Download - Minarcik robbins 2013_ch26-ortho
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BONE
JOINT
SOFT TISSUE
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Modeling/RE-modeling
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CELLS of BONE• OSTEOPROGENITOR (“STEM”)(TGFβ)• OSTEOBLASTS (surface of spicule), under
control of calcitonin to take blood calcium and put it into bone.
• OSTEOCYTES (are osteoblasts which are now completely surrounded by bone)
• OSTEOCLASTS (macrophage lineage), under control of PTH to chew up the calcium of bone and put it into blood
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Proteins (organic) of BONE• Type 1 (TYPE [B]ONE) collagen (90%)• Cell adhesion proteins, i.e. CAMs: Osteopontin,
fibronectin, thrombospondin• Calcium-binding proteins: Osteonectin, sialoprotein• Proteins involved in mineralization: Osteocalcin • Enzymes: Collagenase, Alk. Phos.• Growth factors
– IGF-1, TGF-β, PDGF
• Cytokines– Prostaglandins, IL-1, IL-6, RANKL
• Proteins Concentrated from Serum– β2 –microglobulin Albumin– IGF, insulin-like growth factor– TGF, transforming growth factor– PDGF, platelet-derived growth factor– IL, interleukin– RANKL, RANK ligand
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Minerals (IN-organic) of BONEHYDROXY-APATITE
Ca5(PO4)3(OH) Ca10(PO4)6(OH)2
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ADJECTIVES of BONE•Compact
– Dense– Cortical
•Spongy– Cancellous– Membranous– Endosteal– Spicular
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Woven vs. “Lamellar”
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-BLASTS/-CLASTS
Ca++ PTH
Ca++ Calcitonin
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BONE DISEASES• 1) MALFORMATIONS AND DISEASES CAUSED BY DEFECTS IN NUCLEAR PROTEINS
AND TRANSCRIPTION FACTORS, polydactyly, syndactyly, absence of a bone• 2) DISEASES CAUSED BY DEFECTS IN HORMONES AND SIGNAL TRANSDUCTION
MECHANISMS, achondroplasia, thanatophoria• 3) DISEASES ASSOCIATED WITH DEFECTS IN EXTRACELLULAR STRUCTURAL
PROTEINS– Type 1 Collagen Diseases (Osteogenesis Imperfecta)– Types 2, 10, and 11 Collagen Diseases
• 4) DISEASES ASSOCIATED WITH DEFECTS IN FOLDING AND DEGRADATION OF MACROMOLECULES
– Mucopolysaccharidoses• 5) DISEASES ASSOCIATED WITH DEFECTS IN METABOLIC PATHWAYS (ENZYMES,
ION CHANNELS, AND TRANSPORTERS)– Osteopetrosis
• 6) DISEASES ASSOCIATED WITH DECREASED BONE MASS– Osteoporosis
• 7) DISEASES CAUSED BY OSTEOCLAST DYSFUNCTION– Paget Disease (Osteitis Deformans)
• 8) DISEASES ASSOCIATED WITH ABNORMAL MINERAL (Ca++) HOMEOSTASIS– Ricketts and Osteomalacia– Hyperparathyroidism– Renal Osteodystrophy
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1) MALFORMATIONS AND DISEASES CAUSED BY DEFECTS IN NUCLEAR PROTEINS AND “TRANSCRIPTION FACTORS”
proteinDNAmRNA
• Congenital absence of a, usually single, bone: phalanx, rib, clavicle
• Supernumerary digit (polydactyly)
• Syndactyly
• CRANIORACHISCHISIS
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2) DISEASES CAUSED BY DEFECTS IN HORMONES AND
SIGNAL TRANSDUCTION MECHANISMS
• Achondroplasia, dwarf (non-lethal)• Thanatophoria, dwarf (lethal, FGF-3
mutations)
• a point mutation (usually Arg for Gly375) in the gene that codes for FGF receptor 3 (FGFR3), which is located on the short arm of chromosome 4. In the normal growth plate, activation of FGFR3 inhibits cartilage proliferation, hence the term “achondroplastic”;
• A MUTATION causes FGFR3 to be constantly activated.
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Short arms and extra folds of skin
Achondroplastic “dwarf” Thanatophoric “dwarf”, often lethal
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3) DISEASES ASSOCIATED WITH DEFECTS IN EXTRACELLULAR
STRUCTURAL PROTEINS• OSTEOGENESIS IMPERFECTA TYPES• (“Brittle” bone disease, too LITTLE bone),
BLUE sclerae• Mutations in genes which code for the
alpha-1 and alpha-2 chains of COLLAGEN 1• Mutations of COLLAGEN 2,10, 11 manifest
themselves as CARTILAGE diseases, ranging from joint cartilage destruction to fatal sequelae
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Osteogenesis Imperfecta
BLUE SCLERA
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4) DISEASES ASSOCIATED WITH DEFECTS IN FOLDING AND
DEGRADATION OF MACROMOLECULES(glycosaminoglycans)
• MUCOPOLYSACCHARIDOSIS (one of MANY lysosome storage diseases)
• DECREASES in ENZYMES which degrade:– DERMATAN
– HEPARAN
– KERATAN
• Chiefly CARTILAGE disorders: short, chest wall, malformed bones
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MUCOPOLYSACCHARIDOSES
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5) DISEASES ASSOCIATED WITH DEFECTS IN METABOLIC
PATHWAYS (ENZYMES, ION CHANNELS, AND TRANSPORTERS)
• OSTEOPETROSIS, 4 types
• One common one has a CARBONIC
ANHYDRASE deficiency, i.e., ↓ acid
• DECREASED osteoclast resorption
• “MARBLE” bone, increased bone, brittle, sclerotic bone
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OSTEOPETROSIS
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6) DISEASES ASSOCIATED WITH DECREASED BONE MASS
•OSTEOPOROSIS• “PEAK” bone mass is early adulthood• Normal decline, slow• Osteoporosis is accelerated bone loss• Factors:
– AGE– Physical activity– Estrogen withdrawal (menopause)– Nutrition (Ca++)– Genetics
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Categories of Generalized OsteoporosisPrimary
Postmenopausal Idiopathic
Senile
Secondary
Endocrine disorders Rheumatologic disease
Hyperparathyroidism Drugs
Hypo-hyperthyroidism Anticoagulants
Hypogonadism Chemotherapy
Pituitary tumors Corticosteroids
Diabetes, type 1 Anticonvulsants
Addison disease Alcohol
Neoplasia MiscellaneousMultiple myeloma Osteogenesis imperfecta
Carcinomatosis Immobilization
Gastrointestinal Pulmonary disease
Malnutrition, Malbs., Hepatic Insuf., Vit C,D Homocystinuria
Anemia
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OSTEOPOROSIS
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7) DISEASES CAUSED BY OSTEOCLAST DYSFUNCTION
Paget Disease (Osteitis Deformans)
• Matrix madness, Osteoblasts/-cytes gone wild• THREE PHASES:
– 1) Increased osteoclast resorption– 2) Increased “hectic” bone formation (osteoblasts)– 3) Osteosclerosis
• ELEVATED ALKALINE-PHOSPHATASE • ELEVATED urine HYDROXYPROLINE
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PAGET’s DISEASE (of BONE)
85% MONOSTOTIC, WHOLE BONE
15% POLY-OSTOTIC (skull, pelvis)
“JIGSAW”, NOT LAMINAR, BONE
CLINICAL: PAIN!!!
(MICROFRACTURES)
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PAGET’s DISEASE
NON-Lamellar bone
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8) DISEASES ASSOCIATED WITH ABNORMAL MINERAL
HOMEOSTASIS– Ricketts and Osteo”malacia”
• VITAMIN D deficiency/dysfunction– Hyperparathyroidism, PRIMARY (PTH ADENOMA)
• ENTIRE SKELETON• OSTEITIS FIBROSIS CYSTICA (von Recklinghausen’s
disease (of bone)• “BROWN”* TUMOR
– Hyperparathyroidism, SECONDARY (RENAL) (NOT AS SEVERE AS 1º)
– Renal Osteodystrophy = ANY bone disorder due to chronic renal disease
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PRIMARY HYPERPARATHYROIDISM
OSTEITIS FIBROSA CYSTICA
“BROWN” “TUMOR”
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RENAL OSTEODYSTROPHY
• PHOSPHATE RETENTION
• HYPOPHOSPHATEMIA
• HYPOCALCEMIA
• INCREASED PTH
• INCREASED OSTEOCLASTS
• METABOLIC ACIDOSIS release of HYDROXYAPATITES from matrix
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FRACTURES
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FRACTURES, adjectives
• Complete, incomplete
• Closed, open (communicating)
• Communited (splintered, “greenstick”)
• Displaced (NON-aligned)
• PATHOGENIC, (non-traumatic, 2º to other disease, often metastases)
• “STRESS” fracture
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FRACTURES• THREE PHASES
– HEMATOMA, minutes days PDGF, TGF-β, FGF– SOFT CALLUS (“PRO”-CALLUS), ~1 week– HARD CALLUS (BONY CALLUS), several weeks
• COMPLICATIONS– PSEUDARTHROSIS (non-union)– INFECTION (especially OPEN [communicating]
fractures)
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FRACTURES
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OSTEONECROSIS• Also called AVASCULAR necrosis• Also called ASEPTIC necrosis
• CAUSE: ISCHEMIA– Trauma– Steroids– Thrombus/Embolism– Vessel injury, e.g., radiation– INCREASED intra-osseous pressurevascular
compression– Venous hypertension too
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OSTEONECROSISDisorders Associated with Osteonecrosis
Idiopathic Pregnancy
Trauma Gaucher disease
Corticosteroid administration
Sickle cell and other anemias
Infection Alcohol abuseDysbarism Chronic pancreatitis
Radiation therapy Tumors
Connective tissue disorders
Epiphyseal disorders
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OSTEONECROSIS
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OSTEONECROSIS
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OSTEOMYELITIS• Pyogenic: Staph, E. coli, Pseudom, Kleb,
Salmonella
– Hematogenous
– Contiguous, e.g., from a nearby joint
– Direct implantation
• TB
• Syphilis
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OSTEOMYELITIS• DX: X-ray, Bone scan
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OSTEOMYELITIS• DX: Histology
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OSTEOMYELITIS• COMPLICATIONS
– Subperiosteal abscess
– Draining sinus
– Joint involvement
• SEQUESTRUM (dead bone)
vs.
• INVOLUCRUM (new bone)
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OSTEOMYELITIS• Tuberculous
– Usually blood borne– TB of spine is known as POTTS
disease
• Syphilis– CONGENITAL– TERTIARY, “SABRE” shins
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POTT’s DISEASE
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SABER SHINS
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Classification of Primary Tumors Involving BonesHistologic Type Benign MalignantHematopoietic (40%) Myeloma
Malignant lymphomaChondrogenic (22%) Osteochondroma Chondrosarcoma
Chondroma Dedifferentiated chondrosarcoma
Chondroblastoma Mesenchymal chondrosarcoma
Chondromyxoid fibroma
Osteogenic (19%) Osteoid osteoma Osteosarcoma
OsteoblastomaUnknown origin (10%) Giant cell tumor tumor
Giant cell tumorAdamantinoma
Histiocytic origin Fibrous histiocytoma Malignant fibrous histiocytoma
Fibrogenic Metaphyseal fibrous defect (fibroma) Desmoplastic fibroma
FibrosarcomaNotochordal ChordomaVascular Hemangioma Hemangioendothelioma
HemangiopericytomaLipogenic Lipoma LiposarcomaNeurogenic Neurilemmoma
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BONE TUMORS• BONE
• CARTILAGE
• FIBROUS
• MISC.–Ewing’s “sarcoma”
–Giant Cell Tumor
–METASTASES
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BONE- BONE TUMORS
• OSTEOMA
• OSTEOID OSTEOMA (nidus)
• OSTEOBLASTOMA
• OSTEOSARCOMA (OSTEOGENIC SARCOMA)
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OSTEOMA• SOLITARY
• MIDDLE AGE
• FROM SUBPERIOSTEAL or ENDOSTEAL surfaces
• SKULL, FACE, most common
• Totally BENIGN
• To be distinguished from REACTIVE BONE, (can be difficult)
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Why am I not showing you HISTOLOGY?
FRONTAL SINUS
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OSTEOID OSTEOMA• At least 2 cm in diameter
• Teens, twenties, APPENDICULAR skeleton
• M>>F
• PAINFUL
• Has a NIDUS• Responds to aspirin
• Induces a MARKED bony reaction
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NIDUS
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OSTEOBLASTOMA• AXIAL SKELETON, i.e., SPINE
• NO nidus
• NO bony reaction
• NOT relieved by aspirin
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OSTEOSARCOMA(OSTEOGENIC SARCOMA)
LATE TEENSKNEESMETAPHYSESPAINFUL!!!
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TYPES of OSTEOSARCOMAS• The anatomic portion of the bone from which they
arise (intramedullary, intracortical, or surface) • Degree of differentiation • Multicentricity (synchronous, metachronous[NOT
synchronous]) • Primary (pre-existing bone is unremarkable) or
secondary (e.g., osteosarcoma associated with pre-existing disorders such as benign tumors, Paget disease, bone infarcts, previous irradiation)
• Histologic variants (osteoblastic, chondroblastic, fibroblastic, telangiectatic, small cell, and giant cell)
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The most common subtype is osteosarcoma that arises in the metaphysis of long bones; is primary, solitary, intramedullary, and poorly differentiated; and produces a predominantly bony matrix
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BONE- CARTILAGE TUMORS
• OSTEOCHONDROMA (EXOSTOSIS)
• CHONDROMA
• CHONDROBLASTOMA
• CHONDROMYXOID FIBROMA
• CHONDROSARCOMA
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OSTEOCHONDROMA (EXOSTOSIS)
• Common, Cartilage AND Bone present
• Often MULTIPLE as a hereditary syndrome
• M>>>F
• PELVIS, SCAPULAE, RIBS
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CHONDROMA• Chondroma vs. EN-chondroma• PURE Hyaline Cartilage• MULTIPLE enchondromas = Ollier’s dis.• Maffucci Synd. if hemangiomas present
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CHONDROBLASTOMA• RARE, in teenagers
• M>>F
• KNEES, usually
• Epiphyses
• MUCH LESS matrix than a chondroma
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CHONDROMYXOID FIBROMA• RAREST of all• TEENS, MALES• “MYXOID” concept• “ATYPIA”
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CHONDROSARCOMA• ANATOMY
– INTRAMEDULLARY– JUXTACORTICAL
• HISTOLOGY– CONVENTIONAL
• HYALINE• MYXOID
– CLEAR– DE-DIFFERENTIATED– MESENCHYMAL
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CHONDROSARCOMA
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BONE- FIBROUS TUMORS
• FIBROUS CORTICAL DEFECT/NON-OSSIFYING FIBROMA
• FIBROUS DYSPLASIA
• FIBROSARCOMA/MALIGNANT FIBROUS HISTIOCYTOMA
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FIBROUS CORTICAL DEFECT• COMMON, usually LESS
THAN 1 CM
• CHILDREN >2
• IF MORE THAN 5-6 CM, they are then called NON-OSSIFYING FIBROMA
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FIBROUS “DYSPLASIA”• BENIGN TUMOR
• THREE TYPES– SINGLE BONE (70%)
– POLY-OSTOTIC (27%)
– POLY-OSTOTIC (3%) with café-au-lait and endocrine disorders, especially precocious puberty
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1) CURVED thin spicules
2) LACK of osteoblastic “rimming”
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FIBROSARCOMA/MFH
• METAPHYSES of LONG BONES
• PELVIC FLAT BONES
• LYTIC
• FRACTURES
• OF COURSE, SARCOMATOUS METASTASIS
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FIBROSARCOMA/MFH
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MISC. TUMORS of BONE
• EWING sarcoma/PNET
(Primitive NeuroEctodermal
Tumor)
• GIANT CELL TUMOR
• METASTASES
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EWING/PNET• SAME TUMOR
• SMALL ROUND BLUE CELL TUMOR
• NEUROENDOCRINE CELL ORIGIN
• CHROMOSOME TRANSLOCATION 11&22
• SECOND most COMMON bone malignancy in CHILDREN
• ARISE IN MEDULLARY CAVITY of BONE
• LOOK LIKE LYMPHOMA
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GCT (Giant Cell Tumor), BONE
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METASTASESMALE: PROSTATEFEMALE: BREASTRENAL, THYROID also seek bone early also
LYTIC?BLASTIC?
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SYNOVIAL JOINTS
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TWO KINDS of cells form the synovial intima
• 1) fibroblasts– Hyaluronin
– Lubricin
• 2) macrophagesThe SUB-intima is loose CT or fat
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JOINT DISEASES•“ARTHRITIS”
–DEGENERATIVE (OSTEOARTHRITIS)
–RHEUMATOID– “JUVENILE” RHEUMATOID– NON-INFECTIOUS: Ankylosing Spond.,
Reactive, Psoriasis, IBD– INFECTIOUS: Supp., TB, Lyme, Viral– GOUT (URATE)– PSEUDOGOUT (PYROPHOSPHATE)
• Tumors (all are of synovium)– Ganglion (Synovial Cyst), non-neoplastic– Giant Cell Tumor (Pigmented VilloNodular Synovitis[PVNS]), benign– Synovial Sarcoma, malignant
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“DEGENERATIVE” ARTHRITISaka, “OSTEO”ARTHRITIS
• Etiology/Risk Factors: Age, Trauma, Genes
• Pathogenesis: Progressive EROSION of articular cartilage
• Morphology: X-Ray, “eburnation”, “joint mice”, osteophytes
• Clinical Expression: PAIN, Limitation of motion
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HEBERDEN’S NODES
DIP, NOT MP or PIP
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RHEUMATOID ARTHRITIS Rheumatoid arthritis (RA) is a
chronic systemic inflammatory disorder that may affect many tissues and organs—skin, blood vessels, heart, lungs, and muscles—but principally attacks the joints, producing a nonsuppurative proliferative and inflammatory synovitis that often progresses to destruction of the articular cartilage and ankylosis of the joints.
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TWO KINDS of cells form the synovial intima
• 1) fibroblasts– Hyaluronin
– Lubricin
• 2) macrophagesThe SUB-intima is loose CT or fat
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RHEUMATOID ARTHRITIS• Etiology/Risk Factors: Autoimmune
• Pathogenesis: Progressive SYNOVITIS
• Morphology: Synovial lymphocytes, macrophages, plasma cells, neutrophils,
osteoclasts, “pannus”, hyperemia, rheumatoid “nodules”, vasculitis
• Clinical Expression: PAIN, Limitation of motion, malaise, fatigue, rheumatoid factor IgMIgG-Fc,
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The rheumatoid “nodule” shows “palisading” fibroblasts
HANDSWRISTELBOWS
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DIAGNOSIS• CLINICAL FEATURES (1% of population F>>M)
– MORNING STIFFNESS, MEAN AGE 45 YRS– ARTHRITIS in MORE THAN 3 JOINT AREAS– “TYPICAL” hand findings, MP ULNAR deviation– SYMMETRIC ARTHRITIS– SERUM RHEUMATOID FACTOR– “TYPICAL” X-RAY findings
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“JUVENILE” Rheumatoid Arthritis
• Begins BEFORE age 16, by definition
• Generally LARGER joints than RA
• Often POSITIVE ANA
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“SERONEGATIVE” ARTHRITIDES• ANKYLOSING SPONDYLITIS (aka,
“rheumatoid” spondylitis, or Marie-Strumpell Disease [HLA-B27] (M>>F)
• “REACTIVE” ARTHRITIS (FOLLOWS GU or GI INFECTIONS)– REITER SYDROME (urethral &
conjunctival inflammation too) [HLA-B27]
– Arthritis associated with IBD
• PSORIATIC ARTHRITIS [HLA-B27]
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Ankylosing Spondylitis
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INFECTIOUS ARTHRITIS• From OSTEOMYELITIS• USUALLY SUPPURATIVE
• GC, staph, strep, H. flu, E. coli, (Salmonella in sicklers)
• 4 cardinal signs, fever,
leukocytosis, ESR
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INFECTIOUS ARTHRITIS• TB• LYME Disease, i.e., Borrelia
burgdorferi, from Ixodes ticks• VIRAL
–Parvovirus B19–Rubella–Hepatitis C
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GOUT• Endpoint of HYPERURICEMIA from
ANY cause resulting in JOINT deposition of monosodium urate crystals (TOPHI)– ACUTE– CHRONIC
• 10% of population has hyperuricemia (>7 mg/dl), but only 1/20 of these has gout
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Classification of GoutClinical Category Metabolic Defect
Primary Gout (90% of cases)
Enzyme defects unknown (85%–90% of primary gout)
■ Overproduction of uric acid
Normal excretion (majority)
Increased excretion (minority)
Underexcretion of uric acid with normal production
Known enzyme defects—e.g., partial HGPRT deficiency (rare)
■ Overproduction of uric acid
Secondary Gout (10% of cases)
Associated with increased nucleic acid turnover—e.g., leukemias
■ Overproduction of uric acid with increased urinary excretion
Chronic renal disease ■ Reduced excretion of uric acid with normal production
Inborn errors of metabolism—e.g., complete HGPRT deficiency (Lesch-Nyhan syndrome)
■ Overproduction of uric acid with increased urinary excretion
HGPRT, hypoxanthine guanine phosphoribosyl transferase.
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HYPERURICEMIA GOUT• Age of the individual and duration of the
hyperuricemia are factors. Gout rarely appears before 20 to 30 years of hyperuricemia. M>>F
• Genetic predisposition is another factor. In addition to the well-defined X-linked abnormalities of HGPRT, primary gout follows multifactorial inheritance and runs in families.
• Heavy alcohol consumption predisposes to attacks of gouty arthritis.
• Obesity increases the risk of asymptomatic gout. • Certain drugs (e.g., thiazides) predispose to the
development of gout. • Lead toxicity increases the tendency to develop
gout
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FEATURES• TOPHACEOUS ARTHRITIS
• GOUTY NEPHROPATHY
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GOUTY NEPHROPATHY
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GOUT• Associated with ATHEROSCLEROSIS
• Associated with HYPERTENSION
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Pseudo-GOUT• Gout: Monosodium Urate• Pseudo-GOUT: Calcium Pyrophosphate
• PSEUDOGOUT is also called CHONDROCALCINOSIS, or CPPD (Calcium Phosphate Deposition Disease)
• IDIOPATHIC, HEREDITARY, SECONDARY
–Secondary joint damage, hyperparathyroidism, hemochromatosis, hypomagnesemia, hypothyroidism, ochronosis, and diabetes
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GOUT vs. PSEUDOGOUT
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JOINT TUMORS• BENIGN
– GANGLION (SYNOVIAL CYST)– GIANT CELL TUMOR of TENDON SHEATH,
aka PVNS, Pigmented VilloNodular Synovitis
• MALIGNANT– SYNOVIAL SARCOMA
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GANGLION
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PVNS/GCT
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Synovial Sarcoma
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“SOFT TISSUE” TUMORS
• FAT
• FIBROUS TISSUE
• FIBROHISTIOCYTIC
• SKELETAL MUSCLE
• SMOOTH MUSCLE
• VASCULAR
• PERIPHERAL NERVE• UNCERTAIN: SYNOVIAL SARCOMA, ALVEOLAR
SOFT PART SARCOMA, EPITHELIOD SARCOMA
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CAUSES• MOSTLY UNKNOWN• RADIATION association• CHEMICAL BURN association• THERMAL BURN association• TRAUMA association• VIRUS association (HHV8 for Kaposi)• GENETICS• Parts of many SYNDROMES• MANY TRANSLOCATIONS
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Chromosomal and Genetic Abnormalities in Soft Tissue Sarcomas
Tumor Cytogenetic Abnormality Genetic Abnormality
Extraosseous Ewing sarcoma and primitive neuroectodermal tumor
t(11:22)(q24;q12) FLI-1-EWS fusion gene
t(21:22)(q22;q12) ERG-EWS fusion gene
t(7;22)(q22;q12) ETV1-EWS fusion gene
Liposarcoma—myxoid and round cell type
t(12:16)(q13;p11) CHOP/TLS fusion gene
Synovial sarcoma t(x;18)(p11;q11) SYT-SSX fusion gene
Rhabdomyosarcoma—alveolar type t(2;13)(q35;q14) PAX3-FKHR fusion gene
t(1;13)(p36;q14) PAX7-FKHR fusion gene
Extraskeletal myxoid chondrosarcoma t(9;22)(q22;q12) CHN-EWS fusion gene
Desmoplastic small round cell tumor t(11;22)(p13;q12) EWS-WT1 fusion gene
Clear cell sarcoma t(12;22)(q13;q12) EWS-ATF1 fusion gene
Dermatofibrosarcoma protuberans t(17:22)(q22;q15) COLA1-PDGFB fusion gene
Alveolar soft part sarcoma t(X;17)(p11.2;q25) TFE3-ASPL fusion gene
Congenital fibrosarcoma t(12;15)(p13;q23) ETV6-NTRK3 fusion gene
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SOFT TISSUE TUMORS
• ALL “SPINDLY”
• Deep (desmoid) vs. Superficial (skin)
• Importance of counting MITOSES• Importance of STAGING
• Importance of IMMUNOPEROXIDASE
• Importance of CONSULTATION
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FAT• LIPOMA
• LIPOSARCOMA
NORMAL FAT LIPOMA, encapsulated
LIPOSARCOMA, often retroperitoneal
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FIBROUS TISSUE• NODULAR FASCIITIS
(pseudosarcomatous)• FIBROMATOSES
(plantar, palmar, penile)• FIBROSARCOMA
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MYOSITIS OSSIFICANS• BENIGN FIBROUS TISSUE
PROLIFERATION PLUS OSSEOUS “METAPLASIA”
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FIBROHISTIOCYTIC• FIBROUS HISTIOCYTOMA• DERMATOFIBROSARCOMA
PROTUBERANS• MALIGNANT FIBROUS HISTIOCYTOMA
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SKELETAL MUSCLE• RHABDOMYOMA
• RHABDOMYOSARCOMA
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SMOOTH MUSCLE• LEIOMYOMA
• LEIOMYOSARCOMA
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VASCULAR • HEMANGIOMA
• LYMPHANGIOMA
• HEMANGIOENDOTHELIOMA
• HEMANGIOPERICYTOMA
• ANGIOSARCOMA
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PERIPHERAL NERVE• NEUROFIBROMA
• SCHWANNOMA
• GRANULAR CELL TUMOR
• MALIGNANT (SCHWANNOMA)
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UNCERTAIN• SYNOVIAL SARCOMA
• ALVEOLAR “SOFT PART” SARCOMA
• EPITHELIOD SARCOMA