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Year 4 - Pysch > Dementia > Flashcards

Dementia Flashcards

1
Q

what is an organic psychiatric disorder?

A

results of pathological lesions, medical disorders, drugs leading to alteration of functioning of the brain

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2
Q

what is delirium

A

acute confusional state

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3
Q

aetiology of delirium

A

substance misuse - drugs, alcohol, opiates, sedatives, anticholinergic, diuretics, seriods, digoxin, anticonvulsants, lithium, TCAs, MAOIs, L-dopa

metabolic - renal failure, hepatic failure, resp failure, cardiac failure, electrolyte imbalance (hyponatraemia, hypoalcaemia), dehydration

infective

endocrine - hypoglycaemia, DKA, hypothyroidism, hyperthyroidism, Cushing’s

neurological - stroke, SAH, head injury, space-occupying lesion, epilepsy

hypoperfusion stats - anaemia, cardiac arrhythmias, postoperative states, stress, sleep deprivation, change environment, constipation, urinary retention, vit deff

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4
Q

clinical features

A
  • diurnally fluctuation – pt most settle during the day time and most agitated at night – ‘sundowning’
  • cognitive impairment – concentration, memory, abstract thinking, incoherent speech/thoughts
  • disorientation in time, place and person
  • perceptual abnor – distortions, illusion, hallucinations
  • agitated, psychomotor retardation, emotionally labile and disinhibited
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5
Q

investigation of delirium

A
  • daily assessment of cognition and mental status
  • psych Hx, mental state examination
  • full physical examination
  • delirium screen

FBC, U&E, LFT, TFT, glucose, thiamine, drug screen

infection screen – urine dip, MSU, sputum culture, blood cultures, LP (if necessary)

imaging – CXR, AXR, CT/MRI head

others – ECG

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6
Q

management of delirium

A
  • identify and treat underlying cause
  • nursed in consistent, comfortable, familiar environment
  • encourage family to Continually re orientate and reassure the patient - today’s Monday you’re in Bradford hospital
  • clocks, calendars, familiar objects from home
  • haloperidol/risperidone/lorazepam in extremely agitated patients
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7
Q

definition of dementia

A

• disease of the brain, progressive and chronic deterioration in cognitive function without consciousness impairment.

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8
Q

general symptoms. of dementia

A
  • memory loss  short term memory is more affected than long term memory, impairment in learning of new things and commonly disorientated
  • impaired thinking  concrete thinking, poor judgement, dec flow of ideas, Reduced fluency, struggles to plan, may have delusions
  • language impairment  expressive (Broca’s – frontal) / receptive dysphasia (wernickes  parietal)
  • Deterioration in personal functioning  severe self neglect
  • Disturbed personality and behaviour  euphoria, emotional liability, apathy, irritable, frustrated, disinhibition in social circumstances, can lead to aggression
  • perceptual abnormalities  visual and audio agnosia (an ability to recognise people and places by voice or by sight), prosopagnosia (inability to recognise the faces), hallucinations, illusions, cortical blindness
  • motor impairments  apraxia, spastic paresis, urinary incontinence.
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9
Q

investigation for dementia

A
  • full physical examinations – exclude any organic disorder
  • MMSE/Addenbrooke’s/DemTect = screening/progression tool
  • confusion bloods – FBC, U&Es, LFT, TFT, serum B12 and folate, serum glucose, Ca2+
  • specialised  HIV, syphilis
  • scans  CT/MRI, blood flow imaging (rare)
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10
Q

what is the most common type of dementia

A

Alzheimer’s - 50%

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11
Q

pathology of Alzhimer’s dementia

A

generalised atrophy (cortical), beta amyloid plaque, neurofibrillary tangles, reduced Ach, wide sulci

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12
Q

RF for Alzhimer’s disease

A

age, female, E4 apoliprotein

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13
Q

specific symptoms of Alzhimer’s disease

A

general dementia symptoms but occurs gradually

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14
Q

clinical features of vascular dementia

A

Sudden onset with step wise progression, clinical features dependant on location of infants

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15
Q

pathology of lewy body dementia

A

eosinophilic intracytoplasmic neuronal inclusion bodies (ubiquitin and alpha synuclein) in brainstem and neocortex  neuronal loss leading to cholinergic

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16
Q

clinical features of lewy body dementia

A

marked Fluctuations in cognitive impairment and alertness, vivid visual hallucination and psychotic symptoms, mild parkinsonism, spatial awareness worsening, can develop Parkinsonism
• v.v.v sensitive to antipsychotics – makes dementia worse

17
Q

what medications can make Lewy body dementia worse

A

antipsychotics

18
Q

when is the onset of Frontal Temporal Dementia

A

young

45-60 yrs old

19
Q

clinical features of Lewy body dementia

A

insidious (10-20yrs)

early and prominet mood changes/behavioral abnor/congitive and language impairments

memory often spared

hyperorality

language progressively worsen and eventually becomes mute

20
Q

Non-pharacological management of dementia in general

A
  • general support for patients, carer, social support, OT etc
  • risk management – fire safety, driving, getting loss, finances
21
Q

Pharmacological management of dementia

A

o cholinesterase inhibitors  Donepezil, Rivastigmine, Galantamine
 cholinesterase inhibitors prevent Ach being broken down  inc cholinergic neurotransmission

o Memantine = NMDA receptor antagonist  in more severe cases of dementia

22
Q

side effect of cholinesterase inhibitors

A

N+V, dizziness, syncope, sleepiness, hypersalivation, vivid dreams, stomach ulcers

23
Q

when can Benzo be used in dementia

A

for management of anxiety and agitations

lorazepam / diazepam

24
Q

when should you not use antipsychotics in dementia

A

should avoid in lewy body or frontal-temporal dementia –> severe extrapyramidal side effect

25
Q

what medications are used for motor problem in Lewy Body Dementia

A

Levodopa

26
Q

what is delirium

A

acute confusional state with clouding of consciousness

27
Q

what are the causes of delirium

A

drugs

metabolic –> renal failure, hepatic failure, resp failure, cardiac failure, electrolyte imbalance (hpyponatraemia, hypocalcaemia)
infection

endocrein - hypothyrodisum, DKA, stroke

Neurological - stroke, SAH, head injury, space occupaying lesion, epilepsy

hypoperfusion states

28
Q

clinical features of delirium?

A

sundowning

cognitive impairment - concentration, memory, abstract thinking, incoherent speech/thoughts

cloud consciousness

disorientation in time, place and person

perceptual abnor - disotion, illusion, hallucinations

agitated, psychomotor retardation, emotionally labile and disinhibitied

29
Q

ix for delirium

A
  • daily assessment of cognition and mental status
  • psych Hx, mental state examination
  • full physical examination

• delirium screen
o FBC, U&E, LFT, TFT, glucose, thiamine, drug screen
o infection screen – urine dip, MSU, sputum culture, blood cultures, LP (if necessary)
o imaging – CXR, AXR, CT/MRI head
o others – ECG

30
Q

Mx of delirium

A
  • identify and treat underlying cause
  • nursed in consistent, comfortable, familiar environment
  • encourage family to Continually re orientate and reassure the patient - today’s Monday you’re in Bradford hospital
  • clocks, calendars, familiar objects from home
  • haloperidol/risperidone/lorazepam in extremely agitated patients
31
Q

pathophysiology of alcohol?

A

alcohol is agoinst for GABA (made from glutamien) –> euphoriant and reinforcing effects

32
Q

what is delirium tremens

A

occurs in 24-72 hours

 clouding of consciousness
 Disorientation in time and place
 Impairment in recent memory
 Fear, agitation, restlessness
 Vivid hallucination, delusional thoughts
 insomnia
 Autonomic disturbance – inc HR, BP, hyperthermia, sweating, dilated pupils
 coarse tremor
 N+V, dehydration, electrolyte imbalance
 seizures

33
Q

mx of delirium tremens

A

medical emergnecy

  • dependent on Clinical Institute Withdrawal Assessment for Alcohol (CIWA score)  if > 9 then need mediational help for withdrawal
  • Benzodiazepines (Chlordiazepoxide 20mg QDS  5mg DB over 5 days)
  • correct fluid and electrolyte imbalance
  • thiamine – prevent Wernicke’s/Korsakoff)  Pabrinex IV or oral
34
Q

what is Wernicke-Korsakov syndrome?

A

medical emergency

 very acute onset that can result in dec consciousness and confusion
 Korsakov syndrome  irreversible recent memory impairment

 due to Thiamine (Vit B1), most commonly secondary to alcohol dependence

35
Q

what are the symptoms of Wernicke-Karsakov syndrome

A

 class triad  confusion, ataxia, ocular palsy (nystagmus)

 other presentation  impaired consciousness, confusion, episodic memory impairment, pupillary abnor, peripheral neuropathies

36
Q

mx of Wernicke-Karsakov syndrome

A
  • parenteral thiamine

* 20% recover / 10% die from haemorrhage of brainstem and hypothalamus

Year 4 - Pysch (6 decks)

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