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Pathology > CNS Disorders > Flashcards

CNS Disorders Flashcards

1
Q

Alzheimer’s Disease

A
  • Loss of neurons in hippocampus

- Affects cognition and memory

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2
Q

Pericytes

A
  • Adjacent to endothelial cells, common basement membrane
  • Contribute to microvascular stability
  • Release GFs and angiogenic molecules
  • Smooth muscle lineage, can contract to control blood flow
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3
Q

Blood brain barrier

A

Highly specialized brain endothelial structure of filly differentiated neurovascular system

  • Separates components of blood from neurons
  • Maintain chemical composition of the interstitial space
  • Protection from foreign substances, physiological substances and environmental fluctuations
  • Required for brain function
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4
Q

Glial cells

A
  • All cells that aren’t neurons or vessels
  • Oligodendrocyte (myelin forming)
  • Astrocytes (homeostasis)
  • Microglia (immune surveillance)
  • Ependymal cells (lining of ventricles and central canal)
  • Adult progenitor cells
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5
Q

Oligodendrocytes

A
  • Numerous processes and small amount of cytoplasm
  • Support neuron and synthesize myelin
  • One oligodendrocytes myelinates axons
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6
Q

Astrocytes

A
  • Support and maintain CNS
  • Protoplasmic- in grey matter. Processes spread radially
  • Fibrous- in white matter. Arranged in rows between axon bundles, send processes to nodes of adjacent myelinated axons
  • Endfeet at the ends of processes, contact vessels, ependymal cells, associated with Node of Ranvier, ensheath synapses, associated with nerve cell bodies, communicate with other astrocytes, communicate with oligodendrocytes and microglia
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7
Q

Functions of asstrocytes

A
  • CNS development- neuronal path finding and oligoendrocyte maturation
  • Maintenance of environment at the synapse
  • Synthesis of precursors for transmitters
  • Maintenance of the environment at the Node of Ranvier
  • Supply of energy to neurons
  • Brain water homeostasis
  • Maintenance of BBB integrity
  • Regulation of EC pH
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8
Q

Microglia

A
  • Resident macrophages
  • 10-20% of glial cell population
  • From mesoderm- mononuclear phagocyte precursors
  • Enter brain during early development pre BBB
  • Equal in white and grey matter with regional differences
  • First line of defence against viruses, bacteria, parasitic CNS infections, at BBB and remove debris
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9
Q

Microglia phenotypes

A
  • Ameboid microglia- during development and perinatal period
  • Ramified, under normal conditions in mature CNS
  • Reactive, non-phagocytic microglia- sublethal injury
  • Phagocytic microglia
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10
Q

Neuronal inclusions

A
  • From aging, complex lipids, lipofuscin, proteins and CHOs

- Viral infetion

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11
Q

Intracytoplasmic inclusions

A
  • Neurofibrillary tangles (AD)

- Lewy bodies (parkinson’s)

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12
Q

Astrocytes, gliosis

A
  • Hypertrophy and hyperplasia
  • Up-regulation of GFAP synthesis
  • Extension of processes
  • Stimulated cytokines from activated microglia
  • Release by products of increased biological activity, toxic o the environment
  • May contribute ti further injury
  • Important histological indicator of CNS injury
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13
Q

Rosenthal fibre

A
  • Observed in regions of chronic gliosis
  • Cytoplasmic inclusions of heat shock proteins nd ubiquitin
  • Brightly eosinophilic inclusions, H&E stain
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14
Q

Oligodendrocytes in injury

A
  • Do not respond to injury, but can be injured
  • High potential for repair (relatively), myelin damage doesn’t cause loss of oligodendrocytes
  • Remyelination- thinner thna normal, shorter internodes
  • If oligodendrocytes are lost, replaced from pogenitors until pool is depleted
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15
Q

Microglia in injury

A
  • Become phagocytic
  • Trauma
  • Inflammation
  • Neuronal necrosis
  • Viral & bacterial infections
  • In response to gliomas
  • Graded activation- more severe injury, greater activation
  • They become phagocytic once neuronal death occurs, activated when hey are damaged.
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16
Q

Immunity in CNS

A
  • Limited penetration of BBB by immune system
  • No lymphatic vessels in brain
  • Low levels of MHC in brain
  • Leukocyte trafficking increased with inflammation and disease
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17
Q

BBB and inflammation

A
  • Following injury, activation of endothelial cells and associated
  • Reduced tight junction integrity
  • Formation of transendothelial channels
  • Migration of leukocytes
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18
Q

Inflammation: help/hindrance

A
  • Collateral damage from cytokines and T cells
  • Digestion of myelin by macrophages/microglia
  • Complement-mediated injury
  • Production of ROS and RNS intermediates
  • Proteases
  • Activation of microglia
  • Inflammatory edema-pressure
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19
Q

Raised intracranial pressure

A
  • Injury may increase the volume of the brain. Edoema, increased CSF volume, focally expanding lesion (tumour/haemorrhage)
  • Absence of lymphatic drainage
  • Initially, extra volume compensated by compression of veins and displacement of CSF
  • Raised intracranial pressure
  • Herniation
  • Can be life threatening- resp ad cardiac centres in medulla oblongata
20
Q

Trauma

A
  • Affect depends on location of lesion
  • Limited capacity of brain for repair
  • Consequences clinically silent, severely disabling, fatal
  • Trauma can cause skull fractures, parenchymal injuries (eg concussion), vascular injuries (eg hemtoma)
21
Q

Contusions and lacerations

A
  • A blow to the surface of the brain, lesion at point of contact, diametrically opposed or both
  • Crest of gyri most vulnerable
  • Axonal swelling, close to or distant from site of swelling
  • Haemorrhage, edema
  • Inflammatory response
22
Q

Cerebrovascular disease

A
  • Consequence of altered blood folw
  • Stroke- hypoxia, ischaemia, infarction, caused by thrombosis/embolism
  • Haemorrhage caused by hypertension/ aneurysm
  • Global cerebral ischaemia, generalised loss of cerebral perfusion, cardiac arrest, shock, severe hypotenstion
  • Selective vulnerability-based on metabolic ddemand. Neurons, subpopulations of neurons; cerebral blood supply, metabolic requirements
  • Region in hippocampus
  • Purkinje cells in cerebellum
  • Cortical pyramidal cells
  • Focal cerebral ischaemia- cerebral artery occlusion, outcome determined by the duration of ischaemia, selective vulnerability and adequacy of collateral flow; embolism, thrombosis-atherosclerosis
23
Q

Infection

A
  • Causes damage by direct contact/entry, indirect through microbial toxins, inflammatory/immune response
  • Infection occurs through haematogenous spread, directly-trauma/malformations, local extensions-air sinuses, infected tooth, PNS
  • Meningitis- inflammation of the meninges and CSF
  • Encephalitis- inflammation of the brain parenchyma
24
Q

Bacterial infection of meninges

A
  • Headache, fever, neck stiffness, altered mental status
  • Evasion of host defence systems/invasion nd pathogenesis in CNS. Capsule providing evasion from host, release of edotoxin
  • Proinfammatory mediators in subarachnoid-inflammatory response in CNS, increaesd permeability of BBB, cerebral oedema, increased intracranial pressure
25
Q

Viral infection of microglial

A
  • HIV encephalitis
  • Chronic inflammatory reaction with widely distributed infiltrates of microglial nodules, tissuue necrosis and reactive gliosis
  • Caused by transmission of HIV into the brain by infected monocytes
  • Neuropathological change believed to be associated with viral products and soluble factors produced by infected microglia
26
Q

Demyelinating diseases

A
  • Aqcuired condition characterised by preferential damage of myelin, relative preservation of axons
  • Clinical presentation due to loss of transmission of electrical impulses along axon
  • Immunological (MS)
  • Infection (JC infection oligodendrocytes)
  • Inherited (leukodystrophies)
27
Q

Multiple sclerosis

A
  • Distinct episodes of neurological defect
  • Associated with white matter lesions
  • Genetic and environmental factors
  • Self reactive T cells
  • Breach in intergrity of BBB- allow infiltration of self reactive T-lymphocytes
  • Initiation factor is not understood
28
Q

Neuronal storage disease

A
  • DDeficiency of enzyme involved in catabolism of sphingolipids, mucopolysaccharides and mucolipids
  • Accumulation of substrate within lysosomes causes neural death
29
Q

Leukodystrophies

A
  • Myelin abnormalities (synthesis or turnover)

- Diffuse involvement of white matter

30
Q

Mitochondrial encephalomyopathies

A

-Inherited forms of mitochondrial oxidative phosphorylation, principally presents as muscle disease, but CNS tissue is also affected

31
Q

Tay-Sachs disease

A

Hexosamindase A deficiency

  • GM2 ganglioside accuulation in tissues (heart, liver, spleen, brain)
  • GM2 ganglioside is a lipid essential for neuronal function, neurological defects are the main clinical feature
32
Q

Tumours

A
  • Consequences unique to tumours of CNS. Confined, location, benign vs malignant
  • Gliomas: astrocytomas, oligodendroglioma, ependymoas
  • Neuronal tumours
  • Metastatic tumours
33
Q

Degenerative disorders

A
  • Diseases of grey matter
  • Progressive loss of neurons and secondary white matter change
  • Selected targeting of neuronal groups
  • Symptomatic/ anatomic
  • Pathologic (taupathies, prion disease)
  • Commonly associated with protein aggregates
  • Familial, sporadic and acquired aetiologies
  • Imbalance between protein synthesis and clearance
  • Accumulation of protein in and around neurons
  • Toxic gain or loss of function
34
Q

Alzheimer’s Disease

A
  • Impairment of higher cognitive function associated with pathology in medial temporal lobe (Hippocampus, entorhinal cortex and amygdala)
  • Accumulation of A-beta plaques and Tau tangles
  • Mutations in APP and proteins that cleave APP
35
Q

Parkinson’s Disease

A
  • Characterised by motor dysfunction typical of disturbance of nigostiatal dopaminergic system- tremor, rigidity, bradykinesia
  • Typified by the loss of pigmented catecholaminergic neurons of the substantia nigra and presence of Lewy bodies in neurons-accumulation of alpha-synuclein- correlates with symptoms
  • Progressive disease- begins in brain stem and spreads to cerebral cortex eventually leading to cognitive impairment
  • Evidence supports a “prion -like” spread of protein misfolding
  • Mutation in alpha-synuclein and genes associated with mitochondrial function
36
Q

Toxic and qcquired metabolic diseases

A
  • Vitamin deficiencies
  • Metabolic disturbances- hyperglycaemia -uncontrolled diabetes
  • Toxic disorderes- CO2, ethanol/methanol, radiation. Idiopathic Parkinson’s- toxic exposure to MPTP
37
Q

MPTP induced lesions

A

-Diagnosis. EEG, imaginf (PET/MRI), biomarkers eg CSF, blood

38
Q

Neurogenesis

A
  • Neurons are terminally differentiated,incapable of cell division
  • Brain thought to have limited regenerative capacity
  • Adult neural stem cells (neural progenitor cells)- discrete regions of brain; potential to differentiate into neurons, astrocytes and oligodendrocytes
  • Neurons, astrocytes, oligodendrocytes and ependyma arise from neuroectoderm
  • Microglia arise from mesoderm
39
Q

Potential for repair

A
  • Adult neural stem cell- subventricular zone. In vitro, stem cell potential, self renewing neural spheres, neurons, astrocytes, oligoendocytes. In vivo, low frequency ofdiision, generate neurons.
  • NG2 glia: dispersed throughout human brain parenchyma, differentiate into myelinating oligodendrocytes.
40
Q

Neural stem cell treatment of MPTP-lesion

A

-hNSMs implanted into the striatum showed remarkable migratory ability and were found in the substantia nigra, where a small number appeared to differentiate into dopamine neurons

41
Q

Consequences of traumatic brain injury (TBI)

A
  • An external force that exceeds the protective capacity of the brain
  • Blow, bump, proejctile, blast
  • Bruising, bleeding, brain dysfunction or death
  • Temporary, days, weeks, lifetime
42
Q

TBI- primary cell death

A
  • Mechanicalinjury-shearing,tearing, stretching
  • Affecting neurons, axons, glia cells and blood vessels
  • Acute injury, resulting in cell death and necrosis
43
Q

BBB dysfunction associated with TBI

A
  • Primary injury disrupts the tight junctions, allowing an influx o perippheral immune cells and circling factors that increase osmotic force
  • Affects the interaction between BBB and endothelial cells and astrocytic glial cells, further contributing to the effects of BBB dysfunction by increasing its permeability
44
Q

Excitoxicity

A
  • Injured nerve cells secrete glutamate into the EC space
  • Overstimulates the AMPA and NMDA receptors
  • Activated receptors allow influx of sodium and calcium ions into the cell
  • Cytosolic calcium ions activates enzymes
  • DNA fragmentation, lipid membrane degradation
45
Q

Mitochondrial dysfunction

A
  • Damage to the mitochondrial membrane
  • Mitochondria impaired
  • Increased ROS and calcium
  • Activation of mitochondrial permeability transition pore
  • Decrease ATP production
  • Activation of caspases
46
Q

Oxidative stress

A
  • Accumulation of ROS and RNS
  • Impairment of antioxidants
  • Lipoperoxidation of the cell membrane
  • Fragment DNA, causing mutations
  • Infiltration of neutrophl

Pathology (23 decks)

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