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27 Cards in this Set
- Front
- Back
NSAIDs:
- mechanism of action - reversibility? |
Nonselective COX inhibitor, thus decreasing production of prostaglandins and thromboxanes.
Reversible |
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Differentiate between COX-1 and COX-2.
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COX-1 is ubiquitous
COX-2 is induced by inflammation/injury |
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General Pharmacological Actions of NSAIDs. x8
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Analgesia
Anti-pyretic Anti-inflammatory Anti-thrombotic Induces closure of Ductus Arteriosus Alleviates Dysmenorrhea Tocolytic activity (Indomethacin) Effective against Colorectal CA and Alzheimers |
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What bodily areas are affected by the side effects of NSAIDs?
List specific damages |
GI
(Ulcers, GI distress, diarrhea) Renal (Renal necrosis, nephritis, acute renal failure) |
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What is Misoprostol, and what does it do?
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PGE1 analog
Prevents GI damage from NSAIDs |
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NSAID pharmacokinetics:
- Absorption - Distribution - Metabolism - Excretion |
Fast and complete
Highly bound to proteins (90-95%) By hepatic P450 Renal |
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Salicylates:
- mechanism of action - reversibility |
Nonselectively inhibits COX
(COX-1 and COX-2) IRREVERSIBLE |
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How is salicylates absorbed?
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By passive diffusion (b/c weak acid)
via ion trapping effect |
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What is the major excreted conjugate for salicylates?
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Salicyuric acid
|
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Describe the dose dependency of Salicylates
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Low Dose - 1st order kinetics
High Dose - Saturation kinetics |
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Describe the pH dependency of Salicylates.
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If urine pH below 7.4 -> Absorption
(b/c urine/plasma ratio is < 1) If urine pH above 7.4 -> Excretion (b/c urine/plasma ratio is < 1) |
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What are the common side effects of NSAIDs? x3
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GI bleed
Stimulates respiration Changes Acid/Base balance (respiratory alkalosis -> increased bicarb excretion -> alkalosis compensation) |
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List the Salicylates derivatives. x3
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Methyl Salicylate
Sodium Salicylate Diflusinal |
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Which salicylate derivative is used topically to counter irritants?
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Methyl Salicylate
|
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Which salicylate derivative is least potent when compared to ASA?
|
Sodium Salicylate
|
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Diflusinal:
- Derivative of what? - Potent at? - Weak at? - Side effects? |
Diflusinal
Analgesia + Anti-inflammatory Anti-pyretic Less effects on GI, auditory, thrombotic |
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Acetominophen:
- mechanism of action - reversibility? - occurs where? |
Nonselective COX inhibitor
(COX-1 and COX-2) Reversible More at the CNS (inactive at PNS) |
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Acetominophen:
- Potent at? - Weak at? |
Analgesia + Anti-pyretic
Anti-inflammatory + GI effecs (also anti-thrombotic) |
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Acetominophen:
- toxicity - antidote |
Hepatic Necrosis
N-acetylcysteine (NAC) |
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Acetominophen:
- metabolism/excretion |
With glutathione -> nontoxic
Without glutathione -> hepatotoxic |
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List the Acetic Acid derivatives. x7
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1. Indomethacin
2. Tolmetin 3. Sulindac 4. Ketolorac 5. Fenamates 6. Etodolac 7. Diclofenac |
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List the propionic acid derivatives. x5
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1. Ketoprofen
2. Ibuprofen 3. Naproxen 4. Oxaprozin 5. Fluriprofen |
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Propionic acid derivatives:
- mechanism of action - why use? |
Non selective COX inhibitor
Better tolerated than ASA or indomethacin |
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List the enolic acid derivatives and their mechanism of action. x3
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Piroxicam - (inhibits COX 1)
Meloxicam - (inhibits COX 2) Nabumatone - (inhibits COX 1 and COX 2) |
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COXIBs
- mechanism of action - weak at? - side effects |
COX 2 inhibitors
GI and antithrombotic may cause CV problems |
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Celecoxib:
- metabolized by? - inhibited by? |
CYP2 C9
CYP2 D6 |
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What drugs only inhibit COX-2? x4
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Etodolac
Diclofenac Meloxicam Coxibs |