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Pathology > Vascular Disease + Tumours > Flashcards

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
Q

What are the physical characteristics of a grade 4 glioblastoma?

A

Heterogeneous
Haemorrhage present w/i tumour
Necrosis
Causes midline shift

26
Q

What are the molecular and histology features of oligodendroglioma?

A

Histo:

  • regular branching capillary network
  • round clear cells i.e. have fried egg appearance

Molecular:

  • defined IDH mutation
  • 1q and 19q codeletion
27
Q

Where are ependymoma tumours located?

A

Develop from ependymal cells i.e. radial glial cells
Intramedullary of SC
Ventricles (lined with ependymal cells)
Cerebellum

28
Q

What are the common sites for meningiomas to occur?

A

Parafalcine

Lateral sulcus

Orbits-frontal cortex

Cerebellopontine angle

Thoracic spinal dura

29
Q

What are the possible consequences of local spread of meningiomas?

A

Infiltration of skull i.e. becomes interosseous

Optic nerve involvement i.e. damage to nerve as cancer spreads

30
Q

What are the 3 different types of peripheral nerve sheath tumour? How can you differentiate between them?

A

Neurofibromatosis (type 1 and 2)

Neurofibroma
-fusiform i.e. grows w/i nerve

Schwannoma
-grows outside the nerve

31
Q

What are the different gradings of medulloblastomas? What are these tumours classed as and who is therefore most likely to develop them?

A

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
Q

What are the 3 main classifications of spinal tumour? Give 2 examples of tumours within these classification.

A

Intradural, intramedullary

  • astrocytoma
  • ependymoma

Intradural, extramedullary

  • Meningioma
  • schwannoma

Extradural i.e. do not originate from spinal cord

  • Metastatic carcinoma
  • lymphoma
33
Q

Which people are most likely to develop CNS lymphoma?

A

Elderly= primary large B cell lymphoma
Young adults
Those with severe immune deficiency i.e. AIDS
EBV

34
Q

Bacterial meningitis is a possible cause of CNS infection. What are the different routes of infection?

A

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
Q

What are the signs of meningitis? What are the possible complications?

A

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
Q

What are the possible routes of infection to spread which can then lead to cerebral abscess forming?

A

Haematogenous

  • lung abscess
  • bronchiectasis
  • SBE
  • congenital cyanosis heart disease

Local:

  • middle ear
  • nasal sinuses
37
Q

What are the 3 layers of a cerebral abscess?

A

Pus
Inflamed granulation tissue
Reactive gliosis (external)

38
Q

What is the general pathology of CNS infections? How can they lead to death?

A

Cerebritis with cavitation and pus formation encapsulated by gliosis and granulation tissue

Complications:

  • cerebral swelling
  • ventriculitis
  • meningitis
39
Q

What 2 CNS infections can occur secondary to infection of the sinuses?

A

Subdural empyema I.e. pus in empyema

Epidural abscess i.e slowing growing infection associated with osteomyelitis and sinusitis

40
Q

What is Pott’s puff tumour?

A

Sinusitis which leads to osteomyelitis

41
Q

What are the causes of chronic meningitis? What are the consequences of this type of CNS infection?

A

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
Q

What are the differences between acute and chronic meningitis?

A

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
Q

What are the 3 possible conditions which can be caused by treponema pallidum infection?

A

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
Q

What are the neurological symptoms caused by Lymes disease?

A

Facial nerve palsy
Aseptic meningitis
Mild encephalopathy

45
Q

What are the causes of viral encephalitis?

A

HSV1
-temporal lobe and limbic system

HSV2- more common in neonates

Arboviruses

Adenoviruses

Enteroviruses

46
Q

What different CNS infections associated with the 3 Herpes viruses? Who are these viruses most likely effect

A

HSV1: (children and young adult)

  • haemorrhagic inflammation of front and temporal lobe
  • necrotising encephalitis

HSV2: (adults)
-Viral meningitis

Varicella Zoster (immunosuppressed) 
-HZV encephalitis
47
Q

What virus causes rabies and what are the 2 different types of rabies? What is the time course of the disease?

A

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
Q

What histological feature can be used to diagnosis rabies?

A

Negri bodies= cytoplasmic inclusions in neurones formed of rabies viral protein and RNA

49
Q

What causes encephalomyelitis and what are the consequences of infection? How is post-infectious encephalomyelitis different?

A

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
Q

How can a parasitic infection of tenia solium lead to epilepsy?

A

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

Pathology (12 decks)

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