Mood Disorders I and II Flashcards

You may prefer our related Brainscape-certified flashcards:
1
Q

Why study major depression?

A
  • Common – 8-10% of men; 15-20% of women lifetime prevalence – 1 year prevalence about 7%; 19 million Americans suffering
  • Incidence and prevalence increasing with time – cohort of women born in the 70’s and 80’s– as high as 25% prevalence
  • Burden of Disease – projected to be the 2nd leading cause of disability world wide by 2020 (WHO study) [heart disease #1]
    • cost $100mill USD/yr (2012)
  • Treatable if someone seeks help; many families affected differently
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2
Q

DSM-5 Criteria for Major Depression

A
  • Five or more of the following must be present for TWO WKS and represent a change from previous functioning. Must have 5 of the following 9 symptoms and must include either depressed mood or loss of interest or pleasure (anhedonia)
    • (1) Depressed mood most of the day, nearly every day, as indicated by either subjective report or observation by others (In children and adolescents, can be irritable mood).
    • (2) Markedly diminished interest or pleasure in all, or almost all activities most of the day, nearly every day (as indicated by either subjective account or observation made by others).
    • (3) Significant weight loss when not dieting or weight gain or increased or decreased appetite nearly every day.
    • (4) Insomnia or hypersomnia nearly every day.
    • (5) Psychomotor agitation or retardation (Observable by others).
    • (6) Fatigue or loss of energy nearly every day.
    • (7) Feelings of worthlessness or excessive/inappropriate guilt.
    • (8) Diminished ability to think or concentrate—or indecisiveness.
    • (9) Thoughts of death or suicide.
      • most ppl with depression never become suicidal
  • Above cannot be due to a general medical condition or the direct physiological effects of a substance.
  • Must cause significant impairment or distress in social, occupation, or other areas of functioning
  • Definitions:
    • Mood = what the patient states they are feeling in general
    • Affect = what we observe at the moment
    • Mood:Affect::Climate:Weather
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3
Q

Acronym for NINE DSM criteria

A
  • S(adness)
  • I(nterest)
  • G(uilt)
  • E(nergy)
  • C(oncentration)
  • A(ppetite)
  • P(sychomotor agitation or retardation)
  • S(uicidal thoughts)
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4
Q

Depression RF

A
  • 2W:1M – ration narrows to 1:1 postmenopausal
  • Age onset: peak 20-30 (40?) –decreasing w/ time –some studies suggest that 10% of adolescents may now have depressive symptoms
    • also: second smaller peak >65=elderly indivs with medical issues
  • FHx – moderate genetic risk (heterogenous vs bipolar which is more linked)
    • Parents: 1 rent 10-15%, 2 rents 20-30%
    • MZ twins 50%, DZ twins 15-20%
      • (if take into consideration “Affective Disorder Spectrum” – Major Depression, ETOH**, Somatization, Antisocial personality then genetics more robust)
      • Having an FHx as a genetic base + psychological/environmental disruptions
  • Single, divorced, widowed > married
    • **except in elderly males – high suicide group
  • Income, profession, religion, geography have minimal impact
  • Cultural: some trends – lower in AA men, Asians; higher in
  • Hispanic women and American Indians
  • **Childhood major negative events/trauma are a big risk factor – loss, neglect, abuse
  • Onset of illness usually a series of negative life events, but can also be 1 catastrophic event – death, loss, medical illness, etc.
  • 50% of people with only 1 episode
    • 2 episodes=70% of another
    • 3 episodes or more=95% chance of another
    • for most it’s a reoccurring chronic illness
  • Triggers to relapse over time are less and less (stress vulnerability model)
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5
Q

What are the five possible outcomes that may occur during the THREE phases of tx of Depression

A
  • Three phases of tx:
    • Acute
    • Continuation
    • Maintenance
  • Five Possible Outcomes (5 R’s)
    1. Response
    2. Remission
    3. Relapse
    4. Recovery
    5. Recurrence
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6
Q

How does MD develop?

A
    1. Genetic predisposition – smaller hippocampus, abnml serotonin transport protein
    1. Poor psychological coping strategies or skills- secondary to trauma, loss, dysfunction, societal situations, etc (lack of resiliency)
    1. Triggering events – Biological (could be medicines, substances, diseases), psychological, environmental
    1. Change in brain processes and conceptualization that cause us to interpret external or internal stimuli in different ways - negative cognitions, pessimism, physical changes, withdrawal, retreat, lack of rewards, altered self awareness
    1. These symptoms hinder our ability to reach our previous neurobiological homeostasis/return to nml via neurogenesis through enrichment:
      * Social connection
      * Exercise
      * New learning
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7
Q

MD Pathophys

A
  • neurodegenerative brain disorder, but we do not yet have a biological marker!
    • The closest marker we have is the theory of chronic low level increases in cortisol secondary to stress which causes a disruption in healthy neurogenesis and may add to neurodegeneration.
    • inbalance occurs
  • Genetics and epigenetic are involved and it is a very heterogeneous phenomenon.
  • the longer the depression in untx the greater the chronicity of illness and evidence of physiological brain changes
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8
Q

What are the FOUR theories of MD…NIMS!

A
  1. Monoamine theory
  2. Inflammatory theory
  3. Structural theory
  4. Network hypothesis
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9
Q

Monoamine hypotheses of Depression

A
  • Traditionally the theory of low levels of 3 major neurochemicals involved in emotions…chemical inbalance
  • The monoamines (norepinephrine, dopamine, and serotonin) have been widely implicated in depression.
    • The data are particularly voluminous for serotonin.
  • All present antidepressant drugs affect changes in one or more of these systems
  • this theory is an oversimplification of this heterogenous disorder
  • Serotonin PW: mood, memory processing, sleep, cognition
    • Raphe nucleus
  • DA PW: reward (motivation), pleasure, euphoria, motor fxn (fine tuning), compulsion, perseveration
    • frontal cortex, nucleus accumbens, VTA, striatum
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10
Q

Inflammatory theory

A
  • Low levels of chronic inflammation from a or b produce a TOXIC inflammattory milieu:
    • a. active illness (SLE or CAD)
    • –OR– b. persistent heightened level of corticosteroids from “stress”
  • neurodegeneration increases and neurogenesis is inhibited.
  • IL-6 which interferes w/ serotonin metabolism=main culprit.
  • cytokines also create disruption of other end-organs and create higher risk for heart disease and Alzheimer’s.
  • Hypersecretion of cortisol (Cushing’s dz) can cause acute and more severe depression.
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11
Q

Structural theory

A
  • Depression is caused by abnml changes in brain areas that can be identified premorbidly and are exacerbated in active illness.
  • Atrophy of the prefrontal cortex, amygdala, and hippocampus and enlargement of the insula and anterior cingulated cortex done via MRI suggest this.
  • Enhancing neurogenesis in atrophied areas (BDNF infusion into the rat hippocampus-quickly alleviated depression) or altering GABA (neuronal excitatory/inhibitory) in the insula are areas of exploration.
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12
Q

Network hypothesis

A
  • It is not specifically an altered brain area that causes depression but aberrancies in the tracts between areas.
  • Diffusion tension imagery has revealed white matter abnormalities in the tracts between the medial prefrontal cortex, amygdala, and hippocampus.
    • also PET scans show major changes
  • Glucose activity:
    • REDUCED in the hippocampus and dorsolateral prefrontal cortex
    • INCREASED in the amygdala, ventral striatum, and subgenual cingulated gyrus (an area that is stimulated by deep brain stim).
  • Sertoninergic agents reactivate a juvenile-like plasticity in the neuronal tracts which if also stimulated by nml external phenomenon or psychotherapy = recovery.
  • Depression will only improve if neurogenesis can occure in those tract to return the ineraction and perceptions to nml
  • Depression is therefore a result of miscommunication and misinterpretation of various brain regions involved with interpreting emotions.
    • less neurons, less firing, and less connection
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13
Q

What happens with untreated/undertreated depression?

A
  • The longer the depression the greater the chronicity of illness
    • <6 months=60% chance of remission
    • >24 months=10 –15 % of remission
  • Depression leads to future risk factors for:
    • 1) More Major Depression
    • 2) Other Co-Morbid Psychiatric illnesses
      • 60% of the time – EtOH and anxiety disorders are most common
    • 3) Cardiac events-CAD (cytokines and inflammation)
    • 4) Neurological events-strokes, seizures, Parksonism, dementias (Alzheimers)
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14
Q

Other MD Etiologies

A
  • Psychological: loss, abandonment, lack of nurturing, emptiness, anger turned inward, developmental arrest at a dependent stage with a disordered parent, low self esteem, failures, lack of self object stability and consistency
  • Environmental: poverty, deaths, famine, wars, oppression, abuse, torture, drugs, learned helplessness, side effects of medications, chemical toxins, infectious diseases, medical conditions
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15
Q

Biophysical formulation

A
  • major depression is NOT a homogenous entity, may respond to numerous approaches
  • in order to achieve the best outocme, need to understand the pt and all the variables effecting their presentation
  • empahsis on tx is based on combo of your understanding and their conception of their illness
  • biological, psychological, and/or environmental or social
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16
Q

Condition which may CAUSE or MIMIC MD: Medications

A
  • **Corticosteroids
  • OCP
  • ANTI-psychotics
  • Immunosuppresives (AIDS)
  • Interferons
  • Reserpine
  • Isotretinoin (acne tx-Accutane)
  • Propranolol/Beta-Blockers
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17
Q

Condition which may CAUSE or MIMIC MD: Infectious

A
  • **Mononucleosis (EBV)
  • Tertiary syphilis
  • Toxoplasmosis
  • Influenza
  • Viral hepatitis
  • HIV
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18
Q

Condition which may CAUSE or MIMIC MD: Endocrine and Metabolic/Nutritional

A
  • Endocrine (hyper or hypo):
    • -thyroidism
    • -adrenocortical function
      • Cushing’s and Addison’s
    • -parathyroidism
    • Diabetes
  • Metabolic/Nutritional
    • uremia
    • pellegra
    • anemia
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19
Q

Condition which may CAUSE or MIMIC MD: Neurologic

A
  • Temporal lobe epilepsy
  • Frontotemporal dementia
  • Parkinson’s
  • Huntington’s
  • Subdural hematoma
  • Head trauma
  • Strokes
  • MS
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20
Q

Condition which may CAUSE or MIMIC MD: Neoplasms and Substances

A
  • Neoplasms
    • Lymphomas
    • Abdominal malignancies (**pancreatic CA)
    • Brain tumors
  • Substances
    • **ALCOHOL
    • **HEROIN
    • **MJ
    • prescribed psychotropics (may MIMIC depression):
      • Benzodiazepines
      • Opiates
      • ANTI-psychotics
      • …substance/medication induced MD
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21
Q

Condition which may CAUSE or MIMIC MD

A
  • Medications
  • Infectious
  • Endocrine
  • Metabolic/Nutritional
  • Neurologic
  • Neoplasms
  • Substances
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22
Q

**A GOOD medical work-up**

A
  • Medical work-up is always a good first step even if the symptoms are quite definitive for MD
    • Hx, PE, labs
  • If there is an underlying medical condition it is usually quite obvious from other signs and symptoms
    • Depression and the medial illness may co-exist-cant just tx one alone
  • BUT remember to come back to the depression
  • Whenever you hear hoof beats it’s most likely to be HORSES and not a Zebra
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23
Q

DSM 5 additional specifiers for MD diagnoses

A
  • With anxious distress
  • With mixed features (anxiety and sadness)
  • With melancholic features
    • mood worse in am, terminal insomnia, excessive guilt, marked wt loss, total lack of pleasure (anhedonia)
  • With atypical features
    • wt gain, over-sensitive mood reactivity, oversleeping, leaden paralysis- feel like can’t move arms/legs
  • With mood congruent psychotic features- about 10% of episodes:
    • hallucinations and delusions that have depressive content “I feel like I am rotting, the devil is telling me bad things”
  • With mood in-congruent psychotic features
  • With catatonia
  • With peripartum onset
  • With seasonal pattern
    • 20% in Chicago’s latitude have an element of this
    • worse in winter: wt gain and sluggishness
    • spring: wt loss and hyper
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24
Q

Other disorders and variants on MD

A
  • important to identify other disorders as tx and prognosis may be different
  • in some cases removing the offending agents or condition may make big difference in outcomes
    • Ex: substance-EtOH, dz state-hypOthyroidism
  • diagnosis is ultimately never as important as treating the pt for their unique circumstances
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25
Q

Persistent Depressive Disorder

A
  • accounts for (2-3%)
  • 2 years of duration
  • less common and less responsive to therapy
  • depressed mood for most of the day on more days than not- course tends to be non-remitting
  • TWO of the following Six (lots of similarities to MDD)
    • poor appetite -or- overeating
    • low energy/fatigue
    • insomnia -or- hypersomnia
    • low self-esteem
    • poor concentration -or- difficult decision making
    • feelings of hopelessness
  • Has never been free of symptoms for >2 mo, no signs of other significant mental disorder that would explain symptoms
  • can have Major Depressive Disorder on top of this disorder
26
Q

Premenstrual Dysphoric Disorder

A
  • In the majority of menstrual cycles at least 1 of the following need to be present during the final week before start of menstruation:
    • Marked affective lability
    • Marked irritability and anger or interpersonal conflicts
    • Marked depressed mood, feelings, or hopelessness
    • Marked anxiety, tension, and/ or feeling on edge
  • At least 1 of the following also needs to be present
    • Decreased interest
    • Poor concentration
    • Lethargy
    • Change in appetite
    • Hypersomnia or insomnia
    • Sense of being out of control
    • Physical symptoms-breast tenderness, bloating, muscle pain
  • Must have a total of 5 or more of the above
  • Causes significant distress or impairment
  • Not an exacerbation of another similar disorder- i.e. Major Depression
27
Q

MDD specifiers-Melancholia

A
  • severe type of depression
  • MD but also:
    • lack of reactivity of any pleasure situation
    • early AM mood wordse
    • early morning awakening
    • marked agitation or retardation
    • excessive guilt
  • **use of ANTI-depressants essential
  • DST usually positive-clear HPA axis dysfxn
28
Q

MDD specifier-ATYPICAL

A
  • oversleeping
  • overeating
  • leaden paralysis
  • interpersonal sensitivity
  • mood reactivity-leading to roller-coaster type of mood
29
Q

MDD specifier-Psychotic (10%)

A
  • MDD features but also presence of psychotic element
  • NIHILSM-there is no future-the world will end
  • DELUSIONS-“I am bad”, “I have caused others to be poisoned”, “I have cancer in my bowel-I am rotting from the inside”
  • HALLUCINATIONS-usually negative; usually auditory
  • use of ANTI-psychotic or ECT essential
  • newer agents (SSRIs) may not work as well
  • DO NOT confuse with schizophrenia
  • be careful to rule out Bipolar
30
Q

MDD specifier-Seasonal

A
  • 20% of ppl at this latitude have a seasonal mood fluctuation
  • sxs similar to atypical depression but pts tend to become hyper in the summer
  • worst pt of yr is Oct-Feb
  • light therapy helps 50% (ANTI-depressants just as effective)
31
Q

MDD vs. Bereavement

A
  • Bereavement not classified as a psychiatric disorder
  • For majority of ppl its a nml life rxn – it is expected that someone will feel empty and grieve the loss.
  • may have depressed mood, irritable, take some time off, not sleep well, etc. –
    • These symptoms come in waves but the indiv can still experience pleasure & joy.
  • grieving & mourning is cultural based- expectations are that by 3 mo. many of the symptoms have resolved and the person moves on with their life.
  • However, losses are a precipitant of MDD and one should not hesitate to tx as an MDD if symptoms are severe enough.
  • Complicated (pathological) grief often involves many symptoms of PTSD on top of MDD and bereavement
    • these individuals get stuck on the loss and can’t progress
    • aggressive tx is indicated
  • Stronger (abnml) signals that indicate a more severe condition:
    • guilt about life areas outside of the death
    • worthlessness psychomotor retardation
    • sustained suicidal ideation
    • prolonged fxnl impairment
32
Q

Stages of Bereavement

A
  • numbeness-hours to days (seldome wks)
  • depression-few wks to <1 yr
    • exacerbation son holidays, birthdays, other memorable events
      • insomnia, restlessness, irritability
  • some days good, some bad
  • recovery-usually <6 months
    • accept the loss and return to a pre-morbid level of functioning which might include previous or new roles
  • most ppl start to feel better 6-10 wk after the death
33
Q

Do you treat uncomplicated bereavement?

A
  • most ppl are resilient and do fine
  • if concerned about MDD consider:
    • past hx
    • intensity and duration
    • pervasiveness of symptoms
  • dont wait to normalize-longer the delay to tz the depression the worse the prognosis
34
Q

DSM-5 Adjustment Disorder

A
  • some signs of depression that cause clinical concern (significant emotional or behavioral disturbances) in response to an acute stressor that occurred within 3 months of the onset of symptoms.
  • does NOT meet criteria for other (more significant) disorders
  • once the stressor is removed the symptoms should abate within 6 months
  • can be depressed/anxious/behavioral in nature
  • Usually brief therapy or social interventions are all that is needed
35
Q

Agitated/Anxious

A
  • diagnosis often missed because of absence of sadness
  • high risk of acting out and suicidal or homicidal potential
  • seen often in ELDERLY and ADOLESCENCE
  • watch for substance induced
36
Q

Special Population-ELDERLY Depression

A
  • often masked depression
    • irritable, angry, agitated, (more common than sadness), dont care
    • often somatic in presentation to point of delusional dementia
    • cognitive changes often confused with dementia
  • new incident rate increases past age 65
  • suicide rate highest in elderly males
  • highest growing population
  • misconception that it is a part of aging or is not treatable
  • less likely to seek out help
  • response rate to intervention is just as good as adults
37
Q

Special Population-TEEN Depression

A
  • high risk for impulsive actions
  • often missed because of teenage angst misconception
  • teens aware of what depression is-they dont trust adults
  • high risk suicide group
  • tx intervention available-more controversial and variable (potentially harmful)
  • most severe mental illnesses start now
  • irritability often prominent
  • sadness present but hidden by irritability
  • acting out behavior
  • impulsivity/recklessness
  • substance experimentation, change in friends, grades, behaviors
  • withdrawn
38
Q

Bipolar I Disorder

A
  • Individuals with Bipolar Disorder suffer a life-long illness that can devastate their lives & their families’ lives.
  • classic forms of Bipolar I are relatively uncommon (0.6-0.8% of the general population)
    • if Bipolar variants are included the prevalence may be as high as 4-6% of the pop = significant national health issue.
  • To be diagnosed you must have experienced at least one Manic episode, although most commonly there will be episodes of Major Depression and other mood states in the hx.
  • Diagnosis is often ignored or missed because of lack of good hx taking
    • missing diagnosis leads to morbidity and delay of tx (avg=5 yrs)
    • tx are very helpful if applied
39
Q

What is a manic episode (DSM-5 Criteria)?

A
  • A. A distinct period of abnormally and persistent elevated, expansive, or irritable mood present for most of the day for at least 1 week duration
  • B. During the period of mood disturbance at least 3 of the following are
  • present (FOUR if the mood is only irritable)
      1. Inflated self-esteem or grandiosity
      1. Decreased need for sleep
      1. More talkative than usual or pressure to keep talking
      1. Flight of Ideas or subjective experience of racing thoughts
      1. Distractibility
      1. Increase in goal-directive activities or psychomotor agitation
      1. Reckless behaviors in pleasurable areas (have consequences)– buying, speeding, sexual indiscretions, foolish business ventures
  • C. Marked impairment in functioning in job, social activities, or relationships with others -or- there are psychotic features
  • D. Symptoms not caused by a substance or medical condition
40
Q

Cycling between Mania and Depression

A
  • Individuals usually cycle clearly f/m Mania to Depression over the course of wks to mos.
  • Some pts will end up with a Mixed Bipolar state where they will have symptoms of BOTH mania and depression at the same time.
    • Often these individuals are very refractory to treatment.
  • a cohort of bipolar individuals:
    • 40-45% of time spent in a depressive phase
    • 5-10% hypomanic or manic phase
    • 45% euthymic state
  • 2/3 of pts never make it back to their pre-morbid level of functioning.
    • Even when indivs are euthymic there is evidence of brain fxn abnormalities.
    • math, reasoning, and informational processing abilities are impaired.
    • Verbal memory, attn, and executive functioning < baseline.
  • Life span decreased by 8-10 yrs primarily due to metabolic syndrome co-morbidities and a 15-20x higher risk of suicide.
  • Their insight into their illness is always suspect leading to issues of substance abuse, non-compliance with meds/tx, and potentially challenging life courses
41
Q

Epidemiology (Types) of Bipolar

A
  • Bipolar I: 0.6-0.8% lifetime prevalence
  • Bipolar II: 0.5-0.8% lifetime prevalence
  • Bipolar spectrum: 4-6% lifetime prevalence (controversial)
  • ……………………………………
  • bipolar secondary to medical conditions (depression) or substances
  • M=W
  • **higher socioeconomic
  • onset late adolescence, early adulthood
  • strong genetics:
    • MZ twins: 65-80%
    • DZ twins: 10-15%
    • 1 rent: 10%
    • 2 rents: 50%
  • much greater chance of becoming psychotic
  • pathophys of depressed phase looks v. similar to MDD on neuroimaging
42
Q

What are the hints that a person might be bipolar when presenting with depression?

A
  • Early age onset (before age 20)
  • Psychotic Depression
  • 1st episode of depression is postpartum especially if psychotic
  • Rapid onset and offset of depressive symptoms
  • Recurrent depression with > 5 episodes
    • non-responsive to usual intervention
  • Bipolar FHx
  • Seasonal Mood Disorder
  • Atypical Depression
  • Hypomania associated w/ ANTI-depressants
  • Repeated loss of efficacy of ANTI-depressants over time
  • Trait mood lability, hyperthymic temperament
  • Depression w/ mixed mood states
    • many anxious or mixed hyper features-racing, irritable, hostile
  • Bipolar symptoms (hypomania) can at time be imitated by substances (i.e. cocaine, caffeine, prednisone) or general medical conditions (i.e. hyperthyroidism, closed head injury)
    • good medical work-up is always a first step to diagnosis.
43
Q

Distinguishing Bipolar Disorders

A
  • Bipolar I: a manic episode (depressive episode is not needed, although usually occurs)
  • Bipolar II: hypomanic symptoms-at least 4 days in a row; at least 3 symptoms on mania, but not severe enough to cause impairment in functioning or hospitalization
    • no psychosis, must hv a hx of MDD
  • Cyclothymic Disorder-2 yr duration
    • hypomaniac symptoms at times, but depression never to point of MD or BPI or BPII criteria
  • (BP unspecified:)
    • potential pts who have some symptoms of mania and hypomania at times, but never enough to meet full criteria
    • anyone with significant mood fluctuations and irritabilit that are not induced by substances
44
Q

Bipolar Pathophys-General

A
  • neurodegenerative process even when the mood is stable-evidence of cognitive changes in verbal memory, attn, and executive functioning
  • in depression the neuroimaging looks similar to MD, but mania involves activation of many areas
  • with age there is a cerebral atrophy and the brains look more similar to schizophrenia
  • pts with bipolar have enlarged ventricles and increased white matter HYPERdensities
45
Q

Bipolar cellular pathophys

A
  • use of anticonvulsant leads to theories on calcium or sodium gate abnormalities and stabilization of neuronal pathways
  • some evidence of a specific gene defect associated with chrom 18q or 22q in linkage studies
46
Q

Course of Bipolar illness

A
  • only 1/3 recover at 1 yr out
  • most bipolar will gravitate to the depressive end of the spectrum
  • only 50% were working at 3 yrs after the diagnosis
  • impulsivity, addictions, distractibility lead to high co-morbidity and potential suicide
  • **medications are essential along with support
47
Q

Suicide Epidemiology

A
  • 10th leading cause of death in the US
  • >43k ppl in 2013 in US
    • over 460k suicide attempts documented
  • devastating action that effects both families of the victim (guilt, anger, loss, shame) and for HC providers
  • major emphasis in clinical practice to prevent suicide-lots of screening for this and moos disorders
48
Q

Suicide Statistics/Epidemiology

A
  • 12.9/100,000 per yr in the US
  • Males – 19.9
  • Females-5.5
  • Caucasions-14.1
  • Asians-6.2
  • African-American-5.1
  • Hispanics-5.9
  • Adolescents- 10.5(but often give the least warning and most impulsive)
  • Elderly- 17.6 (often sudden and told of a terminal disease)
  • Middle age(45-64)- 18.6 – now the top risk group demographically
  • Veterans - 34.9 – transition back makes them vulnerable
  • >90% of the time there is the presence of a mental disorder
  • bipolar (15x nml)>Schizophrenia>MDD
    • anxiety disorders, eating disorders, and substance use disorders also high on the list
  • greatest risk of suicide is within inthe 1st yr of diagnosis
49
Q

Suicide Terminology

A
  • suicide ideation
  • suicide plan or intent
  • suicide attempt
  • completed suicide
  • self harm-no desire to die, but instead an attempt to relieve pain or feel smthg real; overlap exists and needs to be explored
  • 34% of those with suicide ideation think of plan
  • 72% of those with a plan try to attempt
    • 51% firearms
    • 25% suffocation- usually hanging
    • 17% poisoning
  • There are probably many more deaths due to suicide that are not documented- single passenger accidents, drowning, accidental OD, stigma preventing MD from listing true reason on death certificate because of the family desire or insurance reasons.
  • 3F:1M attempted suicide
  • 4M:1F successful suicide
50
Q

Suicide Ideation

A
  • relatively common symptom (20% of adolescence will experience this at some pt; 10% of adults in any given year)
  • usually present when someone is under a lot of stress and feels there is no way out.
  • illustrated by statements such as “I wish I were dead”, “The world would be a better place without me”, “I wouldn’t mind if I developed cancer and died”.
  • These thoughts are often fleeting but can begin to persist on a daily basis.
51
Q

Suicidal intent

A
  • Thoughts have moved to thinking about how someone would commit suicide.
  • Looking on websites, asked others, have begun to secure the means to commit suicide or thought out when/how
52
Q

Suicide attempt

A
  • actual carrying out of an act that could end one’s life.
  • The degree to which the attempt might be lethal depends a lot on the means and the place of action.
  • ratio of attempts:completions=12:1.
  • 460k attempts/yr in the US that are evaluated in the ED.
  • Determining whether someone really wanted to die vs just relieve pain or get help is essential in psychiatric triage.
53
Q

Suicide RF

A
  • **70% who die decide in last 10 minutes of life (impulsive decision)
  • currently has a feasible plan in mind
  • x hx of prior attempts
  • x psychosis (especially command hallucinations)
  • x high anxiety
  • x impulsivity
  • x presence of a mental disorder
  • x substance abuse (especially if intoxicated)
  • x hopelessness
  • x lack of support
  • x Fhx of completed suicide
  • x significant negative life event in the last 3 mo
  • x presence of guns in the house
54
Q

Suicide Pathophys

A
  • Lower serotonin receptor numbers
  • Lower serotonin levels in the CNS
    • Both of these are done post mortem=useless
    • some recent PET scans claim that they can identify which individuals are more likely to resort to suicide attempts
  • Lack of effective coping strategies, presence of impulsivity also have strong correlation with attempts.
  • Most ppl who call or show up in the ED for suicidal thoughts are wanting to live and are asking for help.
55
Q

Suicide Prevention

A
    1. Ask- you will never put the thought of suicide into someone’s mind
    1. Use behavioral incidents (as taught in interviewing skills) and appropriate gates– details are important in such a sensitive area
      * “What exactly were you thinking”
      * “Did you actually go out and buy a gun?”
      * “What did you plan to do with it?”
    1. Do a risk analysis based on each patient’s unique situation
    1. Remove the means; triage the pt and make sure theyre safe
    1. Explore each person individually for risk analysis-combination of risks and protective measures
      * support, faith, or religion, on medication, having children
56
Q
A
57
Q
A
58
Q
A
59
Q
A
60
Q
A