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CASE 14

Topic: CHIPS Pre Clinical Revision: Case 14 Trauma & Orthopaedics

Time: Mar 9, 2023 07:00 PM London

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https://cardiff.zoom.us/j/83392140493?pwd=UFZxTlQrc1pkdmNaMUVwS3pPY2svQT09

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Case 14 Tom Griffiths The spine • Made from vertebra and discs • Natural curvatures – cervical and lumbar lordosis, thoracic and sacral kyphosis • Each curvature provide shock absorption • Each spine section has unique vertebrae C1: Atlas C2: axis • Odontoid process extends • Connects to occiput of the skull superiorly into C1 facet • Lateral masses articulate with • Atlanto-axial joint allows occipital condyles head to turn independently • Has a facet for odontoid process of C2 of the torso • Secured by transverse ligament of • Superior articular facets articulate to inferior facets atlas of atlas Cervical vertebrae • Bilateral foramina – vertebral arteries and veins • Bifid spinous processes Thoracic vertebrae • Demi and costal facets articulate with ribs • Long and inferiorly protruding spinous processes to provide more protection • Only T2-T9 have demi facets, T1,10,11 and 12 are atypical vertebrae Lumbar vertebrae • The basic vertebrae with all the normal characteristics • Transverse processes – extend laterally and posteriorly • Pedicles – connect the body to the transverse process • Lamina – connect the transverse and spinous processes • Spinous process – positioned in the center to protect the cord • Articular processes – form joints between vertebraeWhich vertebrae have been fused in the following patient? A.C3-C4 B.C4-C5 C.C5-C6 D.C6-C7 E.T1-T2Which vertebrae have been fused in the following patient? A.C3-C4 B.C4-C5 C.C5-C6 D.C6-C7 E.T1-T2At what level is the fracture present? A.L1 B.L2 C.L3 D.L4 E.L5At what level is the fracture present? What type of fracture is this? A.L1 B.L2 C.L3 D.L4 E.L5Nerve physiology Neurons – Endoneurium Perineurium – Fascicles Epineurium - Nerves Epineurium Endoneurium Perineurium This is made from Several neurons are Covers each neuron grouped together to collagen and protects and surrounds the form a fascicle. The the nerves from myelin sheath fascicle is covered in longitudinal stress. perineurium Made of several fasciclesWhat is the name of the layer that covers fascicles? A.Endoneurium B.Perineurium C.Epineurium D.MyelinWhat is the name of the layer that covers fascicles? A.Endoneurium B.Perineurium C.Epineurium D.MyelinResting potential  Outside - positively charged, Positive +  Inside of the cell - negatively charged  Potential maintained by ATP  The membrane is more permeable to potassium  Negatively charged at rest as it loses more positive ions than it gains negatively charged ones  At rest, the potential is -70mv Negative -Action potential •All or nothing principle •-55mv: the threshold for an action potential to occur •Same action potential no matter whatWhat is the threshold potential required for an actional potential to be propagated? A. +30mv B. -30mv C. -55mv D. +70mv E. +10mvWhat is the threshold potential required for an actional potential to be propagated? A. +30mv B. -30mv C. -55mv D. +70mv E. +10mv Action potential 4 stages 1. Stimulus triggers sodium influx into cell to exceed voltage threshold and cause depolarisation 2. Membrane potential raises to 40 mv, the sodium channels are closed and won’t re-open. They are in the refractory period 3. Potassium gates open, potassium ions actively leave the cell and restore resting potential 4. Hyperpolarisation occurs and is restored by the sodium-potassium co-transporter Pre-synaptic membrane Post-synaptic membrane1. An action potential arrives at the pre-synaptic cleft 2. Voltage-gated calcium channels release calcium into the synaptic terminal 3. Calcium triggers neurotransmitter to bind with postsynaptic membrane 4. Neurotransmitter released into the synaptic cleft 5. Neurotransmitter binds to receptors on the post-synaptic membrane 6. They either cause sodium channels to open or close depending on their effect 7. Enzymes breakdown the neurotransmitter Neurotransmitters Excitatoryneurotransmitters Inhibitoryneurotransmitters ● Excitatory effect ● Inhibitory effect ● Makes the next nerve more ● Causes hyperpolarisation excitable ● Makes exceeding the ● Makes exceeding the requirement threshold more action potential threshold difficult easier to achieve ● Examples: GABA, glycine, ● Examples: Acetylcholine, serotonin glutamate, histamineNeuromuscular blockades Atracarium Suxamethonium • Non-depolarising agent • Depolarising agent • Block the action of Ach • Mimics Ach • Prevents AP at the • Causes a prolonged neuromuscular junction depolarisation • Works in 2 minutes, lasts for 30 • Causes fasciculations then minutes flaccid paralysis • Reversed using acetylcholinesterase inhibitorsNerve injuryCheat Sheet – Seddon classification of nerve injuryPrognosis Advancing Tinel’s test By gently tapping distal to the area of damage, its possible to approximate the progression of nerve regeneration post- injuryA 23-year-old man suffers a crush injury to the arm having been in an accident. The nerve in question has a loss axonal continuity and all the layers are damaged except for the epineurium. What type of injury has occurred? • Seddon type I • Seddon type II • Seddon type III • Seddon type IV • Seddon type VA 23-year-old man suffers a crush injury to the arm having been in an accident. The nerve in question has a loss axonal continuity and all the layers are damaged except for the epineurium. What type of injury has occurred? • Seddon type I • Seddon type II • Seddon type III Seddon type 4 injuries • Seddon type IV are the most severe • Seddon type V type of axonotmesis and usually require surgical interventionWallerian degeneration •Degeneration occurs distal to injury •Axon and myelin breakdown to ellipsoids •Macrophages are recruited to clear debris •Axons align as tunnels to facilitate new growth •The axon regeneratesLocal anaesthetic  Block sodium channels  Bupivacaine and Lidocaine  Lidocaine acts faster for a shorter period  Bupivacaine gets to work slower but lasts longer  Sharp pain – cold- warmth – touch – motor fiber conduction  Maximum doses:  Lidocaine alone – 3mg/kg  Lidocaine with adrenaline – 7mg/kg  Bupivacaine alone – 2mg/kg  Bupivacaine with adrenaline – 2.5mg/kgWhich part of the action potential does lidocaine affect? A. Repolarisation B. Depolarisation C. Resting potential D. Refractory period E. HyperpolarisationWhich part of the action potential does lidocaine affect? A. Repolarisation B. Depolarisation C. Resting potential D. Refractory period E. HyperpolarisationBones • Bone is two thirds mineral and one third organic • Mineral: Hydroxyapatite • Organic: Primarily type one collagen and bone cells Osteoblasts Osteocytes Build new bone tissue by Osteoclasts Point of communication depositing calcium and Responsible for breaking down old bone. The release between osteoclasts and phosphate to form of enzymes breakdown bone blasts. This is the most hydroxyapatite. They are and release calcium and common cell and are old found mostly in the phosphate into the blood osteoblasts embedded in the periosteum matrix that they secrete Paget’s disease Key facts • Caused by bone cell overactivity • Lytic and sclerotic lesions • Deformity, bone pain, usually asymptomatic • Mx: Analgesia, bisphosphonates, osteotomy • Raised ALPTibial bowing and Normal Tam O’Shanter areas of lytic and sign sclerosing lesions Causes Osteoporosis • Smoking • Reduction in bone mass and density • Low BMI • The t-score is the used to assess bone density • Sedentary • It is comparative to the bone density of a healthy young adult • Poor dietary intake of vit D • A t-score of -1 to -2.5 is osteopenia, less than -2.5 is and Calcium osteoporosis • Steroid use • 75% of white females >50 at risk of osteoporotic fracture Management • The goal is to prevent bone loss • Bisphosphonates are bone loss inhibitors • Oestrogen, calcium and vitamin D will all contribute to to bone growth Diet Vitamin D3 and D2 (Cholecalciferol) and sunlight 25-hydroxylase Liver Calcidiol (25(OH) D) 1𝜶 hydroxylase Prox. nephron of the kidney Calcitriol Active form! (1,25(2H) D) • Calcium and phosphate absorbed in GI tract • Increased osteoclastic activityCalcium Low calcium in the blood homeostasis Parathyroid hormone release (Chief cells of the parathyroid) Increase in activity of Kidneys increa3- osteocl2+ts to re3-sorb excretion of PO 4 and Ca and PO 4 converts calcidiol to calcitriol 2+ Calcitriol acts as negative ↑ Ca reabsorbed in the feedback for PTH and GI tract and phosphate stops its secretion secreted by kidneys Increased level of calcium in the bloodCalcium High calcium in the blood homeostasis Calcitonin release (Thyroid) Inhibits osteoclasts, osteoblastic activity presides and absorb Ca Essentially the and P4-from the blood opposite to PTH ↑Increased bone deposition Decreased level of calcium in the bloodHyperparathyroidism Primary • Gland pathology • PTH over-secretion • Hypercalcemia Tertiary • Chronic 2o hyperparathyroidism • Hyperplasia Secondary • Abnormal Ca + PO 3- metabolism 4 • CKD or Vit. D deficiencyThank you!