Dementia, Delirium, Depression - Exam 2 Flashcards
What are 4 common themes when discussing NORMAL aging and cognitive function
Difficulty recalling names but REMEMBER them at a later time
NO functional impairment
SUBTLE deficits in memory function
learning remains intact
Cognitive function in older adults is considered a ______. What are the 3 different phases. What is the goal?
spectrum
early identification of reversible causes
** What are the cognitive impairment critical history points? slide 1
** What are the cognitive impairment critical history points? slide 2
When is the cognitive assessment not a reliable test? What should the general PE focus on?
when the pt has altered LOC or delirium
neuro exam
cardio exam
signs of abuse or neglect
screening for hearing/vision loss
What lab test should you order when thinking about a cognitive impairment? What is the imaging?
B12 and TSH
consider LP if concerned about hydrocephalus or CNS infection
brain CT/MRI w/o
______ is an intermediate state between normal cognition and dementia often seen in older adults. Give 3 characteristics
Mild cognitive impairment (MCI)
subjective memory loss
-Difficulty remembering names and appointments
- Difficulty solving complex problems
- Testing shows abnormal memory but no functional impairment
What should be your approach to mild cognitive impairment?
look for reversible causes: med SE, sleep, depression, vit B12 def, hypothyroid
modify vascular risk factors
nonpharm: regular exercise, cognitive training
** Is dementia reversible?
NO: Dementia is NOT reversible
What is dementia? What are 2 important highlighted things to remember?
A general TERM, not a specific disease, used to describe various conditions in which there are deficits in multiple areas of cognitive function resulting in impairment in daily functioning
**Gradually progressing course
**No disturbances in consciousness
What are the 4 different types of dementia? Which one is MC?
Alzheimer disease - most common
Vascular dementia
Lewy body dementia
Frontotemporal dementia
What is Alzheimer Disease? What 2 cerebral cortex lesions are associated with it?
AD is a neurodegenerative disorder of uncertain cause and pathogenesis; resulting in cognitive and behavioral impairment primarily in older adults.
Amyloid plaques
Neurofibrillary tangles
Under normal neuron circumstances, _____ inside of the _____, transport nutrients, organelles, and other messages from the cell body to the tip of the axon. ______ are the glue that hold the microtubules in place, allowing them to function appropriately
Microtubules
axon
Tau proteins
In a pt with AD, Neurofibrillary tangles occur when the ______ and adhere to each other instead of adhering to the microtubules. What happens as a result?
tau proteins breakdown
This results in inadequate transport from the cell body to the end of the axon, preventing neurons from communicating with one another appropriately
What are the risk factors for AD?
What is the classic triad presentation for AD? Do pts tend to have good insight into their condition?
Difficulty learning and recalling information
Visuospatial problems
Language impairment
pts often LACK insight into their symptoms
What is the order of disorientation that is commonly seen in AD?
time first
then place
then person (self)
in that order
When do you start to see behavioral changes in a pt with AD?
Depression, apathy, irritability early on in disease
Agitation and psychotic symptoms later in disease
AD is a _____ diagnosis. Must rule out _____. What will their brain MRI show?
clinical diagnosis
must rule out delirium
If performed may show diffuse cortical and/or cerebral atrophy ;greater degree of hippocampal atrophy
**What are the first line medications used to tx AD? What drug class?
donepezil (Aricept), galantamine (Razadyne), and rivastigmine (Exelon)
Acetylcholinesterase (Cholinesterase) inhibitors (AchEI)
______ MOA increase Ach at the neuronal synapses in the brain. What effect do they have in AD?
Acetylcholinesterase (Cholinesterase) inhibitors (AchEI): donepezil (Aricept), galantamine (Razadyne), and rivastigmine (Exelon)
slow progression of AD but there is NO evidence of slowing MCI to AD
_________ SE include nausea, anorexia, sleep disturbance and diarrhea. What are the dosing recommendations?
Acetylcholinesterase (Cholinesterase) inhibitors (AchEI)
donepezil
galantamine
rivastigmine
start low and go slow, titrate up every 2 months
______ MOA reduces the destruction of cholinergic neurons and may inhibit β-amyloid production, preserving memory. What drug class?
memantine
N-Methyl-D-Aspartate (NMDA) Receptor Antagonist
What are the indication for memantine?
moderate-to-severe AD, unable to tolerate AchEI’s
What are lecanemab (Leqembi) and donanemab (Kisunla)? When are they used?
Amyloid-targeted therapy → recombinant monoclonal antibodies directed against amyloid beta
-used to AD for those who are mild cognitive impairment or mild dementia
MMSE ≥22; MoCA ≥17
-Amyloid positive patients as documented on PET scan / LP
What are some AD complications?
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
When should you stop AD medications (AchEI and NMDA)?
once the pt is unable to express their needs
_______ a gradual or acute onset of cognitive dysfunction (not related to delirium) with clinical or radiographic evidence of cerebrovascular disease
vascular dementia
What is the clinical presentation of vascular dementia? How does memory impairment and depression compare to AD?
-memory impairment
-Difficulty of timed activities and executive functions
-Behavioral and psychological symptoms as in AD
-depression
-NO focal neurologic deficits
Memory impairment is often LESS severe than AD but depression is MORE severe than in AD
What MRI finding is commonly seen with vascular dementia?
MRI may provide evidence of small infarcts (“white matter lesions”)
What is the tx for vascular dementia?
same as AD: Cholinesterase inhibitors, memantine and nonpharmacological therapy
What are Lewy bodies? Where else are they also seen?
Lewy bodies are deposits of Alpha-synuclein, a protein naturally found at the presynaptic terminals
also seen in Parkinson’s disease
What is the average age of onset for Dementia with Lewy Bodies? male or female? genetic component?
75 years: 50-80
male
mostly sporadic-> very rare occurrence of family history
What are the core features of dementia with Lewy bodies?
Insidious in onset of fluctuating cognitive impairment (day-by-day)
Visuospatial abilities, problem solving, and processing speed are MORE severe than AD early in course and memory is LESS affected
spontaneous parkinsonism
recurrent VISUAL hallucinations
What is the hallmark of DLB?
Spontaneous parkinsonism
Bradykinesia, bilateral limb rigidity, flat affect (mask-like facies), postural instability and gait changes
LESS likely to involve tremors or respond to levodopa
When comparing DLB to AD, _______ is often the first symptom that helps differ from AD. What is it?
Delusional misidentification
mistaking the spouse, friend, or relative as an impostor
What are some suggestive features of DLB?
Rapid eye movement (REM) sleep disorder
Sensitivity to antipsychotics including severe parkinsonism, impaired consciousness and neuroleptic malignant syndrome
What are some features of neuroleptic malignant syndrome?
a life-threatening idiosyncratic reaction to antipsychotic drugs characterized by fever, altered mental status, muscle rigidity, and autonomic dysfunction
What is the criteria called for the dx of DLB? how many do you need of each category?
McKeith criteria
2 core features OR 1 core and 1 supportive feature
**How does the brain MRI of DLB compare to AD?
Less atrophy of the medial temporal with greater atrophy in the basal ganglia structures and the dorsal midbrain
How does the brain MRI of DLB compared to Parkinson’s dz?
More pronounced cortical atrophy than PD
What with SPECT (Single-photon emission computed tomography) show on a pt with DLB?
Reduction in dopamine uptake and perfusion
What is the management for DLB?
What are the atypical antipsychotics used in DLB?
olanzapine (Zyprexa)
quetiapine (Seroquel)
pimavanserin (Nuplazid)
ziprasidone (Geodon)
aripiprazole (Abilify)
paliperidone (Invega)
clozapine (Clozaril)
What is the objective data seen with DLB as the course progresses? What is the prognosis?
A decrease in the MMSE by 4-5 points per year
mean survival is approximately 10 years
What are risk factors for higher mortality in DLB?
Older age, hallucinations, greater degrees of fluctuation, and neuroleptic sensitivity
_______ A group of clinical syndromes that results from degeneration of the frontal and temporal lobes of the brain. What age range?
Frontotemporal Dementia (FTD)
typically presents earlier before the age of 65
_____ most common cause of early-onset dementia (age of onset <65 years old)
Symptoms can begin in the ____
Frontotemporal Dementia (FTD)
40’s
What are the 3 clinical syndromes that are variations of Frontotemporal Dementia (FTD)? Which one is MC?
Behavioral variant (bvFTD)- MC
Semantic primary progressive aphasia variant
Primary progressive aphasia nonfluent/agrammatic variant
Which type of FTD? ________ Apathy, disinhibition, compulsivity, loss of empathy, and overeating, often but not always accompanied by deficits in executive control
Behavioral variant (bvFTD
Which type of FTD? ________ Lose the ability to decode word, object, person-specific, and emotion
Semantic primary progressive aphasia variant
aka cannot interpret words
Which type of FTD? ________ Inability to produce words, often with prominent motor speech impairment
Primary progressive aphasia nonfluent/agrammatic variant
aka cannot speak well
**What is the MRI hallmark finding of FTD?
Hallmark is a focal atrophy of frontal, insular, and/or temporal cortex
Atrophy often begins focally in one hemisphere before spreading to anatomically interconnected cortical and subcortical regions
**MRI findings for different types of FTD. ________ Anterior temporal degeneration
semantic variant PPA
**MRI findings for different types of FTD. ________ Medial and orbital frontal and anterior insula degeneration
Behavioral variant FTD
**MRI findings for different types of FTD. ________ Dominant hemisphere lateral frontal and precentral gyrus atrophy
Nonfluent/agrammatic PPA
What is the management for FTD? What is the prognosis?
from onset of symptoms approx. 8-10 years. shorter for pts with behavioral variant FTD
Look at this chart for comparison of the common types of dementias
______ an accumulation of CSF that causes enlargement of the ventricles in the brain and compression of surrounding structures. What are the 2 different versions?
Normal Pressure Hydrocephalus (NPH)
idiopathic NPH
secondary NPH
_______ underlying condition leads to inflammation and fibrosis at the base of the brain and/or the arachnoid granulations, impairing CSF resorption
secondary NPH
What are the 3 characteristics of NPH? What happens after intervention?
normal pressure hydropcephalus (NPH)
by abnormal gait, urinary incontinence, and dementia
gait often improves but dementia and incontinence do NOT
What is the imaging of choice for NPH? What is the hallmark finding?
MRI/CT- MRI is preferred
Hallmark is ventriculomegaly in the absence of, or out of proportion to, sulcal enlargement
What are the LP results in a pt with NPH?
Normal opening pressure
pt’s gait improves when 30-50 cc of fluids are removed
What is a good prognostic sign for a shunt in pt with NPH?
Improvement in gait is a good prognostic sign for ventricular shunt placement once 30-50 cc of CSF is removed during LP
Where is the MC place to shunt the excessive CSF in NPH? Name one additional option
MC shunting into the abdomen (ventriculoperitoneal)
Less common into the heart (ventriculoatrial)
**What is the big thing to note about delirium?
delirium is reversible
_______ A disorder characterized by an acute change in attention and cognition due to an underlying illness, stressor or precipitant exposure
delirium
What is the greatest predisposing risk factor for delirium?
preexisting cognitive impairment specifically dementia
What is the clinical presentation of delirium?
acute onset (hours to days) of cognitive impairment and functional decline
reduced ability to focus, memory deficits, disorientation
What are some nonpharm strategies for a pt with delirium?
When are pharm strategies used in delirium management? What is the goal?
severely agitated individuals who threaten medically necessary care and pose a safety hazard
to use the lowest dose possible for the shortest period of time with the goal of an awake and manageable pt NOT a sedated one
**What is the BZD of choice for delirium? Why?
lorazepam (ativan) because it has a shorter 1/2 life
**delirium is a ______ condition once the underlying cause is identified. What does it increase your risk of later on down the road?
fully reversible condition
more likely to be diagnosed with dementia at a later date
What are the risk factors for delirium? What are ways to prevent them?
