diag treat mood
TRANSCRIPT
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Diagnosing and Treating
Mood Disorders: The Scienceand Ethics
Chris Trimble, Leo Huizar, Fredah Kabbech,
Megan Sieveke, Brandon Butler
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Mood Disorders
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Depression Can refer to either:
± A mood: a pervasive
and sustainedemotional response
± A clinical syndrome:
a combination of
emotional, cognitiveand behavioral
symptoms
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How To Distinguish
Depression From NormalSadness The mood change is pervasive across situations and
persistent over time
The mood change may occur in the absence of anyprecipitating events
The depressed mood is accompanied by impairedability to function in usual social and occupationalroles
The change in mood is accompanied by a cluster of additional signs and symptoms
The nature or quality of the mood change may bedifferent from that associated with normal sadness
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Four Types of Symptoms
Associated With MoodDisorders Emotional
Cognitive Somatic
Behavioral
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Cognitive Symptoms Involve changes in the way
people think about themselves
and their surroundings Depressed people may have
trouble concentrating and areeasily distracted
Preoccupation with guilt andworthlessness
Manic patients report sped upthoughts and ideas
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Somatic Symptoms Related to basic
physiological or bodily
functions
Include fatigue, aches
and pains, and serious
changes in appetite or sleeping patterns
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Behavioral Symptoms Changes in the things that
people do and the rate at
which they do them Psychomotor retardation
often accompanies the
onset of depression
Manic patients show
energetic, provocative and
flirtatious behavior
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Diagnosing Mood Disorders Defined in terms of
episodes
± discrete periods of time in which the
person¶s behavior is
dominated by either
a depressed or
manic mood
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Major Depressive Episode Five or more of the following symptoms
must have been present during the
same two week period and represent a
change from previous functioning
At least one of the symptoms is either
± Depressed mood
± Loss of interest or pleasure
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Major Depressive Episode
Symptoms Depressed mood most
of the day, nearly everyday
Diminished pleasure inall, or almost allactivities
Significant weight loss
(without dieting) or weight gain
Insomnia or hypersomnia nearlyevery day
Psychomotor agitationor retardation
Fatigue or loss of energy
Feelings of worthlessness or guilt
Diminished ability to
think or concentrate Recurrent thoughts of
death or suicidalideation
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Manic Episode A distinct period of abnormally and
persistently elevated, or expansive
mood, lasting at least one week
During the period of mood disturbance,
three of more of the following symptoms
have persisted and have been presentto a significant degree
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Manic Episode Symptoms Inflated self esteem
or grandiosity
Decreased need for sleep
More talkative than
usual
Flight of ideas
Distractibility (drawn to
unimportant stimuli)
Increase in goaldirected activity
Excessive involvement
in pleasurable activities
that have a high
potential for painful
consequences
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Mood Disorders Two primary types:
± Unipolar mood disorder: the person
experiences only episodes of depression
± Bipolar mood disorder: the person
experiences episodes of mania as well as
depression
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Types of Mood Disorders and
Frequency
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Types of Mood Disorders Unipolar Mood
Disorders
± Major Depressive
Disorder
± Dysthymic Disorder
Bipolar Mood Disorders
± Bipolar I Disorder
± Bipolar II Disorder ± Cyclothymic Disorder
Subtypes
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Major Depressive Disorder One or more major
depressive episodes
No manic or unequivocal hypomanicepisodes
Lifetime prevalence of 15%
Major DepressiveDisorder 15% suicide
mortality VA 1991 Study
± Major DepressiveDisorder mortality 38.7%
± 13% no psychiatricmonitoring
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Major Depressive Disorder Course is variable ± Some having episodes years apart, clusters of
episodes, and some with frequent episodesthroughout life
± Only about 20% have chronic episodes
After the first episode, 50%- 60% chance of asecond , and a 5%-10% chance of a manicepisode (i.e. developing bipolar I disorder)
After second episode, 70% chance of a third
After third episode, 90% chance of a fourth
The greater number of previous episodes is
an important risk factor for recurrence
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Major Depressive Disorder By definition, Major Depressive Disorder
cannot be due to:
± Physical illness, alcohol, medication, or streetdrug use.
± Normal bereavement.
± Bipolar Disorder
± 7Mood-incongruent psychosis (e.g.,Schizoaffective Disorder, Schizophrenia,
Delusional Disorder, or Psychotic Disorder Not
Otherwise Specified).
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Major Depressive Disorder
Co-occurring Disorders Substance Abuse
Anxiety
± 80 to 90% of individuals with Major DepressiveDisorder also have anxiety symptoms (e.g.,anxiety, obsessive preoccupations, panic attacks,phobias, and excessive health concerns).
Cancer, COPD (Chronic ObstructivePulmonary Disease), Pain, eating disorders
Causation: ± Meds: steroids
± Diseases: hypothyroidism
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Dysthymic Disorder Depressed mood for at least two years
Never without at least two of the
following symptoms for more than two
months
± Poor appetite or overeating, insomnia or
hypersomnia, low energy, low self esteem,poor concentration, feelings of
hopelessness
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Dysthymic Disorder No major depressive episode during the
first two years
Lifetime risk of 3%
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Bipolar I Disorder One or more manic episodes
Lifetime risk of 1%
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These positron emission tomography scans of the brain of a person with bipolar disorder show the
individual shifting from depression, top row, to mania, middle row, and back to depression, bottom row,
over the course of 10 days.
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Bipolar II Disorder One or more major depressive episodes
At least one hypomanic episode
± A hypomanic episode is a less severe version of
a manic episode.
No manic episodes
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Subtypes of Mood Disorders Melancholia: describes a particularly
severe type of depression
Psychotic features: when hallucinationsor delusions were present during themost recent episode
Rapid cycling: the person experiencesat least 4 episodes within a 12 monthperiod
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Subtypes of Mood Disorders Postpartum Onset:
when episodes begin
within 4 weeks after
childbirth
Seasonal affective
disorder: when the
onset of episodes is
regularly associatedwith changes in
seasons
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Prevalence of Mood Disorders Depression accounts
for more than 10percent of all disabilities
in the US Younger generations
are experiencing higher rates of depression, andthose who become
depressed are doing soat an earlier age
Depression affects 13-14 million people eachyear
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Prevalence of Mood Disorders Ratio of unipolar to bipolar is at least 5:1
Lifetime prevalence of all mood
disorders is 8%, ranked third behind
substance abuse disorders and anxiety
disorders
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Gender Differences
Women are two or three times more
vulnerable to depression than men
± Sex hormones, stressful life events,
childhood adversity, etc
± May be more likely to seek treatment
± May be more likely to be labeled asdepressed
No differences seen in bipolar disorders
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Children Statistics Up to 2.5% of children
in the US suffer from
depression
Up to 8.3% of
adolescents in the US
suffer from depression
Girls entering puberty
are twice as likely toexperience depression
as boys
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Types of Causes
Environmental Factors Psychological Factors
Biological Factors
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Environmental Factors:
Stress ± Levels of stress may vary from person to
person.
± Depressive episodes can make a personmore vulnerable to further episodes, so
small amounts of stress can activate
depression
³Learner Helplessness´- after experiencing
chronic or repeated stressful events, people
can learn to feel helpless
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Environmental Factors:
Substance Abuse
± Depression that is a result of drug abuse,
medication, or toxin exposure
± Associated with use and withdrawl from: alcohol,
amphetamine, cocaine, hallucinogens, inhalants,
opioids, phencyclidine, sedaitves, hypnotics and
anxiolytics
± Exposure or habitual use of chemicals can alter
brain structure and function resulting in
depression
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Environmental Factors:
Childhood Difficulties
± Depression can develop in children who haveexperienced a traumatic event including but not
limited to: Death of family member or friend
Natural disaster
Divorce
Loss of parent¶s job, home, etc...
± Many of these children are emotionally damagedor lack emotional development and often havedifficulties adjusting
± Traumatic Event may affect the development of the Limibic System
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Depression In Disease
Estimated 1/3 people with
chronic disease have
depression.
Alzheimer¶s
± Boston Study
14% had history of depression
HIV ± 1/3 estimated to have
depression
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C
ontinued« The rate for depression occurring with medical illness*:
± Heart attack: 40-65%
± C
oronary artery disease (without heart attack): 18-20% ± Parkinson's disease: 40%
± Multiple sclerosis: 40%
± Stroke: 10-27%
± Cancer: 25%
± Diabetes: 25%
*Reviewed by the doctors at The Cleveland Clinic Department of Psychiatry and Psychology.
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Psychological Factors Cognitive Vulnerability
± People responding differently to the same
negative experience involving loss, failureand disappointment
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https://www.depressionadvances.com/animation/brainAnimations.htmlhttps://www.depressionadvances.com/animation/brainAnimations.html
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HYPOTHYROIDISM COMMON SYMPTOMS DEPRESSION
Delayed reflexes Depressed mood Weight changes
Cardiac failure Apathy A ppetite problems
Cold intolerance Weight gain Sleep problems
Brittle hair Fatigue
Dry skin Impaired concentration
Thoughts of suicide
Delusions
Decreased appetite
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Biological Factors Neurotransmitters and Neurons
± The signal enters the neuron through the dendriteand proceeds through the cell body to the axonwhere it is switched from a electric signal to achemical one
± Theses chemical signals are calledneurotransmitters
Neurotransmitters can fit into many receptors, butreceptor sites can only receive specific transmitters
Upon release the transmitter is broken down by monoamine oxidase (MAO) or its taken back in by the neuronthat released it, called ³reuptake´
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Biological Factors Of the 30 or so known
neurotransmitters, depression effects
Serotonin, Norepinephrine, andDopamine
Depression has been linked to both low
and elevated Norepinephrineconcentrations.
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Biological Factors:
Serotonin The permissive hypothesis
of serotonin functionpostulates that the deficit incentral serotonergic
neurotransmission permitsthe expression of bipolar disorder but is not sufficientto cause it.
± According to this theory,both the manic and the
depressive phases of bipolar illness arecharacterized by low centralserotonin function but differ in high versus lownorepinephrine activity.
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Biological Factors:
Norepinephrine The catecholamine
hypothesis of affectivedisorders proposes thatsome forms of depression
are associated with adeficiency of catecholamineactivity (particularlynorepinephrine) atfunctionally importantandrengeric receptor sites inthe brain, whereas mania is
associated with a relativeexcess.
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Biological Factors:
Dopamine Evidence is
substantial that
enhanced dopamineactivity may play a
primary role in
psychotic
depression.
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Biological Factors: Hormones
± About one half of all depressed persons have a
high level of the hormone cortisol in their blood
± A person with a depressive mood disorder maynot have their hypothalamus regulating the cortisol
production in the adrenal gland correctly
± Normal cortisol levels peak at 8:00a.m. and
4:00p.m. for non depressed person, while a
person with depression may have the hormonereleased at a constant level
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Biological Factors: Genetics There is a 1.5 to 3% greater chance for a
person to develop a depressive disorder if aparent or sibling has it as well
± 50% of those with bipolar disorder have a parent
with history of clinical depression
± 25% of children of a parent who is bipolar develop
a depressive disorder
± 50-75% of children of two parents with bipolar
disorder develop a depressive disorder
Biological Factors: Twin
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Biological Factors: Twin
Studies If one twin develops depression there is a
76% chance that the other twin will develop a
disorder as well
± When raised apart the percentage is 67%
± Because this number is not closer to 100%, thereis indication that other factors are also responsible
Fraternal twins have a 19% chance of
developing a depressive disorder if the other
develops one
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Bipolar Causes
Relation to Person
w/Bipolar
Risk of Developing
Bipolar
2nd degree relative 1%Sibling 3-7%
Fraternal Twin 15-25%
One Parent 15-30%Both Parents 50-75%
Identical Twin 70%
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Causes of Depression
Depression has been
linked to size/function in
the temporal and frontal
lobes and the cingulate
gyrus. However, it is
unclear as to whether
the depression causes
the abnormalities or thedepression is a result of
the abnormalities.
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Treatments:
Unipolar Mood Disorders ± Cognitive Behavioral Therapy
± Antidepressant Medication
Bipolar Mood Disorders ± Lithium
± Anticonvulsant Medication
± Psychotherapy
Others ± Electroconvulsive Therapy
± Vagus Nerve Stimulation
± Transcranial Magnetic Stimulation
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Cognitive Behavioral Therapy
CBT combines bothcognitive therapy andbehavioral therapy
± Cognitive Therapyteaches a person howcertain thinking patternsare causing their symptoms-by giving thema distorted picture of
what's going on in their life, and making themfeel anxious, depressedor angry for no goodreason, or provokingthem into ill-chosen
actions.
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Cognitive Behavioral Therapy
± Behavioral Therapy helps patients weaken
the connections between troublesome
situations and their habitual reactions tothem. It also teaches them how to calm
their mind and body, so they can feel
better, think more clearly, and make better
decisions
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Cognitive Behavioral Therapy
Identification of Skill Deficits: ± Help patient to identify deficits so that they can
learn better ways to manage life
Evaluation of Life-Experiences ± Help patient develop realistic expectations about
life, and help distinguish between what the patientneeds and what they want
Self-talk ± Help patient identify negative self-talk, teach them
how to combat these thoughts and to replacethem with positive thought
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Cognitive Behavioral Therapy
Automatic thoughts ± Help patient identify negative automatic thoughts
and ways to replace these thoughts with positive
ones
Irrational ideas and Beliefs ± Teach patient how to identify their irrational
thoughts and how to differentiate between
irrational and rational thought Overgeneralizing and Catastrophizing
± Help patient identify and change negativeovergeneralizations
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Cognitive Behavioral Therapy
Cognitive Distortions
± Help patient determine what evaluations
are distortions by providing objectivefeedback of their evaluations of the world
Pessimistic Thinking
± Help patient develop more optimistic viewof world
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Treatment:
Antidepressants Four types of drugs are used in the
treatment of depression and other
associated mood disorders: ± Tricyclic antidepressants
± Monoamine Oxidase Inhibitor
± Selective Serotonin Reuptake
Inhibitors ± Serotonin Norepinephrine
Reuptake Inhibitors
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Tricyclic Antidepressants
From 1960s until late 1980s, tricyclic
antidepressants represented the major
pharmaceutical treatment for depression
They still provide the surest
antidepressant response for moderatelyto severe depression
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Tricyclic Antidepressants
TCAs work by increasing the
concentration of norepinephrine and
serotonin in certain regions of the CNS TCAs impede the reuptake of
norepindephrine and serotonin
They are safe and effective for up to80% of patients
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Tricyclic Antidepressants
There are two broad chemical classes:
± Tertiary Amines
They have a greater effect in boostingserotonin than norepinephrine.
± amitriptyline, imipramine, trimipramine and doxepin
± Secondary Amines
Greater increase of norepinephrine levels ± nortriptyline, desipramine, and protriptyline
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Monoamine Oxidase Inhibitors
MAOIs treat depression by inhibiting theeffect of monoamine oxidase which causesthe concentrations of serotonin,norepinephrine and dopamine to increase
Most doctors will not prescribe MAOIs unlessa patient is not responding to other antidepressants
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Monoamine Oxidase Inhibitors
Definitely Effective ± Atypical Depression
± Major Depression
± Dysthymia ± Melancholia
± Panic Disorder
± Bulimia
± Atypical facial pain
± Anergic Depression ± Treatment-resistant
depression
± Parkinson¶s Disease
Other Possible Uses
± Obsessive-
complusive Disorder ± Narcolepsy
± Headache
± Chronic pain
syndrome ± Generalized anxiety
disorder
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Selective Serotonin Reuptake
Inhibitors SSRIs work by inhibiting the reuptake of
serotonin into the neuron that made it
Includes fluoxetine and paroxetine
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Serotonin Norepinephrine
Reuptake Inhibitors This class of drugs is most recent
addition to the family of antidepressants
and has a structure and chemical profilethat distinguishes them both tricyclic
antidepressants and SSRIs.
Work by increasing levels of Serotoninand Norepinephrine by inhibiting their
re-absorption back into the cell.
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Venlafaxine
Venlafaxine inhibitsserotonin andnorepinephrine
reuptake withoutsignificant effects onmuscarinic, cholinergic,histaminic, or alpha-andrenergic receptors.
Therefore, venlafaxineactivity is similar totricyclics and SSRIs buthas a less adverseside-effect profile.
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Treatments:
Antidepressants 50-65% of people given an
antidepressant show much
improvement over 3 months, comparedto 25-30% of people given a placebo.
± Indicates that although drug is effective,
antidepressants, like most medicines, may
have some benefits due to placebo affect
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Treatments:
Antidepressants Medication must be used every day or
at every time prescribed. If not taken
correctly treatment will not be effectiveand may have adverse effects.
Antidepressants will usually take 1-2
weeks work, however some may takeup to six weeks
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Treatments:
Antidepressants On the basis of clinical research and
experience, the consensus is that most
people can be taken off their antidepressants after six to eight
months of clinical response without
doing worse than patients continuing onthe drug
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Bipolar Treatments
Psychiatric Management
Acute Treatment
Maintenance Treatment
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Psychiatric Management
At this time, there
is no cure for
bipolar disorder; however, treatment
can decrease the
associated morbidity and
mortality.
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Bipolar Treatments:
Lithium Lithium is prescribed to people with
bipolar disorder to even out the ³highs´
and ³lows.´ Because bipolar disorder requires long
term treatment, a patient may have to
take Lithium for many years, often incombination with other antidepressants
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Bipolar Treatments:
Lithium Lithium interferes with the synthesis and
reuptake of chemical messengers by which
nerves communicate with each other (neurotransmitters). Lithium also affects the
concentrations of tryptophan and serotonin in
the brain.
Lithium's effects usually begin within oneweek of starting treatment, and the full effect
is seen by 2 to 3 weeks.
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Bipolar Treatment:
Anticonvulsants Often prescribed to patients who do not
respond to lithium
Include carbamazepine (Tegretol) or valproic acid (Depakene)
More than 50% respond positively tothese drugs
Reduce the frequency and severity of relapse
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Treatments:
Electroconvulsive Therapy ± Patient is put to sleep and temporarily paralyzed,
so that their muscles do not contract and causeinjuries like fractures. An electric current is then
run through the brain to initiate a seizure. ± ECT is sometimes the most effective, rapid
method of treating severe major depressivedisorder (MDD).
for patients with poor response to medications,
poor tolerance of usual antidepressants, severe vegetative symptoms,
or psychotic features
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Treatment:
Vagus Nerve Stimulation VNS stimulates the limbic
system, a group of relatedstructures that affect mood,motivation, sleep, appetite,alertness and other factors
commonly altered bydepression.
VNS is delivered to the leftcervical vagus nerve by theNeuroCybernetic Prosthesis(NCPâ) System which isimplanted just under the skin inthe left chest area. ± Delivers a pre-programmed,
intermittent electrical pulse tocervical vagus nerve 24 hours aday
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Transcranial Magnetic
Stimulation TMS is a procedure in
which the electrical
activity in the brain is
influenced by amagnetic pulse.
This procedure can be
used to alter function of
certain areas of thebrain, especially those
involved in depression
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Side Effects of Treatments
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Side Effects:
Tricyclics Initially:
they cause blurredvision
Constipation Light-headedness when
standing or sitting upsuddenly
Dry mouth
Difficulty urinating
Feelings of confusion
Cognitive Dysfunction
± A small percentage of
people will have other
side effects such as:
sweating, a racingheartbeat, low blood
pressure, allergic skin
reactions or sensitivity
to the sun.
± Side effects usually
disappear oncetherapeutic effects if
medication take hold
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Side Effects:
Tricyclics More serious side effects, although rare,
can be aggravation of narrow angle
glaucoma and seizures Some tricyclic side effects relate to the
fact that these medications have similar
effects on other neurotransmitters in theCNS, notably histamine and
acetylcholine
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Drug Interactions:
Tricyclics Drug Interaction MAOIs Stroke, hypertension
Norepinephrine Large increase in blood
pressure and incidence of arrhyhmias
Phenothiazines Psychosis, agitation
Barbiturates Increase heteocyclicmetabolism
Cimetidine Blocks metabolism of heterocyclics
Haloperidol Can block metabolism of heterocyclics
Methylphanidate Blocks metabolisms of heterocyclics
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Side Effects:
MAIOs Drowsiness
Constipation
Nausea
Diarrhea Stomach upset
Fatigue
Dry mouth
Dizziness
Low blood pressure Lightheadedness, especiallywhen getting up from a lyingor sitting position
Decreased urine output
Decreased sexual function
Sleep disturbances
Muscle twitching Weight gain
Blurred vision
Headache
Increased appetite
Restlessness Shakiness
Trembling
Weakness
Increased sweating
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Drug Interactions:
MAOIs Because of the extensive inhibition of
monoamine oxidase by MAOIs
enzymes raises the potential for anumber of drug interactions.
± Many of these interaction occur with over-
the-counter medications
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Drug Interactions:
MAOIsDrug InteractionOther MAOIS Increase risk for side effect;
covulsions
TCAs, Carbamazepine, Hypertension; convulsions
Cyclobenzaprine
SSRIs Serotonin Syndrome
Stimulants (dextromamphetamine); Increased blood pressure
Busirone
Meperidine Potentially fatal interaction
Dextromethorphan Brief psychosisDirect Sympathomimetics Increased blood pressure
Indirect Sympathomimetics Hypertensive crisis possible
Oral Hypoglycemics (insulin) May worsen hypoglycemia
Fenfluramine, L-Tryptophan Serotonin Syndrome possible
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Food Interactions:
MAOIs MAOIs inhibit
monoamine oxidase in
gut that is responsible
for the break down of tyramine. A build up of
tyramine can lead to a
sudden increase in
blood pressure and a
chance of heart attack
or stroke.
Food Restrictions ± Avoid:
Cheese, overripe agedfruit, fava beans,
sausage, salami, sherry,liquors, sauerkraut,monosodium glutamate,pickled fish, brewer¶syeast, beef and chickenliver, fermentedproducts, red wine
± Used in moderation
Coffee, chocolate,colas, tea, soy sauce,beer, other wines
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Side Effects:
SSRIs loss of appetite, weight loss
increased appetite, weight gain
allergic reactions
dry mouth
irritability / anxiety
sleeplessness drowsiness
headache
shaking
dizziness
fits / convulsions
disturbance of sexual function (but
this is also a feature of depression) sweating
bruising
manic or hypomanic behaviour
shaking
dizziness
fits / convulsions
disturbance of sexual function
(but this is also a feature of depression)
sweating
bruising
manic or hypomanic behaviour
abnormal movements
low sodium level
suicidal ideas abnormal movements
low sodium level
suicidal ideas
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Drug Interactions:
SSRIs
Although the potential for interaction
does exist, SSRIs are not associatedwith many of the interactions are seen
with other antidepressants
± Paroxetine and fluvoxamine have been
associated with increased bleeding when
given with wafarin
± Does not effect Lithium levels
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Suicide and SSRIs
There is evidence that the use of antidepressants, especially SSRIs, can causean increase in suicidal thoughts, however it
does not show an increase in cases. ± A severely depressed patient, or those with bipolar syndrome in a ³low´ phase, usually only have theenergy to focus on their low. As the medicationbegins to take affect they will have an increase in
energy and suicidal thoughts as they transitionfrom their ³low´ or depressed episode. It is thistime when the patient is still in a ³depressed stateof mind,´ that they are able to think more aboutand idealize suicide because oh their higher
energy level.
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Side Effects:
SNRIs Nausea and vomiting
Dizziness
Insomnia
Sleepiness
Abnormal dreams
Constipation
Sweating Dry mouth
Yawning
Tremor
Gas Anxiety
Agitation
Abnormal vision Headache
Sexual dysfunction
Side Effects: Bupropin
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Side Effects: Bupropin
28% of patients will lose five pounds or more
0.04% of patients will experience seizures
± Common: Agitation, constipation, diarrhea,
dizziness, dry mouth, headache, increased
perspiration, insomnia, nausea, vomiting
± Rare: Acne, blurred vision, chest pains, chill,
coordination problems, confusion,
decrease in white blood cell count,
fainting, fever,hair color change
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Withdrawls:
SNRIs Stopping treatment with SNRIs,
especially when done suddenly, can
cause withdrawal-like symptoms: ± nausea, vomiting, anxiety, diarrhea, agitation,
confusion, headaches, nightmares, coordination
changes, or skin-tingling or shock-like sensations
» Sometimes referred to as discontinuation
syndrome
Side Effects:
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Side Effects:
Electroconvulsive Therapy Anxiety or nervousness
Gastrointestinal distress (nausea and diarrhea)
Headache
Insomnia Rash
Slight weight loss
Sexual impotence in men
(about 10%) Lose of interest in sex for
both men and women; inability to achieve orgasm
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The Chris Pittman Case
In 2001, the 12 year
boy shot and killed
his grandparentswhile being under
the influence of
Zoloft, a popular
antidepressant for the previous couple
of days
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The Chris Pittman Case
Defense attorneys argued that Chrissuffered adverse reactions to the drug
including akathisia (a neurologicalreaction characterized by extremeinternal restlessness, which has beenassociated with suicide and violence),
emotional blunting, mania andpsychosis with testimonies by Chris¶saunt and sister
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Ethics
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Ethics
Ethical issue arisesover a depressedpatients ability to make
decisions concerningtreatment.
An elderly patient thathas been diagnosedwith depression has
recently becomegravely ill, requiringdialysis.
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Ethics
If you are not given an effective dosage
of antidepressant medication, suicide
rates increase. Is the hit-or-miss methodof treatment with medication ethical?
Untreated Depression has a high risk of suicide that accompanies the disorder
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Ethics
54% of patients with bipolar disorder aremisdiagnosed as having depression
Misdiagnoses and treatment of patients withbipolar disorder as having a unipolar disorder can magnify the patients symptoms
Many antidepressants can cause a patient with bipolar disorder to have exaggerated and prolonged ³highs´ and³lows´
Should we be quick to treat Depression withmedication when misdiagnosis can haveserious consequences.
References
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References
Downing-Orr, K ristina. Rethinking Depression - Why Current Treatments Fail. 1st ed. New
York: Plenum Press, 1998. Higgins, Edmund S. "Is Depression a Neurochemical or Neurodegenerative?." Current
Psychiatry 3.9 (2004): 39-40.
K line, Nathan S., M.D., Factors in Depression, Rockland State Hospital, Raven Press Books, Inc., 1974
Lazarus, Jeremy A. "Ethics in S plit Treatment." Psychiatric Annals 31.10 (2001): 611-614.
Oltmanns, Thomas F., Case studies in A bnormal Psychology, 3rd, John Wiley and Sons,
Inc., 1991 Oltmanns, Thomas F., and Robert E. Emery. A bnormal Psychology. 5th ed. U pper Saddle
River: Prentice Hall, 2004.
Schatzberg, Alan F., and Charles B. Nemeroff. Textbook of Psychopharmacology. 2nd ed. Washington: American Psychiatric Press Inc., 1998.
S pitzer, Robert L., Psychopathology, A case book, Columbia University, McGraw-Hill, Inc., 1993
Diagnostic and Statistical Manual of Mental Disorders. IV txt revision ed. Washington: American Psychiatric Association, 2000.
"Depression Caused by Chronic Illness."Web MD. July 2005. WebMD Inc.. 02 A pr. 2006 <http://www.webmd.com/content/article/45/1663_51215.htm>.
"Neurotransmitter Animation." Depression Advances. 2006. Eli Lilly and Company. 05 A pr. 2006 <https://www.depressionadvances.com/animation/brainAnimations.html>.
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