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A- Psych > organic psychiatry > Flashcards

organic psychiatry Flashcards

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1
Q

difference between organic and functional disorders

A

Organic psychiatric disorders - caused directly
by a demonstrable physical problem (e.g. brain tumour,
hypothyroidism).

Functional illnesses are those traditionally
have no organic basis (e.g. schizophrenia),

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2
Q

which area of brain is responsible for expression of speech?

where is this found?

A

Broca

in frontal lobe

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3
Q

which area of brain is responsible for comprehension of speech?

where is this found?

A

wernicke

in temporal lobe

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4
Q

which area of brain is responsible for organisation of complex movements?

A

supplementary motor cortex

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5
Q

the following are due to dysfunction of which lobe?

Poor judgement/planning
Inappropriate behaviour/impulsivity
Apathy/decline in self-care
Expressive dysphasia: problems producing language

Telegraphic speech: short words and sentences,
e.g. ‘Want cake’ (I want some cake).
Normal comprehension
Contralateral spastic hemiparesis
Primitive reflexes re-emerge (e.g. sucking, rooting)

A

frontal

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6
Q

the following are due to dysfunction of which lobe?

Contralateral visual defects
Visual agnosia
Cortical blindness

A

occipital

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7
Q

the following are due to dysfunction of which lobe?

Auditory impairment/agnosia
Auditory, olfactory, gustatory hallucinations
Receptive dysphasia

Speech is fluent, but nonsensical with mistakes, additional
sounds/words/neologisms,
Amnesic syndrome
Lability

A

temporal lobe

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8
Q

the following are due to dysfunction of which lobe?

Contralateral sensory impairment
Apraxias
Agnosias

Contralateral sensory neglect
Receptive dysphasia
Dyscalculia = inability to calculate

A

parietal lobe

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9
Q

acute and transient state of global brain

dysfunction with clouding of consciousness is aka?

A

delirium

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10
Q

describe the presentation of delirium?

A

Onset is sudden (hours to days)

symptoms fluctuate throughout the day,

often worsening in the evening or at night.

disorientated with poor attention and short-term memory.

prominent Mood changes —don’t mistake them for depression or mania

Illusions and hallucinations are common (usually visual)

impoverished, pressured, or rambling speech

sleep disturbance - sleepwake cycle reversed

Crowding of conscious

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11
Q

describe the 2 types of behaviour in delirium?

A

Hyperactivity, agitation, aggression.
– Wandering, climbing into other patients’ beds,
pulling out catheters.
– Easily spotted!

• Hypoactivity, lethargy, stupor, drowsiness, withdrawal.
– Quiet delirium, e.g. silently lying in bed.
– Easily missed: these patients appear ‘well-behaved’
to busy staff! (dont confuse with depression)

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12
Q

list some preventative measures for delirium?

A

Good sleep hygiene without medication.
• Minimal moves around the hospital.
• Encouraging mobility.
• Proactive management: minimize dehydration,
pain, constipation, urinary retention, and sensory
problems.

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13
Q

how is delirium managed?

how long to resolve?

A
  1. treat the cause
    - dehydration, pain etc. stop unnecessary meds.
  2. behavioural management
    - frequently orientate to environment; clocks, calender
    - minimize change; moving them around
    - no unnecessary noises eg alarms
    - address sensory issues eg hearing aids
    - avoid over/under stimulation ; SR admission maybe!

(appropriate reorientation and suitable care environment)

  1. Low dose antipsychotic - haloperidol.
    if contraindication then olanzapine is next.

Lecturer says DO NOT give benzo in delirium or dementia as makes things worse!

  1. referal to geri or psych if ongoing problems
    - involve liason psych if unsure of diagnosis

may take days to weeks to resolve

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14
Q

list the OLD AGE dementia’s?

A

Alzheimer’s disease,
vascular dementia,
dementia with Lewy bodies

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15
Q

what are the subcategories of dementia ?

A

cortical - affects cortical function
eg alzhiemers

subcortical - affects subcortical structures eg basal ganglia and thalamus
eg Huntingtons, parkinsons, PSPalsy

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16
Q

in what condition do you find pick bodies?

how to isolate them?

A

Pick’s disease is caused by a buildup of tau proteins, called “Pick bodies,” in the brain.

Pick bodies cause neurological damage in areas where they are present

cause the cells to die. This causes your brain tissue to shrink, leading to the symptoms of dementia.

isolation;
stain with antibodies to hyperphosphorylated tau

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17
Q

what are the 2 pathologies involved in Frontotemporal lobar degenerations (FTLD)?

A
  1. Tau positive; Picks disease - hyperphosphorylated tau
  2. Tau negative; FTLD-U -> tau-negative ubiquinated inclusions

sporadic or autosomal

are cortical dementias

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18
Q

list the 3 clnical forms of Frontotemporal lobar degenerations (FTLD)?

prognosis?

A

Frontotemporal dementia: this 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: this begins with naming
difficulties and progresses to mutism.

Death usually occurs within 5–10 years.

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19
Q

aetiology of huntingtons disease?

A

autosomal dominant inheritance

trinucletoide CAG repeat on huntington gene on chromosome 4

Deposits of abnormal Huntingtin protein cause atrophy
of the basal ganglia and thalamus, as well as some cortical neuron loss, mostly frontal.

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20
Q

clinical presentation of Huntington/

A

Dementia - subcortical
Chorea - limbs, trunk, face, and speech muscles,
and produces a wide-based lurching gait

personality and behavioural changes, sometimes with aggression.
Depression, irritability, or
euphoria are common,

Onset; middle age
more CAG repats = earlier onset and more SEVERE

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21
Q

what is anticipation in huntingtons disease?

A

lengthening occurs with each inheritance, so that onset is younger in subsequent generations (‘anticipation’).

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22
Q

testing and prognosis of huntington disease?

A

Genetic testing

no cure and death usually occurs within 15 years.

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23
Q

what might be seen on imaging ivx for huntington disease?

A

CT/MRI may show caudate
nucleus atrophy

and the EEG may be flat

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24
Q

Reason for chorea in huntington?

A

may be due to a relative excess of dopamine in
the atrophied basal ganglia, and as such, can be thought
of as the ‘opposite’ of parkinsonism

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25
Q

difference between cortical and subcortical dementias?

A

cortical;
older patients
fluent speech
amnesia

subcortical;
earlier onset
changes in their speed of thinking - slow and ability to start activities. 
don't have forgetfulness 
dysarthritic speech
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26
Q

presenting symptoms of hiv dementia?

A

Early apathy and withdrawal progress to a subcortical
dementia, with neurological features such as ataxia, tremor, seizures, and myoclonus.

Depression, mania, psychosis, and other psychiatric
problems are more common in people with HIV.

10% HIV patients ge this

27
Q

aetiology of normal pressure hydrocephalus?

A

meningitis
head injury
50% of cases are idiopathic

28
Q

what is normal pressure hydrocephalus and classic presenting triad?

A

CSF accumulates in the ventricles (hydrocephalus),- see enlarged ventricles on MRI

although CSF pressure remains fairly normal

Distortion of periventricular white matter tracts
produces the classic symptom triad:

  • dementia (subcortical)
  • unsteady gait
  • urinary incontinence.
29
Q

mx for normal pressure hydrocephalus?

A

ventriculo-atrial shunt may allow CSF drainage from

the brain ventricles to the heart

30
Q

Florid plaque is seen in brain biopsys of which patients?

A

vCJD

31
Q

what are the psychaitric symptoms in sporadic CJD and vCJD?

A

SPORADIC;
neurological signs: extra-pyramidal,
pyramidal, cerebellar, myoclonus
Dementia

VARIANT;
prominent psychiatric symptoms: 
dementia, depression,
irritability, psychosis, behavioural changes
Ataxia and sensory symptoms
32
Q

how to differentiate sporadic and variant cjd on non-psych symptoms?

A 
SPORADIC
unkown cause
older patients
raisied 14-3-3 proteins csf
triphasic sharp waves on EEG
VARIANT
eating infected BSE beef
young patients
florid plaque on biopsy
less eeg changes
33
Q

what is amnesic syndrome?

aetiology?

A

anterograde memory loss mainly. other functions in tact.

causes;
hypoxia
encephalitis
CO poisoning
Korsaff syndrome - thiamine/vit b1 deficiency (confabulate etc)
34
Q

presenting sx of Transient global amnesia?

aetiology?

A

global memory loss
ACUTE , lasts 1-24hrs

“where am i”
DO NOT forget identity

aetiology;
stroke, trauma, intoxication, epilepsy

35
Q

prominent feature in psycogenic amnesia?

A

forget their identity

36
Q

executive dysfunction,
innapropriate social behaviour,
personality change and
apathy are part of which condition?

A

frontal lobe syndrome

37
Q

list 2 memeory impariments that can be acquired from head injury?

A

Post-traumatic amnesia (PTA) lasts from the time of
injury until recovery of normal memory. The longer it
lasts, the greater the risk of complications.

• Retrograde amnesia (RA) is memory loss before the
injury (from the last clear memory until the injury
occurred). It is not a good predictor of outcome.

38
Q

which head injuries have somatic sx such as headache fatigue insomnia and noise sensitivity

A

post concussion syndrome

39
Q

list the classic presenting triad in Parkinson?

A

tremor (pill-rolling type)
• rigidity (experienced as stiffness)
• bradykinesia (slowed movement).

40
Q

epidemiology and rx for depression in parkinsons?

A

45% parkinsons patients depressed

same as in depression… ssri 1st line

41
Q

Aetiology of Parkinson’s?

A

Degeneration of dopaminergic cells in the substantia nigra causes depletion of dopaminergic tracts,
leading to the basal ganglia.

42
Q

bradyphrenia is an early sx of?

A

parkinsons dementia

43
Q

drug treatment for for Parkinson/ parkinsons dementia?

A

acetylcholinesterase inhibitors;

Galantamine, rivastigmine, donepezil

improve cognition and behavioural symptoms: SLOWS down rate of decline - doesn’t cure

44
Q

difference between parkinsons dementia and lewy body dementia?

A

parkinsons dementia;
dementia before congitive impairment

Lewy body;
cognitive impariment before dementia

45
Q

what tests can we do in clinic to demonstrate frontal lobe damage?

A

various tests including testing for primitive reflexes.

these would usually be found in babies but are obvious in adults when there is frontal lobe damage.

46
Q

YOU need to know how to do the AMTS for PACES

A

score below 7 suggests cognitive impairment

just a screeening to tell us they need FURTHER assessment

47
Q

what is the temptation to give antipsychotics for LBDementia?

why musnt you?

A

since they have visual hallucinations

cant do so as will make parkinsonian sx worse

48
Q

list some side effects of ACholinestrase inhibitors?

A

common: GI upset,
rare: av/sinoatrial block, EPSE

SLUDGE - salivation, lacrimation urination, diarrhoea/defaction (so all fluids run!) - due to too much acetylcholine around

miosis

49
Q

what are the ivx for dementia?

best imaging choice?

A

screening test:
AMTS - less than 7
MocA - less than 26
MMSE - less than 24 … used less now

ACE III - Addenbrookes cognitive exam (most pop) - dagnostic test (score les than 70) - done by specialists eg neurologists

MRI of brain best than ct

50
Q

list some side effects of ACholinestrase inhibitors?

A

common: GI upset, agitation, fatigue, dizziness, muscle cramps, rash, syncope, headache
rare: av/sinoatrial block, EPSE

if person is getting worse on this drug DO NOT STOP SUDDENLY -> this will accelerate decline

51
Q

what is mild cognitive impairment?

A

a dementia like syndrome

not having effect on daily life

30% develop dementia in 3 years

52
Q

how is capacity assessed?

A

it is decision specific - eg can choose what to eat but not something else.

assess in different situations

53
Q

what type of drug is memantine?

A

Non-competitive Glutamate receptor and antagonist.

54
Q

what are the 3 diagnostic critea for delirium - according to CAM ?

A
  1. Acute onset / fluctauting course of Mental S changes
  2. Inattention

3.Altered consciousness
OR
4. Disordered thinking

Need: 1 + 2 + 3/4

55
Q

Delirium :

lecture by Hardeep Pangli has very good cases!

A

and has good hx for delirium

56
Q

name some RISK FACTORS for delirium, then name causes

A

immobility
sensory impairemnt - eg hearing
poor nutrition
age >65

multi pharmacy
alcohol
lines: urinary catheters

causes:
PINCH ME
pain, infection (pneumonia)
nutrition: dehydration
hyper/hypoglycaemia, hypocalcaemia
contestation, urinary retention
meds - opiods, steroids, anticholinergics!!
environment change
57
Q

what is the prognosis of delirium?

A

43% reversible cognitive impairment

37% die in 6 months

58
Q

how is delirum assessed?

A

Confusion assessment method CAM

physical exam - systemic

bedside ivx - vital signs!, ecg (whatever fits with your suspected ddx)

-> PLEASE dont forget the simple things that as SO common: constipation, dehydration, urinre retention

bloods

59
Q

another name for delirium?

A

acute confusional state

60
Q

A man is having recurrent TIAs, smokes, drinks, has hen. he presents wth symptoms of vascular dementia. how can we manage him?

A

risk factor management:

stop smoking, treat htn - all modifiable things

61
Q

what are obvious signs of dementia on ct/mri head?

A

atrophied brain

very wide sulci

62
Q

list some contraindicatoins of AChEs eg donepezil?

A

gi disease eg pancreatitis

cardiovascular problem eg AV block, copd/asthma, bradycardia, sick sinus syndrome

63
Q

a patient with known alzhiermers dementia, becomes more physically aggressive etc.

what is the ddx?

how to mange this?
caveats of treatment?

A

this is the behavioural and psychological sx of dementia

this is managed as follows:
1.investigations

  1. treatment: Resperidone - low dose antipsychotic -
    short term use - few weeks
    if not responding to non-pharma conditions
    increases risk of strokes 3x
64
Q

what is drug management in behavioural sx of dementia and then delirium?

A

behavioural sx of dementia:
- low dose antipsychotic: resperidone

delirium:
- low dose antipsychotic: haloperidol 1st otherwise olanzapine

A- Psych (24 decks)

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