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SYSTEMIC PATHOLOGY - 1 > 13 - Bone III > Flashcards

13 - Bone III Flashcards

1
Q

What are metabolic bone diseases?

A
  • Generalized or systemic disease of bone caused by various reasons
  • *osteodystrophy: ‘bad bone growth’
  • Unclear why there are different forms
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2
Q

What can metabolic bone disease be caused by?

A
  • Nutritional deficiencies or imbalances
  • Hormonal deficiencies or excesses
  • Toxicities
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3
Q

What are the 3-4 types of metabolic bone disease?

A
  1. Osteoporosis
  2. Osteomalacia and rickets
  3. Fibrous osteodystrophy
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4
Q

What is osteoporosis?

A
  • Most common metabolic bone disease
  • Reduction in bone density or quality
  • Remaining bone is normally mineralized
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5
Q

What do the lesions of osteoporosis include (2)? What is the result?

A
  1. Reduction in trabecular bone with a corresponding increase in medullary cavity
    a. Due to large SA available for resorption
  2. Reduced thickness and increased porosity of cortical bone
    *bone of decreased density: more brittle and easily fractured
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6
Q

What are the causes of osteoporosis?

A
  • Calcium deficiency
  • Starvation/malnutrition
  • Lactation (following pregnancy)
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7
Q

How does calcium deficiency cause osteoporosis?

A
  • Increased demand for circulating calcium=increased secretion of PTH=increase bone resorption
  • *seen in cattle and sheep
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8
Q

What does PTH do?

A
  • Promotes release of Ca from bone by activating osteoclasts and inhibiting osteoblasts
  • Indirectly promotes increased intestinal absorption of Ca
  • Promotes renal tubular reabsorption of Ca and increased renal excretion of phosphates
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9
Q

How does starvation cause osteoporosis?

A
  • Lack of energy, protein and minerals
  • *seen in grazing animals
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10
Q

How dose lactation cause osteoporosis?

A
  • Due to inadequate calcium supplementation during pregnancy and lactation
  • *seen in gilts
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11
Q

What are some less common causes of osteoporosis?

A
  • Primary or secondary copper deficiency
  • Hyperadrenocorticism
    o Chronic glucocorticoid therapy
  • Physical inactivity or disuse
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12
Q

Osteopenia

A
  • Bone deficiency
  • Reduced amount of bone
    o Does not consider the quality of remaining bone=DIFFERS from osteoporosis
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13
Q

Osteoporosis vs. osteopenia (humans)

A
  • Osteoporosis: clinical condition of postmenopausal women defined by decrease BMD (disease that resulted from the osteopenia)
  • Osteopenia: decrease in BMD without clinical disease
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14
Q

Osteomalacia vs. rickets

A
  • Osteomalacia: disease of mature skeleton
  • Rickets: disease of growing skeleton
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15
Q

What are the 2 causes of Osteomalacia and rickets?

A
  • Vitamin D deficiency
  • Phosphorus deficiency
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16
Q

What is the primary lesion of osteomalacia?

A
  • Inadequate mineralization of osteoid leading to abnormally SOFT BONE
    o Leads to deformed bones and fractures
  • Mature animals: defective mineralization is limited to osteoid formed during remodeling
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17
Q

What are the lesions of rickets?

A
  • Also include defective mineralization of cartilage and osteoid at site of endochondral ossification
    o Results in irregular thickening of physes that is most severe in most rapidly growing physes (and enlarged costochondral junctions)
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18
Q

What are the roles of Vitamin D?

A
  • Increase Ca levels in ECF by promoting absorption of Ca in intestines with PTH
  • Mobilization of Ca from bone
  • Reabsorption of calcium by kidneys
  • Promote absorption of phosphorus in intestines
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19
Q

What do the gross changes in Rickets depend on?

A
  • Severity of disease (malacia)
  • Duration of disease
  • Stresses on individual bones
    o Those that bear weight=more likely to deform
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20
Q

What is fibrous osteodystrophy?

A
  • Result of prolonged bone resorption and its replacement with fibrous tissue
  • Produces swelling and weakening of affected bones
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21
Q

What can fibrous osteodystrophy cause?

A

o Lameness
o Deformities
o Infractions
o Pathological fractures

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22
Q

What is osteodystrophy most commonly the result of?

A
  • hyperparathyroidism (primary or secondary)
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23
Q

What is hyperparathyroidism?

A
  • Any condition associated with prolonged elevation of circulating PTH
  • Primary and secondary
24
Q

Primary hyperparathyroidism

A
  • Uncontrolled and excessive release of PTH from parathyroid tissue
  • *characterized by hypercalcemia
  • Rare in domestic animals
25
Q

What kind of cases is primary hyperparathyroidism seen in (2)?

A
  • Parathyroid gland neoplasia
  • Idiopathic parathyroid gland hyperplasia
26
Q

Secondary hyperparathyroidism

A
  • Stimulus to decrease serum calcium AND
  • Compensatory increased production and secretion of PTH
  • *relatively more common in domestic animals: nutritional or renal in origin
27
Q

What is secondary hyperparathyroidism usually characterized by?

A
  • low-normal serum calcium concentration (normocalcemia) OR
  • less commonly: mild hypocalcaemia or mild hypercalcemia
28
Q

Nutritional secondary hyperparathyroidism

A
  • Growing animals diets with deficient calcium and relatively high phosphorous
  • *can get a BIG HEAD: mass of fibrous tissue (fibrosis osteodystrophy)
  • *cattle and sheep develop osteoporosis
29
Q

What kind of diets in pigs cause nutritional secondary hyperparathyroidism?

A
  • All grain diet
30
Q

What kind of diets in horses cause nutritional secondary hyperparathyroidism?

A
  • Cereal hay (ex. oats, barley)
  • Large amounts of grain or bran
31
Q

What kind of diets in dogs and cats cause nutritional secondary hyperparathyroidism?

A
  • All meat (‘organ meat’)
32
Q

Renal secondary hyperparathyroidism

A
  • Kidney doesn’t function properly (chronic, severe, renal disease)
    o Decreased GFR: increase serum phosphorus (‘mass law’)
    o Phosphorus will bind to calcium and deposited in soft tissues
     Decreased serum Ca=increased PTH
  • *older dogs and cats
33
Q

What is the pathogenesis of renal secondary hyperparathyroidism (renal osteodystrophy)?

A
    1. Loss of glomerular function
    1. Inability to excrete phosphate
    1. Hyper-phosphatemia
  • *phosphate reacts with Ca and promotes hypocalcemia
    o Ca-P products precipitates in soft tissues
  • *also get impaired vitamin D metabolism
  • *uremia promotes bone resorption and poor mineralization
34
Q

Osteopetrosis (marble bone disease) is a term used as a

A
  • Syndrome or disease
  • Morphologic diagnosis (descriptive term)
35
Q

What is osteopetrosis?

A
  • Abnormally dense bone in the diaphysis and metaphyses due to DEFECTIVE RESORPTION OF IMMATURE BONE
  • *marble bone disease
36
Q

Osteopetrosis as a disease can be seen in and is a result of

A
  • People and animals
  • Genetic defect in osteoclast production or function
  • Ex. angus calves, Peruvian Paso foals (osteoclasts are ‘upside down’), lab strains of mice
37
Q

Bovine calf: osteopetrosis

A
  • Incompatible with life=still born
  • Impacted molars: all arising from same site
  • Short mandible
  • *really dense bone=no bone marrow cavity
    o Continuous columns of bone: never have been modeled or remodeled
38
Q

Peruvian Paso foal: osteopetrosis

A
  • Born alive, but have bones that fracture more easily than normal
  • Recognized during investigation of spontaneous fractures
  • *develops b/c the resorptive surface of osteoclasts face away from bone surface
39
Q

Why is it believed that osteopetrotic bone is subject to fractures?

A
  1. Weaker, immature, woven bone is NEVER replaced by stronger, mature lamellar bone
  2. Microdamage is NOT properly repaired
  3. Bones do not model in response to biomechanical forces placed on them
40
Q

In which animals does acquired osteopetrosis or osteopetrosis-like lesions occur?

A
  • Those with severe growth retardation lattices
  • Claves with BVD infections
  • Cats with leukemia virus infections
  • Variable degree in congenitally hypothyroid foals
41
Q

What does aseptic (free of infection) necrosis of bone refer to?

A
  • Ischemic necrosis of bone or infarction
    o Ischemia=result of loss of blood supply
42
Q

What are some causes of aseptic necrosis of bone?

A
  • Legg-Calve-Perthe’s disease
  • Neoplasia (including lymphoma)
  • Other
43
Q

Legg-Calve-Perthe’s disease

A
  • Kids and small dogs
  • Ischemic necrosis of head of femur
  • Articular cartilage is spared=may contine to proliferate and become thickened if endochondral ossification is not complete at time of onset of ischemia
    o May become revascularized=allows for removal of dead bone, deposition of new bone or BOTH
    o Turnover may lead to collapse of articular surface
  • *underlying cause and pathogenesis not fully understood
44
Q

What does chronic Legg-Calve-Perthe’s disease result in?

A
  • Degenerative joint disease
45
Q

Calf with lymphosarcoma (LSA)

A
  • Irregular pale areas in bone
    o Pale=due to extra lymphocytes in marrow have lead to collapse of blood vessels due to increased pressure
    *not the sarcoma
46
Q

Osteitis

A
  • Inflammation of bone OR of a bone (ex. pedal osteitis)
47
Q

Osteomyelitis

A
  • Inflammation of bone and bone marrow OR
  • Inflammation of bone with involvement of the metaphysis or medullary cavity
48
Q

Periostitis

A
  • Inflammation of periosteum
49
Q

What often causes osteitis and osteomyelitis?

A
  • Bacteria
  • Fungi, protozoa and viruses can be involved
50
Q

How might a bacteria locate in a bone?

A
  • Direct introduction during traumatic event
  • Extension from soft tissue
  • Extension from a bacterial arthritis
  • Hematogenously
51
Q

What is osteomyelitis often characterized by?

A
  • Chronic disease
  • Necrosis and removal of necrotic bone and production of new bone
    o *2 processes proceed simultaneously
52
Q

Hematogenous osteomyelitis

A
  • *Neonatal farm animals (young piglets, calves and folas)
    o Lack of colostrum
  • Common
  • Metaphyses of LONG bone and vertebrae
    o Can be in any capillary bed with bone
53
Q

Lumpy jaw

A
  • Caused by Actinomyces bovis
    o Enters mandible through breaks in oral mucosa
  • Pyogranulomatous inflammation (bone loss and bone production)
54
Q

Metaphyseal osteopathy

A
  • Aka hypertrophic osteodystrophy
  • Young, large and giant breed DOGS
  • Cause unknown
  • *most recover spontaneously
55
Q

What happens to affected dogs with metaphyseal osteopathy?

A
  • Lame and febrile
  • Swollen, painful metaphyses of long bones
56
Q

Lesions of metaphyseal osteopathy (gross or radiographic)

A
  • Periosteal new bone over metaphyses
  • Lines of increased and decreased bone density adjacent and parallel to physes
57
Q

Lesions of metaphyseal osteopathy (histologically)

A
  • Suppurative inflammation and necrosis of metaphyseal bone and marrow
    o Not often as it is self-limiting and usually get better on their own in 7-10 days

SYSTEMIC PATHOLOGY - 1 (24 decks)

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