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PS25 Psychiatry Toronto Notes 2023

D.the cognitive deficits are not better explained by another mental disorder (e.g. major depressive

disorder,schizophrenia)

Note:if deficits do not interfere (as in B) and cognitive impairments are mild-moderate (asin

A.2), thisis considered “mild neurocognitive disorder;” see Neurology. N22

Specify whether due to:

•Alzheimer'

s disease

•frontotemporal lobar degeneration

•Lewy body disease

•vascular disease

•traumatic brain injury

•normal pressure hydrocephalus

•substance/medication use

•HIV infection

•Prion disease

•Parkinson’s disease

•Huntington'

s disease

•another medical condition (e.g. nutritional deficiency)

•multiple etiologies

•unspecified

•also specify if mild, moderate or severe; major neurocognitive disorder diagnosis requires an

impairment in functioning *

The 7As of Dementia

Amnesia:loss of memory

Aphasia:loss of language ability

Apraxia: loss of ability to carry out

purposeful movement

Agnosia: no longer rccogniics things

through the senses

Anosognosia: not knowing what one

does not know

Apathy:loss of Initiative

Altered perception

Epidemiology

•prevalence increases with age: 5% in patients >65 yr, 35-50% in patients >85 yr

•probability of dementia in an older person with reported memory loss is estimated to be 60%

•prevalence is increased in people with Downs syndrome and head trauma

•Alzheimer's disease comprises >50% of cases; vascular causes comprise approximately 15% of cases

(other causes of dementia neurocognitive disorder - see Neurology. N 23)

•disease course: insidious onset, usually leading to death within 8-10 yr of first symptoms

Subtypes

•with or without behavioural disturbance (e.g.wandering, agitation)

•early-onset:<65 yr,late-onset:>65 yr

Assessment and Investigations (to rule out reversible causes)

•history: consider the 7 A’

s of dementia,significant changes in ADls and IADLS, medication

compliance and substance use, risk factors for dementia and delirium, mood/anxicty and psychotic

symptoms,screen for non-Alzheimer’s dementias, assesssafety and consent/capacity issues

•cognitive tests (e.g. MMSE, Rowland Universal Dementia Assessment Scale, frontal Assessment

Battery, MoCA)

•MoCA 18-25 suggestive of mild neurocognitive disorder (NCD), <18 suggestive of major NCD;beware

of many false positives)

•standard “neurocognitive work-up":see Delirium, PS23

•asindicated: VDRL, HIV, LP,CXR, EEG, SPECT, head CT, or MR1

•indications for head imaging:same as for delirium, plus: age <60, rapid onset (unexplained decline

in cognition or function over 1-2 mo), dementia of relatively short duration (<2 yr),recent significant

head trauma, unexplained neurological symptoms(new onset of severe headache/seizures), bleeding

disorder or use of anticoagulants, Hx of cancer,suspicions of normopressure hydrocephalus, and

presence of unsuspected cerebrovascular disease would change management

Management

•see Neurology. N22 for further management

•treat underlying medical problems and prevent new ones (e.g. treatment of hypertension and B I:

deficiency)

•discontinue cognitively impairing medications (e.g. anticholinergic, benzodiazepines, nonbenzodiazepine (“Z-drugs”))

•provide orientation cuesfor patient (e.g. clock, calendar)

•provide education and support for patient and family (e.g. day programs, respite care,support groups,

home care)

•consider power of attorney/living will and long-term care plan (nursing home)

•inform Ministry of Transportation about patient’sinability to drive safely

•consider pharmacological therapy

•to slow AD:

cholinesterase inhibitors (donepezil (Aricept*, 5-10 mg once daily), rivastigmine, galantamine)

for mild to severe disease

NMDA receptor antagonist (memantine 5 mg once daily to 10 mg BID) for moderate to severe

disease

•to manage AD:

low-dose atypical antipsychoticssuch as olanzapine (2.5-10 mg/d), quetiapine (25-200 mg/d), or

risperidone (0.25-3 mg/d) for severe behavioural disturbances

trazodone (25-100 mg) can be used for night-time agitation

The "Mini Cog” Rapid Assessment

3word immediate recall

Clock drawn to “10 past 11“

3word delayed recall

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PS26 Psychiatry Toronto Notes 2023

• to treat comorbid psychiatric conditions:

• antidepressantssuch as escitalopram can be used for depressive episodes

•

“start low and go slow"

(effective doses can be 1/3 to 1 /2 that of regular adult age patients);

reassess pharmacological therapy every 3 mo

Table 3. Comparison of Dementia,Delirium, and Cognitive Impairment Associated with

Depression

Dementia/Major

Neurocognitive Disorder

Delirium Cognitive Impairment

Associated with Depression Most Common Causes of Dementia

• Alzheimer's disease (up to 50-

60%):predominantly memory and

learning issues,insidious onset/

gradual progression

• Frontotemporal degeneration

(5%):language type (early

preservation),behavioural type

(apathy/disinhibition/self-neglect):

more common among those with

dementia that has onset before age

65; progressive

• Lewy body disease (up to 25%);

early changes in executive and

attention,may fluctuate, well-formed

visual hallucinations (e.g.rabbits),

autonomic impairment (falls,

hypotension).Parkinson's type

EPS that does not respond well to

pharmacotherapy and follows >1yr

after cognitive decline,fluctuating

degree of cognitive impairment,

sleep disturbances

• Vascular disease (15-30%);vascular

risk factors,focal neurological signs,

abrupt onset,stepwise progression,

executive dysfunction > memory

impairment personality and mood

changes (loss of motivation)

. Normal pressure hydrocephalus:

abnormal gait (“magnetic gait”),early

incontinence,rapidly progressive;

dilated ventricles on imaging

6rar)ual.'step-wise decline

Mcrntfis-years

Progressive

Usually irreversible

Normal

Acute (usually hours to days) Subacute

Days-weeks

Fluctuating,reversible,high Recurrent

morbidity,

'

mortality in the elderly Partially reversible

Fluctuatingbetween hyperactive Normal

(agitation) andhypoactive (stupor)

(over 24h)

Impaired Iwandering, easy Difficulty concentrating

distraction)

Impaired (usually to fame and Intact

place),fluctuates

Onset

Duration

Natural History

Variable

Level of Consciousness

Attention Not initially affected

Orientation Intact initially

Behaviour Oismhibition.impairment in ADU

IADI,personality change,loss ol

social graces

Normal

Fragmented sleep at night

labile,anxiety or depression are

commonin the early stages

Decreased executive functioning,

paucity of thought

Recent eventually remote

Typically,lowinsight

Agnosia,aphasia,decreased

comprehension,repetition,

speech (echolalia.palilalia)

Compensatory

Variable

Potential for agitation/retardation Arnedonia.decreased increased

(even severe) sleep,'eating,agitation:

retardation

Slowing or agitation

Early morning awakening

Depressed.pervasive

Psychomotor

Sleep Wake Cycle

Mood andAffect

Fluctuates between extremes

Disturbed sleep wake cycle

Anxious,irritable, fluctuating or

apathetic, withdrawn

Cognition Fluctuating May appear tobe impaired/slowed

Marked recent Recent

More likely to complain

Not affected

Memory Loss

Dysnomia.dysgraphia.speech

rambling,irrelevant,incoherent,

subject changes

Nightmarish and poorly formed

Visual common

Language

Delusions Nihilistic,somatic

Less common:rf present auditory

predominates

Self-deprecatory

Rule out systemic illness,

medications

Hallucinations

Vacuous,bland Frightening,

'

bizarre

Acute illness,drug toxicity

Ouality of Hallucinations

Medical Status Variable

Substance-Related and Addictive Disorders

Overview

• substance use disorder (SUD): a neurobiological disorder involving compulsive drug seeking and drug

taking,despite adverse consequences, with loss of control over drug use (think issues with the “3Cs”:

compulsive,consequences,control)

• it is possible to have a substance use disorder without physiological dependence (i.e.withdrawal

syndrome or tolerance);dependence is the hallmark ofsubstance use disorders and comesin the

following forms:

behavioural:substance-seeking activities and pathological use patterns

physical:physiologic withdrawal effects without use or tolerance

• cognitive:continuous or intermittent cravings for the substance to avoid dysphoria or to attain

the desired effects of the substance

• drug misuse:drug use that deviatesfrom the approved social or medical pattern, usually causing

impairment or disruption to function in self or others

• these disorders are usually chronic with a relapsing and remitting course

• there are 10 separate classes ofsubstances identified in the DSM-5:alcohol; caffeine; cannabis

hallucinogens ( PCP orsimilarly acting arylcyclohexylamines,and other hallucinogens);inhalants;

opioids;sedatives, hypnotics,and anxiolytics (alcohol included);stimulants (amphetamine-tvpe

substances, cocaine, and otherstimulants); tobacco; and other (or unknown) substances

• whereassubstance use disorders imply addiction to substances, addictive disorders include process

(behavioural) addictionssuch as gambling

Epidemiology

• the lifetime prevalence of SUD in Canada is 21.6% lifetime and 10.1% for the last 12 mo;for alcohol use

disorder it is 18.1% and 3.2%;for cannabis use disorder 6.8% and 1.3% and for othersubstances, 4.0%

and 0.7%,respectively (data before the legalization of cannabis use in Canada)

• 47% of those with substance use disorder have mental health problems

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PS27 Psychiatry Toronto Notes 2023

29% of those with a mental health disorder have a substance use disorder

• 47% of those with schizophrenia and 25% of those with an anxiety disorder have a substance use

disorder

Etiology

almost all drugs (and activities) related to dependence, directly or indirectly increase dopamine

release from the ventral tegmental neuronssynapsing onto the nucleus accumbens(known asthe

brain’

s

‘

reward pathway’), an action that contributes to their rewarding properties;with repeated

use,the)'can modulate signaling pathways w'hich further encourages their use,contributing to their

addictive potential

• substance use disorders arise from multifactorial interactions between genetic (neurobiology),

individual (psychological),and environmental factors (low socioeconomic status, peer influence,

adverse childhood or traumatic experiences,social isolation,systemic racism, and chronic stress)

• certain comorbid conditions may also predispose individualsto a substance use disorder (e.g.mental

illness, chronic disease, acute and chronic pain)

• environmental factors play a significant role in the exposure to the substance. For instance, the over

prescription of opioids for pain in North America played a major role in the development of the opioid

use disorder crisis

Diagnosis

• each specific substance is addressed as a separate use disorder and diagnosed utilizing the same

overarching criteria (e.g. a single patient may have moderate alcohol use disorder, and a mild

stimulant use disorder)

• testing for illicit drugsis most commonly done on urine or blood samples

serum toxicology screen measures recent alcohol consumption but has no relation to the

diagnosis of alcohol use disorder

toxicology may be helpful in differentiating withdrawal from other mental disorders

urine drug screens are useful for detecting recent drug use, but not for diagnosing substance use

disorders

• substance use disorders are measured on a continuum front mild to severe based on the number of

criteria met within 12 mo

mild:2-3

moderate:4-5

severe:6 or more

• criteria forsubstance use disorders (PEC WITH MCAT)

use despite Physical or psychological problem (e.g.alcoholic liver disease or cocaine related nasal

problems)

failure to fulfill External roles at work/school/home

Craving or a strong desire to use substance

Withdrawal

continued use despite Interpersonal problems

Tolerance: needing to use more substance to get same effect

• use in physically Hazardoussituations

More substance used or for longer period than intended

unsuccessful attempts toCut down

Activities given up due to substance

excessive Time spent on using or finding substance

Questions to Characterize Substance

Use and Risk Assessment (THE WATER)

• When was the last Time you used?

. How long can you go without using?

• Have you Experienced medical or

legal consequences of your use?

• Any previous attempts to cut down

or quit,and did you experience any

Withdrawal symptoms?

. How has your substance use Affected

your work,school,relationships?

. Are there any Triggers that you know

will cause you to use?

. Substances can be very Expensive,

how do you support your druguse?

• By what Route (oral ingestion,

inhalation (snorting),smoking.IV) do

you usually use?

Table 4. Substance Symptomatology

Drugs Symptoms of Intoxication Symptoms of Withdrawal

CHS Depressants Euphoria,slurred speech,

disinhibition, confusion, poor

coordination, coma (severe)

Alcohol, opioids, barbiturates,

benzodiazepines,GHB

Anxiety, anhedonia,tremor,

seizures, insomnia, psychosis,

delirium, death

‘Crash’, craving,dysphoria,

agitation, anxiety, psychosis suicidality

(especially paranoia),insomnia,

cardiovascular complications

(stroke. Ml,arrhythmias),seizure

Stimulants Amphetamines, methylphenidate, Euphoria,mania,psychomotor

MDMA, cocaine

LSD, mescaline, psilocybin, PCP, Distortion of sensory

ketamine,ibogaine.salvia

Hallucinogens Usually absent

stimuli and enhancementof

feelings, psychosis (+-• visual

hallucinations), delirium,anxiety

(panic), poor coordination

General Approach to Assessment

• a comprehensive evaluation should inquire about drug history including names ofsubstances used,

amount, frequency,duration, routes,last use, injection drug use, needle sharing,symptoms of

withdrawal, consequences of use (medical,social, or personal), previous treatment programs and

medical (e.g. HIV'

, hepatitis B and C, chronic pain), psychiatric (e.g. mood and anxiety disorders), and

social history (e.g.family and housing arrangements, any child safety concerns)

• ask about more socially accepted substances(e.g. nicotine, alcohol) before asking about use of

cannabis, misuse of prescription medicines, and about illicit drugs

• obtaining collateral history is recommended as well as evaluating patient insight into the problem

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PS28 Psychiatry Toronto Notes 2023

Lab Testing

• urine,saliva,sweat,and hair can be tested for the presence of drugs

• urine is most commonly used due to ease of collection and adequate sensitivity and specificity, but it

does not reflectserum concentrations

• proper urine drug testing involves an initial screening test (qualitative) followed by confirmatory

testing forsubstances with positive screening results

• most confirmatory tests use gas or high-performance liquid chromatography

• post-ingestion window of detection with urine test:amphetamine (48 h),barbiturates (1-21 d),shortacting benzodiazepine (72 h), long-acting benzodiazepine (30 d), cocaine (12-72 h), morphine (48-72

h), methadone (72 h), oxycodone (2-4 d), PCP (8 d),cannabis(3d for single use to >30 d for heavy

users)

• limitations: negative tests cannot rule out substance use, and positive results cannot determine how

much or frequency of use

General Approach to Treatment

• approach must be appropriate to the patient’s current state of change (see Public Health and

Preventive Medicine, Health Promotion Strategies,PH11)

• patients will change when the pain of change appearsless than the pain ofstaving the same

• provider can help by providing psychoeducation (emphasize neurobiologic model of addiction),

motivation, and hope

• principles of motivational interviewing (see Psychotherapy, PS-19)

non-judgmental stance

space for patient to talk and reflect

offer accurate empathic reflections back to patient to help frame issue

• encourage and offer referral to evidence based services

social:12-step programs(alcoholics anonymous, narcotics anonymous),family education, and

support

• psychological therapy: addiction counselling,MET,CBT,contingency management, group

therapy,family'therapy, marital counselling

medical management (differs depending on substance):acute detoxification,pharmacologic

agents to aid maintenance. Ontario has the RAAM- Rapid Access to Addiction Medicine clinics

that offer timely,low barrier,specialized services by self-referral

• harm reduction whenever possible:safe-sex practices,avoid driving while intoxicated, avoid

substances with child care,safe needle practices/exchange, pill-testing kits,reducing tobacco use

• comorbid psychiatric conditions:many will resolve with successful treatment of the substance use

disorder but patients who meet full criteria for another disordershould be treated for that disorder

with psychological and pharmacologic therapies

• always consider duty to inform Ministry of Transportation for risk of driving or operating other

vehicles

Nicotine

• see l amilv Medicine. FMI3

Confabulations:the fabrication of

imaginary experiencesto compensate

for memory loss

Alcohol

•see f

amily Medicine, FM15 and Emergency Medicine. ER34

it

History

•Validated screening questionnaire for alcohol use disorders

C ever felt the need to Cut down on your drinking?

A ever felt Annoyed at criticism of your drinking?

G ever feel Guilty about your drinking?

E ever need a drink first thing in the morning (Eye opener)?

for men,a score of >2 is a positive screen;for women, a score of >1 is a positive screen

• if positive CAGE, then assess further to distinguish between problem drinking and alcohol

use disorder

Make sure toask about other alcohols:

mouthwash,rubbing alcohol,methanol,

ethylene glycol aftershave (may be used

as a cheaper alternative)

A "Standard Drink"(SD)

Spirit (40%);1.5 oz.Of 43 ml

Table Wine (12%):5oz.or 142 ml

Fortified Wine (18%):3oz.or 85 ml

Regular Beer (5%):12 oz.or 341 mL

Canada's Low-Risk Alcohol Drinking Guidelines

Moderate Drinking OR

1pint of beer -1.5 SO

1bottle of wine*5SD

1"mickey" “

8SD (375mL)

-2&er-"17 SD (750 mL)

“40 OZ.--27S0

Men:3or less'd (slSfrark) Women:2 or less/d (slO/wk) Elderly:1or less/d r ~t

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Biochemical Markers of Prolonged Alcohol Use

• elevated liver function tests (AST, ALT,GGT), MCV, and carbohydrate-deficient transferrin (CDT)

• ASTrALT ratio>2:1 and elevated GGT are suggestive of alcohol use

Alcohol Intoxication

• throughout Canada, the legal limit for impaired driving is a BAC >0.08% (>80 mg/dL or 17.4 mmol/L)

which istypically reached after 4 drinks in women and 5drinksin men in a 2 h period

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PS29 Psychiatry Toronto N'otcs 2023

•most signs of intoxication are present at over >21.7 mmol/L (100 mg/dL): altered perception, impaired

judgement, ataxia, hyper-reflexia, impaired coordination, changes in mood/personality, prolonged

reaction time, and slurred speech

* respiratory depression and arrest can occur with >60 mmol/L (non-tolerant drinkers) and 90-120

mmol/L (tolerant drinkers)

Management of Alcohol Intoxication

•stabilize patient if there is reduced level of consciousness or vomiting; assess airways and respiratory

function

•administer IV crystalloid fluids if evidence of volume depiction or shock; correct electrolytes and

hypoglycemia

•monitor for signs of alcohol withdrawal following detoxification in patients with alcohol use disorder

Delirium Tremens

(alcohol withdrawal delirium)

. Autonomic hyperactivity (diaphoresis,

tachycardia, increased respiration)

• Hand tremor

• Insomnia

• Psychomotor agitation

. Anxiety

• Nausea or vomiting

. Tonic-clonic seizures

. Visual/tactile/auditory hallucinations

, Persecutory delusions

Alcohol Withdrawal

•medical emergency:occurs within 12-48 h after prolonged heavy drinking and can be life-threatening

•-50% of middle-class,functional individuals with alcohol use disorder have experienced alcohol

withdrawal;80% in hospitalized/homelessindividuals

alcohol withdrawal can be described as having 4 stages, however not allstages may be

experienced:

stage 1 (onset 4-12 h after last drink): “the shakes" tremor, sweating, agitation, anorexia,

cramps, diarrhea,sleep disturbance, anxiety, insomnia, headache.The majority of alcohol

withdrawal presentations are mild to moderate (stage I )

stage 2 (onset 12-24 h): alcoholic hallucinosis: visual, auditory, olfactory, or tactile

hallucinations

stage 3 (onset 12-48 h): alcohol withdrawal seizures, usually tonic-clonic, non-focal, and brief

(can occur as early as 2 h after alcohol consumption)

stage 4 (onset 48-96 h):delirium tremens, conftision/disorientation,delusions,hallucinations,

agitation,tremors,autonomic hyperactivity (diaphoresis,fever, tachycardia, HTN)

•course:almost completely reversible in young; elderly often left with cognitive deficits

•20% mortality rate ofsevere presentations (delirium tremens) if untreated

Management of Alcohol Withdrawal

•monitor using the Clinical Institute Withdrawal Assessment for Alcohol (ClWA-A)scoring system

• areas of assessment include (SHAN'

T AS TAV):

physical (5): paroxysmal Sweats, Headache/fullness in head. Agitation, Nausea and vomiting,

Tremor

psychological/cognitive (2): Anxiety, orientation/clouding of Sensorium

perceptual (3):Tactile disturbances, Auditory disturbances, Visual disturbances

all categories are scored from 0-7 (except:orientation/sensorium 0-4), maximum score of 67

mild <10, moderate 10-20,severe >20

•check for signs of hepatic failure (e.g. ascites, jaundice, and coagulopathy)

Table 5. CIWA-A Scale Treatment Protocol for Alcohol Withdrawal

Diazepam 20 mg PO ql

-2 h PRM until CIWA-A <10 points

Observe1-2 h after last dose and re-assess on CIWA-A scale

Thiamine100- 250 mg IM then 100 mg P0 once dally (or 3d.folk acid

Supportive care (hydration, nutrition, andelectrolyte replacement)

Diazepam 20 mg P0 ql h for minimum of three doses regardless of subsequent CIWA scores

Basic protocol

History of withdrawalseizures

Itage >65or patient hassevere liver disease, Use a short acting benzodiazepine

severe asthma or respiratory failure Lorazepam1-4 mg P0/5UIM q1-2 h

Haloperidol 2-5 mg IM/P0q1-4 h - max 5 doses/d or atypical antipsychotics(olanzapine,

risperidone)

Diazepam 20 mg x 3dosesasseizure prophylaxis (haloperidol lowersseizure threshold)

Still In withdrawal alter >80 mg of diazepam

Delirium tremens, recurrentarrhythmias.or multiple seizures

Medically ill or unsafe to discharge home

If hallucinations are present

Admit to hospital if

Wernicke-Korsakoff Syndrome

• alcohol-induced amnestic disorders due to thiamine deficiency (poor nutrition or malabsorption)

• necrotic lesions:mammillary bodies,thalamus, brainstem

• Wernicke’s encephalopathy (acute and reversible): triad of oculomotor dysfunction such as nystagmus

(CN VI palsy (eye pointing inwards)), gait ataxia, and confusion.If untreated, may progress to

Korsakoff’s syndrome

• Korsakoff'

s syndrome (chronic and only 20% reversible with treatment):anterograde amnesia and

compensatory confabulation; cannot occur only during an acute delirium or dementia and must

persist beyond usual duration of intoxication/withdrawal

• management

Wernicke’s preventative treatment (any patient in withdrawal):thiamine 100-250 mg IM/1V x 1

dose

Wernicke’s acute treatment:thiamine 500 mg IV BID/T1D x 72 h, then reassess

Korsakoff’

s:IV treatment asfor Wernicke’

sfollowed by thiamine 100 mg PO T1D x 3-12 mo

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PS30 Psychiatry Toronto Notes 2023

Treatment of Alcohol Use Disorder

• non-pharmacological

see General Approach to Treatment,PS28

• pharmacological

» naltrexone (Revia*):opioid antagonist,shown to be successful in reducing the “high” associated

with alcohol,moderately effective in reducing cravings,frequency or intensity of alcohol binges;

can be started ifstill consuming alcohol or abstinent but can precipitate withdrawal in those with

physical opioid dependence

acamprosate (Campral*):NMDA glutamate receptor antagonist; useful in maintaining abstinence

and decreasing cravings

disulfiram (Antabuse*):prevents oxidation of alcohol (blocks acetaldehyde dehydrogenase)

and causes an adverse reaction to alcohol (nausea/vomiting, tachycardia,shortness of breath,

headache); if patient relapses, must wait 48 h before restarting Antabuse*; prescribed only when

treatment goal is abstinence; RCT evidence is generally poor or negative due to poor medication

adherence; contraindicated in severe renal disease, pregnancy, psychoses, and cardiac disease

some evidence for the use of gabapentin, topiramate, and ondansetron as anti-craving agents, but

not approved by Health Canada approved for this indication (currently under investigation)

Opioids

•types of opioids:heroin, morphine,oxycodone, Tylenol #3* (codeine), hydromorphone,fentanyl,

methadone,meperidine (Demerol*)

•in addition to working on opiate receptors, opiates also act on the dopaminergic system, which

mediates their addictive properties

•most commonly used are: Percocet* (oxycodone/acetaminophen), Vicodin* (hydrocodone/

acetaminophen), and OxyContin* (oxycodone)

•major risks associated with the use of contaminated needles:increased risk of hepatitis B and C,

bacterial endocarditis, and H1V/A1DS

•recent considerations of inadvertent overdose secondary to contamination with fentanyl in the drug

supply “opioid crisis"

leading to 9000 deaths in Canada between January 2016 and June 2018

Opioid Antagonists

Naltrexone vs. Naloxone

Naltrexone (Revia:

)

• Can be used for EtOH dependence

(although not routinely used)

. Long half-life (>1h)

Naloxone (Narcan )

. Used for life-threatening CNS/

respiratory depression in opioid

overdose

. Short half-life(<1h)

• Very fast acting (min)

• High affinity for opioid receptor

• Induces opioid withdrawal symptoms

Acute Intoxication

•direct effect on receptors in CNS resulting in decreased pain perception,sedation, decreased sex drive,

nausea/vomiting,decreased G1 motility (constipation and anorexia), pupil constriction (e.g. pinpoint

pupils; exception is meperidine), and respiratory depression (can be fatal)

•medical emergency: typical syndrome includesshallow respirations, miosis, bradycardia,

hypothermia, decreased level of consciousness

•management

- ABCs

IV glucose

naloxone hydrochloride (Narcan*): 0.4 mg up to 2 mg IV for diagnosis

treatment:intubation and mechanical ventilation, ± naloxone drip, until patient alert without

naloxone (up to >48 h with long-acting opioids)

•caution:opioids have a longer half-life than naloxone; may need to observe for toxic reaction for at

least 2:24 h

Maintenance Medication foi Opiate Addiction:

The Foundation of Recovery

J Add ct Ois 2012;31:207-225

Maintenance treatment of opioid addiction with

methadone or buprenorptineis associated with

retention in treatment,reduction in illicitopiate use.

decreased craving,and improved socialfunction.

Recently,stridesshowing extended release

naltrexone injections have showed some promise.

Withdrawal

•symptoms: dysphoric mood, insomnia, drug-craving, myalgias, nausea or vomiting, yawning, chills,

lacrimation, rhinorrhea, pupillary dilation, piloerection,sweating, diarrhea, fever; withdrawal

symptoms can be severe but are not life threatening

•onset:6-12 h (depending on half-life of opioid used);duration: 5-10 d

•complications:loss of tolerance (overdose on relapse), miscarriage, premature labour

•management:long-acting oral opioids (methadone, buprenorphine), a-adrenergic agonists (donidine

for symptomatic management of autonomic signs and symptoms of withdrawal)

•monitor withdrawal severity usingClinical Opioid Withdrawal Scale (COWS)

Classic Opioid Overdose Triad (RAM)

Respiratory Depression

Altered Mental Status

Miosis

Treatment of Opioid Use Disorder

•see General Approach to Treatment,RS28

•long-term treatment may include maintenance treatment with methadone (opioid agonist) or

buprenorphine (mixed agonist-antagonist)

•caution:methadone can cause Q'

l

'

c interval prolongation,screening ECG recommended

.Suboxone* formulation includes naloxone in addition to buprenorphine, in an effort to prevent

injection of the drug. When naloxone is injected, it will precipitate opiate withdrawal and block

the opiate effect of buprenorphine. However, it will not have this antagonist action when taken

sublingually

•decreasing risk of overdose: patients with a history of opiate use, and/or friends, family members

and co-workers working with people using opiates should be encouraged to carry a naloxone kit and

educated on ways to limit overdose risk (i.e. use with a friend, avoid mixing drugs). It is a life-saving

strategy

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PS31 Psychiatry Toronto Notes 2023

Cocaine

•street names: blow,C,coke, crack,flake,freebase, rock,snow

•alkaloid extracted from leaves of the coca plant; blocks presynaptic uptake of serotonin (causing

euphoria),dopamine (linked to its addictive effect), norepinephrine and epinephrine (causing

vasospasm, H'

l

'N)

•sodium channel blockade: cocaine slows or blocks nerve conduction and acts as a local anesthetic

by altering recovery of neuronal Na '

channels; it has a similar effect on cardiac Na '

channels and in

overdose can manifest on ECO as prolongation of the QRS complex

•self-administered by inhalation/smoking (crack) (90% bioavailability), insufflation (i.e. intranasal;

80% bioavailability), or intravenous route

•onset and duration of action:onset within seconds if inhaled or IV, lasting 15-30 min; onset in 3-5

min if insufflated, blood levels peak at 10-20 min with effects beginning to fade after 45-60 min;

cocaine has a biologic half-life of I h, thus repeated self-administration is common among users to

maintain an effect

Common Presentations of Drug Use

System filings

tcnefil Weight lou(especially nth

chronic use ol cocaine, heroin)

Injected coniunctira (cannabis)

Pinpoint pupils (opioids)

track marks (injection dings)

frariiM

Viral hepatitis(injection drugs)

Uoerplaiied elevations in All

(injection drugs)

Uissed appointments

non-compliance

Orog-seeUng (especially

bemodiaiepiaes.opioids)

insomnia

fatigue

Depression

Flat affect

(benrodiaiepines,

barbiturates)

Paranoia (cocaine)

Psychosis(cocaine,cannabis,

hallucinogens)

Marital discord

Family violence

Work/schODl

Absenteeism and poor

performance

MSK

Cl

letaiioriral

Intoxication

•elation, euphoria, pressured speech, restlessness,sympathetic stimulation (e.g. tachycardia, mydriasis,

sweating, hypertension)

•prolonged use may result in paranoia and psychosis (including tactile hallucinations)

Psychological

Overdose

•medical emergency: H I N,tachycardia, tonic-clonic seizures, dyspnea, hyperthermia, and ventricular

arrhythmias

•the vasoconstrictive effects of cocaine can also result in stroke,Ml, or intracranial hemorrhage

•treatment with IV diazepam to control seizures

•benzodiazepines may also be used for management of moderate agitation and anxiety, whereassevere

agitation may require antipsychotics

•p-blockers (incl.labetalol or propranolol) are not recommended because of risk from unopposed

a-adrenergic stimulation

Social

Withdrawal

•initial “crash” (1-48 h):increased sleep, increased appetite, dysphoria (non-life threatening)

•withdrawal (1-10 wk):dysphoric mood plusfatigue,irritability, vivid unpleasant dreams,insomnia or

hypersomnia, psychomotor agitation or retardation

•complications:relapse,suicide (significant increase in suicide during withdrawal period)

•management:supportive management

Treatment of Cocaine Use Disorder

•see General Approach to Treatment, PS28

•no pharmacologic agents have widespread evidence or acceptance of use (some evidence for off-label

use of topiramate)

•referral to psychological interventions(e.g. relapse prevention) is the mainstay of long-term treatment

Complications

•cardiovascular:arrhythmias, Ml, cerebrovascular accident, ruptured AAA, chest pain (accountsfor

40% of all cocaine-related ED visits)

•neurologic:seizures

•psychiatric: psychosis, delirium,suicidal ideation

•other: nasal septal deterioration, acute/chronic lung injury "crack lung," possible increased risk of

connective tissue disease

Amphetamines

• includes prescription medications for ADHD e.g. Ritalin" and Adderall" and street drugssuch as

crystal meth

• intoxication characterized by euphoria, improved concentration,sympathetic and behavioural

hyperactivity,and at high doses,(.

'

an mimic symptoms of psychosis or mania; can eventually cause

coma

• chronic use can produce psychosis which can resemble schizophrenia with agitation, paranoia,

delusions, and hallucinations

• withdrawal symptoms include dysphoria, fatigue, and restlessness

• treatment of amphetamine induced psychosis: antipsychotics for acute presentation, benzodiazepines

for agitation, p-blockers for tachycardia, H1N

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PS32 Psychiatry Toronto Xotes 2023

Cannabis

Cannabinoid Hyperemesis Syndrome

An interesting and relatively new

clinical phenomenon associated with

chronic cannabis use characterized

by cyclical,recurrent severe nausea,

vomiting,and colicky pain.Possibly due

to increased potency of available TKC

products. Patients often present to ED

in acute distress with no evidence of

specific 61pathology. Many patients will

successfully sclf-medicate with hot baths

or showers

• psychoactive substance: delta-9-tetrahydrocannabinol (A9-THC)

• general clinical manifestations:intoxication characterized by tachycardia, conjunctival vascular

engorgement, dry mouth,altered sensorium, increased appetite, and muscle relaxation

• neuropsychiatric effects:

altered mood, perception, and thought content increased sense of well-being,euphoria/laughter

impaired cognitive and psychomotor performance:reduced reaction time, impaired attention,

concentration, and short-term memory. It may also impair motor coordination required to

complete complex tasks requiring divided attention. Notably, psvchomotor impairments may

interfere with one'

s ability to operate heavy machinery such as automobiles

• inhaled cannabis: onset of psvchoactive effects occurs rapidly with peak effects felt 15-30 min after

intake and lasting up to 4 h

• acute exacerbation in patients with asthma may be a complication with inhalation

• ingested cannabis:following oral ingestion, psychotropic effects set in with a delay of 30-90 min, reach

their maximum after 2-3h and last for about 4-12 h depending on dose

• high doses can cause depersonalization, paranoia, anxiety and may trigger psychosis and

schizophrenia if predisposed

• chronic use is associated with tolerance and an apathetic, amotivational state;may also exacerbate

respiratory problemssuch as asthma and chronic bronchitis

• assessment:standard urine drug screens

• treatment of cannabis use disorder:see General Approach to Treatment, PS28

cessation following heavy use produces a significant withdrawal syndrome:irritability, anxiety,

insomnia, decreased food intake

Evidence Based Medical Usesof

Cannabis

• Chemotherapy-induced nausea and

vomiting

• Spasticity, muscle spasms (multiple

sclerosis, spinal cord injury)

• Chronic pain (neuropathic pain)

Canabis Use and Risk of Psychotic or Arfectiae

Mental Health Outcomes:a SystematicReview

L axet 2007:370:319-28

Purpose To review the evidence lor cansabs.se and

occurrence of psychotic or affectne mental health

outcomes.

Study Characteristics: I meta-ana yss of 3S

sopdatioo-lased longitudinal studies,or casecootolstudies nested within longitudra designs.

Resolts:There was an increased risk of a"y psyctobc

octcone n individuals whu had ever used catrabs

::c:d ad.csted ON.41,95% Chl.20-1.65).

rndngs were consistent with a dose-response effect.

i4greater rrsk d people who used canrabsnox

frequently (209,95% CM.S4-284).fur tegsfor

depression,su c dal thoughts, andannety outcomes

were less consatent.In both cases(psychou a rd

aSectw outcomes), a substantial con‘

ou*

d *

g effect

was present.

Cooctasions: he find igsare consistent with

“e wen that cannabis increases rtsk of psychotic

outcomes independent of transient rntoncatcr

effects,alth ucgfc evidence is lessstrong for

eSectre outcomes.Although canneha use end the

development of psychosis are strongly associated,

it is AScel!to determine causality and it is possbre

fiat the association results from confounding factors

or bias,the authors did conclude that there is

suScwnterdence to warn young people:hat us ng

cannabscould increase their riskofdevtboga

psychotic illness Idler m life.

Hallucinogens

• types of hallucinogens by primary action

• 5-HT2A agonists: LSD, mescaline ( peyote), psilocybin mushrooms, DMT (avahuasca )

• NMDA antagonists:PCP,ketamine

• K-opioid agonists: salvia divinorum, ibogaine

• 5-HT2A agonists are most commonly used;intoxication characterized by tachycardia,HTN,

mydriasis, tremor, hyperpyrexia, and a variety'of perceptual,mood and cognitive changes (rarely',if

ever, deadly; treat vitalssymptomatically)

• psychological effects of high doses:depersonalization, derealization, paranoia,and anxiety (panic

with agoraphobia)

• tolerance develops rapidly ( hours-days) to most hallucinogensso physical dependency is virtually

impossible, although psychological dependency and harmful use patterns can still occur

• no specific withdrawal syndrome characterized but may experience “flashbacks"

• management of acute intoxication:support, reassurance,diminished stimulation;benzodiazepines

(e.g.lorazepam) or high potency antipsychotics (e.g.haloperidol) seldom required (if used, use small

doses), minimize use of restraints

• long term adverse effects:controversial role in triggering psychiatric disorders,particularly mood or

psychosis, thought to be chiefly in individuals with genetic or other risk factors

• Hallucinogen Persisting Perception Disorder:DSM-5diagnosis characterized by long lasting,

spontaneous, intermittent recurrences of visual perceptual changes reminiscent of those experienced

with hallucinogen exposure

Canabis Use and Psychosis:a Review of Reviews

hrimPsychiatry Clin Neurosci 2019:10.100?.

s 00406-019-01068-1

Purpose lo review theevidence eo carrabs use a:d

se development of psychosis

Methods 1'

isstudy included systematic renews

rd meta- analyses published after 2006.Sidesoc

cantabis use end psychosis were included •

ega'

d ess

of use petsilifetime, past year,past moots,

cfe.ly use.intensive use, occasional ase) andtype

of psychosis(acute psychosis,psychotic tso-drs.

schiaophreuia).

Resalts: 26 systematic rev.ews and meta-analyses

ret inclusion criteria,i dose dependertretatoisnip

was uleotfied between cannabis use and the

development of psychotic illness.Cannabs users also

sad eeriersymptom onset,increased release rate,

more hospitalization,and more posit ve symptoms

compared to non-users.

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PS33 Psychiatry Toronto Notes 2023

“Club Drugs”

Date Rape Drugs

• GHB

. Flumtrarepam (Rohypnol'

)

• Ketamine (sometimes used as it is

tasteless and odourless)

Table 6. The Mechanism and Effects of Common “Club Drugs”

Drug Mechanism Effect Adverse Effects

MDMA

("Ecstasy".“XVEVM",

“Molly")

Acts on serotonergic and

dopaminergic pathways,

properties ola hallucinogen and

stimulant

Enhanced sensorium:feelings ol

well-being,empathy

Diaphoresis,tachycardia,fatigue,

muscle spasms (especially jaw

clenching),ataiia.hyperthermia,

arrhythmias.DIC.rhabdomyolysis.

renal failure,seizures,death

Diaphoresis,tachycardia,fatigue,

muscle spasms (especially jaw

clenching),ataiia

Severe withdrawal from abrupt

cessation of high doses results in

tremor,seizures,psychosis

CNS depression with EtOH

Formication

Tactile hallucination that insects or

snakes are crawling over or under the

skin (especially associated with crystal

meth use but also observed among

some cocaine and PCP users)

Gamma Hydroxybutyrate (GHB. Biphasic dopamine response

“G”,"Liquid Ecstasy")

Euphoric effects,increased

(inhibition then release) and aggression,impaired judgment

releases opiate-like substance

Flunitrazepam

(Rohypnol r

,“Roofies"."Rope", absorption

“The ForgetPill")

Ketamine

("Special K"."Kit-Kat")

Potent benzodiazepine,rapid oral Sedation,psychomotor

impairment,amnestic effects,

decreased sexual inhibition

"Dissociative"state,profound Psychological distress,accidents

amnesiai'analgesia.hallucinations due to intensity of experience and

and sympathomimetic effects lack of bodily control

In overdose:decreased LOC.

respiratory depression,catatonia

Short-term use:high agitation,

rage,violent behaviour,

occasionally hyperthermia and

convulsions

Long-term use:addiction,anxiety,

confusion,insomnia,paranoia,

auditory and tactile hallucinations

(especially formication),

delusions,mood disturbance,

suicidal andhomicidal thoughts,

stroke

May be contaminated with lead,

andIV users may present with

acute leadpoisoning

Amnestic,euphoric,hallucinatory Horizontal/vertical nystagmus,

myoclonus,ataiia.autonomic

instability (treat with diazepam

IV).prolonged agitated psychosis

(treat withhaloperidol)

High-risk for suicide:violence

towards others

High dose can cause coma

Emerging Medical Uses of

Hallucinogens

Many hallucinogens are currently under

investigation for therapeutic benefit

LSD & psilocybin for end of life anxiety.

MDMA for PTSD.ketamine for rapid

treatment of depression,ibogaine

derivatives for addiction

NMDA receptor antagonist,rapidacting general anesthetic usedin

paediatrics and by veterinarians

Rush begins in min.effects

last 6-8 h.increased activity,

decreased appetite,general

sense of well-being,tolerance

occurs quickly,users often binge

and crash

Methamphetamine

("speed”

,

“meth",

“chalk”,

“ice”.“crystal”)

Amphetamine stimulant,induces

norepinephrine,dopamine,and

serotonin release

Malingering:intentional production of

false or grossly exaggerated physical

or psychological symptoms,motivated

by secondary gain- externalreward

(e.g.avoiding work,obtaining financial

compensation,or obtaining drugs)

Factitious Disorder intentional

production or feigning of physical or

psychological signs or symptoms.Unlike

malingering,patients are not motivated

by secondary gain but rather may seek

sympathy,nurturance.and attention

Not understood.used by

veterinarians toimmobilize large

animals

Phencyclidine

(

“

PCP”

,“angel dust") state

Somatic Symptom and Related Disorders

General Characteristics

• physicalsigns and symptomslacking objective medical support in the presence of psychological

factors that are judged to be important in the initiation, exacerbation, or maintenance of the

disturbance (suffering is out of keeping with what would be normally expected)

• cause significant distress or impairment in functioning

• symptoms are produced unconsciously and are not the result of malingering or factitious disorder,

which are disorders of voluntary presentation of symptoms (or intentionally inducing, e.g. injecting

feces) for secondary gain

• primary gain:somatic symptom represents a symbolic resolution of an unconscious psychological

conflict;serves to reduce anxiety and conflict with no external incentive

• secondary gain: the sick role; external benefits obtained, or unpleasant duties avoided (e.g. work)

• theories for root cause: may represent a masked presentation of a psychiatric issue, amplified

perception;social/cultural norms that devalue psychological suffering;lack of ability/language to

express distress in a non-somatic way

Management of Somatic Symptom and Related Disorders

• brief, regular scheduled visits with CiP to facilitate therapeutic relationship and help patient feel

supported (e.g. q4-6 wk)

• good, clear communication among all involved care providers

• limit number of physicians involved in care, minimize medical investigations, coordinate necessary

investigations

• emphasis on mechanism of the symptoms and not on the cause while focusing on what the patient can

change and control; the psychosocial coping skills, not their physicalsymptoms (functional recovery

> explanation ofsymptoms)

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PS3I Psychiatry Toronto Notes 2023

• focus on functional improvement (physiotherapy, occupational therapy) and provide psychoeducation

to validate suffering in the face of medically unexplained symptoms

• psychotherapy:CBT,psychodynamic therapy, mindfulnessinterventions, biofeedback

• minimize psychotropic drugs:anxiolyticsforshort-term use only (associated with worse outcomes),

antidepressantsfor comorbid depression and anxiety

Somatic Symptom Disorder

DSM-5 DIAGNOSTIC CRITERIA FOR SOMATIC SYMPTOM DISORDER

Reprinted withpermissionIrom theDiagnostic andStatistical Manual of Mental Disorders.Sth ed.2013.American Psychiatric Association

A.one or more somatic symptomsthat are distressing or result in significant disruption of daily life

B.excessive thoughts,feelings,or behaviours related to the somatic symptoms or associated health

concerns as manifested by at least one of the following:

1. disproportionate and persistent thoughts about the seriousness of one’

ssymptoms

2. persistently high level of anxiety about health orsymptoms

3. excessive time and energy devoted to these symptoms or health concerns

although any one somatic symptom may not be continuously present, the state of being symptomatic

is persistent (typically >6 mo)

• somatic symptom disorder with predominant pain (previously pain disorder) for those whose

somatic symptom is primarily pain

• patients have physicalsymptoms and believe these symptoms represent the manifestation of a serious

illness

• persistent belief despite negative medical investigations and may develop differentsymptoms over

time

• lifetime prevalence may be around 5-7% in the general adult population

• females tend to report more somatic symptoms than males do; cultural factors may influence sex ratio

• other risk factors include: history of sexual abuse, lower education and socioeconomic status, and

concurrent psychiatric/chronic physical illnesses

• complications: anxiety and depression commonly comorbid (up to 80%), unnecessary medications, or

surgery

• often a misdiagnosis for an insidious illness,so rule out all organic illnesses(e.g.multiple sclerosis)

• DDx:GAD, depressive disorder, delusional disorder, body dysmorphic disorder, obsessive compulsive

disorder, other medical condition

Illness Anxiety Disorder

• preoccupation with fear of having,or the idea that one has a serious disease to the point of causing

significant impairment

• convictions persist despite negative investigations and medical reassurance; however, able to

acknowledge the possibility that feared disease is not present, unlike a delusion,which isfixed and

firm

• somatic symptoms are mild or not present (not acute)

• there is a high level of anxiety about health and the individual is easily alarmed about personal health

status

• person engages in maladaptive behaviour such as excessive physical checking or total healthcare

avoidance

• duration is 26 mo; onset in 3rd-4th decade of life

• epidemiology: 3-5% of patients seen by primary care physicians; increased risk ofsubstance use

problems

• possible role for SSRls astreatment due to generally high level of anxiety

• specifiers:care-seeking type or care-avoidant type

Conversion Disorder (Functional Neurological Symptom

Disorder)

• one or more symptoms or deficits affecting voluntary motor or sensory function that mimic

a neurological or OMC (e.g.impaired coordination,local paralysis, double vision,seizures, or

convulsions)

• does not need to be preceded by a psychological event as per previous DSM criteria;however this

isstill worth exploring as many patients will present after such an event or are related to a medical

diagnosis in a first-degree relative

• incidence of 2-5 in 100000 in general population; up to 20-25% of neurology inpatients and 5% of

psychiatry inpatients

• more common in rural populations and in individuals with little medical knowledge

• spontaneous remission in 95% of acute cases, 50% of chronic cases (>6 mo)

• incompatible findings detected from specific neurological testing can help differentiate between

functional and neurological origin (e.g. Hoover'

ssign and dermatome testing)

• for more details about Conversion Disorder, please consult the DSM-5

Screening questions for somatic

disorders

1. When did the symptoms start?

2.Have you been frustrated with getting

no answers?

3. What has been your experience with

other physicians?

4. What is your understanding of your

symptoms?

5. How have the symptoms affected your

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PS35 Psychiatry Toronto Notes 2023

Table 7. Differential of Somatic Symptom and Related Disorders

Somatic Symptom Illness Anxiety

Disorder

Conversion

Disorder

Factitious

Disorder

Malingering

La belle Indifference: an

inappropriately cavalier patient attitude

in the face of serious symptoms:

classically associated with conversion

disorder but is not diagnostic

Disorder

Somatic Symptoms Present Neurologic, voluntary Psychological or

motor or sensory physical

Unconsciously Consciously

Incompatible Possible, attempts

lo falsify

Psychological or

physical

Consciously

Possible,atlempts

to falsify

Mild or absent

SymptomsProduced Unconsciously

Physical Findings Absent

Unconsciously

Absent Hoover'ssign: involuntary extension of

the “normal" leg occurs when flexing the

contralateral leg against resistance

Dissociative Disorders

General Characteristics

• severe dissociation resulting in breakdoivn of integrated functions of consciousness and perception of

self

• severe stressor traumas are predisposing factorsfor dissociative disorders(e.g.survivors ofsignificant

or chronic trauma, child abuse)

• result in significant distress or impairment in social/occupational functioning

• psychotherapy (psychodynamic,CUT) are the mainstays of treatment; lack ofevidence for use of

medications

• DDx: P'

l