Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

2. Geriatric Psychiatry + Neuroanatomy > Geri One Pagers (Harrison/Bennett) > Flashcards

Geri One Pagers (Harrison/Bennett) Flashcards

1
Q

there is a big spike in dx alzheimer’s disease after what ageq

A

after age 75

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what is the prevalence of alzheimer’s after 60s

A

above 25%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what two brain areas are most affected in early alzheimer’s

A

hippocampus

parietal lobe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is the usual function of tau? how is tis changed in alzheimer’s

A

normal tau–> supports microtubules for function, transport within neuron

abnormal tau–> tau separates from microtubules, tau fragments form tangles and therefor transport within the neuron ceases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

how much is your risk increased if you have a first degree relative with alzheimer’s

A

4x increased risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

why do people with down syndrome develop alzheimer’s

A

have extra chromosome 21, which means they have an extra copy of the amyloid precursor protein and thus high risk of developing alzheimer’s if survive to midlife

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

alzheimer’s is “early onset” if occurs before what age

A

55

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is the strongest risk factor for alzheimer’s

A

age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

list 6 risk factors for alzheimer’s

A

age

sex (female higher risk)

vascular

hx depression

low education

TBI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what are two areas of life which are often the first to be affected in alzheimer’s

A

ability to drive

ability to handle finances

*good to screen for these

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what two areas of functioning are classically affected in alzheimer’s

A
  1. amnestic memory loss/learning–> hippocampus
  2. perceptual/motor dysfunction–> parietal
    (i.e do you get lost?)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what area of functioning is often preserved until late in course in alzheimer’s

A

social cognition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what 3 areas are often first affected when undergoing neuropsych testing in alzheimer’s

A

memory

language/fluency

executive function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what two things would you look for in CT head if suspecting alzheimer’s

A

cortical atrophy

medial temporal lobe atrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what two things would you look for on MRI is suspecting alzheimer’s

A

parietal atrophy

hippocampal atrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what would you look for on PET/SPECT if suspecting alzheimer’s

A

bilateral tempoparietal hypometabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what are the 3 hallmarks of alzheimer’s on postmortem exam of the brain

A

cortical atrophy

amyloid-predominant neuritic plaques

tau-predominant neurofibrillary tangles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what are two ways to look for amyloid early in pathophysiological cascade for alzheimer’s

A

PET amyloid imaging

CSF amyloid beta-42 (low levels)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what is the gene with the greatest known effect on the risk of developing late onset alzheimers

A

APOE (chromosome 19)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what are the two genes associated with EOAD

A

PSEN 1 or 2–> PSEN 1 causes up to 80% of all familial alzheimer’s cases

APP gene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what medication can be used for apathy in alzheimer’s

A

methylphenidate was only agent with benefit, according to cochrane review (small benefit only)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what is a mnemonic for the symptoms of the behavioural variant of frontotemporal dementia

A

HADES

Hyperorality and dietary changes

Apathy or inertia

Disinhibition of behaviour

Empathy or sympathy loss

Stereotyped, perseverative or compulsive/ritualistic behaviour

needs 3/5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what area of functioning is most prominently affected in behavioural variant of frontotemporal dementia

A

prominent decline in SOCIAL COGNITION or EXECUTIVE ABILITIES

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what is relatively spared in FTD

A

learning and memory

perceptual-motor function

*relevant because these are the areas most affected in alzheimers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what is required for “probable” (instead of possible) FTD

A

evidence of a causative genetic mutation from either fam hx or GENETIC TESTING
OR
evidence of disproportionate frontal and/or temporal lobe involvement from NEUROIMAGING

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what % of people with FTD have family hx of early onset NCD

A

about 40%

–10% show autosomal dominant inheritance pattern

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

list 3 genes that may be associated with FTD

A

MAPT

GRN

C9ORF72

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

why dont you treat FTD with cholinesterase inhibitors

A

because the cholinergic system is INTACT in these patients

treating with cholinesterase inhibitors can make behaviours WORSE

(serotonin is mostly affected, maybe some dopamine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what % of those with FTD are diagnosed before age 65

A

75%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what is the classic presentation for FTD

A

progressive development of behavioural and personality change, language impairment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

describe symptoms of behavioural variant of FTD

A

impaired insight

apathy, disinhibition

decreased socialization, self care, personal responsibilities, social appropriateness

changes in social style, religious/political beliefs, hyperorality

COGNITIVE DECLINE IS LESS PROMINENT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

how do language variants of FTD typically present

A

primary progressive aphasia with gradual onset

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

list the 3 subtypes of FTD language variant

A

logopenic

semantic

nonfluent (agrammatic)

34
Q

what is the earliest sign of FTD semantic variant

A

word finding

35
Q

what is the most prominent symptom in FTD semantic variant

A

impaired single word comprehension and object naming

(preserved fluency, repetition, grammar)

36
Q

what is the most prominent symptom in nonfluent/agrammatic FTD variant

A

motor speech deficit, articulatory difficulty

(can understand simple words)

37
Q

what is the most prominent symptom in logopenic FTD

A

impaired single word retrieval, repetition, naming (vague)

*spared grammar

*more linked to alzheimers

38
Q

what would you expect to see on CT/MRI in the behavioural variant of FTD

A

atrophy in frontal lobe (especially medial)

atrophy in anterior temporal lobe

39
Q

what would you expect to see on CT/MRI in the semantic variant of FTD

A

atrophy in middle, inferior and anterior temporal lobe
–> bilateral but more left sided

40
Q

what would you expect to see on CT/MRI in the nonfluent variant of FTD

A

atrophy in left posterior frontal-insular

41
Q

what would you expect to see on CT/MRI in the logopenic variant of FTD

A

left posterior perisylvian or parietal atrophy

42
Q

what medications are used for FTD

A

SSRIs, trazodone, AAPs as alternatives

43
Q

in what areas are the most effects noted in vascular dementia

A

complex attention (including processing speed) and frontal-executive function

44
Q

what is CADASIL

A

cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy

genetic condition

45
Q

in vascular dementia, if there is more of a picture of worsening executive function, where is the stroke more likely to have occurred

A

subcortical

46
Q

in vascular dementia, if there is more of a picture of worsening complex attention, where is the stroke more likely to have occurred

A

cortical

47
Q

describe 4 features of “vascular depression”

A

late onset depressive symptoms

psychomotor slowing

executive dysfunction

progressive small vessel ischemic disease

48
Q

what gene anomaly causes CADASIL

A

NOTCH3 mutation

49
Q

what should you do in patients with a stroke history in order to reduce the risk of post stroke depression

A

lower BP

50
Q

does LBD have more or less of a cholinergic defecit than alzheimers

A

LBD has a MORE PROFOUND cholinergic deficit than in alzheimers

thus they RESPOND BETTER to cholinesterase inhibitors

51
Q

how is the hippocampus affected in LBD compared to AD

A

hippocampus relatively preserved in LBD vs AD

52
Q

what is a major risk factor for LBD

A

presence of REM sleep behaviour disorder

53
Q

at what age do most LBDs present

A

mid 70s

54
Q

what often occurs before diagnosis of LBD

A

prodromal delirium precipitated by illness or surgery

55
Q

what are the 4 cardinal symptoms of LBD

A
  1. fluctuating cognition with variations in attention and alertness
  2. recurrent well formed visual hallucinations (or in other modalities; “feeling of presence” in up to 15%)
  3. REM sleep behaviour disorder (acting out dreams)
  4. parkinsons symptoms like bradykinesia, tremor, rigidity
56
Q

what might you see on EEG in LBD

A

prominent slow wave activity

temporal lobe transient waves

57
Q

what might you see on SPECT/CT perfusion scan in LBD

A

reduced occipital activity

generalized low uptake

low dopamine transporter uptake

58
Q

which NCD population sees the MOST benefit from use of cholinesterase inhibitors

A

LBD–have even more cholinergic deficit than AZ

59
Q

what is the preferred agent for treating hallucinations in LBD

A

quetiapine but often doesnt work (clozapine is best results)

60
Q

what to use in REM sleep behaviour disorder

A

melatonin up to 12mg

trazodone is a good place to start

gabapentin or pregabalin

clonazepam later option with caution in LBD pop

61
Q

list the 4 types of NONfluent aphasias

A

global aphasia

mixed transcortical aphasia

broca’s aphasia

transcortical motor aphasia

62
Q

list the 4 types of FLUENT aphasias

A

wernicke’s aphasia

transcortical sensory aphasia

conduction aphasia

anomic aphasia

63
Q

list the 4 types of aphasia where people CAN repeat words or phrases

A

mixed transcortical aphasia

transcortical motor aphasia

transcortical sensory aphasia

anomic aphasia

64
Q

list the 4 types of aphasia where people CANNOT repeat words or phrases

A

global aphasia

broca’s aphasia

wernicke’s aphasia

conduction aphasia

65
Q

list the 4 types of aphasia where someone CAN understand spoken messages

A

brocas aphasia

transcortical motor aphasia

conduction aphasia

anomic aphasia

66
Q

if someone presents with the following pattern of speech production/comprehension, what type of aphasia do they have?

fluent + comprehends spoken messages + can repeat words or phrases

A

anomic aphasia

67
Q

if someone presents with the following pattern of speech production/comprehension, what type of aphasia do they have?

non fluent + cannot comprehend spoken messages + cannot repeat words or phrases

A

global aphasia

68
Q

if someone presents with the following pattern of speech production/comprehension, what type of aphasia do they have?

fluent + cannot comprehend spoken messages + can repeat words

A

transcortical sensory aphasia

69
Q

if someone presents with the following pattern of speech production/comprehension, what type of aphasia do they have?

fluent + cannot comprehend spoken messages + cannot repeat words

A

wernicke’s aphasia

70
Q

if someone presents with the following pattern of speech production/comprehension, what type of aphasia do they have?

non fluent + can comprehend spoken messages + cannot repeat words

A

broca’s aphasia

71
Q

if someone presents with the following pattern of speech production/comprehension, what type of aphasia do they have?

fluent + can comprehend spoken messages + cannot repeat

A

conduction aphasia

72
Q

if someone presents with the following pattern of speech production/comprehension, what type of aphasia do they have?

non fluent + can comprehend + can repeat

A

transcortical motor aphasia

73
Q

if someone presents with the following pattern of speech production/comprehension, what type of aphasia do they have?

non fluent + cannot comprehend + can repeat

A

mixed transcortical aphasia

74
Q

what is the most severe form of aphasia

A

global aphasia

75
Q

can someone with global aphasia read or write

A

no

76
Q

can someone with broca’s aphasia read or write

A

may be able to read

limited in writing

77
Q

can someone with wernicke’s aphasia read or write

A

often reading and writing is severly impaired

“inability to grasp meaning of spoken words”

78
Q

can someone with anomic aphasia read or write

A

read well

same trouble finding words in writing as in speaking

79
Q

what is the clinical picture of anomic aphasia

A

people who are left wiht a persistent inability to supply the words for the very things they want to talk about (esp. significant nouns and verbs)

speech is full of vague circumlocutions and expressions of frustration

understand speech well

80
Q

what is primary progressive aphasia

A

neurological syndrome in which language capabilities become slowly and progressively impaired

caused by neurodegenerative diseases (unlike other forms of aphasia which are susually caused by stroke or TBI)

results from deterioration of brain tissue responsible for speech and language

81
Q

why does pseudobulbar affect occur

A

due to disconnect between the frontal lobe (which regulated emotions) and the cerebellum and brainstem (which is where basic reflexes are mediated)

LOSS OF INHIBITION from limbic motor neurons in the brain may also be involved

2. Geriatric Psychiatry + Neuroanatomy (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions