Alzheimers disease Flashcards

1
Q

what happens when the number of cholinergic neurons is decreased in the brain?

A

causes AD because there are no neurotransmitters (acetylcholine) sending signals through the synapse.

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2
Q

types of dementia

A

AVHAFCL
- AD (plaques and tangles)
- Vascular dementia (decrease circulation to brain)
- HIV/AID dementia (adv HIV and AIDS)
- Alcohol related dementia (deficient in vitamin B1)
- Front temporal lobar degeneration
- Creutzfeldt-jacob dementia (presence of prion particles)
- Lewy bodies dementia (protein aggregates affecting brain cells)

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3
Q

area of brain affect by AD

A

CBH
Cerebral cortex - thought, language and reasoning
Basal forebrain - personality, movement and judgement
Hippocampus - learning, memory

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4
Q

symptoms of moderate AD?

A

WDI
- worse memory loss
- depression and confusion
- increased relance on family members for decisions

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5
Q

symptoms of late AD?

A
  • loss of long term memory
  • unaware of time and place
  • doesn’t know family
  • unlearn basic motor skills (teeth brushing and hair brushing)
  • death 5-15 years of diagnosis
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6
Q

symptoms of early AD?

A

MHP
- memory loss of recent events
- hard learning new info
- personality change

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7
Q

How do you know if the diagnosis is correct?

A

after death when there is a brain tissue examination.

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8
Q

diagnosis of AD

A

there are no single test to find out if you have AD.

But they would:
- detailed medical history
- physical and neurological examination
- intellectual test
- psychiatric assessment
- neuropsychological test
- multiple types of scans PET, MRI and CT

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9
Q

what is the treatment of AD

A

There is no cure, they just manage the treatment:
- cholinergic (produces acetylcholine) drugs could be used for improving cognitive function in moderate or early AD.
- drugs for depression or deep deprivation
- community support

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10
Q

What is a acetylcholine?

A

it is a type of neurotransmitter, that helps with memory and muscle contraction.

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11
Q

what is amyloid plaque function?

A

extracellular, made up beta amyloid peptide (40 or 42aa), originates from the amyloid precursor protein (695 n 770aa) located on the chromosome 21. 42aa is a harmful peptide

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12
Q

what is the neurofibrillary tangles as hallacks of AD?

A

intracellular, cluster of protein inside the neuron, tau proteins (stabilize microtubules)

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13
Q

what are the effect of cholestral in AD?

A

having high cholesteral can increase the changes of having some type of dementia.

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14
Q

What are the effects of ApoE4 in AD?

A

ApoE4 is a genetic risk factor, that interacts with beta amyloid (toxic 42) and causes an increase in the development of plaques.

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15
Q

what are the financial effects of AD?

A

$1 in every $40 from the Australian health system is spent on AD.
The cost to the economy is at millions per year are spent on AD.

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16
Q

What percentage of change in AD in cause of death from 2000 to 2019?

A

increased by 145.2%

17
Q

what do caregivers support with for AD patients?

A

feeding, dealing with incontinence, bathing showering and getting to and from toilet .

18
Q

how does the abeta plaque process occur?

A

The APP with the beta secretase followed by the gema secretase cutting of the peptide cause a harmful beta amyloid peptide 42aa. Alot is developed and cause the sticking of the plaques together.

The alpha secretase is harmless.

19
Q

how does the neurofibrilliary tangle process occur?

A
  • when the tau protein increase causing the change of microtubules structure which causes the tau to accumulate which ruins the shape of the microtubules causing the tangles.
  • neurotoxcity induces cleavage of p35 to p25 to caplain.
20
Q

what genetic mutations contribute to AD?

A
  • being female
  • if you have down syndrom as you have 3 chromosomes of 21 which increases the chance of developing AD.
21
Q

what is dementia?

A

progressive decline in cognitive function.
due to damage in the brain tissue and it is faster than normal

22
Q

manifestation of dementia?

A

MMD
memory loss
mood swings
deficit in language

23
Q

cause of AD

A

neural loss together with amyloid plaque and neurofibrillary tangles.

24
Q
  1. types of AD
A

Familial (early)- one other family person with the disease.
Sporadic (late)- no one else with the diseases

25
pharmocology of AD includes 2 factors and their role
AN Acetylcholinesterase inhibitors - decrease destruction of acetylcholine. NMDA antagonists - decrease overstimulation of glutamate - their role is to increase acetylchloline levels
26
why do people with down syndrome have AD sooner?
because they have x3 chrom 21 which increases gene for bAPP cause early onset AD.
27
what the main component of the tangle?
hyperphosphoralted tau
28
activation of the protein kinase cdk5 causes
tau phosphorylation and neural apoptosis.