NBB 2 (Psych) Flashcards
Difference in the 3 major theorists:
- Freud
- Jung
- Erikson
- Freud - personality is unconsciously driven; humans are anxious animals because of friction between what we want to do - id (pleasure principle) and what we are supposed to do - super ego (reality principle) - which are equal and opposite of each other
- ego mediates between id and super ego - Jung - also believes that personality is unconsciously driven; but believes humans are one animal (Descended from common ancestor) and share a subconscious –> collective unconscious
- id = shadow, ego = self, no superego equivalent but we have male component animus and female anima - Erikson - we are social animals, and we are not anxious
- development occurs across life cycle, not just in adolescence like Freud says
- 8 stages of Man
I. What are the aspects of personality?
II. What are personality disorders?
III. Etiology of personality disorders
I. Personality:
- Cognition - how you process the world (half glass full or empty) e.g. Orphan Annie
- Affectivity - expressing feeling/emotion e.g. John McEnroe on the tennis court
- Interpersonal functioning - e.g. Elizabeth Taylor married 7+ times
- Impulse control - e.g. Lindsay Lohan stealing a necklace
II. Personality disorder - deficit in 2+ domains across all settings/social situations –> result in impairment in social, occupational, or interpersonal functioning
- stable pattern with adolescent onset
- clinically significant
- primary (not accounted for by another disorder or medical condition)
III. Reich (Freud contemporary) said that we have defense mechanisms –> how ego resolves conflict between id and superego to reduce anxiety
- personality disorders arise when the defense mechanisms are inflexible
Describe Cluster A Personality (Odd and Eccentric) disorders including cardinal signs and underlying defense mechanisms:
- Paranoid
- Schizoid
- Schizotypal
- All are premorbid risk factors for schizophrenia
1. Paranoid personality disorder (ACCUSATORY) - Cardinal sign is pervasive distrust and suspiciousness
- defense mechanism is projection - attribution of one’s undesired impulses onto another
- avoids others due to their distrust
- Schizoid (ALOOF)
- emotional detached from social relationships –> no desire for close relationships and content to live hermit life
- restricted range of emotions
- defense mechanism is fantasy - create inner world to protect from harsh reality
- linked to childhood neglect - Schizotypal (AWKWARD)
- discomfort with close relationships (as with schizoid)
- eccentricity of behavior
- defense mechanism is magical thinking - superstitions/odd beliefs
Describe Cluster B Personality disorders (Dramatic and Emotional) including cardinal signs and underlying defense mechanisms:
- Antisocial
- Borderline
- Histrionic
- Narcissistic
- Antisocial: >18 yo, onset of conduct disorder before age 15
- disregard for and violation of rights of others
- more common in males, inmates (nurture»_space; nature)
- defense mechanism is acting out - direct observable action on an unconscious conflict e.g. assault - Borderline: deficits in interpersonal functioning and impulsivity
- defense mechanisms:
A. Affective instability (splitting into all or nothing thinking and shifting from one extreme to another)
B. suicidal behavior (defense result of passive aggressive turned inward to nihilistic impulse)
C. dissociation
- linked to early sexual / physical trauma in women - Histrionic: Excessive and superficial emotionality
- need for attention
- defense mechanism is dissocation - temporary replacement of unpleasant mood with more pleasant –> Seen as dramatizing and shallow e.g. lying to gain your admiration - Narcissistic: hybrid between histrionic and antisocial
- like histrionic - grandiosity and need for admiration
- like antisocial - low self-esteem and lack of empathy
- more common in men
- defense mechanism is twinship transference “you need me, we are a lot alike” e.g. Batman and Joker
Describe Cluster C Personality disorders (Anxious and Fearful) including cardinal signs and underlying defense mechanisms:
- Avoidant
- Dependent
- Obsessive-Compulsive
- Avoidant (COWARDLY): desire for close relationships but avoid them bc of anxiety produced by sense of inadequacy, desire to avoid humiliation/embarrassment
- defense mechanism is avoidance
- equal in men and women - Dependent (CLINGY): excess need to be taken care of –> need affirmation for next steps
- defense mechanism against aggression and fear of separation is submissive and clinging behavior
- abnormal progression of normal separation anxiety (10-16 mos) - Obsessive-Compulsive OCPD (COMPULSIVE): perfectionist
- more common in men
- different from OCD (obsessions)
- defense mechanism is reaction formation –> inward chaotic and outward perfectionism
- isolate cognitive process from accompanying affect - can remember truth without affect or emotion
What are the 4 personality disorders that are thought to remit with age?
What are treatment approaches for personality disorders?
- Antisocial personality disorder (male prisoners - assault)
- Borderline personality disorder (sexually assaulted women - splitting, suicidal behavior)
- Avoidant personality disorder
- Dependent personality disorder
In general - psychotherapy
for borderline personality disorder in particular - dialectical behavioral therapy
Major developmental milestones during childhood and adolescence for: 1. Language 2. Social development 3. Cognitive development A. Memory B. Emotions
- Language skills - language is inborn, fully verbal by preschool –> toddler years important for language
- suspect language delays in kids with behavior problems - Social development - start social devlpt with attachment to caregiver (they don’t know where they end and caregiver begins) –> adequate attachment provides basis for resilience in face of hardship later in life
- parallel play during toddlerhood -play with same toys but not with each other
- develop friendships during preschool, develop hierarchy - Cognitive development
A. Memory - physical, implicit (tying shoes), explicit (tied to language devlpt ~2-3yo)
B. Emotions - start with pleasure/displeasure –> joy (1-2mos) –> fear (2mos) –> sadness (2-3mos) –> anger (4-6mos) –> empathy (2-3yrs)
Major theories of child cognitive development:
Piaget
Piaget:
0-24 mos - Sensory motor stage –> explore cause and effect
24 mos-7 yrs - preoperational stage –> egocentric thinking, limited sense of time, magical thinking, reality and imagination not separate (don’t realize people have different POVs)
- symbolic and intuitive thought substages
7-11 yrs - concrete operational stage –> logical thinking, inductive reasoning (eg 2 glasses will have same amount of juice even if one is taller and one wider)
11-adult - formal operational stage –> abstract thinking (eg using the rule “hitting feather with glass will break it” in logic, even though you know its not true)
Major theories of child psychological development:
1. Psychodynamic
- Psychodynamic (psychosoexual)
A. Oral: 0-18 mos
B. Anal: 18-36 mos - toilet training
C. Phallic: 36-48 mos - exploration of ones genitals
D. Oedipal: 4-6 yrs - practicing adulthood through rivalry with same sex parent
E. Latency: 7-10 yrs - no devlpt, only obtaining skills
F. Adolescence: 11-20 yrs - puberty, sexual reawakening
G. Adulthood
Major theories of child psychological development:
2. Eriksonian
- Eriksonian - 8 stages of man (compare to Freud and Jung)
0-18 mos: Trust vs mistrust
18 mos - 3 yrs: Autonomy vs shame
3-6 yrs : Initiative vs Guilt
- ability to be independent, function without parental help
6-11 yrs: Industry vs Inferiority
- competence in school and social skills (inferior students cannot do this)
12-18 yrs: Identity vs role confusion
18-35 yrs: Intimacy vs isolation
35-65: Generativity vs stagnation
65-death: Integrity vs despair
- older adults able to accept their lives
Major theories of child moral development: Kohlberg
Kohlberg
A. Premoral: infancy/toddlerhood –> development of conscious, empathy, magical thinking
B. Level 1 Preconventional Morality: 3-6 yrs
- Stage 1 - avoidance of punishment by lying
- Stage 2 - self-serving/self-preservation
C. Level 2 Conventional Morality
- Stage 3 - good intentions/ social norms
- Stage 4 - authority/social order
D. Level 3 Post Conventional Morality
- Stage 5 - social contracts, difference between right and wrong
- Stage 6 - universal ethical principles
Describe major biobehavioral shifts: A. 2-3 mos B. 7-9 mos C. 18-20 mos D. 3-4 yrs E. 6-7 yrs F. 11-13 yrs
A. 2-3 mos: start to development attachment to parents, temperament and personality comes through
B. 7-9 mos: crawling, mobility to explore the world
C. 18-20 mos: language develop, changes relationship to others
D. 3-4 yrs: early childhood, more independent
E. 6-7 yrs: memory improves, formal learning + school
- concrete operational stage (Piaget), latency (psychodynamic), industry vs inferiority (Erikson)
- more linear and less exponential growth
F. 11-13 yrs: puberty, development of sexuality, devlpt of sense of outside world
- Differentiate between normal anxiety / stress response and pathological anxiety
- Differentiate psychic vs somatic anxiety
1A. Anxiety - sense of uneasiness or distress about future uncertainties; universal experience and essential for adaptive functioning
- anxiety performance curve is an upside down parabola
B. Pathological anxiety - excessive, illogical, maladaptive (no survival advantage), incongruent with perceived stressor; may cause inappropriate avoidance
- Anxiety is best manifestation of Mind-body connection
A. Psychic anxiety (mental) - internal uneasiness
B. Somatic anxiety (physical) - GI distress (butterflies), jitters
Behavioral and cognitive theories of anxiety
- Behavioral theory - anxiety may be learned; behavioral treatments aimed at extinguishing avoidance behaviors
- classical conditioning (Pavlov)
- operant conditioning (learning consequences of behavior e.g. action that leads to abuse) –> leads to avoidance behavior - Cognitive theory - anxiety related to cognitive distortions (negative abnormal thoughts)
- e.g. jumping to conclusions, overestimating severity of event, underestimating coping abilities
Biological theory of anxiety
- Key anatomical components of the fear circuit
- Principal neurotransmitters associated with anxiety symptoms
- Substances associated with anxiety
- Withdrawal of which drugs leads to anxiety?
- Fear circuit:
- Sensory afferents (perceptions of external world)
- hippocampus (memories)
- amygdala (Fear/emotion center)
- prefrontal cortex
- hypothalamus - Neurotransmitters:
- GABA –> dampens anxiety
- norepi/dopamine –> increase anxiety
- both high and low (but not intermediate) levels of serotonin –> increase anxiety - Substances:
- stimulants/ caffeine
- decongestants, asthma medications, corticosteroids
- SSRIs (Prozac) - early on, SSRIs can actually increase anxiety
- marijuana
- sodium lactate - can induce panic attack - Substance use/withdrawal
- Alcohol and benzodiazepines withdrawal- both act on GABA
- opiate withdrawal
- cocaine - intoxication is more associated
Features of DSM5 Anxiety disorders:
- Generalized Anxiety disorder
- Panic attacks
- Panic disorder
Recurring exclusion criteria: cannot be better explained by another mental disorder, another medical condition, or a substance (eg cocaine)
- Generalized Anxiety Disorders - persistent, excessive anxiety for everyday stressors
- 6mos+, about multiple issues
- more common in women, onset usually in early 20s
- may present with somatic symptoms (muscle tension, sleep disturbance)
- 80% comorbidity with major depressive disorder (MDD)
- strongly tied to general levels of stress
- kids only need one symptom (restlessness, fatigue, difficulty concentrating, irritability) - Panic attack - abrupt surge of intense fear/discomfort
- short-term, ~10 min
- 4+ symptoms incl:
P- palpitations, paresthesias
A- abdominal distress
N- nausea
I- intense fear of dying or losing control, lIght-headedness
C- chest pain, chills, choking, disConnectedness
S- sweating, shaking, SOB
- common - 30% will have in a given year
- may be specifier to panic disorder or another mental disorder - Panic disorder - recurrent unexpected panic attacks
- panic attacks in panic disorder are spontaneous
- patients usually present first in medical context
- 2x common in women, onset usually in early 20s
- comorbidities with MDD, other anxiety disorders, substance use disorders
Features of DSM5 Anxiety disorders:
- Phobia
- Agoraphobia
- Social phobia (social anxiety disorder)
- Separation anxiety disorder
- Phobia - specific, unreasonable fear of an object or situation (patient realizes fear is excessive)
- animal-type (snakes)
- natural environment (heights, water)
- blood-injection injury (needles, linked to vasovagal)
- situational (airplanes, elevator)
- onset in childhood, F>M, genetic component - Agoraphobia - fear or avoidance of being helpless in place where escape may be difficult/embarrassing
- separated from panic disorder as its own disorder in the new DSM5
- e.g. public transportation, being in a crowd - Social phobia (social anxiety disorder) - fear of social situations with risk of scrutiny by others
- onset in adolescence, F=M
- performance anxiety is a specifier for social phobia
- children - anxiety must also occur in peer settings - Separation anxiety disorder - inappropriate or excessive anxiety around separation from parent/SO
- more common in children, but can be new-onset illness in adults
- 4wks symptoms (kids), 6 mos (adults) to diagnose
- 3+ symptoms: worry, reluctance to go or sleep elsewhere, nightmares, stomachaches when separation occurs or is expected
- Define obsession and compulsion
- Features of DSM5 Anxiety disorders:
A. OCD
B. Hoarding
C. Body dysmorphic disorder
1A. Obsession - recurrent, persistent thought or impulse that is unwanted and provokes anxiety
e.g. compulsion, self-doubt, sexual thoughts, symmetry
B. Compulsion - repetitive behaviors with the goal of reducing anxiety associated with obsessions
e.g. checking, washing, arranging
2A. Obsessive-Compulsive Disorder (OCD) - chronic obsessions and compulsions that cause significant distress, interfere with functioning, or are time-consuming (>1hr/day)
- specifiers - tic-related (comorbid with Tourette’s), insight (do they know its abnormal?)
- 1% prevalence - not v common; F>M
- usual onset in adolescence (younger in M)
- comorbid with MDD as well, not necessarily with Obsessive-Compulsive Personality disorder
- only one that can be treated with neurosurgery (cingulotomy) –> last resort
B. Hoarding - used to be an OCD compulsion
- usual onset in childhood, progressive impairment
- common to hoard animals
C. Body dysmorphic disorder - preoccupation with imagined/exaggerated body defect (Eg nose is too big)
- specifier for delusional level of belief (differentiated from somatic type delusion e.g. emitting foul odor)
- usual onset in early teens
Features of DSM5 Anxiety disorders: 1. Traumatic stress 2. PTSD incl criteria, risk factors, comorbidities, treatment 3. Adjustment disorder
- Traumatic stress - psychological symptoms following severe trauma
- 50% acute stress symptoms after serious trauma, 50% of those have symptoms that persist >1 month
- trauma and stressor disorders include PTSD, acute stress, adjustment, reactive attachment (child) disorders - PTSD
- criteria: long and complicated but requires severe trauma, re-experiencing of trauma, avoidance behavior, hyperarousal (easy startle), and >1 month
- risk factors: severity and nature of trauma, genetic/personality, early traumatic experiences, less supportive environment
- comorbidities: MDD, phobic/anxiety disorders, substance use disorders, 50% PTSD+TBI in Iraq veterans
- trauma: not just anything, its exposure to death, serious injury, or sexual violence that is directly experienced or witnessed, but also can be second-hand knowledge of trauma or repeated exposure to details NOT TV
- treatment: cognitive behavioral therapy, survivor group therapy but risk of harm of single debriefing, eye movement desensitization - Adjustment disorder - clinically significant symptoms in response to identifiable stressor
- not normal bereavement or mental disorder
- v common
- with depressed mood, anxiety, disturbance of conduct, or mixed
- once stressor is over, symptoms stop w/in 6 mos
[Somatic symptom disorders]
- Define somatization
- Explain differences between normal and psychosomatic responses to illness and abnormal illness behavior
- Somatization - behavior related to bodily sensations e.g. limping when knee bothers you, or even saying “my knee hurts”
- can be maladaptive or adaptive
- 60-80% somatize each week
2A. Normal illness behavior (Illness affirming) - both doctor and patients say sick e.g. flu
B. Normal illness behavior (Illness denying) - both doctor and patient say not sick e.g. physical
C. Abnormal illness behavior (illness denying) - doctor says sick, patient says not sick e.g. heart attack
D. Abnormal illness behavior (illness affirming) - doctor says not sick, patient says sick –> somatic symptom disorder
[Somatic symptom disorders]
- Define Somatic Symptom Disorder
- Theory behind etiology
- Risks/harms
- Management/treatment
- Somatic Symptom Disorder (SSD)- someone who is not sick who believes that they are sick
- 1+ somatic symptoms with illness/health anxiety, excessive time/energy devoted
- symptoms >6mos
- specifier is predominant pain
- F»M, presents at any age - Theories:
A. somatic amplification - low threshold for unpleasant body sensations
B. alexithymia - inability to read one’s feelings –> misinterpret body sensations as pain
C. cultural expression of mood/anxiety - Risks
unnecessary tests –> false positives (statistically more likely)
medications –> side effects
procedures/surgeries –> complications - Mgmt/treatment
- exclude other diagnoses
- educate the patients –> treatment is function not cure, their suffering is not in question, not “in their head”
- address psychiatric comorbidities, internal and external reinforcers
- GP with QB (PCP), regularly scheduled visits
[Somatic symptom disorders]
- Illness Anxiety Disorder
- Conversion disorder
- Illness Anxiety Disorder (IAD) -
- preoccupation with illness –> specify if care-seeking or care-avoidant
- usually no somatic symptoms
- > 6 mos
- replaces hypochondria –> 25% are IAD, 75% are SSD - Conversion disorder - neurological symptoms - loss of sensory or motor function (e..g paralysis, blindness, mutism) –> need to prove that the symptoms are incompatible with recognized conditions –> can test with Hoover’s sign
- e.g. pseudo-seizure –> now termed psychogenic non-epileptic seizure disorder; disprove with EEG
- specify if acute or persistent (>6 mos); often transient, associated with stress or trauma
- caused by psychological factors with no obvious external benefit (unlike malingering)
- “la belle indifference” - mood incongruence (affect) e.g. patient is aware of but indifferent towards symptoms
[Somatic symptom disorders]
- What are psychological factors affecting other mental conditions?
- Factitious disorder / Munchausen’s
- Munchausen’s by proxy
- Difference between somatic symptoms disorders, factitious disorder, and malingering
- Emotional or behavioral issues that negatively impact a medical problem
- influence course of illness, interfere with treatment, add risk factors e.g. stress, poor coping styles, noncompliance, denial of symptoms - Factitious disorder / Munchausen’s
- individual intentionally and falsely pretends to be ill, injured –> at risk for serious harm/morbidity
- persists despite lack of obvious external rewards - want the privileges of being sick
- NOT malingering; this is a mental disorder - Factitious disorder by proxy - illness induced in someone else
- goal is to be caregiver for sick child –> child abuse!
- most perpetrators have healthcare background, personality disorder - Malingering is knowingly pretending to be ill for external benefit –> somatic or psychological symptoms but NOT a psychiatric disorder
- inconsistencies with examination, in history/behaviors; atypical symptoms –> use psychological testing
- unlike SSD or factitious disorders where there is no external benefit/ secondary reward, and which ARE psychiatric disorders
- can be adaptive - in legal situations, ERs
- to “diagnose” need evidence from multiple sources
[Sedative hypnotics] Benzodiazepines
A. Clinical Utility
B. Pharmacokinetics
C. MOA
Sedative (anxiolytic) - reduce anxiety and exert calming effect; hypnotic drug produces drowsiness (can be achieved with higher dose)
Benzodiazepine
A. Use - short-term treatment for acute anxiety states producing functional disability (end in “am”)
- generalized anxiety disorder (GAD)
- 7 drugs approved for GAD + midazolam for sedation prior to medical procedures
B. Pharmacokinetics - highly lipophilic, easily cross BBB –> can cross placenta/breast milk so contraindicated in pregnancy and breastfeeding; elderly do not clear drug well
- good for panic attacks bc short time to peak blood level (1-2 hours)
- long duration of action with active metabolites e.g. diazepam / Valium –> should be used short-term or there will be cumulative effects
C. MOA: BZs are GABAergic –> bind to GABAa receptor in CNS neuronal membranes and function as GABA agonists –> increases frequency at which the Cl- channel opens and closes –> promotes GABA inhibition –> more sedation
[Sedative hypnotics]
What are the pros and cons of BZs?
What are toxicological features?
What are dosing considerations?
1A. Advantages: good for acute - rapid onset of action - high TI - low risk of drug interactions based on liver enzyme induction - autonomic system unaffected - minimal effects on respiratory, cardio, etc. B. Cons: - risk of dependence very high - depresses CNS functions - toxic actions
- Toxic actions:
- drowsiness, impaired judgement, and lower motor skills
- dose-related anterograde amnesia, impairs ability to learn new information
- overuse is most common cause of confused states in the elderly
- high doses – lethargy, symptoms of ethanol intoxication - Dosing considerations - write prescriptions for 2-4 weeks max
- do not combine with drowsy medications (antihistamine, anticholinergics, alcohol)
- cut doses for elderly in half
- not many drug interactions
[Sedative hypnotics] - Benzodiazepines
Describe the symptoms and management of:
1. BZ withdrawal from dependence
2. BZ overdose
- Can be psychologically or physiologically dependent bc of drug tolerance
A. Withdrawal symptoms: rebound hyperanxiety, insomnia, CNS excitability (–> seizures)
B. Management: need to taper BZ doses slowly over 1-2 weeks
* those with longer t1/2 cause less severe withdrawal signs bc eliminated more slowly from body - Overdose - BZs one of the most common involved in ODs
A. Symptoms: depresses respiratory drive
B. Management: *Rarely fatal if caught early enough
- ABCs- flumazenil (works for any GABAergic drug)- competitive inhibitor to BZ site of GABAa receptor –> reverses CNS depression of BZ OD and withdrawal; need repeated administration bc it has a short t1/2
[Sedative hypnotics]
Compare uses and MOAs for
1. Antidepressants
2. Buspirone
- Antidepressants equally effective in preventing relapse and recurrence
A. Use - first-line drugs for long-term pharmacology for generalized anxiety disorder esp in presence of depressive symptoms (often comorbid)
- 2 classes: SSRIs and SNRIs
- 2-4 weeks for full effect
B. MOA: unknown, mechanism for sedation is not the same as for depression; thought to activate stress-adaptive neuronal pathways (rather than inhibiting the stress-causing pathways like BZs do) - Buspirone
A. Use - second-line anxiolytic agent (bc of lack of efficacy for concurrent depressive disorder, inconsistent reports of efficacy)
- 2 weeks + for effect (for long-term use)
B. MOA: unknown, binds to D2 and 5-HT receptors
- does NOT interact with GABAergic systems
C. Adverse effects - better toxicology profile than BZs and antidepressants
- tolerance low - can take for a long time
- interacts with CYP3A4 –> difficult to combine with other drugs
[Sedative hypnotics] Compare treatment options for insomnia: 1. GABAergic A. BZs B. Non-BZs
- New Non-GABAergic
A. Ramelteon
B. Suvorexant
- GABAergic -
A. BZs - higher doses than for anxiolytic
- increase sleep time and decrease sleep latency
- can mess with daytime functioning (next day sedation) due to long half-lives / accumulation
- SHORT term bc can result in withdrawal and rebound insomnia; controlled substances
B. Non-BZs (zaleplon/Sonata, zolpidem/Ambien, eszopiclone/Lunesta) most commonly prescribed drugs for insomnia
- bind to same site on GABAa receptor but more selective in binding than BZs
- Zolpidem (Ambien) and eszopiclone (Lunesta) increase total sleep time, zaleplon (Sonata) does not
- rapid onset, short-half lives –> better daytime functioning
- lack anticonvulsant and muscle relaxing of BZs
- less likely to cause tolerance and dependence/withdrawal - New Non-GABAergic
A. Ramelteon (Rozerem) - agonist at melatonin MT1 and MT2 receptors in the brain –> maintain circadian rhythms
- no GABAergic effects in CNS –> no rebound insomnia or dependence
- also used for sleep anea
- decreases sleep latency and increases sleep periods
B. Suvorexant (Belsomra) - antagonist of orexin neurotransmitter receptors in the wake pathway
- no GABAergic effects in CNS
- decreases sleep latency/increases sleep periods but high risk of abuse (controlled substance)
- can cause “sleep-driving,” amnesiac effects, day after somnolence –> overall not v good
[Sedative hypnotics]
- Describe monoamine hypothesis of mood/depression
- Describe major steps in the synthesis and catabolism of serotonin and norepi
- Limitations of monoamine hypothesis and possible explanation
- Monoamine hypothesis: Depression results from decreased transmission of monoamines (serotonin, dopamine, norepi, epi)
- in particular, decreased availability of 5-HT (Serotonin) or norepi or both
2A. Serotonergic neuron hydroxylases tryptophan –> 5-HTP –> decarboxylated to 5-HT (serotonin) –> metabolized by monoamine oxidase in the nerve terminal into 5-HIAA
B. Noradrenergic neuron hydroxylases tyrosine –> Dopa –> decarboxylated to Dopamine –> hydroxylased to Norepinephrine –> metabolized by monoamine oxidase in the nerve terminal –> Epinephrine
- Antidepressants act rapidly but clinical effects require 3+ weeks of therapy –> possibly due to presynaptic autoreceptors (bind to neurotransmitters but do not bring back into the cell) –> they inhibit the production of more neurotransmitters
- during acute treatment, autoreceptors are still inhibiting neurotransmitter release
- during long-term treatment, autoreceptors downregulated and inhibition of neurotransmitters removed
[Sedative hypnotics] SSRI: 1. Clinical uses 2. MOA 3. Adverse effects
SNRI:
- Clinical uses
- MOA
- Adverse effects
SSRI and SNRIs both treat depression, generalized anxiety disorder, panic disorder, and PTSD
Selective Serotonin Reuptake Inhibitors (SSRI) - first line e.g. fluoxetine (Prozac), paroxetine (Paxil), sertraline (Zoloft), escitalopram (Lexapro), citalopram, fluvoxamine
- Clinical uses: OCD, bulimia, social anxiety disorder
- MOA: block 5-HT reuptake receptor (SERT) selectively as compared to NE reuptake
- Adverse effects: elevation of serotonin in peripheral tissues –> GI distress, SIADH, sexual dysfunction, insomnia
Serotonin and Norepinephrine Reuptake Inhibitors (SNRIs) e.g. venlafaxine (Effexor), duloxetine (Cymbalta)
- Clinical uses: major depression, chronic pain, fibromyalgia, menopausal symptoms
- MOA: block both serotonin (SERT) and norepi reuptake channels (NET)
- Adverse effects: sedation, nausea, HTN (particularly with Effexor)
[Sedative hypnotics] TCA: 1. Clinical uses 2. MOA 3. Adverse effects
f:
1. Clinical uses
2. MOA
3. Adverse effects
Tricyclic antidepressant (TCA) e.g. imipramine (5HT»_space;NE), desipramine (NE>5HT), amitriptyline, clomipramine, nortriptyline
1. Clinical uses: treatment-resistant depression, chronic pain (neuropathic pain), second-line for OCD (clomipramine), diabetic neuropathy, migraine prophylaxis (amitriptyline)
2. MOA: block both serotonin (SERT) and norepi reuptake channels (NET) Same as SNRIs
+ block alpha1 adrenergic + H1 histamine + GABAa + muscarinic ACh receptors
- block cardiac fast Na+ channels - widened QRS –> torsades / arrhythmias (treat with sodium bicarb)
3. Adverse effects: interact with many other receptors –> many side effects incl alpha block (orthostatic hypotension), muscarinic block (dry mouth, blurred vision, constipation, confusion), serotonin block (serotonin syndrome), histamine block (weight gain, sedation –> contraindicated in elderly); GABAa block (seizures)
Monoamine oxidase inhibitors (MAOIs) e.g. phenelzine + tranylcypromine + isocarboxazid [MAOa], selegiline [MAOb]
- Clinical uses: treatment-resistant depression, atypical depression (hyperphagic, hypersomnic, leaden paralysis); Parkinson’s (MAOb selegiline)
- MOA: irreversible, non-selective; MAOa breaks down DA, NE, 5-HT; MAOb breaks down DA only
- Adverse effects: HTN crisis in tyramine foods (aged meats, wine, cheese - give phentolamine) –> tachycardia, sweating, vasoconstriction; orthostatic hypotension
- serotonin syndrome when given with TCAs, SNRIs, or SSRIs
[Sedative hypnotics] - Atypical antidepressants 5HT2 Antagonists 1. Clinical uses 2. MOA 3. Adverse effects
Heterocyclics
- Clinical uses
- MOA
- Adverse effects
5HT2 antagonists e.g. nefazodone, trazodone
- Clinical uses: major depression, hypnosis (trazodone)
- MOA: antagonist of 5HT2 receptors in the cerebral cortex –> inhibits reuptake
- Adverse effects: histamine block –> sedation, alpha block –> orthostatic hypotension, sexual dysfunction, hepatotoxicity (nefazodone)
Heterocyclics e.g. bupropion, mirtazapine
1. Clinical uses: major depression, smoking cessation (bupropion), sedation (mirtazapine)
2. MOA:
A. bupropion inhibits presynaptic reuptake of NE and DA
B. mirtazapine blocks presynaptic alpha2 adrenergic receptors on noradrenergic and serotonergic neurons –> enhanced NE and 5HT neurotransmission
- also 5HT2, 5HT3, and H1 receptor antagonist
3. Adverse effects: do NOT cause sexual dysfunction
A. bupropion - lowers seizure threshold, contraindicated in anorexia/bulimia
B. mirazapine - weight gain, disorientation, tachycardia
[Sedative hypnotics]
- Describe pharmacokinetics of antidepressants in general
- ID major drug interactions associated with antidepressants
- List toxic effects of antidepressant OD - TCAs, MAOIs, and SSRIs
- Pharmacokinetics:
- rapid oral absorption
- reach plasma peak concentration in 2-3 hrs
- t1/2 = 0.5-1 day
- tightly bound to plasma proteins, metabolized by liver, eliminated by kidney
(SSRI) fluoxetine metabolite norfluoxetine has long half-life of 7-9 days
(SNRIs) venlafaxine metabolized by CYP2D6 - Drug interactions:
A. Pharmacokinetics: paroxetine and fluoxetine inhibit CYP2D6 while many drugs are substrates for 2D6 e.g. TCAs, beta blockers
- fluvoxamine and others inhibit CYP3A4
B. Pharmacodynamics: sedative effects additive esp with alcohol and BZs
- MAOIs sensitize patients to indirect (tyramine) or direct (ephedrine) sympathomimetics
- SSRI/SNRI + MAO –> serotonin syndrome (increased serotonin –> hyperthermia, HTN, hyperreflexia, myoclonus, altered mental status, fever); treat with cyproheptadine (5HT-2 blocker) - Toxic effects:
TCA- extremely dangerous; no refill basis
MAOs - intoxication rare, requires supportive treatment
SSRIs - OD fatalities rare, requires supportive treatment
[Sedative hypnotics] Lithium: 1. Clinical uses 2. MOA 3. Pharmacokinetics 4. Adverse effects
Lithium:
1. Clinical uses: bipolar affective disorder
- MOA: unknown, may be related to catecholamine (epi, norepi, dopamine) activity
- inhibits IP2 –> IP1 –> inositol regeneration steps (not clear if this is linked to therapeutic benefit) - Pharmacokinetics: enters cells via Na+ channels and subs for Na+ in generating action potentials
- completely absorbed in 6-8 hrs
- distributed in total body water, no protein binding
- completely excreted in urine
- plasma t1/2 = 20 hrs
- narrow TI - Adverse effects:
A. Interactions - diuretics and NSAIDs can decrease renal clearance (i.e. GFR)
B. Toxicity - (acute) GI distress; (chronic) neurological symptoms e.g. tremor, ataxia, hypothyroidism, weight gain, nephrogenic diabetes insipidus –> polydipsia and polyuria; inhibits K+ entry into myocytes –> abnormal repolarization
C. Contraindicated in patients with severe dehydration, sodium depletion, significant cardiovascular disease, renal impairment, during lactation
[Depressive Disorders]
- Describe core symptoms of all mood disorders
- Describe epidemiology of depressive disorders
- Disruptive Mood Dysregulation Disorder
- Mood disorders: persistent emotional state that can be elevated (manic) and/or depressed
- symptoms also in sleep/appetite/cognition(concentration and memory)/behavior
- impairment in functional ability
- are spectrum disorders - lot of gray area - Depressive disorders projected to become 2nd cause of disability by 2020
- increased correlation with chronic medical conditions eg CAD, DM
- $43B costs/year - Disruptive Mood Dysregulation Disorder
- hallmark is severe, recurrent temper outbursts out of proportion in intensity/duration; irritable b/w outbursts (irritability = depression in children)
- >3x/week for 12+ months
- present in 2/3 settings (school/home/peers)
- ages 6-18 for diagnosis
- M»F, no evidence for genetic markers
- lower conversion to bipolar but comorbidity high with oppositional defiant disorder
- do not meet criteria for mania or hypomania
[Depressive Disorders] Major Depressive Disorder 1. Criteria 2. Clinical features 3. Epidemiology
Major Depressive Disorder 1. Criteria: Depressed mood or anhedonia (loss of interest/pleasure) every day during 2+ week period and 4+ add'l symptoms --> S- sleep disturbance (loss or more) I- loss of interest G- guilt E- loss of energy C- concentration problems A- appetite or weight changes P- psychomotor changes (retardation, agitation) S- suicidal thoughts
- Clinical features - hallmark + physical symptoms and NOT sadness, anxiety common
- Epi: lifetime prevalence is 15%, peak incidence in 20s
- 3x more common in F than M
- course is variable - can be one-off or chronic
- recovery w/in 1 year for 80% patients
- risk of chronicity increases with anxiety, personality disorders, substance abuse; severity of 1st episode; younger population
[Depressive Disorders] Major Depressive Disorder 4. Risk factors 5. Differential diagnosis 6. Course/prognosis
- Risk factors:
- negative affectivity
- trauma in childhood
- genetics: 40% heritability
- substance abuse, anxiety, personality disorder, chronic medical disorders - DD:
- (Medical) - drug intoxication/withdrawal, tumor, infection, metabolic disturbance, neurological illnesses, endocrinological disturbance (hypothyroidism)
- (Psychiatric) - substance use, anxiety disorders - Course/prognosis:
- first episode before 40 yo in 50% patients
- 10% of MDD go on to have manic episode
- recurring illness, 25% in 6 mos, 50% in 2 yrs
[Depressive Disorders]
Major Depressive Disorder
7. Neurobiologic correlates
8. Psychosocial etiologies
Etiology of major depression unknown but multifactorial, due to interplay b/w physiologic, psychological, and social factors
- Neurobiologic correlates
- genetics
- monoamine dysfunction and other neurotransmitters
- structural changes in the brain
- alterations in sleep one of the primary psychiatric symptoms –> delayed sleep onset, shortened REM latency, longer initial REM period, abnormal (long wave) delta sleep
8A. Psychological - life events and environmental stressors can change neurotransmitters and brain structures
- Predisposing: personality and temperamental factors, internal conflicts, loss of interpersonal connections
B. Social - occupational and financial stressors, lack of social support, physical health status (e.g. chronic illness), role of spirituality as protective factor
[Depressive Disorders] Major Depressive Disorder 9. Describe specifiers (subsets) of depression A. Anxious distress B. Melancholic features C. Atypical
- Specifiers for depression - IN ADDN TO SIGECAPS
A. Anxious distress (2+ symptoms) V common
- feeling restless, keyed up, tense
- difficulty concentrating
- fear that something awful will happen, will lose control of self
B. Melancholic features most profound depression
- loss of pleasure/reactivity in all activities AND
- 3+: profound despondency, depression worse in AM, early morning awakening EMA, psychomotor retardation (i.e. no eye contact), anorexia, excessive guilt
C. Atypical *most common subtype of depression
- mood reactivity AND
- 2+: weight gain/increase in appetite, hypersomnia, leaden paralysis (heavy feeling in arms/legs), interpersonal rejection sensitivity
[Depressive Disorders] Major Depressive Disorder 9. Describe specifiers (subsets) of depression D. Psychotic E. Peripartum F. Seasonal pattern
D. Psychotic
- delusions and/or hallucinations
- can be mood congruent (e.g. guilt) or incongruent (e.g. paranoia - atypical)
E. Peripartum women need to be screened
- during pregnancy or in 2 wks following delivery
- physically agitated with increased anxiety/panic
- can have psychosis, more likely in 2nd episode or if history of MDD or bipolar
F. Seasonal pattern/ seasonal affect disorder (SADs)
- regular relationship with onset and time of year (fall e.g. October) –> correlation to light
- full remission or switch to hypomania/mania by February
- 2 episodes over past 2 yrs
[Depressive Disorders] Persistent Depressive Disorder 1. Criteria 2. Etiology 3. Course/Prognosis 4. DD 5. Treatment
Persistent Depressive Disorder (PDD i.e. dysthymia)
1. Criteria: Persistent major depression but for 2+ years (1 year in kids); never w/out symptoms for 2+ mos
- more functional, less affected but 2+ symptoms:
C- concentration poor
H- hopelessness
A- appetite change
S- somnia (hypo or hyper)
E- energy low
S- self-esteem low
- risk factors - negative affectivity, substance abuse, conduct disorder, parental loss
- Etiology:
A. biological - decreased REM latency
B. psychosocial - poor interpersonal relationships, abnormal thoughts, personality traits - Course: 50% patients with symptoms before 25 yo, can progress to MDD, bipolar I or II
- 25% never attain remission - DD: double depression, substance abuse, personality disorders
- Treatment: pharmacologic and psychotherapeutic treatments similar to MDD
- include CBT, IPT
[Depressive Disorders] Premenstrual Dysphoric Depressive Disorder 1. Criteria 2. DD 3. Treatment
Premenstrual Dysphoric Depressive Disorder (PDDD)
- Criteria: 5 symptoms in final week before onset of menses and improve after onset –> marked affective lability, irritability, depressed mood, tension/anxiety
- confirmed through 2 cycles of logging these symptoms
- risk factors - stress, trauma, seasonal changes - DD: dysmenorrhea, other mood disorders, hormone use
- Treatment: OCPs, SSRIs, mood charts, monitor caffeine/sugar/sodium, exercise, Calcium/B6, CBT, light therapy
[Depressive Disorders]
Substance/Medication Induced Depressive Disorder
1. Criteria
2. DD
Depressive disorder due to another medical condition
Substance/Medication Induced Depressive Disorder
- Criteria: prominent and persistent disturbance in mood AND symptoms occur after exposure to substance/medication (w/in 1 mo) AND it is capable of producing said mood changes
- substances include alcohol, PCP, inhalants, opioids, amphetamines, cocaine, sedatives
- medications include steroids, OCPs, bp meds, L-dopa, antibiotics, derm agents - DD: substance intoxication/withdrawal, primary depression, depressive disorder due to another medical condition
Depressive disorder due to another medical condition –> linked to Huntington’s, Parkinson’s, TBI, Cushing’s, hypothyroidism
[Depressive Disorders]
- Treatment for major/clinical depression
- Treatment considerations
- Positive predictors to antidepressant response
- Treatment options:
- pharmacotherapy –> moderate-severe symptoms, sleep/appetite problems
- psychotherapy –> motivated patient with mild symptoms and psychosocial stressors
- electroconvulsive therapy
- phototherapy
- transcranial magnetic stimulation - Treatment considerations
- inpatient vs outpatient
- acute (4-8 wks) vs continuation (6-12 mos - remission preserved) vs maintenance (recurrence avoided)
- pt preference, age, cost, treatment history with family members (try a med that worked for pt’s family member), symptom severity, comorbid conditions - Positive predictors to antidepressant response
- sensitivity to side effects
- family history
- acute onset
- psychomotor symptoms
[Depressive Disorders] 1. Describe psychotherapy options for major/clinical depression: A. Interpersonal B. Cognitive C. Behavioral
- Alternative treatments
A. Electroconvulsive therapy (ECT)
B. Transcranial magnetic stimulation
C. Deep brain stimulation
- Psychotherapy - used w/ or w/out meds
A. Interpersonal - our relationships
B. Cognitive - how we think about ourselves and world
C. Behavioral - increase positive reinforcements - Alternatives
A. Electroconvulsive therapy (ECT)
- efficacy superior to antidepressants but not first line treatment
- use for treatment resistance dependence
- unilateral electrode on non-dominant sphere causing seizure
- side effects incl anterograde amnesia and confusion
- contraindication is space-occupying lesion
B. Transcranial magnetic stimulation - magnet to non-dominant sphere
C. Deep brain stimulation - studied in Parkinsons, MDD, and Tourette’s
- area of significant research
[Bipolar Disorders]
- Define manic episode
- Define hypomanic episode
- Etiology of bipolar disorder
- Pharmacologic treatment
- Manic episode: *patients do not perceive they are ill
-mood changes (euphoric/infectious or irritable)
- 3+ symptoms >1 week or hospitalization:
D- distractibility
I- irresponsibility - hedonism e.g. driving fast
G- grandiosity - inflated self-esteem
F - flight of ideas
A- increase in goal directed Activity e.g. spending $, sex
S- decreased need for sleep
T- talkativeness or pressured (faster) speech - Hypomanic episode - same thing as manic episode but lower intensity of symptoms
- usually go undetected, almost always followed by depression
- must be >4 days
- behavior is not characteristics and is observable by others, but does not cause marked impairment - Etiology: less data than with unipolar depression
- heritable
- biopsychosocial factors v important - Mood stabilizers (lithium, antiepileptics, antiseizures), ECT, RARELY antidepressants (could set off mood cycles)
[Bipolar Disorders]
Specifiers for bipolar/related disorders:
1. With anxious distress
2. With mixed features
3. With rapid cycling
4. With catatonia
5. With psychotic features, peripartum onset, or seasonal pattern
- With anxious distress: 2+ symptoms
- feeling keyed up, tense, restless
- difficulty concentrating due to worry
- feeling pt might lose control of self - With mixed features:
- 3+ symptoms of depression within a manic or hypomanic episode –> dysphoria, depressed mood, diminished interest, psychomotor retardation, fatigue, worthlessness/guilt, recurrent thoughts of death/suicide
* having this specifier changes type of treatment
- 3+ symptoms of manic episode within a depressive episode - With rapid cycling: V bad
- presence of 4+ mood episodes in prev 12 mos, either manic, hypomanic, or depressive episodes
- period of partial/full remission 2+ mos - With catatonia: 3+ symptoms
- stupor (no psychomotor activity)
- catalepsy (passive induction of rigid posture)
- waxy flexibility
- mutism
- negativism (opposition to instruction)
- posturing (posturing against gravity)
- mannerism (odd caricatures)
- stereotypy (repetitive, nonsense movements)
- agitation, grimacing, echolalia/echopraxia - With psychotic features, peripartum onset, or seasonal pattern
- same as for depressive episodes
[Bipolar Disorders] Bipolar Type 1 1. Criteria 2. Epi 3. DD 4. Course 5. Prognosis 6. Comorbidity
Bipolar Type 1
1. Criteria: meet criteria for manic episode, may be before/after hypomanic or major depressive episodes
- Epi: low lifetime prevalence (<1%) but higher in higher socioeconomic
- M=F, mean onset 18
- lifetime suicide risk 15x gen pop - DD: major depressive disorders, cyclothymia, generalized anxiety/panic, schizophrenia, ADD/ADHD, personality disorders
- Course:
- 70% of bipolar 1 have depression as first episode
- manic episodes 3 mos and 90% of patients have 1+ episode
- 90% patients never fully remit, 10% are rapid cyclers - Prognosis: poorer than major depression alone
- poorer with young age onset, psychotic features, alcohol dependence, M
- better with short manic episodes, no comorbidity, older age onset, good social support - Comorbidity:
- 75% with anxiety disorders
- 50% with substance abuse
- also ADHD, impulse control disorder, metabolic syndrome, migraines
