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Psych Week 3 > ICL 9.6: Depression > Flashcards

ICL 9.6: Depression Flashcards

1
Q

what is the difference between depression, sadness and grief?

A

sadness is a normal emotion that is appropriate and self limited

grief is a process and has a purpose and leads to emotional reorganization so a person can move past a loss; it occurs in stages following a loss; it is appropriate and self limited

depression serves no purpose, it’s a pathologic state!

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2
Q

what are the types of depressive disorders?

A
  1. Major Depression (single episode/recurrent episode)
  2. Persistent Depressive Disorder (formerly known as Dysthymia)
  3. Premenstrual Dysphoric Disorder
  4. Substance Induced Depression
  5. Due to a General Medical Condition
  6. Other Specified Depressive Disorder
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3
Q

which other conditions should be included in the differential when you think someone has depression?

A
  1. Unipolar versus Bipolar disorder
  2. Dysthymia/Persistent Depressive Disorder
  3. Schizophrenia/schizoaffective disorders
  4. Anxiety disorders
  5. Personality disorders
  6. PTSD
  7. Pseudo-dementia
  8. Due to a General Medical Condition
  9. Substance Induced Mood Disorder
  10. Grief
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4
Q

what is the DSM5 criteria for major depression?

A

CARDINAL SYMPTOMS
1. pervasive sadness: sad, down, blue most of the day nearly every day for at least two weeks

  1. pervasive anhedonia: loss of interest or pleasure in activities that one would normally find pleasurable most of the day nearly everyday for at least 2 weeks
    * must have #1 or #2

5/9 symptoms must be present everyday nearly most of the day for a 2 week period

A. not due to another mental disorder

B. not due to substance use

C. not due to grief

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5
Q

what are the psychological symptoms of depression?

A
  1. pervasive sadness
  2. pervasive anhedonia
  3. feelings of worthlessness
  4. excessive feelings of guilt (may be delusional)
  5. recurrent thoughts of death, dying, or wishing to commit suicide

the psychological symptoms are most sensitive to making the diagnosis of major depression; there are patients that will be medically ill and they frequently have the somatic symptoms that are the same as depression so it’s more reliable to base a diagnosis on psychological symptoms instead of somatic symptoms

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6
Q

what are the somatic symptoms of depression?

A
  1. weight loss/gain
  2. insomnia/hypersomnia
  3. psychomotor retardation/agitation (anxiety or psychosis)
  4. loss of energy/fatigue
  5. difficulty concentrating, thinking, indecisiveness
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7
Q

what are the specifiers of mood disorders?

A
  1. mild = they meet criteria for the condition but they don’t have a functional impairment;
  2. moderate = they meet criteria for the condition and have a slight functional impairment
  3. severe = they are disabled by their condition
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8
Q

what is the difference between full and partial remission?

A

full remission = 8 weeks depression free

vs.

partial remission

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9
Q

what does SIGECAPS stand for?

A 
Sleep
Interest
Guilt
Energy
Concentration
Appetite
Psychomotor
Suicide

this is NOT sufficient to make the diagnosis of major depression because it doesn’t include the cardinal symptoms

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10
Q

what is masked depression?

A

they have no real insight into their own depression because they experience their depression somatically

they have chronic pain, insomnia, chest pain, headaches, irritable bowel syndrome etc. so they’re having somatic symptoms

you see this a lot in the geriatric population; when they experience depression it’s somatized

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11
Q

what are the specific patterns of major depression?

A

can be seen in both unipolar and bipolar disorder

these are the patterns of major depression:

  1. with catatonia
  2. with melancholia
  3. with atypical features
  4. with postpartum onset
  5. with a seasonal pattern
  6. with anxious features
  7. with mixed features
  8. with psychotic features
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12
Q

what is major depressive disorder with catatonia?

A
  1. motoric immobility (stuporous)
  2. excessive motoric activity (excited)
  3. extreme negativism
  4. peculiarities of voluntary movement (catalepsy)
  5. echolalia
  6. echopraxia
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13
Q

what is major depressive disorder with melancholia?

A

profound anhedonia OR lack of reactivity to usually pleasurable stimuli

plus 3 or more of the following:

  1. diurnal variation of mood = they wake up and instantly they feel depressed and anxious; probably related to cortisol levels
  2. terminal insomnia
  3. psychomotor retardation
  4. significant anorexia or weight loss
  5. excessive or inappropriate guilt

respond to all types of treatment!

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14
Q

what is atypical depression?

A

mood reactivity = mood brightens in response to actual or potential positive events

they wake up in the morning and they feel good because they haven’t started dwelling on their anxiousness/fears; their depression worsens throughout the day –> they respond well to CBT because you can change the way they think, and therefore the way they feel

plus 2 or more of the following:

  1. significant wt gain or increased appetite
  2. hypersomnia
  3. leaden paralysis
  4. longstanding history of interpersonal rejection hypersensitivity
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15
Q

what is postpartum depression?

A

severe depression beginning shortly after childbirth, usually within 30 days

most often occurring in women with preexisting psychiatric illness

symptoms include marked insomnia, mood lability, fatigue

frequently associated with psychosis which may endanger the mother and the child

suicidal ideation is common

homicidal and delusional beliefs can occur about the baby

responds best with antipsychotics and antidepressants and ECT

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16
Q

what is seasonal pattern depression?

A

also known as SAD

onset occurs with the shortening of daylight in the fall and progresses through the winter remitting generally by late february

Major Depression characterized by hypersomnia, hyperphagia, craving for sweets, irritability, psychomotor slowing

light Therapy is effective as are antidepressants

17
Q

what is major depression with anxious distress?

A

these patients have a sense of dread, restlessness, poor concentration, tense, fear of losing control with motor agitation

Mild: 2 sx’s

Moderate: 3 sx’s

Moderate : moderate to severe 3-4 sx’s

Severe: 4-5 sx’s

18
Q

what is major depression with mixed features?

A

at least 3/5 symptoms of mania or hypomania

these are patients diagnosed with unipolar depression who are at increased risk of developing BP I or BPII

symptoms are actually signs observable by others

19
Q

what is major depression with mood congruent psychosis?

A

psychotic delusions or hallucinations that are entirely consistent with a depressive theme

ex. guilt, personal inadequacy, disease, death, deserved punishment

responds very well to electroconvulsive therapy

20
Q

what is major depression with mood incongruent psychosis?

A

delusions or hallucinations that do not involve typical themes of depression such as thought insertion, thought broadcasting delusions of control

this type is highly related to schizophrenia and has a worse prognosis

21
Q

what is persistent depressive disorder?

A

it’s major depression or dysthymia (minor depression) lasting >2 years

MDE x 2 yrs or mde x 2 ys

no mood elevations of any kind

same specifiers as major depression except there’s also :
1. early onset

  1. late onset
  2. with pure dysthymic syndrome
  3. with persistent major depressive episode
  4. with intermittent major depressive episodes with current episode
  5. with intermittent major depressive episode without current episode
22
Q

what are adjustment reactions?

A

the development of emotional or behavioral symptoms in response to an identifiable stressor occurring within 3 months of the onset of the stressor(s)

the emotional disturbance are outside the cultural norm but they don’t reach the threshold to meet the criteria by major depressive disorder

the symptoms or behaviors are clinically significant as evidenced by either of the following:

  1. marked distress in excess of what would be expected
  2. significant impairment in social or occupational functioning
23
Q

what are the organic conditions that mimic or cause depression?

A
  1. drugs: steroids, certain antibiotics, progesterone contraceptives, alcohol
  2. infectious: herpes encephalitis, tertiary syphilis
  3. endocrine: premenstrual exacerbation of mood, myxedema madness, Cushing’s, Addison’s, parathyroid adenoma
  4. left frontal lobe stroke
  5. collagen- SLE, Rheumatoid arthritis
  6. neurologic: MS, Parkinson’s Disease
  7. Alzheimer’s Disease, head trauma, complex partial seizures, left frontal lobe stroke, tumors of the 4th ventricle
  8. sleep apnea
  9. nutritional: B12, folate, niacin, thiamine
  10. neoplastic: pancreatic, carcinomatosis of the lung
24
Q

what is the biopsychosocial model of depression?

A

the biopsychosocial model!

the mind and body are one unit and it begins by having a genetic predisposition for certain conditions; genes also code for certain behaviors

we develop maladaptive and adaptive coping strategies – our coping strategies effect the environment – in reverse, our environment also effects our behaviors!

our behavior then changes our brain structure which then modifies our cellular and molecular makeup = epigenetic changes that result due to changes in our environment

so psychiatry can change your personality by doing psychotherapy or we can change their basic brain chemistry/circuitry with medications –> we can’t change the environment though…

25
Q

what are the 3 theories of depression?

A
  1. monoamine theory
  2. neuroendocrine mechanism
  3. neuroplasticity
26
Q

what is the monoamine theory of depression?

A

depression is caused by a functional deficit of monoamine transmitters at certain sites in the brain while mania results from a functional excess

NA or serotonin or dopamine –> 5HT is responsible for regulating obsessions, compulsions, memory; dopamine is responsible for pleasure, reward and motivation/drive; NE is responsible for alertness, concentration and energy

what we actually see is that the brain is perfused by the various NT systems and when we treat people with antidepressants, we’re resetting the firing rates in the origins of the systems! so that would be the locus coeruleus for NE, raphe nuclei for 5HT and the substantia nigra for dopamine

27
Q

what is the neuroendocrine mechanism of depression?

A

hypothalamic-pituitary adrenal axis = increase in cortisol, growth hormone concentration is reduced and prolactin is increased

patients who experience a major stressor will have those experiences reflected to the limbic system, specifically the hypothalamus, where they will produce CRF which then goes to the anterior pituitary gland that releases ACTH which goes to the adrenal cortex and releases cortisol, a stress hormone

cortisol can circulate back to the brain and cause brain damage! the cells lined with glucocorticoid receptors get hyper stimulated and damaged which you can measure in brain scans

another change that occurs is activation of the fight or flight response in the locus coerelus which causes serious changes in behavior like fear, aversion, increased locomotor activity, decreased food intake and sex, disrupted sleep = the stress response

so when we treat patients with MDD, we want to turn off the fight or flight response to limit these effects

CRF also activates the immune system; when cortisol is released by the adrenal cortex is activates macrophages which release inflammatory cytokines, acute phase reactants, etc. which can cross the BBB and activate microglia in the brain which release more cytokines/chemokines etc. which activate astrocytes and oligodendrocytes which effect the myelin sheath protecting our nerve cells –> this leads to
reduced availability of the monoamines, excitotoxicity and down-regulation of the availability of brain-derived neurotrophic factors

so when a patient is suffering from a stress response, they’re literally eating themselves alive! this is a physiologic process that we need to turn off – we’ve activated both the nervous system and immune system and there’s tons of damage being done

28
Q

what is the neuroplasticity mechanism of depression?

A

depression is associated with neuronal loss in the hippocampus and prefrontal cortex

cell loss and breakdown of normal intercellular connections in the hippocampus and the prefrontal cortex lead to impaired function of these structures which are central regulators of mood; this may also explain impairment in catecholamine function

neuroplasticity is at the core of all psychiatric disorders and all biological, psychological and social treatment interventions because symptoms and symptom reduction are presumed to emerge from a change in function of neuronal networks; neuroplasticity shapes the brain!

antidepressant therapies act by inhibiting or actually reversing this loss by stimulating neurogenesis

29
Q

what are some examples of neuroplasticity?

A
  1. neuronal synaptic connections
  2. cell death (apoptosis)
  3. neurogenesis
  4. cell migration
  5. dendritic sprouting
  6. spine formation
  7. axon pruning
  8. axon growth
  9. intracellular changes
  10. cell membrane changes

all of these remodel the brain tissue so that it can function normally

30
Q

what is one of the most important parts of the brain involved in regulating mood?

A

subgenual anterior cingulate cortex

it seems to be controlling sadness and obsessive negative thinking and is probably regulated by serotonin

so when this part of the brain is hyperactive, patients think i’m no good, life is terrible, things are never going to get better etc. and often time this leads to suicidal ideation – as these obsessive rumination occur the other parts of the brain shut down!

31
Q

what is the glutamatergic hypothesis of MDD?

A

a dysfunction of the glutamate neurotransmitter system in MDD is what contributes to depression

a single dose of the glutamate N-methyl-D-aspartate (NMDA) receptor antagonist ketamine produced rapid and large antidepressant effects in patients with treatment-resistant MDD –> inhibitors of glutamate release (e.g., lamotrigine, riluzole) demonstrated antidepressant properties!

abnormal glutamate levels were found in depressed subjects as determined by magnetic resonance spectroscopy and there is evidence for abnormal NMDA signaling in post-mortem tissue preparations

32
Q

what are epigenetic changes?

A

epigenetics is the study of how the environment can influence gene expression and even pass it along through generations without altering the gene structure

so epigenetic changes are the process through which an environmental stimulus during development alters epigenetics marks (DNA methylation, histone modifications, etc.) and thus gene expression altering developmental trajectory and phenotypic expression

these epigenetic changes lead to neuroplasticity! aka changes in structure and function of local brain regions

33
Q

how do we treat depression?

A

it’s a multimodal treatment that includes:

  1. reset the firing rate in the amygdala, locus coeruleus, dorsal raphe nuclei ,subgenual cortex (Brodman Area 25), lateral habenula and anteriomedial OFC
  2. increase BDNF and repair epigenetic damage
  3. turn off the Fight or Flight response
  4. restore function of the hippocampus
34
Q

what is BDNF? what is its importance in MDD?

A

BDNF is growth hormone for your nerve cells and it encourages neurogenesis and repair in nerve tissues

people with MDD have brain tissue loss specifically in the hippocampus and prefrontal cortex

so if you can increase BDNF then you can help regenerate these areas and repair the damage that’s been done by the MDD and the brain rewires and returns to its normal baseline function

Psych Week 3 (11 decks)

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