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Locomotor Yr 1 24/11/2021 Tutors: Olivia Pestrin & Navina SenthilkumarLife Threatening Injuries ATLS A-E AssessmentATLS Advanced Trauma LIfe Support ● Where is it used? Who is it used by? ● What is the approach to ATLS situations?ATLS Advanced Trauma LIfe Support ● Where is it used? ○ Public scene ○ Scene of MCA ○ RTA ○ ED/Resus ● Who is it used by? ○ SAS ○ Emergency doctors ○ Critical Care doctors ○ You ● What is the approach to ATLS situations? ○ ABCDE ○ C-ABCDEA-E C- C-Spine + Catastrophic Bleed ● Assessment of critically unwell patients A - Airway ● Can be used to approach B - Breathing any patient ● Assess in hierarchy of C- Circulatory need D -Disability ○ what will kill you first? E- Exposure ● Universally usedA - Airway ASSESSMENT MANAGEMENT ● Talking & Orientated? ● High Flow Oxygen ● Noises ● Head tilt chin lift OR Jaw thrust ○ Snoring ○ Why would you use tilt vs ○ Stridor thrust? ○ Wheeze ● Physical obstruction ○ No noise ○ manual removal ● Head & Neck Injury? ○ Suction ○ High risk for losing airway ● Low GCS or loss of airway? ○ Skull # 1. Gidel [supraglottic] ● Physical Blockage 2. Nasopharyngeal OR I-Gel ○ Food [oropharyngeal] ○ Blood ○ Vomit 3. Intubation ○ Tongue 4. Surgical airwayB - Breathing ASSESSMENT MANAGEMENT ● Inspection 1. Oxygen ○ chest injury 2. IF RR <10 supplemental bag & mask ○ respiratory effort 3. Treat the cause ○ Asymmetry ● Palpation ○ trachea DIFFERENTIALS ○ chest wall expansion ○ percussion ● Pneumothorax ● Auscultation ○ tension, open, spontaneous ○ symmetrical air entry ● Flail Chest ○ Added sounds? ● Pre-existing condition? ○ No sound? ● Observations ○ SpO2 ○ RR ○ HR ○ BPTension Pneumothorax Internal 1 way valve Signs & Symptoms ● Engorged neck veins ● Reduced lung expansion ● Trachea deviated away ● Decreased breath sounds Investigations CLINICAL DIAGNOSIS Management 1. Immediate needle decompression 2. Definitive chest drainOpen Pneumothorax Suck Chest wound External 1 way valve Air passes into chest through path of least resistance Signs & Symptoms ● Visual ● Reduced lung expansion ● Trachea deviated away ● Decreased breath sounds Investigations CLINICAL DIAGNOSIS Management 1. 3 sided dressing 2. Chest drainFlail Chest 2x2 [2 or more ribs broken in 2 or more places] Separate segment from thoracic cage Paradoxical chest wall movement indrawing on inspiration outwards on expiration Signs & Symptoms ● Visual Investigations CLINICAL DIAGNOSIS Management 1. Stabalization 2. SurgeryC - Circulation ASSESSMENT MANAGEMENT Haemorrhagic Vs Cardiogenic 1. x2 large bore cannula a. take off bloods Floor + 4 More b. Fluid resus ● Inspection 2. ITreat obvious sources ○ Pale a. pelvic binder [closes circuit] ○ Peripheral circulation b. External pressure ● Palpation DIFFERENTIALS ● Auscultation ● Observations ● Pelvic fracture ○ Pulse ● Massive haemothorax ○ BP ● Cardiac tamponade ● Cardiogenic shockMassive Haemothorax Blood into chest cavity >1500mLs Signs & Symptoms ● Chest wall stillness ● Dull to percuss ● Abscent or dull breath sounds Investigations ● CXR ● Pleurocentesis Management 1. Chest drain 2. Blood products 3. SurgeryCardiac Tamponade Fixed space around the heart As it fills compresses heart as so it can’t pump Signs & Symptoms = BECKS Triad ● HOTN ● Raised JVP ● Muffled heart sounds Investigations ● ECHO/USS Management 1. Pericardiocentesis HAEMORRHAGIC Shock Most common in trauma End organ dysfunction Blood Blood Pulse BP Urine Loss Loss o/p Poor perfusion & therefore (%) (ml) (ml/hr) oxygenation Once compensatory mechanisms fail Class <15 <750 <100 N >30 i Types: 15-30 750-15 100-120 N 20-30 ● Hemorrhagic/Hypovolemic Class ● Cardiogenic ii 00 ● Anaphylactic Class 30-40 1500-2 120-140 ↓ 5-15 ● Neurogenic 000 ● Septic iii Class >40 >2000 >140 ↓ neg ivShock Con’t Class 1-3 Body Compensates w/ increasing intervals Compensation fails at stage 4 → Peri arrest RESPIRATORY RATE – increases as lactic acid rises → fails w/ fatigue PULSE – tachycardia to compensate for falling stroke volume → hits max → Brady BLOOD PRESSURE – initial compensation until class iii. → Drops HOTN URINE OUTPUT – falls with renal vasoconstriction → none PERIPHERIES – cool with vasoconstriction → cold & mottled MENTAL STATE – increasing confusionwith reduced cerebral perfusion → comaD - Disability BLOOD GLUCOSE ASSESSMENT GCS [Eyes 4 Verbal 5 Motor 6] BLOOD GLUCOSE AVPU [Alert, Verbal, Pain, Unresponsive] Pupils [reflex, reaction, symmetry] BLOOD GLUCOSE BLOOD GLUCOSED - Disability S E C O ASSESSMENT BLLOD GLUCOSE AVPU [AleDt, Verbal, Pain, Unresponsive] Pupils [reflBLOOD GLUCOSE symmetry] B BLOOD GLUCOSEE- Exposure Commonly missed places ●Back of head Top to ●Perineum ●Axillaolds ToeLife-Threatening Trauma Airway obstruction Tension pneumothorax Open pneumothorax Massive haemothorax Flail chest Cardiac Tamponade Shock Blood glucoseWhat is the first step in ATLS assessment?Patient has 900 mL blood loss HR 110 BP 135/87 and urine output 30ml/hr Classify their shock A. Class I B. Class II C. Class III D. Class IV E. Class VPatient comes into resus after a head on RTA, on assessment of their airway you hear a stridor. What do you do next? A. Head tilt chin lift B. Gidel airway C. Jaw thrust D. Intubate E. I-gel [oropharyngeal]Limb Threatening InjuriesOpen Fracture [Compound] Bone through skin Classification Risks Gustilo-Anderson Classification ● Damage muscle + nerve + vascular Managment 4 R Resuscitate ● Increased risk compartment syndrome ● A-E ● High risk infection ● Fluid or blood products ● Non-union ● IV ABx STAT ● Haemorrhage ○ Cefuroxime 1.5g TDS ○ Clindamycin [pen allergy] History ○ Gentamicin IF increased RF ○ Tetanus booster ● Type of injury Reduce ● Clean bone and area first ● Force ● Traction + relocate ● Environment risks [dirt, chemical, water] ● Surgery ○ debridment ○ IM nail or external fixation Exam ○ Wound closure Restrict ● look + Feel + Move ● Cast & immobilize ● Neurovascular status Rehabilitate ● PTGustilo-Anderson ClassificationArterial Injury MANAGEMENT 1. A-E SURGICAL EMERGENCY 2. Resuscitate the patient 3. Realign fractures [if applicable] kink OR laceration OR a. reassess transect 4. Surgical referral Cause a. vascular b. plastics ● Stabbing/cut c. +/- ortho ● Open fracture ● Crush injury Signs & Symptoms ● cold mottled pale ● painful ● absent pulsesNerve Injury Neurapraxia Compression of nerve Nerve Viable [not dead] Relieve pressure = full recovery Axonotmesis Ischaemia of nerve Distal axon dies Prolonged neurapraxia Possible permanent damage Neurotmesis total transection Surgical repair Risk long term deficitCompartment Syndrome SURGICAL EMERGENCY MANAGEMENT Growing pressure in fascial 1. fasciotomy compartment Fascia = stiff/non-pliable = no where for 2. cut open cast/compression 3. elevate limb pressure to go Swelling → Increased pressure → ischaemia → hypoxia & cell death Signs & Symptoms ● Disproportionate pain to injury ● Pain on passive stretch ● +/- Pulseless distallyWhat is the first step in assessing open fracture?What antibiotic do you give in a clean open fracture? A. Ceftriaxone B. Cefuroxime C. Amoxicillin D. Gentamicin E. Vancomycin What imaging is required in compartment syndrome? A. USS B. CT scan C. MRI D. Pressure gauging E. None of the aboveCommon Paediatric Injuries Plasticity and Elasticity ▶ Adult bones are rigid and brittle and they require more force to break. Occurs in a sudden manner. ▶ Bone breaks completely or into lots of fragments. ▶ Kids bones show elasticity and plasticity (similar to a paperclip). Incomplete fracture ‘Buckle fracture.’ This occurs as the bone is more flexible and the blue part of the bone is under compressive force. ‘Buckles’ under the pressure. Kids Bones Parts of the bone: o Diaphysis = shaft o Metaphysis = change zone between diaphysis and epiphysis o Epiphysis= end zone o Apophysis = outgrowth or projection o Physis = growth plate Weak points: o Physis o Apophysis o Metaphysis Periosteum and Remodelling ▶ Periosteum = coating around the bone ▶ When a bone breaks and the periosteum remains intact – then this makes it easier to reduce the fracture. ▶ Bones don’t displace as much. ▶ Remodelling (occurs in early childhood) ▶ How close the fracture is to a joint and the plane of the fracture. ▶ Wolf’s law- bone will be added to the compressed side (blue) and absorbed from the tension side (red) = almost back to normal. Paediatric Orthopaedics: Physeal • What is a growth plate? • Allows longitudinal growth • Fuse at around 12-14 not a consideration after this age. • Why is a fracture here important? • Risk of growth problems • Partial or complete arrest • +/- articular involvement Salter-Harris This shows articular S involvement A L Type II are the most T common. R Type V has the worst prognosis. III/IV management → Anatomic reduction and fixation. Genu Varum / Valgum: Pathological ▶ Asymmetry (one leg and not other) alerts you to there being a problem. ▶ Resistant – normal varus alignment which is seen in kids ▶ If the degree of varus alignment (i.e. bow-leg) is >11 degrees then this is significant. Alerts you that there was either trauma / infection underlying this. If is it pathological then it requires treatment: Guided growth via an ‘eight plate’. Rotational: in-toeing ▶ True deformity of the foot – is it impairing the child’s ability to run around, are they falling over/ clumsy? Extremities of age (i.e. young children and older adults) 🡪 they have a slight external rotation of their feet. This produces a wider gait which helps with balance/ stability. Femoral Anteversion: Essentially refers to the angle of the head and neck of the femur in relation to the shaft of the femur. It allows for internal rotation of the hip. This is a normal variant and remodels over the period of a child’s life. Persistent femoral anteversion – not remodelled to it’s normal level. Results in internal foot proMetatarsal Adductus (Foot) Medial curve at the inside of the foot. Club Foot (Congenital Talipes Equinovarus) Most common childhood foot deformity Foot turned inwards. Dislocation of the talo-navicular joint (which you can see). Big toe is plantarflexed (points down) – locks the foot in that position. Treated with Ponseti treatment and application of boots and bar.Out-toeing: Tibial Torsion (External / Excessive Tibial Torsion) Results in external foot progression (out-toeing). Patient prone, ankle and foot held neutral and measure the angle between the thigh and the foot. Degree of variability = range in the foot progression angle, tibial torsion angle and internal or external hip rotation. Flat foot (Planovalgus) Most common foot deformity – medial arch collapses on itself. Get the patient up onto their tiptoes = should elicit an arch. Insoles are often not necessary (only if signs of wearing along the midline) or symptomatic. Severe that persists into adolescence = insert a subtalar implant.Persistent In-toeing Persistent Out-toeing 1. Persistent femoral anteversion. 1. Persistent femoral retroversion = requires May have increased internal rotation of the hip. surgery? If it is symmetrical and no pain – observe. No way of guiding growth – fix with plate and Children sitting in ‘W’ formation may lead to this- screws. encourage cross-legged sitting in school. Symptomatic and problems with malalignment to consider surgery. 2. Internal Tibial Torsion Discourage children from sitting on their feet. 2. External Tibial Torsion 3. Miserable Malalignment- can result in patella 3. Planovalgus instability. 4. Metatarsus Adductus - abnormal packaging in the womb. Non-Accidental Injury (NAI) ▶ Quite uncommon but so important to have a high index of suspicion. ▶ NAI is the second most common cause of death in childrRisk Factors for Risk Factors for Adult Child ▶ Soft-tissue injuries (most common type of injury) First born Single parent Disability Unemployment Accidental Premature Substance misuse Unplanned Personal history of abuse ▶ head or face injury is rare in <18 months, bruising of hands, feet and Lower soci - coc tatus. Non-accidental ▶ Lumbar (which is to the back or front of tummy) ▶ Bitemarks (look at the size) ▶ Burn marks (could be accidental, but look for a cigarette burn, lighter burn, or neglect can be seen in sunburn) ▶ BruisingNAI: Fractures Corner of metaphysis Multiple rib fractures (posterior ribs) Femoral fractures (less common in younger children) Multiple fractures at different stages. Conditions which increase susceptibility: - Osteogenesis imperfecta (brittle bone disease) – gives people very fragile bones. Several fractures already by 1 y/o. - Prematurity (risk factor for NAI) OUR ROLE: Recognise unusual injury patterns Liaise with child protection services Always admit the child if you are worried Parents may be distressed, but they will be understanding in the long term.Normal Milestones of Development ▶ Angular deformities Bow legs (Genu varum) Knocked-knee (Genu valgus) ▶ Rotational deformities Feet pointing in or out • Babies are often bow-legged when they are born up. • 2 y/o the child’s legs straighten. • As they grow and begin walking, they begin to develop valgus formation. • Make sure the knee-caps are facing forward.Pathology by Age Toddler (1-2) Younger Child (3-8) Older Child (9-15) Malignancy (leukaemia, Sarcomas) Non-accidental injury Infection Missed DDH Perthes “condition” Slipped capital femoral epiphysis Assessing a child: ▶ History : Acute (sudden onset) – trauma, infection Constant (gradually worse) – tumour, chronic infection Morning pain (inflammatory joint disorders) Pain at night (in infants (2-6) – growing pain, or malignancy) ▶ Examination: Gait, spine, asymmetry, deformity, swelling, tenderness, examine all joints, rotational profile) ▶ Imaging (x-ray / MRI) ▶ PlanRheumatoid ArthritisRheumatoid Arthritis Chronic Autoimmune disorder predominantly affects joints ❑ Demographics ❑ Smoking ❑ 3x more common in females than males ❑ Affects 3 to 5 decades ❑ Familial + environmental trigger ❑ Symptoms ❑ Morning stiffness >30min Extra-Articular MSK ❑ Restriction of joint movement ● Bursitis ❑ pain in joints ● SC nodules ● Tendonitis +/- rupture ❑ symmetrical ● Scleritis ● Pericarditis ❑ Erosive + deforming ▶ telescoping ▶ nodulesRA Pathophysiology 1. citrullination + Trigger → Immunogenic protein 2. B-cell presenting in cartilage + bone 3. T-cell triggered 4. T-cell activated B-cells to release cytokines from synovial macrophages 5. Plasma cells produces auto-antibodies [RF + anti-CCP] 6. T-cell forms +ve feedback loop of inflammatory TNF and cytokine release from liver 7. TNF-alpha activates synovial fibroblasts + RANKL a. RANKL → osteoclast activation → bone erosion b. Synovial fibroblasts → cartilage breakdown c. Synovial fibroblasts → Prostaglandin + NO release from bone → Painful vasodilation Imaging Investigation ● X-ray affected joints ○ joint space narrowing ○ subchondral erosion History ○ ‘gull-wing’ ○ ankylosis Examination ○ subluxation/dislocations ● swollen DAS-28 Score https://nras.org.uk/resource/the-das28-s ● painful ● Pannus core/ ● Hot Bloods ● Rheumatoid factor ● Anti-CCP ● DO NOT DO ANAManagement 1. Short term corticosteroids 1. Physio a. Prednisolone b. Drive into remission 2. OT 3. Podiatry 2. DMARD 4. Social work a. disease modifying b. start early 5. Mental health c. Methotrexate i. sulfasalazine ii.leflunomide iii.hydroxychloroquine 3. NSAID + PPI a. Lowest dose possible b. Pain managementWhat is the most specific antigen serology test for RA? A. Rheumatoid factor B. ANA C. Anti-CCP D. ANCA E. Anti-mitochondrial What occurs in citrilliunation? A. arginine → citrulline B. citrulline → arginine C. Glargine → citrulline D. Citrulline → glargine E. citrulline cross links What occurs in citrilliunation? A. arginine → citrulline B. citrulline → arginine C. Glargine → citrulline D. Citrulline → glargine E. citrulline cross linksWhat causes osteoclast activation? A. TNF-alpha B. synovial cytoblasts C. ADAMTS-5 D. RANKL E. MMPOsteoarthritis Osteoarthritis = joint disease that results from breakdown of cartilage •Multifactorial •Demographics of primary osteoarthritis •In 50s, part of ageing process •By 65years old, 85% of people have evidence of OA – but not necessarily symptoms •Sex•In males, hip joint is commonly affected •In females, knees and hand joints are predominantly affected (DIPs, PIPs) •Can be secondary to joint trauma, congenital abnormality of joint, or obesityOsteoarthritis pathology Pathology of OA Wear. Flare. Repair. ▶ Wear due to overuse, obesity, or malalignment ▶ Flare (I.e. inflammation) ▶ Repair (suboptimal repair processes)Osteoarthritis Radiology ● Joint space narrowing ● Subchondral sclerosis ● Bone cysts ● Osteophytes Osteoarthritis Management Treatment (non-operative) Step-wise management of OA ● Patient education ● Exercises ● Physiotherapy ● Weight loss ● Paracetamol, oral ● Topical NSAIDs ● (Others – opioids, oral NSAIDs, COX-2 inhibitors) ● Intra-articular corticosteroid injections ● Surgery – IF non-operative interventions have been exhaustedMetabolic Bone DiseaseBone cells – Osteoprogenitor cells ❑ Locations: periosteum, endosteum, bone marrow ❑ Fate is determined by environment ❑ Strain (i.e. minimal movement in environment) osteoprogenitor 🡪 pre-osteoblasts 🡪 osteoblasts ❑ More movement osteoprogenitor 🡪 chondrocytes ❑ Lots of movement osteoprogenitor 🡪 fibroblasts Bone cells – Osteoblasts ❑ Origin – osteogenic cell 🡪 pre-osteoblast 🡪 osteoblast ❑ Description – mononuclear cells ❑ Location – periosteum, endosteum, bone surfaces (in their inactive form) ❑ 2 functions: ∙ Bone production by producing non-mineralised matrix o When stimulated by PTH, osteoblasts produce type 1 collagen and ALP (which dephosphorylates molecules, leading to the calcification of the matrix) o When stimulated by vitamin D, osteoblasts produce matrix proteins and ALP ∙ Osteoclast regulation by RANK/OPG axis Bone cells – Osteoblasts ❑ 2 functions: ∙ Osteoclast regulation by RANK/OPG axis ❑ When stimulated by PTH, osteoblasts release RANK-L, which binds to the RANK receptor on osteoclast precursors. This stimulates the production of active osteoclast, which increases bone resorption ❑ Osteoblasts produce OPG, which inhibits bone resorption by binding to RANK-L, thereby inactivating it Bone cells – Osteoblasts ❑ Osteoblasts last around 6 months then have 3 fates: ❑ Apoptosis ❑ Lining cells ❑ Osteocytes – osteoblasts become Entombed in the matrix they have produced Bone cells – Osteocytes ❑ Origin – former osteoblasts that have become ENTOMBED in the matrix they have produced ❑ Description – long cellular processes for signalling ❑ Function ❑ Maintain bone ❑ Regulate calcium and phosphate ❑ Produce RANKL and sclerostin ❑ Sclerostin inhibits osteoblast formation ❑ RANKL activates osteoclastRegulators of bone remodellingMechanotransduction – osteocytes react to stimuli Bone cells – Osteoclasts ❑ Origin – ❑ Description – large multinucleated cell ❑ Function ❑ Resorption of bone ❑ First they dissolve the inorganic hydroxyapatite ❑ Then they dissolve the organic matrix Drugs and bone metabolism ▶ Drugs that affect bone metabolism ▶ Other drugs active on the bone • Corticosteroids – cause adverse effects • Calcitonin • PTH analogues ▶ Drugs that cause therapeutic effects: • Strontium • Bisphosphonates • Oestrogens and analogues • Calcium salts • Vitamin DStages of Bone RemodellingDisorders of Bone Remodelling Disorder Stage of Bone Remodelling Osteoporosis Resorption > Formation Paget’s Disease of Bone Resorption and Formation increased Osteopetrosis Resorption decreasedCalcium homeostasis ▶ Bones ▶ Gut ▶ KidneysOsteoporosisOsteoporosis ▶ Condition of decreased bone density ▶ Resulted in increased bone fragility and increased risk of fragility fracturesPathophysiologyClassificationRisk FactorsPresentationInvestigationManagement - LifestyleManagement - PharmacologicalPharmacology - Side Effects Most Common Form of Osteoporosis? A. Hormone related B. Age related C. Malignancy related D. Obesity related E. None of the above What is the disease modifying treatment of osteoporosis? A. Calcium supplements B. Bisphosphonates C. Vitamin D D. Weight bearing exercises E. Diet and smoking cessation At what age does screening DEXA scan start? A. 55 B. 60 C. 65 D. 70 E. 75MCQ Part 2 - Catching Fire Which ONE of the following statements about OA is TRUE? A. OA can accurately be considered as a single disease B. Ageing and OA have similar effects on the extracellular matrix of cartilage C. The stimulation of the auto-immune response is a primary event in OA D. An increase in joint space is a characteristic feature of OA E. Increased cartilage hydration is an early event in osteoarthritisWhich ONE of the following statements about connective tissue diseases is FALSE? A. Dietary vitamin C is necessary for collagen hydroxylation and assembly B. Osteogenesis imperfecta arises from a deficiency of collagen type I C. Ehlers-Danlos syndrome can arise from several different genetic lesions D. Scurvy is a nutritional disease caused by a lack of vitamin D E. Marfan syndrome is caused by mutations in the gene encoding fibrillin IWhich of the following connective tissue disorders will cause "crumpled bones" in utero? A. Ehler's danlos Syndrome B. Marfan's syndrome C. Scurvy D. Osteogensis Imperfecta type 1 E. Osteogenesis Imperfecta type 2Which of the following connective tissue disorders will cause "crumpled bones" in utero? A. Ehler's danlos Syndrome B. Marfan's syndrome C. Scurvy D. Osteogensis Imperfecta type 1 E. Osteogenesis Imperfecta type 2 What condition is characterised by mutated fibrillin 1? A. Ehler's danlos Syndrome B. Marfan's syndrome C. Scurvy D. Osteogensis Imperfecta type 1 E. Osteogenesis Imperfecta type 2 What condition is characterised by mutated fibrillin 1? A. Ehler's danlos Syndrome B. Marfan's syndrome C. Scurvy D. Osteogensis Imperfecta type 1 E. Osteogenesis Imperfecta type 2Which of the following is/are correct? 1. scurvy results in the failure to secrete, synthesise or deposit collagen 2. scurvy can result in petechial haemorrhages 3. the most severe type of osteogenesis imperfecta is OI type II 4. due to the irregularity of its structure, most mutations in collagen are well tolerated A. 1, 2 B. 2, 3 C. 1, 2, 3 D. 2, 3, 4Which of the following is/are correct? 1. scurvy results in the failure to secrete, synthesise or deposit collagen 2. scurvy can result in petechial haemorrhages 3. the most severe type of osteogenesis imperfecta is OI type II 4. due to the irregularity of its structure, most mutations in collagen are well tolerated A. 1, 2 B. 2, 3 C. 1, 2, 3 D. 2, 3, 4 ▶ What Salter-Harris Classification is this fracture: A. Type I B. Type II C. Type III D. Type IV E. Type V Which of the following is least commonly a sign of NAI? A. Multiple fractures at different stages of healing B. Bruises on legs/ shins C. Femoral fracture in a non-mobilising child D. Bruises to cheeks E. Ripped frenulum What are the functions of these cells? Cell Function Osteoprogenit or cell 1. … Osteoblast 1. … 2. … Osteocyte 1. … 2. … Osteoclast 1. …What condition does osteopetrosis and Paget’s disease commonly co-occur with? A. Gout B. Dementia C. Atrial Fibrillation D. Anaemia Which of these statements about bone remodelling is true? A. Osteoclasts are derived from osteoprogenitor cells B. Sclerostin increases osteoblast activity C. PHT and mechanical stress encourage RANK secretion D. Both osteocytes and osteoblasts secrete RANK-L E. Only osteoclasts secrete RANK-L Which of these statements is FALSE? A. A T-score compares an individual’s bone density to an age-matched, healthy population B. Osteoporosis fractures are most common in bones with >50% trabecular bone C. Osteopetrosis is more commonly inherited than Paget’s disease D. Bone density begins to decrease around age 40 at a rate of 0.7% per year Which of these statements is FALSE? A. A T-score compares an individual’s bone density to an age-matched, healthy population B. Osteoporosis fractures are most common in bones with >50% trabecular bone C. Osteopetrosis is more commonly inherited than Paget’s disease D. Bone density begins to decrease around age 40 at a rate of 0.7% per yearWhich of these statements is TRUE? A. A parathyroid adenoma is a secondary cause of hyperparathyroidism B. Vitamin D is converted to its active form by the liver and the kidney C. Increased absorption of gut material is a cause of vitamin D deficiency D. Rickets is primarily found in adultsWhich of these statements is TRUE? A. A parathyroid adenoma is a secondary cause of hyperparathyroidism B. Vitamin D is converted to its active form by the liver and the kidney C. Increased absorption of gut material is a cause of vitamin D deficiency D. 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