Dementia And Delirium Flashcards
Confusion Confused -Ds
Climical syndromes of cognition
Delirium-impairment >1 aspect of cognition
Dementia
Developmental disability
Deficit (Focal)
Depression- hard to make new memories + concentrate
Delusional state
Dissociative state- somatisatiom disorders- pseudoseizures, not epileptic attacks
When are auditory hallucinations more prominent?
Primary psychic cases
Whats delirium?
A toxic confusional state.
An acute or cpsubacute onset,
Impairement of consciousness (varies in severity and fluctuates compared to dementia) accompined by perception + mood abnormalitites.
Confusion worse at night 🌙⭐️ , accmp by hallucinations, delusions, restlmessness + aggression.
Many diseases can be accmp by delirium esp in elderly.
Commonest: infx + drugs
Managment of delirium
Withdrawal of drugs,mrehydration, pain relief, sedation only if aggressive or at risk of self injury- benzodiazepines ⭐️
Altho severe: IM haloperidol.
What is acute confusion?
Acute onset cognitive impairment, reversible,
Fluctuation
Poor attention: distractibility, impaired working memory, :
disorientation, disturbed diurnal rhythm,
Visual hallucinations
Behav change- withdrawal or aggitation
How do we test for distractibility?
Digit span, poor verbal frequency, poor encoding
What are some predisposing fx for delirium?
Demetia
Eldelry
Sedation drugs
Sensory impairment(vision, hearing, proprioception) Unfamiliar surroundings- encironment Severe illness Infx, dehydration, surgery, hip fracture Physical frality
So: systemic illness- hyperanaemia? Hepatic encephalopathy, hypoxia, paraneoplastic syndrome,…infx, post op
Circulatory: MI,mshock, arrythmia
Structural cranial lesions- neurosurgical- space occupying lesion- blood, CSF, hydrocephalus
So acute confusion is?
Impaired cognitive reserve
Impaired interaction w/ env
F of body to maintain brain
So what are some causes of delirium?
Systemic illness: Drugs: tricyclic antidepressants, Benzodiazepines, Opiates, Anticonvulsants,
Drug/alcohol withdrawal -Metabolic , - Hypoxia, RF, Disorders of electrolytes, Hepatic Failure,
Vit Deficiencies- B1 (Werinke-Korskoff) , Vit B12.
Brain damage: trauma, tumour, abscess, SAH,
Whats Dementia?
Progressive decline of cognitive fx ie loss of mind.
No clouded comsciousness
Over 65s- 10% and 20% >80s
70% Alzheimers. **
Multiple cerebral infraction** Dementia w/ Lewy bodies ** Xs alcohol- werinkes korsakoff syndrome Hypothyroidism Intracranial mass: subdural haem, hydrocephalus Vit B12 def Syphillis Huntingtons Late Parkisnons
What is a simple clinical assesment of the menta state?
Age, time , address, year Place- name of hospital Recognition of 2 ppl- Dr, nurse DOB Year of 1st world war? Monarch? Count backwards from 20-1
Each 1.
Healthy >8
Whats Alzheimers?
1o degenerative cerebral D , unknown aetiology.
Later inset, steady progression.
Most predominant early sx: short temp memory loss
Subsequently: slow disintegration of personality and intellect, all cortical fx affected.
What are Alzheimers plaques made of?
B-amyloid. + granulovacular bodies.
How would you investigate Alzheimers?
Simple assesment of mental state. Exclude treatable causes.
FBC, LFTs, TFTs, B12, folate.
Brain CT in young or those w/ atypical presx.
SH+FH- how vulnerable pt is
How would you manage Alzheimers?
Anxiety and depression must be tx.,
Acetylchoniesterase Inhibiors like donezepil, rivastigmine, galantamine.
Decrease ACh production
Average survival8-10Y
Vascular (multi infract)
2nd most common vause of dementia.hx and CF
- stepwise deterioration with declines dollowed by short periods of stability. Hx of TIAs.
Evidence of arteriopathy
Dementia w/ Lewy bodies
Characterised by fluctuating cognitiom with pronounced variation in attention + alertness.
Prominent and periststent memory loss, not early.m
Impairment in attention, frontal, subcortical and cisuospatial ability is more predominent.
Depression + sleep probs.
Visual hallucinations- frightening nightmares , strange faces
Delusioms with transient loss of consciousness occur.
Cortical lewy bodies on autopsy.
❌❌ neuroleptic drugs
Define Dementia
Progressive, irriversible decline in spcognitive fx w/o i paired consciousness. Can affect all aspects of higher fx, eg concentration, memory, language, personality and emotional control.
What happens in Lewy body dementia?
2 after Alzheimers.
CF: day to day fluctuations of cognitive fx, visual hallucinations,msleep disturbance, transient LOC, recurrent falls, parkinsonian features.
Prone to hallucination, antipsychotics should be avoides since cause ppsevere parkinsonism in 60%.
What are some parkinsosnian features?
Trepmor,
Hypokinesia
Rigidity
Postural instability
What are Lewy bodies?
Abnormalities within the cytoplasm within neurones: proteins + granular material.
Dound in the cerebral cortex of LB dementia and PD.
Whats Creutzfeld disease?
CJD- rapidly progressive dementia caused by prions (infectious agents conposed only by protein) - transmitted by human pituitary hormones + neurosurgical instruments.
Pulvinar sign
What hapoens in Vascular dementia?
Ischaemic disorder characterised by multiple small infracts in cortex and white matter. When >100 mL of infracts occured, dementia is clinically apparent.
Begins in 60s w/ stepwise deterioration f cognitive fx.
Other Features: focal neurology, fits, nocturnal confusion.
RFs(male, smoking, htn, dm, hypercholesterolaemia.
Death usually within 5 years due to stroke or IHD.
Whats Picks disease?
Pick Arnold- Czechoslovakian neurologist and psychiatrist (1852-1924)
Frontotemporal dementia- can only be differentiated from other forms postportum.
CFs: disinhibition, inattention, antisocial behaviour, personality changes. Later, apathy, withdrawal, predominate.
Memory loss + disorientation- late.
Postmortem- atrophy of frontal + tenporal- knife blade atrophy and Picks bodies( tau proteins in cytoplasm)
What happens in. Or al pressure hydrocephalus?
Triad of: 1. Dementia (mainly memory probs) 2. Gait disturbance
3. Urinary inconinence.
Cause: increased vol of CSF, but only a slight increase in pressure cz the ventricles dilate to compensate. Disruption in subarachnoid soace that does not allow CSF reabsorption but allows it to flow theough ventricles into sybaracnhoid space.
Dx- by LP to demonstrate normal CsF opening pressure
Collowed by head CT/MRI (showing wnlarged ventricles).
Tx- ventriculoperitoneal shunting.
