Clinical- 5 Flashcards

1
Q

What is dementia?

A

acquire, generalized + usually progressive impairment of cognitive fxn

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2
Q

What is preserved in dementia, which goes away in coma or confusional states?

A

level of consciousness

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3
Q

What are the cognitive changes with age?

A

slower info processing, impaired learning, reduced word finding/fluency, increased reaction time

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4
Q

What are the neuro-opthalmologic changes with aging?

A

slow pupil, impaired upgaze, impaired convergence

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5
Q

What are the motor changes with aging?

A

atrophy of hand/foot muscles, increased msucle tone, flexion posture, small or board gait

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6
Q

What ar ethe sensory changes with aging?

A

reduced visual,auditory, gustatory, olfactory and vibration acuity

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7
Q

what are the reflex changes with aging?

A

primitive reflexes, absent abdominal and ankle reflexes

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8
Q

What are the 5 reversible causes of dementia?

A

normal pressure hydrocephalus, intracranial mass lesions, B12 deficiency, hypothyroidism, neurosyphilis

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9
Q

What are the 4 dementias with extrapyramidal symptoms?

A

THINGS WITH MOVEMENT PROBLEMS.

dementiawith Lewy bodies, corticobasal ganglionic degeneration, Huntingtions, progressive suprenuclear palsy

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10
Q

What are the 4 diseases withOUT extrapyrimidal symptoms?

A

Alz, Picks, Creutzfeldt-Jacob,normal pressure hydrocephalus

ALL THING WITHOUT MOVEMENT PROBLEMS

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11
Q

Alz- epidemiology

A

60-70% cause of dementia
15% of people >65
45% 85 and older
men = women

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12
Q

Alz- mutation

A

in APP, PS1 or PS2

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13
Q

Which trisomy has an icnreased risk of Alz?

A

Trisomy 21

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14
Q

Why do Downs have an increased risk of Alz?

A

the APP gene is on chromosome 21 –> more APP –> Alz!

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15
Q

Which apolipoprotein has an increased risk of Alz?

A

Apo E4

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16
Q

Which apolipoprotein is PROTECTIVE against Alz??(big board quesiton)

A

ApoE2

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17
Q

How do neuritic plaques form?

A

APP is cleaved by a-secretase or b-secretase incorrectly –> AB42 aggregates (normal is Ab40)

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18
Q

What is the fxn of tau?

A

stabilization of microtubules

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19
Q

What happens to tau in Alz?

A

it becomes hyperphosphorylated

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20
Q

What happens when tau gets phosphoprylated?

A

it dissociates from th microtubules –> aggregates form tangles

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21
Q

What happens if there is synaptic dysfxn?

A

memory loss

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22
Q

Why is the focal cerebral atrophy in Alz?

A

you lose glutamatergic and cholinergic neurons

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23
Q

What are the neurological manifestations of Alz?

A

progressive cognitive impairment, aphasia, anomia and acalculia, depression, apraxia

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24
Q

What are the motor manifestations of Alz?

A

gait disorders- short, slow,shuffling steps with flexedposture

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25
Alz- Tx
no Tx to reverse existing deficits
26
What is the NMDA glutamate R antagonist to Tx Alz?
Mamantine
27
What are the AchEi's to Tx Alz?
Donepazil, tacrine, rivastigmine, galantamine
28
Alz- imagining Dx
CT/MRI for cortical atrophy w/enlarged ventricles PET for hypometabolsim/perfusion in temporal and parietal lobes. can use it wth Pittsburgh compound B which binds to amyloid plaques
29
Alz- CSF Dx
increased CSF levels of AB42, tau, and P-tau
30
Frontotemporal dementia (FD)- etiology
genetically inheirted but most are sporatic with unknown cause
31
FTD- clinical findings
behavior cahnges, altered interpersonal interactions and conduct, semantic dementia (receptive aphasia), progressive nonfluent aphasia (expressive aphasia, brocas)
32
FTD- Dx
MRI for frontal lobe atrophy, PET for hypometabolsim in regions, off Sx.
33
Creutzeldt-Jacob Disease (CJD)- etiology
eating contaminated beef with prions. 85% are sporadic.
34
CJD- Sx
cognitive abnormalities, memory loss, myoclonus, extrapyramidal signs, cerebellar signs
35
CJD- Dx
EEG's show sharp waves/spikes, elevated CSF protein, IMMUNODETECTION OF PRPsc in brain tissue or PRPc in lymphocytes
36
Normal pressure hydrocephalus (NPH)- triad
dementia, gait apraxia + incontinence (wacky, wobble, wet)
37
NPH- clinical findings
magnetic gait, dementia, incontinence
38
NPH- Dx
CT/MRI show enlarged ventricles, normal opening pressure on LP, 30-50mL CSF removal IMPROVES Sx
39
How long is the onset of dementia prior to the 1st motor Sx?
1 year
40
What are the clinical findings to dementia with lewy bodies?
visaul hallucinations, parkinsonism, cognitive decline
41
What are the lewy bodies?
round eosinophilic intracytoplasmic neuronal inclusions that contain a-synclein
42
Vascular dementia- Hx
HTN, abrupt onset
43
Vascular dementia- clinical findings
pseudobulbar palsy with dysarthria, dysphagia and pathological emotionality (woman period Sx)
44
Vascular dementia- Dx
multiple large infarcts of MRI, low density in subcortical white matter
45
What is the most common disorder mistaken for dementia?
depression
46
What are the characteristics of both depression and dementia, which can be confusing to noob Dr.'s (MDs)?
mental slowness, apathy, self-neglect, withdrawal, irritability, difficulty with memory and concentration and changes in behavior + personality
47
Now let's play a quickfire game. I'll say a characteristic and you tell me if it's either depression or dementia. Ready? Abrupt onset
depression
48
Progressive deterioration
dementia
49
Plateau of dysfxn
depression
50
No Hx of depression
dementia
51
Pt unaware of extent of deficits + doesnt complain of memory loss
dementia
52
Somatic complaints or hypochondriases common
depression
53
Variable affect
dementia
54
Somatic complaints uncommon
dementia
55
Insidious onset
dementia
56
Prominent vegetative Sx
depression
57
Impairment worse at night
dementia
58
Neuro exam + labs abnormal
dementia
59
Few vefetative Sx
dementia
60
Impairment not worse at night
depression
61
Neuro exam + labs normal
depression
62
What are the etiologies to cause acute amnesia?
head trauma, ischemia, PCA occlusion, transiet global ischemia, alcoholic blackouts, wernickes encephalopathy, dissociatifve amensia
63
What are the etiologies to cause chronic amnesia?
alcohol korsakoff syndrome, postencephalitic (HSV is big), tumor, paraneoplastic limbic encephalitis