Hypertension, Aneurysms, Stroke Flashcards

1
Q

HYPERTENSION:
What is it?

What are the two types? What are they caused by?

Which vessels control BP?

Where do atheromas commonly form? Where are they more likely to be?

A
  • Sustained elevated BP > 140/90mmHg
  • o Primary; Idiopathic, no identifiable cause
    o Secondary to Renal, Adrenal, Aortic Coarctation, Drugs
  • Arterioles (resistance vessels)
  • In larger systemic vessels; more likely at damaged endothelial sites due to HTN
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2
Q

Organ damage by HTN:
How are the Blood vessels affected?

What is Hyaline Atherosclerosis?

How is the Heart affected?

How are the Lungs affected?

How is the Kidney affected?

What does the Loss of glomeruli cause?

How is the Eye affected? What are the early, moderate, and late signs seen?

How is the Brain affected?

A
  • Can develop Atheroma, Aneurysm and the Small vessels can undergo Elastic duplication (remodelling of elastic lamina)
  • Hyaline Atherosclerosis damage arterioles as plasma exudes deep into wall layers; glassy pink appearance
  • LV Hypertrophy, L-sided Heart Failure (LHF)
  • Pulmonary Oedema; due to LHF
  • Nephrosclerosis, Renal failure
  • Granular cortical atrophy; atrophy of nephron
  • Retinal capillary damage, Haemorrhages, Exudates;
    o Early signs; nicking of retinal veins by overlapping arterioles
    o Moderate signs; flame-shaped haemorrhages, ‘Cotton wool’ spots, Hard exudates
    o Late chronic or Malignant acute; Papilloedema, Haemorrhage
  • Microaneurysms, Stroke, Ischaemic cortical atrophy/Dementia
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3
Q

ANEURYSMS:
What is a True and False aneurysm?

Where do they occur?

What are the 2 types found in the brain? Where are they typically found? What occurs if it ruptures?

What is AAA? What is it secondary to? What occurs if it ruptures?

What is an Aortic Dissecting aneurysm? What are the ways in which it can rupture? Who is it common in?

A
  • o True aneurysm; entire wall bulges, part of wall can tear, and inner layers bulge through the tear
    o False aneurysm; wall punctured (e.g. during angioplasty) and blood leaks
  • At points of weakness due to Atheroma, Inflammation, Connective tissue abnormalities, Trauma
  • o Microaneurysms; In Cerebral arteries in those with HTN, Rupture = IC Haemorrhage
    o Berry aneurysms; At the bifurcations in the Circle of Willis, Rupture = SA Haemorrhage
  • Abdominal Aortic Aneurysm; secondary to Atheroma, Rupture = Intraperitoneal Haemorrhage/Death
  • Tear in t.Intima, so blood enters aortic wall, causing wall layers to separate
    o Can rupture back into aorta (Double-barrelled aorta)
    o Can rupture though adventitia to cause Cardiac Tamponade (in pericardium) or Exsanguination (into mediastinum)
    o Common in elderly with medial degeneration, Marfan’s syndrome (congenital weak t. media)
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4
Q

STROKE:
What is it?

What are the modifiable factors strongly linked with stroke?

What is Liquefaction necrosis?

What is the Watershed Zone? What is it due to?

What are the 2 types of stroke? Which is more common?

What is a Lacunar Infarct? When is it typically seen?

What causes Haemorrhagic stroke?

Why can Thromboembolic strokes appear as haemorrhagic?

A
  • Sudden onset of neurological deficit due to Cardiovascular cause
  • HTN, AF, Smoking, Diabetes, High Cholesterol
  • Makes cerebral lesions soft; cleared by macrophages to leave cystic spaces
  • Infarct at borders between the ACA/MCA/PCA; due to profound Hypoperfusion at boundaries of arterial territories
  • Ischaemic (80%), Haemorrhagic (20%)
  • Occlusion of a single penetrating artery that provides blood to the brain’s deep structures
    o Typically seen in Diabetes and/or HTN with extensive small vessel atheroma
  • Rupture of Cerebral Microaneurysms, secondary to HTN
  • Due to leakage from damaged capillaries at the infarct site
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5
Q

What is the Ischaemic Penumbra?

What can restore the Penumbra territory?

What can make restoration more difficult?

What is a Transient Ischaemic Attack (TIA)? How long does it last?

Why does it need to be investigated immediately after?

A
  • Core of infarct will undergo irreversible necrosis; adjacent territory less ischaemic and there may be some compensation from nearby arteries
  • Restoration of perfusion within 3 hours
  • Ischaemic damage to the endothelium
  • Neurological deficit lasting 12-24 hours
  • It increases the likelihood of a full-blown Stroke
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6
Q

How is a stroke treated?

How is a stroke prevented?

A
  • • Antiplatelets; Aspirin, Clopidogrel, Dipyridamole
    • Thrombolysis; best within 3 hours, but can still be useful within 6 hours - TPA
    • Surgery to remove clot (Thrombectomy)
  • • Aspirin, Warfarin given for AF, fast recognition of TIA
    • Lifestyle changes; Smoking cessation, ↓Salt intake
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7
Q

What are the types of Intracranial Haemorrhages? What are they due to? What can they lead to?

A
  • • Epidural; typically rupture of MMA, presents with LUCID INTERVAL as blood slowly stretches the dura

• Subdural; rupture of veins crossing subdural space, can be acute (Trauma) or chronic (Shrunken brain in dementia makes shearing brain injury more likely)

• Subarachnoid; rupture of Berry aneurysms, high mortality
o Causes Vasospasm of cerebral arteries = Stroke

  • Cerebral Contusion; secondary to trauma
  • Multiple Petechial Haemorrhages; obstruction of small arterioles/capillaries, causing lots of tiny infarcts; secondary to DIC, Malaria
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