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Dementia Delirium
Clinical Medicine II
| Question | Answer |
|---|---|
| Acute (hrs to days) confusional state that is normally transient | Delirium |
| Clinical hallmark signs of delirium | ↓attention span and waxing/waning confusion |
| What is delirium often diagnosed for | dementia or depression |
| What are two things to do to try and miss delirium | thing delirium until proven otherwise, also may have pre-existing dementia (compare to baseline) |
| What are common situations w/ delirium | hospitalized, ICU pt’s, post op, ~80% near death |
| What is the theory cause of delirium | dec. Ach and and excess of dopamine |
| What is the most reversible cause of delirium | medications |
| What is the D.E.L.I.R.I.U.M. causes of it | Dementia, electrolyte d/o, lung, liver, heart, kidney, brain, Infx, Rx drugs, Injury, pain stress, Unfamiliar environment, Metabolic |
| Common drugs that precipitate delirium | Anticholinergics, analgesics (narcotics), benzodiazepines, corticosteroids, antidepressants, parkinson’s medications, dig tox |
| What are 7 RF’s for delirium | Cog impairments, sleep deprivation, immobilization, psychoactive meds, vision impairment, hearing impairment, dehydration |
| What are the three types of delirium | hyperactive, hypoactive, mixed (nocturnal agitation daytime sedation) |
| What are the three diagnostic criteria the DSM states classifies delirium | Disturbance of consciousness, acute (hrs-days), fluctuate throughout the day |
| Sxs of delirium | Clouding of consciousness, difficult maintaining/ shifting attention, disorientation, illusions, hallucinations, fluctuating consciousness |
| What are two cognitive tests for delirium | MMSE: Mini mental status exam and CAM: cognitive assessment method |
| Evaluation of delirium | H&P: compare to baseline, Cognitive tests, Med list, lab evaluation: LFT’s, CMC (infx), BUN/Cr, glucoae and many more depending on the pt |
| What four features are we evaluating with CAM | 1: acute onset w/ fluctuation, 2: inattention, 3: Disorganized thinking, 4: altered level of consciousness |
| With CAM, when can we classify it as deliurm | need 1&2 with either 3 or 4 |
| What is the management of delirium | determine underlying cause and tx it: medical emergency! Tx sxs if necessary (antipsychotic to ↓ agitation), familiarize the room/situation |
| When does delirium usually reside by | 1-2 weeks, lags behind the causative illness |
| How can we prevent delirium | identify high risk pt’s, initiate appropriate interventions |
| An acquired sustained impairment in intellectual fxn w/ compromise in ¼ catagories | dementia |
| What at the spheres of mental activity | memory, language, visuolspatial skills, personality, (other: judgement, calculation, abstraction |
| What are the types of dementia, MC | Alzheimer’s :MC, vascular, mixed, other |
| Types of dementia in late life | alzheimer’s, vascular, lewy body, frontotemporal+pick dz, reversible |
| What does Alzheimer dementia affect | progressive, memory, higher learning, reasoning, behavior, emotion |
| Characteristic signs of alzheimer’s dementia | neurofibrillary tangles and neuritic plaquesdestroy cholinergic and other brain neuronal pathways, also serotnergic and noradrenergic pathways lost |
| 2nd most common type of dementia, cause | Vascular, results from multiple infarcts, ischemia, hypoperfusion, amyloid angiopathy, brain hemorrhage etc. |
| Main different b/w alzheimer’s and vascular dementia | Vascular d/t infarcts, and CNS plaques cause focal neuro sxs |
| What is a lewy body | eosinophilic inclusions in subcortical neurons of pt’s w/ Parkinson’s dz |
| Clinical classifications of DLB | Fluctuations in cognition, visual hallucinations, parkinsonian motor signs |
| What is FTD | Frontotemporal dementia: bilateral frontal lboe atrophy w/ intraneuronal inclusions (Pick bodies) |
| 3 classifications of FTD | Picks dz w/ pick bodies, frontotemporal atrophy w/o picks, and frontotemporal atrophy w/ motor neuron dz |
| What is a dz in the family of transmissible spongiform encephalopathy’s | Creutzfeld-Jakob dz |
| Patho of Alzheimer’s | Plaques: deposits of beta- amyloid precursor proteins Tangles: intracellular accumulations of cytoskeletal protein tau |
| Fxn of tau. Dz? | makes mictrotubles stable in cytoskeleton, hyperphosphorylation of tau causes tangles w/ other tau strands→↓nutrients→nerve cell death |
| Two classifications of AD | early onset 40-64yo late onset >65yo, survival 4-8yrs post dx |
| What is the genetic influence of AD | “susceptibility” gene, Identical twins>fraternal twins, Slibling with AD 40-50%risk |
| How is EOFAD and LAFAD genetically inherited | E: autosomal dominant? PS1,PS2, APP L: “susceptibility gene” |
| What are environmental factors would ↑ development of dementia | head trauma |
| What gene is associated w/ AD | Apolipoprotein E, APOE-4: 3-5fold risk, APOE 2: 2 fold protection (single alleles) worst 4/4 best 2/2 |
| What is the diagnostic criteria for AD | know it :D |
| What is the diagnostic workup doing | r/o other causes |
| Is LOC affected w/ Alzheimer’s | no, but usually is w/ delirium |
| Are neurologic sxs present in AD | can yes with vascular dementia, but not w/ delirium |
Created by:
streetsmarts
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