Test 4: lab 2 bones and blood Flashcards
(42 cards)
Hindlimb and section of ribs from a 1-year-old monkey.
Description:
The tibia and fibula are twisted and have a bowed contour. Several ribs have nodular swellings in the mid-shaft region (blue arrow) (i.e., rib fractures with fracture callus) as well as enlarged, bulbous physes (black arrow) resulting in prominent costochondral junctions.
Name the disease:
Possible causes:
Rickets
In mammals, rickets is most often caused by dietary deficiencies in vitamin D or phosphorus. Insufficient UV light exposure (i.e., during the winter months) can also lead to deficiency in active vitamin D. Other potential causes of rickets include heredita ry errors in vitamin D formation/metabolism, paraneoplastic syndromes affecting phosphorous levels, or malabsorption in the gut (e.g., not enough vitamin D is absorbed, presence of minerals that inhibit PO4 absorption).
What phase of bone remodeling is abnormal in rickets?
Mineral deposition (mineralization of osteoid and/or cartilagenous templates of the growth plates) is deficient in rickets (disease of young growing animals) and osteomalacia (disease of adults). In both juveniles and adults, large seams of unmineralized osteoid are deposited, but osteoclasts can’t resorb unmineralized osteoid and thus can’t remodel “old” bone. Bone eventually fails, resulting in pathologic fractures of trabecular bone (microfractures or infractions, “compression fractures”) and eventually of compact co rtical bone.
In rickets, failure of mineralization of growth plate cartilage leads to growth plate deformities (expanded zone of hypertrophy) and decreased primary bone trabeculae at the ossification front. Physes are enlarged and “flared” because OCLs can’t resorb newly formed trabeculae to taper the metaphyses to the diaphysis in these “cut back” zones. Eventually, bone cortices are affected to the point where they become bowed/deformed because the unmineralized bone is “soft” not brittle.
Tissue from an 18-year-old cat with severe azotemia, anemia, and hyperphosphatemia. The mandible is pliable.
Name the disease:
Pathogenesis:
Fibrous osteodystrophy (specifically, renal fibrous osteodystrophy due to secondary hyperparathyroidism)
Kidney disease with loss of functional nephrons → decreased GFR → decreased phosphorous excretion → hyperphosphatemia → CaPO4 crystallization, precipitation & deposition (uremic mineralization!) → decreased serum ionized calcium → increased PTH secretion → increased osteoclast activation, decreased osteoblast activation, increased fibroblast differentiation → excessive bone resorption with fibrous replacement (rubber jaw!)
Also, remember that:
Kidney failure → reduced Vitamin D activation → decreased calcium!
If this were a young cat, what other metabolic bone disease might occur concurrently with Fibrous osteodystrophy ?
Rickets (due to inadequate generation of active Vitamin D3)
Fibrous osteodystrophy= rubber jaw
renal fibrous osteodystrophy due to secondary hyperparathyroidism
What other lesions might you see in this cat with rickets and Fibrous osteodystrophy (see urinary lectures)?
Small, irregular/shrunken, firm kidneys (chronic kidney disease), bilaterally enlarged parathyroid glands (bilateral parathyroid gland hyperplasia), and uremic mineralization (predilection sites: sublingual tissue, parietal pleura, gastric mucosa, and the left atrium (in dogs).
Femoral head from a 6-year-old German shepherd dog with progressive lameness of both hindlimbs, reduced range of motion and pain on manipulation of both coxofemoral joints. The canine glenohumeral joint is from a different dog but shows similar lesions.
Describe the lesions
Morphologic diagnosis
Describe the lesions: The femoral head is flattened. The articular cartilages are diffusely thinned (eroded) to focally ulcerated with excavations into the subchondral bone. In some ulcerated areas, the subchondral bone has a “polished” appearance (eburnation from bone-on-bone contact). The synovial membrane is discolored tan-to-brown and is markedly thickened with villous projections. The joint capsule is thickened by firm white-tan tissue as well as several palpable 0.5-1.0 cm diameter bony nodules (osteophytes).
Morphologic diagnosis: Glenohumeral and femoral head: Severe chronic degenerative joint disease (or degenerative osteoarthritis) with cartilage ulcers and subchondral eburnation, villous synovial hypertrophy, joint capsule fibrosis, and periarticular osteophytosis.
N.B. from Dr. Engiles - “Don’t worry - I would never make you come up with a morph like this for the exam. Just be able to recognize and anticipate these changes in a severely degenerated joint”
Why is the synovial membrane brown?
Hemarthrosis. Intra-articular hemorrhage is broken down into hemosiderin (brown) pigment by macrophages. Joint fluid should be pale yellow but if there has been hemorrhage from the synovial membrane and/or exposed subchondral bone (ie deep cartilage ulcers) synovial fluid can be red-orange to brown-tinged. In chronic DJD, joint fluid has reduced viscosity due to reduced hyaluronic acid and other proteoglycans
Likely etiology for the femoral head lesions in this German shepherd dog
Congenital canine hip dysplasia → excessive joint laxity.
Tissue from a 14-year-old Standardbred mare that was euthanized for severe, progressive right hind lameness.
Describe the lesions in the stifle joint:
Morphologic diagnosis:
The caudomedial rim of the medial meniscus has a near-complete tear. The fibrocartilage along the margins of the tear is dull yellow and frayed. Two irregular oval ulcers (~3 cm x 2 cm) are centered on the medial femoral condyle and medial tibial plateau. Nodular osteophytes extend along the medial tibial plateau and intercondylar eminence. There is fibrous thickening of the joint capsule and synovial hypertrophy.
Medial meniscal tear with severe chronic degenerative joint disease (or degenerative osteoarthritis).
The medial meniscal tear resulted in severe instability that initiated the degenerative process in the other tissue components of the joint.
Bones from the elbow of a senior-aged goat that had difficulty ambulating and rising to stand. Note how these bones do not come apart, and the joint is effectively fused due to severe bridging osteophytosis (worse on the lateral side than medial side). Provide the term for “self fusion” of an end-stage degenerative joint:
Ankylosis
Provide the term for surgical fusion of a join
Arthrodesis
The MC3 (third metacarpal bone) of a 3-year-old Thoroughbred racehorse that sustained an incomplete, simple lateral condylar fracture that was repaired by surgical fixation using cortical bone screws placed in lag fashion, which resulted in good compression o f the fracture fragment.
Which stage of healing (early or late) is this fracture in? How did you make that judgement?
This fracture is in the early stages of healing. Although the fracture fragment is in close anatomic apposition to the parent bone, there still remains a narrow gap that was likely spanned by granulation tissue (or possibly unmineralized osteoid) without adequate time to form a mineralized bony callus before the horse was euthanized (in this case, for aspiration pneumonia - an unfortunate complication of general anesthesia during the fracture repair surgery).
The benefit of internal fixation is that by placing the fracture fragment in close apposition to the parent bone, it minimize s the size of the bony callus needed to stabilize and heal the fracture and thus markedly reduces healing time compared to conservative managem ent. If the fragments are immediately apposed, direct bone healing can occur (fracture healing without a bony callus) minimizing the time to heal.
Contrast the MC3 fracture to that of the beef cow that sustained a complete, severely displaced oblique diaphyseal humeral fr acture. Note the size of this fracture fragment, the size of the callus and the distortion of the diaphysis and distal metaphysis/epiphysis.
This bovine humerus represents the extreme version of a common complication of fracture healing - which one?
This is a wonderful example of a bony malunion. Although there is abundant bony callus stabilizing the fracture fragment, the severe distal and oblique displacement of the diaphysis has resulted in severe shortening and distortion of the bone. Given the oste ophytes surrounding the distal epiphysis of the humerus, this fracture likely created aberrant biomechanical forces on this joint tha t led to secondary DJD.
The amount and smooth quality of the bone that formed the callus is not compatible with osteomyelitis, which would be much mo re porous (like “Swiss cheese” quality of bone seen we saw with ‘bovine lumpy jaw’ from the alimentary lectures).
These are the antebrachia (radius and ulna) from the left and right forelimbs of a 4-month-old gilt (female juvenile pig) that was euthanized for severe bilateral fore- and hindlimb lameness of 2-weeks duration. Autopsy reveals these lesions as well as severe fibrinosuppurative arthritis of the left and right hind tarsocrural joints with an opaque, yellow-pink exudate (see associated image).
The farmer reports this gilt had Salmonella enterocolitis at 3 months of age but had recovered. At this point, the viscera are within normal limits.
Describe the lesions you see in the distal ulnar metaphyseal physes (hint: you can compare the ulnar growth plates to the growth plates of the distal radii):
Morphologic diagnoses:
Expanding and effacing both distal ulnar physes are friable pink-tan exudates. The exudates extend into the metaphyses and form an irregularly scalloped margin where they partially efface and abut medullary trabecular bone (bone lysis).
Severe bilateral chronic septic physitis
These are the antebrachia (radius and ulna) from the left and right forelimbs of a 4-month-old gilt (female juvenile pig) that was euthanized for severe bilateral fore- and hindlimb lameness of 2-weeks duration. Autopsy reveals these lesions as well as severe fibrinosuppurative arthritis of the left and right hind tarsocrural joints with an opaque, yellow-pink exudate (see associated image).
The farmer reports this gilt had Salmonella enterocolitis at 3 months of age but had recovered. At this point, the viscera are within normal limits.
Given the history and autopsy findings what is the likely etiopathogenesis of the lesions in the hock and these growth plates?
Salmonella enterocolitis → intestinal vascular invasion with bacteremia → hematogenous dissemination → bacterial seeding of the joints and capillaries at the ossification front of the growth plates → fibrinosuppurative polyarthritis and physitis
Given these lesions in the gilt, what other anatomic locations of the bones are commonly involved in this process?
What is a predisposing cause of neonatal sepsis?
Epiphyses. In addition to septic arthritis (polyarthritis) and metaphyseal physitis, septic epiphysitis is another common manifestation of hematogenous spread of bacteria in young, fast-growing animals.
Failure of passive transfer (inadequate amounts of colostrum or ingestion of poor-quality colostrum → inadequate transfer of material antibodies). Common routes of entry include the umbilicus and the gastrointestinal and respiratory tracts.
These gross specimens represent the same disease process in two different dogs. Both bones are examined in cross-section and are regionally effaced by an expansile, multilobulated, firm to hard mass that partially fills the medullary cavity and extends into the
surrounding tissue. The mass does not extend through the articular cartilage into the joint space.
Diagnosis:
Osteosarcoma
What are the critical diagnostic features of Osteosarcoma ?
What is the biologic behavior of these neoplasms?
The three main critical diagnostic features of this neoplasm are osteolysis (lytic foci), osteoproliferation, and production of tumor osteoid by neoplastic osteoblasts.
Malignant and highly aggressive with rapid metastasis to lungs and other organs or bones. Metastases are often present at the time of diagnosis, and surgical excision alone is seldom curative.
What is the difference between a traumatic fracture and a pathologic fracture?
A traumatic fracture is the result of excessive force applied to a bone. A pathologic fracture is the result of disease weakening the bone such that it can break even under normal physiologic conditions.
Even though this osteosarcoma is producing a mineralized osteoid matrix, the tumor matrix is often more haphazard and more sparse than “reactive” woven bone and is also often poorly mineralized (the radiograph shows the poorly mineralized “lytic” foci of the neoplasm). This and the extensive destruction of the bone’s normal architecture (cortex as well as medulla), predisposes to fracture. Oftentimes dogs will present with acute lameness due to the pathologic fracture prior to diagnosis of the neoplasm.
Bone marrow myeloid hyperplasia, high M:E, and left shift
Anemia with erythroid hyperplasia
Anemia with erythroid hypoplasia
Bone marrow plasma cells greater than 30%, Bence-Jones proteins in urine
Bone marrow myeloid hyperplasia, high M:E, and left shift - b
Anemia with erythroid hyperplasia - a
Anemia with erythroid hypoplasia - c
Bone marrow plasma cells greater than 30%, Bence-Jones proteins in urine - d multiple myeloma??
Explain your decisions:
Bone marrow myeloid hyperplasia, high M:E, and left shift
This is consistent with an increased demand for inflammatory cells, with high demand for neutrophils resulting in release of immature stages (left shift). This can be seen in an acute bacterial infection, matching the acute suppurative bronchopneumonia.
explain why
Anemia with erythroid hyperplasia
This is a regenerative response in response to blood loss, such as a hemoabdomen. With hemorrhage, you can also expect to see megakaryocyte hyperplasia and a decreased M:E ratio.
Anemia with erythroid hypoplasia
This is a non-regenerative response to blood loss, consistent with anemia of chronic disease. In addition to the chronic inflammation, chronic renal disease can also lead to decreased erythropoietin, further exacerbating the decrease in red blood cell production.
