dementia and delirium Flashcards
Mild cognitive impariment
cognitive decline greater than the expected for pts age and educational level but does not interfere with functioning.
Midlife htn and hypercholesterolemia increase risk of mci as well as lack of exercise.
Presetnation - ℅ memory problems, family member notices.
TX - acetylcholinesterase inhibitors may delay.
Course - more than half develop dementia within 5 years.
Greater if olfactory deficits, memory impairment.
Dementia
- Cortical- involve cortex and cx by prominent memory impairment, language deficits.
- Subcortical - involve areas below cortex (thalamus, basal ganglia, brainstem). due to HIV, parkinson, hunting tons, wilsons, MS.
s/s recall and memory problems, decreased verbal fluency, bradyphrenia (slow thinking), depressed mood, affective lability, apathy, difficulty concentrating, deficits in social judgment.
Both can be vascular dementia, mixed dementia, lewy bodies, or trauma.
Subtypes of dementia:
q. AD
b. vascular
c. Lewy bodies
r. frontotemporal demetnia
Dementia associ with cognitive functioning impairment severe enough to cause limitation of memory, self care, and othe social functioning.
Disrupts QOL and safety.
prealence doubles every 5 years after age 55.
AD account for majority of dementia cases.
Onset - early onset before age 65.
late onset after age 65.
S/s in EOD not common in LOD are delusions and hallucinations, aggressive, difficulties finding right worlds, problems concentration.
Risk - advanced age, higher in women, APOE e4
Middle aged - trauma, untreated HTN, DM, ^ cholesterol, low education, physical.metnal, and social inactivity. obesity
Diet - Mediterranean diet have lower risk
Clinical presentation
Apathy, irritability, anxiety, and depression. Features common to all dementias: cognitive deficits, inability to store, retain, or recall new knowledge, aphasia, apraxia(inability to perfrom purposeful acts), agnosia( loss of ability to recognize familiar objects) disturbances in executive functioning difficutly multitasking apathy and withdrawal emotional disinhibiton anxieyt and fearfulness sleep disturbances decreased self awareness agitation psychotic symptoms
Diagnosis
Labs: CBC, homocysteine , lipid, thryorid, vit b12, folate, rpr, hiv, uds, ua. ecg cxray
Assessments:
MMSE, Clock drawing test, demetia rating scale, mini-cog.
TX
psychotherapy
pharmacotherapy used for patients to maintain cognitive function. Cholinesterase inhibitors (donezipil, rivastigmine, galantine).
Antipsychotic med fo hallucinations, delierum, agitaion.
Antidepressatn - irritability
AD
signifciant cognitive changes in semantic cognition and conceptual congition 12 hrs before Ad diagnosed.
Risk - age, female, ethnicity. African Americans. genetic vulnerability, smoking, alcohol, medical conditions, obesity, dm, cvs, TBI, lifestyle practices.
EOD - familiarl, rapidly progressive,dyphasia and dypraxia.
LOD - 95% of AD, genetic, TBI, low educational achievement, diet high in saturated fats, lack of mental and physical activity.
Lewy body
Risl of sever adverse reaction to antipsychotic mediations.
Cx by progressive decline to limit social and work functioning and pseudo delirium.,
repeated falls, syncope, depression.
In contrasts with AD, short term memory may be good!!
Daytime drowsiness. verbal skills not impaired. Depression is common. EPS common.
Age on onset - 75=80.
Bio - lewy bodies, NO nuerofibrillay tangles as in AD.
No pharmacotherapy approved by FDA except for cholinesterase.
Vascular dementia
Often in males.
Gait disturbance, mood swings, decreased executive functioning, Parkinsonmina symptoms.
Rapid onset.
Only certain areas of brain are affected.
Presentation - anxiety, depression, confusion, and wandering are common, apathy, irritability,
FTD
Result from atrophy of frontal and anterior temporal lobes of brain. between age 50-60.
Slow progressing, behavioral or language disturbances and changes in personality but with memory and spatial orientation remaining intact in early stage.
Onset is subtle and insidious. Possible thyroid.
43% had fx hx.
Genetic influences - TAu protein.
Clinical presetnation - social withdrawal and din inhibition. apathy, perseveration, depression, anxiety, sleep disturbances, psychosis.
Main forms: behavioral symptoms (disinhibition) with personality changes, problems with language.
Tx - atnipsychotics, SSRI, trazodone.
Delirium
Acute brain d. and potential lethal, impairment of consciousness, reduced ability to focus or martin attention, rapid changes in cognition, fluctuations in mental status.
Key features - attn impairment, sleep wake diturbaces, changes in motor acitivyt, decreased activity.
- Altered state of conciousess and change in cognition
- rapid onset
- fluctation of symptoms during the day
- result of medical condition
Rsk - advanced age, genetic vulnerability, AD, VaD, depression, CVA, rbi, low thiamine, htn, dm, ca, chronic illness.
Precipitating factors, benzos psychotropics, opiates muscle relaxants nsaids antacids
Etiology hedydration heat stroke hypoxia pain medications polypharmacy drug intoxication myocardial infarction infectons stroke tbi, brain tumors; seizures disrupted sleep
R PFC, NT abnormalities like acetylcholine.
Presetnation -
a. hyperactive type - restless, agitation, hypervigilant.
b. hypoactive type - slowed speech, movmemtes, apathy, lethargy, sleepiness, reduced alertness. withdrawn, lethargic, depressed.
Mixed delirium hs both features and is most common and have poorer prognosis.
Difficutly sustaining attention, disoriented to time and place but not person, visual hallucinations, delusions, fluctuation level sod consciousness, disturbances of psychomotor state.
mood and anxiety symptoms, fear, anger, depression, apathy, anxiety, and euphoria.
Confusion Assesment method. MMSE.
Tx prevention, antipsychotic to decrease dopamine levels, olanzapine and risperidone. .
Symptoms may profess to delirium 1-3 days and duration between 1 week to 2 monthss.