Term
| What three effects are characteristic of NSAIDS? |
|
Definition
*Analgesic
*Antipyretic
*Anti-inflammatory |
|
|
Term
| What enzyme do NSAIDS inhibit? |
|
Definition
| *Non-selective inhibitors of the enzyme cycloxygenase (1&2) |
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|
Term
| What does cycloxygenase do? |
|
Definition
| *Catalyzes prostaglandins and thromboxane from arachadonic acid. |
|
|
Term
| What do prostaglandins do? |
|
Definition
| *They are messenger molecules in the process of inflammation. |
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|
Term
| What will NSAIDS do to the inflammatory process? |
|
Definition
*Inhibition of chemotaxis
*Down regulation of interleukin-1
*Decreases free radicals |
|
|
Term
| Are NSAIDS acids or bases? |
|
Definition
|
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Term
| What protein will NSAIDS bind to? Why? |
|
Definition
*Albumin
*Because they are weak acids |
|
|
Term
| What is the pKA of most NSAIDS? |
|
Definition
|
|
Term
| *What % of NSAIDS are protein bound? |
|
Definition
| *Highly protein bound in plasma >98% |
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Term
| Cox-1 is considered the ________ pathway. |
|
Definition
|
|
Term
| COX-1 Prostaglandins are associated with: |
|
Definition
*GI mucosal integrity
*Platelet function
*Renal function
*An extremely important pathway for protection |
|
|
Term
| COX-2 Prostaglandins are associated with: |
|
Definition
*Pain
*Fever
*Inflammation |
|
|
Term
| What can NSAIDS release that lead to neurodegeration in neurons and neuroinflammation in glia cells? |
|
Definition
|
|
Term
| Where are NSAIDS metabolized? |
|
Definition
|
|
Term
| How are NSAIDS metabolized? |
|
Definition
| *By oxidation and conjugation in the liver to inactive metabolites. |
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|
Term
| How are NSAIDS eliminated after metabolism? |
|
Definition
|
|
Term
| What are adverse GI effects of NSAIDS? |
|
Definition
|
|
Term
| What are the adverse cardiac effects from NSAIDS? |
|
Definition
|
|
Term
| What are the adverse renal effects associated with NSAIDS? |
|
Definition
|
|
Term
| How do NSAIDS cause GI upset? |
|
Definition
*Acidic molecules of the drugs directly irritate the gastric mucosa
*Inhibition of COX-1 reduces the levels of protective prostaglandins on gastric mucosa. |
|
|
Term
| What are the S&S of GI complications with NSAID use? |
|
Definition
*Hemoptysis
*Black Tarry Stools
*GIB |
|
|
Term
| How much do NSAIDS increase risk of heart failure? |
|
Definition
|
|
Term
| NSAIDS put the patient at high risk for MI excluding _______. |
|
Definition
|
|
Term
|
Definition
| *Secondary to decreased prostaglandin levels which lead to decreased vasodilation and constricted arteries. |
|
|
Term
| Describe the cascade leading to Heart failure: |
|
Definition
*Perceived reduction in circulating volume and pressure
*Decreased LV function, decreased BP
*Increased sympathetic tone
*Increased Renin-Angiontensin-Aldosterone release
*increased arginine vasopressin release
*Vasoconstriction
*Salt and water retention
*Signaling for hypertrophic growth and remodeling
*Left ventricle dysfunction
*Hypertension, viral infection, myocardial ischemia |
|
|
Term
| What effects do NSAIDS have on the renal system? |
|
Definition
*Na and water retention
*HTN (Angiotensin II) d/t promotion of blockade of ARBs and metabolism of AT2
*Decreased prostaglandin level--> decreased vasodilation--> decreased blood flow--> decreased GFR |
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|
Term
| What pregnancy class are NSAIDS? |
|
Definition
|
|
Term
| What can use of NSAIDS during the 3rd Trimester cause? |
|
Definition
| *Premature closing of fetal ductus arteriosus |
|
|
Term
| What does the use of ASA during pregnancy cause? |
|
Definition
*Preterm birth
*Reyes Syndrome |
|
|
Term
| What effects do Ketorolac have on COX? How are its effects measured comparatively to others? |
|
Definition
*COX-1 and COX-2 inhibitor
*Mainly an analgesic with decreased anti-inflammatory effects as compared to others. |
|
|
Term
| When given with an opioid, Ketorolac decreases opioid requirements by__________. |
|
Definition
|
|
Term
| How many Mg of Morphine is Ketorolac equal to and for how long? |
|
Definition
|
|
Term
| How does Naproxen effect COX? |
|
Definition
|
|
Term
| How does Naproxen metabolism differ in men and women? |
|
Definition
| *The free % is higher in women than men |
|
|
Term
| What type of protein binding does Napoxen have? |
|
Definition
*Highly protein bound to albumin
*Long DOA 12-18 hours |
|
|
Term
| What is the major drawback of Naproxen? |
|
Definition
| *2x the GI bleeding than ibuprofen |
|
|
Term
| How does Tylenol effect platelets? |
|
Definition
*Inhibits platelets competitively
*Reversible |
|
|
Term
| How does Aspirin affect platelets? |
|
Definition
*Inhibits platelets noncompetitively
*Irreversible for platelet life |
|
|
Term
| What are some specific characteristics of selective COX-2 inhibitors? |
|
Definition
*Do not effect platelet function, may PROMOTE platelet aggregation
*Increases edema, HTN, & cardiovascular thrombotic events.
*has black box warning
*Ex. Celebrex |
|
|
Term
| What class is Lyrica (pregabalin)? |
|
Definition
| *Anticonvulsant & Antiepileptic |
|
|
Term
| *Whta is Lyrica used for? |
|
Definition
*Neuropathic pain regime (3rd line)
*Used to treat anxiety and fibromyalgia (1st line) |
|
|
Term
| What is pregabalin's MOA? |
|
Definition
*Binds to voltage-dependent calcium channel
*Decreases calcium influx into nerve terminals
*Decreases release of NT: glutamate, substance P & noradrenaline |
|
|
Term
| What does pregabalin cause a dose dependent increase in? |
|
Definition
| *Glutamic acid decarboxylase |
|
|
Term
| What does glutamate + glutamic acid decarboxylase =?? |
|
Definition
*GABA
*pregabalin decreases amount of glutamate so there isn't a large increase in GABA formation. |
|
|
Term
| What drug does pregabalin potentiate? |
|
Definition
|
|
Term
| How is pregabalin metabolized? |
|
Definition
| *Pregabalin is not metabolized but is excreted in urine unchanged |
|
|
Term
| What advantage does pregabalin have due to the lack of metabolism? |
|
Definition
| *There is no hepatic upregulation with its use. |
|
|
Term
| What is the half life of pregabalin? |
|
Definition
|
|
Term
|
Definition
| *Centrally acting analgesic, synthetic opioid |
|
|
Term
| What receptors do Tramadol act at? |
|
Definition
|
|
Term
| What is Tramadol used for? |
|
Definition
*Trigeminal neuralgia
*Depression
*Anxiety Disorders |
|
|
Term
| What is the maximum daily dose of Tramadol? |
|
Definition
|
|
Term
| Is Tramadol fully reversed with Narcan? |
|
Definition
|
|
Term
| How is Tramadol metabolized? |
|
Definition
|
|
Term
| Which drugs should you use with caution when using Tramadol? |
|
Definition
*SSRI
*Ketamine
*Tricyclic Antidepressants (Contraindicated)
*Opioids (potentiation)
|
|
|
Term
| What pregnancy class is Tramadol? |
|
Definition
|
|
Term
| What are some disadvantages of Tramadol? |
|
Definition
*Tolerance and abuse is high
*Up-regulation is common |
|
|
Term
| What is the half life of tramadol? |
|
Definition
|
|
Term
| What is the analgesic duration of Tramadol? |
|
Definition
|
|
Term
| What is the % protein binding of Tramadol? |
|
Definition
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