Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Neurology > Pathology > Flashcards

Pathology Flashcards

(79 cards)

Start Studying
1
Q

cellular responses to injury

A

rapid necrosis

slow atrophy

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

what is Nissl substance

A

large granular body in neurons - RER

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

when is a red neuron found

A

in acute neuronal injury

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

how does a red neuron arise

A

hypoxia/ischaemia

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

when are red neurons visible

A

12-48 hours after irreversible insult to cell

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

why is a red neuron called what it is

A

intensely red cytoplasm

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

list other neuronal responses to injury

A

axonal
chronic degeneration
sub cellular alterations - inclusions

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

What is Wallerian degeneration

A

axonal response to injury where there is degeneration of myelin and axon distal to site of injury

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

give an example of subcellular alterations / inclusions

A

neurofibrillary tangles in Alzheimers

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

What is the main cell involved in repair and scar formation

A

astrocytes

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

what is gliosis

A

astrocyte damage

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

what are the early stages of gliosis

A

hyperplasia and hypertrophy of astrocytes

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

what is the most important histopathological indicator of CNS injury regardless of cause

A

gliosis

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

what does damage to oligodendrocytes result in

A

demyelination

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

what are oligodendrocytes sensitive to

A

hypoxia

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

Ependymal cells have a limited response to injury, true or false

A

true

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

M2 microglia are anti/pro inflammatory

A

ANTI inflammatory

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

causes of nervous system injury

A 
hypoxia 
trauma 
toxins 
metabolic abnormalities 
nutritional deficiencies 
infections 
genetics 
ageing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Why is excitotoxicity important

A

important mediator of neuronal injury

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

what is excitotoxicity

A

hypoxia leads to reduced ATP production and so reduced energy followed by neuronal depolarisation
glial cells fail to reuptake glutamate resulting in a glutamate storm
this excites post synaptic GluR resulting in rapid Ca2+ accumulation in post synaptic neuron

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

what are the 3 outcomes of Ca2+ accumulation in excitotoxicity

A

protease activation
mitochondria dysfunction
oxidative stress

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

what is cytotoxic oedema

A

accumulation of Na and Cl in the CELL resulting in a shift of water to the cell also

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

causes of cytotoxic oedema

A

alcohol intoxication
Reye’s
hypothermia

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

what is ionic/osmotic oedema

A

movement of Na, Cl and water into interstitium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
causes of ionic oedema
SIADH | increased water uptake
26
what is vasogenic oedema
disruption of BBB resulting in larger molecules like albumin bringing in water
27
causes of vasogenic oedema
``` trauma tumours inflammation infection encephalopathy ```
28
what is haemorrhagic conversion
BBB is majorly disrupted that RBCs enter
29
in global hypoxic ischaemic damage, what does the MAP fall below
50mmHg
30
define stroke
sudden disturbance of cerebral function of vascular origin that causes symptoms lasting more than 24 hours
31
what can cause cerebral infarction
thrombus from atherosclerosis - commonly MCA | embolus - from internal carotid artery or from the heart
32
what type of necrosis occurs in the brain
liquefactive necrosis
33
consequences of hypertension in the brain
lacunar infarct strokes vascular dementia ruptured aneurysms and intra-cerebral haemorrhage hypertensive encephalopathy
34
what are lacunar infarcts
small infarcts in deep cerebral white matter, basal ganglia or pons
35
what type of necrosis do you get in blood vessels
fibrinoid necrosis
36
what is hypertensive encephalopathy
HTN and raised ICP brain herniation global cerebral oedema petechiae
37
what illicit drugs can cause intra cerebral haemorrhage
cocaine | alcohol
38
what is amyloid angiopathy
accumulation of abnormal B sheet proteins resulting in stiffened vessels and HTN
39
cellular constituents of CSF
``` clear fluid No WBC low protein no RBCs glucose >2.2 ```
40
what is hydrocephalus
accumulation of excessive CSF in ventricular system of brain
41
3 main causes of hydrocephalus
obstruction of CSF flow decreased CSF resorption CSF overproduction
42
hydrocephalus calssification
communicating | non-communicating
43
what is non-communicating hydrocephalus
obstruction to CSF flow withIN the ventricular system
44
what is communicating hydrocephalus
obstruction to CSF flow OUTwith the ventricular system
45
what is hydrocephalus ex vacuo and in which degenerative condition is it seen in
loss of brain parenchyma resulting in secondary ventricular dilatation and increase in CSF Alzheimer's disease
46
causes of raised ICP
tumour / SOL hydrocephalus oedema
47
consequences of raised ICP
brain herniations CN palsies visual distrubances
48
list some causes of SOL
tumour abscess haemorrhage oedema
49
what is the most common primary malignant tumour in: adults children
adults - astrocytoma | children astrocytoma and medulloblastoma
50
what is the most common primary benign tumour in: adults children
adults - meningioma | children - craniopharyngioma
51
medulloblastoma is radio/chemosensitive
radiosensitive
52
what is demyelination
preferential damage to myelin sheath with relative preservation of axons
53
examples of primary demyelination in the CNS
MS acute disseminated encephalomyelitis acute haemorrhagic leukoencephalitis
54
secondary causes of demyelination in CNS
viral - JC virus metabolic toxic
55
describe MS plaques
well demarcated irregularly shaped vary in size non-symmetrical distribution
56
commonly affected areas by MS plaques
``` lateral ventricle area corpus callosum optic nerves and chiasm brainstem ascending and descending tracts cerebellum spinal cord ```
57
describe the histology of active plaques in MS
perivascular inflammatory cells microglia ongoing demyelination
58
describe the histology of inactive plaques in MS
gliosis little remaining myelinated axons reduced number of oligodendrocytes and axons
59
macroscopically, what colour are active plaques
yellow/brown | ill defined edge
60
macroscopically, what colour are inactive plaques
grey/brown | well demarcated
61
what is the immunopathology of MS
lymphocytic infiltration oligoclonal bands in CSF HLA DRB1 Th1 and Th27 cells
62
is dementia a normal part of the ageing process
no it is always pathological
63
list primary causes of dementia
Alzheimer's Lewy body dementia Frontotemporal dementia/Pick's disease Huntington's disease
64
list secondary causes of dementia
``` vascular/multi infarct infection trauma metabolic drugs and toxins SOLs ```
65
what is the most common cause of dementia in the elderly
Alzheimer's disease
66
genetics of Alzheimer's disease
APP presenalin 1+2 trisomy 21 ApoE4
67
macroscopic appearance of Alzheimer's disease
cortical atrophy - frontal, parietal, temporal lobes widened sulci and narrowed gyri hydrocephalus ex vacuo
68
microscopic features of Alzheimer's disease
simple neuronal atrophy gliosis neurofibrillary tangles amyloid plaques/neuritic plaques
69
what are neurofibrillary tangles
intracellular bundles of Tau protein
70
what is amyloid angiopathy
extracellular eosinophilic accumulation of Abeta sheets
71
appearance of amyloid with congo red stain
apple green birefringence
72
features of Lewy body dementia DLB
progressive hallucinations fluctuating levels of attention
73
all DLB get PD but not all PD get DLB, true or false
true
74
what are lewy bodies
a-synuclein aggregrates + ubiquitin
75
what is frontotemporal dementia FTD also known as
Pick's disease
76
onset of FTD
early <65 yo
77
symptoms of FTD
social disinhibition personality change rapidly progressive
78
atrophy of what happens in FTD
frontal and temporal lobes
79
what are Pick's bodies
intracytoplasmic filamentous inclusions seen in Pick's disease

Neurology (25 decks)

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