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CABS - Neuro > Neurocognitive disorders > Flashcards

Neurocognitive disorders Flashcards

1
Q

How are AMS classified

A

change in consciousness and cognition
*important to make sure to know what their baseline is

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2
Q

What are the two major pathways of AMS

A

diffuse dysfunction compromise and focal lesions

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3
Q

What are red flags for AMS

A

sudden onset
elderly
headache
drug use
trauma
fever
AMS - symptom not diagnosis

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4
Q

What needs to be assessed for a patient presenting with AMS

A

great history
great physical exam - naked, accurate temp, GLUCOSE

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5
Q

what is AVPU

A

Assessment of mental status
Alter, or responsive to Verbal stimuli
Unresponsive, or responsive only to Painful stimuli

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6
Q

what are the baseline labs used for AMS

A

IMMEDIATE BGL
CBC
CMP - sodium/uremia(kidney), Liver
Lactate
UA
Urine drug screen
Urine pregnancy
ABG or VBG
TSH
LP
PT/PTT

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7
Q

What is delirum

A

acute change in attention/awareness and cognitive status with disturbance of sleep-wake cycle

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8
Q

Dementia

A

chonic state of AMS with slow, progressive onset

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9
Q

psychosis

A

patient will have delusions, hallucinations, disorganized thinking, abnormal behavior or negative symptoms

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10
Q

What are the common causes of delirium

A

Drugs
ETOH/Drug withdrawal
metabolic disorder
TBI
encephalitis

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11
Q

What is the reticular activating system

A

source of consciousness (wakefulness, sleep/wake and attention)
consists of the nuclei within the brain as well as fibers that send the sensory input to the cerebral cortex

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12
Q

What is the pathophysiology of hyperactive delirium

A

hyperactive autonomic system
decreased ach and melatonin
excess dopamine, norepi, glutamate
will affect specific areas of the brain leading to the expressed symptoms

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13
Q

what happens when there is increased excitability with change in neurotransmitters?

A

inflammation. decreased BBB function, change in CBF and CNS metabolic derangements

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14
Q

what is hyperactive delirium with

A

associated with withdrawal, infection, sepsis, electrolyte, abnormalities, metabolic abnormalities

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15
Q

what is hyperactive delirium presentation

A

tremor
hallucinations
difficulty concentrating
insomnia
irritability
restlessness
dilated pupils
tachycardia
fever
sweating

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16
Q

what is Agitated Delirium

A

aka excited delirium syndrome
increased dopamine activity - cocaine, thyroid storm, methamphetamines
AMS, combative, aggressive, high temp, poor awareness, superhuman strength, indefatigable
Can lead to death

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17
Q

what is hypoactive delirium

A

often associated with right-sided frontal-basal ganglion disruption
associated with CNS depressants, metabolic disorders
will have decreased levels of alterness, decreased attention span, forgetful and apathy
intact perception and interpretation of surroundings

18
Q

What is the active form of Thyamine

A

TTP

19
Q

what is Wernicke-korsakoff syndrome

A

lack of sufficient thiamine - complication of long term ETOH abuse
hallmarked by paralysis of eye movement, ataxic gait, changes in consciousness
acute syndrome

20
Q

What is Korsakoff’s syndrome:

A

hallmarked by memory loss, confusion, confabulation - lesions in mammillary body
Chronic result

21
Q

what is the pathophysiology of Wernicke encephalopathy

A

decreased thiamine
increased vascular congestion
increased macrophage activation
petechial hemorrhages
demyelination
neuronal damage is most common in the thalamus
atrophy of mamillary bodies

22
Q

What is Wernickes encephalopathy triad

A

encephalopathy
oculomotor dysfunction
gait ataxia (often first symptom)

23
Q

what is dementia

A

acquired decline in cognition. may affect many facets including memory, learning, executive functioning, social cognition, motor skills

24
Q

What is the pathophysiology of dementia

A

genetic predisposition with environmental triggers

25
Q

what does dementia lead to

A

neuron degeneration
compression/deformation of brain parenchyma
head trauma
vascular abnormalities
infectious etiologies
inflammatory issues

will ultimately lead to nerve degeneration and brain atrophy

26
Q

What is broca’s aphasia

A

expressive - cannot find words.
comprehension is intact - unable to repeat or write
supplied by MCA

27
Q

What is wernickes aphasia

A

receptive aphasia. will have meaningless, inappropriate expression. cannot recognize errors. comprehension impaired, cannot repeat, cannot read or write

affects left posteriosuperior temporal lobe
fed by inferior division of MCA

28
Q

What is alzheimers disease

A

most common cause of severe dementia
affects elderly
plaques and tangles are most common in cerebral cortex and hippocampus - frontal and temporal lobe atrophy

29
Q

what are risk factors for alzheimers

A

family history
DM
female
HTN
TBI
sedentary lifestyle

30
Q

What is vascular dementia

A

associated with decreased vascular flow in the brain
may be associated with ischemia or hemorrhagic infarcts
similar in presentation to Alzheimers

31
Q

what is the presentation of vascular dementia

A

memory more intact (initially)
associated with other CVA symptoms (focal weakness, ambulatory disfunction)
anxiety and apathy
presents with cognitive slowing

32
Q

What is frontotemporal dementia

A

aka picks disease
onset <60 yo
3 varients: behavioral, progressive nonfluent aphasia (bracas aphasia), semantic dementia
associated with degenerative changes in the frontal lobe
mutation in the tau protein

33
Q

what is the presentation of frontotemporal dementia

A

loss of language
difficulty with understanding speech prior to memory deficitis
emotional disturbances with apathy, emotional blunting, inappropriate conduct and loss of judgement and depression

34
Q

What is Lewy Body dementia

A

similar presentation to vascular dementia or alzheimers
brain atrophy - frontal, temporal and parietal lobes

35
Q

how do you diagnose lewy body dementia

A

histology post mortum

36
Q

what is the presentation of Lewy Body depenta

A

initial loss of concerntation/attention
memory and cognition will follow
increased risk of delirium
may have visual hallucinations, sleep disorder
may have motor deficits similar to Parkinsons

37
Q

What is Creutzfeldt-Jakob disease

A

“mad cow disease”
considered a rapidly progressive degenerative dementia
prion related disease
pts typically die wtihin a year

38
Q

what are priors

A

infectious misfolded protein particles - they replace normal prion proteins thought to typically play a role in memory and sleep

39
Q

what are the types of Creutzfeldt-jakob disease

A

Sporadic CJD
variant CJD
genetic CJD
latrogenic CJD

40
Q

what is the presentation of CJD

A

mental status change is variable may have frontal/executive dysfunction memory impairment
depression, anxiety and decreased cognitive function

CABS - Neuro (15 decks)

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