Case 14 Flashcards
What shape are babies spine at birth and what is this caused by ?
Straight or C shaped from depression in the uterus
What are the 3 major functions of the spine ?
Movement, support and protection of the spinal cord
How does bone growth occur during embryological development ?
Centrum and 2 halves of the arch form from mesoderm in utero by week 14.
How and when does horizontal and vertebral growth of the vertebrae occur ?
Horizontal - periosteal ossification first 7 years
Vertical - sup/inf growth plates first 5 years
Name the atypical vertebrae ?
C1 (atlas) which rotates around C2 (axis) , C7 (vertebra prominens)
What is the difference between sublaxation and dislocation ?
Partial discontinuity of joint surface = sub
Full discontinuity = dislocation
What is the path of the vertebral artery and vein ?
Go through the foramen transversum until C7 when it’s just the artery.
What muscle allows tension of the neck, causing it to protrude ?
Platysma muscle
What vein overlies the sternocleidomastoid ?
Jugular vein
What structures make up the middle and deep layers of the anterior neck ?
Middle - pre tracheal and carotid sheath
Deep - pre vertebral
What nerves control the voice box ?
Sup laryngeal controls pitch. Recurrent laryngeal controls the rest.
What is the muscle that opens the vocal chords and what is its innervation ?
Posterior cricoarytenoid muscles
Innervated by the recurrent laryngeal nerve
Which nerves have the potential to loop in their path?
Median, ulnar, vagus and recurrent laryngeal.
What is necessary for venous cannulation and where would it be placed ?
internal jugular and subclavian need to be known.
Either between 2 heads of SCM or underneath clavicle (medial 2/3 lateral 1/3) under US guidance
What syndrome arises from damage to the sympathetic trunk and what is its triad of sx ?
Horner’s syndrome
Myosis (small pupil) , anhydrosis (abnormal sweating, usually seen one half of face) , ptosis
At what spinal level do the common carotid arteries bifurcate ?
C4.
How would you distinguish between thoracic and cervical vertebrae ?
Thoracic are larger with larger spinous processes. Flatter vertebral bodies on left side (aorta).
Nerves correspond to vertebrae unlike cervical.
How do the different vertebrae articulate with the ribs ?
1, 11, 12 articulate solely with named vertebra.
2-10 with rostral neighbour, articulate with anterior transverse process.
What is the difference between removing 1 and 5 ribs ?
One has little effect on structure and stability
5 leads to disruption of ring so segments of rib suck in during inhalation -> lung can’t inflate.
Name the erector spinae muscles and identify which compartment they are in ?
Superficial
Iliocostalis , Longissimus, spinalis
What compartment are the elevator rostrum and multifidus muscles found ?
Intermediate
What muscles are supplied by the posterior primary rami?
All muscles of the back apart form in the superficial compartment.
What is the multifidus ?
Intermediate stabilising muscle the originates form spinous process and inserts on mamillary process 1 level below.
What structures make up the body of the vertebral disc ?
Nucleus polposus, hydrated centre with glycosaminoglycans
Annulus fibrosus, fibrocartiliganous structure with different mesh layers.
What adjustments can the doctor/GP impose on a fit note regarding return to work ?
Altered hours, altered activities (eg. less manual labour) , regular breaks (to sit/lie down)
When is a fit note required ?
After 7 days off work, prior to this the px can self refer.
How long does SSP last ?
Statutory sick pay lasts up to 28 weeks if deemed unable to work.
What is health related worklessness ?
People out of work for long term basis (4+ weeks) due to chronic illness or disability.
What is the difference between somatic and parasympathetic NS?
Somatic; voluntary motor functioning
Autonomic; involuntary motor, sympathetic, parasympathetic function
Where do the CNs arise ?
1-2 = Cerebral hemisphere 3-4 = midbrain 5-8 = Pons 8-12 = medulla
What is the significance of the nodes of Ranvier ?
Allow for saltatory conduction, large conc of voltage gated Na channels. ^ R to flow elsewhere
What is the significance of an ‘all or nothing’ response during AP production ?
AP always the same size but vary in frequency
What is the difference between +/- ions during AP propagation?
+ve cause partial depolarisation (excitatory) so exceeding the threshold is easier
-ve cause hyperpolarisation (inhibitory) so exceeding is more difficult
Name two types of summation?
Temporal; lots of APs in short succession build up to depolarisation
Spatial; 1+ at same time so together cause AP
What are the functions of LA?
Neuromuscular blockade, good analgesic so decreases pain post op. Stops sensory conduction.
What are the possible downsides of LA ? (4)
Toxicity (max dose of LA) causes cardioresp depression, allergic reactions (rare) , vasoconstriction so may miss structures -> possible ischemia (fingers/toes). given IV to reduce risk of cardiac arrhythmias
What is often given alongside LA ?
Adrenaline eg. Xylocaine (v weak) , px fells anxious/panic.
What is the proper name for Botox and what is it’s function?
Botulinum, blocks ACh release. spasticity and hypertonic muscles. lasts about 3 months (hence repeat injections)
What the more common of the non depolarising agents used as a neuromuscular blockade ?
Atracurium, blocks synaptic transmitter (post) without depolarising/activating them.
What drug may be used as an LA that leads to px twitchy/fits as they’re sedated ?
Suxamethonium. Binds to receptor and activates it but has ^ affinity and ^ half life so not broken down by ACh esterase.
What is the clinical difference between non depolarising and depolarising agents ?
Non depolarising; competitive antagonist, block action of ACh, not broken down no fasciculation’s
Depolarising; single type use, competitive agonist, act in addition to Each, broken down slowly, fasciculations
What condition is shown when the px hears everything during a surgery ?
Anaesthetic awareness, px paralysed and ‘goes to sleep’ no wise but still aware.
How can an axon be damaged? (5)
Pressure (compression) , laceration, traction , chemical, thermal
What is the Seddon classification of nerve injury?
Normal
Neurapraxia (myelin damage)
Axonotmesis (axon damage within the fibre)
Neurotmesis (whole nerve transection)
How would axonotmesis with a lost endoneurium but intact perineum scale on the Sunderland classification ?
grade 3 , loss of axonal continuity no conduction
What is the Sunderland classification ?
I = neurapraxia, myelin damage II = loss of axonal conductivity no conduction, with; III (endo lost) and IV (endo+peri lost) V = nerve trunk divided no conduction (neurotmesis) VI = mixed, injury varies fascicle to fascicle
What response is triggered when a fibre is cut ?
Fibre death 4-6 days post injury. Distal to injury macrophages recruited to clear remnants of the nerve fibre including myelin.
How does regeneration of fibre occur ?
Regrows proximal -> distal through attraction of nerve fibres (neurotropism) from proximal end. Fibres travel down specific tunnel
What happens to motor end plates after damage ?
12-24 months the muscle fibres atrophy. Some function restorable but can disappear even when supply returns.
List the anatomical landmarks of the femur from knee to ankle joint …
Physical scar (corresponds to physis) Metaphysis (proximal) Diaphysis Metaphysis (distal) Physeal scar
Describe the features of corticol bone
Outer bone ^ density so ^ resistance. Present in longer bones, cells organised into Haversian systems which surround Haversian canal (blood/nerve supply in the centre)
What is the other type of bone (apart from corticol) and give some features …
Trabecular bone, inner spongy ^ metabolic activity. Present in vertebral bodies in spine, wrist, foot
What are the components of bone on cellular level ?
Collagen arranged in fibrils for mineral deposition between layers.
Ca/PO4 forms round outside to give strength (hydroxyapatite)
What is the non collagenous protein that helps form bone ?
Glycosaminoglycans
What is the name of articular cartilage and where is it present ?
Hyaline, joint surface 2-4 mm thick. Thickest in ankle, thinnest around hand.
What is the composition of hyaline cartilage ?
H20, collagen (type 2), proteoglycans and sparsely distributed chondrocytes.
What is the rate of healing for hyaline cartilage and why ?
Very slow if at all due to a lack of BV supply.
What substances form the hydrophilic structure to attract H2O into the gaps in cartilage ? What effect does this have ?
Conjointin and keratin
walking/weight through cartilage squeezes H2O out into space, picks up nutritional elements and brings them back on return
What are the 5 main functions of bone ?
Structural support, protection, locomotion, metabolic, haematopoesis (in bone marrow)
What is the normal range of free Ca ?
2.2-2.6 mmol/L
What do the abnormal levels of Ca lead to?
Hypocalcaemia, channels open spontaneously -> nerve/muscle cells hyperactive -> tetany (muscle spasm)
Hyper, channels shut -> NS function down and deposition of Ca, PO4 (kidney stones)
When testing Ca levels what other substance would you test for ?
Albumin to check you’re not deficient. If you were this would show less free Ca.
Has is dietary Ca distributed throughout the body ?
200mg enters CSF (absorption in duo and upper jejunum). Kidney excretes Ca in urine. Majority out through faeces
What does an hour of sunlight produce and what is it then converted to ?
Produces 7-dehydrocholesterol which is converted to Vit D
How is inactive Vit D activated ?
Converted in the liver to 25-0H-Cholecalciferol then goes to kidney -> 1,25-di-OH-cholecalciferol
What are the two major functions of activated vit D ?
Stimulates absorption of Ca in the intestines
Stimulates osteoclast function in bone
What is the homeostatic mechanism induced when Ca levels drop?
Recognised by the parathyroid which secretes PTH.
Stimulates hydroxylation ^ Ca reabsorption in the kidney and ^ PO4 urine excretion (this frees up more Ca)
Stimulates osteoclast function in bone
When are where is Calcitonin released and what is its function ?
Secreted when Ca ^ from C cells in the thyroid. Inhibits osteoclasts so Ca down.
What is primary hyperparathyroidism ?
Enlargement in 1+ parathyroid glands. PTH hyper secretion -> Ca ^ -> adenoma (benign)
What are the sx of primary hyperparathyroidism ?
Bones, Stones (renal/kidney) , groans (abdo pain) , moans (psych disturbance/depression)
Px recently had surgery, presents with tetany and paraesthesia around mouth/feet. What’s wrong ?
Hypoparathyroidism, injury to parathyroid glands usually from surgery. Ca down with assoc problems; muscle spasm, tetany (hypocalcaemic).
What are osteocytes and how are they formed ?
Cytoplasmic processes that extend through matrix in canaliculi. They are from osteoblasts that remained in newly formed osteoid.
How are strains/microfractures detected in bone ?
Canaliculi break so dendritic process is disturbed. Osteocytes transmit info to induce remodelling and repear.
What immediate response immediately post fracture helps give structural stability for new bone ?
Inflammation last several days. Bleeding -> inflammation and clotting at site.
How is a new haemotoma formed ?
^ Capillary permeability allows ^ local inflammatory mediators -> differentiation/proliferation of stem cells -> new bone formation and repair
What are the inflammatory mediators that are attracted to damaged site in bone healing?
IL, IGF, hormones
When does bone production start ?
Clotted blood from inflammation replaced with fibrous tissue and cartilage (soft callus)
What is the function of soft callus and what process does it undergo ?
Bridges gap from break periosteally and intramedullary. Undergoes ossification -> hard callus , takes weeks.
What fx promote healing of bone ?
Good blood supply, mechanical stability, once adequate weight bearing ^ remodelling
What fx inhibit healing of bone ? (4)
malnutrition (callus drops) , smoking (inhibits osteoblasts, nicotine -> vasoconstriction so blood supply down) , diabetes (collagen content down, defective cross linking) , infection
What is primary bone healing ?
analogous -> bone remodelling in non fractured bone. no callus, bones put together with micro screws. Short length reduction. difficult to monitor.
What is osteoporosis ?
Decreased bone mass and micro architectural deterioration of bone tissue -> ^ bone fragility and ^ fracture risk.
What are the risk fx for OP? (7)
Age, gender, gentics, lifestyle, low BMI, physical inactivity, Oestrogen down post menapausal.
What are the causes of OP ?
imbalance in remodelling bone resorption > bone production. Trabecular bone down so loss connectivity between adjacent bone plates -> ^ fracture risk.
How would you diagnose OP and in which site ?
BMD using DEXA scan (dual energy X-ray absorptiometry usually on hip bone.
What is the difference between a Z and T score for bone mineral density ?
Z is matched for age, gender and ethnicity
T score = healthy 30 y/o (gender and ethnicity matched)
When are the T and Z scores used for bone mineral density , what are the parameters ?
Z used for non post menopausal women
T, everyone else. Need to be >2.5 SDs below T
What is osteopenia and how is it indicated on bone mineral density charts ?
Area between bold (normal) and dotted (OP) line. indicates ‘pre’ OP
What is the first line drug tx for OP? give 3 examples and the MOA ?
Bisphosphonates; Alendronate, Ibandronate, Risedronate. Decrease bone breakdown to inhibit osteoclast function and induce apoptosis of osteoclasts.
What drug tx for OP is used less than bisphosphonates and why ?
PTH analogues (eg. Teriparatide). Varying effects and expensive.
What is the MOA of Teriparatide ?
^ bone formation through ^ osteoblast activity
What is osteomalacia and what are the key features ?
Vit D deficiency leads to Low Ca poor mineralisation. Decrease Ca/PO4 so new osteoid can’t be mineralised. Bones go softer and ^ pliable so more prone to deformation/fracture.
What are the causes of Vit D def? (6)
lack of sunlight, poor diet (lactose, vegan) , malabsorption (SB resection, CF) , medication (rifampicin phenytoin) , poor levels in breast milk , abnormal metabolism (liver/renal disease).
What are the tx for Vit D deficiency ?
oral D2/3 (requires renal function) eg. Fultium D3, Caloichew D3 forte , 600-2000 IV vit D daily maintenance.
Oral 1-alfacalcidol (longer half life, less demand on kidney)
What disease is characterised by disorder bone metabolism; osteoclast overactivity followed by compensatory osteoblast activity
Paget’s disease. Disorded woven mosaic bone that’s weaker than normal
What are the direct sx of Paget’s disease ?
Bone pain (deep, constant boring, worse on weight) , patho feature, sarcomatous change
What fx of Paget’s are described as indirect?
^ CO, compression affects (depends on site)
What are the tx for Paget’s disease ? When would you tx ?
only when symptomatic, in danger of nerve compression, around a weight bearing joint.
Risedronate; 30mg/day for 2 months
Zoledronate; 5mg x 1 infusion
What are the cancers which may metastasise to the bone ?
Breast, kidney, Thyroid, Prostate, Lung
How do you class metastasis ?
Lytic (destructive) , sclerotic (^abnormal bone formation) or mixture of both
What chemical changes are seen with Osteomalacia ?
decreased Ca and PO4 (decreased Vit D, bones more likely to break)
Normal or high, Alk Phos and PTH (unaffected, may ^ to try and ^ Ca)
Can osteoporosis be diagnosed using biochemical tests ?
No , all the tests should be in the normal range
What biochem marker would ^ in Paget’s disease ?
Alkaline phosphatase
What condition is indicated by; ^ Ca, normal PO4 and Alk Phos, ^ PTH ?
Primary hyperthyroidism
What biochem changes are seen in renal osteodystrophy ?
Low/normal Ca
increased ; PO4, Alk Phos, PTH
What is the cause of secondary hyperparathyroidism ?
Chronic decrease Ca from renal dysfunction.
Goals of spinal trauma ? (5)
Protection, detection, optimise conditions for neural recovery, maintain/restore spinal alignment (decrease loss of spinal motility), rehabilitation.
How many people should you have for transfers during spinal cord injury ?
6 but minimum 4 for log rolls
How do you mobilise the spine ?
Triple immobilisation
Born keeps spine straight for lifting
Blocks stop head movement side to side
Neck brace fixes the position and allows for access to airway.
What is the downside of being on the board for too long ?
Pressure sores
What conditions do you have to be aware of when using a bord ?
Ankylosing spondylitis, straightening the spine causes more damage
How would you assess an SCI in an unconscious px ?
Flaccid areflexia, diaphragmatic breathing, pain response above clavicle, bradycardia/hypotension, priapism
What is shock ?
State of inadequate organ perfusion and tissue oxygenation
What are the types of shock ? (8)
Hypovolemic, haemorrhage or fluid loss, tension pneumothorax, cardiac tamponade, cardiogenic (less blood) , neurogenic, septic (BP down) , anaphylactic
What are the characteristics of spinal shock?
flaccid paralysis, lack of sensation 2ndry to physiological spinal cord ‘shut down’
How does spinal shock normally resolve ?
Usually within 24 hours when reflex arcs caudal (post/tail of body) to injury return.
What is the characteristic feature of neuro shock and what are the other presentations ?
Bradycardia from decreased cardiac stimulation. Decreased sympathetic outflow (T1-L2) with resultant unopposed vagal tone. Hypotension from loss of BV tone with venous pooling.
What is clinical instability of the spine ?
Loss of ability of spine under physiological loads to maintain displacement pattern so there’s no neuro deficit, deformity or incapacitating pain
When is an erect X ray used ?
normally done in collar. after a CT showing ‘stable injury’ checks for development of load bearing deformity and ligament injury.
When is a dynamic X ray used ?
done 2 weeks post injury check for stability or after tx in collar to check for instability. Flexion and extension x rays taken.
What is SCIWORA ?
Without radiographic abnormality; no fragment, no ligament injury, no extra neural compression.
Oedema, concussion, haemorrhage, infarct, transection
What are the consequences of untreated SCI?
Paralysis, inadequate ventilation, abdo evaluation compromised, occult compartment syndrome
How would you manage hypotension clinically ?
Assume haemorrhage shock until proven otherwise, consider neurological problems, monitor urine output
What is autonomic dysreflexia ?
distention of bladder causes ^ impulse to spinal cord -> ^BP, seizures, inter cranial bleeds/stroke
How is autonomic dysreflexia triggered and what are the sx ?
Sustained stimuli at T6 or below triggers occurrence at T6 and above.
^BP, red face, HR down, sweating, vasodilation above injury and vasoconstriction below; pale cool no sweat
What is the chemical cause of autonomic dysreflexia ?
Chemical cause BV constriction -> ^BP (baroreceptor detection). Brain; parasympathetic (vagus nerve) to slow HR, sends down spinal cord to open BV but cord injury stops messages so not enough to overcome constricted vessels to BP ^
What is the tx plan for px with autonomic dysreflexia ?
Monitor BP frequently (systolic 90-110) , sit px up and lower legs, check catheter.
What are you checking for in the catheter with autonomic dysreflexia ?
kinks, folds, obstructions, placement. If blocked irrigate bladder with 10-15 ml. if fails remove and replace.