Cerebrovascular Disease Flashcards
List 3 types of glial cells in CNS, glial cells come from ectoderm
Astrocytes,
Oligodendrocytes,
Ependymal cells
List 3 types of cells of CNS and 3 supporting structures
Neurons, glial cells, microglia
& connective tissue, meninges and blood vessels
Microglia is the ____ of the CNS
Macrophage
What is nissl substance and where is it
Is in cell body, has granular appearance and consists of endoplasmic reticulum and ribosomes
What is Red Neuron?
Pathological hallmark of severe acute neuron injury, usually in context of hypoxia/ischaemia
Red Neuron changes seen within how many hours after irreversible insult to cell?
12-24hrs
Red neuron pattern changes?
Shrinking and angulation of nuclei,
Loss of nucleolus,
Intensely red cytoplasm
Axonal injury reaction (3)
Cell body swelling and enlarged nucleolus due to increased protein synthesis,
Chromatolysis - disolving of Nissl granules,
Degeneration of axon and myelin sheath distal to injury
Simple neuronal atrophy - chronic degeneration, morphology and which cells does it occur in?
Shrunken, angulated neurones, lost neurons, small dark nuclei, lipofuscin pigment, reactive gliosis Happens to functionally related groups of neurones.
3 instances where inclusions appear in brain?
Common in neurodegenerative conditions,
Accumulate with ageing,
In viral infections affecting the brain
What inclusions do you get in Alzheimer’s disease?
Neurofibrillary tangles
What are inclusion bodies in neurons?
Aggregates of protein
Oligodendrocytes have relatively limited reaction to injury but are sensitive to what type of damage?
Oxidate damage
Damage to the myelin sheath can lead to? (2)
Conduction reduced & axons exposed to injury
List two structures the astrocytic processes envelop?
Envelop synaptic plates,
Wrap around vessels and capillaries within the brain
What are the 3 main roles of astrocytes?
Ionic, metabolic and nutritional homestasis,
Help maintain BB barrier,
Main cell for repair and scar formation (cos no fibroblasts)
Astrocytic response is the most import histopathological indicator of CNS injury. What is the name of the astrocytic response to CNS injury?
Gliosis
Describe early gliosis histopathologically
Astrocyte hyperplasia and hypertrophy,
nucleus enlarges, becomes vesicular,
the nucleolus becomesprominent,
Cytoplasmic expansion with extension of processes
Describe old lesions of gliosis
Are translucent and nuclei become small & dark & lie in glial fibrils which are dense network of processes
Ependymal cells line what in the brain?
Ventricular system
Ependymal cells have a limited reaction to injury. True/false?
True
Ependymal cells can cause problems in what 2 ways?
Can undergo tumour transformation and block CSF production,
Can be involved in infection as infection spreads through CSF
Injured ependymal cells scar in what way?
Local proliferation of sub-ependymal astrocytes into ependymal granulations
How do microglia respond to injury?
Proliferate and form aggregates around areas of necrotic and damaged tissues
What is the difference between M1 and M2 microglia?
M1 are pro-inflammatory and more chronic,
M2 are anti-inflammatory, phagocytic and more acute
List 8 causes of nervous system injury
Hypoxia, Trauma, Toxic insult, Metabolic abnormalities, Nutritional deficiencies, Infections, Genetic abnormalities, Ageing
Brain consumes approximately what percentage of total body resting O2 consumption?
Approx. 20%
What enzyme is thought to consume 70% of the brains energy?
Na+/K+ channel ATPase
Cerebral blood flow can only increase by how much to maintain oxygen delivery?
Can only double
After onset of ischaemia, what happens in terms of ATP?
Mitochondrial inhibition of ATP synthesis leads to ATP reserves being consumed within few minutes
Excitotoxicity occurs in neurons in the case of energy failure which can occur in hypoxia, trauma and some neurodegenerative conditions. Outline what occurs in excitotoxicity.
Hypoxia and hypogylcaemia
- > neuronal depolarisation so glutamate released + inhibition of astrocytes reuptake of glutamate
- > glutamate storm and excitation
- > increased Ca+ going into post-synaptic membrane
- > protease activation + mitochondrial dysfunction + oxidative stress
- > apoptosis
Oedema also mediates injury in CNS. 4 main types?
Cytotoxic oedema
Ionic oedema,
Vasogenic oedema,
Haemorrhagic conversion
Cytotoxic oedema occurs how and is this swelling?
Extracellular ions e.g. sodium and chloride move into cells and bringing in water by osmosis - no swelling occurs because there is no outside fluid coming in its just moving from one area to another within a confined space
Ionic oedema is the first dysfunction of the BB barrier. How does cytotoxic oedema lead to ionic oedema?
Cytotoxic oedema means lack of sodium in extracellular space and so sodium ions cross BB barrier and this drives chloride ions across too, this creates osmotic gradient for water to move in.
How does vasogenic oedema happen?
Breakdown of BBB due to disruption of endothelial tight junctions which leads to plasma proteins e.g. albumin crossing into extracellular space which are very osmostically active so water in too!
In both ionic and vasogenic oedema substances move across the blood brain barrier. However in which type of oedema does the BB barrier still maintain its integrity?
Ionic
In vasogenic oedema the BBB is still intact enough for RBCs to not pass through. What is it called when BBB is very dysfunctional and RBCs begin to pass through BBB? This happens in 30-40% of what?
Haemorrhagic conversion, happens in 30-40% of ischaemic strokes
