Cerebrovascular Disease Flashcards Preview

Neurology > Cerebrovascular Disease > Flashcards

Flashcards in Cerebrovascular Disease Deck (68):
1

what are bridging veins

perforate through the arachnoid and dura, very delicate and can rupture in trauma

2

what are the types of glial cells and their functions

astrocytes- supporting structures in brain
oligodendrocytes- myelination
ependymal cells - ciliated cuboidal/ columnar epithelium that lines the ventricles
microglia- immune monitoring and antigen presentation

3

what can damage to nerve cells lead to

rapid necrosis with sudden acute functional failure
slow atrophy with gradually increasing dysfunction

4

what is nissl substance

material consisting of granular endoplasmic reticulum and ribosomes that occurs in nerve cell bodies and dendrites

5

what is acute neuronal injury/ red neurone

occurs due to hypoxia/ ischaemia
results in neuronal cell death
-shrinking and angluation of nuclei
-loss of the nucleolus
-intensely red cytoplasm

6

what are the axonal responses to nerve injury

increased protein synthesis (cell body swells, enlarged nucleus)
chromatolysis (margination and loss of nissl substance)
degeneration of axon and myelin sheath distal to injury (wallerian degeneration)

7

what happens in neuronal atrophy (chronic degeneration)

shrunken, angulated and lost neurones, small dark nuclei, accumulation of lipofuscin pigment, reactive gliosis

8

what are sub cellular alterations (inclusions) cell damage

happen in neurodegenerative conditions
inclusions accumulate with ageing/ in viral infections

9

what type of damage are oligodendrocytes sensitive

oxidative damage

10

what cell type is damage in demyelinating disorders

oligodendrocyte

11

what does damage to the myelin sheath cause

reduced conduction and exposition of the axon

12

what do astrocytic processes do

envelop synaptic plates
wrap around vessels and capillaries within the brain (how they control BBB and cerebral blood flow)

13

what is the role of astrocytes

ionic, metabolic and nutritional homeostasis (do anaerobic glycolysis and give lactate to neurones. also moderate glutamate production)
work in conjunction with endothelium to maintain BBB
repair and scar formation (as no fibroblasts to do this)

14

what is gliosis

an astrocytic response that indicated CNS damage
astrocyte hyperplasia and hypertrophy
nucleus enlarges, becomes vesicular, nucleolus is prominent
cytoplasmic expansion

old lesions (equivalent to scarring)- meshwork of glial fibrils

15

what do ependymal cells provide a pathway for

ascending infection (line ventricles)

16

what are the possible causes of nervous system injury

Hypoxia
Trauma
Toxic insult (exogenous and endogenous due to metabolic sustances within brain)
Metabolic abnormalities
Nutritional deficiencies
Infections
Genetic abnormalities
Ageing

17

what can cause CNS hypoxia

cerebral ischaemia, infarct, haemorrhage, trauma, cardiac arrest, cerebral palsy

18

how much of total body resting oxygen does the brain consume

20%

19

how much can cerebral blood flow increase to maintain oxygen consumptoms

only two fold

20

what happens after onset of ischaemia in the brain

mitochondria inhibit ATP synthesis
ATP reserves consumed within a few minutes

21

what is excitotoxicity

In context of energy failure- neuronal depolarisation causing glutamate release
At same time re uptake of glutamate by astrocytes is inhibited due to energy failure causing accumulation in synaptic space creating a glutamate store which leads to excitation of the post synaptic glutamate receptors= rapid accumulation of Ca in post synaptic neurone what causes;
protease activation
mictochondrial dysfunction
oxidative stress

these things are the main mediators of injury

22

what are the types of oedema

cytotoxic (pre morbid process, accumulation of Na and Cl in neurones moves water from interstitium into cell)

ionic (water goes into interstitium because of deficiency caused by cytoxic oedema)

vasogenic (large molecules like albumin enter interstitium from vessels (more marked swelling that ionic)

haemorragic (blood cells cross BBB if vessel damage bad enough)

23

what helps to maintain blood brain flow

autoregulatory mechanisms
dilatation and constriction of cerebral vessels

24

what is the definition of cerebrovascular disease

any abnormality of brain caused by a pathological process of blood vessels

25

what are the main manifestations of cerebrovascular disease

brain ischaemia and infarction
haemorrhages
vascular malformations
aneurysms

26

what is global hypoxic ischaemic damage

generalised reduction in blood flow/ oxygenation
causes:
-cardiac arrest
-severe hypotension (hypovolaemic shock)
-trauma

27

what is focal cerebral ischaemia and infarction

where the is restriction of blood flow to a localised area of the brain
e.g. a vascular obstruction

28

what are the watershed areas

zone between two arterial territories
particular sensitive to loss of BP

29

what cell type is most sensitive to hypoxia in brain

neurones, especially in neocortex and hippocampus

30

a blood pressure below what leads to hypoperfusion in the brain

50 mmhg

31

what is a stroke

sudden disturbance of cerebral function of vascular origin that causes death or lasts over 24 hours

32

what causes a infarction stroke

interuption of blood flow due to thrombosis or emboli

33

are men or women more likely to have an infarction stroke

men

34

what causes a thrombotic stroke

thrombosis in an atherosclerotic segment
mostly middle cerebral artery

35

what causes an embolic strole

from atheroma in internal carotid or aortic arch or heart

36

what are the rarer causes of cerebral infarction stroke

osteophytes compressing vertebral circulation, vasculitis, septal defects (e.g. left to right shunt creates emboli)

37

what are the risk factors for an infarction stroke

atheroma (intracranial -esp basilar- and extracranial- esp carotid and aorta)
hypertension (risks atheroma and atherosclerosis)
serum lipids, obesity, diet
diabetes mellitus
heart disease
diseases of neck arteries
drugs
smoking
septal defects

38

in a cerebral infarction what is the extent of damage determined by

arterial territory of the affected artery
timescale of occlusion
extend of collateral circulatory relief
systemic perfusion pressure

39

what happens to the brain after 48hrs of an infarction

become gelatinous and friable

40

what is the most common cell type in area of damage after 2 days of an infarction

microglia

41

when does gliosis begin

after a week of infarction

42

when does a gliotic scar form

a few weeks after infarction

43

what is a haemorrhagic infarct

In the context of an infarct the BBB deteriorates
haemorhagic conversion happens

44

what happens if you thrombolyse an infarct too late

BBB will be damaged too much and will cause a haemorrhage

45

localise the vascular lesion:
contra‐lateral weakness or sensory loss. If dominant hemisphere, may be aphasia or apraxia

carotid artery disease

46

localise the vascular lesion:
weakness predominantly contralateral face and arm

middle cerebral artery

47

localise the vascular lesion:
weakness and sensory loss in contralateral leg

anterior cerebral artery

48

localise the vascular lesion:
vertigo, ataxia, dysarthria, and dysphasia

(brain stem syndromes)
vertebro-basilar artery disease

49

how does hypertension increase risks of stroke

accelerates atherosclerosis
creates lacunes (CSF cavity in basal ganglia/ white matter- leads to lacuna infarcts)
micro aneurysms (charcot bouchard) in small arteries (esp basal ganglia)
fibrinoid necrosis of vessel walls if severe

50

what are the different consequences of HPTx in the brain

lacunar infarcts (atheroma, embolism in small penetrating vessels leads to occulsion (esp in basal ganglia)
multi infarct dementia
ruptured aneurysms and intracerebral haemorrhage
hypertensive encephalopathy (in acute malignant hptx)
(global cerebral oedema, tentorial and tonsilar herniation, petechiae and arteriolar fibrinodnecrosis)

51

what are lacunar infarcts

small lake like infarcts due to occulsion of small penetrating vessels
particularly affect basal ganglia
when multiple can contribute to multi infarct dementia

52

what is seen clinically in hypertensive encephalopathy

severe hypertension
symptoms of raised ICP

53

what is found pathologically in hypertensive encephalopathy

global cerebral oedema
tentorial and tonsilar haemorrhages
ateral fibrioid necrosis
petechiae

54

what are the types of spnotaneous intracranial haemorrhage

intracerebral
sub arachnoid
haemorrhagic infarct

55

what are the types o traumatic intracranial haemorrhage

extra dural
sub dural
contusion (surface bruising)
intracerebral
sub arachnoid

56

what are the contributing factors to a intracerebral haemorrhage

Hypertension

Aneurysms

Systemic coagulation disorders
Iatrogenic anticoagulation

Vascular malformations

Amyloid deposits (cerebral amyloid angiopathy)

Open heart surgery
Neoplasms
Vasculitis (infectious and non‐infectious)

causes of vascular injury/ disease
-hptx
-amyloid
-diabetes
-drugs, cocaine, alcoholism
-vascullitis

57

where do intracerebral haemorrhages most commonly occur

basal ganglia
thalamus
cerebral white matter
cerebellum

58

what usually surrounds an intracerebral haemorrhage and causes more damage

oedema
adjecent tissue also softens
can cause herniations

59

what happens in amyloid angiopathy

beta sheet of amyloid stick together, form a plaque and make vessels unable to respond to changes in BP= rupture = intracerebral haemorrhage

60

what does amyloid angiopathy happen in

Alzheimers and in old age

61

what types of vascular malfnormations cause intracranial haemorrhages

AVM
cavernous angiomas
venous angiomas
capilary teleangectases

62

what else in brain can vascular malformations cause

headaches, seizures and focal neurological deficits

63

describe an anteriovenous malformation in the brain

abnormal tortuous vessels (conglomeration of arteries and veins)
shunting from artery to vein which:
-undergoes hypertrophy
-is not compliant and ruptures easily
-forms aneurysms- rupture

64

what is the most common cause of a subarachnoid haemorrhage

rupture of a saccular aneurysm (berry aneurysm)
-905 in ICA territory
-10% in vertebrobasilar

65

what causes a berry aneurysm

arise in aterial bifurcations arising from circle of willis
acquired degenerative lesion due to chronic haemodynamic injury to the vessel
associated with genetic PCKD and hormone abnormalities

66

what is seen pathologically after the rupture of a berry aneurysm

Intracerebral haematomas adjacent to aneurysms

Infarcts of brain parenchyma may also develop – due to arterial spasm

Mass effect of haematoma and features of raised ICP.

Hydrocephalus: acute and chronic (accumulation of CSF as poor flow across surface)

67

what are the risk factor for a subarachnoid haemorrhage

(berry aneurysm)
smoking
hptx
kidney disease

68

what is the clinical features of a sub arachnoid haemorrhage

severe headache
vomiting
loss of consciousness
women> men
survivors at risk of hydrocephalus