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PMCOL 200 > Psychosis > Flashcards

Psychosis Flashcards

1
Q

what do psychotic disorders all share?

A

involve symptoms of psychosis

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2
Q

what is psychosis?

A

mental disorders where there’s loss of contact w/ reality, affecting a person’s ability to think, feel and act

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3
Q

what are 3 examples of psychotic disorders?

A

schizophrenia, schizoaffective disorder (manic depression), substance-induced psychotic disorder

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4
Q

what is schizophrenia?

A

severe psychotic disorder wherein individual exhibits 2 or more positive, negative or cognitive symptoms for 6 months (min)

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5
Q

what are positive symptoms of schizophrenia?

A

mental phenomena that aren’t in healthy individuals (hallicinations/delusions)

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6
Q

what are negative symptoms of schizophrenia?

A

loss/impairment of normal psychological functioning (decr motivation/social withdrawal)

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7
Q

what are 3 ex of cognitive symptoms of schizophrenia?

A

poor conc., disorganized thinking, poor memory

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8
Q

what most likely causes schizophrenia?

A

genes (can interact w/ enviro stimuli to alter neurochem. or structural causes)

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9
Q

when does schizophrenia manifest in life?

A

early adulthood (predisposed but symptoms arise at this time)

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10
Q

what 4 enviro factors can interact w/ genes to cause schizophrenia?

A

prenatal infections of mother, perinatal hypoxia, adolescent drug abuse, trauma/stress

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11
Q

what is the theory that suggests NTs cause schizophrenia?

A

biochemical theory of schizophrenia

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12
Q

what is the dopamine hypothesis for schizophrenia?

A

symptoms of schizophrenia are due to hyperactivity of dopamine system

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13
Q

what inferential evidence supports the dopamine hypothesis? (2)

A

drugs that incr dopamine (amphetamine, cocaine, cannabis) can cause hallucinations/delusions at high doses; drugs that block dopamine are effective antipsychotics (1st gen antipsychotics)

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14
Q

what 2 areas in the midbrain contain the largest population of dopamine neurons?

A

ventral tegmental area/VTA and substantia nigra

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15
Q

what is the mesocortical/mesolimbic system?

A

dopamine neurons protruding from VTA to striatum and prefrontal cortex

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16
Q

what does the mesocortical/mesolimbic system mediate? (4)

A

memory, learning, mood (aka affect), thought organization

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17
Q

hyperactivity in what system contributes to psychotic symptoms according to the dopamine hypothesis?

A

mesocortical/mesolimbic system

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18
Q

what kind of receptors are dopamine receptors?

A

GPCRs

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19
Q

what are the 2 classes of dopamine receptors?

A

D1 and D2

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20
Q

what is the difference btwn D1 and D2 dopamine receptors? (2 each)

A

D1: Gs GPCR (unlikely to contribute to antipsychotic action of drugs)
D2: Gi GPCR (directly related to clinical antipsychotic potency)

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21
Q

what 2 other pathways does inhibiting dopamine transmission by antipsychotic drugs affect?

A

nigrostriatal system, tuberoinfundibular system

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22
Q

what is the nigrostriatal system?

A

dopamine neurons that project from substantia nigra to striatum

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23
Q

what is the nigrostriatal system responsible for?

A

initiating movement

24
Q

inhibiting the nigrostriatal system can cause what? (long-term use of some antipsychotics)

A

tardive dyskinesia (involuntary movements of face and body)

25
Q

what is the tuberoinfundibular system?

A

dopamine neurons in arcuate nucleus that control hormone release in pituitary

26
Q

dopamine release from the tuberoinfundibular system inhibits secretion of what 2 hormones from the pituitary?

A

prolactin and growth hormone

27
Q

how does long-term use of antipsychotic drugs cause hyperprolactinemia?

A

antipsychotics inhibit dopamine release (inhibits prolactin), therefore, disinhibits prolactin secretion and causes incr prolactin

28
Q

what is hyperprolactinemia associated w/? (3)

A

amenorrhea, decr libido and infertility (from antipsychotics)

29
Q

what is the glutamate hypothesis?

A

symptoms of schizophrenia are linked to deficiencies in glutamate signalling (in cortex)

30
Q

what inferential evidence supports the glutamate hypothesis?

A

substances that are NMDA antagonists (phencyclidine, PCP/Angel dust and ketamine) produce hallucinations/paranoid delusions

31
Q

what does the glutamate hypothesis suggest causes schizophrenia?

A

hypofunctional NMDA receptors on GABA interneurons in cerebral cortex causes overreaction of glutamate signalling downstream to VTA (causes symptoms)

32
Q

how do dopamine, GABA and glutamate normally function vs in schizophrenia patients?

A

Glu binding to NMDARs on GABA interneurons usually inhibits Glu neurons and decr dopamine release, this doesn’t occur in ppl w/ schizophrenia so Glu neurons incr activity and incr dopamine release

33
Q

what is the serotonin hypothesis?

A

symptoms of schizophrenia are due to incr serotonin signalling

34
Q

what inferential evidence supports the serotonin hypothesis? (2)

A

some 5HT agonists are hallucinogenic (LSD); 5HT antagonists decr positive symptoms of schizophrenia

35
Q

what is 5HT?

A

serotonin

36
Q

which 5HT neurons in prefrontal cortex cause hallucinations?

A

5HT-2A

37
Q

how does activation of 5HT-2A receptors cause hallucinations?

A

enhance excitation of glutamate neurons (activate mesolimbic dopamine system)

38
Q

how are the serotonin and glutamate hypothesis similar and different?

A

excitation of Glu neurons causes schizophrenia symptoms but Glu hypothesis states upstream control is by hypofunction of NMDA on GABA interneurons vs Ser hypothesis states upstream control is by 5HT

39
Q

what do 5HT-2A antagonists do?

A

block glutamate release (by blocking 5HT) in cortex and decr hallucinations and other positive symptoms of schizophrenia

40
Q

what are 1st gen/typical antipsychotics? 2 ex?

A

drugs that target D1 and D2 dopamine receptors but efficacy relates to D2 antagonism; haloperidol, chlorpromazine

41
Q

what are 2nd gen/atypical antipsychotics? 2 ex?

A

antagonists at 5HT, D1 and D2 receptors (efficacy relates to D2) but have lower affinity to D receptors than 1st gen (less dopamine/extrapyramidal side effects) and more effective at treating negative side effects; clozapine, risperidone

42
Q

what are extrapyramidal symptoms?

A

Parkinson-like effects of ~80% D2 receptor occupancy (substantia nigra pathway)

43
Q

what D2 receptor occupancy is required to produce antipsychotic effects? (1st and 2nd gen)

A

60-80%

44
Q

what 3 side effects are there for 1st gen antipsychotics? (80% D2 receptor occupancy)

A

extrapyramidal symptoms, hyperprolactinemia and tardive dyskinesia

45
Q

do 1st gen or 2nd gen antipsychotics have a higher therapeutic index?

A

2nd gen

46
Q

what does Kd =?

A

Koff ÷ Kon (ligand and receptor)

47
Q

what is the difference btwn NT (dopamine) action in the mesolimbic/nigrostriatal pathway vs tuberoinfundibular pathway?

A

M/N: dopamine released into synaptic cleft (decr d, incr receptor rebinding)
T: dopamine secreted into bloodstream, crosses BBB by hypophyseal portal system to pituitary (incr clearance by blood flow, decr receptor rebinding)

48
Q

what are the effects of fast on/slow off antipsychotics? ex?

A

incr D2 receptor binding in striatum (fast on) and pituitary (slow off), therefore incr extrapyramidal effects and hyperprolactinemia; haloperidol

49
Q

what are the effects of fast on/fast off antipsychotics? ex?

A

incr D2 receptors binding in striatum (fast on) but decr at pituitary (fast off) therefore incr extrapyramidal symptoms but no hyperprolactinemia; chlopromazine

50
Q

what are the effects of slow on/fast off antipsychotics?

A

still have D2 receptor binding in striatum (slow on but in synaptic cleft) but decr at pituitary (fast off) therefore decr extrapyramidal symptoms and hyperprolactinemia;

51
Q

what causes other side effects of 1st and 2nd gen antipsychotics?

A

have affinity for multiple other receptors

52
Q

what is a unique effect of clozapine?

A

has affinity for D4 receptor (on WBCs) and causes agranulocytosis (loss of WBCs) therefore incr infection rate and death (not 1st line therapy for schizophrenia)

53
Q

when do antipsychotics start to work vs reach their full effect?

A

start to work within hours/days (dopamine receptor occupancy reaches 65% quickly) but 4-6 weeks to see any antipsychotic effects

54
Q

what % of ppl w/ schizophrenia are treatment resistant?

A

30% (don’t respond after ≥2 trails)

55
Q

what % of ppl stop taking antipsychotics due to adverse side effects?

A

50%

56
Q

what are adverse side effects of 1st vs 2nd gen antipsychotics?

A

1st gen: extrapyramidal, dyskinesias, hyperprolactinemia

2nd gen: cardiovascular effects, metabolic syndrome, diabetes, weight gain

PMCOL 200 (27 decks)

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