dementia, delirium, depression Flashcards
what are the functions of glia cells
support neurons by providing insulation, supplying nutrients, and removing pathogens
what isthe function of epindymal cells
create membrane around the brain and spinal cord
what are the functions of astrocytes
connect the blood vessels and supply nutrients
what is the function of microglial cells
destroy pathogens and remove cellular debris
what are the functions of oligodendrocytes
create myelin sheaths that insulate the axon of the neuron
what does damage to microglia cells result in
chronic pain
what are implications of decreased numbers of neurons and increase in size and number of neuroglial cells
increased risk for neuro probs including CVA
what are implications of change with decline in nerves and nerve fibers
- parkinsonism
- slower conduction of fibers across the synapses
what are the implications of atrophy to the brain and increase in cerebral dead space
- modest decline in short term memory
- alteration in gait pattern
what are implications of change with thickened leptomeninges in the spinal cord
- increased risk of hemorrhage before symptoms present
what does damage to oligodendrocytes result in
multiple sclerosis
what does damage to neurons result in
- ALS
- Alzheimers
- parkinsons
what are the results of the normal aging process regarding neurons
-neurons decrease in number
-glial cells decrease in size and number
-damage in DNA
-malfunctioning DNA damage response
-decline in nerves and nerve fibers
what is cerebral atrophy
loss in neurons and the connections between them
what is the difference between generalized and focal atrophy
- gen - brain shrinks
- focal - affecting only a limited area of the brain
what occurs to leptomeninges in the normal aging process
they thicken
what is a possible result of thickening leptomeninges of the spinal cord
compression of nerves
what are symptoms of cerebral atrophy
- dementia
- seizures
- aphasias
what are aspects of normal aging in regards to cognitive function
- difficult recalling names or locations
- subtle deficits in memory
T/F in normal aging, 3 word recall remains intact
TRUE
T/F dementia is different in each person
True
what are the two innermost layers of tissue (meninges) that cover the brain and spinal cord
- pia mater (inner layer)
- arachnoid mater (outer layer)
- CSF flows between these
how do you obtain hx from a patient w a cog impairement
- hx should be obtained from pt and verified from a reliable source
t/f you cannot rely on results of a cognitive assessment if the patient as altered levels of consciousness or delirium
True
what are labs that you should obtain in a patient w cognitive impairment
- Vit B12 and TSH
- Lumbar puncture
what diagnostic imaging can be ordered for a patient with cog impairment
- noncontrast CT/MRI to r/o causes of dementia
what are possible differential dx for cog dysfunction
-alzheimers
-dementia with lewy body
-depression
-substance abuse
what are indications of mild cognitive impairment
- Intermediate -intermediate stage between normal cognition and dementia
- difficulty remembering names, appointments, and solving complex issues
what are the test results of mild cognitive impairment
abnormal memory but NO functional impairment
what is the management of mild cognitive impairment
- look for reversible causes
- regular exercise
- cognitive training
what are some reversible causes of mild cognitive impairment
- medication side effects
- sleep disturbances
- depression
- vitamin B12 deficiency
- hypothyroidism
what is dementia
the general term used to describe various conditions in which there are deficits in multiple areas of cognitive function resulting in impairment in daily functioning
at what age does the prevelance of dementia start doubling every 5 years
60 years
what are the types of dementia
- alzheimers
- vascular dementia
- dementia with lewy bodies
- frontotemporal dementia
what is alzheimers disease
neurodegenerative disorder of uncertain etiology and pathogenesis resulting in cognitive and behavioral impairment
where does the damage of alzheimers appear
hippocampus and entorhinal cortex
what occurs to the size of the brain in alzheimers brain
it shirn ks:)
what are the 2 types of cerebral cortex lesions associated with alzheimers
- amyloid plaques
- neurofibrillary tangles
what are amyloid precursor protein
protein found on the membrane of various cells throughout the body and concentrated in the synapse of the neuron
what is beta amyloid protein
sticky fragment of the APP that is released when various enzymes are present
what is beta amyloid plaque
lesion consisting of beta amyloid proteins that occurs between neurons and thought to affect neuronal communication
what is the result of amyloid plaque formation
inhibition of dendrites from communicating w eachother
what are the jobs of the microtubules in the axon
transport nutrients, organelles, and other messages from the cell to the tip of the axon
what are tau proteins
glue that holds the microtubules in place, allowing them to function appropriately
what are neurofibrillary tangles
tau proteins breakdown and adhere to each other instead of adhering to the microtubules, resulting in inadequate transport from the cell body to the end of the axon , preventing neurons from communicating.
what are risk factors for alzheimers
- age
- female
- hx of head trauma
- diabetes
- family history
- vascular disease
what are clinical presentations of alzheimers disease
- difficulty learning and recalling information
- visuospatial problems
- language impairment
what is the order of disorientation of alzheimers
- time
- place
- person
t/f alzheimers patients often have insight into their symptoms
False
what are behavior changes in alzheimer
- early: depression, apathy, irritability
- later: agitation and psychotic symptoms
presentation of mild alzheimers
- recalling new names
- word recall
- losing items
- recognizing familiar faces
what is the presentation of moderate alzheimers
- disoriented to place and time
- behavioral changes
- psychotic symptoms
- difficulty recognizing family and friends
- easily lost
what is the presentation of severe alzheimers
- completely dependent on others for care
- death
how is alzheimers diagnosed
clinical diagnosis with with evidence of cognitive dysfunction leading to functional impairment after ruling out other causes of dementia
t/f imaging of alzheimers is not diagnostic
True
what is the 1st line therapy for alzheimers disease
acetylcholinesterase inhibitors
MOA of acetylcholinesterase inhibitors
increases acetylcholine at the neuronal synapses in the brain
what is the effect of acetylcholinesterase inhibitors
slows progression of alzheimers
what are the acetylcholinesterase inhibitors
- donepezil
- Rivastigmine
- galantamine
SE of acetylcholinesterase inhibitors
- nausea
- anorexia
- sleep disturbances
- diarrhea
what is the most serious SE of acetylcholinesterase inhibitors
bradycardia
what is the counseling point for acetylcholinesterase inhibitors
take with food
what is the MOA of NMDA receptor antagonists
reduces to destruction of cholinergic neurons and may inhibit B-amyloid production, thereby preserving memory
what are the NMDA antagonists
memantine
what are SE of memantine
- dizziness
- HA
- Confusion
- Constipation
what is the combo drug for donepezil and memantine
namzaric
nonpharmacologic interventions for alzheimers
- physical activity
- mentally stimulating activities
- social activities
what should you do when the patient is unable to express their needs?
discontinue AchEI and NMDA
how do you test for executive functions in vascular dementia
one minute semantic test
Behavioral management of alzheimers disease
- SSRIs
- Trazodone
what does advanced alzheimers lead to
- poor nutritional intake
- urinary incontinence
- skin breakdown
- infections
what are the s/s of spontaneous parkinsonism
- bradykinesia
- shuffled gait
- tremors
- very visual dreams
first symptoms that helps differ dementia with lewy bodies from alzheimers
delusional misidentification
what is the criteria for diagnosing dementia w lewy bodies
Probable
-two or more core clinical features of DLB with or without biomarkers
-only one clinical feature with biomarkers
Possible
-one clinical feature with no biomarkers
-one or more biomarker with no clinical features
what would you see on an MRI w lewy bodies
-hippocampus atrophy
-atrophy of the basal ganglia structures and the dorsal midbrain
what is the definitive diagnostic study of dementia w lewy bodies
lewy bodies present on autopsy
t/f frontotemporal dementia has a strong family history component
True
what is frontotemporal dementia
clinical syndrome that results from degeneration of the frontal and temporal lobes of the brain
what is the clinical presentation of frontotemproal dementia
-behavioral variant
-semantic primary progressive aphasia variant
-primary progressive aphasia
what is “behavioral variant” in frontotemporal dementia
- changes in personality
- apathy
- compulsivity
- loss of empathy
how to diagnose behavioral frontotemporal dementia
medial and orbital frontal degeneration on MRI
how to diagnose primary frontotemporal dementia
lateral frontal lobe and precentral gyrus atrophy
how do you manage frontotemporal dementia
- regular exercise
- speech therapy
- behavioral therapy
what is the primary progressive aphasia variant of frontotemporal dementia
- inability to produce words
- affects brocas area
what is the diagnostic finding for semantic frontotemporal dementia
anterior temporal degeneration on MRI
what is the semantic primary progressive aphasia variant of frontotemporal dementia
the loss of ability to recall words or objects
what is normal pressure hydrocephalus
accumulation of CSF that causes enlargement of the ventricles in the brain and compression of surrounding structures
what is the pathophysiology of normal pressure hydrocephalus
CSF builds up in the brain
what is hte clinical presentation of nromal pressure hydrocephalus
- abnormal gait
- urinary incontinence
- dementia
after intervention for normal pressure hydrocephalus, _________ often improves but ______ do not
gait; dementia and incontinence
what is the diagnostic finding of normal pressure hydrocephalus
- MRI shows ventriculomegaly (HALLMARK)
- high volume lumbar puncture
where is the most common area to shunt CSF to in normal pressure hydrocephalus?
abdomen
how do you manage normal pressure hydrocephalus
ventricular shunting
clinical presentation of delirium
-acute onset
-attention deficits
-cognitive impairment
what is vascular dementia
gradual or acute onset of cognitive dysfunction with clinical or radiographic evidence of cerebrovascular disease
what is the pathophysiology of vascular dementia
pathophysiologic, small, micro-ischemic changes in the brain
clinical presentation of vascular dementia
-memory impairment less severe than AD
-difficulty of times activities and executive functions
-behavioral symptoms
-depression
what does imaging show in vascular dementia
MRI showing small infarcts and white matter lesions
how do you manage vascular dementia
same as alzheimers
what things are important to identify and treat in vascular dementia
- HTN
- smoking
- DM
- statins
- antiplatelets
what is dementia with lewy bodies
dementia identified by the presence of lewy bodies on histopathology of the brain tissue
what is the etiology of dementia w lewy bodies
deposits of alpha-synuclein in the cell body
what is the average onset for dementia w lewy bodies
75
t/f dementia with lewy bodies has a strong family history component
false! its sporadic
what is the hallmark sign of dementia w lewy bodies
spontaneous parkinsonism
bradykinesia, BIL limb rigidity, flat affect, gait changes, postural instability
what is the clinical presentation of dementia w lewy bodies
- insidious onset
- memory is less affected
- visuospatial abilities, problem solving, and processing speed are more severe
- parkinson like symptoms
- visual hallucinations
- delusional misidentification
t/f there is more atrophy of the medial temporal lobe in dementia with lewy bodies than alzheimers
False
In lewy bodies you will see greater atrophy in the basal ganglia structures and the dorsal midbrain as well as more pronounced cortical atrophy.
what would a SPECT of dementia with lewy bodies show
reduction in dopamine uptake and perfusion
what is the clinical course of dementia with lewy bodies
- decrease in MMSE by 4-5 years per year
- mean survival is 10 years
how do you manage dementia w lewy bodies
cholinesterase inhibtors
memantine +/-
antipsychotics if psychosis is severe
SSRI for depression
melatonin for REM disorder
Sinemet for parkinsonsim
fludrocortisone for orthostatic hypotension
what are risk factors for higher mortality in dementia with lewy bodies
- older age
- hallucinations
- greater degrees of fluctuation
- neuroleptic sensitivity
what is the MCC of early onset dementia
frontotemporal dementia
what is delerium
disorder characterized by an acute change in attention and cognition
what is the greatest predisposing risk for delirium
preexisting cognitive impairment
what is the management of delirium
- identification and treatment of the underlying medical cause
- eradication of contributing factors
- management of delirium
goal for management of delirium symptoms
an awake and manageable patient, not a sedated patient
