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Neuropsychopharmacology > Lecture 11: Antipsychotics > Flashcards

Lecture 11: Antipsychotics Flashcards

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1
Q

emotional symptoms of depression

A

pessimism, low self esteem, loss of motivation

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2
Q

biological symptoms of depression

A

slowness of thought & action, loss of libido, sleep disturbance & loss of appetite

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3
Q

two types of depression

A

unipolar & bipolar

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4
Q

duration of unipolar depression

A

6+ months, w/ 1+ month of active-phase symptoms

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5
Q

key symptoms of unipolar depression (at least 2)

A

delusions, hallucinations, disorganized speech, grossly disorganized or catatonic behavior

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6
Q

bipolar depression difference from unipolar depression

A

at least one manic episode (which may be preceded or followed by hypomanic or depressive episodes)

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7
Q

manic episode duration criteria

A

at least 1 week (or any duration if hospitalization is required)

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8
Q

manic episode mood disturbance criteria

A

abnormally & persistently elevated, expansive, or irritable mood

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9
Q

symptoms of manic episode (at least 3+)

A
  • inflated self-esteem/grandiosity
  • decreased need for sleep
  • more talkative
  • racing thoughts
  • distractibility
  • increased goal-directed activity
  • risky activities
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10
Q

bipolar disorder

A

mental illness characterized by extreme shifts in mood, energy, and activity levels, ranging from periods of mania or hypomania to periods of depression

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11
Q

manic episodes

A

periods of intense, often euphoric or irritable mood, accompanied by increased energy, activity, & racing thoughts

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12
Q

depressive episodes

A

periods of sadness, hopelessness, & a lack of interest in daily activities, along with low energy, sleep disturbances, & changes in appetite or weight

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13
Q

what genetic variations are associated w/ increased risk for bipolar

A

neurotransmitter systems, Ca2+ signaling, & synaptic function
- no single “bipolar gene”exists - it’s polygenic

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14
Q

two types of bipolar

A

bipolar I disorder, bipolar II disorder

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15
Q

bipolar I mood disorder characteristics

A
  • at least 1 manic episode, which may be preceded or followed by hypomanic or depressive episodes
  • manic episode is severe & can lead to hospitalization
  • depressive episodes are common but not required for diagnosis
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16
Q

bipolar II disorder characteristics

A
  • 1+ major depressive episode & 1+ hypomanic episode
  • no full manic episodes
  • misdiagnosed as depression bc hypomania is less noticable
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17
Q

hypomania

A

milder form of mania
- elevated or irritable mood & increased energy or activity, but without severe impairment or psychosis in mania

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18
Q

duration of hypomania vs mania

A

hypomania: 4+ days
mania: 7+ days (or any duration if hospitalization is needed)

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19
Q

impairment of hypomania vs mania

A

hypomania: noticeable but not severe
mania: severe functional impairment

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20
Q

psychosis in hypomania vs mania

A

hypomania: absent
mania: may be present

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21
Q

hospitalization in hypomania vs mania

A

hypomania: rarely needed
mania: often required

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22
Q

psychosis

A

loss of contact w/ reality
- causes hallucinations, delusions, disorganized thinking, severely impaired insight & judgement

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23
Q

treatment for bipolar disorder

A

mood stabilizers, can be used w/ antidepressants or antipsychotics

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24
Q

mood stabilizer function

A

control mood swings in manic depressive illness

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25
what was the most common drug to control mania
lithium
26
what drugs are more common to treat mania now
carbamazepine, valproate, & gabapentin
27
lithium
inorganic ion taken orally - takes 3-4 weeks to have effect - controls mania, not depression
28
neuroprotective effects of lithium
preserves or increases the volume of brain structures involved in emotional regulation - prefrontal cortex, hippocampus, amygdala
29
mechanism of lithium on ions
replaces Na+ in excitable tissue but is not pumped out of the cell w/ Na/K-ATPase so it accumulates inside excitable cells disrupting depolarization
30
mechanism of lithium on cell signaling
depletes accumulation of intracellular inositol phosphate, resulting in inhibition of agonist stimulated IP3 - also inhibits PKC
31
how does lithium affect glutamate activity
inhibits its release, increases its reuptake, and decreases post-synaptic activation of NMDA receptors, which are crucial for excitability
32
how does lithium affect dopamine activity in the brain
reduces it, particularly in the prefrontal cortex, which is involved in mood regulation
33
how does lithium affect GABA neurotransmission
increases, causing inhibitory effects to stabilize mood by counteracting effects of excitatory NTs
34
toxicity & side effects of lithium
- nausea - tremor - renal effects such as polyuria - thyroid enlargement - weight gain
35
what is polyuria
excessive urine production
36
carbamazepine and valproic acid use
treat acute mania & prevention of recurrance
37
carbamazepine mechanism
induces the metabolism of CYP3A4 substrates - voltage-gated Na+ channel blocker - one of the most commonly used antiseizure medications - stabilizes the channel & prevents them from returning to a state where they can be reopened
38
typical management plan for a severe manic episode in bipolar disorder
1. hospitalization - may be necessary for safety, stabilization, & medication re-initiation 2. pharmacologic treatment - mood stabilizer (lithium, valproate, or carbamazepine) - antipsychotic (for agitation or severe mania, such as Olanzapine, Risperidone) 3. monitor serum levels, renal & thyroid function (for lithium), liver enzymes (for valproate or carbamazepine)
39
what are antipsychotic drugs (neuroleptics) used to treat
individuals who experience psychotic symptoms as in schizophrenia - provide symptomatic relief from some of the disease symptoms
40
what molecular basis has been linked to schizophrenia
dysfunction of monoaminergic & amino acid transmitters (primarily dopamine) in the brain
41
brain chemistry in schizophrenia
DA, glut, GABA - both excess & deficient - neuroinflammation, immune activation
42
neuronal changes in schizophrenia
dendritic apoptosis, decreased neuronal plasticity, synaptic pruning
43
symptoms of schizophrenia
hallucinations, delusions, disorganized thinking, lack of motivation, anhedonia
44
environmental triggers for schizophrenia
infections, childhood & adolescent stressors, malnutrition, cannabis or drug abuse at a young age
45
neurodevelopmental disorder
brain develops abnormally long before symptoms appear
46
how does abnormal brain development in adolescence unmask schizophrenia symptoms
due to synaptic pruning, hormonal changes, or stress
47
dopamine hypothesis
- excess DA activity in the mesolimbic pathway is linked to positive symptoms - reduced dopamine activity in the prefrontal cortex is linked to negative symptoms & cognitive deficits
48
other NT systems involved in schizophrenia
- glutamate - GABA - serotonin
49
how does glutamate dysfunction affect schizophrenia
may contribute to cognitive deficits & negative symptoms like social withdrawal
50
how does GABA affect schizophrenia
inhibitory deficits may cause cognitive & negative symptosm
51
how does serotonin affect schizophrenia
modulates mood, cognition
52
what four pieces of circumstantial evidence is the DA hypothesis based on
1. most anti-psychotic drugs block D2 receptors 2. drugs that increase dopaminergic activity aggravate schizophrenia or produce psychosis 3. D2 receptors are increased in untreated schizophrenic brains 4. successful treatment of schizophrenic patients have altered metabolite of DA in CSF, plasma, & urine
53
what may increased dopamine receptor density in the brain be due to
chronic neuroleptic drug therapy (receptor upregulation by chronic D2 receptor blockade)
54
support for the glutamate hypothesis
1. blockade of other transmitter receptors (eg NMDAR antagonists) precipitates negative symptoms of schizophrenia in non-psychotic patients 2. hypofunction of L-glutamatergic neurotransmission in cortical & hippocampal regions produces symptoms of schizophrenia - hypoactivity of glutamate in limbic brain may underlie schizophrenia 3. some biochemical studies show reduced levels of L-gluamate in brains of scizophrenics
55
evidence for serotonin dysfunction in schizophrenia
LSD produces schizophrenia-like symptoms
56
brain structure & function in schizophrenia
- enlarged ventricles (suggesting brain volume loss) - reduced gray matter volume (in prefrontal cortex, temporal lobes, hippocampus, amygdala - abnormal connectivity between brain regions
57
environmental & social factors toward schizophrenia
- psychosocial stress - urban upbringing, social adversity, childhood trauma - birth complications - substances
58
positive symptoms of schizophrenia
- delusions, paranoid thinking - hallucinations - thought disorder - abnormal behaviors
59
thought disorder
conflicting thoughts, wild trains of thought, garbled sentences, irrational conclusions
60
negative symptoms of schizophrenia
- apathy - poor socialization - sense of self - affective flattening - attentional deficits
61
when does schizophrenia usually begin
in adolescence or young adult life
62
two major classes of neuroleptic drugs
typical/classical and atypical
63
how do neuroleptic drugs act
by modifying activity of monoamine transmitters (dopamine & serotonin) in the limbic brain
64
typical neuroleptic drugs
chlorpromazine, haloperidol
65
downside of typical neuroleptic drugs
causes a high incidence of extrapyramidal side effects
66
atypical neuroleptic drugs
clozapine, risperidone
67
receptor potency of chlorpromazine
D2 > D1
68
receptor potency of Haloperidol
D2 >> D1
69
receptor potency of Clozapine
5-HT2 > D1 = D2
70
receptor potency of Respirodone
5-HT2 > D2 (no effect on D1)
71
side effect profiles of atypical vs typical
atypicals have lower side effects - less risk of parkinsonism & tardive dyskinesias
72
atypicals vs typicals in treatment efficacy
atypicals have greater efficacy
73
atypicals vs typicals in treatment of negative symptoms
atypicals are more effective
74
how do antipsychotic drugs affect activity of midbrain DAergic neurons in SN & VTA
initially increase & later decrease electrical activiy
75
which pathways correlate w/ antipsychotic effects
mesolimbic/mesocortical DA pathways
76
which pathways correlate w/ unwanted motor effects
nigrostriatal pathways
77
D1 receptor mechanism
increases in cAMP
78
D1 receptor locations
located in putamen, NAc, and olfactory tuberbcule
79
D2 receptor mechanism
decreases cAMP, blocks Ca2+ channels, opens K+ channels
80
where are D2 receptors located
both pre- and post-synaptically on neurons in caudate putamen, NAc, and olfactory tubule
81
atypical vs typical receptor interference
atypical drugs have greater ability to alter 5HT2A receptors than interfere w/ D2 action
82
adverse effects of anti-psychotics on the autonomic nervous system
- dry mouth, difficulty urinating, constipation (muscarinic cholinergic receptor blockade) - orthostatic hypertension, impotence, failure to ejaculate (alpha adrenergic receptor blockade)
83
symptoms of adverse effects on the central nervous system
- parkinson's syndrome (dopamine receptor blockade) - tardive dyskinesia (super-sensitivity of dopamine receptors) - toxic-confusional state (muscarinic blockade)
84
adverse effects of anti-psychotic drugs on endocrine system
infertility, impotence (DA receptor blockade resulting in hyperprolactinemia)
85
possible clinical consequences of muscarinic receptor blockade
- blurred vision - constipation - urinary retention - memory dysfunction - dry mouth - tachycardia
86
what is the effectiveness of long term treatment of schizophrenia
effective in preventing recurrence of schizophrenic attacks, & this is a major factor in allowing individuals to lead normal life
87
are drugs effective at treating negative symptoms
no

Neuropsychopharmacology (17 decks)

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