Meds Flashcards
Mefanamic acid (Ponstel)
Category
MOA
SE
Category: NSAID Class: Fenamic acid
MOA: primary anti-inflammatory with some analgesics, antipyretic NON-cox selective
SE: nvd, ulcers, headaches, drowsiness, hematopoietic toxicity
Ibuprofen (Motrin, Advil) Category Max dose MOA Metabolism Excretion SE Other drug interactions? Why?
Category: NSAID class: profens Max dose = 3200mg MOA (generally considered to be cox1 selective except for naproxen) Metabolism: liver Excretion: kidneys (as inactive metabolites) SE: less GI than ASA, headache, dizziness, fluid retention edema Other drug interactions: highly bound to plasma proteins
COX-1 inhibition side affects are?
COX-1 inhibiton decreases protective cardiovascular effects, GI bleeding
Perixicam (Feldine) Meloxicam (Mobic) Cagtegory MOA Metabolized Excreted
Category: NSAID Class: Enolic acid (oxicam) derivatives MOA: higher cox2 selective Metabolized: liver Excreted: kidneys
Naproxen (aleve) Ketoprofin (Orudis) Category MOA Metabolism Excretion SE Other drug interactions? Why?
Category: NSAID Class: propionic acid/profens Max dose: 1000mg MOA: analgesic, antipyretic (naproxen more selective to cox2) Metabolism: liver Excretion: kidneys (as inactive metabolites) SE: less GI than ASA, headache, dizziness, fluid retention edema Other drug interactions: highly bound to plasma proteins
What are the considerations for NSAID use?
–age > 65 –use of anticoagulant therapy –hx GI bleed –Acute PUD –Concomitant use of glucocorticoids –renal failure –liver cirrhosis —CHF, nephrotic syndrome —-HTN patients (NSAIDs block prostagandin synthesis at kidneys, decrease GFR which then increases blood volume and pressure)
Indomethacin Ketorolac (Toradol) Limits? Category MOA Metabolism Excretion SE
Category: NSAID Class: acetic acid ** only use toradol for 5 days MOA: indomethacin= cox1 selective, primarily anti-inflammatory Ketorolac= primary analgesic, but has anti-inflammaotry, antipyretic Metabolism:Toradol = liver Indomethacin Excretion:Torado = liver SE: Indomethacin = cns toxicity–> headaches to delusions to psychosis, thrombocytopenia) Toradol: inhibits platelet function
Phenytoin (Dilantin) Category MOA Metabolism SE CI
Category: anti-epileptic/anticonvulsant MOA: Na+ channel antagonist, slows seizure activity Characteristics: lipid soluble, highly protein bound, CYP inducer Metabolism: Liver SE: nystagmus, ataxia, cognitive impairment CI: hepatic disease, heart block, bradycardia
Vancomycin Category MOA Metabolism Excreted SE CI
Category: glycopeptide MOA: bacterial cell lysis Metabolism: NONE Excreted: kidneys, fecal if orally administered SE: redmans syndrom, ototoxicity, nephrotoxicity CI: renal disease
What are the side affects of NSAIDS?
–GI: n/v/d, heartburn, ulcers/bleeding –Photosensitivity –Renal: NA+/H2O retention, HTN, damaging with other nephrotoxic drugs –Platelet aggregation (interferes for 2-4 days) – can cause acute kidney injury in : chronic kidney disease patients( decrease GFR), volumed depleted patients, CHF, nephrotic syndrome, cirrhosis, old age
Acetaminophen (Tylenol) Category MOA DOSE Absorbed Metabolized SE CI
Type: analgesic MOA: weak cox1/2 inhibitor (decreases pain) anti-pyretic, NO inflammatory effect Dose: max 4gm Absorbed: GI Metabolized: liver (relatively non-toxic) SE: liver toxicity, dizziness, disorientation, renal damage CI: ETOH abuse or with more than 2 drinks, liver disease, can decrease INR **drug of choice in treating minor, noninflammatory pain especially in pts at risk for GI bleeding
ASA (salicylic acid) Bayer, excedrin Category MOA Absorbed Metabolized Eliminated SE CI/toxic levels
Category: NSAID, analgesic Class: salicylates MOA: potent anti-inflammatory, antipyretic, analgesic, irreversibly inhibits cox1/2 and platelet aggregation, decreases risk of heart attack and stroke (cox1 selective) Absorption: sm. intestine, stomach Metabolized: liver to salicylic acid Eliminated: kidneys SE: gastric upset/ulcers, heartburn, asthma, rashes, renal toxicity, hepatotoxicity CI: hx of bleeding disorders, asthma, hypersensitivity to NSAIDS Toxic levels: metabolic acidosis, respiratory depression, cardiotoxicity, ototoxicity Reyes disease in children,
Celecoxib (Celebrex) Category MOA Metabolism Excretion
Category: NSAID MOA:COX-2 inhibitor, analgesic, antipyretic, anti-inflammatory, DO NOT inhibit platelet aggregation, minimal renal and CV side effects Less GI toxicity GOOD for treating arthritis short term Metabolized: liver Excreted: urine
What do prostaglandins do?
- Activate inflammatory response
- Elicitation of pain and fever
- Contraction and relaxation of smooth muslce
4 .Inhibition of acid synthesis and increased secretion of protective mucus in the stomach
- increased blood flow to the kidneys
Lorcarserin (Belvaq)
MOA ( dont worry about)
SE
CI
How long can pt use for?
MOA: selective agonist of serotonin C2 receptors which decrease appetite
SE: HA, nausea, dizziness, nasopharyngitis, back pain
CI: pregnancy and other use of serotonin meds
can be habit forming
Can only be used for 3-4-6 months and usually weight comes back on
Orlistate (Xenical, Alli)
MOA
SE
CI
How long can pt use?
MOA: lipase inhibitor, ihibits the aboroption of dietary fats
SE: oily spotting, flatus w/ discharge, fecal urgency, oily stools, increased defecation, fecal incontinence
Forces pts to eat low fat diet or get side effects
Can use long term