Bone Pathology

61 flashcards · Other · by Jared Blackwell

  1. Pagets Disease Top arrow points to sclerosis of coritcal bone (more dense) Bottom is thickening of trabecula.

  2. Primary Paget Disease Lytic lesions from osteoclasts.

  3. Describe Pagets disease

    Non-integrated cycles of bone formation. Middle-age and Elderly Pagetoid bone THICK. 1st stage: Osteoclast activation 2nd stage: Osteoblasts lay down osteoid type I collage rapidly. Thick, woven, disorganized bone Temporal bone -> decreased hearing High output CHF increased vascularity within bone Increase in osteogenic sarcoma

  4. Paget disease of pelvis Right has abnormal. Left is normal.

  5. Paget Disease Nuclear scan shows increased flow and laying down of bone concentrates the radioactive material.

  6. What are the diagnostic blood exams for bone resorption?

    1) Urinary hydroxyproline measures collagen I breakdown 2) C-Telopeptide for collage I x-linked peptides 3) Pyridinoline

  7. What are the diagnostic blood exams for bone formation?

    1) Alkaline Phosphatase - osteoblast enzyme 2) Osteocalcin - noncollagen protein in dentin and bone. Use for anti-resorptive therapy. Produced by osteoblasts Alkal in biliary canculi in liver, if no jaudice etc, coming from bone.

  8. Osteopetrosis

    Abnormal CA2 gene for carbonic anydrase. Inhibits osteoclast function. Leads to unopposed osteoblast function. Bone of marble.

  9. Bone of Marble - Osteopetrosis Dense Very brittle

  10. Rickets Osteomalacia in child with open growth plates. Vit D. deficiency decreases Ca2+ absorption, Increases PTH, and decreases Phosphate. Calcification of chondrocytes

  11. Importance of phosphate with bone growth?

    Apoptosis of chondrocytes dependent on Phosphate. Also closure of growth plate. Rickets may occur with low phosphate.

  12. What are the lab values of rickets?

    HIGH alkaline phosphatase = AP increased because measure of osteoblast formation (it is an enzyme). HIGH PTH level "off the wall" Low calcium and phosphate.

  13. Osteogenesis Imperfecta

    Type 1: normal procollagen I but reduced. Type 2: replacement of Glycine. Brittle bones *Blue sclera *Dentin enamel abnormal. Treat with bisphosphates to promote mineralization of bone.

  14. Primary osteoporosis

    Ageing decreases osteoblast acitivity. Thinning of trabeculae. Loss of Estrogen increases IL-1 and IL- 6 which stimulates osteoclasts. Without estrogen, OPG not stimulated, upregulated RANKL and osteoclasts.

  15. Secondary osteoporosis

    Steroid use, vit. D deficient, malabsorption of fat soluble vitamins, HPT, Testosterone deficient

  16. Describe secondary HPT

    Renal failure decreases GFR to clear phosphate. High serum Phosphate increases PTH Norma Ca2+ because no hydroxylation of vitamin D

  17. Describe Osteomalacia

    Common in black people and northeast. No vit. D. Low Phosphate Low calcium HIGH PTH IBD like Crohn's

  18. Transverse Stress Displaced/oblique Greenstick Comminuted

  19. What does PTH do?

    Responds to low calcium and high phosphate. Interacts with osteoblast to activate osteoclasts. Increases renal clearance of phosphate. Stops OPG

  20. What does calcitonin do?

    Directly inhibits osteoclasts.

  21. Steps of healing bone fracture?

    1) Hematoma, granulation tissue 2) Soft callus with new cartilage 3) Hard callus with new bone 4) Remodeling

  22. Common causes of bacterial osteomyelitis?

    S. aureus (80-90%) E.Coli, Psudomonas, Klebsiella (IV drug users) H. influenzae, group B strep (neonates) Salmonella (sickle cell disease)

  23. Describe spread of baterial osteomyelitis

    Extends through haversian canal and out beneath periosteum. Over time, a sleeve of new bone called involucrum is formed which surrounds dead bone sequestrum.

  24. Acute bacterial osteomyelitis Many neutrophils in bone marrow cavity. Open circle (top left) with no nuclei is dead bone = sequestrum.

  25. Granulomatous osteomyelitis (coccidiodomycosis) Giant cells, epitheloid cells. Granulomatous osteomyelitis of spine (tuberculosis). Casesous necrosis.

  26. Describe granulomatous osteomyelitis

    M. tuberculosis and coccidioides Usually hematogenous "seeding" (esp. lung) To spine, knee, wrist Granulomas form when body attempts to wall off something foreign but can't eliminate it.

  27. Coccidioides spherules (GMS stain) "bag of marble"

  28. Granulomatous arthritis (coccidioides) *Second has GMS stain. Shows fungal wall

  29. What is this?

    Avascular necrosis of femoral head

  30. Avascular necrosis of femoral head. *Necrotic subchondral bone in red outline.

  31. Superficial fat Full of fluid or fat density in joint capsule. Occurs with inter-articular fracture with bone marrow fat going into joint space. Benign bone tumor.

  32. What causes bone infection? 1) IV drug users 2) Sickle Cell Disease 3) Neonates 4) Most common

    1) Gram negative bacteria: E.coli, Pseudomonas, Klebsiella 2) Salmonella 3) H. influenzae 4) S. auerus - 85% (vancomyocin).

  33. Osteoid Osteoma - Benign Teenagers Femur & tibia Lesion less than 2cm. Sclerotic rim Random arranged trabecula of woven bone.

  34. Osteochondroma Long bones Teenagers Stops growing when growth plate closes. Cartilagenous cap over normal bone.

  35. Osteosarcoma Child & Teens, and young adults Around the knee. Periosteal "sunburst" reaction. Metaphysis. Codman sign lifting up periosteum. RB gene chromosome 13. --Bright mass trying to invade skeletal muscle --Gross: Gray white mass --HISTO: Bright pink osteoid matrix. Large osteocytes purple irregular.

  36. Describe hyperparathyroidism

    Primary is due to hyperplasia or tumor of parathyroid gland which oversecretes PTH Secondary is due to hypocalcemia which results in increased PTH.

  37. Chondroma Enchondroma=medullary cavity. Juxtacortical=surface of bone. Hands and Feet. Young adults

  38. Chondrosarcoma Older adults Ribs, pelvis, femur/humerus Speckled calcification Translucent bluish gray gross appearance. Gray chondroid matrix

  39. Giant Cell Tumor Young adults Osteoclast derive (osteoclastoma) Many giant cells. Knee, starts at metaphysis and extends to epiphysis.

  40. Ewing Sarcoma Children and young adults Mesenchymal derived Around the knee, Large tissue mass. Epiphysis. "Small blue round cell tumor." Translocation at 11:22

  41. Multiple myeloma Malignant plasma cells Older adults In FLAT BONES like skull, ribs, pelvis.

  42. X-Ray Bone Soft tissue Fluid/Fat Air

  43. Transverse Oblique/displaced Segmented Spiral Comminuted

  44. Describe the fracture:

    Right closed intra-articular, comminuted distal radius and ulnar fracture.

  45. Salter Harris fracture

  47. Primary fracture healing

    Intramembranous ossification, relies on rigid fixation. Should not see fracture gaps. Direct bone formation. Fracutre lines should NOT be visible after fixation. If you can see the fracture osteoclasts can't jump across it.

  48. Secondary fracture healing

    Endochondral ossification, relies on periosteum and soft tissue. Just like bone growth. Cartilage intermediary to bone formation. Relies on periosteium & soft tissue.

  49. Describe fracture and how to fix:

    Right/Left: Right Open/Closed: Closed Joint involvement: Intra-articular Fracture type: Comminuted Location: Proximal Periprosthetic: No Bone: Tibia "Right closed intra-articular, comminuted proximal tibia fracture." Image w/ XR+ CT (CT because intra-articular and comminuted). Treat with surgery to bring rigid fixation for primary fracture healing. DO NOT want callus for joints.

  50. Great saphenous vein varicosities without pain. Unilateral pitting edema. What is this ultrasound pointing to?

    DVT

  51. Calcaneofibular ligament Anterior talofibular ligament Calcaneous Talus (no tendons)

  52. Describe a lateral ankle sprain

    Involves the Anterior talofibular ligamtent ATFL with or without the Calcaneol fibular ligament CFL. Radiograph needed with point palpation tenderness and inability to bear weight. ATFL main ankle sprain ligament. Pain with inversion.

  53. Describe high ankle sprain

    External rotation injury. Injury to tibiofibular syndesmosis Interosseous membrane and anterior/posterior tibiofibular ligament. Connects fibula to tibia. Distal osseous includes AITFL, PITFL, Transverse ligament, interosseous ligament. Prognosis is much longer.

  54. Anterior drawer exam of ankle?

    Move ankle up and down and in and out. Use for Lateral ankle sprain. *Never on recent sprain

  55. How to test for high ankle sprain.

    Ask to cross legs and it hurts because its squeezing sprain.

  56. Treatment for high ankle sprain

    Mortise intact: Non-weight-bearing in cast or boot. Mortise widened: operative stabilization. Screws between tibia and fibula so ligaments heal at right length. Take screws out later. *Mortise is space between tibia and fibula.

  57. What is the most common knee injury? Describe it

    Meniscus tear. Occurs with twisting of knee. Tear with femur grinding down on them. Femur tears meniscus. Complain of pop, click, locking, catching, "giving out." McMurray's test: Push tibia and femur together and rotate side to side. Regular meniscus

  58. ACL injury

    Mostly valgus - medial injury while decelerating. May hear a pop. Hemarthrosis, limited ROM. Lachman's- flex knee 30 degrees and move knee back and forth. Anterior directed force on tibia. Pivot Shift- Trying to get tibia to come partly out of joint. Push up on knee with valgus force and internal rotation and feel tibia put out and back in. Anterior Drawer test- pull forward at knee with 90 degrees. Tibia will come forward. Anterior force on tibia.

  59. Describe ACL physical exam

    Lachman's Test 82% sensitive 97% specific. Anterior Drawer 40% sensitive 95% specific Pivot shift test 82% sensitive 98% specific

  60. d

    Females have natural valgus to hips and knees. If you tear edge of meniscus it has vascularity and will heal.

  61. What is pes cavus?

    High arch of foot that does not flatten with weight bearing.