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73 Cards in this Set
- Front
- Back
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Amyloidosis |
Broadrange of fibrillary proteins that stain pink on HE and green on Congo Red. Beta-2Microglobulin: often the culprit protein Causes; Infection, RA, MM, Genetic types, CRF. Manifestations CTS, Bone cyst, Pathological #, Arthritis, Renal calculi, Tendinous deposits. |
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AVN / Osteonecrosis |
AS IT TIPS C Stages; Necrosis, Inflamation, Repair (creeping substitution). Creeping substitution.
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Location of AVN FH and HH. |
Anterosuperolateral femoral head Central dome of humeral head |
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Double line AVN on T2 |
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AVN XR |
- Initialmottling - Sclerotic line at junction of deadbone 2nd to:o 1 Ca++ of dead marrow 2 Surrounding Osteopenia 3 Creeping substitution 4 Collapse of dead trabeculae 5 Subchondral fracture |
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Dystrophic Calcification |
Nserum calcium Occurs in damagedtissues - Dead or degenerative Depositsamorphous & non-crystalline Hydroxyapatite crystals may form:Mayprogress to Ossification Fat Necrosis, Infarcts, Thrombi CPPD, Chondrocalcinosis, Atherosclerosis |
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Metastatic Calcification |
Occursin N tissue whenever there is hyperCa++. Mechanism unknown. Immobilisationo High bone turnover o Malignancyo 1° HyperPTHo Renalfailure c 3° hyperPTH MilkAlkali Syndrome |
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CREST |
Calcinosis, Reynauds, Esophageal Dysmotility, Sclerodactyly and telangiectasis |
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Tumoural calcinosis |
Formation of large, painless, juxta-articularmasses often at pressure points. HAdeposition disease May have increased Pi, 1,25-Vit D Larger crystals in deposits, with more perfectstructure than normal bone |
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Charcot joints aetiology |
SadTulip Spina Bifida Alcoholism DM - No 1 cause Tabesdorsalis - Syringomyelia (UL) Leprosy (UL) Cong Indifferenceto pain Peripheralnerve lesions: drugs, etoh, vit b12 deficiency |
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Charcot joints Defn. |
Chronicprogressive degenerative arthropathy of vertebral and appendicular joints as aresult of disturbance of normal sensory innervation |
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Charcot joints Stages. |
Eichenholz I: Dissolution = hyperaemia, demineralisation NWB, castwhen swelling decreases. II: Coalescence = Fragmentation of bone. PWB –TCC III – Consolidation = healing, mayulcerate, Brace |
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Haemophilia |
Haemophilia– X-linked, factor VIII, different severities. Rx give factors VIII. Haematoma ensure Factor VIII 30% Haemarthrosis + ST surgery FactorVIII 50% Haemarthrosis + Bone Surgery, Need Factor VIII levels 100% for 1/52 post op |
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Haemophilic joint XR |
Widening of distal femur Squaring of femoral condyles Osteopaenia #s |
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Christmas dis |
Christmas dis – X-linked, Factor IX. Clinically identical to Haemophillia, APTT increased, PT normal. Give factor IX. |
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Von Willebrand |
platelets can’t stick to endothelium, prolonged bleeding time, platelets OK. Rx ç Cryoprecipitate or DDAVP |
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Hyperparathyroidism + Brown’s Tumours |
disorder of metabolism secondary to increasd PTH. Increased PTH lead to increas Ca, decre PO4 & increased bone turnover. Stones, Bones, Abdominal Groans, Psychic Moans increased Overall Bone Turnover OsteitisFibrosa Cystica Middle age, old women. Ortho
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Hyperparathyroidism causes |
Primary, Excessive secretion PTH by Parathyroid. (usually adenoma) Secondary, Hypocalcaemia leads to incre level PTH leads to hypertrophy parathyroids, HPT. Tertiary, CRF, and Vit D deficiency. |
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Investigations Hyperparathyroidism |
Increase Ca decrease Pi increase PTH increase AlkPhos increase Urate XR 10% Have Skeletal Manifestations |
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Boney erosions Hyperparathyroidism |
Outer 1cmof clavicle Prox humerus Pubic symphysis SIJ Salt + Pepper Skull Radial sided Phalangeal Erosions Codfish Vertebrae: Biconcave vertebraedue to compression #s Chondrocalcinosis |
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Brown’s Tumours |
Brownishtumour like-masses in bone Highly Vascular May be seen in renal disease +2nd PTH Composed of:
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Hyperphosphatasia |
Autosomal Recessive Subperiostealbone formation: loss of corticomedullary differentiation Due toloss of OPG genes à RANKLactivity + Osteoclastic activity present<2yrs old Multiple #s Deaf Rx Anti-resorptive, Recombinant OPG Bowed/Widened long bonesà disfiguring |
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Gout |
Inbornerror of purine metabolism characterised by hyperuricaemia and recurrentattacks of acute arthritis. Dx confirmed by Monosodium Urate in the neutrophils in the synovial fluid Other features:
Negatively birefringent under polarised light |
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Gout pathology |
Prerequisiteis Hyperuricaemia at some stage Oxidation of Purine bases Via Xanthine Oxidase in to Uric acid. Excreted in Urine and GIT. Primary Gout
Develop Monosodium Urate in synovial and released into joint. Precipitates. crystals cause inflamm. |
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Gout XR |
Punched out lytic appearance Sub-articulartypically medial side 1st MT Overhanging sclerotic margin Periarticular erosions at site of capsular attachments |
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Gout Mx |
Cochicine. Inhibits Neutro migration. 1mg initially then 0.5mg q2h Max (6mg) Indomethacin 50mg q6h. Steriods. Prophylaxis. LOW, hydration, precipitant avoidance, Probenecid, Allopurinol ( XanthineOxidase Inhibitor), |
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Pseudogout-CPPD |
Pseudogout is an inflammatory arthritis caused by Ca++Pyrophosphate Dihydrate crystals in the joint. PARTIALLYPOSITIVE PURPLE” rhomboidal crystals, weakly +vely birefringent. Deposited in, Joint capsule, Articular Cartilage, Fibrocartilage (Menisci) |
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Causes CPPD |
“WHIPADOG” Wilson’s disease Hypothyroidism, Haemochromatosis, Hyperparathyroidism,Hypophosphatasia, Hypomagnesia Idiopathic (familial) PerniciousAnaemia DM Onchronosis Gout – joint traumatised. |
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CPPD NHx |
AsymptomaticChondrocalcinosis Rx Rest, treat cause, NSAID, Colchicine (sev) Pseudogout = acute synovitis, usually large joints ChronicCPPD Arthropathy = chronic, degenerative. pseudo OA, polyarticular disease. |
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Reiter’s Syndrome |
Reactivearthritis with classic history of sacroiliitis, iritis and urethritis Affects men. 20-40 usually follows episode of non-gonococcal urethritis, maybe dysentery. HLA-B27 pos in 80%. Polyarthritisis asymmetrical and involves LL. Enthesopathy (TA/PF) pustulardermatitis of the feet. Cardiac problems with AV block Treatment of the inciting infection. NSAIDs Can go on for some time. |
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Rheumatoid Arthritis |
Chronic, systemic, autoimmune inflammatory disease of unknown Aetiology RhF –heterogenous mainly IgM (80% +ve) Synovitis, T cell in origin, but synovial fluid rich in Neutrophils RF positive in 80% HLADR4 - 70 % positive in RA |
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Rheumatoid Arthritis diagnostic criteria |
Dx Crtieria 1987 AmCollege of Rheumatology Need 4/7 MAX RANS 1. MorningStiffness 2. Arthritisof 3 areas > 6/52 3. X-raychanges 4. Rh factor 5. Arthritisof Hand > 6/52 6. Nodules 7. SymmetricArthritis > 6/52 |
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RA pathology |
Triggernot identified Exogenous agent alters Fc part of IgG to become antigenic Helper T cells activate B Cellsto become plasma cells PlasmaCells produce RF's (IgM) directed against IgG. Synovium acts as lymphoid organ AB-Antigen complexes formed 2° destructive inflam cascade(Lymphokines, IL-1) |
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Homocystinuria |
Inborn error ofmetabolism AR- Enzyme deficiency. Accumulate - Methionine - Homocystine Marfanoid habitus. Inferior lens dislocation Tight joint Osteopenia Thromboembolic, Retard Bowing tibia Erlenmeyer flask |
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Heterotopic Ossification |
Extra-Skeletal bone formation in periarticulartissues Brooker classification. 1 - 4. RF; hip, male,CNS, previous HO, DISH ,AS, #, Haematoma, Infection, hypertrophic OA. Mesenchymalcells diff in o'blasts, Osteoid, mineralisation. Rx Early Resection = Recurrence. Wait 18mths. Until fully mature, no progression cold on BS. Prophylaxis. |
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MyositisOssificans Traumatica (Circumscripta) |
PathologicalBone formation in soft tissues. Occurs proximally. Usually single or multiple traumatic event. Difficult to differenate from sarcoma. Ossification from peripherally. Avoid OT. Lesion can spontaneously regress. OT if NV issue, decrease ROM. |
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Myositis Ossificans Progressiva |
OSSIFICATIONOF CONNECTIVE TISSUE. UsuallyAffects Muscles and Ligs of Back and Major joints Rare Symmetrical. Die from restrictive lung disease. |
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Osteoarthritis |
PrimaryOA: Idiopathic Secondary OA: Traumatic, Inflammatory, Metabolic, endocrine, Neuropathic, developmental. |
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Change in Cartilage OA |
Loss of cell height, cellularity, decrease hydration lead to increasedstiffness. Telomeres Shorten Increase Chondroitin + decrease Collagen. Stages,
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Osteochondroses |
Sclerosis, fragmentation ofossification at time of greatest growth, looks like AVN. Occurs at time of greatest growth. Crushing= Kohler’s (Navicular), Freiberg, Panner Pulling= Osgood Schlatters Splitting = OCD Knee/Ankle/Hip Features on XR
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Osteogenesis Imperfecta |
Heterogenous group of genetic disorders which result in increased bonefragility. 90%genetic mutation COL 1 Gene Ch 17 encode for type 1 pro-collagen. Unable to form helix and cross link. OI Type I: quantitative defect in AMOUNTof collagen OI Type II – IV: qualitative defectin collagen. Bone thin cortices, little lamellar bone, usually woven, poor H system. Abnormal Endochondral and Intramembranous |
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OI Classification |
Sillence1981 bad2 are AR & mild 2 are AD Mnemonic:Mike's Little Squashed Mate Type 1 : Mild/Tarda – 70% Type 2: Leathal 2% Type 3: Severe/Classic 20% Type 4: Moderate |
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OI clinical features |
Triangular face Brownish translucent teeth Blue sclerae Genu Valgum Grossly Osteopenic Narrowdiaphyses +Broadened Metaphysis Trefoil shape Coxa Vara Protrusio Acetabuli Short Scoliosis Pectus Carinatum/Excavatum Ligamentouslaxity (Type 1 collagen) |
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OI treatment |
Rx Mutli D team (paeds, endocrine, genetic). Bisphosphonates decrease # and pain. Manage # and prevent deformity. #, ambulate and WB! If treat use IMN. |
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Osteolysis |
Lossof bone around the prosthesis due to wear debris stimulation of macrophages orinfection. Wear leads to particulate debris. Macrophages phagocytose wear particles and activate osteoclast. Prosthesis micromotion leads to increased wear Increased hydrostatic presure leads to increased effective joint space. |
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Harris signs loosening |
Subsidence Mantle # Line > 1mm |
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Particle effect |
Local (UHMWPE)
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Biological effects of particles |
Small enough phagocytized <10um Ti is less irritative than CoCrMo Butis worse bc macrophages don’t die whereas CoCr is toxic to the macrophages andthey die so CoCr has less osteolysis effects |
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Engh classification Uncemented THR |
I stable bony ingrowth: canhave ‘spot welds’ II stable fibrous ingrowth III unstable fibrous ingrowth |
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Osteomalacia |
A metabolic bone disease where defectivemineralization results in a large amount or unmineralized osteoid.
malaise +fatigable bone pain+ tenderness Proximalmuscle weakness |
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Osteomalacia Risk factors |
vitamin-D deficient diets malabsorption e.g. celiac disease, IBD renal osteodystrophy (Phosphate leaks) hypophosphatemia chronicalcoholism tumors (tumor-induced osteomalacia, see below) drugs VitaminD Dependent Rickets 5 Major Categories
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Osteomalacia Bloods |
Low or low-N Ca++ Low PO4- Ca++ /PO4 index low Ca++ x PO4 < 2.4 (N> 3) --> diagnostic High ALP – high turnover PTH N or high Low [25-D3] |
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Osteomalacia xr |
Changes less evident. indistinct trabeculae (ground glass), bowing, #. Bone resorption rad border middle finger. Three characteristic features
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Codfish Vertebrae |
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Looser line |
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Osteoporosis |
Osteoporosis is ischaracterized by a decrease in the apparent density of the normally mineralizedmatrix Definition: BMD<2.5 x STD deviations below that of young adult reference population RF age, genetics, Environmental, Chronic disease, hormones. |
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Osteoporosis Classifications |
Primary
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Osteoporosis Ix |
Bloods normal - primary OP DEXA FBE& diff ESR ALP(increased turnover) Protein,Albumin (malnutrition) Ca (lowlevels may be stripping bone), PO4- Creat(Renal failure) Glucose –diabetes 25-hydroxyvitamin D, 1,25(OH)2 vit D (deficiencies) thyroid fxn tests (Hyperthyroid) sex steroids (menopause) PTH(hyperparathyroidism) Bence Jones protein |
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Osteoporosis Rx |
HRT increases BMD by 4-7% Bisphosponates increases BMD by 4-9% Exercise 1-3% Ca 1500mg/day Vit D 400 Int units/d~ Active |
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Paget’s Disease |
Idiopathic focaldisorder of skeletal remodelling AD, viral inclusion bodies in nuclei and cytoplasmof giant cells ? caused by Paramyxovirus Polyostotic or monostotic Abnormalosteoclasts make large holes Osteoblastshave normal response, new bone laid (WOVEN) |
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Pagets Histology |
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Pagets phases |
Active
Bone deformity persists, turnover returns to normals. Bone is enlarged, brittle, sclerotic, deformed. |
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Pagets - Orthopaedic deformity |
- Coxa vara - Protrusioacetabuli - Femoralbowing - Increasesize & abN shape of bones o Thicker cortex o Bow along stress lines o Femora bow ant & lat o Tibia bow ant = Saber Shin - Skull enlargement Hats don't fit - ThoracicKyphosis Arthrokatadysis |
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Pagets complications |
CVS - High-outputcardiac failure Malignant change - OS or Chondrosarcomaor MFH MetabolicAbnormalities CNS - Neural impingement. Fractures on convex side. |
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THR in Paget’s |
Pro op Want ALP < 700 Airway issues with neck ext. CVS issue with High output failure Intra op Bleed a lot correct deformity seating and reaming difficult due to bone Cement implants (helps with stasis) Protrusio cages + offset liners Post op Higherrate of loosening Higher HO rate 23-50% use indocid |
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Causes of periosteal reaction |
- Trauma - Tumour (including lung) - Infection - Infarction |
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Peripheral Neuropathy |
DINTMII Developmental - HSMN, Freidrich Inflam - RA, SLE, Guillain Barre Neoplastic - Pareneo, sarcoid Traumatic - compression neuropathies Metabolic - Alco, DM, Amyloid, B12 folate. Infective - Polio, leprosy, herpes, HIV Iatrogenic - Drugs, Cipro, Chemo. |
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Renal Osteodystrophy |
Rickets/Osteomalaciaand 2°Hyperparathyroidism due to chronic glomerular failure. Decrease filtration leads to increase phosphate Plus Decreased tubular mass laeds to decrease 1,25 vit D synthesis, decreased Ca absorbed from filtered urine, lead t odecrease Ca2+ and secondary hyperparathyroidism. |
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Renal Osteodystrophy features |
Osteomalacia etc. SUFE Patchy osteosclerosis Periosteal bone formation in MT and pelvis. Rugger jersey spine. Browns tumours Ectopic calcifications. |
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Rickets |
defect in mineralization of osteoid matrixcaused by inadequate Ca + P. Brittle bones with physeal widening and cupping. Long bone bowing Rachitic rosary, costal cartilage enlargement. Looser zones |
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Rickets causes |
Nutritional - decreased Vit D. Vit D resistant rickets (familial / X linked) Vit D Dependant rickets. type 1 and 2. Drug induced. Fanconi syndrome. |
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Sarcoidosis |
Young patients. Non caseating granuloma. 5% have bone involvement Typically small bones of hands/feet: permeative/lytic lesions withcystic appearance |
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Synovial Chondromatosis |
Proliferativesynovial disease that is associated with cartilaginous METAPLASIA resulting inmultiple intra-articular loose bodies. Monoarticular Knee most common. Hip, elbow, ankle. Synovectomyand loose body resection |
