Organic disorders Flashcards

1
Q

what do we mean by mental disorder?

A

are “due to common, demonstrable aetiology in cerebral disease, brain injury, or other insult leading to cerebral dysfunction”

  • ACQUIRED
  • distinction from functional mental illness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Primary vs secondary mental disorders?

A

Primary – direct effect on the brain

Secondary – systemic diseases that affect the brain in addition to other systems/organs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Some examples of disorders with an organic base

A

Schizophrenia, bipolar affective disorder, melancholia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Cognitive features?

A

Memory
Intellect
Learning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Sensorium features affected?

A

Consciousness

Attention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

affective changes examples

psychotic change examples

A

Depression
Elation
Anxiety

Hallucinations
Delusions

Personality & behavioural disturbance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is acute organic brain syndrome?

A

mental impairment, as a result of intoxication, drug overdose, infection, pain, and many other physical problems affecting mental status
- is often temporary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Examples of acute brain syndrome

A

Delirium
Organic mood disorder
Organic psychotic disorder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Examples of chronic brain syndrome

A

Dementia
Amnesic syndrome
Organic personality change

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is chronic brain syndrome

A
  • long term
  • chronic drug and alcohol dependence
  • dementia from stroke eg Alzheimers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Management depends on?

A
  • Correct diagnosis
  • Medication usually not that useful except for acute situations
  • Requires MDT approach
  • Management of environment important
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Features of delirium tremors

A
can complicate acute alcohol withdrawal
fluctuating confusion 
disorientation in time & place
memory impairment
psychotic phenomena, e.g. hallucinations, delusional thinking
Treatment with benzodiazepines
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Wernike’s Encephalopathy signs

A

Acute Confusional State
Ataxia
Opthalmoplegia
Nystagmus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

cause of Wernike’s Encephalopathy

A

acute insufficiency of Thiamine (vitamin B1)

- missing meals etc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Acute phase of Wernike’s Encephalopathy can last?

A

2 weeks, 84% develop Korsakoff psychosis

15% mortality

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What can take longer to be treated in Wernike’s Encephalopathy?

A

nystagmus, neuropathy and ataxia may be prolonged or permanent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Treatment of Wernike’s Encephalopathy?

A

High potency parenteral B1 replacement IV or IM - rambabronex
3-7 days
Oral thiamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

All patients with symptoms of Wernike’s encephalopathy or at high risk should be treated with ?

A

parenteral thiamine, others undergoing detoxification or under investigation should be commenced on oral thiamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What should you avoid with Wernike’s encephalopathy

A

carbohydrate load

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what treatment for alcohol withdrawal

A

benzodiazepine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Alcohol Amnesic Syndrome (Korsakoff’s psychosis) is characterised by

A

characterised by marked impairment of anterograde memory (ability to learn new information), disturbance of time sense

  • 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 with prolonged abstinence
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Hepatic encephalopathy features

A
  • normally seen in advanced alcohol liver disease
  • general psychomotor retardation, drowsiness
  • fluctuating levels of confusion
  • related to build up of toxic products (e.g. ammonia)
  • improves if and as liver function recovers
23
Q

How can alcohol brain damage occur?

A

neurotoxic effects of alcohol, head injury, vitamin deficiencies, cerebrovascular disease, hypoxia, hypoglycaemia, seizures

24
Q

when do women tend to present with alcohol brain damage ?

A

40-50’s

25
Q

50-80% heavy drinkers display?

A

cognitive impairment when sober

- Impairment in short-term memory, long-term recall, new skill acquisition, set-shifting ability

26
Q

ARBD visuospatial ability decline is?

A

greater than language ability decline

27
Q

what might you seen on imaging on a patient with ARBD?

A

cortical atrophy (mainly white matter loss) and ventricular enlargement

28
Q

Adults with Incapacity (Scotland) Act 2000 -unable to make a decision if?

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

depressive illness that could be dementia?

A

pseudodementia

30
Q

What is dementia?

A

progressive and chronic

- global cognitive impairment

31
Q

Different types of dementia

A
Alzheimer 
Vascular
(Mixed)
Lewy body 
Frontotemporal
Due to other brain disorders
Huntington’s chorea 
Head injury 
Parkinson’s disease
32
Q

Steroid induced psychosis features?

A

Mild-moderate psychiatric symptoms in 28% patients

- 6% = severe

33
Q

Steroid induced psychosis - the dosage is related to?

A

incidence but not timing, duration or severity

34
Q

Management of Steroid induced psychosis?

A

Taper the steroids

  • consider an antipsychotic or mood stabiliser for duration of treatment
  • olanzapine, Quetiapine
35
Q

Endocrine and metabolic disorders , how may patients present?

A

GP/General medicine but some conditions (i.e. Hypothyroidism, Addison’s disease) may present first to psychiatry and there is risk of mistaken diagnosis

36
Q

Neurological investigations for acute psychosis?

A

MRI
EEG
biochemistry tests

37
Q

what is Anti-NMDA Receptor encephalitis?

A

Autoimmune disease that targets NMDA receptors

38
Q

What is an NMDA receptor?

A

Ionotropic glutamate receptor involved in synaptic plasticity and memory function

39
Q

Anti-NMDA Receptor encephalitis is often associated with what malignancy

A

50% - ovarian teratoma

40
Q

Anti-NMDA Receptor encephalitis can present with

A

psychiatric symptoms

41
Q

treatment of Anti-NMDA Receptor encephalitis

A

Immunotherapy and tumour resection if indicated
IVIg, plasmapheresis, rituximab
- benzodiazepines and antipsychotics symptomatically

42
Q

what is delirium?

A

nonspecific syndrome characterised by concurrent disturbances of consciousness and attention, perception, thinking, memory, psychomotor behaviour, emotion, and the sleep-wake cycle

43
Q

Presenting features of delirium?

A

Impairment of consciousness and attention
Global disturbance of cognition - delusions, hallucinations
hypoactive
Psychomotor disturbances
Disturbance of sleep-wake cycle
Emotional disturbance

44
Q

Delirium presents with

A

rapidly
often worse at night
Diurnally fluctuating

45
Q

Physical signs of delirium

A

Due to underlying cause

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

Dysgraphia often evident

46
Q

Toxic and metabolic disturbances perhaps prone to ?

A

to listlessness and apathy

47
Q

Infective processes and alcohol withdrawal to?

A

hyperactivity and hallucinations

48
Q

Mechanisms of delirium - why does it happen?

A
  • GABAergic and cholinergic neurotransmitter systems?

Central cholinergic deficiency?
Increased risk associated with GABAa agonists and anticholinergic drugs

Increased dopaminergic activity?

Direct neurotoxic effect of inflammatory cytokines?

49
Q

Correct factors contributing to delirium: (11)

A
Disorientation
Dehydration
Constipation
Hypoxia
Immobility/limited mobility
Infection
Multiple medications
Pain
Poor nutrition
Sensory impairment
Sleep disturbance

-stop opiates and anticholinergic drugs

50
Q

Management - environmental

A

Education of relatives, medical and nursing staff
Make environment safe
Optimise stimulation
Orientation

51
Q

Delirium - medications

A

Avoid sedation unless required to maintain safety
Evidence base and guidelines do not support use of medications in delirium

Antipsychotics
Benzodiazepines
Promethazine

52
Q

Delirium antipsychotics?

A

Risperidone 0∙5 – 1mg
Quetiapine 25-50mg
If IM required – consider olanzapine/aripiprazole

53
Q

Delirium - benzodiazepines

A

first choice - can prolong an episode
- Lorazepam 0∙5 – 1mg
Use in withdrawal states – diazepam/chlordiazepoxide; caution in liver failure

54
Q

Avoid antipsychotics in alcohol/drug withdrawal states unless ?

A

patient well covered with benzodiazepines due to lowering of seizure threshold
- give dopamine