Neuropathology 1, basic principles & Cerebrovascular disease Flashcards
what makes up the peripheral NS?
the 31 pairs of spinal nerves and 12 cranial nerves
Give the layers of the CNS?
Dura
tough, fibrous, bridges crevices, attached to skull
Arachnoid
delicate sealed bag for CSF, bridges crevices
Arachnoid trabeculae
ropes across subarachnoid space
pia mater
delicate and dips into crevices
what are the cellular components of the CNS?
Neurones Glial cells Blood vessels Microglia Connective tissue (meninges)
What are glial cells?
-examples? (3)
supporting system for neurones and their dendritic and axonal processes
astrocytes
(regulate transmission of electrical impulses)
oligodendrocytes
(wrap around axons forming myelin sheath)
ependyma
(line the ventricular system)
what are the 4 ways in which neurones respond to injury?
acute neuronal injury
simple neuronal atrophy (in hypoxia)
Sub-cellular alterations
Axonal reaction
Hypoxic damage to CNS
-what occurs in neurones?
-activation of glutamate receptors and uncontrolled Ca entry into cell
they can’t use anaerobic glycolysis
neuronal degeneration
- what is an axonal reaction?
- what is the response to axonal injury? (7)
-a reaction within the cell body that is associated with axonal injury
-inc RNA and protein synthesis swelling of cell body peripheral displacement of nucleus enlargement of nucleolus central chromatolysis anterograde degeneration of axon occurs distal to sire of injury breakdown of myelin sheath
Gliosis
- what is it?
- indicates what?
- what happens to astrocytes?
- nuclear and cytoplasmic changes?
- appearance of old lesions?
- a nonspecific reactive change of glial cells in response to damage to the central nervous system
- CNS injury
- undergo hyperplasia and hypertrophy
-N: enlarges, becomes vesicular and nucleolus prominent
C: expansion with extension of ramifying processes
-nuclei become small and dark and lie in a dense net of processes
Oligodendrocytes
- function?
- reaction to injury
- injured in what?
- wrap around axons of neurones to from myelin sheath
- limiters reaction
- demyelinating disorders
Ependymal cells
- function?
- rection to injury?
- what occurs when these cells are disrupted?
- what produces changes in these cells?
- line the ventricular system
- limited
- local proliferation of sub-ependymal astrocytes to produce small irregularities on the ventricular surfaces termed ependymal granulations
- infectious agents e.g. viruses
Microglia
- function?
- response to injury? (4)
-fixed macrophage system
-proliferating
developing elongated nuclei (rod cells)
forming aggregates around small foci of tissue necrosis (microglial nodules)
Congregate around portions of dying neurones (neuronophagia)
Vascular supply to the NS
- brain receives what % of CO and O2?
- needs what from of energy?
- what maintains cerebral blood flow?
- what vessels supply blood to brain?
- 15% of CO and 20%of O2 consumed by body
- brain requires active aerobic metabolism of glucose
-autoregulatory mechanisms
(vasculature constricts on response to abnormally high pressure and dilates in response to hypotension)
-internal carotid and vertebral arteries = circle of willis
-
consequences of an anterior cerebral artery blockage? (3)
-frontal lobe dysfunction
contralateral sensory loss in foot & leg
paresis of arm & foot, relative sparing of thigh & face
consequences of an middle cerebral artery blockage?
-depends on whether its dominant of non dominant cortex contralateral hemiparesis contralateral hemisensory loss Aphasia/dysphasia apraxia
what areas does the vertebrobasilar artery supply? (3)
brain stem
Cerebellum
Occipital lobe
Brainstem
- components?
- syndromes resulting from damage to these components?
-Midbrain, Pons, Medulla
-Midbrain Webers syndrome Pons medial &lateral inferior pontine syndromes Medulla Lateral medullary syndrome
What occurs with occipital lobe damage?
homonymous hemianopia with macular sparing
symptoms that occur with cerebellar dysfunction?
DANISH dysdiadokinesis Ataxia Nystagus Intention tremor slurred speech Hypotonia
Cerebrovascular disease:
-name the 3 types
brain ischaemia and infarction
Haemorrhages
Vascular malformations and developmental abnormalities
brain ischaemia and infarction
- difference between the 2?
- what are parenchymal injuries associated with?
- below what BP does autoregulation fail?
- name the 3 grades of ischaemia and their consequences
- what is infarction?
-global hypoxia-ischaemic damage
Focal infarcts- due to local vascular obstruction
- generalised reduction in blood flow, global hypoxic ischaemic encephalopathy
- systolic 50
-Mild:
preferential loss of selectively vulnerable neurones
Moderate:
selective neuronal necrosis, glial and endothelial cells preserved
Complete:
pannecrosis
-prolonged interruption of blood flow leading to irreversible ischeamic injury
Hypoxic-ischaemic damage
- What cells are the most vulnerable to hypoxia?
- can occur due to what?
- what are watershed areas?
- neurones (glial resistant)
- resp obstruction, lung and heart disease, CO poisoning, cardiac arrest etc.
- junctions or arterial territories and the first to be deprives of blood supply in hypotension
e. g. superior cerebral convexities, posterior aspects of the cerebellar hemispheres
Stroke -definition? -classification: severity? (3) Mechanism? (2-5)
-Sudden disturbance of cerebral function of vascular origin that causes death or lasts over 24 hours
-TIA
evolving strokes
complete strokes
-Infarction:
Thrombotic or Embolic
Haemorrhagic:
intracerebral
subarachnoid
Bleeding into infarct
Cerebral infarction: -cause? -risk factors? (8) -describe the changes in morphology of the brain that occur at the following times after continued infarction? 4-12 hours? 15-12 hours? 24-36 hours? 36-48 hours? day 3? 1-2 weeks? months?
-local interruption of cerebral, blood flow due to thrombosis or emboli
-Atheroma Hypertension Serum lipids, obesity, diet Diabetes mellitus Heart disease Diseases of neck arteries Drugs Smoking
-4-12 brain may appear normal 15-20 ischaemic neuronal changes develop, defined margin between normal brain 24-36 inflammatory reaction, extravasation of RBCs, activation and microglia 36-48 necrotic area visible, becomes swollen and softer than surrounding tissue day 3 macrophages infiltrate into area 1-2 weeks liquefaction of tissue and gloisis months cavitation and completion of glial scar
Subarachnoid haemorrhage
- causes? (2)
- morphology? (3)
- presentation? (4)
-spontaneous (rupture of saccular aneurysm, generally on internal carotid)
or traumatic
-bleeding into subarachnoid space
intracerebral hematomas adjacent to aneurysms
infarct of brain parenchyma due to arterial spasm
-acute onset, no precipitating factors
severe headache
vomiting
LOC
Hypertension and the brain
- what changes can be seen? (4)
- what pathological conditions occur? (4)
-inc atheroma
hyaline arteriosclerosis
Microaneurysms
autoregulatory curve shifts to right
-lacunar infarcts
intracerebral haemorrhage and haematoma formation
multi infarct dementia
hypertensive encephalopathy
