Raised ICP Pathology Flashcards Preview

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Flashcards in Raised ICP Pathology Deck (52)
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1
Q

What is normal ICP?

A

5-13mmHg

2
Q

What is normal number of lymphocytes in CSF?

A

<4 cells/ml

3
Q

What is the normal protein in CSF?

A

<0.4g/l

4
Q

What is normal glucose in the CSF

A

> 2.2mmol/l

5
Q

What are hte causes of hydrocephalus?

A

obstruction of CSF eg inflammation, pus and tumours; decreased resoption of CSF- post SAH or meningitis; overproduction of CSF- rare- tumours of choroid plexus

6
Q

How is hydrocephalus classified?

A

non-communicating adn communicating hydrocephalus

7
Q

What is non-communicating hydrocephalus?

A

obstruction to flow of CSF occurs within ventricular system

8
Q

What is communicating hydrocephalus?

A

obstruction to flow of CSF outside of ventricular system eg in subarachnoid space or arachnoid granulations

9
Q

What happens to the brain with hydrocephalus?

A

expansion of hte ventricles; flattening of the dyrae; fullness of the sulci and riased ICP

10
Q

What is hydrocephalus ex vacuo?

A

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

11
Q

What is a subfalcine hernation?

A

unilateral or asymmetric expansion of cerebral hemisphere displaces the cingulate gyrus under the falx cerebri

12
Q

What happens in a tentorial hernation?

A

medial aspect of temporal lobe (hippocampus) herniates over the tentorium cerebelli

13
Q

What is tonsillar herniation?

A

displacement of cerebellar tonsila through the foramen magnum

14
Q

What is the consequences of tonsillar hernation?

A

brainstem compression and vital respiratory centresi nthe medulla

15
Q

What is a consequence of tentorial herniation?

A

compression ipsilateral CNIII and its parasympathetic fibres

16
Q

What is a consequence of subfalcine hernation?

A

compression of the anterior cerebral artery and weakness and /or sensory loss in leg

17
Q

What are the features of an ICP induced headache?

A

worse on lying down; coughing; sneezing and straining

18
Q

Where do tumours o the brain in children arise?

A

mostly below the tentorium cerebelli

19
Q

Where do CNS tumours in adults tend to arise?

A

above the tentorium cerebelli

20
Q

What are hte most common origins of brain metastates?

A

breast; bronchus; kidney; thryoid; colon and melanoma

21
Q

What is the most common priamry malignant intracranial tumour in adults and children?

A

astrocytoma

22
Q

what is the second most common malignant primary intracranila tumour in children?

A

medulloblastoma

23
Q

hwat is the most common primary benign intracranial tumour in adults?

A

meningioma

24
Q

What is the most common benign intracranial tumour in children?

A

craniophayrngioma

25
Q

What type of astrocytoma do only children get?

A

grade 1 pilocytic astroctyoma

26
Q

What do tumour cells relase that leads to neoangiogenesis?

A

VEFG secretion

27
Q

Where are medulloblastomas found?

A

midline of the cerebellum

28
Q

What is the treatment for medulloblastoma

A

is very radiosensitive- radiotherpay

29
Q

What do medulloblastomas look like histopathologically?

A

undifferentiated embryonic/fetal cells

30
Q

What tends to cause single abscesses?

A

local extension or direct implantation- tend to occur adjacent to source

31
Q

what causes multiple brain abscesses?

A

haematogenous spread

32
Q

Where can abscesses locally ectend from?

A

chronic otitis media; mastoiditis; paranasla sinusitis

33
Q

How does e.coli appear on gram stain?

A

gram ive rods

34
Q

How does h.influenzae appear on gram stain?

A

gram negative cocco-baciili

35
Q

How does neisterria meningitides appear on gram stain?

A

gram negative diplococci

36
Q

How does strep. pneumoniae appear on gram stain?

A

gram +ve cocci in chains

37
Q

How does listeria monocytogenes appear on gram stain?

A

gram +ve rods

38
Q

What happens with high veolcity head injury?

A

cavitation occurs- small bubbles appearing at low pressure

39
Q

How are non-missile injuries caused?

A

sudden acceleration and/or deceleration

40
Q

What are primary injuries to the brain?

A

shear injury to axons and contusions due to compressive strain, cavitation or surface lacerations of brain parenchyma

41
Q

What is a linear skull #?

A

striaght sharp # line, that may cross sutures(diastatic #)

42
Q

WHat is a compound skull #?

A

associated with full thickness scalp lacs

43
Q

What does a linear # increase the chance of?

A

a haematoma being present

44
Q

What are coup and contracoup injuries?

A

coup injury occurs at point of impact whereas contracoup occur diametrically opposite the point of impact

45
Q

Are coup or contracoup injuries usually worse?

A

contracoup

46
Q

What is the most importnant type of brain damage due to blunt injury?

A

diffuse axonal injury

47
Q

what is diffuse axonal injury?

A

widespread disruption of axons due to shear strains tearing axons at the immediate time of acceleration/deceleration

48
Q

Wher does diffuse axonal injury most commonly happen?

A

in central structures due to cerebral hemispheres moving a different rates relative to each other when exposed to forces

49
Q

Waht is the pathological hallmark of diffuse axonal injury?

A

axonal bulbing and blebbing of the truncated axons

50
Q

What is a burst lobe?

A

a gross contusion that involves disruption of much of the frontal and temporal lobes and is associated iwth a significant degree of haemorrhage

51
Q

Why are the elderly more at risk of subdural haemorrhage?

A

age related strophy of hte brain puts more pressure on the briding veins and brain is more mobile in cranium meaning higher chance of rupture of one of these bridging veins

52
Q

What are the chronic subdural haemorrhages composed of?

A

liquefied blood/yellow-tinged fluid separated from inner surface of dura mater and underlying brain by a neomembrane (granulation tissue and mature collagen)