psychosocial approaches to mental illness 1. Sigmund Freud -> () 2. B.F. Skinner -> ()

1. psychoanalysis 2. behaviorism

Chapter 22: Mental Illness Flashcards by Apphia Trillo

Branch of medicine concerned with the diagnosis and treatment of nervous system disorders

neurology

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neurological disorders Help illustrate the role of () in normal brain function

physiological processes

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Branch of medicine concerned with the diagnosis and treatment of disorders that affect the mind or psyche

psychiatry

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an individual is said to me “mentally ill” at the point when the person has a diagnosable disorder of (3) that causes distress or impaired functioning

thought (e.g. schizo), mood (affective), or behavior (e.g. anxiety)

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human behavior is ultimately the product of ()

brain activity

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the brain is the product of 2 mutually interacting factors:

heredity, environment

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earlier belief regarding illness (in context of body and mind)

illness in body -> for doctors
illness in mind -> for religion

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current belief on mental illness

Most disorders of mood, thought, and behavior have biological explanations.

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psychosocial approaches to mental illness

Sigmund Freud -> ()
B.F. Skinner -> ()

psychoanalysis
behaviorism

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2 assumptions that form the basis for Freud’s psychoanalysis

much of mental life is unconscious
past experiences, particularly in childhood, shape how a person will feel and respond throughout life

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accdg. to Freud’s psychoanalysis, mental illness arises when ()

unconscious and conscious elements of psyche come into conflict

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accdg. to Freud’s psychoanalysis, treatment for mental illness involves ()

unearthing hidden secrets of unconscious

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accdg. to behaviorism, Many behaviors are () -> basis of mental illness

learned maladaptive responses to the environment

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accdg. to behaviorism, mental illness is treated by ()

“unlearning” maladaptive behaviors through behavior modification

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The use of verbal communication to help patient
* Only tools available until the revolution of biological
psychiatry

Psychotherapy

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Former major disorder: () ->10-15% of institutionalized patients
Symptoms: mania, cognitive deterioration

general paresis of the insane

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general paresis of the insane is caused by ()

infection with Treponema pallidum (syphilis)

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aside from infections, () can also cause or confer risk for psychiatric disease

psychiatric disorders also occur in infection-free indivs

gene mutations

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approach of using genetic info to develop treatment

new approach for treating psychiatric diseases)

molecular medicine

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discovery of an abnormal physiological condition

pathophysiology

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Challenges of Psychiatric Diseases

Mental disorders are diagnosed by clinicians based on (1), not by (2) -> Same diagnosis may arise from many causes

how the appear or are described by the patient (signs and symptoms)
knowledge of their underlying cause (etiology)

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Challenges of Psychiatric Diseases

(): not all mental illnesses have a clear genetic basis, and for those that do, a large number of genes have been implicated

Genetic complexity

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a radical new approach to overcoming the challenges od psych. diseases is to study the () from individual patients

pathophysiology of neurons

neurons from individual patients using skin cells that are transformed into induced pluripotent stem cells (iPSCs)

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– Caused by inappropriate expression of fear
– Most common of psychiatri cdisorders (>15% of Americans in a given year)

fear: adaptive response to threatening situations

anxiety disorder

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(): sudden feelings of intense terror that occur without warning

Panic attacks

(): reoccurring unexpected panic attacks

Panic disorder

Severe anxiety about being in situations where escape might be difficult or embarrassing; leads to avoidance of situations irrationally perceivd as threatening

agoraphobia

Overwhelming and unreasonable fear of objects or situations that pose little real danger but provoke anxiety and avoidance

specific phobias

Several disorders that are no longer classified as “anxiety disorders” are nevertheless characterized by increased anxiety. Two of the most common are ()

PTSD, OCD

long-lasting consequence of psychological trauma

Post-traumatic stress disorder (PTSD)

(): repetitive behaviors or mental acts to reduce the anxiety associated with obsessions (e.g., repeated hand-washing, checking to make sure that something is not out of place ...)

Compulsions

(): recurrent, intrusive thoughts, images, ideas, or impulses (e.g., contamination with germs ...)

Obsessions

# Biological Bases of Anxiety Disorders 2 major causes for anxiety disorders

genetic predisposition, occurence of stressful life events

Anxiety disorders: occurrence of an inappropriate stress response when a () is absent or when it is not immediately threatening ## Footnote () - threatening stimulus

stressor

coordinated reaction to threatening stimuli

stress response

() orchestrates humoral, visceromotor, and somatic motor responses in stress response

Hypothalamus

the stress response is characterized by (4)

1. avoidance behavior 2. increased vigilance and arousal 3. activation of symapthetic ANS 4. cortisol release from adrenal glands

humoral component of the stress response is mediated by ()

Hypothalamic-Pituitary-Adrenal Axis

() may degenerate hippocampus -> less inhibition of HPA axis -> less reguation of stress response

Chronic stress ## Footnote decreased hippocampal volume in some PTSD patients

# Treatments for Anxiety Disorders – gradually increase the exposure to threatening stimuli – learning that the stimuli are not dangerous

Psychotherapy

# Treatments for Anxiety Disorders act by altering chemical synaptic transmission in brain

Anxiolytic medications

# Treatments for Anxiety Disorders: Anxiolytic medications – (1) (binds to site in GABA receptor to make GABA more effective if producing inhibition) – (2) (effective for OCD; effect develops slowly) ## Footnote *virtually all drugs enhancing GABA actions are anxiolytic

1. Benzodiazepines 2. Serotonin-selective reuptake inhibitors (SSRIs)

# Treatments for Anxiety Disorders * Target for new drugs: () -> if inactive, can't activate cortisol release

CRH receptors

Repeated episodes of mania, or mixed episodes of mania and depression

Bipolar (Manic-Depressive) Disorder

– A distinct period of abnormally and persistently elevated, expansive, or irritable mood – Symptoms: inflated self-esteem or grandiosity; a decreased need for sleep; increased talkativeness; impaired judgement

Mania

# Bipolar Disorder * Type I: () (1%) * Type II: () (0.6%)

1. mania 2. hypomania

– a milder form of mania – often associated with increased productivity or creativity – always associated with episodes of major depression

hypomania

() can enhance cognitive processes, creative thinking, and linguistic skills

Hypomania

() states reduce the need for sleep, foster intense concentration, create unmitigated self-confidence, and eliminate concern for social norms

Manic

# Biological Bases of Affective Disorders Deficit in central diffuse modulatory systems (NE, 5-HT)

monoamine hypothesis

# The Monoamine Hypothesis (): for high blood pressure; causes severe depression (20%); depletes central DA, NE and 5-HT

Reserpine

# The Monoamine Hypothesis (): for tuberculosis; causes mood elevation

Monoamine oxidase (MAO) inhibitors

# The Monoamine Hypothesis (): antidepressant; inhibits reuptake of 5-HT and NE

Imipramine

treatment of depression based on monoamine hypothesis: focus on ()

central 5-HT and/or NE synapses

# Biological Bases of Affective Disorders Genetic predisposition + other stress factors (especially during early childhood)

The Diathesis-Stress Hypothesis ## Footnote Genetic predisposition = diathesis

accdg. to the Diathesis-Stress Hypothesis, () is the main site where genetic and environmental factors converge to cause mood disorders

HPA axis

Brain () injection in animals induces depression symptoms (insomnia, low appetite, high anxiety ...)

CRH

# Biological Bases of Affective Disorders Resting-state metabolic activity in anterior cingulate cortex increased in depression; decreased by treatment

Anterior Cingulate Cortex Dysfunction

activity in the Anterior Cingulate Cortex is increased by (1) and decreased by (2)

1. sad memory recall 2. depression treatment

(): localized electrical stimulation – Unknown mechanism in relieving depression – Affects temporal lobe – Advantage: quick relief of depression, mania – Adverse effect: loss of prior memories, impaired storage of new information

Electroconvulsive therapy (ECT)

(): Help patients overcome negative views. – Effective for mild to moderate depression – Helps patients overcome negative view – Neural basis of the treatment unknown

Psychotherapy

examples of antidepressants

MAO inhibitors, tricyclics, and SSRIs

The nature of adaptive changes unknown, but antidepressants dampen hyperactivity of the () in humans

HPA system and ACC

# Antidepressants: animal studies long-term () → glucocorticoid receptor elevation in the hippocampus → suppression of HPA and ACC

serotonin

SSRIs increase () in the hippocampus

neurogenesis

# Antidepressants: new drug target (): rapid action; for suicidal patients; psychotic side effects

Ketamine ## Footnote act on CRH receptors

basis of lithium treatment for bipolar disorder

Mechanisms unknown, but lithium enters neurons and inhibits PIP2 turnover and adenylate cyclase activity

basis of deep brain stimulation as treatment for severe depression ## Footnote used only when patient fails to respond to other treatments

implanted electrode delivers electrical stim.; decreases activity in brain circuits that are chronically active ## Footnote technically kind of brain surgery -> last resort

Severe mental disorder—loss of contact with reality

schizophrenia

Schizophrenia () in ways that healthy people find difficult to understand

distorts thoughts and perceptions

3 possible biological bases of schizophrenia

* Genes and the Environment * The Dopamine Hypothesis * The Glutamate Hypothesis

describe how genes and the environment explain onset of schizophrenia

faulty genes (roles in synaptic transmission) -> vulnerability to environmental factors (viral infection; poor maternal nutrition; marijuana) ## Footnote explains physical changes in schizophrenia patient brains

describe how the dopamine hypothesis explains onset of schizophrenia

psychotic episodes triggered by activation of dopamine receptors

() overdose can lead to psychotic episodes with positive symptoms indistinguishable from those of schizophrenia

Amphetamine ## Footnote Neuroleptic drugs (antipsychotic drugs)—potent blockers of dopamine D2 receptors

describe how the glutamate hypothesis explains the onset of schizophrenia

Schizophrenia reflects diminished activation of NMDA receptors in the brain ## Footnote NMDA recpetor inhibitors (ketaine, phenylcyclidine) -> don't affect dopaminergic transmission

involuntary lips and jaw movements

Tardive dyskinesia

basic treatment for schizophrenia

Drug therapy combined with psychosocial support

(1) neuroleptics, such as chlorpromazine and haloperidol, act at (2) -> Reduce the positive symptoms of schizophrenia

1. Conventional 2. D2 receptors

c.f. conventional neuroleptics, () have less side effects when used for schizophrenia treatment

atypical neurleptics

newest focus for schizophrenia drug research

NMDA receptors