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Material Type: Notes; Class: Pathophysiology; Subject: Biology; University: Missouri Western State University; Term: Unknown 1989;
Typology: Study notes
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Pathophysiology
A fracture is a break in the rigid structure and continuity of a bone The fracture may be: Complete fracture Incomplete fracture Open fracture Closed fracture
Simple Comminuted Compression Impacted Pathologic Stress Depressed Others
Five stages: Hematoma Granulation tissue Procallus Bony callus remodeling
Muscle spasms Infections Ischemia Compartment syndrome Fat emboli Nerve damage Failure to heal Osteoarthritis or stunted growth
A dislocation is the separation of two bones at a joint with loss of contact between the articulating bone surfaces Usually only one of the bones is out of position If the bone is only partially displaced, with partial loss of contact between the surfaces it is termed subluxation.
Two forms of osteoporosis Primary including postmenopausal, senile and idiopathic osteoporosis Secondary following a specific primary disorder like Cushing’s Syndrome Both men and women are affected although the frequency and severity is more pronounced in women
Bone is a hard connective tissue
Matrix about 1/3 organic (mostly bone collagen)
Matrix about 2/3 inorganic (mostly calcium phosphate and calcium carbonate; some fluoride, magnesium and sodium)
Osteoblasts deposit minerals from blood into bone matrix after meal Osteoclasts remove and release minerals from bone into blood during fasting Dietary deficiency of Calcium causes demineralization of osseus tissue
Quantity of bone matrix decreases with age because matrix formation becomes slower than matrix resorption May begin as early as age 20 but by age 30 most people are losing matrix By age 35, everyone has begun to lose bone at a substantial rate
At first, only trabecular bone is removed
The trabeculae become thinner and weaker Trabeculae can become thicker and stronger again if osteoblasts can be stimulated to replace missing matrix (e.g. increase in exercise) Some trabeculae disappear completely and cannot be replaced; some disconnect from others and matrix becomes weaker The weakening at that spot is permanent
Decline in cortical bone is not detected until about age 40 and is quite slow After age 45 the rate increases but remains about half the rate of trabecular loss Loss of cortical bone occurs only on the inside of the bone and so the layer of cortical bone becomes thinner and weaker
Rates of both trabecular and cortical bone loss increases in women after menopause
Menopause usually occurs between 45- but the level of estrogen declines even before this
Combined effects of aging and menopause result in a loss of 15-20 percent of the trabecular bone in the 10 years after menopause
This is 2-3 times the rate of loss in women before menopause or the rate of loss in men Very old women may have only half the trabecular bone they had at age 25 Men have lost only 2/3 as much trabecular bone as women during the same period
Cortical bone loss also accelerates because of menopause with a loss of 10- 15 percent in the decade after menopause
This is a 3-4 fold increase over the rate in the years before menopause
Very elderly women have only about half the cortical bone they had at age 25
Women begin with less bone matrix than men and suffer greater losses with aging
Increase in spontaneous fractures and breaks from accidents with age Fractures heal more slowly in the aged This can lead to complications such as infection, bedsores, blood clots and pneumonia The prolonged immobility leads to an increase in the rate of matrix loss increasing the risk of another fracture
With age there is a general decline in bone mass (loss of bone mineral and collagen) If the loss of bone mass is serious enough to compromise bone structure resulting in easy fractures (crush fractures and broken bones) condition called osteoporosis.
The cause of loss of bone matrix with aging is not known Much has been learned about factors that modify the rate of loss Best strategy is to develop as much bone matrix as possible during youth and then slow losses during adulthood It is much more difficult to reverse bone loss than to slow it
Results in soft bone and rickets in children often with deformities including “bow legs”. Height is usually abnormal
Results in soft bone and osteomalacia in adults resulting in compression fractures
Renal rickets refers to osteomalacia associated with severe renal failure
Progressive bone disease occurring in adults over 40 years.
Cause not well understood but may include a slow virus and heredity
Includes excessive bone destruction with replacement by fibrous tissue and abnormal bone
Pathologic fractures are common
Bone deformities of the long bones, vertebrae, pelvis and skull occur
When the vertebrae are involved, compression fractures with kyphosis result
Also causes cardiovascular disease and heart failure
Egil apparently had Paget’s disease He had many of the physical characteristics Stories of his prowess as a warrior taking direct blows to the skull from an ax
Most primary bone tumors are malignant Bone is also a common site for secondary tumors Particularly the spine and pelvis Metastases usually have spread from breast, lung or prostate
Osteosarcoma (osteogenic sarcoma) Primary malignant neoplasm Usually develops in metaphysis of femur, tibia or fibula in children or young adults More common in males than females Steady, severe and persisting pain with rest and activity
Muscular Dystrophy (MD) is a group of inherited disorders characterized by degeneration of skeletal muscle
The disorders differ in: Type of inheritance Area affected Rate of progression
This is a group of disorders characterized by pain and stiffness affecting muscles, tendons and surrounding soft tissues (not joints) Specific trigger points where pain may be stimulated
No obvious signs inflammation or degeneration in the tissues No cause is known but appears to be related to altered central neurotransmission resulting in increased soft tissue sensitivity to substance P
Gate Control Theory says that control systems or “gates” are built into normal pain pathways in the nervous system that can modify the entry of pain into the spinal cord and brain Gates can be open at synapses allowing pain to ascend the spinal cord to the brain Gates can be closed, reducing or modifying the passage of pain impulses
Incidence higher in women aged 20-
Often history of prior trauma or osteoarthritis
Aggregating factors include: Sleep deprivation Stress fatigue
Osteoarthritis Degenerative or “wear and tear” Non inflammatory joint disease Articular cartilage especially in weight bearing joints (hips and knees) is damaged from excessive mechanical stress Sometimes the breakdown is from unknown causes
Surface of cartilage becomes rough and worn and interferes with smooth joint movement Tissue damage appears to cause enzyme release that accelerates breakdown of cartilage Eventually, the bone underlying the cartilage is exposed and damaged and cysts and bone spurs develop along the margin of the bone
Pieces of the bone spur and cartilage break off inside the synovial cavity and cause further irritation No systemic effects are typically seen in osteoarthritis
Primary form of osteoarthritis is considered to by idiopathic Secondary type follows injury or abuse Commonly seem after participation in sports and some physically demanding occupations Once cartilage is damaged, a vicious cycle ensues Pain is mild and incidious in the beginning Pain becomes more severe and degeneration progesses
