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

Explanations - Test Number Five

Question 1. A. Blocking the H1 receptor leads to weight gain and sedation. You should also be familiar with the effects of blocking some other receptors. Blocking acetylcholine receptors leads to dry mouth, constipation, blurry vision, urinary retention, and cognitive dysfunction. Blocking alpha 1 adrenergic receptors leads to orthostatic hypotension and drowsiness. Blocking dopamine receptors can lead to EPS and elevated prolactin.

  Basic Neuroscience

  K&S Ch. 3

Question 2. C. The diagnostic evaluation of myasthenia gravis (MG) is multifaceted. Timed endurance tasks such as prolonged upgaze, holding outstretched arms in abduction, or vital capacities are useful office-based physical examination evidence of fatigability. Weakness improvement upon edrophonium chloride (Tensilon) injection is a useful sign, though false-negative and false-positive results are known to occur. The detection of acetylcholine receptor antibodies (AChR-ab) in serum is another useful corroborative test that has 70% sensitivity in ocular myasthenia and 80% sensitivity in generalized disease.

  Repetitive nerve stimulation by needle EMG may demonstrate a decrementing response: a reduction of the compound muscle action potential, potentiated after one minute of exercise, consistent with a polysynaptic transmission defect. The sensitivity of repetitive stimulation is about 75%. The demonstration of increased “jitter” by single-fiber EMG is the most sensitive test for MG. The sensitivity ranges from 80% in ocular myasthenia to close to 100% in moderate generalized MG. Using AChR-ab, repetitive stimulation and single-fiber EMG identifies all MG cases.

  Neurology

  B&D Ch. 78

Question 3. E. This question may be a bit odd, but it covers an important point nonetheless. It is asking you to compare NMS and serotonin syndrome. This can be a very tricky task as they both present with many of the same symptoms. Both present with mental status changes, autonomic instability, diaphoresis, and mutism. Both can have elevated CPKs but high CPKs are more common in NMS because of the muscular rigidity. To make the decision between the two the key point is that serotonin syndrome presents with myoclonus, hyper-reflexia and GI symptoms, whereas NMS presents with muscle rigidity. Now some may argue that serotonin syndrome can present with rigidity also…and they’re right. But when we take the whole clinical picture into account the myoclonus, GI symptoms and normal CPK would push the decision in the direction of the serotonin syndrome over NMS. In the real world hopefully the patient’s family members or doctor could tell you what the new medication was, which would greatly influence your diagnosis.

  Psychopharmacology

  K&S Ch. 36

Question 4. A. Classically, MRI studies of the brains of patients with Huntington’s disease (HD) reveal caudate and cerebral atrophy. Besides taking a fastidious family history, blood should be drawn and DNA testing conducted for the Huntington’s genetic anomalies. HD is caused by a mutation on chromosome 4 causing an unstable expansion of CAG repeats.

  The atrophy of the caudate alters the appearance and configuration of the frontal horns of the lateral ventricles, because the inferolateral borders do not reveal the typical bulge formed by the head of the caudate nucleus. Also, in general, the ventricles are diffusely enlarged. Further discussion of HD can be found in other questions in this volume.

  Neurology

  B&D Ch. 71

Question 5. D. This question tests how well you know your DSM criteria for somatization disorder. For somatization disorder you need four pain symptoms, two GI symptoms, one sexual symptom and one pseudoneurological symptom. These symptoms may present over a period of several years. The illness must begin before age 30. The symptoms either cannot be explained by a medical condition or are out of proportion to the symptoms/impairment one would expect given the medical condition. The symptoms are not intentionally produced or feigned. More women get the illness than men, and it often presents as a dramatic patient who is very vague about details of their symptoms.

  Somatic Symptom Disorders

  K&S Ch. 17

Question 6. B. The core features of dementia with Lewy bodies (DLB) include visual hallucinations, fluctuating cognition and parkinsonism. Two features are required to diagnose clinically probable DLB and one is required to diagnose clinically possible DLB. Rapid eye movement (REM) sleep behavior disorder, and neuroleptic sensitivity, as well as low uptake in basal ganglia on fluorodopa PET and SPECT scans are now considered “suggestive” clinical criteria. In general, the clinical picture of mild parkinsonism with more severe dementia and marked visual hallucinations and paranoid delusions should trigger consideration of the diagnosis of DLB.

  Parkinsonian features of DLB may respond well to L-dopa therapy, but usually only temporarily and sometimes with the undesirable side effect of causing agitated delirium or hallucinations. Some patients also suffer from orthostatic hypotension. There is no definitive diagnostic test for DLB, although PET scans sometimes reveal reduced activity in the posterior parietal cortical regions.

  Neurocognitive disorders

  B&D Ch. 66

Question 7. B. All of the choices listed are inhibitors of CYP450 1A2 except tobacco, which is an inducer. Other inducers of 1A2 include charbroiled meats, and cruciferous vegetables.

  Psychopharmacology

  K&S Ch. 3

Question 8. A. Intracranial metastatic carcinoma is more frequently seen than primary brain tumors. Most carcinomas metastasize to the brain via hematogenous spread. About one-third of brain metastases originate in the lung and about half that number originate in the breast. The third most frequent source is melanoma, followed by the gastrointestinal tract, in particular the colon and the rectum. This is followed in frequency by cancers of the kidney. The remainder are accounted for by cancers of the thyroid, liver, gallbladder, testicle, pancreas, uterus, and ovaries.

  Neurology

  B&D Ch. 52F

Question 9. B. Fiduciary duty is the obligation to work in the patient’s best interests. Beneficence is an obligation to help patients and relieve suffering. Nonmaleficence is the duty to do no harm. Altruism is putting the needs of others before your own needs. Parens patriae is a doctrine that allows the state to intervene and act as a surrogate parent for those who cannot take care of themselves.

  Ethics

  K&S Ch. 58

Question 10. C. Most subdural hematomas occur over the convexity of the cerebral hemispheres. Bleeding into the subdural space is usually a result of tearing of one or more of the bridging veins that cross the space to reach the venous sinuses. In 50–80% of patients there is a history of head trauma. Headache due to subdural hematoma can occur due to chronic expansion of the lesion. Other symptoms that can be caused by chronic subdural hematoma include cognitive deficits, personality changes, subacute dementia, dizziness and excessive sleepiness. Headache is the single most common symptom and is more common in younger patients, who have less atrophy than the elderly. In the presence of atrophy a larger collection of blood can accumulate before it expands and deforms pain-sensitive structures.

image

  The photo attached to this question most likely represents a subacute subdural hematoma. An acute bleed would initially be hyperdense, but gradually becomes more isodense after a period of one or more weeks. The fluid then becomes more hypodense (with respect to the cortex) over a period of two to six weeks.

  Neurology

  B&D Ch. 69

Question 11. E. This question compares schizophreniform disorder with brief psychotic disorder to see if you know some of the key differences. Both disorders present with schizophrenia-like symptoms (i.e., criteria A symptoms). In both disorders the patient returns to baseline functioning after the disturbance resolves. In brief psychotic disorder there is often a stressor which precedes the episode, but there does not need to be one. In making the diagnosis the DSM allows us to describe the episode as “with marked stressor”, “without marked stressor”, or “with postpartum onset.” The key point to keep in mind is the time difference. Brief psychotic disorder lasts from 1 day to 1 month. Schizophreniform disorder lasts from 1 month to 6 months. After 6 months the psychosis can be called schizophrenia (assuming schizophrenia criteria are met). Either diagnosis is ruled out if there is a medical condition present that could be causing the symptoms. In that case one would diagnose psychotic disorder secondary to a medical condition.

  Psychotic Disorders

  K&S Ch. 14

Question 12. D. The core features of Parkinson’s disease are resting tremor, rigidity, postural instability and hypokinesia/bradykinesia. The classic parkinsonian tremor is seen in the initial presentation of about seventy percent of patients with the disease. The 4 to 6-per-second characteristic “pill-rolling” tremor of thumb and fingers is seen in about half of the patients with Parkinson’s disease. The tremor is typically seen when the hands are still (hence the term resting tremor).

  The most replicable finding in idiopathic Parkinson’s disease is loss of pigmented cells in the substantia nigra and other pigmented dopaminergic tracts. Recall that there must be a loss of at least 80% of dopaminergic cell bodies before the clinical symptoms and signs of Parkinson’s disease begin to manifest.PD traditionally has been considered a non-genetic disorder; however, around 15% of individuals with PD have a first-degree relative who has the disease. At least 5% of people are now known to have forms of the disease that occur because of a mutation of one of several specific genes.

  Mutations in specific genes have been conclusively shown to cause PD. These genes code for alpha-synuclein (SNCA), parkin (PRKN), leucine-rich repeat kinase 2 (LRRK2 or dardarin), PTEN-induced putative kinase 1 (PINK1), DJ-1 and ATP13A2. In most cases, people with these mutations will develop PD. In terms of pathophysiology, PD is considered a synucleinopathy due to an abnormal accumulation of alpha-synuclein protein in the brain in the form of Lewy bodies, as opposed to other diseases such as Alzheimer’s disease where the brain accumulates tau protein in the form of neurofibrillary tangles. Nevertheless, there is clinical and pathological overlap between tauopathies and synucleinopathies. A classical Lewy body is an eosinophilic cytoplasmic inclusion that consists of a dense core surrounded by a halo of 10-nm wide radiating fibrils, the primary structural component of which is alpha-synuclein. These are found pervasively in the substantia nigra of patients with Parkinson’s disease.

  Neurology

  B&D Ch. 71

Question 13. B. The answer to this question is bipolar II disorder because the patient meets criteria for hypomania as well as major depressive episodes. The important learning point here is to distinguish mania from hypomania. To qualify for mania one needs symptoms for at least a week. If the core symptom is euphoria, three additional symptoms are needed. If the core symptom is irritability, four additional symptoms are needed. Additional symptoms can include grandiosity, decreased need for sleep, pressured speech, flight of ideas, distractibility, increased goal directed activity, or excessive involvement in pleasurable activities. One must demonstrate impairment in social or occupational functioning, need for hospitalization, or presence of psychosis as part of the picture of mania.

  Hypomania lasts for at least 4 days. The same criteria for symptoms apply, but the patient does not experience disturbance in social or occupational functioning, require hospitalization, or become psychotic as part of the symptom picture.

  To qualify for cyclothymic disorder a patient must have 2 years with periods of hypomania and depressive symptoms that don’t meet criteria for MDD.

  Major depressive disorder is not the correct answer choice because the patient meets criteria for a bipolar diagnosis based on her hypomanic episodes. Schizoaffective disorder is ruled out by the absence of any psychotic symptoms in the patient’s description. Bipolar I disorder is incorrect because the patient does not meet criteria for manic episodes.

  Bipolar Disorders

  K&S Ch. 15

Question 14. B. Wilson’s disease (hepatolenticular degeneration) is a rare heredodegenerative disorder affecting 1–2/100 000 individuals. It is an autosomal recessive disorder of copper metabolism localizing to mutations on chromosome 13, in the ATP7B gene. Many patients present in childhood with signs and symptoms of liver dysfunction that span the spectrum from cirrhosis to fulminant liver failure. Some patients present with hemolytic anemia, hypersplenism and kidney failure. Neurological signs and symptoms can be seen in up to half of patients with Wilson’s disease. These CNS manifestations can include parkinsonism, postural and kinetic tremor, ataxia, titubation, chorea, seizures, dysarthria, and dystonia. Dementia may be present and is most often mild. Psychiatric manifestations can also be seen and include mood and personality disorders, behavioral changes and psychosis. When neurologic manifestations are seen, ophthalmological exam almost inevitably demonstrates the presence of Kayser–Fleischer rings due to copper deposition in Descemet’s membrane. Treatment is classically accomplished by copper chelation with D-penicillamine. Note that answer B is correct because the classic 4–6 Hz intention tremor is generally associated with idiopathic Parkinson’s disease and not Wilson’s disease.

  Neurology

  B&D Ch. 71

Question 15. E. The school-age years (ages 5–12) include many important milestones. All of those listed are correct with the exception of choice E. The ability to think abstractly usually develops during adolescence and coincides with the stage that Piaget coined “formal operations.” In this stage the person can manipulate data and emotions in the environment in a constructive manner using their own experience and a hypothetical or “what if” framework. It is not a skill that usually develops during the school-age years.

  Human Development

  K&S Ch. 2

Question 16. E. This answer refers to what is currently termed childhood-onset generalized primary dystonia. This disease entity was formerly known as Oppenheim’s dystonia or dystonia musculorum deformans. The disease prevalence is about 1.4 in 100 000. Most cases that start early in childhood are DYT1 dystonia, resulting from a mutation in the torsin A gene (TOR1A) on chromosome 9q32-34. The prevalence of DYT1 is as high as 20 to 30 per 100 000 and is commonly seen in individuals of Ashkenazi Jewish decent. Early symptoms are characterized by an action-induced dystonia of the leg or the arm. In about 70% of affected individuals, dystonic movements spread to the trunk and other limbs and the condition generalizes over about 5 years. Laryngeal and pharyngeal dystonia remain rare in this disorder. Cognition is generally intact. The other four movement disorders in answers A through D are all associated with a dementing process. These disorders are described in other questions in this volume.

  Neurology

  B&D Ch. 71

Question 17. B. Ten to fifteen percent of the general population has a diagnosable personality disorder.

  Personality disorders

  K&S Ch. 27

Question 18. A. Approximately 1% of tuberculosis infections are complicated by neurologic disease, such as intracerebral tuberculoma, tuberculous meningitis, or tuberculous spine involvement with myelopathy (Pott’s disease).TB meningitis usually follows a subacute course with low-grade fever, headache and intermittent nausea and vomiting. This is followed by more severe headache, neck stiffness, altered mentation, and cranial nerve palsies. The diagnosis is made by identifying tubercle bacilli on CSF acid-fast bacilli (AFB) smear or culture. CSF examination reveals normal or elevated opening pressure, elevated protein (80–400 mg/dL), low glucose (<40 mg/dL), and pleocytosis (averaging 200 to 400 WBC/µL with lymphocytic predominance). Tuberculomas, the parenchymal form of TB, are single or multiple brain or spinal cord lesions. CT or MRI may show low- or high-intensity lesions with ring enhancement. The other answer choices, B through E, are among the most common CNS manifestations of HIV disease. These diseases do not classically present with ring-enhancing lesions on neuroimaging. Be sure to read up on these other AIDS-related disorders, as they do appear frequently on standardized examinations.

  Neurology

  B&D Ch. 53C

Question 19. C. The finding of thin gyri, wide sulci and enlarged ventricles on neuroimaging studies is typically indicative of cortical atrophy. With normal aging, there is mild to moderate progressive enlargement of the ventricles, sulci and cisternal spaces. In neurodegenerative disorders, such as Alzheimer’s disease, atrophy is excessive and premature. Chronic alcoholism and drug abuse can cause early cerebral atrophy. More typically though, chronic alcohol use causes cerebellar atrophy which can result in truncal ataxia due to the preferential involvement of the vermis over the cerebellar hemispheres. The classic symptoms of cerebellar atrophy due to alcohol use are gait unsteadiness and a wide-based gait. Brain imaging of patients with schizophrenia can also reveal generalized cortical atrophy with enlargement of the ventricular spaces. Trisomy 21 (Down’s syndrome) leads to an early onset of Alzheimer-like changes in the brain. Trisomy 21 leads to increased levels of amyloid precursor protein (APP), because it is expressed on chromosome 21. Increase in amyloid deposition occurs as a result of the increase in APP. A single lacunar infarct of the subcortical white matter would not be expected to be accompanied by generalized cortical atrophy.

  Neurology

  B&D Ch. 66

Question 20. A. Middle cerebral artery (MCA) infarction is one of the most common types of strokes. The clinical picture varies depending on whether the site of occlusion is in the stem, superior division, inferior division, or lenticulostriate branches.

  A stem occlusion typically produces a large hemispheric infarction with contralateral hemiplegia, conjugate eye deviation towards the side of the infarct, hemianesthesia and homonymous hemianopia. Associated global aphasia occurs if the dominant hemisphere is involved. Hemineglect occurs in cases of nondominant hemispheric involvement.

  A Broca-type aphasia is more common in upper division MCA infarcts because of the preferential involvement of the anterior branches of the upper division when occluded. Answer choice A is the best response to this question because a perisylvian infarct would almost certainly impair naming and repetition, producing a perisylvian aphasia. Answer B is incorrect because a dominant hemisphere infarct in the MCA territory would almost certainly involve some kind of language functioning impairment. Answer choice C is incorrect because the left MCA territory stroke would cause a right hemiparesis with face and arm weakness that is worse than the leg. This is so, because the anterior cerebral artery irrigates the part of the motor strip responsible for lower extremity movement. Answers D and E are features of a Wernicke-type aphasia. Wernicke’s area is indeed within the MCA territory, particularly the inferior branch, but is less likely to be affected than Broca’s area.

  Neurology

  B&D Chs 12A&51A

Question 21. D. There is only one ethical answer here, and that is to transfer the patient’s care to another psychiatrist. There are no exceptions to the rule prohibiting sex between psychiatrist and patient. Regardless of circumstances, his processing of the matter or what he tells the patient, having a sexual relationship is prohibited. He can no longer serve a neutral therapeutic role in this case. It must be transferred to another psychiatrist.

  Ethics

  K&S Ch. 58

Question 22. B. Pure alexia without agraphia is classically caused by a stroke in the left posterior cerebral artery (PCA) territory, particularly in the splenium of the corpus callosum. This syndrome was initially described by Dejerine in 1892. Patients can write, but they cannot read their own writing. Speech, auditory comprehension and repetition are intact. Naming, particularly for colors, may be deficient. Dejerine postulated that this syndrome was due to a disconnection between the intact right visual cortex and left hemisphere language centers. Associated signs may include: right hemianopia or superior quadrantanopia, short-term memory loss and the absence of motor and sensory signs.

  Neurology

  B&D Ch. 12A

Question 23. C. A binary variable has two possible values …such as yes or no, positive or negative, male or female. A continuous variable will fall somewhere on a range, such as age, height, or weight. Independent Variables (predictor variables) are contributing factors to a result or predictors of a certain outcome within an experimental study. They are the variables that are manipulated by the experimenter. Dependent variables (outcome variables) are the outcomes that the independent variables contributed to or predicted. A dependent variable is the variable that is not manipulated by the experimenter.

  To answer this type of question, first ask yourself two more questions. How many variables are there? Are they binary or continuous? Then consider the following:

  The Chi-Square test is used for 1 binary predictor variable and 1 binary outcome variable. The T-test is used for 1 binary predictor variable and 1 continuous outcome variable. The ANOVA test is used for 2 or more binary predictor variables and 1 continuous outcome variable. Correlation is used for 1 continuous predictor variable and 1 continuous outcome variable. Regression Analysis is used with two or more continuous or binary variables and 1 continuous outcome variable.

  Statistics

  K&S Ch. 4

Question 24. A. Homocystinuria is an inborn error of amino acid metabolism. Three types of enzymatic deficiencies are possible: homocysteine methyltransferase, methylene tetrahydrofolate reductase and cystathione-β-synthetase. The accumulation of homocysteine in the blood leads to endothelial injury and premature atherosclerosis. Patients can present with marfanoid habitus, livedo reticularis, malar flush, ectopia lentis, glaucoma, myopia, optic atrophy, mental retardation, spasticity, seizures, psychiatric problems, osteoporosis, and a high likelihood of intracranial arterial or venous thrombosis. Death can result from myocardial infarction, stroke or pulmonary embolism. Raised plasma homocysteine levels may be an independent risk factor for coronary artery disease, cerebrovascular disease, or peripheral artery occlusive disease. Elevated homocysteine levels can effectively be lowered by administration of folic acid, sometimes needing the addition of pyridoxine (vitamin B6) and vitamin B12.

  Phenylketonuria is an amino acidopathy resulting from an enzyme deficiency, specifically phenylalanine hydroxylase. The pattern of inheritance is autosomal recessive. Other symptoms may include: delayed mental and social skills, head size significantly below normal, hyperactivity, jerking movements of the arms or legs, mental retardation, seizures, skin rashes, tremors, and unusual positioning of hands. If the condition is untreated or foods containing phenylalanine are not avoided, a “mousy” or “musty” odor may be detected on the breath and skin and in urine. The unusual odor is due to a buildup of phenylalanine substances in the body.

  Tay–Sachs disease is the infantile form of hexosaminidase-A deficiency. The pattern of inheritance is autosomal recessive. It is caused by a mutation in the HEXA gene on chromosome 15. Infants with the disorder appear to develop normally for the first 6 months after birth. Then, as nerve cells become distended with gangliosides, a relentless deterioration of mental and physical abilities occurs and progresses inexorably. The child becomes blind, deaf, unable to swallow, and develops atrophy and paralysis. Death usually occurs before age four. The disease has no known treatment or cure.

  Metachromatic leukodystrophy (MLD) is yet another lysosomal storage disease of infancy. This disorder results from a deficiency in arylsulfatase A. Again, its pattern of inheritance is autosomal recessive. In the late infantile form, which is the most common form of MLD (50–60%), affected children begin having difficulty walking after the first year of life, usually at 15–24 months. Symptoms include muscle wasting and weakness, muscle rigidity, developmental delays, progressive loss of vision leading to blindness, convulsions, impaired swallowing, paralysis, and dementia. Children may become comatose. Untreated, most children with this form of MLD die by age 5, often much sooner. There is no cure for MLD, and no standard treatment. It is a terminal illness. Treatment options for the future are currently being investigated. These include gene therapy, enzyme replacement therapy (ERT), substrate reduction therapy (SRT), and potentially enzyme enhancement therapy (EET).

  Neurology

  B&D Chs 51A&62

Question 25. A. Knowing childhood developmental stages is important for standardized psychiatry exams. A child is capable of running well without falling, building a tower of six cubes, and engaging in parallel play by 18 months of age.

  Human development

  K&S Ch. 2

Question 26. B. Niemann–Pick disease is a sphingomyelinase deficiency that is categorized as a lysosomal storage disease of infancy. The pattern of inheritance is autosomal recessive. There are essentially 2 types of Niemann–Pick disease that are further categorized in subtypes A, B, C and D, depending on specific genetic loci of mutation. Symptoms are related to the organs in which they accumulate. Enlargement of the liver and spleen (hepatosplenomegaly) may cause reduced appetite, abdominal distension and pain as well as thrombocytopenia secondary to splenomegaly. Sphingomyelin accumulation in the central nervous system (including the cerebellum) results in unsteady gait (ataxia), slurring of speech (dysarthria) and discoordinated swallowing (dysphagia). Basal ganglia dysfunction causes abnormal posturing of the limbs, trunk and face (dystonia) and upper brainstem disease results in impaired voluntary rapid eye movements (supranuclear gaze palsy). The type A disease has a very poor prognosis, with most cases resulting in death by age 18 months. Patients with types B and C disease often live into their adolescent years with a better prognosis. Current and future treatment research focuses on enzyme replacement therapy and gene therapy.

  Hexosaminidase-A deficiency is Tay–Sachs disease. Arylsulfatase-A deficiency is metachromatic leukodystrophy. Phenylalanine deficiency is phenylketonuria. Hypoxanthine guanine phosphoribosyltransferase (HGPRT) deficiency results in hyperuricemia and Lesch–Nyhan syndrome. Lesch–Nyhan syndrome, unlike the other diseases noted in this question, is an X-linked recessive disease. It is a disorder of purine and pyrimidine metabolism. These diseases of inborn errors in metabolism are all explained further in other questions in this volume.

  Neurology

  B&D Ch. 62

Question 27. D. Depakote has the potential to cause pancreatitis which will lead to an increased serum amylase and the symptoms described in this question. Another concern with valproic acid would be hepatitis, for which one would want to look at liver function tests but hepatitis would most likely present with right upper quadrant pain, nausea, vomiting, diarrhea, fever, coca-cola urine and jaundice.

  Psychopharmacology/Lab Tests in Psychiatry

  K&S Ch. 36

Question 28. E. The disease described in answer choice E is that of fragile X syndrome. Fragile X syndrome is the most common inherited cause of infantile mental retardation and the most common single-gene cause of autism. Of course, this question is constructed to try to trick you by not giving you the disease name, but forcing you to extrapolate the disease name from its presenting symptoms. Fragile X results in a spectrum of intellectual disability ranging from mild to severe as well as physical characteristics such as an elongated face, large or protruding ears, and larger testes (macro-orchidism), behavioral characteristics such as stereotypical movements (e.g. hand-flapping), and social anxiety.

  Fragile X syndrome is associated with the expansion of the CGG trinucleotide repeat affecting the Fragile X mental retardation 1 (FMR1) gene on the X chromosome, resulting in a failure to express the fragile X mental retardation protein (FMRP), which is required for normal neural development. Depending on the length of the CGG repeat, an allele may be classified as normal (unaffected by the syndrome), a premutation (at risk of fragile X associated disorders), or full mutation (usually affected by the syndrome). A definitive diagnosis of fragile X syndrome is made through genetic testing to determine the number of CGG repeats. The mode of transmission is X-linked dominant.

  There is currently no drug treatment that has shown benefit specifically for fragile X syndrome. However, medications are commonly used to treat symptoms of attention deficit and hyperactivity, anxiety, and aggression. Supportive management is important in optimizing functioning in individuals with fragile X syndrome, and may involve speech therapy, occupational therapy, and individualized educational and behavioral programs.

  Neurology

  B&D Ch. 40

Question 29. D. The signs and symptoms of Down’s syndrome (trisomy 21) are characterized by the neotenization of the brain and body to the fetal state. Down’s syndrome (DS) is characterized by decelerated maturation (neoteny), incomplete morphogenesis (vestigia) and atavisms. Individuals with Down’s syndrome may have some or all of the following physical characteristics: microgenia (abnormally small chin), oblique eye fissures with epicanthic skin folds on the inner corner of the eyes (formerly known as a mongoloid fold), muscle hypotonia (poor muscle tone), a flat nasal bridge, a single palmar fold, a protruding tongue (due to small oral cavity, and an enlarged tongue near the tonsils) or macroglossia, “face is flat and broad”, a short neck, white spots on the iris known as Brushfield spots, excessive joint laxity including atlanto-axial instability, excessive space between large toe and second toe, a single flexion furrow of the fifth finger, a higher number of ulnar loop dermatoglyphs and short fingers. They also tend to have a single palmar crease (also called a “simian crease” for its resemblance to that in apes and monkeys). Growth parameters such as height, weight, and head circumference are smaller in children with DS than with typical individuals of the same age. Adults with DS tend to have short stature and bowed legs – the average height for men is 5 feet 1 inch (154 cm) and for women is 4 feet 9 inches (144 cm). Individuals with DS are also at increased risk for obesity as they age and tend to be “round in shape”. Individuals with trisomy 21 often develop early-onset Alzheimer’s type dementia and die young from its complications. This occurs because the amyloid precursor protein gene is expressed on chromosome 21 which these patients possess in triplicate. Stunted growth and mental retardation are seen in virtually 100% of trisomy 21 patients. Small genitalia are seen in at least 75% of cases and in most cases these individuals are sterile.

  Neurology

  B&D Chs 40&66

Question 30. B. Answer choice B refers to Williams’ syndrome. The syndrome is a result of an autosomal microdeletion on chromosome 7q11. Features of the disorder include cardiac valvular stenosis, hypotonia, hyperacusis, short stature and “elfin” facies, low nasal bridge, unusual ease with strangers and pleasant demeanor, developmental delay and strong language skills. Prevalence is 1 in 7500 to 20 000 births. The disorder has no known cure and is strongly associated with attention deficit–hyperactivity disorder.

  The distracters in this question are described in greater detail in other questions in this volume. Trisomy 21 is of course, Down’s syndrome. Deletion in chromosome 15q is Angelman syndrome. Deletion of 45 XO refers to Turner’s syndrome. Klinefelter’s syndrome is a result of an extra sex chromosome 47 XXY.

  Neurology

  B&D Ch. 7

Question 31. B. Right unilateral placement of the electrodes in ECT has been shown to minimize cognitive impairment and memory deficits. If unilateral electrode placement fails to improve the patient’s symptoms after four to six treatments the placement may be switched to bilateral, which can be more effective but carries a higher risk of side effects.

  Diagnostic and Treatment Procedures in Psychiatry

  K&S Ch. 36

Question 32. C. Marfan’s syndrome is an inherited autosomal dominant connective tissue disease associated with defects in fibrillin. Features include arachnodactyly, joint laxity, extreme limb length, pectus carinatum or excavatum, aortic valvular insufficiency and subluxation of the lens. Marfan’s syndrome is also associated with dilatation of the aortic root and coarctation of the aorta, mitral valve prolapse and mitral annulus calcification with regurgitation. Dissection of the ascending aorta is also a possible occurrence, following from dilatation of the aortic root. Saccular intracranial aneurysms or carotid artery dissection are also possible. Patients with Marfan’s syndrome are recommended to undergo annual echocardiogram screening and to avoid contact sports.

  The other answer choices are all inherited disorders that present with either mental retardation, autistic features, or both, and they are explained in the answer material of other questions in this volume. Marfan’s syndrome is not associated with either mental retardation or autism.

  Neurology

  B&D Ch. 51A

Question 33. A. Lithium can prolong seizure activity during ECT and should be discontinued. Antipsychotics are fine during ECT, with the exception of clozapine which causes late appearing seizures during ECT. TCAs and MAOIs are fine to continue during ECT.

  Diagnostic and Treatment Procedures in Psychiatry

  K&S Ch. 36

Question 34. A. The major features of tuberous sclerosis (TS) include facial angiofibromas or forehead plaque, nontraumatic ungual or periungual fibroma, hypomelanotic macules (ash leaf spots), shagreen patch, multiple retinal hamartomas, cortical tuber, subependymal nodule, subependymal giant astrocytoma, cardiac rhabdomyoma, lymphangiomyomatosis and renal angiomyolipoma. The predominant neurologic manifestations of TS are seizures, mental retardation and behavioral abnormalities. Seizures of various types occur in eighty to ninety percent of patients with TS. Tuberous sclerosis comes up quite a bit on standardized examinations and you should know the major features, imaging appearance and genetic facts of this disorder. These are reviewed in other questions in more detail.

  Cutaneous and conjunctival telangiectasias are seen in the disorder known as ataxia–telangiectasia (AT). This is a neurodegenerative disorder that begins in childhood as slowly progressing ataxia. Later, other features develop, in particular, telangiectasias (small dilated blood vessels), immunodeficiency and sensitivity to ionizing radiation. The telangiectasias typically involve the earlobes, sclera, bridge of the nose and less commonly, the eyelids, necks, antecubital and popliteal fossae. AT is an autosomal recessive neurocutaneous disorder, affecting both sexes equally with a prevalence of 1 in 40 000 to 100 000. Nearly all patients with AT have elevated alphafetoprotein levels and about 80% have reduced serum IgA, IgE or IgG. The gene associated with AT is the large gene at chromosome 11q22-23. Approximately 10 to 15% of AT patients develop a lymphoid malignancy by early adulthood.

  Neurology

  B&D Ch. 65

Question 35. A. Sublimation is a mature defense mechanism. Displacement and repression are neurotic defense mechanisms. Hypochondriasis and introjection are immature defense mechanisms. For your exam you must not only know what each defense mechanism is but also be able to say which are mature and which are immature.

  Psychological Theory and Psychometric Testing

  K&S Ch. 4

Question 36. D. Thalamic lesions are usually responsible for sensory deficits of cerebral origin. The thalamus receives its blood supply from the thalamoperforate branches of the posterior cerebral arteries. In some individuals, both thalami are supplied by one posterior cerebral artery, thus unilateral arterial occlusion may result in bilateral thalamic infarction. Thalamic pain syndrome sometimes results following thalamic sensory stroke. The pain is typically spontaneous and localized to the distal arm and leg and is exacerbated by contact and stress.

  Neurology

  B&D Ch. 28

Question 37. C. When a forensic psychiatrist is evaluating a case they are doing so for a third party, such as the court. As such there is no assumption of confidentiality the way there normally would be with a psychiatrist. The forensic psychiatrist should tell the patient this at the beginning of the interview. The information collected is expected to be shared with a third party and is not expected to remain confidential. If there is no confidentiality and no therapeutic alliance there is no doctor–patient relationship. Both evaluations should include a medication history and basic elements of the mental status exam and mini mental status exam such as memory, as would any complete psychiatric examination regardless of setting. Both evaluations will contain recommendations. ER recommendations will focus on the next step in treatment whereas forensic recommendations will focus on the particular legal issues being decided and the impact of the patient’s illness upon those issues.

  Forensics

  K&S Ch. 58

Question 38. D. The typical EEG findings in Creutzfeldt–Jakob disease (CJD) are periodic sharp wave complexes (PSWCs) which may be preceded by less specific frontal intermittent rhythmical delta activity. These characteristic EEG abnormalities can be seen in about 70% of patients with CJD.

  EEG findings in Alzheimer’s dementia are dependent on timing. Early in disease course, the EEG may be normal, or show an alpha rhythm at or just below normal. As the disease progresses, generalized slowing ensues. Delirium is most often characterized by generalized slow wave activity on EEG. If triphasic waves are seen, these are indicative of a metabolic cause in an unresponsive patient. Previously, it was thought that these triphasic waves were diagnostic of hepatic encephalopathy, but other metabolic causes such as uremia, hypoxia, hyponatremia and hyperosmolarity can also produce this EEG abnormality. There are no particular classic EEG abnormalities associated directly with either Parkinson’s disease or HIV-related dementia.

  Neurology

  B&D Chs 32A&66

Question 39. A. The classic triad of dementia, urinary incontinence and gait apraxia is the clinical picture of normal pressure hydrocephalus (NPH). The gait problems resemble those in Parkinson’s disease, though they abate after gait is initiated. Cognitively, patients can present with deficits in speed of mental processing, decreased memory functioning, poor abstraction and difficulty with set-shifting tasks. Other common features include depression, hypersomnia, abulia and apathy. The gait disturbance and incontinence are believed to be a result of pressure on and distortion of descending white matter pathways. The cognitive symptoms are thought to be due to pressure on anterior cortical structures. Neuroimaging studies usually show ventricular enlargement of the lateral, third and fourth ventricles. Treatment of NPH is placement of a ventricular peritoneal shunt. Successful response to shunting ranges from 25 to 80% of cases. The other distracters in answers B through E are explained in detail in other questions in this volume.

  Neurology

  B&D Ch. 66

Question 40. B. The clinical picture here is that of the epidural hematoma. Notice that nowhere in this question is the phrase “epidural hematoma” mentioned. You are asked to extrapolate this from the data given. Epidural hematomas are located between the inner table of the skull and the dura. They typically occur when a skull fracture tears the middle meningeal artery or one of its branches. Epidural hematomas have a lens-shaped appearance and smooth inner border, because as they enlarge, they strip the dura away from the inner table of the skull. The classic clinical presentation is as described in this question: a brief loss of consciousness, followed by an intercurrent period of lucidity and then a later deterioration. Recall that damage to the bridging veins usually causes a subdural hematoma, which is often seen in alcoholics who have head injury that goes undetected. An intracranial aneurysmal rupture would present as a subarachnoid hemorrhage and “the worst headache of my life” scenario. Damage to the reticular activating system (in the brainstem) would likely cause unconsciousness and, if protracted, coma. Frontal lobe damage from traumatic brain injury, for example, can result in loss of executive functioning and planning ability, impulsivity, inappropriate behavior and mood swings.

  Neurology

  B&D Ch. 50B

Question 41. A. Because it is an often asked developmental milestone, it is good to know that pat-a-cake occurs for most children around 10 months.

  Human Development

  K&S Ch. 2

Question 42. E. This is a great question, because it takes you through the commonest CNS manifestations of AIDS. The best answer here is HIV-related dementia (AIDS-related dementia complex or ARDC). ARDC is the commonest complication of late untreated HIV disease. Early symptoms usually consist of problems with attention and concentration. Many patients have a slowness of thought (bradyphrenia). Complex tasks may become difficult to accomplish and may take longer due to these problems. Social withdrawal, apathy, depression and fatigue are all commonly seen in ARDC. There are generally psychomotor deficits noted as well. These can include gait incoordination and rigidity and slowness of gait. Fine and skilled hand and finger movements are affected early in the course of ARDC.

  Diffuse cerebral atrophy is almost always seen on brain MRI and CT imaging in ARDC patients. In some patients, MRI may show nonspecific white matter abnormalities in the hemispheres and less commonly in the thalamus and basal ganglia. CSF examination in ARDC reveals mild mononuclear pleocytosis and mildly elevated protein in about 60% of cases. Specialized CSF studies may also reveal intrathecal IgG synthesis and a presence of oligoclonal bands. These findings are seen in other conditions such as multiple sclerosis and so their diagnostic value in ARDC is uncertain. Please note that the other four answer choices, A through D, are explained in other questions in this volume. Do study them, because they can and do appear on standardized examinations.

  Neurology

  B&D Ch. 53A

Question 43. B. The CYP450 2D6 enzyme has a long list of substrates. All of the choices listed in the question are substrates except bupropion, which is an inhibitor. Other inhibitors include citalopram, duloxetine (this is both a substrate and an inhibitor), escitalopram, fluoxetine, methadone, paroxetine, sertraline, and TCAs. Bupropion is a substrate of 2B6.

  Psychopharmacology

  K&S Ch. 3

Question 44. D. This is a simple question really, but some will find it tricky because it asks about the less common symptoms and signs of Parkinson’s disease (PD). You can never study Parkinson’s disease enough for standardized examinations in psychiatry. This topic comes up time and time again on neurology questions, because there is a strong overlap with behavioral and psychiatric presentation in this disorder. We’ve discussed the disorder in many questions in this book BUT we want to give you some of the essential bullet points now:

• Pathology = depigmentation and neuronal loss in the substantia nigra and presence of Lewy bodies and pale bodies

• Pathologic hallmark is dopaminergic underactivity in the striatum

• 60 to 85% of striatal dopamine and nigral neurons must be lost before symptoms of PD arise

• Prevalence is 100 to 200 per 100 000 population

• Cardinal features = resting tremor (4 to 7 Hz), rigidity, postural instability and bradykinesia

• Tremor is called “pill-rolling” as it resembles the rolling of the finger tips over a pill surface

• Festination, or a festinating gait, refers to the tendency of the patient to propulse involuntarily while standing or walking, or to retropulse and fall.

• Manifestations are usually asymmetrical early in the disease and become bilateral later on in the course

• Levodopa–carbidopa is the mainstay of therapy. Other important antiparkinsonian agents include dopamine agonists, monoamine oxidase inhibitors, anticholinergics.

  Remember that alcoholic cerebellar atrophy presents with truncal ataxia for the most part, because the cerebellar vermis is preferentially affected. The vermis is responsible for truncal balance and smooth movement around the midline.

  Neurology

  B&D Ch. 71

Question 45. C. When compared to men, women have less alcohol dehydrogenase in their gut. As such men metabolize more alcohol in their gut leading to lower blood alcohol levels. Women have a lower body water content compared to men so that the alcohol is distributed in less water and is therefore more concentrated. The question said they both drank the same amount, so choice A is wrong. There is no evidence that Susan urinates more than Billy or that it can be assumed that a woman would urinate more than a man. The question stem says nothing about either of their weight so we can’t make any assumptions. If you chose answer choices A, D, or E, you made assumptions about data that was not provided in the question stem. This is a common way that people get questions wrong. Never insert data into the question that the test writer didn’t give you.

  Substance Abuse

  K&S Ch. 12

Question 46. B. Here we have another question that asks you to jump directly to appropriate management from symptom presentation only. The question bypasses asking you what the disease entity is, because that would clearly be too simple: temporal arteritis. Temporal arteritis (TA) is a vasculitis found in the elderly patient. If left undiagnosed and untreated it can frequently lead to permanent blindness. Headache is the most common symptom, experienced by about 72% of patients at some point during this condition and seen in one-third of patients on initial presentation. More than half of the patients with TA present concomitantly with polymyalgia rheumatica, which consists of aching in proximal and axial joints, proximal myalgias and often significant morning stiffness. Jaw claudication is a common associated symptom and presents initially in about 4% of patients with TA. Amaurosis fugax is one the most ominous symptoms as it evolves to partial or total blindness in 50% of cases, if left untreated. The most often recognized lab abnormality in TA is the erythrocyte sedimentation rate (ESR) which is elevated in most cases (85±32 mm). Diagnosis is then confirmed by temporal artery biopsy. Nevertheless, it is essential to treat early, even before biopsy is done or results are known, with high-dose oral prednisone, to avoid the onset of irreversible visual loss. Prednisone should be initiated at 40 to 60 mg daily and maintained for at least 1 month before beginning a cautious taper.

  Neurology

  B&D Ch. 69

Question 47. B. Low levels of folate can lead to fatigue, agitation, delirium, dementia, psychosis, and paranoia. It is seen commonly in alcoholics. Low folate does not cause panic attacks.

  Lab Tests in Psychiatry

  K&S Ch. 10

Question 48. A. This is a simple question. Answer choices B through E are all preventative (prophylactic) treatments of migraines. Divalproex sodium and topiramate are both in fact FDA-approved for preventative therapy of migraine headache. Desipramine is of course a tricyclic antidepressant that is used off-label for neuropathic pain. It is also effective in the prevention of migraine and this is an off-label use, as well. Gabapentin is an anticonvulsant agent, FDA-approved for seizure and post-herpetic neuralgia. It too is used off-label for the prevention of migraine. The triptans, including sumatriptan, naratriptan, eletriptan, rizatriptan, are abortive agents for migraines. Their mechanism of action is as agonists at 5-HT1B and 5-HT1D receptors. These agents modulate the excitability of cells in the trigeminal nucleus caudalis (TNC), which receives input from the trigeminal nerve.

  Neurology

  B&D Ch. 69

Question 49. C. This patient is clearly hypothyroid. If you miss that fact and treat the depression and not the thyroid you will get the question wrong and mistreat the patient. Symptoms of hypothyroidism include depression, weakness, stiffness, poor appetite, constipation, menstrual irregularities, slowed speech, apathy, impaired memory, hallucinations, or delusions. This is a very common test question. Make sure you get it right when it shows up on an exam near you!

  Somatic Symptom Disorders

  K&S Ch. 10

Question 50. E. Rupture of an intracranial aneurysm or AVM results in a subarachnoid hemorrhage, which may extend into the brain parenchyma. The headache associated with this bleed is usually sudden in onset and explosive. It’s often described by patients as “the worst headache of my life.” The headache is often accompanied by vomiting. Hydrocephalus may develop, resulting from intraventricular blood that distorts the midline structures. Noncontrast head CT confirms the diagnosis by revealing blood in the subarachnoid cisterns or in the parenchyma. If CT confirms the presence of blood in the subarachnoid spaces, lumbar puncture should be avoided to prevent a possible herniation or further bleeding. Subarachnoid hemorrhage generally indicates the need for cerebral angiography. Note that 80 to 85% of aneurysms arise from the arteries of the anterior circulation: the anterior communicating artery, posterior communicating artery or middle cerebral artery. In contrast, 15 to 20% of aneurysms arise from the posterior circulation. The majority of these aneurysms are found at the bifurcation of the basilar artery or at the origin of the posterior inferior cerebellar artery on the vertebral artery.

  Neurology

  B&D Chs 49,51C&69

Question 51. C. Damage to the medial longitudinal fasciculus (MLF) between the third and sixth cranial nerve nuclei interrupts transmission of neural impulses to the ipsilateral medial rectus muscle. Adducting saccades of the ipsilateral eye are impaired. The nystagmus-like movement of the typical abduction is in fact overshoot dysmetria. Upward-beating and torsional nystagmus are often present. The classic cause of this lesion is a demyelinating lesion of the brainstem in multiple sclerosis. There are many other possible causes of internuclear ophthalmoplegia (INO). These include pontine stroke, intrinsic tumor, drug intoxication, and chemotherapy with radiation therapy. INO can be caused by myasthenia gravis and progressive supranuclear palsy, but certainly less often than in multiple sclerosis.

  Neurology

  B&D Ch. 36

Question 52. D. When focal injury to myelin arises, conduction along the affected nerve fibers may alter. This can result in conduction slowing or conduction block along the nerve fibers. This conduction defect can be seen on nerve conduction studies. More than 50% decrement of both the compound muscle action potential (CMAP) amplitude and area across the lesion usually is the criterion for definite conduction block.

  Fibrillation potentials are the electrophysiological markers of muscle denervation. These are elicited on needle electromyographic (EMG) studies and are usually seen with positive sharp waves. Based on their distribution, they are useful in localizing lesions to the anterior horn cells of the spinal cord, ventral root, plexus, or peripheral nerve. Positive sharp waves may appear within 2 weeks of acute denervation; however, fibrillation potentials do not become full until about 3 weeks after axonal loss.

  After acute focal axonal damage, the distal nerve segment undergoes Wallerian degeneration. Nerve conduction studies classically demonstrate unelicitable or low CMAP amplitudes. Decremental response to slow repetitive stimulation is a hallmark of postsynaptic neuromuscular junction disorders like myasthenia gravis.

  Neurology

  B&D Ch. 32B

Question 53. B. Signs of cannabis intoxication include conjunctival injection, increased appetite, dry mouth, and tachycardia. Impaired motor coordination, euphoria, anxiety, sensation of slowed time, impaired judgment, and social withdrawal may also be found. Diuresis is not one of the side effects.

  Substance Abuse and Addictive Disorders

  K&S Ch. 12

Question 54. C. Huntington’s disease (HD) is an autosomal dominant neurodegenerative disorder characterized by progressive movement disorder associated with psychiatric and cognitive decline, culminating in a terminal state of dementia and immobility. Prevalence is about 10 per 100 000. HD usually begins between ages 30 and 55 years. About 60% of patients present initially with motor signs, about 15% with behavioral signs and about 25% with both motor and behavioral signs. A change in the ability to generate saccadic eye movements and their speed is often the earliest sign. Eventually, a blink or head thrust may be required to initiate saccadic eye movements. The motor disorder usually begins with clumsiness and fidgetiness that evolves into chorea. In addition to chorea, HD patients have bradykinesia and motor impersistence, with difficulty sustaining ongoing movement. The gait often resembles a marionette, lurching, swaying, dipping and bobbing. Dysarthria and dysphagia progressively impair communication and nutrition. Mean survival is 17 years. Most patients wind up wheelchair or bedbound and perish from complications that include pneumonia and head injury. HD is dominantly inherited and caused by an unstable expanded CAG trinucleotide repeat in exon 1 of the HD gene on the tip of the short arm of chromosome 4. Essentially all patients with 40 or more CAG repeats in the HD gene will develop the clinical illness. The direct DNA test for the CAG repeat expansion in the huntingtin (HD) gene, formerly called IT15, is highly sensitive and specific. The pathology of HD includes prominent neuronal loss and gliosis in the caudate nucleus and putamen, along with regional and more diffuse atrophy. No treatment has yet been proven to improve disease progression. The use of tetrabenazine has been found to be effective in reducing chorea in HD patients and is now FDA-approved and available in the USA for this labeled use.

  Neurology

  B&D Ch. 71

Question 55. C. Carbamazepine will interact with all of the drugs listed in this question. Erythromycin will increase carbamazepine levels. Phenobarbital and theophylline will decrease carbamazepine levels. Carbamazepine will decrease doxycycline and cyclosporine levels.

  Psychopharmacology

  K&S Ch. 36

Question 56. C. Extracranial vertebral artery dissection presents with high cervical pain sometimes radiating to the occipital region, as well as posterior circulation transient ischemic attacks (TIAs) or stroke. Vertebral artery dissection can occur spontaneously, but most commonly, it is due to trauma, which can be dramatic (cervical fractures and dislocation) or subtle (abrupt turning of the neck, chiropractic manipulation, or simple hyperextension of the neck such as sometimes used for shaving under the chin). Anticoagulation is the mainstay of treatment for extracranial vertebral dissection, when there is ischemic symptomatology. The results are usually favorable, unless the patient already has a fixed deficit.

  Pain in the arm can result from damage to the brachial plexus. Infiltrative or inflammatory lesions of the brachial plexus produce severe brachialgia, with pain radiating down the arm and spreading into the shoulder region. Radiation to the ulnar two fingers suggests origin in the lower brachial plexus, and radiation to the upper arm, forearm, and thumb suggests an upper brachial plexopathy. Causes of brachial plexopathy include traction and heavy impact. Sporting injuries in bicycling, football, snowmobiling, skiing, and horseback riding can all cause plexus injury. Rucksack paralysis is another form of brachial plexus injury from the traction and pressure on the brachial plexus exerted by heavy backpack straps to the shoulders. Other plexus injuries can be caused by metastatic disease or radiation-induced injury in the cancer patient.

  Sacroiliac joint syndrome is a major source of low back pain. Pain can present on one side of the lower back and radiate down to the hip or thigh. Pain often worsens upon walking up stairs. Patrick’s test or single leg standing test often exacerbates the pain. NSAIDs are first-line therapy in patients with joint inflammation. Sacroiliac joint corticosteroid injection can provide temporary pain relief.

  Anterior spinal artery syndrome results in spinal cord infarction and has been seen more frequently because of increased numbers of invasive surgical procedures, such as vascular and thoracoabdominal surgeries. The anterior horns and anterolateral tracts are affected (corticospinal tract involvement below the level of the lesion), resulting in loss of bowel and bladder control and sexual dysfunction. A sensory deficit develops, sparing the posterior columns, involving only the spinothalamic tracts. Spinal shock with areflexia is expected initially, followed by later onset of spasticity.

  Neurology

  B&D Chs 24,29,44&46

Question 57. A. Bell’s palsy is a self-limited, monophasic facial nerve palsy of acute or subacute onset. In 60% of patients, pain accompanies the facial weakness, impaired lacrimation in 60%, taste changes in 30 to 50% and hyperacusis in 15 to 30%. MRI of the internal auditory canal often demonstrates enhancement of the facial nerve, most often at the geniculate ganglion. Eighty five percent of patients recover normal facial function within 3 weeks. Bell’s palsy occurs with increased frequency during pregnancy and is associated with a poorer recovery rate. Residual abnormalities after Bell’s palsy occur in 12% of patients, persistent severe facial weakness in 4%, and synkinetic contraction and twitching of the upper and lower facial muscles in 17%. Aberrant regeneration involving the lacrimal gland may lead to tearing with facial muscle contraction (syndrome of “crocodile tears”), particularly during eating. The finding of spontaneous fibrillation in facial muscles on EMG 10 to 14 days after onset of facial weakness is a predictor of poor outcome. Bell’s palsy can be recurrent, but in these cases other causes such as Lyme disease or sarcoidosis must be considered. Bilateral facial palsy is also common with acute inflammatory demyelinating polyneuropathy. Bell’s palsy is considered to be idiopathic, but herpes simplex virus and varicella zoster virus reactivation in the geniculate ganglion have been implicated in its pathogenesis. Early administration of corticosteroids and acyclovir is common practice and may enhance recovery.

  The classic triad of Horner’s syndrome from sympathetic dysfunction is that of ipsilateral ptosis, miosis and facial anhidrosis. Later medullary syndrome (Wallenberg’s syndrome) typically results from occlusion of the posterior inferior cerebellar artery and produces sensory loss on the ipsilateral face, from trigeminal involvement, plus loss of pain and temperature sensation from the contralateral body, from damage to the ascending spinothalamic tract. Motor findings include ipsilateral cerebellar ataxia, bulbar weakness resulting in dysarthria and dysphagia, and Horner’s syndrome.

  Neurology

  B&D Chs 16,28&70

Question 58. E. The pain of postherpetic neuralgia (PHN), described as continuous deep aching, burning sharp, stabbing, and shooting, and triggered by light touch over the affected dermatomes, is often debilitating and difficult to treat. Tricyclics (amitriptyline or desipramine), selective serotonin reuptake inhibitors (sertraline or nefazodone hydrochloride), anticonvulsants (carbamazepine and gabapentin), oral opioids (oxycodone), and topical capsaicin cream or lidocaine patches are helpful in about 50% of patients. Note that gabapentin is the best answer to this question because it is specifically FDA-approved for PHN and carbamazepine and desipramine are used off-label.

  PHN occurs in anywhere from 8 to 70% of patients following herpes zoster (the shingles, which is varicella-zoster virus reactivation of the dorsal root ganglion). Herpes zoster is characterized by sharp or burning radicular pain sometimes associated with fever, malaise and rash. The cutaneous eruption begins as an erythematous maculopapular rash and progresses to grouped clear vesicles that continue to form for 3 to 5 days. These become pustules by 3 to 4 days and form crusts by 10 days. Pain usually disappears as the vesicles fade.

  Neurology

  B&D Ch. 75

Question 59. B. Carbon monoxide exposure occurs mainly in miners, gas workers, and garage employees. Other exposures occur with poorly ventilated home heating systems, stoves and suicide attempts. The neurotoxic effects of carbon monoxide relate to intracellular hypoxia. Carbon monoxide binds to hemoglobin with high affinity to form carboxyhemoglobin. Acute toxicity leads to headache, disturbances of consciousness and other behavioral changes. Motor abnormalities can occur with pyramidal and extrapyramidal deficits. Seizures may occur and focal cortical deficits sometimes develop. Pathological examination shows hypoxic and ischemic damage in the cerebral cortex as well as in the hippocampus, cerebellar cortex, and basal ganglia. Lesions are also present diffusely in the cerebral white matter.

  Neurology

  B&D Ch. 58

Question 60. D. In approximately 80% of patients with stiff-person syndrome, the disorder develops as non-paraneoplastic phenomenon in association with diabetes and polyendocrinopathy and, often, antibodies to glutamic acid decarboxylase. Characteristic of stiff-person syndrome is fluctuating rigidity of the axial musculature with superimposed spasms. Muscle stiffness primarily affects the lower trunk and legs, but it can extend to the arms, shoulders and neck. The usual precipitating factors of muscle spasms are emotional upset and auditory or somesthetic stimuli. The rigidity disappears during sleep and after local or general anesthesia. The paraneoplastic form of stiff-person syndrome is usually associated with breast and lung cancers and Hodgkin’s disease. The main autoantigen of the paraneoplastic form of stiff-person syndrome is amphiphysin. Treatment of the tumor and the use of corticosteroids may improve paraneoplastic stiff-person syndrome. IVIg is useful in patients with non-paraneoplastic stiff-person syndrome. GABA-enhancing agents, such as benzodiazepines, gabapentin, and baclofen, provide symptomatic relief.

  Neurology

  B&D Ch. 52G

Question 61. B. Mirtazapine has 5-HT3 receptor antagonism which is thought to be responsible for its antinausea effect. This same receptor antagonism is responsible for the antinausea properties of ondansetron.

  Psychopharmacology

  K&S Ch. 36

Question 62. D. The clinical manifestations of a medulloblastoma, located in the fourth ventricle, are the result of increased intracranial pressure (ICP) and obstructive hydrocephalus. Headache is the most common initial symptom and usually precedes diagnosis by 4 to 8 weeks. Intractable nausea and vomiting occur frequently, characteristically in the morning. Personality changes, namely irritability, are an early feature. Lethargy, diplopia, head tilt and truncal ataxia are other features that can help lead to diagnosis. Common signs on physical examination are papilledema, ataxia, dysmetria, and cranial nerve involvement. Abducens nerve palsy, secondary to increased ICP, is a cause of diplopia and head tilt. Torticollis can be a sign of cerebellar tonsil herniation.

  Neurology

  B&D Ch. 52E

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Question 63. D. In 50% of families where a child dies, parental divorce follows.

  Depressive Disorders

  K&S Ch. 28

Question 64. B. For the individual to be rendered unconscious by a traumatic brain lesion, either the reticular activating system must be involved or diffuse injury to both hemispheres. The functioning of the awake mind requires the ascending inputs referred to as the reticular activating system, with its way stations in the brainstem and thalamus, as well as an intact cerebral cortex. Bilateral lesions of the brainstem or the thalamus produce coma. Very diffuse lesions of the hemispheres produce an “awake” patient who shows no responsiveness to the environment, a state sometimes called coma vigil or persistent vegetative state, as in the recent Terry Schiavo case. Patients with very slight responses to environmental stimuli are said to be in a minimally conscious state.

  Neurology

  B&D Ch. 6

Question 65. B. Neuroimaging of schizophrenics demonstrates increased size of the lateral ventricles. PET scan and fMRI of schizophrenics will show decreased metabolic activity in the frontal lobes. Know these facts for your exam.

  Laboratory Tests in Psychiatry

  K&S Ch. 13

Question 66. A. Symptoms of cervical radiculopathy often appear suddenly. Acute trauma is often the cause of nerve root contusion or disk herniation that results in cervical radiculopathy. In patients younger than age 45, disk herniation is more likely to be the cause. With increasing age, degenerative changes resulting in neural foraminal stenosis are more likely to be the causative factors. Pain is usually in the neck with radiation to an arm. Headache may also be a symptom. The C5, C6, and C7 roots are the ones most commonly involved in cervical spondylosis, because they are at the level of greatest mobility. Lesions at the C4–C5 level affect the C5 root, causing pain, paresthesias and sometimes loss of sensation over the shoulder, with weakness of the deltoid, biceps, and brachioradialis muscles. The biceps and supinator reflexes may be lost. Lesions at the C5–C6 level affect the C6 root and cause paresthesias in the thumb or lateral distal forearm and weakness in the brachioradialis, biceps or triceps. The biceps and brachioradialis reflexes may be diminished or inverted. Lesions at the level of C6–C7 affect the C7 root and cause paresthesias, usually in the index, middle or ring fingers, and weakness in C7-innervated muscles, such as the triceps and pronators. The triceps tendon reflex may be diminished. Remember that myelopathy (compromise of the spinal cord) generally causes hyperreflexia and not diminished or absent reflexes, particularly early on in the course of the condition.

  Typical findings in cervical myelopathy are a combination of leg spasticity, upper extremity weakness or clumsiness, and sensory changes in the arms, legs or trunk. Some patients experience leg or trunk paresthesia induced by neck flexion (Lhermitte’s sign).

  Neurology

  B&D Ch. 73

Question 67. C. Narcolepsy consists of irresistible attacks of sleep that occur daily for at least 3 months. They involve cataplexy (loss of muscle tone during attacks often associated with strong emotion) and REM sleep during episodes often leading to hypnopompic or hypnagogic hallucinations and sleep paralysis. Catalepsy is also known as waxy flexibility and is seen in catatonic schizophrenia.

  Sleep Wake Disorders

  K&S Ch. 24

Question 68. C. Subacute combined degeneration (SCD) refers to the combination of spinal cord and peripheral nerve pathology associated with vitamin B12 (cobalamin) deficiency. Patients often complain of unsteady gait and distal paresthesias. The neurologic examination may demonstrate evidence of posterior column, pyramidal tract and peripheral nerve involvement. Cognitive, behavioral and psychiatric manifestations can also occur. Personality change, cognitive dysfunction, mania, depression and psychosis, have all been reported. Dementia is often comorbid with cobalamin deficiency; however the causative association is unclear. Cobalamin deficiency-associated cognitive impairment is more likely to improve when impairment is mild and of short duration.

  Neurology

  B&D Ch. 9

Question 69. D. Extensor plantar responses (Babinski signs) are indicative of a lesion of the corticospinal tracts i.e. upper motor neuron involvement. The other four answers are clearly cardinal features of a dementia of the Alzheimer type. Alzheimer’s dementia does not typically involve lesions to the descending motor tracts, unless some other ischemic or hemorrhagic process is accompanying the dementia. That is not to say that vascular dementia does not present with aphasia, apraxia, agnosia or memory loss. Vascular dementia (or multi-infarct dementia as it was formerly called) typically includes a history of clinical strokes with focal neurological signs and symptoms and “stepwise” cognitive decline. Epidemiological studies find that the prevalence of vascular dementia ranges from 3 to 21%. In autopsy studies of late-life dementia, 15 to 20% of the patients are reported to have had vascular dementia.

  Neurology

  B&D Ch. 66

Question 70. A. This scan and the question vignette are indicative of a frontotemporal dementia (FTD), one of which is Pick’s disease. The scan demonstrates classic preferential atrophy of the frontal and temporal lobes with occipitoparietal sparing. This kind of imaging finding is known as “knife-edge” atrophy of the frontal and temporal lobes and was characterized histologically by ballooned cells and intraneuronal inclusions (Pick cells and Pick bodies). Criteria focus on loss of insight, easy distractibility, reduced concern or empathy for others, emotional lability or withdrawal, impulsiveness, poor self-care, perseveration, features of the Klüver–Bucy syndrome, and diminished verbal output. There is a second type of presentation of FTD, which is characterized by early and progressive change in language, with problems of expression of language or severe naming difficulty and problems with word meaning. Males and females are affected equally. Mean duration of illness is approximately 8 years, with a range from 2 to 15 years. FTD makes up 10–15% of the neurodegenerative dementias in clinical autopsy series.

  Neurology

  B&D Ch. 66

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Question 71. A. The potassium-sensitive periodic paralysis and myotonias are associated with mutations in the α-subunit of the sodium channel; the gene is located on chromosome 17q. Inheritance of potassium-sensitive periodic paralysis is autosomal dominant, with strong penetrance and involvement of both sexes. Symptom onset occurs in infancy or early childhood. An infant may cry in an altered or unusual manner, or may be found lying quietly in the crib. The first attack often occurs during the first few weeks of school because of the enforced sitting. The predominant symptom is weakness provoked by potassium exposure. Myotonia may be present, but the overwhelming difficulty is recurrent bouts of paralysis. Many patients have two kinds of attacks, light and heavy. A light attack is characterized by fatigue and mild weakness usually dissipates in under an hour. A heavy attack, in contrast, may be associated with more severe paralysis, during which the patient may not be able to rise from a chair or a bed. The frequency can vary from two or three mild attacks a day to episodes months apart.

  Neurology

  B&D Ch. 79

Question 72. C. CSF findings on their own cannot make or exclude the diagnosis of MS. The CSF is grossly normal in MS, being clear, colorless and under normal pressure. Total leukocyte count is normal in two thirds of patients. CSF protein (or albumin) level is normal in the majority of patients with MS. Albumin levels are elevated in only 20–30% of patients. A common finding in MS is an elevation of CSF immunoglobulin levels. The increase is predominantly IgG, but the synthesis of IgA and IgM is also increased. Oligoclonal bands (OCBs) have been found in 85 to 95% of patients with clinically definite MS. The presence of OCBs in monosymptomatic patients predicts a significantly higher rate of progression to MS than the absence of bands: 25% versus 9% at 3 years’ follow-up. The pattern of banding remains relatively consistent in individual patients during the disease course, though bands may be added over time.

  Neurology

  B&D Ch. 54

Question 73. B. Mirtazapine works via alpha 2 antagonism on the presynaptic neuron. This blocks a feedback loop causing more serotonin and norepinephrine to be released into the synaptic cleft.

  Psychopharmacology

  K&S Ch. 36

Question 74. B. Cluster headache is classified by at least five repeated attacks that are severe or very severe unilateral, orbital, supraorbital and/or temporal pain lasting 15 to 180 minutes if left untreated. The headache must be accompanied by one of the following: ipsilateral conjunctival injection or lacrimation; ipsilateral nasal congestion and/or rhinorrhea; ipsilateral eyelid edema; ipsilateral forehead and facial swelling; ipsilateral miosis and/or ptosis; a sense of restlessness or agitation. Attacks have a frequency from one every other day to eight per day. Cluster headache is predominantly a disease of men. Onset typically begins in the third decade of life. Periodicity is a cardinal feature of cluster headache. The first cluster of attacks tends to last, on average, for 6 to 12 weeks and is followed by a remission period that lasts from months to years.

  The pain is strictly unilateral and almost always remains on the same side of the head from cluster to cluster. The pain is felt generally in the retro-orbital and temporal regions (upper syndrome) but may be maximal in the jaw or cheek (lower syndrome). It is often described as being boring or stabbing in nature, like a hot poker going through the eye or poking the eye. During the episode, patients tend to avoid the recumbent position because lying down tends to exacerbate the pain.

  The pathogenesis of cluster headache is not entirely understood. The pain is likely mediated by the activation of trigeminal nerve pathways and the autonomic symptoms are due to parasympathetic outflow and sympathetic dysfunction. The periodicity suggests a defect in CNS cycling mechanisms that is likely related to hypothalamic dysfunction.

  Acute symptomatic therapy is best accomplished by administering of oxygen, subcutaneous sumatriptan, and subcutaneous or intramuscular DHE. Oxygen delivered at a flow rate of 8 to 10 L/min via a nonrebreathing face mask can be dramatically effective for aborting a cluster attack. Methysergide is utilized as maintenance prevention of cluster attacks. It is dosed from 4 to 10 mg per day and prevents cluster headache in about 60% of patients. Typically, NSAIDs, butalbital combination preparations, and oral narcotics are not particularly effective in aborting cluster attacks.

  Neurology

  B&D Ch. 69

Question 75. A. Hemicrania continua is characterized by a continuous unilateral headache of moderate intensity. The female to male ratio is about 2 to 1 and the average age of onset is 28 years. The disorder is usually continuous and unremitting; however, in certain cases it can resemble a prolonged unilateral migraine attack of several days to weeks in duration, with headache-free remissions. The continuous headache is typically punctuated by painful unilateral exacerbations lasting twenty minutes to several days. These periods of increased pain intensity are accompanied by one or more autonomic features. Primary stabbing headache (“ice-pick headache”) is often a feature of this disorder, usually on the ipsilateral side, and usually during a period of exacerbation. Hemicrania continua patients respond completely to prophylactic indomethacin. Cases of hemicrania continua have been reported that have not recurred after stopping indomethacin. It is therefore reasonable to withdraw treatment periodically. Other agents that may produce a response include: methysergide, acetaminophen with caffeine, lamotrigine, gabapentin, topiramate, verapamil, melatonin, dihydroergotamine, corticosteroids, and lithium.

  Neurology

  B&D Ch. 69

Question 76. D. Lacunar infarcts are small ischemic infarctions in the deep regions of the brain or brainstem that range in diameter from 0.5 to 15.0 mm. Lacunes usually occur in patients with longstanding arterial hypertension, current cigarette smoking and diabetes mellitus. The most frequent sites of involvement are the putamen, basis pontis, thalamus, posterior limb of the internal capsule and the caudate nucleus. Multiple lacunar infarcts are strongly associated with arterial hypertension and diabetes mellitus. Studies indicate that arterial hypertension leads to microvascular changes characterized by fibrinoid angiopathy, lipohyalinosis, and microaneurysm formation. Control of hypertension, prevention of microangiopathy, and use of platelet antiaggregants are essential in the management of patients with lacunar infarcts.

  Neurology

  B&D Ch. 51A

Question 77. C. The Dandy–Walker malformation consists of a ballooning of the posterior half of the fourth ventricle, often but not always associated with nonopening of the foramen of Magendie. In addition, the posterior cerebellar vermis is aplastic, and there may be heterotopia of the inferior olivary nuclei, pachygyria of the cerebral cortex, and other cerebral and sometimes visceral anomalies. Obstructive hydrocephalus usually ensues, but if treated promptly, the prognosis may be good. Neurological handicaps, such as spastic diplegia and mental retardation, probably relate more to the associated malformations of the brain than to the hydrocephalus.

image

  Chiari malformations involve a displacement of the tonsils and posterior vermis of the cerebellum through the foramen magnum, compressing the spinomedullary junction. The simple form is termed Chiari type I malformation. Type II involves an additional downward displacement of a distorted lower medulla and dysplasia of medullary nuclei and is a constant feature of lumbosacral meningomyelocele. Chiari type III malformation is actually a cervical spina bifida with cerebellar encephalocele.

  Anencephaly is a failure of the closing of the anterior neuropore at 24 days’ gestation. Death in utero occurs in approximately 7% of anencephalic pregnancies, 34% are born prematurely and 53% at term. Stillbirth occurs in 20% of these deliveries. The prenatal diagnosis of anencephaly is by examination of amniotic fluid for elevation of alpha-fetoprotein and confirmation is by sonographic imaging as early as 12 weeks’ gestation.

  Neurology

  B&D Ch. 60

Question 78. A. Prader–Willi syndrome (PWS) is a genetically defined mental retardation syndrome. It is caused by a deletion on chromosome 15q11–q13. If the individual inherits the deletion from a maternal chromosome 15, the result is Angelman’s syndrome; if the mutation is on a paternal chromosome 15, the result is PWS. Mean IQ range in PWS is 70, with a spectrum ranging from profound mental retardation to average intelligence. Language function is impaired by oromotor dysfunction. PWS patients have a knack for doing jigsaw puzzles and demonstrate good visuospatial strength. Executive functioning is impaired and characterized by obsessive skin picking. There is a high likelihood of autism in PWS patients. Social functioning is often impaired by the internalizing and externalizing of problems, as well as by ADHD. With maternal uniparental disomy, psychosis and aggressive behaviors can be seen in young adults with PWS. Hypothalamic dysfunction in PWS results in overeating behavior leading to truncal obesity in many patients. The other four answer choices to this question are also genetically defined mental retardation syndromes. Explanations of these can be found in other questions in this volume.

  Neurology

  B&D Ch. 61

Question 79. C. Creutzfeldt–Jakob disease (CJD) is a rapidly progressive spongiform degeneration of the brain secondary to the accumulation of misfolded prion proteins. Three other human prion diseases have been described: kuru (in New Guinea), Gerstmann–Straussler–Scheinker syndrome, and fatal familial insomnia. Because these diseases are now believed to be caused by a “proteinaceous infectious particle”, they are often referred to as prion diseases. Do read up on these other prion diseases; they do appear once in a while on board-style examinations. CJD affects men and women equally and typically manifests in late middle age. Peak incidence is in the 55–70-year age group. Symptoms can appear gradually over a period of weeks, or more suddenly. Approximately one-third of patients exhibit mental deterioration, one-third exhibit physical disabilities (especially incoordination), and another third exhibit mixed mental and physical abnormalities. Memory loss, accompanied by either cerebellar or visual–oculomotor signs are frequent at the disease onset. As the illness evolves, these symptoms are joined by pyramidal and extrapyramidal signs and a variety of involuntary movements, especially myoclonus. A small number of patients present with sleep and autonomic disorders that mimic familial fatal insomnia. Progressive mental deterioration terminates in mutism and global dementia. Death commonly occurs within 6 months of disease onset. Three laboratory tests are used to aid the diagnosis: EEG, CSF analysis, and brain MRI. In its most pathognomonic form, when the disease is fulminant, the EEG reveals a one- or two-cycle per second slow-wave triphasic spiking activity. The CSF is analyzed in two ways: for 14-3-3 protein kinase inhibitor and for tau protein. The presence of elevated levels of either one of these two markers has a sensitivity and specificity for CJD in the 90% range. Finally, in sporadic disease, the MRI may reveal a symmetrical or sometimes unilateral hyperintense signal in the basal ganglia. The other distractors are discussed elsewhere in other questions in this volume. Please do study them as well; they do pop up on standardized tests a great deal.

  Neurology

  B&D Ch. 66

Question 80. D. The JC virus is a polyomavirus and is ubiquitous; up to 85% of individuals have antibodies to the virus by age 9 years. The JC virus is the etiological agent of progressive multifocal leukoencephalopathy (PML). The kidneys are thought to be the site of latent JC viral persistence. Reactivation of the virus associated with immunosuppression results in hematogenous spread of the virus to the brain. Foci of PML are frequently located in proximity to blood vessels. PML occurs in patients with impaired cell-mediated immunity such as those with AIDS, chronic lymphocytic leukemia, Hodgkin’s disease, other lymphomas, sarcoidosis, organ transplantation, and lupus. The JC virus preferentially infects myelin-producing oligodendrocytes, resulting in cell lysis and demyelination. Focal neurologic deficits, seizure activity and cognitive impairment characterized by memory impairment, psychomotor retardation, and inattentiveness characterize the clinical presentation of PML. There is no proven therapy for PML, but clinical trials are ongoing. The average length of survival from the onset of symptoms to death is 1 to 4 months, but a small percentage of patients reportedly have improved spontaneously and survived for several years.

  The etiologic agent responsible for CNS lymphoma is Epstein–Barr virus (EBV). EBV is detectable from a majority of primary CNS lymphomas in AIDS patients and to a lesser degree from primary CNS lymphomas in immunocompetent individuals. The clinical presentation is that of progressive personality changes, seizures, and signs of increased intracranial pressure. The other answer choices to this question are discussed in greater detail elsewhere in this volume. Do study all of these CNS manifestations of HIV, because you are likely to come upon these questions on your board-style examination.

  Neurology

  B&D Ch. 53B

Question 81. B. The major morbidity associated with idiopathic intracranial hypertension (aka pseudotumor cerebri), is visual loss related to optic nerve dysfunction. Patients should satisfy the modified Dandy’s criteria: (1) signs and symptoms due to increased intracranial pressure; (2) a normal result on neurological examination except for an abducens palsy; (3) neuroimaging excluding a mass lesion or other cause of elevated intracranial pressure; and (4) normal CSF parameters, except an elevated opening pressure (>250 mmH2O). Patients are usually young, obese females who may complain of headache, transient visual obscurations (seconds), pulsatile intracranial noises, or double vision. Almost uniformly, patients have papilledema. Typically, visual acuity and color are preserved, but optic nerve-related visual field defects, which are best detected with computerized threshold perimetry, are present in more than 90% of patients and include enlarged blind spots, generalized constriction, and inferior nasal field loss. Hypervitaminosis A is one of many purported causes of idiopathic intracranial hypertension. Treatment involves reducing intracranial pressure. Acetazolamide is an inhibitor of carbonic anhydrase that lowers CSF production and pressure. It is given in a dose of 250 mg twice daily, which can be increased to 1 g/day. Some patients undergo repeated lumbar punctures with CSF removal to maintain lower CSF pressures. If vision is threatened, surgery is usually contemplated. Lumboperitoneal shunting and optic nerve sheath fenestration are the procedures of choice, although the latter has not been proven beneficial in follow-up studies.

  Neurology

  B&D Ch. 59

Question 82. A. Here is yet another look at Piaget’s theory of development. This material comes up very frequently on standardized tests so it is imperative to study and memorize. The developmental stage of concrete operations refers to ages 7 to 11 years. During this period, children are able to act on real, concrete and perceivable objects and events that surround them. Egocentric thought (characteristic of the stage of preoperational thought), is replaced by operational thought. Children gain the ability to see things from other people’s perspectives. Conservation and reversibility are the two abilities that children demonstrate in the stage of concrete operations. Conservation refers to the ability to recognize that although the shape of objects may change, the objects still maintain or conserve characteristics that enable them to be recognized as the same. Reversibility is the ability to understand the relation between things, that one thing can turn into another and then back again.

  Human Development

  K&S Ch. 4

Question 83. C. Men do not lose their sex drive as they age, unless there are specific physical and/or psychological factors underlying this problem. As is the case with women, lack of desire in men can be of either physical or psychological origin.

  Physical causes:

• Alcoholism – quite common. Tobacco use: frequent and its role is underestimated in loss of sexual drive

• Abuse of drugs such as cocaine

• Obesity – quite common; slimming down will often help

• Anemia – unusual, unless the man has been bleeding for any reason

• Hyperprolactinemia – a rare disorder where the pituitary gland produces too much of the hormone prolactin

• Prescribed drugs – particularly Proscar, a tablet used for prostate problems

• Low testosterone level – contrary to what many people think, this is rare, except in cases where some injury or illness has affected the testicles

• Any major disease such as diabetes

  Psychological causes:

• Depression – very common

• Stress and overwork

• Hang-ups from childhood

• Latent homosexuality

• Serious relationship problems with your partner

  Sexual desire has been described as a “longing for sexual union”, it associates with certain behaviors that are more linked to arousal and states of fear, concern and enhanced attention to others, and sexual cue displays such as lip biting and touching. In keeping with the correlation between sexual desire and arousal, sexual desire is mediated by gonadal estrogens and androgens.

  Enhanced focus, concern and attention toward the desired other has not only been associated with increased arousal by means of testosterone, but also with elevated concentrations of central dopamine and norepinephrine, and decreased levels of central serotonin. Other forms of physiological arousal associated with enhanced levels of dopamine include increased energy, exhilaration, euphoria, sleeplessness, loss of appetite, trembling, pounding heartbeat, and accelerated breathing. This same increased arousal is also a feature of attraction, and is the suggested cause of feelings of exhilaration, ecstasy, intrusive thinking about the love object, regarding them as unique, and a craving for emotional union with this partner or potential partner.

  Human development

  K&S Ch. 21

Question 84. D. Attachment theory was first set forth by John Bowlby, a British psychoanalyst. Attachment is defined as the emotional tone between children and caregivers, manifested by the infant’s seeking and clinging to the caregiver closely, such as the mother. It is well-accepted that a person’s psychological health and sense of well-being depend to a great extent on the quality of relationships and attachments to others, particularly those attachments that were laid down in childhood with caregivers. People with a secure attachment style are highly invested in relationships and tend to behave without much possessiveness or fear of rejection.

  Human Development

  K&S Ch. 4

Question 85. E. Heinz Kohut, an Austrian-born American psychoanalyst was best known for his development of self psychology, an influential school of thought within psychodynamic/psychoanalytic theory which helped transform the modern practice of analytic and dynamic treatment approaches. Though he initially tried to remain true to the traditional analytic viewpoint with which he had become associated and viewed the self as separate but coexistent to the ego, Kohut later rejected Freud’s structural theory of the id, ego, and superego. He then developed his ideas around what he called the tripartite (three-part) self. According to Kohut, this three-part self can only develop when the needs of one’s “self states,” including one’s sense of worth and well-being, are met in relationships with others. In contrast to traditional psychoanalysis, which focuses on drives (instinctual motivations of sex and aggression), internal conflicts, and fantasies, self psychology thus placed a great deal of emphasis on the vicissitudes of relationships. Kohut demonstrated his interest in how we develop our “sense of self” using narcissism as a model. If a person is narcissistic, it will allow him to suppress feelings of low self-esteem. By talking highly of himself, the person can eliminate his sense of worthlessness.

  Kohut initially proposed a bipolar self compromising two systems of narcissistic perfection: (1) a system of ambitions and, (2) a system of ideals. Kohut called the pole of ambitions the narcissistic self (later, the grandiose self), while the pole of ideals was designated the idealized parental imago. According to Kohut, these poles of the self represented natural progressions in the psychic life of infants and toddlers.

  Kohut argued that when the child’s ambitions and exhibitionistic strivings were chronically frustrated, arrests in the grandiose self led to the preservation of a false, expansive sense of self that could manifest outwardly in the visible grandiosity of the frank narcissist, or remain hidden from view, unless discovered in a narcissistic therapeutic transference (or self-object transference) that would expose these primitive grandiose fantasies and strivings. Kohut termed this form of transference a mirror transference. In this transference, the strivings of the grandiose self are mobilized and the patient attempts to use the therapist to gratify these strivings (this is essentially what is displayed between child and mother in this examination question).

  Kohut proposed that arrests in the pole of ideals occurred when the child suffered chronic and excessive disappointment over the failings of early idealized figures. Deficits in the pole of ideals were associated with the development of an idealizing transference to the therapist who becomes associated with the patient’s primitive fantasies of omnipotent parental perfection.

  Kohut believed that narcissistic injuries were inevitable and, in any case, necessary to temper ambitions and ideals with realism through the experience of more manageable frustrations and disappointments. It was the chronicity and lack of recovery from these injuries (arising from a number of possible causes) that he regarded as central to the preservation of primitive self systems untempered by realism.

  Human Development

  K&S Ch. 6

Question 86. C. Margaret Mahler, was a pioneer in object-relations psychoanalysis. Her six stages of separation–individuation come up on almost every standardized examination in psychiatry. Here is the list in correct order:

1. Normal autism (birth to 2 months): sleep periods predominate over arousal periods. This stage hearkens back to fetal and intrauterine life for the infant.

2. Symbiosis (2 to 5 months): Mother–infant is perceived as a single fused entity. Developing perceptual abilities gradually enable infants to distinguish the inner from the outer world.

3. Differentiation (5 to 10 months): Distinctness from mother is appreciated. Progressive neurological development and increased alertness draw the infant’s attention away from self to the outer world.

4. Practicing (10 to 18 months): The ability to move autonomously increases the child’s exploration of the outer world.

5. Rapprochement (18 to 24 months): Children move away from their mothers and come back for reassurance. As they slowly realize their helplessness and dependence, the need for independence alternates with the need for closeness.

6. Object constancy (2 to 5 years): Children gradually comprehend and are reassured by the permanence of mother and other important people, even when not in their presence.

  Human Development

  K&S Ch. 2

Question 87. B. Memory can be divided into three system categories: episodic, semantic and procedural. Episodic memory is mediated by the medial temporal lobes, anterior thalamic nuclei, mamillary bodies, fornix and prefrontal cortex. It involves explicit, declarative awareness. An example of episodic memory would be remembering what you ate for a meal a day earlier, or what you did on your last vacation. Semantic memory is mediated by the inferolateral temporal lobes. It too involves explicit, declarative awareness. Examples of semantic memory include knowing who the first President of the United States was, or knowing the difference between a bus and a train. Procedural memory is mediated by the basal ganglia, cerebellum and supplementary motor area. It involves either implicit or explicit, nondeclarative awareness. Examples of procedural memory include operating a motor vehicle (explicit) or learning how to type your telephone number without thinking about it (implicit).

  Neurocognitive Disorders

  K&S Ch. 3

Question 88. A. Burrhus Frederic “B. F.” Skinner, was an American behaviorist, author, inventor, social philosopher and poet. Skinner invented the operant conditioning chamber, innovated his own philosophy of science called radical behaviorism, and founded his own school of experimental research psychology – the experimental analysis of behavior. Skinner’s theory of learning and behavior is known as operant conditioning. In operant conditioning, an animal is active and behaves in a way that produces a reward. Thus, learning occurs as a consequence of action. Gambling behavior occurs due to the reinforcement schedule known as a variable–interval schedule. Reinforcement in this schedule, occurs after variable intervals (of time). As such, the response rate does not change between reinforcements. The animal responds at a steady rate to get the reward when it is available.

  Human Development

  K&S Ch. 4

Question 89. B. Selective perception (or attention) is a broad term to identify the behavior all people exhibit to tend to “see things” based on their particular frame of reference. Selective perception may refer to any number of cognitive biases in psychology related to the way expectations affect perception. For instance, several studies have shown that students who were told they were consuming alcoholic beverages (which in fact were non-alcoholic) perceived themselves as being “drunk”, exhibited fewer physiological symptoms of social stress, and drove a simulated car similarly to other subjects who had actually consumed alcohol. The result is somewhat similar to the placebo effect. A cognitive bias is a pattern of deviation in judgment that occurs in particular situations, leading to perceptual distortion, inaccurate judgment, illogical interpretation, or what is broadly called irrationality.

  Learned helplessness, as a technical term in animal psychology and related human psychology, means a condition of a human person or an animal in which it has learned to behave helplessly, even when the opportunity is restored for it to help itself by avoiding an unpleasant or harmful circumstance to which it has been subjected. Learned helplessness theory is the view that clinical depression and related mental illnesses may result from a perceived absence of control over the outcome of a situation. Organisms which have been ineffective and less sensitive in determining the consequences of their behavior are defined as having acquired learned helplessness. Martin Seligman’s experiments and theory of learned helplessness began at the University of Pennsylvania in 1967, as an extension of his interest in depression. Quite by accident, Seligman and colleagues discovered that the conditioning of dogs led to outcomes that opposed the predictions of B.F. Skinner’s behaviorism, then a leading psychological theory. In the learned helplessness experiment an animal is repeatedly hurt by an adverse stimulus which it cannot escape. Eventually the animal will stop trying to avoid the pain and behave as if it is utterly helpless to change the situation. Finally, when opportunities to escape are presented, this learned helplessness prevents any action. The only coping mechanism the animal uses is to be stoical and put up with the discomfort, not expending energy getting worked up about the adverse stimulus.

  Cognitive distortions are exaggerated and irrational thoughts, identified in cognitive therapy and its variants, which in theory perpetuate some psychological disorders. The theory of cognitive distortions was presented by David Burns in The Feeling Good Handbook in 1989, after studying under Aaron T. Beck. Eliminating these distortions and negative thoughts is said to improve mood and discourage maladies such as depression and chronic anxiety. The process of learning to refute these distortions is called “cognitive restructuring”. Magnifying or minimizing a memory or situation such that they no longer correspond to objective reality, is one of many types of cognitive distortion. This is common enough in the normal population to popularize idioms such as “make a mountain out of a molehill.” In depressed clients, often the positive characteristics of other people are exaggerated and negative characteristics are understated. There is one subtype of magnification: catastrophizing, which is the inability to foresee anything other than the worst possible outcome, however unlikely, or experiencing a situation as unbearable or impossible when it is just uncomfortable.

  Psychological Theory and Psychometric Testing

  K&S Chs 15&35

Question 90. D. Sensitivity and specificity are statistical measures of the performance of a binary classification test, also known in statistics as classification function. Sensitivity (also called recall rate in some fields) measures the proportion of actual positives which are correctly identified as such (e.g., the percentage of sick people who are correctly identified as having the condition). Specificity measures the proportion of negatives which are correctly identified (e.g., the percentage of healthy people who are correctly identified as not having the condition). These two measures are closely related to the concepts of type I and type II errors. A perfect predictor would be described as 100% sensitivity (i.e., predict all people from the sick group as sick) and 100% specificity (i.e., not predict anyone from the healthy group as sick), however theoretically any predictor will possess a minimum error bound known as the Bayes error rate. For any test, there is usually a trade-off between the measures. The sensitivity of a test is the proportion of people who have the disease who test positive for it. It is calculated by taking the number of true positives and dividing by the number of true positives plus the number of false negatives. It is the probability of a positive test given that the patient is ill. If a test has high sensitivity then a negative result would suggest the absence of disease.

  Specificity relates to the ability of the test to identify negative results. Consider the example of the medical test used to identify a disease. The specificity of a test is defined as the proportion of patients who do not have the disease who will test negative for it. Specificity is calculated by taking the number of true negatives and dividing by the number of true negatives plus the number of false positives. It is the probability of a negative test given that the patient is well. If a test has high specificity, a positive result from the test means a high probability of the presence of disease.

  Statistics

  K&S Ch. 4

Question 91. A. Atypical antipsychotics are the most thoroughly studied class of medications for patients with dementia who are agitated, and are the most common drugs used in clinical practice. They are better tolerated than typical neuroleptic agents, with less risk of causing extrapyramidal syndrome (EPS). In the absence of contraindications such as serious extrapyramidal dysfunction (e.g., EPS, parkinsonism), an atypical neuroleptic agent should be initiated at the lowest effective dosage and titrated weekly. Tremor, rigidity, dystonia, and dyskinesia are identified in a significant number of patients at baseline and may be exacerbated by the use of atypical antipsychotics, particularly when these agents are taken at higher dosages. Physicians must use caution when increasing dosages and observe the patient closely for the emergence of EPS. Although the use of the conventional antipsychotic agent haloperidol (Haldol) is discouraged in long-term care facilities, it is widely used in the management of delirium and acute agitation in other settings. Haloperidol has been used with acceptable side effects in the management of behavior disorders of dementia. If used, it should be prescribed at low dosages and for short periods (typically days), after which the patient should be switched to another agent such as an atypical antipsychotic. Benzodiazepines should not be considered first-line therapy for management of chronic behavior disorders of dementia, even in patients with prominent anxiety. Chronic benzodiazepine use may worsen the behavior abnormality because of the amnestic and disinhibitory effects of these drugs. In clinical practice, benzodiazepine use should be limited to management of acute symptoms that are unresponsive to redirection or other agents. Anticonvulsant agents typically are used when psychotic behaviors result in aggressive behavior. Increasing evidence supports the use of divalproex (Depakote) or carbamazepine (Tegretol). These drugs are recommended as second-line agents in patients with inadequate response to antipsychotic agents. Tricyclic antidepressants should be avoided in demented patients, and in particular those with agitation, because of their anticholinergic effects, which can worsen both the agitation and the underlying dementia.

  Psychopharmacology

  K&S Ch. 10

Question 92. C. Psychiatrists are held to ethical principles and standards by the American Psychiatric Association that are higher than other physicians are held to by the American Medical Association. On occasion, psychiatrists are asked to render an opinion about individuals who are public figures, or individuals who have revealed information about themselves through the public media. Psychiatrists are permitted to share their expertise about psychiatric issues in general with the public. However, it is unethical for psychiatrists to offer a professional opinion about a specific individual unless they have examined the individual and been granted proper authorization for such a statement.

  Ethics

  K&S Ch. 59

Question 93. C. Transcranial magnetic stimulation (TMS) is a noninvasive method to cause depolarization or hyperpolarization in the neurons of the brain. TMS uses electromagnetic induction to induce weak electric currents using a rapidly changing magnetic field; this can cause activity in specific or general parts of the brain with minimal discomfort, allowing the functioning and interconnections of the brain to be studied. A variant of TMS, repetitive transcranial magnetic stimulation (rTMS), has been tested as a treatment tool for various neurological and psychiatric disorders including migraines, strokes, Parkinson’s disease, dystonia, tinnitus, depression and auditory hallucinations. In 2008 Neuronetics, Inc, a privately held company in the United States received FDA clearance for its NeuroStar TMS device for the in-office treatment of major depressive disorder. The treatment protocol involves the application of electromagnetic stimulation to the standardized treatment location which is over the left prefrontal cortex, determined by moving the TMS coil 5 cm anterior to the MT location along a left superior oblique plane with a rotation point about the tip of the patient’s nose. Treatment for depression involves 20–30 sessions of about 40 minutes each over a 4–6 week period.

  Diagnostic and Treatment Procedures in Psychiatry

  www.neuronetics.com

Question 94. A. NeuroStar TMS Therapy is indicated for the treatment of major depressive disorder in adult patients who have failed to achieve satisfactory improvement from one prior antidepressant medication at or above the minimal effective dose and duration in the current episode. NeuroStar TMS Therapy noninvasively stimulates the left prefrontal cortex of the brain to treat the symptoms of major depression. It requires 4 to 6 weeks of treatment. Transcranial magnetic stimulation (TMS) is a noninvasive method to cause depolarization or hyperpolarization in the neurons of the brain. TMS uses electromagnetic induction to induce weak electric currents using a rapidly changing magnetic field; this can cause activity in specific or general parts of the brain with minimal discomfort, allowing the functioning and interconnections of the brain to be studied. A variant of TMS, repetitive transcranial magnetic stimulation (rTMS), has been tested as a treatment tool for various neurological and psychiatric disorders including migraines, strokes, Parkinson’s disease, dystonia, tinnitus, depression and auditory hallucinations. In 2008 Neuronetics, Inc, a privately held company in the United States received FDA clearance for its NeuroStar TMS device for the in-office treatment of major depressive disorder.

  Diagnostic and Treatment Procedures in Psychiatry

  www.neuronetics.com

Question 95. C. This patient has acute stress disorder. Remember that depersonalization and derealization are part of the criteria for ASD, but not PTSD. ASD lasts for 2 days to 4 weeks, whereas PTSD must last for 4 weeks or more. Major symptom clusters for both disorders include re-experiencing, avoidance, and increased arousal.

  Anxiety Disorders

  K&S Ch. 16

Question 96. B. The mechanisms behind atypical antipsychotic (AAP) action are not clear. All antipsychotics work on the dopamine system but all vary in regards to the affinity to the dopamine receptors. There are five types of dopamine receptors in humans. There are the “D1-like” group which are types 1 and 5 which are similar in structure and drug sensitivity. The “D2-like” group includes dopamine receptors 2, 3 and 4 and have a very similar structure but very different sensitivities to antipsychotic drugs.

  The “D1-like” receptors have been found to not be clinically relevant in therapeutic action. If D1 receptors were a critical component of the mechanism of AAP blocking just the D1 receptor would improve the psychiatric symptoms that are exhibited. If D1 receptor binding was a critical component of the action of antipsychotics they would need to be present in maintenance dosages. This is not seen. They are not present or present in low or negligible levels which would not even maintain the elimination of the symptoms that are seen.

  The “D2-like” group of dopamine receptors are classified together based on structure but not drug sensitivity. It has been shown that D2 receptor blockade is necessary for action. All antipsychotics block D2 receptors to some degree, but the affinity of the antipsychotics vary from drug to drug and it has been hypothesized that it is the varying in affinities that causes a change in effectiveness.

  One theory for how atypicals work is the “fast-off” theory. This theory of antipsychotic action is that AAP have low affinities for the D2 receptor and only bind loosely to the receptor and are rapidly released. In fact, the AAP bind more loosely to the D2 receptor than dopamine itself. The AAP effectively interfere with the phasic release of endogenous dopamine. The AAP transiently bind and rapidly dissociate from the D2 receptor to allow normal dopamine transmission. It is this transient binding that keeps prolactin levels normal, spares cognition and obviates EPS.

  From a historical point of view there has been interest in the role of serotonin and treatment with the use of antipsychotics. Experience with LSD suggests that 5-HT2A receptor blockade may be a promising method of treating schizophrenia. One problem with this is the fact that psychotic symptoms caused by 5-HT2 receptor agonists differs substantially from the symptoms of schizophrenic psychoses. One promising factor of this is where the 5-HT2A receptors are located in the brain. They are localized on hippocampal and cortical pyramidal cells and have a high density in the fifth neocortex layer where the inputs of various cortical and subcortical brain areas are integrated. This makes the blocking of this receptor an interesting area considering these areas in the brain are of interest in the development of schizophrenia. This is an area of research that could prove convincing but has not yielded any convincing results. Evidence points to the fact that serotonin is not sufficient to produce an antipsychotic effect but serotonergic activity in combination with D2 receptor blockade may be responsible.

  Psychopharmacology

  K&S Ch. 36

Question 97. B. Conversion disorder is highest among rural populations, those with little education, low intelligence, low socioeconomic status, and military personnel who have had combat exposure.

  Somatic Symptom Disorders K&S Ch. 17

Question 98. D. Serotonin is involved in the mechanism of action of two major substances of abuse: LSD (lysergic acid diethylamide) and MDMA (ecstasy; methylenedioxymethamphetamine). The serotonin system is the major site of action of LSD, but exactly how it exerts its hallucinogenic effects is not well-understood. MDMA has dual effects: blocking the reuptake of serotonin and inducing the massive release of the serotonin contents of serotonergic neurons. In animals, it is well understood that MDMA produces selective, long-lasting damage to serotonergic nerve terminals. Users of MDMA show differences in neuroendocrine responses to serotonergic probes, and studies of former MDMA users show global and regional decreases in serotonin transporter binding, as measured by positron emission tomography.

  Substance Abuse and Addictive Disorders

  K&S Chs 3&12

Question 99. C. The MMPI has several validity and clinical scales. There are three validity scales, the lie scale (L scale), the infrequency scale (F scale), and the suppressor scale (K scale). The infrequency scale is useful in identifying malingering, illiteracy, confusion, psychosis, and panic. The lie scale focuses on socially desirable behaviors that are rarely practiced to test if the patient is being honest in answering the questions. The suppressor scale is used to decrease false positives and false negatives. There are 10 clinical scales which focus on specific symptom clusters.

  Psychological Theory and Psychometric Testing

  K&S Ch. 5

Question 100. C. Thyroid hormone can be used in psychiatry on its own, or as an augmenting agent for depressive or bipolar disorder. Liothyronine (Cytomel) is the synthetic oral replacement of endogenous T3 (tri-iodothyronine). Several controlled trials have demonstrated that liothyronine can convert about 50% of antidepressant nonresponders into responders. The dosage of liothyronine is 25 to 50 µg a day added to patient’s antidepressant regimen. Adverse events occur infrequently with liothyronine when given at the dosage noted above. The most common adverse effects are weight loss, palpitations, transient headache, abdominal cramps, diarrhea, sweating, tachycardia, and increased blood pressure. Thyroid hormones should not be taken by patients with cardiac disease, angina, or hypertension. The hormones are contraindicated in thyrotoxicosis and uncorrected adrenal insufficiency and in patients with acute myocardial infarctions. Thyroid hormones can potentiate the effects of warfarin. They can increase the insulin requirements of diabetic patients and the digitalis requirements of patients with cardiac disease. Coadministration of thyroid hormones with SSRIs, tricyclics, lithium or carbamazepine can mildly lower serum thyroxine and raise serum thyrotropin levels. Thus, close serum monitoring is warranted in these patients that may require an increase in dosage of or initiation of thyroid hormone supplementation.

  Psychopharmacology

  K&S Ch. 36

Question 101. B. Eszopiclone is probably best known to most of us as Lunesta. It is a non-benzodiazepine hypnotic medication. It is only indicated for sleep (not depression or anything else for that matter). It does not lead to tolerance over time. Both zolpidem (Ambien) an eszopiclone can lead to hallucinations, sleep walking or other abnormal behaviors. So given this patients sleep walking, eszopiclone may not be the best alternative. As for choice C… the sleep medication famous for being a melatonin agonist is ramelteon (Rozerem). I’m sure you will come across it again elsewhere in this book!

  Psychopharmacology

  K&S Ch. 36

Question 102. D. GGT (gamma-glutamyl transpeptidase) is the most sensitive marker for alcohol abuse. In can be elevated in as many as ¾ of patients with alcohol dependence. It can also be increased by obesity, fatty liver, medications, as well as other types of liver disease. It usually takes up to 8 weeks for the GGT to return to normal following cessation of alcohol consumption.

  Laboratory Tests in Psychiatry

  K&S Ch. 12

Question 103. C. You cannot lie to the insurance company. That would be simply unethical. The important therapeutic work to do is to understand the request and why the patient is making it, and help him explore his feelings about it. Giving a different false diagnosis is no more ethical than calling it an adjustment disorder, and kicking the patient out of your office is abdication of your responsibility as a therapist to help the patient cope with their illness.

  Ethics

  K&S Ch. 58

Question 104. C. Adrenal insufficiency (a.k.a. Addison’s disease) is a condition in which there is decreased production of mineralocorticoids, glucocorticoids, and sex hormones by the adrenal gland. There are primary, secondary and tertiary causes. Primary comes from direct damage to the adrenal gland. Secondary comes from pituitary disease. Tertiary comes from malfunction of the hypothalamus. This condition is fair game for a psychiatry exam because it can present with psychiatric symptoms. Most commonly these include depression, apathy, and irritability, but psychosis and delirium are also possible. Mania is not a common presentation. Patients may also experience fatigue, weight loss, hyperpigmentation, hypotension, nausea, vomiting, salt craving, dizziness, joint and muscle pain. Treatment consists of IV hydrocortisone in acute cases and treatment with prednisone or oral hydrocortisone in chronic cases.

  Somatic Symptom Disorders

  K&S Ch. 28

Question 105. A. When giving lamotrigine and valproic acid together lamotrigine levels are elevated and valproic acid levels are decreased. When giving lamotrigine and carbamazepine together lamotrigine levels are decreased. Valproic acid will increase carbamazepine levels. Because lithium is cleared renally it will not affect the levels of lamotrigine, valproic acid, or carbamazepine.

  Psychopharmacology

  K&S Ch. 36

Question 106. D. This question touches on the neurochemical changes that we associate with aggression. In aggressive patients we would expect to find increased dopamine, decreased serotonin, decreased GABA, increased testosterone, and increased acetylcholine.

  Basic Neuroscience

  K&S Ch. 3

Question 107. C. This question tests your knowledge of motor development during infancy. Choice C is incorrect because the grasp and tonic neck reflexes begin to recede between 2 to 6 months. All other choices are correct and are good markers to keep in mind to measure normal development. Motor development should be looked at in conjunction with cognitive and social development when evaluating a young child for psychiatric reasons.

  Human Development

  K&S Ch. 2

Question 108. D. Tardive dyskinesia (TD) is a delayed effect of antipsychotics. It is rarely seen until after 6 months of treatment. The disorder manifests as abnormal, involuntary, irregular choreoathetoid movements of the muscles of the trunk, limbs and head. Perioral movements are the most common and manifest as darting, twisting and protruding movements of the tongue, as well as chewing, lateral jaw movements, lip puckering and facial grimacing. In severe cases, torticollis, retrocollis, pelvic thrusting and trunk twisting can be seen. Dyskinesia disappears during sleep and is exacerbated by stress and anxiety. TD develops in about 10 to 20% of patients treated for more than a year. About 20 to 40% of patients with long-term psychiatric hospitalization have TD. Women are more likely to develop TD than men. Children, patients over 50 years of age and those with brain damage or mood disorders, are also at greater risk. Between 5 and 40% of all cases of TD remit and between 50 and 90% of all mild cases of TD remit. TD is less likely to remit in elderly patients than in young patients, however.

  Management in Psychiatry

  K&S Ch. 36

Question 109. A. This question tests some important facts about commonly used benzodiazepines. Let’s review the data. Clonazepam has a rapid rate of absorption, a half-life of 34 hours, and is considered long acting. Alprazolam has a medium rate of absorption, a half-life of 12 hours, and is considered short acting. Diazepam has a rapid rate of absorption, a half-life of 100 hours, and is considered long acting. Lorazepam has a medium rate of absorption, a half-life of 15 hours, and is considered short acting.

  Psychopharmacology

  K&S Ch. 36

Question 110. D. For most anxiety disorders the rates are higher for women than for men.

  The only anxiety disorder with equal rates between men and women is obsessive–compulsive disorder.

  Anxiety Disorders

  K&S Ch. 16

Question 111. E. Appropriate monitoring of WBC count for patients on clozapine is as follows. First get a baseline WBC before the drug is started. Then monitor WBC weekly for the first 6 months…then biweekly for the next 6 months…then monthly thereafter. Following discontinuation of clozapine monitor weekly WBC for 4 consecutive weeks.

  Laboratory Tests in Psychiatry

  K&S Ch. 36

Question 112. D. Common side effects of lithium include sedation, confusion, tremor, hair loss, nephrogenic diabetes insipidus, polyuria, polydipsia, acne, weight gain, nausea, diarrhea, and hypothyroidism. Lithium toxicity can lead to coma, seizures and death. Neural tube defects are caused in fetuses when the mother takes Depakote. When pregnant women take lithium it causes Ebstein’s anomaly, which is a cardiac malformation of the tricuspid valve. Risk of Ebstein’s anomaly are greatest when lithium is taken during the first trimester.

  Psychopharmacology

  K&S Ch. 36

Question 113. E. This question looks at management of alcohol withdrawal. During alcohol withdrawal it is preferable to use long acting benzodiazepines such as chlordiazepoxide. As such alprazolam, which is short acting, is not a good choice. It would also have to be dosed more frequently than BID to actually cover the patient for 24 hours. IV thiamine and dextrose should be given for the first 3 days then switch to PO thiamine. Some argue that after the first IV dose, that the doses for the remainder of the 3 days can be given IM then switched to PO. Regardless of which method you advocate, giving the meds IV for 9 days is clearly wrong. Disulfiram is an aversive treatment used to stop a patient from drinking again who is currently detoxed and sober. It will make the patient sick if they have a drink while on the medication. It is not used to manage withdrawal. In a hepatically impaired patient one would choose lorazepam over clonazepam. This can be remembered by the phrase “Tolerated by Our Liver” or TOL – which stands for Temazepam, Oxazepam, Lorazepam – the three benzos safe to use in hepatic impairment. When using lorazepam for alcohol withdrawal it should be dosed QID for even coverage, then tapered off over three days.

  Substance Abuse and Addictive Disorders

  K&S Ch. 12

Question 114. C. Acute dystonia is a rapid onset spastic contraction of discrete muscle groups such as the neck, eyes, back or tongue. Akathisia is a sensation of restlessness and an irresistible urge to move parts of the body. Tardive dyskinesia is a choreoathetoid movement of the tongue, mouth, face, extremities or trunk that is involuntary and irregular. Blepharospasm is an involuntary spasm of the muscles surrounding the eye.Tardive dystonia is a slow sustained twisting movement of the limbs, trunk and neck. It usually occurs late in onset following treatment with antipsychotics.

  Psychopharmacology

  K&S Ch. 12

Question 115. D. All choices listed are inducers of CYP450 3A4 except fluoxetine, which is an inhibitor. Other inhibitors include calcium channel blockers, cimetidine, grapefruit juice, and antifungals.

  Psychopharmacology

  K&S Ch. 3

Question 116. C. Asking the patient to consent to treatment is an example of respecting a patient’s autonomy. Autonomy is the belief that a patient has a right to control what happens to their own bodies and make decisions freely and without coercion. All of the other choices are legal or ethical terms which will be the subject of their own questions throughout this text. Pay attention to them the next time you see them.

  Ethics

  K&S Ch. 58

Question 117. B. On average depressed patients require 6–12 ECT treatments to treat depression. Some cases may require as many as 30 treatments, but these are the exception rather than the rule. Treatments are often given three times per week with one seizure per treatment. The use of more than one seizure per episode has no proven advantages. The preference is for unilateral electrode placement because it lessens memory impairment from the procedure. If a patient fails to improve after six unilateral treatments then bilateral electrode placement should be considered.

  Diagnostic and Treatment Procedures in Psychiatry

  K&S Ch. 36

Question 118. C. The SCID does not include functional impairment. However functional impairment is covered in the SCAN (Schedule for Clinical Assessment in Neuropsychiatry) and the SCAN is thought to give a broader assessment of psychosocial function than the SCID. The SCID covers the following topics: General overview (demographics, medical, psych services and med use histories), mood episodes, psychotic symptoms, psychotic disorders differential, mood disorders differential, substance use, anxiety disorders, somatoform disorders, eating disorders, and adjustment disorders.

  Diagnostic and Treatment Procedures in Psychiatry

  K&S Ch. 5

Question 119. D. Self-disclosure by the therapist is only acceptable when it is done solely for the benefit of the patient. It must be the patient’s needs that drive the disclosure. The therapist must be very careful not to disclose things for their own benefit. Whether the disclosures are true is irrelevant. The focus of therapy should always be on the patient. That’s what matters.

  Psychotherapy

  K&S Ch. 1

Question 120. D. To boil this question down to its most basic facts, you have an elderly patient who is looking delirious and is on carbamazepine. Though there are a myriad of possible explanations for why an elderly patient can be delirious, the astute psychiatrist knows that carbamazepine has a vasopressin-like effect which can lead to hyponatremia. Therefore one of the first things you would want to look for in a confused patient on carbamazepine is the basic metabolic panel, more specifically the sodium level.

  Psychopharmacology

  K&S Ch. 36

Question 121. C. Of all the medications listed all are metabolized by the liver except paliperidone (Invega). Paliperidone is 80% excreted through the kidney so you must be careful in using it in patients with renal impairment. It is a good choice for patients with hepatic impairment however. Paliperidone is the active metabolite of risperidone. Risperidone is metabolized through the liver.

  Psychopharmacology

  K&S Ch. 36

Question 122. A. Validity is the degree to which an instrument measures what it is intended to measure. There are different types of validity. Face validity means a diagnosis is based on a general consensus among experienced clinicians and researchers. Descriptive validity means that a diagnosis is based on characteristic features that distinguish it from other disorders. Predictive validity means that a diagnosis will allow clinicians to accurately predict treatment response and clinical course. Construct validity means that a diagnosis is based on an understanding of the underlying pathophysiology. Positive Predictive Power is the ability of a positive test result to predict disease. It is calculated as true positives divided by true positives plus false positives.

  Statistics

  K&S Ch. 4

Question 123. E. Desvenlafaxine extended release tablets are approved for treatment of MDD in adults. Desvenlafaxine is an SNRI. The usual dosage is 50 mg PO QD. Care must be taken with the dose in renally compromised patients and in the elderly. Side effects include orthostasis, hyponatremia (especially in the elderly) and hypertension, much like venlafaxine. There is a black box warning to monitor for suicidality especially for children and teens, as there is with all of the SSRIs and SNRIs.

  Psychopharmacology

  Physicians Desk Reference, 64th edition 2010, PDR Network LLC, Montvale NJ USA, p 3564

Question 124. D. This patient would qualify for a GAF of 35, which represents impaired reality testing or communication and major impairment in functioning in several areas. The GAF scale is fair game for standardized exams. We will not reproduce the whole scale here but you should spend some time familiarizing yourself with the details before your exam. Some rough guidelines are that anyone above 60 has minor symptoms and is mostly functioning well. Anyone below 20 is either persistently dangerous to self or others or has severely impaired functioning. A score of 30 to 50 fit in between these extremes. Just knowing these rough landmarks you could have answered this question without memorizing every detail of the whole scale. Make sure you have some landmarks of your own in mind before your exam!

  Diagnostic and Treatment Procedures in Psychiatry

  K&S Ch. 7

Question 125. E. A large proportion of the elderly population complains of difficulty in initiating and maintaining sleep, early-morning awakening, unrefreshing sleep, and daytime sleepiness. Many resort to napping. Polysomnographic investigations have supported these findings, and have revealed a gradual decrease in stages 3 and 4 sleep (delta sleep; aka slow-wave sleep) and an increase in stage 1 sleep. There may also be a decreased amount of REM sleep in the elderly. Additionally, sleep efficiency progressively decreases and the propensity for daytime napping increases, although it is still a matter of investigation as to whether the elderly are truly sleepier during the day. There also appears to be a progressive advance in the sleep/wake times with aging, related to a gradual phase advance in the internal biological clock; this may explain the common complaint of seniors that they fall asleep early in the evening, yet awaken much earlier than desired in the morning and cannot fall back to sleep easily. Because aging is also associated with an increased risk for medical and psychiatric disorders, which can also disrupt sleep, it may be difficult to ascertain, in any individual case, whether the sleep-related alterations are a “normal” consequence of the aging process itself or secondary to other disorders.

  Sleep Wake Disorders

  K&S Ch. 24

Question 126. B. Atomoxetine is a norepinephrine reuptake inhibitor approved for the treatment of ADHD in both children and adults (ages 6 years and above). It may take up to 10 weeks after starting treatment to reach optimal effect. Once daily dosing works well for most patients. Most common side effects include dizziness, reduced appetite, and dyspepsia. Similar to the SSRIs, atomoxetine carries a black box warning for suicidality. It is metabolized primarily by the liver and reports suggest that combination of atomoxetine with stimulants is well tolerated and effective.

  Psychopharmacology

  K&S Ch. 36

Question 127. B. The theory that empathic failures in the mother lead to developmental arrest in the child at a stage when the child needs others to help perform self-object functions is the work of Heinz Kohut. He specifically applied this theory to narcissism and later expanded it to other pathology as well. He viewed the development of self-esteem and self-cohesion as more important than sexuality or aggression. 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. Other famous therapists listed in this question are the subject of their own questions elsewhere in this text.

  Psychological Theory and Psychometric Testing

  K&S Ch. 4

Question 128. D. Vivitrol (naltrexone extended release injectable suspension) is a long acting injection of naltrexone used to control cravings in alcohol dependence. Naltrexone pills are often used to control alcohol craving in those trying to maintain sobriety and this injectable form of naltrexone aims to increase compliance and lower rates of relapse. It is given as a 380 mg IM injection every 4 weeks. Vivitrol was FDA-approved for opioid relapse prevention in 2010.

  Psychopharmacology

  http://www.vivitrol.com/

Question 129. B. The HAM-D (Hamilton depression rating scale) is used to evaluate depression. The GAF (Global Assessment of Functioning) rates overall level of functioning and is not linked to any one illness. The PANSS (Positive and Negative Symptom Scale) rates severity of psychosis. The BPRS (Brief Psychiatric Rating Scale) rates severity of psychosis. The CAGE is a questionnaire used to evaluate alcohol abuse.

  Diagnostic and Treatment Procedures in Psychiatry K&S Ch. 5

Question 130. E. The medication described in the question stem is Duloxetine (Cymbalta). It inhibits reuptake of both serotonin and norepinephrine. It has an indication for neuropathic pain. It lacks significant cholinergic, antihistaminic and alpha adrenergic effects. The side effect profile is similar to the SSRIs, however it is worth noting that abrupt discontinuation will give clear withdrawal symptoms (yes, paroxetine is known for this as well) and unlike the other SNRI venlafaxine, hypertension is not common with duloxetine. Of note, duloxetine is also FDA-approved for treatment of fibromyalgia.

  Psychopharmacology

  K&S Ch. 36

Question 131. D. Patients taking an MAOI have dietary restrictions to avoid hypertensive crisis. All of the foods listed in the question are restricted except for vodka. Small amounts of clear alcohol may be used, but patients should avoid tap beer, red wines, some white wines, and aged sherry.

  Psychopharmacology

  K&S Ch. 36

Question 132. D. This is a case of inhalant intoxication. This patient has been sniffing something out in the garage. The perioral rash should be a big clue. When inhalants contact the skin it dries out leading to small cracks which allow bacteria to enter. A dermatitis can develop which looks like a nonspecific contact hyperactivity reaction or perioral eczema. It is known as a “huffer’s rash.” Criteria for inhalant intoxication include recent exposure to volatile inhalants followed by change in behavior. The patient often becomes agitated, belligerent, assaultive, or apathetic. If bad enough this state can progress into a delirium, coma, or be fatal. The patient also must have 2 of a possible 13 neurologic signs. These signs include dizziness, nystagmus, incoordination, slurred speech, unsteady gait, lethargy, depressed reflexes, psychomotor retardation, tremor, muscle weakness, blurry vision, stupor, and euphoria.

  Substance Abuse and Addictive Disorders

  K&S Ch. 12

Question 133. B. Narcolepsy is a sleep disorder characterized by excessive daytime sleepiness with sleep attacks, as well as other characteristics that are manifested by the intrusion of REM sleep into wakefulness. The onset of the disorder in most cases is in adolescents and young adults, with a peak incidence between ages 15 and 30. The classic sleep attack, which occurs in virtually 100% of narcoleptic patients, is an irresistible desire to fall asleep in inappropriate circumstances and at inappropriate places (e.g., while talking, driving, eating, playing, walking, running, working, sitting, listening to lectures, watching television or movies, during sexual intercourse, or when involved in boring or monotonous circumstances). These spells last for a few minutes to as long as 20 to 30 minutes. The patient generally feels refreshed on waking. There are wide variations in frequency of attacks, anywhere from daily, weekly, monthly, or every few weeks to months. Attacks generally persist throughout the patient’s lifetime, although fluctuations and rare temporary remissions may occur. Patients often show a decline in performance at school and work and encounter psychosocial and socioeconomic difficulties as a result of sleep attacks and excessive daytime sleepiness (EDS). Sudden loss of tone in all voluntary muscles except the respiratory and ocular muscles characterizes cataplexy. The attacks are triggered by emotional factors such as laughter, rage, or anger more than 95% of the time. The attacks may be complete or partial and are rarely unilateral. Most commonly, the patient may momentarily have head nodding, sagging of the jaw, buckling of the knees, dropping of objects from the hands, dysarthria, or loss of voice, but sometimes they may slump or fall forward to the ground for a few seconds. The duration is usually a few seconds to a minute or two, and consciousness is retained completely during the attack. An EEG recording shows evidence of wakefulness during brief cataplectic spells, but if the attack lasts longer than 1 to 2 minutes, the EEG shows REM sleep. This is indicative of decreased REM latency during attacks. In approximately 25 to 50% of patients, sleep paralysis is noted, generally months to years after the onset of narcoleptic sleep attacks. The sudden apparent paralysis of one or both sides of the body or one limb occurs either during sleep onset (hypnagogic) or on awakening (hypnopompic) in the morning. The patient is unable to move or speak and is frightened, although he or she retains consciousness. The attacks last from a few minutes to 15 to 20 minutes. In 20 to 40% of narcoleptic patients, hypnagogic hallucinations occur either at sleep onset or on awakening in the morning and generally appear months to years after the onset of sleep attacks. Hallucinations are most commonly vivid and visual (and often fear-inducing), but are sometimes auditory, vestibular, or somesthetic in nature. In 30% of patients, three of the four major manifestations of the narcoleptic tetrad (sleep attacks, cataplexy, sleep paralysis, and hypnagogic hallucinations) occur together, and in about 10% of cases all four major features occur together. Disturbed night sleep is commonly noted in 70 to 80% of patients. In approximately 20 to 40% of cases, automatic behavior, characterized by repeated performance of a single function such as speaking or writing in a meaningless manner or driving on the wrong side of the road or to a strange place without recalling the episode, is noted. These episodes of automatic behavior may result from partial sleep episodes, frequent lapses, or microsleeps. In patients with narcolepsy, HLA typing may be performed because most of the patients with narcolepsy show positivity for HLA DR2DQ1, and DQB1*0602 antigens.

  Sleep Wake Disorders

  K&S Ch. 24 and B&D Ch. 72

Question 134. C. Jimmy is moderately mentally retarded. The ranges you should memorize for the exam are as follows. Above 70 is not mentally retarded; 50–70 is mild mental retardation; 35–50 is moderate mental retardation; 20–35 is severe mental retardation. Less than 20 is profound mental retardation.

  Neurodevelopmental and Pervasive Developmental Disorders

  K&S Ch. 5

Question 135. D. This question covers some important facts about clozapine. Doses greater than 600 mg/day substantially increase the chance of developing seizures than lower doses. Clozapine is very anticholinergic and antihistaminic and has high likelihood of leading to weight gain and metabolic syndrome. NMS occurs rarely but adding lithium to clozapine increases the chances of developing NMS. Agranulocytosis can occur at any dose and is not dose related. Because of its impact on the CYP450 system, smoking can decrease clozapine levels.

  Psychopharmacology

  K&S Ch. 36

Question 136. B. In delusional disorder the patient usually has a non-bizarre delusion of at least 1 month duration. They do not have any other psychotic symptoms that would classify them as schizophrenic. As such, criteria A are not met and there is a relative preservation of function. In some cases the patient may have olfactory or tactile hallucinations but these are directly linked in some way to the delusional theme. The DSM specifies several subtypes. These subtypes are erotomanic, grandiose, jealous, persecutory, somatic, mixed and unspecified.

  Psychotic Disorders

  K&S Ch. 14

Question 137. E. Most people do not experience PTSD symptoms, even when faced with severe trauma. The lifetime prevalence of PTSD is about 6.7%, as per the National Comorbidity Study. As per that same study about 60% of males and 50% of females had experienced some significant trauma. Evidence points to a “dose–response” relationship between the degree of trauma and the likelihood of symptoms. The subjective meaning of the trauma to the individual is also extremely important. The predisposing vulnerability factors in PTSD are as follows:

1. Presence of childhood trauma.

2. Borderline, paranoid, dependent, or antisocial personality disorder traits.

3. Inadequate family or peer supports.

4. Female gender.

5. Genetic predisposition to mental illness.

6. Recent life stressors.

7. Perception of an external locus of control to the trauma (natural cause) as opposed to an internal one (human cause).

8. Recent alcohol abuse.

  Anxiety Disorders

  K&S Ch. 16

Question 138. B. Schizophrenic patients are no more likely to commit homicide than anyone in the general population at large. When a schizophrenic patient does commit murder, it may be for unpredictable or bizarre reasons due to delusions and/or hallucinations. Predictors of future homicidal behavior include a prior history of violence, dangerous behavior while hospitalized, and delusions or hallucinations involving this kind of violence. By contrast, schizophrenic patients are more prone to suicide attempts and completed suicide than the general population at large. Suicide attempts are made by 20 to 50% of schizophrenic patients. Long-term rates of suicide among schizophrenic patients are estimated at 10 to 13%. This reflects about a 20-fold increase in the suicide rate over the general population. The most important predictor of suicide in schizophrenic patients is the presence of a major depressive episode.

  Psychotic Disorders/Public Policy

  K&S Ch. 13

Question 139. D. This is a tricky question that can easily fool you if you are not familiar with the symptoms of Sheehan’s syndrome. Sheehan’s syndrome is a postpartum pituitary necrosis that can lead to chronic symptoms which can easily be mistaken for depression and misdiagnosed. Symptoms of Sheehan’s syndrome include failure to lactate, hypotension, weight loss, loss of secondary sex characteristics, scant menses, constant fatigue, and diminished libido. These symptoms can develop months or even years after the birth. Diagnosis of Sheehan’s syndrome is made by first looking for history of failure to make breast milk or failure to resume menstruation after birth. If suspected, pituitary hormone levels are checked followed by MRI to examine the pituitary. Important to keep in mind is that DSM criteria for postpartum depression states that it must onset within 4 weeks of the birth. When we consider this patient in light of our knowledge of Sheehan’s it is clear that an endocrine workup to rule out the disease must be our first step, especially considering her failure to produce breast milk. To immediately treat the situation as if she has a major depressive disorder or anxiety disorder from the stress of the new baby would be missing a very important diagnostic rule out. There is no evidence of child abuse given here and as such child protective services should not be called.

  Somatic Symptom Disorders

  K&S Ch. 3

Question 140. D. This question focuses on avoidant personality disorder. Patients with this disorder tend to avoid interpersonal interaction out of fear of shame and ridicule. They are hypersensitive to negative evaluation by others. They are unwilling to get involved with others without certainty of being liked. They are inhibited interpersonally because of fears of inadequacy. They see themselves as inferior to others. They are often misdiagnosed as dependent personality disorder and in some cases are very hard to distinguish from generalized social phobia.

  Other answer choices reflect characteristics of other personality disorders:

  “These patients tend to be indifferent to praise or criticism” – schizoid.

  “Affective instability is a key component of the disorder” – borderline.

  “These patients are unable to discard worthless objects” – OCPD.

  Personality Disorders K&S Ch. 27

Question 141. B. Acute intermittent porphyria is one of the medical illnesses that is fair game for a psych exam because of the prominence of psychiatric symptoms in its presentation. It is a disorder of heme synthesis which leads to a buildup of porphyria. This leads to the classic triad of abdominal pain, peripheral neuropathy, and psychiatric disturbance. Psychiatric symptoms may come in the form of delirium, psychosis, depression, or anxiety (sorry, no dementia). The diagnosis is confirmed by looking for metabolites of porphyrins in the urine. This is the illness thought responsible for the “madness” of King George III.

  Somatic Symptom Disorders

  K&S Ch. 10

Question 142. D. Most studies point to a prevalence of Alzheimer’s disease of about 20–40% in the 85 years and over age range. Other statistics of note include the fact that 50 to 60% of patients that are demented have Alzheimer’s disease. The second most common type of dementia is vascular dementia which accounts for approximately 15 to 30% percent of all dementia cases. Alzheimer’s disease is slightly more prevalent in women than in men throughout the life cycle, about 1.3 to 1. Vascular dementia is more prevalent in men than women and is most common in the 60 to 70 age range. About 10 to 15% of patients have comorbid Alzheimer’s disease and vascular dementia.

  Neurocognitive Disorders/Public Policy

  K&S Ch. 10

Question 143. E. It is important to understand legal issues surrounding the suicidal patient. The law does not impose liability on the psychiatrist whenever a patient commits suicide. It asks whether the suicide was foreseeable and how a reasonable psychiatrist would have addressed the likelihood of harm. All potential harm is not viewed as foreseeable or predictable. The standard of care calls for documentation of risk assessment and implementation of appropriate precautions to protect the patient. No-harm contracts between therapist and patient do not protect the therapist from liability in the event of a suicide.

  Forensic Psychiatry

  K&S Ch. 57

Question 144. D. The definition of “disability” under the Americans with Disabilities Act (ADA) reflects the intent of Congress to prohibit the specific forms of discrimination that persons with disabilities face. While individuals with disabilities may experience the types of discrimination that confront other groups, they also may encounter unique forms of discrimination because of the nature of their disabilities and the effect that their present, past, or perceived conditions have on other persons. The purpose of the ADA is to eliminate discrimination that confronts individuals with disabilities. Since the definition of the term “disability” under the ADA is tailored to the purpose of eliminating discrimination prohibited by the ADA, it may differ from the definition of “disability” in other laws drafted for other purposes. For example, the definition of a “disabled veteran” is not the same as the definition of an individual with a disability under the ADA. Similarly, an individual might be eligible for disability retirement but not be an individual with a disability under the ADA. Conversely, a person who meets the ADA definition of “disability” might not meet the requirements for disability retirement.

  The statutory definition – with respect to an individual, the term “disability” means

  (A)a physical or mental impairment that substantially limits one or more of the major life activities of such individuals;

  (B)a record of such an impairment; or

  (C)being regarded as having such an impairment.

  A person must meet the requirements of at least one of these three criteria to be an individual with a disability under the Act.

  Public Policy

  K&S Chs 2&8

Question 145. E. The homeless mentally ill are a significant public policy concern. Their population continues to grow with large numbers of homeless people carrying a psychiatric diagnosis. Many of them are also dependent on substances. Street dwellers tend to be schizophrenic with substance abuse. Episodically homeless tend to have personality disorders, substance abuse, and mood disorders. These of course are generalizations and exceptions can be found. Traditional mental health delivery systems often fail to successfully treat the homeless due to a variety of factors. Successful treatment for this population is often very non-conventional including street outreach programs.

  Public Policy

  K&S Ch. 4

Question 146. E. This is an easy one. No sex with patients or former patients…ever, under any circumstances. No former sexual partners as current patients either.

  Ethics

  K&S Ch. 58

Question 147. E. Varenicline (Chantix) is a partial nicotine agonist that decreases withdrawal and cravings as well as blocks the reinforcing effects of nicotine. Whereas nicotine replacement and bupropion have been shown to double quit rates, varenicline triples quit rates. Take note of its warning for behavioral changes such as hostility, agitation, depression, suicidal thoughts either during treatment of after stopping treatment. The most common side effect is nausea.

  Psychopharmacology

  K&S Ch. 12

Question 148. A. Treatment of organophosphate poisoning 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. The dose of pralidoxime can be repeated if no obvious benefit occurs, but in refractory cases it may need to be given by intravenous infusion, the dose being titrated against clinical response. Functional recovery may take approximately 1 week, although acetylcholinesterase levels take longer to reach normal levels. Measurement of paraoxonase status may be worthwhile as a biomarker of susceptibility to acute organophosphate toxicity; this liver and serum enzyme hydrolyzes a number of organophosphate compounds and may have a role in modulating their toxicity.

  Chelation therapy with either water-soluble derivatives of dimercaprol (DMSA or DMPS) or penicillamine is effective in controlling the systemic effects of acute arsenic poisoning and may prevent the development of neuropathy if it is started within hours of ingestion. Lead encephalopathy is managed supportively, but corticosteroids are given to treat cerebral edema, and chelating agents (dimercaprol or 2,3-dimercaptopropane sulfonate) are prescribed also.

  Poisoning

  B&D Ch. 58

Question 149. E. HIPAA stands for Health Insurance Portability and Accountability Act. It contains rules to protect the transmission and confidentiality of patient information. The privacy rule is one that is very relevant to psychiatric practice. It applies to all protected health information whether on paper, electronic, or spoken. Some of the important points to keep in mind are as follows: Patients have a right to a written copy of their privacy rights. They also have a right to know how their protected information will be stored and disclosed. Patients have a right to a copy of their medical record. This does not include psychotherapy notes. Authorization must be obtained from the patient for release of their health information. Exclusions to this rule involve routine uses such as treatment, obtaining payment from the insurance company, or health care operations. Patients do have the right to dictate how their information is communicated. For example they can tell a doctor not to call their home phone number and only call their cell phone in order to protect their privacy, or dictate a specific address to which all confidential information must be sent.

  Forensic Psychiatry

  K&S Ch. 57

Question 150. A. To answer this question correctly you needed to know the mechanism of action of Mirtazapine. Mirtazapine works through antagonism at presynaptic alpha-2 receptors thereby potentiating the actions of serotonin and norepinephrine. It does NOT block reuptake of serotonin or norepinephrine. It is a potent H1 antagonist which explains why it is sedating and causes increased appetite and weight gain. It has minimal sexual side effects.

  Psychopharmacology

  K&S Ch. 36