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201 Cards in this Set
- Front
- Back
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positive agonist opiods
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most mu- produce analgesia
act at specific opiod receptor sites |
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antagonist
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block opiod receptors
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agonist PK
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well absorbed via SC, IM, PO routes
1st pass effect variable protein binding metabolized by the liver, renally excreted |
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phenylpiperidines
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opiod agonist- cyp450 metabolism
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agonist CI/caution
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allergies, diarrhea caused by toxic poisons/ respiratory depression, recent GI/GU surgery, ulcerative colitis, head injury, alcoholism, liver/renal dysfunction, pregnancy or lactation
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opiod agonist adverse effects
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sedation, respiratory depression, n/v, postural hypotension, constipation, urinary retention, pruritis, allergic reactions
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Opiod tolerance
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Chronic toxicity: neuroadaptation by the body during chronic use
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opiod physical dependence
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Chronic toxicity: seen only when opiates are stopped suddenly or dose is markedly decreased
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opiod addiction
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chronic toxicity: dysfunctional pattern of use for purposes other than the alleviation of pain
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hydromorphone
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opiod agonist, more potent, better oral absorption
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oxymorephone
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opiod agonist, active metabolite of oxycodone, no pharmacological advantages
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codeine
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opiod agonist, prodrug of morphine, often combined with other compounds
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hydrocodone
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opiod agonist, used in combination products, pharmacological properties similar to morphine
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oxycodone
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opiod agonist, good analgesia when combined with peripherally acting nonopiod agent
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morphine
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opiod agonist, prototype
PK: 1/2 life 2 hrs, converted to active metabolite that's 2x more potent, excreted by kidneys |
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meperidine
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opiod agonist, pharmacological profile similar to morphine
-not as potent, shorter duration - metabolite accumulates with high doses and in renal failure -causes CNS excitability --> seizures |
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fentanyl
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opiod agonist, high potency and high lipid solubilty
-transdermal patch, oral transmucosal, parenteral and lozenge -metabolized by CYP3A4 |
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methadone
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opiod agonist, synthetic, similar to morphine
- longer 1/2 life= more sedation -extended duration of action - DOA prolonged with repeated doeses |
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Mixed agonist/ antagonist opiods
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stimulate one receptor, block another
- produce analgesia and respiratory depression but has ceiling effect= plateau -lower abuse potential -effect dependent on previous opiate exposure- dependent= withdrawal symptoms |
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mixed agonist/antagonist pharmicokinetics
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readily absorbed, metabolized by the liver, excreted in urine or feces
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mixed agonist/ antagonist opiods adverse effects
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respiratory depression, n/v, constipation, dizziness, anxiety, hallucinations
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pentazocine
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mixed agonist/ antagonist opiod
-significant CV effects: high doses increase BP, HR -can cause dizziness. hallucinations, nightmares -mostly used in anesthesia |
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buprenorphine
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mixed agonist/antagonist opiod
-used in detox -less sedation, respiratory depression and hypotension -long DOA, respiratory depression CANNOT be reversed, nausea, dizziness |
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nalbuphine and butorphanol
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mixed agonist/ antagonist opiods
- limited role in chronic pain - no CV effects |
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opiod antagonists
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-MOA: compete with endogenous and exogenous opiods @ mu receptor sites= prevent or reverse opiod induced side effects
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opiod antagonist adverse effects
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acute narcotic abstinence syndrome, CNS excitement, increased heart rate, BP changes, pulmonary edema
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Naloxone
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opiod antagonist
- binds competitively to opiod receptors but no analgesia - used to reverse toxic effects of agonist/mixed narcotics -repeated dosing req. to reverse coma and respiratory depression |
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naltrexone
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opiod antagonist
-longer DOA - hepatotoxic |
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tramadol
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-MOA: weak opiod receptor binding (mu), inhibition of NA and serotonin reuptake
- less respiratory depression and constipation - PO only -can cause seizures - used with chronic pain b/c less dependence and tolerance |
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acetominophen
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non opiod agent
-alternative to aspirin - minimal anti-inflammatory effects, -no effect on platelets -MOA: weak prostaglandin inhibitor in CNS -PK: well absorbed, peak concentration 30-60 min -AE: overdose assoc w/ fatal hepatic necrosis |
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NSAIDS method of action
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MOA: inhibits COX-1- protective prostaglandins (kidney and GI function) and COX-2- inflammatory prostaglandins
- anti inflammatory, analgesic, antipyretic and anti-platelet effects |
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NSAIDs pharmacokinetics
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different potency and 1/2 life- lower for milder pain, higher for more severe
-absorbed rapidly from GI, metabolized in liver, excreted in urine |
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NSAIDs cautions/contraindications
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allergies, history of peptic ulcer, GI bleeding, bleeding, surgery associated blood loss, asthma, renal impairment, dehydration, hypersensitivity to aspirin, renal/hepatic dysfunction
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NSAIDs adverse effects
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dyspepsia, d/n/v, gastric bleeding, ulceration, acute renal insufficiency, rashes, bronchospasm, bleeding, fluid retention, peripheral edema
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ibuprofen
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NSAID
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naproxen
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NSAID
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diclofenae
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NSAID
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indomethacin
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NSAID
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ketorolac
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NSAID
-parenteral, short term management of moderate- severe pain -associated with severe bleeding post op -increases liver enzymes, limit therapy to maximum of 5 days |
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celecoxib
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NSAID
-COX-2 inhibitor - decreases GI toxicity, doesn't effect platelet aggregation -CI in pts with sulfa allergy - increase risk for CV event |
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aspirin
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NSAID
- irreversible inhibition of COX enxyme -AE: Gi, dizziness, deafness, tinnitus, Reyes Syndrom in kids w/ viral infections, increased risk of bleeding with warfarin |
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nonspecific analgesic
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absorptive therapy for migraines
- not considered 1st line for migraines b/c of adverse effects - ibuprofen, aspirin, opiods, other NSAIDs, acetominophen |
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ergot derivative
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- used to treat migraines
- precise MOA unknown |
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ergot derivative adverse effects
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hallucinations, alters prolactin release, vasoconstriction, uterine stimulation, n/v/d
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ergot derivative pharmacokinetics
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metabolized by liver and excreted by kidneys
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ergot derivative contraindications
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cardiac, peripheral and cerebral vascular disease, liver disease, pregnancy- category x b/c of uterine stimulation
-interaction w/ triptans |
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dihydroergotamine
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ergot derivative
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ergotamine
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ergot derivative
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triptans
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1st line in migraine treatment
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triptan MOA
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selective stimulation of serotonin 1b and 1d receptors, relieve pain by constricting intracranial blood vessels and suppress release of inflammatory neuropeptides
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triptan pharmacokinetics/ contraindications/ adverse effects
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-metabolized by liver, excreted by urine, variable 1/2 life
- CI: hypertension, peripheral vascular disease, CAS, MI, angina -AE: n/v, malaise, dizziness, injection site pain, chest pressure |
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beta lactams
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antibacterial
Cell wall synthesis inhibitor MOA: interfere with the last step og bacterial cell wall synthesis- prevent cross linkage - time dependent killing |
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penicillins method of action
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antibacterial
beta lactams interfere with the ability of susceptible bacteria to build their walls when they're dividing (cross linkage) |
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penicillin PK
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inhibit cell wall synthesis: beta lactam
- absorption variable, most incomplete - distributed well into most body tissues, not well in eye, CSF or prostate - mostly excreted by kidneys - metabolism: only semisynthetic hepatically metabolized and excreted in bile |
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penicillin adverse effects
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inhibit cell wall synthesis: beta lactam
hypersensitivity, diarrhea, interstital nephritis, CNS effects, increased liver enzymes |
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natural penicilins
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antibacterial
inhibit cell wall synthesis: beta lactam penicillin G- IM/IV and penicillin V-PO - narrow spectrum of activity: gram+/-, few anaerobes, few spirocettes -DOC for syphillis |
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penicillin-resistant penicillins
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antibacterial
inhibit cell wall synthesis:beta lactams narrow spectrum- gram + only, use limited to MSSA |
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nafcillin
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antibacterial
inhibit cell wall synthesis: beta lactam parenteral penicillin |
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oxacillin
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antibacterial
inhibit cell wall synthesis: beta lactam parenteral penicillin |
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cloxacillin
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antibacterial
inhibit cell wall synthesis: beta lactam oral penicillin |
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dicloxacillin
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antibacterial
inhibit cell wall synthesis: beta lactam oral penicillin |
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aminopenicillins
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beta lactam-penicillin
narrow spectrum: some gram+/- |
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amoxicillin
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antibacterial
inhibit cell wall synthesis: beta lactam aminopenicillin |
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ampicillin
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antibacterial
inhibit cell wall synthesis: beta lactam aminopenicillin |
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antipseudomonal penicillins
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antibacterial
inhibit cell wall synthesis: beta lactam penicillin broad spectrum- increased activity against gram - - used to treat pseudomonas infections |
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ticarcillin
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antibacterial
inhibit cell wall synthesis: beta lactam antipseudomonal penicillin |
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pipercillin
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antibacterial
inhibit cell wall synthesis: beta lactam antipseudomonal penicillin |
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beta lactamase inhibitors
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antibacterial
inhibit cell wall synthesis: beta lactam -used with penicillin to expand spectrum of action -mimic beta lactam, bind to enzymes and inhibit their activity -broad spectrum: dependent on parent beta lactam- gram +/-, anaerobes |
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clavulonic acid
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antibacterial
inhibit cell wall synthesis: beta lactam beta lactamase inhibitor |
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sulbactam
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antibacterial
inhibit cell wall synthesis: beta lactam beta lactamase inhibitor |
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tazobactam
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antibacterial
inhibit cell wall synthesis: beta lactam beta lactamase inhibitor |
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cephalosporin
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antibacterial
inhibit cell wall synthesis: beta lactam - all end in cef -1st generation treats gram + w/ narrow spectrum ---> 4th gen treats gram - with broad spectrum - well absorbed, widely distributed, some into CSF, metabolized in liver, renal excretion |
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cephalosporin adverse effects
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antibacterial
inhibit cell wall synthesis: beta lactam hypersensitivity, IM admin painful, diarrhea, interstitial nephritis, CNS effects, billiary sludge |
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monobactam
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antibacterial
inhibit cell wall synthesis monocyclic beta lactam -narrow spectrum: gram --, pseudomonas -used in pts with PCN allergy -PK: IM/IV only, not absorbed in GI, wide distribution, renal excretion, 1/2 life 2 hrs -AE: rash |
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carbapenems
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antibacterial
inhibit cell wall synthesis: beta lactam - differ in 5 member ring structure -used in serious and life threatening infections and polymicrobial infections -broad spectrum: gram +/--, anaerobes -broadest of all beta lactams -PK: well distributed, renal excretion -AE: hypersensitivity, diarrhea, seizures |
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doripenem
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antibacterial
inhibit cell wall synthesis: beta lactam carbapenem |
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ertapenem
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antibacterial
inhibit cell wall synthesis: beta lactam carbapenem |
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imipenem-cilastin
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antibacterial
inhibit cell wall synthesis: beta lactam carbapenem |
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meropenem
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antibacterial
inhibit cell wall synthesis: beta lactam carbapenem |
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glycopeptides
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antibacterial
cell wall synthesis inhibitor |
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vancomycin
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antibacterial
inhibit cell wall synthesis: glycopeptide -MOA:inhibits 2nd stage of peptidoglycan- cell wall -broad spectrum: gram + only, incl. MRSA -poorly absorbed in gut, IV systemic distribution, excreted by kidney - measure trough levels for therapeutic levels -AE: red man syndrome: infusion related, red rash of head, face, neck and upper trunk, hypotension, nephrotoxicity, ototoxicity - time dependent killin |
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inhibit protein synthesis
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antibacterial
inhibit the binding of 50s and 30s (combine to form 70s) ribosome to mRNA |
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chloraphenicol
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antibacterial
protein synthesis inhibitor -spectrum: gram +/-, anaerobic -MOA: bind to 50s ribosomal subunit -PK: well absorbed, widely distributed incl CSF, hepatically metabolized, metabolite excretion in urine - bacteriostatic -AE: hypersensitivity, reversible bone marrow supression, fatal anemia, gray baby syndrome |
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tetracyclines
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antibacterial
protein synthesis inhibitor -MOA: bind to 30s subunit, block incoming tRNA -narrow spectrum: some gram +/- - PK: widely distributed incl CSF, excreted in bile and urine -bacteriostatic -AE: GI irritation, diarrhea, photosensitivity, kidney and liver toxicity, permanent brown discoloration of teeth |
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demeclicycline
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antibacterial
inhibit cell wall synthesis: tetracycline |
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doxycycline
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antibacterial
inhibit cell wall synthesis: tetracycline -complete oral absorption -excreted in feces |
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minocycline
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antibacterial
inhibit cell wall synthesis: tetracycline -complete oral absorption -metabolized by the liver |
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glycylcycline
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antibacterial
protein synthesis inhibitor -broad spectrum: gram +/--, anaerobes, NO pseudomonas - PK: IV only, large distribution, elimated through feces -AE: n/v, hepatic toxicity |
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tigecycline
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antibacterial
protein synthesis inhibitor- glycylcycline |
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macrolides
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antibacterial
protein synthesis inhibitor -MOA: binds to 23s subunit- component 50s -narrow spectrum: gram+/- -widely distributed except CSF -AE: GI intolerance, cholestatic hepatitis, ototoxicity, cardiac arrythmias |
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azythromycin
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antibacterial
protein synthesis inhibitor:macrolide |
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clarithromycin
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antibacterial
protein synthesis inhibitor: macrolide |
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dirithromycin
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antibacterial
protein synthesis inhibitor: macrolide |
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erythromycin
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antibacterial
protein synthesis inhibitor: macrolide |
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clindamycin
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antibacterial
protein synthesis inhibitor -MOA: binds to 50s - narrow spectrum: gram+, anaerobes -PK: almost completely absorbed, distribute everwhere excp CSF -bacteriostatic -AE: diarrhea, rash |
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licosamide
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antibacterial
protein synthesis inhibitor- clindamycin |
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streptogramins
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antibacterial
protein synthesis inhibitor -quinupristin/dalofopristin- combo, ehance activity of each other -MOA: binds to 50s in 2 places -narrow spectrum: gram +- used in serious infections (MRSA,VRE) -PK: IV only, incompatible w/ saline, no CSF, hepatic metabolism, biliary excretion -bacteriostatic, together may be bacteriocidal -AE: thrombophlebitis, muscle and joint pain, increased liver enzymes and hyperbilirubinemia |
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oxazolidinones
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antibacterial
protein synthesis inhibitor -synthetic -MOA: binds to 50s- inhibits formation of initiation complex -broad spectrum: gram +only -PK: complete absorption PO, widely distributed incl CSF, metabolized in liver -bacteriostatic - AE: n/v/d, bone marrow suppression |
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linezolid
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antibacterial
protein synthesis inhibitor: oxazolidinones |
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aminoglycosides
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antibacterial
protein synthesis inhibitor MOA: interfere w/ initiation @ 30s -broad spectrum: gram-- only, in combo for gram+ - distributed only in lean body mass -rapidly bacteriocidal, concentration dependent -post antibiotic effect:bacteria fail to grow despite concentration falling below MIC -AE: nephrotoxicity (reversible), ototoxicity (irreversible), neuromuscular blockade -extended interval dosing |
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amikcan
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antibacterial
protein synthesis inhibitor: aminoglycosides |
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gentamicin
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antibacterial
protein synthesis inhibitor: aminoglycosides |
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kanamycin
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antibacterial
protein synthesis inhibitor: aminoglycosides |
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momycin
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antibacterial
protein synthesis inhibitor: aminoglycosides |
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streptomycin
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antibacterial
protein synthesis inhibitor: aminoglycosides |
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tobramycin
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antibacterial
protein synthesis inhibitor: aminoglycosides |
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fluorquinolones
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antibacterial
alter nucleic metabolism -MOA: inhibits activity of topoisomerase- interferes with replication - spectrum: gram --, some pseudomonas -concentration dependent, bactericidal -PK: well absorbed except w/ multivalent cations, wide distribution, metabolized by liver, excreted by kidneys - AE: n/v, rashes, photosensitivity, atropathy, tendonitis, increased liver enzymes, cardiac arrhythmias, dizziness, seizures, hallucination |
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ciprofloxacin
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antibacterial
alter nucleic acid metabolism: fluorquinolones |
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gemifloxacin
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antibacterial
alter nucleic acid metabolism: fluorquinolones |
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levofloxacin
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antibacterial
alter nucleic acid metabolism: fluorquinolones |
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lomefloxacin
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antibacterial
alter nucleic acid metabolism: fluorquinolones |
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moxifloxacin
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antibacterial
alter nucleic acid metabolism: fluorquinolones |
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norfloxacin
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antibacterial
alter nucleic acid metabolism: fluorquinolones |
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ofloxacin
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antibacterial
alter nucleic acid metabolism: fluorquinolones |
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trimethoprim/sulfamethoxazole
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antibacterial
inhibit folate metabolism -MOA: inhibits synthesis of tetrahydrofolic acid= unable to synthesize DNA,RNA and proteins -spectrum: limited gram +/- -DOC for immunosuppressed -PK: analogs of PABA, well absorbed, widely distributed, excreted via kidneys -AE: hypersensitivity, rashes, stevens johnson syndrome (sloughing of skin), hematologic abnormalities, kidney inflammation, hepatitis, pancreatitis, encephalopathy in infants |
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metronidazole
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antibacterial
-MOA: binds to and breaks DNA- inhibits synthesis -anaerobic bacteria only- treats C.Diff -PK: high bioavailability PO and distribution incl CSF, liver metabolism, metabolites excreted by kidneys -AE: ataxia, dysarthia, dizziness, confusion, excitation, depression, seizures, peripheral neuropathy, metallic taste, alcohol=vomiting |
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daptomycin
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antibacterial
-MOA: Ca dependent binding and insertion of the lipophilic tail into gram + membrane--> ion leakage and collapse--> cell death -PK: IV only, small distribution, , renal elimination -concentration dependent bactericidal -AE: reverse myositis |
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polymyxins
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antibacterial
B and E -MOA: cause permability changes in gram - - used in ear/eye, multi resistant gram- -PK: concentration dependent killing, tightly bound to tissues, poorly distribution into lung, CSF, bone -AE: renal toxicity, neurotoxicity |
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amphotericin B
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antifungal
-MOA: binds to ergosterol in fungal cell membrane -PK: poor oral absorption, IV over 2-4 hrs, wide distribution, slow excretion via kidneys -AE: infusion rlated rxns- fever, chills, vomitting; nephrotoxicity, electrolyte imbalance |
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flucytosine
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antifungal
-MOA: inhibits thymidylate--> inhibits DNA synthesis -combo -PK: PO only, excreted by kidneys -AE: bone marrow suppression, hepatoxicity |
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echinocandins
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antifungals
-MOA: inhibits cell wall synthesis -PK: IV only, liver metabolism -AE: thrombophlebitis, abnormal liver enzymes |
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anidulafungin
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antifungal
echinocandin |
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caspofungin
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antifungal
echinocandin |
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micafungin
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antifungal
echinocandin |
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azoles
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antifungal
-MOA:inhibit synthesis of ergosterol- cell membrane component -PK: variable absorption PO, hepatic metabolism CYP 450 3A4 -AE: local irritation, hepatotoxicity, visual disturbances -inhibitor of CYP 450 |
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fluconazole
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antifungal
azole |
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itraconazole
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antifungal
azole |
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ketoconazole
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antifungal
azole |
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posaconazole
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antifungal
azole |
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voriconazole
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antifungal
azole |
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griseofluvin
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antifungal
-active against dermatophytes -MOA: disrupts microtubule function and inhibits mitosis -PK: PO only, increase absorption with high fat meal, metabolized by liver -AE: GI, hepatitis, phototoxicity, possibly carcinogenic |
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terbinafine
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antifungal
-treats superficial dermatophyte infections -MOA: inhibits ergosterol synthesis -PK: 40% bioavailability, due to 1st pass effect, highly protein bound, extensive liver metabolism, long 1/2 life -AE: GI disturbances, rash, dizziness, joint and muscle pains, hepatotoxicity |
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nystatin
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antifungal
-polyene -limited to direct contact surfaces- topical and PO swish |
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nucleoside analogs
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antiviral-herpes
-MOA:prodrug, prevents synthesis of viral DNA -PO, topical, IV -PK: eliminated in kidneys -AE: GI, headache, rash, neutropenia, thrombocytopenia, |
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acyclovir
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antiviral-herpes
nucleoside analogue -poor bioavailability |
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cidofovir
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antiviral-herpes
nucleside analogue -IV only -long 1/2 life, dose 1-2 weeks - AE: bone marrow suppression, very toxic |
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famiciclovir
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antiviral-herpes
nucleside analogue -best bioavailability |
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ganciclovir
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antiviral-herpes
nucleside analogue -IV, PO, poor bioavailability -AE: bone marrow suppression- very toxic |
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valcyclovir
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antiviral-herpes
nucleside analogue -prodrug, metabolized to be acyclovir |
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valganciclovir
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antiviral- herpes
nucleside analogue -PO -AE: bone marrow suppression- very toxic |
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foscarnet
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antiviral-herpes
-pyrophosphate derivative -MOA: prevents attachment of nucleotide precursors to DNA -Main use CMV, IV only, renal excretion -AE: toxic- nephrotoxicity, anemia, seizures, arrythmias, electrolyte imbalances |
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neuraminidase inhibitors
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antiviral-influenza
-MOA: prevents release of new virons -decreases symptoms and vaccine -AE: GI discomfort, nausea, respiratory tract irritation |
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oseltamivir
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antiviral-influenza
neuraminidase inhibitor - PO active prodrug, rapidly hydrolyzed in liver, eliminated unchanged in urine |
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zanamivir
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antiviral-influenza
neuraminidase inhibitor -eliminated unchanged in urine, absorbed through respiratory tract |
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carbonic anhydrase inhibitors
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diuretic
-MOA: inhibits carbonic anhydrase- req for Na resorption in PT- increases excretion of Na, H2O, HCO3 -used more for glaucoma and altitude sickness -AE: metabolic acidosis, hypokalemia |
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acetzolamide
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diuretic
carbonic anhydrase inhibitor |
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methazolamide
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diuretic
carbonic anhydrase inhibitor |
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loop diuretics
|
-most potent
-PO, IV -MOA: inhibits Na/K symporter in ascending LOH -increases excretion of Na and H2O by 25% and other electrolytes -high bioavailibilty, short 1/2 life -CI: allergy, electrolyte depletion, renal failure -AE: hypotension, hyponatremia, hypochloremia, hypokalemia, hypomagnesia, hypocalcemia, ototoxicity |
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furosemide
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loop diuretic
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burnetamide
|
loop diuretic
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torsemide
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loop diuretic
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ethacrynic acid
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loop diuretic
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thiazide diuretics
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-MOA: inhibits Na/Cl symporter in the distal tubule, up to 10% Na, H2O and other electrolyte excretion
-PK: absorbed in GI, metabolized in liver, excreted in urine -CI: sulfa allergy, fluid and electrolyte imbalances, severe renal disease -effectiveness decreases when creatinine clearance falls below 30ml/min -AE: low BP, hyponatremia, hypokalemia, hypomagnesia, hypocalemia, increased uric acid and plasma levels |
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hydrochlorothiazide,
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thiazide diuretic
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chlorothiazide
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thiazide diuretic
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metolazone
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thiazide diuretic
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chlorothalidone
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thiazide diuretic
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indapamide
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thiazide diuretic
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potassium sparing diuretics
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-limited usefulness as a diuretic
-MOA: at collecting duct, up to 2% Na and H2O excretion -PK: well absorbed, metabolized in liver, excreted in urine -AE: lethargy, confusion, hypotension, hyperkalemia |
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amiloride
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potassium sparing diuretic
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spironolatone
|
potassium sparing diuretic
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triamterene
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potassium sparing diuretic
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histamine (H2) receptor antagonists
|
treat GERD and ulcers
-available as OTC- moderate effectiveness -MOA: reversibly inhibit gastric acid secretion by competitively antagonizing H2 receptors on parietal cells- only blocks one receptor out of 3 -PK: well/rapidly absorbed from GI, 1/2 life 1-4 hrs, DOA 12 hrs, -AE: GI discomfort, diarrhea, constipation, sedation and delirium in elderly, gynecomastia and impotence in men -intrxns: drugs requiring gastric acid for absorption |
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cimetidine
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treat GERD and ulcers
histamine (H2) receptor antagonists -hepatically metabolized -CYP 450 inhibitor |
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famotidine
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treat GERD and ulcers
histamine (H2) receptor antagonists -hepatically metabolized |
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nizatidine
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treat GERD and ulcers
histamine (H2) receptor antagonists -eliminated renally, good for ppl with liver disease |
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ranitidine
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treat GERD and ulcers
histamine (H2) receptor antagonists -hepatically metabolized |
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proton pump inhibitors (PPI)
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treat GERD and ulcers
-MOA:admin as inactive prodrug, activated by acid-inhibits active proton pump by irreversibly binding to H/K ATPase enzyme across the parietal cell -PK: take w/food- oral bioavailibility decreases w/food, DOA 24 hrs, CYP 2C19 metabolism -AE: diarrhea, headache, abdominal pain, dizziness -intrxns: drugs via CYP 450 and requiring gastric acid for absorption |
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dexiansoprazole
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treat GERD and ulcers
proton pump inhibitor (PPI) |
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esomeprazole
|
treat GERD and ulcers
proton pump inhibitor (PPI) |
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lansoprazole
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treat GERD and ulcers
proton pump inhibitor (PPI) -approved to treat under 18 |
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omeprazole
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treat GERD and ulcers
proton pump inhibitor (PPI) -available OTC |
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pantoprazole
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treat GERD and ulcers
proton pump inhibitor (PPI) |
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raberprazole
|
treat GERD and ulcers
proton pump inhibitor (PPI) |
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antacids
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treat GERD and ulcers
-least effective- only treat symptoms -MOA: weak bases that react with acid to neutralize pH -PK: multiple doses daily- short DOA -intrxns: affect absorption of other drugs by binding to the drug b/c multivalent cation or by increasing pH-may cause enteric-coated to release early |
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aluminum salts
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treat GERD and ulcers
antacid -AE: constipation -used in combo products w/ magnesium |
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calcium salts
|
treat GERD and ulcers
antacid -AE:diarrhea, if absorbed: n/v, sedation - used in combo products w/ aluminum |
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sodium bicarbonate
|
treat GERD and ulcers
antacid -AE: bloating, belching, exacerbates: fluid retention, hypertension, kidney disease, heart failure |
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calcium salts
|
treat GERD and ulcers
antacid -AE: bloating, belching, hypercalcemia, constipation, rebound acid secretion |
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sucralfate
|
treat GERD and ulcers
GI protectant -MOA: in H2o or acid, forms viscous paste- binds to damaged, ulcerated tissue forming a protective barrier -PK: tablet or oral suspension, not absorbed, excreted in feces -AE: constipation, dry mouth, nausea, rash, renal dysfunction= CNS effects, diarrhea -intrxns: alter absorption of other PO drugs |
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misoprostol
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treat GERD and ulcers
prostaglandin -semi-synthetic- used only in prevention of gastric ulcer in pts w/ long term NSAID use -MOA: inhibits gastric acid secretion and promotes the scretion of mucus and bicarbonate -PK: rapid absorption, metabolized in liver, excreted in urine, 1/2 life-30 min -CI: pregnancy- stimulates uterine contractions- category X -AE: diarrhea, abdominal pain |
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phenothiazine
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treats nausea and vomitting
-antipsychotic drugs that are can be used for antiemetic and sedative properties -MOA: inhibits muscarinic and dopamine receptors (CTZ)- cause sedation by blocking histamine -PK: IV/PO- onset 30 min, PR-60 min -AE: sedation, hypotension, tardive dyskinesia, restlessness, muscular spasms, dryness, urinary retenion, constipation, pupil dilation, double vision, agitaion, tachycardia |
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promethazine
|
treats nausea vomiting
phenothiazine |
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prochiorperazine
|
treats nausea vomiting
phenothiazine |
|
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metoclopramide
|
treats nausea vomiting
nonphenothiazine -MOA: inhibits dopamine and serotonin receptors in CTZ -PK: PO/IV, rapidly absorbed, metabolized in liver, excreted in urine -CI: GI tract obstruction -AE: sedation, confusion, seizures, diarrhea |
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serotonin (5HT3) antagonists
|
treats nausea vomiting
-used for chemo induced and postoperative n/v -MOA: competitively blocks 5-HT3 receptors in the CTZ and GI tract -PK: 1/2 life of 4-9 hrs -AE: infrequent- headache, sedation, dizziness, constipation |
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doiasetron
|
treats nausea vomiting
serotonin (5HT3) antagonist |
|
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granisetron
|
treats nausea vomiting
serotonin (5HT3) antagonist |
|
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ordansetron
|
treats nausea vomiting
serotonin (5HT3) antagonist |
|
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palonosetron
|
treats nausea vomiting
serotonin (5HT3) antagonist -1/2 life of 40hrs- weekly dose |
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chemical stimulants
|
laxatives
-MOA: directly act on intestinal mucosa to alter fluid secretion--> stimulate perstalsis- increases amt of fluid in stool -PK: 6-10 hr onset PO, PR 15min-2hr -CI: appendicitis, fecal impaction, intestinal obstruction -AE: n/v, cramping, flatulence, urine discoloration, dependence |
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bisacodyl
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laxative
chemical stimulant |
|
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senna
|
laxative
chemical stimulant |
|
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bulk stimulants
|
laxative
-used to prevent constipation-safe for daily use -MOA: absorbs liquid in GI tract--> causes stool to swell --> facilitates peristalsis and motility -PK: begins in 12-24 hrs, full effect at 3 days -CI: intestinal perforation/obstruction, inability to drink adequate amt of fluid -AE: flatulence, bloating, cramps, n/v |
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psyllium
|
laxative
bulk stimulant |
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methylcellulose
|
laxative
bulk stimulant |
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polycarpophil
|
laxative
bulk stimulant |
|
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docusate
|
laxative-lubricant
-MOA: decreased surface tension of liquid in stool, causes additional liquid to be incorporated into feces -prevents constipation in cardiac pts and opiod users -1-3 day onset -AE: stomach upset, diarrhea |
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loperamide
|
antidiarrheal
-MOA: direct action on muscle of GI to slow activity -PK: PO only- poorly absorbed -AE: constipation, abdominal discomfort, n/v, dry mouth |
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diphenoxylate/atropine
|
antidiarrheal
-MOA: activates opiod receptors in the GI tract- decreases intestinal motility- more time for fluid and electrolytes to be reabsorbed -chem related to opioids, but doesn't exhibit analgesic except at high doses- mixed w/ atropine to discourage abuse -PK: PO only -AE: at high doses CNS effects- light headedness, hallucinations |
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bismuth subsalicylate
|
antidiarrheal
-MOA: decreased motility of GI tract through direct action on the lining to inhibit local reflexes -coats ulcers and erosions- protective layer -PK: subsalicyclate >90% absorbed, bismuth < 1%- converted to salicyclic acid and bismuth salts in GI, bismuth excreted in feces, subsalicylate in urine -caution/CI: aspirin, warfarin, allergy -AE: constipation, blackening of stool, darkening of tongue, toxicity in high doses |
