Psych Flashcards

1
Q

What neurotransmitters play a primary role in mental health alterations?
What medication class is used?
Which subclass do we use to treat each specifically?
625

A

Dopamine: Tricyclic Antidepressants (TCA)

Serotonin: Selective serotonin reuptake inhibitors (SSRI)

Norepinephrine: selective norepinephrine reuptake inhibitors (SNRI)

All are MAOIs

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2
Q

Define mood vs affective state
When is it a disorder?
623

A

Mood is sustained emotional state
Affective state is brief emotional feelings

Disorder when emotional states become chronic and uncontrollable

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3
Q

Unipolar Depression
What population
623-624

A

Unipolar refers to major depression. Dysphoric mood or intensely painful mood is frequently accompanied with insomnia, loss of appetite and weight, and reduced interest in pleasurable activities and interpersonal relationships.

UNIPOLAR DEPRESSION IS THE MOST COMMON MOOD DISORDER

Women > Men AFTER adolescence; kids = prevalence by gender 2-6% of kids affected.

Bipolar mixture of depression and mania

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4
Q

Bipolar 1&2
Definition of mania
Definition of Hypomania
623, 627-628

A

Mania: elevated levels of euphoria and self esteem and feelings of grandiosity. Energy is greatly enhanced after only a few hours of sleep. However, does not lead to organized plans or thoughts. Instead they show poor judgement spending money, hypersexuality, or poor business commitments; have excessive, rapid, loud and pressured speech.

Hypomania: Mania behaviors however, less severe

Bipolar 1: experiences at least one manic episode that may be preceded or followed by hypomania or major depressive episodes. Men and women = prevalence

Bipolar 2: experiences one major depressive episode for at least 2 weeks and at least one hypomanic episode for at least 4 days. Women > Men

ALL WITH BIPOLAR HAVE INCREASED RISK OF CV DISEASE, OBESITY, DM AND THYROID DISEASE

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5
Q

Is there a genetic component to mood disorders?
Environmental?
624

A

YES
Bipolar & Schizophrenia linked with chromosomes 18 & 22

Study results in twin and adoptees show strong correlation with the development of mood disorders with family history of them.

Lecture says there is a strong correlation with psychosocial stress (environment) and precipitation and severity of the mental disorder

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6
Q

What is the monoamine hypothesis of depression?
624

A

a deficit in the concentration of brain norepinephrine, dopamine and or serotonin is the underlying cause of depression, in contrast to mania that results from elevated concentration of monoamines.

This theory is supported by studies showing a reduction of monoamine metabolites in the CSF of depressed people.

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7
Q

What symptoms are associated with alterations in each neuroCHEMICAL alteration?
626 Lecture

A

Dopamine: fatigue, low energy (associated with schizophrenia)
–Depression
–ADHD
–Psychotic disorders

Norepinephrine: attention, concentration, sleep and arousal difficulties, and depression
–Anxiety
–Depression
–Post-Traumatic Stress

Serotonin: emotionality, and intolerance to aversive experiences. Depletion may precede depression
–Depression
–Anxiety
–Eating disorders

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8
Q

What is neuroENDOCRINE dysregulation?
624-625

A

Alteration in hypothalamic-pituitary-adrenal (HPA) system that plays a critical role in the ability to cope with stress. Dysregulation is also associated with activation of proinflammatory cytokines, decreased monoamine levels, decreased TSH and response to thyrotropin releasing hormone.

Chronic stress induced activation resulted in elevated glucocorticoid secretion in 30-70% of people with major depression.
Antidepressant drugs that are effective in normalizing the HPA system are associated with good clinical response to depression.

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9
Q

What are the neuroANATOMIC changes with psychopathology?
626

A

Structures:
Prefrontal Cortex: reduced activity or structural change -> depression and decreased emotional regulation

Amygdala: hyperactivity-> anxiety, mood dysregulation

Hippocampus: reduced volume-depression, may impair stress and emotional responses

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10
Q

Anxiety Disorder Definition
630-631

A

Fear and anxiety that are too intense, therefore prevent daily functioning.

MOST COMMON PSYCHIATRIC ILLNESS 10-30% OF PEOPLE

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11
Q

Social Anxiety
Definition
Onset
Mechanism
632

A

Fear and avoidance of social situations. Suffers significant distress or impairment that interferes with ordinary routines in everyday social settings as work or school.
Very common (6-12% prevalence)

Onset often adolescence

May be related to serotonin and GABA in amygdala
Possibly Oxytocin as well (newer research suggests has antianxiety properties and recues HPA activation, promotes social attachment, and maternal behavior and increasing empathy and trust.

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12
Q

General Anxiety Disorder
Definition?
Prevalence?
Symptoms?
Patho?
632-633

A

Excessive and persistent worries about life events such as marital relationships, job performance, health, money, or social status.

Lifetime prevalence is 4-6%, Women > Men
Onset usually in early 20’s

Symptoms: restlessness, muscle tension, irritability, easily fatigued, difficulty concentrating, and difficulty sleeping

Patho: Genetic link suspected but no genes identified, norepinephrine and serotonin abnormalities.

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13
Q

Post-Traumatic Stress Disorder
633

A

Exposure to a terrifying or life-threatening event, such as threat of death, serious injury, or sexual violation.

Occur hours to years after event

4 diagnostic clusters:
-Re-experiencing: flashbacks or nightmares
-Avoidance: distressing memories, feelings or external
reminders of the traumatic event
-Negative cognitions and mood: persistent and distorted
sense of blame of self or others, from estrangement
from others or diminished interest in activities
-Arousal: aggressive, reckless, or self-destructive behavior,
sleep disturbances, hypervigilance.

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14
Q

Substance Use Disorder
Definition
Prevalence
Etiology
(NOT IN BOOK AT ALL)

A

Mental and physical dependence that results from long-term exposure to substances.

Common: 20.4 million people over 12yo in 2019

Etiology:
–Genetics: 70+ genes associated, early exposure increases misuse likelihood
–Psychological: ADHD, anxiety, depression
–Biological: how body processes substance
–Socio-cultural: peer pressure
–Environmental: stress, parental drug use (high association with kids using in the future)

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15
Q

Substance use disorder
Patho
Brain cycle
(NOT IN BOOK)

A

All addictive substances produce a surge of DOPAMINE that acts on the basal ganglia (reward center), but each substance has a different mechanism

Developed tolerance drive increased use and increased dependence.

Affects amygdala and prefrontal cortex making it harder to quit. They develop conditioning (pavlov themselves into using in a situational setting).

Cycle
Basal Ganglia: binge/intoxication
Extended Amygdala: withdrawal/negative affect
Prefrontal cortex: preoccupation/anticipation

Eventually they use not to get the high but to avoid the negative effects of withdrawal.

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16
Q

Three types of substance dependence
Factors predictive of relapse
(NOT IN BOOK)

A

Physical: physiologic effects of multiple uses

Psychological: craving the use of and avoidance of the dysphoric state

Behavioral: substance seeking behavior

Factors:
–Level of dependence
–motivation for abstinence
–treatment timeframe
–genetics
–severity of craving
–how the individual copes during stressful situations