NSAIDS Flashcards
Names of NSAIDS
**Aspirin
Diclofenac , ketorolac**
(blue fan holding sign “ go BLAC sox”)
Indomethacin
(green fan holding sign “ don’t mess with indigo sox”)
Meloxicam , Piroxicam
(big screen in stadium streaming from “SOX CAM”)
Naproxen
(big screen in stadium saying :” apPROXimately 110 mph”)
what is the COX (1,2) Pathway ? what are the effects of the resultant products ?
COX 1
cell membrane →(PLA2)→AA→(COX1)→
-
TXA2 ⇒ platelet activation , vasconstriction
(batter’s box says “ SOX A2”) -
Prostaglandins
⇒ gastric cytoprotective
(proslugger protects catcher with GI pads)
⇒dilate afferent arteriole
COX 2 FOUND IN ENDOTHEL , ACTIVE DURING INFLAMMATION
cell membrane →(PLA2)→AA→(COX2)→
-
Prostacyclin (PGI2)
⇒ vasodilation
⇒inhibition of platelet aggregation - Prostaglandins-inflammation
⇒increase vascular permeability
⇒increase pain sensitivity
⇒induce fever
⇒dilate afferent arteriole
——————————————————————————–
Both COX 1 +2 synthesize prostaglandins that can dilate the afferent arteriole
what is the difference between COX 1 and COX 2?
COX 1 - is constitutively expressed
COX 2 - expression is induced by inflammation
NSAIDs MOA
Reversible inhibition of COX 1,2
(“anti inflammatory fire extinguisher aiming towards head coach and assistant coach “)
Diclofenac
Ketorolac
(“BLAC sox”)
Indomethacin
(“INDIGO Sox “)
Piroxicam
Meloxicam
(“Sox Cam”)
Naproxen
(“approximately 110 mph”)
Irreversible inhibition of COX 1,2
Aspirin (“ASA umpire”)
- acetylates COX-1 and COX-2 resulting in irreversible inhibition
Reversible COX 2 inhibitor
Celecoxib
(“Celebrating catcher in the dugout drenching the assistant coach”)
Non-Anti Inflammatory COX2 Inhibitor
Acetaminophen
(“Icy-medicine spray on assistant coach”)
NSAIDs Side Effects
inhibition of COX-1
-can cause gastric inflammation, erosions, and ulceration
(“Burned hole in the gastrointestinal pads”)
-inhibition of COX-1 by NSAID’s can cause GI bleeding
(“Ketchup on the gastrointestinal pads”)
-inhibition of COX-1 by NSAIDs can prolong bleeding time
(“Ketchup on clock”)
——————————————————————————–
NSAIDs in General
-can increase blood pressure due to COX inhibition in the kidney, decreasing sodium excretion
(“Bursting from high pressure”)
-can cause acute interstitial nephritis
(“Baseball-filled kidney shaped containers”)
-NSAID’s cause afferent arteriole vasoconstriction, decreasing GFR ACE inhibitors will effect GFR greatly when used with NSAIDS due to the great decrease of GFR
(“Contracted proximal end of fire extinguisher hose”)
-cause renal papillary necrosis (sloughing of renal papillae)
(“Sloughing of cleat spikes”)
-NSAIDs can increase serum lithium concentrations
(“Elevated “lift-ium” balloons”)
-NSAIDs (indomethacin generally) can cause aplastic anemia
(“Plastic bone-shaped balloon”)
-NSAIDs will cause Impaired renin secretion leading to hyporaldosteronism (decreased mineralcorticoids) that will lead to hyperkalemia, type IV RTA
(“player number 4 falling into the depleted “mineral mine”, entrance of the mine has a “big K”)
Risk managment
-minimize NSAID use in patients of risk for acute kidney injury, because it can exacerbate renal insufficiency, same with MI, or any other issue that may decrease renal perfusion
(“Fire extinguisher behind cracked kidney-shaped glass”)
-avoid NSAIDs in 3rd trimester due to risk of premature closure of ductus arteriosus (highest risk with indomethacin and ibuprofen)
(“Exiting pregnant lady with 3 on her shirt “)
what is the difference between most NSAIDs and Aspirin ?
Aspirin irreversibly inhibits COX 1 ,2
in which cases is Aspirin therapy useful?
- useful in Kawasaki’s disease (the most common vasculitis in children) manifests as fever, conjunctivitis, erythema of lips and oral mucosa, rash, and cervical lymphadenopathy
(“Child on Kawasaki’s ATV”)
Aspirin Side Effects
-aspirin use in children can lead to development of Reye’s syndrome
(“kid next to ATV wearing shirt with rays pattern”)
-Reye’s syndrome occurs when a child is given aspirin in the setting of a viral illness. Consists of rapidly progressive encephalopathy with hepatic dysfunction after apparent recovery of a viral illness
(“Cerebral baseball cap , Fat liver spot on cow”)
(“Tissue box”)
———————————————————————————aspirin toxicity can cause an anion gap metabolic acidosis
(“play sitting on Mudpile”)
-aspirin causes respiratory alkalosis priorto metabolic acidosis
(“ player sitting on mudpile blowing “OH-“”)
-aspirin can cause tinnitus
(“Tin Cans on ground”)
what can be used to control aspirin in the setting of acute toxicity ?
-activated charcoal , can be used to absorb aspirin in setting of acute toxicity
(“Charcoal lines on fan’s face”)
-alkalinization of the serum and urine with a basic solution (sodium bicarb) increases the renal excretion of aspirin
(“Base loaded hose sprinkles on ASA umpire”)
Celecoxib Properties
-celecoxib is a sulfa drug
(“Rotten sulfa eggs”)
-has reduced ulcer and bleeding risk by avoiding COX-1 inhibition
(“Clean gastrointestinal pads”)
-celecoxib may increase the risk of ischemic cardiovascular disease, avoid in acute MI and stable angina
(“spilled Thrombus ice cubes”)
Acetaminophen Properties
- NOT anti- inflammatory
- acting as an antipyretic and analgesic used for mild to -moderate pain, osteoarthritis and some Rheumatoid arthritis
-acetaminophen causes hepatotoxicity.
(“Liver spot on goat”)
- toxic levels of acetaminophen deplete glutathione in the liver since glutathione will inactivate the toxic metabolite NAPQI
(“Goat scared by the icy medicine”)
what is the Antidote for Acetaminophen toxicity
N-acetylcysteine restores hepatic glutathione stores to treat acetaminophen hepatoxicity
(“Goat attracted to N-Flower seeds
-activated charcoal can be used to absorb acetaminophen in setting of acute toxicity
(“Charcoal lines on the fan above acetaminophen spray”)
