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Psychiatry > First Pass Miss Exam 2 > Flashcards

First Pass Miss Exam 2 Flashcards

1
Q

What are the two subtypes of ADHD, and how many symptoms do you have to have in that category in order to qualify for that subtype (or combined = affected by both)

A

Inattentive subtype
Hyperactive / impulsive subtype

Need at least 6 for children and 5 for adults

Must be present at least 6 months, symptoms first appearing before 12 years of age

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2
Q

What areas of the brain seem to have lower activity in ADHD? What neurotransmitters are affected?

A 
Prefrontal cortex (impulse control) 
Caudate & Globus pallidus (basal ganglia, motor control)

Neurotransmitters include dopamine and NE

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3
Q

What things are commonly cormorbid with ADHD?

A

ODD/CD
Learning disability
Anxiety / Mood disorders

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4
Q

What are first line, second line, and third line pharmacotherapies for ADHD?

A

First line: Stimulants - Methylphenidate and dextroamphetamine

Second line: Alpha-2 agonists - Guanfacine, Clonidine
NRI - Atomoxetine

Third line: TCAs, Bupropion

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5
Q

What are the important side effects of stimulants?

A

Appetite suppression / weight loss -> may lead to growth delay
Mood disturbance in withdrawal -> will realize they are hungry
Elevated HR / BP
Can cause insomnia if taken at night, also GI / headache

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6
Q

What are some other indications for stimulants?

A

Exogenous obesity and binge-eating disorder (appetite suppressant)

Adjunct for Obstructive Sleep Apnea

Narcolepsy (treats insomnia via keeping you awake)

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7
Q

What are some conditions which may be mis-diagnosed at ADHD (on the differential)?

A

Anxiety -> will be fidgety
Depression -> lack of motivation
BPAD -> looks like hypomanic symptoms
Conduct disorder -> playing with scissors might look like conduct disorder but actually be ADHD

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8
Q

What are atomoxetine’s drug interactions of concern?

A

Metabolized by CYP2D6 - increased levels with paroxetine, fluoxetine, and TCAs

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9
Q

What is the mechanism of action of alpha agonists in ADHD?

A

Enhance NE input from locus coeruleus and stimulate post-synaptic alpha 2A receptors -> improves functional connectivity of prefrontal cortex networks

side effects include the pre-synaptic effects:
Drowsiness / sedation
Decreased BP / pulse -> discontinuation = rebound hypertension, tachycardia, anxiety / panic attacks

Take 4-6 weeks to work (same as Atomoxetine)

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10
Q

Give a couple key biological, individual, family, and social/school risk factors for development of DBDs?

A

Biology - male sex, perinatal complications, genetic

Individual - Below average IQ, reading problems, aggression / ADHD

Family - Parental antisocial behavior, single parent w/ lack of supervision, excessive control, early motherhood

Social - Peer rejection / being bullied / victimized, low SES, exposure to media violence

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11
Q

What are the three categories for ODD diagnosis? How long must it be present?

A

For >6 months - pattern of negativistic / hostile / defiant behavior

  1. Angry / Irritable Mood
  2. Argumentative / Defiant Behavior
  3. Spiteful / Vindictive

Basically: Mood, Behavior, and Vindictive behavior

Usually starts before age 8, average age 6

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12
Q

What is the treatment for ODD? What is most important?

A

There is NO pharmacotherapy

  • > Early treatment via psychosocial therapies MUST involve parents
  • > Individual or family therapy NOT effective
  • -> Parent Management Training or Problem Solving Collaboration / Communication therapy is indicated*
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13
Q

When is conduct disorder diagnosed and what is it generally?

A

Repetitive & persistent pattern of behavior in which basic rights of others or major age-appropriate societal norms / rules are violated

Diagnosed until 18, or after age 18 if criteria for antisocial personality disorder are not met

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14
Q

What are the four categories of misconduct in conduct disorder?

A

TARD: Theft, aggression, rules violation, destruction of property

  1. Aggression towards people & animals
  2. Destruction of property
  3. Deceitfulness or theft
  4. Serious violations of rules (parental or school)
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15
Q

What are three specifiers of conduct disorder?

A
  1. Childhood onset -> at least one criteria before age 10
  2. Adolescent onset -> absence of criteria before age 10
  3. With limited prosocial emotions -> lack of remorse, guilt, empathy, shallow affect, and unconcern about performance
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16
Q

What are the three evidence-based psychosocial treatments for CD and which one shows a long-term reduction in arrest / incarceration?

A
  1. Parent Management Training
  2. Probleming-Solving Skills Training
    (First two are same as ODD)
  3. Multisystemic Therapy (MST) -> leads to a reduction in re-arrest. Includes involvement of school, home, justice system, etc.
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17
Q

What conditions are most frequently comorbid with ODD / CD?

A 
ADHD (10x) 
Major Depression (7x) 
Substance Abuse (4x) -> although behavior must not be CAUSED by substance use
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18
Q

What are the three levels of ASD severity?

A

Level 1 - least severe, requires some support. Will have decreased interest in social interactions and difficulties switching between activities, with poorer independence

Level 2 - requires substantial support, marked deficits, reduced or abnormal social responses, and repeated behaviors are obvious to casual observer

Level 3 - Most needy, very limited social interactions / social responses, restricted behavior interferes with functioning in all spheres

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19
Q

What are the diagnostic features of ASD?

A
  1. Poor social interactions, social communication deficits

2. Repetitive / ritualized behaviors, and restricted interests.

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20
Q

What neurobiological abnormalities are known to be associated with ASD? One important environmental exposure?

A

Neurobiological - EEG abnormalities & seizure disorders
Environmental - Fetal exposure to valproate

Poor prognosis involves ASD associated with grand mal seizures.

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21
Q

What are the typical avenues to accomplish the treatment goals of ASD?

A

Language remediation for speech delay -> speech therapy
Educational interventions -> classroom changes
**Applied Behavior Analysis (ABA) ** -> teach them learning
OT/PT, and sensory integration therapy

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22
Q

How can ASD social developmental deficits be seen in childhood and adults?

A

Childhood - Difficult playing with peers due to awkward / inappropriate social behavior, cannot detect feelings of others

Adults - lack of relationships

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23
Q

What is an example of hypo / hyper-reactivity to the environment?

A

Apparent indifference to pain / temp (wont even care if they bang their head)

Will have adverse response to specific sounds, or be fascinated by lights / movement

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24
Q

What is Asperger’s basically?

A

A subset of ASD, with no language or intellectual impairment, but clearly marked decrease in social interactions which can lead to teasing / bullying

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25
Q

What causes Rett syndrome and who gets it?

A

X-linked dominant MECP2 gene mutation -> homozygous lethal in males

MeCP2 gene = Methyl Cytosine-binding Protein 2 -> needed for brain development
-> cases are usually de novo, but some are rarely asymptomatic (not penetrant)

Seen in females only

Encephalopathy beginning between 6 months and 2 years (normal development early)

Loss of purposeful hand movements, with stereotypic hand-wringing, ataxia, head circumference growth deceleration, loss of language skills

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26
Q

What are the common manifestations of social or pragmatic communication disorder?

A

Deficits in using appropriate communication for context / listener needs. Cannot understand the implied meaning or multiple meanings of words and phrases very well.

Sometimes when things are said, you mean to imply many things “We are going to the store, remember it’s raining” -> need them to infer you need to put on your raincoat, etc. They have difficulty understanding whats not explicitly stated.

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27
Q

What are the pharmacological treatments of ASD for?

A

Targeting specific symptoms / common comorbidities

If aggression -> Risperidone
SSRIs for comorbid depression / anxiety
Stimulants for comorbid ADHD

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28
Q

How is restricted, repetitive behavior characterized in ASD?

A
  1. Stereotyped / repetitive movements and in use of objects / speech - stereotypies
  2. Insistence on sameness, inflexibility / ritualized behavior - i.e. extreme distress at small changes
  3. Highly restricted, fixated interests which are abnormal in intensity / focus -> way too focused on one thing, possible savantism
  4. Hypo/hyper reactivity to environment
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29
Q

What are three types of complex vocal tics which may involve speaking? There are three words for these.

A
  1. Palilalia - repeating one’s own words
  2. Echolalia - repeating someone else’s words
  3. Coprolalia - Obscenities uttered (rare)
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30
Q

What are the criteria for Tourette’s Disorder (TS)?

A
  1. 2+ motor AND 1+ vocal tics present during illness, but not necessarily at same time
  2. Tics must persist for greater than 1 year since onset (though the tics can change during this time)
  3. Must occur before age 18
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31
Q

What is a provisional tic disorder?

A

Single or multiple motor tick and/or vocal tics

Any tics presenting for <1 year since onset, before age 18

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32
Q

What neuroanatomic abnormalities occur in TS?

A

Basal ganglia dysfunction, with defective cortical input to striatum, and thalamocortical abnormalities.

-> small caudate volumes, larger PFC, increased dopamine (D1 for direct pathway = GalphaS) receptor density in striatum in general to make them hypermobile

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33
Q

What is the typical progression of tic disorders?

A

Simple, transient motor tics arise around age 4-6
Rostrocaudal progression of tics
Phonic tics appear ages 8-15 (does not happen in all, but if you have a phonic tic you most likely have a motor tic)
Tics severity peaks age 10-12
Waxing / waning is normal

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34
Q

What is the best psychotherapy for tic disorders?

A

Habit Reversal Training (HRT)
-> Teaches awareness of tic, and “competing response practice” -> channel the urge into a less functionally impairing tic which cannot be seen

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35
Q

What are three classes of drugs used in treatment of tic disorders?

A
  1. Alpha-2 receptor agonists - first line (clonidine, guanfacine)
  2. D2 receptor antagonists - neuroleptic drugs like haloperidol, risperidone, and pimozide (typical antipsychotics mostly)
  3. Botox - for very severe motor / vocal
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36
Q

What are the typical etiologies of primary vs secondary enuresis and what does this mean? Which is more common?

A

Primary - never gained continence -> usually due to maturational delay. Represents 80% of patients.

Secondary enuresis - lost continence after at least 1 year of continence -> usually due to a stressor. Less common, starts between 5-8

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37
Q

What is the DSM diagnosis of enuresis? What developmental must be met?

A

Involuntary or intentional voiding into bed or clothes, at least 2x a week for >=3 consecutive months, or presence of distress / impairment

Developmental age >= 5 years (better than 90% will have bladder control by this point)

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38
Q

What are the pharmacotherapies available for enuresis if there is a major functional impairment? Major risks?

A

Imipramine - tricyclic with anticholinergic properties, cardiac arrhythmia is a concern

DDAVP - desmopressin - reduces urine production, may lead to hyponatremia and seizure due to water intoxication

Best treatment: Enuresis alarm

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39
Q

What condition must be ruled out before making a diagnosis of encopresis and starting normal treatment?

A

Psychogenic megacolon

pathology:
- > children hold feces voluntarily or because of defecation pain
- > rectal distention leads to loss of rectal tone / desensitization
- > children do not need to defecate -> leads to OVERFLOW encopresis
- > need GI to decompact the bowel for treatment

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40
Q

What is the DSM criteria for encopresis? What must you specify?

A

Involuntary or intentional passage of feces at least 1x per month for at least 3 months
-> chronological age of at least 4 (vs 5 with enuresis)

-> must specify if due to overflow incontinence or not

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41
Q

What are the DSM criteria of separation anxiety disorder (SAD)?

A

Inappropriate, excessive anxiety concerning separation from attachment figures (i.e. Meghan), lasting for 1 month (>4 weeks).

Distress from separation, worry about attachment figure, refusal or fear to leave home or be alone, refusal to sleep away from home or without attachment figure. Nightmares w/separation themes common.

Starts after a life stress, usually ages 7-9 years.

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42
Q

What is the DSM criteria for selective mutism?

A

For >1 month (not the first month of school), failure to speak in specific social situations despite speaking in others. Interferes with function, not simply due to language / developmental issue

-> explains high incidence of social phobia / anxiety later in life

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43
Q

Why does encopresis typically arise?

A

Arises usually as secondary encopresis (>1 yr of continence) with constipation and excessive fluid overflow (overflow incontinence) -> will be small liquid stool. Often precipitated by life events and in reaction to a stressor / anxiety.

Can also be primary due to lack of proper toilet training.

This is opposite to enuresis which tends to arise as primary, secondary is less common. (It’s unlikely that you will have never figured out how to hold your poops).

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44
Q

What is considered moderate, at risk, and heavy drinking for males? This is, number of drinks per day. Females?

A

Moderate = 2 drinks a day
At risk = 4+ drinks a day
Heavy = 5+ drinks a day

Females is 1 less than this in all categories.

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45
Q

What is the rough timeline of withdrawal symptoms for alcohol?

A

6 hours - tremor
8 - 12 hours - visual hallucinations
12-24 hours - seizures
72 hours - delirium tremens (preventable)

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46
Q

What liver enzymes suggest alcoholic liver damage vs viral hepatitis?

A

Elevated AST > ALT, ratio of AST:ALT is increased.

Also, elevated GGT levels

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47
Q

What are the most common features of Cannabis Withdrawal Syndrome?

A

3+ behavior symptoms: Decreased appetite, Irritability, Sleep difficulty
+
1+ physical symptoms: like sweating, tremors, headache

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48
Q

Can opiate withdrawal be fatal and how long does it last?

A

Q.
Can opiate withdrawal be fatal and how long does it last?

A.
Lasts 7-10 days, peaking at 2-3 days

NOT fatal (like delirium tremens would be)

Remember: Nicotine withdrawal peaks at 2-3 days as well, but lasts 1-3 months! gg!

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49
Q

What are the common behavioral effects of cannabis?

A

Decreased goal-directed mental activity, relaxation, slowed sense of time, heightened sensitivity to external stimuli (smell, sound, taste), anterograde amnesia, increased appetite

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50
Q

How does cocaine cause stroke?

A

Major vasoconstriction -> nonhemorrhagic cerebral infarct

  • > can also cause hemorrhagic
  • > also liable to cause MI / arrhythmias due to myocardial ischemia from vasoconstriction + sympathetic hyperstimulation
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51
Q

What are two quite diagnostic physical changes for amphetamine overuse (i.e. methamphetamine or other sympathomimetics)

A
  1. Bruxism - teeth grinding
  2. Weight loss (appetite suppressant)

-> otherwise it looks just like cocaine use

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52
Q

How can an LSD trip be told apart from an acute psychotic episode?

A

Absence of auditory hallucinations in LSD (visual only)

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53
Q

Does a withdrawal syndrome exist for hallucinogens? How do they differ from dissociative drugs?

A

NO

Differ from dissociative drugs because they expand your consciousness

Dissociative drugs distort your consciousness and detach you from it

Both will act on NMDA receptors

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54
Q

What is the mechanism of action of MDMA?

A

Amphetamine analog -> stimulant properties, but also mild hallucinogenic properties by acting on serotonergic receptors

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55
Q

How do kids these days typically deal with the negative effects of MDMA use?

A
  1. Pacifier - can cause bruxism (similar MoA as methamphetamine)
  2. Water bottles - can cause diaphoresis, dehydration, and hyperthermia
    - > can lead to hyperthermia, heart, kidney failure due to extreme heat stroke
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56
Q

What can cannabis do to the lungs, to the psyche, and to the reproductive system?

A

Lungs - decreased lung capacity and increased infection risk
Psyche - Increased risk for anxiety / depression, worse mood disorders
Reproductive system - Decreased testosterone / gynecomastia. Reduced fertility

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57
Q

What is the medical name of roofies and its mechanism of action? How long do effects last?

A

Rohypnol - Flunitrazepam

Mechanism of action - GABA-A agonist, similar to other benzos. 7-10x as potent as diazepam, with effects lasting 4-6 hours

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58
Q

What is “entering the K hole” or “going to K land”?

A

Descriptions of entering an alternate plane of existence, perceptual distortion and feelings of disconnection from self and environment. Can lead to terrifying sensations of loss of time and identity.

59
Q

What are the three types of control delusions? Most common type of delusion overall?

A
  1. Insertion - Someone is inserting thoughts in my head
  2. Withdrawal - someone is taking thoughts out of my head
  3. Broadcasting - someone is letting everyone hear my thoughts

Most common delusion: Persecutory / paranoid

60
Q

What is meant by catatonic behavior in psychosis?

A 
Decrease in reactivity 
Includes (possibly): 
1. Negativism - resistance to instruction or doing the exact opposite 
2. Rigid / bizarre posture (catalepsy) 
3. Mutism 
4. Lack of motor response - stupor 
5. Stereotypes like grimacing, staring 
6. Echolalia/Echopraxia 
7. Purposeless or excessive motor activity - catatonic excitement
61
Q

What are the criteria for Schizophrenia?

A

For greater than 1 month (or less if treatment), presence of 2+

Hallucinations 
Delusions 
Disorganized speech 
Disorganized or catatonic behavior 
Negative Symptoms

At least 1 of the 2 has to come from first three (the first three are positive symptoms).

Must have a decreased functioning in some aspect of life, and symptoms persist for at least 6 months which are at least prodromal, residual, attenuated, or negative symptoms of Criterion A.

That is, even when Criterion A symptoms are treated, you still have not returned to baseline for 6 months.

62
Q

Why is life expectancy decreased in Schizophrenia?

A

Increase in cardiovascular problems
Weight gain and diabetes are common side effects of atypical antipsychotics
Substance abuse
Insufficient counseling / screening by doctors
Suicide / Violence

Basically boils down to: The drugs they’re taking, what their disorder does to them, and how that becomes the only thing people care about

63
Q

What are the features of “psychotic” behavior?

A

Delusions
Hallucinations
Disorganized speech
Disorganized and catatonic behavior

64
Q

What are some factors which indicate good prognosis in schizophrenia?

A

Female (tend to be diagnosed later, also have higher incidence of mood disorder)
Later onset
Precipitating event or stressor with acute onset
Paranoid features
Family history of mood disorder, and associated mood change in illness
Good interepisode function
No gross brain abnormality

65
Q

What is the strongest genetic association with schizophrenia, and what neurological process is this thought to underlie?

A

Strongly associated with the major histocompatibility complex

  • > process of errant and excessive synaptic pruning during adolescence and early adulthood may underlie brain volume decrease and prodromal impairments in emotional, cognitive, and motor function
  • > explains ventriculomegaly with decreased dendritic branching / atrophy of cortex in schizophrenia
66
Q

What are some factors which indicate poor prognosis in schizophrenia?

A

Physical illness comorbid
Substance abuse comorbid
Family history of schizophrenia (less related to mood disorders)
High emotional conflicts at home (stress = worse outcome)
Low treatment compliance
Experience side effects w/ antipsychotics

67
Q

By what mechanism are positive and negative symptoms in schizophrenia thought to be controlled

A

Mesocortical pathway (ventral tegmental area to prefrontal cortex) is thought to lead to cognitive and negative symptoms, and this is due to a decrease in dopamine.

Increased dopamine to mesolimbic pathway (VTA to NAcc) leads to positive symptoms

68
Q

What is the unifying NMDA theory of schizophrenia?

A

Hypofunction of the glutamate NMDA receptor underlies schizophrenia.

In the Mesolimbic system, there is an interneuron which is improperly activated when glutamate function is low. As a result, this GABA interneuron cannot inhibit dopamine release to NAcc -> Increased dopamine.

In the Mesocortical system, there is no interneuron. We simply cannot stimulate the dopamine releasing neuron to the prefrontal cortex properly because NMDA receptors are not working. Thus, there is decreased dopamine in the prefrontal cortex.

69
Q

How is schizophreniform disorder diagnosed?

A

Same diagnostic criteria as schizophrenia, although the prodromal, active, and residual phases have gone on less than 6 months at this point.

ALSO

Decline of function is not required at this point.

-> better prognosis = acute delirium features, and more acute onset (less prodromal symptoms)

70
Q

What is Brief Psychotic Disorder?

A

Same diagnostic criterion A as schizophrenia, MINUS the negative symptoms.

Duration at least 1 day to less than 1 month.

Premorbid level of functioning will return, associated with personality disorders

Modifiers:
1. With marked stressor - occur shortly after very stressful event

  1. With postpartum onset - within 4 weeks postpartum
71
Q

What is Schizoaffective Disorder? (Diagnostic criteria)

A
  1. Period of major depressive or manic episode
    AND
  2. Criteria A for Schizophrenia (full)
    AND
  3. 2+ week period of delusions / hallucinations in absence of major mood symptoms has occurred
    AND
  4. Minimum duration of one month

Vs major mood disorder with psychotic features - this two week period will exist

72
Q

What is Delusional Disorder?

A

Presence of delusions for >1 month in absence of otherwise bizarre behavior and functional deficits.

Hallucinations may present if in accordance to delusions

-> most commonly persecutory or jealous delusions

73
Q

How is the diagnosis of psychotic disorder due to another medical condition made? What factors would make you lean towards this diagnosis

A

Prominent hallucinations or delusions with evidence from history, physical exam, or labs which show it is the direct physiological consequence of another medical condition

Factors: 
Atypical age of onset 
Documented in literature 
Non-auditory hallucinations (usually visual) 
Absence of personal or family history
74
Q

What psychotic features are associated with amphetamine and cocaine intoxication?

A
  1. Persecutory delusions
  2. Distortion of body image
  3. Formication
  4. Wicked bad nightmares
75
Q

What type of seizures are alcohol withdrawal seizures, and who is predisposed?

A

Generalized tonic-clonic with loss of consciousness

  • > predisposed = hypokalemia, hypomagnesia, epilepsy
  • > prevent with chlordiazepoxide or lorazepam
76
Q

What is the mechanism of action of Acamprosate? What is it used to treat? How is it excreted?

A

Second line drug behind naltrexone for treatment of alcohol use disorder

Mechanism: NMDA antagonist, GABA-A agonist - “normalizes neurotransmitter systems”
-excreted by the kidney, so better in liver problems

Topiramate also reduces drinking days

77
Q

How do you treat PCP / Ketamine intoxication?

A

Keep patients in a calm environment for them to come down

Give benzodiazepines / antipsychotics to calm them

78
Q

How is opioid withdrawal typically managed?

A

Methadone or buprenorphine (partial agonist) until there are no withdrawal symptoms, then taper

Manage withdrawal symptoms via medication:
Ibuprofen for muscle aches
Dicyclomine for diarrhea
Clonidine for autonomic changes / sweating / insomnia

79
Q

What are the consequences of prolactinemia caused by dopamine blockade going to the infundibulum?

A
  1. Galactorrhea - lactation, even in males
  2. Amenorrhea, fertility problems, and sexual dysfunction due to inhibition of FSH / LH
  3. Osteoporosis, especially in post-menopausal women
80
Q

What are the EPS from typical antipsychotics and how do you treat all of them?

A

Parkinsonism: Benztropine

Acute dystonia: Anticholinergics once stable, following anticholinergic antihistamine: diphenhydramine

Akathisia: Beta blockers, benzos, and anticholinergics

81
Q

How is TD diagnosed? Treated?

A
  1. A 2 measure brief screen - hands out and wiggle the fingers while checking for mouth movements
  2. AIMS scale - abnormal involuntary movement

Use Valbenazine - a VMAT2 inhibitor preventing the packaging of dopamine in nigrostriatal neurons

82
Q

What features characterize neuroleptic malignant syndrome (NMS)? What labs go with it?

A

Life-threatening reaction to D2 antagonism

  • > Severe muscle rigidity (“Lead pipe rigidity”)
  • > Hyperthermia (guys face is bright red)
  • > autonomic instability - tachycardia, confusion, diaphoresis, labile blood pressure

Lab findings - Increased CPK and myoglobin due to rhabdomyolysis

83
Q

What side effects are particularly associated with chlorpromazine?

A

Photosensitivity

Also weight gain and dyslipidemia / DM like atypicals (especially clozapine and olanzapine)

84
Q

What is the mechanism of action of aripiprazole / brexiprazole / cariprazine? What is the side effect associated with them?

A 
D2 partial agonist (blocks dopamine if there's alot) 
5HT2A antagonism (accounts for effects) 
5HT1A partial agonist -> like buspirone

More activating than other antipsychotics

85
Q

Which atypical is thought to have a pro-cognitive effect due to 5HT7 antagonism (like vortioxetine)?

A

Lurasidone

-> lubricates ur brain

86
Q

Why is Risperidone considered like a borderline typical antipsychotic? What drug is an active metabolite of it?

A

Becomes more like typical above 6mg daily -> EPS side effects

  • > also raises prolactin even at low doses
  • > Paliperidone is an active metabolite with fewer side effects
87
Q

What atypical is associated with DRESS (drug reaction with eosinophilia and systemic syndromes)?

A

Ziprasidone (think of pretty lady with a zipper wearing a DRESS)
-> also associated with QT prolongation next to the guide tape, along with Iloperidone

88
Q

What are the major side effects of concern for clozapine other than agranulocytosis?

A

Myocarditis - heart with a sandglass in it in sketchy
Seizures - shaking clock
Anticholinergic effects - tea party painting behind clozapine closet

-> decreases suicidality like lithium

89
Q

What drug is used for blind patients unable to obtain a normal circadian rhythm?

A

Tasimelteon (melatonin agonist, same as ramelteon)

-> patients with a non-24 hour sleep-wake disorder

90
Q

What tricyclic is used for treatment of insomnia and why?

A

Doxepin - strongly anti-H1 effects at low doses

91
Q

What are the two somatic diagnoses when the patient is consciously producing symptoms (lying)?

A
  1. Factitious disorder - patient wants to play the sick role
  2. Malingering - patient wants to get something (i.e. drugs, time off work)
92
Q

What are the four somatic diagnoses when the patient will unconsciously produce their symptoms?

A
  1. Somatic symptom - preoccupation with symptoms.

Predominant pain is a subtype with long history of medical / surgical care, comorbid OUD and MDD

  1. Illness anxiety - preoccupation with disease, somatic symptoms are often absent.
  2. Conversion - symptoms appear neurologic and may be motor or sensory. La belle indifference -> doesn’t seem to care that they can’t feel or move a body part.
  3. Pseudocyesis - False belief of being pregnant which is nondelusional and actually associated with objective signs, including abdominal enlargement, reduced menstrual flow / amenorrhea, feeling fetal movement, nausea, breast engorgement / secretions, and labor pains at expected delivery date
93
Q

How do you explain a somatic symptom disorder to a patient?

A

Explain symptoms are not caused by a serious disease, refrain from confrontation

94
Q

Are patients with Factitious disorder willing to be treated? How will you know they’re lying?

A

Yes -> they will undergo multiple procedures and tamper with test data.

Condition is most commonly seen in healthcare workers.

You will know they’re lying when their condition defies conventional understanding, not responding to usual treatment, and they can predict the course (they are making it up)

95
Q

How should factitious disorder be treated?

A

Remember that they are MENTALLY ILL

  • > do not confront, be empathetic
  • > refer to PCP as a gatekeeper
  • > avoid unnecessary tests and procedures (basically just ignore it)
  • > treat underlying mood / anxiety conditions
  • > monitor your countertransference
96
Q

What personality disorder is closely associated with malingering? How can you tell its probably this?

A

Antisocial personality disorder

-> most likely patient will not be compliant with diagnosis and treatment

97
Q

What two interventions have been shown to decrease suicide mortality? How can we find out if they are going to?

A
  1. Physician education in risk assessment
  2. Restriction of lethal means - i.e. less guns available

Ask them if they are considering it, and ask them if they have access to the means

98
Q

What family genes are thought to correlate to increased suicide risk?

A
  1. Tryptophan hydroxylase - serotonin production

2. Serotonin transporter

99
Q

What are the static risk factors for suicide? Include descriptions of these qualifiers.

A
  1. Gender - male - women attempt more, males complete more
  2. Age - Increasing age increases risk, but 45-64 is currently highest rate
  3. Personal or family history of suicide - genetic
  4. Previous events - trauma / abuse
  5. Race - being native american / white
  6. Marital status - being single
100
Q

What are some mental disorders which increase risk of suicide? Are most suicides tied to mental illness?

A

90% of suicides are
MDD
Schizophrenia with increased academic achievement -> will see how much they are going to lose
Substance use disorder
Anxiety disorder
Borderline and Antisocial Personality Disorders (aggressive, impulsive)

101
Q

What are some neurobiological markers associated with suicide?

A
  1. Decreased serotonin metabolites in CSF
  2. Inflammation in CSF / periphery
  3. Low cholesterol (how serotonin is transported across membranes)
  4. HPA axis dysfunction
102
Q

What therapies can be used for suicidality?

A

Repeated visits to PCP

Cognitive behavioral therapy
Especially: dialectical behavioral therapy -> reduce self-injurious behavior (used commonly in borderline PD)

103
Q

What are the three stages of violence?

A
  1. Anxiety / agitation
  2. Verbal threats -> with menacing posture / swearing / demanding specific threats
  3. Overt aggression -> hitting / physical damage to things / throwing things in the room
104
Q

When is involuntary commitment allowed? Give three reasons.

A
  1. Risk of intentionally or unintentionally harming oneself or others
  2. Made serious threats to harm others
  3. Unable to take care of basic physical needs (i.e. schizophrenic patient not wearing a coat in the winter)
105
Q

How can you treat mild and severe agitation?

A

Mild - benzos and antipsychotics
Severe - Physical restraints, high potency antipsychotic (Haloperidol - can use if patient is in danger of harming self or others)

106
Q

What biological treatments can be used for treatment of suicidality?

A
  1. Lithium
  2. Clozapine - Schizophrenia / Schizoaffective disorder
  3. ECT or ketamine - decreased suicidality acutely
  4. Antidepressants can be used, but beware of initial suicidality increases in younger people (black box warning)
107
Q

What physical illnesses are correlated with impairment of sexual functioning?

A

Erectile dysfunction - cardiovascular illness, diabetes mellitus, MS, spinal cord injury

Decreased libido - hypothyroidism

108
Q

Describe the effects on sexual functioning of the following drugs: alcohol, amphetamines, cocaine, ecstasy.

A

Alcohol - long term impotence / testicle atrophy in men, hypoactive sexual desire in women

Amphetamines - good in short-term, but inhibits in longterm

Cocaine - same as amphetamines, with impotence longterm

XTC - increased desire, but erectile failure

109
Q

What is Female orgasmic disorder?

A

Delay in, marked infrequency of, or absence of orgasm, and/or markedly reduced intensity of orgasmic sensations
-> based on clinical judgment, since there is so much variability in how much triggers organism

110
Q

How is paraphilic disorder distinguished from paraphilias in general? How long must they be present?

A

Disorder causes distress or impairment to individual or paraphilia which involves personal harm or risk of harm to others

Must be present at least 6 months, each disorder will cause intense sexual arousal in the given situation

-> frequently co-morbid with ASPD

111
Q

What are the courtship disorders? (A subset of anomalous activity preference)

A

Voyeuristic disorder - Peeping nonconsenting people, must be at least 18 yrs for diagnosis

Exhibitionistic disorder - Exposure of one’s genitals to an unsuspecting person

Frotteuristic disorder - touching or rubbing against nonconsenting person - basically sexual assault

112
Q

What are the algolagnic disorders? (A subset of anamalous activity preference)

A

They involve pain:

Sexual Masochism - humilitation or being beaten, bound, etc
Sexual Sadism - humilitating, beating, or binding another person

113
Q

What are the four phases of the sexual response cycle? What sex does this cycle typically describe and why?

A
  1. Desire (libido)
  2. Excitement (arousal)
  3. Orgasm
  4. Resolution

Typically males -> women can experience more than one orgasm per cycle

114
Q

What is Female Sexual Interest / Arousal Disorder?

A

Reduced interest, fantasies, lack of initiation / response to partner’s initiation, reduced excitement / pleasure in engaging in almost all or all encounters, reduced sensations.

  • > females cannot separate the two.
  • > men can have hypoactive sexual desire, or they can have delayed ejaculation / erectile disorder
115
Q

What are the anomalous target preference disorders?

A
  1. Pedophilic Disorder - >16 yo, at least 5 years older than child or children, generally 13 or younger, specify male, female, both, or incest only
  2. Fetishistic Disorder - Arousal from nonliving objects or a highly specific focus on non-genital parts (i.e. toe), not sex toys or clothes
  3. Transvestic Disorder - Sexual arousal from cross-dressing

Specify with fetishism (as well) or autogynephilia (man aroused by thinking he is a woman)

116
Q

What are the treatment mainstays for sexual dysfunctions and paraphilic disorders?

A

Primarily psychotherapy
Sex therapy and CBT for sexual dysfunctions

-> can also treat underlying mood, anxiety, or SUD

117
Q

What is the hormonal treatment of Female Sexual Interest/Arousal Disorder in postmenopausal women? What are the risks?

A

Testosterone increases libido + sexual functioning, especially postmenopausal

Risks:
Hirsutism, enlarged clitoris, deepening of voice

-> also used in Male Hypoactive Sexual Desire Disorder if Testosterone levels are low

118
Q

What drug treats female hypoactive sexual desire in premenopausal women?

A

Flibanserin - 5HT1A agonist

119
Q

What is the treatment for premature ejaculation?

A

Behavioral: Squeezing tip of penis or start/stop
Pharmacological: Serotonergic antidepressions like clomipramine and sertraline -> cause sexual dysfunction
Lidocaine - local anesthetic, but can interfere with woman

120
Q

What are the two processes of sleep which are being balanced? Which type of sleep is independent of this?

A

Process S - homeoStatic process
Process C - Circadian arousal process

REM sleep is independent of this - offsets process S for homeostatic dysregulation (increased variability in HR, BP, and respiratory rate)

121
Q

What is insomnia disorder / how long must it be present?

A

At least 3 nights a week for at least 3 months, sleep difficulty occurs despite adequate opportunity to sleep, which is not attributable to a substance or other medical condition

122
Q

Who is suvorexant contraindicated in?

A

Narcolepsy

123
Q

What is hypersomnolence disorder and what should it be differentiated from? How to treat?

A

Differentiated from fatigue. Basically, this is chronic fatigue which causes sleep, with a myriad of causes AND presentations.

  • Prolonged sleep duration
  • Persistent daytime drowsiness
  • daytime lapses into microsleep, with sleep attacks
  • > increases risk for MVAs

Treat with: Polysomnogram and Multiple Sleep Latency Test (MSLT), and treating the underlying cause (i.e. sleep apnea, mood disorder, circadian rhythm disorder, others).

124
Q

What are the criteria for diagnosing narcolepsy?

A

3x per week x3 months, recurrent episodes of irresistable need to sleep or napping occurring in the same day

Presence of cataplexy - few times per month

  • >
    1. Bilateral loss of muscle tone with maintained consciousness which is precipitated by laughing
  1. Jaw-opening episodes with tongue thrusting or global hypotonia (spontaneous grimaces without any emotional triggers)
125
Q

What are two important lab findings in Narcolepsy?**

A
  1. Hypocretin deficiency - orexin-1 is less than 110 pg/mL in CSF
  2. REM sleep latency in less than 15 minutes (normal is 90 min)
126
Q

What are the pharmacological treatments for narcolepsy?

A

Stimulants (methylphenidate, amphetamines) to control daytime sleepiness, anticataplexy drugs -> TCAs, sodium oxybate - also used in insomnia

127
Q

What are the biomarkers in the CSF for dementia?

A

Low CSF A-beta42 (aggregates do not cross BBB into CSF very well)

Elevated CSF tau (hyperphosphorylated tau accumulates)

128
Q

What are the major cognitive domains?

A
  1. Complex attention
  2. Executive function
  3. Learning and memory
  4. Language
  5. Perceptual-motor
  6. Social cognition

CELLPS

129
Q

What gene is a primary risk factor for Late Onset Alzheimer’s Disease and why?

A

ApoE4 - E4 variant causes ineffective removal of amyloid peptides, leading to amyloid plaque formation

130
Q

Give one type of dementia other than acute delirium which can cause prominent fluctuations in the level of consciousness or cognitive abilities.

What are the features of Lewy Body dementia?

A

Dementia with Lewy bodies

Decreased attention / fluctuating cognition
Visual hallucinations
Motor features of parkinsonism
Lewy bodies in cerebral cortex

131
Q

How does Alzheimer’s generally prevent differently than other dementias?

A

AD: Has a much slower (insidious) onset, with prominent early memory loss. Motor coordination / strength are generally preserved. Atrophy seen on MRI (especially medial temporal lobe = hippocampus).

Other dementias have a rapid or stepwise progression, generally occur younger than 65 years old, and affect focal CNS / motor systems far more than memory.

132
Q

What is pseudo-dementia / what causes it?

A

Memory complains which are misdiagnosed as dementia, but are actually due to depression
-> need to be sure to ask about sadness or anhedonia

-BEWARE: depressive symptoms can be a precursor to dementia

133
Q

What is the most common cause of Frontotemporal dementia and what are its symptoms?

A

Pick’s disease

aphasia, apathy, impulse control

Prominent behavior changes w/ disinhibition (loss of prefrontal cortex)

Language disturbances -> aphasia, from loss of Broca’s and Wernicke’s.

Neuroimaging shows focal atrophy, PET will show decreased perfusion before this occurs

134
Q

What is dementia now called in the DSM 5, and what are its diagnostic criteria?

A

Major Neurocognitive Disorder

Significant decline in 1+ cognitive domains, as assessed by clinical assessment. They interfere with daily life and do not occur exclusively in delirium or as a part of another psych disorder.

Dementia itself includes memory + 1+ cognitive domains

135
Q

What are the common side effects of all acetylcholinesterase inhibitors?

A

DUMBBELS

Diarrhea
Urination
Miosis
Bradycardia
Bronchorrhea
Emesis (vomiting)
Lacrimations
Salivation 
Sweating

Weight loss & abnormal dreams

136
Q

Which cholinesterase inhibitor is approved for the treatment of cognitive impairment in PD? Why else was it developed?

A

Only Rivastigmine - also developed to have less GI side effects via using transdermal patch

137
Q

What is BPSD and what are some common reversible precipitants?

A

Behavioral and Psychological Symptoms in Dementia -> acting out in dementia

  • > Environmental changes (being in a nursing home)
  • > Medication side effects or withdrawal
  • > Pain
138
Q

What drugs are first line for treatment of BPSD, and some second line options?

A

First line: SSRIs or SNRIs

Second line options: 
Anticonvulsants 
Beta blockers 
Buspirone 
Trazodone 
BENZOS 
Gabapentin
139
Q

What are the diagnostic criteria for delirium?

A

A. Disturbance in attention and awareness
B. Change in cognition (memory, orientation, language, visuo-spatial ability, perception)
C. Happens over a short period of time and tends to fluctuate in severity during the day

140
Q
  1. Hyperactive - hypervigilant, hyperactive, decreased sleep, appear manic and may have more overt psychosis (looks like PTSD / manic BPAD)
  2. Hypoactive - “quiet” - slowed, unaware, somnolent, withdrawn, may even look depressed
A
  1. Hyperactive - hypervigilant, hyperactive, decreased sleep, appear manic and may have more overt psychosis (looks like PTSD / manic BPAD)
  2. Hypoactive - “quiet” - slowed, unaware, somnolent, withdrawn, may even look depressed

Common to both: Distractibility / irritability, and hallucinations / paranoia

141
Q

How can medications induce delirium? What types of medications most often do?

A

Often intoxication or withdrawal from a drug can precipitate it

Most often polypharmacy, especially with benzodiazepines, anticholinergic burden, and opiates

142
Q

What are two neurotransmitters are involved in delirium?

A
  1. Acetylcholine - decreased (like Alzheimer’s)

2. Dopamine - increased (like Schizophrenia)

143
Q

How can delirium be prevented?

A
  1. Hydrate well
  2. Limit use of physical restraints - cause confusion
  3. Avoid indwelling catheters (cause the UTI / sepsis)
  4. Correct sleep deprivation
  5. Avoid problem drugs (opiates, benzos, anticholinergics)

Psychiatry (23 decks)

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