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phase 2a mine > neuro middle tier > Flashcards

neuro middle tier Flashcards

1
Q

are primary or secondary brain tumours more common

A

secondary

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2
Q

risk factors for primary brain tumours

A

Ionising radiation
Immunosuppression
Family history, genetics
Vinyl chloride

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3
Q

adults vs children. where are most primary brain tumours

A

Adults: majority = supratentorial
Children: majority = in posterior fossa

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4
Q

grading gliomas

A

1: pilocytic astrocytoma (paeds)
2: diffuse astrocytoma (benign)
3: anaplastic astrocytoma (malignant)
4: glioblastoma multiforme (GBM) - given enough time, all will progress to this except 1

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5
Q

types of brain tumour

- which is most common

A
  • gliomas - astrocytomas (most common) and oligodendrogliomas
  • Meningiomas
  • Lymphomas
  • Neurofibromas
  • Ependymmomas
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6
Q

where do secondary brain tumours metastasise from

A 
Lung, bronchus
Breast
Melanoma
GI tract
Kidney
Thyroid
Stomach
Prostate
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7
Q

common and less common cause of astrocytomas

A

Common (esp under 50): genetic error in glycolysis due to isocitrate dehydrogenase enzyme mutation. This causes instability in glial cells causing inappropriate mitosis

Less common (more common over 60): different mutation (no isocitrate dehydrogenase). Catastrophic. Poor prognosis

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8
Q

differential diagnosis of brain tumours

A 
Other causes of space occupying lesion
Aneurysm
Abscess
Cyst
Haemorrhage
Idiopathic intracranial hypertension
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9
Q

presentation of brain tumour in frontal lobe

A

personality change, hemiparesis, broca’s dysphasia, loss of smell, decreased verbal fluency, lack of initiative, unable to plan

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10
Q

presentation of brain tumour in temporal lobe

A

dysphasia, amnesia, contralateral homonymous hemianopia,

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11
Q

presentation of brain tumour in parietal lobe

A

hemisensory loss, dysphasia (wernicke’s), sensory inattention

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12
Q

presentation of brain tumour in occipital lobe

A

contralateral visual field defects, palinopsia (image remains seen for longer than it is present), polyopia (multiple images either side of object at fixation)

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13
Q

presentation of brain tumour in cerebellum

A

dysdiadochokinesia (impaired ability to do rapid alternating movements), dysmetria (uncoordinated - problems judging distance), ataxia, nystagmus, intention tremor, slurred speech, hypotonia, gait

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14
Q

presentation of brain tumour as a result of raised ICP

A

Headaches - worse on walking, lying down, bending forward, coughing
Vomitting
Papilloedema (swelling of optic discs)
drowsiness

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15
Q

other features of brain tumours (not specific to location or raised ICP)

A

Seizures, epilepsy (focal or generalised)

General cancer symptoms :
Weight loss
Malaise
Anaemia

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16
Q

brain tumour investigation

and what in contraindicated

A

CT/MRI/ PET – to find masses

Biopsy (via skull bore) - confirm cancer and grade it

Bloods : FBC, LFTS, U/Es, B12

Contraindicated = lumbar puncture (may provoke immediate coning- brain stem compressed through foramen magnum)

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17
Q

brain tumour management

A

Surgery - Removal or debulk where possible

Radiotherapy - Good for gliomas and radiosensitive masses

Chemo - for glioma and post op

Cerebral oedema /inflammation reduced with corticosteroids

Epilepsy treated with anticonvulsants

Palliative therapy

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18
Q

complications of giant cell arteritis

A

blindness if untreated

stroke

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19
Q

giant cell arteritis treatment

A

High dose steroids immediately - oral prednisolone

  • 2 years. Can be tapered eventually once disease is suppressed
  • Reduced risk of complete blindness
  • IV methylprednisolone if vision loss is progressing/occuring
  • Low dose aspirin
  • Bone protective drugs to prevent osteoperosis should be considered
  • PPI (medications are associated with GI toxicity)
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20
Q

investigations for giant cell arteritis

- inc diagnosis criteria

A

Diagnosis = 3 of 5 :

  • Age >50
  • New headache
  • Temporal artery =tender / decreased pulsation
  • ESR elevated (50/50 rule – over 50 with ESR over 50)
  • Biopsy of temporal artery abnormal. (Histology may be normal if it a ‘skip lesion’ is sampled – arteritis is patchy)
  • CPR elevated
  • High ALP (liver/ gallbladder)
  • Platelets elevated
  • Haemoglobin reduced
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21
Q

symptoms of giant cell arteritis

A
  • Headache- Abrupt onset
  • Tender temporal artery. May be palpable, firm, tender and pulseless
  • Jaw / tongue claudication
  • Visual symptoms- unilateral blindness (amaurosis fugax) in 25% of untreated
  • Scalp tenderness (from skin ischemia)
  • Systemic features
  • –Weight loss
  • –Malaise
  • –Fever
  • –Morning muscle stiffness - polymyalgia rheumatica (esp shoulders)
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22
Q

what condition is associated with giant cell arteritis

A

Associated with polymyalgia rheumatica (PMR) in 50%

  • Muscle pain, stiffness, inflammation in the shoulder, neck, hips
  • Morning stiffness worse
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23
Q

giant cell arteritis risk factors

A

Age (over 55)
Family history
Polymyalgia rheumatica (shoulder inflam muscle pain)

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24
Q

giant cell arteritis pathophysiology

A
  • Large vessel vasculitis
  • Granulomatous arteritis
  • Chronic inflammation of the medium-large arteries( aorta, carotid and its extracranial branches)
  • Blindness = inflammation and occlusion of the ciliary or central retinal artery
  • Onset can be insidious or abrupt
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25
Q

complications of cauda equina/ spinal cord compression

A

persistent neurological deficit

26
Q

management of cauda equina

A

Emergency lumbar decompression (surgical decompression) - remove causative agent

27
Q

management of spinal cord compression

A
  • Corticosteroids (dexamethasone) - if malignancy. Reduced oedema around the lesion
  • Chemotherapy
  • Radiotherapy
  • Surgery : decompressive laminectomy
28
Q

investigations into cauda equina / spinal cord compression

A
  • MRI
  • Biopsy / exploration of any masses
  • Chest X ray - look for primary lung cancers (spinal cord compression)
  • Also, in cauda equina - Anal tone reduced (PR exam) and anal wink reflex reduced
29
Q

how to distinguish cauda equina and spinal cord compression

A

In cauda equina, leg weakness is flaccid and areflexic (LMN)

In spinal cord compression, leg weakness is spastic and hyperreflexic (UMN)

30
Q

cauda equina presentation

A

Develops progressively : coming/going over weeks/months

  • Loss of anal tone (on PR examination)
  • Loss of sensation around the saddle region (groin, upper inner thighs, genitals, bum)- saddle anasthesia
  • Loss of anal wink reflex (contraction)
  • Urinary retention, overflow incontinence
  • Bilateral muscular leg pain and loss of power (weakness), and sensory deficit (paraesthesia /numbness) - LMN
  • Impotence - sexual dysfunction
  • Nerve root pain - sharp, stabbing (Sciatica : this pain down both sciatic nerve in legs)
  • Gait disturbance
  • Lower back pain - severe , rapid
31
Q

spinal cord compression presentation

A

Onset = hours to days

At level of lesion:

  • Localised back pain
  • Nerve root pain - typically shooting/sharp/ burning/ radiating
  • Numbness
  • Paraesthesia
  • LMN signs

Below the level of the lesion: (this is the key part! )

  • UMN signs!
  • Sensory loss
  • Progressive motor loss - BI lateral- legs/arms depending on where in spine → eventual paralysis

May also have sphincter disturbance- loss of bowel and bladder control. Manifests as hesitancy, frequency and later, as painless retention

32
Q

causes of cauda equina compression

A
  • Disk prolapse (herniation)
  • Tumour
  • Infection (osteomyelitis)
  • Bleeding
  • Trauma
  • Inflammatory conditions - ankylosing spondylitis
33
Q

causes of spinal cord compression

A
  • Spondylosis (spine degeneration)
  • Disc prolapse (herniation)
  • Spondylolisthesis (one vertebra slips forward on another)
  • Spinal tumours = main! Metastases from lung, breast, prostate, or myeloma
  • Spinal stenosis
  • Spinal abscess
  • Spinal tuberculosis
34
Q

age for cauda quina/ spinal cord compression

which is a medical emergency

A

can occur at any age

both

35
Q

risk factors for spinal cord compression

A 
Osteoporosis
Trauma
Tumour
Rheumatoid arthritis
Ankylosing spondylitis
36
Q

risk factors for cauda equina

A

Obesity

Heavy lifting

37
Q

nerve root lesion symptoms

A

Tingling in the affected dermatome
Pain
Paraesthesia
weakness

38
Q

nerve root lesion management

A

Steroid injection in nerve root

Surgical decompression

39
Q

carpals tunnel

  • age
  • gender
A

f>m
- Females have narrower wrists but similar sized tendon
Usually over 30y

40
Q

risk factors for carpals tunnel

A 
Usually idiopathic
Associated with
- Hypothyroidism
- Diabetes
- Pregnancy
- Obesity
- Rheumatoid arthritis
- Amyloidosis 
- Acromegaly
41
Q

tinnels sign

A

lightly tap over nerves. Patient feels tingling sensation

carpals tunnel

42
Q

phalen’s test

A

flex wrist 90deg (prayer hands). Sensation on medial nerve region.

carpals tunnel

43
Q

carpals tunnel presentation

A
  • Intermittent and gradual onset of symptoms
  • Pain
  • Aching
  • Loss of sensation of median nerve
  • Paraesthesia - worse at night– Relieved by hand over side of bed
  • Weakening and wasting of thenar eminence
  • tinnels sign
  • phalens sign
44
Q

carpals tunnel investigation

A

Electromyography
Slower conduction velocity in median sensory nerves
Confirms site and severity

45
Q

carpals tunnel management

A

Surgical decompression
Nocturnal splint - pain relief
Steroid injections - pain relief

46
Q

myasthenia crisis =

treatment

A

= weakness of respiratory muscles

Treatment = Plasmaphereisis (antibody removal) + imunoglobulin

47
Q

MG treatment

A

Anticholinesterase eg pyridostigmine

Relapses
– Immunosuppressant drugs eg azathioprine
If anticholinesterase fails
– Prednisolone

Thymectomy

  • Young onset
  • Anticholinesterase fails
48
Q

MG investigation

A

Serum antibodies

  • antiAChR
  • anti-MuSK - this is less important, look when antiAChR is neg

Nerve stimulation test = electromyography

  • Reduction in evoked potential following motor nerve stimulation, slower response
  • Esp in repetitive stimulation

Ice test = ptosis improves with ice pack

CT thymus - look for tumour/hyperplasia /atrophy

Test fatigability

  • Count to 50: as they continue, their voice becomes quieter
  • Ask the patient to raise eyes, not head, to finger. They will eventually be unable to maintain this
49
Q

MG symptoms

A
  • Diurnal variability (in the day) – improves after rest
  • Increasing Muscular weakness (fatiguing)
  • Fatigability of ocular (ptosis, double vision), bulbar (swallowing - dysphagia, chewing, dysarthria, myasthenic snarl on smiling), and proximal limbs
  • Myasthenia crisis= weakness of respiratory muscles
50
Q

MG pathophysiology

A

Autoimmune - antibodies to nicotinic ACh receptors (anti-AChR antibodies)

  • Immune complex deposition at postsynaptic membranes
  • Depletion of working postsynaptic receptor sites
  • B cells and T cells involved
  • ACh less able to activate neuromuscular junction - excitatory effect blocked

Antibodies to Muscle specific tyrosine kinase (anti -MuSK) at the postsynaptic membrane of the neuromuscular junction – causing receptor blockade /loss

51
Q

what conditions is MG associated with

A 
Associated with other autoimmune conditions eg SLE, RA
Associated with 
thymic hyperplasia (esp under 50) 
Thymic tumour (esp if over 50) 
Thymic atrophy (esp if over 50)
(thymus)
52
Q

MG age and gender

A

Overall f>m

  • But m> f over 50
  • F peak = 30y
  • M peak = 60y
53
Q

6 causes nerve malfunction

A
  1. Demyelination
    - Due to Schwann cell damage
    - Conduction slows
    - Eg guillain barre
  2. Axonal degeneration
    - Axon damage causes nerve fibre to die
    - Toxic neuropathies
  3. Compression
    - Focal demyelination at compression site
    - Causes disruption of conduction
    - Eg entrapment neuropathies (Carpals tunnel)
  4. Infarction
    - Micro-infarction of vasa nervorum
    - Diabetes, polyarteritis nodosa
  5. Infiltration
    - By inflammatory cells (leprosy), neoplastic cells, and granulomas (sarcoid)
  6. Wallerian degeneration
    - Nerve fibre lesion causes axon distal to this degenerates (separated from neuron cell body)
54
Q

list 5 causes of peripheral neuropathies

A 
guillain barre syndrome (acute)
diabetes (chronic)
alcohol (chronic)
leprosy
RA
renal failure
syphillis
sarcoidosis
malignancy
polyarteritis nodosa
hypothyroidism
hypoglycaemia
HIV
lyme disease
lead
arsenic
drugs
nutritional defects
55
Q

Mononeuritis multiplex =

A

2 or more individual nerves are affected

causes tend to be systemic eg RA, diabetes, AIDs, leprosy, carcinoma, sarcoidosis, polyarteritis

56
Q

polyneuropathy characteristics

eg

A

widespread, symmetrical disease, usually commencing peripherally/distally (glove and stocking).

eg leprosy, guillain barre

57
Q

sensory neuropathy symptoms

A
  • numbness
  • paraesthesia eg pins and needles, burning
  • Affects extremities/peripheral first - glove and stocking
  • May have dexterity issues eg buttons
  • May have signs of trauma that indicate sensory loss eg cuts, burns, joint deformation
  • — Often presents as foot ulcers
  • Pain
  • — Esp alcoholic and diabetic neuropathies
58
Q

motor neuropathy presentation

A
  • Often progressive (May be rapidly so)
  • Weakness, clumsiness
  • Wasting
  • walking/ gait issues eg stumbling, falling
  • Breathing issues - reduced vital capacity
59
Q

autonomic neuropathy presentation

A

incontinence

sexual dysfunction

60
Q

treatment for neuropathic pain

A

amitriptyline

phase 2a mine (38 decks)

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