organic disorders Flashcards

1
Q

what is an organic mental disorder

A

mental disorders that are due to common, demonstratable aetiology in cerebral disease, brain injury or other insult leading to cerebral dysfunction

they are acquired and are different from functional mental illnesses

can be:
1y - direct effect on the brain
2y - systemic diseases that affect the brain in addition to other systems/organs

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2
Q

problems when defining organic mental illnesses

A

many (if not all) psychiatric disorders have an organic basis - sz, BPAD, melancholia

many mental disorders present w/ a mixture of mental and physical features

physical disorders also have an effect on psychological functioning

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3
Q

common features to organic mental disorders

A

cognitive - memory, intellect, learning

sensorium - consciousness, attention

mood - depression, elation, anxiety

psychotic - hallucinations, delusions

personality and behaviour disturbance

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4
Q

onset of organic mental disorders

A

any age

most tend to start in adult or later life

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5
Q

prognosis for organic mental disorders

A

some irreversible and progressive

some transient/respond to treatment

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6
Q

acute/sub-acute organic mental disorders - 3 examples

A

delirium

organic mood disorder

organic psychotic disorder

  • recently appearing state of mental impairment as a result of intoxication, drug OD, infection, pain etc
  • often temporary
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7
Q

3 examples of chronic organic mental disorders

A

dementia

amnesic syndrome

organic personality change

-

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8
Q

what can cause chronic organic mental disorders

A

chronic drug/alcohol dependence - due to their long lasting toxic efffects

vascular problems - strokes

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9
Q

management of organic mental disorders

A

varies depending on cause

key points:

  • correct diagnosis
  • medication not usually that useful (except acute)
  • MDT approach
  • management of environment
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10
Q

triad of symptoms in Wernicke’s encephalopathy

A

acute confusional state
ataxia
opthalmoplegia

nystagmus

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11
Q

what causes wenicke’s encephalopathy

A

relataed to acute thiamine deficiency (B1)

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12
Q

what is wernicke’s encephalopathy often confused with

A

delirium tremens

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13
Q

prognosis of wernicke’s encephalopathy

A

untreated acute phase lasts ~ 2wks
84% develop korsakoff psychosis
- 15% mortality in untreated pts

w/ treatment: confusional state and opthalmoplegia can resolve within days

nystagmus, neuropathy and ataxia may be prolonged or permanent

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14
Q

treatment of wernicke’s encephaloptahy

A

high potency parenteral B1 replacement
- 3-7 days, oral thiamine

avoid carb load until thiamine replacement completed

all pts w/ WE symptoms or at high risk: parenteral thiamine
other undergoing detox/under investigation should be commenced on oral thiamine

concurrent treatment for alcohol withdrawal

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15
Q

what characterises alcohol amnesic syndrome (Korsakoff’s psychosis)

A

marked impairment of anterograde memory (ability to learn new info)

disturbance of time sense

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16
Q

features of korsakoff’s psychosis

A

no clouding of consciousness, absence of defect in immediate recall or global impairment

variable degrees of cognitive impairment

personality changes, apathy, loss of initiative

confabulation in the early stage

can improve w/ prolonged abstinence

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17
Q

differential diagnosis for wernicke’s encephalopathy

A

hepatic encephalopathy

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18
Q

where is hepatic encephalopathy usually seen

A

advanced alcoholic liver disease

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19
Q

features of hepatic encephalopathy

A

general psychomotor retardation, drowsiness

flucutating levels of confusion

related to build up of toxic products e.g. ammonia

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20
Q

when does hepatic encephalopathy improve

A

if and as liver function improves§

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21
Q

what type of illness is alcohol related brain damage

A

part of a spectrum of alcohol relate medical disorders

not a specific diagnosis

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22
Q

what causes alcohol related brain damage

A

neurotoxic effects of alcohol

head injury

vitamin deficiencies

cerebrovascular disease

hypoxia

hypoglycaemia

seizures

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23
Q

how common is alcohol related brain damage

A

35% of alcohol dependent persons will exhibit post-mortem evidence

prevalence is increasing - increased awareness/increased prevalence

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24
Q

when does alcohol related brain damage present

A

women tend to present 40-50y/o
- usually a decade younger than men

trend towards people presenting earlier than in the past

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25
Q

features of alcohol related brain damage

A

50-80% of heavy drinkers display cognitive impairment when sober

impairment in short term memory, long term recall, new skill application, set-shifting ability

visuospatial ability decline > language ability decline

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26
Q

features of alcohol related brain damage on imaging

A

cortical atrophy (mainly white matter loss)

ventricular enlargement

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27
Q

when can alcohol related brain damage improve

A

may recover spontaneously w/ abstinence/greatly reduced drinking

28
Q

adults w/ incapacity act

when is a person unable to make a decision

A

a person is unable to make a decision for themselves if, due to mental disorder or inability to communicate because of physical disability, they are incapable of:

acting or
making decisions or 
communicating decisions or 
understanding decisions or 
retaining the memory of decisions
29
Q

what is dementia

A

syndrome characterised by global cognitive impairment which is chronic in nature

30
Q

underlying pathology in dementia

A

variable

usually, but not always progressive

31
Q

what are the different types of dementia

A
alzheimer
vascular 
mixed
Lewy body 
frontotemporal 
due to other brain disorders - huntington's, head injury, parkinson's
32
Q

difference between dementia and depressive pseudodementia

A
33
Q

how common is steroid induced psychosis

A

mild-moderate psychiatric symptoms in 28% pts treated w/ steroids

~6% severe reaction

34
Q

factors affecting severity of steroid induced psychosis

A

dosage related to incidence but not timing, duration or severity

subsequent events not predicted by previous (or lack of previous) reaction

35
Q

management of steroid induced psychosis

A

consider tapering steroids - might not be possible due to medical condition being treated

consider antipsychotic/mood stabiliser

36
Q

endocrine and metabolic disorders - presentation

A

wide variety of clinical presentations

likely to 1st present to GP/general medicine but some conditions (hypothyroidism, addison’s) may present 1st to psychiatry - risk of mistaken diagnosis

37
Q

link between CNS and endocrine/metabolic issues

A

CNS requires stable biochemical and metabolic environment for proper functioning

38
Q

how reversible are endocrine/metabolic presentations

A

psychiatric presentations may be reversible if detected

39
Q

what is anti-NMDA receptor encephalities

A

AI disease that targets NMDA receptors

  • ionotropic glutamate receptor involved in synaptic plasticity and memory function
40
Q

presentation of anti-NMDA receptor encephalitis

A

~1/2 associated w/ malignancy - typically ovarian teratoma in women

often presents initially w/ psychiatric symptoms

41
Q

management of anti-NMDA receptor encephalitis

prognosis

A

immunotherapy and tumour resection if indicated
- IVIg, plasmapheresis, rituximab

prognosis w/ treatment generally good
- can be longer lasting cognitive and neuropsychiatric symptoms in a minority

42
Q

what is delirium

A

aetiologically non-specific syndrome

characterised by concurrent disturbances of: 
consciousness and attention
perception 
thinking 
memory 
psychomotor behaviour 
emotion 
sleep-wake cycle
43
Q

presenting features of delirium

A
impairment of consciousness and attention 
global disturbance of cognition 
psychomotor disturbances
disturbance of sleep-wake cycle 
emotional disturbance
44
Q

timing of presentation of delirium

A

rapid onset

diurnally fluctuating

duration <6mths

45
Q

physical signs of delirium

A

due to underlying cause

autonomic activation: tachycardia, hypertension, diaphoresis, dilated pupils, fever

dysgraphia often evident

46
Q

causes of delirium

A

medication

druga buse

withdrawal syndromes

metabolic

vitamin deficiencies

endocrinopathies

infections

neurological

toxins and industrial exposures

other

47
Q

medication causes of derlirum

A

anticholinergic drugs - atropine, TCAs, antipsychotics, anti-histamines, OTC hypnotics, anti-vertigo, anti-spasmodics

sedative hypnotics - esp w/ long 1/2 life e.g. flurazepam

decongestants

anti-asthmatics

other sympathomimetics

cimetidine, digitalis, L-dopa, meperidine, methyldopa, glucocorticoids

48
Q

drug abuse causes of delirium

A

amphetamines

cocaine

PCP

hallucinogens

inhaled drugs - glue, NO

49
Q

withdrawal syndrome causes of delirium

A

alcohol

benzodiazepines - esp alprazolam

barbiturates

other sedative hypnotics

50
Q

metabolic causes of delirium

A

hepatic encephalopathy

uraemia

hypoglycaemia

hypercalcaemia

hypo/hypermagnesaemia

porphyria

51
Q

vitamin deficiency causes of delirium

A

thiamine - wernicke-korsakoff syndrome

vit B12

nicotinic acid - pellagra

52
Q

endocrinopathy causes of delirium

A

hypo/hyperthyroidism

hypo/hyperparathyroidism

cushings

addisons

hypopituitarism

53
Q

infectious causes of delirium

A

any systemic infection in the elderly

esp w/ co-existing dementing process

meningitis, encephalitis, brain abscess, neurosyphilis

AIDS encephalopathy

54
Q

neurological causes of delirium

A

head injury - post-concussive syndromes, bleeds

stroke

hypertensive encephalopathy

intracranial neoplasm - esp frontal and temporal

complex partial status epilepticus

post-ictal states

55
Q

toxins and industrial exposure causes of delirium

A

CO

carbon disulphide

organic solvents

heavy metals

56
Q

other causes of delirium

A

SLE - lupus cerebritis

cerebral vasculitis - temporal arteritis, periarteritis nodosa

paraneoplastic syndromes - limbic encephalitis

hyperviscosity syndromes

57
Q

mechanism of delirium

A

pathophysiology unclear
- GABAergic and cholinergic NT systems?

  • central cholinergic deficiency? - increased risk associated w/ GABA agonists and anticholinergic drugs
  • increased dopaminergic activity?
  • direct neurotoxic effect of inflammatory cytokines?
58
Q

delirium vs dementia

A
59
Q

delirium vs functional psychosis

A
60
Q

implications of delirium

A

disruption of other pts and anxiety of clinical staff

prolonged hospital stays

increased risk of institutionalisation

~£13000 per admission

61
Q

prognosis for delirium

A

fluctuating course

gradual resolution of symptoms w/ effective treatment of underlying cause - may improve more quickly at home

slower symptom resolution in the elderly

often patchy amnesia for delirious period following recovery

mortality

may be a marker for subsequent dementia

62
Q

mortality rates for delirium

A

20% die during this admission

up to 50% at 1yr

63
Q

management of delirium

A

correct contributing factors (disorientation, dehydration, constipation, hypoxia, immobility/limited, infection, polypharmacy, pain, poor nutrition, sensory impairment, sleep disturbance)

enviornmental and supportive measures - education of relatives and healthcare staff, safe environment, optimise stimulation, orientation

medications

64
Q

medications for management of delirium - things to remember

A

avoid sedation unless required to maintain safety (severely agitated or required to facilitate investigation/treatment)

evidence base and guidelines don’t support use of medications in delirium

medications sometimes have to be used for acute distress and to maintain safety: antipsychotics, benzodiazepines, promethazine

use single medication, start low and assess response - slow doses in frail elderly

65
Q

cautions to take with medications in delirium

A

antipsychotics - lower seizure threshold, be cautious if suspected withdrawal case

benzodiazepines - safer first choice (interact w/ fewer things), can prolong delirious episode

promethazinde - can ultimately worsen delirium

66
Q

drugs to use when managing delirium

A

ANTIPSYCHOTICS:
- risperidone 0.5-1mg
- quetiapine 25-50mg
if IM required - consider olanzapine/aripiprazole
avoid in withdrawal state unless pt well covered w/ benzodiazepines - lower seizure threshold

BENZODIAZEPINES:
can prolong delirium
- lorazepam 0.5-1mg
use in withdrawal states - diazepam/chlordiazepoxide, caution in liver failure

PROMETHAZINE:

  • oral/IM 10-25mg
  • off licence use
  • caution: in elderly (anticholinergic effect), prolonged QTc, lower seizure threshold