Aneurysms, hypertension and stroke

Question 1

What is hypertension?

Answer 1

Sustained elevation of systolic and diastolic blood pressure (> 140/90mmHg)

Question 2

What are primary and secondary causes of hypertension?

Answer 2

• No identifiable primary cause - idiopathic
• Secondary - renal disease, adrenal tumours, aortic coarctation, steorid Rx

Question 3

How can hypertension cause organ damage? (vessels, heart, lungs, kidney, eye, brain) [brief]

Answer 3

• Vessels - atheroma, aneurysm, elastic reduplication
• Heart - left ventricular hyeprtrophy, LHF
• Lungs - pulmonary oedema due to LHF
• Kidney - nephroscelerosis, renal failure
• Eye - retinal capillary damage, haemorrhages, exudates
• Brain - microaneurysms, stroke, ischaemic cortical atrophy

Question 4

What is hypertensive heart disease?

Answer 4

When increased load causes concentric left ventricular hypertrophy. This can lead to heart failure.

Question 5

What happens in hypertensive nephropathy?

Answer 5

Granular cortical atrophy due to nephrosclerosis - loss of a glomerulus causes atrophy of the nephron.

Question 6

What happens in hypertensive retinopathy as it gets worse?

Answer 6

• Early - nicking of retinal veins by overlying arterioles, normally they run alongside.
• Moderate - straightened, wider capillaries, flame shaped haemorrhages, ‘cotton wool’ spots, hard exudates around macula
• Late chronic/malignant - Papilloedema, haemorrhage

Question 7

What change in parameter of an arteriole can alter the systemic arterial blood pressure, thus causing hypertension?

Answer 7

Luminal diameter - resistance of flow is equiv to the fourth power of the diameter.

Question 8

What is the difference between atherosclerosis and arteriosclerosis?

Answer 8

Atherosclerosis is the narrowing of the artery because of plaque build-up, a disease of the intima.

Arteriosclerosis refers to the general hardening/thickening of the artery walls, so atherosclerosis is a type of it.

Question 9

Does atheroma cause hypertension?

Answer 9

Atheroma tends to affect larger blood vessels so does not increase TPR, so unlikely to cause hypertension. The two diseases are often encountered together though.

Question 10

What happens to blood vessels (arterioles) in hypertension? What is hyaline arteriosclerosis?

Answer 10

Resistance arterioles show elastic duplication in hypertension.

Plasma exudes into the intima and deeper layers of the wall (media), causing hardening and a ‘pink glassy’ structure. This is ‘hyaline arteriosclerosis’.

The endothelium in hypertension is subject to damage by shearing forces applied by high cardiac output: atheroma is likely to develop at sites of endothelial damage due to hypertension.

Question 11

What 3 things stimuate renin release by the kidney juxtaglomerular complex?

Answer 11

• Low renal blood flow/pressure
• Low blood Na+
• Sympathetic NS

Question 12

How do you get from renin to angiotensin II?

Answer 12

• Angiotensinogen cleaved to angiotensin I
• By enzyme renin
• Angiotensin I activated to angiotensin II
• by ACE (from lung)

Question 13

How does angiotensin II increase blood pressure?

Answer 13

• Vasoconstriction of resistance vessels
• • ALDOSTERONE -> inc water reabsorption
• • ADH -> inc water reabsorption
• • thirst -> inc blood volume
• • cardiac hypertrophy
• • SNS -> noradrenaline inc

Question 14

What signals negative feedback in the renin-angiotensin-aldosterone system?

Answer 14

Natriuretic peptides (ANP, BNP) released by the heart

Question 15

How can ACE inhibitors (-pril) result in a dry cough as a side-effect?

Answer 15

As ACE is released from the lung surfaces, ACE inhibitors result in bradykinin build up within the lung and cause irritation resulting in a dry cough.

Question 16

What is an aneurysm?

Answer 16

A bulge in the wall of a blood vessel

Question 17

What is the difference between a ‘true’ and ‘false’ aneurysm?

Answer 17

True anuerysm is when all 3 layers of the blood vessel are affected, a false aneurysm is when not all 3 are affected, eg. it might be a punctured wall causing the bulge/expansion.

Question 18

Describe ‘berry’ (saccular) aneurysms

Answer 18

• Typically occur at bifurcations of arteries - circle of willis
• Rupture -> subarachnoid haemorrhage

Question 19

Describe microaneurysms

Answer 19

• Typically occur in cerebral arteries
• Patients with hypertension
• Rupture -> intracerebral haemorrhage

Question 20

What is a cause of abdominal aortic aneurysm? What can rupture cause?

Answer 20

• Usually secondary to atheroma
• Rupture -> intraperitoneal haemorrhage -> death
• Can also throw off clots -> ischaemia / gangrene

Question 21

What types of aneurysms result in a stretched aortic ring?

Answer 21

• Aortic dissection ‘dissecting aneurysm’
• Syphillitic aneurysm

Rupture -> haemopericardium and cardiac temponade

Question 22

Why may an aneurysm not present as pulsatile?

Answer 22

Diminished due to thrombus or severe atheromatous thickening

Question 23

At which locations do aneurysms occur?

Answer 23

In arteries and occasionally left ventricle (post MI) but very rarely in veins

Question 24

What are points/factotrs of weakness that increase susceptiblity to aneurysms?

Answer 24

• usually due to atheroma
• sometimes inflammatory damage (eg syphilis)
• occsionally due to connective tissue abnormalities (Marfan’s)
• sometimes follow trauma eg. traffic accident

Question 25

What are complications of aneurysms?

Answer 25

* Rupture * Thrombosis * Thromboembolism

Question 26

Who is more likely to have aortic dissection ('dissecting aneurysm') in the population?

Answer 26

Elderly w/ medial degeneration or Marfan's syndrome - a congenitally weak media

Question 27

Describe aortic dissection and its consequences upon rupture

Answer 27

* **Tear in the intima**, typically aortic root, allows **blood to enter the aortic wall** and form a parallel track * this may rupture **back into aorta** OR **rupture through adventitia**, causing cardiac tamponade (into pericardium) or exsanguination (into mediastinum)

Question 28

Define 'stroke'

Answer 28

Sudden onset of neurological deficit due to cardiovascular cause

Question 29

What are modifiable risk factors associated with stroke?

Answer 29

* Hypertension * Atrial fibrilation * Smoking * Diabetes mellitus * High cholesterol

Question 30

What are the two major types of stroke?

Answer 30

* Ischaemic (80%) * Haemorrhagic (20%)

Question 31

Describe the 3 types of ischaemic stroke

Answer 31

* **Thrombo-embolic**: eg thrombus over atheroma at carotid bifurcation; can be a mural thrombus from the heart (over MI) * Primary occlusion of intracerebral artery/arteriole * Lacunar (25%): occlusion of single penetrating artery, tiny lesions, silent, associated with white matter lesions and vascular dementia

Question 32

What is the most common cause of haemorrhagic strokes?

Answer 32

Rupture of cerebral microaneurysm secondary to hypertension

Question 33

What is the ischaemic penumbra?

Answer 33

The core of an infarct will undergo irreversible necrosis. The adjacent territory (penumbra) is only relatively ischaemic, as there may be a degree of compensation from nearby blood supplies. We are trying to save the penumbra!

Question 34

What is the timeframe for the 'ischaemic penumbra' to be salvaged if arterial perfusion is restored?

Answer 34

Within 3 hours, but some benefit to treatment up to 6 hours

Question 35

What 3 factors do clinical effects of stroke depend on?

Answer 35

* Site * Size * Speed (of restoration of circulation of clot)

Question 36

What are the 3 main sites at which herniation of the brain can occur in response to a space occupying lesion (massive bleed) in the brain?

Answer 36

* Beneath the FALX CEREBRI * Through the TENTORIUM CEREBELLI * Through the FORAMEN MAGNUM

Question 37

What happens after liquefication necrosis of brain tissue due to strokes?

Answer 37

Macrophages clear the area, cystic spaces remain -\> scarring

Question 38

Describe lacunar infarcts

Answer 38

* Seen in diabetes, hypertension + extensive small vessel atheroma * Affect deep penetrating arterioles - basal ganglia, brainstem, thalamus + deep white matter * Not space occupying lesions * Minimal additional symptoms due to small calibre vessels involved

Question 39

What is a TIA?

Answer 39

* transient ischaemic attack - neurological deficit lasting 12-24 hours * temporary but indication for immediate investigation and intervention

Question 40

What constitutes the stroke management in hyperacute stroke units?

Answer 40

* Antiplatlet therapy (aspirin, clopidogrel, dipyridamole) * Thrombolysis (best within 3 hours, may have functional benefit up to 6 hours later) * Evacuation of clot

Question 41

How can we prevent stroke in the population?

Answer 41

* Cigarette tax * Aspirin for those at risk (Red of 25%) * decrease salt intake * treat atrial fib - warfarin * fast recognition of TIA

Question 42

Why is subarachnoid haemorrhage not considered a stroke on technical grounds?

Answer 42

As it involves vessels which are external to the brain itself. However, can produce spasm in cerebral arteries.

Question 43

What are the types of intracranial haemorrhage?

Answer 43

* Extradural * Subdural * Subarachnoid * Cerebral contusion * Multiple petechial

Question 44

What is the difference between subarachnoid and subdural haemorrhage?

Answer 44

Subarachnoid often follows ruptured berry aneurysm; blood is confined beneath pia/arachnoid and follows brain contours. Subdural formation is result of trauma. Blood clot lies between arachnoid and dural meninges.

Question 45

Watershed zone infarcts occur due to hypoperfusion at the boundaries of arterial territories. In what 3 organs are they most common?

Answer 45

* Colon * Heart * Brain

Question 46

What are the 3 areas affected by watershed zone infarctions in the brain?

Answer 46

* Anterior, middle and posterior cerebral artery territory