Dementia Flashcards

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1
Q

What are the risk factors for dementia ?

A

Increased age
Cardiovascular disease
Infections
Lifestyle factors - smoking, obesity
Neaurological diseases
Trauma head injuries
Environmental toxins
Hormonal

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2
Q

Non-modifiable risk factors for dementia. ?

A

Age, sex, gender
Ethnicity
Genetics cognitive impairment in childhood

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3
Q

Modifiable risks for dementia ?

A

Obesity
Cardiovascular disease
Smoking and alcohol use
Traumatic brain injury (TBI)
Infection

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4
Q

What is dementia ?

A

Brain disorder that effects the thinking, behaviour and ability of a person to preform tasks and brain functions

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5
Q

What’s the most common type of dementia ?

A

Alzheimer’s disease (40-70%)

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6
Q

What are Tau proteins ?

A

These proteins are found within the brain and they stabilise microtubules, abundant in the neurons of the nervous system and are less common everywhere else

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7
Q

What happens when astrocytes are impaired ?

A

If they become impaired and become injured then they trigger/exacerbate changes in Tau and amyloid-beta (AB) pathologies

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8
Q

What does loss of astrocyte function and deficit in Tau probations lead to ?

A

The formation of amyloid and neurofibrillary tangles (NFTs) as well as neuronal dysfunction

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9
Q

What cells medicate neuroinflammation ?

A

Medicated by activated microglial cells which are a source of Cytokines

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10
Q

Describe and explain the inflammatory process with effects towards Alzheimer’s disease ?

A

Neuroinflammation activated cytokines
Disturbances in cerebral glucose metabolism also effects AD
Increase in circulating Interleukins and tumour necrosis factor-alpha (A) buildup
C-reactive protein and interleukins-6 can predict congnative decline
Microglia circulate the brain looking for infection or inflammation caused by toxic proteins that might damage neurons
The result: more and more damaged neurons which can lead to the onset of AD

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11
Q

What are Cytokines and what role do they play ?

A

They are key compound in the brains inflammatory response.
They are triggered by pro-inflammatory and anti inflammatory events, stimulated by injury, ischaemia and beta-amyloid toxicity.
Cytokines (interleukin 1) and tumour necrosis cause ongoing inflammatory responses, such as the amyloid cascade.
Inflammatory process also increases the presence of vascular injury, hypertension, atherosclerosis and high blood cholesterol.
Presence of Chromic inflammatory cells (Neutrophils, T cells CD4 and CD8 positive T cells and Macrophages) all within the walls of the blood vessels in the brain

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12
Q

What are Beta-Amyloid plaques and what role do they play ?

A

Amyloid beta proteins (APP) are proteins found in the cell membrane at the synapse of the neuron - regulate synapse formation
In AD the abnormal process of APP results in the formation of beta-amyloid which is toxic, they come from larger proteins found in the fatty membrane o surrounding nerve cells.
Beta-amyloid is “sticky” and clumps together to form plaques, the abnormal clusters of proteins buildup between nerve cels and block the cel to cell signalling at synapses.
They also activate the immune system cells (microbial) trigger inflammation and destroy the synapse.

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13
Q

What two types of neurotransmitters are affected in AD ?

A

Subcortical - Acetylcholine, noradrenaline, serotonin

Cortical - somatostatin, glutamate

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14
Q

What is the role of Acetylcholine ?

A

Plays a crucial role in information processing and memory

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15
Q

In AD the brain shows …

A

Loss of cholinergic neurons in the basal forebrain, decreased acetylcholine levels and a decrease in the acetylcholine synthesising enzyme choline acetyltransferse (CHAT) in the cerebral cortex

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16
Q

What do the destruction of neurons lead to ?

A

Further reduction in neurotransmitters.
Neurodegeneration leads to neurotransmitters depletion, which leads to further neurodegeneration

17
Q

Explain the mode of action and side effects for Acetycholinesterase inhibitors

A

Mode of action - improve cognitive functions by inhibiting acetylcholineesterase from breaking own the neurotransmitter acetylcholine into chlorine and acetate
Increasing levels and duration of action of acetylcholine in central nervous system. Shown to improve cognitive functions

Side effects -
Vomiting
Muscle cramps
diarrhoea

18
Q

Examples of Acetylcholinesterase inhibitors

A

Donepezil
Glantamine
Rivastigmine

19
Q

Explain the mode of action and the side effects of Gluatmate-receptor antagonist

A

Mode of action - improve cognitive function by reducing the amount of of glutamate. Prevents entry of calcium ions into the neurons, excess calcium damages neurons and prevents receiving messages from other neurons
In AD lots of glutamate leaks out of damaged cells interfering with learning and memory

Side effects -
Headache
Dizziness
Heartache
Allergies

20
Q

An example of a Glutamate-receptor antagonist

A

Memantine

21
Q

When would an Atypical antipsychotic be used ?

A

When behavioural and psychological symptoms are severe and resist other treatments - side effects can be significant

22
Q

Describe the mode of action and side effects for atypical antipsychotics

A

Mode of action - they increase monoamine neurotransmitters in the brain, serotonin, dopamine, norepinephrine and histamine

Side effects -
Drowsiness
Stiff muscles
Increased risk of stroke, TIA and death

23
Q

What three diary supplements can help reduce the onset of AD ?

A

Low vitamin B 12
Omega 3 supplements
Balanced diet

24
Q

What are the 10 warning signs associated with AD ?

A
  1. Memory changes
  2. Withdrawal from usual activities
  3. Disorientation to time and place
  4. Visual-spatial difficulties
  5. Decrease in written or verbal communication
  6. Challenges in problem solving and planning
  7. Personality and mood changes
  8. Misplacing items frequently
  9. Decline in judgement
  10. Difficulty preforming familiar tasks
25
Q

What should you expect in late stage dementia ?

A

Unable to speak
Bed-required round the clock care
Unable to walk or sit up without assistance
Loss of facial expression
Problems with everyday activities like bathing, dressing and eating

26
Q

What are the 5 A’s of Alzheimer’s

A

Amnesia - memory loss
Aphasia - impaired communication
Apraxia - impaired motor skills
Agnosia - difficulty understanding information
Associated features (BPSD)

27
Q

What are associated features (BPSD) ?

A

Apathy
Aggression
Agitation
Depression
mania
Psychosis

28
Q

What tests and investigations can be preformed for cognitive function ?

A

Mini mental state examination (MMSE)
Montreal cognitive assessment
Blessed dementia scale (BDS)

29
Q

What are the different types of brain scans called ?

A

Magnetic resonance imaging (MRI)
Computed tomography (CT)
Single-photon emission computerised tomography (SPECT)
Positron emission tomography (PET)
Electroenchepphalpogram (EEG)

30
Q

What laboratory tests can be taken out ?

A

Blood tests - rule pout liver, kidney, thyroid disease
Detect key protein biomarkers - phospho-tau 181

Lumber puncture - collect CSF, rule out infection, test for presence of dementia biomarkers - beta-amyloid 42, tau, phospho-tau

Urinalysis - to detect biomarkers - isoprostanes and exclude infection