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Med School > Psychosis > Flashcards

Psychosis Flashcards

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
Q

Personality Disorder DSM-5
Which personality disorders are most common?

A
  • 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
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26
Q

Cluster A Personality Disorders

A
  • 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
Q

Cluster B Personality Disorders

A
  • 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
Q

Cluster C Personality Disorders

A
  • Anxious-Fearful
  1. Avoidant - sensitive, hesitant, feel inadequate
  2. Dependent - submissive, clingy, need reassurance
  3. Obsessive-Compulsive - perfectionist, controlling
29
Q

Motor Circuit

A
  • 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
Q

Associative Circuit

A
  • 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
Q

Limbic Circuit

A
  • 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
Q

How do D1 and D2 differ?

A
  • D1 is excitatory, G-protein mechanism increases CAMP which increases intracellular Ca
  • D2 is inhibitory, G-protein mechanism blocks CAMP
33
Q

What leads to catalepsy symptoms due to anti-DA meds in schizophrenia?

A
  • D2 receptor blockade on cholinergic neurons present in the indirect pathway
34
Q

How is reward wired? How does schizophrenia affect this?

A
  • 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
Q

Gambling disorder DSM-5
Tx?

A
  • 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
Q

How does gambling disorder affect other things? Possible etiology?

A
  • 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
Q

What is the pathophysiology behind addiction?

A
  • 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
Q

Role of serotonin
Role of glutamate

A

Serotonin - mood, sleep, memory, cognition
- raphe nucleus/NA/HC/PFC
- seen to decrease in the cerebral cortex after ecstasy

Glutamate - craving, learning, memory

39
Q

Effect of:
Nicotine
Opioids
Alcohol
Cocaine
Methamphetamine
Cannabis

A

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
Q

Impulsivity vs compulsivity?

A

Impulsivity –> effort to obtain arousal/ gratification (NE and DA)

Compulsivity –> effort to reduce anxiety (5HT)

41
Q

SUD DSM-5
What is considered remission?
Which substance is most addictive?

A
  • 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
Q

Treatments for SUD?

A
  • 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
Q

What is considered high risk for drinking? What causes flushing/tachycardia/HTN/nausea? Chronic consequences?

A
  • 7+ drinks a week
  • acetaldehyde
  • hepatosplenomegaly, caput medusa, macro anemia, hepatitis
44
Q

What does alcohol withdrawal look like?
What is delirium tremens?
What is Wernicke Korsacoff?

A
  • 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
Q

THC vs CBD

A

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
Q

Where are CB1 and CB2 expressed?

A

CB1 –> widely expressed in CNS/PNS, psychotropic effects (THC)

CB2 –> expressed in immune tissues (macrophages, B and T cells, GI), cytokine release

47
Q

Side effects of weed

A
  • 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
Q

Evidence of benefit for weed?

A

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
Q

What causes tolerance and withdrawal?

A
  • over time receptors become less sensitive
  • body can no longer produce enough endogenous opioids
50
Q

How does pupil size vary in relation to drugs?

A
  • Dilated if withdrawal
  • Constricted if opioid overdose
51
Q

Risk factors for OUD

A
  • 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
Q

Social vs structural vs self stigma

A

Social –> negative labels/images, ignoring
Structural –> barriers to care (witholding until better managed)
Self –> u hate urself

53
Q

Ways to avoid OUD

A
  • 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
Q

Demographics of suicide

A
  • 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
Q

Unintentional Self-Injury
Self-Injurious Behaviour
Non-Suicidal Self-Injury
Suicide Gesture
Suicide Attempt
Suicide

A

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

56
Q

Etiology behind NSSI

A
  • 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
Q

4 Cs of Suicide

A

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

58
Q

Risks of Suicide (SAD PERSONS)

A
  • 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
Q

Motivations for Suicide

A
  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
Q

What should you also test for to rule out secondary causes of psychosis?

A
  • syphilis - neurosyphilis can cause psychotic-like symptoms
  • urinalysis for drugs that could be induced psychosis
61
Q

BC Mental Health Act

A
  • 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
Q

Substance Induced Psychotic Disorder

A
  • delusions and/ or hallucinations
  • evidence of onset after use/ withdrawal
  • not better explained by another illness
63
Q

Stimulant Withdrawal

A
  • dysphoria and 2 of:
  • fatigue, unpleasant dreams, insom/hypersomnia, increased appetite, pyschomotor agitation and retardation

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