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Pharmacology > NSAIDS > Flashcards

NSAIDS Flashcards

1
Q

what type of activities do NSAIDs have

A

antipyretic, analgesic, anti inflammatory activities

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2
Q

mechanism of NSAIDs

A

inhibitor of COX so both inhibition of both prostaglandins and thromboxanes

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3
Q

difference between COX-1 and COX-2

A
  • COX-1 is a constitutively active enzyme that is expressed in most tissues and is main source of cytoprotective prostaglandin formation
  • COX-2 is inducible and is main source of prostanoids in inflammation and cancer
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4
Q

where in the body is COX-2 constitutively active

A

kidney and brain as it is the main source of vascular prostacyclin

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5
Q

why has there been a search for selective COX-2 inhibitors versus COX-1 inhibitors

A

inhibition of COX-1 causes inability to form protective prostaglandin leading to gastric damage as a side effect

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6
Q

What are the non selective COX inhibitors

A

PINK AID

Piroxicam
Ibuprofen
Naproxen
Ketorolac
Aspirin
Indomethacin
Diclofenac
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7
Q

what are the COX-2 inhibitors

A

Celecoxib

Meloxicam

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8
Q

how do NSAIDs produce their analgesic action

A

they decrease PGE2 synthesis hence repressing the sensation of pain

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9
Q

dominant source of prostaglandins that mediate the rise in temperature

A

COX-2 hence why both selective and non selective are consistent with antipyretic clinical efficacy of both subclasses of NSAIDs

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10
Q

therapeutic effects of NSAIDs

A
  • antipyretic, anti inflammatory, analgesic
  • tx for mild to moderate pain
  • pain arising from inflammation (usually not visceral pain with exception to menses)
  • tx of musculoskeletal disorders
  • rheumatoid arthritis, gout, osteoarthritis, ankylosing spondylitis, dysmenorrhea
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11
Q

NSAIDs used to treat gout

A
  • Indomethacin

- Other NSAIDs excluding AST (Aspirin, Salicylates, Tolmetin) used for acute gout

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12
Q

NSAIDs that decreases the risk of colon cancer

A

Aspirin

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13
Q

how do NSAIDs help with tolerating Niacin

A
  • with increased dose or first dose, Niacin causes flushing which is mediated by release of PGD2 from the skin
  • this release can be inhibited by COX inhibitor NSAIDs
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14
Q

NSAID used for closure of ductus arteriosus

A

Indomethacin

FUN FACT: Alprostadil is used to keep patent ductus arteriosus from closing

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15
Q

what are the GI effects caused by using NSAIDs

A
  • inhibition of COX-1 in gastric epithelial cells depresses mucosal cytoprotective prostaglandins (PGI2 and PGE2)
  • local irritation from contact of NSAIDs with gastric muxosa
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16
Q

what does PGI2 and PGE2 do

A

inhibit acid secretion by the stomach, enhance mucosal blood flow, promote secretion of cytoprotective mucus in the intestine

this is all inhibited by blocking COX-1

less side effects with selective COX-2 inhibitor

17
Q

which one of the NSAIDs has the lowest risk and which has highest risk of GI adverse effects

A

lowest - Celecoxib

highest - Piroxicam

18
Q

adverse effects of NSAIDs other than GI adverse effects

A
  • increase cardiovascular risk
  • decrease in renal blood flow
  • analgesic nephropathy from long term use
  • aspirin hypersensitivity
  • hypersensitivity to sulfa since Celecoxib is a sulfonamide
19
Q

what do COX-1 and COX-2 produce and inhibition of which one has more of a cardiovascular risk and why?

A
  • COX-1 produces vasoconstricting, platelet aggregating thromboxane A2
  • both COX-1 and COX-2 produce vasodilating, platelet inhibiting prostacyclins

-COX-2 selective inhibitors have more of a cardiovascular risk because COX-1 is left to produce vasoconstriction, platelet aggregation, and thrombosis

20
Q

how do NSAIDs cause a decrease in renal blood flow

A
  • it only affects persons with CHF, chronic kidney failure, or those with hypoperfusion to the kidney
  • they rely on the vasodilative effects of COX to maintain the GFR so its inhibition leads to decreased GFR, sodium and water retention, edema, high BP, hyperkalemia, and acute renal failure
21
Q

what is aspirin hypersensitivity associated with

A

increased synthesis of leukotrienes reflecting diversion of arachidonate to LOX metabolism due to COX inhibition

22
Q

NSAIDs interaction with other drugs

A
  • ACEIs prevent breakdown of bradykinin which stimulates PG production and NSAIDs prevent PG production. Together they decrease antihypertensive effect of ACEIs
  • diuretics effects reduced
  • with corticosteroids, increases severity GI ulceration
  • increases bleeding with warfarin
23
Q

what is triple whammy when it comes to NSAIDs

A

use of ACEIs (or ARBs) with NSAIDs and diuretics

NSAIDs constrict the afferent arteriole and reduce GFR. ACEIs (or ARBs) dilate the efferent arteriole and reduce GFR. Diuretics decrease plasma volume and GFR. Together, they all lead to acute renal failure.

24
Q

contraindication of NSAIDs

A
  • Pregnancy close to term
  • Reye’s syndrome –> aspirin and other salicylates are contraindicated in children or those less than 20 with fever and viral illnesses (give them acetaminophen or ibuprofen)
25
Q

the only COX-2 inhibitor

A

celecoxib since meloxicam preferentially does COX-2 over COX-1 but not selective for COX-2

26
Q

what makes aspirin different from the other NSAIDs

A

it a salicylate that irreversibly acetylates COX thus inactivating it

27
Q

how does aspirin become a salicylate

A

it is deacetylated in the body by esterases which makes it a salicylate

28
Q

actions of aspirin on respiration and platelets

A
  • at therapeutic level, it increases alveolar ventilation because salicylates uncouples oxidative phosphorylation leading to elevated CO2 and respiration
  • higher doses, hyperventilation and resp alkalosis
  • toxic doses, respiratory paralysis
  • low doses, irreversibly inhibits thromboxane
  • inhibits COX but action doesn’t last long because of production of new COX molecules
  • low dose PGI2 not affected so vasodilation still occurring and platelet aggregation inhibition
29
Q

uses of aspirin

A
  • anti inflamm, analgesic, antipyretic
  • inhibit platelet aggregation so at low doses is used prophylactically for cardiovascular applications
  • decreases risk of colon cancer
30
Q

dosage of salicylates

A

low doses are analgesic and antipyretic and high doses are anti inflammatory

31
Q

how is aspirin metabolized in the body

A
  • it is metabolized by esterases in tissue to salicylate and acetic acid then salicylate is converted by liver to conjugates with glycine and glucuronate, which is then eliminated by first order kinetics
  • high doses over 1g is eliminated by zero order kinetics because conjugation enzymes are saturated, until it comes back down to 300mg then it is eliminated by first order
32
Q

adverse effects of aspirin

A
  • GI epigastric distress
  • risk of hemorrhage for those with bleeding disorders since it inhibits platelet aggregation
  • those with Reye’s syndrome can be fatal
  • uses same transport as uric acid –> hyperuricemia
  • causes hepatic injury
  • pregnancy in later trimester
33
Q

who is aspirin contraindicated in

A

Reyes Syndrome

Chronic liver disease

34
Q

what happens with salicylate poisoning - mild and severe

A

mild - salicylism which includes headache, mental confusion, tinnitus, hyperventilation, diarrhea etc

severe - mixed respiratory alkalosis and metabolic acidosis –> respiratory depression –> respiratory failure

35
Q

what is acetaminophen classified as in terms of mechanism and what are its actions

A

it is NOT AN NSAID though it has weak COX-1 and COX-2 inhibition

analgesic and anti pyretic action but no anti inflammatory action or anti platelet effects

36
Q

who do you give acetaminophen to

A
  • those to relieve pain and fever especially children with flu like symptoms
  • safe for pregnant women
  • not useful for inflamm conditions like RA
37
Q

adverse effects of acetaminophen

A
  • severe hepatic injury especially with overdose when all the glutathione stores are used and NAPQI causes hepatotoxicity
  • narrow therapeutic window for alcoholics or those with liver disease
38
Q

what is used to treat acetaminophen overdose

A

N-acetylcysteine because it replenishes glutathione stores

Pharmacology (79 decks)

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