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303: Neurology > Neuropathology > Flashcards

Neuropathology Flashcards

0
Q

What cells of the nervous system are most sensitive to hypoxia?

A

Neurons
Neuroglia
Microglia cells

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1
Q

What are two responses neurones have to injury?

A

Hypoxia

Neuronophagia

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2
Q

Describe the neuronal response to hypoxia

A

Shrinking of the cell body, becoming eosinophilic and angular with loss of Nissl substance
Changes occur within 12 hours
Affected neuron surrounded by clear space (swelling of astrocyte processes)
Nucleus becomes dark and pyknotic (triangular) and loss of nucleolus

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3
Q

Describe the neuronal response of neuronophagia.

A

Irreversible damage

Phagocytosis of affected cell

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4
Q

When does neuronophagia often occur?

A

Rapid neuronal death in hypoxia or viral infection

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5
Q 
Terminology:
Polio-
Leuko-
Encephalo-
Myelo-
Malacia-
A 
Polio = grey matter
Leuko = white matters
Encephalo = brain
Myelo = spinal cord
Malacia = necrosis
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6
Q

What is the term used to describe the reaction if the neuron cell body to axonal damage?

A

Central chromatolysis

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7
Q

Does central chromatolysis occur in the CNS, PNS or both?

A

Both

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8
Q

What occurs in the axonal reaction to damage?

A

central chromatolysis
Swelling, nucleus becomes peripheral, Nissl substance (rough endoplasmic reticulum) disperses
Pallor (pale colour to cell body)

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9
Q

What is the duration of the axonal reaction (central chromatolysis)?

A

Within a day, may persist for months

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10
Q

What is known as secondary demyelination?

A

Axonal (Wallerian) degeneration

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11
Q

What is the term used to describe the reaction that follows axon disruption?

A

Axonal (Wallerian) degeneration/secondary demyelination

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12
Q

Describe the axonal (Wallerian) degeneration process

A

24hr after injury: proximal and distal axonal stumps swell
Distal axon degenerates and fragments
1 month: axonal debris removed by phagocytosis
Myelin breaks down
Week(s): removal of myelin debris in PNS by macrophages (months/years in CNS)
PNS axon regrows (Schwann cell proliferation) 5-10mm/day - only occurs if connective tissue support remains suitably intact

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13
Q

What happens to the regeneration of axon sprouts in the PNS during axonal (Wallerian) degeneration process if there is loss of connective tissue integrity?

A

Fibres are unable to regenerate

Functional loss

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14
Q

When are viral inclusion bodies produced?

A

In viral infections e.g. Herpes simplex encephalitis and rabies

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15
Q

Where are viral inclusion bodies most likely found?

A

Neurons in specific locations: pyramidal cells of hippocampus/adjacent temporal cortex, Purkinje cells of cerebellum

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16
Q

What are interneuronal deposits?

A

Substances that accumulate within neurons

Permanent nature of cells make them prone to accumulating particular substances

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17
Q

Give an example of an intraneuronal deposit

A

Lewy bodies (Parkinson’s disease)

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18
Q

What disease are levy bodies present in?

A

Parkinson’s disease

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19
Q

What are Lewy bodies?

A

Abnormally phosphorylated neurofilaments in the substantia nigra/locus coerulus

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20
Q

What is a typical feature of spongiform encephalopathy?

A

Neuronal vacuolation

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21
Q

What is a vacuolated neuron?

A

Affected neuron with specific anatomic disruptions and vacuoles in the surrounding neuropil (due to swelling of astrocyte processes)

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22
Q

What causes vacuoles in the neuropil?

A

Swelling of astrocyte processes

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23
Q

What are the glial cells (neuroectodermal derivatives) of the nervous system?

A

Astrocytes
Oligodendrocytes
Ependyma

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24
What are the functions of Astrocytes?
``` Formation of blood brain barrier Secretion of growth factors and chemokines (modulation of inflammation in CNS) Metabolic buffering Detoxification Nutrient supply Glucose transport Uptake of neurotransmitters Electrical insulation Antioxidant roles ```
25
What is the function of oligodendrocytes?
Formation of myelin sheaths in CNS
26
What is the function of expendyma cells?
Lines ventricles
27
What is gliosis?
Astrocytes response to injury (aka astrogliosis/astrocytosis) Increased glial cell number and size Fill small cavities/scars, wall off tumor/abscess
28
What is the result of oligodendrocyte damage?
Demylination - pale area | Poor proliferation/regeneration
29
What are the bone marrow derivatives of the nervous system?
Microglia
30
What are the functions of microglia?
Fixed macrophages in CNS (dead cells and lipids)
31
What are the main causes for increased intracranial pressure?
Focal space-occupying lesions (tumour, abscess, haematoma, encephalitis Increase CSF volume (hydrocephalus) Compression in spinal cord (disc herniation, unstable vertebral articulations)
32
What is a common response to increased intracranial pressure?
Herniation: movement of parts of the brain through natural openings into a different anatomical compartment
33
What are the various types of herniations of the brain that can occur due to increased ICP?
Subfalcine: medial portion of cerebral hemisphere (cingulate gyrus) moves laterally under falx cerebri Transtentorial: medial temporal lobe moves under the tentorium cerebelli Tonsillar/coning: protrusion of cerebellar tonsils causally through foramen magnum
34
What is the consequence of increased ICP in infants (neonates)?
Sutures and frontanelles allow expansion
35
What are the clinical presentations of increased intracranial pressure?
Headache, dullness, nausea, vomiting (papilledema)
36
Describe what a subfalcine herniation is.
Movement of the cingulate gurus (medial part of cerebral hemisphere) underneath falx cerebri - can compress on anterior cerebral artery
37
Describe what a transrentorial herniation is.
Movement of the incus of the hippocampus and medial parts of temporal lobe beneath the tentorium Can produce a grossly visible groove
38
What are the possible consequences of a transrentorial herniation?
Movement mid brain compression - coma Oculomotor nerve compression - ipsilateral pupil dilation Aqueduct compression - further ICP increase Posterior cerebral artery compression - occipital infarction - blindness Arterial and venous tears in brain stem - haemorrhage (Mass effect in one or both cerebral hemispheres)
39
What are the consequences of cerebral oedema?
Herniation due to raised CSF, fixed volume of CNS compartment and lack of effective lymphatic drainage
40
What are the possible causes of cerebral oedema?
Vascogenic Cytoxic Interstitial hypo-osmotic
41
What is the most common form of oedema?
Vascogenic oedema
42
What causes Vascogenic oedema?
Increased vascular permeability from trauma/vascular necrosis within infarcts/tumours Second impact syndrome
43
What causes cytoxic oedema?
Intracellular fluid accumulation due to toxins or ischemia and water overload
44
What causes interstitial oedema?
Build up of fluid due to obstructive hydrocephalus (peri ventricular regions)
45
What is hypo-osmotic oedema?
Oedema caused by water intoxication
46
Which form of oedema can be treated by reducing brain swelling using diuretic agents?
Vascogenic
47
What is hydrocephalus?
Increased CSF volume within cranial cavity
48
How often is CSF renewed?
3-5 times per day
49
What are the various types of hydrocephalus?
Internal (ventricular) External (subarachnoid) Communicating (ventricles and subarachnoid space) Active Arrested Compensatory (increased CSF secondary it reduced volume of brain substance)
50
What is the cause of hydrocephalus?
Obstruction of CSF flow
51
What is the result of an obstruction at the foramen of Munro?
Unilateral ventricular hydrocephalus
52
What is the result of an obstruction at the third ventricle or mesencephalic aqueduct?
Hydrocephalus of lateral ventricles
53
What is the result of an obstruction at the foramina of Luschka (lateral apertures of fourth ventricle)?
Affects whole ventricular system
54
What is the result of an obstruction of the subarachnoid?
While ventricular system and communicating
55
Where do the obstructive materail causing hydrocephalus arise from?
Masses: neoplasms Congenital malformations: non-patent mesencephalic aqueduct Iflammation Hernias
56
What are causes of hydrocephalus by destroying arachnoid villi?
Vitamin A deficiency | Severe meningitis
57
What are some of the ceerebral signs of hydrocephalus?
``` Headache Nausea Blurred vision Dullness Confusion Memory loss Irritability Poor intellectual performance Urinary incontinence ```
58
Are neurons more tolerable of hypoxia or ischemia?
Hypoxia
59
Define the term malacia.
Necrosis in CNS (breakdown of Blood Brain Barrier) Due to cardiac arrest, anesthetic accidents, atherosclerosis
60
What is a "stroke"
Clinical term used for the syndrome resulting from infarction and haemorrhage in the CNS
60
What are some of the causes of stroke
Aphasia, hemiplegia, blindness | Dependant on site affected
60
What are some of the causes of arterial obstruction in CNS?
``` In situ thrombosis (atherosclerosis) Embolism of cardiac thrombi Tumor Air/fat Arterial compression from herniation/masses ```
60
What is excitocity?
Imbalance in stimulatory neurotransmitters seen in CNS disease, hypoxia/ischemia (glucose deprivation) resulting in penumbral death Increased release of glutamate and aspartate Reversible acute swelling of depolarised neuron (influx of sodium ions, chloride ions and water) NDMAR opened by glutamate - Ca influx - generation of reactive oxygen and nitrogen species
60
How can Astrocytes moderate the damage of exocitoxicity?
Convert glutamate to glutamine (neutralising free radicals)
61
What aids in protecting the CNS from infections.
Bone, dura, blood brain barrier, microglia
62
What are the possible routes for infectious agents to reach the CNS?
Haematogenous (bacteria) Local extension (osteitis, sinusitis, tooth roots, vertebral abscesses, middle ear infections) Direct implantation (skull fracture, penetrating injuries, grafts, surgical exposure) Neural (rabies, tetanus toxin, prions)
63
What happens if an infectious agent does gain access to the CNS?
Rapid dissemination via the ventricular system (CSF), aided by poor fibrous response and low degree of immuno-surveillance
64
What are the two key bacterial infections?
Meningitis | Abscessation
65
What are the key features of meningitis?
Subarachnoid purulent exudate (neutrophils) More apparent in basal cisterns and sulci CSF obstruction and hydrocephalus (oedema) Superficial cortical necrosis and encephalitis Some diffuse brain swelling
66
What are the key features of abscessation?
Clinically appears to be SOL - surrounding oedema | Only thin capsule (collagen and astrocytosis

303: Neurology (7 decks)

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