Psychosis Flashcards

(63 cards)

1
Q

Definition of Schizophrenia

A
  • Need 2 or more of for 6 months:
  • Delusions, hallucinations, disorganized speech, disorganized/catatonic behaviour, negative symptoms (flat affect, alogia, avolition, anhedonia)
  • Also affects attention, conecntration, memory
  • Onset in late teens/ 20s, earlier onset in men
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2
Q

Etiology of schizophrenia

A
  • environmental (maternal infection, nutrient deficiency, adversity, immigrant, cannabis, decreased motor/ cognitive/ social function)
  • genetics (higher risk in twins/ children/ siblings)
  • Over 150 associated SNPs i.e 22q11.2 deletion
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3
Q

Pathophysiology of schizophrenia

A
  • drugs that increase DA
  • increases in mesolimbic pathway leads to positive symptoms
  • decreases in mesocortical pathway leads to negative symptoms and cognitive impairment
  • decreased cortical thickness
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4
Q

What are the 4 dopamine pathways?

A
  1. Nigrostriatal
  2. Mesolimbic
  3. Mesocortical
  4. Tuberoinfundibular
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5
Q

What makes up the striatum? What 3 pathways run towards it?

A
  • Caudate nucleus and Putamen
    1. Limbic - emotion and motivation
    2. Associative (DA release is increased here in schizo) - higher level cognition
    3. Sensorimotor - body and eye movements

*info from the cortex flows through these 3 pathways to the striatum, which integrates output to the thalamus for feedback to the cortex

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6
Q

DDx for delusions/ hallucinations

A
  • epilepsy, frontal lobe tumors, SLE, hypoxia, B12/thiamine deficiency, levodopa, prednisone, cannabis, cocaine, benzo withdrawal, bipolar
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7
Q

How to distinguish primary vs secondary psychosis

A
  • Primary (i.e. schizophrenia) has normal consciousness i.e. will be able to tell you the date
  • Prominent visual hallucinations are more common in secondary psychosis
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8
Q

Distinguishing schizophrenia vs drug induced vs medically induced

A

Schizo –> gradual, normal consciousness, multiple auditory hallucinations, remitting and relapsing

Substance –> sub/acute, consciousness and orientation may be altered, SUD, resolves

Medical –> variable onset, acute, Px findings, consciousness may be altered, orientation impaired, resolves

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9
Q

Common symptoms characteristic of schizophrenia?

A

audible thoughts, arguing voices, voices commenting on actions, somatic passivity (being controlled), thought withdrawal and broadcasting

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10
Q

Psychotic disorders and their criteria

A

Schizophrenia - over 6 months
Schizophreniform - 1 to 6 months
Brief psychotic disorder - 1 day to 1 month

Schizoaffective - psychosis and a mood disorder (depression or mania)
Delusional disorder - only delusions
Substance/ Medication induced psychosis

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11
Q

Prognosis after first schizophrenic episode

A
  • decline is more pronounced in early stages
  • relapse rate is 2 years post 1st episode
  • life span is decreased 10 years (not only suicide!)

Worse prognosis if chronically progressive
Better prognosis if remitting/ relapsing

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12
Q

What are risk factors of schizophrenia? What factors lead to a poor prognosis?

A
  • male, decreased cognition, older paternal age, obstetric complications
  • low SES, SUD, early onset, longer time untreated, increased lateral ventricle
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13
Q

Describe the mesocortical pathway

A
  • VTA to the PFC
  • cognition, emotion, affect
  • issues here lead to the (-) sx of schizophrenia
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14
Q

Describe the mesolimbic pathway

A
  • VTA to the nucleus accumbens
  • memory, emotional behaviours, reward
  • activity here leads to the (+) sx of schizophrenia
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15
Q

Describe the nigrostriatal pathway

A
  • SN to the basal ganglia
  • controls motor movement
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16
Q

Describe the tuberoinfundibular pathway

A
  • hypothalamus to the infundibular area
  • controls prolactin secretion
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17
Q

1st Generation Antipsychotics
- MOA
- drawbacks
- side effects
- examples, and which ones are high/low potency for D2

A
  • antagonize D2, H1, A1, M1 receptors
  • antagonism of mesolimbic D2 treats (+) sx
  • BUT antagonism of mesocortical D2 may lead to (-) sx (neuroleptic induced deficit syndrome), as well as extrapyramidal sx in nigrostriatal, and increased prolactin via inhibition of the TI pathway
  • anti-H (sedation and weight gain), anti A (dizziness and lower BP), anti M (dry mouth, constipation, blurry vision, and urinary retention)
  • Chlorpromazine low potency for D2
  • Haloperidol high potency for D2
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18
Q

2nd Generation Antipsychotics
- MOA
- examples

A
  • antagonize D2, H1, A1, M1, 5HT2A and some are partial agonists of 5HT1A
  • 5HT2A receptor normally inhibits the release of DA, so antagonizing this receptor increases release of DA which can improve (-) sx as well as extrapyramidal sx and help inhibit prolactin release
  • Clozapine, Quetiapine, Risperidone
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19
Q

3rd Generation Antipsychotics
- MOA
- Examples

A
  • antagonize H1, A1, M1, 5HT2A and partial agonists of D2, D3 and 5HT1A
  • partial agonism helps with extrapyramidal sx and inhibiting prolactin secretion, also lessens orthostatic hypoTN/ sedation/ dizziness/ dry mouth/ constipation
  • Apriprazole (which has the most partial agonist activity)
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20
Q

What are the treatment guidelines for schizophrenia?

A
  • Initially start with an SGA or TGA and evaluate over 2 weeks
  • If no response, switch to a different drug (Clozapine) or increase the dose, consider a long acting injectable
  • If the patient doesn’t show 20% sx decrease in the first 2 weeks it is unlikely it will work, but can wait up to 6-8 weeks to fully evaluate
  • Threshold should be low for choosing to switch bc of side effects, but keep in mind that some side effects will decrease with time so consider waiting a bit if there is a therapeutic benefit
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21
Q

Unique side effects of clozapine?
What factors increase or decrease its plasma concentration?
What should you consider if refractory (+)/(-)/ aggression?

A
  • agranulocytosis, myocarditis
  • increase –> female, pregnant, old, CYP1A2 inhibitors (valproic acid), infection, asian, obese, rapid titration
  • decrease –> smoking, inducers (carbamazepine, valproic acid)
  • apiprazole/ ECT for (+) sx
  • anti-depressant/ ECT for (-) sx
  • mood stabilizer or anti-psychotic for aggression
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22
Q

What are general side effects of anti-psychotics? Treatment options

A
  • pseudo-parkinsonism (anticholinergics)
  • akathisia (benzos, propranolol, mirtazapine)
  • tardive dyskinesia (TGA, cloz/quet)
  • hyperprolactinemia (can lead to ED, gynecomastia, hirsutism, acne, etc.)
  • weight gain, HTN, insulin insensitivity
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23
Q

Personality

A
  • internal characteristics, consistent over time, based in patterns of behaviour
  • can be affected by situation
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24
Q

5 Factor Model of Personality

A

Openness to experience (intellect, insight, creativity)
Conscientiousness (organized, dependable)
Extraversion (sociable, expressive, energetic)
Agreeableness (cooperative, empathic, respectful)
Neuroticism (insecure, touchy, excitable, anxious)

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25
Personality Disorder DSM-5 Which personality disorders are most common?
- enduring pattern of behaviour that deviates from expectation of one's culture, distress and impairment - must affect at least 2 areas: cognition, affect, impulse, interpersonal - must be pervasive across time and situation - late adolescence/ early adulthood onset - OC, antisocial, schizotypical and paranoid are most common
26
Cluster A Personality Disorders
- Odd-Eccentric, shared schizophrenia vulnerability 1. Paranoid - distrust, self-righteous 2. Schizoid - detached, does not connect 3. Schizotypical - relationship discomfort, blurring of reality and fantasy, perceptual distortions, eccentric
27
Cluster B Personality Disorders
- Dramatic-Emotional 1. Borderline - impulsive, unstable in relationships and mood, suicidal, self harm 2. Histrionic - excessive emotions, attention seeking 3. Antisocial - disregard for others, superficially charming 4. Narcissistic - need admiration, lack empathy
28
Cluster C Personality Disorders
- Anxious-Fearful 1. Avoidant - sensitive, hesitant, feel inadequate 2. Dependent - submissive, clingy, need reassurance 3. Obsessive-Compulsive - perfectionist, controlling
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Motor Circuit
- regulation of gaze and eye orientation - putamen receives input from sensory/motor areas, then sends input to the thalamus via VA/VL which sends info back to the motor cortex
30
Associative Circuit
- planning complex motor activity - when an action is well-learned, activity in this circuit decreases and will increase in the motor circuit - input from SN, nucleus accumbens and caudate nucleus project to the thalamus
31
Limbic Circuit
- postures/ gestures/ expressions related to emotion, anticipatory reward, incentive based learning, rich in DA neurons, - amygdala and hippocampus --> nucleus accumbens --> thalamus --> frontal association areas, orbitofrontal lobe, and anterior cingulate
32
How do D1 and D2 differ?
- D1 is excitatory, G-protein mechanism increases CAMP which increases intracellular Ca - D2 is inhibitory, G-protein mechanism blocks CAMP
33
What leads to catalepsy symptoms due to anti-DA meds in schizophrenia?
- D2 receptor blockade on cholinergic neurons present in the indirect pathway
34
How is reward wired? How does schizophrenia affect this?
- VTA (midbrain), nucleus accumbens, SN - motivation and reward are combined to create goal oriented behaviour - VTA --> motivation, executive functioning, drug seeking, emotion, reward - in schizophrenia, get altered reward (DA) signalling in the mesolimbic pathway leading to distorted salience of stimuli - in a non-addicted person, the PFC can inhibit drive while conditioned clues and saliency can stimulate it - in an addicted person, saliency can override the PFC and will no longer be inhibited by it
35
Gambling disorder DSM-5 Tx?
- 12 months - at least 4 of: - increased amounts, restless, cant quit, preoccupied, distressed, lying about extent, affects life, rely on other for $ - CBT, motivational interviewing, no meds approved - Screen with South Oaks Gambling Screen/ LIE/ BET
36
How does gambling disorder affect other things? Possible etiology?
- affects SUD tx (often coincide), increases intimate partner violence - though to have DA basis --> increased bottom-up ventral striatal DA release to cues/gambling tasks/reward prediction, decrease of top down orbitofrontal influence - increased compulsivity with DA agonists
37
What is the pathophysiology behind addiction?
- dopamine! - mesolimbic system involved in behavioural reinforcement/ drive - reward pathway: VTA --> NA --> PFC - amygdala activates when seeing craved substance - D2 receptors are LOWER in addiction, more likely to find methylphenidate pleasant - more stress = better response to drugs - new environments can lead to overdose
38
Role of serotonin Role of glutamate
Serotonin - mood, sleep, memory, cognition - raphe nucleus/NA/HC/PFC - seen to decrease in the cerebral cortex after ecstasy Glutamate - craving, learning, memory
39
Effect of: Nicotine Opioids Alcohol Cocaine Methamphetamine Cannabis
Nicotine --> increases DA and NE Opioids --> increase DA and decrease NE Alcohol --> increases GABA (inhibitory) and decreases glutamate (excitatory), also increases DA and 5HT Cocaine --> reuptake inhibitor of NE, DA, 5HT Methamphetamine --> dumps NE, DA, 5HT into the cleft by reversing transport Cannabis --> increase DA and 5HT *withdrawal is the opposite
40
Impulsivity vs compulsivity?
Impulsivity --> effort to obtain arousal/ gratification (NE and DA) Compulsivity --> effort to reduce anxiety (5HT)
41
SUD DSM-5 What is considered remission? Which substance is most addictive?
- 12 months, 2 of the typical criteria - 3-12 months is early remission, 12+ months is sustained remission (can still have cravings) - tobacco is most addictive (nicotine is a gateway drug) - earlier age = higher risk of addiction *this exact criteria is same for Cannabis use disorder and OUD
42
Treatments for SUD?
- Agonists --> methadone for OUD, nicotine patch for smoking - Partial agonists --> buprenorphine for OUD, varenciline for smoking - Antagonists --> naltrexone for OUD - Aversion --> disulfiram for AUD - Sx Mitigators --> benzos for alcohol withdrawal - Behavioural --> CBT, MI, SMART, mindfulness
43
What is considered high risk for drinking? What causes flushing/tachycardia/HTN/nausea? Chronic consequences?
- 7+ drinks a week - acetaldehyde - hepatosplenomegaly, caput medusa, macro anemia, hepatitis
44
What does alcohol withdrawal look like? What is delirium tremens? What is Wernicke Korsacoff?
- insomnia, irritability, anxiety - high BP and HR, tremor, hyperreflexia Delirium tremens --> hallucinations, tremor, seizures, disorientation, anxiety 3-4 days after, EMERGENCY Wernicke Korsacoff --> encephalopathy, ataxia, hallucinations, psychosis, memory impairment, low vitamin B, EMERGENCY
45
THC vs CBD
THC --> psychoactive, lipophilic, partial agonist of CB1 - euphoria, relaxation, psychomotor and memory deficits, increased appetite, tachycardia, analgesia - slower onset and longer lasting if ingested CBD --> non-intoxicating, low affinity for CB1/2 - somnolence, lethargy, insomnia, suicidal thoughts, GI - approved for epilepsy
46
Where are CB1 and CB2 expressed?
CB1 --> widely expressed in CNS/PNS, psychotropic effects (THC) CB2 --> expressed in immune tissues (macrophages, B and T cells, GI), cytokine release
47
Side effects of weed
- acute --> nausea, vomitting, transient psychosis, anxiety, paranoia - higher risk with polysubstance use and ingestion, young males - chronic --> increased risk of developing schizophrenia, impaired learning/ attention/ working memory/ coordination, poor social functioning, potentially IQ decline but could be due to SES
48
Evidence of benefit for weed?
Substantial - chronic pain, antiemetic in chemo, MS spasticity, decreasing opioid use (enhances the analgesic effects of opioids) Moderate - sleep Meh - tourette's, anxiety, PTSD, increase appetite in HIV
49
What causes tolerance and withdrawal?
- over time receptors become less sensitive - body can no longer produce enough endogenous opioids
50
How does pupil size vary in relation to drugs?
- Dilated if withdrawal - Constricted if opioid overdose
51
Risk factors for OUD
- 40+, male, current or past Hx of SUD, family hx, depression/ anxiety/ PTSD/ ADD, chronic pain and being prescribed an opioid for it, trauma, ACEs (alter the HPA axis) - 5-15% of chronic pain patients on opioids have OUD
52
Social vs structural vs self stigma
Social --> negative labels/images, ignoring Structural --> barriers to care (witholding until better managed) Self --> u hate urself
53
Ways to avoid OUD
- don't dispense more than 30 days at a time - do not co-Rx with benzodiazepines - assess for other SUD - supervised injection sites, OAT, support programs - don't use alone, don't mix, don't inject *if overdose --> ventilation BEFORE chest compressions (respiratory issue)
54
Demographics of suicide
- starts at 10, increases until 24 and remains high, peaks at 50 and then decreases until 70 - continued decline in women, severe rebound in men - overrepresented in indigenous (but NOT a risk factor) - immigrants commit less suicide
55
Unintentional Self-Injury Self-Injurious Behaviour Non-Suicidal Self-Injury Suicide Gesture Suicide Attempt Suicide
USI --> risky behaviour (alcohol overdose, firearms) SIB --> hair pulling, skin picking, intellectual disabilities NSSI --> intentional but not wanting to die, cutting/burning/purging Gesture --> suicidal behaviour/ communication, doesn't need intent Attempt --> intent of death w action Suicide --> resulting in death
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Etiology behind NSSI
- genetic susceptibility --> TRAUMA --> increased opioid release and decreased sensitivity --> NSSI to release opioids - those with a history of suicidality and NSSI have less endorphins in spinal fluid - those who self-injure report greater euphoria when given opioids - those who self-injure have lower stress/ cortisol levels
57
4 Cs of Suicide
Collateral --> ask other people about history, perception of reality, distortion of time, reactionary nature Confidence --> how well do you know the patient, patient is confident in themself, poor enagement Common Sense --> careful history taking, active vs passive ideation Changeability --> NOT: age, sex, fam hx, prior attempts YES: access, mental health, support, meds
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Risks of Suicide (SAD PERSONS)
- sex: male - age under 19 or over 45 - depression - previous attempts/ psychiatric care - excessive alcohol/ drugs - single/ widowed/ divorced - no support - organized/ serious attempt (2) - stated future intent (2) - rational thinking loss (2) 8+ --> hospital admission 0-5 --> maybe discharge +ASARI - assessment of suicide and risk inventory
59
Motivations for Suicide
1. Isolated (egoistic) --> LGBT, trauma, divorced 2. Hopeless (fatalistic) --> chronic illness, hardship 3. For others (socioistic) --> remorse, shame, revenge, protecting others 4. Pressure (anomic) --> school/social pressure, family loss/change *most suicide interventions address anomic ideation
60
What should you also test for to rule out secondary causes of psychosis?
- syphilis - neurosyphilis can cause psychotic-like symptoms - urinalysis for drugs that could be induced psychosis
61
BC Mental Health Act
- allows patients to be admitted involuntarily 1. Have a mental disorder 2. Require tx in a facility to prevent deterioration/ protect themselves and others 3. Cannot suitably be admitted voluntarily
62
Substance Induced Psychotic Disorder
- delusions and/ or hallucinations - evidence of onset after use/ withdrawal - not better explained by another illness
63
Stimulant Withdrawal
- dysphoria and 2 of: - fatigue, unpleasant dreams, insom/hypersomnia, increased appetite, pyschomotor agitation and retardation