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Flashcards in Dementia Deck (39):
1

Dementia is a term used to describe

a group of related chronic, organic, brain disorders. They all share a common characteristic of deterioration of cognitive function leading to gradual decrease in intellectual capacity

2

Dementia is a term used to describe

a group of related chronic, organic, brain disorders

3

Cognitive decline is

a significant decline from what was normal for an individual in any of the following
- consciousness
- memory
- concentration + attention
- insight
- self awareness
- general knowledge
- intellectual performance
- orientation
- judgement

4

What are the types of dementia?

Dementia of Alzheimer's Type Early onset
Dementia of Alzheimer's Type Late onset
Vascular Dementia
Lewy body/ Parkinson's Disease Dementia
Others - Pick's Disease, Huntington's Chorea

5

Neuropathology of AD

- Generalised atrophy, especially frontal, parietal and temporal lobes
- Widespread deposition of neurofibrillary tangle and amyloid plaques
- Depletion of NT levels, especially ACh
- Loss of brain volume - upto 15% enlargement of sulci and ventricles
- Dramatic loss of central neurones

6

Neuropathology of AD; NFTs and Amyloid plaques

NFTS:
- remains of defective neurones
- normal part of ageing, greater number in AD
- number on post mortem correlates with duration and severity of AD
Neuritic/ Senile plaques:
- Clumps of dying nerve axons and dendrites
- appear where neurone loss is most severe

7

Wha is the neurotransmitter hypothesis

Cholinergic systems are critical for normal memory and other cognitive functions.
A selective loss of cholinergic cells from the basal forebrain.
Depletion of neurones in this area results in memory and cognitive decline.
By the time mild symptoms are detectable, there is already a significant loss of ACh
Post mortem shows there are reduced levels of synaptosomal ACh and low levels of acetylcholesterase and acetyltransferase.

8

What is the inflammatory hypothesis.

-

9

What is the inflammatory hypothesis.

- individuals on long term anti inflammatory drugs have lower incidence of AD
- Insult to brain results in neuronal damage and debris deposition
- Cascade process is set up leading to neuronal death and starts inflammatory response
- Anti inflammatory prevent further propagation of process

10

What is the oxidative hypothesis?

- AD is due to free radical mediated cell damage
- Oxidative stress leads to tissue inflamation

11

Progression and Staging of AD:
1st stage is between:
2nd stage is between:
3rd stage is between:

What happens in each stage?

1st: first three years; recent memory impairment, ADL impairment, forgetting names, losing direction when out, depression, language difficulties
2nd: 2nd and 10th year; amnesia, aphasia, calculation/ problem solving difficulties, personality, behavioural and psychiatric changes, inability to perform ADL
3rd: 8th and 12th year; short and long term memory loss, muted or nonsensical speech, rigid posture, complete dependence on others

12

Vascular dementia occurs when neuronal death is brought about by

hypoxia or other damage secondary to stroke.
It presents with sudden onset and follows step wise progression
No association between choline acetyltransferase and degree of cognitive decline
Frequent Hx of hypertension, stroke
Damage can be focal
Assessment tools used to differentiate

13

Lewy Body Dementia is progressive dementia distinguished from AD by

fluctuating course and presence of psychotic symptoms.

14

Lewy Body Dementia is progressive dementia distinguished from AD by

fluctuating course and presence of psychotic symptoms.
characterised from parkinsons symptoms and extreme sensitivity to EPSE from antipsychotics.
like AD, widespread reduction in choline acetyltransferase.
Also reduction in Dopamine
Lewy bodies are detectable intracellular masses found on post mortem
Senile plaques may be found but not NFTs
Lewy bodies are found in non demented patients but in different brain region to demented PD patients.

15

Diagnosis of AD can only be made when:

other general medical conditions have been excluded,
other psychiatric disorders have been excludes and
other neurological conditions and reversible causes have been excluded

16

Criteria for diagnosis of probable AD:

- onset between 40-90 years
- absence of systemic or neurological disorders
- objective testing e.g. MMSE
- decline in two or more cognitive areas
- progressive worsening of memory + other cognitive functions
- no disturbance of consciousness

17

What is the MMSE?

Mini Mental State Examination
- Clinical screening tool that tests memory, attention and calculation
- quick to perform, widely used and understood
- fairly crude, considered insensitive to change but sensitive to effects of cholinesterase inhibitors
- each questions tests different aspect of cognition

18

What does MMSE test?

1. orientation
2. registration
3. reading and writing
4. recall and STM
5. concentration and attention
6. constructional ability
7. learning, naming objects and repeating words
8. three stage command

19

What are the MMSE scores?

mild: 21-26
moderate: 10-20
moderately severe: 10-14
severe: less than ten

20

What is the class of drugs prescribed for dementia? How do they work? What do they improve?

AChE- inhibitor
inhibit breakdown by cholinesterase
improve cholinergic transmission, possible slowing down neuronal degeneration

21

AChEIs most commonly prescribed?

Donepazile
Rivastigmine
Galantamine

22

AChEIs most commonly prescribed?

Donepezil
Rivastigmine
Galantamine

23

What drugs act on AChE in brain?

Donepezil
Rivastigme

24

Rivastigme inhibits

AChE and BuchE

25

Which drugs are selective inhibitors of AchE?

Donepezil and Galantamine

26

Which drugs are selective inhibitors of AchE?

Donepezil and Galantamine

27

Galantamine acts on

both AchE (inhibits) and Nicotinic receptors (excites to indirectly release Ach)

28

Predictable side effects of AChEIs?

Nausea/ Vomiting
Diarrhoea
Sweating
Dizziness
Insomnia

29

ACheEiS can exacerbate

Peptic Ulcer Disease
Asthma
COPD

30

Which drug is not a substrate for hepatic metabolism?

Rivastigmine

31

Which drugs are metabolised by CYP 3A4 and 2D6?

Donepezil and Galatamine

32

What is Memantine? What class of drugs?

non competitive NMDA receptor antagonist

33

Patients intolerant or have a contraindication to AChEI are prescribed

memantine

34

Patients with moderate or severe AD are prescribed

memantine

35

What is Memantine? What class of drugs? What does it target?

non competitive NMDA receptor antagonist
targets glutamate

36

Memantine works by blocking

the pathological activation of glutamate receptors without blocking physiological) activation (memory function

37

Side effects of memantine?

Hallucinations
Confusion
Dizziness
Headache
Vomiting

38

How are behavioural symptoms of dementia treated? What is the problem with using this class of drugs?

Antipsychotics
Little evidence that it is efficient
Has side effects of falls due to sedation/ hypotensive effects, EPSE (even with some SGAs), concerns over cardiac side effects e.g stroke

39

What would be the most suitable antipsychotic in terms of a patient who is at high risk of CVD?

Quetiapine