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S1Secrets Case1Contents 1. Anatomy of lower limb 2. Bone physiology 3. Haemostasis 4. Skin and inflammation 5. Pain and analgesiaAnatomy of lower limb SBA Mr Jones, a marathon runner, comes into the GP surgery with pain and tenderness on his medial left knee. The GP suspects pes anserine bursitis. Which muscles form the pes anserine tendon? A Semitendinosus, semimembranosus, adductor magnus To remember: Say Grace before Tea B Sartorius, Gracilis, Gracilis, adductor longus, biceps femoris semiTendinosus C Sartorius, gracilis, semitendinosus D Rectus femoris, sartorius, semimembranosus SBA Which muscle of the lower limb is labelled in this MRI scan? A Vastus medialis B Rectus femoris C Sartorius D Vastus lateralis SBA Mr Evans is a construction worker who has had an accident at work where a concrete block fell onto his lower leg. Upon examination, the doctor suspects damage to the deep fibular nerve. Which movement of the lower limb is Mr Evans most likley to struggle performing? A Foot dorsiflexion B Foot inversion C Foot plantar flexion D Foot eversion SBA A patient suffers a displaced, intracapsular femoral neck fracture after a car crash. The doctor is concerned that this injury will lead to avascular necrosis of the femoral head if not treated soon. What blood vessels are most likely damaged? A Superior and inferior gluteal arteries B Medial and lateral circumflex arteries medial circumflex C deep femoralcumflex Deep femoral artery D Obturator artery Anterior compartment Anatomyoflowerlimb Muscle Action Innervation Bloodsupply Tibialis anterior Dorsiflexion, Deep fibular Anterior tibial inversion nerve artery Extensor Dorsiflexion, Deep fibular Anterior tibial digitorum extension of nerve artery longus digits2-5 Extensor Dorsiflexion, Deep fibular Anterior tibial hallucis longus extension of nerve artery digit1 tibialis Fibularis tertius Dorsiflexion, Deep fibular Anterior tibial eversion nerve artery anterior extensor digitorum longus extensor hallucis longus fibularis tertius Anatomyoflowerlimb Lateral compartment Muscle Action Innervation Blood supply Fibularis longus Plantarflexion, Superficial fibular Perforating eversion nerve branches of anterior tibial and fibulararteries Fibularis brevis Eversion Superficial fibular Perforating nerve branches of anterior tibial and fibulararteries fibularis longus fibularis brevis Posterior compartment – superficial Anatomyoflowerlimb muscle group Muscle Action Innervation Blood supply Gastrocnemius Plantarflexion, Tibial nerve Posterior tibial and knee flexion fibulararteries Soleus Plantarflexion Tibial nerve Posterior tibial and fibulararteries Plantaris Plantarflexion, Tibial nerve Posterior tibial and knee flexion fibulararteries plantaris heads of gastrocnemius soleus gastrocnemius soleus calcaneal tendon calcaneal tendon calcaneus Posterior compartment – deep muscle Anatomyoflowerlimb group Muscle Action Innervation Blood supply Popliteus Stabilisesand Tibial nerve Posterior tibial and unlocksknee fibulararteries joint Flexor digitorum Flexionof digits Tibial nerve Posterior tibial and longus 2-5 fibulararteries Flexor hallucis Flexionof digit1 Tibial nerve Posterior tibial and longus fibulararteries Tibialis Plantarflexion, Tibial nerve Posterior tibial and popliteus posterior inversion, fibulararteries supports medial arch of foot tibialis posterior flexor digitorum longus flexor hallucis longus Muscleattachmentsthatyouneed Anatomyoflowerlimb toknow! Muscle Proximal Distal Sartorius Anterior superioriliacspine Medial surface of tibiajust inferomedialto tibialtuberosity Gracilis External surface of body of pubis, inferiorpubic ramus, ischial ramus Medial surface of proximal tibia Rectus femoris Anterior inferioriliacspine,area of iliumimmediatelysuperiorto acetabulum Patellaviaquadricepsfemoristendon Biceps femoris Long head = ischial tuberosity Head of fibula Short head = lateral lipof lineaaspera Semitendinosus Ischial tuberosity Medial surface of proximal tibia Semimembranosus Ischial tuberosity Medial tibial condyle Gastrocnemius Medial head = medialfemoral condyle Calcaneusviacalcaneal tendon Lateral head = lateral femoral condyleBone physiology SBA Mrs Edwards, an 81-year-old woman, suffers a hip fracture after slipping on the kitchen floor. She has a history of osteoporosis. What type of cell is overactive in osteoporosis? A Osteoblast B Osteoclast C Monocyte precursor cell D Osteocyte Bonestructure • Cells embedded in layers of collagen and minerals • Osteocytes found in lacunae • Lacunae connected by canaliculi to transport nutrients and waste products • 2 types – spongy and compact Spongy bone Compact bone • Porous interior • Hard exterior • Trabeculae make a lattice • Made up of osteons • Osteons = rings of bone called • Cavities in between trabeculae contain lamellae, with Haversian canal in red bone marrow the middle for blood supplyBonestructure BONE Cells Extracellular matrix Osteoid Minerals Osteocytes Osteoblasts Osteoclasts Type 1 collagen Hydroxyapatite Glycoproteins ProteoglycansBonecells Osteoblasts Osteoclasts Osteocytes • Deposit new bone • Resorb bone • Detect microfractures to trigger • Secrete RANKL to activate • Drill holes into bone remodelling osteoclasts called Howship’s lacunae • Maintains bone tissue • Formed from fusion of monocyte precursor cells Boneremodeling 1 Osteoblasts secrete RANKL to activate osteoclasts 2 Osteocytes resorb bone by secreting enzymes to digest collagen and HCl to dissolve hydroxyapatite 3 Osteoblasts lay down new osteoid 4 Osthe bone, turning into osteocytes Osteoporosis • Imbalance in remodeling, osteoclasts more active than osteoblasts • Increased bone resorption, decreased bone formation Normal bone • = low bone mass • Risk factors include ageing, menopause and corticosteroids • Treated with bisphosphonates (which inhibit osteoclasts) Osteoporotic bone Osteomalacia • Normal bone mass, but mineral component is reduced • Called rickets in children • Caused by vitamin D deficiency • Insufficient calcium and phosphate means new bone cannot be mineralized, = soft bone • Fractures and deformations like knock knees • Treated with vitamin D supplementsHaemostasis SBA A child comes into A and E with prolonged bleeding after cutting their finger. They have a history of haemophilia B. The doctor gives the child an injection of the medication nonacog alfa to treat their prolonged bleeding. Using your knowledge of clotting disorder deficiencies, what is nonacog alfa a synthetic version of? A Coagulation factor IX B Von Willebrand factor C Coagulation factor VIII D Coagulation factor XI SBA A bruise forms on a patients toe after stubbing their foot on the hospital bed. After 2 weeks, the bruise has changed colour reason for this colour change?/brown colour. What is the A Albumin breakdown B Melanocyte proliferation C Melanocyte apoptosis D Haemoglobin breakdownHaemostasis overview 1 The overall process through which blood loss is prevented Split into primary haemostasis (formation of clot) and secondary 2 haemostasis (stabilisation of clot) 3 based modelaemostasis has 2 models – the classical model and the cell-Classicalmodel Intrinsic pathway Text Extrinsic pathway pathway Classicalmodel Tissue Factor is EXTRINSIC to the blood!ClassicalmodelCell-basedmodel Initiation CFs X, VII and II diffuse across blood vessel wall and interact with tissue factor CF V too big to diffuse across So small amount of IIa producedCell-basedmodel Amplification When blood vessel is damaged, blood flows into surrounding tissue IIa produced in initiation activates other CF and plateletsCell-basedmodel Propagation Platelets have a negatively charged surface IXa.VIIIa and Xa.Va complexes bind to platelets Complexes now much more active and brought close together – pathway flows = thrombin burst Bruisesandcolourchanges Bruises occur when capillaries just blow the skin burst and clots form Red Purple Green Yellow Remember: You cannot tell how old a bruise is by the colour! Biliverdin Bilirubin Blood under skin Haemoglobin breakdown Haemostasis Clottingdisorders Haemophilia A Haemophilia B Haemophilia C Coagulation factor IX Coagulation factor VIII Coagulation factor VIII deficiency/dysfunction deficiency/dysfunction deficiency/dysfunction A sounds like 8 B is 9, benign Just have to remember this one! No IXa.VIIIa complex formed Not enough fibrin produced to stabilise soft clotSkin and inflammation SBA A cyclist falls of their bike and cuts their knee. In the hours that follow, neutrophils release enzymes to kill bacteria and degrade damaged tissue in the wound. What are these enzymes referred to as? A Thromboxane B Platelet-derived growth factor beta C Neutrophil elastase D Matrix metalloproteinase SBA A patient’s wound has stopped bleeding and is now entering the proliferative phase of wound healing. In order to replace the lost tissue, fibroblasts found in the dermis secrete extracellular matrix. Which substance does not make up the extracellular matrix? A Collagen B Glycosaminoglycans C Proteoglycans D Aminoglycosides Stagesofwoundhealing Inflammation Proliferation Remodeling granulation tissue cytokines vasodilation angiogenesis improve tensile organise new and and fibroplasia strength ECM chemokines permeabilityStagesofwoundhealing Angiogenesis Hypoxia leads to HIF1 expression Upregulation of pro-angiogenic genes Migrating tip follows the concentration gradient of VEGF PDGF beta recruits pericytes which block VEGF New blood vessel is covered by smooth muscle cells SBA A patient notices a new mole on their neck and visits the GP. The GP suspects the patient has a melanoma. In which layer of the skin did these malignant cells originate from? A Stratum basale B Dermis C Epidermis D Stratum granulosumStructureoftheskinSkinreceptors Howcanwoundheal? • Wound edges held together • Faster healing • Less scarring Primary intention Howcanwoundheal? • Wound edges not held together • Tissue healing occurs from the bottom of the wound upwards • Slower healing Secondary intention • More scarringPain and analgesia SBA A child touches a hot pan. What type of nociceptive nerve fibre is stimulated? A A fibre B C fibre C A-delta fibre D C-beta fibreNociceptivenervefibres Nociceptivenervefibres A-delta fibre C fibre Nociceptive nerve endings Aδ fibre C fibre • Myelinated axons • Unmyelinated axons • Fast conduction speed • Slow conduction speed • Intense mechanical • Intense mechanical stimulus, cold temp stimulus, >42˚ temp, irritant chemicals • Sharp pain • Dull pain SBA What is the mechanism of action of aspirin? A Competitive inhibitor of cyclo-oxygenase domain of prostaglandin H synthase B synthasele inhibitor of peroxidase domain of prostaglandin H C Irreversible inhibitor of cyclo-oxygenase domain of prostaglandin H synthase D Irreversible inhibitor of prostaglandin H synthaseProstaglandinproduction NSAIDs Ibuprofen → competitive inhibition Aspirin → irreversible inhibitionImportantNSAIDcontraindications Contraindicated if… Reye’s syndrome Already on NSAID/allergic Pregnant Paracetamol Adverse drug reactions • Overdose-related hepatotoxicity Contraindications • Liver failure • Acute alcohol intoxication Codeine Adverse drug reactions codeine • Constipation • Dizziness • Dependence • Drowsiness Contraindications • Acute respiratory depression • Coma Thank You!/Break/ Questions? Follow our Socials: Instagram: @cu_cardiosoc Facebook: Cardiff University Cardiovascular Society Cardiovascularsociety@outlook.com