NSAIDs Flashcards
What is the main target of NSAIDs (Non-steroidal Antiinflammatory Drugs)?
Therapeutic uses by class:
Which one has a reversible inhibition of COX 1 and 2 and has analgesic, antipyretic, and anti-inflammatory effects?
Which one has a reversible inhibition of COX 2 and has analgesic, antipyretic, and anti-inflammatory effects?
Which one has reversible inhibition of COX-2 in the CNS and has no anti-inflammatory effects at the site of injury?
Which one has an irreversible inhibition on both COX 1 and 2, and and it is the only one with anti-platelet effects?
Side effects by class:
Which one has reversible binding to COX2 in the CNS causes NO GI upset, bleeding, decreased renal function, decreased labor, or increase in clotting?
Which one irreversibly bind to COX 1 and 2 and causes all the side effects mentioned before except an increase in clotting?
Glucocorticoids and NSAIDs both inhibit what?
Which prostaglandins are important for pain sensitization, inflammationm, and fever?
COX-2 Eicosanoids: Induced - Up-Regulated Actions
Which are actions that are diminished by NSAID use:
Which cytokine produces pain?
In the hypothalamus, which prostaglandin produces fever?
•Tissue Damage–> Pain / Inflammation [PGE2 / PGI2] (induced)
- Edema formation - leukocyte infiltration via vasodilation
- Potentiation of bradykinin pain-producing activity
•Hypothalamus–> Fever [PGE2] (induced)
–>Increase in heat generation and decrease in heat loss
COX-2 Eicosanoids: Induced - Up-Regulated Actions
Actions that are diminished by NSAID use:
•Kidneys [____1_______] (constitutively up-regulated)
- Adaptation to stresses via maintenance of RBF.
- Most critical in elderly – deteriorating renal function
•Endothelial cells [__2__] (up-regulated by shear stress)
-Vasodilation and anti-aggregatory platelet effects.
•Uterine smooth muscle [___3____] (induced)
-Contributes to labor contractions near parturition
•Ductus arteriosus [___4___] (induced)
–>Maintenance of patent ductus arteriosus via vasodilation
1- PGE2 / PGI2
2- PGI2
3-PGE2 / PGF2
4- PGE2
Physiology of COX1 and COX2 eicosanoid mediators
Which one produces prostaglandins and thromboxanes?
Which one produces gastroprotection, platelet aggregation, and renal function?
Which one produces protaglandins?
Which one is has an effect in producing fever, pain, tissue repair, renal function, reproduction, development and inflammation?
COX-1 Eicosanoids: Constitutive Actions
Actions that are diminished by NSAID use:
What effect do COX 1 eicosanoids have on the GI tract? Which prostaglandins?
What about in smooth muscle? Which prostaglandins?
What has an effect on platelet aggregation?
What is their action on the kidneys? Which prostaglandin?
In vascular smooth muscle, which prostaglandins produce vasodilation? What about vasoconstriction?
Adverse drug events due to inhibition of what COX?
Four main groups:
Major therapeutic uses:
Analgesia is due to inhibition of which COX at site of injury? What dose is usually required? How often?
Antipyretic is due to inhibition of which COX and where? What dose?
Anti-inflammatory is due to inhibition of which COX and where? What is special of the dose required?
Antithrombic effect related to which COX? How is the dose required?
Mechanism of analgesic actions of COX inhibitors:
With central cytokine release, COX2 upegulation on ____________ leads to protagranding production (PGE2), which acts on receptors on _________ to enhace depolatization of secondary sensory neurons.
What cytokine binds to peripheral receptors to cause inflammation?
Antipyretic actions of COX inhibitors
Anti-inflammatory actions of COX inhibitors
Pharmacology of COX1 and COX2 inhibitors
Inhibition of COX 1 decreases GI cytoprotection and leads to _________.
Inhibition of COX 1 decreases platelet aggregation and leads to_________.
Inhibition of inducible effects of COX2 allows decrease in ______, ______ and ______.
Common side effects:
Renal dysfuncton can be related to inhibiton of ________.
Delay in labor can be attributed to inhibition of _________.
Increased thrombotic events [unopposed inhibition of _______ in vascular endothelial cells]: Potential for increased cardiovascular events, including myocardial infarction and strokes
Traditional NSAIDS
They can reversibly bind to _____ and ______.
They have analgesic effects based on inhibiting _____ in CNS.
They have anti-pyretic effects based on inhibiting _____ in CNS
They have anti-inflammatory effects based on inhibiting _____ in at injury site.
Clinical uses:
•Pain of inflammatory origin (muscle-dental-arthritis) - as effective or superior to ______ or ________.
Are they effective against dysmenorrhea?
Which one is available via an IV for post-surgical pain?
For antipyretic effects which one is available as a solution for pediatrc patients?
•For their anti-inflammatory effect they are a component of__________ treatment.
Traditional NSAIDs
Side Effects - GI Tract
Interfere with ___________ by inhibition of COX-1 PGE synthesis –> dyspepsia and gastric ulceration.
They are contraindicated for patients with risk of peptic ulcer disease (PUD) such as: ______, _______, _______.
What can help in lessen dyspepsia?
What will protect against gastroduodenal toxicity?
Traditional NSAIDS
Side effects- Platelets
Interfere with platelet aggregation by inhibition of COX-1 ______synthesis –> promotion of bleeding
How long does aspirin side effects last? In platelets?
NSAIDs use should be avoided in which patients/people?
If taking low-dose aspirin for cardioprotective effect – take NSAIDs for pain-inflammation ____ hour after.
Traditional NSAIDs
Side efffects- Kidney
All NSAIDs cause _______, which is why it is important for use in patients at risk of cardiovascular disease.
Safety comparisson of NSAIDs:
For gastrointestinal issues, inhibiting ________ poses a greater risk than ______.
Is the risk for gastrointestinal issues greater for male or female?
Which medication has the lowest risk for GI issues? Which one has the highest?
For cardiovascular issues, inhibiting _______ poses a greater risk than ______.
Which one is the safest?
Safety comparisson of NSAIDs:
For renal failure risk inhibition of both ____ and ______ has the same effect.
Which patients shoud avoid NSAIDs? For short or long term use?
What are some NSAID alternatives to consider?
In what patients should NSAIDs be avoided?
COX-2 selective
Celecoxib
Does it cause GI issues?
Does it cause bleeding?
Does it cause clotting?
Clinical uses:
Celecoxib
What effects does it have that are similar to ASA and tNSAIDs?
What is it used for?
Beneficial in patients who cannot tolerate GI side effects from______.
Side effects of Celecoxib in GI tract:
Celecoxib is an option for patients requiring chronic NSAID treatment at high risk for gastric complications such as?
What are other safe options for those patients?
Side effects of Celecoxib in platelets:
Selective inhibition of COX-2 could reduce antithrombic PGI2 activity, which means that it could lead to?
Celecoxib increases risk of _____2______in a dose-dependent manner - similar to non-selective NSAIDs
increase in clotting
ischemic CVD and HF
Different NSAIDs and celecoxib in different side effect toxicities:
For increased Gastrointestinal side effects:
naproxen>ibuprofen>celecoxib
For CVD?
For CVD it is reversed
Celecoxib side effects:
What are the greatest concerns? Why?
–> Celecoxib is a sulfonamide so use cautiously in patients with sulfa hypersensitivity
Acetaminophen
Clinical uses:
How is its efficacy in comparisson to tNSAIDs and ASA?
What in terms of antipyretic effects?
Anti-inflammatory effects?
Acetaminophen pharmacokinetics
Acetaminophen side effects:
In supra-therapeutic doses, what is a major concern?
What is the problems of acetaminophen with opioids combo?
How does acetaminophen toxicity gets treated?
Aspirin (Acetyl Salycic Acid)
Clinical uses:
For what kind of pain it is not effective?
What is the requiement for arthritis?
Aspirin
Where is it highest prior to hepatic metabolism?
Aspirin
In elimination of ASA what enzymes eliminate it from blood?
When do you see first order kinetics? Zero order kinetics?
Aspirin side effects:
Contraindications for use of ASA:
ASA oversode:
