Neurocognitive Flashcards

1
Q

onset/course of delirium

A

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

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2
Q

9 subcategories of dementia (NCD)

A

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

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3
Q

4 categories of cognition

A

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

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4
Q

common neurological s/s of delirium

A

tremor
asterixis
nystagmus
incoordination
incontinence

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5
Q

what is the primary neurotransmitter involved in delirium

A

acetylcholine

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6
Q

beclouded dementia

A

delirium in a dementia patient

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7
Q

major neuroanatomical area and pathway affected in delirium

A

reticular formation of the brain stem

dorsal tegmental pathway

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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

major neuroanatomical area associated with delirium

A

reticular formation of the brainstem

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10
Q

what is the principle area for regulating attention and arousal

A

reticular formation of the brainstem

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11
Q

major pathway associated with delirium

A

tegmental

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12
Q

what increases recovery time from delirium

A

lengthier delirium
older patient

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13
Q

delirium recall

A

spotty, like a dream or a nightmare

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14
Q

what are the 3 aspects of delirium that may require medication

A

psychosis
agitation
insomnia

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15
Q

what antipsychotic is not appropriate for delirium and why

A

ziprasidone as it can be activating

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16
Q

when in delirium can use benzodiazepines

A

alcohol-induced delirium
other types they may worsen confusion

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17
Q

what medication is approved for parkinson’s psychosis

A

pimavanserin

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18
Q

Principle goal of delirium treatment

A

treat underlying cause

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19
Q

which dementias have an insidious onset

A

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

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20
Q

which dementia have rapid onset

A

head trauma, cardiac arrest, stroke, encephalitis

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21
Q

catastrophic reaction

A

marked agitation d/t subjective awareness of cognitive deficits under stressful circumstances

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22
Q

sundowner syndrome

A

characterized by drowsiness, confusion, ataxia, and falls

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23
Q

average survival for Alzheimer’s

A

8 years
range is 1-20

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24
Q

what are the cholinesterase inhibitors

A

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

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25
How do cholinesterase inhibitors work
reduce the inactivation of acetylcholine which increases its cholinergic effects to cause modest improvement in memory
26
how does memantine (Namenda) work
protects neurons from cytotoxic excessive glutamate
27
which cholinesterase inhibitor is best tiolerated
donepezil
28
what are the two most common types of dementia
Alzheimers followed by vascular
29
what neurotransmitters are hypoactive in dementia
acetylcholine and norepinephrine
30
which enzymes are decreased in dementia and what do the do
choline acetyltransferase which is critical for acetylcholine synthesis
31
what neuroactive peptides are decreased in dementia
somatostatin and corticotropin
32
what is the dementia that was recently discovered and what is the typical age of onset
familial multiple system tauopathy onset in 40-50s
33
Neuropathology of Alzheimer's dementia
diffuse atrophy with flattened cortical sulci and enlarged cerebral ventricles
34
what can be a differentiating factor between Alzheimer's and frontotemporal dementia
in early stages, there are more behavioral sx in frontotemporal and cognition is better preserved
35
what is a differentiating factor between Alzheimer's and Lewy body dementia
Lewy body commonly presents with hallucinations, parkinsonian sx, and EPS s/s
36
differentiating factors between Alzheimer's and Huntington's dementia
Huntington's has more motor sx and memory/language/insight remains intact in early phases
37
anterograde amnesia
inability to learn new things
38
retrograde amnesia
inability to recall previously learned information
39
what is an amnestic disorder
neurocognitive disorder due to another medical condition
40
what are some medical conditions that can cause amnestic disorders
cerebrovascular disease MS Korsakoff syndrome Alcoholic blackouts ECT Head injury transient global amnesia
41
what causes korsakoff syndrome
thiamine deficiency usually seen in alcoholics
42
other causes of thiamine deficiency besides alcoholism
poor nutrition gastric carcinoma hemodialysis hyperemesis gravidarum gastric plication
43
Does administering thiamine reverse cognitive impairment in korsakoff syndrome
it can prevent additional sx but does not reverse severe sx
44
definition of transient global amnesia
abrupt loss of ability to recall recent events or learn new information
45
how long do episodes of transient global amnesia typically last
6-24 hours
46
Diencephalic structures involved in major neurocognitive disorder
-dorsomedial and midline nuclei of the thalamus -midtemporal lobe structures of hippocampus, mamillary bodies, and amygdala
47
what causes seizures
excessive and spontaneous neural firing
48
what are the types of general seizures
tonic-clonic absence
49
what are the types of partial seizures
simple complex
50
characteristics of absence seizures
no convulsions lose touch w/ reality but not consciousness
51
when do absence seizures usually develop
between 5-7 and often disappear with puberty
52
what is the difference between general and partial seizures
general involves entire brain and partial involves a focal region
53
main characteristic of simple partial seizure
no alteration of consciousness
54
main characteristic of complex partial seizure
alteration in consciousness
55
what is the most common form of epilepsy in adults
complex partial
56
autonomic sensations of the preictal state
stomach full, blushing, change in respiration
57
cognitive sensations of preictal state
deja-vu forced thinking dreamy state
58
affective symptoms of preictal state
fear panic depression elation
59
automatisms of preictal state
lip-smacking, rubbing, chewing
60
what are some symptoms of interictal state
personality disturbance psychotic symptoms violence mood disorder symptoms
61
what should be done about seizure patients who develop new psychiatric symptoms
evaluation of seizure control eval for other psych sx
62
what are some sx that should cause a suspicion of epilepst
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
63
first line tx for tonic-clonic seizures
valproate and phenytoin
64
first line for partial seizures
carbamazepine, oxcarbazepine, phenytoin
65
first line for absence seizures
ethosuximide and valproate
66
demyelinating disorders that can cause neurocognitive sx
MS ALS
67
infectious diseases that can cause neurocognitive sx
herpes simplex encephalitis rabies encephalitis neurosyphilis chronic meningitis subacute sclerosing panencephalitis Lyme disease prion disease
68
symptoms of meningioma
focal symptoms from compression of a limited region of the cortex
69
symptoms of gliomas
more likely to be diffuse
70
what typer of brain tumor is typically associated with incontinence
frontal lobe tumor
71
what type of brain tumor is frequently associated with abnormalities in memory/speech
temporal lobe tumor
72
signs of Lyme disease
bullseye rash at bite site followed by flu-like symptoms
73
treatment of lyme disease
14-21 day course of doxycycline
74
what causes prion diseases
transmission of infectious protein called prion
75
types of prion diseases
Creutzfeldt-Jakob disease variant CJD (mad cow disease) Kuru Gerstmann-Straussler-Scheinker fatal familiar insomnia
76
when can you break confidentiality with an HIV patient
if you know they are putting others at risk
77
manifestations of cruetzfeldt jacob disease
fatigue flue-like symptoms cognitive impairment
78
how do you dx cruetzfeldt jacob disease antemortem
by examining tonsils
79
expected survival for cruetzfeldt jacob disease
rapidly progressive and fatal in 2-3 years
80
what does development of dementia in an HIV patient mean
typically death in 6 months
81
different course for AIDS mania
cognitive slowing/dementia more irritable than euphoric severe presentation malignant course chronic with infrequent remissions
82
endocrine disorders that can cause neurocognitive sx
thyroid disorders parathyroid disorders adrenal disorders pituitary disorders
83
Basic definition of SLE
autoimmune disease that involves inflammation of multiple organs
84
physical sx of hyperthyroid
-fatigue/general weakness -weight loss with increased appetite -insomnia, palpitations, sweating
85
neuropsych sx of hyperthyroidism
-confusion/anxiety -impairments in memory, concentration, and judgment -manic excitement, delusions, hallucinations
86
physical sx of hypothyroidism
weight gain deep voice thin/dry hair loss of lateral eyebrow facial puffiness cold intolerance impaired hearing
87
neuropsych sx of severe hypothyroidism
paranoia depression hypomania hallucinations
88
what causes parathyroid disorders
abnormal regulation of calcium metabolism
89
disorder of adrenal insufficiency
Addison's disease
90
disorder of adrenal excess
Cushing syndrome
91
metabolic disorders with neurocognitive symptoms
hepatic encephalopathy uremic encephalopathy hypoglycemia encephalopathy diabetic ketoacidosis acute intermittent porphyria
92
nutritional disorders that can cause neurocognitive symptoms
niacin deficiency thiamine deficiency cobalamin deficiency
93
"5D's" course of niacin deficiency
dermatitis, diarrhea, delirium, dementia, death
94
treatment of niacin deficiency
nicotinic acid
95
toxins that cause neurocognitive symptoms
mercury lead manganese arsenic
96
only drug approved for moderate-severe dementia
memantine
97
donepezil peak concentration, half-life, and steady state
peak concentration: 3-4 hours Half-life: 70 hours steady state: 2 weeks
98
effect of food on rivastigmine
delays peak concentration
99
effect of food on galantamine
decreases max concentration by 25%
100
rivastigmine peak concentration, half-life
peak concentration: 1 hour half-life: 1 hour
101
why can rivastigmine be dosed BID if half-life is only 1 hour
it remains bound to cholinesterase so dose is therapeutic for 10 hours
102
galantamine peak concentration, half-life
peak concentration: 30min-1 hour half-life: 6 hours
103
what SSRI should you not use with cholinesterase inhibitors and why
paroxetine because it's the one with the most anticholinergic properties
104
what decreases concentration of donepezil by increasing metabolism
dilantin, carbamazepine, dexamethasone, rifampin, and phenobarbital
105
what increases the concentration of donepezil
paroxetine, ketoconazole, erythromycin
106
drug interactions for rivastigmine
none because it is relatively unbound
107
dosage for donepezil
initial 5mg and increase to 10mh in 4 weeks
108
food with donepezil
w/ or w/o food
109
dosage for rivastigmine
initial 1/5mg BID x 2weeks then increase by 1.5mg every 2 weeks to 6mg in divided doses (3mg BID)
110
enzymes that metabolize donepezil and galantamine
2D6 3A4
111
food with rivastigmine
yes to lessen GI side effects
112
dosage for galantamine
start 8mg daily x4 weeks and can raise every 4 weeks target dose 16-32mf in divided doses
113
memantine peak concentration and half-life
peak concentration: 3-7 hours half-life: 60-80 hours
114
what other drugs are eliminated by tubular secretion that can interfere with concentrations of memantine
HCTZ triamterene (Dyrenium) cimetadine (tagamet) ranitidine (Zantac) quinidine nicotine
115
what happen to memantine in an alkaline urine environment (pH8)
clearance is reduced so concentration may increase
116
dosage of memantine
start 5mg daily and increase by 5mg weekly to 20mg
117
how often do you dose memantine
once daily at 5mg any dose above 5mg should be BID
118
which cholinesterase inhibitor can cause weight loss
donepezil
119
which muscarinic receptors are stimulating to downstream second messengers
M1 M3 M5
120
which muscarinic receptors are inhibitory to downstream second messengers
M2 M4
121
donepezil inhibits which enzyme(s)
AChE only
122
which enzyme(s) are inhibited by rivastigmine
AChE BuChE
123
How does pimavanserin work
blocks excitatory input of serotonin in the psychosis network at 5HT2A receptors