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Neurology_Clinical Medicine > Neurocognitive Disorders > Flashcards

Neurocognitive Disorders Flashcards

1
Q

What functions are impacted in delirium?

A

Attention, awareness (consciousness), cognition (thinking) and memory are impacted

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2
Q

What is the onset timing of delirium?

A

Acute onset, often fluctuating, 24 hour period

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3
Q

Can patients with delirium return to baseline?

A

Yes

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4
Q

When is the onset or complication of delirium most commonly associated with?

A

Post-op complication and new diagnosis during an inpatient stay

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5
Q

What unit within the hospital has higher rates of delirium?

A

ICU

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6
Q

Who is at high risk for delirium?

A

Older age
Polypharmacy (anesthetics, anticholinergics, opioids)
Multiple medical co-morbidities
Sensory impairment (vision, hearing)
Substance or alcohol use

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7
Q

What are the top three things that can cause delirium?

A

Drug toxicity, infection, dehydration

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8
Q

What is included in the mental status exam?

A

Appearance
Attitude
Behavior (motor movements, overall arousal)
Speech
Mood (how the patient feels- subjective)
Affect (how you perceive their mood)

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9
Q

What is the difference between a full mental status exam vs. the mini-mental status exam?

A

Full mental status exam is more subjective and the mini-mental status is more objective

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10
Q

What is the DSM-5 Diagnostic Criteria for Delirium?

A
  1. Disrupted attention and awareness
  2. Develops over a short period of time and fluctuates
  3. Acute change in cognition
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11
Q

Can a patient have dementia and delirium?

A

Yes

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12
Q

What is typical the first thing to go in dementia?

A

Short term memory

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13
Q

What are the differentiating factors for dementia and delirium?

A

Onset (acuity)
Course (fluctuating vs. gradual)
Awareness (impaired vs. often clear until advanced stage)
Attention (disturbed vs. often good until advanced stage)

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14
Q

What is the treatment for delirium?

A

Treat underlying cause and remove/treat any exacerbating factors

Prevention is key!

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15
Q

What is a medication that can treat agitation in delirium patients?

A

Haloperidol- antipsychotics (IM/IV)

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16
Q

What is the treatment of choice for delirium due to withdrawal?

A

Benzos (PO or IV)

17
Q

What is the first step of the continuum of Wernicke-Korsakoff Syndrome?

A

Wernicke’s Encephalopathy (WE)

18
Q

Why is Wernicke Encephalopathy often mis-diagnosed?

A

We don’t ask about ETOH abuse and mimics delirium (misdiagnosed in 80% of patients)

19
Q

Is WE reversible?

A

Yes, with appropriate treatment. If left untreated will progress to Korsakoff’s which is irreversible.

20
Q

What is the pathophysiology of WE?

A

Inadequate thiamine (B1) –> ETOH leads to GI tract inflammation reducing absorption and poor nutritional intact

21
Q

How long does your body store thiamine under normal conditions?

A

4-6 weeks

22
Q

Why is thiamine important in the Krebs Cycle?

A

Needed to break down Pyruvate and enter aerobic metabolism (Krebs Cycle). Without it body goes into anerobic cycle (lactic acid formation)

23
Q

What is the classic triad of symptoms in WE?

A
  1. Altered mental status
  2. Gait ataxia
  3. Opthalmoplegia (weakness/paralysis)
24
Q

Are serum thiamine levels used for diagnosis of WE?

A

No, they are unreliable because there is no single threshold and doesn’t correlate with clinical symptoms

25
Q

Is imaging necessary to diagnose WE?

A

No it is not necessary, but may see mammillary body atrophy

26
Q

What is the initial treatment of WE?

A

IV thiamine

27
Q

What is the problem if we give glucose first in WE?

A

Glucose will be immediately utilized for energy (ATP) production, further preventing ATP to enter Kreb’s cycle –> lactic acid buildup

28
Q

What is the average age of onset for Crutzfeldt-Jakob Disease (CJD)?

A

60 years

29
Q

What is the sole presentation of Crutzfeldt-Jakob Disease?

A

Rapidly Progressive Dementia

30
Q

What is needed for definitive diagnosis of CJD?

A

Histology (biopsy or autopsy)

31
Q

What are some supportive laboratory findings for CJD?

A

EEG abnormalities (sharp wave complexes)
Brain MRI abnormalities (cerebellar atrophy)
CSF analysis (14-3-3 protein testing)

32
Q

What is the treatment for CJD?

A

No curative treatment, 100% fatality. Tx is palliative.

Neurology_Clinical Medicine (13 decks)

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