Psychiatry Flashcards

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1
Q

What is the DSM-5 criteria for OCD?

A

Experiencing obsessions and/or compulsions that are time-consuming (e.g., >1 hr/day) or cause significant distress or dysfunction.

Not caused by the direct effects of a substance, another mental illness, or another medical condition.

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2
Q

What are obsessions?

A

Recurrent, intrusive, anxiety-provoking thoughts, images, or urges that the patient attempts to suppress, ignore, or neutralize by some other thought or action (i.e., by performing a compulsion).

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3
Q

What are compulsions?

A

Repetitive behaviors or mental acts the patient feels driven to perform in response to an obsession, or a rule aimed at stress reduction or disaster prevention. The behaviors are excessive and/or not realistically connected to what they are meant to prevent.

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4
Q

What is PANDAS?

A

Pediatric autoimmune neuropsychiatric disorder associated with group A strep. Produces antibodies that damage caudate. These infections in kids can lead to severe OCD overnight!

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5
Q

What are the risk factors for OCD?

A

o Genetic: neurological dysfunction, family history
o Environmental: adverse childhood experiences (i.e. abuse, behavioural inhibition), exposure to traumatic events, group A streptococcal infection

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6
Q

What is the etiology of OCD?

A

o Significant genetic component: Higher rates of OCD in first-degree relatives and monozygotic twins than in the general population. Higher rate of OCD in first-degree relatives with Tourette’s disorder.
o Elevated CSF glutamate in OCD

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7
Q

1st line treatment for OCD?

A

CBT: exposure and response prevention (tolerate, don’t avoid and don’t use avoidance strategies)

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8
Q

Medical treatment for OCD?

A

o SSRIs: fluoxetine, fluvoxamine, sertraline; faster titration! Wait longer (8-12 weeks at therapeutic doses). Benzos – use early then taper – cover temporary worsening of anxiety.
▪ Step 1: SSR1 (2-3 types if necessary)
▪ Step 2: trial of clomipramine >250mg.
▪ Step 3: add antipsychotic (risperidone, aripiprazole, etc.), esp. if co-morbid tics.

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9
Q

What is the DSM-5 criteria for dysmorphic disorder?

A

o Preoccupation with one or more perceived defects or flaws in physical appearance that are not observable by or appear slight to others.
o In response to the appearance concerns, repetitive behaviors (e.g., skin picking, excessive grooming) or mental acts (e.g., comparing appearance to others) are performed.
o Preoccupation causes significant distress or impairment in functioning.
o Appearance preoccupation is not better accounted for by concerns with body fat/weight in an eating disorder.

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10
Q

Treatment for dysmorphic disorder?

A

SSRIs and/or CBT may reduce the obsessive and compulsive symptoms in many patients.

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11
Q

What is the DSM-5 criteria for hoarding disorder?

A

o Persistent difficulty discarding possessions, regardless of value.
o Difficulty is due to need to save the items and distress associated with discarding them.
o Results in accumulation of possessions that congest/clutter living areas and compromise use.
o Hoarding causes clinically significant distress or impairment in social, occupational, or other areas of functioning.
o Hoarding is not attributable to another medical condition or another mental disorder.

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12
Q

Treatment for hoarding disorder?

A
  • Very difficult to treat.
  • Specialized CBT for hoarding.
  • SSRIs can be used.
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13
Q

What is the DSM-5 criteria for trichotillomania?

A
  • Recurrent pulling out of one’s hair, resulting in hair loss.
  • Repeated attempts to decrease or stop hair pulling.
  • Causes significant distress or impairment in daily functioning.
  • Hair pulling or hair loss is not due to another medical condition or psychiatric disorder.
  • Usually involves the scalp, eyebrows, or eyelashes. May include facial, axillary, and pubic hair.
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14
Q

Trichotillomania and excoriation disorder are driven by ____?

A

Impulsions - feeling of anxiety/boredom/tension

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15
Q

What do you need to rule out for trichotillomania?

A

Rule out: Rule out dermatological condition, body dysmorphic disorder

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16
Q

Treatment for trichotillomania?

A
  • Treatment includes SSRIs, bupropion, second-generation antipsychotics, lithium, or N-acetylcysteine.
  • Specialized types of cognitive-behavior therapy (e.g., habit reversal training).
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17
Q

What is the DSM-5 criteria for excoriation disorder?

A
  • Recurrent skin picking resulting in lesions.
  • Repeated attempts to decrease or stop skin picking.
  • Causes significant distress or impairment in daily functioning.
  • Skin picking is not due to a substance, another medical condition, or another psychiatric disorder.
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18
Q

What do you need to rule out for excoriation disorder?

A

Rule out: scabies, substance use (i.e. cocaine), psychotic disorder (delusions, tactile hallucinations), body dysmorphic disorder, stereotypic movement disorder, non-suicidal self-injury

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19
Q

Treatment for excoriation disorder?

A
  • Specialized types of cognitive-behavior therapy (e.g., habit reversal training).
  • SSRIs have shown some benefit.
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20
Q

What should be asked when taking a sleep history

A

BEARS – bedtime, excessive daytime somnolence, awakenings, restlessness(?) , snoring. Duration, meds, concurrent illnesses, mental health!

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21
Q

What are the two sleep-wake disorder groups?

A
  • Dyssomnias

- Parasomnias

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22
Q

DSM-5 criteria of insomnia disorder?

A
  • Complaint of dissatisfaction with sleep quantity or quality – difficulty initiating sleep or maintaining sleep or early-morning awakening with inability to return to sleep
  • Causes significant distress
  • At least 3 nights/week and for at least 3 months
  • There is adequate opportunity for sleep
  • Other medical conditions, sleep-wake disorders or substances can’t explain the cause
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23
Q

Clinical features of insomnia disorder?

A
  • Difficulty initiating sleep (initial or sleep-onset insomnia).
  • Frequent nocturnal awakenings (middle or sleep-maintenance insomnia).
  • Early morning awakenings (late or sleep-offset insomnia).
  • Waking up feeling fatigued and unrefreshed (nonrestorative sleep).
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24
Q

Etiology of insomnia disorder

A
  • Subclinical mood and/or anxiety disorders.
  • Preoccupation with a perceived inability to sleep.
  • Bedtime behavior not conducive to adequate sleep (poor sleep hygiene).
  • Idiopathic
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25
Q

____ is the most common PTSD symptom.

A

Insomnia

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26
Q

What are the diagnoses that fall under dyssomnias?

A
  • Insomnia Disorder
  • Hypersomnolence Disorder
  • Breathing-related sleep disorders
  • Narcolepsy
  • Circadian rhythm sleep-wake disorders
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27
Q

Definition of insomnia disorder?

A

Refers to a number of symptoms that interfere with duration and/or quality of sleep despite adequate opportunity for sleep.

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28
Q

Definition of dyssomnias?

A

Abnormalities in the amount, quality or timing of sleep.

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29
Q

Treatment of insomnia disorder?

A
  • Meds – trazodone (can cause priapism) and zopiclone. As effective as CBT during short periods of treatment (4-8 weeks); insufficient evidence to support long-term efficacy. Mirtazapine (in low doses) is often used to promote sleep in patients with coexisting depressive disorders. Releases norepinephrine and serotonin
  • CBT-I – mostly good sleep hygiene
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30
Q

Side effects of trazodone?

A

Side effects include development of tolerance, addiction, daytime sleepiness, and rebound insomnia.

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31
Q

DSM-5 criteria of hypersomnolence disorder?

A
  1. Self-reported excessive sleepiness despite a main sleep period lasting at least 7 hours, with at least one of the following symptoms:
    - Recurrent periods of sleep or lapses into sleep within the same day.
    - A prolonged main sleep episode of more than 9 hours per day that is nonrestorative (i.e., unrefreshing).
    - Difficulty being fully awake after abrupt awakening.
  2. The hypersomnolence occurs at least three times per week, for at least 3 months.
  3. The hypersomnolence is accompanied by significant distress
  4. Other medical conditions, sleep-wake disorders or substances can explain the cause
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32
Q

Etiology of hypersomnolence disorder?

A
  • Viral infections (e.g., HIV pneumonia, infectious mononucleosis, Guillain-Barre).
  • Head trauma.
  • Genetic-may have autosomal dominant mode of inheritance in some individuals.
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33
Q

Treatment of hypersomnolence disorder?

A

Life-long therapy with modafinil or stimulants such as methylphenidate; amphetamine-like antidepressants such as atomoxetine are second-line therapy.

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34
Q

Diagnostic criteria for obstructive sleep apnea hypopnea?

A
  1. Evidence by polysomnography of at least five obstructive apneas or hypopneas per hour of sleep and either of the following sleep symptoms:
    - Nocturnal breathing disturbances: snoring, snorting/gasping, or breathing pauses during sleep.
    - Daytime sleepiness, fatigue, or unrefreshing sleep despite sufficient opportunities to sleep that is not better explained by another mental disorder
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35
Q

Diagnostic criteria for central sleep apnea?

A
  • Evidence by polysomnography of five or more central apneas per hour of sleep.
  • The disorder is not better explained by another current sleep disorder.
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36
Q

Diagnostic criteria for sleep-related hypoventilation?

A

Polysomnography demonstrates episodes of decreased respiration associated with elevated CO2 levels

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37
Q

Clinical features of sleep-related hypoventilation?

A

Individuals report frequent arousals, morning headaches, insomnia, and excessive daytime sleepiness.

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38
Q

___ of chronic opioid users have central sleep apnea.

A

30%

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39
Q

Treatment of central sleep apnea?

A
  • Treat the underlying condition.
  • CPAP/BiPAP.
  • Supplemental O2.
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40
Q

What are the breathing-related sleep disorders?

A
  • Obstructive sleep apnea hypopnea
  • Central sleep apnea
  • Sleep-related hypoventilation
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41
Q

Risk factors of obstructive sleep apnea hypopnea?

A

Obesity, increased neck circumference, airway narrowing.

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42
Q

Treatment of obstructive sleep apnea hypopnea?

A
  • Positive airway pressure: continuous (CPAP) and in some cases bilevel (BiPAP).
  • Behavioral strategies such as weight loss and exercise.
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43
Q

Diagnosis (DSM-5 Criteria) of narcolepsy?

A
  1. Recurrent periods of an irrepressible need to sleep, lapsing into sleep, or napping occurring within the same day. These must have been occurring at least three times per week over the past 3 months.
  2. The presence of at least one of the following:
    - Cataplexy - a medical condition in which strong emotion or laughter causes a person to suffer sudden physical collapse though remaining conscious.
    - Hypocretin deficiency in the CSF
    - Nocturnal sleep polysomnography showing rapid eye movement (REM) sleep latency (time to reach REM sleep) less than or equal to 15 minutes (normal is 90-120 mins).
  3. Hallucinations and/or sleep paralysis at the beginning or end of sleep episodes are common (Not included in the DSM-5)
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44
Q

Pathophysiology of narcolepsy?

A
  • Linked to a loss of hypothalamic neurons that produce hypocretin.
  • May have autoimmune component.
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45
Q

Treatment of excessive daytime sleepiness from narcolepsy?

A
  • Amphetamines (d-amphetamine, methamphetamine).
  • Non-amphetamines such as methylphenidate, modafinil, sodium oxybate, and pitolisant (a novel histamine H3 receptor inverse agonist that is effective for both daytime sleepiness and cataplexy).
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46
Q

Treatment of cataplexy from narcolepsy?

A
  • Sodium oxybate (drug of choice).
  • Tricyclic antidepressants (TCAs): Imipramine, desipramine, and clomipramine.
  • REM suppression drugs such as selective serotonin reuptake inhibitor (SSRI)/serotonin-norepinephrine reuptake inhibitor (SNRI): Fluoxetine, duloxetine, atomoxetine, venlafaxine.
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47
Q

Treatment of circadian rhythm sleep-wake disorders?

A

Melatonin

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48
Q

Definition of circadian rhythm sleep-wake disorders?

A

Sleep disruption that is primarily due to an alteration of the circadian system or to a misalignment between the endogenous circadian rhythm and the sleep-wake schedule required by an individual’s physical environment or social or professional schedule

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49
Q

Definition of parasomnias?

A

Abnormal behaviour in sleep

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50
Q

What are the diagnoses that fall under parasomnias?

A
  • Non-rapid eye movement (NREM) sleep arousal disorder
  • Nightmare disorder
  • Rapid eye movement (REM) sleep behavior disorder
  • Restless legs syndrome
  • Substance/Medication-Induced Sleep Disorder
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51
Q

What are the diagnoses that fall under non-rapid eye movement (NREM) sleep arousal disorder?

A
  • Sleepwalking

- Sleep terrors

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52
Q

What is the definition of non-rapid eye movement (NREM) sleep arousal disorder?

A

Repeated episodes of incomplete arousals that are brief and usually occur during the first one-third of the sleep episode

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53
Q

Clinical features of sleepwalking

A
  • Behaviors may include sitting up in bed, walking around, eating, and in some cases “escaping” outdoors.
  • Eyes are usually open with a blank stare and “glassy look.”
  • Difficulty arousing the sleepwalker during an episode.
  • Dreams aren’t remembered and there is amnesia for the episode.
  • Episodes usually end with patients returning to bed or awakening (briefly) confused and disoriented.
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54
Q

Treatment of sleepwalking

A
  • Most cases do not need to be treated.
  • Patients may benefit from education, reassurance, addressing precipitating factors, ensuring a safe environment, and proper sleep hygiene.
  • Refractory cases may respond to low-dose benzodiazepine (e.g., clonazepam)
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55
Q

Etiology of sleepwalking

A
  • Unknown.
  • Family history in 80% of cases.
  • Usually not associated with any significant underlying psychiatric or psychological problems.
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56
Q

Clinical features of sleep terrors?

A
  • Recurrent episodes of sudden terror arousals, usually beginning with screaming or crying, that occur during slow-wave sleep.
  • Signs of autonomic arousal, including tachycardia, tachypnea, diaphoresis, and mydriasis.
  • Difficulty arousing during an episode.
  • After episode, patients usually return to sleep without awakening.
  • Dreams aren’t remembered and there is amnesia for the episode.
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57
Q

Treatment of sleep terrors?

A
  • Reassurance that the condition is benign and self-limited.

- Same as for sleepwalking.

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58
Q

Define of nightmare disorder?

A
  1. Repeated occurrences of extended, extremely dysphoric, and well-remembered dreams that usually involve efforts to avoid threats to survival, security, or physical integrity
    - On awakening from the dysphoric dreams, the individual rapidly becomes oriented and alert.
    - This occurs during REM sleep
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59
Q

Treatment of nightmare disorder?

A
  • Not always needed. Reassurance may help in many cases.
  • Desensitization/Imagery rehearsal therapy (IRT) involves the use of mental imagery to modify the outcome of a recurrent nightmare, writing down the improved outcome, and then mentally rehearsing it in a relaxed state.
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60
Q

Diagnostic criteria of rapid eye movement (REM) sleep behavior disorder?

A
  1. Repeated episodes of arousal during sleep associated with vocalization and/or complex motor behaviors, occurring during REM sleep.
    - Upon awakening from these episodes, the individual is completely awake, alert, and not confused or disoriented.
    - Either of the following:
    o REM sleep without atonia on polysomnographic recording.
    o A history suggestive of REM sleep behavior disorder and an established synucleinopathy diagnosis (e.g., Parkinson’s disease, multiple system atrophy).
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61
Q

Risk factors of rapid eye movement (REM) sleep behavior disorder?

A
  • Older age, generally more than 50 years.
  • Psychiatric medications such as TCAs, SSRIs, SNRIs, and B-blockers.
  • Narcolepsy.
  • Highly associated with underlying neurodegenerative disorders, especially Parkinson’s, multiple system atrophy, and neurocognitive disorder with Lewy bodies.
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62
Q

Treatment of rapid eye movement (REM) sleep behavior disorder?

A
  • Discontinuation of likely causative medications if possible.
  • Clonazepam is efficacious in most patients.
  • Melatonin may also be helpful.
  • Ensure environmental safety such as removing potentially dangerous objects from the bedroom and sleeping on the ground until behaviors can be managed effectively.
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63
Q

Diagnostic criteria of restless leg syndrome?

A
  1. An urge to move the legs, usually accompanied by or in response to uncomfortable and unpleasant sensations in the legs, characterized by all of the following:
    - The urge to move the legs begins or worsens during periods of rest or inactivity.
    - The urge to move the legs is partially or totally relieved by movement.
    - The urge to move the legs is worse in the evening or at night than during the day, or occurs only in the evening or at night.
    - At least 3x/wk for 3 months
    - Characterized by significant distress
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64
Q

Risk factors of restless leg syndrome?

A
  • Increases with age.
  • Strong familial component.
  • Iron deficiency.
  • Antidepressants, antipsychotics, dopamine-blocking antiemetics, and antihistamines can contribute to or worsen symptoms.
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65
Q

Treatment of restless leg syndrome?

A
  • Behavioral strategies including regular exercise, reduced caffeine intake, and avoiding aggravating factors have been shown to be beneficial.
  • Responds well to pharmacologic treatments.
  • Remove offending agents if possible.
  • Iron replacement if low ferritin.
  • Dopamine agonists and benzodiazepines are first-line treatments.
  • Gabapentin, gabapentin enacarbil (prodrug to gabapentin), and pregablin are also used.
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66
Q

Diagnostic criteria of substance/medication-induced sleep disorder

A
  1. A prominent and severe disturbance in sleep.
  2. There is evidence from the history, physical examination, or laboratory findings of both (1) and (2):
    - The symptoms in Criterion A developed during or soon after substance intoxication or after withdrawal from or exposure to a medication.
    - The involved substance/medication is capable of producing the symptoms in Criterion A.
  3. The disturbance is not better explained by a sleep disorder that is not substance/medication-induced. Such evidence of an independent sleep disorder
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67
Q

Contributors to eating disorder risk?

A

Temperament, eating dysregulation, attachment issues, poor self-regulation, childhood abuse (BN especially), sociocultural ideas of health/beauty.

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68
Q

Triage for danger zone/when to admit?

A
  • <75% of IDEAL BODY WEIGHT = STARVATION.
  • Correct K (<3 cause prolonged QTc), P, Mg, NA. ECG/lytes (including Phosphorous) is critical!
  • Vitals: BP<85/50 or HR <40
  • ECG: Prolonged QTc
  • Be careful of refeeding syndrome – can cause hypophosphatemia, fluid/MSK issues.
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69
Q

Diagnostic criteria for anorexia?

A

Restriction of energy intake leading to significantly low body weight (behaviour), intense fear of gaining weight/fat or persistent behaviour that interferes with weight gain (psychopathology), and disturbance in the way one’s body weight OR shape is experienced/self-evaluated.

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70
Q

Anorexic patients normally have cluster __ traits

A

C

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71
Q

Anorectic symptoms are ego-____

A

Syntonic

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72
Q

What defines the restricting type of anorexia?

A

During the last 3mo, individual has not engaged in binge/purging. Just fasting/restriction or excessive exercise

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73
Q

What defines the binge/purge type of anorexia?

A

During the last 3mo, engaged in recurrent binging/purging. If your weight is LOW and you fulfill these criteria, you are NOT bulimic, still anorexic.

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74
Q

Physical complications of restricting/malnutrition (anorexia):

A
  • Bone: osteopenia/porosis, fractures
  • Brain: enlarged ventricles
  • Cardiac: bradycardia, hypotension, orthostasis, hypothermia, arrhythmia, QTc prolongation, and ST-T wave changes on electrocardiogram
  • Derm: lanugo hair (indicative of anorexia), dry skin, edema, hair loss, brittle nails
  • GI: constipation
  • Heme: pancytopenia
  • Endo: sick euthyroid (low TSH), hypoglycemia, low LH/FSH/estrogen/testo
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75
Q

Treatment of anorexia?

A
  • Weight restoration (FOOD and lots of it) - BMI 20 in teens
  • Family intervention - non-blaming, wt restoration under parental control → return control → address delays → relapse prevention. ONLY FOR TEENS, otherwise CBT.
  • Meds - Premeal anxiolytic (such as alprazolam) can help encourage eating by decreasing anticipatory anxiety. Quetiapine can be used for sedation and appetite stimulation. Treatment for constipation. Vitamin and mineral supplementation
  • CBT
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76
Q

What is refeeding syndrome?

A

Refers to electrolyte and fluid shifts that occur when severely malnourished patients are refed too quickly. Look for fluid retention and decreased levels of phosphorus, magnesium, and calcium

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77
Q

Bulimic patients normally have cluster __ traits

A

B

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78
Q

Diagnostic criteria for bulimia?

A
  • Recurrent episodes of binge eating (eating more than average in a 2hr period/an amount of food that is larger than most people would eat and a sense of lack of control over eating during the episode)
  • Recurrent inappropriate compensatory behaviour to prevent weight gain (vomiting, laxatives, fasting, excess exercise)
  • At least 1x/wk for 3mo with body shape/weight influencing self-evaluation.
  • Does not occur exclusively during an episode of anorexia nervosa.
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79
Q

Bulimic symptoms are ego-____

A

Dystonic
- Many bulimic patients feel like failed anorexics because they would like to have the self control to restrict their food intake

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80
Q

Signs of purging?

A

Electrolytes abnormal (low K) Russel’s sign – more in bulimia (cuts on knuckles when putting fist into mouth to vomit), moth-eaten teeth erosion/caries, salivary gland swelling (Chipmunk Cheeks).

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81
Q

Laboratory/imaging abnormalities of purging?

A

Hypochloremic hypokalemic alkalosis (purging), metabolic acidosis (laxative abuse), elevated bicarbonate (compensation), hypernatremia, increased BUN, increased amylase, altered thyroid hormone, cortisol homeostasis, esophagitis

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82
Q

Pathophysiology of bulimia?

A
  • ADDICTIVE DISORDER – high prevalence of substance use in these (30%). Involves dopaminergic system.
  • Childhood obesity and early pubertal maturation increase risk for bulimia nervosa.
  • Psychodynamic theories: Masochistic displays of control and displaced anger over one’s body.
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83
Q

Treatment of bulimia

A
  • CBT is BEST (20 sessions over 5 mo) and/or FLUOXETINE (60-80mg OD – good for short term). Vysanse (Dexedrine stimulant) can decrease binging!
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84
Q

What is the difference between binge-eating disorder and bulimia/anorexia?

A

Patients with binge-eating disorder suffer emotional distress over their binge eating, but they do not try to control their weight by purging or restricting calories, as do individuals with anorexia or bulimia. Unlike in anorexia and bulimia, patients with binge-eating disorder are not as fixated on their body shape and weight.

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85
Q

Diagnostic criteria of binge eating disorder?

A
  1. Recurrent episodes of binge eating, marked distress associated with ≥3 of the following for at least 1/wk for 3mo but NO COMPENSATORY BEHAVOUR (vomiting) as in BN or ANOREXIA:
    - Eating more rapidly than normal
    - Eating till uncomfortable full
    - Eating large amounts when not feeling hungry
    - Eating alone due to embarrassment by amount of food
    - Feeling disgusted with oneself/depressed/guilty after
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86
Q

Physical exam findings of binge eating disorder

A

Patients are typically obese and suffer from medical problems related to obesity including metabolic syndrome, type 2 diabetes, and cardiovascular disease.

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87
Q

Which stimulant suppresses appetite and is used in the treatment of binge eating disorder?

A

Lisdexamfetamine (Vyvanse)

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88
Q

Treatment of binge eating disorder?

A
  • Individual (cognitive-behavioral or interpersonal) psychotherapy with a strict diet and exercise program coordinated by a registered dietician. Comorbid mood disorders or anxiety disorders should be treated as necessary.
  • SSRIs are first-line treatment due to their efficacy and tolerability.
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89
Q

What is pica?

A

Persistent eating of non nutritive, non food substances for at least one month

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90
Q

What is avoidant restrictive food intake disorder?

A

An eating or feeding disturbance lack of interest in eating and food based on the secondary characteristics of food or about aversive consequences of eating. There is no concern about body weight and shape

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91
Q

What is rumination disorder?

A

Repeated regurgitation of food over at least one month – rechewed, reswallowed or spit out.

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92
Q

Differential diagnosis of anxiety?

A
  • Cardiac: angina, post/impending-MI, arrhythmias, cardiac tamponade
  • Endocrine: hyper(para)thyroidism, hyperadrenocorticism, diabetes, pheochromocytoma
  • GI: gastroesophageal reflux disease, irritable bowel syndrome, peptic ulcer disease, acute alcohol withdrawal
  • Metabolic: hyperkalemia, hyperthermia, hypoglycemia, hyponatremia, hypoxia, porphyria, or substance ingestion/overdose.
  • Respiratory: asthma, PE, COPD
  • Psychiatric: somatoform/psychotic disorders, mood disorders (depression/bipolar), personality disorders (OCPD)
  • D – Drugs: EtOH/benzo withdrawal, amphetamines, caffeine, OTC for colds/decongestants
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93
Q

Investigations for anxiety?

A
  • ECG* + CXR + CBC*
  • TSH*, Ca2+, cortisol, fasting glucose/A1C, 24hr metanephrines
  • Liver enzymes
  • PFTs, D-dimer*
  • Tox screen
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94
Q

What physical symptoms might a child display if anxious?

A

Headaches, stomach aches, muscle tension and muscle twitches, sleep problems

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95
Q

Most anxiety disorders benefit from which class of medications?

A

Sertraline (or any other SSRI)

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96
Q

What could you augment with if no benefit from >12weeks of SSRI for anxiety?

A
  • Antipsychotics (risperidone in OCD, PTSD) – esp. if co-morbid tics; usually see improvement in first 4 weeks.
  • Consider clonazepam, buspirone – short term use (OCD, GAD, panic, SP)
  • Gabapentin (panic, SP, PTSD pain, bipolar anxiety),
  • Lamotrigine (OCD, PTSD, bipolar depression), valproic acid.
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97
Q

How should you titrate SSRI/SNRI for anxiety?

A

Start low (1/2 normal starting dose), go slow (4-6 weeks titration – OCD faster), aim sufficient (higher doses than MDD), and wait longer (8-12 weeks at therapeutic doses).

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98
Q

Side effects of SSRI/SNRI?

A

Headache, irritability, GI complaints, insomnia, fatigue, sexual dysfunction, weight gain

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99
Q

____ has proven effective for anxiety disorders. It examines the relationship between anxiety-driven cognitions (thoughts), emotions, and behavior.

A

Cognitive behavioral therapy (CBT)

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100
Q

Types of panic attacks?

A
  • Unexpected = panic disorder

- Situational = everything else!

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101
Q

Symptoms of panic attacks?

A

Da PANICS

  • Dizziness, disconnectedness, derealization (unreality), depersonalization (detached from self)
  • Palpitations, paresthesias
  • Abdominal distress
  • Numbness, nausea
  • Intense fear of dying, losing control or “going crazy”
  • Chills, chest pain, choking
  • Sweating, shaking, shortness of breath
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102
Q

Define panic attacks?

A

An abrupt surge of intense fear or discomfort that reaches a peak within minutes, during which time => 4 sx occur

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103
Q

Diagnosis (DSM-5 Criteria) of panic disorder?

A
  • Recurrent, unexpected panic attacks without an identifiable trigger.
  • One or more of panic attacks followed by >1 month of continuous worry about experiencing subsequent attacks or their consequences, and/or a maladaptive change in behaviors (e.g., avoidance of possible triggers).
  • Not caused by the direct effects of a substance, another mental disorder, or another medical condition.
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104
Q

Etiology of panic disorder?

A
  • Genetic factors: Greater risk of panic disorder if a first-degree relative is affected.
  • Psychosocial factors: increase incidence of stressors (especially loss) prior to onset of disorder; history of childhood physical or sexual abuse.
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105
Q

Course/prognosis of panic disorder?

A
  • Panic disorder has a chronic course with waxing and waning symptoms.
  • Relapses are common with discontinuation of medication.
  • Only a minority of patients have full remission of symptoms.
  • Up to 65% of patients with panic disorder also have major depression.
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106
Q

Treatment of panic disorders

A
  • First-line: SSRIs (e.g., sertraline, citalopram, escitalopram) – there’s a lower dose of sertraline for panic disorder specifically
  • SNRIs (e.g., venlafaxine) are also efficacious.
  • If above options are not effective, can try TCAs (e.g., clomipramine, imipramine).
  • Can use benzodiazepines (e.g., clonazepam, lorazepam) as scheduled or PRN, especially until the other medications reach full efficacy.
  • Use beta-blockers
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107
Q

Define agoraphobia?

A

Agoraphobia is an intense fear of being in public places where escape or obtaining help may be difficult. It often develops with panic disorder.

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108
Q

Diagnosis (DSM-5 Criteria) of agoraphobia?

A
  1. Intense fear/anxiety about more than two situations due to concerns of difficulty escaping or obtaining help in case of panic or other humiliating symptoms:
    - Outside of the home alone.
    - Open spaces (e.g., bridges).
    - Enclosed places (e.g., stores).
    - Public transportation (e.g., trains).
    - Crowds/lines.
  2. The triggering situations cause fear/anxiety out of proportion to the potential danger posed, leading to endurance of intense anxiety, avoidance, or requiring a companion. This holds true even if the patient suffers from another medical condition such as inflammatory bowel disease (IBS) which may lead to embarrassing public scenarios.
  3. Symptoms cause significant social or occupational dysfunction.
  4. Symptoms last >6 months.
  5. Symptoms not better explained by another mental disorder.
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109
Q

Epidemiology of agoraphobia?

A

Mean age of onset 17 (without preceding panic disorder, onset is 25-29). Persistent and chronic. Without treatment, complete remission is rare (10%). More than 1/3 completely housebound and unable to work.

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110
Q

Etiology of agoraphobia?

A
  • Strong genetic factor: Heritability about 60%.

- Psychosocial factor: Onset frequently follows a traumatic event.

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111
Q

Treatment of agoraphobia?

A

Although SSRIs are considered the first-line agents for treatment of panic disorders with or without agoraphobia, the tricyclic drugs clomipramine (Anafranil) and imipramine (Tofranil) are the most effective in the treatment of these disorders. Therapies: supportive psychotherapy, behaviour therapy, cognitive therapy and virtual therapy. Benzodiazepines have the most rapid onset of action against panic.

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112
Q

Define a specific phobia.

A

A phobia is defined as an irrational fear that leads to endurance of the anxiety and/or avoidance of the feared object or situation. A specific phobia is an intense fear of a specific object or situation (i.e., the phobic stimulus).

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113
Q

Diagnosis (DSM-5 Criteria) of a specific phobia?

A
  • Persistent, excessive fear elicited by a specific situation or object which is out of proportion to any actual danger/threat.
  • Exposure to the situation triggers an immediate fear response.
  • Situation or object is avoided when possible or tolerated with intense anxiety.
  • Symptoms cause significant social or occupational dysfunction.
  • Duration >6 months.
  • Symptoms not solely due to another mental disorder, substance (medication or drug), or another medical condition.
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114
Q

___ are the most common psychiatric disorder in women and second most common in men (substance-related is first).

A

Phobias

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115
Q

Treatment of specific phobias

A

CBT Model for Specific Phobia: exposure is highly effective. More effective if sessions are grouped closely together, exposure if prolonged, real (not imagined), and provided in multiple different settings.

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116
Q

Epidemiology of social anxiety

A

12-14% lifetime prev, F>M in epi samples, F:M in clinical samples. Age of onset ~ mid-teens (13).

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117
Q

Define social anxiety

A

Social anxiety disorder (social phobia) is the fear of scrutiny by others or fear of acting in a humiliating or embarrassing way. The phobia may develop in the wake of negative or traumatic encounters with the stimulus. Social situations causing significant anxiety may be avoided altogether, resulting in social and academic/occupational impairment.

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118
Q

Diagnosis (DSM-5 Criteria) of social anxiety

A
  • The diagnostic criteria for social anxiety disorder (social phobia) are similar to specific phobia except the phobic stimulus is related to social scrutiny and negative evaluation. The patients fear embarrassment, humiliation, and rejection. This fear may be limited to performance or public speaking, which may be routinely encountered in the patient’s occupation or academic pursuit. NOT due to impaired capacity for socialization as in ASD
  • For youth: Children must experience discomfort with peers, not only with adults
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119
Q

Treatment of social anxiety

A
  • Treatment of choice: CBT.
  • First-line medication, if needed: SSRIs (e.g., sertraline, fluoxetine) or SNRIs (e.g., venlafaxine) for debilitating symptoms.
  • Benzodiazepines (e.g., clonazepam, lorazepam) can be used as scheduled or PRN.
  • Beta-blockers (e.g., atenolol, propranolol) for performance anxiety/public speaking. Also can use benzos
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120
Q

Diagnosis (DSM-5 Criteria) of separation anxiety disorder

A
  1. Excessive and developmentally inappropriate fear/anxiety regarding separation from attachment figures, with at least three of the following:
    - Separation from attachment figures leads to extreme distress.
    - Excessive worry about loss of or harm to attachment figures.
    - Excessive worry about experiencing an event that leads to separation from attachment figures.
    - Reluctance to leave home, or attend school or work.
    - Reluctance to be alone.
    - Reluctance to sleep alone or away from home.
    - Complaints of physical symptoms when separated from major attachment figures.
    - Nightmares of separation and refusal to sleep without proximity to attachment figure.
  2. Lasts for >4 weeks in children/adolescents and >6 months in adults.
  3. Symptoms cause significant social, academic, or occupational dysfunction.
  4. Symptoms not due to another mental disorder.
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121
Q

At what age does separation anxiety disorder occur?

A

Tends to peak around 9-18 months and decrease after age 2. Can increase again at age 4-5 when starting school

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122
Q

Treatment of separation anxiety disorder

A
  • Psychotherapy: CBT, family therapy.

- Medications: SSRIs can be effective as an adjunct to therapy.

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123
Q

Define selective mutism

A

Selective mutism is a rare condition characterized by a failure to speak in specific situations for at least 1 month, despite the intact ability to comprehend and use language.

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124
Q

Diagnosis (DSM-5 Criteria) of selective mutism

A
  • Consistent failure to speak in select social situations (e.g., school) despite speech ability in other scenarios.
  • Mutism is not due to a language difficulty or a communication disorder.
  • Symptoms cause significant impairment in academic, occupational, or social functioning.
  • Symptoms last >1 month (extending beyond first month of school).
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125
Q

Treatment of selective mutism

A
  • Psychotherapy: CBT, family therapy.

- Medications: SSRIs (especially with comorbid social anxiety disorder).

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126
Q

Epidemiology of Generalized Anxiety Disorder

A

6% lifetime prev F>M 2:1. Median age at onset 30 but spread over broad range (GAD sx often in childhood).

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127
Q

Diagnosis (DSM-5 Criteria) of Generalized Anxiety Disorder?

A
  • Excessive, anxiety/worry about various daily events/activities ‚>6 months.
  • Difficulty controlling the worry.
  • Associated >3 symptoms (BESKIM): blank mind/impaired concentration, easily fatigued, restlessness, fatigue, irritability, muscle tension, insomnia.
  • Symptoms are not caused by the direct effects of a substance, or another mental disorder or medical condition.
  • Symptoms cause significant social or occupational dysfunction.
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128
Q

Treatment of Generalized Anxiety Disorder?

A
  • CBT
  • SSRIs (e.g., sertraline, citalopram) or SNRIs (e.g., venlafaxine).
  • Can also consider a short-term course of benzodiazepines or augmentation with buspirone.
  • Much less commonly used medications are TCAs and MAOIs
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129
Q

Define Posttraumatic stress disorder (PTSD)

A

Posttraumatic stress disorder (PTSD) is characterized by the development of multiple symptoms after exposure to one or more traumatic events: intrusive symptoms (e.g., nightmares, flashbacks), avoidance, negative alterations in thoughts and mood, and increased arousal. The symptoms last for at least a month and may occur immediately after the trauma or with delayed expression.

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130
Q

Diagnosis (DSM-5 Criteria) of Posttraumatic stress disorder (PTSD)

A

A – Exposure to death, serious injury or sexual violence (1/4)
- Witness, Repeated occupational exposure to aversive situations, learning about someone close to the person, directly
B – Re-experiencing (1/5)
- Recollections, revieller, reliving, resembling cues cause distress, reactivity of body
C – Avoidance associated w/ stimuli (1/2)
- Thoughts/feelings, people/places/conversations
D - Negative change cognitions/mood (2/7)
- Inability to remember, negative beliefs, blames themselves (common in children), loss of interest in activities
E - Alterations in arousal/reactivity (2/6) – behaviour, sleep disturbance, hypervigilance, irritable, task completion, startled (acryonym: BSHITS)
- Those in D and E are not specific for PTSD – E can be confused for mania
F - Lasts >1mo.

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131
Q

Epidemiology of Posttraumatic stress disorder (PTSD)

A

M>F for trauma exposure, but women exposed 2x likely to develop PTSD (lifetime prev. 2x, 10.4%) – due to the type of trauma (rape), 20% soldiers.

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132
Q

Etiology/Risk Factors of Posttraumatic stress disorder (PTSD)

A
  • Pretrauma (temperamental/physiological/genetic – prior mental disorders, female, enviro – lower SES/intelligence, exposure to prior trauma, family psychiatric history)
  • Peritrauma (type, severity)
  • Posttrauma (poor coping, social support, subsequent adverse life events).
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133
Q

Pathophysiology of Posttraumatic stress disorder (PTSD)

A

Hippocampal volume reduction (failure to distinguish between safe and dangerous) + increased amygdala activation + decreased activation of ratio of PFC (extinction memory) LOWER:ACC (fear memory) HIGHER. Therefore failure of top-down learning (insufficient top-down modulation of amygdala).

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134
Q

Pharmacological treatment of Posttraumatic stress disorder (PTSD)

A
  • First-line antidepressants: SSRIs (e.g., sertraline, citalopram) or SNRIs (e.g., venlafaxine).
    • Step 1: any of above for 8 weeks
    • Step 2: add risperidone or olanzapine (mixed results)
    • Step 3: add anti-convulsant esp. if mood lability or anger (lamotrigine or topiramate)
  • Prazosin, alpha-receptor antagonist, targets nightmares and hypervigilance.
  • May augment with atypical (second-generation) antipsychotics in severe cases.
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135
Q

Psychotherapy treatment of Posttraumatic stress disorder (PTSD)

A
  • Specialized forms of CBT (e.g., exposure therapy, cognitive processing therapy).
  • Supportive and psychodynamic therapy.
  • Couples/family therapy.
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136
Q

What are delusions?

A

Delusions are fixed, false beliefs that persist despite evidence to the contrary and that do not make sense within the context of an individual’s cultural background.

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137
Q

What are delusions of persecution/paranoid delusions

A

Irrational belief that one is being persecuted. Example: “The Central Intelligence Agency (CIA) is monitoring me and tapped my cell phone.”

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138
Q

What are ideas of reference

A

Belief that cues in the external environment are uniquely related to the individual. Example: “The TV characters are speaking directly to me.”

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139
Q

What are delusions of control

A

Includes thought broadcasting (belief that one’s thoughts can be heard by others) and thought insertion (belief that outside thoughts are being placed in one’s head).

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140
Q

What are delusions of grandeur

A

Belief that one has special powers beyond those of a normal person. Example: “I am the all-powerful son of God and I shall bring down my wrath on you if I don’t get my way.”

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141
Q

What are delusions of guilt

A

Belief that one is guilty or responsible for something. Example: “I am responsible for all the world’s wars.”

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142
Q

What is an illusion

A

Misinterpretation of an existing sensory stimulus (such as mistaking a shadow for an evil spirit).

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143
Q

What are somatic delusions

A

Belief that one has a certain illness or health condition. Example: A patient believing she is pregnant despite negative pregnancy tests and ultrasounds.

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144
Q

Differential diagnosis of psychosis?

A
  • Psychotic disorder due to another medical condition.
  • Substance/Medication-induced psychotic disorder.
  • Delirium/Major neurocognitive disorder (dementia).
  • Bipolar disorder, manic/mixed episode.
  • Major depression with psychotic features.
  • Brief psychotic disorder.
  • Schizophrenia.
  • Schizophreniform disorder.
  • Schizoaffective disorder.
  • Delusional disorder.
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145
Q

What are hallucinations?

A

Sensory perception without an actual external stimulus.

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146
Q

Investigations for psychosis?

A
  • CBC, electrolytes (including extended lytes), creatinine, glucose, urinalysis, urine drug screen, TSH, Vit B12
  • LFTs, fasting lipids, HbA1C to obtain baseline levels prior to antipsychotic initiation
  • ECG (several antipsychotics affect cardiac conduction)
  • If clinically indicated, order infectious work-up, inflammatory markers, brain imaging
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147
Q

What kind of hallucinations are most commonly exhibited by schizophrenic patients?

A

Auditory

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148
Q

Which type of hallucination may accompany drug intoxication, drug and alcohol withdrawal, or delirium?

A

Visual

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149
Q

Epidemiology of schizophrenia

A
  • Disease of youth (onset late teens-mid30s). 1% lifetime prevalence. Equally prevalent in men and women - Onset is earlier in men than in women.
  • Modal age of onset is between 18 and 25 for men and between 25 and 35 for women, with a second peak (bimodal for women) occurring around menopause/middle age i.e. >40 (>45 = late onset). Only 50% obtain treatment
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150
Q

First-degree biological relatives of persons with schizophrenia have a ___ greater risk for developing the disease than the general population.

A

Ten times

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151
Q

Persons who develop schizophrenia are more likely to have been born in the ___ and ____ and less likely to have been born in late spring and summer.

A
  • Winter

- Early spring

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152
Q

Epidemiological data show a high incidence of schizophrenia after prenatal exposure to ____ during several epidemics of the disease

A

Influenza

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153
Q

The lifetime prevalence of any drug abuse (other than tobacco) in schizophrenia is often greater than ____

A

50 percent

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154
Q

Diagnosis of schizophrenia

A
  • A: 2 (or more) of the following for at least one month period (but at least 1 criteria in red): delusions, hallucinations, or disorganized speech. Grossly disorganized/catatonic behaviour. Negative symptoms (avolition, alogia, apathy, asociality).
  • B: Also need a social/occupational decline in function. Cognitive, depressive sx can also occur but not in DSM.
  • C: 6mo sx (with at least 1mo of criterion A unless successfully treated)
  • D: Schizoaffective and Mood Disorder exclusion.
  • E: Substance use/other medical condition exclusion.
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155
Q

What are the dopamine pathways

A
  • Mesolimbic (originates in the VTA and innervates limbic system)
  • Mesocortical (originates in the VTA and projects to the frontal cortex)
  • Nigrostriatal (projects from substantia nigra to the striatum)
  • Tuberinfundibular (connects hypothalamus to the pituitary gland)
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156
Q

Mesolimbic hyperactivity is the cause of ___ in schizophrenics

A

Mesolimbic hyperactivity is the cause of positive symptoms. Evidence – paranoia can be induced by constant stimulant abuse. Therefore, want to block this hyperactivity using dopamine (D2) blockade.

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157
Q

Mesocortical (originates in the VTA and projects to the frontal cortex) – dopamine deficiency here (prefrontal cortex) may be responsible for the ___ in schizophrenics

A

Negative/cognitive symptoms. Thus – dopamine receptor blockade could lead to worsening of negative/cognitive symptoms

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158
Q

The medication we give for schizophrenia affect this area and cause Parkinson-like symptoms

A

Nigrostriatal

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159
Q

Medications used for schizophrenia also affect here, and cause excess prolactin secretion

A

Tuberinfundibular

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160
Q

Too much mesolimbic dopamine causes ___ and too little mesocortical dopamine causes ____.

A

+ve sx
–ve/cognitive sx

Since this is the case, we need agents that decrease mesolimbic dopamine to reduce +ve sx and increase mesocortical to treat –ve sx.

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161
Q

Neuropathology findings in schizophrenics?

A
  • Loss of brain volume widely reported in schizophrenic brains appears to result from reduced density of the axons, dendrites, and synapses that mediate associative functions of the brain
  • Functional Neuroimaging – Hypofrontality
  • Structural Neuroimaging - Temporal lobe reductions in grey matter. Enlarged ventricles due to hippocampal loss in volume.
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162
Q

Neurodevelopmental hypothesis for schizophrenia?

A
  • 2nd trimester defect in neuronal migration. Neuronal loss due to hypoxia-associated obstetric complications
  • Excessive synaptic pruning occurring during adolescence leading to psychosis (too little connections)
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163
Q

The classic feature of the catatonic type is a marked disturbance in ______

A

The classic feature of the catatonic type is a marked disturbance in motor function; this disturbance may involve stupor, negativism, rigidity, excitement, or posturing.

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164
Q

Subtypes of schizophrenia?

A
  • Paranoid Type
  • Disorganized Type
  • Catatonic Type
  • Undifferentiated Type
  • Residual Type
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165
Q

Classically, the paranoid type of schizophrenia is characterized mainly by the presence of

A

Delusions of persecution or grandeur

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166
Q

Patients who clearly have schizophrenia cannot be easily fit into one type or another

A

Undifferentiated Type

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167
Q

What is the residual type of schizophrenia?

A

The residual type of schizophrenia is characterized by continuing evidence of the schizophrenic disturbance in the absence of a complete set of active symptoms or of sufficient symptoms to meet the diagnosis of another type of schizophrenia

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168
Q

The classic feature of the catatonic type of schizophrenia is a marked disturbance in ______

A

The classic feature of the catatonic type is a marked disturbance in motor function; this disturbance may involve stupor, negativism, rigidity, excitement, or posturing.

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169
Q

What is the disorganized type of schizophrenia?

A

The disorganized type of schizophrenia is characterized by a marked regression to primitive, disinhibited, and unorganized behavior and by the absence of symptoms that meet the criteria for the catatonic type

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170
Q

What is the disorganized type of schizophrenia?

A

The disorganized type of schizophrenia is characterized by a marked regression to primitive, disinhibited, and unorganized behavior and by the absence of symptoms that meet the criteria for the catatonic type

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171
Q

What are delusions of influence?

A

Body or actions are being acted on by an outside influence

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172
Q

What is tangential speech?

A

In which the train of thought of the speaker wanders and shows a lack of focus, never returning to the initial topic of the conversation.

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173
Q

What is derailment (loosening of association) speech?

A

No logical connections b/w topic changes

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174
Q

What is neologism?

A

Words that only have meaning to the person using them, either made up words or real words that they believe have meanings other than their common meaning

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175
Q

What are the positive symptoms of schizophrenia?

A
  • Hallucinations
  • Delusions
  • Disorganized speech
  • Disorganized behaviour
  • Motor
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176
Q

What is automatic obedience?

A

Individual obeys all orders, commands, and instructions from another person without question or concern.

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177
Q

What is catalepsy?

A

A medical condition characterized by a trance or seizure with a loss of sensation and consciousness accompanied by rigidity of the body.

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178
Q

What are the negative symptoms of schizophrenia?

A
  • Avolition - decreased motivation to start or perform purposeful activities
  • Alogia - inability to speak or reduction in the amount of speech
  • Anhedonia - inability to feel pleasure
  • Asociality - preference for solitary activities, inability to engage in social interactions
  • Secondary “negative symptoms” – depression, pre-existing PD, SUD, hypothyroidism
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179
Q

What are the cognitive symptoms of schizophrenia?

A

SMARTS (speed of processing, memory, attention, reasoning, tact and synthesis. Good working memory, NOT reducing positive symptoms, helps improve social recovery. NEGATIVE SYMPTOMS AND COGNITIVE IMPAIRMENT strongly affects functional outcomes

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180
Q

____ is the most frequent prodromal symptom appearing 4 years prior to the 1st hospital admission.

A

Depression

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181
Q

Risk factors of suicidal behaviours in schizophrenics?

A

Presence of a major depressive episode, early age onset, high SES/IQ, deteriorating course with relapses/hospital dependence. Greater insight associated with higher risk of being suicidal (shaming, self-blame) – therefore insight needs to be monitored as part of suicide risk. Also having negative beliefs about psychosis

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182
Q

Risk factors of hostile symptoms in schizophrenics?

A

Exhibiting violent behaviour? A victim of violence in past 6 months. Male, young, nonadherence to meds. Persecutory delusions, prior antisocial behaviour prior to psychosis

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183
Q

What eye findings are found in schizophrenics?

A

The disorder of smooth ocular pursuit (saccadic movement), patients with schizophrenia have an elevated blink rate. The elevated blink rate is believed to reflect hyperdopaminergic activity.

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184
Q

Investigations for schizophrenias?

A

Tox screen, GGT, rule out med causes (CBC, lytes, BUN, LFT, TSH, VDRL (for neurosyphilis), CT – not routine – used if massive change in neurological presentation)

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185
Q

Comorbidities of schizophrenia

A
  • Obesity - This is due, at least in part, to the effect of many antipsychotic medications, as well as poor nutritional balance and decreased motor activity
  • Diabetes Mellitus – clozapine. Insulin resistance. Glucose tolerance
  • Cardiovascular Disease
  • HIV
  • COPD – smoking
  • Less likely to get RA
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186
Q

Relapse of psychotic symptoms in schizophrenia occurs in up to ___ of patients within 2 years of being hospitalised

A

40-60%

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187
Q

Men are more likely to be impaired by _____ (worse prognosis), and women are likely to have better premorbid social functioning than men, and are more likely to have _____

A

Negative symptom

Positive symptoms

188
Q

Good prognostic factors for schizophrenia?

A

acute onset, shorter prodromal period, treatment compliant, female gender, good pre-morbid cognitive function, good pre-morbid social functioning, positive symptoms, precipitants, older age of onset, no family history, presence of affective symptoms, good response to drug, good support system

189
Q

______ is the major effect of antipsychotics

A

Dopamine (D2 blockage)

190
Q

Antipsychotics help the ____ symptoms but not the ____ symptoms in schizophrenia?

A

Positive, negative

These do not help negative sx since they only block the mesolimbic path

191
Q

What is the dopamine D2 receptor blockage target?

A

> 65%

192
Q

What can happen if the dopamine D2 receptor blockage is >72% or >78%.

A

However, blockage leads to other collateral damage: >72% block = hyperprolactinemia (tuberoinfundibular tract), >78% block = Parkinsonism + extrapyramidal symptoms (nigrostriatal tract) Nigrostriatal tract is involved in motor planning and purposeful movement - can lead to involuntary movement)!

193
Q

Examples of 1st gen typical antipsychotics

A
  • Haloperidol – high potency, used for acute agitation,
  • Methotrimeprazine, chlorpromazine – low potency,
  • Loxapine – medium potency
194
Q

What causes neuroleptic malignant syndrome?

A

Caused from dopamine blockade

195
Q

Side effects of 1st gen typical antipsychotics

A
  • Acute dystonia
  • Parkinsonism
  • Akathisia
  • Tardive dyskinesia
196
Q

What is acute dystonia?

A

Characterized by involuntary contractions of muscles which may include writhing, or torsional movement and VERY painful rolling eyes into their head – oculogyric crisis, arching back – retrocollis and craning neck to one side – torticollis.

197
Q

When does acute dystonia occur?

A

Occurs a few days after starting med (5days)

198
Q

Treatment of acute dystonia?

A

Anticholinergic (benztropine) or antihistamine (diphenhydramine), diazepam 3Bs

199
Q

What is tardive dyskinesia?

A

Causes stiff, jerky movements of your face and body that you can’t control. Sometimes doesn’t go away even if off the drug

200
Q

Treatment of tardive dyskinesia?

A

Decrease dose, Vit E, atypical, botox? CLOZAPINE

201
Q

When does tardive dyskinesia occur?

A

Occurs a 3 months after starting med.

202
Q

What are the symptoms of Parkinsonism

A

Coarse, rhythmic, resting tremor affecting limbs, head, mouth and tongue. Bradykinesia. TRAP (tremor, rigidity, akinesia, postural instability).

203
Q

What is akathisia

A

Movement disorder that makes it hard for you to stay still/restless.

204
Q

When does Parkinsonism occur

A

Occurs within a few weeks of starting med.

205
Q

When does akathisia occur?

A

Occurs a 4 weeks after starting med – worse with Abilify.

206
Q

Treatment of Parkinsonism?

A

Decrease dose, anticholinergic – D/C AC in 2-3 weeks

207
Q

Treatment of akathisia?

A

B-blocker, anticholinergic, lorazepam

208
Q

What are the symptoms of neuroleptic malignant syndrome?

A

FARM (fever, autonomic instability, rigidity and mental change)

209
Q

Diagnosis of neuroleptic malignant syndrome?

A

Antipsychotic + muscle rigidity + hyperthermia + 2..

  • Labs: CK or WBC
  • Autonomic instability: labile BP, diaphoresis, tachycardia
  • Neuro: tremor, confusion, fluctuating levels of consciousness
210
Q

Treatment of neuroleptic malignant syndrome?

A

D/c antipsychotic and wait 2 weeks. ICU, supportive – hydrate, temp control. BROMOCRIPTINE or DANTROLENE

211
Q

Examples of 2nd gen typical antipsychotics

A

Clozapine, risperidone (most like the typicals), ziprasidrone, paliperidone, quetiapine, olanzapine (short acting, use in acute situations)

212
Q

MOA of 2nd gen typical antipsychotics

A

Serotonin-dopamine antagonists

213
Q

Side effects of 2nd gen typical antipsychotics

A
  • Metabolic – weight gain, dyslipidemia, orthostatic hypotension (alpha blocker), somnolence/sedation (antihistamine)
  • Clozapine and Olanzapine have the most metabolic side effects (don’t give to big ppl/high BP/high sugars)
214
Q

Examples of 3rd gen typical antipsychotics

A

Aripiprazole

215
Q

MOA of 3rd gen typical antipsychotics

A

Partial dopamine agonists

216
Q

How should you start antipsychotics?

A

START AP, wait 2 weeks. If poor response, med adherence? Substance use? If no response after 4 weeks at optimal dose than change AP, If partial response wait up until 8 wks. If no response with 2 APs then trail of clozapine. If you discontinue meds – continue monitoring for s/s of relapse for at least 2 years.

217
Q

____ is the only antipsychotic that reduces suicide risk to normal

A

Clozapine

218
Q

Which antipsychotic has less weight gain and EPS and no sexual symptoms?

A

Aripiprazole

219
Q

Side effects of clozapine?

A
  • Increased threshold of seizure, agranulocytosis, cardiac, sedation/wt/sialorrhea/anticholinergic (constipation!).
  • Need to do CBC weekly for 6 months and then monthly thereafter
220
Q

Psychosocial therapies for schizophrenia?

A
  • Social Skills Training
  • Assertive Community Treatment: .
  • Group therapy is effective in reducing social isolation, increasing the sense of cohesiveness, and improving reality testing for patients with schizophrenia.
  • CBT: Cognitive behavioral therapy has been used in schizophrenia patients to improve cognitive distortions, reduce distractibility, and correct errors in judgment.
  • Vocational Therapy: Enabling patients to become gainfully employed is both a means toward, and a sign of, recovery.
221
Q

What is assertive community treatment?

A

These include home delivery of medications, monitoring of mental and physical health, in vivo social skills, and frequent contact with family members. There is a high staff-to-patient ratio (1:12). ACT programs can effectively decrease the risk of rehospitalization for persons with schizophrenia, but they are labor-intensive and expensive programs to administer

222
Q

Ways to improve compliance with antipsychotics?

A
  • Establish links between treatment and attainment of goals, avoid S/E, involve patient and family in med decisions, improve anxiety, depression and sense of well-being. Can use a depot (injectable antipsychotic)
  • Long-acting forms of risperidone, paliperidone, aripiprazole, and olanzapine are also available.
  • CTO
223
Q

What is schizophreniform disorder

A

Schizophreniform disorder differs from schizophrenia in that the symptoms have a duration of at least 1 month but less than 6 months

224
Q

Prognosis of schizophreniform disorder

A

One-third of patients recover completely; two-thirds progress to schizoaffective disorder or schizophrenia.

225
Q

Diagnosis (DSM-5 Criteria) of schizoaffective disorder

A
  • Meet criteria for either a major depressive or manic episode during which psychotic symptoms consistent with schizophrenia are also met.
  • Delusions or hallucinations for 2 weeks in the absence of mood disorder symptoms (this criterion is necessary to differentiate schizoaffective disorder from a mood disorder with psychotic features).
  • Mood symptoms present for a majority of the psychotic illness.
  • Symptoms not due to the effects of a substance (drug or medication) or another medical condition.
226
Q

Treatment of schizoaffective disorder

A
  • Hospitalization (if necessary) and supportive psychotherapy.
  • Medical therapy: Antipsychotics (second-generation medications may target both psychotic and mood symptoms); mood stabilizers, antidepressants, or electroconvulsive therapy (ECT) may be indicated for treatment of mood symptoms.
227
Q

What are the two subtypes of schizoaffective disorder and who is more likely to have them?

A
  • Bipolar type (+manic) – young, better prognosis

- Depressive type (-manic) – old, worse prognosis

228
Q

Treatment of Brief Psychotic Disorder

A

Brief hospitalization (usually required for workup, safety, and stabilization), supportive therapy, course of antipsychotics for psychosis, and/or benzodiazepines for agitation.

229
Q

Diagnosis (DSM-5 Criteria) of brief psychotic disorder

A
  • Patient with psychotic symptoms as in schizophrenia; however, the symptoms last from 1 day to 1 month, and there must be eventual full return to premorbid level of functioning. Symptoms must not be due to the effects of a substance (drug or medication) or another medical condition
  • There may also be a precipitating traumatic event.
230
Q

Risk factors of delusional disorder

A

Delusional disorder occurs more often in middle-aged or older patients (after age 40). Immigrants, the hearing impaired, and those with a family history of schizophrenia are at increased risk.

231
Q

Diagnosis (DSM-5 Criteria) of delusional disorder

A
  • A: One or more delusions (fixed and firm) for 1 month
  • B: Hallucinations if present are not prominent and related to delusional theme
  • C: Apart from the impact of delusions, functioning is not markedly impaired and behaviour is not obvious or bizarre
232
Q

Treatment of delusional disorder

A

Difficult to treat, especially given the lack of insight and impairment. Antipsychotic medications are recommended despite somewhat limited evidence. Supportive therapy is often helpful.

233
Q

Define drug abuse

A

Drug use that deviates from the approved social or medical pattern, usually causing impairment or disruption to function in self or others

234
Q

Pathophysiology of substance disorders?

A

Almost all drugs (and activities) of abuse increase dopamine in the nucleus accumbens, an action that contributes to their euphoric properties and, with repeated use, to their ability to change signaling pathways in the brain’s reward system

235
Q

What are the different forms dependence can manifest?

A
  • behavioural: substance-seeking activities and pathological use patterns
  • physical: physiologic withdrawal effects without use
  • cognitive: continuous or intermittent cravings for the substance to avoid dysphoria or attain drug state
236
Q

Etiology of substance disorders?

A

Substance use disorders arise from multifactorial interactions between genes (personality, neurobiology) and environment (low socioeconomic status, substance-using peers, abuse history, chronic stress)

237
Q

Diagnosis (DSM-5 Criteria) of substance use disorders?

A

PEC WITH MCAT

  • use despite Physical or psychological problem (i.e. alcoholic liver disease or cocaine related nasal problems)
  • failures 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 Hazardous situations
  • More substance used or for longer period than intended
  • unsuccessful attempts to Cut down
  • Activities given up due to substance
  • excessive Time spent on using or finding substance
238
Q

Investigations of substance use disorders?

A
  1. Stimulant toxidrome
    - Urine General Toxicology Panel (UGTP)
    - Blood glucose
    - Acetaminophen and salicylate levels (ACET, SAL)
    - ECG
    - Pregnancy test in women of childbearing age
  2. Alcohol intoxication
    - Blood Alcohol Level (ETOH)
    - Electrolytes and Blood glucose
  3. Diagnostic tools
239
Q

Treatment options for substance use disorder?

A
  • Behavioral counseling should be part of every substance use disorder treatment.
  • Psychosocial treatments are effective and include motivational intervention (MI), cognitive-behavioral therapy (CBT – SMART recovery), contingency management, and individual and group therapy.
  • Reddit subgroup – stopdrinking
  • Poundmaker’s or Henwood treatment programs
  • Ponoka Concurrent Disorders Program
  • Twelve-step groups such as Alcoholics Anonymous (AA) and Narcotics Anonymous (NA) should also be encouraged as part of the treatment.
  • Al-Anon Family Groups
240
Q

Nicotine withdrawal symptoms?

A

Intense craving, dysphoria, anxiety, poor concentration, increase in appetite, weight gain, irritability, restlessness, and insomnia.

241
Q

Nicotine use disorder treatments?

A
  • Varenicline (Chantix):
  • Bupropion (Zyban or Wellbutrin):
  • Nicotine replacement therapy (NRT): Available as transdermal patch, gum, lozenge, nasal spray, and inhaler.
  • Behavioral support/counseling should be part of every treatment. Relapse after abstinence is common.
242
Q

MOA of varenicline (Chantix)?

A

Partial nicotinic receptor agonist, and partial nicotinic receptor competitive antagonist

243
Q

Side effects of varenicline (Chantix)?

A

Nausea, vomiting, constipation, headache, dream disorder, insomnia, increased risk of psychosis, depression, suicidal ideation

244
Q

MOA of bupropion (Zyban or Wellbutrin)?

A

Inhibits re-uptake of dopamine and/or norepinephrine

245
Q

Side effects of bupropion (Zyban or Wellbutrin)?

A

Insomnia, dry mouth

246
Q

Contraindications of bupropion (Zyban or Wellbutrin)?

A

Seizure disorder, Eating disorder, MAOI use in past 14 d, Simultaneous use of bupropion (Wellbutrin®) for depression

247
Q

Use NRT cautiously with?

A

Use with caution: immediately post-MI, worsening angina, arrhythmia

248
Q

Asians often have less _____, resulting in flushing and nausea with alcohol use.

A

Aldehyde dehydrogenase

249
Q

What is the CAGE questionnaire?

A
  • 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 morning (Eye opener)?

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

250
Q

Most adults will show some signs of intoxication with BAL ___ and obvious signs with BAL ____.

A

> 100 mg/dL

> 150 mg/dL

251
Q

Stage 1 (onset 4-12 h after last drink) alcohol withdrawal?

A

“The shakes” tremor, sweating, agitation, anorexia, cramps, diarrhea, sleep disturbance, anxiety, insomnia, headache

252
Q

Stage 2 (onset 12-24 h) alcohol withdrawal?

A

Alcoholic hallucinosis: visual, auditory, olfactory or tactile hallucinations

253
Q

Treatment of alcohol intoxication

A
  • Parenteral thiamine (to prevent or treat Wernicke’s encephalopathy) and folate. Remember thiamine must be given before glucose, as it’s a necessary cofactor for glucose metabolism.
  • Naloxone may be necessary to reverse effects of co-ingested opioids.
  • A computed tomography (CT) scan of the head may be necessary to rule out subdural hematoma or other brain injury.
  • Severely intoxicated patients may require mechanical ventilation with attention to acid-base balance, temperature, and electrolytes while they are recovering.
254
Q

Risk factors of delirium tremens?

A
  • A history of sustained drinking
  • A history of alcohol withdrawal seizures
  • A history of DT
  • Age greater than 30
  • The presence of a concurrent illness
  • The presence of significant alcohol withdrawal in the presence of an elevated blood alcohol concentration
  • A longer period since the last drink
255
Q

Stage 3 (onset 24-48 h) alcohol withdrawal?

A

Alcohol withdrawal seizures, usually tonic-clonic, non-focal, and brief

256
Q

Symptoms of delirium tremens?

A

DT is defined by hallucinations, disorientation, tachycardia, hypertension, hyperthermia, agitation, and diaphoresis in the setting of acute reduction or abstinence from alcohol.

257
Q

Stage 4 (onset 48-72 h) of alcohol withdrawal?

A

Delirium tremens, confusion, delusions, hallucinations, agitation, tremors, autonomic hyperactivity (fever, tachycardia, HTN)

258
Q

Onset of delirium tremens?

A

DT typically begins between 48 and 96 hours after the last drink and lasts one to five days

259
Q

Clinical Institute Withdrawal Assessment for Alcohol (CIWA-A) scoring system, areas of assessment include:

A
  • physical (5): nausea and vomiting, tremor, agitation, paroxysmal sweats, headache/fullness in head
  • psychological/cognitive (2): anxiety, orientation/clouding of sensorium
  • perceptual (3): tactile disturbances, auditory disturbances, visual disturbances
260
Q

Basic treatment protocol for alcohol withdrawal

A
  • Diazepam 20 mg PO q1-2h prn until CIWA-A <10 points
  • Thiamine 100 mg IM then 100 mg PO OD for 3 d
  • Supportive care (hydration and nutrition)
  • Hypomagnesemia may predispose to seizures; thus, it should be corrected promptly.
261
Q

If age >65 or patient has severe liver disease, severe asthma or respiratory failure use what for alcohol withdrawal

A
  • Use a short acting benzodiazepine Lorazepam PO/SL/IM 1-4 mg q1-2h
262
Q

If history of withdrawal seizures use what for alcohol withdrawal

A
  • Diazepam 20 mg PO q1h for minimum of three doses regardless of subsequent CIWA scores
263
Q

What is Wernicke-Korsakoff Syndrome?

A

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

264
Q

Korsakoff’s syndrome symptoms?

A

Anterograde amnesia and confabulation (unconsciously making up answers when memory has failed); cannot occur during an acute delirium or dementia and must persist beyond usual duration of intoxication/withdrawal

265
Q

Wernicke’s encephalopathy triad?

A

Triad of oculomotor dysfunction such as nystagmus (CN VI palsy), gait ataxia, and confusion

266
Q

Management of Wernicke-Korsakoff Syndrome?

A
  • Wernicke’s preventative treatment (any patient in withdrawal): thiamine 100-250mg IM/IV x 1 dose
  • Wernicke’s acute treatment: thiamine 500 mg IV BID/TID x 72,h then reassess
  • Korsakoff’s: IV treatment as for Wernicke’s followed by thiamine 100mg PO TID x3-12mo
267
Q

Investigations of alcohol use disorder?

A
  • BAL
  • GGT and MCV for baseline and follow-up monitoring
  • AST, ALT (usually AST:ALT approaches 2:1 in an alcoholic)
  • CBC (anemia, thrombocytopenia), INR (decreased clotting factor production by liver)
268
Q

Treatment of alcohol use disorder?

A
  • Naltrexone: Effective in reducing EtOH consumption (IF STILL DRINKING) but less effective in promoting abstinence
  • Acamprosate: Major advantage is that it can be used in patients with liver disease.
  • Disulfiram - enhances negative effects of EtOH by inhibiting acetaldehyde dehydrogenase ‚ acetaldehyde accumulation when EtOH consumed ‚adverse symptoms (flushing, tachycardia, hypotension, sweating, SOB, nausea, vomiting)
  • Topiramate – used for maintenance, helps reduce cravings
269
Q

MOA of naltrexone

A

mu-opioid antagonist, blocks dopaminergic response involved with EtOH consumption, reduces positive reinforcement effects of EtOH.

270
Q

MOA of acamprosate

A

NMDA glutamate receptor antagonist

271
Q

Symptoms of opioid intoxication

A

Drowsiness, nausea/vomiting, constipation, slurred speech, constricted pupils, seizures, and respiratory depression, which may progress to coma or death in overdose.

272
Q

Treatment of opioid intoxication

A
  • ABCs
  • IV glucose
  • naloxone hydrochloride (Narcan): 0.4 mg up to 2 mg IV for diagnosis
  • Intubation and mechanical ventilation, ¬± naloxone drip, until patient alert without naloxone (up to >48 h with long-acting opioids)
273
Q

____ is the exception to opioids producing miosis.

A

Meperidine is the exception to opioids producing miosis. “Demerol Dilates pupils”

274
Q

Opioid withdrawal symptoms?

A

Dysphoric mood, insomnia, drug-craving, myalgias, nausea or vomiting, yawning, chills, lacrimation, rhinorrhea, pupillary dilation, piloerection, sweating, diarrhea, fever

275
Q

Onset of opioid withdrawal symptoms?

A

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

276
Q

Treatment of opioid withdrawal?

A
  • Moderate symptoms: Symptomatic treatment with clonidine (for autonomic signs and symptoms of withdrawal), nonsteroidal anti- inflammatory drugs (NSAIDs) for pain, loperamide for diarrhea, dicyclomine for abdominal cramps, etc.
  • Severe symptoms: Detox with buprenorphine or methadone.
277
Q

Treatment of opiate use disorder?

A
  • Buprenorphine (1st line) - can precipitate withdrawal if used too soon after full opioid agonists. comes as Suboxone, which contains buprenorphine and naloxone; this preparation prevents intoxication from intravenous injection.
  • Methadone (2nd line) - Restricted to federally licensed substance abuse treatment programs.
  • Naltrexone - precipitates withdrawal if used within 7 days of heroin use. Either daily oral medication or monthly depot injection. It is a good choice for highly motivated patients such as health care professionals
  • Naloxone – full antagonist. Works minutes to hours. No restrictions
278
Q

MOA of buprenorphine?

A

Partial opioid receptor agonist

279
Q

Can cause Qtc interval prolongation: screening electrocardiogram is indicated

A

Methadone

280
Q

MOA of methadone?

A

Long-acting opioid receptor agonist

281
Q

MOA of naltrexone?

A

Competitive opioid antagonist

282
Q

MOA of cocaine

A

Cocaine blocks the reuptake of dopamine, epinephrine, and norepinephrine from the synaptic cleft, causing a stimulant effect.

283
Q

Signs and symptoms of cocaine intoxication?

A

Euphoria, heightened self-esteem, increase or decrease in blood pressure, tachycardia or bradycardia, nausea, dilated pupils, weight loss, psychomotor agitation or depression, chills, and sweating.

284
Q

Signs and symptoms of a cocaine overdose?

A

Seizures, cardiac arrhythmias, hyperthermia, paranoia, and hallucinations (especially tactile). Since cocaine is an indirect sympathomimetic, intoxication mimics the fight-or-flight response.

285
Q

Management of cocaine overdose/intoxication?

A
  • For mild-to-moderate agitation and anxiety: Reassurance of the patient and benzodiazepines (IV diazepam)
  • For severe agitation or psychosis: Antipsychotics (e.g., haloperidol).
  • Symptomatic support (i.e., control hypertension, arrhythmias).
  • Temperature of >102F should be treated aggressively with an ice bath, cooling blanket, and other supportive measures.
286
Q

Signs and symptoms of cocaine withdrawal?

A
  • Initial “crash” (1-48h): increased sleep, increased appetite, dysphoria
  • Withdrawal (1-10wk): dysphoric mood plus fatigue, irritability, vivid unpleasant dreams, insomnia or hypersomnia, psychomotor agitation or retardation
287
Q

Symptoms of amphetamine intoxication

A

Euphoria, dilated pupils, increased libido, tachycardia, perspiration, grinding teeth, and chest pain, psychomotor agitation or retardation

288
Q

Symptoms of amphetamine overdose

A

Cause hyperthermia, dehydration (especially after a prolonged period of dancing in a club), rhabdomyolysis, and renal failure (monitor CK and for acute kidney injury). Amphetamine withdrawal can cause prolonged depression.

289
Q

Treatment of amphetamine intoxication?

A

Rehydrate, correct electrolyte balance, and treat hyperthermia.

290
Q

Symptoms of amphetamine withdrawal?

A

Dysphoric mood and 2+ of the following developing within a few hours to days

  • Fatigue
  • Vivid, unpleasant dreams
  • Insomnia or hypersomnia
  • Increase appetite
  • Psychomotor retardation or agitation
291
Q

What is sexual desire?

A

Energy that allows an individual to initiate or respond to sexual stimulation

292
Q

What is sexual arousal?

A

Physical and emotional stimulation leading to breast and genital vasodilation and clitoral engorgement

293
Q

What is an orgasm?

A

Physical and emotional stimulation is maximized, allowing the individual to relinquish their sense of control

294
Q

What is sexual resolution?

A

Most of the congestion and tension resolves within seconds, complete resolution may take up to 60 min

295
Q

Criteria for sexual dysfunction disorders?

A
  • The disorder causes clinically significant distress.
  • The dysfunction is not better explained by a nonsexual mental disorder, as a consequence of severe relationship distress or other stressors, and not attributable to the effects of a substance/medication or another medical condition.
296
Q

Etiology of erectile or orgasmic dysfunctions

A
  • Psychological or emotional - depression, abuse
  • Neurologic dysfunction - spinal cord injury
  • Vascular insufficiency – diabetes, atherosclerosis
  • Drug adverse effects - B-blockers
  • Aging
297
Q

Diagnostic criteria for erectile disorder?

A

Marked difficulty obtaining or maintaining an erection, or marked decreased in erectile rigidity for more than 6 months. Commonly referred to as erectile dysfunction (ED) or impotence.

298
Q

Non-invasive treatment of erectile disorder?

A
  • lifestyle changes (alcohol, smoking), psychological (sexual counselling and education)
  • change precipitating medications
  • treat underlying causes (DM, CVD, HTN, endocrinopathies)
299
Q

Pharmacological treatment of erectile disorder?

A

Phosphodiesterase-5 inhibitors (e.g., sildenafil) are given orally, which enhance blood flow to the penis; they require psychological or physical stimulation to achieve an erection. Alprostadil, either injected into the corpora cavernosa or transurethral, acts locally; it produces an erection within 2 to 3 minutes and works in the absence of sexual stimulation.

300
Q

Diagnostic criteria of premature (early) ejaculation

A

Recurrent pattern of ejaculation during sex within 1 minute and before the individual wishes it for more than 6 months.

301
Q

Treatment of premature (early) ejaculation

A

SSRIs and tricyclic antidepressants (TCAs) pro-long the time from stimulation to orgasm – common side effect of SSRIs. Squeeze technique

302
Q

Diagnoistic criteria of genito-pelvic pain or penetration issues (dyspareunia)

A

Persistent or recurrent difficulties in one of the following: vaginal penetration during intercourse, marked vulvovaginal or pelvic pain during intercourse or penetration, marked anticipatory fear or anxiety about vulvovaginal or pelvic pain, or marked tensing or tightening of pelvic floor muscles during attempted vaginal penetration for more than 6 months.

303
Q

Etiology of genito-pelvic pain or penetration issues (dyspareunia)

A
  • Trauma - episiotomy
  • Hormonal - vulvovaginal atrophy postmenopause – decreased levels of estrogen
  • Other pelvic pathology - endometriosis, pelvic inflammatory disease (pelvic adhesions), vaginismus, vulvodynia
304
Q

Treatment of genito-pelvic pain or penetration issues (dyspareunia)

A
  • Kegel and reverse Kegel exercises
  • dilator treatment
  • comfort with self-exam
  • psychotherapy, other behavioural techniques
  • female on top position: allows for control of speed and duration
  • vestibulitis: remove local irritants, change in contraceptive methods, dietary changes (increased citrate, decreased oxalate), and vestibulectomy (rare)
  • vulvodynia: local moisturization, cold compresses, systemic nerve-blocking therapy (amitriptyline, gabapentin) orally or topically, topical anesthetics, estrogen cream
  • pain clinic
  • removal of environmental factors: bubble baths, soaps, perfumes, sanitary pads with plastic lining
305
Q

Etiology of substance- or medication-induced sexual dysfunction

A
  • Alcohol, sedatives
  • Antihypertensives, anticholinergics, antidepressants (especially selective serotonin reuptake inhibitors [SSRIs]), and anti psychotics
306
Q

Diagnosis (DSM-5 Criteria) of gender dysphoria?

A
  • A marked incongruence between one’s experienced/expressed gender and assigned gender, of at least 6 months’ duration, as manifested by at least two of the following:
    1. A marked incongruence between one’s experienced/expressed gender and primary and/or secondary sex characteristics (or in young adolescents, the anticipated secondary sex characteristics).
    2. A strong desire to be rid of one’s primary and/or secondary sex characteristics because of a marked incongruence with one’s experienced/expressed gender (or in young adolescents, a desire to prevent the development of the anticipated secondary sex characteristics).
    3. A strong desire for the primary and/or secondary sex characteristics of the other gender.
    4. A strong desire to be of the other gender (or some alternative gender different from one’s assigned gender).
    5. A strong desire to be treated as the other gender (or some alternative gender different from one’s assigned gender).
    6. A strong conviction that one has the typical feelings and reactions of the other gender (or some alternative gender different from one’s assigned gender).
  • The condition is associated with clinically significant distress or impairment in social, occupational, or other important areas of functioning.
307
Q

Requirements to have gender affirmation surgery covered by Alberta Health

A
  • Permanent resident of Canada and in Alberta for at least 12 months
  • > 18 YOA
  • Registration of intent form submitted by psychiatrist
  • Diagnosed with gender dysphoria by a psychiatrist
  • Preliminary surgeries completed (?hysterectomy, mastectomy, etc)
  • Completion of at least 12 months appropriate hormone therapy
  • Completion of at least 12 months of “real-life experience” (incl name change)
  • Letters from 2 psychiatrists that confirm patient is physically fit, psychologically prepared for surgery, no substance abuse, adequate support network
  • Must not have an axis 1 psychiatric disorder (anxiety, major depression) that is symptomatic or likely to become so
  • Must not have significant problems with personality disorder (acting out, antisocial)
308
Q

Hormonal treatment for male transition to female?

A

Antiandrogen therapy (spironolactone or cyproterone acetate) or GnRH agonist therapy, combined with estrogen therapy (transdermal or oral 17-beta-estradiol).

309
Q

Hormonal treatment for female transition to male?

A

Either testosterone esters (IM or SQ) or testosterone gels, depending upon pt preference. Higher testosterone levels are more easily achieved with parenteral therapy

310
Q

Define paraphilic disorders?

A

Intense and persistent sexual arousal that is elicited by something other than genital stimulation or preparatory fondling with phenotypically normal, physically mature, consenting human partners

311
Q

Treatment paraphilic disorders?

A
  • anti-androgen drugs
  • behaviour modification
  • psychotherapy
312
Q

Diagnostic criteria for female sexual interest/arousal disorder

A

Absence or reduced sexual interest, thoughts/fantasies, initiation of sex, sexual excitement/pleasure, sexual arousal, and/or genital/nongenital sensations during sex for more than 6 months (unclear prevalence of DSM-5 disorder, but low sexual desire in up to 26-43% of women).

313
Q

Diagnostic criteria for male hypoactive sexual desire disorder

A

Absence or deficiency of sexual thoughts, desire, or fantasies for more than 6 months (occurs in 5% of men).

314
Q

Treatment of male/female arousal disorders

A

Testosterone is used as replacement therapy for men with low levels. Low doses may also improve libido in women, especially in postmenopausal women. Low-dose vaginal estrogen replacement may improve vaginal dryness and atrophy in postmenopausal women.

315
Q

Diagnostic criteria of female orgasmic disorder

A

Marked delay in infrequency/absence/reduced intensity of orgasm for more than 6 months.

316
Q

Diagnostic criteria of delayed ejaculation

A

Marked delay in infrequency/absence of ejaculation for more than 6 months. Estimated prevalence likely less than 1%.

317
Q

Treatment of female orgasmic disorder

A

Self-exploration/pleasuring, relationship therapy if needed, bridging techniques (different sexual positions, clitoral stimulation during intercourse)

318
Q

What are the types of mood disorders

A
  • depressive (major depressive disorder, persistent depressive disorder)
  • bipolar (bipolar I/II disorder, cyclothymia)
  • induced by or due to (“secondary to”) a general medical condition, substance, medication, other psychiatric condition
319
Q

Medical workup of mood disorder

A
  • Routine screening: physical exam, CBC, extended electrolytes, renal, liver and thyroid function tests, drug screen, medications list
  • Additional screening: B12 (in older people), neurological consultation, chest X-ray, ECG, head imaging
320
Q

DSM-5 Diagnostic Criteria for major depressive episode

A
  • Criterion A: > 5 Sx must include depressed OR loss of interest/pleasure for 2 wks: Depressed mood + SIGECAPS (suicidality [thoughts/plan/intent], interest/pleasure (loss of), guilt (worthlessness, hopelessness, psychosis), energy (loss of), concentration (loss of/indecisive), appetite/weight changes, psychomotor retardation/agitation, sleep changes (insomnia/hypersomnia).
  • B. the symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning
  • C. the episode is not attributable to the direct physiological effects of a substance or a GMC
321
Q

DSM-5 Diagnostic Criteria for manic episode

A
  • Criterion A: Manic episode (Need to have one for Bipolar I) involves a distinct period of abnormal/persistent elevated, expansive or irritable mood + abnormally increased goal-directed activity or energy for at least 1 week present for most of the day, nearly every day
  • Criterion B: with ≥3sx or ≥4sx if irritable mood: DIGFAST – distractibility, increased goal-directed activity, grandiosity, flight of ideas/racing, activities pleasurable with painful consequences (e.g. spending lots), talkative, sleep (rested after 3h).
  • Criterion C: The mood disturbance is sufficiently severe to cause marked impairment in social or occupational functioning or to necessitate hospitalization to prevent harm to self or others, or there are psychotic features.
  • Criterion D: The episode is not attributable to the physiological effects of a substance (e.g., a drug of abuse, a medication, or there are psychotic features.
322
Q

Hypomanic episode criteria:

A
  • Criterion A: A distinct period of abnormally and persistently elevated, expansive, or irritable mood and abnormally and persistently increased activity or energy, lasting at least 4 consecutive days and present most of the day, nearly every day.
  • Criterion B: with ≥3sx or ≥4sx if irritable mood: DIGFAST – distractibility, increased goal-directed activity, grandiosity, flight of ideas/racing, activities pleasurable with painful consequences (e.g. spending lots), talkative, sleep (rested after 3h).
  • Criterion C: The episode is associated with an unequivocal change in functioning that is uncharacteristic of the individual when not symptomatic.
  • Criterion D: The disturbance in mood and the change in functioning are observable by others.
  • Criterion E: The episode is not severe enough to cause marked impairment in social or occupational functioning or to necessitate hospitalization. If there are psychotic features, the episode is, by definition, manic.
323
Q

DSM-5 Diagnostic Criteria for Major Depressive Disorder (MDD)

A
  • Criterion A. presence of a MDE
  • Criterion B: major depressive episode not better explained by schizophrenia spectrum/psychotic disorders
  • Criterion C: there has never been manic/hypomanic episode (this exclusion does not apply if episodes substance-induced or attributable to another condition)
324
Q

Which SIGECAPS symptoms are more common in younger and older patients?

A

Hypersomnia + hyperphagia more common if younger vs. psychomotor disturbances if older

325
Q

What is the definition of MDE with mood-congruent psychotic features

A

The content of all delusions and hallucinations is consistent with the typical depressive themes of personal inadequacy, guilt, disease, death, nihilism, or deserved punishment.

326
Q

What is the definition of MDE with mood-incongruent psychotic features

A

The content of the delusions or hallucinations does not involve typical depressive themes of personal inadequacy, guilt, disease, death, nihilism, or deserved punishment, or the content is a mixture of mood-incongruent and mood-congruent themes.

327
Q

What is the definition of MDE with catatonia

A

The catatonia specifier can apply to an episode of depression is catatonic features are present during most of the episode.

328
Q

What is the definition of MDE with peripartum onset

A

This specifier can be applied to the current of, if full criteria are not currently met for a major depressive episode, most recent episode of major depression if onset of mood symptoms occurs during pregnancy or in the 4 weeks following delivery.

329
Q

Strongest predictor of PDD is ______

A

MDD during pregnancy

330
Q

Treatment of MDE with peripartum onset

A

Meds used when risk to mom/fetus of MDD outweighs risk of pharmacotherapy (sertraline low levels in breast milk, if smoker bupropion, use whatever has worked in the past as first line!)

331
Q

What is recurrent MDD?

A

Recurrent is classified as the patient having two or more distinct MDE episodes; to be considered separate the patient must have gone 2 consecutive months without meeting criteria

332
Q

Epidemiology of Major Depressive Disorder (MDD)?

A

Lifetime prevalence 12% (highest prevalence out of all psychiatric disorders), 2x higher incidence in women, mean onset is 40s - 50 percent of all patients having an onset between the ages of 20 and 50 years. More common in rural than urban areas

333
Q

Biological etiology of Major Depressive Disorder (MDD)?

A
  • genetic: 65-75% MZ twins; 14-19% DZ twins, 2-4 fold increased risk in first-degree relatives
  • neurotransmitter dysfunction: decreased activity of 5-HT, NE, and DA at neuronal synapse; changes in GABA and glutamate; various changes detectable by fMRI
  • neuroendocrine dysfunction: abnormal HPA axis activity
  • neuroanatomy and neurophysiology: decreased hippocampal volume, increased size of ventricles; decreased REM latency and slow-wave sleep; increased REM length
  • immunologic: increased pro-inflammatory cytokines IL-6 and TNF
  • secondary to medical condition, medication, substance use disorder
334
Q

Psychosocial etiology of Major Depressive Disorder (MDD)?

A
  • cognitive (i.e. distorted schemata, Beck’s cognitive triad: negative views of the self, the world, and the future)
  • environmental factors (i.e. job loss, bereavement, history of abuse or neglect, early life adversity)
  • comorbid psychiatric diagnoses (i.e. anxiety, substance abuse, developmental disability, dementia, eating disorder)
335
Q

Risk factors of Major Depressive Disorder (MDD)?

A
  • sex: F>M, 2:1
  • family history: depression, alcohol abuse, suicide attempt or completion
  • childhood experiences: loss of parent before age 11, negative home environment (abuse, neglect)
  • personality: neuroticism, insecure, dependent, obsessional
  • Recent stressors: illness, financial, legal, relational, academic
  • Lack of intimate, confiding relationships or social isolation
  • Low socioeconomic status
336
Q

Unique clinical features of depression seen in elders?

A

Somatic complaints, anhedonia, apathy, psychomotor retardation, cognitive changes

337
Q

Comorbidity of Major Depressive Disorder (MDD)?

A
  • Anxiety, a common symptom of depression, affects as many as 90 percent of all depressed patients. Social anxiety disorder, OCD, panic disorder
  • Alcohol use disorder
  • Depressed patients often use stimulants, such as cocaine and amphetamines, to relieve their depression
338
Q

Treatment of depression in elderly?

A
  • Biological: SSRI or mirtazapine – usually start at ½ the regular dose, titration is slower, osteoporosis and bleeding are some S/E to watch out for, ECT is a valid option
  • Psychological: CBT
  • Social: Day Programs, Support Groups
339
Q

Treatment of MDD in pregnancy?

A
  • Mild/moderate MDD – CBT or IPT (2nd line meds listed next).
  • Severe MDD – Sertraline (first line), citalopram. Psychotherapy as monotherapy NOT recommended, ECT not first-line but considered if psychotic or treatment-resistant
340
Q

Children and adolescents can have ___ mood instead of depressed mood to fulfill MDD criteria

A

irritable

341
Q

Depression with atypical features may be more common in youth

A

Mood reactivity (mood brightens in response) 2 or more of: significant weight gain or increase in appetite, hypersomnia, leaden paralysis, longstanding pattern of interpersonal rejection sensitivity

342
Q

Treatment of depression in children and youth?

A
  • CBT and IPT are first line for mild and moderate
  • SSRIs are for more severe – fluoxetine (level 1). Escitalopram and sertraline (level 2)
  • SNRIs usually avoided
343
Q

First line treatment for MDD?

A
  • Selective serotonin reuptake inhibitors (SSRIs)
  • Venlafaxine (Effexor), Desvenlafaxine (SNRI) – dose-dependent effects for depression: serotonin effects <150mg, norepinephrine effects >150mg. HTN and sweaty at higher doses. Better for depression than anxiety
  • NE/DA reuptake inhibitor (NDRI): bupropion lower SE profile; can be added to SSRIs but worsens anxiety!
344
Q

Side effects of SSRIs?

A

GI upset, insomnia, headache. Weight gain, sexual dysfunction. Withdrawal syndrome, serotonin syndrome, hyponatremia, RLS

345
Q

Examples of selective serotonin reuptake inhibitors (SSRIs)?

A
  • Fluoxetine (Prozac) – longest half-life (one week), effective for bulimia, first line SSRI for youth age 10-21. Weight neutral.
  • Sertraline – most diarrhea of SSRIs
  • Citalopram (SSRI) – least drug interactions, can’t use citalopram > 40mg or escitalopram > 20 mg→ increased QT interval→ Torsades de pointes. Can cause seizures
346
Q

S/E profile of bupropion?

A

No sexual SE, less weight gain, no emotional blunting/anhedonia, facilitates smoking cessation

347
Q

Lifestyle treatments for MDD?

A

Increased aerobic exercise, mindfulness-based stress reduction

348
Q

Second line treatment for MDD?

A

Tricyclic antidepressants (TCAs): (imipramine, nortriptyline (norepinephrine), amitriptyline - sedation, clomipramine (serotonin) - OCD)

349
Q

Side effects of tricyclic antidepressants (TCAs)?

A

Anticholinergic SEs, cardiac toxicity lethal if OD.

350
Q

Third line treatment for MDD?

A
  • Monoamine oxidase inhibitors (MAOIs): stops monoamines from being broken down (phenelzine, tranylcypromine)
  • Maca root (women) and SAMe (men) may help sexual SE
  • Modafinil: may help with fatigue + apathy
  • Used in treatment resistant
351
Q

Monoamine oxidase inhibitors (MAOIs) side effects?

A

Hypertension crisis, temp, increased HR + arrhythmia, must avoid tyramine containing foods (aged cheese, fermented/dried meat, beers on tap, soy)

352
Q

Psychotherapy for MDD?

A

CBT or IPT alone can be used for mild depression; combined with SSRI for mod/severe

353
Q

First-line recommendation to patients with MDD who failed at least 1 AD

A

rTMS

354
Q

Side effects of ECT

A

Possible loss of memory, anesthesia complications.

355
Q

When to use ECT?

A

Not responding to/not wanting meds, prior favourable response, need a rapid fix (acute suicidal, catatonic), needing acute changes during pregnancy (suicidal, catatonic, severe sx…) or in general, any psychotic MDD!

356
Q

What is discontinuation syndrome?

A

FINISH (flu-like symptoms, insomnia, neurological symptoms, irritability, sensory symptoms, hyperactivity).

357
Q

What is serotonin syndrome?

A

SHIVERS (shivering, hyperreflexia, increased temperature, vital sign instability, encephalopathy, restlessness and sweating)

358
Q

Severe discontinuation syndrome with which antidepressants?

A

Severe discontinuation with paroxetine (Paxil) and venlafaxine (SNRI):

359
Q

Approach to starting antidepressants for MDD?

A

Try the above SSRIs, then reassess every 1-2 weeks for 3-4 weeks; full response? Continue

360
Q

For Partial/Non-Response after 3-4 weeks on antidepressants for MDD?

A
  • Optimize dose, then reassess regularly for 4-8 weeks; full response? Continue
  • No-Response: change class
  • Partial Response: add agent (bupropion or other SN or SSRI) or augment (risperidone, quetiapine-XR, aripiprazole, lithium)
  • Switch vs Adjunctive: Consider switch AD when: first trial, poorly tolerated, no response to initial AD, more time to wait for response
361
Q

How long should antidepressant treatment should be maintained for in MDD?

A

Antidepressant treatment should be maintained for at least 6 months or the length of a previous episode, whichever is greater. Ongoing management should include assessment in key domains (school, home, social settings), reassessment and referral recommended if no improvement after 6-8 weeks of treatment

362
Q

DSM-5 Diagnostic Criteria for Persistent Depressive Disorder

A
  • Criterion A: Depressed mood for most of the day, for more days than not, as indicated by either subjective account or observation by others, for at least 2 years.
  • Criterion B: Presence, while depressed, of two (or more) of the following:
    • Poor appetite or overeating.
    • Insomnia or hypersomnia.
    • Low energy or fatigue.
    • Low self-esteem.
    • Poor concentration or difficulty making decisions.
    • Feelings of hopelessness.
  • Criterion C: During the 2-year period (1 year for children or adolescents) of the disturbance, the individual has never been without the symptoms in Criteria A and B for more than 2 months at a time.
  • Criterion D: Criteria for a major depressive disorder may be continuously present for 2 years
  • Absence of manic/hypomanic episodes, not better explained by schizophrenia/substances/illnesses
363
Q

Treatment of Persistent Depressive Disorder

A
  1. Psychological
    - traditionally, psychotherapy was the principal treatment for persistent depressive disorder; recent evidence suggests some (but generally inferior) benefit for pharmacological treatment. Combinations of the two may be most efficacious
  2. Biological
    - antidepressant therapy: SSRIs (i.e. sertraline, escitalopram), TCAs (i.e. nortiptyline)
364
Q

In distinguishing grief from a major depressive episode (MDE), it is useful to consider that in grief the predominant affect is feelings of ____, while in MDE it is ____.

A
  • emptiness and loss

- persistent depressed mood and the inability to anticipate happiness or pleasure.

365
Q

Bereavement/Grief vs MDE

A
  • The dysphoria in grief is likely to decrease an intensity over days to weeks and occurs in waves, the so-called pangs of grief. These waves tend to be associated with thoughts or reminders of the deceased.
  • The depressed mood of MDE is more persistent and not tied to specific thoughts or preoccupations.
  • The pain of grief may be accompanied by positive emotions and humor that are uncharacteristic of the pervasive unhappiness and misery characteristic of MDE.
  • The thought content associated with grief generally features a preoccupation with thoughts and memories of the deceased rather than the self-critical or pessimistic ruminations seen in MDE.
  • In grief, self-esteem is generally preserved, whereas in MDE feelings of worthlessness and self-loathing are common.
  • If a bereaved individual thinks about death and dying, such thoughts are general focused on the deceased and possibly “joining” the deceased, whereas in MDE, such thoughts are focused on ending one’s own life because of feeling worthless, undeserving of life, or unable to cope with the pain of depression.
366
Q

What is Bipolar I disorder

A
  • Disorder in which at least one manic episode has occurred
  • if manic symptoms lead to hospitalization, or if there are psychotic symptoms, the diagnosis is BP I
  • commonly accompanied by at least 1 MDE but not required for diagnosis
367
Q

What is Bipolar II disorder

A

Disorder in which there is at least 1 MDE, 1 hypomanic episode, and no manic episodes

368
Q

What are the 6 S’s you should ask about in Bipolar II disorder

A

6S’s – sex, sleep, socializing, spending, speeding, special projects

369
Q

What is bipolar disorder with melancholic features

A

Melancholia is sometimes referred to as “endogenous depression” or depression that arises in the absence of external life stressors or precipitants.

370
Q

What is bipolar disorder with catatonic features

A

The hallmark symptoms of catatonia—stuporousness, blunted affect, extreme withdrawal, negativism, and marked psychomotor retardation

371
Q

What is bipolar disorder with rapid cycling

A

Likely to be female and to have had depressive and hypomanic episodes. Patient must have at least four episodes within a 12-month period.

372
Q

Manic episodes are more common in __, and depressive episodes are more common in ___.

A

men

women

373
Q

Risk factors for switching from BP2 to mania:

A

2+ prior depressions, rapid cycling, Hx of suicide attempts, younger age, earlier age at onset. More manic symptoms during depressive episode

374
Q

Risk Factors for bipolar disorder?

A
  • Genetic: 60-65% of bipolar patients have family history of a major mood disorder, especially bipolar disorder
  • Clinical features of MDE history favouring bipolar over unipolar diagnosis: early age of onset (<25yr), increased number of MDEs, psychotic symptoms, postpartum onset, anxiety disorders (especially separation, panic), antidepressant failure due to early “poop out” or hypomanic symptoms, early impulsivity and aggression, substance abuse, cyclothymic temperament
375
Q

What is the suicide risk in bipolar disorder?

A

Suicide risk is 15-20x general pop

376
Q

Mood stabilizers used for the treatment of acute bipolar mania

A
  • Lithium
  • Valproic Acid
  • Carbamazepine
377
Q

Side effects of lithium

A
  • LITH: Leukocytosis, Insipidus (polyuria/dipsia – dose only once a day at bedtime (kidneys not as active overnight)), Tremor, Hypothyroidism
  • Others: GI upset (N/V), weight gain, cognitive slowing
378
Q

Lithium monitoring

A

Creatinine, TSH, Calcium. Within 9-12hours after dose, then 4-5d for steady state + check lithium levels. Pregnancy test, ECG (if >40) – brugada pattern. Do this 2x first 6months then 1x/year

379
Q

Which drugs will increase lithium levels

A

CANT drugs (Ca blockers, ACEi, NSAID, thiazides)

380
Q

Valproic acid monitoring

A

Need to follow: LFTs and platelets (thrombocytopenia). Do this 2x first 6months then 1x/year

381
Q

Side effects of valproic acid?

A

GI upset (nausea), sedation, tremor, alopecia

382
Q

Symptoms of lithium toxicity?

A

Symptoms may include a tremor, increased reflexes, N/V, trouble walking, kidney problems, and an altered level of consciousness

383
Q

Treatment of lithium toxicity?

A

Treat by stopping the lithium, rehydrating. Lithium levels drop by 50% in 24 hours. Severe toxicity use dialysis

384
Q

Side effects of carbamazepine

A

Rash - SJS, GI upset, sedation, ataxia, hyponatremia, hepatic inducer, agranulocytosis, teratogenic

385
Q

What should be checked with carbamazepine

A

CBC (agranulocytosis) + LFTs

386
Q

____ are first line treatment in someone who is acutely manic and are used in the short term while the mood stabilizers are titrated to therapeutic doses

A

Atypicals

387
Q

Examples of atypical antipsychotics?

A
  • Risperidone, Quetiapine, Aripiprazole (less weight gain), Ziprasidone, Asenapine, Lurasidone (Latuda)
  • Quetiapine: 1st line treatment, consider if diagnostic uncertainty and there are psychotic symptoms and sleep disturbances
388
Q

ECT can be considered first in acute bipolar mania if?

A

High suicide risk, psychotic bipolar depression, or if mood stabilizers are contraindicated – pregnancy, elderly, epileptic patients, CV disease

389
Q

1st line treatment of acute bipolar depression?

A

Lithium, Lamotrigine (good for younger females), Lurasidone.

390
Q

2nd line treatment of acute bipolar depression?

A

DVP, SSRI/bupropion – best antidepressant (adjunctive – don’t give antidepressant without a mood stabilizer. ADs added to a mood stabilizer probably cause no harm and can help treat co-morbid anxiety disorders).

391
Q

For a BP1 patient, you would never use an ____ without also using lithium or another mood stabilizer. For a BP2 patient, you might just use an ____ if that’s their primary symptom right now.

A

antidepressant
antidepressant
Bottom line is that you can safely use antidepressants on their own for BP2 and might start with them cause less S/E

392
Q

Alternative & psychosocial treatments of bipolar disorder

A
  • Psychoeducation – the only first-line psychosocial intervention for the maintenance phase
  • CBT, IPT and family – help as an adjunct to pharmacotherapy
  • Social: time off work, AISH, life skills training
393
Q

What treatments are indicated for BPI in pregnancy?

A

Lithium probably safest, for Li nonresponders use lamotrigines or ECT if needing quick treatment

394
Q

Women of childbearing age should NOT be on ____ for BPI as it has the highest risk of ____

A
  • Divalproex

- Ebstein’s anomaly

395
Q

Predictors of poorer response in bipolar disorder?

A

Male, mixed states, AUD, depressive features between the mania and depression, prior exposure to antidepressants, anticonvulsants, poorer adherence to Rx at 3 months

396
Q

An untreated manic episode can last __ months, treatment can cut that in half

A

3-6

397
Q

Diagnosis of cyclothymic disorder

A
  • Presence of numerous periods of hypomanic and depressive symptoms (not meeting criteria for full hypomanic episode or MDE) for >2 yr; never without symptoms for >2 mo
  • Never have met criteria for MDE, manic or hypomanic episodes
  • Symptoms not better explained by any psychotic disorder (including schizoaffective, schizophrenia, schizophreniform, delusional disorder, or other specified/unspecified)
  • Symptoms are not due to the direct physiological effects of a substance or GMC
  • Symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning
398
Q

Treatment of cyclothymic disorder

A

Similar to Bipolar I: mood stabilizer ± psychotherapy, avoid antidepressant monotherapy, treat any comorbid substance use disorder

399
Q

What is primary gain?

A

Goal of patient is to assume the ‘sick role’ in the absence of any obvious external advantages.

400
Q

What is secondary gain

A

Goal is to avoid a financial, societal or interpersonal obligation.

401
Q

What is somatization?

A

The process by which psychological distress manifests/are converted to physical symptoms. It is unconscious and a normal phenomenon. Considered pathological when it becomes primary mode of behaving and gets in the way of function.

402
Q

Diagnosis (DSM-5 Criteria) of somatic symptom disorder

A
  • ≥1 somatic symptom that is distressing/impairing function.
  • 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’s symptoms
    2. persistently high level of anxiety about health or symptoms
    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 (>6 mos).
403
Q

Epidemiology of somatic symptom disorder

A

Starts early, F>M (20:1), more common in lower SES (more stress, less stability), familial or antisocial personality in male relatives, associated with sexual abuse, substance abuse, depression, GAD, phobias as well as histrionic, borderline, and dependent personality disorders.

404
Q

Management of somatic symptom disorder

A
  • The patient should have regularly scheduled visits with a single primary care physician, who should minimize unnecessary medical workups and treatments.
  • Address psychological issues slowly. Patients will likely resist referral to a mental health professional.
  • Not cure and use non-invasive tx (CBT, physio), praise and validate adaptive behaviour/coping.
405
Q

Diagnosis (DSM-5 Criteria) of conversion disorder

A
  • ≥1 symptoms of altered voluntary motor or sensory function
  • Findings provide evidence of incompatibility between symptom and recognized neurological condition.
  • Not better explained by physical or mental issue
  • Causes significant distress or impairment in social or occupational functioning or warrants medical evaluation.
406
Q

Common symptoms of conversion disorder

A

Paralysis, weakness, blindness, mutism, sensory complaints (paresthesias), seizures, globus sensation (globus hystericus or sensation of lump in throat).

407
Q

Epidemiology of conversion disorder

A
  • More common in females.
  • Onset at any age, but more often in adolescence or early adulthood.
  • High incidence of comorbid neurological, depressive, or anxiety disorders.
408
Q

Management of conversion disorder

A
  • Main 3 modalities of tx for motor symptoms:
    1. Withdraw medical/social attention from movements/gait (ignore behaviour)
    2. PT and OT to retrain patient.
    3. CBT targeted at developing methods of coping with stress.
  • Often is short-lived (no preoccupation with the somatic symptoms), responds to almost any therapy, may require social intervention, might need hypnosis or benzo to even interview.
409
Q

Diagnosis (DSM-5 Criteria) of Illness Anxiety Disorder

A
  • Preoccupation with having or acquiring illness with excessive health-related behaviour for ≥6mo.
  • NONE or mild SOMATIC SYMPTOMS – high anxiety about health.
  • Heightened awareness of bodily sensation, excessive worry with that.
  • Specify whether care-seeking type or care-avoidant type
410
Q

Epidemiology of Illness Anxiety Disorder

A

F=M. Generally dissatisfied with care received, believe not taken seriously. Can result in countertransference. 2/3 have a least one other comorbid major psychiatric disorder

411
Q

Management of Illness Anxiety Disorder

A

Therapeutic alliance (AVN). Limit your investigations (arrange for regular, timed appointments). CBT

412
Q

Diagnosis (DSM-5 Criteria) of Psychological Factors Affecting Other Condition

A

A present medical condition (not mental) whose course is adversely affected by psychological factors that interfere with treatment/well-being of the individual (not better explained by any other disorder).

413
Q

Management of Psychological Factors Affecting Other Condition

A

Psychoeducation (discuss nature/cause), response prevention (refrain from behaviours that maintain health anxiety), stress/behaviour mgmt., SSRIs, treat psych co-morbidities, mindfulness approaches, CBT

414
Q

Diagnosis (DSM-5 Criteria) of Factitious Disorder

A
  • Falsification of physical signs or symptoms, or induction of injury or disease to SEEK CARE, associated with identified deception (false hx, simulation, exaggeration, aggravation – contaminating own wounds, self induction).
  • Evident even if no obvious external rewards.
  • Specify if single episode or recurrent
415
Q

Commonly feigned symptoms of Factitious Disorder

A
  • Psychiatric-hallucinations, depression.

- Medical-fever (by heating the thermometer), infection, hypoglycemia, abdominal pain, seizures, and hematuria.

416
Q

Epidemiology of Factitious Disorder

A
  • More common in women.
  • Higher incidence in hospital and health care workers (who have learned how to feign symptoms).
  • Associated with personality disorders.
  • Many patients have a history of illness and hospitalization, as well as childhood physical or sexual abuse.
417
Q

Management of Factitious Disorder

A

Hard to diagnose. Avoid confrontation and tx same way as somatic symptom disorder. Tempting to fire them

418
Q

The fundamental difference between malingering and factitious disorder is in the intention of the patient; in malingering, the motivation is ___, whereas in factitious disorder, the motivation is ____.

A

external

internal

419
Q

What is malingering

A

Malingering involves the intentional reporting of physical or psychological symptoms in order to achieve personal gain.

420
Q

Presentation of malingering

A
  • Patients usually present with multiple vague complaints that do not conform to a known medical condition.
  • They often have a long medical history with many hospital stays.
  • They are generally uncooperative and refuse to accept a good prognosis even after extensive medical evaluation.
  • Their symptoms improve once their desired objective is obtained.
421
Q

Is malingering more common in men or women

A

Significantly more common in men than women.

422
Q

Management of malingering

A
  • In your assessment, remember your ABCS (avoid accusations, beaware of countertransference, clarification and security measures
423
Q

Criteria for personality disorder

A
  1. Enduring pattern of behavior/inner experience that deviates from the person’s culture and is manifested in two or more of the following ways (CAPRI):
    - Cognition
    - Affect
    - Interpersonal functioning
    - Impulse control
  2. The pattern:
    - Is pervasive and inflexible in a broad range of situations.
    - Is stable and has an onset no later than adolescence or early adulthood.
    - Leads to significant distress in functioning.
    - Is not accounted for by another mental/medical illness or by use of a substance.
424
Q

What are the cluster A personality disorders

A

Schizoid, schizotypal, and paranoid

425
Q

What are the cluster B personality disorders

A

Antisocial, borderline, histrionic, and narcissistic

426
Q

What are the cluster C personality disorders

A

Avoidant, dependent, and obsessive-compulsive

427
Q

What is projection (transference)?

A

Reacting to unacceptable inner impulses as though they were outside self. Involves taking our own unacceptable qualities or feelings and ascribing them to other people. Transference is commonly used to describe this – transferring feelings about someone who was a figure from early life like your dad to another (e.g. a psychiatrist).

428
Q

What is countertransference?

A

Clinician’s emotional reaction to the patient – e.g. reacting to the transference with a strong emotional reaction.

429
Q

What is splitting?

A

Dividing emotions/relationships into all good or all bad – have a hard time dealing with grey. Can lead to staff splitting too – some are thought to be awesome, some not leading to divides in treatment teams.

430
Q

What is acting out?

A

Expressing unconscious impulse through action to avoid being conscious of a feeling.

431
Q

Diagnosis (DSM-5 Criteria) of paranoid personality disorder?

A
  1. Pervasive distrust/suspiciousness of others thought to be malevolent. e.g. Dwight from the Office.
  2. At least four of the following must also be present:
    - Suspicion (without evidence) that others are exploiting or deceiving him or her.
    - Preoccupied with unjust doubts
    - Reluctant to trust others
    - Interpretation of benign remarks as threatening or demeaning.
    - Persistence of grudges.
    - Perception of attacks on his or her character that is not apparent to others; quick to counterattack.
    - Suspicions regarding fidelity of spouse or partner.
432
Q

Treatment of paranoid personality disorder?

A
  • Psychotherapy is the treatment of choice, although, as stated above, patients rarely initiate treatment.
  • Group psychotherapy should be avoided due to mistrust and misinterpretation of others’ statements.
433
Q

Diagnosis (DSM-5 Criteria) of schizoid personality disorder

A
  • Pervasive pattern of detachment from social relationships and restricted range of expression of emotions in interpersonal settings.
  • At least 4 of: neither desires nor enjoys human interaction, usually chooses solitary activities, little interest in sex, lacks close friends, appears indifferent to praise/criticism of others, emotional coldness.
434
Q

Treatment of schizoid personality disorder

A
  • Hard to tease apart from autism.
  • Lack insight for individual psychotherapy, and may find group therapy threatening; may benefit from day programs or drop-in centers.
  • Antidepressants if comorbid major depression is diagnosed.
435
Q

Diagnosis (DSM-5 Criteria) of schizotypal personality disorder

A
  • A pattern of social deficits marked by eccentric behavior, cognitive or perceptual distortions, and discomfort with close relationships, beginning by early adulthood and present in a variety of contexts.
  • Indicated by at least 5 of: ME PECULIAR
  • M magical thinking or odd beliefs
  • E experiences unusual perceptions
  • P paranoid ideation
  • E eccentric behaviour or appearance
  • C constricted or inappropriate affect
  • U unusual thinking and speech
  • L lacks close friends
  • I ideas of reference (excluding delusions of reference).
  • A anxiety in social situations
436
Q

Schizotypal personality disorder vs schizophrenia?

A

Unlike patients with schizophrenia, patients with schizotypal personality disorder are not frankly psychotic (though they can become transiently so under stress), nor do they have fixed delusions.

437
Q

Schizotypal personality disorder vs schizoid personality disorder?

A

Patients with schizoid personality disorder do not have the same eccentric behavior seen in patients with schizotypal personality disorder.

438
Q

Treatment of schizotypal personality disorder

A
  • Psychotherapy is the treatment of choice to help develop social skills training.
  • Short course of low-dose antipsychotics if necessary (for transient psychosis). Antipsychotics may help decrease social anxiety and suspicion in interpersonal relationships.
439
Q

Diagnosis (DSM-5 Criteria) of antisocial personality disorder

A
  1. Antisocial: pervasive pattern of disregard/violation of rights of other since 15.
  2. Patients must be at least 18 years old for this diagnosis; history of behavior as a child/adolescent must be consistent with conduct disorder
  3. Need 3 or more of: CORRUPT
    - C cannot follow law
    - O obligations ignored
    - R remorselessness,
    - R reckless disregard for safety,
    - U underhanded (deceitful)
    - P planning deficit (impulsive)
    - T temper (irritable, aggressive)
440
Q

Treatment of antisocial personality disorder

A
  • Psychotherapy is generally ineffective.
  • Before treatment can begin, firm limits are essential. Therapists must find ways of dealing with patients’ self-destructive behavior. And to overcome patients’ fear of intimacy, therapists must frustrate patients’ desire to run from honest human encounters. In doing so, therapists face the challenge of separating control from punishment and of separating help and confrontation from social isolation and retribution.
  • Pharmacotherapy may be used to treat symptoms of anxiety or depression, but use caution due to high addictive potential of these patients.
441
Q

Diagnosis (DSM-5 Criteria) of borderline personality disorder?

A
  1. A pervasive pattern of instability of interpersonal relationships, self-image, and affects, and marked impulsivity, beginning by early adulthood and present in a variety of contexts, as indicated by five (or more) of the following: AM SUICIDE
    - A abandonment avoidance
    - M mood instability (marked reactivity of mood)
    - S suicidal (or self-mutilating) behaviour
    - U unstable and intense interpersonal relationships characterized by alternating between extremes of idealization and devaluation.
    - I impulsivity in at least two areas that are potentially self-damaging (e.g., spending, sex, substance abuse, reckless driving, binge eating)
    - C control of anger
    - I identity disturbance: markedly and persistently unstable self-image or sense of self.
    - D dissociative (or paranoid) symptoms that are transient and stress related
    - E emptiness
442
Q

Clinical features of borderline personality disorder?

A
  • Mood swings are common. Patients can be argumentative at one moment, depressed the next, and later complain of having no feelings.
  • Patients can have short-lived psychotic episodes (so-called micropsychotic episodes) - circumscribed, fleeting, or doubtful
  • The painful nature of their lives is reflected in repetitive self-destructive acts. Such patients may slash their wrists and perform other self-mutilations to elicit help from others, to express anger, or to numb themselves to overwhelming affect.
  • Patients with borderline personality disorder cannot tolerate being alone
  • Functionally, patients with borderline personality disorder distort their relationships by considering each person to be either all good or all bad. BLACK OR WHITE THINKING
  • Patients can exhibit defence mechanisms, splitting (idealization)!
443
Q

Treatment of borderline personality disorder?

A
  • Dialectical Behaviour Therapy - Duration: A full round takes about 6 months to complete
  • Pharmacotherapy should be considered an adjunct to psychotherapy. Various medications (e.g., mood stabilizers, antipsychotics, antidepressants) have been found to be somewhat effective in treating certain symptoms of BPD.
444
Q

Borderline personality disorder is diagnosed three times more often in ___ than ___.

A

women

men

445
Q

Diagnosis (DSM-5 Criteria) of histrionic personality disorder

A
  1. Pervasive pattern of excessive emotionality and attention-seeking, beginning in early adulthood.
  2. Need 5 or more of: PRAISE ME
    - P provocative behaviour
    - R relationships considered more intimate than they are
    - A attention (uncomfortable when not centre of attention)
    - I influenced easily
    - S style of speech (impressionistic, lacks detail)
    - E emotions (rapidly shifting and shallow)
    - M made up (uses physical appearance to draw attention)
    - E emotions exaggerated
446
Q

Treatment of histrionic personality disorder

A
  • Psychotherapy (e.g., supportive, problem-solving, interpersonal, group) is the treatment of choice.
  • Pharmacotherapy to treat associated depressive or anxious symptoms as necessary.
447
Q

Diagnosis (DSM-5 Criteria) of narcissistic personality disorder

A
  • Pervasive pattern of grandiosity, need for admiration, lack of empathy. E.g. Steve Carell in the Office.
  • Need 5 of: grandiose sense of self-importance, preoccupied with fantasies of success/power/brilliance, believes he/she is special or unique, requires excessive admiration, sense of entitlement, lacks empathy, is interpersonally exploitive, envious of others, arrogant/haughty.
448
Q

Narcissistic personality disorder vs antisocial personality disorder

A

Both types of patients exploit others, but NPD patients want status and recognition, while antisocial patients want material gain or simply the subjugation of others. Narcissistic patients become depressed when they don’t get the recognition they think they deserve.

449
Q

Treatment of narcissistic personality disorder

A
  • Psychotherapy is the treatment of choice.

- Psychotropics may be used if a comorbid psychiatric disorder is also diagnosed.

450
Q

Diagnosis (DSM-5 Criteria) of avoidant personality disorder?

A
  1. Pervasive pattern of social inhibition, feeling inadequate, hypersensitive to negative evaluation beginning in early adulthood. Need 4 of: CRINGES
    - C certainty of being liked before willing to get involved with others
    - R rejection or criticism preoccupies ones’ thoughts in social situations
    - I intimate relationships (restraint in intimate relationships due to hear of being shamed)
    - N new interpersonal relationship (is inhibited in)
    - G gets around occupational activity
    - E embarrassment prevents new activity or taking personal risks
    - S self viewed (as socially inept)
451
Q

Avoidant personality disorder vs schizoid personality disorder?

A

Patients with avoidant personality disorder desire companionship but are extremely shy, whereas patients with schizoid personality disorder have little or no desire for companionship.

452
Q

Avoidant personality disorder vs social anxiety disorder (social phobia)

A

Both involve fear and avoidance of social situations. If the symptoms are an integral part of the patient’s personality and have been evident since adolescence, personality disorder is the more likely diagnosis. Social anxiety disorder involves a fear of embarrassment in a particular setting (speaking in public, urinating in public, etc.), whereas avoidant personality disorder is an overall fear of rejection and a sense of inadequacy. However, a patient can have both disorders concurrently and should carry both diagnoses if criteria for each are met.

453
Q

Treatment of avoidant personality disorder?

A
  • Psychotherapy, including assertiveness and social skills training, is most effective.
  • Group therapy may also be beneficial.
  • Selective serotonin reuptake inhibitors (SSRIs) may be prescribed for comorbid social anxiety disorder or major depression.
454
Q

Diagnosis (DSM-5 Criteria) of dependent personality disorder?

A
  • Pervasive and excessive need to be taken care of that leads to submissive/clinging behaviour and fear of separation.
  • Need 5 of: difficulty with decisions without reassurance needs others to assume responsibility, difficulty disagreeing, difficulty initiating projects, excessive lengths to obtain nurturance/support from others, feels uncomfortable/helpless when alone, seeks another relation as a source of care/support when one ends, fearful of taking care of oneself
455
Q

Treatment of dependent personality disorder?

A
  • Psychotherapy, particularly cognitive-behavioral, assertiveness, and social skills training, is the treatment of choice.
  • Pharmacotherapy may be used to treat associated symptoms of anxiety or depression.
456
Q

Diagnosis (DSM-5 Criteria) of obsessive compulsive personality disorder

A
  1. Pervasive pattern of orderliness, perfectionism, mental/interpersonal control at the expense of flexibility, openness, efficiency.
  2. Need 4 or more of:
    - Preoccupation with details, rules, lists, and organization such that the major point of the activity is lost.
    - Perfectionism that is detrimental to completion of task.
    - Excessive devotion to work.
    - Excessive conscientiousness and scrupulousness about morals and ethics.
    - Will not delegate tasks.
    - Unable to discard worthless objects.
    - Miserly spending style.
    - Rigid and stubborn
457
Q

Obsessive-compulsive disorder (OCD) vs obsessive compulsive personality disorder

A

Patients with OCPD do not have the recurrent obsessions or compulsions that are present in OCD. In addition, the symptoms of OCPD are ego-syntonic rather than ego-dystonic (as in OCD); OCD patients are aware that they have a problem and wish that their thoughts and behaviors would go away.

458
Q

Narcissistic personality disorder vs obsessive compulsive personality disorder

A

Both personalities involve assertiveness and achievement, but NPD patients are motivated by status, whereas OCPD patients are motivated by the work itself.

459
Q

Treatment of obsessive compulsive personality disorder

A
  • Psychotherapy is the treatment of choice. Cognitive-behavior therapy may be particularly useful.
  • Pharmacotherapy may be used to treat associated symptoms as necessary.
460
Q

What is passive suicidal ideation

A

Would rather not be alive but has no active plan for suicide. e.g. “I’d rather not wake up” or “I would not mind if a car hit me”

461
Q

What is active suicidal ideation

A

Thoughts of actively ending life

462
Q

What should you consider when assessing suicide intent

A

Assessed based on planned vs impulsive attempt, precautions against being found, seeking help after act/reaction to survival, dangerousness of method and presence of “final act”, expectation of lethality/dying, substances use/intoxication

463
Q

Risk factors for suicidality?

A

SADPERSONS: sex (male), age (men peaks at 45, women peaks after 65, rapid rise in males 15-24), depression (50% of all people who kill themselves are depressed, 15% of people who have depression commit suicide), previous attempt, EtOH, rational thinking loss (psychosis), social supports lacking, organized plan, no spouse, sickness//chronic illness (schizophrenia, BPT, anxiety disorders, dementia)

464
Q

What is the ratio of attempted: completed suicides

A

Attempted: completed = 20:1

465
Q

Management of higher risk suicidal patient?

A
  • Patients with a plan and intention to act on the plan, access to lethal means, recent social stressors, and symptoms suggestive of a psychiatric disorder
  • Do not leave patient alone; remove potentially dangerous objects from room
  • If patient refuses to be hospitalized, complete form for involuntary admission (Form 1)
466
Q

Management of lower risk suicidal patient?

A
  • Patients who are not actively suicidal, with no plan or access to lethal means
  • Discuss protective factors and supports in their life, remind them of what they live for, promote survival skills that helped them through previous suicide attempts
  • *Suicide contracts are not effective