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Flashcards in Deck 5a - neuro Deck (18)
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1
Q

Q. What does the Glasgow Coma scale access?

A

A. Level of consciousness

B. Motor response (obeys commands, localises pain, flexors to pain, extends to

pain, none), Sensory response to pain, Best eye opening response – brain stem

(not accurate in first one hour)

2
Q

Q. Name 3 ways a patient’s neurological state can be tested?

A

A. Glasgow coma scale, pupil reactivity (fixed dilated pupil?), lateralising signs –

response to pain stimuli – (obeys commands, localises pain, flexes to pain,

extends to pain, none)

B. (Other vital signs – BP, RR, oxy sat, temp, pulse)

3
Q

Q. How do subdural/extradural haematoma appear on imaging?

A

A. Concave – subdural

B. Convex - epidural

4
Q
  1. Who is at a greater risk of suffering from chronic subdural haematoma?
A

A. The elderly and alcoholics – smaller brain – following small head injury there is a

low pressure bleed, the blood sucks in fluid and forms a mass

B. Days-weeks later pt is confused, falls

C. Tx: surgery – decompression – drill hole in skull

5
Q

Q. Define a) disability/limitation of activity b) Handicap/participation

A

A. Disability/ Limitation of activity: Any restriction or lack of ability to perform an

activity in manner or within the range considered as normal

B. Handicap/ Participation: A disadvantage for a given individual resulting from an

impairment or disability that limits or prevents the fulfilment of a role that is

normal for that individual

6
Q

Q. Name 3 different treatments/ways to manage the symptoms of MS e.g.

spasticity

A

A. Physiotherapy – special seating, moving and handling, stretching

B. Drugs – anti-spasticity drugs e.g. baclofen

C. Surgery

D. Botulinum Toxin

E. Psych, nurses, social workers

7
Q

Q. Name 6 symptoms of raised ICP (tumour)

A

A. Headache, reduced consciousness level, nausea and vomiting, may also present

with progressive neurological deficit, or epilepsy

B. Stage 1: no symptoms

C. Stage 2: headache, confusion, drowsiness

D. Stage 3: coma

E. Stage 4: death

8
Q

Q. Name two features of raised ICP headache

A

A. Worst on waking from sleep in the morning, increased by coughing, straining,

bending forwards

9
Q

Q. Name a cardinal physical sign of raised ICP – name 4 features seen

A

A. The cardinal physical sign: is papilloedema – due to obstruction of venous return

from the retina - Loss of crisp optic nerve head margins, Venous enlargement,

Retinal oedema, Haemorrhages

10
Q
  1. Q. What neurological deficits may be seen due to ICP?
A

A. Wide range – motor, sensory, speech, visual deficit, deafness, deteriorating memory, personality change

11
Q

Q. What features of epilepsy are suggestive of raised ICP/brain tumour?

A

Recent onset – focal seizures (motor, sensory, temporal lobe pattern – often

associated with olfactory aura, or deja vue, funny feeling in gut/stomach)

12
Q

Q. Where do most secondary brain tumours originate?

A

A. 24% non-small cell lung cancer, 15% small-cell lung cancer, 17% breast,

11% melanoma, 6% renal cell, 6% GI, unknown primary 5%

B. Surgery + RT

13
Q

Q. What cell origin are the majority of primary brain tumours?

A

Glial cell in origin: 85-90% are astrocytoma, 5% are oligodendroglioma

(favourable prognosis, eventual transformation into WHO III, can transform into

GBM WHO IV – genetic defect in chromosomes 1 and 19)\

14
Q

Q. What are the 4 WHO grades of glioma? Which are most common?

A

A. Grade I (pilocytic astrocytoma) is a ‘paediatric’ tumour

B. Grade II (‘benign’) is a premalignant tumour – not benign (!)

C. Grade III is called ‘anaplastic astrocytoma’ = Cancer

D. Grade IV = GLIOBLASTOMA MULTIFORME (GBM) - THE MOST COMMON

PHENOTYPE (necrosis seen within tumour – histologically)

15
Q

Q. What are the two common pathways to malignant glioma?

A

Common – genetic error of glucose glycolysis – mutation of isocitrate

dehydrogenase 1 (IHD-1) results in excessive build up of 2-hydroxyglutarate,

which triggers genetic instability in glial cells and subsequent inappropriate

mitosis

B. No IDH mutation – catastrophic genetic mutations – very poor prognosis

16
Q

Q. Name 5 positive and 5 negative prognostic factors for glioblastoma?

A

A. Good: <45-50yrs, aggressive surgical therapy, good performance post surgery,

tumour that was previously low grade, MGMT mutation – should respond to

chemoRx

B. Bad: >50yr, poor neuro function (drowsy, headache, focal neuro) post surgery,

non radial surgery tx, ‘primary’ GMB (catastrophic genetic mutation), MGMT

‘wild type’ – no predicted response to chemoRx

17
Q
  1. Q. How is glioblastoma treated?
A

A. Resective surgery, adjuvant chemo with temozolomide at time of RT

B. Followed by temozolomide chemoRx

18
Q

Q. Who is most commonly affected by ‘benign’ gliomas? How does it present?

A

A. Disease of young adults – commonly presents with seizues

B. Deterioration due to: tumour transformation to malignant phenotype,

progressive mass growth, or progressive neurological deficit from functional

brain destruction by tumour