organic psychiatry

Question 1

difference between organic and functional disorders

Answer 1

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),

Question 2

which area of brain is responsible for expression of speech?

where is this found?

Answer 2

Broca

in frontal lobe

Question 3

which area of brain is responsible for comprehension of speech?

where is this found?

Answer 3

wernicke

in temporal lobe

Question 4

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

Answer 4

supplementary motor cortex

Question 5

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)

Answer 5

frontal

Question 6

the following are due to dysfunction of which lobe?

Contralateral visual defects
Visual agnosia
Cortical blindness

Answer 6

occipital

Question 7

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

Answer 7

temporal lobe

Question 8

the following are due to dysfunction of which lobe?

Contralateral sensory impairment
Apraxias
Agnosias

Contralateral sensory neglect
Receptive dysphasia
Dyscalculia = inability to calculate

Answer 8

parietal lobe

Question 9

acute and transient state of global brain

dysfunction with clouding of consciousness is aka?

Answer 9

delirium

Question 10

describe the presentation of delirium?

Answer 10

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

Question 11

describe the 2 types of behaviour in delirium?

Answer 11

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)

Question 12

list some preventative measures for delirium?

Answer 12

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

Question 13

how is delirium managed?

how long to resolve?

Answer 13

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)

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

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

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

may take days to weeks to resolve

Question 14

list the OLD AGE dementia’s?

Answer 14

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

Question 15

what are the subcategories of dementia ?

Answer 15

cortical - affects cortical function
eg alzhiemers

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

Question 16

in what condition do you find pick bodies?

how to isolate them?

Answer 16

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

Question 17

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

Answer 17

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

sporadic or autosomal

are cortical dementias

Question 18

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

prognosis?

Answer 18

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.

Question 19

aetiology of huntingtons disease?

Answer 19

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.

Question 20

clinical presentation of Huntington/

Answer 20

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

Question 21

what is anticipation in huntingtons disease?

Answer 21

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

Question 22

testing and prognosis of huntington disease?

Answer 22

Genetic testing

no cure and death usually occurs within 15 years.

Question 23

what might be seen on imaging ivx for huntington disease?

Answer 23

CT/MRI may show caudate
nucleus atrophy

and the EEG may be flat

Question 24

Reason for chorea in huntington?

Answer 24

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

Question 25

difference between cortical and subcortical dementias?

Answer 25

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 ```

Question 26

presenting symptoms of hiv dementia?

Answer 26

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

Question 27

aetiology of normal pressure hydrocephalus?

Answer 27

meningitis head injury 50% of cases are idiopathic

Question 28

what is normal pressure hydrocephalus and classic presenting triad?

Answer 28

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.

Question 29

mx for normal pressure hydrocephalus?

Answer 29

ventriculo-atrial shunt may allow CSF drainage from | the brain ventricles to the heart

Question 30

Florid plaque is seen in brain biopsys of which patients?

Answer 30

vCJD

Question 31

what are the psychaitric symptoms in sporadic CJD and vCJD?

Answer 31

SPORADIC; neurological signs: extra-pyramidal, pyramidal, cerebellar, myoclonus Dementia ``` VARIANT; prominent psychiatric symptoms: dementia, depression, irritability, psychosis, behavioural changes Ataxia and sensory symptoms ```

Question 32

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

Answer 32

``` 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 ```

Question 33

what is amnesic syndrome? aetiology?

Answer 33

anterograde memory loss mainly. other functions in tact. ``` causes; hypoxia encephalitis CO poisoning Korsaff syndrome - thiamine/vit b1 deficiency (confabulate etc) ```

Question 34

presenting sx of Transient global amnesia? aetiology?

Answer 34

global memory loss ACUTE , lasts 1-24hrs "where am i" DO NOT forget identity aetiology; stroke, trauma, intoxication, epilepsy

Question 35

prominent feature in psycogenic amnesia?

Answer 35

forget their identity

Question 36

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

Answer 36

frontal lobe syndrome

Question 37

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

Answer 37

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.

Question 38

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

Answer 38

post concussion syndrome

Question 39

list the classic presenting triad in Parkinson?

Answer 39

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

Question 40

epidemiology and rx for depression in parkinsons?

Answer 40

45% parkinsons patients depressed same as in depression... ssri 1st line

Question 41

Aetiology of Parkinson's?

Answer 41

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

Question 42

bradyphrenia is an early sx of?

Answer 42

parkinsons dementia

Question 43

drug treatment for for Parkinson/ parkinsons dementia?

Answer 43

acetylcholinesterase inhibitors; Galantamine, rivastigmine, donepezil improve cognition and behavioural symptoms: SLOWS down rate of decline - doesn't cure

Question 44

difference between parkinsons dementia and lewy body dementia?

Answer 44

parkinsons dementia; dementia before congitive impairment Lewy body; cognitive impariment before dementia

Question 45

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

Answer 45

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.

Question 46

YOU need to know how to do the AMTS for PACES

Answer 46

score below 7 suggests cognitive impairment just a screeening to tell us they need FURTHER assessment

Question 47

what is the temptation to give antipsychotics for LBDementia? why musnt you?

Answer 47

since they have visual hallucinations cant do so as will make parkinsonian sx worse

Question 48

list some side effects of ACholinestrase inhibitors?

Answer 48

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

Question 49

what are the ivx for dementia? best imaging choice?

Answer 49

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

Question 50

list some side effects of ACholinestrase inhibitors?

Answer 50

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

Question 51

what is mild cognitive impairment?

Answer 51

a dementia like syndrome not having effect on daily life 30% develop dementia in 3 years

Question 52

how is capacity assessed?

Answer 52

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

Question 53

what type of drug is memantine?

Answer 53

Non-competitive Glutamate receptor and antagonist.

Question 54

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

Answer 54

1. Acute onset / fluctauting course of Mental S changes 2. Inattention 3.Altered consciousness OR 4. Disordered thinking Need: 1 + 2 + 3/4

Question 55

Delirium : lecture by Hardeep Pangli has very good cases!

Answer 55

and has good hx for delirium

Question 56

name some RISK FACTORS for delirium, then name causes

Answer 56

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 ```

Question 57

what is the prognosis of delirium?

Answer 57

43% reversible cognitive impairment 37% die in 6 months

Question 58

how is delirum assessed?

Answer 58

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

Question 59

another name for delirium?

Answer 59

acute confusional state

Question 60

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

Answer 60

risk factor management: | stop smoking, treat htn - all modifiable things

Question 61

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

Answer 61

atrophied brain very wide sulci

Question 62

list some contraindicatoins of AChEs eg donepezil?

Answer 62

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

Question 63

a patient with known alzhiermers dementia, becomes more physically aggressive etc. what is the ddx? how to mange this? caveats of treatment?

Answer 63

this is the behavioural and psychological sx of dementia this is managed as follows: 1.investigations 2. treatment: Resperidone - low dose antipsychotic - short term use - few weeks if not responding to non-pharma conditions increases risk of strokes 3x

Question 64

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

Answer 64

behavioural sx of dementia: - low dose antipsychotic: resperidone delirium: - low dose antipsychotic: haloperidol 1st otherwise olanzapine