Stahl's Self-Assessment Examination in Psychiatry

3rd Edition - 9781108710022

This book features 150 new and updated questions derived from Dr Stahl's Online Master Psychopharmacology Program which will help readers prepare for formal tests, including American Board of Psychiatry and Neurology examinations, and achieve CME and MoC credits towards ABPN reaccreditation. The self-assessment questions also offer detailed explanations of correct and incorrect answers.

Stahl's Self-Assessment Examination in Psychiatry

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Disclaimer
Introduction/Preface
CME Information
TOC
Optional Posttests and CME Certificates
Index

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Introduction/Preface

As many readers know, Essential Psychopharmacology started in 1996 as a textbook (currently in its fourth edition) on how psychotropic drugs work and then expanded to a companion Prescriber’s Guide in 2005 (currently in its sixth edition) on how to prescribe psychotropic drugs . In 2008, a website was added ( stahlonline.org ) with both of these books available online in combination with several more, including an Illustrated series of several books covering specialty topics in psychopharmacology. In 2011 a case book was added, called Case Studies: Stahl’s Essential Psychopharmacology that shows how to apply the concepts presented in these previous books to real patients in a clinical practice setting . Now comes a comprehensive set of questions and answers that we call Stahl’s Self-Assessment Examination in Psychiatry: Multiple Choice Questions for Clinicians , designed to be integrated into the suite of our mental health/psychopharmacology books and products in the manner that I will explain here.

Why a question book?

Classically, test questions are used to measure learning, and the questions in this new book can certainly be used in this traditional manner, both by teachers and by students, and especially in combination with the companion textbook in this suite of educational products, Stahl’s Essential Psychopharmacology . That is, teachers may wish to test student learning following their lectures on these topics by utilizing these questions and answers as part of a final examination. Also, readers not taking a formal course may wish to quiz themselves after studying specific topics in the specific chapters of the textbook. The reader will also note that documentation of the answers to each question in this book refers the reader back to the specific section of the textbook where that answer can be found and explained in great detail; outside references for the answers to the questions in the book are also provided.

Do questions just document learning?

For the modern self-directed learner, questions do much more than just document learning; they can also provide beacons for what needs to be studied and the motivation for doing that even before you read a textbook. Thus, questions are also tools for pre-study self-assessment. If you want to know whether you have already mastered a certain area of psychopharmacology, you can ask yourself these self-assessment questions BEFORE you review any specific area in the field. Many reading a textbook of psychopharmacology are not novices, but lifelong learners, and are likely to have areas of strength as well as areas of weakness. Getting correct answers will show you that a specific area is already well understood. On the other hand, getting lots of incorrect answers not only informs the self-motivated learner that a specific area needs further study, but can provide the motivation for that learner to fill in the gaps. Failure can be a powerful focuser for what to study and an energizing motivator for why to study.

“Adults don’t want answers to questions they have not asked”

The truth of this old saying is that taking a test AFTER study tends to feel like being forced to answer questions that the teacher has asked. However, modern readers with the mind-set of a self-directed learner want to focus on gaps in their knowledge, so looking at these same questions PRIOR to study is a way of asking the questions of yourself and thus owning them and their answers.

What is a “knowledge sandwich?”

Ideally, self-directed learners organize their study as a “knowledge sandwich” of meaty information lying between two slices of questions. The questions in this book can be the first slice of questioning, followed by consuming the “meat” of the subject material in any textbook, including Stahl’s Essential Psychopharmacology , or if you prefer, from a lecture, course (such as the integrated Neuroscience Education Institute’s annual Psychopharmacology Congress), journal article, whatever. At the end of studying, another slice of testing shows whether learning has occurred, and whether performance has improved. You can utilize, for example, the continuing medical education (CME) tests that accompanies Stahl’s Essential Psychopharmacology to test yourself after studying and document your learning (available at neiglobal.com ). The rationale for this instructional design is also discussed in another one of our books, Best Practices in Medical Teaching , published in 2011. The self-assessment questions, additional “meaty” content on all the subject areas, plus posttests are also available as the “Master Psychopharmacology Program” at neiglobal.com for those who prefer online learning rather than a textbook.

Recertification/maintenance of certification by the American Board of Psychiatry and Neurology (ABPN)

Utilizing self-assessment questions as the first “slice” of the learning “sandwich” is not just theoretical, but is gaining prominence among expert educators these days, and indeed is now part of the requirements for maintenance of certification (MOC) in a medical specialty in the USA, including by the ABPN, which has accepted the questions in this book not only for ABPN CME requirements but also for their SA/self-assessment activity requirement, a sort of pretest.

Is your learning unforgettable?

Finally, and perhaps most importantly, tests prevent forgetting. Thus, the self-assessment questions here actually create long-term remembering, and do not just document that initial learning has occurred. It is a sorry fact that learning that occurs following one exposure/reading of material is rapidly forgotten. We have discussed this in the accompanying book in this series Best Practices in Medical Teaching . Perhaps 50% of what you learn after a single exposure to new, complex information is forgotten in 3–8 days, with some studies suggesting that little or nothing is remembered in 2 months! Exposing yourself to new material over time in bite-sized chunks and encountering the material again at a later time leads to more retention of information than does learning in a large bolus in a single setting, a concept sometimes called interval learning or spaced learning. Research has shown that when the re-exposure is done not as a review of the same material in the same manner, but as a test, retention is much enhanced. This results in the most efficient way of learning because the initial encoding (reading the material or hearing the lecture the first time) is consolidated for long-term retention much more effectively and completely if the re-exposure is in the form of questions. Thus, questions help you remember, and we hope that you utilize this book to maximize the efficiency of your learning to leverage the time you are able to put into your professional development.

How do you use this book?

To use this book, simply look on every right-hand page where you will see the question appear with a multiple choice format for the answer. Read the question, answer the question either in your head, on the page, or on another piece of paper. Then, turn the page and on the left hand will appear not only the correct answer, but also an explanation of why the correct answer is correct, why the incorrect answers are incorrect, and references that document the correct answers, both in the companion textbook Stahl’s Essential Psychopharmacology and elsewhere. The reader will also see at this time what peers who have already taken this test thought was the correct answer. While taking a test, the examinee is usually curious about how (s)he is doing, how many peers get a question right, and, if the wrong answer was selected, how many peers also selected that answer wrongly. Such information can provide motivation, either as reinforcement for correct answers (yes!) or to drive the reader to understand the correct answer and never to feel the sting of missing that question again (ouch!).

So, it is with the greatest wishes for your successful journey throughout psychiatry and psychopharmacology that I present this question book to you as one of the tools for your professional development, as well as for your fascination, learning, and remembering!

Stephen M. Stahl, MD, PhD

In memory of Daniel X. Freedman, mentor, colleague, and scientific father.

CME Information

Release/expiration dates

Released: October, 2018
CME credit expires: December 31, 2020

Overview

These case-based questions, divided into 10 core areas of psychiatry, will help you identify areas in which you need further study. Each question is followed by an explanation of the answer choices and a list of suggested reference materials (recommended resources).

Learning objectives

After completing the entire book, you should be better able to:

Diagnose patients presenting with psychiatric symptoms using evidence-based standards
Optimize the use of available psychiatric treatments to improve patient outcomes
Integrate recent advances in diagnostic and treatment strategies into clinical practice

Accreditation and credit designation statements

The Neuroscience Education Institute (NEI) is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide continuing medical education for physicians.

NEI designates this enduring material for a maximum of 16.0 AMA PRA Category 1 Credits™. Physicians should claim only the credit commensurate with the extent of their participation in the activity. A posttest score of 70% or higher is required to receive CME credit.

The American Society for the Advancement of Pharmacotherapy (ASAP), Division 55 of the American Psychological Association, is approved by the American Psychological Association to sponsor continuing education for psychologists. ASAP maintains responsibility for this program and its content.

The American Society for the Advancement of Pharmacotherapy designates this program for 16.0 CE credits for psychologists.

Nurses and Physician Assistants : for all of your CE requirements for recertification, the ANCC and NCCPA will accept AMA PRA Category 1 Credits™from organizations accredited by the ACCME. The content of this activity pertains to pharmacology and is worth 16.0 continuing education hours of pharmacotherapeutics.

A certificate of participation for completing this activity is available.

The content of this print monograph also exists as an online learning activity under the title “NEI Master Psychopharmacology Program Self-Assessments, 2018–2020 Edition.”

ABPN–Maintenance of Certification (MOC)

The American Board of Psychiatry and Neurology (ABPN) has reviewed Stahl’s Self-Assessment Examination in Psychiatry: Multiple Choice Questions for Clinicians, Third Edition enduring activity and has approved this program as part of a comprehensive lifelong learning and self-assessment program, which is mandated by the American Board of Medical Specialties (ABMS) as a necessary component of maintenance of certification. This activity awards 16.0 Self-Assessment Category 1 CME credits.

More information about ABPN’s Maintenance of Certification Program for psychiatry is available at www.abpn.com/maintain-certification

Instructions

The chapters of this book can be completed in any order. You are advised to read each question carefully, formulate an answer, and then review the answer/explanation on the following page. The estimated time for completion of the entire activity (including optional posttests and CME evaluations) is 16.0 hours.

Optional posttest and CME credit instructions

The optional posttests with CME credits are available online for a fee (waived for NEI members). For participant ease, each chapter has its own posttest and certificate. NOTE : the book as a whole is considered a single CME activity and credits earned must be totaled and submitted as such to other organizations.

To receive a certificate of CME credit or participation:

1. Complete a chapter posttest : available only online at neiglobal.com/CME (under “Book” )
2. Print the chapter certificate: if a score of 70% or more is achieved

Questions? call 888-535-5600, or email CustomerService@neiglobal.com

Peer review

The content has been peer-reviewed by an MD specializing in psychiatry (excepting “Dementia and Cognitive Function and its Treatment,” peer-reviewed by a PhD specializing in dementia) to ensure the scientific accuracy and medical relevance of information presented and its independence from commercial bias. NEI takes responsibility for the content, quality, and scientific integrity of this CME activity.

Disclosures

All individuals in a position to influence or control content are required to disclose any financial relationships. Although potential conflicts of interest are identified and resolved prior to the activity being presented, it remains for the participant to determine whether outside interests reflect a possible bias in either the exposition or the conclusions presented.

Disclosed financial relationships with conflicts of interest have been reviewed by the NEI CME Advisory Board Chair and resolved.

(From original online learning activity “NEI Master Psychopharmacology Program Self-Assessments, 2018–2020 Edition” )

Authors

Meghan M. Grady, BA
Director, Content Development, Neuroscience Education Institute, Carlsbad, CA
No financial relationships to disclose.
Elizabeth S. Lukins, BS
Medical Writer Associate, Neuroscience Education Institute, Carlsbad, CA
No financial relationships to disclose.
Debbi A. Morrissette, PhD
Adjunct Professor, Biological Sciences, Palomar College, San Marcos, CA
Senior Medical Writer, Neuroscience Education Institute, Carlsbad, CA
Editor, E-Cronicon Psychology and Psychiatry
No financial relationships to disclose.
Sabrina K. Segal, PhD
Adjunct Professor, Department of Psychology, Arizona State University, Tempe, AZ
Adjunct Professor, Department of Psychology, California State University Channel Islands, Camarillo, CA
Adjunct Professor, Biological Sciences, Palomar College, San Marcos, CA
Medical Writer, Neuroscience Education Institute, Carlsbad, CA
No financial relationships to disclose.

Peer reviewer

Donna M. Wilcock, PhD
Sweeney-Nelms Professor, Alzheimer’s Disease Research Center, Sanders-Brown Center on Aging, Department of Physiology, University of Kentucky College of Medicine, Lexington, KY
Research/Grant: Lilly
Speakers Bureau: AC Immune, Alector
The remaining Peer Reviewers have no financial relationships to disclose.

Disclosure of off-label use

This educational activity may include discussion of unlabeled and/or investigational uses of agents that are not currently labeled for such use by the FDA. Please consult the product prescribing information for full disclosure of labeled uses.

Cultural and linguistic competency

A variety of resources addressing cultural and linguistic competency can be found at this link: nei.global/cmeregs

Providers

This activity is provided by NEI.

Additionally provided by the ASAP.

Support

This activity is supported solely by NEI.

Chapter 1	Chapter 6
Basic Neuroscience	Chronic Pain and its Treatment
Chapter 2	Chapter 7
Psychosis and Schizophrenia and Antipsychotics	Disorders of Sleep and Wakefulness and Their Treatment
Chapter 3	Chapter 8
Unipolar Depression and Antidepressants	Attention Deficit Hyperactivity Disorder (ADHD) and its Treatment
Chapter 4	Chapter 9
Bipolar Disorder and Mood Stabilizers	Dementia and Cognitive Function and its Treatment
Chapter 5	Chapter 10
Anxiety Disorders and Anxiolytics	Substance Use and Impulsive Compulsive Disorders and their Treatment

Optional Posttests and CME Certificates

Index

Instructions and Study Guide

CME Credit Expires: December 31, 2020.

Posttests will remain available indefinitely, for your personal enrichment.

The optional online posttests with CME credits are available for a fee (waived for NEI members). For participant ease, each chapter has its own posttest and certificate. NOTE: the book as a whole is considered a single CME activity and credits earned must be totaled and submitted as such to other organizations.

To receive a certificate of CME credit or participation:

1. Complete a chapter posttest: available only online at neiglobal.com/CME (under “Book” )
2. Print the chapter certificate: if a score of 70% or more is achieved

Questions? call 888–535-5600, or email CustomerService@neiglobal.com

Study guide for online posttests

The posttest questions have been provided below solely as a study tool to prepare for your online submissions. Posttests can only be submitted online. If you do not have access to a computer, contact customer service at 888-535-5600.

Basic Neuroscience

1. A signal transduction cascade passes its message from an extracellular first messenger to an intracellular second messenger. In the case of the G-protein-linked systems, the second messenger is a:

A. Ion

B. Hormone

C. Chemical

D. Kinase enzyme

2. A receptor with four transmembrane regions changes conformation as GABA binds. Which system is this process describing?

A. Presynaptic transporter

B. Ligand-gated ion channel

C. Voltage-sensitive ion channel

3. Which of the following are involved in regulating neurotransmission via excitation–secretion coupling?

A. Voltage-sensitive sodium channels

B. Voltage-sensitive calcium channels

C. Both A and B

D. Neither A nor B

4. What are the molecular mechanisms of epigenetics?

A. Molecular gates are opened by acetylation and/or demethylation of histones, allowing transcription factors access to genes, thus activating them.

B. Molecular gates are opened by deacetylation and/or methylation, allowing transcription factors access to genes, thus activating them

C. Molecular gates are closed by deacetylation and/or methylation, preventing access of transcription factors to genes, thus silencing them.

D. A and C

Psychosis and Schizophrenia and Antipsychotics

1. A 21-year-old man has just been diagnosed with schizophrenia. What pattern of cognitive functioning prior to psychosis onset would you be most likely to find?

A. Normal cognitive functioning during premorbid and prodromal phases

B. Impaired cognitive functioning that is stable across premorbid and prodromal phases

C. Impaired cognitive functioning premorbidly with further decline during the prodromal phase

2. A major current hypothesis for the cause of schizophrenia proposes that N -methyl- d -aspartate (NMDA) receptors may be:

A. Hypofunctional

B. Hyperfunctional

3. A 34-year-old man is initiated on an atypical antipsychotic for the treatment of schizophrenia. The majority of atypical antipsychotics:

A. Have higher affinity for dopamine 2 receptors than for serotonin 2A receptors

B. Have higher affinity for serotonin 2A receptors than for dopamine 2 receptors

4. A 44-year-old woman with schizophrenia has developed tardive dyskinesia after taking haloperidol 15 mg/day for 2 years. Which of the following would be the most appropriate pharmacologic mechanism to manage her tardive dyskinesia?

A. Antagonism at serotonin 2A receptors

B. Antagonism of beta adrenergic receptors

C. Inhibition of vesicular monoamine transporter 2

Unipolar Depression and Antidepressants

1. A patient with major depressive disorder has not responded to two adequate trials of antidepressant monotherapy. Which of the following has the best evidence of efficacy for augmenting antidepressants in patients with inadequate response?

A. Atypical antipsychotic

B. Buspirone

C. Stimulant

2. A 31-year-old married man has been taking an SSRI for his depression. He discloses that although his mood has improved, he is experiencing sexual dysfunction that is affecting his relationship with his wife. What pharmacological treatment option might be appropriate to address his sexual dysfunction?

A. 5HT2 antagonist

B. 5HT3 antagonist

C. 5HT6 antagonist

3. Symptoms of reduced positive affect (depressed mood, anhedonia, loss of energy) are hypothetically more likely to respond to agents that enhance:

A. Dopamine and possibly norepinephrine

B. Norepinephrine and possibly serotonin

C. Serotonin and possibly dopamine

4. Which of the following foods must be avoided by patients taking MAOIs?

A. Aged cheeses

B. Bottled beer

C. Fresh fish

D. All of the above

E. None of the above

Bipolar Disorder and Mood Stabilizers

1. Sam is a 31-year-old patient who presents with a major depressive episode. He has previously been hospitalized and treated for a manic episode but is not currently taking any medication. The agents with the strongest evidence of efficacy in bipolar depression are:

A. Lamotrigine, lithium, quetiapine

B. Olanzapine–fluoxetine, lurasidone, lamotrigine

C. Quetiapine, olanzapine–fluoxetine, lurasidone

D. Lurasidone, lamotrigine, lithium

2. Patricia is a 39-year-old patient with bipolar I disorder. She has been maintained on 1200 mg/day of lithium. She was doing well for a long time and had even been able to lose the weight she had initially gained with lithium. She lost her job as a postal service worker 6 months ago and has been feeling depressed ever since. You augment her with 300 mg/day of quetiapine, but after several weeks she complains of weight gain and wants to change medications. Blockade of which two receptors was most likely responsible for this weight gain induced by quetiapine?

A. Serotonin 2C and histamine 1

B. Serotonin 2A and muscarinic 3

C. Muscarinic 1 and serotonin 6

D. Dopamine 2 and alpha 1 adrenergic

3. Diane is a 31-year-old patient with bipolar I disorder who frequently exhibits impulsive symptoms of mania including risk-taking and pressured speech during her manic episodes. Compared to a healthy brain, neuroimaging of this patient’s brain during a no-go task (designed to test response inhibition) would likely show:

A. Increased activity in the dorsolateral prefrontal cortex

B. Increased activity in the orbitofrontal cortex

C. Decreased activity in the orbitofrontal cortex

4. Steven is a 29-year-old patient with bipolar II disorder who tends to endorse some manic symptoms during depressive episodes. Of the following symptoms, which is the most common subsyndromal mania symptom in patients during a major depressive episode with mixed features?

A. Psychomotor agitation

B. Decreased need for sleep

C. Inflated self-esteem

D. Elevated mood

E. High-risk behavior

Anxiety Disorders and Anxiolytics

1. A 51-year-old male veteran with chronic PTSD has agreed to begin pharmacotherapy for his debilitating symptoms of arousal and anxiety associated with his experiences in Iraq 2 years ago. Which of the following would be appropriate as first-line treatment?

A. Paroxetine

B. Paroxetine or lorazepam

C. Lorazepam or quetiapine

D. Paroxetine, lorazepam, or quetiapine

2. Which of the following pharmacotherapy options has been theorized as a potential pre-emptive treatment to the development of PTSD?

A. N -methyl- d -aspartate (NMDA) agonist such as d -cycloserine

B. Alpha 2 delta ligand such as pregabalin

C. Beta adrenergic blocker such as propranolol

D. Benzodiazepine such as diazepam

3. Which of the following drugs can diminish anxiety but does NOT have sedative, hypnotic, anticonvulsant, or musculoskeletal relaxing activity?

A. Diazepam

B. Buspirone

C. Mirtazapine

D. Haloperidol

Chronic Pain and its Treatment

1. A young man arrives at the emergency room in great pain after receiving a chemical burn during an accident at work. Which primary afferent neurons would have responded to the chemical stimulus to produce nociceptive neuronal activity?

A. A beta fiber neurons

B. A delta fiber neurons

C. C fiber neurons

2. Does the official diagnosis of fibromyalgia require a tender point diagnosis?

A. Yes

B. No

3. Which of the following statements is true?

A. SSRIs may have inconsistent effects on pain because serotonin can both inhibit and facilitate ascending nociceptive signals

B. SSRIs may worsen pain because serotonin can facilitate but not inhibit ascending nociceptive signals

C. SSRIs generally alleviate pain because serotonin can inhibit but not facilitate ascending nociceptive signals

D. SSRIs generally have no effect on pain because serotonin neither facilitates nor inhibits nociceptive signals

Disorders of Sleep and Wakefulness and their Treatment

1. A 52-year-old female patient with shift work disorder exhibits excessive daytime sleepiness that is interfering with her ability to perform duties as a firefighter. She is initiated on armodafinil with good therapeutic response. Modafinil, and its R -enantiomer armodafinil, are hypothesized to promote wakefulness and increase alertness by:

A. Decreasing norepinephrine

B. Decreasing hypocretin/orexin

C. Increasing histamine

D. All of the above

E. None of the above

2. Sheila is a 41-year-old woman who recently underwent diagnostic testing for obstructive sleep apnea. Results show that this patient has an apnea–hypopnea index (AHI) of 37. An AHI of 37 is indicative of:

A. No sleep apnea

B. Mild sleep apnea

C. Moderate sleep apnea

D. Severe sleep apnea

3. A clinician is planning to prescribe eszopiclone for a 51-year-old male patient with insomnia. What is the correct starting dose for this patient?

A. 0.5 mg/night

B. 1 mg/night

C. 2 mg/night

D. 3 mg/night

4. A 13-year-old male patient has been brought to the clinic by his parents for evaluation. The patient typically sleeps for 11 or more hours a day (yet still exhibits excessive daytime sleepiness), eats excessive amounts of food, and demonstrates disinhibited behaviors. This patient most likely has:

A. Idiopathic hypersomnia

B. Narcolepsy without cataplexy

C. Kleine–Levin syndrome

Attention Deficit Hyperactivity Disorder (ADHD) and its Treatment

1. According to DSM-5 criteria, what is the maximum age threshold for symptom onset when making a diagnosis of attention deficit hyperactivity disorder (ADHD)?

A. 8

B. 10

C. 12

D. 14

2. Which of the following drugs are transported into neurons via the dopamine transporter?

A. Amphetamine

B. Atomoxetine

C. Methylphenidate

D. A and B

E. A, B, and C

3. Aggregate data suggest that, at the class level, the effect size of stimulants is:

A. Smaller than that of non-stimulants

B. Approximately the same as that of non-stimulants

C. Larger than that of non-stimulants

Dementia and Cognitive Function and its Treatment

1. Mike is a 50-year-old accountant with a family history of Alzheimer’s disease. He recently had amyloid positron emission tomography (amyloid PET) neuroimaging done and, although he currently exhibits no behavioral symptoms of Alzheimer’s disease, Mikes’s amyloid PET scans revealed accumulation of beta amyloid protein throughout cortical and limbic areas of his brain. Although much research is yet to be done, data indicate that the normal physiological role of amyloid beta protein may include:

A. Blood vessel repair functions

B. Antimicrobial functions

C. Both of the above

2. Harriet is a 69-year-old patient recently diagnosed with probable Alzheimer’s disease. This patient would like to start treatment with a cholinesterase inhibitor; however, she has been a chain smoker for over 50 years and refuses to give up the habit. Which of the following medications would not be appropriate for this patient, given her smoking habit?

A. Donepezil

B. Galantamine

C. Rivastigmine

D. None of these medications should be prescribed to a patient who smokes

E. There are no contraindications due to smoking for these medications

3. Pete is a 46-year-old man with progressive amnesic memory loss and cognitive deficits beginning approximately 1 year ago. Neuropsychiatric testing shows moderate cognitive impairment not attributable to any medical or psychiatric condition. Amyloid PET imaging indicates that this patient has amyloid beta protein accumulation in his brain and genetic testing has revealed that he carries an Alzheimer’s-associated mutation in the presenilin gene. What would be the most likely diagnosis for this patient according to the National Institute on Aging and Alzheimer’s Association 2011 diagnostic criteria for dementia?

A. Possible Alzheimer’s dementia

B. Probable Alzheimer’s dementia with increased level of certainty

C. Alzheimer’s dementia

Substance Use and Impulsive Compulsive Disorders and their Treatment

1. Your 16-year-old son is thrilled when he wins the 100-meter dash in an important high school competition. This “natural high” is most likely associated with inducing dopamine release in his mesolimbic pathway and in his:

A. Hypothalamus

B. Amygdala

C. Hippocampus

D. Cerebellum

E. Motor cortex

2. Lisa, who is 13, has been staying up later than usual, complaining that she can’t sleep. Sometimes during the day, she locks herself in her room for hours, only coming out to use the bathroom. Recently, her mother discovered boxes of hidden cereal, chips, and cookies in her closet. Her mother suspects that Lisa has an eating disorder, but she is not sure if Lisa is vomiting or not, and her weight appears to be normal. Upon psychiatric evaluation, Lisa has negative affect, functional impairment, elevated thin-ideal internalization, and body dissatisfaction. She says she is dieting, but that she is not fasting. Which eating disorder is she at high risk for?

A. Anorexia nervosa

B. Bulimia nervosa

C. Binge-eating disorder

3. A 28-year-old painter presents with a severe drinking problem and you affirm the need for pharmacotherapy. When you suggest naltrexone, the curious artist would like to know how this will help. Which might you use as part of your explanation?

A. Naltrexone blocks mu-opioid receptors to reduce the euphoria you might normally experience with heavy drinking

B. Naltrexone blocks metabotropic glutamate receptors (mGluR) to reduce the euphoria you might normally experience with heavy drinking

C. Naltrexone stimulates mu-opioid receptors to the euphoria you might normally experience with heavy drinking

D. Naltrexone stimulates mGluR receptors to the euphoria you might normally experience with heavy drinking

4. Clara is at a party with some friends and decides to try “Molly.” She was told that “Molly” is the pure form of Ecstasy (3,4-methylenedioxymetamphetamine), lacking many of the harmful additives that can be found in Ecstasy. Upon taking the pill, Clara notices that while she is in a state of excited delirium, she has a nosebleed, she is sweating profusely, and she feels nauseous. She is disoriented, and wonders why she is feeling so horrible after taking the pure form of the drug. Her symptoms are most likely attributed to:

A. A synthetic cathinone, such as methylone

B. Caffeine

C. Methamphetamine

Index

A-beta fiber neurons

A-beta peptides

A-delta fiber neurons

A4 clinical trial

–

absolute neutrophil count (ANC)

acetaminophen

acetylcholine

Alzheimer’s disease

action potential

ion flow

propagation

acute pain

ADHD see attention deficit hyperactivity disorder

adrenocorticotropic hormone (ACTH)

aerobic exercise, ADHD

affect

aggressive behavior

agitation

,

agnosia

agomelatine

agonists

–

,

akathisia

alcohol abuse

,

ADHD

,

reduced-risk drinking

treatment

alcohol withdrawal syndrome

allodynia

alpha 1 adrenergic receptor antagonists

,

alpha 2 adrenergic receptor agonists

alpha 2 delta ligands

alprazolam

Alzheimer’s disease

,

acetylcholine

amyloid PET

bacteriuria

biomarkers

,

depression

diagnosis

,

immunotherapy

–

presymptomatic stage

smoking

,

treatment

,

amantadine

amitriptyline

amnesiac mild cognitive impairment

AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) receptors

amphetamine

,

ADHD

amygdala

,

amyloid beta

,

–

,

amyloid positron emission tomography (amyloid PET)

,

anaerobic exercise, ADHD

anhedonia

,

anorexia nervosa

antagonists

anterior cingulate cortex

anticholinergic medication

antidepressants; see also ; SNRIs

bipolar disorder

overdose

pregnancy

side effects

,

therapeutic effects

tricyclic

antioxidants

antipsychotics

,

; see also specific drugs

atypical

,

high doses

long-acting injectable

oral

plasma levels

polypharmacy

properties

side effects

,

switching

anxiety disorder

,

treatment

,

apathy

,

aphasia

apnea–hypopnea index (AHI)

,

apoptosis

appetite-affecting hormones

apraxia

,

aripiprazole

bipolar disorder

,

major depressive disorder

schizophrenia

,

armodafinil

,

asenapine

,

atomoxetine

,

ADHD

,

attention deficit hyperactivity disorder (ADHD)

,

alcohol abuse

cortical brain development

diagnosis

dopamine transporter defect

drug release

inattentive subtype

,

maximum age threshold

,

substance abuse

treatment

,

–

,

atypical antipsychotics

,

; see also specific drugs

auditory hallucinations

,

axonal zone

–

back pain, chronic

,

bacteriuria

behavioral changes

benign ethnic neutropenia (BEN)

benzodiazepines

,

beta adrenergic blockers

beta amyloid

,

–

,

binge-eating disorder

,

bipolar disorder

atypical antipsychotics

brain activity

children

,

cognitive impairment

lithium

,

mood stabilizers

pattern of episodes

pregnancy

quetiapine

rapid-cycling

side effects of treatment

symptoms

,

treatment

,

withdrawal dyskinesias

bipolar storm

brain-derived neurotrophic factor (BDNF)

,

breast secretions

brexpiprazole

bulimia nervosa

buprenorphine

,

bupropion

–

,

teratogenicity

–

buspirone

anxiety

major depressive disorder

C fiber neurons

C-reactive protein

caffeine

calcium channels

blocking

voltage-sensitive

–

,

cannabidiol

cannabinoid receptors

cannabinoids, synthetic

carbamazepine

cardiac arrhythmia

cariprazine

,

catechol-O-methyltransferase (COMT)

cathinones, synthetic

cheese, tyramine in

–

chemical neurotransmission

chlorpromazine

cholinesterase inhibitors

dementia

,

chronic obstructive pulmonary disease (COPD)

circadian rhythms

disruption

phase-advanced

citalopram

clomipramine

OCD

side effects

–

clonazepam

,

–

clonidine

clozapine

,

cocaine addiction

cocaine vaccine

codeine

cognitive-behavioral therapy

OCD

cognitive functioning

,

ADHD

bipolar disorder

impairment

restructure

schizophrenia

slowing

combined central nervous system (CNS) depression

comorbidity

compulsivity

congenital heart defects

–

cortical brain development, ADHD

corticotropin-releasing hormone (CRH)

cortisol

Crh gene

cyclobenzaprine

cycloserine

PTSD

,

CYP450 1A2

CYP450 2D6

CYP450 3A4

cytokines

–

role in depression

d-cycloserine see cycloserine

daytime sleepiness

,

deacetylation

delirium tremens

dementia

,

; see also Alzheimer’s disease

comorbid illnesses

differential diagnoses

frontotemporal

Lewy bodies

dendritic membrane

–

dentate gyrus, hippocampus

depression; see also major depressive disorder

Alzheimer’s disease

late-onset

SSRIs

treatment

depression-executive dysfunction

desipramine

diabetic peripheral neuropathy

Diagnostic and Statistical Manual of Mental Disorders (DSM-5)

,

DIAN-TU clinical trial

–

diazepam

,

distractibility

disulfiram

dizziness

antipsychotics

PTSD

tricyclic antidepressants

donepezil

,

dopamine

deficiency

natural highs

,

role in depression

dopamine D2 receptors

blockade

,

partial agonists

prolactin release

upregulation

dopamine reuptake transporters (DAT)

ADHD

,

cocaine addiction

defect

dorsal striatum

dorsolateral prefrontal cortex

,

doxepin

,

DSM-5

,

duloxetine

,

hepatitis, chronic

pain relief

PTSD

dyskinesias

early life stress

eating disorders

,

Ecstasy (3,4-methylenedioxymetamphetamine)

,

electrical communication

electrocardiography (ECG)

electroconvulsive therapy (ECT)

emotional blunting

epigenetics

,

escitalopram

OCD

eszopiclone, insomnia

,

excitation–secretion coupling

–

excitotoxicity

exercise, ADHD

extrapyramidal side effects

,

fear extinction

fear response

fibromyalgia

diagnosis

,

treatment

treatment-resistant

5-HT see serotonin

fluoxetine

,

major depressive disorder

OCD

side effects

–

side effects in pregnancy

–

flupenthixol

fluphenazine

flurazepam

fluvoxamine

OCD

food addiction

free polysomes

–

free radicals

frontotemporal dementia

G-protein-linked signal transduction cascade

,

GABA (gamma-aminobutyric acid)

binding

–

,

inactivation

wakefulness promotion

GABA-A receptors

gabapentin

,

hepatitis

galactorrhea

galantamine

,

gastrointestinal disorder

generalized anxiety disorder see anxiety disorder

genetic testing

genetics

ghrelin

glutamate

inhibition of release

release, effects of serotonin

–

traumatic memory formation and extinction

glycine

glycogen synthase kinase 3b

goal-directed activity

Golgi apparatus

–

guanfacine

hallucinations

auditory

,

visual

haloperidol

,

anxiety

schizophrenia

,

hepatitis, chronic

hippocampus

,

dentate gyrus

volume

histamine

inactivation

histamine H1 receptors

blockade

,

sleep/wake cycle

histones

Huntington’s disease

hydrocodone

,

hyperactivity

hyperalgesia

hypersomnia

,

hypertensive crisis

hypnotics

,

hypomania

,

hypotension

hypothalamic pituitary adrenal (HPA) axis

hypothalamus

food addiction

sleep/wake

idiopathic hypersomnia

,

iloperidone

,

immune system

immunotherapy clinical trials, Alzheimer’s disease

–

impulsivity

,

ADHD

inattention

inflammatory markers

inositol monophosphatase (IMPase)

insomnia

,

interleukin 1

interleukin 6

internal restlessness

ion channels see ; ligand-gated ion channels

irritability

ketamine

Kleine–Levin syndrome

lamotrigine

,

bipolar disorder

,

major depressive disorder

lateral tegmental nucleus

leptin

levetiracetam

Lewy body dementia

ligand-gated ion channels

–

,

lithium

bipolar disorder

,

mechanism of action

monitoring

pregnancy

long-tern potentiation (LTP)

lorazepam

lurasidone

bipolar disorder

,

schizophrenia

magnesium

maintenance of wakefulness tests

major depressive disorder

,

; see also depression

hypomania

inflammatory markers

perimenopausal patients

response/remission/recovery/relapse/recurrence

SSRI-induced indifference

symptoms

treatment

,

treatment-resistant

,

mania

,

MAOIs (monoamine oxidase inhibitors)

,

foods to avoid

–

,

marijuana

ADHD

melatonin

early morning

receptor agonists

suprachiasmatic nucleus

memantine

,

–

,

menopause

meperidine

mesolimbic pathway

metabotropic glutamate receptors

methadone

methamphetamine

methylation

methylenedioxymetamphetamine

,

methylenetetrahydrofolate reductase (MTHFR)

methylone

methylphenidate

,

ADHD

midbrain central gray

migraines

mild cognitive impairment

,

milnacipran

mirtazapine

,

mitochondria

–

dysfunction

modafinil

,

monoamine oxidase inhibitors see MAOIs

mood stabilizers

,

morphine

multiple sleep latency tests

muscarinic M1 receptor blockade

,

muscarinic M3 receptor blockade

naloxone

,

naltrexone

,

narcolepsy

,

natural highs

,

necrosis

neurogenesis

,

neuropathic pain

,

; see also fibromyalgia

diabetic peripheral neuropathy

treatment

neuropeptide inactivation

neurotransmission

chemical

excitation–secretion coupling

–

retrograde

–

signal integration

–

synaptic

–

,

–

volume

–

neurotransmitters see specific neurotransmitters

nicotine replacement therapy

NMDA (N-methyl-d-aspartate) agonists

NMDA receptors

,

role in schizophrenia

,

nociception

,

nociceptive pain

,

non-stimulants

,

noradrenergic pathways

norepinephrine

reuptake inhibitors

role in depression

role in sleep

norepinephrine reuptake transporters (NET)

ADHD

,

nucleus accumbens

,

nucleus reticularis pontis caudalis

obsessive compulsive disorder (OCD)

,

obstructive sleep apnea

,

olanzapine

,

bipolar disorder

,

major depressive disorder

schizophrenia

,

olanzapine–fluoxetine

olfactory bulb

opioids

addiction

,

receptors

orbital frontal cortex

,

aggressive behavior

orexin

,

receptor antagonists

orthostatic hypotension

pain; see also fibromyalgia

acute

chronic

,

inhibiting transmission

neuropathic

,

nociceptive

,

widespread pain index

paliperidone

,

panic disorder

,

parabrachial nucleus

parkinsonism

,

paroxetine

OCD

PTSD

side effects

–

teratogenicity

–

periaqueductal gray

periodic limb movements

perphenazine

,

persistent pulmonary hypertension of the newborn (PPHN)

–

pharmacokinetics

phasic firing

pipothiazine

polysomnography

positive affect, reduced

positive allosteric modulation (PAM)

postnatal adaptation syndrome (PNAS)

–

posttraumatic stress disorder (PTSD)

pre-emptive treatment

prolonged exposure treatment

treatment

,

treatment-resistant

,

potassium, action potential

prazosin

prefrontal motor cortex

,

pregabalin

,

hepatitis, chronic

PTSD

pregnancy

antidepressants, adverse effects

bipolar disorder

OCD

prescription opiate addiction

presynaptic reuptake transporters

–

presynaptic transporters

,

presynaptic zone

–

primary motor cortex

prolactin

prolonged exposure treatment, PTSD

propranolol

,

protein kinase C

psychomotor retardation

psychosis

,

; see also schizophrenia

synthetic cannabinoids

PTSD see posttraumatic stress disorder

pyramidal glutamate neuron

–

quazepam

quetiapine

,

bipolar disorder

,

major depressive disorder

pregnancy

PTSD

,

schizophrenia

,

ramelteon

dopamine D2 receptors

receptors, upregulation

,

; see also ; ; dopamine D2 receptors

response/remission/recovery/relapse/recurrence, depression

retrograde neurotransmission

–

ribosomes, membrane-bound

–

risperidone

,

rivastigmine

,

rough endoplasmic reticulum

–

schizoaffective disorder

schizophrenia

,

cognitive functioning

,

drug-switching

prodromal phase

role of NMDA receptors

,

tardive dyskinesia

treatment

,

second messengers

,

sedation

benzodiazepines

,

hypnotics

tricyclic antidepressants

selective attention

selective serotonin reuptake inhibitors see SSRIs

selegiline

serotonergic pathways

–

,

serotonin serotonergic pathways

–glutamate interactions

–

inactivation

neurotransmission see serotonergic pathways

role in depression

role in sleep

serotonin 2 antagonists

serotonin 2A receptors

blockade

,

prolactin release

serotonin 2C receptors

blockade

serotonin 3 antagonists

,

serotonin 3 receptors

serotonin 6 receptor blockade

,

serotonin 7 receptor blockade

–

serotonin and norepinephrine reuptake inhibitors see SNRIs

sertraline

,

OCD

,

–

sexual dysfunction

,

SSRIs

shift-work disorder

,

treatment

,

signal transduction cascade

–

,

G-protein-linked

,

sleep cycle disorders

daytime sleepiness

,

idiopathic hypersomnia

insomnia

,

Kleine–Levin syndrome

narcolepsy

,

obstructive sleep apnea

,

periodic limb movements

phase-advanced

shift work

,

sleep/wake regulation

smoking

Alzheimer’s disease

,

cessation

SNRIs (serotonin and norepinephrine reuptake inhibitors)

,

; see also specific drugs

major depressive disorder

social anxiety disorder

sodium, action potential

sodium channels, voltage-sensitive

–

,

soma

–

spice (synthetic cannabinoid)

SSRIs (selective serotonin reuptake inhibitors); see also specific drugs

indifference induced by

major depressive disorder

,

pain relief

,

serotonin syndrome

sexual dysfunction

side effects

startle response, increased

stimulants

,

striatum

,

substance abuse

; see also specific substances

ADHD

substantia nigra

suicidal ideation

supplementary motor area

suprachiasmatic nucleus (SCN)

,

sustained attention

suvorexant

symptom severity scale (SS)

synaptic neurotransmission

–

,

–

synaptogenesis

synthetic cannabinoids

synthetic cathinones

tardive dyskinesia

,

tau protein

temazepam

tender point criteria

teratogenicity

–

,

theophylline

tonic firing

topiramate

transcranial magnetic stimulation (TMS)

transcription factors

,

tranylcypromine

–

traumatic memory formation and extinction

trazodone

,

OCD

triazolam

tricyclic antidepressants

; see also specific drugs

trigeminal/facial motor nerve

tumor necrosis factor-alpha

tyramine

–

ultradian cycles

unipolar depression

; see also major depressive disorder

valproate

bipolar disorder

,

pregnancy

vasomotor symptoms

venlafaxine

,

side effects in pregnancy

–

ventral striatum

,

ventromedial prefrontal cortex

vesicular monoamine transporter 2 (VMAT2), selective inhibitors

vilazodone

visual hallucinations

voltage-sensitive ion channels

–

,

volume neurotransmission

–

vortioxetine

wakefulness promotion

weight gain

antidepressants

,

antipsychotics

bipolar disorder

widespread pain index (WPI)

withdrawal dyskinesias

zaleplon

ziprasidone

,

zolpidem

,

zuclopenthixol

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Information on this title: www.cambridge.org/9781108710022

DOI: 10.1017/9781108590570

This publication is in copyright. Subject to statutory exception and to the provisions of relevant collective licensing agreements, no reproduction of any part may take place without the written permission of Cambridge University Press.

First published 2012

Second edition 2016

Third edition 2019

Printed in the United Kingdom by TJ International Ltd. Padstow Cornwall

A catalogue record for this publication is available from the British Library.

Library of Congress Cataloging-in-Publication Data

Names: Stahl, Stephen M., 1951–author.

Title: Stahl’s self-assessment examination in psychiatry : multiple choice questions for clinicians / Stephen M. Stahl ; editorial assistant, Meghan M. Grady.

Other titles: Self-assessment examination in psychiatry

Description: Third edition. | Cambridge, United Kingdom ; New York, NY : Cambridge University Press, 2019. | Includes index.

Identifiers: LCCN 2018042772 | ISBN 9781108710022 (paperback)

Subjects: | MESH: Mental Disorders | Nervous System Physiological Phenomena | Psychiatry–methods | Examination Questions

Classification: LCC RC457 | NLM WM 18.2 | DDC 616.890076–dc23

LC record available at https://lccn.loc.gov/2018042772

ISBN 978-1-108-71002-2 Paperback

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Every effort has been made in preparing this book to provide accurate and up-to-date information that is in accord with accepted standards and practice at the time of publication. Although case histories are drawn from actual cases, every effort has been made to disguise the identities of the individuals involved. Nevertheless, the authors, editors, and publishers can make no warranties that the information contained herein is totally free from error, not least because clinical standards are constantly changing through research and regulation. The authors, editors, and publishers therefore disclaim all liability for direct or consequential damages resulting from the use of material contained in this book. Readers are strongly advised to pay careful attention to information provided by the manufacturer of any drugs or equipment that they plan to use.

Stahl's Self-Assessment Examination in Psychiatry

3rd Edition - 9781108710022

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Introduction/Preface

Why a question book?

Do questions just document learning?

“Adults don’t want answers to questions they have not asked”

What is a “knowledge sandwich?”

Recertification/maintenance of certification by the American Board of Psychiatry and Neurology (ABPN)

Is your learning unforgettable?

How do you use this book?

Release/expiration dates

Overview

Learning objectives

Accreditation and credit designation statements

ABPN–Maintenance of Certification (MOC)

Instructions

Optional posttest and CME credit instructions

Peer review

Disclosures

Authors

Peer reviewer

Disclosure of off-label use

Cultural and linguistic competency

Providers

Support

Table of Contents

Disclaimer

Introduction/Preface

CME Information

Optional Posttests and CME Certificates

Index

Instructions and Study Guide

Study guide for online posttests

Basic Neuroscience

Psychosis and Schizophrenia and Antipsychotics

Unipolar Depression and Antidepressants

Bipolar Disorder and Mood Stabilizers

Anxiety Disorders and Anxiolytics

Chronic Pain and its Treatment

Disorders of Sleep and Wakefulness and their Treatment

Attention Deficit Hyperactivity Disorder (ADHD) and its Treatment

Dementia and Cognitive Function and its Treatment

Substance Use and Impulsive Compulsive Disorders and their Treatment

Index

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