Neurocognitive Flashcards
onset/course of delirium
sudden onset, brief fluctuating course, rapid resolution once cause is treated
9 subcategories of dementia (NCD)
-Alzheimer’s
-vascular
-HIV
-TBI
-frontotemporal
-Prion disease
-Substance-induced
-multiple etiologies
-unspecified
4 categories of cognition
-memory
-visuospatial/construction abilities
-reading/writing/math
-abstraction ability
common neurological s/s of delirium
tremor
asterixis
nystagmus
incoordination
incontinence
what is the primary neurotransmitter involved in delirium
acetylcholine
beclouded dementia
delirium in a dementia patient
major neuroanatomical area and pathway affected in delirium
reticular formation of the brain stem
dorsal tegmental pathway
how do you differentiate delirium from schizophrenia
schizophrenia:
-delusions/hallucinations are more constant and better organized.
-usually no change in LOC/orientation
major neuroanatomical area associated with delirium
reticular formation of the brainstem
what is the principle area for regulating attention and arousal
reticular formation of the brainstem
major pathway associated with delirium
tegmental
what increases recovery time from delirium
lengthier delirium
older patient
delirium recall
spotty, like a dream or a nightmare
what are the 3 aspects of delirium that may require medication
psychosis
agitation
insomnia
what antipsychotic is not appropriate for delirium and why
ziprasidone as it can be activating
when in delirium can use benzodiazepines
alcohol-induced delirium
other types they may worsen confusion
what medication is approved for parkinson’s psychosis
pimavanserin
Principle goal of delirium treatment
treat underlying cause
which dementias have an insidious onset
Alzheimer’s, vascular, endocrinopathies, brain tumors, metabolic disorders
which dementia have rapid onset
head trauma, cardiac arrest, stroke, encephalitis
catastrophic reaction
marked agitation d/t subjective awareness of cognitive deficits under stressful circumstances
sundowner syndrome
characterized by drowsiness, confusion, ataxia, and falls
average survival for Alzheimer’s
8 years
range is 1-20
what are the cholinesterase inhibitors
donepezil (Aricept)
rivastigmine (exelon)
galantamine (Razadyne)
Tacrine
How do cholinesterase inhibitors work
reduce the inactivation of acetylcholine which increases its cholinergic effects to cause modest improvement in memory
how does memantine (Namenda) work
protects neurons from cytotoxic excessive glutamate
which cholinesterase inhibitor is best tiolerated
donepezil
what are the two most common types of dementia
Alzheimers followed by vascular
what neurotransmitters are hypoactive in dementia
acetylcholine and norepinephrine
which enzymes are decreased in dementia and what do the do
choline acetyltransferase which is critical for acetylcholine synthesis
what neuroactive peptides are decreased in dementia
somatostatin and corticotropin
what is the dementia that was recently discovered and what is the typical age of onset
familial multiple system tauopathy
onset in 40-50s
Neuropathology of Alzheimer’s dementia
diffuse atrophy with flattened cortical sulci and enlarged cerebral ventricles
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
what is a differentiating factor between Alzheimer’s and Lewy body dementia
Lewy body commonly presents with hallucinations, parkinsonian sx, and EPS s/s
differentiating factors between Alzheimer’s and Huntington’s dementia
Huntington’s has more motor sx and memory/language/insight remains intact in early phases
anterograde amnesia
inability to learn new things
retrograde amnesia
inability to recall previously learned information
what is an amnestic disorder
neurocognitive disorder due to another medical condition
what are some medical conditions that can cause amnestic disorders
cerebrovascular disease
MS
Korsakoff syndrome
Alcoholic blackouts
ECT
Head injury
transient global amnesia
what causes korsakoff syndrome
thiamine deficiency usually seen in alcoholics
other causes of thiamine deficiency besides alcoholism
poor nutrition
gastric carcinoma
hemodialysis
hyperemesis gravidarum
gastric plication
Does administering thiamine reverse cognitive impairment in korsakoff syndrome
it can prevent additional sx but does not reverse severe sx
definition of transient global amnesia
abrupt loss of ability to recall recent events or learn new information
how long do episodes of transient global amnesia typically last
6-24 hours
Diencephalic structures involved in major neurocognitive disorder
-dorsomedial and midline nuclei of the thalamus
-midtemporal lobe structures of hippocampus, mamillary bodies, and amygdala
what causes seizures
excessive and spontaneous neural firing
what are the types of general seizures
tonic-clonic
absence
what are the types of partial seizures
simple
complex
characteristics of absence seizures
no convulsions
lose touch w/ reality but not consciousness
when do absence seizures usually develop
between 5-7 and often disappear with puberty
what is the difference between general and partial seizures
general involves entire brain and partial involves a focal region
main characteristic of simple partial seizure
no alteration of consciousness
main characteristic of complex partial seizure
alteration in consciousness
what is the most common form of epilepsy in adults
complex partial
autonomic sensations of the preictal state
stomach full, blushing, change in respiration
cognitive sensations of preictal state
deja-vu
forced thinking
dreamy state
affective symptoms of preictal state
fear
panic
depression
elation
automatisms of preictal state
lip-smacking, rubbing, chewing
what are some symptoms of interictal state
personality disturbance
psychotic symptoms
violence
mood disorder symptoms
what should be done about seizure patients who develop new psychiatric symptoms
evaluation of seizure control
eval for other psych sx
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
first line tx for tonic-clonic seizures
valproate and phenytoin
first line for partial seizures
carbamazepine, oxcarbazepine, phenytoin
first line for absence seizures
ethosuximide and valproate
demyelinating disorders that can cause neurocognitive sx
MS
ALS
infectious diseases that can cause neurocognitive sx
herpes simplex encephalitis
rabies encephalitis
neurosyphilis
chronic meningitis
subacute sclerosing panencephalitis
Lyme disease
prion disease
symptoms of meningioma
focal symptoms from compression of a limited region of the cortex
symptoms of gliomas
more likely to be diffuse
what typer of brain tumor is typically associated with incontinence
frontal lobe tumor
what type of brain tumor is frequently associated with abnormalities in memory/speech
temporal lobe tumor
signs of Lyme disease
bullseye rash at bite site followed by flu-like symptoms
treatment of lyme disease
14-21 day course of doxycycline
what causes prion diseases
transmission of infectious protein called prion
types of prion diseases
Creutzfeldt-Jakob disease
variant CJD (mad cow disease)
Kuru
Gerstmann-Straussler-Scheinker
fatal familiar insomnia
when can you break confidentiality with an HIV patient
if you know they are putting others at risk
manifestations of cruetzfeldt jacob disease
fatigue
flue-like symptoms
cognitive impairment
how do you dx cruetzfeldt jacob disease antemortem
by examining tonsils
expected survival for cruetzfeldt jacob disease
rapidly progressive and fatal in 2-3 years
what does development of dementia in an HIV patient mean
typically death in 6 months
different course for AIDS mania
cognitive slowing/dementia
more irritable than euphoric
severe presentation
malignant course
chronic with infrequent remissions
endocrine disorders that can cause neurocognitive sx
thyroid disorders
parathyroid disorders
adrenal disorders
pituitary disorders
Basic definition of SLE
autoimmune disease that involves inflammation of multiple organs
physical sx of hyperthyroid
-fatigue/general weakness
-weight loss with increased appetite
-insomnia, palpitations, sweating
neuropsych sx of hyperthyroidism
-confusion/anxiety
-impairments in memory, concentration, and judgment
-manic excitement, delusions, hallucinations
physical sx of hypothyroidism
weight gain
deep voice
thin/dry hair
loss of lateral eyebrow
facial puffiness
cold intolerance
impaired hearing
neuropsych sx of severe hypothyroidism
paranoia
depression
hypomania
hallucinations
what causes parathyroid disorders
abnormal regulation of calcium metabolism
disorder of adrenal insufficiency
Addison’s disease
disorder of adrenal excess
Cushing syndrome
metabolic disorders with neurocognitive symptoms
hepatic encephalopathy
uremic encephalopathy
hypoglycemia encephalopathy
diabetic ketoacidosis
acute intermittent porphyria
nutritional disorders that can cause neurocognitive symptoms
niacin deficiency
thiamine deficiency
cobalamin deficiency
“5D’s” course of niacin deficiency
dermatitis, diarrhea, delirium, dementia, death
treatment of niacin deficiency
nicotinic acid
toxins that cause neurocognitive symptoms
mercury
lead
manganese
arsenic
only drug approved for moderate-severe dementia
memantine
donepezil peak concentration, half-life, and steady state
peak concentration: 3-4 hours
Half-life: 70 hours
steady state: 2 weeks
effect of food on rivastigmine
delays peak concentration
effect of food on galantamine
decreases max concentration by 25%
rivastigmine peak concentration, half-life
peak concentration: 1 hour
half-life: 1 hour
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
galantamine peak concentration, half-life
peak concentration: 30min-1 hour
half-life: 6 hours
what SSRI should you not use with cholinesterase inhibitors and why
paroxetine because it’s the one with the most anticholinergic properties
what decreases concentration of donepezil by increasing metabolism
dilantin, carbamazepine, dexamethasone, rifampin, and phenobarbital
what increases the concentration of donepezil
paroxetine, ketoconazole, erythromycin
drug interactions for rivastigmine
none because it is relatively unbound
dosage for donepezil
initial 5mg and increase to 10mh in 4 weeks
food with donepezil
w/ or w/o food
dosage for rivastigmine
initial 1/5mg BID x 2weeks then increase by 1.5mg every 2 weeks to 6mg in divided doses (3mg BID)
enzymes that metabolize donepezil and galantamine
2D6
3A4
food with rivastigmine
yes to lessen GI side effects
dosage for galantamine
start 8mg daily x4 weeks and can raise every 4 weeks
target dose 16-32mf in divided doses
memantine peak concentration and half-life
peak concentration: 3-7 hours
half-life: 60-80 hours
what other drugs are eliminated by tubular secretion that can interfere with concentrations of memantine
HCTZ triamterene (Dyrenium)
cimetadine (tagamet)
ranitidine (Zantac)
quinidine
nicotine
what happen to memantine in an alkaline urine environment (pH8)
clearance is reduced so concentration may increase
dosage of memantine
start 5mg daily and increase by 5mg weekly to 20mg
how often do you dose memantine
once daily at 5mg
any dose above 5mg should be BID
which cholinesterase inhibitor can cause weight loss
donepezil
which muscarinic receptors are stimulating to downstream second messengers
M1
M3
M5
which muscarinic receptors are inhibitory to downstream second messengers
M2
M4
donepezil inhibits which enzyme(s)
AChE only
which enzyme(s) are inhibited by rivastigmine
AChE
BuChE
How does pimavanserin work
blocks excitatory input of serotonin in the psychosis network at 5HT2A receptors
