Cerebrovascular disease Flashcards

1
Q

Define the following conditions: Stroke, TIA, Amaurosis Fugax?

A

Stroke: a clinical syndrome caused by a thrombo-embolic or haemorrhagic event, characterised by rapidly developing signs of focal or global disturbance of cerebral functions, lasting for more than 24 hours or leading to death.

Transient Ischaemic Attack: same clinical presentation of a stroke which resolves within 24 hours

Amaurosis Fugax: a transient monocular vision loss that appears as a “curtain coming down vertically into the field of vision in one eye;” a specific type of TIA

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2
Q

List the risk factors leading toward the development of thromboembolic and haemorrhagic stroke?

A
Thromboembolic:
Male (irreversiblle)
Smoking
Hypertension
Obesity and Hypercholestrolaemia
Diabetes
AF
IE
Medication: POC
Haemorrhagic:
Medication (warfarin etc)
Bleeding disorders
Hypertension
Smoking
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3
Q

Describe the pathological causes of stroke?

A

Thrombo-embolic infarction: (~70%)
A combination of atherosclerosis of vertebral/intracerebral aa and emboli from:
-AF (leads to stasis forming a clot which can embolise)
-Ulcerated carotid plaques
-Mural plaque
-Infective endocarditis

Haemorrhagic:
Haemorrhage of an intracerebral vessel
SAH account for 5%

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4
Q

Describe the clinical features of a sub arachnoid haemorrhage, and the most common cause?

A

A sudden onset severe headache (peak pain almost immediately).
Worst headache ever.
Usually in the occipital region.

May be focal neurology and meningisms.

Most commonly due to a ruptured berry aneurysm in teh circle of willis.

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5
Q

Describe the clinical features of meningisms?

A

Neck stiffness, photophobia and headache.

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6
Q

Describe the vascular abnormalities which may predispose a patient developing a SAH?

A

Berry aneurysms: congenital weakness in the elastic lamina of aa, often develop at weak branch points in the circle of willis.
40% occur at the internal carotid aa
30% occur at the anterior communicating aa
20% occur at the middle communicating aa

Arteriovenous malformations: Congenital defect in which there are abnormal anastomoses between the arterial and venous system without capillaries due to the abnormal pressure difference these are more likely to bleed.

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7
Q

What are the complications of SAH?

A

The blood may spread through the sub arachnoid space leading to raised ICP.

There may be focal neurology due to infarction at the site of rupture.

If left untreated it will lead to death.

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8
Q

Describe the cause subdural haemorrhage?

A

Head trauma.
Occurs in a 1/3 of serious head traumas.

Often occurs in acceleration deceleration (blunt head trauma) when there has been damage to one of the bridging veins draining the blood from the cortex into one of the central venous sinuses.

Bleeding from a damaged cortical aa.

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9
Q

Describe the clinical presentation of an acute and chronic subdural haemorrhage?

A

Acute:
Usually presents shortly after a moderate to severe head trauma.
There may be a loss of consciousness.
There may be a lucid period of a few hours where the patient seems relatively well before deteriorating and losing consciousness as a haematoma forms.

Chronic:
Usually presents 2-3 weeks after the trauma, which may have been relatively uneventful (think of this in groups with a high bleeding risk)

Often a hx of progressive symptoms including:
Anorexia, nausea and vomiting.
Focal neurology such as limb weakness, speech difficulties, confusion or personality change.
May be a progressively worsening headache (should really raise suspicion)

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10
Q

Describe the predisposing factors making a patient vulnerable to developing a subdural haemorrhage?

A

Anything increasing bleeding risk.

Anticoagulants
Liver failure
Alcoholism (poor clotting and brain atrophy)
Inherited haemophilias
Infants and elderly (brain atrophy)
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11
Q

Describe what symptoms would be seen total anterior circulation and a partial anterior circulation stroke?

A

Higher cortical dysfunction (agnosia, neglect, dysphasia)
Hemianopia
Motor or sensory deficit

Note: hemianopia is on the same side as the hemiparesis

In a total anterior stroke all three are present in a partial 2 of the 3 are present.

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12
Q

Describe what symptoms would be seen in a posterior circulation stroke?

A
Isolated hemiapnopia
OR
Cerebellar ataxia
OR
Cranial nn lesions
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13
Q

Describe what symptoms would be seen in a lacunar stroke?

A

One motor or sensory deficit.

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14
Q

What is the name used to classify strokes?

A

Bamford classification.

Splits different strokes up into TACS, PACS, POCS and Lacunar based on the symptoms.

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15
Q

Which is the most serious stroke you can have and what is the 1 year mortality for the different strokes?

A

Right TACS as it will effect the left dominant hemisphere.

TACS 60%
PACS 15%
LACS 10%
Posterior circulation 20%

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16
Q

Describe the acute management of a suspected stroke?

A

A-E

  • O2 only if sats are less than 95%
  • BP only give antihypertensives in a hypertensive crisis 185/110
  • BM should be between 4-11

Emergency head CT scan to rule out a haemorrhagic stroke.

17
Q

In a CT confirmed NON haemorrhagic stroke what is the initial management?

A

The window of opportunity for effective thrombolysis is four and a half hours from the onset of the stroke.

This can only be used in confirmed diagnoses of stroke.

In this case the thrombolytic altepase should be used.

18
Q

What is the follow on management of non haemorrhagic stroke?

A

Once the window for thrombolysis has passed then

  • Aspirin 300mg should be started.
  • Standard hospital anticoagulants should NOT be started for 2 weeks
  • Statins offered after 48hrs, regardless of cholesterol

MDT approach:

  • SALT with a focus on a safe swallow (likely they may initially need an NG or thickened fluids)
  • Physiotherapy
  • Occupational therapist

With a view to discharging to intermediate care if necessary.

19
Q

How should a haemorrhagic stroke be managed?

A

Stop any anticoagulants.

Look for causes of the bleed on imaging.

MDT approach:

  • SALT with a focus on a safe swallow (likely they may initially need an NG or thickened fluids)
  • Physiotherapy
  • Occupational therapist
20
Q

Outline the secondary prevention measures used in stroke?

A

Lifestyle changes: including smoking cessation, physical activity, diet, weight control and avoiding excess alcohol.

Regular review and treatment of risk factors for vascular disease.

Antithrombotic treatment (warfarin/NOAC): if there is history of persistent or paroxysmal AF in a non haemorrhagic stroke.

If a non haemorrhagic stroke not due to AF then all patients should be started on clopidogrel.

All patients should be started on a statin if not contraindicated.

Note: patients who have had a TIA should be on secondary prevention, should also not drive for 1 month post episode.

21
Q

How is suspected carotid aa stenosis investigated?

A

Initial investigation should be with a colour duplex ultrasound as it is a quick cheap investigation.

Further assessment before invasive treatment is needed by using CT or MR angiography.

22
Q

How is carotid aa stenosis treated?

A

Carotid endarterectomy (surgical removal of the fatty deposits and blood clots from inside the carotid artery wall)

Or

Carotid aa angioplasty and stenting with an emboli protection device.

23
Q

What is venous sinus thrombosis?

A

It is cerebral infarction caused by thrombosis in the cerebral venous sinuses.

They are quite rare in comparison to arterial infarcts.

24
Q

What are the risk factors for venous sinus thrombosis?

A

Pro-thrombotic states:

  • Pregnancy
  • Malignancy
  • Dehydration
  • Coagulopathies

Local infection: sinusitis

25
Q

What is the clinical presentation of venous sinus thrombosis and how does it differ to arterial infarctions clinically?

A

May present with stroke symptoms.

May present with severe headache mimicking a subarcahnoid haemorrhage.

May present with status epilepticus.

May present with signs of raised intracranial pressure.

May have several of these symptoms.

Clinically differentiated on CT/MRI scans