Psychopathology and Mental Health Exam 2

Dysthymic Disorder

Depressed mood for at least 2 years, never without symptoms for more than 2 months during 2 year period. No major depressive episode. Lifetime prevalence: 3%

Depression epidemiology

~16-17%, leading cause of disability (10%) more prevalent in recent generations

Depression course

Onset: adolescence and young adulthood. Earlier onset = more severe

Gender and Depression

2x more common in women—> more likely to present at health clinics

Depression Environmental Factors

Stressful life events, lack of social support

Depression Biological Factors

HPA axis, genetics, brain function, neurochemicals

Depression Psychological Factors

Information processing bias, cognitive distortions, rumination, personality

HPA Axis

Central regulator of stress response, improper regulation of cortisol could lead to depression

Brain Regions where decreased functioning/volume relates to depression

OFC = reward

DLPFC = cognitive control

ACC = selective attention

Hippocampus = learning and memory

Barin region where increased function relates to depression

Amygdala = emotion and threat

Beck’s Negative Cognitive Triad

Critical incident leads to core belief formed in early experience to be activated which leads to negative thoughts about self, future, and world

Negative Attribution Style

Internal, global, stable

Negative Schemata

tend to view world negatively, process information in negative ways as a result

Unipolar Disorders Treatments

Cognitive Therapy, Interpersonal therapy, Behavioral activation treatment

Cognitive Therapy

Replacing self defeating thoughts with rational statements

Interpersonal Therapy

Focuses on current relationships and improving them via communication

Behavioral Activation Treatment

Plan positive activities and force self to go

Antidepressant Medications

SSRI, SNRI, MAO, TCA

SSRI

Selective serotonin reuptake inhibitors, preferred

50% or larger reduction of symptoms

Prozac, Paxil

Problems: nausea, insomnia

SNRI

Serotonin and norepinephrine reuptake inhibitors

MAO

Monoamine Oxidase Inhibitors - inhibit enzymes that break down serotonin and norepinephrine

TCA

Tricyclic Antidepressants - inhibit norepinephrine reuptake(and serotonin in small amounts)

TMS(transcranial magnetic stimulation)

Stimulates brain regions to increase or decrease activity. Increasing left PFC activity is beneficial for depression

Suicide Epidemiology

Highest rate in white men over 50, increased among adolescents. Males more lethal

Durkheim’s Classification

Egotistic: alienated and lost

Altruistic: sacrifice for society

Anomic: breakdown for social order

Fatalistic: unbearable life circumstances

Suicide Psychosocial factors

Impulsivity, Aggression, Pessimism, Family psychopathology, genetics, sociocultural factors

David Klonsky’s framework

Starts with ideation then progresses to attempts. Most people with ideation don’t attempt.

Thomas Joiner’s Approach to Suicide

Being a burden, social isolation, acquired ability to inflict lethal self injury

Bipolar I

At least one manic episode

Bipolar II

At least one major depressive episode

At least one hypomanic episode

No manic episodes

Cyclothymia

No manic of MD episodes but rapid fluctuations in mood

Manic episode

A period of elevated, expansive, or irritable mood

last about a week

Grandiosity/inflated self esteem, talkative, distractible, goal oriented activity

Causes significant distress of impairment

Bipolar Epidemiology

Occurs equally in males and females, starts in adolescence or young adulthood, average age of onset 22 years, 3x as many depressed days as manic/hypomanic

Bipolar Environmental Factors

Stressful life events, goal attainment, schedule disruption, lack of sleep

Bipolar biological factors

Genetic vulnerability, brain fucntion

Bipolar psychological factors

Cognitive distortions, grandiose thinking

Bipolar and Brain function

Hypoactivation of reward circuit to small gains

Treatment for Bipolar Disorders

Lithium = effective for mania, 40% don’t improve, side effects cause noncompliance

Anticonvulsants = Tegretol, Depakene, ~50% respond, used for rapid cycling, gastrointestinal side effects

Psychotherapy and Bipolar Disorders

Can supplement biological intervention but is not effective alone. Cognitive Therapy combined works better than meds alone

Anxiety Social Factors

Stressful life events involving danger, insecurity, family discrod

Childhood adversity

Exposed to more anxiety in parents

Anxiety Biological Factors

Genetics, behavioral inhibition temperament, stronger amygdala response

Insula

Connected to autonomic nervous system, critical for interception, bodily perception, increased activity in anxiety

Specific Phobia

Marked and persistent fear that is excessive or unreasonable cued by presence or anticipation of a specific object or situation. Avoidance, interfered with daily life

Specific Phobia Epidemiology

Lifetime prevalece ~12%, more common in women

Etiology of Specific Phobias

Evolutionary adaptation, classical conditioning

Preparedness Theory of Phobias

Biologically prepared for associations, learned in one trial and are difficult to extinguish, easy to condition fear to snakes or spiders and more difficult for neutral objects

Fear-Avoiaence Hierarchy

Start with thinking about stimulus and end with interacting with it closely

Social Anxiety Disorder

Marked and persistent fear of one or more social or performance situations. Situations are avoided or endured with great distress and they interfere with functioning

Specific SAD

one to three feared situations

Generalized SAD

4 or more feared situations

SAD Prevalence

~12.1% lifetime prevalence, higher rates in women, age of onset childhood to mid-adolescence.

SAD Environmental Risks

Bullying in childhood, childhood neglect/abuse, maternal overprotection

Cognitive Behavioral Theory of SAD

Beliefs: negative evaluation is likely, being liked is important

Hyper-vigilance: heightened attention to signs of social threat(eye tracking)

SAD Treatment

SSRIs and sometimes benzodiazepines

Group or individual CBT, attention Bias retraining

Panic Disorder

Recurrent and unexpected panic attacks, persistent concern about having an additional panic attack

Agoraphobia

Anxiety in situations from which escape might be difficult. Mostly female

Panic Disorder Prevalence

3.5% lifetime prevalence, twice as common in females, Chronic, age of onset 23-34

Catastrophic Misinterpretation

Panic attacks triggered by internal stimuli, anxious mood leads to physiological sensations, narrowed attention and increased awareness of bodily sensations, person misinterprets bodily sensations as catastrophic event(fear of fear)

Panic disorder Treatment

Interoceptive exposure = deliberate exposure to feared internal situations

Cognitive therapy = target catastrophic automatic thoughts

Psychoeducation

GAD Prevalence

Lifetime: 5.7%

Age of onset 31 or 33

High comorbidity with MDD

Tri-partite model of mood and anxiety disorders

Negative Affect (shared by mood and anxiety disorders)

Positive affect (MDD)

Physiological hyper-arousal (anxiety)

GAD specific symptoms

Worry, cognitive biases, intolerance of uncertainty, GABA/benzodiazepine receptor dysfunction

GAD Treatements

SSRIs, benzodiazepines

CBT

Treatments that target avoidance of emotion = Interpersonal and emotional processing therapy, mindfulness-based CBT for GAD, emotion regulation therapy

CBT for GAD

Self monitoring, antecedent cognitive reappraisal, prevention of emotional avoidance = emotional awareness training

Obsessions

Recurrent and persistent thoughts, impulses, causes anxiety, person attempts to suppress and recognizes thoughts are from their own mind

Compulsions

Repetitive behaviors or mental acts that person feels driven to preform in response to obsession

ODC Epidemiology

Lifetime prevalence 2.3%, affects both genders equally, begins in adolescence or early adulthood, comorbid with mood and anxiety disorders and body dysmorphic disorder

OCD Psychological Factors

Avoidance learning: neutral stimuli associated with frightening thoughts through classical conditioning.

Once associated, anxiety is reduced with compulsive behavior

Thought suppression

OCD Genetics

moderate heritability

OCD Treatment

Exposure and prevention

SSRIs