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NUR 243 Opioids, Nsaids, Glucocorticoids, Peptic Ulcer Drugs Notes $10.99   Add to cart

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NUR 243 Opioids, Nsaids, Glucocorticoids, Peptic Ulcer Drugs Notes

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This is a comprehensive and detailed note on Opioids, Nsaids, Glucocorticoids, Peptic Ulcer Drugs for NUR 243. *Essential Study Material!!

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  • September 18, 2024
  • 5
  • 2020/2021
  • Class notes
  • Prof. patricia
  • All classes
All documents for this subject (28)
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anyiamgeorge19
;Sedative Hypnotics: depress CNS function, anxiety and insomnia, dosage dependent
Benzodiazepines: works on GABA, high lipid solubility - BBB cross,
IV can cause issue w/ BP (hypotension and resp depres.) - NO alc or opioids
Dependency w/ long term issues,
Benzo- like: most widely used, no apparent tolerance or increase of adverse effects
Drowsiness and dizziness - can intensify effects with alc and benzos
Ramelton: melatonin antag, not controlled substance, activate melatonin receptors, chronic insomnia,
rapid onset. Adverse effect: dizziness, nausea, fatigue, headache

Opioids: mu, kappa , delta = receptors, peptides = enkephalins, endorphins, dynorphins
Pure agonist = morphine, codeine - activate mu and kappa; analgesia, euphoria, sedation, resp depress,
physical dependence, constipation; tranquility, depresses swallow and cough reflex. First pass effect,
stored in liver, not lipid soluble - no BBB, Methylnaltrexone (Relistor)- Used to treat opioid-induced
constipation, a peripheral opioid antagonist. Orthostatic htn, urinary retention,
agonist-antag = pentazocine - mu = antag, kappa = agonist. Will throw pt into withdrawal instantly,
partial agonist = buprenorphine - mu = partial agonist, kappa = antag, some dependency some analgesia
also opioid addiction, sublingual = best
pure antag = naloxone/narcan = REVERSAL of OPIOIDS

Opioid Use Disorder: Tolerance=a larger dose is required to produce the same response that could be
produced with smaller amounts (prolonged use), Physical Dependence=an abstinence syndrome will
occur if drug abruptly stopped (long term use), CNS resets
Heroin = highly soluble, BBB cross in 15s



NSAIDS: blocks COX 1 and 2, synthesis to prostaglandins is impaired, for inflammation, fever,
analgesia.
First gen: inibit cox 1 and 2, anti-inflam disorder, mild to mod pain, suppress fever, inflam - risk for harm
Aspirin: nonselective for cox, suppression of platelet aggregation - reduce MI, helpful for periods, cancer
prevention. MI, CVA = 75-81 mg; fever = 325-625mg (max4g) adverse: GI bleeding, bleeding, renal
impair, salicylism, reyes syndrome - no children, hypersensitivity; interactions Anticoagulants: Warfarin
and heparin, Glucocorticoids, Alcohol, Ibuprofen, ACE inhibitors and ARBsAnticoagulants
Nonaspirin = ibuprofen, naproxen - do not protect against MI and CVA
2nd gen: celecoxib- lower risk for GI, can impair renal and cause HTn and edema, increased risk Mi and
CVA. adverse = dyspepsia, abdominal pain, renal impairment, sulfa allergy
Avoid use in older adults,
Acetaminophen: analgesic and fever reduce, inhibits prostaglandin synthesis, steven johnson syndrome,
hepatic necrosis in OD

, Glucocorticoids
● Nearly identical to steroids produced by the adrenal gland
● In low doses, controls glucose metabolism for adrenocortical insufficiency -- Addison’s disease
● In high doses, suppresses inflammation
● Cortisol is released from the adrenal cortex in times of stress
○ Ex: trauma, surgery, stress, etc.
○ Also plays a role in maintaining BP
● Addison’s Disease -- adrenal dysfunction/ endocrine dysfunction
○ Low dose steroids taken everyday
○ If stress response is triggered - need exogenous cortisol
● Effects of glucocorticoids on body
○ Metabolism
■ Carbohydrate metabolism = gluconeogenesis
■ Protein metabolism = breakdown into amino acids
■ Lipid metabolism = increase in breakdown of fatty acids
○ Body fluids
■ Play role in fluid volume status
■ Help to maintain water, can hold onto salt and water and excrete it
■ Can see problems with hypokalemia and hyponatremia
■ Can act on kidney to promote retention of sodium and water while promoting
potassium secretion
■ Long term use = hypernatremia, hypokalemia and edema
● Glucocorticoids in nonendocrine disorders
○ Decrease inflammatory and immune responses
■ Suppress phagocytes and proliferation of lymphocytes
○ Can be used in rheumatoid arthritis, lupus, IBD, and other inflam disorders
■ Goal of treatment is to decrease chronic inflammation and prevent destruction of
bones and joints
■ Suppress widespread destruction of connective tissues
● Leads to bowel issues, IBD, chronic kidney disease
○ Can be used in allergic conditions (decrease hypersensitivity), asthma, dermatologic
disorders (eczema, psoriasis), neoplasm, suppression of allograft rejection, prevention of
respiratory distress syndrome in preterm infants
● Mechanism of action
○ Inhibiting/suppressing synthesis of inflammatory mediators -- prostaglandins,
leukotrienes, histamine
○ Suppresses infiltration of phagocytes
○ Suppress proliferation of lymphocytes
● Acute onset - steroids get inflammation down
● Goal is not long term -- must be weaned to lowest possible therapeutic dose
● Metabolic effects
○ elevates blood glucose

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