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Psychiatry > Organic Psychiatry > Flashcards

Organic Psychiatry Flashcards

1
Q

What are organic psychiatry disorders

A

Organic psychiatry disorders are directly caused by demonstrable physical illnesses or structural problems of the brain e.g space occupying lesions. Traditionally and conversely functional illnesses were though to have no organic basis e.g schizophrenia, thought they are now being shown to have underlying physical causes.

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2
Q

Function and symptoms of dysfunction of the fronatl lobe

A

Function:

  • Executive function
  • Personality/ social behaviour
  • Initiatve/ motivation
  • Speech production: Broca’s area= dominant lobe
  • Motor cortex: suppression of primitive reflexes

Symptoms of Dysfunction:

  • Poor judgment and planning
  • Innapropriate behaviour and impulsivity
  • Apathy or decline in self-care
  • Telegraphic speech: short words and sentances
  • Normal comprehension
  • Contralateral spastic hemiparesis
  • Primitive re-flexes re-emerge e.g sucking or rooting
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3
Q

Function and symptoms of dysfunction of temporal lobe

A

Function:

  • Auditory, olfactory, gustatory perception
  • Understanding of speech : Wernicke’s area= dominant lobe
  • Memory and emotional regulation

Symptoms of dysfunction:

  • Auditory impairment and agnosia
  • Auditory, olfactory and gustatory hallucinations (temporal lobe epilepsy)
  • Receptive dysphasia- speech is fluent but nonsensical with mistakes and additional words/sounds/neologisms
  • Lability
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4
Q

Function and symptoms of dysfunction of parietal lobe

A

Function:

  • Somatosensory perception
  • Integration of sensory perception, allowing awareness and movemnt of body
  • Communication between Broca’s and Wernicke’s areas
  • Calculation

Symptoms of dysfunction:

  • Contralateral sensory impairment
  • Apraxia
  • Agnosia (inability to recognise a sensory stimulus despite normal peripheral sensation)
  • Contralateral sensory neglect
  • Receptive dysphasia
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5
Q

Function and symptoms of dysfunction of occipital lobe

A

Function: Visual perception and interpretation

Symptoms of dysfunction: Contralateral visual defects, visual agnosia and cortical blindness

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6
Q

Definition of delirium and who it affects

A

An acute and transient state of confusion which arises due to an underling physical problem. Patients are often unaware of their surroundings. It affects up to:

  • 30% of medical inpatients
  • 50% of postoperative patients
  • 80% of patients admitted to intensive care
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7
Q

Risk factors for delirium

A

older age, male sex, pre-existing physical/mental illness (especially dementia), substance misuse, polypharmacy, malnutrition, pain, sensory impairment and immobility.

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8
Q

Causes of delirium

A

Aetiology: VITTAMIN

  • Vascular: stroke or heart attack
  • Infections: Urinary tract/ chest infection, encephalitis, sepsis
  • Traumatic: Head injury, burns, fractures
  • Toxic: drug or alcohol intoxication/ withdrawal, poisoning, overdose
  • Autoimmune: SLE, MS
  • Metabolic: liver/renal failure, electrolyte imbalance, hypoglycaemia
  • Iatrogenic: ‘Deliriogenic’ medications include sedatives, anticholinergics, opiates and steroids
  • Neoplastic: Space occupying lesion
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9
Q

Onset and presentation of delirium

A

The onset is sudden (hours to days) though symptoms may fluctuate throughout the day, with brief lucid moments. Altered consciousness can range from drowsiness or stupor to clouded consciousness to vigilance and hyper-alertness. Symptoms are often worse at night:

  • Mood changes are prominent and may resemble depression or mania
  • Global cognitive impairment includes inattention, disorientation, and poor memory
  • Thinking may be disorganised (illogical/rambling) or impoverished
  • People may experience transient, often persecutory delusions, illusions and hallucinations (most commonly visual).
  • Behavioural changes
    • Hyperactivity, agitation and aggression. Wandering, climbing into other patients’ beds, pulling out catheters, easily identified
    • Hypoactivity, lethargy, stupor, drowsiness and withdrawal. ‘Quiet delirium’ which is easily missed
  • CAM- delirium bedside testing
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10
Q

Investigations for delirium

A

Requires a full physical examination and observations (BP, HR, RR, SpO2, temperature.) A DRE must be included if there is a history of constipation. Also must get a collateral history and perform a MSE. It is important to consider a cognitive assessment since delirium is often comorbid with dementia. Essential testing includes: FBC, U&Es, LFTs, TFTs, CBG (both hypos and hypers cause confusion), Vit B + Folate, Bone profile, BBV, septic screen, MSU, CT, UDS.

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11
Q

Management of delirium

A

Need to treat the cause and any exacerbating factors. Stop any unnecessary medications. Optimise nutrition and ensure dentures fit etc. Behavioural management includes:

  • Frequent reorientation: clocks, calendars
  • Good lighting and addressing sensory problems e.g. hearing aids. Avoiding over or understimulation (e.g silencing any unnecessary noises)
  • Minimise change
  • Remove things that can be thrown or tripped over
  • Allow safe wandering
  • If agitated behaviour is risky (e.g aggression), or if there is extreme distress, consider short-term, low-dose medication e.g antipsychotic (haloperidol or olanzapine) or a benzodiazepine if antipsychotics are contraindicated
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12
Q

Complications of delirium

A

Delirium is associated with increased mortality, longer and repeated admissions and subsequent nursing home placements. There is also an increased risk of developing subsequent dementia

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13
Q

Classification of dementia

A

Dementia may be cortical (Alzheimers) which affects cortical functions such as memory and language, or subcortical (Huntington’s) which affects subcortical structures (thamaus, basal ganglia) and causes problems including bradyphrenia (mental slowing), bradykinesia, depression, movement disorders and executive dysfunction.

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14
Q

Patients most commonly affected by frontotemporal dementia + pattern of inheritance

A

Most commonly diagnosed in 45–65 year-olds. Most cases are ‘sporadic’ but around 1/3 of cases are familial, with autosomal dominant inheritance.

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15
Q

Hallmarks of frontotemporal dementia

A

The hallmarks include asymmetrical anterior temporal and/or frontal lobe atrophy, cortical atrophy, neuronal loss and gliosis.

FTD includes Pick disease, which involves collection of hyperphosphorylated tau protein (pick bodies) and ballooned neurones (pick cells) on biopsy

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16
Q

Variants of frontotemporal dementia

A

Initially there are TWO main variants:

  • Behavioural variant FTD: prominent disinhibition and personality change (‘frontal lobe syndrome’)
  • Primary progressive aphasia: worsening speech and language problems which progresses to aphasia

Eventually, particularly later, these syndromes overlap and present with memory problems

17
Q

Cause and onset of Huntington’s disease

A
  • An autosomal dominant disease which causes dementia and chorea.
  • Caused by the CAG repeat in the huntingtin gene on chromosome 4
  • Get deposit of abnormal huntingtin protein cause atrophy of the basal ganglia, thalamus and some cortical neurone loss (mostly frontal).
  • Onset is usually in middle age, however each inheritance lengthens the repeat causing earlier onset.
18
Q

CT/ MRI and EEG changes in Huntington’s disease

A

CT/MRI may show caudate nucleus atrophy and the EEG may be flat

19
Q

Clinical presentation of Huntington’s disease

A
  • Personality and behavioural changes such as depression, euphoria, irritability and aggression. Subcortical dementia may develop later on.
  • Chorea affectsthe limbs, trunk, face and speech muscles. It produces a wide-based, lurching gait.
  • Causes death within 15 years
20
Q

Causes and presentation of HIV encephalopathy

A
  • HIV associated neurocognitive disorder (HAND)
  • The risk of developing HAND increases with age, CVD factors and substance misuse
  • HIV encephalopathy may occur after progression from HIV to AIDS
  • Causes early apathy and withdrawal progressing to subcortical dementia (get ataxia, tremor, seizures, myoclonus.)
    *
21
Q

Normal pressure hydrocephalus causes and presentation. What is the definitive treatment

A
  • Rare but potentially reversible cause of dementia affecting older adults which may be caused by
    • meningitis
    • head injury
    • haemorrhage
    • idiopathic (50%)
  • Caused by impaired CSF absorption in subarachnoid space leading to ventricular CSF accumulation without raised ICP
  • Produces a TRIAD of symptoms treated by placing a ventriculo-atrial shunt:
    • Dementia (subcortical)
    • Unsteady gait
    • Urinary incontinence
22
Q

What is a prion disease. What is the most common prion diseaes seen in humans. What are the causes of prion disease in humans?

A
  • A rare condition causing rapidly progressive neurological and psychiatric symptoms
  • Normal human prion protein changes into abnormal insoluble form, which appears to act as a template for further transformation of normal to abnormal prion
  • The main form in humans is Creutzfeldt-Jakob Disease (CJD)
  • Accumulations of abnormal prion protein are linked to spongiform and amyloid changes in the cerebrum, basal ganglia and cerebellum. The main type is sporadic CJD which occurs due to spontaneous prion misfolding. But may also be variant CJD, from eating BSE-infected meat.
23
Q

What is amnestic disorder (what is the characteristic defecit)

A

Amnestic disorder is characterised by relatively circumscribed and profound anterograde amnesia- the inability to lay down new memories after a brain insult

Can also get some retrograde loss, though procedural memory will be intact and they can often learn new skills. Patients will confabulate. However, all other brain functions will be relatively intact.

24
Q

What are the causes of amnestic disorder

A

Damage affects limbic structures dealing with explicit memory – hippocampus, mammillary bodies, parts of the thalamus and surrounding cortex. Causes include:

  • Hypoxia
  • Encephalitis
  • CO poisoning
  • Korsakoff’s syndrome = most common type of amnesic syndrome. Due to thiamine (B1) deficiency secondary to alcohol misuse or anorexia nervosa
25
Q

What is working memory

A

Briefly holding onto information into its original state. Fleeting and limited (lottery numbers). Information then consolidates into short-term and long-term memory

26
Q

How can explicit and implciit memory be differentiated

A

Content can be explicit memories (memories that can be put into words) or implicit (non-declarative) memories (hard to verbalise and learned and accessed unconsciously)

27
Q

What is transient global amnesia, what are its causes

A

Acute global memory loss, lasting from 1-25 hours (anterograde memory also affected). Patients are usually over 50 and otherwise healthy. They are often bewildered – in psychogenic amnesia patients don’t forget their identity. Causes are unclear but linked to transient ischaemia, physical or emotional stress (could also be migrainous or epileptic.)

28
Q

What is frontal lobe syndrome, how does it present? How can it be managed

A

Any damage (head injury, dementia, stroke) can cause frontal lobe syndrome. This results in deficits in:

  • Executive function: poor judgment, reasoning and problem solving, planning and decision making
  • Social behaviour (personality change): Get inappropriate behaviour (irresponsible, disinhibited, aggressive), impulsivity and euphoric or ‘fatuous’ mood. Mood is labile. Also get apathy (no motivation), self-neglect and repetitive or compulsive behaviours.

People with FLS tend to either be apathetic (dorsolateral damage) or impulsive and disinihibited (orbitofrontal damage.) MRI may be helpful but formal occupational therapy and neuropsychological testing will give insight into functional impairment. Management is supportive and focuses on rehabilitation.

29
Q

How can traumatic brain injury be characterised. How does each category present

A

Can be open (skull is penetrated causing local cerebral damage) or closed (caused by acceleration, deceleration or shearing forces.) TBI severity is graded as mild, moderate or severe. This often relies on GCS, duration of coma and post-traumatic amnesia

Deficits are more likely to be focal following open head injuries and global following closed head injuries. Typically, attention, concentration, memory, processing speed and problem-solving are affected. Can get circumscribed amnesia and amnestic syndrome. Depression and anxiety occur in up to 50% of head injury survivors and can persist.

30
Q

Definition of post-raumatic amnesia and retrograde amnesia

A

Post-traumatic amnesia= time of injury until time of recovery of memory

Retrograde amnesia= memory loss before the injury

31
Q

What is post concussion syndrome

A

Occurs in 20-50% of people after a mild head injury. Symptoms include: Mood: depression, anxiety, irritability, Cognitive: poor concentration and memory, Somatic: headache, dizziness, fatigue, insomnia, noise sensitivity

32
Q

Parkinsons disease definition and causes

A
  • A progressive, idiopathic movement disorder
  • Genetic and environmental factors (exposure to pesticides) can increase the risk.
  • Caused by degeneration of dopaminergic cells in substantia nigra > depletion of dopaminergic tracs leading to the basal ganglia. Abnormal deposits of the protein alpha-synuclein form in affected cells as Lewy bodies
33
Q

How does PD present

A

Presents with the classic TRIAD of:

  • Tremor: pill-rolling
  • Rigidity (experienced as stiffness)
  • Bradykinesia (slowed movements)

Other symptoms include: Stooped posture, Shuffling gait, Mask-like facies, Recurrent falls, Constipation, Urinary problems. Mood symptoms commonly precede motor symptoms

34
Q

What are some causes of Parkinsonism

A
  • Drug-induced e.g. antipsychotics
  • Multiple cerebral infarcts
  • Repeated head injury (Boxing Encephalopathy/Punch-drunk syndrome)
  • Parkinson plus syndromes (neurodegenerative disorders comprising PD, with additional defects) e.g. progressive supranuclear palsy, corticobasal degeneration, multiple system atrophy
35
Q

What are some complications of Parkinson’s disease, how can they be treated

A

Depression:

  • Affects 45% of parkinson’s patients and can be difficult to diagnose since depression symptoms can overlap e.g. lack of smiling
  • Tx is same as primary depression

Parkinson disease dementia:

  • 80% of Parkinson’s patients eventually develop dementia. This is associated with an increased mortality, carer stress and nursing home admission
  • Early symptom = bradyphrenia
  • Presence of PD before cognitive impairment = NOT lewy body dementia
  • Acetylcholinesterase inhibitors can be used in the treatment of both conditions

Psychotic symptoms:

  • Can affect up to 40% of people with PD, and can also be a side effect of dopaminergic anti-Parkinson medication. Strongest predictor of nursing home admission
  • Visual hallucinations are common
  • Dopaminergic drugs can be slowly withdrawn, or cautious doses of atypical antipsychotics can be tried, but both can exacerbate Parikinsonism
36
Q

What is multiple sclerosis, what causes it and how does it present

A

Characterised by episodes of inflammation, demyelination and plaque formation occurring at different sites and at different times, within the white matter of the CNS

  • May run a relapsing and remitting course
  • Then become progressive
  • May be progressive from the start – less common
  • 50% of MS patients suffer from depression and have a substantial increase in risk of suicide
  • Mania is also common
  • Memory and concentration problems can exacerbate either illness and dementia affects 60% in late stages of MS
37
Q

How can epilepsy be defined, what are some psychiatric complications

A

Defined as recurrent (2+) seizures, unproved by an immediate identifiable cause

  • Significantly increased risk of psychiatric disorders, particularly in treatment-resistant or temporal lobe epilepsy
  • High psychosocial burden and stigma
  • Depression is common and suicide is 4x higher than general population

Psychiatry (15 decks)

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