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Neuro: Sem 3 > Aneurysms, Hypertension and Stroke > Flashcards

Aneurysms, Hypertension and Stroke Flashcards

1
Q

What is hypertension?

A

sustained elevation of systolic and diastolic blood pressure > 140/90 mmHg

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2
Q

primary causes of hypertension

A

No identifiable cause

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3
Q

secondary causes of hypertension

A
  • renal disease
  • adrenal tumours
  • aortic coarctation
  • Rx/Antiangiogenic drugs
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4
Q

blood vessel damage by hypertension

A

contribute to all aspects of hypertensive organ damage. Blood vessels themselves undergo atheroma and aneurysm formation in large vessels, elastic reduplication in small vessels.

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5
Q

heart damage by hypertension

A

left ventricular hypertrophy, left heart failure (LHF)

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6
Q

lung damage by hypertension

A

pulmonary oedema due to LHF

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7
Q

kidney damage by hypertension

A

nephrosclerosis, renal failure

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8
Q

eye damage by hypertension

A

retinal capillary damage, haemorrhages, exudates

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9
Q

brain damage by hypertension

A

: microaneurysms and stroke, ischaemic cortical atrophy/ dementia.

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10
Q

what is hypertensive heart disease?

A

Increased load causes concentric left ventricular hypertrophy

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11
Q

what is hypertensive neuropathy?

A
  • Granular cortical atrophy due to nephrosclerosis – loss of a glomerulus causes atrophy of the nephron.
  • thickened renal arterioles
  • glomerulosclerosis
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12
Q

early hypertensive retinopathy

A

‘Nicking, of retinal veins by overlying arterioles, normally they run alongside

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13
Q

moderate hypertensive retinopathy

A
  • Straightened, wider capillaries
  • Flame shaped haemorrhages
  • ‘Cotton wool’ spots
    (later) ‘Hard’ exudates around macula
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14
Q

late chronic/malignant hypertensive retinopathy

A

papilloedoma

haemorrhage

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15
Q

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

A

Blood pressure is controlled by the arterioles, especially the latter – they are the ‘resistance vessels’ which can constrict or relax to alter the peripheral resistance.

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16
Q

atheroma

A

= bigger vessels

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17
Q

hypertension

A

= smaller vessels

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18
Q

how does blood vessel change in hypertension

A
  • Resistance arterioles show elastic duplication

‘Hyaline arteriosclerosis’ damages arterioles as plasma exudes into the intima and deeper layers of the wall, sometimes out of the smaller vessels – glassy pink appearance on histology

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

(Atheroma tends to affect larger blood vessels, so does not increase peripheral resistance sufficiently to cause hypertension. However the two diseases are encountered together most of the time

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19
Q

what is an aneurysm

A

bulge in the wall of a blood vessel

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20
Q

what is a true aneurysm?

A

when the entire wall of the vessel bulges. Sometimes part of the wall is cut or torn, usually by trauma, and the inner layers bulge through the tear – some people would term this a false aneurysm because not all layers are affected

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21
Q

what is a false aneurysm?

A

occur if the artery wall is punctured (eg during an arteriogram or angioplasty) and blood tracks out into adjacent tissue, but is contained locally by scar tissue. This expands as further blood is pumped out of the vessel wall.

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22
Q

why are aneurysms pulsatile?

A

Due to arterial blood flow, but this effect may be diminished by thrombus or severe atheromatous thickening

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23
Q

where do aneurysms occur?

A

arteries and occasionally the left ventricle but rare in veins

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24
Q

why do aneurysms occur at points of weakness?

A

due to atheroma or due to inflammatory damage (e.g. syphilis), occasionally due to connective tissue abnormalities and sometimes following trauma

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25
Q

what is a berry (saccular) aneurysm?

A

typically occur at the bifurcations of the arteries in the Circle of Willis.
Their rupture usually causes subarachnoid haemorrhage

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26
Q

what is a microaneurysms

A

typically occur in cerebral arteries in patients with hypertension.
Their rupture causes intracerebral haemorrhage

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27
Q

what is an abdominal aortic aneurysm?

A

This is usually secondary to atheroma and may:

  • Rupture, causing intraperitoneal haemorrhage and death
  • Throw off thromboemboli, causing ischaemia and gangrene
28
Q

what is a stretched aortic ring aneurysm?

A

This can be due to
-Aortic dissection (‘dissecting aneurysm’)
-Syphilitic aneurysm
Both develop due to weakening of the media and may rupture, causing haemopericardium and cardiac tamponade

29
Q

what do aneurysms look like?

A

Most aneurysms are secondary to atheroma and are fusiform (spindle shaped)

30
Q

when do saccular aneurysms occur?

A

after focal damage to a vessel (e.g. infection where bacteria may lodge in an atheromatous plaque)

31
Q

what do berry aneurysms look like?

A

saccular due to focal vessel wall weakness at point of bifurcation

32
Q

what are the complications of aneurysms?

A
  • rupture
  • thrombosis
  • thromboembolism
33
Q

what is a stroke?

A

sudden onset of neurological deficit, due to cardiovascular cause.

34
Q

who are strokes most common in?

A

elderly men

35
Q

what are the modifiable factors associated with stroke?

A

hypertension, atrial fibrilation, smoking, diabetes mellitus, high cholestrol

36
Q

NHS budget spent on stroke?

A

7%

37
Q

how many strokes are ischaemic?

A

80%

38
Q

what is an ischemaic stroke?

A

Thrombo-embolic: sources include thrombus over atheroma at carotid bifurcation; mural thrombus from heart (e.g. after myocardial infarction “mural thrombus” or, in atrial fibrillation, from atrial appendage)
Primary occlusion of intracerebral artery/arteriole
Lacunar: occlusion of single penetrating artery (lenticulostriate). ~ ¼ of ischaemic strokes fall into this category. Tiny lesions 0.2-15mm diameter, can be silent, associated with white matter lesions and ‘vascular’ dementia, or catastrophic, e.g. brainstem.

39
Q

how many strokes are haemorrhagic?

A

20%

40
Q

what is an haemorrhagic stroke?

A

most commonly due to rupture of cerebral microaneurysm secondary to hypertension

41
Q

why do thrombo-embolic strokes appear haemorrhagic?

A

due to leakage from damaged capillaries at sites of infarction

42
Q

what is the ischameic penumbra?

A

The core of an infarct will undergo irretrievable and irreversible necrosis
The adjacent territory is only relatively ischaemic, as there may be a degree of compensation from nearby blood supplies

43
Q

within how many hours should arterial perfusion be restored to salvage penumbra territory?

A

3 hours, though some benefit within 6 hours

44
Q

why are cerebral lesions due to stroke soft?

A

due to liquefaction necrosis of the brain tissue. When this is cleared by macrophages, cystic spaces remain in the brain.

45
Q

where are lacunar infarcts seen?

A

in diabetes and/or hypertension, usually with extensive small vessel atheroma.

46
Q

what do lacunar infarcts affect?

A

deep penetrating arterioles – typically to basal ganglia, brainstem, thalamus and deep white matter, small lesions 2-15mm.

47
Q

what can occur from a tiny cystic infarct?

A

if internal capsule is involved a 2mm infarct could cause a dense hemiplegia. white matter can be clinically silent but contribute to vascular dementia

48
Q

what is TIA?

A

‘Transient ischaemic attack’ – neurological deficit lasting < 12-24 hours

49
Q

likelihood of stroke after TIA?

A

within 5 years = 30%
within 90 days = 4-20%
within 48 hours = 50%

50
Q

risk factors of TIA

A

Age, Blood Pressure, Clinical Symptoms, Duration > 1 hour, Diabetes

51
Q

how is stroke managed in stroke units?

A

anti-platelet therapy (aspirin, clopidogrel, dipyridamole), thrombolysis (best within 3 hours), evacuation of clot

52
Q

stroke prevention measures?

A
  • smoking tax
  • aspirin for those at risk
  • decrease salt intake
  • treat atrial fibrilation (warfarin) or new direct oral anticoagulant
  • fast TIA detection
53
Q

what is a subarachnoid haemorrhage?

A

often considered together with occlusive or haemorrhagic strokes.

54
Q

why is SAH not a stroke technically?

A

it involves vessels which are external to the brain itself. However, SAH can induce spasm in cerebral arteries, one reason for the high mortality and morbidity in this condition.

55
Q

types of intracranial haemorrhage other than stroke

A
  • extradural haemorrhage
  • subdural haemorrhage
  • subarachnoid haemorrhage
  • cerebral contusion
  • multiple petechial haemorrhages
56
Q

Extradural haemorrhage

A

Typically parietal due to rupture of middle meningeal artery, often acute. ‘Lucid interval’ common after initial unconsciousness because tough dura takes time to stretch.

57
Q

subdural haemorrhage

A

(eg rupture of veins crossing subdural space; may be acute (post trauma, similar to extradural) or chronic - typical in dementia as shrunken brain renders shearing injury more likely.)

58
Q

subarachoid haemorrhage

A

(eg rupture of Berry aneurysm). SAH is often considered together with stroke, since brain damage/death can occur secondary to the haemorrhage due to spasm of cerebral blood arteries.

59
Q

cerebral contusion

A

(trauma – may be ‘contre-coup’ injury)

60
Q

Multiple petechial haemorrhages

A

(obstruction of small arterioles and capillaries eg falciparum malaria, DIC). Capillary obstruction causes multiple tiny infarcts but because the disease is not primarily of cerebral blood vessels and disseminated through the body, this is not a stroke.

61
Q

subarachoid haemorrahge often follows what?

A

ruptured berry aneurysm so blood confined beneath pia/arachnoid following brain contours

62
Q

what is subdural haematoma result of?

A

trauma. blood clot lies between arachnoid and dural meninges

63
Q

why does watershed zone infarction occur?

A

due to hypoperfusion at the boundaries of arterial territories

64
Q

where does watershed zone infarction occur?

A

at border between middle and anterior cerebral artery supply in patient with profound hypotension due to MI

65
Q

how does infarction occur?

A

If the blood pressure suddenly drops profoundly, eg following profuse haemorrhage, tissue at the periphery of adjacent arterial territories may be starved of oxygen and undergo infarction.

Neuro: Sem 3 (3 decks)

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