PATHOLOGY- cerebrovascular disease Flashcards
layers of the scalp?
SCALP
Skin subcutaneous
Connective tissue
Aponeurotic
Loose areolar connective tissue
Pericranium (periosteum)
what are the meninges?
Pia mater
Arachnoid Mater
Dura Mater
what are the cellular components of the CNS?
-Nerve cells (neurons)
-Glial cells
-Microglia
-Supporting structures (connective tissue, meninges, blood vessels)
What are examples of Glial cells?
-astrocytes
-Oligodendrocytes
-Ependymal cells
what can damage to nerve cells and/or their processes lead to in the brain?
Rapid necrosis with sudden acute functional failure (as seen in “stroke”)
Slow atrophy with gradually increasing dysfunction (as seen in age-related cerebral atrophy)
what is red neurone?
- 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
what is a red neurone pattern?
-shrinking and angulation of nuclei
-loss of necleolus
-intensely red cytoplasm
how do neurons respond to axonal injury?
Increased protein synthesis -> cell body swelling, enlarged nucleolus
Chromatolysis – margination and loss of Nissl granules
Degeneration of axon and myelin sheath distal to injury
how do axons respond to chronic degeneration?
simple neuronal atrophy
-shrunken, angulated and lost neurons, small dark nuclei, lipofuscin pigment, reactive gliosis
when are inclusions seen in the brain?
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
what wraps around the axons of the CNS forming myelin sheath?
Oligodendrocytes
what reaction fo Oligodendrocytes have to injury?
-variable patterns of demyhelination
-variable degrees of demyelination
-apoptosis
what occurs to oligodendrocytes in demyelinating disorders?
oligodendrocytes are damaged
what can damage to the myelin sheath result in?
-reduced conduction
-axons are exposed and so are more likely to be injured
where are astrocytes foubd?
-in the CNS
-astrocyte processes envelope synaptic plates and wrap around vessels and capillaries within the brain
role of astrocytes?
-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
what is the most important histopathological indicator of CNS injury?
Gliosis (an astrocyte response)
describe what happens in gliosis
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)
where are Ependymal cells located?
-line the ventricular system
what is the reaction that ependymal cells that to injury?
-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
what is the clinical relevence of ependymal cells?
-infectious agents including viruses produce changes in ependymal cells
-often site of tumour formation which can obstruct the flow of CSF
where are microglia derived from?
-embryologically derived
what is the role of microglia cells?
-function as a macrophage system, phagocytosis
what reaction do microglia have to injury?
-microglia proliferate
-recruited through inflammatory mediators
-form aggregates (around areas of necrotic and damaged tissues)
why are microglia clinically relevent?
Important mediators in acute nervous system injury:
M2- anti inflammatory, phagocytic, more acute
M1- pro inflammatory, more chronic
what occurs to blood flow during hypoxia of the brain?
-it can increase by two fold to maintain o2 delivery
what occurs if the brain doesnt manage to get enough oxygen and increasing blood flow doesnt work?
-after onset of ischaemia, mictochondrial inhibition of ATP synthesis leads to ATP reserves being consumed within a few minutes
what supplies the red portion of the brain?
middle cerebral artery
what supplies the yellow portion of the brain?
anterior cerebral artery
what supplies the blue portion of the brain?
posterior cerebral artery
what is the commonest cause of adult disability?
cerebrovascular disease
what 2 processes does cerebrovascular disease involve?
- hypoxia ischaemia infarction from impairement of blood and oxygen getting to the tissue
- haemorrhage from rupture of CNS vessels
what can cerebral ischaemia be classed as?
Global or focal
describe the 2 classes of cerebral ischaemia
- 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 - FOCAL HYPOXIC ISCHAEMIC DAMAGE
→ Vascular obstruction
what cells are most sensitive and get damaged first in global hypoxic ischaemic damage?
- Watershed areas are most sensitive (the zone between 2 territories)
- Glial cells
- Neurons in neocortex and hippocampus
- other neurones
definition of stroke
sudden disturbance of cerebral function of vascular origin that causes death or lasts over 24 hours
what are the 2 types of stroke and which is more common?
Infarction and Haemorrhage stroke
Infarction is more common (around 80%)
what causes a cerebral infarction?
caused by interruption of blood flow due to thrombosis or emboli
who most commonly experiences a cerebral infarction?
men > women
> 70 yrs
old men
where does a thrombotic cerebral infarction typically originate?
-in an atherosclerotic segment
-more commonly in middle cerebral artery territory
where does an embolic cerebral infarction typically originate?
-originate from atheroma in internal carotid and aortic arch
-originate from the heart
what vessel is the biggest risk factor for atheroma formation intracranially?
basilar
what vessel is the biggest risk factor for atheroma formation extracranially?
-carotid
-aorta
what determines the location, distribution and extent of parenchymal damage?
-arterial territory of the affected artery
-timescale of occlusion
-extent of collateral circulatory relief
-systemic perfusion pressure
how does a cerebral infarction appear micro and macroscopically from 1-12 hours?
-little visible micro and macroscopically
how does a cerebral infarction appear microscopically from 12-24 hours?
-red neuron
-oedema (cytotoxic and vasogenic)
-generalised cell swelling
how does a cerebral infarction appear macroscopically from 12-24 hours?
-pale, soft and swollen with ill defined margin between injured and normal brain
how does a cerebral infarction appear microscopically from 24-48 hours?
-increasing neutrophils
-extravasation of red blood cells (haemorrhagic conversion)
-activation of astrocytes and microglial
how does a cerebral infarction appear macroscopically from 2-14?
-brain becomes gelatinous and friable
-a reduction in the surrounding tissue oedema demarcates the lesion
how does a cerebral infarction appear microscopically from 2-14?
-microglia become predominant cell type
-myelin break down (in picture)
-reactive gliosis begins from as early as 1 week
how does a cerebral infarction appear macroscopically after several months?
-increasing liquification apparent
-eventual formation of cavity lined by dark grey tissue
how does a cerebral infarction appear microscopically from 2-14?
-ongoing phagocytosis brings increasing cavitation and surrounding gliotic scar formation
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??
carotid artery
Patient has a haemorrhagic infarct and is experiencing:
-weakness predominantly contralateral face and arm
What vessel is affected??
middle cerebral artery
Patient has a haemorrhagic infarct and is experiencing:
-weakness and sensory loss in contralateral leg
What vessel is affected??
anterior cerebral artery
Patient has a haemorrhagic infarct and is experiencing:
-vertigo
-ataxia
-dysarthria and dysphasia
What vessel is affected??
Vertebro- basilar artery
(complex brain stem syndromes)
what causes Hypertensive Encephalopathy
-severe hypertension
how does hypertensive encephalopathy present in pathology?
-global cerebral oedema (most important)
-tentorial and tonsillar herniation
-arteriolar fibrinoid necrosis
-petechiae
how does hypertensive encephalopathy present?
-severely hypertensive
-symptoms of raised intracranial pressure
how may intracranial haemorrhages be classed and give examples of each?
Can be classed as
Spontaneous:
-intracerebral haemorrhage
-SAH
-Haemorrhagic Infarct
Traumatic:
-Extra dural haematoma
-sub sural haematoma
-Contusion (surface bruising)
-Intracerebral haemorrhage
-Sub arachnoid
causes/ risk factors of intracerebral haemorrhage
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
where does intracerebral haemorrhage commonly occur?
-Basal ganglia (most common)
-Thalamus
-Cerebral white matter
-Cerebellum
morphology on cut surface of intracerebral haemorrhage?
-asymmetrically distortion
-various shifts and herniations are common
-well demarcated intra parenchymal haematomas
-softening of adjacent tissue
-surrounding oedema
what is amyloid angiopathy linked to?
Alzheimers and increase in age
role of oligodendrocytes?
-wrap around axons forming myelin sheath in the CNS
-locally confining neuronal depolarisation
-protecting axons
-forming nodes of ranvier
