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Neurology > Mood Disorders: Depression and Bipolar > Flashcards

Mood Disorders: Depression and Bipolar Flashcards

1
Q

Reactive sadness

A

Transient emotional reaction to a minor event

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2
Q

Grief

A

Normal response to a major interpresonal loss, can be prolonged

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3
Q

Clinical Depression

A

Persistent sadness that interferes with normal functioning
* loss of interest
* Low-self esteem

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4
Q

What are the signs and symptoms of depression?

A
  • Persistent sad, anxious, or “empty” feelings
  • Feelings of hopelessness or pessimism
  • Feelings of guilt, worthlessness, or helplessness
  • Irritability, restlessness
  • Loss of interest in activities or hobbies once pleasurable
  • Fatigue and decreased energy
  • Difficulty concentrating, remembering details, and making decision
  • Insomnia, early-morning wakefulness, or excessive sleeping
  • Overeating, or appetite loss
  • Thoughts of suicide, suicide attempts
  • Aches or pains, headaches, cramps, or digestive problems that do not ease even with treatment
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5
Q

What are the risk factors for depression?

A
  • Female (particularly in adolescence, post-partum, and in older age)
  • Prior depressive episodes
  • Medical comorbidity
  • Substance use disorder
  • Lack of social support
  • Stress
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6
Q

What are the DSM-V criteria for depression?

A
  • Must have 5 or more symptoms in same 2 week period
  • Must include depressed mood and/or anhedonia
  • Must represent change from previous functioning
  • Cause social or occupational impairment
  • Not be due to an organic disorder or other cause
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7
Q

What is a manic episode?

A

Consists of a persistent elevated or irritable mood that is extreme, which lasts for at least one week
* And at least three (four if only irritable mood) other features are also involved:
- Inflated self-esteem for sleep
- Decreased need for sleep
- More talkative than usual or compelled to keep talking
- Experiencing racing thoughts or ideas
- Easily distracted
- Increase in goal-oriented activity or excessive movements
- Excessive involvement in potentially risky pleasurable behavior

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8
Q

Monoamine hypothesis

A

Decreased synaptic concentrations of monoamines results in sustained depression

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9
Q

Dysregulation hypothesis

A

Dysregulation of neurotransmission release results in changes in pre- and post- synaptic receptors, which ultimately result in sustained depression

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10
Q

Neuroendocrine hypothesis

A

Dysregulation of thyroid and HPA axis result in sustained depression

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11
Q

What were the findings of depressed patients that support the monoamine deficiency hypothesis?

A
  • Relapse of depression with tyrosine hydroxylase inhibitors or depletion of dietary tryptophan
  • Increase mutation in the brain specific form of tryptophan hydroxylase (TPH-2)
  • Increase MOA ligand binding
  • Subsensitive 5-HT1A receptors
  • Malfunction in 5-HT1B receptors
  • Polymorphisms of the serotonin-reuptake transporter
  • Inadequate response of G proteins to monoaminergic signals
  • Decrease levels of cAMP, inositol and CREB in postmortem brains
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12
Q

What are the findings in depressed patients that support the endocrine hypothesis?

A
  • Cortisol level are sometimes increased in severe depression; non-suppression of cortisol by dexamethasone (dexamethasone suppression test. DST), reversed by antidepressants
  • Size of anterior pituitary, adrenal cortex is increased
  • CRH levels in CSF and CRH expression in the limbic brain regions are increased
  • Hippocampal size and numbers of neurons and glia decrease (due to decrease BDNF?)
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13
Q

What are the general mechanism of increasing neurotransmission including increasing the “synpatic residence time”?

A
  • Blocking the reuptake of NE, 5-HT, and DA into nerve terminals (reuptake inhibitors)
  • Blocking the metabolism of NE and 5-HT in nerve terminals (monoamine oxidase inhibitors)
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14
Q

What is the onset of therapeutic?

A
  • Week 1 – sleep, appetite, energy, anxiety
  • Weeks 1-3 – activity, drive, concentration, memory
  • Weeks 4-6 – mood, hopelessness
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15
Q

What is an adequate trial of antidepressant?

A

Approximately 6-8 weeks

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16
Q

Name the class of antidepressants

A
  • TCAs
  • MAOIs
  • SSRIs
  • SNRI
  • NDRI
  • 5-HT and/or NE modulators
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17
Q

What are the disvantages of tricyclic antidepressants?

A
  • Toxic in overdose
  • Side effects
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18
Q

What are the side effects of tricyclic depressants?

A
  • Orthostatic hypotension
  • Tachycardia
  • EEG changes
  • Anticholinergic effects
  • Seizure threshold lowered
  • Weight gain
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19
Q

T/F: Tricyclic are not stimulants

A

T

20
Q

What are the mechanism of action of tricylic depressants?

A
  • Block reuptake of monoamines (both NE and 5-HT) to varying degrees
  • Neurotransmitter levels in the synaptic cleft increase, but clinical effect are delayed around 2-3 weeks
  • Also bind to histamine (H1 & H2), alpha 1 & 2, GABA-A, and muscurinic receptors, which accounts for many side effects
21
Q

What are the pharmacokinetics of tricylic depressants?

A
  • Well absorbed orally and have long half-lives. Highly protein-bound
  • Cause sedation–dose at. bedtime
  • Drug inactivation by hepatic metabolism
22
Q

T/F: Tricyclic depressants used to be the first most common cause of overdose fatalities in developed countries

A

F; second

23
Q

Why aren’t tricyclic depressant not first line?

A

Anticholinergic and cardiac side effects

24
Q

What is the mechanism of MAOIs?

A
  • Increase neurotransmission by increasing NE, 5-HT, and DA levels in nerve terminal
  • Inhibition of MAOIs is irreversible
25
Q

EmSam (selegiline transdermal)

A
  • Approved for treatment of Major Depressive Disorder
  • More selective for MAO-B; avoids inhibition of intestinal MAO-A enzyme
26
Q

What are some safety issues that limit use of MAO inhibitors?

A

Hepatic and intestinal MAO serve to inactivate biogenic amines present in food (tyramine) as well as biogenic amines administered as drugs (sympathomimetic decongestants in OTC cold remedies)
* must avoid foods high in tyramine (not necessary with EmSam)

27
Q

What are some side effects of MAOI?

A
  • Orthostatic hypotension
  • Insomnia
  • Anticholinergic
  • Serotonin Syndrome when combined with SSRIs or if overdose
28
Q

Citalopram (Celexa)

A
  • Most selective of the SSRIs
  • Low inhibition of cytochrome P450s
  • Combination with MAOIs can be fatal
  • Escitalopram: active S-enantiomer of citalopram
29
Q

What are the side effects of SSRIs?

A
  • GI disturbances
  • CNS excitation
  • Anorexia and weight loss during early treatment; possible weight gain with long-term use
  • Decreased libido and significant sexual dysfunction
30
Q

What are the symptoms of SSRI Discontinuation Syndrome?

A
  • Flu-like symptoms
  • GI effects
  • Dizziness
  • Paresthesia
  • Mood, appetite, and sleep changes
31
Q

Bupropion (Wellbutrin)

A
  • Norepinephrine/dopamine reuptake inhibitor (NDRI)
  • Weak blocker of DA uptake, even weaker blocker of NE uptake and affinity no effect 5-HT uptake
  • Used for ADHD (Aplenzin) and for smoking cessation
32
Q

What are the side effects of Bupropion (Wellbutrin)?

A
  • Generally well tolerated due to little or no muscurinic, alpha-adrenergic, and histamine receptor effects
  • Nausea, restlessness, insomnia, anxiety
  • Low incidence of sedation, hypotension, weight gain, sexual side effects
  • High risk of seizure activity at doses of 450 mg/day
  • May precipitate psychotic episodes
33
Q

Venlafaxine (Effexor)

A
  • SSRI at low doses but inhibits NE uptake at higher doses
  • Little affinity for muscurinic, cholinergic, H1-histaminic, or alpha-adrenergic receptors
34
Q

Duloxetine (Cymbalta)

A
  • Used in patients with neuropathic pain
  • Unproven claims that it works faster (1-2 weeks)
35
Q

What are some Serotonin Antagonist and Reuptake Inhibitors (SARIs)?

A
  • Trazodone (Oleptro)
  • Nefazodone (Serzone)
36
Q

Trazodone (Oleptro)

A
  • Acts as 5-HT2 antagonist and 5-HT reuptake blocker
  • Very sedating (not effective as an antidepressant)
37
Q

Nefazodone (Serzone)

A
  • Analogue of trazodone withe less sedating and postural hypotension)
  • Acts much like trazodone
38
Q

Mirtazapine (Remeron)

A
  • Noradrenergic and specific serotoninergic antidepressant (NSSA)
39
Q

What are the mechanism of action of Mirtazapine (Remeron)

A

Serotonin and norepinephrine modulator
* Blocks alpha 2 autoreceptors resulting in increased NA release
* Antagonize 5-HT2 receptors
* Enhances activity at 5-HT1 receptors
* Blocks H1 and muscarinic receptors

40
Q

What are the side effects of Mirtazapine (Remeron)?

A
  • Sedation due to blockade of histamine receptors
  • Increased appetite
  • Significant weight gain
41
Q

What are the non-pharmacologic therapies of depression?

A
  • Electroconvulsive Therapy (ECT)
  • Light therapy
  • Psychotherapy
  • Transcranial Magnetic Stimulation (TMS)
  • Vagus Nerve Stimulation (VNS)
  • Deep Brain Stimulation (DBS)
  • Exercise
42
Q

What are some augmentation strategies of depression?

A
  • Lithium
  • Thyroid supplementation
  • Stimulants
  • Atypical antipsychotics
  • Anticonvulsants
  • Esketamine
43
Q

Thyroid Supplementation

A
  • T3 (liothyronine): 20-25 mcg/day
  • May accelerate response or result in improvement of residual symptoms
  • May work best in patients with sub-clinical hypothyroidism
44
Q

Ketamine

A
  • Dissociative anesthetic
  • Non-competitive NMDA receptor antagonist
  • Most commonly used anesthetic in the world
  • Plays an essential role in surgeries in low-resource countries and in emergencies
45
Q

Esketamine (Spravato)

A
  • The S (+) enantiomer of ketamine
  • Received Breakthrough Therapy Designation from FDA for treatment-resistant depression
  • Also acts as a partial DA reuptake inhibitor
46
Q

What are the only two atypicals with FDA approval as adjunctive treatment for MDD in combination with current antidepressant therapy?

A

Ariprazole (Abilify) and Quetiapine (Seroquel XR)

Neurology (21 decks)

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