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84 Cards in this Set
- Front
- Back
The prefrontal cortex is a major area for ___________________
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Judgment, EF, decision making
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Primary divisions of the PFC include...
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Dosolateral Prefrontal Cortex (DLFPC)
cognitive fucntioning (EF, prob. solv., analyze) Orbito Frontal Cortex (OF) Impulses, compulsions, drives Anterior Cingulate Cortex (ACC) Top (dorsal) related to selective attention Lower (ventral or subgenual) related to emotions such as depression and anx Ventromedial PFC Emotional processing |
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Secondary divisions of the PFC include....
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Hippocampus - memory, neurgenesis
Amygdala - fear processing (emotion) NT Nodes cell bodies in brainstem etc projections to PFC etc Some overlap, some are unique |
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What activity can help determine how well the PFC is fx'ing?
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Stroop Color Word Task
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DA projections are primarily ascending or descending?
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Ascending
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What are the two DA projections?
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Ventral tegmental area
thalamus |
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What does the ventral tegmental area regulate?
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movement, pleasure and reward, cognition, psychosis (esp. positive symptoms)
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NE projections are primarily ascending or descending?
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Both
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The ascending NE pathway begins with what/where and regulated what?
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Locus Coeruleus,
mood, arousal, cogntions |
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5HT projections are primarily ascending or descending?
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Both
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5HT projections are involved in....
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mood, anxiety, sleep, pain
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what are the two primary AcH pathways?
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brain stem, basal forebrain
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AcH medications are commonly a treatment for what diagnosis?
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Alzheimer's
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Describe the biological components of PTSD
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Hippocampus has stored traumatic memories that can trigger the amygdala. The amygdala releases cortisol which changes breathing
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Histamine (HA) projections begin in the________and continue to the
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Tuberomammilary nucleus (TMN) in Hy to PFC, SC
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HA is related to the control of
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Arousal, wakefulness and sleep
can make you sleep but make it difficult to stay asleep |
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What is the NT and route in the pain pathway?
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Primarily NE, but also 5HT
from lateral tegmental NE cell system, descending into spinal cord, in brain stem |
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"Classic neuro-transmission occurs via
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G-protein linked receptors
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Most psychotropic drugs target _________ or ______________
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transporters or G-protein linked receptors
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the purpose of transporters is to
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transport NT across membranes and/or facilitate re-storage of NT in vesicles
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Plasma membrane transporters are AKA _____________ and are classified as ____________________
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reuptake pump
SLC6 (NT's besides Glu) or SLC1 (Glu only) SLC = solute carrier |
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How are SSRI's selective?
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selective in its affinity for allosteric sites; when something binds allosterically in prevents the NT from binding and it is not taken back up into the cell
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Where does the energy for NT transport come from?
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sodium pumps (Na+) constantly pumping sodium out of the cell
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True/Fale: Transporters only have binding sites for NA
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False, they also have monoamine sites and allosteric sites
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What process and chemical(s) can cause increased concentrations of GABA in the synapse?
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GAT1 targeting SNRIs like anitconvulsant tiagabine/Gabitril; also alcohol
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What results from inhibited Glu?
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Potential for lower levels of excitation, cell damage
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Which NT does not have a transport system? How does it work?
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Histamine: it targets other actions, such as enzymatic destruction
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Why do amphetamines have a phasic burst?
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Targets DATs and NETs (presynaptic pumps) as well as VMATs (intracellular synaptic vesicle transporter) causing a reversal of reuptake pump action and a flood of DA into synapse
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True/False: Constitutive activity = no activity
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False: it = no CHANGE in activity, i.e. baseline
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What is required for an antagonist to alter effects of a chemical?
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Presence of an agonist; otherwise it is neutral (prevents change while maintaining baseline)
EX. GABA-A antagonist Flumazenil -used for Benzo OD bc it blocks PAM -unmedicated, non anxious ppl, show no response (silent agonist) -unmedicated anxious ppl show increase panic/anx bec inhibition of GABA stops |
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What is the opposite of an agonist?
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inverse agonist
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What are the types of ion channels, what is the difference b/w them?
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Ligaand-gated - opened by NTs
Voltage sensitive - opened by charge |
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Which is faster, ligand-gated or G-protein linked channels?
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Ligand-gated; though both begin with 1st messenger NTs
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Explain net effects
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eg - partial agonist = net agonist in presence of full agonist; antagonist = net agonist in presence of inverse agonist
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Why is it ok/not ok to drink alcohol with benzos?
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Its not b/c Benzos increase GABA activity as does alcohol
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What is the difference between positive/negative allospheric modulation?
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PAM boosts NT effect, opens more and more often than a full agonist alone, but only in the presence of the NT
Ex - benzo's + alcohol NAM blocks/reduces NT effect; closes more/more often than NT alone |
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What are some of the basics for understanding tolerance, withdrawal, drug interactions, cross dependence?
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Desensitization - prolonged exposure to agonist
Inactivation - stablized closed after inverse agonist Net effects Speed of ion channels vs G-protein linked Competitive binding vs allosteric |
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Explain excitation-secretion coupling
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sodium channels first activation on the axon, later calcium opens which pulls in vesicles towards the membrane , all the positive NTs are pumped in; part of signal transduction
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What percent of meds target enzymes? Are they usually inhibitory/excitatory?
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10%, inhibitory
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True/false: enzyme inhibition is permanent?
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False
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Describe the rational approach to treatment outlined by Stahl. What are its shortfalls?
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Construct a diagnosis
Deconstruct the diagnosis into its component symptoms Match each symptom to its hypothetically malfunctioning circuit Consider the NTs that theoretically regulate each circuit Select a tx that targets the NT regulating the circuit Add or switch to another tx if the symptom is not relieved Repeat for each sx until the pt is asymptomatic or in remission Shortcomings: knowing when to switch vs combine how long to wait to combine difficulty interpreting/predicting interaction effects working from clinical experience/intuition to research questions |
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What are the 5 levels of mood descriptors?
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Mania
Hypomania Euthymic Dysthymia Depression |
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What are the 3 temperaments?
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Hyperthymic (above normal but not psychopathic)
Depressive (bw euthymic and dysthymic, not pathological) Cyclothymic |
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Malfunctioning circuits associated with Major Depressive Episode
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PFC - concentration, interest, pleasure, psycho-motor, mental fatigue, guilt, suicidal, worthlessness, mood
Amygdala - guilt, suicidality, worthlessness, mood Striatum - psychomotor fatigue Hypothalamus - sleep, appetite (only sxs not caused by PFC) Cerebellum - psychomotor NA - concentration, interest, pleasure |
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What is the difference b/w MAOI’s, tricyclic antidepressants, and SSRI’s?
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MAOI's are Dopamine-Epinepherine-Norepinephrine-Seratonin agonists
Tricylcic Anti-d's are Norephinephrine-Serotonin agonists SSRIs are Serotonin agonists |
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Name some brand name SSRI’s
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Prozac, Zoloft, Paxil
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Name some name brand SNRIs
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Effexor, Cymbalta
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Name some name brand NDRI's
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Wellbutrin, Zyban
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What is a name brand NRI
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Strattera
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most likely consequence of neuroleptic drugs
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Tardive dyskinesia
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Chlorpromzaine
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aka Thorazine
neuroleptic drug |
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Tricyclic drugs
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imipramine
clomipramine amitryptyline |
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SSRI's
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fluoxetine
sertraline paroxetine Straterra Lexapro Cymbalta Saragem Luvox Celexa Paxil |
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fluoxetine
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Prozac
SSRI |
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sertraline
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Zoloft
SSRI |
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paroxetine
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Paxil
SSRI |
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MAOI's
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phenelzine
tranylcypromine |
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Nardil
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phenelzine
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Parnate
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tranylcypromine
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what class of drugs are most widely prescribed for anxiety?
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Benzodiazepines
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diazepam
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Valium (benzo)
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alprazolam
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Xanax (benzo)
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clonazepam
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Klonopin (benzo)
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lorazepam
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Ativan (benzo)
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triazolam
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Halcion (benzo)
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Barbituates
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replaced by benzo's for anxiety bc they're safer
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Thiopental
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barbituate
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amabarbital
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Barbituate
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secobarbital
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Barbituate
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conventional antipsychotics are more useful in treating what symptoms of schizophrenia?
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positive
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Haloperiodal
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aka Haldol
conventional antipsychotic |
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OCD medications
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Anafranil (clomipramine)
Prozac (fluoxetine) Luvox (fluvoxamine) Paxil (paroxetine) Zoloft (sertraline) Celexa (citalopram) |
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serotonin hypothesis of OCD
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medications that reduce OCD sx's increase available levels of serotonin
serotonin antagonists (atypical antipsychotics) increase OCD sx's in patients, but not in controls |
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Anticholinergic Effects
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block Ach
dry mouth blurred vision constipation memory impairment urinary retention confusional states |
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extrapyramidal effects
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dopamine blockade in basal ganglia
Parkinson=like effects: ridigity, shffling gaint, tremor, flat affect, lethargy dystonias: spasms in neck and other muscle groups akathisia: intense, uncomfortable sense of inner restlessness tardive dyskinesia: often a persistent movement disorder (lip smacking, writhing movements, jerky movements) |
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autonomic effects
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especially orthostatic hypotension, which can cause dizziness and imbalance, and in the elderly esp can cause falls and fractures
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unclassified antidepressant
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does not work selectively on serotonin levels
Wellbutrin |
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Lithium is prescribed to treat
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Bopilar I
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Buspar is prescribed to treat
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anxiety disorders
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haloperidol is prescribed to treat
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Schizophrenia and Tic Disorders
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withdrawal from ____________ (type of drug) can be fatal is done abruptly
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benzodiazepine (Valium)
has a potential for addiction |
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withdrawal from alcohol can include
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dangerous seizures
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tricyclic antidepressants
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block the reuptake of norep. and serotonin
cause anticholinergic side effects more side effects than SSRIs |
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MAOIs
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block the enzyme that breaks down norep. and serotonin
have to avoid foods with thyramine (red wine, cheeses, etc) |