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VMS 2007 > Neuropathology: Circulatory Diseases > Flashcards

Neuropathology: Circulatory Diseases Flashcards

1
Q

What is the glymphatic system?

A

waste clearance system that utilises a unique system of perivascular channels formed by astroglial cells

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2
Q

What is the function of the glymphatic system?

A
  • efficent elimination of soluble proteins and metabolites from the CNS
  • Helps distribute non-waste compounds

may be supressed in certain diseases

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3
Q

What is vasogenic oedema?

A

Injury to the vascular endothelium -> breakdown of the blood-brain barrier -> permeability and leakage -> fluid spreads between cells

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4
Q

Name 5 causes of vasogenic oedema

A
  1. Inflammation
  2. Tumours
  3. Haemorrhage/ Contusions
  4. Infarcts
  5. Hypertension
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5
Q

What does intracellular cytotoxic oedema look like

A

hydropic degeneration
* astrocytes, neurons, endothelial cells, swelling of the cytoplasm

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6
Q

What causes cytotoxic intracellular oedema?

A

Cellular injury with disruption of the membrane- ATP-dependent NA+/ K+ pumps

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7
Q

What is cytotoxic oedema related to?

A
  • decrease in energy supply
  • Ischaemia
  • Hypoxia
  • Metabolic inhibitors
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8
Q

What is hydrostatic oedema?

A

Accumulation of fluid in the interstitial space

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9
Q

What is hypo-osmotic oedema?

A
  • Over consumption of water leading to dilution of plasma
  • Fluid moves to brain plasma causing salt poisioning
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10
Q

What is primary traumatic brain injury?

A
  • Mechanical disruption of tissue
  • Microvascular lesions
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11
Q

What is secondary traumatic brain injury?

A
  • Occurs within hours to days after injury
  • Changes lead to ischaemia
  • Frequently fatal
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12
Q

What supplies oxygen to the brain?

A

O2 is supplied to the brain from the internal carotid and vertebral arteries which anastamose ventral to the brainstem and at the circle of willis

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13
Q

What is an ‘end-artery’ ?

A

an arterial branch that penetrates the brain

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14
Q

What is a cerebral infarction?

A

sudden occlusion of the arterial branch

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15
Q

What causes a cerebrovascular accident ‘stroke’?

A

Central haemorrhage or infarction

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16
Q

What is ischemic myelopathy?

A

herniation of the fibrocartilage from the intervertebral disc into the vasculature, forming occlusive emboli

17
Q

What does cytotoxic oedema look like?

A

Sweling of the cytoplasm +/- the nucleus
related to a decrease in energy supply (ischaemia, hypoxia, decreased metabolic inhibitors)

18
Q

What are the three sites where herniation occurs?

A
  • Foramen magnum
  • Falx cerebri
  • Tentorium cerebelli
19
Q

Give 4 possible causes of vasogenic oedema

A
  1. Oedema disease
  2. Focal symetrical encephalomalacia
  3. Mulberry heart disease
  4. Thiamine deficiency
20
Q

Give two possible causes of cytotoxic oedema

A
  1. Early stages of hypoxic-ischaemic injury
  2. Ammonia toxicity in hepatic and renal encephalopathy
21
Q

What cells in the brain are the most susceptible to injury?

A
  • Neurones (high metabolic activity) and high energy use
  • Endothelial cells are the least sensitive
22
Q

What causes impaired cell utilisation of O2?

A

cyanide poisoning or fluroacetate

23
Q

Where do small emboli tend to lodge in the brain?

A

tend to lodge close to the grey/ white matter junction

24
Q

Where do the venous sinuses of the dura mater empty into?

A

Jugular veins and also communicate with the cranial bones

25
Q

Give 4 causes of cerebral infarction

A

Thromboembolism
2. Feline cardiomyopathy
3. Septic thrombosis
4. Parasitic (dirofilaria immitis)
5. Fibrocartilaginous emboli

26
Q

What does the consequence of vascular osbtrcution depend on?

A
  • Type and size of the obstructed blood vessel
  • Speed and onset
  • Existence and capacity of the collateral circulation
27
Q

What do CNS infarcts tend to undergo?

A
  • Liquefactive necrosis
  • Softening (malacia)
  • Swelling
28
Q

What colour do grey arterial infarcts tend to be?

A

red/ haemorrhagic

29
Q

What colour do white arterial infarcts tend to be?

A

pale

30
Q

What is fibrocartilaginous embolic myelopathy?

A

Herniation of fibrocartilage from the intervertebral disc into the vasculature, forming occlusive emboli
Trauma to the nucleus pulposus causes it to fragment and the pressure of the trauma forces small fragments into damaged veins, venous plexus or small arterioles

embolised fibrocart material resembels nucleus pulposus -> infarction

31
Q

Where does water in the brain come from?

A
  • Water comes from the blood and ultimately returns to it by re-entry at the venous ends of the capillaries
  • little water passes through cerebrospinal fluid
32
Q

What are dura mater lymphatics?

A

Network of lymphatics in the meninges running alongside the dural venous sinuses and extending upon the dura mater surrounding the brain

33
Q

What are the three sites of herniation?

A
  1. Falx cerebri
  2. Tentorium cerebelli
  3. Foramen magnum
34
Q

What is the pathophysiology of oedema?

A
  • Compression and disrupted vessels go on to cause ischaemia
  • excitatory neurtransmitters
  • increased intracellular calcium
  • proteloytic enzymes -> neuronal necrosis
  • high levels of inflammatory mediators
  • vasospasm
35
Q

What are the 5 causes of hypoxic brain injury?

A
  1. Vascular obstruction
  2. Complete cessation of cerebral circulation
  3. Sustained hypotension
  4. Hypoxaemia
  5. Impaired cell utilisation of O2
36
Q

What do abrupt changes in the calibre of the pia-arachnoid arterial vessels lead to?

A

large emboli to become trapped in leptomeningeal vessels

37
Q

Why are strokes less common in dogs?

A
  • Difference in arterial supply
  • Decreased incidence of atherosclerosis
38
Q

Name 4 causes of cerebral infarction

Thromboembolism

A
  1. Feline cardiomyopathy
  2. Septic thrombosis
  3. Parasitic
  4. Fibrocartilaginous emboli

VMS 2007 (28 decks)

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