Term
|
Definition
| Risk of depression, mania or psychosis during pregnancy or postpartum, especially if susceptible |
|
|
Term
|
Definition
Highest risk at 4-6 wks postpartum
No prior depression -- 8-10%
Hx of depression -- 25%
Hx of postpartum depression -- 50%
Sleep deprivation is a major factor.
Take naps if necessary. |
|
|
Term
|
Definition
Use psychotherapy w/o meds whenever possible, especially during 1st trimester and 1-2 mos before delivery
ADs generally considered fairly safe, but infant withdrawal sxs may occur
If must use an AD, use fluoxetine (but avoid paroxetine [Paxil])
Breast feeding not recommended |
|
|
Term
| Bipolar or psychosis during pregnancy |
|
Definition
Generally, SGAs are preferred over lithium & anticonvulsants during pregnancy.
Valproate preferred over lithium; other anticonvulsants preferred over valproate
Generally, breast feeding is not recommended. |
|
|
Term
| Lithium and anticonvulsants in pregnancy |
|
Definition
Try to avoid during 1st trimester and use lowest possible dose
Birth defects - Ebstein’s anomaly (abnormal tricuspid valve, which separates right atrium from right ventricle), hypotonicity
Breast feeding – not recommended |
|
|
Term
|
Definition
Neural tube defects; withdrawal sxs in infant
(irritability/jitteriness, abnormal tone, feeding
difficulties, seizures) - Rx folate, 1 mg/d
Rx vitamin K, last 6 wks to prevent bleeding
Breast feeding – considered safe but watch for irritability, sedation |
|
|
Term
| Increasing DA & NE in circuits involving basal ganglia and prefrontal cortex |
|
Definition
Improves attention, executive function
Decreases hyperactivity & impulsivity
May decrease depression, fatigue, sleepiness. |
|
|
Term
| Psychostimulants generally used for |
|
Definition
|
|
Term
|
Definition
Most used/studied, FDA approved 6 yrs & older
Increases DA > NE by blocking reuptake |
|
|
Term
| Immediate release stimulants |
|
Definition
(RitalinTM, Methylin®, Focalin®)
Effects within 30-60 minutes; peak in 1-3 hrs; lasts 3-5 hrs; so requires 2-3 doses/day |
|
|
Term
|
Definition
Causes reuptake transporter to work in reverse
Increases release of DA & NE
Blocks reuptake of DA & NE
Effects within 30-60 minutes; peak in 1-3 hrs for tablets and 8-10 hrs for spansules; lasts 4-6 hrs; bid or tid |
|
|
Term
| lisdexamfetamine (Vivanse) |
|
Definition
A prodrug that is absorbed by GI tract and converted to dextroamphetamine
Peak in 3.5 hrs; lasts 10-12 hrs; qam |
|
|
Term
| Mixed amphetamines (Adderall®, Adderall XR®) |
|
Definition
4 salts of d-amphetamine & l-amphetamine
is being abused to lose weight by pts who “fake” ADHD sx |
|
|
Term
| Mixed amphetamines (Adderall®, Adderall XR®) |
|
Definition
4 salts of d-amphetamine & l-amphetamine
is being abused to lose weight by pts who “fake” ADHD sx |
|
|
Term
| Advantages to sustained-release formulations: |
|
Definition
Decrease SEs and possibly improve therapeutic effects by smoothing out peaks & troughs
Decrease abuse potential by increasing tonic (steady) DA & NE signals while not excessively increasing phasic signals
Phasic signals (pulses of DA) lead to rapid, frequent DA in mesolimbic pathway lead to increased reinforcement/addiction
Immediate-release drugs & stimulants when abused have rapid onset and higher peaks leading to such phasic signaling. |
|
|
Term
|
Definition
Restlessness, anxiety, behavior disturbance, slurred speech, psychosis, insomnia, somnolence
Anorexia, growth inhibition (temporarily)
Headache
Abdominal pain, nausea, vomiting
May unmask underlying tic disorder and will increase tics in Tourette’s disorder 50% of time
Hypertension, tachycardia, risk of cardiovascular events (“Black Box” warning)
Seizure
Tolerance & dependence when abused |
|
|
Term
|
Definition
atomoxetine (Straterra®)
Non-amphetamine NRI (selective NE reuptake inhibitor) |
|
|
Term
|
Definition
At low-moderate doses, decreases inattention, hyperactivity, impulsivity via:
Increased NE at postsynaptic 2A receptors in prefrontal cortex
Increased DA in prefrontal cortex
DA is inactivated by NET (this area has few DAT’s) |
|
|
Term
| Why is Strattera (SNRI) not considered a stimulant. |
|
Definition
It does not increase DA in mesolimbic tract.
Nucleus accumbens has DAT’s but few NET’s
DA does not increase in nucleus accumbens
Less abuse potential; not a controlled substance |
|
|
Term
|
Definition
| increase NE at α2A postsynaptic receptors & enhance cognition |
|
|
Term
|
Definition
| activating α1 receptors (and α2B receptors in thalamus), causing sedation & impaired cognition (lowering dose may help) |
|
|
Term
|
Definition
|
|
Term
|
Definition
slow onset, long duration (much longer than 5-hr half-life), perpetual NET inhibition leading to restoration of tonic D1 & a2A signaling.
Downregulates phasic NE & DA actions and desensitizes postsynaptic NE & DA receptors
Decreases chronic overactivaton of HPA axis |
|
|
Term
|
Definition
|
|
Term
|
Definition
clonidine (Kapvay, Catapres)
Kapvay - qd or bid
Catapres® - tid or qid
May be helpful w/ pts w/ comorbid tic disorders
Can cause sedation & hypotension (α2B, imidazoline receptors) |
|
|
Term
| What happens if abrupt D/C of these α2A agonists |
|
Definition
| Possible rebound HTN, nervousness/anxiety, headache, tachycardia, nausea |
|
|
Term
| Drugs to Treat Aggression |
|
Definition
Atypical antipsychotics (SGAs) are the most often used (including children).
Other drugs used:
Anticonvulsants (e.g., divalproex [Depakote])
β-blockers (e.g., propranolol [Inderal])
buspirone [BuSpar])
clonidine (Kapvay, Catapres)
lithium
SSRIs
BDZs should only be used very temporarily and only if psychotherapy (e.g., behavioral) has not been successful or practical. |
|
|
Term
|
Definition
Impairment of memory and of at least one other cognitive domain
May have abnormal behaviors and personality changes
Must R/O delirium
can apply to reversible, chronic, or degenerative disorders |
|
|
Term
|
Definition
Vascular dementias
Alzheimer’s disease (AD)
Dementia with Lewy bodies
Frontotemporal dementia (frontotemporal lobar degeneration) |
|
|
Term
| The “amyloid cascade hypothesis” |
|
Definition
Beta-amyloid plaques in extracellular space lead to inflammation lead to release of cytokines & free radicals from activated microglia & astrocytes
Cause hyper-phosphorylation of tau proteins and conversion of intracellular microtubles into neurofibrillary tangles lead to synaptic and neurotransmitter dysfunction in nucleus basalis of Meynert lead to decreased release of ACh lead to abnormal synapses in hippocampus lead to memory dysfunction
Eventually neuronal loss of:
Cholinergic neurons & medial temporal lobe neurons further memory deficits
Neurons throughout cortex other cognitive dysfunctions (dementia) |
|
|
Term
| Treatment of AD (Alzheimer's) |
|
Definition
| Inhibition of acetylcholinesterase (which metabolizes ACh) ACh in cleft |
|
|
Term
| Drugs that inhibit acetylcholinesterase |
|
Definition
donepezil (Aricept®)
Mild, moderate, or severe AD
Most common SEs are GI-related (usually transient); qhs dosing
galantamine (Razadyne, Razadyne ER)
Also improves action of nicotinic cholinergic receptors
Mild-moderate AD
Most common SEs are GI-related (usually transient); qhs dosing |
|
|
Term
|
Definition
| Inhibition of acetylcholinesterase and butyrylcholinesterase (particularly present in glia) |
|
|
Term
| Drugs that Inhibit acetylcholinesterase and butyrylcholinesterase |
|
Definition
rivastigmine (Exelon®)
Mild-moderate AD
May have greater effect
Blocks both enzymes
Greater affinity for ACh in cortex & hippocampus compared to rest of brain
GI SEs more common than w/ Aricept but may be transient); bid dosing
Exelon Patch given qd may be more effective and w/ fewer GI SEs. |
|
|
Term
|
Definition
|
|
Term
| Drug that reduces excitotoxicity |
|
Definition
memantine (Namenda®)
Moderate-severe AD
Is a weak NMDA Glu antagonist |
|
|
Term
|
Definition
Amyloid plaques may increase NMDA-Glutamate receptor activity lead to excitotoxicity lead to excessive free radicals lead to neuronal damage or cell death
Weakly blocking NMDA-Glu receptors may decrease this process, thereby slowing degeneration |
|
|
Term
|
Definition
| acetylcholinesterase inhibitor and memantine (Namenda®) |
|
|
Term
|
Definition
Most commonly abused drug. Bind to opiod receptors (mu, kappa, delta) and relieve pain.
Mu receptor - strongest analgesia, most abuse potential
Analgesia, relaxed euphoria, sedation, tranquility/reduced apprehension, reward, respiratory depression, suppression of cough reflex, pupillary constriction (miosis [“pinpoint pupils”]), constipation, nausea/vomiting, reduced libido in men, menstrual irregularities/infertility, itching, allergic reactions (bronchoconstriction) |
|
|
Term
|
Definition
| strongest analgesia, most abuse potential |
|
|
Term
|
Definition
| mimic effects of drugs extracted from opium poppy and of endorphins (endogenous morphines) |
|
|
Term
|
Definition
the main drug extracted from opium and the gold standard for analgesia
Injection (most common), oral, rectal
MS-Contin – time-release |
|
|
Term
| Examples of Opiod agonists |
|
Definition
| morphine, thebaine, codeine, and Semi-synthetic derivatives of morphine |
|
|
Term
| Semi-synthetic derivatives of morphine |
|
Definition
| hydromorphone (Dilaudid, Palladone, Exalgo) and oxymorphone (Numorphan, Opana-ER) |
|
|
Term
|
Definition
semi-synthetic derivative of morphine
Compared to morphine, is more fat-soluble and can cross blood-brain barrier 3X faster
In brain, is converted into morphine
Taken IV (“mainlined”, least expensive), smoked, snorted (most potent form and most expensive) |
|
|
Term
| Heroine smoked w/ “crack” cocaine |
|
Definition
Leads to increased euphoria, decreased anxiety/paranoia (often occurring w/ cocaine) and decreased depression after effect of cocaine wears off
Causes multi-drug addiction that is difficult to Tx |
|
|
Term
|
Definition
extracted from opium but w/ little analgesia
Synthetic derivatives include:
oxycodone (OxyContin)
Percodan – oxycodone + aspirin
Percocet – oxycodone + acetaminophen
Epidemic abuse of OxyContin – “poor man’s heroin,” “oxy,” “OC,” “killer”
Crush pills (destroys time-release mechanism) and snort, smoke or inject
hydrocodone
Vicodin – hydrocodone + acetaminophen |
|
|
Term
|
Definition
extracted from opium
Relieves cough (antitussive)
Relieves mild-moderate pain
40% of use associated w/ dependence
Often w/ comorbid depression
Tylenol w/ Codeine #3 – acetaminophen + codeine (300/30)
Tylenol w/ Codeine #4 – acetaminophen + codeine (400/60) |
|
|
Term
|
Definition
opiod agonists not derived from or structurally similar to endorphins or morphine:
fentanyl (Sublilmaze, Durapatch, Fentora, Actiq) and methylfentanyl (manufactured illegally)
“china white” – street name for fentanyl
Abuse has caused many fatalities
meperidine (Demerol) |
|
|
Term
| Mechanisms of reinforcement of drugs of abuse |
|
Definition
In VTA, opiods bind to mu receptors on GABA-neurons lead to inhibition of those neurons lead to disinhibition of dopaminergic neurons projecting mainly to nucleus accumbens (mesolimbic pathway).
Abuse or addiction more likely if there is intense and phasic DA firing immediately after taking drug.
Such excessive mesolimbic activity is involved in all drugs of abuse and behavioral addictions. |
|
|
Term
| More mechanisms of reinforcement and abuse |
|
Definition
Positive and negative reinforcement
Gradual dependence from alleviation of preexisting dysphoria or painful states (self-medicating)
Correction of deficient endorphin or reinforcement systems (in some)
Need to continue use due to downregulation of endorphin or reinforcement systems
Associative learning/conditioning - drug effects & withdrawal become linked w/ cues & mood states |
|
|
Term
| Dependence (physical dependence) |
|
Definition
| physical or psychological withdrawal sxs occur when drug is discontinued due to neurochemical changes in CNS |
|
|
Term
|
Definition
|
|
Term
|
Definition
| (DSM-IV TR) = “addiction” |
|
|
Term
|
Definition
| depends on pharmacology of drug, quantity used, frequency of use, route of administration (speed of onset), phasic DA firing in mesolimbic pathway; and psychological & sociocultural context of use |
|
|
Term
|
Definition
| will develop tolerance & dependence but usually not abuse or addiction |
|
|
Term
|
Definition
| opiods when in pain whereas abusers or addicts use when not in pain |
|
|
Term
|
Definition
| cause tolerance, dependence, withdrawal sxs, abstinence syndrome and have abuse potential |
|
|
Term
| Opiod Agonists Withdrawal sxs |
|
Definition
generally opposite to opiod effects
Reduced DA release and increased NE release
Craving, dysphoria, restlessness, anxiety, irritability, rhinorrhea (runny nose), piloerection (“goosebumps”), sympathetic hyperactivity (tachycardia, panting, sweating, pupillary dilation, tremor), fever, chills, retching & vomiting, cramping, explosive diarrhea, intense aches & pains, (see Table 10.3, p 337 in textbook)
Severity depends on dose, frequency of use and duration of use
Not life-threatening (unlike alcohol)
Treatments for acute withdrawal/detoxification (modestly successful)
clonidine-assisted detoxification
Alpha-2 adrenergic agonist to decrease sympathetic physical sxs
Used alone, w/ naltrexone or w/ tapering meds
methadone taper, over 3-180 days
buprenorphine taper |
|
|
Term
| Rapid anesthesia-aided detoxification (RAAD) |
|
Definition
pt is asleep for 72 hrs while detoxified
Antagonist (naloxone or naltrexone)
clonidine (Catapres), given IV
Anesthesia
Expensive but no more effective than other methods |
|
|
Term
|
Definition
from end of withdrawal period for up to 6 months
Drug craving, depression, decreased coping w/ stressors, decreased self-esteem, anxiety
Comorbid disorders include antisocial personality disorder and MDD. |
|
|
Term
| Treatments for acute withdrawal/detoxification (modestly successful) |
|
Definition
clonidine-assisted detoxification
Alpha-2 adrenergic agonist to decrease sympathetic physical sxs
Used alone, w/ naltrexone or w/ tapering meds
methadone taper, over 3-180 days
buprenorphine taper |
|
|
Term
|
Definition
| methadone – used in methadone clinics & to treat pain |
|
|
Term
|
Definition
Principal drug for preventing abstinence syndrome in dependent pts (in federally licensed methadone maintenance programs)
Combined w/ psychotherapy to rehab pts by decreasing illicit use, crime and needle-associated diseases
Effective, but only 20-25% of pts are being treated; and laws often dictate max doses even though doses must be individualized.
methadone is being diverted for abuse.
Numerous fatalities due to diversion and many DDIs (metabolized by 5 CYP isoenzymes) |
|
|
Term
|
Definition
naloxone (Narcan)
Rapidly causes withdrawal; no analgesia or abuse
Not absorbed from oral mucosa or GI tract (must be injected)
Used to reverse respiratory depression 2O to opiod intoxication or in newborns of opiod-dependent mothers
Lasts only 15-30 minutes
naltrexone (ReVia, Vivitrol)
To maintain pt in treatment instead of giving an agonist (e.g., methadone)
Taken orally, lasts 24 hrs; can cause nausea and hepatotoxicity
Poor adherence because pt must choose between drug and illicit opiod
Vivitrol – long-acting (30 days) injectable for decreasing craving in recovering alcoholics
Better for adherence
Used to decrease self-injurious behavior
Embeda – naltrexone + morphine
Pellets of morphine for extended-release analgesia surrounding core of naltrexone
If abused (crushed or chewed), naltrexone will cause withdrawal sxs
A drug that combines oxycodone w/ naloxone or naltrexone is badly needed in U.S.
nalmefene (Revex) – to treat acute respiratory depression due to overdose |
|
|
Term
|
Definition
buprenorphine (Subutex)
Suboxone = buprenorphine + naloxone (an opiod antagonist) to prevent preventing abstinence syndrome in dependent pts or for detox
When taken sublingually (duration of action is 24 hrs), buprenorphine prevents withdrawal in pt who is not abusing (naloxone does not cause withdrawal because it is not absorbed)
If abused (crushed, dissolved & injected), naloxone will be absorbed withdrawal
Can be used in private practice – no need to go daily or to a methadone clinic
tapentadol (Nucynta) – partial opiod agonist, NRI
tramadol (Ultram) - partial opiod agonist, SNRI |
|
|
Term
| Mixed agonist-antagonist opiods |
|
Definition
agonists at kappa receptors, weak antagonists at mu receptors
Will precipitate withdrawal in opiod-dependent pts and can cause hallucinations (leading to illicit use)
pentazocine (Talwin), pentazocine + acetaminophen (Talacen)
Being abused, especially when combined w/ tripelennamine (an antihistamine) (“Ts and blues”) – can cause seizures, psychosis
Talwin NX – pentazocine + naloxone to prevent abuse
butorphanol (Stadol, Stadol NS) – being abused |
|
|
Term
| Addiction to opiods time frame |
|
Definition
|
|
Term
|
Definition
| not realistic in large number of addicts. |
|
|
Term
| Optimal tx goal for opiod addiction |
|
Definition
prolonged agonist/antagonist maintenance (w/ Suboxone or Embeda)
But maintained dependence (methadone) or detoxification (via an antagonist) may be better for some. |
|
|
Term
| Best tx for opiod addiction |
|
Definition
| Pharmacotherapy + psychotherapy, support services, random drug screens and structure are critical |
|
|
Term
|
Definition
| leading cause of preventable death in US and of mobidity & premature mortalitiy in world |
|
|
Term
| Number of nicotine-dependent Americans have another psychiatric disorder; many are in low socioeconomic classes |
|
Definition
|
|
Term
|
Definition
Leads to increased cardiac rate/contractility & blood pressure (BP).
w/ CO2 Lead to atherosclerosis & thrombosis (clotting)
CO decreases oxygen (O2) to cardiac muscle (all cells) because CO replaces O2 in hemoglobin
Above factors risk of angina pectoris, myocardial infarction (MI, heart attack) and stroke
Smoking greatly increases risk of chronic bronchitis, emphysema, pulmonary infections.
The major cause of death from cancers of lung, mouth/larynx/throat and bladder; and increases risk of cancer of pancreas, cervix |
|
|
Term
|
Definition
the active ingredient in tobacco that leads to acute effects & dependence
Passes BBB, placental barrier and into breast milk
Activates nicotinic cholinergic receptors
Nicotine activates alpha-4 beta-2 postsynaptic receptor intense, phasic firing of DA neurons in mesolimbic pathway immediately after taking drug
Cigarette – clever but evil delivery system of nicotine to brain very quickly and soon after behavior and many times during day |
|
|
Term
| Activation of alpha-4 beta-2 postsynaptic receptor |
|
Definition
| Leads to intense, phasic firing of DA neurons in mesolimbic pathway immediately after taking drug (nicotine) |
|
|
Term
| Activation alpha-7 presynaptic receptor |
|
Definition
Leads to increased release of DA, Glu & ACh leading to improved psychomotor activity, attention, memory, cognition, sensorimotor performance
Reduces appetite, may decrease depression, decreases afferent impulses from muscles (helps person feel relaxed) |
|
|
Term
| Therapies for nicotine dependence |
|
Definition
Pharmacotherapy + counseling better than either alone
Nicotine-replacement
Gum, inhaler, nasal spray, patch
Replace nicotine, then slowly reduce level
bupropion (Zyban, Wellbutrin), nortriptyline (Pamelor)
Both are NDRIs
bupropion reduces smoking relapse and causes less wt gain
varenicline (Chantix) – a partial nicotine receptor agonist (NPA)
Selective alpha-4 beta-2 nicotinic ACh partial agonist
Gives a low level of DA to prevent withdrawal and craving, but continued smoking is less satisfying
Significantly improves chances of quitting and maintaining abstinence for ≥ 12 mos compared to nicotine-replacement, bupropion, placebo or no Tx
Often combined w/ CBT (e.g., GETQUIT)
SEs – nausea, possible neuropsychiatric sxs (depression, agitation, hostility, suicidality) |
|
|
Term
|
Definition
“Snorting” “lines” of 25-100 mg of (“crystal,” “snow”) – usually by occasional users
Snorting or smoking the freebase form – heavy users for dose of 250-1000 mg
Inject 100-1000 mg - regular users
All methods cause high-dose, rapid effects and rapid toxicity & dependence |
|
|
Term
|
Definition
Blocks reuptake of DA, NE, 5-HT (somewhat)
intense, phasic release of DA in nucleus accumbens
Leads to euphoria & “high” w/ one of the greatest potential for abuse and dependence
Increases NE ascending activating system, causing global CNS arousal
Leads to alertness, but can also lead to paranoia and seizures
Increases NE sympathetic activity
Dilated pupils (mydriasis)
Increased heart rate (HR), BP leads to increased risk of heart attack, stroke, damage to heart valves (even many yrs after D/C of drug)
See Table 12.2, p 406 in textbook |
|
|
Term
|
Definition
when cocaine is combined w/ ethyl alcohol
Inhibits reuptake of DA, NE & 5-HT
Compared to cocaine alone:
More & longer euphoria (inhibits reuptake of DA more potently)
T1/2 longer (150 mins vs 15-30 mins)
More cardiotoxic |
|
|
Term
|
Definition
No pharmacotherapies have been proven effective or FDA-approved.
CBT & contingency management methods are useful. |
|
|
Term
|
Definition
a synthetic drug abused for its “rush”
Causes reuptake transporter to work in reverse
Increases release of DA, NE, 5-HT
Blocks reuptake of DA, NE, 5-HT
leading to intense, phasic release of DA in nucleus accumbens, causing reinforcement & dependence
Increased DA in basal ganglia causes stereotyped behavior (constant, repetitive, meaningless acts) |
|
|
Term
|
Definition
more potent than amphetamine (“speed,” “crystal,” “crank,” “ice” when smoked; can be injected)
T1/2 longer than cocaine (12 hrs vs 15-30 mins)
Chronic user
Outbursts of aggression, paranoid delusions/ psychosis (can last days-wks), severe anorexia, poor physical health
Very taxing to body, especially with repeated cycles of extreme activity w/o proper nutrition & sleep followed by extreme exhaustion (“wasted”)
Physiological effects similar to cocaine |
|
|
Term
| tetrahydrocannabinol (THC) |
|
Definition
the active ingredient in marijuana obtained from Cannabis sativa
Acts on CB1 receptors, which are receptors for endocannabinoids
Can function as retrograde messengers modulating release of neurotransmitters from presynaptic terminals |
|
|
Term
|
Definition
an endocannabinoid that plays a role in forgetting by inhibiting adenyl cyclase so that brain is not overwhelmed w/ information
Increase DA in mesolimbic pathway leading to reinforcement via opiod receptors |
|
|
Term
|
Definition
May suppress appetite and reduce pain sensitivity
May lower BP, reduce nausea and decrease intraocular pressure in glaucoma
Research may provide drugs w/ the beneficial effects but w/o the harmful effects of marijuana.
Eventually, leads to downregulation, which in turn leads to craving and withdrawal sxs
Chronic use of cannabis causes memory deficits, which may persist long after use.
May cause hypomotivational syndrome, paranoid ideation, psychosis, worsening of respiratory diseases and possibly cancer
Current cannabis is many times more potent than that of few years ago. |
|
|
Term
|
Definition
Often leads to executive disinhibition, extremely poor judgment, MVAs, date rape, unprotected sex, spousal or child abuse, aggression, crime and death
Initially depresses cortex, especially prefrontal cortex, resulting in difficulty exercising judgment, performing abstract reasoning and inhibiting inappropriate acts.
Occurs before other obvious signs of intoxication
Also depresses activity of cerebellum leads to incoordination, clumsiness, slowed psychomotor functions, slurred speech |
|
|
Term
|
Definition
the concept that alcohol represents time out from the usual rules of daily behavior that govern behavior
These rules are specific to culture, group, and setting.
Helps explain how behavior under the influence can vary from one context to another |
|
|
Term
|
Definition
after imbibing alcohol, local and immediate cues govern behavior
Due to executive disinhibition, in that lesions in prefrontal cortex cause a patient to be abnormally drawn to a stimulus |
|
|
Term
|
Definition
causes CNS inhibition/depression
Is a PAM of GABAA receptor
Inhibits NMDA-Glu receptor
Blocks reuptake of adenosine (an inhibitory neurotransmitter)
Stimulates opioid and cannabinoid receptors
KNOW: Increases DA release in mesolimbic pathway by stimulating opiod & cannabinoid receptors in VTA – so is reinforcing and increases craving |
|
|
Term
|
Definition
cause cognitive decline, particularly in memory
Main effect is inhibition of NMDA-Glu receptors, involved in LTP
Can get neuropsychological deficits
Can lead to alcoholic dementia
Korsakoff’s dementia – profound anterograde amnesia |
|
|
Term
| Fetal Alcohol Syndrome (FAS): |
|
Definition
Small brains, learning disabilities, low IQ’s, hyperactivity, physical abnormalities
Worse if mother drinks during 1st trimester, particularly if binge drinks or smokes cigarettes
Even one drink per day causes lowered IQ’s
The leading cause of mental retardation |
|
|
Term
|
Definition
| increased HR & BP, tremor, anxiety, delirium & hallucinations (DTs), seizures |
|
|
Term
| Treatment for alcohol withdrawal sxs |
|
Definition
Enhance inhibitory actions of GABA and inhibit excitatory actions of Glu since Glu activity is disinhibited when alcohol is D/C
Glu can cause potentially fatal seizures (especially in 1st 72 hrs, w/o warning/other sxs)
Taper w/ a long-acting, minimally reinforcing BZD (e.g., Librium, Valium) because all sedative-hypnotics are cross-tolerant |
|
|
Term
| Tx for maintenance of alcohol abstinence |
|
Definition
| naltrexone (ReVia, Vivitrol) – reduces consumption of alcohol because alcohol stimulates opiod receptors in VTA, which in turn leads to DA release |
|
|
Term
| Tx for Alcohol Absentism/Detox |
|
Definition
acamprosate (Campral) – binds to mGlu receptors leads to decreased excitatory Glu neurotransmission and increased inhibitory GABA neurotransmission
Can reduce Glu excitotoxity that may occur following withdrawal, thereby decreasing brain damage that may occur during detox
Best when combined w/ naltrexone and behavioral, educational and/or supportive therapy in groups or as an individual |
|
|
Term
| Findings of COMBINE study |
|
Definition
Best to combine pharmacotherapies w/ cognitive behavioral intervention (CBI) and medical management (MM)
MM + naltrexone + acamprosate = best (if cost justifies adding acamprosate) |
|
|
