Aneurysms, hypertension and stroke Flashcards

1
Q

What is hypertension?

A

sustained elevation of systolic and diastolic BP (>140/90mmHg)

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2
Q

Whats the difference between primary and secondary hypertension?

A
  • primary (idiopathic) - no identifiable cause

- secondary (to) - renal disease, adrenal tumours, aortic coarction, steroid use

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3
Q

What effect does hypertension have on organs?

A
  • Heart - LV hypertrophy, left heart failure
  • Lungs - pulmonary oedema from LHF
  • Kidneys - nephrosclerosis, renal failure
  • eye - retinal capillary damage, haemorrhages, exudates
  • Brain - microaneurysms, stroke, ischaemia, dementia
  • BVs - atheroma
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4
Q

What is hypertensive nephropathy?

A
  • loss of a glomerulus causes atrophy of the nephron
  • renal arteries thicken
  • glomerulosclerosis
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5
Q

What is hypertensive retinopathy?

A
  • Early - nicking of retinal veins by overlying arterioles
  • moderate - flame shaped haemorrhages; cotton wool spots; hard exudates around macula; straightened, wider capillaries.
  • Late - papilloedema, haemorrhage
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6
Q

Which vessels control BP?

A
  • BP is controlled by the arterioles, they are the resistance vessels which can constrict or relax to alter the TPR
  • Change in lumen’s diameter is the most important factor
  • a 50% decrease in diameter gives a 16-fold increase in pressure
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7
Q

How do atheromas form?

A
  • resistance arterioles show elastic duplication
  • damaged arterioles leak plasma into the vessel wall and cause hardening of the media
  • shear force appiled by high pressure CO on endothelium - likely to develop atheroma
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8
Q

How do we monitor BP?

A
  • Baroreceptors in the carotid sinus sense stretch, stimulates vasodilation/constriction in response
  • chemoreceptors in the carotid and aortic bodies respond to reduced oxygen tension, increased CO2 and increased hydrogen ions
  • RAAS system - renin released by juxtoglomerular complex
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9
Q

What is the RAAS system?

A
  • renin cleaves angiotensinogen into angiotensin I

- Lung capillary endothelia cells secrete ACE, which converts AngI to AngII

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10
Q

What does Angiotensin 2 cause?

A
  • constriction of resistance vessels
  • stimulate aldosterone and ADH release - increase water reabsorption by kidney
  • stimulate thirst
  • stimulate cardiac hypertrophy
  • increase NA release and decrease reuptake - enhances sympNS
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11
Q

What is an aneurysm?

A
  • bulge in the BV wall
  • true aneurysm is when the entire wall bulges
  • false aneurysm is when the artery wall is punctured and blood tracks out into adjacent tissue - expands as further blood is pumped out
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12
Q

What are the 4 main types of aneurysm?

A
  • Berry (typically occur at the bifurcations of CoW arteries. Rupture causes subarachnoid haemorrhage)
  • Abdominal aortic aneurysm (secondary to atheroma - cause ischaemia by throwing off thromboemboli, intraperitoneal haemorrhage and death)
  • Microaneurysm (cereberal arteries of hypertensive patients - causes intracerebral haemorrhage if rupture)
  • Stretched aortic ring - due to aortic dissection, syphilitic aneurysm.
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13
Q

Name 3 complications from aneurysms

A
  • rupture
  • thrombosis
  • thromboembolism
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14
Q

What is a stroke?

A
  • sudden onset of neurological deficit due to cardiovascular cause
  • commonest in elderly men
  • factors are: hypertension, AF,smoking, diabetes mellitus and high cholesterol
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15
Q

What are the 2 types of stroke?

A
  • Ischaemic (80%) - thromboembolic, primary occlusion of intracerebral artery/arteriole
  • Haemorrhagic (20%) - most commonly caused by rupture of cerebral microaneurysm.
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16
Q

What is the ischaemic penumbra?

A
  • the core of an infarct will undergo irreversible necrosis
  • adjacent territory is only relatively ischaemic - may get compensation from nearby vessels
  • if we can restore perfusion within 3 hrs, penumbra territory may be salvaged
17
Q

What 3 factors affect clinical effects of stroke?

A
  • site
  • size
  • speed of restoration of circulation/ evacuation of clot
18
Q

Where can herniation occur due to SOL?

A
  • beneath falx cerebri
  • through tentorium cerebelli
  • through foramen magnum
19
Q

What is liquefaction necrosis?

A

A type of necrosis which results in a transformation of the tissue into a liquid viscous mass

20
Q

What are Lacunar infarcts?

A

Small lesions affecting deep penetrating arterioles (in basal ganglia, brainstem etc)
- typically seen in diabetes and/or hypertension

21
Q

What is TIA?

A
  • Transient ischaemic attack - neurological deficit lasting less than 12-24hrs
  • 30% likelihood of stroke in next 5 years
  • 4-20% within 90 days
  • Factors: age, BP, diabetes
22
Q

What stroke management strategies are there?

A
  • Antiplatelet therapy - aspirin, Clopidogrel, Dipyridamole
  • Thrombolysis (best within 3 hours)
  • Evacuation of clot
23
Q

How can we try to prevent stroke?

A
  • Cigarette tax
  • Aspirin for those at risk (decreases risk by 25%)
  • Decrease salt intake
  • Treat AF - warfarin
  • Fast recognition of TIA
24
Q

Name 5 other types of intracranial haemorrhage

A
  • Extradural haemorrhage
  • subdural haemorrhage
  • subarachnoid haemorrhage
  • cerebral contusion
  • petechial haemorrhages
25
Q

What is extradural haemorrhage?

A
  • Haemorrhage outside the dura
  • typically parietal due to middle meningeal artery rupture
  • common lucid interval after initial consciousness - dura takes time to stretch
26
Q

What is subdural haemorrhage?

A
  • rupture of veins crossing subdural space
  • can be acute due to trauma
  • or chronic - typical in dementia due to shrinking
27
Q

What is subarachnoid haemorrhage?

A
  • rupture of berry aneurysm

- SAH is often considered together with a stroke as it can lead to spasm of cerebral arteries causing damage/death

28
Q

What is cerebral contusion?

A

Bruise of brain tissue after trauma

- usually opposite side to where the trauma was

29
Q

What are petechial haemorrhages?

A
  • obstruction of small arterioles and capillaries
  • multiple tiny infarcts from capillary obstruction
  • isnt a stroke as it isnt primarily cerebral blood vessels
30
Q

What is the difference between subarachnoid and subdural haemorrhage?

A
  • SAH - blood is confined between pia/arachnoid and follows contour of brain
  • Subdural - clot lies between arachnoid and dural meninges
31
Q

What is an infarction?

A

Tissue necrosis due to compromised blood supply

32
Q

What is a watershed infarction?

A
  • if BP suddenly drops, tissue at the periphery of adjacent arterial territories may be starved of oxygen and infarct
  • eg. splenic flexure of colon and watershed zones of CoW