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PDA Block 3 > Intro to Neuropsychopharmacology Part 1 > Flashcards

Intro to Neuropsychopharmacology Part 1 Flashcards

1
Q

where are the neuron cell bodies containing norepinephrine located

A

neurons containing norepinephrine are located in the locus coeruleus and innervate nearly every part of the CNS

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2
Q

Where are neurons containing serotonin located

A

neurons containing serotonin are located in two groups of raphe nuclei and project to most of the brain

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3
Q

where are neurons containing dopamine located

A
  • dopaminergic (DA) pathways in the brain are responsible for the beneficial and adverse effects of many antipsychotic drugs
  • Mesolimbic and Mesocortical pathways
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4
Q

GABA localization in brain

A
  • substantia nigra
  • globus pallidus
  • hippocampus
  • limbic structures: Amgydala
  • hypothalamus
  • spinal cord
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5
Q

List the Bipolar and related disorders

A
  • bipolar I
  • Bipolar II
  • cyclothymic disorder
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6
Q

List the depressive disorders

A
  • disruptive mood dysregulation disorder
  • major depressive disorder
  • persistant depressive disorder
  • premenstrual dysphoric disorder
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7
Q

Criteria for MDD

A
  • depressed mood
  • diminished interest or pleasure
  • weight change
  • insomnia/hypersomnia
  • fatigue or loss of energy
  • feelings of worthlessness
  • inappropriate guilt
  • agitation/retardation
  • difficulty concentrating
  • preoccupation with death/suicidal ideation
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8
Q

Describe the monoamine theory of depression and how we think of it today

A
  • the theory results from functionally deficient monoamine (NE and or 5-HT) transmission in the CNS
  • based on pharmacological evidence
  • known antidepressant drugs (TCAs and MAO inhibitors) facilitate monoaminergic transmission
  • drugs such as reserpine that depletes amines to cause depression
  • however other pharmacological evidence fails to support eh traditional monoamine hypothesis (takes 2 weeks for drugs to work0)
  • simple monoamine hypothesis is no longer tenable as an explanation of depression, BUT pharmacological manipulation of monoamine transmission remains the most successful approach to treating depression
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9
Q

Classical Biogenic amine theory of MDD

A

depression is due to a deficiency of NE and/or 5HT

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10
Q

Effect of tricyclic antidepressants on noradrenergic transmission

A
  • blockade of neurotransmitter uptake NE and 5-HT

- or acts on receptors and second messengers

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11
Q

Current status of Monoamine Theory –

A

Depression is due to a biogeneic amine receptor or transmission imbalance. the various drugs that we are discussing today act to change the imbalance and restore a more normal affect

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12
Q

Serotonin Specific Reuptake Inhibitors

A
  • Block SERT so serotonin isn’t taken up and there is more available in the cleft
  • antidepressant actions are similar in efficacy and time course to those of CTAs
  • acute toxicity is less than that of a TCA and monoamine oxidase inhibitor therefore overdose risk is reduced
  • side effects include nausea, insomnia, and sexual dysfunction
  • no food reactions, but dangerous “serotonin reaction” (hyperthermia, muscle rigidity, cardiovascular collapse) can occur if given with MAOIs
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13
Q

SSRI WIthdrawal

A

-dizziness
-ligt headedness
-vertigo/feeling faint
-shock-like sensations
-paresthesia
-anxiety
fatigue
-gait instability
-headache
-insomnia
-irritabilit
-nausea or vomiting
-tremor
-visual disturbances

-symptoms appear within 1-7 days after stopping an SSRI

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14
Q

SSRI approved uses

A
  • Major depression
  • OCD
  • Panic disorder
  • social anxiety disorder
  • PTSD
  • Generalized anxiety disorder
  • PMS now PDD (premenstraul dysphoric disorder)
  • hot flashes associated with menopause
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15
Q

Fluoxetine

A

-Frist SSRI on the market
effects on drug metabolism
-long half life active metabolite (7 days or more)
-now available as sustained release product for PDD

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16
Q

Sertraline

A

similar in action to fluoxetine with less effects on drug metabolism

  • shorter half life
  • OCD
  • Panic attacks
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17
Q

SNRI drugs

A
  • block both 5-HT and NE reuptake
  • side effect profile is more SSRI like than TCA like
  • ex: Duloxetine
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18
Q

Duloxetine

A
  • 12-18 hour half life
  • also approved for neuropathic pain syndromes, fibromyalgia, back pain and osteoarthritis pain
  • use with caution in patients with liver disease
  • can produce withdrawal symptoms
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19
Q

Norepinephrine synapse

A
  • Tyr enters the cell and is converted to DOPA which is converted to Dopamine
  • dopamine enters the vacuole and is converted to NE
  • NE is released from the cell and can act on the alpha receptor or the B receptor
  • NE is taken up by NAT into the axon.
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20
Q

SNRI Drugs

A
  • mechanism of action
  • inhibition of 5HT and NE reuptake
  • treatment of neuropathic pain
  • treatment of depressive disorders
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21
Q

TCA

A
  • same stuff as SNRIs
  • but also receptor blockade
  • muscarinic receptors=blurred vision, xerostomia, urinary retention, constipation, narrow angle glaucoma
  • histamine H1 receptors=sedation
  • alpha adrenergic receptors=orthostatic hypotension, dissiness, reflex tahcycardia
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22
Q

Atypical antidepressants

A
  • drugs without typical tricycli structure or SSRI or SNRI action. may or may not block catecholamine uptake
  • Bupropion
  • Mirtazapine
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23
Q

Bupropion

A
  • atypical antidepressant
  • also approved for nicotine withdrawal and seasonal affective disorder.
  • weakly blocks NE and Dopamine uptake
  • no weight gain or sexual dysfunction
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24
Q

Mirtazapine

A
  • blocks presynaptic apha2 receptors in brain

- increase appetite for AIDS patients with AIDS wasting syndrome

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25
Q

Tricyclic antidepressants

A
  • first highly effective drugs for the treatment of depression
  • block NE and 5-HT reuptake
  • now used secondarily to SSRIs and other newer compounds
  • long plasma life
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26
Q

Pharmacological properties of TCAs

A
  • produces elevation of mood in depressed patients after about 2 to 3 weeks
  • decreases REM and increases stage 4 sleep
  • prominent anticholinergic effects
  • sedation
  • cardiac abnormalities-due to anticholinergic effects and increased NE concentrations palpitations, tachycardia and arrhythmias
  • overdoses-acute toxicity-symptoms include hyperpyrexia, hyper or hypotension, seizures, coma, and cardiac conduction defects
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27
Q

Drug interactions of TCAs

A
  • sympathomimetic drugs-particularly indirect acting agents

- effects absorption and metabolism of other drugs

28
Q

therapeutic uses of TCAs

A
  • major depressive disorder
  • enuresis in childhood-imipramine
  • chronic pain: amitriptyline
29
Q

MAO Inhibitors mechanism of action

A
  • block the oxidative deamination of naturally occuring biogenic amines, such as NE, DA and 5-HT and ingested amines.
  • monoamine oxidase is found in neurons and also in the liver, lungs and other organs
  • two forms A, and B. antidepressant action is probably due to A
  • irreversible inhibitor is Phenelzine
30
Q

MAO Inhibitors function/use/side effect/how long does ti take to begin working

A
  • antidepressant action takes 2 weeks or more
  • produces mood elevation in depressed patients. May progress to hypomania particularly in bipolar disease
  • coorrects sleep disorders in depressed patient
  • may produce stimulation in normals
  • acute toxicity can produce agitation, hallucinations, hyperpyrexia, convulsions and changes in blood pressure
31
Q

MAO Inhibitors and food

A

if you eat tyramine then you can overwhelm the MAO inhibitors

32
Q

Therapeutic uses of MAOI

A

Major depression-although not drug of first choice

Narcolepsy

33
Q

MOA Amitriptyline

A

-nonspecific blockers of NE and 5-HT Reuptake

34
Q

MOA Fluoxetine and Sertraline

A

SSRI

35
Q

MOA Duloxetine

A

SNRI

36
Q

MOA Phenelzine

A

MAOI

37
Q

MOA Bupropion Mirtazapine

A

other monoamine mechanisms

38
Q

Psychosis

A
  • derangement of personality
  • loss of contact with reality
  • delusions
  • hallucinations
39
Q

Schizophrenia central criteria

A

two or more symptoms during a one month period, at least one must be a core positive symptom, and there are no subtypes

40
Q

core positive symptoms of schizophrenia

A
  • delusions
  • hallucinations
  • disorganized speech
41
Q

other symptoms of schizophrenia

A
  • grossly disorganized or catatonic behavior
  • negative symptoms
  • blunted affect
  • lack of spontaneity
  • poor abstract thinking
  • poverty of thought
  • social withdrawal
42
Q

Dopamine hypothesis of schizophrenia

A
  • schizophrenia results from hyperactivity of dopaminergic neurons or their receptors, particularly those with terminals in limbic areas of the brain
  • abnormal dopamine neurotransmission in frontal cortical areas may be responsible for negative symptoms
  • mechanism of action: All effective antipsychotics interact with dopamine systems
43
Q

DA Mesolimbic tract

A
  • originates in A10
  • arousal, memory, stimulus processing, locomotor activity, motivational behavior
  • dopamine hyperactivity results in positive symptoms of schizophrenia
44
Q

mesocortical tract

A
  • originates in A10
  • cognition, communication, social activity,
  • altered dopaminergic activity leads to negative symptoms of schizophrenia
45
Q

Nigrostriatal pathway dopamine

A
  • originates in A9
  • dopamine blockade increase EPS
  • blockade of 5HT2a decrease EPS, parkinsonism
46
Q

Tuberoinfundibular tract

A

-dopamine blockade leads to increase in prolactin release

47
Q

Dopamine receptors

A

D1 like family:

  • subtypes D1 and D5
  • activation is coupled to G alpha “s” receptor. which activates adenylate cyclase which leads to increase in concentration of cAMP

D2 like family:

  • includes D2, D3, and D4
  • activation is coupled to G alpha “i”, inhibits adenylyl cyclase leading to decrease in concentration of cAMP
48
Q

Atypical Antipsychotics

A
  • most of the newer drugs such as clozapine, risperidone etc have an additional neurochemical effect in addition to DA receptor blockade
  • block 5-HT receptors in the forebrain. often with greater potency than for DA receptors
49
Q

Actions of the Antipsychotic Drugs

A
  • Decrease in psychotic behavior
  • typical drugs differ only in potency
  • the negative symptoms of schizophrenia are not well treated by the older typical agents
  • Atypical drugs in addition to treating positive symptoms, may be more effective in treating negative symptoms

-sedation

  • Extrapyramidal effects
  • dystonias
  • parkinsonism (early reactions more with typicals)
  • akthisia
  • tardive dyskinesia (late reaction may be frequent with atypicals
50
Q

Acute dystonia

A
  • onset is 1-5 days
  • spasm of muscle of tongue, face neck, and back
  • opisthotonus
51
Q

Parkinsomism

A
  • onset 5 to 30 days

- bradykinesia, mask-like facies, tremor, rigidity, shuffling gait, drooling, cogwheeling, stooped posture

52
Q

Akathisia

A
  • 5 to 60 days

- compulsive restless movemnts, symtoms of anxiety, agitation

53
Q

Later reaction-tardive dyskinesia

A
  • months to years

- oral-facial dyskinesias, choreoathetoid movements

54
Q

Actions of antipsychotic drugs-neuroendocrine

A

result of dopamine receptor blcokade

55
Q

Actions of antipsychotic drugs-anticholinergic

A

dry mouth, blurred vision, urinary retention

56
Q

side effects of antipsychotic drugs

A
  • neuroendocrine
  • anticholinergic
  • orthostatic hypotension
  • decreased seizure threshold- particularly clozapine
  • weight gain: diabetes related events are more common with atypicals particulary olanzapine, risperidone clozapine and quetiapine
57
Q

Neuroleptic Malignant Syndrome

A
  • a potentially lethal hypodopaminergic side effect of antipsychotic drugs
  • hyperthermia, parkinson-like tremor symptoms (muscular rigidity and tremor) mutism and possible death
  • treatment includes cooling and hydration, bromocriptine and dantrolene
58
Q

Available typical antipsychotic drugs

A
  1. Phenothiazines
    - Chlorpromazine: low to medium potency, sedative with pronounced anticholinergic actions (aiphatic side chain)
    - Fluphenazine (piperazine side chain)
  2. Thioxanthine Derivatives
  3. Butyrophenone
    - Haloperidol: not chemically related to the phenothiazines but is pharmacologically similar to the high potency piperazine derivatives
59
Q

List the 5 atypical antipsychotic drugs

A
  • clozapine
  • olanzapine
  • risperidone
  • quetiapine
  • aripiprazole
60
Q

advantages of atypical antipsychotics over typical antipsychotics

A
  • lower incidence of extrapyramidal symptoms (better compliance)
  • possible lower incidence of tardive dyskinesia
  • helps with negative symptoms
  • improve positive symptoms in many antipsychotic-resistant or refractory patients
  • less impact on cognitive function
61
Q

Clozapine

A
  • Blocks D4 and 5-HT2 receptors
  • little effect on D2
  • muscarinic antagonist
  • improves positive symptoms even in patients not helped by other drugs
  • improves negative symptoms
  • lowers seizure thresholds more than other antipsychotics (5-10% incidence)
  • can cause fatal agranulocytosis: requires monitoring
62
Q

Olanzapine

A
  • related to clozapine
  • potent 5-HT2 antagonist
  • D1 and 2 antagonist some D4
  • few extrapyramidal symptoms (5HT>D)
  • less seizure incidence than clozapine
  • no agranulocytosis
  • weight gain and diabetes related adverse events
  • reports of olanzapine abuse
63
Q

risperidone

A
  • combined D2 and 5-HT2 antagonist
  • greater reduction in negative symptoms and less extrapyramidal symptoms than traditional antipsychotics
  • less seizure activity and less antimuscarinic than clozapine
  • paliperidone is the active metabolite of risperidone
  • both are available as intramuscular depot preparations
64
Q

Quetiapine

A
  • structurally related to clozapine
  • similar to risperidone and olanzapine in effects on schizophrenia symptoms and side effects
  • shorter half life
  • approved for augmentation in depression
65
Q

Aripiprazole

A
  • a paritial D2 agonist and 5 HT 2 antagonist also approved as an adjunct in depression (augmentation) and for bipolar I disorder
  • long acting forms available (one month or more)
  • brexpiprazole is a similar drug partial agonsit at D2 and 5 HT1 A receptors; 5 HT2 antagonist
66
Q

uses of antipsychotic drugs

A
  • acute psychotic episodes
  • chronic schizophrenia
  • manic episodes, bipolar disorder: apripiprazole, olanapine, quetiapine, ziprasidone, risperidone, asenapine, ,lurasidone, cariprazine
  • schizoaffective disorder-paliperidone
  • augmentation in depression-aripiprazole, olanzapine, quetiapine
  • tourette’s syndorme-haloperidol, aripiprazole and pimozide
  • antiemesis

PDA Block 3 (16 decks)

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