Case 14 Flashcards

1
Q

What are the 3 different principles for spinal injury operations?

A

Decompress
Realign
Stabilise

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2
Q

What are examples of conservative treatment of spinal injury?

A

Halo vest
Braces
Cervical colar

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3
Q

When would conservative treatment of spinal injury be indicated?

A

Stable fracture
Some polytraumas
Unfit for surgery
Osteoporotic bones

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4
Q

What can be used to immobilise the entire spine?

A

Semi-rigid collar
Sandbags either side of head
Spinal board - only used for transport to avoid pressure sores

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5
Q

What is flaccid areflexia?

A

Loss of motor, sensory, reflex and autonomic function

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6
Q

What is priapism?

A

Persistent often painful erection

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7
Q

What could suggest a spinal cord injury in the unconscious patient?

A
Flaccid areflexia 
Diaphragmatic breathing 
Pain response above clavicle 
Bradycardia/ hypotension 
Priapism
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8
Q

What is shock?

A

Cellular hypoxia from inadequate:
Organ perfusion
Tissue oxygenation

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9
Q

When does spinal shock usually resolve by?

A

24 hours of cord injury

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10
Q

What occurs in spinal shock?

A

Below the level of injury you get:
Flaccid paralysis
Areflexia
Lack of sensation

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11
Q

What causes spinal shock?

A

Physiologic spinal cord shut down in response to injury

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12
Q

What indicates end of spinal shock and how is this elicited in practise?

A

Return of reflexes - occurring in caudal to cranial direction
Test bulbocavernosus reflex (anal sphincter contraction in response to glans penis squeezing)

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13
Q

What causes neurogenic shock?

A

Reduced sympathetic outflow T1-L2

= unopposed vagal tone

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14
Q

What are the signs of neurogenic shock?

A

Flaccid paralysis
Hypotension
Bradycardia

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15
Q

What causes the hypotension and bradycardia in neurogenic shock?

A

Reduced sympathetic stimulation causes:
Hypotension - loss of blood vessel tone
Bradycardia - reduced cardiac stimulation

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16
Q

What is transient neurapraxia and what is it caused by?

A

Temporary loss of motor/ sensory function in the absence of structural changes
Caused by blunt injury, compression and ischaemia

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17
Q

What is complete spinal cord injury and when can it be confirmed?

A

No sensation or voluntary motor function below the level of the injury
Only confirmed after resolution of spinal shock - when reflex activity has returned

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18
Q

What is sacral sparing?

A

Presence of sacral sensation, voluntary rectal tone and great toe movement
Potential for recovery

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19
Q

How are the different parts of the lateral spinothalamic and corticospinal tracts distributed?

A

Cervical (medial) - arms
Thoracic
Lumbar - legs
Sacral (lateral)

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20
Q

What are the features of CENTRAL cord syndrome?
How common is it?
What’s the prognosis?

A

Motor and sensory
Most common cord syndrome
Fair prognosis

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21
Q

What are the features of ANTERIOR cord syndrome?
How common is it?
What’s the prognosis?

A

Motor, some sensory
Common
Poor prognosis

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22
Q

What are the features of POSTERIOR cord syndrome?
How common is it?
What’s the prognosis?

A

Posterior column tetraparesis
Uncommon
Poor prognosis

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23
Q

What are the features of Brown-Sequard cord syndrome?
How common is it?
What’s the prognosis?

A

Ipsilateral motor, contralateral pain and temp
Uncommon
Good prognosis

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24
Q

What are the features of COMPLETE cord syndrome?
How common is it?
What’s the prognosis?

A

Total loss below level
Uncommon
Poor prognosis

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25
Q

How would you manage a patient recovering from central cord injury?

A

Lie flat for 6 weeks

Then tilt table to avoid postural hypotension that can cause further neurological deterioration

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26
Q

What radiological tests need to be carried out if spinal injury suspected?

A

Lateral cervical spine - detects 85% of cervical fractures

Entire spine - 10% with 1 fracture have another non-contiguous injury

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27
Q

What does ABDCE stand for when assessing a lateral C spine X-ray?

A
Adequacy/ alignment 
Bone 
Cartilage
Dens 
Extra-axial soft tissue
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28
Q

The ADI (atlas dens distance) should be less than 5mm, if it is greater what does it indicate?

A

Transverse and accessory ligament rupture

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29
Q

What is divided up into thirds according to steel’s rule of thirds?

A

1/3 dens, 1/3 space, 1/3 spinal cord

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30
Q

If the space between the dens and spinal cord closes in and begins to compress the spinal cord, what’s wrong?

A

Atlanto-axial instability

Alar ligaments have failed

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31
Q

How is static instability inferred?

A

Imaging

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32
Q

What is dynamic instability?

A

Deformity that worsens under physiologic loads

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33
Q

What would be observed in posterior ligamentous complex injury on X-ray? and MRI?

A

> 50% loss of vertebral height
30 degree kyphosis
MRI - disrupted PLC

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34
Q

What can erect cervical X-rays show?

A

Load bearing deformity

Ligament injury/ instability

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35
Q

What do dynamic X-rays show?

A

Physiological instability

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36
Q

Why are steroids not used in SCI?

A

They’re osteoporotic

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37
Q

What is SCIWORA and what causes it?

A

Spinal cord injury without radiological abnormality
Oedema, haemorrhage, infarct, transection, concussion
Rare - no factor, ligament injury or extra neural compression

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38
Q

What are the possible complications of spinal cord injury?

A
Pneumonia 
Postural hypotension 
DVT/ PE
Autonomic dysreflexia = acute, uncontrolled hypertension 
Renal failure 
Pseudo-obstruction 
Sexual dysfunction 
Pressure sores
Psychological problems 
Inadequate ventilation - C3,4,5 damage
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39
Q

What is ankylosis?

A

Abnormal stiffening and immobility of a joint due to fusion of the bones

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40
Q

What sort of SCI does partial preservation zone apply to?

A

Complete injuries

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41
Q

What is tetraplegia?

A

Paralysis resulting in partial/ total use of all limbs/ torso

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42
Q

What is paraplegia?

A

Paralysis similar to tetraplegia but arms are spared

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43
Q

What is spondylosis?

A

Degeneration of the intervertebral discs - painful

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44
Q

How common is cauda equina syndrome, what’s the usual cause, what’s important to remember in examination?

A

Rare
Canal filling disc compressing on entire cauda equina
Check sphincter disturbance, time important (diagnosis and treatment)

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45
Q

What does the spectrum of cauda equina syndrome consist of?

A
Low back pain 
Uni/ bilateral sciatica 
Saddle anaesthesia 
Motor weakness in lower extremities
Variable rectal/ urinary symptoms
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46
Q

Which reflex is tested at the ankle?

A

S1

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47
Q

Which reflex is tested at the knee?

A

L4

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48
Q

Which reflex is tested at the wrist?

A

C6

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49
Q

What reflexes are tested for near the elbow?

A

Biceps - C5

Triceps - C7

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50
Q

What myotome is tested by elbow flexion?

A

C5

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51
Q

What myotome is tested by wrist extension?

A

C6

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52
Q

What myotome is tested by elbow extension?

A

C7

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53
Q

What myotome is tested by finger flexion?

A

C8

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54
Q

What myotome is tested by finger abduction?

A

T1

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55
Q

What myotome is tested by hip flexion?

A

L2

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56
Q

What myotome is tested by knee extension?

A

L3

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57
Q

What myotome is tested by ankle dorsiflexion?

A

L4

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58
Q

What myotome is tested by big toe extension?

A

L5

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59
Q

What myotome is tested by ankle plantar flexion?

A

S1

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60
Q

What are the gradings of power?

A

0 - total paralysis
1 - palpable/visible contraction
2 - active movement gravity eliminated
3 - active movement against gravity
4 - active movement against some resistance
5 - active movement against full resistance

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61
Q

What’s the difference between paraparesis and hemiparesis?

A

Paraparesis - partial paralysis of lower limbs (spinal injury)
Hemiparesis - weakness of entire body on 1 side (head injury)

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62
Q

What are the serious causes of back pain to exclude?

A

(ATIT)
AAA, pancreatitis, malignancy
spinal Trauma, Infection, Tumour

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63
Q

Which cranial nerves come off the cerebral hemispheres?

A

I Olfactory

II Optic

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64
Q

Which cranial nerves come off the midbrain?

A

III Oculomotor

IV Trochlear

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65
Q

Which cranial nerves come off the pons?

A

V Trigeminal
VI Abducens
VII Facial

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66
Q

Which cranial nerves come off the junction between pons and medulla?

A

VIII Vestibulocochlear

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67
Q

Which cranial nerves come off the medulla?

A

IX Glossopharyngeal
X Vagus
XI Accessory
XII Hypoglossal

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68
Q

Which connective tissue sheath encloses fascicles?

A

Epineurium

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69
Q

Which connective tissue sheath surrounds individual fascicles?

A

Perineurium

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70
Q

Which connective tissue sheath separates individual fibres?

A

Endoneurium

71
Q

What do Pacinian corpuscles respond to?

A

Pressure

72
Q

What do Meissener’s corpuscles respond to?

A

Light touch

73
Q

What’s the difference between malunion and nonunion?

A

Malunion: when a fracture heals in a non optimal position
Nonunion: failure to heal, common in the tibia

74
Q

What’s an osteoclast?

A

Large cells that dissolve the bone

75
Q

What’s an osteoblast?

A

Form new bone

76
Q

What’s an osteocyte?

A

Cells inside the bone
Formed from osteoblasts
Their long branches connect them to the other osteocytes
Sense pressures/ cracks in the bone and help to direct where osteoclasts will dissolve the bone

77
Q

Explain the difference in manifestations of injuries to different segments of the dorsal column

A

Gracile fascicles - Ipsilateral loss of proprioception and fine touch from the leg

Cuneate Fasciculus - Ipsilateral loss of proprioception and fine touch from the arm

78
Q

At resting potential, where are K+ and Na+ greatest in concentration? Which pump maintains this gradient?

A

More Na+ outside
More K+ inside
Na+/K+ pump (Mr Nasty out, K+ in)

79
Q

How do local anaesthetics work?

A

Bind to Na+ channels

Stop sensory conduction

80
Q

What does the toxicity of local anaesthetics mainly involve?

A

CNS

Cardiovascular system

81
Q

What are the CNS toxicity of local anaesthetics?

A
Feeling of inebriation 
Lightheadedness
Drowsiness 
Numbness of tongue and perioral region 
Restlessness 
Paraesthesia 
Dizziness 
Blurred vision 
Tinnitus 
Headache 
Nausea 
Vomiting 
Muscle twitching 
Tremors 
Convulsion
82
Q

What are the cardiovascular system toxicities of local anaesthetics?

A

Myocardial depression

Peripheral vasodilation - hypotension and bradycardia

83
Q

What does adrenaline do to blood vessels?

A

Vasoconstrictor

84
Q

How does vasoconstriction desirable in local anaesthetic administration?

A

Diminishes local blood flow

Slows rate of absorption - prolonging anaesthetic effect

85
Q

Inhibition of which fibres cause a loss of cold sensation?

A

C fibres

86
Q

Inhibition of which fibres cause a loss of pinprick sensation?

A

A delta fibres

87
Q

Inhibition of which fibres cause a loss of touch sensation?

A

A beta fibres

88
Q

What is the action of Botulinum?

A

Blocks ACh release

89
Q

What is the action of Atracurium?

A

Non-depolarising

90
Q

What is the action of Suxamethonium?

A

Depolarising

91
Q

How do depolarising agents work and do they cause fasciculations?

A

Competitive agonists of ACh at postsynaptic nicotinic receptor (causing depolarisation)
Fasciculations

92
Q

How do non-depolarising agents work and do they cause fasciculations?

A

Competitive antagonists of ACh at postsynaptic nicotinic receptor (preventing depolarisation)
No fasciculations

93
Q

What is damaged in neurapraxia (seddon)/ I (sunderland)?

A

Myelin sheath

94
Q

What is damaged in axonotmesis (seddon)/ II, III and IV (sunderland)?

A

II Axons
III Axons and endoneurium
IV Axons, endoneurium and perineurium

95
Q

What is damaged in neurotmesis (seddon)/ V (sunderland)?

A

Complete severance of nerve

96
Q

Out of neurapraxia, axonotmesis, neurotmesis, which results in no conduction?

A

Axonotmesis, neurotmesis

neurapraxia is just slowed conduction

97
Q

What does sunderland class VI nerve injury describe?

A

Mixed - injury varies fascicle to fascicle

98
Q

What nerve is affected in carpal tunnel syndrome and which muscles does is supply?

A
Median nerve 
LOAF (OAF - thenar eminence)
Lumbricals 1 and 2 
Opponens pollicis 
Abductor pollicis brevis
Flexor pollicis brevis
99
Q

Which nerve injuries have a tinel’s sign and advancing tinel’s sign/ recover?

A

Tinel’s sign - axonotmesis II, III, IV, neurotmesis V

Advancing tinel’s/ recover - axonotmesis II, III

100
Q

Which nerve injuries require treatment?

A

Axonotmesis III - internal neurolysis
Axonotmesis IV - repair/ graft
Neurotmesis V - repair/ graft

101
Q
Group the following words describing bone in terms of meaning:
Cortical 
Spongy 
Trabecular 
Compact 
Cancellous
A

Trabecular/ Spongy/ Cancellous - 20% of total skeleton

Cortical/ Compact - outer, dense, strength-providing for weight bearing, 80% of total skeleton

102
Q

What is bone made up of?

A

Water
Hydroxyapatite (mineral form of calcium apatite)
Collagen type I
Non-collagenous proteins

103
Q

Why does cartilage heal slower than bone?

A

Cartilage doesn’t have blood vessels

104
Q

What type of collagen does hyaline cartilage contain?

A

Type II collagen

105
Q

What type of cartilage is articular cartilage?

A

Hyaline

106
Q

What are the differences between the layers of hyaline/ articular cartilage?

A

Superficial zone - tangentially orientated collagen fibrils, flattened discoid shaped chondrocytes
Middle zone - highest proteoglycan content
Deep zone - radially orientated collagen fibrils
Calcified zone

107
Q

What happens to the density of chondrocytes moving from superficial to deep zones of hyaline/ articular cartilage?

A

Decreases

108
Q

What is the normal plasma calcium level?

A

2.2-2.6 mmol/L
Less than 2.2 = hypocalcaemia
Greater than 2.6 = hypercalcaemia

109
Q

What are the possible consequences of hypercalcaemia?

A

Voltage gated ion channels don’t open as easily
Depressed nervous system function
Deposition of excess calcium and phosphate
Kidney stones
Respiratory arrest

110
Q

Calcium metabolism and exchange between ECF and intestine/ bone/ kidney are under the hormonal influence of?

A

Vitamin D

PTH

111
Q

How are calcium levels increased if they become too low?

A

Calcitriol (active form of vitamin D) promotes absorption of calcium from GI tract
PTH increases osteoclast no and activity, decreases calcium loss in urine, stimulates formation of calcitriol - increasing Ca2+ in blood

112
Q

How are calcium levels decreased if they become too high?

A

Parafollicular cells in thyroid gland secrete calcitonin

Calcitonin inhibits osteoclast activity, promotes bone formation decreasing blood Ca2+

113
Q

Is D3 active?

A

No - inactive

114
Q

How is D3 activated?

A

25-hydroxylation in liver

Additional hydroxylation in kidney under regulation of calcium, phosphorus and PTH

115
Q

What is the role of 1,25-dyhydrocyvitamin D?

A

Stimulates intestinal calcium and phosphate resorption - raising serum calcium and phosphate levels
Decreases PTH levels

116
Q

What is the role of PTH?

A

Stimulates bone turnover
Renal phosphate excretion - decreasing serum phosphate levels
Renal calcium absorption - raising serum calcium levels
Raise 1,25-dyhydrocyvitamin D levels

117
Q

What condition is the mnemonic moans, groans, stones and bones used for?

A

Hypercalcaemia e.g. from hyperparathyroidism

Psychiatric moans, abdominal groans, stones, painful bones

118
Q

What does primary hyperparathyroidism result in?

A

PTH hypersecretion leading to hypercalcaemia (moans, groans, stones and bones)

119
Q

What are the possible consequences of hypocalcaemia?

A

Voltage gated ion channels open spontaneously
Tetany
Paraesthesia around mouth/ feet
Cardiac arrest

120
Q

What’s in the centre of an osteon?

A

Haversian canal

121
Q

What surrounds the haversian canal in an osteon?

A

Osteocytes

122
Q

Briefly explain the bone remodelling cycle

A
Resorption by osteoclasts 
Osteoclasts apoptosed/ removed 
Reversal by osteoblasts 
Formation 
Mineralization
123
Q

What are the 3 stages of bone fracture healing?

A

Inflammation
Repair
Remodelling

124
Q

What happens in the inflammation stage of fracture healing?

A

Blood vessel crossing fracture line broken - haematoma formation
Infiltration of inflammatory mediators (interleukins, growth factors, hormones)
Proliferation and differentiation of stem cells stimulated
Minutes to days

125
Q

What happens in the repair stage of fracture healing?

A

Periosteal fibrocartilaginous callus formation - fibroblasts produce collagen and chondroblasts to make fibrocartilage which ossifies
Bony callus formation - osteoblasts produce spongy bone trabeculae
Lasts weeks

126
Q

What happens in the remodelling stage of fracture healing?

A

Dead portions resorbed by osteoclasts
Compact bone replaces spongy around periphery of fracture
Lasts months

127
Q

How does smoking inhibit bone healing?

A

Vasoconstriction - poor blood supply

Directly inhibits osteoblasts

128
Q

What is osteoporosis?

A

Low bone mass - less osteoblast activity than osteoclast
More so in trabecular rich sites e.g. skin and hip as remodelling rates higher in trabecular bone than cortical
Loss of connectivity between adjacent bone plates
Fragility and increased fracture risk

129
Q

What effect do oestrogens and testosterone have on bone?

A

Stimulate osteoblast activity

130
Q

What are the risk factors for osteoporosis?

A
Increases with age
Women 
Family history 
Smoking, alcohol, diet low in calcium and vit D
Low MBI
Physical inactivity 
European/ Asian 
Prednisolone (steroid) use 
Reduced oestrogen in women (post menopause/ hysterectomy/ late menarche/ early menopause)
131
Q

Does T or Z score relate more to fracture risk?

A

T score - SDs away from mean, relative to young normals

Z relative to normal people of SAME age

132
Q

Although there is no true fracture threshold, what would be classed as osteoporosis?

A

2.5 SDs from young normal mean or lower

133
Q

For every drop in SD from young normal, what happens to the fracture risk?

A

Fracture risk doubles for every SD reduction

134
Q

What’s the 1st line treatment for osteoporosis?

A
Ca2+ and colecalciferol (vit D3) 
and Bisphosphonate (alendronate/ risendronate/ ibandronate) - antireabsorptive drugs (inhibit osteoclast function, induce osteoclast apoptosis)
135
Q

What is the adult form of rickets?

A

Osteomalacia

136
Q

What causes osteomalacia/ rickets?

A

Inadequate calcification of extracellular bone matrix
Usually caused by vitamin D deficiency
Insufficient calcium and phosphate so new osteoid

137
Q

Where does the spinal cord end?

A

Adult: L1/2
Child: L3/4

138
Q

What are the symptoms of MS?

A
MS is an Upper Motor Neuron lesion
UMN lesions typically present with 
-diffuse wasting
-no wasting
-increased reflexes
-increased tone
-no fasiculations
-babinski maybe present (absent in LMNL's)
139
Q

What are the erector spinae muscles?

A

Iliocostalis
Longissimus
Spinalis

140
Q

In sociology what are the 4 different coloured flags and what do they stand for?

A

Red - biomedical factors
Yellow - psychological/ behavioural factors
Blue - social/ economic factors
Black - occupational factors

141
Q

What is Spondylolysis?

A

Congenital or acquired deficiency of the pars interarticularis of the neural arch of a particular vertebral body, usually affects L4/ L5

142
Q

What is Spondylolisthesis?

A

Slippage of one vertebra on another

143
Q

What is spondylosis?

A

Degenerative disc degeneration or facet joint degeneration

144
Q

Which osteoporosis treatment is described as dual action and why?

A

Strontium ranelate - increases deposition of new bone by osteoblasts and reduces the resorption of bone by inhibiting osteoclasts

145
Q

What does the trauma triad of death include?

A

Hypothermia, acidosis and coagulopathy

146
Q

How is osteomalacia/ rickets treated?

A

Vitamin D

Exposure to moderate sunlight

147
Q

How is the amount of bone and ration of matrix to bone mineral altered in osteoporosis and osteomalacia?

A

Osteoporosis - decreased amount, ratio the same

Osteomalacia - normal amount, ratio of matrix to bone mineral increased (more matrix, less mineral)

148
Q

What effect does calcitriol have on calcium, phosphate and PTH levels?

A

Increases Ca2+
Increases phosphate
Decreases PTH

149
Q

What effect does PTH have on calcium, phosphate and calcitriol levels?

A

Increases Ca2+
Decreases phosphate
Increases calcitriol

150
Q

What is the urinary marker of bone turnover?

A

Hydroxyproline

151
Q

What would the blood profile of someone with Paget’s disease be like?

A

High ALP

Normal Ca2+, phosphate, vit D and PTH

152
Q

How may Paget’s disease be diagnosed?

A

X ray
Blood test: high ALP (normal Ca2+, phosphate, vit D and PTH)
Increased urinary Hydroxyproline (urinary marker of bone turnover)
Increased uptake of isotope bone scan

153
Q

What happens in Paget’s disease?

A

Osteoclast overactivity
Compensatory osteoblast activity
Disordered, woven, mosaic bone
Weaker as higher proportion of spongy to compact bone

154
Q

What are the symptoms of Paget’s disease?

A
70-90% asymptomatic 
Deep, constant, boring, worse on weight-bearing bone pain 
Fracture 
High CO 
Possible compression
155
Q

Which people with Paget’s disease need to be treated and with what?

A

Symptomatic
In danger of nerve compression
Around weight-bearing joint

Bisphosphonates

156
Q

What are the 2 different forms of bone mets?

A

Lytic: destructive
Sclerotic: increased abnormal bone formation

157
Q

How may someone with bone mets present?

A

Pain
Fracture
Spinal cord compression
Elevated ALP and calcium

158
Q

How is bone mets treated?

A

Bisphosphonates and radiotherapy for pain
Surgical
Chemo/ hormone therapy

159
Q

What are the blood levels of Ca2+, phosphate, ALP and PTH in osteomalacia?

A

Ca2+: LOW
Phosphate: LOW
ALP: high/ normal
PTH: high/ normal

160
Q

What are the blood levels of Ca2+, phosphate, ALP and PTH in osteoporosis?

A

All normal

161
Q

What are the blood levels of Ca2+, phosphate, ALP and PTH in primary hyperparathyroidism?

A

Ca2+: high/ normal
Phosphate: low (PTH decreases it)/ normal
ALP: high/ normal
PTH: HIGH

162
Q

What are the blood levels of Ca2+, phosphate, ALP and PTH in bone mets?

A

Ca2+: high
Phosphate: high
ALP: high
PTH: low

163
Q

What does the posterior root carry?

A

Sensory afferents

164
Q

What does the anterior root carry?

A

Motor efferents

165
Q

What does the posterior and anterior rami supply?

A

Posterior: synovial joints of vertebral column, deep back muscles and overlying skin
Anterior: much larger remaining area

166
Q

Which 3 muscle groups make up the transversospinales?

A

Semispinalis
Multifidus
Rotatores

167
Q

What are the intervertebral discs made of?

A

Fibrous anulus fibrosus around periphery

Gelatinous nucleus pulposus in centre

168
Q

How can pain from a degenerative disc be differentiated from facet joint pain?

A

Degenerative disc - bending forward worsens pain

Facet joint - bending forward relieves pain, bending backward worsens pain

169
Q

What does the Babinski reflex test for?

A

Abnormal big toe extension - upper motor neurone lesion

170
Q

What proves a complete spinal cord injury?

A

Absence of sacral sparing

  • No voluntary anal contraction or deep anal pressure sensation
  • All S4-5 sensory scores = 0
171
Q

What is the ASIA impairment scale?

A
A = complete
B = sensory incomplete (sensory function preserved)
C = motor incomplete (motor function preserved, half or more key muscle function grade less than 3)
D = motor incomplete (motor function preserved, half or more key muscle function grade 3 or more) 
E = normal
172
Q

What does the denticulate ligaments attach to?

A

Attach pia mater to arachnoid and dura

173
Q

What structure coming off the spinal cord does the sympathetic chain attach to?

A

Ventral/ anterior ramus

174
Q

What does the pia continue as below the conus medullaris?

A

Filum terminale - descends all the way to the coccyx, anchoring the spinal cord