Condition Major Depression – Sad mood & Mania / Bipolar Disorder Generalized Anxiety Post–Traumatic Stress Schizophrenia &

ized Anxiety Post–Traumatic Stress Schizophrenia & Psychotic Disorders Spectrum

tearfulness Disorder Disorder
Epidemiology  Sex: ♀ > ♂ (F > M) ~1–3% of general population; M = F Most common anxiety Lifetime prevalence: 6–9% Prevalence: < 1%
 Lifetime prevalence: 10–20% 1st – degree relative with bipolar disorder: up to 10% disorder among the Sex:♀>♂ (F:M = 4:1) Sex: ♂ = ♀(M = F)
 Age of onset: 3rd decade of life Monozygotic twin: 40–70% elderly population Age of onset: late teens to mid–30s
Lifetime prevalence: 5– o Men: typically early 20s
10% o Women: typically late 20s
♀ > ♂(F:M = 2:1) Genetic factors – family history
o One schizophrenic parent: ∼ 10%
o Two schizophrenic parents: ∼ 40%
o Concordance rate
 monozygotic twins: 30–40%
 dizygotic twins: 10–15%
 ↓ Dopamine in prefrontal cortex / mesocortical
pathway may cause negative symptoms of psychosis
→ typical antipsychotics generally makes negative
symptoms worse
 ↑ Dopamine in mesolimbic pathway may lead to
positive symptoms of psychosis.
Symptoms Depressed mood + ‘SIGECAPS’*  ‘DIG FAST’ ‘WATCHERS’ ‘DREAMS’ Positive symptoms – Exaggerated distortion of
 Sleep disturbance (Insomnia or  Distractibility Worry   Disinterest in usual activities normal functioning
Always ask Hypersomnia)   Indiscretion / Impulsivity & Poor Judgement Anxiety  o Emotional detachment  Disorganized – speech, behaviour
Duration of  Interest – Loss of interest (anhedonia) o High–risk behavior seeking pleasure without  Tension in muscles  (alexithymia) o Thinking disturbed, neologisms
symptoms  Guilt or worthlessness (not a major regard for consequences (e.g., engaging in  Concentration difficulty  o Numb emotionally  Hallucinations, typically auditory
criteria) unrestrained buying sprees, sexual indiscretions /  Hyperarousal or o Negative mood  Delusions & Reduced contact with reality
 Energy decreased (fatigue) hypersexuality, or foolish business investments) irritability  Re–experience (Nightmares &  Catatonic (Severe immobility)
 Concentration Difficulties &  Grandiosity & Inflated self–esteem (euphoria)  Energy loss (Fatigue) Flashbacks, intrusive  Emotional control affected – incongruous affect
Indecisiveness  Flight of ideas  Restlessness  or feeling memories)  Arousal may lead to worsening of symptoms
 Appetite disturbance (increased or  Activity increase Keyed–up or on edge  Event preceding symptoms Negative symptoms – ‘LESS’ & the A’s
decreased) or weight loss o Increase in goal–directed activity or psychomotor  Sleep disturbance with emotional effects  Avolition–apathy
 Psychomotor Retardation or Agitation agitation (distress, unsafe, fear) o Under–activity, social withdrawal
o Subjective AND observable feelings  Sleep – decreased need for sleep  Avoidance of triggering o Lack of drive and energy
o Restlessness & fidgeting (agitation) or  Talkativeness or pressured speech stimuli / reminders,  Affective blunting or flattening (lack of facial
o Loss of spontaneous movement & Dissociative Amnesia expression)
reactivity (retardation) e.g. blank Other symptoms:  Month duration or longer of  Alogia – Speech reduced, monosyllabic
staring into space Poor judgement symptoms (Duration ≥ 1  Anhedonia – Asociality (social withdrawal and
 Suicidal thoughts  Inflated self-esteem month) diminished interest in relationships)
Spending sprees & unwise financial decision making  Sympathetic Hyperactivity  Slowness in movement & thought, psychomotor
 Seen on Polysomnography – Shortened Increased sex drive (Insomnia, hypervigilance, retardation
REM latency, more frequent REM, Increased drive to achieve goals irritability); exaggerated
decreased slow–wave sleep Careless or dangerous use of drugs or alcohol startle response The social causation hypothesis asserts that
Delusions (psychosis) experiencing economic hardship increases the risk of
 Decreased hippocampal and frontal lobe Intrusive symptoms subsequent mental illness – has been criticized
volumes N.B. If symptoms occur for 1st time in 75 y/o patient Distressing memories &
→ look for medical cause *Right frontal hemisphere dreams of or related to The social drift hypothesis (downward drift
 Associated with subclinical increased stroke* traumatic event(s) hypothesis) posits that mental illness can inhibit
 serum cortisol concentration (due to
hyperactivity of the hypothalamic–
pituitary–adrenal axis)
 Atypical Depression (i.e. MDD with
Atypical features – ↑ sleep
(hypersomnia), ↑ appetite & weight gain
o Hypersensitivity to rejection
o Leaden paralysis in morning (“Legs
like cement blocks”; heavy sensation
of limbs)
o Mood reactivity (positive
responsiveness to pleasant events)
o Tx – MAOIs
 N.B. C/I with SSRIs, TCAs, St. John’s
wort, meperidine,
dextromethorphan, linezolid (risk
of serotonin syndrome).
 Wait 2 weeks after stopping
MAOIs before starting
serotonergic drugs or stopping
dietary restrictions.
 Melancholic subtype of MDD
o Weight loss
o Insomnia
o Pervasive anhedonia
o Inability to respond to positive
events
Criteria for Major Depressive Episode:
 ≥ 5 / 9 major symptoms every day for
TWO (2) WEEKS
 ≥ 1 symptom is either 1) Depressed
Mood or 2) Loss of interest
 Absence of history of mania
Criteria A
Dissociative reactions (e.g. socioeconomic attainment and lead people to drift
Avoid SSRIs and TCAs (can trigger antidepressant– flashbacks) into the lower social class or never escape poverty.
induced hypomania/mania) Intense or prolonged
o Suggested by atypical rapid improvement in psychological distress at Neuroimaging often show enlarged lateral cerebral
depression after 2 days (typical time of onset of exposure to symbolic internal ventricles (schizophrenia associated with loss of
effect is 2 weeks) or external cues of the cortical tissue volume [e.g. decreased amygdala &
o Tx – immediate discontinuation of antidepressant ± traumatic event hippocampus] with ventricular enlargement)
addition of mood stabilizer (e.g. lithium, valproate) Marked physiological
or an antipsychotic (e.g. quetiapine) if manic reactions to cues
symptoms persists
Negative mood & cognitions:
Bipolar + ↑AFP in a 20wk preggo? – Could be Persistent horror, anger, guilt,
Valproate or Carbamazepine → Neural Tube Defect negative beliefs about self &
o Teratogenicity the world, decreased interest
o Switch to lamotrigine, a mood stabilizer with a in activities, emotional
favourable pregnancy safety profile, in euthymic detachment, amnesia of
patients who wish to get pregnant and discontinue event
valproate
 Pregnancy should be delayed for 3 – 6 months Arousal symptoms:
to assess the efficacy of the medication Sleep disturbance,
 If affective stability is maintained with the hypervigilance, hyperarousal,
new medication, pregnancy can be attempted irritability, impaired
concentration
 History of early–onset depression, poor tolerability
to previous trial of antidepressant therapy, and a Common comorbidities:
depressive episode characterized by lethargy and depression, substance use
hypersomnia are especially characteristic of disorders (frequently use
unrecognized bipolar disorder, & should warrant substances to self–medicate),
careful assessment for period of mood elevations somatic symptom disorder
(e.g. discrete periods of uncharacteristically good or
irritable moods, excessive energy, decreased need
for sleep, racing thoughts, & risk–taking behaviour)
Criteria for Manic Episode Excessive anxiety and Triggers = exposure to actual  ≥ 2 of 5 of following for at least x1/12 (i.e. psychosis
 ≥ 1 week – Abnormally and persistently elevated, worry (apprehensive or threatened trauma, serious ≥ 1 month):
expansive, or irritable mood and abnormally & expectation), occurring injury, or sexual violence o Delusions
persistently increased goal–directed activity or more days than not for (either through direct o Hallucinations
energy ≥ 6 months, about a experience or as a witness) o Disorganized speech (e.g. frequent derailment or
 Present most of the day, nearly every day with number of events or Sexual abuse (most common) incoherence)
markedly impaired functioning – Significant activities (such as work Physical abuse o Grossly disorganized or catatonic behaviour
dysfunction (work/school; grossly disorganized or school performance). Accidents o Negative Symptoms
behaviour), patient requires hospitalization (risk of Natural disasters
harm to self or others), or there are psychotic C.f. Adjustment disorder War (civilians or combatants):
features – anxiety symptoms < 6 duration of combat exposure
Criteria for Hypomanic Episode months directly proportional to risk
 ≥ 4 days duration of PTSD
 Does not cause significant dysfunction, Diagnosis of a severe disease
hospitalization or psychotic features
 Clinically significant distress or impairment in ≥ 3 of 7 symptoms (4 if mood is only irritable) Difficult to control worry ≥ 1 intrusive symptom Impaired level of functioning in one or more of the
Criteria B social, occupational, or other important areas representing noticeable change in behaviour associated with prior major areas: work, interpersonal relations or self–
of functioning traumatic event care
Not Attributable to physiologic effects of Mood disturbance is sufficiently severe to cause marked Uncontrollable worry + Persistent avoidance of Duration for Schizophrenia – > 6/12
substance abuse or other medical condition impairment in social or occupational functioning or to ≥ 3 of 6 italized stimuli associated with  Must include x1/12 of Criteria A (active–phase
necessitate hospitalization to prevent harm to self or others, symptoms above (i.e. traumatic event(s) symptoms – i.e. psychosis ≥ 1 month)
N.B. Depressive Episode = Criteria A – C or there are psychotic features
last 6 bullet points  Signs of disorder for > 6 months;
For a diagnosis of MDD, the following two
criteria must also be present: the symptoms above) o Active Psychos is often preceded by prodromal
are not due to another psychiatric disorder phase
AND there is no history of a manic or N.B. only 1 additional  Social withdrawal
Criteria C hypomanic episode. symptom is sufficient in  Loss of interest in school or work
children  Hygiene and grooming deteriorate
 Angry outbursts
 Unusual behavior
 May include prodromal or residual periods
(attenuated symptoms of odd beliefs or unusual
perceptual experiences; or negative symptoms
only)
Not attributable to the physiological effects of a substance Significant distress and A lot more criteria I will not be Rule out Schizoaffective and depressive or bipolar
Criteria D (e.g., a drug of abuse, a medication, other treatment) or to functional impairment typing…. disorder
another medical condition Criteria D - H
Not attributable to the Disturbance is not attributable to the physiological
physiological effects of a effects of a substance (e.g., a drug of abuse, a
substance (e.g., a drug of medication) or another medical condition.
Criteria E abuse, a medication, other
treatment) or to another
medical condition (e.g.
hyperthyroidism)
Not better explained by Additional specific criteria if autism or
Criteria F
another mental disorder communication disorder of childhood onset present
Differentials  Unipolar Depression Disorders:  BPD I – At least 1 manic episode or mixed episode ±  Panic Disorder (≥ 1 month)  Brief Psychotic Disorder (x1/7 – 1/12)
o Major Depressive Disorder hypomanic or depressive episode (typically; can be o Lifetime prevalence: ~ 5%  Schizophreniform Disorder (x1/12 – 6/12)
 ‘Typical’ or ‘Melancholic’ Depression separated by any length of time)) o aged 26 – 34 years  Schizophrenia (> 6/12)
– ↓ sleep (insomnia) & appetite  BPD II – Recurrent Major Depressive Episode + o ♀ > ♂ (2:1)  Schizoaffective, depressive Type or bipolar type –
 With Atypical features (see above) Hypomania (less severe symptoms, i.e. no history of o Associations – Agoraphobia, Substance use, (Schizophrenia + Mood symptoms)
o Dysthymia / Persistent Depressive manic episodes) Depression, Bipolar Disorder o > 2/52 of pure psychosis prior to onset of mood
Disorder / Cyclothymic (Sxs > 2yrs & < o Hypomania = elevated mood, increased energy & o Symptoms symptoms (either hypomanic or depressive)
5 SIGECAPS; > 1 year in children / productivity at work, flight of ideas and decreased  Recurrent unexpected panic attacks – Episodes of o when mood symptoms are present, psychotic
adolescents) need for sleep lasting ≥ 4 days; occupational intense fear & discomfort lasting minutes; fear of symptoms are more dominant
 ≥ 2 of the following: appetite functioning is either improved or mildly impaired dying; o Delusions generally incongruent with mood
disturbance, sleep disturbance, low  Cyclothymia (symptoms at least half the time ≥ 2 Overstimulation of sympathetics o Tx – Atypical antipsychotics
energy, low self-esteem, poor years [1 year in children], with any remission ≤ 2 o Sweating, palpitations, Dyspnea, tachycarida  ± SSRI if depression
concentration, hopelessness months) o Paresthesias, ABD pain, nausea, light–  ± Lithium if manic.
 Specifiers: o Mild hypomanic & depressive symptoms with headedness, chest pain, dyspnea, choking  Mood Disorder (either MDD or BPD) with
 with pure dysthymic syndrome fluctuation between the two; symptoms do not sensation, impending doom psychotic features
 With intermittent major meet criteria for hypomanic or major depressive  Concern about future attacks & their o Mood or depressive symptoms > 2/52 exclusively
depressive episodes episodes consequences, &/or a significant change in
  With persistent major depressive  Mood Disorder due to GMC behavior related to the attacks, ≥ 1 month. prior to onset on psychotic symptoms
episodes o Autoimmune–induced o Associated with ↑ sensitivity to lactate infusion o Psychotic symptoms appear exclusively during
o MDD with psychotic features o Neurosyphilis o Treatment manic or depressive episodes; usually mood–
o Depression with seasonal pattern / o Lyme Disease  Acute panic attack – Short–acting BZDs (e.g. congruent delusions in severe depression/mania
Seasonal Affective Disorder (fall & o HIV alprazolam, lorazepam) is abortive o Delusions typically mood congruent in MDD with
winter) o Subacute Combined Degeneration 2O B12  If hyperventilation: breathing in a paper bag psychotic features – Tx w/ Atypical antipsychotic
 Depressed phase of BPD deficiency  Long–term management - maintenance + SSRI or ECT (especially in pregnant)
 Adjustment Disorder with depressed o Hyperthyroidism  CBT  Delusional Disorder (Non–bizarre delusions)
mood o Wilson’s Disease  Antidepressants: SSRIs, SNRIs, TCAs o ≥ 1 type of delusion (fixed, false beliefs) ≥ 1
o Anxiety symptoms within 3 months of  Substance–Induced Mania  Benzodiazepines may be used until month without any other psychotic symptoms
onset of identifiable stressor & o Steroid–induced antidepressants take effect (e.g., hallucinations, disorganized speech,
inappropriate subjective distress (e.g. o Stimulants – cocaine, methamphetamine  Acute Stress Disorder (3 – 30 days) – similar symptoms negative symptoms)
bad break–up, death of a pet, cancer o Drug–induced to PTSD o Hallucinations only occur during delusional
diagnosis successfully treated) o Exposure to actual or threatened trauma episodes
o Anxiety symptoms < 6 months o Symptoms from the following categories: o Types of delusions
following termination of stressor  Avoidance of internal memories or external  Grandiose
o Symptoms must be distressing &/or reminders  Jealous
impairing but insufficient to meet other  Intrusion (e.g. nightmares, flashbacks)  Erotomanic
diagnostic criteria for mood disorder  Dissociation (e.g. amnesia of event, derealization)  Somatic
o Marked distress &/or impairment in  Arousal (e.g. insomnia, hypervigilance, startle)  Persecutory
social and occupational functioning  Negative mood  Psychosis due to General Medical Condition
(impaired concentration affecting  PTSD (> 1 month) o Delirium, Dementia
work, social isolation)  Specific Phobias (≥ 6 months) – intense fear of phobic o Cushing syndrome
o Tx – psychotherapy & counselling stimulus – such as specific situations (e.g. o Thyroid disorder (e.g., thyrotoxicosis)
 Disruptive mood dysregulation disorder claustrophobia), objects (e.g. arachnophobia - spiders) o Vitamin B12 deficiency
(DMDD) or agoraphobia (intense fear of public spaces / crowds, o Systemic lupus erythematosus
o Symptoms ≥ 12 months duration closed spaces, public transportation, lines) o Neoplasm (e.g., brain tumor)
o Severe temper outbursts (verbal or o Egodystonic (aware of problem which is deemed o Epilepsy (e.g., temporal lobe epilepsy)
behavioral) ≥ 3 times/week unhealthy) o Wilson disease
o Irritability or anger in between o Agoraphobia is comorbid with panic disorder o Porphyria
outbursts o Tx – CBT with exposure to phobic stimulus (1st line;  Substance–Induced Psychotic Disorder
o Diagnosis can only be established in systemic desensitization therapy) o Hallucinogens
children UNDER 18 years of age o Alternative: BZDs or SSRIs when CBT not available o N.B. very rare so don’t say it. It would mean u
 Depressive Disorder due to General Medical Condition (GMC) or when phobic stimulus infrequently encountered smoke now & act crazy, 4 hours later your back
o HIV, Lyme, Hypothyroidism,  Social Anxiety Disorder (previously Social Phobia) to normal and never go crazy again until you
o Porphyria, Uremia, Cushing’s Disease, Liver disease, o Anxiety restricted to social & performance situations, smoke again and the cycle begins. So your
o Huntington’s, MS, Lupus, L–MCA stroke fear of scrutiny and embarrassment normal all the time except once you smoke.
 Substance / Medication–Induced Depressive Disorder o Persistent anxiety and poor eye contact during  Cluster A Personality disorders
o IFN, beta–blockers interactions o Schizotypal personality disorder
o α–methyldopa, L–dopa, OCPs, o Management  Odd and eccentric behavior
o EtOH, marijuana  Maintenance: SSRIs / CBT  Magical thinking (inventing causal
o Cocaine /amphetamine withdrawal  Performance: Beta blockers relationships between behaviors &
o Opiates, Corticosteroids  Abortive: Benzodiazepines (BZDs) events with no evidence e.g.
 Depression–related Cognitive impairment (pseudodementia)  Obsessive Compulsive Disorder, OCD (see below) superstitions, clairvoyance); inconsistent
o Deficits in attention, concentration, memory & executive function  Generalized Anxiety Disorder (≥ 6 months) with the patient's cultural norms
 Pathologic grief / Persistent Complex Bereavement Disorder (Prolonged grief, Complex Grief) o Panic attacks may also occur in GAD  Discomfort in close relationships
 o Loss of loved one > 12 months ago; risk associated with unexpected or violent death of a loved o Panic symptoms in GAD are generally precipitated by  Aloof, dresses weirdly
one and death of a spouse of child the uncontrolled escalation of anxiety/worry rather  Lacks delusions / hallucinations
o Sadness, anxiety, apathy than occurring spontaneously or acutely in specific  Malignant personality disorder i.e. has
o Functional impairment present situations as in panic disorder. highest likelihood of transitioning to
o Suicidal Ideation, i.e. Wants to die NOT just to be with deceased (c.f. Normal Bereavement) o Individuals with GAD tend to be more concerned with actual psychotic disorder
o Treatment – psychotherapy to re–engage in meaningful life without deceased the future; individuals with depressive disorders are o Schizoid personality disorder
 Normal Grief (Uncomplicated Bereavement) more past–oriented.  NO interest in social relationships (c.f.
o Up to 12 months after death of loved one o Mood swings & suicidal ideation are uncommon avoidant personality that wants
o Sadness, anxiety, apathy  Adjustment Disorder with anxiety relationships but scared & embarrassed)
o NO functional impairment o Emotional or behavioural disturbances within 3  Restricted emotional expression &
o Acceptable to have auditory hallucinations of loved ones months of onset of stressor anhedonia
o No suicidal ideation* (other than wanting to be with the deceased)  Medical illness – e.g. angina, arrhythmias, hypoglycemia,  Seclusive to self (“Loner”); works night
o No treatment indicated typically thyrotoxicosis, pheochromocytoma time jobs
 Other Psychiatric illness – e.g. Schizophrenia, Mood o Paranoid personality disorder
disorders, Avoidant personality disorder  Distrustful of others
 Substance-Induced Anxiety Disorder e.g. Caffeine,  Suspicious of friends and family
sympathomimetics, BZD withdrawal  Superficial relationships
o Tx –
 Discontinuation of the substance/medication
 CBT & SSRIs/SNRIs
Treatment  Most antidepressants requires > 4 weeks  Psychotherapy Anxiety Disorders: Psychotic disorders
to be therapeutic (6 – 8 weeks typically o Appreciate stressors, social intervention  Antidepressants ± Anxiolytics  Psychosocial Interventions, Psychoeducation
for response); initial tx 6 – 12 weeks  Acute Mania or Hypomania o 1st line – SSRI or SNRI o Cognitive, Vocational & Psychosocial rehabilitation
o If in remission, continue o Mild to moderate mania: lithium monotherapy or o BZDs < 2 – 4 wks; NOT for chronic anxiety  Antipsychotics
antidepressants for ≥ 4 – 9 months atypical antipsychotics (olanzapine, quetiapine,  Psychotherapy – CBT o Acute psychosis – High–potency 1st
following remission (continuation lurasidone) o Deep breathing training generation antipsychotics (e.g.,
phase). N.B. the dose that achieves  Target lithium blood level should be high normal o Relaxation haloperidol) & high–potency 2nd
remission should be maintained; therapeutic level (i.e. levels closer to 1.0 – 1.2 o Systemic desensitization for phobias generation antipsychotics (e.g.,
subtherapeutic doses associated mEq/L) often needed for acute mania o Trauma–focused CBT for PTSD & Acute risperidone, olanzapine, aripiprazole,
with increased risk of recurrence o Severe mania: mood stabilizer (lithium or Stress Disorder quetiapine, ziprasidone)
o Due to high risk of recurrence, valproate) PLUS 2nd generation antipsychotic (e.g. Tx of Generalized Anxiety Disorder o Maintenance – long–acting injectable
maintenance phase indicated if early quetiapine) is 1st line combination therapy First–line: psychotherapy, pharmacotherapy, or both antipsychotics e.g. Olanzapine,
age of onset (≤ 18 years), ≥ 2  If no response within 1–3 weeks, continue o Psychotherapy: CBT, applied relaxation therapy, Risperidone, Haloperidol, Fluphenazine
episodes, persistent residual antipsychotic but switch lithium to valproate or biofeedback o Typicals
depressive symptoms, and comorbid vice versa. o Pharmacotherapy: SSRIs/SNRIs  Butyrophenones – e.g. Haloperidol
psychiatric disorders; → continued  If still not responsive, switch the antipsychotic Second–line  Phenothiazene – e.g. Chlorpromazine
for ~1–3 years.  If still refractory, D/C pharmacotherapy, & ECT o BZDs can be used until SSRIs take effect but should o Atypicals
o If decision is made to discontinue o Urine toxicology – rule out cocaine or other never be used for long–term management, as they  E.g. Clozapine, Risperidone,
medication, a gradual taper over stimulant use increase the risk of benzodiazepine dependence. Quetiapine (Seroquel)
several weeks to months is o Mania/hypomania in pregnancy: typical o Buspirone (5HT–1a partial agonist): requires  Olanzapine (Zyprexa)
preferable with close monitoring and antipsychotics (e.g., haloperidol) or ECT (if severe or consistent, daily intake for ≥ 2 weeks due to its Pharmacotherapy
early reinstitution of refractory mania)  Acute psychotic episode: short–acting
delayed onset of action
pharmacotherapy if necessary o Management of agitation: rapid–acting IM atypical antipsychotics + adjunctive BZDs for agitation
 give BZDs to bridge the 2–3 weeks
o If highly recurrent illness (≥ 3 prior antipsychotics (olanzapine, aripiprazole) or BZDs  ADRs – dizziness, orthostatic hypotension  Acute manic episode: mood stabilizers (e.g.,
MDEs) or severe episodes (e.g., (e.g., lorazepam, clonazepam) o Antipsychotics only for refractory cases lithium, valproate, carbamazepine)
including suicide attempt or  Mood Stabilizers – long–term maintenance  1st – line treatment: 2nd-generation antipsychotics
st
o 1 line – (e.g., risperidone, quetiapine), which are
 psychosis) or severe ongoing
psychosocial stressors, or chronic
episodes (≥ 2 years) → continue
antidepressants indefinitely
o Tapering off medications should be
done over 6–8 weeks; may help to:
 Decrease the risk of relapse
 Prevent antidepressant
discontinuation syndrome
(results from abrupt withdrawal
after taking meds ≥ 4 weeks): flu–
like symptoms, nausea, insomnia,
hyperarousal, & sensory
disturbances
 Most common w/ sertraline &
fluvoxamine
 MDD with psychotic features –
combination of antidepressant +
antipsychotic
 Mild –Psychotherapy (Cognitive Behaviour
Therapy and Interpersonal
Psychotherapy)
 Moderate & Severe – Psychotherapy +
Antidepressant
o 1st line – SSRIs (e.g. escitalopram;
also indicated in OCD, bulimia,
anxiety, PTSD or premature
ejaculation)
o Alternatives
 Atypical Features – MAOIs e.g.
phenelzine
 ADR – sedation, weight gain,
drug & food interactions
(serotonin syndrome,
tyramine hypertensive crisis)
 Requires a 2 week washout
period of SSRI (5 weeks for
fluoxetine due to its longer
half–life) prior to use, due to
risks of hypertensive crisis or
serotonin syndrome
 SNRIs (e.g. venlafaxine – assoc.
with tachycardia & ↑ BP)
 Avoid in HTN &/or post–MI –
Venlafaxine (SNRI). Don’t take
w/ St. Johns Wart
 Lithium – if predominantly manic
 MOA – modulation of phosphonositol
pathway
 ADRs – Reversible Nephrogenic DI, Hyper– or
Hypothyroidism, Teratogenic (Epstein
anomaly), CKD, Chronic interstitial nephritis,
Cardiotoxicity (arrhythmias – sinus node
dysfunction)
 N.B. Lithium – induced hypothyroidism not an
indication to stop. This is particularly
important if severe mood episodes that
respond preferentially to lithium
o TFTs every 6 – 12 months
o Add levothyroxine
 Thiazide diuretics, NSAIDs (except aspirin),
and ACE inhibitors have been associated with
increased lithium levels
 Valproate (Valproic Acid (Dilvaproex, Epilim) if
frequent fluctuations between mania and
depression; preferred over lithium in cases of
renal insufficiency as valproate is not nephrotoxic
– ADRs:
 N/V/D, Skin rash, hepatotoxicity
(transaminitis within 1st 6 months of
treatment; rare), pancreatitis,
thrombocytopenia, tremor, alopecia
 Teratogen – neural tube defects (e.g.
anencephaly, myelomeningocele)
 Carbamezapine (Tegretol; AED) – MOA: Blocks
Na channels; risk of agranulocytosis,
Dermatologic (skin rash [most common],
pruritus) & SJS (less common); GI (nausea,
vomiting), neurologic (drowsiness, blurred vision)
 If ANC <2000? – weekly CBC
 If ANC <1000? – D/C CBZ
 CBZ toxicity can manifest with cerebellar
findings and anticholinergic symptoms
 Lamotrigine (AED) if predominantly depressive –
risk of SJS (Steven Johnson Syndrome)
 MOA – Glutamate inhibition, Voltage–Gated
Na Channel inhibition
o If refractory, (lithium or valproic acid) + atypical
antipsychotics (e.g. quetiapine, aripiprazole,
olanzapine, risperidone)
o Severe depression or predominantly depressive BPD
II: Antidepressants may be started after initiating
mood stabilizers.
Tx of Acute Stress Disorder
Trauma focused, brief CBT (1st line)
BZDs can be administered to reduce agitation, intense
anxiety or sleep disturbance
Monitor for PTSD (symptom duration > 1 month)
Tx of PTSD
Psychotherapy: first-line treatment; with or without
adjunctive pharmacotherapy
o Trauma–focused cognitive-behavioral therapy
 Exposure therapy (e.g., showing war veterans
images of war, returning to scene of an accident)
 Cognitive processing therapy
o Eye movement desensitization and reprocessing:
 Under the guidance of a therapist, the patient
recalls traumatic images while following the
therapist's fingers with their eyes from left to right.
Pharmacotherapy
o Antidepressants – SSRIs (sertraline or paroxetine),
SNRIs
o Prazosin: for PTSD-related nightmares and sleep
disturbance
o Consider atypical antipsychotics to augment SSRIs
and SNRIs.
o BZDs such as lorazepam are not effective for PTSD
and are rarely used for hyperarousal and anxiety.
BZDs use should be closely monitored because many
patients with PTSD are at risk for drug dependence.
Prognosis – In addition to PTSD, sexual assault victims are
at increased life-time risk for major depression, and
contemplation of suicide and actual attempts; also at
increased risk for medical problems, including STDs,
pelvic pain, fibromyalgia, functional gastrointestinal
disorders, and cervical cancer (which may be linked to an
avoidance of pelvic examinations)
Tx of Adjustment Disorder
Psychotherapy (usually sufficient without
pharmacotherapy)
o 1st-line treatment: CBT or psychodynamic
psychotherapy
o May be provided as individual, family, or group
support therapy
o Interpersonal psychotherapy
Pharmacotherapy
o SSRIs (e.g. paroxetine): for depressed mood
o Benzodiazepines: for anxiety or panic attacks
especially effective at treating positive psychotic
symptoms & less likely to cause extrapyramidal
side effects
 Alternative treatment: 1st–generation
antipsychotics in depot form for those at risk of
poor adherence (e.g., fluphenazine, haloperidol,
chlorpromazine)
o Treatment–resistant schizophrenia, or
schizophrenia / schizoaffective disorder with
recurrent suicidality → clozapine for
persistent positive symptoms (i.e., delusions,
hallucinations, &/or disorganized speech)
despite trials of ≥ 6 weeks of 2 different
antipsychotics at their maximum doses
o Treatment during pregnancy: 1st generation
antipsychotics (e.g., haloperidol) – 1st–line
o Treatment of depression: SSRIs or tricyclic
antidepressants (e.g., sertraline, imipramine)
o Treatment of anxiety: SSRIs
 Negative symptoms are more difficult to treat and
often persist even after the resolution of positive
symptoms.
o Social skills training is an effective
augmentation strategy to target negative
symptoms
Prognostic factors in schizophrenia
 Good (Favourable prognostic factors in
schizophrenia)
o Later onset (age ≥ 40)
o Female sex
o Acute onset of symptoms (no prodrome)
o Identifiable precipitant
o Presence of mood symptoms
o Predominantly positive (rather than negative)
symptoms
o Good pre–morbid functioning
o No family history of schizophrenia
o Short duration of active symptoms
 Poor
o Onset in childhood or adolescence
o Male sex
o Gradual onset (prodrome), no precipitant
o Predominantly negative symptoms (i.e. flat
affect, loss of motivation, anhedonia)
o Family history of psychotic illness
  Atypical antidepressants
 Bupropion (; an activating
antidepressant): lowers seizure
threshold, results in less sexual
dysfunction than SSRIs, and can
also treat tobacco dependence
 If erectile dysfunction with
SSRIs → switch to Bupropion
(dual NE reuptake inhibitor, &
Dopamine agonist activity)
 Has stimulatory effects
(‘activating’); no weight gain
or sexual side effects), thus
preferred if persistent fatigue
& weight gain with SSRIs
 Contraindications – Bulimia,
alcoholics, epileptics
 Mirtazapine: significant weight
gain, sedation / somnolence, ↑
appetite
 preferred choice if patient has
poor appetite &/or poor sleep
 does not cause sexual
dysfunction
 Trazodone (serotonin–
modulator): used primarily for
insomnia; higher dose is
required when used as an
antidepressant
 ADRs – sedation, nausea,
priapism, postural
(orthostatic) hypotension
 Erection lasting > 3 hours –
likely trazoDONE which gives
us a “BONEr”
 Other Serotonin modulators
(e.g. vilazodone)
 Paroxetine – has most drug–
drug interactions
 Citalopram – fewest drug–drug
interactions
 N.B. Don’t have to tapper when
stopping fluoxetine
 TCA and MAO inhibitors: cause
more side effects than SSRIs
o Augmenting agents: lithium, 2nd–gen
antipsychotics (e.g., aripiprazole),
Obsessive Compulsive Disorder o Benzodiazepines or other sedative-hypnotic agents o Long duration of untreated psychosis
 High prevalence of vocal–motor ticks and 5–7% of (e.g., zolpidem): for insomnia
OCD pts have full blown Tourette Syndrome
 Often begins in childhood or adolescence
 Clinical Features
o Obsessions
 Recurrent, intrusive, anxiety–provoking
thoughts, urges, or images that causes severe
distress, & is not related to another mental
disorder
o Compulsions
 Response to obsessions with repetitive,
intentional behaviors or mental acts (e.g.
checking &/or counting; repeating words [such
as counting down from 5 to 1]) in an attempt
to get rid of thoughts or images, and to
alleviate the anxiety caused by a particular
obsession.
 Behaviors not connected realistically with
preventing feared event
o Time–consuming (>1 hr/day) or causing
significant distress or impairment, with
interference with daily routine
 Associated with structural abnormalities in the
orbitofrontal cortex and basal ganglia
 Pregnancy & postpartum period are associated with
increased risk for new onset, recurrence, or
exacerbation of OCD
o The obsessional thoughts and compulsions often
relate to the health and safety of the baby
 Tx – psychotherapy and/or pharmacotherapy
o Cognitive–behavior therapy (exposure &
response prevention)
o SSRIs (e.g., sertraline, paroxetine, fluoxetine,
fluvoxamine)
 Fluoxetine, fluvoxamine and sertraline have
been shown to be safe and effective
treatment in pediatric OCD
o Alternatively, TCAs with serotonergic action (e.g.,
clomipramine)
 thyroid hormones
 For patients with partial response (25 –
50% symptom improvement) to 1st line
treatment and are tolerating their
current medication, major augmentation
strategies include adding an
antidepressant, with a different
mechanism of action, a 2nd generation
antipsychotic (e.g. aripiprazole), lithium,
triiodothyronine, or psychotherapy
 Unlike partial responders, non-responders
(i.e. patients with little to no
improvement or unacceptable tolerability
to first–line therapy) generally benefit
from switching to a different
antidepressant
 Bright light therapy for Seasonal
Depression (10,000-Lux light box shortly
after awakening) + antidepressants
 Electroconvulsive therapy for depression
o Induces a 30- to 60-second generalized
tonic-clonic seizure under general
anesthesia. Typically administered 3
times per week for a course of 6-12
treatments
o Indications
 Treatment resistance to multiple
medical trials
 Psychotic features
 Emergencies – pregnancy, refusal to
eat or drink [malnutrition /
dehydration], persistent suicidality
o Safety
 No absolute contraindications
 Increased risk
 Severe cardiovascular disease,
recent MI
 Space-occupying brain lesion
 Recent stroke, unstable aneurysm

 Buspirone is primarily used to treat anxiety disorders. It may be used as augmentation for major depression when augmentation with a second antidepressant is ineffective.
Treatment Resistant Depression
Non–responder – consider switching Partial Responder – consider augmentation
 Monotherapy with a different antidepressant (e.g.  Augmentation agents:
phenelzine) o Second – generation antipsychotic (e.g. aripiprazole)
 Psychotherapy
 Electroconvulsive therapy o Antidepressant with different mechanism of action
 Repetitive transcranial magnetic stimulation o Lithium
o Thyroid hormone
o Psychotherapy

Pharmacotherapy for Smoking Cessation

Treatment Indications Adverse Effects / Contraindications
 More effective than either buproprion or
Varenicline  Disordered sleep and abnormal dreams
combination nicotine replacement therapy
Long–Acting Nicotine Replacement Therapy  ↓ Cravings & daytime withdrawal symptoms
 No significant effects, safe in almost all
(nicotine patch)  Long – acting ay be combined with short –
patients
Short–Acting Nicotine Replacement Therapy acting nicotine replacement therapy (“patch
 Skin irritation from patch
(nasal spray, gum, lozenges, inhaler) plus regimen”) to improve efficacy
 ↓ Post–cessation weight gain  Contraindicated in patients with seizure
Buproprion  Good choice for patients with unipolar disorder or eating disorders
depression  Can worsen HTN

 Classification of antidepressants-
o Selective serotonin (5–HT) reuptake (SSRIs) – fluoxetine (Prozac®), paroxetine (Paxil ®), sertraline (Zoloft®), citalopram (Celex®), escitalopram (Lexapro®), fluvoxamine (luvox®)
 Citalopram is associated with dose-dependent QT–prolongation
 Common early ADRs of SSRIs – headache, nausea, insomnia/sedation, anxiety, dizziness
 Long–term ADRs – sexual dysfunction, weight gain
 N.B. Patients aged 18 – 24 should be informed that studies of their age group have demonstrated an increased risk of suicidality during initial weeks of SSRI treatment; however this information should be
tempered with information about risks of untreated mental illness
 SSRI discontinuation syndrome (e.g. anxiety, dysphoria, flu–like syndrome) – due to abrupt discontinuation or missed doses of SSRIs
 4-6 weeks to respond to SSRI therapy on average; response may be as early as 2 weeks
o Selective serotonin – noradrenergic reuptake inhibitors (SNRIs) – venlafaxine, desvenlafaxine, duloxetine, milnacipran
 Abrupt discontinuation of short – acting serotonergic antidepressants (e.g. paroxetine, venlafaxine, duloxetine) may lead to discontinuation syndrome
 Physical symptoms – dizziness, fatigue, headaches, and myalgias
 Neurologic symptoms may also occur – perceptual changes, paresthesias and “electric shock” sensations
o Tricyclic antidepressants (TCAs) – imipramine, amitriptyline, desipramine, nortriptyline, clomipramine
 Amitriptyline exerts its therapeutic effects by inhibiting the reuptake of norepinephrine and serotonin
 Generally reserved for treatment–refractory patients (non–responders to multiple and different classes of first–line antidepressants) due to less favourable side effect profile
 ADRs of Amitriptyline
o Muscarinic (M1) receptors, leading to anticholinergic symptoms – dry mouth, constipation, urinary retention, blurred vision (2 O to mydriasis), confusion
o Histamine receptors – lethargy
o Alpha adrenergic receptors – orthostatic hypotension (particularly common, even at low doses)
o Cardiotoxicity (QRS prolongation), Lethality in overdose
o Atypical Antidepressants – Antidepressant therapies that are not categorized as SSRIs, TCAs, or MAOIs
 Heterocyclic (Tetracyclic & Unicyclic) Antidepressants –
 Bupropion = norepinephrine & dopamine reuptake inhibitor; no serotonergic effects
o It is activating, does not cause weight gain, and has no sexual side effects
o Preferred choice in depressive symptoms including hypersomnia and weight gain
o Contraindicated in eating disorders
 Other = mirtazapine, amoxapine, maprotiline
 Serotonin modulator – vortioxetine
 5-HT2 receptor antagonists – e.g. trazodone
o Monoamine oxidase inhibitors (MAOIs) – for treatment–resistance depression
  Irreversible, non–competitive inhibitors e.g. phenelzine, tranylcypromine
 Reversible, MAO-A- selective inhibitors e.g. moclobemide
 Dietary restrictions (avoid foods containing tyramine)
 Low levels of 5–hydroxyindlacetic acid (5–HIAA) in CSF is associated with suicidal behaviour. 5–HIAA is the primary metabolite of serotonin, which is one of the most important neurotransmitters
responsible for modulating mood and behaviour
o Low levels of CSF 5–HIAA are thought to represent dysfunction of the serotonin syndrome
o Serotonin is the target of SSRIs, the class of drugs considered 1 st line for depressive disorders
 ANTIPSYCHOTICS
o Antipsychotic medication effects (dopamine antagonism) in dopamine pathways
 Mesolimbic pathway – Antipsychotic efficacy
 Mesocortical – dopamine hypofunctioning may be responsible for negative symptoms in schizophrenia
 Nigrostriatal Pathway – Extrapyramidal symptoms: Acute dystonia, akathisia, parkinsonism
 Tuberoinfundibular Pathway – Hyperprolactinemia (sexual dysfunction and gynecomastia in men, menstrual irregularities e.g. amenorrhea &/or oligomenorrhea, infertility, galactorrhea)
 Antipsychotics with highest potential for increasing prolactin are high–potency , 1 st generation medications (e.g. haloperidol, fluphenazine) and 2 nd generation agents risperidone
and paliperidone (a metabolite of risperidone)
 Among 2nd gen antipsychotics, aripiprazole (a partial D2 agonist) and quetiapine (a low–potency D2 antagonist) are two of the least likely drugs to produce hyperprolactinemia
o Most antipsychotics act as dopamine antagonists (or partial dopamine agonists) at D2 receptors, decreasing activity in this pathway by preventing dopamine from binding to D2 receptors.
 Low–potency agent chlorpromazine has been associated with cholestatic jaundice
 2nd generation antipsychotic risperidone is a serotonin–dopamine antagonist that has moderately high affinity for D2 receptors.
 Most newer agents (Atypical antipsychotics) act as 5–HT2A receptor antagonists e.g. clozapine, olanzapine, quetiapine, risperidone, ziprasidone
 Tend to be limbic–specific thus improving adverse drug side-effect profile
 Serotonergic–dopamine antagonist; have low affinity for D2 receptors in mesocortical, nigrostriatal and tuberoinfundibular tract
 Aripiprazole is a D2 partial agonist
 New agents have varied effects on alpha and H1 receptors
o Weight neutral but prolongs the QTc? – Ziprasidone
o Weight neutral but increases akathesia? – Aripiprazole
o All atypical (2nd generation) antipsychotics—ADRs prolonged QTc, fewer EPS and anticholinergic side effects than typical antipsychotics
 2nd generation antipsychotics have affinities for other receptors (e.g. alpha adrenergic, muscarinic, histaminic) to varying degrees, resulting in different ADRs
 Muscarinic receptor antagonism may result in anticholinergic effects – dry mouth, constipation
 Histaminic antagonism and metabolic dysfunction contributes to sedation and weight gain, dyslipidemia, hyperglycemia (including new–onset DM)
 Most associated with weight gain? (but #1 S/E is sedation) – Olanzapine
 “–apine”—metabolic syndrome (weight gain, diabetes, dyslipidemia).
 Causes orthostasis (alpha blocking properties) and cataracts? – Quetiapine
 Quetiapine has mixed serotonin–dopamine antagonist activity by binding at both serotonin 2A & dopamine 2 receptors
 Addition of serotonin antagonism, and low binding affinity for dopamine when compared to 1 st generation antipsychotics, is believed to contribute to
the decreased risk of extrapyramidal side effects
 Risperidone— ADRs: hyperprolactinemia (amenorrhea, galactorrhea, gynecomastia), extrapyramidal side effects
 Clozapine, Olanzapine
 Clozapine tx guidelines / indications – Treatment–resistant / Refractory schizophrenia & Schizoaffective disorder, Schizophrenia–associated with
suicidality
 ADRs
o Most common – Sedation, Metabolic syndrome (lowers insulin sensitivity → weight gain, hyperglycemia, hyperlipidemia)
o Most dangerous / Serious ADRs
 Neutropenia / Agranulocytosis (clozapine only), decreased seizure threshold (clozapine); risk is dose–dependent, although
clozapine–induced seizures may occur at any level (clozapine lowers seizure threshold); tonic– clonic seizures are the most common
seizure type observed
 Myocarditis
  Ileus, Constipation
 Orthostatic Hypotension
 Pulmonary Embolism (clozapine)
o Monitoring – baseline & regular follow–up
 Clozapine – CBC → Absolute Neutrophil Count weekly for 6mo and q4–weekly thereafter
 D/C if WBCs<3000 or ANC<1500
 Risk of Agranulocytosis or neutropenia higher with clozapine >>> olanzapine (rare)
 BMI should be monitored monthly, 3–monthly, then annually
 Fasting glucose & lipids
 Blood pressure
 Waist circumference
 Earlier and more frequent monitoring is recommended for patients with diabetes or those who have gained > 5% of initial weight

Second–generation antipsychotic side effects Antipsychotics & Risks for Drug–Induced Parkinsonism
Weight gain / Extrapyramidal Prolonged QTc
Antipsychotic Parkinsonism Risk D2 antagonism
metabolic syndrome side effects
Aripiprazole Low Low Low Haloperidol +++ High
Clozapine Very High Low Medium Risperidone ++ High
Lurasidone Low Medium Low Olanzapine ++ Intermediate
Olanzapine Very High Low Medium Clozapine + Low
Quetiapine High Low Medium Quetiapine + Low
Risperidone High High Medium Pimavanserin + None
Ziprasidone Low Low High

 General Approach to acute Psychosis – Rule out medical or substance use disorder by performing the following tests:
o Urine toxicology
o Serum
 CBC, U&Es, LFTs, TSH, and fasting glucose
o ECG to assess:
 Presence or absence of metabolic syndrome
 Baseline QTc interval before starting antipsychotic
Antipsychotic Extrapyramidal Effects (EPS) – particularly at risk with high potency 1st generation antipsychotics (e.g. Pharmacotherapy*
haloperidol, fluphenazine) & high–risk atypicals aka 2nd generation (e.g. risperidone, lurasidone), and the antiemetic Discontinue causative agent if feasible
metoclopramide (prokinetic drug that acts on central and peripheral D2–receptor blocker)
 Low potency (e.g. Chlorpromazine & Thioridazine) – Less EPS, more anticholinergic ADRs
o Chlorpromazine – Purple grey metallic rash over sun–exposed areas and jaundice, corneal deposits
o Thioridazine – Prolonged QTc and pigmentary retinopathy (reTinal deposits)
Acute dystonia (< 12  Also seen with anticonvulsants (e.g. Carbamazepine) & metoclopramide (antiemetic)  Anticholinergics – Benztropine, trihexyphenidyl
hours)  Sudden, sustained contraction of the neck, mouth, tongue & eye muscles  Antihistamine with significant anticholinergic activity – Diphenhydramine
o Oculogyric crisis – forced, sustained upward gaze deviation
o Torticollis
o Blepharospasm
o Trismus
Akathisia  Subjective restlessness, inability to sit still (clinician must differentiate from psychotic  Beta blocker (e.g. propranolol) – 1st line
agitation) o May work by blocking noradrenergic and serotonergic inputs on
 After 30 – 90 days of antipsychotic dopamine pathways
  Benzodiazepine (lorazepam) – associated with increased mortality in
schizophrenia and is not the preferred option for long–term treatment of
akathisia unless 1st line measures have failed
 Benztropine
Parkinsonism  Gradual–onset tremor, rigidity & bradykinesia  Benztropine (or DPH)
 > 6 months  Amantadine (or bromocriptine)
Tardive dyskinesia  Abnormal involuntary hyperkinetic movement disorder with gradual onset after prolonged  Valbenazine or Deutetrabenazine
therapy (> 6 months) with antipsychotics or metoclopramide: dyskinesia of the mouth, face, o Reversible inhibitors of the vesicular monoamine transporter 2
(usually after several trunk & extremities (VMAT2)
years) o Orofacial dyskinesia (tongue protrusion, lip smacking, grimacing)  Taper and discontinue antipsychotic and switching to an atypical / 2 nd gen
o Limb dyskinesia (dystonic postures, foot tapping, chorea) (e.g. clozapine, quetiapine)
o Trunk dyskinesia (rocking, thrusting, shoulder shrugging)  N.B. anticholinergic drugs (e.g. benztropine) are ineffective and may
o Greater risk with 1st gen antipsychotics worsen tardive dyskinesia
* Management may include reducing the dose or switching to another antipsychotic, depending on the clinical scenario

Postpartum Blues, Depression & Psychosis

Postpartum Blues Postpartum Depression Postpartum psychosis
Prevalence  40 – 80%  8 – 15%  0.1 – 0.2%
Onset  2–3 days (resolves within 14  Typically within 4 – 6 weeks (can be up to 1 year)  Variable: Days to weeks (generally within the first 2 weeks)
days)
Clinical  Mild depression, tearfulness,  ≥ 2 weeks of moderate to severe depression, sleep or appetite  Delusions, hallucinations, thought disorganization, bizarre behaviour
features irritability disturbance, low energy, psychomotor changes, guilt, concentration o Content frequently related to the infant
 Typically peaks at day 5 difficulty, suicidal ideation  Most often seen in patients with a history of other psychiatric disorders, most
postpartum commonly bipolar disorder
o Depressed and/or manic moods, severe insomnia, agitation, disorganized
behaviour
Management  Reassurance & monitoring  Antidepressants, psychotherapy  Antipsychotics + treatment of underlying mood disorder (Antidepressants,
Mood stabilizers) if necessary
 Hospitalization (do not leave mother alone with infant due to risk of infanticide)

 Hoarding Disorder – New DSM-5 disorder distinct from obsessive-compulsive disorder

o Characterized by accumulation of a large number of possessions that may clutter living areas to the point that they are unstable
o Patients experience intense distress when trying to discard possessions regardless of their actual value
o Social isolation due to embarrassment (e.g. being unable to invite people to their homes) may also occur
o Extreme cases may be associated with unsanitary conditions and fire risk due to blocked exits
o Management – Cognitive Behaviour Therapy specifically targeted to hoarding behaviours
 Education, Motivational interviewing, skills training in organization, and decision-making, cognitive restructuring of dysfunctional thoughts, and gradual exposure to discarding
possessions
 ± SSRIs (adjunct to CBT) – limited efficacy in treating hoarding disorder without obsessive compulsive disorder; helpful in treating comorbid depression and anxiety disorders
 Catatonia
o Syndrome (not a specific disorder) of marked psychomotor disturbance that occurs in severely ill patients with mood disorders with psychotic features, psychotic disorders, autism spectrum
disorder, and medical conditions (infectious, metabolic, neurologic, rheumatologic)
o Clinical Features
 Immobility or excessive purposeless activity
 Mutism, stupor (decreased alertness & response to stimuli)
 Catatonia can range from stupor to marked agitation (“catatonic excitement”), which contributes to difficulty in recognition
  Negativism (resistance to instructions & movement)
 Posturing (assuming positions against gravity)
 Waxy flexibility (initial resistance, then maintenance of new posture)
 Echolalia, echopraxia (mimicking speech & movements)
o Management
 Benzodiazepines (most commonly lorazepam)
 N.B. a lorazepam challenge test (IV lorazepam 1–2 mg) resulting in partial , temporary relief within 5 – 10 minutes confirm diagnosis
 Generally responds to lorazepam within a week
 Electroconvulsive therapy – if refractory to BZDs
 N.B. Antipsychotics can worsen catatonia and should be avoided. Treatment of any psychotic features with antipsychotics should be deferred until catatonia resolves with lorazepam
o
Psychiatric Emergencies
Serotonin Syndrome Neuroleptic Malignant Hyperthermia Hypertensive Crisis Lithium Toxicity (> 1.5 mEq/L typically) Tricyclic Antidepressant Toxicity
Malignant Syndrome
Etiology and Any drug that ↑ 5-HT Antipsychotics (typical Triggered by inhaled volatile Eating tyramine–rich foods (eg.  Acute toxicity – Intentional overdose  TCAs inhibit 5–HT and NE reuptake
Pathophysiology (Serotonin), especially in > atypical) + genetic anesthetics (e.g. halothane), chocolate, aged cheeses,  Chronic toxicity (decreased renal perfusion o Antidepressant MOA: blockade of
combination predisposition succinylcholine, excessive smoked/cured meats, & consequent ↓ lithium clearance [renally monoamine reuptake, at both
 Drug interactions – Typically occurs early heat alcoholic beverages & wine, excreted]) noradrenergic and serotonergic nerve
serotonergic in treatment, and not Autosomal dominant genetic dried fruits) while taking o Dehydration (vomiting, diarrhea, fever, endings.
medication & MAOI or likely to appear in mutation of skeletal muscle MAOIs (e.g. Selegiline – diuresis), gastrointestinal illness  3° TCAs (amitriptyline) have more
linezolid patients who have receptors which alters selective MAO-B inhibitor, o Reduced GFR anticholinergic effects than 2° TCAs
 Serotonergic drug been stable for years control of intracellular Phenelzine – non– selective o Drug Interactions: (nortriptyline); 3° TCAs avoided in
overdose on a particular calcium; leading to MAO-A/MAO-B inhibitor)  Thiazide diuretics elderly
 Psychiatric drugs: antipsychotic hypermetabolism  Tyramine displaces other  NSAIDs (except aspirin)  Indications for TCAs
o MAOIs (e.g. Due to dysregulation Consequently marked, neurotransmitters [eg, NE] in  ACE inhibitors, ARBs o MDD (3rd or 4th line)
phenelzine) + SSRIs of dopamine caused excessive calcium release the synaptic cleft → ↑  Tetracyclines, Metronidazole o Neuropathic pain (e.g., peripheral
e.g. fluoxetene, by D2 receptor sympathetic stimulation (α 1-  Antiepileptics (e.g. carbamezapine, neuropathy, diabetic neuropathy,
SNRIs e.g. antagonism (MOA of adrenergic receptors) → phenytoin) postherpetic neuralgia)
venlafaxine, TCAs, 1st gen and most 2nd vasoconstriction, & HTN  Non – DHP CCBs (e.g. Verapamil) o Chronic pain (including fibromyalgia)
vilazodone, gen antipsychotics)  SSRIs o Migraine prophylaxis
vortioxetine, or Symptoms develop Narrow Therapeutic index 0.8 – 1.2 mEq/L o OCD: clomipramine
buspirone over course of days Lithium MOA – suppresses inositol o Nocturnal enuresis: imipramine
o E.g. switching from triphosphate (modulation of phosphoinositol
MAOI to SSRI with an pathway)
< 2–week washout Contraindications to Lithium
period. o Severe Renal Disease / Renal Impairment
o N.B. due to o MI
fluoxetine’s long half o Diuretics or digoxin
– life, its o Myasthenia Gravis
recommended o Pregnancy or breastfeeding (Ebstein
washout period is at anomaly)
least 5 weeks before
switching from Lithium monitoring
fluoxetine to MOAI o Requires evaluation of TFTs and Kidney
 Non–psychiatric drugs: Function before initiation of therapy
o tramadol, o Creatinine & TFTs are monitored
ondansetron, periodically (e.g. every 3 – 6 months) in
triptans, linezolid, lithium – treated patients due to risks of
MDMA (ecstasy), hypothyroidism and renal toxicity
dextromethorphan,
meperidine, St.
John’s wort
Manifestations  Fever (Hyperthermia)  Presents within 1 hr of  Pounding headache, flushing, Manifestations of Li Toxicity Respiratory depression, hyperpyrexia +
 Tachycardia anesthesia induction or nausea, myoclonus after  Acute toxicity Tri-CyCliC’s:
 Hypertension during maintenance of eating cheese, drinking red o GI – Nausea, Vomiting, Diarrhea o Convulsions
 Diaphoresis anesthesia wine, taking decongestant or o Late neurologic sequelae o Coma
 Generalized Muscle rigidity merperidine o Cardiotoxicity (arrhythmia due to
 Masseter muscle spasms  Hypertension blockade of cardiac fast Na+
  3 A’s:
o ↑ Neuromuscular
hyperActivity
(neuromuscular
irritability; e.g. tremor,
MYOCLONUS,
HYPERREFLEXIA,
bilateral Babinski
signs, hypertonia,
rigidity, seizures,
ocular clonus [slow,
continuous,
horizontal eye
movements]),
o Autonomic instability
(e.g., hyperthermia
although fever not as
high as in NMS,
vomiting, diaphoresis,
DIARRHEA &
hyperactive bowel
sounds)
o Altered mental status
(e.g. anxiety,
restlessness, agitated
delirium)
o Hyponatremia (due to
drug–induced SIADH +
excessive water intake
to reduce
hyperthermia)
o Mydriasis
Treatment  Cooling, sedation with  Stop antipsychotics or  Respiratory / ventilatory
benzodiazepines,
supportive
management (e.g.  Supportive care –
hydration)
 Cyproheptadine (5-HT2
receptor antagonist) if  Dantrolene (↓ rigidity
severe or if supportive
measures fail
 Immediate sedation,  Dopamine agonist
paralysis, & tracheal
intubation if
temperature > 41.1 OC
(106 OF)
 Acute Benzodiazepine withdrawal
 Malignant FEVER:  Sinus tachycardia  Can lead to intracranial  Chronic toxicity channels; prolonged QTc; wide QRS
o Myoglobinuria  Hypercarbia resistant to haemorrhage, stroke or death o Neuromuscular – complex)
o Fever (> 40 OC increased minute Coarse tremor – fasciculations,  QRS duration > 100 msec is
common) ventilation (tachypnea) myoclonic jerks associated with ↑ risk for
o Encephalopathy,  Haemodynamic instability in Altered Mental Status – Confusion, ventricular arrhythmia & seizures
confusion immediate intra– and lethargy, agitation and is used as an indication for
o Vitals unstable & postoperative period Ataxia, Nystagmus, Slurred speech sodium bicarbonate therapy
diaphoretic  Rhabdomyolysis with Seizures, psychomotor impairment, and ADRs (think “HAM”)
(autonomic myoglobinuria coma o H1 receptor inhibition –
instability)  Hyperkalemia  Acute renal failure  Sedation, lethargy, drowsiness
o ↑ WBC, ↑ CPK  Respiratory & metabolic  ECG – T–wave flattening/depressions (most o α1–blocking effects
(rhabdomyolysis) acidosis common) or inversion + U waves  Postural hypotension (major cause
o Diffuse muscle  Hyperthermia / High fever (>  ADRs of Lithium – of mortality)
RIGIDITY 40 OC [104 OF]) – late o Fine Action symmetric tremor (common; o Muscarinic – anticholinergic toxicity
(generalized; “lead manifestation can be treated with β –blockers if (3O amines > 2O amines)
pipe” & persistent)  CVS: tachycardia, arrhythmia
bradykinesia – st
o Ebstein anomaly (1 trimester of (including ventricular fibrillation;
dopamine pregnancy; teratogenicity 0.1%) wide QRS; QTc prolongation)
antagonism in o Nephrogenic Diabetes Insipidus  CNS: confusion, hallucinations,
nigrostriatal o Hypothyroidism (25%) – fatigue, sedation, coma, grand mal seizures,
pathway) – c.f. constipation, bradycardia, myalgias myoclonic and choreoathetosis
hyperkinesia of  Baseline TFTs & repeat every 6–12  GI: intestinal ileus (decreased bowel
serotonin months sounds), constipation
syndrome  Tx with levothyroxine (T4) rather than  GU: urinary retention
discontinuation of lithium  General: xerostomia, mydriasis,
hyperthermia (hyperpyrexia), dry
mucous membranes, dry & flushed
skin
 Tx – Phentolamine 5mg IV Lithium levels every 2 – 4 hours Supportive treatment
restart dopamine support IV hydration (except those with specific Activated charcoal within 2 hours of
agents  Immediate cessation of contraindications, e.g. decompensated CHF) ingestion
causative anesthetic D/C Lithium ECG monitoring
cooling blankets,  Dantrolene (skeletal muscle Bowel irrigation (asymptomatic acute Sodium Bicarbonate, NaHCO3 (helps
hydration, ICU relaxant) overdose) metabolic acidosis improves systolic BP,
Hemodialysis – indications: prevents arrhythmia [cardioprotective],
and hyperthermia) – o if > 4 mEq/L and narrows QRS complex)
1st line if refractory o > 2.5 mEq/L with prominent signs of o Increases TCA protein binding, and
toxicity or renal failure (Cr > 2.0 mg/dL) reduces the binding affinity of TCA in
(e.g. bromocriptine) – AMS, seizures, &/or life–threatening the sodium channel → neutral form
– 2nd line if refractory arrhythmias of TCA is less available to bind
o Increasing levels despite IV fluids sodium channels
Ventilatory support if required BZDs for seizures
o Clinical Features
  Convulsions / Seizures, Pyrexia / Fever, Confusion, HTN  Body Dysmorphic Disorder
 Autonomic nervous system o Clinical Features
 Sweating  Preoccupation with ≥ 1 perceived physical defects
 Nausea, vomiting, and anorexia  Defects not observable or appear slight to others
 Hypertension  Repetitive behavior or mental acts performed in response to the
 Neurological preoccupation
 Seizure  Significant distress or impairment
 Tremors, tremulous, anxious  Variable insight (good, poor, absent/delusional beliefs)
 Memory impairment  BDD with absent insight/delusional beliefs
 Psychiatric  BDD with poor insight
 Withdrawal psychosis with optic and auditory hallucinations  BDD with good insight
 Depressive moods o Management
o Similar to Delirium Tremens.  Antidepressants (SSRIs e.g. escitalopram) & Cognitive Behavior Therapy
o Tx  Delusional Disorder
 Diazepam or chlordiazepoxide + haloperidol if psychotic o Clinical Features
 Carbamazepine – Seizure prophylaxis  ≥ 1 delusion ≥ 1 month
 Catatonic excitement: antipsychotics (e.g., haloperidol)  Other psychotic symptoms absent or not prominent
 Behaviour not obviously odd or bizarre; ability to function apart from
delusion’s impact
 Subtypes – erotomanic, grandiose, jealous, persecutory, & somatic
o Differential Diagnosis
 Schizophrenia – prominent psychotic features & greater functional
impairment
 Personality Disorders: pervasive pattern of suspiciousness (paranoid);
grandiosity (narcissistic), odd beliefs (schizotypal), but no clear delusions
o Treatment
 Antipsychotics & Cognitive Behaviour Therapy
 Challenging to engage in treatment due to their lack of insight
 Social Anxiety Disorder (Social Phobia)
o Diagnosis
 Marked Anxiety about ≥ 1 social situations for ≥ 6 months
 Fear of scrutiny by others, humiliation, embarrassment
 Social situations avoided or endured with intense distress
 Marked impairment (social, academic, occupational)
 E.g. refusing job promotion due to fear of increased requirement
for social interactions with clients
 Subtype specifier: performance only
 Self-medication with alcohol is a common complication of social anxiety
o Treatment
 SSRI (e.g. paroxetine) / SNRIs (e.g. venlafaxine) – first line; used in
treatement of non-performance type social anxiety, or if comorbid
depression
 CBT – social skills training, cognitive reframing of anxious thoughts,
systemic desensitization
 Beta-blocker (e.g. propranolol) or BZDs (e.g. diazepam, lorazepam) for
performance-only subtype
  Due to their addictive potential, BZDs less preferred in non-  Despite earlier concerns, does not appear to increase suicidality or
performance type social anxiety disorder and personal or family depression compared with placebo
history of substance-use disorder. In addition, they are not o Bupropion
preferred when performance could be impaired by sedation and  Antidepressant
cognitive side effects (e.g. giving a presentation)  MOA – Norepinephrine-dopamine reuptake inhibitor
 Beta blockers on as-needed basis help control autonomic  ADRs – increases seizure threshold, mild stimulant effects → increased
response (e.g. tremors, tachycardia, diaphoresis) wakefulness, energy and concentration
 Binge–Eating Disorder  Contraindicated in seizure disorder and bulimia
o Clinical Features o Counselling and supportive therapy
 Recurrent episodes of binge eating  Gender Dysphoria
 ≥ 1 episode per week of binge eating over 3 months o Clinical Features
 No inappropriate compensatory behaviors  Experiences persistent (≥ 6 months) incongruence between assigned & felt
 Lack of control during eating; eating rapidly until uncomfortably full, eating gender
when not hungry, eating alone due to embarrassment, and distress,  Desires to be another gender
depression, disgust, or guilt after overeating  Dislikes own anatomy, desires sexual traits of another gender
o Treatment  Believes feelings / reactions are of another gender
 CBT  Feels significant distress / impairment
 Behavioral weight-loss therapy  Increased prevalence of comorbid psychopathology, especially mood
 SSRI disorders, anxiety disorders, and suicidality
 Lisdexamfetamine, topiramate o Initial management (Tailored to individual’s needs)
 Pharmacotherapy for Smoking Cessation  Assessment of safety
o Nicotine Replacement Therapy  Support; psychotherapy (individual, family)
 Transdermal patch and gum or lozenge  Referral to specialists services (medical and mental health
o Varenicline multidisciplinary)
 Alpha-4 beta-2 nicotinic acetylcholine receptor partial agonist  Hormonal therapy
 Gender-affirming surgery
 Key Features of Somatic Symptom and Related Disorders (Somatoform Disorders) – Symptoms tend not to match up with clinical picture
 Excessive anxiety & preoccupation with ≥ 1 unexplained symptoms
 Criteria:
o ≥ 6 months duration
o ≥ 1 real physical / somatic symptom(s) causing distress & functional (social and occupational) impairment
o Psychosocial impairment due to worrying about symptoms; excessive thoughts or behaviours related to somatic symptoms
Somatic  Unwarranted, persistent thoughts about seriousness of symptoms
symptom  Persistent anxiety about health or symptoms
disorder  Excessive time & energy devoted to symptoms
 Clues:
(formally known o F > M; Multitude of diagnostic test done, i.e. often make extensive use of medical services
as somatization  Management
disorder in DSM o Regularly scheduled visits with the same provider
IV) o Limit unnecessary workup & specialist referrals
o Reassure that serious illness has been ruled out
o Legitimize symptoms but make functional improvement the goal
 Focus on stress reduction
 Improve coping strategies
o Mental health referral only once physician–patient relationship is well established and if patient will accept
 Fear of having a serious illness despite few or no prominent somatic symptoms & consistently negative evaluation
o Predominant concerns are restricted to health and disease
Illness Anxiety
 Criteria same as Somatic Symptom disorder except symptoms are usually absent or mild
Disorder
o Rarely reassured by negative findings on physical investigation or laboratory testing
(previously
o In contrast to delusional disorder – somatic type, patients are able to acknowledge the possibility that they don’t have the disease in question
known as
 Preoccupies patient’s life leading to high health care utilization, repeated self–checking for signs of illness, and catastrophic interpretations of minor, non–specific physical sensations (e.g. thinking that eye
hypochondriasis)
fatigue and cramping after prolonged muscle use could signify a serious disease)
 Tx – scheduling regular visits, limiting diagnostic tests and referrals, and focusing on coping and functional improvement
Conversion  Typically preceded by emotional trigger and characterized by unexplained NEUROLOGIC symptoms that are incompatible with recognized neurologic conditions
Disorder  Criteria:
o ≥ 6 months duration
(Functional o ≥ 1 abnormal neurologic sign / symptom and loss of function NOT better explained by another diagnosis (i.e. inconsistent with a known disease)
neurologic o Psychosocial impairment due to worrying about symptoms
symptom  Clues:
disorder) o 10 – 35 years old; No external incentive and symptoms are not intentionally produced
Factitious  Intentional falsification or feigning of illness / symptoms in the absence of obvious external rewards
Disorder  Criteria:
o Goal is to assume “sick role” with no apparent secondary gain
(Previously  Clues:
called o Atypical or dramatic presentation, long medical record
Munchausen o Vague historical details; Inconsistencies between reported symptoms and objective findings; an atypical course of illness
syndrome) o Associated Personality Disorder
o Health Care Experience, complex knowledge of medicine
o May resort to extreme and dangerous measures to generate signs of disease (e.g. self–inflicted trauma, manipulating laboratory tests, injecting fecal matter). Some may undergo numerous surgeries,
resulting in scarring and adhesions
o Unusual acquiescence to invasive procedures, and unexplained medical supplies in the patient’s possession
 o Not content with negative results; usually demanding & typically become upset when confronted, often discharging against medical advice & seeking care at another medical facility to start over cycle
 Falsification or exaggeration of symptoms to obtain external rewards (“secondary gain” such as financial compensation, leave from work, narcotics)
 Clues:
o M>F
Malingering o Irregularities of reported symptoms
o Patient doesn’t cooperate, refuses complete examination
o Patient not happy with negative results or reassurances
o Invasive procedures are typically avoided in malingering but eagerly accepted in factitious disorder

EATING DISORDERS
 N.B. Bupropion contraindicated in eating disorders
o lowers the seizure threshold
o Patients with eating disorders would be at further increased risk of developing seizures secondary to dehydration and electrolyte imbalances
 Binge–eating disorder
o Recurrent episodes of binge–eating, but no inappropriate compensatory behaviours (unlike Bulimia)
 Both binge–eating disorder & bulimia nervosa are characterized by episodes of excessive, uncontrollable eating within a specified period (1 – 2hr) that occur ≥ once per week for 3 months
o Lack of control during eating
o Treatment –
 Cognitive–behaviour therapy, behavioural weight loss therapy
 SSRI (e.g. fluoxetine)
 lisdeamfetamine, topiramate
Anorexia Nervosa Bulimia Nervosa
Epidemiology Sex: ♀ > ♂ (10:1) Sex: ♀ > ♂ (> 90% of affected individuals are young women)
Peak age: 10–25 years of age Peak age: 20–24 years of age
Clinical Patients ≤ 20 years of age: BMI < 5th – 10th percentile for sex & age is considered the underweight threshold Recurrent binge eating
Features Patients > 20 years of age, BMI < 18.5 kg/m2 Recurrent compulsive compensatory behavior to counteract weight
Significant deliberate reduction in body mass (BMI) using strategies that include restrictive eating, purging, and excessive exercise. gain
Intense fear of weight gain motivates compensatory behavior that promotes weight loss, even if patient already has low body o Most frequent: self–induced vomiting after binge eating
weight o Laxative abuse
Body image disturbance (distorted views of body weight & shape) o Transient starvation periods
o Excessive concern about weight and body shape, despite being considerably underweight o Other weight–loss measures
o Lack of awareness of the seriousness of low body weight Binge eating and compulsive compensatory behavior both occur at
Subtypes: least once a week > 3–month period.
o Restricting type Sense of self–worth pathologically influenced by the perception of
 No binge eating or purging > 3–month period physical appearance (body weight & shape)
 Suggests weight loss is achieved by excessive dieting, exercise, or fasting Binging and purging do not occur exclusively during episodes of
o Binge–eating/purging type anorexia
 Presence of binge eating or purging > 3–month period
 Purging behaviours = self–induced vomiting, diuretic and laxative abuse, or enemas
Complications of treatment: Refeeding syndrome—often occurs in significantly malnourished patients (starvation catabolic state)
with sudden ↑ calorie intake
o Starvation catabolic state → ↓ insulin, ↑ glucagon, ↑ Cortisol → ↓ Ketone bodies use in muscle, ↑ ketone bodies use in the
brain → ↑ glycogenolysis, lipolysis, & protein catabolism → depletion of fat, protein, vitamins, minerals, & intracellular
electrolytes → Start Refeeding: Anabolic State→ ↑ insulin →
 ↑ glycogen synthesis, ↑ protein synthesis, & ↑ intracellular uptake of phosphorus, potassium, magnesium & thiamine → ↓
 PO43−, ↓ K+, ↓ Mg2+ → Clinical manifestations:
 Cardiac complications – inadequate ATP & thiamine contribute to tissue hypoxia, resulting in myocardial dysfunction
o Torsades de pointes & other arrhythmias (2O hypokalemia & hypmagnesia)
o Congestive heart failure – a weak atrophic heart that cannot handle fluid and electrolyte shifts
 Rhabdomyolysis
 Seizures, Ataxia
 Wernicke’s Encephalopathy
o Treatment: electrolyte substitution – oral phosphate preferred over IV phosphate as the latter can lead to life–threatening
hyperphosphatemia (e.g. hypocalcemia, acute renal injury, arrhythmias)
o Prophylaxis: monitor electrolyte levels, limit initial dietary intake to 1000–1500 kcal/day
Other  CVS: myocardial atrophy, bradycardia, hypotension, arrhythmias Normal or elevated BMI (≥ 18.5 kg/m2 or ≥ 10th percentile for
Features o Orthostatic hypotension (decrease in SBP ≥ 20 mmHg and in DBP ≥ 10 mmHg with standing) pediatric patients)
 Renal: poor urinary concentration, dehydration Dental status: dental caries and perimolysis due to frequent vomiting
 Neurological: seizures, cognitive impairment Gastrointestinal tract
o Hypothermia o Esophagitis and/or gastritis; Mallory–Weiss Syndrome
o Cortical pseudoatrophy with enlargement of the subarachnoid space → possible organic psychosyndrome → disturbed o Salivary (Parotid) gland Hypertrophy (parotitis)
concentration and memory, changes in personality Metabolic imbalances
o Seizures o ↓ Potassium, ↓ sodium, ↓ chloride, and ↓ calcium
 Endocrine: o ↑ Blood pH (metabolic alkalosis)
o Stress hormones: ↑ cortisol, ↑ adrenaline Skin
o Thyroid: euthyroid sick syndrome (T3 &/or T4 may be low, TSH normal or low) o Calluses on the knuckles (Russell sign)
o Secondary amenorrhea (severe weight loss suppresses hypothalamic–pituitary–gonadal axis → hypogonadotropic o Dry skin and brittle nails
hypogonadism) o Peripheral edema due to third spacing of retained fluid
o Impaired glucose tolerance Cardiovascular symptoms
 Dermatological: o Cardiac arrhythmias
o Dry skin, wound healing disorders, hair loss, lanugo body hair o Hypotension
o Russell sign (calluses on dorsal aspect of MCP joints i.e. knuckles) – seen in purging type CNS: seizures
 Gynecological: secondary amenorrhea, infertility
 Gastrointestinal: gastroparesis, constipation
 Hematological: cytopenias
 Other: electrolyte depletion (e.g. hypokalemia), osteopenia, hypercholesterolemia, hypercarotenemia
 Bones: secondary osteoporosis and stress fractures (hypercortisolism, growth hormone resistance, various endocrine
abnormalities)
 Salivary glands: sialadenosis with dystrophy
 Dental status: caries and perimolysis due to frequent vomiting
Investigations Pancytopenia ECG - arrhythmias
Hypoglycemia (pathologic tolerance of low glucose levels) U&Es:
U&Es: o Hyponatremia, Hypochloremia, Hypokalemia
o Hyponatremia, Hypochloremia, Hypokalemia, Hypophosphatemia, Hypomagnesemia o Hypocalcemia
o ↑ bicarbonate (metabolic alkalosis), ↓ creatinine o ↑ bicarbonate (metabolic alkalosis)
o Pre-renal azotemia – elevated bun–to–creatinine ≥ 20:1  ± ↑ serum amylase (salivary gland)
Hypercholesterolemia (↑ cholesterol – accelerated metabolism of cholesterol) Increased aldosterone due to upregulation of RAAS because of
LFTs: ↑ AST/ALT dehydration and volume contraction
 ↑ Serum α–amylase
High cortisol, low LH/FSH, low estrogen
 hypoproteinemia, hypoalbuminemia
ECG – arrhythmia
Treatment Psychotherapy (1st line; CBT & Psychodynamic therapy) Psychotherapy (first-line): cognitive behavioral therapy
Nutritional rehabilitation (monitor weight gain, establishing a structured and consistent meal pattern) Nutritional rehabilitation
N.B. little evidence to support the use of fluoxetine as a first line treatment in anorexia nervosa Pharmacotherapy:
Olanzapine if no response to the above o treatment with SSRIs (e.g., fluoxetine) may help decrease
Indications for hospitalization: binging/purging cycles
o < 70% ideal body weight or BMI < 15 kg/m2
o Unstable vital signs / Hemodynamic instability
 Hypothermia (< 35.5°C (96° F))
 Bradycardia (< 40 bpm)
 Hypotension (BP < 80/60 mmHg) or symptoms of lightheadedness
o Acute medical complications (e.g., syncope, seizures, pancreatitis, liver failure)
o Hypoglycemia, Acute food refusal
o Suicidality, Psychosis
o Severe refeeding syndrome
 Electrolyte derangements, marked dehydration
 Dysrhythmia / Arrhythmia
 Severe edema
Prognosis Chronic, relapsing disease course with varying outcomes (complete recovery, symptom fluctuation & relapses, progressive The disease course is chronic with relapses.
deterioration) Mortality: 2–8x higher than the general population
Mortality Increased risk of psychological comorbidities
o Cumulative mortality rate (∼ 5% per decade) o Most common: depression, anxiety, and panic disorders
o Most commonly due to severe cachexia/starvation, cardiac failure, or suicide (particularly social phobias)
Increased risk of comorbidities o Attention deficit hyperactivity disorder
o Mood disorders (e.g., depression, bipolar disorder) o Alcohol and drug addiction or abuse
o Anxiety disorders (e.g., generalized anxiety disorder, social anxiety disorder)
o Personality disorders
o Obsessive–compulsive disorder

Suicide Risk Assessment & Management– ‘SAD PERSONS’  Ethanol or drug abuse = 1
 Scored out of 10
o All drugs of abuse really
o 0 – 3 very low risk;
 Rational thinking loss = 1
o 4 – 6 intermediate or moderate risk
o Psychosis, impulsivity
o 7 – 10 high risk
 Separated / Divorced / Widowed = 1
 Sex – Male = 1
o Risk – Single > Divorce > Widowed
 Age - ≤ 19 or ≥ 45 = 1
 Organized plan or serious attempt to commit suicide = 1
 Depression or hopelessness = 1
 No social support = 1
 Previous attempt = 1
 Availability of lethal means
o Greatest risk within x3/12 of previous attempt
 Sickness or injury (presence of chronic or debilitating illness) = 1

 Suicide Risk Factors / Homicide Risk Factors

o Psychiatric disorders, prior suicide attempts (strongest single factor)
 Patients with previous suicide attempt(s) are 5 – 6 times more likely to make another attempt than those who have not had a previous attempt
o Hopelessness
o Never married, divorced or separated
 o Living alone
o Elderly white man (> 65 years), Adolescent / Young Adults (age 15 – 24)
o Unemployed or unskilled, impoverished
o Physical illness
o Family History of suicide, family discord
o Access to firearms
o Substance abuse
o impulsivity
o Antisocial personality disorder
o History of violence or criminality
 Suicide Protective Factors
o Social support / family connectedness
o Pregnancy
o Parenthood
o Religion & participation in religious activities
 Assessment and Management of Suicidality
o High imminent risk (ideation, intent, & plan)
 Ensure safety: hospitalize immediately (involuntary if necessary)
 Remove personal belongings & objects in room that may present self–harm risk
 Constant observation & security may be required to hold against will
o High non–imminent risk (ideation, intent, but no plan to act in near future)
 Ensure close follow–up
 Treat modifiable risk factors (underlying depression, psychosis, substance abuse, pain)
 Recruit family or friends to support patient
 Reduce access to potential means (secure firearms, medications)

 Alcoholism / Alcohol Use Disorder

o Sedation causing disinhibition
o Alcohol use (abuse) screening
 Single – item screening
 How many times in the past year have you had ≥ 5 (≥ 4 for women) drinks in a day?
 If positive on single screen, subsequently assessed further for symptoms of DSM 5 substance use disorder (i.e. evidence of withdrawal, tolerance and craving)
 AUDIT – C
 How often do you drink alcohol?
 How many drinks do you have on a typical day when you are drinking?
 How often do you have ≥ 6 (≥ 4 for women) drinks on 1 occasion?
 AUDIT (Alcohol Use Disorder Identification Test)
 10 – item screen assessing frequency, number of drinks, and psychosocial consequences
 CAGE Questionnaire – Can be used to follow up a positive single item screen to identify more severe problems. No longer recommended as an initial screen because they fail to identify
the full spectrum of unhealthy use. Any more than one positive answer may suggest alcohol abuse:
 Cut down? – Have you ever felt the need to cut down on your drinking?
 Annoyed? – Have you ever felt annoyed by criticisms of your drinking?
 Guilty? – Have you ever felt guilty about drinking?
 Eye–opener – Have you ever felt the need to have a drink first thing in the morning?
o Metabolism of EtOH by alcohol dehydrogenase & aldehyde dehydrogenase reduces NAD+ to NADH and ↑ NADH/NAD+ ratio → inhibition of pathways requiring NAD+ including gluconeogenesis
 in particular reaction driven in reverse direction from pyruvate toward lactate
  Additionally, excess NADH inhibits conversion of malate to oxaloacetate
 Excess NADH inhibits free fatty acid oxidation, thereby diverting free fatty acids away from lipolysis to the formation of triglycerides → contributes to hepatic steatosis in alcoholics
o Complications
 GI—
 Gastritis, esophagitis, PUD
 Alcoholic liver disease (alcoholic hepatitis, cirrhosis, portal HTN)
o AST:ALT > 2:1 (DeRitis Ratio)
o ↑ GGT (inducible enzymes; 24 hours to 2 weeks of heavy alcohol consumption and return to normal within 2 to 6 weeks of abstinence)
o Esophageal varices
 Pancreatitis (acute & chronic)
 Mallory–Weiss tears
 N.B. In initial phase of binge drinking, euglycemia is maintained by hepatic glycogenolysis. Hypoglycemia not typically seen unless hepatic glycogen stores are depleted.
 Cardiac—
 Alcoholic dilated cardiomyopathy
o Signs of right sided failure – S3, elevated JVP, Peripheral Edema, tender hepatomegaly
o Atrial fibrillation
 Essential HTN (more than three drinks per day significantly increases BP)
 CNS
 Wernicke encephalopathy—often reversible
o Caused by thiamine deficiency
o Associated conditions
 most often associated with alcoholism –
 risk of WE progressing to Korsakoff syndrome is much higher in alcohol use disorder than in other WE–associated conditions
 Malnutrition (e.g. anorexia nervosa, short gut syndrome)
 Hyperemesis gravidarum (a severe, persistent nausea and vomiting of pregnancy that results in weight loss & dehydration)
o Triad of
 Oculomotor Dysfunction
 Horizontal Nystagmus
 internuclear ophthalmoplegia (bilateral abducens nerve palsy [lateral rectus])
 Motor Ataxia – Postural & gait ataxia
 Confusion
o Can be precipitated by administering glucose in alcoholics without first giving thiamine (Vitamin B1) replacement
 Korsakoff psychosis—irreversible
o Caused by thiamine deficiency
o Alcohol–induced amnestic disorder
o Develops in up to 80% of patients with alcohol use disorder who have WE develop Korsakoff syndrome. It occurs less frequently in WE patients who are non–abusers
 N.B. In some patients who abuse alcohol, KS may develop without a recognized acute episode of WE
o Mostly affects short–term memory (permanent memory loss); confabulation is common
 Anterograde & retrograde Amnesia (anterograde > retrograde)
 Mamillary body atrophy on MRI
 Brain MRI: T2–weighted hyperintense lesions in the mammillary bodies, midbrain tectal plate, dorsomedial nuclei of the thalamus, cerebellum, and
around the aqueduct and the 3rd ventricle
o Recovery from Korsakoff Syndrome is rare, even in spite of thiamine supplementation
 Wernicke-Korsakoff syndrome—damage to anterior and medial dorsal nucleus of thalamus as well as the corpus callosum;
o Neuropathologic findings in WE include mammillary body atrophy and dorsomedial thalamic neuron loss
o Presentation is combination of two
  Treatment: IV vitamin B1 (aka thiamine) before dextrose
o IV thiamine improves ocular abnormalities within hours, but confusion and gait ataxia may persist for days or weeks; many patients never fully recover
 Pulmonary—pneumonia, aspiration
 Unable to protect airway when intoxicated and somnolent
 Nutritional deficiencies (vitamins, minerals)—likely due to poor nutritional intake, alcohol–induced renal losses, and diarrhea
 Thiamine (B1) deficiency
 Hypomagnesemia
o commonly occurs together with hypokalemia
o Well–known cause of refractory hypokalemia
 intracellular magnesium is thought to inhibit potassium secretion by renal outer medullary potassium (ROMK) channels in the collecting tubules of the kidney
 Therefore low intracellular magnesium concentrations result in excessive renal potassium loss and refractory hypokalemia
 Normalization of magnesium levels restores ROMK channel potassium transport regulation, decreases renal potassium losses, and allows for successful
correction of hypokalemia with oral (preferred) or intravenous potassium replacement
 Folate deficiency
 Hypophosphatemia – when severe can result in weakness, rhabdomyolysis, paresthesias, and respiratory failure
 Haematology – macrocytosis
 Peripheral neuropathy—due to thiamine deficiency
 Sexual dysfunction—impotence, loss of libido
 Psychiatric—depression, anxiety, insomnia
 Increased risk of malignancy—esophagus, oral, liver, lung
 Frequent falls, minor injuries, motor vehicle accidents
 Fetal Alcohol Syndrome
 Smooth Upper lip & philtrum
 Low nasal bridge with short nose
 Short palpebral fissure length
o Laboratory Findings in Alcoholics
 Anemia
 Macrocytic (most common)—due to folate deficiency
 Microcytic—due to GI bleeding
 LFTs—increased GGT; AST–ALT ratio is 2:1
 Hypertriglyceridemia
 Hyperuricemia, hypocalcemia
 Thiamine deficiency
 Decreased testosterone level
 Carbohydrate–deficient transferrin (most specific test for alcohol consumption in past 10 days)
o Tx of Alcoholism
 Psychosocial treatment
 Mutual Help Groups e.g. Alcoholics anonymous
 Motivational Interviewing
 Cognitive Behaviour Therapy
 Residential Treatment / Rehabilitation
 Pharmacotherapy for moderate to severe alcohol use disorder
 Naltrexone is a good first–line drug that improves abstinence rates by reducing the craving for alcohol
o Mu–opioid receptor antagonist → decreased pleasure
o Associated with hepatotoxicity. Contraindicated in patients taking opioids as it can precipitate withdrawal, and those with acute hepatitis or liver failure
o Shown to reduce alcohol craving, reduce heavy drinking days (> 5 drinks for men, & > 4 for women), and increase days of abstinence
o Can be initiated while the patient is still drinking
  Acamprosate indicated with liver disease or opioid use (where naltrexone contraindicated)
o NMDA–receptor mediator (glutamate modulator) → decreased cravings
o Excreted mostly unchanged by the kidney; requires dosage adjustment for renal failure
o Primarily used to maintain abstinence
 Other options: baclofen, disulfiram, topiramate, gabapentin, SSRIs, and ondansetron
o Disulfiram (Antabuse) inhibits aldehyde dehydrogenase and leads to the accumulation of acetaldehyde → increased side effects when alcohol is consumed
(tachycardia, flushed skin, headache, nausea, vomiting)
 2nd line agent in highly motivated patients. Can only be used in abstinent patients
 A few minutes after drinking alcohol, patient experiences shortness of breath, flushing, palpitations, and tachycardia.
 If more alcohol is consumed, headache and nausea/vomiting ensue.
 Symptoms last about 90 minutes.
 It is appropriate for short–term use and should not be taken chronically
 It is contraindicated in patients with heart disease
 Drugs for alcohol withdrawal—benzodiazepines—best to use long–acting agents (diazepam)
 Fomepizole is an alcohol dehydrogenase inhibitor used as an antidote to treat methanol or ethylene glycol poisoning
 Correction of fluid imbalance, vitamin supplementation (thiamine, folate, multivitamins)
o Alcohol Withdrawal from chronic alcohol use
 Pathophysiology – rebound CNS overexcitation upon sudden alcohol cessation in a chronic alcoholic
 Alcohol is a strong CNS depressant that enhances GABA (inhibitory) signaling and inhibits NMDA (excitatory) signaling.
 New homeostasis in patients with alcohol use disorder whereby the depressant effects of alcohol required to counterbalance innate CNS excitatory signaling
 Clinical Manifestations / Stages (begins 6 – 24 hours of alcohol cessation / reduction)
 Occult alcohol use disorder and alcohol withdrawal should be suspected when these symptoms emerge early during the course of hospitalization (i.e. 6 – 24 hours after last
drink)
 Minor Withdrawal (6 – 24 hours after last drink) – sympathetic nervous system activation (e.g. agitation, tachycardia, hypertension)
o Tremor
o Insomnia
o Anxiety, palpitations, and sweating
o Gastrointestinal upset
o Headache
o Intact orientation
o Duration: 24–48 hours
 Withdrawal Seizures (12 – 48 hours after last drink)
o Brief, generalized tonic – clonic seizure (usually a single episode; can be multiple)
 Alcoholic hallucinosis (12 – 48 hours after last drink)
o Consciousness is usually intact & Normal (stable) vital signs (c.f. DT – see below)
o Auditory &/or visual hallucinations are common (tactile hallucinations are also possible; prominently involve insects or animals)
o Delusions
o NO Disorientation (intact orientation)
o Duration: 24–48 hours after onset
 Goal is to prevent progression to delirium tremens (DT), which is a medical emergency (mortality rate, 20%).
o DT occurs in 5% of alcoholic withdrawals
o Delirium tremens (48–96 hours [2 – 4 days] after last drink) – persistent alteration of consciousness and sympathetic hyperactivity due to alcohol withdrawal
 altered mental status
 Rapid onset delirium, Confusion, Agitation
 Impaired consciousness and disorientation ; acute confusion, restlessness
 Visual / tactile hallucinations (usually small moving objects, e.g., mice, crawling insects)
  Increased suggestibility
 Autonomic instability (Dysautonomia)
 Fever
 Tachycardia
 Hypertension
 Sweating / Diaphoresis
 Nausea
 Neurological impairment
 Generalized tonic–clonic seizures (N.B. different from Withdrawal seizures)
 Rest and intention tremor (first high–frequency, then low–frequency)
 Hyperreflexia
 Duration: 1–5 days
 Fatal ~5% of cases
 Risk factors are pancreatitis, hepatitis, or other illness. DT is rare in healthy people.
 Tx of alcohol withdrawal
 Give long–acting benzodiazepines (e g, chlordiazepoxide, oxazepam, diazepam) if withdrawal symptoms are present.
 Prevention of DT is the best treatment.
 IV fluid therapy and electrolyte disbalance correction
 Frequent monitoring of vital signs
 Thiamine followed by Dextrose: for Wernicke encephalopathy prophylaxis or treatment (administer thiamine BEFORE glucose)
 Folate and multivitamins, nutritional support
o Diet is important in treatment (high in calorie, high in carbohydrates, multivitamins).
 IV benzodiazepines for control of psychomotor agitation and seizures
o Long–acting (e.g., diazepam [t½ = 80 hr], chlordiazepoxide [t½ = 120 hr]) if no liver disease
 Active metabolites risk buildup and toxicity in patients with liver dysfunction and consequent over–sedation
o Short–acting (e.g., lorazepam [intermediate–acting BZD], oxazepam): especially for patients with liver disease (e.g. chronic hepatitis C, elevated INR, low platelets)
 Lorazepam, Oxazepam, and Temazepam are preferred in those who drink a LOT because they are not metabolized by the liver and therefore safe in alcoholic
liver disease.
 These BZDs lack active metabolites and undergo hepatic metabolism via phase II glucuronidation instead of phase I cytochrome P450 reaction
o In the case of alcohol withdrawal seizures, benzodiazepines are preferred over other anticonvulsants to prevent further seizures.
 Anticonvulsants: if seizures persist despite benzodiazepines administration
o Carbamezapine may be used to treat symptoms of mild alcohol withdrawal, but is not first line
o Phenobarbital used as an adjunct to BZDs in treatment–refractory alcohol withdrawal and withdrawal–related seizures
 Antipsychotics (e.g., haloperidol, risperidone)
o May be used for management of psychotic symptoms (never as independent medication)
o Should be avoided, if possible, or administered in low doses
o N.B. Haloperidol decreases seizure threshold.
 Marchiafava – Bignami Disease
o Presents with Dementia, motor dysfunction & dysarthria
o Associated with severe damage to the corpus callosum and surrounding white matter in the context of chronic, alcohol use disorder and attendant malnutrition
 Delirium
o Acute confusional state consistent with reduced or fluctuating level of consciousness and inability to sustain attention and arousal (e.g. from shouting to drowsy within minutes)
o One of the most common disorders seen in elderly
o Etiology of Delirium
 Predisposing risk factors
 Dementia
  Parkinson disease
 Prior stroke
 Advanced age (> 65 years)
 Sensory impairment
 Precipitating factors
 Metabolic diseases & Systemic Illness → metabolic encephalopathy (most common cause; also referred to as metabolic encephalopathy)
o Liver or kidney failure
o Diabetes mellitus / Hyperglycemia
o Hyperthyroidism or hypothyroidism
o Vitamin deficiencies (e.g., vitamin B12, folic acid, or thiamine deficiency)
o Electrolyte abnormalities (e.g. hyponatremia, hypocalcemia, diuretics)
o Malignancy
 Drugs and toxins → toxic encephalopathy (e.g. opioid narcotics, sedatives, antihistamines, antimuscarinics, muscle relaxers, BZD, polypharmacy)
 Infections (e.g. UTI, pneumonia, meningitis)
 Central nervous system conditions (e.g. seizure, stroke, head injury, subdural haematoma)
 Hypoxia (e.g. anemia, Congestive Heart Failure, COPD, Pulmonary Embolism)
o Clinical Features
 Main symptom is an acute (hours to days) alteration in the level of awareness and attention
 Associated with anxiety, agitation and combativeness
 Delirium–induced psychosis including visual hallucinations and/or illusions
 Sleep and behavioural changes – Reversal of the sleep-wake cycle
 Recent Deficits in memory
 Emotional lability
 Severity of symptoms fluctuates throughout the day and worsens in the evening (termed sundowning).
 The duration of symptoms depends on the underlying illness
 C.F. primary psychotic disorders where sensorium is clear
o Investigations
 CBC with differential, U&Es, RBG & GMR, TFTs (TSH), LFTS
 Urinalysis ± Urine Culture & Blood Cx
 Urine toxicology & serum drug levels
 CXR – if pneumonia suspected
 ECG – MI, arrhythmias
 LP to rule out meningitis/encephalitis
 vitamin B12, folate level, VDRL (syphilis), HIV screening, and Neuroimaging (CT scan or MRI Brain) – e.g. normal pressure hydrocephalus
 EEG: usually shows diffuse slowing of background activity in patients with delirium; also useful in patients with a history of head trauma, stroke, or brain lesions
 Depression screen
o Treatment
 Primary treatment is identification and treatment of underlying condition
 Discontinue possible offending agents
 Supportive Care
 Management of Agitation
o Short-term, low-dose IM Haloperidol for agitation
o Alternative: atypical antipsychotics (e.g., olanzapine)
 Maintain adequate hydration and nutrition.
 Reduce pain, preferably with nonopioid medications.
 Prevent aspiration, incontinence, and skin breakdown.
  N.B. Restraints can worsen delirium and should be reserved as a last resort when the patient’s safety is in jeopardy

Depersonalization / Derealization
disorder
Dissociative Amnesia
Dissociative Identity Disorder
Dissociative Disorders
 Persistent or recurrent experiences of 1 or both (feelings of detachment or unreality):
o Depersonalization (feelings of detachment from, or being an outside observer of one’s self)
o Derealization (experiencing surroundings as unreal)
 Intact reality testing and intact autobiographical memory
 Inability to recall important personal or autobiographical information, usually of a traumatic or stressful nature
o Can be localized or selective amnesia for a particular event, or
o More generalized amnesia for personal identity or history
 Not explained by another disorder (e.g. substance abuse, post-traumatic stress disorder)
 Sudden onset and preceded by overwhelming or intolerable events
 If amnesia is associated with traveling or wandering, the term “dissociative fugue” is used as a specifier for dissociative amnesia
 Marked discontinuity in identity & loss of personal agency with fragmentation into ≥ 2 distinct personalities that alternate in assuming
control of the patient’s behaviour
 Transition from one personality to another can be sudden and is usually precipitated by stress
 Often have chronic auditory hallucinations that have been present since childhood, and perceived as inside the head (as opposed to
psychotic disorders, in which voices seem to come from outside the head)
 Associated with severe prolonged childhood trauma or abuse (e.g. physical, sexual, or emotional abuse, neglect)
 Tx – long-term trauma-focused therapy

DSM-5 Personality Disorders

 Paranoid  Suspicious, distrustful, hypervigilant
Cluster A
 Schizoid  Prefers to be a loner, detached, unemotional
Odd/Eccentric
 Schizotypal  Unusual thoughts, perceptions & behaviour
Cluster B  Disregard, & violation of the rights of others
Dramatic / Erratic  Violates rights of others, social norms, laws
 Impulsive, irritable, aggressive (fights, assaults) behaviours designed to intimidate
 Consistently irresponsible, lies, is deceitful
 Exploitation of others for personal gain, Lack of remorse
 Antisocial  unstable unemployment history
 Age ≥ 18
 Evidence of conduct disorder before age 15
 Management
o Psychotherapy for milder forms (monitor for manipulation of therapeutic relationship)
o Treat comorbid psychiatric disorders (e.g. substance use, depression)
 Borderline  Pervasive pattern of behaviour beginning at early adulthood; ≥ 5 of the following:
o Markedly & persistently unstable self–image
o Feelings of emptiness
o Unstable relationships – Chaotic relationships, abandonment fears, inner emptiness
 Pervasive interpersonal difficulties; frantic efforts to avoid abandonment
o Abandonment Fears
o Mood instability (marked mood reactivity; intense reactivity lasting hours to days); labile mood
 Mood shifts in response to situational stressors and typically last minutes to hours (as opposed to days to weeks required to diagnose manic and depressive
episodes in primary mood disorders)
o Inappropriate and intense anger
 o Transient stress–related paranoia or dissociation (e.g. depersonalization)
o Impulsivity in ≥ 2 areas that are potentially self-damaging (substance abuse, binge eating)
o Repetitive non–suicidal self-injury & self–mutilation (e.g. cutting)
 Splitting (i.e. feeling herself or others to be all good or all bad), disturbance of self–identity, suicidal threats
 Like antisocial, may exhibit manipulative and impulsive behaviour, but their motivation is to avoid abandonment and maintain relationships
 Treatment
o Primary treatment is psychotherapy (several types effective; best evidence for dialectical behaviour therapy, which focuses on treating emotional dysregulation
and self–harm behaviours, behaviour modification and the building of skills)
 Establishment of appropriate boundaries, validation of a patient’s experience, assumption of responsibility for one’s own actions, management of feelings on
both sides, promotion of reflecting before acting rather than being impulsive, reduction of tendency to engage in splitting, and the setting of limits on self –
destructive behaviours
o Adjunctive pharmacotherapy to target mood instability & transient psychosis (2 nd gen antipsychotics, mood stabilizers e.g. lithium, valproate)
o Antidepressants if comorbid mood or anxiety disorder
 Pattern of excessive emotionality & attention–seeking behaviour since early adulthood
 Inappropriate, sexually seductive or provocative behaviour; uses appearance to draw attention; superficial, theatrical, attention–seeking
 Shallow, rapidly–shifting, dramatic emotions (e.g., easily becoming “extremely upset”, bursting into tears)
 Impressionistic, vague speech (“real friends don’t stab you in the back like that”)
 Histrionic
 Suggestible (easily influenced)
 Overly dramatic communication (e.g., crossing arms dramatically, exaggerated facial expressions and hand gestures)
 Excessive emotionality, overestimate of closeness of relationships, use of seductive behaviour to get their needs met
 Considers relationships more intimate than they really are
 Narcissistic  Grandiosity, need for admiration, sense of entitlement, lack of empathy. Inflated self – esteem
 Avoidant  Avoidance due to fear of criticism & rejection
 Submissive, clingy, needs to be taken care of
 Dependent
Cluster C  Pervasive, psychological dependence on others to meet their emotional and physical needs
Anxious / fearful  Obsessive–  Rigid, controlling, perfectionist
Compulsive  OCPD – Hoarding and orderliness is egosyntonic (i.e. patient deems behaviour as rational; problem is with somebody else)
(OCPD)  C.f. obsessive compulsive disorder (OCD), where hoarding and orderliness is egodystonic (i.e. patient deems behaviour as unwanted or unhealthy)

 Conduct Disorder
o Age < 18 – Middle childhood to adolescence
o Childhood psychiatric disorder characterized by behaviours that violate societal norms (e.g. excessive absenteeism, consistently staying out past curfew) or the rights of others (e.g. often initiating
fights)
o M>F
o Greater risk of developing antisocial personality disorder in adulthood
o Clinical Features – BREAKS THE LAW
 Pattern of violating major societal norms or rights of others over the previous 12 months
 Aggression & cruelty towards people and animals
 Destruction of property, setting fires
 Serious violation of rules (truancy, running away)
 Deceitfulness &/or theft (lying, stealing)
 Impact functioning (e.g. failing to graduate high school)
o Treatment
 Cognitive Behaviour therapy, family therapy
 Parent management training
 Oppositional Defiant Disorder
 o Age < 18 – Onset is usually during late preschool or elementary school years
o Epidemiology –
 Before puberty ♂ > ♀; after puberty ♂ = ♀
 Frequent comorbidity of ADHD, anxiety, mood disorders, and/or learning disorders
 ODD can precede development of conduct disorder, and it increases risk of adult antisocial behaviour, impaired impulse control, substance abuse, anxiety, and depression
 ODD more troublesome, but don’t break the law
 C.f. conduct disorder – more severe and aggressive behaviours & BREAK THE LAW (e.g. physical aggression or cruelty towards people or animals, destruction of property, lying,
stealing)
o Diagnosis
 Pattern of angry / irritable mood, argumentative / defiant behaviour, or deliberately annoying behaviour, vindictiveness for ≥ 6 months
 Argumentative, vindictive, and defiant behavior toward adults and authority figures (e.g., teachers, parents), refuses to follow rules
 Deliberately annoys others
 Blames others for own mistakes or misbehavior
 Easily annoyed, Angry, irritable mood, resentful, or vindictive
 Not due to another mental disorder
 Duration of symptoms: ≥ 6 months
o Treatment –
 Parent management training to reward prosocial behaviour and use brief, non-aversive consequences of behaviour
 Psychotherapy (anger management, problem-solving, social skills training)
 No pharmacotherapy for ODD but assess for comorbid ADHD & treat if present
o Prognosis: often precedes onset of conduct disorder
 Disruptive Mood Dysregulation Disorder
o Temper outburst out of proportion to the stimulus and inconsistent with developmental age
o Symptoms manifest prior to age 10
 Severe outbursts of anger (verbal or behavioral) ≥ 3 times/week
 Severe, persistent irritability or anger in between outbursts
 Duration of symptoms: ≥ 12 months
o Treatment
 Psychotherapy (individual and family), parent management training
 Pharmacotherapy to address irritability and mood problems (e.g., stimulants, antidepressants, atypical antipsychotics)
o Prognosis: Individuals with DMDD are at increased risk of developing major depressive disorder or anxiety disorders in adulthood.
 Intermittent Explosive Disorder
o Sudden, aggressive outbursts (verbal or physical) grossly disproportionate to the stressor
 ≥ 2 times/week for a period of 3 months without physical injury to humans or animals and no destruction of property
 OR ≥ 3 times/year with physical injury to humans or animals and/or destruction of property
o Outbursts cause severe distress or result in financial and/or legal consequences.
o Individuals with intermittent explosive disorder are at increased risk of self-harm.
 Attention Deficient Hyperactivity Disorder (ADHD)
o Epidemiology
 M>F
 One– to two–thirds of children diagnosed with ADHD will experience persistent ADHD symptoms in adulthood
 If left untreated, ADHD is associated with increased risk of academic underachievement, underemployment, antisocial behaviours, substance use, and motor vehicle accidents
o Clinical Features – DSM–5 criteria
 ≥ 6 Inattentive &/or ≥ 6 hyperactive / impulsive symptoms for ≥ 6 months
 Inattentive symptoms –
o Cannot listen or follow instructions, gets sidetracked, unable to finish tasks
 o Difficulty organizing tasks (disorganized work, poor time management)
o Avoids tasks requiring sustained concentration
o Forgetful (chores, appointments)
o Loses / Misplaces objects required to perform tasks (e.g. book, phone, keys)
o Easily distractible by extraneous stimuli, Difficulty focusing
 Hyperactive / impulsive symptoms –
o Fidgety
o Unable to sit still
o Physically active ALL the time (as if “driven by a motor”)
o runs or climbs inappropriately
o Cannot perform activities quietly
o Hyper–talkative – talks constantly
o Interrupts / intrudes when others are busy or speaking
o Blurts out answers, completes others’ sentences
o Difficulty awaiting turn (e.g. in line)
 Several symptoms present before age 12
 Symptoms occur in at least two settings (e.g. home, school)
 Functional impairment (social, academic)
 Subtypes –
 Predominantly inattentive (F > M)
 Predominantly hyperactive / impulsive
 Combined type
 Children with ADHD often have increased conflict with peers, teachers, &/or parents as their inattention is often considered volitional
 ADHD is one of the most common childhood neuropsychiatric disorders and often persists into adulthood. Some patients may not seek clinical attention until adulthood and it often goes
unrecognized, untreated or misdiagnosed as a mood or anxiety disorder
 In adulthood, overt physical symptoms (e.g. excessive running, climbing) often subside, and hyperreactivity / impulsivity is typically manifested as restlessness, verbal
impulsivity, and rash decisions
 Emotional dysregulation (e.g. mood lability, irritability, anger outbursts, low frustration tolerance) and executive dysfunction (e.g. difficulty focusing on, prioritizing, and
completing tasks; disorganization; poor time management) are common and impairing.
 ADHD has been associated with higher levels of unemployment, reduced educational achievement and work productivity, increased risk of accidents, and substance abuse.
o Treatment
 Initially – Behavioral therapy in preschool age children (3 – 5; i.e. < 6)
 Improves problem behaviours and parent – child relationships
 Involves teaching parents to consistently implement effective behavioral techniques (e.g. rewards, and non–punitive consequences to shape behaviour, calm limit setting,
structured daily activities, minimizing distractions
 Medication in pre-school children should only be considered when behaviour therapy fails or the child’s function is severely impaired (e.g. repeatedly expelled from day care or
school, risk injuring others)
 Stimulants (methylphenidate, dextroamphetamine, amphetamines) – 1st line for adolescents and school – aged children (age ≥ 6)
 MOA of Amphetamines (e.g. Adderall)– Reuptake inhibitor + agonist of norepinephrine & dopamine
 MOA of Methylphenidate (e.g. Ritalin) – reuptake inhibitor of norepinephrine & dopamine
o N.B. Methylphenidate does not show up on drug screen whereas amphetamines show up on drug screens
 ADRs of stimulants– decreased appetite, weight loss, insomnia; less commonly jitteriness, irritability and emotional lability (moodiness)
o Clinically significant increases in heart rate, or blood pressure are rare; may have small elevations in heart rate (3 – 10 /min), systolic blood pressure (3 – 8 mmHg),
and diastolic blood pressure (2 – 14 mmHg)
o Appetite suppression / weight loss concerns can be mitigated against by giving medications after nutrient–dense meals.
 Potential for misuse or addiction, especially in patients with a history of substance use disorder
 o However, history of substance use and family history of alcohol abuse are NOT CONTRINDICATIONS to stimulant therapy
 May be a consideration in medication selection (e.g. choosing longer – acting preparations or a methylphenidate patch with less risk of abuse)
 Prior to initiating stimulant therapy, a comprehensive cardiac history and examination, baseline weight, and vital signs should be obtained
o If history and examination show no cardiac disease, then routine electrocardiogram (ECG) screening is NOT indicated
 Non–stimulants
 Atomoxetine [a norepinephrine reuptake inhibitor] – if strong family preference against stimulant medication; some physicians may favour it when patient history of illicit drug
use / substance use disorders
 Alpha–2–adrenergic agonist [e.g. guanfacine, clonidine] – used when there are intolerable ADRs to stimulants or if coexistent Tic disorders
o Utility in children and adolescents; limited efficacy in adult ADHD
 Other non–stimulant options with efficacy in adult ADHD include bupropion and tricyclic antidepressants
 Reactive Attachment Disorder
o May develop in young children when abuse, neglect, prolonged institutionalization, or inconsistent care (e.g. frequently moving foster homes) disrupts the development of a healthy, secure
attachment to caregivers.
o These patients seldom seek comfort and do not respond to attempts to comfort them
o Other symptoms include lack of social responsiveness, lack of positive emotions, and episodes of unexpected irritability or sadness in response to non-threatening encounters
o History of neglect and hoarding (which is common in those who have suffered neglect)
 Disinhibited Social Engagement Disorder
o Also possible outcome of early neglect
o Characterized by overfamiliarity and an unhesitant approach to unfamiliar adults
 Other disturbances commonly seen in children with a history of abuse or neglect include poor emotion regulation, toileting and sleeping difficulties, anxiety, aggression, hyperactivity and/or impulsivity
DSM V
 Diagnosis
o Record Mental health disorder, personality disorder & general medical conditions
 List those most important to understanding mental health first
 Psychosocial and Environmental Problems or Conditions
 Functioning or Severity Measures

Assessment – Check out these two DSM V Reporting Examples

1. Diagnosis:
 Schizoaffective Disorder – Bipolar type
o Multiple Episodes, Continuation of acute manic episode

Psychosocial & Environmental stressors:

 Poor insight into mental illness; non-compliance with medication
 Provokation &amp; stigmatization by other newspaper vendors
 Financial shortcomings and obsession over well-being of two children
 Poor performance in secondary school (highest education level)
 Problems with primary support group – tenuous relationships with mother, and children’s respective fathers
 Loss of half-sister to medical illnesses
 Raped by cousin during childhood
 Physical abuse from immediate family members during childhood

Disability/Impairment:
 Mania – Severe
 Patient has marked impairment in her social and occupational functioning, mood and judgement due to her delusions, hallucinations, irritability and social and sexual disinhibition

2. Diagnosis (Medical and Mental Health Disorder):

 Diabetes Mellitus Type II
 Dry gangrene 2o to Critical Limb Ischemia
 Hypertension - Essential
 Other Specified Depressive Disorder - Depressive episode with insufficient symptoms or Mild Depression
 Specific Learning Disorder with impairment in Mathematics (Dyscalculia) - Moderate to  Severe impairment

Psychosocial & Environmental stressors:

 Impending amputation procedure to right foot / lower extremity and consequent decrease in mobility and self-reliance (autonomy)
 Loss of Loved ones: Aunt during late adolescence + Recent death of Son from HIV/AIDs
 Rape incident during adolescence
 Tenuous relationships with mother and brother; Estranged father

Disability/Impairment: Mild Depression + Severe Dyscalculia