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Neuro 4 week 1 > Pharm of psychoses > Flashcards

Pharm of psychoses Flashcards

1
Q

Explain the dopamine theory of schizophrenia

A

Abnormality of brain function in schizophrenics is due to overactivity in brain dopaminergic pathways, especially in the mesolimbic pathway.

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2
Q

chlorpromazine*

A

typical antipsychotic, D2 block, increased EPSE

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3
Q

haloperidol*

A

typical antipsychotic D2 block, increased EPSE

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4
Q

clozapine*

A

atypical antipsychotic, reduced EPSE, poor D2 block, good 5HT2a block, hypersalivation, Agranulocytosis

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5
Q

risperidone

A

atypical antipsychotic, reduced EPSE, poor D2 block, good 5HT2a block

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6
Q

olanzapine

A

atypical antipsychotic, reduced EPSE, poor D2 block, good 5HT2a block

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7
Q

aripiprazole

A

atypical antipsychotic, reduced EPSE, poor D2 block, good 5HT2a block

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8
Q

Describe the relationship between receptor blocking potency-selectivity (esp. 5HT vs DA), efficacy in schizophrenia, and side effect profile for typical and atypical antipsychotic agents.

A

typical have more D2 block, atypical have more 5HT2a block. less EPSE in atypicals but clozapine does have a couple (agranulocytosis, hypersalivation)

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9
Q

Describe the catecholamine hypothesis of depression and its limitations and how it may relate to the neurodegenerative hypothesis of depression.

A

Initial observation: Reserpine depleted brain NE and 5HT induced depression
Additional support: Effective antidepressant drugs share property to enhance NE-5HT-(DA) availability in synapse
BUT – does not totally explain etiology of depression
Effect on amines immediate – mood elevating effect delayed 2-3 weeks
Direct evidence in support largely lacking

Dysregulation of pre-and post-synaptic control of NE-5HT neurotransmission
Synaptic changes produced by antidepressants then lead to alterations of gene expression
Time frame for these changes correlates with onset of mood changes

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10
Q

amitriptyline*

A

TCAD, blocks SERT and NET, high sedation and antimuscarinic

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11
Q

imipramine

A

TCAD, blocks SERT and NET, med. sedation and antimuscarinic

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12
Q

desipramine

A

TCAD, only blocks NET, little sedation, little antiM

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13
Q

fluoxetine*

A

SSRI, blocks SERT

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14
Q

paroxetine*

A

SSRI, blocks SERT

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15
Q

sertraline

A

SSRI, blocks SERT

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16
Q

bupropion*

A

NDRI, blocks NET and DAT

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17
Q

venlafaxine*

A

SNRI along with duloxetine blocks SERT and NET

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18
Q

trazodone*, S/E

A

blocks SERT, high sedation used as sleeping med
Drowsiness
Dizziness, nausea, agitation
“Black Box Warning” for liver failure with nefazodone

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19
Q

phenelzine*

A

(MAOI) antidepressant and anxiolytic. non-selective MAOI

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20
Q

electroconvulsive therapy

A

Most rapid and effective (70-90%) treatment for severe acute depression
Can be life-saving if patient is suicidal
Usually 6-12 treatments at a frequency of 2-3 per week

Adverse effects
Medical cardiopulmonary events, fractures, orodental injuries, headache
Cognitive acute confusion, retrograde and anterograde amnesia

21
Q

lithium*

A 
mood stabilizer, used to augment antidepressants, narrow therapeutic window
Slow onset (10-21 d) – necessary to accumulate Li+  in cell

Effects greatest on cells with highest level of activity (use-dependence)

Enhance 5HT action and/or diminish NE and DA effect – most favored MOA:

Interference with PIP recycling (Gq protein: IP3 and DAG)
S/E
In thyroid anti-TSH hypothyroidism
In kidney anti-ADH polyuria-polydipsia

Competes with Na+ for reabsorption

increase dietary Na+ decreaseLi+ plasma levels

Na+ restriction increases Li+ plasma levels

22
Q

valproic acid

A

anti convulsants

23
Q

carbamazepine

A

Carbamazepine (Tegretol)
primarily in the treatment of epilepsy and neuropathic pain.
not effective for absence seizures or myoclonic seizures. may be used in schizophrenia along with other medications and as a second line agent in bipolar disorder.

24
Q

Explain the limitations of the dopamine theory of schizophrenia

A
  • Block of D2 receptors immediate – onset of psychoses improvement 3-6 wks
  • Clozapine weak D2 blocker but extremely effective antipsychotic
  • If DA system completely responsible, D2 blockers would be more effective
  • Evidence exists for role of glutamate and serotonin and acetylcholine systems
25
Q

describe the mechanism of antipsychotic drug action

A

Virtually all antipsychotic drugs block dopamine D2 receptors. Drugs that increase dopaminergic activity produce or aggravate psychosis

26
Q

Mesolimbic pathway

A

Subserve the integration of sensory input and motor responses with affective or emotional data
+++++++

27
Q

Mesocortical pathway

A

Involved in communication and social abilities

———-

28
Q

Nigrostriatal pathway

A

Part of basal ganglia (aka extrapyramidal tract) plays a central role in planned, coordinated movement

29
Q

Tuberoinfinduibular pathway

A

Hypothalamic neurons release DA in pituitary to inhibit prolactin release

30
Q

Serotonin Hypothesis

A
31
Q

Glutamate Hypofunction Hypothesis

mesocortical and mesolimbic

A

Cortical Glu neurons activate cortical GABA neurons to produce a tonic inhibition of cortical Glu excitation of mesolimbic DA neurons
Hypofunction in cortical NMDA-Glu neurons  remove GABA inhibition  activate DA Neurons  positive symptoms of schizophrenia

Cortical Glu neurons activate GABA to inhibit cortical Glu to inhibit VTA GABA to produce a tonic excitation of mesocortical DA neurons
Hypofunction in cortical NMDA-Glu neurons  remove inhibition of VTA GABA  inhibit mesocortical DA  negative symptoms of schizophrenia

32
Q

Positive symptoms of schizophrenia (delusions, hallucinations) are believed to result from:

A

Overactivity of dopamine neurons in the mesolimbic system

Underactivity of glutamate neurons in the prefrontal cortex

33
Q

Quetiapine*

A

atypical antipsychotic, reduced EPSE, poor D2 block, good 5HT2a block

34
Q

Atypical antipsychotic agents such as clozapine (Clozaril) or olanzapine (Zyprexa) are distinguished from typical agents such as haloperidol (Haldol) because they are associated with a lower incidence of:

A

Extrapyramidal side effects

35
Q

side effects of D2 block

A

tardive dyskinesia in elderly females (involuntary orofacial mvts)
Pseudoparkinsons- treat with anticholinergics

36
Q

Antipsychotic agents exert both therapeutic actions and side effects as a result of dopaminergic receptor blocking activities in various brain regions. Appetite increase, weight gain and diabetes are common side effects of antipsychotic use that result from block of dopamine receptors at which site?

A

hypothalamus

37
Q

Agranulocytosis (low white blood cell count) can predispose patients to infections. Which of the following agents used in the pharmacotherapy of mental illnesses is associated with the highest incidence of agranulocytosis as a side effect?

A

clozapine

38
Q

*Which of the following therapeutic actions or side effects of antipsychotic agents does NOT result from blockade of dopamine receptors?

A

Orthostatic hypotension

39
Q

Monoamine Theory of Depression

A

Dysregulation of pre-and post-synaptic control of NE-5HT neurotransmission
Synaptic changes produced by antidepressants then lead to alterations of gene expression
Time frame for these changes correlates with onset of mood changes

40
Q

SSRI S/E

A

Nausea-diarrhea [5HT3] (increased serotonin effects in GI tract)
Activation-insomnia (commonly)
Restlessness [5HT2] (akathisia), somnolence possible
Weight gain
!Sexual dysfunction [5HT3]
Cognitive blunting
Very low likelihood of fatalities in overdose
Withdrawal (discontinuation) symptoms
Flu-like or neurologic symptoms severity related to half-life (shorter > longer [paroxetine > fluoxetine])

41
Q

SNRI side effects

A

Venlafaxine - Duloxetine
Hypertension, anxiety, nausea, somnolence, sweating, dizziness, sexual dysfxn!!
More rapid appearance of withdrawal symptoms than with SSRIs

42
Q

Norepinephrine Dopamine Reuptake Inhibitors (NDRIs) S/E

A

Bupropion
Dizziness, dry mouth, tremor, insomnia, anxiety, aggravation of psychosis
Potential for seizures at high doses

43
Q

TCAD S/E

A

Sedation: Lassitude, fatigue, sleepiness [Amitriptyline
Antimuscarinic Effects:
Blurred vision, constipation, dry mouth, urinary hesitancy, fuzzy thinking
Higher doses-aggravation of narrow angle glaucoma, paralytic ileus, urinary retention, delirium
Orthostatic hypotension (α1 blockade)
EKG abnormalities arrhythmias sudden death in overdose
Neurologic: Tremor, paresthesias, can see seizures in overdose

44
Q

Monoamine Oxidase Inhibitors S/E

A

Postural hypotension via chronic increase in false neurotransmitter formation
Seizures, shock, hyperthermia in overdose

45
Q

what drug class do u worry about a Tyramine reaction (hypertensive crisis)?

A

beer wine cheese fava beans, MAOI

46
Q

Which of the following statements concerning the side effects and toxicities of antidepressant drug use is FALSE?

A Concomitant use of SSRIs and MAOIs may result in a serotonin syndrome.
B SSRIs (e.g., fluoxetine) can induce hypomania in patients with bipolar disorder.
C Tricyclic antidepressants (e.g., amitriptyline) have a higher incidence of anticholinergic side effects than SSRIs.
D Inhibitors of dopamine and norepinephrine reuptake (e.g., bupropion) have been observed to cause anxiety and restlessness due to their mild stimulant action.
E None of the above (All are TRUE).

A

B

47
Q

serotonin syndrome

A

SSRIs + MAOIs  serotonin syndrome

Hyperthermia, muscle rigidity, myoclonus

Rapid changes in mental status (confusion / agitation) and vital signs (hypertension and tachycardia)

Also SSRIs + opioids: analgesics [meperidine-tramadol] and antitussive [ dextromethorphan]

48
Q

Which of the following statements concerning the treatment of bipolar disorder with lithium is accurate (TRUE)?
A Lithium will alleviate the manic phase of bipolar disorder within 24 hours.
B Excessive intake of sodium chloride will decrease lithium plasma levels.
C Lithium dosage may need to be decreased in patients taking thiazide diuretics.
D Lithium does not cross the blood brain barrier.
E Lithium does not cross the placental barrier.
F Lithium is a safe drug with a wide therapeutic index.

A

Excessive intake of sodium chloride will decrease lithium plasma levels.
Lithium dosage may need to be decreased in patients taking thiazide diuretics.

Neuro 4 week 1 (14 decks)

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