1. Dementias As of 4Feb2015. All items from DSM-IV, DSM-5, APA Practice Guidelines, Taman/Mohr Text, or Sadock/Sadock/Ruiz Text unless otherwise indicated.

2. Dx criteria Q. What is the outline of the DSM dx criteria of dementia?

3. Dx criteria - general Ans. 1. Multiple cognitive deficits. 2. Gradual onset and decline 3. Not part of another Disorder

4. Dx criteria – Specific Cognitive deficits Q. What cognitive deficits are part of the DSM criteria of dementia?

5. Dx – specific cognitive deficits Ans. 1. Memory impairment AND 2. At least one of the following: –Aphasia –Apraxia –Agnosia –Executive functioning deficits

6. Early onset Q. What is the dividing line between early and late onset dementia?

7. Early Onset Ans. < or = 65, early onset > 65, late onset

8. Reasons to hospitalize Q. List reasons to hospitalize pts with dementia.

9. Reasons to hospitalize Ans. 1. Symptom severity: –Dangerousness to self or others, including inability of caretakers to care for the pt 2. Intensity of care and treatment needed: -- evaluations or treatments that cannot by done on outpt basis.

10. Follow-up Q. If you have a “routine” pt with Alzheimer’s, how often should the pt be monitored by you?

11. Follow-up Ans. Every 3 to 6 months.

12. MMSE Q. What is the MMSE? And What does it evaluate?

13. MMSE Ans. MMSE = Mini-mental status examination. MMSE tests cognitive functioning.

14. CT or MRI Q. When is CT or MRI advised as part of the initial eval of people with dementia?

15. CT or MRI Ans. Some would say in all, but the question is more likely to focus on when one of these tests is more indicated than most pts with dementia: –Early onset –Relatively rapid onset –High vascular risk factors suggested –Neurological exam suggests local lesions

16. Neuropsych testing Q. When is neuropsych testing indicated?

17. Neuropsych testing Ans. When questions arise as to whether the individual actually has a “dementia.” [Keep in mind that only Mental Retardation and Learning Disorders has psychological testing as part of a DSM criteria set.]

18. Gene testing Q. Is gene testing recommended?

19. Gene testing Ans. Gene testing is not recommended. Dx is clinically based regardless of genes. [See exceptions infra]

20. Apolipoprotein E-4 Q. What is the significance of apolipoprotein E-4 (APOE-4)?

21. Apolipoprotein E-4 Ans. Apolipoprotein E-4 [APOE-4], on chromosome 19, is more common in individuals with Alzheimer’s – but not diagnostic.

22. Suicidal Q. At what stage of a dementia is suicidal ideation most common?

23. Suicidal Ans. Most common when the disease is still mild.

24. Suicide and gender Q. Which gender is suicide most common in this illness?

25. Suicide and gender Ans. Men [In answering exam questions as to “successful” suicides, keep in mind that men do so far more often than women, and that is even more true in the elderly.]

26. Falls Q. Give one of major ways a physician can reduce the chances of falls in pts with dementia.

27. Falls Ans. Review and considered discontinuance of meds associate with falls.

28. Driving Q. Should a physician report their patient who has dementia to the state department of motor vehicles?

29. Driving Ans. Varies by state. Required in some, forbidden in others.

30. Dosing in the elderly Q. What are the principles of medicating in the elderly?

31. Medicating the elderly Ans. -- lower starting doses. -- longer intervals between dose increases. -- smaller dose increase

32. Medicating rules - why Q. Why the go-slow approach with the elderly?

33. Medicating rules - why Ans. slower hepatic metabolism decreased renal clearance

34. Goal of medicating Q. What is the goal of medicating a patient with Alzheimer’s?

35. Goal of medicating Ans. Delay progression of the disease. No med reverses.

36. FDA for Alzheimer’s Q. What meds have been approved for Alzheimer’s?

37. FDA for Alzheimer’s Ans. donepezil galantamine memantine rivastigmine tacrine

38. FDA – med action Q. Which of the five is/are cholinesterase inhibitors? Which is/are NMDA antagonist?

39. Meds - actions Ans. donepezil, galantamine, rivastigmine, and tacrine are cholinesterase inhibitors. memantine is a noncompetitive N-methyl- aspartate antagonist, glutamate antagonist.

40. Vitamin E Q. What about high doses of Vitamin E for Alzheimer’s?

41. Vitamin E Ans. Not proven to be useful and high doses may be associated with increased risk of heart failure. Vitamin E must be avoided in patients with vitamin K deficiencies.

42. Q. Selegiline 1] Selegiline’s usefulness in dementia? 2] Especially problematic?

43. Ans. Selegiline 1] Not proven to be useful. 2] Should not be given to pt on an antidepressant.

44. Tacrine Q. Tacrine status?

45. Tacrine Ans. Regarded as less preferred to donepezil, rivestigmine, and galantamine because of tacrine’s hepatic toxicity.

46. ECT Q. Indications for ECT in pts with Alzheimer’s?

47. ECT Ans. Indicated for pts with moderate to severe depression and Alzheimer’s and who do not respond to or cannot tolerate antidepressant meds.

48. Delusions and hallucinations Q. Pt is moderately impaired from Alzheimer’s, has delusions and hallucinations and is not distressed or agitated, meds?

49. Hallucinations and delusions Ans. No meds, instead reassurance, redirection and distractions.

50. Hallucinations and delusions Q. Alzheimer’s pt with hallucinations and delusions and combative, meds?

51. Hallucinations and delusions Ans. Low dose antipsychotic. [This is true of the Guides. Recent FDA warnings would suggest ordering antipsychotics at quite low levels to begin - - given the increased death rate of the elderly on antipsychotics.]

52. Profoundly impaired Q. What meds help the cognition of the severely impaired?

53. Profoundly impaired Ans. Memantine is approved for the profoundly impaired. Cholinesterase inhibitors are not.

54. Meds & Delirium Q. What classes of meds can cause delirium in those with Alzheimer’s?

55. Delirium & meds Ans. Virtually all psychotropic meds, even more so, those having anticholinergic activity.

56. Anticholinergic Q. What are some meds psychiatrists use that have anticholinergic activity?

57. Anticholinergic Ans. Tricyclics, low-potency antipsychotics, and diphenhydramine.

58. Dopaminergic meds Q. Dopaminergic meds used in Parkinson’s disease in pt who also has Alzheimer’s predisposes that pt to?

59. Dopaminergic meds Ans. Visual hallucinations

60. Vascular dementia Q. Treatment for vascular dementia?

61. Vascular dementia Ans. -- control BP -- low-dose aspirin [2 of 3 trials with donepezil found some positive results, but the 3 rd trial lack of effectiveness probably precludes it being the correct answer.]

62. Fronto-temporal dementia Q. What med has been shown to decrease problematic behaviors of fronto-temporal dementia, e.g., agitation?

63. Fronto-temporal dementia Ans. Trazodone. [If trazodone is not one of the choices, amantadine has some anecdotal support.]

64. Caregivers and depression Q. To what degree does depression occur in caregivers?

65. Caregivers and depression Ans. 30% of spousal care-givers experience a depressive disorder. 22-37% of adult children care-givers, the higher percentage, > 30%, in those with a prior hx of a mood disorder.

66. Federal Regulation Q. A major law, passed in 1987, that regulates the use of physical restraints and use of meds in nursing home is?

67. Federal Regulation Ans. The Omnibus Budget Reconciliation Act of 1987 [OBRA].

68. Gender Q. In Alzheimer’s, which gender is more frequent?

69. Gender Ans. More common in women.

70. African Americans Q. Relative to Caucasians, Which dementias do African Americans have more and which do they have less?

71. African Americans Ans. More vascular dementia [could guess from their higher hypertension rate] and less Parkinsonian dementias.

72. Family Hx Q. If Mrs. X has Alzheimer’s, what the chances of her siblings or children getting Alzheimer’s?

73. Family hx Ans. Two to four times that of the general population.

74. Genes – early onset Q. What are the three genes that have an increased association with early on-set Alzheimer’s?

75. Genes – early onset Ans. 1. Amyloid precursor protein [APP] on chromosome 21 2. Presenilin 1 [PSEN1] on chromosome 14 3. Presenilin 2 [PSEN2] on chromosome 1

76. Vascular dementia Q. Onset and course of vascular dementia?

77. Vascular dementia Ans. Acute onset and step-wise decline.

78. Alzheimer’s onset - age Q. Give the approximate onset of Alzheimer’s per the age of the individual, such as % per year of: < 65 65-70 70-75 75-80 80-85 >85

79. Alzheimer’s onset - age < 65 – rare 65-70 – 0.5%/ year [i.e., one in 200 will develop Alzheimer’s within a year] 70-75 – 1% 75-80 – 2% 80-85 – 3% >85 – 8% [Means that the odds of someone who does not have Alzheimer’s at 85 has an 8% chance of having the onset over the next 12 months. The jump from 3% to 8% doesn’t seem correct for 85 y/o compared to 84 y/o, so the “8” percent must be based on the average of all over 85. I’m not sure.]

80. Mild cognitive impairment Q. Criteria for “mild cognitive impairment”?

81. Mild cognitive impairment 1. Subjective memory complaints 2. Objective cognitive deficits on testing 3. Functioning OK

82. Vascular dementia - onset Q. Relative to age, what is the incidence of the onset of vascular dementia?

83. Vascular dementia - onset Ans. Gradually increases with age, so forms an increased percentage of those with neurocognitive disorders with age, such as those >85. More common in men.

84. Lewy body disease Q. Lewy body disease differs in clinical presentation from Alzheimer’s in what ways?

85. Lewy body disease Ans. Differs: -- early and more prominent visual hallucinations -- early and more prominent Parkinsonian features [leading to falls] -- more rapid decline

86. Lewy body disease - meds Q. When you decide to prescribe antipsychotic medications to someone with Lewy body disease has, what prominent signs are your concern?

87. Lewy body disease - meds Ans. Very sensitive to extrapyramidal signs.

88. Frontotemporal dementia Q. Characteristics of frontotemporal dementia in comparison to Alzheimer’s?

89. Frontotemporal dementia Ans. -- personality change early -- apathy early -- emotional blunting early -- disinhibition early -- language abnormalities early -- memory problems late -- apraxia late [the examiner may use “Pick’s disease” for this entity] [Hard to remember all 7 items, but recalling that memory is relatively late may get you the correct answer.]

90. Frontotemporal dementia - onset Q. Common age of onset?

91. Frontotemporal dementia - onset Ans. Onset tends to be between 50 and 60.

92. Huntington’s disease - gene Q. Genetic aspect of Huntington’s?

93. Huntington’s - genes Ans. Autosomal dominate.

94. Huntington’s - pathology Q. Pathology of Huntington’s?

95. Huntington’s - pathology Ans. While there is damage to many subcortical structures, the answer they are probably looking for is “basal ganglia.”

96. Creutzfeldt-Jakob disease - etiology Q. What two etiologies are seen in this disease?

97. Creutzfeldt-Jakob disease - etiology Ans. -- slow virus OR -- a prion [proteinaceous infectious particle]

98. Tardive Diskinesia risks Q. Relatively to age, gender, and dementia, what are TD risks when using antipsychotics?

99. TD risks Ans. Relative to use of antipsychotics, increased risk: 1. in women, 2. increased risk in the elderly and 3. increased in those with dementia

100. delirium Q. What meds used in psychiatry are associated with delirium when used with people with Alzheimer’s?

101. delirium Ans. “Virtually all” [Practice Guideline]

102. Exercise Q. Role of exercise in pts with Alzheimer’s?

103. Exercise Ans. Reduces depression in addition to other health benefits.

104. MMSE & “moderate level” Q. Moderate level of dementia is associated with what MMSE score?

105. MMSE & “moderate level” Ans. 9 -18.

106. Alzheimer’s Neuropathology?

107. Ans. Alzheimer’s Neuropathology 1] Flattened cortical sulci 2] Enlarged cerebral ventricles 3] Senile plaques 4] Neurofibrillary tangles 5] Neuronal loss, especially in the cortex and hippocampus 6] Granulovascular degeneration in the neurons

108. Also seen in? Neuropathology of Alzheimer’s also seen in?

109. Ans. Also seen in. 1] Down’s 2] Dementia pugilistica 3] Parkinson-dementia complex of Guam 4] Hallervoren-Spatz Disease 5] Familial Multiple System Taupathy 6] Normals as they age

110. Senile Plaques Composed of?

111. Senile Plaques Composed of Beta/A4

112. Neurotransmitters Often Implicated in Alzheimer’s?

113. Neurotransmitters Often Implicated in Alheimer’s 1] Acetylcholine, hypoactive 2] Norepinephrine, hypoactive

114. Cholinergic Antagonists? Two cholinergic antagonists that impair cognitive ability?

115. Cholinergic Antagonists 1] Scopolamine 2] Atropine [Not complete, but likely to reach questions.]

116. Cholinergic Agonists? Name of cholinergic agonists that would enhance cognition?

117. Cholinergic Agonist Physostigmine

118. Vascular Dementia Seen In? Gender? Medical History?

119. Vascular Dementia Is Seen In Men with hypertension

120. Binswanger’s Disease? Pathology of Binswanger’s Disease?

121. Binswanger’s Disease Many small infarcts of the white matter that spares the cortical region.

122. Pick’s Disease Pathology?

123. Pick’s Disease Pathology Also called Frontotemporal Dementia. Atrophy in the frontotemporal region where neuronal loss, gliosis, and masses of cytoskeletal elements are most present.

124. What is Kluver-Bucy Syndrome?

125. Kluver-Bucy Syndrome 1] Hypersexuality 2] Placidity 3] Hyperorality

126. Kluver-Bucy Syndrome Caused By?

127. Kluver-Bucy Syndrome Caused By Damage to both medial temporal lobes.

128. Bradyphrenia? Means? And seen in?

129. Bradyphrenia Bradyphrenia is a neurological term referring to the slowness of thought common to many disorders of the brain. Disorders characterized by bradyphrenia include Parkinson's disease and forms of schizophrenia. Bradyphrenia can also be a side effect of psychiatric medicationsParkinson's disease schizophrenia

130. Sundowner Syndrome? 1] Clinical picture? 2] Causes?

131. Sundowner Syndrome Clinical picture: confusion and ataxia. Causes: in demented patients when external stimuli, light or interpersonal cues are diminished.

132. Step-wise Cognitive Deterioration? Seen in?

133. Step-wise Deterioration Seen in vascular dementia

134. Alcohol withdrawal? Manifestations? Treatment?

135. Alcohol withdrawal Manifestations Irritability, nausea, vomiting, insomnia, malaise, autonomic hyperactivity, shakiness

136. Alcohol withdrawal treatment Fluids, sedate with benzodiazepines, 100 mg thiamine IM

137. Idiosyncratic Alcohol Intoxication? 1] manifestation? 2] treatment?

138. Idiosyncratic Alcohol Intoxication, Manifestation Marked aggressive and assaultiveness.

139. Idiosyncratic Alcohol Intoxication - treatment Protective environment.

140. Q. Alzheimer’s Diagnostic Markers

141. Ans. Alzheimer’s Diagnositc Markers 1] cortical atrophy 2] amyloid-predominant neuritic plaques 3] tau-predominant neurofibrillary tangles

142. Q. Markedly Diminished in Alzheimer’s

143. Ans. Markedly Diminished in Alzheimer’s Choline acetyltransferase Acetylcholine

144. Q. If need a benzodiazepine in treating Alzheimer’s

145. Ans. If needing a benzodiazepine in treating Alzheimer’s Go with short acting, lorazepam or oxazepam

146. Q. If Needing to use an antipsychotic? In pts with Alzheimer’s

147. Q. If needing to use an antipsychotic Ans. Select with low anticholinergic activity

148. Q. Pathology of Parkinsonian’s Disease?

149. Ans. Pathology of Parkinsonian’s Disease Pathology is especially seen in substantia nigra

150. Q. Parkinson’s Halluncinations?

151. Ans. Parkinson’s Hallucinations Visual

152. Q. Head Trauma Physical Findings

153. Ans. Head Trauma Physical Findings Ans. 1.Blood behind tympanic membrane 2.Subconjunctival ecchymosis [raccoon eye sign] 3.Pupillary abnormalities

154. Q. Wilson’s genetic finding? Which chromosome?

155. Ans. Wilson’s Genetic Finding Ans. On chromosome 13

156. Q. Chronic Traumatic Encephalopathy – signs?

157. Ans. Chronic Traumatic Encephalopathy - signs 1] Dysarthric speech 2] Emotional liability 3] Slow thinking 4] Impulsivity

158. Q. Compare as to cognitive severity Amyloid-predominant neuritic plaques? Tau-predominant neurofibrillary tangles?

159. Ans. Compare as to Severity The plaques are more a sign of severity than the tangles

160. Q. Apolipoprotein?

161. Ans. Apolipoprotein Risk factor for Alzheimer’s but neither necessary or sufficient factor.

162. Q. Frontotemporal Neurocognitive Disorder Pathology? Name two types and associated pathology.

163. Ans. Frontotemporal Neurocognitive Disorder Behavioral-variant has both frontal lobes and anterior temporal lobes are atrophied Semantic language-variant has temporal lobe atrophy at the middle, inferior, and anterior parts of that lobe

164. Q. Wing-beating tremor? Seen in?

165. Ans. Wing-beating tremor, Seen In Wilson’s

166. Q. Lewy Body Pathology?

167. Ans. Lewy Body The underlying neurodegenerative disease is synucleinopathy due to alpha-synuclein misfolding and aggregation.

168. Q. Tramantic Brain Injury Neurological/Mental Signs?

169. Ans. TBI loss of consciousness posttraumatic amnesia Disorientation and confusion Neurological signs, e.g., seizures

170. Q. Creutzfeldt-Jakob A form of?

171. Ans. Creutzfeldt-Jakob One of the prion diseases

172. Q. Huntington’s Disease Diagnostic marker?

173. Ans. Huntington’s Disease Genetic testing for trinucleotide CAG on chromosome #4.

174. Q. Hirano’s bodies?

175. Ans. Hirano’s bodies Seen in Alzheimer’s. Hirano bodies are intracellular aggregates of actin and actin-associated proteins first observed in neurons (nerve cells) by Asao Hirano in 1965.[1]actinneuronsAsao Hirano[1] Hirano bodies are found in the nerve cells of individuals afflicted with certain neurodegenerative disorders, such as Alzheimer's disease and Creutzfeldt-Jakob disease.[2]neurodegenerative disordersAlzheimer's diseaseCreutzfeldt-Jakob disease[2] Hirano bodies are often described as rod-shaped, crystal-like, and eosinophilic. Hirano bodies have been noted as a function of age without obvious underlying neurodegeration