Flashcards in Dementia And Delirium Deck (25):
Confusion Confused -Ds
Climical syndromes of cognition
Delirium-impairment >1 aspect of cognition
Depression- hard to make new memories + concentrate
Dissociative state- somatisatiom disorders- pseudoseizures, not epileptic attacks
When are auditory hallucinations more prominent?
Primary psychic cases
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,
Poor attention: distractibility, impaired working memory, :
disorientation, disturbed diurnal rhythm,
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?
Sensory impairment(vision, hearing, proprioception)
Unfamiliar surroundings- encironment
Infx, dehydration, surgery, hip fracture
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,
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
Intracranial mass: subdural haem, hydrocephalus
Vit B12 def
What is a simple clinical assesment of the menta state?
Age, time , address, year
Place- name of hospital
Recognition of 2 ppl- Dr, nurse
Year of 1st world war?
Count backwards from 20-1
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
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
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?
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.
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)