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PATHOLOGY- cerebrovascular disease Flashcards

1
Q

layers of the scalp?

A

SCALP

Skin subcutaneous
Connective tissue
Aponeurotic
Loose areolar connective tissue
Pericranium (periosteum)

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2
Q

what are the meninges?

A

Pia mater
Arachnoid Mater
Dura Mater

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3
Q

what are the cellular components of the CNS?

A

-Nerve cells (neurons)
-Glial cells
-Microglia
-Supporting structures (connective tissue, meninges, blood vessels)

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4
Q

What are examples of Glial cells?

A

-astrocytes
-Oligodendrocytes
-Ependymal cells

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5
Q

what can damage to nerve cells and/or their processes lead to in the brain?

A

Rapid necrosis with sudden acute functional failure (as seen in “stroke”)

Slow atrophy with gradually increasing dysfunction (as seen in age-related cerebral atrophy)

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6
Q

what is red neurone?

A
  • a pathological hallmark of lethal injury to the neurone
    -typically occurs in hypoxia/ischaemia
    -it is usually visible 12 to 24 hours after an irreversible ‘insult’ to the cell and results in neuronal cell death

basically a dying neurone

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7
Q

what is a red neurone pattern?

A

-shrinking and angulation of nuclei
-loss of necleolus
-intensely red cytoplasm

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8
Q

how do neurons respond to axonal injury?

A

Increased protein synthesis -> cell body swelling, enlarged nucleolus

Chromatolysis – margination and loss of Nissl granules

Degeneration of axon and myelin sheath distal to injury

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9
Q

how do axons respond to chronic degeneration?

A

simple neuronal atrophy

-shrunken, angulated and lost neurons, small dark nuclei, lipofuscin pigment, reactive gliosis

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10
Q

when are inclusions seen in the brain?

A

sub cellular alterations (inclusions)=
-common in neurodegenerative conditions e.g. neurofibrillary tangles in Alzheimer’s disease
-viral infections affecting the brain
-appear to accumulate with age

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11
Q

what wraps around the axons of the CNS forming myelin sheath?

A

Oligodendrocytes

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12
Q

what reaction fo Oligodendrocytes have to injury?

A

-variable patterns of demyhelination
-variable degrees of demyelination
-apoptosis

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13
Q

what occurs to oligodendrocytes in demyelinating disorders?

A

oligodendrocytes are damaged

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14
Q

what can damage to the myelin sheath result in?

A

-reduced conduction
-axons are exposed and so are more likely to be injured

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15
Q

where are astrocytes foubd?

A

-in the CNS
-astrocyte processes envelope synaptic plates and wrap around vessels and capillaries within the brain

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16
Q

role of astrocytes?

A

-Ionic, metabolic and nutritional homeostasis

-Work in conjunction with endothelial cells to maintain the blood brain barrier

-The main cell involved in repair and scar formation given the lack of fibroblasts

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17
Q

what is the most important histopathological indicator of CNS injury?

A

Gliosis (an astrocyte response)

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18
Q

describe what happens in gliosis

A

Gliosis occurs due to injury to the CNS

-Astrocyte hyperplasia and hypertrophy
* Nucleus enlarges, becomes vesicular and the nucleolus is prominent
* Cytoplasmic expansion with extension of ramifying processes
Old lesions – translucent, nuclei become small and dark and lie in a dense net of processes (glial fibrils)

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19
Q

where are Ependymal cells located?

A

-line the ventricular system

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20
Q

what is the reaction that ependymal cells that to injury?

A

-limited reaction to injury

-important for infection (infection can pass from one set of ependymal cells to another through CSF)

-disruption of these cells often associated with a local proliferation of sub ependymal astrocytes to produce small irregularities on the ventricular surfaces termed ependymal granulations

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21
Q

what is the clinical relevence of ependymal cells?

A

-infectious agents including viruses produce changes in ependymal cells

-often site of tumour formation which can obstruct the flow of CSF

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22
Q

where are microglia derived from?

A

-embryologically derived

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23
Q

what is the role of microglia cells?

A

-function as a macrophage system, phagocytosis

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24
Q

what reaction do microglia have to injury?

A

-microglia proliferate
-recruited through inflammatory mediators
-form aggregates (around areas of necrotic and damaged tissues)

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25
Q

why are microglia clinically relevent?

A

Important mediators in acute nervous system injury:

M2- anti inflammatory, phagocytic, more acute

M1- pro inflammatory, more chronic

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26
Q

what occurs to blood flow during hypoxia of the brain?

A

-it can increase by two fold to maintain o2 delivery

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27
Q

what occurs if the brain doesnt manage to get enough oxygen and increasing blood flow doesnt work?

A

-after onset of ischaemia, mictochondrial inhibition of ATP synthesis leads to ATP reserves being consumed within a few minutes

28
Q

what supplies the red portion of the brain?

A

middle cerebral artery

29
Q

what supplies the yellow portion of the brain?

A

anterior cerebral artery

30
Q

what supplies the blue portion of the brain?

A

posterior cerebral artery

31
Q

what is the commonest cause of adult disability?

A

cerebrovascular disease

32
Q

what 2 processes does cerebrovascular disease involve?

A
  1. hypoxia ischaemia infarction from impairement of blood and oxygen getting to the tissue
  2. haemorrhage from rupture of CNS vessels
33
Q

what can cerebral ischaemia be classed as?

A

Global or focal

34
Q

describe the 2 classes of cerebral ischaemia

A
  1. GLOBAL HYPOXIC ISCHAEMIC DAMAGE
    → Generalised reduction in blood flow/oxygenation and autoregulatory mechanisms cannot compensate (MABP falls below 50mmHg)
    → E.g. cardiac arrest or hypovolaemic shock
  2. FOCAL HYPOXIC ISCHAEMIC DAMAGE
    → Vascular obstruction
35
Q

what cells are most sensitive and get damaged first in global hypoxic ischaemic damage?

A
  1. Watershed areas are most sensitive (the zone between 2 territories)
  2. Glial cells
  3. Neurons in neocortex and hippocampus
  4. other neurones
36
Q

definition of stroke

A

sudden disturbance of cerebral function of vascular origin that causes death or lasts over 24 hours

37
Q

what are the 2 types of stroke and which is more common?

A

Infarction and Haemorrhage stroke

Infarction is more common (around 80%)

38
Q

what causes a cerebral infarction?

A

caused by interruption of blood flow due to thrombosis or emboli

39
Q

who most commonly experiences a cerebral infarction?

A

men > women

> 70 yrs

old men

40
Q

where does a thrombotic cerebral infarction typically originate?

A

-in an atherosclerotic segment
-more commonly in middle cerebral artery territory

41
Q

where does an embolic cerebral infarction typically originate?

A

-originate from atheroma in internal carotid and aortic arch
-originate from the heart

42
Q

what vessel is the biggest risk factor for atheroma formation intracranially?

A

basilar

43
Q

what vessel is the biggest risk factor for atheroma formation extracranially?

A

-carotid
-aorta

44
Q

what determines the location, distribution and extent of parenchymal damage?

A

-arterial territory of the affected artery
-timescale of occlusion
-extent of collateral circulatory relief
-systemic perfusion pressure

45
Q

how does a cerebral infarction appear micro and macroscopically from 1-12 hours?

A

-little visible micro and macroscopically

46
Q

how does a cerebral infarction appear microscopically from 12-24 hours?

A

-red neuron
-oedema (cytotoxic and vasogenic)
-generalised cell swelling

47
Q

how does a cerebral infarction appear macroscopically from 12-24 hours?

A

-pale, soft and swollen with ill defined margin between injured and normal brain

48
Q

how does a cerebral infarction appear microscopically from 24-48 hours?

A

-increasing neutrophils
-extravasation of red blood cells (haemorrhagic conversion)
-activation of astrocytes and microglial

49
Q

how does a cerebral infarction appear macroscopically from 2-14?

A

-brain becomes gelatinous and friable
-a reduction in the surrounding tissue oedema demarcates the lesion

50
Q

how does a cerebral infarction appear microscopically from 2-14?

A

-microglia become predominant cell type
-myelin break down (in picture)
-reactive gliosis begins from as early as 1 week

51
Q

how does a cerebral infarction appear macroscopically after several months?

A

-increasing liquification apparent
-eventual formation of cavity lined by dark grey tissue

52
Q

how does a cerebral infarction appear microscopically from 2-14?

A

-ongoing phagocytosis brings increasing cavitation and surrounding gliotic scar formation

53
Q

Patient has a haemorrhagic infarct and is experiencing:

-contra lateral weakness or sensory loss
-if in dominant hemisphere may be aphasia or apraxia

What vessel is affected??

A

carotid artery

54
Q

Patient has a haemorrhagic infarct and is experiencing:

-weakness predominantly contralateral face and arm

What vessel is affected??

A

middle cerebral artery

55
Q

Patient has a haemorrhagic infarct and is experiencing:

-weakness and sensory loss in contralateral leg

What vessel is affected??

A

anterior cerebral artery

56
Q

Patient has a haemorrhagic infarct and is experiencing:

-vertigo
-ataxia
-dysarthria and dysphasia

What vessel is affected??

A

Vertebro- basilar artery

(complex brain stem syndromes)

57
Q

what causes Hypertensive Encephalopathy

A

-severe hypertension

58
Q

how does hypertensive encephalopathy present in pathology?

A

-global cerebral oedema (most important)
-tentorial and tonsillar herniation
-arteriolar fibrinoid necrosis
-petechiae

59
Q

how does hypertensive encephalopathy present?

A

-severely hypertensive
-symptoms of raised intracranial pressure

60
Q

how may intracranial haemorrhages be classed and give examples of each?

A

Can be classed as

Spontaneous:
-intracerebral haemorrhage
-SAH
-Haemorrhagic Infarct

Traumatic:
-Extra dural haematoma
-sub sural haematoma
-Contusion (surface bruising)
-Intracerebral haemorrhage
-Sub arachnoid

61
Q

causes/ risk factors of intracerebral haemorrhage

A

Causes of vascular injury/disease:
-hypertension
-Amyloid deposits (cerebral amyloid angiopathy)
-diabetes
-Drugs (cocaine, alcoholism)
-Vasculitis (infectious and inflammatory)

Aneurysms

Vascular malformations

Systemic coagulation disorders/ iatrogenic anticoagulation

Open heart surgery

Neoplasms

62
Q

where does intracerebral haemorrhage commonly occur?

A

-Basal ganglia (most common)
-Thalamus
-Cerebral white matter
-Cerebellum

63
Q

morphology on cut surface of intracerebral haemorrhage?

A

-asymmetrically distortion
-various shifts and herniations are common
-well demarcated intra parenchymal haematomas
-softening of adjacent tissue
-surrounding oedema

64
Q

what is amyloid angiopathy linked to?

A

Alzheimers and increase in age

65
Q

role of oligodendrocytes?

A

-wrap around axons forming myelin sheath in the CNS

-locally confining neuronal depolarisation

-protecting axons

-forming nodes of ranvier

neuro (44 decks)

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