PSYCHIATRY
OME + UWORLD
SchizoCat
Table of Contents
ANXIETY DISORDERS
2
IMPULSE CONTROL DISORDERS
7
OCD AND RELATED DISORDERS
9
POST-TRAUMATIC STRESS DISORDER
12
MOOD DISORDERS
15
PSYCHOTIC DISORDERS
27
EATING DISORDERS
34
PERSONALITY DISORDERS
38
DEFENSE MECHANISMS
42
DISSOCIATIVE DISORDERS
45
CATATONIA
47
PSYCH PHARM
51
ADDICTION
62
SLEEP PHYSIOLOGY & DISORDERS
77
GENDER DYSPHORIA
82
ABUSE
83
SOMATIC SYMPTOM DISORDERS
85
PSYCHOTHERAPY
89
1
Anxiety disorders
Expression of anxiety is different from one person to the other. However, it is congruent in that
person.
C/P:
•
•
•
•
•
•
•
•
Worry.
Fear.
Hypervigilance.
Palpitations.
Perspirations.
Dyspnea.
Chest pain.
Women>men.
Can be associated with mood disorders.
Some people self-medicate with alcohol.
Generalized anxiety disorder:
•
•
Chronic and insidious amount of anxiety.
Criteria:
o Constant state of worry.
o About most things.
o On most days.
o At least 6 months in duration.
2
3 or more somatic complaints.
 Change in sleep.
 Change in weight.
 Irritability.
 Concentration.
Clinical diagnosis.
Treatment:
o Psychotherapy>pharmacotherapy.
o Pharmacotherapy:
 Chronic: SSRI.
 Acute anxiety: benzodiazepines.
o Avoid benzodiazepines in patients with a history of substance abuse or
significant comorbid depression.
o Buspirone (non-benzodiazepine anxiolytic-5HT1a receptor partial agonist) can be
used in patients with a high risk of benzodiazepine abuse.
o
•
•
Panic disorder:
•
•
•
•
•
Acute, overt, and catastrophic.
20s, women.
Lasts for 20-30 minutes.
Used to be called: dacosta’s syndrome, cardiac neurosis, and CVS asthenia.
Most common presentation: palpitations and sense of impending doom.
o Hyperventilation  dizziness  tremors  tetany  fainting.
3
•
•
•
•
•
•
•
•
Characteristics:
o Recurrent and unpredictable.
o Not restricted to any situation/circumstances.
o Attacks last for a few minutes (sometimes longer).
o Often accompanied by agoraphobia.
o Presence of 1 or more months of worry about future attacks or change in
behavior.
o Another criterion: 4 attacks per month.
o If they don’t meet criteria  recurrent panic attacks.
C/P: STUDENTS PANIC: 4 or more of the following.
o Shortness of breath.
o Trembling.
o Unsteady.
o Dissociative symptoms: depersonalization or derealization.
o Excessive heart rate (tachycardia).
o Numbness.
o Tingling.
o Sweating.
o Palpitation.
o Abdominal pain.
o Nausea.
o Intense fear.
o Chest pain.
Diagnosis:
o Rule out acute coronary syndrome: ECG.
o Rule out thyroid: TSH.
o Rule out asthma: wheezing.
To assess the biopsychosocial effect: ask if his life has been affected or his job.
Treatment:
o Pharmacotherapy>> psychotherapy.
 Cognitive behavioral therapy; repeated graded exposure, cognitive
restructuring, breathing training, and muscle relaxation.
 Acute: reassurance, distraction, deep breaths or breathing into a bag, and
benzodiazepines.
• Benzodiazepines avoided for long term use due to risk of
dependence, cognitive impairment, depression, and respiratory
depression.
• Avoid benzodiazepines in those who smoke marijuana daily and
exceeds the recommended limit of 14 alcoholic drinks per week.
 Chronic: SSRI.
 First line treatment: CBT + SSRI.
 Beta blockers should be avoided.
Prophylaxis:
o Biopsychosocial.
Can be associated with agoraphobia; anxiety and avoidance of 2 or more situations in
which it may be difficult to escape or get help in the event of a panic attack for 6 or more
months.
Side note: 10% of healthy people have a panic attack per year.
4
Phobia:
•
•
•
•
Exaggerated or irrational or both.
Against an object or situation.
Specific phobia:
o Examples:
 Heights.
 Flying.
 Spiders.
 Animals.
 Driving.
 Blood.
 Injections.
 Clowns.
 Snakes.
o Treatment:
 CBT: flooding (overload them with the fear) and systemic desensitization
(slowly add the fear).
• Control the anxiety during flooding using benzodiazepines.
Social phobia:
o Public speaking or public peeing.
o Treatment:
 Nonselective beta blockers to control the tremors and the cracked voice.
• Avoid in asthmatics.
5
6
Impulse control disorders
Stressor that is anxiety inducing that causes an impulse and patient commit an action. The
action decreases the anxiety, gives relief, and causes sexual arousal.
Intermittent explosive disorder:
•
•
•
•
Stressor is anything.
Action is violence.
o Degree of violence is disproportionate to the stressor.
C/P:
o Men>women.
o Decreases with age.
o Outbursts last less than 30 seconds.
o Mild: no harm to a person.
 2 outbursts per week for 3 months.
o Severe: harm to person.
 3 outbursts in 12 months.
o Episodes followed by remorse, dysphoria, and embarrassment.
o Functional impairment.
Treatment:
o CBT and SSRI.
Kleptomania:
•
•
•
•
•
Stressor: sight of an object.
Action: steal.
o Little or no value.
o Can afford.
Reaction is guilt. But it reduced her anxiety.
o Gifting.
o Hoarding.
o Returning.
Diagnosis:
o Rule out theft.
Treatment:
o Psychotherapy: CBT.
o Medications: SSRI, opioid antagonists, lithium, and anticonvulsants.
7
Pyromania:
•
•
•
•
•
No stressor.
Lighting fires to increase sexual arousal.
C/P:
o Men>women.
o 2 or more occasions.
o Motivation: decreased anxiety and increased arousal.
Diagnosis:
o Rule out arson.
Treatment:
o Medications and psychotherapy are useless.
o No need to incarcerate, but they usually get incarcerated.
8
OCD and related disorders
Obsessive compulsive disorder:
•
•
•
•
•
•
Obsessions: anxiety provoking.
o Internal, intrusive. No trigger.
o Unwanted.
o Thoughts or preoccupations.
Compulsions: anxiety relieving.
o Behavior or ritual.
Ego-dystonic.
Examples:
o Safety  checking locks.
o Contamination  washing and cleaning.
o Symmetry  order and counting.
o Aggressive and sexual impulses.
Clinical diagnosis.
o It has to impair functionality.
Treatment:
o Psychotherapy> medications.
 Cognitive behavioral therapy.
• ERP: the therapist would guide the patient to practice checking
the obsession once and then prevent her from checking repeatedly.
Initially, anxiety increases.
 SSRIs.
 Don’t use benzodiazepines unless patient also has panic attacks.
Disorder
Preoccupation
(obsession)
Compulsion
Effect
Hoarding disorder
Throwing away
anything
Keep the items
(trash)
Unsafe
Body dysmorphic
disorder (female)
Some part of the
body; skin, hair, nose,
breast
Check appearance,
unnecessary
surgeries
-
9
Muscle dysphoria
(male)
Increasing muscle
size
Excessive exercise
and use anabolic
steroids
Rhabdomyolysis,
road rage, acute
renal failure
“copper” “testicular
atrophy”
Trichotillomania
Anything
Pull out hair
Alopecia (varying
length)
Rule out fungus
Bezoars (pulls out
hair and eats it)
Hoarding disorder:
•
•
•
•
•
Accumulation of a large number of possessions that may clutter living areas to the point
that they are unusable.
Patients experience distress when attempting to discard possessions regardless of their
actual value.
Social isolation due to embarrassment may also occur.
Extreme cases may be associated with unsanitary conditions and fire risk due to blocked
exits.
Treatment:
o CBT; education, motivational interviewing, skills training in organization and
decision making, cognitive restructuring of dysfunctional thoughts, and gradual
exposure to discarding possessions.
o SSRI effect is limited.
Body dysmorphic disorder:
10
Trichotillomania:
11
Post-traumatic stress disorder
Stressor  disorder:
•
•
•
Life-threatening severe event  PTSD.
Non-life-threatening severe event  adjustment disorder.
Neglect and abuse  reactive attachment disorder, disinhibited social engagement
disorder.
Post-traumatic stress disorder:
•
•
•
•
•
•
•
Can occur immediately after trauma, however, there is often a delay of months or years.
Stressors:
o Actual death.
o Threatened death.
o Combat.
o Survivors of assault/raped; highest risk of developing MDD and contemplating
suicide.
o Abused/neglect.
Exposure:
o Experienced (self).
o Witnessed (others).
o Learned (loved one).
o Repeated exposure of the aftermath (responders).
C/P:
o Intrusion.
o Mood change.
o Dissociation.
o Avoidance.
o Arousal.
Clinical diagnosis.
o Duration:
 Acute stress disorder if 3 days to 1 month.
 PTSD if more than 1 month.
Treatment:
o Psychotherapy: group therapy. Educate about physical & emotional response to
trauma.
o SSRI/SNRI.
o Panic attacks: benzodiazepines.
o Nightmares: prazosin.
Can be associated with mood disorders or substance abuse.
12
Reactive attachment disorder/ disinhibited social engagement disorder:
•
•
•
•
•
•
•
Abuse or neglect in infancy.
RAD: pairs too little.
DSED: pair too much.
Diagnosis must be made in those less than 5 years old.
o Rule out autism.
o RAD: seldom seek comfort, lack of social responsiveness and positive emotions,
and episodes of unexpected irritability or sadness.
Treatment:
o Caregiver  parent better.
o Or foster care.
Associated with mood disorders, anxiety, and substance abuse.
Associated with learning disabilities.
13
Adjustment disorder:
•
•
•
•
•
Non-life-threatening event  mood disorder.
Onset must be within 3 months of the event.
Duration cannot be longer than 6 months.
No suicidal/homicidal ideation.
Treatment of choice: psychotherapy.
14
Mood disorders
At one end of the spectrum there is mania, on the other end there is depression.
Check if they are presenting with catatonia (mostly with depression) and (mood-congruent)
psychotic features.
Major depressive disorder:
•
•
Depressed mood or loss of interest (anhedonia) and duration for at least 2 weeks.
Five of the SIGECAPS:
o Sleep.
 Usually less.
o Interest.
o Guilt.
o Energy.
o Concentration.
o Appetite.
 Usually less.
o Psychomotor retardation.
o Suicide.
•
•
Hyperactivity of the HPA axis  increased cortisol.
Decreased hippocampal and frontal lobe volumes and changes in sleep architecture.
REM sleep latency and slow-wave sleep (stage 3 and 4) are decreased.
Older patients and children present with somatic complaints such as insomnia.
Atypical depression: increased sleep, increased appetite, and leaden paralysis.
•
•
15
•
•
•
•
After diagnosis of depression  assess for suicidal ideation.
o What to do depends on how close to suicide are they.
 Has a plan and the means to carry out the plan  hospitalize.
 No plan and no means to carry out the plan  contract safety.
Assess for psychotic features such as delusions and hallucinations with depressive
themes.
o Treatment: antidepressants + antipsychotics or ECT.
Rule out mania prior to initiating antidepressants.
Treatment:
o SSRI/SNRI.
 Titrate the dose until you reach the maximum tolerable dose and
continue for 2 months.
 Adequate trial: adequate dose and duration for 6 or more weeks.
 Patients with minimal to no improvement with initial antidepressant
treatment can be switched to another antidepressants.
• Options:
o SSRI to SNRI.
o Or bupropion, mirtazapine, or serotonin modulators
(vitazodone).
• Washout period of 2 weeks.
 Failed several trials  TCA or MAO inhibitors (after washout of 5
weeks).
o Psychotherapy.
o Best treatment: electroconvulsive therapy.
 Used for refractory cases, catatonia, or psychosis.
 Premedicate with atropine, methohexital, and succinylcholine.
 ADRS: amnesia.
16
Differential diagnosis of depressed mood:
Dysthymia:
•
•
•
•
•
Depressed mood within a 2-year period or longer.
Never without symptoms for 2+ months.
Get TSH to rule out hypothyroid.
Treatment: SSRI, psychotherapy, or combination.
Note: if mania or hypomania occurred then it is bipolar or cyclothymia respectively.
17
Bipolar 1:
•
•
•
•
Manic predominant.
Elevated/irritable mood and increased energy plus 3 of the following (4 if the mood is
irritable) for 7 or more days with functional impairment:
o Distractibility.
o Insomnia.
o Grandiosity.
o Flight of ideas/racing thoughts.
o Activities/agitation.
o Sexual exploit/sleep (decreased need).
o Talkative/pressured speed.
Diagnosis:
o Rule out stimulus.
o Rule out bipolar 2 and cyclothymia.
Treatment:
o Lifelong illness that requires maintenance pharmacotherapy to reduce the risk of
recurrent mood episodes.
 Lifelong maintenance indicated for those with severe course (suicide
attempt, frequent episodes, severe symptoms, hospitalization).
o First line for acute mania: antipsychotics, lithium, and anticonvulsant mood
stabilizers (valproate).
o Agitated (emergency department): antipsychotics or benzodiazepines (can be
given IM).
o Mood stabilizers: lithium (mania > depression).
 Second choice: valproic acid (mixed affective).
 Third choice: carbamazepine (rapid cyclers) or lamotrigine (depression >
mania).
o First line medications for treatment of acute bipolar depression  second
generation antipsychotics such as quetiapine and lurasidone.
o Monotherapy for all patients.
o Inadequate response to monotherapy, severe episodes  lithium or valproate and
second-generation antipsychotic.
18
Bipolar 2:
•
•
•
Hypomania+ major depressive disorder.
Hypomania criteria:
o 4 or more days of elevated/irritable mood, increased energy and 3 or more of the
following:
 Grandiosity.
 Decreased need for sleep.
 Talkativeness.
 Racing thoughts.
 Distractibility.
 Hyperactivity.
 Risky behavior.
o If there were psychotic features  mania.
Rule out catatonia and rule out psychosis.
19
•
•
No functional impairment.
Usually seen after MDD takes SSRI  you reveal hypomania.
Cyclothymia:
•
Hypomania and MDD without meeting criteria of either.
Rapid cycling:
•
•
4 or more switches in mood in 1 year.
2 months in between attacks if they are the same (mania to mania or depression to
depression) or 1 month when the attacks are different.
Mixed affective:
•
Depression and mania develop at the same time (few hours in between).
Grief:
•
Stages:
20
•
•
o Denial.
o Depression.
o Bargaining.
o Anger.
o Acceptance.
PTSD/ASD: unexpected and violent stimulus.
o Fear and anxiety.
Adjustment disorder: non-life-threatening disorder  adjustment.
o Not death or dying.
o Can’t be defined as bereavement.
Grief
Persistent
Complex
Bereavement
Disorder (PCBD)
MDD
<12 months (since
the loss of the
person)
Symptoms last for 12
months or more.
Grief for more than
12 months 
consider MDD
Focus of
dysphoria, guilt,
anhedonia
Focus on the
deceased
Same as grief
Pervasive and global
Depressed mood
when?
Waxes and wanes
Same as MDD
Persistent
Behaviors
Talking to the
deceased
Onset and
duration
Started 6 months
after
Can imagine a time
in the future where
they can be happy
Cannot imagine a
time in the future
where they can be
happy
Same as MDD
Praying at them
Psychotic features
Visiting the grave
No insight
There is insight.
Suicide
To go to deceased 
normal, don’t treat
In relation to
hallucinations
(auditory, visual)
Same as grief
Hopeless
Negative reflection of
self
Despondent
21
Treatment
-
Psychotherapy
SSRI/SNRI
SSRI/SNRI
Postpartum:
•
•
•
Postpartum blues:
o First baby.
o Mum cares.
o Onset and duration: within 2 weeks.
Postpartum depression:
o After the first.
o Doesn’t care about the baby.
o Neglect.
o Onset within one month.
o Duration is ongoing.
o Treatment: SSRI.
Postpartum psychosis:
o Not in the first baby.
o History of bipolar disorder or who are later diagnosed with bipolar.
o Fears baby.
o Kills baby.
o Within first month.
o Ongoing.
o Psychosis predominates.
o Treatment: antipsychotics.
22
•
Screening for PPD with edinburg postnatal depression scale (EPDS).
Premenstrual syndrome:




A symptom diary over 2 menstrual cycles should demonstrate recurrence of symptoms
during the luteal phase (1-2 weeks prior to menses) and resolution during the follicular
phase (onset of menses or a few days after).
Symptom severity must reach a point of socioeconomic impact to qualify as PMS or the
more severe variant, premenstrual dysmorphic disorder.
Eliminate other mood disorders and hypothyroidism.
Treatment: SSRIs. Another treatment would be OCPs.
o Keep a menstrual diary.
Poststroke depression:
23
•
•
•
Associated with a reduced quality of life, decreased adherence to treatment, poor
functional outcomes, and increased mortality.
Etiology:
o Inflammation.
o Cerebrovascular dysregulation.
o Altered neuroplasticity.
o Altered glutamate neurotransmission.
Treatment:
o Antidepressants and psychotherapy improves outcomes.
o SSRIs are the pharmacotherapy of choice.
Seasonal affective disorder:
•
•
•
MDD with seasonal patten.
o Fall-winter onset and spring-summer remission.
C/P: atypical features
o Increased sleep.
o Increased appetite.
o Carbohydrate craving,
o Weight gain.
Treatment:
o Antidepressants and bright light therapy (10,000 lux light box shortly after
awakening).
 Improvement in 1-4 weeks and continue treatment throughout the fall or
winter until spontaneous remission in the spring or summer.
Suicidality:
•
•
Low levels of 5-HIAA in the CSF are associated with suicidal behavior.
Elderly white men are at a high risk of suicide.
24
25
Homicide:
26
Psychotic disorders
Agitation:
•
•
Management:
1. Prioritize their evaluation.
2. Verbal de-escalation.
3. Benzodiazepine IM.
4. First or second generation antipsychotic.
5. Coadministration of benzodiazepine and antipsychotic for severely agitated,
combative patients.
Basic medical workup:
o Physical examination.
o Mental status examination.
o CBC.
o Urine toxicology screen.
o Syphilis.
o HIV,
o Vitamin b12 level.
o Thyroid function.
o ANA.
o Neuroimaging.
27
Schizophrenia:
•
•
•
•
•
•
Thought disorder.
Genetic component.
o One parent with schizo: 12% risk.
o Two parents with schizo: 25% risk.
o Sibling with schizo: 8% risk.
Epilepsy is associated with schizophrenia: 2.5% risk (80% of the 2.5% have temporal lobe
epilepsy).
Neuroimaging: loss of cortical tissue volume with ventricular enlargement (lateral
ventricles especially).
Stages of schizophrenia:
o Prodromal: decline in function.
o Psychotic: positive symptoms.
o Residual: negative symptoms.
C/P:
28
Positive symptoms: excess dopamine in mesolimbic pathway.
Negative symptoms: excess dopamine in prefrontal cortex.
Two or more symptoms, and one of them must be from 1-3 for at least 6 months.
 Positive symptoms:
1. Delusions; persecution or grandiosity.
2. Hallucinations; auditory.
o Other types: visual (organic), tactile (substance), or
olfactory (epilepsy).
o Command hallucinations: tells the patient what to do.
3. Disorganization; speech or behavior.
 Negative symptoms:
1. Flat affect.
2. Alogia.
3. Avolition (apathy).
4. Anhedonia.
5. Asociality.
 Cognitive impairment/delay.
o Usual presentation: psychotic break.
 Every time they have a break  they get more cognitively impaired.
 Change of behavior and thought.
Diagnosis:
o Rule out drugs.
o Duration and presence of mood disorders.
Treatment:
o Risk assessment,
o Assess the need of admission depending on risk.
o Antipsychotics for life.
o Cognitive behavioral therapy.
o Family therapy (reduces risk of relapse) and psychoeducation.
 Reduce the risk of rehospitalization.
 Critical, hostile, or overinvolved family members have a higher
risk of relapse.
o Vocational rehabilitation.
o Social skills training.
o
o
o
•
•
29
Brief psychotic disorder:
•
•
•
Duration of more than 1 day to less than 1 month.
Includes postpartum psychosis.
Treatment for only a month.
Schizophreniform:
•
•
Duration is for more than 1 month to less than 6 months.
Treatment: 3 to 6 months of treatment.
Schizoaffective disorder:
•
•
Psychosis predominates plus mood features.
Treatment:
o Treat the mood first.
30
Delusional disorder:
•
•
•
•
•
Delusions: fixed, false belief not compatible with cultural ideas.
o Categorized as bizarre or nonbizarre.
 Usually nonbizarre in this disorder and bizarre in schizophrenia.
o Types of delusions:
 Erotomaniac: another person is in love with them.
 Grandiose: having great talent.
 Somatic: physical.
 Persecutory.
 Jealous.
 Mixed: more than one of the above.
 Unspecified: none of the above.
o Themes of delusions:
 Persecution/paranoid.
 Ideas of reference: cues in the external environment are uniquely related
to the individual.
 Control:
• Thought broadcasting: thoughts can be heard by others.
• Thought insertion: thoughts inserted into head.
• Thought withdrawal.
 Grandeur.
 Guilt.
 Somatic.
No bizarre delusion.
No impairment.
Treatment:
o Gentle confrontation.
o Normal schizophrenic: use atypical; quetiapine, olanzapine, risperidone.
o Combative in the ED: typical; haloperidol.
o Noncompliant: depot; haloperidol.
o When everything fails; clozapine.
o Antipsychotics cause neuroleptic malignant syndrome  dantrolene.
Folie a deux (a shared psychotic disorder):
o Same delusions who share a close relationship.
o Dominant individual in the pair becomes delusional and transfers the delusion
onto the second.
o Intervention:
 Separate the pair.
 Dominant individual gets psychiatric treatment (sometimes inpatient).
 Submissive individual gets formal treatment.
31
Dhat syndrome:
•
•
•
•
Cultural-bound syndrome.
South Asian cultures.
Sufferers attribute a range of psychological and somatic complaints to the loss of semen
via various methods (loss in urine, excess masturbation).
Approach to the treatment of unfamiliar culture-bound syndromes is from a patientcentered approach.
o Ask open-ended question.
Medications/substance induced psychosis:
•
Can be caused by:
o Glucocorticoids.
o OTC cold preparations contain antihistamines and anticholinergics.
o Dextromethorphan.
Medical causes of psychosis:
32
33
Eating disorders
Methods:
•
•
Restriction(anorexia): reducing caloric intake (diet and fast) and increased caloric
expenditure (exercise).
Purge (bulimia): emesis (dental erosions, hand scars, parotid swelling, electrolyte
imbalances (low potassium and magnesium), metabolic alkalosis) or laxative abuse
(diarrhea, metabolic acidosis).
Trends:
•
•
•
•
Female to male ratio is 10:1.
Occurs in the teens to twenties.
Restriction associated with anorexia.
Purge associated with bulimia.
Anorexia
Bulimia
Body weight
Underweight
Normal
Self-image
Low
Low
Anxiety
Fearing of being fat
Binge
No insight
There is insight
Method
Restriction
Binge-purge
Signs and symptoms
Malnourished; lanugo,
amenorrhea, cold intolerance,
emaciated
Normal patient
Hospitalize
When anorexia is extreme:
BMI<15, <85% of their ideal
body weight, electrolyte
disorders (bradycardia and
hypotension), amenorrhea,
severe psychiatric
comorbidity (severe
depression/suicidality)
-
Treatment
Hospitalize; force feed and IV
fluids
SSRI/SNRI + CBT
Signs of purge (russel signcalluses)
34
Outpatient; psychotherapy,
nutritional rehabilitation,
antipsychotics (olanzapine)
F/u
Associated with OCD and
MDD- indication to treat
with SSRI
Never use bupropion due to
increased risk of seizures
Anorexia nervosa:
35
Bulimia nervosa:
•
At least once a week for 3 months.
Binge-eating disorder:
•
•
•
•
Obese.
Binge but no purge.
At least once a week for 3 months.
Treatment:
o Mainstay is psychotherapy, CBT.
o Medications: SSRI, lisdexamfetamine, and topiramate.
Refeeding syndrome: Can also occur in chronic alcoholics.
36
37
Personality disorders
Personality disorders: ego syntonic and impairs functionality. Treated by psychotherapy.
Clustered traits: when it doesn’t impair functionality.
38
Cluster A:
•
Paranoid:
Cluster B:
•
Borderline:
o Can present as depression or a suicidal attempt.
39
•
Histrionic:
•
Antisocial:
Cluster C:
•
Obsessive-compulsive (anankastic):
o Maintains a sense of control; preoccupied with details and rigid rules.
o Stubbornness, excessive devotion to work, inability to delegate tasks to others,
and a miserly spending style.
40
•
o Limited insight into his behavior and ego syntonic.
Dependent:
o Clingy and submissive.
o Fearful of being left to care for themselves.
o They may seek medical attention with somatic symptoms that are an expression
of their distress.
o Struggle to make decisions.
41
Defense mechanisms
42
43
44
Dissociative disorders
Dissociation of thought, memory, and identity. Functionality impaired.
Occurs after severe and prolonged stressors.
Diagnosis:
•
•
Rule out malingering.
Rule out substance abuse.
Treatment:
•
Psychotherapy.
•
•
Not severe  recover.
More severe  less likely to recover.
f/u:
Dissociative identity disorder:
•
•
•
Two or more distinct identity states.
C/P;
o Self:
 Memory gaps/blackouts.
 History of severe trauma.
 Other dissociative signs and symptoms.
o Other:
 Additional identity faces the trauma.
 Paradoxical behaviors.
• Women having changes in sexual preferences and drug use.
• Women physically might look different.
o Look for other psychotic disorders.
Treatment:
o Trauma-focused psychotherapy.
o MDD or PTSD: SSRI.
o Mutilation: naltrexone.
o Nightmares: prazosin.
45
Dissociative amnesia:
•
•
With or without fugue (travel).
Amnesia of
o the stressor or the event or
o loss of everyday occurrences or routines or
o entire biography.
Depersonalization/derealization:
•
•
•
•
Depersonalization from the body.
o Can happen when you give ketamine to kids.
o Déjà vu.
Derealization from the environment.
o Experiencing things as if it’s a dream.
Intact reality testing.
Occur in nonsevere trauma or stressor in adolescence.
46
Catatonia
Not a disease. Modifier of an illness.
Mood disorders like depression, bipolar disorder like mania are more associated with catatonia
than schizophrenia.
C/P:
•
3 or more of the following symptoms:
o Retarded catatonia:
 Stupor.
 Catalepsy.
 Waxy flexibility.
 Negativism; resistant to commands.
 Mutism.
o Excited catatonia:
 Stereotyping (verbal and movement repetition).
 Agitation and grimace.
 Echolalia.
 Echopraxia.
Clinical diagnosis.
•
Lorazepam challenge test: IV lorazepam 1-2 mg results in temporary relief within 5 to
10 minutes confirms the diagnosis.
Treatment: lorazepam.
f/u: watch out for malnutrition (check albumin), give enteral and parenteral nutrition, LMWH
(DVT), or rhabdomyolysis (check CK).
Drug induced catatonia:
47
Disorder
Precipitant
Signs and
symptoms
Malignant
catatonia
Psychiatric disease
underlying
Hypertonicity and
hyperreflexia
No medications
Elevated CK
Increased resistance
to movement
ANS dysfunction:
increased HR, BP,
temperature
Neuroleptic
malignant
syndrome
Psychiatric disease
underlying
Serotonin
syndrome
Psychiatric disease
underlying
On anti-psychotics
On SSRI
Malignant
hyperthermia
“
Neuromuscular
rigidity
“
Neuromuscular
irritability
(tremor,
hyperreflexia,
myoclonus)
No psychiatric illness
“
Exposed to
anesthesia
(halothane gas)
Ask for FHx of
reactions to
anesthesia
Neuroleptic malignant syndrome:
•
•
•
•
•
•
•
•
Type B adverse drug reaction; independent of drug dose.
o Type A is dependent on drug dose.
Idiosyncratic reaction to dopamine antagonist medication.
o Central dopamine receptor blockage; autonomic dysregulation.
o Dopamine antagonism in the nigrostriatal pathway  lead-pipe rigidity.
Tetrad (in the table).
Young, muscular men.
Autonomic dysregulation; labile BP.
Associated with leukocytosis and electrolyte abnormalities.
Muscle necrosis from the hyperthermia and rigidity.
Treatment:
o Bromocriptine or amantadine can be used for those who do not respond to
supportive care and withdrawal of medication.
48
49
Serotonin syndrome:
•
•
Can be triggered by dextromethorphan.
Management includes:
o Short-acting antihypertensives (esmolol).
o IV hydration, and evaporative and convective cooling (fanning or water mist).
 Antipyretics are useless since the fever is due to the sustained muscle
contraction.
50
Psych pharm
Antidepressants:
•
Which drug to pick?
o Trial and error SSRI/SNRI.
 Attempt a single dose for 6 weeks to see if its effective or not.
 Once you find an effective dose  treat depression for 6 months.
(continuation-phase treatment)
 3-6 weeks of washout between drugs to decrease drug interactions.
 Maintenance-phase treatment is defined as continuing antidepressant
medication past the initial continuation phase. Maintenance for 1-3 years
is appropriate for those with high risk of recurrence or persistent residual
depressive symptoms.
• 3 or more lifetime episodes, chronic episodes for 2 or more years,
strong family history, or severe episodes (suicidal attempts) 
maintenance treatment indefinitely.
• Other indications for maintenance therapy: early age of onset,
greater severity, suicidality, and the presence of severe, ongoing
psychosocial stressors or persistent residual depressive symptoms.
o Partial response: 25% to 50% improvement on a single drug. Add another
antidepressant with a different MoA, a second-generation antipsychotic, lithium,
triiodothyronine, or psychotherapy.
o Side note: combination of psychotherapy and pharmacotherapy is better than
pharmacotherapy alone.
51
•
•
•
•
•
SSRI:
o Drugs:
 Citalopram.
• Avoid due to risk of QT prolongation.
 Escitalopram.
 Fluoxetine. (washout is 5 weeks)
 Paroxetine.
 Sertraline.
o ADRS:

 Early: headache, nausea, insomnia/sedation, anxiety, and dizziness.
• Anxiety: temporary dose reduction with a gradual increase to a
therapeutic level over several weeks.
 Late:
• Sexual dysfunction.
o Decreased libido.
o Prolonged ejaculation.
• Weight gain.
• QT prolongation with citalopram.
SNRI:
o Drugs:
 (DES)Venlafaxine; associated with dose-dependent hypertension; usually
above 225 mg daily.
• At low doses  higher affinity to the serotonin transporter rather
than norepinephrine transporter. Acts on the norepinephrine
transporter at higher doses; which explains why HTN occurs with
larger doses.
• Monitor BP regularly.
• If hypertension: dose reduction or switch to another
antidepressant.
 Duloxetine: used for those with diabetic neuropathy and neuropathic
pain.
o Better and cleaner but cost more money.
Atypicals:
o Bupropion: norepinephrine-dopamine reuptake inhibitor.
 Helps in smoking cessation and no weight gain and no sexual ADRs.
 Should not be used in bulimia  seizures.
 Should not be used in those with seizure disorders.
 Recent use of monoamine oxidase inhibitors (past 2 weeks) 
hypertensive crisis.
Serotonin modulators:
o Drugs:
 Mirtazapine; appetite stimulants. And a sleep aid.
 Trazodone; can be used a sleep aid.
• Causes priapism.
Medications which were used to treat depression:
o TCA (“-triptylines” + imipramine + doxepin):
 Used for their side effects.
• Enuresis (imipramine).
• OCD (clomipramine).
• Neuropathic pain (doxepin).
52

• Also used for migraines (amitriptyline).
• 3 C’s; convulsions, cardiotoxicity and coma.
Overdose:
• Inhibition of fast sodium channels in His-purkinje and
myocardium.
• C/P:
o Mental status changes.
o Seizures.
o Tachycardia.
o Hypotension.
o Cardiac conduction delay; leads to prolongation of the QRS
(>100 msec) and risk of ventricular arrhythmia.
 Give IV sodium bicarbonate.
o Anticholinergic effects.
•
•
o
Management:
o Charcoal in 2 hours.
o Sodium bicarbonate.
 Increases serum pH makes the TCA less active.
 Increasing extracellular sodium concentration
raises the electrochemical gradient across cardiac
cell membranes.
 Also improves TCA-induced hypotension caused by
alpha-1-adrenergic receptor antagonism in
combination with cardiac toxicity, and is leading
cause of mortality in TCA overdose.
o Benzodiazepine.
o Anticholinergic toxicity: physostigmine.

MAO inhibitors (tranylcypromine, isocarboxazid, selegiline and phenelzine):
53
Hypertensive crisis when the patient consumes wine or cheese or aged
meats or fermented soy products, or overripe fruits(tyramine).
• C/P:
o Headache.
o Intracranial bleeding.
o Stroke.
o Death.
• Treatment: nitroprusside or phentolamine.
 Can lead to serotonin syndrome if SSRI/SNRI started within 2 weeks of
discontinuation.
• 5 weeks if fluoxetine.
 Can lead to neuroleptic malignant syndrome if antipsychotic is started
afterwards.
 Useful in atypical depression but not the first line.
o Agomelatin: useful for insomnia.
Stimulants (such as methylphenidate) can be used in geriatric and terminally ill
patients.
Antidepressant discontinuation syndrome:
o C/P:
 Fatigue.
 Dysphoria.
 Insomnia.
 Myalgias.
 Dizziness.
 Flu-like and GI symptoms.
 Tremors.
 Neurosensory disturbances (electric shock and rushing sensations in the
head, paresthesia, hyperresponsivity to light and noise, vivid dreams).
o Due to abruptly stopping the treatment or rapidly tapering it.
o Serotonergic antidepressants (paroxetine, venlafaxine) with a shorter
elimination half-life, higher doses, and longer duration of treatment are
associated with more severe discontinuation symptoms.
o Treatment:
 Re-institute the same antidepressant and taper the dose gradually over 24 weeks.
 Alternate management of SSRI discontinuation is to substitute
fluoxetine, which is more easily tapered due to its long half-life.
In patients less than the age of 25; they should be informed about the small risk of
becoming suicidal during initial anti-depressant treatment. However, the benefits of use
still outweighs the risk.

•
•
•
Mood stabilizers:
•
•
Acute mania: lithium/valproate + atypical antipsychotic.
o If they resolve on those medications  leave them on it for maintenance.
Lithium:
o First line for acute and maintenance.
o Manic predominance.
o Teratogen.
54
Narrow therapeutic index (0.6-1.2).
Tremor:
 Lithium-enhanced physiological tremor.
 Symmetric physiological tremor.
 Nonprogressive.
 Decreases over time with no dosage reduction.
o Nephrotoxic.
o Nephrogenic DI.
o Hypothyroidism.
 Monitor TFT every 6 to 12 months.
o Chronic tubulointerstitial nephritis
o Ebstein anomaly.
o Kidney and thyroid function tests should be monitored.
o In toxicity:
 Irregular coarse tremor involving multiple body parts.
 Hemodialysis is the treatment of choice for patients with lithium levels
>2.5 mEq/L and prominent signs of toxicity or patients with levels >4
mEq/L and creatinine >2.0 mg/dl should generally be prescribed dialysis
regardless of symptoms.
Valproate: (50-150)
o First line.
o Mixed affective.
o Teratogen.
o Pancreatitis.
o Decreased platelets.
o Agranulocytosis.
o Hepatotoxicity.
o Alopecia.
o Used if there is renal insufficiency thus inability to use lithium.
o Periodic screening of platelet count and liver function test is necessary.
Quetiapine:
o Second line.
o Weight gain.
o Prolongation of QT-get an ECG.
o Somnolence.
Lamotrigine:
o Second line.
o SAFE IN PRENANCY.
 Pregnancy should be delayed 3-6 months to assess efficacy of the
medication.
o Depressive > manic.
o ADRS: drug rash (mild), SJS and TEN (severe).
 Discontinue once rash starts.
Carbamazepine:
o Third line.
o Manic > depressive.
o Useful for rapid cycling.
o Used for trigeminal neuralgia.
ECT is the best treatment for a manic pregnant woman.
Patient with a history of postpartum mania should be provided prophylaxis with mood
stabilizers in the subsequent pregnancies.
o
o
•
•
•
•
•
•
55
Anti-anxiety:
•
Chronic anxiety (GAD):
o Psychotherapy.
o SSRI/SNRI.
 Risk of serotonin syndrome.
 Start at low dose and then gradually increase because initially they may
worsen the anxiety.
56
•
•
Acute anxiety (panic disorders):
o Anxiolytic: benzodiazepines.
 Chronic use creates dependance (lorazepam or alprazolam) and
withdrawal (diazepam, chlordiazepoxide, similar to alcohol withdrawal).
 Can be used temporarily to bridge patients until long-term medication
becomes effective.
Public speaking: B-blockers (propranolol, nadolol, atenolol).
Antipsychotics:
•
•
•
Typical antipsychotics:
o Potent: haloperidol and fluphenazine(impaired thermoregulation).
o Non-potent: thioridiazine (retinal pigmentation (retinitis pigmentosa)) and
chlorphenazine (lens and cornea pigmentation).
o MoA: antagonizes mesolimbic system  decreases positive signs and symptoms.
o Increased potency  increased extrapyramidal side effects (nigrostriatal).
 Tuberoinfundibular  gynecomastia (males), amenorrhea, and
galactorrhea.
 ACh side effects: dry mouth and urinary retention.
Atypical antipsychotics:
o Drugs:
 Quetiapine: can be used for insomnia, bipolar/mania.
 Olanzapine: weight gain and DM.
 Clozapine- best drug but causes agranulocytosis (fatal). Used in refractory
cases.
• Regular monitoring of the absolute neutrophil count before
dispensing the drug.
• Other ADRs: weight gain, metabolic syndrome, seizures, ileus,
myocarditis, and hypotension.
• Least likely to cause extrapyramidal symptoms or tardive
dyskinesia.
 Risperidone: blocks serotonin 2A and dopamine D2 receptors.
 Ziprasidone: low metabolic risk profile.
 Aripiprazole.
o Both positive and negative symptoms.
o Decreased extrapyramidal side effects.
o All cause QT prolongation.
o BMI should be measured monthly. Fasting plasma glucose and lipids, blood
pressure, and waist circumference should be assessed at baseline, 3 months, and
then annually.
o Earlier and closer monitoring for patients with diabetes or those who have
gained >5% of initial weight.
o Hyperprolactinemia:
 Antipsychotics highly associated with hyperprolactinemia: high-potency
first-generation medications (haloperidol, fluphenazine) and second
generations (risperidone and paliperidone (metabolite of risperidone)).
 Least associated: quetiapine and aripiprazole.
Choice of drugs:
o Normal: atypicals.
57
Noncompliant:
 Agitated: IM risperidone or ziprasidone or olanzapine or haloperidol.
 Dysphagia: oral dissolving tablets olanzapine or risperidone.
 Chronic noncompliant: depot olanzapine or risperidone (LONG ACTING
INJECTABLE).
• Given intramuscularly every 2-4 weeks.
o Failed everything: clozapine.
o Scenarios:
 Young patient with positive symptoms and weight loss  olanzapine.
 Patient with the lack of motivation and poverty of thoughts 
aripiprazole.
Duration of treatment:
o 1 episode: 2 years.
o 2 episodes: 5 years.
o 3 episodes: life-long.
o
•
58
Extrapyramidal symptoms: dopamine antagonists and antiemetics such as metoclopramide and
prochlorperazine.
•
•
Management:
o Reducing the dose.
o Change to an antipsychotic with less potential to cause extrapyramidal
symptoms.
o Adding an anticholinergic.
Akathisia: urge to move; restless.
o Decrease the dose.
59
Management:
 Reducing the antipsychotic dosage.
 Change to an antipsychotic with less potential to cause extrapyramidal
symptoms.
 Adding a beta blocker, anticholinergic, or less commonly, benzodiazepine.
Acute dystonia: any contraction of a major muscle group. More common with high
potency FGAs.
o Oculogyric crisis or torticollis.
o Management:
 Discontinuation of agent.
 Use anticholinergics (benztropine or diphenhydramine).
 Airway protection.
Parkinsonism:
o Options to manage:
 Reducing the dose.
 Switching to another antipsychotic with less potential to cause EPS.
 Use anticholinergics (benztropine or diphenhydramine) when the
antipsychotic is working well and there is concern for destabilizing the
patient with a dose reduction or switching to a new antipsychotic.
Tardive dyskinesia:
o After prolonged use of antipsychotics (>6 months) in older women.
o Chronic and lifelong.
o Orofacial dyskinesias: rhythmic movements of the face, lips, and tongue.
o Choreoathetoid movements of the trunk and the extremities.
o Can’t be reversed.
o It gets worse with treatment.
o Screen for it and stop medication once it starts.
o Treatment options:
 Valbenazine: VMAT-2 inhibitor.
 Benzodiazepines.
 Botulinum toxin.
 Benztropine is contraindicated since it worsens the symptoms.
o
•
•
•
60
61
Addiction
Substance use disorder;
•
•
•
Criteria:
o Control:
 Too much.
 Inability to cut down when you want to.
 Spending too much time trying to get the substance.
 Cravings.
o Social impairment:
 Inability to feel obligations at work or school.
 Relationships.
 Activities.
o Risk taking behaviors:
 Hazardous-sex or driving.
• Having sex to obtain the drugs.
 Complications-health or legal.
o Physical (pharm):
 Tolerance.
 Withdrawal.
Clinical diagnosis.
o Screening:
 CAGE:
• Cutdown.
• Angry.
• Guilty.
• Eye opener. (need it to start the day)
 CRAFFT:
• Car (used while driving).
• Relax.
• Alone.
• Friendships (losing friends).
• Forget.
• Trouble.
o Severity:
 2-3 is mild.
 4-5 is moderate.
 6+ severe.
Treatment:
o Pharmacology.
o Group therapy (alcohol anonymous).
o Psychotherapy.
 FRAMES:
• Feedback.
• Responsibility.
• Advice.
• Menu of options.
• Empathy.
62
Stages:
 Precontemplation. (denial)
 Contemplation. (acceptance)
 Preparation. (first steps)
 Action. (actual behavior change)
 Maintenance. (sustain behavioral changes)
o Addiction: neurobiological predilection to acquire a
substance in order to feel normal.
• Self-efficacy.
Relapse is common.
o
o
Alcohol:
•
Intoxication:
o C/P:
 Altered mental status.
 Disinhibition.
 Slurred speech.
 Cerebellar dysfunction.
 Nausea and vomiting.
 Coma and death.
o Diagnosis:
 Breathalyzer.
 Blood alcohol content (definitive) maximum is 0.08.
63
o
•
• Usually intoxicated at 0.2.
• If chronic alcohol user  0.3.
Treatment:
 Acute: IVF and time.
 Coma: thiamine  D50  naloxone.
Chronic alcohol use:
o Women of all ages and men age 65 or more consuming >7 drinks in a week or >3
in a day.
 For men aged less than 65  >14 drinks in a week or >4 drinks in a day.
o Diagnosis supported by history of GERD and HTN.
o They usually present with sleep disturbance and/or anxiety symptoms from mild
withdrawal.
o All patients should be screened for unhealthy alcohol use.
 All identified should receive a brief counseling intervention geared to the
patient’s level of awareness of the problem and degree of motivation to
change.
 Motivational interviewing: connecting the alcohol use to negative effects.
o C/P:
 Brain Wernicke encephalopathy & Korsakoff.
 Liver  cirrhosis and a ratio of 2:1 AST: ALT.
 GIT  GI bleeds and gastritis.
 Blood  macrocytosis.
 Coma; “found down”.
• Give coma cocktail; which treats both alcohol and opioid overdose,
o Thiamine, D50, and naloxone.
o Treatment:
 Alcohol anonymous.
 Moderate to severe alcohol use  naltrexone (mu-opioid receptor
antagonist) and acamprosate (glutamate modulator).
• Naltrexone decreases alcohol cravings and reduce heavy drinking
days (defined as >5 drinks for men and >4 for women).
o Contraindicated in those taking opioids since it can cause
withdrawal. And in those with acute hepatitis or liver
failure.
64
o Can be initiated while patients are still drinking.
Acamprosate is used to maintain abstinence.
o Glutamate modulator.
o Should be avoided in significant renal impairment.
Disulfiram (Antabuse): aldehyde dehydrogenase inhibitor.
• Causes an unpleasant physiological effect (tachycardia, flushing,
headache, nausea, and vomiting) when alcohol is consumed.
• Can only be used in abstinent patients.
• Candidates for this treatment should be highly motivated or
taking it under a supervised setting.
• Used when naltrexone or acamprosate are contraindicated or
ineffective.
•

•
Withdrawal:
o
o
o
The choice of benzodiazepines depends on the preferred route of administration
as well as pharmacokinetic and metabolic considerations.
 Liver disease  preferred benzodiazepines are those that lack active
metabolites and undergo hepatic metabolism via phase II glucuronidation
instead of CYP 450  lorazepam, oxazepam, and temazepam.
• Most commonly used: diazepam, lorazepam, and chlordiazepoxide.
• Diazepam and lorazepam available in IV formulations.
• Chlordiazepoxide and diazepam can be used for alcohol
withdrawal as well but they have long half-lives and active
metabolites that risk buildup and toxicity in patient with liver
dysfunction.
Moderate to severe alcohol withdrawal management:
 Benzodiazepines to control agitation and prevent progression of
withdrawal.
Delirium tremens management:
 Rule out other causes of delirium.
 Nutritional and electrolyte supplementation.
 Administering benzodiazepines.
 Lorazepam, oxazepam, and temazepam  safe for alcoholic liver.
 Banana bag: thiamine, folic acid, and multivitamins.
65
Benzodiazepines:
•
•
•
•
•
Same as alcohol.
o CIWA score to monitor withdrawal.
Clinical diagnosis.
Treatment:
o Intoxication: endotracheal intubation + flumazenil.
 It lowers the threshold for seizure thus give prophylactic carbamazepine.
o Withdrawal:
 Long acting benzodiazepines and taper.
 Rapid acting benzodiazepines.
Adverse effects:
o Elderly: increased risk of confusion and falls.
o Paradoxical agitation: recurrent episodes of confusion and agitation shortly after
taking dose.
 C/P:
• Increased agitation, confusion, aggression, and disinhibition.
 Important to recognize as increasing the dose might worsen the condition.
 Treatment: taper and discontinue.
Sedative-hypnotic overdose:
o Alongside the signs of benzodiazepines overdose, there will be signs of CNS
depression such as bradycardia, hypotension, respiratory distress, and
hyporeflexia.
o Hypnotic is most likely to be alcohol.
66
Opioids:
•
•
•
•
Starts of as prescription drugs  heroin.
IV use  leads to HIV, hepatitis C, and infective endocarditis.
Risk factors of prescription drug misuse:
o Age <45.
o Psychiatric disorder.
o Personal or family history of substance use disorder or a legal history.
Reduce the risk by checking the prescription drug-monitoring program data for
undisclosed co-prescriptions, performing random urine drug screening, and scheduling
follow-up visits (at least once every 3 months).
67
•
•
•
•
Novel abuse-deterrent formulations only deter certain routes of abuse (e.g. crushresistant formulations deter insufflation).
C/P:
o Intoxication:
 Euphoria.
 Coma.
 Decreased respiratory rate.
 Constricted pupils (doesn’t develop tolerance).
 Constipation.
o Withdrawal:
 Pain.
 Nausea and vomiting.
 Diarrhea.
 Irritable.
Clinical diagnosis.
o Get urine toxicology.
 Only detects natural opioids.
 Cannot detect synthetic and semisynthetic such as oxycodone,
hydrocodone, hydromorphone, fentanyl, meperidine, methadone, or
tramadol.
o Naloxone challenge.
 Might trigger withdrawal.
• So just give enough to increase the RR (>12/min).
Treatment:
o Intoxication: naloxone.
o Chronic: narcotics anonymous and medical assisted therapy (methadone).
 Diarrhea (loperamide), myalgias (ibuprofen), muscle cramps (baclofen).
 Clonidine for anxiety, restlessness, and hypertension.
68
Cocaine:
69
•
•
Produces increased energy, decreased appetite, and reduced need for sleep.
C/P:
o Euphoria and irritability.
o Weight loss secondary to decreased appetite.
o Erythema of the nasal mucosa.
o Severe cases  perforation.
o Crash (due to abrupt cessation):
 Depression.
 Fatigue.
 Hypersomnia.
 Increased dreaming.
 Hyperphagia.
 Drug craving.
 Impaired concentration.
 Suicidal ideation.
 Resolves within 1-2 weeks.
Amphetamines: “meth” “crystal” “ice” “glass”
•
•
•
•
Increase in synaptic NE, dopamine, and serotonin.
Can be misused by high-school students and university students.
Types:
o MDMA: synthetic amphetamine known as “molly” or “ecstasy”.
 Causes hyponatremia.
 Used by college students to increase sociability, empathy, and sexual
desire.
o Bath salts (synthetic cathinones) are amphetamine analogs.
 Sold as a white powder in small packages labeled as “bath salts”, “plant
food”, “cleaners”, or other substances.
 Can be ingested orally, inhaled, or injected.
 They cause agitation, combativeness, acute psychosis, delirium,
myoclonus, and rarely seizures.
 Increased BP and HR.
 Prolonged duration of effect; may last for a week.
 Less likely to cause hyponatremia.
 Cannot be detected by urine toxicology.
C/P:
o Delusions.
o Tactile hallucinations (bugs crawling under the skin).
o Aggressive behavior.
o Severe insomnia.
o Poor dentition.
o Bruxism.
o Weight loss.
70
Excoriations due to chronic skin picking.
Meth mouth: brown discoloration, tooth decay, cracked teeth, and dry mouth.
Amphetamine toxicity: hypertension, tachycardia, mydriasis, and hyperthermia.
 Severe cases: paranoid psychosis.
o Serotonin toxicity: serotonin syndrome and hyponatremia.
Can develop chronic psychosis.
Decongestant pseudoephedrine and the antidepressants bupropion and selegiline can
cause false positive on urine toxicology testing.
o Can be verified by gas chromatography/mass spectrometry.
Treatment:
o Long term management: cognitive behavioral therapy + antipsychotic.
o Benzodiazepines  lorazepam.
o
o
o
•
•
•
LSD:
•
C/P:
o
o
o
o
o
Hallucinations.
Distorted time perception.
Anxiety & agitation.
Paranoid delusions.
Sympathomimetic effect: tachycardia, hypertension, & mydriasis.
Barbiturates:
GHB:
•
•
Direct agonist of GABA.
C/P:
71
•
o Amnesia.
o Nausea.
o Respiratory depression.
o Date rape drug.
Supportive.
PCP: “angel dust”
•
•
Activates NMDA (psychotic and excitatory), dopamine, norepinephrine, serotonin
(dopaminergic and adrenergic), and sigma receptor complex (psychotic and
anticholinergic).
Intoxication:
o C/P:
 Severe agitation.
 Delusions of enhanced strength.
 Dissociative amnesia.
 Violent behavior.
 Psychosis.
 Analgesia.
 Aggression.
 Multidirectional nystagmus.
 Severe: hyperthermia, hypertension, ataxia, muscle rigidity, seizures, and
coma.
o Treatment:
 Supportive management.
 Benzodiazepines if agitated.
Cannabis (“dronabinol” “marijuana”):
•
•
•
Causes psychomotor impairment
Intoxication:
o Impaired reaction time.
o Dry mouth.
Withdrawal:
72
o
o
Symptoms: irritability, anxiety, depressed mood, insomnia, increased appetite.
Examination findings: no significant findings.
Caffeine intoxication:
•
•
C/P:
o Insomnia.
o Anxiety.
o Palpitations.
o Hypertension.
o Tremors.
o Headache.
o GI symptoms.
o Panic attacks.
o Psychosis.
o Seizures.
Due to excessive consumption of energy drinks.
o Safe: <400 mg of caffeine daily.
o One energy drink: 50 to 500 mg.
Inhalant abuse:
•
•
•
Commonly abused inhalants: glue, toluene, nitrous oxide (“whip-its”), amyl nitrite
(“poppers”), and spray paints.
Inhalants may be abused by sniffing, huffing (inhaled from a saturated cloth), or
bagging (bag over mouth or nose).
C/P:
o Boys between 15 and 17 years of age.
o Transient euphoria.
o Psychiatric: irritability, mood swings, aggression, and grandiosity.
o Neurological: tremor, disorientation, headaches, slurred speech, and
hallucinations.
o Gastrointestinal: stomach cramps and nausea.
o Cardiovascular: arrhythmia.
o Respiratory: wheezing and cough.
73
Chronic: weight loss, anorexia, neurocognitive impairment, cerebellar
dysfunction, and peripheral neuropathy.
o Dermatitis (“glue sniffer’s rash”) can be seen around the mouth or nostrils.
o Vitamin B12 deficiency and resultant polyneuropathy in chronic abuse of nitrous
oxide.
Inhalants produce an immediate effect that lasts 15 to 45 minutes.
They are CNS depressants and may cause death.
o
•
•
Gambling disorder:
•
•
•
•
Persistent and maladaptive gambling behavior that results in impairment and distress.
It is considered a nonsubstance behavioral addiction.
Criteria: 4 or more of the following:
o Gambling when distressed, depressed, or anxious.
o Increased gambling to achieve the desired excitement.
o Frequently returning to gambling to recover past losses.
o Preoccupation with gambling.
o Irritability and distress when trying to cut back on gambling,
o Repeated unsuccessful attempts to cut back.
o Trying to conceal the extent of behaviors.
o Damaging relationships or jeopardizing employment.
o Relying on others to make up for financial losses.
Treatment:
o CBT.
o Self-help programs.
o SSRI and opioid antagonists.
Smoking:
•
Smoking cessation treatment:
o Nicotine replacement therapy replaces the nicotine from tobacco to decrease
nicotine withdrawal and aid in smoking cessation.
 Methods of administration: transdermal patch, gum, lozenge, inhaler,
nasal spray).
 Preferred combination: transdermal patch and gum or lozenge.
o Varenicline: alpha-4-beta-2 nicotinic acetylcholine receptor partial agonist, can
diminish nicotine cravings.
74
Does not increase the risk of suicidality or depression compared with
placebo.
 Increases the risk of CVS events in those with preexisting CVS disease.
Bupropion: norepinephrine-dopamine reuptake inhibitor, effective smoking
cessation aid.
 Contraindicated in seizure patients or in any patient with bulimia.
All treatments should be combined with counselling and supportive treatment.

o
o
Withdrawal syndromes:
75
76
Sleep physiology & disorders
Stages of sleep:
•
•
•
The longer the sleep the shorter the NREM and the longer the REM.
NREM:
o N1:
 Theta waves.
 Absent alpha waves.
o N2:
 K complexes.
 Sleep spindles.
o N3:
 Delta waves.
 Not arousable.
 Most restful.
REM:
o Rapid eye movement.
o Memory processing.
o Awake brain.
o Atonia.
o Female and male erections.
Sleep latency:
•
•
Time from putting your head down to N1.
Increased in insomnia and decreased in deprivation.
REM latency:
•
•
Time from entering sleep into REM.
Decreased in narcolepsy and decreased in deprivation (OSA and alcohol).
REM rebound:
•
Increased REM after REM deprivation.
Neurotransmitters of sleep:
•
SAND:
o Serotonin.
 Increases sleep.
o Acetylcholine.
 Increases dreaming.
77
o
o
•
Norepinephrine.
 Increased arousal.
Dopamine.
 Increased arousal.
GABA:
o Decreases sleep latency and N3.
o Stimulated by alcohol, benzodiazepines, or zolpidem.
 Avoid alcohol and benzodiazepines for sleep help.
• Patient can be dependent and increased risk of REM rebound.
 Zolpidem can be used.
Sleep hygiene:
•
•
•
•
•
•
•
Avoiding late afternoon naps.
Avoid nicotine, caffeine, and alcohol.
Avoid heavy meals in the evening.
Adhere to a regular sleep schedule.
Avoid using electronics before bedtime.
Cool, dark, and quiet bedroom environment.
If cannot sleep:
o Do not look at the clock ticking.
o Stimulus control therapy: go to another room and do something relaxing until
feeling drowsy.
Delayed sleep-wake phase disorder:
•
•
•
Sleep-onset insomnia and excessive morning sleepiness.
Occurs due to misalignment of the circadian rhythm with a person’s desired sleep time.
“night owls”.
Advanced sleep-wake phase disorder:
•
Early morning insomnia and inability to stay awake in the evening.
Shift work disorder:
•
Recurrent pattern of sleep interruption due to shift work; difficulty initiating and
maintaining sleep and producing daytime sleepiness.
Age-related sleep changes:
•
•
Decreased total sleep time.
Increased nighttime awakenings.
78
•
•
•
•
•
Phase advance (becoming sleepy earlier in the evening and awakening earlier).
Increased nighttime sleep latency.
Decreased REM latency.
Decreased slow-wave sleep.
No unusual tiredness in the evening.
Nightmares:
•
•
•
•
•
•
•
•
Dreams gone bad.
REM.
No tone.
Easy to wake up – arousal.
Can happen at any age.
They can remember it.
Diagnosis is clinical.
No treatment; just reduce stressors.
Night terrors:
•
•
•
•
•
•
•
•
•
Active behaviors.
In N3.
Has tone.
Appears that they have awoken.
“Screaming during sleep”.
Flushed face, sweating, and tachycardia are common.
They don’t remember it.
Clinical diagnosis.
No treatment; just reassurance it will resolve in 1-2 years.
REM sleep behavior disorder:
•
•
•
•
Older adult men.
Complex motor behaviors that occur during REM sleep.
Dream enactment can occur if the muscle atonia that usually accompanies REM is
absent or incomplete.
Usually occurs in the latter part of the night. At least 90 minutes after sleep onset.
79
•
•
•
•
Can be awakened quickly and after a period of transient confusion can become fully
alert.
If frequent and recurrent it may be a prodromal sign of neurodegeneration in patients
with Parkinson disease or dementia with Lewy bodies.
Can be associated with subtle motor deficits such as changes in gait, insomnia, and
constipation.
Narcolepsy and antidepressant medication initiation are also associated with RBD.
Narcolepsy:
•
•
•
•
•
Associated with low CSF levels of orexin-A/hypocretin-1.
Startled  rapid REM and loss of tone.
C/P:
o Decreased sleep latency.
o 3 times per week for 3 months.
o Waking refreshed.
o Cataplexy: loss of tone and paralysis.
o Hallucinations:
 Hypnogogic: going to sleep.
 Hypnopompic: waking from sleep.
Diagnosis:
o Polysomnography.
Treatment:
o Schedule naps.
o Use stimulants throughout the day  modafinil.
o Cataplexy  REM sleep-suppressing drugs such as TCA antidepressants and
sodium oxybate (drug of choice).
Insomnia:
•
•
•
•
Defined as trouble sleeping.
Either a product of having trouble falling asleep or reawakening.
3 times a week for 3 months.
Determine if they’re having enough sleep which is 6 hours per day.
80
o
o
6 or more sleep  jet lag or normal sleep.
 Reorientation or use phototherapy.
Less than 6 hours  sleep hygiene.
 Good sleep hygiene  and it’s a primary insomnia (not a product of
another disorder  diphenhydramine, trazodone, quetiapine, triazolam,
or zolpidem.
 Bad sleep hygiene  use bed for sex and sleep only, lights off, avoid
stimulus (caffeine, nicotine), avoid alcohol, avoid exercise 4 to 6 hours
before sleep.
• Fails  use above mentioned medications.
• Other forms of treatment:
o CBT.
o Chronotherapy.
81
Gender dysphoria
Terminology:
•
•
•
•
•
Assignment: phenotype.
Identity: mind.
Transgender is identity is incongruent with phenotype.
Transsexual is someone who made the switch from a gender to the other through body or
social status.
Transvestism is someone who cross-dresses but not transgendered.
Gender dysphoria:
•
•
•
•
•
•
•
Identity incongruent with assignment.
Causes a distress.
C/P:
o Lasts for 6 or more months.
o Identity is incongruent with assignment.
o Desires to be or be treated like the opposite sex.
o To rid themselves of secondary sexual characteristics.
o Believes they are the opposite sex.
Clinical diagnosis.
Treatment: psychotherapy and gender identity-affirming surgery.
Differentiate from gender nonconformity; individuals do not conform to stereotypical
gender roles but still identify with their assigned gender.
Kids:
o Rejection of same sex roles or acceptance of the opposite sex roles.
o Lasts for 6 months.
o Causes distress.
82
Abuse
Elder abuse:
Sexual assault:
83
•
Most cases occur between acquaintances and involve intoxication of alcohol or use of
date rape drugs (flunitrazepam (Rohypnol)) that causes LOC and amnesia.
84
Somatic symptom disorders
Somatoform disorder:
•
•
•
•
Real symptoms, patient distress about disease, but there is no organic cause.
C/P:
o Multiple physicians.
o Many tests.
o Anxiety disorder or depression.
o Might ask for procedures.
Diagnosis:
o Rule out organic disease.
o Rule out factitious and malingering.
Treatment:
o Psychotherapy and setting boundaries.
Disorder
Signs and
symptoms
Preoccupation
Motivation
Illness anxiety
disorder
None
Acquiring illness
despite repeated
reassurance
Unwanted
Somatic symptom
disorder
Somatic (pain or
fatigue)
Somatic symptom
Unwanted
May be related to a
medical disease
Disproportionate to
the medical disease
Conversion
disorder
Neurological sign
None; won’t hurt
themself
Unwanted
Factitious (by
proxy-imposed on
someone else)
Any symptoms;
inconsistencies
between reported
symptom and
objective findings
Attention
Intention to deceive
Malingering
Any symptoms
Intention to deceive
85
Illness anxiety disorder (hypochondriasis):
•
•
•
•
Absence of prominent somatic symptoms.
Unfounded fear of having a serious illness.
High health care utilization, repeated self-checking for signs of illness, and catastrophic
interpretations of minor physical sensations.
Management:
o Scheduling regular visits, limiting diagnostic tests and referrals, and focusing on
coping and functional improvement.
Somatic symptom disorder:
86
•
•
They don’t respond to reassurance.
Difficulty in expressing emotions; alexithymia.
Conversion disorder:
•
•
La belle indifference (indifferent attitude towards severe symptoms) occurs with equal
frequency in both conversion and true neurological disorders and is therefore not a
reliable indicator.
Psychogenic nonepileptic seizures:
o C/P:
 Forceful eye closure.
 Side-to-side head or body movements.
 Rapid alerting.
 Reorienting.
 Memory recall of the event.
 Infront of witnesses.
o Models their behavior after a friend or a relative with epilepsy.
o Not associated with abnormal cortical activity.
o Video-EEG is gold standard for diagnosis.
87
Factitious disorder:
88
Psychotherapy
89
•
Insight-oriented psychotherapy:
o Focuses on uncovering unconscious patterns originating in childhood
experiences.
o Initially causes anxiety.
90
Stages of change:
91