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(page 1438) "Pathophysiology

When a bone is broken, the periosteum and blood vessels in the cortex, marrow, and
surrounding soft tissues are disrupted. Bleeding occurs from the damaged ends of the
bone and from the neighboring soft tissue. A clot (hematoma) forms within the medullary
canal, between the fractured ends of the bone, and beneath the periosteum. Bone tissue
immediately adjacent to the fracture dies. This necrotic tissue along with any debris in the
fracture area stimulates an intense inflammatory response characterized by vasodilation,
exudation of plasma and leukocytes, and infiltration by inflammatory leukocytes and
mast cells. [for information on the pathophysiology of the immune response, see
http://allnurses.com/forums/f50/histamine-effect-244836.html]". Within 48 hours after
the injury, vascular tissue invades the fracture area from surrounding soft tissue and the
marrow cavity, and blood flow to the entire bone is increased. Bone-forming cells in the
periosteum, endosteum, and marrow are activated to produce subperiosteal procallus
along the outer surface of the shaft and over the broken ends of the bone. Osteoblasts
within the procallus synthesize collagen and matrix, which becomes mineralized to form
callus (woven bone). As the repair process continues, remodeling occurs, during which
unnecessary callus is resorbed and trabeculae are formed along lines of stress. Except for
the liver, bone is unique among all body tissues in that it will form new bone, not scar
tissue, when it heals after a fracture."

From Pathophysiology: A 2-in-1 Reference for Nurses by Springhouse, Springhouse


Publishing Company Staff, page 399)
"BONE GROWTH
Bone formation is ongoing and is determined by hormonal stimulation, dietary factors,
and the amount of stress put on the bone. It's accomplished by the continual actions of
bone-forming osteoblasts and bone-reabsorbing cells called osteoclasts. Osteoblasts are
present on the outer surface of and within bones. They respond to various stimuli to
produce the bony matrix, or osteoid. As calcium salts precipitate on the organic matrix,
the bone hardens. As the bone forms, a system of microscopic canals forms around the
osteocytes (mature bone cells). Osteoclasts are phagocytic cells that digest old, weakened
bone section by section. As they finish, osteoblasts simultaneously replace the cleared
section with new, stronger bone.

Vitamin D supports bone calcification by stimulating osteoblast activity and calcium


absorption from the gut to make it available for bone building. When serum calcium
levels fall, the parathyroid gland releases parathyroid hormone, which then stimulates
osteoclast activity and bone breakdown, freeing calcium into the blood. Parathyroid
hormone also increases serum calcium by decreasing renal excretion of calcium and
increasing renal excretion of phosphate ions

Phosphates are essential to bone formation; about 85% of the body's phosphates are
found in bone. The intestine absorbs many phosphates from dietary sources, but adequate
levels of vitamin D are necessary for their absorption. Because calcium and phosphates
interact in a reciprocal relationship, renal excretion of phosphates increases or decreases
in inverse proportion to serum calcium levels. Alkaline phosphatase (ALP) influences
bone calcification and lipid and metabolite transport. Osteoblasts contain an abundance of
ALP. A rise in serum ALP levels can identify skeletal diseases, primarily those
characterized by marked osteoblastic activity such as bone metastasis of Paget's disease.
It can also identify biliary obstruction or hyperparathyroidism, or excessive ingestion of
vitamin D.

In children and young adults, bone growth occurs in the epiphyseal plate, a layer of
cartilage between the diaphysis and epiphysis of long bones.

Osteoblasts deposit new bone in the area just beneath the epiphysis, making the bone
longer; osteoclasts model the new bone's shape by reabsorbing previously deposited
bone. These remodeling activities promote longitudinal bone growth, which continues
until the epiphyseal growth plates, located at both ends, close during adolescence. In
adults, bone growth is complete, and this cartilage is replaced by bone, becoming the
epiphyseal line."

This information will help you to determine the related factors in forming your 3-part
nursing diagnostic statements. It also helps you to understand some of the signs and
symptoms the patient is having (pain, swelling) and why they may be at risk for things
like fat or pulmonary embolism, neurovascular impairment. Some of this information
should also give you some ideas of some of the nursing interventions you should be
including in your care plan, particularly regarding dietary replacement of calcium and
magnesium.

The local separation of a bone into two or more pieces under the action of stress. Strong
force is required to produce a fractured tibia. As a result, soft tissue damage,
devascularization, and open fracture are frequent. The tibia is one of the more common
sites of a stress fracture. Complications are compartment syndrome, fat embolism,
problems associated with bony union, and possible infection associated with open
fracture.