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PR3136 PT IV > Depression (Blue Deck) > Flashcards

Depression (Blue Deck) Flashcards

1
Q

What are the symptoms of depression (emotional and other domains)?

A

Emotional:

  • Misery, apathy, and pessimism
  • low self-esteem (feelings of guilt, inadequacy and ugliness)
  • indecisiveness, loss of motivation

Other domains:

  • retardation of thought and action
  • loss of libido
  • sleep disturbances and loss of appetite
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2
Q

What are the 2 major types of depression?

A
  • unipolar depression: mood swings always in same direction

- bipolar depression/affective disorder: alternating depression and mania

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3
Q

What are the two different types of unipolar depression?

A
  • reactive depression

- endogenous depression

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4
Q

What is reactive depression associated with and accompanied by what symptoms?

A
  • non-familial
  • associated with life-events
  • accompanied by smx of anxiety and agitation
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5
Q

What is endogenous depression associated with and accompanied by what symptoms?

A
  • familial pattern

- not directly related to external stress

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6
Q

FYI what are the manifestations of bipolar depression?

A
  • depression alternates with mania
  • periodicity of oscillations in mood vary but usually occur over several weeks
  • usually appears in early adulthood
  • strongly familial
  • some studies suggest genetic similarities to susceptibility to SCHIZOPHRENIA
  • Drugs used to treat depressive smx still usually include ANTIDEPRESSANTS
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7
Q

What is the monoamine theory?

A
  • deficits in monoamine neurotransmitters (NA and 5-HT) cause depression
  • Basis of most successful pharmacological strategies for treatment of depression
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8
Q

What are the limitations of the monoamine theory?

A
  • formulated for NA first, but later emphasis shifted to 5-HT
  • inconsistent and equivocal results
  • the hypothesis alone is inadequate to explain all pharmacological actions in depression
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9
Q

5-HT is brokwn down mainly by

A

MAO-A

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10
Q

NA and dopamine is broken down by

A

MAO-A and MAO-B; MAO-B more selective on dopamine

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11
Q

What is the MOA of MAOIs?

A
  • increase biological availability of monoamines

- e.g. phenelzine

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12
Q

What is phenelzine?

A
  • non-selective for MAO-A vs MAO-B

- an irreversible MAO inhibitor

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13
Q

What are the adverse effects of MAOIs?

A
  • Postural hypotension: due to sympathetic block produced by accumulation of dopamine in the cervical (neck) ganglia, where it acts as an inhibitory transmitter
  • Restlessness and insomnia due to CNS stimulation
  • Shouldn’t be combined w or other drugs enhancing serotoninergic function (e.g. pethidine): hyperexcitability, inc muscular tone, myoclonus (jerking, involuntary movements), loss of consciousness
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14
Q

What is the cheese reaction?

A
  • Drug-food interaction
  • acute HTN –> throbbing HA, and occasionally intracranial haemorrhage
  • major danger from cheeses and concentrated yeast products (marmite)
  • amines (tyramine) in foods (cheese) are usually broken down by MAO in the intestines and liver
  • MAOIs can lead to accumulation of tyramine and a sympathomimetic effect
  • Dangerous food interactions w MAO blockers (e.g. acute HTN)
  • Tyramine taken up into adrenergic terminals and competes w NA for vesicular compartment –> inc release of NA into synapses
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15
Q

What are tricyclic antidepressants? (TCAs)

A

1st gen monoamine reuptake inhibitor antidepressants

(tri) ringed (cyclic) chemical structure

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16
Q

What is Nortripytline?

A

2nd gen TCA
Milder SE compared to amitriptyline
Improved compliance

17
Q

What are the adv effects of TCAs? ( 4 effects)

A
  • Sedation (due to h1 histamine receptor antagonism); tolerance to sedation can develop in 1-2wks
  • Postural hypotension: due to a-adrenoceptor sympathetic block
  • Dry mouth, blurred vision, constipation: due to muscarinic receptor antagonism
  • DDI: Plasma protein bound; rely on hepatic metabolism for elimination
18
Q

What are the examples of TCAs?

A

Imipramine
Amitriptyline
Nortriptyline

19
Q

What are selective serotonin reuptake inhibitors (SSRIs)?

A
  • greater 5-HT reuptake selectivity than TCAs
  • 50 to -1000- fold selectivity for 5-HT over NA
  • Fluoxetine approximately 50-fold selectivity for 5-HT
  • Citalopram approximately 1000- fold selectivity for 5-HT
  • Fewer adv effects than TCAs
20
Q

What are the advantages of SSRIs?

A
  1. Low affinity for a-adrenoreceptors –> lack of Cardiovascular effects, safer in overdose
  2. Lack of effect at histamine receptors –> reduced sedation
  3. low affinity for muscarinic cholinergic receptors –> minimal anticholinergic side effects (e.g. dry mouth and constipation)
21
Q

What are the adv effects of SSRIs?

A
  • Nausea
  • Insomnia
    ~ Nausea and Insomnia - maybe be discontinuation/rebound smx of withdrawal when plasma levels of drug drop btw doses
  • Sexual dysfunction
22
Q

What is the issue with SSRI-induced sexual dysfunction?

A

men = delayed ejaculation
women = delayed or blocked orgasm (anorgasmia)
reported by up to 50% of pts on SSRIs
But rarely (<10%) leads to discontinuation
Due to inc stimulation of 5HT2 receptors

23
Q

What is a serotonin syndrome?

A
  • severe reaction can result from DDI with other drugs increasing serotoninergic activity (MAOIs)

effects include: tremor, hyperthermia, cardiovascular collapse

No MAOI with SSRI
After a few weeks of SSRI, whether pt feel hot, or BP high, or shaking

24
Q

What are noradrenaline reuptake inhibitors? (NARIs)

A
  • greater NA reuptake selectivity than TCAs
  • approx 1000-fold selectivity for NA over 5-HT
  • Reboxetine approx 1000-fold selectivity for NA
  • fewer adv effects than TCAs and SSRIs
25
Q

Adv effects of reboxetine? (NARIs)

A
  • new drug so adv effects not well described
  • dry mouth and constipation due to anticholinergic effects
  • insomnia: probably due to incrased NA activiy in CNS
  • Tachycardia (inc availability of NA at sympathetic FFF synapses)
26
Q

What are serotonin and NA reuptake inhibitors? (SNRIs)

A

similar dual 5-HT and NA reuptake inhibition profiles to non-selective TCAs
- issue of additional receptor antagonism is controversial

  • Venlafaxine, Desvenlafaxine (synthetic metabolite of venlafaxine), and Duloxetine are examples in clinical use
27
Q

Advantages of Venlafaxine? (SNRIs)?

A
  • different structure to TCAs and fewer adv effects than TCAs
  • claimed to work slightly faster than other antidepressants
  • claimed to work better in treatment-resistant pts
28
Q

What are the adv effects of SNRIs?

A
  • serotoninergic adv effects similar to SSRIs: nausea, insomnia, sexual dysfn
  • serotonin syndrome when combined w other serotoninergic drugs and MAOIs
  • withdrawal effects may be more common and stronger than for SSRIs and TCAs

PR3136 PT IV (17 decks)

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