Depression Flashcards

(56 cards)

1
Q

Mood disorder that has high worldwide prevalence.

Wide range of severity of symptoms (mild -> disabling)

A

Depression

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2
Q

DSM-IV diagnosis

A

presence of 2 or more symptoms affecting energy level, sleep, appetite, self-esteem, concentration, and decision making

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3
Q

Major Depression Symptoms

A

low mood
loss of interest, motivation, libido
feeling of helplessness/hopelessness
sleep disturbance
suicidal thoughts
eating disturbance
pessimism

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4
Q

depression and suicide

A

8th leading cause of death in adults
2nd in 15-29
3rd in children 5-14

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5
Q

increased risk of other diseases

A

Reduced CV health (MI)
Ostreoporosis, PUD, DM
Increased Cortisol levels

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6
Q

Chronicity of disease

A

depression persists without appropriate treatment

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7
Q

Common features of all depressive disorder classifications

A

Sadness, emptiness, or irritable mood accompanied by somatic and cognitive changes that significantly affect the individual’s capacity to function

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8
Q

2 major categories of depression

A

Major Depressive Disorder

Dysthymic

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9
Q

Symptoms for 2 or more weeks (sadness, emptiness, irritable)

A
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10
Q

Mild chronic depression

Presence of more depressive moments than not for at least 2 YEARS and persistence of the depression for longer than 2 MONTHS

A

Dysthymic Disorder

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11
Q

diagnosis can be challenging since there are no

A

biologic markers

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12
Q

Multifactorial including _____, ______, ______, and _____ factors

A

genetic, social, lifestyle, environmental

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13
Q
A
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14
Q

Etiology: Factors leading to higher rates of depression

A
  • First-degree relatives
  • many diseases and disorders
  • life events and hassles
  • environmental factors (violence, abuse, neglect, poverty)
  • traumatic events
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15
Q

Pathophysiology of depression

A

exact pathogenesis not completely understood

  • monoamine hypothesis
  • receptor downregulation, sensitivity changes
  • neuroplasticity hypothesis
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16
Q

deficiency or imbalance of monoamines (serotonin, NE, dopamine)

Limiting reuptake of NTs appears to reduce depression symptoms
- TCS, SSRI’s, SNRI’s reduce reuptake
- MAOI’s inhibit monoamine breakdown

A

monoamine hypothesis

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17
Q

secondary adaptive changes

may explain why it takes weeks for drugs to show clinical changes in pts

A

receptor downregulation, sensitivity changes

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18
Q

neurohistological changes lead to a disorder of the hardwiring of the brain

antidepressants reverse structural and functional consequences of stress in hippocampus and prefrontal cortex

A

neuroplasticity hypothesis

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19
Q

D: Pharmacological Treatment

A

Antidepressant meds (SSRI + TCA)
- effective for mod-severs but are not 1st line of treatment for mild cases
- shouldn’t be used for children

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20
Q

D: non-pharmacological/ psychosocial therapy

A
  • effective in mild w/o med
  • uses with med in mod-severe

includes:
- cognitive behavior therapy (CBT)
- problem solving therapy (PST)
- exercise
- socialization

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21
Q

Antidepressant MOA

A

Block reuptake of serotonin or NE
- excess NT accumulates in synaptic cleft
- downregulation of receptors (relief)

Desensitization of autoreceptors
- autoreceptors act as “shut-off” switch when there is excess NT
- drug desensitization of these receptors blocks their action = continued NT release

Enhancement of NE release
- increases serotonergic cell firing
- elevated NT concentration leads to downregulation of receptors

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22
Q

Accumulation of high levels of serotonin, usually via therapeutic use of serotonergic drugs

variable symptoms from mild to life threatening

A

Serotonin Syndrome

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23
Q

Mild SS symptoms

A

HTN
Tachycardia
Mydriasis
Diaphoresis
Shivering
Tremor
Myoclonus
Hyperreflexia; usually afebrile

24
Q

Mod SS symptoms

A

all mild plus hyperthermia-104, hypereactive bowels, mild agitation

25
Severe SS symptoms
all mild and mod plus hyperthermia-106, dramatic HR/BP swings, delerium, muscle rigidity Life-threatening cases often include >101.3, peripheral hypertonicity, truncal rigidity that progresses to respiratory failure
26
SS treatments
may include benzos, serotonin antagonist, cardiac monitoring, and discontinuation of serotonergic agent
27
Antidepressant Therapy
Goal: reduce acute symptoms, return to baseline level of function, prevent further episodes, prevent suicide attempts 2 wks to see improvement in physical symptoms (sleep, eat, energy) 6-8 wks to see improvement in emotional symptoms may require med changes or additiong to achieve goals
28
5-HT
serotonin
29
DA
dopamine
30
Antidepressant Monitoring and Risks
5-HT, NE, and DA receptor subtypes throughout outside CNS can contribute to AE Monitor DDI - interactions due to CYP metabolism, anticholinergic effects, .... SS - risk varies by how much the drug increases 5-HT but is true for all meds - MAOIs have highest risk - avoid other serotonergic meds Boxed warning: increased risk of suicidality in pts < 24 yrs - immediatley report clinical worsening, suicidality, or unusual changes in behavior
31
Selective Serotonin Reuptake Inhibitors (SSRI)
Prozac, Celexa, Lexapro, Zoloft, Paxil Typically 1st in line due to efficacy and tolerability
32
SSRI MOA
inhibit reuptake of 5-HT in CNS less anticholinergic and CV effects than other classes
33
SSRI AE's
Common: HA, N/V/D, insomnia, sexual side effects most are activating (take in AM) but some are sedating (paroxetine) Less common: hyponatremia, bleeding (impaired platelet aggregation)
34
SSRI Other Uses
eating disorder PTSD anxiety OCD bipolar disorder vasomotor menopausal sym
35
Serotonin/NE Reuptake Inhibitors (SNRI)
Effexor, Pristiq, Cymbalta, Fetzima May be 1st line, especially if concomitant neuropathic pain or fibromyalgia
36
SNRI MOA
inhibit reuptake of 5-HT and NE in CNS
37
SNRI AEs
HA, nausea, dry mouth, sweating, sexual dysfunction, insomnia
38
SNRI Other Uses
anxiety, OCD, panic disorder, PTSD, vasomotor menopausal symptoms, fibromyalgia, neuropathic pain, migraine prevention
39
Atypical Agents (action at multiple sites, do not fit into other classes)
Bupropion (Wellbutrin)
40
Wellbutrin
Class: NE/DA reuptake inhibitor MOA: inhibits NE and DA reuptake commonly used, often adjunct to reduce sexual dysfunction AE: HA, nausea, significant insomnia, tremor, dry mouth, decreased appetite risk of seizures, especially at high doses or with electrolyte abnormalities Also used for: ADHD, stop smoking, weight loss
41
Tricyclic Antidepressants
Amitripyline, .............. Less commonly used as safer options are available
42
Tricyclic Antidepressants MOA
inhibit reuptake of 5-HT and NE in CNS; other receptor blockade contributes to AE
43
Tricyclic Antidepressants AE
wt gain, sexual dysfunction, sedation (histamine receptors), anticholonergic effects (muscarinic receptors), hypotension/dizziness (alpha receptors)
44
Tricyclic Antidepressants has a serious risk in overdose
cardiac conduction abnormalities may be fatal due to blocking cardiac Na+ channels
45
Tricyclic Antidepressants other uses
neuropathic pain, migraine prevention, insomnia
46
Ketamine
for highly treatment resistant depression Spravato - nasal spray (appr. 2019) only administered in office sue to risks (sedation, dissociation, abuse) 2nd gen antipsychotic
47
Ketamine features
Is a nonbarbiturate dissociative anesthetic Unique disociative action and partial agonism of opiate µ-receptors permit painful procedures in a consistent state of sedation and comfort
48
Ketamine antidepressant efficacy possibly mediated by
A secondary increase in structural synaptic connectivity mediated by a neuronal response to the ketamine-induced "hyper-glutamatergic state"
49
Ketamine elevates level of ____ in the brain
Glutamate stimulating synaptogenesis and elevated levels of BDNF
50
Ketamine antagonistic action on NMDA works rapidly in controlling
symptoms of depression and acute suicidal ideation
51
Overall Antidepressant AE
HE, GI Upset, sexual dysfunction, insomnia, BP issues TCA's are anticholinergic!
52
Antidepressant Therapeutic Concerns
SSRIs: good for depression and fatigue but diminish libido Continuous treatment best, intermittent may diminish efficacy. Should keep taking when symptoms improve. Be aware of AE especially with SS Monitor BP and HR TCAs and SSRIs may cause tremor AE like sedation and decreased alertness may hinder PT participation
53
Higher intensity exercise associated with
greater mental improvements. increased expression of neurotropic factors, increased 5-HT and NE, regulate hypothalamic/pituitary/adrenal activity, reduce systemic inflammation
53
Physical activity positively affects mental well being by increasing release of
Endorphins
54
Longer duration exercise
not as important as intensity when compared to short and mid duration
55
Suggested ex prescription
60 mins, 3x wk, for 24 wks