Neurodegeneration 2 Flashcards

giggles

1
Q

Glial produce inflammatory cytokines that activate…

A

astrocytes and death receptors on neurons

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

Mitochondrial uncoupling causes

A

increased MNDA sensitivity

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

Central Integrative State (CIS) increases because

A

sitting in a pool of glutamate

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

neurologic failure as a result of this?

A

stoke essentially with no imaging

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

serotonin issue

A

triptins work great and help stimulate serotonin receptors

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

why shouldn’t you piss off astrocytes?

A

they make and uptake glutamate

and regulate extracellular potassium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Increased extracellular potassium can _____ and_____ activity

A

depolarize cells

epileptform

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

increases ____ can activate microglial cells and lead to degeneration due to firing greater than metabolic rate

A

K

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

glycosylated end products

what does it mean if they are elevated for a prolonged period of time

A

homocysteine
A1C

they need to be reduced because the process of TND has already started

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

increased A1c=

A

bbb dysfunctions and microglial activity

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

increased homocysteine means

A

bbb dysfunctions and excitotoxicity

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

apigenin
luteolin
curcumin

A

modulate cytokines, NO, prostaglandin, lipopolysaccharide, mitosen protein degeneration
decreases activation of death receptors

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

rutin

A

good for brain

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

catechin

A

good for brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

alzheimers factors to consider

A
optimize methylation
modulate stress
control diabetes/blood glucose levels
prostaglandin balance
antioxidants for inflammation
control associated lymphoid tissue
optimize control TB cell activity
Control/optimize NT levels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

methylation

A

BBB
small vessel damage
energy landed excitotoxins
homocysteine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

patient comes in with depression

A

1.energy
2.bbb
3.inflammation
4. activate
5. decrease excitotoxins
allergens/immune
NT pprecursors
drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Challenges

A

exotic
mito
inflammatory
allergens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Tau diseases

A

fronto temporal dementia
progressive super nuclear palsy
cortico bacilar degeneration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Trinuclear disorders

A

huntington

spinocerebellar ataxia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

alpha synuclein disorders

A

Dementia
Parkinsons
protein folding
multisystem

22
Q

amyloid and tau pathology

A

alzheimers

23
Q

ALS is a ____ _____ disease

A

ventral horn

24
Q

how do you manage ALS?

A

high doses of antioxidants and neuroprotective stuff B/C ALS is massive, unregulated free radical damage

25
Q

ALS in upper extremity

A

characteristics of upper motor neuron lesion

  • fasiculations
  • atrophy, hands and move proximal
  • decreases reflexes un upper extremities
26
Q

ALS in lower extremity

A

characteristics of lower motor neuron lesion

  • hyperreflexia
  • pathological reflexes
  • clonus
27
Q

ALS has no ____ or ____ changes

A

visual or sensory

28
Q

How is MS typical managed?

A

down regulate immune system that doesn’t like myelin anymore

29
Q

first sign of MS

A

optic findings “pain behind eye, hurts when moved”

30
Q

lose central vision in MS

31
Q

typical neurologic patter of MS

A

none since multiple areas can be demylinating

32
Q

Causes of Big pupils

A

oculomotor lesion
lesion to sympathetic chain
internuclear ophthalmoplegia

33
Q

Internuclear opthalmoplegia

A

double vision (side by side, not stacked or vertical)
MS every single time
aDduction bad
can still converge

34
Q

lesion to sympathetic chain

A

smaller on opposite side

35
Q

Occulomotor lesion

A

deviation and pupillary change

lid change

36
Q

will increase by 4x before 2050

A

alzheimers

37
Q

first signs of alzheimers

A

memory deficit
aphasia: loss in purposeful speaking
apraxia slow performance: speaking/moving
Agnosia: can’t recognize things

38
Q

Aphasia receptive vs expressive

A

spot localization ok=expressive

39
Q

first sign of dementia

A

loss of smell because deposits occur in olfactory nerve first

extra pyramidal signs:tremors

40
Q

first signs of front temporal demise

A

hyperoral
disinhibition
no tremor

41
Q

common triggers of neurodegeneration (DX is final condition but not cause)

A

Neuro inflammation of bowel
HPA axis
Mesencephalon firing in inflammatory situation

42
Q

Neuroinflammation in bowel

A

damages enteric NS and decreases function

GALT activation increase inflammatory cytokines and causes energy linked excitotoxicity

Altered GI functions will up regulate HPA axis and oxidative stress from this decreases pituitary function and immune system weakening

decreases serotonin and dopamine

43
Q

_____ ganglia in the gut degenerate prior to dopaminergic ones in enteric NS in ______

A

autonomic

Parkinsons

44
Q

HPA axis

A

cortisol destroys hippocampus
decreases enzymes to make T3 from T4
unregulates IML
increases catecholamines

45
Q

destruction of hippocampus=

A

short term memory bad and depression

46
Q

increases in catecholamine due to HPA axis does what?

A

depolarizes C fibers and increases substance P (inflames nerves)

47
Q

what can cause the mesencephalon to spontaneously fire?

A

pro inflammatory situation

48
Q

RAS does what?

A

fires up to the cortes and doesn’t let it shut down. Increases anxiety. (happens when mesencephalon spontaneously fires)

49
Q

signs of dementia

A
saccadic abnormality 
optic abnormality
memory loss
loss in speech and affect
executive function loss
mood swings 
difficulty learning 
loss in smell
50
Q

eye symptoms of dementia

A

lose vertical saccades and eye movements

51
Q

horizontal eye movements

52
Q

vertical eye movements