Neurocognitive Disorders Flashcards
What functions are impacted in delirium?
Attention, awareness (consciousness), cognition (thinking) and memory are impacted
What is the onset timing of delirium?
Acute onset, often fluctuating, 24 hour period
Can patients with delirium return to baseline?
Yes
When is the onset or complication of delirium most commonly associated with?
Post-op complication and new diagnosis during an inpatient stay
What unit within the hospital has higher rates of delirium?
ICU
Who is at high risk for delirium?
Older age
Polypharmacy (anesthetics, anticholinergics, opioids)
Multiple medical co-morbidities
Sensory impairment (vision, hearing)
Substance or alcohol use
What are the top three things that can cause delirium?
Drug toxicity, infection, dehydration
What is included in the mental status exam?
Appearance
Attitude
Behavior (motor movements, overall arousal)
Speech
Mood (how the patient feels- subjective)
Affect (how you perceive their mood)
What is the difference between a full mental status exam vs. the mini-mental status exam?
Full mental status exam is more subjective and the mini-mental status is more objective
What is the DSM-5 Diagnostic Criteria for Delirium?
- Disrupted attention and awareness
- Develops over a short period of time and fluctuates
- Acute change in cognition
Can a patient have dementia and delirium?
Yes
What is typical the first thing to go in dementia?
Short term memory
What are the differentiating factors for dementia and delirium?
Onset (acuity)
Course (fluctuating vs. gradual)
Awareness (impaired vs. often clear until advanced stage)
Attention (disturbed vs. often good until advanced stage)
What is the treatment for delirium?
Treat underlying cause and remove/treat any exacerbating factors
Prevention is key!
What is a medication that can treat agitation in delirium patients?
Haloperidol- antipsychotics (IM/IV)
What is the treatment of choice for delirium due to withdrawal?
Benzos (PO or IV)
What is the first step of the continuum of Wernicke-Korsakoff Syndrome?
Wernicke’s Encephalopathy (WE)
Why is Wernicke Encephalopathy often mis-diagnosed?
We don’t ask about ETOH abuse and mimics delirium (misdiagnosed in 80% of patients)
Is WE reversible?
Yes, with appropriate treatment. If left untreated will progress to Korsakoff’s which is irreversible.
What is the pathophysiology of WE?
Inadequate thiamine (B1) –> ETOH leads to GI tract inflammation reducing absorption and poor nutritional intact
How long does your body store thiamine under normal conditions?
4-6 weeks
Why is thiamine important in the Krebs Cycle?
Needed to break down Pyruvate and enter aerobic metabolism (Krebs Cycle). Without it body goes into anerobic cycle (lactic acid formation)
What is the classic triad of symptoms in WE?
- Altered mental status
- Gait ataxia
- Opthalmoplegia (weakness/paralysis)
Are serum thiamine levels used for diagnosis of WE?
No, they are unreliable because there is no single threshold and doesn’t correlate with clinical symptoms
Is imaging necessary to diagnose WE?
No it is not necessary, but may see mammillary body atrophy
What is the initial treatment of WE?
IV thiamine
What is the problem if we give glucose first in WE?
Glucose will be immediately utilized for energy (ATP) production, further preventing ATP to enter Kreb’s cycle –> lactic acid buildup
What is the average age of onset for Crutzfeldt-Jakob Disease (CJD)?
60 years
What is the sole presentation of Crutzfeldt-Jakob Disease?
Rapidly Progressive Dementia
What is needed for definitive diagnosis of CJD?
Histology (biopsy or autopsy)
What are some supportive laboratory findings for CJD?
EEG abnormalities (sharp wave complexes)
Brain MRI abnormalities (cerebellar atrophy)
CSF analysis (14-3-3 protein testing)
What is the treatment for CJD?
No curative treatment, 100% fatality. Tx is palliative.
