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pathology Flashcards

1
Q

what does damage to nerve cells and their process lead to

A

-rapid necrosis with sudden acute functional failure
-slow atrophy with gradually increasing dysfunction

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2
Q

what does hypoxia cause to happen to a red neuron

A

acute neuronal injury
-shrinking and angulation of nuclei
-loss of nucleolus
-intensely red cytoplasm

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3
Q

axons response to injury/disease

A

-increased protein synthesis
-chromatolysis (margination and loss of Nissl granules)
-degeneration of axon and myelin sheath distal to injury

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4
Q

what are cellular inclusions and what causes them

A

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

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5
Q

oligodendrocytes role

A

wrap around axons forming myelin sheath

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6
Q

oligodendrocytes reaction to injury

A

-variable patterns and degrees of demyelination
-apoptosis
-damage is a feature of demyelinating disease

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7
Q

what can damage to the myelin sheath result in

A

-conduction reduced
-axons exposed to injury

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8
Q

role of astrocytes

A
  • 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
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9
Q

what is gliosis

A

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

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10
Q

what happens in gliosis

A
  • Astrocyte hyperplasia and hypertrophy
  • Nucleus enlarges, becomes vesicular and the nucleolus is prominent
  • Cytoplasmic expansion with extension of ramifying processes
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11
Q

what produces changes in ependymal cells

A

infectious agents including viruses

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12
Q

microglia response to injury

A
  • Microglia proliferate
  • Recruited through inflammatory mediators
  • Form aggregates around areas of necrotic and damaged tissues
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13
Q

M1 mediator in acute nervous system injury

A

pro-inflammatory, more chronic

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14
Q

M2 mediators in acute nervous system injury

A

anti-inflammatory. phagocytic, more acute

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15
Q

what can cause hypoxia in the nervous system

A

-cerebral ischaemia
-infarct
-haemorrhages
-trauma
-cardiac arrest
-cerebral palsy

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16
Q

what is excitotoxicity

A

energy failure leads to buildup of glutamate and excitation of post-synaptic NMDA receptors, which causes Ca2+ buildup → protease activation, mitochondrial dysfunction, oxidative stress

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17
Q

pathophysiology of oedema

A
  • 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
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18
Q

how does raised ICP occur

A

-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

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19
Q

causes of increased ICP

A

-increased CSF (hydrocephalus)
-focal lesion in brain (space occupying lesion)
-diffuse lesion in brain (e.g. oedema)
-increased venous volume
-physiological (hypoxia, hypercapnia, pain)

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20
Q

causes of hydrocephalus

A

-obstruction to flow of CSF
-decreased resorption of CSF (post SAH or meningitis)
-overproduction of CSF

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21
Q

non-communicating hydrocephalus

A

obstruction to flow of CSF occurs within ventricular system

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22
Q

communicating hydrocephalus

A

obstruction to flow of CSF outside of the ventricular system
-e.g. in the subarachnoid space or at the arachnoid granulations

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23
Q

what happens if hydrocephalus develops before closure of cranial sutures

A

then cranial enlargement occurs

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24
Q

what happens if hydrocephalus develops after closure of the cranial sutures

A

there is expansion of ventricles and increase in intracranial pressure

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25
Q

hydrocephalus ex vacuo

A

dilatation of the ventricular system and a compensatory increase in CSF volume secondary to a loss of brain parenchyma

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26
Q

effects of raised ICP

A

-intracranial shifts and herniations
-midline shift
-distortion and pressure on cranial nerves and vital neurological signs
-impaired blood flow
-reduced level of consciousness

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27
Q

clinical signs of increased ICP

A

-papilloedema
-headache
-nausea and vomiting
-neck stiffness

28
Q

where are mets tumours commonly seen

A

at the boundaries between grey and white matter

29
Q

what is the most common primary intracranial tumour

A

astrocytoma

30
Q

what is the astrocytoma grading system

A

pilocytic - grade I
well differentiated - grade II
anaplastic - grade III
glioblastoma - grade IV

31
Q

medulloblastoma

A

2nd most common tumour in children after pilocytic astrocytomas
-poorly differentiated/embryonal
-occurs in midline of cerebellum

32
Q

describe an abscess

A

central necrosis, oedema, fibrous capsule

33
Q

symptoms of an abscess

A

-fever
-symptoms of raised ICP
-symptoms of underlying cause

34
Q

diagnosis of abscess

A

CT or MRI
-aspiration for culture and treatment

35
Q

what does missile or non-missile head trauma mean

A

penetrating or blunt

36
Q

penetrating trauma

A

-focal damage
-lacerations in region of brain damage
-haemorrhage
-high vs low velocity

37
Q

non-missile injury to brain

A

-sudden acceleration/deceleration of head
-smaller the contact time the larger the force
-brain moves within the cranial cavity and makes contact with the inner table of the cranium and bony protrusions

38
Q

primary injury of head trauma

A

-scalp lesions
-skull fractures
-surface contusions
-surface lacerations
-diffuse axonal injury
-diffuse vascular injury

39
Q

what are the three types of skull fracture

A

linear - straight, sharp fracture line
compound - associated with full thickness scalp lacerations
depressed

40
Q

what is a coup injury

A

occurs to the brain on the side of the impact

41
Q

what is a contracoup injury

A

diametrically opposite point of impact

42
Q

what usually causes traumatic extradural haematomas

A

-usually a complication of fracture in tempero-parietal region that involves middle meningeal artery
-immediate brain damage often minimal
-but untreated leads to midline shift- compression and herniation

43
Q

what is a subdural haemorrhage

A

-collections of blood between the internal surface of dura mater and arachnoid mater
-caused by disruption of bridging veins that extend from the surface of the brain into subdural space

44
Q

acute subdural haemorrhage features

A

-clear history of trauma
-unilateral or bilateral
-gyral contours preserved - pressure evenly distributed
-swelling of cerebrum on side of haematoma
-non-treated, non fatal haematomas become liquefied and form a yellowish neomembrane

45
Q

chronic subdural haematoma

A

-often associated with brain atrophy
-composed of liquefied blood/yellow-tinged fluid separated from inner surface of dura mater and underlying brain by neomembrane

46
Q

what do oligodendrocytes do

A

insulate axons
-locally confining neuronal depolarisation
-protecting axons
-forming nodes of ranvier

47
Q

what do nodes do

A

precipitate rapid saltatory conduction

48
Q

what are some primary demyelinating diseases

A

-MS
-acute disseminated encephalomyelitis
-acute haemorrhagic leukoencephalitis

49
Q

what are secondary demyelinating diseases

A

viral - progressive multifocal leukoencephalopathy
metabolic - central pontine myelinosis
toxic - CO, organic solvents, cyanide

50
Q

definition of multiple sclerosis

A

auto-immune demyelinating disorder characterised by distinct episodes of neurological deficit, separated in time, and which correspond to spatially separated foci of neurological injury

51
Q

what does the brain look like in MS

A

-principally a white matter disease
-extensor surface of brain seems normal
-cut surface of brain shows plaques

52
Q

active plaques

A

-perivascular inflammatory cells
-microglia
-ongoing demyelination

53
Q

inactive plaques

A

-gliosis
-little remaining myelinated axons
-oligodendrocytes and axons reduced in number

54
Q

what degenerative diseases are in the cerebral cortex

A

-alzheimer’s
-pick disease
-CJD

55
Q

what degenerative diseases are in the basal ganglia and brain stem

A

-parkinson’s disease
-progressive supranuclear palsy
-multiple system atrophy
-huntington disease

56
Q

what degenerative diseases are in the spinocerebellar

A

spinocerebellar ataxias

57
Q

what are neurodegenerative diseases characterised by

A

-progressive loss of neurons
-typically affecting functionally related neuronal groups

58
Q

what are the primary dementias

A

-alzheimer’s
-lewy body dementia
-pick’s disease (fronto-temporal)
-huntingtons disease

59
Q

pathology of the brain in Alzheimer’s

A

-decreased size and weight
-frontal, temporal and parietal lobe atrophy
-widening of sulci
-narrowing of gyri
-dilatation of ventricles
-brainstem and cerebellum normal

60
Q

what mutations can cause familial alzheimers disease

A

the E4 allele of the apolipoprotein E gene, point mutations in the APP gene, and mutations in presenilin (PS)-1 and 2

61
Q

what is amyloid angiopathy

A

a condition in which proteins called amyloid build up on the walls of the arteries in the brain

62
Q

what is seen in amyloid angiopathy

A

-extracellular eosinophillic accumulation
-stains congo red
-disrupts blood brain barrier causing: serum leaking, oedema, local hypoxia

63
Q

what type of condition is parkinsonism seen in

A

conditions which affect the nigro-striatal dopaminergic pathway

64
Q

pathology of lewey body dementia

A

degeneration of substantia nigra

65
Q

histological hallmarks of fronto-temporal dementia

A

-picks cells (swollen neurons)
-intracytoplasmic filamentous inclusions known as pick’s bodies

neuro (26 decks)

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