Aneurysms, hypertension and stroke Flashcards

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1
Q

What is hypertension?

A

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

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2
Q

What are primary and secondary causes of hypertension?

A
  • No identifiable primary cause - idiopathic
  • Secondary - renal disease, adrenal tumours, aortic coarctation, steorid Rx
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3
Q

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

A
  • 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
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4
Q

What is hypertensive heart disease?

A

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

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5
Q

What happens in hypertensive nephropathy?

A

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

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6
Q

What happens in hypertensive retinopathy as it gets worse?

A
  • 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
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7
Q

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

A

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

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8
Q

What is the difference between atherosclerosis and arteriosclerosis?

A

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.

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9
Q

Does atheroma cause hypertension?

A

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.

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10
Q

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

A

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.

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11
Q

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

A
  • Low renal blood flow/pressure
  • Low blood Na+
  • Sympathetic NS
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12
Q

How do you get from renin to angiotensin II?

A
  • Angiotensinogen cleaved to angiotensin I
  • By enzyme renin
  • Angiotensin I activated to angiotensin II
  • by ACE (from lung)
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13
Q

How does angiotensin II increase blood pressure?

A
  • Vasoconstriction of resistance vessels
    • ALDOSTERONE -> inc water reabsorption
    • ADH -> inc water reabsorption
    • thirst -> inc blood volume
    • cardiac hypertrophy
    • SNS -> noradrenaline inc
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14
Q

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

A

Natriuretic peptides (ANP, BNP) released by the heart

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15
Q

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

A

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.

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16
Q

What is an aneurysm?

A

A bulge in the wall of a blood vessel

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17
Q

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

A

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.

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18
Q

Describe ‘berry’ (saccular) aneurysms

A
  • Typically occur at bifurcations of arteries - circle of willis
  • Rupture -> subarachnoid haemorrhage
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19
Q

Describe microaneurysms

A
  • Typically occur in cerebral arteries
  • Patients with hypertension
  • Rupture -> intracerebral haemorrhage
20
Q

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

A
  • Usually secondary to atheroma
  • Rupture -> intraperitoneal haemorrhage -> death
  • Can also throw off clots -> ischaemia / gangrene
21
Q

What types of aneurysms result in a stretched aortic ring?

A
  • Aortic dissection ‘dissecting aneurysm’
  • Syphillitic aneurysm

Rupture -> haemopericardium and cardiac temponade

22
Q

Why may an aneurysm not present as pulsatile?

A

Diminished due to thrombus or severe atheromatous thickening

23
Q

At which locations do aneurysms occur?

A

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

24
Q

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

A
  • usually due to atheroma
  • sometimes inflammatory damage (eg syphilis)
  • occsionally due to connective tissue abnormalities (Marfan’s)
  • sometimes follow trauma eg. traffic accident
25
Q

What are complications of aneurysms?

A
  • Rupture
  • Thrombosis
  • Thromboembolism
26
Q

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

A

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

27
Q

Describe aortic dissection and its consequences upon rupture

A
  • 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)
28
Q

Define ‘stroke’

A

Sudden onset of neurological deficit due to cardiovascular cause

29
Q

What are modifiable risk factors associated with stroke?

A
  • Hypertension
  • Atrial fibrilation
  • Smoking
  • Diabetes mellitus
  • High cholesterol
30
Q

What are the two major types of stroke?

A
  • Ischaemic (80%)
  • Haemorrhagic (20%)
31
Q

Describe the 3 types of ischaemic stroke

A
  • 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
32
Q

What is the most common cause of haemorrhagic strokes?

A

Rupture of cerebral microaneurysm secondary to hypertension

33
Q

What is the ischaemic penumbra?

A

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!

34
Q

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

A

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

35
Q

What 3 factors do clinical effects of stroke depend on?

A
  • Site
  • Size
  • Speed (of restoration of circulation of clot)
36
Q

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?

A
  • Beneath the FALX CEREBRI
  • Through the TENTORIUM CEREBELLI
  • Through the FORAMEN MAGNUM
37
Q

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

A

Macrophages clear the area, cystic spaces remain -> scarring

38
Q

Describe lacunar infarcts

A
  • 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
39
Q

What is a TIA?

A
  • transient ischaemic attack - neurological deficit lasting 12-24 hours
  • temporary but indication for immediate investigation and intervention
40
Q

What constitutes the stroke management in hyperacute stroke units?

A
  • Antiplatlet therapy (aspirin, clopidogrel, dipyridamole)
  • Thrombolysis (best within 3 hours, may have functional benefit up to 6 hours later)
  • Evacuation of clot
41
Q

How can we prevent stroke in the population?

A
  • Cigarette tax
  • Aspirin for those at risk (Red of 25%)
  • decrease salt intake
  • treat atrial fib - warfarin
  • fast recognition of TIA
42
Q

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

A

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

43
Q

What are the types of intracranial haemorrhage?

A
  • Extradural
  • Subdural
  • Subarachnoid
  • Cerebral contusion
  • Multiple petechial
44
Q

What is the difference between subarachnoid and subdural haemorrhage?

A

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.

45
Q

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

A
  • Colon
  • Heart
  • Brain
46
Q

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

A
  • Anterior, middle and posterior cerebral artery territory