Handbook of Psychiatry 2021

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Simply Psych EDU © Handbook of Psychiatry

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SAMPLE
HANDBOOK OF
PSYCHIATRY
2021
Michael T. Ingram, M.D.
Michael T Ingram Psychiatry Inc. 2021

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CONTENTS
Psychiatric Evaluation ............................... 17

Components of the evaluation ............. 17
Mental Status Examination ....................... 19
Emergency Psychiatry ............................... 22
Acute Agitation ..................................... 22
Drugs of Abuse ...................................... 23
Urine Toxicology: .............................. 23
False Positives: .................................. 23
Alcohol .................................................. 24
Medical complications of chronic
alcohol use ........................................ 24
Alcohol Withdrawal Timeline ............ 25
Alcoholic Hallucinosis:....................... 25
Alcohol withdrawal syndrome: ......... 25

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Alcohol withdrawal seizures: ............ 26

Alcohol withdrawal delirium (Delirium
tremens):........................................... 26
Wernicke Korsakoff Syndrome (WKS):
.......................................................... 27
Alcohol Intoxication/Poisoning: ........ 27
Benzodiazepines for Alcohol
Withdrawal ....................................... 28
Alcohol Withdrawal Treatment Table
.......................................................... 28
Serotonin Syndrome & NMS ................. 29
Lithium Toxicity ..................................... 30
Catatonia ............................................... 31
Presentation:..................................... 31
Causes: .............................................. 31
Treatment: ........................................ 31

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Suicide Risk Assessment........................ 32

RISK FACTORS.................................... 32
PROTECTIVE FACTORS ....................... 32
Risk FACTORS FOR VIOLENCE: ............... 33
Consultation Liaison Psychiatry ................ 34
Delirium|Altered Mental Status ........... 34
General Concepts: ............................. 34
Predisposing factors:......................... 34
Precipitating factors: ......................... 35
Behavioral Management:.................. 35
Pharmacological Management: ........ 35
Physical restraints: ............................ 36
Geriatrics ............................................... 36
General Comments: .......................... 36
Delirium/Dementia Management:.... 37

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Depression in the Elderly: ................. 37

Psychopharmacology in medically complex
patients ..................................................... 38
Patients with Cardiovascular Disease 38
Patients with Liver Disease ............... 45
Patients with Renal Disease .............. 46
Patients with Respiratory Disease .... 47
Patients with Neurological Disease ... 48
Capacity................................................. 50
Capacity Vs. Competence ................. 50
Criteria for Decision-Making Capacity
.......................................................... 51
Documenting Capacity ...................... 51
Pregnancy & Post-Partum Period ......... 53
Inpatient Psychiatry .................................. 55
Treating common patient complaints:.. 55

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Insomnia ........................................ 55
Break-through anxiety ................... 56
Pain ................................................ 56
Pruritus .......................................... 56
Akathisia ........................................ 56
Dystonic reactions ......................... 56
Parkinsonism .................................. 57
Tardive Dyskinesia ......................... 57
Psychopharmacology ................................ 58
Drug Schedules ..................................... 58
Terms & Definitions: ............................. 58
Drug Levels, Labs, & Monitoring ........... 60
Antipsychotics ....................................... 61
SIDE EFFECTS (LEAST TO MOST) ........ 61
Benzodiazepines ................................... 61

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Benzodiazepine Equivalency Table: .. 64

Treating Extrapyramidal Symptoms ...... 64
Drug Interactions Table......................... 65
High Yield Psychopharmacology concepts
.................................................................. 67
General Concepts .................................. 67
Lithium .................................................. 71
Antidepressants .................................... 73
Antipsychotics ....................................... 76
Mood Stabilizers ................................... 79
Important Drug-Drug Interactions ............ 81
Valproic acid (VPA) + Lamotrigine:........ 81
Carbamazepine (CBZ) is an inducer of
CYP3A4 .................................................. 81

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Lithium + NSAIDs (not aspirin), ACE

Inhibitors, Thiazide diuretics, low sodium
diet: ....................................................... 82
Lithium + caffeine, theophylline, high
sodium diet: .......................................... 82
Grapefruit Juice ..................................... 82
Smoking Tobacco cigarettes: ................ 83
Tyramine ............................................... 83
Fluoxetine, Paroxetine, and Bupropion
are potent inhibitors of CYP2D6 ........... 83
Antimicrobial-Psychotropic Drug
Interactions: .......................................... 84
Other Interactions/Adverse Reactions: 84
Medication Quick Reference..................... 86
Fluoxetine (Prozac) ............................... 86
Sertraline (Zoloft) .................................. 88

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Paroxetine (Paxil) .................................. 90

Fluvoxamine (Luvox) ............................. 92
Citalopram (Celexa)............................... 94
Escitalopram (Lexapro) ......................... 96
Duloxetine (Cymbalta) .......................... 98
Venlafaxine (Effexor)........................... 100
Desvenlafaxine (Pristiq) ...................... 103
Levomilnacipran (Fetzima) .................. 105
Bupropion (Wellbutrin) ...................... 106
Mirtazapine (Remeron) ...................... 108
Trazodone (Desyrel) ........................... 110
Vortioxetine (Trintellix) ...................... 112
Tricyclic Antidepressants (TCAs) ......... 114
Buspirone (Buspar) ............................. 117
Gabapentin (Neurontin)...................... 119

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Pregabalin (Lyrica)............................... 121

Lithium ................................................ 123
Valproic Acid (Depakote) .................... 126
Carbamazepine (Tegretol) .................. 129
Lamotrigine (Lamictal) ........................ 131
Topiramate (Topamax) ....................... 134
Methylphenidate (Ritalin, Concerta) .. 137
(D,L) Amphetamine (Adderall) ............ 140
(D) Amphetamine (Dexedrine) ............ 142
Lisdexamfetamine (Vyvanse) .............. 144
Typical Antipsychotics ......................... 147
Side Effects of Typical Antipsychotics
........................................................ 148
Receptors and side effects .............. 148
Atypical Antipsychotics ....................... 151

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Side Effects of Atypical Antipsychotics

........................................................ 152
Clozapine (Clozaril).............................. 154
Risperidone (Risperdal) ....................... 156
Olanzapine (Zyprexa) .......................... 157
Quetiapine (Seroquel) ......................... 160
Aripiprazole (Abilify) ........................... 162
Ziprasidone (Geodon) ......................... 164
Asenapine (Saphris) ............................ 165
Lurasidone (Latuda) ............................ 167
DSM-5 Diagnostic Criteria ....................... 168
Psychotic Disorders ............................. 168
Schizophrenia .................................. 168
Schizophreniform Disorder ............. 170
Brief Psychotic Disorder .................. 171

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Schizoaffective Disorder ................. 171

Delusional Disorder ......................... 172
Mood Disorders .................................. 174
Major Depressive Disorder ............. 174
Bipolar Disorder .............................. 176
Disrupted Mood Dysregulation
Disorder (DMDD) ............................ 180
Persistent Depressive Disorder
(Dysthymia) ..................................... 182
Premenstrual Dysphoria Disorder
(PMDD)............................................ 184
Anxiety Disorders ................................ 187
Generalized Anxiety Disorder ......... 188
Separation Anxiety Disorder ........... 189
Specific Phobia ................................ 191
Social Anxiety Disorder ................... 193

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Panic Disorder ................................. 194

Panic Attack Specifier...................... 196
Agoraphobia.................................... 196
OCD and Related Disorders ................. 198
Obsessive Compulsive Disorder ...... 198
Body Dysmorphic Disorder ............. 199
Hoarding Disorder ........................... 200
Hair Pulling Disorder (Trichotillomania)
........................................................ 200
Excoriation (Skin-Picking) Disorder . 200
Attention Deficit Hyperactivity Disorder
(ADHD) ................................................ 201
Eating disorders .................................. 203
Bulimia Nervosa .............................. 203
Anorexia Nervosa ............................ 204
Post Traumatic Stress Disorder ........... 205

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ICD-10 Codes ........................................... 209

Neurodevelopmental Disorders .......... 209
ADHD ................................................... 210
Somatic Symptom and Related Disorders
............................................................ 212
Psychotic Disorders ............................. 212
Bipolar Disorders................................. 216
Dissociative Disorders ......................... 218
Feeding and Eating Disorders ............. 218
Depressive Disorders .......................... 220
Impulse-Control and Conduct Disorders
............................................................ 222
Medication Induced Movement Disorders
and Other Adverse Effects of Medications
............................................................ 223
Anxiety, OCD, and Trauma Disorders.. 224

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Substance Use Disorders..................... 229

References .............................................. 237

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PSYCHIATRIC EVALUATION
COMPONENTS OF THE EVALUATION
SAMPLE
Patient Identification Name, Age, Gender identity
Chief Complaint Reason for visit/admission

Symptom(s) onset, duration, severity,
aggravating and alleviating factors,
History of Present additional stressors.
Illness
Depression (SIGECAPS)*
Manic/Hypomanic Symptoms
(DIGFAST)**
Psychiatric Review of Anxiety Symptoms
Symptoms Psychotic Symptoms
Drug name(s), Date of first use,

Substance Use History Quantity, Frequency, Duration, Longest
period of sobriety (LPOS), Last use
Outpatient treatment history
Inpatient treatment history
Past Psychiatric History Previous medication trials
History of self-harm, suicide attempts,
and violence
Medical problems, Past Surgeries,

Past Medical History
Medications, Allergies
Psychiatric Disorders, Suicide attempts,

Family History
completed suicide, substance use
Birthplace
Early parental figures
Social History Developmental Milestones
Education history

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Relationship History
Marital status
Social Support
Religious preference
Trauma and/or Abuse history
Current Living Situation
Employment History
SAMPLE
Legal History (arrests, DUIs, prison time)
Constitutional
Skin
HEENT
Neck
Cardiovascular
Medical Review of Pulmonary
Systems Gastrointestinal
Genitourinary
Musculoskeletal
Lymphatic
Endocrine
Neurological
Mental Status Exam
Physical Examination Neurological Exam
Neurobehavioral Exam
*SIGECAPS: Sleep disturbances, lack of Interest, low Energy, Concentration

problems, Appetite changes, Psychomotor changes, Suicidal thoughts
**DIGFAST: Distractibility, Impulsivity, Grandiosity, Flight of Ideas, Agitation, lack

of Sleep, Talkative/pressured speech

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MENTAL STATUS EXAMINATION

VITAL SIGNS Temperature, Heart Rate, Blood Pressure,
Respiratory Rate, Oxygen Saturation, Weight,
Height
SAMPLE
ALERTNESS/ORIENTATION Is the patient awake, alert, and oriented to
person, place, time, date, situation? Is the
patient drowsy, confused, sedated, or lethargic?
APPEARANCE Does the patient appear his or her age? Is the

patient wearing appropriate attire? Is the patient
disheveled? How is the patient’s hygiene? Are
there any physical abnormalities or
distinguishing features such as tattoos, hairstyle,
scars, or unusually smells? How is the patient’s
posture?
BEHAVIOR Is the patient cooperative? Does the patient

make appropriate eye contact? Behavioral
descriptors include guarded, evasive, angry,
seductive, bored, distracted, disinterested,
indifferent/apathetic, pleasant, preoccupied,
sarcastic, passive-aggressive, hostile,
threatening, crying, tearful, smiling, laughing
(inappropriate laughing, giggling, smiling).

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MOTOR Is the patient’s motor activity slowed/decreased

(e.g., parkinsonian, catatonic) or
hyperactive/agitated/increased (e.g., restless,
fidgety, chorea, pacing, foot tapping, hand
wringing, skin picking)? Any abnormal
movements present such as tics, dystonia,
SAMPLE
rigidity, tardive dyskinesia, athetoid, akathisia?
Does the patient have a normal gait?
SPEECH How is the patient’s speech rate, rhythm,

volume, quantity, articulation? Does the patient
speak fluently and spontaneously?
MOOD How does the patient describe their mood state?
AFFECT How does the patient’s mood appear to you (i.e.,

affect is the outward expression of the patient’s
emotional state)? Note the Stability, Range,
Appropriateness, Intensity, and Quality
(depressed, sad, happy, angry, euphoric, irritable,
anxious, neutral, fearful, apathetic, pleasant)
THOUGHT CONTENT Does the patient have suicidal ideations (passive,

active), homicidal ideations, depressive
cognitions, obsessions, compulsions,
ruminations, phobias, ideas of reference,
paranoid ideation, magical ideation, delusions,
overvalued ideas? Are there any recurrent major
themes discussed by the patient?

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THOUGHT PROCESS Is the patient’s thought process linear, logical,

and goal-directed or is it circumstantial,
tangential, illogical, perseverative, and
incoherent? Does the patient have disorganized
thoughts, flight of ideas, loose associations, clang
associations, neologisms, or thought blocking?
PERCEPTION Does the patient report Hallucinations, Illusions,

Depersonalization, Derealization, Déjà vu, Jamais
vu? Is the patient responding to internal stimuli?
INTELLECT Average, above average, below average?
INSIGHT Does the patient demonstrate adequate

understanding of their illness and the current
situation?
JUDGEMENT Does the patient have good judgement? Ask a

question RELATED TO THE CURRENT SITUATION
(e.g., hypothetical scenarios, etc.).
IMPULSE CONTROL Is the patient impulsive and unpredictable?

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 Diazepam has a rapid onset of action due to its rapid
absorption and distribution (very lipid-soluble)
 Diazepam has a shorter duration of clinical action than
lorazepam after one dose
 Intramuscular administration of diazepam and
chlordiazepoxide have unreliable and unpredictable
absorption
 Benzodiazepines are all positive allosteric modulators of the
GABA-A Receptor
 Benzodiazepines that preferentially bind to the α1 subunit of
the GABA-A receptor are thought to have more
sedative/hypnotic effects while those that preferentially bind
to the α2 and α3 subunits of the GABA-A receptor are thought
to have anti-anxiety effects (but there is little evidence to
support this at this time)
 Benzodiazepines increase the binding affinity of GABA for its
receptor and increase the frequency of opening of the
chloride channel embedded within the GABA-A receptor.
 This leads to increased chloride influx and hyperpolarization
of the dendritic portion of neurons bearing GABA-A
receptors).
 When benzodiazepines are given to an individual suffering
from acute stress disorder, the probability of conversion to
PTSD is roughly doubled (i.e., benzodiazepines may interfere
with post trauma adaptation).
 Exposure therapies for anxiety disorders and PTSD do not
work as well if performed in the presence of a
benzodiazepines.

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 Short course of benzodiazepines are commonly prescribed
when starting SSRIs/SNRIs in patients with high anxiety to
minimize activating side effects that can occur when initiating
these agents
 The following benzodiazepines have little, if any, phase 1
metabolism in the liver and primarily undergo
glucuronidation (and therefore they are preferred for
individuals with hepatic impairment):
• Oxazepam
• Temazepam
• Lorazepam
 Benzodiazepines have been associated with:
• Tolerance, physical dependence, withdrawal
• Abuse potential
• Ataxia
• Diminished attention
• Failure of memory consolidation
• Increased risk of falls in the elderly
• Increased risk of delirium in the elderly

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BENZODIAZEPINE EQUIVALENCY
TABLE:
Dosage Elimination
Equivalency half-life (hrs)
(mg)
Alprazolam (Xanax) 0.5 6-20

Chlordiazepoxide (Librium) 10 30-100
Clonazepam (Klonopin) 0.25 18-50
Diazepam (Valium) 5 30-100
Lorazepam (Ativan) 1 10-20
Midazolam (Versed) -- 2-3
Oxazepam (Serax) 15 8-12
Temazepam (Restoril) 30 8-20
TREATING EXTRAPYRAMIDAL
SYMPTOMS
Side Effect Treatment Options
Acute Akathisia Propranolol (30mg-90mg/day)
Benzodiazepines
Diphenhydramine
Parkinsonism Reduce dose
Benztropine 1-2mg/day
Tardive Dyskinesia Reduce dose
Discontinue
Ingrezza
Hyperprolactinemia Reduce dose
(symptomatic) Discontinue
Acute Dystonia Benztropine 1mg-2mg IM

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DRUG INTERACTIONS TABLE

Substrates Inhibitor Inducer
1 Caffeine Fluvoxamine Cimetidine Phenobarbital Modafinil
A Theophyline Fluoxetine Omeprazole Secobarbital Tobacco
2 TCAs Paroxetine Fluoroquinol. Carbamazepine Charcoal-
Ropinirole Sertraline Ticlopidine Phenytoin grilled meat
Duloxetine Rifampin
Mirtazapine
Clozapine
Haloperidol
Olanzapine
Asenapine
Tacrine
Zolmitriptan
2 Warfarin Valproic acid Fluconazole Secobarbital Rifampin

C Losartan Fluoxetine Miconazole Carbamazepine
9 NSAIDs Amiodarone
Glipizide
ARBs
2 BZDs Fluvoxamine Ketoconazole Carbamazepine Rifampin

C PPIs Fluoxetine Cimetidine Valproic acid
1 SSRIs (citalopram) Omeprazole Phenobarbital
9 Amitriptyline Lansoprazole Phenytoin

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2 β-blockers Bupropion Terbinafine None None

D Class 1C Fluoxetine Quinidine
6 antiarrhythmics Paroxetine Cimetidine
Codeine Duloxetine Amiodarone
Amitriptyline Sertraline Mibefradil
Sertraline Citalopram Ritonavir
Haloperidol Escitalopram
TCAs Haloperidol
Risperidone Thioridazine
Iloperidone
Tramadol
Venlafaxine
Duloxetine
Aripiprazole
3 Acetominophen Fluvoxamine Clarithromycin Carbamazepine Rifampin

A BZDs Nefazodone Erythromycin Phenytoin Ritonavir
4 Statins Troleandomycin Phenobarbital Indinavir
Macrolides Fluconazole St. John’s Wort Efavirenz
Quinidine Ketoconazole Morphine Pioglitazone
Indinavir, Ritonavir Itraconazole Nicotine Glucocortic
Amlodipine, Indinavir Topiramate oids
Felodopine Cimetidine Felbamate
Diltiazem Verapamil
Atorvastatin Diltiazem
Buspirone
Sertraline
Venlafaxine
Mirtazapine
Haloperidol
Iloperidone
Trazodone

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U FGAs Diclofenac Carbamazepine Rifampin

G SGAs NSAIDs Phenytoin Carbapene
T TCAs Probenecid Phenobarbital ms
NSAIDs Valproic acid Lamotrigine
Carvedilol
Furosemide
Morphine
Tramadol
Lorazepam
Oxazepam
H I G H Y I EL D P S Y C H OP H A R M A C OL O G Y C O NC EP T S
GENERAL CONCEPTS
1) Elderly patients in general require lower doses of
medications due to normal changes in total body water
(TBW), muscle mass, fat %, and kidney/liver function
associated with aging.
2) In patients with hepatic impairment, adjust dose by
calculating the Child-Pugh Score (see above).
3) AST, ALT, and Alkaline Phosphatase are not reliable
indicators of hepatic function.
4) Young men with increased muscle mass who abuse
stimulants (methamphetamine) might be at higher risk for
extrapyramidal symptoms after administering high
potency antipsychotics (Minimal empirical evidence
supporting this, but mainly anecdotal support)

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5) Seasonal Affective Disorder (SAD) can be treated with
light therapy. Bupropion is also effective.
6) Avoid beta blockers, if possible, in patients with COPD or
asthma
7) Oxazepam, Temazepam, and Lorazepam are typically used
in patients with hepatic impairment as they do not
undergo Phase 1 metabolism and primarily undergo
glucuronidation. (“Outside The Liver”)
8) Zolpidem (Ambien) and Zaleplon can case dissociative-like
state (sleep walking, binge eating, aggressive outbursts,
night driving) and the patient will not remember doing
any of those things
9) Restless Leg Syndrome: Replete iron if deficient. 1st line
treatment are dopamine agonists (levodopa, ropinirole,
pramipexole, rotigotine); Alternatives
are benzodiazepines (clonazepam), gabapentin,
anticonvulsants, opioids.
10) In patients who are overweight, obese, or who have a
large neck circumference: Think Obstructive Sleep Apnea
(OSA) if presents with excessive daytime sleepiness,
fatigue, irritability, or memory problems. Order a sleep
study.
11) Stimulants (Amphetamines, Methylphenidate), non-
stimulants (atomoxetine, a norepinephrine reuptake
inhibitor), and modafinil are used to treat ADHD and
narcolepsy
12) Stimulants can be used in terminally ill elderly patients
with depression and/or demoralization syndrome.

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13) Stimulants in children/adolescents: side effects include
insomnia, anorexia, and tics
14) Remelteon is a good for initial insomnia due to short half
life.
15) Benzodiazepine overdose treated with flumazenil (may
precipitate seizures in those with pre-existing seizure
disorders)
16) Naloxone (Narcan) is used for opioid overdose. Has a
short half life so must give in intervals or patient may
revert back to opioid/opiate induced coma/respiratory
depression.
17) Anticholinergic agents (benztropine, atropine,
diphenhydramine, doxepin, low-potency antipsychotics)
can cause cognitive impairment, worsen dementia, and
precipitate delirium in the elderly.
18) Electroconvulsive therapy (ECT) is has shown efficacy for
severe refractory depression, depression during
pregnancy, psychosis, mania, catatonia, malignant
catatonia, and treatment refractory NMS
19) There are no absolute contraindications to ECT. Avoid ECT
in patients with intracranial masses (due to increased
intracranial pressure and risk of herniation). ECT alters
cerebral hemodynamics.
20) Ethanol is broken down to acetaldehyde by alcohol
dehydrogenase. Acetaldehyde is broke down to Acetyl
CoA by acetaldehyde dehydrogenase. Disulfiram inhibits
acetaldehyde dehydrogenase causing accumulation of
acetaldehyde (facial flushing, nausea, vomiting, etc.).
These reactions can occur with over the counter cough

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syrups or anything with alcohol in it. It is most effective
for motivated patients with a good support system.
21) Narcolepsy (sudden REM sleep with loss of muscle
tone/cataplexy) is diagnosed by Multiple Sleep Latency
Test and treated with stimulants or modafinil.
22) Steady state of oral drugs is usually reached after 4-5 half-
lives (Example: Li takes ~5 days to reach steady state after
initiation or dose change)
23) Chronic alcoholic patients should always receive
parenteral thiamine before administering
glucose/dextrose
24) Treatment of Catatonia: Benzodiazepines (IV lorazepam
first line) or ECT
25) ECT side effects: musculoskeletal pain, amnesia, headache
26) Seizures: Potential culprits are clozapine, chlorpromazine,
clomipramine, bupropion, lithium (toxicity), abrupt
withdrawal from benzodiazepines or anticonvulsants.
Flumazenil also reduces seizure threshold.
27) Therapeutic Index (TI) = TD50/ED50
28) Propranolol (Inderal) is effective for social phobia (public
speaking), akathisia, and essential tremor

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LITHIUM
1) Lithium is toxic to the thyroid gland
2) 5-10% of patients on lithium develop hypothyroidism, >30%
of lifetime lithium patients have elevated TSH
3) Check TSH levels prior to starting lithium, at 6 months, then
annually
4) Lithium Toxicity: Emergency dialysis indicated with
symptoms of toxicity (tremors, ataxia, slurred speech, AMS)
and Lithium levels > 2.5
5) Lithium is not protein bound and therefore is easily
dialyzed.
6) Dialysis is not a contraindication for using lithium. Dose
lithium immediately after dialysis only.
7) Lithium worsens skins conditions such as Acne and Psoriasis
8) Lithium’s mechanism of action is incompletely understood
but thought to interact with signal transduction pathways
(e.g., IP3 pathway)
9) Lithium and ECT: Lithium dose should be reduced or
discontinued in patients undergoing ECT (may cause
prolonged seizures)
10) Lithium use during pregnancy (especially 1st trimester)
increases risk of Epstein’s anomaly (congenital downward
displacement of tricuspid valve into the right ventricle)
11) Lithium level normal range is 0.6-1.2 (for acute mania target
should be 1.0-1.5)

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12) Decreased lithium levels with: Theophylline, caffeine,
osmotic diuretics, acetazolamide, increased sodium intake
13) Increased lithium levels with: Na depletion, Diuretics,
NSAIDs (not aspirin), COX-2 inhibitors, Tetracycline, ACE
inhibitors
14) Lithium is also known to be a potential precipitant of
serotonin syndrome in people concurrently on serotonergic
medications such as antidepressants, buspirone, and
certain opioids such as pethidine (meperidine), tramadol,
oxycodone, fentanyl and others.
15) Lithium co-treatment is also a risk factor for neuroleptic
malignant syndrome in people on antipsychotics and other
anti-dopaminergic medications.
16) Lithium causes acquire nephrogenic diabetes insipidus in
about 50% of patients on long term Lithium treatment
17) Lithium treatment and EKG changes: T-wave flattening or
inversion
18) Lithium interferes with AV conduction and the pace making
activity of the sinus node (avoid in sick sinus syndrome).
Also avoid in Brugada syndrome (genetic defect of cardiac
sodium channels)

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ANTIDEPRESSANTS
1) In Elderly patients with depression or anxiety: Use
SSRIs due to minimal side effects.
2) In Elderly patients with depression or anxiety: Avoid
tricyclic antidepressants (TCAs), if possible, due to
anticholinergic side effects (constipation, urinary retention,
cognitive impairment, delirium risk), cardiovascular side
effects, cognitive impairment, and orthostatic hypotension)
3) Selective Serotonin Reuptake Inhibitors (SSRIs) are first line
treatments for Obsessive Compulsive Disorder but usually
require higher doses than would be prescribed for
depression.
4) Clomipramine is most serotonergic of the Tricyclic
Antidepressants (TCAs) and therefore is a good choice for
SSRI-refractory Obsessive Compulsive Disorder.
5) All SSRIs, except maybe paroxetine, are very safe to use
during pregnancy. Sertraline and Fluoxetine are the best
first choices for pregnant patients as these have the most
data for safety.
6) Paroxetine and Sertraline are minimally secreted in
breastmilk and are the best choices for individuals who are
breastfeeding
7) SSRIs and the reported risk of persistent pulmonary
hypertension of the newborn during 2nd and 3rd trimesters
is controversial.
8) Safest SSRIs during pregnancy: Sertraline, Fluoxetine,
Citalopram

74
9) Safest SSRIs during breast feeding: Paroxetine, Sertraline,
Fluoxetine, Citalopram
10) Paroxetine is not a the best first choice as an
antidepressant and anxiolytic during pregnancy due to a
small risk of congenital defects
11) Paroxetine should be dosed once daily at bedtime due to
anticholinergic and antihistamine properties (usually
sedating)
12) Fluoxetine and Sertraline are generally considered more
“activating” SSRI antidepressants (but not always).
13) Paroxetine does not have an active metabolite and has a
relatively short half-life and therefore often causes
withdrawal syndrome when abruptly stopped.
14) Paroxetine has anticholinergic properties and a potent
inhibitor of CYP2D6
15) Sertraline (Zoloft) is a weight neutral SSRI
16) SSRIs have shown effectiveness in premenstrual dysphoria
and irritability. Also for “hot flashes” in perimenopause.
17) Bupropion is a good choice for patients who smoke or have
low libido.
18) Bupropion is a good choice for SSRI induced sexual side
effects.
19) Bupropion is a good choice for seasonal affective disorder.
20) Bupropion should be used with caution in patient’s with a
history of seizure disorders and/or eating disorders
(appears to lower the seizure threshold)

75
21) Bupropion is the least likely of the studied antidepressants
to induce mania or cause rapid cycling in depressed
patients with bipolar disorder
22) TCAs cause slowing of cardiac conduction leading to a
widening of the QRS complex and fatal heart blocks.
SAMPLE
23) Antidepressants with noradrenergic properties may be the
best choice for patients with depression and neuropathic
pain.
24) SNRIs be dosed in the morning as they can cause insomnia
if dosed too late in the day (but not always).
25) For patients with TCA overdose, the treatment of choice is
NaHCO3 (sodium bicarbonate)
26) Monoamine Oxidase Inhibitors (MAOIs) carry a risk for
hypertensive crises when used in combination with
tyramine rich foods (aged cheese, red wine, deli meats,
sausage, sauerkraut) as well as other catecholaminergic
drugs (ephedrine, pseudoephedrine, amphetamines, and
other monoamine antidepressants).
27) A discontinuation syndrome occurs most frequently with
Paroxetine, Sertraline, duloxetine, and venlafaxine when
abruptly stopped.
28) Fluoxetine is rarely associated with a discontinuation
syndrome due to its very long half-life (fluoxetine is often
used for SSRI discontinuation syndrome).
29) Trazodone: Risk of priapism “traza-BONE”
30) Trazodone has minimal anticholinergic activity and is a good
choice for elderly patients (but there is a risk for falls due to

76
alpha 1 antagonism and associated orthostatic
hypotension)
31) In patients with Bipolar Depression: Best choices are
Lithium, Quetipaine, Olanzapine-Fluoxetine combination,
Lurasidone, Lamotrigine, or Aripiprazole.
32) Before increasing the dose of antidepressants, ensure that
the antidepressant treatment has been administered for a
sufficient duration and at a sufficient dose. At least four (4)
weeks are needed before it can be concluded that a patient
is partially responsive or unresponsive to a specific
intervention. No treatment should continue unmodified if
there has been no symptomatic improvement after four (4)
weeks.
33) Serotonin Syndrome: Seen with TCAs, MAOIs, SSRIs, SNRIs,
Triptans, Linezolid, Methylene blue, meperidine, tramadol,
dextromethorphan, fentanyl, St johns wort, MDMA
ANTIPSYCHOTICS
1) Clozapine ANC Monitoring: Weekly for 6 months, then
biweekly for 6 months then monthly after 12 months
2) Neuroleptic Malignant Syndrome (NMS): Patient starts
typical or atypical antipsychotic then develops delirium,
fever, muscle rigidity, and extremely elevated CPK.
3) NMS can be caused by antipsychotics, phenothiazine
antiemetics (promethazine, prochlorperazine),
metoclopramide, or abrupt discontinuation of L-dopa.

77
4) NMS Treatment: Stop antipsychotic and administer
intravenous fluids (IVF). Also, use cooling blankets,
dantrolene, and/or bromocriptine if needed
5) Antipsychotics increase risk of extrapyramidal symptoms
(EPS). Typical antipsychotics are associated with higher
risk compared to atypical antipsychotics.
6) EPS includes Acute Dystonia, Pseudoparkinsonism,
Akathisia, and Tardive Dyskinesia.
7) Acute dystonia (painful muscle spasms and contractions)
can be lethal if laryngeal muscles involved.
8) Treatment of acute dystonia: Intramuscular benztropine
(Cogentin) or diphenhydramine (benadryl)
9) Tardive dyskinesia: Repetitive, involuntary movements
of the limbs, torso, and fingers. Grimacing, tongue
movements, lip smacking, lip puckering, pursing of lips,
excessive eye blinking
10) Treatment of Tardive Dyskinesia: Decrease dose or stop
the offending agent. Try one of the new treatments
available. If this is not possible, try clozapine.
11) Akathisia: Restlessness, can’t sit still, feel like they
always need to be moving, rocking back and forth in
chair.
12) Treatment of Akathisia: Propranolol.
13) Clozapine and Olanzapine are the most likely to cause
metabolic syndrome (insulin resistance, glucose
abnormalities, dyslipidemia), worsen diabetes, or even
precipitate diabetic ketoacidosis.

122
SIDE EFFECTS: Peripheral Edema, Dizziness, Fatigue, Ataxia,
Weight Gain
RARE SIDE EFFECTS: Hypersensitivity skin reactions,

angioedema, rhabdomyolysis
NOTABLE INTERACTIONS: Reduced absorption with antacids;

Additive sedative effects when used with other sedating
medications
PREGNANCY: More safety data needed
BREASTFEEDING: More safety data needed
FDA INDICATIONS:
1) Diabetic Peripheral Neuropathy
2) Neuropathic Pain
3) Post-herpetic neuralgia
4) Partial Seizures
5) Fibromyalgia
Off label: Generalized Anxiety Disorder, Alcohol withdrawal,
Benzodiazepine withdrawal, cannabis use disorder, and
restless leg syndrome
ADDITIONAL INFORMATION:
• Pregabalin is structurally similar to Gabapentin but more
potent with greater bioavailability.
• Pregabalin is a schedule V controlled substance due to
potential for abuse/dependence (abrupt withdrawal can
cause insomnia, nausea, diarrhea, headache)

123
LITHIUM
HALF-LIFE: 18-24 hours
INITIAL DOSE: 300mg-600mg PO per day (divided doses)
TARGET DOSING RANGE: 600mg-1,200mg per day (Target

level 0.8-1.0 mEq/L)
BEST TIME TO DOSE: Any
HOW TO DOSE: Initial 300mg-600mg at bedtime or divided in

two doses. Gradually increase dose to target serum level of
0.6-1.0 mEq/L. Max dose is generally 2,400mg/day.
SIDE EFFECTS: Nausea, diarrhea, upset stomach, frequent

urination, increased thirst, tremors, headache, fatigue,
lethargy, emotional blunting/flatness, Increased white blood
cell count
PREGNANCY: Avoid if possible (but not a contraindication) –

Risk of Epstein Anomaly (cardiac defect)
BREASTFEEDING: Avoid if possible (but not a contraindication)

124
FDA INDICATIONS:
1) Acute mania
2) Bipolar Disorder Maintenance in children and adults
LITHIUM’S INTERACTIONS WITH THE BRAIN ARE COMPLEX

AND INCLUDE:
 Desensitizing presynaptic 5ht-1a auto receptors in the
raphe nuclei and thereby increasing serotonin release
 Decoupling g-protein linked production of second
messengers
 Directly increasing transcription of fast response genes
(e.g. Kreb, phos, and jun)
PROPOSED MECHANISMS OF ACTION OF LITHIUM:

 Alters sodium transport in myocytes/neurons
 Alters metabolism of catecholamines (da, ne,
epinephrine)
 Alters intracellular signaling via second messengers
(ip 3 and pkc pathways)
• Lithium is a cation metal first used in the 19th century to
treat gout and discovered by John Cade in 1949 to exert
anti-manic effects
• Lithium does not undergo metabolism and is not protein
bound. It is cleared via the kidneys.
• Benign leukocytosis is common due to demarginalization of
WBCs
• Despite being highly effective, lithium is not widely used
due to its narrow therapeutic index. Optimal plasma
concentrations for treatment of bipolar mood disorder are
0.8 to 1.2 meq/L, however, toxic signs and symptoms may
begin at concentrations as low as 1.5 meq/L and serious

125
toxicity with risk of permanent neurological injury may
occur at concentrations as low as 2.0 meq/L.
• Lithium may worsen skin conditions such as acne and
psoriasis
• Lithium use during the first trimester of pregnancy may be
associated with an increased risk of Epstein’s anomaly
(downward displacement of tricuspid valve into a
malfunctioning right ventricle) although this is
controversial. Note that lithium has been safely used in
pregnancy in select patients.
• Lithium is easily dialyzed and can be administered to
patients on hemodialysis (Give dose after dialysis
treatment)
• Caffeine may decrease lithium levels
• Lithium + Haloperidol may increase the risk of NMS and
delirium
• Lithium may cause abnormal involuntary movements
• Lithium may increase the risk of serotonin syndrome if
administered with serotonergic agents
• An increase or decrease of 300mg/day changes serum Li
levels approximately 0.25 mEq/L (rough estimate)
• Effective for chronic suicidal thoughts in bipolar and
unipolar depression
• Effective for aggressive and violent behaviors
• Increased risk of nephrogenic diabetes insipidus (usually
reversible) – may be reduced with once daily dosing
• Propranolol is an effective treatment for tremors associated
with lithium
• Bradycardia, cardiac arrhythmia, sinus node dysfunction
may be seen with lithium therapy

126
VALPROIC ACID (DEPAKOTE)
STARTING DOSE: 250mg-500mg per day
TARGET DOSING RANGE: 1000mg-1500mg PO daily
BEST TIME TO DOSE: Bedtime (for Extended release)
HOW TO DOSE: Initial 250mg-500mg PO QHS. Increase rapidly

to effective dose. Alternatively: Initial 15-20 mg/kg/day (twice
daily dosing). Target range 1000mg-1500mg daily. Target
serum level: 50mcg/mL – 125mcg/mL. Max dose generally
4000mg/day
SIDE EFFECTS: Sedation, Tremor, Dizziness, Ataxia, Asthenia

(muscle weakness), Headache, Abdominal Pain, Nausea,
Vomiting, Weight gain, Alopecia
PREGNANCY: Avoid due to Neural Tube Defects

127
PREGNANCY RISKS: Neural tube defects (spina bifida,
anencephaly, etc), Low IQ, Developmental delay
NOTE: Valproic should not be used during pregnancy except

in special cases (consult a perinatal psychiatrist). There is
little evidence that folate supplementation prevents or
SAMPLE
protects against neural tube defects (but it has not been
shown to be harmful so not a bad idea to use)
BREASTFEEDING: Avoid
FDA INDICATIONS:
1) Seizures
2) Acute Mania associated with Bipolar Disorder
3) Migraine prophylaxis
MECHANISM(S) OF ACTION:
• Blocks voltage sensitive sodium channels
• Increases brain concentrations of GABA
• Unlike many other medications, lithium and the
antiepileptics alter brain signal transduction by dampening
axonal signal transmission and by inhibiting cellular
response to excitatory signals. Part of this is mediated by
partial blockade of voltage-dependent sodium
channels. This property alone is not sufficient as anti-
epileptics which DO NOT show benefit in bipolar illness
also exhibit inhibitory effects at voltage-dependent sodium
channels.
• To date, the property best correlated with prophylaxis of
mood cycling has been depletion of the second-messenger,
triphosphoinositol (IP3).

128
• Another candidate mechanism is increased guanine
synthase kinase, type 3, activity. This enzyme plays a role in
modulating both voltage and ligand-gated sodium channels.
LABS TO OBTAIN BEFORE STARTING VALPROIC ACID:

Pregnancy test, Liver function tests, Platelet count
SAMPLE
• Valproic acid (Valproate) is considered an anticonvulsant
with mood stabilizing properties
• Use of anticonvulsants in mood disorders developed out of
research looking at the effects of anticonvulsants on seizure
activity and the process of “kindling” in mice (i.e.,
repeatedly inducing seizures via electrical stimulation
results in seizure activity even in the absence of any
stimulation).
• Valproic acid (Depakote) was found to be superior to
lithium in type II bipolar illness and in rapid cycling illness
(but anticonvulsants and lithium together showed additive
benefits)
• In manic patients, plasma levels greater than 45 ug/mL may
be required for antimanic effects (levels up to 100-125
ug/mL are often tolerated in manic patients)
• There is no consensus on the therapeutic plasma level
range for valproic acid but likely between 50-100 ug/mL
• Valproate inhibits Lamotrigine metabolism
• Combination of valproate and lamotrigine increases
lamotrigine levels and increases risk of rash and SJS/TEN
• The dose of lamotrigine must be decreased by half the
normal dose when given in combination with valproic acid
(valproic acid inhibits lamotrigine metabolism).
• Valproic acid associated with dose-related
thrombocytopenia in ~24% of patients

129
• Commonly associated with elevated liver enzymes
• Valproic acid has been associated with encephalopathy,
specifically from elevated ammonia levels
• Valproic acid + Topiramate increases risk of encephalopathy
• Valproic acid metabolized primarily by liver but by
NonCYP450 enzymes
• Valproic acid associated with Polycystic Ovarian Syndrome
(10% of women)
• Valproic acid has been shown to be effective in neuropathic
pain
CARBAMAZEPINE (TEGRETOL)
HALF-LIFE: Initially 25-65 hours, then 15 hours after 2-4 weeks
STARTING DOSE: 200mg PO BID
TARGET DOSING RANGE: 400mg-600mg PO BID

130
HOW TO DOSE: Initial 200mg PO BID. Increase by 200mg/d
every 3-4 days to target dose. Max dose 800mg PO BID
NOTABLE SIDE EFFECTS: Sedation, Fatigue, Nausea, Dizziness,

Ataxia, Diplopia, muscle incoordination, nystagmus,
Leukopenia, Thrombocytopenia, Rare Aplastic Anemia (fever,
fatigue, pallor, bleeding gums), Risk of Aplastic Anemia
increased by coadministration with clozapine, Rare
Agranulocytosis, Rash (increased risk of SJ/TEN in Asians with
HLA-B1502 allele (recommend testing for this allele prior to
prescribing carbamazepine to individuals of Asian descent),
Syndrome of Inappropriate ADH (Hyponatremia), Very rare
hepatotoxicity, Cardiac arrythmias (slows cardiac conduction),
Elevated GGT (not concerning unless >3x normal limit).
PREGNANCY: AVOID
BREASTFEEDING: AVOID
FDA INDICATIONS:
1) Seizures
2) Trigeminal Neuralgia
3) Acute mania associated with Bipolar Disorder (Equetro)
MECHANISM(S) OF ACTION: Blocks voltage sensitive sodium

channels
DRUGS THAT INCREASE CARBAMZEPINE LEVELS: Cimetidine,

Ciprofloxacin, Diltiazem, Fluoxetine, Fluvoxamine, Doxycycline,
Erythromycin (and other macrolide antibiotics), Fluconazole,
Grapefruit juice, Isoniazid (INH), Ketoconazole, TCAs,
Valproate, Warfarin, Norfloxacin, Verapamil

131
DRUGS WHOSE BLOOD LEVELS ARE DECREASED BY
CARBAMAZEPINE: Atypical antipsychotics (olanzapine,
risperidone, clozapine), Benzodiazepines, Doxycycline,
Ethosuximide, Fentanyl, Glucocorticoids, Haloperidol,
Methadone, Oral contraceptives, Phenothiazines, Phenytoin,
Sertraline, TCAs, Theophylline
• Reports of CNS toxicity (dizziness, diplopia) associated with
combination of carbamazepine and lamotrigine
• Metabolized primarily by CYP3A4 and also induces its own
metabolism by inducing CYP3A4
• Induces multiple other CYP450 isozymes as well as P-
Glycoprotein
• May test positive (false positive) for tricyclics (TCAs)
LAMOTRIGINE (LAMICTAL)

With valproic acid: 48-70 hours
With Carbamazepine: 13-14 hours
STARTING DOSE: 25mg PO daily

132
TARGET DOSING RANGE: 50mg-200mg per day
BEST TIME TO DOSE: Any (causes insomnia in some patients)
HOW TO DOSE:
If dosing without valproic acid:
>Initial 25mg PO Daily for two weeks
>Increase to 25mg PO BID for two weeks
>Increase to 50mg PO BID for two weeks
>If tolerated, can consolidate to once daily dosing
>Max dose without valproate typically 200mg per day
If dosing with valproic acid:

>Initial 25mg PO every other day for two weeks
>Increase to 25mg PO daily for two weeks then 50mg PO
daily
>Max dose with valproate typically 100mg per day
*RESTART TITRATION IF STOPPED/MISSED FOR >5 HALF
LIVES*
SIDE EFFECTS: Rash (benign), Steven-Johnson’s Syndrome/TEN,

Fatigue, Insomnia, vivid dreams, headache, nausea, upset
stomach, diarrhea, hyponatremia, DRESS Syndrome
PREGNANCY: Minimal data on safety in humans. Must weigh

risk of discontinuing vs risk of teratogenicity (which is low)
BREASTFEEDING: Minimal data on safety in

humans. Recommend bottle/formula feeding

133
FDA INDICATIONS:
1) Bipolar Disorder (maintenance/preventing mood episodes)
2) Seizures in adults and children
• Lamotrigine shows prophylactic and antidepressant
SAMPLE
properties, but is no better than placebo in treating mania
• Lamotrigine has been shown to reduce glutamate release
and modulate reuptake of monoamines including serotonin
and dopamine
• Lamotrigine has been shown to increase the time between
both depressive and manic episodes
• May be a good add-on medication with lithium for bipolar
depression
• Mostly case reports and open labeled trials support
lamotrigine in rapid cycling bipolar disorder, bipolar
depression, and mixed episodes but RCTs have not
consistently demonstrated efficacy for these conditions
• Lamotrigine carries a risk of both benign rash and Steven
Johnson’s Syndrome/TEN
• Rash associated with rapid dose escalation
• Reduce dose and slow titration if benign rash develops
• Interaction between valproic acid and lamotrigine: Valproic
acid inhibits lamotrigine metabolism; dose of lamotrigine
must be decreased by half the normal dose when given in
combination with valproic acid
• Many hormonal contraceptives decrease lamotrigine levels
– Caution during contraceptive-free “pill-free” periods as
lamotrigine levels may rise substantially. Conversely,
lamotrigine may decrease levels of hormonal
contraceptives
• Carbamazepine decreases lamotrigine levels

134
• If lamotrigine stopped/missed for >5 half-lives then strongly
consider restarting titration
TOPIRAMATE (TOPAMAX)
SAMPLE
STARTING DOSE: 12.5mg-25mg per day

HOW TO DOSE: Initial 12.5mg-25mg per day. Increase dose by

25mg per week. Max dose usually 400mg/day.
For weight loss/prevent weight gain: 50mg-150mg/day
For Mood effects: 100mg-200mg per day in divided doses

135
SIDE EFFECTS: Psychomotor slowing, Decreased

concentration, Somnolence, Fatigue, Anorexia, Kidney stone
formation, cognitive side effects (“dope-a-max” or
topamax “fog”) is a common reason for discontinuing
PREGNANCY: Minimal data on safety.
BREASTFEEDING: Minimal date on safety.
FDA INDICATIONS:
1) Epilepsy
2) Prophylaxis of Migraine headaches
Off Label: Antipsychotic-induced weight gain (usually 50mg-

150mg daily), Neuropathic pain, Borderline personality
disorder, Alcohol use disorders, Cocaine use disorders
MECHANISM(S) OF ACTION:
 Blocks voltage sensitive sodium channels
 Inhibits glutamate release
 Potentiates activity of GABA
 Blocks calcium channels
 Topiramate inhibits carbonic anhydrase (increased risk of
metabolic acidosis and kidney stones)
 Topiramate may have prophylactic properties, but
appears to exert little benefit during acute bipolar
depression or mania.
• Used in children with Lennox-Gastaut Syndrome
• Carbamazepine increases elimination of topiramate
• Topiramate may increase plasma levels of phenytoin

136
• Topiramate is a weak inhibitor of CYP219
• Topiramate is weak inducer of CYP3A4
• Alcohol enhances sedation and may increase risk of seizures

137
METHYLPHENIDATE (RITALIN,
CONCERTA)
*IR (INSTANT RELEASE) | XR (EXTENDED RELEASE)
SAMPLE
Generic Name Brand Name Usual Typical
Starting Daily Dose
Dose Range
Long-acting MPH Ritalin SR 20mg QAM 10-140mg
Ritalin LA 20mg QAM 20-120mg
Concerta 18mg QAM 18-144mg
Metadate CD 10-20mg 10-120mg

QAM
Short-acting MPH Methylphenidate 10mg q4hrs 10-140mg
Methylin 10mg q4hrs 10-140mg
Ritalin 10mg q4hrs 10-140mg
D-methylphenidate Focalin 5mg q4- 10-80mg

6hrs
Focalin XR 5-10mg 10-80mg

QAM
SAMPLE
MPH, Methylphenidate;
XR, Extended Release;
SR, Sustained Release;
LA, Long-Acting
TIME TO EFFECT: IR ~15-30min | Concerta/LA/SR ~1-2 hours

138
PEAK IN PLASMA: IR 1-2 hours | Concerta/LA/SR ~5-8 hours
DURATION OF CLINICAL ACTION: IR 4-5 hours

|Concerta/LA/SR ~ 8-12 hours
METABOLISM: Primarily Liver and Gut
WITH/WITHOUT FOOD: Methylphenidate is absorbed at a

faster rate in the presence of food
BEST TIME TO DOSE: Morning
HOW TO DOSE: (See Table Above)
SIDE EFFECTS: Insomnia, Headache, Anxiety/Nervousness,

Abdominal Pain, Anorexia, Nausea, Vomiting, Dry Mouth,
Weight loss, Seizures (rarely with PO), Psychosis (rarely with
PO), Elevated Blood Pressure, Tachycardia, Sudden death has
been reported in patients with preexisting cardiac structural
abnormalities
PREGNANCY: Avoid if possible (discuss with a medical

professional)
BREASTFEEDING: Avoid if possible (discuss with a medical

professional)
DRUG INTERACTIONS: Desipramine should be used with

extreme caution if used with methylphenidate. Antacids
increase absorption of methylphenidate. Dopamine
antagonists such as haloperidol and chlorpromazine as well as
lithium may inhibit stimulant effects. Avoid using with

139
monoamine oxidase inhibitors (MAOIs) due to risk of
hypertensive crises and malignant hyperthermia
FDA INDICATIONS:
1) Attention deficit hyperactivity disorder in children and
adults
2) Narcolepsy (R139italin, Concerta, 139Ritalin-sr,
R139italin-la)
Off label: chronic fatigue, fibromyalgia, cognitive/memory

problems
• Methylphenidate has four (4) possible stereoisomers

because it has two (2) stereoactive
centers. Dexmethylphenidate (brand name Focalin) is the
most biologically active form and also 2x more potent than
methylphenidate. Methylphenidates generally have fewer
adverse effects compared to
amphetamines. Methylphenidate was synthesized by CIBA
(now Novartis) pharmaceuticals by chemist Leandro
Panizzon, whose wife, Rita, used it for her chronic low
blood pressure. Leandro named the drug “Ritaline” after his
wife.

140
(D,L) AMPHETAMINE (ADDERALL)

*IR (INSTANT RELEASE) | XR (EXTENDED RELEASE)
TIME TO EFFECT: IR ~1 hour | XR ~1-2 hours
PEAK IN PLASMA: IR 3 hours | XR 7 hours
DURATION OF CLINICAL ACTION: IR 6-9 hours | XR 6-10 hours
WITH/WITHOUT FOOD (PO): Taking with food may delay peak

actions. pH of food alters absorption and elimination of
amphetamines. GI and urinary Acidifying agents decrease
plasma levels of amphetamines. GI and urinary alkalinizing
agents increase plasma levels of amphetamines.
STARTING DOSE: 5mg-10mg
BEST TIME TO DOSE: Morning (but depends on formulation)
HOW TO DOSE:
>IR: Initial 5mg twice daily. Increase dose by 5mg-10mg per

day each week based on response and tolerability. Typically
dose every 4-6 hours. Maximum daily dose generally 40mg-
60mg. Some patients may require higher dosages.

141
>XR: Initial 10mg every morning. Increase dose by 5mg-

10mg at weekly intervals based on response and
tolerability. Maximum daily dose generally 30mg-60mg.
Some patients may require higher dosages.

abnormalities

professional)

professional)
FDA INDICATIONS:
1) ATTENTION DEFICIT HYPERACTIVITY DISORDER IN
CHILDREN AND ADULTS
2) NARCOLEPSY
3) EXOGENOUS OBESITY

problems
NOTABLE INTERACTIONS:
• GI/Urinary Acidifying agents decrease plasma levels of
amphetamine
• GI/Urinary Alkalinizing agents increase plasma levels of
amphetamine

142
• Desipramine should be used with extreme caution if used
with amphetamine
• Dopamine antagonists such as haloperidol and
chlorpromazine as well as lithium may inhibit the stimulant
effects of amphetamines
• Amphetamines increase the pain relieving effects of
meperidine
• Avoid using with monoamine oxidase inhibitors (MAOIs)
due to risk of hypertensive crises (extremely high blood
pressures) and malignant hyperthermia (extremely high
body temperatures)
• Adderall is a mixture of the two isomeric forms of
amphetamine (D and L Amphetamine) in a ratio of 3 to 1 (D
to L)
(D) AMPHETAMINE (DEXEDRINE)

*IR (INSTANT RELEASE) | ER (EXTENDED RELEASE)
TIME TO EFFECT: IR ~1 hour | ER ~1-2 hours
PEAK IN PLASMA: IR 3 hours | ER 7 hours
DURATION OF CLINICAL ACTION: IR 3-9 hours | ER 6-10 hours

143
WITH/WITHOUT FOOD (PO): Taking with food may delay peak
actions. pH of food alters absorption and elimination of
amphetamines. GI and urinary Acidifying agents decrease
plasma levels of amphetamines. GI and urinary alkalinizing
agents increase plasma levels of amphetamines.
BEST TIME TO DOSE: Morning (but depends on formulation)
HOW TO DOSE:
>IR: Initial 5mg twice daily. Increase dose by 5mg-10mg per

day each week based on response and tolerability. Typically
dose every 4-6 hours. Maximum daily dose generally 40mg-
60mg. Some patients may require higher dosages.
>ER: Initial 5mg-10mg every morning. Increase dose by

5mg-10mg at weekly intervals based on response and
tolerability. Maximum daily dose generally 20mg-40mg.
Some patients may require higher dosages.

abnormalities. Anecdotally, patients experience less peripheral
sympathetic side effects (anxiety, tachycardia, tremors) with
dextroamphetamine compared to Adderall (also less irritability
at the end of the day)

144

professional)

professional)
FDA INDICATIONS:
adults
2) Narcolepsy

problems
• Dexedrine contains ONLY the dextro isomer of
amphetamine
LISDEXAMFETAMINE (VYVANSE)
HALF-LIFE: lisdexamfetamine (prodrug): <1 hour |

dextroamphetamine (active metabolite): 10-13 hours
(dextroamphetamine)
TIME TO EFFECT: Variable. But generally longer than other

amphetamine formulations
DURATION OF CLINICAL ACTION: Variable

145
WITH/WITHOUT FOOD (PO): Food does not affect absorption

of lisdexamfetamine, but like other amphetamines,
acidification of the urine or GI tract results in more rapid
clearance.
SAMPLE
BEST TIME TO DOSE: Morning
HOW TO DOSE: Initial 20mg-30mg every morning. Increase

dose by 10mg-20mg at weekly intervals based on response and
tolerability. Maximum daily dose generally 70mg. Some
patients may require higher dosages.

abnormalities. Anecdotally, patients experience less peripheral
sympathetic side effects (anxiety, tachycardia, tremors) with
dextroamphetamine formulations compared to amphetamine
mixed salts (also less irritability at the end of the day)
NOTABLE INTERACTIONS: Same as other amphetamines

professional)

146
professional)
FDA INDICATIONS:
adults
2) Binge eating disorder

problems
• Lisdexamfetamine is an inactive prodrug, which means it
needs to be metabolized in order for it to be active
• Lisdexamfetamine is metabolized primarily by
gastrointestinal (gut) enzymes to the active metabolite
dextroamphetamine.
• Snorting or injecting lisdexamfetamine will not result in
“highs” and therefore there is less abuse potential overall
• Anecdotally, patients experience less peripheral
sympathetic side effects and anxiety with lisdexamfetamine
(likely related to slower onset/offset of action but may also
be due to stereospecificity of dextroamphetamine (active
metabolite).
• Lisdexamfetamine 70mg is approximately equivalent to
30mg of D,L-Amphetamine (Adderall)
• Some evidence suggests lisdexamfetamine may be
beneficial for residual depressive symptoms (but
controversial as RCTs failed to show separation from
placebo in treatment resistant depression)

147
TYPICAL ANTIPSYCHOTICS
Generic Name Brand Name
SAMPLE
Chlorpromazine Thorazine
Fluphenazine Prolixin
Haloperidol Haldol
Loxapine Loxatane
Perphenazine Trilafon
Pimozide Orap
Thiothixene Navane
Trifluoperazine Stellazine
 The Typical (first-generation) antipsychotics are derived

from a number of chemical classes but differ in their affinity
(or potency) for binding to dopamine (D2) receptors in the
brain. High Potency antipsychotics include Haloperidol and
Fluphenazine whereas Low Potency antipsychotics include
Chlorpromazine.
 Unfortunately, the lower potency antipsychotics such as

chlorpromazine (Thorazine) target more than just
dopamine receptors which means they also cause a lot of
other side effects.

148
SIDE EFFECTS OF TYPICAL

ANTIPSYCHOTICS
 Sedation
 Weight Gain
SAMPLE
 Increased Appetite
 Blood Pressure Changes and Lightheadedness
 Dry Mouth
 Urinary Retention/Difficulty Urinating
 Constipation
 Blurry Vision
 Cognitive Impairment
 Slowed Movements (Parkinsonism)
 Emotional “Blunting” or “Flattening”
 Seizures (rare)
 Cardiac Arrhythmias (rare)
 Tardive Dyskinesia
RECEPTORS AND SIDE EFFECTS
 Blockade of Histamine (H1) receptors causes sedation and

weight gain
 Blockade of Adrenergic (α1) receptors causes sedation

and blood pressure changes
 Blockade of Muscarinic cholinergic (M1) receptors causes

dry mouth, urinary retention, constipation, blurry vision,
and cognitive impairment/memory impairment.

149
 High-potency antipsychotics such as fluphenazine and

haloperidol show far less sedation, hypotension, and
anticholinergic side effects, but because they are strong
dopamine blockers, they are more likely to cause side
effects from blocking dopamine (slowed movements,
cognitive problems, emotional flattening, dystonic
reactions, prolactin elevations, and tardive dyskinesia).
TARDIVE DYSKINESIA (TD)
 Tardive Dyskinesia (TD) is a hyperkinetic movement

disorder associated with long term use of antipsychotics
and/or the rapid withdrawal of antipsychotic medications.
 Symptoms include involuntary movements such as lip

smacking, eye blinking, grimacing, tongue movements, or
writhing movements of the extremities or trunk.
 All first-generation antipsychotics induce tardive dyskinesia

(TD) at an incidence rate of about 3% to 5% per year of
exposure up to 60% lifetime prevalence.
 TD is mild and non-progressive in majority of cases.
 TD results from chronic blockade of dopamine receptors in

the brain and the body’s response to such blockade over
time.

150
 Once TD is well-established, withdrawal of the offending
agent does not typically result in a return of the
nigrostriatal pathway to baseline signal transduction, i.e.
movements tend to persist.
 TD is treated by reducing the dose of the antipsychotic,

switching to an atypical antipsychotic, or using new
medications such as Valbenazine (Ingrezza).
 Clozapine has been shown to reduce TD symptoms in some

patients.
 In general, extrapyramidal symptoms are treated by

reducing the dose of antipsychotic, switching to an atypical
antipsychotic with lower dopamine blocking properties,
and/or administering an anticholinergic agent such as
benztropine (Cogentin) or diphenhydramine (Benadryl).
NEUROLEPTIC MALIGNANT SYNDROME

(NMS)
 First generation antipsychotic medications, especially high-

potency medications, may rarely induce a condition called
neuroleptic malignant syndrome (NMS). Note that
immediate withdrawal of dopamine agonists (such as L-
Dopa or Bromocriptine) can also lead to NMS.
 NMS is characterized by delirium/confusion, muscle rigidity,

rhabdomyolysis (muscle break down), fever, seizures, and
renal failure.

206
4. Intense or prolonged psychological distress at exposure
to internal or external cues.
5. Marked physiological reactions to internal or external
cues.
C. Avoidance symptoms, persistent (one or both):
1. Avoidance of or efforts to avoid distressing memories,
thoughts, or feelings about or closely associated with
the traumatic event(s).
2. Avoidance of or efforts to avoid external reminders
(people, places, conversations, activities, objects,
situations) that arouse distressing memories, thoughts,
or feelings about or closely with the traumatic event(s).
D. Negative alterations in cognitions and mood as evidenced
by two (or more) of the following:
1. Inability to remember an important aspect of the
traumatic event(s) (typically due to dissociative amnesia
and not to other factors such as head injury, alcohol, or
drugs).
2. Persistent and exaggerated negative beliefs or
expectations about oneself, others, or the world.
3. Persistent, distorted cognitions about the cause or
consequences of the traumatic event(s) that lead the
individual to blame himself/herself or others.
4. Persistent negative emotional state (e.g., fear, horror,
anger, guilt, or shame).
5. Markedly diminished interest or participation in
significant activities.
6. Feelings of detachment or estrangement from others.
7. Persistent inability to experience positive emotions (e.g.,
inability to experience happiness, satisfaction, or loving
feelings).

207
E. Marked alterations in arousal and reactivity as evidenced by
two (or more) of the following:
1. Irritable behavior and angry outbursts (with little or no
provocation) typically expressed as verbal or physical
aggression toward people or objects.
2. Reckless or self-destructive behavior.
3. Hypervigilance
4. Exaggerated startle response.
5. Problems with concentration.
6. Sleep disturbance (e.g., difficulty falling or staying asleep
or restless sleep).
F. Duration of the disturbance (Criteria B, C, D and E) is more
than one month.
G. The disturbance causes clinically significant distress or
impairment in social, occupational, or other important areas of
functioning.
H. The disturbance is not attributable to the physiological
effects of a substance (e.g., medication, alcohol) or another
medical condition.
Specify whether:
With dissociative symptoms:
Depersonalization: Persistent or recurrent experiences of
feeling detached from, and as if one were an outside
observer of, one’s mental processes or body (e.g., feeling
as though one were in a dream; feeling a sense of
unreality of self or body or of time moving slowly).
Derealization: Persistent or recurrent experiences of

unreality of surroundings (e.g., the world around the

208
individual is experienced as unreal, dreamlike, distant, or
distorted).
With Delayed Expression:

If the full diagnostic criteria are not met until at least 6
months after the event (although the onset and
expression of some symptoms may be immediate).

209
ICD-10 CODES
NEURODEVELOPMENTAL DISORDERS
Intellectual Disability
• mild F70
• moderate F71
• severe F72
• profound F73
Global dev’al delay F88
Unsp’d intel’al disabil. F79
Communication Disorders
Language disorders F80.9
Speech Sound do F80.0
Childh onset flu’cy do F80.81
Social (Pragmatic)
communication do F80.89
Unspec’d commun. Do F80.9
Autism spectrum do F84.0

237
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3) Bear, Mark F.,, Barry W. Connors, and Michael A.
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4) Berman RM, Cappiello A, Anand A, Oren DA, Heninger GR, Charney
DS, Krystal JH. Antidepressant effects of ketamine in depressed
patients. Biological Psychiatry. 2000;47:351–354.
5) Berman RM, Sanacora G, Anand A, Roach LM, Fasula MK, Finkelstein
CO, et al. Charney DS. Monoamine depletion in unmedicated
depressed subjects. Biological Psychiatry. 2002;51:469–473.
6) Bernard R, Kerman IA, Thompson RC, Jones EG, Bunney WE, Barchas
JD, et al. Watson SJ. Altered expression of glutamate signaling,
growth factor, and glia genes in the locus coeruleus of patients with
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7) Blumenfeld, Hal. Neuroanatomy Through Clinical Cases. 2nd ed.
Sunderland, Mass.: Sinauer Associates, 2010.
8) Burgdorf J, Zhang Xl, Nicholson KL, Balster RL, David Leander J,
Stanton PK, et al. Moskal JR. GLYX-13, a NMDA receptor glycine-site
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9) Chandley MJ, Szebeni A, Szebeni K, Crawford JD, Stockmeier CA,
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11) Cooper, J. R., Bloom, F. E., & Roth, R. H. (2003). The biochemical
basis of neuropharmacology (8th ed.). New York, NY, US: Oxford
University Press.
12) Higgins, E. S., & George, M. S. (2019). The neuroscience of clinical
psychiatry: the pathophysiology of behavior and mental illness.
Philadelphia: Wolters Kluwer.
13) Hillhouse, T. M., & Porter, J. H. (2015). A brief history of the
development of antidepressant drugs: from monoamines to
glutamate. Experimental and clinical psychopharmacology, 23(1), 1–
21. doi:10.1037/a0038550
14) Iversen, L. L., Iversen, S. D., Bloom, F. E., & Roth, R. H.
(2009). Introduction to neuropsychopharmacology. Oxford: Oxford
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15) Levenson, J. L. (2019). The American Psychiatric Association
Publishing textbook of psychosomatic medicine and consultation-
liaison psychiatry. Washington, D.C.: American Psychiatric
Association Publishing.
16) Mendez, M. F., Clark, D. L., Boutros, N. N. (2018). The Brain and
Behavior: An Introduction to Behavioral Neuroanatomy. United
States: Cambridge University Press.
17) Papakostas GI, Thase ME, Fava M, Nelson JC, Shelton RC. Are
antidepressant drugs that combine serotonergic and noradrenergic
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Psychiatry. 2009;16(Suppl 4):16–24.
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Simply Psych EDU © Handbook of Psychiatry

Michael T. Ingram, M.D.

Michael T Ingram Psychiatry Inc. 2021

Psychiatric Evaluation ............................... 17

Michael T Ingram Psychiatry Inc. 2021

Alcohol withdrawal seizures: ............ 26

Michael T Ingram Psychiatry Inc. 2021

Suicide Risk Assessment........................ 32

Michael T Ingram Psychiatry Inc. 2021

Depression in the Elderly: ................. 37

Michael T Ingram Psychiatry Inc. 2021

Michael T Ingram Psychiatry Inc. 2021

Benzodiazepine Equivalency Table: .. 64

Michael T Ingram Psychiatry Inc. 2021

Lithium + NSAIDs (not aspirin), ACE

Michael T Ingram Psychiatry Inc. 2021

Paroxetine (Paxil) .................................. 90

Michael T Ingram Psychiatry Inc. 2021

Pregabalin (Lyrica)............................... 121

Michael T Ingram Psychiatry Inc. 2021

Side Effects of Atypical Antipsychotics

Michael T Ingram Psychiatry Inc. 2021

Schizoaffective Disorder ................. 171

Michael T Ingram Psychiatry Inc. 2021

Panic Disorder ................................. 194

Michael T Ingram Psychiatry Inc. 2021

ICD-10 Codes ........................................... 209

Michael T Ingram Psychiatry Inc. 2021

Substance Use Disorders..................... 229

Michael T Ingram Psychiatry Inc. 2021

COMPONENTS OF THE EVALUATION

Chief Complaint Reason for visit/admission

Drug name(s), Date of first use,

Medical problems, Past Surgeries,

Psychiatric Disorders, Suicide attempts,

Michael T Ingram Psychiatry Inc. 2021

*SIGECAPS: Sleep disturbances, lack of Interest, low Energy, Concentration

**DIGFAST: Distractibility, Impulsivity, Grandiosity, Flight of Ideas, Agitation, lack

Michael T Ingram Psychiatry Inc. 2021

MENTAL STATUS EXAMINATION

APPEARANCE Does the patient appear his or her age? Is the

BEHAVIOR Is the patient cooperative? Does the patient

Michael T Ingram Psychiatry Inc. 2021

MOTOR Is the patient’s motor activity slowed/decreased

SPEECH How is the patient’s speech rate, rhythm,

MOOD How does the patient describe their mood state?

AFFECT How does the patient’s mood appear to you (i.e.,

THOUGHT CONTENT Does the patient have suicidal ideations (passive,

Michael T Ingram Psychiatry Inc. 2021

THOUGHT PROCESS Is the patient’s thought process linear, logical,

PERCEPTION Does the patient report Hallucinations, Illusions,

INTELLECT Average, above average, below average?

INSIGHT Does the patient demonstrate adequate

JUDGEMENT Does the patient have good judgement? Ask a

IMPULSE CONTROL Is the patient impulsive and unpredictable?

Michael T Ingram Psychiatry Inc. 2021

Michael T Ingram Psychiatry Inc. 2021

Michael T Ingram Psychiatry Inc. 2021

Alprazolam (Xanax) 0.5 6-20

Michael T Ingram Psychiatry Inc. 2021

DRUG INTERACTIONS TABLE

2 Warfarin Valproic acid Fluconazole Secobarbital Rifampin

2 BZDs Fluvoxamine Ketoconazole Carbamazepine Rifampin