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Flashcards in Delirium vs. Dementia Deck (67)
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1
Q

What are the differences in delirium vs. dementia in terms of their: Time course?

A
  • Delirium = acute

* Dementia = chronic

2
Q

What are the differences in delirium vs. dementia in terms of their: Attention?

A

• Delirium = impaired

Dementia = normal

3
Q

What are the differences in delirium vs. dementia in terms of their: Level of consciousness?

A
  • Delirium = fluctuating

* Dementia = normal

4
Q

What are the differences in delirium vs. dementia in terms of their: Memory

A
  • Delirium = poor registration

* Dementia = amnesia

5
Q

What are the differences in delirium vs. dementia in terms of their: Reversibility

A
  • Delirium = common

* Dementia = uncommon

6
Q

What are the differences in delirium vs. dementia in terms of their: Toxic and metabolic causes

A
  • Delirium = typical

* Dementia = unusual

7
Q

What are the differences in delirium vs. dementia in terms of their: Speech and language

A
  • Delirium = inchoherent speech

* Dementia = aphasia

8
Q

What is the definition of delirium?

A
  • From latin “off the track”
    • Rapidly developing disorder of attention characterized by an inability to maintain a coherent line of thought
    • Acute confusional state
    • Toxic-metabolic encephalopathy
    • Incorporates the more rare but visual delirium tremens - to describe the hyperaroused, agitated, hallucinatory state
    • MORE COMMON is underaroused, lethargic, somnolent state
9
Q

What is meant by “clouded dementia”?

A
  • The phenomenon where demented patients more easily and quickly become delierious
    • This can reflect poor outcomes in these older, demented patients and contribute to progression of dementia
10
Q

What are most vulnerable neurons to delirium?

A
  • Chonlinergic, dopaminergic, histaminergic, noradrenergic and serotonergic
    • Note NOT GABA or glutamate systems
11
Q

What is the pathophysiology of delirium?

A
  • Perturbations in the metabolic environment of the brain…and the brain freaks out
    • Represents diffuse brain dysfunction related to a disruption of normal brain homeostasis
    • The neuronal dysfunction is widespread affecting arousal systems in the brainstem and diencephalon as well as cortical regions
    • There is usually an underlying shift in the brain’s environment that causes the delirium, and removal of that cause can often reverse the condition
12
Q

What psychiatric disorders go on the differential for delirium?

A

• Schizoprenia and psychotic diseases
○ Main differentiator here is the fluctuations in level of consciousness
• Mania and depression
○ No fluctuation in level of consciousness like there is in delirium though
○ And also there is change in affect usually (not in delirium)

13
Q

What might cause delirium?

A
• Anything that would mess with the metabolic environment of the brain
	• Most often drugs and toxins
		○ OTC drugs, recreational drugs, illicit substances
		○ Intoxication AND withdrawal
	• Infectious and inflammatory disease
		○ Meningitis
		○ Encephalitis
		○ CNS vasculitis
		○ Systemic infection
	• Structural lesions
		○ TBI, stroke
	• Seizure disorders
14
Q

What are the routine laboratory tests for delirium?

A
• Complete metabolic panel
	• Complete blood count
	• Urinalysis
	• Urinary toxicology screen
	• Electrocardiogram
	• Chest radiograph
	• Image of brain
		○ CT or MRI
	• LP is required if brain infection is suspected
	• EEG can be helpful for confirmin non-convulsive status epilepticus
15
Q

What always starts your evaluation of the delirium patient?

A

History, physical exam, neurologic exam

*not necessarily the mini mental status exam which is usually unrewarding with the confused state of the patient

16
Q

What is the most important rule of delirium treatment?

A

• Find the cause, and reverse/treat the cause
• You can enhance normal cognitive function during treatment:
○ Clock and calendar (environmental manipulations)
○ Provision of adequate sleep and restore the sleep-wake cycle
○ Calming medications such as the atypical neuroleptics

17
Q

What causes dementia (etiology)?

A
• Reversible (10-20%) and irreversible (80-90%)
	• Reversible
		○ Drugs and toxins
		○ Mass lesions
		○ Normal pressure hydrocephalus
		○ Hypothyroidism
		○ Vitamin B12 deficiency
		○ Neurosyphilis
		○ CNS inflammatory disease (like SLE)
		○ Systemic infection/inflammation
		○ Severe depression
		○ Mild traumatic brain injury
	• Irreversible
		○ Alzheimer
		○ Frontotemporal dementia
		○ Vascular dementia
		○ Huntington
		○ Parkinson
		○ Lewy body dementia
		○ Creutzfeldt-jakob
		○ Multiple sclerosis
		○ HIV-associated dementia
		○ Severe traumatic brain injury
18
Q

What are the reversible causes of dementia we discussed?

A
• Reversible (10-20%) and irreversible (80-90%)
	• Reversible
		○ Drugs and toxins
		○ Mass lesions
		○ Normal pressure hydrocephalus
		○ Hypothyroidism
		○ Vitamin B12 deficiency
		○ Neurosyphilis
		○ CNS inflammatory disease (like SLE)
		○ Systemic infection/inflammation
		○ Severe depression
		○ Mild traumatic brain injury
19
Q

what are the irreversible causes of dementia we discussed?

A
• Reversible (10-20%) and irreversible (80-90%)
	• Irreversible
		○ Alzheimer
		○ Frontotemporal dementia
		○ Vascular dementia
		○ Huntington
		○ Parkinson
		○ Lewy body dementia
		○ Creutzfeldt-jakob
		○ Multiple sclerosis
		○ HIV-associated dementia
		○ Severe traumatic brain injury
20
Q

What is the definition of dementia?

A

• “down from the mind” - latin
• Acquired and persistent impairment in intellectual function with deficits in at least three:
○ Memory
○ Language
○ Visuospatial skills
○ Emotion and personality
○ Complex cognition
• Must interfere with usual social and occupational activities (be actual pathology)
• Need not be either progressive or irreversible by definition, though it largely is

21
Q

What is the most important objective of the demential work-up?

A
  • Find, if possible, a reversible cause and treat it

* Rare-ish to find, but you need to look for it

22
Q

What tests/procedures are considered in the dementia work up?

A

• History and physical exam (neuro, mental status, physical)
• CMP
• CBC
• TSH
• B12
• RPR - rapid plasma reagin - screen for syphilis
• MRI/CT scan
• Only in select cases:
○ HIV, EEG, ESR, antibody for autoimmune dementia, heavy metal screen, angiography and biopsy

23
Q

What are the two most common cortical dementias?

A
  • These are neurodegenerative dementias
    • Alzheimer
    • FTD or frontotemporal dementia
24
Q

What are the clinical features of alzheimer’s disease?

A

• Know that AD has a defined clinical profile that helps make this dx
• Stage I - amnesia is notable
• Stage II - dementia is obvious
• Stage III - mental and physical incapacity
• MCI - mild cognitive impairment - is associated with age but can convert to true AD (10-15% per year)
○ 1-2% of non-MCI elderly convert
• Most common in older individuals with 5-10% prevalence after 65 and near 40% over 85

25
Q

What must be present on neuropathology to confirm the AD dx?

A
  • AD is characterized by cerebral atrophy and amyloid plaques and neurofibrillary tangles
    • Sufficient plaques and tangles either on brain biopsy or at autopsy
    • Brain biopsy is rarely done, the clinical features are pretty telling
    • 90% accuracy with probable AD dx (clinical)
26
Q

What causes AD?

A

• Largely unknown, but it is a mix of environmental and genetic factors

27
Q

What are the genetic factors in AD?

A
  • Not tested for much b/c can’t do much if you get a positive result
    • Trisomy 21 - overexpression of APP or amyloid precursor protein
    • Early-onset - APP, presenilin-1 (chromosome 14) and presenilin-2 (chromosome 1)
    • Late-onset - APOE gene, epsilon-4 allele presence
28
Q

What is the cholinergic hypothesis of AD?

A
  • Ach is relatively deficient in AD
    • Loss of cholinergic cells in basal forebrain is correlated with cognitive impairments in AD
    • Donepezil, rivastigmine and glantamine are ache inhibitors approved for AD
    • The other drug is memantine, an NMDA antagonist
29
Q

What is the standard drug treatment for AD?

A
  • Ache inhibitor and memantine

* Memantine = NMDA antagonist

30
Q

What’s up with frontotemporal dementia?

A
  • FTD = frontotemporal dementia
    • Most salient features are changes in behavior and comportment
    • NOT changes in memory
    • Once was “pick’s disease”
    • Disinhibition, apathy, executive dysfunction while memory is still normal
31
Q

In addition to dementia, what do the subcortical dementias share?

A
  • Some variety of abnormal movement in additinon to dementia

* Disease in which subcortical gray matter structures are affected

32
Q

What is LBD?

A
  • lewy body dementia
    • Related disorder to PD
    • Dementia, parkinsonism, visual hallucinations and fluctuating confusion
    • Hard to treat as PD drugs worsen psychosis while neuroleptics worsen parkinsonism
33
Q

What’s up with Parkinson’s Disease?

A
  • PD resting tremor, bradykinesia, rigidity, postural instability are CLASSIC signs
    • Lewy bodies in substantia nigra are characteristic histopatholoic finding
    • Dopamine deficiency is the movement disorder cause
    • Subset is LBD or lewy body dementia
34
Q

What are the two subcortical dementias we talked about?

A
  • Parkinson’s Disease (PD)

* Huntington’s Disease (HD)

35
Q

What structures are affected in subcortical dementia?

A

• Basal ganglia
• Thalamus
• Brainstem nuclei
○ Subcortical gray matter

36
Q

What are the manifestations and cause of Huntington Disease?

A
  • HD - huntington’s disease
    • Autosomal dominant disease that involves dementia and chorea, with either presenting
    • Many have premonitory (like a premonition, or a warning sign) personality changes
    • Also present are a variety of neuropsychiatric features
    • Caudate atrophy is commonly seen on neuroimaging reflecting a major site of neuronal loss
    • CAG triplet repeat disease (basis of genetic test)
    • Chorea = a neurological disorder characterized by jerky involuntary movements affecting especially the shoulders, hips, and face.
37
Q

Tetrabenazine is used in what disease?

A
  • HD-related chorea Can be treated with neuroleptic drugs and tetrabenazine
    • Chorea = a neurological disorder characterized by jerky involuntary movements affecting especially the shoulders, hips, and face.
    • This is one of the presenting signs of HD
38
Q

What is chorea and what should it make you think?

A
  • Chorea = a neurological disorder characterized by jerky involuntary movements affecting especially the shoulders, hips, and face.
    • This is one of the presenting signs of HD
    • Can be treated with neuroleptic drugs and tetrabenazine
39
Q

What are the given examples of white matter dementia?

A
  • Binswanger’s Disease (BD)

* Normal Pressure Hydrocephalus (NPH)

40
Q

What’s up with BD?

A
  • BD - binswanger’s disease
    • Form of vascular dementia in which long-standing hypertension leads to the development of ischemia an dlacunar infarction that falls heavily on the cerebral white matter
    • White matter dementia
    • Often underdiagnosed
    • Course is typical of widespread white matter problems
41
Q

What’s up with NPH?

A
  • NPH - normal pressure hydrocephalus
    • Reversible dementia
    • Present with dementia, gait disorder and urinary incontinence and have enlarged ventricles with normal sulci on neuorimaging indicating hydrocephalus and neuopatholgy affecting the periventricular white matter
    • If patients respond well to large volume spinal tap they may be candidates for a ventricular or lumbar shunt to divert CSF
    • NPH is rare, and shunting even more so
    • Large tap is 30-55cc of CSF
42
Q

What are the given examples of mixed dementia?

A
  • Multi-infarct dementia

* CJD or creutzfeldt-Jakob

43
Q

What’s up with multi-infarct dementia?

A
  • Vascular dementia, contrast with BD
    • Repeated strokes erode cognitive function so that eventually enough brain tissue is destroyed to cause dementia
    • Can be large vessel ischemic infarcts affecting cerebral cortex
    • Can be small vessel lacunar infarcts involving subcortical gray and white matter
    • Some patients have both
    • Only treatment is stroke prevention
44
Q

While CJD is potentially transmissible, what percentage of cases are sporadic in origin?

A
• 85-90%
	• Remainder are familial. SUPER uncommon  is a case of transmissibility
		○ Dura mater grafts
		○ Neurosurgical instruments
		○ Corneal transplantation
		○ Cadaveric pituitary growth hormone
		○ EEG depth electrodes
	• Present with dementia that progresses over weeks to months
	• Ofen confusion or spychotic features
	• Myoclous
	• Cortical or subcortcial hyperintenstities on diffusion weighted MRI
	• Death in 4-12 months
45
Q

What drugs should be avoided in dementia?

A
  • These drugs can make things worse
    • Benzodiazepines
    • Anticholinergic drugs
46
Q

What conditions warrant use of atypical antipsychotics in AD patients?

A
• Neuropsychiatric syndromes:
		○ Delusions, 
		○ Hallucinations
		○ Paranoia
		○ agitation
47
Q

What are the pharm treatments for AD?

A

• Ache inhibitors
• Tacrine was first but superseded by donepezil
○ Standard of care with efficacy and well tolerated)
• Rivastigmine
• Galantamine
• Rivastigmine can be given transdermally to reduce GI side effects
• Memantine is an NMDA antagoinst with similar efficacy to ache
• With psychiatric syndromes use atypical antipsychotics

48
Q

What drugs can you use in dementia?

A
• Low-dose atypical antipsychotic drugs
		○ Quetiapine
		○ Risperidone
	• For disruptive neuropsychiatric syndromes
	• SSRI's for depression is helpful
49
Q

Should you use the term confused when discussing a patient’s care?

A

• No, this term is used in too many places and therefore has very little clinical meaning

50
Q

What’s the “pyramid” of basic cognition?

A
  • Base = arousal
    • Attention
    • Language
    • Memory
    • Praxis
    • gnosia
    • Tip = executive function
51
Q

Where can you expect to see delirium?

A
  • 10-40% of hospitalized elderly
    • 80% of terminally ill
    • 51% post-op cases
    • Presenting feature in 30% of bacteremia in elderly
    • Indicator of increased morbidity and mortality, as well as worse outcome
    • Consider this a vital organ failure and sign of underlying serious disease
52
Q

What are the DSM-5 criteria for the diagnosis of delirium?

A
  • Disturbance in attention and awareness (to environment)
    • Develops over a short period of time (hours to days), fluctuates and is a change from baseline
    • Additional disturbance in cognition (memory, language, visuospatial)
    • The disturbances are not due to another preexisting or established neurocognitive disorder
    • Evidence exists that there is an underlying cause (drugs, withdrawal, toxin, etc)
53
Q

What is gnosia?

A

• 1. The perceptive faculty enabling one to recognize the form and the nature of people and things; the faculty of perceiving and recognizing.

54
Q

What is praxis?

A

• Learned skills and the performance of skills learned through practice

55
Q

What are the two ends of the spectrum that is delirium?

A
• Hyperactive and hypoactive
	• Hyperactive is more "classic"
		○ Irritable, angry, laughing, euphoric (emotional lability)
		○ Wandering
		○ Distractible, tangential
	• Hypoactive
		○ Can easily be missed as the patients are quiet
		○ Apathetic, lethargic
		○ Slow of speech and movement,
		○ staring off
56
Q

What are the clinical characteristics of delirium?

A
  • Fluctuating arousal
    • Attention deficits
    • Alterations in memory, language, construction, perception and mood
    • Spontaneous speech may be incoherent, rambling, shifting topics
57
Q

How can you use a patient’s writing as diagnostic help for delirium?

A
  • There is a marked impairment in writing and constructional abilities
    • “agraphia”
    • Illegible, abnormal spacing, agrammatical, spelling errors, omissions, substitutions, and duplication errors
    • Distorted or unrecognizable drawing of shapes or figures
58
Q

What is meant by “patient is perseverative”?

A

• Some initial stimulus will get a patient started on something, but they will continue to repeat themselves, even after the stimulus is gone

59
Q

What are the psychosis manifestations of delirium?

A
  • If they do hallucinate, they tend to be silent fully formed visual hallucinations
    • Auditory is less common
    • Range from simple and transient to complex and rigid
    • Frequent affective alterations with lability
60
Q

What neurological motor disturbances would be something to look for in delirium?

A
  • Asterixis
    • Altered tone
    • Myoclonus
    • hyperrreflexia
61
Q

What is asterixis?

A
  • Extended wrists, push back on them and notice an unconscoious/uncontrolled flapping movement
    • Can be synchronous or not
    • Indicative of encephalopathy or altered mental status
62
Q

What are some other neurological things you should look for in the delirium patient?

A
  • Autonomic disturbances

* Neurological motor disturbances

63
Q

What autonomic disturbances might surface in the delirium patient?

A
  • (sympathetic drive)
    • Tachycardia
    • Diaphoresis
    • Pupillary dilation
64
Q

A pitfall to remember in the delirium patient (pharm)…?

A
  • Unless alcohol withdrawal, avoid the pitfall of giving a patient benzos
    • Results in paradoxical agitation
    • Physical restraints are dangerous. Only use during the acute agitation episode and remove them as soon as they calm down
65
Q

What does the state of delirium do to a patient’s long-term outcomes?

A
  • In non-demented patients up to 8x increased risk of future dementia after delirium
    • In AD patients, decline 2x faster for up to 5 years after delirium
66
Q

What are the DSM-5 criteria for dementia?

A
  • Evidence of significant cognitive decline from a prior level of performance in one or more cognitive domains
    • Deficits interfere with independence in everyday activities
    • Do not occur in the context of delirium alone
    • Not better explained by another disorder
67
Q

Delirium is a “bottom up” impairment while dementia…?

A
  • Dementia is a top-down impairment
    • Executive function is first
    • Gnosia, praxis, memory, language, attention, arousal
    • In that descending order
    • Think of the pyramid of cognitive function

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