Biopsychology of Psychiatric Disorders Flashcards

1
Q

For schizophrenia diagnosis: 2 of the following for atleast 6 months

A

delusions: unjustifiable beliefs
-hallucinations
-disorganized speech
-disorganized behaviour
-weak or absent signs of emotions, speech, or socialization.
Prevalence: approx. 1.3%

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2
Q

type I schizophrenia

A

Positive symptoms (behavioural excesses, such as hallucinations and agitated movements);
Possibly due to a dopaminergic dysfunction associated with acute onset, good prognosis, and a favourable response to neuroleptics

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3
Q

type II schizophrenia

A

Negative symptoms (behavioural deficits, such as reduction in motivation, catatonia) and associated with chronic (stabilized) affliction, poor prognosis, poor response to neuroleptics, cognitive impairments, enlarged ventricles, and cortical atrophy, particularly in the frontal cortex

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4
Q

cognitive symptoms of schizophrenia

A

Slow processing speed
Impaired long-term memory
Difficulty perceiving others’ emotions from their facial expressions and body language
Errors in perceiving others’ intentions and beliefs.
Abnormalities in the Wernickes area, auditory areas, subcortical areas, hippocampus, and dorsolateral prefrontal cortex

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5
Q

the neurodevelopmental hypothesis

A

Abnormalities occurred in prenatal or neonatal nervous system development can produce abnormalities in the developing brain that predispose to schizophrenia.

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6
Q

the two-hit hypothesis

A

A combination of a genetic predisposition and environment in prenatal/neonatal development, later in life, or both

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7
Q

Dopamine hypothesis

A

Schizophrenia results from excess activity at dopamine synapses in certain areas of the brain.
Substance-induced psychotic disorder
Research indicates increased activity, specifically at the D2 receptor

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8
Q

second generation (atypical) antipsychotics

A

Clozapine, Amisulpride, Risperidone, Olanzapine
Weakly block D2 receptors so there are fewer Parkinson-like effects
But its atypical because it also blocks D1, D4, and serotonin 5-HT2 receptors
-5-HT is serotonin
Improves motivation and reduces agitation, but may result in weight gain

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9
Q

glutamate hypothesis

A

Deficient activity at glutamate synapses, especially in the prefrontal cortex
Dopamine inhibits glutamate release
Or, glutamate stimulates neurons that inhibit dopamine release
Increased dopamine can produce the same effects as decreased glutamate

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10
Q

ketamine

A

Has hallucinogenic properties and is used in some clinical settings (mostly by vets) as a dissociative anesthetic (i.e., you feel separate from the body, and it reduces pain)
The difference between the “correct” dose and a potentially lethal overdose is on the order of milligrams.
Date rape drug

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11
Q

monoamine oxidase (MAO) inhibitors

A

Block the enzyme MAO from degrading neurotransmitters such as dopamine, noradrenaline, and serotonin.
Thus, these drugs increase amounts of dopamine, noradrenaline, and serotonin for release

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12
Q

tricyclic antidepressants

A

First-generation antidepressants with a chemical structure characterized by three rings that block reuptake transporter proteins
Block transporter proteins that reabsorb serotonin, dopamine, and norepinephrine into the presynaptic neuron after release; therefore, more norepinephrine, dopamine and serotonin are available.
E.g., Amitriptyline

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13
Q

second-generation antidepressants

A

Action is similar to first-generation antidepressants but is more selective in its action on the serotonin reuptake transporter proteins
Selective Serotonin Reuptake Inhibitors (SSRIs)
Block the reuptake of serotonin by the presynaptic terminal
E.g. Prozac (fluoxetine)- prescribed for depression

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14
Q

SNRIs

A

Serotonin and norepinephrine reuptake inhibitors
Block reuptake of serotonin and norepinephrine
E.g., desvenlafaxine (Pristiq), duloxetine (Cymbalta), levomilnaciprin (Fetzima), venlafaxine (Effexor XR),

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15
Q

Atypical antidepressants

A

Miscellaneous group of drugs with antidepressant effects and milder side effects
E.g., bupropion (Wellbutrin)
Inhibits the reuptake of dopamine and, to some extent, norepinephrine, but not serotonin

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16
Q

antidepressants

A

Most people with depression have normal levels of neurotransmitters
Decreasing serotonin in control groups does not provoke depression
Drugs affect neurotransmitters in synapses quickly (minutes to hours)
Result improving mood often requires weeks

17
Q

Cognitive Behavioural Therapy

A

Cognitive-behavioural Therapy
It has been shown to be equally effective for all levels of depression
Causes increased metabolism in same brain areas as antidepressants
More likely to reduce relapse months or years later
Combination of antidepressant drugs and psychotherapy shows more rapid improvement

18
Q

bipolar disorder

A

Manic episodes interspersed with depressive episodes
Bipolar disorder I: characterized by full-blown episodes of mania
Bipolar II: characterized by much milder manic phases, called hypomania
Brains use of glucose increases during periods of mania

19
Q
A