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4th Year Surgery Block > Neurosurgery > Flashcards

Neurosurgery Flashcards

1
Q

List 8 red flags for back pain?

A
  • Age: >60 or <20 years old
  • Pain not improved by rest
  • Pain that wakes the patient up at night
  • Urinary retention/incontinence and faecal incontinence
  • Saddle anaesthesia
  • History of malignancy
  • Unexplained weight loss.
  • Fever, immunosuppression or IV drug abuse
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2
Q

List the ligaments of the spine from superficial to deep

A

supraspinous ligament
interspinal ligament
ligamentum flavum
posterior longitudinal ligament
anterior longitudinal ligament

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3
Q

Explain what a radiculopathy is and radiculopathy vs radicular pain?

A
  • A radiculopathy is a conduction block in the axons of a spinal nerve or its roots, with impact on motor axons causing weakness and on sensory axons causing paraesthesia and/ or anaesthesia
    There is a distinction between radiculopathy versus radicular pain:
  • Radiculopathy = a state of neurological loss and may or may not be associated with radicular pain
  • Radicular pain = pain deriving from damage or irritation of the spinal nerve tissue, particularly the dorsal root ganglion
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4
Q

Causes of radiculopathy?

A
  • Intervertebral disc prolapse: the lumbar spine is predominantly affected by repeated minor stresses that predispose to rupture of the annulus fibrosus and sequestration of disc material (the nucleus pulposus)
  • Degenerative diseases of the spine: leading to neuroforaminal or spinal canal stenosis, the cervical spine is the most mobile segment of the spine and degenerative change is a normal part of the ageing process
  • Fracture: either trauma or pathological
  • Malignancy: most commonly metastatic
  • Infection: such as extradural abscesses, osteomyelitis (most commonly TB), or herpes zoster
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5
Q

Clinical features of a radiculopathy?

A
  • Sensory symptoms in the corresponding demeratome and weakness in the corresponding myotome
  • Sensory features are paraesthesia and numbness and motor features are weakness
  • Radicular pain is often also present, typically described as a burning, deep, strap-like, or narrow pain, it is not uncommon for radicular pain to be intermittent
  • Important to ask about red flag symptoms for cauda equina
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6
Q

Management of a radiculopathy?

A
  • Definitive long term management depends on the underlying cause
  • In general the only condition that requires emergency surgical treatment is cauda equina syndrome
  • Most IV disc prolapses can be managed non-operatively, but indications for surgical treatment include unremitting pain despite non-surgical management, progressive weakness, and new or progressive myelopathy (compression of the spinal cord)
  • Symptomatic management is with analgesia, amitriptyline is usually first line or pregabalin and gabapentin as alternatives, if the patient suffers from muscle spasms these can be managed with benzodiazepines or baclofen, physiotherapy is an important part of management
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7
Q

What is the cauda equina and what is cauda equina syndrome?

A
  • This is a surgical emergency caused by compression of the cauda equina
  • The spinal cord ends at L1-L2
  • The cauda equina is a bundle of nerves situated inferior to the spinal cord
  • Cauda equina contains motor and sensory fibres to the lower limbs, motor innervation to the anal sphincters and parasympathetic innervation for the bladder
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8
Q

The spinal cord ends at

A

L1-L2

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9
Q

Causes of cauda equina syndrome? peak age of onset?

A
  • Peak onset between 40-50 years
  • Most common cause is disc herniation
  • Other causes include trauma, neoplasms, infection, chronic spinal inflammation or iatrogenic e.g. haematoma secondary to spinal anaesthesia
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10
Q

Clinical features of cauda equina?

A
  • Reduced lower limb sensation
  • Bladder or bowel dysfunction
  • Lower limb weakness
  • Severe back pain
  • Impotence
  • Saddle paraesthesia and anaesthesia
  • Need to do a PR exam to assess for reduced anal tone
  • Post void bladder scan to assess urinary retention
  • Full peripheral neurological examination including upper limbs is required to look for spinal pathologies higher up along the spine than cauda equina
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11
Q

Investigations for cauda equina?

A
  • Emergency lumbar-sacral spine MRI
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12
Q

Management and prognosis of cauda equina?

A
  • Neurosurgical decompression
  • Prognosis is variable depending on aetiology and time from symptom onset to surgery
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13
Q

What is lumbar spinal stenosis?

A
  • Narrowing of the spinal canal which compresses the lowest most spinal cord, conus medullaris and nerve roots leading to symptoms of neurogenic claudication
  • Mainly occurs in patients older than 50 yo
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14
Q

Causes of lumbar spinal stenosis?

A
  • Hypertrophy of facet joints and ligamentum flavum
  • Protruding intervertebral discs
  • Spondylolisthesis
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15
Q

Clinical features of lumbar spinal stenosis?

A
  • Insidious and progressive over many months or years
  • Unilateral or bilateral hip, buttock or lower extremity pain or burning sensation precipitated by standing or back extension and relieved by sitting, lumbar flexion or walking uphill
  • Anthropoid posture (flexion of the waist)
  • Neurogenic intermittent claudication: leg weakness, tingling and numbness accompanied by paraesthesia
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16
Q

Neurogenic vs vascular claudication?

A
  • Neurogenic is dermatomal, variable amount of exercise illicit pain, can come on with prolonged standing at rest (vascular does not)
  • When resting it takes a while to resolve, whereas vascular immediately resolves
  • Burning pain in neurogenic vs cramping in vascular
  • Peripheral pulses are normal in neurogenic but diminished or absent in vascular
  • Neurogenic claudication is relieved on walking uphill whereas vascular is not
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17
Q

Investigations for lumbar spinal stenosis?

A
  • Neurogenic claudication is often a clinical diagnosis but can be confirmed with MRI lumbosacral spine
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18
Q

Management of lumbar spinal stenosis?

A
  • Conservative treatment first off (physio and analgesia)
  • If symptoms worsen/ intolerable surgery can be done
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19
Q

What is cervical spondylosis?

A

Degenerative arthritic process of cervical spine and affecting intervertebral discs and zygapophyseal joints
Will either present as a radiculopathy or myelopathy
Different surgeries for it

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20
Q

Myelopathy vs radiculopathy?

A

Myelopathy – compressing on spinal cord itself – upper motor neuron signs
Radiculopathy – compressing the spinal nerves or their roots – lower motor neuron signs

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21
Q

What is degenerative cervical myelopathy? Why is it importantn?

A
  • Spinal cord compression in the cervical region
  • Causes UMN signs more prominent in the lower limbs
  • Occurs in the elderly and causes a deterioration in a patient’s gait and thus is an important cause of falls in the elderly
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22
Q

Features of degenerative cervical myelopathy?

A

Progressive symptoms:
* Imbalance and disturbance of gaits
* Clumsy hands e.g. difficulty with buttons, or holding fork or tingling in fingertips
* Urinary or faecal incontinence (rare)
* Pain in a non-dermatomal distribution
* Legs jump at night due to hyperreflexia

On examination:
* UMN signs
* Weakness, hyperreflexia and spasticity
* Positive babinksi
* Loss of finger dexterity

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23
Q

Investigation for degenerative cervical myelopathy

A

MRI cervical spine

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24
Q

Management of degenerative cervical myelopathy?

A
  • Early treatment = best recovery but most patients present too late
  • Decompressive surgery is best, this prevents deterioration but does not improve symptoms
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25
Q

Describe anterior cord compression syndrome?

A
  • Cord infarction by area of anterior spinal artery
  • Loss of pain and temperature below level but preserved vibration and proprioception
  • ie. You lose the spinothalamic which is ventral but keep the DCML as its dorsal
  • also keep your corticospinals which are dorsal
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26
Q

Describe complete cord transection syndrome?

A
  • All motor and sensory modalities below lesion
  • Initially flaccid areflexic paralysis (spinal shock) but then UMN signs will appear
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27
Q

Describe brown sequard syndrome?

A
  • Penetrating injury probably
  • Ipsilateral UMN paralysis and loss of proprioception and vibration (because it crosses over at the medulla)
  • Contralateral loss of pain and temperature (because spinothalamic crosses over at the spinal cord)
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28
Q

Describe central cord syndrome?

A
  • Acute extension injury to already stenotic neck or syringomyelia or tumour
  • Predominantly bilateral upper limb weakness > lower limbs
  • Capelike spinothalamic sensory loss
  • Dorsal columns preserved
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29
Q

The incidence of metastatic neoplasm is ______
metastates appear as ___________
the most common sites are _________

A
  • The incidence of metastatic neoplasms in the brain is much higher than that of a primary cerebral neoplasm
  • The common appearance of metastatic brain tumours is multiple, well-delineated spherical nodules that are randomly distributed
  • The two most common primary sites are the lung and breast but any malignant tumours can metastasise to the brain
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30
Q

List some categories of brain tumours

A

gliomas
tumours of neuronal cell types
tumours arising from mesoderm
tumours of nerve sheath
germ cell tumours
pituitary gland tumours

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31
Q

Describe astrocytomas?

A
  • These are gliomas that arise from astrocytes
  • They are histologically graded from grade I-IV
  • Grade I astrocytomas grow very slowly over many years while grade IV cause death within several months
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32
Q

What is a glioblastoma multiforme?

A

grade 4 astrocytoma - v aggressive

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33
Q

What is the most common glial tumour?

A

glioblastoma multiforme

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34
Q

Describe oligodendrogliomas?

A
  • These are gliomas that arise from oligodendrocytes
  • They grow very slowly over several decades and calcification is common
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35
Q

Describe tumours of neuronal cell type and different types?

A
  • Fully differentiated neurons can neither multiply nor give rise to neoplasms
  • Tumours of this type are therefore derived from primitive nerve precursors (blast cells) and seen in infancy and childhood before completion of differentiation
  • Depending on their site of origin they are given different names (but the tumour is mainly composed of the same cells which are blast cells- blast cells are basically a precursor to mature neurons)

Medulloblastoma
* Tumour arising from cerebellum

Retinoblastoma
* Tumour arising from the retina

Neuroblastoma and Ganglioneuroma
* These are tumours that arise from sympathetic ganglia
* In ganglioneuromas the tumour is derived from blast cells but as the tumour grows the neurons actually mature

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36
Q

Describe menigiomas?

A

arise from arachnoid granulations most commonly adjacent to venous sinuses
slow growing and essentially benign
can occassionally arise in the spine

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37
Q

2 types of nerve sheath tumour?

A

schwannomas/ neuromas (derived from schwann cells)
neurofibromas (derived from endoneurium- connective tissue that surounds myelin sheaths in PNS )

38
Q

Describe germ cell tumours?

A
  • These occasionally arise in midline structures and are derived from embryologically misplaced germ cells
  • Can have these misplaced cells in your brain your whole life and not find out or only find out if you get a tumour arising from these cells!
  • E.g. teratoma
39
Q

potential symptoms of tumour in frontal lobe?

A

1) Precentral gyrus: Contralateral weakness, the part of the body that the weakness is in will depend on the position along the gyrus, it will correspond with the motor homunculus
2) Broca’s area (inferior frontal gyrus): expressive dysphasia where the patient can still comprehend words but produces faulty sentences
3) Frontal eye fields (Middle frontal gyrus): abnormalities of gaze
4) Micturation inhibition centre: incontinence
5) Personality changes, disinhibition and cognitive slowing

40
Q

Potential symptoms of tumour in temporal lobe?

A

1) Auditory Cortex and Wernickes Area (superior temporal gyrus): damage to auditory cortex can lead to loss of awareness of sound, wernicke’s area is located on the superior temporal gyrus in the dominant hemisphere and damage can lead to receptive dysphasia in which an individual has impaired comprehension and produces jargon (word salad) but their speech is fluent
2) Memory deficits
3) Contralateral superior quadrantanopia

41
Q

Potential symptoms of tumour in occipital lobe?

A

1) Visual Cortex: visual hallucinations, contralateral homonymous hemianopia

42
Q

Potential symptoms of tumour in parietal lobe?

A

1) Postcentral gyrus: contralateral sensory loss, part of body will depend on location along gyrus, it will correspond with the sensory homunculus
2) Contralateral inferior quadrantopia
3) If dominant lobe affected (left in most people): dyscalculia (difficulty understanding maths), dysgraphia (difficulty writing), finger agnosia (inability to distinguish between and recognise all fingers), left-right disorientation
4) If non-dominant lobe affected (right in most people): neglect (deficit in awareness of one side of the body), dressing apraxia (inability to dress yourself automatically), constructional apraxia (inability to build, assemble or draw objects)

43
Q

Potential symptoms of tumour in cerebellum?

A
  • Dysdiadochokinesia: impairment of rapid alternating movements e.g. quick alternating, pronation, supination of the hand
  • Ataxia: broad based gait
  • Nystagmus: involuntary, uncontrollable eye movements
  • Intention tremor: tremor that gets worse as you approach the end point of a guided movement, finger to nose test can show this
  • Scanning dysarthria: patients speaks slowly with poor articulation of speech
  • Hypotonia: reduced tone
44
Q

Direct effects of brain tumours

A

raised ICP causing headaches and papilloedema
seizures due to uspet of electrical pathways

45
Q

Investigations for brain tumour?

A
  • MRI is the investigation of choice
  • CT may be done first though if MRI is not possible right away
  • Biopsy is carried out to ascertain the histology
  • Since metastases are more common than primary tumours, routine tests such as chest x-ray should be performed
46
Q

Treatment of low grade astrocytomas?

A

removed as it has been shown that these tumours if left have the potential to de-differentiate (reverse differentiation and lose specialised characteristics) into a high-grade malignancy

47
Q

Treatment for glioblastoma?

A
  • The gold standard treatment for glioblastomas is surgery, radiotherapy and chemotherapy, despite these treatments these tumours unfortunately still have a poor prognosis
48
Q

What is SAH and what are main causes?

A
  • Subarachnoid haemorrhage refers to extravasation of blood in the SA space between the pia and arachnoid membrane
  • It can be caused by head trauma or be non traumatic
  • The main cause of non traumatic SAH is rupture of a intracranial (berry) aneurysm
49
Q

thunderclap headache?

A

SAH

50
Q

Clinical features of SAH?

A
  • Sudden onset of “thunderclap headache” patients claim it is the worst headache of their life
  • Neck stiffness and photophobia due to meningeal irritation
  • Headache is often accompanied by nausea or vomiting due to increased ICP or meningeal irritation
  • If the aneurysm is of the posterior communicating artery then a third nerve palsy may occur
  • Sometimes confusion, seizures and loss of consciousness can occur
  • Sometimes can get vitreous haemorrhage associated with SAH
51
Q

Investigations for SAH?

A
  • Diagnosis is usually confirmed with an unenhanced CT scan where a large volume of acute blood which appears white is seen in the suprasellar cistern, sylvian fissures and sulci
  • Lumbar puncture may be performed if doubt remains after CT and would be checking the CSF for signs of blood
  • When SA blood is found in the absence of a history of trauma CT cerebral angiography is performed to look for the underlying berry aneurysm
52
Q

Management of SAH?

A
  • Immediate treatment of SAH involves bed rest and supportive measures. Hypertension should be controlled. Nimodipine, a calcium-channel blocker given for 3 weeks, reduces mortality
  • Nearly half of SAH cases are either dead or moribund before reaching hospital. Of the remainder, a further 10–20% rebleed and die within weeks. Failure to diagnose SAH – for example, mistaking SAH for migraine – contributes to this mortality
  • Where angiography demonstrates an aneurysm (the cause of the vast majority of SAHs), endovascular treatment by placing platinum coils via a catheter in the aneurysm sac, to promote thrombosis and ablation of the aneurysm, is now the first-line treatment
  • Endovascular coiling has a lower complication rate than surgery but direct surgical clipping of the aneurysm neck is still required in some selected cases
53
Q

Complications of SAH?

A
  • Vasospasm occurs because blood in the SA space is very irritant to vessels. Treatment for vasospasm includes the use of nimodipine (to prevent spasmodic effects) and blood pressure control
  • Re-bleed: The risk of re-bleeding is highest in the first 2 weeks and is increased in elderly patients and patients with hypertension. It can be managed with surgical clipping or coiling.
  • Hydrocephalus
  • Seizures
  • Hyponatraemia - SIADH can be a complication
54
Q

What is SDH and what causes it?

A
  • This is a collection of blood between the dura and the arachnoid layer, typically caused by a traumatic event
  • Acute SDH is due to high impact head trauma which results in rupture of the bridging veins (these are the veins in the subarachnoid space which puncture the dura matter to drain into the dural venous sinuses hence if these are ruptured because they are going from the SA space to the dura they will bleed under the dura)
  • Chronic SDH is associated with brain atrophy (due to age, chronic alcoholism or dementia), brain atrophy causes the bridging veins to be stretched meaning that even minor trauma can cause them to rupture, the leaky vessels cause blood to accumulate in the space
55
Q

Presentation of SDH?

A
  • Acute SDH forms quickly and the patient becomes almost immediately symptomatic following the head trauma
  • Chronic SDH can take longer for symptoms to develop
  • Patients with acute SDH typically present with severely decreased state of consciousness
  • Patients with chronic SDH can present with a more insidious course, common symptoms are of headache and confusion but other symptoms include urinary incontinence, weakness, seizures, cognitive dysfunction and gait abnormalities
56
Q

Investigations for SDH?

A

unenhanced ct

57
Q

Semilunar shape on ct

A

sdh

58
Q

Lens shape on ct

A

edh

59
Q

CT appearance of SDH?

A
  • SDH appears as a semilunar shape because the blood is not bounded by the fissures like it is in extradural haemorrhage
  • Acute SDH appears as a crescent shape hyperdensity and chronic as a hypodense crescent shaped appearance
60
Q

Management of SDH?

A
  • May not need immediate treatment but it is important to involve neurosurgery
  • Even large collections can resolve on their own
  • Serial imaging is required to assess progress
  • If needed they can be drained surgically
61
Q

What is EDH and what is most common cause?

A
  • Accumulation of blood between dura and bone usually caused by separation of dura and bone following a shearing stress from head trauma with disruption of vessels
  • The most common source of bleeding is from the middle meningeal artery from a temporoparietal fracture because this runs under the thinnest part of the skull called the pterion
62
Q

Presentation of EDH?

A
  • Typically presents in a young adult after head trauma
  • Classically presents with a brief loss of consciousness, followed by a lucid interval after that the patient further deteriorates, exhibiting symptoms such as headache, vomiting, contralateral hemiparesis (stalks that attach the cerebrum to the brainstem and contain a lot of the ascending and descending tracts) and ipsilateral pupillary dilatation (due to temporal lobe herniating and compressing the oculomotor nerve)
63
Q

loss of consciousness followed by lucid interval followed by deterioration?

A

EDH

64
Q

Investigation for EDH? Apperance?

A
  • Unenhanced CT is imaging modality of choice
  • Extradural haematoma has a lens shaped appearance (because it is bounded by the fissures as the haemorrhage is above the dura)
  • It is acute so the blood appears white
65
Q

Management of EDH?

A
  • Expanding extradural haematomas need immediate neurosurgical evacuation
  • Conservative management is sometimes considered in neurologically intact patients with small haematomas
66
Q

What is an aneurysm? What are the 2 types?

A
  • An aneurysm is defined as an abnormal dilatation of a blood vessel by more than 50% its normal diameter
    saccular more common = dilatation on one side
    fusiform less common = symmetrical dilatation
67
Q

Where do intracranial aneurysms tend to form?

A
  • They form at sites where blood vessels bifurcate or merge as such the majority form around the Circle of Willis
68
Q

Risk factors for developing an aneurysm?

A
  • Female gender
  • Family history
  • Hypertension
  • Smoking
  • Autosomal dominant polycystic kidney disease
  • Marfans
69
Q

Risk factors for aneurysm rupture?

A
  • Location (posterior circulation highest rupture risk)
  • Size (bigger the more likely to rupture)
70
Q

Clinical features of aneurysms?

A
  • Most small unruptured produce no symptoms and are found incidentally on MRI
  • Unruptured symptomatic aneurysms can cause headaches or nausea, in rarer cases focal neurological deficits, seizures or isolated nerve palsies
  • Ruptured aneurysms will present most commonly as a SA haemorrhage
71
Q

Investigations for aneurysms?

A
  • For diagnosis will be CT angiogram, then magnetic resonance angiography may be useful for operative planning
72
Q

Management for aneurysms?

A
  • Depends on patient factors
  • All should have modifiable risk factors managed e.g. hypertension and smoking
  • Majority of aneurysms are monitored only with regular interval imaging
  • For those requiring surgical intervention may stay is surgical clipping or endovascular coiling
73
Q

Idiopathic intracranial hypertension typically occurs in?

A
  • Typically develops in younger, overweight females many of whom have polycystic ovaries
74
Q

Features of IIH?

A

include those of raised intracranial pressure e.g. headache worse in morning, headache with nausea and vomiting, headache with visual obscurations due to papilloedema

75
Q

Investigations for IIH?

A
  • MRI is usually normal
  • Lumbar puncture shows elevated CSF pressure but normal constituents
76
Q

Management of IIH?

A
  • Treatment involves monitoring visual fields, encouraging weight loss, acetozalmide and thiazide diuretics can be used to reduce CSF production
  • Sometimes ventriculoperitoneal shunt insertion or optic nerve sheath fenestration to protect vision is sometimes necessary
77
Q

What is hydrocephalus? types

A
  • Hydrocephalus is an excessive accumulation of CSF within the head, caused by disturbance of formation, flow or absorption
  • High pressure and ventricular dilatation result
  • Hydrocephalus can be congenital or acquired
  • Communicating hydrocephalus occurs when CSF is inefficiently absorbed back into the blood stream, causes include meningitis or subarachnoid haemorrhage
  • Non-communicating hydrocephalus is obstructive, CSF is blocked from flowing between one of the passage that connects the ventricles e.g. tumours and other lesions
78
Q

What are some congenital abnormalities that cause hydrocephalus

A

arnold-chiari - cerebelum and medulla bulge through foramen magnum
congenital stenosis or atresia of duct of sylvius
atresia of formaina of magendie and luschka

79
Q

Acquired causes of hydrocephalus?

A
  • Posterior fossa and brainstem tumours
  • Subarachnoid haemorrhage
  • A 3rd ventricle colloid cyst
  • Choroid plexus papilloma (rare)
80
Q

Presentation of hydrocephalus?

A
  • In the infant and young child, the pliable skull expands to accommodate the enlarging brain
  • There is great enlargement of the head with prominent scalp veins and forehead overhanging the eyes, the fontanelles remain open
  • In the older child and adult, enlargement of the brain is prevented by the inability of the skull to expand
  • The main change is dilatation of the ventricles associated with the effects on the brain of increased intracranial pressure
  • E.g. cognitive impairment, headache, visual disturbance, nausea and vomiting, ataxia
81
Q

Management of hydrocephalus?

A
  • Ventriculoperitoneal or lumbar peritoneal shunting is necessary when progressive hydrocephalus causes symptoms
  • Removal of tumours is carried out when appropriate
  • Endoscopic 3rd ventriculostomy may be performed
82
Q

Describe normal pressure hydrocephalus?

A
  • A syndrome of enlarged ventricles in elderly patients- causes not really understood
  • Triad of symptoms: gait apraxia, dementia, urinary incontinence
  • CSF pressures tend to intermittently be high
  • Shunting may be required
83
Q

Gait apraxia, dementia, urinary incontinence?

A

normal pressure hydrocephalus

84
Q

4 questions for cervical myelopathy?

A

Do you struggle with fine finger movements/ fingers feel fat like bunch of bananas?
Clumsy – are you dropping things?
Do your legs jump at night?
Do you fall over/ have poor balance if you close your eyes?

85
Q

Explain what hoffmans sign is?

A

basically if positive suggests cervical myelopathy

this is an UMN sign and suggests corticospinal tract dysfunction localised to cervical segments of spinal cord – flicking nail – is positive if adduction of thumb and flexion of index finger

86
Q

Patients with intracerebral bleed who becomes unresponsive needs _____

A

urgent CT to check for hydrocephalus

87
Q

To detect a SAH by LP it should be done _____

A

12 hrs post onset of headache
because you want to look for old blood, cant test for new blood because cant distinguish whether it is bleeding from the LP or bleeding actually in CSF
also need to keep it in the dark

88
Q

Describe 2 types of brain herniation and how they may present?

A

herniation is due to raised ICP

tonsilar herniation - cerebellar tonsils down through the foramen magnum - will cause cardiorespiratory arrest

transtentorial herniation - will cause a third nerve palsy

89
Q

Explain what neurogenic shock is and how it presents?

A

this is caused by trauma or injury to the spine

low HR alongside warm flushed peripheries. There is loss of sympathetic outflow resulting in hypotension and bradycardia as well as warm peripheries due to vasodilation and inability to vasoconstrict

(spinal shock is not circulatory and is loss of all sensation below level of the injury)

90
Q

Spondylosis vs spondylolisthesis?

A

Spondylosis is degeneration of the IV discs, mainly wear and tear

Spondylolisthesis is when part of the vertebra slips forwards can be due to trauma or wear and tear

4th Year Surgery Block (11 decks)

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