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Diagnosis_Management 1 > Neurocognitive > Flashcards

Neurocognitive Flashcards

1
Q

definition of delirium

A

acute decline of LOC and cognition w/ particular impairment in attention

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2
Q

onset/course of delirium

A

sudden onset, brief fluctuating course, rapid resolution once cause is treated

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3
Q

9 subcategories of dementia (NCD)

A

-Alzheimer’s
-vascular
-HIV
-TBI
-frontotemporal
-Prion disease
-Substance-induced
-multiple etiologies
-unspecified

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4
Q

4 categories of cognition

A

-memory
-visuospatial/construction abilities
-reading/writing/math
-abstraction ability

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5
Q

common neurological s/s of delirium

A

tremor
asterixis
nystagmus
incoordination
incontinence

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6
Q

what is the primary neurotransmitter involved in delirium

A

acetylcholine

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7
Q

beclouded dementia

A

delirium in a dementia patient

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8
Q

how do you differentiate delirium from schizophrenia

A

schizophrenia:
-delusions/hallucinations are more constant and better organized.
-usually no change in LOC/orientation

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9
Q

what increases recovery time from delirium

A

lengthier delirium
older patient

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10
Q

delirium recall

A

spotty, like a dream or a nightmare

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11
Q

what are the 3 aspects of delirium that may require medication

A

psychosis
agitation
insomnia

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12
Q

what antipsychotic is not appropriate for delirium and why

A

ziprasidone as it can be activating

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13
Q

when in delirium can use benzodiazepines

A

alcohol-induced delirium
other types they may worsen confusion

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14
Q

what medication is approved for parkinson’s psychosis

A

pimavanserin

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15
Q

which dementias have an insidious onset

A

Alzheimer’s, vascular, endocrinopathies, brain tumors, metabolic disorders

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16
Q

which dementia have rapid onset

A

head trauma, cardiac arrest, stroke, encephalitis

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17
Q

what are the cholinesterase inhibitors

A

donepezil (Aricept)
rivastigmine (exelon)
galantamine (Razadyne)
Tacrine

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18
Q

How do cholinesterase inhibitors work

A

reduce the inactivation of acetylcholine which increases its cholinergic effects to cause modest improvement in memory

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19
Q

how does memantine (Namenda) work

A

protects neurons from cytotoxic excessive glutamate

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20
Q

which cholinesterase inhibitor is best tiolerated

A

donepezil

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21
Q

what are the two most common types of dementia

A

Alzheimers followed by vascular

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22
Q

what neurotransmitters are hypoactive in dementia

A

acetylcholine and norepinephrine

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23
Q

which enzymes are decreased in dementia and what do the do

A

choline acetyltransferase which is critical for acetylcholine synthesis

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24
Q

what neuroactive peptides are decreased in dementia

A

somatostatin and corticotropin

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25
Q

what is the dementia that was recently discovered and what is the typical age of onset

A

familial multiple system tauopathy
onset in 40-50s

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26
Q

what can be a differentiating factor between Alzheimer’s and frontotemporal dementia

A

in early stages, there are more behavioral sx in frontotemporal and cognition is better preserved

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27
Q

what is a differentiating factor between Alzheimer’s and Lewy body dementia

A

Lewy body commonly presents with hallucinations, parkinsonian sx, and EPS s/s

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28
Q

differentiating factors between Alzheimer’s and Huntington’s dementia

A

Huntington’s has more motor sx and memory/language/insight remains intact in early phases

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29
Q

anterograde amnesia

A

inability to learn new things

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30
Q

retrograde amnesia

A

inability to recall previously learned information

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31
Q

what is an amnestic disorder

A

neurocognitive disorder due to another medical condition

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32
Q

what are some medical conditions that can cause amnestic disorders

A

cerebrovascular disease
MS
Korsakoff syndrome
Alcoholic blackouts
ECT
Head injury
transient global amnesia

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33
Q

what causes korsakoff syndrome

A

thiamine deficiency usually seen in alcoholics

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34
Q

definition of transient global amnesia

A

abrupt loss of ability to recall recent events or learn new information

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35
Q

what causes seizures

A

excessive and spontaneous neural firing

36
Q

what are the types of general seizures

A

tonic-clonic
absence

37
Q

what are the types of partial seizures

A

simple
complex

38
Q

characteristics of absence seizures

A

no convulsions
lose touch w/ reality but not consciousness

39
Q

when do absence seizures usually develop

A

between 5-7 and often disappear with puberty

40
Q

what is the difference between general and partial seizures

A

general involves entire brain and partial involves a focal region

41
Q

main characteristic of simple partial seizure

A

no alteration of consciousness

42
Q

main characteristic of complex partial seizure

A

alteration in consciousness

43
Q

what is the most common form of epilepsy in adults

A

complex partial

44
Q

autonomic sensations of the preictal state

A

stomach full, blushing, change in respiration

45
Q

cognitive sensations of preictal state

A

deja-vu
forced thinking
dreamy state

46
Q

affective symptoms of preictal state

A

fear
panic
depression
elation

47
Q

automatisms of preictal state

A

lip-smacking, rubbing, chewing

48
Q

what are some symptoms of interictal state

A

personality disturbance
psychotic symptoms
violence
mood disorder symptoms

49
Q

what should be done about seizure patients who develop new psychiatric symptoms

A

evaluation of seizure control
eval for other psych sx

50
Q

what are some sx that should cause a suspicion of epilepst

A

abrupt psychosis in healthy person
abrupt delirium w/o a cause
hx of similar episodes w/ abrupt onset and recovery
hx of unexplained falls/fainting

51
Q

first line tx for tonic-clonic seizures

A

valproate and phenytoin

52
Q

first line for partial seizures

A

carbamazepine, oxcarbazepine, phenytoin

53
Q

first line for absence seizures

A

ethosuximide and valproate

54
Q

demyelinating disorders that can cause neurocognitive sx

A

MS
ALS

55
Q

infectious diseases that can cause neurocognitive sx

A

herpes simplex encephalitis
rabies encephalitis
neurosyphilis
chronic meningitis
subacute sclerosing panencephalitis
Lyme disease
prion disease

56
Q

signs of Lyme disease

A

bullseye rash at bite site followed by flu-like symptoms

57
Q

what causes prion diseases

A

transmission of infectious protein called prion

58
Q

types of prion diseases

A

Creutzfeldt-Jakob disease
variant CJD (mad cow disease)
Kuru
Gerstmann-Straussler-Scheinker
fatal familiar insomnia

59
Q

when can you break confidentiality with an HIV patient

A

if you know they are putting others at risk

60
Q

what does development of dementia in an HIV patient mean

A

typically death in 6 months

61
Q

different course for AIDS mania

A

cognitive slowing/dementia
more irritable than euphoric
severe presentation
malignant course
chronic with infrequent remissions

62
Q

endocrine disorders that can cause neurocognitive sx

A

thyroid disorders
parathyroid disorders
adrenal disorders
pituitary disorders

63
Q

disorder of adrenal insufficiency

A

Addison’s disease

64
Q

disorder of adrenal excess

A

Cushing syndrome

65
Q

metabolic disorders with neurocognitive symptoms

A

hepatic encephalopathy
uremic encephalopathy
hypoglycemia encephalopathy
diabetic ketoacidosis
acute intermittent porphyria

66
Q

nutritional disorders that can cause neurocognitive symptoms

A

niacin deficiency
thiamine deficiency
cobalamin deficiency

67
Q

toxins that cause neurocognitive symptoms

A

mercury
lead
manganese
arsenic

68
Q

only drug approved for moderate-severe dementia

A

memantine

69
Q

donepezil peak concentration, half-life, and steady state

A

peak concentration: 3-4 hours
Half-life: 70 hours
steady state: 2 weeks

70
Q

rivastigmine peak concentration, half-life

A

peak concentration: 1 hour
half-life: 1 hour

71
Q

why can rivastigmine be dosed BID if half-life is only 1 hour

A

it remains bound to cholinesterase so dose is therapeutic for 10 hours

72
Q

galantamine peak concentration, half-life

A

peak concentration: 30min-1 hour
half-life: 6 hours

73
Q

what SSRI should you not use with cholinesterase inhibitors and why

A

paroxetine because it’s the one with the most anticholinergic properties

74
Q

what decreases concentration of donepezil by increasing metabolism

A

dilantin, carbamazepine, dexamethasone, rifampin, and phenobarbital

75
Q

what increases the concentration of donepezil

A

paroxetine, ketoconazole, erythromycin

76
Q

drug interactions for rivastigmine

A

none because it is relatively unbound

77
Q

dosage for donepezil

A

initial 5mg and increase to 10mh in 4 weeks

78
Q

food with donepezil

A

w/ or w/o food

79
Q

dosage for rivastigmine

A

initial 1/5mg BID x 2weeks then increase by 1.5mg every 2 weeks to 6mg in divided doses (3mg BID)

80
Q

food with rivastigmine

A

yes to lessen GI side effects

81
Q

dosage for galantamine

A

start 8mg daily x4 weeks and can raise every 4 weeks
target dose 16-32mf in divided doses

82
Q

memantine peak concentration and half-life

A

peak concentration: 3-7 hours
half-life: 60-80 hours

83
Q

what other drugs are eliminated by tubular secretion that can interfere with concentrations of memantine

A

HCTZ triamterene (Dyrenium)
cimetadine (tagamet)
ranitidine (Zantac)
quinidine
nicotine

84
Q

what happen to memantine in an alkaline urine environment (pH8)

A

clearance is reduced so concentration may increase

85
Q

dosage of memantine

A

start 5mg daily and increase by 5mg weekly to 20mg

86
Q

how often do you dose memantine

A

once daily at 5mg
any dose above 5mg should be BID

Diagnosis_Management 1 (11 decks)

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