Psychiatry Flashcards

1
Q

Serotonin is synthesized from _______ and metabolized by ________.

A

Serotonin is synthesized from tryptophan and metabolized by monoamine oxidase (MAO).

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2
Q

What is the principal site of serotonergic neuronal cell bodies?

A

Raphe nuclei in the brainstem

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3
Q

What receptor does ondansetron affect?

A

Ondansetron is a 5HT3 serotonin antagonist (primarily affects the area postrema).

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4
Q

What receptors do triptans act on?

A

5HTD1 serotonin receptors to inhibit neuronal transmission and trigeminal neurogenic inflammatory peptide release

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5
Q

Where do dopaminergic neurons originate?

A

The ventral tegmental area and substantia nigra

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6
Q

What is the major inhibitory neurotransmitter in the brain? How is it synthesized?

A

GABA is the major inhibitory neurotransmitter in the brain. It is synthesized from glutamic acid by glutamic acid decarboxylase (GAD). This is why GAD dysfunction results in overactivity of the CNS and clinical phenotypes like stiff person syndrome.

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7
Q

What is the difference between GABAa and GABAb receptors? Name one medication that acts on each type of receptor.

A

GABAa: ionotropic receptor - leads to activation of chloride channels

GABAb: metabotropic receptor - coupled to an inhibitory G protein, inhibiting adenylyl cyclase

Benzodiazepines are GABAa agonists. Baclofen is a GABAb agonist.

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8
Q

Which CNS receptors are activated by glutamate?

A

NMDA, AMPA, and kainic acid receptors

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9
Q

What is the mechanism of action of memantine?

A

NMDA antagonist used in the treatment of dementia

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10
Q

What is the role of glycine in the nervous system? Where does it primarily act?

A

Glycine is an inhibitory neurotransmitter located primarily in the spinal cord, brainstem, and retina. When glycine receptors are activated, chloride enters the neuron.

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11
Q

What are the diagnostic criteria for major depressive disorder?

A

At least 2 major depressive episodes at least 2 months apart. A major depressive episode is defined as symptoms of depressed mood for 2+ weeks in addition to 2 of several other domains, including sleep, appetite, cognition, energy level, hope.

MUST have significant functional impact for diagnosis.

Persistent depressive disorder is a more chronic form in which patients are depressed more days than not for 2 years (adults) or 1 year (children/ado).

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12
Q

What neurotransmitter is found in the locus ceruleus?

A

Norepinephrine

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13
Q

Name 5 classes of therapies for depression

A
  1. Antidepressant medications
  2. Therapy
  3. Electroconvulsive therapy (ECT)
  4. Transcranial magnetic stimulation
  5. Vagus nerve stimulation
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14
Q

What regions of the brain are affected in depression?

A

Dorsolateral prefrontal cortex is hypometabolic.

Orbitofrontal cortex is hypermetabolic.

Subcallosal cingulate gyrus is metabolically overactive in depression; connects the frontal and subcortical regions.

Hypothalamic-pituitary-adrenal axis is thought to be involved: patients with depression have elevated corticotropin-releasing hormone.

Can have hippocampal volume reductions.

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15
Q

Are depressive episodes required to diagnose bipolar disorders?

A

No. Bipolar I can be diagnosed after a single manic episode and Bipolar II can be diagnosed after a single hypomanic episode (hypomania is distinguished from mania by the fact that in hypomania the patient has insight and is not significantly functionally impaired).

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16
Q

What is a panic attack?

A

Discrete episode of symptoms including intense fear, palpitations, diaphoresis, trembling, sense of choking, nausea, and dizziness

WITH associated derealization (feeling of unreality), depersonalization (feeling of detachment from self), fearing of losing control and/or dying.

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17
Q

What is obsessive compulsive disorder? In what other disease is it a common comorbidity?

A

Obsessions and compulsions are time consuming and affect function.

Obsessions: persistent ideas, thoughts, or impulses that provoke significant anxiety and distress

Compulsions: repetitive physical or mental acts that are meant to counteract the distress caused by the obsession.

About 50% of people with Tourette syndrome have OCD.

18
Q

What distinguishes PTSD from acute stress reactions?

A

Duration. PTSD symptoms are >1 month, acute stress reactions <1 month.

19
Q

Name the four classes of medications that are FDA-approved for treatment of anxiety disorders

A

SSRIs

SNRIs

Azaspirodecanedione class ( = buspirone)

Benzodiazepines

20
Q

What are positive and negative symptoms in schizophrenia?

A

Positive symptoms: hallucinations, delusions, disorganized thought

Negative symptoms: blunting, alogia or empty speech, apathy, reduced communicativeness

21
Q

What is the difference between brief psychotic disorder, schizophreniform disorder, and schizophrenia?

A

TIME

brief psychotic disorder is < 1 month (commonly after significant stressor or post-partum)

schizophreniform disorder is 1-6 months (2/3 go on to have schizophrenia, 1/3 recover or have other diagnoses)

schizophrenia > 6 months (affects about 1% of the population)

22
Q

What features distinguish conduct disorder from intermittent explosive disorder?

A

Conduct disorder is highlighted by lack of empathy or remorse for actions such as chronic and pervasive violation of rules (theft and destruction of property), other’s rights (aggression to people/animals), and age-appropriate societal norms.

Intermittent explosive disorder can be characterized by similar behaviors and outburts, but the patient expresses remorse and regret between episodes.

23
Q

What is trichotillomania?

A

Recurrent pulling of one’s hair, leading to gratification

24
Q

Describe Cluster A personality disorders

A

“Odd or eccentric”

Paranoid

Schizoid (lack of interest in social relationships/intimacy, and lack of enjoyment of social interaction)

Schizotypal (magical or bizarre thinking, prefer social isolation)

25
Q

Describe Cluster B personality disorders

A

“Dramatic”

Antisocial (disrespect of the law, lacking remorse)

Narcissistic (grandiose, fearful of others seeing flaws, manipulative)

Borderline (unstable relationships, fear of abandonment, splitting)

Histrionic (attention seeking behaviors, particularly using physical attributes)

26
Q

Describe Cluster C personality disorders

A

“Fearful/anxious”

Avoidant (want friends but avoid relationships, hypersensitive to criticism)

Dependent (need to be taken care of, seek new relationships urgently if one ends)

Obsessive-compulsive personality disorder (rigid, inflexible, unproductive preoccupation with orderliness and perfection)

27
Q

Which drug is a benzodiazepine antagonist?

A

Flumazenil

28
Q

What are the most common side effects of SSRIs? Some rarer side effects? What is the black box warning?

A

Common: Nausea/vomiting, sexual dysfunction, irritability, sleep problems

Rare: Hyponatremia (typically older adults with diuretic use)

Black box: May increase the risk for suicidal thinking/behavior in adolescents

Common SSRIs are fluoxetine, paroxetine, citalopram, escitalopram, fluvoxamine, sertraline

29
Q

Describe serotonin syndrome.

A

Results from over-stimulation of brainstem serotonin receptors. Symptoms include encephalopathy, autonomic hyperactivity, myoclonus, hyperreflexia, and tremor.

(Myoclonus is not a feature of NMS so can be a helpful distinction.)

Common with concomitant use of SSRIs with MAOIs.

30
Q

Distinguish between factitious disorder, Munchausen’s sydrome, and malingering.

A

Factitious disorder: Signs/symptoms are intentionally feigned, internal movtivation to be the patient

Munchausen’s syndrome: Chronic, severe form of factitious disorder in which extensive, deceptive means are often employed in feigning physical symptoms

Malingering: Factitious symptoms, but secondary gain is an external incentive (ie money)

31
Q

What class of medications are duloxetine and venlafaxine? What are common side effects?

A

SNRIs, used for depression/anxiety as well as pain disorders. Side effects are similar to SSRIs, but tend to have relatively less sexual dysfunction. Can cause hypertension.

32
Q

Mechanism and uses of buspirone

A

Anxiolytic agent WITHOUT sedative-hypnotic

MoA: partial agonism at 5HT1a; some activity at dopaminergic D2

33
Q

Mechanism and uses of mirtazapine

A

Noradrenergic and specific serotonergic antidepressant

Mechanism: Antagonist at pre-synaptic alpha-2 receptors, increasing release of NE and 5HT. Antagonist at 5HT2 and 5 HT3 receptors. Potent antagonism at histamine receptors accounts for its sedating effects.

34
Q

Mechanism, uses, side effects of bupropion

A

Inhibits reuptake of NE and dopamine and increases presynaptic release of these NTs without direct effects on the serotonin system.

At high doses, it increases the risk of seizures.

Can be used for treatment of depression - decreased risk for sexual dysfunction than SSRIs.

35
Q

Mechanism, uses, side effects of trazodone

A

MoA: Antagonist at post-synaptic 5HT2 receptor. Also a potent alpha 1 antagonist.

Initially used as an antidepressant but is used today as sedative/sleep aid. Can INCREASE REM sleep time.

Adverse effect: priapism

Minimal side effect on libido.

36
Q

What are some of the side effects of stimulant medications for ADHD?

A

Usually dose dependent: Could worsen tics, Decreased appetite, Abdominal discomfort, Headache, Irritability / slight increase in risk of mood issues, Anxiousness, Sleep problems, Slight reduction in height velocity, Cardiac problems (conflicting evience), slight risk of HTN.

37
Q

What are the side effects of non-stimulant medications for ADHD?

A

Atomoxetine (Strattera): somnolence, GI upset, reduce appetite

Guanfacine (Tenex), Clonidine: sedation, hypotension, bradycardia

38
Q

What are self-psychotherapy options that you can provide families with?

A

Coping Cat - CBT workbooks for kids

Therapist Aid - Free CBT workbooks

Headspace - Mindfulness meditation app

Insight Timer - Mindfulness meditation app

39
Q

To which class of antidepressants does mirtazapine belong?

A

Mirtazapine is a tetracyclic (NOT tricyclic) antidepressant that acts by inhibition of presynaptic alpha-2-adrenergic receptors which causes 5HT1A activation and increased dopamine release.

40
Q

What are the two mechanisms of action of methadone?

A
  1. mu-receptor agonist
  2. NMDA-receptor antagonist