NBB 2 (Psych)

Question 1

Difference in the 3 major theorists:

1. Freud
2. Jung
3. Erikson

Answer 1

1. 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
2. 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
3. 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

Question 2

I. What are the aspects of personality?
II. What are personality disorders?
III. Etiology of personality disorders

Answer 2

I. Personality:

1. Cognition - how you process the world (half glass full or empty) e.g. Orphan Annie
2. Affectivity - expressing feeling/emotion e.g. John McEnroe on the tennis court
3. Interpersonal functioning - e.g. Elizabeth Taylor married 7+ times
4. 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

Question 3

Describe Cluster A Personality (Odd and Eccentric) disorders including cardinal signs and underlying defense mechanisms:

1. Paranoid
2. Schizoid
3. Schizotypal

Answer 3

• 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

2. 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
3. Schizotypal (AWKWARD)
   - discomfort with close relationships (as with schizoid)
   - eccentricity of behavior
   - defense mechanism is magical thinking - superstitions/odd beliefs

Question 4

Describe Cluster B Personality disorders (Dramatic and Emotional) including cardinal signs and underlying defense mechanisms:

1. Antisocial
2. Borderline
3. Histrionic
4. Narcissistic

Answer 4

1. Antisocial: >18 yo, onset of conduct disorder before age 15
   - disregard for and violation of rights of others
   - more common in males, inmates (nurture&raquo_space; nature)
   - defense mechanism is acting out - direct observable action on an unconscious conflict e.g. assault
2. 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
3. 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
4. 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

Question 5

Describe Cluster C Personality disorders (Anxious and Fearful) including cardinal signs and underlying defense mechanisms:

1. Avoidant
2. Dependent
3. Obsessive-Compulsive

Answer 5

1. 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
2. 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)
3. 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

Question 6

What are the 4 personality disorders that are thought to remit with age?

What are treatment approaches for personality disorders?

Answer 6

1. Antisocial personality disorder (male prisoners - assault)
2. Borderline personality disorder (sexually assaulted women - splitting, suicidal behavior)
3. Avoidant personality disorder
4. Dependent personality disorder

In general - psychotherapy
for borderline personality disorder in particular - dialectical behavioral therapy

Question 7

Major developmental milestones during childhood and adolescence for: 
1. Language
2. Social development
3. Cognitive development
A. Memory
B. Emotions

Answer 7

1. Language skills - language is inborn, fully verbal by preschool –> toddler years important for language
   - suspect language delays in kids with behavior problems
2. 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
3. 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)

Question 8

Major theories of child cognitive development:

Piaget

Answer 8

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)

Question 9

Major theories of child psychological development:

1. Psychodynamic

Answer 9

1. 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

Question 10

Major theories of child psychological development:

2. Eriksonian

Answer 10

2. 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

Question 11

Major theories of child moral development: Kohlberg

Answer 11

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

Question 12

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

Answer 12

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

Question 13

1. Differentiate between normal anxiety / stress response and pathological anxiety
2. Differentiate psychic vs somatic anxiety

Answer 13

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

2. Anxiety is best manifestation of Mind-body connection
   A. Psychic anxiety (mental) - internal uneasiness
   B. Somatic anxiety (physical) - GI distress (butterflies), jitters

Question 14

Behavioral and cognitive theories of anxiety

Answer 14

1. 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
2. Cognitive theory - anxiety related to cognitive distortions (negative abnormal thoughts)
   - e.g. jumping to conclusions, overestimating severity of event, underestimating coping abilities

Question 15

Biological theory of anxiety

1. Key anatomical components of the fear circuit
2. Principal neurotransmitters associated with anxiety symptoms
3. Substances associated with anxiety
4. Withdrawal of which drugs leads to anxiety?

Answer 15

1. Fear circuit:
   - Sensory afferents (perceptions of external world)
   - hippocampus (memories)
   - amygdala (Fear/emotion center)
   - prefrontal cortex
   - hypothalamus
2. Neurotransmitters:
   - GABA –> dampens anxiety
   - norepi/dopamine –> increase anxiety
   - both high and low (but not intermediate) levels of serotonin –> increase anxiety
3. Substances:
   - stimulants/ caffeine
   - decongestants, asthma medications, corticosteroids
   - SSRIs (Prozac) - early on, SSRIs can actually increase anxiety
   - marijuana
   - sodium lactate - can induce panic attack
4. Substance use/withdrawal
   - Alcohol and benzodiazepines withdrawal- both act on GABA
   - opiate withdrawal
   - cocaine - intoxication is more associated

Question 16

Features of DSM5 Anxiety disorders:

1. Generalized Anxiety disorder
2. Panic attacks
3. Panic disorder

Answer 16

Recurring exclusion criteria: cannot be better explained by another mental disorder, another medical condition, or a substance (eg cocaine)

1. 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)
2. 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
3. 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

Question 17

Features of DSM5 Anxiety disorders:

1. Phobia
2. Agoraphobia
3. Social phobia (social anxiety disorder)
4. Separation anxiety disorder

Answer 17

1. 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
2. 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
3. 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
4. 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

Question 18

1. Define obsession and compulsion
2. Features of DSM5 Anxiety disorders:
   A. OCD
   B. Hoarding
   C. Body dysmorphic disorder

Answer 18

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

Question 19

Features of DSM5 Anxiety disorders:
1. Traumatic stress
2. PTSD
incl criteria, risk factors, comorbidities, treatment 
3. Adjustment disorder

Answer 19

1. 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
2. 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
3. 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

Question 20

[Somatic symptom disorders]

1. Define somatization
2. Explain differences between normal and psychosomatic responses to illness and abnormal illness behavior

Answer 20

1. 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

Question 21

[Somatic symptom disorders]

1. Define Somatic Symptom Disorder
2. Theory behind etiology
3. Risks/harms
4. Management/treatment

Answer 21

1. 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
2. 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
3. Risks
   unnecessary tests –> false positives (statistically more likely)
   medications –> side effects
   procedures/surgeries –> complications
4. 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

Question 22

[Somatic symptom disorders]

1. Illness Anxiety Disorder
2. Conversion disorder

Answer 22

1. 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
2. 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

Question 23

[Somatic symptom disorders]

1. What are psychological factors affecting other mental conditions?
2. Factitious disorder / Munchausen’s
3. Munchausen’s by proxy
4. Difference between somatic symptoms disorders, factitious disorder, and malingering

Answer 23

1. 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
2. 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
3. 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
4. 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

Question 24

[Sedative hypnotics] Benzodiazepines
A. Clinical Utility
B. Pharmacokinetics
C. MOA

Answer 24

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

Question 25

[Sedative hypnotics] What are the pros and cons of BZs? What are toxicological features? What are dosing considerations?

Answer 25

``` 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 ``` 2. 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 3. 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

Question 26

[Sedative hypnotics] - Benzodiazepines Describe the symptoms and management of: 1. BZ withdrawal from dependence 2. BZ overdose

Answer 26

1. 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 2. 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

Question 27

[Sedative hypnotics] Compare uses and MOAs for 1. Antidepressants 2. Buspirone

Answer 27

1. 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) 2. 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

Question 28

``` [Sedative hypnotics] Compare treatment options for insomnia: 1. GABAergic A. BZs B. Non-BZs ``` 2. New Non-GABAergic A. Ramelteon B. Suvorexant

Answer 28

1. 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 2. 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

Question 29

[Sedative hypnotics] 1. Describe monoamine hypothesis of mood/depression 2. Describe major steps in the synthesis and catabolism of serotonin and norepi 3. Limitations of monoamine hypothesis and possible explanation

Answer 29

1. 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 3. 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

Question 30

``` [Sedative hypnotics] SSRI: 1. Clinical uses 2. MOA 3. Adverse effects ``` SNRI: 1. Clinical uses 2. MOA 3. Adverse effects

Answer 30

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 1. Clinical uses: OCD, bulimia, social anxiety disorder 2. MOA: block 5-HT reuptake receptor (SERT) selectively as compared to NE reuptake 3. 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) 1. Clinical uses: major depression, chronic pain, fibromyalgia, menopausal symptoms 2. MOA: block both serotonin (SERT) and norepi reuptake channels (NET) 3. Adverse effects: sedation, nausea, HTN (particularly with Effexor)

Question 31

``` [Sedative hypnotics] TCA: 1. Clinical uses 2. MOA 3. Adverse effects ``` f: 1. Clinical uses 2. MOA 3. Adverse effects

Answer 31

Tricyclic antidepressant (TCA) e.g. imipramine (5HT >>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] 1. Clinical uses: treatment-resistant depression, atypical depression (hyperphagic, hypersomnic, leaden paralysis); Parkinson's (MAOb selegiline) 2. MOA: irreversible, non-selective; MAOa breaks down DA, NE, 5-HT; MAOb breaks down DA only 3. 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

Question 32

``` [Sedative hypnotics] - Atypical antidepressants 5HT2 Antagonists 1. Clinical uses 2. MOA 3. Adverse effects ``` Heterocyclics 1. Clinical uses 2. MOA 3. Adverse effects

Answer 32

5HT2 antagonists e.g. nefazodone, trazodone 1. Clinical uses: major depression, hypnosis (trazodone) 2. MOA: antagonist of 5HT2 receptors in the cerebral cortex --> inhibits reuptake 3. 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

Question 33

[Sedative hypnotics] 1. Describe pharmacokinetics of antidepressants in general 2. ID major drug interactions associated with antidepressants 3. List toxic effects of antidepressant OD - TCAs, MAOIs, and SSRIs

Answer 33

1. 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 2. 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) 3. Toxic effects: TCA- extremely dangerous; no refill basis MAOs - intoxication rare, requires supportive treatment SSRIs - OD fatalities rare, requires supportive treatment

Question 34

``` [Sedative hypnotics] Lithium: 1. Clinical uses 2. MOA 3. Pharmacokinetics 4. Adverse effects ```

Answer 34

Lithium: 1. Clinical uses: bipolar affective disorder 2. 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) 3. 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 4. 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

Question 35

[Depressive Disorders] 1. Describe core symptoms of all mood disorders 2. Describe epidemiology of depressive disorders 3. Disruptive Mood Dysregulation Disorder

Answer 35

1. 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 2. Depressive disorders projected to become 2nd cause of disability by 2020 - increased correlation with chronic medical conditions eg CAD, DM - $43B costs/year 3. 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

Question 36

``` [Depressive Disorders] Major Depressive Disorder 1. Criteria 2. Clinical features 3. Epidemiology ```

Answer 36

``` 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 ``` 2. Clinical features - hallmark + physical symptoms and NOT sadness, anxiety common 3. 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

Question 37

``` [Depressive Disorders] Major Depressive Disorder 4. Risk factors 5. Differential diagnosis 6. Course/prognosis ```

Answer 37

4. Risk factors: - negative affectivity - trauma in childhood - genetics: 40% heritability - substance abuse, anxiety, personality disorder, chronic medical disorders 5. DD: - (Medical) - drug intoxication/withdrawal, tumor, infection, metabolic disturbance, neurological illnesses, endocrinological disturbance (hypothyroidism) - (Psychiatric) - substance use, anxiety disorders 6. 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

Question 38

[Depressive Disorders] Major Depressive Disorder 7. Neurobiologic correlates 8. Psychosocial etiologies

Answer 38

Etiology of major depression unknown but multifactorial, due to interplay b/w physiologic, psychological, and social factors 7. 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

Question 39

``` [Depressive Disorders] Major Depressive Disorder 9. Describe specifiers (subsets) of depression A. Anxious distress B. Melancholic features C. Atypical ```

Answer 39

9. 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

Question 40

``` [Depressive Disorders] Major Depressive Disorder 9. Describe specifiers (subsets) of depression D. Psychotic E. Peripartum F. Seasonal pattern ```

Answer 40

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

Question 41

``` [Depressive Disorders] Persistent Depressive Disorder 1. Criteria 2. Etiology 3. Course/Prognosis 4. DD 5. Treatment ```

Answer 41

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 2. Etiology: A. biological - decreased REM latency B. psychosocial - poor interpersonal relationships, abnormal thoughts, personality traits 3. Course: 50% patients with symptoms before 25 yo, can progress to MDD, bipolar I or II - 25% never attain remission 4. DD: double depression, substance abuse, personality disorders 5. Treatment: pharmacologic and psychotherapeutic treatments similar to MDD - include CBT, IPT

Question 42

``` [Depressive Disorders] Premenstrual Dysphoric Depressive Disorder 1. Criteria 2. DD 3. Treatment ```

Answer 42

Premenstrual Dysphoric Depressive Disorder (PDDD) 1. 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 2. DD: dysmenorrhea, other mood disorders, hormone use 3. Treatment: OCPs, SSRIs, mood charts, monitor caffeine/sugar/sodium, exercise, Calcium/B6, CBT, light therapy

Question 43

[Depressive Disorders] Substance/Medication Induced Depressive Disorder 1. Criteria 2. DD Depressive disorder due to another medical condition

Answer 43

Substance/Medication Induced Depressive Disorder 1. 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 2. 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

Question 44

[Depressive Disorders] 1. Treatment for major/clinical depression 2. Treatment considerations 3. Positive predictors to antidepressant response

Answer 44

1. Treatment options: - pharmacotherapy --> moderate-severe symptoms, sleep/appetite problems - psychotherapy --> motivated patient with mild symptoms and psychosocial stressors - electroconvulsive therapy - phototherapy - transcranial magnetic stimulation 2. 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 3. Positive predictors to antidepressant response - sensitivity to side effects - family history - acute onset - psychomotor symptoms

Question 45

``` [Depressive Disorders] 1. Describe psychotherapy options for major/clinical depression: A. Interpersonal B. Cognitive C. Behavioral ``` 2. Alternative treatments A. Electroconvulsive therapy (ECT) B. Transcranial magnetic stimulation C. Deep brain stimulation

Answer 45

1. 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 2. 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

Question 46

[Bipolar Disorders] 1. Define manic episode 2. Define hypomanic episode 3. Etiology of bipolar disorder 4. Pharmacologic treatment

Answer 46

1. 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 2. 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 3. Etiology: less data than with unipolar depression - heritable - biopsychosocial factors v important 4. Mood stabilizers (lithium, antiepileptics, antiseizures), ECT, RARELY antidepressants (could set off mood cycles)

Question 47

[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

Answer 47

1. With anxious distress: 2+ symptoms - feeling keyed up, tense, restless - difficulty concentrating due to worry - feeling pt might lose control of self 2. 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 3. 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 4. 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 5. With psychotic features, peripartum onset, or seasonal pattern - same as for depressive episodes

Question 48

``` [Bipolar Disorders] Bipolar Type 1 1. Criteria 2. Epi 3. DD 4. Course 5. Prognosis 6. Comorbidity ```

Answer 48

Bipolar Type 1 1. Criteria: meet criteria for manic episode, may be before/after hypomanic or major depressive episodes 2. Epi: low lifetime prevalence (<1%) but higher in higher socioeconomic - M=F, mean onset 18 - lifetime suicide risk 15x gen pop 3. DD: major depressive disorders, cyclothymia, generalized anxiety/panic, schizophrenia, ADD/ADHD, personality disorders 4. 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 5. 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 6. Comorbidity: - 75% with anxiety disorders - 50% with substance abuse - also ADHD, impulse control disorder, metabolic syndrome, migraines

Question 49

``` [Bipolar Disorders] Bipolar Type 2 1. Criteria 2. Epi 3. DD 4. Course 5. Prognosis ```

Answer 49

Bipolar Type 2 1. Criteria: meet criteria for hypomanic episode 2. Epi: onset in mid-20s - mixed data on gender prevalence - 1/3 patients report suicide, lethality higher in 2>>1 3. DD: major depressive disorders, cyclothymia, generalized anxiety/panic, schizophrenia, ADD/ADHD, personality disorders 4. Course: - 10% ultimately develop manic episode - first episode may be depressive - occupational/cognitive decline - more lifetime episodes 5. Prognosis: - poorer with rapid cycling - better with later age of onset, higher education, and marriage

Question 50

``` [Bipolar Disorders] Cyclothymia 1. Criteria 2. Epi 3. DD 4. Course 5. Comorbidity ```

Answer 50

Cyclothymia - equivalent of PDD for clinical depression 1. Criteria: 2+ years duration, periods of hypomanic symptoms and periods of minor depression - periods are brief, unpredictable, and change abruptly - different from bipolar 2 bc depression is minor, and not major - longest gap between periods is 2 mos 2. Epi: M>>F, onset in early 20s - diagnosis that is rarely made in clinical practice 3. DD: bipolar 1 or 2, substance use, ADD/ADHD, personality disorders 4. Course: 50% risk that patient will eventually develop bipolar 1 or 2 5. Comorbidity: substance use, sleep disorders

Question 51

Mood disorders in primary care 1. Most common 2. Factors associated with depression 3. Assessment

Answer 51

1. Most common: - major depressive disorder - dysthymic disorder - mood disorder due to medical condition - substance induced mood disorder - bipolar *see but will not treat 2. Factors associated with depression - complaints in multiple organ systems (neuro, GI, cardiac) - recurrent emotionality - sleep disturbances - frequent/urgent visits - chronic pain 3. Assessment - good history + mental status exam - PHQ-9 - tells you you need to do better screening for depression - rule out medical conditions related to depression esp thyroid disease

Question 52

1. Define: A. Behavior B. Learning 2. Major theories of learning: A. Classical conditioning B. Operant conditioning C. Social learning theory

Answer 52

1A. behavior - function of individual and environmental interaction B. learning - permanent change in behavior due to experience; process by which behavior is altered through environmental interaction 2. Theories of learning A. Classical conditioning - learning based on associations, more frequently things are paired --> stronger connection e.g. Pavlov's dogs B. Operant conditioning - learning based on consequences --> behaviors with good consequences are repeated and vice versa i. reinforcement - increases frequency of behavior; - positive reinforcement - something good added eg candy - negative reinforcement - something bad taken away eg taking drugs to reduce depression ii. punishment - decreases frequency of behavior - positive punishment - something bad introduced eg teacher yelling - negative punishment - something good taken away eg timeout C. Social learning theory - based on combination of associations, consequences, observation, cognitive mediation - king of learning theories - gives importance to role of thoughts

Question 53

1. Describe Cognitive behavioral therapy (CBT) | 2. Examples of therapeutic techniques utilized

Answer 53

1. CBT - evidence based psychotherapy - largely based on social learning theory, heavily incorporates operant and classical conditioning - not situation itself that creates negative emotional state - it is meaning, interpretation that leads to negative behavioral response/maladaptive functioning - targets thoughts and behaviors related to onset and maintenance of psychopathology --> focuses on how a person is thinking about things (meaning, interpretation) --> provides patients with new learning experiences so they can develop adaptive coping skills - target cognitive/behavioral and have spillover effects into biological areas 2. Case study- Parkinson's - behavioral focus first: A) socially connected? B) exercising? C) self-soothing? associated with positive feelings -anxiety mgmt and relaxation - sleep hygiene - Cognitive interventions: thought monitoring and logging --> want them to be balanced/realistic

Question 54

[Suicide] When to do suicide assessment What is a suicide assessment

Answer 54

1. Suicide assessment - new patient - suicide attempt or convo - negative affect and increased energy - when you think someone is depressed 2. Suicide assessment:  Demographic risk factors (M, LGBT, anything not married, adolescent/geriatric, social isolation)  Clinical risk factors (chronic pain, HIV/AIDS, dialysis, comorbidity, mental disorder)  Individual risk factors (history of prior attempts, family history)  Psychological state (hopeless/helpless/hapless, cognitive states)  Presence of warning signs  Suicide ideation, method, intent and actions How specific, lethal, available is the method?

Question 55

[Suicide] | Suicide warning signs

Answer 55

- HOPELESSNESS - Talking about suicide, death, no reason to live - Withdrawal and social isolation - Recent/threatened severe (perceived) LOSS - Making final arrangements - Prior suicide attempt - Risk-taking behaviors - Increased use of drugs or alcohol - Unwilling to “connect” to potential helpers ``` IS PATH WARM Ideation Substance abuse Purposelessness Anxiety Trapped Hopelessness Withdrawn Anger Recklenessness Mood change ```

Question 56

``` [Suicide] 1. Interview techniques A. Normalization B. Gentle assumption C. Behavioral incidence ``` 2. Interventions A. Biologic B. Social

Answer 56

1. Interview techniques A. Normalization - "sometimes people in similar situations have had thoughts... have you?" B. Gentle assumption - assume something has it occurred, don't ask whether it has occurred C. Behavioral incidence - ask for detailed behavior, not patient's opinion 2. Interventions A. Biologic - treat underlying psychiatric disorder, medicine for agitation or pain, active consultation/mgmt, ECT B. Social - assess social isolation, involve/education SOs, reduce access to lethal means, increase support

Question 57

1. Define neuroanatomical correlates for mood disorders in general 2. Define neuroanatomical correlates for depression 3. Define neuroanatomical correlates for PTSD

Answer 57

1. Neuroanatomical correlates - hippocampus and prefrontal cortex - cognitive abnormalities, memory impairments, hoplessness, worthlessness, guilt - amygdala - anxiety and fear - nucleus accumbens - anhedonia and decreased motivation - hypothalamus - neurovegetative symptoms (sleep, appetite) 2. Anatomical observations in depression - increase in ventricles, CSF, periventricular intensity - reduction in caudate and basal ganglia, hippocampus, frontal cortex, gyrus rectus - MDD/anxiety correlates with thinner left medial cortex and thicker orbitofrontal and subgenual cortex 3. PTSD - smaller hippocampus predisposes to PTSD - smaller pregenual anterior cingulate cortex volume may result from PTSD

Question 58

# Define neuroanatomical correlates and neuronal activity for: 1. Depression 2. OCD 3. Panic disorder

Answer 58

1. Depression - areas mediating emotional and stress response are activated --> thalamus, amygdala, orbital PFC, medial PFC incl subgenual cingulate cortex cg25 - areas mediating attention and sensory processing are deactivated --> anterior cingulate cortex 2. OCD - increased activity in head of caudate nucleus, anterior cingulate gyrus, orbitofrontal cortex (i.e. orbital PFC) * can reduce activity with head of caudate equally with medication or psychotherapy * OCD, Tourette's and Huntington's have same pathways affected (excited prefrontal cortex --> more movement) * PANDAS attack basal ganglia leading to increase in activity in the caudate --> OCD-liked symptoms 3. Panic disorder - fewer GABA receptors --> more hyperactivity - BZs, barbiturates (e.g. alcohol) bind to GABA receptor and increase affinity of receptor for GABA --> relieve symptoms which is why people self-medicate by drinking

Question 59

Describe hypotheses of depression including evidence for and against: 1. Monoamine

Answer 59

1. Monoamine - depression is decreased availability of 5-HT (serotonin), dopamine, and/or norepinephrine A. evidence for: metabolic levels in CSF, plasma, urine - mania --> increased dopamine - anxiety --> increased NE, 5-HT and decreased GABA B. evidence against: -only 30% patients respond to treatment fully - increased monoamine transmission can increase memories of bad life event - long delay of efficacy (~3 wks) due to neuronal adaptation (Eg neurogenesis, gene expression) and/or desensitization of presynaptic 5-HT inhibitory autoreceptors

Question 60

Describe hypotheses of depression: 2. HPA axis 3. Neurotrophin 4. Neurotrophic

Answer 60

2. HPA Axis - problems in glucocorticoid receptor GR feedback mechanism that cause mood disorders - paraventricular nucleus in hypothalamus (CRF) --> pituitary (ACTH) --> adrenal cortex (Glucocorticoids) which negatively feedback on both - decreased GR expression in pituitary and hypothalamus --> damaged feedback loop --> continuously release more glucocorticoids *fail dexamethasone test* - hippocampus --> inhibits hypothalamus (less negative feedback when smaller/damaged) 3. Neurotrophin - levels of growth factors (E.g. BDNF) mediate neuroanatomical changes during stress and anti-depressant treatment - high levels of glucocorticoids inhibit BDNF --> lower BDNF leads to fewer dendrites/synaptic connections in hippocampus --> damage to hippocampus --> further loss of negative feedback - treatment with monoamines allows more branches/synapses to form 4. Neurotrophic - - dentate gyrus of hippocampus is 1 of 2 places where there is adult neogenesis - neurogenesis increased by running, learning, deep brain stimulation, antidepressants, neurotrophins - decreased by stress, drugs of abuse - lack of neurogenesis result in depression-like behavior Long delay of efficacy of antidepressants bc they target not only serotonin receptors but also enhance GR function and expression in hypothalamus and pituitary --> increase BDNF --> hippocampal repair and neurogenesis --> these underlying mechanisms take time

Question 61

Describe hypotheses of depression: 5. neurotransmission 6. immune

Answer 61

5. Altered neurotransmission hypothesis - reduced GABAergic neurotransmission causes depression - reduced glutamate neurotransmission causes depression --> ketamine is a strong antidepressant which increases AMPA (GluR1) receptor levels --> 60% of SSRI treatment resistant patients respond to ketamine treatment 6. Immune/cytokine - humoral mediators of immunity affect mood - increased stress, inflammation --> increased cytokines --> activated HPA axis, altered monoamines --> depression - patients with autoimmune diseases often suffer from depression - antidepressants have anti-inflammatory effects

Question 62

Describe possible causes for mood disorders: | 1. Genetic

Answer 62

1. Genetic - depression 2-5x higher among relatives (50% concordance for monozygotic twins) - bipolar 25x higher among relatives (80% concordance for monozygotic twins) - panic disorders 3-5x higher among relatives ( 30% concordance for monozygotic twins) - polygenic, some candidate genes include: monoamine - 5HT transporter promotor, 5HT1A receptor, TPH2 HPA axis - protective alleles are CRH receptor 1 and glucocorticoid cochaperone neurotrophin - protective and risk BDNF alleles

Question 63

Describe possible causes for mood disorders: | 2. Environmental

Answer 63

2. Environmental - stress - estrogen - mood disorders more common in women than men; estrogen receptors in hippocampus and amygdala and BDNF enhances synaptogenesis in hippocampus - exercise - increases neurogenesis - maternal care - tactile stimulation increases glucocorticoid receptor expression --> better HPA feedback mechanisms --> better stress response as adults

Question 64

Describe possible causes for mood disorders: 3. Epigenetics A. Maltreatment B. Stress

Answer 64

3. Epigenetics - interaction between genetics and environment A. Maltreatment - 5HT transporter promoter gene --> short form and long form of transporter - severe maltreatment as child + short form of transporter --> 2x increase of depression - connection between maltreatment as child and the serotonin transporter that results in ability to stave off depression as adult B. Stress - stress increases histone and DNA methylation --> Reduced transcription of genes involved in antidepressant affects (BDNF, glucocorticoid receptor) - histone acetylation is permissive to transcription

Question 65

``` Describe new approaches for treating mood disorders based on alternative hypotheses (i.e. non-SSRIs) 1. Pharmacologic 2. Non-pharmacologic A. ECT B. DBS ```

Answer 65

1. Pharmacologic - Monoamine --> 5HT receptor agonists - HPA axis --> CRH receptor antagonist - Neurotrophin --> BDNF receptor agonist and antagonists - neurotransmission --> sub-anesthetic doses of ketamines - immune --> IL-1beta antagonist (to prevent cytokine activation) - epigenetic --> HDAC inhibitors (transmission of genes that respond to stress) 2. Non-pharmacologic: A. electroconvulsive therapy (ECT) - induce grand mal seizure --> increases sensitivity and number of 5HT receptors + increases neurogenesis --> used for antidepressent non-responders, suicidal, elderly patients bc of fast onset B. deep brain stimulation (DBS) - of subgenual cingulate cortex (Cg25), VTA/NAc, or anterior limb of internal capsule (for MDD and OCD) *stimulate hyper-active area to cause deactivation --> bc of GABA neuron activation, synaptic failure due to high frequency stimulation, or interrupted cortical inputs

Question 66

Intellectual developmental disorder (prev known as mental retardation) 1. List major criteria for diagnosing intellectual disability 2. Difference between mild, moderate, severe 3. Etiology

Answer 66

Intellectual disability - onset in adolescence; low intelligence and need for special help to cope with life in conceptual, social, practical domains 1. Criteria - 3+ of following: - deficit in intellectual functioning confirmed by both clinical assessment and individualized, standardized intelligence testing - inability to meet standards for social responsibility and indpt learning --> communication, social participation, or indpt living across environments 2A. Mild: IQ of 55-70 - can conform socially and self-support in adulthood B. Moderate: IQ 35-55 - 2nd grade ceiling - can live semi-independently with support C. Severe: IQ 20-40 - non-functional across all 3 domains (immature, gullible, cannot read social cues, not independent) 3. Etiology A. Organic - insults from antenatal period --> 50% B. Genetic - 750+ genetic causes --> genetic conditions with known behavioral patterns and intellectual disability

Question 67

Describe common chromosomal abnormalities associated with intellectual disability: 1. Prader-Willi 2. Angelman 3. Down syndrome 4. Fragile X

Answer 67

1. Prader-Willi - absent paternal gene 15q11-13 deletion - hyperphagic - obese - mild-moderate intellectual disability (ID) 2. Angelman - absent maternal gene deletion at 15q11-13 - moderate-severe ID - motor delays, abnormal gait, epilepsy 3. Down syndrome - Trisomy 21 (21q21.1) - most common chromosomal etiology of ID - mild-moderate ID - flattened nasal bridge, short hands, facial depression 4. Fragile X - 2nd most common chromosomal etiology - mild-moderate ID - connective tissue dysplasia - gaze aversion, macroorchidism (big testes), big ears

Question 68

[Communication Disorders] ID and distinguish between major categories of communication disorders and describe info needed to make specific diagnoses: 1. Language disorder 2. Social (Pragmatic) communication disorder

Answer 68

Communication disorders manifest in early developmental period 1. Language disorder - persistent problem in using written and spoken language - reduced vocab compared to peers, sentences gramatically incorrect, trouble understanding sentences and words - disability in school, work, social situations - DD includes autism, sensory impairment, intellectual disability, learning disorder 2. Social communication disorder - persistent difficulties in the social (pragmatic as opposed to semantic) use of language - has adequate vocab and ability to create sentences - v commonly misdiagnosed as autism spectrum (which has deficit in communication/interaction but ALSO restricted repetitive behaviors/interests/activities) - cannot use or change communication to fit social context, don't understand non-verbal/implicit communication - NOT secondary to poor grammar, intellectual disability, autism spectrum

Question 69

1. Describe Specific Learning Disorder | 2. Course of learning disorder

Answer 69

1. Specific Learning Disorder - difficulty in learning and using academic skills inconsistent with intelligence (IQ) level e.g. dyslexia; 1+ difficulties >6 mos despite interventions: - spelling - written expression (content) - mastering math - number sense or calculations, mathematical reasoning - inaccurate/slow and effortful word reading - NOT secondary to intellectual disability, sensory deficits, language proficiency problems, poor education 2. Course - poor outcome w/out recognition and intervention - high risk for other psychiatric disorders - persists throughout lifetime - needs change with developmental stage

Question 70

``` [ADHD] 1. Describe ADHD and criteria for diagnosis 2. Clinical presentation of symptoms A. Inattention B. Hyperactivity ```

Answer 70

1. ADHD: impaired executive functions, M>>F - complex genetic disorders due to several genes interacting with environment; multiple biological correlates - spectrum of symptoms - persistent pattern of inattention (6+ symptoms >6mos) and/or hyperactivity (6+ symptoms >6mos) * only need 5 symptoms for ages 17+ - symptoms present before 12 yo and in 2+ settings 2. Symptoms A. Inattention: *NOT due to oppositional defiance - careless mistakes, fails to finish things - difficulty sustaining attention, don't listen when directly spoken to - loses things, easily distracted, forgetful B. Hyperactivity: - fidgets, squirms, leaves seat - restlessness, "on the go" - talks excessively, blurts out answers, interrupts, difficulty waiting

Question 71

[ADHD] 3. Anatomical changes 4. DD 5. Comorbid disorders

Answer 71

3. Anatomical changes - delayed devlpt of basal ganglia - contraction of ventral striatum surfaces - nucleus accumbens (reward processing regions) - contraction of dorsal striatum - putamen and caudate nucleus (executive function and motor planning regions) - small % outgrow ADHD by 16 yo - due to repeat allele - lower cerebral volume, in particular frontal lobe 4. DD - many disorders present with ADHD symptoms incl - sleep apnea - endocrine esp hyperthyroid - elevated lead levels - neurological eg seizure, tumor - toxins (herbicides, pesticides) 5. Comorbid - 30% have just ADHD - learning and language disorders - oppositional defiant disorder - anxiety disorder - conduct disorder - depression - bipolar - tourette's

Question 72

[ADHD] 6. Course 7. Management

Answer 72

6. Course - persists into adulthood - social skills problems - less educational achievement, lower occupational status - risk of developing antisocial personality disorder - untreated teens more likely to have substance abuse, 4x risk of STDs, 3x risk of unemployment, 2x risk of divorced/arrested - increased risk motor vehicle accidents when unmedicated 7. Management - - biopsychosocial approach - medication - psychological factors, self-control strategies - social factors - need lots of structure/support

Question 73

``` ADHD treatments incl MOA and clinical uses: 1. Stimulants A. Methylphenidate (Ritalin) B. Dextroamphetamine (Adderall) C. Adverse effects ``` ``` 2. Non-stimulants A. atomoxetine B. guanfacine C. clonidine D. antidepressants e.g. fluoxetine (Prozac), buproprion (Welbutrin) ```

Answer 73

1. Stimulants - first line therapy; habit-forming A. Methylphenidate (Ritalin) - block transporters and thus inhibits DA and NE reuptake; used for ADHD and narcolepsy (not first line) B. Dextroamphetamine (Adderall) - substrate for DA transporter, uses DAT to gain entry into presynpatic neuron (thereby blocking DA reuptake); blocks storage vesicles --> increased release of presynaptic NE and DA in synapses - used for ADHD, weight control + narcolepsy (not first line) *other stimulants include Vyvanse, Concerta C. Side effects - weight loss --> high calorie meal for bfast/dinner - stomachache, headache --> give with food - insomnia --> give dose early in day and taper - rebound symptoms --> longer-acting drug - irritability --> assess for comorbid, reduce dosage 2. Non-stimulants - use as adjuncts to stimulants for ADHD or alone when stimulants cannot be tolerated; less effective but no abuse potential A. atomoxetine - NE uptake inhibitor; used more in adults bc lag time (2 wks) is too long for children B. guanfacine - alpha2 adrenergic agonist - stimulates prefrontal cortex --> better executive function and working memory C. clonidine - alpha2 adrenergic agonist D. antidepressants - DA and NE reuptake inhibitors

Question 74

1. Define Substance abuse disorders 2. Treatment of addiction 3. Treatment of withdrawal

Answer 74

1. Substance use/abuse disorders - self-administration of a drug for prolonged periods or in excessive amounts leading to physical and/or psychological dependence - alcohol, CNS depressants (narcotic analgesics, marijuana), CNS stimulants (cocaine, meth, nicotine), hallucinogens (LSD) - other abused CNS stimulates are GHB (Date rape drug), ecstasy (Derivative of meth), and bath salts (cathinones) 2. Treatment of addiction - no approved or effective treatment for addiction - best treatment is prevention, then CBT 3. Treatment of withdrawal - alpha1 adrenergic antagonists (prazosin) to relieve withdrawal symptoms - antipsychotics (chlorpromazine, haloperidol) - anxiolytics (lorazepam, diazepam) - antidepressants (fluoxetine, desipramine)

Question 75

``` Cocaine 1. MOA 2. Effects 3. Pharmacokinetics 4. Overdose A. Symptoms B. Treatment ```

Answer 75

Cocaine - CNS stimulant; physiologically NOT physically addictive; used as topical anesthetic (like lidocaine) 1. MOA - blocks DA, NE, 5-HT reuptake transporters (DAT, NET, SERT) --> increased synapse activity 2. Effects: euphoria, increased sympathetic drive--> increase energy, tachycardia, vasoconstriction, increase bp, mydriasis, hyperthermia - Depressed, fatigued, drowsy as drug wears off 3. Pharmacokinetics - absorbed quickly through BBB, t1/2 ~60 min due to rapid enzymatic breakdown - fastest onset is IV and smoked forms - cocaine + alcohol --> cocaethylene (psychoactive) - cocaine + heroin (depressant)--> speedballing (intense euphoria, v addictive and dangerous) 4. Overdose *greater risk for cardiotoxicity than with methamphetamines A. Symptoms - agitation, HTN, tachycardia, paranoid psychosis, hallucinations, hyperthermia, MI, seizures, coma, death *withdrawal leads to apathy, anxiety, disorientation, depression B. Treatment - no antidote for OD; give antipsychotics (haloperidol, chlopromazine) for psychosis; benzos (diazepam, lorazepam) for seizures and sedation - need detox and psychiatric counseling

Question 76

``` Methamphetamines 1. MOA 2. Effects 3. Pharmacokinetics 4. Overdose A. Symptoms B. Treatment ```

Answer 76

Methamphetamines - CNS stimulant, used for ADHD, narcolepsy, weight reduction; "poor man's cocaine" 1. MOA - substrate for DA transporter, uses DAT to gain entry into presynpatic neuron (thereby blocking DA reuptake); blocks storage vesicles --> increased release of presynaptic NE, DA, and 5-HT 2. Effects - fast CNS penetration --> immediate euphoria --> higher potential for addiction/abuse - dose-related effects, tolerance can develop 3. Pharmacokinetics - longer half life (8-12 hours) compared to 1-2 hours for cocaine 4. Overdose - permanent psychosis (cocaine is reversible) and oral damage ("meth mouth") A. Symptoms - similar to cocaine --> mydriasis, paranoia, psychosis, tachycardia, HTN, insomnia *hyperthermia more associated with cocaine - severe convulsions --> respiratory/cardiovascular collapse --> coma/death - withdrawal leads to paranoia which lasts days following drug cessation (cocaine lasts hours) B. Treatment - same as cocaine

Question 77

[Disruptive, Impulse Control, Conduct Disorders] 1. Describe this group of disorders 2. Describe Intermittent Explosive disorder

Answer 77

1. Disruptive, Impulse Control, Conduct Disorders - forms of impaired self-regulation - most common disorders presenting to psychiatrists - M>>F - due to imbalance of 5-HT (Serotonin) - orbitofrontal cortex (orbital PFC) most affected 2. Intermittent Explosive disorder - recurrent behavioral outbursts representing failure to control aggressive impulses A. Mild - verbal physical aggression not resulting in damage/injury; 2x week for 3+ mos B. Severe - outbursts with damage/injury; 3 incidents over 12 mos period - outbursts are not premeditated, out of proportion to trigger, and cause functional impairment - >6 yrs - usually seen in younger, less educated, exposure to trauma, genetic component - treatment: SSRIs, CBT

Question 78

[Disruptive, Impulse Control, Conduct Disorders] 1. Pyromania 2. Kleptomania 3. Internet addiction 4. Compulsive shopping

Answer 78

Impulse control disorders: 1. Pyromania - deliberate, purposeful fire setting - tension/arousal before act - after setting fire --> pleasure, relief, gratification - not intention of causing harm 2. Kleptomania - recurrent failure to resist impulses to steal objects that are not needed for personal use/monetary value - tension before act --> pleasure/gratification at time and after act 3. Internet addiction - excessive or poorly controlled computer use --> impairment or distress - urge to use computer when offline - tension/arousal before logging on --> depressed/guilty after spending too much time online 4. Compulsive shopping - irresistible urge to buy items that are unneeded/unwanted - this is the one impulsive disorder seen in women

Question 79

[Disruptive, Impulse Control, Conduct Disorders] | Oppositional defiant disorder

Answer 79

Oppositional defiant disorder - onset usually <8 yo; recurrent pattern of 4+ symptoms: - angry/irritable mood - loses temper, touchy, resentful - argumentative/defiant behavior - argues with authority figures, refuses to comply with rules, blames others for their misbehavior - vindictiveness - 1+ incident/week for >6mos - causes distress and functional impairment - specifiers for settings: mild (1), moderate (2), severe (3 settings) - comorbid with ADHD and conduct disorder - increased risk of suicide - M>>F - treatment: social skills training, cognitive problem solving training , family therapy

Question 80

``` [Disruptive, Impulse Control, Conduct Disorders] Conduct disorder I. Criteria for diagnosis II. Specifiers III. Treatment ```

Answer 80

Conduct disorder - repetitive and persistent behavior pattern in which basic rights of others and social norms/rules are violated I. Criteria: 3+ symptoms in past 12 mos, AND 1+ in past 6 mos 4 main categories: 1. Aggressive conduct towards people/animals - bullying, initiating fights, using a weapon, physically cruel to people/animals, mugging/robbery 2. Destruction of property +/- fire setting 3. Deceitfulness or theft - broken into someone's house/car, shoplifting, lying to obtain goods 4. Serious rule violations - staying out at night, running away, truancy - impairment in social/academic functioning II. Specifiers: A. Onset - childhood (<10 yrs), adolescent (>10 yrs), or unspecified B. "Limited prosocial emotions" IF >2: lack of remorse/guilt, callous, unconcerned about performance, or shallow/deficient affect C. Severity - mild (minor harm), moderate (stealing, vandalism), severe (serious harm, forced sex, weapon) III. Treatment: v difficult to treat - family therapy, psychotherapy - medication - treat comorbidities

Question 81

Autism spectrum disorder (ASD) | 1. Core features

Answer 81

1. Core features of autism A. Communication impairment - verbal and nonverbal; delay/loss in language acquisition, repetitive vocalizations, echolalia, Asperger's subtype (no impairment but difficulty with conversations) B. Social deficits - cannot pick up on social cues, socially/emotionally immature C. Repetitive behaviors and restricted interests - (low functioning) stereotypies and self-stimulation, (high functioning) intense, unusual interests D. Associated features: i. difficulty regulating emotions ii. sensory integration difficulty iii. cognitive difficulties - can have any IQ, mismatch bw strengths and weaknesses (e.g. good at math but poor at reading) iv. neurological/physical difficulties - gross/fine motor abilities, seizures w/ bimodal onset (<3 yo and at puberty)

Question 82

``` Autism spectrum disorder (ASD) 2. Neurobiology A. Anatomy B. Functional anatomy C. Biochemical ```

Answer 82

``` 2. Neurobiology A. Anatomy - large head size due to poor pruning of neurons (increased gray:white matter) - abnormalities in the cerebellum B. Functional anatomy - abnormal circuitry and resting state - fMRI at rest shows fewer connections, more localized functioning (poor global and better local connectivity) C. Biochemical abnormalities (heterogenous) - serotonin - oxytocin low - GABA - glutamate - omega 3 FAs - ACh ```

Question 83

Autism spectrum disorder (ASD) 3. Rating Scales 4. Etiology

Answer 83

3. Rating Scales M-CHAT: Modified Checklist for Autism in Toddlers --> sensitive but not v specific CARS and CARS II: Childhood Autism Rating Scales --> more specific ADI: Autism Diagnostic Interview --> gold standard but v long (3+ hrs), need to be trained; interview with parents ADOS: Autism Diagnostic Observation Scale --> interview with children *Asperger's no longer exists as a diagnosis in DSMV 3. Etiology - genetic - 90% monozygotic twin concordance for autistic traits - 60% monozygotic twin concordance for autism - multigenetic - 100+ genes, but only a few needed for syndrome --> heterogeneity of the syndrome - M>>F - environmental factors e.g. pregnant woman who give dogs flea baths have higher % - toxins - insecticides - parental age at birth - M>>F

Question 84

``` Autism spectrum disorder (ASD) 5. Treatment A. Behavioral B. Educational C. Alternative medicine D. Medication ```

Answer 84

5. Treatment A. Behavioral - earlier intervention the better - applied behavioral analysis - teach them how to learn (looking at teacher, reading, etc) based on reinforcements which are later extinguished; works for majority of kids and is gold standard - floortime - used as adjunct, way of connecting with kids B. Educational - TEACCH - focuses on communication, not used as much - rapid prompting - v intense C. Alternative medicine - DAN procedures - believe autism is caused by viruses and can be treated with chelation, 02 therapy - supplements (little evidence) - vitamins, diets (e.g. gluten free), secretin, chelation E. Medication - atypical antipsychotics - risperidol and aripiprozale are approved, also olanzapine (weight gain) - CNS stimulants - used as adjuncts - SSRIs - not used as much due to side effects (agitation) - anticonvulsants - if child has seizure disorder Other therapies: social skills, speech, occupational, physical

Question 85

[Substance Use Disorders] 1. What are substance abuse disorders? 2. DSM-5 criteria for diagnosis

Answer 85

1. Substance abuse disorders - chronic medical conditions - genetic susceptibility (genetic risk is 50%, environmental is 50%) - chronic pathophysiologic changes - no longer using terms abuse/dependence --> more of continuum, not two separate groups - substance-induced mental disorders when someone uses chronically (delirium, dementia, anxiety, psychosis) 2. DSM5 Criteria - substances include alcohol, opioids, sedative hypnotics, weed, caffeine, CNS stimulants, tobacco - 2+ symptoms in past 12 mos: A. Pharmacologic e.g withdrawal, tolerance B. Impaired control e.g. unsuccessful efforts to cut down, cravings C. Risky use e.g. use despite physical problems (like drinking with liver disease), use when hazardous (like driving) D. Social impairment e.g. use despite problems in relationships, failure to fulfill roles (work/school/home) - specifiers: (mild) 2-3; (moderate) 4-5; severe (6+ symptoms) *this has replaced abuse/dependence*

Question 86

[Substance Use Disorders] 1. Alcohol use disorder (AUD) 2. Role of screening for substance use disorders A. CAGE B. MAST (Michigan Alcohol Screening Test) 3. Assessment of AUD

Answer 86

1. AUD - repeated alcohol consumption - M>>F (3:1), but F have more medical consequences - onset 16-30 - increased risk factors: tobacco, depression, antisocial personality disorder, gambling, family history 2. Screen everyone bc substance use disorders are under-recognized and under-treated (only 15%) - looking for at-risk drinking (7+/week for F, 14+/week for M --> 1 in 4 will have alcohol use disorder) A. CAGE (1 Y- suspicious; 2 Ys- positive test) C- have you ever felt you should cut down on your drinking? A- have people annoyed you by criticizing your drinking? G- have you ever felt bad or guilty about your drinking? E- eye opener = have you ever had a drink first thing in the morning to get rid of a hangover B. MAST - many questions incl about consequences of drinking - have you ever attended AA? - have you ever had a DWI? - do you think you're a normal drinker? 3. Assessment - clinical interview about amount, type, frequency - consequences - informing you about use disorder with functional impact --> functional, medical, psychological, social, legal "Tell me about your use of alcohol" - physical exam and labs

Question 87

[Substance Use Disorders] 1. Physical signs of alcohol use A. Early-medium B. Late-end stage

Answer 87

``` 1. Signs of alcohol use A. Early-medium - gastritis - fatty liver (almost all heavy drinkers, reversible) - abdominal obesity - vitamin/electrolyte deficiencies -fall/trauma/subdural hematoma B. Late-end stage - cardiomyopathy - chronic pancreatitis - cirrhosis/portal HTN (later stage - irreversible) - hepatitis - dementia, Wernicke-Korsakoff syndrome - peripheral neuropathy ```

Question 88

[Substance Use Disorders] 2. Physical sequelae of chronic alcohol use A. Due to portal HTN B. Due to liver detoxification impairment C. Due to liver synthesis impairment D. Due to liver storage function impairment

Answer 88

2. Physical sequelae A. Portal HTN - blood builds up and causes: - caput medusae (umbilical vein) - esophageal varices (esophageal veins) - hemorrhoids (internal hemorrhoidal veins) - hepatosplenomegaly (splenic vein) B. Liver detoxification impairment i. decreased androgens --> testicular atrophy, spider angioma ii. Ammonia --> asterixis (bird flapping hand tremor), delirium C. Due to liver synthesis impairment i. glucose metabolism ii. low albumin --> ascites (belly swelling), edema iii. Vit K Coagulation factors (II, VII, IX, X) --> ecchymoses (bruises) iv. bilirubin --> jaundice, scleral icterus D. Due to liver storage function impairment - B1 --> Wernicke encephalopathy (reversible) with ataxia, confusion, ophthalmoplegia Korsakoff (chronic, irreversible) with impaired memory loss, confabulation - folate - macrocytic anemia and pallor - B6 - anemia and pallor

Question 89

[Substance Use Disorders] 3. Associated lab findings 4. BAC and clinical findings 5. Features of alcohol intoxication 6. Treatment

Answer 89

3. Associated lab findings - urine - alcohol in urine for only few days; urine drug screen incl cocaine, PCP, marijuana, opiates, barbs, amphetamine, but NOT alcohol, MDMA, or methodone - LFTs - GGT>35, AST:ALT >2 and elevated - MCV elevated --> macrocytic anemia due to folate deficiency - triglycerides high, platelets low - carb deficient transferrin (CDT>20g/l) ``` 4. BAC and clinical findings 100-150 mg/dl - loss of coordination 150-250 - slurred speech, ataxia >250 - pass out >300 - stupor, respiratory depression, death - 1 drink = 15 mg/dl ``` 5. Alcohol intoxication - 1+ of: - slurred speech - incoordination - unsteady gait - memory or attention impairment - stupor or coma - nystagmus 6. Treatment I- intervention II- detoxification III- rehabilitation

Question 90

``` [Substance Use Disorders] 7. Alcohol withdrawal syndrome A. Range of severity of substance withdrawals B. Criteria C. Course D. Predictors of severity E. Treatment ```

Answer 90

7. Alcohol withdrawal - varies by substance A. Types - life-threatening syndome: alcohol, sedative hypnotics - severe discomfort: opiates - milder: cocaine, tobacco, amphetamine, weed - no physiological dependence: hallucinogens - decreased GABAa receptor function in withdrawal --> excitation - chronic use - decreased GABAa-R sensitivity --> tolerance B. 2+ symptoms after cessation/reduction: - insomnia, flushing, tremor, nausea/vomiting - physical agitation, anxiety, sweating, hyperreflexia - grand mal seizures C. Course: peaks severity at 36 hrs post last drink 12-48 hrs - 90% of alcohol withdrawal seizures 48-72 hrs - increased stage 1 symptoms 72-105 hrs - delirium tremens (preceded by seizure, medical emergency, can be lethal due to autonomic instability) >7 days - protracted withdrawal D. Predictors - severity of drinking - older age - history of prior AW - sedative/hypnotic use E. Treatment - benzodiazepine taper (increased GABAaR, reduce risk for seizure) --> first line - fluid/electrolytes - frequent vitals

Question 91

[Substance Use Disorders] 1. Opioid intoxication 2. Heroin-associated morbidity 3. Opioid withdrawal 4. Withdrawal treatment

Answer 91

opioid - entire family of opiates incl natural, synthetic e.g. oxycodone, heroin, morphine 1. Opioid intoxication (everything closes) - miosis - hypotension, bradycardia - hypothermia - constipation - slurred speech - OD --> respiratory depression --> coma *Cause of death* * give naloxone, naltrexone is orally available and used for relapse prevention 2. Heroin associated morbidity - HIV/AIDS - endocarditis/sepsis - tetanus, TB - osteomyelitis, cellulitis - pneumonia, abscess 3. Opioid withdrawal (everything opens) --> flu-like syndrome - diaphoresis, lacrimation - mydriasis, piloerection, myalgia ("hurting all over") - GI: nausea, vomiting, diarrhea, cramps - anxiety, yawning 4. Withdrawal treatment - NOT life-threatening - symptomatic relief - detox with phenergan (entiemetics), benzos, clonidine (alpha adrenergic), muscle relaxant - not common - methodone (full agonist) --> ILLEGAL to prescribe methodone for addiction, only through federally qualified facility - buprenorphine (partial agonist) + naloxone (antagonist) for early withdrawal/office-based treatment

Question 92

[Substance Use Disorders] 1. What are hallucinations? 2. Hallucinogens 3. OD/withdrawal

Answer 92

1. Hallucinations - changes in thoughts, perceptions, mood but with minimal sedation and NO change in memory, intellectual function 2. Hallucinogens - include peyote, ketamine (glutamate receptor agonist), marijuana, herb salvia, MDMA (amphetamine-hallucinogen hybrid), PCP, LSD - serotonergic - act via 5HT2 receptors 3A. intoxication - lethal OD rare B. no withdrawal syndrome --> no detoxification needed - people can be psychologically dependent but NOT physically dependent - most are not in urine drug screen except PCP, marijuana

Question 93

``` [Substance Use Disorders] Describe drug incl intoxication, OD, withdrawal 1. PCP 2. Marijuana 3. Cocaine 4. Methamphetamine ```

Answer 93

1. PCP "angel dust"- dissociative anesthetic (schedule II) - long half life - Intoxication: PCP induces state presents similar to schizophrenia - acute psychosis + vertical nystagmus (classic sign) - autonomic effects make it more dangerous than others - MOA: NMDA receptors --> Affect glutamate systems --> led to schizophrenia research in this area 2. Marijuana - cannabis sativa - plants have been genetically altered to increase THC active chemical - Withdrawal: not life threatening --> craving, anxiety, depression, tremor, insomnia, irritability - aging - tend to stop on their own as they get older - medical use (via dronabinol): antiemetic, anti-cancer analgesic, appetite stimulation 3. Cocaine - CNS stimulant - Intoxication: hyperalertness, restless, talkative, aggression, elation, impulsivity, paranoid psychosis, hyperthermia, chest pain (MI) - Withdrawal is non-specific: agitation, depression, fatigue, malaise, craving - no withdrawal syndrome --> no detoxification needed 4. Methamphetamine "speed" "chalk" - CNS stimulant - oral, intranasal, injection, or smoked (as "ice," "Crystal") - Schedule II stimulant- used for ADHD, narcolepsy - Intoxication: high levels of DA and NE --> increased wakefulness, HR, BP, irregular heartbeat, irritability, tremors, convulsions + cardiovascular collapse (OD) - chronic use --> changes brain structure and function, damages neuron cell endings --> cognitive problems (paranoia, memory loss, hallucinations, delusions --> permanent psychosis), poor dentition "meth mouth"

Question 94

[Antipychotics] 1. Describe the dopamine hypothesis of schizophrenia 2. Limitations to the dopamine hypothesis of schizophrenia 3. Dopamine pathways in the brain responsive to drugs used to treat psychosis

Answer 94

1. Dopamine hypothesis of schizophrenia - schizophrenia results from increased and disregulated levels of dopamine neurotransmission - drugs that increase dopaminergic activity (L-dopa) aggravate schizophrenia - increased dopamine receptor density in untreated schizophrenic patients 2. Limitations: - all evidence circumstantial - antipsychotic drugs only partly effective in most patients - 2nd gen drugs (clozapine, olanzapine, quetiapine) not potent D2 antagonists but ARE clinically effective 3. Dopamine pathways - A. nigrostriatal: substantia nigra to dorsal striatum (caudate + putamen) --> motor control *increased dopamine in striatum linked to neurocognitive deficits in schizophrenia (memory, executive functioning) B. tuberoinfundibular: hypothalamus to pituitary --> hormonal regulation, maternal behavior, sensory processes *normally dopamine suppresses prolactin --> hypoactivity leads to hyperprolactinemia C. mesolimbic: VTA to D4 receptors in ventral striatum (nucleus accumbens) --> reward, addiction *hyperactivity results in positive symptoms e.g. hallucinations, hearing voices D. mesocortical: VTA to prefrontal, cingulate cortexes --> motivation, cognitive function *hypoactivity results in negative symptoms e.g. flat affect, alogia (poverty of speech) + worsening cognition (memory)

Question 95

[Antipsychotics] 1. Differentiate typical from atypical antipsychotic drugs re side effects, therapeutic benefit 2. Pharmacokinetics: A. Absorption B. Preparations available C. Metabolism incl potential for drug interactions

Answer 95

1. Typical vs atypical determined by side effects A. Typical - substantial risk of extrapyramidal symptoms; reduced positive but NOT negative symptoms B. Atypical - reduced risk of extrapyramidal symptoms; reduced positive AND negative symptoms - positive symptoms (delusions, catatonic behavior, disorganized speech) --> hyperactivity of mesolimbic D2 receptors *why typicals alleviate positive symptoms - negative symptoms --> hypoactivity of mesocortical neurons (D2 receptor antagonism) 2. Pharmacokinetics A. Absorption: oral - readily but incompletely absorbed - high first pass transformation --> low availability = lipid soluble, readily enter CNS, - extensively bound due plasma proteins Preparations: - 1x daily dosing bc half-lives are ~24 hours - all drugs available orally but sometimes better to use IM (Acute psychosis) or depot (uncompliance) or extended release/oral disintegration (elderly) C. Metabolism - metabolites not important for action EXCEPT mesoridazine (more active than parent thioridazine) - atypicals metabolized by CYPs 3A4 and 2D6

Question 96

``` [Antipsychotics] Toxicities of antipsychotics and how to treat them A. EPS B. Tardive dyskinesia C. Neuroleptic malignant syndrome D. Endocrine + metabolic effects E. Additional ```

Answer 96

Toxicity A. Extrapyramidal symptoms (reversible neurological effects) 1st gen high potency >> 1st low >> 2nd gen i. 4 hr acute dystonia (writhing muscle spasms) --> focal dystonia treated with botox ii. 4 day akathisia (motor restlessness) --> treat with beta blockers iii. 4 wk parkinsonism (bradykinesia, tremor, rigidity) --> decrease dose and use antimuscarinics (benztropine) to treat B. 4 mos Tardive dyskinesia - movements of muscles of lips and buccal cavity; irreversible - due to upregulation of dopamine receptors - to treat - switch meds to clozipine; add diazepam to enhance GABAergic activity C. Neuroleptic malignant syndrome - muscle rigidity, diaphoresis, hyperpyrexia/fever, autonomic instability - most severe, fatal in 10% - treat with muscle relaxant (dantrolene) and D2 agonist (bromocriptine) D. Endocrine + metabolic effects - - D2R blockage in pituitary (lose tonic suppression)--> hyperprolactinemia, amenorrhea, infertility - weight gain, hyperglycemia, hyperlipidemia, diabetes (due to antagonism of 5HT2C receptors or leptin levels) * 2nd gen >> 1st gen E. Additional: STOMAS (capitalized below) - histamine block --> Sedation - ventricular arrhythmia --> QT prolongation --> Torsades de pointes - alpha1 block --> Orthostatic hypotension - Metabolic - Anticholinergic block --> dry mouth, constipation - Seizures

Question 97

``` [Antipsychotics] - Typical 1. MOA of typical antipsychotics 2. ID typical antipsychotics A. High potency B. Low potency 3. Clinical uses 4. Pharmacological effects ```

Answer 97

1. MOA - blocks D2 receptors on postsynaptic cells in CNS, esp in mesofrontal areas - some also block D2 receptors on presynaptic cell - binding at D2 receptors correlated to clinical dose for controlling schizophrenia 2. Typicals: A. High potency - trifluoperazine, fluphenazine, haloperidol B. Low potency - chlorpromazine, thioridazine 3. Uses: positive symptoms of schizophrenia, acute psychosis, acute mania (bipolar), acute agitation, Tourette's 4. Pharmacologic effects A. High >> low potency: D2R blockade -> extrapyramidal symptoms - haloperidol --> NMS, tardive dyskinesia B. Low >> high potency: STOMAS (sedation, torsades, orthostatic hypotension, metabolic, anticholinergic, seizures) - chlorpromazine --> corneal deposites - thioridazine --> retinal deposits side effect order: EPS, hyperprolactinemia, STOMAS

Question 98

[Antipsychotics] - Atypical 1. MOA of atypical antipsychotics 2. ID atypical antipsychotics 3. Clinical uses 4. Pharmacological effects 5. Clozapine unique pharmacodynamics + toxicity 6. Aripiprazole unique pharmacacodynamics

Answer 98

1. MOA: block D2 receptors weakly; higher 5-HT2 block relatively and compared to typicals; also block alpha and H1 receptors 2. Atypicals: quetiapine, olanzapine, risperidone, aripiprazole, ziprasidone, clozapine (quiet, only whispering from A to Z closely) - cannot be grouped chemically 3. Uses: positive and negative symptoms of schizophrenia, treatment resistant depression, OCD (adjunct with SSRIs), Tourette's 4. Pharmacologic effects - D2R blockade weak --> fewer, less common EPS - Alpha2 block and M block --> intermediate autonomic effects - QT interval prolongation --> torsade de pointes; NMS; - dyslipidemia, weight gain, hyperglycemia, diabetes - risperidone increases prolactin 4. Clozapine - strong D4 block (expressed in limbic system), low affinity for D2 receptors - unique toxicity --> agranulocytosis - also seizures, significant weight gain - only used in those with treatment-resistant schizophrenia 5. Aripiprazole - partial D2 agonist, rather than antagonist - diminish subcortical dopamine by competition + enhancing transmission in prefrontal cortex - does not completely eliminate dopamine signaling side effect order: STOMAS, hyperprolactinemia, EPS

Question 99

[Psychotic disorders] 1. What are psychoses and what do they have in common? 2. Describe catatonia 3. Explain role of selective mutism in the exacerbation of an acute psychotic episode

Answer 99

1. Psychoses - aka delirium - dopamine is the final common pathway for all psychoses - direct physiologic result of general medical condition or substance - psychoses from withdrawal of alcohol, sedative hypnotics, or hallucinogens 2. Catatonia - marked behavioral (psychomotor) disturbance; inability to move normally ` - decreased engagement i. moderate - negativism ii. severe - mutism - abnormal motor behavior i. decreased - (moderate) catalepsy, (severe) stupor ii. excessive - (simple) agitation, (complex) stereotypy, mannerism iii. peculiar 3. Selective mutism - type of anxiety disorder; >1 month of consistent failure to speak in specific social situations; clinically significant

Question 100

``` [Psychotic disorders] Schizophrenia A. Criteria for schizophrenia B. Psychological determinants C. Social determinants ```

Answer 100

Schizophrenia: causes functional impairment, talk to patients family A. Criteria- 2+ symptoms for 1+ month: i. Positive symptoms: delusions, hallucinations, disorganized speech, disorganized or catatonic behavior ii. Negative symptoms: 5 A's (via PLANT mnemonic) - aPathy - aLogia - poverty of speech - Affective flattening - aNhedonia - withdrawal, loss of interest - aTtention deficit B. Psychological determinants - Defense mechanism --> projection; becomes fixed due to damage to frontal lobe C. Social determinants - i. downward drift - schizophrenia causes poverty (not other way around) ii. Stress-diathesis model - genetics may predispose, but precipitants are psychosocial stimuli; we are ALL on the spectrum (can all become psychotic with enough stress) - MYTH: double-bind theory --> that schizophrenia is due to contradictory familial interactions (not genetic) - MYTH: schizophrenia inherited from mother

Question 101

[Psychotic disorders] Describe the following symptoms of schizophrenia (prev referred to as First Rank symptoms) ``` 1. Delusional beliefs A. Delusions B. Delusional perceptions (ideas of reference) C. Somatic passivity D. Thought insertion E. Thought withdrawal F. Thought broadcasting ``` 2. Hallucination 3. Illusion

Answer 101

1. Positive A. Delusions - deficit of thought content --> thought/belief that is not bound by reality and is fixed/rigid *FBI is after me* do NOT realize that it is a product of your own mind B. Delusional perceptions (ideas of reference) - real life stimulus/cue with a delusional interpretation *dangerous e.g. etiology of subway pushers C. Somatic passivity - believe they are passive recipient of bodily sensations from external force *devil made me do it* D. Thought insertion - believe thoughts are being put into their mind by an external force E. Thought withdrawal - believe thoughts are being removed from their mind by an external force F. Thought broadcasting - believe their thoughts are being transmitted to others *hand in hand with paranoia 2. Hallucination - perceptual disturbance without any environmental cue 3. Illusion - perceptual disturbance; misinterpretation of environmental cue

Question 102

``` [Psychotic disorders] 1. Describe difference between A. Brief psychotic disorder B. Schizophreniform disorder C. Schizophrenia ``` ``` 2. Describe exclusion criteria for schizophrenia A. Autism B. Substance use C. General medical conditions D. Schizoaffective/mood disorder ```

Answer 102

1. Main difference is the time course A. Brief psychotic disorder - total duration 1 day- 1 month - ONLY positive symptoms - presence of negative symptoms implies schizophrenia caught early in its course - usually precipitated by a stressor e.g. childbirth - full return to premorbid functioning B. Schizophreniform disorder - total duration 1-6 mos C. Schizophrenia - total duration > 6mos 2. Exclusion criteria A. Autism spectrum disorder - disorganized speech/behavior symptoms also seen in schizophrenia B. Substance use i. intoxication of all substances except nicotine, opioids, caffeine (only induces anxiety, insomnia) ii. withdrawal of alcohol (delirium tremens DTs), sedative hypnotics, or hallucinogens C. General medical condition - general medical conditions that can present as psychosis - use I<3 LADY MACBETH D. Schizoaffective/mood disorder - concurrent schizophrenic and mood symptoms throughout entire duration - clinical presentation of patient the same, BUT: - if depression comes first --> MDD with psychotic - if schizophrenia comes first --> schizophrenia superimposed with MDD - if schizophrenia + depression at same time for whole duration --> schizoaffective

Question 103

``` [Psychotic disorders] 1. Describe delusional disorder 2. List subtypes of delusional disorder 3. Describe syndromes seen within the "unspecified" subtype of delusional disorder A. Capgras Syndrome B. Fregoli's Syndrome C. Cotard Syndrome ```

Answer 103

1. Delusional disorder - 1+ delusions for >1 month in individual with no prior history of schizophrenia - functioning is not impaired (apart from direct effect of delusion) 2. Subtypes - erotomanic - fixed belief that individual is in love with you - jealous - persecutory - grandiose - somatic - mixed, unspecified 3. Subtypes of delusional disorder A. Capgras syndrome - belief that people close to you have been replaced by imposters e.g. spouse - may accompany other psychotic disorders like schizophrenia B. Fregoli's Syndrome - belief that people can assume other disguises (intermetamorphoses) e.g. Neo in the Matrix - variant of Capgras C. Cotard Syndrome - belief that individual has lost part of themselves - physical (heart) or metaphysical (courage) e.g Wizard of Oz

Question 104

``` [Sleep] 1. Describe stages of sleep: A. Wakefulness B. Stage 1 C. Stage 2 D. Stages 3 + 4 E. REM sleep ```

Answer 104

1. Sleep stages: A. Wakefulness - higher frequency, low amplitude beta waves; when calm you see alpha waves (lower frequency) B. Stage 1 - theta waves, very light sleep and easy to wake up; hypnic myoclonia (jerks) C. Stage 2 - theta waves continue with sleep spindles and K complexes: HR slows and body temp drops D. Stages 3 + 4 - low frequency, high altitude delta waves; deep, restorative sleep - bedwetting, night terrors, sleep walking E. REM sleep - alpha and beta waves; 90+ min post falling asleep; dreaming

Question 105

[Sleep] 1. What are the drivers behind the sleep-wake cycle? (The 2-Process Model) 2A. Describe sleep-wake cycle over the course of the day B. role of neurotransmitters C. role of orexin

Answer 105

1. Two-process model A. Homeostatic drive to sleep - driven by buildup of energy metabolite adenosine; related to how much sleep debt you have *caffeine blocks adenosine buildup* B. Circadian rhythms - sleep independent, tied/entrained to light-dark cycle - regulated by suprachiasmatic nucleus (SCN) in hypothalamus 2A. Over the course of the day, we accumulate sleep debt/adenosine, but circadian alerting system (SCN) opposes the sleep debt --> stay awake - Melatonin starts being produced by pineal gland when dark --> turns off circadian system (SCN) --> sleep debt is unopposed --> fall asleep Over course of the night, adenosine is cleared out of the brain --> reduces sleep debt + when its light out, melatonin goes away --> awake B. balanced system - GABA produced by ventrolateral preoptic nucleus (VLPO) of hypothalamus promotes sleep NE (locus ceruleus), 5-HT (raphe nuclei), histamine (tuberomamillary nucleus) promote wakefulness C. orexin - peptide produced in hypothalamus --> promotes wakefulness by exciting neurotransmitters

Question 106

``` [Sleep] Primary sleep disorders incl A. Etiology B. signs / symptoms C. comorbidities D. treatment ``` 1. [Noise] Sleep apnea 2. [Movement] REM behavior disorder

Answer 106

Primary sleep disorders 1. Sleep apnea - M>>F, more common A. MOA: obstruction of airway --> pauses or gaps in breathing B. Signs/symptoms: snoring (noise is the vibration from the movement of air through constricted space), choking, gasps, no breathing (brain goes up to stage 1 sleep so you can exert voluntary control over muscles) - *classic symptom* excessive daytime sleepiness --> spend less time in restorative deep sleep (stages 3/4) C. Comorbidities - obesity. HTN, CAD, MI, stroke D. Treatment - CPAP (continuous positive airway pressure) 2. REM behavior disorder A. MOA: lack of muscle atonia --> act out on dreams --> can lead to physical harm to themself or bed partner B. Signs/symptoms: most common in M>60 yo C. Comorbidities: significant % develop neurological disorders incl Parkinson's, lewy body dementia D. Treatment - clonazepam (benzo)

Question 107

``` [Sleep] Primary sleep disorders incl A. Etiology B. signs / symptoms C. comorbidities D. treatment ``` 3. [Movement] Parasomnia 4. Narcolepsy

Answer 107

3. Parasomnia - sleepwalking, eating, night terrors A. MOA: happens during non-REM sleep, transition between sleeping and walking B. Signs/symptoms: most common in children, risk for self-injury C. Comorbidities: sleep deprivation, sedative use, alcohol, stress D. Treatment: avoid sedative use, keep person safe in sleep environment 4. Narcolepsy A. MOA: discoordination of REM and wakefulness due to loss of orexin neurons in hypothalamus - diagnosed with polysomnagram and multiple sleep latency test (MSLT) B. Signs/symptoms: *tetrad* i. excessive daytime sleepiness ii. sleep paralysis (waking and unable to move) iii. cataplexy (loss of muscle tone) with strong emotion iv. hypnagogic (going to sleep) and hypnapompic (waking up) hallucinations --> conscious but still seeing your dreams C. Comorbidities: N/A D. Treatment: recognition, reassurance, meds (modafinil, stimulants, antidepressants)

Question 108

``` [Sleep] - Insomnia 1. Medications known to cause insomnia 2. Define idiopathic insomnia 3. Approaches to insomnia A. Non-pharmacologicc B. Pharmacologic ```

Answer 108

1. Antidepressants (SSRI, SNRI, MAOI), nasal decongestants, antiparkinsonian drugs (L-dopa), antihypertensives (beta blockers), bronchodilators (theophylline), corticosteroids (prednisone) 2. Idiopathic insomnia - not due to primary sleep disorder or a byproduct of general medical / psychiatric condition --> no known cause - can be difficulty falling asleep, staying asleep, waking up too early, or poor quality - must have next-day consequences for insomnia diagnosis (decreased ability to function, accidents, increased healthcare utilization) - chronic insomnia due to predisposing, precipitating, perpetuating factors (napping, conditioning) - Risk factors - F>M, increased prevalence in elderly (>65) 3. Approaches to insomnia - people most commonly use alcohol (GABA agonist but short half-life), OTC sleep aids (contain antihistamines) A. Non-pharmacologic - sleep hygiene (using bed for sleep), exercise, relaxation, CBT (stress control, stimulus control) B. Pharmacologic - sedating antidepressant e.g. doxepin (Silenor) --> most antihistaminic, or use Benadryl - suvorexant - orexin blocker used for insomnia - sedative hypnotics e.g. GABA agonists (benzo or non-benzos) --> work well for acute insomnia but risk for tolerance/dependence and can produce odd nighttime behaviors/daytime sedation

Question 109

[Cognitive Assessment] 1. Purpose of intelligence testing 2. Issues with intelligence testing 3. Most common IQ tests 4. Difference between achievement vs aptitude and tests used

Answer 109

Intelligence testing 1. Purpose - get sense of cognitive aptitudes and weaknesses --> predicts short-term academic achievement; use in educational/occupational counseling; diagnosis of learning disabilities - no accepted definition of intelligence 2. Nature vs nurture (nature sets range, nurture determines where we fall within that) - weak relationship to occupational status, job performance, success in life - cultural/gender bias, stereotyped due to performance - misuse of scores, outcome (Vs process) oriented 3. 16-89 years --> WAIS-IV (Wechsler Adult Intelligence Scales); mean 100, SD 15 with 10 core subtests 6-16 years --> WISC-IV (Wechsler Scales for Children) 4. Achievement - assess what has been learned in the past --> final exams, AP exams, Wide Range Achievement Test (WRAT-4) Aptitude test - predictor of future behavior --> GRE, MCAT, IQ test, Wechsler Individual Achievement Test (WIAT - maps directly onto IQ scores)

Question 110

``` [Cognitive Assessment] - Intelligence testing Core subtests for WAIS-IV I. Verbal comprehension II. Perceptual reasoning III. Working memory IV. Processing speed ```

Answer 110

Core subtests for WAIS-IV I. Verbal comprehension 1. vocabulary - *most stable*, best indicator of premorbid functioning; general mental ability 2. information - "what continent is brazil on"; general mental ability 3. Similarities - abstract reasoning "how are apple and banana alike" II. Perceptual reasoning 4. block design - use colored blocks to replicate design in picture book; culture-neutral, spatial perception + nonverbal reasoning 5. matrix reasoning - explaining how you would solve the puzzle/problem; abstract + spatial reasoning 6. visual puzzles - actually solving puzzles; spatial reasoning III. Working memory 7. Digit span - repeating numbers forward and backwards; attention + concentration 8. Arithmetic - concentration and mental math IV. Processing speed 9. Symbol search - matching symbols; visual perception and analysis 10. Coding - motor + mental speed, visual working memory

Question 111

``` [Cognitive Assessment] 1. Goals of Neuropsych testing 2. Issues with testing 3. Types of neuropsych batteries A. fixed B. flexible C. Mixed ```

Answer 111

Neuropsych testing 1. Goals - screen/diagnose/track neurological disorders; determine if problem behavior is organic (physical injury) or functional (e.g. due to depression); evaluate cognitive functions; informs treatment planning 2. Issues - balancing false negatives vs false positives - consider variables - age, education, disabilities, ethnicity - selecting type of battery 3. Types of neuropsych batteries A. fixed - everybody gets same tests --> good for research, outcome focused and time-consuming B. flexible - tailor tests to referral question --> process focused and time efficient C. Mixed - everybody does same 1-2 tests, others are tailored to client/referral question

Question 112

[Cognitive Assessment] - Neuropsych testing 4. Describe areas assessed with neuropsych batteries incl brain regions affected, disorders, and tests used A. Attention B. Language C. Visual-Spatial D. Memory E. Executive functioning

Answer 112

Neuropsych testing 4A. Attention - frontal lobes; affected in ADHD, depression, dementia - tests - digit span, arithmetic, trail test, stroop test (name color ink that the word is written in) B. Language - frontal and temporal lobes; speech production is Broca's (frontal) and comprehension is Wernicke's (temporal) - tests - Boston-Naming (picture book), COWA (list words that begin with F), category fluency (e.g. list animals), boston diagnostic aphasia exam C. Visual-spatial - parietal and occipital lobes; affected in visual neglect, visual agnosia, prosopagnosia - tests - benton test of visual attention, block design, object assembly, copying pictures D. Memory - temporal and frontal lobes, affected in Alzheimer's dementia, depression, normal aging - tests - Wechsler memory scale, Hopkins verbal learning test (recall list of words after 20 min delay), digit span, information, bender/benton E. Executive functioning - frontal lobe; affected in alcoholism, depression, autism, ADHD, schizophrenia, parkinson's - tests - Wisconsin card sort, letter number sequencing, trail test, stroop test

Question 113

[Dissociative Disorders] 1. Define dissociation 2. Neurobiology of dissociation 3. Most common comorbid psychiatric conditions

Answer 113

1. Dissociation - complex psychobiological process along a continuum from normal (day dreaming) to pathological (failure to integrate into coherent sense of consciousness) 2. Neurobiology of dissociation - NMDA, 5-HT, endogenous opioid dysregulation - increased tone/blunted stress reactivity of HPA axis - disruptions in sensory cortex - frontal inhibition of limbic structures --> hypo-emotional - PFC, subcortical, parietal --> memory suppression 3. Difference between having dissociative symptoms (eg in PTSD, panic disorder, delirium, Alzheimer's, temporal lobe disease) and dissociative disorder Most common comorbid psychiatric conditions: MDD, PDD/dysthymia, substance use, generalized anxiety disorder, eating disorders, personality disorders (borderline, OCD, avoidant)

Question 114

[Dissociative Disorders] 1. Define Dissociative symptoms 2. Symptoms to ask about in diagnostic interview 3. Dissociative experiences scale

Answer 114

1. Dissociative symptoms - unwanted intrusions into awareness and behavior; disruption in integration of memories, perceptions, emotions, sense of self, motor control/behavior, consciousness - occur in context of trauma and are an attempt to maintain equilibrium 2. Symptoms: blackouts, fugues (Travel without remembering), unexplained possessions, changes in relationships, fluctuations in skills/knowledge, fragmentary recall of personal history - passive influence (feeling that your thoughts are not your own) - negative hallucinations (not hearing/seeing what others heard/saw) - analgesia (any other person would have felt pain/emotion that you did not eg trauma on battlefield) ``` 3. Dissociative experiences scale - screening tool; 28 item scale 5-15: normal 25: suspicious >30: amnesia/fugue or depersonalization >45: likely dissociative disorder ```

Question 115

[Dissociative Disorders] Describe including criteria for diagnosis, symptoms, subtypes, and differential 1. Dissociative amnesia

Answer 115

1. Dissociative amnesia - inability to recall important autobiographical information, usually related to trauma, patients not in distress - risk factors are repeated trauma, severity of trauma A. Subtypes - subtype with dissociative fugue - travel associated with amnesia - subtypes: (localized) failure to recall events during specific time e.g. when attacked; (selective) recall some but not all of the events of a specific time; (generalized) complete loss of memory for personal identity - semantic or procedural; (systemized) - loss of memory in one category e.g. family; (continuous) B. differential - delirium/dementia, memory loss due to head trauma, seizure disorder, transient global amnesia, somatoform disorder, PTSD, substance use, catatonic stupor

Question 116

[Dissociative Disorders] Describe including criteria for diagnosis, symptoms, subtypes, and differential 2. Depersonalization/derealization disorder

Answer 116

2. Depersonalization/derealization disorder - high levels of distress, common symptom but uncommon syndrome - depersonalization (feel detached from body anatomically, unreal/absent self, emotional/physical numbness) - derealization (feel detached from environment - things appear distorted, foggy, bigger/smaller) - history of emotional abuse/neglect (trauma) - mean age of onset = 16 yo - last from days to years, sudden or gradual onset - Differential - neurological (seizure, infection, vascular, degenerative), toxic/metabolic (endocrine, substance, infectious), psychiatric (schizophrenia, mood, anxiety, or personality disorders)

Question 117

[Dissociative Disorders] Describe including criteria for diagnosis, symptoms, subtypes, and differential 3. Dissociative identity disorder (formerly Multiple Personality Disorder)

Answer 117

3. Dissociative identity disorder - disruption of identity with 2+ distinct personality states (Avg 5-10); discontinuity in sense of self (shifting b/w personalities v quickly) - related to ongoing stressors/trauma (physical / sexual childhood abuse) - F>>M --> women present with classic dissociative, men with criminal/violent behavior - alteration in sense of self and agency (not in charge) and recurrent dissociative amnesia - possession by "alters" (not normal possession associated with religious observance) - most chronic and severe; 70% attempt suicide - differential: dissociative amnesia, MDD, bipolar, psychotic disorder, borderline personality, malingering, complex partial seizures

Question 118

``` [Dissociative Disorders] 4. Describe other specific dissociative disorders A. Identity disturbance B. Acute dissociative reaction C. Dissociative trance ``` 5. Treatment for dissociative disorders

Answer 118

4. Other specific dissociative disorders A. Identity disturbance - due to prolonged and intense persuasion e.g. brainwashing, torture B. Acute dissociative reaction - resolve <1 month after trauma C. Dissociative trance - completely separated from environment/not conscious; can happen normally in religious context *hypnosis requires dissociation 5. Treatment for dissociative disorders - v rare disorders - not a lot of data, no controlled studies - behavioral interventions (positive reward) - psychotherapy e.g. CBT - no medications but treat comorbid conditions

Question 119

[Eating Disorders] Anorexia Nervosa 1. Diagnostic criteria 2. Associated features 3. Medical complications 4. Treatment

Answer 119

Eating disorders have highest mortality rates of all psychiatric disorders Anorexia Nervosa *often do not want help* 1. Criteria: restriction of energy intake - v low body weight; intense fear of weight gain despite being underweight 2. Features: food preoccupations, bizarre eating habits, increased irritability/depression, impaired sleep/concentration, social isolation * secondary effects of starvation* 3. Medical complications: low BP, amenorrhea, osteoporosis, GI problems, edema, cardiac irregularities 4. Treatment: family therapy, psychotherapy, nutritional treatment, no drugs available

Question 120

[Eating Disorders] Bulimia Nervosa 1. Diagnostic criteria 2. Associated features 3. Medical complications 4. Treatment

Answer 120

Bulimia Nervosa *want help to be thin* 1. Criteria: recurrent episodes of binge eating (lack of control and eating a lot fast when not hungry/until uncomfortably full) with inappropriate compensatory behavior to prevent weight gain (purging, laxatives, exercise) 2. Features: occur at least weekly for 3 mos - overemphasis on shape/weight - negative body image 3. Medical complications: electrolyte imbalance --> Cardiac irregularities, dental problems, damage to throat/esophagus/stomach, GI problems 4. Treatment: family therapy, psychotherapy, nutritional treatment, antidepressants e.g. fluoxetine/Prozac

Question 121

[Eating Disorders] Binge Eating Disorder 1. Diagnostic criteria 2. Associated features 3. Medical complications 4. Treatment

Answer 121

Binge Eating Disorder *want help with weight but maintain food intake* most common, M=F 1. Criteria: recurrent episodes of binge eating without compensatory behavior 2. Features: eating alone due to embarrassment, feeling disgusted with oneself, marked distress 3. Medical complications: high BP, high cholesterol, increased risk diabetes, weight gain - weight cycling is more dangerous than staying at a higher weight - don't want to flip binge eaters into becoming anorexic 4. Treatment: family therapy, psychotherapy, nutritional treatment, Vyvanse (CNS stimulant)