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19 Psychiatry > Psychopharma > Flashcards

Psychopharma Flashcards

1
Q

3 dimensions of neurotransmission

A

space, time, and function

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2
Q

anatomical vs chemical addressed nervous system

A

anatomical: chemical communication, electrical is converted to chemical signals at synapse
chemical: volume neurotransmission (diffusion to non-targeted receptors), pulsatile fashion

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3
Q

time dimension of neurotransmission

A

fast onset: glutamate and gaba

slow onset: ne and serotonin, neuromodulators (can last for days)

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4
Q

pre-synaptic events

A

excitation/secretion coupling

read 1-4

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5
Q

when pre-synaptic neurons use monoamine nts, they create:

A
  • enzymes for monoamine synthesis
  • receptors for reuptake and regulation
  • synaptic vesicles loaded with monoamine nts
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6
Q

7 steps in nt action

A

read

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7
Q

points on neurodevelopment and neuroplasticity

A
  • myelination and arborization = adolescence
  • synaptogenesis = lifetime
  • apoptosis = throughout life cycle and under certain conditions
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8
Q

___ is the foundation of psychopharmacology

A

chemical neurotransmission

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9
Q

agonistic drug effects

A
  • increases synthesis of nt
  • destroy degrading enzymes = increase number of nt
  • increase release of nt
  • blocks inhibitory effect of autoreceptors
  • binds postsynaptic receptors (activate/increase effect)
  • block degradation/reuptake
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10
Q

antagonistic drug effects

A
  • blocks synthesis of nt
  • causes nt to leak from vesicles to be degraded
  • blocks release of nt
  • activates autoreceptors and inhibits nt release
  • receptor bloacker
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11
Q

five r’s of antidepressant therapy

A
  • response: at least 50% reduction in symptoms
  • remission: all symptoms go away
  • recovery: remission for 6-12 mos
  • relapse: worsens before complete remission
  • recurrence: worsens after complete recovery
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12
Q

indications for treatment for depression for >1 year

A
  • severe episodes
  • psychotic symptoms
  • elderly
  • response but not remission
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13
Q

those with __ require lifetime treatment

A

more than one episode

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14
Q

monoamine hypothesis

A
  • deficiency in epi and serotonin = depression
  • mao-i = increase monoamine nts
  • tca = block nt reuptake pump = more nt
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15
Q

ne deficiency syndrome

A
  • impaired attention
  • difficulty concentrating
  • deficiency in working memory
  • slow information processing
  • depressed mood
  • psychomotor retardation
  • fatigue
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16
Q

ne pathways

A

LOCUS CERULEUS

  • LC-fc1: mood
  • LC-fc2: attention, concentration, cognitive functions
  • LC-limbic cortex: emotions, energy, fatigue, psychomotor agitation and retardation
  • LC-cerebellum: motor movements (tremors)
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17
Q

other ne pathways

A
  • brainstem in cardio centers: bp
  • sns from spinal cord = cv function (beta-1 receptors)
  • sns from spinal cord = bladder emptying (alpha-1 receptors)
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18
Q

serotonin deficiency syndrome

A
  • depressed mood
  • anxiety
  • panic
  • phobia
  • obsessions and compulsions
  • food craving; bulimia
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19
Q

serotonin pathways

A

RAPHE NUCLEUS

  • frontal cortex: mood
  • basal ganglia: movements, obsessions, compulsions
  • limbic areas: anxiety and panic
  • hypothalamus: appetite and eating
  • brainstem sleep centers: sleep
  • spinal cord: sexual response
  • brainstem: vomiting
  • gut: appetite and gi mobility
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20
Q

classical antidepressants

A
  • mao-i (irreversible)
  • reversible inhibitors of mao (rima) are safer
  • tca
21
Q

inhibition of mao a can cause

A

rise in bp, intracerebral hemorrhage, death

22
Q

what are tcas

A
  • block reuptake pumps for se and ne
  • blockade of muscarinic cholinergic receptors
  • blockade of h1 histamine receptors
  • blockade of a1 adrenergic receptors
  • block na channels in heart and brain = cardiac arrythmia and seizure
23
Q

moa of ssris

A
  • blocks serotonin reuptake pump
  • increase in se = autoreceptors are desensitized / down regulated
  • downregulation = neuron release more 5ht at axon
24
Q

side effects of ssri

A
  • 2a/c in limbic cortex: acute mental agitation, anxiety
  • 2a in basal ganglia: motor movements
  • 2a in sleep centers: myoclonus, disrupt slow wave sleep
  • 2a in spinal cord: reflexes, orgasm, ejaculation
  • libido
25
Q

examples of ssris

A
  • fluoxetine = longest half life
  • sertaline
  • citalopram/ escitalopram
  • fluvoxamine, paroxetine = short half life
26
Q

what are nris

A
  • selective noradrenergic reuptake inhibitor

- inhibition greater than se without side effects of tcas

27
Q

what are ne and dopamine reuptake blockers (ndri)

A
  • bupropion

- more of pro-drug

28
Q

what are snris

A
  • combines ssri and nris

- shares ne and 5ht

29
Q

what are nassa

A
  • dual 5ht and ne actions via alpha 2 antagonism
  • increase 5ht and ne levels by blocking alpha 2 receptors
  • side effects: sedation and weight gain
  • mirtazapine = sedating, weight gain
30
Q

drug with least weight gain

A

fluoxetine

31
Q

gold standard mood stabilizer

A

lithium!!

  • site of action: inositol monophosphatase (phosphatidyl inositol system)
  • bipolar depression, rapid cycling or mixed episodes
  • many side effects
32
Q

moa of anticonvulsants

A
  • ion channels (na, k, ca)

- modulate effects of gaba: augmenting synthesis/release, inhibiting breakdown, reducing reuptake

33
Q

valproic acid

A
  • inhibit na or ca channel, boost gaba, reduce glutamate action
  • side effects: hair loss, weight gain, sedation
34
Q

carbamazepine

A

effective against manic phase but not approved

cause sedation, hema abnormalities, sjs

35
Q

lamotrigine

A
  • inhibit na channels, inhibit release of glutamate

- biploar depression

36
Q

gabapentin

A
  • gaba transporter: enhance gaba and reduce glutamate
37
Q

topiramate

A
  • interferes with na and ca channels
  • weak inhibitor for carbonic anhydrase
  • weight loss
38
Q

five symptom dimension in schizophrenia

A
  • positive
  • negative
  • cognitive
  • aggressive/hostile
  • depressive or anxious
39
Q

mesolimbic pathway

A

mesoLOOK AT ALL THIS DOPAMINE

  • vta to limbic areas of brain (nucleus accumbens)
  • positive symptoms: hallucination and delusions
  • dopamine excess
40
Q

mesocortical pathway

A

meso-CULANG

  • vta to cerebral cortex (limbic cortex)
  • negative and/or cognitive symptoms
  • dopamine deficit
41
Q

nigrostriatal pathway

A
  • substantia nigra
  • regulating movements
  • dopa deificient: parkinsonism
  • dopa excess: hyperkinetic movements
42
Q

tuberoinfundibular pathway

A

TUBERS = POTATOES IN BRAIN = PITUITARY = PROLACTIN

  • hypothalamus to anterior pituitary
  • regulates prolactin secretion
  • galactorrhea, gynecomastia, amenorrhea
43
Q

conventional antipsychotics

A

dopamine 2 receptor blockers

  • mesolimbic dopamine pathways
  • reduces hyperactivity that causes positive symptoms
44
Q

other effects of d2 receptor blockers

A
  • mesocortical: neuroleptic-induced deficit syndrome
  • nigrostriatal: extrapyramidal symptoms, tardive dyskinesia
  • tuberoinfundibular: prolactinemia
45
Q

serotonin effects on nigrostriatal pathway

A
  • level of serotonergic innervation of substantia nigra
  • level of axon terminals arriving from raphe synapse on cell bodies and dendrites of dopaminergic cells
  • serotonin 2a reverses d2 antagonism
  • blocking 5ht2a promote da release
46
Q

serotonin effects on mesocortical pathway

A
  • reverses d2 antagonism, net increase in da activtiy

- for negative symptoms

47
Q

serotonin effects on tuberoinfundibular pathway

A
  • serotonin 2a antagonism reverses d2 antagonism
  • serotonin promotes prolactin release
  • mitigates hyperprolactinemia
48
Q

serotonin effects on mesolimbic pathway

A
  • d2 blockade on positive symptoms
49
Q

atypical antipsychotic drugs

A
  • clozapine: treatment resistant cases
  • risperidone
  • olanzapine
  • quetiapine
  • ziprasidone: can cause arrythmias (torsades)
  • apiprazole
  • asenapine

19 Psychiatry (9 decks)

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