57
Piroxicam A/E?
light‐headedness, dizziness, insomnia, headache, gastritis, bronchospasm, rash, renal failure
58
Piroxicam Kinetics?
E= t 1/250 hr
59
Mefenamic acid I?
post‐traumatic conditions, dysmenorrhea
60
Mefenamic acid CI?
GI bleeding/perforation/ulceration, IBD, heart failure, known hypersensitivity to NSAIDs
61
Mefenamic acid A/E?
light‐headedness, dizziness, insomnia, headache, gastritis, bronchospasm, rash, renal failure
62
Mefanamic Kinetics
A= bioav. Extensiveonsetrapid, D=↑protein‐bound M=in liver via oxidation/conjugation E= t 1/22 hr; dialysable; 66% urine; 20‐25% feces
63
Reversible COX inhibitors?
Selective COX‐2 inhibitors
64
Selective COX‐2 inhibitors?
Celecoxib etoricoxib parecoxib meloxicam
65
Selective COX‐2 inhibitors MOA?
selectively (‐) COX‐2 → ↓prostaglandins synthesis → ↓pain + inflammation
66
Selective COX‐2 inhibitors decreases risk of what?
↓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
Celecoxib I?
symptomatic treatment of inflammation & pain in osteoarthritis and rheumatoid arthritis; pain after dental surgery
68
Celecoxib CI?
hypersensitivity to sulphonamides, severe renal/hepatic impairment, asthma, allergy to NSAIDs, risk to cardiovascular disease, pregnancy
69
Celecoxib A/E?
dyspepsia, abd. pain, diarrhea, N&V, flatulence, SJS
70
Celecoxib Kinetics?
A= bioav. undetermined D=97% protein‐bound M=in liver via CYP2C9 E= t 1/211 hr; inactive metabolites in urine and feces
71
Etoricoxib I?
osteoarthritis, rheumatoid arthritis, gouty arthritis, primary dysmenorrhea
72
Etoricoxib CI?
hypersensitivity to sulphonamides, severe renal/hepatic impairment, asthma, allergy to NSAIDs, risk to cardiovascular disease, pregnancy
73
Etrocicoxib kinetics?
A= bioav. undetermined D=97% protein‐bound M=in liver via CYP2C9 E= t 1/211 hr; inactive metabolites in urine and feces
74
Etoricoxib I?
osteoarthritis, rheumatoid arthritis, gouty arthritis, primary dysmenorrhea AE:dizziness, headache, palpitations, bronchospasm, gastritis, SJS, tinnitus
74
Etoricoxib CI?
hypersensitivity to sulphonamides, severe renal/hepatic impairment, asthma, allergy to NSAIDs, risk to cardiovascular disease, pregnancy
75
Etoricoxib A/E?
AE:dizziness, headache, palpitations, bronchospasm, gastritis, SJS, tinnitus
76
Parecoxib I?
I: preoperative pain
77
COX-1 Inhibits what?
Decreases production of thromboxane
78
COX-2 decreases production of PGs
COX-2 decreases production of PGs
79
Names of common NSAIDS?
CAIN Caused pain lol Celebrax Aspirin Indomethicin/Ibuprofen Naproxen
80
Names od common NSAIDS?
NSAIDS Naproxen Salicylate Advil Ibuprofen/Indomethicin Diclofenac Sulindac
81
Reversible COX-Inhibitions self-separation to distinguish CI?
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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