Cerebrovascular disease Flashcards
(108 cards)
1
Q
What are the three types of glial cells?
A
Astrocytes Oligodendrocytes Ependymal cells
2
Q
What are the supporting structures of the CNS?
A
Connective tissue Meninges Blood vessels
3
Q
What does damage to nerve cells and/or their processes lead to?
A
Rapid necrosis with sudden acute functional failure (as seen in stroke) Slow atrophy with gradually increasing dysfunction (as seen in age-related cerebral atrophy)
4
Q
How are neurones organised?
A
- aggregates: nuclei, ganglia - columns/layers - assigned functional domains
5
Q
What is the perikaryon and its variation in size?
A
The cell body of a neurone- can vary from 10 to 50um
6
Q
When does acute neuronal injury occur?
A
Context of hypoxia/ischaemia
7
Q
When does a red neurone become visible?
A
Typically 12-24 hours after an irreversible ‘insult’ to the cell
8
Q
What does acute neuronal injury result in?
A
Neuronal cell death
9
Q
What pattern is seen in acute neuronal injury?
A
- shrinking and angulation of nuclei - loss of the nucleolus - intensely red cytoplasms
10
Q
What are the axonal reactions to injury/disease?
A
- increased protein synthesis -> cell body swelling, enlarges nucleolus -chromatolysis- margination and loss of nissl granules - degeneration of axon and myelin sheath distal to injury ‘‘wallerian degeneration’’
11
Q
What is simple neuronal atrophy?
A
Chronic degeneration - shrunken, angulated and lost neurons, small dark nuclei, lipofuscin pigment, reactive gliosis
12
Q
What are sub cellular alterations- inclusions?
A
Common in neurodegenerative conditions, e.g. neurofibrillary tangles in Alzheimers disease Inclusions appear to accumulate with ageing Also get inclusion in viral inflectional affecting the brain
13
Q
Describe the shape of astrocytes?
A
Star shaped with multipolar cytoplasmic processes
14
Q
What do astrocytic processes do?
A
Envelop synaptic plates Wrap around the vessels and capillaries within the brain
15
Q
What are the roles of astrocytes?
A
- Ionic, metabolic and nutritional homeostasis - work in conjunction with endothelial cells to maintain the BBB - the main cell involved in repair and scar formation given the lack of fibroblasts
16
Q
What is the most important histopathological indicator of CNS injury regardless of cause?
A
Gliosis
17
Q
Describe the process of gliosis?
A
Astrocyte hyperplasia and hypertrophy Nucleus enlarges, becomes vesicular and the nucleolus is prominent Cytoplasmic expansion with extension of ramifying processes
18
Q
Describe old lesions which have undergone gliosis?
A
Nuclei become small and dark and lie in a dense net of processes (glial fibrils)
19
Q
What is the role of oligodendrocytes?
A
Wrap around axons forming myelin sheath
20
Q
How to oligodendrocytes react to injury?
A
-variable patterns of demyelination - variable degrees of demyelination - apoptosis
21
Q
Oligodendrocytes are particularly sensitive to which type of damage?
A
Oxidative damage
22
Q
Oligodendrocyte damage is a feature of which disorders?
A
Demyelinating disorders
23
Q
Where are ependymal cells found?
A
Lining the ventricular system
24
Q
How to ependymal cells react to injury?
A
Limited reaction to injury
25
What is disruption of ependymal cells associated with?
Local proliferation of sub-ependymal astrocytes to produce small irregularities on the ventricular surfaces termed ependymal granulations
26
What produces changes in ependymal cells?
infectious agents including viruses
27
What is the function of microglia?
Function as macrophage system: phagocytosis
28
How do microglia respond to injury
- microglia proliferate - recruited through inflammatory mediators - form aggregates (around areas of necrotic and damaged tissues)
29
What are the types of microglia?
M2- anti-inflammatory, phagocytic, more acute M1- pro-inflammatory, more chronic
30
What can occur as a result of hypoxia?
Cerebral ischaemia, infarct, haemorrhages, trauma, cardiac arrest, cerebral palsy
31
Brain consumes \_\_% of total body resting oxygen consumption
Brain consumes 20% of total body resting oxygen consumption
32
Cerebral blood flow can increase only ______ to maintain oxygen delivery
Cerebral blood flow can increase only twofold to maintain oxygen delivery
33
After the onset of ischaemia, mitochondrial inhibition of ATP synthesis leads to ___ reserves being consumed within \_\_\_\_\_\_
After the onset of ischaemia, mitochondrial inhibition of ATP synthesis leads to ATP reserves being consumed within minutes
34
Describe the process of excitotoxicity?
When there is energy failure n**euronal depolarisation** occurs (releasing **glutamate**) in addition to **astrocyte reuptake becoming inhibited** (**failure of glutamate reuptake**). This results in a **glutamate** **storm** and **excitation**/ An excess of **Ca ions** in the postsynaptic neurone results in **protease activation**, **mitochondrial dysfunction** and **oxidative stress**
35
What kind of oedema occurs in cerebrovascular disease?
* cytotoxic oedema
* ionic oedema
* vasogenic oedema
36
What causes cytotoxic oedema?
Intoxication, Reye's and severe hypothermia
37
What causes ionic oedema?
*Also known as osmotic oedema*
Occurs in hyponatraemia and excess water intake (SIADH)
38
What causes vasogenic oedema?
Trauma
Tumours
Inflammation
Infection
Hypertensive encephalopathy
39
The brain recieves \_\_% of CO and uses \_\_% of oxygen consumed by the body
The brain recieves 15% of CO and uses 20% of oxygen consumed by the body
40
The brain requires what to function?
Active aerobic metabolism of glucose
41
\_\_\_\_\_\_\_ mechanisms help to maintain blood flow at a _______ rate by ______ and ______ of cerebral vessels
Autoregulatory mechanisms help to maintain blood flow at a constant rate by dilatation and constriction of cerebral vessels
42
What is cerebrovascular disease?
Any abnormality of brain caused by a pathological process of blood vessels
43
What are the 4 main
What are the 4 main pathologies of cerebrovascular disease?
* brain ischaemia and infarction
* Haemorrhages
* Vascular malformations
* Aneurysms
44
Cerebral ischaemia and infarction can be either ____ hypoxic ischaemic damage or ____ damage.
Cerebral ischaemia and infarction can be either global hypoxic ischaemic damage or focal damage.
45
What causes global hypoxic ischaemic damage?
- generalised reduction in blood flow/oxygenation
- cardiac arrest
- severe hypotension, e.g. trauma with hypovolaemic shock
46
what causes focal damage?
Vascular obstruction
47
What areas are particularly sensitive to global hypoxic ischaemic damage?
Watershed areas- zone between two arterial territories - e.g. parieto-occipital
48
Severe ischamia leads to ...
pan-necrosis
49
Which neurons are more sensitive than others?
Neocortex and hippocampus
50
What is the definition of a stroke?
Sudden disturbance of cerebral function of vascular origin that causes death or lasts over 24 hours
51
What is the most common type of infarction
Thrombotic 53%
Embolic 31%
52
What are the most common types of haemorrhages?
Intracerebral 10%
Subarachnoid 6%
Bleeding into infarct 1%
53
Who is most at risk for cerebral infarction?
\>70 years old
Men \> Women
- atheroma
- hypertension
- serum lipids, obesity, diet
- Diabetes mellitus
- Heart disease
- Diseases of neck arteries
- Drugs
- Smoking
54
What is thrombosis and where is it most common?
An atherosclerotic segment
Middle cerebral artery territory
55
What is the most common embolic infarction?
From atheroma in internal carotid and aortic arch
Tends to affect the heart
56
What determines the location, distribution and extend of parenchymal damage after a cerebral infarction?
- arterial territory of affected artery
- timescale of the occlusion
- extent of collateral ciruclatory relief
- systemic perfusion pressure
57
When does gliosis begin?
After a week
58
What is a what can occur after thrombolysis for embolic/thrombotic infarct?
Haemorrhagic infarct - Occlusion of a vessel usually by an embolus, with reperfusion and leakage through a damaged capillary bed following lysis of the embolus
59
Where is the vascular lesion?
Contra-lateral weakness or sensory loss. If dominant hemisphere, may be aphasia or apraxia.
Carotid artery disease
60
Where is the vascular lesion?
Weakness predominantly contralateral face and arm
Middle Cerebral artery
61
Where is the vascular lesion?
Weakness and sensory loss in contralateral leg
Anterior cerebral artery
62
Where is the vascular lesion?
Vertigo, ataxia, dysarthria and dysphasia
Vertebro-basilar artery
63
What are lacunar infarcts?
A consequence of hypertension
Atheroma, embolism of small penetrating vessels leading to occlusion
Affects basal ganglia
64
What is hypertensive encephalopathy?
Consequence of hypertension
Global cerebral oedema, tentorial and tonsilar herniation, petechiae and arteriolar fibrinoid necrosis
65
What are the consequences of hypertension?
- lacunar infarcts
- multi-infarct dementia
- ruptured aneurysms and intra-cerebral haemorrhage
- hypertensive encephalopathy
66
What are the spontaenous intracranial haemorrhages?
- intracerebral haemorrhage
- subarachnoid haemorrhage
- haemorrhagic infarct
67
What intracranial haemorrhages occur as a result of trauma?
Extra-dural haematoma
Sub-dural haematoma
Contusion (surface bruising)
Intracerebral haemorrhage
Sub-arachnoid
68
What factors contribute to intracerebral haemorrhage?
* hypertension
* aneurysms
* systemic coagulation disorders
* anticoagulation
* vascular malformations
* amyloid deposits (cerebral amyloid angiopathy)
* open heart surgery
* neoplasma
* vasculitis (infectious/non-infectious)
69
What is the most common locations for intracerebral haemorrhage?
Basal ganglia
70
What (morphology) would be seen on cut surface after intracerebral haemorrhage?
* asymmetrically distorted
* various shifts and herniations
* well demarcated intra-parenchymal haematoma
* softening of adjacent tissue
* surrounding oedema
71
What are the various types of vascular malformations?
AV malformations
Cavernous angiomas
Venous angiomas
Capillary telangectases
72
Which vascular malformations bleed?
- AV malformations
- Cavernous angiomas
73
What do vascular malformations cause clinically other than bleeding?
Headaches, seizures and focal neurological deficits
74
What happens in AVM that causes rupture?
Shunting from artery -\> vein
Undergoes SM hypertrophy
Is not compliant and ruptures easily
Also can form aneurysms
75
What is the most common cause of subarachnoid haemorrhages?
Where do these occur
Saccular aneurysm (berry aneurysm)
90% ICA territory
10% vertebro-basilar circulation
76
where do berry aneurysms occur?
Arterial bifurcations
77
What are the clinical features of subarachnoid haemorrhages?
* severe headache
* vomiting
* loss of consciousness
* abrupt onset
78
What are the risk factors for SA haemorrhages?
- Smoking
- Hypertension
- Kidney disease
79
What is the prognosis of SA haemorrhage?
50% die within several days of onset
Survivors at risk of hydrocephalus
80
What must be known in order to give the full diagnosis of a stroke?
* type of stroke
* size of stroke
* laterality of stroke
* cause of stroke
81
How can the type of stroke be determined?
CT brain
82
What is TACS?
Total anterior circulation syndrome
- hemiplegia involving at least two of face, arm and leg +/- hemisensory loss
- homonymous hemianopia
- cortical signs (dysphasia, neglect)
83
What is PACS?
Partial anterior circulation syndrome
2/3 features present in TACS or;
Isolated cortical dysfunction such as dysphasia or;
Pure motor/sensory signs less severe than lacunar syndrome (e.g. monoparesis)
84
What is LACS?
Lacunar syndrome
Small infarcts in the deeper parts of the brain (basal ganglia, thalamus, white matter) and in the brain stem.
85
What causes LACS?
Occlusion of a single deep penetrating artery. Affect 2 of face, arm and leg.
86
Which stroke has the best prognosis?
LACS- 60% of patients alive and independent at 1 year
87
What is POCS?
Posterior circulation syndrome
- cranial nerve palsies
- bilateral motor/sensory deficits
- conjugate eye movement disorders
- isolated homonymous hemianopia
- cortical blindness
- cerebellar deficits without ipsilateral motor/sensory signs
88
Dominant hemisphere (left) cortical events often affect \_\_\_\_\_
Non-dominant hemisphere (right) cortical events affect _____ \_\_\_\_\_\_\_
Dominant hemisphere (left) cortical events often affect language
Non-dominant hemisphere (right) cortical events affect spatial awareness
89
What is Type 1 Small vessel disease?
**Type 1**. Ateriosclerotic (age/risk factor related)
- fibrinoid necrosis
- lipohyalinosis
- microatheroma
- microaneurysm
90
What is Type 2 Small vessel disease?
**Type 2**. Sporadic and hereditary cerebral amyloid angiopathy
91
What is Type 3 small vessel disease?
**Type 3.** Genetic small vessel disease distinct from cerebral amyloid angiopathy
e.g. CADASIL
92
What is type 4 small vessel disese?
**Type 4.** Inflammatory and immunologically mediated
e.g. churgg-strauss, wegeners granulomatosis
93
What is type 5 small vessel disease?
**Type 5.** Venous collagenosis
94
What is type 6 small vessel disease?
**Type 6.** Other small vessel disease
e.g. post radiation angiopathy
95
AF is associated with a \_fold increase in stroke risk
AF is associated with a 5 fold increase in stroke risk
96
Primary intracerebral haemorrhage is due to;
- hypertension
- amyloid angiopathy
97
Secondary cerebral haemorrhage is due to
AV malformation
Aneurysm
Tumour
98
Intracerebral haemorrhages as a result of amyloid angiopathy tend to be ____ in location
Intracerebral haemorrhages as a result of amyloid angiopathy tend to be lobar in location
99
What is the ABC of stroke prevention?
**A-** Antithrombotic therapy
* antiplatelet*
* anticoagulant*
**B-** blood pressure
**C-** cholesterol
**D-** Diabetes
**D-** Don't smoke
100
What score can be used to calculate risk of stroke?
CHA2DS2VASc score
Max= 9
101
The bleeding risk on warfarin is _____ \_\_\_\_\_ as the bleeding risk on aspirin
The bleeding risk on warfarin is the same as the bleeding risk on aspirin
102
Anticoagulate or not?
Patient may need to fall about 300 times/year for the risk of bleeding to outweigh the benefit of coagulation.
103
What system is used to evaulate bleeding risk?
HAS-BLED
- hypertension
- abnormal renal and liver functin
- stroke
- bleeding
- labile INRs
- elderly \>65
- drugs or alcohol
104
What should you treat stroke with?
Perindopril based regimen
105
Carotid endartectomy provides what % absolute risk reduction?
15.9%
106
How should dysphagia be managed?
- initial swallow screen
- if abnormal -\> assessment by a SLT
- may need NG tube placement or textured diet and thickened fluids depending on swallow
107
What are the options for nutrition treatment?
* oral intake (soft diet and normal fluids)
* textured modified diets (TMD)/thickened fluids
* patient eats/drinks with knowledge of aspiration risk
* patient refuses food/fluid
* oral nutritional support including food first/oral nutrition supplements
* artificial nutrition support
* nil by mouth
108
