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80 Cards in this Set

  • Front
  • Back
Key reward area involved in addiction
nucleus accumbens
Dependence involves
tolerance
withdrawal
larger amounts/longer period of time
inability to cut down or control
great deal of time spent on obtaining, using or recovering
reduced other important activities
using despite probelms causes or exacerbated by use
physiological dependence involves
tolerance
withdrawal
tolerance
the phenomenon of decreased effect with prolonged exposure to a drug
acute tolerance
occurs in the time course of a single dose
chronic tolerance
occurs with repeated use of the drug
reverse tolerance
need less of drug for effect with chronic use (marijuana after first use)
postive reinforcers of addiction
increase DA release in nucleus accumbens
negative reinforcers of addiction
taking away a withdrawal syndrome
In intracranial self stimulation electrodes are placed on medial forebrain of rat and
drugs of abuse (morphine and barbs) decrease amount of current needed to experience reward while haloperiodal (D2 blocker, antipsychotic) increase the current needed for reward
Opoids + reinforcement
act on Mu-1 receptor and cause DA release in Nucleus accumbens
-euphoria
-mental clouding
Opoids - reinforcement
withdrawal symptoms:
-diaphoresis
-lacrimation
-rhinorrhea
-piloerection
-diarrhea
-yawning
-insomnia
-muscle aches
clonidine
reduces withdrawal symtpoms form opoid addiction
Clonidine is a centrally acting alpha2-agonist hypotensive agent
Clonidine treats high blood pressure by stimulating α2 receptors in the brain, which decreases cardiac output and peripheral vascular resistance, lowering blood pressure. It has specificity towards the presynaptic α2 receptors in the vasomotor center in the brainstem. This binding decreases presynaptic calcium levels, and inhibits the release of norepinephrine (NE). The net effect is a decrease in sympathetic tone
Clonidine is beneficial in opiate withdrawal because
it treats symptoms that are commonly associated with that condition (watery eyes and nose, diarrhea, irritability). For this condition, clonidine is often used alone. For the treatment of alcohol withdrawal, clonidine is usually combined with benzodiazepine tranquilizers such as Librium, Valium, Xanax, or Ativan.
opoid subsitution treatment
Another key component of the comprehensive package is the provision of drug dependence treatment and particularly of opioid substitution therapy (OST). OST has proven to be effective in the treatment of opioid dependence as well as in the prevention of HIV transmission, and improving treatment with antiretroviral therapy (ART).
methadone for opoid subsitution therapy
60-120 mg/day
buprenorphine for opoid subsitution therapy
low dose - prophylaxis agaisnt withdrawal
high dose - induces withdrawal

avaible in SL w/naloxone (can't INJ)
Coaine
naturally occuring alkaloid
increases DA in nuclues accumbens
short t1/2
coaine does NOT caue
life-threatening withdrawal syndrome
cocaine abuse is often comorbin with
depression
Phase I cocaine withdrawal
CRASH: wihtin hrs-days
-depression
-cravings
-fatigue
-agitation
Phase II cocaine withdrawal
WITHDRAWAL: 1-10 wks
-low/high cravings
-low anxiety
-anhedonia
anhedonia
is an inability to experience pleasurable emotions from normally pleasurable life
piloerection
the erection of the hairs on the surface of the skin
lacrimination
production of tears
cocaine withdrawal phase III
EXTINCTION: indefinite
-episodic craving
tx symptomatic anxiety in cocaine withdrawal
BZDs or SSRIs
longer lasting than cocaine(short t1/2)
D-amphetamine, methamphertamine, and methylphenidate
amphetamines
increase DA in nucleus accumbens
in withdrawal cause severe depression & lethargy
very high repeated doses of amphetamines can cause
paranoid schizophrenia
Barbs MOA
The principal mechanism of action of barbiturates is believed to be their affinity for the GABAA receptor (Acts on GABA : BDZ receptor Cl- channel complex). GABA is the principal inhibitory neurotransmitter in the mammalian central nervous system (CNS). Barbiturates bind to the GABAA receptor at the alpha subunit, which are binding sites distinct from GABA itself and also distinct from the benzodiazepine binding site. Like benzodiazepines, barbiturates potentiate the effect of GABA at this receptor. In addition to this GABA-ergic effect, barbiturates also block the AMPA receptor, a subtype of glutamate receptor. Glutamate is the principal excitatory neurotransmitter in the mammalian CNS. Taken together, the findings that barbiturates potentiate inhibitory GABAA receptors and inhibit excitatory AMPA receptors can explain the CNS-depressant effects of these agents. At higher concentration they inhibit the Ca2+-dependent release of neurotransmitters.[9] Barbiturates produce their pharmacological effects by increasing the duration of chloride ion channel opening at the GABAA receptor (pharmacodynamics: this increases the efficacy of GABA), whereas benzodiazepines increase the frequency of the chloride ion channel opening at the GABAA receptor
BZD & Barb MOA
indirectly increase GABA by facilitating its binding to its receptor
abilify
Aripiprazole (Abilify, Abilify Discmelt) is an atypical antipsychotic and antidepressant used in the treatment of schizophrenia, bipolar disorder, and clinical depressionAripiprazole's mechanism of action is different from those of the other FDA-approved atypical antipsychotics (e.g., clozapine, olanzapine, quetiapine, ziprasidone, and risperidone). Rather than antagonizing the D2 receptor, aripiprazole acts as a D2 partial agonist.[19][20] Aripiprazole is also a partial agonist at the 5-HT1A receptor, and like the other atypical antipsychotics displays an antagonist profile at the 5-HT2A receptor
buspar
Buspirone functions as a serotonin 5-HT1A receptor partial agonist.[4] It is this action that is thought to mediate its anxiolytic and antidepressant effects. Additionally, it functions as a dopamine D2, as well as α1, and α2-adrenergic receptor antagonist to a lesser degree, though these properties are generally undesirable in an anxiolytic and likely only contribute to side effects.
buprenorphine
Buprenorphine is a semi-synthetic opiate with partial agonist actions at the mu opioid receptor and ORL1/nociceptin receptor and antagonist actions at the kappa opioid receptor.
examples of partial agonists
buspirone, aripiprazole, buprenorphine
Barbs & BZDs withdrawal
Barb>BZD
similar to alchohol withdrawal
-insomnia
-anxiety
-tremulousness
severe withdrawal can proceed to seizures & death
anabolic steriods
maximum anabolic properties
AEs: acne, abnormal LFTs, feminzation, virilization, premature closure of epiphysical plates, behavioral changes, cardiomyopathy
pituary and synthetic gonadotropins
increase testerone
anti-estrogenic
AEs: ovarian cytsts
corticotropins
increase testerone
AEs: rare & related to corticosteriod use: pitutiarysuppression, decreased immunity, osteroporosis, hyperglycemia
growth hormone
increase muscle mass & decrease fat
AEs: gigantism, acromegaly, hypothyroidism, cardiac disease, myopathies, arthritis, DM, impotence, & osteoporosis
acromegaly
disease involving hormone overproduction: overproduction of growth hormones, resulting in enlarged bones in the hands, feet, jaw, nose, and ribs of adults
amphetamines & ephedrine
CNS stimulants
increase DA in nucleus accumbens
AEs: HT, agina, vomiting, abdominal pain, cerebral hemorrhage, dependence, death
Erythropoeietin (EPO)
stimulates RBC production
increases O2 carrying capacity
blood dopaing
RBC transfusion, arificial O2 carriers, increases O2 carrying capacity
allergic reactions
sludging of blood
tx alchohol addiction
withdrawal: BZDs
abstinecne: naltrexone, acmprosate or combination
naltrexone
Naltrexone is an opioid receptor antagonist used primarily in the management of alcohol dependence and opioid dependence. It
tx opiate addiction
withdrawal: clonidine
abstinence: buprenophrine or methadone
acamprosate
Acamprosate, also known by the brand name Campral, is a drug used for treating alcohol dependence.

Acamprosate is thought to stabilize the chemical balance in the brain that would otherwise be disrupted by alcoholism, possibly by blocking glutamatergic N-methyl-D-aspartate receptors, while gamma-aminobutyric acid (GABA) type A receptors are activated.[2] Reports indicate that acamprosate only works with a combination of attending support groups and abstinence from alcohol.[3] Certain serious side effects include allergic reactions, irregular heartbeats, and low or high blood pressure, while less serious side effects include headaches, insomnia, and impotence.[4] Acamprosate should not be taken by people with kidney problems or allergies to the drug.[5]
methadone
Methadone (also known as Symoron, Dolophine, Amidone, Methadose, Junkie Juice, Physeptone, Heptadon, Phy and many other names) is a synthetic opioid, used medically as an analgesic, antitussive and a maintenance anti-addictive for use in patients on opioids.
tx cocaine addiction
withdrawal: maintain comfort
smoking cessastion tx
1st line: bupropion SR & NRT
at risk drinking for men
>14 drinks/week
5 or more drinks/occasion
at risk drinking for women
> 7 drinks per week
4 or more drinks/occasion
ethyl alchohol PKs
not abosrbed by body fat
cross BBB rapdily
metabolized in liver via lacohol dehydrogenase
some eliminated through sweat, urine, and breath
zero order metabolism
CAGE ?s
cut down attempts
annoyed others with drinking
guilty about drinking
had an eyeopener
pharmacotherapy for alcohol addiction
disulfiriam
naltresone
acamprosate
BZDs
SSRIs
disulfiram
Disulfiram is a drug used to support the treatment of chronic alcoholism by producing an acute sensitivity to alcohol.
alcohol withdrawal
day 1 = anxiety
day 2 = increased BP & pulse
hallucination
day 3 = seizures
day 4 = delirium tremens & hyperthermia
delirium
craze: state of violent mental agitation
Wernicke-Korsakoff
Wernicke-Korsakoff syndrome (also called wet brain, Korsakoff psychosis, alcoholic encephalopathy, Wernicke's disease, and encephalopathy - alcoholic) [1] is a manifestation of thiamine (vitamin B1) deficiency, or beriberi. This is usually secondary to alcohol abuse. It mainly causes vision changes, ataxia and impaired memory.
alcohol withdrawal is
life threatening
DOC for alcohol withdrawal
BZDs
in alcohol withdrawal need to monitor
vital signs
hyperactivity in CNS
standard detoxification in alcohol withdrawal
day 1 lorazepam 2 mg PO/IM Q 8 hours
day 2 2 mg Q 12 hr
day 3 1 mg Q 12 hr
day 4 1 mg QHS
day 5 D/C
- can add PRN BZDs for breakthrough symptoms
symptom triggered alcohol withdrawal
clincial insititue withdrawal assessment for alcohol (CIWA)
typical plan: lorazepam 2 mg Q 1 hr PRN
can use ____ in conjunction with BZDs to tx alcohol withdrawal
beta-blockers
clonidine
carbamazepine
neuroleptics (if used alone with decrease seizure threshold) usually use atypical antipsychotics (D2 blockers) for agitiation/hallucinations
carbamazepine
arbamazepine (CBZ) is an anticonvulsant and mood stabilizing drug used primarily in the treatment of epilepsy and bipolar disorder, as well as trigeminal neuralgia. It is also used off-label for a variety of indications, including attention-deficit hyperactivity disorder (ADHD), schizophrenia, phantom limb syndrome, paroxysmal extreme pain disorder, and post-traumatic stress disorder.
Voltage-gated sodium channels are the molecular pores that allow brain cells (neurons) to generate action potentials, the electrical events that allow neurons to communicate over long distances. After the sodium channels open to start the action potential, they inactivate, essentially closing the channel. Carbamazepine stabilizes the inactivated state of sodium channels, meaning that fewer of these channels are available to subsequently open, making brain cells less excitable (less likely to fire). Carbamazepine has also been shown to potentiate GABA receptors made up of alpha1, beta2, gamma2 subunits.[7]
thiamine deficiency is common in
chronic alcoholics due to inadequate intake and malabsorption
supplement with 100 mg thiamine/day, multivitamine and 1 mg/day of folic acid
FDA approved meds for alcohol dependence
disulfiram (antabuse)
naltrexone (ReVia)
acamprosate (Campral)
disulfiram MOA
inhibits aldehyde dehydrogenase causing N/V, tachycrdia, facial flushing, dizziness
DIs: ampreanvir and lopinavir/tironavir PO solutions
need to monitor LFTs (hepatotoxicity)
ethyl alchocol is converted to acetaldehyde by alcohol dehydrogenase and acetaldehyde is covered to CO2 + H2) by aldehyde dehydrogenase
naltrexone
ReVia
opiod competitive antagonist
inhibits dopamine release thus blocking the reward pathway
do not administer naltrexone until
patient is opiod free for 7-10 days
naltrexone dose
50-100 mg PO

AEs: insomina, nervousness, HDs, N/V, joint & muscle pain
monitor LFTs
DI: opiods
Acramposate MOA
blocks glutamamte in nuclues accumbens
normalizes GABA in nucleus accumbens
increases taurine in ECF which contribute to GABA/glutamate balance
similar structure to glutamate & taurine
acamprosate dosing
666 mg TID PO
reduce dose when ClCr < 50 ml/min
D/C when ClCr < 30 ml/min

NO DIs
alcohol addiction meds with grade A efficacy
naltrexone
acamprosate
combination therapy for alcohol addiction
disulfiram + acamprosate (more efficacious than acamprosate alone)
ondansetron + naltrexone + CBT
acamprosate + natrexone (more effective than either agent alone but not statistically different than naltrexone is latest RCT)
add pyschological tx
Vivitrex
long acting IM naltrexone
flumanezil + BZD
Flumazenil should be used with caution in patients with chronic benzodiazepine use, prior seizure history, or when a mixed overdose is suspected. Flumazenil may unmask tricyclic antidepressant-induced seizures by antagonizing the antiepileptic effect of concomitantly ingested benzodiazepine.