25 Delirium & Dementia Flashcards

1
Q

Describe alzheimers

A

loss of cerebral cortical neruons, neuritic plaques of B-amyloid, and neurofibrillary tangles

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2
Q

What is hallmark cognitive change in AD?

A

memory decline

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3
Q

In alzheimer’s does parietal lobe have more tangles or plaques?

A

more plagues than tangles

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4
Q

What genes are involved in early onset, autosomal dominant Alzheimers? What percentage of disease patients is this responsible for?

A

chromosomes 21, 14 and 1 mutations on amyloid precurso protein (APP), presenilin 1 and 2 (aka AD1, AD3 and AD4). Only 5-10% of all alzheimers pateints

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5
Q

What gene is associated with late onset, sporadic alzheimers? What percentage of disease patients is sporadic responsible for? What percentage of sporadic is the gene mutation responsible for?

A

chromosome 19 abnormality (AD2) that codes for APOE4. Sporadic accounts for 90-95% of all alzheimers patients. APOE4 is present in 50% of those cases

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6
Q

What happens to neurotransmitter levels in alzheimer’s? What nucleus is involved in the pathology?

A

nucleus basalis is atrophied, then it no longer sends Acetylcholine to neocortex. (provides heavy innervation to neocortex

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7
Q

What enzyme inhibitor drug can be given to help aleviate symptoms of alzheimers?

A

AchE inhibitors to increase neuronal neocortex activity. also butrylcholinesterase (BuChE) inhibitors to do the same thing.

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8
Q

What is contraindicated treatment for lewy body dementia?

A

neuroleptic drugs that may be prescribed for hallucinations (extremely sensitive to it and react)

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9
Q

What is the hallmark histology of FTDs?

A

neurofibrillary tangles and/or Pick bodies comprised of ubiquitin and hyper-phosphorylated tau protein. (tauopathies)

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10
Q

What are presenting symptoms of FTD?

A

prominent personality and behavioral changes with LESS prominent memory loss early in course. Loss of pwerosnlal awareness, socal comportment, disnhibition, impulsive, distracted, orality,
Prominent primitive or frontal reflexes.

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11
Q

Patient has loss of judgment, disinhibition, social and sexual misconduct and loss of language, but memory is still workable. Diagnosis? What chromosome mutation is a common cause?

A

Pick’s disease caused by chromosome 17 mutation involving tau protein gene.
Cognitive defects out of proportion to memory loss

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12
Q

What does atrophy pattern of Pick’s disease look like?

A

frontal and temporal atrophy, with parietal lobe spared

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13
Q

What will temporal lobe atrophy cause?

A

fluent (semantic) aphasia and emotional flatness/apathy

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14
Q

What is the minimum acceptable score on Folstein mini-mental status exam? (score that doesn’t raise concern)

A

scores < 27 / 30

Exam has you name date/time, name and remember 3 objects, serial subrtractions, say “no ifs, ands or buts”, write a sentance, etc.

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15
Q

What lab workups should be ordered for dementia?

A

neuropsych battery, chem profile (liver, renal, PTH), thyroid, folate B1,6, and 12, RPR or VDRL for neurosyphilis, lumbar punture, head CT/MRI, PET, APOE4, and AD1,3,4 genes.

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