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

Explanations - Test Number Six

Question 1. D. Trazodone is metabolized by the CYP 3A4 enzyme.

  Psychopharmacology

  K&S Ch. 36

Question 2. C. Acute and subacute transverse myelitis (TM) is defined as the development of isolated spinal cord dysfunction over hours or days in patients in whom no evidence exists of a compressive lesion. Approximately 37% of patients reported a preceding febrile illness. TM is an acute myelopathic process that is presumed to be autoimmune in origin. Patients present with motor and sensory deficits below the lesion, usually in the form of a paraplegia. The abnormalities are typically bilateral but may be asymmetrical. MRI may show enhancement in the spinal cord, which has an appearance that differs subtly from that in involvement in multiple sclerosis. CSF analysis is nondiagnostic. TM is a clinical diagnosis. The primary differential diagnosis is between multiple sclerosis and neuromyelitis optica. Only about 7% of patients with TM go on to develop multiple sclerosis by clinical criteria.

  Anterior spinal artery infarction usually causes paraparesis and spinothalamic sensory loss below the level of the lesion. Dorsal column function is preserved. Rarely, one segmental branch of the anterior spinal artery can be involved with unilateral spinal cord damage and monoparesis or hemiparesis. Spinal metastasis can cause a central cord deficit, but this is unusual in a young patient such as the one presented in this question!

  Neurology

  B&D Chs 23&54

Question 3. C. Lamotrigine has FDA approval for bipolar maintenance and has demonstrated efficacy in both mania and depression. Topiramate is approved for seizures and migraines but is used off label for mania. Carbamazepine is approved for treatment of acute mania. Valproic acid has been demonstrated to be effective for acute mania. Gabapentin is approved for seizures, post-herpetic neuralgia, and neuropathic pain.

  Psychopharmacology K&S Ch. 36

Question 4. D. Somnambulism (sleepwalking) is a parasomnia. It is common in children between ages 5 and 12. Sometimes it persists in adulthood or rarely begins in adults. Sleepwalking begins with the abrupt onset of motor activity arising out of slow-wave sleep (stage IV) during the first one-third of sleep. Episodes generally last less than 10 minutes. There is a high incidence of positive family history. Injuries and violent activity have been reported during sleepwalking episodes, but generally, individuals can negotiate their way around the room. Rarely, the occurrence of homicide has been reported and sometimes abnormal sexual behavior occurs. Sleep deprivation, fatigue, concurrent illness, and sedatives may act as precipitating factors. Treatment involves taking appropriate precautions to prevent wandering and troublesome behaviors. Medications that may improve the condition include imipramine and benzodiazepines. Remember also, that sleep terrors occur during the same stage of sleep as sleepwalking (stage IV, also called slow-wave sleep).

  Neurology

  B&D Ch. 68

Question 5. C. The pregnancy categories are as follows:

  Category A – Controlled studies show no risk. Generally considered safe.

  Category B – Animal studies show no risk. No human studies available. Caution advised.

  Category C – Animal studies show adverse fetal effect. No human studies available. Weigh risks and benefits.

  Category D – Positive evidence of human fetal risk. Weigh risk and benefit.

  Psychopharmacology

  K&S Ch. 36

Question 6. A. In Wernicke’s aphasia, expressive speech is fluent but comprehension is impaired. The speech pattern is effortless and sometimes even excessively fluent (logorrhea). Speech is devoid of meaning, containing verbal paraphasias, neologisms, and jargon productions. This speech pattern is referred to as paragrammatism. Naming in Wernicke’s aphasia is deficient, often with bizarre, paraphasic substitutions for the correct name. Auditory comprehension is impaired, sometimes even for simple nonsense questions. Deficient semantics is the major cause of the comprehension disturbance in Wernicke’s aphasia, along with disturbed access to the internal lexicon. Repetition is impaired. Reading comprehension usually is affected in a fashion similar to that observed for auditory comprehension, but occasional patients show greater deficit in one modality than in the other. Writing also is impaired, but in a manner quite different from that of Broca’s aphasia. The patient usually has no hemiparesis and can grasp the pen and write easily. The lesions of patients with Wernicke’s aphasia usually involve the posterior portion of the superior temporal gyrus, sometimes extending into the inferior parietal lobule.

  In 1909, Balint described a syndrome in which patients act blind, yet can describe small details of objects in central vision. The disorder is usually associated with bilateral hemisphere lesions, often involving the parietal and frontal lobes. Balint’s syndrome involves a triad of deficits: (1) psychic paralysis of gaze, also called ocular motor apraxia, or difficulty directing the eyes away from central fixation; (2) optic ataxia, or incoordination of extremity movement under visual control (with normal coordination under proprioceptive control; and (3) impaired visual attention. These deficits result in the perception of only small details of a visual scene, with loss of the ability to scan and perceive the “big picture.” Patients with Balint’s syndrome literally cannot see the forest for the trees. Some but not all patients have bilateral visual field deficits.

  A second partial Balint’s syndrome deficit is simultanagnosia, or loss of ability to perceive more than one item at a time, first described by Wolpert in 1924. The patient sees details of pictures, but not the whole. Many such patients have left occipital lesions and associated pure alexia without agraphia; these patients can often read “letter-by-letter,” or one letter at a time, but they cannot recognize a word at a glance.

  Anomic aphasia refers to aphasic syndromes in which naming, or access to the internal lexicon, is the principal deficit. Spontaneous speech is normal except for the pauses and circumlocutions produced by the inability to name. Comprehension, repetition, reading, and writing are intact, except for the same word-finding difficulty in written productions. Isolated, severe anomia may indicate focal left hemisphere pathology. The angular gyrus is the purported site of lesions producing anomic aphasia, but lesions there usually produce other deficits as well, including alexia and the four elements of Gerstmann’s syndrome: agraphia, right–left disorientation, acalculia, and finger agnosia, or inability to identify fingers.

  Conduction aphasia is an uncommon but theoretically important syndrome that can be recognized by its striking deficit of repetition. Most patients have relatively normal spontaneous speech, although some make literal paraphasic errors and hesitate frequently for self-correction. Naming may be impaired, but auditory comprehension is preserved. Repetition may be disturbed to seemingly ridiculous extremes, such that a patient who is capable of self-expression at a sentence level, and can comprehend conversation, may be unable to repeat even single words. Associated deficits include hemianopia in some patients; right-sided sensory loss may be present, but right hemiparesis usually is mild or absent. The lesions of conduction aphasia usually involve either the superior temporal or inferior parietal region. Conduction aphasia has been advanced as a classical disconnection syndrome. Wernicke originally postulated that a lesion disconnecting Wernicke’s and Broca’s areas would produce this syndrome; Geschwind later pointed to the arcuate fasciculus, a white matter tract traveling from the deep temporal lobe, around the sylvian fissure, to the frontal lobe, as the site of disconnection.

  Most psychotic patients speak in an easily understood, grammatically appropriate manner, but their behavior and speech content are abnormal. Only rarely do schizophrenics speak in “clang association” or “word salad” speech. Sudden onset of fluent, paraphasic speech in a middle-aged or elderly patient should always be suspected of representing a left hemisphere lesion with aphasia.

  Neurology

  B&D Ch. 12A

Question 7. C. Accepting a small gift from a patient is acceptable under certain circumstances. The details of the case are important in determining whether or not to accept the gift. Exploitation involves using the therapeutic relationship for personal gain, such as hiring a patient, or going into business with a patient. You can not have any business interactions with a patient aside from their paying you for treatment. Charging for missed visits is considered ethical. Releasing information to the patient’s insurance company is ethical. You should only release as much information as is necessary to process the claim or pre-approve the visit etc. It is ethical to keep a separate set of psychotherapy notes for your therapy patients that are not part of the medical record and to which the patient is not entitled access.

  Ethics

  K&S Ch. 58

Question 8. B. Anterior cerebral artery (ACA) territory infarctions are uncommon. They occur in patients with vasospasm after subarachnoid hemorrhage caused by ACA or anterior communicating artery aneurysm. Excluding these causes, the percentage of acute cerebral infarcts that are in the ACA territory is less than 3%. The characteristics of ACA infarction vary according to the site of involvement and the extent of collateral blood flow. Contralateral weakness, involving primarily the lower extremity and, to a lesser extent, the arm, is characteristic of infarction in the territory of the hemispheric branches of the ACA. Other characteristics include abulia, akinetic mutism (with bilateral mesiofrontal damage), impaired memory or emotional disturbances, transcortical motor aphasia (with dominant hemispheric lesions), deviation of the head and eyes toward the lesion, paratonia (gegenhalten), discriminative and proprioceptive sensory loss (primarily in the lower extremity), and sphincter incontinence. An anterior disconnection syndrome with left arm apraxia caused by involvement of the anterior corpus callosum can be seen. Pericallosal branch involvement can cause apraxia, agraphia, and tactile anomia of the left hand. Infarction of the basal branches of the ACA can cause memory disorders, anxiety, and agitation. Infarction in the territory of the medial lenticulostriate artery (artery of Heubner) causes more pronounced weakness of the face and arm without sensory loss caused by this artery’s supply of portions of the anterior limb of the internal capsule.

  The anterior choroidal artery syndrome is often characterized by hemiparesis caused by involvement of the posterior limb of the internal capsule, hemisensory loss caused by involvement of the posterolateral nucleus of the thalamus or thalamocortical fibers, and hemianopia secondary to involvement of the lateral geniculate body or the geniculocalcarine tract. The visual field defect with anterior choroidal artery syndrome infarcts is characterized by a homonymous defect in the superior and inferior visual fields that spares the horizontal meridian. In a small number of patients, left spatial hemineglect with right hemispheric infarctions and a mild language disorder with left hemispheric infarctions may occur. With bilateral infarctions in the anterior choroidal artery syndrome territory, there can be pseudobulbar mutism and a variety of other features, including facial diplegia, hemisensory loss, lethargy, neglect, and affect changes.

  Other answer choices are discussed in detail elsewhere in this volume.

  Neurology

  B&D Ch. 51A

Question 9. E. Of the choices given only gabapentin is excreted unchanged in the urine. It has no interaction with the CYP 450 system and no liver metabolism. The other choices are first metabolized in the liver and their metabolites are subsequently excreted in the urine and/or feces.

  Psychopharmacology

  K&S Ch. 36

Question 10. E. Transient amnesia is a temporary version of amnestic syndrome. The most striking example of transient amnesia is the syndrome of transient global amnesia, lasting from several to 24 hours. In this syndrome, an otherwise cognitively intact individual suddenly loses memory for recent events, asks repetitive questions about his or her environment, and sometimes confabulates. During the episode, the patient has both anterograde and retrograde amnesia, as in the permanent amnestic syndrome. As recovery occurs, however, the retrograde portion “shrinks” to a short period, leaving a permanent gap in memory of the brief retrograde amnesia before the episode and the period of no learning during the episode. The syndrome is of unknown cause but can be closely imitated by disorders of known etiology, such as partial complex seizures, migraine, and possibly transient ischemia of the hippocampus on one or both sides. Studies do not prove an ischemic etiology for transient global amnesia; rather, they indicate transient dysfunction in the hippocampus or its connections. Drug intoxication, alcoholic “blackouts,” and minor head injuries can also produce transient amnesia.

  Neurology

  B&D Ch. 6

Question 11. C. Nefazodone inhibits CYP3A4 thereby increasing trazodone levels.

  Psychopharmacology

  K&S Ch. 36

Question 12. B. Psychogenic nonepileptic seizures are episodes of movement, sensation, or behaviors that resemble epileptic seizures, but do not have a neurologic origin; rather, they are somatic manifestations of psychologic distress. Inpatient video-electroencephalography monitoring is the gold standard for the diagnosis of nonepileptic seizures. Definitive diagnosis is made when a patient is observed having typical seizures without accompanying EEG abnormalities. From 5 to 10% of outpatient epilepsy patients and 20 to 40% of inpatient epilepsy patients have psychogenic nonepileptic seizures. Such patients inevitably have comorbid psychiatric illnesses, most commonly depression, post-traumatic stress disorder, other somatoform and dissociative disorders, and character pathology, especially borderline personality disorder or traits. Many patients have a history of sexual or physical abuse. Up to 40% of patients with nonepileptic seizures also have true epileptic seizures. Between 75 and 85 percent of patients with psychogenic nonepileptic seizures are women. Treatment involves discontinuation of antiepileptic drugs in patients without concurrent epilepsy and referral for appropriate psychiatric care. As an auxiliary investigation of suspected psychogenic seizures, plasma prolactin concentrations may provide additional supportive data. Plasma prolactin concentrations frequently are elevated after tonic–clonic seizures and less frequently after complex partial seizures. Serum prolactin levels almost invariably are normal after psychogenic seizures, although such a finding does not exclude the diagnosis of true epileptic seizures. Elevated prolactin levels, however, also may be present after syncope and with the use of drugs such as antidepressants, estrogens, bromocriptine, ergots, phenothiazines, and antiepileptic drugs. Although a number of procedures are employed to help distinguish epileptic from nonepileptic seizures, none of these procedures have both high sensitivity and high specificity. No procedure attains the reliability of EEG-video monitoring, which remains the standard diagnostic method for distinguishing between the two.

  Neurology

  B&D Ch. 2

Question 13. D. Beta blockers are first line treatment for akathisia. Benzodiazepines may also help in some cases. Anticholinergics like benztropine are not helpful. Bromocriptine is a mixed dopamine agonist/antagonist useful in neuroleptic malignant syndrome, Parkinson’s disease, elevated prolactin, and cocaine withdrawal. Nimodipine is a calcium channel blocker (useless for akathisia). Clonidine is an alpha 1 agonist which is useful in treating hypertension, aggression, attention deficit hyperactivity disorder, and opiate withdrawal.

  Psychopharmacology

  K&S Ch. 36

Question 14. D. Characteristic of trigeminal neuralgia (TN), tic douloureux, is paroxysmal lancinating attacks of severe facial pain. TN has an incidence of approximately 4 per 100 000, with a large majority of cases occurring spontaneously. Both genders experience the disorder with a slight female predominance, and it is most common after the age of 50. Characteristics of classic TN include an abrupt onset and termination of unilateral brief electric shock-like pain. Pain often is limited to the distribution of one or two (commonly the second and third) divisions of the trigeminal nerve. Trivial stimuli, including washing, shaving, smoking, talking, and brushing the teeth (trigger factors), can evoke the pain. Some areas in the nasolabial fold or chin may be particularly susceptible to stimulation (trigger areas). In individual patients, stereotypical pain attacks recur with the same intensity and distribution. Most affected patients are symptom-free between attacks and clinical examination is usually normal. Attacks of TN occur in clusters and remissions can last for months. The cause of the pain attacks is unknown. Compression of the trigeminal nerve by benign tumors and vascular anomalies may play a role in the development of clinical symptoms.

  Carbamazepine is the drug of first choice for treatment of TN. Both controlled and uncontrolled studies confirm its clinical efficacy. Carbamazepine monotherapy provides initial symptom control in as many as 80% of the patients. Of those initially responding to the drug, approximately 75% will continue to have long-term control of pain attacks. Controlled studies demonstrate that baclofen and lamotrigine are superior to placebo for treatment of TN. In the experience of many clinicians, baclofen is just as effective as carbamazepine and often better tolerated. Baclofen could be an alternate choice for initial drug therapy. Other medications that may be effective include oral gabapentin, clonazepam, oxcarbazepine, topiramate, and phenytoin. If a patient is not satisfied with single-medication therapy, adding another oral medication may offer additional benefit. Intravenous lidocaine or phenytoin may be effective for some severe refractory cases of TN. These treatments carry additional risks, however, and require close cardiovascular monitoring. Opioid analgesics are not effective for TN.

  Neurology

  B&D Ch. 44

Question 15. A. Aspirin, the oldest and most commonly used nonprescription drug in the world, is the standard medical therapy for prevention of stroke in patients with transient cerebral ischemia, as well as for reducing the risk for recurrent stroke and postoperative strokes after carotid endarterectomy (CEA). Aspirin is effective, inexpensive, and safe if started within 48 hours of acute ischemic stroke. Meta-analyses have shown that aspirin reduces the combined risk for stroke, MI, and vascular death by approximately 25%. The optimal dose of aspirin remains a source of controversy among neurologists. The range of acceptable management includes daily doses ranging between 50 and 1300 mg of aspirin. There is a suggestion that aspirin is also effective in doses as low as 30 mg daily. The mechanism of action of aspirin is the irreversible inhibition of platelet function by inactivation of cyclo-oxygenase. The antiaggregant effect is seen within 1hour after administration. Aspirin is also anti-inflammatory, antioxidant, and may increase fibrinolytic activity up to 4 hours after administration. The main side effect of aspirin is gastric discomfort. Gastrointestinal hemorrhage occurs in 1 to 5% of cases.

  Evidence from several clinical studies favors the use of platelet antiaggregants as the first line of therapy in patients at high risk for stroke. These agents are indicated for secondary prevention of stroke. There appears to be no evidence to support the use of aspirin in primary prevention of stroke among low-risk middle-aged people. Results of primary prevention trials do not support the use of aspirin for primary stroke prevention. However, aspirin 81 mg every other day was effective in primary prevention of stroke in older women. Although aspirin did not offer a long-term protective effect among 372 asymptomatic patients with carotid bruits and greater than 50% carotid stenosis on duplex ultrasonography, many physicians continue its use in patients with carotid bruits or asymptomatic carotid stenosis under the assumption that it may be effective. Data regarding intraplaque hemorrhage caused by platelet antiaggregants are conflicting.

  Oral anticoagulation with warfarin is indicated for primary and secondary prevention of stroke in patients with nonventricular atrial fibrillation. Ticlopidine and clopidogrel are structurally related thienopyridines that have antiplatelet effects. Ticlopidine reduces the relative risk for death or nonfatal stroke by 12% in comparison with aspirin. Ticlopidine acts primarily by irreversibly inhibiting the adenosine 51 diphosphate pathways of the platelet membrane. It also reduces plasma fibrinogen levels and increases erythrocyte deformability. The recommended dosage of ticlopidine, in most of the world, is 250 mg twice a day. Ticlopidine has more side effects than aspirin, including diarrhea, nausea, dyspepsia, and rash. The Clopidogrel versus Aspirin in Patients at Risk of Ischemic Events study (CAPRIE) assessed the relative efficacy of clopidogrel (75 mg daily) and aspirin (325 mg daily) in reducing the incidence of ischemic stroke, MI, or symptomatic atherosclerotic peripheral arterial disease. The results of this study showed that clopidogrel was modestly more effective (8.7% relative risk reduction) than aspirin in reducing the combined risk for ischemic stroke, MI, and vascular death in patients with atherosclerotic vascular disease. Clopidogrel is a platelet adenosine diphosphate receptor antagonist. Overall, the tolerability of clopidogrel was excellent, with no increased incidence of neutropenia, and a lower incidence of gastrointestinal hemorrhage and peptic, gastric, or duodenal ulcers when compared with aspirin. Despite this evidence, Aspirin is still the recommended treatment of choice 48 hours following an ischemic cerebrovascular event.

  Neurology

  B&D Ch. 51A

Question 16. C. Carpal tunnel syndrome is by far the most common entrapment neuropathy. This entrapment occurs in the tunnel through which the median nerve and flexor digitorum tendons pass. Because the transverse carpal ligament is an unyielding fibrous structure forming the roof of the tunnel, tenosynovitis or arthritis in this area often produces pressure on the median nerve. Symptoms consist of nocturnal pain and paresthesias, most often confined to the thumb, index, and middle fingers. Patients complain of tingling numbness and burning sensations, often awakening them from sleep. Referred pain may radiate to the forearm and even as high as the shoulder. Symptoms are often worse after excessive use of the hand or wrist. Objective sensory changes may be found in the distribution of the median nerve, most often impaired two-point discrimination, pinprick and light touch sensation, or occasionally hyperesthesia, in the thumb and index fingers, with sparing of the thenar eminence. Thenar (abductor pollicis brevis muscle) weakness and atrophy may be present with prolonged entrapment (see photo below).

image

Thenar atrophy in chronic bilateral carpal tunnel syndrome

  The syndrome is frequently bilateral and usually of greater intensity in the dominant hand. A positive Tinel’s sign, in which percussion of the nerve at the carpal tunnel causes paresthesias in the distribution of the distal distribution of the median nerve, is present in approximately 60% of affected patients, but is not specific for carpal tunnel syndrome. Flexing the patient’s hand at the wrist for 1minute (Phalen’s maneuver) or hyperextension of the wrist (reversed Phalen’s maneuver) can reproduce the symptoms.

  Approximately one in five pregnant women reports nocturnal hand paresthesias, primarily during the last trimester, often associated with peripheral edema. Excessive weight gain and fluid retention increase the occurrence of these complaints. This irritation can be expected to disappear spontaneously within weeks after parturition. During pregnancy, conservative therapy is indicated. Splinting of the wrist in the neutral position is helpful. Additionally, some physicians inject corticosteroids into the carpal tunnel. When hand muscles supplied by the median nerve weaken, surgical decompression using fiberoptic techniques is indicated.

  Although it is frequently (mis)diagnosed, neurogenic thoracic outlet syndrome is a rare entity, seen only once or twice a year in busy EMG laboratories. Most patients are women. The mean age at onset is 32 years, but patients as young as 13 and as old as 73 years have been reported. Pain is usually the first symptom, with either aching noted on the inner side of the arm or soreness felt diffusely throughout the limb. Tingling sensations accompany pain and are felt along the inner side of the forearm and in the hand. In many cases, cervical spine roentgenograms disclose small bilateral cervical ribs or enlarged down-curving C7 transverse processes.

  Arm pain and weakness are the cardinal manifestations of idiopathic brachial plexopathy. It occurs in all age groups, particularly between the third and seventh decades of life. Men are affected two to three times more often than women; there appears to be a higher incidence among men engaged in vigorous athletic activities, such as weight lifting, wrestling, and gymnastics. Although half of the cases seem unrelated to any precipitating event, in others the plexopathy follows an upper respiratory tract infection, a flu-like illness, an immunization, surgery, or psychological stress, or it occurs postpartum. The illness begins with the abrupt onset of intense pain, described as sharp, stabbing, throbbing, or aching, located in a variety of sites, including the shoulder, scapular area, trapezius ridge, upper arm, forearm, and hand. The pain may last from hours to many weeks, and then it gradually abates. Lessening of pain is associated with the appearance of weakness. This may have been present during the painful period but was not appreciated because the pain prevented the patient from moving the limb. Weakness may progress for 2 to 3 weeks after the onset of pain. Although pain subsides in most patients, it may continue for several weeks after weakness has reached its peak, and, rarely, it recurs episodically for a year or more. On examination, approximately one half of patients have weakness in muscles of the shoulder girdle, one third have weakness referable to both upper and lower parts of the plexus, and approximately 15% have evidence of lower plexus involvement alone. The natural history of brachial plexus neuropathy is benign; improvement occurs in the vast majority of patients, even in those with considerable muscle atrophy.

  Neurology

  B&D Chs 75,76&81

Question 17. D. Specific phobia is the most common anxiety disorder. It is the most common mental disorder among women and the second most common among men (after substance abuse). This fact takes many psychiatrists by surprise however, because most patients with specific phobia do not seek medical attention.

  Statistics

  K&S Ch. 16

Question 18. B. Neurofibromatosis (NF) is actually two separate diseases, each caused by a different gene. NF type 1 (NF1), or von Recklinghausen’s disease, is the most common of the neurocutaneous syndromes, occurring in approximately 1 in 3000 people. NF type 2 (NF2) is characterized by bilateral vestibular schwannomas and often is associated with other brain or spinal cord tumors. NF2 occurs in only 1 in 35 000 to 50 000 people. Inheritance for both is an autosomal dominant pattern, but approximately half of NF1 cases result from a spontaneous mutation. The clinical features of both conditions are highly variable. A mutation of the 60-exon NF1 gene on chromosome 17q causes NF1. The NF1 gene product, neurofibromin, is a GTPase-activating protein, functioning to inhibit ras-mediated cell proliferation. Despite identification of approximately 100 mutations of NF1 in various regions of the gene, none correlates to a specific clinical phenotype. Several patients have developed a somatic NF1 mutation affecting only a limited region of the body. With this segmental NF, one extremity may have café-au-lait lesions, subcutaneous neurofibromas, and other signs of NF, but the rest of the body is unaffected. Similarly, some patients with only gonadal mosaicism have no outward manifestations of NF1 but have multiple affected offspring. A mutation of the NF2 gene on chromosome 22 causes NF2. The NF2 protein product is schwannomin or merlin. The NF2gene suppresses tumor function. Dysfunction of the NF2 gene accounts for the occurrence of multiple central nervous system (CNS) tumors in patients with NF2. The diagnostic criteria for NF1 and NF2 are as follows:

Neurofibromatosis Type 1 (any two or more)

• Six or more café-au-lait lesions more than 5 mm in diameter before puberty and more than 15 mm in diameter afterward

• Freckling in the axillary or inguinal areas

• Optic glioma

• Two or more neurofibromas or one plexiform neurofibroma

• A first-degree relative with neurofibromatosis type 1

• Two or more Lisch nodules

• A characteristic bony lesion (sphenoid dysplasia, thinning of the cortex of long bones, with or without pseudarthrosis)

Neurofibromatosis Type 2

• Bilateral VIII nerve tumor (shown by magnetic resonance imaging, computed tomography, or histological confirmation)

• A first-degree relative with neurofibromatosis type 2 and a unilateral eighth nerve tumor

• A first-degree relative with neurofibromatosis type 2 and any two of the following lesions: neurofibroma, meningioma, schwannoma, glioma, or juvenile posterior subcapsular lenticular opacity

  Lisch nodules are pigmented iris hamartomas that are pathognomonic for NF1. Lisch nodules do not cause symptoms; their significance lies in their implications for the diagnosis of NF1. Lisch nodules are often not apparent during early childhood; therefore, their absence does not exclude the diagnosis of NF1. Rarely, children with NF1 have retinal hamartomas, but these usually remain asymptomatic. Optic nerve gliomas are the most common CNS tumors caused by NF1. About 15% of patients with NF1 have unilateral or bilateral optic glioma. Patients with NF2 have few cutaneous lesions. To meet criteria for NF2, patients must go on to develop bilateral schwannomas of the auditory nerve (acoustic neuromas), proven on neuroimaging or by postexcisional biopsy.

  Neurology

  B&D Ch. 65

Question 19. E. Culture correlates most with ethnicity. People can be of the same race, age, gender, or nationality and have very different cultures.

  Cultural Issues in Psychiatry

  K&S Ch. 4

Question 20. A. The porphyrias are caused by enzymatic defects in the heme biosynthetic pathway. Porphyrias with neuropsychiatric symptoms include acute intermittent porphyria (AIP), variegated porphyria (VP), hereditary mixed coproporphyria (HMP), and plumboporphyria (extremely rare and autosomal recessive), which may give rise to acute episodes of potentially fatal symptoms such as neurovisceral crisis, abdominal pain, delirium, psychosis, neuropathy, and autonomic instability. AIP, the most common type reported in the United States, follows an autosomal dominant pattern of inheritance and is due to a mutation in the gene for porphobilinogen deaminase. The disease is characterized by attacks that may last days to weeks, with relatively normal function between attacks. Infrequently, the clinical course may exhibit persisting clinical abnormalities with superimposed episodes of exacerbation. The episodic nature, clinical variability, and unusual features may cause symptoms to be attributed to somatization, conversion, or other psychiatric conditions. Attacks may be spontaneous, but are typically precipitated by a variety of factors such as infection, alcohol use, pregnancy, anesthesia, and numerous medications that include antidepressants, anticonvulsants, and oral contraceptives.

  Porphyric attacks usually manifest with a triad consisting of abdominal pain, peripheral neuropathy, and neuropsychiatric symptoms. Seizures may also occur. Abdominal pain is the most common symptom, which can result in surgical exploration if the diagnosis is unknown. A variety of cognitive and behavioral changes can occur, including anxiety, restlessness, insomnia, depression, mania, hallucinations, delusions, confusion, catatonia, and psychosis. The diagnosis can be confirmed during an acute attack of AIP, HMP, or VP by measuring urine porphobilinogens. Acute attacks are treated with avoidance of precipitating factors (e.g., medications), intravenous hemin, intravenous glucose, and pain control.

  Neurology

  B&D Chs 9&62

Question 21. C. Lithium is cleared through the kidneys. It is reabsorbed in the proximal tubules with sodium. When a thiazide diuretic is added it leads to sodium depletion which in turn causes the reabsorbtion of sodium and lithium in the proximal tubules. This increased lithium reabsorbtion added to the lower fluid levels as a result of the diuretic can lead to an increased lithium level and lithium toxicity. Valproic acid and clozapine are metabolized through the liver and would not be effected by a thiazide diuretic.

  Psychopharmacology

  K&S Ch. 36

Question 22. B. The first medication approved by the FDA for use in MS was recombinant interferon beta-1b (Betaseron). Interferon beta-1b is administered subcutaneously every other day by self-injection. Side effects include influenza-like symptoms, which usually diminish over weeks to months, depression, and reactions at the injection site. The mechanism of action of interferon beta-1b is currently unknown, but may relate to antiproliferative effects, cytokine changes, effects at the blood-brain barrier, and alterations of T-cell subsets.

  Glatiramer acetate (formerly known as copolymer 1) (Copaxone) is a synthetic polypeptide administered by daily sub-cutaneous injection. Patients receiving glatiramer acetate have a 29% reduction in relapse rate over 2 years. The mechanism by which glatiramer acetate may work in humans is unknown, but may relate to interference with antigen presentation and induction of regulatory cells (Th2) that traffic to the CNS and induce bystander suppression of immune responses.

  Tizanidine and Lioresal are muscle relaxing agents that are used to relieve some of the spasticity caused by multiple sclerosis. These are not disease-modifying agents. Prednisone, an oral corticosteroid, is given following an acute MS exacerbation to reduce the disease burden of an acute attack. Acute attacks are typically treated with intravenous corticosteroids. Indications for treatment of a relapse include functionally disabling symptoms with objective evidence of neurological impairment. Thus, mild sensory attacks are typically not treated. In the past, corticotropin and oral prednisone were primarily used. More recently, treatment with short courses of intravenous methylprednisolone, 500 to 1000 mg daily for 3 to 7 days, with or without a short prednisone taper, has commonly been used.

  Neurology

  B&D Ch. 54

Question 23. A. The most likely effects of ipecac abuse are cardiomyopathy, enlarged heart, increased QTc interval, increased CK-MB, decreased ejection fraction, tricuspid or mitral valve insufficiency, dysrythmia, low WBC, and increased LFTs. One would not expect pancreatitis (leading to an increase in amylase) or infection.

  Feeding and Eating Disorders/Lab Tests in Psychiatry

  K&S Ch. 23

Question 24. D. Subcortical arteriosclerotic encephalopathy (SAE), also known as Binswanger’s disease, is a form of subcortical vascular dementia. Originally described in younger patients with hypertension (age 50 to 65), this disorder is characterized by a gradual (or stepwise) progressive dementia associated with frequent clinical strokes, motor and sensory deficits and seizures, multiple subcortical infarcts, and white matter lesions (WML; leukoaraiosis). Clinically, it may be difficult to differentiate from the état lacunaire described by Pierre Marie in patients with multiple subcortical ischemic lesions, including gray matter structures. SAE, however, is associated with more extensive WMLs, with ventricular enlargement. Both syndromes can have cortical infarcts and état crible, dilatation of the penetrating arteries’ perivascular spaces. Although once believed to be rare, SAE is detected easily on CT or MRI, and the diagnosis is entertained more frequently when patients with cognitive decline have scans that show extensive subcortical WMLs. MRI can document that white matter abnormalities accompany the subcortical lacunes in a majority of cases. Therefore, the term used to describe this entity is subcortical ischemic vascular dementia, which incorporates subcortical WMLs and lacunar infarctions under the same subtype.

  Gradual onset of cognitive difficulties is the first sign in more than half of the cases. Memory deficits, apathy, and slowed thinking are prominent. These memory deficits tend to be most prominent for delayed recall, with relative sparing of recognition memory, at least in comparison with this aspect of cognitive function in vascular dementia. Acute episodes of neurological dysfunction may occur at the onset or during the course; weakness, discoordination, and slurred speech are typical. Frequent falls often are reported. In some instances, these variable neurological signs and symptoms are absent, and the patient experiences only slowly progressing mental deterioration; such cases initially may be diagnosed as neurodegenerative disease such as Alzheimer’s disease (AD).

  Because the clinical picture is similar to that of MID (multi-infarct dementia with cortical strokes), cases with Binswanger’s disease probably are included as MID in population studies. The population incidence and prevalence are unknown.

  Neurology

  B&D Ch. 66

Question 25. B. At 23 months children can respond to simple directions and understand pronouns. They can also follow action commands and begin to understand complex sentences.

  Human Development

  K&S Ch. 2

Question 26. E. Essential tremor (ET) is one of the most common movement disorders. In population-based studies, the prevalence increases steadily with age, occurring in up to 10% of patients older than age 60 years. The prevalence is higher in men than in women and in whites than in nonwhites. In its purest form, ET is a monosymptomatic illness characterized by gradually increasing amplitude postural and kinetic tremor of the forearms and hands (with or without involvement of other body parts), in the absence of endogenous or exogenous triggers or other neurological signs.

  The typical patient becomes aware of a barely perceptible postural or action tremor, usually in the distal arms and hands. The head and lower limbs are less commonly affected. Head tremor (titubation) is milder than limb tremor and is predominantly of a side-to-side, “no-no” type. Tremor of the face, trunk, and voice are rarely seen. The kinetic tremor is higher in amplitude than the postural tremor and is the major determinant of disability. Handwriting is particularly troublesome. A striking improvement after ingestion of a small amount of ethanol is seen in 50% of patients and may be helpful in diagnosis. Over time, the tremor worsens, causing increasing functional disability. Only a fraction of affected persons seek medical attention, and there is often a long latency from onset to presentation for care. ET is thought to be a monosymptomatic illness without changes in cognition, strength, coordination, or muscle tone, and the results of the neurological examination are usually normal.

  As many as two thirds of patients give a positive family history of tremor, and first-degree relatives of patients with ET are 5 to 10 times more likely to have ET than first-degree relatives of control subjects.

  Patients with mild ET whose main source of disability is tremor during meals and whose tremors respond to ethanol often benefit from a cocktail before meals. The two most commonly used pharmacological treatments are beta-adrenergic blockers and primidone.

  Stereotactic thalamotomy has been reported to suppress contralateral tremor as much as 75% in up to 90% of cases. The effect appears to be long lasting. Side effects of this procedure are relatively common, although most are transient, and bilateral thalamotomy may cause speech difficulty, so it should be avoided. Thalamic deep brain stimulation has shown very good efficacy in controlling ET. Tremor improves as much as 80% contralateral to the implantation, and bilateral stimulation can be performed safely with long-lasting benefits. DBS should be considered for cognitively intact, otherwise healthy patients with disabling medication-resistant tremor.

  Neurology

  B&D Ch. 75

Question 27. E. In the “communication stage” from 55 months onward, a child can use language to tell a story, share ideas, and discuss alternatives. They can understand concepts such as number, speed, time, space, and left vs. right. Their speech at this stage is 100% intelligible.

  Human Development

  K&S Ch. 2

Question 28. B. Wernicke’s encephalopathy is due to thiamine deficiency. Although the most common clinical setting for this disorder is chronic alcoholism, a large number of cases occur in other conditions, with the only prerequisite being a poor nutritional state, either from inadequate intake, malabsorption, or increased metabolic requirement. Wernicke’s encephalopathy may be precipitated acutely in at-risk patients by intravenous glucose administration or carbohydrate loading.

  Wernicke’s original description of the clinical triad of confusion, ophthalmoplegia, and ataxia is still valid. The confusional state develops over days or weeks and is characterized by inattention, apathy, disorientation, and memory loss. Stupor or coma is rare. Ophthalmoplegia, when present, commonly involves both lateral recti, either in isolation or together with palsies of other extraocular muscles. Patients may have horizontal nystagmus on lateral gaze, and many also have vertical nystagmus on upgaze. Sluggish reaction to light, light-near dissociation, and other pupillary abnormalities are sometimes seen. Truncal ataxia is common, but limb ataxia is not, findings similar to those seen in alcoholic cerebellar degeneration.

  The clinical findings reflect the localization of pathological abnormalities in this disease; namely, the prominent involvement of periventricular structures at the level of the third and fourth ventricles. Lesions of the nuclei of cranial nerves III, VI, and VIII are responsible for the eye findings. The truncal ataxia is probably caused by the vestibular dysfunction and involvement of the superior cerebellar vermis.

  Wernicke’s encephalopathy is a clinical diagnosis, although brain MRI can be helpful. MRI may show signal abnormalities on T2-weighted, fluid-attenuated inversion recovery, and diffusion-weighted images in the periaqueductal regions, medial thalami, and bilateral mammillary bodies.

  Patients suspected of Wernicke’s encephalopathy should receive thiamine before administration of glucose to avoid precipitation of acute symptom worsening. Thiamine is the only treatment known to alter the outcome. A dose of 50 to 100 mg should be given parenterally in the acute stage because intestinal absorption is unreliable in debilitated and alcoholic patients. Thiamine can then be continued daily through the acute period.

  If left untreated, Wernicke’s encephalopathy is progressive. The mortality, even with thiamine treatment, was 10 to 20% in the early studies. With treatment, the majority of ocular signs resolve within hours, although a fine horizontal nystagmus persists in approximately 60% of patients.

  In Korsakoff’s syndrome, memory is impaired out of proportion to other cognitive functions. This is due to the selective localization of the lesions in the diencephalon and temporal lobes. Injury to these regions regardless of cause (e.g., infarction, trauma, tumors, or herpes encephalitis) can produce a syndrome indistinguishable from the amnesia syndrome seen in alcoholic patients.

  The memory impairment is characterized by the presence of both anterograde and retrograde amnesia. Confabulation can be a prominent feature, especially in the early stages, although it may be absent in some patients.

  Despite treatment with thiamine, improvement in memory function is slow and may be incomplete. Those who improve usually do so after a 1-month delay or longer. Occasionally, patients may not achieve maximal improvement for more than a year.

  In 1903, Marchiafava and Bignami, two Italian pathologists, described a syndrome of selective demyelination of the corpus callosum in alcoholic Italians who indulged in large quantities of red wine. The disease seems to affect severe and chronic alcoholics in their middle or late adult life, with a peak incidence between ages 40 and 60. Because of the background history of alcohol abuse, a nutritional cause has been invoked, but no nutritional factor has been identified. A toxic cause, such as direct toxicity of ethanol or other constituents, seems equally plausible. The neurological presentation is that of a variable combination of mental and motor slowing, personality and behavior changes, incontinence, dysarthria, seizures, and hemiparesis. Occasionally patients present with coma. The most common is a frontal lobe or dementing syndrome. Sucking, grasping, and gegenhalten may be prominent. Pathologically, there is selective involvement of the central portion of the corpus callosum; the dorsal and ventral portions are spared or affected to a much lesser degree. There also may be symmetrical involvement of other white matter tracts. MRI is valuable for premortem visualization of these white matter lesions. Treatment should be directed at nutritional support and rehabilitation from alcoholism. In those patients who recovered, it is not clear whether improvement was a result of vitamin supplementation or merely a reflection of the disease’s natural history.

  Neurology

  B&D Ch. 57

Question 29. D. The Judgment of Line Orientation Test is useful in detecting right hemisphere disease. This test involves matching lines of the same slope. A patient with right hemisphere disease will have a very hard time with this, whereas a patient with only left hemisphere disease can complete the task without difficulty. The Boston diagnostic aphasia examination is just that…an exam for aphasia. The sentence completion test is used to test the patient’s associations with areas of interest by having the patient complete sentences. Responses that are particularly emotional or are repeated are noted by the examiner. The Thematic Apperception Test has patients create a story based on pictures they are presented with. The stories the patient generates tell the examiner about their thoughts, feelings, organization, assumptions etc.

  Psychological Theory and Psychometric Testing

  K&S Ch. 5

Question 30. D. First described in 1964 by Steele, Richardson, and Olszewski as a progressive illness characterized by vertical supranuclear ophthalmoplegia, axial rigidity, pseudobulbar palsy, and mild dementia, progressive supranuclear palsy (PSP) is the second most common form of neurodegenerative atypical parkinsonism. PSP typically begins in the sixth to seventh decades of life with gait disorder and falling. Patients develop an akinetic-rigid state with symmetrical signs and prominent axial rigidity. In contrast to the flexed posture of patients with PD, those with PSP may have an extended trunk or retrocolic neck posture. A characteristic facial appearance with a wide-eyed stare, furrowing of the forehead, and deepening of other facial creases allows experienced clinicians to make an instant diagnosis. Pseudobulbar palsy with dysarthria and dysphagia lend the patient a characteristic dysarthria with spasticity, hypokinesia, and ataxia and often “silent” aspiration. Frontal lobe features are common. There is striking executive dysfunction early in the disease course; concrete thought, difficulty shifting set, decreased verbal fluency, and personality changes such as impulsivity and poor judgment are nearly universal. Although considered a clinical hallmark of PSP, supranuclear vertical gaze palsy may not appear until later in the disease course, and some patients may never develop gaze palsy. Abnormal vertical saccades, best demonstrated by examination for opticokinetic nystagmus, compared to horizontal saccades, is one of the earliest ophthalmological signs of PSP. PSP almost always occurs sporadically, yet an increasing number of familial cases suggest a genetic etiology in some cases. There is growing support for the notion of altered regulation of tau gene expression in PSP. No toxic, viral, or other environmental risk factors have been described.

image

Typical facial expression of a patient with progressive supranuclear palsy, illustrating worried or surprised appearance, with furrowed brow and fixed expression of lower face.

  Dopaminergic agents, particularly levodopa (LD), may provide temporary improvement in bradykinesia in approximately 40% of patients, but LD usually does not improve dysarthria, gait, or balance problems. The prognosis of PSP is poor, with serious impact on quality of life and a median duration of survival of approximately 8 years.

  Pseudobulbar palsy (or spastic bulbar palsy) develops when there is disease involvement of the corticobulbar tracts that exert supranuclear control over those motor nuclei that control speech, mastication, and deglutition. The prefix “pseudo-” is used to distinguish this condition from “true” bulbar palsy that results from pure LMN involvement in brainstem motor nuclei. Articulation, mastication, and deglutition are affected in both pseudobulbar and bulbar palsies, but the degree of impairment in pseudobulbar palsy is generally milder. Spontaneous or unmotivated crying and laughter uniquely characterize pseudobulbar palsy. This is also termed emotional labilityhyperemotionalitylabile affect, or emotional incontinence and is often a source of great embarrassment to the patient. A patient advocacy group has suggested a new term, involuntary emotional expression disorder, to prevent the possible misconception that the “pseudo” in pseudobulbar palsy implies that it is not a true disorder.

  Neurology

  B&D Ch. 71&74

Question 31. B. Of all the answer choices, only introjection is an immature defense. All other choices in this question are mature. Other immature defenses include acting out, blocking, hypochondriasis, regression, passive–aggressive behavior, somatization, projection, and schizoid fantasy. We will not take the space to define all 12 defenses listed in this question and answer explanation, but suffice it to say they are all fair game for a standardized exam and you should take the time to learn any that are unfamiliar to you. You may also see questions on several of them elsewhere throughout this book.

  Psychological Theory and Psychometric Testing

  K&S Ch. 6

Question 32. C. The prevalence of adult-onset primary focal or segmental dystonia is 12.9 per 100 000. Cervical dystonia and blepharospasm are most commonly represented. The focal and segmental primary dystonias generally begin in adulthood with dystonic movements in the hand and arm, neck, or face. When spread occurs, the ultimate distribution tends to maintain a segmental pattern. Cervical dystonia is the most frequently diagnosed form of focal dystonia, accounting for about half of focal dystonia cases. Patients with cervical dystonia present with neck pain, difficulty maintaining a normal head position, and sometimes tremor. Dystonic tremor, which may be present not only in patients with cervical dystonia, but also in those with limb dystonia, is usually an irregular oscillatory movement that stops when the patient is allowed to place the head or limb in the position of the dystonic pulling, the so-called null point. There is a directional preponderance to dystonia movements, which is usually maintained throughout the course of the disease. Many studies have suggested that focal and segmental dystonia might have a genetic basis. Approximately 25% of adult-onset focal or segmental dystonia patients have a positive family history of dystonia, which would be consistent with an autosomal dominant condition with low penetrance. The locus has been mapped to chromosome 18. Medical treatment of adult-onset primary focal and segmental dystonia is difficult and employs those agents typically used in generalized dystonia. Adults are less able to tolerate effective doses of these agents, so the response to therapy is somewhat more disappointing than that seen in children. Botulinum toxin injections, on the other hand, are very helpful in the treatment of focal and segmental dystonia. Botulinum toxin is injected subcutaneously over the facial muscles or directly into larger deeper muscles that underlie pain and inappropriate movement in other focal dystonias. Many, though not all, clinicians use EMG to help guide toxin injection. Botulinum toxin injections have been proven effective in the treatment of blepharospasm and other facial dystonias, as well as cervical dystonia. Clinical experience suggests they are useful in the treatment of oromandibular, laryngeal, truncal, and limb dystonia. Overall, more than 75% of treated patients report moderate to marked improvement in dystonic pain or posture. The procedure is generally well tolerated, with excessive weakness of injected muscles or occasionally neighboring muscles the most often reported side effect. The mechanism of action of botulinum toxin appears complex.

  Neurology

  B&D Ch. 75

image

A patient with cervical dystonia (torticollis) with head rotation to the right demonstrating marked hypertrophy of the left sternocleidomastoid muscle.

Question 33. E. This question is really about orgasmic disorder. In order to properly diagnose orgasmic disorder you must rule out possible medical causes including medications. Some common causes of anorgasmia include alcohol, marijuana, SSRIs, TCAs, benzodiazepines, diabetes, spinal cord damage, hormones, pelvic injury, cardiac problems, liver disease or kidney disease.

  Orgasmic disorder is defined as a recurrent delay in or absence of orgasm following a normal excitement phase. It must cause marked distress. The DSM divides the diagnosis into male and female orgasmic disorder. It occurs more frequently in women than in men.

  Sexual Dysfunction

  K&S Ch. 21

Question 34. A. Juvenile myoclonic epilepsy (JME) accounts for 4–10% of all cases of epilepsy, but the diagnosis often is delayed and the prevalence is underestimated because symptoms are not recognized. Other names for JME are impulsive petit maljerk epilepsy, and myoclonic epilepsy of adolescence. Age at onset usually is between 12 and 18 years, but onset may occur from 8 to 30 years. The characteristic feature is sudden, mild to moderate myoclonic jerks of the shoulders and arms that usually occur after awakening. Generalized tonic–clonic seizures develop in 90% of cases, and approximately one third of the patients have absence seizures. Myoclonic seizures precede generalized tonic–clonic seizures in approximately one half of the patients. Initially, myoclonic jerks are mild and explained as nervousness, clumsiness, or tics. They may be unrecognized as seizures until a generalized tonic–clonic seizure brings the patient to medical attention. Sleep deprivation, alcohol intake, and fatigue precipitate seizures. Affected persons are of normal intelligence, and neurological deterioration does not occur. A seizure disorder with onset between ages 1 and 5 years has been recognized that may represent a bridge between benign myoclonic epilepsy of infancy and JME. Development and intelligence are normal. Even though JME manifests as a clinically well-defined disorder with some variation, different genetic and pathophysiological mechanisms seem to be responsible for the condition. Multiple different genetic abnormalities and mechanisms may be responsible for influencing neuronal excitability in JME.

  The interictal EEG in JME consists of bilateral, symmetrical spike and polyspike-and-wave discharges of 3 to 5 Hz, usually maximal in the frontocentral regions. The EEG correlate of the myoclonic jerks is a burst of high-voltage, 10–16-Hz polyspikes followed by irregular 1-Hz slow waves and single spikes or polyspike discharges. Focal EEG abnormalities occur in a significant number of patients with JME.

  Valproic acid controls the seizures, but lifetime treatment is necessary. Lamotrigine, levetiracetam, topiramate, and zonisamide may be considered in patients who do not tolerate valproic acid. In some situations, lamotrigine may exacerbate myoclonus. Ethosuximide is useful to treat uncontrolled absence seizures.

  Benign childhood epilepsy with centrotemporal spikes (BECTS) also is referred to as benign rolandic epilepsy. Seizures begin between 3 and 13 years of age with a peak onset at 9 to 10 years of age. The typical seizure characteristics are somatosensory disturbance of the mouth, preservation of consciousness, excessive pooling of saliva and tonic or tonic–clonic activity of the face, and speech arrest when the dominant hemisphere is affected. The somatosensory or motor activity may spread to the arm. Secondary generalization may occur, especially when the seizures are nocturnal. Seizures typically occur shortly after sleep onset, just before awakening, and with naps. Seizures can occur during the day. Headache and vomiting may be associated. Development, neurological examinations, and neuroradiological studies at the time of diagnosis typically are normal. Seizures usually stop in adolescence, and the outcome is favorable. Some children with BECTS have cognitive or behavioral problems, particularly difficulty with sustained attention, reading, and language processing. A family history of epilepsy is present in approximately 10% of cases.

  The EEG consists of a normal background with midtemporal and central, high-amplitude, often diphasic spikes and sharp waves with increased frequency during sleep. The spikes and sharp waves are usually unilateral, but they may be bilateral. Because the overall prognosis for benign childhood epilepsy is good, treatment is not required after the first or even the second seizure, and some children never require treatment. Most anticonvulsant drugs are effective as monotherapy.

  Neurology

  B&D Ch. 67

Question 35. B. The practice described in the question is called “fee splitting” and is considered unethical. As a physician you cannot receive financial compensation for referring patients to other doctors, nor can you pay for such referrals. Such an arrangement puts the doctor’s interests (the financial incentive to refer) over the best interests of the patient and leads to inappropriate referrals.

  Ethics

  K&S Ch. 58

Question 36. B. Advances in medical and surgical techniques in liver transplantation have improved long-term post-transplantation survival, with reported 5-year survival rates of 80–90%. Liver transplantation has become the accepted standard of care in children with end-stage liver disease. Congenital biliary atresia is the most common reason for liver transplantation in children. Other causes are biliary micronodular cirrhosis, viral hepatitis, Alagille syndrome, and several rare genetic disorders.

  Neurological problems occur in 48% of pediatric orthotopic liver transplant recipients. A majority involve seizures, mental status changes, or coma. Three fourths of comatose patients had significant intracerebral hemorrhage on brain imaging. Neurological complications constitute a significant source of mortality and morbidity in these patients. A recent study reviewed data for 41 adults and pediatric patients who underwent liver transplantation. Encephalopathy occurred in 62% with either immediate or delayed onset. Seizures (multifocal myoclonus, focal, or status epilepticus) occurred in 11% and were associated with the presence of encephalopathy. Three patients had neuropathy. Other complications were headache, tremor, fatigue, restlessness, enuresis, dizziness, critical illness myopathy, and detached retina. Brain imaging revealed atrophy, subarachnoid hemorrhage, intracerebral hemorrhage, and infections.

  Neurology

  B&D Ch. 49B

Question 37. A. Erikson developed the concept of the epigenetic principle. The epigenetic principle states that human development occurs in sequential, clearly defined stages, and that each stage must be properly resolved for development to proceed normally. Other famous therapists listed in this question are the subject of their own questions elsewhere in this text.

  Human Development K&S Ch. 4

Question 38. C. An isolated, painful abducens palsy may represent microvascular ischemia, especially in older patients with vascular risk factors. Spontaneous resolution over 8 to 12 weeks is typical. In the absence of complete, spontaneous resolution, neuroimaging is essential. Head trauma, even if mild, is another relatively common cause of abducens palsy. Impaired ability to abduct the eye past midline or bilateral presentation predicts poor spontaneous recovery. The abducens nerve is the cranial nerve most commonly affected bilaterally in isolation. This occurs most often from trauma and increased intracranial pressure.

  A third-nerve palsy is the most commonly encountered diabetic cranial mononeuropathy. Pupillary sparing, the hallmark of diabetic third-nerve palsy, results from ischemic infarction of the centrifascicular oculomotor axons due to diabetic vasculopathy of the vasa nervorum. The peripherally located pupillary motor fibers are spared as a result of collateral circulation from the circumferential arteries. With decreasing frequency, the fourth, sixth, and seventh nerves are also affected. Patients with Bell’s palsy have a significantly higher frequency of diabetes than an age-matched population. Most make a full recovery in 3 to 5 months.

  Neurology

  B&D Chs 70&76

Question 39. E. Appropriate specifiers for substance induced anxiety disorder include “with generalized anxiety”, “with panic attacks”, “with obsessive–compulsive symptoms”, and “with phobic symptoms”. Other specifiers include “with onset during intoxication” and “with onset during withdrawal”. “With delayed onset” is not appropriate to use with this diagnosis. Though some may think this question is picky or unfair, the details of the DSM are indeed fair game for a test of general psychiatric knowledge. The small details of the DSM give the test writer ample opportunity to form tricky questions. Know your DSM well!

  Anxiety Disorders

  K&S Ch. 16

Question 40. D. Herpes simplex virus-1 encephalitis (HSE) is the most common cause of sporadic, fatal encephalitis in the United States, accounting for approximately 10% of all cases of encephalitis and occurring with a frequency of about 1 case/250 000 population/year. Early recognition is important because the antiviral drug acyclovir (ACV) is effective in reducing morbidity and mortality. HSV-1 strains are causal agents in over 90% of cases of HSE in adults. Type 2 strains are more commonly isolated in monophasic or recurrent meningitis and congenitally acquired neonatal HSV meningoencephalitis. Fever is present in approximately 90% and headache in about 80% of patients with biopsy or polymerase chain reaction (PCR)-proven HSE. Other common features include disorientation (70%), personality change (70–85%), focal or generalized seizures (40–67%), memory disturbance (25–45%), motor deficit (30–40%), and aphasia (33%). The presence of olfactory hallucinations should also suggest the possibility of HSE.

  Examination of CSF is the single most important diagnostic test in suspected cases of HSE. CSF is usually under increased pressure, with a lymphocytic pleocytosis of 10 to 1000 white blood cell count (WBC) per microliter. More than 95% of PCR- or biopsy-proven cases of HSE have a CSF pleocytosis, although rare cases with an initial acellular CSF have been reported. HSE is often hemorrhagic, and both red blood cells and xanthochromia can occur in the CSF, although neither feature occurs with significantly greater frequency in HSE than with other causes of focal encephalitis. CSF protein is usually moderately elevated, and glucose is normal in more than 90% of cases. Virus cannot be cultured from CSF in more than 95% of cases of HSE; however, HSV DNA can be detected in the CSF with PCR techniques. Amplification of HSV DNA from CSF by PCR testing has a sensitivity and specificity of greater than 95% for the diagnosis of HSE compared with brain biopsy and is the diagnostic procedure of choice for HSE. MRI is significantly more sensitive than CT and is the neuroimaging procedure of choice in patients with suspected HSE. Approximately 90% of patients with PCR-proven HSE will have MRI abnormalities involving the temporal lobes. The electroencephalogram (EEG) may be abnormal early in the course of disease, demonstrating diffuse slowing, focal abnormalities in the temporal regions, or periodic lateralizing epileptiform discharges (PLEDs). EEG abnormalities involving the temporal lobes are seen in approximately 75% of patients with PCR-proven HSE. Because of its safety, empiric therapy with ACV should be started immediately in cases of suspected focal encephalitis. The mortality rate in untreated cases of HSE is about 70%, which is reduced to 19–28% in patients treated with ACV.

  Neurology

  B&D Ch. 53B

Question 41. E. This question is really asking why pain disorder is a psychiatric condition rather than a medical one. And the answer, of course, is that in pain disorder the pain is thought to be mediated by psychological factors. In chronic pain syndromes, which are in the domain of medicine and not psychiatry, there is thought to be a physical cause for the pain even if that cause cannot be identified. In pain disorder there is believed to be no medical cause or the pain is grossly disproportionate to any pathological findings. In pain disorder psychological factors are felt to play a major role in the precipitation, maintenance or exacerbation of the pain. Any of the other choices could be true for either condition and are not the key difference used to differentiate the two.

  Somatic Symptom Disorders

  K&S Ch. 17

Question 42. B. Inclusion body myositis (IBM) is the most common myopathy in patients over the age of 50 years. Only rarely does it occur in people less than 50 years of age. Unlike dermatomyositis, polymyositis, and other autoimmune disorders, inclusion body myositis is much more common in men than in women. The disease weakens the distal muscles of the arms and legs. The deep finger flexors, including the flexor pollicis longus, and wrist flexors are involved early. They are usually more involved than the wrist and finger extensors. In the legs, early involvement of the quadriceps and anterior tibial muscles occurs. Profound atrophy is appreciable in the flexor forearms and quadriceps. The disease generally has a chronic progressive course and is considered unresponsive to prednisone and other immunosuppressive (e.g., methotrexate) and immunomodulating (e.g., IVIG) therapies. The clinical history and examination are the basis for suspecting the diagnosis of IBM. Muscle biopsy is confirmatory. The CK concentration may be normal or only mildly elevated (<10 times the upper limit of normal). The EMG demonstrates fibrillation potentials and positive sharp waves. The muscle biopsy demonstrates endomysial inflammation and invasion of non-necrotic muscle fibers similar to polymyositis. In addition, characteristic “rimmed” vacuoles may be profuse.

  Dermatomyositis is an illness in which weakness is associated with a characteristic skin rash. It is the common form of myositis occurring in childhood through middle adult life. The rash usually occurs with onset of muscle weakness, although it may develop during the course of the disease. It is characteristically a purplish discoloration of the skin over the cheeks and eyelids. It often has a butterfly distribution and blanches on pressure. The weakness is symmetrical and affects the proximal more than distal muscles of the arms and legs. Muscle pain is noted, but not in all patients. The serum CK concentrations are usually elevated in dermatomyositis but can be normal earlier in the course or in patients with a very indolent course. Serum CK levels do not necessarily reflect activity of the disease. The characteristic histological feature on muscle biopsy is perifascicular atrophy (a crust of small fibers surrounding a core of more normal-sized fibers deeper in the fascicle).

  Polymyositis is an acute or subacute illness that occurs in adults. Cases of polymyositis in infants and children probably represent muscular dystrophies with inflammation. It is more frequent in women than in men, as are other autoimmune diseases. As in dermatomyositis, weakness is symmetrical and affects the proximal more than distal muscles of the arms and legs. Systemic symptoms are common at onset, such as malaise, fever, and anorexia. A viral prodrome sometimes precedes the illness, but such events are sufficiently common enough that the association may be coincidental. The diagnostic studies in polymyositis are similar to those in dermatomyositis and include serum CK concentrations, serum autoantibodies, EMG, and muscle biopsy. Serum CK concentration should always be elevated in polymyositis, unlike dermatomyositis or inclusion body myositis, in which the CK concentration may be normal.

  Neurology

  B&D Ch. 79

Question 43. D. This question tests the four most commonly asked neural pathways on standardized psych exams. The tuberoinfundibular pathway goes from the hypothalamus to the anterior pituitary. It is important in the regulation of prolactin secretion. The nigrostriatal pathway goes from the substantia nigra to the basal ganglia. It is important in the development of extrapyramidal symptoms. The mesocortical pathway goes from the ventral tegmental area to the frontal cortex and is involved in the negative symptoms of schizophrenia. The mesolimbic pathway goes from the ventral tegmental area to the nucleus accumbens and is involved in positive psychotic symptoms. The ventral amygdalofugal pathways are a distracter. They are not commonly asked on exams and are part of the limbic system, running from the amygdala to the thalamus and hypothalamus.

  Basic Neuroscience

  K&S Ch. 3

Question 44. C. Mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS) is a maternally inherited encephalomyopathy clinically characterized by stroke-like episodes, vascular headaches, vomiting, seizures, and lactic acidosis. The stroke deficits are sometimes transient but can be permanent and cause progressive encephalopathy with dementia. Unusual clinical patterns include focal seizures, sometimes prolonged, which can herald a stroke. The unique radiological feature is that the stroke involves the cerebral cortex, sparing the white matter, mostly in the parietal and occipital regions. Neuroimaging may show additional lesions that have no clinical correlates. The onset is generally in childhood or early adult life. Most patients have RRF on muscle biopsy, but only rarely is there clinical weakness or exercise intolerance. The finding of excessive mutation load in the endothelium and smooth muscle of cerebral vessels has been suggested as the likely cause of stroke episodes and migraine headaches in these patients.

  Myoclonic epilepsy with ragged-red fiber myopathy (MERRF) is another maternally inherited encephalomyopathy characterized by myoclonus, epilepsy, cerebellar ataxia, and myopathy with RRF. Onset is usually in childhood or early adulthood. The syndrome begins generally with myoclonic epilepsy in childhood, and other seizure patterns are added soon thereafter. Worsening ataxia and mental retardation is seen in later childhood.

  The clinical deficit in Leber’s hereditary optic neuropathy (LHON) is usually an isolated bilateral optic neuropathy. LHON is expressed predominantly in males of the maternal lineage, but the greater susceptibility of males to vision loss in LHON remains unexplained. The age of onset is typically between 15 and 35 years, and the vision loss is painless, central, and usually occurs in one eye weeks or months before involvement of the other eye. Funduscopic abnormalities may be seen in patients with LHON and in their asymptomatic relatives. Especially during the acute phase of vision loss, there may be hyperemia of the optic nerve head, dilatation and tortuosity of peripapillary vessels, circumpapillary telangiectasia, nerve fiber edema, and focal hemorrhage. Vision loss in LHON affects central or centrocecal fields and is usually permanent. A minority of patients show objective improvement, sometimes to a dramatic degree. In most LHON patients, vision loss is the only manifestation of the disease. Some families have additional members with associated cardiac conduction abnormalities, especially pre-excitation syndromes. There may also be a movement disorder or other minor neurological or skeletal abnormalities.

  Kearns–Sayre syndrome (KSS) is defined by the triad of progressive external ophthalmoplegia (PEO), onset before age 20, and at least one of the following: short stature, pigmentary retinopathy, cerebellar ataxia, heart block, and elevated CSF protein (>100 mg/dL). Many patients with KSS are physically or mentally subnormal. Some clinical features of MELAS and MERRF may overlap with KSS. The clinical course in KSS is progressive, and most patients with associated mental retardation die in the third or fourth decade.

  Neurology

  B&D Ch. 63

Question 45. E. This question covers the paraphilias. Sexual masochism is a preoccupation with fantasies or urges of being beaten, bound or humiliated. Fetishism is being sexually fixated on and aroused by inanimate objects like shoes or pantyhose. Voyeurism is preoccupation with fantasies of observing an unsuspecting person who is naked or involved in sexual activity. Transvestic fetishism involves fantasies and sexual urges to dress in clothing of the opposite gender in order to obtain sexual arousal. Frotteurism involves rubbing ones genitals against a nonconsenting person in order to obtain sexual arousal.

  Paraphilias

  K&S Ch. 21

Question 46. A. Botulinum toxin blocks acetylcholine release at peripheral synapses, leading to the paralytic and autonomic clinical manifestations of botulism. Botulinum toxin causes irreversible blockade at peripheral cholinergic synapses. Recovery requires sprouting of new nerve terminals, accounting for the protracted clinical course of botulism.

  Neurology

  B&D Ch. 53C

Question 47. C. Signs of nicotine withdrawal include depressed mood, insomnia, irritability, anxiety, poor concentration, restlessness, decreased heart rate, and increased appetite. To meet DSM criteria for nicotine withdrawal four of the above symptoms must be present within 24hours of cessation of nicotine.

  Substance Abuse and Addictive Disorders

  K&S Ch. 12

Question 48. E. If stroke patients meet appropriate criteria, thrombolytic therapy may be administered. Thrombolytic therapy is able to recanalize acute intracranial occlusions, but the question remains whether thrombolytic therapy can recanalize occlusions of large extracranial or other large intracranial vessels (e.g., carotid terminus). A strong correlation has been shown between arterial recanalization and neurological improvement in acute cerebral ischemia.

  In June 1996, the Food and Drug Administration (FDA) approved the use of intravenous tissue plasminogen activator (t-PA) for ischemic stroke within 3hours of symptom onset. Intravenous t-PA administration requires close adherence to protocol guidelines. The management of patients following t-PA administration requires close neurologic and blood pressure monitoring as well as capabilities to handle potential hemorrhagic complications associated with thrombolytic therapy by physicians experienced in the management of cerebrovascular disease. Centers that do not have these capabilities can still administer intravenous t-PA in partnership with tertiary care facilities by starting the drug and transferring the patient. Successful centers have treated up to 15–20% of ischemic strokes with thrombolytic therapy, although nationally only a few percent of patients are likely to be treated with thrombolytic therapies. The most recent operational change in stroke care is formal certification of stroke centers, and a model that mirrors the trauma system with primary and comprehensive designated stroke centers is under development in the United States. Inclusion criteria for administration of t-PA in the NINDS t-PA trial were acute ischemic stroke with a clearly defined time of onset (<3 hours), neurological deficit measurable on the NIH Stroke Scale, and CT scan without evidence of intracranial hemorrhage. Patients who awoke from sleep had symptom onset defined as “when last seen awake and normal.” Exclusion criteria for administration of t-PA were rapidly improving or isolated minor neurological deficits, seizure at the onset of stroke, prior intracranial hemorrhage, symptoms suggestive of subarachnoid hemorrhage, blood glucose level less than 50 mg/dL (2.7 mM) or greater than 400 mg/dL (22.2 mM), gastrointestinal or genitourinary bleeding within the 3 weeks before stroke, recent MI, current use of oral anticoagulants (PT>15seconds or INR>1.5), a prolonged aPTT or use of heparin in the previous 48hours, platelet count less than 100 000/μL, another stroke or serious head injury in the previous 3 months, major surgery within the previous 14 days, arterial puncture at a noncompressible site within the previous 7 days, or pretreatment SBP greater than 185 mmHg or DBP greater than 110 mmHg.

  Neurology

  B&D Ch. 51A

Question 49. D. In hypochondriasis the patient is convinced that they have a serious disease based on misinterpretation of bodily symptoms and despite assurance that they are not ill. In somatization disorder the patient presents with multiple physical complaints involving several organ systems that are not explained by any medical disorder. In malingering the patient is intentionally feigning symptoms for external incentives. In factitious disorder the patient is intentionally feigning symptoms for the benefits of the sick role. This patient does not have Lou Gehrig’s disease or he would not have had several negative workups.

  Somatic Symptom Disorders

  K&S Ch. 17

Question 50. C. The cervical spinal column includes 37 joints that are continually in motion throughout life. Cervical osteoarthritis and spondylosis are ubiquitous with increasing age. Myelopathy caused by compression of the cervical spinal cord by the changes of spondylosis and osteoarthritis usually develops insidiously, but it may be precipitated by trauma or progress in stepwise fashion. Typical findings are a combination of leg spasticity, upper extremity weakness or clumsiness, and sensory changes in the arms, legs, or trunk. Either spinothalamic tract-mediated or posterior column-mediated sensory modalities may be impaired. Sphincter dysfunction, if it occurs, usually is preceded by motor or sensory findings. Neck pain is often not a prominent symptom, and neck range of motion may or may not be impaired. Some patients experience leg or trunk paresthesia induced by neck flexion (Lhermitte’s sign).

  The anterior–posterior diameter of the cervical spinal cord is usually 10 mm or less. Patients rarely develop cervical spondylotic myelopathy if the congenital diameter of their spinal canal exceeds 16 mm. In congenitally narrow canals, disk protrusion, osteophytes, hypertrophy of the ligamentum flavum, ossification of the posterior longitudinal ligament, and vertebral body subluxations can combine to compress the spinal cord. MRI or CT myelography provide excellent images of the relation between the spinal canal and the spinal cord. MRI provides more intramedullary detail such as secondary cord edema or gliosis. CT provides better images of calcified tissues. The natural history of cervical spondylotic myelopathy is variable. Some patients have stable neurological deficit for many years without specific therapy, whereas other patients have gradual or stepwise deterioration. Some patients improve with treatments such as bed rest, soft collars, or immobilizing collars, but these treatments have not been assessed in controlled trials. Many patients with cervical spondylotic myelopathy are treated by surgical decompression with variable surgical results. Surgical and nonsurgical treatment results are best when the neurological deficit is mild and present for less than 6 months and when the patient is younger than 70 years. Anterior cervical diskectomies are generally performed for spondylotic lesions at a limited number of levels, whereas posterior laminectomy, sometimes with an expanding “open-door” laminoplasty, is generally performed for congenital spinal canal stenosis.

  Neurology

  B&D Ch. 73

Question 51. B. Female sexual arousal disorder involves inability to attain an adequate lubrication–swelling response of normal sexual excitement. In sexual aversion disorder the patient has extreme aversion to or avoidance of sexual contact with a partner. In female orgasmic disorder there is a delay in or absence of orgasm following a normal excitement phase. Vaginismus is involuntary muscle spasm of the outer third of the vagina which interferes with sexual intercourse. Dyspareunia is recurrent genital pain associated with intercourse in either a male or female.

  Sexual Dysfunction

  K&S Ch. 21

Question 52. E. Nonarteritic anterior ischemic optic neuropathy (AION) is the most common cause of unilateral optic nerve swelling in adults older than 50 and commonly is associated with vascular risk factors such as diabetes or hypertension. Other risk factors include a crowded optic nerve head and nocturnal hypotension, possibly precipitated by antihypertensive therapy. Prognostically, many patients will have a stable deficit, although some may experience progression over a month, and the expected rate of spontaneous improvement is high. In 30–40% of patients, subsequent involvement of the fellow eye occurs, and this rate is increased by the presence of vascular risk factors. Recurrence in an affected eye, however, is very rare. There does not appear to be a significantly higher rate of stroke in patients with nonarteritic ischemic optic neuropathy. Posterior (retrobulbar) ischemic optic neuropathy is rare, but is often a sign of giant cell arteritis. The workup should therefore include an evaluation for arteritis, as well as for inflammatory and infiltrative conditions. Sometimes ischemic optic neuropathy without significant disk edema can occur after severe blood loss and shock. Arteritic anterior ischemic optic neuropathy usually is related to temporal arteritis and always associated with disk swelling. Rarely, this entity can affect the nerve only proximal to the lamina cribrosa and manifest without disk swelling; this situation is termed arteritic posterior ischemic optic neuropathy. The prevalence of temporal arteritis increases with age, and most patients are older than 70 years of age. Acute vision loss is the presenting symptom in 7–60% of cases and generally is significantly more severe than in nonarteritic AION. In approximately 25% of cases, vision is limited to perception of hand motion only, or light perception is absent.

  Neurology

  B&D Ch. 15

Question 53. E. Phencyclidine, inhalants, sedative hypnotics, and alcohol can all cause nystagmus during intoxication.

  Substance Abuse and Addictive Disorders

  K&S Ch. 12

Question 54. B. A thorough knowledge of the criteria for brain death is essential for the physician whose responsibilities include evaluation of comatose patients. Despite differences in state laws, the criteria for the establishment of brain death are fairly standard within the medical community. These criteria include the following:

  Coma. The patient should exhibit an unarousable unresponsiveness. There should be no meaningful response to noxious, externally applied stimuli. The patient should not obey commands or demonstrate any verbal response, either reflexively or spontaneously. Spinal reflexes, however, may be retained.

  No spontaneous respirations. The patient should be removed from ventilatory assistance and carbon dioxide should be allowed to build up because of the respiratory drive that hypercapnia produces. The diagnosis of absolute apnea requires the absence of spontaneous respiration at a carbon dioxide tension of at least 60 mmHg. A safe means of obtaining this degree of carbon dioxide retention involves the technique of apneic oxygenation, in which 100% oxygen is delivered endotracheally through a thin sterile catheter for 10minutes. Arterial blood gas levels should be obtained to confirm the arterial carbon dioxide pressure.

  Absence of brainstem reflexes. Pupillary, oculocephalic, corneal, and gag reflexes all must be absent, and there should not be any vestibulo-ocular responses to cold calorics.

  Electrocerebral silence. An isoelectric EEG should denote the absence of cerebrocortical function. Some authorities do not regard the performance of an EEG as mandatory in assessing brain death and instances of preserved cortical function, despite irreversible and complete brainstem disruption, have been reported.

  Absence of cerebral blood flow. Cerebral contrast angiography or radionuclide angiography can substantiate the absence of cerebral blood flow, which is expected in brain death. These tests are considered confirmatory rather than mandatory. On rare occasions, in the presence of supratentorial lesions with preserved blood flow to the brainstem and cerebellum, findings on cerebral radionuclide angiography may be misleading.

  Absence of any potentially reversible causes of marked CNS depression. Such causes include hypothermia (temperature 32°C [89.6°F] or less), drug intoxication (particularly barbiturate overdose), and severe metabolic disturbance.

  The American Academy of neurology has determined that a positive apnea test is an absolute necessity for the declaration of brain death.

  Neurology

  B&D Ch. 5

Question 55. C. To get this question right you must know the difference between an inhibitor and an inducer of the CYP450 system. An inhibitor decreases the enzyme activity leading to an increase in the plasma concentration of the drug. An inducer increases the enzyme activity leading to a decrease in the plasma concentration.

  The question also touches on some other important concepts. For example there are some patients or ethnic groups who because of a genetic polymorphism in the CYP450 genes will have either increased or decreased enzyme activity. This can change them into slow or rapid metabolizers.

  Paroxetine and fluoxetine are potent CYP2D6 inhibitors. Great caution must be shown mixing them with TCAs, Mellaril, codeine, beta blockers, Risperdal, clozapine, and aripiprazole. Thioridazine is contraindicated with CYP2D6 inhibitors.

  The most important CYP450 enzymes for the psychiatrist to understand are CYP2D6, CYP1A2 and CYP3A4. You will no doubt see more questions about them all throughout this book and on your exam.

  Psychopharmacology K&S Ch. 36

Question 56. D. Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder of undetermined etiology that primarily affects the motor neuron cell populations in the motor cortex, brainstem, and spinal cord. It is progressive and most patients eventually succumb to respiratory failure. Between 5 and 10% of ALS is familial rather than sporadic, the most common inheritance pattern being autosomal dominant. The incidence and prevalence rates for non–Western Pacific ALS are surprisingly uniform throughout the world. The incidence is estimated at 0.86 to 2.4 per 100 000 (∼2 per 100 000 in the United States) and the prevalence is about 6 per 100 000. Perhaps the most significant breakthrough in understanding the cause of ALS (be it sporadic or familial) came in 1993, when Rosen and colleagues identified mutations in the gene encoding an enzyme called copper/zinc superoxide dismutase (SOD1) in patients with familial ALS. SOD1 mutations are identified in up to 20% of all patients with familial ALS. A significant body of basic and clinical research lends strong support to a theory of ALS pathogenesis, which proposes selective motor neuron damage from a complex chain of injurious events involving excitotoxins, oxidative stress, neurofilament dysfunction, altered calcium homeostasis, mitochondrial dysfunction, enhanced motor neuron apoptosis, and proinflammatory cytokines. Onset of muscle weakness is more common in the upper than the lower extremities (classic, spinal ALS), but in approximately 25% of patients, weakness begins in bulbar-innervated muscles (bulbar-onset ALS). Pseudobulbar palsy may present with inappropriate or forced crying or laughter, which is often a source of great emotional distress for patients. The median duration of ALS from clinical onset ranges from 22 to 52 months, and the mean duration from 23 to 43 months, with an average 5-year survival rate of 22% (roughly 1 in 5) and a 10-year survival rate of 9.4% (roughly 1 in 10). The diagnosis of clinically definite ALS can sometimes be reached based on the history and clinical examination alone, but, owing to the seriousness of the diagnosis, ancillary investigations are necessary to exclude other possibilities. The EMG examination characteristically reveals a combination of acute (positive sharp waves and fibrillation potentials) and chronic (reduced neurogenic firing pattern with evidence of increased amplitude and duration, polyphasic motor unit potentials) changes in a widespread distribution that is not in keeping with any single root or peripheral nerve distribution. Fasciculation potentials are usually identified; their absence should prompt an investigation for another disorder. In 1996, riluzole (Rilutek) was approved by the US Food and Drug Administration as the first specific drug for the treatment of ALS. It is believed to principally function as an antiglutamate agent, although its mechanism of action is not yet fully understood. The care of patients with ALS has become increasingly complex. As a consequence, many patients receive the care of a multidisciplinary team in a specialized ALS center, rather than by a single treating physician. Explanations of the other answer choices to this question can be found in other question explanations in this volume.

  Neurology

  B&D Ch. 74

Question 57. E. Females develop tardive dyskinesia more commonly than males. Patients over the age of 50 are more likely to develop tardive dyskinesia than those younger. Patients with brain damage and young children are more likely to develop tardive dyskinesia than older healthier counterparts.

  Psychopharmacology

  K&S Ch. 36

Question 58. B. Brain tumors account for approximately 4% of epilepsy cases. Seizures are a common presenting symptom of brain tumors. The incidence of seizures is greater in primary low-grade brain tumors than in brain metastases or high-grade primary tumors. A study of 132 adult patients with newly diagnosed glioblastoma reported that seizures were the presenting symptom in 31% of patients. In a series of patients with low-grade supratentorial gliomas, seizures occurred in association with 75.5% of astrocytomas, 60.8% of mixed gliomas, and 62.5% of oligodendrogliomas. Seizures are sometimes focal, reflecting tumor location, but many become secondarily generalized at onset. Patients with temporal lobe tumors frequently describe auras: epigastric sensations and psychological phenomena such as déjà vu and depersonalization are common. Complex partial seizures and secondarily generalized tonic–clonic seizures are common.

  Neurology

  B&D Ch. 52C

Question 59. B. Valproic acid will increase lamotrigine levels. Oral contraceptives will decrease lamotrigine levels. Phenobarbital and Phenytoin will decrease lamotrigine levels.

  Psychopharmacology

  K&S Ch. 36

Question 60. D. Positron emission tomography (PET), like SPECT, depends on detection of emitted radioactivity (derived from injection of a radiolabeled tracer). Positrons are highly unstable particles and travel only a short distance in space before colliding with an electron. The resulting annihilation reaction results in the formation of two gamma rays of 511 keV traveling at 180° to each other. PET is based on the detection of these coincident gamma rays. PET utilizes the selective binding or uptake and retention of a variety of radiopharmaceuticals. These tracers may provide general information about physiological function, such as regional cerebral blood flow (usually assessed with H215O) or cerebral glucose metabolism, assessed with [18F]fluoro-2-deoxyglucose (FDG). FDG undergoes phosphorylation but, because of the 2-deoxy modification, cannot proceed further along the glycolytic pathway; as a result, glucose uptake is physiologically trapped. Brain glucose metabolism is correlated with synaptic activity, and FDG PET therefore provides a good measure of neural activity, but without specifying the particular neuronal subtype involved. The other major application of PET is in the labeling of pharmaceuticals that are substrates for specific enzymes, such as those involved in neurotransmitter synthesis or breakdown – examples are 6-[18F]fluoro-L-dopa as a measure of dopamine synthesis and N-[11C]methylpiperdin-4-yl propionate ([11C]PMP) to measure acetylcholinesterase activity – or that bind to specific neurotransmitter receptors or transporters. It is this capacity of PET to study specific neurochemical processes that is its unique strength. Other advantages of PET include the generally preferable spatial resolution and quantifiability over those of SPECT (although some more recent SPECT cameras have vastly improved resolution).

  SPECT is the nuclear medicine equivalent of computed tomography, similarly combining a series of two-dimensional images obtained by moving the gamma camera on a gantry in a circular or elliptical orbit around the patient. The information from this series of images is then combined into a three-dimensional volume. Unlike PET, SPECT is based on the detection of single gamma rays, rather than coincident detection of simultaneously emitted photons. Like PET, brain SPECT can be used to study general physiological functions such as perfusion, as well as in labeling neurotransmitter receptors and transporters. Brain perfusion often is measured using SPECT with 99 mTc-hexamethylpropyleneamine oxime (HMPAO).

  In addition to its superior spatial resolution, MRI takes advantage of changes in the paramagnetic properties of deoxyhemoglobin compared with oxygenated hemoglobin to deduce the degree of blood oxygenation (the so-called blood oxygenation level-dependent [BOLD] technique). As blood flow increases, oxygen extraction decreases, so the levels of deoxyhemoglobin decline and MRI signal intensity increases. This effect has been widely exploited in a large number of research settings in order to examine regional activation associated with a variety of cognitive processes, including language, reward processing, decision making, fear, and altruistic behavior and empathy, as well as motor and sensory processing. Functional MRI can provide valuable insights into brain plasticity and reorganization after injury such as trauma or stroke. Functional MRI has vastly superior temporal resolution compared with PET or SPECT and is widely available—most current commercial scanners have the capacity to perform such studies. The spatial resolution also is favorable, although not as good as with structural MRI, and comparable to that achieved with the best PET scanners. In contrast with PET, which permits a quantifiable absolute measure (e.g., blood flow, metabolic rate, ligand-binding potential), fMRI allows estimation of only the relative change in regional blood flow.

  Neurology

  B&D Ch. 33C

Question 61. A. The random movements of chorea are accentuated and often most noticeable during walking. The superimposition of chorea on the trunk and leg movements of the walking cycle gives the gait a dancing quality, and there is an exaggerated motion of the legs and arm swing. Chorea can also interrupt the walking pattern, leading to a hesitant gait. Additional voluntary compensatory movements appear in response to perturbations from the chorea. Chorea in Sydenham’s chorea or chorea gravidarum may be sufficiently violent to throw patients off their feet; severe chorea of the trunk may render walking impossible. The chorea of Huntington’s disease usually causes a lurching or stumbling and stuttering gait with frequent steps forward, backward, or to the side. Walking is slow, the stance is wide-based, the trunk sways excessively, and steps are variable in length and timing. Spontaneous knee flexion and leg-raising movements are common. Haloperidol reduces chorea but does not improve gait in Huntington’s disease. Balance and equilibrium usually are maintained until the terminal stages of Huntington’s disease, when an akinetic-rigid syndrome may supervene. Stereotactic thalamotomy is of course a neurosurgical technique designed to alleviate symptoms of Parkinson’s disease. Pramipexole and benztropine are antiparkinsonian medications. Lioresal (Baclofen) is a potent muscle relaxant used in the treatment of muscle spasticity, for example in stroke and multiple sclerosis patients.

  Neurology

  B&D Ch. 22

Question 62. C. The most common akinetic-rigid gait disturbance is that encountered in Parkinson’s disease. The posture is stooped with flexion of the shoulders, neck, and trunk. During walking, there is little associated or synergistic body movement. Arm swing is reduced or absent, and the arms are held immobile at the sides or slightly forward of the trunk. Tremor of the upper limbs frequently increases when walking (but parkinsonian tremor of the legs rarely affects walking). The gait is slow and shuffling, with small, shallow steps on a narrow base. The posture of generalized flexion of the patient with Parkinson’s disease exaggerates the normal tendency to lean forward when walking. To maintain balance when walking and avoid falling forward, the patient may advance with a series of rapid, small steps (festination). Retropulsion and propulsion are similar manifestations of a flurry of small, shuffling steps made in an effort to preserve equilibrium. Instead of a single large step, a series of small steps are taken to maintain balance. Falls occur in Parkinson’s disease when festinating steps are too small to restore balance.

  Astasia–abasia refers to the inability to either stand or walk in a normal manner. Patients exhibit an unusual and dramatic gait disturbance, lurching wildly in various directions and falling only when a nearby physician, family member, or soft object will catch them. Astasia refers to the inability to maintain station (stand upright) unassisted. Abasia refers to lack of motor coordination in walking. The term literally means that the base of gait (the lateral distance between the two feet) is inconstant or unmeasurable. When seen in conversion disorder, the gait is bizarre and is not suggestive of a specific organic lesion: often the patient sways wildly and nearly falls, recovering at the last moment. However, an acquired total inability to stand and walk can be seen in true neurological diseases, including stroke, Parkinson disease, damage to the cerebellum, Guillain–Barré syndrome, normal pressure hydrocephalus and many others. In normal pressure hydrocephalus for example, when the condition remains untreated, the patient’s gait becomes shortened, with frequent shuffling and falls; eventually standing, sitting, and even rolling over in bed become impossible. This advanced state is referred to as “hydrocephalic astasia–abasia”.

  Neurology

  B&D Ch. 22

Question 63. E. Bacterial meningitis may be defined as an inflammatory response to bacterial infection of the pia-arachnoid and cerebrospinal fluid (CSF) in the subarachnoid space. Because the subarachnoid space is continuous over the brain, spinal cord, nerves, and nerve roots, infection in this space generally extends throughout the cerebrospinal axis. The incidence of bacterial meningitis is between 2 and 4 per 100 000 people per year in the United States. More than 1500 deaths due to bacterial meningitis are reported annually in the United States. Worldwide, three main pathogens, Haemophilus influenzaeStreptococcus pneumoniae, and Neisseria meningitidis, account for 75–80% of cases after the neonatal period. Group B streptococci, Escherichia coli and other enteric bacilli, and Listeria monocytogenes are major pathogens in neonatal meningitis. The most common bacteria that cause meningitis, S. pneumoniae and N. meningitides, initially colonize the nasopharynx by attaching to nasopharyngeal mucosa. At any time, S. pneumoniaecan be isolated from 5–10% healthy adults and from 20–40% healthy children. Bacterial meningitis occurs when pathogens colonizing the nasopharynx cause bacteremia and breach the blood–brain barrier to reach into the brain.

  The classical clinical presentation of adults with bacterial meningitis comprises headache, fever, and neck stiffness, often with signs of cerebral dysfunction; these manifestations are found in more than 85% of patients. Nausea, vomiting, myalgia, and photophobia are also common. The neck stiffness may be subtle or marked, accompanied by Kernig’s or Brudzinski’s signs (or both). These signs are elicited in over half of adults, but less in neonates and elderly; absence of clinical meningeal signs does not rule out the diagnosis of bacterial meningitis. Cerebral dysfunction is manifested by confusion, delirium, and a declining level of consciousness that ranges from lethargy to coma. Seizures occur in approximately 40% of cases. Cranial nerve palsies involving cranial nerves III, VI, and VII are found in 10–20% of cases and result from direct damage to the nerve by the surrounding infection or endarteritis of the vasa nervorum.

  Neurology

  B&D Ch. 53C

Question 64. A. In 1916, Guillain, Barré, and Strohl emphasized the main clinical features of GBS: motor weakness, areflexia, paresthesias with minor sensory loss, and increased protein in CSF without pleocytosis (albuminocytological dissociation). The frequent finding of motor conduction block and reduced nerve conduction velocities provided further electrophysiological confirmation of the widespread demyelination. Approximately two thirds of patients report a preceding event, most frequently an upper respiratory or gastrointestinal infection, surgery, or immunization 1 to 4 weeks before the onset of neurological symptoms. The agent responsible for the prodromal illness often remains unidentified. Specific infectious agents linked to GBS include cytomegalovirus (CMV), Epstein–Barr virus, varicella zoster virus, hepatitis A and B, HIV, Mycoplasma pneumoniae, and Haemophilus influenzae. The most common identifiable bacterial organism linked to GBS and particularly its axonal forms is Campylobacter jejuni, a curved Gram-negative rod that is a common cause of bacterial enteritis worldwide. Patients with classic GBS may initially present with weakness, with or without paresthetic sensory symptoms. The fairly symmetrical weakness of the lower limbs ascends proximally over hours to several days and may subsequently involve arm, facial, and oropharyngeal muscles, and, in severe cases, respiratory muscles. Hyporeflexia or areflexia are the invariable features of GBS but may be absent early in the course of the disease. Cranial nerve involvement has occurred in 45–75% of cases in different series. Facial paresis, usually bilateral, is found in at least one half of patients. In the first week of neurological symptoms the CSF protein may be normal but then becomes elevated on subsequent examinations. In approximately 10% of cases, the CSF protein remains normal throughout the illness. Abnormalities of electrophysiological studies are found in approximately 90% of established cases and reflect an evolving picture of multifocal demyelination associated with secondary axonal degeneration. The most common electrophysiological abnormalities include prolonged distal motor and F-wave latencies, absent or impersistent F waves, conduction block, reduction in distal CMAP amplitudes with or without temporal dispersion, and slowing of motor conduction velocities. Conduction block of motor axons is the electrophysiological correlate of clinical weakness and is recognized by a decrease of greater than 50% in CMAP amplitude from distal to proximal stimulation in the absence of temporal dispersion. Among specific therapeutic interventions aimed at mitigating the harmful effects of autoantibodies, plasma exchange and high-dose intravenous immune globulin (IVIG) infusions have been shown to be equally effective.

  Neurology

  B&D Ch. 76

Question 65. E. The clinical presentation of intracerebral hemorrhage (ICH) has two main elements: symptoms that reflect the effects of intracranial hypertension and those that are specific for the location of the hematoma. The general clinical manifestations of ICH related to increased intracranial pressure (ICP) (headache, vomiting, and depressed level of consciousness) vary in their frequency at onset of ICH. CT is sensitive to the high-density fresh blood in the brain parenchyma, along with associated features of local mass effect and ventricular extension. MRI adds further precision, especially in determining the time elapsed between onset and time of MRI examination. Cerebellar hemorrhage represents approximately 5–10% of the cases. Its clinical presentation is characteristic, with abrupt onset of vertigo, headache, vomiting, and inability to stand and walk, with absence of hemiparesis or hemiplegia. The physical findings that allow its clinical diagnosis are the triad of appendicular ataxia, horizontal gaze palsy, and peripheral facial palsy, all ipsilateral to the hemorrhage. The clinical course in cerebellar hemorrhage can be difficult to predict at onset. There is a notorious tendency for abrupt deterioration to coma and death after a period of clinical stability under hospital observation. The neurologist must be able to recognize when neurosurgical intervention, which is frequently life saving and function restoring for these patients, is indicated. To this effect, it is convenient to classify the clinical stages seen in this condition: (1) an initial “cerebellar” stage, in which the only clinical deficits detected are referable to the cerebellum; (2) an intermediate stage, in which, in addition to cerebellar signs, there are signs and symptoms referrable to hydrocephalus; and (3) the final stage, brainstem compression. Neurosurgical intervention is indicated when the first signs and symptoms of hydrocephalus develop. The prognosis for good functional recovery is excellent in patients with cerebellar hemorrhage who have had a timely suboccipital decompression before they have lapsed into coma. Even comatose patients, however, can make an excellent functional recovery, provided that the decompression is carried out expeditiously and soon after the onset of coma.

  Neurology

  B&D Chs 46&51B

Question 66. C. Stiff-person syndrome (SPS) is rare and no information is available about its epidemiology. SPS is a syndrome of progressive rigidity of axial and proximal appendicular muscles with muscle hypertrophy and extreme lumbar lordosis. Intense spasms are superimposed on a background of continuous muscle contraction. Gait is slow and stiff legged. Spasms and stiffness improve with sleep and are eliminated by general anesthesia and neuromuscular blocking agents. Clinical criteria for diagnosis include insidious development of limb and axial (thoracolumbar and abdominal) stiffness, clinical and electrophysiological confirmation of co-contraction of agonist and antagonist muscles, episodic spasms superimposed on chronic stiffness, and no other underlying illness that would explain the symptoms. EMG examination shows continuous firing of normal motor units. SPS is associated with autoimmune disorders, such as type I diabetes, thyroiditis, myasthenia gravis, pernicious anemia, and vitiligo. High titers of antibodies to the 65-kD fraction of glutamic acid decarboxylase and to other antigens are present. It is thought that SPS results from dysfunction of descending suprasegmental pathways possibly secondary to immune-mediated inhibition of GABA synthesis. Paraneoplastic SPS has been reported with breast and lung cancers and Hodgkin’s disease. Untreated, SPS progresses to extreme disability. Diazepam at doses of 20 to 400 mg/day is the most effective symptomatic treatment. Clonazepam, baclofen, valproic acid, clonidine, vigabatrin, and tiagabine have also been reported to be effective. Intrathecal baclofen and local intramuscular injections of botulinum toxin have been helpful in some cases. Plasmapheresis, IVIg, and immunosuppression have been reported to have variable effects on the condition.

  Neurology

  B&D Chs 52G&71

Question 67. D. Simple partial seizures of temporal lobe origin often are difficult to recognize as epileptic events. The report of symptoms by the patient may be the only clear evidence of the event. Complex partial temporal lobe seizures may begin with impairment of consciousness, or by a simple partial seizure, or an aura. Auras vary in duration from seconds to several minutes before impairment of consciousness. Most complex partial seizures last longer than 30 seconds, usually up to 1 to 2 minutes; few last less than 10 seconds, which is a distinguishing characteristic from absence seizures. Postictal recovery usually is slow, with significant confusion that may last for several minutes or longer. Some have suggested that clinical symptomatology at the very onset of the seizure occasionally provides clues about the site of ictal onset in the temporal lobe. These may include auditory or olfactory hallucinations, emotional or psychic symptoms, sensations of movement or rotation, or autonomic symptoms. The focus usually is in the superior temporal gyrus. The cause of olfactory seizures (uncinate fits), usually an unpleasant odor, is discharges in the medial temporal lobe. The cause of gustatory seizures is discharges deep in the sylvian fissure or the operculum. Epigastric sensations of nausea, “butterflies,” emptiness, or tightness usually are caused by temporal lobe activity. Emotional changes and psychic phenomena, often attributed to simple partial seizures of temporal lobe origin, more commonly are associated with complex partial seizures.

  Neurology

  B&D Ch. 67

Question 68. A. Carotid artery dissection commonly manifests with neck, face, and head pain ipsilateral to the dissection, frequently is associated with an ipsilateral Horner’s syndrome, and often follows head or neck trauma. A dissection is produced by subintimal penetration of blood in a cervicocephalic vessel with subsequent longitudinal extension of the intramural hematoma between its layers. Most dissections involve the extracranial segment of the internal carotid artery or extracranial vertebral arteries. Intracranial dissections are usually subintimal and may follow trivial trauma, closed head trauma, basilar skull fracture, or penetrating injuries. Diagnosis is based on arteriographic findings, although high-resolution MRI and magnetic resonance angiography (MRA), computed tomographic angiography (CTA), and extracranial and transcranial Doppler ultrasound are rapidly replacing contrast angiography for the diagnosis of cervicocephalic arterial dissections, particularly in cases of carotid artery involvement. Features on arteriography include the presence of a pearl and string sign; double-lumen sign; short, smooth, tapered occlusion; or pseudoaneurysm formation. Therapeutic interventions have included immediate anticoagulation with heparin followed by a 3–6-month course of warfarin, and platelet antiaggregants instead of, or following, warfarin.

  Neurology

  B&D Chs 18&51A

Question 69. B. Tolosa–Hunt syndrome (THS) is a painful syndrome of idiopathic, self-limited inflammation of the cavernous sinus, typically responsive to corticosteroids. Inflammation associated with systemic rheumatologic disease, metastatic or nasopharyngeal neoplastic infiltration, carotid–cavernous fistulas, and compression from an intracavernous internal artery aneurysm or meningioma may also cause a cavernous sinus syndrome. Pituitary apoplexy should be considered in the differential diagnosis for sudden onset, painful unilateral or bilateral oculomotor palsies, with or without accompanying visual loss. THS is a rare disorder characterized by severe and unilateral headaches with extraocular palsies, usually involving the third, fourth, fifth, and sixth cranial nerves, and pain around the sides and back of the eye, along with weakness and paralysis (ophthalmoplegia) of certain eye muscles. Symptoms are usually limited to one side of the head, and in most cases the individual affected will experience intense, sharp pain and paralysis of muscles around the eye. Symptoms may subside without medical intervention, yet recur without a noticeable pattern. In addition, affected individuals may experience paralysis of various facial nerves and drooping of the upper eyelid (ptosis). Other signs include double vision, fever, chronic fatigue, vertigo or arthralgia. Occasionally the patient may present with a feeling of protrusion of one or both eyeballs (exophthalmos). MRI scans of the brain and orbit with and without contrast, magnetic resonance angiography or digital subtraction angiography and a CT scan of the brain and orbit with and without contrast may all be useful in detecting inflammatory changes in the cavernous sinus, superior orbital fissure and/or orbital apex. Treatment of THS is usually completed using corticosteroids (often prednisone) and immunosuppressive agents (such as methotrexate or azathioprine). Corticosteroids act as analgesia and reduce pain (usually within 24–72hours), as well as reducing the inflammatory mass, whereas immunosuppressive agents help reduce the autoimmune response. Treatment is then continued in the same dosages for a further 7–10 days and then tapered slowly. The prognosis of THS is usually considered good. Patients usually respond to corticosteroids, and spontaneous remission can occur, although movement of ocular muscles may remain damaged. Roughly 30–40% of patients who are treated for THS experience a relapse.

  Neurology

  B&D Ch. 70

Question 70. A. Lorazepam (initially marketed under the brand names Ativan and Temesta) is a high-potency short-to-intermediate-acting 3-hydroxy benzodiazepine drug that has all six intrinsic benzodiazepine effects: anxiolytic, amnesic, sedative/hypnotic, anticonvulsant, antiemetic and muscle relaxant. Lorazepam is used for the short-term treatment of anxiety, insomnia, acute seizures including statusepilepticus and sedation of hospitalized patients, as well as sedation of aggressive patients. Lorazepam is considered to be a short-acting drug which, similar to other benzodiazepines, exerts its therapeutic as well as adverse effects via its interaction at benzodiazepine binding sites, which are located on GABA receptors in the central nervous system. After its introduction in 1977, lorazepam’s principal use was in treating anxiety. Among benzodiazepines, lorazepam has a relatively high addictive potential. Lorazepam also has abuse potential; the main types of misuse are for recreational purposes or continued use against medical advice. Lorazepam may be safer than most benzodiazepines in patients with impaired liver function. Like oxazepam, it does not require hepatic oxidation, but only hepatic glucuronidation into lorazepam-glucuronide. Therefore, impaired liver function is unlikely to result in lorazepam accumulation to an extent causing adverse reactions. Similarly renal disease has minimal effects on lorazepam levels. The three benzodiazepines that are metabolized via glucuronidation are lorazepam, oxazepam, and temazepam and these come up often in this context on standardized examinations in psychiatry (mnemonic LOT).

  Psychopharmacology

  K&S Ch. 36

Question 71. C. Most of the body’s serotonin is in the gastrointestinal (GI) tract. This is why serotonergic drugs typically cause varying degrees of stomach pain, nausea, vomiting, flatulence and diarrhea. These side effects are mediated mostly through effects on the serotonin 5HT-3 receptor. Sertraline and fluvoxamine produce the most intense GI symptoms. In most cases these side effects are transient, but in a small percentage of individuals, these effects never abate and a switch to another class of antidepressant must be made. The most effective way to offset these side effects is to use initial low doses of these agents or to use delayed-release preparations. Up to one-third of patients taking SSRIs will gain weight. This effect is mediated through a metabolic mechanism, increase in appetite, or both. It happens slowly over time and is resistant to diet and exercise regimens.

  Psychopharmacology

  K&S Ch. 36

Question 72. E. The standard and classic treatment for obsessive–compulsive disorder (OCD) is via pharmacotherapy, behavior therapy, or a combination of the two. SSRIs and clomipramine (Anafranil) are the pharmacologic agents of choice in OCD. Behavioral therapy techniques have been shown to be effective for OCD. These include exposure and response prevention, desensitization, thought-stopping, flooding, implosion therapy, and aversive conditioning. In behavior therapy, patients have to be truly committed to their own improvement. Family and group therapy are often helpful in supporting the family and improving relationships in patients with OCD. For extreme cases that are unresponsive to all these therapies, electroconvulsive shock therapy (ECT) and psychosurgery are considerations. ECT is not as effective as psychosurgery, but it should still be tried before psychosurgery. Cingulotomy is a common psychosurgical procedure for extreme OCD and is effective in 25–30% of otherwise treatment-unresponsive patients. Another surgical procedure that may also help intractable OCD is subcaudate tractotomy, also known as capsulotomy. The most common complication of psychosurgery is the development of seizures. Some patients who do not respond to psychosurgery following failure of prior pharmacotherapy and/or behavior therapy, may respond to these interventions after the psychosurgery is done.

  Anxiety Disorders

  K&S Ch. 16

Question 73. B. Lithium has myriad side effects that crop up in multiple choice questions on psychiatry examinations. Among its neurologic side effects, Lithium can cause dysphoria, lack of spontaneity, slowed reaction time and memory difficulties. Patients often complain of “altered creativity” and this is a well-described adverse effect of lithium. These are usually benign side effects that can occur even when the serum lithium level is below the toxic range. Lithium can also cause tremor, peripheral neuropathy, benign intracranial hypertension, lowered seizure threshold and a myasthenia gravis-like syndrome. Other common non-neurologic side effects of lithium include: weight gain, fluid retention, appetite loss, nausea, vomiting, diarrhea, nephrogenic diabetes insipidus (polyuria/polydipsia), hypothyroidism, hyperparathyroidism, benign T-wave changes, acne, rash, psoriasis, and hair loss.

  Psychopharmacology

  K&S Ch. 36

Question 74. D. Affective disorders (MDD + Bipolar) accounts for 50% of completed suicides. The other potentially tricky choice listed was personality disorders, which only account for 5% of completed suicides despite their many attempts and gestures. Of the personality disorders, 4 to 10% of borderlines commit suicide, and 5% of antisocial personality disorders commit suicide. Mixing the personality disorder with major depression or substance abuse greatly increases the risk. The risk of completed suicide in affective disorders is 30 times greater than that for the general population. Drug and alcohol abuse account for 25% of completed suicides and 5–10% of patients with schizophrenia complete suicide.

  Management in Psychiatry

  K&S Ch. 34

Question 75. E. The therapist’s tasks in a group therapy setting include determining the size and setting of the group, choosing frequency and length of sessions, deciding on an open vs. closed group, formulating appropriate goals, selecting patients and building a therapeutic environment for the group that can identify and deal with problems within the group. We do not want to suppress catharsis, we want patients to speak about their feelings and emotions and feel relief after doing so.

  Psychological Theory and Psychometric Testing

  K&S Ch. 35

Question 76. C. Carbamazepine, in its extended-release form (Equetro), was finally FDA-approved in the US for treatment of bipolar disorder in 2004. It was first used to treat partial and generalized-onset epilepsy and trigeminal neuralgia. Carbamazepine is structurally similar to the tricyclic antidepressants. Carbamazepine is believed to cause blockade of type 2 sodium channels and have activity at A1 adenosine receptors. Carbamazepine absorption is slow and unpredictable. This results, at least partially, from autoinduction of its own metabolism via hepatic CYP450 3A4 enzymes. Carbamazepine has numerous side effects. Those that are dose-dependant include blurred vision, vertigo, gastrointestinal disturbances, and task-performance impairment. Idiosyncratic adverse effects (which are not dose-dependant) include agranulocytosis, Stevens–Johnson syndrome, aplastic anemia, hepatic failure, rash and pancreatitis. The drug’s hematologic effects are not dose-dependant. Severe blood dyscrasias (aplastic anemia and agranulocytosis) occur in about 1 in 125 000 persons treated with carbamazepine. Patients should be warned that symptoms such as fever, rash, petechiae, sore throat, bruising and easy bleeding, may herald serious blood dyscrasia and they should be urged to seek medical attention immediately. Routine blood monitoring of the complete blood count is recommended at 3, 6, 9, and 12 months. If no evidence of bone marrow suppression is noted at 12 months, most clinicians would reduce the interval of monitoring.

  Psychopharmacology

  K&S Ch. 36

Question 77. E. The grammar development stage is 36–54 months. At around 40 months children can use a wide range of grammatical forms such as plurals, past tense, negatives and questions. Children of this age can also understand prepositions, cause and effect, and know up to 5500 words.

  Human Development

  K&S Ch. 2

Question 78. A. Clozapine should not be taken in conjunction with any other drug that is associated with the development of agranulocytosis or bone marrow suppression. Such agents include carbamazepine, phenytoin, propylthiouracil, sulfonamides, and captopril. Lithium combined with clozapine can increase risk of seizures, confusion and movement disorders. Lithium should not be taken with clozapine in patients who have previously experienced an episode of neuroleptic malignant syndrome. Clomipramine can increase the seizure risk by lowering the seizure threshold and by increasing clozapine plasma concentrations. Fluoxetine, paroxetine, risperidone and fluvoxamine can all increase the serum levels of clozapine. Also, paroxetine may trigger clozapine-associated neutropenia.

  Psychopharmacology

  K&S Ch. 36

Question 79. D. Memantine is a low to moderate affinity NMDA receptor antagonist. It is FDA-approved in the USA for treatment of moderate to severe Alzheimer’s disease. It is purported that overexcitation of NMDA receptors by the neurotransmitter glutamate may play a role in Alzheimer’s disease, because glutamate plays an integral part in the neural pathways associated with learning and memory. Excess glutamate overstimulates NMDA receptors to allow too much calcium into nerve cells, leading to cell death that is observed in Alzheimer’s disease. Memantine is believed to have neuroprotective effects by partially blocking NMDA receptors associated with abnormal transmission of glutamate, while allowing for physiologic transmission associated with normal cell functioning. Galantamine, donepezil, tacrine, and rivastigmine are all inhibitors of acetylcholinesterase.

  Psychopharmacology

  K&S Ch. 36

Question 80. E. Organophosphorus poisoning mnemonics:

  DUMBELS

  D = Diarrhea

  U = Urination

  M = Miosis

  B = Bradycardia

  E = Emesis

  L = Lacrimation

  S = Salivation / Sweating / Secretion

  Organophosphates are used mainly as pesticides and herbicides but are also used as petroleum additives, lubricants, antioxidants, flame retardants, and plastic modifiers. Most cases of organophosphate toxicity result from exposure in an agricultural setting, not only among those mixing or spraying the pesticide or herbicide but also among workers returning prematurely to sprayed fields. Absorption may occur through the skin, by inhalation, or through the gastrointestinal tract. Organophosphates inhibit acetylcholinesterase by phosphorylation, with resultant acute cholinergic symptoms, with both central and neuromuscular manifestations. Symptoms include nausea, salivation, lacrimation, headache, weakness, and bronchospasm in mild instances and bradycardia, tremor, chest pain, diarrhea, pulmonary edema, cyanosis, convulsions, and even coma in more severe cases. Death may result from respiratory or heart failure. Treatment involves intravenous administration of pralidoxime (1 g) together with atropine (1 mg) given subcutaneously every 30 minutes until sweating and salivation are controlled. Pralidoxime accelerates reactivation of the inhibited acetylcholinesterase, and atropine is effective in counteracting muscarinic effects, although it has no effect on the nicotinic effects such as neuromuscular cholinergic blockade with weakness or respiratory depression. It is important to ensure adequate ventilatory support before atropine is given.

  Poisoning

  B&D Ch. 58

Question 81. B. Clostridium tetani secretes tetanospasmin, also known as tetanus toxin, and tetanolysin. The toxicity of tetanolysin is uncertain; tetanospasmin blocks release of inhibitory neurotransmitters by spinal interneurons, causing the dramatic muscle contractions that characterize tetanus. Tetanospasmin inhibits release of gamma-aminobutyric acid and glycine, which are inhibitory neurotransmitters in the brainstem and spinal cord. A single type of tetanus neurotoxin exists, in contrast to the multiple serotypes of botulinum toxin. The typical incubation period is 2 weeks but can range from hours to a month or more. Cardinal features include muscle rigidity and spasms, which may be accompanied by autonomic hyperactivity. Local tetanus, in which symptoms remain limited to a limb, is a rare form. Far more common is generalized tetanus, also called lockjaw, as trismus heralds the disorder in over 75% of cases. Sustained contraction of facial muscles causes a sneering grimace known as risus sardonicus. Other early symptoms include dysphagia and axial muscle involvement, such as neck stiffness, abdominal rigidity, and back pain. Early involvement of face, neck, and trunk muscles has been ascribed to the shorter axons of motor neurons supplying cranial and axial muscles, as compared with the limbs. Laryngospasm compromises ventilation and makes intubation extremely difficult. Sustained contraction of back muscles causes opisthotonos, an arching posture of the back. As tetanus progresses, reflex muscle spasms develop, triggered by sensory stimuli, movement, or emotion. Examination can be difficult, as it may prompt spasms. Therapeutic goals include protecting the airway, neutralizing circulating tetanospasmin and preventing its further production, managing spasms and dysautonomia, and general supportive care. Initial treatment of most patients with generalized tetanus includes endotracheal intubation, because laryngospasm may appear abruptly even in mild cases. Human tetanus immune globulin, given as a single dose of at least 500 IU intramuscularly, neutralizes circulating toxin. Infected wounds should be debrided after human tetanus-immune globulin administration, because the procedure may release further toxin. Metronidazole or penicillin should be given to eradicate C. tetani.

  Poisonings

  B&D Ch. 53C

Question 82. B. Sleep is composed of five distinct phases or stages: non-REM (NREM) sleep, which is divided into Stages I through IV and REM sleep. Each phase has its own unique characteristics when measured in three ways: electroencephalogram (EEG), electrooculogram (EOG) and electromyogram (EMG). The following table breaks down these phases into their distinct characteristics.

image

  Sleep Wake Disorders

  K&S Ch. 24

Question 83. D. In the neonatal period, REM represents more than 50% of total sleep time and the EEG goes directly into REM phase without passing first through stages I through IV. Newborns sleep about 16 hours a day. By about 4 months of age, the sleep pattern shifts. Infants now pass through NREM sleep before their first REM episode and REM sleep drops to less than 40% of total sleep time. By young adulthood, NREM makes up about 75% of total sleep time. This 75% is divided as follows: Stage I 5%; Stage II 45%; Stage III 12%; Stage IV 13%. Thus, in adulthood, REM makes up about 25% of total sleep time. This distribution remains relatively constant into older age, although there is usually a reduction in both slow-wave sleep and REM sleep in the elderly.

  Sleep Wake Disorders

  K&S Ch. 24

Question 84. C. Phentolamine is a parenteral medication usually reserved for hospital use in intensive care unit or cardiac care unit settings. Its primary action is vasodilation due to α1 blockade. It also can lead to reflex tachycardia because of hypotension and α2 inhibition, which increases sympathetic tone. The primary application for phentolamine is for the control of hypertensive emergencies, most notably due to pheochromocytoma. It also has usefulness in the treatment of cocaine induced hypertension, where one would generally avoid beta blockers and where calcium channel blockers are not effective. Beta blockers (e.g., metoprolol) or combined alpha and beta adrenergic blocking agents (e.g., labetalol) should be avoided in patients with a history of cocaine abuse. They can cause an unopposed alpha-adrenergic mediated coronary vasoconstriction, causing the worsening of myocardial ischemia and hypertension. It is also used in the treatment of pheochromocytoma prior to the administration of beta blockers to avoid unopposed alpha-stimulation. In this context it is probably most safely given by infusion since bolus doses have a propensity towards causing precipitous falls in blood pressure. When given by injection it causes blood vessels to expand, thereby increasing blood flow. Phentolamine has a very short half-life of approximately 20-minutes duration. Monoamine oxidase inhibitor (MAOI) induced hypertensive crisis should be treated with alpha-adrenergic antagonists, such as phentolamine or chlorpromazine. These agents lower blood pressure within five minutes. Intravenous furosemide (Lasix) can be used to reduce the fluid load and beta-adrenergic receptor antagonists can be used for controlling tachycardia. A sublingual dose of nifedipine (Procardia) can be given and repeated in 20 minutes. MAOIs should not be taken by patients with pheochromocytoma or thyrotoxicosis. Bromocriptine and dantrolene are dopamine agonists and are used in the treatment of neuroleptic malignant syndrome. They have no place in the treatment of MAOI-induced hypertensive crisis and in fact bromocriptine should be used with extreme caution in patients on MAOIs, as it can interact adversely with MAOIs, worsening hypertensive crisis. Sedative-hypnotic agents, like diazepam, should also be used with caution in patients taking MAOIs.

  Diagnostic and Treatment Procedures in Psychiatry

  K&S Ch. 36

Question 85. D. Concurrent administration of an SSRI with an MAOI antidepressant or Lithium can raise plasma serotonin to toxic levels, producing a serotonin syndrome. Serotonin syndrome is serious and can, in some cases, be fatal. Symptoms tend to occur in the following order as the condition worsens: (1) diarrhea; (2) restlessness; (3) extreme agitation, hyperreflexia and autonomic instability, with possible rapid fluctuations in vital signs; (4) myoclonus, seizures, hyperthermia, uncontrollable shivering, and rigidity; and (5) delirium, coma, status epilepticus, cardiovascular collapse, and death. Treatment consists of promptly removing the offending agents and immediately instituting comprehensive supportive care with nitroglycerine, cyproheptadine, methysergide, cooling blankets, chlorpromazine, dantrolene, benzodiazepines, anticonvulsants, mechanical ventilation, and paralytic agents.

  Management in Psychiatry

  K&S Ch. 36

Question 86. A. The overwhelming factor that correlates with childhood physical abuse is poverty and psychosocial stress, especially financial stress. Abuse and neglect of children also correlates with less parental education, underemployment, poor housing, single parenting and welfare reliance. Risk of child abuse increases in families with many children and is also increased by other risk factors, such as physical handicap, mental retardation, and prematurity. Parental mental illness, parental substance abuse (in particular alcoholism), social isolation, and domestic violence also correlate with childhood abuse and neglect. Families in which there are many of these problems coexisting tend to be more prone to child abuse and neglect.

  Public Policy

  K&S Chs 32&55

Question 87. B. Interpersonal therapy (IPT) is a time-limited (acutely, 12–16 weeks) treatment with three phases: a beginning (1–3 sessions), middle, and end (3 sessions). The initial phase requires the therapist to identify the target diagnosis (MDD) and the interpersonal context in which it presents. In diagnosing major depression, the therapist follows DSM-IV criteria and employs severity measures such as the Hamilton Depression Rating Scale (Ham-D) or Beck Depression Inventory (BDI) to reify the problem as an illness rather than the patient’s idiosyncratic defect. The therapist also elicits an “interpersonal inventory”, a review of the patient’s patterns in relationships, capacity for intimacy, and particularly an evaluation of current relationships. A focus for treatment emerges from the last: someone important may have died (complicated bereavement), there may be a struggle with a significant other (role dispute), or the patient may have gone through some other important life change (role transition); in the relatively infrequent absence of any of these, the default focus is on interpersonal deficits, a confusing term that really denotes the absence of a current life event.

  The therapist links the target diagnosis to the interpersonal focus. This formulation defines the remainder of the therapy. The connection between mood and life events is practical, not etiological: there is no pretense that this is what “causes” depression. With the patient’s agreement on this focus, treatment moves into the middle phase.

  Other facets of the opening phase include giving the patient the “sick role”, a temporary status recognizing that depressive illness keeps the patient from functioning at full capacity, and setting treatment parameters such as the time limit and the expectation that therapy will focus on recent interpersonal interactions.

  In the middle phase of treatment, the therapist uses specific strategies to deal with whichever of the four potential problem areas is the focus. This might involve appropriate mourning in complicated bereavement, resolving an interpersonal struggle in a role dispute, helping a patient to mourn the loss of an old role and assume a new one in a role transition, or decreasing social isolation for interpersonal deficits. Whatever the focus, the therapy is likely to address the patient’s ability to assert his or her needs and wishes in interpersonal encounters, to validate the patient’s anger as a normal interpersonal signal and to encourage its efficient expression, and to encourage taking appropriate social risks. In the last few sessions, the therapist reminds the patient that termination is nearing, helps the patient to feel more capable and independent by reviewing his or her often considerable accomplishments during the treatment, and notes that ending therapy is itself a role transition, with inevitable good and painful aspects. Since IPT has also demonstrated efficacy as a maintenance treatment for recurrent MDD, and since patients who have had multiple episodes are very likely to have more, therapist and patient may decide to end acute treatment as scheduled and then to recontract for ongoing treatment, perhaps of less intensive dosage: e.g., monthly rather than weekly sessions.

  The IPT therapist’s stance is relaxed and supportive. The goal is to be the patient’s ally. The acute time limit pressures the patient to take action. No formal homework is assigned, but the goal of solving the focal interpersonal problem area provides an overall task. Treatment centers on the patient’s outside environment, not on the therapy itself. The scheduling of sessions once weekly accentuates that the emphasis is on the patient’s real life, not the office. In sessions therapist and patient review the past week’s events. When the patient succeeds in an interpersonal situation, the therapist acts as a cheerleader, reinforcing healthy interpersonal skills. When the outcome is adverse, the therapist offers sympathy, helps the patient to analyze what went wrong in the situation, brainstorms new interpersonal options, and role plays them with the patient in rehearsal for real life. The patient then tests them out. Given this emphasis on interpersonal interaction, it is not surprising that depressed patients learn new interpersonal skills from IPT that they have not seen with pharmacotherapy. Note that psychotherapy questions come up frequently on psychiatry examinations and candidates often find themselves underprepared for these important questions. Do make it a point to look up IPT along with other psychotherapy modalities, to maximize your understanding of them.

  Psychotherapy

  K&S Ch. 35

Question 88. E. The “dialectical” in dialectical behavioral therapy (DBT) refers to the way in which it uses a broad way of thinking that emphasizes the limitations of linear ideas about causation. It substitutes “both/and” for “either/or” and sees truth as an evolving product of the opposition of different views. The use of dialectical ideas in DBT arises largely from the clinical observation of the mixed and shifting nature of human emotion and experience in general and in patients with borderline personality disorder (BPD) in particular. Interaction with such a patient is unlikely to have the characteristics of a logical argument or even an orderly conversation. It is more likely to be akin to a dance to rapidly changing music. The person with BPD is seen as having difficulties in being detached from his or her experience and is often overwhelmed by it. Developing the capacity for being mindful and living in the moment allows a greater potential for feeling appropriately in charge of the self. A related concept is the balance between acceptance and change. The most difficult idea for some is that the world is as it is. But again there is some paradox in the notion that acceptance – for instance, of unchangeable traumatic events in the past – may be necessary for change to be possible.

  Psychotherapy

  K&S Ch. 35

Question 89. E. Most patients with obsessive–compulsive disorder (OCD) have both obsessions and compulsions – up to 75% according to some studies. Some psychiatrists feel that this statistic is closer to 100%, if the patient is properly assessed for both mental and behavioral compulsions. Nevertheless, as per DSM-IV-TR, a patient need not have both obsessions and compulsions to meet criteria for OCD; one or the other is sufficient. Obsessions are intrusive thoughts and compulsions are intrusive behaviors. In OCD, an idea or impulse intrudes insistently and persistently into a person’s conscious awareness. Remember that by DSM diagnostic standards, compulsions are defined as repetitive behaviors or mental acts that the person feels driven to perform in response to an obsession, or according to rules that must be applied rigidly. These behaviors (or mental acts) are targeted at reducing distress or anxiety, and are clearly excessive in their nature. In this particular question, the patient presents with compulsive orderliness, alphabetizing and color-coding behaviors. There is no mention of obsessions, though the criteria for OCD are met without that stipulation in this case.

  Obsessive Compulsive and Related Disorders

  K&S Ch. 16

Question 90. B. By DSM-IV-TR criteria, pedophilia is defined as recurrent, intense sexually arousing fantasies, sexual urges, or behaviors involving sexual activity with a prepubescent child or children, generally 13 years of age or younger, persisting over at least 6 months. The perpetrator either has acted on these sexual urges, or the urges or fantasies must cause significant distress or interpersonal difficulty. The perpetrator must be at least 16 years of age and at least 5 years older than the victim. When a perpetrator is a late adolescent involved with a 12- or 13-year-old, the pedophilia diagnosis does not apply. Ninety-five percent of pedophiles are heterosexual and 50% are found to be using alcohol at the time of the incident.

  Paraphilias

  K&S Ch. 21

Question 91. D. The mainstay of pharmacologic treatment of childhood ADHD is the stimulant medication class of agents. Methylphenidate and amphetamine preparations are dopamine agonists. Methylphenidate has been shown to be effective in about 75% of all children with ADHD. Common side effects of the stimulants are: headaches, GI discomfort, nausea and insomnia. Of course stimulants also suppress appetite and can induce weight loss. Some children experience a rebound effect following the wearing-off of the stimulant, during which period they become irritable and hyperactive. Motor tics can also be exacerbated by the use of stimulants, which warrants caution when the medications are given in this specific population of children. Methylphenidate is also associated with growth stunting or suppression. This effect seems to be offset when children are given drug holidays during the summer months when they are not in school. About 75% of students on stimulant medications demonstrate improvement in attention as measured by objective tests of their academic performance. Dextroamphetamine and dextroamphetamine/amphetamine salt combinations (Adderall) are generally the second choice when methylphenidate fails.

  Disruptive, Impulse Control, Conduct Disorders, and ADHD

  K&S Chs 43&54

Question 92. B. The predominant disturbance in dissociative fugue is sudden, unexpected travel away from home or one’s customary place of work, with inability to recall one’s past. There is also confusion about one’s personal identity or the assumption of a new identity. The symptoms must cause significant distress or impairment in social, occupational, or other important areas of functioning. The fugue state must not occur during a period of substance abuse or as part of dissociative identity disorder, or as a consequence of a medical condition. These fugue episodes can last from minutes to months in duration. Traumatic circumstances leading to an altered state of consciousness with a wish to flee, are generally the underlying cause of most fugue states. The disorder is seen more commonly during natural disasters, wartime, or during times of terrorism or social upheaval. Dissociative fugue is usually treated with psychodynamic psychotherapy, attempting to help the patient recover lost memory of their identity and recent experiences. Hypnotherapy is at times also helpful in the process of recovery following fugue states.

  Dissociative Disorders

  K&S Ch. 20

Question 93. C. Eating disorders occur in about 4% of adolescents and young adults. Anorexia nervosa has its most common age of onset in the mid-teenage years, but up to 5% of cases begin in the twenties. The most common age of onset is between 14 and 18 years of age. Anorexia nervosa is estimated to occur in about 0.5 to 1% of adolescent girls. The disorder occurs about 10 to 20 times more frequently in women than in men. It is most frequent in developed countries and it is seen with highest frequency in women whose profession requires thinness, such as acting and modeling and dance. Anorexia is associated with depression in about 65% of cases.

  Feeding and Eating Disorders

  K&S Ch. 23

Question 94. A. Encopresis is defined by DSM as the repeated passage of feces into inappropriate places, such as clothes or the floor, whether intentionally or involuntarily. The child must be 4 years of age, or older. The episodes must occur at least monthly for 3 months or more. Encopresis is not due to a general medical condition. The behavior must cause the child significant distress or social or academic impairment. Males are found to have encopresis six times more frequently than females. Encopresis has been shown to develop with much greater frequency in children with a known history of sexual abuse. Some studies have associated encopresis with measures of maternal hostility and punitive and harsh parenting.

  Elimination Disorders

  K&S Ch. 47

Question 95. E. The defining feature of the paranoid subtype of schizophrenia is the presence of auditory hallucinations or prominent delusional thoughts about persecution or conspiracy. However, people with this subtype may be more functional in their ability to work and engage in relationships than people with other subtypes of schizophrenia. The reasons are not entirely clear, but may partly reflect that people suffering from this subtype often do not exhibit symptoms until later in life and have achieved a higher level of functioning before the onset of their illness. People with the paranoid subtype may appear to lead fairly normal lives by successful management of their disorder. People diagnosed with the paranoid subtype may not appear odd or unusual and may not readily discuss the symptoms of their illness. Typically, the hallucinations and delusions revolve around some characteristic theme, and this theme often remains fairly consistent over time. A person’s temperaments and general behaviors often are related to the content of the disturbance of thought. For example, people who believe that they are being persecuted unjustly may be easily angered and become hostile. Do review the five subtypes of schizophrenia thoroughly, as questions about them do appear with regularity on standardized tests. Also be sure to review the good and poor prognosticating factors of schizophrenia. These too are often tested on psychiatry examinations.

  Psychotic Disorders

  K&S Ch. 13

Question 96. D. In order to be diagnosed with pathological gambling, an individual must present with persistent and recurrent maladaptive gambling that causes economic problems and significant disturbances in personal, social, or occupational functioning with at least five of the following symptoms:

1. Preoccupation. The subject has frequent thoughts about gambling experiences, whether past, future, or fantasy.

2. Tolerance. As with drug tolerance, the subject requires larger or more frequent wagers to experience the same “rush”.

3. Withdrawal. Restlessness or irritability associated with attempts to cease or reduce gambling.

4. Escape. The subject gambles to improve mood or escape problems.

5. Chasing. The subject tries to win back gambling losses with more gambling.

6. Lying. The subject tries to hide the extent of his or her gambling by lying to family, friends, or therapists.

7. Loss of control. The person has unsuccessfully attempted to reduce gambling.

8. Illegal acts. The person has broken the law in order to obtain gambling money or recover gambling losses. This may include acts of theft, embezzlement, fraud, or forgery.

9. Risked significant relationship. The person gambles despite risking or losing a relationship, job, or other significant opportunity.

10. Bailout. The person turns to family, friends, or another third party for financial assistance as a result of gambling.

  Studies have pointed towards a neurobiological determinant in pathological gamblers’ risk-taking behaviors. Theories have focused on both serotonergic and noradrenergic receptor systems. Evidence supports the probability that male pathological gamblers have low plasma MHPG concentrations, as well as increased CSF MHPG concentrations and increased urinary output of norepinephrine. Chronic gamblers also have decreased platelet MAO activity, which is a marker of serotonergic dysfunction, which is linked to difficulties with inhibition and impulse control. Epidemiologic studies point to a prevalence rate of about 3 to 5% of problem gamblers in the general population at large and about 1% who meet criteria for pathological gambling.

  Disruptive, Impulse Control, Conduct Disorders, and ADHD

  K&S Ch. 25

Question 97. C. Conduct disorder is defined, as per DSM-IV-TR, as a repetitive and persistent pattern of behavior in which the basic rights of others or major age-appropriate societal norms or rules are violated, as manifested by the presence of three (or more) of the following criteria in the past 12 months, with at least one criterion present in the past 6 months:

  Aggression to people and animals:

• often bullies, threatens, or intimidates others

• often initiates physical fights

• has used a weapon that can cause serious physical harm to others (e.g., a bat, brick, broken bottle, knife, gun)

• has been physically cruel to people

• has been physically cruel to animals

• has stolen while confronting a victim (e.g., mugging, purse snatching, extortion, armed robbery)

• has forced someone into sexual activity

  Destruction of property:

• has deliberately engaged in fire setting with the intention of causing serious damage

• has deliberately destroyed others’ property (other than by fire setting)

  Deceitfulness or theft:

• has broken into someone else’s house, building, or car

• often lies to obtain goods or favors or to avoid obligations (i.e., “cons” others)

• has stolen items of nontrivial value without confronting a victim (e.g., shoplifting, but without breaking and entering; forgery)

  Serious violations of rules:

• often stays out at night despite parental prohibitions, beginning before age 13 years

• has run away from home overnight at least twice while living in a parental or parental surrogate home (or once without returning for a lengthy period)

• is often truant from school, beginning before age of 13 years

  The disturbance of behavior causes clinically significant impairment in social, academic, or occupational functioning. Many biopsychosocial factors contribute to the manifestation of childhood conduct disorder. Some of these factors include harsh, punitive parenting; family discord; low socioeconomic status; lack of proper parental supervision; and lack of social competence. The problems must begin to manifest before 13 years of age. In some children with conduct disorder, low plasma levels of dopamine-beta-hydroxylase have been found. This finding supports the notion of decreased noradrenergic functioning in conduct disorder. Also, a recent Canadian study demonstrated greater right frontal EEG activity at rest correlated with violent and aggressive behavior in children. There is also little doubt that children chronically exposed to violence and abuse have a higher risk for being violent themselves.

  Disruptive, Impulse Control, Conduct Disorders, and ADHD

  K&S Ch. 44

Question 98. E. Rett’s disorder presents with normal development up until 5 months of age. Then the child experiences a loss of previously acquired motor, social, and language skills as well as deceleration of head growth. Rett’s disorder is always seen in girls. Childhood disintegrative disorder has a similar loss of skills but the decline starts later (around 2 years of age), it can occur in both genders and there is no change in head circumference. In autism the child has severe deficits in social interactions, communication, and develops stereotyped patterns of behavior. The autistic child never develops appropriate verbal and social skills unlike Rett’s and childhood disintegrative disorder where those skills are developed then lost. Asperger’s disorder is an autism-like picture where the child has normal language development. Autistic children do not have normal language development. In pervasive developmental disorder NOS there is a clear disturbance of normal development and deficits in motor, social, communication or other areas, but the picture does not meet criteria for one of the other developmental disorders.

  Neurodevelopmental Disorders K&S Ch. 42

Question 99. D. Carl Jung expanded on Freud’s work with concepts such as archetypes, the collective unconscious, complexes, introverts, extroverts, anima and animus, the persona, and individuation. Erich Fromm defined five personality types that he felt were common to and determined by Western society. Kurt Goldstein gave us the term self-actualization which refers to people using their creative powers to fulfill their potential. Edith Jacobson proposed theories regarding an infant’s experience of pleasure or lack of pleasure and its impact on the mother–infant relationship. Otto Kernberg did a great deal of work concerning object relations and borderline personality organization.

  Psychological Theory and Psychometric Testing

  K&S Ch. 6

Question 100. E. Only opium and organophosphorus insecticides out of the options cause miosis. Organophosphate poisons irreversibly inhibit acetylcholinesterase and cause accumulation of acetylcholine at muscarinic and nicotinic receptors. Muscarinic effects of organosphosphorus poisons are :

• miosis and blurred vision

• increased sweating, salivation, lacrimation

• increased bronchial secretions, bronchoconstriction

• abdominal cramps, diarrhea, nausea, vomiting

• urinary frequency and incontinence

  Nicotinic effects of organophosphorus poisons are :

• on striated muscles – twitching, fasciculations, cramps and muscle paralysis

• on sympathetic ganglia – hypertension and tachycardia

  CNS effects of organophosphorus poisons are:

• anxiety, restlessness and confusion

• seizures and coma

  This child presents with tachycardia and hypertension which are nicotinic manifestations. Sometimes the presentation can vary due to the muscarinic effect on cardiovascular system which causes bradycardia and hypotension, but this occurs due to severe organophosphorus poisoning.

  n-Hexane is used as a solvent in paints, lacquers, and printing inks and is used especially in the rubber industry and in certain glues. Workers involved in the manufacturing of footwear, laminating processes, and cabinetry, especially in confined, unventilated spaces, may be exposed to excessive concentrations of this substance. Exposure to this chemical by inhalation or skin contact leads to a progressive distal sensorimotor axonal polyneuropathy; partial conduction block may also occur. Optic neuropathy or maculopathy and facial numbness also have followed n-hexane exposure.

  The major symptoms of botulism are blurred vision, dysphagia and dysarthria. Pupillary responses to light are impaired, and reduction of tendon reflex responses is variable. Weakness progresses for several days and then reaches a plateau. Fatal respiratory paralysis may occur rapidly. Most patients have symptoms of autonomic dysfunction, such as dry mouth, constipation, or urinary retention. The edrophonium test is positive in approximately one third of patients and does not distinguish botulism from other causes of neuromuscular blockade. Wound cultures and serum assay for botulinum toxin confirm the diagnosis of wound botulism. Treatment consists of bivalent (type A and B) or trivalent (A, B, and E) antitoxin. Antibiotic therapy is not effective because the cause of symptoms (in all but infantile botulism) is the ingestion of toxin rather than organisms. Otherwise, treatment is supportive; the need for respiratory assistance is unusual. Acetylcholinesterase inhibitors are not beneficial. Recovery takes many months but usually is complete.

  Poisoning

  B&D Chs 58&78

Question 101. C. Oxazepam, lorazepam, and temazepam are only phase II metabolized (via glucoronidation) and as such have no active metabolites prior to excretion. The other benzos first undergo phase I metabolism (oxidation via the Cytochrome P450 system) which generates active metabolites that then go on to be phase II metabolized and excreted.

  Psychopharmacology

  K&S Ch. 36

Question 102. D. Benzodiazepines are pregnancy category D. Category D indicates positive evidence of human fetal risk. Weigh risk and benefit of using medication in a pregnant patient.

  Psychopharmacology

  K&S Ch. 36

Question 103. C. Some of the most common reasons for psychiatric malpractice suits include suicide attempt or completion by a patient, incorrect or negligent treatment, medication error or drug reaction, and incorrect diagnosis. Though other choices in this question are causes for malpractice suits suicide is the most common.

  Forensic Psychiatry

  K&S Ch. 57

Question 104. A. SSRIs delay ejaculation. Yohimbine, alprostadil and sildenafil can be used for impotence. Testosterone can increase sexual desire but is masculinizing.

  Sexual Dysfunction

  K&S Ch. 21

Question 105. B. Obsessive–compulsive disorder occurs in equal rates in men and women. All other choices listed in this question occur more in males. Don’t forget this important fact for your exam.

  Statistics

  K&S Ch. 16

Question 106. B. Here are commonly asked forensics terms. You must know them all.

  A socially harmful act is not enough to have committed a crime. To be found guilty the accused must also have mens rea (evil intent) and actus reus (voluntary conduct). In the case of many mentally ill patients that commit socially harmful acts they lack one of these elements.

  Parens patriae is a doctrine that allows the state to intervene and act as a surrogate parent for those who are unable to care for themselves.

  Respondeat superior holds that a person occupying a high position in a hierarchy is responsible for those in lower positions.

  Substituted judgment is when a surrogate makes a decision on the basis of what the patient would have wanted, taking into account their wishes and values.

  Justice is the equitable distribution of social resources and benefits.

  Forensic Psychiatry

  K&S Ch. 57

Question 107. E. Studies support CBT as the best therapy for panic disorder. SSRIs are also considered first line because of their effectiveness, safety, and low side effect profile. Studies also support the fact that CBT plus an SSRI will deliver better results than either treatment given alone.

  Anxiety Disorders

  K&S Ch. 16

Question 108. B. Disorders that are frequently comorbid with social phobia include other anxiety disorders, affective disorders and substance abuse disorders. About 1/3 of patients with social phobia will meet criteria for major depressive disorder. There is no significant comorbidity with the somatoform disorders in general and conversion disorder in particular.

  K&S Ch. 16

  Anxiety Disorders

Question 109. E. The addition of a benzodiazepine to a patient on an SSRI for panic disorder will lead to a more rapid resolution of the anxiety. The SSRI will take 2 to 4 weeks to work in most cases. The benzodiazepine can effectively control the patient’s symptoms until the SSRI is fully working. The other choices will take longer to titrate or become effective and are not good choices for rapid resolution of panic symptoms. Propranolol is only indicated for performance anxiety and should not be used in other anxiety disorders.

  Anxiety Disorders

  K&S Ch. 16

Question 110. C. Carbamazepine acts like a vasopressin agonist and has antidiuretic actions. As such it can cause hyponatremia, especially in the elderly. The other choices are not known for this particular side effect.

  Psychopharmacology/Lab Tests in Psychiatry

  K&S Ch. 36

Question 111. D. Risperidone does not affect thyroid function tests but may alter the other choices listed as part of a metabolic syndrome. In addition the clinician may wish to consider an EKG if the patient has significant cardiac risk factors, as well as HbA1c.

  Psychopharmacology/Lab Tests in Psychiatry

  K&S Ch. 36

Question 112. D. The psychotherapist should maintain neutrality with his or her patients. Personal information should be limited and only given if it is to help the patient in some way. In this case his telling the patients is more about his grief than about the needs of the patients. It is therefore a boundary violation. Whenever revealing personal information the therapist should ask him or herself if they are doing it for the patient or themselves. Choices A and B are too much of a black and white statement to be true. There may be situations where a therapist can reveal personal information, but must examine why they are doing it first. Choice E misses the central issue in the ethical dilemma.

  Ethics

  K&S Ch. 58

Question 113. D. Kappa is a number that is used for binary data and tells us whether a given procedure or test produces reliable or reproducible results. It is often used to measure the degree of agreement between raters in a study. Correlation coefficient indicates reliability for non-binary data such as continuous measurements. Point prevalence is the number of cases at a specific point in time divided by the population at the same time. Period prevalence looks at the number of cases both existing and new during a specific time period. Lifetime prevalence reflects the proportion of people who have ever had a specific condition during their lifetimes.

  Statistics

  K&S Ch. 4

Question 114. C. This is a common case of countertransference which is expected to develop in the course of psychodynamic psychotherapy. The patient is reenacting her relationship with her mother with the therapist. The therapist is not rejecting the patient, her schedule does not allow her to meet three times per week. Nor is there evidence to suggest that countertransference on the part of the therapist is the issue here. There is no evidence of psychosis, or delusion, or of an erotomanic theme to the therapy. We have no evidence that the patient is stalking the therapist nor would it be reasonable to assume that this is the case given the information provided. Displacement is taking the emotional energy from one object and placing it onto another unrelated object. The patient is not doing that in this question.

  Psychotherapy

  K&S Ch. 1

Question 115. E. Neuroimaging is not considered standard of care for mania. It should be considered in all of the other scenarios listed in this question as well as before initial ECT treatments, with acute mental status change following head trauma, and in dementia of unknown etiology.

  Lab Tests in Psychiatry

  K&S Ch. 7

Question 116. A. Exposure with response prevention is considered the “gold standard” for treatment of OCD. Make sure you know this fact before you sit for your exam!

  Anxiety Disorders

  K&S Ch. 16

Question 117. B. The abnormal formation of the tricuspid valve you should be concerned with here is Ebstein’s anomaly. It is the result of giving lithium during pregnancy, especially during the first trimester. Also worth noting is that valproic acid given during pregnancy causes neural tube defects in the fetus.

  Psychopharmacology

  K&S Ch. 36

Question 118. D. For many women libido increases during pregnancy and it is incorrect to say that most women experience absence of sexual desire during pregnancy. The other choices are part of normal adjustment to pregnancy. Many women experience pregnancy as a means of self realization, project hope onto the child, are afraid of inadequate mothering or have unconscious fears and ambivalence regarding the impact of the relationship with the child’s father.

  Human Development

  K&S Ch. 2

Question 119. E. Competence is decided by the court. Capacity is decided by the psychiatrist. The four standards of capacity are:

1. Ability to communicate a choice

2. Ability to understand the information presented

3. Ability to understand how information applies to ones own circumstances

4. Ability to reason in a logical manner (even if most people wouldn’t agree with the final decision)

  Forensic Psychiatry

  K&S Ch. 57

Question 120. A. The Benton visual retention test is one in which a patient is presented with geometric figures for 10 seconds then asked to draw them from memory. It is a test of short term memory. The Weschler Memory Scale is the most widely used memory test for adults. The Bender visual motor gestalt test is a test of visuomotor coordination and is useful in testing maturational levels in children. The Wisconsin Card Sorting Test assesses abstract reasoning and difficulty in problem solving.

  Psychological Theory and Psychometric Testing

  K&S Ch. 5

Question 121. B. Schizoid fantasy is indulging in autistic-like retreat to resolve conflict. Interpersonal intimacy is avoided and others are driven away by eccentricity. It is an immature defense. Anticipation is planning for future inner discomfort, and is mature. Altruism is using service to others to undergo an internally gratifying experience, and is mature. Humor is using comedy to express feelings without becoming uncomfortable or causing discomfort in others, and is mature. Suppression is consciously postponing attention to an impulse or conflict, and is mature.

  Psychological Theory and Psychometric Testing

  K&S Ch. 6

Question 122. B. Lithium has been associated with hyperplasia and adenomas of the parathyroid glands leading to hyperparathyroidism and hypercalcemia. Neutropenia is associated with clozapine. Pancreatitis is a rare but potentially deadly side effect of valproic acid. Hepatic failure is associated with valproic acid, hence the black box warning in the PDR. Eosinophilic colitis is associated with clozapine. Though these drugs are certainly not the only causes of these conditions these associations would be useful for the prudent student to know.

  Psychopharmacology

  K&S Ch. 36

Question 123. E. In order to be a good candidate for brief psychodynamic therapy the patient must be able to identify and discuss their feelings. The best candidates are highly motivated, have an area of focus for the therapy, and have at least one solid relationship. You are looking for psychological-mindedness and the ability to learn through relationships. Patients who are too concrete, regressed, and have no meaningful relationships are usually not good candidates. The ability to take a daily medication is not particularly relevant.

  Psychotherapy

  K&S Ch. 35

Question 124. A. Object relations theory is best represented by the work of Melanie Klein. Object relations theory is known for the schizoid, paranoid and depressive positions as well as tension between the true and false self. The other notable therapists listed in this question will undoubtedly be the subject of other questions throughout this book.

  Psychotherapy

  K&S Ch. 4

Question 125. C. Motivational enhancement therapy is a treatment that has proven successful at treating drug addiction, especially in cases where there is denial and ambivalence on the part of the substance abuser. The patient does not suffer from depression or anxiety so fluoxetine is not appropriate. There is no evidence that Joe is a borderline so dialectical behavior therapy is not warranted. ECT is used for depression, psychosis, and mania, not crack addiction. We don’t have adequate information to make a judgment call about involuntary hospitalization.

  Substance Abuse and Addictive Disorders/Psychotherapy

  K&S Ch. 12&35

Question 126. B. It is considered unethical to have any business involvement with patients or former patients. It is unethical to get patients to leave you anything in their will or to solicit them to leave anything to anyone in their will. As such the answer here is that you will not ask any of your current or former patients to make donations in any way.

  Ethics

  K&S Ch. 58

Question 127. C. In its most basic form interpretation is making something that was unconscious conscious. It is an explanatory statement that links a feeling thought, behavior or symptom to its unconscious meaning. Confrontation is addressing something the patient does not want to accept. Clarification is reformulating what the patient has said to create a coherent view of what has been communicated. Empathic validation is a demonstration of the therapist’s empathic understanding of the patient’s internal state. Affirmation is giving succinct comments in support of the patient’s statements or feelings.

  Psychological Theory and Psychometric Testing

  K&S Ch. 35

Question 128. B. This is a common ethical situation encountered by physicians. Accepting gifts from a drug representative is a conflict of interest and is ethically questionable. There is evidence that gifts influence physician behavior, which is why drug companies try to give you things! They’re not just giving you things to be nice. They know it will influence prescribing habits. The monetary value of the gift is not the determining factor in whether it is unethical. Physicians have done very poorly at self-regulating with regard to this issue. Doctors are just as influenced by gifts as anyone else in the office.

  Ethics

  K&S Ch. 57

Question 129. B. The proper way to work with an interpreter is to look at and direct questions to the patient. The interpreter should then translate the discussion for both sides. Don’t look at the interpreter. She is not your patient. Having the family in the room is problematic because they may misinterpret or answer the questions without asking the patient and their involvement may pose a problem in terms of patient confidentiality. Shouting at people who do not speak English is common but unsuccessful. They’re not deaf, they can’t speak English no matter how slowly or loudly you say it!

  Psychotherapy

  K&S Ch. 1

Question 130. B. Epigenetic is a term used to describe Erikson’s stages of development. Each stage contains a psychological crisis which must be negotiated before moving on to the next phase. Levinson’s theories divided adult development up into four stages, each lasting about 25 years. Vaillant found that a happy childhood correlated with positive traits in middle life and that adaptive styles mature over time. He postulated that this maturation was dependant on internal development rather than changes in the environment. Neurodevelopmemtal theory concerns itself with physical brain development, formation and connection of neurons and brain plasticity. In normality-as-process, changes in personality over time are an essential part of the developmental process. Emphasis is placed on the changes one undergoes over time rather than labeling where a person should be at a given age.

  Human Development

  K&S Ch. 2

Question 131. C. Routine monitoring for patients on lithium includes all of the choices except urine for creatinine and protein. However, this test should be considered in patients who have renal disease and are on lithium. Additional tests one might consider include pregnancy tests for women of childbearing age.

  Psychopharmacology/Lab Tests in Psychiatry

  K&S Ch. 36

Question 132. C. DSM criteria for panic disorder state that the patient must have either recurrent attacks or one attack followed by 1 month or more of persistent concern about having more attacks, or worry about the implications of the attack or its consequences, or a significant change in behavior related to the attacks.

  Anxiety Disorders

  K&S Ch. 16

Question 133. C. The DSM states that a diagnosis of major depression should not be made following a death unless a patient’s symptoms are severe and persist for 2 months following the loss. Sadness, sleep disturbance, and appetite disturbance are part of normal grief. The clinician should be on the lookout for MDD when presented with feelings of excessive guilt unrelated to the deceased, suicidality, morbid preoccupation with worthlessness, or psychomotor retardation. Psychosis is also not part of the normal bereavement process.

  Depressive Disorders

  K&S Ch. 15

Question 134. D. Methylenedioxymethamphetamine (ecstasy) is known for a hyperthermic syndrome that can progress to disseminated intravascular coagulation, rhabdomyolysis, liver and kidney failure, and death. Adverse effects of ecstasy are not dose related so this syndrome can occur at any dose. This is one of those facts that you must know for your exam and need to just memorize. Just in case you weren’t sure flunitrazepam is Rohypnol. The other drugs mentioned are found in questions throughout this book.

  Substance Abuse and Addictive Disorders

  K&S Ch. 12

Question 135. D. When treating social anxiety disorder combining CBT and pharmacotherapy does not show a clear benefit over using just one or the other for most initial treatment. There is evidence however, that there are some refractory cases that do respond better to a combination of both.

  Anxiety Disorders

  K&S Ch. 16

Question 136. D. When considering the choices given, hopefully lamotrigine jumped out at you. The other choices are all very well known for causing significant weight gain. Clozapine and olanzapine cause some of the most weight gain of all the antipsychotics and carry high rates of metabolic syndrome. Valproic acid and lithium are both known to cause significant weight gain, amongst other troublesome side effects. Lamictal however, is relatively weight neutral and significant weight gain is rare.

  Psychopharmacology

  K&S Ch. 36

Question 137. D. Skills training is part of a cognitive behavioral approach to substance abuse. Patients are helped to change beliefs, improve interpersonal communication, resist social pressure, increase assertiveness, and better manage stress. Unconscious symbolism is part of a psychodynamic approach to therapy, not part of a cognitive behavioral approach.

  Substance Abuse and Addictive Disorders

  K&S Ch. 12

Question 138. B. Only MDs can order the start of a new seclusion once the previous seclusion order has ended. The nurse cannot extend the time on her own. All other answer choices are correct.

  Forensic Psychiatry

  K&S Ch. 54

Question 139. D. The lowest effective methadone dose for most patients is 50 mg per day. The average methadone dose for opiate addiction is 80 mg per day. Doses of 80 mg per day are twice as likely to lead to successful outcomes as doses of 50 mg or less.

  Substance Abuse and Addictive Disorders

  K&S Ch. 12

Question 140. E. Patients who have a high likelihood to go into the delirium tremens based on history should be detoxified inpatient. This is a major safety concern as the delirium tremens can be life threatening. As such this takes precedence over other considerations.

  Substance Abuse and Addictive Disorders

  K&S Ch. 12

Question 141. E. The best medication for this patient would be an SSRI to control the OCD symptoms and a dopamine blocker to control the tics. When we look at the choices the one that fits is choice E. Fluvoxamine is an SSRI with proven efficacy in treating OCD. Haloperidol is a strong dopamine blocker that can effectively control tics. Benzos, buspirone, and naltrexone are not used for tics.

  Psychopharmacology

  K&S Ch. 36

Question 142. B. The DSM criteria for hypomania specifically state that there are no psychotic features. If psychosis exists then the mood episode would be considered mania. Major depression, mania, mixed episodes and delirium can all involve psychosis. In addition it should be noted that dementia can also present with psychosis.

  Bipolar Disorders

  K&S Ch. 15

Question 143. E. In order to meet criteria for Bipolar I one must have at least one manic episode. So Bipolar I is out in this case. For Bipolar II one must have one hypomanic episode and one episode of major depressive disorder. So Bipolar II is out in this case because we have no depressive symptoms. To meet Cyclothymic disorder one must have hypomanic symptoms as well as depressive symptoms which do not meet criteria for major depression that go on for at least 2 years. This patient has no depressive symptoms so Cyclothymic disorder is out. There is no evidence of any substance abuse in the question stem so substance induced mood disorder is out. The correct answer is Bipolar disorder NOS which includes patients with clear bipolar symptoms who do not meet criteria for any specific bipolar disorder.

  Bipolar Disorders

  K&S Ch. 15

Question 144. E. Symptoms of pheochromocytoma can include anxiety, panic, tremulousness, flushing, feeling of impending doom, hypertension, and tachycardia. It can be mistaken for panic disorder. Hyperparathyroidism presents as constipation, polydipsia, nausea, depression, paranoia and confusion. Hypothyroidism presents with cold intolerance, weight gain, brittle hair, goiter, constipation, dry skin, lethargy, depressed affect, hallucinations, and paranoia. Raynaud’s phenomenon presents with idiopathic paroxysmal bilateral cyanosis of the digits and can be exacerbated or triggered by stress. Crohn’s disease does not have psychiatric manifestations.

  Somatic Symptom Disorders

  K&S Ch. 28

Question 145. D. When compared to the general population patients with social phobia tend to have fewer friendships, lower levels of education, higher rates of suicide, and less success in career advancement. They also have poorer marital function.

  Anxiety Disorders

  K&S Ch. 16

Question 146. C. Regularly scheduled primary care appointments are a crucial and standard part of treating hypochondriasis. In hypochondriasis the patient is convinced that they have an illness that they don’t have. If they are not followed closely by their primary care physician they will go doctor shopping. While regularly following with the primary care doctor they should also be engaged in psychotherapy to work on the underlying psychological causes of the condition. None of the other disorders listed require regular follow-up by the primary care doctor. That is not to say these patients should not regularly follow up for routine medical care, but that it is not a crucial component of the treatment for the psychiatric condition.

  Somatic Symptom Disorders

  K&S Ch. 17

Question 147. C. Alcohol dependence, being widowed, being unemployed, and being socially isolated are all factors which increase chances of suicide in the elderly. Add to that list male gender, chronic illness, depression, irritation, rage, violence, and affective instability.

  Management in Psychiatry

  K&S Ch. 34

Question 148. B. For a patient on clozapine who develops a white count between 2000 and 3000 the correct action is to stop the clozapine. The clozapine may be tried again when the patient’s white count improves. Monitor the WBC daily until it is over 3000. For a patient whose WBC count is between 3000 and 3500 you can switch to twice weekly monitoring until it is back above 3500. If the WBC count is lower than 2000 the patient can not be re-challenged on clozapine.

  Psychopharmacology

  K&S Ch. 36

Question 149. E. QTc interval is normally less than 450 milliseconds. Prolongation of the QTc interval longer than 500 milliseconds increases the risk for torsade de pointes. Under these circumstances any medication which may be increasing the QTc must be considered carefully and possibly discontinued, changed, or decreased.

  Psychopharmacology

  K&S Ch. 36

Question 150. A. Interferon is well known to exacerbate depression. Side effects include depressed mood, suicidality, suicidal ideation, insomnia, fatigue, and cognitive inefficiency. The other medications listed are not known to cause the exacerbation of depressive symptoms listed in this question.

  Psychopharmacology

  K&S Ch. 36