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Year 3 - Mental Health Conditions > Dementia - Yr 4 > Flashcards

Dementia - Yr 4 Flashcards

4th Year - Flashcards relating to Alzheimer's, Vascular and Lewy Body dementia.

1
Q

What is the pathophysiology behind dementia?

A

Alzheimers- amyloid plaques and neurofibrillary tangles -> loss of function

Vascular - stroke-related –> single or multiple infarcts

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2
Q

What are the risk factors for Alzheimer’s dementia?

A
  • age
  • genetics
  • sex
  • female
  • head injury
  • high cholesterol
  • decreased brain activity
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3
Q

What are the risk factors for vascular dementia?

A

smoking
hypertension
diabetes
cholesterol

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4
Q

What are the symptoms of dementia?

A
  • loss of memory
  • disorientation
  • change in logic/reasoning
  • change in personality
  • change in speech and communication
  • physical problems
  • change in thinking and concentration
  • change in mood
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5
Q

How is alzeihmers dementia managed?

A
  • acetylcholinesterase inhibitors
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6
Q

what is the prevalence of Dementia?

A

6% prevalence over the age of 65.

20% prevalence over the age of 80.

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7
Q

Describe the pathological findings of Alzheimer’s dementia.

A

1) Cerebral atrophy
2) Senile Plaques (made of beta-amyloid) deposited in the cortex.
3) Amyloid deposition in cortex and cerebral blood vessels.
4) Tau containing neuro-fibrillary tangles.

…. Leads to damaged synapses and neuronal death. Synaptic damage also leads to decreased neurotransmitters incl. acetylcholine.

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8
Q

In Alzheimer’s dementia senile plaques, amyloid deposition and Tau containing neuro-fibrillary tangles damage synapses and lead to neuronal death; thereby decreasing levels of acetylcholine. What is the role of acetylcholine in the brain?

A

Acetylcholine is important in :

  • sustaining attention
  • learning and memory
  • also promotes REM sleep
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9
Q

What are the typical findings of Alzheimer’s dementia on a CT scan?

A

Alzheimer’s dementia leads to progressive degeneration of the cortex. This can be seen by widspread cortical atrophy (shrunken brain) on a CT scan.

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10
Q

What is the commonest cause of senile ( late onset / 65+) dementia in the UK?

A
  • Alzheimer’s disease accounts for 54% of dementias in those aged over 65 years.
  • Dementia with Lewy bodies = 20%
  • Vascular Dementia = 16%
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11
Q

What are the genetic risk factors for Alzheimer’s dementia?

A

The genetic risk factors for Alzheimer’s dementia include:

  • having a 1st degree relative with AD confers a doubled lifetime risk.
  • Downs syndrome (trisomy 21 chromosome contains 3 copies of the amyloid precursor protein (APP) gene. This leads to excess amyloid deposition.
  • PS1 and PS2 gene mutations are involved in rare, early onset forms.
  • Inheritance of the E4 allele of the apolipoprotein E gene confers increased risk (2-3X of AD). Inheriting two copies of the E4 allele leads to a 6-8X risk of AD)
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12
Q

What is the ratio of Alzheimer’s in Men and women?

A

Female to Male ratio of AD = 2:1

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13
Q

What are the biological risk factors for Alzheimer’s dementia?

A

1) increased age
2) head trauma
3) cardiovascular risk factors (smoking, obesity, diabetes, HBP, high cholesterol)
4) history of depression
5) latent herpes simplex infection (in people with ApoE4 allele)

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14
Q

what are the protective factors of Alzheimer’s?

A

1) healthy + engaged lifestyle
2) increased educational attainment
3) NSAIDs, HRT, Vit C, Vit E

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15
Q

what is the definition of dementia?

A

Dementia is the global IMPairment of Intellect, Memory and Personality

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16
Q

how does Alzheimer’s Dementia present?

A

1) it is slow and gradual
2) memory problems, repetitive phone calls, changes in behaviour and decreased self care.
3) The 5A’s = Amnesia, Agnosia, Aphasia, Apraxia, Associated behaviours

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17
Q

Amnesia, Agnosia Aphasia, Apraxia and Associated behaviours are the 5 As of Alzheimer’s dementia.
Describe how amnesia may present in a patient with AD.

A

1) Amnesia
- a slow, but progressive decrease in memory.
- starts with forgetfulness
- failure to retain new info
- difficulty laying down new memories + retrieving old ones.
- AD patients adopt strategies to help like like getting family and friends to tasks they could do before e.g. paying bills.
- distant memories are preserved e.g. childhood. But can get confused and believe that they live in the past.
- Patient is disorientated and can lose track of time (days, seasons, years) and place (decreased awareness of surroundings can cause them to wander)

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18
Q

Agnosia is one of the 5As seen in Alzheimer’s dementia. Describe how Agnosia may present in AD.

A

Angnosia is inability to recognise external sensory stimuli such as people or objects.

1) Initially this will start with the inability to recognise peoples names and faces.
2) It can lead to the inability to recognise family members and mistake them for intruders. –> increased risk of attacks.
3) They may not be able to recognise themselves or everyday objects e.g. toilet –> so may use bins etc.

This is all made worse by decreased vision and hearing.

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19
Q

Apraxia is one of the 5As seen in Alzheimer’s dementia. Describe how Apraxia may present in AD.

A

Apraxia is the inability to carry out motor tasks.

It affects activities of daily living such as dressing, writing, feeding, drinking.

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20
Q

aphasia is one of the 5As seen in Alzheimer’s dementia. Describe how Aphasia may present in AD.

A

Aphasia is an impairment of language that affects the production and comprehension of speech.

  • it usually presents in late AD.
  • initially pts might find it difficult to paritcipate in convo as they can’t find the words to express themselves and forget word for objects.
  • brocas aphasia is difficulty getting the words out but it makes sense
  • wernickes aphasia is when individuals can physically speak but it makes little sense.
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21
Q

“Associated behaviours/symptoms” are one of the 5As of Alzheimer’s dementia. Describe how the changes may present (Psychological , behavioural, personality)

A

Psych:

  • depression in 20% (irritable, apathetic, agitation)
  • Delusion in 15%
  • visual and auditory hallucinations in 10-15%
Behaviour
 wandering
- aggression
- social / sexual disinhibition
- decreased appetite leading to weight loss
- incontinece

Personality

  • more egocentric
  • sexual disinhibition
  • antisocial behaviour
  • emotional blunting with outburst of anger
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22
Q

what type of dementia accounts for up to 20% of presenile (<65 yrs) dementia cases?

A

frontotemporal dementia

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23
Q

What are the four genes which can lead to
a) late onset
b) early onset
of Alzheimers?

A

late onset = apoE 4 allele
early onset = amyloid precursor protein on chromosome 21, Presenilin 1 (PS1) on chromosome 14, Presenilin 2 on chromosome 1(PS2).

*high chance of early onset gene leading to AD. However late-onset sporadic AD accounts for the majority of AD cases.

24
Q

What tools can be used to assess a patient with Alzheimer’s dementia?

A

1) Mini mental state exam
2) 6 item cognitive impairment (6-CIT)
3) 7 minute screen
4) mental state exam (MSE)

use ICD-10 and DSM-5 or NINCDS-ADRDA Alzheimers criteria to help diagnose.

25
Q

What investigations can be done for Alzheimer’s dementia?

A

1) Do CSF if CJD ( creutzfeldt jacob disease) is suspected.
2) Imaging (can help to distinguish between different types of dementia)
- CT (shows cortical atrophy) or SPECT scan
- MRI (shows grey matter atrophy)
3) Bloods
- FBC, LFT, U+Es, glucose, ESR, phosphate
- syphillis, HIV, B12/folate deficiency

26
Q

What is the treatment for (alzheimers) dementia?

A

1) treat reversible causes
2) Acetylcholinesterase inhibitors to enhance affect of Ach at synapses.
3) NMDA receptor antagonists e.g. memantine monotherapy (effective in more advanced disease)
4) social treatment alongside medical: emotional support, cognitive rehab/stimulation, carer support, occ therapy input / social care

27
Q

what are the social risk factors for Alzheimer’s disease?

A

1) hearing loss
2) untreated depression (though depression can also be one of the symptoms of Alzheimer’s disease)
3) loneliness or social isolation
4) a sedentary lifestyle

28
Q

Acetylcholinesterase inhibitors are uses to treat mild to moderate Alzheimers disease. What are the 3 drugs recommended as monotherapies by NICE guidelines?

A

1) Donepezil (5-10mg OD)
2) Rivastigmine (24hr patch)
3) galantamine

All 3 are 2nd generation Ach inhibitors.

29
Q

How do NMDA receptor partial antagonists suchs as memantine help to treat moderate to severe Alzheimers?

A

memantine protects neurons from glutamate mediated toxicity.

“If you have Alzheimer’s disease, your cells can make too much glutamate. When that happens, the nerve cells get too much calcium, and that can speed up damage to them. NMDA receptor antagonists make it harder for glutamate to “dock” – but they still let important signals flow between cells. “
https://www.webmd.com/alzheimers/guide/nmda-receptor-antagonists#1

30
Q

why should you be wary of treating Lewy Body Dementia with antipsychotics?

A

Antipsychotics could induce a severe parkinsonism reaction, impaired consciousness, increase in mortality and severe autonomic symptoms in those with Lewy Body dementia.

31
Q

Describe the half life, action, benefits and limitations of Donepezil ( a first line acetylcholinersterase used to treat mild to moderate Alzheimer’s disease)

A

Donepezil:

  • 1/2 life is long (70hrs)
  • it is a highly selective drug and only acts centrally

Benefits

  • no liver toxicity
  • 1X daily dosage

Limitations:

  • GIT side effects at high dose
  • bradycardia
  • GIT bleed (rare)
  • contraindicated in Asthma
32
Q

Rivastigmine is one of the acetylcholinesterase inhibitors used to treat mild to moderate Alzheimer’s disease. Describe the half-life, action, benefits and limitations of this drug.

A

Rivastigmine:

  • half-life is short (12 hrs)
  • action - inhibits AChE and butyrylcholinesterase in CNS
  • benefits - not metabolised by the liver, least likely to cause drug-drug interactions, available in modified release OD form or 24hr patch.
  • limitations - GIT side effects, 2x daily dosage
33
Q

What is the half-life, action and site of metabolism of Galantamine (AChE inhibitor)

A

Galantamine (acetylcholinesterase inhibitor used to treat mild to moderate Alzheimers)

  • half-life = 5 hours
  • selectively inhibits AChE
  • metabolised in liver
  • needs twice daily dosage
34
Q

What are the risk factors for developing vascular dementia?

A

Risk factors for vascular dementia are :

  • male
  • smoking
  • previous stroke
  • hypertension
  • diabetes
  • history of MI
  • carotid artery stenosis
  • valvular disease
  • hypocholesterolaemia
  • Hypercoagulation disorders
35
Q

What is the 2nd most common type of dementia in the over 65s?

A

Vascular dementia is the 2nd most common type of dementia >65 and accounts for 20% of cases

36
Q

Apraxic gait disorder, urinary incontinence and pyramidal signs are common additional features of what type of dementia?

A

vascular dementia

*pyramidal signs include increased muscle tone in lower extremities, positive Babinski sign, hyperreflexia and decrease in fine motor coordination.

37
Q

What is the neuropathology of vascular dementia?

A

1) cognitive defects following a single stroke
2) multiple small infarct dementia (multiple strokes –> stepwise deterioration in cognitive function. Between strokes there are periods of stability.)

3) Progressive small vessel disease / biswanger’s disease
- (multiple microvascular infarcts of perforating vessels lead to lacunae formation –> white matter ischaemic changes on MRI)
- gradual decrease in intellect, generalised slowing, motor problems & gait disturbance.

38
Q

What are the clinical features / presentation of vascular dementia?

A
  • abrupt onset
  • stepwise progression
  • difficulty concentrating
  • seizures
  • emotional and personality changes
  • cognitive defects (fluctuating in severity)
  • depression with confusion
  • anxiety
  • rigidity, amnesia, brisk reflexes, pseudobulbuar palsy
  • 10% have siezures
  • often weakness on one side of the face and not the other.
39
Q

What investigations should be done for vascular dementia?

A
  • Mental state exam
  • cognitive assessment
  • cholesterol clotting screen, CRP, renal function,
  • ECG, CXR, CT and MRI
40
Q

what treatment should be given for vascular dementia?

A
  • treat underlying condition (cardiovascular)
  • consider anticoagulants
  • lifestyle changes e.g. exercise, diet, smoking, Hypertension and diabetes control.
  • social care, support + carer
  • OT and physio
  • DO NOT USE Ach inhibitors, NMDA antagonists.
41
Q

What are the clinical differences between vascular and Alzheimer’s disease?

A

1) step wise course with relatively sudden onset / deterioration following onset is typical of vascular. Alzheimer’s has a more insidous onset and gradual progession.
2) Vascular has loss of insight an personality later than alzheimers.

3) Vascular = patchy cognitive deficits.
Alzheimer’s = global cognitive deficits.

4) Vascular = hard neurological signs ( e.g. parkinonism or old cerebovascular accident.
Alzheimers = soft signs only

5) vascular has a history cardiovascular disease.

42
Q

Describe an overall management plan for someone with dementia?

A

1) Treat the underlying condition (e.g. cardiovascular risk factors, hypothyroidism)
2) Treating associated disorders or complications (e..g. aggression or agitation with antipsychotics, depression with antidepressants)
3) Address functional problems (kitchen skills, financial management, social isolation)
4) advice and support for carers
5) symptomatic treatment for Alzheimer’s with Acetylcholiniesterase inibitors e.g. donepezil.

43
Q

What is the prognosis of dementia?

A

the course of dementia is progressive and invariably
fatal.

The duration of survival from time of diagnosis:
Alzheimers = 7 - 9yrs
Vascular = variable but usually less than alzheimers
Lewy bodies (similar to AD) = 5 - 8 yrs
Frontotemporal = 8 - 11 yrs
huntington's = 12 - 16 yrs
CJD = 6 - 8 months
44
Q

what are the presenting features of Dementia with Lewy bodies/

A
  • Fluctuating cognitive impairment in attention and alertness.
  • 60% Recurrent visual hallucinations ( of people & animals)
  • 20 % have auditory hallucinations
  • 70% have parkinsonism (rigidity, bradykinesia, tremor)
  • recurrent falls and syncope
  • loss of consciousness –> *this is not observed in AD
  • memory impairment
  • sleep disturbance (vivid dreams)
  • extreme sensitivity to antipsychotics (induces parkinsonism)
  • 40 % have major depression episodes.
45
Q

what is the treatment for dementia with lewy bodies?

A
  • **Ach inhibitors (e.g. donepezil, rivastigmine and galantamine) may help with hallucinations, sleepiness and confusion
  • AVOID ANTIPSYCHOTICS!
  • Memantine (for moderate to severe DLB)
  • Levodopa may be given to help with some of the motor problems but needs to be monitored carefully as can worsen other symptoms.
  • antidepressants (if depressed)
  • clonazepam (can be used if experiencing disturbed sleep, however part of the benzo family so be cautious with the length of time on the drug)
46
Q

what is the prevalence of lewy body dementia?

A

15 - 20 %

47
Q

what is the age of onset and age of death for patients with Lewy body dementia?

A

Lewy body dementia
age of onset = 50 - 83 yrs
age of death = 68 - 92 yrs

48
Q

Describe the neuropathology of Lewy body dementia?

A
  • Subcortical (& some cortical structures) are involved.
  • Lewy bodies ( inclusions containing protein a-synclunein) are found in the cortex.
  • neurofibrillary tangles may be present but lack amyloid core.
  • neuronal loss leads to lower Ach, but there is minimal cortical atrophy.
49
Q

Visual hallucinations, fluctuating cognition with variation in alertness and attention, as well as sleep disorders are characteristic of Dementia with lewy bodies. What type of visual hallucinations are common in DBL?

A

Visual hallucinations take the form of people or animals or the sense of a presence.

50
Q

what are the differentiating features between Parkinson’s disease dementia and dementia with Lewy body?

A

1) DLB cognitive features dominate and parkinsonism may evolve later and is usually mild,
2) PDD cognitive problems are a late feature, at least 1 year and usually occur after the age of 75.

51
Q

what investigations should be done for dementia with Lewy Bodies?

A

1) Basic Dementia screen
- routine haematology (FBC, ferritin, Vitamin B12, folate)
- biochemistry ( U+Es, LFTs, renal, calcium, glucose)
- Thyroid function test
- Midstream specimen of urine (MSU)
- CXR / ECG where clinically indicated

2) CT/ MRI will show generalised atrophy with sparing of temporal lobes. (look to exclude other causes of dementia.)
3) SPECT / PET scan show decreased dopamine transporter uptake

52
Q

What are the degenerative, vascular, metabolic and endocrine causes of dementia?

A 
Dementia causes:
Degeneratidve=
1) Alzheimer's
2) Lewy Bodies
3) Frontotemporal dementia
4) Huntingtons
5) Parkinson's
6) Prion diseases e.g. creutzfeldt-jacob

Vascular=

1) vascular dementia
2) cerebral vasculitis (rare)

Metabolic=

1) Uraemia
2) Liver failure

53
Q

What are the toxic, vitamin deficiency and traumatic causes of dementia?

A

Causes of Dementia :

Toxic=

1) Alcohol
2) Solvent abuse
3) heavy metals

Vitamin deficiency=
1) B12 and thiamine

Traumatic=
1) severe or repeated brain injury

54
Q

What are the intracranial lesions, infections and endocrine conditions that can lead to dementia?

A

Causes of dementia

Intracranial lesions:

1) Subdural haematoma
2) tumours
3) Hydrocephalus

Infections:

1) HIV
2) Neurosyphilis
3) Whipple’s disease
4) Tuberculosis

Endocrine:

1) Hypothyroidism
2) Hypoparathyroidism

55
Q

Formulate a management plan for a patient with lewy body dementia

A

1) Refer to a specialist
2) Talk to the main carer to maximise patient’s indepenence in activities of daily living.
3) Make sure carers understand diagnosis and prognosis.
4) social interventions include music therapy, art, dance etc (according to patient’s interests)

5) involve psych social workers / carer support early.
6) Patients with DLB must NOT DRIVE!
7) medication : Ache inhibitors e.g. rivastigmine at daily dose of 6mg and above.

Year 3 - Mental Health Conditions (9 decks)

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