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Geriatrics Exam 2 > Dementia, Delirium, Depression > Flashcards

Dementia, Delirium, Depression Flashcards

1
Q

What are neuronal components of the normal aging process?

A
  • Neurons decrease
  • Glia increase in size and number
  • Decline in nerves and nerve fibers
  • Atrophy of brain and increase in cranial dead space
  • Thickened leptomeninges in spinal cord
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2
Q

What is the implication of the decreased number of neurons and increase in size and number of neuroglial cells in aging?

A

Increased risk for neurological problems or cerebrovascular accident

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3
Q

What is the implication of the decline in nerves and nerve fibers during aging?

A
  • Parkinsonism
  • Slower conduction of fibers across the synapses
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4
Q

What is the implication of the atrophy of the brain and increase in cranial dead space during aging?

A
  • Modest decline in short-term memory
  • Alterations in gait pattern: wide based, shorter stepped, and flexed forward
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5
Q

What is the implication of thickened leptomeninges in spinal cord during aging?

A
  • Increased risk of hemorrhage before symptoms are apparent
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6
Q

What is the function of the glial cells?

A
  • Support the neurons
  • Remove pathogens
  • Supply nutrients
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7
Q

What is the function of ependymal cells?

A
  • Control production and flow of CSF, brain metabolism, and waste clearance
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8
Q

What is the function of astrocytes?

A
  • Perform metabolic, structural, homeostatic and neuroprotective tasks including stabilizing and regulating the blood brain barrier
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9
Q

What is the function of microglial cells?

A
  • Specialized macrophages that remove damaged neurons and infections, maintaining the heal of the CNS
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10
Q

What are oligodendrocytes?

A
  • Myelinating cells of the CNS
  • Proliferate, migrate, differentiate, and myelinate to produce the insulating sheath of the axon
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11
Q

What happens to DNA during normal aging?

A
  • DNA damage
  • Malfunctioning DNA damage response (DDR)
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12
Q

What does increased size and # of neuroglial cells lead to?

A
  • Reduced microglia migration and activation –> chronic pain
  • Oligodendrocytes reducing myelin –> leukodystrophy, MS, or neuromyelitis optics
  • Reduced astrocyte function (supply nutrients)
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13
Q

What does decreased # of neurons lead to?

A

ALS, parkinson’s disease, stroke, traumatic injury

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14
Q

What is cerebral atrophy?

A

A loss of neurons and the connections between them

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15
Q

What are the 2 types of cerebral atrophy?

A

Generalized and focal

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16
Q

What diseases are associated with cerebral atrophy?

A
  • Stroke and TBI
  • Alzheimer’s disease, Pick’s disease, and fronto-temporal dementia
  • Cerebral palsy (lesions may impair motor coordination)
  • Huntington’s disease (genetic mutations)
  • Leukodystrophies (destroys myelin sheath around axons)
  • Mitochondrial encephalomyopathies (interferes with basic function of neurons)
  • MS (inflammation, myelin damage, and lesions in cerebral tissue
  • Infectious diseases (encephalitis, neurosyphilis, AIDS; infectious agents or the inflammatory reaction)
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17
Q

What are symptoms of cerebral atrophy?

A
  • Dementia
  • Seizures
  • Aphasia
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18
Q

What is dementia?

A
  • Progressive impairment of memory and intellectual function severe enough to interfere with social and work skills
  • Memory, orientation, abstraction, ability to learn, visual-spatial perception, and higher executive functions such as planning, organizing and sequencing may also be impaired
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19
Q

How can seizures due to cerebral atrophy present?

A
  • Disorientation
  • Repetitive movements
  • Loss of consciousness
  • Convulsions
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20
Q

What are aphasias?

A

Disturbances in speaking and understanding language

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21
Q

How does receptive aphasia present?

A

Impaired comprehension

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22
Q

How does expressive aphasia present?

A

Odd choices of words, the use of partial phrases, disjointed clauses, and incomplete sentences

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23
Q

What is a leptomeninge?

A

Arachnoid mater and pia mater (2 innermost meninges that cover brain and spinal cord)

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24
Q

What are normal aging and cognitive function changes?

A
  • Difficulty recalling names or locations of placed objects, often to remember at a later time without functional impairment
  • Subtle deficits in memory function that are not severe enough to disturb/delay life
  • Learning remains intact: 3 word recall
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25
Q

What is the spectrum of cognitive impairment in older adults?

A

Normal cognitive changes seen with aging –> mild cognitive impairment (MCI) pathology –> dementia

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26
Q

What is the goal of assessment of cognitive impairment?

A

Early identification of reversible causes

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27
Q

How should the history be obtained from cognitively impaired older adults?

A

From the patient and verified by a reliable source

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28
Q

What diagnostic labs can be performed for cognitive impairment in an elderly adult?

A
  • Vit B12 and TSH
  • Additional labs on case-by-case basis: LFT, rapid plasma reagent (RPR-syphilis), HIV serology, paraneoplastic antibodies (autoimmune encephalitis)
  • Lumbar puncture (R/O normal pressure hydrocephalus and CNS infections
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29
Q

What imaging can be performed for cognitive impairment in an elderly adult? Why?

A

Noncontrast CT/MRI
Helps rule out/in stroke, small vessel disease, tumor, subdural hematoma, normal pressure hydrocephalus

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30
Q

What are characteristics of mild cognitive impairment?

A
  • Intermediate state between normal cognition and dementia
  • Trouble remembering names and appointments
  • Difficulty solving complex problems
  • Testing shows abnormal memory but no functional impairment
  • Subjective complaints of memory loss by family
  • d/t age-related neurodegenerative disease
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31
Q

How is mild cognitive impairment managed?

A
  • Look for reversible causes (medication side effects, sleep disturbances, depression, vitamin B12 deficiency, hypothyroidism)
  • Identify and modify vascular risk factors
  • Nonpharmacologic strategies
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32
Q

What nonpharmacological strategies can be used for mild cognitive impairment?

A
  • Regular exercise
  • Cognitive training: jigsaw puzzle, reading cards, read and look up unfamiliar words, encourage activities that use senses, learn a new skill, teach a new skill, listen to or play music
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33
Q

What are types of dementia?

A
  • Alzheimer’s
  • Vascular
  • Lewy Body
  • Frontotemporal
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34
Q

What is the definition of dementia?

A
  • Conditions in which there are deficits in multiple areas of cognitive function resulting in impairment in daily functioning (at any level)
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35
Q

What is the epidemiology of dementia?

A
  • 5 million people with dementia in 2014 and increasing
  • Prevalence doubles every 5 years after 60
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36
Q

What is Alzheimer disease?

A
  • Neurodegenerative disorder
  • Uncertain etiology and pathogenesis
  • Damage to hippocampus and entorhinal cortex that are essential in memory formation\
  • As neurons die, brain begins to shrink
  • By final stage, brain shrunk significantly
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37
Q

What is the pathophysiology of alzheimer disease?

A
  • 2 types of cerebral cortex lesions: amyloid plaques and neurofibrillary tangles
  • Unknown if lesions cause or result from AD
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38
Q

What is the pathophysiology of neurofibrillary tangles?

A
  • Tau protein breakdown and adhere to each other instead of the microtubules
  • Results in inadequate transport from the cell body to end of axon, preventing neuron communication

Tau proteins =glue that holds microtubules in place
Microubule = functions in transportation in axon

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39
Q

What is a amyloid precursor?

A
  • Protein found on membrane of cells throughout the body and concentrated in synapse of neuron
  • Enzymes cut these proteins
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40
Q

What is a beta amyloid protein?

A

Sticky fragment of the APP that is released when enzymes present

APP = amyloid precursor protein

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41
Q

What is a beta amyloid plaque?

A
  • Lesion consisting of beta amyloid proteins that occurs between neurons and thought to affect neuronal communication
  • Prevents dendrites from communicating with each other
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42
Q

What are risk factors for Alzheimer disease?

A
  • Increasing age
  • Female sex
  • Apo e (epsilon)4 gene on chromosome 19
  • Hx of head trauma
  • Lower education level
  • Vascular disease
  • Diabetes
  • Down syndrome
  • Family history

chromosome 19 APO e4 gene helps with cholesterol transport
Down syndrome has extra APP gene on chromosome 21 –> make more proteins

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43
Q

What is the classic triad in Alzheimer’s disease?

A
  • Difficulty learning and recalling information
  • Visuospatial problems
  • Language impairment
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44
Q

In addition to the classic triad, what clinical presentation may be present in Alzheimer’s disease?

A
  • Disorientation to time –> place –> person
  • Behavioral changes: early- depression, apathy, irritability; late- agitation and psychotic symptoms (delusion, hallucinations, paranoia)
  • Slow progression
  • Family often associate with normal aging
  • Patients often lack insight into symptoms
  • Interferes with social, occupational, or daily functioning
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45
Q

What is the clinical presentation of mild AD?

A
  • Often first noticed by those close to individual
  • Longer time to perform daily tasks
  • Recognize familiar places
  • Recall new names
  • Paying bills or handling money
  • Word recall
  • Losing or misplacing items
  • Planning or organizing
  • Remember new reading material
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46
Q

What is the clinical presentation of moderate AD?

A
  • Symptoms more pronounced
  • Recalling demographics (phone #)
  • Easily lost
  • Disoriented to place/time
  • Short attention span
  • Disorganized thought processes
  • Repetitive statements
  • Difficulty recognizing family/friends
  • Choosing appropriate clothing
  • Loss of new learning
  • Psychotic symptoms
  • Behavioral changes
  • Trouble reading, writing
47
Q

What is the clinical presentation of severe AD?

A
  • Completely dependent on others for care
  • All sense of “self” is gone
  • Absent recognition of family/friend
  • Weight loss
  • Increased sleeping
  • Increased infections: aspiration pneumonia MC
  • Death often due to complicating illness
  • Loss of bowel/bladder control
  • Trouble swallowing
  • Unable to communicate effectively
48
Q

How is alzheimer disease diagnosed?

A
  • R/O delirium and other causes of dementia
  • Imaging: CT or MRI can r/o mass, monitor progression
49
Q

What can be seen on CT or MRI of a patient with Alzheimer disease?

A
  • Diffuse cortical and/or cerebral atrophy
  • Greater degree of hippocampal atrophy
  • Progressive atrophy of medial temporal lobes
50
Q

What can be seen on CT/MRI of a patient with frontotemporal dementia? Vascular dementia?

A
  • Frontotemporal = diffuse cortical or cerebral atrophy of frontal lobe
  • Vascular pathology = vascular dementia
51
Q

How is alzheimer disease managed?

A
  • Acetylcholinesterase inhibitors = first line at any stage of disease
  • If moderate-to-severe or unable to tolerate cholinesterase inhibitors, NMDA receptor antagonists
  • Nonpharmacologic interventions
  • Behavioral management
52
Q

What is the MOA of acetylcholinesterase inhibitors?

A

Works as a neurotransmitter to increase acetylcholine at neuronal synapses

53
Q

What is the effect of acetylcholinesterase inhibitors?

A

slows the progression of AD

54
Q

What are the FDA approved acetylcholinesterase inhibitors?

A
  • Donezepril
  • Galantamine
  • Rivastigmine
  • Aricept and Razadyne (po only)
  • Exelon (po and transdermal)
55
Q

What are the MC side effects of acetylcholinesterase inhibitors?

A
  • Nausea
  • Anorexia
  • Sleep disturbance
  • Diarrhea; take with food
56
Q

What are serious side effects of acetylcholinesterase inhibitors?

A
  • Bradycardia
  • AV nodal block
  • Syncope
57
Q

How should acetylcholinesterase inhibitors be dosed?

A

Start low and go slow! Titrate up q 2 months until therapeutic dose achieved

58
Q

What is the mechanism of action of NMDA receptor antagonists?

A
  • reduces the destruction of cholinergic neurons and may inhibit B-amyloid production, thereby preserving memory
59
Q

What is the effet of NMDA receptor antagonists on AD?

A

Slows the progression of the disease

60
Q

What is the name of the NMDA receptor antagonist?

61
Q

What is the combo NMDA/cholinesterase inhibitor?

A
  • Namzaric
  • Indicated for moderate to severe AD
62
Q

What are nonpharmacologic interventions for AD?

A
  • Physical activity and exercise
  • Mentally stimulating activities
  • Social activities
63
Q

What is behavioral management for AD?

A
  • Nonpharmacologic therapy –> music therapy, exercise, remove extraneous noise and clutter, simplify tasks, develop daily routine
  • Pharmacologic therapy –> SSRI for depression, agitation, sexual inappropriateness; trazodone to improve sleep wake cycle
  • Refer to geriatric psychiatrist if unable to control symptoms
64
Q

What is patient (family) education for AD?

A
  • Assess driving safety, pill box, electronic reminders
  • Appropriate supervision or limited use of stove, woodworking equipment, firearms
  • Medical alert systems
  • 24 hour supervision if patient can’t identify what to do in an emergency
  • Home care services to assist with ADL’s
  • Caregiver support
  • Increased risk for depression, work absence, and health problems
  • Educational resources: NIA, Caring for AD, Communication strategies, legal and financial planning
  • Respite care services and adult daycare: NIA
  • Local support groups: alzheimer’s association
65
Q

What are complications of Alzheimer disease?

A
  • Worsening of comorbid conditions due to treatment adherence issues
  • Increased risk of developing delirium in response to medical illness or surgery
  • Advanced AD leads to poor nutritional intake, urinary incontinence, skin breakdown, and infections
66
Q

What should you know about the course of AD?

A
  • Rate of progression depends on patient
  • Discontinue AchEI and NMDA once patient unable to express their needs
67
Q

What is the definition of vascular dementia?

A
  • Gradual or acute cognitive dysfunction
  • Clinical or radiographic evidence of cerebrovascular disease, often with AD
68
Q

What is the pathophysiology of vascular dementia?

A
  • Pathophysiologic, small, micro-ischemic changes in brain
  • Not enough for focal deficits but lots can damage neuro function
69
Q

What is the clinical presentation of vascular dementia?

A
  • Memory impairment, often less severe than AD
  • Difficulty of timed activities and executive functions (one minute semantic test)
  • Behavioral and psychological symptoms as in AD
  • Depression often more severe than AD
  • Focal neuro deficits not commonly seen
70
Q

What imaging can be performed and its result for vascular dementia?

A

MRI showing small infarcts white matter lesions

71
Q

How is vascular dementia managed?

A

Same as AD
Cholinesterase inhibitors, memantine, nonpharmacological therapy

72
Q

What are vascular risks to identify and treat with vascular dementia?

A
  • HTN
  • Smoking
  • DM
  • Statins
  • Antiplatelets (if hx of TIA or ischemic stroke)
73
Q

What is the definition of dementia with lewy bodies?

A
  • Dementia with lewy bodies on histopathology of brain tissue
74
Q

What is the etiology of dementia with lewy bodies?

A
  • Lewy bodies are deposits of alpha-synuclein
  • Alpha-synuclein is naturally found at presynaptic terminals and plays role in neurotransmitter release
75
Q

What is the pathophysiology of dementia with lewy bodies?

A
  • Exact not understood
  • Unknown if alpha-synuclein deposits cause damage or form as protective response
  • Similar lesions in Parkinson’s disease
76
Q

What is the epidemiology of dementia with lewy bodies?

A
  • Average age of onset is 75 but range from 50-80
  • Slight male predominance
  • Mostly sporadic- very rare occurance of family history
  • Occur concomitantly with AD in 40% of patients
77
Q

What is the core clinical presentation of dementia with lewy bodies?

A
  • Insidious fluctuating cognitive impairment (day to day)
  • Memory less affected than AD
  • Visuospatial abilities, problem solving, and processing speed more severe than AD
  • Spontaneous Parkinsonism
  • Visual hallucinations (rare in AD)
  • Delusional misidentification
78
Q

What is the hallmark of dementia with lewy bodies?

A

Spontaneous parkinsonism
* Bradykinesia, bilateral limb rigidity, flat affect, postural instability, gait changes
* Less likely to involve tremors or respond to levodopa

79
Q

What is often the first symptoms of dementia with lewy bodies that helps distinguish from AD?

A

delusional misinterpretation

80
Q

What are additional presentations that may occur in dementia with lewy bodies?

A
  • REM sleep disorder
  • Vivid and scary dreams (may be acted out verbally or motorically)
  • Sensitivity to antipsychotics (symptoms get worse, severe parkinsonism, NMS, life threatening rxn)
  • Repeated falls
  • Orthostatic hypotension, syncope, transient loss of consciousness
  • Autonomic dysfunction
  • Hypersomnia
  • Hyposmia
  • Apathy, anxiety, depression

hyposmia = decreased sense of smell

82
Q

What diagnostics are used in dementia with Lewy bodies?

A
  • R/o other causes
  • MRI
  • SPECT
83
Q

What will be seen on MRI of DLB?

A
  • Greater atrophy in basal ganglia structures and dorsal midbrain in DLB
  • More pronounced cortical atrophy than PD
  • Lewy bodies in pathohistological brain autopsy post mortem

Greater atrophy of medial temporal lobe in AD
Hippocampus atrophy more prominent in AD

84
Q

What is the McKeith Criteria for DLB?

A

Probable DBL
* two or more clinical features of DLB are present, with or without indicative biomarkers
* OR only one core clinical feature is present, but with one or more indicative biomarkers
* Probable DLB should not be diagnosed on the basis of biomarkers alone

Possible DBL
* Only one core clinical feature of DLB is present, with no indicative biomarker evidence
* OR one or more indicative biomarkers are present, but there are no core clinical features

85
Q

What is a SPECT and what are findings with dementia with lewy bodies?

A
  • Nuclear imaging scan that integrates CT and radioactive tracer
  • Reduction in dopamine uptake and perfusion
86
Q

What is dementia with lewy bodies managed?

A
  • Cholinesterase inhibitors
  • +/- memantine - evidence mixed
  • Atypical antipsychotics in very small doses only if psychosis severe
  • SSRIs for depression
  • Low doses of melatonin for REM disorders
  • Parkinsonism treated same as PD: carbidopa-levodopa
  • Fludrocortisone for orthostatic hypotension
87
Q

What is the clinical course and prognosis of dementia with lewy bodies?

A
  • Decrease in MMSE by 4-5 points per year
  • Mean survival appx 10 years
  • Risk factors for higher mortality include older age, hallucinations, greater degrees of fluctuation, and neuroleptic sensitivity
88
Q

What is frontotemporal dementia?

A
  • Umbrella term for clinical syndromes due to degeneration of the frontal and temporal lobes of the brain
  • MC cause of early onset dementia (can begin in 40s)
  • Often has family history
89
Q

How is frontotemporal dementia diagnosed?

A
  • MRI showing focal atrophy of frontal, insular, and/or temporal cortex
  • Atrophy begins in one hemisphere and spreads to anatomically interconnected cortical and subcortical regions
90
Q

What does behavioral variant FTD look like on MRI?

A

Medial and orbital frontal and anterior insula degeneration on MRI

91
Q

What does non-fluent/agrammatic primary progressive aphasia look like on MRI?

A

Dominant hemisphere lateral frontal and precentral gyrus atrophy

92
Q

What are the 3 clinical syndromes in frontotemporal dementia?

A
  • Behavioral variant
  • Semantic primary progressive aphasia variant
  • Primary progressive aphasia
93
Q

What is the clinical presentation of behavioral variant frontotemporal dementia?

A
  • Insidious onset
  • Changes in personality, do things they wouldn’t normally do
  • Apathy, disinhibition, compulsivity, loss of empathy, overeating
94
Q

What is the clinical presentation of semantic/primary progressive aphasia variant?

A
  • Loss of ability to decode/recall words, object, person-specific
95
Q

What is the clinical presentation of primary progressive aphasia FTD variant?

A
  • Inability to produce words, often with prominent motor speech impairment
  • Affects broca’s area
96
Q

How is frontotemporal dementia managed?

A
  • Safety and driving as in AD
  • Regular exercise
  • Behavioral therapy
97
Q

What are components of behavioral therapy for frontotemporal dementia?

A
  • Non-pharm first line: distraction, redirection, offer simple choices, avoid overstimulation
  • Pharmacologic only if behavioral modification fails with SSRI or trazodone (start low, go slow)
98
Q

What is the prognosis of frontotemporal dementia?

A
  • Survival from symptom onset is approximately 8-10 years
  • Often shorter in patients with the behavioral variant FTD
99
Q

What is the definition of normal pressure hydrocephalus?

A
  • accumulation of CSF that causes enlargement of the ventricles in the brain and compression of the surrounding structures
100
Q

What is the pathophysiology of normal pressure hydrocephalus?

A
  • CSF build up inside the brain
  • Idiopathic NPH: no cause identified
  • Secondary NPH: underlying condition leads to inflammation and fibrosis at base of brain and/or arachnoid granulations, impairing CSF resorption
101
Q

What is the clinical presentation of normal pressure hydrocephalus?

A
  • Abnormal gait
  • Urinary incontinence
  • Dementia
  • After intervention, gait often improves but dementia/incontinence do not
102
Q

How is normal pressure hydrocephalus managed?

A
  • Ventricular shunting into the abdomen (MC) –> fluid gets absorbed
  • Into the heart to enter circulation (LC) –> fluid enters circulation
103
Q

How is normal pressure hydrocephalus diagnosed?

A
  • MRI/CT (MRI preferred)
  • High-volume lumbar puncture
104
Q

What are findings of normal pressure hydrocephalus on MRI/CT?

A
  • Ventriculomegaly in absence of or out of proportion to sulcal enlargement
  • Applies pressure to cerebral cortex causing symptoms
105
Q

What are findings on high-volume lumbar puncture for normal pressure hydrocephalus?

A
  • Normal opening pressure
  • Remove 30-50 cc of CSF
  • Assess gait prior to procedure and 30-60 mins after
  • Improvement in gait is good prognostic sign for ventricular shunt placement
106
Q

What is the definition of delirium?

A
  • Acute change in attention and cognition due to underlying illness, stressor or precipitant exposure
  • May be only sign of underlying illness in older patients
107
Q

What is the greatest predisposing risk for delirium?

A

preexisting cognitive impairment, specifically dementia

many predisposing risk factors are present

109
Q

What is the clinical presentation of delirium?

A
  • acute onset of cognitive impairment and functional decline
  • symptoms fluctuate throughout day
  • Attenion deficits: reduced ability to direct, focus, sustain, and shift attention
  • Cognitive impairment: memory deficit, disorientation, lagnuage, visuospatial ability, perception
110
Q

How is delirium managed?

A
    1. identification and treatment of underlying medical cause
    1. eradication or minimization of contributing factors
    1. management of delirium symptoms
111
Q

how is the underlying cause of delirium identified and treated?

A
  • H&P
  • Review of meds
  • Kidney and liver function assessment for metabolci processes
  • Lab/radiologic screening tests such as TSH, B12, hepatic enzymes
  • Evaluate for occult infection with CBC, UA, FO
112
Q

How are delirium symptoms managed non-pharmacologically?

A
  • Frequent reorientation
  • Environment optimization
  • Sensory deficit correction
  • Avoiding restraints
  • Mobility/self-care
  • Sleep hygiene
113
Q

How are delirium symptoms managed pharmacologically?

A
  • Reserve for severely agitated individuals who threaten medically necessary care/pose a safety hazard
  • Start at lowest dose possible and for shortest period d/t risk of worsening confusion
  • Goal: awake and manageable, not sedated
  • Antipsychotics used: haloperidol, olanzapine, quetiapine, risperidone
  • Benzodiazepines (lorazepam is choice due to decreased half life)
114
Q

What is the clinical course and prognosis of delirium?

A
  • fully reversible once cause identified and treated
  • Patients with delirium are more likely to be diangosed with dementia later

Geriatrics Exam 2 (1 decks)

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