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BS450 > Chapter 22: Mental Illness > Flashcards

Chapter 22: Mental Illness Flashcards

1
Q

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

A

neurology

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2
Q

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

A

physiological processes

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3
Q

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

A

psychiatry

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4
Q

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

A

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

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5
Q

human behavior is ultimately the product of ()

A

brain activity

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6
Q

the brain is the product of 2 mutually interacting factors:

A

heredity, environment

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7
Q

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

A

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

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8
Q

current belief on mental illness

A

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

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9
Q

psychosocial approaches to mental illness

  1. Sigmund Freud -> ()
  2. B.F. Skinner -> ()
A
  1. psychoanalysis
  2. behaviorism
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10
Q

2 assumptions that form the basis for Freud’s psychoanalysis

A
  1. much of mental life is unconscious
  2. past experiences, particularly in childhood, shape how a person will feel and respond throughout life
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11
Q

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

A

unconscious and conscious elements of psyche come into conflict

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12
Q

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

A

unearthing hidden secrets of unconscious

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13
Q

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

A

learned maladaptive responses to the environment

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14
Q

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

A

“unlearning” maladaptive behaviors through behavior modification

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15
Q

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

A

Psychotherapy

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16
Q

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

A

general paresis of the insane

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17
Q

general paresis of the insane is caused by ()

A

infection with Treponema pallidum (syphilis)

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18
Q

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

psychiatric disorders also occur in infection-free indivs

A

gene mutations

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19
Q

approach of using genetic info to develop treatment

new approach for treating psychiatric diseases)

A

molecular medicine

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20
Q

discovery of an abnormal physiological condition

A

pathophysiology

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21
Q

Challenges of Psychiatric Diseases

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

A
  1. how the appear or are described by the patient (signs and symptoms)
  2. knowledge of their underlying cause (etiology)
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22
Q

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

A

Genetic complexity

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23
Q

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

A

pathophysiology of neurons

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

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24
Q

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

fear: adaptive response to threatening situations

A

anxiety disorder

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24
Q

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

A

Panic attacks

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24
Q

(): reoccurring unexpected panic attacks

A

Panic disorder

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25
Q

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

A

agoraphobia

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26
Q

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

A

specific phobias

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27
Q

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

A

PTSD, OCD

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28
Q

long-lasting consequence of psychological trauma

A

Post-traumatic stress disorder (PTSD)

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29
Q

(): 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 …)

A

Compulsions

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29
Q

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

A

Obsessions

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30
Q

Biological Bases of Anxiety Disorders

2 major causes for anxiety disorders

A

genetic predisposition, occurence of stressful life events

31
Q

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

() - threatening stimulus

A

stressor

32
Q

coordinated reaction to threatening stimuli

A

stress response

33
Q

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

A

Hypothalamus

33
Q

the stress response is characterized by (4)

A
  1. avoidance behavior
  2. increased vigilance and arousal
  3. activation of symapthetic ANS
  4. cortisol release from adrenal glands
34
Q

humoral component of the stress response is mediated by ()

A

Hypothalamic-Pituitary-Adrenal Axis

35
Q

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

A

Chronic stress

decreased hippocampal volume in some PTSD patients

36
Q

Treatments for Anxiety Disorders

– gradually increase the exposure to threatening
stimuli
– learning that the stimuli are not dangerous

A

Psychotherapy

36
Q

Treatments for Anxiety Disorders

act by altering chemical synaptic transmission in brain

A

Anxiolytic medications

37
Q

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)

*virtually all drugs enhancing GABA
actions are anxiolytic

A
  1. Benzodiazepines
  2. Serotonin-selective reuptake inhibitors (SSRIs)
38
Q

Treatments for Anxiety Disorders

  • Target for new drugs: () -> if inactive, can’t activate cortisol release
A

CRH receptors

39
Q

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

A

Bipolar (Manic-Depressive) Disorder

40
Q

– 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

A

Mania

41
Q

Bipolar Disorder

  • Type I: () (1%)
  • Type II: () (0.6%)
A
  1. mania
  2. hypomania
42
Q

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

A

hypomania

43
Q

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

A

Hypomania

44
Q

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

A

Manic

45
Q

Biological Bases of Affective Disorders

Deficit in central diffuse modulatory systems (NE, 5-HT)

A

monoamine hypothesis

46
Q

The Monoamine Hypothesis

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

A

Reserpine

47
Q

The Monoamine Hypothesis

(): for tuberculosis; causes mood elevation

A

Monoamine oxidase (MAO) inhibitors

48
Q

The Monoamine Hypothesis

(): antidepressant; inhibits reuptake of 5-HT and NE

A

Imipramine

49
Q

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

A

central 5-HT and/or NE synapses

50
Q

Biological Bases of Affective Disorders

Genetic predisposition + other stress factors (especially during early childhood)

A

The Diathesis-Stress Hypothesis

Genetic predisposition = diathesis

51
Q

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

A

HPA axis

52
Q

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

A

CRH

53
Q

Biological Bases of Affective Disorders

Resting-state metabolic activity in anterior cingulate cortex increased in depression; decreased by treatment

A

Anterior Cingulate Cortex Dysfunction

54
Q

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

A
  1. sad memory recall
  2. depression treatment
55
Q

(): 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

A

Electroconvulsive therapy (ECT)

56
Q

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

A

Psychotherapy

57
Q

examples of antidepressants

A

MAO inhibitors, tricyclics, and SSRIs

58
Q

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

A

HPA system and ACC

59
Q

Antidepressants: animal studies

long-term () → glucocorticoid receptor elevation in
the hippocampus → suppression of HPA and ACC

A

serotonin

60
Q

SSRIs increase () in the hippocampus

A

neurogenesis

61
Q

Antidepressants: new drug target

(): rapid action; for suicidal patients; psychotic side effects

A

Ketamine

act on CRH receptors

62
Q

basis of lithium treatment for bipolar disorder

A

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

63
Q

basis of deep brain stimulation as treatment for severe depression

used only when patient fails to respond to other treatments

A

implanted electrode delivers electrical stim.; decreases activity in brain circuits that are chronically active

technically kind of brain surgery -> last resort

64
Q

Severe mental disorder—loss of contact with reality

A

schizophrenia

65
Q

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

A

distorts thoughts and perceptions

66
Q

3 possible biological bases of schizophrenia

A
  • Genes and the Environment
  • The Dopamine Hypothesis
  • The Glutamate Hypothesis
67
Q

describe how genes and the environment explain onset of schizophrenia

A

faulty genes (roles in synaptic transmission) -> vulnerability to environmental factors (viral infection; poor maternal nutrition; marijuana)

explains physical changes in schizophrenia patient brains

68
Q

describe how the dopamine hypothesis explains onset of schizophrenia

A

psychotic episodes triggered by activation of dopamine receptors

69
Q

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

A

Amphetamine

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

70
Q

describe how the glutamate hypothesis explains the onset of schizophrenia

A

Schizophrenia reflects diminished activation of NMDA receptors in the brain

NMDA recpetor inhibitors (ketaine, phenylcyclidine) -> don’t affect dopaminergic transmission

71
Q

involuntary lips and jaw
movements

A

Tardive dyskinesia

72
Q

basic treatment for schizophrenia

A

Drug therapy combined with psychosocial support

73
Q

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

A
  1. Conventional
  2. D2 receptors
74
Q

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

A

atypical neurleptics

75
Q

newest focus for schizophrenia drug research

A

NMDA receptors

BS450 (11 decks)

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