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47 Cards in this Set
- Front
- Back
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Analgesics used for? |
Pain control
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NSAIDS, salicylates, ibuprofen, naproxen, & celecoxib are all non-narcotics used ONLY for ______________. |
tissue injury |
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Non-narcotics (NSAIDs, salicylates, ibuprofen, naproxen, & celecoxib) act via? |
COX enzyme inhibition (inhibition of PGE and inflammation-->mechanical pain) |
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Opioids (Morphine & Codeine) are part of which class and are used for which types of injuries? |
Narcotics. Tissue & Acute injury. |
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Narcotics (opioids) act via what mechanism? |
mu receptor agonist |
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Anticonvulsants (Gabapentin) and Antidepressants (amitryptilene & duloxetine) are used for what kinds of injury? |
Nerve injury |
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Anticonvulsants (gabapentin) act how? |
Ca++ channel antagonists |
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Antidepressants (amitryptilene & duloxetine) act how? |
NE re-uptake inhibitors |
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Which prostaglandin in Renal Artery? |
PGE2 (also in connective tissue, GI, & stomach) |
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Which prostaglandin in blood vessels? |
PGI2 (prostacyclin)-->vasodilation and decreased platelet aggregation |
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What does TxA2 (thromboxane) do? |
Vasoconstriction & increased platelet aggregation |
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Aspirin & diflunisal are ____________. |
salicylates |
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PGE2 has what roles in the joints/connective tissue vs gut? |
inflammation of MSK but protection of the gut. Hence, ulcers or GI issues. |
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Which salicylate is 2 salicylates hooked together? |
Diflunisal |
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3 categories of anti-inflammatories |
NSAIDs, Coxibs, Salicylates |
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COX-1 vs COX-2. Similarities? |
Same substrates (AA), same products (PGs), both have a role in inflammation, both have a physiological role in renal function |
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**Which cox has a prominent role responding to physiological stimuli? (hint: constitutive: expressed in all tissues all the time & also responds to any pathological stimuli that release AA from cells-inflammation) |
COX-1 |
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**Which cox has a prominent role responding to pathological stimuli? It especially has a physiological role in the kidney (hint: induced: in some tissues at some times-responds to pathological stimuli) |
COX-2 |
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Which COX for local inflammation? |
COX1. Inflammation stimulates AA release. COX-1 converts AA into PGE2. PGE2 causes symptoms (erythema, local edema *capillary leak*, pain) |
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Which COX amplifies symptoms? |
COX2. |
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NSAIDs block which COX? |
Both constitutive COX1 & Induced COX2 |
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Patient presents with Ulcers, bleeding, peripheral edema, high BP. What drug has he been excessively taking? |
tNSAIDS (ibuprofen, naproxen, diclofenac) |
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Which prostaglandins and COX forms are responsible for each of the side effects of tNSAIDs? |
Ulcer (PGE2, COX-1) Bleeding (TxA2 COX-1) Peripheral Edema & htn (PGE2 & PGI2)--kidney |
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Who would you prescribe an NSAID to with caution? |
Renal disease or cardiac disease (constricts renal artery) |
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Which patients are contraindicated for NSAID use? |
Asthmatics Pts w/ gut inflammation (gastritis, colitis, pancreatitis, hepatitis) Surgery--we need inflammation |
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Slective inhibitors of COX2 |
Coxibs *Rx* (celecoxib, valdecoxib) |
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What is the use of Rofecoxib or Celecoxib? |
COX2 selective inhibitor--> GI sparing |
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Rofecoxib & Valdecoxib are selective for what? |
COX2 300-1000 fold selective |
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Delecoxib & Diclofenac selective for what? |
COX2 10-30 fold selective |
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Ibuprofen & Naproxen selective for what? |
COX1 3 fold selective |
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***What is the only anti-inflammatory that is given parenterally and is a very strong COX-1 inhibitor? |
Ketorolac |
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Who gets Ketorolac? |
Patients who can't swallow or are NPO |
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**What are the risks of COXIBS? |
Same effects on renal artery. Increased peripheral Edema and increased blood pressure. |
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**What is a major adverse reaction to Celecoxib? Who can't take it? |
Stevens-Johnson syndrome (&TEN) It is a sulfonamide. Not for those with sulfa allergy |
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What are the COX-independent toxicities of Salicylates? |
Acid-base disturbances, tinnitus, hypersensitivity, Reye's syndrome (hepatic collapse & coma in kids w/ viral infx) |
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Aspirin Dosage for antiplatelet effect? |
80-160mg |
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Aspirin Dosage for analgesic/antipyretic effect? |
325-1000mg |
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Aspirin dosage for Anti-inflammatory effects (tinnitus possible)? |
325mg-6g |
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***Signs of aspirin toxicity (>6g) |
Respiratory alkalosis followed by metabolic acidosis, fever, dehydration |
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Why not give aspirin to kids <19 with fever? give what instead? |
Reye's syndrome (w/ influenza-like illnesses such as chicken pox, colds, etc.) Give ibuprofen instead |
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Why does low dose aspirin (81mg) have durable (3-5 days) anti-thrombotic effects? |
acetylsalicylic acid irreversible binding platelets: no nucleus=no induction of cox2 or regeneration of cox1. COX acetylated=inactive mesenteric portal circulation: just needs to circulate in liver. |
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Does aspirin prevent heart attacks? |
Maybe. But it is recommended after the first heart attack. So not for PRIMARY prevention due to risk of ulcer. |
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Why are coxibs bad for CV health? |
With atherosclerosis, there is COX-2 which is releasing prostacyclin (PGI2) which is an anti-thrombotic and actually having protective effects. Valdecoxib & Rofecoxib are selective for COX2. |
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**All NSAIDs have a black box warning for what? Who is relatively contraindicated? |
Cardiovascular risks. High or bad cholesterol, high bp, etc. |
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Switch between families of tNSAIDS for GI problems. (Selectivity is relative b/w pts) |
Indole Acetic acids: Indomethacin, sulindac Heteroaryl Acetic acids: Diclofenac, ketorolac Aryl Propionic Acids: Ibuprofen, Naproxen Anthranilic Acids: Mefenamic acid Enolic Acids: Pirox-, tenox-, melox-icam Alkanones: Nabumetone |
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Can acetaminophen be used as an anti-inflammatory agent? |
No. Doesn't inhibit COX. Solely analgesic. |
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Risk of acetaminophen? |
Hepatotoxicity |
