Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Psychiatry > Y4 - Dementia > Flashcards

Y4 - Dementia Flashcards

1
Q

What is required for the diagnosis of dementia?

A

Evidence of cognitive decline (e.g. MOCA/MMSE) and functional decline with a clear consciousness and duration > 6months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are some examples of cognitive dysfunctions common in dementia?

A

Dysmnesia (tends to be short term)
Dysphasia
Dysgnosia
Dyspraxia
Problems with orientation (in time, place, person)
Constructional ability issues
Executive dysfunction (initiation, inhibition, abstraction, problem solving etc.)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What activities of daily living may be affected in dementia?

A 
Finances
Food - eating food that is in date? buying food? cooking? 
Care of children/pets
Health/medication 
Use of telephone/television 
Basic ADL - washing, dressing, eating
Driving
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

When assessing someone’s functional ability for a diagnosis of dementia what must you do?

A

Consider a change from baseline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What must you do in relation to driving when someone is diagnosed with dementia?

A

Tell them to inform the DVLA

If they do not, you can go above their head if you feel their driving would put them/others at risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Name some reversible types of dementia

A 
Normal pressure hydrocephalus 
Subdural haematoma (tends to be fluctuating) 
Tumours
Neurosyphillis/HIV
Vitamin deficiencies 
Hypothyroidism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

When might you think of a vitamin deficiency causing a reversible dementia?

A

Poor cognition, low mood

This is why GPs must always check haematinics and FBC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What vitamin deficiencies can lead to a reversible dementia?

A

B12

Folate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How are dementias typed?

A

Based on clinical decision

Scans may be used to back it up

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the types of dementia?

A 
Alzheimer's
Vascular
Mixed AD and VD
Lewy body dementia 
Frontotemporal/Pick's
Alcohol related brain damage - e.g. Korsakoff's
Subcortical, e.g. Parkinson's, Huntington's, HIV
Prion protein, e.g. CJD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is typical in the presentation of Alzheimer’s?

A

Progressive deterioration over a long period of time
V. little insight
Confabulation
Memory issues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is typical in the presentation of vascular dementia?

A

Step wise deterioration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is typical in the presentation of Lewy body dementia?

A

Dementia
Parkinsonism
Hallucinations (visual)
Fluctuation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is Pick’s disease?

A

Type of frontotemporal dementia
Neurodegeneration of frontal and temporal lobes due to accumulation of proteins in the brain

Tends to affect behaviour and personality a lot (e.g. become hypersexualised, rude)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What causes ARBD?

A

Thiamine deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the pathology of Alzheimer’s?

A

Abnormal accumulation of proteins (beta-amyloid plaques, tau tangles)
Atrophy of key brain regions (temporal in Alzheimer’s)
Neurochemical disruption - acetylcholine is reduced

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the aetiology of Alzheimer’s?

A

Genetic and environmental factors

Early onset more associated with genetic factors, late onset more associated with environmental factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are RFs for Alzheimer’s?

A

Age
F>M
Vascular RFs
Head injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are risk factors for vascular dementia?

A 
Age
HTN 
Smoking
Hyperlipidaemia
M
IHD
DM
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How do you treat vascular dementia?

A

No specific Rx

Modify RFs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the difference between LBD and dementia in Parkinson’s?

A

Onset of motor and cognitive decline within 1y = LBD

Onset of cognitive decline 1y after motor symptoms = DPD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the pathology of LBD?

A

Lewy body accumulation leads to reduced dopamine due to alpha synucleic protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Why can people with LBD get differing symptoms?

A

Predominant site in brain confers symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are classical features of LBD?

A

Visual hallucinations
Fluctuating course
Parkinsonism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What drug should be avoided in those with LBD?
Antipsychotics | Makes motor symptoms a lot worse
26
How do you treat LBD?
Cholinesterase inhibitors (e.g. rivastigime)
27
What are some differentials for dementia?
Normal Delirium Depression Mild cognitive impairment
28
What things may make you lean towards delirium as a diagnosis as opposed to dementia?
``` Rapid onset & decline Very fluctuant Worse at night Psychomotor disturbance Disrupted sleep wake cycle Florid psychotic symptoms Clouding of consciousness ```
29
What things may make you lean towards depression as a diagnosis as opposed to dementia?
``` Trigger/life event Subjective complaints of memory loss Sleep/appetite disturbance Worse in morning Distressed & unhappy 'Don't know answers' ```
30
What is involved in the clinical assessment of someone with suspected dementia?
``` Hx, collateral Hx Functional ability Ex - physical, MSE, cognitive Ex Risks Bloods - FBC, UE, LFTs, glucose, B12, folate CT/SPECT ```
31
How should you treat Alzheimer's?
Anticholinesterase inhibitors for mild to moderate AD (MMSE 10+) NMDA antagonist, GABA for moderate to severe AD (14 or less on MMSE) or second line if AChI not tolerated
32
How do anticholinesterases work?
Reduce breakdown of ACh
33
What are the anticholineasterases?
Donepezil Galantamine Rivastigime
34
What is the NMDA antagonist used for moderate-severe Alzheimer's?
Memantime
35
How is the severity of dementia assessed/
``` Consider functional level MMSE: Mild - 21-30 Moderate - 10-20 Moderately severe - 10-14 Severe <10 ```
36
What are BPSD?
Behavioural and psychological symptoms in dementia Challenging behaviours (unreasonable and challenging the norms and rules of the context in which they occur)
37
What are the kinds of BPSD?
Lack of behaviour Exaggerated normal behaviour Abnormal/undesirable behaviours
38
What are the five major BPSD symptoms?
Agitation (restlessness, wandering) Psychosis Affective (depression, lability, anxiety, hypomania, apathy) Disinhibition (aggression, sexual) Behaviour (eating, toileting, dressing, sleep wake cycle)
39
What is involved in BPSD management?
``` Hx, Obs, monitoring Environment Personal history and personality Physical health Intervention ```
40
What is the ABC approach to BPSD management?
Antecedent - circumstances & precipitating factors at onset of behaviour Behaviour - description of behaviour Consequences - what occurs after behaviour, how everyone responds to behaviour
41
How is BPSD managed pharmacologically?
Antipsychotics, e.g. risperidone
42
What are the SEs of using antipsychotics in dementia patients?
Sedation, falls, confusion, postural hypotension Make EPSE worse
43
Which part of the brain does Alzheimer's largely affect?
Temporal lobes
44
What are the two main theories of Alzheimer's pathology?
Beta-amyloid plaques which interfere with neuronal signalling, cause inflammation --> neuron damage, and deposit in BVs weakening their walls and predisposing to haemorrhage TAU tangles - TAU proteins become misshapen, cannot support the cytoskeleton & clump together to form neurofibrillary tangles Non-functioning neurons cannot signal and undergo apotosis --> brain atrophy, sulci and ventricles widen, gyri shrink
45
What are the main clinical features of Alzheimer's?
``` Loss of short term memory Loss of motor skills Language problems Long term memory problems Disorientation Bed ridden ```
46
How is the definitive diagnosis of Alzheimer's made?
Brain biopsy on autopsy
47
What is Parkinson's?
Movement disorder where dopamine producing neurons in the substantia nigra undergo degeneration
48
Give two risk factors for PD
Pesticide exposure | DNA variants in genes
49
Where are the SN?
One either side of midbrain They are part of the basal ganglia
50
What is the role of the basal ganglia?
Control movement via its connections to the motor cortex
51
What part of the brain tends to disappear in PD?
Substantia nigra
52
What is the pathophysiology of PD?
Lewy bodies appear in the affected substantia nigra before they die
53
What are Lewy bodies?
Eosinophilic, round lesions made of alpha synuclein proteins
54
What other disease are Lewy bodies found in?
LBD among others
55
What are the two parts of the SN?
Pars reticulata - receives signals from the striatum, relays messages via GABA neurons to the thalamus Pars compacta - sends messages to the striatum via dopamingeric neurons (nigrostriatal pathway)
56
What is the nigrostriatal pathway involved in?
Stimulating cerebral cortex to initiate movement and calibrating/fine tuning movement
57
What is the striatum?
Caudate and putamen
58
What are some clinical features of PD?
``` Resting, asymmetric, pill rolling tremor Cogwheel rigidity Stooped posture Expressionless face Bradykinesia, hypokinesia, akinesia Shuffling gait Postural instability (can lead to falls) ``` Depression, dementia, sleep disturbances/difficulties
59
What are some PD treatments?
``` Levodopa/carbidopa Amantadine Dopamine agonists COMT inhibitors MAO-B inhibitor Anticholingerics Deep brain stimulation ```
60
Can dopamine cross the BBB?
No but levodopa (its precursor can)
61
How is levodopa converted into dopamine?
By dopa decarboxylase in the nigrostriatal neurons NB peripheral dopa decarboxylase is found elsewhere in the body
62
What may lead to some of the unwanted SEs associated with levodopa?
May be broken down elsewhere in the body to adrenaline, which can lead to arrhythmias
63
What drug is levodopa always given with and why?
Carbidopa (dopa decarboxylase inhibitor that can't cross the BBB to stop it breaking down before it reaches the brain)
64
How does amatadine work?
Increases endogenous dopamine production
65
Give examples of dopamine agonists?
Bromocriptine Pramiprexole Ropinirole
66
What does the COMT enzyme do?
Degrade dopamine and levodopa
67
When are COMT inhibitors given?
With levodopa | Used to prevent it being broken down outside the CNS
68
How do MAO-B inhibitors work?
MAO-B is an enzyme that metabolises dopamine
69
Why might anticholingeric drugs be given in the treatment of PD?
Relative increase in amount of ACh compared to dopamine This tries to reset the balance Often helps the tremor
70
What is deep brain stimulation?
Implanted device that directly sends electrical signals to the basal ganglia that counteracts the aberrant signalling in PD
71
What is parkinsonism?
Symptoms of Parkinson's, e.g. in other diseases or due to drugs, e.g. antipsychotics or metacloperamide
72
What is vascular dementia?
Progressive loss of brain function due to long term poor blood supply (usually a series of strokes)
73
What are the functions of the frontal lobe?
``` Movement Personality Counting Spelling Decision making ```
74
What are the functions of the parietal lobe?
Processes sensory information to allow us to know where we are physically Guides movement in 3D space
75
What are the functions of the temporal lobe?
Hearing Smell Memory Recognition of faces
76
What is the main function of the occipital lobe?
Visual information processing
77
What is the pathophysiology of vascular dementia?
Neurons are aerobic & have no longer term energy supply Atherosclerosis leads to gradual decrease in BF to the brain --> chronic ischaemia Small parts of atherosclerosis can break off & occlude small arteries Once tissue demand > supply ==> ischaemic stroke & tissue damage (which can undergo liquefactive necrosis) --> loss of mental function
78
What is atherosclerosis?
Build up of plaque that thickens the artery wall
79
What are the symptoms of vascular dementia like?
Depends on area affected | Symptoms appear suddenly and function decreases with each stroke
80
How do you diagnose vascular dementia?
Neuropsychological tests | CT/MRI can show multiple cortical/subcortical infarct & atrophy confirming ischaemia
81
What causes lewy body dementia?
Misfolded alpha-synuclein proteins that aggregate to form Lewy bodies that deposit in neurons, especially those in the cortex/SN
82
What are the symptoms of LBD?
Early cognitive - difficulty focusing, poor memory, visual hallucinations, disorganised speech, depression Later motor - resting tremor, stiff movements, reduced facial movements Sleep disorders
83
How is the definitive diagnosis of LBD made?
Brain biopsy
84
How do you manage LBD?
Alzheimer's meds for the cognitive aspects, e.g. donepezil PD medications for the motor aspects, e.g. levodopa

Psychiatry (26 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions