Psych Flashcards
Depression Symptoms
AS
Anhedonia
Sadness
EASY Energy Appetite Sleep Yearning
ACID
Activity
Concentration
InDecisiveness
SUGR Suicide Unworthiness Guilt Rumination
SIGECAPS Sleep (increased or decreased) Interest (loss of) Guilt (or other negative thoughts) Energy (loss) Concentration problems Appetite (increased or decreased) Psychomotor activity (retardation or agitation) Suicidal thoughts
Depression DDx (14)
Adjustment disorder w/ disturbance of mood Persistent depressive disorder Cyclothymic disorder Bipolar disorder Major depressive episode secondary to substance use or substance withdrawal Major depressive episode secondary to medical condition AD(H)D Disruptive mood dysregulation disorder Generalized anxiety disorder PTSD Premenstrual dysphoric disorder Normal periods of sadness Psychotic disorders Borderline personality disorders
Psychoanalytic theory of depression:
Dysfunction
Precipitant
Key Features
Dysfunctional maturation
Real, threatened or perceived loss
Loss leads to anger and low self esteem; depression is “anger turned inward”
Behavioral theory of depression:
Dysfunction
Precipitant
Key Features
Dysfunctional social skills
Decrease in response contingent positive reinforcement (RCPR)
Not enough reward. dysphoria; clinical depression is a result of the secondary gain
Cognitive/behavioral theory of depression:
Dysfunction
Precipitant
Key Features
Dysfunctional attitudes and beliefs
Environmental stressor
Activation of depressogenic schema trigger negative interpretations of self/future which in turn cause other symptoms of depression
Learned helplessness theory of depression:
Dysfunction
Precipitant
Key Features
Dysfunctional attributional style
Negative events
Frequent “punishment” can cause an internalized, stable, and global interpretation of the world: specifically, a belief that your future actions will have no effect on outcome
Attachment theory of depression:
Dysfunction
Precipitant
Key Features
Dysfunctional object relations
Disrupted affectional bonds between mother and infant
Abnormal mother-infant bonding leads to disruptions in the development of object constancy, which may predispose to marked dependency needs and depression
MDD:
Male/Female
Age of Onset
Risks (3)
Genetic?
Female
30
Poverty
Life stress
Personality disorder
Yes
Approach to evaluating & treating mood disorders
DETRE
Diagnose
- consider other diagnoses
Educate
- side effects, response, treatment, prognosis
Treat
- SSRI, SNRI, DRI, 5-HT, Li, Lamotrigine, Psychotherapy
Re-Evaluate
- adherence, improvement, side effects, dose adjustment
Cumulative Risk Model
molecular and cellular factors interact with environmental and behavioral factors, with risks accumulating sufficiently in some individuals to produce clinical phenotypes
Serotonin (5-HT):
Origins
Involved Structures
Relevant Disorders
Dorsal raphe
Cortex (esp. frontal) Thalamus Midbrain Basal ganglia Cerebellum
Depression
Anxiety
Norepinephrine (NE):
Origins
Involved Structures
Relevant Disorders
Locus ceruleus
Limbic system (amygdala, hypothalamus)
Cortex
Thalamus
Depression
Anxiety
Dopamine (DA):
Origins
Involved Structures
Relevant Disorders
Ventral tegmental area (VTA)
Substantia nigra –> striatum
Tubulo-infidibular (pituitary)
Midbrain –> limbic/cortex
Nucleus accumbens
Schizophrenia
Addiction
HPA Axis
Hypothalamus –> [CRH] –> Anterior Pituitary –> [ACTH] –> Adrenal Cortex –> [Cortisol] –> Hypothalamus & Anterior Pituitary (negative feedback)
When we’re stressed & have to respond, HPA is stress response system
- in Depression, HPA turns on but doesn’t turn off
Yerkes-Dodson Law
Inverted U-shaped curve whereby low levels of anxiety yield low performance, some anxiety enhances performance, while high anxiety lowers performance again
Syndrome
A set of signs & symptoms that occur together, representative of a morbid condition
Known phenomenology
Disorder
A morbid condition w/o a known basis or pathology
Known syndrome w/ time + characteristic associations
Disease
A morbid condition w/ characteristic signs & symptoms, w/ a known etiology, pathology, or physiology
DSM Diagnosis
(1) Identify presenting symptom(s)
(2) Determine if the symptom(s) is/are clinically significant (is it a mental disorder?)
(3) Rule out secondary causes
(4) Determine specific primary disorder
(5) Add subtypes & specifiers
Mini-Mental State Exam
Component of a full mental status exam that ssess only cognitive functions
Anorexia Nervosa:
Epidemiology
Course
Etiology
2nd decade (13-18), female, Caucasian, upper/middle social classes
most lethal, chronic, depression/anxiety comorbidity, improve w/ treatment
familial, serotonin abnormalities, HPA axis abnormalities, multifactorial (psychological, social, cultural, biological/genetic), 5HT abnormalities –> dysphoria
Bulimia Nervosa:
Epidemiology
Course
Etiology
mid-adolescence to late 20s, diverse socioeconomic class, female
substance use problems, fluctuating symptoms w/ varying cycles of remissions & exacerbations, seasonal, psychiatric comorbidity
multifactorial (psychological, social, cultural, biological/genetic), 5HT abnormalities –> dysphoria
Binge-Eating Disorder:
Epidemiology
Course
Etiology
similar to bulimia nervosa, but less severe
impulsive eating w/ no compensatory weight loss efforts
multifactorial (psychological, social, cultural, biological/genetic), 5HT abnormalities –> dysphoria
Monoamine Hypothesis
Depression / anxiety results, in part, from inadequate monoamine neurotransmitter activity in the brain (serotonin, norepinephrine, dopamine)
All antidepressnats work, theoretically, by boosting the availability of one or more of these NTs in certain circuits of the brain
Torsades de pointes
Fatal arrhythmiadue to TCA overdose (no risk in SSRIs)
Hypertensive crisis: “cheese reaction”
Potential problem when prescribing MAOIs
Too much dietary tyramine –> abrupt increase in pulse & BP –> acute onset of hypertension
Treat by stopping MAOI & giving meds to reduce BP
Serotonin Syndrome
Dangerously high serotonin levels when mix MAOIs w/ other antidepressants
–> elevated pulse & BP, confusion, muscle stiffness, & fever
Dopamine Hypothesis
SCZ
- Excess DA neurotransmission –> positive symptoms (hallucinations, delusions, disorganization of thought)
- Deficit in DA transmission –> negative symptoms (apathy, alogia, anhedonia, amotivation, asociality)
All antipsychotics block DA receptors (esp D2)
DA Pathways:
Mesolimbic
Associated with…
DA receptor activity in SCZ
DA receptor activity in SCZ w/ D2 blockade
Consequence
Positive symptoms
Elevated
Balanced
Reduction of hallucinations, delusions
DA Pathways:
Mesocortical
Associated with…
DA receptor activity in SCZ
DA receptor activity in SCZ w/ D2 blockade
Consequence
Negative symptoms
Reduced
Further reduced
Worsens negative symptoms
DA Pathways:
Nigrostriatal
Associated with…
DA receptor activity in SCZ
DA receptor activity in SCZ w/ D2 blockade
Consequence
Basal ganglia, movement disorders
Normal
Reduced
Induces Parkinsonism (extrapyramidal symptoms, EPS)
DA Pathways:
Tuberoinfundibular
Regulates…
DA receptor activity in SCZ
DA receptor activity in SCZ w/ D2 blockade
Consequence
Prolactin
Normal
Reduced
Can cause hyperprolactinemia
Atypical vs. Typical Antipsychotics
Decreased extrapyramidal symptoms (temporary, treat w/ anticholinergics)
Decreased tardive dyskinesia (s/t permanent writhing/chorea movement, switch to milder antipsychotic)
Decreased neuroleptic malignant syndrome (all-ver muscle rigidity due to high creatinine kinase, treat w/ benzos (muslce relaxants) & DA receptor agonist)
Decreased acute dystonic reaction (sudden single muscle group contraction, treat w/ intramuscular anticholinergic)
Elevated metabolic syndrome (elevated serum glucose, serum triglycerides, & body weight, risk of diabetes)
Major Depressive Episode:
Minimum duration of symptoms
Minimum number of symptoms
Symptoms cause marked impairment?
Psychosis may occur?
Hospitalization may occur?
May be caused by drugs or other medical conditions?
2 weeks
5
Yes
Yes
Yes
No
Manic Episode:
Minimum duration of symptoms
Minimum number of symptoms
Symptoms cause marked impairment?
Psychosis may occur?
Hospitalization may occur?
May be caused by drugs or other medical conditions?
1 week (unless hospitalized)
3 (4 if the mood is only irritable)
Yes
Yes
Yes
No
Hypomanic Episode:
Minimum duration of symptoms
Minimum number of symptoms
Symptoms cause marked impairment?
Psychosis may occur?
Hospitalization may occur?
May be caused by drugs or other medical conditions?
4 consecutive days
3 (4 if the mood is only irritable)
No
No
No
No
Striatum D2/3 receptors
Decreased in number in patients w/ addiction
- less DA synthesis & transmission –> fewer DA receptors –> experience less reward, no reinforcement from natural reinforces (food, etc.)
Low receptor availability: risk factor for addiction
Main problems with stimulants (cocaine, amphetamines)
Cardiovascular (hypertension, vasospasm, arrhythmias, sudden cardiac death)
Cocaethylene production if cocaine is used w/ alcohol (neurotoxic & increased risk of cardiac death, alcohol increased blood levels of cocaine by 30%)
Main problem with opiates
Overdose risk
Substance Use Disorder Recovery
a process of change through which an individual achieves abstinence and improved health, wellness and quality of life
Efferent Copy Proposal
Hallucinations result from a breakdown in the monitoring of internal speech
We’re usually able to readily distinguish b/n external verbal material & our own internally-generated “inner speech” by making an “efference copy” that serves as a monitor
Pts w/ SCZ may not be making efferent copies & thus can’t tell the difference b/n internal/external speech, perceiving the inner speech as “alien”
Misplaced Salience Hypothesis
Salience (the sense that something is important) may be driven by amygdala & other limbic inputs
In delusions, there may be a misrepresentation of salience that corresponds biologically to NMDA receptor dysfunction & the role of DA in controlling signal to noise
Pts w/ SCZ attach greater salience on events or situations which contributes to increased arousal & scanning, further reinforcing the delusional beliefs
Cognitive dysfunction –> thought disorganization in SCZ
Dysfunctional excitatory-inhibitory circuits in the prefrontal cortex give rise to impairments in working memory
Pts w/ SCZ lose track of the general idea that prompted their speech and hence jump from one thought to another, without a connecting, overarching theme or goal
speech appears like “loose associations”
Suicide Risks
Male White Old > teen Unmarried Protestant MDs > dentists Rural West
Somatic Symptom:
Mechanism (conscious / unconscious)
Motivation (conscious / unconscious)
Unconscious
Unconscious
Factitious
Mechanism (conscious / unconscious)
Motivation (conscious / unconscious)
Conscious
Unconscious
Malingering
Mechanism (conscious / unconscious)
Motivation (conscious / unconscious)
Conscious
Conscious
NE abnormalities in specific personality traits
Emotional reactivity
Arousal
Extraversion
5HT abnormalities in specific personality traits
Inhibition of impulse / affect
ACh abnormalities in specific personality traits
Lethargy
Depression
Decreased exploration
DA abnormalities in specific personality traits
Novelty-seeking
Histrionic (theatrical) traits
