substance abuse psychosis - rawalpindi medical university media club/3rd year/pharmacology/9... ·...
TRANSCRIPT
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Substance abuse psychosis
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psychosis
(Scientifc mystery& personal disaster)
• Psychosis is a severe mental illness
characterized by distorted or non-existent
sense of reallity
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Antipsychotics/Major Tranqullizers/Neuroleptics
or
Anti-schizophrenic drugs
• Psychosis
1. Schizophrenia
2. Affective/mood disorders with psychotic
features
Depression
Mania
Manic depressive illness (bipolar
depression)
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• Substance-induced
•
• Psychotic symptom associated with
diseases e.g dementia
•
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• Etiology:
• Not known
• Strong but incomplete genetic pre-
disposition
• 1st degree relatives – 10%)
• 2nd monozygotic twin – 50%)
• Neurodevelopmental disorder
• Envionmental factor
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• Symptoms:
• 1.Positive symptom: (result from
Neurochemical Abnormality)
• Increase do paminergic transmission
Respond well to Rx
1)Delusions (thought disorder)
• often paranoid
cann’t be rectified by reasoning
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• Hallucinations:(perception disorder)
• They may be
• Visual
• Auditory –more common
• Tactile (CD Canine bugs)
•
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• c) Thought disorder
Wild train of thoughts
irrational conclusion with the feeling
that thoughts are inserted or withdrawn by
an outside agency.
• Usually not like to be interfered, flight of
ideas from one thought to other thought.
• Broadcast of ideas.
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• d) Abnormal stereotypical behavior,
usually aggressive.
• e) Defectiveness in selective attention
disorganized speech, and disorganized or
agitated behavior
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• 2. Negative Symptoms:
• seen in schizophrenia typically
Result from brain atrophy
• 10% of patient commit suicide,don’t
respond / less responsive to Rx
,
Emotional blunting.
Poor Socialization
avolition
alogia
apathy
amotivation
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Cognitive dysfunction
• (strongest predictor of functional
impairment among schizophrenia)
• particularly seen in
• working memory,
• processing speed,
• social cognition,
• problem solving below population norms
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• Neurochemical Basis:
• 1) Dopamine Theory
• positive symptoms ---Dopamine
hyperactivity in mesolimbic and
mesocortical pathway & amygdale
• Inc dopaminergic activity–produce these
symptoms e.g levodopa,apomorphine
• Blockade of Dopamine recp Improve
the symptoms
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• 2) Glutamate Theory
– Glutamate----- excite GABA ergic striatal
neurons
– DA---- inhibit GABA ergic striatal neurons
which project to thalamus and constitute
―sensory Gate‖
Glutamate NMDA (N-methyl deaspartate)
recep antagonists produce psychotic synd
e.gPhencyclidine ,Katamine
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• 3) 5 – HT Theories:
• 5 – HT dysfxn
• LSD & 5-HT2 Receptors agonists
produced schizophrenia like syndrome.
• Mostly of Anti-psychotics in addition to
affect dopamine also back serotonin
receptors.
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• 4) Current views:
• Combination of DA hyperactivity with 5-
HT & glutamate dysfxn.
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• 1) Nigrostriatal Pathway:
• 75% of dopamine in brain
•
• 2) Mesolimbic mesocortical pathway:
• Projects from neurons near S.N to limbic
system & Neocortex
• Behaviorial effects
• Hyperactivity leads to schizophrenia.
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• 3) Tuberoinfundibular (Tubrohypophy
Scal) Pathway:
• Connects arcuate nuclei &
paraventricular nuclei hypothalamus
and post pituitary. Regulation endocrine
control – control MSH, GH, Prolactin.
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• 4) Medullary Periventricular Pathway:
• From neurons of Motor Nucleus of Vagus
___ Periventricular nuclei
Eating behavior regulation
Satiety center ___ Bolimia Nervosa
Appetite Cetre ___ Anorexia Nervosa
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• 5) Incertohypothalamic Pathway:
• From medial zone incerta to hypothalamus
& Amygdala.
• Sexual drive, Microvasculatory function
and temperature regulation.
• 6) Many local Dopaminergic Neurons in
olfactory cortex & retina:
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• 7) Dopaminergic transmission in
periphery:
• - Renal Vasculatory
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ANTIPSYCHOTIC DRUGS
• Produce improvement in the mood &
behavior of a psychotic patient without
excessive sedation & addiction
• (Greek----- take hold of nerves)
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Classification of Antipsychotic
Drugs
• A) Classical Typical Neuroleptics:
• 1. Phenothiazines:
• a) Aliphatic Comp
• (less potent,sedation & weight gain)
• Chloropromazine (Largactil)
• Promazine
• Triflupromazine
• promethazine
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• b) Piperidine Derivative: • Thioridazine (Melleril, less potent, Anti-Cholinergic)
• Mesoridazine (metabolite of thioridazine)
• Mepazine
• piperacetazine
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• c) Piperazine Derivative: Fluphenazine (I/V preparation,slowly release),
Perphenazine
Trifluperazine
Prochlorperazine(stemetil)
Thioperazine
Acetophenazine
carphenazine .
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• 2. Thioxanthines: (also available as
DEPOT preparation)
Thiothixene
Clopenthixol
Flupenthixol
Chlorprothixine
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• 3. Butyrophenones(highly potent)
Haloperiodol
Droperidol
Benperidol
trifluoperidol
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• B) Atypical Neuroleptics:
• (MOA different from anti-psychotics)
1-Loxapine
2-Clozapine(agranulocyctosis ,bone marrow
,depre)
3-Olanzapine (agranulocytosis)
4-Ziprasidone(patients resistant to other drugs. Also Rx of
negative effects)
5-Molindone
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• 5-Risperidone ( commonly used D2, 5HT2 selective
activity for D4 receptors
• 6-Sulpirdie (D2 selective)
Remazopride
Remoxipride
• 7-Pimozide (D2 selective,long acting indole)
• 8-Quetiapine
• 9-Aripiprazole(partial agonist at D2&5HT1a,alpha
antagonist)
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• FIRST GENERATION(typical,low potency)
chlorpromazine
prochlorperazine
thioridazine
First GENERATION (typical,highly potent)
fluphenazine
haloperidol
thiothixine
pimozide
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Phenothiazines • Chemistry & Structure
• 3 ring structure
• 2 benzene rings linked together by S at 5
• &N at 1 position
• Pharmacokinetics
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• PARMACOKINETIC
• highly lipophilic,
• highly membrane- or protein-bound,
accumulate in the brain, lung, and other
tissues with a rich blood supply
• Cross placenta, secreted in milk
• extensive meta by CYPs and subsequent
glucuronidation, sulfation, and other
conjugations
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MOA
Act on a variety of CNS & Peripheral receptors
– Post synaptic D2 receptor blockade in
mesolimbic ,mesocotical pathway
– 5 HT2 receptor blockade
– Alpha-1 adrenergic blockade
– Muscarinic receptor blockade
– Ganglion blockade
– Quinidine like effects
– Local anaesthetic like activity
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Pharmacological Actions
• CNS
• NORMAL (NON -PSYCHOTICS)
• unpleasant feelings due to
Sleepiness, restleseness
• Autonomic effects : b/c of muscarinic
blockade
•
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IN PATIENTS:
EFFECT ON BEHAVIOR & INTELLECT
• No loss of intellectual functions and performance
(clear sensorium)
• Alteration of deranged thought process
• Emotional quietening&Psychomotor slowing
• Decreased paranoid idea
• Decrease initiative
• Decrease aggressiveness in agitated person
• Indifference to enviornment &pain sensation
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2. Effect on motor activity
a. Decreased spontaneous activity
b. Extra Pyramidal symptoms
Acute dystonias (acute)
tonic contractions of postural muscles e.g torticollis
Akinesia
Akathisia
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Tardive Dyskinesia
(Prolifiration of D2 receptors in C. striateum
Disabling repetitive purposeless involun movements of Face, tongue, trunk, pelvis
Perioral tremor (Rabbit syndrome
Neuroleptic malignant syndrome
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Effect on CTZ
suppresses nausea, vomiting
Endocrinal Effect
↑ prolactin
↓ Gonadotrophins ,ACTH &growth
hormone
Disturbed temp regulation
Hypothermia/ Hyperthermia
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EFFECT ON ANS
• a) ANTICHOLINERGIC
• b) ADRENOCEPTORS BLOCKADE
• Orthostatic hypotension
• c) WEAK GANGLIONIC BLOCKADE:
• Both symp and P/symp ganglionic
blockade .
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• RESP. CONTROL:
• Depressant effect ,sig in resp dis
• No prominent effect in N individual
• No prominent effect in psychotic pt having
N respiration
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• vi) ENDOCRINE EFFECT:
• hyperprolactinemia and inflextility DA,
control prolactin (check its release),if block
hyper prolactinemia manifested by
Gynecomastia in infertility in male and
female
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• ix) ANTIEMETIC ACTION:
• Because of DA recep blockade in CRTZ.
Useful in drug induced vomiting and other
vomiting except motion sickness and
vomiting in pregnancy
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• 2) CVS
i-Effects due to ANS
dec stroke volume & TPR
dec CO
dec B.P
(may cause reflex tachycardia due to
postural hypotension
ii- direct -ve inotropic effects
iii- quinidine like effect,increase QT interval
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.
4. MISCELLANEOUS
LA effect
Renal effects
Effect on Liver
Antihistaminic action
(H1 blocker)
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Adverse effects
1-Neurological side effects-
• drowsiness, lethargy ,sedation( in many
cases desirable)
• Feels depressed( pseudo depression)
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Parkinson’s like synd
• 1- switch to drug with less EPS(when possible)
2- anticholinergic
diphenhydramine ,benztropine ( IM)
3-non-anticholinergic ----Amantadine
Perioral tremor (Rabbit syndrome)
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EPS
• 1-Acute dystonias( within few hrs to5 days)
• More who have never before taken antipsychotic drugs, adolescents, and young adults.
• Start with initial lower dosages
• 2-Akathisia ( days&weeks) Doesn’t respond to antiparkinsonian drugs
Improved by clonazepam and propranolol
3- Akinesia
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•
• Tardive Dyskinesia
(supersensitivity ,D2high recep)
elderly 5 times more susceptible stereotyped, repetitive, painless, involuntary,
quick choreiform (tic-like) movements of the face,
more common in affective disorder
withdrawal-emergent dyskinesias
tolerate high doses of potent D antagonists with limited EPS
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• Neuroleptic malignant syndrome
homicidal less common suicidal less
chances occure in extreme of disease.
• Rarely fatal except thio & mesoridazine
duer jto cacdio depressive neuro musculal,
excitability. Convulsions.
• Pt. comatosed.
• Hypothermia, miosis, deep
• Tendon reflexes.
• Tachycacdia
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DECREASE SEIZURE THRESHOLD:
• High dose:
cause convulsion cause
epileptic patients
aggravate epilepsy
inc dose req
latent epileptic
Potentiate cause of seizure
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2. ANS effects
anticholinergic—dry mouth(Tolerance develops to anticholinergic effects)
ECG Changes
(No Physical Dependence,tolerance to antipsychotic effect)
Reverse Tolerance or super sensitivity.
Cholestatic Jaundice
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5. Endocrinal effects
galactorrhea( in females)
gynaecomastia(in males)
infertility,
6- failure of ejaculation
Hypothermia / Hyperthermia
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METABOLIC EFFECTS weight gain---
d/tH1 blockade,inc appetite
hypertriglyceridemia --- weight-independent
occurs within weeks &resolves within 6
weeks after medication discontinuation
result of derangements in glucose-insulin
homeostasis
Hyperglycemia
result of derangements in glucose-insulin
homeostasis,reversible after
discontinuation
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5. DermatITIS ,photosensitivity
6. Opacities in lens and cornea
accentuate th normal process of aging of
lens
5. increased risk of all-cause mortality
elderly dementia patients,e.g cvs
events,pneumonia,
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• NEUROLEPTIC POISONING:
• Can be homicidal less common suicidal
less chances occure in extreme of
disease.
• neuro musculal, excitability. Convulsions.
• Pt. comatosed.
• Hypothermia, miosis, deep
• Tendon reflexes.
• Tachycacdia
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• Monitor vital functions.
• * Gastric lavage with activated charcoal
• *Saline catharsis (Na2SO4Mgo)
• * Fluid replacement
• * Pressor agents.
• Diaqzepam for seizerres I/V.
•
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Senile agitation
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Therapeutic Uses
A. Treatment of Psychiatric patient
1. Schizophrenia
2. Organic Psychosis
3. Bipolar depression
B. Nausea & vomiting
C. Alcoholic hallucinition
D. Intractable Hiccough
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• *
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• PIPERIDINE DERIVATIVE:
• THIORIDAZINE:
– Block D2,x-1 & 5HT-2
– .B.A (20-30%)
– Metabolite mesoridaine more active
– More cacdiotoxic
– Less extra pyramidal eff.
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– More potent anti muscacinics
• Extrapyramidal (packinsonian) symptoms
due to blockade of D2 and balance is
disturbed, in this case balance is notr
distubedf when cholinergicx activity es
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• cvsQUINIDINE LIKE effects,cardiac conduction
defects,&sudden death
• OCULAR adverse effectsDeposit in retina,
browning of vision.
• Picture resemble that of retinitis pigmentosa pt.
• Over dose
• pupils constricted
hyotension ,hypothermia
neuromuscular excitability,convulsions
,later dec tendon reflexes
fatal cardiac arrythmias&death
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HALOPERDOL
highly potent
oral1/2----1 to 2 days
haloperidol decanoate has a t1/2 of 21
days less ANS effects
no weight gain
rarely jaundice
used for acute
schizopherinia,huntington’s
disease,Tourette syd
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STE OF ACTION ,PFC
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D2 affinity of atypical agents
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ATYPICAL ANTIPSYCHOTICS MOA
• antagonism exerts the greatest effect on
prefrontal and basal ganglia DA release
and midbrain noradrenergic outflow, with
recent data implicating 5-HT2A receptor
polymorphisms
• 60-75% D2 rece occupancy--antipsychotic
efficacy
• > 78% of D2 recep in the basal ganglia ----
-----risk of EPS
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CLINICAL USES
• PSYCHOTIC DISORDER
1- schizophrenia spectrum disorders,
• 2- mania & hypomania----olanzapine
• Levo-Dopa induced psychosis----
clozapine,quietapine
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• 3-Manic phase ofBipolar disorder---
• -Olanzapine/risperidone with lithium
/valproic acid
continued many months after the
resolution of psychotic and manic
symptoms, typically in combination with a
mood stabilizer such
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• NON-PSYCHOTIC MENTAL ILLNESS
I- Anxiety disorder
i- non manic excited states( withBZ)
ii-OCD obsessive compulsive disorder
iii- PTSD (post-traumatic stress
disorder)
iv-GAD---quietapine, risperidone
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• II-Tourette's disorder &tic disorder
risperidone and aripiprazole, ziprasidone
III- Huntington's disease --suppress the
severity of choreoathetotic movements
IV- Autism-- risperidone
(Disruptivebehavior,irritabity,mental
retardation)
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• V-Agitated patients of Alzhiemer’s
&parkinsonism
• VI-Major depression----aripiprazole(as
adjunctive in SSRI resistant major )
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ADVERSE EFFECTS
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CLOZAPINE
• Bind D2 with less affinity& for shorter
duration ,easily diplaced
• 51-63% D2 recep blocked
• highest ratio of 5-HT2A/D2 binding
Binds with high affinity & blocks
D1,D4,5HT2,M& alpha rec
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CLOZAPINE
• D4 &5HT2, alpha and H1 blockerD2 51-
63% receptors selective
• CYPs 1A2, active metabolite N-
desmethylclozapine
• Enzyme inducer of CYP1A2 e.g
carbamazepine,smoking
dec dose by 50%.
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1-Twice more potent antag at 5HT2 than D2
2-also block D1,D3,D4,H1& alpha 1
3-potent antimuscarinic
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– NOT USED IN MANIA
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• ADVERSE EFF
• Sialorrhea(inc salivation,paradoxical)
• Seizures
• 0.8 % agranulocytosis ,immunemediated
• initial 6 months ---- highest risk
TLC/DLC wkly for 6 mths then every 3 wks
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• metabolic
Weight gain,
diabetes
hypercholestroemia
CVS
myocarditis
• ANS
• M1 blockade,
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OLANZAPINE
• Twice more potent at HT2 than D2
• Also has ntidepressent eff
USES
• Epileptogenic
• Wt gain
• sedation
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• metabolic
Weight gain,
diabetes
hypercholestroemia
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• USES
PSYCHOSIS
manic phase of bipolar disorder
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ARIPIPRAZOLE
• Partial agonist
• I/M, if emergeny
• Meta—dehydroaripiprazole more active
• most weight and metabolically neutral
atypical agents,
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Partial agonist verse antagonist
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• Clinical use
• adjunctive use in antidepressant
nonresponders
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quetiapine'
1) efficacy for bipolar depression
2)Unipolar major depresson---primary
metabolite, norquetiapine, is a potent
norepinephrine reuptake inhibitor