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Psychiatry > Organic Psychiatry > Flashcards

Organic Psychiatry Flashcards

1
Q

What is the difference between organic psychiatric disorders and functional illnesses?

A
  • Organic Psychiatric Disorders are those caused directly by a demonstrable physical problem (e.g. brain tumour, hypothyroidism)
  • Functional Illnesses are traditionally viewed as having NO organic basis (e.g. schizophrenia)
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2
Q

Outline the main functions of the frontal lobe & some main symptoms of dysfunction

A

Executive funciton
Personality/social behaviour
Speech production (Broca’s area)
Motor cortex

Poor judgement/planning
Inappropriate behaviour/impulsivity
Expressive dysphasia
Contralateral hemiparases

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3
Q

Outline the main functions of the temporal lobe & some main symptoms of dysfunction

A

Auditory, olfactory, gustatory (taste) perception
Understanding of speech (Wernicke’s area)
Memory
Emotional regulation

Auditory impairment/agnosia
Auditory, olfactory and gustatory hallucinations
Receptive dysphasia
Amnesic syndrome
Lability
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4
Q

Outline the main functions of the parietal lobe & some main symptoms of dysfunction

A

Somatosensory perception
Communication between Broca’s and Wernicke’s

Contralateral sensory impairment
Apraxias and agnosia (inability to recognise sensory stimulus despite normal peripheral sensation)

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5
Q

Outline the main functions of the occipital lobe & some main symptoms of dysfunction

A

Visual perception and interpretation

Contralateral visual defects
Visual agnosia

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6
Q

What is the definition of delirium?

A

Acute and transient global brain dysfunction with clouding of consciousness (acute confusional state)

It is a manifestation of a physical problem so always search for an underlying cause

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7
Q

Give some causes for delirium

A

Trauma (e.g. head injury)

Hypoxia (cardiovascular, respiratory)

Infection (e.g. intracranial infection or systemic (septicaemia))

Metabolic (e.g. liver failure, renal failure, electrolyte imbalance)

Endocrine (e.g. hypoglycaemia)

Nutritional (e.g. Wernicke’s encephalopathy)

CNS pathology (e.g. raised intracranial pressure)

Drugs and alcohol (e.g. intoxication, withdrawal)

Medication (e.g. anticholinergics, opiates)

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8
Q

Give the clinical onset and symptoms of delirium

A

Onset is sudden (hours to days) and symptoms fluctuate often worsening in the evening/night

  • Disorientated: poor attention and short term memory
  • Mood changes (can be mistaken for depression or mania)
  • Illusions
  • Hallucinations
  • May have delusions
  • Sleep disturbances: insomnia, reversal of sleep-wake cycle
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9
Q

What are the two types of behavioural changes present in delirium?

A

HYPERactivity
• Agitation and aggression

HYPOactivity
• Lethargy, stupor, drowsiness and withdrawal

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10
Q

What investigations would you do for delirium?

A

o Physical examination
o Collateral history (what is the baseline?)
o Check the drug chart

Essentials: 
•	FBC  
•	U&Es  
•	Glucose  
•	Calcium  
•	MSU  
•	Oxygen saturation 
•	ECG  
•	CXR  
•	Septic screen 
o	Consider: LFTs, blood cultures, CT head, CSF, EEG
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11
Q

Outline the management for delirium

A

Treat the cause
• Manage aggravating factors (e.g. pain, dehydration, constipation)
• Stop unnecessary medications

Behavioural Management
• Frequent reorientation (e.g. clocks, calendars, verbal reminders)
• Good lighting (gloomy conditions increase risk of hallucinations/illusions)
• Address sensory problems (e.g. hearing aids, glasses)

Medication
• Small night-time dose of benzodiazepines could promote sleep
• If short-term sedation is needed, low-dose typical antipsychotics (e.g. haloperidol) or benzodiazepines can be used

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12
Q

What are frontotemporal lobar degenerations?

A

Asymmetrical frontal and/or anterior temporal lobe atrophy

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13
Q

Outline 3 types of frontotemporal lobar degeneratoins

A

Frontotemporal Dementia
• Causes frontal lobe syndrome with prominent disinhibition and social/personality changes

Semantic Dementia
• Progressive loss of understanding of verbal and visual meaning

Progressive Non-Fluent Aphasia
• Begins with naming difficulties progressing to mutism

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14
Q

Outline the pathophysiology of Huntington’s disease

A
  • Autosomal dominant
  • Caused by CAG trinucleotide repeat in the Huntingtin gene on chromosome 4
  • Deposits of abnormal Huntingtin protein causes atrophy of the basal ganglia and thalamus as well as some cortical lobe loss (particularly frontal lobe)
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15
Q

Which factors influence the severity and time of onset of Huntington’s?

A

Severity: more CAG repeats
Earlier onset: lengthening of CAG repeats occurs with each inheritance so onset is younger in subsequent generations (anticipation)

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16
Q

What are the clinical features of Huntington’s?

A

o Personality and behavioural changes (sometimes aggression)
o Depression, irritability and euphoria are common
o Chorea affects limbs, trunk, face and speech muscles
o Wide-based lurching gait

17
Q

Outline the causes and clinical features of normal pressure hydrocephalus

A

Causes: Meningitis, Head injury, Idiopathic
• CSF absorption is impaired with normal communication between ventricles (i.e. not obstructed)
• CSF accumulates in the ventricles (hydrocephalus) but the CSF pressure remains fairly normal as CSF production adjusts to compensate

Clinical features, triad:
o Dementia (subcortical)
o Unsteady gait
o Urinary incontinence

18
Q

Outline the pathophysiology of prion diseases

A

Tranmissable spongiform encephalopathies (e.g mad cow disease)

Most common is sporadic CJD (Creutzfeldt-Jakob disease)
• Normal prion protein changes into an insoluble form which appears to act as a template for further transformation of normal to abnormal prion
• Accumulation of abnormal prion proteins leads to spongiform and amyloid changes

19
Q

Outline the causes and key clinical features of amnesic syndromes

A

Anterograde memory loss - an inability to lay down new memories from the time of brain damage onwards

Causes:  
o	Hypoxia  
o	Encephalitis  
o	Carbon monoxide poisoning 
Korsakoff Syndrome is the most common type of amnesic syndrome  
o	Caused by thiamine (B1) deficiency  
o	Usually secondary to alcohol abuse
20
Q

Outline the key clinical features of transient global amnesia

A

Acute global memory loss , lasting from 1-24 hours

  • May be due to transient ischaemia of memory structures
  • Anterograde memory is particularly affected
  • Patient does NOT forget their identity
  • Consciousness and cognition re normal
  • NO signs of neurological disease
21
Q

Outline the key clinical features of frontal lobe syndrome

A

Caused by anything that can damage the frontal lobe (e.g trauma, dementia, stroke)

Executive Dysfunction
o Poor judgement
o Poor planning and decision-making

Social Behaviour and Personality Change
o Loss of social awareness: irresponsible/disinhibited, inappropriate behaviour
o Impulsivity
o Euphoric or fatuous mood, lability

Apathy
o Lack of motivation and initiative
o Decline in self-care

22
Q

Differentiate between open and closed head trauma

A
  • Open: skull is penetrated causing local cerebral damage

* Closed: no penetration but brain damage is caused by acceleration/deceleration and shearing forces

23
Q

What symptoms are commonly seen with head trauma?

A
  • Post-Traumatic Amnesia: lasts from the time of injury until recovery of normal memory
  • Retrograde Amnesia: memory loss before the injury. NOT a good predictor of outcome
  • Previous personality traits may be exaggerated
  • Depression and anxiety occur in up to 50%
• Post-Concussional Syndrome may follow head injury with loss of consciousness  
o	Mood (e.g. depression, anxiety, irritability) 
o	Cognitive (e.g. poor concentration and memory) 
o	Somatic (e.g. headache, dizziness, fatigue, insomnia, noise sensitivity)
24
Q

Outline the pathology of Parkinson’s disease and its key clinical features

A

• Degeneration of dopaminergic neurones in the substantia nigra

TRIAD of extrapyramidal symptoms:
o Tremor (pill-rolling)
o Rigidity (stiffness)
o Bradykinesia

Other features: stooped posture, shuffling gait, hypomimic face, recurrent falls, constipation, urinary problems, sleep disturbance

25
Q

Give some complications of Parkinson’s disease

A

• Depression
• Dementia in Parkinson’s Disease (occurs in 80% of cases)
NOTE: In PD dementia the PD comes first, In LBD the dementia comes first
• Secondary Forms of Parkinsonism (e.g drug induced, PSP syndromes)
• Psychotic Symptoms (visual hallucinations, can result from use of dopaminergic anti-Parkinson’s drug

26
Q

Outline the pathology of MS and give some common complications

A

Episodes of inflammation and demyelination occurring at different sites, and at different times, within the white matter tracts of the CNS (relapsing-remitting)

Complications
• Depression
• Cognitive impairment (late stages)

27
Q

What psychiatric complication can occur following stroke

A

• Depression

Treat as same as primary depression

28
Q

Define epilepsy and give some of its complications

A

Tendency to recurrent, unprovoked seizures
• Cognitive impairment, psychotic symptoms and learning disabilities
• Depression, and suicide rates are 4 x higher than the general population

Psychiatry (14 decks)

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