CNS degenerative disorders Lecture #2 Flashcards

1
Q

What does Huntington’s disease affect?

A

-The GABA pathway (it wipes it out)

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

What are the clinical manifestations of Huntington’s disease?

A

-Early onset (around 30-40 yrs)

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

Huntington’s disease is associated with abnormal moves, what are they?

A
  • Chorea forms (sudden/jerky movements)

- Facial grimacing/oral facial movements

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

What drives the abnormal movements in Huntington’s disease?

A

-You have too much Dopamine

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

If you get the huntington’s gene will you get huntington’s?

A

-Yes it is a genetic disorder

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

What is the progressive intellectual dysfunction associated with huntingtons disease?

A
  • Decreased judgement
  • Withdrawl from others
  • Depression
  • Schizophrenia
  • Become compulsive
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the incidence of huntingtons disease?

A

-.01%

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

What is the duration of diagnosis till death?

A

-5-10 yrs

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

What are the features of the pathophysiology of huntingtons disease?

A
  • To much dopamine and cholinergic activity in the striatum
  • To little GABA projections
  • Lose cell bodies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

The lateral ventricles in brain of a person with huntington’s disease are enlarged, why is this the case?

A

-Because the loss of caudate neurons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the cause of huntington’s disease?

A

-A gene known as huntington gene (deals with NMDA and AMPA receptors)

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

What happens if you activate NMDA receptors?

A

-Ionotropic Ca2+ release (causing problems with GABA if too much Ca2+)

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

How do you diagnose of huntingtons disease?

A

-Genetic screening for diagnosis

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

What is the pharmacological treatment for Huntington’s disease?

A
  • DA antagonists (antipsychotics) (D2 antagonists)
  • Dopamine agonists for bradykinesia/rigidity
  • DA depletion (reserpine) for choreiform movement
  • SSRIs for depression
  • Antipsychotics for hallucination/delusions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is haloperidol?

A

-D2 antagonist

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

What is Olanzepine?

A

-atypical anti-psychotic

17
Q

What can haloperidol lead to?

A

-Parkinsonism because of the lack of Dopamine

18
Q

What is the most common degenerative brain disease?

A

-Alzheimer’s disease (3-4 million)

19
Q

What is the life expectancy for a person diagnosed with alzheimer’s disease?

A

-5-20 yrs

20
Q

What are the three categories of Alzheimer’s disease?

A
  • Early
  • Moderate
  • Late
21
Q

How is early memory loss characterized?

A

-Short term memory

22
Q

What do you see in early alzheimer’s disease?

A
  • Short term memory loss
  • annoying
  • Don’t like change
23
Q

What do you see in moderate alzheimer’s disease?

A
  • Decreased function
  • Stop working
  • Stop remembering the important things
24
Q

What do you see in late alzheimer’s disease?

A
  • Decreased motor
  • No judgement
  • Immobile
  • Stop eating
25
Q

What is the epidemiology of alzheimer’s disease?

A
  • Old age
  • Family history
  • Inflammatory disease
26
Q

What are three places in the brain the you can see alzheimer’s disease?

A
  • Hippocampus (memory)
  • Cortex (function)
  • Nucleus basalis
27
Q

What neurons are severely damaged in alzheimers?

A

-The neurons from the nucleus basalis to the hippocampus (causes a deficiency in cholinergic activity)

28
Q

What histologies are associated with alzheimers?

A
  • Senile plaques

- Neurofibrillary tangles

29
Q

What do senile plaques have in them?

A

-Beta amyloid (is abnormal form of amyloid and becomes sticky)

30
Q

What protein is associated with the neurofibrillary tangles?

A

-Tau protein (microtubule protein)

31
Q

What is the precursor protein for beta amyloid?

A

-APP

32
Q

What happens to cholinergic activity when you have senile plaques?

A

-It decreases acetyl choline and muscarinic receptors

33
Q

What types of drugs do you use for alzheimers?

A

-Acetylcholinesterase inhibitors

34
Q

What type of genes do you see in alzheimers patients?

A
  • Apolipoproteins that turn into the APP that turn into the Beta amyloid
  • Chromosome #21
35
Q

When there is a protein aggregate in the brain what is usually associated with it?

A

-Inflammation

36
Q

What cholinesterase inhibitor drugs are used for the treatment of Alzheimers?

A
  • Donepezil (Aricept)
  • Galantamine
  • Rivastigmine
37
Q

What is the only way you can have a definitive diagnosis of Alzheimers disease?

A

-Post mortem look at the brain

38
Q

What are the functional consequences of alzheimers?

A
  • Diminish capacity of the brain so you’re not able to do multiple tasks concurrently
  • Protein aggregates that cause inflammation
39
Q

What are antipsychotics used for alzheimers?

A
  • Olanzapine
  • Quetiapine
  • Risperidone
  • Ziprasidone