pathology Flashcards
what does damage to nerve cells and their process lead to
-rapid necrosis with sudden acute functional failure
-slow atrophy with gradually increasing dysfunction
what does hypoxia cause to happen to a red neuron
acute neuronal injury
-shrinking and angulation of nuclei
-loss of nucleolus
-intensely red cytoplasm
axons response to injury/disease
-increased protein synthesis
-chromatolysis (margination and loss of Nissl granules)
-degeneration of axon and myelin sheath distal to injury
what are cellular inclusions and what causes them
various nutrients or pigments that can be found within the cell, but do not have activity like other organelles
-neurodegenerative disease
-accumulate with age
-viral infections
oligodendrocytes role
wrap around axons forming myelin sheath
oligodendrocytes reaction to injury
-variable patterns and degrees of demyelination
-apoptosis
-damage is a feature of demyelinating disease
what can damage to the myelin sheath result in
-conduction reduced
-axons exposed to injury
role of astrocytes
- Ionic, metabolic and nutritional homeostasis
- Work in conjunction with endothelial cells to maintain the BBB
- The main cell involved in repair and scar formation given the lack of fibroblasts within the CNS
what is gliosis
a nonspecific reactive change of glial cells in response to damage to the central nervous system (CNS
-most important histopathological indicator of CNS injury, regardless of the cause
what happens in gliosis
- Astrocyte hyperplasia and hypertrophy
- Nucleus enlarges, becomes vesicular and the nucleolus is prominent
- Cytoplasmic expansion with extension of ramifying processes
what produces changes in ependymal cells
infectious agents including viruses
microglia response to injury
- Microglia proliferate
- Recruited through inflammatory mediators
- Form aggregates around areas of necrotic and damaged tissues
M1 mediator in acute nervous system injury
pro-inflammatory, more chronic
M2 mediators in acute nervous system injury
anti-inflammatory. phagocytic, more acute
what can cause hypoxia in the nervous system
-cerebral ischaemia
-infarct
-haemorrhages
-trauma
-cardiac arrest
-cerebral palsy
what is excitotoxicity
energy failure leads to buildup of glutamate and excitation of post-synaptic NMDA receptors, which causes Ca2+ buildup → protease activation, mitochondrial dysfunction, oxidative stress
pathophysiology of oedema
- Cytotoxic oedema e.g. intoxication, Reye’s, severe hypothermia
- Ionic oedema e.g. hyponatraemia, excess water intake (e.g. in SIADH)
- Vasogenic oedema - most important, occurs in e.g. trauma, tumours, inflamamtion, infection, hypertensive encephalopathy
- Haemorrhagic conversion
how does raised ICP occur
-if the brain enlarges, some blood +/- CSF must escape from cranial vault to avoid rise in pressure
-once this process is exhausted, venous sinuses are flattened and there is little or no csf
-any further increase in brain volume results in rapid increase in ICP
causes of increased ICP
-increased CSF (hydrocephalus)
-focal lesion in brain (space occupying lesion)
-diffuse lesion in brain (e.g. oedema)
-increased venous volume
-physiological (hypoxia, hypercapnia, pain)
causes of hydrocephalus
-obstruction to flow of CSF
-decreased resorption of CSF (post SAH or meningitis)
-overproduction of CSF
non-communicating hydrocephalus
obstruction to flow of CSF occurs within ventricular system
communicating hydrocephalus
obstruction to flow of CSF outside of the ventricular system
-e.g. in the subarachnoid space or at the arachnoid granulations
what happens if hydrocephalus develops before closure of cranial sutures
then cranial enlargement occurs
what happens if hydrocephalus develops after closure of the cranial sutures
there is expansion of ventricles and increase in intracranial pressure
