Cerebrovascular disease

Question 1

What are to modes of response that nerve cell/ their processes have to injury?

Answer 1

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

Question 2

When does acute neuronal injury occur?

Answer 2

after hypoxia/ischaemia

Question 3

When is acute neuronal injury visible after an injury to the cell?

Answer 3

12-24 hours

Question 4

What is seen in acute neuronal injury?

Answer 4

shrinking and angulation of nuclei; loss of the nucleolus and intensely red cytoplasm

Question 5

What is Wallerian degeneration?

Answer 5

antegrade degeneration of axona and myelin sheath distal to injury

Question 6

What happens to the cell body when there is damage to the axon?

Answer 6

increased protein synthesis causing cell body swelling and an enlarged nucleolus; chromatolysis- migration and loss of Nissl granules

Question 7

When does simple neuronal atrophy occur?

Answer 7

with chronic degradation eg in MS or Alzheimers

Question 8

What is seen cellularly with simple neuronal atrophy?

Answer 8

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

Question 9

What are common examples of inclusions in neurones?

Answer 9

can accumulate with age; common in neurodegenerative conditions eg neurofibrillary tangles in Alzheimers and in viral infections

Question 10

What is a difference between the metabolism of astrocytes and neurones?

Answer 10

astrocytes carry out anaeriobic glycolysis

Question 11

What is the main cell involved in repair and scar formation in the brain?

Answer 11

astrocytes

Question 12

What is the most important indicator of CNS injury?

Answer 12

gliosis

Question 13

What occurs in gliosis?

Answer 13

astorpcyte hyperplasia nad hypertrophy; get enlarged vesicular nuclei with prominent nucleoli; cytoplasmic expansion with extension of ramifying processes

Question 14

How do old gliotic lesions appear?

Answer 14

nuclei become small and dakr and lie in a dense net of glial fibrils

Question 15

How are Schwann cells involved with axonal loss in the PNS?

Answer 15

Schwann cells can assist the regrowth of axons through organising a neural tube

Question 16

What type of damage are oligodendrocytes sensitive to?

Answer 16

oxidative damage

Question 17

What does disruption of ependymal cells lead to?

Answer 17

a local proliferation of sub-ependymal astrocytes to produce small irregularities on the ventricular surfaces termed ependymal granulation

Question 18

What are the two typees of microglial cell?

Answer 18

M1 and M2

Question 19

What is the function of M1 microglial cells?

Answer 19

pro-inflammatory, more chronic

Question 20

what is the function of M2 microglial cells?

Answer 20

anti-inflammatory, phagocytic and moreacute

Question 21

What is thought to be large reason the brain has such high energy demands?

Answer 21

neuronal membrane sodium/potassium ATPases for APs

Question 22

What is the maximum that cerebral blood flow can increase to maintain oxygen delivery?

Answer 22

twofold

Question 23

Why are neurones so vulnerable CNS cells?

Answer 23

metabolically dependent on oxidative phosphorylation

Question 24

What happens to the neurone with hypoxia nad hypoglycaemia and therefore energy failure?

Answer 24

there is neuronal depolarisation and astrocyte reuptake is inhibited so there is a glutamate soterm and excitation

Question 25

What does a glutamate storm lead to?

Answer 25

influx of calcium into the cell which results in protease activation; mitochondrial dysfunction; oxidative stress; apoptosis and necrosis

Question 26

What happens in cytotoxic oedmea?

Answer 26

osmotically active extracellular ions eg sodiu mand clhoride move into dying cells

Question 27

What does cytotoxic oedema lead to?

Answer 27

ionic and vasogenic oedema

Question 28

What causes ionic oedema?

Answer 28

because of cytotoxic oedema, the extracellular space is relatively devoid of sodium so sodium crosses the BBB, driving chloride entry and water

Question 29

What causes vasogenic oedema?

Answer 29

when there is deterioration and breakdown of the BBB albumin passes into the axtracellular space bringing water- not RBCs

Question 30

What is haemorrhagic conversion?

Answer 30

when integrity of the BBB is completely lost and blood enters the extracellular space

Question 31

What parts of the brain does the anterior cerebral artery sjupply?

Answer 31

media frontal and parietal lobes

Question 32

What areas does the middle cerebral artery supply?

Answer 32

the lateral frontal and temporal lobes

Question 33

Where does the posterior cerebral artery supply?

Answer 33

the occipital lobe

Question 34

What would be affected by a blockage in the anterior cerebral artery?

Answer 34

trunk legs sensory and motor abnormalities; frontal lobe dysfunction and higher cognitive dysfunction

Question 35

What would be affected by a blockage in the middle cerebral artery?

Answer 35

major bulk of the sensory and motor cortices would be affected

Question 36

What is global hypoxic ischaemia damage?

Answer 36

systemic compromise to circulation which cannot be compensated for by CNS autoregulation

Question 37

What is focal ischaemia?

Answer 37

restriction of blood flow to a localised area of the brain

Question 38

What are watershed areas?

Answer 38

zone between 2 arterial territories

Question 39

Which areas of the brain are most sensitive to global hypoxic ischaemic damage?

Answer 39

watershed areas

Question 40

Which neurones are most sensitive within the brain?

Answer 40

those within neocortex; hippocampus and purkinje cells of the cerebellum

Question 41

What is the most common area for thrombosis in the cerebral bloodsupply?

Answer 41

middle cerebral artery

Question 42

What is seen between 12-24 hours after cerebral infarction?

Answer 42

pale soft and swollen with illdefined margin between injured and normal brain; red neuron; cytotoxic and vasogenic oedema with generalised cell swelling

Question 43

What is seen 24-48 horus post infarction?

Answer 43

increasing neutrophils; extravasation of RBCs and activation of astrocytes and microglia

Question 44

What is seen 2-14 days post infarction?

Answer 44

brain is gelatinous and friable; oedeam demarcates lesion; microglia become predominant cell type; myelin breakdown; reactive gliosis

Question 45

What is seen several months post-infarction?

Answer 45

increasing liquification; eventual cavity lined by dark grey tissue; ongoing phagocytosis brings cavitation and surroung gliotic scar

Question 46

What is a gliotic scar characterised by?

Answer 46

astrocytes with abundant fine cytoplasmic processes

Question 47

What are the two causes of a haemorrhagic infarct?

Answer 47

haemorrhagic conversion and ischaemia; reperfusion results in haemorrhage thorugh damaged vessels

Question 48

What symtpoms are seen with middle cerebral artery lesions?

Answer 48

weakness predominantly contralateral face and arm

Question 49

What symptoms are seen with anterior cerebral artery lesions?

Answer 49

weakness and sensory loss in contralateral leg

Question 50

What symptoms are seen with vertebro-basilar artery disease?

Answer 50

vertigo; ataxia; dysarthrai and dysphagia- brainstemsyndrome

Question 51

What is name of the micro-aneurysms that develop with chronic hypertension?

Answer 51

Charcot-Bouchard

Question 52

Where are Charcot-Bouchard lesions often found?

Answer 52

in small MCA branches most commonly within the basal ganglia

Question 53

What are lacunar infarcts?

Answer 53

infarcts of deep cerebral white matter; basal ganglia or pons from a single small penetrating vessel

Question 54

What do lots of lacunar infarcts lead to?

Answer 54

multi-infarct dementia

Question 55

What are the causes of spontaneous intracranial haemorrhage?

Answer 55

intracerebral haemorrhage; sub-arachnoid haemorrhage and haemorrhagic infarct

Question 56

What is an important risk factor in spontaneous haemorrhage?

Answer 56

HT

Question 57

What are contributing factors to intracerbral haemorrhage?

Answer 57

aneurysm; systemic coagulation disorder; vascular malformation; amyloid deposits; vasculitis; neoplasm

Question 58

How does amyloid angiopathy lead to haemorrhage?

Answer 58

deposition of protein leads to vessels becoming less compliant and more likley to rupture and lead to a lobar intracerebral haemorrhage

Question 59

What are the most common vascular malformations leading to haemorrhage?

Answer 59

AV malformations; cavrnous angioma

Question 60

As well as bleeding what else are AV malformations implicated in?

Answer 60

are SOLs which can lead to focal neuro deficits; seizrues and headaches

Question 61

Where are AVMs most commonly founjd?

Answer 61

in cerebral hemispheres in MCA territory

Question 62

What is the most common cause of a subarachnoid haemorrhage?

Answer 62

rupture of a saccular aneurysm eg Berry

Question 63

Where are the majority of subarachnoid haemoorhages?

Answer 63

in the territory of the ICA, at arterial bifurctions

Question 64

What happens due to the mass effecti nthe ubsarachnoid space?

Answer 64

CSF is obstructed leading to hydrocephalus

Question 65

What are the symtpoms of subarachnoid haemorrhahge ?

Answer 65

severe headache; vomiting and LOC; meningeal signs