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ABPN 2022 > Psychiatry > Flashcards

Psychiatry Flashcards

1
Q

Major depressive disorder

A

DSM-5 criteria
Depressed mood &/or anhedonia PLUS ≥5 symptoms during the same two week period
-Sleep: Insomnia or hypersomnia
-Interest: Markedly diminished interest/pleasure in activities
-Guilt: Feeling worthless or excessive/inappropriate guilt
-Energy: Fatigue
-Concentration: Decreased concentration or indecisiveness
-Appetite: Significant weight loss/gain, or decreased/increased appetite
-Psychomotor: Psychomotor agitation or retardation
-Suicidal ideation: Recurrent thoughts of death or suicidal ideation
AND significant stress or impairment, substances and other medical & psychiatric conditions ruled out, no history of (hypo)manic episodes

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2
Q

Persistent depressive disorder (dysthymia)

A

DSM-5 criteria
Depressed mood for most of the day, more days than not, for at least two years PLUS ≥2 symptoms while depressed
- Sleep: Insomnia or hypersomnia
- Energy: Fatigue
- Concentration: Poor concentration or indecisiveness
- Appetite: Poor appetite or overeating
- Low self-esteem
- Feelings of hopelessness
AND substances and other medical & psychiatric conditions ruled out, no history of (hypo)manic episodes

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3
Q

Seasonal affective disorder SAD

A

MDD with seasonal pattern
Responsive to light therapy

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4
Q

Post-partum depression

A

MDD beginning during pregnancy or within four weeks following delivery
Distinct from “baby blues,” which is short-lasting (1-2 weeks), does not interfere with daily activities, and resolves without treatment

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5
Q

Melancholic depression

A

Marked anhedonia and lack of mood reactivity, insomnia (early morning awakening), worse in the mornings
Tx: Tricyclic antidepressants

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6
Q

Atypical depression

A

Hypersomnia, hyperphagia, leaden paralysis, interpersonal rejection sensitivity
Tx: MAOIs

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7
Q

Depression treatment

A

SSRIs: Citalopram, escitalopram, sertraline, paroxetine, fluoxetine, fluvoxamine
SNRIs: Venlafaxine, duloxetine
TCAs: Amitriptyline, nortriptyline, doxepin, amoxapine, desipramine, clomipramine, imipramine
MAOIs: Selegiline, phenelzine, tranylcypromine, isocarboxazid
DNRIs: Bupropion
SRI & 5-HT-2A antagonists: Trazodone
Alpha-2 receptor antagonists: Mirtazepine**
Electroconvulsive therapy**
Treat for ≥6 mo before tapering!

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8
Q

Serotonergic side effects

A

SSRIs: Citalopram, escitalopram, sertraline, paroxetine, fluoxetine, fluvoxamine
SNRIs: Venlafaxine, duloxetine

Transient side effects upon initiation

  • Jitteriness, anxiety
  • GI disturbance
  • Sleep disturbance

Long-term side effects

  • Sexual side effects: Dose dependent, does not decrease over time***
  • Weight gain
  • Bleeding risk: Especially upper GI bleeds
  • SIADH: Primarily in the elderly within 2 weeks of starting SSRI
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9
Q

Serotonin syndrome

A

Vitals: Fever, diaphoresis, autonomic instability
Behavior: Altered mental status, agitation
Exam: Tremors, hyperreflexia, inducible or spontaneous clonus, ocular clonus

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10
Q

Serotonin withdrawal

A

Flu-like symptoms, agitation, nausea, unsteadiness, dysphoria, electric shock sensation
Risk factors: Medication with shorter half-life, >2 months of treatment, no taper
Treat with fluoxetine

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11
Q

SSRI pearls

A

SSRIs: Citalopram, escitalopram, sertraline, paroxetine, fluoxetine, fluvoxamine

Citalopram, escitalopram
- Most pure SSRIs, least off-target side effects*
Sertraline
- Most GI side effects
Paroxetine
- Most sedation, weight gain, insomnia, and sexual side effects
- The only SSRI contraindicated in pregnancy
Fluoxetine
- Prominent insomnia, but least weight gain

The SSRIs include fluoxetine, fluvoxamine, sertraline, paroxetine, citalopram, and escitalopram. They inhibit reuptake of serotonin through inhibition of the serotonin transporter, leading to increased availability of serotonin at the postsynaptic membrane. The antidepressant and/or anxiolytic effect of SSRIs may not become apparent for several days to weeks because their mechanism of action involves pre- and postsynaptic receptor changes that are not immediate.

The SSRIs are metabolized by the hepatic cytochrome P450 system and have various drug–drug interactions, with the extent varying with each of the SSRIs. Citalopram and escitalopram have the least potential for drug–drug interactions.

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12
Q

SNRI pearls

A

SNRIs: Venlafaxine, duloxetine

Venlafaxine
- Mainly an SSRI, no NE effects until 150mg dose
- May increase BP (5%), usually mild
- Prominent discontinuation effects
Duloxetine**
- More robust evidence for neuropathic pain than depression
- FDA approved for diabetic neuropathy, fibromyalgia, and chronic musculoskeletal pain
- Rare incidence of fulminant hepatic failure

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13
Q

Tricyclic antidepressants

A

TCAs: Amitriptyline (3), nortriptyline (2), doxepin (3), amoxapine (2), desipramine (2), clomipramine (3), imipramine (3)

Mechanism
- Blocks 5-HT & NE re-uptake -> increases synaptic concentration of 5-HT & NE
- Also blocks muscarinic, alpha-1 adrenergic, and histamine-1 receptors: Most prominent in tertiary amines (3), secondary amines (2) have fever side effects, are less sedating, and are safer in overdose
Particularly useful for melancholic depression

The tricyclic antidepressants (TCAs) are among the oldest antidepressants and are still commonly used to treat depression. The TCAs with a tertiary amine side chain such as amitriptyline, doxepin, and imipramine inhibit reuptake of both serotonin and norepinephrine, whereas some such as clomipramine predominantly inhibit reuptake of serotonin. The TCAs do not directly inhibit reuptake of dopamine, though they may indirectly facilitate the effects of dopamine.

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14
Q

Tricyclic antidepressant side effects

A

TCAs: Amitriptyline, nortriptyline, doxepin, amoxapine, desipramine, clomipramine, imipramine

Anti-cholinergic: Blind as a bat (blurry vision), dry as a bone (dry mouth), full as a flask (urinary retention, constipation), mad as a hatter (confusion); slowed cardiac conduction (AV block, arrhythmias); lowers seizure threshold***
Anti-alpha-1 adrenergic: Orthostatic hypotension
Anti-histamine: Sedation, weight gain*
Serotonergic: Sexual dysfunction

Overdose
Can be lethal!
Cardiotoxicity: Slowed cardiac conduction (AV block, arrhythmias)
Neurotoxicity: Agitation, delirium, coma

Withdrawal
Irritability, dizziness, nausea, diaphoresis, insomnia

All TCAs have some activity at muscarinic, histaminergic, and α1-adrenergic receptors, though to varying degrees. Because of these effects at noncatecholaminergic receptors, they are used for various disorders not limited to depression and anxiety, including urinary retention and neuropathic pain.

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15
Q

MAOIs

A

MAOIs: Selegiline, phenelzine, tranylcypromine, isocarboxazid

Mechanism
Monoamine oxidase metabolizes monoamines (5-HT, NE, DA)
MAOIs irreversibly inhibit MAO-A & MAO-B: increases 5-HT, NE, DA
Also blocks alpha-1 adrenergic & histamine-1 receptors
Particularly useful for atypical depression

Side-effects
Anti-alpha-1 adrenergic: Orthostatic hypotension
Anti-histamine: Sedation, weight gain
Serotonergic: Sexual dysfunction, insomnia, myoclonus
Hepatotoxicity (rare)
Tyramine-induced hypertensive crisis: Tyramine is normally broken down in the GI tract by MAO-A. On MAOIs, it isn’t broken down, so more is absorbed into the bloodstream. Activates adrenergic pathways, precipitating catastrophic rise in BP. Must avoid high tyramine foods (wine, aged cheese, fava beans, liver).

Phenelzine and isocarboxazid are nonselective monoamine oxidase inhibitors (MAOIs) and are among the oldest antidepressants, rarely used in clinical practice today due to their side effect profile. Because nonselective MAOIs block metabolism of tyramine, found in certain foods such as cheese and wine, a lethal reaction resulting from hyperadrenergic state can occur with use of MAOIs, particularly when taken with other agents that increase serotonin.

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16
Q

Bupropion**

A

DNRI
Blocks NE & DA reuptake
Avoids anti-cholinergic, anti-alpha-1 adrenergic (orthostatic hypotension), anti-histaminergic (weight gain) and serotonergic (sexual dysfunction) side effects**
Decreases seizure threshold, contraindicated in eating disorders
Also used for smoking cessation**

It inhibits reuptake of norepinephrine and dopamine and increases presynaptic release of these neurotransmitters, without direct effects on the serotonin system.

Different from busprinone: Buspirone is an anxiolytic agent without sedative–hypnotic activity. Its mechanism of action involves partial agonism at serotonergic (5-HT1A) receptors. It also has some activity at dopaminergic D2 receptors.

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17
Q

Trazodone

A

SRI & 5-HT2A receptor antagonists
Mainly blocks reuptake of serotonin
Anti-alpha-1 adrenergic: Orthostatic hypotension, priapism
Anti-histaminergic: Sedation (helpful for insomnia)

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18
Q

Mirtazepine**

A

Alpha-2 receptor antagonists
Stimulates alpha-1 receptors, blocks alpha-2 receptors, and blocks 5-HT-2A receptors, overall increasing 5-HT & NE release
Anti-histaminergic: Sedation (helpful for insomnia), weight gain (helpful for stimulating appetite)**

Mirtazapine has complex pharmacology; it acts as an antagonist at presynaptic α2-receptors, increasing release of norepinephrine and serotonin, and also acts as an antagonist at 5-HT2 and 5-HT3 receptors. Its potent antagonism at histamine receptors accounts for its sedating effects.

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19
Q

Mania

A

DSM-5 criteria
Abnormally elevated, expansive, or irritable mood & persistently goal-directed behavior or energy, lasting at least one week PLUS ≥3-4 of the following symptoms
- Distractibility
- Impulsivity
- Grandiosity
- Flight of ideas or racing thoughts
- Activity: Increase in goal-directed activity or psychomotor agitation
- Sleep: Decreased need for sleep yet feels rested
- Talkative: More talkative than usual or pressure to keep talking
AND marked impairment or psychotic features, substances and other medical conditions ruled out

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20
Q

Bipolar disorder I vs II

A
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21
Q

Treatment of bipolar disorder

A
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22
Q

Mood stabilizer - S/Es and pregnancy

A
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23
Q

Lithium side-effects/toxicity

A

S/E’s
Most common: Polyuria & thirst, weight gain, tremor*
Neuro: Decreased cognition, tremor, incoordination
Cardiac: Decreases sinoatrial node conduction (avoid in sick sinus syndrome)
Renal: Polyuria (antagonistic effect on ADH)
GI: Nausea, vomiting, anorexia, dyspepsia, diarrhea
Endo: Weight gain, hypothyroidism
Skin: Hair loss, acne, psoriasis
Heme: Benign leukocytosis

Toxicity
Narrow therapeutic index
Not metabolized; excreted in urine
Levels can become toxic due to:
- Renal insufficiency
- Dehydration (fever, excessive sweating, GI illness)**
- Decreased sodium intake (lithium reabsorption in proximal tubule)**
- Drug-drug interactions: NSAIDs, thiazide diuretics, ACE inhibitors
Acute toxicity
- Nausea, vomiting, diarrhea -> dehydration & compromised renal function
- Confusion, tremor, seizures (including nonconvulsive status)
- Arrhythmia (rare)

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24
Q

Causes of secondary mania

A

Neurological
- Stroke (right prefrontal),* subdural hematoma, tumor, multiple sclerosis, Huntington’s disease, dementia, seizures
Medical
- Hypothyroidism, hyperthyroidism, carcinoid syndrome, sleep apnea, delirium
Substance-induced
- Dopamine agonists, anabolic and corticosteroids, sympathomimetics (PCP, amphetamines, pseudoephedrine)

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25
Q

Catatonia

A

Inability to move normally with decreased reactivity to environment
- Akinetic mutism, catalepsy (waxy flexibility), echolalia, echopraxia, utilization behavior
May occur in the context of many psychiatric & medical disorders
- Most commonly bipolar disorder or psychotic depression
Treat with benzodiazepines or ECT
Avoid using dopamine blocking drugs

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26
Q

Generalized anxiety disorder

A

Excessive worrying for ≥6 months
Associated somatic symptoms: Headache, muscle tension, GI upset

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27
Q

Panic disorder

A

Recurrent panic attacks associated with one of the following: Worrying about consequences of attack, concern about additional attacks, change in behavior**
Treatment: Exposure therapy, CBT

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28
Q

Anxiolytics - list

A

SSRIs
Benzodiazepines
Buspirone
Clonidine
Antihistamines (hydroxyzine)
Anticonvulsants (gabapentin)
Beta blockers (propranolol)
Atypical antipsychotics (quetiapine, risperidone)

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29
Q

Benzodiazepines

A

Mechanism: Enhances GABA activity
Uses: PRN for situational anxiety, helpful for reducing initial SSRI-induced activation and acting as a bridge until anxiolytic onset

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30
Q

Buspirone

A

Mechanism: Partial agonist of 5-HT-1A receptors, indirect effect on DA
Benefits: Non-sedating, no potential for dependence
Drawbacks: No immediate effect on anxiety (not useful for panic disorder)
Uses: GAD, adjunctive use in MDD

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31
Q

Clonidine

A

Mechanism: Alpha 2 adrenergic agonist, feduces firing at the locus coeruleus**

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32
Q

Hydroxyzine

A

Mechanism: Primarily anti-histaminergic
Uses: GAD

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33
Q

Positive and negative symptoms

A

Positive symptoms
- Hallucinations
- Delusions
- Disorganized speech & behavior
Negative symptoms
- Flat affect
- Lack of speech
- Inability to initiate goal-directed activities

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34
Q

Primary vs secondary psychosis

A

Primary psychosis (diagnosis of exclusion)
- Schizophrenia spectrum
- Other psychiatric illnesses: Schizoaffective, MDD with psychotic features, bipolar mania, normal grief reaction with auditory hallucinations*
Secondary psychosis
- Infectious: Acute HIV, cerebral malaria, toxoplasmosis, neurocysticercosis, sleeping sickness
- Neoplastic: Anterior temporal lobe mass**
- Degenerative: Lewy body dementia
- Autoimmune: NMDAR encephalitis, Hashimoto encephalitis, SLE
- Toxins/meds: Steroids, antibiotics, toluene
- Endocrine/metabolic: Thyroid disease, B12, porphyria, Wilson’s, Tay-Sachs

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35
Q

Schizophrenia spectrum

A

Schizophrenia spectrum
- ≥2 psychotic symptoms (at least 1 must be positive), present for a significant portion of the time and disrupting normal functioning
Duration
- <1 month: brief psychotic disorder
- 1-6 months: schizophreniform disorder
- >6 months: schizophrenia: strong heritability, suicide in 10-15%

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36
Q

Schizoaffective disorder

A

Schizophrenia + MDD or bipolar mania
Psychotic symptoms in the absence of mood symptoms for ≥2 weeks

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37
Q

MDD with psychotic features

A

Psychotic symptoms only during depressive episodes

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38
Q

Bipolar mania

A

Psychotic symptoms only during manic episode

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39
Q

Delusional disorder

A

1+ non-bizarre delusions for ≥1 month
Apart from impact of delusions, daily functioning and behavior are not affected

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40
Q

Normal grief reactions

A

Can include auditory hallucinations

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41
Q

Capgras delusion

A

Belief that a loved one has been replaced by an identical imposter, usually with malevolent intent; frequently seen in neurodegenerative diseases, and occasionally in schizophrenia***

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42
Q

Fregoli delusion

A

Opposite of Capgras; sense of familiarity with strangers, but cannot recognize them because they are in disguise**

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43
Q

Metamorphosis

A

Belief that people in the environment swap identities with each other while maintaining the same appearance

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44
Q

Mirror sign

A

Belief that one’s reflection in the mirror is some other person

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45
Q

Subjective doubles:

A

Belief that there is a double of the patient carrying out independent actions*

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46
Q

Reduplicative paramnesia

A

Belief that a place or location has been duplicated, existing in 2+ places simultaneously; can occur with R frontal, temporal, or parietal lesions*

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47
Q

Cotard delusion

A

Patient believes that he is dead

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48
Q

Anti-D2 in different pathways+other side-effects

A

Anti-D2 in different pathways
Mesolimbic pathway* -> therapeutic efficacy against positive symptoms
Mesocortical pathway* -> worsens negative & cognitive symptoms
Nigrostriatal pathway -> extrapyramidal symptoms
Tuberoinfundibular pathway -> hyperprolactinemia (F amenorrhea, M gynecomastia & impotence)

OTHER
Anti-cholinergic: Blind as a bat (blurry vision), dry as a bone (dry mouth), full as a flask (urinary retention, constipation), mad as a hatter (confusion); tachycardia; lowers seizure threshold
Anti-alpha-1 adrenergic: Orthostatic hypotension
Anti-histamine-1: Sedation, weight gain
QT prolongation**

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49
Q

Typical vs atypical antipsychotics

A

Typical: greater anti-dopaminergic>other side effects
Atypical: fewer anti-dopaminergic side effects, compared to other side effects

Why? Atypical antipsychotics blocks serotonin, which blocks mesocortical, nigrostriatal, and tuberoinfundibulum pathways, so there are fewer anti-dopaminergic side-effects

EPS: extrapyramidal symptoms

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50
Q

Antipsychotics in Parkinson’s disease

A

Parkinson’s disease

1) Initial step in treating new onset psychosis is to adjust dopaminergic meds
2) Pimavanserin**: 1st line on RITE: Inverse agonist & antagonist of 5-HT-2A, avoids EPS but very expensive
3) Clozapine: 2nd line on RITE: Avoids EPS but requires intensive monitoring due to risk of agranulocytosis
4) Quetiapine: 3rd line on RITE: Relative avoidance of EPS, often used first line in reality

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51
Q

Antipsychotics in dementia

A

Increased mortality risk in those started on an antipsychotic

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52
Q

Dementia with Lewy bodies

A

Rivastigmine**
Cholinesterase inhibitors treat hallucinations & behavioral disturbances, and improve cognition

Pimavanserin is only FDA-approved antipsychotic for treatment in LBD (specifically for PD psychosis) (RITE 2021)

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53
Q

Antipsychotic: EPS

A

2/2 antidopaminergic effects in nigrostriatal pathway

Acute dystonia

  • Oculogyric crisis, torticollis
  • Develops within hours
  • Tx: Benztropine (anti-muscarinic), diphenhydramine,** hydroxyzine (anti-histamine)

Akathisia

  • Feeling of restlessness, inability to sit still
  • Develops within days
  • Tx: Benzodiazepines, propranolol

Parkinsonism

  • Develops within weeks to months
  • Tx: Benztropine (anti-muscarinic), amantadine (dopaminergic), propranolol
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54
Q

Tardive dyskinesia

A

Involuntary choreoathetoid movements; often permanent and can be debilitating
Develops within months to years
Tx: Stop offending agent, consider switching to clozapine; can try benztropine (anti-muscarinic)

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55
Q

Neuroleptic malignant syndrome

A

Life-threatening condition of hyperpyrexia, autonomic instability, muscle rigidity, and delirium
Dose-dependent
Typically develops within 2 weeks of medication onset, but may develop at any time
Tx: Dantrolene (muscle relaxant), bromocriptine (dopamine agonist),** amantadine (dopaminergic)

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56
Q

Conversion disorder:

A

1+ neurological symptoms of altered voluntary motor or sensory function**

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57
Q

Somatic symptom disorder

A

Excessive thoughts, feelings, or behaviors related to 1+ somatic symptoms**
…with predominant pain: Previously pain disorder

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58
Q

Body dysmorphic disorder

A

Preoccupation with 1+ perceived flaws in physical appearance

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59
Q

Illness anxiety disorder

A

Preoccupation with having or acquiring a serious illness, mild or no somatic symptoms

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60
Q

Factitious disorder and malingering

A

Intentional falsification of physical or psychological signs or symptoms, or intentional induction of injury or disease
For primary gain (to play the sick role) = factitious disorder**
For secondary gain (money, shelter, meds, etc.) = malingering***

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61
Q

ADHD

A

Persistent pattern of inattention &/or hyperactivity-impulsivity that interferes with functioning or development
Symptoms started before age 12 & present in 2+ settings
Treatment: Stimulants (1st line), atomoxetine (2nd line, NRI), bupropion (DNRI) or TCA (3rd line)**

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62
Q

Tourette syndrome

A

2+ motor tics & 1+ vocal tic, not necessarily at the same time
Tics started before age 18 & present for at least one year
Often co-morbid with ADHD, OCD, &/or mood disorders***
Treatment: Comprehensive behavioral intervention for tics (CBIT) / habit reversal training (HRT), antidopaminergic meds (tetrabenazine, fluphenazine, risperidone)**

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63
Q

OCD

A

Obsessive thoughts/impulses +/- compulsive behaviors to reduce distress
Patient usually aware that obsessions/compulsions are unreasonable
Often co-morbid with Tourette’s***
Treatment: SSRIs (1st line; fluoxetine, fluvoxamine), TCAs (clomipramine)**

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64
Q

PTSD

A

Three clusters of symptoms: Re-experiencing (flashbacks, distressing dreams), avoidance, hyperarousal**
- If these occur for <1 month, diagnosis is acute stress reaction
Treatment: Prazosin for nightmares (alpha-1 blocker),** propranolol or clonidine for hyperarousal symptoms

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65
Q

Dissociative identity disorder**

A

Amnestic episodes associated with the presence of distinct identities or personality states**
Often the result of severe emotional trauma and abuse in childhood

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66
Q

Behavioral manifestations of systemic disease

A
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67
Q

Cluster A personality disorder

A
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68
Q

Cluster B personality

A
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69
Q

Cluster C personality disorder

A
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70
Q

Transferance

A

Thoughts, feelings, emotions and behaviors of a patient towards the therapist that are based on issues specific to the patient’s life and past relationships

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71
Q

Countertransference

A

The therapist’s responses (thoughts, feelings, emotions, and behaviors) towards a patient that express the therapist’s personal background issues more that they express an appropriate response to the patient

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72
Q

Adaptive behaviors level defense mechanisms

A

– Anticipation, Affiliation, altruism, humor, self-assertion, self-observation,
– Sublimation: transfer of emotion to healthy activity- e.g. sports for aggression)
– Suppression: consciously choosing to expel thoughts/feelings from awareness

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73
Q

Mental inhibition level defense mechanisms

A

– Dissociation: breakdown in usual integrated fxns of consciousness, memory, sense of self/environment, or sensory/motor behavior
– Intellectualization: excessive use of abstract thinking or the making of generalizations to control or minimize disturbing feelings
– Isolation of affect: separations of ideas/cognition elements from the feelings associated with them
– Displacement: attributing feelings about one object to (less powerful) other
– Reaction formation: warding off thought by espousing opposite thought
– Repression: unconscious expulsion of unacceptable wishes/feelings from awareness
– Undoing: behaviors designed to symbolically negate unacceptable feelings/thoughts

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74
Q

Minor Image Distorting Level (regulates self-esteem) defense mechanisms

A

– Devaluation: attributes exaggerated negative qualities to others
– Idealization: attributes exaggerated positive qualities to others
– Omnipotence: ascribing special powers to the self/superiority to self

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75
Q

Disavowal Level (keeps unwanted impulses/thoughts/feelings out of awareness) defense mechanism

A

– Denial: refusing the acknowledge external realities or subjective experiences
– Rationalization: dealing with issues through self-assuring, but incorrect, explanations
– Projection: falsely attributing one’s own unacceptable thoughts/feelings to another

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76
Q

Major Image Distorting Level (gross distortion of image of self/others) defense mechanism

A

– Autistic fantasy: excessive daydreaming as a substitute for actual relationships or effective problem-solving
– Projective Identification: starts as projection, then the person attributes their own feelings as a justifiable response to the projected feelings. Often, this induces the projected feelings in the recipient
– Splitting: positive and negative qualities of self or others are not integrated

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77
Q

Action level defense mechanism

A

– Acting out: using actions to express internal emotional conflict
– Apathetic withdrawal: lack of participation as a way to avoid internal conflicts
– Help-rejecting complaining: requesting help for problems then rejecting all advice/help
– Passive Aggression: indirectly expressing anger

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78
Q

Defensive Dysregulation Level (failure of defense mechanisms leads to break with objective reality) defense mechanism

A

– Delusional projection
– Psychotic denial
– Psychotic distortion

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79
Q

Prevalence vs incidence

A

Prevalence: proportion of individuals in a population who have a disease at a specific instant in time (i.e. estimate of probability)
- Period prevalence
- Lifetime prevalence
Incidence: number of new events or cases of a disease that develop in a population of at-risk individuals in a specified time interval
- Cumulative incidence
- Incidence rate

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80
Q

Uncomplicated alcohol withdrawal

A

Majority of Pts with alcohol WD
Symptoms start within 6 hours after last drink
Increase BP (>140/100), pulse>90, T>101 F, nausea, sweat, insomnia, anxiety, brisk reflexes, and fine tremor
If withdrawal does not progress, usually resolves in 24 hours

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81
Q

Alcohol withdrawal seizure

A
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82
Q

Alcohol hallucinosis

A
83
Q

Complicated alcohol withdrawal, DTs

A
84
Q

Risk factors for DTs

A
85
Q

Management of alcohol withdrawal with CIWA

A
86
Q

Management of DTs

A
87
Q

Wernicke’s Korsakoff syndrome

A
88
Q

Fetal alcohol spectrum disorder

A
89
Q

Treatment of alcoholism

A
90
Q

Disulfram

A
91
Q

Naltrexone

A
92
Q

Acamproste

A
93
Q

Psychosocial and self-help for alcohol use disorders

A
94
Q

Nicotine addiction - epidemiology

A

Kills > 430,000 people annually (1/3 of all cancers)
Pediatric disease- typically starts at 12 years old
85% of alcoholics smoke
Self-imposed abstinence = 4% at 1 year

95
Q

Treatment of nicotine dependence

A

Nicotine Replacement Therapies (NRT) Varenicline and Bupropion generally safe in pts
with psychiatric illness, cardiovascular disease
NRT plus behavioral support is best National Toll Free Hotline 1-800-QUITNOW

96
Q

Pharmacology of cocaine

A

Cocaine Hydrochloride: Powder, IV, or intranasal - Snorting peak in blood 30 minutes, Half-life 60 minutes, reload in 45 minutes

Freebase cocaine: No cocaine ion, smoked, DIY: boil hydrochloride in water and baking soda, Crack retail: $3-5/vial, vial last 5-20 minutes

Metabolism of cocaine: Plasma and liver cholinesterase’s to benzyl ecgonine, usually lasts in urine drug screen 3 days, longest 7-10 days from body stores

97
Q

Cocaine pharmacology

A
98
Q

Cocaine pharmacology

A

CNS stimulant - blocks presynaptic catecholamines: DA, NE and serotonin and blocks DA receptors

Euphoria/reinforcement via mesolimbic pathway (dopamine) in ventral tegmentum, which projects to reward cells in the hippocampus

99
Q

Adverse neurological/psychiatric effects of cocaine

A
  1. Cocaine+EtOH=cocaethylene: sudden deaths
  2. Seizures 3.5% of users, usually single, generalized
  3. MI
  4. AKI, over failure
  5. If laced with levamisole →agranulocytosis, cutaneous vasculitis; levamisole is a veterinary antihelminth
100
Q

Maternal/fetal effects of cocaine

A

Mother: 1) premature birth, rupture of membrane 2) placental separation 3) miscarriage, infant stroke

Infant: 1) Decreased attention, alertness, IQ, motor skills from birth to 2 years of age 2) Results are at low end of normal tests, well-controlled

101
Q

Cocaine withdrawal

A

DSM-IV withdrawal: fatigue, unpleasant dreams, increased appetite, sleep disturbance, psychomotor retarding or agitation

102
Q

Cocaine treatment

A
103
Q

Treating benzodiazepine withdrawal

A
104
Q

Opiate withdrawal

A

Acute withdrawal 8-12 hours after last use, peaks at 3 days, usually last 5 days

Mydriasis, sweats, bone pain, diarrhea, yawing, rhinorrhea, lacrimation, goose-flesh

Activates NE in locus ceruleus (autonomic hyperactivity) thus, tx with clonidine (alpha agonist)

Activates serotonin and DA (craving)

105
Q

Treatment of opiate use disorder

A

Methadone taper or clonidine symptom supression

  1. Relapse prevention: Naltrexone - ineffective for most street addicts, effective for professionals - MDs, lawyers, pilots, etc.
  2. Medication assisted therapy: Methadone, Suboxone (buprenorphine, naloxone)
106
Q

Methadone

A

x

107
Q

Buprenorphine (subutex)

A
  1. High potency, partial Mu opiate receptor agonist
  2. Competes with other opioids and blocks their effects
  3. Slow dissociation from mu opioid receptor and a prolonged therapeutic effect for MAT
108
Q

Suboxone

A

Combined buprenorphine plus naloxone

Oral SL tablet, dissolvable film (SL and buccal)

Addition of naloxone to buprenorphine to decrease diversion (selling of drug)

Buprenorphine equally effective as moderate doses of methadone (e.g., 60 mg per day)

8 hr certification necessary for license

109
Q

Marijuana

A
110
Q

MDMA (Molly)

A
111
Q

MDMA medical harm

A
112
Q

PCP

A
113
Q

PCP side-effects

A
114
Q

Salvia Divinorum

A
115
Q

Spice/K2

A
116
Q

Bath salts

A
117
Q

Gamma hydroxybutyrate

A
118
Q

Toulene

A
119
Q

Toulene and neuroimaging

A
120
Q

General predictors of success in addiction treatment

A
121
Q

Major depressive episode vs disorder

A

A diagnosis of major depressive disorder is made after the occurrence of at least two major depressive episodes that occurred at least 2 months apart.

122
Q

Major depression epidemiology

A

Depression is the most common mood disorder. Depression carries with it significant morbidity, and is a common cause of disability. It is approximately twice as common in females as compared to males across all age groups. Its incidence peaks in the third and fourth decades of life, but it can occur at any age. It is more common among lower socioeconomic populations and in those living in urban as compared to rural areas.

There are no differences in the occurrence of depression among different races if social class, education, and area of residence are controlled for.

123
Q

Genes associated with mood disorders

A

Patients with specific polymorphisms of a serotonin transporter have an increased chance of developing a mood disorder following negative life events.

Other genes include the genes that encode for dopamine transporters, the gene for brain-derived neurotrophic factor, and the cyclic-AMP response element-binding protein gene.

While genetic factors explain approximately 50% to 70% of the etiology of mood disorders, environmental factors also play a large role. For example, traumatic childhood events predispose to mood disorders later in life.

124
Q

Functional imaging in depression

A

The dorsolateral prefrontal cortex has been shown to be hypometabolic in patients with depression, whereas the orbitofrontal cortex is hypermetabolic, and pharmacologic therapies have been shown to reverse these changes.

The subcallosal cingulate gyrus is metabolically overactive in depression.

125
Q

Depression and HPA

A

Patients with depression have elevated levels of corticotropin- releasing hormone and other abnormalities of the HPA axis.

126
Q

Panic attacks vs disorder, agoraphobia

A

Panic attacks are discrete episodes of symptoms that include a sense of intense fear, associated with other physical and/or psychiatric symptoms. Physical symptoms seen in panic attacks include palpitations or chest discomfort, diaphoresis, trembling, dyspnea, feeling of choking, nausea or abdominal pain, paresthesias, chills or hot flashes, and dizziness. Psychiatric symptoms include derealization (a feeling of unreality) or depersonalization (a feeling of being detached from oneself), fear of losing control, and fear of dying. Other types of panic attacks are cued, being situationally bound: occurring in relation to a specific internal or external trigger. P

Panic disorder is diagnosed when recurrent panic attacks occur. Panic disorder may occur in isolation or may be associated with agoraphobia.

Agoraphobia is characterized by a fear of being in places or situations where escape would be difficult or embarrassing, or in which help would be difficult to obtain, as depicted in question 8. Agoraphobia may occur in isolation as well. The course of panic disorder is typically variable, with periods of exacerbations and remissions. Improvement occurs with age.

127
Q

Separation anxiety disorder

A

Separation anxiety disorder is an anxiety disorder of childhood characterized by excessive and inappropriate fear of being away from home or from familiar figures such as parents or siblings. It usually presents around 6 months of age and declines by ages 2 to 3 years, but may persist and/or recur during ages 6 to 12 years.

128
Q

Dissociative amnesia

A

dissociative amnesia. Dissociative amnesia is one of the dissociative disorders and is characterized by extreme amnesia, far out of what would be considered normal forgetfulness. There is typically a loss of personal experiences. The information forgotten usually relates to a stressful event. Some patients regain memory of the event, whereas others remain chronically amnestic for it.

129
Q

Depersonalization

A

Depersonalization disorder is another dissociative disorder in which there are intermittent or constant feelings of detachment from oneself as if a person is viewing him- or herself as an outside observer.

130
Q

Dissociative identity disorder

A

In dissociative identity disorder (commonly known as “multiple personality disorder”), a person exists in two or more distinct identities or states, with these identities each unaware of the other and with each separately taking control of the person’s behavior over different time periods.

131
Q

Dissociative fugue

A

Patients with dissociative fugue suddenly and unexpectedly travel away from their environment and are then unable to recall their past or their identity, and may assume a partial or completely new identity.

132
Q

BBB

A

Serum concentrations of a medication do not necessarily reflect brain concentrations.

This is in large part related to the blood– brain barrier (BBB) and blood–CSF barrier, which are selectively permeable barriers to diffusion or transport of substances from the bloodstream into the CNS.

  • The BBB is formed from continuous _tight junctions (not gap junctions) between brain capillary endothelial cell_s and also results from unique characteristics of pericapillary glial cells.
  • The blood–CSF barrier is formed from tight junctions between epithelial cells in the choroid plexus.
  • When intact, the BBB limits diffusion of most macromolecules and allows selective permeation of some small charged molecules (including neurotransmitter precursors and metabolites, and some drugs) through specific transport systems.
  • Nonionized molecules and lipophilic (lipid-soluble) drugs have higher penetration into the CNS.
  • Transport systems may also allow penetration of drugs into the CNS. The BBB also contains transport systems that allow efflux of substances out of the CNS.
  • Metabolites of neurotransmitters are cleared through an acid transport system in the choroid plexus. The BBB does not exist in the peripheral nervous system, and is absent or less prominent in the circumventricular organs: the median eminence, area postrema, pineal gland, subfornical organ, and subcommissural organ. The BBB is disrupted by ischemia and inflammation, or can be intentionally disrupted with drugs such as mannitol, allowing access of substances that would not normally penetrate into the brain.
133
Q

Brief psychotic disorder vs schiophreniform disorder and schizophrenia

A

The main distinguishing feature between brief psychotic disorder (discussed in question 62) schizophreniform disorder, and schizophrenia (discussed in questions 24 and 25) is symptom duration, being up to 1 month in brief psychotic disorder, more than 1 month but less than 6 months in schizophreniform disorder, and 6 or more months in schizophrenia. Patients with these three disorders are typically managed similarly once the appropriate diagnostic workup has been completed (as discussed in question 45).

Of patients with schizophreniform disorder, two-thirds eventually meet diagnostic criteria for schizophrenia and one-third recover within 6 months of symptom onset. Predictors of good prognosis include occurrence of psychotic symptoms within 4 weeks of change in behavior or functioning, presence of prominent positive symptoms, disorganization of thought, confusion, and good premorbid function.

134
Q

OCD vs obsessive compulsive personality

A

Obsessive-compulsive disorder (OCD) is one of the anxiety disorders, and the main features of it are obsessions and compulsions that are time consuming and affecting function. Obsessions are persistent ideas, thoughts, or impulses that provoke significant anxiety and distress. Compulsions are repetitive physical or mental acts that are meant to counteract the distress caused by an obsession. Adult patients with OCD recognize that their obsessions or compulsions are unreasonable or excessive.

OCD typically begins in adolescence or early adulthood, but can begin in childhood. It is equally common in males and females, though males have an earlier age of onset. Other psychiatric conditions that are frequently comorbid with OCD include depression, attention-deficit hyperactivity disorder, and eating disorders. Approximately 50% of patients with Tourette’s syndrome also suffer from OCD. Deep brain stimulation of the ventral portion of the anterior limb of the internal capsule for the treatment of OCD is being studied with promising results.

Although obsessive-compulsive disorder may coexist with obsessive-compulsive personality disorder, distinct and definable obsessions and compulsions are absent in the latter, distinguishing the two.

135
Q

PTSD

A

Posttraumatic stress disorder (PTSD) is an anxiety disorder characterized by the occurrence of specific symptoms after experiencing a traumatic event involving threat of death or injury to oneself or others, resulting in intense fear or horror. These symptoms include reexperiencing the traumatic event (such as through nightmares or flashbacks), avoiding any stimuli associated with the event, and experiencing symptoms of autonomic arousal (such as increased startle reflex, insomnia, hypervigilance, and irritability). A diagnosis of PTSD is made only after symptoms have been occurring for more than 1 month; within a 1-month period of symptom onset, a diagnosis of acute stress reaction is made. The majority of patients with PTSD develop complete remission; however, up to a fourth of patients develop a chronic disorder.

136
Q

Somatic symptom disorder

A

As with the patient in question 20, somatic symptom disorder (previously known as somatization disorder) is characterized by the occurrence of multiple recurrent symptoms, affecting various systems, and cannot be fully explained by physical factors. In some cases, pain is the predominant symptom. Patients fixate on symptoms, and devote considerable thought, time, and energy to them, recurrently seeking medical attention, often resulting in excessive nondiagnostic testing and unnecessary medical treatments. Age of onset is typically prior to age 30.

137
Q

Conversion disorder

A

As with the patient depicted in question 21, conversion disorder is characterized by acute loss of motor or sensory function that cannot be explained by a neurologic or other medical condition. The symptoms often resemble neurologic syndromes, such as hemiparesis, cerebellar ataxia, or seizures. Nonneurologic symptoms such as blindness, deafness, or false pregnancy (pseudocyesis) also occur. Conversion disorder is also classified as a dissociative disorder in some texts.

137
Q

Illness anxiety disorder

A

In illness anxiety disorder (which encompasses a disorder previously known as hypochondriasis), there is chronic and pervasive preoccupation with physical symptoms and fear of having a serious disease, often resulting from misinterpretation of physical symptoms, even after diagnostic testing and exclusion of the condition of concern or any other identifiable medical condition.

138
Q

Body dysmorphic disorder

A

As with the patient in question 22, patients with body dysmorphic disorder experience a chronic and intense preoccupation with a perceived defect of appearance or over- concern with minor physical abnormalities. Such patients often seek unnecessary and repeated surgical procedures to correct their perceived deformity.

139
Q

Monoamine hypothesis disorder of depression

A

Postulates that deficiencies or dysfunctions in the monoamines serotonin, dopamine, and norepinephrine are implicated in the pathogenesis of depression. Although there is evidence to support this hypothesis, this is yet to be unequivocally proven, and some studies have not found alterations in monoamines in depressed patients. Evidence to support the monoamine hypothesis includes the induction of depression by reserpine, which depletes monoamines, increased risk for depression in carriers of specific serotonin transporter promoter gene polymorphisms, and response of depression to medications that increase levels of monoamines.

140
Q

Neutrophic hypothesis of depression

A

However, another theory of depression pathogenesis, the neurotrophic hypothesis, holds that depression results from loss of neurotrophic support by nerve growth factors such as brain-derived growth factor.

141
Q

Schizophrenia - epidemiology

A

Schizophrenia affects 1% of the world’s population. It is more prevalent in lower socioeconomic populations, but the relationship between schizophrenia and socioeconomic status is complex. Low socioeconomic status is likely an effect rather than a cause of schizophrenia, relating to the “downward drift” effect, in which during the prodromal phase of schizophrenia an individual drifts down into a lower socioeconomic class. Schizophrenia is equally common in males and females, though males typically have a younger age of onset. Schizophrenia typically manifests in adolescence and early adulthood, though late-onset forms, with symptom onset after the age of 45, have also been described. Premorbidly (prior to the onset of positive symptoms), 25% of patients have abnormalities in social or cognitive function, with some features of schizoid personality disorder (discussed in question 41–43). Both positive and negative symptoms may occur simultaneously. Positive symptoms predominate in the earlier stages of the illness and may diminish overtime; positive symptoms are more responsive to typical antipsychotics compared to negative symptoms.

142
Q

Treatment of depression in older adults

A

The tricyclic antidepressants (TCAs), as discussed in question 50, have various side effects including cardiac conduction abnormalities and drug–drug interactions that make them undesirable for the treatment of depression in older adults. A selective serotonin reuptake inhibitor is more favorable than a TCA in this patient. Fluvoxamine has a high risk for drug–drug interactions, whereas escitalopram does not. Fluvoxamine also has high protein binding, and can therefore interact with anticoagulant medications, such a warfarin. Therefore, of the medications listed, escitalopram is the most appropriate in this patient. In older adults, psychotropic medications should be started at a low dose and titrated up slowly to the lowest effective dose.

143
Q

Conduct disorder

A

Conduct disorder, which is characterized by a chronic and pervasive violation of rules (including deceit, theft, and destruction of property), of others’ rights (including physical aggression to people or animals), and age-appropriate societal norms. Individuals with this disorder show little empathy or remorse. Conduct disorder is more common in males. Risk factors for conduct disorder include psychopathology in parents, dysfunctional family environment and poor parenting practices, exposure to physical, sexual, or emotional abuse or neglect, and exposure to violence. A diagnosis of antisocial personality disorder (discussed in questions 64–67), cannot be given to those younger than 18 years of age; some individuals with conduct disorder go on to meet criteria for antisocial personality disorder in adulthood, whereas in others, the conduct disorder remits and they are able to achieve adequate social and occupational adjustment. Management of conduct disorder centers primarily around institution of early multimodal psychosocial interventions to prevent conduct disorder when there are early signs of aggression or deviance in a child.

144
Q

Oppositional defiant disorder

A

Question 28 depicts oppositional defiant disorder. This is marked by a dysfunctional pattern of hostile and defiant behavior that cannot be explained by a mood or psychotic disorder. Oppositional defiant disorder most frequently emerges between ages 6 and 8, and is more common in males and those of lower socioeconomic status and in urban dwellers.

145
Q

Sertonin metabolism

A

Serotonin, or 5-hydroxytryptamine (5-HT), is synthesized from tryptophan (not tyramine) in a two-step process.

The first step is catalyzed by tryptophan hydroxylase, which converts the essential amino acid tryptophan into an intermediate that is subsequently converted into serotonin by action of the enzyme aromatic L-amino acid decarboxylase.

Serotonin is metabolized by action of monoamine oxidase (MAO) into 5-hydroxyindoleacetaldehyde, which by action of aldehyde dehydrogenase is transformed to 5- hydroxyindoleacetic acid. MAO-A is the predominant isoform in the metabolism of serotonin. MAO-B, along with MAO-A, metabolizes dopamine and tryptamine; low-dose selegiline is a selective inhibitor of MAO-B.

146
Q

Serotonin receptors

A

There are at least seven classes and 14 subtypes of 5-HT receptors. The 5-HT1, 5-HT2, and 5-HT4 subtypes are coupled to G- proteins (which either inhibit or activate adenylyl cyclase, depending on the subtype). The 5-HT3 receptor is a ligand-gated ion channel.

147
Q

Raphe nucleus

A

In the CNS, the principle site of serotonergic neuronal cell bodies is in the raphe nuclei of the brainstem, with diffuse projections to the brain and spinal cord. Serotonin has various actions both in the CNS and systemically.

148
Q

Serotonin effects

A

In the CNS, serotonin has a role to play in the sleep-wake cycle; serotonin deficiency leads to insomnia, and tryptophan (a serotonin precursor) promotes sleep. Serotonin has also been implicated in violent behavior; low CSF levels of the serotonin metabolite 5-hydroxyindole acetic acid (5-HIAA) have been associated with aggressiveness and violent impulsivity. Serotonin deficiency has also been implicated in both anxiety and depression. Regarding the nonpsychotropic effects of serotonin, the 5-HT1B receptors elicit vasoconstriction and the 5-HT1D receptors inhibit neuronal transmission and trigeminal neurogenic inflammatory peptide release. Triptan medications such as sumatriptan are agonists at these latter receptors. Action of serotonin at 5-HT2A receptors leads to platelet aggregation. Serotonin acts at 5-HT3 in the area postrema and the antiemetic ondansetron is an antagonist at this receptor. Serotonin is released by enterochromaffin cells in the intestines where it increases intestinal motility. It also induces bronchoconstriction, and patients with malignant carcinoid syndrome, in which there is excessive production of serotonin, manifest many of the symptoms of a hyperserotonergic state, including wheezing and diarrhea.

149
Q

Type of delusion

A

His delusional disorder can therefore be classified as the erotomanic type. Other types of delusional disorder include the following:

  • Grandiose type, in which there are delusions of inflated worth, power, knowledge, or identity.
  • Jealous type, in which there are delusions that an individual’s significant other is unfaithful. -Persecutory type, in which the delusion is one of being persecuted by someone.
  • Somatic type, delusions of having a physical defect or medical problem of some sort.

The absence of psychotic features such as hallucinations, bizarre delusions, changes in affect, and changes in function distinguish delusional disorder from other psychotic disorders such as brief psychotic episode (discussed in question 62) and schizophrenia (discussed in questions 24 and 25). Schizoaffective disorder is discussed in question 69 and atypical depression in question 3.

150
Q

Suicide

A

It is a more common cause of death in males, though females attempt suicide more often than males.

The rate of suicide increases with increasing age among Caucasians; in African Americans beyond the fourth decade, the rate of suicide decreases.

Caucasians have a higher rate of suicide as compared to African Americans. Native Americans have the highest rate of suicide among all races/ethnicities in the United States.

Approximately 60% to 70% of patients who have committed suicide were suffering from a mood disorder; patients with schizophrenia are also at an increased risk of suicide.

Substance abuse and panic disorder are frequent comorbidities in patients who commit suicide. Among patients with personality disorders, those with borderline personality disorder (discussed in question 64–67) are most likely to attempt suicide.

151
Q

Serotonin metabolism

A

Serotonin, or 5-hydroxytryptamine (5-HT), is synthesized from tryptophan (not tyramine) in a two-step process. The first step is catalyzed by tryptophan hydroxylase, which converts the essential amino acid tryptophan into an intermediate that is subsequently converted into serotonin by action of the enzyme aromatic L-amino acid decarboxylase. Serotonin is metabolized by action of monoamine oxidase (MAO) into 5-hydroxyindoleacetaldehyde, which by action of aldehyde dehydrogenase is transformed to 5- hydroxyindoleacetic acid. MAO-A is the predominant isoform in the metabolism of serotonin. MAO-B, along with MAO-A, metabolizes dopamine and tryptamine; low-dose selegiline is a selective inhibitor of MAO-B.

152
Q

Serotonin receptors

A

There are at least seven classes and 14 subtypes of 5-HT receptors. The 5-HT1, 5-HT2, and 5-HT4 subtypes are coupled to G- proteins (which either inhibit or activate adenylyl cyclase, depending on the subtype). The 5-HT3 receptor is a ligand-gated ion channel.

153
Q

Raphe nuclei

A

In the CNS, the principle site of serotonergic neuronal cell bodies is in the raphe nuclei of the brainstem, with diffuse projections to the brain and spinal cord. Serotonin has various actions both in the CNS and systemically.

154
Q

Serotonin effets

A

In the CNS, serotonin has a role to play in the sleep-wake cycle; serotonin deficiency leads to insomnia, and tryptophan (a serotonin precursor) promotes sleep.

Serotonin has also been implicated in violent behavior; low CSF levels of the serotonin metabolite 5-hydroxyindole acetic acid (5-HIAA) have been associated with aggressiveness and violent impulsivity.

Serotonin deficiency has also been implicated in both anxiety and depression.

Regarding the nonpsychotropic effects of serotonin, the 5-HT1B receptors elicit vasoconstriction and the 5-HT1D receptors inhibit neuronal transmission and trigeminal neurogenic inflammatory peptide release. Triptan medications such as sumatriptan are agonists at these latter receptors.

Action of serotonin at 5-HT2A receptors leads to platelet aggregation.

Serotonin acts at 5-HT3 in the area postrema and the antiemetic ondansetron is an antagonist at this receptor.

Serotonin is released by enterochromaffin cells in the intestines where it increases intestinal motility. It also induces bronchoconstriction, and patients with malignant carcinoid syndrome, in which there is excessive production of serotonin, manifest many of the symptoms of a hyperserotonergic state, including wheezing and diarrhea.

155
Q

Dopamine pathways

A

Dopaminergic pathways include the mesolimbic and mesocortical pathways (which project from the midbrain to the limbic system and neocortex), nigrostriatal pathway (which consists of neurons projecting from the substantia nigra to the dorsal striatum, including the caudate and putamen), and tuberoinfundibular system (which arises from the hypothalamus and projects to the pituitary; dopamine released by these neurons inhibits prolactin release from the pituitary). It is the limbic and cortical–subcortical pathways (mesolimbic and mesocortical pathways) that are thought to be overactive in psychosis, rather than the nigrostriatal and tuberoinfundibular pathways.

156
Q

Dopamine receptors

A

There are five dopamine receptors identified, D1 to D5. It is mainly the D2 receptor that is implicated in the dopamine hypothesis of schizophrenia. Support for the dopamine hypothesis comes from evidence that there is increased dopamine receptor density in the brains of schizophrenics postmortem and increased D2 receptor occupancy in the brains of schizophrenics on functional imaging. Improvement of psychosis with D2 antagonism and worsening of psychosis with dopaminergic agonists such as levodopa, amphetamines, and dopamine agonists further lend support to this theory.

However, the dopamine hypothesis only partially explains the many features of schizophrenia and other psychotic disorders. For example, reduced dopaminergic activity in specific cortical areas including the medial temporal lobe and dorsolateral prefrontal cortex as well as the hippocampus is thought to underlie the negative symptoms of schizophrenia.

The serotonin hypothesis of schizophrenia postulates a role for excessive serotonergic activity, particularly at serotonergic 5-HT2A receptors, in the pathogenesis of hallucinations and other symptoms of psychosis. The occurrence of hallucinations with exposure to lysergic acid diethylamide (discussed in Chapter 17), a serotonin agonist, lends support to this theory, as does the efficacy of atypical antipsychotics, which have serotonergic antagonism in addition to antidopaminergic activity.

Underactivity of glutamate pathways, which normally excite inhibitory GABA pathways, has also been implicated in the pathogenesis of schizophrenia and other psychotic disorders, as evidenced by the ability of phencyclidine and ketamine (noncompetitive NMDA receptor antagonists, discussed in Chapter 17) to exacerbate cognitive dysfunction and psychosis in patients with schizophrenia.

157
Q

Intermittent explosive disorder

A

This patient’s history is consistent with intermittent explosive disorder (IED), an impulse control disorder characterized by several episodes of verbal or physical aggression that is out of proportion to an instigating event. In between episodes, patients may express remorse or regret for their actions. IED typically starts in adolescence or early adulthood and is more common in men. Treatment of IED includes psychotherapy, as well as pharmacotherapy with mood stabilizers, antipsychotics, or selective serotonin reuptake inhibitors.

158
Q

Impulse control disorders

A

Kleptomania is an impulse control disorder and is defined as recurrent impulses to steal objects because of a sense of pleasure or gratification from the act of stealing, with the object being of little personal use or value. Kleptomania typically begins in adolescence, and is more common in women.

Other impulse control disorders include trichotillomania (recurrent pulling of one’s hair resulting in hair loss and a sense of pleasure or gratification), pyromania (deliberate setting of fires, a fascination with fire, and pleasure or gratification when setting fires or observing their aftermath), and pathologic gambling.

159
Q

Anorexia nervosa

A

A disorder characterized by restricted energy intake relative to the requirements and resulting in a significantly low body weight. In an individual with anorexia nervosa there is disturbed perception of one’s body weight/shape, an intense fear of gaining weight, and an impaired self-perception of weight (such as denial of the seriousness of low body weight). Anorexia nervosa is of two types: The first is a restricting type, which occurs in approximately 50% of patients, in which there is self-induced starvation and often compulsive exercising without binge eating or purging behaviors. The second type is a binge eating/purging type, in which the patient regularly engages in binge eating followed by purging. Anorexia nervosa is treated at least initially in the inpatient setting to allow for medical stabilization and initiation of nutrition under close supervision. Later, outpatient therapy revolves mainly around psychotherapy, with pharmacologic management of comorbid mood or anxiety disorders.

160
Q

Bulimia

A

In bulimia nervosa, depicted in question 38, patients binge and subsequently partake in compensatory behaviors to prevent weight gain such as excessive exercise, induction of emesis or misuse of laxatives, diuretics, or other medications. In contrast to anorexia nervosa, patients with bulimia nervosa typically maintain a normal body weight. In patients with bulimia nervosa, self-assessment is unduly influenced by body weight and shape. Treatment of bulimia nervosa involves psychotherapy combined in some cases with selective serotonin reuptake inhibitors.

161
Q

Binge eating

A

In binge eating disorder, binge eating occurs over discrete periods. During episodes of binge eating, there is a sense of lack of control, embarrassment (by how much one is eating), and/or guilt. Bulimia nervosa is distinguished from binge eating disorder in that

in the latter, inappropriate compensatory behaviors do not occur. In patients with eating disorder not otherwise specified, patients may avoid food, binge with or without purging or participating excessively in exercise, and partake in other methods of minimizing weight loss, but the patient’s weight is maintained within the normal range. Menstruation remains regular. The binge eating form of eating disorder not otherwise specified is the most common eating disorder, followed by bulimia and anorexia

162
Q

Epidemiology of eating disorders

A

Peak onset of eating disorders is in the teenage years, though they may begin at any age. Eating disorders are more common in females than in males, with a 3:1 ratio, though males are likely underdiagnosed. The pathophysiology relates to be both environmental and genetic factors; there is a 50% to 80% concordance rate among monozygotic twins. Comorbid mood, anxiety, and personality disorders are common among patients with eating disorders.

163
Q

Specific learning disability.

A

This is marked by difficulties learning and acquiring academic skills out of proportion to any developmental, mental, or neurologic disorders and despite interventions to target those difficulties. Domains affected include reading, writing, or math skills. Individuals affected with learning disability perform below what would be expected for the individual’s chronologic age.

In individuals with specific learning disability, capabilities in other domains are typically average or may be above average, though the various learning disabilities frequently co-occur.

164
Q

Mental retardation

A

Mental retardation is defined by significantly subaverage general intellectual functioning, in more than one domain, as assessed by standardized tests. Mild mental retardation is defined by an intelligence quotient (IQ) of 55 to 70, moderate mental retardation by an IQ of 35 to 55, severe mental retardation by an IQ of 20 to 35, and profound mental retardation by an IQ of less than 20. R

165
Q

Receptive aphasia

A

Receptive aphasia is marked by inability to understand language in its written or spoken form.

166
Q

Acquired dyslexia

A

Acquired dyslexia is a loss of language skills that were previously acquired, as may occur in patients with traumatic brain injury.

167
Q

Caveat to personality disorders

A

The caveat to the diagnosis of personality disorders is that the features do not occur in the context of signs or symptoms that are part of a mood, anxiety, impulse control, or psychotic disorder, or any other psychiatric disorder as the primary underlying illness. Personality traits are patterns of behavior or thinking about oneself and the environment that are relatively consistent over time, but they do not lead to a diagnosis of personality disorder unless they are maladaptive or cause functional impairment or distress. The personality disorders are categorized into clusters A, B, and C. Different personality disorders may co-occur in the same individual.

Patients with personality disorders lack insight into their pathology, but may be asked to seek care from a psychiatrist by family members or others in the setting of dysfunction in relationships, occupation, or otherwise.

168
Q

A shared psychotic disorder, or folie à deux,

A

A type of disorder in which a psychotic belief develops in an individual that is similar to that held by a close relation.

169
Q

Typical antipsychotics - high vs low potency

A

The typical antipsychotics, first brought into clinical use in the 1950s, include chlorpromazine and thioridazine, which have low potency at D2 (dopamine) receptors and higher antagonism at muscarinic, adrenergic, and histaminergic receptors. They are therefore more likely to cause side effects related to antagonism at these receptors, such as dry mouth, orthostasis, and sedation, respectively.

Those with higher potency at D2 receptors, such as haloperidol and fluphenazine, have activity at muscarinic, adrenergic, and histaminergic receptors as well and can lead to similar side effects, but are less likely to do so. On the other hand, they are more likely to lead to extrapyramidal side effects (EPS), which result from D2- antagonism in the nigrostriatal pathway.

The EPS can be divided into acute reactions such as acute dystonia, which are in general reversible with treatment with antimuscarinic agents such as benztropine, and tardive dyskinesia (such as the orolingual dyskinesias depicted in question 55, or tardive cervical dystonia), which are in general irreversible but may be treatable with botulinum toxin or deep brain stimulation to the globus pallidus interna.

170
Q

Functional and anatomical imaging in schizophrenia

A

Whole-brain and CSF volume studies in patients with schizophrenia have shown reduced brain volumes and higher CSF volumes compared to normal controls. There is evidence of ventricular enlargement, particularly of the third and lateral ventricles, with sulcal widening.

There is atrophy of areas of the frontal and temporal lobes, as well as the hippocampus and thalamus.

PET studies have shown hypometabolism of the dorsolateral prefrontal cortex during activation tasks. PET studies have not shown resting regional cerebral blood flow abnormalities in patients with schizophrenia compared to controls.

*Similar to depression

171
Q

Hyponatremia with SSRIs

A

Hyponatremia is an established side effect of therapy with selective serotonin reuptake inhibitors (SSRIs). Risk factors include older age, female sex, and concomitant use of diuretics. Hyponatremia resulting from SSRIs typically occurs within the first month of therapy, but may not occur until several months after initiation of therapy. Among the SSRIs, fluoxetine and paroxetine are more likely to lead to hyponatremia.

The pathophysiology of SSRI- induced hyponatremia is thought to be at least in part related to the syndrome of inappropriate antidiuretic hormone, resulting from excessive release of antidiuretic hormone mediated by activation of serotonergic receptors. Although there are no definitive data to support routine monitoring of serum sodium in patients started on an SSRI, any change in mentation or other symptoms potentially suggesting hyponatremia should prompt a laboratory evaluation for this complication. In isovolemic hyponatremia due to SSRIs, the treatment is discontinuation of the SSRI along with fluid restriction. In more severe symptomatic hyponatremia, treatment with intravenous sodium chloride may be indicated. Rechallenge with SSRIs may not necessarily lead to recurrent hyponatremia, though it can.

172
Q

Serotonin syndrome

A

Results from overstimulation of brainstem serotonin receptors.

Symptoms include encephalopathy, autonomic hyperactivity manifesting as hypertension, tachycardia, and diaphoresis, as well as myoclonus, hyperreflexia, and tremor. Serotonin syndrome can occur with any agent that increases serotonin, and has even been reported with monotherapy, but is more likely to occur with a combination of therapies that increaseserotonin, and particularly with concomitant use of nonselective monoamine oxidase inhibitors. Treatment generally includes supportive care and withdrawal of the offending agent.

173
Q

Serotonin withdrawal

A

Serotonin withdrawal syndrome can occur with abrupt discontinuation of serotonergic medications such as selective serotonin reuptake inhibitors. Symptoms include dizziness, paresthesias, dysphoria, and in some cases encephalopathy. Therefore, gradual tapering of such medications is generally recommended.

174
Q

Inhibitory neurotransmitter

A

GABA is an inhibitory transmitter in the CNS. Glycine is also an inhibitory amino acid neurotransmitter and plays a prominent role in the brain and spinal cord.

GABA is synthesized from glutamic acid by action of the enzyme glutamic acid decarboxylase. Disorders of this enzyme lead to a deficiency in GABA and subsequently overactivation in the CNS, as is seen in stiff person syndrome.

The GABAA receptor is an example of an ionotropic receptor, activation of which leads to opening of chloride channels. The GABAB receptor is an example of a metabotropic receptor, which is coupled to an inhibitory G- protein, inhibiting adenylyl cyclase.

Baclofen is an example of a selective aclofen is an example of a selective GABAB receptor agonist; benzodiazepines act at GABAA receptors.

175
Q

SNRIs

A

Duloxetine and venlafaxine are serotonin–norepinephrine reuptake inhibitors (SNRIs): They inhibit reuptake of both serotonin and norepinephrine by inhibiting serotonin and norepinephrine transporters, respectively. The SNRIs and tricyclic antidepressants (TCAs), because they increase both norepinephrine and serotonin, are useful in the treatment of pain disorders. Unlike the TCAs, the SNRIs are relatively selective and have little activity at muscarinic, histaminergic, and α-adrenergic receptors.

176
Q

Trazodone and nefazodone

A

Act primarily by antagonism at the 5- HT2 receptor; trazodone was initially used as an antidepressant, but its primary use today is as a hypnotic (sedative) because it is highly sedating and little tolerance develops to its sedating effect over time. An adverse effect that may occur with trazodone therapy is priapism or prolonged painful erection.

177
Q

Schizoaffective disorder vs depression

A

Schizoaffective disorder is distinguished from depression (discussed in questions 1 and 2) or mania (discussed in questions 10 and 11) with psychotic features in that in schizoaffective disorder, there must be at least a 2-week period during which psychotic symptoms are present without prominent symptoms of a mood disorder.

178
Q

Treatment of BPSD

A

Atypical antipsychotic agents (discussed in questions 72–74) can be efficacious in the treatment of behavioral and psychotic symptoms of dementia (BPSD), which include agitation and hallucinations. In this patient population, they carry significant risks, including increased mortality and increased risk of both arterial (stroke) and venous thrombosis and thromboembolic events. Despite these risks, in some patients, when BPSD pose a significant risk to the patient and his or her caregivers, as depicted in this case, their use may be indicated. Nonpharmacologic measures and medications besides atypical antipsychotic agents should be tried when feasible, though data regarding use of the latter in the treatment of BPSD is not robust. When necessary, atypical antipsychotic agents should be started at the lowest possible dose, and need for them should be reassessed regularly.

179
Q

Trial of antidepressants

A

The treatment of major depressive episode includes both pharmacologic therapy and nonpharmacologic therapy, the latter mainly including psychotherapy. Electroconvulsive therapy (discussed in question 80) can be effective after 8 to 12 sessions, but is often reserved for medication-resistant depression because of cognitive side effects.

180
Q

Atypical antipsychotics

A

The second generation of antipsychotics, so-called atypical antipsychotics, includes clozapine, olanzapine, quetiapine, risperidone, ziprasidone, and aripiprazole. These agents do have antagonistic activity at D2 (dopamine) receptors, however, their clinical antipsychotic effect results in large part from antagonism at serotonergic 5-HT2A receptors.

Studies to date have not shown overall superior efficacy of the atypical antipsychotics over the typical ones, though atypical antipsychotics may be more effective at treating some of the negative symptoms of schizophrenia. Because they have less antagonism at D2 receptors, they are less likely to cause extrapyramidal side effects (EPS), but certainly can.

181
Q

Antipsychotic side-effects to know

A

As a class, the atypical antipsychotics carry with them an increased risk of weight gain, diabetes, and dyslipidemia. Patients being treated with these medications should therefore periodically be assessed for such side effects. Clozapine and olanzapine are most likely to lead to weight gain. Ziprasidone and aripiprazole are less likely to cause weight gain than the others.

Some of the typical and atypical antipsychotics including thioridazine, haloperidol, ziprasidone, and quetiapine have negative ionotropic action on the heart and a quinidine-like effect, leading to QT prolongation with the potential for arrhythmias. Aripiprazole is least likely to do so.

Other cardiac side effects include myocarditis, which can rarely be seen with clozapine.

The atypical antipsychotics also have activity at muscarinic, adrenergic, and histaminergic receptors, and several side effects result from activity at these sites.

Clozapine can lead to agranulocytosis in 1% to 2% of patients, and patients being treated with this medication are required to have periodic complete blood counts checked. Clozapine also leads to a dose-dependent increased risk of seizures. Clozapine is least likely of all the atypical antipsychotics to lead to EPS. Because of the side effect profile of clozapine, its use is usually limited to treatment of patients who have failed trials of other typical and atypical antipsychotics.

Among the atypical antipsychotics, olanzapine has the highest antimuscarinic activity, and side effects resulting from this include dry mouth, urinary retention, confusion, and constipation. Clozapine also has significant antimuscarinic activity. Quetiapine has significant antihistaminergic activity, and along with olanzapine, is the most likely to lead to sedation.

182
Q

Treatment of overdose

A

Flumazenil is an antagonist of benzodiazepines and other sedative– hypnotic agents such as zolpidem and eszopiclone (the latter two agents are used in the treatment of insomnia). Flumazenil does not however antagonize the action of barbiturates.

Naloxone and naltrexone are used in the treatment of opioid overdose. Thiamine and dextrose are used in the treatment of thiamine deficiency and hypoglycemia as is seen in alcoholics or other chronic states of malnourishment .

183
Q

Glutamate neurotoxicity

A

Glutamate and aspartate are excitatory neurotransmitters. The glutamate receptors are divided into NMDA receptors, those at which NMDA acts as an agonist, and non-NMDA receptors, which include AMPA and kainic acid receptors, named according to the substances that act as agonists at these receptors. Specific patterns of activation of NMDA receptors can lead to induction of long-term. potentiation, which is a prolonged increase in a postsynaptic response resulting from a finite presynaptic stimulus and is thought to be involved in memory formation. High concentrations of glutamate lead to neuronal cell death triggered by excessive glutamate receptor activation, with excessive calcium influx into cells. Glutamate excitotoxicity has been implicated in neuronal damage seen in ischemia and hypoglycemia.

Memantine is an NMDA antagonist used in the treatment of dementia.

184
Q

Psychiatri medic

A

Both bupropion (discussed in question 68) and clozapine (discussed in questions 72–74) have been associated with increased risk of seizure at higher dosages.

Olanzapine (discussed in questions 72– 74) is less likely to cause seizures, but can do so; other atypical antipsychotics rarely cause seizures.

Amitriptyline, which is a tricyclic antidepressant (discussed in question 39) is also associated with increased seizure risk with acute toxicity.

Flumazenil, by inducing a state of benzodiazepine withdrawal, can lead to increased risk of seizures, particularly in patients with a prior history of seizures.

185
Q

ECT

A

Electroconvulsive therapy can be a highly effective therapy for depression. It is most commonly used for major depression refractory to medications but is also used acutely in depression (without a prior drug trial) when necessary. Suicide is not a contraindication for ECT. Other indications for ECT include schizoaffective disorders, schizophrenia, and mania (particularly in bipolar patients with a mixed episode [of both mania and depression] or rapidly cycling bipolar disorder). In ECT, an electric current is applied to the scalp in an anesthetized patient, with the goal of inducing a nonconvulsive seizure. The mechanism of action of the antidepressant effects of ECT is not well understood. Sideffects include retrograde amnesia, which can be partially irreversible.

186
Q

TMS

A

In TMS, a rapidly changing magnetic field is applied to the scalp and is thought to affect the superficial layers of the cerebral cortex, locally inducing small electric currents. Single-pulse TMS is generally considered safe but seizures are nevertheless a potential risk, even in individuals without a prior history of epilepsy. Application of TMS to the left dorsolateral prefrontal cortex improves symptoms in major depression.

187
Q

VNS

A

n VNS, intermittent electrical stimulation is directly applied via an electrode to the left cervical vagus nerve. The current is provided by a pulse generator, a pacemaker-sized device that is implanted in the chest and is connected to the electrode. Stimulation of the afferent vagus nerve fibers leads to changes in several brainstem nuclei that are involved in the pathophysiology of depression, such as the nucleus of the tractus solitarius and raphe nuclei, leading to alterations in serotonergic activity in cortical and limbic structures. VNS is used as adjunctive therapy for chronic or recurrent depression in individuals with either unipolar depression or bipolar disorder.

188
Q

Duration of symptoms distinguishing schizophrenia, scizophreniform disorder, and brief psychotic disorder

A

Brief psychotic disorders ≤1 month, schizophreniform 1-6 months, schizophrenia≥ 6 months

189
Q

Secondary gain in factious disorder imposed of self

A

Assumption of role of patient

190
Q

Secondary gain in malingering

A

External incentive such as money

191
Q

Duration of symptoms distinguishing acute from PTSD

A

Acute stress reaction ≤ 1 month, PTSD≥ 1 month

192
Q

Pathological stealing

A

Kleptomania

193
Q

Pathological impulse to start fires

A

Pyromania

194
Q

Cluster A personality disorder

A

Paranoid: paranoid, distrustful

Schizoid: loner, unsociable

Schizotypal: weird, odd, eccentric

195
Q

Cluster B personality disorders

A

Narcissistic: conceited, grandiose

Antisocial: cruel, reckless, unremorseful

Borderline: unstable relationships, self-injurious behavior, splitting

Histrionic: dramatic, emotional, attention=seeking

196
Q

Cluster C personality disorder

A

Avoidant: hypersensitivity to criticism, feelings of inadequacy

Dependent: clingy, submissive

Obsessive-compulsive: perfectionist, too organized but not necessarily productive, rigid

197
Q

Antidepressants→convulsions, coma, cardiac arrhthymias (three Cs) in toxicity

A

TCAs

198
Q

Antidepressants that lead to hyponataremia

A

SSRIs

199
Q

Antipsychotic that cures agranulocytosis

A

Clozapine

200
Q

MOA of haloperidol and other typical antipsychotics

A

Antagonism at D2 (dopamine) receptors

201
Q

MOA of risperidone and other atypical antipsychotics

A

Antagonists at 5-HT2A receptors (main effect) and D2 receptors

202
Q

Mood-stabilizing agents that lead to thyroid dysfunction, tremor, and nephrogenic DI with hypernataremia

A

Lithium

203
Q

Benzodiazepine antagonists

A

Flumazenil

ABPN 2022 (26 decks)

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