S3: Aneurysms, Hypertension and Stroke Flashcards

1
Q

Definition of hypertension and types

A

Hypertension is sustained elevation of systolic and diastolic blood pressure above 140/90 mmHg. Primary hypertension is also known as idiopathic or essential hypertension. this is when the cause isn’t known and this makes up the bulk of hypertension (90%).
Secondary hypertension is when there is an identifiable cause so secondary to renal disease, adrenal tumours, aortic coarctation, steroids etc.

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2
Q

Describe the effect hypertension can have on our different organs

A
  • Blood vessels: The blood vessels themselves undergo atheroma, aneurysms in large vessels and elastic reduplication (remodelling of vessel, elastic lamina) in small vessels. The blood vessels also will contribute to all aspects of hypertensive organ damage.
  • Heart: Can get LV hypertrophy, L heart failure due to increase work on the heart.
  • Pumonary Oedema: Due to left sided heart failure.
  • Kidneys: Nephrosclerosis, renal failure (reciprocal regulation with kidney and high BP in vessels).
  • Eye: Retinal capillary damage, haemorrhages, exudates.
  • Brain: Micro-aneurysms and stroke.
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3
Q

Describe hypertensive heart disease

A
  • Increased load on the heart causes a concentric left ventricular hypertrophy.
  • There is thickening of the muscle that is consistent throughout the ventricle therefore it is concentric.
  • Significantly weakened or damaged ventricles can lead to heart damage.
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4
Q

Describe hypertensive neuropathy

A
  • The kidneys can be badly affected by hypertension, there is thickening of the renal arterioles (fibrosis and scarring) and hardening of the glomerulus called glomerulosclerosis.
  • There can also be endothelial cell dysfunction and changes to cells leading to apoptosis and cell death in the wall of vessels.
  • There is then reduced oxygen and ischaemic tissue and eventually there may be atrophy which can lead to loss of function and failure of kidney tissue.
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5
Q

Describe hypertensive retinopathy

A

This can be classified into three different degrees of severity:

  1. Early hypertensive retinopathy sees nicking of retinal veins due to compression by overlying arterioles which cross over veins.
  2. Moderate hypertensive retinopathy sees flame haemorrhages (spots of bleeding), ‘cotton wool’ sports (white patches) and later there are hard exudates (due to lipid leakage of vessels around the macula).
  3. Late chronic or malignant acute hypertensive retinopathy can lead to severe haemorrhage and papilloedema.
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6
Q

Which blood vessels are involved in hypertension and which in atheroma?

A
Blood pressure is controlled by arterioles which are also called resistance vessels as they can constrict or relax to alter peripheral resistance.
Atheromatic plaques (atheroma) tend to be found in larger vessels and they do not develop in veins. Because atheroma tends to be found in larger blood vessels they do not sufficiently increase TPR enough to cause hypertension.
- However, the two diseases are often encountered together.
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7
Q

Describe blood vessel changes in hypertension

A
  • In hypertension, the resistance arterioles show elastic duplication in the lamina.
  • Hyaline arteriosclerosis affects more of the media of the vessel and we see hardening of the arterioles so they becomes less elastic so they cannot respond properly to physiological needs. Plasma may exude into the media and deeper into the vessel wall.
  • The endothelium in hypertension is also subject to damage by shearing forces applied by the high pressure. Where there is endothelial damage, atheroma is more likely to develop.
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8
Q

Difference atherosclerosis and arteriosclerosis

A

Atherosclerosis is a type of arteriosclerosis. Atherosclerosis is more of a condition affecting the intima because this is where we see the build up of plaque formation in the larger vessels.

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9
Q

What is a true aneurysm?

A

This is when the entire wall of the vessel is dilated outwards. Sometimes part of the wall is cut or torn, usually by trauma causing the inner layers to bulge out.

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10
Q

What is a false aneurysm?

A

This is when there is a breach in the vessel wall such that blood leaks out but is contained in the adventitia or surrounding tissue. The aneurysm will expand as blood is pumped out of the vessel wall.

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11
Q

Describe the typical sites and shapes of aneurysms

A
  • ‘Berry’ (saccular) aneurysms typically occur at the bifurcations of the arteries of the circle of willis. They look like a berry and their rupture usually causes subarachnoid haemorrhage.
  • Microaneurysms typically occur in the cerebral arteries in patients with hypertension. Their rupture causes intracerebral haemorrhage.
  • Abdominal aortic aneurysms are usually secondary to atheroma (often seen together in the vessel). Rupture of the aneurysm can cause intraperitoneal haemorrhage and death. They can also throw off thromboemboli causing ischaemia and gangrene.
  • Stretched aortic ring can be caused by an aortic dissection (a dissecting aneurysm), or can be due to infection such as a syphilitic aneurysm. Rupture can cause cardiac tamponade.
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12
Q

What can reduce anuerysms being pulsatile?

A

Aneurysms are usually pulsatile due to the arterial blood flow but thrombus or severe atheromatous thickening may diminish this effect. It is important to remember that aneurysms occur in arteries and occasionally the left ventricle (post MI) but are very rare in veins!

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13
Q

What usually causes aneurysms?

A

Aneurysms occur at points of weakness:

  • These points are usually due to atheroma (leads to damage to vessel wall, thrombosis and then dilatation).
  • They sometimes occur due to inflammatory damage e.g. syphilis.
  • Occasionally due to connective tissue abnormalities.
  • Sometimes they may follow truama.
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14
Q

What do aneurysms look like?

A

There are a lot of physical changes that occur in vessels with aneurysms:

  • Most aneurysms are secondary to atheroma and are fusiform (spindle shaped) and these would be seen in the aorta.
  • Saccular aneurysms often occur after focal damage to a vessel e.g. infection. ‘Berry’ aneurysms are saccular.
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15
Q

3 complications of aneurysms

A
  1. Rupture
  2. Thrombosis
  3. Thromboembolism (due to thrombosis)
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16
Q

List special types of aneurysms

A
  • Aortic dissection
  • Cerebral micoraneurysm
  • Berry aneurysm
17
Q

Describe aortic dissection (dissecting aneurysm)

A
  • These are typically found in elderly people with medial degeneration or in individuals with Marfan’s syndrome where they have a congenitally weak media.
  • A dissecting aneurysm can occur when there is a tear in the intima so the blood enters into the aortic wall and forms a parallel track.
  • This causes the vessel to dilate and may rupture through the adventitia causing death by cardiac tamponade (bursts into pericardium) or exsanguination (blood loss e.g. into the mediastinum).
18
Q

Describe a cerebral microaneurysm

A

These are typical of hypertension and also a precursor to intracerebral haemorrhage.

19
Q

What is a stroke?

A

it is the sudden onset of neurological deficit, likely due to cardiovascular cause.

20
Q

List some risk factors for stroke

A
  • Old
  • Men
  • Hypertension
  • Atrial fibrillation
  • Smoking
  • Diabetes
  • High cholesterol
21
Q

What factor determine the clinical effects of a stroke?

A

The site of damage, extent of damage size) and the speed of interventional treatment determine the effects of a stroke.

22
Q

What are the two broad categories of strokes?

A

We can classify stokes into two broad categories of ischaemic due to lack of blood flow (making up 80% of strokes) and haemorrhagic due to bleeding (20%).

23
Q

Describe causes of ischaemic strokes

A
  • Thromboembolic –> thromboembolic sources include a thrombus over an atheroma at the carotid bifurcation and a mural thrombus from the heart (due to AF).
  • Primary occlusion of intracerebral artery/arteriole (thrombus) –> this is occlusion of a cerebral vessel by a thrombus forming in the intracerebral vessel itself around an atheroma.
  • Lacunar –> This is where there is a penetrating artery that gets occluded (e.g. lenticulostriate). These are caused by tiny lesions and may be silent, they are associated with white matter lesions and ‘vascular dementia’ (poor blood supply leads to dementia) or can be catastrophic e.g. if brainstem is deprived.
24
Q

Describe causes of harmorrhagic stroke

A
  • Most commonly due to rupture of cereberal microaneurysm, secondary to hypertension.
  • Thromboembolic strokes appear haemorrhagic due to leakage from damaged capillaries at the sites of infarction.
  • Haemorrhagic stroke will often show compression,
25
Q

Describe the ischaemic penumbra

A
  • The core of an infarct will undergo irretrievable and irreversible necrosis. However the adjacent territory will be only relatively ischaemic as there may be a degree of compensation from nearby blood supplies.
  • We want to be able to save as much of this adjacent territory as we can when a person has a stroke, this is called the ‘penumbra’ territory. If arterial perfusion can be restored within 3 hours, much of the penumbra territory may be salvaged, there is also benefit in treatment up to 6 hours later.
  • The faster we restore circulation to these tissues the better the patient will be.
    Do note however that ischaemic damage to the endothelium may render newly perfused vessels leaky, so restoration of function of them may not be as good as hoped and re-bleeding may even occur.
26
Q

List acute and chronic feature of a stroke

A

Acute features of a stroke would be headache, neurological deficit (abnormal function of a body area due to weaker function of brain, spinal cord, muscles or nerves) e.g. inability to speak. Also confusion, coma and death.
The chronic features of a stroke are site-dependent.

27
Q

Describe space occupying lesion caused by stroke

A

A massive bleed acts as a space occupying lesion, in the brain this can cause herniation of the brain called ‘coning’ which can cause death.

28
Q

Describe liquefaction necrosis in the brain caused by stroke

A

Cerebral lesions caused by strokes are soft due to liquefaction necrosis of the brain tissue, this will form cysts. When this is cleared by macrophages cystic spaces remain in the brain.
As well as this gliosis will likely be seen which is the brains equivalent of scarring.

29
Q

Describe lacunar infarcts caused by stroke

A

Lacunar infarcts affect the deep penetrating arterioles, typically the ones supplying the basal ganglia, brainstem, thalamus and deep white matter e.g. lenticulostriate.
These infarcts are typically seen in diabetes and or hypertension, usually accompanied with extensive small vessel atheroma.
Lacunar infarcts are not space occupying lesions as they don’t take up a huge amount of space. Nonetheless they can still be devastating, for example if the internal capsule is involved a 2mm infact may cause a dense hemiplegia. If the white matter is affected it can be clinically silent but contribute to vascular dementia.
There are minimal additional symptoms due to the small caliber vessels involved.

30
Q

What is a transient ischaemic attack?

Describe it

A

A transient ischaemic attack (TIA) is neurological deficit lasting less than 12-24hrs. It is not a stroke, but the risk of a full-blown stroke occurring is now high.
- Risk within 5yrs is 30%. There is a 4-20% incidence of full-blown stroke within 90 days. Risk is influenced by age, blood pressure, diabetes etc. So these must be monitored.

31
Q

Describe stroke management in hyperacute stroke units

A

The immediate management of a stroke may differ in accordance to age of victim
(the below are for ischaemic stroke).
Most likely will be put on antiplatelet therapy:
- Aspirin
- Clopidogrel
- Dipyridamole
Thrombolytic drugs will be given for ischaemic stroke (tPa), these are best given within 3 hours, but may have functional benefit up to 6 hours.
In other cases, there may be evacuation of the clot.

32
Q

List stroke prevention

A
  • Smoking cessation
  • Give aspirin to those at risk
  • Decrease salt intake (a drop in BP by 5mmHg should reduce strokes by 40%)
  • Treat atrial fibrillation, can do this using warfarin (offers 70% protection compared to aspirin, however there is greater risk of haemorrhagic complications). Note though that new direct anticoagulants have been developed
  • Fast recognition of a TIA
33
Q

Describe a subarachnoid haemorrhage

A

The term ‘ stroke’ only applies to sudden intracerebral vascular events due to vascular occlusion (due to a thrombus or thromboembolus) or intracerebral haemorrhage.
If a haemorrhage occurs in the space around the outside of the brain, this is called a subarachnoid haemorrhage (SAH).
SAH is not a stroke on technical grounds since it involves vessels that are external to the brain itself.
However SAH can induce spasm in the cerebral arteries which is one reason for the high mortality and morbidity for this condition.

34
Q

List types of intracranial haemorrhage (other than stroke)

A

Extradural/epidural = Occurs between the two layers of dura mater, often due to middle meningeal artery.
Subdural haemorrhage = In between dura and arachnoid, often caused by trauma as veins go up from cortex to bone layer and so cross open space. If brain shrinks, it is much easier for the brain to knock around in the cranium and this makes shearing of the vessel much more likely.
Subarachnoid = under the arachnoid mater, in the subarachnoid space e.g. due to berry aneurysm, this would produce a “red CSF”.
Intracerebral = within the brain.
Multiple petechial haemorrhages = caused by things like malaria, occlusion of capillary causes multiple tiny infarcts but because disease is not primarily of cerebral blood vessels and disseminated through the body this is not a stroke.

35
Q

Describe watershed zone infarction

A
  • There are some tissues which are at the boundaries of arterial territories. Examples of these areas include being in the brain, colon and heart.
  • If blood pressure drops suddenly, the tissue at the periphery of two or more arterial territories is vulnerable to hypoperfusion and likely to undergo infarction.
  • The zones between territories of the arteries of the Circle of Willis are at risk of being hypoperfused.