Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Pathology Term 4 > Week 3 - DEMENTIA > Flashcards

Week 3 - DEMENTIA Flashcards

Alzheimer's, Parkinson's, Multiple Sclerosis, Others (75 cards)

Start Studying
1
Q

What is the commonest neuronal degeneration?

A

Alzheimer’s

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

What are examples of selective/system primary neuronal degenrations?

A
  • parkinsons
  • huntingtons
  • MND
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are global primary degenerations characterised by?

A

*alzheimer’s, lewy body, fronto-temporal

–> DEMENTIA

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

What is dementia?

A
  • loss of higher cognitive function (ability to process information –> emotions, language) –> things that make us HUMAN
  • preserved consciousness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the limbic system?

A
  • controls emotions and instinctive behaviour

- includes the hippocampus and parts of the cortex

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

What is the hippocampus?

A
  • part of the brain where short-term memories are converted to long-term memories
  • part of the limbic system
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the thalamus?

A

-part of the brain which receives sensory and limbic information, processes it, and sends it to the cerebral cortex (COGNITION) –> gives us understanding

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

Why is there an increasing incidence in Alzheimer’s?

A
  • ageing, toxins, diet, pollution ??

- >45% of adults over 85y are demented

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

When does the brain start degenerating?

A
  • after 30yrs

- rapid >70yrs

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

What is the most important feature of alzheimer’s?

A
  • recent memory loss (hippocampus)
  • pts. remember past memories (childhood friends, etc.) but cannot remember where they parked their car, what they ate for breakfast, etc.
  • also: aphasia + agnosia + apraxia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is agnosia?

A

inability to interpret sensations and hence recognise things

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

What is apraxia?

A

speech disorder in which person has trouble saying what he/she wants to say correctly + consistently

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

What is aphasia?

A

impairment of language, affecting production/comprehension of speech and the ability to read/write

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

What is the commonest etiology of alzheimer’s?

A
  • sporadic (90%) >60yrs

- genetic/familial (10%) early

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

What is the commonest genetic association with alzheimer’s?

A
  • trisomy 21 (Downs syndrome)
  • excess APP (amyloid precursor proteins)
  • early alzheimer’s disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the pathology of alzheimer’s and what are the 3 microscopic characteristic features?

A
  • cortical atrophy, limbic, temporal, hippocampus –> DEMENTIA
    1. neurofibrillary (NF) tangles (tau) –> intracellular
    2. neuritic plaques (Abeta amyloid) –> extracellular
    3. amyloid angiopathy around BVs –> narrowing + ischaemia

**tau + amyloid are neurotoxic –> atrophy of neurons + reactive gliosis

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

What are neurofibrillary tangles and what is the pathogenesis of them within neurons (intracellular)?

A
  • abnormal clumps of tau protein
  • breakage of normal binding tau protein leads to collapse of microtubules and tau protein clumps –> NF tangles
  • tau proteins normally stabilise the microtubules**
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What stain is used to identify NF tangles?

A
  • nissl stain

- appear as dark spots within neurons

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

What enzymes normally breakdown/cleave amyloid precursor protein?

A
  • alpha + gamma secretase

- broken down into 3 recyclable fragments

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

What is the pathogenesis of amyloid plaques (extracellular) in alzheimer’s?

A
  • abnormal cleavage (into 2 fragments) of APP due to presence of beta-secretase enzyme
  • A-beta peptides produced –> insoluble + non-digestable
  • over years these A-beta proteins accumulate and form abnormal filaments (amyloid fibrils) –> AMYLOID PLAQUES
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the gross features of alzheimer’s disease?

A
  • atrophy of neuronal tissue (limbic system, temporal lobe + cortex - advanced)
  • dilatation of ventricles (compensatory)
  • narrowing of gyri
  • widening of sulci
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the first sign of alzheimer’s?

A

memory loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Outline progression of alzheimer’s

A
  1. memory loss = 1st sign
  2. confusion, poor judgement
  3. language and thoughts, restlessness, agitation
  4. inability, dependence on others
  5. wt. loss, seizures, loss of bladder + bowel control
  6. infections, groaning, moaning + grunting
  7. death usually occurs from aspiration pneumonia, respiratory failure or septicemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is parkinson’s disease (characteristic triad)?

A

“shaking palsy”

  • tremor
  • rigidity
  • bradykinesia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Damage to what causes parkinson's disease?
damage to nigrostriatal dopaminergic system (movement)
26
What are the 3 components of the dopaminergic system?
1. nigro-striatal (movement) 2. mesolimbic/mesocortical (behaviour) 3. tuberoinfundibular (prolactin)
27
What is the difference between parkinsons disease and parkinsonism?
PD --> primary atrophy of substantia nigra (origin of dopaminergic system) Parkonsonism --> secondary (drugs, toxins, other dis.)
28
What are lewy body inclusions?
dopaminergic nerves with alpha-synuclein
29
What is the early sign of PD?
-diminished facial expressions
30
What are the clinical features of PD?
- diminished facial expressions - stooped posture - festinating gait - bradykinesia - rigidity of muscles (cogwheel rigidity) - fine rolling resting tremors (pill-rolling) - micrographia - dementia in SOME cases
31
What is it called when dementia arises <1yr of onset of PD (motor Sx.)?
Lewy body dementia (LBD) --> PD + AD
32
What are the gross and microscopic features of PD?
Gross: - atrophy of substantia nigra - loss of neuromelanin pigment in substantia nigra Micro: - markedly decreased pigmented neurons - lewy bodies in neurons --> rounded inclusion of alpha-synuclein within neurons
33
What is a characteristic finding in diffuse lewy body dementia (DLD) that helps differentiate between just PD or AD?
visual hallucinations - usually pleasant (e.g animals, etc) - not scary
34
What is parkinsonism?
- clinical syndrome - "anti-dopaminergic effects" - drugs: dopamine antagonists, MPTP toxin in heroin, pesticides - NORMAL substantia nigra
35
What is atypical parkisonism and what 3 disorders fall under it?
*other neurodegenerative disorders with parkinson features 1. progressive supranuclear palsy (PSP) - tau, nuchal dystonia, falls 2. corticobasal degeneration (CBD) - jerking movement of limbs 3. multiple system atrophy (MSA) - PD + autonomic abnormalities (orthostatic hypotension) + cerebellar atrophy (ataxia)
36
What does selective myelin damage in myelin disorders lead to?
axon damage --> defective transmission of impulse
37
True or False? | Grey matter is affected more in myelin disorders
False | -white matter as this is where the myelin is stored (AXONS)
38
What are the 2 types of myelin disorders?
1. demyelinating (increased destruction) | 2. dysmyelinating (decreased production)
39
What is the commonest demyelinating disorder? and what is the other?
Immune --> multiple sclerosis (MS)** commonest! also: -metabolic --> central pontine myelinolysis (osmotic; alcohol)
40
How would an MS patient typically present?
- recurrent limb weakness - paraesthesia - vision abnormalities * remission + relapses, progressive damage (no healing) --> death in years
41
What are the gross and microscopic features of MS?
Gross: -multiple soft pink plaques (MS plaques) of demyelination --> commonly around ventricles (periventricular), optic nerve, cerebellum, spinal cord and throughout white matter Micro: -myelin stain - marked loss of myelin around BVs (decreased blue stain) --> perivascular demyelination - inflammation - lymphocytes
42
What stain is used to detect MS?
myelin stain
43
What are the etiological factors for MS?
1. genetic - twins, family, HLA DR2 2. environment - virus, EBV? 3. autoimmune - Th1/Th17** PROVED --> inflamm. (IFN-gamma, IL-23, IFN-beta)
44
What is increased in MS pts. CSF?
increased IgG in CSF (oligoclonal)
45
What are the 4 MS plaque types?
1. macrophages; clear border 2. complement; clear border 3. diffuse; apoptosis 4. non-apoptotic
46
True or False? | When a pt. comes in with hyponatremia (severe vomiting, dehydration, etc.) it should be corrected rapidly
False - should be corrected slowly so as to prevent central pontine myelinolysis - rapid correction causes myelinolysis in the base of the pons WITHOUT inflammation
47
How does central pontine myelinolysis occur?
-2-6 days following RAPID correction of hyponatremia* OR -rapid changes in osmolality, alcoholism, malnutrition, etc.
48
What are the features of central pontine myelinolysis?
- rapidly evolving quadriplegia, may be fatal | - locked in syndrome: - fully conscious yet unresponsive patients (vegetative-like state)
49
What are the dysmyelinating disorders?
- vitamin deficiency (B12) - infections --> JC virus - PML in immunosuppressed - genetic --> leukodystrophy (dysmyelinating)
50
What is the difference between age-related/senile degeneration and alzheimer's?
exactly the same yet occuring at a later age (slow progress) - NF tangles/A-beta plaques still present like alzheimers* - hippocampus/cerebral cortex affected like alzheimers
51
What is Fronto Temporal Lobre Dementia (FTLD) AKA?
Picks Disease | -second commonest dementia following alzheimers
52
What are the subtypes of FTLD?
Picks disease -FTLD-tau (tau deposition) - common FTLD-U -ubiquitin deposition (next common)
53
What are the characteristic features of FTLD?
- affects personality, behaviour and SPEECH - younger pts. - memory NOT affected until late (c.f. alzheimers where memory loss is the first sign) - semantic dementia --> progressive language problems - aphasia predominate - selective frontotemporal degeneration (rest of brain is normal) --> knife blade atrophy*
54
Why is FTLD known as knife blade atrophy?
-atrophy is so severe in the frontotemporal lobes that the gyri become v thin and look like knife blades
55
What are the gross + microscopic features of FTLD?
Gross: - frontotemporal lobe degenration --> knife blade atrophy - rest of brain is normal Micro:-neurons with round intracytoplasmic inclusions - Pick's bodies (tau protein)
56
What is the difference in the intracellular inclusions in alzheimers vs. FTLD?
alzheimers have NF tangles (abnormal tau protein) which appear irregular/tangled; whereas in FTLD the intracytoplasmic inclusions known as Pick's bodies (also abnormal tau proteins) are rounded
57
What anatomical structures are characteristically degenerated in huntington's disease?
Striatum - putamen - caudate nucleus **makes ventricle look OVAL SHAPED
58
What are the features of Huntington's disease?
- dementia - depression - choreiform (dance like) movements --> JERKING DEMENTIA - writhing (twisting) movements of limbs* *5th decade, progressive --> death in 15yrs
59
What gene mutation is responsible for huntingtons disease?
- autosomal dominant | - huntington gene on Chromosome 4p - protein huntington
60
What is associated with increased severity of huntingtons disease?
excess CAG tandem repeats
61
What is dementia pugilistica?
- punch drunk syndrome boxers --> TRAUMA - chronic traumatic encephalopathy - progressive dementia, tremor, focal neurological deficits - degeneration in septum pellucidum, thinning of corpus callosum and substantia nigra - NF tangles + A-beta amyloid accumulation --> SECONDARY ALZHEIMER'S *Muhammad Ali*
62
What is vascular dementia?
- multi-infarct dementia --> HTN, DM, AS, etc. - varying clinical features (location/size of infarcts) - mixed alzheimer and vascular lesions - common
63
What is binswanger disease?
small vessel damage --> HTN, DM, etc (vascular dementia)
64
What is the commonest type of MND?
ALS | -amyotropic lateral sclerosis
65
Wha are the features of ALS?
- progressive motor neuron loss - muscle weakness - fasciculations - spasticity (UMN lesion) - normal sensation (confined to MOTOR neurons)
66
What cells are associated with degeneration of UMN in ALS?
Betz cells in motor cortex
67
What vitamin deficiency is responsible for alcohol-associated CNS disorders?
B1 (thiamine) | -chronic alcoholics + also seen in pts with malabsorption syndromes
68
What is wernicke encephalopathy?
- thiamine deficiency (chronic alcoholics/malabsorption) - ataxia - confusion - double vision *mamillary body + 3rd ventricle haemorrhage
69
What is Korsakoff psychosis?
- thalamus - memory loss with confabulations (pt. tries to make up bits of stories due to inability to remember actual story) - hallucinations
70
What CNS features are associated with chronic alcoholism?
- wernicke encephalopathy - korsakoff psychosis - cortical atrophy - central pontine myelinolysis - atrophy of vermis of cerebellum --> ataxia
71
What does B12 deficiency cause with regards to CNS features?
- subacute combined degeneration of cord (SCDC) - both ascending + descending tracts (motor + sensory) - spastic ataxia - lower limb numbness - tingling
72
What vitamin deficiencies can cause neuropathies?
B12, B1 (thiamine), B2, B6, E
73
What is the difference between MS and MND?
MND: - progressive - bilateral demyelination - increased in males MS: - recurrent/episodic - irregular, patchy demyelination - increased in females
74
What is the pathogenesis of MS?
autoimmune condition --> Th1 + Th17 cells against myelin | *IgG in CSF (oligoclonal antibody)
75
What is Lhermitte's sign?
- shock like sensation that travels down the neck down the spinal cord - clinical finding in MS pts.

Pathology Term 4 (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions