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Clinical Neuro Exam 2 > Neurology: Dementia and Delirium > Flashcards

Neurology: Dementia and Delirium Flashcards

0
Q

What structures are affected in subcortical dementias and what are the symptoms?

A

Frontostriatal Pathways affected

  • slowed thinking
  • executive dysfunction: difficulty with goal formation, planning, self-monitoring, attention
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1
Q

What are two examples of cortical dementia and what are the signs associated with general cortical dementias?

A

Alzheimer Disease and CJD

-memory loss, aphasia, apraxia, agnosia

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2
Q

What is meant by extrapyramidal?

A

Motor system with fibers originating from the basal nuclei and cerebellum.
-caudate, putamen, globus pallidus, subthalamus, substantia nigra

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3
Q

What is dementia?

A

Acquired, persistent decline of intellectual functioning including memory and at least one other cognitive domain:

  • aphasia
  • apraxia
  • agnosia
  • executive function
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4
Q

What is the difference between dementia and Mild Cognitive Impairment?

A

MCI only involves memory impairment with no other dementia symptoms. Activities of daily living (ADLs) are intact.

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5
Q

What genetic disease is associated with development of Alzheimer Disease?

A

Down Syndrome

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6
Q

What enzyme plays a significant role in the metabolism and deposition of the amyloid proteins in AD?

A

Beta-secretase

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7
Q

What contributes to the cognitive deficits seen in AD?

A

Cholinergic Deficiency

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8
Q

How does glutamate lead to neuronal cell death in AD?

A

Overstimulation of glutamate receptors leads to excitotoxicity and activation of proteases that degrade neuron proteins.

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9
Q

Late onset AD is most common, which chromosome is most associated with AD?

A

19

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10
Q

How is AD diagnosed?

A

Almost 100% clinical thru H&P.

-definitive diagnosis has to be done with brain biopsy on autopsy.

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11
Q

Name 4 AChase inhibitor drugs used to treat AD.

A
  1. Donepezil: treats cognitive symptoms of AD
  2. Rivastigmine: treats cognitive symptoms of AD and dementia related to parkinson disease.
  3. Tacrine: treats cognitive symptoms but leads to liver toxicity
  4. Galantamine: treats cognitive symptoms of AD.

All can lead to N/V/D, anorexia, bradycardia, insomnia

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12
Q

Name 1 NMDA receptor antagonist used for AD.

A

Memantine: treats moderate to severe dementia.

Can lead to constipation, hypertension, dizziness, headache

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13
Q

What is the triad associated with Diffuse Lewy Body Dementia (DLBD)?

A
  1. Parkinsonism
  2. Visual Hallucinations
  3. Fluctuating Cognitive Impairment
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14
Q

What medications should not be given to patients with DLBD and why?

A

Neuroleptics due to extreme sensitivity to extrapyramidal side effects.

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15
Q

What is normally found in H&P to diagnose a patient with a multi-infarct dementia?

A

History of at least 1 stroke

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16
Q

What is Binswanger Disease?

A

Subcortical arteriosclerotic encephalopathy.

-caused by multiple infarcts in white matter in the brain

17
Q

What medication is best to treat motor symptoms of Diffuse Lewy Body Dementia?

A

Carbidopa/Levodopa

18
Q

How can Parkinson Disease be differentiated from Diffuse Lewy Body Dimentia?

A

In PD the dementia symptoms manifest after the parkinsonian motor symptoms.

In DLBD the dementia and parkinsonian motor symptoms occur almost simultaneously.

19
Q

What is CADASIL?

A

A form of a hereditary stroke disorder that causes migraine attacks with aura and mood disorders.

20
Q

What is Pick Disease?

A

A frontotemporal dementia that is similar to AD but manifests earlier in life and progresses much faster. Often linked with ALS due to chromosome 9 location.

21
Q

When does dementia manifest during the disease process of Parkinson Disease?

A

Usually in the second half of the progression in a setting of “well-established parkinsonism”.

22
Q

What are unique factors to Progressive supranuclear palsy compared to other movement disorders?

A

Symmetric onset of bradykinesia and rigidity (PD is usually unilateral)

Falls tend to occur backwards due to increased postural lordotic compensation (PD falls occur forward)

Vertical supranuclear gaze affected mostly DOWNWARD gaze.

23
Q

What is the triad seen in Normal Pressure Hydrocephalus?

A

Wet, Wacky, Wobbly

  1. Dementia
  2. Ataxia/Apraxia
  3. Incontinence
24
Q

What is the characteristic gait and treatment for normal pressure hydrocephalus?

A

Magnetic Gait

Treat with a shunt to remove excess CSF.

25
Q

What can be found in the CSF to indicate Creutzfeldt-Jakob Disease?

A

14-3-3 protein

26
Q

What is one example of a pseudodimentia?

A

Depression

27
Q

What is the triad for Chronic Traumatic Ecephalopathy?

A
  1. Cognitive Impairment
  2. Depression
  3. Irrational and Impulsive Emotional Behavior
28
Q

If a physician suspected a reversible dementia and wanted to test B12 levels, what other molecule should be tested for a complete diagnosis?

A

Methylmalonic Acid levels

29
Q

What is the 1st step in treating dementias?

A

Treat the cognitive symptoms.

30
Q

What is sundowning?

A

Term meaning that patients with dementia tend to have worse behavioral problems in the evening and at night.

31
Q

What is delerium?

A

An acute, transient, potentially reversible confusional state.

  • disturbed consciousness and altered cognition that has a high mortality rate
  • the cause needs to be treated immediately
32
Q

What 3 things can be done to treat delerium?

A
  1. Eliminate the underlying cause
  2. Alter the environment to help with orientation (clocks, calendar, lighting)
  3. Medications (thiamine, haloperidol, atypicals, benzos)
33
Q

What is the treatment for Delirium Tremens?

A

Results from alcohol withdrawal (insomnia, agitation, increased sympathetic activity).

Give benzodiazepines throughout the duration symptoms.

34
Q

Why is Thiamine (B12) so important for proper nervous system function?

A

Major Point:
-it is necessary for oxidative phosphorylation and energy production in cells (especially neurons which use lots of energy)

Minor Point:
-is one of the component needed to make GABA

35
Q

What is Wernicke Encephalopathy?

A

Diffuse axonal, neuronal, and myelin loss from a thiamine deficiency. Alcoholics are at high risk.

Results in truncal ataxia and abnormal eye movements with nystagmus.

36
Q

Treatment for Wernicke Ecephalopathy.

A 
IV thiamine
(don't wait for tests if you suspect this)
37
Q

What is Korsakoff Syndrome?

A

Condition that can manifest if Wernicke Encephalopathy is untreated.

Patients suffer severe amnesia due to mammillary body degradation, as well as lesions in the dorsomedial nucleus of the thalamus and brain stem.

38
Q

What is Hepatic Encephalopathy?

A

Liver dysfunction leads to increased ammonia levels in the blood which is toxic to the brain. Patients have disturbed sleep, bradykinesia, asterixis, rigidity, and hyperactive deep tendon reflex.

!Asterixis is very diagnostic of metabolic encephalopathies!

39
Q

Describe the 4 stages of Hepatic Encephalopathy.

A
  1. Euphoria, confusion, sleep disorder
  2. Lethargy, confusion, asterixis
  3. Marked confusion, slurred speech, sleepy
  4. coma
40
Q

What is the treatment for hepatic encephalopathy?

A

Remove the underlying cause

Treat the serum ammonia

  • lactulose
  • neomycin

Clinical Neuro Exam 2 (13 decks)

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