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Neuro Block 5 > Mood Disorders > Flashcards

Mood Disorders Flashcards

0
Q

What are the known neurochemical effects of monoamine oxidase inhibitors (MAOIs)?

A

Irreversibly blocks oxidative deamination of monoamines

Block both MOA a and MOA b

Occurs within 24-48hrs, clinically takes 3+ weeks to begin

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1
Q

What are the known neurochemical effects of tricyclic antidepressants?

A

Block reuptake of NE and/or 5-HT

OTHER:

  • Block H1 receptor (weight gain, drowsy)
  • block muscarinic receptor (dry mouth, constipat)
  • block alpha 1 receptor (low BP, light headedness)
  • Block Na channels (arrhythmias, cardiac arrest and seizures)
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2
Q

What are the known neurochemical effects of second generation antidepressants?

A

Increase NE, 5-HT and possible DA

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3
Q

What are the major adverse effects associated with MAOIs?

A

Mess with SSRIs

Serotonin syndrome

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4
Q

What are the main adverse effect associated with tyramine?

A

Tyramine is completely metabolized by MAO hepatic

  • Accumulation induces NE and Epinephrine release
  • -> increase BP dangerously –> crisis
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5
Q

What are potential advantages of some of the newer antidepressant drugs?

A

Less effects Cholinergic receptors

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6
Q

What are the clinical uses of using lithium to treat mood disorders?

A
  • manic phases of bipolar disorder
  • prevention of mood swings
  • antidepressant in some patients
  • effective in 60-80% of treated Pxs
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7
Q

What are the neurochemical effects of lithium?

A
  • unsure
  • most likely postsynaptic
  • IP3 release and production and DAG
  • inhib NEnsensitive ardenylyl cyclase
  • uncouple receptor recognition site from GTP-binding protein by competing with Mg
  • alters gene expression implicated in long-term neuroplastic events that could underlie long-term mood stabilization
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8
Q

What is the toxicity of lithium?

A
  • 95% excreted by kidneys! therefore effected by water and electrolyte balance
  • fatigue, muscle weakness, slurred speech, ataxia, fine tremor of the hands at therapeutic doses
  • coma, muscle rigidity, hyperactive deep reflexes, tremor, muscle fasciculations, symptomatic treatment, at toxic levels
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9
Q

What other drugs besides lithium are used to treat bipolar mood disorder?

A

Anticonvulsants: valproic acid, carbamazepine

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10
Q

Why should SSRIs not be given to bipolar patients who do not receive a mood stabilizer?

A

Because rapid onset of mania may occur

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11
Q

What is key in distinguishing depressive disorder from bipolar disorder?

A

Mania

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12
Q

What is the rate of suicides for depression and bipolar disorder?

A

~15% in depression

~25% in bipolar disorder

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13
Q

When does unipolar depression occur?

A

Once, everyday at least 2 weeks

Recurrent episodes separated by periods of euthymia

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14
Q

What do Pxs with bipolar disorder alternate between?

A

Depression, mania, either separated by euthymia or rapid cycles

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15
Q

What is depression?

A
  • Heterogenous disease
  • depressed mood and/or anhedonia (no interest in pleasure)
  • disruptions in sleep, weight gain or loss, psychomotor retardation, fatigue, indecisiveness, and or suicidal thoughts
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16
Q

What areas of the brain are linked to depression?

A
  • Monoaminergic brain areas
  • dorsal raphe nucleus in midbrain
  • other limbic structures
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17
Q

What is the monoamine hypothesis?

A
  • depression associated with changes in serotonin or NE signaling in he brain (or both) with significant downstream effects
  • other neurochemicals associated downstream
  • depression occurs if receptors are insensitive or if amine synthesis, storage, or release is deficient
  • mania occurs of excess amines
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18
Q

What is the problem with the amine theory of depression?

A

Mismatch between time course

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19
Q

What is the neurotrophic hypothesis of mood disorders?

A
  • Nerve growth factors (BDNF) are critical for function
  • Depression is associated with the loss of neurotrophic support
  • increase this support in cortical areas such as the hippocampus
  • antidepressants are associated with an increase in BDNF in animal models
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20
Q

What are the drug classes for mood disorders?

A
  • antidepressants
    1. Tricyclic antidepressants
    2. MAOIs
    3. SSRIs
    4. Dual mechanism drugs
  • mood stabilizers
    1. Lithium carbonate
    2. Anticonvulsants
    3. Atypical antipsychotics
21
Q

What are the clinical effects of TCAs?

A

Normal Pxs: no mood effects, antimuscarinic effects, sleepiness and light headedness

Depressed Pxs: elevation on mood after 2-3 weeks
Used always

22
Q

What TCA blocks NE reuptake selectively?

A

Desipramine

23
Q

What TCA blocks NE/5-HT reuptake?

A

Imipramine

24
Q

What are adverse effects of TCAs?

A
  • orthostatic hypotension - blockade of alpha adrenoceptors
  • Antimuscarinic effects (confusional state, constipation, glaucoma)
  • weight gain
  • tachycardia - increased chances for arrhythmia with high doses
25
Q

What is fluoxetine (Prozac)and what does it inhibit?

A

SSRI

Inhibits CYP2D6 which metabolizes TCAs

26
Q

What is the TI of TCAs?

A

5-10

Well absorbed and long half life
Do not give more than a weeks worth to a depressed Px

27
Q

When are TCAs used?

A

In depression that is unresponsive to SSRIs and SNRIs

Relatively poor tolerability
Lethality in overdose

28
Q

What MAOI should you remember?

A

Phenelzine

29
Q

What does MAO a do?

A

Metabolizes NE and 5-HT

30
Q

What does MAO b do?

A

Metabolizes DA

31
Q

Why should you wait 14 days before you start an SSRI upon discontinuation of treatment with an MAOI?

A

To allow for MAO regeneration so serotonin does not build to toxic levels

Same with reverse (5 weeks for fluoxetine)

32
Q

What is the TI of MAOIs?

A

Less than 5

33
Q

What is serotonin syndrome?

A 
Hyperthermia
Muscle rigidity
Tremors
Autonomic instability 
Confusion
Irritability
Agitation 
- coma --> death
- treatment is to antagonize serotonin
Also caused by MDMA
34
Q

What should you avoid while on MAOIs?

A

Foods rich in tyramine and sympathetomimics

  • aged cheese, red wine, beer, beans, bananas, avocados, yogurt, sour cream, chocolate
  • cold meds - ephedrine, pseudophedrine
35
Q

What type of MAOI is it ok to have some tyramine?

A

Selective and reversible MAO a inhibitors

36
Q

What are the three main SSRIs?

A

Fluoxetine (Prozac)
Sertraline (Zoloft)
Escitalopram (Lexapro)

37
Q

What is the mechanism of SSRIs?

A
  • Clinical improvement is associated with 5-HT 2A
  • also 3 and 2c for GI/sex problems and agitation/restlessness
  • down reg of postsynaptic, autoreceptors, and heteroreceptors
38
Q

What are adverse effects of SSRIs?

A
  • nusea, dirrhea, and weight loss
  • stimulating rather than sedating
  • sexual dysfunction
  • alone they flip from depressed state into manic in bipolar Pxs
  • increase suicidality
39
Q

What drugs lead to weight loss and gain?

A

Loss: SSRIs
Gain: TCAs

40
Q

What is the mechanism of Venlafaxine?

A

Serotonin-NE reuptake inhibitor
Maybe DA

  • similar to TCAs but does not effect H1, adrenergic, or Cholinergic receptors
  • do not used with MAOIs
41
Q

What does raising the dose of Venlafaxine do?

A

Determines the monoamine effected (blocked reuptake)

Low - 5-HT
Med - NE
High - DA

42
Q

What is Desvenlafaxine?

A

Active metabolite of Venlafaxine

  • about the same as Venlafaxine
43
Q

What does Mirtazapine do?

A

Blocks presynaptic alpha2 therefore increasing NE and 5-HT

Autoreceptors (adrenergic)
Heteroceptors (serotonergic)

44
Q

What are alpha 2 receptor on?

A

Adrenergic neuron presynaptically

45
Q

What is Buproprion?

A

Enhances NE and DA (not 5-HT) reuptake inhibition
Maybe also involves release of NE and DA

Side effect - stimulation

Combine with an SSRI

Also for smoking cessation

46
Q

What is Ketamine?

A
  • injectable anesthetic
  • antagonist of NMDA
  • single dose improves symptoms of depression in less than 2 hours and lasts at least one week
  • possibly hallucinations and nightmares
  • AZD6765
47
Q

What area of neurons may be involved in depression treatment?

A

Dorsal RAPHE nucleus

mPFC –> dorsal raphe nucleus

48
Q

What is Lurasidone?

A

Atypical antipsychotic used for bipolar disorder

DA and 5-HT receptor antagonism

49
Q

What is wake therapy and why is it useful?

A
  • keeping patients awake at night and from sleeping during the day
  • alleviates signs of depression and may jump start the effectiveness of an anti-depressant

Neuro Block 5 (20 decks)

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