Session 9 - Lecture 1: Dementia and toxic insults Flashcards

1
Q

What are the cognitive symptoms of dementia?

A

Impairment of memory (temporal lobe), reduced orientation (parietal lobe), reduced learning capacity (parietal lobe) and reduced sense of judgement (frontal lobe).

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2
Q

What are the non-cognitive symptoms of dementia?

A

Behavioural change i.e. agitation, aggression, wandering, sexual disinhibition, depression and anxiety.
Psychotic symptoms i.e. visual and auditory hallucinations (false perception with lack of external stimuli) and persecutory delusions (fixed false belief with paranoia).
Sleep symptoms i.e. insomnia and daytime drowsiness.

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3
Q

How can a diagnosis of dementia be deduced?

A

Based on excluding other conditions i.e. hyperthyroidism, hypercalcaemia (moans, groans and stones), vitamin B12 deficiency and normal pressure hydrocephalus (raised CSF with normal ICP). If individuals present with cognitive decline, these conditions must be excluded as a possible diagnosis.

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4
Q

In addition to the previous lecture on dementia, describe in more detail the pathophysiology behind Alzheimer’s disease.

A

APP is broken down to Abeta protein by secretes enzyme which is specifically deposited to produce senile plaques. Neurofibrillary tangles are a result of hyperphosphorylated Tau proteins which aggregate and deposit within neurones leading to a global reduction of neurotransmitters within the brain. Both of these processes lead to enlargement of the third and fourth ventricles within the brain. There is a steady decline in cognition whereas in vascular dementia, the decline is stepwise.

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5
Q

Describe the pathophysiology of Lewy body dementia.

A

Increased aggregation of alpha-synuclein protein (spherical in shape), this leads to intracytoplasmic deposition within the substantia nigra, temporal lobe, frontal lobe and cingulate gyrus. Presentation includes fluctuating cognition and alertness, vivid visual hallucinations, spontaneous features of Parkinson’s disease, repeated falls and sensitivity to neuroleptic malignant syndrome.

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6
Q

Why is the order in which symptoms of Parkinson’s disease and Lewy body dementia appear relevant to the diagnosis?

A

If cognitive symptoms precede Parkinson’s symptoms then an individual will have Lewy body dementia, if the Parkinson’s symptoms precede then an individual will have Parkinson’s disease with Lewy body dementia.

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7
Q

What is neuroleptic malignant syndrome and what is it caused by?

A

NMS is usually caused by antipsychotic drug use, symptoms include fever, encephalopathy, vital signs unstable, elevated creatinine phosphokinase and rigidity.

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8
Q

Describe frontotemporal dementia.

A

Atrophy of frontal and temporal lobes of the brain, symptoms include loss of inhibitions, inappropriate social behaviour, loss of motivation without depression, repetitive/ritualistic behaviours and non-fluent aphasia.

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9
Q

Describe AIDs dementia complex.

A

HIV infected macrophages enter the brain and cause indirect damage to neurones, insidious onset with rapid progression. Presentation includes cognitive impairment, psychomotor retardation, tremor, ataxia, dysarthria (slurred speech) and incontinence.

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10
Q

What is the management for dementia?

A

Biopsychosocial model including acetylcholinesterase inhibitors such as donepazil, rivastigmine and galantine. Can also use NMDA antagonists such as memantine to reduce the overstimulation of glutamate activity.

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11
Q

Describe the basis of delirium.

A

Insult to the brain that leads to acute neuronal cell damage caused by hypoxia with or without inflammation. Onset is acute and rapid, consciousness is clouded, the course is fluctuating with or without transient visual hallucinations.

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12
Q

What are the types of delirium?

A

Hypoactive –> withdrawn, quiet and sleepy.
Hyperactive –> restless, agitated and aggressive.
Symptoms are worse at dawn/dusk.

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13
Q

What is the management for delirium?

A

Treat the underlying cause.

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14
Q

What is the prognosis of delirium?

A

Increased risk of dementia, higher risk of mortality, increased length of stay in hospital, risk of new admission into long term care.

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