depressive disorder Flashcards

1
Q

what is depression

A

severe or persistent enough to interfere with normal functioning
- depressed mood, psychomotor dysfunction, fatigue, decreased
interest or pleasure in activities

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2
Q

what is the etiology of depression

A
  • exact ‘cause’ is not well understood and likely involves multiple factors
  • genetic (e.g. single nucleotide polymorphisms)
  • altered neurotransmitter levels (monoamines)
  • altered neuroendrocrine function
  • psychosocial factors
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3
Q

what is the Major depressive disorder

A
  • depressive symptoms every day for two weeks
  • at least 5 depressive symptoms from a list of 9, and must include
    depressed mood, or loss of interest or pleasure
  • other symptoms include sleep disturbance, fatigue, suicidal thoughts
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4
Q

what is the Persistent depressive disorder

A

at least two depressive symptoms persist for two years

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5
Q

what is the interaction between the limbic system activity and cognitive control

A

there is reciprocal interconnection between the limbic system activity and the cognitive control as the limbic system activity increase the cognitive control decrease

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6
Q

what is the anterior cingulate cortex

A

has connection to both the limbic area of the brain and the cortical brain network

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7
Q

what are the cortical region

A

dorsaltral
ventromedial
ventrolateral

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8
Q

what is the limbic system structure

A

thalamus
amygdala
hippocampus

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9
Q

how do Tricyclic Antidepressants work

A

act by blocking reuptake of 5-HT and NE

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10
Q

which receptors do the Tricyclic Antidepressants block

A

also bind and antagonize many other receptor targets: 5-HT (2A, 2C, 6, 7),
alpha1, NMDA, histamine H1 and H2, muscarinic acetylcholine

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11
Q

what are the side effects of the Tricyclic Antidepressants

A

many more including anxiety, nausea, drowsiness, cardiac
(tachycardia and bradycardia)

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12
Q

give me a name of the Tricyclic Antidepressants medication

A

clomipramine

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13
Q

how do Monoamine oxide inhibitors (MOAIs) work

A

inhibit the oxidative deamination of 5-HT, NE, and DA

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14
Q

give two medications that are MOAIs

A

Nardil ( phenelzine) and Manerix ( moclobemide)

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15
Q

what is the hypertensive crisis in the MOAIs

A

when MOAIs are ingested along with food containing
tyramine or dopamine

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16
Q

which medication is a new reversible MOAI that is selective for MOA-A

A

Manerix

17
Q

give some meds of SSRIs

A

fluoxetine (Prozac), sertraline, citalopram, escitalopram

18
Q

how does SSRIs work

A

(1) SSRI – increased amount of 5-HT in the synaptic cleft
(2) desensitization of the presynaptic 5-HT 1A autoreceptor
- increased 5-HT 1A autoreceptor in postmortem studies
- chronic SSRI treatment may downregulate these autoreceptors
(3) desensitization of the postsynaptic 5-HT 2A receptor
(4) anti-inflammation: downregulation of pro-inflammatory cytokines:
IL-1β, IL-6, interferon-γ, tumor necrosis factor α

19
Q

what is the The Inflammation Hypothesis

A

an imbalance to the interaction between the immune system and brain

20
Q

what are the evidences for the Inflammation Hypothesis

A
  • major depressive disorder occurs more often with chronic inflammation
    (e.g. diabetes or rheumatoid arthritis)
  • systemic administration of interferon-γ, or elevation to tumor necrosis
    factor α and IL-6, correlate with depressive symptoms
  • in many cases, levels of these cytokines are increased in the
    cerebrospinal fluid of patients with major depressive disorder
  • these same cytokines can upregulate the function of monoamine
    reuptake pumps such as the 5-HT transporter
21
Q

which neurotransmittors does Inflammation Hypothesis affects

A

an imbalance to
serotonin and
glutamate
neurotransmission

22
Q

what are SNRIs

A

similar to the tricyclic antidepressants, inhibit reuptake of 5-HT and NE
- very similar clinical efficacy and adverse effects as SSRIs
- some adverse effects (e.g. sexual dysfunction) may be milder

23
Q

give two meds of the SNRIs

A

effector ( venlavaxine), cymbalta ( Duloxetine)

24
Q
A