Clin Med Exam 1 Meds

MOA: bind to G protein opioid receptors in the CNS, which inhibits ascending pain pathways = analgesia

opioids

AE: sedation, nausea, respiratory depression, cough suppressant, pinpoint pupil, truncal rigidity

opioid

AE: constipation, urinary retention, bronchospasm, reduced GI motility, itching

opioids

morphine (MC Contin)

strong u agonist

oxycodone (Oxycontin)

strong u agonist

fentanyl (Duragesic)

strong u agonist

hydromorphone (Dilaudid)

strong u agonist

hydrocodone/hydrocodone with acetaminophen (Vicodin)

strong u agonist

active metabolites even if normal renal function

strong u agonist

not to be used if opioid naive

fentanyl

codeine

mild-moderate u agonists

prodrug, may be used as an antitussive

codeine

weak u and k agonist and inhibits reuptake of NE and serotonin

tramadol

less risk of dependence, increases risk of seizures

tramadol

naloxone (narcan)

reversal agent

competitive antagonist at opioid receptors. possesses its highest affinity for the u receptor, allowing it to rapidly reverse life threatening respiratory depression and euphoria with less impact on baseline analgesia

naloxone (Narcan)

propofol

general anesthesia

exact MOA unknown; creates less “hangover” effect

inhaled general anesthesia

quick onset, quick recovery; often preferred for induction

IV general anesthesia

slightly sedated, but a whole region is blocked

regional anesthesia

lidocaine

regional and local

central block, peripheral nerve block, field block

regional

reversibly bind a receptor site within the pore of the Na+ channels in nerves —> block ion movement through the pore —> blocks the AP for nerve conduction

local

quick recovery, low toxicity, action mostly confined to nerves

local

incomplete analgesia, longer time to anesthesia

local

AE: RARE — CNS stimulation (tremors, confusion, seizures), respiratory depression, CV (arrhythmia, bradycardia, hypotension, cardiac arrest)

local

falls risk, decrease cough

anesthesia

fluoxetine (Prozac)

SSRIs

escitalopram (Lexapro)

SSRIs

selectively inhibits the serotonin reuptake transporter in the CNS, leaving more serotonin in the synaptic gap

SSRIs

headache, nausea, diarrhea, insomnia, sexual side effects, less common = low sodium and increased bleeding risks

SSRIs

should be taken in the AM

SSRIs

venlafaxine (Effexor)

SNRIs

duloxetine (Cymbalta)

SNRIs

inhibition of both serotonin and NE reuptake transporters in the CNS

SNRIs

AE: headache, nausea, dry mouth, excessive sweating, insomnia, sexual dysfunction

SNRIs

first line option if pt presents with concomitant neuropathic pain or fibromylagia

SNRIs

bupropion (Wellbutrin)

NDRIs — atypical agents

NE/dopamine reuptake inhibitor, blocking NE and DA reuptake pumps

NDRIs

AE: headache, nausea, tremor, dry mouth, decreased appetite, significant insomnia

NDRIs

risk of seizures, does not cause sexual dysfunction

NDRIs

MOA: inhibit reuptake of serotonin and NE in the CNS. they concurrently block histamine, muscarinic Ach, alpha adrenergic receptors

tricyclic antidepressants (TCAs)

AE: weight gain, sexual dysfunction, sedation, anticholinergic effects (dry mouth/urinary retention), OH/dizziness

TCAs

highly dangerous in overdose and arrhythmias

TCAs

esketamine (Spravato)

NMDA antagonists

increases glutamate —> increased BDNF

NMDA antagonists

alprazolam (Xanax)

benzos

clonazepam (Klonopin)

benzos

bind to BZD receptor sites on GABA gated chloride channels, enhancing the binding affinity of GABA to increase inhibitory chloride influx

benzos

acute/short term rescue for anxiety

benzos

AE: ataxia, sedation, memory problems. elderly patients prone to severe toxicity

benzos

maintenance treatment for anxiety

buspirone (Buspar)

binds directly to central serotonin and dopamine receptors

buspirone (Buspar)

carries no risk of abuse, induces no physiological dependence or withdrawal, causes limited motor, memory, or concentration impairment

buspirone (Buspar)

AE: dizziness, 3 weeks to see impact, may cause initial increase in anxiety

buspirone (Buspar)

long term panic attacks and as a targeted PRN med for phobias

propranolol

acts peripherally to block beta adrenergic receptors, directly shutting down sympathetic autonomic stimulation to eliminate physical heart palpitations and tremors

propanolol

encourage rapid neuroplasticity by stimulating the growth of entirely new structural connections between neurons

psychedelic assisted therapies

haloperidol (Haldol)

FGA

aripiprazole (Abilify)

SGA

quetiapine (Seroquel)

SGA

risperidone (Risperdal)

SGA

aggressive dopamine inhibitors

FGA

neurological, motor, extrapyramidal symptoms

FGA

UV exposure, thermoregulation, cardiac

FGA

gently blocks dopamine, mainly blocks serotonin

SGA

metabolic dysfunction, weight gain, high blood sugar, lipid abnorms

SGA

inability to stay still

akathisia

bradykinesia, rigidity, tremor, shuffle gait

psuedoparkinsonism

involuntary movement of face, mouth, tongue

tardive dyskinesia

lithium AE

levels, increased urination, thirsty/tremors, hair thinning/hypothyroidism, interactions, upset stomach, muscle weakness, skin

valproic acid

anticonvulsants

carbamazepine

anticonvulsants

lamotrigine

anticonvulsants

MOA: selectively bind a2 receptors in CNS to ↓ release of excitatory NTs from presynaptic terminals and ↓ excitability of postsynaptic neurons

alpha 2 adrenergic agonist — tizanidine (Zanaflex)

centrally acting drug class approved to manage spasticity, used off label for spasms

a2 adrenergic agonist — tizanidine (Zanaflex)

AE: drowsiness, dizziness, asthenia (abnormal weakness/lack of energy)

sedation within 30 mins of dose, peak 1.5 hours after dose

a2 adrenergic agonist — tizanidine (Zanaflex)

Indications: acute, painful MSK conditions rather than spasticity

cyclobenzaprine (Flexeril) and metaxolone (Skelaxin)

centrally acting antispasmodics

MOA: depress CNS activity and reduce excitability of spinal and supraspinal motor pathways, resulting in decreased muscle spasm and muscle guarding

cyclobenzaprine (Flexeril) and metaxolone (Skelaxin)

centrally acting antispasmodics

AE: sedation, dizziness

long-term or excessive use may contribute to tolerance and physical dependence

cyclobenzaprine (Flexeril) and metaxolone (Skelaxin)

centrally acting antispasmodics

all on beers list due to increased risk of sedation, fractures, some with anticholinergic effects, may have limited efficacy at tolerable doses

cyclobenzaprine (Flexeril) and metaxolone (Skelaxin)

centrally acting antispasmodics

indications: primarily used to manage spasticity and can also treat muscle spasms

diazepam (Valium) —> benzodiazepines

centrally acting antispasmodic

MOA: binds to GABAergic interneuron, blocks Ca+ influx into presynaptic terminal = ↓ NT release

diazepam (Valium) —> benzodiazepines

centrally acting antispasmodic

AE: sedation, ataxia, memory problems

diazepam (Valium) —> benzodiazepines

centrally acting antispasmodic

beers list: increased risk for active metabolites to remain in the body for days, heightened CNS sensitivity, severe sedation, falls

diazepam (Valium) —> benzodiazepines

centrally acting antispasmodic