Clinical Psych

ADHD characteristics

* hyperactivity
* impulsivity
* inattention

ADHD prevalence

* 5% children, 2.5% adults
* more common in males
* found across cultures

ADHD biological explanations

* genetic susceptibility
* smaller brain, abnormal activity in prefrontal cortex, striatum, and cerebellum
* prenatal birth
* abnormalities in serotonin, dopamine, epinephrine, and norepinephrine

ADHD treatments

* stimulant drugs
* behavioral techniques (CBT)

ASD characteristics

* impairment in social interaction, communication, and repetitive patterns of behavior
* echolalia (immediate imitation of words/sounds), pronoun reversal, stimming

theory of mind

how the mind works, ability to interpret others’ emotions

cognitive empathizing

knowing how others feel/think

emotional empathizing

feeling/intuition of others’ feelings

ASD biological explanations

* genetic contribution


* abnormalities in serotonin and dopamine
* larger brain, large ventricles, poor neural connectivity

ASD treatments

* drug treatments (SSRI, atypical antipsychotics, stimulants)
* behavioral training
* inclusive strategies

ASD prevalence

* 0.1-0.2% of people
* much more common in males

eating disorder

persistent disturbance in eating behavior

anorexia characteristics

* intense fear of gaining weight
* restricting energy
* restrictive type or binge/purge type
* underweight
* disturbed body image

anorexia prevalence

* 0.9% adult women, 0.3% adolescent girls
* 0.3% males

bulimia characteristics

* uncontrolled binge-eating followed by behavior to prevent weight gain
* normal weight/overweight
* realistic body image

bulimia prevalence

* 0.5% adults, 0.9% adolescents
* more common in women
* more common in western cultures

binge eating disorder characteristics

* uncontrolled binge eating, without purging
* overweight

binge eating disorder prevalence

* 2-3.5% of population
* slightly more common in women

eating disorder diagnostic crossover

* high crossover between binge/purge and restricting anorexia
* crossover between binge/purge anorexia and bulimia
* crossover between bulimia and BED
* no crossover between anorexia and BED

biological factors for eating disorders

* genetics (moderate heritability)
* brain mechanisms (lateral hypothalamus, frontal cortex, temporal cortex)
* set points (hunger impulse repressed in anorexia)
* serotonin

environmental factors for eating disorders

* family (eating habits, comments, behavior of parents)
* perfectionism
* thin-ideal body image
* dieting

anorexia psychological treatment

* CBT: confronts over-evaluation of thinness, rewards contingent on weight gain, relaxation techniques
* family: family takes control of eating, autonomy restored with weight gain

bulimia and BED psychological treatment

* CBT: monitor cognitions around eating, adaptive attitudes toward weight and body shape, eating “forbidden” foods, confront irrational thoughts
* IPT: interpersonal problems related to ED solved
* behavioral: monitor food intake, reinforce eating avoided foods, coping strategies

eating disorder biological treatment

SSRIs reduce symptoms, fails to restore normal eating habits

phobia

persistent and inappropriate fear of specific object/situation

fear vs anxiety

anxiety doesn’t trigger fight or flight, more focused on avoidance, can appear in moderation

specific phobia

intense, irrational fear of something that poses little to no actual danger

blood-injection-injury phobia

* fear of blood, injections, or injuries
* more somatic than other phobias
* 12% of population, more common in women

psychological factors of specific phobias

* learning theory (classical/operational conditioning)
* individual experiences
* inflation effect (another traumatic event with same phobia happens)
* cognitive bias
* evolutionary prepared learning

biological factors of specific phobias

* genetics and temperament
* heritability
* serotonin neurotransmission

agoraphobia

fear of public spaces

agoraphobia prevalence

* 4.7% in US
* more common in women

agoraphobia epidemiology

genetics, usually acquired after a panic attack

agoraphobia treatment

* anxiolytics
* antidepressants
* CBT

social phobia

fear of being exposed to the scrutiny of others, of being humiliated (general social phobia and performance phobia)

social phobia prevalence

* 12% lifetime
* more common in women

social phobia epidemiology

* learned behavior
* evolutionary factors
* traumatizing experiences
* perception of lack of control
* cognitive biases
* genetics

social phobia treatments

* CBT
* antidepressants

anhedonia

lost interest to anything in life

symptoms of MDD

depressed mood, diminished interest in activities, abnormal sleep and appetite, feelings of worthlessness or guilt

anxious distress

prominent anxiety

mixed features

at least 3 manic.hypomanic symptoms, but not a manic episode

melancholic features

physiological symptoms of MDD

psychotic features

mood-congruent or mood-incongruent delusions

catatonic features

no active relation to environment

atypical features

odd assortment of symptoms

seasonal pattern

MDD symptoms occurring during season

peripartum onset

MDD symptoms during pregnancy or 4w after

MDD prevalence

* 16% USA
* onset 18-29 yo, decreasing, increasing at 85
* 2.5% children, 8.3% adolescents
* women 2x as likely as men

biological etiology MDD

* genetics: serotonin transporter gene → dysfunction in serotonin regulation
* neurotransmitters: monoamine function disrupted
* abnormalities in prefrontal cortex, anterior cingulate, hippocampus, amygdala
* elevated cortisol and chronic hyperactivity in HPA axis

psychological etiology MDD

* behavior: depression as reaction to neg life events (reduces pos reinforcers)
* cognitive: ignoring good events and exaggerating bad ones
* interpersonal: difficulties and losses trigger depression

learned helplessness theory

uncontrollable neg life event lead to depression because they lead people to believe they are helpless to control important outcomes in environment

negative cognitive triad

neg view of themselves, the world, and the future

reformulated learned helplessness theory

neg events being viewed internal, stable, and global→ self-blame, expectations of recurrence

rumination

focus on feelings and their causes with no focus on solution

rejection sensitivity

heightened need for approval and support from others

bipolar disorder

mania followed by depression in a cyclical pattern

manic episode symptoms

inflated self-esteem, distracted, talkative, racing thoughts, painful activity, less need for sleep

bipolar I disorder

full manic episodes, unnecessary to have depressive episodes

bipolar II disorder

severe depressive episodes, milder manic episodes

hypomania

manic episode symptoms present that aren’t severe enough to impair functioning

bipolar disorder prevalence

* 0.6% bipolar I, 0.4% bipolar II
* men and women equally likely

biological etiology bipolar disorder

* genetic factor, no specific abnormality found
* abnormal structure in amygdala, prefrontal cortex, striatum
* dysregulation in dopamine system

psychological etiology bipolar disorder

* sensitivity to reward
* stress can trigger new episodes
* change in bodily rhythm/routine

biological treatments for MDD or BD

* selective serotonin reuptake inhibitor (MDD)
* selective serotonin norepinephrine reuptake inhibitor (MDD)
* norepinephrine reuptake inhibitor (MDD)
* tricyclic antidepressants (MDD, no longer used)
* monoamine oxidase inhibitors (MDD, no longer used)
* lithium (BD)
* anticonvulsant and antipsychotic medication (BD)
* repetitive transcranial stimulation
* vagus nerve stimulation
* deep brain stimulation

psychological treatments for MDD or BD

* behavioral therapy (pos reinforcers, interaction w environment)
* CBT (change patterns of thinking, solve problems)
* IPT (solve 4 types of interpersonal problems)
* interpersonal and social rhythm therapy (combine IPT with behavior techniques for BD)
* family therapy (for BD, focus on interpersonal stress within family, communication and problem solving skills)

gender dysphoria

incongruence between experienced gender and sex assigned at birth, resulting in significant distress

gender incongruence

incongruence between experienced gender and sex assigned at birth, not necessarily resulting in distress

gender dysphoria biological etiology

* exposure to unusual levels of prenatal hormones
* high heritability
* brain structure is more similar to that of experienced gender

gender dysphoria psychological etiology

* absence in mother-child interaction
* distressing punishments

gender dysphoria psychological support

* psychoeducation of family to support child
* taking steps to interventions
* peer group support

gender dysphoria biological treatment

* pubertal suppression
* gender affirming hormonal treatment
* gonadal suppressive treatment
* sex reassignment surgery

paraphilic disorder

atypical sexual preference leading to distress/social impairment/harm of self or others

pedophilic disorder

* sexual focus on prepubescent children
* can be diagnosed whether or not urge is acted upon
* must be at least 16-18yo for diagnosis

exhibitionistic disorder

* sexual gratification by exposure of genital to *unsuspecting* individual(s)
* must be with non-consenting people, present for 6mo
* high frequency, begins late teens/early 20s

voyeuristic disorder

sexual gratification by watching *unsuspecting* individuals engage in sexual activity

fetishistic disorder

use of non-living objects/parts for sexual gratification, cannot be aroused w/o it

partialism

arousal by a specific body part

frotteuristic disorder

* sexual gratification by rubbing clothed genitals against an *unsuspecting* person
* can be diagnosed whether or not urge is acted upon
* begins in early adulthood

sexual masochism

sexual urges of suffering pain/being humiliated

sexual sadism

sexual urges to inflict physical/psychological pain on others

* 4 types: restriction, humiliation, administration of pain, hypermasculinity

transvestic disorder

cross-dressing for sexual arousal

paraphilia biological etiology

* high levels of testosterone
* left temporal lobe dysfunction (amygdala and hippocampus)

paraphilia social etiology

* low self-esteem
* ignorance/lack of understanding of sexuality
* early crossing of sexual boundaries
* abuse
* lack of consistent parental environment
* inappropriate sexual partners

paraphilia psychological etiology

* lovemap (representation of sexual preferences) gone wrong
* more likely to have been abused earlier in life

paraphilia treatment

* aversion therapy: pair sexual stimulus with unpleasant stimulus (not common anymore)
* CBT
* anti-androgen drugs (lower testosterone)
* SSRI (diminish deviant sexual interest and social anxiety)
* tritorelin (reduced testosterone, deviant fantasies, and paraphilic behavior)
* empathy training

psychosis

inability to tell the difference between what’s real and what’s not

positive symptoms of SP

* represent overt expressions of unusual perceptions, thoughts, behaviors
* delusion
* hallucination
* disorganized thought
* disorganized/abnormal motor behavior

delusions

* ideas the individual believes are true but are highly unlikely/impossible
* persecutory delusion
* delusion of reference
* grandiose delusion
* delusion of being controlled
* thought broadcasting
* thought insertion
* thought withdrawal
* delusion of guilt/sin
* somatic delusion

hallucination

* unreal perceptual experiences
* tactile: outside body
* somatic: inside body
* can be tied to any of 5 senses (auditory and visual common)

disorganized thought and speech

* unpredictable and untriggered agitation
* trouble organizing daily routine
* socially unacceptable behavior
* catatonia

negative symptoms of SP

* loss of certain qualities of person
* restricted affect and avolition/asociality

restricted affect

severe reduction in/absence of emotional expression

avolition/asociality

* avolition: inability to initiate/persist at common, goal-directed activity
* asociality: lack of desire to interact with other people

cognitive deficits of SP

* memory, attention, processing speed
* focusing/maintaining attention
* working memory
* distinguishing relevant and irrelevant info

diagnosis of SP

* develops at early age
* 2+ symptoms of psychosis, 1 must be delusion, hallucination, or disorganized speech

prognosis of SP

* severe and debilitating
* lower life expectancy, higher rates of suicide
* stabilize 5-10yrs after first episode, few to no relapse
* women tend to have better prognosis
* functioning tends to improve with age
* more benign course in developing countries

stages of SP

1. prodromal stage: more cognitive symptoms, social withdrawal
2. acute stage: typical symptoms
3. stabilization stage: more stable and manageable with treatment
4. residual stage: reduction in normal functions

biological etiology SP

* genetic component, no specific abnormality found
* brain structure: reduction in gray matter, enlarged ventricles, reduction/abnormalities in white matter, abnormal activity in prefrontal cortex, abnormal activation, volume, and shape of hippocampus
* damage to developing brain (viruses, injury, perinatal hypoxia)
* different types of dopamine receptors and different levels of dopamine in brain (excess in mesolimbic pathway, less in prefrontal area)

psychosocial etiology SP

* social drift (impaired functioning moves them down social class)
* more likely to be born in large city
* stress can trigger new episodes
* expressed emotion in family
* limited cognitive skills → conservation → biases and thinking styles