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Neurology > Cerebrovascular disease > Flashcards

Cerebrovascular disease Flashcards

1
Q

What are the three types of glial cells?

A

Astrocytes Oligodendrocytes Ependymal cells

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2
Q

What are the supporting structures of the CNS?

A

Connective tissue Meninges Blood vessels

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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)

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4
Q

How are neurones organised?

A
  • aggregates: nuclei, ganglia - columns/layers - assigned functional domains
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5
Q

What is the perikaryon and its variation in size?

A

The cell body of a neurone- can vary from 10 to 50um

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6
Q

When does acute neuronal injury occur?

A

Context of hypoxia/ischaemia

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7
Q

When does a red neurone become visible?

A

Typically 12-24 hours after an irreversible ‘insult’ to the cell

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8
Q

What does acute neuronal injury result in?

A

Neuronal cell death

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9
Q

What pattern is seen in acute neuronal injury?

A
  • shrinking and angulation of nuclei - loss of the nucleolus - intensely red cytoplasms
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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’’
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11
Q

What is simple neuronal atrophy?

A

Chronic degeneration - shrunken, angulated and lost neurons, small dark nuclei, lipofuscin pigment, reactive gliosis

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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

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13
Q

Describe the shape of astrocytes?

A

Star shaped with multipolar cytoplasmic processes

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14
Q

What do astrocytic processes do?

A

Envelop synaptic plates Wrap around the vessels and capillaries within the brain

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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
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16
Q

What is the most important histopathological indicator of CNS injury regardless of cause?

A

Gliosis

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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

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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)

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19
Q

What is the role of oligodendrocytes?

A

Wrap around axons forming myelin sheath

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20
Q

How to oligodendrocytes react to injury?

A

-variable patterns of demyelination - variable degrees of demyelination - apoptosis

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21
Q

Oligodendrocytes are particularly sensitive to which type of damage?

A

Oxidative damage

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22
Q

Oligodendrocyte damage is a feature of which disorders?

A

Demyelinating disorders

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23
Q

Where are ependymal cells found?

A

Lining the ventricular system

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24
Q

How to ependymal cells react to injury?

A

Limited reaction to injury

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25
Q

What is disruption of ependymal cells associated with?

A

Local proliferation of sub-ependymal astrocytes to produce small irregularities on the ventricular surfaces termed ependymal granulations

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26
Q

What produces changes in ependymal cells?

A

infectious agents including viruses

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27
Q

What is the function of microglia?

A

Function as macrophage system: phagocytosis

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28
Q

How do microglia respond to injury

A
  • microglia proliferate - recruited through inflammatory mediators - form aggregates (around areas of necrotic and damaged tissues)
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29
Q

What are the types of microglia?

A

M2- anti-inflammatory, phagocytic, more acute M1- pro-inflammatory, more chronic

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30
Q

What can occur as a result of hypoxia?

A

Cerebral ischaemia, infarct, haemorrhages, trauma, cardiac arrest, cerebral palsy

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31
Q

Brain consumes __% of total body resting oxygen consumption

A

Brain consumes 20% of total body resting oxygen consumption

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32
Q

Cerebral blood flow can increase only ______ to maintain oxygen delivery

A

Cerebral blood flow can increase only twofold to maintain oxygen delivery

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33
Q

After the onset of ischaemia, mitochondrial inhibition of ATP synthesis leads to ___ reserves being consumed within ______

A

After the onset of ischaemia, mitochondrial inhibition of ATP synthesis leads to ATP reserves being consumed within minutes

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34
Q

Describe the process of excitotoxicity?

A

When there is energy failure neuronal 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

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35
Q

What kind of oedema occurs in cerebrovascular disease?

A
  • cytotoxic oedema
  • ionic oedema
  • vasogenic oedema
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36
Q

What causes cytotoxic oedema?

A

Intoxication, Reye’s and severe hypothermia

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37
Q

What causes ionic oedema?

A

Also known as osmotic oedema

Occurs in hyponatraemia and excess water intake (SIADH)

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38
Q

What causes vasogenic oedema?

A

Trauma

Tumours

Inflammation

Infection

Hypertensive encephalopathy

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39
Q

The brain recieves __% of CO and uses __% of oxygen consumed by the body

A

The brain recieves 15% of CO and uses 20% of oxygen consumed by the body

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40
Q

The brain requires what to function?

A

Active aerobic metabolism of glucose

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41
Q

_______ mechanisms help to maintain blood flow at a _______ rate by ______ and ______ of cerebral vessels

A

Autoregulatory mechanisms help to maintain blood flow at a constant rate by dilatation and constriction of cerebral vessels

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42
Q

What is cerebrovascular disease?

A

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

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43
Q

What are the 4 main

What are the 4 main pathologies of cerebrovascular disease?

A
  • brain ischaemia and infarction
  • Haemorrhages
  • Vascular malformations
  • Aneurysms
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44
Q

Cerebral ischaemia and infarction can be either ____ hypoxic ischaemic damage or ____ damage.

A

Cerebral ischaemia and infarction can be either global hypoxic ischaemic damage or focal damage.

45
Q

What causes global hypoxic ischaemic damage?

A
  • generalised reduction in blood flow/oxygenation
  • cardiac arrest
  • severe hypotension, e.g. trauma with hypovolaemic shock
46
Q

what causes focal damage?

A

Vascular obstruction

47
Q

What areas are particularly sensitive to global hypoxic ischaemic damage?

A

Watershed areas- zone between two arterial territories - e.g. parieto-occipital

48
Q

Severe ischamia leads to …

A

pan-necrosis

49
Q

Which neurons are more sensitive than others?

A

Neocortex and hippocampus

50
Q

What is the definition of a stroke?

A

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

51
Q

What is the most common type of infarction

A

Thrombotic 53%

Embolic 31%

52
Q

What are the most common types of haemorrhages?

A

Intracerebral 10%

Subarachnoid 6%

Bleeding into infarct 1%

53
Q

Who is most at risk for cerebral infarction?

A

>70 years old

Men > Women

  • atheroma
  • hypertension
  • serum lipids, obesity, diet
  • Diabetes mellitus
  • Heart disease
  • Diseases of neck arteries
  • Drugs
  • Smoking
54
Q

What is thrombosis and where is it most common?

A

An atherosclerotic segment

Middle cerebral artery territory

55
Q

What is the most common embolic infarction?

A

From atheroma in internal carotid and aortic arch

Tends to affect the heart

56
Q

What determines the location, distribution and extend of parenchymal damage after a cerebral infarction?

A
  • arterial territory of affected artery
  • timescale of the occlusion
  • extent of collateral ciruclatory relief
  • systemic perfusion pressure
57
Q

When does gliosis begin?

A

After a week

58
Q

What is a what can occur after thrombolysis for embolic/thrombotic infarct?

A

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
Q

Where is the vascular lesion?

Contra-lateral weakness or sensory loss. If dominant hemisphere, may be aphasia or apraxia.

A

Carotid artery disease

60
Q

Where is the vascular lesion?

Weakness predominantly contralateral face and arm

A

Middle Cerebral artery

61
Q

Where is the vascular lesion?

Weakness and sensory loss in contralateral leg

A

Anterior cerebral artery

62
Q

Where is the vascular lesion?

Vertigo, ataxia, dysarthria and dysphasia

A

Vertebro-basilar artery

63
Q

What are lacunar infarcts?

A

A consequence of hypertension

Atheroma, embolism of small penetrating vessels leading to occlusion

Affects basal ganglia

64
Q

What is hypertensive encephalopathy?

A

Consequence of hypertension

Global cerebral oedema, tentorial and tonsilar herniation, petechiae and arteriolar fibrinoid necrosis

65
Q

What are the consequences of hypertension?

A
  • lacunar infarcts
  • multi-infarct dementia
  • ruptured aneurysms and intra-cerebral haemorrhage
  • hypertensive encephalopathy
66
Q

What are the spontaenous intracranial haemorrhages?

A
  • intracerebral haemorrhage
  • subarachnoid haemorrhage
  • haemorrhagic infarct
67
Q

What intracranial haemorrhages occur as a result of trauma?

A

Extra-dural haematoma

Sub-dural haematoma

Contusion (surface bruising)

Intracerebral haemorrhage

Sub-arachnoid

68
Q

What factors contribute to intracerebral haemorrhage?

A
  • hypertension
  • aneurysms
  • systemic coagulation disorders
  • anticoagulation
  • vascular malformations
  • amyloid deposits (cerebral amyloid angiopathy)
  • open heart surgery
  • neoplasma
  • vasculitis (infectious/non-infectious)
69
Q

What is the most common locations for intracerebral haemorrhage?

A

Basal ganglia

70
Q

What (morphology) would be seen on cut surface after intracerebral haemorrhage?

A
  • asymmetrically distorted
  • various shifts and herniations
  • well demarcated intra-parenchymal haematoma
  • softening of adjacent tissue
  • surrounding oedema
71
Q

What are the various types of vascular malformations?

A

AV malformations

Cavernous angiomas

Venous angiomas

Capillary telangectases

72
Q

Which vascular malformations bleed?

A
  • AV malformations
  • Cavernous angiomas
73
Q

What do vascular malformations cause clinically other than bleeding?

A

Headaches, seizures and focal neurological deficits

74
Q

What happens in AVM that causes rupture?

A

Shunting from artery -> vein

Undergoes SM hypertrophy

Is not compliant and ruptures easily

Also can form aneurysms

75
Q

What is the most common cause of subarachnoid haemorrhages?

Where do these occur

A

Saccular aneurysm (berry aneurysm)

90% ICA territory

10% vertebro-basilar circulation

76
Q

where do berry aneurysms occur?

A

Arterial bifurcations

77
Q

What are the clinical features of subarachnoid haemorrhages?

A
  • severe headache
  • vomiting
  • loss of consciousness
  • abrupt onset
78
Q

What are the risk factors for SA haemorrhages?

A
  • Smoking
  • Hypertension
  • Kidney disease
79
Q

What is the prognosis of SA haemorrhage?

A

50% die within several days of onset

Survivors at risk of hydrocephalus

80
Q

What must be known in order to give the full diagnosis of a stroke?

A
  • type of stroke
  • size of stroke
  • laterality of stroke
  • cause of stroke
81
Q

How can the type of stroke be determined?

A

CT brain

82
Q

What is TACS?

A

Total anterior circulation syndrome

  • hemiplegia involving at least two of face, arm and leg +/- hemisensory loss
  • homonymous hemianopia
  • cortical signs (dysphasia, neglect)
83
Q

What is PACS?

A

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
Q

What is LACS?

A

Lacunar syndrome

Small infarcts in the deeper parts of the brain (basal ganglia, thalamus, white matter) and in the brain stem.

85
Q

What causes LACS?

A

Occlusion of a single deep penetrating artery. Affect 2 of face, arm and leg.

86
Q

Which stroke has the best prognosis?

A

LACS- 60% of patients alive and independent at 1 year

87
Q

What is POCS?

A

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
Q

Dominant hemisphere (left) cortical events often affect _____

Non-dominant hemisphere (right) cortical events affect _____ _______

A

Dominant hemisphere (left) cortical events often affect language

Non-dominant hemisphere (right) cortical events affect spatial awareness

89
Q

What is Type 1 Small vessel disease?

A

Type 1. Ateriosclerotic (age/risk factor related)

  • fibrinoid necrosis
  • lipohyalinosis
  • microatheroma
  • microaneurysm
90
Q

What is Type 2 Small vessel disease?

A

Type 2. Sporadic and hereditary cerebral amyloid angiopathy

91
Q

What is Type 3 small vessel disease?

A

Type 3. Genetic small vessel disease distinct from cerebral amyloid angiopathy

e.g. CADASIL

92
Q

What is type 4 small vessel disese?

A

Type 4. Inflammatory and immunologically mediated

e.g. churgg-strauss, wegeners granulomatosis

93
Q

What is type 5 small vessel disease?

A

Type 5. Venous collagenosis

94
Q

What is type 6 small vessel disease?

A

Type 6. Other small vessel disease

e.g. post radiation angiopathy

95
Q

AF is associated with a _fold increase in stroke risk

A

AF is associated with a 5 fold increase in stroke risk

96
Q

Primary intracerebral haemorrhage is due to;

A
  • hypertension
  • amyloid angiopathy
97
Q

Secondary cerebral haemorrhage is due to

A

AV malformation

Aneurysm

Tumour

98
Q

Intracerebral haemorrhages as a result of amyloid angiopathy tend to be ____ in location

A

Intracerebral haemorrhages as a result of amyloid angiopathy tend to be lobar in location

99
Q

What is the ABC of stroke prevention?

A

A- Antithrombotic therapy

  • antiplatelet*
  • anticoagulant*

B- blood pressure

C- cholesterol

D- Diabetes

D- Don’t smoke

100
Q

What score can be used to calculate risk of stroke?

A

CHA2DS2VASc score

Max= 9

101
Q

The bleeding risk on warfarin is _____ _____ as the bleeding risk on aspirin

A

The bleeding risk on warfarin is the same as the bleeding risk on aspirin

102
Q

Anticoagulate or not?

A

Patient may need to fall about 300 times/year for the risk of bleeding to outweigh the benefit of coagulation.

103
Q

What system is used to evaulate bleeding risk?

A

HAS-BLED

  • hypertension
  • abnormal renal and liver functin
  • stroke
  • bleeding
  • labile INRs
  • elderly >65
  • drugs or alcohol
104
Q

What should you treat stroke with?

A

Perindopril based regimen

105
Q

Carotid endartectomy provides what % absolute risk reduction?

A

15.9%

106
Q

How should dysphagia be managed?

A
  • initial swallow screen
  • if abnormal -> assessment by a SLT
  • may need NG tube placement or textured diet and thickened fluids depending on swallow
107
Q

What are the options for nutrition treatment?

A
  • 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
Q
A

Neurology (41 decks)

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