Dementias Flashcards
What is the most common form of dementia?
Alzheimer’s
What causes Alzheimer’s?
Accumulatino of proteins (amyloidosis) in the brain the leads to reduced levels of neurotransmitters, loss of connections between cells and death of nervous tissue
What is the first presenting symptoms in Alzheimer’s?
Forgetfulness - names, appointments, getting lost
What is the pathology seen in Alzheimer’s?
- Globally you see generalized atrophy, disproportionate hippocampal atrophy
- The underlying pathology is an accumulation of amyloid plaques and hyperphosphorylated tau tangles (tau usually binds to microtubules and stabilizes them) – interrupt synaptic transmission and damage to neurons and brain tissue, leading to cell death.
- Senile plaques – enlarged axons and nerve terminals with amyloid depositions at the centre
- There are reduced levels of neurotransmitters
- Amyloid deposition is due to 3 mutations on chromosome 21 hence why it is more common in individuals with trisomy 21 as they have an extra chromosome where the mutation could occur.
Describe the three stages of Alzheimer’s
• Early stage o Mislaying items o Forgetting recent events o Word-finding difficulties o Difficulty/slowness to grasp new ideas o Disorientation to day and date o Poor judgement o Can’t judge distance o Lack of interest in activities
• Middle stage o Require more support with ADLs o Begin not to recognize people o Disorientation to place o Wandering behaviour o Mixing up day and night o Agitation and disinhibition o Delusions and hallucinations
• Late stage o Weak & unsteady on feet o Difficulty eating and swallowing o Weight loss o Incontinence o Gradual loss of speech o Often pneumonia is the cause of death
What is the investigation for Alzheimer’s (confusion screen)?
• Full blood count – infection, anaemia (such as pernicious anaemia)
• Urea and electrolytes
• Liver function tests
• CRP
• Glucose
• Calcium
• TFTs
• B12
• Folate
• Urine dipstick
• Mental state examination – for other mental health problems
• Mini mental state examination
• MRI head – cerebral atrophy, ventricular dilatation, hippocampal atrophy
o Single photon emission CT can sometimes be used also (SPECT scan)
What is the management for Alzheimer’s?
Drugs don’t cure Alzheimer’s disease, but the drugs improve the symptoms for 6-12 months, after which the patient starts to deteriorate again. Medication can help with anxiety, reduced motivation, memory, concentration, and improve the ability to carry out ADLs.
Acetylcholinesterase inhibitors for mild/moderate Alzheimer’s
NMDA receptor antagonists (memantine) for severe Azlheimer’s
Describe acetyl cholinesterase inhibitors, MOA, examples, ADRs.
Increase the levels of acetylcholine in the synapse – they are used in mild – moderate Alzheimer’s disease. Examples include donepezil, rivastigmine and galantamine. They are beneficial in 40-70% of people. The ADRs are significant and include bradycardia, which increases falls risk in the elderly, and Steven’s Johnson syndrome (rare toxic epidermal necrolysis), as well as seizures, urinary retention, sleepiness, GI symptoms and headache.
Describe NMDA receptor antagonists, MOA, example, ADR
Antagonize overactive NMDA receptors in severe Alzheimer’s disease. They are thought to reduce neuronal damage. E.g. memantine. Side effects include sleepiness, dizziness, constipation, headache, shortness of breath, hallucinations, confusion, vomiting, abnormal gait.
How should you manage a patient who is acutely confused?
If someone is acutely confused, try to initially treat the environment they are in (the other patients, the ward layout, access to the toilet, levels of noise) and their physical health (delirium, alcohol withdrawal, hypoglycaemia, pain, urinary retention), before considering sedation (for example with haloperidol, an antipsychotic, or benzodiazepines), as sedation carries risks of falls and infections. Give IM and start with a low dose, monitor vital signs.
What is vascular dementia?
Results from infarction of brain tissue – either post stroke, or multiple small infarcts. Can get mixed dementia with Alzheimer’s disease. Early stages show less prominent memory loss and more problems with planning, thinking, periods of acute confusion, language, visuospatial skills, apathy, and depression and anxiety.
Treatment is control of the cardiovascular risk factors – lipids, blood pressure etc.
What is Front-temrpoal dementia?
It is due to abnormal protein build up – presents with loss of inhibition, loss of interest, loss of sympathy and empathy, repetitive and compulsive behaviour, cravings of food, problems with speech, forget meanings of words & word finding difficulties, agnosia.
There is no available treatment.
What is Pick’s disease?
Fronto-temporal lobe dementia type
Describe levy body dementia. Associated with? Treatment?
Issues with attention and alertness, which fluctuate quickly, visual hallucinations, delusions, movement difficulties and sleep disturbance. There is no specific treatment, by donepezil and rivastigmine can help with psychotic symptoms.
What is Creutzfeld-Jakob disease? Presentation?
Prion (abnormal protein) disease – most commony sporadic CJD in the over forties. New variant CJD from eating meat from cattle with BSE – affects younger adults – it is linked to traditional butchery, since prions are not eradicated by sterilization and auroclaving. New variant CJD may incubate for 15+ years. It presents with:
• Minor lapses of memory, mood change, loss of interest, clumsiness, muddledness, unsteady walking, slow and slurred speech, dystonia, tremors, hypertonia, incontinence, paralysis
• Death within six months
Prion protein is a normal constituent of synapses, mutated prion protein (which can be sporadic, familial or ingested) interacts with normal prion protein which undergoes a post-translational conformational change. It is then in a very stable structure which forms aggregates which causes neuronal death and “spongy” grey matter.
