Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

neurology > pathology III > Flashcards

pathology III Flashcards

1
Q

Dementia triad

A

Aphasia, apraxia, agnosia

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

What is apraxia

A

inability to perform preprogrammed motor tasks

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

What is agnosia?

A

inability to correctly interpret senses -cant recognize people, full bladder, pain

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

Presentation of parkinsons disease

A 
tremor
rigidity
akinesia (or bradykinsea)
postural instability
shuffling gait
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Which drug contaminant presents similarly to parkinsons disease?

A

MPTP - metabolized to MPP+ which is toxic to substantial nigra

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

histological findings of parkinsons disease

A

loss of dopaminergic neurons of substantia nigra pars compacta AND lewy bodies

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

What are lewy bodies?

A

intracellular eosinophilic inclusion composed of alpha-synuclein seen in Parkinson disease

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

Cause of huntingtons disease

A

Autosomal dominant trinucleotide repeated (CAG) expansion gene on chromosome 4

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

Symptoms of huntingtons disease

A

chorea, athetosis, aggression, depression, dementia

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

pathophys of huntingtons

A

Increased dopamine, decreasd GABA and Ach

Neuronal death via NMDA-R binding and glutamate excitotoxicity

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

Gross findings in huntington disease

A

Atrophy of caudate and putamen with ex vacuo ventriculomegaly

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

Why do down syndrome patients have increased risk of Alzheimer disease?

A

APP is located on chromosome 21

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

ApoE2 is associated with..

A

DECREASED risk of the sporadic form of Alzheimers

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

ApoE4 is associated with…

A

INCREASED risk of the sporadic form of Alzheimers

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

What are the familial altered proteins seen in Alzheimers disease

A

APP, presenilin-1, presenilin-2

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

Gross findings of Alzheimers

A

widespread cortical atrophy especially in the hippocampus. Narrowing of gyri and widening of sucli

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

Histological findings of alzheimers

A

senile plaques in gray matter: extracellular B-amyloid core; may cause amyloid aniopathy ->intracranial hemorrhage
Neurofibrillary tangles: intracellular hyperphosphorylated tau protein

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

What are neurofibrillary tangles

A

intracellular hyperphosphorylated tau protein - insoluble cytoskeletal elements; number of tangles correlates with degree of dementia

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

frontotemporal dementia aka

A

picks disease

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

presentation of frontotemporal dementia

A

Early chagnes in personality and behaviour (behavioural variant) or aphasia

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

Gross findings of frontotemporal dementia

A

frontotemporal lobe degeneration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Histological findings of frontotemporal dementia

A

inclusions of hyperphosphoryalted tau (round pick bodies) or ubiquinated TDP-43

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

Lewy body dementia presentation

A

visual hallucinations, dementia with fluctuating cognition/alerntess, REM sleep behaviour disorder and parkinsonism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

histological findings of lewy body dementia

A

intracellular lewy bodies primarily in cortex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
vascular dementia presentation
multiple arterial infarcts or chronic ischemia lead to a stepwise decline in cognitive ability with late-onset memory impairment
26
MRI/CT findings of vascular dementia
multiple cortical and/or subcortical infarcts
27
Creutzfeldt-Jakob disease presentation
Rapidly progressive dementia with myoclonus and ataxia
28
What will you see on an EEG of Creutzfeldt-Jakob disease?
periodic sharp waves
29
What will you find in the CSF of someone with Creutzfeldt-Jakob disease?
increased 14-3-3 protein
30
gross findings of Creutzfeldt-Jakob disease?
spongiform cortex
31
histological findings of Creutzfeldt-Jakob disease?
Prions (PrPc->PrPsc sheet results in beta pleated sheet resistant to proteases)
32
Idiopathic intracranial hypertension aka
pseudotumour cerebri
33
risk factors for idiopathic intracranial hypertension
female, tetracyclines, obesity, vitamin A excess, danazol
34
clinical findings of idiopathic intracranial hypertension
headache, tinnitus, diplopia, no change in mental status. Impaired optic nerve axoplasmic flow - > papilloedema. Enlarged blind spot and peripheral constriction. Lumbar puncture with increased opening pressure that provides temporary relief of headaches
35
treatment of idiopathic intracranial hypertension
weight loss, acetazolamide, invasive procedures for refractory cases (CSF shunt, optic nerve sheath fenestration surgery)
36
What causes communicating hydrocephalus?
Decreased CSF uptake from arachnoid granulations (eg. arachnoid scarring post-meningitis)
37
Presentation of communicating hydrocephalus
Increasd ICP, papilledema, herniation
38
Presentation of normal pressure hydrocephalus
urinary incontenence, gait apraxia, cognitive dysfunction
39
Treatment of normal pressure hydrocephalus
CSF shunt placement
40
What causes normal pressure hydrocephalus?
Usually idiopathic, but expansion of the ventricles results in distortion of the fibers in the corona radiata
41
What causes noncommunicating hydrocephalus?
structural blockage of CSF
42
Ex vacuo ventriculomegaly presentation
Appearance of increased CSF on imaging but its ACTUALLY due to decreased brain tissue and neuronal atrophy
43
Causes of ex vacuo ventriculomegaly
azheimers, advanced HIV, pick disease, huntington disease
44
Presentation of aquaductal stenosis
enlarging head circumference
45
Aquaductal stenosis cause
X-linked congenital narrowing | Can be from inflammation in utero
46
What is multiple sclerosis?
autoimmune inflammation and demyelination of CNS with axonal damage
47
Possible presentations of multiple sclerosis
Acute optic neuritis Brain stem/cerebellar syndromes Pyramidal tract demyelination Spinal cord syndromes
48
How does acute optic neuritis present?
painful unilateral vision loss associated with Marcus Gunn pupil
49
How do spinal chord syndromes present?
electric shock-like sensations, neurogenic bladder, paraparesis, sensory manifestations
50
Who is multiple sclerosis most common in?
Women aged 20 to 30 and farm from the equator
51
Symptoms of multiple sclerosis may present with what?
increased body temp (hot back, exercise)
52
findings in CSF of someone with multiple sclerosis
Increased IgG level and myelin basic protein | Oligoclonal bands - DIAGNOSITC
53
What will be seen on MRI of someone with MS?
periventricular plaques and multiple white matter lesions disseminated in space and time
54
Treatment of multiple sclerosis
Disease modifying therapies - B-interferon, glatiramer, natalizumab. Treat acute flares with IV steroids. Symptomatic treatment for neurogenic bladder, spasticity and pain
55
What is cerebral amyloid angiopathy?
Recurrent hemorhagic strokes from B-amyloid deposits in artery walls (that make them weak and prone to rupture)
56
Osmotic demyelination syndrome aka
Central pontine myelinosis
57
Pathophys of osmotic demyelination syndrome?
massive axonal demylination in pontine white matter secondary to rapid osmotic changes - most commonly from correction of hyponatremia but can be from shifts of other osmolytes
58
Presentation of osmotic demylination syndrome
acute paralysis, dysarthria, dysphagia, diplopia, loss of consciousness - causes locked in syndrome
59
if you raise sodium too fast what happens?
osmotic demyelination syndrome
60
if you decrease sodium too fast what happens?
cerebral edema/herniation
61
most common type of acute inflammatory demyelinating polyradiculopathy
guillain-barre syndrome
62
What cell type is destroyed in GBS?
Schwann cells
63
Pathophys of GBS
autoimmune destruction of schwann cells via inflammation and demyelination of motor fibers, sensory fibers, peripheral nerves. Facilitated by molecular mimicry and triggered by inoculations or stress.
64
GBS may be associated to which pathogen?
Campylobacter jejuni
65
Presentation of GBS
symmetric ascending muscle weakness/paralysis and depression/absent distal tendon reflexes Facial paralysis and respiratory failure common May present with autonomic dysregulation (cardiac irregularities, hypertension, hypotension) or sensory abnormalities.
66
CSF findings in GBS
increased protein with normal cell count (albuminocytologic dissociation)
67
Treatment of GBS
respiratory support is critical until recovery. Disease-modifying treatment; plasmapheresis or IV immunoglobulins.
68
Acute disseminated (postinfectious) encephalomyelitis pathophys
Multifocal inflammation and dyemylination after infection or vaccination
69
Presentatino of acute disseminated (postinfectious) encephalomyelitis
rapidly progressive multifocal neurologic symptoms and latered mental status
70
Charcot-Mari-Tooth disease aka
hereditary motor and sensory neuropathy
71
Deformities seen in Charcot-Mari-Tooth disease?
pes cavus, hammer tow
72
other symptoms seen in Charcot-Mari-Tooth disease?
foot drop/lower extremity weakness and sensory deficts
73
What causes Charcot-Mari-Tooth disease?
Autosomal dominant disorder caused by defective production of proteins involved in peripheral nerves
74
Most common type of Charcot-Mari-Tooth disease?
CMT1A
75
Mutation in CMT1A?
PMP22 gene duplication
76
What is progressive multifocal leukoencephalopathy?
demylination of CNS due to destruction of oligodendrocytes (from reactivation of JC virus)
77
Which virus causes progressive multifocal leukoencephalopathy?
JC virus
78
Which population gets progressive multifocal leukoencephalopathy?
aids patients with CD4 <200
79
outlook of progressive multifocal leukoencephalopathy?
Rapidly progressive and usualyl fatal
80
which brain areas are involved in progressive multifocal leukoencephalopathy?
parietal and occipital - visual symtpoms common
81
which drug is associated with progressive multifocal leukoencephalopathy?
natalizumab

neurology (9 decks)

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