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Dementias

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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. – PowerPoint PPT presentation

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Title: Dementias


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.
  • lt or 65, early onset
  • gt 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 Alzheimers,
    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
    Alzheimers 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
    Alzheimers?

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

36
FDA for Alzheimers
  • Q. What meds have been approved for Alzheimers?

37
FDA for Alzheimers
  • 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
    Alzheimers?

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 Selegilines 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
    tacrines hepatic toxicity.

46
ECT
  • Q. Indications for ECT in pts with Alzheimers?

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

48
Delusions and hallucinations
  • Q. Pt is moderately impaired from Alzheimers,
    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. Alzheimers 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 Alzheimers?

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 Parkinsons disease
    in pt who also has Alzheimers 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 3rd 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, gt 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 Alzheimers, 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 Alzheimers, what the chances of
    her siblings or children getting Alzheimers?

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
    Alzheimers?

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
Alzheimers onset - age
  • Q. Give the approximate onset of Alzheimers per
    the age of the individual, such as per year of
  • lt 65
  • 65-70
  • 70-75
  • 75-80
  • 80-85
  • gt85

79
Alzheimers onset - age
  • lt 65 rare
  • 65-70 0.5/ year i.e., one in 200 will develop
    Alzheimers within a year
  • 70-75 1
  • 75-80 2
  • 80-85 3
  • gt85 8 Means that the odds of someone who does
    not have Alzheimers at 85 has an 8 chance of
    having the onset over the next 12 months. The
    jump from 3 to 8 doesnt 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. Im 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 gt85. More
    common in men.

84
Lewy body disease
  • Q. Lewy body disease differs in clinical
    presentation from Alzheimers 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 Alzheimers?

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 Picks 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
Huntingtons disease - gene
  • Q. Genetic aspect of Huntingtons?

93
Huntingtons - genes
  • Ans. Autosomal dominate.

94
Huntingtons - pathology
  • Q. Pathology of Huntingtons?

95
Huntingtons - 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
    Alzheimers?

101
delirium
  • Ans. Virtually all Practice Guideline

102
Exercise
  • Q. Role of exercise in pts with Alzheimers?

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
Alzheimers Neuropathology?
107
Ans. Alzheimers 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 Alzheimers also seen in?

109
Ans. Also seen in.
  • 1 Downs
  • 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 PlaquesComposed of?
111
Senile PlaquesComposed of
  • Beta/A4

112
Neurotransmitters Often Implicated in
Alzheimers?
113
Neurotransmitters OftenImplicated in Alheimers
  • 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 DementiaIs Seen In
  • Men with hypertension

120
Binswangers Disease?
  • Pathology of Binswangers Disease?

121
Binswangers Disease
  • Many small infarcts of the white matter that
    spares the cortical region.

122
Picks DiseasePathology?
123
Picks DiseasePathology
  • Also called Frontotemporal Dementia.
  • Atrophy in the frontotemporal region where
    neuronal loss, gliosis, and masses of
    cytoskeletal elements are most present.

124
What isKluver-Bucy Syndrome?
125
Kluver-Bucy Syndrome
  • 1 Hypersexuality
  • 2 Placidity
  • 3 Hyperorality

126
Kluver-BucySyndrome 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 medications

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 withdrawalManifestations
  • Irritability, nausea, vomiting, insomnia,
    malaise, autonomic hyperactivity, shakiness

136
Alcohol withdrawaltreatment
  • Fluids, sedate with benzodiazepines, 100 mg
    thiamine IM

137
Idiosyncratic AlcoholIntoxication?
  • 1 manifestation?
  • 2 treatment?

138
Idiosyncratic AlcoholIntoxication, Manifestation
  • Marked aggressive and assaultiveness.

139
Idiosyncratic Alcohol Intoxication - treatment
  • Protective environment.

140
Q. Alzheimers Diagnostic Markers
141
Ans. Alzheimers Diagnositc Markers
  • 1 cortical atrophy
  • 2 amyloid-predominant neuritic plaques
  • 3 tau-predominant neurofibrillary tangles

142
Q. Markedly Diminishedin Alzheimers
143
Ans. Markedly Diminishedin Alzheimers
  • Choline acetyltransferase
  • Acetylcholine

144
Q. If need a benzodiazepinein treating
Alzheimers
145
Ans. If needing a benzodiazepine in treating
Alzheimers
  • Go with short acting, lorazepam or oxazepam

146
Q. If Needing to use an antipsychotic?
  • In pts with Alzheimers

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

148
Q. Pathology ofParkinsonians Disease?
149
Ans. Pathology of Parkinsonians Disease
  • Pathology is especially seen in substantia nigra

150
Q. Parkinsons Halluncinations?
151
Ans. Parkinsons Hallucinations
  • Visual

152
Q. Head TraumaPhysical Findings
153
Ans. Head TraumaPhysical Findings
  • Ans.
  • Blood behind tympanic membrane
  • Subconjunctival ecchymosis raccoon eye sign
  • Pupillary abnormalities

154
Q. Wilsons genetic finding?
  • Which chromosome?

155
Ans. Wilsons 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. Compareas to cognitive severity
  • Amyloid-predominant neuritic plaques?
  • Tau-predominant neurofibrillary tangles?

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

160
Q. Apolipoprotein?
161
Ans. Apolipoprotein
  • Risk factor for Alzheimers 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
  • Wilsons

166
Q. Lewy BodyPathology?
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. Huntingtons Disease
  • Diagnostic marker?

173
Ans. Huntingtons Disease
  • Genetic testing for trinucleotide CAG on
    chromosome 4.

174
Q. Hiranos bodies?
175
Ans. Hiranos bodies
  • Seen in Alzheimers.
  • Hirano bodies are intracellular aggregates of
    actin and actin-associated proteins first
    observed in neurons (nerve cells) by Asao Hirano
    in 1965.1
  • 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
  • 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
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