Term
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Definition
Indic: Refractory CINV and AIDS associated anorexia
MOA: pure isomer of THC
AE: euphoria, impaired cognition, drowsiness
DDI; CNS dep and other cannabinoids |
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Term
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Definition
Indication: refractory CINV
MOA: synthetic analog of THC
AE: euphoria, drowinses, ataxia and vertigo
DDI: cns dep and other cannabinoids |
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Term
| Two endogenous cannabinoids: synthesis and release and degradation |
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Definition
AP releases glutamate -- binds post synaptically on glutamate receptor which induces Ca channels to open. Ca accumulation -- release of endocannabinoids from mb lipids.
This binds to CB1 receptor on the presynaptic (RETROGRADE RELEASE)
incr in CA triggers activation of NAT.. the rate limiting step
1) Anandamide -- fatty acid amide hydrolysis FAAH (located post synaptically)
2) 2-AG -- monoacylglycerol lipase (MAGL) -- located pre synaptically |
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Term
| Second messenger involved for CBR... and location of CB1 |
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Definition
secondary msg = cAMP - which causes decr in glutamate and NT release bc works on Gi
location: cerebellum, medulla, spinal cord, HT HC cerebral cortex BG (7) |
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Term
| Toxic effects of cannabinoids |
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Definition
initial stimulant phase: euphoria, sensation of slowed time, impaired judgment, decr appetite
later sedative phase: lethargy and increased appetite
Others blood shot eyes and tachycardia |
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Term
Cannabinoids decr release of glutamate and GABA how and
where does this occur |
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Definition
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Term
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Definition
Adddiction: PSYCHOLOGICAL DEPENDENCE --> inability to stop using a drug
Dependence : PHYSICAL -- body adapts to drug and requires more to get an effect (tolerance) and eliciting drug specific phys/mental sx if drug isnt used (withdrawal) |
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Term
| what part of brain does psychostimulants cause increased dopaminergic transmission |
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Definition
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Term
| 3 prominant pharmacotherapies for ADHD ? MOA and major NT affected |
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Definition
MP affects DAT and NET
Adderall does DAT, NET, SERT
- levo = vasoconstriction
- dextro = inhibits DAT MAO and reversal of DAT direction |
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Term
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Definition
insufficient NE DA and 5HT in synapse for adequate receptor activity
dep = deficiency in these
limitations
1) tpx lag. incr NT within hrs of taking med but effects not seen for 6 wks
2) depleting NT in normal ppl dont cause them to be depressed |
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Term
| monoamine NT: enz responsible and reuptake |
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Definition
5HT: MAO, SERT
NE: MAO COMT NET
DA: MAO COMT DAT |
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Term
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Definition
phenelzine, tranylcypromine, selegiline
MOA: monoamine NT accumulate so that more is released
AE: HTN CRISIS: TYRAMINE FOOOOOD tyramine is usu degraded by MAO. so since not degraded this incr NE/EPI |
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Term
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Definition
secondary: nortrip, desipramine, protripyline
tertiary: amitrip, imipramine, clomipramine, doxepin, trimipramine
MOA: NET SERT H1 M1 A1 blocks Na/K/Ca channels in heart
secondary = more selective for NET
AE
M1 blockade: anticholinergic -- blurry vision dry mouth constip glaucoma
a1: ortho hotn, reflex TC
H1 blockade: sedation
CARDIOTOXICITY
sexual dysfn and wt gain
DDI: QT prolonging and SEROTONIN SYNDROME
CI: GLAUCOMA, BPH, CVDz, SEIZ, concurrent use of MAOI |
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Term
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Definition
block sert: incr serotonin
class AE: GI, sleep, sex dysfn, bleeding
BBW: suicide ideation
w/d syndrome (flu like sx eshock like)
ss (tachycardia, hyperreflexia, HTN)
fluoxetine more activating, sertraline more diarrhea
paroxetine: worse GI, wt gain, sedation, more sx dysfn
DDI: fluox and parox for 2d6 , citalo = QT prolongation! |
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Term
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Definition
MOA: SERT and NET
class AE: HTN, GI, dry mouth, sweating insomnia, sexual dysfn, bleeding
DULOX: HEPATOTOXICITY
BBW: suicide ideation, w/d, SSRI
CI: HTN< hepatic impairmetn (dulox), and narrow angle glaucoma |
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Term
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Definition
MOA:
high doses: inhibits SERT and can agonize 5HT1A
low doses: angaonizes 5HT 2A/2C
also does a1 h1 m1
SE: sedation, orthostasis PRIAPISM, QT prolongation
DDI: MAOI and 2D6 Inhibitors (mcPP accumulation leading to panic attakcs)
CI: cardiac dz, QT prolong, glaucoma
NEFAZODONE: HEPATOTOIXICITY |
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Term
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Definition
MOA: a2 autoreceptor antagoniz: to incr NE and 5HT
does H1 and alpha 1 too
SE: sedation and wt gain
DDI sedatives, EtOH and MAOI (serotonin sndrome) |
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Term
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Definition
MOA: NET DAT inhibition and nicotinic recpetor antagonist
AE: insomnia, agitation, SEIZURES and rash
DDI: 2B6 inhibitors and inducers, 2D6 substrates
CI: seizure and eating disorders |
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Term
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Definition
AE: N/V/Constipation
DDI: Cyp2D6 |
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Term
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Definition
2nd have fewer antichol, a1, h1, and CV AE's... because they are more selective for NET
HIGHER AVAILABILITY
3rd = MORE BBB (LIPOPHILICITY) |
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Term
| Treat cardiotoxicity from TCA |
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Definition
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Term
| "emotional" brain circuits and association withd epressed mood, anxiety, and loss of pleasure |
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Definition
medial prefrontal cortex, anterior cingulate cortex, orbitofrontal cortex: depressed mood and anxiety (guilt, worthless, suicidality)
Amygdala and Hippocampus: Anxiety, hypersensitivity to stress
Nucleus accumbens: loss of pleasure (feeling worthless, guilt, suicidality) |
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Term
| new antidepressant with less SE and min wt gain |
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Definition
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Term
| Psychosis and Schizophrenia |
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Definition
psychosis: thoughts/emotions are distorted/ "loss of contact w/ reality"
SCHIZO:
POS: 4 Ds... auDitory halluc, delusions, disorganized speech, disorganized hbeaiovr
this ALLL OCCURS IN ALL PSYCHOTIC DISORDERS
NEG SX: UNIQUE TO SCHIZO --> social withdrawal, no motivation |
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Term
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Definition
MESOLIMBIC: hyperactivity --> pos sx (D2 blockade fixes this)
MESOCROTICAL: hypoact --> neg sx (D2 blockade worsens this) --> but if u hae a sertonin being blocked the dopamine isnt decreasing so less neg sx w/ second gen (serotonin inhibits dopamine.. so if u inhibit receptor theres more dopamine in mesocortical)
NIGROSTRIAL: motor moement..
D2 blockade causes EPS
TUBEROINFUNDIBULAR: controls prolactin levels (d2 blockade increases this) |
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Term
| rationale for 1st and 2nd aaps |
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Definition
reduces EPS (5HT2 in nitrostriatal: less serotonin happening, more DA in synapse)
neg sx: 5HT2-R in mesocortical
less prolactin: 5HT2R in tuberoinfundibular
BUTTTT more wt gain compared to 1st gen bc 5HT-2 R antagonism
Location of 5HT2A = in NIGROSTRITAL PATHWAY: so LESS EPS!!!!!!! |
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Term
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Definition
haloperidol and fluphenazine and pimozide!! ALL high potency
halo and pimo can be used for tourette's
haloperidol can be used for ADHD
Chlorpromazine and thioridazine has low potency
AE for all: QT prolongation, seizures, prolactinemia, EPS (acute dystonia, akathesia, park, TD), sedation, wt gain, orthostasis (alpha 1), and muscarinic 9AC side fe
HIGH POTENCY = MORE EPS
LOW POTENCY = all the other stuff
DDI: antichol, anti HTN, QT prolonging/EPS, CYP 3A4 and 2D6 (incr risk for QT/EPS) |
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Term
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Definition
Clozapine: refractory schizo ----- myocarditis, sialorrhea, agranulocytosis, seizures, metabolic SE, sedation, ACH SE, orthostatic HOTN, tachycardia
- CYP1A2 2D6 and 3A4
Olanzapin: weight gain!!!
Quetiapine: sedative
Risperidone: high prolactin levl and EPS at doses > 6 mg/day
Lurasidone and Aripirpazole = low metabolic se
ARIP; 5HT2A antagonist and D2 partial agonist |
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Term
| 1st generation AAPs: potencies |
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Definition
HIGH POTENCY: HALOP PIMO FLUPHEN: more EPS, less H1 (sedation, wt gain), alpha 1 (orthostasis) and antichol
low potency = all that stufffff |
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Term
| Aripiprazole vs Haloperidol |
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Definition
Arip:
- 5HT2A antagonist, weak partial agonist at presynaptic D2
- antagonist at postsynaptic D2
- high affinity to other D3 D4 5HT2C 5HT7 alpha 1 H1
Haloperidol: angoanist postsyn D2
- low affinity antag at H1, M and and alpha 1 |
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Term
| AAPs and highest probability for SE |
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Definition
METABOLIC: CLOZA AND OLANZAPINE
EPS: 1st gen more than 2nd... and in first gen = high potency, Risperidone
HYPERPROL: 1st >2nd, and Risper
QT prolongation: ALL OF 1st one, and most 2nd.. ONLY LURASIDONE DOESNT
Wt gain: 1st = H1 antagonism, 2nd gen: due to metabolic syndrome (5HT2C) |
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Term
| BAC: diff methods of measuring |
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Definition
% of ethanol in blood, measured in untis of mass per volume of blood
BAC of .1% = .1 g alcohol/ dL blood
measure w/ blood draw, breathalyzer, standard drink chart |
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Term
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Definition
Alc releases dopamine in nucleus accumbens (MESOLIMBIC PATHWAY) -- processes rewarding or reinforcing stimuli which leads to addiction
acts within CNS by INCR GABA and DECR GLUTAMATE
acts on mu opioid recpetors in these synapses or cuase release of endogenous opioids (enkephalins) |
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Term
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Definition
2E1 and alcohol dehydragenase
in chronic alc consumpion u incr leels of 2#1 and dpeles NADPH.. so u deplete glutathione stores so theres more toxic metabolite if u also take APAP and glutathione isnt there to remove it from APAP toxic metabolite
w/ acute; its not a risk factor for hepatotoxicity -- it can actually be protectie by competing w/ APAP |
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Term
| alcohol and antidepressants |
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Definition
TCAs:
- PD; additive sedation
- PK: intereferes with TCA metabolism so leads to more toxicity
MAOI: tyramine containing alcohols -- tyramine incr
Atypical antidepressants: additive sedation, impaired cognition, der motor perf |
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Term
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Definition
MOA: competitive mu opioid receptor antagonist -- decr reward pathway and therefore decr urge to drink
SE:
- CNS (HA, weakness, depression)
- Injection site rxn, nausea, diarrhea, musculoskeletal, anorexia
CI:
- concurrent use of opioids -- leads to acute hepatitis |
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Term
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Definition
inhibits aldehyde hydrogenase -- incr acetaldhyde so disulfuram effect = flushing sweating palpitations SOB, hypervent, HR, HOTN, vomiting
SE: HEPATITIS, SKIN ERUP, NEUROTOXICITY (optic neuritis, p neuropathy, polyneuritis)
CI: cardiac dz, psycohsis, ethanol intoxication |
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Term
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Definition
"artifical alcohol" reduces excitototxicity by enhancing GABA sys and inhibits glutamate system
SE: anxiety, depression, insomnia, diarrhea, impotence, rash, HTN, palpitations |
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Term
| BZDs vs Barbs on GABA a channel |
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Definition
BZDs: bind to GAMMA subunit --- allosteric modification that incr GABA recpeotr activity incr the frequency of channel opening events which leads to incr in Cl conductance and inhibition of aciton potential
incr gaba = less excitability
BARBS: Potentiate gaba aciton on cl entry into neuron by prolonging Cl channel opening. (more toxicity) -- doesnt need presence of GABA
use = GAD, social phobia, OCD, PTSD, panic, phobias |
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Term
| Alcohol on heart, GI, posterior pituitary and liver |
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Definition
heart: incr CO, SBP, HR, cardiomyoapthy after heavy chronic use
GI: gastritis, incr acid production by parietal cells in stomach, elyte/fluid imbalance
posterior pituitary: inhibits ADH secr ---- DEHYDR/HYPONATREMIA
liver: alcoholic hepattitis, fatty liver, cirrhosis |
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Term
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Definition
long acting = daytime sleepiness: fluraze and diazepam
short acting = rebound insomnia = triazolam and midazolam
DACLO |
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Term
| PK prop diff in anti anxiety and hypontic |
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Definition
HYPNOTIC =
rapid absnorption, high lipophilicity, no actie metabolites, and short acting |
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Term
| current binge and heavy alcohol use |
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Definition
current: at least 1 drink in past 30 days
binge: 5 or more in 1 occasion in past 30 days. BAC is > .08%
heavy: same as aboe for at least 5 diff days in past 30 days |
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Term
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Definition
M: inhibits DAT NET SERT by blcoking reuptake
can directly agonize central 5HT receptors: calming effect
interferes with VMAT too... so depleted vesicles = more NT in cytoplasm
Effects:
- acute: euphoria, wt loss, tremor/muscle twiching, speed psychosis
Toxicity: sleep dist, growth impairment, tic disorder
w/d of amphet, cocaine, MP: craving, anxiety, hypersomnolence, anhedonia |
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Term
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Definition
PNS: blocks fast sodium channels (local anesthetic effect)
CNS: blocks reuptake of DA, NE and 5HT (stimulant effects) - DAT NAT and SERT
more dapmine = rewarding effects
short term : euphoria, hyperstim, loss of appetite, incr HR/BPP/Temp,
long : halluinations, severe depression, organ damage, disor apathy confused exhaustion
w/d:
initial acute sx: crash --> depression, fatigue, craving, hypersom, anx, anhedonia
dysphoria/anhedonia can persist for weeks |
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Term
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Definition
MOA: DAT and NET inhibitor --> prolongation of NT effects --
metnal > motor activity
toxicity = nervousness, insomnia, decr appetite |
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Term
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Definition
SNRI
nonstimulant treatment for ADHD
NO ABUSE POTENTIAL
tox: SBP and HR,
kids/ teens: upset stomach, vomiting, tired
aduls: dry mouth, sex dysfunction |
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Term
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Definition
MOA: UNKNOWN inhibits DA reuptake, actiates glutam while inhibiting GABA and inhibtion of noradrenaline reuptake and orexin activation
used for nacrolepsy
serious AEs rash, mental sx (suicidal mania dep), heart prob (OB)
low abuse potential |
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Term
| cocaine and route of administration |
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Definition
snorted: peak in 30 min, e/s within 2 min
IV: peak in few min, 15-30 sec
snorted: within 6-8 seconds -- MOST RAPID |
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Term
| psychotropic leads to rebound |
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Definition
antianxiety: hyperexcitability/seizure
antipsychotic: TD
antidep: depression like sx |
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Term
| Addiction, pseudoaddition |
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Definition
compulsion to seek/take, loss of control in intake
- sx when px access
phys dep = w/d sx
dependence with little d: w/d sx
big Dependence = imairs fn
pseudoaditction: drug seeking behaivor to achieve pain relief
addiction = compulsive + impulsive |
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Term
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Definition
1) Binge/itnoxication: desire to take in more --> nucelus accumbens / ventral striatm (has DA?Opioids
2) withdrawal: extended amygdala -- antireward of drug dependence
decreases DA, opioid, and incr CRF and NE
3) preocc/anticip: persistent phys/psychologic problems aka craving -- prefrontal cortex
glutaminergic |
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Term
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Definition
+ reinfrocement: presence of drug increases probability of response (nondep drug taking)
- reinforcement: removal of a stimulus increases probability of response (dep induced drug taking) |
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Term
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Definition
promotes wakefulness through inhibiting NET and DAT
ae: insomnia
ddi: psychostimulants and grapefruit juice |
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Term
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Definition
schedule III - restricted distribution program
MOA: gaba analog that improves night sleep
ae: bed wetting, sleepwalking, resp depression |
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