Alzheimers and Dementia Flashcards
- Define amnesia, aphasia, apraxia, agnosia and executive dysfunction.
ii. Amnesia: impairment of either the ability to store new memories or to recall previous stored memories or both (distinct from transient global amnesia), is the central
symptom of Alzheimer’s disease and other dementias
1. Anterograde: inability to form new memories
2. Retrograde: inability to retrieve information that was encoded premorbidly
iii. Aphasia: loss of the ability to comprehend and or produce language, common in dementia
iv. Apraxia: manifests as impaired performance despite person being physically able and willing to do so
v. Agnosia: inability to recognize or identify objects despite intact sensory function
vi. Executive dysfunction: dysfunction of planning, organizing, decision-making, strategizing, cognitive flexibility, impulse control, sequencing, abstract reasoning and socially appropriate behavior (gauged by activities of daily living)
- Describe the different types of memory and their molecular, cellular and neuroantomic substrates.
PFC contributes to both LTM and STM, lesions caused less effective encoding/ retrival; 1. Neurodegeneration of the hippocampus and medial temporal lobe with disruption of cholinergic transmission; aphasia, viso-spatial problems and executive dysfunction, paraphasic substitutions, disinhibition
Substrates: long-term potentiation results from a complex cascade of events that evolve over different time scales (near-instantaneous phosphorylation of intracellular proteins to the insertion or membrane spanning neurotransmitter receptors to protein synthesis-dependent structural changes)
consolidation reflects the number of times that a piece of information is re-remembered (multiple traces)
Discuss the pathological findings in a patient with alzheimers disease.
Amyloid plaques: networks of fibrillary material in loose, disjointed arrangement, composed of swollen, degenerated neuronal processes around a central deposit of amyloid with close association with small vessel (rupture is common)
Neurofibrillary tangles: accumulations of large numbers of paired helical filaments in the cytoplasm of neurons (birefringent under polarized light/silver stain)
AD dementia related to loss of neurons and synapses, autosomal dominant forms
- Correlate the neuropathological changes found in Alzheimer’s disease with its clinical manifestations, in particular, amnesia.
- Decreases acetylcholine and Somatostatin
- Apoplipoprotein E found in the plaque and being a carrier of apoE-e4 allele is associated with AD while apoE-e2 is protective
- Vascular disease causes degeneration and loss of neurons
- Microglia function helps to clear plaques, low grade inflammation found in AD, microglia lose ability to take up and degrade AB and show increased expression of inflammatory cytokines
- List the diagnostic criteria for Alzheimer’s disease.
Met criteria for major or mild neurocognitive disorder, insidious onset and gradual progression of impairment in at least 2 cognitive domains.
1. Evidence of a causative Alzhemier’s disease genetic mutation from FH or testing
- All: clear evidence of decline in memory and learning, steadily progressive gradual decline in cognition without plateaus, no evidence of mixed etiology
- Describe the epidemiology f Alzheimer’s disease, vascular dementia, Lewy body disease and frontotemporal dementia.
Risk factors: age, others include TBI, length of education, late-life depression, CV risk factors, abstinence or excessive alcohol consumption
ii. Mild cognitive impairment, STM is affected, eventually LTM is affected in a gradient
- Contrast the clinical presentation, course, and prognosis of the principal types of dementia, including Alzheimer’s disease, vascular dementia, Lewy body disease and frontotemporal dementia.
Alzheimers: progressive decline in ability to perform activities of daily living, emotional and psychological disturbances (depression, anxiety, irritability, apathy, insomnia, paranoid delusions, visual hallucinations, restlessness, and aggression); Dx usually between 75 and 85 yo, 6-12 years between diagnosis and death
Vascular dementia due to cerebrovascular disease (ie. stroke) usually with step-wise development of symptoms, dx 65-75yo; slow progression via tx with cognitive enhancer and addressing vascular risk factors, (episodic, MRI signs)
Lewy body diseases:
Parkinson’s disease dementia: cognitive symptoms at least one year after the onset of motor symptoms
Dementia with Lewy bodies: fluctuating symptoms, visual hallucinations, cognitive impairment, less severe parkinsonian symptoms than in Parkinson’s disease (LB found in cerebral cortex)
Frontotemporal Dementia (collection of syndromes including Pick’s dz): Presence of tau inclusion bodies on histological exam, Lobar degeneration of frontal/temporal lobe, Behavioral disturbance and/or aphasia, repetitive actions, visual; Onset between 50 and 65, may be dx as MDD due to apathy, amotivation, anergia or mania due to dis-inhibition, impulsivity or irritability; death occurs within 5 years
Discuss medical and substance causes of dementia
Huntington’s disease, Creutfeldt-Jakob, neurosyphilis, Wernicke-Korsakoff syndrome, repeated head trauma, CNS tumor and HIV/AID, depression, hypothyroidism, B12 deficiency, normal pressure hydrocephalus (wet, wobbly and whacky) and subdural hematoma, thiamine
- List the treatments available for dementia, including psychotropic medications, psychosocial interventions and caregiver interventions.
Cognitive enhancing: donepezil, galatamine rivastigmine or memantine used to delay cognitive decline, may benefit in vascular dementia and dementia with Lewy bodies
Behavioral interventions (redirecting, distracting), or SSRI, antidepressants and atypical antipsychotics (increased mortality in elders with dementia) to address depression, anxiety, psychosis and agitation
Planning for the future early on the course of dementia is important
- List methods used to assess cognition in patients suspected of having a neurocognitive disorder.
Mini mental state exam: orientation to time and place, registration and recall of 3 objects, attention, naming, repetition, reading comprehension, writing a sentence, copying a figure and following a three-step command
SLUMS: orientation to place and time, registration and recall of five objects, calculation, naming animals, attention, drawing a clock and ID a shape, recall a story
montreal cognitive assessment: for mild cognitive impairment, assessment of visuospatial function, executive function, naming, immediate and delayed recall, attention, language, abstraction and orientation
Animal naming test, 15 or more is normal (tests executive function)
Clock drawing: test of visuospatial and executive function
Mini-cog: clock-drawing, 3 object recall (quick cognitive screen)
- Describe the epidemiology, pathophysiology, and risk factors of delirium.
common in terminally ill (80%), nursing home residents (60%) and patients with cancer (25%); delririum has a high mortality rate (sign of more severe underlying condition)
final common pathway is a disturbance in the reticular activating system (associated with arousal and attention and facilities sensory input to the cortex via cholinergic projections form the brainstem to the thalamus)
Toxic: sedative-hypnotic medications, medications with anticholinergic properties, opiates, steroids, antibiotics (quinolones)
Alcohol withdrawal (delirium tremens), sedative-hypnotic withdrawal
Metabolic: electrolytes (hyponatremia, hypernatremia, hypocalcemia and hypercalcemia); hypoxia or hypercapnia; hypoglycemia/hyperglycemia
Infectious: UTI, pneumonia, meningitis, encephalitis, sepsis, CNS abscess
Other: TBI, stroke, epilepsy, cardiac ischemia or arrhythmia
- Describe the clinical presentation, and prognosis of delirium.
waxing and waning of symptoms:
impairment of attention, altered level of consciousness
associated disorientation, disturbance of sleep-wake cycle, perceptual disturbance (visual hallucinations) paranoia, memory loss, emotional disturbances
What is the diagnostic criteria for delirium?
- Disturbance in attention (ability to direct, focus, sustain and shift attention) and awareness (reduced orientation to the environment)
- Disturbance develops over a shot time, tends to fluctuate in severity
- Additional disturbance in cognition (memory deficit, disorientation, language, visuospatial ability or perception)
a. Not better explained by another preexisting or established condition or from another medical condition
- Distinguish between delirium and dementia.
duration, onset, course and whether its reversible (also different causes)
- Describe the management of delirium.
treatment of underlying medical condition
breif trial of an antipsychotic medication (BZD avoided unless delirium tremens)
sere quill can shorten the length of delirium
