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PMCOL II > Psychosis > Flashcards

Psychosis Flashcards

1
Q

Positive Symptoms

A

Mental phenomena that are normally absent in healthy individuals
(Hallucinations and Delusions)

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2
Q

Negative Symptoms

A

Loss or impairment of normal physiological functions
(Loss of motivation and social withdrawal)

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3
Q

Cognitive Symptoms

A

Poor concentration, disorganized thinking, poor memory

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4
Q

What influences the development of schizophrenia

A

Highly influenced by genes

Environmental factors can also trigger neurochemical and structural changes leading to schizophrenia

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5
Q

Dopamine Hypothesis of Schizophrenia

A

Symptoms caused by hyperactivity of dopamine system

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6
Q

Inferential evidence of Dopamine hypothesis

A

Drugs that increase synaptic dopamine can cause delusions and hallucinations at high doses
Drugs that block dopamine receptors are effective antipsychotics

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7
Q

Where is the largest population of dopamine neurons located

A

Midbrain

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8
Q

Where are the Mesocortical and mesolimbic systems located

A

Ventral tegmental area (VTA)

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9
Q

Hyperactivity of the dopamine receptors in the VTA causes?

A

Contributes psychotic symptoms

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10
Q

Blocking dopamine transmission can treat what kind of symptoms

A

Positive symptoms of schizophrenia

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11
Q

What do the mesocortical and mesolimbic system mediate

A

Memory, learning, thought organization

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12
Q

What are D1 receptors, what are their effects

A

Gs coupled receptors
Increase AC, increase cAMP

Do not contribute to therapeutic effect of antipsychotic drugs

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13
Q

What are D2 receptors, what are their effects

A

Gi coupled receptors
Inhibits AC, decrease cAMP
Inhibiting an inhibitory GABAergic interneuron that is regulating Dopamine release through inhibition –> Thus, increases dopamine
Causes antipsychotic effects

Inhibition of D2 is related to antipsychotic effects, stops disinhibition of GABAergic interneurons and allows them to inhibit and regulate dopamine levels

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14
Q

Nigrostriatal System

A

This dopamine system contains dopamine neurons in the substantia nigra and project to the striatum

initiates movement
Inhibiting this pathway produces extrapyramidal symptoms (movement disorders)

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15
Q

Tardive dyskinesias

A

Involuntary movement of face and moth

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16
Q

Tuberoinfundibular System

A

This dopamine system contains dopamine neurons in the arcuate nucleus

Controls hormone release in the pituitary
Dopamine inhibits the secretion of prolactin and growth hormone

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17
Q

How does long term use of antipsychotics affect the Tuberoinfundibular System

A

Antipsychotics lower dopamine –> Nothing to inhibit prolactin release –> Hyperprolactinemia

Decreased libido, infertility, amenorrhea

18
Q

Glutamate Hypothesis of Schizophrenia

A

Symptoms are caused by deficiencies in glutamate signaling

19
Q

Evidence for Glutamate Hypothesis Hallucinogens

A

NMDA ( glutamate receptor) antagonists produce hallucinations

20
Q

Theory behind mechanism of Glutamate Hypothesis

A

Associated with hypofunctional (decrease in function) NMDA receptors on GABA interneurons in the cerebral cortex.

Decreased function of GABA interneurons mean less inhibition of downstream glutamate receptors. These glutamates receptors will start to activate dopamine.

Summary: Overactivation of downstream glutamate signaling to the VTA

21
Q

Serotonin Hypothesis of schizophrenia

A

Symptoms caused by an increase in serotonin signaling

22
Q

Evidence for serotonin hypothesis

A

5HT agonists (5HT = Serotonin) are hallucinogenic
5HT antagonists improves positive symptoms of schizophrenia

23
Q

Theory behind mechanism of Serotonin Hypothesis

A

5HT-2A receptors in the prefrontal cortex are activated enhancing the excitation of glutamate neurons activating mesolimbic dopamine systems

5HT-2A antagonists block glutamate release in the cortex, reduces hallucinations

24
Q

First Generation Antipsychotics or _____

A

Typical Antipsychotics

25
Q

Second Generation Antipsychotics or ___

A

Atypical Antipsychotics

26
Q

What are First Generation Antipsychotics effects

A

Targets D1 and D2 dopamine receptors

Efficacy focuses on D2 receptor antagonism

27
Q

What are Second Generation Antipsychotics effects

A

Antagonists for both D2 receptors (dopamine) and 5HT receptors (serotonin)

Lower affinity to dopamine receptors than first gen, produces less dopamine related side effects

28
Q

Haloperidol

A

First Generation Antipsychotic

Fast on, Slow off

29
Q

Chlorpromazine

A

First Generation Antipsychotic

30
Q

Clozapine

A

Second Generation Antipsychotic

Also binds to D4 dopamine receptors, and causes agranulocytosis (loss of white blood cells)

31
Q

Risperidone

A

Second Generation Antipsychotic

32
Q

What is the Therapeutic Margin of Typical Antipsychotics
(Percentage and side effect)

A

60-80% of D2 receptors need to be occupied to produce antipsychotic effect

80% of D2 occupancy will lead to side effects like extra pyramidal symptoms (movement disorder) and hyperprolactinemia (elevated prolactin)

33
Q

What is the Therapeutic Margin of Typical Antipsychotics
(Dose-Response Curve)

A

Has a narrow window between antipsychotic effects and neuroleptic threshold

Curves are both close to each other

34
Q

What is the Therapeutic Margin of Atypical Antipsychotics
(Percentage and side effect)

A

Has a wide therapeutic window between antipsychotic effects and neuroleptic threshold

Curves are far apart from each other

35
Q

What has more receptor rebinding mesolimbic/nigrostriatal pathway or tuberoinfundibular pathway

A

mesolimbic/nigrostriatal has a high degree of receptor rebinding due to dopamine being in a tight space when it lets go, nowhere for it to go so it rebinds to the receptor

In the tuberoinfundibular pathway blood flow will clear out dopamine

36
Q

Kinetics of Haloperidol

A

Fast on, Slow off

High receptor binding potential
High extrapyramidal side effects and increased prolactin release

37
Q

Kinetics of Chlopromazine

A

Fast on, Fast off

Fast on = high extrapyramidal effects (High affinity for binding at nigrostriatal and higher rebinding potential)

Fast off = normal prolactin release (Lets go of receptor and is cleared by blood)

38
Q

Kinetics of Clozapine

A

Slow on, fast off

Slow on = low extrapyramidal effects (lower rebinding potential)

Fast off = normal prolactin release (Lets go of receptor and is cleared by blood)

39
Q

What are the side effects of first generation antipsychotics

A

Extrapyramidal symptoms, dyskinesis, prolactin release

40
Q

What are the side effects of second generation antipsychotics

A

Cardiovascular effects, metabolic syndrome, diabetes, weight gain

PMCOL II (10 decks)

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