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Head and Neck > Elective Neurosurgery > Flashcards

Elective Neurosurgery Flashcards

1
Q

Typical site of primary intracerebral haemorrhage

A

Basal ganglia

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2
Q

Cause of primary intracerebral haemorrhage

A

Rupture of microaneurysms of Charcot-Bouchard of the perforating arteries supplying the basal ganglia

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3
Q

List the risk factors associated with subarachnoid aneurysms

A
  • HTN
  • Smoking
  • Cocaine
  • Polycystic kidney disease
  • Marfans
  • Ehlers-Danlos
  • Neurofibromatosis type 1
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4
Q

What is associated with mycotic subarachnoid aneurysms

A

Infective endocarditis

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5
Q

List the complications of SAH

A
  • Rebleeding - 3% in first 24 hours
  • Hyponatraemia
  • Vasospasm
  • Hydrocephalus
  • Seizures
  • Cardiac abnormalities
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6
Q

What is the aim of surgery in SAH

A

Prevent rebleeding

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7
Q

How is hyponatraemia secondary to SAH managed

A

Triple ‘H’ therapy:

  • Hypervolaemia (3L saline per day)
  • Hypertension
  • Haemodilution
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8
Q

List the risk factors for chronic subdural haematoma

A
  • Age
  • Alcohol
  • Dementia
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9
Q

How are chronic subdural haematomas managed

A

Burr hole drainage (posterior frontal and posterior parietal)

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10
Q

What is the most common brain tumour

A

Cerebral metastases

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11
Q

What is the most common primary brain tumour

A

Glioblastoma multiforme (Glioma)

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12
Q

What is the most common childhood brain tumour

A

Astrocytoma (Glioma)

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13
Q

Where do cerebral metastases typically seed

A

At the interface between grey and white matter

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14
Q

List the common origins of cerebral metastases

A
  • Lung
  • Bowel
  • Breast
  • Renal
  • Melanoma
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15
Q

If no primary tumour is identified by non-invasive means, how should you proceed

A
  • Stereotactic brain biopsy

- Excision biopsy

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16
Q

List the brain tumours of glial cell origin (gliomas)

A
  • Astrocytoma
  • Oligodendroglioma
  • Ependymoma
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17
Q

Describe the macroscopic appearance of Glioblastoma multiforme

A
  • Grey-ish ill-defined mass

- Areas of necrosis and haemorrhage

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18
Q

List the diagnostic histological features of Glioblastoma multiforme

A
  • Vascular proliferation and thrombosis

- Necrosis

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19
Q

What WHO grade is Glioblastoma multiforme

A

4

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20
Q

What WHO grade is anaplastic astrocytoma

A

3

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21
Q

Why are both glioblastoma multiforme and anaplastic astrocytoma non-resectable

A

Due to tumour cell migration to some distance from the original lesion

22
Q

Describe the macroscopic appearance of anaplastic astrocytoma

A

White ill-defined mass, sometimes expanding into the gyrus

23
Q

From where do meningiomas arise

A

Arachnoid cap cells

24
Q

With regards to position relative to the tentorium cerebelli, what is the difference between paediatric and adult CNS tumours

A
  • Paediatric = most infratentorial

- Adult = most supratentorial

25
Q

What WHO grade are meningiomas

A

1

26
Q

Describe the macroscopic appearance of meningiomas

A
  • Rubbery, round, lobulated mass

- Firmly attached to the dura

27
Q

What are the indications for stereotactic radiotherapy in CNS lesions

A
  • AVM
  • Vestibular schwannoma
  • Metastasis
28
Q

When is de-bulking surgery indicated in CNS tumours

A

For young patients <65 with GBM and AA:

  • Decrease mass effect for symptom relief
  • Reduce ICP
  • Remove lesion causing motor symptoms
29
Q

How are pituitary tumours divided

A
  1. Functional (secrete hormones)
  2. Non-functional

OR

  1. Microadenomas <10mm
  2. Macroadenomas >10mm
30
Q

List the indications for surgery in pituitary tumours

A
  • Non-functional tumours with mass effect
  • Cushing’s disease
  • Acromegaly
  • Acute visual deterioration
  • Pituitary apoplexy (infarction/haemorrhage of the gland)
31
Q

How are prolactinomas managed

A

Most shrink with dopamine agonists

32
Q

What is the typical surgical approach to pituitary tumours

A

Trans-sphenoidal

33
Q

How does pituitary apoplexy present (bleeding/infarction)

A
  • Sudden-onset headache
  • Sometimes visual disturbance
  • Deteriorating conscious level
  • Panhypopituitarism with addisonian crisis
34
Q

How is SIADH managed

A
  • Fluid restriction <1L/day

- Monitor sodium

35
Q

How is hydrocephalus categorised

A
  1. Communicating

2. Non-communicating (obstructive)

36
Q

Describe communicating hydrocephalus

A
  • CSF resorption at the arachnoid granulations is arrested or slowed e.g. secondary to SAH
  • All CSF spaces are increased in volume
37
Q

Describe non-communicating hydrocephalus

A

Block to CSF flow proximal to the arachnoid granulations

38
Q

How do you determine the difference between communicating and non-communicating hydrocephalus

A

CT/MRI

39
Q

Why is it important to distinguish the difference between communicating and non-communicating hydrocephalus

A
  • LP is life-saving in communicating hydrocephalus

- LP can cause coning in non-communicating hydrocephalus

40
Q

Describe normal-pressure hydrocephalus

A

Clinical triad of:

  1. Dementia
  2. Gait dyspraxia
  3. Incontinence
41
Q

How is normal-pressure hydrocephalus managed

A

Ventriculo-peritoneal shunt

42
Q

Describe ventriculo-peritoneal shunts

A
  • Ventricular catheter inserted into occipital horn of the lateral ventricle via burr hole
  • Peritoneal catheter is tunnelled under the skin to insert into the peritoneal cavity at the costal margin
43
Q

What bacteria complicate ventriculo-peritoneal shunts

A

Staphylococcus epidermiidis and staphylococcus aureus

44
Q

How may non-communicating hydrocephalus be managed

A

Third ventriculostomy

45
Q

What is the main pathogen in cerebral abscesses

A

Streptococci mainly

46
Q

How may cerebral abscesses present

A
  • Symptoms of raised ICP
  • Seizure
  • Focal neurology
47
Q

From what sites does haematogenous spread cause cerebral abscesses

A
  • Bronchiectasis
  • Bacterial endocarditis
  • Dental abscess and caries
48
Q

From where does local spread cause cerebral abscesses

A
  • Middle-ear (esp. cholesteatoma)
  • Frontal and sphenoid sinusitis
  • Skull base bone erosion
49
Q

How are cerebral abscesses managed

A
  • Needle drainage

- Antibiotics

50
Q

From where does subdural empyema develop from

A

Spread from paranasal sinuses

51
Q

How is subdural empyema managed

A

Surgical drainage via burr hole or craniotomy

Head and Neck (7 decks)

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