Hypertension, Aneurisms, Stroke

Question 1

What are the causes of hypertension?
1 primary + 4 secondary

Answer 1

> 140/90 mmHg. Causes:
primary (idiopathic/essential)= no identifiable cause

Secondary:
renal disease
adrenal tumours
aortic coarctation (birth defect in which a part of the aorta is narrower than usual)
Antiangiogenic drugs

Question 2

What does this show?

Answer 2

Question 3

What do these images show?

Answer 3

Question 4

compare early, moderate and late hypertensive retinopathy. Use this diagram to help

Answer 4

Early hypertensive retinopathy: ‘Nicking’/compression, of retinal veins by overlying arterioles, normally they run alongside.

Moderate hypertensive retinopathy:
Straightened, wider capillaries
Flame shaped haemorrhages
‘Cotton wool’ spots

(later)‘Hard’ exudates around macula

Question 5

What happens in late chronic hypertensive retinopathy?

Answer 5

Late chronic or ‘malignant’ acute hypertensive retinopathy:
Papilloedema
Haemorrhage

Question 6

Outline the blood vessel changes in hypertension

what do resistance arterioles show?
what does hyaline arteriosclerosis damage?

Answer 6

Atheroma is likely to develop at sites of endothelial damage due to hypertension

Question 7

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

Answer 7

Arterioles constrict/relax to regulate TPR + arterial BP
Resistance of flow= diameter to the power of 4. Therefore, a 50% decrease in the lumen= 16-fold increase in BP.

(Atheroma tends to affect larger blood vessels, so does not increase TPR sufficiently to cause hypertension. Still, both diseases are often encountered together).
in layman terms → atheroma cannot rly lead cause hypertension; hypertension can lead to atheroma via endothelial damage

Question 8

An aneurysm is a bulge in the wall of a blood vessel

compare true vs false aneurysm?

Answer 8

True aneurysms: entire vessel wall bulges. Sometimes part of the wall is cut (trauma) and the inner layers bulge through the tear – could be false aneurysm because not all layers are affected.

False aneurysms: artery wall is punctured (e.g. during angioplasty) and blood tracks out into tissue, but is contained locally by scar tissue. - This then further expands as blood is pumped out the vessel wall

Question 9

Why are aneurysms pulsatile?

Answer 9

Aneurysms are usually pulsatile due to arterial blood flow, but this effect may be diminished by thrombus or severe atheromatous thickening

Question 10

Where do aneurysms occur? + 4 causes

Answer 10

Aneurysms occur in arteries and occasionally the LV (post MI), v rare in veins - they essentially occur at points of weakness.
Causes:
Atheroma
Inflammatory damage (e.g. syphilis)
Connective tissue/ medial vessel wall abnormalities (e.g. Marfan’s)
Trauma, e.g. partial medial tear

Question 11

compare 2 types of aneurysms that occur in the brain?

Answer 11

‘Berry’ (saccular) aneurysms: occur at vessel wall weaknesses- e.g points of bifurcation in the Circle of Willis. Their rupture causes subarachnoid haemorrhage (bleeding into subarac. space )

Microaneurysms occur in cerebral arteries in hypertensive patients - Their rupture causes intracerebral haemorrhage OR haemorrhagic stroke (only 20% tho)

Question 12

compare 2 types of aneurysms which occur in the heart?

What can the 2nd type be due to? What are the 2 causes?

Answer 12

AAA, often secondary to atheroma + may:
-Rupture, causing intraperitoneal haemorrhage + death OR throw off thromboemboli, causing ischaemia + gangrene

Stretched aortic ring, can be due to
-Aortic dissection (‘dissecting aneurysm’)
-Syphilitic aneurysm
Both develop due to media weakening and may rupture, causing haemopericardium + cardiac tamponade

Question 13

What do aneurysms look like?
What are saccular aneurysms caused by?

Answer 13

Most aneurysms are caused by atheroma and are fusiform (spindle shaped)

However, ‘Berry’ aneurysms are saccular - Saccular aneurysms are caused by focal damage to a vessel, eg infection ( bacteria may lodge in an atheromatous plaque)

Question 14

3 Complications of aneurysms?

Answer 14

.

Question 15

Special types of aneurysm inc Aortic dissection (‘Dissecting aneurysm’). Describe this - where is typical, scenario

What are the 2 consequences of aortic dissection?

Answer 15

Typical in elderly w medial degeneration
or Marfan’s (congenitally weak media)

Scenario: tear in the intima (typically aortic root). This tear allows blood to enter between the layers of the aorta + form a parallel track in the wall!

This may rupture back into aorta (‘double-barrelled aorta’) OR rupture thru adventitia -> death by Cardiac tamponade (into pericardium) or Exsanguination (eg into the Mediastinum)

Question 16

compare and contrast 3 subtypes of Ischaemic strokes . Describe each of these and sources for them

Answer 16

Thrombo-embolic: thrombus over atheroma at carotid bifurcation; mural thrombus from heart (e.g. after MI or, in AF). If these thrombi break off + lodge in cerebral arteries -> stroke

Primary occlusion of intracerebral artery/arteriole (atheroma w/in cerebral vessel itself!)

Lacunar: occlusion of single penetrating lenticulostriate artery. Tiny lesions 0.2-15mm

Question 17

Explain The ‘ischaemic penumbra’
however what can ischaemic damage still result in?

Answer 17

When the core of an infarct undergoes irreversible necrosis - but adj territory is compensated for by local blood supplies - therefore if arterial perfusion can be restored within 3-6hrs max the ‘penumbra’ area may be salvaged!

BUT, ischaemic damage to endothelium may render newly perfused vessels leaky, so restoring function not as good + re-bleeding may occur.

Question 18

What kind of texture do cerebral lesions have?

What is left when liquefaction necrosis is cleared up?

Answer 18

Cerebral lesions due to strokes are soft due to liquefaction necrosis of the brain tissue
When this is cleared by macrophages, cystic spaces remain in the brain + nearby gliosis is the brain’s equivalent of scarring.

Question 19

What are lacunar infarcts?
where are they typical, what do they affect, 2 bad outcomes?

Answer 19

Typical in diabetes/hypertension, usually w extensive small vessel atheroma.
Small lesions 2-15mm, affecting deep penetrating arterioles of basal ganglia, brainstem, thalamus and deep white matter.

Tiny cystic infarcts may be devastating, eg if internal capsule is involved=hemiplegia
If white matter= can be silent or lead to vascular dementia.

Question 20

What is TIA? What are the risk factors of TIA causing a stroke?

Answer 20

‘Transient ischaemic attack’ – neurological deficit lasting < 12-24 hours
Likelihood of full blown stroke v high after this
Risks: Age, BP, Clinical Symptoms, Duration > 1 hour, Diabetes
Immediate intervention to prevent subsequent strokes

Question 21

3 parts of Hyperacute stroke management?

Answer 21

Antiplatelet therapy:Aspirin, Clopidogrel, Dipyridamole
Thrombolysis (best within 3 hrs, may have functional benefit up to 6 hours later) tPa
Evacuation of clot

Question 22

5 parts of Stroke prevention?

? cessation: ?
? for at risk (risk reduction for stroke 25%)
Decrease ?
Treat ?: ?, but greater risk of ? - therefore New direct ? developed!
Fast recognition of ?

Answer 22

Smoking cessation: tax on cigarettes.
Aspirin for at risk (risk reduction for stroke 25%)
Decrease salt intake
Treat atrial fibrillation: warfarin (70% protection vs aspirin, but greater risk of haemorrhagic complications) - therefore New direct oral anticoagulants developed!
Fast recognition of TIA

Question 23

Explain and compare Subarachnoid vs subdural haemorrhage

Answer 23

Question 24

How can we get infarctions in the watershed zone?

Answer 24

Massive drops in BP can starve tissue at border zones between the anterior, posterior and middle cerebral arteries (watershed zone)

In the watershed zone, the blood supply is already limited compared to other brain areas. The reduced blood pressure further makes watershed zone becomes more susceptible to ischemia and infartion