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Medications and Behavior > Chapter 5 Test (Psychotic Disorders) > Flashcards

Chapter 5 Test (Psychotic Disorders) Flashcards

1
Q

Amphetamine challenge

A

Scanning for radioactive markers of dopamine receptor occupancy following the administration of amphetamine. A measure of dopamine activity in the brain.

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2
Q

Amphetamine induced psychosis

A

A psychotic state similar to schizophrenia, induced by amphetamine overdose.

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3
Q

Antipsychotic

A

A drug that is used to treat symptoms of schizophrenia and other psychotic disorders

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4
Q

Atypical antipsychotics

A

Antipsychotic drugs that different in their mechanism of action from their predecessors, the phenothiazines.

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5
Q

What was the first Atypical antipsychotic widely used?

A

clozapine (Clozaril)

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6
Q

dopamine hypothesis

A

Excessive dopamine activity in the mesolimbic-cortical systems of the brain underlie schizophrenia and its symptoms.

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7
Q

Electric shock therapy

A

The induction of a severe seizure in a patient by delivering electric shocks to the head. Used as a treatment for drug resistant schizophrenia and depression.

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8
Q

Extrapyramidal symptoms

A

Severe motor impairment following disruptions to neurons outside of the major pyramidal tracks descending from the medulla. These symptoms are often caused by long-term use of phenothiazine drugs.

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9
Q

Frontal lobotomy

A

Separating the prefrontal areas from the remainder of the frontal cortex by knife cuts or by destroying these areas with ice picks inserted behind the eyes. Used as an early treatment for sever psychosis.

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10
Q

Insulin shock

A

A comatose state induced by severe hypoglycemia following an injection of insulin. Used as an early treatment for schizophrenia.

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11
Q

Negative symptoms

A

Symptoms of schizophrenia characterized by features removed from normal behavior and functioning.

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12
Q

What are the Negative symptoms of Schizophrenia

A

1) Lack of affect
2) Social Withdrawal
3) cognitive impairment
4) Muscle rigidity

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13
Q

Positive Symptoms

A

Symptoms of schizophrenia that are characterized by features that are added to normal behavior and functioning.

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14
Q

What are the positive symptoms of Schizophrenia?

A

1) Delusions
2) Hallucinations
3) Motor Symptoms
4) Emotional Turmoil

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15
Q

Prepulse Inhibition

A

The ability to inhibit a startle response to a strong stimulus if given a warning signal or prepulse stimulus. Schizophrenic patients show deficits in prepulse inhibition.

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16
Q

Do Schizophrenic patients show a deficit or abundance of prepulse inhibition.

A

A deficit

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17
Q

Receptor competition

A

The ability of a drug to compete with a neurotransmitter for receptor binding is measured by its capacity to displace a radioactive ligand.

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18
Q

What is used to predict drug effectiveness against schizophrenic symptoms?

A

Receptor competition

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19
Q

Tardive dyskinesia

A

Involuntary movements and motor tics.

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20
Q

Where does tardive dyskinesia often appear?

A

1) Mouth
2) tongue

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21
Q

After what does tardive dyskinesia appear?

A

After long-term phenothiazine use.

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22
Q

What is the most common type of hallucination?

A

Auditory (in Wernicke’s)

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23
Q

When does Schizophrenia typically emerge?

A

Early adulthood and is life-long for most

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24
Q

What is the lifetime prevalence of Schizophrenia?

A

1%

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25
Q

Where is the greatest incidence of Schizophrenia?

A

Among African-Caribbeans in England

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26
Q

Is there a consensus on what gene or genes are involved in Schizophrenia?

A

No

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27
Q

Do sons and daughters have a higher chance of getting Schizophrenia if their parents have it?

A

Yes it is tenfold

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28
Q

Does environment or genetics play a greater role in the etiology of Schizophrenia?

A

Environmental

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29
Q

How long do symptoms need to be present before diagnosis of schizophrenia?

A

one month

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30
Q

How many symptoms need to be present for diagnosis of Schizophrenia?

A

Two

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31
Q

When were antipsychotic drugs discovered?

A

1950s

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32
Q

What were early treatments for Schizophrenia?

A

1) Physical restraints
2) Insulin shock

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33
Q

What was the most widely used surgical procedure for Schizophrenia?

A

Frontal lobotomy

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34
Q

By who and when were frontal lobotomies introduced?

A

By Antonio Moniz in late 1930s

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35
Q

In the dopamine hypothesis, where is there an excessive activity of dopamine?

A

The striatum and mesolimbic pathways

36
Q

In the dopamine hypothesis, where is there an decrease activity of dopamine?

A

prefrontal cortex

37
Q

What is amphetamine psychosis?

A

When large doses or prolonged use of things such as cocaine and amphetamines induce psychotic symptoms indistinguishable from schizophrenic symptoms.

38
Q

What is the only predictor of a drug’s antipsychotic efficacy?

A

Its ability to block dopamine receptors

39
Q

Is the correlation between clinically effective doses of antipsychotic drugs with their ability to compete for and block D2 receptors found in other receptor types?

A

NO

40
Q

Are there other neurotransmitters implicated in schizophrenia?

A

Yes

41
Q

What are the positive symptoms of schizophrenia associated with?

A

The hyperdopamine activity in striatum and mesolimbic

42
Q

What are the negative symptoms of schizophrenia associated with?

A

the hypodopaminergic activity in mesocortical pathways to the prefrontal cortex.

43
Q

How dose the lack of dopamine in the prefrontal cortex affect the dopamine in the mesolimbic area?

A

It may result in increased dopamine activity

44
Q

What glutamate NMDA receptor antagonists produce effects that mimic schizophrenia? (Pos and neg)

A

phenylcyclidine and ketamine

45
Q

Schizophrenic patients have ——- numbers of NMDA receptors in the thalamus and the hippocampus

A

depressed

46
Q

Glutamate dysfunction is associated with pos or neg symptoms of Schizophrenia?

A

negative

47
Q

Where is there a loss of cell volume in Schizophrenia?

A

1) frontal lobes
2) hippocampus
3) amygdala

48
Q

When were phenothiazines discovered?

A

1950s

49
Q

What was chlorpromazine (Thorazine) originally used for?

A

antiemetic (antinausea)

50
Q

chlorpromazine (Thorazine) has what kind of properties?

A

Sedative

51
Q

When was the first use of it for a psychotic patient?

A

France 1952

52
Q

What is the pathology of phenothiazines?

A

They compete for dopamine receptors (mostly D2)and decrease dopamine neural transmission

53
Q

What percent of D2 receptors need to be occupied by phenothiazines to have a therapeutic effect?

A

70 - 80%

54
Q

What is the initial response to phenothiazine treatment?

A

An increase in dopamine synthesis and release due to auto receptor antagonism.

55
Q

Do phenothiazines block other receptors?

A

Yes, norepinephrine, muscarinic, histamine

56
Q

What are the side effects when phenothiazines block norepinephrine?

A

1) hypotension
2) tachycardia
3) sedation

57
Q

What are the side effects when phenothiazines blocks muscarinic receptors?

A

1) dry mouth
2) dry eyes
3) dilated pupils
4) blurred vision
5) decrease sweating
6) memory impairment

58
Q

What are the side effects when phenothiazines block histamine receptors?

A

sedative effects

59
Q

What happens when phenothiazines block D2 receptors in the basal ganglia?

A

Serious and often debilitating motor effects

60
Q

What is the first non-phenothiazine used for treatment of psychotic disorders?

A

haloperidol (Haldol)

61
Q

haloperidol (Haldol) Pathology/facts

A

1) Competes for and blocks D2 receptors as effectively as phenothiazines
2) Produces severe extrapyramidal side effects
3) Has less affinity for H1 receptors so sedation is not as problematic as with phenothiazines

62
Q

Non-phenothiazines developed in 1970s

A

1) loxapine
2) molindone
3) pimozide

63
Q

What is different about loxapine?

A

It also competes for and antagonizes serotonin 5-HT receptors

64
Q

What is the decade of the brain?

A

1990s

65
Q

What was the first atypical antipsychotics introduced in the 1990s?

A

clozapine (Clozaril)

66
Q

While most atypicals vary slightly in mechanism, what do most antagonize to some extent?

A

dopamine D2 and 5-HT 2a

67
Q

What is the first antipsychotic that appeared to improve symptoms of schizophrenia without causing severe extrapyramidal effects?

A

clozapine (Clozaril)

68
Q

Does clozapine compete weakly or strongly with D2 receptors?

A

weakly

69
Q

How much of dopamine receptors does clozapine transiently occupy?

A

75 - 80%

70
Q

What receptors does clozapine antagonize?

A

D2 and 5-HT2a

71
Q

What are the side effects of clozapine (Clozaril)?

A

1) sedation
2) dizziness
3) hypotention
4) high hearth rate
5) dry mouth and eyes
6) constipation
7) HYPERGLYCEMIA
8) DIABETES

72
Q

What is the most serious side effect of clozapine (Clozaril)

A

agranulocytosis (in about 0.8% of patents)

73
Q

What has risperidone (Risperdal) been used to treat?

A

1) schizophrenia
2) bipolar disorders
3) autism
4) disruptive behaviors

74
Q

What does resperidone (Risperdal) competitively block?

A

D2, 5-HT2a, and noradrenergic

75
Q

How does resperidone (Risperdal) compete with dopamine receptors on a low therapeutic dose?

A

weakly

76
Q

Does resperidone (Risperdal) have a high or low risk of extraprymidal side effects a a low therapeutic dose?

A

low risk

77
Q

amisulpride (Solian) facts

A

1) Not approved by FDA in USA for schizophrenia
2) as effective as other atypical antipsychotics
3) more effective in treating depression associated with psychotic symptoms

78
Q

What is different about amisulpride (Solian)?

A

1) acts preferentially in low doses on presynaptic autoreceptors
2) does NOT block 5-HT2a receptors
3) causes less weight gain
4) minds weekly to dopamine receptors resulting in less extrapyramidal effects

79
Q

What is the most predictive factor of an antipsychotic’s propensity to cause extrapyramidal symptoms?

A

How tightly it competes for dopamine D2 receptors in basal ganglia

80
Q

What is unique about aripiprazole (Abilify)?

A

it agonizes and antagonizes dopamine

81
Q

When was aripiprazole (Abilify) approved for adults? adolescents?

A

1996, 2007

82
Q

What does NMDA stand for?

A

N-methyl D-aspartate

83
Q

glutamate dysfunction in the thalamus and hippocampus leads to what in the cortex and the development of what in schizophrenia?

A

1) excitotoxic glutamate activity in cortex
2) development of negative symptoms late in schizophrenia

84
Q

How do you increase glutaminergic NMDA activity?

A

By directly increasing NMDA activity with glutamate agonists

85
Q

How do psychotic patients filter extraneous stimuli?

A

they can’t always distinguish what is important info and what isn’t

86
Q

Are atypical or phenothiazine treatments more effective in reinstating prepulse inhibition?

A

Atypical antipsychotics (specifically risperidone)

Medications and Behavior (40 decks)

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