Computer generated transcript

Warning!
The following transcript was generated automatically from the content and has not been checked or corrected manually.

PRECLINEAZY Case 1 Agbo Pethiyagoda Case 1 Todays Session will cover Lower Limb Anatomy Pain Pathway and Pain Physiology Analgesics (NSAIDs)Lower Limb Anatomy Bones Lower Limb Regions; Posterior Anterior 1. Gluteal Region 2. Thigh 3. Leg 4. Foot Upper Margin; 1. Iliac Crest 2. Superior Iliac Spine 3. Pubic Tubercle Anatomy Femur Clinical Relevance Injuries; Head Greater Trochanter 1. Posterior hip dislocation – short, Neck adducted, internally rotated 2. Spiral fracture of femur – one leg Lesser Trochanter shorter than the other Shaft(body) Extracapsular fracture – Fix hip rather than replace (Dynamic Medial epicondyle Lateral epicondyle Hip Screw) Intracapsular fracture – Head of femur necrosis and requires Medial condyle Lateral condyle hemiarthroplasty Anatomy Knee Clinical Relevance ACL damage = “Pop” sound, rapid joint swelling, Positive Lachman’s test PCL damage = Caused by direct blow Gastrocnemius to knee/ hyperextension bursa Unhappy triad; 1. ACL 2. Medial Collateral Pre-patellar bursa 3. Medial meniscus Subcutaneous Infra- Pre-patellar = common bursitis patellar bursa (Housemaid’s Knee) Deep Infra-patellar bursa Anatomy Leg Foot Lateral Condyle Medial Condyle Head of Tall - Talus Camels – Calcaneus Fibula Interosseous Membrane Never - Navicular Consume – 3 Fibula Tibia(shinbone) Cuneiforms Cubes - Cuboid Lateral Malleolus Medial Malleolus Anatomy Musculature Anterior Medial Posterior Thigh Flexion Thigh Adduction Thigh Extension Extension of leg at Knee Flexion knee Anterior Lateral Posterior Dorsi flexion Plantar flexion Plantar flexion Extension of Digits Eversion Eversion Inversion Flexion of the Digits Anatomy Innervation Anterior Medial Posterior Femoral Nerve Obturator Nerve Sciatic Nerve Posterior Anterior Lateral Deep fibular nerve Superficial Fibular Tibial Nerve Nerve Question 1 Bruce Lee was seen fighting at the ICU games and during one A Posterior thigh & Sciatic nerve of his kicks, he ended up damaging his leg. On examination, it can be seen that he can no longer kick forwards (extend at B Medial thigh & Fibular nerve the knee joint). What group of muscles and/or what nerve may have been C Anterior thigh & sciatic nerve damaged resulting in this loss of motion? D Posterior thigh & femoral nerve E Anterior thigh & femoral nerve Question 1 Bruce Lee was seen fighting at the ICU games and during one A Posterior thigh & Sciatic nerve of his kicks, he ended up damaging his leg. On examination, it can be seen that he can no longer kick forwards (extend at B Medial thigh & Fibular nerve the knee joint). What group of muscles and/or what nerve may have been C Anterior thigh & sciatic nerve damaged resulting in this loss of motion? D Posterior thigh & femoral nerve E Anterior thigh & femoral nerve Question 1 After this incident, Bruce was taken into surgery. At the end ofA Sciatic nerve the surgery, the surgeon accidentally cuts through a nerve. On recovery, Bruce is unable to flex his toes. Which nerve B Fibular nerve may been damaged? C Medial nerve D Femoral nerve E Tibial nerve Question 1 After this incident, Bruce was taken into surgery. At the end ofA Sciatic nerve the surgery, the surgeon accidentally cuts through a nerve. On recovery, Bruce is unable to flex his toes. Which nerve B Fibular nerve may been damaged? C Medial nerve D Femoral nerve E Tibial nerve Anatomy Blood Supply Clinical Relevance Deep veins sometimes follow arteries (venae Dorsal Pedal pulse = sits commitantes) à aids with venous return. on top of foot and is checked to ensure that leg Superficial veins are has a good blood supply. subcutaneous and do not follow arteries. No pulse = something à Drain into deep veins wrong (eg- compartment syndrome) à prone to varicosities Anatomy Femoral triangle SIA Popliteal Fossa Semitendinosus Biceps femoris Semimembranosus Popliteal nerve Inguinal Ligament Popliteal artery Popliteal vein Lateral head of Adductor longus Sartorius gastrocnemius Medial head of N - Nerve A - Artery gastrocnemius V - Vein Y - Lymph Medial Lateral Serve and volley next ball Anatomy Flexor Retinaculum Contents; Tom, Dick And Very Nervous Harry Tibialis posterior Flexor digitorum longus Tibial Artery Vein Nerve Flexor Hallucis LongusPain Pathway and Physiology Pain Duration Nature Chronic Acute Recent onset & limited duration Persistent after healing time and in absence of Caused by activation of nociceptive sensory injury Lasting for 3+ months neuronesx Often no identifiable cause (pain lasts after normal healing) Pain Duration Nature Nociceptive Non-nociceptive Somatic Visceral (from Neuropathic Sympathetic (from skin) organs) (nerve) (unexplained) Obvious Tissue Injury Nervous system damage Types of Nerve Fibres A-delta C A-beta • Fast, myelinated • Slow, unmyelinated • Fastest, myelinated • Respond to; • Respond to • Respond to; - Heat - Chemical - Non-noxious - Pressure - Mechanical stimuli • 1 “sharp” sensation - Thermal - Light touch nd - Vibrations • 3-30m/s • 2 “throbbing”, “burning” pain • “Comforts you” sensation • 33-75m/s • 0.5-2m/s Pain Gate theory Opens gate – A delta, C Closes gate – A beta Inhibitory descending pathway Eg – TENS therapy stimulates A-beta fibres Ascending pain pathway Pain Pain Gate Fast A delta fibres A beta fibres Slow C fibres Injury TouchPhysiology of Pain 1. Transduction 2. Transmission 1. Tissue injury 1. Nociceptive input enters CNS at Nociception 2. Chemicals released dorsal horn 2. Substantia gelatinosa receives 3. Pain receptors stimulated input • Occurs in 4 main 3. Nerves synapse 4. Signals travel to A-delta 4. 2 nerve travels up opposite side phases of spinal cord towards the brain and C fibres 4. Modulation 3. Perception 1. Descending pathway 1. Thalamus is the 2 relay station from brain to dorsal 2. Connections to many parts of the brain horn 3. Experience painà emotional 2. Usually decreases & subjective pain signal 4. Pain perception occurs in the pain-management-by-Gautam-Das-reprinted-with_fig1_324776320ourtesy-basics-of- cortex Pain Pain Modulation (PAG) 1. Receives information from ascending pain tracts 2. Stimulation of the PAG activates enkephalin releasing neurone 3. Raphe nucleus releases serotonin 4. Interneurones in the substantia nigra release opioid neurotransmitters 5. Bind to Mu-opioid receptors 6. Inhibition of substance P bindingAnalgesics Analgesics NSAID Mechanism PGE2 - Pain sensitizer Membrane - Inflammatory mediator phospholipids - GI mucosa & renal protection Cleaved PG-E2 synthase - Uterine contraction Via to form Phospholipase Prostaglandin H synthase TXA2 A2 (PLA2) - Platelet aggregation - Local vasoconstriction Arachidonic Acid (AA) synthase COX Peroxidase PGH2 PGG2 PGI2 PG-I2 synthase - Inhibits platelet aggregation O2 - Local vasodilation Analgesics NSAID Mechanism NSAID Mechanism 1. All inhibit COX Domain Membrane 2. Resulting in no phospholipids subsequent Cleaved conversions (no PGG2 Via to form and PGH2 formed) Phospholipase Prostaglandin H synthase A2 (PLA2) Arachidonic Acid (AA) Therefore no PGH2 binding COX Peroxidase PGH2 at tissues causing; 1. Reduced extent and PGG2 duration of None formed inflammation O2 2. Less vasodilation 3. Less vascular permeability Non-steroidal Anti-Inflammatory Drugs Aspirin Paracetamol Ibuprofen • Competes with AA • Acetylates the • Not a NSAID • May be chosen before for COX domain serine residue in NSAIDs à it can have • Reversible inhibitor the COX domain better analgesic & • Irreversible antipyretic effects (but inhibitor very little anti- inflammatory activity). • Unknown mechanism (may inhibit Peroxidase domain activity) NSAIDs ADRs Contraindications • Gastric Ulceration • Pregnant • NSAID allergy/ sensitized to salicylates • Already on a NSAID • Renal function impaired • Younger than 16 years old (aspirin use à associated with Reye’s Syndrome) Question 2 You have a medical student as a Acts as a competitive inhibitor of AA for the cycle- A oxygenase domain of PGHS-1 and PHGS-2. patient and prescribe aspirin as a painkiller. Acts as an irreversible inhibitor of PGHS enzyme by B causing acetylation of the serine residue. They ask about the mechanism of Acts as a reversible inhibitor of PHGS action of aspirin. What would be C the correct explanation? peroxidase domain. D Acts as an opioid receptor agonist. Acts as a glucocorticoid steroid receptor E agonist. Question 2 You have a medical student as a Acts as a competitive inhibitor of AA for the cycle- A oxygenase domain of PGHS-1 and PHGS-2. patient and prescribe aspirin as a painkiller. Acts as an irreversible inhibitor of PGHS enzyme by B causing acetylation of the serine residue. They ask about the mechanism of Acts as a reversible inhibitor of PHGS action of aspirin. What would be C the correct explanation? peroxidase domain. D Acts as an opioid receptor agonist. Acts as a glucocorticoid steroid receptor E agonist. • Diamorphine, fentanyl, sedation Severe agony • Stronger Opioids Strong pain WHO Pain Ladder • Weaker Opioids Moderate to strong pain • Cocodamol Mild Pain • Paracetamol & NSAIDs Question 2 Harry Potter has fallen off his broom during sports A Aspirin practices. He is in immense pain and he asks the doctor for pain relief. The doctor starts by prescribing a pain B Ibuprofen killer, but he finds out that this has no effect on Harry. So he goes up the ladder and he has just found out that C Codeine Co-codamol also has no effect on Harry. D Fentanyl Which drug would he prescribe next? E Morphine Question 2 Harry Potter has fallen off his broom during sports A Aspirin practices. He is in immense pain and he asks the doctor for pain relief. The doctor starts by prescribing a pain B Ibuprofen killer, but he finds out that this has no effect on Harry. So he goes up the ladder and he has just found out that C Codeine Co-codamol also has no effect on Harry. D Fentanyl Which drug would he prescribe next? Codeine – a weak opioid E Morphine THANKS FOR WATCHINGPLEASE FILL OUT THE FEEDBACK FORM PLEASE TUNE IN TO OUR REMAINING SESSIONS THIS WEEK