Vascular Disease + Tumours Flashcards

1
Q

What pressure is classified as raised intracranial pressure?

A

Over 200 mM

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2
Q

What are the different types of herniation that can occur as a result of RICP?

A
Subfalcine/cingulate= midline shift causing cingulate gyrus to pass under the falx cerebri 
Tonsillar= cerebellar tonsils through foramen magnum 
Uncal= uncus of temporal lobe moves across supratentorial notch  
Central/trans-tentorial = decent of diencephalon and BS i.e. can compress resp and CVS centres of BS
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3
Q

What are the complications associated with uncal herniation?

A

CNIII compression
-fixed dilated pupils (unilateral)

Compression of posterior cerebral artery
-leads to occipital lobe infarct which leads to occipital blindness

CNX compression

Midbrain/BS
-altered consciousness or coma

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4
Q

What are the cardinal signs of uncal herniation?

A

Acute loss of consciousness

Ipsilateral pupil dilation

Contralateral hemiparesis

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5
Q

What is the definition of a stroke?

A

Abrupt onset of neurological deficits lasting more than 24 hours that are attributable to focal vascular disease, where no other cause is apparent

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6
Q

What are the two broad classification of stroke? What are the 2 subtypes which come under these classifications? Give brief details.

A
Ischaemic 
-thrombotic 
Eg thrombus forms inside intracranial vessels (cerebral venous sinus thrombosis) 
-embolic 
Eg Artherosclerotic plaque from CCA 

Haemorrhagic
-intracerebral
Eg intraparenchymal or intraventricular vessel rupture
-subarachnoid
Eg rupture of cerebral arteries in subarachnoid space

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7
Q

What is global anoxia and which cells are most vulnerable?

What parts of the CNS can be affected?

A

Ischaemic changes due to circulatory collapse which leads to loss of neurones

Neurones more than glial cells due to being more vulnerable to ischaemic changes

Cerebral cortex= layer 3, 4 and 6
Hippocampus= CA1, CA3, CA4
Purkijne cells of cerebellum

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8
Q

What is watershed zone infarction and when does it occur?

A

Infarction in cerebral cortex which occurs at the boundaries of different arterial zones

With less severe hypoperfusion

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9
Q

What is an infarction and what are the possible causes?

A

Occlusion of artery leading to loss of blood supply and ischaemia

Causes:

  • atherosclerosis
  • Embolism
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10
Q

What are the 2 different origins of embolisms which can lead to an infarction? How can you differentiation between the 2?

A

Atheroma of extracranial arteries

  • Bifurcation of carotid arteries
  • origin of vertebral arteries
  • ascending aorta
  • arch of aorta

Cardiac:
-due to conditions which increase the risk of emboli formation:
Eg AF and endocarditis

Cardiac emboli will appear red due to subsequent bleeding

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11
Q

What are the risk factors associated with atherosclerosis? What other condition do these risk factors put you at risk of?

A
Cigarette smoke 
Hypertension 
DM
Hyperlipoproteinaemia 
Obesity 
Increasing age
Male sex
Low HDL level 

STOKE!!!

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12
Q

What are the consequences of an infarct in the internal capsule?

A

Capsular stroke

Genu of internal capsule can be damage (MOTOR)= corticobulbar tracts
- contains the UMN for CNV and CNVII
Eg contralateral loss of muscles of mastication and facial expression

Posterior limb of internal capsule (SENSORIMOTOR)= Corticospinal and thalamocortical projections
-loss of connection between ventral posterior nucleus and primary somatosensory cortex
Eg contralateral sensory loss

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13
Q

What is the possible precipitating event to venous infarction?

A

Sagittal sinus thrombosis

Eg clots can lead to para-sagittal infarcts

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14
Q

What are the different risk factors associated with intracerebral haemorrhage?

A
Hypertension 
Smoking 
Aneurysm 
Arterio-venous malformation 
Amyloid angiopathy 
Tumour 
Trauma
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15
Q

What are the 4 broad types of intra-cranial haemorrhage? What causes them and what are their characteristic features?

A

Epidural:
-MMA i.e. trauma at pterion
-Features:
Initial loss of consciousness followed by lucid period and then rapid deterioration
Lentiform on CT which doesn’t cross suture lines

Subdural:
-bridging veins
-Features:
Symptoms follow weeks after injury i.e. headache/dizziness/confusion/LOC
Cresentric on CT which does cross suture lines

Subarachnoid:
-cerebral arteries in subarachnoid space 
-rupture of berry aneurysm:
Anterior communicating a
Internal carotid artery + MCA
Basilar artery 
Cerebellar arteries
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16
Q

How can you differentiate between a ischaemic and haemorrhagic CVA on a CT scan? How does their treatment differ and why?

A
Ischaemic:
-darker region visible due to ischaemia 
-loss of sulcal patter due to associated oedema 
TX
-Anteplase (thrombolytic) w/i 3-4 hrs 
-thrombectomy 

Haemorrhagic:
-white lesion
TX
-Craniotomy to release pressure and access bleed
-ventricle shunt to treat complication of hydrocephalus
NO THROMBOLYSIS i.e. will exaggerate the problem

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17
Q

What are features of normal brain histology?

A

6 layers of neocortex
Glial cells
Pyramid-shaped spinal motor nuclei with large nuclei
Ependymal Ciliated cells lining the ventricles

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18
Q

What are common sites for metastatic cerebral tumours to originate from?

A

Lung
Breast
Skin- malignant melanoma
Kidney

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19
Q

What is the difference in prognosis between diffuse astrocytic and other astrocytic tumours?

A

Diffuse have higher grade (around grade 4) meaning they have worse prognosis than other astrocytic tumours which are well circumcised (grade 1 )

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20
Q

What is used on addition to histology to grade CNS tumours?

A

Molecular parameters

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21
Q

What 3 molecular mutations can influence the prognosis of glial tumours?

A

Isocitrate Dehydrogenase (IDH)= improves prognosis

06 methyl guanine methyl transferase (MGMT) methylation status:

  • methylated= increased response to chemo
  • non-methylated= decreased response to chemo

Loss of heterozygosity at 1q and 19q

22
Q

What is the most common primary CNS malignancy?

A

Glioblastoma

23
Q

What are examples of astrocytic tumours for each of the 4 different grades of severity?

A

Grade 1= pilocytic astrocytoma
Grade 2= diffuse astrocytoma
Grade 3= anaplastic astrocytoma
Grade 4= glioblastoma

24
Q

Would someone with a IDH-mutation or wild type astrocytoma have a better prognosis?

How does the cancer progress and change over time?

A

IDH mutant= better prognosis

Transform to anaplastic astrocytoma after 5-10 years
Develop into secondary glioblastoma in 4/5th decade of life

25
What are the physical characteristics of a grade 4 glioblastoma?
Heterogeneous Haemorrhage present w/i tumour Necrosis Causes midline shift
26
What are the molecular and histology features of oligodendroglioma?
Histo: - regular branching capillary network - round clear cells i.e. have fried egg appearance Molecular: - defined IDH mutation - 1q and 19q codeletion
27
Where are ependymoma tumours located?
Develop from ependymal cells i.e. radial glial cells Intramedullary of SC Ventricles (lined with ependymal cells) Cerebellum
28
What are the common sites for meningiomas to occur?
Parafalcine Lateral sulcus Orbits-frontal cortex Cerebellopontine angle Thoracic spinal dura
29
What are the possible consequences of local spread of meningiomas?
Infiltration of skull i.e. becomes interosseous Optic nerve involvement i.e. damage to nerve as cancer spreads
30
What are the 3 different types of peripheral nerve sheath tumour? How can you differentiate between them?
Neurofibromatosis (type 1 and 2) Neurofibroma -fusiform i.e. grows w/i nerve Schwannoma -grows outside the nerve
31
What are the different gradings of medulloblastomas? What are these tumours classed as and who is therefore most likely to develop them?
Group1= WNT activated Group 2= Sonic hedgehog (SHH) activated Group 3+4= non-WNT and non-SHH activated Embryonal Tumourd I.e. children most likely to develop them
32
What are the 3 main classifications of spinal tumour? Give 2 examples of tumours within these classification.
Intradural, intramedullary - astrocytoma - ependymoma Intradural, extramedullary - Meningioma - schwannoma Extradural i.e. do not originate from spinal cord - Metastatic carcinoma - lymphoma
33
Which people are most likely to develop CNS lymphoma?
Elderly= primary large B cell lymphoma Young adults Those with severe immune deficiency i.e. AIDS EBV
34
Bacterial meningitis is a possible cause of CNS infection. What are the different routes of infection?
Haematogenous i.e. blood and sepsi Middle ear Air sinuses Direct implantation i.e. malformation or trauma causing skull fracture PNS i.e. extension from PN into CN
35
What are the signs of meningitis? What are the possible complications?
Neck stiffness Fever Bacteria in CSF (different bacteria depending on age of person) Complications: - cerebral swelling - infective thrombophlebitis i.e. venous infarction - hydrocephalus - CN defects i.e. deafness
36
What are the possible routes of infection to spread which can then lead to cerebral abscess forming?
Haematogenous - lung abscess - bronchiectasis - SBE - congenital cyanosis heart disease Local: - middle ear - nasal sinuses
37
What are the 3 layers of a cerebral abscess?
Pus Inflamed granulation tissue Reactive gliosis (external)
38
What is the general pathology of CNS infections? How can they lead to death?
Cerebritis with cavitation and pus formation encapsulated by gliosis and granulation tissue Complications: - cerebral swelling - ventriculitis - meningitis
39
What 2 CNS infections can occur secondary to infection of the sinuses?
Subdural empyema I.e. pus in empyema Epidural abscess i.e slowing growing infection associated with osteomyelitis and sinusitis
40
What is Pott’s puff tumour?
Sinusitis which leads to osteomyelitis
41
What are the causes of chronic meningitis? What are the consequences of this type of CNS infection?
TB (from TB granuloma) Cryptococcal infection i.e. associated with immunosuppressed/compromised patients Poorly treated bacterial meningitis Complications: (due to pus collecting at base of brain) - hydrocephalus - venous thrombosis
42
What are the differences between acute and chronic meningitis?
Chronic: - pus collects at base of brain - disease time course= weeks - insidious onset Acute: - pus collects on top of brain - associated with acute infection rather than chronic or immunocompromised state - disease time course= days
43
What are the 3 possible conditions which can be caused by treponema pallidum infection?
Meningovascular neurosyphillis - leads to obliterate endarteritis (inflammation of inner lining of artery) - occurs at base of brain or spinal cord Paretic neurosyphillis -dementia caused by damage to frontal lobe i.e. glial proliferation, gliosis and iron deposition by the bacteria Tabes Dorsalis -demyelination of DCMLs i.e. loss of proprioception, vibration and complete ataxia
44
What are the neurological symptoms caused by Lymes disease?
Facial nerve palsy Aseptic meningitis Mild encephalopathy
45
What are the causes of viral encephalitis?
HSV1 -temporal lobe and limbic system HSV2- more common in neonates Arboviruses Adenoviruses Enteroviruses
46
What different CNS infections associated with the 3 Herpes viruses? Who are these viruses most likely effect
HSV1: (children and young adult) - haemorrhagic inflammation of front and temporal lobe - necrotising encephalitis HSV2: (adults) -Viral meningitis ``` Varicella Zoster (immunosuppressed) -HZV encephalitis ```
47
What virus causes rabies and what are the 2 different types of rabies? What is the time course of the disease?
Rhabdovirus ``` Furious= associated with brainstem encephalitis Paralytic= associated with cerebral encephalitis ``` 1-6 month incubation period for the infection to travel along the axons
48
What histological feature can be used to diagnosis rabies?
Negri bodies= cytoplasmic inclusions in neurones formed of rabies viral protein and RNA
49
What causes encephalomyelitis and what are the consequences of infection? How is post-infectious encephalomyelitis different?
Poliovirus 1/2/3 via an infection in GI tract Mostly asymptomatic Paralysis if infection affects anterior MN i.e. loss of LMN -signs of LMN disorder i.e. poliomyelitis when associated polio Occurs after viral infection such as measles, varicella, rubella and mumps
50
How can a parasitic infection of tenia solium lead to epilepsy?
End stage infection of tenia solium leads to larvae leaving the GI lumen and migrating to the brain and subarachnoid space which causes structural damage