Nsaid

Front 1

Action of IL1

Back 1

Fever - blocks cyclooxygenase

Front 2

Salicylic acid

Back 2

inhibits COX - nothing but aspirin

Front 3

DMARD

Back 3

acute symptoms of RH Atritis

Front 4

PG F2

Back 4

inflammation

Front 5

PGH

Back 5

mediate platelet aggregation

Front 6

PGE2

Back 6

mediate Gastric mucus production and decreases gastric acid production

Front 7

PG I2

Back 7

in endothelial cells …inhibits platelet aggregation

Front 8

What is the significance of irreversible inhibition (proloned duration of inhibition)?

Back 8

Only Aspirin irreversibly inhibit both cox 1 and 2
Aspirin acetylates (irreversible inhibition ) cox-1 and cox-2 enzymes. Acetylation of COX-1 enzyme in platelets leads to reduced formation of TXA2 by platelets. So platelets cannot aggregate…no clot formation until new platelets are formed

Front 9

why do non selective cox cause peptic ulcers

Back 9

due to cox 1 inhibition hence PGE2 synthesis - no gastric mucus secretion - increase gastric acid - peptic ulcer

Front 10

Why are selective cox-2 inhibitors are relatively safe to be used in a patient with peptic ulcers

Back 10

They don’t inhibit COX-1 in gastric cells. Inhibit only COX-2 , thus inhibits only inflammation without causing peptic ulcers. So reletively safe in peptic ulcers

Front 11

Why NSAIDs precipitate bronchial asthma

Back 11

Archidonic acid now diverted to production of LTs which mediates bronchial constriction

Front 12

DOC of PDA and rational behind

Back 12

Indomethacin
Decrease in PGs during birth causes closure of ductus arteriosus however if they stay open NSAIDS are given to cause decrease in PGs thereby closure

Front 13

Rational behind the use of NSAID in dysmenorrhea

Back 13

PGs are considered to be involved in uterus inflammation during menstruation. NSAIDs by inhibiting PGs reduces uterus inflamation

Front 14

DOC in MI/TIA and MOA

Back 14

Aspirin , antiplatelet
irreversible inhibition of Cox-1 in platelets (not in endothelial cells)

Front 15

DOC Acute rheumatic fever

Back 15

Aspirin - high doses -irreversible inhibition of cox-2

Front 16

Peptic ulceration and bleeding

Back 16

both irreversible/reversible inhibition of cox-1 by selective/non selective NSAIDS

Front 17

Treatment of most general inflammatory conditions

Back 17

Ibuprofen or Diclofenac or naproxen

Front 18

Treatment of acute Rheumatic fever

Back 18

Aspirin in high dose

Front 19

Treatment of thrombotic diseases like MI and TIA

Back 19

low dose Aspirin

Front 20

R.Arthritis

Back 20

Indomethacin

Front 21

GOUT

Back 21

Indomethacin

Front 22

PDA

Back 22

Indomethacin

Front 23

osteoarthritis

Back 23

Indomethacin

Front 24

ketorolac

Back 24

DOC Moderate to severe postoperative pain

Front 25

Acetaminophen

Back 25

fever, mild to moderate pain and absence of inflammation

Front 26

NSAID in a patient with peptic ulcers/ gastritis

Back 26

any coxib (celecoxib or valdecoxib)

Front 27

NSAID in a patient allergic to sulfa drugs

Back 27

avoid celecoxib because it is a sulfa related drug

Front 28

if you have to use NSAID, but patient has peptic ulcers and allergic to coxibs

Back 28

use the required NSAID along with misoprostol , a PG analogue used to treat and prevent NSAID induced peptic ulcers

Front 29

General ADR of NSAIDs

Back 29

Gastric ulcers
Nephrotoxicity
Asthma

Front 30

Why is Aspirin contraindicated in children with viral fever

Back 30

Reye’s syndrome

Front 31

Acute overdose or poisoning of of aspirin

Back 31

Vomiting, dehydration, metabolic acidosis ,delirium, hyperthermia, convulsions , coma and death due to respiratory failure

Front 32

Treatment of aspirin poisoning

Back 32

External cooling by tepid sponging, IV fluids, NaHCO3, gastric lavage, forced alkaline diuresis, antacids , ranitidine and haemodialysis

Front 33

Clinical features of Salicylism

Back 33

Vomiting, Tinnitus, Vertigo, loss of hearing

Front 34

Acetaminophen overdose

Back 34

liver cell necrosis
due to increase metabolite(N-acetyl benzoquinone ) and not enough glutathione in the body to detoxify

Front 35

how can u treat acetaminophen poisoning

Back 35

Treat with specific antidote N-acetyl cysteine. This acts by replenishing the glutathione store in body and donating –SH groups.

Front 36

DOC to modify the course of disease progress in RA

Back 36

DMARDs - methotrexate (an anticancer drug )

Front 37

TNF-alpha antagonists

Back 37

DMARDs like Infliximab (a monoclonal antibody) and etanarcept

Front 38

Sulfasalzine - DNARDs

Back 38

Sulfasalazine is metabolized to two byproducts in the body :
a. Sulfapyridine
b. 5-Amino Salicylic Acid (5-ASA)
Sufapyridine : is the active moiety when treating R.arthritis
5-ASA: is the active moiety when treating Inflammatory Bowel Disease (ulcerative colitis and Chrohn’s disease) but not in R.arthritis

Front 39

when do u use cordticosteroids as RA treatment

Back 39

when Acute or chronic conditions not controlled by NSAIDs

Front 40

acute swelling of great toe

Back 40

acute gout - treatment by NSAIDs or Colchicine
Colchicine acts by inhibiting release of glycoproteins

Front 41

swelling of small joints, presence TOPHI and incrased uric acid level with hisotry of more than 5 acute attacks
treatment strategy

Back 41

chronic gout - reduce the blood uric acid level which cannot be achieved by NSIADs or colchicine

Front 42

DOC and MOA in tretment of chronic gout

Back 42

probenacid or allopurinol
• MOA of Probenecid : Probenecid acts by promoting Excretion of uric acid
• MOA of Allopurinol: By inhibiting the enzyme Xanthine oxidase ,Allopurinol prevents the conversion of Hypoxanthine to uricacid

Front 43

used to prolong the duration of action of Penicillins and METHOTREXATE

Back 43

probenacid

Front 44

used to potentiate the action of anticancer drugs like 6-mercaptopurine and Azathioprine

Back 44

Allopurinol