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Flashcards in NSAIDS - Slattery Deck (15):

What is the most potent COX inhibitor?
Why isn't it often used?
What should you use it for when you do?


It has significant toxicity
(GI distress, abdominal pains, ulcers, blood loss, headache)

Used when other NSAIDS are ineffective
(fevers, arthritis not controlled by other NSAIDS)
(Congential disorder ductus arteriosis)


Why is acetaminophen not an NSAID?

It is NOT anti-inflamaotry.
It is analgesic and antipyretic


ADvantage vs Disadvantage of acetaminophen?

Advatnage: Minimal GI irritation , no effect on bleeding, no effect on respiration

Disadvantage: therapeutic index much lower than other OTC drugs

Too high of doses can causes hepatic necrosis especially when combined with alcohol


How does acetaminophen cause hepatotoxicity, how does N-acetylcystein treat it?

A free radical is created when the dose is too high, which reacts with cells to create hepatic necrosis

N-acetylation is a scavenger drug that can pick up those free radicals
-Exogenous equivalent of glutathione (nice!)


Pros and Cons of NSAIDS vs Opioids:

-inflammation pain gone
-few adverse effects
-Only mild or moderate pain

-Intense ain
-phys. dependence
-abuse potential
-resp depression


What are differences between the two forms of Cyclooxygenase

COX1: normal physiology
Gastric cytoprotection, vasodilation, platelet aggregation

COX2: inducible
Induced by acute inflammation
Inhibited by glucocorticoids

NSAIDs inhibit both COX1 and COX2


How is temperature elevated in infection?

How does NSAID lower it again?

Hypothalamus sets body temperature
-Temperature elevation mediated by cytokines
-COX2 induction and PGE2 synthesis, in epithelial cells of brain vasculature
-PGE2 crosses BBB, promotes elevation of body temperature by hypothalamus

NSAIDs decrease prostaglandin synthesis (PGE2) = decrease body temperature


Why can NSAIDS create gastrointestinal distress?

NOT hypersensitivity

Its cuz prostaglandins inhibit secretion of gastric acid and promote mucus secretion

SO, you get too much acid and not enough mucus when NSAIDs block prostaglandin synthesis

Capillary damage leads to necrosis and bleeding


Cyclooxygenase generates what? from arachidonic acid?

Prostaglandins - to modify nociception threshold
Thromboxane - To increase platelet aggregation
Prostacyclin - Inhibits platelet aggreagation


How can high doses of NSAIDS cause respiratory and electrolyte disturbances?

Hyperventilation - caused by stimulation of medulla respiratory center

Metabolic Acidosis - High doseuncouples oxidative phosphorylation, causing lactic acid to accumulate in blood and decrease pH

Body hyperventilates more in order to blow off acid through CO2


Treatment for aspirin overdose:

Gastric decontamination

Sodium carbonate to balance pH

Tranfusion or dialysis?


What causes asprinin hyersensitivity

Probably due to shunting of arachidonic acid into the leukotriene pathway

Treat with epinephrine


Why is aspirin use not reccommended in kids with chicken pox?

Slight possibilty of Reye's syndrome.

Caused by asprinin use in the presence of a viral infection. Mechanism not known


What cox-inhibitor is used for arthritic diseases?



What drug is a selective Cox-2 inhibitor?
Why is this an advantage?

Celecoxib (Celebrex)

COX2 inhibition responsible for NSAID therapeutic effects

The cox-1 inhibition is wht is responsible for side effects.

Unfortunately there are complications with heart attacks and stroke...