Depression (Midterm II) Flashcards

1
Q

how do patients describe depression

A
  • like the world lacks colour
  • stuck in their own negativity and can’t escape
  • can’t get out of bed
  • food doesn’t taste good anymore
  • lack of purpose, low mood; patients interpret symptoms on a deeper level, connected to personality and their whole life
  • it’s a loop of thinking that they can’t get out of
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2
Q

DSM-V criteria for depression

A

in a two week period, 5/9 following symptoms:

  • depressed mood most of the day
  • diminished interest or pleasure
  • decrease or increase in appetite
  • insomnia or hypersomnia
  • psychomotor agitation or retardation
  • fatigue or loss of energy
  • feelings of worthlessness or excessive/inappropriate guilt
  • recurrent thoughts of death/suicidal ideation without a specific plan
  • diminished ability to concentrate nearly every day
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3
Q

core and associated symptoms of depression

A
  • emotional symptoms (feelings of guilt, suicidal thoughts lack of interest, sadness)
  • physical symptoms (lack of energy, decreased concentration, changes in appetite, sleep and psychomotor skills)
  • associated symptoms (brooding, obsessive rumination, irritability, excessive worry over physical health, pain, tearfulness, anxiety or phobias
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4
Q

psychological theories of depression

A
  • psychodynamic: anger directed inward
  • behavioural: classical and operant conditioning
  • cognitive: negative self-schemas and thinking patterns
  • interpersonal theory
  • learned helplessness
  • evolutionary theory
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5
Q

biological theories of depression

A
  • monoamine
  • neuroendocrine
  • inflammatory
  • genetic
  • stress diathesis
  • glutamatergic
  • neuroimaging connectomics (bc neurons that fire together wire together)
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6
Q

effects of reduced monoamine neurotransmission

A
  • 5HT plays a role in obsessions, compulsions, and memory
  • NE plays a role in alertness, concentration and energy
  • DA plays a role in pleasure, reward, and motivation/drive
  • all three contribute to mood and cognitive function
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7
Q

serotonin

A
  • produced from tryptophan in the median and dorsal raphe nuclei
  • implicated in sleep, memory and learning, mood regulation, temperature regulation, sexual function, aggression and impulsivity
  • receptors found in CNS, GI system, platelets and vessel walls
  • linked to a number of psychiatric disorders, the most common being anxiety and depression
  • studies find that the CSF of indv who are depressed or have committed suicide have low lvls of 5HIAA, a 5HT metabolite
  • drugs that deplete monoamines also mimic depression
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8
Q

noradrenaline

A
  • produced in the locus coeruleus (an area implicated in panic attacks) (directly from DA, but the pathway precursor is tyrosine)
  • receptors are found in the CNS and systemically
  • implicated in the pathophysiology of depression bc depression is sometimes responsive to medications affecting the brain’s noradrenergic activity
  • suggests that medications with dual 5HT and NE actions may be more efficacious
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9
Q

dopamine

A
  • produced from tyrosine which is converted to L-DOPA
  • linked to the production of psychotic symptoms and chlorpromazine, a DA receptor blocker, was the first antipsychotic agents
  • DA also linked bc of the psychotic effects of stimulants (cocaine, meth, amphetamines, etc) which increased DA lvls
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10
Q

absorption

A
  • some medications are better absorbed with food, which increased blood flow, changes pH, and changes gut motility
    ex. ziprasodone, lurasidone, vilazodone
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11
Q

metabolism

A
  • some medications have active metabolites, and others are broken down and activated by metabolism (prodrugs)
  • interactions may occur when two drugs use the same enzyme
  • there is also variation in enzymes among people that can have predictive value
  • phase 1 metabolic oxidative metabolism of many substances and psychotropic drugs is performed by the cytochrome P450 system; these evolved from animals to deactivate plant toxins and induce a liver pigment that absorbs light at peak 450 nm ; they’re classified into 8 families and subfamilies based on similarity in AA sequence
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12
Q

SSRIs

A
  • most commonly prescribed type of antidepressant
  • principle action through inhibition of 5HT reuptake
  • time of onset usually 3-6 weeks, but side effects begin immediately
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13
Q

SNRIs

A

-similar side effect profiles to SSRIs, but dual action with NE effects at higher doses

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14
Q

NDRIs

A

ex. bupropion
- act on both NA and DA
- effects on smoking cessation and attention related disorders such as ADHD (which are DA related)
- see less sexual dysfunction and weight gain (which are as’d with 5HT inhibition)
- may cause more initial agitation (Possibly a NA effect)

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15
Q

MAOIs

A

ex. phenelzine, tranylcypromine
- mandate a low tyramine diet (the drug prevents its breakdown, which leads to an excess of NA that can cause a hypertensive crisis)

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16
Q

glutamate

A
  • the predominant excitatory NT
  • principle receptor is NMDA, which has lots of ubiquitous functions
  • linked to psychosis, agitation, anxiety, dementia, depression
  • complete NMDA blockage from large doses of agents like ket/PCP can lead to a hyperactive state that mimics schizophrenia
  • some medications that slow the progression of dementia work on Glu
17
Q

other treatments of depression

A
  • medication
  • therapy
  • neuromodulation (ECT, rTMS, VNS (vagus nerve stim), DBS (deep brain stim))
  • social interventions
  • complementary and alternative methods (light therapy, exercise, diet)
18
Q

novel treatments of depression: ketamine therapy

A
  • ketamine is a agent that completely blocks the NMDA receptor at high doses, leading to decreased excitatory Glu signaling
  • ketamine is a drug of abuse, and the party range of dosing, which produces desired dissociative/psychedelic effects is just slightly lower than an anesthetic or even toxic dose
  • at sub-party thresholds though, we can see a paradoxical increase in Glu at what is called the antidepressant range
  • it seems that at different concentrations, ket has a different affinity for differed locations
  • at low doses, it seems to effect interneurons, inhibiting the release of inhibitory GABA
  • the additional Glu can then get involved with BDNF, which is implicated in spinal synapse number and increasing function by growing back neurons
  • while other antidepressants can take 4-6 weeks, ket can take effect in days