Brainscape's Knowledge GenomeTM

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


See full index

Medicine > Neurodegenerative disorders > Flashcards

Neurodegenerative disorders Flashcards

1
Q

what are neurodegenerative diseases

A

ensemble of conditions primarily affecting the neurons in the human brain

frequently culminate in neuronal cell death

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

what are neurons prone to

A

o2 lack- 3 mins to death (VASCULAR)
degenerative triggers
-stress
-immuno-sensitive
-toxic aggregates
-trauma
-age

POOR REGENERATIVE POWERS

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

when is dementia conventionally diagnosed

A

when progressive cognitive decline has occurs
this has had a noticeable impact upon a persons ability to carry out important everyday activities
defined according to the EXTENT of brain failure

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

when do the pathological changes of dementia start

A

likely commenced well in advance to symptoms presenting
(15-30 years)
therefore how do you reverse cell death that has already occurred

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

define cognition in relation to brain function
what are the 5 DOMAINS of cognition

A

the mental action or process of acquiring knowledge and understanding through thought, experience, and the senses

  1. learning and memory
  2. language
  3. visuo-spatial function
  4. executive function
  5. psychomotor abilities
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what are 10 signs of dementia

A

poor/ decreased judgement
difficulty with simple tasks
problems communicating
misplacing things
dat-to-day forgetfulness
problems with language
difficulty solving problems
confusion of time/place
changes in personality

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

what is dementia
diagnosis
treatment

A

chronic
often global
irreversible deterioration of cognition

rule out vascular/tumour cause
but cant differentiate between different kinds of dementia
-lab and imaging
POST MORTEM ONLY DEFINITICE DIAGNOSTIC

lack reliable biomarkers

SUPPORTIVE treatment (no cure/reversing treatment)

CHOLINESTERASE INHIBITORS- temporarily improve cognition

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

what is dementia
diagnosis
treatment

A

chronic
often global
irreversible deterioration of cognition

rule out vascular/tumour cause
but cant differentiate between different kinds of dementia
-lab and imaging
POST MORTEM ONLY DEFINITICE DIAGNOSTIC

lack reliable biomarkers

SUPPORTIVE treatment (no cure/reversing treatment)

CHOLINESTERASE INHIBITORS- temporarily improve cognition

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

what test do you do for frontal lobe
-sequencing, verbal fluency

A

luria hand sequencing task
verbal fluency 1 minute words

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

what test do you do for temporal lobes
-memory, speech

A

address test
object recall
serial 7s (100-7)

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

what test do you do for parietal lobes
-spatial awareness (R)
-language (L)

A

clock face
naming objects
drawing cube, interlocking infinity
agnosia (name object with closed eye)

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

what screening tests are there for detecting dementia

A
  1. MINI-MENTAL STATE EXAMINATION (MMSE)
    -not good at discriminating (have to be very demented)
  2. ADDENBROOKE’S COGNITIVE EXAMINATION III
    -good differentiation between dementia, MCI and controls but not dementia subtypes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is the difference between sensitivity and specificity
AND MMSE vs ACE III

A

sensitivity- TRUE POSITIVE
specificity- TRUE NEGATIVE

ace has higher sensitivity and specificity

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

what is mild cognitive impairment

A

(grey zone)
cognitive impairment greater than age related impairment
decline in function of 1 or more of the 5 cognitive domains

no ADL impairment

it might progress to dementia

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

is alzheimers predominant in female or men
and how does it present

A

female

early memory disturbance
progress to dyspraxia and dysphasia
eventually immobile and mute

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

what are the signature proteins of AD
(aggregates)

A

INTRACELLULAR in cytoplasm
-phosphorylated TAU proteins
-neurofibrillary tangles

EXTRACELLULAR
-amyloid plaques
-AB peptides

16
Q

what are the risk factors of dementia

A

less education
hypertension
hearing impairment
smoking
obesity
depression
physical inactivity
diabetes
infrequent social contact
(xs alcohol, TBI, air pollution)

12 modifiable risk factors account for 40% of worldwide dementias
–could theoretically be prevented or delayed

17
Q

what are specific recommended actions to reduce risk of dementia

A

maintain BP (130 or less)
use of hearing aids- reduce noise induced hearing loss
reduce air pollution exposure, second hand tobacco smoke
reduce head injury
limit alcohol use <21 units a week
avoid smoking
provide primary and secondary education

18
Q

how do amyloid precursor peptide cleavage patterns determine plaque formation

A

-Membrane protein processed
in secretory pathway
-Cleaved by secretases
-If beta secretase acts Abeta
fragments with 38-42 amino
acids generated
-Less soluble and aggregate
extracellularly to make
fibrils/plaques

19
Q

what are some major risk genes associated with AD
in particular familial alzheimers

A

ApoE4- membrane trafficking
TREM2- recycling
SORL1-sorting

ENDOSOMAL MEMBRAINE TRAFFICKING PROBLEMS

familial forms:
changes in amyloid precursor protein
and presemilin gene

20
Q

what is the retromer complex
and what happens in AD patients

A

involved in endosomal protein sorting back to surface for reuse

key components of retromer are depressed in hippocampus of AD patients
–causes mixing of B secretase and APP, aberrant trafficking
this causes AB production and TAU increases

21
Q

what are some biomarkers

A

structure:
CT, MRI

functional PET
amyloid PET
tau PET

EXPENSIVE, DONT PROVIDE A SCREENING TOOL

CSF studies- why if cant differentiate and cant treat, why put patient through that

peripheral blood samples- more accessible, promising

MAINLY CLINICAL

22
Q

Ach and dementia
what drug can you use

A

marked loss of Ach (mainly responsible for memory and learning defect)
-related to neuronal loss from nucleus basalis of Meynert

DONEPEZIL (most affective in mild-moderate)

MEMANTINE (moderate to severe)

23
Q

what does MEMANTINE target

A

glutamate is off target from astrocytes
on extra-synaptic NMDA (glutamate receptors)
stimulate death pathways

so block flow though glutamate channels
affect function of receptors and block death pathways

NMDA receptor antagonists

24
Q

what is ADUHELM

A

immunoglobulin gamma 1
antibody against amyloid beta (rid aggregates)
clinical effectiveness questionable
probs wont be approved in uk

25
Q

discuss vascular dementia

A

often mixed with AD
can identify vascular features

history of stroke/vascular disease/ risk factors

26
Q

what is the toxic aggregate found in parkinsons

A

a-synuclein accumulation

also found in lewy body dementia

27
Q

what is the difference between parkinsons and lewy body dementia

A

parkinsons
usually start with movement disorder
can develop into dementia

lewy body
starts with dementia and parkinsonism movement disorder

both have a-synuclein accumulation

28
Q

what is common with alzheimers and parkinsons

A

membrane sorting components defect

difficulty to degrade aggregates

29
Q

what is amyotrophic lateral sclerosis

A

both upper and lower motorneurones die

  • fasciculations (muscle twitches) in the arm, leg, shoulder, or tongue
  • muscle cramps
  • tight and stiff muscles (spasticity)
  • muscle weakness affecting an arm, a leg, neck or diaphragm.
  • slurred and nasal speech
  • difficulty chewing or swallowing.

overlaps with frontotemporal dementia

30
Q

what are some genes found in ALS
and mechanisms

A

5-10% familial

C9orf72 is most common mutation
(also found in FTD)

CAUSES AGGREGATION OF TDP-43
-causes stress and glutamate toxicity related death

protein aggregates (SOD1)
Excitoxicity- glutamate transport is reduced (EAAT2), glutamate increased in CSF
mitochondrial dysfunction caused by SOD1- DNA damage
astrocytes play a role in neuron toxicity via SOD1 mechanisms

31
Q

what is RILUZOLE

A

reduces glutamate release
increases astrocyte glutamate uptake
decrease levels

inhibits TDP43 metabolism
improve glutamate transporter EAAT2

32
Q

what are treatments for ALS

A

RILUZOLE
EDARAVONE

33
Q

what are some types of motorneurone disease

A

amyotrophic lateral sclerosis UMN/LMN (lou gehrig’s disease)

progressive muscular atrophy LMN

primary lateral sclerosis UMN

spinal muscular atrophy

Medicine (54 decks)

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