Pathology Flashcards

1
Q

What is concussion?

A

A clinical term, usually describes instantaneous loss of consciousness, temporary respiratory arrest and loss of reflexes, following sudden change in the momentum of the head

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2
Q

What are secondary effects of traumatic injury?

A

Ischaemia, hypoxia, cerebral swelling (increased ICP), infection, epilepsy

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3
Q

What are the characteristics of an extradural haemorrhage?

A

Haemorrhage between the dura mater and skull

  • related to an arterial bleed
  • often trauma
  • may have a lucid period after injury but then deteriorates very quickly
  • “lemon” shaped
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4
Q

What are the characteristics of a subdural haemorrhage?

A

Haemorrhage between dura mater and the brain

  • related to tearing of the veins that bridge between the brain and venous dural sinuses
  • usually develop slowly
  • “banana” shaped
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5
Q

How does the brain heal after injury?

A

Over time contusions shrink as macrophages phagocytose the dead tissue and haemorrhage
- brain is left with a haemosiderin stained area of tissue

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6
Q

What are the consequences of raised intracranial pressure?

A

Brain can move through some areas (eg foramen magnum, coning [compression of medullary centres])

  • initial response to expanding brain lesion is expulsion of as much CSF and venous blood as possible, after that ICP starts to rise
  • brain herniates through dural openings
  • as ICP approaches arterial pressure, brain perfusion ceases
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7
Q

What features of the PNS allow it to regenerate?

A

Simple structure, degeneration of distal axon and myelin in quick, Schwann cells support axon regrowth, nerve structures often remain intact, macrophages phagocytose debris, Schwann cells and macrophages are the only cells present, neurons survive

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8
Q

What features of the CNS are inhibitory for regrowth?

A

Complex structure, degeneration of distal axon and myelin is slow, oligodendrocyte inhibits axonal regrowth, neural structure often destroyed, macrophages can enhance inflammatory response, complex cellular environment, neurons often die

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9
Q

What are the 3 most common bacterial causes of meningitis in adults?

A

Neisseria meningitidis
Streptococcus pneumonia
Haemophilis influenza typeb
** all have a capsule –> can evade immune response

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10
Q

What are the common causes of bacterial meningitis in neonates/infants

A

E. coli and other gram -ve bacilli
Group B streptococcus
Listeria monocytogenes

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11
Q

What are the clinical features of meningitis?

A

Fever, vomiting, headache, stiff neck, altered mental state, photophobia, seizures, non-blanching rash

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12
Q

What are the key features of CSF in a bacterial meningitis diagnosis?

A

Pressure (raised), appearance (cloudy), white cell count (high), gram stain (positive), protein (raised), glucose (low)

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13
Q

What is a stroke?

A

Development of a focal or global neurological deficit related to a vascular event

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14
Q

What are the risk factors for stroke?

A

Ageing, hypertension, cardiac disease, hyperlipidaemia, diabetes mellitus, hypercoagulable sates, smoking, obesity

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15
Q

What are the two main types of pathologic processes involved in stroke?

A

Infarction (75%) - death of tissue due to inadequate blood supply
Haemorrhage (20%) - tissue injury due to escape of blood from vessel/s
Subarachnoid haemorrhage (5%) - escape of blood primarily into the subarachnoid space

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16
Q

What is cerebral infarction?

A

Necrosis of cerebral tissue in a particular vascular distribution due to vessel occlusion or severe hypoperfusion
- usually related to an arterial obstruction, but primary problem may be at the level of arterioles, veins, heart

17
Q

What is the pathogenesis of cerebral infarction?

A

Cardiac causes: vegetations on valves can be thrown off, probe-patent interatrial septum
Large artery occlusion: thrombotic or embolic (embolic most common)
Small vessel occlusion: thrombotic or embolic
Venous occlusion: thrombotic

18
Q

What is the macroscopic appearance after cerebral infarction?

A

Brain swells due to cytotoxic oedema

  • membranes are not maintaining a proper electrolyte fluid passage
  • also get vasogenic oedema because blood vessels are leaky/not working properly
    • after 36 hours can see that the whole hemisphere is markedly expanded
19
Q

What is the histological appearance after cerebral infarction?

A

Initially - viable neurons centrally, surrounded by anoxic-ischaemic neurons
Later - macrophages start to migrate in, liquefactive necrosis, macrophages phagocytose the dead tissue and take it away, leaving a space in the brain where tissue used to be

20
Q

Why do people with cerebral infarction die?

A
  • Involvement of vital centres (brainstem)
  • Cerebral swelling
  • Pneumonia
  • CV disease
  • Pulmonary thromboembolism
    • patients usually survive the initial event but are then susceptible to other things in the sub acute phase
21
Q

What are the causes of intracerebral haemorrhage?

A

Hypertensive small vessel disease, amyloid angiopathy, blood disorders, tumour, vasculitis, vascular malformation, frugs

22
Q

What is cerebral amyloid angiopathy?

A

Deposition of beta-amyloid in walls of superficial supratentorial blood vessels

  • associated with superficial haemorrhages, often multiple
  • associated with Alzheimer’s disease
23
Q

What are causes of non-traumatic subarachnoid haemorrhage?

A

Rupture of vessels in the subarachnoid space –> saccular “berry” aneurysm
Rupture of other types of aneurysm
Extension of intracerebral haemorrhage