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Sem 4: Nervous System > 9a.) Confusion in the Elderly > Flashcards

9a.) Confusion in the Elderly Flashcards

1
Q

State some possible causes of confusion in the elderly

A
  • Dementia
  • Depression
  • Drugs
  • Delirium
  • Metabolic

4 D’s and the M

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2
Q

What is delirium?

A

Acute onset of altered mental status with a flucutating course, often involves:

  • Inattention
  • Disorgnaised thinking/confusion
  • Altered level of consciousness
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3
Q

What is depression?

A

Change in mood and feeling of self-worth

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4
Q

Broadly speaking, what is dementia?

A

Cognitive decline due to disease of brain; it is chronic, progessive and has an insidious (graudual) onset

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5
Q

What is cognition?

A

The mental action or process of acquiring knowledge and understanding through thought, experience, and the senses

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6
Q

State some drugs which can cause confusion

A
  • Morphine
  • Cocaine
  • Alcohol
  • Zopiclone (sleeping tablet)
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7
Q

State some metabolic causes of confusion

A
  • Hypothyroidism
  • Hypercalcaemia
  • Vit B12 deficiency
  • Normal pressure hydrocephalus
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8
Q

Describe dementia, include:

  • It is a decline in…
  • What impairments it leads to?
  • Impact on everyday life
A
  • Decline in higher cortical function
  • Impairment of memory, intellect and personality
  • Individual fails to cope with everyday life
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9
Q

Dementia can be broadly divided into two categories (NOTE: this is not referring to the different types of dementia); what are the 2 categories and what determines which category you are in

A
  • Early onset: symptoms manifest before 65
  • Late onset: symptoms manifest after 65
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10
Q

State the 5 types of dementia

A
  • Alzheimer’s dementia
  • Dementia with Lewy body
  • Vascualr dementia
  • Fronto-Temporal dementia
  • AIDS-Dementia complex
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11
Q

An 80 year old man is brought into GP by his daugher who is concerned that there has been a steady decline of his cognitive function over the last year; state 3 tests you could do to test his cognition?

A
  • MMSE: mni mental state examination (ACUTE)
  • MOCA: Montreal cognitive assessment (NEUROLOGY CLINIC)
  • Ask to draw a clock and a specific time on that clock

*The top two test things such as memory, calculation, laguage, orientation, visuospatial

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12
Q

Describe the macroscopic changes in Alzheimer’s disease

A
  • Global atrophy of brain lobes, mostly: frontal, parietal & temporal (not so much in occipital)
  • Sulcus widening (due to brain atrophy)
  • Enlarged 3rd & 4th ventricle spaces (due to brain atrophy)
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13
Q

Describe microscopic changes in Alzheimer’s dementia

A
  • Amyloid beta plaques
  • Neurofibrillary tau tangles

These plaques and tangles kill neurones; since neurogoenesis in limited in CNS the neurones that die are unlikely to be replaced

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14
Q

Describe the pathophysiology of Alzhemier’s dementia

(3 main points)

A

Plaques

  • Amyloid precursor protein in usually found in membrane; it is thought to have a role in growth & repair after injury
  • When it’s broken down & recycled, if wrong enzymes do this the degradation products are insoluble amyloid beta
  • Amyloid beta aggregates to form plaques outside neuron which can:
    • Interrput neurone signalling
    • Cause inflammation and hence damage to other neurones
    • Deposit aroudn blood vessels weakening walls and increasing risk of haemorrhage

Neurofibrillary tangles

  • TAU protein usually binds & stabilises microtubles
  • Kinase phosphorylates TAU
  • TAU changes shape
  • Aggregtes with othehr TAU proteins to form neurofibrillary tangles WITHIN the neuron

Increase in ACh esterase enzyme leading to decreased ACh neurotransmitter

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15
Q

What are teh 4 groups of neurones predominatly affected in Alzheimer’s dementia?

A
  • Cholingergic (treatment targets this)
  • Noradrenergic
  • Serotonergic
  • Those expressing somatostatin
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16
Q

There have been genes identified for both early onset and late onset Alzheimer’s disease:

  • State the 3 genes for early onset
  • State the 1 gene for late onset
A

Early onset:

  • Beta-amyloid precursor protein (beta-APP)
  • Presenilin 1
  • Presenilin 2

Late onset

  • Apolipoprotein E gene
  • **All genes affect beta amyloid*
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17
Q

Describe the typical presentation of someone with Alzheimer’s disease

A
  • Deterioration in memory
  • Deterioration in spatial navigation
  • Difficulty in executive functions:
    • Language
    • Visuospatial functioning
    • Calculation
  • Daily life activities affected
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18
Q

Drugs used to treat Alzheimer’s can be broadly categorised into two categories based on their target/mechanism of action; state the two mechanisms of action

*ALSO, for each include what they are good for treating

A
  • Acetylcholine esterase inhibitors (mild to moderate Alzheimer’s)
  • NMDA (glutamate receptor) antagonists (useful for agitation and severe Alzheimer’s)
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19
Q

Give an example of a drug that is an:

  • ACh esterase inhibitor
  • NMDA antagonist
A
  • AChE= donepezil, galantamine, rivastigmine
  • NMDA antagonist= memantine
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20
Q

Describe the pathophysiology of Demetia with Lewy Bodies, include:

  • What Lewy bodies are
  • Where they are found in the neurones
  • Where Lewy Bodies are found in the brain
  • Brainstem changes
A
  • Lewy bodies are spherical aggregations of alpha-synuclein protein which are found in cytoplasm of neurones?
  • Lewy bodies are found in substantia nigra, temporal lobe, frontal lobe and cingulate gyrus
  • Branstem changes mirror those in Parkinson’s (degeneration of dopaminergic neurones in substantia nigra compacta)
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21
Q

State the 3 core clinical features of Dementia with Lewy Bodies

A
  • Fluctuating cognition with variations in attention and alertness
  • Visual hallucinations
  • Features of parkinsonism (which may lead to frequent falls): shuffling gait & flexed posture (ONLY)

*** As you can see, dementia with Lewy bodies has some quite distinct features

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22
Q

Discuss how you could distinguish between Dementia with Lewy bodies and Parkinsons dementia

A
  • Dementia with Lewy bodies: if dementia precedes movement disorder we call it dementia with Lewy bodies
  • Parkinson’s disease: if movement disorder appears before dementia then we call it Parkinson’s
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23
Q

How do we treat dementia with Lewy bodies?

A
  • Same as for Alzheimer’s we can use AChE inhibitors or NMDA antagonists
24
Q

How can we detect presence of alpha synuclein in brain (when investigating if pt has dementia with Lewy bodies)?

A

Alpha synuclein antibodies and then advanced imaging techniques

25
Q

What drugs must you NOT give to someone with dementia with Lewy bodies and why?

A
  • DO NOT give antipsychotics (dopamine antagonists) as they can cause neuroleptic malignant syndrome (a life threatening reaction to anti-psychotics)which is a psychiatric emergency- symptoms include:
    • Fever
    • Encephalopathy (leading to confusion)
    • Vital signs instability (tachycarida, tachypnoea if very sensitive, fluctuation BP)
    • Elevate creatien phosphokinase
    • Rigidity (caused by dopamine antagonism)
26
Q

Which dementia is the 2nd most common cause of early-onset dementia?

A

Fronto-temporal dementia

27
Q

Describe the pathophysiology of fronto-temporal dementia

A

Atrophy of frontal & temporal lobes

28
Q

Describe the symptoms/typical presentation of someone with fronto-temporal dementia

A

Symptoms are based on lobe dysfunction and most are related to frontal lobe:

  • Altered behaviour e.g. personality changes, social conduct etc
  • Behavioural disinhibition e.g. impulsive
  • Loss of motivation without depression (due to damage to anterior cingulate cortex)
  • Repetitive/ritualistic behaviours
  • Primitive reflexes e.g. grasp reflex & palmomental reflex
  • Short & long term memory impairment
  • Language disorders: WERNICKES OR BROCAS?
29
Q

Describe the pathophysiology of vascular dementia

A

Cerebrovascular disease causing impaired perfusion to areas of brain leading to congnitive impairment (can be thought of as multiple small strokes)- impaired perfusion could be ischaemic or haemorrhagic

*NOTE: this can be diffuse small vessel cerebovascular disease, large vessel disease leading to mutliple infarcts or a global persusion failure

30
Q

State some risk factors for vascular dementia

A

Risk factors are same as those for any vascular disease:

  • Previous stroke/MI
  • Hypertension
  • Hypercholesterolaemia
  • Diabetes
  • Smoking
31
Q

Describe the typical presentation of someone with vascular demetia

A

Step-wise deterioration of cognitive function potentially with focal neurological symptoms

*by focal neurological symptoms means we can relate them to the area of brain that has most likely suffered inadequete perfusion

32
Q

Describe how we treat vascular dementia

A
  • Manage their risk factors for vascular disease e.g. stop smoking, treat hypertension, reduce alcohol, weight loss etc…
  • Only consider an AChE inhibitor or NMDA antagnoist if you suspect they also have another type of dementia or Parkinson’s
33
Q

Suggest why AIDS-Dementia Complex (ADC) is becoming more prevalent

A

Patients with HIV infections are living longer due to modern treatments hence the chance of HIV patients developing AIDS-Dementia complex is increasing

34
Q

Describe the pathophysiology of AIDS-Dementia Complex

A
  • HIV infected macrophages enter brain
  • Cause indirect damage to neurones
35
Q

Describe the progression/deterioration of AIDS-Dementia Complex

A
  • Insidious (gradual) onset
  • BUT once established it has rapid progression
36
Q

Describe some symptoms of/typical presentation of AIDS-Complex Dementia

A

Features related to global damage hence features can be vague; but there may also be some manifestations of cerebellar involvement:

  • Cognitive impairment
  • Psychomotor retardation (slow thoughts & movements- also seen in depression)
  • Tremor
  • Ataxia
  • Dysarthria
  • Incontinence
37
Q

How do we treat AIDS-Complex Dementia?

A

Treat their AIDS (anti-virals)

*NOTE: I have put treat their AIDS as AIDS-Complex dementia is an AIDS defining illness

38
Q

State some investigations that need to be done when you are diagnosing someone with dementia and briefly summarise why these tests must be done

A

Need to do these investigations to rule out any other causes of confusion:

  • FBC
  • U&E
  • ESR or CRP (inflammtory biomarkers)
  • TFTs
  • LFTs
  • Random blood sugar
  • Vit B12 & folate

*Routine syphilis testing is not done but should be done if you identifiy they are at risk when taking a history

39
Q

We manage patients with dementia using the bio-psycho-social model; we have already discussed the biological treatment (drugs). What is psychological treatment for patients with dementia?

A

Few psychological treatments are available for dementia due to it’s progressive nature

40
Q

We manage dementia patients using bio-psycho-social model; managing them socially is probably the main form of managment offered. Discuss what may be involved in the social management of someone with dementia

A
  • Explain diagnosis sensitively
  • Talk about problems that will arise and how they will be managed
  • Give results of any special investigations
  • Driving- dificult topic as pateints want to keep their independence
  • Mobility problems
  • Activities of daily living
  • Finances: wills, power of attorney
  • Day care & respite care
  • Residential/nursing home placement
41
Q

What is delirium sometimes called?

A

Acute confusional state

42
Q

Delirium is often reversible and due to an organic cause; true or false?

A

True

43
Q

What is the main difference between dementia and delirium?

A

In delirium there is an altered level of consciousness. There is not an altered level of consciousness in dementia

44
Q

Dementia does NOT predispose to episodes of delirium; true or false?

A

FALSE; dementia does predispose to episodes of delirium

45
Q

State 5 features of delirium

A
  • Rapid onset
  • Clouded consciousness (may be drowsy)
  • Fluctuating course
  • Maybe transient visual hallucinations
  • Often exaggerated emotional responses (e.g. aggression)
46
Q

State, and describe symptoms for each, the two types of delirium

A

Hypoactive

  • Withdrawn
  • Sleepy
  • Quiet

(Hence it is more likely to be missed/confused with something else)

Hyperactive

  • Restless
  • Agitated
  • Aggressive
  • Mood may rapidly fluctuate
  • Persecturoy delusions
  • Symptoms worse at start and end of day
47
Q

Why may delirium be worse at start and end of day?

A

May be related to changes in endogenous cortisol levels

48
Q

State some possible causes of delirium

A

Causes are associated iwth insults to brain which can cause neuronal damage & inflammation:

  • Drugs toxicity
    • Intoxication
    • Withdrawal (alcohol, coffee, cocaine, benzodiazepine)
  • Endocrine:
    • Hypo/hyperthryroidism
    • Addison’s disease
    • Cushing’s disease
    • Pancreas
  • Liver failure
  • Intracranial:
    • Stroke
    • Haemorrhage
    • Abscess
    • Epilpesy
  • Renal failure
  • Infections:
    • Pneumonia
    • UTI
    • Sepsis
    • Meningitis
  • Urinary retention/faecal retention
  • Metabolic:
    • Electrolyte imbalance
    • Hypoxia
    • Vitamin deficiencies
49
Q

How do you treat delirium?

A
  • Treat underlying cause!!!!!
  • Calm environment
  • Rehydration
  • Haloperidol (ONLY IF ESSENTIAL- it is a drug for aggitation)
50
Q

Discuss the prognosis of delirium

A

It is reversible but it can:

  • Increase risk of dementia
  • Associated with mortality
  • Lengthy hospital stays & high risk of re-admission
51
Q

State some investigations you may do for someone with delirium

A
52
Q

Compare dementia & delirium, include:

  • Onset
  • Decline
  • Hallucinations?
  • Speech?
  • GCS
  • Consciousness?
A
53
Q

Remind yourself of the GCS system

A
54
Q

Discuss how you would assess a patient who in unconscious

A
55
Q

State some of the generic symptoms of dementia

A
  • Cognitive symptoms:
    • Impaired memory (temporal lobe)
    • Impaired orientation (temporal lobe)
    • Impaired learning capacity (temporal lobe)
    • Impaired judgement (frontal lobe)
  • Non-cognitive symptoms:
    • Behavioural:
      • Agitation
      • Aggression (frontal lobe)
      • Wandering
      • Sexual disinhibition (frontal lobe)
    • Depression & anxiety
    • Psychotic features:
      • Visual & auditory hallucinations
      • Persecutory delusions
    • Sleep symptoms:
      • Insomnia
      • Daytime drowsiness (due to decrersed cortical activity)
56
Q

How do you diagnose dementia?

A

By exclusion!! Need to exlcude things like:

  • Hypothyroidism
  • Hypercalcaemia
  • B12 deficiency
  • Normal pressure hydrocephalus
57
Q

What is normal pressure hydrocephalus?

State some symptoms

A

Excess CSF in ventricles however CSF pressure stays normal (or is only slightly raised) because the ventricular system expands. This can cause intracranial pressure to increase and compression of surroudning structures in brain. Symptoms include:

  • Abnormal gait
  • Incontinence
  • Confusion

Sem 4: Nervous System (21 decks)

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