Psychiatry Test Preparation and Review Manual: Expert Consult, 2nd Ed.

Explanations

Vignette One

1. C. Post-traumatic stress disorder is the best explanation for the scenario in this vignette. In PTSD the person experienced or witnessed an event which involved actual or threatened death or serious injury and they responded with fear, helplessness, or horror. They then need at least one symptom of reexperiencing, three symptoms of avoidance and two symptoms of increased arousal to meet DSM criteria. In this case the nightmares are a symptom of reexperiencing. The restricted range of affect (low mood, unable to be happy), sense of foreshortened future, and avoiding people associated with the trauma all count as avoidance symptoms. Irritability and outbursts of anger with his family and the nurses, and difficulty staying asleep are considered symptoms of increased arousal.

  Although he may have some symptoms of depression he does not meet MDD criteria and the overall picture is better explained by PTSD. There is more going on symptom wise than would be explained by an adjustment disorder with depressed mood. Although he no doubt has several medical issues at this point mood disorder secondary to a medical condition does not fully account for the full picture we are seeing. The most comprehensive explanation is found with PTSD.

  K&S Ch. 16

2. ABD. Most patients with PTSD receive both medication and therapy. SSRIs and SNRIs are first line for PTSD. CBT is the type of therapy with the most evidence of effectiveness for PTSD. Psychodynamic psychotherapy does not have significant evidence of effectiveness in PTSD. Dialectical behavior therapy is first line for borderline personality disorder, not PTSD. Benzodiazepines should be avoided in PTSD both because of the high risk for potential addiction and because some studies have shown that benzodiazepines slow recovery rates for PTSD. Patients take longer to recover when they are on benzodiazepines so they are not a good choice. In this vignette, family therapy is certainly a good idea given the stress the family is under and the patient’s reaction to them.

  K&S Ch. 16

3. DE. Rapid onset of symptoms, strong social supports, absence of other psychopathology or substance abuse, short duration of symptoms (less than 6 months), and good premorbid functioning would all be considered good prognostic factors for PTSD. The opposite of any of these would be considered poor prognostic factors. As a general rule, the very old and very young have the highest likelihood of developing PTSD with those in the middle of life faring best.

  K&S Ch. 16

4. D. Alexithymia is an inability to describe feeling states and can be a symptom of PTSD. Tactile hallucinations and thyroid abnormalities are not usually associated with PTSD. We see increased norepinephrine turnover in the locus coeruleus in PTSD, not decreased.

  K&S Ch. 16

5. ABCE. Overcoming denial, use of imaginal techniques or in vivo exposure, encouragement and help for proper sleep, and learning cognitive approaches to stress can all be helpful to patients with PTSD as part of a successful therapeutic approach. Cathartic expression of aggression is not a common component of PTSD treatment and patients are encouraged to verbalize feelings rather that act them out aggressively.

  K&S Ch. 16

6. AB. Hallucinations and restriction of affect can occur in both schizophrenia and PTSD. Restricted affect would be considered a symptom of avoidance in PTSD. Decreased need for sleep is characteristic of mania. A sense of foreshortened future is a symptom of avoidance seen in PTSD.

  K&S Ch. 16

7. ABC. Decreased sleep and most importantly decreased need for sleep can be seen in bipolar I disorder. Generalized anxiety disorder may present with sleep disturbance as one of the physical symptoms (the others are muscle tension and fatigue). PTSD can present with difficulty falling or staying asleep as part of the increased arousal symptoms. OCD does not have a sleep disturbance as part of its DSM criteria.

  K&S Ch. 16

8. C. This is an example of classical conditioning. Classical conditioning is when a neutral (conditioned) stimulus is paired with a stimulus that evokes a response (unconditioned stimulus) such that over time the neutral stimulus eventually elicits the same response as the unconditioned stimulus. In this case the unconditioned stimulus was the fire and the reaction was fear and horror. In time the neutral stimulus of the chainsaw takes on the power to generate the fear originally caused by the fire. Classical conditioning is part of the behavioral model for PTSD.

  In operant conditioning voluntary behavior is modified as the patient actively tries different behaviors to see which will deliver a desired reward. Learned helplessness is a model of depression in which a patient repetitively fails at a task and eventually stops trying, adopting a hopeless apathetic position. Premack’s principle states that behavior engaged in at a high frequency can be used to reinforce behavior that occurs at a low frequency.

  K&S Chs 4&16

9. C. Feelings of detachment from others is considered a symptom of avoidance when diagnosing PTSD. All other choices in the question are symptoms of increased arousal.

  K&S Ch. 16

10. ABCD. The differential diagnosis for PTSD should include all of the choices mentioned in this question except schizotypal personality disorder. Panic disorder can present with symptoms which could be considered in line with avoidance and hyperarousal. Substance abuse can mimic anxiety symptoms and there is a high overlap between PTSD and substance abuse, especially alcohol. Major depressive disorder presents with symptoms similar to the avoidance symptoms of PTSD (restricted affect, diminished interest in activities, feelings of detachment). Borderline personality disorder may present with mood lability, irritability and angry outbursts which could be mistaken for hyperarousal symptoms in PTSD.

  K&S Ch. 16

Vignette Two

1. B. This question asks you to focus on the most clinically appropriate maneuver in this case. You could certainly send the patient home with yet another medication trial, but the fact that she has already failed multiple medication trails makes the prognosis for success very poor. Clearly, her daughter has done the patient no harm so there is no question here of reporting her to state authorities as a case of possible elder abuse. ACT teams are an excellent treatment modality principally for patients who have poor insight into their mental disorder and, as a result, are poorly adherent to medication regimens that would prevent decompensation. ACT teams, because of their mobility and their high staff to patient ratio, are able to service such patients in their home environment and at the same time ensure that the medications are filled and taken appropriately. ACT teams are not a substitute for skilled nursing care or skilled nursing facility placement. Such teams are unable to handle and manage patients at home who have multiple medical problems and need structure and help with basic activities of daily living, such as shopping, cooking, and cleaning. Such patients are much better served by skilled nursing facility placement, or if less severe, by visiting nurse services complemented by home healthcare assistance. In this particular case though, placing the patient in a skilled nursing facility is not the best immediate maneuver. The patient is profoundly depressed and in need of intensive psychiatric care prior to nursing home placement. If placed in such a facility in her present mental state, the patient will surely not be able to be managed by a nursing home consulting psychiatrist, given the profound severity of her depression and disintegration of her activities of daily living. The best maneuver in this case would be to convince the patient and her daughter that a voluntary psychiatry inpatient admission would be best for the patient. Consideration of electroshock therapy, once admitted, is quite appropriate, given the patient’s failure to improve with numerous trials of antidepressant medications. The most common indication for ECT is major depressive disorder, for which ECT is the fastest and most effective available therapy. ECT should be given consideration when patients have failed multiple medication trials, are acutely suicidal, homicidal, or psychotic, or have severe symptoms of stupor or agitation.

  K&S Ch. 36

2. ABD. The pretreatment evaluation for ECT includes physical examination, neurological examination, anesthesia consultation, and complete medical and surgical history. Laboratory testing should include blood and urine chemistries, chest radiography, and an electrocardiogram. A dental exam is advisable, particularly in the elderly who may have poor dentition or poor dental hygiene. Spine radiography should be done only if there is history or suspicion of preexisting spinal disorder. Brain CT or MRI scan should be done if there is history or suspicion of a seizure disorder or a space-occupying lesion. In this particular vignette, the patient may well have a brain tumor of some sort that is causing her refractory depression. Even though a brain tumor is not an absolute contraindication to ECT, a brain scan should be performed in this case to rule out that possibility. Thyroid function tests and routine electroencephalogram are not needed for pretreatment ECT evaluation.

  K&S Ch. 36

3. E. Electroshock therapy has no absolute contraindications. Patients with situations that put them at increased risk merely need closer and more careful monitoring before, during, and after the procedure. Pregnancy is not a contraindication for ECT. Patients with space-occupying brain lesions are at risk for brain edema and herniation following the procedure. Those patients with smaller mass lesions can be premedicated with dexamethasone (Decadron), which reduces the risks following the procedure. Patients with recent myocardial infarction are a high-risk group, but the risk is diminished two weeks after the myocardial infarction and even further diminished 3 months following the infarction. Patients with hypertension should be well-stabilized on their antihypertensive medications prior to ECT being administered.

  K&S Ch. 36

4. C. For a seizure to be effective in the course of ECT, it should last at least 25 seconds. Proper objective seizure monitoring must be undertaken by the physician conducting the ECT. There must be evidence that a bilateral generalized seizure has taken place after the electrical stimulation has been applied. The EEG and electromyogram enable this to be monitored objectively.

  K&S Ch. 36

5. DE. The most worrisome side effect of ECT is memory loss. About 75% of patients given ECT complain that memory impairment is the worst adverse effect. Most patients with memory impairment report a return to baseline within 6 months following treatment. Fractures and muscle or back soreness are possible with ECT, but with routine use of muscle relaxants, fractures of long bones do not generally occur. A minority of patients experience nausea, vomiting and headache following ECT. Mortality rate with ECT is about 0.002% per treatment and 0.01% for each patient. Hypertension can occur during the seizure, but can be controlled by antihypertensive agents administered at that time. Hypertension is not typically a long-term adverse effect of ECT.

  K&S Ch. 36

6. ACD. The indications for maintenance ECT treatments are: severe medication side effects and intolerance, psychotic or severe symptoms, and rapid relapse after a successful initial round of treatments. Maintenance ECT should always be considered after a remission of symptoms from a first round of treatment, because initial positive response is rarely maintained and relapses often occur despite an initial response to a first round of treatments.

  K&S Ch. 36

7. CEF. Benzodiazepines should be tapered and withdrawn prior to ECT because of their anticonvulsant properties. Lithium must be withdrawn prior to ECT because it can cause a postictal delirium and can prolong seizure activity. Clozapine and bupropion should also be withdrawn prior to ECT, because they are known to be associated with late-appearing seizures. Antidepressants in the class of the SSRIs, SNRIs, tricyclics and MAO inhibitors are not contraindicated with ECT.

  K&S Ch. 36

8. D. Methohexital (Brevital) is the most commonly used anesthetic agent for ECT because of its shorter duration of action and lower association with postictal arrhythmias. Etomidate (Amidate) is sometimes used in elderly patients, because it does not increase the seizure threshold and it is well understood that seizure threshold increases as patient’s age. Ketamine (Ketalar) is sometimes used because it doesn’t raise the seizure threshold. It is however associated with the emergence of psychotic symptoms following anesthesia. Alfentanil (Alfenta) is used concomitantly with barbiturates in some cases, because it allows for lower dosing of the barbiturates which lowers the seizure threshold further. It is however associated with an increased incidence of nausea. Propofol (Diprivan) is less useful as an anesthetic agent in ECT because it raises the seizure threshold.

  K&S Ch. 36

9. C. Electrode placement for ECT can either be unilateral or bilateral. Bilateral placement leads to a more rapid therapeutic response in most cases, but it also results in a higher frequency of memory impairment. Most practitioners will begin treatment with unilateral ECT because of its more favorable adverse effect profile. If the patient does not improve after four to six unilateral treatments, most clinicians will strongly consider moving to bilateral electrode placement thereafter. Initial bilateral electrode placement is considered in cases of severe depressive symptoms, with catatonic stupor, acute suicide risk, manic symptoms, treatment-resistant schizophrenia and in cases of marked agitation.

  K&S Ch. 36

Vignette Three

1. C. Cathy would best be described as having bipolar II disorder. To meet criteria for bipolar II requires at least 1 MDD episode and 1 hypomanic episode. Cathy clearly meets MDD criteria. Hypomania is defined by a clear period of irritable, expansive, or elevated mood lasting for at least 4 days but does not cause marked impairment in functioning. In addition there must be at least 3 of the same symptoms which define manic episodes (pressured speech, decreased need for sleep, grandiosity, flight of ideas, distractability, increased goal directed activity, excess involvement in behaviors with high potential for harmful consequences). Cathy fits this profile. If she were to have mania her symptoms would continue for 1 week or more and/or she would have marked impairment in functioning, neither of which are true in this case. Major depressive disorder is incorrect because it does not explain the entire picture we are seeing. Cyclothymic disorder is defined as hypomania plus subthreshold depressive symptoms for a period of 2 years or longer. This doesn’t fit Cathy’s case. Substance induced mood disorder would certainly be included in a differential for Cathy, but would not be the best choice because we have given you no data on the connection between substance abuse and mood changes. She also denies the use of substances, which would likely precipitate a manic episode around the time of her sister’s wedding (cocaine).

  K&S Ch. 15

2. C. Key differentiating factors between hypomania and mania would include the time period (4–6 days for hypomania vs. 7+ days for mania) and the presence or absence of marked impairment in social or occupational functioning. Irritable mood, decreased need for sleep and flight of ideas could be present in either.

  K&S Ch. 15

3. ABCD. Psychosis, rapid cycling, severity of symptoms and pregnancy are all valid concerns which would impact the choice of medications in the bipolar patient. For a patient in their 30s age wouldn’t be a major factor.

  K&S Chs 15&36

4. AB. ECT for bipolar has been proven very effective in severe mania with psychosis and in pregnancy. Mania secondary to a medical condition or substance abuse would not necessarily lead to ECT and would most likely be treated with medications.

  K&S Chs 15&36

5. ABC. Glioma, Cushing’s disease, and multiple sclerosis have all been associated with mania. Thiamine deficiency is not associated with mania but is a crucial component of Wernicke–Korsakoff syndrome seen in alcoholics.

  K&S Ch. 15

6. ABCD. Isoniazid, cimetidine, metoclopramide and steroids can all cause a manic episode. Of course there are others such as bronchodilators, antidepressants, anticonvulsants, stimulants, barbiturates and several drugs of abuse. Benzodiazepines would tend to lessen mania, not cause it.

  K&S Ch. 15

7. ACD. Cocaine use causes rapid dopamine and norepinephrine reuptake inhibition. It increases dopamine in the mesolimbic and mesocortical pathways and decreases dopamine in the corpus striatum.

  K&S Ch. 12

8. D. Sequelae of cocaine use include hallucinations, paranoia, euphoria, increased energy, hypersexuality, and irritability. With heavy cocaine use patients can experience a shower of lights in their central vision, as well as visual hallucination of black dots on their skin and in the environment (coke bugs). Itching and respiratory depression come from opiate abuse, not cocaine.

  K&S Ch. 12

9. ABC. Treatment for cocaine overdose can include cold blankets and ice packs for hyperthermia, IV diazepam for seizures, IV phentolamine for malignant hypertension and both haloperidol and lorazepam for agitation. Clonidine is useful in treating the autonomic effects of opiate withdrawal, but is not used in cocaine overdose.

  K&S Ch. 12

10. C. Sixty percent of patients with bipolar disorder have a co-occurring substance abuse disorder. As such Cathy is not unusual in this regard. It means that it is very important to screen for substance abuse in any bipolar patients.

  K&S Ch. 15

Vignette Four

1. B. Susan has borderline personality disorder. Characteristics of the disorder include frantic efforts to avoid abandonment, unstable and intense interpersonal relationships, idealization and devaluation, unstable self image, impulsivity in self damaging ways, affective instability, chronic feelings of emptiness, intense inappropriate anger, and transient stress related paranoia or dissociation. In Susan’s case we see impulsivity in self damaging ways, unstable interpersonal relationships, intense inappropriate anger, efforts to avoid abandonment, affective instability, and unstable self image.

  K&S Ch. 27

2. ABDE. Characteristics of Susan’s diagnosis are frantic efforts to avoid abandonment, unstable and intense interpersonal relationships, idealization and devaluation, unstable self-image, impulsivity in self-damaging ways, affective instability, chronic feelings of emptiness, intense inappropriate anger, transient stress related paranoia or dissociation. Grandiosity is not a characteristic of borderline personality disorder but can be seen in bipolar disorder and psychotic disorders.

  K&S Ch. 27

3. C. Perceived rejection is the centerpiece of many borderline suicide attempts and is certainly the precipitating factor in Susan’s case.

  K&S Ch. 27

4. C. The treatment of choice for borderline personality disorder is dialectical behavior therapy.

  K&S Ch. 27

5. ABC. Borderline patients may only be in touch with reality on a basic level, have limited capacity for insight, and use primitive defenses such as splitting. They do not have an integrated sense of self. Their unstable sense of self is an important part of the disorder.

  K&S Ch. 27

6. DE. Acting out and splitting are two of the defenses most commonly associated with borderline personality disorder. The others have no particular association with borderline personality disorder.

  K&S Ch. 27

7. BCD. Patients with borderline personality self-harm in order to express anger, elicit help from others, and numb themselves to overwhelming affect. Their goal is not to socially isolate themselves and they may feel quite dependent on others, despite the fact that they eventually do drive others away by their extreme behavior.

  K&S Ch. 27

8. D. Projective identification is a defense mechanism used by borderline patients which was first described by Otto Kernberg. Intolerable aspects of the self are projected onto another person. The other person is then induced to play the projected role. This is of particular concern for psychiatrists working with borderline patients as they can be pulled into this dynamic if they lose their neutral stance. Displacement is a defense mechanism where emotional energy is taken from one object and placed onto another unrelated object. Rationalization is using rational explanations to justify beliefs and attitudes that would otherwise be socially unacceptable. Splitting is seeing other people or situations as either all good or all bad. It is a commonly used defense of the borderline patient.

  K&S Chs 6&27

9. ABC. Impulsive behaviors are certainly part of the borderline picture. Prolonged psychotic episodes are not. Borderline patients may have brief episodes of psychosis when under significant stress but prolonged psychosis is something seen on Axis I. Marked peculiarity of thinking is more a descriptor of schizotypal personality disorder than of borderline. Extreme suspiciousness is more a descriptor of paranoid personality disorder than of borderline. That is not to say that a borderline patient may never be suspicious, but extreme suspiciousness is not one of the defining DSM criteria.

  K&S Ch. 27

10. ABCD. All of the choices except stimulants may have a role in treating Susan’s condition. Antipsychotics have been used for anger, hostility, and brief psychotic episodes. SSRIs have been used for depressive features and aggression. Anticonvulsants are helpful for mood lability and aggression. MAOIs have been helpful in modulating impulsive behavior in some patients. Stimulants are not considered effective treatment for borderline personality disorder.

  K&S Ch. 27

Vignette Five

1. B. During the initial contact the doctor wishes to establish rapport quickly, put the patient at ease, and show respect. If the patient wishes to have someone else in the initial session with them then that should be respected. Patients have a right to know the position and professional status of the people involved in their care. As such introducing yourself is important. The answer choice which best addresses all of these issues is choice B.

  K&S Ch. 1

2. AC. Starting the interview with an open ended question is best. It allows the patient to describe what has brought them in and signals to them that you are interested in hearing what they have to say. Choices A and C are open ended and allow the patient to tell Dr. Smith what is wrong in her own words. Choices B and D are too closed ended and specific for an opening question. They are both phrased so directly the patient may interpret them as rude.

  K&S Ch. 1

3. D. A patient may be frightened or anxious at the beginning of an interview. The first step in addressing this is by acknowledging the patient’s anxiety and offering reassurance. Of the choices given the one that does this best is choice D. Choices A and B have an accusatory tone which may make the patient shut down more. Choice C is ignoring the dynamic in the room and talking about a completely unrelated subject that does not address the patient’s underlying discomfort.

  K&S Ch.1

4. ACD. The content of an interview is what gets said between doctor and patient, such as subjects discussed and topics mentioned. The process of the interview is what happens nonverbally, such as body language, behaviors, or avoidance of difficult topics.Choices A, C, and D are all behaviors, body language, or avoidance of difficult topics. Choice B is a topic which was spoken about in the session and as such is content.

  K&S Ch. 1

5. C. In clarification the therapist tries to get more details about what the patient has already said. That is what Dr. Smith is doing in this question. Confrontation is pointing out something that the patient is missing or denying. Facilitation is using both verbal and nonverbal cues to encourage a patient to keep talking. Explanation is when the doctor describes the treatment to the patient in clear understandable language and gives them opportunity to ask questions.

  K&S Ch. 1

6. B. In transition the doctor lets the patient know that they have gathered enough information on one subject and encourage them to move on to another subject. In reassurance the patient informs them of their condition in a way that leads to increased trust and compliance and is experienced by the patient as empathic and caring. In positive reinforcement the doctor makes the patient feel as if they are not upset no matter what the patient says so as to facilitate an open exchange of information. In advice the doctor recommends a course of action to the patient. This should always be done after the patient has had time to speak freely about their problems. If done before this it can be received as inappropriate or intrusive.

  K&S Ch. 1

7. ABCD. In ending the session it is important to give patients a chance to ask questions and explain future plans and next steps. You should thank the patient for sharing information. Any prescriptions should be reviewed and the patient should understand why they are being given medication and how to take it. Patients should be encouraged to call with questions if they need clarification of their treatment, if anything emergent arises, or if they have side effects to medications and need guidance.

  K&S Ch. 1

8. ABCD. Putting the patient at ease, expressing compassion for pain, showing expertise, and establishing authority as a physician are all necessary parts of developing rapport with a patient. To do this well the doctor must balance the roles of empathic listener, expert, and authority. Doctors are not expected to be all knowing and should be honest with the patient when they do not know the answer to a patient’s question.

  K&S Ch. 1

9. BC. Decreased rates of patient compliance have been proven to be associated with increased complexity of the treatment regimen and an increased number of behavioral changes required for the treatment to succeed. Intelligence, gender, marital status, race, religion, socioeconomic status, and education level have not been proven to correlate with compliance rates.

  K&S Ch. 1

10. B. All of these answer choices represent different models of the doctor–patient relationship. In the teacher–student model the physician’s dominance is emphasized. The physician is paternalistic and controlling. The patient’s role is one of dependence and acceptance. In the active–passive model patients assume no responsibility for their care and take no part in their treatment. This is appropriate for patients who are unconscious or delirious. In the mutual participation model there is equality between both parties and each depends on the other for cooperation and input. Long-term management of chronic diseases often leads to this model. In the friendship model patient and doctor become friends. This is an arrangement that is considered unethical and dysfunctional. It often reflects psychological problems on the part of the physician.

  K&S Ch. 1

Vignette Six

1. BCE. Gender identity disorder is defined as a strong and persistent cross-gender identification. In adolescents and adults, the disturbance is manifested by symptoms such as a stated desire to be the other sex, frequent passing as the other sex, desire to live or be treated as the other sex, or the conviction that he or she has the typical feelings and reactions of the other sex. There is a persistent discomfort with his or her sex or sense of inappropriateness in the gender role of that sex. In adolescents and adults, the disturbance is manifested by symptoms such as preoccupation with getting rid of primary sex characteristics or belief that he or she was born the wrong sex.

  Transvestic fetishism is a disorder in a heterosexual male who, over at least a 6-month period, has recurrent, intense sexually arousing fantasies, sexual urges, or behaviors involving cross-dressing. Pearl would not be considered a heterosexual male in this case and so does not meet criteria for this disorder. Partialism, also called oralism, is categorized under paraphilias not otherwise specified. People with this disorder concentrate their sexual activity on one part of the body to the exclusion of all others. The typical presentation involves preference for oral sex without intercourse. Urophilia is also a paraphilia not otherwise specified. Pearl does meet criteria for urophilia as it involves the intense desire to urinate on a partner or be urinated on. In both men and women, this may also be associated with sexual arousal via the insertion of foreign objects into the urethra for the purpose of sexual stimulation.

  Sexual sadism and sexual masochism are two different paraphilias, but they are related. The former involves at least 6 months of recurrent, intense sexually arousing fantasies, sexual urges, or behaviors involving acts in which psychological or physical suffering of the victim is sexually exciting to the person. The latter involves at least 6 months of similar fantasies, urges or behaviors involving acts of being humiliated, beaten, bound, or otherwise made to suffer. It would seem that Pearl and her partner meet criteria for these paraphilias. Fetishism is again a paraphilia of at least 6 months’ duration, during which time the person has recurrent, intense sexually arousing fantasies, urges, or behaviors involving the use of nonliving objects (for example, female undergarments, or fake rubber penises). Pearl does not seem to have a fetishistic paraphilia.

  K&S Ch. 21

2. A. Poor prognosis for paraphilias is associated with early age of onset, a lack of guilt or shame about the act, a high frequency of acts, and concomitant substance abuse. The prognosis is also better when there is a history of the act of coitus with the paraphilia and when the patient is self-referred rather than referred by a legal agency.

  K&S Ch. 21

3. BCF. Good prognostic indicators for paraphilias include normal intelligence, the absence of substance abuse, the absence of personality disorders, the presence of normal adult attachments and relationships, the absence of concomitant axis one mental disorders, and the presence of only one paraphilia.

  K&S Ch. 21

4. AD. There are essentially five types of psychiatric intervention used to treat paraphilias. These include reduction of sexual drives, external control, treatment of comorbid conditions, dynamic therapy and cognitive-behavioral therapy. Prison is an external control mechanism to prevent sexual crimes, but it does not usually involve a treatment element. Interpersonal psychotherapy is not usually useful in helping prevent paraphiliac behaviors, urges and fantasies. Sex therapy can be effective and is considered an adjunctive modality to dynamic therapy. Twelve-step programs based on the Alcoholics Anonymous model are of course useful in supporting individuals with sexual addiction and troublesome behaviors. Antiandrogen therapy may reduce sex drive and aberrant sexual behavior by decreasing serum testosterone levels to subnormal concentrations.

  K&S Ch. 21

5. E. Most patients with gender identity disorder (GID) are males. Men present with the disorder at a rate of about 1 in 30 000 and women present with disorder at a rate of about 1 in 100 000. Prospective studies of children with GID indicate that few become transsexuals and want to change their sex. Adult transsexuals typically complain of being uncomfortable wearing the clothes of their assigned sex and so they prefer to wear clothes of the opposite sex and act in ways compatible with the opposite sex. They find their own genitals to be repugnant, which may lead to their repeated requests for gender-reassignment surgery and hormone therapy. About two-thirds of adult men with GID are sexually attracted to men only. Therefore, Pearl would be counted among the minority one-third of male patients with GID who are exclusively attracted to female partners.

  K&S Ch. 22

6. B. At this time, there is no evidence that indicates that psychological or psychiatric intervention for children with GID can change their future sexual orientation. Also, there are no particular hormonal or psychopharmacological treatments for GID in childhood. Adolescents with GID can now be given cross-sex hormones in pre-pubescence to slow down or arrest pubertal development and begin the cross-over to the opposite gender at that time. No drug therapy has been shown to reduce cross-gender desires in adult patients with GID. When adult patients suffer from severe gender dysphoria, sex-reassignment surgery may be the best solution.

  K&S Ch. 22

Vignette Seven

1. AEF. This is a classic, though complex, case scenario. It comes up frequently in day-to-day practice for the forensic psychiatric consultant. As a psychiatric expert witness for the defense, you are engaged by the defense lawyer to help the accused in his defense. You must act within the scope and expertise of your profession and practice. You must evaluate the defendant and any pertinent collaterals, as well as examine the circumstances surrounding the alleged acts, and then produce a written report that supports the defense attorney’s stance in his defense of his client. You cannot skew the facts or perjure yourself in an attempt to help the defense team and their client.

  Note that ethically there is no reason that you cannot participate as an expert witness in this case. The fact that the defendant is also a psychiatrist has no bearing on the experts who may be brought forth to defend him. The only conflict of interest that may arise would stem from a situation in which Dr. Daniels and you were best friends, relatives, business partners, or had other past or present collaborations or combined interests that would render your judgment in the case unnecessarily biased in his favor. In such a case, you would have to decline the case and refuse to participate in it.

  Your job begins with a thorough consultation with the defense attorney to discuss the facts of the case, as well as the defense team’s stance and approach to the defense. Is the defense seeking a psychiatric defense: i.e. applying the M’Naghten Rule looking for a “not guilty by reason of insanity” plea on any or all of the charges? Is the defense seeking mitigation of the charges on the basis of psychiatric incapacitation or deficits? Does the defense attorney feel that there are mitigating circumstances in the defendant’s behavior that reflect a mental status that was not sound at the time the alleged events took place? Who are the collateral people that can be interviewed who might lend weight in evidence to the desired defense? Are there facts in the defendant’s psychiatric and/or medical history that may help in establishing mitigation of guilt? Does the attorney himself feel that his client is competent to stand trial and has this issue been brought to bear by the defense, the prosecution, or the judge?

  All of these (and many more) questions need to be answered before you can begin to approach this case. Once you are satisfied that you have enough background data and information to begin work on the case, your next step is to interview and examine Dr. Daniels thoroughly. This may need to take place over several different sessions held over a period of time, in order for you to gather as complete details as you can, and also to establish his recollection and redaction of the facts as he sees them. You may feel that medical and neurologic assessment should be part of the defense investigation and suggest this to the defense attorney, if you think it would be helpful to the client’s defense. Part of your interview and assessment (and part of your function in this case) is to assess the defendant’s current competency to stand trial. The defense attorney may not ask you to do this formally, because he may have no doubts about the fact that the good doctor has full capacity to stand trial. Even so, you must ask the classic questions of the defendant to be sure that you as a consultant have no doubts about his ability to stand trial. The defendant must demonstrate knowledge of the charges brought to bear against him, knowledge of the circumstances on which the charges are based, knowledge of the important persons involved in the playing out of the case, knowledge of the possible outcomes of the various types of pleas that the defense may enter in his behalf. Above all, the defendant must demonstrate an ability to collaborate with his lawyer in his own defense. Note that the defendant’s current mental status is what is assessed in competency to stand trial, and not his mental status at the time the alleged acts were committed.

  In order to assess for mitigation of responsibility or for a “not guilty by reason of insanity” plea, you must evaluate Dr. Daniels mental status at the time the alleged incidents occurred. You must establish (if you can) intent to harm versus lack of such intent, as this will mitigate or implicate his responsibility if it is deemed that the alleged acts were committed. Obtaining information from collateral persons who may have been involved around these events may be a crucial maneuver in trying to piece together the defendant’s mental status at that time.

  Should you recommend functional brain imaging studies to help in the client’s defense? This type of recommendation and evidence is extremely controversial and very new to the process. Generally speaking, such evidence is not really contemplated unless there are some clear-cut facts in the neurologic or medical history that would warrant such studies to be done. Neuropsychological testing may also reveal deficits that might warrant such imaging, depending on the history. Brain injury, stroke, brain tumor, seizure history, severe and chronic substance use, are but some of the historical factors that may trigger an expert witness to suggest that brain imaging might be helpful. Even if such imaging is conducted on the defendant, and even if the results show brain abnormalities, the evidence, as it is presented to prosecutors, the judge and perhaps eventually a jury, may not be helpful because of its complexity and the lack of good precedents in the law annals to help support the data as a mitigating factor to the defendant’s guilt.

  There is no case scenario (expect perhaps in the case of a mute or profoundly mentally retarded defendant) in which neuropsychological testing should not be conducted. Even if the testing reveals nothing to help the defendant (i.e., a thorough battery shows he has an above-average intelligence with no dangerous personality characteristics, nor any deficits in executive functioning or reasoning), this will not necessarily hurt the defense. How is this possible? Once the testing is complete, the consulting neuropsychologist must colleague with the defense team verbally before writing up a final report. If upon discussion, the defense attorney feels that the testing results would not be helpful (or may even be a hindrance) to the defense, he can certainly request that a report not be written at that time. Certainly, the prosecution team must be told of the neuropsychological testing, and they can subpoena the neuropsychologist to testify at trial, if the case goes that far, but a noncontributory report need not be immediately presented, because it certainly can then be used by the prosecution against the defendant. This is indeed a legal “game” that is often played out between defense and prosecution, in order to spin or skew the evidence in one direction or another. Most of these cases never get to trial and wind up either being dropped by prosecutors if evidence if too weak, or even thrown out by the judge before moving forward to pre-trial, if the judge feels the charges and allegations are frivolous or unsubstantiated! If the charges are neither dropped nor thrown out of court, a trial may still never come to pass, as many cases are settled as a plea bargain by both sides before the case can go further.

  Should Dr. Daniels be practicing his profession (if the state permits him to do so) between now and his future court date? This is a matter that falls between him and his defense attorney, who will no doubt advise and guide him. In certain situations, it is deemed best for the defendant to continue “business as usual” in the interim, as it points to a professional who is currently unimpaired and who can carry on working without a problem in his chosen profession. In other circumstances, his defense attorney may feel it best for him not to continue practicing, because it may help the defense mount a psychiatric plea that points more towards impairment and the need for mitigation of responsibility. Again, these are lawyers’ tactics that are outside the purview of the psychiatric expert witness. Of course, you are entitled to your opinion as an expert witness, based on your findings, and you should impart this opinion to the defense team, but they are the ones who will finally advise and guide their client accordingly.

  K&S Chs 58&59

2. BDF. The commission of a criminal act has two components: voluntary conduct (actus reus) and evil intent (mens rea). Evil intent cannot be present if the offender’s mental status is so impaired or diseased as to have deprived the offender of the rational intent to commit the act. The law can only be invoked in the presence of evil or malicious intent. Intent to do harm is not sufficient on its own as grounds for criminal action. The M’Naghten Rule is the statute derived from the 1843 case of Daniel M’Naghten in the British courts. This is known as the right–wrong rule or test. The question brought to bear in this rule is “did the defendant understand the nature and quality of the act and the difference between right and wrong with respect to the act” at the time the act was committed. If a mental illness causes the defendant to be unaware of the consequences of his/her acts, or if he/she was incapable of understanding that these acts were wrong, the person could then be absolved of criminal responsibility for the acts. Ford v. Wainwright is a landmark case in the matter of competence to be executed and has nothing to do with the case in this vignette. The duty to warn and protect derives from the case of Tarasoff v. Regents of the University of California, which was the landmark case setting the precedent for clinicians to be responsible for warning and protecting intended victims of patients expressing intent to harm others.

  K&S Ch. 58

3. BDE. The standard for competence to stand trial is set quite low to enable as many defendants to have their day in court as possible. This standard was set by the US Supreme Court in the landmark case of Dusky v. United States. The defendant must be able to demonstrate knowledge of the charges brought against him. He must demonstrate knowledge of the penalties associated with being found guilty of each of these charges. He must demonstrate a knowledge and recognition of the various persons involved in his case: his attorneys, the prosecuting attorneys, the judge, the witnesses who will be called, the jury. He must be able to collaborate with his attorney with a reasonable degree of rational understanding of the proceedings against him. Note that the defendant’s current mental status (and not his mental status at the time the alleged acts were committed) is what is brought to bear in determining his competency to stand trial.The defendant does not have to recall every minute detail of the acts that he is alleged to have committed. The defendant does not have to be able to take the stand as a witness in his own defense. The defendant does not have to have an opinion on what kind of plea his defense team should enter on his behalf. Defense and prosecuting attorneys usually have the discretion to hire and appoint their own psychiatric expert witness to attest to the defendant’s competency to stand trial. The judge has the final word on which, if any of these opinions, he/she is willing to hear and entertain in the decision-making process on competency to stand trial. The judge also has the discretion to appoint his/her own psychiatric expert witness(es) to lend further weight to the decision in cases where the defendant’s competency to stand trial may be difficult to determine.

  K&S Ch. 58

4. E. This is a tough, tough question, particularly if you have little or no experience in the forensic arena. The answer, upon reflection, is simple. Judges have the final word on how anything will play out in their courtroom. In this vignette, as it is presented, both sides will undoubtedly want a crack at this all-important witness. Remember that she is not the one on trial here and she is not a plaintiff here either. She is merely the accuser in a criminal trial brought against Dr. Daniels by state prosecutors. So Selena can be a key witness for either side, and of course her testimony may be the most important factor in this case, but the judge is the only one who can dictate how that is to be conducted. Of course, prosecutors and judges work together to represent the best interests of “the people of the state” when trying criminal cases; the results are not always fair and unbiased, unfortunately. After all, judges and prosecutors are usually elected political officials in the US, and they seek to maintain popularity among their voters and constituents by winning high-profile criminal cases that demonstrate their keen abilities to serve and protect the people.

  So, to get off the political soap-box and back to psychiatric test preparation, it would be ideal if you could interview Selena and thus lessen her credibility as a witness. This would help you defend your client, Dr. Daniels. It’s unlikely that the prosecution will allow that to happen and they will certainly petition the judge to prevent this. They may ask the judge to let the prosecution first appoint their own psychiatric expert witness and have Selena be examined by that expert. The prosecution may try to block Selena from being examined all together, but again the judge will determine if that should be upheld or overruled. Mr. Wolff can certainly try to subpoena Selena to be psychiatrically examined for the defense, but prosecutors can ask the judge to block this for the reasons already mentioned. The prosecution can try to protect their case against Dr. Daniels by trying to petition the judge not to allow Selena to submit to an examination by a defense-appointed psychiatrist, but again, the judge decides. If the judge allows the prosecution to call a witness, in the interest of fairness and good judicial practice, he/she will usually allow the defense the opportunity to do the same. That said, judges can act and rule however they like (and have been known to do so in these cases) and their decisions are indemnified against any retaliation or accusation of wrongdoing or unprofessionalism for the most part.

  K&S Ch. 58

5. BCD. If Dr. Daniels’ defense team has put in a psychiatric plea on all three charges and the prosecution has allowed this to go to trial before a jury, then there is almost certainly a psychiatric impediment in the good doctor’s case. If the jury finds the good doctor not guilty by reason of insanity on all three counts, then there was certainly some compelling reason for the doctor’s mental status to have been clouded during these events, given that the jury felt he did not know right from wrong at the time these acts were committed. With this knowledge alone, we know that Dr. Daniels needs psychiatric treatment of some kind. We don’t know why his mental status was clouded, but a psychiatric disorder was likely the root cause at that time.

  Based on these facts, there is little doubt that the judge will mandate Dr. Daniels to some sort of psychiatric treatment. Dr. Daniels is highly unlikely to be permitted to return to psychiatric practice immediately without some sort of treatment mandate. Dr. Daniels will not be classified as a sex-offender because he was found not guilty of these charges, albeit by reason of psychiatric incapacitation. The decision to remove or maintain the doctor’s license comes not from the court, but from the state licensing department, who, upon reviewing the facts of the case, will determine the destiny of the doctor’s practice privileges. It is absolutely possible (though it may come as a shock) that the state licensing department could allow the doctor to return to practice after treatment is successfully completed, despite the nature of these charges.

  K&S Ch. 58

Vignette Eight

1. D. Thought process refers to the form of the patient’s thoughts. Descriptions of thought process would include the terms goal directed, linear, circumstantial, tangential, loosening of associations, flight of ideas, thought blocking, neologisms, racing thoughts, or word salad. Thought content includes delusions, preoccupations, obsessions, compulsions, phobias, hypochondriacal symptoms or antisocial urges. Perceptions primarily refers to hallucinations, be they auditory, visual, tactile, olfactory, or gustatory. In this case the only statement that is both correct and accurate is that the perceptions section of the mental status exam should include auditory hallucinations.

  K&S Ch. 7

2. A. The beliefs that Steven is having qualify as delusions. A delusion is a fixed false belief that is not supported by social norms. They are listed under the thought content section of the mental status exam.

  K&S Ch. 7

3. B. The GAF stands for global assessment of functioning. It is a 100 point scale of functioning which is included as Axis V in a full five axis diagnosis.This question is testing to see if you know some of the landmarks on the GAF. A GAF of 10 represents persistent danger of hurting self or others or persistent inability to maintain personal hygiene. A GAF of 20 represents some danger of hurting self or others or occasionally fails to maintain personal hygiene. A GAF of 40 represents some impairment in reality testing or communication or major impairment in several areas such as work or school. A GAF of 60 represents moderate symptoms or moderate difficulty in social or occupational functioning.

  K&S Ch. 9

4. BD. Concentration may be impaired in several psychiatric disorders. It is tested by asking the patient to start at 100 and count backwards by 7s or by asking them to spell the word world backwards and forward. Attitude in the mental status exam describes the patient’s attitude towards the examiner. Words commonly used include cooperative, friendly, interested, seductive, defensive, hostile, evasive, apathetic, ingratiating, and guarded. Memory would be tested by giving the patient three words to remember then coming back to them in 5 minutes and see if he remembered them. Abstract thinking is tested through the use of proverbs. It is a reflection of the patient’s ability to handle concepts.

  K&S Ch. 7

5. B. A delusion of grandeur is a person’s exaggerated conception of his importance, identity, or power. Pseudologia phantastica is a type of lying in which a person appears to believe in the reality of their fantasies and acts on them. Algophobia is the dread of pain. A nihilistic delusion is a false feeling that self or others are nonexistent or that the world is coming to an end.

  K&S Ch. 8

6. D. The mesocortical pathway which is responsible for the negative symptoms of schizophrenia begins at the ventral tegmental area and extends to the frontal lobes.

  K&S Ch. 3

7. ABD. Positive symptoms in schizophrenia are most associated with frequency of hospitalization but are not good predictors of long-term functional outcome. Cognitive symptoms have the strongest correlation with long-term functional outcome. Schizophrenia is associated with a 10% suicide rate. Most schizophrenics who commit suicide do so in the first few years of their illness and are therefore young.

  K&S Chs 13&34

8. BCD. Residual schizophrenia is defined by the absence of prominent delusions, hallucinations, disorganized speech or grossly disorganized or catatonic behavior. It is possible for them to have negative symptoms or positive symptoms in an attenuated form such as odd beliefs or unusual perceptual experiences.

  K&S Ch. 13

9. ABCD. All of the choices given except bright clothing are commonly seen in schizophrenics. Lack of spontaneous movement, odd stiffness or clumsiness, echopraxia (imitation of posture or behavior of the examiner), agitation, and bizarre posture are all possible in addition to tics and stereotypies.

  K&S Ch. 13

10. ACD. Thought form (a.k.a. thought process) of schizophrenic patients can include verbigeration (meaningless repetition of specific words or phrases), word salad (incomprehensible connection of thoughts with loss of normal grammatical structure) and mutism (voicelessness without any physical impediments of speech). Ideas of reference are part of thought content, not thought form.

  K&S Ch 8

Vignette Nine

1. ABC. Anorexia nervosa can be divided into restricting type and binge-eating–purging type. Refusal to maintain body weight above 85% of the expected body weight for height and age is an essential criterion. In addition the anorexic patient has an intense fear of becoming fat, has a disturbance in the way their body is experienced, and presents with amenorrhea. Binge eating and purging can occur in either anorexia or bulimia.

  K&S Ch. 23

2. ABCDE. Medical complications associated with anorexia include but are not limited to bradycardia, pancytopenia, lanugo, osteopenia, metabolic encephalopathy, arrhythmias, elevated LFTs, elevated BUN, decreased T3 and T4, parotid gland enlargement, seizures, and peripheral neuropathy.

  K&S Ch. 23

3. ABC. Indications that anorexia should be managed inpatient include significant hypokalemia, weight loss to under 75% of expected weight for height and age, growth arrest, risk of self-harm or development of psychosis, rapid weight loss, or the failure of outpatient management.

  K&S Ch. 23

4. B. BMI (body mass index) is calculated as weight (kg)/height (m)2. Other choices are just distractors and are nothing you should memorize.

  K&S Ch. 23

5. ABCD. Treatment for anorexia should address psychiatric, medical and nutritional issues. Weight restoration is a major goal. Psychopharmacology can include the use of both antipsychotics and antidepressants. Psychotherapy and family therapy are important and there is evidence for the use of cognitive behavioral therapy in all eating disorders, especially bulimia. The most effective psychotherapy focuses on helping the patient develop alternative coping strategies and defenses as well as changing problematic eating behaviors. Bupropion should be avoided in patients with eating disorders as it lowers the seizure threshold which can increase risk of seizures during periods of electrolyte disturbances which eating disorder patients are prone to.

  K&S Ch. 23

6. ABC. Complications of self-induced vomiting found in anorexia or bulimia can include esophagitis, scars and abrasions on the back of the hand (Russell’s sign), Mallory–Weiss syndrome (bleeding from tears in the esophageal mucosa caused by repetitive retching), Barrett’s esophagus, erosion of tooth enamel, parotid gland swelling, increased serum amylase, hypokalemia, and an increased rate of spontaneous abortion and low birth weight during pregnancy. Atonic colon can be found in anorexics but is a result of laxative abuse, not self-induced vomiting.

  K&S Ch. 23

7. ACD. Abuse of ipecac syrup can lead to skeletal muscle atrophy, prolonged QTc interval, cardiomyopathy, and tachycardia. Rectal prolapse can be seen in eating disorders following severe laxative abuse.

  K&S Ch. 23

8. AD. The risk of anorexia is higher in families that contain anorexics. Anorexia is unrelated to paranoid personality disorder. Eating disorder patients tend toward personality traits that are rigid and perfectionistic. They tend to be emotionally inflexible. Adolescence is a time of heightened risk. Patients may control eating as a reaction to other changes in their lives that are outside of their control.

  K&S Ch. 23

9. ABCD. Disorders which may be misdiagnosed as an eating disorder, or vice versa, include all listed in this question except brief psychotic disorder. In MDD weight loss often accompanies loss of appetite, sometimes severe weight loss. A thorough evaluation for symptoms of MDD should be done including an understanding of how the patient feels about the weight loss. In MDD the patient is not afraid of gaining weight. In anxiety disorders patients may lose weight due to changes in appetite due to anxiety, or issues surrounding obsessions. These patients should be screened carefully for areas in which anxiety may impede normal eating.Bulimia may be misdiagnosed as anorexia especially in cases of binge eating–purging anorexia. Keep the patient’s body weight in mind as an important marker. Below 85% of expected body weight is considered anorexia whether they are purging or not. Substance abuse can often come along with severe weight loss as patients do not eat properly and become malnourished. These patients do not fear gaining weight as an anorexic does.

  K&S Ch. 23

10. BCD. There are a whole range of medical considerations which come along with anorexia. Combinations of estrogen and progesterone have not been shown to be successful at reversing osteopenia in anorexia. Dental follow-up is essential particularly for those who purge because the stomach acid eats away at tooth enamel over time and greatly increases risk of caries and tooth decay. Electrocardiogram is important as many anorexics develop hypokalemia leading to arrhythmias as well as changes in QTc interval. Correcting hypokalemia is necessary to prevent significant cardiac issues. Checking all electrolytes, administering vitamin supplementation, checking a CBC, and evaluation for severity of bone loss due to osteopenia are some of the other measures which should be considered.

  K&S Ch. 23

Vignette Ten

1. ACD. Lisa clearly has some form of anxiety disorder based on the symptoms given in the vignette. As such, panic disorder, social phobia, and GAD should be included in a differential diagnosis and more questions should be asked to better determine the correct diagnosis. There is no mention of psychosis in the vignette, so schizoaffective disorder should not be included.

  K&S Ch. 16

2. ABC. Based on Lisa’s history the most likely diagnosis is social anxiety disorder. First line pharmacotherapy consists of SSRIs and SNRIs. Benzodiazepines can also be very effective at decreasing anxiety when the patient has to function in a specific social situation. Lisa has already been tried on sertraline with poor results. However we don’t know what dosage was tried and for how long she was on the medication. She has also tried bupropion which tends to be very activating and can make anxiety worse. Our best bet would be to return to first line treatments and make sure they are given adequate therapeutic trials. Paroxetine and citalopram would both be considered first line. Clonazepam is a very reasonable add-on to one of these medications to control acute anxiety in specific social situations. Bupropion should be avoided for its potential to make anxiety worse.

  K&S Ch. 16

3. A. Cognitive behavioral therapy has solid evidence behind its use in social anxiety disorder as well as other anxiety disorders. The other answer choices do not. CBT should be considered the first line psychotherapy for social anxiety disorder.

  K&S Ch. 16

4. AB. Social anxiety disorder can overlap with or easily be misdiagnosed as schizoid personality disorder or avoidant personality disorder. Important to keep in mind is that in social phobia the patient fears embarrassment in social situations. In avoidant personality disorder the person fears rejection in relationships. In schizoid personality disorder the patient does not desire close relationships and is very happy without them.

  K&S Ch. 16

5. C. Patients with social phobia can demonstrate avoidance of public restrooms and this is clearly mentioned in the DSM IV. Their fear is not a specific phobia of the sink, toilet, or room. Their fear is of being embarrassed if someone hears, sees, or smells them using the bathroom. As such it is a form of social phobia.

  K&S Ch. 16

6. C. The non-generalized subtype of social phobia is performance anxiety. Successful treatment consists of beta adrenergic antagonists such as propranolol. These will decrease the physical manifestations of the anxiety. Always keep in mind that beta blockers are contraindicated in asthma due to their ability to cause bronchoconstriction. As such if given an asthmatic with performance anxiety one could choose a low dose benzodiazepine or SSRI (which would be considered second line agents for social phobia) but don’t give them a beta blocker. Also be careful with benzodiazepine doses if they have to speak publicly because of cognitive impairment.

  K&S Ch. 16

7. D. Fear of embarrassment is the major fear of those with social phobia. It is present in all situations that they fear, whether it is using a public restroom or talking at a party. Fear of rejection is found most prominently in those with avoidant personality disorder. They often don’t form relationships for fear of rejection. The need for someone to be with the patient in stressful or anxiety producing situations is a part of agoraphobia. The example is the person who won’t leave their front gate without a friend or family member with them. Having someone with them doesn’t help the avoidant or social phobia patient. Avoidance of relationships is most characteristic of the schizoid personality disorder patient, who neither has nor seeks close relationships. He is a loner and is happy that way. One could argue that avoiding relationships could also describe the avoidant patient, but the underlying motivation is different.The avoidant patient wants relationships but is afraid of rejection. The schizoid patient doesn’t want them at all.

  K&S Chs 16&17

8. D. According to DSM criteria, if the patient is under 18 years old the symptoms of social anxiety disorder must last for 6 months before the diagnosis is made. This makes sense as discomfort in social situations can be a normal part of adolescent development and we don’t want to diagnose anyone prematurely or inappropriately.

  K&S Ch. 16

9. ABC. Blushing, dry mouth, and sweating are all commonly seen in social phobia, as are muscle twitching and anxiety over scrutiny and embarrassment. Fear of dying is a more severe symptom which is seen in panic attacks, as would be dizziness and a sense of suffocation. Panic attacks can co-occur with social phobia but should be diagnosed as such if present. They are not a necessary part of the social phobia picture.

  K&S Ch. 16

10. A. As many as one third of patients with social anxiety disorder also meet criteria for major depressive disorder. Many social phobia patients also have alcohol problems. This makes sense when you think about the availability of alcohol in social situations and its ability to take the edge off of their anxiety and allow them to better tolerate social interaction.

  K&S Ch. 16

Vignette Eleven

1. AB. Of the choices given, the most likely to be in Carl’s differential are sleep apnea and major depressive disorder. Carl is experiencing decreased energy, fatigue, decreased concentration and poor sleep. Sleeping longer hours is not making him feel rested or better. Both of these diagnoses can present this way. The warning signs suggesting sleep apnea are Carl’s obesity and the snoring which drove his wife out of their bedroom. Sleep apnea can include morning headaches, long pauses without breathing during sleep, and waking up gasping for air. Because of the impact on mood and irritability it can masquerade as a psychiatric disorder and should be considered in overweight people who present looking depressed. Treatment for the disorder is a CPAP machine (continuous positive airway pressure).

  Klein–Levin syndrome is a rare condition characterized by hypersomnia and hyperphagia. These patients can have mood changes but also show confusion, lack of sexual inhibitions, hallucinations, disorientation, memory impairment and incoherent speech. Periods of excessive sleeping can extend from days to months. This is not the picture we are seeing with Carl.

  Narcolepsy is a pattern of excessive daytime sleepiness, sleep attacks, cataplexy, hypnagogic/hypnopompic hallucinations, and direct descent into REM sleep during sleep attacks. Sleep attacks are most common during heightened emotional states.

  K&S Ch. 24

2. AD. A workup for Carl should include thyroid function tests, as thyroid disorders can mimic mood disorders and must be ruled out. Nocturnal polysomnography (sleep study) is the test of choice to diagnose sleep apnea. A periodic limb movements of sleep test is not a real test. There is a periodic limb movements of sleep disorder (restless legs syndrome). It is diagnosed with nocturnal polysomnography, but there is not a special test with that name. CPAP is the machine used to treat sleep apnea. It does not diagnose sleep apnea. Therefore it would not be used as part of a workup.

  K&S Ch. 24

3. ABD. Possible complications of sleep apnea include decreased mood, increased risk of stroke, and cardiovascular complications. Patients with obstructive sleep apnea may have large necks but the sleep apnea doesn’t cause their neck to get bigger. The big neck contributes to the collapse of airway when they’re asleep.

  K&S Ch. 24

4. B. Sleep apnea is considered a dyssomnia. Dyssomnias are disorders relating to duration, quality, or timing of sleep. They can lead to too much sleep or too little sleep. Examples would be narcolepsy, sleep apnea, and circadian rhythm disorder. Parasomnias are disorders in which undesired behaviors occur during sleep or sleep transitions. Examples would be nightmare disorder, sleep terrors, or sleepwalking. Modafinil is used for narcolepsy, not sleep apnea. An increased risk for Parkinson’s disease is seen in REM behavior disorder, not in sleep apnea.

  K&S Ch. 24

5. D. The differential diagnosis for sleep apnea should include insufficient sleep, gastroesophageal reflux, and nighttime panic attacks. Pavor nocturnus is another name for sleep terror disorder. It presents as sudden arousal from sleep with behavior indicative of extreme fear. The patient may be awake but disoriented. They won’t remember the event the next day. Somnambulism is another name for sleepwalking disorder. It is more common in males. It can include retrograde amnesia as well as confusion. Treatment primarily involves maintaining safety for the patient. Jactatio capitis nocturna is a rhythmic movement disorder which includes head banging during sleep. Treatment involves preventing injury.

  K&S Ch. 24

6. AD. In obstructive sleep apnea airflow ceases during episodes and respiratory effort increases. This is in contrast to central sleep apnea where airflow stops and respiratory effort decreases. To be diagnosed with sleep apnea, the apnic episodes must last for 10 seconds or longer and occur a minimum of 30 times per night. In severe cases the patient may have as many as 300 episodes per night.

  K&S Ch. 24

7. ABD. Complications of obstructive sleep apnea include pulmonary and cardiovascular death, arrhythmias, transient alterations in blood pressure during each episode, pulmonary hypertension, and over time, an increase in systemic blood pressure which may be mistaken for essential hypertension.

  K&S Ch. 24

8. BC. REM sleep behavior disorder is a chronic progressive condition which is most often seen in men. There is a loss of atonia during REM sleep which leads to sometimes violent behaviors in which the patient acts out their dreams. Serious injury to the patient and those sleeping next to them is a risk. It tends to get worse with the use of stimulants, tricyclics and fluoxetine. Clonazepam and carbamazepine have proven effective in decreasing the symptoms.

  K&S Ch. 24

9. ABC. Sleep-related gastroesophageal reflux can cause awakening from sleep due to burning substernal pain or a sense of tightness in the chest. Coughing and choking sensations can occur repeatedly. Despite all of these symptoms airflow is not impeded as it is in sleep apnea. However given the symptoms, it is clear how this could be mistaken for sleep apnea.

  K&S Ch. 24

10. ABD. Sleep hygiene measures should be instituted in all patients with primary insomnia. They consist of arising at the same time each day, limit daily time in bed, discontinue any CNS activating drugs such as caffeine, avoid daytime naps, exercise, avoid evening stimulation, take hot baths before bed, avoid regular meals near bedtime, practice evening relaxation routines, and maintain comfortable sleeping conditions. The use of medication for sleep is considered treatment for insomnia but is not considered part of sleep hygiene.

  K&S Ch. 24

Vignette Twelve

1. ABCE. Ryan is a complex case with a great deal of missing information. As such there are several diagnoses to be included on the differential. Schizophrenia should definitely be considered as a result of his command auditory hallucinations and aggression history. Substance-induced psychotic disorder should be included as he has a significant alcohol history and we don’t have a urine toxicology on him so can’t say for sure that he hasn’t been using other drugs. Post-traumatic stress disorder needs to be explored because he has a very clear trauma history. He denies current flashbacks, but that is not enough data to rule out the diagnosis. Dementia NOS should be included because he only remembers one out of three objects on memory testing. This is clearly a poor result, but we have no idea what is causing it. He clearly had a concussion/head trauma in the past, he could have memory impairment due to chronic alcohol use or his poor performance on the exam could be a result of thought disorganization due to psychosis. His medical and cardiovascular risk factors place him at higher risk for vascular dementia. We don’t have a clear understanding of his executive functioning. We just don’t have enough information to know. As such, dementia NOS should be included until more information can be collected and we can clearly understand the pattern of symptoms we are seeing. The only disorder in the question that should not be included is generalized anxiety disorder. The vignette does not mention a single symptom of GAD.

  K&S Chs 10,13&16

2. ABCDE. A workup for Ryan should include, but is not limited to the following items. Thyroid function tests to rule out a biological cause for a mood disorder which could be presenting with psychotic symptoms. (We don’t have enough info in the vignette to rule this out as a possibility at this point.) Thiamine level should be included due to the possibility for Wernike–Korsakoff given the picture of heavy alcohol use and memory impairment. Head CT should be included to rule out possible organic cause of hallucinations and memory impairment, particularly with a history of head trauma. EKG should be included because of the need to treat CAH with antipsychotic medication and the need to monitor cardiac status during this process.In addition his hypertension, hypercholesterolemia, and diabetes put him at higher risk for heart disease. Urine toxicology should be included to rule out the possibility that other substances have been involved in this complex picture. The only one that should not be considered is prolactin level. The patient is not on any medication which would elevate prolactin at this point and as such there is no current need to monitor it.

  K&S Chs 10,13&16

3. CD. If we were to treat Ryan with ziprasidone the most likely side effects would include sedation and cardiac effects. Ziprasidone does not cause significant weight gain or extrapyramidal symptoms like some of the other antipsychotics. The patient should be instructed to take ziprasidone with food for adequate absorption.

  K&S Ch. 36

4. D. There is evidence that heavy cannabis use during early adolescence increases the relative risk of developing schizophrenia to as much as 6 times that of the general population.

  K&S Ch. 13

5. BD. Criteria A for schizophrenia is defined as two or more of the following for 1 month: delusions, hallucinations, disorganized speech, disorganized behavior, and negative symptoms. Only one is needed if the initial psychotic symptom is a bizarre delusion, voices commenting directly on behavior, or two voices conversing. Psychosis lasting longer than a month that does not meet criteria A for schizophrenia can either be a delusional disorder or psychosis NOS. All of the other diagnostic options would meet criteria A. Schizotypal personality disorder is characterized by bizarre, odd, and magical thinking but florid psychosis is not part of the picture. As such it is not the right choice.

  K&S Ch. 13

6. A. This question is important because it is antagonism at the 5HT2A receptor that makes the atypical antipsychotics atypical. It is through this mechanism that they help with negative symptoms rather than worsen them. Haloperidol is a typical neuroleptic and has no action on the 5HT2A receptor. Aripiprazole can be confusing because it is a partial agonist at D2 and 5HT1A but antagonizes 5HT2A.

  K&S Ch. 36

7. CD. In delusional disorder auditory or visual hallucinations are not present but tactile, olfactory or gustatory hallucinations may be if related to the patient’s delusions. Delusions are non-bizarre in delusional disorder. There is no memory impairment as in dementia (which may also present with psychosis). If the patient has delusional disorder somatic type then unnecessary medical interventions are quite likely.

  K&S Ch. 14

8. D. In brief psychotic disorder symptoms last between one day and one month after which the patient returns to normal functioning. It may be characterized by hallucinations, delusions, paranoia, disorganized speech and behavior, even catatonia. Antipsychotics are used to treat the episode while it is ongoing. There are no known primary preventative measures.

  K&S Ch. 14

9. ABCD. All of the following statements are true. Tactile hallucinations are more common in medical and neurologic conditions than in schizophrenia. Illusions are sensory misperceptions of actual stimuli. Delusions are fixed false beliefs which are not supported by cultural norms. Word salad is the violation of basic rules of grammar seen in severe thought disorder. Cataplexy is the sudden loss of muscle tone seen in narcolepsy attacks. Catalepsy is synonymous with waxy flexibility.

  K&S Chs 13&14

10. ABCD. The differential diagnosis for new onset psychosis should include many medical conditions. Among them are systemic lupus erythematosus, temporal lobe epilepsy, neurosyphilis, Wilson’s disease, AIDS, B12 deficiency, heavy metal poisoning, delirium, dementia, Huntington’s disease, pellagra, tumor, stroke, or bleed, herpes encephalitis, or autism. Phymatous rosacea is a skin disorder that has nothing to do with psychosis.

  K&S Chs 13&14

Vignette Thirteen

1. BE. This is a straightforward case with respect to initial early management. The predominant determinant of your actions as an emergency room psychiatrist is based on the principles of maintaining staff and patient safety and collecting more data, before approaching more complex workup and disposition decisions. As an emergency room psychiatrist it is imperative to collect as much history and collateral information as possible. The primary source of that information in this case is from police and emergency medical technicians, because there are no identified family members or collaterals from whom one might obtain information. Once a proper history of events is obtained, further workup, management and disposition planning can be made.

  Even before obtaining a history though, the psychiatrist must ensure that the patient and staff in the emergency room are safe. Safety of patient and others comes before all in an acute or emergency room setting. To this end, the psychiatrist’s first maneuver should be to have the agitated or aggressive patient restrained and medicated so that no acute harm comes to the patient or the staff that are attending to him. Haloperidol, with or without lorazepam, when given intramuscularly, is an excellent choice of management. The initial dosage depends upon the age and body size of the individual, as well as the severity of the agitation. An initial dose of haloperidol 5 mg intramuscularly can be repeated every 20–30 minutes (with or without addition of lorazepam) until sedation ensues. With the advent of short-acting, atypical antipsychotic agents, such as aripiprazole, ziprasidone and olanzapine, strong consideration should be given to these agents, given their superior safety and tolerability profile.

  K&S Ch. 4

2. CD. There are many well-described risk factors for aggressive behavior in patients. Many major mental illnesses predispose the patient to potential acting out and acts of violence directed against others. These conditions include: mental retardation; ADHD; conduct disorder; delirium; dementia; psychotic disorders; mood disorders; intermittent explosive disorder; adjustment disorder with disturbance of conduct and cluster B personality disorders. The likelihood of violence to others increases during periods of decompensation in major mental disorders. Acute use of alcohol or other substances of abuse can also trigger acute dangerousness to others. The frequency of violence among males outweighs that in females, when it comes to homicide, assault and battery, or rape. With respect to domestic violence episodes, the rates of outward violence are about equal in both sexes. The most tell-tale predictor of violence is, of course, a history of prior violent behavior. Being a battered, underprivileged child predisposes the individual to a future likelihood of violent behavior. Low educational level, having poor family supports, unstable housing, unemployment, and poor coping skills or a lack of resources for help, can all be contributors to homicidality and violence. Medical problems, unless they involve acute or chronic physical pain, do not typically predict violent acts of aggression in individuals.

  K&S Ch. 4

3. ACD. The psychiatrist should attempt to conduct an assessment with a potentially violent patient in a way that promotes containment of the behavior and limits the potential for harm. There are several steps that a psychiatrist can take to try to minimize the patient’s agitation and potential risk. The interview should be conducted in a calm, quiet and nonstimulating area. Sufficient physical space should be available for both patient and psychiatrist, with no physical barrier to leaving the room for either one. The psychiatrist should avoid any kind of behavior that might be misconstrued by the patient as threatening, such as standing over the patient, touching the patient, or staring at the patient. The psychiatrist should ask whether the patient is carrying weapons, but should not ask the patient to hand over any weapons. Assistance from security personnel, as well as physical or chemical restraints, may be helpful if the psychiatrist deems these to be appropriate.

  K&S Ch. 7

4. BEF. The patient is voicing homicidal ideation and perhaps even intention, directed at his mother. Psychiatrists can be sued for failing to protect society from the violent acts of their patients if it was reasonable for the psychiatrist to have known about the patient’s violent tendencies and if the psychiatrist could have done something to safeguard the public. The landmark case of Tarasoff v. Regents of the University of California, resulted in the California Supreme Court ruling that mental health professionals have a duty to protect identifiable, endangered third parties from threats of imminent and serious harm made by their outpatients. In this case, the psychiatrist is certainly acting quite responsibly in wanting to contact the patient’s mother to inform her of the patient’s feelings and possible intentions of harm directed against her. Of course, the psychiatrist in this case, should not discharge the patient, particularly if the patient continues to voice these feelings and intentions.

  In this case, the most conservative course of action would be to admit the patient to the psychiatry unit, most likely on an involuntary basis, given his lack of cooperation with you in the emergency room. This would enable safety, stabilization and further history taking to take place simultaneously in a confined clinical setting, with the highest level of care and clinical attention to the patient. It would not be wrong to detain the patient overnight in the emergency room so that a social work consultation can be obtained in the morning, focused on obtaining more detailed history and collateral information about the patient and also adding more weight to the disposition plan for the patient. There is no evidence in this vignette that the police have intentions to arrest and charge the patient with a crime once he is psychiatrically cleared in the emergency room. Typically, police officers will inform the psychiatrist or the triage nurse of this so that they can be contacted to pick the patient up upon discharge to bring the patient to the police station for booking. Starting aripiprazole and divalproex sodium is pre-emptive and presumptive of a psychotic or bipolar disorder that warrants ongoing medication management of this kind. There is no indication of any such diagnosis in this vignette given that too little symptomatic information is presented.

  K&S Ch. 58

5. AB. Given the patient’s refusal of oral medication, the psychiatrist should begin thinking about the need for a long-acting, injectable antipsychotic agent to ensure the patient’s compliance and stability. Of the six agents listed in answers A through F, only olanzapine and risperidone have long-acting injectable formulations (Zyprexa Relprevv and Risperdal Consta). These would be the two agents of choice in this case, given the current presentation of patient’s refusal to take oral medications on a voluntary basis. Olanzapine and risperidone also come in oral disintegrating tablet formulation (Zydis and M-tabs, respectively). This may be an advantage to the psychiatrist, if the patient eventually agrees to take oral medication. The melting tablets can be given by nursing staff while the patient is directly observed. This formulation prevents the cheeking or spitting out of medication once it has been placed in the oral cavity. If the patient is not acutely agitated, but refuses oral medication, a court petition for medication-over-objection may need to be presented to a judge, depending on the state.

  K&S Chs 36&58

6. BCD. In this case, the patient needs a higher level of outpatient mental health care than a simple outpatient clinic setting. This stems from the fact that he has failed this level of care previously and has relapsed numerous times in the past. He also has a history of noncompliance with medication and very poor insight and judgment with respect to his mental illness and how to cope with it. The assertive community treatment team (ACT team) model exists in most states in the USA. It is truly the highest level of outpatient mental health care because the treatment team visits the patient at the patient’s residence multiple times every month. The team helps the patient with medication monitoring and management and in many cases can prevent patient noncompliance that may result in an acute decompensation. The program was developed in the 1970s by researchers in Madison, Wisconsin. The patient is assigned to a treatment team that is composed of a psychiatrist, nurse, social workers, case managers and other possible interventionists. The team can provide care and clinical coverage virtually 24 hours a day, 7 days a week. The high staff-to-patient ratio (anywhere from 6 to 12 staff per patient) enables the ACT team to help the patient with a rich variety of case management modalities and options.

  Partial hospital programs are useful for refractory patients who are discharged from the hospital. These programs are designed to be time-limited and are a step-down from the acute inpatient setting for the patient. These partial hospitals offer a less restrictive level of care for the chronic psychiatric patient, while maintaining a well-structured framework that is close to that offered on an inpatient hospital unit. The patient sleeps at home and comes to the partial hospital each day to attend programming and get physician and nursing care during the day, as well as case management and psychotherapy. Classically, patients can spend up to 12 to 16 weeks in these programs following an acute hospitalization. They should then be discharged to a less-restrictive outpatient level of care for ongoing maintenance care.

  The continuing day treatment program for the chronically mentally ill is also an excellent choice for the patient presented in this vignette. These programs run 5 to 7 days a week and provide a less structured, though comprehensive, treatment modality for these patients. Patients sleep at home and attend the program during the day, where they receive a similar array of therapies to that which is available in the partial hospital setting. Key to this modality (and that of the partial hospital as well) is the fact that nursing staff can administer oral and injectable medication on site and while directly observing the patient. The census of a day program is usually greater than that of a partial hospital program, due to the fact that the psychiatrist will usually see and evaluate the patient less often in the day treatment program setting.

  K&S Ch. 13

Vignette Fourteen

1. DE. Attitude in the mental status exam describes the patient’s attitude towards the examiner. Words commonly used include cooperative, friendly, interested, seductive, defensive, hostile, evasive, apathetic, ingratiating, and guarded. Based on the information in this vignette the patient is best described as cooperative and friendly.

  K&S Ch. 7

2. B. Affect is the patient’s present emotional responsiveness based on facial expressions and expressive behavior. It may or may not be congruent with mood. Words used to describe affect include full range (within normal range), constricted, blunted, and flat. Full range would be considered normal. Flat would be used to describe a patient who is showing no signs of affective expression. A patient with constricted affect shows less emotion than someone who is full range but more than someone who is blunted. Someone who is blunted shows less emotion than someone who is constricted but more than someone who is flat.

  K&S Ch. 7

3. DE. Thought process refers to the form of the patient’s thoughts. Examples of this would be goal directed, linear, circumstantial, tangential, loosening of associations, flight of ideas, thought blocking, neologisms, racing thoughts, or word salad. In this case Robert’s thoughts are completely normal and as such the best description would be linear or goal directed.

  K&S Ch. 7

4. A. Impulse control refers to the patient’s ability to control sexual, aggressive and other impulses. It may be determined based on recent history and the patient’s behavior during the interview. It is often rated as good, fair, or poor.

  K&S Ch. 7

5. A. Insight is the patient’s understanding and awareness of his or her own illness. It can be rated as good, fair, or poor.

  K&S Ch. 7

6. A. Judgment is reflection of the patient’s capacity for good social judgment. What kind of decisions are they making? Do they understand the outcome of their behavior? Can they predict what they would do in imaginary situations? It can be rated as good, fair, or poor.

  K&S Ch. 7

7. A. Perceptions primarily refers to hallucinations, be they auditory, visual, tactile, olfactory, or gustatory. In Robert’s case there are none present. Choices B, C, D, and E may be true for Robert but they were never asked about in the vignette and Robert never mentioned any of them. Therefore we have no evidence of whether he is experiencing them or not.

  K&S Ch. 7

8. A. Sialorrhea (excessive drooling) is a common and predictable side effect of clozapine. Robert and his doctor should keep an eye on it but it is not a reason to stop the medication if the patient can tolerate it. It may get worse with a dosage increase.

  K&S Ch. 7

9. C. The appropriate schedule for measuring WBC/ANC in a patient on Clozapine would include a baseline WBC/ANC, weekly WBC/ANC for the first 6 months, biweekly WBC/ANC for the next 6 months, and monthly WBC/ANC thereafter.

  K&S Ch. 36

10. ABCDEFG. All of the tests listed except an echocardiogram would be appropriate to monitor in Robert over time. EKG is important for anyone on antipsychotics, paying special attention to the QTc interval. Clozapine is metabolized through the liver so LFT’s are important. A clozapine level to ensure a therapeutic dose is important. Fasting glucose, weights, waist circumference, triglycerides, and cholesterol are all important parts of monitoring for metabolic syndrome, which we know clozapine has a high likelihood to cause.

  K&S Ch. 36

Vignette Fifteen

1. AC. There are very few studies on dissociative identity disorder (DID), so very little epidemiological data exists on the subject. Studies have pointed towards a female to male ratio of diagnosed cases as somewhere between 5 and 10 to 1. The disorder is principally linked to severe early childhood trauma experiences, usually abuse, neglect, or maltreatment. The rates of reported trauma in adult sufferers of DID range from 85 to 97%. Physical and sexual abuse are most frequently reported as the type of childhood trauma sustained by sufferers of DID. Studies have not, up until now at any rate, demonstrated much in the way of a genetic component to the disorder. About 70% of DID patients also meet criteria for post-traumatic stress disorder (PTSD). A key DSM criterion for DID is the inability of the patient to recall important personal information that is too extensive to be explained by ordinary forgetfulness. About 40 to 60% of DID patients also meet criteria for somatization disorder. Psychotherapy is a key component in the progress and recovery of the DID patient. Those modalit ies that have been seen to be useful to DID patients include supportive psychotherapy, dynamic psychotherapy, cognitive therapy and hypnotherapy.

  K&S Ch. 20

2. BF. Group psychotherapy can be very useful in DID, but it is better conducted only with patients with this disorder because of the tendency of other patients to be overly fascinated or frightened by these patients. Prognosis of DID is poorer in patients with comorbid organic mental disorders, psychotic disorders, and severe medical illnesses. Refractory substance abuse disorders and eating disorders are also thought to worsen the prognosis of patients with DID. As far as appropriate medication choices are concerned, patients with DID may benefit from a low-dose benzodiazepine, which may help to diminish anxiety, hyperarousal, panic, and intrusive symptoms suffered by these patients. A proper substance abuse history should be taken prior to starting any benzodiazepine of course. Patients that are able to maintain a high level of daily functioning tend to do better with this condition than those that are lower functioning.

  K&S Ch. 20

3. D. There are many valid choices of medication to address the myriad of symptoms that may accompany DID. Lithium is not one of them. It has no place as a mood stabilizer in DID, unless there is a concomitant diagnosis of bipolar disorder. On the other hand the anticonvulsant and antipsychotic mood stabilizing agents are excellent choices for DID patients. These include: divalproex sodium, lamotrigine, gabapentin, topiramate, carbamazepine, risperidone, quetiapine, olanzapine, and ziprasidone. The SSRI class of antidepressants also has been shown to be efficacious in reducing the symptoms associated with DID. These of course include fluoxetine, paroxetine, sertraline, citalopram, and escitalopram. These are useful for depressive symptoms and mood lability, but may be less effective for the intrusive hyperarousal symptoms of PTSD often associated with DID.

  K&S Ch. 20

4. E. Dissociative identity disorder is conceptualized as a trauma spectrum disorder. Many patients with DID, up to 70%, meet criteria for PTSD. About 40 to 60% of patients with DID also meet criteria for somatization disorder. Many DID patients also meet criteria for a mood disorder, in particular the depressive disorders. Frequent rapid mood swings are also seen commonly in DID patients. These mood swings are not believed to be bipolar in nature, but are believed to be post-traumatic and dissociative in nature and not true cyclic mood disorder.

  K&S Ch. 20

5. CE. Patients with dissociative identity disorder must be ruled out for malingering, factitious disorder, conversion disorder and somatoform disorders. The following indicators may point a clinician away from DID as a diagnosis and towards one of these psychosomatic disorders: increased symptoms when under observation, refusal to allow collateral contacts, symptom exaggeration, outright lies, using fabricated symptoms to excuse antisocial behavior, or a history of legal issues. Patients with veritable DID are generally conflicted, confused, ashamed and distressed by their symptoms. Patients with nongenuine DID often show little dysphoria about their disorder.

  K&S Ch. 20

Vignette Sixteen

1. CE. Mr. Moran is showing the signs and symptoms of progressive memory and executive function decline that are compatible with a dementia. Dementia is defined as a progressive loss of cognitive functioning in the presence of a clear sensorium. The basic faculties that are affected include memory, thinking, attention and comprehension. Dementia can be caused by different etiological factors, and can be multifactorial. About 15% of demented patients have reversible illness if treatment is rendered prior to the development of irreversible damage. Mr. Moran’s presentation could well be that of a dementia of the Alzheimer type. He has been confused and forgetful, which are cardinal features of Alzheimer’s dementia. He has also been wandering aimlessly and cannot remember his way around familiar territory. This is essentially a visual agnosia; is presented with places that are familiar to him, but he does not remember them or recognize them and he cannot negotiate his way around them. Part of the essential criteria for Alzheimer’s dementia are the classic cognitive disturbances of aphasia, apraxia, agnosia and disturbance in executive functioning. A patient must have at least one of these four deficits, with marked memory impairment, in order to meet criteria for dementia of the Alzheimer type. Mr. Moran also forgets the names of household items. This is both an agnosia (he cannot name/recognize objects) and an apraxia (he has forgotten how to use certain common items).

  Now, Mr. Moran could certainly be suffering from a vascular dementia, or a combination of a vascular dementia with Alzheimer’s dementia. The differential diagnosis of vascular dementia presents itself in this case by the patient’s medical history. The patient, we are told, has a history of hypertension, diabetes, hyperlipidemia, and cardiovascular disease. He is a vasculopath and certainly these cardiovascular risk factors are also stroke risk factors. He could be having repeated silent strokes that eventually begin to compromise his cognitive functioning. The medical and neurological examination and work-up will help you clarify which type of dementia is the more likely to be the culprit of his decline in functioning in this case.

  Note that there is no mention in this vignette of any manifestation of depression or anxiety, which make these two answers incorrect in this case. As for the possibility of a dementia due to diffuse Lewy-body disease or a frontotemporal dementia, these are very specific dementing entities that present with their own specific set of symptoms and signs, none of which are really mentioned in this vignette. We urge you to refer to other question explanations in this volume that elaborate on these two special types of dementias. They do appear frequently on standardized examinations and it is essential to know their features.

  K&S Ch. 10

2. CFG. A medical and neurological workup are essential for this patient to help you clarify your differential diagnosis. You should be thinking about a dementia of the Alzheimer type, a vascular dementia, or a dementia with features of both Alzheimer and vascular types. An outpatient brain imaging study is essential. The MRI is best, as it affords the most anatomic detail and its sensitivity to ischemic lesions is much greater than CT scan. A brain tumor is not completely out of the realm of possibility in this case, and the MRI can be performed with gadolinium contrast administration to see if there is a presence of any enhancing space-occupying lesion that could be responsible for this patient’s cognitive impairment.

  Neuropsychological consultation for a testing battery can be extremely valuable in a case such as this. A thorough battery includes testing for cognitive and executive functioning and is highly sensitive to subtle deficits in cognition, visuospatial abilities, and multitasking and reasoning skills. In the face of a negative or nonspecific medical workup, such a battery may lend weight to a subtle diagnosis of Alzheimer’s dementia.

  An electroencephalogram is not a high priority in this case. There is no evidence of seizure activity, or anything remotely resembling ictal events, from the history given in this vignette. For such a test to be useful, a picture of repeated discrete events that involve waxing and waning of attention and awareness should be a part of the presenting history, which it is not in this case.

  Starting medication can be useful for this patient, but which one(s)? There is no evidence of depressive symptoms or sleep disturbance presented in this case history. Therefore, sertraline and trazodone would not be very helpful at this juncture. On the other hand, the case history points strongly in the direction of a dementia, and donepezil would be an excellent choice to start, even before a workup is conducted and a diagnosis solidified. Donepezil (Aricept) is FDA-approved for Alzheimer’s dementia and it may have efficacy in vascular dementia as well, though the FDA did not approve the agent for this indication. The dosing is simple: 5 mg daily for the first month, increasing to 10 mg daily thereafter. New evidence suggests further titration to the new 23 mg daily dose may be more beneficial in maintaining cognition than the former 10 mg dosing. Donepezil can always be stopped if the diagnosis of Alzheimer’s dementia is brought into question once a workup has been completed on this particular patient.

  K&S Ch. 10

3. BCF. This patient is getting to be too much to handle at home, without outside support, assistance and guidance. Soon, his daughter will become a patient herself, because her emotional and physical burden of caring for the patient will cause her caregiver burnout. Thus, referring the patient’s daughter to caregiver support programming and groups is a wise thing to do. Obtaining a visiting nurse consultation in the patient’s home is also an excellent maneuver in this case. A homecare nurse can assess the patient’s basic homecare needs and make appropriate recommendations to his physicians for these services. Ultimately, if around the clock homecare is not feasible for the patient and his family members, consideration will have to be given to skilled nursing facility placement, if his condition continues to deteriorate, which we might expect to happen in this particular case.

  An ACT team referral is quite inappropriate in this case. Such teams are unable to provide the broad-based medical, nursing and homecare that this patient will eventually need. ACT teams are based on a psychiatric model and are charged with the responsibility of helping mental health patients to maintain their stability in the outpatient setting, despite a lack of insight and ability to do so themselves. Medical issues that are deeply complex, such as in this case, are far too burdensome for ACT teams, that have only a psychiatric nurse and a psychiatrist among their team members. Family members can certainly provide coverage at home for this patient, if he begins to become home-bound. This, however, is not ideal, as family members are not usually trained to this intense medical task and they generally have to sacrifice their own lives and well-being to tend to their relative. A subacute rehabilitation facility is hardly an appropriate placement for this patient. Such facilities are geared towards patients that need intensive physical therapy to restore their ambulatory functioning. These placements are deemed to be temporary and the expectation is that these patients will recover functional ability and eventually make their way home, whenever possible.

  K&S Ch. 10

4. C. Alzheimer type dementia has an average survival expectancy of about 8 years from the time of initial onset of the disease. Studies typically point to a range from about 5 to 10 years of survival for these patients. Note that more than 50% of nursing home beds in the USA are occupied by patients with Alzheimer’s dementia.

  K&S Ch.10

5. ADG. Alzheimer’s dementia is treated with either an acetylcholinesterase inhibitor, a NMDA antagonist, or both together. The three acetylcholinesterase inhibitors currently in use in the US include donepezil, rivastigmine and galantamine. The NMDA antagonist that is FDA-approved for Alzheimer’s dementia is memantine.

  With respect to the treatment and prevention of vascular dementia, the approach is to treat modifiable underlying risk factors for cerebrovascular disease. These measures include prescribing antiplatelet aggregants such as aspirin, clopidogrel, or aspirin/dipyridamole combination therapy (Aggrenox). Antihypertensive medication, antidiabetic medications and insulin, as well as lipid-lowering medications all have a place in the treatment and prevention of further worsening of cerebrovascular disease. Smoking cessation is ultimately a very important recommendation to patients in this regard as well.

  The other agents mentioned in answer choices B, C, E and F have no real place in the treatment of dementia itself, though they may be useful in treatment associated comorbid symptoms and problems.

  K&S Ch. 10

6. F. Dementia is often accompanied by other devastating symptoms that are associated with cognitive decline. Patients can often be seen to exhibit subtle or gross personality changes that are uncharacteristic for them when at baseline. They may become depressed and unmotivated for self care, even if they still have the cognitive capacity to engage in this behavior. Aggression and violent verbal and physical outbursts can be seen in moderate to late-stage Alzheimer’s dementia. Sundowner syndrome can also be seen, which occurs when day–night cycle is disrupted by a lack of external light or lack of cues as to the date, season and time of day. Patients in this instance can become delirious, aggressive, agitated and acutely more confused as the day proceeds and may need sedation to abort such episodes. Such episodes may also be accompanied by frank delusions and hallucinations. Mania, however, is not typically seen in dementing patients, unless they have a history of bipolar or schizoaffective disorder with such episodes in the past.

  K&S Ch. 10

7. DE. Benztropine (Cogentin) and diphenhydramine (Benadryl) are dangerous in the demented patient because their anticholinergic properties can worsen cognitive impairment and cause greater confusion in these patients. Patients exposed to these agents may also develop an anticholinergic delirium and may require sedation due to agitation and disinhibition of their behavior. The rest of the medication choices listed are all viable therapies for the patient presented in this vignette.

  K&S Ch. 10

Vignette Seventeen

1. AE. Wanda of course is suffering from a delirium. Delirium is characterized by a waxing and waning of level of consciousness and a cognitive impairment that evolves over a short period of time. Common associated psychiatric symptoms include mood disturbance, perceptual disturbance, and behavioral disturbance. Delirium usually evolves rapidly over a period of hours or days.Irritability, impulsivity, anger, and rage, can all be seen at times within the constellation of symptoms that make up a delirium. Cognitive deficits can manifest as memory and language impairment. There may be noted incoordination (apraxia) in certain cases of delirium as well. Patients with delirium often have disturbance of sleep and/or of the sleep-wake circadian cycle. Identification and reversal of underlying causes of delirium are the cornerstones of treatment of the disorder.

  K&S Ch. 10

2. ADE. Wanda is of course suffering from an acute delirium. Delirium is defined as an acute onset of waxing and waning level of consciousness, with impairment in cognitive functioning. Recognizing a delirium is important so that identifying the underlying causes can be undertaken and appropriate measures taken to treat and prevent these causes. Delirium prevalence is highest in postcardiotomy patients. Some studies point to these rates as high as 90%. Advanced age is a risk factor for delirium, but generally in the over 70-year-old population. About 30 to 40% of hospitalized patients over age 65 have an episode of delirium. Preexisting brain damage or disease is a serious risk factor for delirium. This patient has multiple sclerosis and is in the midst of an acute exacerbation of that disease. This certainly predisposes her to an acute delirium. A history of alcohol abuse or tobacco smoking is also a risk factor for an acute delirium. Diabetes, cancer, blindness and malnutrition are also delirium risk factors. Hypertension, in and of itself, is not a risk factor for delirium. According to DSM-IV-TR, the male gender is an independent risk factor for delirium. Intoxication or withdrawal from pharmacologic or toxic agents is certainly a strong risk factor for delirium. The fact that Wanda is on interferon at home and methylprednisolone in the hospital, can predispose her to a delirium. Classic medications that can predispose patients to a delirium include narcotic painkillers, steroids, anesthetic agents, antineoplastic agents and anticholinergic agents and antibiotics, antifungals and antiviral agents.

  K&S Ch. 10

3. D. The exact pathophysiology of delirium is not well-understood. The major neuroanatomical area implicated in delirium is the reticular formation. The reticular formation is the area of the brainstem responsible for regulation of attention and arousal. The major pathway implicated in the etiology of delirium is the dorsal tegmental pathway. This pathway projects from the mesencephalic reticular formation to the tectum and thalamus.

  K&S Ch. 10

4. B. The complex pathophysiology of delirium is not well understood. Studies tend to point towards decreased acetylcholine activity in the brain as a causative factor in delirium. The delirium associated with alcohol withdrawal has been associated with hyperactivity of noradrenergic neurons in the locus ceruleus. Serotonin and glutamate have also been implicated in the pathophysiology of delirium.

  K&S Ch. 10

5. C. The EEG characteristically shows generalized background slowing in delirium. Triphasic waves are mostly specific for a hepatic encephalopathy and not for delirium of other etiologies. PLEDS is the characteristic EEG finding in herpes simplex virus encephalitis. Temporal lobe spikes would be indicative of a seizure focus in the temporal lobe. Hypsarrhythmia is an EEG pattern of high amplitude waves and spikes on a chaotic disorganized background that is characteristic of infantile spasms.

  K&S Ch. 10

6. CE. Psychosis and insomnia are the two major symptoms of delirium that are likely to warrant medication management. Haloperidol, a butyrophenone antipsychotic agent, is the most commonly used sedative agent used in cases of hospital-based delirium. It can be given orally, intramuscularly or intravenously, though the intravenous route of administration is not FDA-approved. Despite that fact, intravenous haloperidol is standard of care for this type of patient in an intensive care unit setting. Note that a monitored bed is essential when giving intravenous haloperidol because of the risk of torsades de pointes, a potentially fatal cardiac arrhythmia. Use of atypical antipsychotics such as risperidone, olanzapine, quetiapine and aripiprazole are felt to be effective in delirium management, though there is a dearth of studies to lend evidence to this management. Anticholinergic drugs like diphenhydramine and benztropine, along with phenothiazine antipsychotics such as chlorpromazine, are very poor choices in delirium management. Use of such drugs can prolong or even worsen the delirium, rather than improve it, and so they are to be avoided in delirium management. Insomnia can be treated with short or intermediate half-life benzodiazepines such as lorazepam. However, any benzodiazepine can have a paradoxically agitating effect on patients with delirium. Thus the use of these agents is generally reserved for patients with known alcohol-withdrawal delirium (delirium tremens).

  K&S Ch. 10

7. BEF. Even though the onset of delirium is usually acute and sudden in nature, premonitory or prodromal symptoms can be seen in the days (not months!) preceding the onset of florid symptoms. The symptoms of delirium usually persist while causally relevant factors are present, though typical duration of episodes is usually about 1 week. The more advanced the age of the patient and the longer the delirium episode lasts, the longer the delirium usually takes to resolve. Delirium is known to increase patient mortality within the first year following an episode. This is due mostly to the serious nature of the concomitant medical problems that lead to the delirium. Controlled studies have not been conducted to demonstrate that delirium typically progresses to a dementia. Nevertheless, many clinicians believe this to be the case. It is however well understood that periods of delirium may lead to symptoms of depression or post- traumatic stress disorder in the aftermath of the episode.

  K&S Ch. 10

Vignette Eighteen

1. D. Allan is of course suffering from body dysmorphic disorder (BDD). The cause of this disorder is unknown. There is a high comorbidity with depressive disorders. Patients with BDD often have family histories of mood disorders and obsessive-compulsive disorder. In many patients with BDD, the symptoms are responsive to serotonin-specific medications, which leads researchers to feel that the disorder itself is related to imbalances in serotonin.

  K&S Ch. 17

2. C. All of the answers are valid psychodynamic explanations for adulthood neurosis. However, the most accurate explanation of BDD symptoms falls under the defense mechanism of a displacement of sexual or emotional conflict onto body parts unrelated to the issue. The defense mechanisms of repression, projection, distortion, dissociation and symbolization also are in play in this dynamic.

  K&S Ch. 17

3. AC. Data indicate that BDD typically has its initial onset between the ages of 15 and 30 years. In this regard, Allan is quite typical. Women are more affected than men, though slightly. So in this regard, Allan would be considered atypical. Most sufferers of BDD are unmarried and in this regard Allan is among the majority. The fact that Allan has never suffered a major depressive episode in the past is quite atypical of BDD. There is a high comorbidity of BDD with mood and depressive disorders. One study found that 90% of BDD sufferers had experienced a major depressive episode in their lifetimes. The fact that Allan is high-functioning and spends a lot of money on himself and his appearance has no bearing on his BDD at all.

  K&S Ch. 17

4. ACE. Pharmacotherapy for BDD is usually approached first-line with serotonergic agents such as SSRIs, MAOIs, or TCAs. These serotonergic agents are typically effective at reducing symptoms in about 50% of patients. Augmentation with buspirone, lithium, methylphenidate, or an atypical antipsychotic is appropriate if first-line therapy is ineffective.

  K&S Ch. 17

5. C. BDD usually begins during the adolescent years. The onset can be gradual or abrupt. The disorder usually has an undulating course with few symptom-free intervals. The part of the body on which concern is focused may remain the same or it may change over time. The preoccupation with imagined defects is almost always associated with significant distress and impairment.

  K&S Ch. 17

Vignette Nineteen

1. CEF. Of course, Grace meets DSM criteria for a somatization disorder and not for a conversion disorder. Remember that a somatization disorder begins before age 30 and symptoms persist over a period of years. The somatization disorder diagnosis requires the presence of the specific list of symptoms from multiple systems at any time during the course of the disorder. Specifically, the patient must have at least four pain symptoms, two gastrointestinal symptoms, one sexual symptom and one pseudoneurological symptom. Conversion disorder differentiates from somatization disorder by manifesting as only a pseudoneurological symptom or symptoms, which typically involve motor or sensory functioning. Other bodily systems, gastrointestinal and sexual are not part of the clinical picture of conversion disorder. Note that pain symptoms fall in a nebulous category that encompasses both the physical and neurological and so could be a part of either a somatization or conversion disorder. Recall that conversion and somatization disorders are both disorders in which the patient’s symptoms are not being voluntarily produced. They are manifested involuntarily as a product of psychological distress and interpersonal problems. Most often, these triggering conflicts are subconscious, though patients may at times be able to identify stressors and triggers when asked about them. Another classic difference between these two disorders is the way in which patients react emotionally to their symptoms. Somatization disorder patients often describe their symptoms in a more histrionic, emotional, and exaggerated fashion. Conversion disorder patients typically display la belle indifference, which is simply an inappropriately cavalier attitude towards serious symptoms and a marked unconcern regarding what may appear to be serious impairment.

  K&S Ch. 17

2. ACF. There are multiple etiological theories that attempt to explain the complexity of somatization disorder. Certainly, psychosocial factors can play a great role in the presentation of this disorder. Many such patients are found to originate from unstable homes, with histories of physical abuse. Psychodynamically, the symptom presentation may be conceptualized as a manifestation of repressed instinctual impulses. Biological factors seem to point to a neuropsychological relation of somatization disorder to attention deficit symptoms or disorders. Studies using evoked potentials have proposed a link between the somatic symptoms and those of excessive distractibility, inability to habituate to repetitive stimuli, and lack of stimulus selectivity. A small number of neuroimaging studies have demonstrated decreased frontal lobe and nondominant hemisphere metabolism.

  Genetic factors may also play a role in the etiology of somatization disorder. The disorder tends to run in families and occurs in approximately 10 to 20% of the first degree female relatives of probands of patients with somatization disorder. One study demonstrated a 29% concordance rate of somatization disorder in monozygotic twins and 10% in dizygotic twins. Male relatives of women with somatization disorder show an increased risk of antisocial personality disorder and substance-related disorders. The other answer choices have no proven relationship to the etiology of somatization disorder and are merely nonsense distracters.

  K&S Ch. 17

3. ACD. Women with somatization disorder tend to outnumber men with the disorder by about 5 to 20 times. The lifetime prevalence of the disorder in the general population is about 1 or 2%. Among general primary care patients, patients with somatization disorder may number about 5 to 10%. The disorder is inversely related to social position and occurs most often in patients with low income and little education. Somatization disorder must begin before age 30 and typically begins in the teenage years. Two disorders that are not more commonly seen in patients with somatization disorder include bipolar I disorder and substance abuse.

  K&S Ch. 17

4. BCD. Somatization disorder is a chronic, undulating and relapsing disorder that rarely remits completely. Patients with the disorder are no more likely to develop another medical illness in the next 20 years than patients who do not have somatization disorder. A patient with somatization disorder has about an 80% chance of being diagnosed with the disorder 5 years later. It is unusual for patients with somatization disorder to be symptom-free for more than a year. The prognosis of the disorder overall is poor to fair at best.

  K&S Ch. 17

5. D. Both individual and group psychotherapy seems to be the most useful strategy for somatization disorder, as these have been shown to reduce patients’ personal health expenditure by 50%. This is so because psychotherapy helps to decrease rates of hospitalization in these patients. Giving psychotropic medications to these patients, even when somatization disorder is accompanied by a mood or anxiety disorder, is a risk. This is because these patients are notorious for marginal or poor compliance with such medications. There is very little data that exists to support the use of psychotropic medications in somatization disorder when it is not comorbid with other mental disorders.

  K&S Ch. 17

Vignette Twenty

1. ACF. Pain and opioid dependence, when they coexist, make up one of the most delicate and difficult disease combinations to treat effectively. This is even more complex when alcohol and cannabis abuse cloud and complicate the clinical scenario. Detoxification of the patient off of the painkillers, as well as alcohol and cannabis, on an inpatient basis is certainly an excellent maneuver. Once the patient comes out of the inpatient facility, a subsequent referral to pain management and perhaps physiatry would be ideal, because the patient will certainly need to have his pain addressed at that point. Outpatient narcotic tapers typically don’t work well for a number of reasons. The patient is not being monitored and so is being asked to use his judgment and willpower to adjust the medication on his own. We already know that Kerry has a problem with abuse and dependence on a variety of substances. Asking him to monitor his own home-based taper off narcotics is a bit naïve on the part of any good clinician. There is no doubt that he will fail to manage such a taper appropriately, because of chronic pain and a lack of willpower and a predisposition to addictive behavior. Also, giving Kerry naltrexone long-acting monthly injections (Vivitrol) is a pipe-dream. This medication is FDA-approved for both alcohol and opioid relapse prevention, but it has no analgesic properties whatsoever. Naltrexone will certainly reduce the cravings for both narcotics and alcohol; however, one cannot take narcotics with Vivitrol because at best, they won’t work because they will be blocked by the antagonistic effect of the Vivitrol and at worst, the combination of narcotics with Vivitrol could induce a precipitated withdrawal state. Guidelines dictate that at least 5 days must elapse between the last dose of a short-acting narcotic (or 10 days if a long-acting narcotic is being taken) and the first dose of naltrexone.

  Sending Kerry to a specialized pain clinic is an outstanding option. Pain specialists, who are neurologists, psychiatrists, internists, anesthesiologists and physiatrists, are well-poised to put Kerry on a strict painkiller regimen that will be tailored to his abusive tendencies. Options for this include fentanyl transdermal patch therapy or methadone for chronic pain.They will also recommend ancillary services like physical therapy to help Kerry improve his condition and his pain.

  Continuing Roxicodone is absolutely not an option in this case. Kerry will merely continue to overuse and abuse this medication, which is a short-acting opioid narcotic useful for only short-term, acute treatment of intense pain, such as post-operative pain. Disulfiram (Antabuse) cannot be given to Kerry until he abstains from alcohol for several days to at least a week. Recall that Antabuse blocks aldehyde dehydrogenase in the liver, which is the hepatic enzyme responsible for alcohol metabolism. Thus, levels of acetaldehyde build up in the bloodstream. As such, if alcohol is consumed while the patient is on Antabuse, an aversive reaction of nausea, vomiting, hypertension, headache, flushing, thirst, sweating and dyspnea is the result. For Antabuse to be started, Kerry must either be detoxed off the alcohol first, or be abstinent of his own accord in order to avoid this adverse reaction. The minimum safe duration off alcohol before starting to take disulfiram is 12 hours.

  Orthopedic and neurologic consultations are useful, but they won’t help Kerry in the immediate with his substance dependence and abuse issues, or with his pain management. These are more pressing issues in the moment and these consultations can take place after both pain and addiction are directly addressed.

  Methadone and acamprosate calcium (Campral) are excellent choices for outpatient management of Kerry’s problems with narcotic painkillers and alcohol. Methadone is along-acting synthetic narcotic that can be prescribed lawfully in an outpatient office when it is given for chronic pain. When methadone is prescribed only as opioid replacement therapy for narcotic addiction, it can only be given in a federally-licensed and regulated methadone clinic. Methadone is thought to be most effective for opioid relapse prevention at or above doses of 60 mg daily. Campral is a wonderful medication for alcohol relapse prevention. Campral effectively reduces cravings for alcohol consumption. Campral’s mechanism of action is believed to involve the antagonism of glutamate and the NMDA receptor. In order for Campral to be effective, the patient must have already stopped drinking alcohol for a short period, perhaps about one week.

  K&S Ch. 36

2. C. The correct dosing strategy for disulfiram (Antabuse) is to start the patient on 500 mg daily for the first 1-2 weeks, and then lower the maintenance dose to 250 mg daily. Disulfiram should not be administered until the person has abstained from alcohol for at least 12 hours.

  K&S Ch. 36

3. BCE. Suboxone (buprenorphine/naloxone) is a sublingual tablet or disintegrating film strip that is rapidly absorbed under the tongue. It comes in two strengths: 8/4 mg and 2/0.5 mg. The first digit is the dose of buprenorphine and the second digit is the dose of naloxone. The unique property of buprenorphine is that is both an agonist and antagonist at the µ-opiate receptor site. This property makes buprenorphine a very modest painkiller and it also renders the medication very difficult to abuse. At doses above 40 mg daily, buprenorphine gates the µ-opiate receptor and no further agonistic effects occur. This essentially breaks up most of the medication’s potential for building tolerance and inducing euphoria. Also, if full opioid agonists are consumed in conjunction with Suboxone, the user may well experience a disturbing precipitated withdrawal syndrome.

  The naloxone content of Suboxone is a failsafe mechanism to prevent the diversion of the product by intravenous opiate users for the purposes of self-injection for recreational purposes. When absorbed by the two large veins under the tongue, the naloxone has no real clinical effect; however, if the product is emulsified and injected intravenously, the naloxone component of the medication acts as a potent and rapid opioid antagonist and abusers can experience a significant precipitated withdrawal if any attempt is made to inject it.

  Suboxone tablets and film strips must be taken under the tongue in order to be fully effective. Typical maintenance doses for opioid relapse prevention range from 4 to 16 mg daily.

  K&S Ch. 36

4. ABC. Among the agents that can decrease methadone blood levels are: phenytoin, hypericum, dextromethorphan, abacavir, carbamazepine, cocaine, dexamethasone, nevirapine, rifampin, spironolactone, and tobacco products. Among the agents that can increase methadone blood levels are: ciprofloxacin, erythromycin, disulfiram, verapamil, dihydroergotamine, grapefruit, moclobemide, Echinacea.

  K&S Ch. 36

5. D. Cannabis intoxication produces memory impairment, perceptual distortions, decreased problem-solving ability, loss of coordination, increased heart rate, anxiety, and panic attacks. Abrupt cessation of cannabis after prolonged heavy use may cause a characteristic withdrawal syndrome that encompasses insomnia, irritability, drug craving, restlessness, depressed mood, nervousness and anxiety. This can be followed by anxiety, nausea, tremors, muscle twitches, sweating, myalgia, and general malaise. Typically, the withdrawal syndrome begins about 24 hours after the last use, peaks at about 2 to 4 days, and diminishes after about 2 weeks.

  K&S Chs 36&52


Previous
Page
Next
Page