Brainscape's Knowledge GenomeTM

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


See full index

Scientific Basis of Clinical Practice > CNS Pathology > Flashcards

CNS Pathology Flashcards

1
Q

describe the function of neurones

A

cells specialised for rapid communication

connected to one another by a series of synapses through the transfer of neurotransmitters

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

describe the function of neuroglia

A

form the scaffolding of the nervous system

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

describe macroglia and their subtypes

A

a subtype of neuroglia
oligodendrocytes; form myelin and aid impulse transport down the axon
astrocytes; metabolic buffers, detoxifiers, supply nutrients, electrical insulators, involved in repair and scar formation
ependymal cells; line the ventricle system

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

describe microglia and their function

A

another subtype of neuroglia

a fixed macrophage system within the CNS and respond to injury

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

describe the pathway of CSF

A

produced b the choroid plexus of the lateral 3rd and 4th ventricles
exits through the foramina of luschka and magendie into the subarachnoid space between the arachnoid and Pia mater
descends into the spine or ascends to the cerebellum and cerebral hemispheres
absorbed in the superior sagittal sinus

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

what are the causes of hydrocephalus?

A

posterior fossa/brain stem tumours
colloid cysts
resolving arachnoid haemorrhage
chiari malformations; defect in the posterior fossa or cerebellum
dandy-walker syndrome; cerebellar hypoxia and cyst formation
choroid plexus papilloma; excess CSF production

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

describe hydrocephalus ex vacuo

A

compensatory CSF seen in certain dementias

ventricular enlargement due to loss of brain parenchyma

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

what are the normal cranial contents?

A

brain; 70%
CSF; 15%
blood; 15%

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

what are the main causes of raised intracranial pressure?

A

tumours
abscesses
areas of infarction
haemorrhage

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

what are the symptoms and signs of raised intracranial pressure?

A 
headache
vomiting
confusion
focal neurological signs; paralysis, hemianopia, dysphagia
depressed conscious level
respiratory depression
bradycardia
seizures
papilloedema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what are the stages of raised intracranial pressure?

A

spatial compensation; one of the cranial contents expands
ICP rises slowly; systemic arterial pressure rises to maintain cerebral perfusion (Cushing’s response)
ICP rises rapidly as cerebral perfusion drops
cerebral vasomotor paralysis; cerebral circulation ceases

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

what re the consequences of raised ICP?

A

flattening of the gyral pattern of the cerebral hemispheres
unilateral lesion; compression of the ventricular system and a shift of the midline structures
herniation of the brain matter; through the foramen magnum, flax cerebri and tentorial incisura

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

what re the types of internal herniation?

A

supracallosa/subfalcine; cingulate gyrus herniates under falx cerebri

uncal herniation; 3rd CN or posterior cerebral artery compression, haemorrhage of midbrain and pons

tonsillar herniation; cerebellar tonsils displaced down foramen magnum, brain stem compression (life threatening)

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

what are the signs of 3rd CN compression?

A

dilated pupils

loss of eye movements

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

what are the consequences of posterior cerebral artery compression?

A

infarction of its supplied territory

secondary haemorrhage into the brain stem

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

what are the types of cerebral oedema?

A

vasogenic; disruption of the brain barrier, adjacent to a tumour, haemorrhage or abscess or due to sepsis
cytotoxic; increase in intracellular fluid secondary to an insult (hypoxia or ischaemia)
interstitial; increase in water content with in the periventricular tissue (acute hydrocephalus)

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

what is the treatment of cerebral oedema?

A

based on the cause
steroids; tumours
surgery; haemorrhage

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

describe the types of cerebral ischaemia

A

focal; involvement of a territorial artery

global/diffuse; ischaemia due to decreased cerebral perfusion across the entire brain (cardiac arrest, severe shock)

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

define stroke

A

rapidly progressive clinical symptoms of focal/global los of cerebral function
>24hrs or leading to death
no apparent cause other than vascular origin

TIA; <24hrs

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

describe the macroscopic brain changes in a stroke

A

6hrs; minimal change
48hrs; tissue becomes pale, soft and swollen, less of a sharp margin between grey and white matter
2-10 days; area becomes gelatinous and friable
3 weeks; tissue liquifies into a cavity

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

describe the microscopic brain changes in a stroke

A

12hrs; red neurones and oedema
48hrs; inflammatory response, compromising neutrophil polymorphs
2-3 weeks; increasing numbers of microglia or macrophages, reactive astrocytosis surround area of infarction

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

what conditions are associated with mural thrombosis?

A

previous MI; blood stasis and thrombus formation
valve disease; turbulent flow
AF

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

what are the causes of emboli?

A 
ventricular septal defects
AF
previous MI
valve disease
cardiac surgery
tumour
air
debris from infected valves in acute bacterial endocarditis
trauma; multiple fractures
aggressive cardiopulmonary resuscitation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

describe intracerebral haemorrhage

A

haemorrhage into the parenchyma or tissue
usually from rupture of the small intraparenchymal blood vessels
most common cause; hypertension
second most common cause; amyloid angiopathy
can be caused by trauma
diffuse axonal injury; acceleration and deceleration forces on the head
>2hrs; stain for beta-APP on histology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

describe Charcot Bouchard aneurysms

A

caused by weakening by hyaline arteriosclerosis

predisposing lesion to vessel rupture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what are the effects of hypertension on the CNS?

A 
large vessel disease
small vessel disease
charcot Bouchard aneurysms
lacunar infarcts
slit haemorrhages
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

describe the pathophysiology of amyloid angiopathy

A

the media of the small penetrating vessels is replaced by amyloid
staining; amyloid immunological stain, Congo red stain (shows up apple green)
causes weakening in the vessel walls
increases the likelihood of rupture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what are the causes of non-traumatic intracerebral haermorrhage?

A 
hypertension
amyloid angiopathy
anticoagulant therapies; warfarin
tumours
vasculitic diseases
AV malformation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

describe AV malformations

A

can cause intracerebral and subarachnoid haemorrhages
most common in the 3rd/4th decade
more common in males

30
Q

what are the types of non-traumatic intracranial haemorrhage?

A

intracerebral

subarachnoid

31
Q

what are the causes of non-traumatic subarachnoid haemorrhages?

A

berry aneurysms

AV malformations

32
Q

describe berry aneurysms

A

most commonly found near the major arterial branch points of the cerebral arteries
40%; between the anterior communication and anterior cerebral arteries
associated with PKD, neurofibromatosis, marfan’s syndrome

33
Q

name the types of haemorrhage

A

extradural
subdural
subarachnoid
intracerebral

34
Q

describe extradural haemorrhages

A

blood collects between the skull and the dura
a squamous temporal fracture tearing the middle meningeal artery
slow accumulation of blood
compensatory mechanisms can slow the rise of ICP; lucid interval between injury and death
death; cerebral compression and herniation

35
Q

describe subdural haemorrhages

A

resulting from the tearing of bridging veins; typically during a fall where the brain moves relative to the dura
haemorrhage between the dura mater and the arachnoid mater
increased risk in patients with cerebral atrophy; elderly, alcoholics
presentation; minor injury, headache, confusion developing over 48hr, abrasion of the back of the scalp

36
Q

describe subarachnoid haemorrhages

A

bleeding beneath the arachnoid matter
most commonly caused by a ruptured berry aneurysm
associated with severe contusions, fractured skull, blood from an intraventricular haemorrhage, neck blows
rapid loss of conscious and death

37
Q

name some of the symptoms and signs of brain tumours

A 
new onset epilepsy
hydrocephalus
focal neurological deficit
balance and gait problems
visual field defects in pituitary tumours
38
Q

what are the first line investigations to diagnose a brain tumour?

A

radiological; CT or MRI

confirm diagnosis; brain biopsy or brain smear

39
Q

what is the treatment of brain tumours?

A

surgery; depends on whether the deficit is worth it
chemoradiotherapy; blood brain barrier makes this difficult, affects cognitive ability and vision
proton beam therapy; precisely targeted and reduces damage to surrounding tissues and organs

40
Q

what are the causes of a black eye/orbital contusion?

A

direct blow; punch
injury to the front of the scalp; bruising
basal skull fracture; racoon eyes

41
Q

describe scalp lacerations

A

the skin is crushed onto the rigid skull during a blunt impact
can be located on the back of the scalp following backwards falls
stellate laceration just above the occipital protuberance

42
Q

what are the types of scalp surface injury?

A 
bruises/contusions
abrasions/grazes
lacerations/cuts
incisions/slashes
stab/penetrating wounds
43
Q

what are the types of skull fracture?

A 
linear
comminuted
depressed
contra-coup
hinge
ring
pond; ripple/spider web
diastatic
44
Q

what are the common areas of cerebral contusion?

A

frontal poles
orbital surfaces of the frontal poles
temporal poles
cortex adjacent to the Sylvian fissure

45
Q

define coup and contrecoup

A

coup; cerebral injury at the point of contact

contrecoup; injury to the surface opposite the point of contact, after sudden deceleration

46
Q

describe traumatic subarachnoid haemorrhage

A

a rare cause of death following a single blow
causes a tear within the vertebral basilar arterial system
may chronically cause hydrocephalus due to CSF blockage

47
Q

describe diffuse axonal injury

A

blunt impact or severe acceleration/deceleration forces may cause tearing of tiny blood vessels
widespread axonal damage
immediately unconscious and remain in a vegetative state

48
Q

describe the histology of diffuse axonal injury

A

widespread axonal swelling duet B-APP

highlighted by silver impregnation techniques

49
Q

what are the effects of raised ICP?

A

flattening of the gyro pattern
compression of the ventricular system
internal herniations
if caused by a space-occupying lesion (extradural/subdural haemorrhage); lateral shift of the midline structures

50
Q

what are the features of age-related cerebral atrophy?

A

flattening of the general pattern across the cerebral hemispheres
widening of the sulk
compensatory enlargement of the ventricular system
hippocampus affected in Alzheimer’s disease
substantia nigra affected in Parkinson’s disease

51
Q

what are the characteristics of neurodegeneration?

A

progressive neuronal dysfunction and death
degeneration often affects specific systems implying some form of selective vulnerability
incidence tends to increase with age

52
Q

describe dementia

A

a global impairment of higher intellectual function; intellect, reason and personality, through alterations in mood and behaviour
increases with age
affects more females

53
Q

describe the gross changes of Alzheimer’s disease

A

brain weight <1000g
global atrophy; particularly the frontal and parietal lobes
compensatory enlargement of the ventricular system
widening of the sulci due to cortical atrophy

54
Q

describe the microscopic changes of Alzheimer’s disease

A

neurofibrillary tangles
senile (neuritic) plaques
amyloid angiopathy
varying degrees of neuronal loss and reactive astrocytosis

55
Q

what are the histological findings of Alzheimer’s disease?

A

deposition of amyloid beta subtype protein within the brain parenchyma
concentrated in the hippocampus and neocortex
stained suing conga red stain; apple green
neurofibrillary tangles; largely composed of protein tau which can be highlighted by silver staining
amyloid enruopathy
varying degrees of neuronal loss and reaction; astroycytosis

56
Q

describe vascular/multi-infarct dementia

A 
stepwise progression corresponding to the episodes of infarction
hypertension-driven arteriosclerosis
more common in males
characterised by lacunar infarcts
cortex and basal ganglia involvement
57
Q

what are the types of dementia?

A 
alzheimer's disease
vascular dementia
Lewy body dementina
pick's disease
CJD
58
Q

describe pick’s disease

A

rare
presents between 25-90
<1000g brain
early onset behavioural and personality changes; selective frontal lobe atrophy
language disturbances; temporal lobe atrophy
neuronal loos most severe in the outer 3 layers of the cortex; neuronal swelling (Pick cells)

59
Q

define Creutzfeldt jakob disease

A

rapid progression dementia recently accompanied by myoclonus and clinical evident cerebellar degeneration

60
Q

describe creutzfeldt Jakob disease

A

transmissible spongiform encephalopathy (prion disease)
prions; abnormal form of a normal cell protein, capable of replication and causing infection
can be sporadic or familial
rapidly progressive
associated with myoclonus and ataxia
death; usually 3-12 months after onset

61
Q

describe the gross and histological findings of Creutzfeldt Jakob disease

A

gross; brain may be normal

histology; vacuoles/spongiosis in grey matter

62
Q

what are the clinical features of Parkinson’s disease?

A 
diminished facial expressions
stooped posture
pill rolling tremor
rigidity
bradykinesia
festinating gait
63
Q

describe Parkinson’s disease

A

degeneration fo the dopaminergic neurones of the substantia nigra
severity proportional to the drop in dopamine
early symptoms can be managed by L-dopa

microscopy; pallor of the substantia nigra and locus cereleus
lewy bodies; alpha synuclein and ubiquitin

64
Q

what are the clinical features of Huntington’s disease?

A

chorea
rigidity
cognitive decline
often associated with cognitive impairment

65
Q

what are the gross and histological features of Huntington’s disease?

A

gross; cerebral atrophy and striking atrophy in caudate nucleus and putamen
microscopically; loss of striata neurones, reactive astrocytosis

66
Q

describe multiple sclerosis

A

characterised by plaque formation within the CNS
clinically; fluctuates with periods of relapse and remission
affects more females
peak onset; 22-40yrs

67
Q

what are the causes of multiple sclerosis?

A

more frequent in northern geographical regions
genetic link
immunological; possibly precipitated by a viral infection

68
Q

what are the clinical features of multiple sclerosis?

A

unilateral visual impairment due to optic nerve impairment
brain stem involvement; ataxia, nystagmus, diplopia
spinal cord involvement; parasthesia, sensory impairment, muscle spasms, incontinence

69
Q

what are the CSF findings in multiple sclerosis>

A

60%; increased protein concentration
40%; IgG increase
oligoclonal bands on electrophoresis

70
Q

what are the gross and microscopic features of multiple sclerosis?

A

gross; grey-tan irregular plaques in white matter

microscopy; perivascular inflammation and macrophage reaction in association with myelin breakdown
reduction in oligodendrocytes with relative preservation of axons

Scientific Basis of Clinical Practice (10 decks)

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