Dementia Flashcards
Cognitive screening
6 questions which test function
First 3: year?month? tests for temporal orientation
Time.count back tests for attention
Repeat address tests for short term memory
Dementia
Several aspects of cognitive function impaired accompanied by changes in emotional control social behavior depression and co morbidity
Worsens with age
Alzheimer’s
Most common type
Gradual onset
Starts with memory and progresses to mood problems social
Treated with ach inhibitors and memantine
Vascular dementia
Step by step progression associated with strokes and blockage of blood vessels
Gait disturbance
Personality changes
Bladder problems
Associated with cardiovascular issues such as diabetes and hypocholesterolaemia
Lewy body dementia
Visual hallucinations
Parkinsonian symptoms
Sleep disorder
Fluctuating awareness and attention
Memory problems appear later in disease
Caused by Lewy body deposits in brain (alpha synuclein deposits)
Treated with acetylcholinesterase inhibitors
Frontal temporal dementia
Group of disorders that cause degradation of frontal and temporal lobes due to presence of phosphorylation tau or TDP-43
Has autosomal dominant inheritance
Effects speech
Lack of empathy
Behavioral inappropriateness
Disinhibition
CTE- chronic traumatic encephalopathy
Linked to multiple concussions
Form of dementia
Neuronal death
Mistakes within genes lead to proteins in the cell being the wrong shape. This damages the cells in the brain which causes the cells in the brain to die
Amyloid plaque
Amyloid precursor protein is usually cleaved by alpha-secretase.
In plaque formation, it is cleaved improperly by beta and gamma secretases.
This results in an excessive amount of amyloid-beta peptides.
The AB peptides form oligomers and fibrils with beta-pleated sheet structures.
These fibrils become deposited in insoluble plaques outside neurons (extracellular).
Amyloid plaque arguments for and against
Genes involved in early onset Alzheimer’s include genes involved in generation metabolism and movement of amyloid
These genes are the genes for amyloid precursor protein, presenilin 1, presenilin 2 and ApoE genes
However amount of plaque doesn’t correlate with severity of impairment
Neurofibrillary tangles
Tau is a protein involved in the formation of microtubules.
Microtubules are important in neurone shape, development, transport of molecules within the cell and communication between neurones.
When tau is hyperphosphorylated, it forms oligomers.
The oligomers aggregate into filamentous neurofibrillary tangles (NFTs) inside the neurones (intracellular).
NFTs disrupt the microtubular system, resulting in impaired neurone growth, transport and communication between neurones.
Where are NFTs deposited
- Hippocampus
- Medial temporal lobe
- Frontal cortices (covers frontal lobe)
- Lateral parietotemporal region
Acetylcholine deficiency
There is particular loss of neurones in the nucleus basalis of Meynert.
These neurones are particularly rich in acetylcholine, which they supply the hippocampus, amygdala and neocortex with.
Therefore neuronal death in this region leads to acetylcholine deficit in these areas.
Acetylcholine is involved in memory
Acetylcholinesterase inhibitors such as donezapil prescribed
Serotonin deficiency
Death of neurones in the brainstem’s median raphe results in a decrease in serotonin levels.
Noradrenaline deficiency
Death of neurones in the locus coeruleus results in a decrease in noradrenaline levels.
Sertotonin and noradrenaline deficiencies contribute to the mood and sleep effects of Alzheimer’s.
Synaptic deterioration
Synapses lost so fewer connections
Cerebro cortical atrophy
Shrinkage of brain associated with loss of neurons in the nucleus of basalis of meynert which also decreases ach
Limbic system
First area affected
Regulates emotion behavior and memory
Posterior cingulate cortex,hippocampus and anterior thalamus affected
Posterior cingulate cortex
Involved in orientation awareness of time and space
Hypothalamus
Involved in short term memory
Anterior thalamus
Involved in attention
MDT
Physiotherapist
- Social workersIdentify practical needs, and what kind of additional social care services Mrs Wilkins might need. Eg: if she progresses and needs carers
- Community mental health nursesVisit the home and provide advice on to the patient and carers on optimizing health and quality of life.
- District nursesHelp with dressings, medications, etc.
- Optometrists and AudiologistsOptimize sensory input to minimize confusion and isolation.
- Speech and language therapists
- DieticiansAssess dietary intake.Provide advice on poor appetite, what sort of diet a patient can follow and what sort of food a patient can prepare themselves.
- Continence nursesAid with any continence issues (ability to control bladder and bowel).
- Volunteers
Mental capacity act
Does the person have an impairment
Does the impairment mean the person can’t make a specific decision
If yes then team decides if no then patient decides
Mental health act
If decision is concerned with disorder of the mind itself then patients can be treated without agreement if at risk of harm to themselves
Mild cognitive impairment
Cognitive decline beyond expected for age and education without interfering with normal function
Of memory loss occurs known as amnestic MCI
MCI vs dementia
MCI:associated with normality of ageing,no underlying pathophysiology,doesn’t interfere with normal activity,no treatment
Dementia:not normal,chronic from pathophysiologies,interferes with daily life,many drug treatments such as cholinesterase inhibitors
When is referral made
0-7 is normal
8-9 mild cognitive impairment
10-28 severe cognitive impairment
Similarities between MCI and dementia
Don’t impact consciousness
Impact cognitive inability
Types of loss
Amnesia is short term memory loss
Anomia is the inability to name objects
Apraxia is the loss of dexterity
Agnosia is the inability to recognize things
Aphasia is the inability to talk
