Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathophys > CNS 4c > Flashcards

CNS 4c Flashcards

1
Q

HAND (HIV-Associated neurocognitive disorders)

A

HIV: infection of helper T cells; immune deficiency
immune-mediated degeneration in CNS
-infected imm une cells enter CNS early in infection
cell death-> progressive cognitive decline

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

HAND mechanism

A

-HIV infected mo attracted to brain
-Neurotoxic viral proteins
-microglia-> chemokines, cytokines
-neuronal injury/death
synaptic pruning- reduced signaling(loss of branches like naked tree)

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

HAND manifestation

A

Cognitive symptoms:
progressive dementia
memory loss
disorientation
behvior changes
problems with thinking, reasoning, language

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

HAND tx

A

no tx for cognitive decline
-combined anti-retoviral treatment: supress viral load (CART)

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

most common neurogenerative disease

A

alzheimers

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

Alezheimers

A

leadin cause of demntia
incidence increases with age
biggest contributer: cerebrovascular dx
other risk factors: genetics, dm, htn

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

2 hallmarks of alzheimers

A

neuritic plaques and neurofibrillay tangles

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

Neuritic plaques

A

no (or reduced) ability to discardamyloid B protein
develop amyloid B plaques
disrupt glutamate uptake -> excitatory -> cell death

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

Neurofibrillary tangles

A

tau- structural protein, forms large intracellular tangles
axon -> instability -> cell death

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

alzheimers mechanism

A

vascular dyfxn and damage precede neuronal death
APOE gene mutation: important for vascular and neuron health
lipid metab, cholstrol transport, amyloid B protein degradation
strong correlation btwn APOE mutation and alzheimers, esp with diabetics

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

alzheimers cognitive sysmtoms

A

memory loss
mood and behavior changes
(preservation of motor /sensory fxn)

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

anatomical changes

A

neuronal loss mostly in cerebral cortex and hippocampus
brain atrophy, decrease in volume

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

Cholinesterase inhibitors

A

cholinesterase: enzyme that degrades acetylcholine (Ach)
-inhibiting breakdown of ACh increases amount of it
improves cognitive fxns, delays dementia progression

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

NDMA receptor antagonists

A

-block affects of glutamate (can block excitotoxicity)
-important with learning, memory
when liagand binds, ca channels open
in AD, excess glutamate-> excess Ca-> excitotoxicity

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

huntingtons dx

A

inherited neurodegnerative condtion with motor and cognitive symptoms
-autosomal dominant
onset not until mid-life
-atrophy of basal ganglia, enlargment of ventricles

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

Huntingtons dx mechanism

A

Huntington protein on chromsome 4
widely expressed, interacts w/ other proteins
mutation = repeat explansion -> makes protein toxic to neurons
protein tangles and collects inside cells
-may induce excitoxic pathways within cell

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

in huntingtons- severe degeneration of basal ganglia:

A

targets GABAergic neurons
-prefrontal cortex, hippocampus, hypothalamus

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

Motor symptoms of hunt.

A

involuntary jerking movements (chorea)
slow writhing movements of limbs (athetosis

19
Q

cognitive symptoms

A

decline in thinking and reasoning abilities
memory loss
psychiatric disturbances

20
Q

huntingtons tx

A

no cure or way to slow progression
tetrabenazine: for uncontrolled movement
antipsychotics: for uncontrolled movemnts, mood stabilizing
antidepressants: for pysch symptoms
PT/OT- to maintain funcitaion and independence

21
Q

Parkinsons dx

A

most common caus eof parkinsonism
selective degeneration of neurions in brainstem and basal ganglia, especially dopaminergic cells of substania nigra
cytoplasmic inclusions (Lewy bodies)

22
Q

Parkinsonism:

A

clinical syndrome of rigidity, bradykinesia, tremor, postural instability: can result from encephalitis, repeated head trauma, exposure to toxins, certain drugs

23
Q

parkinsons mechanism-Genetic:

A

PARK1(a-synuclein)- fxn ? but hangs put in synaptic terminals
PARK2 (parkin)
PARK5 (ubiguitin hydrolase)<-degrades misfolded damages proteines normally
Glucocerebrosidase <- lysomal processing

24
Q

lewy bodies

A

abnormal accumulation of protein inside neurons:
a-synuclein
ubiquitin
tau
a B crytallin

25
Q

parkinsons mechanism: toxic exposure

A

agent orange: herbicide
rotenine: pesticide
polychloriinated biphenyls (PBCs_
disrupts mitchondiral fxn–> decr ATP prod and incr ROS accumulation

26
Q

Parkinsins manifesrtions

A

Sensor: loss of smell
Motor: tremor, rigidity, bradykinesia, postural instability
cognotive: dementis (lewy body), memory loss, halluciatio, mood disorders, sleep disorder (REM behavior disorder)

27
Q

dopamine precursoe

A

levodope: converted into dopamine by enzyhmes in the brain
most effective PD tx (can be used in dx)

28
Q

dopamine agonsits

A

COMT/MAO-B inhibitors
prolong effect of other drugs by blocking dopamine metabolism

29
Q

deep brain stimulation

A

electrodes implanted into brain, connected to generator (chest)
sends electrical signals - invasive

30
Q

Multiple sclerosis

A

autoimmune demylinating and neurogenerative dx
progession varies
4 types: clinically isolated syndrome
relapsing-remitting
primary progressive
secondary progressive

31
Q

MS mechanism

A

autoreactive Th cells activate in periphery
proinflamm cells migrate to CNS
B cells: auto-antibodies against CNS
Cytotoxic T cells attack oligodendrocytes
Mo release proinflamm cytokines
T cell reactivated by mylein fragments

32
Q

loss of myelin ____
loss of neurons_____

A

lesions
atrophy
(both seen on MRI)

33
Q

MS manifestations

A

sensory: numbness, pain, tingling in limbs, loss of vision
motor: weakness, tremor/spasms, slurred speech, incontinence
cognitive: depression, anxiety

34
Q

MS treatments

A

depend on progression and frequcny of attacks

35
Q

Acute attacks of MS tx

A

corticosteriods
plasmapheresis

36
Q

AD tx-slow progession by affecting immune syestem

A

IFN-beta
monoclonal antibodies (natalizumab)
immunosuppressant (mitoxantrone)

37
Q

Amyotrophic lateral sclerosis

A

degeneration of motor neurons in motor cortex and spinal cord
-neurons show cytoskeletal dysfxn- little inflamm

38
Q

ALS

A

familial- inherited 5-10%
sparodic
theeories:
gene mutations
excess glutamate levels
disorganized immune response
protein mishandling

39
Q

ALS mechanisms

A

-common mutations: superoxide dismutase 1 SOD1
excess ROS -> neural death
20% of familial cases
-peripherin; neurofilament
cytoskeleton proteins that maintain axon structure (motor neurons have very long axons)
mutation casues aggregation -> distruption of axonal transport-> cell death
-glutamate cytotoxicity
decr fxn of ternnaporter tht removes glutamate from synapse
excess glutamaye excess Ca (toxic)
only in motor neurons!

40
Q

ALS manifestation

A

cognitive: depression, sleep disorders, inappropiate affect (outburts laughing/crying)
motor: extremities affected first, dx spreads
-early on weakness, clumsiness, tripping, falling, cramps, spasms
late: paralysis, breathing difficulties-> respitory failure

41
Q

ALS TX

A

no cure, tx for symptoms
antidepressants: psych sumptoms, sleep problems
Riluzole (only FDA approved tx)
slows progression of dx, glutamine inhibitor
does not reverse damage to motoe neurons

42
Q

inflammtion and neurodegeneration

A

`chronic NSAIDs use may dcr risk for AD
may slow progression of dx

43
Q

contributors to chronic inflammtion thoiught to incr risk of neurodegen

A

gram-neg bacterial endotoxin (gut bacteria)
certain viral infectiooj s(EBV, HIV, Herpes simple)
toxin exposure (incr cell damage-> death) pestoscides, herbicides
endothelial cell damge

44
Q
A

Pathophys (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions