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Neuro > Delirium and Dementia B&B > Flashcards

Delirium and Dementia B&B Flashcards

1
Q

dementia vs delirium

A

dementia = chronic, progressive cognitive decline, irreversible, abnormal EEG

delirium = acute, waxing/waning, usually reversible (secondary to fever, etc), normal EEG

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2
Q

What is the most common reason for altered mental state in the hospital?

A

dementia patients in an unknown setting become delirious (orient themselves by becoming familiar with their surroundings)

Classically a dementia patient with pneumonia

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3
Q

what drug can be used to treat delirium?

A

first, fix underlying cause (infection, withdrawal, O2 levels, etc)… then, place patient in calm/quiet environment

if drug is needed: haloperidol (called “vitamin H”) - neuroleptic which blocks D2 receptors (main effect)

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4
Q

what kind of drugs are trifluoperazine, fluphenazine, thioridazine, and chlorpromazine? what is their MOA?

A

neuroleptics: main effect is to block CNS dopamine D2 receptors

help calm patients with schizophrenia, psychosis, mania

also block ACh (M), alpha1, and histamine receptors —> side effects

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5
Q

What is the mechanism in clinical use of haloperidol?

A

neuroleptic: main effect is to block CNS dopamine D2 receptors

Used to calm patients with schizophrenia, psychosis, and mania (often in hospital setting)

Also blocks ACh (M), alpha1, and histamine receptors —> side effects

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6
Q

name 3 high potency and 2 low potency neuroleptic agents

A

High potency: more neurologic side effects + extrapyramidal side effects
1. Haloperidol.
2. Trifluoperazine.
3. Fluphenazine.
[HAL TRIed the FLUte?]

Low potency: more non-neurologic side effects
1. Thioridazine
2. Chlorpromazine.

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7
Q

pyramidal vs extrapyramidal side effects

A

pyramidal = corticospinal tract —> weakness/paralysis

extrapyramidal = basal ganglia, rubrospinal, tectospinal (modulation of movement) —> movement disorders (movement you don’t want or uncoordinated)

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8
Q

what are the four extrapyramidal side effects of haloperidol and the order in which they occur?

A
  1. Dystonia (acute): involuntary muscle contractions (spasms, stiffness), can tx with benzotropine (anti-ACh)
  2. Akathisia (days): restlessness, can tx with lower dose/ benzos/ propranolol
  3. Bradykinesia (weeks): drug-induced Parkinsonism, can tx with benzotropine
  4. tardive dyskinesia (months-years): irreversible chorea - lip smacking, grimacing

[neuroleptic: main effect is to block CNS dopamine D2 receptors - blockage causes side effects above]

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9
Q

what are the side effects of haloperidol besides the four extrapyramidal symptoms? (5) [hint: think of all the receptors it blocks!]

A
  1. D2 block —> hyperprolactinemia, galactorrhea
  2. ACh M block —> dry mouth, constipation
  3. alpha1 block —> hypotension
  4. histamine block —> sedation
  5. QT prolongation (risk of Torsade de Points!)

[neuroleptic: main effect is to block CNS dopamine D2 receptors; Also blocks ACh (M), alpha1, and histamine receptors]

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10
Q

name 5 side effects that are more common with low potency neuroleptic agents (thioridazine and chlorpromazine) than high potency agents (haloperidol, trifluoperazine, fluphenazine)

A
  1. D2 block —> hyperprolactinemia, galactorrhea
  2. ACh M block —> dry mouth, constipation
  3. alpha1 block —> hypotension
  4. histamine block —> sedation
  5. QT prolongation (risk of Torsade de Points!)

[recall non-neurological side effects are more common with the low potency agents]

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11
Q

what occurs with neuroleptic malignant syndrome (NMS)? how does it present? to what other syndrome is it similar?

A

rare, dangerous reaction to neuroleptics usually 7-10 days after treatment

—> fever, rigidity, encephalopathy, HTN/tachycardia (autonomic instability), elevated CK, myoglobinuria (acute renal failure from rhabdo)

Very similar to malignant hyperthermia/ also treated with dantrolene (muscle relaxant), and in addition bromocriptine (dopamine agonist)

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12
Q

how is neuroleptic malignant syndrome (NMS) treated? (2)

A

rare, dangerous reaction to neuroleptics usually 7-10 days after treatment

—> fever, rigidity, encephalopathy, HTN/tachycardia (autonomic instability), elevated CK, myoglobinuria (acute renal failure from rhabdo)

treated with dantrolene (muscle relaxant) + bromocriptine (dopamine agonist)

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13
Q

Pt in the ICU develops a fever and mental status changes. Vitals show HTN and tachycardia. Blood work shows an elevated CK and myoglobinuria. Pt was admitted 1 week prior for mania and treated with haloperidol (brand name Haldol). How should you treat the patient right now?

A

neuroleptic malignant syndrome (NMS): rare, dangerous reaction to neuroleptics usually 7-10 days after treatment

—> fever, rigidity, encephalopathy, HTN/tachycardia (autonomic instability), elevated CK, myoglobinuria (acute renal failure from rhabdo)

treated with dantrolene (muscle relaxant) + bromocriptine (dopamine agonist)

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14
Q

inpatient being treated with neuroleptics develops fever and rigid muscles =

A

neuroleptic malignant syndrome (NMS): rare, dangerous reaction to neuroleptics usually 7-10 days after treatment

—> fever, rigidity, encephalopathy, HTN/tachycardia (autonomic instability), elevated CK, myoglobinuria (acute renal failure from rhabdo)

treated with dantrolene (muscle relaxant) + bromocriptine (dopamine agonist)

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15
Q

what is the classic triad of dementia?

A
  1. aphasia: inability to communicate effectively, forget words, can’t comprehend
  2. apraxia: inability to complete motor tasks
  3. agnosia: inability to correctly interpret senses, can’t recognize people, can’t interpret full bladder/pain/etc
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16
Q

what is the molecular hallmark of Alzheimer’s disease?

A

loss of ACh cortical activity due to deficiency of choline acetyltransferase —> generalized degeneration of cortex

most prominent in basal nucleus of Meynert and hippocampus

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17
Q

which allele puts patients at risk for Alzheimer’s? Which is neuroprotective? and why?

A

apolipoprotein E (ApoE) epsilon 4 allele = higher risk, causes more amyloid precursor protein (APP) to be broken down to beta breakdown product, facilitating formation of alpha-beta (AB) amyloid

apolipoprotein E (ApoE) epsilon 2 allele = neuroprotective, decreases formation of beta breakdown product

[4 is HIGHER than 2 = HIGHER risk]

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18
Q

Describe two ways in which amyloid is visualized in imaging

A
  1. Congo red stain
  2. apple-green birefringence under polarized light

applies to amyloid in any disease process anywhere in the body! (amyloid = extracellular protein deposits)

19
Q

what are 2 causes of early onset Alzheimer’s Disease?

A
  1. Down syndrome - amyloid precursor protein (APP) is on chromosome 21
  2. familial form - due to gene mutations in presenilin 1&2
20
Q

what type of hydrocephalus do patients with Alzheimer’s develop and why does this make sense?

A

hydrocephalus ex vacuo: ventricles appear larger due to atrophy of the gyri

21
Q

what are the 2 histology findings of Alzheimer’s?

A
  1. beta amyloid plaques
  2. neurofibrillary tangles of hyper-phosphorylated Tau protein (within neuron cell bodies)
22
Q

how is memantine used to treat Alzheimer’s?

A

memantine: noncompetitive NMDA receptor antagonist

NMDA (N-methyl-D-aspartate) = glutamate receptor

side effects: dizziness, confusion, hallucinations

May also be effective for dementia with Lewy bodies and vascular dementia

23
Q

name 3 acetylcholinesterase inhibitors used to treat Alzheimer’s

A
  1. donepezil
  2. galantamine
  3. rivastigmine

side effects: nausea, dizziness, insomnia

24
Q

what is the cause/risk factors of multi-infarct dementia?

A

dementia after multiple strokes (step-wise cognitive decline following each one)

risk factors: HTN, high cholesterol, smoking

25
Q

What is contained in a Lewy body and when does it cause Parkinson’s versus Lewy body dementia?

A

Lewy body = alpha-synuclein

found in basal ganglia —> Parkinson’s

found in cortex —> LB dementia (dementia + Parkinson’s symptoms + hallucinations)

[patients can develop symptoms of both, but diagnosis is named after whichever came first]

26
Q

what is the triad of Lewy body dementia?

A

Lewy bodies (alpha-synuclein) accumulate in cortex —>
1. dementia
2. Parkinson’s symptoms
3. hallucinations

27
Q

Pick’s Disease

A

rare cause of dementia affecting frontal and temporal lobes —> change in personality + aphasia

pathology shows Pick bodies - spherical tau protein (as opposed to tangles in AD)

(aka frontotemporal lobe degeneration, FTLD)

28
Q

histology taken from patient with dementia shows spherical tau proteins … what is the diagnosis? which areas of the brain are affected?

A

Pick’s Disease: rare cause of dementia affecting frontal and temporal lobes —> change in personality + aphasia

pathology shows Pick bodies - spherical tau protein (as opposed to tangles in AD)

29
Q

what is the cause of Creutzfeldt-Jakob disease? what are the etiologies (3)?

A

aka spongiform encephalopathy - rare dementia characterized by intracellular vacuoles (brain looks like a sponge)

caused by PrPSC prion - either sporadic, familial, or transmitted (from beef = Mad Cow Disease)

30
Q

what causes normal prion proteins to become abnormal/disease-causing?

A

PrP(c) = normal prion
PrP(sc) = abnormal

PrP(sc) can convert normal prions to abnormal prions (duplicate itself) and aggregate into abnormal beta-pleated sheets

31
Q

what are 3 classic features of Creutzfeldt-Jakob dementia? describe the prognosis

A

aka spongiform encephalopathy, due to abnormal prions

RAPID (weeks!) development of dementia, death within 1 year

  1. ataxia
  2. ”startle myoclonus” - startled by small stimuli
  3. spike-wave complexes on EEG
32
Q

pt rapidly develops signs of dementia within weeks + spike-wave complexes on EEG =

A

Creutzfeldt-Jakob dementia: aka spongiform encephalopathy, due to abnormal prions

classic features:
1. ataxia
2. ”startle myoclonus” - startled by small stimuli
3. spike-wave complexes on EEG

33
Q

where does atrophy occur in Lewy Body dementia (specifically)?

A

posterior parietal and hippocampal areas

histology shows alpha-synuclein plaques/ neurofibrillary tangles

34
Q

on which chromosomes do the following precursor mutations for Alzheimer’s occur?
a. beta-amyloid precursor protein mutations (early onset)
b. apolipoprotein E4 polymorphism (high genetic risk)
c. Presenilin 1 mutation (early onset)
d. Presenilin 2 mutation (early onset)

A

a. beta-amyloid precursor protein mutations - chromosome 21 (high risk in Down’s patients)

b. apolipoprotein E4 polymorphism - chromosome 19, mutation creates less stable protein —> impaired alpha-beta42 clearance, promoting aggregation

c. Presenilin 1 mutation - chromosome 14

d. Presenilin 2 mutation - chromosome 1

35
Q

what are the respective roles of the following genes which may be linked to sporadic Alzheimer’s Disease?
a. clusterin/Apolipoprotein J
b. CR1
c. PICALM

A

a. clusterin/Apolipoprotein J: similar to ApoE4, regulates alpha-beta42 aggregation

b. CR1: complement related protein, may play role in alpha-beta42 clearance

c. PICALM: involved in endocytosis, may regulate APP trafficking in cells

36
Q

what are the 3 variants of frontotemporal lobar degeneration (FTLD)?

A
  1. behavioral (Pick’s disease): apathy, disinhibition, compulsions, social withdrawal, executive dysfunction
  2. semantic dementia: loss of semantic knowledge, memory loss
  3. progressive non-fluent aphasia: decreased verbal fluency —> agrammatism, phonemic paraphasias, apraxia of speech
37
Q

Pt is 76yo M presenting to their GP with concern of multiple falls in the past 2 months. PE reveals postural instability and a vertical gaze palsy. An MRI is performed, which shows a “Mickey mouse sign.” What type of dementia is this?

A

progressive supranuclear palsy: tauopathy affecting subthalamic nucleus, substantia nigra, globus pallidus

MRI may also show “hummingbird sign”, histology shows tufted astrocytes

38
Q

describe the pathology and clinical presentation of chronic traumatic encephalopathy

A

due to recurrent sub-concussive head trauma

pathology shows perivascular accumulations of phosphorylated tau in neurons and astrocytes

clinical presentation: memory impairment, executive dysfunction, impaired attention, depression, explosively (often violent)

39
Q

describe the clinical features of limbic-predominant age-related TDP-43 encephalopathy (LATE)

A

due to TDP-43 accumulation from amygdala to limbic regions, then neocortex

presents with amnestic dementia which progresses slower (LATEr) than AD

diagnosed as isolated syndrome - memory-predominant dementia with hippocampal atrophy in absence of tau or amyloid biomarkers

40
Q

what is the cause of vascular dementia?

A

accumulation of recurrent or chronic low-level ischemia (2nd most common cause of dementia)

—> step-wise decline in cognitive function - executive dysfunction and slowed processing speed, memory impairment (late)

imaging shows small vessel ischemic disease and/or multiple infarcts

41
Q

what is the mechanism of action of the following dementia drugs?
a. Rivastigmine.
b. Donepezil
c. Galantamine.

A

Rivastigmine and donepezil are both noncompetitive (covalent but reversible) cholinesterase inhibitors

Galantamine is a competitive cholinesterase inhibitor

Used to treat mild to moderate Alzheimer’s disease

may cause N/V, bradycardia, syncope (raise ACh - this makes sense!)

42
Q

what are aducanumab and lecanemab used to treat?

A

mAb to platforming beta amyloid peptide - FDA approved for mild cognitive impairment or mild dementia

Both reduce amyloid plaques in the brain (disease modifying!!), only lecanemab has showed statistically significant slowing in rate of cognitive decline thus far

May cause amyloid related imaging abnormalities (ARIA): cerebral edema, microhemorrhages

43
Q

What are three classes of drugs that should be avoided in patients with dementia?

A
  1. anticholinergics.
  2. Benzodiazepines.
  3. sedatives/hypnotics.

These aggravate cognitive impairment

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