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Pharmacology > Alzheimer's Disease > Flashcards

Alzheimer's Disease Flashcards

1
Q

What is dementia?

A

Progressive deterioration of memory and cognitive function.

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2
Q

What is reversible dementia?

A

Theoretically treatable underlying cause.

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3
Q

What is irreversible dementia?

A

Caused by incurable condition.

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4
Q

What are some causes of reversible dementia?

A

Brain tumors, vitamin B-12 deficiency.

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5
Q

What are some causes of irreversible dementia?

A

Alzheimer’s, strokes.

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6
Q

What is the most common type of dementia?

A

Alzheimer’s Disease.

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7
Q

What gross findings are found in Alzheimer patients?

A

Cortical atrophy.

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8
Q

What historical findings were thought to be only associated with Alzheimer’s Disease?

A

Amyloid Plaques and neurofibillary tangles

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9
Q

What are amyloid plaques?

A

Contains primarily aggregated (fibrillary) forms of beta amyloid.

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10
Q

What are neurofibillary tangles?

A

Contain primarily abnormal tau.

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11
Q

What is cortical atrophy?

A

Caused by cell death and loss of neurons.

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12
Q

What 3 genes are associated with early-onset Alzheimer’s disease?

A

APP, PSEN1, PSEN2.

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13
Q

What is now thought to be the major driver of Alzheimer’s disease?

A

Smaller soluble A(beta) oligomers. They can block neurotransmitters, may trigger inflammation, may be toxic to neurons.

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14
Q

How could soluble A(beta) oligomers cause Alzheimer’s disease?

A

They can block neurotransmitters, may trigger inflammation, may be toxic to neurons.

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15
Q

What are the two main drug groups used to treat Alzheimer’s disease?

A

Acetylcholinesterase Inhibitors and Glutamate receptor partial antagonist. Or both together.

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16
Q

What is the role of acetylcholine in Alzheimer’s?

A

Loss of acetylcholine cells results in some of the symptoms of AD.

17
Q

What does Acetylcholinesterase do?

A

It breaks down Acetylcholine.

18
Q

How do Acetylcholinesterase Inhibitors help those with AD?

A

It stops the breakdown of ACh by Acetylcholinesterase, allowing for more ACh to be available.

19
Q

Do Acetylcholinesterase Inhibitors alter the course of the disease?

A

No, but they may slow cognitive decline.

20
Q

What are the 3 Acetylcholinesterase Inhibitors?

A

Donepezil (Aricept), Rivastigmine (Exelon), and Galantamine (Razadyne).

21
Q

How does Donepezil (Aricept) work? Are its effects reversible? When can it be used?

A

It is a reversible inhibitor of AChE. It can used for all stages of AD.

22
Q

What are the pros of using Donepezil (Aricept)?

A

Long half-life, fewer GI side effects.

23
Q

How does Rivastigmine (Exelon) work? Are its effects reversible? When can it be used?

A

Inhibition of AChE, slowly reversible “Psuedo irreversible”. It can be used for mild-moderate AD.

24
Q

What are the pros of using Rivastigmine (Exelon)?

A

Patch available (all stages AD, mild-moderate PD).

25
Q

What are the cons of using Rivastigmine (Exelon)?

A

More GI side effects than Donepezil (Aricept) (oral dosing).

26
Q

How does Galantamine (Razadyne) work? Are its effects reversible? When can it be used?

A

Reversible ACHE inhibition. May also have actions at Nicotinic receptors.

27
Q

What is the role of glutamate in creating the symptoms of Alzheimer’s disease? How do plaques play a role?

A

Glutaminergic excitotoxicity. Too much glutamate, or too much glutamate signaling can have toxic affects a neurons. Plaques may make neurons release too much glutamate.

28
Q

How does Memantine (Namenda) work? When is it used?

A

It is a glutamate NMDA-type receptor non-competitive partial antagonist. It can be used in moderate to severe AD.

29
Q

What is the one drug that is a Glutamate receptor partial antagonist?

A

Memantine (Namenda).

30
Q

How does the NMDA channel normally work if excited?

A

Normal excitatory transmission: glutamate released.

31
Q

When glutamate is absent, what block the NMDA receptor?

A

Mg ions.

32
Q

When does the NMDA channel open?

A

NMDA (Ca) channel opens if: neuron is depolarized, glutamate is bound, and co-transmitter glycine is also bound.

33
Q

What effects occur if you chronically block NMDA receptors?

A

It can interfere with memory formation and plasticity.

34
Q

How does Memantine (Namenda) work, specifically, on NMDA channels?

A

With excitotoxicity, the channel is mainly open. Memantine basically only blocks the channel when it is open, that block is quickly reversible.

35
Q

What is Ginko biloba? What effects did it have on AD patients?

A

Extract from ginko tree used as a supplement. There were no benefits for AD patients.

36
Q

What is the goal of immunotherapy?

A

To get the body’s immune system to react to A(beta), thus preventing worsening of plaques, could lead to clearance of plaques and potentially reverse disease.

37
Q

How could immunotherapy work?

A

Create anti Ab antibodies to get eaten by macrophages.

38
Q

What are the two types of ways Immunotherapy can work for AD?

A

Actively (vaccination) and passively (supply antibodies).

39
Q

Does the passive way of immunotherapy (supplying antibodies) work? What is the name?

A

No efficacy in AD trials. Solanezumab.

Pharmacology (20 decks)

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