CRAM BUDDY: BGH PSYCHIATRY (FAST FACTS… )

MENTAL HEALTH

WHO DEFINITION: Mental health is defined as a state of well-being in which every individual realizes his or her own potential, can cope with the normal stresses of life, can
work productively and fruitfully, and is able to make a contribution to her or his community.

Model A: Mental Health as Above Normal

• This first perspective differs from the traditional medical approach to health and illness. In this medical model, if one were to put all individuals on a continuum,
normality would encompass the major portion of adults, and abnormality would be the small remainder.

Model B: Mental Health as Maturity

• Unlike other organs of the body that are designed to stay the same, the brain is designed to be plastic. Therefore, just as optimal brain development requires
almost a lifetime, so does the assessment of positive mental health.
• The association of mental health to maturity is probably mediated not only by progressive brain myelination into the sixth decade but also by the evolution of
emotional and social intelligence through experience. Erik Erikson conceptualized that such development produced a "widening social radius."

IDENTITY -Allows to become separate from their parents, for mental health and adult development cannot evolve through a false
self
-Task: mastering the last task of childhood: sustained separation from social, residential, economic, and ideological
dependence on family of origin

INTIMACY -Developed by young adults, permits them to become reciprocally, and not selfishly, involved with a partner
-mastery of intimacy may take very different guises in different cultures and epochs, but “mating-for-life” and “marriage-
type love” are developmental tasks built into the developmental repertoires of many warm-blooded species, including
ours.

CAREER CONSOLIATION -task that is usually mastered together with or that follows the mastery of intimacy
-Mastery of this task permits adults to find a career as valuable as they once found play.

GENERATIVITY -demonstration of a clear capacity to care for and guide the next generation
-means to be in a caring relationship in which one gives up much of the control that parents retain over young children
-Its mastery is strongly correlated with successful adaptation to old age.

INTEGRITY -task of achieving some sense of peace and unity with respect both to one’s life and to the whole world.
-Erikson described integrity as “an experience which conveys some world order and spiritual sense. No matter how dearly
paid for, it is the acceptance of one’s one and only life cycle as something that had to be and that, by necessity, permitted
of no substitutions.”

Model C: Mental Health as Positive or ''Spiritual '' Emotions

• This model defines both mental and spiritual health as the amalgam of the positive emotions that
bind us to other human beings. Love, hope, joy, forgiveness, compassion, faith, awe, and gratitude
comprise the important positive and "moral" emotions included in this model.
• Negative emotions originating in the hypothalamus such as fear and anger are elaborated in the
human amygdala (larger in humans than in other mammals). Of tremendous importance to
individual survival, the negative emotions are all about "me." In contrast, positive emotions,
apparently generated in the limbic system and unique to mammals, have the potential to free the
self from the self. People feel both the emotions of vengeance and of forgiveness deeply, but the
long-term results of these two emotions are very different. Negative emotions are crucial for survival
in present time. The positive emotions are more expansive and help us to broaden and build.

Model D: Mental Health as Socioemotional Intelligence

• High socioemotional intelligence reflects above-average mental health in the same way that a high
intelligence quotient (IQ) reflects above-average intellectual aptitude. Such emotional intelligence
lies at the heart of positive mental health.
• Aristotle defined socioemotional intelligence as follows : "Anyone can become angry-that is easy.
But to be angry with the right person, to the right degree, at the right time, for the right purpose, and
in the right way-that is not easy."

Model E: Mental Health as Subjective Well-Being

• Positive mental health does not just involve being a joy to others; one must also experience
subjective well-being. Long before humankind considered definitions of mental health, they
pondered criteria for subjective happiness.
• Subjective well-being is not just the absence of misery, but the presence of positive contentment.
 PSYCHIATRIC HISTORY TAKING AND MSE

• PATIENT-PHYSICIAN RELATIONSHIP: CORE OF THE PRACTICE OF The History: OUTLINE

MEDICINE • Presenting Complaint
• Safety and comfort: advisable for the interviewer to have a • History of presenting complaint
clear,unencumbered exit path • Family History
• Time and number of sessions: 45 to 90 minutes for the initial interview • Personal History
• Interview room: patient and psychiatrist should be seated 4 to 6 feet apart • Past Psychiatric History
• Past Medical History
• Substance Use
General Principles of History Taking • Drug History
• Aim to understand problems/symptoms and effect on life • Forensic History
• To put presenting problems into context by enquiring about background history • Personality
and previous treatment • Current Social Situation
• Is followed by Mental Status Examination (MSE)
• Enables formulation to be reached – psychodynamic occurrences, General Data: name, age, marital status, educational attainment, current
psychopathology address, birthday, birthplace, religion, race
• Is therapeutic in itself – ventilating emotions and problems
Presentation/Referral and Presenting Complaint(s)
Preparing The Setting • Who referred patient and what is their concern/request
• Safety • Where is patient being seen.
• Privacy • What is their problem, in their own words – Recommendation in Medicine, chief
• Try to avoid interruptions complaints should be written in medical term. In Psychiatry, we still use the
• Arrange seating so sitting at angle to patient words of the patients to know the background of what the he is feeling inside.
• Writing materials
• Box of tissues. History of presenting complaint
• Nature of problem
Starting the Interview • Precipitant
• Put patient at ease – stablish rapport with the patient • Onset, time span, development of symptoms, fluctuations, factors worsening or
• Introduce yourself and explain role improving
• Introduce to anyone who is accompanying patient • Degree of functional impairment
• Inform them about the length of interview • Level of distress
• Treatments trialled (eg. Traditional healers)
• Need to take notes
• Confidentiality
We still use OPQRST in Psychiatric Facility:
o Onset
Interview Style
• Relaxed even if under time pressure o Provocation or Palliation
o Quality
• Appropriate eye contact, appear interested
• Begin with a general question eg “tell me about your problem” o Region and Radiation
o Severity
• Have a systematic but flexible plan – at beginning can be helpful to take a list of
headings as prompt o Time (History)
• Keep in control. May need to interrupt “I’m sorry but I need to move on to other
Family History
things” “We can come back to this if we have time later”
• Parent: age (now or at death), occupation, relationship with patient
Interview Techniques • Siblings: as above
• Use of open questions where possible, especially at beginning eg “How is your • Psychiatric history in family members (genetic and effect on home life).
appetite?” Substance use, suicide.
• Closed questions are useful if time is short eg “is your appetite good?” • Genogram
• Avoid leading questions eg “You have a poor appetite, don’t you?”
Personal history or Anamnesis
• Encourage patient by leaning forward, nodding, saying “go on” “tell me more
• Mother’s pregnancy, birth
about…..”
• Early development, illness
• Help them talk about painful or embarrassing subjects by being non-judgmental,
• Childhood separation, emotional problems
acknowledging distress and explaining why you are asking, eg “I can see this is
• Relationships with family members, atmosphere at home
difficult to talk about…”
• Schooling – academic performance and peer relationships. (Bullying, school
• Summarise key points to check understanding refusal, shyness, conduct disorders)
• As experience grows start to select questions according to emerging diagnostic • Qualifications. Further education
possibilities and management options. This is becomes more important when • Occupation(s), work performance
time is limited or patient uncooperative • Sexual relationships, marriage, children
• Don’t take words at face value eg “paranoid” • History of abuse (physical, sexual, emotional) in childhood or adulthood
• Pick up non-verbal cues • Sexual History – starts from having the desire to masturbation. It has a brief to
• Watch experienced clinicians and get them to watch you! the psychiatric patient. (Learn to control hesitations when asking patients about
• Video yourself sexual history.)

Interviewing Informants Past Psychiatric History

• Always useful and more so if patient is cognitively impaired, patient is
concealing information
• Gain patient consent
• Often best to see patient alone first and then informant
• Establish confidentiality (and limits)
• Ascertain informants concerns as well as gain information.
• May need to help informant if stressed carer (carer assessment)
• History of similar or other symptoms in past (genetics)
• Previous diagnosis
• History of treatment – include from primary care, counselling, CAMHS,
complementary therapy as well as mental health services
• Previous hospitalisation, MHA, medications, ECT.
• Recovery between episodes
• Previous DSH and suicide attempts

Interviewing patients from other cultures (Cultural competency) ***Developmental and social history-developmental and social history reviews
• Interview patients in first language where possible. May need interpreter. the stages of the patient’s life. It is an important tool in determining the context of
• Using interpreter is skill. Discuss approach first. Manageable chunks of psychiatric symptoms and illnesses and may, in fact, identify some of the major
information. 2nd person, direct translation is most useful. factors in the evolution of the disorder.
• Distress is shown via different symptoms eg physical rather then psychological
symptoms Past Medical History
• Cultural beliefs may include ideas that appear delusional but are culturally • Chronology of illness and treatment
acceptable eg witchcraft.
Need collateral information. Substance Use
• Treatment expectations may differ • Alcohol, other substances, tobacco.
• Pattern of use
• Age at onset • Tardive dyskinesia
• Relationship to symptoms • Akathisia
• Harmful use
• Psychological dependency Speech
• Physical dependency
• Previous detox • Elements:
• Patient view • Fluency
o Refer to whether the patient has full command of the
Drug History language
• Current medications o Issues: stuttering, word finding difficulties, paraphasic
• Allergies errors
o Attempt should be made to assess if fluent in other
Forensic History languages
• Record all offences – convicted or not. • Amount
• Violence/Anger, sexual offences particularly important o Normal: suggestive of hypomania or mania
• Persistent offending o Increased
• Probation o Decreased: anxiety, disinterest, thought blocking or
• Relationship to symptoms psychosis
• Rate/Speed
Personality o Slowed
• Hard to assess at one-off interview and collateral information should be sought. o Rapid (pressured)
o Speech
• GP may have useful information
• Tone
• Ask patient how others see them/would describe them • Volume
• Prevailing mood; how they get on with people; deal with stress; hobbies; o Descriptive terms:
standards. ▪ Irritable
▪ Anxious
• Impulsive
▪ Dysphoric
• Prone to worry ▪ Loud
• Strict, fussy
• Seek attention Mood
• Untrusting, resentful
• Irritable • Patient’s internal and sustained emotional state
• Sensitive • Subjective
• Suspicious • Best to use patient’s own words
• Argumentative • Accompanying symptoms
• Lack concern for others o Depression: early morning wakening, diurnal variation,
Current social circumstances anhedonia, loss of appetite, loss of weight, fatigue, loss of
• Who they live with concentration, hopelessness, Suicidal thoughts, plans,
• Current employment intent
• Stressors o Anxiety: palpitations, dry mouth, sweating, tremor
• Social supports o Elation: Overactivity, excessive self-confidence, reduced
• Typical day sleep, distractibility, increased libido

MENTAL STATE EXAMINATION

What is the MSE Affect
• “Here and now” record of presentation
• History will give clues as to likely symptoms • Expression of mood or what the patient’s mood appears to be to the
clinician
• Systematic
• Described to ff elements:
• Until more experienced carry out full mental state
o Quality (tone)
• Be observant but also learn the terminology to describe symptoms/signs
o Quantity
• Use conventional headings to structure examination – other colleagues and o Range
examiners will expect it o Appropriateness
o Congruence - Agreement/compatibility with patient’s
GENERAL FEATURES mood or thought content
Appearance and Behavior
Thought Content- Essentially what thought are occurring to the patient
• General overview of how the patient looks and acts during the
interview • Refers to what a person is actually thinking about: ideas, beliefs,
• Age preoccupations, obsessions
• Style of dressing, appropriate for context • What patient spontaneously expresses, the responses to specific
• Physical features questions aimed at eliciting particular pathology
• Style of interaction o Obsessive thoughts- Unwelcome and repetitive
• Appearance thoughts that intrude into the pt’s consciousness;
• Examples to note Generally ego alien, resisted by patient
• Clothing o Compulsions- Repetitive, ritualized behaviors that
• Hygiene patient feels compelled to perform to avoid an increase
• Grooming in anxiety or some dreaded outcome
• Behavior o Delusion- False, fixed ideas not shared by others
o Suicidality
Motor Activity o Homicidality

• Normal Thought Process- Does not describe what person is thinking but HOW the
• Bradykinesia (slowed) thoughts are formulated, organized, and expressed; Refers to the way in which a
• Hyperkinesia (agitated) person puts together ideas and associations, the form in which a person thinks
• Give clues to diagnosis (depression or mania)
• Posture • Normal: Linear, organized, and goal-directed
• Pacing • Flight of ideas- Rapidly moves from one thought to another, at a
pace that is difficult for the listener to keep up with but are logically
• Poise
connected
• Gait
• Circumstantial- Overincludes details and materials not directly
• Freedom of movement
relevant to subject; With connections between sequential statements
• Hand wringing
• Tangential Never returns to original point or question; Irrelevant and
• +/- tics, jitteriness, tremors, restlessness, lip-smacking, tongue
related in a minor, insignificant manner
protrusions
• Loose thoughts or Association- Difficult or impossible to see
• Parkinsonian features
connections between sequential content
 • Perseverations-Tendency to focus on specific idea or content w/o
ability to move on to other topics
• Thought blocking- Sudden disposition of thought or a break in flow
of ideas
• Neologism- Refer to a new word or condensed combination of
several words
• Word salad- is speech characterized by confused, and often
repetitious, language with no apparent meaning or relationship
attached to it.
o A person can have normal thought process with
significantly delusional thought content
o May have generally normal thought content but
significantly impaired thought process
Perceptual Disturbances
• Hallucinations- Perceptions in the absence of stimuli
o • Can occur in any sensory modality: auditory, visual,
olfactory, gustatory, tactile, deep sensation
o • Visual: more likely in organic conditions
o • Gustatory: unpleasant taste. In schizophrenia, TLE.
May lead to delusion is being poisoned
o • Olfactory: Schizophrenia, organic, TLE. May believe
result of gas being pumped into dwelling
o • Tactile: touched, pricked, insects crawling on skin
(formication, drug withdrawal/cocaine addiction)
o • Deep Sensation: often in schizophrenia. May be
sexual.
o HYPNOGAGIC IS NORMAL
• Delusion- fixed, false beliefs out of keeping with the patient's cultural
background
• Illusion-Misperceptions of a stimuli
• Derealization- Feeling that one is not oneself or that something has
changed
o Derealization is a feeling that one's environment has
changed in some strange way that is difficult to describe
Cognition
• Alertness
• Orientation- time, place and person
• Concentration- serial 7’s, WORLD, days of the week then vice versa
• Memory (short and long)
• Short Term Memory (STM) – name and address recall after 3
mins eg. Mango, Table, Coin
• Long Term Memory (LTM) – history
• Calculation
• Fund of knowledge
• Abstract reasoning- Ability to shift back and forth between general
concepts and specific examples
o Assessment:
▪ Identifying similarities between objects
▪ Interpreting proverbs
• Insight- Refers to the patient's understanding of how he or she is
feeling, presenting, and functioning as well as the potential causes of
his or her psychiatric presentation
o LEVELS OF INSIGHT
o Insight is rated on a 6-point scale from one to six
▪ 1 – complete denial of illness
▪ 2 – slight awareness of being sick and
needing help but denying it at the same time
▪ 3 – awareness of being sick but blaming it on
others, on external factors, or on organic
factors
▪ 4 – awareness that illness is due to something
unknown in the patient
▪ 5 – intellectual insight (Admission of ill ness
and recognition that symptoms or failures in
social adjustment are due to irrational feelings
or disturbances, without applying that
knowledge to future experiences)
▪ 6 – true emotional insight (Emotional
awareness of the motives and feelings within,
of the underlying meaning of symptoms;
does the awareness lead to changes in
personality and future behavior; openness to
new ideas and concepts about self
and the important persons in his or her life)
• Judgement- Person's capacity to make good decisions and act on
them
o The level of judgment may or may not correlate to the
level of insight.
o A patient may have no insight into his or her illness but
have good judgment.
 NEUROTRANSMITTER SYSTEM AND PHARMACOLOGY

CHEMICAL NEUROTRANSMISSION

• It is the process involving the release of a neurotransmitter by one neuron and the binding of the neurotransmitter molecule to a receptor on another neuron.

• The process of chemical neurotransmission is affected by most drugs used in psychiatry.

NEUROTRANSMITTER

– A molecule must meet ALL of the criteria to be classified as a neurotransmitter.

▪ The molecule is synthesized in the neuron.
▪ The molecule is present in the presynaptic neuron and is released on depolarization in physiologically significant amounts.
▪ When administered exogenously as a drug, the exogenous molecule mimics the effects of the endogenous neurotransmitter.
▪ A mechanism in the neurons or the synaptic cleft acts to remove or deactivate the neurotransmitter.

CLASSIFICATION – -Serotonin -Epinephrine

– -Histamine -Acetylcholine
1) BIOGENIC AMINES
2)AMINO ACIDS: GABA, Glycine, Glutamate
– -Dopamine -Norepinephrine
3) PEPTIDES: TRH, Neurotensin, CCK-S

PSYCHOTROPIC DRUGS – Antidepressants

– Mood Stabilizers
CLASSIFICATION: – Anxiolytics
– Antihistamine
– Antipsychotics/Neuroleptics – Anticholinergic

– Drugs efficacy is noted after 2-3 weeks

 DOPAMINE ▪ Risperidone – increase Prolactin (Lactation & Gynecomastia)

• 4 CNS DOPAMINERGIC TRACTS ANTIDEPRESSANTS

• NIGROSTRIATAL TRACT – MAOIs

– TCAs
• Projects from its cell bodies in the substantia nigra to the corpus – SSRI
striatum. (substantia nigra corpus striatum) – SNRI
• When the D2 receptors at the end of this tract are blocked by classic
antipsychotic drugs, parkinsonian side effects emerge. *** BIOGENIC AMINE THEORY OF MOOD DISORDERS
• Control of motor and mood
– In Parkinson's disease the nigrostriatal tract degenerates, • In Depression, Norepinephrine and Serotonin are the two most
resulting in the motor symptoms of the disease. implicated in mood disorders
– Because of the significant association between
Parkinson's disease and depression, the nigrostriatal tract – DECREASED Norepi and Serotonin in post-synaptic
may somehow be involved with the control of mood, in receptors
addition to its classic role in motor control
– D2 receptors in the caudate nucleus suppress the activity NOREPINEPHRINE
of the caudate nucleus. The caudate neurons regulate
motor acts by gating, in which intended acts are actually – Compact locus ceruleus in the pons
carried out. The absence of D2 receptor activity allows the – Norepinephrine along with Epinephrine and Dopamine constitute the
caudate to dampen motor activity excessively, resulting in catecholamines.
the bradykinesia that typifies parkinsonism. – Once norepinephrine is formed, it is taken through specific transporter
proteins into synaptic vesicles, from which it is released on depolarization
• MESOLIMBIC of the axonal terminal.
– As with dopamine, the two major routes of deactivation are:
– projects from its cell bodies in the ventral tegmental area ▪ uptake back into the presynaptic neuron (re-uptake) and
(VTA), which lies adjacent to the substantia nigra, to most ▪ metabolism by MAO and COMT.
areas of the cerebral cortex, and to the limbic system • *The MAOA subtype preferentially metabolizes
– VTA  Neocortex & Limbic System norepinephrine and epinephrine, as well as
– Associated with positive symptoms of Schizophrenia serotonin.
• Delusion
• Hallucination MAOI
• Disorganized Speech
• Disorganized Behavior or Catatonic Behavior – Blocks the enzyme
monoamine oxidase which
• MESOCORTICAL: Associated with negative symptoms of breaks down
Schizophrenia neurotransmitters dopamine,
serotonin and
– Flat affect Norepinephrine
– Social withdrawal – Clinical Use:
– Lack of motivation (avolition) Depression & Parkinson’s
– Lack of speech or thought (alogia) Disease
– Example: Phenelzine
• TUBEROINFUNDIBULAR (Nardil), Isocarboxazid
(Marplan), Tranylcypromine
– Arcuate Nucleus & Periventricular Area of Hypothalamus (Parnate), Selegiline (Eldepryl)
 Infundibulum & Anterior Pituitary Gland Selegiline – effective inhibitor of MAOb use for the ttt of
– Dopamine acts as a release-inhibiting factor in the tract Parkinson’s Dse
by inhibiting the release of Prolactin
– Endocrine Effects ***PIC: GOAL: Increase NTs (NE, Serotonin) in the postsynaptic neuron (bec the
px in depression is decrease/lack of NTs available in the postsynaptic site);
***DOPAMINE HYPOTHESIS OF SCHIZOPHRENIA MAO-metabolizes these NTs before reaching the postsynaptic neuron; TCA,
SSRI, SNRI – blocks reuptake
– Remains the leading neurochemical hypothesis for schizophrenia
– blockade of dopamine receptors reduces psychotic symptoms • What to avoid during MAOI treatment?
– may also be involved in the pathophysiology of mood disorders
-Food containing tyramine (e.g. liver and fermented substances such as alcoholic
ANTIPSYCHOTICS beverages and aged cheese as well as pizza!)

– Also known as neuroleptics or major tranquilizers are a class of psychiatric • What is the consequence if one happens to ingest one of the
medication primarily used to treat the symptoms of psychosis, such as contraindicated food?
hallucinations and delusions which are seen in:
▪ Schizophrenia – Hypertensive Crisis (aka “cheese effect”) will result!
▪ Schizoaffective disorder • Hypertensive Crisis – HPN + acute impairment of
▪ Bipolar Disorder one or more organ systems (CNS, CVS and/or
Renal)
2 MAJOR GROUP OF ANTIPSYCHOTIC • ttt: IV Na Nitroprusside Injection
• The exact mechanism by which tyramine causes H.
1) TYPICAL ANTIPSYCHOTICS/1st GEN/DRA Crisis is not well understood but it is postulated that
tyramine displaces Norepinephrine from the storage
o MOA: Dopamine (D2) Receptor Antagonist (DRA) vesicles into the extracellular space that trigger
o Clinical Use: Schizophrenia (primarily positive symptoms), Psychosis, H.Crisis.
Acute Mania, Tourette Syndrome
o Example: Haloperidol*, Fluphenazine, Chlorpromazine, Thioridazine TRICYCLIC ANTIDEPRESSANTS
o more prone to neurologic side effect (EPS & NMS)
• Blocks transported site of norepinephrine and serotonin, thus increasing
2) ATYPICAL ANTIPSYCHOTIC/2ND GEN/SDA the synaptic concentration of these neurotransmitters.
• SIDE EFFECTS:
– -MOA: Not completely understood but has serotonin-dopamine antagonism – Histamine Blockade: Sedation
effect. – Cholinergic Blockade: Dry Mouth, Constipation, Blurring of
– -Clinical Use: Schizophrenia (both positive & negative symptoms), OCD, Vision, Urinary Retention
Bipolar D/O – Autonomic Effect: Orthostatic Hypotension
– -Example: Clozapine*, Olanzapine, Risperidone, Quetiapine • Desipramine FEWEST S/E
– -Fewer EPS S/E • Nortriptylline
– ***Clozapine – must watch closely • Imipramine
▪ Fewer s/e but Clozapine & Olanzapine may cause significant • Doxepin
weight gain • Amitriptylline MOST S/E
▪ Clozapine – Agranulocytosis
 SSRI – Prototype: Diazepam
– Others: Alprazolam, Chlordiazepoxide, Clonazepam, Lorazepam,
– Increase the extracellular level of neurotransmitter serotonin by inhibiting Oxazepam (-pam)
its reuptake into the presynaptic cell, increasing the level of serotonin in – *Flumazenil – antidote for benzodiazepine toxicity
the synaptic cleft available to bind to the postsynaptic receptor.
– First line agents for the treatment of depression, OCD, and panic BARBITURATE
disorder
– Depression: efficacy is the same with TCA’s but their side effect profile is – MOA: increase the duration of GABA-mediated chloride ion channel
markedly better. opening
– Example: – Prototype: Phenobarbital
o Fluoxetine (Prozac) – Others: Amobarbital, Pentobarbital, Secobarbital, Thiopental (-tal)
o Citalopram (Celexa) – No direct antidote for Barbiturate overdose
o Escitalopram (Lexapro) o No direct antidote for overdosage  IV Naloxone, NGT, Mech Vent
o Paroxetine (Paxil) o Bremegide – analeptic (CNS stimulant that stimulates breathing
o Sertraline (Zoloft) muscles  improve respiration)
o Fluvoxamine (Luvox)
o *PCL PZL ANTICHOLINERGIC/ANTIPARKINSON

SNRI • BIPERIDEN (Akineton)- Indication: used to treat EPS

– aka Non-tricyclic Serotonin & Norepinephrine Reuptake Inhibitors ANTIHISTAMINE

– Dual reuptake inhibitors have low affinity at neuronal receptors of the other
neurotransmitters which results in a low adverse effects, compared with the • DIPHENHYDRAMINE- Indication: Use to treat neuroleptic-induced acute
TCAs dystonia and Parkinson’s and also as a hypnotics and anxiolytics
– Example:
o Venlafaxine (Effexor)
o Duloxetine (Cymbalta) EPS TIME OF MANIFESTATION/S TREATMENT/S
o Desvenlafaxine (Pristig) ONSET
▪ *Venlafaxine – increase BP, Mydriasis, Abnormal
Bleeding (RANGE)

MOOD STABILIZERS
ACUTE DYSTONIA 4 Muscle Spasm Diphenhydramine
– Lithium hours (Torticollis)
– Valproic Acid –4
– Carbamazepine days Stiffness
– Lamotrigine (Trismus)

o Valproic, Carbamazepine, Lamotrigine – anticonvulsants Oculogyric Crisis

LITHIUM
PARKINSONISM 4 days – Cogwheel Rigidity Anticholinergic
– MOA: Unknown. Theories: 4 Drug
o block the enzyme inositol-1 phosphatase within neurons, inhibition months Shuffling Gait
results in decreased cellular responses to the NTs that are linked to Biperiden
the PI second messenger Pill Rolling (Akineton)
o Increase the release of serotonin in the brain
– First line treatment for Bipolar Disorder Stooped Posture
– Teratogenic (EBSTEIN ANOMALY)
– Example: Eskalith, Lithobid
TARDIVE 4 Stereotypical oral- There’s no single
– Lithium therapeutic index: 0.6 -1.2 mEq/L, could be considered 1st line
DYSKINESIA months facial movements effective
treatment for bipolar d/o except for nephrotoxicity
–4 treatment
– Manic pregnant patients: don’t give mood stabilizers (Na Divalproex): side
years (potentially
effect: Neural tube defects
irreversible) Lower the
dosage or Switch
to SDA
VALPROIC ACID

– Anticonvulsant AKATHISIA anytime A subjective feeling Decrease dose

– blocks voltage-dependent sodium channels and increased brain levels of of muscular
gamma-aminobutyric acid (GABA) discomfort that can Beta Adrenergic
– The GABAergic effect is believed to contribute towards the anti-manic cause patients to be Antagonist
properties of valproate. agitated, pace (Propralnolol)
– Teratogenic relentlessly,
– Example: Depakote alternately sit and
stand in rapid
CARBAMAZEPINE & LAMOTRIGINE succession, and feel
generally dysphoric
– Anticonvulsants
– Bind to voltage dependent Na channels in the inactive state and prolonging
their inactivation NMS anytime FEVER Immediate
– Reduction of currents through NMDA glutamate receptor channels discontinuation
– Carbamazepine – Teratogenic (More prone to NTDs) F-ever
– Lamotrigine – Non-teratogenic (DOC as mood stabilizer for Pregnant Dantrolene
Women) E-ncephalopathy
– Example: Carbamazepine (Tegretol), Lamotrigine (Lamictal) Bromocriptine
– Important A/E: V-itals unstable
o Carbamazepine – aplastic anemia & agranulocytosis
o Lamotrigine – SJS and TEN E-nzymes
ANXIOLYTICS R-igidity of muscles
– MOA: increase the frequency of GABA mediated chloride ion channel
opening
 PSYCHODYNAMICS
• ATTACHMENT THEORY: JOHN BOWLBY
o ATTACHMENT: child to mother, gives infants feelings of security
o BONDING: concerns the mother’s feelings for her infant
• SIGMUND FREUD: CLASSIC PSYCHOANALYSIS

MATCHING TYPE:

• ERIK H. ERIKSON: EPIGENETIC PRINCIPLE

• HEINZ KOHUT: SELF-PSYCHOLOGY
• JOHN BOWLBY: ATTACHMENT THEORY
 PERSONALITY DISORDER

– An enduring pattern of inner experience and behavior that deviates markedly from the expectations of the individuals culture
– When personality traits are inflexible and maladaptive and cause significant functional impairment or subjective distress
– Has an onset in adolescence or early adulthood
– Is stable over time

General Personality Disorder Criteria

A. An enduring pattern of inner experience and behavior that deviates markedly from the expectations of the individual’s culture. This pattern is manifested in two (or
more) of the following areas:
1. Cognition
2. Affectivity
3. Interpersonal functioning
B. The enduring pattern is inflexible and pervasive across a broad range of personal and social situations
C. The enduring pattern leads to clinically significant distress or impairment in social, occupational, or other important areas of functioning.
D. The pattern is stable and of long duration, and its onset can be traced back at least to adolescence or early adulthood
E. The enduring pattern is not better explained as a manifestation or consequence of a substance or another medical condition
 CLUSTER A: Odd or eccentric

CLUSTER B: Dramatic, emotional or erratic

CLUSTER B Clinical Features Treatment

Antisocial personality -Inability to conform to the social norms -Psychotherapy: Lack of motivation disappears when they feel that they are among
disorder peers
-Continual antisocial or criminal acts but
not synonymous with criminality -Pharmacotherapy: anxiety, rage and depression

• Psychostimulants (methylphenidate): ADHD

• Carbamazepine or valproate: control impulsive behavior

Borderline personality -Stand on border of neurosis and -Psychotherapy

disorder psychosis
-Pharmacotherapy:
-Unstable affect, mood, behavior, object
relations, and self-image • Antipsychotics: control anger, hostility and psychotic episodes

• Antidepressants

• MAO inhibitors: impulsive behavior

Histrionic personality -Unaware of their own feelings -Psychotherapy: clarification of their inner feelings
disorder
-Excitable and emotional and behave in a -Pharmacotherapy: adjunct when symptoms are targeted
colorful, dramatic, extroverted fashion

Narcissistic personality -Heightened sense of self-importance and -Psychotherapy: group therapy for them to learn to share their own feelings
disorder grandiose feelings of uniqueness
-Pharmacotherapy

• Lithium: mood swings

• Antidepressants (Serotonergic drugs☺ tolerate rejection poorly and are

prone to depression

CLUSTER C: Anxious or fearful

CLUSTER C Clinical features Treatment

Avoidant personality -Extreme sensitivity to rejection and lead to a socially withdrawn -Psychotherapy:
disorder life
• Trust
 -Shy but not antisocial and show a great desire for • Group therapy
companionship, but they need unusually strong guarantees of
uncritical acceptance -Pharmacotherapy

-Inferiority complex • Beta adrenergic receptor antagonist (Atenolol): manage

autonomic nervous system hyperactivity

Dependent personality -Subordinate their own needs to those of others, get others to -Psychotherapy:
disorder assume responsibility for major areas of their lives
• Insight oriented
-lack self-confidence
-Pharmacotherapy:
-intense discomfort when alone for more than a brief period
• Benzodiazepines and Serotonergic agents

Obsessive-compulsive -Emotional constriction, orderliness, perseverance, stubborness, -Psychotherapy

personality disorder and indecisiveness
• Group and behavior therapy
-Pervasive pattern of perfectionism and inflexibility
-Pharmacotherapy

• Clonazepam, Clomipramine

Personality Change due to Another Medical Condition

A. A persistent personality disturbance that represents a change from the individual’s previous characteristic personality pattern

B. There is evidence from the history, physical examination, or laboratory findings that the disturbance is the direct pathophysiological consequence of another
medical condition

C. The disturbance is not better explained by another mental disorder

D. The disturbance does not occur exclusively during the course of delirium

E. The disturbance causes clinically significant distress or impairment in social, occupational, or other important areas of functioning

Other specified Personality Disorder

 Symptoms characteristic of a personality disorder that cause clinically significant distress or impairment in social, occupational, or other important areas of
functioning predominate but do not meet the full criteria for any of the disorders in the personality disorders diagnostic class

 The other specified personality disorder category is used in situations in which the clinician chooses to communicate the specific reason that the presentation does
not meet the criteria for any specific personality disorder

Unspecified Personality Disorder

 Symptoms characteristic of a personality disorder that cause clinically significant distress or impairment in social, occupational, or other important areas of
functioning predominate but do not meet the full criteria for any of the disorders in the personality disorders diagnostic class

 The unspecified personality disorder is used in situations in which the clinician chooses not to specify the reason that the criteria are not met for a specific
personality disorder, and includes presentations in which there is insufficient information to make a more specific diagnosis

MAJOR DEPRESSIVE DISORDER

• Major Depressive Disorder

o Borderline personality d/o most likely associated with depression
o foliecirculaire: patients experience alternating moods of depression and mania
o Karl Kahlbaum: term cyclothymia: described mania and depression as stages of the same illness
o Lifetime prev of major dep: 5-17%
o Alterations of sleep neurophysiology:
▪ associated with a premature loss of deep (slow-wave) sleep and an increase in nocturnal arousal.
▪ Four types of disturbance:
(1) an increase in nocturnalawakenings,
(2) a reduction in total sleep time,
(3) increased phasic rapid eye movement (REM) sleep,
(4) increased core body temperature
o reduced REM latency: combination of increased REM drive and decreased slow-wave sleep results in a significantreduction in the first period of non-
REM (NREM) sleep
o Psychosocial factors:
▪ Life events: most compelling data indicate that the life event mostoften associated with development of depression is losing a parent before
age 11 years
▪ Personality disorder: OCD, histrionic, and borderline—may be at greater risk for depression than persons with antisocialor paranoid
personality disorder
ETIOLOGY  SEROTONIN: most commonly assoc with
depression
 BIOLOGICAL/ NEUROTRANSMITTERS
 depletion of serotonin may
➢ Serotonin, Norepinephrine, Dopamine: decreased precipitate depression

 NORE: downregulation of b adrenergic  Low CSF level of serotonin

receptors and clinical antidep metabolites suicidal tendencies

 Activation of B2 receptors
decreased NorE
  DOPAMINE: decreased activity; reserpine  Neg view of self- negative self
(decrease dopamine concentration), percept;
parkinson’s disease depressive sx
 Envt: tendency to experience the
 - Increase conc: tyrosine, world as hostile and demanding
amphetamine, wellbutrin
 Future: expectation of suffering
 Mesolimbic dopamine pathway; hypoactive and failure
dopamine D1 receptor
➢ LEARNED HELPLESSNESS
 GENETIC FACTORS
 Depression is associated with experience of
➢ 1st degree relatives of MDD: 1.5-2.5 times likelihood- uncontrollable events
bipolar I; 2-3 times- MDD
 Internal causes of depression produce loss of
➢ Wider degree of relationship: lesser likelihood to be self-esteem after adverse external events
affected
 Improvement: sense of control and mastery of
➢ 1 parent with MDD: 10-25% risk of child with MDD the environment

➢ 2 parents with MDD: 50-75% ➢ LIFE EVENTS AND ENVIRONMENTAL STRESS

 PSYCHOSOCIAL FACTORS  Stressful events precede mood disorders

➢ PSYCHOANALYTIC (FREUD)  Loss of parent before 11 y/o: most often assoc

with development of depression
 Internalized ambivalence towards love object
produces depression if the object is lost  Loss of spouse: most often assoc with onset
of an episode of depression
➢ PSYCHODYNAMICS
 Unemployment: 3x likelihood to have
 Introjection of ambivalently viewed lost love symptoms
object leads to depression
➢ PERSONALITY FACTORS
 Psychodynamic understanding of
depression by S.F: classical view of ➢ OC, histrionic, borderline: greater risk
dep- involves 4 key points:
➢ Recent stressful events: most powerful predictor of onset
1. infant-mother relt during the oral phase
(first 10-18 mos) predispose to  Different presentations:
subsequent vulnerabiloity to dep
Prepubertal Som
2. Depression can be linked to real or
imagined object loss

3. Introjection of the departed objects: Adolescence Substance ab

defense mechanism invoked to deal
with distress connected with the object’s
loss Elderly Cog

4. Lost obj is regarded with a mixture of love and COURSE AND PROGNOSIS
hate feelings of anger directed inward at the
self  Onset: 50% of patients undergoing 1st major depressive d/o exhibited
significant depressive symptoms before the first identified episode
 Bowlby: damaged early attachments and
traumatic separation in childhood predispose ◦ Early identification and treatment
to depression
◦ 50%: before age 40
 Adult losses revive these
childhood loss adult depression ◦ Later onset: (-) family history of mood d/o, antisocial
personality d/o, alcohol abuse
 Edward Bibring: depression is a
phenomenon that occurs when a person Duration: untreated- 6-13 months
becomes aware of the discrepancy b/w high
deals and inability to meet them ◦ Treated: 3 months
 Negative thoughts create negative feelings
and one acts based on those feelings;
◦ Withdrawal of antidepressants before 3 months
therefore, treat first the way one thinks
through psychotherapy
◦ Development of manic episodes
 *Arieti: many depressed people have lived
their lives for someone/something else-
◦ 5-10% with initial dx of MDD have manic episode 6-10
dominant other. Depression sets in when pts
years after the first depressive episode
realize that the person/ideal for whom they
have been living is never going to respond in
a manner that will meet their expectations ◦ 32 y/o

➢ COGNITIVE TRIAD OF AARON BECK ◦ After 2-4 depressive episodes

 Depressogenic schemata: cognitive ◦ Prognosis

distortions
 Negative view of self, environment and future*
 Cognitive distortions:
depressogenic schemata-
cognitive templates that perceive
both the internal and external data
in ways altered by early
experiences
◦ Chronic, tendency to relapse
◦ 1st hospitalization: 50% chance of recovery in the first
year
◦ Recurrences: common
◦ 25%: recurrence after 1st 6 months after
release from hosp
 ◦ 30-50%: first 2 years
◦ 50-75%: 5 years
◦ PROGNOSTIC INDICATORS
◦ Good:
◦ Mild episodes, absence of psychotic
symptoms, short hospital stay
◦ History of solid friendship during adolescence,
stable family functioning and sound social
functioning
◦ Absence of comorbid psychiatric d/o and
personality d/o
◦ No more than 1 previous hospitalization for
MDD
◦ Advanced age of onset
◦ Poor:
◦ Alcohol abuse and other substances
◦ Anxiety d/o
TREATMENT
➢ COGNITIVE THERAPY
• Short- term management aimed at correcting
negative cognitions and unconscious
assumptions that underlie them
• Based on Aaron Beck’s theory (Cognitive
triad)
• Challenge thoughts, not delusions
• Correct thought  correct feeling  correct
behavior
➢ BEHAVIORAL THERAPY
• Based on learning theory (classic and
operant)
• Short- term, aimed at specific undesired
behaviors
• Operant conditioning technique of positive
reinforcement (reward a patient)
➢ INTERPERSONAL THERAPY
• Short- term treatment for non- psychotic
depressed outpatients
• Emphasis on on- going, current interpersonal
issues as opposed to unconscious,
intrapsychic dynamics
➢ PSYCHOANALYTICALLY- ORIENTED THERAPY
• Insight- oriented therapy of indefinite length
• Aim is to achieve understanding of
unconscious conflicts that may be fuelling
depression
➢ SUPPORTIVE THERAPY
• Primary aim is to provide emotional support
• Indicated in acute crisis such as grief or when
patient is recovering from depression but
unable to engage in more demanding
interactive therapy
• Counseling, giving of advice
➢ FAMILY THERAPY
• Indicated when patient’s depression is
disrupting family stability, depression is
related to family events or when it is
supported by family patterns
➢ PHARMACOLOGIC
➢ TRICYCLIC ANTIDEPRESSANTS
• Block transport site of serotonin and
norepinephrine by blocking their receptors,
thereby increasing their concentration in the
synaptic cleft
➢ MONOAMINE OXIDASE INHIBITORS
• Degrade norepinephrine, serotonin, dopamine
and tyramine
• Tyramine- induced hypertenive crisis
(Haloperidol can be given)
• Must not be administered for 2-5 weeks after
using another serotonergic agent (Serotonin
Syndrome)
➢ SELECTIVE SEROTONIN REUPTAKE INHIBITORS
• Most popular mode of treatment; safest
• Blocks serotonin reuptake  increased
concentration in the synaptic cleft
• Early anxiogenic effects may aggravate
suicidal ideations  “Paradoxical Suicide”
(may use anxiolytics (benzodiazepines) for the
1st few days)
➢ SEROTONIN- NOREPINEPHRINE REUPTAKE
INHIBITORS
• Inhibits reuptake of serotonin and
norepinephrine
➢ ELECTROCONVULSIVE TREATMENT
➢ MOA: Down-regulation of B- adrenergic receptors
(norepinephrine)  fewer receptors  high concentration
of neurotransmitters
➢ Use of anticholinergics (decrease salivation), anesthesia,
muscle relaxants (reduce risk of bone fractures) before
administration of electrical stimulus
➢ No absolute contraindications
➢ TRANSCRANIAL MAGNETIC STIMULATION
➢ Uses very short pulses of magnetic energy to stimulate
nerve cells in the brain
 SELF-HARM/SUICIDE

TERMS COMPRISING SUICIDAL IDEATION AND BEHAVIOR

• Aborted suicide attempt: Potentially self-injurious behavior with explicit or implicit evidence that the person intended to die but stopped the attempt before
physical damage occurred.

• Deliberate self-harm: Willful self-inflicting of painful, destructive, or injurious acts without intent to die.

• Lethality of suicidal behavior: Objective danger to life associated with a suicide method or action. Note that lethality is distinct from and may not always coincide
with an individual's expectation of what is medically dangerous.

• Parasuicide: patients who injure themselves by self-mutilation (e.g., cutting the skin), but who usually do not wish to die.

• Suicidal ideation: Thought of serving as the agent of one's own death; seriousness may vary depending on the specificity of suicidal plans and the degree of
suicidal intent.

• Suicidal intent: Subjective expectation and desire for a self-destructive act to end i n death.

• Suicide attempt: Self-injurious behavior with a nonfatal outcome accompanied by explicit or implicit evidence that the person intended to die. Suicide: Self-
inflicted death with explicit or implicit evidence that the person intended to die.

RISKS FOR SUICIDE

 -Among men, suicides peak after age 45; among women, the greatest number of completed suicides occurs after age 55 .
 -Men commit suicide more than four times as often as women, regardless of age or race, despite the fact that women attempt suicide or have suicidal thoughts
three times as often as men.
 -Single, never-married persons register an overall rate nearly double that of married persons. Divorce increases suicide risk, with divorced men three times more
likely to kill themselves as divorced women.
 -Work, in general, protects against suicide. Among occupational rankings, professionals, particularly physicians, have traditionally been considered to be at
greatest risk. The suicide rates increase during economic recessions and depressions and decrease during times of high employment and during wars. Among
physicians, psychiatrists are considered to be at greatest risk, followed by ophthalmologists and anesthesiologists, but all specialties are vulnerable.
 -Factors associated with illness that contribute to both suicides and suicide attempts are loss of mobility, especially when physical activity is important to
occupation or recreation; disfigurement, particularly among women; and chronic, intractable pain.
 -Depressive disorders account for 80 percent of this figure, schizophrenia accounts for 10 percent, and dementia or delirium for 5 percent
 NEUROBIOLOGICAL ASPECT

 Diminished central serotonin plays a role in suicidal behavior.

 low concentrations of the serotonin metabolite 5-hydroxyindoleacetic acid (5-HIAA) in the lumbar
cerebrospinal fluid (CSF) were associated with suicidal behavior
 modest decreases in serotonin itself or 5-HIAA in either the brainstem or the frontal cortex of suicide
victims
 Postmortem receptor studies :significant changes in presynaptic and postsynaptic serotonin binding
sites in suicide victims.

Genetic factors

 Suicidal behavior tends to run in families.

 A family history of suicide increases the risk of attempted suicide and that of completed suicide in most
diagnostic groups

MOLECULAR GENETICS STUDY

 Tryptophan hydroxylase (TPH) is an enzyme involved in the biosynthesis of serotonin

 Such individuals may have alterations in genes controlling serotonin synthesis and metabolism.
 a history of multiple suicide attempts was found most often in subjects with the LL genotype and to a lesser extent among those with the UL genotype
 This led to the suggestion that the L allele was associated with repetitive suicidal behavior. The presence of one TPH*L allele may indicate a reduced capacity to
hydroxylate tryptophan to 5-hydroxytryptophan in the synthesis of serotonin, producing low central serotonin turnover and, thus, a low concentration of 5-HIAA in CSF.
CARE FOR THE PATIENT WITH SELF-HARM

• Treat people who have self-harmed with the same care, respect and privacy given to other people, and be sensitive to the emotional distress associated with self-
harm.
 • Include the carers if the person wants their support during assessment and treatment;

• if possible, the psychosocial assessment should include a one-to-one interview between the person and the health worker, to explore private issues.

• Provide emotional support to carers/family members if they need it.

• Ensure continuity of care.

• Hospitalization in non-psychiatric services of a general hospital is not recommended for the prevention of self-harm.

• However, if admission to a general (non-psychiatric) hospital is necessary for the management of the medical consequences of self-harm, monitor the
person closely to prevent further self-harm in the hospital.

• If prescribing medication:

– Use medicines that are the least hazardous, in case of intentional overdose.

– Give prescriptions as short courses (e.g. one week at a time).

OFFER AND ACTIVATE PSYCHOSOCIAL SUPPORT

• Offer support to the person

• Explore reasons and ways to stay alive.

• Focus on the person’s strengths by encouraging them to talk of how earlier problems have been resolved.

• Consider problem-solving therapy to help people with acts of self-harm within the last year, if sufficient human resources are available.

• Activate psychosocial support

– Mobilize family, friends, concerned individuals and other available resources to ensure close monitoring of the person as long as the risk of self-harm/suicide
persists.
– Advise the person and carers to restrict access to means of self-harm/suicide when the person has thoughts or plans of self-harm/suicide.
– Optimize social support from available community resources. These include informal resources, such as relatives, friends, acquaintances, colleagues and
religious leaders or formal community resources, if available, such as crisis centres, and local mental health centres.

CARERS SUPPORT

– Inform carers and family members that asking about suicide will often help the person feel relieved, less anxious, and better understood.
– Carers and family members of people at risk of self-harm often experience severe stress. Provide emotional support to them if they need it.
– Inform carers that even though they may feel frustrated with the person, they should avoid hostility and severe criticism towards the vulnerable person at risk
of self-harm/suicide.

PSYCHOEDUCATION

– Key messages to the person and the carers

o If one has thoughts of self-harm/suicide, seek help immediately from a trusted family member, friend or health care provider.
o It is okay to talk about suicide. Talking about suicide does not provoke the act of suicide.
o Suicides are preventable.
o Having an episode of self-harm/suicide is an indicator of severe emotional distress. The person does not see an alternative or a solution. Therefore, it is
important to get the person immediate support for emotional problems and stressors.
o Means of self-harm (e.g. pesticides, firearms, medications) should be removed from the home.
o The social network, including the family and relevant others, is important for provision of social support.

BIPOLAR PATIENTS

*** Bipolar disorder is a serious mental illness that is characterized by extreme
mood swings from mania to depression. Mania is an abnormally elevated mood,
while depression is an abnormally low mood.
***MSE
– Manic patients are excited, talkative, sometimes amusing, and frequently
hyperactive. At times, they are grossly psychotic and disorganized and
require physical restraints and the intramuscular injection of sedating
drugs.
– Mood, Affect, and Feelings
o Manic patients classically are euphoric, but they can also be irritable,
especially when mania has been present for some time. They also
have a low frustration tolerance, which can lead to feelings of anger
and hostility. Manic patients may be emotionally labile, switching from
laughter to irritability to depression in minutes or hours.
– Speech
o Manic patients cannot be interrupted while they are speaking, and
they are often intrusive nuisances to those around them. Their
speech is often disturbed. As the mania gets more intense, speech
becomes louder, more rapid, and di􀉽cult to interpret. As the activated
state increases, their speech is filled with puns, jokes, rhymes, plays
on words, and irrelevancies. At a still greater activity level,
associations become loosened, the ability to concentrate fades, and
􀉽ight of ideas, clanging, and neologisms appear. In acute manic
excitement, speech can be totally incoherent and indistinguishable
from that of a person with schizophrenia.
– Perceptual Disturbances. Delusions occur in 75 percent of all manic
patients. Mood-congruent manic delusions are often concerned with
great wealth, extraordinary abilities, or power. Bizarre and mood-
incongruent delusions and hallucinations also appear in mania.
– Thought. The manic patient’s thought content includes themes of
self-confidence and self-aggrandizement. Manic patients are often
easily distracted, and their cognitive functioning in the manic state is
characterized by an unrestrained and accelerated flow of ideas.
– Sensorium and Cognition. Although the cognitive deficits of patients
with schizophrenia have been much discussed, less has been written
about similar deficits in patients with bipolar I disorder. These deficits can
be interpreted as reflecting diffuse cortical dysfunction; subsequent work
may localize the abnormal areas. Grossly, orientation and memory are
intact, although some manic patients may be so euphoric that they answer
questions testing orientation incorrectly. Emil Kraepelin called the symptom
“delirious mania.”
– Impulse Control. About 75 percent of all manic patients are assaultive
or threatening. Manic patients do attempt suicide and homicide, but the
incidence of these behaviors is unknown.
– Judgment and Insight. Impaired judgment is a hallmark of manic
patients. They may break laws about credit cards, sexual activities, and
finances and sometimes involve their families in financial ruin. Manic
patients also have little insight into their disorder.
– Reliability. Manic patients are notoriously unreliable in their
information. Because lying and deceit are common in mania,
inexperienced clinicians may treat manic patients with inappropriate
disdain.
Roles and Relationships
– Rarely can fulfill role responsibilities
– Have trouble at work or school---too distracted and hyperactive to pay
attention to children or ADLs
– Begins many tasks or projects but completes few
– Have a great need to socialize but little understanding of their excessive,
overpowering, and confrontational social interactions,
– Their need for socialization often leads to promiscuity
– Invades the intimate space and personal business or others
– Labile emotions
– Can become hostile to others whom they perceive as standing in way of
desired goals
– Cannot postpone or delay gratifications
Physiologic and self-care considerations
– Can go days w/o sleep or food and not even realize they are hungry or tired
– Unwilling to stop or unable to rest or sleep even on the brink of physical
exhaustion
– Ignores personal hygiene as “boring” when they have “more important
things” to do
– Throws away possessions or destroy valued items
– May physically injure themselves
– Tend to ignore or be unaware of health needs
Psychoanalytic Approach
– Cause of both manic/depressive episodes arise from a low self-concept
– Depressive episodes represent this, while manic episodes represent a
defense against the low self-concept.
Trait Approach
❖ Mania:Excessive happiness, irritability, less need for sleep, racing
thoughts, increased energy, etc.
❖ Depression: Sadness, loss of energy, increased need for sleep,
change in appetite, thoughts of death/suicide, etc.
Biological Approach
– The biological approach to bipolar disorder suggests that high or low levels
of neurotransmitters such as dopamine, serotonin, or norepinephrine is the
cause.
Humanistic Approach
- When circumstances stop or hinder a person and force them to loose
there drive toward self-actualization, and the ultimate fulfillment of
one’s dreams, desires, and potential.
Behavioral and Social Learning Approach
– The behavioral/social learning approach to bipolar disorder suggests that
these behaviors are learned and therefore can be unlearned.
Cognitive Approach
• - Individuals in a manic phase often have grandiose thoughts, such as one
being capable of doing anything. Those in a depressive phase often have
self-deprecating thoughts, such as “I am terrible at this, or why can’t I do
anything right?”
Treatment
Three types of short-term psychotherapies—cognitive therapy,
interpersonal therapy, and behavior therapy
– Thus, treatment should address the number and severity of stressors in
patients’ lives postulated to be present in major depressive disorder. Such
distortions include selective attention to the negative aspects of
circumstances and unrealistically morbid inferences about consequences.
For example, apathy and low energy result from a patient’s expectation of
failure in all areas.
– COGNITIVE THERAPY: The goal of cognitive therapy is to alleviate
depressive episodes and prevent their recurrence by helping patients
identify and test negative cognitions; develop alternative, flexible, and
positive ways of thinking; and rehearse new cognitive and behavioral
responses.
– INTERPERSONAL THERAPY. Interpersonal therapy, developed by Gerald
Klerman, focuses on one or two of a patient’s current interpersonal
problems. This therapy is based on two assumptions. First, current
interpersonal problems are likely to have their roots in early dysfunctional
relationships. Second, current interpersonal problems are likely to be
involved in precipitating or perpetuating the current depressive symptoms.
o The interpersonal therapy program usually consists of 12 to 16
weekly sessions and is characterized by an active therapeutic
approach. Intrapsychic phenomena, such as defense mechanisms
and internal con􀉽icts, are not addressed. Discrete behaviors—such
as lack of assertiveness, impaired social skills, and distorted
thinking—may be addressed but only in the context of their meaning
in, or their effect on, interpersonal relationships.
– BEHAVIOR THERAPY. Behavior therapy is based on the hypothesis that
maladaptive behavioral patterns result in a person’s receiving little positive
feedback and perhaps outright rejection from society. By addressing
maladaptive behaviors in therapy, patients learn to function in the world in
such a way that they receive positive reinforcement.

DSM 5 CRITERIA: Bipolar I Disorder

For a diagnosis of bipolar I disorder, it is necessary to meet tlie following criteria for a manic episode. The manic episode may have been preceded by and may be
followed by hypomanic or major depressive episodes

Manic Episode
A. A distinct period of abnormally and persistently elevated, expansive, or irritable mood and abnormally and persistently increased goal-directed activity or energy, lasting at
least 1 week and present most of the day, nearly every day (or any duration if hospitalization is necessary).
B. During the period of mood disturbance and increased energy or activity, three (or more) of the following symptoms (four if the mood is only irritable) are present to a significant
degree and represent a noticeable change from usual behavior:
1. Inflated self-esteem or grandiosity.
2. Decreased need for sleep (e.g., feels rested after only 3 hours of sleep).
3. More talkative than usual or pressure to keep talking.
4. Flight of ideas or subjective experience that thoughts are racing.
5. Distractibility (i.e., attention too easily drawn to unimportant or irrelevant external stimuli), as reported or observed.
6. Increase in goal-directed activity (either socially, at work or school, or sexually) or
psychomotor agitation (i.e., puφoseless non-goal-directed activity).
7. Excessive involvement in activities that have a high potential for painful consequences (e.g., engaging in unrestrained buying sprees, sexual indiscretions, or foolish business
investments).
C. The mood disturbance is sufficiently severe to cause marked impairment in social or occupational functioning or to necessitate hospitalization to prevent harm to self or
others, or there are psychotic features.
D. The episode is not attributable to the physiological effects of a substance (e.g., a drug of abuse, a medication, other treatment) or to another medical condition.
Note: A full manic episode that emerges during antidepressant treatment (e.g., medication, electroconvulsive therapy) but persists at a fully syndromal level beyond the
physiological effect of that treatment is sufficient evidence for a manic episode and, therefore, a bipolar I diagnosis.
Note: Criteria A-D constitute a manic episode. At least one lifetime manic episode is required for the diagnosis of bipolar I disorder.

Hypomania Episode
A. A distinct period of abnormally and persistently elevated, expansive, or irritable mood and abnormally and persistently increased activity or energy, lasting at least 4
consecutive days and present most of the day, nearly every day.
B. During the period of mood disturbance and increased energy and activity, three (or more) of the following symptoms (four if the mood is only irritable) have persisted, represent
a noticeable change from usual behavior, and have been present to a significant degree:
1. Inflated self-esteem or grandiosity.
2. Decreased need for sleep (e.g., feels rested after only 3 hours of sleep).
3. More talkative than usual or pressure to keep talking.
4. Flight of ideas or subjective experience that thoughts are racing.
5. Distractibility (i.e., attention too easily drawn to unimportant or irrelevant external stimuli), as reported or observed.
6. Increase in goal-directed activity (either socially, at work or school, or sexually) or psychomotor agitation.
7. Excessive involvement in activities that have a high potential for painful consequences (e.g., engaging in unrestrained buying sprees, sexual indiscretions, or foolish business
investments).
C. The episode is associated with an unequivocal change in functioning that is uncharacteristic of the individual when not symptomatic.
D. The disturbance in mood and the change in functioning are observable by others.
E. The episode is not severe enough to cause marked impairment in social or occupational functioning or to necessitate hospitalization. If there are psychotic features, the
episode is, by definition, manic.
F. The episode is not attributable to the physiological effects of a substance (e.g., a drug of abuse, a medication, other treatment).
Note: A full hypomanie episode that emerges during antidepressant treatment (e.g., medication, electroconvulsive therapy) but persists at a fully syndromal level beyond the
physiological effect of that treatment is sufficient evidence for a hypomanie episode diagnosis. However, caution is indicated so that one or two symptoms (particularly increased
irritability, edginess, or agitation following antidepressant use) are not taken as sufficient for diagnosis of a hypomanie episode, nor necessarily indicative of a bipolar diathesis.
Note: Criteria A-'F constitute a hypomanie episode. Hypomanie episodes are common in bipolar I disorder but are not required for the diagnosis of bipolar I disorder.

Major Depressive Episode

A. Five (or more) of the following symptoms have been present during the same 2-week period and represent a change from previous functioning; at least one of the symptoms
is either (1) depressed mood or (2) loss of interest or pleasure.
Note: Do not include symptoms that are clearly attributable to another medical condition.
1. Depressed mood most of the day, nearly every day, as indicated by either subjective report (e.g., feels sad, empty, or hopeless) or observation made by others (e.g., appears
tearful). (Note: 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).
3. Significant weight loss when not dieting or weight gain (e.g., a change of more than 5% of body weight in a month), or decrease or increase in appetite nearly every day.
(Note: In children, consider failure to make expected weight gain.)
4. Insomnia or hypersomnia nearly every day.
5. Psychomotor agitation or retardation nearly every day (observable by others; not merely subjective feelings of restlessness or being slowed down).
6. Fatigue or loss of energy nearly every day.
7. Feelings of worthlessness or excessive or inappropriate guilt (which may be delusional) nearly every day (not merely self-reproach or guilt about being sick).
8. Diminished ability to think or concentrate, or indecisiveness, nearly every day (either by subjective account or as observed by others).
9. Recurrent thoughts of death (not just fear of dying), recurrent suicidal ideation without a specific plan, or a suicide attempt or a specific plan for committing suicide.
B. The symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.
C. The episode is not attributable to the physiological effects of a substance or another medical condition.
Note: Criteria A-C constitute a major depressive episode. Major depressive episodes are common in bipolar I disorder but are not required for the diagnosis of bipolar I disorder.
Note: Responses to a significant loss (e.g., bereavement, financial ruin, losses from a natural disaster, a serious medical illness or disability) may include the feelings of intense

SCHIZOPHRENIA SPECTRUM

-The limbic system has been particularly implicated in neuropathological studies of schizophrenia.
-Eugen Bleuler’s well known four A’s of schizophrenia—affect, associations, ambivalence, and autism—refer to brain functions served in part by limbic structures
-coined the term schizophrenia
-Benedict Morel: démenceprécoce: to describe deteriorated patients whose illnesses began in adolescence
-Emil Kraepelin: dementia precox, a term that emphasized the change in cognition (dementia) and early onset (precox) of the disorder.
-paranoia: persistent persecutory delusions
-Lifetime prevalence:1%
-Men=Women, onset earlier in men than women, peak: 10 to 25 years for men and 25 to 35 years for women.
-Etiology:
Genetics: monozygotic twins: 50%, 4-5x concordance in dizygotic twins,
Biochemical factors: too much dopaminergic activity
-serotonin excess: cause of both positive and negative symptoms
-norepinephrine: anhedonia
-Psychoanalytic theories:
-Sigmund Freud: developmental fixations early in life defects in ego development
-Family dynamics:
-double bind: formulated by Gregory Bateson and Donald Jackson to describe a hypothetical family in which children receive conflicting parental
messages about their behavior, attitudes, and feelings.
-schisms and skewed families: Theodore Lidz
Subtypes:
a. Paranoid: characterized by preoccupation with one or more delusions or frequent auditory hallucinations. Classically, the paranoid type of schizophrenia is
characterized mainly by the presence of delusions of persecution or grandeur
b. Disorganized type: characterized by a marked regression to primitive, disinhibited, and unorganized behavior and by the absence of symptoms that meet the
criteria for the catatonic type.
-onset: before 25 y/o
c. Catatonic: marked disturbance in motor function; this disturbance may involve stupor, negativism, rigidity, excitement, or posturing
d. Undifferentiated type:
e. Residual type: characterized by continuing evidence of the schizophrenic disturbance in the absence of a complete set of active symptoms or of sufficient
symptoms to meet the diagnosis of another type of schizophrenia.
• Schizophrenia: 6 months
• Schizoaffective disorder: features of both schizophrenia and mood disorders
o Lifetime prev: <1%
• Schizophreniform: symptoms more than one month but less than 6 months
• Brief Psychotic disorder: symptoms more than one day but less than 1 month
 ALCOHOL USE DISORDER

Table 12.2-2 Epidemiological Data for Alcohol-Related Disorders

Race and Ethnicity • Whites have the highest rate of alcohol use
• Hispanics and blacks have similar rate of binge use, but is lower among blacks than among whites
Gender • Men are much more likely than women to be binge drinkers and heavy drinkers
Region and • Alcohol use is highest in western states and lowest in southern states
Urbanicity • North central and northeast regions are about the same
• The rate of past month alcohol use was 56 percent in large metropolitan areas, 52 percent in small metropolitan areas, and 46 percent
in nonmetropolitan areas.
• Little variation seen in binge and heavy alcohol use rates by population density.

Impairment likely to be seen at different blood alcohol concentrations

Level (mg/dL) Likely impairment
20-30 Slowed motor performance and decreased thinking
ability
30-80 Increases in motor and cognitive problems
80-200 Increases in coordination and judgment errors
Mood lability
Deterioration in cognition
200-300 Nystagmus, marked slurring of speech, and alcoholic
blackouts
>300 Impaired vital signs and possible death

• Alcohol is metabolized by two enzymes: alcohol dehydrogenase (ADH) and aldehyde dehydrogenase. ADH catalyzes the conversion of alcohol into acetaldehyde, which
is a toxic compound; aldehyde dehydrogenase catalyzes the conversion of acetaldehyde into acetic acid. Aldehyde dehydrogenase is inhibited by disulfiram (Antabuse),
often used in the treatment of alcohol-related disorders. Some studies have shown that women have a lower ADH blood content than men; this fact may account for
woman's tendency to become more intoxicated than men after drinking the same amount of alcohol.
DIAGNOSTIC TESTS FOR ALCOHOLISM
• The most direct test available to measure alcohol consumption cross-sectionally is blood alcohol concentration, which can also be used to judge tolerance to
alcohol
• One sensitive laboratory indicator of heavy drinking is a modest elevation or high-normal levels (>35 units) of gamma-glutamyltransferase (GGT).
• At least 70% of individuals with a high GGT level are persistent heavy drinkers (i.e., consuming eight or more drinks daily on a regular basis).
• A second test with comparable or even higher levels of sensitivity and specificity is carbohydrate-deficient transferrin (CDT), with levels of 20 units or higher useful
in identifying individuals who regularly consume eight or more drinks daily.
• Liver function tests (e.g., alanine aminotransferase [ALT] and alkaline phosphatase) can reveal liver injury that is a consequence of heavy drinking