Hannah Friedman

Psychiatry final 6 year

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 Hannah Friedman

Psychiatry Topic List

A Topics – General Psychiatry
1. The concept and history of psychiatric diseases
2. Classification in Psychiatry
3. Taking psychiatric history
4. Genetic background and the role of neurotransmitters in psychiatric disorders
5. The examination and disturbances of consciousness
6. The examination and disturbances of orientation
7. The examination and disturbances of attention and concentration
8. The examination and disturbances of memory
9. The examination and disturbances of thinking
10. The examination and disturbances of perception
11. The examination and disturbances of affect and mood and affect
12. The idea and disorders of intelligence. Intelligence testing
13. Aggression in psychiatric disorders
14. Laboratory tests in psychiatry
15. Psychiatric rating scales
16. Psychological testing of personality
17. Neuroimaging in psychiatry
18. Forensic psychiatry
19. Defence mechanisms
20. Psychosocial treatment and rehabilitation
21. Consultation-liaison psychiatry
22. Theories of personality and psychopathology
B Topics – Diseases
1. The classification of organic mental syndromes
2. Depressive pseudodementia
3. Reversible dementia, amnestic disorders
4. Alzheimer’s dementia, neurodegenerative disorders
5. Delirium
6. Alcohol abuse and dependence
7. Epidemiology and aetiology of alcohol-related disorders
8. Psychiatric morbidity in alcohol-related disorders
9. Alcohol intoxication, idiosyncratic alcohol intoxication
10. Alcohol withdrawal syndrome and delirium tremens
11. Alcohol-induced psychotic disorder
12. The bases of substance addiction
13. Illicit drug-related disorders
14. Benzodiazepine - abuse and dependence
15. The aetiology of schizophrenia
16. Clinical features of schizophrenia
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17. The subtypes and course of schizophrenia

18. The differential diagnosis of schizophrenia and other psychotic disorders
19. Schizoaffective disorders
20. The aetiology of delusional disorders
21. Delusional psychosis
22. Postpartum blues, depression and psychosis
23. Biological and genetic factors of mood disorders
24. The clinical features, diagnosis and course of depression
25. Bipolar disorders, dysthymia, cyclothymia
26. Obsessive-compulsive disorders
27. Panic disorder and agoraphobia
28. Specific phobias, social phobia
29. Generalized anxiety disorder, mixed anxiety-depressive disorder.
30. Acute stress disorder, PTSD, adjustment disorders
31. Dissociative disorders
32. Somatoform disorders
33. Sleep disorders
34. Pathology of human sexual behaviour and gender identity
35. Impulse control disorders
36. The aetiology and significance of personality disorders
37. Cluster A personality disorders: odds and eccentrics
38. Cluster B personality disorders: dramatics
39. Cluster C personality disorders: anxious
40. Anorexia nervosa. Bulimia nervosa
41. The overview and treatment of psychosomatic diseases
42. Mental retardation.
43. The most common psychiatric disorders in childhood
44. Geriatric psychiatry
45. Depression in old age
46. Psychotic disorders in old age
47. Suicide: Alarming signs and Prevention
48. Suicide, Crisis, “Cry for help”
49. Psychiatric features of neurological diseases (excluding epilepsy)
50. Ictal and Interictal psychiatric symptoms in epilepsy
51. Psychiatric symptoms in general medical conditions
C Topics – Treatments
1. The treatment of dementia
2. The treatment of alcohol dependence
3. The management of acute alcohol intoxication
4. The management of alcohol withdrawal syndromes
5. Wernicke-Korsakoff syndrome and its treatment
6. The complex treatment of drug-related disorders
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7. The complex treatment of schizophrenia (pharmaco-psycho-sociotherapy)

8. The complex therapy of anxiety disorders
9. The principles of anxiolytic therapy
10. The pharmacotherapy of depression
11. The side effects of antidepressants
12. Non-pharmacological therapies of depression
13. Treatment of bipolar disorders
14. Mood stabilizers
15. The classification of antipsychotics
16. Clinical use of antipsychotics
17. The side effects of antipsychotics
18. The symptoms and treatment of neuroleptic malignant syndrome.
19. Electroconvulsive therapy
20. The idea and principles of psychotherapy
21. Major psychotherapy schools
22. Group psychotherapy, family therapy
23. The treatment of postpartum psychosis
24. The treatment of personality disorders
25. The treatment of specific phobias and social phobia
26. The treatment of sleep disorders
27. Psychiatric emergencies. The treatment of violence
28. The treatment of patients after a suicide attempt
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Topic 1: The concept and history of psychiatric diseases

Concept:
 Psychiatry is the medical specialty devoted to the study and treatment of mental
disorders - including affective, behavioral, cognitive and perceptual disorders.
 Psychiatric assessment typically starts with a mental status examination and case
history. Psychological tests and physical examination may be conducted, including on
occasion the use of neuroimaging or other neurophysiological techniques.
 Mental disorders are diagnosed in accordance with criteria listed in diagnostic manuals
such as Diagnostic and Statistical Manual of Mental Disorders (DSM), published by the
American Psychiatric Association, and the International Classification of Diseases (ICD)
edited and used by the World Health Organization. The 5th edition of DSM (DSM-5) will
be released in 2013, and is expected to have significant impact on many medical fields.
 Psychiatric treatment uses different modalities, including medication, psychotherapy
and a wide range of other techniques such as transcranial magnetic stimulation.
 Treatment may be as inpatient or outpatient, according to severity of function
impairment/the disorder in question.

History:
The term psychiatry was first coined by the German physician Johann Christian Reil in 1808
and literally means "medical treatment of the mind".

Ancient
 Egypt – mental illnesses thought to be due to magical forces of the deities. The therapists
were pristes who used magico-religious treatment.
 Greek and Roman – mental illness were viewed as mainly psychological, somatic or
combination of both.
Middle age
 Number of hospitals known as bimaristans were built throughout Arab countries beginning
around the early 9th century, with the first in Baghdad.
19th century
 1808 German physician Johann Christian Reil coined the term "psychiatry". [
 1812 American physician Benjamin Rush became one of the earliest advocates of humane
treatment for the mentally ill with the publication of Medical Inquiries and Observations
Upon Diseases of the Mind,the first American textbook on psychiatry.
 1821 The element lithium was first isolated from lithium oxide and described by English
chemist William Thomas Brande
 1844 American Psychiatric Association (APA), was founded in Philadelphia, Pennsylvania.
 1893 German psychiatrist Emil Kraepelin clinically defined "dementia praecox", later
reformulated as schizophrenia.
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 1895 Sigmund Freud and Josef Breuer of Austria published Studies on Hysteria, based on the
case of Bertha Pappenheim (known as Anna O.), developing the Talking Cure; Freud and
Breuer later split over Freud's obsession with sex.
 1899 dementia praecox (schizophrenia) was introduced in the 6th edition of Emil Kraepelin's
famous Lehrbuch
20th century
 1900 Russian neurologist Vladimir Bekhterev discovered the role of the hippocampus in
memory.
 1901 German psychiatrist Alois Alzheimer identified the first case of what later became
known as Alzheimer's disease.
Sigmund Freud published The Psychopathology of Everyday Life.
 1905 French psychologists Alfred Binet and Theodore Simon created the Binet-Simon
Scale to assess intellectual ability, marking the start of standardized psychological testing.
 1906 Russian physiologist Ivan Pavlov published the first Conditioning studies.
 1908 The term "Schizophrenia" was coined by Swiss psychiatrist Paul Eugen Bleuler.
 1910 Sigmund Freud founded the International Psychoanalytical Association (IPA), with Carl
Jung as the first president, and Otto Rank as the first secretary.
 1911 Alfred Adler left Freud's Psychoanalytic Group to form his own school of thought,
accusing Freud of overemphasizing sexuality and basing his theory on his own childhood.
 1920 Swiss psychiatrist Hermann Rorschach developed the Rorschach Inkblot Test.
 1921 Sigmund Freud published Group Psychology and the Analysis of the Ego.
 1923 German pharmacologist Otto Loewi and English neuroscientist Sir Henry
Dale discovered Acetylcholine, the first neurotransmitter to be described, winning them the
1936 Nobel Prize.
 1924 German neuropsychiatrist Hans Berger discovered human Electroencephalography.
 1933 Hungarian psychiatrist Sándor Ferenczi (Freud’s student) published a paper claiming
that patient accounts of childhood sexual abuse are true, providing a psychological
explanation, causing Freud to break with him. (VERY IMPORTANT!)
 1944 Ritalin (Methylphenidate) was synthesized.
 1950 The World Psychiatric Association was founded.
 1952 The first monoamine oxidase inhibitor (MAOI) antidepressant iproniazid was
discovered.
 1960s Aaron T. Beck developed cognitive therapy.
 1977 The ICD-9 was published by the WHO.
21th century
 2013 DSM-5 was published by the American Psychiatric Association.
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Topic 2: Classification in Psychiatry (SOLLA)

There are two major classification systems used in psychiatry:
 Diagnosis and Statistical Manual of Mental Disorders (DSM)
o Current edition is called DSM-5 (released in May 2013)
- Published by the American Psychiatric
Assosiation (ASA)
o Most text books still follow the older version
DSM IV TR (2000)
- TR (text revision)
o In these notes I will describe DSM IV TR but
also list the major changes that were applied
in DSM-5
 International Classification of Diseases (ICD)
o Current edition is called ICD-10 - Published by WHO
o Chapter V deals with Mental and Behavioral disorders

DSM IV TR

 Used by all mental health professionals to diagnose psychiatric disorders

 Contains diagnostic criteria for 17 major categories of
mental disorders, comprising 375 discrete illnesses
DSM IV TR organized each psychiatric diagnosis into 5 axes
relating to different aspects of disorder or disability:
 Axis I: All psychological diagnostic categories except
mental retardation and personality disorder
o E.g. Depression, anxiety disorders, bipolar
disorders, ADHD, autism spectrum disorders,
anorexia n., bulimia, schizophrenia
 Axis II: Personality disorders and mental retardation
o E.g. Paranoid-, schizoid-, schizotypal-,
borderline-, antisocial, narcissistic-, histrionic-,
avoidant-, dependent- and obsessive-
compulsive personality disorders + intellectual
disabilities
 Axis III: General medical condition, acute and physical disorders
o E.g. Brain injuries or other medical/physical disorders
 Axis IV: Psychosocial & environmental factor contributing to the disorder
 Axis V: GAF or children’s global assessment scale for children <18 years

Major categories of DSM IV TR:

1. Disorders usually first diagnosed in infancy, childhood, or adolescence

 Mental retardation, learning difficulties, motor skill disorders, communication disorders,
pervasive developmental disorders (autism, Asbergers), attention-deficit and disruptive
behavior disorders, feeding and eating disorders of infancy or early childhood, tic
disorders, elimination disorders etc.
2. Delirium, dementia, amnestic and other cognitive disorders
 Characterized by change in brain structure and function that results in impaired learning,
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orientation, judgment, memory and intellect

3. Mental disorders due to a general medical condition
4. Substance-related disorders
5. Schizophrenia and other psychotic disorders
 Schizophrenia (5 subtypes), delusional disorder, brief psychotic disorder,
schizophreniform disorder, schizoaffective disorder, shared psychotic disorder, psychotic
disorder resulting from a general medical condition, substance-induced psychotic
disorder, atypical psychosis
6. Mood disorders
 Bipolar disorder, depressive disorders, major depressive disorder
7. Anxiety disorders
 Generalized anxiety disorder, panic disorder, phobias, OCD, acute stress disorder, PTSD,
medical or substance related anxiety
8. Somatoform disorders
 Marked by preoccupation with the body and fear of disease
o Somatization disorder, conversion disorder, hypochondriasis, pain disorder, body
dysmorphic disorder
9. Factitious disorders
 Characterized by the intentional production or feigning of psychological or physical
symptoms (or sometimes both) to assume the role of a sick person (Munchausen
syndrome)
10. Dissociative disorders
 Characterized by sudden, temporary change in consciousness or identity – dissociative
amnesia, fugue or identity disorder
11. Sexual and gender identity disorders
 Paraphilias, gender identity disorders and sexual dysfunctions
12. Eating disorders Anorexia nervosa, bulimia nervosa
13. Sleeping disorders
 Dyssomnias, parasomnias, narcolepsy, breathing related sleep disorders, circadian
rhythm sleep disorder, medical/substance related
14. Impulse-control disorders not elsewhere classified
 Covers disorders in which persons cannot control impulses & act out
 Intermittent explosive disorder, kleptomania, pyromania, trichotillomania, pathological
gambling
15. Adjustment disorders
 Maladaptive reaction to a clearly defined life stress – 6 subtypes
16. Personality disorders
 Paranoid-, schizoid-, schizotypal-, obsessive-compulsive-, histrionic-, avoidant-,
antisocial-, narcissistic-, borderline- & dependent personality disorders
17. Other conditions that may be a focus of clinical attention
 Psychological factors affecting physical condition (psychosomatic)
o Atopic dermatitis, backache, asthma, HTN, migraine, ulcers, irritable bowel
syndrome, colitis
 Medication induced movement disorders
o Parkinsonism, neuroleptic malignant syndrome, acute dystonia, acute akathisia,
tardive dyskinesia and postural tremor - related to dopamine R antagonists
(Chlorpromazine)
 Relational problems
o Parent-child problems, marriage problems etc.
 Problems related to abuse (physical/sexual) or neglect
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Major changes seen in DMS-5

 Multiaxial system (described above) for mental disorders was removed

 Mental retardation has a new name:
o Intellectual disability or intellectual developmental disorder
 Phonological disorders are now called communication disorders
 Autism spectrum disorders incorporate Asperger
disorder, childhood disintegrative disorder and
pervasive developmental disorder not otherwise
specified (NOS)
o So Asperger syndrome was dropped as a distinct classification
 Motor disorders (new subcategory) includes
developmental coordination disorder, stereotypic
movement disorder and tic disorders (Tourette)
 All subtypes of Schizophrenia were removed in DMS-5
 A major mood episode is required for schizoaffective disorder
 Catatonia in all contexts required 3 of total 12 symptoms
 Bereavement exclusion in DMS IV was removed
from depressive disorders in DMS-5
 New addition: Disruptive mood dysregulation disorder in children <18
 Premenstrual dysphoric disorder became a disorder
 Dysthymia should be called persistent depressive disorder
 Panic disorder and agoraphobia became separate
 New chapter on obsessive-compulsive and related disorders
o Includes four new disorders:
 Excoriation disorder, hoarding disorder,
substance- or medication induced OC
and related disorder and OC and related
disorder due to other medical condition
 Trichotillomania moved to obsessive-compulsive disorders
 Posttraumatic stress disorder (PTSD) is now in a
new section titled “Trauma- and stressor related
disorders”
 Somatoform disorders are now somatic symptom & related disorders
 Binge eating disorder is now a diagnosis
 Criteria for anorexia nervosa does not include amenorrhea anymore
 Name change for gender identity disorder into gender dysphoria
 Gambling disorder and tobacco use disorder were added
into substance related and addictive disorders

ICD-10 section V – Mental and behavioral disorders:

1. Organic, including symptomatic, mental disorders

2. Mental and behavioral disorders due to psychoactive substance use
3. Schizophrenia, schizotypal and delusional disorders
4. Mood (affective) disorders
5. Neurotic, stress-related and somatoform disorders
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6. Behavioral syndromes asso. w. physiological disturbances & physical factors

7. Disorders of adult personality and behavior
8. Mental retardation
9. Disorders of psychological development
10. Behavioral and emotional disorders with onset usually
occurring in childhood and adolescence
11. Unspecified mental disorders
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Topic 3: Taking psychiatric history (Psychiatric department)

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Topic 4: Genetic background and the role of neurotransmitters in psychiatric disorders

Genetic:
o Mental illness tend to run in families.
o There is no gene that cause psychiatric disorders.

Neurotransmitters - Endogenous chemicals that enable neurotransmission. It is a type of chemical messenger

which transmits signals across a chemical synapse. Include:
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Summary:
Alzheimer's: ↓Ach, ↑Glutamate, ↓NE
Parkinson: ↓Dopamine, ↑Ach
Huntington: ↓GABA
Depression: ↓Serotonin, ↓Dopamine, ↓Norepi, ↑Ach
Schizophrenia: ↑Dopamine, ↓Glutamate
Alcohol: ↑GABA (CNS depression), ↑5HT (pleasure), ↓Glutamate
Anxiety: ↓Serotonin, ↑NE, ↓GABA
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Topic 5: The examination and disturbances of consciousness

*Don’t forget GCS –

clinical measure of
conscious level.
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Topic 6: The examination and disturbances of orientation

Orientation: Continuous, correct judgement of the connection between the individual and their outer world.
Examination:
a) Autopsychic – refers to patient’s own mind or self - consciousness
- What’s your name?
- How old are you?
- When and where were you born?
- What’s your occupation?
- Are you married?
- Where do you live? (city)

a) Allopsychic – refers to the patients mind in relations to the outside world

- What’s my occupation? (doctor, student)
- Who are those people in the same room as you? (patients)
- Who takes care of you? (nurses)

a) in time
- What’s the date today? (day, month)
- What day of the week is it?
- What year are we in?

d) in space
- Where are we now, what is this room? (examining room)
- What is this building, what is this institution?: (hospital, university, psychiatry)
- In which town, in which country are we in?: (Debrecen, Hungary)

Disorder: disorientation - partial

- total

Occurence of disorder:
- disorders of intelligence (total or partial)
- Korsakov’s syndrome (disorientation in time and space)
- schizophrenia (autopsychic)
- organic psychosyndromes: - Delirium (in time and space)
- Intoxications, fever, strokes, after epileptiform
convulsions
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Topic 7: The examination and disturbances of attention and concentration

Attention: the ability to focus on the matter in hand. It selects among stimuli, might be called the filter of the
mind.

Characteristics:
- alertness
- capacity
- intensity
- tenacity (for how long the patient can focus it)
- vigilance (how easily the patient can change its object)

Examination:

a) Serial sevens test: ask the patient to subtract 7 from l00 and then take 7 from the reminder repeatedly
and observe the time and the number of errors)
b) Ask the patient to tell the days of the week or the months of the year in reverse order.
c) Bourdon test: the patient has to underline the letter “e” in a text written in a foreign language. Assessment:
time needed, number of mistakes.
“Krąpielowate (Taccaceae Dumort.) – monotypowa rodzina roślin z rzędu pochrzynowców (Dioscoreales),
obejmująca jeden rodzaj – krąpiel (Tacca J.R.Forst. & G.Forst.), liczący 15 gatunków, występujących w
strefie klimatu tropikalnego i subtropikalnego. Rośliny zaliczane do tej rodziny charakteryzują się
specyficznymi kwiatostanami, zbudowanymi z liściowatych podsadek, nitkowatych przysadek i
szypułkowych kwiatów, przeważnie w ciemnych, bordowo-purpurowych kolorach. Rośliny z tej rodziny
znajdują szerokie zastosowanie, przede wszystkim jako rośliny lecznicze i spożywcze, a w ostatnich latach
również jako rośliny ozdobne.”

Disorders:
- reduction of each characteristic
- hypertenacity + hypovigilance (depression, epileptic, personality disorder)
- hypotenacity + hypervigilance (mania, schizophrenia)
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Topic 8: The examination and disturbances of memory

Memory: the psychological function that forms, stores and recalls imagery.

Process:
1. imprinting
2. storing
3. recalling

Types:
- short-term memory
- long-term memory (general knowledge, recall the curriculum)

Characteristics:
- capacity
- durability
- accuracy

Examination:
a) Short-term memory:
Ziehen’s test: Ask a multiplication (e.g. 9x7), then ask the patient to repeat 2 sequences of numbers, then
ask what the multiplication was.
Ranschburg-Ziehen test: ten pair of words, recall immediately and after 5 minutes, assessment: %
lake - river table - chair
pen - paper scarf - cap
boy - girl door - handle
needle - thread button - coat

b) Long-term memory: Ask for data the patient learnt at school and general knowledge.
Pay attention to the educational level!

Disorders:
a) Quantitative:
- disorders of durability: - hypomnesia (dementia)
- disorders of capacity: - hypermnesia (high fever dreams, hypnagogic states)
- Hypomnesia
- Amnesia (head injuries, repression), it can be retrograde and
anterograde
b) Qualitative:
- disorders of accuracy: - paramnesia (the patient is convinced of the authenticity of their distorted
memory).
- déjà vu, jamais vu (diseases of the temporal lobe)
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Topic 9: The examination and disturbances of thinking

Thinking: The way in which a person puts together ideas and associations.
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Topic 10: The examination and disturbances of perception

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Topic 11: The examination and disturbances of affect and mood and affect
Emotion: a complex feeling state with psychic, somatic, and behavioural components that is related to
affect and mood.
Emotions: a subjective relation
Affect: a sudden, powerful expression of emotion
Mood: “thymia” – a pervasive and sustained diffuse emotional background, subjectively experienced
and reported by the patient, as well as observed by others.

Examination:
The patient’s mood can be judged more or less by their behaviour, facial expressions and gestures. We have to
be very careful in order to determine whether the patient is dissimulating. The patient’s facial expressions and
gestures have to be written down carefully. It is also noteworthy if there is any discrepancy between the topic in
question and the patient’s behaviour.

What to do:?
- write down our objective observations
- write down the patient’s subjective account (How do you feel now? How would you describe your mood?)
- ask for how long the symptoms have been present
- ALWAYS ask whether the patient has had / has any suicidal thoughts or intentions or attempts (This is a
compulsory question which may indicate an endangering state that requires institutional treatment.)

Disorders:

I. Disorders of affect
 inadequate expression of powerful emotions
 lability

II. Disorders of mood

 hyperthymia (excessively elevated mood)
 dysthymia (slightly depressed mood)
 moria (empty cheerfulness which indicates a frontobasal process in the brain)
 apathy (empty indifference which indicates the lesion in the convexity of the frontal lobe)
 alexithymia (the inability to express emotions)
 prolonged grief
 anhedonia (the inability to feel joy)

III. Other affective disorders

 anxiety
 fear
 agitation
 ambivalence (the simultaneous presence of conflicting emotions towards a subject)
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Topic 12: The idea and disorders of intelligence. Intelligence testing

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Topic 13: Aggression in psychiatric disorders

Violence - has extreme physical harm, such as injury or death, as its goal .
Aggression - as behavior that is intended to harm another individual who does not wish to be harmed.

Physical aggression is aggression that Nonphysical aggression is aggression that does

involves harming others physically—for not involve physical harm. Nonphysical aggression
instance hitting, kicking, stabbing, or includes:
shooting them.  Verbal aggression (yelling, screaming,
swearing, and name calling)
 Relational or social aggression, which is
defined as intentionally harming another
person’s social relationships, for instance,
by gossiping about another person,
bullying.
 Nonverbal aggression also occurs in the
form of sexual, racial, and homophobic
jokes and epithets, which are designed to
cause harm to individuals.
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Topic 14: Laboratory tests in psychiatry

Psychiatry depends more on the clinical examination and the patient’s signs and symptoms to make an
diagnosis than do other medical specialists.

No laboratory tests in psychiatry can confirm or rule out diagnosis such as schizophrenia, bipolar I
disorder, and major depressive disorder. However, laboratory tests have become increasingly valuable
for clinical psychiatrists.

In clinical psychiatry, laboratory tests can help rule out potential underlying organic causes of
psychiatric symptoms - for example impaired copper metabolism in Wilson’s disease and a positive
result on antinuclear antibody (ANA) in systematic lupus erythematosus (SLE).

Laboratory work then is used to monitor treatment, such as measuring the blood levels of
antidepressants medication and assessing the effects of lithium on electrolytes, thyroid metabolism and
renal function. However laboratory data can serve only as an underlying support for the essential skill of
clinical assessment.

BASIC SCREENING TESTS

These tests are made in order to:
 rule out organisity
 screen for concurrent diseases
 establish baseline values of functions to be monitored

ELECTROLYTES Sodium (Na+)  Disturbance distribution of sodium in

depression and bipolar disorder.
 Changes in levels of sodium during
treatment with carbamazepine and
lithium (higher sensitivity for lithium
when sodium level is decreased).
 Sodium is measured in diagnosis of
cognitive disorders
Potassium (K+)  Decreased level in: anorexia nervosa
and bulimia
 Disturbance distribution of potassium
in depression and bipolar disorder
 Hyperkalemia in anxiety disorders
 Decreased level in hepatic cirrhosis
e.g. in alcoholism
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Chlorides (Cl-) panic disorder bulimia

Magnessium (Mg2+) alcohol dependence
low levels
associated with
agitation, delirium
and seizures
HEMATOLOGY -
CBC
NEUROENDOCRINE THYROID FUNCTION TEST depression
TESTS Many other (than thyroid)
hormones affect behavior:
prolactin
growth hormone
somatostatin
gonadotrophin releasing
hormone the sex steroids
melatonin (connected with
seasonal affective disease).
On the basis of unspecified
changes in endocrine function
some symptoms of anxiety or
depression may by explained.
LIVER FUNCTIONS bilirubin phenothiazine or Phenobarbital
TESTS tricyclic medication,
alcohol and other
abuse substances
KIDNEY FUNCTION Method of estimation of Serum BUN and creatine levels must be
TESTS kidney functions: monitored in patients taking lithium - high
- serum level of creatinine risk of damage of kidneys.
- level of blood urine nitrogen
(BUN)
- creatinine clearance (24-
hour urine) urinalysis
- FGR (gromerular filtration
rate)
- inuline clearance
- urinalysis
BLOOD TESTS FOR syphilis Mood disorder, cognition impairment,
SEXUALLY delusions, hallucinations.
TRANSMITTED
DISEASES
DRUGS - patients all antipsychotic (except leukocytosis, leucopenia, impaired platelet
receiving clozapine) function, mild anemia (both aplastic and
psychotropic hemolytic) and agranulocytosis
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medication it is Clozapine Agranulocytosis

necessary to CBC is determined each week during first 6
measure regularly months of treatment, after this time CBC is
the concentration determined each 2 weeks.
of the prescribed Lithium leukocytosis, hypothyroidism, disturbances
drugs in plasma. in urine concentration
Carbamazepine anemia (both aplastic and hemolytic),
agranulocytosis, thrombocytopenia,
leucopenia
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Topic 15: Psychiatric rating scales (SOLLA)

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Topic 16: Psychological testing of personality

Personality - Maladaptive Patterns of Interacting.
Personality Disorders - are characterized by an enduring pattern of thinking, feeling, and behaving which is
significantly different from the person’s culture and results in negative consequences.

Personality test can give you a great deal of insight about the core components that make up who you are.
There are 2 types of personality tests:

1.Objective test: uses simple stimuli e.g. a question and you don’t need any clinical experience to do the test.
Since the stimulus is simple, you are going to have limited number of answers possible (true/false questions).

The most common type is the self-report inventory, also commonly referred to as objective personality
tests. Self-report inventory tests involve the administration of many questions/items to test-takers who
respond by rating the degree to which each item reflects their behavior and can be scored objectively. The
term 'item' is used because many test questions are not actually questions; they are typically statements on
questionnaires that allow respondents to indicate level of agreement.

A sample item on a personality test, for example, might ask test-takers to rate the degree to which they
agree with the statement "I talk to a lot of different people at parties" by using a scale of 1 ("strongly
disagree") to 5 ("strongly agree").

Minnesota multiphasic personality inventory - The MMPI is currently commonly administered in one of
two forms

 the MMPI-2, which has 567 true/false questions, the MMPI-2 is still the more widely used test
because of its existing large research base and familiarity among psychologists.

 Newer MMPI-2-RF, published in 2008 and containing only 338 true/false items. While the MMPI-
2-RF is a newer measure and takes about half the time to complete (usually about 40 to 50
minutes).

 Another version of the test — the MMPI-A — is designed exclusively for teenagers.

2. Projective testing: This kind of test relies on one of the defense mechanisms proposed by Freud—projection—
as a way to assess unconscious processes.

During this type of testing, a series of ambiguous cards is shown to the person being tested, who then is
encouraged to project his feelings, impulses, and desires onto the cards by telling a story, interpreting an
image, or completing a sentence.
No true/false answers.
Some of projective tests are:
 Hannah Friedman

 Rorschach Inkblot Test was developed in 1921 by a Swiss psychologist named Hermann Rorschach
(pronounced “ROAR-shock”). It is a series of symmetrical inkblot cards that are presented to a client by a
psychologist. Upon presentation of each card, the psychologist asks the client, “What might this be?”.
Effective in measuring depression, psychosis, and anxiety.

https://quizly.co/inkblot-test-personality/ - TRY IT!

 Thematic Apperception Test (TAT), created in the 1930s by Henry Murray, an American psychologist, and a
psychoanalyst named Christiana Morgan. A person taking the TAT is shown 8–12 ambiguous pictures and
is asked to tell a story about each picture. The stories give insight into their social world, revealing hopes,
fears, interests, and goals.

 Rotter Incomplete Sentence Blank (RISB) developed by Julian Rotter in 1950. There are three forms of this
test for use with different age groups: the school form, the college form, and the adult form. The tests
include 40 incomplete sentences that people are asked to complete as quickly as possible. The average
time for completing the test is approximately 20 minutes, as responses are only 1–2 words in length. This
test is similar to a word association test, and like other types of projective tests, it is presumed that
responses will reveal desires, fears, and struggles.
 Hannah Friedman

Topic 17: Neuroimaging in psychiatry

Neuroimaging methodologies allow measurement of the structure, function, and chemistry of the living human
brain. Have provided information about the pathophysiology of psychiatric disorders that may be useful for
diagnosing illness and for developing new treatments.

CT/MRI PET
Schizophrenia  Consistent lateral and third ventricular  Hypofrontality
enlargement
 Reduced volumes of cortical gray matter
 Frontal lobe abnormalities in prefrontal gray
matter and orbitofrontal regions.
 Parietal lobe abnormalities, particularly of the
inferior parietal lobule
 Reduced symmetry in several brain areas in
schizophrenia, including the temporal, frontal,
and occipital lobes.
Mood disorder:  Increased frequency of abnormal  decreased anterior brain
hyperintensities in subcortical regions, such as metabolism
Depression
periventricular regions, the basal ganglia, and
the thalamus.
 Also present in bipolar I disorder.
 Ventricular enlargement, cortical atrophy, and
sulci widening also have been
 Reduced hippocampal or caudate nucleus
volumes, or both
OCD  Bilaterally smaller caudate.  Increased metabolism in the
 Significantly more cerebral grey matter & less the orbitofrontal cortex,
white matter volume than normal controls. caudate nucleus, anterior
 Decreased volume of left orbital frontal cortex. cingulate cortex, thalamus,
 Abnormality in length of corpus callosum. and parietal cortex.
 Abnormality in pituitary volume.  Cortico-striatal-thalamic-
 Larger anterior cingulate volumes - increased cortical (CSTC) Increased
OCD symptom severity activity in these circuits both
at rest, and on exposure to
feared stimuli.
 Pharmacological and
behavioral treatments
reportedly reverse these
abnormalities.
Anxiety  smaller OFC, putamen, and temporal lobe  Altered resting-state regional
volume, and lower gray matter density in cerebral blood flow (rCBF).
disorders
parahippocampal cortex Specifically, patients show
 Intrinsically exaggerated amygdala altered function in
hyperresponsivity and abnormal structure or parahippocampal gyrus,
function in the hippocampus. hippocampus, superior
temporal gyrus.
Dementia:  Cerebral atrophy (typical dilatation of lateral  Reduced blood flow and
ventricles & widening of cortical sulci) metabolism in parietal,
Alzehimer
particularly in posterior temporal & parietal posterior temporal, and
regions posterior cingulate cortices,
 Change in global (whole brain and ventricles) with variable reductions in
and regional (entorhinal cortex, hippocampus, other cortical regions.
corpus callosum) volumes
 Hannah Friedman

 MRI evidence of medial temporal lobe (MTL)

atrophy.
ADHD  Increased cortical grey & white matter  Lower glucose metabolism
volumes from 5 yrs of age with peak at 12-15  Lower CBF and metabolic
yrs of age. rates in the frontal lobes
 Decrease in the volume of posterior inferior  Less striatal activation during
cerebellar vermis (region involved in attention cognition inhibition tasks.
processing).
 Hannah Friedman

Topic 18: Forensic psychiatry

Forensic psychiatry is a branch of medicine which focuses on the interface of law and mental health. It may
include psychiatric consultation in a wide variety of legal matters
Forensic psychiatry deals with 3 distinct but overlapping areas:
1. General forensic psychiatry
• Criminal areas:
◦ Expert witness or testifying - Expert witnesses give their opinion about a specific issue
associated with psychiatry and explain the basis for that opinion which includes important
concepts, approaches and methods used in psychiatry.
◦ Dangerous or long-term offender applications
◦ Fitness to stand trial
◦ Probation and Parole
◦ Review boards
• Civil areas:
◦ Divorce and custody evaluations
◦ Negligence and malpractice
◦ Personal injury
◦ Workman's compensation boards
◦ Workplace violence
2. Clinical criminology
• Developmental delay issues
• Impulse control disorders
• Interpersonal violence
• Paraphilias and Sex offences
• Psychopathy
• Risk assessment and management
• Major mental illness within the forensic setting such as psychosis, schizophrenia or mood
disorders
• Personality disorders within the forensic setting
• Substance abuse within the forensic setting
• Treatment programming within the forensic setting
3. Psychiatry and Law
• Capacity of the person to consent to treatment, to manage property, to consent to
emergency treatment, etc...
• Informed consent
• Confidentiality of patient records
• Duty to care and to warn
• Involuntary hospitalization
• Substitute decision making and patient's intrinsic rights.
 Hannah Friedman

Topic 19: Defence mechanisms

Definition:
 Primary tools of the ego used to cope with external stressors to avoid or reduce anxiety, restrict impulses,
and avoid unpleasant feelings
 Mostly unconscious; may be healthy if used in moderation or unhealthy if used excessively.
Classification:
 Pathological/Narcissistic: seen in children or patients with personality disorders.
 Immature: seen in children, adolescents, psychotic patients, or patients with personality disorders.
 Neurotic: seen in obsessive-compulsive or anxious patients.
 Mature: seen in normal adults.
Hannah Friedman
 Hannah Friedman

Topic 20: Psychosocial treatment and rehabilitation

Psychosocial refers to the close connection between the psychological aspects of people with their social
environments.
Psychosocial treatment involves making use of the social treatment to improve and help with restoration of
psychological health.

Psychosocial interventions include:

• Behavior therapy
◦ Behavior therapy is for helping a patient deal with their current problems
◦ Desired behaviors are positively reinforced in order to have the patient display the correct
behavior outside of the hospital
• Group therapy
◦ Focus is on support and social skills development
◦ Groups are very good for decreasing social isolation and increasing the
efficacy of reality testing
• Family therapy
◦ Can significantly decrease the relapse rates for a schizophrenic
• Supportive psychotherapy
◦ For schizophrenics, the traditional insight-oriented psychotherapy is not so good as their
egos are too fragile
◦ Supportive therapy includes things like advice, reassurance and education.
◦ A special type of supportive therapy known as personal therapy relies heavily on the
doctor-patient relationship
• Social skills training
◦ Attempting to improve social skill problems such as poor eye contact
◦ This training is usually done in group settings and incorporates things like homework,
videotapes and role playing
• Case management
◦ Case managers participate in treatment coordination between various providers
◦ Such people help patients make appointments, get housing, jobs, etc...
• Individual therapy
• Support groups
Any of these treatment modalities can be made in an inpatient or an outpatient setting!
 Hannah Friedman

Psychosocial rehabilitation is for all patients that suffer from a severe and persistent mental condition

The goal is to help these people develop the emotional, social and intellectual skills needed to live, learn
and work with the least amount of professional support
There are two overall strategies to this rehabilitation process:
1. Developing the patient's skills to deal with a stressful environment
2. Creating an environment or designing resources to reduce potential stressors

When is there a need for psychosocial rehabilitation?

1. Majority of schizophrenics
2. Drug rehab
 Hannah Friedman

Topic 21: Consultation-liaison psychiatry

Is the branch of psychiatry that specializes in the interface between general medicine and psychiatry, Most liaison
psychiatrists provide a service across three broad areas of the hospital:

 the emergency department

 hospital wards
 outpatient clinics

Psychiatry act as "Consults" (guide). Follow any psychiatric treatment needed, questions about a patient's mental
health, or how that patient's mental health is affecting his or her care and treatment. In this fashion the
psychiatric team works as a "liaison" (bridge) between the medical team and the patient. Issues that arise include
capacity to consent to treatment, conflicts with the primary care team, and the intersection of problems in both
physical and mental health, as well as patients who may report physical symptoms as a result of a mental
disorders.

Liaison psychiatrists must be ready to offer assessment and treatment to people with any psychiatric
disorder. Commonly encountered problems and disorders are self-harm, delirium, depression, anxiety, acute
psychosis, addictions and dementia. They also see people with medically unexplained symptoms,
neuropsychiatric disorders, perinatal mental health problems, eating disorders and almost any other psychiatric
disorder.
 Hannah Friedman

Topic 22: Theories of personality and psychopathology

Sigmund Freud (1856-1939):
Sigmund Freud (1856-1939) Born in Moravia, Czech Republic on May 6 th 1856 Died in London, 23 rd Sep 1939

Freud’s theories
1. Levels of Awareness:

2. Personality structure
 Id
- Energy constantly striving to satisfy basic drives (Pleasure Principle)
- Is the only component of personality that is present from birth.
- This aspect of personality is entirely unconscious and includes all of the instinctive and
primitive behaviors.
 Ego
- Component of personality that is responsible for dealing with reality (Reality Principle).
- This is the “self”, or who you view yourself as.
- Defense Mechanisms Function: Used by ego to defend against anxiety Involves distortion of
reality
 Super Ego
- Superego Operates on “ideal principle”.
- The superego represents the conscience.
- It is the “should” of human beings - Begins forming at 4-5 yrs of age.
- Internalized conventions and morals.
- The superego provides guidelines for making
judgments.

3. Freud's theory of psychosexual development:

- Stages of development in which conflict over Id’s impulses plays out
- Ego must control these impulses If not resolved, psychological issues can emerge later in life .
Hannah Friedman
 Hannah Friedman

Others theories
Hannah Friedman
 Hannah Friedman

B
Topic 1: The classification of organic mental syndromes

Organic psychiatric disorders are those due to a recognized medical cause or pathology.
Organic mental disorders are disturbances that may be caused by known specific organic cause,
injury or disease affecting brain tissues as well as by chemical or hormonal abnormalities. Exposure
to toxic materials, neurological impairment, or abnormal changes associated with aging can also
cause these disorders.

The major organic disorders: dementia and delirium, are defined like other psychiatric syndromes
by their characteristic clinical features. However, unlike other syndromes they are known to arise
from different diseases with various aetiologies and pathologies .
 Hannah Friedman

Other organic disorders are simply psychiatric disorders of any type that appear in a particular case to be caused by
an identifiable medical condition.

Amnesia Korsakoff's syndrome

Head trauma
Cerebrovascular disease
Brain tumor
Brain surgery
Systemic conditions: e.g., hypoxia (CO poisoning) and
hypoglycemia
Substance related
Hallucinations Visual –drugs
-epilepsy
- occipital lobe injury
Auditory –pontine lobe injury
Olfactory –migraines
Gustatory –temporal lobe injury
Anxiety disorder Epilepsy
Drugs – amphetamines
Stroke
Thyrotoxicosis
Brain tumor
Pheochromocytoma
Personality disorder Head injury
Mood disorder Brain tumor
Alzheimer’s disease
 Hannah Friedman

Topic 2: Depressive pseudodementia

Reversible cognitive impairment in depressed geriatric patients is known as pseudodementia. Patients may
appear demented, however their symptoms are only secondary to their underlying depression.

*it can be difficult to differentiate the two.

*pseudodementia respond well to antidepressants OR electroconvulsive therapy (ECT).
 Hannah Friedman

Topic 3: Reversible dementia, amnestic disorders

Reversible dementia 10-20% -> conditions that may well be associated with cognitive or behavioral
symptoms that can be resolved once the primary etiology is treated.

Etiology:
Drugs (anticholinergics)
Endocrine
Metabolic (electrolyte imbalance)
Emotional (Depression)
Nutritional deficiencies (folate. Vit B12)
Trauma/tumor
Infections (syphilis, HIV)
Alcohol, arteriosclerosis

Irreversible 80-90%
 Alzheimer disease (> 50% of dementia cases)
 Parkinson disease
 Frontotemporal dementia
 Dementia with Lewy bodies
 Progressive supranuclear palsy
 Huntington disease

Amnestic disorders -> characterized by deficit in memory caused by brain damge/disease. (E.g., time,
content)
Causes:
* Acute –Drugs (BNZ)
-ECT
-Trauma, head injury
* Chronic –Infections
-Brain tumor
-Neurodegenerative
-Nutritional deficiencies
-Psychosocial events.
Clinical features:
Isolated memory loss doesn't affect a person's intelligence, general knowledge, awareness, attention span,
judgment, personality or identity. People with amnesia usually can understand written and spoken words
and can learn skills such as bike riding or piano playing. They may understand they have a memory
disorder.
 Hannah Friedman

The two main features of amnesia are:

 Difficulty learning new information following the onset of amnesia (anterograde amnesia)
 Difficulty remembering past events and previously familiar information (retrograde amnesia)

 False memories (confabulation), either completely invented or made up of genuine memories misplaced in
time

Types:
 Retrograde amnesia: loss of memory-access to events that occurred and/or information acquired prior to the
incident.
 Anterograde amnesia: loss of memory-access to events that occurred and/or information acquired after the
incident.
 Global amnesia: loss of memory-access to events that occurred and/or information acquired prior and after
the incident.
 Drug induced: injection for surgery.
 Dissociative: psychological/distress events.
 Post-traumatic amnesia: generally due to a head injury (example: a fall, a knock on the head).
 Lacunar amnesia: loss of memory about one specific event.

Diagnosis:
Clinical history
Lab –vitamins, infections
Imaging – MRI,CT to check for brain damage or abnormalities.

Treatment:
Treatment for amnesia focuses on techniques and strategies to help make up for the memory problem, and
addressing any underlying diseases causing the amnesia.
 Occupational therapy
 Memory training
 Smart technology, such as a smartphone or a hand-held tablet device
 Low-tech memory aids include notebooks, wall calendars, pill minders, and photographs of people
and places
No medications are currently available for treating most types of amnesia .
 Hannah Friedman

Topic 4: Alzheimer’s dementia, neurodegenerative disorders

Alzheimer disease (AD) is a chronic neurodegenerative disease and the leading cause of dementia.

Etiology:
Gene defects (e.g., amyloid precursor protein gene mutations)
Other risk factors:
 Age
 Family history of dementia
 Low socioeconomic and/or educational status
 Diabetes, obesity, dyslipidemia
 Hypertension, peripheral atherosclerosis, and cerebrovascular disease
 Lack of physical activity (independent risk factor)
 Traumatic brain injuries
 Environmental factors (e.g., secondhand smoke)
 Sleep deprivation

Pathophysiology:
The following pathophysiological mechanisms contribute to AD:
1. Extracellular senile plaques (neuritic plaques) in the grey matter of the brain
 Aβ protein is the main component of the plaques.
 Enzymatic cleavage of transmembranous APP by β-secretase and γ-secretase → Aβ
peptide aggregation → formation of insoluble plaques together with tau protein and microglia →
neurotoxic effect .
2. Intracellular neurofibrillary tangles
 Tangles are composed of hyperphosphorylated tau protein(a microtubule-associated protein).
 Increased phosphorylation (hyperphosphorylation) of tau → formation of intracellular fibrils →
neurotoxic effect .
3. Overall reduction of cholinergic function.

Clinical features:
Cognitive:
Common symptoms of cognitive impairment
 Short-term memory impairment (insidious onset, slow progress with episodic memory affected first)
 Language impairment
 Temporal and spatial disorientation (patients are usually not oriented to person, place, time, or events)
 Impairment of executive functions and judgment

Less common symptoms

 Primary progressive aphasia
 Apraxia
 Alexia
 Agnosia
 Acalculia
 Hannah Friedman

Non cognitive:
 Behavioral changes
 Apathy
 Aggression, irritability, and agitation
 Mood disorders (e.g., symptoms of depression)
 Anxiety and mutism
 Hallucinations and paranoia
 Hyposmia
 Insomnia
 Urinary incontinence
 Myoclonus
 Seizures

Diagnosis:
To diagnose dementia in patients with memory loss, cognitive and/or functional decline:
 neuropsychological testing (e.g., Mini-Mental State Examination, Montreal Cognitive Assessment)
 Rule out reversible causes of dementia.
 Review medications.
 Laboratory tests (rule out hypothyroidism and vitamin B12 deficiency)
 Neuroimaging (rule out vascular dementia, hydrocephalus, tumors)
 Clinical assessment for depression to rule out pseudodementia: See diagnostic criteria for major
depressive disorder.
 AD can only be definitively diagnosed with neurohistopathological examination, which is only conducted
post mortem.

Diagnosis finding:
1.Synopsis of diagnostic criteria
 Insidious onset (symptoms are often first noticed by the patient's relatives)
 Objectively confirmed progressive loss of function in at least two cognitive domains (usually including
memory impairment)
 Impaired activities of daily living (e.g., difficulties at the workplace)
 No other plausible explanation (e.g., delirium)
2.Cerebrospinal fluid
 Increased phospho-tau protein
 Decreased β-amyloid proteins Aβ1-42
3.CT/MRI
 Signs of generalized or focal cerebral atrophy: enlarged ventricles (ventriculomegaly), narrowing of gyri,
and prominent cerebral sulci (hydrocephalus ex vacuo)
 Disproportionate atrophy of the hippocampus and/or medial temporal lobe
4.EEG: slower basic rhythm
 Evoked potentials: long latency
5.PET
 FDG-PET: temporoparietal hypometabolism
 Amyloid PET: increased amyloid uptake signal
 Hannah Friedman

Treatment: There is currently no curative therapy; only symptomatic therapies are available.
1. Pharmacological
 Mild-moderate (determined by neuropsychological
testing): donepezil, galantamine, rivastigmine (acetylcholinesterase inhibitors)
 Moderate-severe (may be given in addition to acetylcholinesterase inhibitors): memantine (NMDA-
receptor antagonist)
 Aggression and psychosis: low dose antipsychotics
2. Suppurative care (non pharmacological)
 Lifestyle modifications: e.g., adhering to a regular sleep schedule, maintaining a familiar environment,
removing ambient noise
 Cognitive rehabilitation: memory training (e.g., puzzles, interactive games) to support memory retention
and strategies to compensate for cognitive and functional decline
 Physical activity: improves physical strength, which slows functional decline
3. Associate symptoms - In patients who have not adequately responded to supportive care, the following
classes of drugs may be considered:
 Atypical antipsychotics (e.g., risperidone): in patients with agitation, hallucinations, insomnia
 SSRIs (e.g., citalopram): in patients with depression

Major neurodegenerative disorders

Acquired disorder of cognitive function that is commonly characterized by impairments in memory, speech,
reasoning, intellectual function, and/or spatial-temporal awareness.

Causes:
*Neurodegenerative brain diseses:
 Alzheimer disease (> 50% of dementia cases)
 Parkinson disease
 Frontotemporal dementia
 Dementia with Lewy bodies
 Progressive supranuclear palsy
 Huntington disease
*Additional causes:
 Cerebrovascular disease (20% of dementia cases) - Multi infarct dementia, subcortical
arteriosclerotic encephalopathy
 Hypoxic brain damage
 Normal pressure hydrocephalus
 After head trauma, intracranial bleeding or brain tumors
 Drug/alcohol-related (e.g., Wernicke-Korsakoff syndrome)
 Wilson disease
 Vitamin deficiencies (thiamine, B6, B12, folate)
 Metabolic: exsiccosis, uremia, electrolyte
imbalances, hypothyroidism and hyperthyroidism, hypoparathyroidism, and hyperparathyroidism
 Environmental toxins
 Inflammatory/infectious (syphilis,HIV, Creutzfeldt-Jakob disease)
 Hannah Friedman

Clinical features:
 Memory impairment
 Additional cognitive impairment
-Speech: aphasia, word-finding difficulties, semantic paraphasia
-Intellectual capacities, reasoning, planning capabilities, and self-control
-Spatial-temporal awareness (however, the awareness of oneself remains stable for a long time)
-Apathy
 Changes in personality, mood, and behavior
-Early stages: depression
-Later stages: seemingly unconcerned mood and cognitive impairment is downplayed

Diagnosis:
 Personal and collateral history of cognitive and behavioral changes
 Drug history
 Screening for depression
 Physical and neurological examination
 DSM5

Differential diagnosis:
 Hannah Friedman

C Topic 1: The treatment of dementia

1. Memory training
 Cognitive capabilities can be improved through targeted stimulation (e.g., practicing image recognition,
completing arithmetic or combinatorial problems).
 Recalling past memories

2. Pharmacology
 Memantine
*Recommendations
o Particularly moderate to advanced cases of Alzheimer disease or vascular dementia
o Memantine may be used in combination with cholinesterase inhibitors.
*Effect: NMDA-receptor antagonism
*Adverse side effects: mostly affect the central nervous system
o Headaches and dizziness
o Confusion and hallucinations
o Epilepsy

 Cholinesterase inhibitors - donepezil, rivastigmine, galantamine

*Recommendation:
o Particularly mild to moderate cases of Alzheimer dementia or vascular dementia
o May be beneficial in cases of dementia with Lewy bodies, frontotemporal dementia, and Parkinson
disease
*Drugs: donepezil, rivastigmine, galantamine
*Effect: Reversible cholinesterase inhibition leads to increased acetylcholine (ACh) concentration and can
thus improve symptoms of some types of dementia.
*Adverse side effects: symptoms of cholinergic crisis
 Hannah Friedman

Topic 5: Delirium
Delirium (also known as acute confusional state or acute brain syndrome) is a neurocognitive disorder
characterized by impaired attention, awareness (reduced orientation to the environment), and other disturbed
cognitive functions (e.g., memory, language, or perception).

Causes:
I WATCH DEATH: Infection, Withdrawal, Acute metabolic disorder, Trauma, CNS
pathology, Hypoxia, Deficiencies, Endocrine, Acute vascular, Toxins/drugs, Heavy metals.

Clinical features:
 The main symptom is an acute (hours to days) alteration in the levelof awareness and attention.
 Other features may include:
- Illusions
- Hallucinations
- Deficits in memory
- Reversal of the sleep-wake cycle
- Emotional lability
- Agitation, combativeness
 The severity of symptoms fluctuates throughout the day and worsens in the evening (termed sundowning).
 The duration of symptoms depends on the underlying illness.

Diagnosis:
 If the cause of delirium is not obvious based on the patient history and physical findings:
- Start with complete blood count, serum glucose, electrolytes, and urinalysis.
- If medication or substance use is suspected: urine toxicology or serum drug levels
- If a metabolic etiology is suspected: serum creatinine, BUN, liver function tests, arterial blood gas
- If pneumonia is suspected: chest x-ray
- If a cardiac etiology (e.g., myocardial infarction, arrhythmia) is suspected: ECG
 If the patient has focal neurological deficits or the initial workup is negative, further tests may include:
- Neuroimaging (CT, MRI)
- Lumbar puncture: to rule out meningitis/encephalitis
- EEG: usually shows diffuse slowing of background activity in patients with delirium; also useful in patients
with a history of head trauma, stroke, or brain lesions
 Further diagnostics that may be considered:
- Blood culture
- HIV; syphilis serology
- Thyroid function tests
- Vitamin B12, folate, and thiamine levels

Treatment:
 Identify and treat the underlying cause.
 Discontinue the causative medications (e.g., benzodiazepines and anticholinergics).
 Supportive medical care
 Hannah Friedman

- Manage agitation initially with nonpharmacologic strategies (see “Prevention” below).

- Administer antipsychotics if the patient is agitated and/or poses harm to themselves or others.
- Haloperidol is used most commonly; however, it should not be used in patients with delirium that is due
to alcohol or benzodiazepine withdrawal because it lowers the seizure threshold.
- Alternative: atypical antipsychotics (e.g., olanzapine)
- Maintain adequate hydration and nutrition.
- Reduce pain, preferably with nonopioid medications.
- Prevent aspiration, incontinence, and skin breakdown.

Prevention:
*Nonpharmacologic approach
 Reduce exposure to modifiable risk factors.
 Reorient the patient regularly.
 Arrange for regular visits from family and friends.
 Arrange for constant observation, preferably by a family member or friend.
 Reduce the amount of noise, procedures, and medication administration occurring at night.
 Provide physical and occupational therapy to mobilize the patient as soon as possible.
 Minimize the use of restraints as much as possible.
 Provide visual and hearing aids for patients with impairments.
*Pharmacologic
 Dexmedetomidine
 Cholinesterase inhibitors (e.g., rivastigmine, donepezil)
 Second-generation antipsychotics
 Melatonin
 Hannah Friedman

Topic 6: Alcohol abuse and dependence

Abuse Dependence
 Drinking alcohol in excessive amount  Strong craving for alcohol.
but not in a daily/weekly basis.  4 main symptoms:
 Repetitive problems with alcohol in - Craving, strong need
any one of four life areas: - Impaired control, inability to stop
 social - Physical dependence (withdrawal
 interpersonal symptoms)
 Legal - Tolerance – increase the amount
 Occupational in order to feel the same effect.
 Repeated use in hazardous situations
such as driving while intoxicated in
an individual who is not alcohol
dependent.

DSM 5 The alcohol abuse diagnosis is no longer

At least three out of seven of the
used in the DSM-5 , it is now part of
following criteria must be manifest during
the alcohol use disorder diagnosis.
a 12-month period:

 Tolerance
 Withdrawal symptoms or clinically
defined alcohol withdrawal syndrome
 Use in larger amounts or for longer
periods than intended
 Persistent desire or unsuccessful
efforts to cut down on alcohol use
 Time is spent obtaining alcohol or
recovering from effects
 Social, occupational and recreational
pursuits are given up or reduced
because of alcohol use
 Use is continued despite knowledge of
alcohol-related harm (physical or
psychological)

Etiology  Social pressure

 Genetics
 Neurobiological changes
 Desire to relax
 Coping mechanism for anxiety
 Depression
 Tension
 Hannah Friedman

 Loneliness
 Self-doubt or unhappiness
 Family history of abusing alcohol
Diagnosis screening

Laboratory test
 Hannah Friedman

C Topic 2: The treatment of alcohol dependence

1. Alcoholics Anonymous—self-help group
2. Disulfiram (Antabuse)—aversive therapy; inhibits aldehyde dehydro-genase, causing violent retching when
the person drinks
3. Psychotherapy and selective serotonin reuptake inhibitors (SSRIs)
4. Naltrexone—though an opioid antagonist, helps reduce cravings for EtOH
 Hannah Friedman

Topic 7: Epidemiology and aetiology of alcohol-related disorders

Epidemiology
 Alcohol consumption results in > 3 million deaths worldwide per year.
 About 10% of women and 20% of men have met the diagnostic criteria for alcohol abuse and half of
these (5% and 10%) met the criteria for alcohol dependence
 Caucasians have the highest rate of alcohol use
 Peak incidence: 21–34 years
 Higher education = More likely the use of alcohol; opposite situation for illicit drugs

Etiology
 Genetic factors
Twin studies have shown a high concordance of AUD in monozygotic twins, which indicates that genetic
factors contribute significantly to the development of the disorder.
 Neurobiological factors
Dysregulation of the endogenous dopaminergic reward system.
 Psychosocial factors
 Family history of AUD
 Environmental influence: e.g., social pressure to consume alcohol
 Hannah Friedman

Topic 8: Psychiatric morbidity in alcohol-related disorders

C Topic 5: Wernicke-Korsakoff syndrome and its treatment

Alcohol starts to disrupt brain chemicals (NTs) and interface with hormonal system – link to progression of most
mental disorders.

We can divide psychiatric consequences of alcoholism into 3 groups:

1.Disorders related to direct effects of alcohol on the brain
 Alcohol intoxication, Withdrawal with/without delirium, Hallucinosis
2.Behaviour disorders related to alcohol
 Alcohol abuse and Dependence
3.Disorders with persisting effects
 Alcohol-induced persisting amnestic disorder
 Dementia
4.Alcohol-induced persisting amnestic disorder
Features disturbances in short-term memory from prolonged, heavy drinking
Two forms:

Wernicke encephalopathy Korsakoff syndrome

Is an acute, reversible condition Is a late development, chronic
and irreversible condition.

Etiology Wernicke encephalopathy and Korsakoff syndrome are caused by a severe deficiency
of thiamine (vitamin B1).
Thiamine deficiency can be due to:
 Chronic heavy alcohol use (most common) → inadequate intake, absorption, and
hepatic storage of thiamine
 Inadequate intake
-Thiamine-deficient diets
-Anorexia nervosa, starvation
-Malabsorption
 Increased demand (hypermetabolic states)
-Pregnancy and lactation
-Hyperthyroidism
 Systemic diseases
-Malignancy
 Increased loss
-Diarrhea
-Hyperemesis
-Dialysis
 Hannah Friedman

Clinical  Should be suspected in any patient with a Korsakoff syndrome is a late

features history of chronic heavy alcohol use who development in patients with
presents with one/more symptoms of the persistent vitamin B1 deficiency.
classic triad of Wernicke encephalopathy It is most often seen
1. Confusion (most common) in thiamine deficiency due to
2. Oculomotor dysfunction chronic heavy alcohol use.
 Gazeinduced horizontal/vertical nystagmus  Confabulation: Patients
(most common) produce fabricated
 Diplopia memories to fill in lapses
 Conjugate gaze palsy of memory.
3. Gait ataxia: wide-based, small steps  Anterograde and
 Other manifestations retrograde
 Autonomic amnesia (anterograde >
dysfunction: hypotension, syncope, retrograde)
Peripheral neuropathy: paresthesia, foot  Personalitychanges (in fro
drop, decreased deep tendon reflexes ntal lobe lesions): apathy,
 Cardiovasculardysfunction: tachycardia, exe indifference, decrease in
rtional dyspnea executive function
 Diencephalic involvement: vegetative  Disorientation to time,
disorders (coma and stupor) place, and person
 Hallucinations

Diagnosis Usually a clinical diagnosis

In ambiguous cases:
 Laboratory tests
↓ Serum thiamine levels
↓ Erythrocyte transketolase activity (thiamine dependent)
↑ Serum lactate and pyruvate
Evidence of alcohol-related liver dysfunction in patients with chronic heavy
alcohol use
 Brain MRI: T2-weighted hyperintense lesions in the mammillary
bodies, midbrain tectal plate, dorsomedial nuclei of the thalamus, cerebellum,
and around the aqueduct and the third ventricle

Treatment  immediate IV administration of high-  Oral thiamine supplementati

dose vitamin B1/thiamine upon suspicion on to prevent further
of Wernicke encephalopathy until symptoms progression to irreversible
recede, followed by a lower dose complications
 Long-term oral replacement of vitamins B1, B6,  Abstinence from alcohol
B12, and folic acid (vitamin B complex)  Psychiatric and psychological
 Abstinence from alcohol therapy
 Memory strengthening
exercises and aids
 Hannah Friedman

 The use of signs and arrows

at home can help
with orientation.

Prognosis Oculomotor dysfunction resolves, in general, within Symptoms are often irreversible.
hours, ataxia within days, and confusion within
weeks.
 Hannah Friedman

Topic 9: Alcohol intoxication, idiosyncratic alcohol intoxication

Alcohol intoxication
Definition: a temporary condition in which excessive consumption of alcohol alters a person's consciousness,
cognition, perception, judgment, affect, and/or behavior
Pathophysiology:
The majority of alcohol consumed is absorbed by the proximal small intestine. Only a small amount of alcohol
gets absorbed by the oral, esophageal, and/or gastric mucosa.

Clinical features:

Idiosyncratic alcohol intoxication

Variant of alcohol intoxication characterized by sudden and extreme changes in personality, mood, and behavior
following the ingestion of a small amount of alcohol which usually not cause intoxication.
Results in aggression, impaired consciousness, prolonged sleep, transient hallucinations, illusions, and delusions.

C Topic 3: The management of acute alcohol intoxication

1.Agitation and/or aggression management
- Sedation with benzodiazepines or typical antipsychotics (e.g., haloperidol)
- Mechanical restraints may be used for individuals who pose a danger to themselves and/or others if de-
escalation and medication strategies have been unsuccessful.
2.Aggressive fluid therapy
3.Thiamine: for Wernicke encephalopathy prophylaxis or treatment
4.Correction of electrolyte disbalance, hypoglycemia, and hypothermia
5.Thorough assessment for occult trauma (e.g., imaging), if suspected
 Hannah Friedman

Topic 10: Alcohol withdrawal syndrome and delirium tremens

Caused by a sudden reduction or cessation of alcohol intake after a prolonged period of heavy drinking. Onset
and duration vary among different syndromes.

Delirium tremens is the most severe form

of alcohol withdrawal

C Topic 4: The management of alcohol withdrawal syndromes

Hannah Friedman
 Hannah Friedman

Topic 11: Alcohol-induced psychotic disorder

Alcohol chronic consumption/intoxication/withdrawal can lead to psychosis.
*Typically seen in people who were dependent on alcohol for 10 years or more.

Chronic consumption – very intoxication withdrawal

similar to schizophrenia
 Hallucination  Unusual aggression  Anxiety
 Alcohol paranoia  Delusion  Mood changes
 Wernicke korsakoff syndrome  Illusion  Agitation
 Hallucinations  Autonomic symptoms
 Impaired consciousness

Topic 12: The bases of substance addiction

Addiction is the repeated and increased use of a substance and the deprivation of the substance in question leads
to symptoms of distress and an irresistible urge to use the agent again.

Substance use disorder are complex conditions that affect the reward, reinforcement, motivation,
and memory systems of the brain. They are characterized by impaired control over usage; social impairment,
involving the disruption of everyday activities and relationships, and craving.

A person with an addiction uses a substance, or engages in a behavior, for which the rewarding effects provide a
compelling incentive to repeat the activity, despite detrimental consequences. Addiction may involve the use of
substances such as alcohol, inhalants, opioids, cocaine, and nicotine, or behaviors such as gambling .

Because addiction affects the brain’s executive functions, centered in the prefrontal cortex, individuals who
develop an addiction may not be aware that their behavior is causing problems for themselves and others.

Topic 13: Illicit drug-related disorders

C Topic 6: The complex treatment of drug-related disorders
 Hannah Friedman

Substance-related disorders are a class of psychiatric disorders characterized by a craving for, the development of
a tolerance to, and difficulties in controlling the use of a particular substance or a set of substances, as well as
withdrawal syndromes upon abrupt cessation of substance use.
Hannah Friedman
 Hannah Friedman

Topic 14: Benzodiazepine - abuse and dependence

BNZ belongs to Sedative-hypnotics class of drugs that cause a dose-dependent depression of the CNS function,
inducing sedation, sleep, and unconsciousness with increasing dose.

Mechanism of action:
Benzodiazepines are indirect GABA A agonists that bind to GABA-A receptors → ↑ affinity of GABA to bind
to GABAA receptors → ↑ GABA action → ↑ opening frequency of chloride channels → hyperpolarization of the
postsynaptic neuronal membrane → decreased neuronal excitability.

Abuse/misuse – Clinical features Treatment

Is the use of BNZ without a CNS depression: 1.Supportive therapy
prescription, often for -Lethargy, somnolence - activated charcoal if
recreational purpose. -Respiratory depression the patient is fully
Risk of dependence, withdrawal -Mild hypotension conscious and presents
and other long term effect. -Hypotonia and hyporeflexia within 30 minutes of
-Ataxia overdose
-Slurred speech - fluid resuscitation
Drowsiness, sleepiness - GCS ≤ 8: endotracheal
Blunted affect intubation
Increased appetite 2. Antidote: flumazenil
Next-day hangover effect
Anterograde amnesia
Drug tolerance
Paradoxical excitability

BNZ dependence- Rebound phenomenon: 1.Nonpharmacological

A condition that develops reemergence of symptoms measures: psychotherapy,
following using of (e.g., depression, insomnia, and inpatient care
benzodiazepines for several anxiety) that were previously 2.Pharmacological measures:
 Hannah Friedman

weeks. Since the condition can absent or controlled Dose tapering

be life-threatening, rapid by benzodiazepine therapy (Benzodiazepines should not be
recognition and treatment is when the medication is stopped suddenly)
essential. discontinued for a few days. Seizure prophylaxis
(e.g., carbamazepine)
Patients can develop withdrawal Antipsychotics (e.g., haloperidol)
symptoms such as sweating,
nausea, vomiting, anorexia,
hypertension, tremors,
hallucinations and even
seizures upon discontinuing
benzodiazepines.
 Hannah Friedman

Topic 15: The aetiology of schizophrenia

Severe psychiatric disorder characterized by chronic or recurrent psychosis. The majority of individuals with
schizophrenia initially experience symptoms in their 20s.

Etiology:
The exact mechanism is unknown but is thought to relate to increased dopaminergic activity in
the mesolimbic neuronal pathway and decreased dopaminergic activity in the prefrontal cortical pathway.

Risk factors:
*Genetic factors: risk significantly increased if relatives are also affected
 One schizophrenic parent: ∼ 10%
 Two schizophrenic parents: ∼ 40%
 Concordance rate in monozygotic twins: 30–40%
 Concordance rate in dizygotic twins: 10–15%
*Environmental factors
 Stress and psychosocial factors
 Frequent use of cannabis
 Urban environment
 Birth in late winter or early spring
 Advanced paternal age at conception

Pathophysiology:
*Dysregulation of neurotransmitters
 ↓ Dopamine in prefrontal cortical pathway may cause negative symptoms of psychosis.
 ↑ Dopamine in mesolimbic pathway may lead to positive symptoms of psychosis.
 ↑ Serotonergic activity and ↓ dendritic branching
 ↓ Glutamatergic neurotransmission may lead to psychosis.
 ↓ GABA leads to ↑ dopamine activity.
 Hannah Friedman

Topic 16: Clinical features of schizophrenia

Schizophrenia typically manifests with a prodrome of negative symptoms and psychosis (e.g., social withdrawal)
that precedes the positive psychotic symptoms (e.g., hallucinations and bizarre delusions)
Hannah Friedman
 Hannah Friedman

Topic17: The subtypes and course of schizophrenia

*DSM-5 omits subtypes of schizophrenia previously included in DSM-IV (disorganized, paranoid, catatonic,
undifferentiated, residual) because they are no longer thought to reflect the heterogeneity of schizophrenia.

C Topic 7: The complex treatment of schizophrenia (pharmaco-psycho-sociotherapy)

1.General considerations
 Establish a therapeutic alliance when taking care of patients with delusions.
 Acknowledge the patient's emotional state.
 Avoid validation of delusions or confronting patients about the delusional nature of their symptoms.
 Initial response to treatment during the first 2–4 weeks is associated with a better long-term response.
 Hospitalization if acutely psychotic
2.Pharmacotherapy
 Acute psychotic episode: short-acting antipsychotics
 Acute manic episode: mood stabilizers (e.g., lithium, valproate, carbamazepine)
 First-line treatment: second-generation antipsychotics (e.g., risperidone, quetiapine), which are especially
effective at treating positive psychotic symptoms
 Alternative treatment: first-generation antipsychotics in depot form for those at risk of poor adherence
(e.g., fluphenazine, haloperidol, chlorpromazine)
 Hannah Friedman

 Treatment-resistant schizophrenia: clozapine for persistent positive symptoms

(i.e., delusions, hallucinations, and/or disorganized speech) despite trials of ≥ 6 weeks of 2
different antipsychotics at their maximum doses
 Treatment during pregnancy: first-generation antipsychotics (e.g., haloperidol) as a first-line treatment
 Treatment of depression: SSRIs or tricyclic antidepressants (e.g., sertraline, imipramine)
 Treatment of anxiety: SSRIs
 See antipsychotics for more details.
3.Psychoeducation (used as an adjunct to avoid relapse)
 Patient, family, and group psychosocial therapy and education
 Cognitive-behavioral therapy
 Supportive social measures
 Hannah Friedman

Topic 18: The differential diagnosis of schizophrenia and other psychotic disorders

Other causes of psychosis:

PTSD
Personality disorder
Organic causes of psychosis
 Delirium
 Dementia
 Cushing syndrome
 Substance use disorder (e.g., hallucinogens)
 Thyroid disorder (e.g., thyrotoxicosis)
 Vitamin B12 deficiency
 Systemic lupus erythematosus
 Neoplasm (e.g., brain tumor)
 Epilepsy (e.g., temporal lobe epilepsy)
 Wilson disease
 Porphyria
 Hannah Friedman

Topic 19: Schizoaffective disorders

Schizoaffective disorder is a chronic mental health condition characterized primarily by symptoms of

schizophrenia, such as hallucinations or delusions, and symptoms of a mood disorder, such as mania and
depression.
Combination of schizophrenia and a mood disorder and cannot be diagnosed as either one separately

Diagnosis (DSM4):

The diagnosis of schizoaffective disorder is made in patients who:

Meet criteria for either major depressive episode, manic episode, or mixed episode (during which criteria for
schizophrenia are also met).
Have had delusions or hallucinations for 2 weeks in the absence of mood disorder symptoms (this condition
is necessary to differentiate schizoaffective disorder from mood disorder with psychotic features) Have
mood symptoms present for substantial portion of psychotic illness.
Symptoms not due to general medical condition or drugs.

Treatment:
Hospitalization and supportive psychotherapy
Medical therapy: Antipsychotics as needed for short-term control of psychosis; mood stabilizers, antidepressants,
or electroconvulsive therapy (ECT) as needed for mania or depression.

Prognosis:
Better than schizophrenia but worse than mood disorder.
 Hannah Friedman

Topic 20: Etiology of delusional disorder

Delusional disorder is classified as a psychotic disorder, a disorder where a person has trouble recognizing reality.
Formerly called paranoia or paranoid disorder.

Delusion is a false belief that is based on an incorrect interpretation.

Delusions may involve circumstances that

 NON bizarre - could occur in reality even though they are unlikely (for example, the family next door
plotting to kill you, poisoned.
 Bizarre - for example, feeling controlled by an outside force or having thoughts inserted into your head.
Etiology:
1. unknown
2. family history
3. biological factors (neurological disease, conditions that affect the limbic sys and basal ganglia)
4. imbalance in neurotransmitters
5. environmental factors (drug abuse, excessive stress, being married, being employed, low socioeconomic
status)

Clinical feature:
Patients are further categorized based on the types of delusions they experi-ence:
 Erotomanic – Delusion of a special, loving relationship with another person, usually someone famous or of
higher standing. (This kind of delusion is sometimes at the root of stalking behavior.)
 Grandiose – Delusion that the person has a special power or ability, or a special relationship with a
powerful person or figure, such as the president, a celebrity or the Pope.
 Jealous – Delusion that a sexual partner is being unfaithful.
 Persecutory – Delusion that the person is being threatened or maltreated.
 Somatic – Delusion of having a physical illness or defect.

Treatment:
Psychotherapy may be helpful. Antipsychotic medications are often ineffec-tive, but a course of them should be
tried (usually a high-potency traditional antipsychotic or one of the newer atypical antipsychotics is used).
 Hannah Friedman

Topic 21: Delusional psychosis

 Hannah Friedman

Topic 22: Postpartum blues, depression and psychosis

Postpartum psychiatric illness is typically divided into three categories:

BLUES DEPRESSION PSYCHOSIS

Onset Begin within a few days Usually begins between two weeks The most severe
of childbirth and often to a month after delivery but can symptoms last from 2
peak by day 4/5 and occur any time in the first year to 12 weeks, and
may last a few days up postpartum. recovery takes 6
to two weeks. months to a year.
If symptoms last more
than two weeks, the ! Used to describe
individual must be a psychiatric
evaluated emergency !
for postpartum
depression
Incidence 70-80% 10% 0.1-0.2%
Symptoms Mild Severe Severe + psychosis
Emotional The symptoms vary
 Tearfulness or and can change
crying "for no  Persistent sadness, quickly.
reason" anxiousness or "empty" mood
 Mood swings  Severe mood swings  high mood and
 Irritability  Frustration, irritability, racing thoughts
 Anxiety restlessness, anger (mania)
 Questioning one's  depression
 Feelings of hopelessness
ability to care for  severe confusion
 Guilt, shame, worthlessness
the baby  losing inhibitions
 Low self-esteem
 Difficulty making  paranoia
 Numbness, emptiness
choices  Hallucinations and
 Exhaustion delusions.
 Loss of appetite
 Inability to be comforted
 Fatigue
 Trouble bonding with the
 Difficulty sleeping baby
 Difficulty  Thoughts of self-harm or
concentrating suicide
 Negative mood
Behavioral
symptoms
interspersed with
 Lack of interest or pleasure in
positive symptom
usual activities
 Low or no energy
 Low libido
 Changes in appetite
 Hannah Friedman

 Fatigue, decreased energy and

motivation
 Poor self-care
 Social withdrawal
 Insomnia or excessive sleep

 Lack of concentration, poor

memory

C Topic 23: The treatment of postpartum psychosis

Treatment Support and education  Psychological and behavioral  Antipsychotic medi
therapy cations
 Medications used to treat  Hospitalization
major depressive disorder might be indicated,
especially if there is
a risk of infanticide.

*Most antidepressants cross the placenta and should, therefore, be avoided, unless the patient has severe or
relapsing depression. In lactating patients, there is minimal or no risk of exposing the baby
to antidepressants via breastmilk, especially with SSRIs.

*SSRI - fluoxetine, citalopram and sertraline are safe during pregnancy.

 Hannah Friedman

Topic 23: Biological and genetic factors in mood disorders

Also known as mood affective disorders, is a group of conditions where a disturbance in the
person's mood is the main underlying feature.

Causes:
1. Psychosocial factors Life events and environmental stress
2. Personality factors
3. Genetics
4. Biological
A) Biogenic Amines
 Norepinephrine. decreased sensitivity of β-adrenergic receptors and clinical antidepressant
responses indicates a direct role for the noradrenergic system in depression. – clinical
effectiveness of antidepressant drugs with noradrenergic effects e.g. Venlafaxine
 Serotonin. Depletion of serotonin may precipitate depression, and some patients with suicidal
impulses have low CSF concentrations of serotonin metabolites and low concentrations of
serotonin uptake sites on platelets. – SSRIs highly effective in treating depression
 Dopamine. dopamine activity may be reduced in depression. Drugs that increase dopamine
concentrations reduce sx of depression.
B) Alterations in sleep neurophysiology
 Depression is associated with a premature loss of deep (slow-wave) sleep and an increase in
nocturnal arousal, with reduction in total sleep time.
 Patients manifesting a characteristically abnormal sleep profile have been found to be less
responsive to psychotherapy and to have a greater risk of relapse or recurrence and may benefit
preferentially from pharmacotherapy.
C) Immunological Disturbance.
Depressive disorders are associated with several immunological abnormalities, including decreased
lymphocyte proliferation in response to mitogens and other forms of impaired cellular immunity.
D) Oher Neurotransmitter disturbances
 Acetylcholine. Cholinergic agonists can exacerbate sx in depression; can induce changes in
hypothalamic-pituitary-adrenal (HPA) activity and sleep that mimic those associated with severe
depression.
 GABA has an inhibitory effect on ascending monoamine pathways, esp the mesocortical and
mesolimbic systems. Reductions have been observed in plasma, CSF, and brain GABA levels in
depression
 Drugs that antagonize NMDA receptors (where glutamate and glyicine bind) have antidepressant
effects.
 Hannah Friedman

E) Alterations of Hormonal Regulation:

Lasting alterations in neuroendocrine and behavioral responses can result from severe early stress.
 Thyroid axis activity. Approximately 5 to 10% of people evaluated for depression have previously
undetected thyroid dysfunction
 Growth Hormone. Decreased CSF GH levels have been reported in depression. GH is secreted from
the anterior pituitary after stimulation by norepinephrine and dopamine.
 Hannah Friedman

Topic 24: The clinical features, diagnosis and course of depression

Major depressive disorder (MDD) is an episodic mood disorder primarily characterized by depressed mood
and anhedonia lasting for at least 2 weeks.
The etiology is multifactorial, including both biological and psychological factors. Reduced levels
of neurotransmitters (serotonin, noradrenaline, dopamine) are believed to be the pathophysiological basis in most
cases.

Clinical features + diagnosis:

 Hannah Friedman

Topic 25: Bipolar disorders, dysthymia, cyclothymia

https://www.youtube.com/watch?v=KSvk8LLBo2g&t=227s OSMOSIS

Bipolar disorder -> Bipolar disorder is a psychiatric illness characterized by episodes of mania (or hypomania) and
major depression, interspersed with periods of normal mood and functioning.

Etiology:
Multifactorial origin
 Strong genetic component → increased risk if first-degree relative is affected
 ↑ Paternal age → ↑ mutations during spermatogenesis → ↑ risk of bipolar disorder in offspring
Triggers
 Childhood traumatic experiences
 Psychosocial stress
 Sleep disturbances
 Physical illness

Clinical features:

Types
 Hannah Friedman

Persistent depressive disorder (dysthymia)

Is a mood disorder consisting of the same cognitive and physical problems as depression , with less severe but
longer-lasting symptoms (chronic).
Symptoms are present for ≥ 2 years
Depressed mood, in addition to the presence of ≥ 2 of the following symptoms:
 Poor appetite or overeating
 Insomnia or hypersomnia
 Low energy or fatigue
 Low self-esteem
 Poor concentration or difficulty making decisions
 Feelings of hopelessness

C Topic 13: Treatment of bipolar disorders

Pharmacotherapy
Lithium—mood stabilizer
Anticonvulsants (carbamazepine or valproic acid)—also mood stabilizers, especially useful for rapid cycling bipolar
disorder and mixed episodes Olanzapine—a typical antipsychotic

Psychotherapy
Supportive psychotherapy, family therapy, group therapy (once the acute manic episode has been controlled)

ECT
Works well in treatment of manic episodes
Usually requires more treatments than for depression
 Hannah Friedman

Topic 26: Obsessive-compulsive disorders

Is characterized by persistent and recurring thoughts,
urges, or images (obsessions) that lead to repetitive
behaviors or mental acts (compulsions).
Since obsessions are experienced as intrusive and
involuntary as well as undesirable and unpleasurable, they
generally cause anxiety or distress. While compulsive
actions are generally not experienced as pleasurable, their
performance may provide relief from the distress and
anxiety caused by an obsession.

Etiology:
The etiology of OCD is multifactorial. Factors that have been associated with OCD development include:
 Genetic: familial transmission (high concordance rate of 0.57 in monozygotic twins)
 Neurobiological: abnormalities in the orbitofrontal cortex, anterior cingulate cortex, and striatum
 Serotonin level imbalance may play a role.
 Infection: pediatric autoimmune neuropsychiatric disorder associated with streptococcal infections
(PANDAS)
 Psychological trauma

Clinical features:
 Egodystonic: behavior patterns are not in agreement with ideal self-image
 Obsessions: recurring and intrusive thoughts
 Compulsions: repetitive actions to provide relief from anxiety caused by obsessions

Treatment:
A combination of pharmacotherapy and psychotherapy has been proven effective in the treatment of OCD.
 Cognitive-behavioral therapy (CBT)
 Cognitive therapy techniques
 Exposure therapy
 Pharmacotherapy
 Antidepressants
 SSRIs are the preferred treatment (e.g., sertraline, paroxetine, fluoxetine, fluvoxamine).
 Alternatively, tricyclic antidepressants with serotonergic action (e.g., clomipramine)
 Atypical antipsychotics (e.g., risperidone, aripiprazole, quetiapine)
 Hannah Friedman

Topic 27: Panic disorder and agoraphobia

Panic disorder is characterized by the experience of panic attacks accompanied by persistent fear of having
additional attacks. Recurrent spontaneous and unexpected panic attacks that often occur without a known trigger
Most common in patients aged 26–34 years

Associations:
 Agoraphobia
 Substance use
 Depression
 Bipolar disorder

Panic attacks are discrete periods of heightened anxiety that classically occur in patients with panic disorder;
however, they may occur in other mental dis-orders, especially phobic disorders and posttraumatic stress
disorder.

Panic attacks often peak in several minutes and subside within 25 minutes. They rarely last > 1 hour. Attacks may
be either unexpected or provoked by specific triggers. They may be described as a sudden rush of fear.

DIAGNOSIS AND DSM-IV CRITERIA

A panic attack is a discrete period of intense fear and discomfort that is ac-companied by at least four of the
following:
Palpitations
Sweating
Shaking
Shortness of breath
Choking sensation
Chest pain
Nausea
Light-headedness
Depersonalization (feeling detached from oneself)
Fear of losing control or “going crazy”
Fear of dying
Numbness or tingling
Chills or hot flushes

Treatment:
 Acute panic attack
 Short-acting benzodiazepine (e.g. alprazolam)
 If hyperventilation: breathing in a paper bag
 Long-term management
 Hannah Friedman

 CBT
 Antidepressants: SSRIs, SNRIs, TCAs
 Benzodiazepines may be used until antidepressants take effect.

Agrographia
Definition: pronounced fear or anxiety of being in situations that are perceived as difficult to escape from or
situations in which it might be difficult to seek help
Clinical features:
 Fear, anxiety, or even panic attacks over a period of ≥ 6 months in ≥ 2 of the following 5 situations:
 Using public transportation
 Being in open spaces
 Being in enclosed places
 Standing in line or being in a crowd
 Being outside of the home alone
 Active avoidance of these settings unless a companion is present
 Some patients can have comorbid panic disorder.
Treatment:
 CBT
 SSRIs

C Topic 8: The complex therapy of anxiety disorders

Anxiety disorders cover a broad spectrum of conditions characterized by excessive and persistent fear (an
emotional response to imminent threats), anxiety (the anticipation of a future threat), worry (apprehensive
expectation), and/or avoidance behavior.
Therapy typically consists of a combination of pharmacotherapy, especially selective serotonin reuptake
inhibitors (SSRIs), and psychotherapy, especially cognitive-behavioral therapy (CBT).
 Hannah Friedman

Topic 28: Specific phobias, social phobia

A phobia is a type of anxiety disorder defined by a persistent and excessive fear of an object or situation.

Specific phobia Social phobia

Persistent and intense fears of one or Also called social anxiety disorder) is a fear of
more specific situations or objects social situations in which embarrassment can
occur.
animal: spiders (arachnophobia), insects
(entomophobia), dogs (cynophobia) Phobias speaking in public

Eating in public
Natural environment: heights (acrophobia), Using public restrooms
storms (astraphobia)

Blood-injection-injury: blood
(hematophobia), needles (blenophobia), dental
procedures (odontophobia), fear of injury
(traumatophobia)

Situational: enclosed places

(claustrophobia), flying (aviophobia)

Other: fear of vomiting (emetophobia),

the number 13 (triskaidekaphobia), costumed
characters (masklophobia), fear of clowns

Etiology:

The cause of phobias is most likely multifactorial, with the following components playing important parts:
 Genetic: Fear of seeing blood often runs in families and may be associated with an inherited,
exaggerated vasovagal response. First-degree relatives of patients with social phobia are three times
more likely to develop the disorder.
 Behavioral: Phobias may develop through association with traumatic events. For example, people who
were in a car accident may develop a specific phobia for driving.
 Neurochemical: An overproduction of adrenergic neurotransmitters may contribute to anxiety
symptoms.

DIAGNOSIS AND DSM-IV CRITERIA

The diagnostic criteria for specific phobias is as follows:

1. Persistent excessive fear brought on by a specific situation or object

2. Exposure to the situation brings about an immediate anxiety response.
3. Patient recognizes that the fear is excessive.
 Hannah Friedman

4. The situation is avoided when possible or tolerated with intense anxiety.

5. If person is under age 18, duration must be at least 6 months.

The diagnosis of social phobia has the same criteria as above except that the feared situation is related to social
settings in which the patient might be embarrassed or humiliated in front of other people.

C Topic 25: The treatment of specific phobias and social phobia

Specific Phobia
 Supportive psychotherapy are often useful.
 If necessary, a short course of benzodiazepines or beta blockers may be used during desensitization to help
control autonomic symptoms.
 Systemic desensitization: Gradually expose patient to feared object or situation while teaching relaxation
and breathing techniques.

Social Phobia
 Paroxetine (Paxil), an SSRI.
 Beta blockers are frequently used to control symptoms of performance anxiety.
 Cognitive and behavioral therapies are useful adjuncts .
 Hannah Friedman

Topic 29: Generalized anxiety disorder, mixed anxiety-depressive disorder

Generalized anxiety disorder (GAD)

Prolonged and excessive anxiety that is either unspecific or revolves around certain themes (e.g., health,
work); not focused on a single specific fear

Clinical fetures:
 Prolonged (≥ 6 months, occurring more days than not) and excessive anxiety
 Anxiety causes clinically significant distress
 Not caused by substance use, medication, or underlying medical condition
 Fatigue and muscle tension
 Restlessness and irritability
 Sleep disturbances and difficulty concentrating

Treatment:
First-line: psychotherapy, pharmacotherapy, or both
 Psychotherapy: CBT, applied relaxation therapy, biofeedback
 Pharmacotherapy: SSRIs/SNRI
Second-line
 Benzodiazepines can be used until SSRIs take effect but should never be used for long-term management,
as they increase the risk of benzodiazepine dependence.
 Buspirone: requires consistent, daily intake for at least two weeks because of its delayed onset of action
 Antipsychotics only for refractory cases

Mixed anxiety–depressive disorder (MADD)

Patients who have both anxiety and depressive symptoms of limited and equal intensity accompanied by at least
some autonomic features.

Risk factors:
 Having a family history of mental health disorders, including substance abuse disorders
 Living in poverty or struggling financially
 Lacking familial or social support
 Having a serious or chronic illness
 Having low self-esteem
 Having had a form of childhood trauma
 Having to deal with an increased amount of daily stress

DIAGNOSIS AND DSM-IV CRITERIA

 A dysphoric mood is chronic or recurring for a minimum of 4 weeks and has at least 4 of the following
symptoms:
 Hannah Friedman

-troubles concentrating or with memory

-disturbed sleep
-tiredness or lack of energy
-feeling irritable
-worrying
-crying easily
-enhanced sensory stat
-expecting the worst
-feeling hopeless or pessimistic, or having low self-esteem/feeling worthless.
 The symptoms presented are not caused by medications, drugs, or a health condition.
 The symptoms cause significant impairments or distresses in aspects of daily life.
 The symptoms do not meet the criteria for different and separate mental health disorders. Around 60% of
individuals with major depressive disorder also experience a form of anxiety disorder, so the disorders are
often comorbid.

Treatment:
 CBT
 Medication – SSRI, antidepressive
 Hannah Friedman

Topic 30: Acute stress disorder, post-traumatic stress disorder and adjustment disorder
Trauma and stressor related disorders
Trauma and stressor related disorders are a group of psychiatric disorders that arise following a stressful or
traumatic event. They include acute stress disorder, post-traumatic stress disorder, and adjustment disorder.
These three conditions often present similarly to other psychiatric disorders, such as depression and anxiety,
although the presence of a trigger event is necessary to confirm a diagnosis.

Acute stress disorder

Definition: distressing symptoms related to the traumatic event that last between 3 days to 1 month following the
exposure.
Epidemiology:
 Occurs in ∼ 50% of individuals experiencing interpersonal traumatic events (e.g., assault, rape)
 Occurs in up to ∼ 13% of individuals involved in motor vehicle accidents
 Hannah Friedman

Risk factors:
 Pre-existing mental disorder
 Poor social support

Dagnostic criteria (according to DSM-5)

Exposure to death (actual or threatened), injury, or sexual abuse that occurs in ≥ 1 of the following:
 Direct experience of these events
 Witnessing these events
 Hearing about these events happening to close friends or family
 Repeated exposure to unpleasant details of traumatic events occurring to others
At least 9 of the following 14 symptoms are present:
A)Intrusion
1) Recurrent distressing memories
2) Recurrent distressing dreams
3) Flashbacks
4) Severe psychological distress or physiological responses to internal or external cues related to the event
B)Negative mood
5) Inability to feel positive emotions (e.g., happiness, satisfaction, or love)
C)Dissociation
6) Altered sense of reality
7) Loss of memory with regards to important details of the event
D)Avoidance
8) Avoidance of memories, thoughts, or feelings related to the event
9) Avoidance of external reminders (e.g., places, people, conversations, objects) related to the event
E)Arousal
10) Sleep disturbance
11) Irritable behavior
12) Hypervigilance
13) Poor concentration
14) Heightened startle reflex
Duration: Symptoms last from 3 days to 1 month following the traumatic event.
The affected individual has been experiencing significant distress or impaired social and/or occupational
functioning since the traumatic event.
Symptoms are not explained by substance misuse or another medical condition.

Treatment:
Benzodiazepines should be used with caution because of the risk of comorbid substance-use
 Cognitive-behavioral therapy is the first-line treatment.
disorders, especially among patients with active or previous alcohol or substance use disorder.
 Benzodiazepines can be administered to reduce agitation or sleep disturbance.
 Hannah Friedman

Post-traumatic stress disorder (PTSD)

Definition: distressing symptoms related to a specific traumatic event and lasting > 1 month following the event

Etiology:
Triggers: exposure to traumatic events (either through direct experience or as a witness)
 Sexual abuse (most common)
 Physical abuse
 Accidents
 Natural disasters
 War: The duration of combat exposure, by either combatants or civilians, is directly proportional to the risk
of developing PTSD.
 Diagnosis of a severe disease

Risk factors:
 Psychiatric comorbidities
 Lower socioeconomic status
 Younger age at time of trauma
 Lack of social support
 Prior traumatic exposure and/or subsequent reminders, including childhood experiences
 Initial severe reaction to the traumatic event
 Common comorbidities: depression, substance use disorders, somatic symptom disorder
Initial severe reaction to the traumatic event

Diagnostic criteria (according to DSM-5)

Experience of a traumatic event involving death (actual or threatened), serious injury, or sexual
violence that occurs in ≥ 1 of the following ways:
 Direct experience of these events
 Witnessing these events
 Hearing about these events happening to close friends or family
 Repeated exposure to unpleasant details of traumatic events occurring to others
≥ 1 of the following intrusion symptoms that begin after the traumatic event:
 Intrusive thoughts: recollection of psychotraumatic events
 Recurrent, distressing dreams
 Flashbacks: reexperiencing the traumatic event. Flashbacks can last from seconds to days.
 Intense and persistent distress due to internal or external cues related to the traumatic event
 Physiological reactions due to internal or external cues related to the traumatic event
Avoidance of triggering stimuli following the event in ≥ 1 of the following ways:
 Avoidance of memories, thoughts, or feelings associated with the event
 Avoidance of external reminders (e.g., places, people, conversations, objects) related to the event
Negatively affected mood and cognition that begins or worsens after the event in ≥ 2 of the following ways:
 Inability to remember important details of the event
 Severe negative thoughts or expectations about oneself or the world
 Distorted memories of the cause and/or consequences of the event
 Constant negative emotions (e.g., fear, guilt)
 Hannah Friedman

 Reduced or absent interest in important life activities

 Detachment from others
 Inability to feel positive emotions (e.g., happiness, satisfaction, or love)
Altered reactivity or arousal beginning or worsening after the event in ≥ 2 of the following ways:
 Irritability or angry outbursts
 Self-destructive behavior
 Hypervigilance
 Heightened startle reflex
 Poor concentration
 Sleep disturbance
Duration: Symptoms in groups B–E last > 1 month following the traumatic event.
The affected individual has been experiencing significant distress or impaired social and/or occupational
functioning since the traumatic event.
Symptoms are not explained by substance misuse or another medical condition.

Treatment:
1.Psychotherapy: first-line treatment; with or without adjunctive pharmacotherapy [4]

 Trauma-focused cognitive-behavioral therapy

 Exposure therapy (e.g., showing war veterans images of war, returning to the scene of an accident)
 Cognitive processing therapy
 Eye movement desensitization and reprocessing: Under the guidance of a therapist, the patient recalls
traumatic images while following the therapist's fingers with their eyes from left to right.
2.Pharmacotherapy
 SSRIs, SNRIs
 Prazosin: for nightmares
 Consider atypical antipsychotics to augment SSRIs and SNRIs.
 Benzodiazepines are rarely used for hyperarousal and anxiety. Their use should be closely monitored
because many patients with PTSD are at risk for drug dependence.

Prognosis: Approximately 60% of patients have reported a full recovery within an average of 4.5 years following
the event with psychotherapy and/or pharmacotherapy.

To remember the features of PTSD, think of “TRAUMMA”: Traumatic event, Reexposure, Avoidance,
Unable to function, More than a Month of duration, Arousal is increased
 Hannah Friedman

Adjustment disorder
Definition: a maladaptive emotional or behavioral response to a stressor, lasting ≤ 6 months following resolution
of the stressor.

Etiology: a combination of intrinsic and extrinsic stressors (e.g., divorce, losing a job, academic failure, difficulties
with peer group)

Diagnostic criteria (according to DSM-5)

 Emotions or behaviors in response to a stressor that occur within 3 months of onset
 Clinically significant responses that include ≥ 1 of the following:
 A level of distress that is disproportionate to the expected response to the stressor
 Impaired functioning in social, occupational, and/or other important areas
 Symptoms are not explained by another mental disorder.
 Symptoms are not explained by a normal response to grief.
 Symptoms last ≤ 6 months following resolution of the stressor.

Differential diagnosis: normal stress reaction

Treatment:
1.Psychotherapy
 First-line treatment: cognitive-behavioral therapy or psychodynamic psychotherapy
 May be provided as individual, family, or group support therapy
 Interpersonal psychotherapy
2.Pharmacotherapy
 SSRIs: for depressed mood
 Benzodiazepines: for anxiety or panic attacks
 Benzodiazepines or other sedative-hypnotic agents (e.g., zolpidem): for insomnia

*Although psychotherapy alone is usually sufficient in patients with adjustment disorder who have no other
disabling symptoms, pharmacotherapy may be used when psychotherapy has little or no effect.
 Hannah Friedman

Topic 31: Dissociative disorders

https://www.youtube.com/watch?v=XF2zeOdE5GY&t=377s OSMOSIS

Mental disorders that involve experiencing a disconnection and lack of continuity between thoughts, memories,
surroundings, actions and identity. People with dissociative disorders escape reality in ways that are involuntary
and unhealthy and cause problems with functioning in everyday life.

Dissociative disorders according to the DSM-IV TR include:

1. Dissociative amnesia
Epidemiology: most common dissociative disorder (lifetime prevalence ∼ 7%); more common
in women than in men.

Diagnostic criteria:
1) Inability to recall autobiographical information, typically of a traumatic or stressful event , that is
distinct from ordinary forgetting
 Can be described as localized (i.e. amnesia of a single event or time period), selective
(i.e. amnesia of a specific aspect of an occurrence), or generalized (i.e. amnesia of personal history
and identity)
2) Symptoms cause significant social or occupational impairment.
3) Symptoms are not due to substance use or another medical condition.
4) Symptoms cannot be explained better by another psychiatric disorder (e.g., dissociative identity
disorder, acute stress disorder, or posttraumatic stress disorder).
5) May present with dissociative fugue: wandering or purposeful travel; associated with amnesia of
identity or autobiographical information

Treatment: psychotherapy; no effective pharmacotherapy available

Prognosis:
 Temporarily inaccessible memories are often retrievable or return naturally
 Rarely generalizes, but can cause complete memory loss
 Associated with concurrent major depressive disorder and increased risk for suicide
 Hannah Friedman

2. Dissociative identity disorder (Multiple personality disorder)

Epidemiology:
 Rare (prevalence < 1%)
 More prevalent in women
 May manifest at any age
 Very common in patients with a history of physical/sexual abuse and/or neglect during childhood (90%
of patients)

Diagnostic criteria:
 Alternation of at least two separate personality states that cause identity disruption and dominate at
different times
 Involves discontinuity in sense of self (depersonalization) and agency; altered affect, memory, behavior,
perception, consciousness, cognition and/or sensory-motor functioning (derealization)
 Frequent gaps in recall of normal daily events or personal information that are significantly different
from ordinary forgetfulness
 Symptoms cause the patient significant social or occupational impairment.
 Symptoms are not related to substance use, another medical condition, or a broadly accepted religious
or cultural practice.

Treatment: psychotherapy; SSRIs for comorbid conditions (depression, PTSD)

Prognosis:
 Chronic disease course with fluctuations in severity
 Increased risk of other psychiatric conditions (major depression, borderline personality disorder, PTSD,
eating disorders, substance use disorders)
 High rates of self-harm and suicide
 Hannah Friedman

3. Depersonalization/Derealzioation disorder
Epidemiology: lifetime prevalence ∼ 2%; average age at onset 16 years

Diagnostic criteria:
1. Recurrent or persistent episodes of depersonalization and/or derealization
 Depersonalization: sense of unreality with detachment from oneself (e.g., body perception, feelings,
thoughts, actions)
 Derealization: sense of unreality with detachment from one's environment
2. Reality testing is intact during these episodes.
3. Symptoms cause significant social or occupational impairment.
4. Symptoms are not due to substance use or another medical condition.
5. Symptoms cannot be better explained by another psychiatric disorder (e.g., schizophrenia, major
depressive disorder, panic disorder, acute stress disorder, PTSD, other dissociative disorders)

Treatment: cognitive behavioral therapy, hypnotherapy, psychodynamic therapy

Prognosis:
 Often persistent, with fluctuations in severity
 Increased risk for concurrent major depression and anxiety disorders
 Hannah Friedman

Topic 32: Somatoform disorders

A somatic symptom disorder, formerly known as a somatoform disorder, any mental disorder that manifests as
physical symptoms that suggest illness or injury, but cannot be explained fully by a general medical condition or
by the direct effect of a substance, and are not attributable to another mental disorder.
Patients with somatoform disorders present with physical symptoms that have no organic cause.

The following were conditions under the term Somatoform Disorders:

1) Conversion disorder: A somatic symptom disorder involving the actual loss of bodily function such as
blindness, paralysis, and numbness due to excessive anxiety
2) Somatization disorder
3) Hypochondriasis
4) Body dysmorphic disorder: wherein the afflicted individual is concerned with body image, and is manifested as
excessive concern about and preoccupation with a perceived defect of their physical appearance.
5) Pain disorder
6) Undifferentiated somatic symptom disorder – only one unexplained symptom is required for at least six
months.
 Hannah Friedman

1
 Hannah Friedman

Topic 33: Sleep disorders

 Hannah Friedman

C Topic 26: The treatment of sleep disorders

Sleep is a physiologically recurring state of rest characterized by relative suspension of consciousness and
inaction of voluntary muscles. It is regulated by the circadian rhythm and typically runs through 4–5 cycles of
three stages of non-rapid eye movement sleep and one stage of rapid eye movement (REM) sleep.
They may be primary, i.e., due to an intrinsic problem with the sleep-wake cycle, or secondary to an underlying
medical condition.

Causes of sleep disorders include:

 Medical conditions (pain, metabolic disorders, endocrine disorders, etc.)
 Physical conditions (obesity, etc.)
 Sedative withdrawal, use of stimulants (caffeine, amphetamines, etc.)
 Major depression (causes early morning awakening or hypersomnia)
 Mania or anxiety
 Neurotransmitter abnormalities:
- Elevated dopamine or NE causes decreased total sleep time
- Elevated acetylcholine causes increased total sleep time and increased
proportion of rapid eye movement (REM) sleep
- Elevated serotonin causes increased total sleep time and increased
proportion of delta wave sleep

Sleep disorders may be further subdivided into:

1. Dyssomnias: Disturbances in the amount, quality, or timing of sleep

 Primary insomnia, primary hypersomnia, narcolepsy, breathing-related disorders,
circadian rhythm sleep disorder
2. Parasomnias: Abnormal events in behavior or physiology during sleep
 Nightmare disorder, night terror disorder, sleepwalking disorder
(somnambulism)

1. Dyssomnias
Insomnia
Etiology:
 Poor sleep hygiene
 Subclinical mood or anxiety disorders

Classification:
 Acute or transient: < 3 months (associated with stress or a disrupted sleep schedule)
 Chronic: ≥ 3 months (associated with an increased risk of psychiatric illness and functional impairment)

Clinical features:
 Initial or sleep-onset insomnia: difficulty initiating sleep
 Middle or sleep-maintenance insomnia: frequently waking from sleep
 Late or sleep-offset insomnia: awakening early in the morning
 Hannah Friedman

 Nonrestorative sleep: feeling fatigued after waking

DSM-5 diagnostic criteria (primary insomnia is a diagnosis of exclusion)

 Problems initiating or maintaining sleep, or awakening in the early morning and being unable to return to
sleep
 Symptoms occur ≥ 3 days/week for ≥ 3 months
 Symptoms cause functional impairment or distress
 Symptoms are not caused by an underlying substance or medication use
 Symptoms occur despite having enough time to sleep
 No underlying or coexisting psychiatric or medical disorder that explains symptoms
Treatment:
1.Improve sleep hygiene
 No alcohol 4–6 hours preceding sleep
 No stimulants (caffeinated drinks and nicotine should be avoided 3–4 hours before bedtime)
 Quiet, dark, pleasantly cool bedroom and a comfortable bed
 No large meals before bedtime
 Regular exercise is beneficial but should be avoided 6 hours before bedtime.
2.Stimulus control therapy: Insomnia disorder may cause the bed and bedroom to become cues for arousal rather
than sleep. Stimulus control instructions aim to correct this by re-establishing the association of the bed and
bedroom with sleep.
 Advise waking up at regular times (also during the weekend and holidays).
 Discourage engaging in other activities in bed such as working or reading.
 Leave the bedroom when unable to fall asleep within 20 minutes (e.g., to read or listen to music) and
return only when sleepy.
 Advise against afternoon naps; if taken, this should not take place after 3 pm and naps should be no
longer than 1 hour.
 Sleep restriction therapy: A cognitive behavior therapy for patients with chronic insomnia, where the
amount of time spent in bed is restricted to their average estimated sleep time. When sleep efficacy (total
sleep divided by time spent in bed) is greater than 90%, the amount of time spent in bed is increased. This
has been shown to reduce sleep latency.
3.Cognitive-behavioral therapy (CBT): preferred treatment for chronic insomnia
4.Pharmacotherapy (use sparingly and short-term)
 Benzodiazepines
 ↓ Sleep latency; ↓ awakenings during sleep
 For sleep onset insomnia: short-acting agent, e.g., triazolam
 Antidepressants: trazodone (most commonly prescribed antidepressant for chronic insomnia and
depressive symptoms) or amitriptyline
 Non-benzodiazepine sedatives
 Zolpidem, eszopiclone, zaleplon

Hypersomnolence

Age of onset: 15–25 years of age

Etiology:
 Genetic (may be autosomal dominant)
 Hannah Friedman

 Head trauma
 Viral infections (e.g., HIV)
Classification:
 Acute: < 3 months
 Chronic: ≥ 3 months
Clinical features:
 Excessive sleep (with decreased sleep quality)
 Difficulty awakening from sleep
 Sleep inertia (impaired alertness or excessive fatigue after waking)
 Automatic behaviors (with no memory of the episode after waking)
DSM-5 Diagnostic Criteria
 Excessive sleepiness despite ≥ 7 hours of sleep with:
 Recurrent periods of sleep on the same day, and/or
 > 9 hours of sleep that is nonrestorative, and/or
 Impaired alertness after awakening
 Symptoms occur ≥ 3 days/week for ≥ 3 months
 Symptoms cause functional impairment or distress
 Symptoms not caused by an underlying substance or medication use
 Symptoms occur despite having enough time to sleep
 No underlying or coexisting psychiatric or medical disorder that explains symptoms
Treatment:
 Regularly scheduled naps
 First-line therapy: modafinil or methylphenidate
 Second-line therapy: atomoxetine

Circadian rhythm sleep-wake disorders

Delayed sleep phase disorder -> recurrent delay in sleep onset and waking times
Risk factors: associated with puberty, stimulant use (e.g., caffeine), and irregular sleep
Treatment:
 Phototherapy in the morning
 Melatonin receptor agonist (e.g., ramelteon, administered at night)
 Chronotherapy - behavioral treatment in which the sleep time is progressively delayed by 3 hours until a
final earlier bedtime schedule is achieved and maintained.

Jet leg disorder -> insomnia or hypersomnia due to travel across time zones
Risk factor: sleep deprivation prior to travel
Treatment: resolves spontaneously

Shift work disorder -> misaligned circadian rhythm due to nightly working hours and sleep deprivation
Risk factors: shifts > 16 hours and/or night shifts
Treatment:
 Modafinil if severe
 Bright light therapy at night to adapt to work shift
 Hannah Friedman

Breathing-Related Disorders
Characterized by sleep disruption and excessive daytime sleepiness caused by abnormal
sleep ventilation from either obstructive or central sleep apnea. Breathing disturbances
include apneas, hypoapneas and oxygen desaturation.

 Obstructive: Caused by cessation of airflow through nose or mouth

 Common in middle-age overweight males (Pickwickian syndrome)
 Freq. in patients with micrognatia, acromegaly & hypothyroidism
 Main symptom is load snoring with intervals of apnea
 Excessive daytime sleepiness, severe morning
headaches, morning confusion, depression and anxiety
 Each event last 10-20 seconds and usually 5-10 episodes per/hr
 Occurs both in REM and nonREM sleep
 Treatment consists of nasal CPAP, uvulopharyngoplasty, weight
loss, buspirone, SSRIs and TCAs (to reduce REM periods)
 Avoid sedatives or alcohol as they might exacerbate the condition
 Central: Loss of airflow secondary to lack or respiratory effort
 Rare and usually occurs in the elderly
 Treatment is nasal CPAP and mechanical ventilation
 Strong correlation with heart failure
 Mixed: Elements of both obstructive and central apnea

Nacrolepsy
Narcolepsy is a disorder that is characterized by repeated, sudden attacks of sleep in the daytime for at
least 3 months, associated with:
 Excessive daytime somnolence
o Distinguishable from fatigue by irresistible sleep attacks of short duration (<15
minutes)
o Sleep attacks may be precipitated by monotonous or sedentary activity – and when the
patient wakes up he/she feels refreshed
 Cataplexy: Collapse due to sudden loss of muscle tone
o Occurs in 70% of patients
o Associated with emotion, particularly laughter
 Short REM latency
 Sleep paralysis: Brief paralysis upon awakening (50% of patients)
 Hypnagogic & hypnopompic hallucinations
o Dreamlike experience during transition from wakefulness to sleep and vice versa with vivid
auditory or visual hallucinations or illusions – can be seen in 30% of patients
 Increased incidence of:
o Periodic leg movement, sleep apnea (mainly central), short sleep latency and frequent
nighttime arousals, memory problems, ocular symptoms (blurring, diplopia, flickering) &
depression

2.Parasominas

Seep walking disorder

Non-REM sleep arousal disorder (no memory of dream)
Epidemiology
 Discrete episodes are common (up to 7% of adults and 30% of children), but the disorder is rare.
 Hannah Friedman

 Associated with sleep deprivation, irregular sleep schedules, some medications

Etiology: idiopathic or genetic (inherited in 80% of cases)
Risk factors:
 Stress or fatigue
 Obstructive sleep apnea
 Nocturnal seizures
 Fever
 Drugs (e.g., lithium)
Clinical features:
 Recurrent episodes during the first third of the sleep cycle, including sitting up, walking, or eating (rarely,
violence)
 Blank stare and difficulty arousing patient during the episode
 Followed by amnesia of the event
Treatment:
 Education and reassurance
 Ensuring safe sleep environment to reduce the risk of physical harm or wandering outdoors
 In refractory cases, benzodiazepines

Sleep terror disorder

Non-REM sleep arousal disorder (no memory of dream)
Epidemiology: Discrete episodes of sleep terrors are relatively common (up to 2% of adults and 20% of children),
but the disorder is rare.
Etiology: unknown; thought to be genetic (family history)
Risk factors:
 Stress or fatigue
 Obstructive sleep apnea
 Nocturnal seizures
 Fever
 Drugs (e.g., lithium)
Clinical features:
 Screaming or crying suddenly upon awakening
 Intense fear and agitation
 Tachypnea, diaphoresis, tachycardia during episodes
 Difficulty arousing patients during episodes; patients will often return to sleep and not remember the
episode the next day
Treatment:
 Education and reassurance (disorder is usually self-limited)
 Remove dangerous objects from bedroom to reduce risk of self-injury
 In refractory cases, benzodiazepines

Nightmare disorder
REM sleep arousal disorder (patient remembers the dream)
Epidemiology:
 Prevalence: up to 2% of adults, most common in early adulthood
 Hannah Friedman

Risk factors: post-traumatic stress disorder (PTSD)

Clinical features:
 Recurrent frightening dreams during the second half of sleep cycle (middle of the night or early in the
morning)
 Patient remembers the dream after awakening
 Causes functional impairment or distress
Treatment:
 Reassurance if the disorder is mild
 Imagery rehearsal therapy: involves modifying a recurrent nightmare by writing it down and rehearsing
new endings that make nightmares less frightening when they occur again
 Antidepressants if associated with PTSD
 Hannah Friedman

Topic 34: Pathology of human sexual behaviour and gender identity

Sex: a collection of biological features, including sex chromosomes and internal and external reproductive organs,
that allow an individual to be categorized as male, female, or intersex.

The 4 phases of the Whipple and Brash-McGreer sexual response cycle

1. Desire phase
 Interest in sexual activity
 Manifests as sexual fantasies
2. Arousal phase
Excitement phase: initiation of physiological changes
 ↑ Heart rate, blood pressure, respiratory rate
 Nipples become erect
 ♂: penis becomes erect, testes become congested and elevated, scrotum tightens (see
also physiological erection)
 ♀: swelling of the clitoris, labia, and vagina; the vagina produces transudate; uterus becomes elevated
within the pelvis
Plateau phase: enhanced physiological changes with persistent sexual excitement
3. Orgasm phase
 Climatic phase of physical arousal
 Involuntary muscle contractions in the genital and anal regions
 ♂: ejaculation
 ♀: contractions of the proximal labia minora, distal vagina, and uterus
4. Resolution phase
 The body returns to its physiological baseline

Sexual disorders are characterized by abnormal sexual desires or functioning that cause significant distress
and/or impaired social functioning.

Sexual desire disorders

Divided into:
 Hypoactive
- Lack of sexual fantasies or desire for sex
- Lack of desire may be used to protect the patient against any unconscious fears they have
about sex
- Lack of desire may be seen along with chronic anxiety or depression
- Women are more commonly affected than men

 Sexual aversion
- Avoidance of genital sexual contact with a partner OR an avoidance of masturbation
Sexual arousal disorders
Divided into:
 Female sexual arousal disorder
- Features persistent or recurrent inability to maintain or attain the lubrication needed to
 Hannah Friedman

complete the sexual act

- May reflect psychological conflicts
- Possibly hormone related (thyroid, prolactin, testosterone, estrogen, serotonin)

 Male erectile disorder

- Features the persistent or recurrent inability to maintain or attain an erection
- We should determine whether this problem is organic (ex. Prostatectomy side- effect) or
functional (i.e. Psychological)
▪ This is accomplish with the use of monitoring nocturnal penile tumescence (stamp test)

Orgasmic disorders
 Female orgasmic disorder (anorgasmia)
- Recurrent or persistent delay in or absence of an orgasm during sex
- Psychological factors include fear of impregnation, fear of rejection by partner, hostility
towards men, feelings of guilt towards sexual impulses or marital conflicts

 Male orgasmic disorder

- If ejaculation does occur at all during sex, it is done so with great difficulty
- A life-long anorgasmia indicates a more severe psychopathology
- Most common organic reason is the use of SSRIs, which causes delayed orgasms

 Premature ejaculation
- Main complaint of men being treated for sexual disorders
- Constant achievement of an early, unintended orgasm
- Common in younger men, men with a new partner, and college-educated m

Sexual pain disorders

 Vaginismus
- Involuntary muscle constriction of outer 1/3 of vagina that interferes with penile entry and
sex
- Usually seen with women in higher social classes
- Sexual trauma such as rape or childhood abuse can also be a cause
- Women with psychosexual conflicts may see the penis as a weapon
 Dyspareunia
- Recurrent or persistent genital pain occurring before, during or after sex

Sexual dysfunction caused by a general medical condition

- Male erectile disorder: Atherosclerotic disease, Klinefelter's syndrome, MS, DM, Hyperthyroidism, Perineal
prostatectomy, Addison's disease
- Dyspareunia: Endometriosis, Cervicitis, Vaginitis
- Hypoactive sexual desire disorder: Surgical procedure that lowers body image (ex. Mastectomy)
 Hannah Friedman

Substance-induced sexual dysfunction

- Greater evaluation studies done with men than with women
- Common drugs causing male sexual dysfunction include:
- SSRIs, Lithium, Anti-hypertensives (ex. Clonidine and methyldopa), Alcohol, Anti-parksonian
agents, Digoxin

Treatment:
1.Individual cognitive behavioral and psychodynamic therapy
2.Sex therapy
 Short-term therapy for individuals or couples
 Addresses psychological and physical barriers to a healthy sexual relationship
 Involves exercises to increase sexual sensory awareness and progressively heighten levels of sexual contact
3.Pharmacotherapy
 Male hypoactive sexual desire disorder: testosterone replacement therapy
 Female sexual interest/arousal disorder: low-dose testosterone and/or vaginal estrogen replacement
therapy (postmenopausal women)
4.Mechanical therapy
 Female orgasmic disorder: education and exercises to enable women to orgasm through self-stimulation

Paraphilic disorder
Definition: characterized by abnormally intense and persistent sexual interests (manifested as urges, fantasies, or
behaviors) accompanied by significant distress or functional impairment of the affected individual.

Diagnostic criteria (according to DSM-5):

1. Abnormally intense and persistent sexual interests occur over a period of at least 6 months
2. Result in significant distress or impairment in important areas of functioning (e.g., social, occupational) to
the individual or they harm or have the potential to harm others (e.g., children, nonconsenting adults).

Pedophilia: Sexual gratification from fantasies or behaviors involving sexual acts with
children (most common paraphilia)
Voyeurism: Watching unsuspecting nude individuals (often with binoculars) in order to
obtain sexual pleasure
Exhibitionism: Exposure of one’s genitals to strangers
Fetishism: Sexual preference for inanimate objects (e.g., shoes or pantyhose)
Transvestic fetishism: Sexual gratification in men (usually heterosexual) from wearing
women’s clothing (especially underwear)
Frotteurism: Sexual pleasure in men from rubbing their genitals against unsuspecting
women; usually occurs in a crowded area (such as subway)
Masochism: Sexual excitement from being humiliated or beaten
Sadism: Sexual excitement from hurting or humiliating another
Necrophilia: Sexual pleasure from engaging in sexual activity with dead people
Telephone scatologia: Sexual excitement from calling unsuspecting women and engaging in
sexual conversations with them.
 Hannah Friedman

Treatment:
 Psychotherapy and cognitive behavioral therapy
 Pharmacological treatment to suppress sex drive (e.g., antiandrogens, antidepressants such as SSRIs, mood
stabilizers)
 Group therapy (therapist-led group therapy)
 12-step program
 Social skills training

Gender identity (Gender dysphoria)

Gender: the set of socially constructed, culturally-specific attitudes and behaviors deemed appropriate for men
and women by a given society.

Gender identity: an individual's sense of self as male, female, or a combination of both, or neither.

According to DSM 5:

Treatment:
1.Psychotherapy
2.Hormone therapy
 Estrogen or antiandrogen therapy may be used to feminize transgender women (i.e., increase body fat,
reduce male hair pattern growth, induce breast growth)
 Testosterone therapy may be used for transgender men (i.e., reduces female secondary sex
characteristics → masculinization).
3.Sexual reassignment surgery
 Hannah Friedman

Topic 35: Impulse control disorders

Impulse control disorders are characterized by an inability to resist behaviors that may bring harm to oneself or to
others. Patients may or may not try to suppress their impulses and may not feel remorse or guilt after they have
acted out. Anxiety or tension is often experienced prior to the impulse, and relief or satisfaction results after the
behavior is completed.

Impulse control disorders are not caused by another mental condition, general medical problem, or substance use .

Include:
Pyromania
 Individuals cannot control the impulse to set fire, resulting in multiple episodes of intentional fire setting.
 Individuals experience internal tension before setting a fire and relief after starting or witnessing a fire.
 The fire setting is not aimed at secondary gains such as money, not driven by sociopolitical factors, not an
expression of anger or vengeance, and not a response to a delusion or hallucination

Kleptomania
 Individuals cannot control the impulse to steal objects, which are not needed for personal use or for their
monetary value.
 Individuals experience internal tension before stealing and relief at the time of committing theft.
 The stealing is not motivated by anger or vengeance and is not in response to a delusion or hallucination.
Treatment:
 CBT
 There is currently no pharmacotherapy available.

Intermittent explosive disorder

A condition characterized by outbursts of impulsive aggression (verbal or physical) that are intermittent,
unplanned, and out of proportion to the circumstances, causing the individual significant distress, and impairing
psychosocial functioning
Age at onset: 14–17 years

Etiology: associated with genetic, neurobiological, inflammatory, infectious ( Toxoplasma gondii), psychological,
and/or social factors (e.g., history of abuse)

Diagnostic criteria (according to DSM-5)

 Sudden aggressive outbursts (verbal or physical) either:
 ≥ 2 times/week for a period of 3 months with no physical injury to humans or animals and no destruction
of property
 OR ≥ 3 times/year with physical injury to humans or animals and/or destruction of property
 The aggressive behavior is grossly disproportionate to the stressor.
 The patient has to be at least 6 years of age for this diagnosis to be considered.
 Adjustment disorder should be excluded in children 6–18 years of age.
 The disturbance causes significant distress or negatively impacts the individual's functioning and legal or
financial situation.
 Hannah Friedman

Treatment
 CBT
 Pharmacotherapy (e.g., SSRIs or mood stabilizers)

Trichotillomania
Recurrent pulling out of one’s hair, resulting in visible hair loss
Usually involves scalp, but can involve eyebrows, eyelashes, and facial and pubic hair
Tension present before the behavior, and pleasure or relief resulting af-terwards causes significant distress or
impairment in daily functioning

Treatment:
 SSRIs, antipsychotics, lithium
 Hypnosis, relaxation techniques
 Behavioral therapy, including substituting another behavior and/or pos-itive reinforcement (viewing hair
pulling as simply a habit)
 Hannah Friedman

Topic 36: The aetiology and significance of personality disorders

Personality is one’s set of stable, predictable emotional and behavioral traits.

Personality disorder - Pervasive, inflexible, and maladaptive personality patterns that lead to significant distress
or functional impairment and are stable over time. Differ significantly from the expected and accepted norms of
an individual's culture.

Diagnostic criteria:
 At least two or more of the following deviate significantly from cultural expectations:
1. Cognition (e.g., perceives events, others, or self in an inappropriate way)
2. Affectivity
3. Interpersonal functioning
4. Impulse control
 Begins in early adulthood and is stable over time
 Leads to significant distress and impaired functioning in important areas of life (e.g., social, occupational)
 Is not caused by another mental disorder, substance abuse, or other medical condition
 Can be diagnosed in individuals < 18 years of age if features have been present for ≥ 1
year (except antisocial personality disorder)

C Topic 24: The treatment of personality disorders

1.Psychotherapy, dialectical behavior therapy, group therapy, and/or cognitive therapy
2.Symptomatic medical therapy
 Mood stabilizers: valproate, topiramate, and lamotrigine
 Antipsychotics: especially for symptoms of delusion
 Antidepressants: selective serotonin reuptake inhibitors (SSRIs)
 Hannah Friedman

Topic 37: Cluster A personality disorders: odds and eccentric

Paranoid, schizoid, and schizotypal. These patients are perceived as being eccentric and “weird.”
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Topic 38: Cluster B personality disorders: dramatics

Includes antisocial, borderline, histrionic, and narcissistic personality disorders. These patients are often emotional,
impulsive, and dramatic.
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Topic 39: Cluster C personality disorders: anxious

Includes avoidant, dependent, and obsessive–compulsive personality disorders. These patients appear anxious and
fearful.
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 Hannah Friedman

Topic 40: Anorexia nervosa. Bulimia nervosa

Eating disorders are psychological conditions characterized by abnormal eating habits, disturbed body image,
and, in most of these disorders, weight loss. Adolescent girls and young women are most commonly affected.

Anorexia nervosa -> Patients with anorexia nervosa are preoccupied with their weight, their body image, and
with being thin.

Etiology:
The etiology of anorexia nervosa is multifactorial and not entirely understood. Several factors are thought to
contribute to the development of the disease:
 Genetic factors: There is a higher concordance of anorexia in identical twins than in fraternal twins.
 Neurobiological factors: a disorder of the endogenous reward system
 Psychiatric factors: associated with OCD, anxiety disorders, and mood disorders
 Psychosocial factors
 Traumatization
 Poor ability to handle/resolve conflicts
 Difficulty establishing autonomy and gaining control (e.g., separation from parents)
 High-pressure careers and sports (e.g., modeling, ballet, gymnastics, wrestling )
 Unrealistic standards of beauty

Features:
 Peak age: 10–25 years of age
 Significant deliberate reduction in body mass (as measured by BMI) using strategies that include restrictive
eating, purging, and excessive exercise.
 Fear of weight gain motivates compensatory behavior that promotes weight loss, even if the patient
already has low body weight.
 Body image disturbance
- Excessive concern about weight and body shape, despite being considerably underweight
- Lack of awareness of the seriousness of low body weight

 Amenorrhea, electrolyte abnormalities (hypochloremic hyperkalemic alkalo-sis), hypercholesterolemia,

arrhythmias, cardiac arrest, lanugo (fine body hair), melanosis coli (darkened area of colon secondary to
laxative abuse), leukopenia, osteoporosis

Subtypes:
Restricting type
 No binge eating or purging over a 3-month period
 Suggests weight loss is achieved by excessive dieting, exercise, or fasting

Binge-eating/purging type
 Presence of binge eating or purging over a 3-month period
 Suggests weight loss is achieved by vomiting, diuretic and laxative abuse, or enemas
 Hannah Friedman

Diagnosis:
History
Physical exam: BMI < 18.5
Laboratory studies
 Electrolyte imbalances: ↓ potassium, ↓
sodium, ↓ chloride, ↓ phosphate, ↓ magnesium, ↑ bicarbonate (metabolic alkalosis)
 ↓ Glucose , pathological tolerance of low glucose levels
 Liver enzymes: ↑ AST/ALT
 ↑ Serum α-amylase
 Renal function parameters: ↓ creatinine
 Lipids: ↑ cholesterol
 Proteins: hypoproteinemia, hypoalbuminemia
 Blood count: pancytopenia

Treatment:
1.Psychotherapy (first-line)
 Cognitive behavioral therapy
 Psychodynamic psychotherapy
2.Nutritional support
 Monitor weight gain and provide nutritional support; usually through oral intake

Bulimia nervosa -> Bulimia nervosa involves binge eating combined with behaviors intended to counteract weight
gain, such as vomiting, use of laxatives or diuretics, or excessive exercise. Patients are embarrassed by their
bingeing and are overly concerned with body weight. However, unlike patients with anorexia, they usually maintain
a normal weight (and may be overweight).

There are two subcategories of bulimia:

Purging type—involves vomiting, laxatives, or diuretics

Nonpurging type—involves excessive exercise or fasting

Etiology:
 The etiology of bulimia nervosa is multifactorial and not entirely understood.
 Obesity during childhood and early puberty

Clinical features:
Peak age: 20–24 years of age
 Recurrent binge eating
 Recurrent compulsive compensatory behavior to counteract weight gain
- Most frequent: self-induced vomiting after binge eating
- Laxative abuse
- Transient starvation periods
- Other weight-loss measures
 Hannah Friedman

 Binge eating and compulsive compensatory behavior both occur at least once a week over a 3-
month period.
 Sense of self-worth pathologically influenced by the perception of physical appearance (body weight and
shape)
 Binging and purging do not occur exclusively during episodes of anorexia nervosa
 By definition, the BMI in individuals with bulimia is normal or elevated (≥ 18.5 kg/m 2 or ≥
10th percentile for pediatric patients)
Dental status: caries and perimolysis due to frequent vomiting
Gastrointestinal tract
 Esophagitis and/or gastritis
 Salivary gland swelling (parotitis)
Metabolic imbalances
 ↓ Potassium, ↓ sodium, ↓ chloride, and ↓ calcium
 ↑ Blood pH (metabolic alkalosis)
Skin
 Calluses on the knuckles (Russell sign)
 Dry skin and brittle nails
Cardiovascular symptoms
 Cardiac arrhythmias
 Hypotension
CNS: seizures

Treatment:
Treatment should be initiated as early as possible to avoid chronification:
1.Psychotherapy (first-line): cognitive behavioral therapy
2.Nutritional rehabilitation
3.Pharmacotherapy: treatment with selective serotonin reuptake inhibitors (e.g., fluoxetine) may help decrease
binging/purging cycles.
 Hannah Friedman

Topic 41: The overview and treatment of psychosomatic diseases

Psychosomatic means mind (psyche) and body (soma). A psychosomatic disorder is a disease which involves both
mind and body.
Some physical diseases are thought to be particularly prone to be made worse by mental factors such as stress
and anxiety (Your current mental state can affect how bad a physical disease is at any given time).

Etiology:
 Stress factors - Prolonged stress + organ that genetically vulnerable to stress
 Neurotransmitter response – Catecolamines, serotonin, dopamine
 Endocrine response – Cortisol
 Immune response - Cytokines , increase glucocorticoids
 Physiological factors – General adaption syndrome; stress affect HPA axis

Clinical presentations of Psychosomatic Disorders:

1. Skin: Neurodermatitis & alopecia areata.
2. Musculoskeletal system: Backache, myalgias and tension headaches.
3. Respiratory system: Bronchial asthma and hiccough.
4.Cardiovascular system: Paroxysmal tachycardia, essential hypertension, migraine, and coronary artery diseases.
5.Gastrointestinal system: Heartburn, peptic ulcer, constipation, ulcerative colitis and spastic colon.
6. Genitourinary system: Disturbances in menstruation and micturition, dyspareunia and impotence.
7. Special senses: Tinnitus or blurring of vision.
8. Immune system: Lupus Erythematosus, Rheumatoid Arthritis.
9. Endocrinal system: Thyrotoxicosis, Diabetes Mellitus.

Treatment:
 Mild cases could be handled by the patient’s own general practitioner, physician or surgeon
 The behavioral approach includes desensitization; biofeedback techniques are also partially included in
cognitive therapy.
 Autonomic blockers (as Beta blockers) are also useful and they could be helpful to cut the vicious circle of
autonomic arousal.
 Underlying psychiatric disorders need to be treated promptly, e.g., giving antidepressants for depression.
 analgesia
 Treat the underlying physical cause.
 Hannah Friedman

Topic 42: Mental retardation

Is a generalized neurodevelopmental disorder characterized by significantly impaired intellectual and adaptive
functioning (Significant impairments in adaptive behaviours and life skills)

Mental retardation is defined by the DSM-IV as:

 Significantly subaverage intellectual functioning with an IQ of 70 or below
 Deficits in adaptive skills appropriate for the age group
 Onset must be before the age of 18.

Mental retardation is defined by the DSM-V as:

Intellectual disability is a disorder with onset during the developmental period that include both intellectual and
adaptive functioning deficits in 3 domains:
 Conceptual domain: language, reading, writing, maths, reasoning, knowledge, memory
 Social domain: empathy, social judgement, interpersonal communication skills, making & retaining
friendships
 Practical domain: personal care, job responsibilities, money, recreation, organising school & work
tasks Diagnosis based on severity of deficits in adaptive functioning.
Etiology:
 Genetic condition
 Down syndrome
 Klinefelter syndrome
 Fragile X syndrome
 Gross disease of brain
 Tuberous scleroses
 Neurofibromatosis
 Epilepsy
 Problems during pregnancy (TORCH, intoxication, DM,placental dysfunction, hypoxia)
 Malnutrition

Clinical features:
 Failure to achievedevelopmentalmilestones
 Deficiency in cognitivefunctioning such asinability to followcommands or directions
 Failure to achieveintellectualdevelopmental markers
 Reduced ability to learnor to meet academicdemands
 Expressive or receptive
 Psychomotor skilldeficit
 Difficulty performingself-esteem
 Irritability whenfrustrated or upset
 Depression or labilemoods
 Acting-out behavior
 Persistence of infantile behavior
 Hannah Friedman

Diagnosis:
 History collection from parents & caretakers
 Physical examination
 Neurological examination
 Assessing milestones development
 EEG, especially if seizure are present
 CT scan or MRI brain, for example, in tuberoussclerosis
 Investigations
– Urine & blood examination for metabolic disorders
– Culture for cytogenic & biochemical studies
– Amniocentesis in infant chromosomal disorders
– chorionic villi sampling
– Hearing & speech evaluation
– Thyroid function tests when cretinism is suspected
 Psychological tests like Stanford Binet IntelligenceScale & Wechsler Intelligence Scale for Children’s(WISC),
for categorizing the child’s level of disability.
 DSM three criteria must be met for a diagnosis of intellectual disability and significant limitations in one or
more areas of adaptive behavior. Adaptive behavior - refers to behavior that
enables a person to get along in his or her
environment with greatest success and least
Treatment:
conflict with others.
 Behavior management
 Environmental supervision
 Monitoring the child’s development needs & problems.
 Programs that maximize speech, language, cognitive, psychomotor, social, self-care, & occupational skills.
 Ongoing evaluation for overlapping psychiatric disorders, such as depression, bipolar disorder, & ADHD.
 Family therapy to help parents develop coping skills & deal with guilt or anger.
 Early intervention programs for children younger than 3 with mental retardation
- Provide day schools to train the child in basic skills, such as bathing & feeding.
- Vocational training
 Hannah Friedman

Topic 43: The most common psychiatric disorders in childhood

Etiology Diagnosis Treatment

ADHA The etiology of ADHD 1) At least six symptoms Pharmacotherapy:

is multifactorial, involving CNS stimulants—
including: inattentiveness, methylphenidate (Ritalin) is
 Genetic factors first-line therapy,
hyperactivity, or both
 trauma/toxin dextroamphetamine
that have persisted for
exposure (Dexedrine), and pemoline
at least 6 months:
(Cylert) SSRIs/tricyclic
 Neurochemical  Inattention—problems antidepressants (TCAs)—
factors
listening, adjunctive therapy
(dysregulation of
concentrating, paying
peripheral and
attention to details, or Individual psychotherapy
central nor-
organizing tasks; easily
adrenergic
distracted, often Parental counseling
systems)
forgetful (education and parenting
 Neurophysiologic
 Hyperactivity– skills training)
al factors.
 Psychosocial impulsivity—blurting
out, interrupting, Group therapy—to help
factors
(emotional fidgeting, leaving seat, patient improve social
deprivation, etc.) talking excessively, and skills, self-esteem, etc.
so on
2) Onset before age 7
3) Behavior inconsistent
with age and
development

Learning types of learning Remedial education

disorders disorders include: tailored to the child’s
- Reading disorder specific needs
- Mathematics
disorder
- Disorder of
written
- Expression

Learning disorders
may be caused by
genetic factors,
abnormal
development,
perinatal injury, and
neurological or
medical conditions
 Hannah Friedman

Disruptive conduct disorder -A multimodal treatment

A pattern of behavior that
behavioral involves violation of the approach is most
disorders include: basic rights of others or of effective. It is important to
social norms and rules, with strucure the child’s
at least three acts within the environment with firm
following categories during rules that are consistently
the past year: enforced.
1. Aggression toward -Individual psychotherapy
people and animals that focuses on behavior
2. Destruction of modification and
property problem-solving skills is
3. Deceitfulness
often useful.
4. Serious violations of
-pharmacotherapy may be
rules
helpful, including
antipsychotics or lithium
for aggression and
selective serotonin re-
uptake inhibitors (SSRIs)
for impulsivity, irritability,
and mood lability.

oppositional defiant Treatment should involve

At least 6 months of
disorder individual psychotherapy
negativistic, hostile, and
defiant behavior during that focuses on behavior
which at least four of the modification and
following have been
problem-solving skills as
present:
well as parenting skills
1. Frequent loss of
training.
temper
2. Arguments with
adults
3. Defying adults’ rules
4. Deliberately
annoying people
5. Easily annoyed
6. Anger and
resentment
7. Spiteful
8. Blaming others for
mistakes or
misbehaviors

Mood disorder
 Hannah Friedman

Eating disorder
Anxiety
abuse

ADHD:
 Hannah Friedman

Topic 44: Geriatric psychiatry

Is a subspecialty of psychiatry dealing with the study, prevention, and treatment of mental
disorders in humans with old age.
The diagnosis, treatment and management of dementia and depression are two areas of this field:

Normal Aging
Factors associated with normal aging include:
Decreased muscle mass/increased fat
Decreased brain weight/enlarged ventricles and sulci
Impaired vision and hearing
Minor forgetfulness (called benign senescent forgetfulness)

- Alzheimer's disease is one of the five leading causes of death in the elderly
- About 25% of the elderly have significant psychiatric problems
- Adults over 75 have one of the highest risks for suicide
- The most common psychiatric disorders of old age are:
 Depressive disorders
 Dementias
 Phobic disorders
 Alcohol use disorders
- Other disorders include:
 Schizophrenia
 Delusional disorder
- Can occur under physical or psychological stress
- Usually seen before age 40
- Most commonly they are persecutory delusions
 Anxiety disorder
- Phobias and obsessions and compulsions are usually less severe than those in younger
patients
 Sleep disorder

Psychiatric History
 Benign senescent forgetfulness- age associated memory impairments of no significance.
 childhood and adolescent history:
– provide information about personality organization
– give important clues about coping strategies and defense mechanisms used under stress
 Hannah Friedman

Topic 45: Depression in old age

Major depression is a common mental disorder in the geriatric population, and the elderly are twice as likely to
commit suicide as the general population. Depressive symptoms are present in 15% of nursing home residents.

Causes of depression in older adults:

 Health problems. Illness and disability, chronic or severe pain, cognitive decline, damage to your body
image due to surgery or sickness can all be contributors to depression.
 Loneliness and isolation. Factors such as living alone, a dwindling social circle due to deaths or relocation,
decreased mobility due to illness or a loss of driving privileges can trigger depression.
 Reduced sense of purpose. Retirement can bring with it a loss of identity, status, self-confidence, and
financial security and increase the risk of depression. Physical limitations on activities you used to enjoy
can also impact your sense of purpose.
 Fears. These include a fear of death or dying as well as anxiety over financial problems or health issues.
 Recent bereavements. The death of friends, family members, and pets, or the loss of a spouse or partner
are common causes of depression in older adults.
 Side effect of medication
 Blood pressure medication (e.g. clonidine)
 Beta-blockers (e.g. Lopressor, Inderal)
 High-cholesterol drugs (e.g. Lipitor, Mevacor, Zocor)
 Tranquilizers (e.g. Valium, Xanax, Halcion)
 Calcium-channel blocker

Symptoms of major depression in the elderly often include problems with memory and cognitive functioning;
because this clinical picture may be mistaken for dementia, it is termed pseudodementia.
Pseudodementia is the presence of apparent cognitive deficits in patients with major depression. Patients may
appear demented; however, their symptoms are only secondary to their underlying depression. It can be difficult to
differ-entiate the two.
 Hannah Friedman

Topic 46: Psychotic disorders in old age

Bereavement
The elderly are more likely to experience losses of loved ones or friends. It is important to be able to distinguish
normal grief reactions from pathological ones (depression).

Normal grief may involve:

Feelings of guilt and sadness
Mild sleep disturbance and weight loss
Illusions (briefly seeing the deceased person or hearing his or her voice—these tend to be culturally related,
i.e., in some cultures this is the norm, not the exception)
Attempts to resume daily activities/work
Symptoms that resolve within 1 year (worst symptoms within 2 months)

Abnormal grief (major depression) may involve:

Feelings of severe guilt and worthlessness
Significant sleep disturbance and weight loss
Hallucinations or delusions
No attempt to resume activities
Suicidal ideation
Symptoms persist more than 1 year (worst symptoms more than 2 months).

Sleep disturbance
The incidence of sleep disorders increases with aging. Elderly people often re-port difficulty sleeping, daytime
drowsiness, and daytime napping. The causes of sleep disturbances may include general medical conditions,
environment, and medications, as well as normal changes associated with aging.

Changes in sleep structure:

The structure of sleep changes normally with aging:

Rapid eye movement (REM) sleep: Increased number of REM episodes throughout the night. These episodes
are redistributed throughout the sleep cycle and are shorter than normal. Total amount of REM sleep re-mains
about the same as with younger adults.
Non-REM sleep: Increased amount of stage 1 and 2 sleep with a de-crease in stage 3 and 4 sleep (deep sleep);
increased awakening after sleep onset

Causes of sleep disorders in the elderly include:

Primary sleep disorder (most common is primary insomnia; others include nocturnal myoclonus, restless leg
syndrome, and sleep apnea)
Other mental disorders
General medical conditions
Social/environmental factors (alcohol consumption, lack of daily structure, etc.)

Treatment:
Sedative-hypnotic drugs are more likely to cause side effects when used by the elderly, including memory
impairment, ataxia, paradoxical excitement, and rebound insomnia. Therefore, other approaches should be tried
first, including alcohol cessation, increased structure of daily routine, elimination of daytime naps, and treatment
of underlying medical conditions that may be exacerbating sleep problems. If sedative-hypnotics must be
 Hannah Friedman

prescribed, medications such as hydroxyzine (Vistaril) or zolpidem (Ambien) are safer than the more sedating
benzodiazepines.

Elder abuse
Incidence:

Ten percent of all people 65 years old; underreported by victims Perpetrator is usually a caregiver who lives
with the victim.

Types:

Physical abuse, sexual abuse, psychological abuse (threats, insults, etc.), ne-glect (withholding of care), and
exploitation (misuse of finances)

Care for the eldery

Restraints

Restraints are often overused in nursing homes and hospitals. Patients who are restrained suffer both physically
and psychologically. Always try alterna-tives such as closer monitoring or tilted chairs.

Medications

Many older people are on multiple medications. They suffer from more side effects because of decreased lean body
mass and impaired liver and kidney function. When confronted with a new symptom in an elderly patient on multiple
medications, always try to remove a medication before adding one.
 Hannah Friedman

Topic 47: Suicide: Alarming signs and Prevention

Warning Signs
The warning signs of suicide are indicators that a person may be in acute danger and may urgently.
 Looking for a way to kill oneself
 Talking about feeling hopeless or having no purpose
 Talking about feeling trapped or being in
unbearable pain
 Talking about being a burden to others
 Increasing the use of alcohol or drugs
 Acting anxious, agitated, or reckless
 Sleeping too little or too much
 Withdrawing or feeling isolated
 Showing rage or talking about seeking revenge
 Displaying extreme mood swings
 Talking about wanting to die or to kill oneself

Suicide prevention is a collection of efforts to reduce

the risk of suicide. These efforts may occur at the individual, relationship, community, and society level. [2] Suicide
is often preventable.
 Hannah Friedman

Topic 48: Suicide, Crisis, “Cry for help”

Suicide
Suicide refers to the act of intentionally killing oneself. If that action fails, it is called a suicide
attempt. Suicide and suicide attempt can be summed up under the term suicidal behavior. Suicidal behavior
requires a mental process that includes both general thoughts about suicide and concrete, deliberate plans to act
upon those ideas (suicidal ideation).

While attempted suicide is more common in women, successful suicide is significantly more common in
men. Suicidal ideation is almost always a symptom of psychiatric illness (e.g., major depressive disorder).

Etiology:
The biggest risk factors for suicidal behavior are:
 Previous suicide attempt(s)
 Other psychiatric disorders (e.g., major depressive disorder, alcohol or substance abuse, psychotic
symptoms, history of aggressive behavior)
 Other chronic and/or serious diseases (e.g., cancer or chronic pain)
 Age > 45 years Peak incidence: 45–64 years
 Male sex
 Possession of firearms
 Social factors: unemployment, no spouse, poor social support/few social contacts, early loss of a parent

Diagnosis:
 General psychiatric evaluation (e.g., mood disorders, substance abuse, recent severe psychic
stress/trauma)
 Ask specifically and directly about suicidal ideation and concrete intent/plans to act on such thoughts
and evaluate whether the patient is in a position to act on them (e.g., whether the patient possesses a
firearm).
 Ask about previous suicide attempts (also within the family), feelings of despair, and ambivalence towards
death.
 If there is any reason to suspect suicidal ideation, ask the patient about it!

Cry for help: An expression of suicidal intent in the hope of receiving help and being rescued.
A cry for help may take many different forms such as a telephone call, a message left on an answering phone, a
note left in a conspicuous place, or an e-mail message. It may also be a symbolic gesture such as a superficial cut
on the wrist.

Suicidal crisis or potential suicide: a situation in which a person is attempting to kill themselves or is seriously
contemplating or planning to do so.
 Hannah Friedman

C Topic 28: The treatment of patients after a suicide attempt.

Acute management
Imminent risk of suicidal behavior (suicidal ideation, intent and concrete plan)
 Immediately reduce the risk, actively prevent the patient from suicidal behavior and assure the patient's
safety.
 Hospitalization (even against the patients will If both clear suicidal ideation and concrete plan/intent
are present) )
 Remove objects from the patient's environment that could be used in a suicide attempt.
 Do not leave the patient alone or even with his family.
 If necessary, involve authorities (e.g., local police).
Elevated risk of suicidal behavior (suicidal ideation and intent but no concrete plan)
 Involve the family of the patient and inquire about the patient's psychological and social situation (e.g.,
history of suicidal ideation, access to firearms, social connections).
 Take measures to increase the patient's social contacts and interaction with medical professionals.

Long term management
 Treat underlying psychiatric disorders.
 Lithium is an especially effective mood stabilizer in suicidal patients with depression.
 If possible, avoid treatment with tricyclic antidepressants, MAO-inhibitors, and venlafaxine since these
medications may easily cause lethal overdoses.
 Improve social circumstances that constitute risk factors for suicidal behavior (e.g., change living
conditions and increase social contacts).

Follow up
 After a suicide attempt, the risk for a new attempt can fluctuate depending on several factors (e.g.,
changing social situation, medications).
 The risk of suicide is increased in the first weeks following discharge from psychiatric care → soon (ideally
within 7 days after discharge) and frequent follow-ups are vital to prevent recurrence of suicidal behavior.
 Hannah Friedman

Topic 49: Psychiatric features of neurological diseases (excluding epilepsy)

Brain Tumors
 Brain tumors can produce pretty much any psychiatric symptom
 For example, suicidal ideation is seen in 10% of patients
 Slow growing tumors create personality changes whereas rapidly growing tumors produce cognitive
changes
Frontal lobe tumors can feature depression, inappropriate affect, disinhibition, dementia impaired coordination
and psychotic symptoms
Temporal lobe tumors can feature anxiety, depression and hallucinations (especially gustatory and
olfactory). Impaired memory or speech may be present
Parietal lobe tumors have fewer psychiatric symptoms and can be mistaken for hysteria

Multiple Sclerosis
 Multiple sclerosis frequently shows psychiatric symptoms
 Depression is seen early on:
-Frontal lobe involvement can feature disinhibition and euphoria
-Memory loss can be mild OR be as severe as dementia
-Can be psychosis
-Hysteria is common, especially later in the disease

CNS Infections
 Rabies encephalitis shows hydrophobia in 50% of patients
 AIDS has a wide variety of psychiatric syndromes that it can cause:
o Delirium
o Anxiety disorders; especially GAD, PTSD and OCD
o Adjustment disorder with anxiety or depressed mood in about 15% of AIDS patients
o Depressive disorders
o Mania
o Psychotic disorder (usually seen as part of late stage HIV infection complications)
o Substance abuse
o Suicide
 Lyme disease of the brain is associated with impaired cognition and mood changes
 Neurosyphilis generally affects the frontal lobes and results in personality changes, poor judgement,
irritability and decreased care for self
 HSV encephalitis usually affects the frontal and temporal lobe
 Symptoms usually include olfactory and gustatory hallucinations and personality changes
 May show bizarre and psychotic behaviours

Creutzfeldt-Jakob disease shows a wide variety of psychiatric symptoms such emotional lability,
anxiety, euphoria, depression, delusions, hallucinations or significant personality changes
Hannah Friedman
 Hannah Friedman

Topic 50: Ictal and Interictal psychiatric symptoms in epilepsy

Epilepsy
 Recurrent unprovoked seizure
 Caused by uncoordinated neuronal discharge
- Epilepsy is the most common chronic neurological disease
- Its not a disease, should be considered as a symptom of brain diseases
- Psychiatric co morbidity is common in epilepsy
- 30 to 50 percent of epileptics have psychiatric difficulties sometime during the course of
their illness
- The most common behavioral symptom of epilepsy is a change in personality
Ictal - during a seizure Interictal - between seizures.
 Brief, disorganized, and 1. Personality Disturbances : patients with epilepsy of
uninhibited behavior characterizes  Religiosity
the ictal event - increased participation in overtly religious
 The cognitive symptoms include activities
amnesia for the time during the - unusual concern for moral and ethical issues
seizure and a period of resolving - preoccupation with right and wrong
delirium after the seizure - heightened interest in global and
 Transient confusional state, philosophical concerns.
affective disturbances, anxiety, - sometimes seem like the prodromal
automatism. symptoms of schizophrenia
 Psychosis-  Viscosity of personality
- Sudden onset & - Slow, serious, ponderous, overly replete with
termination of nonessential details, and often circumstantial
disturbances - The speech tendencies, often mirrored in
- Olfactory & Gustatory the patient's writing, result in a symptom
hallucination known as hypergraphia, which some
- Relative lack of first rank clinicians consider virtually pathognomonic
symptoms for complex partial epilepsy
- Amnesia for the period of  Changes in sexual behavior
disturbances - Hypersexuality: deviations in sexual interest,
transvestism
- Hyposexuality: both by a lack of interest in
sexual matters and by reduced sexual
arousal
2. Psychotic Symptoms
 Interictal psychotic states are more common than
ictal psychoses
 Hannah Friedman

 Schizophrenia-like interictal episodes can occur in

patients with temporal lobe epilepsy
 The most characteristic symptoms of the
psychoses are hallucinations and paranoid
delusions
3. Violence
 especially epilepsy of temporal and frontal lobe
origin.
4. Mood Disorder Symptoms
 such as depression and mania
 The mood disorder symptoms that do occur tend
to be episodic and appear most often when the
epileptic foci affect the temporal lobe of the
nondominant hemisphere
 The importance of mood disorder symptoms may
be attested to by the increased incidence of
attempted suicide in people with epilepsy.
 Hannah Friedman

Topic 51: Psychiatric symptoms in general medical conditions

Endo Hyperthyroidism Anxiety

Over activity
Restlessness
Hypothyroidism Delirium
Depression
Mild memory impairment
Adison disease Apathy
Depression
Delirium
DM Anxiety
Delirium
Depersonalization
Metabolic Electrolyte disturbance Drowsiness
Impaired concentration
Vit b1 deficiency
Infections Delirium
Anxiety
Dementia

CNS See topic 49

 Hannah Friedman

C
Topic 9: The principles of anxiolytic therapy
An anxiolytic (also antipanic or antianxiety agent) is a medication, or other intervention, that inhibits
anxiety.

Anxiolytic medications including benzodiazepines, barbiturates, and buspirone, are the most widely
prescribed psychotropic medications. In general, they all work by diffusely depressing the CNS, causing
a sedative effect. Common indications for anxiolytics/hypnotics include:
Anxiety disorders
Muscle spasm
Seizures
Sleep disorders
Alcohol withdrawal
Anesthesia induction

Benzodiazepines (BDZs)

Benzodiazepines are first-line anxiolytics. Advantages include safety at high doses (as opposed to
barbiturates). A significant limitation is imposed on the duration of BDZ use due to their potential for
tolerance and dependence after prolonged use. Benzodiazepines work by potentiating the effects of
GABA.

EXAMPLES OF BDZS

Long Diazepam (Valium)—rapid onset, used in treatment of anxiety and seizure control
Flurazepam (Dalmane)—rapid onset, treatment of insomnia

Intermediate Acting (10 to 20 Hours) Alprazolam (Xanax)—treatment of panic attacks

Clonazepam (Klonopin)—treatment of panic attacks, anxiety Lorazepam (Ativan)—treatment of
panic attacks, alcohol withdrawal Temazepam (Restoril)—treatment of insomnia

Short Acting (3 to 8 Hours)

Oxazepam (Serax)
Triazolam (Halcion)—rapid onset, treatment of insomnia
Acting (1 to 3 Days)
Chlordiazepoxide (Librium)—used in alcohol detoxification, presurgery anxiety

Side effects:

Drowsiness, impairment of intellectual function, reduced motor coordination.

Toxicity: Respiratory depression in overdose, especially when combined with
alcohol
 Hannah Friedman

Zolpidem (Ambien)/Zaleplon (Sonata)

Used for short-term treatment of insomnia

Selectively bind to benzodiazepine binding site on GABA receptor
No anticonvulsant or muscle relaxant properties
No withdrawal effects
Minimal rebound insomnia
Little or no tolerance/dependence occurs with prolonged use Sonata—newer, has shorter half-life than
Ambien Chemically not a BDZ, although same effect

Buspirone (BuSpar)

Alternative to BDZ or venlafaxine for treating generalized anxiety dis-order

Slower onset of action than benzodiazepines (takes 1 to 2 weeks for ef-fect)
Anxiolytic action is at 5HT-1A receptor (partial agonist)
Does not potentiate the CNS depression of alcohol (useful in alco-holics)
Low potential for abuse/addiction

Propranolol

This beta blocker is particularly useful in treating the autonomic effects of panic attacks or
performance anxiety, such as palpitations, sweating, and tachycardia. It can also be used to treat
akathisia (side effect of typical an-tipsychotics).
 Hannah Friedman

Topic 10: The pharmacotherapy of depression

Topic 11: The side effects of antidepressants
Antidepressants are used primarily to treat major depressive disorder (MDD), although they are also
indicated for the treatment of many other neuropsychiatric conditions.

Classes of antidepressants

Drugs Indication Side effects

SSRIs: selective serotonin Fluoxetine Generalized anxiety disorder (GAD)  Sexual

reuptake inhibitors Paroxetine Obsessive-compulsive dysfunction (e.g.,
Sertraline disorder (OCD) anorgasmia,
Mechanism of Citalopram Post-traumatic stress erectile or
action: inhibition Escitalopram disorder (PTSD) ejaculatory
of serotonin reuptake Fluvoxamine Panic disorder dysfunction, ↓
in synaptic Premature ejaculation libido)
cleft → ↑ serotonin levels Premenstrual dysphoric disorder  Diarrhea, nausea,
Binge-eating disorder vomiting
Bulimia nervosa  Agitation
Gambling disorder  Insomnia
Somatic symptom disorder  Headache
 Serotonin
syndrome

SNRIs: serotonin- Venlafaxine Major depressivedisorder (second-  Similar profile

norepinephrine reuptake Duloxetine line therapy) to SSRIs
inhibitors Desvenlafaxine GAD  Increased blood
Levomilnacipran Neuropathic pain pressure
Mechanism of Milnacipran Fibromyalgia: duloxetine  Sedation
action: inhibition Social anxiety disorder, OCD, panic  Nausea
of serotonin and norepinephri disorder
ne reuptake in synaptic
cleft → ↑ serotonin and
norepinephrine levels
SARIs: serotonin antagonist Trazodone Insomnia  Priapism
and reuptake inhibitors Nefazodone Major depressive disorder  Sedation (due
to H1 antagonism)
 Orthostatic
hypotension
 Hannah Friedman

Mechanism of action  Nausea

 Block postsynaptic type

2 serotonin receptors (5-
HT2)
 Weak inhibition
of serotonin reuptake
→ ↑ serotonin levels
 Antagonist of H1 and α1-
adrenergic receptors

MAOIs: monoamine oxidase Tranylcypromin Major depressive disorder  CNS stimulation

inhibitors Phenelzine Parkinson disease: selegiline  Sexual
Selegiline dysfunction
Mechanism of action: Isocarboxazid  Orthostatic
hypotension
Inhibition of monoamine  Weight gain
oxidase → ↓breakdown of  Hypertensive
epinephrine, norepinephrine, crisis with
and serotonin → ↑levels of epi ingestion of foods
nephrine, norepinephrine, containing
and serotonin. tyramine (e.g.,
aged cheeses,
Selegiline: selective MAO-B smoked/cured
inhibitor → ↑ meats, alcoholic
levels of dopamine beverages).

TCAs: tricyclic 2nd amines MDD  Orthostatic

antidepressants Nortriptyline Neuropathic pain hypotension
Desipramine Chronic pain (including  Cardiotoxicity due
Mechanism of action: Protriptyline fibromyalgia) to Na+ channel
inhibitionof serotonin and Amoxapine Migraine prophylaxis inhibition in
norepinephrine reuptake 3rd amines OCD: clomipramine the myocardium:
in synapticcleft → ↑ serotonin Amitriptyline changes in cardiac
and norepinephrine levels. Clomipramine conductivity
Doxepin velocity,
Imipramine prolonged QT
Trimipramine interval.
 Tremor
 Respiratory
depression
 Hannah Friedman

 Hyperpyrexia

Atypical antidepressants -> Bupropion Smoking cessation  Reduction of

mixed group of agents that Increase Major depressive disorder seizure threshold
have actions at several dopamine and  Tachycardia, palpi
different sites. norepinephrine tations
levels via  Dry mouth
reuptake  Weight loss
inhibition  Neuropsychiatric
symptoms:
insomnia,
agitation, headach

Vilazodone MDD  Headaches

Mechanism of  Nausea, diarrhea
action:  Sleep
Inhibition disturbances
of serotonin  Sexual
reuptake dysfunction
in synaptic  Dry mouth
cleft →
↑ serotonin leve
5HT1A receptor
partial agonist

Varenicline smoking cessation  Mood

Mechanism of disturbances
action:  Sleep
disturbances
Nicotinic ACh  Seizures
receptor partial
agonist.

Stimulates dopa
mine activity →
decreases nicoti
ne cravings and
withdrawal.
 Hannah Friedman

Topic 12: Non-pharmacological therapies of depression

Psychotherapy:
 Cognitive
 Behavioural
 Interpersonal: Emphasis on ongoing current interpersonal issues
 Psychoanalytically oriented: Understanding the patient's unconscious mind and the
conflicts or motivations that lay there that may be fuelling their depression
 Supportive
 Group
 Family
Electroconvulsive therapy
 Hannah Friedman

Topic 14: Mood stabilizers

Mood stabilizers are also known as antimanics and are used to treat acute mania and to help prevent
relapses of manic episodes. Less commonly, they may be used for:
 Potentiation of antidepressants in patients with major depression refractory to
monotherapy
 Potentiation of antipsychotics in patients with schizophrenia
 Enhancement of abstinence in treatment of alcoholism
 Treatment of aggression and impulsivity (dementia, intoxication, mental retardation,
personality disorders, general medical conditions

Drugs that can be used as mood stabilizers are:

DRUG INDICATION SIDE EFFECTS
1.lithium  First-line therapy Side effects occur at therapeutic levels (0.8-1.2 mEq/L)
for bipolar disorder but tend to be more severe at peak serum concentration
 Mood stabilization in of the drug.
patients
with acute mania  Fine tremor
 Maintenance therapy  One of the most common side effects of lithium
 Augmentation in use
treatment-resistant  Symmetric, fine action tremor
depression  Can be treated with beta
blockers (e.g., propranolol) if persistent
 Nausea, diarrhea
Absolute contraindications  Polyuria, polydipsia
 Advanced renal  Weight gain
failure (creatinine  Worsens psoriasis
clearance < 30  Muscle weakness
mL/minute)  Dry oral mucosa
 Severe cardiovascular  Leukocytosis
disease  Hair thinning
Relative contraindications  ECG changes: T-wave depressions (most
 Concurrent diuretic use common), Uwaves, repolarization abnormalities
 Dehydration, sodium  Sinus node dysfunction (bradycardia)
depletion  Hypothyroidism
 First trimester  Goiter
of pregnancy  Hyperparathyroidism causing hypercalcemia
 Nephrogenic diabetes insipidus
 Clinical features: polyuria, nocturia,
and polydipsia → increased risk
of dehydration and subsequent lithium toxicity
 Hannah Friedman

 Chronic interstitial nephritis (lithium-associated

nephropathy)
 Interstitial fibrosis, focal nephron atrophy,
tubular cysts with chronic use
 Can progress to chronic kidney disease
 Teratogenicity: cardiac malformations, in
particular Ebstein anomaly (0.1% risk)

2.Anticonvulsant Carbamazepine  Nausea

drugs:  Skin rash
 Hyponatremia, hyperhydration, and edema
 Blood count abnormalities
(e.g., agranulocytosis, aplastic anemia)
 Teratogenicity during the first
trimester (see pharmacotherapy during pregnancy)
 Diplopia
 Ataxia
 Hepatotoxicity
 Stevens-Johnson syndrome

Valproate  Gastrointestinal upset (e.g., abdominal discomfort)

 Teratogenicity
 Tremor
 Sedation
 Ataxia
 Skin rash
 Agranulocytosis
 Weight gain

Lamotrigine  Exanthema, exfoliative dermatitis, Stevens-

Johnson syndrome
 Blurry vision
 Gastrointestinal symptoms

3.BNZ
4.Antipsychotic Haloperidol
Clozapine
 Hannah Friedman

Topic 15: The classification of antipsychotics

Topic 16: Clinical use of antipsychotics
Antipsychotics are a heterogeneous group of substances used primarily to teat schizophrenia,
psychosis, mania, delusions, and states of agitation.
The term neuroleptics was formerly used interchangeably with antipsychotics because early
antipsychotic drugs induced apathy, quiescence, and reduced psychomotor activity, but newer
antipsychotic drugs no longer have these effects.
The antipsychotic effect of first-generation (typical) antipsychotics (e.g., haloperidol) is based
on D2 antagonism, while second-generation (atypical) antipsychotics interact with several receptors
(e.g., D2, D3, D4, 5-HT).
 Hannah Friedman

Topic 17: The side effects of antipsychotics

 Hannah Friedman

Topic 18: The symptoms and treatment of neuroleptic malignant syndrome

Neuroleptic malignant syndrome (NMS) is life-threatening neurological disorder usually associated

with antipsychotics that is characterized by a tetrad of features: fever, muscle rigidity, autonomic
instability, and mental status changes. As well as rhabdomyolysis and elevated creatine kinase.

Etiology:
 Reaction to antipsychotic drugs (especially high-potency antipsychotics), other agents that affect
the CNS (e.g., carbamazepine, lithium).
 Genetic predisposition.
 A connection between NMS and the duration of therapy or therapeutic dose has not been
established.

Pathophysiology: The underlying mechanism is not well understood; disruption of

numerous neurotransmitter pathways is suspected.
 Central D2 receptor blockade in the nigrostriatal pathway and hypothalamus, resulting in
movement disorders and impaired thermoregulation.
 Increased sympathetic tone disrupts autonomic regulation and increases muscle tone and
metabolism.
 Increased release of calcium from the SR of striated muscle cells, resulting in increased
contractility and muscle breakdown.

Clinical features: Onset usually occurs within 2 weeks of the first dose.
 Muscle rigidity, akinesia, tremor
 Hyperthermia
 Autonomic instability (tachycardia, labile blood pressure, tachypnea, diaphoresis, dysrhythmias)
 Mental status change: confusion, delirium, reduced vigilance, stupor
 Diagnostics
 ↑↑ Creatine kinase
 Leukocytosis
 Metabolic acidosis
 Myoglobinuria
 Electrolyte abnormalities (hypocalcemia, hyperkalemia, hyponatremia or hypernatremia)
 Hannah Friedman

Treatment:
 Discontinuation of the antipsychotic drug!
 Supportive measures (e.g., ICU care)
 Pharmacotherapy
 Dantrolene (ryanodine receptor antagonist): prevents the release of calcium from
the sarcoplasmic reticulum of striated muscle → reduced muscle rigidity and hyperthermia
 Benzodiazepines can be administered to treat psychomotor agitation.
 Hannah Friedman

Topic 19: Electroconvulsive therapy

Electroconvulsive therapy (ECT) involves unilateral (sometimes bilateral) electrode placement over the
nondominant hemisphere to induce tonic-clonic seizures under sedation. Although not fully
understood, ECT likely causes anticonvulsant effects, brain remodeling, and improves brain perfusion.
ECT is indicated for refractory cases, life-threatening symptoms (e.g., suicide risk), or special patient
groups (e.g., pregnant patients) with certain mental disorders; including depression, schizoaffective
disorder, and bipolar mood disorder.

Procedure:
1. General preparation and procedure
 Unilateral electrode placement over the nondominant hemisphere
 EEG as well as constriction of the contralateral arm via blood pressure cuff for monitoring
the seizure
 Administration of oxygen via face mask + preparation for emergency intubation if necessary
 ECG and pulse oximetry allow for monitoring further vital signs.
2. Administration of premedications:
 Anticholinergic (e.g., atropine) to reduce dysrhythmias and oral/respiratory secretions
 A mild sedative and hypnotic (e.g., methohexital) to relieve anticipatory anxiety
3. Short-term general anesthesia, including a muscle relaxant (e.g., succinylcholine) to avoid risk
of fractures
4. An electric current is passed from one side of the cerebral cortex to the other.
5. 6–12 sessions in total consisting of generalized tonic-clonic convulsions lasting 25–30
seconds, usually 2–3 times per week
6. Treatment sessions can be discontinued once symptoms improve.
7. Maintenance may be implemented once every 1–8 weeks.

Indications contraindications
 Depression (most common) No absolute contraindications. [4] Relative contraindications
 Schizoaffective disorder include:
 Schizophrenia with catatonia
 Bipolar mood disorder (e.g., manic  Elevated intracranial pressure and space-
episodes) occupying lesions in the brain
 Highly suicidal or pregnant  Recent myocardial infarction (within the last 3 months)
depressed patients (not usually first-  Severe arterial hypertension
line)  Narcotic intolerance
 Neuroleptic malignant syndrome  Acute glaucoma
 Changes in the cerebral arteries, e.g., aneurysm, angioma
 Hannah Friedman

Side effects:
More common
 Reversible memory loss: retrograde more often than anterograde amnesia
 Tension headache
 Nausea
 Transient muscle pain
Less common
 Skin burns
 Temporary, short-term functional disorders (such as amnesic aphasia)
 Prolonged seizure
 Hannah Friedman

20. The idea and principles of psychotherapy

Psychotherapy -> A process which attempts to help the patient relieve symptoms, resolve
problems or seek personal growth through a structured relation (i.e. specified goals and methods) with
a trained professional therapist.
The therapist may be a psychiatrist, a psychologist, a nurse, etc... Psychotherapy
 Hannah Friedman

21. Major psychotherapy schools

Psychotherapy is the use of psychological methods to assist people to modify undesirable emotions,
attitudes, and behaviors. Types of psychotherapy include:

Technique School
Psychoanalysis Sigmund Freud

Goal of Psychoanalysis: to release the tension of repression and resolving

unconscious inner conflicts.

Typical duration: Weekly sessions for 6 months to years

Free association: the patient speaks freely about memories, dreams,

feelings.

Interpretation: the therapist suggests unconscious meanings and underlying

wishes, to help the client gain insight and release tension.

Psychodynamic
Derived from Psychoanalytic Tradition, but compared Psychoanalysis:
 Fewer sessions per week rooted in past and fewer years relationships.
 Less theory about sex
 Client now faces therapist
 Focus is on the present,not just the past

 The focus is on improved but self-awareness and insight into

unconscious thoughts and feelings which may be rooted in past.
 In addition to insight, therapists suggest changes in patterns of thinking
relating to others
 Hannah Friedman

 Therapists help reveal resolve the dynamics, the forces and changes, in
the individual
Humanistic therapy Abraham Maslow and
Emphasizes the human potential for growth, self-actualization, and personal Carl Rogers (“Client-
fulfillment. centered therapy”)
Humanistic therapy attempts to support personal growth by helping people
gain self-awareness and self-acceptance.
Behavioral therapy B.F. Skinner and Ivan
Behavioral therapy seeks to treat psychiatric disorders by helping patients Pavlov
change behaviors that contribute to their symptoms. It can be used to
extinguish maladaptive behaviors (such as phobias, sexual dysfunction,
compulsions, etc.) by replacing them with healthy alternatives.

2 types:

1. Conditioning
Classical conditioning: A stimulus can eventually evoke a conditioned re-
sponse. (Example: Pavlov’s dog would salivate when hearing a bell because
the dog had learned that bells were always followed by food.)
Operant conditioning: Behaviors can be learned when followed by positive or
negative reinforcement. (Example: Skinner’s box—a rat happened upon a
lever and received food; eventually it learned to press the lever for food)
2. Deconditioning
Systemic desensitization: The patient performs relaxation techniques while
being exposed to increasing doses of an anxiety-provoking stimulus.
Gradually, he or she learns to associate the stimulus with a state of
relaxation. Commonly used to treat phobic disorders. (Example: A patient
who has a fear of spiders is first shown a photograph of a spider, followed
by a stuffed animal, a videotape, and finally a live spider.)
Flooding and implosion: Through habituation, the patient is confronted with
a real (flooding) or imagined (implosion) anxiety-provoking stimulus and not
allowed to withdraw from it until he or she feels calm and in control.
Relaxation exercises are used to help the patient tolerate the stimulus.
Commonly used to treat phobic disorders. (Example: A patient who has a
fear of flying is made to fly in an airplane [flooding] or imagine flying
[implosion].) Aversion therapy: A negative stimulus (such as an electric
shock) is repeatedly paired with a specific behavior to create an unpleasant
response. Commonly used to treat addictions or paraphilias. (Example: An
alcoholic patient is prescribed Antabuse, which makes him ill every time he
drinks alcohol.)
 Hannah Friedman

 Token economy: Rewards are given after specific behaviors to

positively reinforce them. Commonly used to encourage showering,
shaving, and other positive behaviors in disorganized or mentally
retarded individuals.
 Biofeedback: Physiological data (such as heart rate or blood pressure
measurements) are given to patients as they try to mentally control
physiological states. Commonly used to treat migraines,
hypertension, chronic pain, asthma, and incontinence. (Example: A
patient is given her heart rate and blood pressure measurements
during a migraine while being instructed to mentally control visceral
changes that affect her pain.)

Cognitive therapy Albert Ellis’s rational-

Practice Cognitive therapy helps people alter the negative thinking that emotive behavior therapy
worsens depression and anxiety. – challenging irrational
Therapists might suggest other thoughts that the clients could have about beliefs and assumptions.
their lives, or at least point out when clients jump to conclusions that make
them feel worse. Aaron Beck’s cognitive
therapy for depression
correcting cognitive
distortions.

Donald Meichenbaum’s
stress inoculation
training practicing
healthier thinking before
facing a stressor,
disappointment, or
frustration
Cognitive Behavioral therapy
Typical duration: 6 weeks to 6 months

Cognitive behavioral therapy [CBT] works to change both cognitions and

behaviors that are part of a mental health disorder. Using cognitive
behavioral therapy, people with OCD are led to resist the urge to act on their
compulsions, as well as to learn to manage obsessional thinking.
 Hannah Friedman

22. Group psychotherapy, family therapy.

Group therapy
Three or more patients with a similar problem or pathology meet together with a therapist for group
sessions. Any of the psychotherapeutic techniques may be employed, including psychoanalytical,
behavioral, cognitive, educational, and so on.

Certain groups are leaderless (self-Help group = including 12-step groups like Alcoholics Anonymous)
and do not have a therapist present to facilitate the group. These groups meet to discuss problems,
share feelings, and provide support to each other.

Group therapy is especially useful in the treatment of substance abuse, adjustment disorders, and
personality disorders. Advantages of group therapy over individual therapy include:
-Patients get immediate feedback from their peers.
-Patients may gain insight into their own condition by listening to others with similar problems.
-If a therapist is present, there is an opportunity to observe interactions between others who may
be eliciting a variety of transferences.

The benefits include:

 Less cost per person.
 More interaction, feedback, and support.
 Clients realize others share their problems and they are not alone.

Family therapy
Family therapy is useful as an adjunctive treatment in many psychiatric conditions because:
1. A person’s problems usually affect the entire family. He or she may be viewed differently and
treated differently after the development of psychopathology, and new tensions and conflicts
within the family may arise.
2. Psychopathology may arise partly or entirely from dysfunction within the family unit. These
conditions are most effectively treated with the entire family present.

The goals of family therapy are to:

 Reduce conflict
 Help members understand each other’s needs (mutual accommodation)
 Help the unit cope with internally destructive forces.

Boundaries between family members may be too rigid or too permeable, and “triangles” may result when
two family members form an alliance against a third member. The therapist may assist in correcting
these problems as well.
Example of boundaries that may be too permeable: Mother and daughter smoke marijuana together and
share intimate details about their sexual activities.
 Hannah Friedman

27. Psychiatric emergencies. The treatment of violence (LECTURE)

Psychiatric emergencies are acute changes in behavior that negatively impact a patient's ability to
function in his or her environment. Often such patients are in a state of crisis.

Psychiatric Emergencies -> any disturbances in thoughts, feelings, or actions, which if not rapidly
attended to may result in harm to a patient or others. Arise in context of:
 Acute psychiatric illness (e.g. psychosis, mania)
 Consequence of medical illness that presents with psychiatric symptoms
 Intoxication
 Adverse drug reaction
 Drug interaction
 Crisis, most commonly with suicide and violent behavior

Common medical conditions that often present as psychiatric emergencies:

 Hypothyroidism
 Hyperthyroidism
 Diabetic ketoacidosis
 Hypoglycemia
 Urinary tract infection
 Pneumonia
 AIDS
 Heart failure (chronic or acute as MI)
 Chronic obstructive pulmonary disease
 Acute liver disease (or decompensated LC)
 Alcohol intoxication

Violence -> is the use of physical force so as to injure, abuse, damage, or destroy .

Actively violent patients must first be restrained by:

 Physical means
 Drugs (chemical restraint)
 Both
Such interventions are done to prevent harm to patients and others and to allow evaluation of the
cause of the behavior (eg, by taking vital signs and doing blood tests).
 Hannah Friedman

Close monitoring, sometimes involving constant observation by a trained sitter, is required. Although
clinicians must be aware of legal issues regarding involuntary treatment, such issues must not delay
potentially lifesaving interventions.

Potentially violent patients require measures to defuse the situation. Measures that may help reduce
agitation and aggressiveness include:
 Moving patients to a calm, quiet environment (e.g. a seclusion room, when available)
 Removing objects that could be used to inflict harm to self or others from patients
 Expressing sympathetic concern for them and their complaints
 Responding in a confident yet supportive manner
 Speaking directly mentioning that patients seem angry or upset, asking them if they intend to
huff someone acknowledges their feelings and may elicit information; it does not make them
more likely to act out.