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171 Cards in this Set
- Front
- Back
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cholinesterase inhibitors used in treatment of dementia |
donepezil, rivastigmine, galantamine |
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indications for donepezil? |
alzhemiers dementia, all stages |
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indications for rivastigmine |
alzheimers dementia, mild to moderate parkinsons disease dementia |
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indications for galantamine |
alzheimers dementia, mild to moderate |
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side effects of cholinesterase inhibitors |
primary: GI (nausea, vomiting, diarrhea, anorexia) secondary: insomnia, vivid dreams, bradycardia, syncope |
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drug interactions with donepezil and galantamine |
CYP2D6 and 3A4 hepatic metabolism |
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drug interactions for rivastagmine |
non-hepatic metabolism |
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glutaminergic antagonist used for dementia |
memantine |
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mechanism of action for memantine |
low-moderate affinity, voltage dependent antagonist of NMDA receptor activity (which play a role in long term potentiation in the hipposcampus, which underlies synaptic plasticity involved in learning) -it is thought that excessive stimulation of receptors results in excessive Ca influx into cells which leads to excitatotoxicity |
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indications for memantine |
moderate to severe alzheimers disease (not mild) |
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side effects of memantine |
headaches, constipation, agitation |
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drug interactions for memantine metabolism for memantine |
interactions: decreases metabolism of buproprion and trihexylphenidyl (anticholinergics used for parkinsons tremor) metabolism: non-hepatic (p450), decrease dose with renal insufficiency |
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through which mechanisms can you stop or prevent seizures? |
decrease excitatory synpatic neurotransmission (decreased glutamate) increased inhibitory synaptic neurotransmission (increased GABA) alteration in voltage gated ion channels to favor polarization (alterations in neuronal sodium and calcium channels) |
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which drugs are used to treat status elipticus but are classified as anixiolytic/hypnotic drugs rather than anti-epilepsy drugs? |
benzodiazepines, pentobarbital, propofol |
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neuronal voltage gated sodium channel binders (extend inactivated phase) |
carbemazepine phenytoin lamotrigine valproate topirimate |
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what are indications for carbamazepine? |
trigeminal neuralgia, mood stabalization in type 1 bipolar disorder (second line therapy) |
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side effects of carbamazepine |
toxic levels: decreased consciousness, N/V, double vision, ataxia leukopenia (anemia and pancytopenia happen too) hepatototoxicity hyponatremia all AEDs: dose related sedation, cognitive impairment, dizziness, potential for long term bone demineralization, tertogens, stevens-johnson syndrome |
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what are side effects of all AEDs? |
all AEDs: dose related sedation, cognitive impairment, dizziness, potential for long term bone demineralization, tertogens, stevens-johnson syndrome |
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carbamazepine metab and drug interaction |
metabolized in liver p450 inducer
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indications for phenytoin |
epilepsy
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mechanism of action for phenytoin |
binds to voltage gated sodium channels, which prolong inactivated phase, but they also affect resting memrane potential, synaptic transmission, and second messenger systems |
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side effects of phenytoin |
toxic levels: decreased consciousness, N/V, double vision, ataxia ALL AEDS: dose-related sedation, cognitive impairment, dizziness, potential for long term bone demineralization teratogenecity, stevens johnson syndrome many AEDs: bone marrow suppression, hepatotoxicity specific to PHT: gingival hyperplasia IV PHT: significant hypotension, cardiac arrhythmias, venous irritation-- led to dvlpmnt of fosphenytoin-- used for IV |
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metab and drug interactions for phenytoin |
metabolized in liver p450 inducer |
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lamotrigine |
known to inactivate neuronal voltage dependent Na channels, but they selectively influence neurons that synthesize excitatory NT such as glutamate |
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indications for lamotrigine |
epilepsy, mood stabilization in bipolar disorder |
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side effects of lamotrigine |
toxic levels: dizziness, somnolence all AEDs: dose related sedation, cognitive impairment, potential for long term bone demineralization, teratogenicity, stevens johnson LTG: terrible problems with life threatening rash valporate increases plasma conc of LTG and incresaes change of rash bone marrow suppression and hepatotoxicity are uncommon antidepressant effect |
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metab of lamotrigine and drug interaction |
metabolized in liver ESTROGEN and with other AEDs because of effects on the p450 system |
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ethosuximide (valproate) |
affects alpha subunit of neuronal voltage gated calcium channels heavily expressed in thalamic neuron populations (t type Ca channels) first line agent in absence of epilepsy |
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what are the GABA agonists? |
phenobarbitol (also valproate and topiramate work in many ways, but this is one of them) |
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mechanism of action for phenobarbital |
bind to GABA receptor, augmenting the effect of GABA by extending the duration of GABA mediated chloride chanel openings net effect: neuronal hyperpolarization |
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indication for phenobarbitol |
epiplepsy, tremor (primidone is used for treatment of essential tremor) |
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side effects of phenobarbitol |
at toxic levels: decreased conscoiusness, N/V, double vision, ataxia all AEDs: dose related sedation, cognitive impairment (limits its use except in status epilepticus, neonatal seizures, and refractory epilepsy) diizziness, long term bone demineralization, teratogenecity, steves johnson syndrome many AEDs: bone marrow suppression, hepatotoxicity specific to phenobarbitol: hyperactivity, addiction |
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metab of phenobarbitol and drug interactions |
metabolized in liver p450 inducer |
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which drugs have multiple mechanisms |
valproate (Na channel binder, Ca channel binder, GABA agonist) topiramate (Na channel binder, glutamate antagonist, GABA agonist) |
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valproate |
VPA blocks voltage dependent sodium channels (different site of phenytoin and carbamazepine) incresaes GABA conc by an unknown mechanism acts against T type calcium channels |
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indications for valproate |
epilepsy, mood stabalization in bipolar disorder, migraine prophylaxis |
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side effects of valproate |
toxic levels: decreased conciousness, N/V, ataxia all AEDs: dose-related sedation, cognitive impairment, dizziness, nausea/vomiting, teratogenicity (high risk of neuronal tube defects-- reduced with folate supp) long term bone demineralization, steven johnson syndrome hepatotoxicity-- esp in kids specific to valproate: tremor, weight gain, hair thinning, pancreatitis |
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topiramate MOA |
blocks voltage dependent Na channels, enhance action of GABA non-benzodiazepine site on GABA alpha, and antagonizes NMDA glutamate receptor |
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indications for topiramate |
epilepsy, migraine prophylaxis |
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side effects of topiramate |
cognitive impairment all the others that apply to all AEDS bone marrow suppression and hepatotoxicity are UNCOMMON specific to topiramate: weight loss, inc risk of kidney stones, dec. sweating, paresthesiasis, mood disturbances, metabolic acidosis |
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metabolism of topiramate |
70% excreted unchanged by kidney, 30% metabolized in liver |
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garbapentin indication |
epilepsy, chronic pain, neuropathic pain |
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gabapentin side effects |
toxic levels: dec consciousness, ataxia same as all AEDs no associated with hepatotox or bone marrow suppression specific to gabapentin: peripheral edema and weight gain |
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how is gabapentin metabolized? what are drug interactions? |
100% excreted unchanged in the urine (needs to have dose adjusted in kidney disease) need to be taken two hours after antacids which impair its bioavailability |
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levetiracetam |
MOA not well understood (binds SV2A protein in pre synaptic NT vesicle, modulate neuronal Ca channels used for epilepsy |
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levetiracetam side effects |
same as all AEDs, but its not assoc with hepatotox or bone marrow suppression has very few serious side effects |
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what are the main enzyme inducers and what effects do they have on other drugs? |
carbamezepine, phenytoin, phenobarbital increase metabolism of other drugs and reduce plasma concentrations and efficacy drugs: chemo agents, antivirals, benzos, corticosteroids, cyclospoorine, gireseofulvin, haloperidol, theophylline, TCAs, oral contraceptive pills/ERT, warfarin |
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which AED is an enzyme inhibitor? |
valproate-- dec metabolism of drugs and increases plasma concentrations (so you can experience toxicity) |
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which two drugs should a female watch out for? |
topiramate and lomotrigine both have interactors with oral conraceptives topiramate decreases efficacy of OCPs and then OCPs induce metabolism of lamotrigine and decrease plasma conc, so when you go on the sugar pill you have inc levels of lamotrigine |
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what should be prescribed with antiepileptic drugs for women? |
folate-- reduce risk of fetal malformations also, women who want to get pregnant should transition to monotherapy with any agent EXCEPT valproate |
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which drug do you use to treat absence seizure? |
ethosuximide |
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which drug do you use to treat primary generalized seizures? |
valproate |
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drugs used to treat partial seizures |
carbamazepine, phenytoin |
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drugs used to treat neonatal seizures |
phenobarbitol |
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which drugs can treat all seizure types? |
lamotrigine, levetiracetam, topiramate, valproate |
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which drugs have a narrow spectrum? (simple partial, complex partial, secondarily generalized seizures) |
carbamazepine, gabapentin, pregabalin, phenobarbital, phenytoin |
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which drug has a narrow spectrum and only treats absence seizure? |
ethosuximide |
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benzodiazepines (what do they end in?) |
alprazolam, clonazepam, diazepam, lorazepam, midazolam, oxazepam, tamezepam |
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what is mechanism of benzos? |
GABA-A enhancement |
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what are indications for benzodiazepines? |
anxiety disorder, panic disorder, insomnia (short term), pre-anesthetic, status epilepticus (anticonvulsant), alcohol withdrawal |
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side effects of benzodiazepines |
common: drowsiness, memory impairment, reduced motor coordination, somnolence severe: potential for addiction/abuse, respiratory depression, teratogen (cleft lip), neonatal toxicity |
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which drugs only require glucuronide conjugation (not hepatic oxidation) and have no active metabolites and are generally shorter acting (so preferred for elderly and those with liver impairments)? |
lorazepam, oxazepam, temazepam (LOT) |
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which drugs have shorter half life + higher potency? |
TOMAL: tamezepam, oxazepam, maidazolam, alprazolam, lorazepam |
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longer half life + lower potency |
clonazepam, diazepam |
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contraindications for benzos: |
acute narrow-angle glaucoma, respiratory insufficiency, sleep apnea |
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other precautions for benzos: |
abrupt discontinuation can lead to withdraw, active or history of alc abuse can lead to addition co admin with other CNS depressants can lead to respiratory depression |
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flumazenil-- what does it do? risk? |
benzo receptor antagonist that competitively inhibits activity at benzo recognition site on gaba/benzo receptor complex-- can reverse effect of benzos on CNS use for benzo overdose or toxicity abrupt benzo withdrawal--> seizures |
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busiprone MOA |
serotonin receptor partial agonist |
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indications for busiprone |
generalized anxiety disorder, chornic anxiety (in pt with subst. abuse) INEFFECTIVE at treating acute anxiety |
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side effects of busiprone, durg interactions, metabolism |
side effects: dizziness, drowsiness, headaches hepatic meatbolism, oral absorption half life 2-11 hrs so administer BID |
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non-benzodiazepine hypnotics |
zolpidem, zaleplon, eszopiclone |
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mech of action of non-beno hypnotics (zolpidem, zaleplon, eszopiclone) |
bind to GABA receptor subtypes that specifically modulate sleep-- thought to have less unwanted side effects |
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indications for zolpidem, zaleplon, eszopiclone |
short term treatmnet of insomnia sleep onset insomnia: zolpidem and zaleplon sleep onset and sleep maintenance insomnia: zolpidem and eszopiclone |
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how do side effects of non-benzo hypnotics compare to benzos? |
shorter duration of action than benzo, less likely to have next day sedation (still can have drowsiness, dizziness, unsteady gait, rebound insomnia, memory impairment) less likely to be abused |
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metabolism and drug interactions of non-benzo hypnotics |
metabolized by p450 system, affected by inducers/inhibitors of system
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melatonin receptor agonists indications, MOA, side effects? |
ramelton agonizes M1 and M2 melatonin receptors in suprachiasmatic nucleus of hypothalamus used to sleep onset insomnia side effects: head ache, dizziness, drowsiness, fatigue, nausea |
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where do antipsychotics exert their effects? 1st generation? 2nd generation? |
at the mesocortical and mesolimbic dopminergic pathwyas first generation (typical) have high affinity to antagonize dopamine D2 receptors second generation (atypical) antipsychotics are slightly weaker D2 receptor antagonists as well as strong serotonin receptor antagonists |
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first generation (typical) antipsychotics |
haloperidol- high potency perphenazine: mid-potency chlorpromazine: low potency |
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second generation (atypical) antipsychotics: |
olanzapine clozapine quetiapine risperidone aripiprazole ziprasidone its atypical for old closets to quietly risper from A to Z |
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indications for antipsychotics |
schizophrenia and schizoaffective disorders and psychosis secondary to mood disorders, delerium, and intoxication |
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what is clozapine used for? |
for efficacious for schizophrenia, but it has a life-threatening side effect (agranulocytosis) which makes it a second-line agent so its used for refractory schizophrenia |
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general side effects of antipsychotics |
delay cardiac conduction (prolong QT interval)-- pts can develop torsades de pointes black box warnign that they increase rate of death in elderly patients with dementia related psychosis |
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anticholinergic effects of antipsychotics |
lower potency antipsych (chlorpromazine) have more anticholinergic effects: blurred vision, constipation, dry mouth, orthostatic hypotension, sedation, urinary retention higher potency antipschy (haloperidol) exhibit stronger DA antagonism and have more extrapyramidal symptoms (nigrastriatal pathway) |
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what are the extrapyramidal symptoms (in haloperidol for example) |
along nigrastriatal pathway acute dystonic reaction-- develop over hours to days, sustained contraciton of muscles (usu in neck, mouth, toungue) tx: IM diphenhydramine, benztropine akathisia: develop over days to weeks, defined as feeling of inner restlessness (you get anxiety/agitation but also pacing, rocking) parkinsonism (dv over weeks to months)-- tx: diphenhydramine, benztropine tardive dyskinesia: after 6+ months of D2 blockade-- hyperkinetic movement, perioral movements (tongue, facial grimacing, lip puckering)-- if using 1st line gen, switch to 2nd, and if usig 2nd, switch to clozapine |
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what is hyperprolactinemia? what stimulates it? |
excessive DA blockade along tuberoinfundibular pathway stimulates prolactin release can result in osteoporosis, amenorrhea, galactorrhea, gynecomastia, sexual side effects haloperidol, risperidone are most commonly cause this |
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metabolic effects of antipsychotics |
2nd gen antipsychs assoc w/ metabolic syndrome (weight gain, diabetes, hyperlipidemia, hypertension) drugs induce insulin resistance and dyslipidemia independent of associated weight gain-- elevate CV risk factors |
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neuroleptic malignant syndrome |
rare of potentially fatal idiosyncratic rxn to DA blockade (usually occur in 1st week) -- confusion, vital sign instability, extreme hyperthermia, rhabdomyolysis, renal failure, CV collapse, and eventually death from first aid:: FEVER Fever, Encepalopathy, Vitals unstable, Enzymes elevated, Rigidity of muslces |
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what causes malignant hyperthermia? what causes malignant syndrome? |
malignant hyperthermia: rxn to succinylcholine or inhaled anesthetics malignant syndrome: antipsychotics in NMS, muscle rigidity due to DA blockade in brain in MH, pathophys of rigidity occurs at level of muscle |
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what is treatment for malignant hyperthermia and malignant syndrome? |
dantrolene |
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which antipsych drugs are first line? |
second gen are first line for psychosis to lessen risk of extrapyramidal symptoms (but do carry risk of metabolic syndrome) clozapine is high risk (agranulocytosis, metab side effects, myocarditis) and high reward (high efficiacy, low risk of EPS) |
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what is the black box warning for antidepressants? |
increase suicidal thinking and behavior in children, adolescents, an dyoung adults with major depressive disorders and other psych disorders |
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which drugs at MAO inhibitors? |
phenelzine and tranycypromine |
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MOA of MAO inhbitors (phenelzine and tranycypromine) |
irreversibly inhibits monoamine oxidase enzyme that breaks down monoamine NTs (5-HT, NE, DA) |
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indications of MAO inhibitors |
first line tx for atypical depression, anxiety and for MDD after other tx options have failed |
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side effects of MAO inhibitors |
orthostatic hypotension, sedation, sexual dysfunction |
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important drug interactions |
admin of multiple sertonergic agents (MAOIs, SSRIs) can result in serotonin syndrome due to additive effect |
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what is serotonin syndrome? |
diarrhea, restlessness, hyperreflexia, autonomic instability, hyperthermia, rigidity, delerium distinguish it from neuroleptic malig syn by HYPERREFLEXIA |
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what drugs are contraindicated with MAOis? |
methylodpa, other classes of antidpepressants (need 14 day washout, 5 wk for fluoxetine), sympathomimetics, meperidine, dextromethorphan (cough supressant in OTC meds), appetite supressants, carbamazepine, triptans |
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tyramine induced hypertensive crisis |
tyramine is potent releaser of NE-- causes vasoconstriction and elevated BP tyramine is normally degraded by MAOa ,and when its inhibited by MAOIs, small amounts of tyramine in diet can cause hypertensive crisis
symptoms: N/V, occipital headache, stiff neck, sweating dont eat aged/fermented meats, sausages, pickled herring, lima beans, tap beer, cheese, red wine, soybean |
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selective serotonin reuptake inhibitors |
citalopram, escitalopram, fluoxetine, fluvoxamine, paroxetine, sertraline work by blocking presynaptic reabsorption of serotonin, increase levels
Flashbacks Paralyze Senior Citizens Fluoxetine, Paroxetine, Sertraline, Citalopram |
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indications for SSRIs |
MDD, various anxiety disorders |
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side effects of SSRIs |
nausea/loose bowel, resolve after 1st week of therapy sexual: dec. libido, delayed ejaculation, anorgasmia paroxetine: associated with weight gain |
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how are SSRIs metabolized? drug interactions? |
metab: hepatic fluoxetine has longest half life (2 wks) fluvoxamien and paroxetine have shortest-- likely to induce discontinuation syndrome that has flu like symptoms, irritability, dizziness, vivid dreams CONTRAINDICATED with pimozide |
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serotonin-norepinephrine reuptake inhibitors |
venlafaxine, desvenlafaxine, duloxetine |
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MOA of SNRIs |
blocks the reuptake of presynaptic serotinin and NE-- at low doses they function as SSRIs, and at higher doses they block reupatkes of NEs as well |
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indications for SNRIs |
MDD, various anxiety disorders, neuropathic pain |
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side effects of SNRIs (venlafaxine, desvenlafaxine, duloxetine) |
GI: nausea/loose bowel movements-- resolves after first week of therapy sexual: dec libido, delayed ejaculation, anorgasmia (50% incidence) increase in diastolic BP (HTN) |
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metabolism of SNRIs and drug interactions |
be careful when prescribing wiht other serotonin drugs in risk of serotonin syndrome metab: hepatic (CYP450) duloxetine-- moderate CYP450 inhibitor |
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tricyclic antidepressants |
amitriptyline, nortriptyline, imipramine (end in triptyline or ipramine) |
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MOA of tricyclic antidepressants |
blocks 5-HT and NE transporters-- inc. conc of these NT in the synaptic cleft blocks histamine receptors and muscarinic acetylcholine receptors with high affinity |
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what are indication for triclyclic antidepressants? |
MDD, chronic pain headaches (prophylaxis and treatment) nocturnal enuresis (imipramine)-- inability to control bladder |
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side effects of TCAs |
anticholinergic: blurred vision, constipation, dry mouth, orthostatic hypotension, sedation, urinary retention CV: tachycardia, prolonged QT interval overdoses are lethal |
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atypical antidepressants |
bupropion, mirtazapine, amoxapine, trazodone |
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bupropion MOA and indications |
unicyclic antidressant-- inhibits reuptake of DA and NE, preferred over SSRIs by many pts bc of lack of sexual side effects indications: MDD, seasonal affective disorder, smoking cessation side effects: constipation, headache, nausea, anxiety severe-- seizures, pyschosis |
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mirtazapine and amoxapine |
tetracycline-- increases conc of NE and 5-HT indications: more sedating than other antidepressants-- also used to treat insomnia in addition to MDD side effects: weight gain, sedation severe: agranulocytosis |
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drug interactions for atypical antidepressants |
avoid co-admin with MAOis due to hypertensive crisis bupropion-- use caution with other DA agents |
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trazodone |
complex-- increase serotonergic activity via poorly understood mechanisms indications: more sedating than other antidepressants-- also used to treat insomnia in addition to MDD side effects: anticholinergic symptosm (dizziness, dry mouth, orthostatic hypotension, sedation severe-- priapism (think trazobone) |
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lithium |
mood stabilizer that alters cation transport across cell membranes in nerve and muscle cells, influences reuptake of serotonin and NE used for bipolar disorder |
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what are side effects of lithium? |
very effective, but very toxic, narrow therapeutic window common: cognitive slowing, GI upset, polyuria, tremor severe: cardiac conduction delays, diabetes insipidus, ebstesins anomaly, hypothyroidism moderate tox: twiching, slurred speech, lethargy, hyperreflexia, vertigo, GI upset (tx: supportive measures-- stop lithium, fluids) severe tox: seizures, stupor, coma, CV collapse, death tx: hemodialysish
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how is lithium metabolized? |
100% renally excreted co-admin with NSAIDs (except salicylate), diuretics (thiazides), or ACE inhibitors are dangerous due to risk of lithium toxicity |
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anticonvulsants |
valproate, carbamezpine, lamotrigine |
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what is valproate used for? |
to treat manic and maintenance phases of bipolar disorder-- preferred treatment for rapid cyclinc bipolar patients and patients with mixed episodes (depressive and manic symptoms present) |
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carbamazepine used for? |
to treat manic phase of bipolar disorder, may be effective for maintenance phase too |
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lamotrigine |
used to treat maintenance phase of bipolar disorder |
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alcohol signs of intox where in body does alc have effect? |
signs of intox: ataxia, incoord, slurred speech, euphoria, impaired attention, irritability, mood changes, sedation, nystagmus neuro, GI, CV, hem/onc, endocrine |
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alcohol withdrawal |
autonomic hyperactivity (sweating or pulse >100 bpm) hand tremor insomnia, n/v, transit visual. tacitle, auditory hallucinations or illusions psychomotor agitation, anxiety, seizures |
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alcohol use disorder |
tolerance and withdrawal are potential but not required symptoms -- alc taken in at larger amounts, unsuccessful at cutting back, craving it, dec time at friends or work, physical hazards |
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alcohol induced diosrders |
substance/med induced depressive diosrder, anxiety disorder, psych disorder, bipolar diosrder symptoms resolve within 1 mo of drug discontinuation specify if related to intox or withdrawal |
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what quantifies at risk drinking? |
femal: >3 drinks in one sitting, <7 in week male: >4 drinks in one sitting, >14 in week pregnant: any drinking male/female younger than 14:any drinking male>65: >3 drinks in one sitting, 7/week |
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alcohol screening for adults? for adolescents? |
CAGE- cut down,annoyed others with drinking, guilt, eye opener alcohol drink in morn CRAFFT- in car with anyone driving while drinkign R: drink to relax? A- drink alone? F-family/friends tell you to cut down F- forget things while drinking? Trouble? due to drinking/using |
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BACs and effects? |
0-100 (mg/dL)- well being, sedated, tranquil 100-150: irritable, incoordinated 150-250: slurred speech, ataxia >250: unconcious |
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what lab tests can you do to detect someone's alcohol use? |
ehtyglucuronide (EtG) and ethyl sulfate (can see past days) carbohydrate deficient transferrin (equivalent of HbA1c in diabetics--see past month's use LFTs (GGT, AST, ALT are increased) increase lactate dehydrogenase, inc MCV, inc uric acid, decrease BUN high HDL and low LDL
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alcohol withdrawal |
N/V, tremor, hallucinations, agitation, seizures delerium tremens, insomnia, irritability, HTN, tachycarida, nausea, sweating |
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when does delirium tremens |
onset 48-96 hours after last drink hyperactivity/excitation increased HR/inc BP, fever frightening hallucinations disorientation fluctuating level of conciousness can be fatal if severe med problems must rule out other causes of delerium
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what is the triad in wernickes encephalopathy? |
confusion, ataxia, opthalmoplegia due to low thiamine (B1) emergency if untreated --> death in 20% treat by IV thiamine (always give thiamine before glucose) |
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korsakoff syndrome |
impaired memsry in otherwise alert, responsive patient retrograde and anterograde memory loss mammilary bodies, thalamus |
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tx of alcohol withdrawal |
benzodiazepine LOT have less hepatic metabolism (lorazepam, oxazepam, temazepam) also give thiamine, multivitamin, folate |
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what do you give if alc withdrawal pt goes into hepatic failure or hepatic encepalopathy? |
lorazepam or oxazepam |
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what do you give if alc withdrawal starts having seizures? hallucinations? |
seizures: full court press benzodiazepines add anticonvulsant hallucinations: low dose haloperidol |
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disulfiram |
antabuse-- given to alcoholic. blocks step in metabolism of EtOH, increases acetaldehyde drink ETOH--> N/V, sweating, headache, low BP- psychological and pharmacological deterrent |
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acamprosate |
campral, oral , NMDA receptor antagonist, reduces cravings associated with post withdrawal negative effects |
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naltrexone |
oral (24 hr half life), injectable (monthly) opioid receptor antagonist reduces cravings associated with rewarding effects of alcohol |
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flumazenil |
reverses effects of benzodiazepines (but watch out for withdrawal-- can be life threatening withe benzos |
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benzodiazepine and bartibuate withdrawal |
altered perceptions, insomnia, irritability, seizures, HTN, tachy
(like ethanol, but no nausea or sweating, no tremor, instead you get muscle cramps and twitching)wh |
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ich two drug withdrawals are potentially fatal? |
ethanol and benzodiazepine |
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opioid withdrawal |
altered perceptions, insomnia, irritability, seizures, muscle aches, HTN, tachy, nausea, sweating, fever, mydriasis (DILATED pupils), diarrhea, yawning, pilo-erection (goosebumps) (resembles flu-- muscle aches, sweating, chills) |
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MOA for ethanol, barbituates, benzo |
potentiating GABA receptor ethanol potentiates gamma amniobutyric acid |
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alcohol metabolism |
alcohol dehydrogenase breaks ethanol into acetylaldehyde (hangover feeling) aldehyde dehydrogenase breaks acetylaldehyde into acetate ethanol at higher doses undergoes oxidation by cytochrome P450 enzymes (CYP2E1) |
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CNS stimulants sign of intoxication |
caffeine, nicotine, amphetamines, cocaine
amphetamine: behavior: grandiosity, euphoria, hypervigilance, paranoia, agitation autonomic symptoms: hypertenion, tachy, chills, mydriasis (DILATED PUPIL), nystagmus, sweating
cocaine: tactile hallucinations of bug crawling on skin |
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tx of amphetamine and cocaine overdose |
lorazepam (agitation) cardiac monitoring and support haloperidol for psychosis |
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signs of ampetamine/cocaine withdrawal |
increased appetite, bradycardia, depression/dysphoria, drowsiness/fatigue |
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symptoms of nicotine withdrawal |
increased appetite, bradycardia, dysphoria, anxiety, irritability, restlessness |
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caffeine withdrawal signs |
anxiety, depression, impaired concentration, headache, malaise |
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cocaine MOA |
inhibits neuronal reuptake of NE and DA |
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caffeine MOA |
indirectly enhances DA neurotransmission by blocking adenosine receptors throughout the CNS |
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nicotine |
activates cholinergic nicotinic receptors in both CNS and PNS |
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amphetamine |
increase synaptic concentrations of NE and DA |
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lSD |
psychotic symptoms: hallucinations, delusions neuro: ataxia and tremo autonomic: mydriasis (dilated pupils), tachy and sweating (activates serotonin receptors in neocortex, brainstem, limbic system) |
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PCP |
psychotic symptoms: hallucinations and delusions with euphoria and violent behavior neuro: muscle rigidity and nystagmus autonomic: miosis, tachy, sweating blocks NMDA receptors |
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what is emergent treatment of intox/overdose of PCP and LSD? |
lorazepam for agitation minimize sensory input support vital functions haloperidol for psychosis |
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signs of marijuana intoxication |
rapid speech, conjuncitivitis, hallucinations, jocularity, hypertension and tachycardia, increased appetite, tightness in chest, euphoria and sensory intensification, dry mouth treat overdose (agitation) with lorazepam |
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what are symptoms of withdrawal from marijuana? |
irritability, mild agitation, sleep disturbances, nausea, stomach cramps treatment is unnecessary |
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marijuana MOA |
THC (delta-9-tetrahydrocannabinol) binds to cannabinoid receptors, activates adenylyl cyclase and cAMP, which modulates activity of Ach, DA, serotonin marijana can lower testosterone, decrease ovulation, lead to low birth weight in neonates |
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what do you to manage opioid overdose/intoxication? withdrawal? |
cardiac monitoring, naloxone (quick opioid antagonist) withdrawal-- not life threatening, but help with symptoms: clonidine-- autonomic instability NSAIDs- pain muscle relaxants-- muscle pain antidiarrheal/anticholinergic-- GI symptoms consider methadone/burprenorphine taper
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pharm tx for opioid addiction |
naltrexone: opioid antagonist methadone: long acting opioid, daily clinic visits buprenorphine/naloxone: partial opioid agonist + opioid antagonist office based, need DEA waiver |
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stimulants |
cocaine, amphetamine, methamphetamine, bath salts, (caffeine and nicotine) effects: mood elevation, insomnia, psychosis, dec. appetite, CV (inc BP and P), inc GI, dilated pupils |
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stimulant withdrawal withdrawal tx? |
depression, irritability, lethargy, fatigue, headaches, inc. appetite, CV (dec BP and P), dec GI activity, dec neuro activity (cardiac monitoring, benzodiazepines, antipsychotics) |
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drug interactions of nicotine |
CYP 1A2 dec effects of antipsych agents, antidepressants, tacrine, theophylline, caffeine oral when combined with contraceptives: MI, CVAs, thromboembolism to withdrawal: buproprion and varenicline |
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hallucinogens |
marijuana, spice, hashish, salvia, LSD, psiolocybin, MDMA (ecstasy) effects: hallucinations (visual >> auditory), synethesia (can feel colors), hyperalertness, clear sensorium, memory INTACT, reality testing can be intact |
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dissociatives: NMDA antagonists |
PCP, ketamine, dextromethorphan, nitrous oxide dissociation, hallucinations, sensory isolation, mental distortion, invulnerability, agitation, violence, nystagmus, hyperreflexia, confusion, increased BP and P, coma and seizure rare |
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inhalants |
fules, pain, household substance, amyl nitrate, anesthetics, Nitrous oxide euphoria, disinhibition, dizziness, lightheadedness, drowsiness, slurred speech, ataxia, accidents/injuries, muscle/joint pain, respiratory depression, asphyxia, chest pain, dysrthymias, cardiac arrest, neuro, cognitive |
