Unit 9 Musculoskeletal System and Unit 10 Multi

Paratenonitis- Table 44-2 p.1546

"Inflammation" of the outer layer of the tendon (paratenon) alone whether or not the paratenon is lined by synovium -mucoid degeneration if the areolar tissue is seen -a scattered mild mononuclear infiltrate with or without focal fibrin deposition and fibrinous exudate.

Osteochondrosis p.1604

-Avascular diseases of the bone; insufficient blood supply to growing bones -Several types -Activity-related pain of the affected region that improves with rest

Legg-Calve-Perthes Disease p. 1604

-Blood supply to the femoral head is interrupted. -Ossification center first becomes necrotic, collapses, and then is gradually remodeled by live bone. -classically thought to be an osteochondrosis -self-limited disease of the hip is presumably produced by recurrent interruption of the blood supply to the femoral head -the ossification center first becomes necrotic and collapses and then is gradually remodeled by live bone --the cause of decreased blood supply to the head of the femur is unknown -several theories have been proposed, including trauma, infection and protein C and S deficiencies, which cause a hypercoagulable state or vascular anomalies -a plausible theory is that acute synovitis (infection of the synovial membrane) and increased hydrostatic pressure in the hip joint compress blood vessels that supply the femoral head. -constitutional factors definitely play a role -skeletal maturation is delayed an average of 2 years in children with this and affected children are between 2.5-7cm shorter than unaffected children of the same age -familiar occurrence is 30-40%

Fractures p.1540

-Broken bone can damage the surrounding tissue, periosteum, and blood vessels in the cortex and marrow. -Bone is unique: After a fracture it will heal with normal tissue, not scar tissue. -Healing occurs in phases. -a break in the continuity of a bone -a break occurs when force is applied that exceeds the tensile or compressive strength of the bone -these of healthy bones, particularly the tibia, clavicle, and lower humerus, tend to occur in young persons and are often the result of trauma -these of the hands and feet are usually caused by accidents in the workplace -the incidence of these of the upper femur, upper humerus, vertebrae, and pelvis is highest in older or older adults and is often associated with osteoporosis. -classified as complete or incomplete and open or closed -also classified according to the direction of the fracture line -further classified as pathologic, stress, or transchondral.

Classic Inflammatory Joint Disease p.1568

-Commonly called arthritis -Inflammatory damage or destruction in the synovial membrane or articular cartilage -Systemic signs of inflammation -Fever, leukocytosis, malaise, anorexia, and -hyperfibrinogenemia -Infectious or noninfectious

Potential causes of osteoporosis

-Decreased levels of estrogen and testosterone -Decreased activity level -Inadequate levels of vitamins D and calcium or magnesium -Alterations in the osteoprotegerin (OPG), receptor activator of nuclear factor kappa B (κB) ligand (RANKL), and receptor activator of nuclear factor κB (RANK): OPG/RANKL/RANK system -Postmenopausal osteoporosis: Increased osteoclast activity, changes in OPG, insulin-like growth factor (IGF), and family history -Glucocorticoids: Increase RANKL expression and inhibit OPG production by osteoblasts, leading to lower bone density

Osteogenesis imperfecta p.1597

-Defect in bone and/or vessel collagen production -Sillence classification: Types I through IV, based on severity -brittle bone disease -spectrum of disease caused by genetic mutation in the gene that codes for type I collagen, the main component of bone and blood vessels -osteoporosis. With fractures and skeletal deformities -Sillence classification is based on both models of inheritance and clinical findings -in the most severe form of this disorder, the child is usually stillborn or dies soon after birth, although some survive into childhood -in its more severe form is evident at birth because fractures and deformities have occurred in utero -the less severe forms may not become evident until the child begins to walk -some children with this milder form experience numerous fractures and can be mistaken for non accidental trauma until the diagnosis is made. -inheritance is usually autosomal dominant but can be autosomal recessive. ?? is a disorder caused by genetic mutation in the gene that encodes for type I collagen, the main component of bone and blood vessels. The Sillence classification defines four types. Types I and IV are milder forms and are inherited in an autosomal dominant pattern. Types II and III are more severe and are inherited in a recessive pattern. The classic clinical manifestations of osteogenesis imperfecta are osteopenia and an increased rate of fractures. Type IV can be subtle with more normal stature and fractures often not occurring until children are older; however, it can be misdiagnosed as child abuse. A bone scan may be useful in subtle injuries, especially rib fractures. Posterior rib fractures are especially likely to be the result of abuse. Nonaccidental trauma requires the child undergo skeletal survey, especially if the child is less than 2 years of age, and have a complete physical examination to evaluate for pattern bruising, burns, or multiple soft tissue injuries. Nonaccidental trauma necessitates early consultation with child protective services.

Bursitis p.1545

-Inflammation of a bursa -Is caused by repeated trauma. -Small sacs lines with synovial membrane and filled with synovial fluid; they are located between tendons, muscles and bony prominences -primary function is to separate, lubricate and cushion these structures -when irritated or injured, theses sacs become inflamed and swell -because most lie outside joints, joint movement is rarely compromised with bursitis -acute occurs primarily in the middle years and is often caused by trauma, repetitive irritation can cause chronic bursitis -septic is caused by wound infection or bacterial infection of the skin overlying these -commonly occurs in the shoulder, hip, knee and elbow -typical is an inflammation that is reactive to overuse or excessive pressure -the inflamed sac becomes engorged, and the inflammation can spread to adjacent tissues -the inflammation may decrease with rest, heat, and aspiration of fluids -shoulder (subacromial) - repetitive overhead activities -elbow (olecranon) - rheumatoid arthritis, gout, tuberculosis, leaning on elbow -hip (greater trochanter) - acute trauma, chronic stress -ischial (weaver's bottom) - overuse (runner, ballet dancer, lumbosacral disease, RA, OA) -knee - prepatellar (housemaid's knee) - trauma frequent kneeling, infection -pies anserine (medial knee) - obesity, long distance runner, OA, type 2 diabetes -heel (calcaneal) - poorly fitting footwear, Achilles tendinitis

Osteomalacia p.1557

-Deficiency of vitamin D lowers the absorption of calcium from the intestines. -Bone formation progresses to osteoid formation, but calcification does not occur; result is soft bones. -Metabolic disease characterized by inadequate and delayed mineralization of osteoclast in mature compact and spongy bone -the remodeling cycle proceeds normally through osteogenesis formation, but mineral calcification (hydroxyapatite formation) does not occur -bone volume remains unchanged, but the replaced bone consists of soft osteoid instead of rigid bone -result is abnormal bone matrix mineralization -rickets is similar to this in pathogenesis, but it occurs in the growing bones of children, whereas this occurs in adult bone -chronically low serum phosphate levels can be caused by tumors resulting in this -fibroblast growth factor-23 plays a significant role in maintaining normal serum phosphate levels -primarily produced by osteocytes, FGF-23 functions to inhibit absorption of phosphate in the renal proximal tubule. -these diseases occur in older adults, in premature infants of very low birth weights, and individuals adhering to rigid macrobiotic vegetarian diets -breast fed black infants who don't receive vitamin D supplementation have been shown to be at trick for developing nutritional rickets. -many factors contribute to the development of this but the most important is a deficiency of vitamin D -the major causes of vitamin D deficiency are diets deficient in vit D, decreased endogenous production of vit D, intestinal malabsorption of vit D, renal tubular diseases, and anticonvulsant therapy -disorders of the small bowel, kidneys, hepatobiliary system, and pancreas do cause vit d deficiency -in malabsorptive disease of the small bowel, vit D and calcium absorption are decreased, so vit D is lost in feces -liver disease interferes with the metabolism of vit D to its more active form and diseases of the pancreas and biliary system cause a deficiency of bile salts, which are necessary for normal intestinal absorption of vitamin D. -the mechanism by which anticonvulsant drug therapy results in decreased bone mineral density is not completely understood, but appears to be from direct impact on bone or effects on other regulations of bone metabolism such as calcium, vit d, and parathyroid hormone -the anticonvulsants phenobarbital and phenytoin interferes with calcium absorption and increase degradation of vit D metabolism in the liver through activation of the cytochrome P-450 pathway.

Scoliosis p.1600

-Idiopathic: No known cause -Onset: Infant, juvenile, adolescent -a rotational curvature of the spine most obvious in the anteroposterior plane -can be classified as nosntructural or structural -nonstructural results from a cause other than the spine itself, such as posture, leg length discrepancy or pain -structural is curvature of the spine associated with vertebral rotation -nonstructural can become structural if the underlying cause is not found and treated. -structural can result from curvature associated with vertebral rotation, congenital skeletal abnormalities, contracture, bone infections that involve the vertebrae, metabolic bone disorders (rickets, osteoporosis, osteogenesis imperfecta), joint disease and tumors, neuromuscular disease, trauma, extraspinal contractures, -most cases of structural have no known cause, although genetic factors are suggested -structural with no known cause is termed idiopathic, accounts for 70% of cases. -idiopathic is classified as infantile, juvenile, or adolescent, depending on this child's age at the time of onset -in infantile, spinal curvature develops during the first 3 years of life; in juvenile, curvature develops between the skeletal age of 4 and the onset of adolescence, and in adolescent scoliosis, it develops after the skeletal age of 10 -adolescent idiopathic is the most common

osteomyelitis in children- patho/clinical manifestations p.1601/1602/1603

-Infection spreads under the periosteum and along the bone shaft or into the bone marrow. -Sequestra: Sections of dead bone from periosteal separation -Involucrum: Periosteal new bone -Is significantly less common after the epiphyseal plates are closed, except in the vertebral body. -Infection may develop in any part of a bone, and abscesses spread slowly. -Destruction of the cortex in a localized area may result in a pathologic fracture. *patho: -usually begins as a bloody abscess in the metaphysics of the bone -the abscess ruptures under periosteum and spreads along the bone shaft or into the bone marrow cavity if untreated -infection rarely spreads down the medullary cavity of the bone but rather first gains entrance to the subperiosteal space in the metaphysis -the bone cortex in this area is porous, allowing easier entry for the bacteria than the shaft of the bone -because of the accumulation of debris caused by the infection, the periosteum may separate and form a shell of new bone around the infected portion of the shaft -because the periosteum is separated from an adequate blood supply of the bone die; these pieces of dead bone are called sequestra -the periosteum that maintains a blood supply generates new bone and is responsible for the appearance of the periosteum new bone or involucrum -the presence of the sequestra and involucrum indicates that the disease is highly aggressive or established. -in infants is often associated with septic arthritis bc the infant's bone has blood vessels that perforate the growth plate -bc of the unique nature of the blood supply to an infants bones the occurrence of this and septic arthritis in combination is higher than 50% -normal anatomic variations in infants allow infection to spread directly to the epiphysis, which causes both joint disease and permanent injury to the growth plate. -multiple sites of this are also common in children younger than 2 years of age -other areas of this and possible septic arthritis must be evaluated through a bone scan of the entire skeleton. -children are susceptible to joint involvement for several reasons -in the immature infant, there is no epiphyseal plate or an ossification nucleus at the end of the bone and the cartilage precursor of bone is penetrated by vascular channels -in these infants the infection begins in the vulnerable cartilage precursor of the end bone itself and results in rapid destruction of the joint and arrested growth of the bone -for this reason the early detection and treatment of this are crucial if the infant's joint is to be saved from destruction -as the child matures and the epiphyseal or growth plate forms a temporary barrier is established against infection because the arterioles end beneath the epiphyseal plate. -in children older than 2 years, the epiphyseal plate prevents the spread of a metaphyeal abscess into the epiphysis and the cortex of the metaphysis is thicker -these anatomic differences increase the likely hood that the metaphyseal abscess will extend into the diaphysis and the blood supply of the bone will be disrupted -the periosteum is also more difficult to perforate in older children; this may lead to a larger subperiosteal abscess that could endanger the periosteum blood supply as well -this process results in extensive sequestrum formation and chronic this. -much less common after the physeal plates are closed, except in the vertebral body -infection may develop in any part of a bone, and abscesses spread slowly -destruction of the cortex in a localized area may result in a pathologic fracture. -spread of infection to contiguous joints is related to the child's age -metaphyeal infection may spread to contiguous joints if the fibrous joint capsule includes the metaphysis and epiphysis -this special situation exists at the hip joint, distal femur, proximal humerus and radius, and lateral ankle -careful clinical vigilance helps protect children with this from suffering permanent joint injury -unlike bone, the articular cartilage of joints is unable to repair after injury from infection. *clinical manifestations: Clinical manifestations of osteomyelitis are age-dependent and are related to differing vascular patterns found in the skeletal system at various ages. Three distinct groups can be identified- 1)Infants younger than one year 2)children from one year of age to puberty 3)adolescence after cessation of bone growth and adults infants: May be an acute illness characterized by fever and failure to move the affected limb (pseudoparalysis). Infant osteomyelitis is characterized by involvement of multiple sites within the same bone or in multiple bones. if untreated involvement of the adjacent growth plate can result in growth arrest. children: Between ages of one year and puberty is characterized by fever and systemic signs of toxicity. The illness is sometime subacute with the child complaining of swelling, fever, tenderness, and decrease in ability to bear weight on or move the affected area. Onset can be abrupt. Osteomyelitis during childhood most often affects the long bones but also may be found in the pelvis and spine. Manifestations are usually accompanied by elevated white blood cell counts and elevated erythrocyte sedimentation rates. When the level of C-reactive protein (CRP) is elevated it is a sensitive sign of osteomyelitis and can rapidly decrease with appropriate treatment. Evidence of infection using roentgenograms can be delayed but bone scan is positive within 48 hours. adolescents and adults: In addition to the sites previously mentioned osteomyelitis in adolescents and adults may involve the vertebrae. Back pain with a duration of several weeks may be the only clinical complaint. This age group is less often affected then younger populations.

Rhabdomyolysis p.1547

-Life-threatening complication of severe muscle trauma with muscle cell loss -Crush syndrome versus crush injuries -Compartment syndromes -myoglobinuria -rapid breakdown of muscle that causes the release of intracellular contents, including protein pigment myoglobin, into the extracellular space and bloodstream -physical interruptions in the sarcolemmal membrane, called delta lesions, suggest that the sarcolemmal membrane is the rout through which muscle constituents are released -myoglobinuria refers to the presence of the muscle protein myoglobin in the urine -more recently, myoglobinuria has been resported in individuals found unresponsive and immobile for long periods, such as drug and alcohol overdoses -classic triad: Muscle pain, weakness, and dark urine (from myoglobin)

Osteoarthritis p.1565

-Inflammatory joint disease -Loss of articular cartilage, sclerosis of underlying bone, and formation of bone spurs (osteophytes) -Also called degenerative joint disease -Incidence increases with age -common age-related disorder of synovial joints -characterized by local areas of damage and loss of articulate cartilage, new bone formation of joint margins (osteophytosis), subchondral bone changes, variable degrees of mild synovitis and thickening of joint capsule -commonly classified as noninflammatory joint disease -it is clear that specific markers of inflammation are present in this and inflammation is an important feature -the use of MRI and arthroscopy has mad it clear that changes are not defined by changes noted on X-ray films alone -the exact cause is uncertain, pathology centers on load-bearing areas -advancing disease reveals narrowing of the joint space because of cartilage loss, bone spurs (osteophytes), and sometimes changes in the subchondral bone -uncommon in people younger than 40 but rises in incidence with age -low-grade inflammation, calcification of articulate cartilage, genetic alterations and metabolic disorders combines with the interaction of transcription factors, cytokines, growth factors, matrix molecules and enzymes affect development and progression -generally distributed throughout the peripheral and central joints of the body (hips, hands, knees, and spine) -with aging, the quality and quantity of the proteoglycans in cartilage decrease in direct proportion to the severity of this. -can be caused by any condition that damage cartilage directly; subjects the joint surfaces or underlying bone to chronic, excessive or abnormal forces; or causes instability in the joint.

Rheumatoid Arthritis p.1568

-Inflammatory joint disease -Presence of rheumatoid factors (RFs): RA or RF test -Antibodies (immunoglobulin G [IgG] and IgM) against antibodies -Joint fluid with inflammatory exudate -a chronic, systemic inflammatory autoimmune disease distinguished by joint swelling and tenderness and destruction of synovial membranes and joints, leading to disability and premature death -the first joint to be affected is the synovial membrane which lines the joint cavity -multiple immunoregulatory cytokines (such as interleukins, B cells, and matrix metalloproteinases) contribute to joint damage -inflammation may spread to the articular cartilage, fibrous joint capsule, and surrounding ligaments and tendons, causing pain, joint deformity and loss of function -the joints most commonly affected are in the fingers, feet, wrists, elbows, ankles and knees, but the shoulders, hips, and cervical spine also may be involved, as well as the tissues of the lungs, heart, kidneys and skin. -the frequency increases with age -can also cause fever, malaise, rash, lymph node or spleen enlargement and Raynaud phenomenon (transient lack of circulation to the fingertips and toes). -the cause remains obscure -it is likely a combo of genetic factors interacting with inflammatory mediators -the intricate interplay of chemokines (powerful mediators of inflammation) is largely responsible for this chronic inflammatory characteristics -ligand/receptor chemokines attract T cells and produce inflammatory changes. -environmental factors including geographic area of birth, length of breastfeeding, socioeconomic status, and especially smoking have been identified as risk factors -higher prevalence among women -hormones and genetics play a role as shown by symptom improvement during pregnancy and flares with breastfeeding

Gout p.1574

-Is a metabolic disorder that disrupts the body's control of uric acid production or excretion. -exhibits high levels of uric acid in the blood and other body fluids. -Occurs when the uric acid concentration increases to high enough levels to crystallize. -Crystals deposit in connective tissues throughout the body. -If prolonged in joints: Gouty arthritis -Tophi: Small, white visible nodules -a syndrome caused by an inflammatory response to uric acid production or excretion resulting in high levels of uric acid in the blood (hyperuricemia) and in other body fluids, including synovial fluids -although hyperuricemia is essential for the development of this, into not the only factor -other factors include age (rare before 30), genetic predisposition (X-linked alteration of the enzyme HGPRT), excessive alcohol consumption, obesity, certain drugs (thiazides), and lead toxicity -when the uric acid concentration is >6.8 mg/dl in fluids it crystallizes and forms insoluble precipitates of mono sodium irate that are deposited in connective tissue throughout the body -crystallization in synovial fluid causes acute, painful inflammation of the joint and triggers an inflammatory response by macrophages -when macrophages phagocytize MSU crystals, they form a protein scaffold known as an inflammasome -inflammasome so then convert inactive interleukins of IL-1B and IL-18 into their active forms -prolonged accumulation results in joint damage, a condition known as thisy arthritis -with time, crystal deposition in subcutaneous tissues causes the formation of mall, white nodules or tophi that are visible through the skin -crystal aggregates deposited into the kidneys can form irate renal stones and lead to renal failure.

Nonunion p.1543

-Is the failure of the bone ends to grow together. -Gap between the broken ends of the bone fills with dense fibrous and fibrocartilaginous tissue. -Occasionally, fibrous tissue contains a fluid-filled space that resembles a joint: Referred to as a false joint or a pseudarthrosis.

Osteomyelitis p.1558

-Is usually caused by a staphylococcal infection. -Is often outside the body (exogenous); can be from a bloodborne (endogenous) infection. -Infection spreads under the periosteum and along the bone shaft or into the bone marrow. -In adults: Affects the cortex -Sequestra: Sections of dead bone from periosteal separation -Involucrum: Periosteal new bone -Acute versus subacute versus chronic -bone infection most often caused by bacteria; however, fungi, mycobacteria, parasites and viruses can infect bone -exogenous is an infection that enters from outside the body, for example, through opens fractures, penetrating wounds, or surgical procedures -infection spreads from soft tissues into adjacent bone -endogenous is caused by pathogens carried in the blood from sites of infection elsewhere in the body -hematogenous, infection spreads from bone to adjacent soft tissues -commonly found in infants, children and older adults -common complication of sickle cell anemia and low oxygen tension. -s. Aureus (including MRSA) is the primary cause of hematogenous -other microorganisms include group B strep, H. Influenzae, salmonella, and gram negative bacteria -group B strep and H influenzae tend to infect young children; salmonella infection is associated with sickle cell anemia; and gram-negative infections are most common in older adults and individuals with impaired immunity -mycobacterial and fungal infections occur in immunocompromised individuals. -cutaneous, sinus, ear and dental infections are the primary sources of bacteria in hematogenous type -soft tissue infections, disorders of the GI tract, infection of the GU system and respiratory tract infections are also sources of bacterial contamination -infections contracted after total joint replacement surgeries can be causes of this -the vulnerability of specific bone depends on the anatomy of its vascular supply -in adults, hematogenous type is more common in the spine, pelvis, and small bones. -microorganisms reach the vertebrae through arteries, veins, or lymphatic vessels -the spread of infection from pelvic organs to the vertebrae is well documented -vaginal, uterine, ovarian, bladder and intestinal infections can lead to iliac or sacral OM. -exogenous type can be caused by human bites or fist blows to the mouth -superficial animal or human bites inoculate local soft tissue with bacteria that later spread to underlying bone -deep bites can introduce microorganism directly onto bone -the most common infecting organism in human bites is s. Aureus -in animal bites the most common infecting organism is Pasturella multocida, which is a part of the normal mouth flora of cats and dogs. -direct contamination of bones with bacteria also can occur in open fractures or dislocations with an overlying skin wound -intervertebral disk surgery and operative procedure involving I plantations of large foreign objects, such as metallic plates or artificial joints, are associated with exogenous type -local injections and venous punctures are significant causes of exogenous type -exogenous type of the arm and hand bones tends to occur in drug abusers -s. Aureus is the most common pathogen -persons who are chronically ill, have diabetes, or alcoholism, or are receiving large doses of corticosteroids or immunosuppressive drugs are particularly susceptible to exogenous type or recurring episodes of the disease.

Osgood-Schlatter Disease p. 1605

-Mild tendinitis to a complete separation of the anterior extension of the tibial epiphysis -tendinitis of the anterior patellar tendon, within which the patella is embedded and associated osteochondrosis of the tubercle of the tibia -occurs most often is preadolescents and adolescents who participate in sports -incidence higher in boys than girls, increased outward tibial fusion.

Tendinosis p.1545

-Painful degradation of collagen fibers -Intratendinous degeneration (commonly due to aging, micro trauma, muscular compromise) -collagen disorientation, disorganization and fiber separation by an increase in mucoid ground substance, increased preponderance of cells and vascular spaces with or without neovascularization and focal necrosis or calcification

Osteoporosis p.1550

-Poorly mineralized bone -Primary versus secondary -Bone density: Normal bone: 833 mg/cm2 -Osteopenic bone: Decreased bone mass: 833 to 648 mg/cm2 -Osteoporosis: <648 mg/cm -porous bone -Types: Perimenopausal, Iatrogenic, Regional, Postmenopausal, Glucocorticoid-induced, Age-related bone loss -disease in which bone tissue is normally mineralized but the mass - density of bone - is decreased and the structural integrity of trabecular bone is impaired -two types are generally considered -postmenopausal, or primary, is most common -secondary is caused by other conditions, including hormonal imbalances (endocrine disease, diabetes, hyperparathyroidism, hyperthyroidism) medications (such as heparin, corticosteroids, phenytoin, barbiturates, lithium) and other substances (including tobacco and ethanol) -other conditions including rheumatoid disease, HIV, malignancies, malabsorption syndromes, liver or kidney disease, also increase the risk for developing -cortical bone becomes more porous and thinner, making bone weaker and prone to fractures. -the WHO has defined it based on bone density: 1) Normal bone mass is greater than 833 mg/cm2 2) osteopenia, or decreased bone mass is 833-648 mg/cm32 3) this is bone mass less than 648 mg/cm2 -complex, multi factorial chronic disease that often progresses silently for decades until fractures occur -it is the most common disease that affects bone -it is not necessarily a consequence of the aging process because some older adults retain strong, relatively dense bones -old bone is being reabsorbed faster than new bone is being made, causing the bones to lose density, becoming thinner and more porous -a progressive loss of bone mass may continue until the skeleton is no longer strong enough to support itself -eventually, bones can fracture spontaneously -as bone becomes more fragile, fractures occur from falls or bumps that would not previously have caused fracture. -severe or established this is identified when there has been a fragility fracture -the disease can be 1) generalized, involving major portions of the axial skeleton, 2) regional, involving only one segment of the appendicular skeleton -the major risks for persons with this are fractures -men lose bone density with aging but be hey begin with a higher bone density, they reach osteoporotic levels at an older age than women do. -vertebral fracture are the most common type of fracture but may be asymptomatic -even if the fracture doesn't cause pain, vertebral fractures can cause deformity, reduced pulmonary function, and loss of height. -black women remain at a high risk because of factors such as decreased dietary Ca intake, a high percentage of lactose intolerance, and increased prevalence of disease, such as sickle cell disease and lupus that increases the risk of developing this -decreased bone strength with aging is partly due to lower bone mass, but other factors such as deterioration of type 1 collagen likely contribute to increased fracture risk.

osteoporosis- patho/clinical manifestations p.1550/1551/1552/1553/1554/1555

-Reduced bone mass or density and an imbalance of bone resorption and formation -Bone histologic anatomy: Usually normal but lacks structural integrity -develops when the remodeling cycle - the process of bone resorption and bone formation - is disrupted, leading to an imbalance in the coupling process -the explosion of new info in the field of bone biology has led to new understanding of the roles of hormones, growth, and signaling factors and cellular biology in this -although hormonal influences remain important in maintaining bone health, genetic factors and the role of oxidative stress are receiving increased attention as critical determinants of bone homeostasis -reactive oxygen species are normal byproducts of aerobic metabolism and although they can cause cell damage, at levels below which they cause OS, ROS serve as signaling molecules for many cell types, including osteocytes, osteoblasts, and osteoclasts -when excess ROS accumulate, OS accounts and can result in loss of bone mass and bone strength. *clinical manifestations: The specific clinical manifestations of osteoporosis depend on the bones involved. The most common manifestations however is bone deformity. Pain tends to occur only when there is a fragility fracture. Fractures are likely to occur because the trabeculae of spongy bone becomes thin and sparse and compact bone becomes porous. As the bones lose volume they become brittle and weak and may collapse or become misshapen. Vertebral collapse causes kyphosis (hunchback) and diminished height. Fractures of the long bones particularly the femur and humorous, distal radius, ribs, and vertebrae are most common. The most serious fractures associated with osteoporosis are hip fractures because of their resultant chronic pain, disability, diminished quality-of-life, and premature death. Fracture of the neck of the femur (intertrochanteric fracture) tends to occur in older adult women with osteoporosis. Fatal complications or fractures include fat or pulmonary embolism hemorrhage and shock. approximately 20% of persons with a hip fracture die as a result of surgical complications.

gout- patho/clinical manifestations p.1574/1575/1576/1577/1578

-Related to purine metabolism -Causes: Purine synthesis or breakdown is accelerated -Poor uric acid secretion in the kidneys -Mechanisms for crystal deposition: Low body temperatures -Decreased albumin or glycosaminoglycan levels -Changes in ion concentration and pH -Trauma -Primary versus secondary -Clinical stages: Asymptomatic hyperuricemia: Urate level is high with no symptoms. -Acute gouty arthritis: Attacks develop. -Tophaceous gout: Urate crystal deposits (tophi) appear in cartilage, synovial membranes, tendons, and soft tissues. *patho: -closely linked to purine metabolism and kidney function -at the cellular level, purines are synthesized to purine nucleotides, which are used in the synthesis of nucelic acids, adenosine triphosphate, cyclic adenosine monophasphate and cyclic guanosine monophasphate -uric acid is a breakdown product of purine nucleotides -some individuals with this have an accelerated rate of purine synthesis accompanied by an overproduction of uric acid -other individuals break down purine nucleotides at an accelerated rate that also results in an overproduction of uric acid -a deficiency of the enzyme HGPRT can lead to an increased production of uric acid -a complete absence of HGPRT is uncommon but can occur in X-linked Lesch-Nyhan syndrome, with males at risk for hyperuricemia, neurological alterations and sometimes this arthritis -the majority of individuals with this have an unknown metabolic defect, which is referred to as primary -when the etiology is known, it is referred to as secondary -most uric acid is eliminated from the body through the kidneys. -urate is filtered at the glomerulus and undergoes reabsorption and excretion within the proximal renal tubules -in primary, urate excretion by the kidneys is sluggish; this may be the result of a decrease in glomerular filtration of urate or acceleration in urate reabsorption -MSU crystals deposited in renal tubules can cause acute nephropathy. -MSU crystals can stimulate and perpetuate the inflammatory response -the presence of MSU crystals triggers the acute inflammatory response -initiation of the complement system activates cytokines and produces other substances called chemoattractants, that draw neutrophils out of the circulation- begin phagocytizing (ingesting) the crystals. -a variety of inflammatory mediators are released during the crystal/cell response, of which IL-1B appears to be of prime important -other factors including chemotactic factors, lysosomal enzymes, eicosanoids, prostaglandin E, reactive oxygen species and collagenase are also released -some of these mediators stimulate the influx of neutrophils, monocytes, and lymphocytes. -within the joint fluid, urate crystals react particularly with neutrophils and monocytes -tissue damage begins to occur, principally when the neutrophils release the contents of their phagolysosomes -these contents also perpetuate inflammation -at an early phase of an acute gouty attack, synovial microtophi have been demonstrated -as the process continues, numerous microtophi may be present on the synovial membrane. *clinical manifestations: gout is manifested by: 1) an increase in serum uric concentration (hyperuricemia) 2)recurrent attacks of monoarticular arthritis (inflammation of a single joint) 3)deposits of monosodium urate monohydrate (tophi) in and around the joints 4)renal disease involving glomerular, tubular, and interstitial tissues and blood vessels 5)the formation of renal stones these manifestations appear in 3 clinical stages: -asymptomatic hyperuricemia- The serum urate level is elevated but arthritic symptoms, tophi, and renal stones are not present, may persist throughout life. -Acute gouty arthritis: attacks develop with increased serum uric concentrations, tend to occur with sudden or sustained increases of hyperuricemia but also can be triggered by trauma, drugs, and alcohol. -tophaceous gout: The third and chronic stage of disease can begin as early as three years or as late as 40 years after the initial attack of gouty arthritis. Progressive inability to excrete uric acid expands the urate pool until urate crystal deposits (tophi) appear in cartilage synovial membranes, tendons, and soft tissue. Attacks of gouty arthritis occur abruptly usually in a peripheral joint. The primary symptom is severe pain. Approximately 50% of the initial attacks occur in the metatarsalphalangeal joint of the great toe. The other 50% involve the heel, ankle, and instep of the foot, knee, wrist, or elbow. The pain is usually noticed at night. Within a few hours the affected joint becomes hot red and extremely tender and may be slightly swollen. Lymphangitis and systemic signs of inflammation (leukocytosis, fever, elevated sedimentation rate) occasionally are present. Untreated mild attacks usually subside in several hours but may persist for 1 to 2 days. Severe attacks may persist for several days or weeks. After recovery the symptoms resolve completely. Intervals between acute attacks of gouty arthritis are called intercritical periods. Some individuals never have a second attack, others experience subsequence attacks within days to as long as 5 to 10 years after the first. The helix of the ear is the most common sight of tophi, which are the characteristic diagnostic lesion of chronic gout. Each tophus consists of a deposit of urate crystals surrounded by a granuloma made up of mononuclear phagocytes (macrophages) that have developed into epithelial and giant cells. Tophaceous deposits produce irregular swellings of the fingers, hands, knees, and feet. Tophi commonly form lumps along the ulnar surface of the forearm, the tibial surface of the leg, the Achilles tendon, and the Olecranon bursa. Tophi may produce marked limitation of joint movement and eventually cause grotesque deformities of the hands and feet. Although tophi themselves are painless they often cause progressive stiffness and persistent aching of the affected joint. Tophi in the upper extremities may cause nerve compression such as carpal tunnel syndrome in the lower extremities tophi may cause tarsal tunnel syndrome. They also may erode and drain through the skin. Renal stones are 1000 times more prevalent in individuals with primary gout than in general population. Renal stones conform in the collecting tubules, pelvis, or ureters causing obstruction, dilation, and atrophy of the more proximal tubules and leading eventually to acute renal failure. Stones deposited directly in renal interstitial tissue initiate an inflammatory reaction that leads to chronic renal disease and progressive renal failure.

Developmental dysplasia of the hip p.1594

-Subluxated or dislocated or acetabular dysplasia -formerly known as congenital dislocation of the hip, is an abnormality in the development of the proximal femur, acetabulum or both -although most often present at birth, it may occur at any time in the newborn or infant period -the left hip is affected in 60% of cases. -risk factors include family history, female gender, metatarsus adductus, torticollis, oligohydramanios, first pregnancy, and breech presentation -first pregnancies and oligohydramanios (deficient volume of amniotic fluid) are thought to limit fetal movement and breech presentation not only limits movement but also places the hips in a position of flexion and adduction, which creates a more shallow socket, or acetabulum -maternal hormones that reportedly increase joint laxity also have an effect on this, although the exact mechanism is unknown -more common in cultures that swaddle infants with the hips in extension and adduction -it is almost unknown in African cultures where infants are carried, with legs abducted on the back.

Strain- p.1545

-Tear or injury to a tendon -major trauma can tear or rupture a tendon at any site in the body -most often injured are the tendons of the hands and feet, the knee (patellar), the upper arm (biceps and triceps), the thigh (quadriceps), the ankle, and the heel (Achilles) -lifting excessive weight with the arms can cause traumatic rupture of the biceps tendon -rupture of the Achilles' tendon occurs when forced dorsiflexion is applied to the foot when it is in plantar flex ion -spontaneous tendon ruptures can occur in individuals receiving local corticosteroid injections or fluoroquinolones and in persons with rheumatoid arthritis or SLE

Uric acid p.1575 (left column 4th para)

-a byproduct of protein metabolism that normally assists with removal of nitrogen waste from the body -at loser levels it is an important antioxidant but at high levels it acts as a pro-oxidant where it increases levels of free radicals and causes other inflammatory changes -when ionized, it can form salts with various cations but 98% of extracellular this is in the form of monosodium urate (uric acid salt) -at any time, the proportion of this or urate is pH dependent, so the ratio of these two forms varies considerably in urine. -the solubility of urate and this is critical to the development of crystals -urate is more soluble in plasma, synovial fluid, and urine than in aqueous solutions; solubility in urine rises dramatically as the pH increases to more than 4 -there is little change however, in the solubility or urate within the normal pH range that exists in the plasma, synovial fluid and other tissues -decreasing temperatures cause both urate and this solubility to fall

Rheumatoid factors p.1569

-a key genetic element has been localized to the human leukocytes antigen-death receptor 4, HLA-DRB1 (death receptor beta), and HLA-DP genes of the major histocompatibility complex in all ethnic groups -a surprising new discovery is the presence of T-cell abnormalities in individuals with RA, indicating a defect in telomere repair that may result in faster aging of telomeres with subsequent loss of efficient immune function -with long term or intensive exposure to the antigen, normal antibodies (immunoglobulins) become autoantibodies - antibodies that attach host tissues (self-antigens) -because they are usually present in individuals with RA, the altered antibodies are termed this -usually consist of two classes of immunoglobulin antibodies (IgM and IgG) but occasially involve antibodies for IgA -their main antigenic targets are portions of the immunoglobulin molecules -these bind with their target self-antigens in blood and synovial membrane, forming immune complexes.

Burn shock

-a phenomenon consisting of both a hypovolemic cardiovascular component and a cellular component -results from massive fluid losses from the circulating blood volume -hypovolemia is caused by increased capillary permeability with massive fluid losses from blood volume -altered cell membrane permability and loss of electrolyte homeostasis contribute -cardiac contractility is decreased during the first 24 hours with shunting of blood away from the liver, kidney and gut -fluid resuscitation, such as with LR solution, involves infusion of fluid at a rate faster than the loss of circulating volume -the most reliable criterion for adequate resuscitation is urine output -capillary seal is the term used to indicate the end of this -a major burn injury, is a systemic Pathophysiologic issue that requires therapeutic intervention to sustain life -the immediate (acute) physiologic consequence of a major burn injury, center around the profound, life-threatening hypovolemic shock that occurs in conjunction with cellular and immunologic disruption within a few hours of injury

Osteomyelitis in children p 1601

-an infection of the bone -Is often associated with septic arthritis because an infant's bone has blood vessels that perforate the growth plate. -Begins as a bloody abscess in the metaphysis of the bone. -Vertebrae may be involved in adolescents and adults. These age groups are affected less often than younger populations. -bacteria enter the bone through the bloodstream and lodge in the medullary cavity, where a rich phagocytic mechanism often prevents most of the bacteria from establishing an infectious state -in some cases, the bacteria may lodge at the end of the venous loops beneath the epiphyseal plate, and infection then develops because there are no phagocytic cells present to remove the bacteria. -the microorganism responsible for this varies and is related to the age of the child. -in the newborn, it is primarily caused by staphylococcus aureus. -Group B strep and E. Coli infections are responsible for some cases, esp those of multiple bone involvement and in high risk infants. -S. Aureus is responsible microorganism for 80-90% of this in older children -H. Influenzae a previously common cause of this in children less than 5 years of age has become rare -causes of MRSA have risen alarmingly in the past 5 years -MRSA now causes up to 30% of new cases -Gram-negative microorganisms account for an increasing number of infections of the vertebrae where salmonella infections are associated with sickle cell disease. -factors that predispose an individual to the development of this include impetigo, furunculosis, infected lesions of varicella, infected burns, cerebral abscesses, immunization with BCG vaccine, prolonged IV and central parenteral alimentation, drug addiction and direct trauma to the area adjacent to the site of OM.

Transient regional osteoporosis p.1552 (right column last para)

-associated with the 3rd trimester of pregnancy or the immediate postpartum period -typically self-limiting syndrome affecting the lower extremity joints of middle-aged men and women -the etiology is unknown and although most cases spontaneously resolve, some occurrences of bone demineralization may be related to osteogenesis

Postmenopausal osteoporosis p.1552

-bc bone density related to quantity of bone, bone quality is not accurately identified by bone density testing -bone density testing may or may not accurately identify individuals with increased fracture risk -an online tool called FRAX incorporates clinical risk factors with BMD at the femoral neck to predict an individual's 10 year probability of fracture -this occurs in middle aged and older women -it can occur because of estrogen deficiency as well as estrogen-independent age-related mechanisms (secondary causes such as hyperparathyroidism and decreased mechanical stimulation) -recent studies indicate that increased oxidative stress and increased intracellular reactive oxygen species play a significant role in the development of age related bone loss, as well as other age-related changes in the body -hormonal deficiency also can increase with stress, excessive exercise, and low body weight -changes include a substantial increase in bone turnover - an imbalance between the remodeling activity of osteoclasts and osteoblasts -increased formation and longevity of osteoclasts results in increased bone resorption and is associated with a cascade of proinflammatory cytokines -increased cytokines activation, especially TNF, can occur with declining estrogen levels -estrogen helps protect against the effects of OS and osteoclast apoptosis -biologically these processes involve the receptor activator nuclear factor kB ligand (RANKL), transcription factors such as forehead proteins, the Wnt and osteoprotegerin, signaling pathways, and insulin-like growth factor -other causes may include a combo of inadequate dietary calcium intake and lack of vitamin D, possibly decreased Mg level, lack of exercise, low body mass, and family history -IGF is known the help in fracture healing and collagen synthesis and improves conditions for bone mineralization -IGF levels significantly decline by age 60 -characterized by increased bone resportion relative to the rate of bone formation, leading to sustained bone loss resulting from estrogen deficiency -bone loss resulting from estrogen deficiency also contributes to osteoporosis in men

Septic shock

-begins with impaired cellular metabolism caused by uncontrolled septicemia -the infecting agent triggers the inflammatory and immune response -it is part of a continuum known as SIRS -mortality for this is very high -a condition caused by systemic infection that results in decreased tissue perfusion and oxygenation and can lead to MODS and death

Torus fracture p.1541

-buckle -the cortex buckles but doesn't break -a relatively stable fracture

Neurogenic shock in children

-caused by a loss of vasomotor tone after severe injury to the spinal cord -clinical manifestations include warm skin, hypotension with a low diastolic blood pressure, and power systemic perfusion -tachycardia is not present -a form of hypovolemic and vasogenic (maldistribution) shock -caused by a loss of vasomotor tone after severe head or spinal cord injury -massive vasodilation and loss of sympathomimetic tone result in a relative hypovolemia and hypotension -the loss of sympathetic tone prevents compensatory tachycardia

Hypoxia and ischemia in shock in children

-causes tissue inadequate blood flow and inadequate oxygen delivery that leads to acidosis and cell dysfunction -oxygen delivery may be inadequate because arterial oxygen content or cardiac output is low or because there are increased metabolic requirement or impaired cellular use of oxygen -these are primary insults to cells

Glucocorticoid (cortisone) inducing osteoporosis p.1553

-characterized by increased bone resportion and decreased bone formation -increase RANKL expression and inhibit OPG production by osteoblasts - the use of immunosuppressive drugs (cyclosporine A) to reduce rejection of transplanted organs also alters the OPG/RANKL/RANK system and can lead to post transplantation osteoporosis -other conditions affected by OPG/RANKL/RANk include RA, myeloma, vascular disease, and skeletal metastasis from neoplastic disorders

Warm shock

-characterized by peripheral vasodilation, warm skin with flash capillary refill,, bounding pulses and wide pulse pressure -thought to be associated with hyper dynamic cardiovascular function and high cardiac output -characteristics are most commonly seen in adults with septic shock

Cardiogenic shock in children

-decreased cardiac output, is observed most commonly after cardiovascular surgery or with inflammatory diseases of the heart, such as cardiomyopathy and myocarditis -it is also found in children with obstructive congenital heart disease and those with drug toxicity or severe electrolyte or acid-base imbalances -clinical manifestations include inadequate systemic perfusion despite adequate intravascular volume -cardiac output is typically low -adrenergic compensatory mechanisms, including peripheral vasoconstriction and decreased urine volume are similar to those found in hypovolemic shock -results from impairment of myocardial function -this and hypovolemic shock blood flow distribution is reduced to skin, gut and kidney to maintain blood flow to the heart and brain

Burns

-classified according to depth and extent of injury -first degree involve the superficial skin without loss of protective function -secondary degree are superficial (blister formation) or superficial involving partial skin thickness with a waxy white appearance and no involvement of dermal appendages -third degree involve full skin thickness and other underlying tissues -painless and can be life-threatening as a result of hypovolemic shock and metabolic and immunologic responses -the TBSA burned is estimated using either the rule of nines or the Lund and Browder chart -hypovolemia associated with this shock is caused by increased capillary permeability with massive fluid losses from blood volume -altered cell membrane permeability and loss of electrolyte homeostasis contribute to this shock -cardiac contractility is decreased during the first 24 hours with shunting of blood away from the liver, kidney and gut -fluid resuscitation, such as with LR, involves infusion of fluid at a rate faster than the loss of circulating volume -the most reliable criterion for adequate resuscitation of this shock is urine output -capillary seal is the term used to individative the end of this shock -transmembrane potentials are altered in cells not directly damaged by heat, with impairment of the Na-K pump and loss of Mg and phosphate -the stress of a major burn activates the sympathetic nervous system with release of catecholamines, cortisol, glucagon, and insulin -this injury produces a hyper metabolic state that persist until wound closure and is related to a higher therm regulatory set point -the local inflammatory response at the site releases cytokines, oxygen-free radicals, chemotactic factors and eicosanoids, which lead to a systemic inflammatory response and contributes to hyper metabolism -a posttraumatic hypermetabolic response is associated with increased visceral heat production -alterations in clotting factors produce a hypercoagulable state following major burns -the immune response following this is immediate, prolonged, and severe -numerous alterations in inflammatory cytokines are evident in the immediate burn period, affecting cellular immunity, antibody production, and attraction of neutrophils and contributing to the vasodilation and increased capillary permeability associated with burn shock -white blood cells are altered, and there is decreased opsonization and phagocytosis, contributing to the development of sepsis -changes in intestinal wall integrity lead to translocation of bacteria, endotoxemia and septic shock -loss of intact skin with a major this results in significant evaporative water loss contributing to hypovolemia -tx of major these involves meticulous wound management, adequate fluids and nutrition, early surgical excision and grafting, modulation of the hypermetabolic state and pain mgmt -The three essential elements of survival after a major burn are (1) meticulous wound management, (2) adequate fluids and nutrition, and (3) early surgical excision and grafting.

Open fracture p.1541

-compound -if the skin is broken -communicating wound between bone and skin

Regional osteoporosis p.1552

-confined to a region or segment of the appendicular skeleton, usually has a known cause -no known etiology, is characterized by bone marrow edema, and can cause severe pain -the lower extremity is most often affected, but other areas may be involved -it is usually self-limited -tends to occur in middle aged men and women in their late second or third trimester of pregnancy -characterized by bone marrow edema, seen on MRI and areas of localized bone demineralization on radiographs -tx is primarily symptomatic and the condition usually resolves spontaneously over 3-6 months with no long term-adverse effects -classic type is associated with disuse or immobilization of a limb because of fractures, motor paralysis or bone or joint inflammation -a negative calcium balance develops early and continues throughout the period of immobilization -after 8 weeks of immobilization, significant this is present, although it may develop earlier in persons younger than 20 years or older than 50 years -a uniform distribution of this also has been observed in astronauts and in individuals treated with air suspension therapy as a result of weightless ness and lack of mechanical strain

Signaling pathways and OA p.1567 (left column top para)

-crosstalk between these contributes to the development and progression of this -some of the enzymes that degrade collagen (chemokines and metalloproteinases) are produced by the synovium -chondrocytes apoptosis is increased in this cartilage and is directly correlated with hydroxyapatite crystal deposition -nitric oxide stimulates apoptosis in chondrocytes -the resultant cartilage destruction initiates the IL01B and TNF-a types of inflammation -genetic deficiencies of inhibitors of calcification also may contribute to "run away" calcification -collagen breakdown destroys the fibrils that give articular cartilage its tensile strength and exposes the chondrocytes to mechanical stress and enzyme attach -thus a cycle of destruction begins that involves all the components of articular cartilage - proteoglycans, collagen fibers, and chondrocytes

osteomalacia- patho/clinical manifestations p.1557

-crystallization of minerals in osteoid required adequate concentrations of Ca and phosphate -when the concentrations are too low, crystallization (and hence ossification) doesn't proceed normally -vit D deficiency disrupt is mineralization because vit D normally regulation and enhances the absorption of calcium ions from the intestine -a lack of vit D causes the plasma Ca concentrations to fall -low plasma ca levels stimulate increased synthesis and secretion of parathyroid hormone -although the increase in the level of circulating PTH raises the plasma ca concentration, it also stimulated increased renal clearance of phosphate -when the concentration of phosphate in the bone decreases below a critical level, mineralization cannot proceed normally. -abnormalities occur in spongy as well as compact bone -trabeculae in spongy bone become thinner and fewer, whereas haversian systems in compact bone develop large channels and become irregular -bc osteoid continues to be produced but not mineralized, abnormal quantities of osteoid accumulate, coating the traveculae and the linings of the Haversian canals -excessive osteoid also can accumulate in areas beneath the periosteum -the excess of osteoid leads to gross deformities of the long bones, spine, pelvis and skull. *clinical manifestations: Osteomalacia causes varying degrees of diffuse skeletal pain and tenderness. bone pain is typically between joints rather than within them. Pain is noted particularly in the hips and the individual may be hesitant to walk. Muscular weakness particularly of the proximal muscles is common and may contribute to a waddling gate. Facial deformities and bowed legs or knock knees may be present. Bone fractures and vertical collapse occur with minimal trauma. low back pain may be an early complaint but pain also may involve ribs feet or other areas of the vertebral column and other sites. uremia may be present in renal osteodystrophy.

Insufficient fractures p.1541

-fragility fractures of osteoporosis and osteomalacia, and occur in bones lacking normal ability to deform and recover (normal weight bearing or activity fractures the bone)

Transchondral fracture p.1541

-fragmentation and separation of a portion of the articulate cartilage that covers the end of a bone at a joint -the fragments may consist of cartilage alone or cartilage and bone -typical sites are the distal femur, the ankle, the kneecap, the elbow, and the wrist -most prevalent in adolescents -separation of cartilaginous joint surface from the main shaft of the bone

Hypotensive shock

-if systolic hypotension is associated with inadequate tissue perfusion, the child is in this -formally called decompensated

Pseudogout p.1575

-in classic gouty arthritis, mono sodium urate crystals form and cause joint inflammation -this is caused by the formation of calcium pyrophosphate dihydrate crystals -the effect of either crystal is the same, the onset of a cytokines-mediated acute inflammatory response

Tendinitis p.1545

-inflammation of a tendon -symptomatic degeneration of the tendon with vascular disruption and inflammatory repair response -degenerative changes as noted in tendinosis with superimposed evidence of tear, including fibroblastic and myofibroblastic -inflammatory fluid accumulates causing sweeling of the tendon and its enclosing sheath -inflammatory changes cause thickening of the sheath, which limits movements and cause pain -micro tears cause bleeding, edema and pain in the involved tendons or surrounding structures -at times, after repeated inflammations, calcium may be deposited in the tendon origin area, causing a calcific type.

Epicondylitis p.1546

-inflammation of a tendon where it attaches to a bone (at its origin) -Tennis elbow: Lateral -Golfer's elbow: Medial -most tendon pathology, however, is caused by tissue degeneration rather than inflammation -areas of the humerus, radius or ulna and the area around the knee are most often involved -related to smoking, obesity, and work activities that involve forceful or repetitive cyclic flexion and extension of the elbow, or cyclic pronation, supination, extension and flexion of the wrist that generates loads to the elbow and forearm region

scoliosis- patho/clinical manifestations p. 1600/1601

-it has been hypothesized that in individuals with adolescent type, there is an abnormality of the CNS involving the balance mechanism (reticular system) in the midbrain -a genetic component is also suggested because 30% occur in families. -experimentally it also have been shown that individuals with adolescent idiopathic scoliosis I have an abnormality in the function of the posterior columns of the spinal cord -this results in abnormal proprioceptive and isn't evident clinically except in the presence of scoliosis -the exact cause remains elusive. -the earliest pathologic changes, which are probably secondary changes, occur in the soft tissues -the muscle, ligaments, and other soft tissues become shortened on the concave side of the curve -vertebral deformity occurs as asymmetric forces are applied to the epiphyseal center of the ossification by shortened and tight soft tissues on the concave side of the curve -true curves involve not only bending but also twisting of the torso leading to the rib hump seen when the child bends forward. -the curves increase most rapidly during periods of rapid skeletal growth -if the curve is less than 40 degrees at skeletal maturity, the risk of progression is quite small -in curves greater than 50 degrees, the spine is bio mechanically unstable, and the curve usually progresses even after the cessation of growth -curves in the thoracic spine greater than 80 degrees result in decreased pulmonary function, whereas the most common complicated of large curves in the lumbar spine is back pain. *clinical manifestations: Non-structural scoliosis are mild spinal curvature with prominence of one hip or rounded shoulders. The curvature disappears with forward flexion of the spine, lying down, or traction of the head. Treatment for nonstructural scoliosis is correction of the underlying disorder. The clinical manifestations of structural scoliosis include asymmetry of hip height, asymmetry of shoulder height, shoulder and scapular (shoulder blade) prominence, and rib prominence.

Obstructive shock

-low cardiac output is caused by mechanical obstruction to blood flow, such as cardiac tamponade, tension pneumothorax, critical left heart or aortic obstruction, or pulmonary embolus -difficult to distinguish from cardiogenic shock because both may present with signs of low cardiac output and evidence of systemic or pulmonary venous congestion -prompt detection and treatment are critical to survival -inadequate cardiac output caused by an impediment to blood flow to or from the heart into the pulmonary or systemic circulation -causes in children include congenital heart defects (such as critical aortic stenosis and those with ductal-dependent pulmonary or systemic blood flow), tension pneumothorax, and PE -obstruction to blood flow results in low cardiac output and circulatory collapse, typically with signs of peripheral vasoconstriction as adrenergic stimulation attempts to reduce blood flow to the skin, gut and kidney and maintain adequate blood flow to the heart and brain -signs of systemic or pulmonary venous obstruction are observed

Bone mineral density p.1552 (left column 2nd para)

-measuring this by using DXA continues to be the most common method of estimating bone mass -bone quality relates not just to bone mass (as measured by this) but also to the micro architecture of the bone -other variables include crystal size and shape, brittleness, vitality of the bone cells, structure of the bone proteins, water volume, integrity of the trabecular network, vascular supply, and the ability to repair tiny cracks

Hypovolemic shock in children

-most common type of shock in children and it most frequently results from dehydration and trauma -also may result from expansion of the vascular space, producing inadequate intravascular volume relative to the vascular space -clinical manifestations include inadequate systemic perfusion associated with intravascular fluid loss -adrenergic compensatory mechanisms can produce tachycardia, redistribution of blood flow, peripheral vasoconstriction, cool extremities, delayed capillary refill and oliguria -caused by inadequate intravascular volume relative to the vascular space

rheumatoid arthritis- patho/clinical manifestations p.1569/1570/1571/1572

-no specific events (such as trauma, illness or environmental conditions) have been identified that would cause immune abnormalities to develop into localized tissue and joint inflammation, the pathology of this is fairly well understood -during inflammation, arginine (an a-amino acid) can be enzymatically modified into another a-amino acid, citrulline -this process (citrullination) changes the structure and function of the protein -other proteins, like fibrin and vimentin, can become citrullinated during cell death and tissue inflammation -the citrullinated proteins can be seen as antigens by the body's immune system -both T and B cells play a role in the autoimmune response -T cells express RANKL, which promotes osteoclast formation causing bony erosion. -inflammatory cytokines, particular TNF-a, IL-1B, IL-6, 7, and 21, that induce enzymatic (metalloproteinases) breakdown of cartilage and bone and T cells also interact with synovial fibroblasts (synoviocytes) through TNF-a, converting synovium into a thick abnormal layer of granulation tissue known as pannus -composed of these macrophages, plus osteoclasts and fibroblast-like synoviocytes , the pannus acts like a locally invasive tumor -macrophages, components of pannus, stimulate the release of IL-1, PDGF and fibronectin. -several types of leukocytes are attracted out of the circulation and into the synovial membrane -the phagocytes of inflammation (neutrophils and macrophages) ingest the immune complexes and in the process of doing so release powerful enzymes that degrade synovial tissue and articular cartilage -the immune system's B and T lymphocytes are also activated -the B lymphocytes are stimulated to produce more RFs, and the T lymphocytes eventually cause release of enzymes that amplify and perpetuate the inflammatory response -cartilage destruction is mediated by matrix metalloproteinases that activate the synoviocytes to invatde and attack the synovium and matrix -RANKL is expressed by various cells in the synovium and induces osteoclast maturation and activation, thus producing increased bone resportion. -inflammatory and immune processes have several damaging effects on the synovial membrane -along with the swelling caused by leukocyte infiltration, the synovial membrane undergoes hyperplastic thickening as its cells proliferate and become abnormally large -as synovial inflammation progresses to involve its blood vessels, small venues become occluded by the hypertrophied endothelial cells, fibrin, platelets and inflammatory cells which decrease vascular flow to the synovial tissue -compromised circulation, coupled with increased metabolic needs because of hypertrophy and hyperplasia, causes hypoxia and metabolic acidosis -acidosis stimulates the release of hydrolytic enzymes from synovial cells into the surrounding tissue, initiating erosion of the articular cartilage and inflammation in the supporting ligaments and tendons -inflammation causes hemorrhage, coagulation and fibrin deposition on the synovial membrane, in the intracellular matrix, and in the synovial fluid. *clinical manifestations: The onset of RA is usually insidious although as many as 15% of cases have an acute onset. RA begins with general systemic manifestations of inflammation including fever, fatigue, weakness, anorexia, weight-loss, and generalized aching and stiffness. Local manifestations also appear gradually over weeks or months. Typically the joints become painful, tender, and stiff. Pain early in the disease is caused by pressure from swelling, later it is caused by sclerosis of subchondral bone and new bone formation. Stiffness usually lasts for about one hour after rising in the morning and may be caused by synovitis. Initially most commonly involved joints are the metacarpophalangeal (MCP), proximal interphalangeal (PIP), and wrists, with later involvement of larger weight bearing joints. Widespread and symmetric joint swelling is caused by increasing amounts of inflammatory exudate (leukocytes, plasma, plasma proteins) in the synovial membrane, hyperplasia of inflamed tissues, and formation of new bone. On palpation the swollen joint feels warm and the synovial membrane feels boggy. the skin over the joint may have a ruddy or cyanotic hue and may look thin and shiny. An inflamed joint may lose some of its mobility even mild synovitis can lead to loss of range of motion. Extension becomes limited and is eventually lost if flexion contractures form. Chronic synovitis weakens ligamentous structures leading to deformities of the fingers, toes, and limbs including ulner deviation of the hands, boutonniere, and swan neck deformity of the finger joints, plantar subluxation of the metatarsal heads of the foot and hallux valgus (angulation of the great toe toward the other toes). Flexion contractures of the knees and hips are also common. Joint deformities cause the physical limitations experienced by persons with RA. Loss of joint motion is quickly followed by secondary atrophy of the surrounding muscles. With secondary muscle atrophy the joint becomes unstable which further aggravates joint pathology. Two complications of chronic RA are caused by an excessive amount of inflammatory exudate in the synovial cavity. One complication is the formation of cysts in the articular cartilage of subchondral bone. Occasionally these cysts communicate with the skin surface (usually the sole of the foot) and can drain through passages called fistulae. The second complication is rupture of the cyst or of the synovial joint itself usually caused by strenuous physical activity and that places excessive pressure on the joint. Extrasynovial rheumatoid nodules or swelling's are observed in areas of pressure or trauma and 20% of individuals with RA. Each nodule is an aggregate of inflammatory cells surrounding a central core of fibrinoid and cellular degrees. T lymphocytes are the predominant leukocytes in the nodule, B lymphocytes, plasma cells, and phagocytes are found around the periphery. Nodules are found most often in subcutaneous tissue over the extensor surfaces of elbows and fingers. Less common sites are the scalp, back, feet, hands, buttocks, and knees. Rheumatoid nodules also may invade the skin, cardiac valves, pericardium, pleura, lung parenchyma, and spleen. These nodules are identical to those encountered in some individuals with rheumatic fever and are characterized by central tissue necrosis surrounded by proliferating connective tissue. Also noted are large numbers of lymphocytes and occasional plasma cells. Acute glaucoma may result with nodules forming on the sclera. Pulmonary involvement may result in diffuse pleuritis or multiple intraparenchymal nodules. Together the occurrence of pulmonary nodules and pneumoconiosis (chronic inflammation of the lungs from inhalation of dust) creates caplan syndrome. Diffuse pulmonary fibrosis may occur because of immunologically mediated immune complex deposition. Rheumatoid nodules within the heart may cause valvular deformities particularly of the aortic valve leaflets. Pericardial effusion or other pericardial problems occur in almost 50% of individuals with RA. Lymphadenopathy of the nodes close to the affected joints may develop. Rheumatoid nodules within the spleen results in splenomegaly. Involvement of blood vessels results in an acute necrotizing vasculitis, characteristic of that noted in other immunologic/inflammatory states. thrombosis of such involved vessels may give rise to myocardial infarction, cerebrovascular occlusions, mesenteric infarction, kidney damage, and vascular insufficiency in the hands and fingers (raynaud phenomenon). Vascular changes are noted primarily in individuals receiving corticosteroid therapy, thus there is some concern that the therapy may play a role in initiating these lesions. Changes in skeletal muscle are often noted in the form of nonspecific atrophy, secondary to joint dysfunction.

Stress fractures p.1541

-occur in normal or abnormal bone that is subjected to repeated forces, such as occurs during athletics -microfracture -Fatigue and insufficiency -Transchondral

Shock

-occurs when the cardiovascular system fails to perfuse tissue, cells and organs adequately, causing a widespread impairment of cellular metabolism and tissue function -a downward physiologic spiral, that if not reversed, can lead to MODS -types are cardiogenic, hypovolemic, neurogenic or vasogenic, anaphylactic I and septic -the final common pathways in all types of this is impaired cellular metabolism and cells switch from aerobic to anaerobic metabolism -energy stores drop and cellular mechanisms relative to membrane permeability, action potentials, and lysozyme release fail -anaerobic metabolism results in activation of the inflammatory response, decreased circulatory volume, and decreased pH -impaired cellular metabolism results in cellular inability to use glucose because of impaired glucose delivery or impaired glucose intake, resulting in a shift of glycogenylysis, gluconeogenesis, and lipolysis for fuel generation -glycogenylysis is affected for up to 10 hours -gluconeogenesis results in the use of proteins necessary for structure, function, repair, and replication that leads to more impaired cellular metabolism -lipolysis is ineffective because of a lack of transport serum proteins -gluconeogenesis contributes to lactic acid, uric acid, and ammonia buildup; interstitial edema; and impairment of the immune system as well as general muscle weakness leading to decreased respiratory function and cardiac output -Gluconeogenesis causes proteins to be used for fuel. The breakdown of proteins can result in increased lactic acid, uric acid, interstitial edema, and ammonia, as well as impairment of the immune system. Tachycardia is a compensatory shock mechanism focused on oxygen delivery. -a condition in which the circulatory system is unable to provide adequate circulation to the body tissues because of inadequate pumping by the heart, a reduction in blood volume or a reduction in blood pressure -it results in slowing of vital functions and possibly death

Burns in children

-often the result of inadequate supervision, curiosity, inability to escape the burning agent or intentional abuse -scald injuries are commonly seen in young children and result from exposure to hot water grease or other hot liquids, whereas flame types are more prevalent among older children -a child's skin is thinner and this more susceptible to injury than adult skin -the kitchen and bathroom are common sites of injury -approximately 10% of all forms of child abuse cases in the US result from this injury -flame type involving flammable liquids, most notably gasoline are more common in older children -risk-taking behaviors in young males can lead to electrical type -children may be exposed to chemical injury by swallowing caustic agents at home -use of the standard Rule of Nine results in inaccurate calculation of the percentage of TBSA in children -a modified Rule of Ninces deducts 1% from the head and adds 0.5% to each leg for each year of life after two years of age -major trauma involves all of body systems and the consequences of injury include shock, infection, hyper metabolism, organ failure, and functional limitations -these effects can be magnified in the pediatric population as a result of physiologic immaturity and age-related variation in tx modalities -infection, trauma, or applying ice to the area may convert a partial-thickness injury to a full-thickness one, esp in young children, who have thinner more delicate skin -marked reduction in cardiac output occurs immediately after injury and is accompanied by an initial increased in systemic vascular resistance -the inefficient and labile peripheral circulation of the infant complicated management of the shock phase of tx -constriction of the chest and impairment of respiratory excursion may occur in the very young child because of the increased pliability of the rib cage -younger children are also more susceptible to increased intra-abdominal pressure -the leading cause of death in children after injury, as in adults, is inhalation injury -children require fluid resuscitation for smaller ones than does the adult population as a result of limited physiologic reserves -colloid replacement may be required in the very young child who fails to respond to fluid replacement -children younger than 2 years lack the ability to concentrate urine because of the immaturity of the renal system and are therefore at increased risk for dehydration -because children have a relatively larger body surface area in relation to weight than ducts, they require proportionately increased fluid during shock resuscitation to compensate for evaporative water losses -some children exhibit immunosuppressive for a prolonged period after wound closure -a biphasic pattern of physiologic responses is evident in the injured child -the initial ebb phase occurs during the immediate post this period and continues for 3-5 days -this phase is characterized by reduced oxygen consumption, impaired circulation and cellular shock -after this phase and the restoration of volume, the metabolic response shifts to a catabolic, or flow, phase -this phase is characterized by hyper metabolism with an increased oxygen consumption and elevation of catecholamines, glucocorticoids and glucagon -glycogen stores are limited in children making it hard for them to meet the increased energy demands of the burn -this prolonged metabolic dysfunction may lead to loss of lean body mass and increased morbidity -although age was not found to be a predictor of hypertrophic scarring, children have greater skin tension and an accelerated rate of collagen synthesis -children require specialized management to ensure optimal functional and cosmetic results -long-term scar and contracture management is necessary because of changes in the body composition as the child grows and matures

Septic shock in children

-once this is present, immediate tx is urgently needed -therapy in the first hour includes aggressive fluid resuscitation (typically 60-80ml/kg administered in first hour of therapy, and approximately 200-240ml/kg in the first 8 hours of therapy -if the child doesn't response to volume administration alone, vasoactive support must be initiated within the first hour of tx -antibiotics also must be administered within the first hour -goals of therapy are to rapidly normalize the heart rate and BP for age and to normalize capillary refill to less than 2 seconds -the child's shock index (heart rate/systolic BP) should fall during the first hour of management if therapy is effective -fluid and vasoactive therapy should support high cardiac output and oxygen delivery, maintains the SVO2 at approx 70% -the development of this is heralded when the child with severe sepsis develops signs of cardiovascular dysfunction -the child may become hypotensive despite adequate fluid rescucitation or require vasopressors to maintain BP -is heralded in the child with sepsis by the development of cardiovascular dysfunction -this may characterized by hypotension despite adequate fluid resuscitation or by the need for vasopressors to maintain BP -children tend to develop hypotension only late in the course of any shock, this should be identified when the child develops more subtle signs of poor perfusion despite adequate fluid resuscitation -when the child with sepsis does develop hypotension plus signs of poor perfusion, hypotensive/decompensated type is present and mortality may be as high as 30%

Nutrition and osteoporosis p.1552 (right column 1st para)

-poor this and insufficient intake or malabsorption of dietary minerals, particularly calcium absorption from the intestine decreases with age and studies of individuals with this show that their Ca intake is lower than that of age-matched controls -deficiencies of vitamins particularly C, D, E, and K also contribute to bone loss

Shock in children

-present when there are signs of poor systemic perfusion, regardless of BP -lactic acidosis (rise in serum lactate) may be the most sensitive indicator of inadequate systemic perfusion in children -effective therapy should eliminate lactic acidosis -the general goals of tx for this are maximization of oxygen delivery and minimization of oxygen demand -this requires support of airway, oxygenation, and ventilation -support of CV function requires support of appropriate heart rate and rhythm, adequate intravascular volume, good myocardial function and appropriate vascular resistance and distribution of blood flow -the child should be kept warm but fever must be treated promptly -the signs of this should lessen or disappear if management of shock is effective -the warmth of the child's extremities, briskness of cap refill, quality of peripheral pulse, LOC, and responsiveness, urine volume, oxygenation, ventilation and acid-base status should improve through therapy -a condition of acute and progressive circulatory dysfunction that results in inadequate delivery of oxygen and nutrients to the tissues -most often results from hemorrhage, severe dehydration, progressive heart failure, or sepsis -may also complicate the care of the child with congenital heart disease, pulmonary hypertension (cor pulmonale), drug toxicity, electrolyte or acid-base imbalance, dysrhythmias, or multiple organ failure -present when there are signs of poor systemic perfusion, regardless of the BP - may be present with normal, high or low BP

Duchenne Muscular Dystrophy p. 1607

-progressive weakness associated with large calf muscles said to be pseudohypertrophic, because they consisted of fat and connective tissue rather than muscle -most common type -occurs only in boys and has a history of X-linked inheritance in half the cases -age is about 3 years -usually distributes in hips, shoulders, quadriceps femoris, gastrocnemius -progresses rapidly -frequently mental retardation present

Third spacing of fluids

-relative hypovolemia may be caused by a decrease in the intravascular volume relative to the vascular space -this may be associated with the vasodilation of sepsis, anaphylaxis or neurogenic shock or with B2-adrenergic drug toxicity -a relative hypovolemia also may be caused by increased capillary permeability with a redistribution of intravascular volume such as with burns, anaphylaxis or sepsis -the translocation of extravascular fluid to a location that is neither intravascular or intracellular, as in edema, is termed this

MODS in children

-reperfusion and inflammatory injury stimulate free oxygen radicals that can damage cell membranes, denature proteins, and disrupt chromosomes -this process likely affects endothelial cells and the microvasculature causing this -the simultaneous failure of at least two organs resulting from a single cause -may be either primary or secondary -primary is directly attributable to the insult and typically occurs soon (3-7 days) after an insult -secondary typically occurs later an may be associated with more sequential development or organ dysfunction -risk factors include severe or prolonged shock, sepsis, trauma, cardiopulmonary arrest, congenital heart disease, and liver and bone marrow transplantation -children with chronic disease have an increased risk and increased mortality

Reperfusion injury

-restoration of adequate blood flow and oxygen delivery may trigger the development of this, a secondary problem characterized by an exaggerated inflammatory response that may produce cellular death and organ failure -reoxygenation -cell damage caused by the restoration of blood flow and physiologic concentration of oxygen to cells that have been exposed to injurious but no lethal hypoxic conditions -ischemia causes changes in transmembrane permeability to sodium and calcium and damage to intracellular organelles -this damage triggers a proinflammatory and procoagulant response that can be very similar to that described for septic shock

Fragile fracture p.1541

-results from a low-level trauma (one that would normally not cause a fracture) -often seen in osteoporosis

Neurogenic (vasogenic) shock

-results from massive vasodilation that results from an imbalance between parasympathetic and sympathetic stimulation of vascular smooth muscle -it causes a relative hypovolemic (even though cardiac output may be high) and results in impaired cellular metabolism -a type of shock caused by the sudden loss of the sympathetic nervous system signals to the smooth muscle in vessel walls, causing the vessels to relax and a decrease in peripheral vascular resistance and BP -imbalance between sympathetic and parasympathetic stimulation -> massive vasodilation -> decreased vascular tone -> decreased SVR -> inadequate cardiac output -> decreased tissue perfusion -> impaired cellular metabolism

Cardiogenic shock

-results from persistent hypotension and tissue hyoperfusion caused by cardiac dysfunction in the presence of adequate intravascular volume and left ventricular filling pressure -a condition resulting from decreased cardiac output caused by heart disease in which the heart is unable to pump blood through the body, usually because of MI

Legg-Calve-Perthes Disease- patho/clinical manifestations p.1604/1605

-run its natural course in 2-5 years -in the initial stage the soft tissues of the hip (synovial membrane and joint capsule) are swollen, edematous and hyperemic, often with fluid present in the joint -the joint space widens and the joint capsule bulges -the first stage lasts only a few weeks -in the second stage, called fragmentation, the entire epiphysis or the anterior half of the epiphysis of the femoral head loses blood supply and the metaphyeal bone at the junction of the femoral neck and capital epiphyseal plate is softened because of decalcification -soon granulation tissue (procallus) and blood vessels invade the dead bone -this stage lasts several months to 1 year. -the third (or regenerative healing) stage ordinarily lasts 2 to 3 years -the dead femoral head is replaced by procallus and new bone is laid down -collapse and flattening of the femoral head occur and the femoral neck becomes short and wide. -in the fourth (or healed) stage, remodeling takes place and the newly formed bone is organized into a live spongy bone -children less than 6 years of age at onset have more time to remodel the damage this has caused and have the best outcome -recents studies, using the Herring "lateral pillar" classification, have shown the hips younger than 6 with no involvement of the lateral femoral head (type A) do better than those with involvement of the lateral femoral head -those children with complete collapse of the lateral femoral head (type C) have the worse prognosis -long term studies of type c hips show that 70-90% progress to OA by 40 years of age. *clinical manifestations: Injury or trauma precedes the onset of clinical manifestations in approximately one third of children with LCP. disease onset of symptoms is insidious unless trauma aggravates the disease process. The pain often is referred to the knee and can lead to misdiagnosis as knee injury. The inner thigh and groin also can be painful. In some children pain may be absent or minimal. If pain is present it is usually aggravated by activity and relieved by rest. The typical physical findings include spasm on inward rotation of the hip and a limitation of internal rotation flexion and abduction. If the child is walking- an abnormal gait termed a Trendelenburg gate or abductor lurch is apparent. The child dips the trunk towards the affected side with stance to compensate for week abductor musculature. If the hip pain or length has been present for a prolonged period, muscles of the hip and thigh atrophy. a limb length inequity may be present if the proximal femoral physis is involved.

SIRS (systemic inflammatory response syndrome)

-sepsis is a systemic response to infection -it is present when manifestations of this are observed -this is present when the child demonstrates two or more of the following as an acute change from baseline values: altered temperature, altered heart rate, altered respiratory rate, and alteration in the WBC count -the newborn often develops hypothermia rather than fever as a sign of infection and may develop bradycardia instead of tachycardia -severe sepsis is present when there is evidence of this and signs of organ dysfunction, hypoperfusion or hyptotension -represents a nonspecific response to a variety of insults, including trauma, burns, pancreatitis, or infection -fever (greater than 38.5 or hypothermia less than 36 -tachypnea or in infants Bradycardia -need for mechanical ventilation -leukocyte, leukopenia or an increase in the % of immature or band forms of WBC -The most common sites of infection from sepsis are primary bloodstream (25%) and respiratory tract (37%) infections.

Distributive shock

-septic, anaphylactic, and neurogenic shock -blood flow is unregulated throughout the skin and organ systems and vasodilation and increased capillary permability are typically present, so a normal cardiac output is likely to be inadequate to maintain sufficient perfusion of all tissue beds -volume administration nis necessary to ensure that the intravascular volume is adequate relative to the vascular space, and vasoactive drugs are needed to support adequate cardiac output and oxygen delivery

Extracellular signal regulated kinases (ERKs) p.1553

-sex steroids (estrogen( exert anti-apoptotic effects on osteoblasts but exert pro-apoptotic effects on osteoclasts; in both scenarios this is accomplished by activation this -estrogen activates this outside the nucleus; they then accumulate in the nucleus and activate downstream transcription factors -this confusing and complicated data eventually revealed that the important determinant of whether pro-apoptosis or anti-apoptosis was exhibited was the length of time that the phosphorylated this remained in the nucleus -prolonged nuclear accumulation of activated these converted the anti-apoptotic effect of estradiol to pro-apoptotic -RANKL promotes the anti-apoptotic effects on osteoclasts, thus increasing their life span -Wnt signaling induces a biochemical series of events that increases osteoblast and bone formation -alterations in Wnt signaling account for critical Patho changes in most acquired metabolic bone disease including postmenopausal osteoporosis, aging effects, and glucocorticoid (cortisone) excess -agents such as parathyroid hormone and biphosphonates, used for treatment of bone loss, exert their positive effects by altering the formation of osteoblasts or osteoclasts or by inducing osteoclast apoptosis.

Hormones and osteoporosis p.1552 (left column last para)

-sex type, esp estrogen and testosterone are significant in premenopausal bone maintenance, however, when estrogen levels drop after menopause, it appears that circulating androgens become significant effectors on bone metabolism -data have suggested that serum androgens influence bone density in pre- peri- and postmenopausal women -androgen have long been recognized to stimulate bone formation

Hypotension in children

-sign of severe (preterminal), decompensated shock, referred to as hypotensive shock

Closed fracture p.1541

-simple -if the skin isn't broken -the skin overlying the bone is intact

Endocrine and osteoporosis p.1552 (right column 2nd para)

-skeletal homeostasis depends on a very narrow range of plasma Ca and phosphate concentrations, which are maintained by this -this dysfunction ultimately can cause metabolic bone disease -hormones most commonly associated with this are parathyroid hormone, cortisol, thyroid hormone, and growth hormone -excessive intakes of caffeine alcohol and nicotine along with low body fat have been considered risk factors -significant differences in the levels of trace elements (zinc, copper, manganese) were noted in in the bones and hair of unaffected individuals compared with those with this -development of selective androgen receptor modulators promises novel treatment for this through increaseing bone formation and building more muscle mass -selectively affecting bone, muscle mass, and other desired sites while not affecting lipid or estrogen levels or blood pressure, side effects can be controlled but since the direct effects of SARMS on bone are not yet known

rhabdomyolysis- patho/clinical manifestations p.1547/1548/1549/1550

-sometimes incorrectly used interchangeable with crush injury (a description of injuries resulting from crushing of a body part), compartment syndrome (the consequences of increased intracompartmental pressures of a muscle), or crush syndrome (the Pathophysiologic events caused by this, primarily involving the kidneys and coagulation syndrome) -relatively rare -has many causes and can result in serious complications, including hyperkalmia (because of the release of intracellular K into the circulation),, metabolic acidosis (from liberation of intracellular phosphorus and sulfate), acute renal failure (myoglobin precipitates in the tubules, obstructing flow through the nephron and producing injury), and even DIC (likely caused by activation of the clotting cascade by sarcolemmal damage and release of intracellular components from the damaged muscles -even the weight of a limp extremity can generate enough pressure to produce muscle ischemia. -malignant hyperthermia is a potentially life-threatening hereditary disorder of skeletal muscle ryanodine receptors, allowing large quantities of calcium to be released from the sarcoplasmic reticulum after exposure to certain volatile anesthetics -the sustained elevation of Ca concentration allows excessive stimulation of aerobic and anaerobic glycolytic metabolism, causing a hyper metabolic state resulting in respiratory and metabolic acidosis, muscle rigidity, altered cell permeability, and hyperkalemia -dantrolene, a skeletal muscle relaxant, inhibits Ca release from the SR and is used to reverse the effects of MH. -compartment syndromes occur when blood flow to the affected area is compromised because of increased venous pressure, leading to decreased arterial inflow, ischemia, and edema -emergency treatment may be required to save an affected limb -classic sx of compartment syndrome are: 1)pain out of proportion to the injury 2)paresthesia 3)pallor 4)pulselessness (uncommon) 5)paralysis (a late finding) -pain is the most sensitive clinical sign -when clinical evaluation is inconclusive, the rising compartment pressure can be directly measured by inserting a wick catheter, needle, or slit catheter into the muscle -immediate fasciotomy and debridement are advocated for reducing elevated intracompartmental pressures -compartments frequently affected are the compartments of the leg, the collar compartment of the hand, the abdomen, and the gluteal compartments. *clinical manifestations: Classic triad of muscle pain, weakness, and dark urine is considered typical of rhabdomyolysis but those affected may have no complaints of pain or muscle weakness. abnormally dark urine caused by myoglobinurea may be the first and only sign. The renal threshold for myoglobin is low (approximately 0.5 mg/dL) so only 200g muscle need to be damaged to cause visible changes in the urine. Myoglobin is rapidly cleared and levels may return to normal within 24 hours of injury. Along with the release of myoglobin, creatinine kinase (CK), and other serum enzymes are released in massive quantities. The efflux of proteins and enzymes also includes loss of potassium, phosphate, nucleotides, creatinine, and creatine. Serum hypocalcemia is seen early in the course of myoglobinuria and is followed by late hypercalcemia.

duchenne muscular dystrophy- patho/clinical manifestations p.1607/1608

-the X-linked inherited type is thought to be caused by deletion of a segment of DNA or a single gene defect on the short arm of the X chromosome -a protein encoded by this gene, called dystrophin, has been identified. -dystrophin is present in normal muscle cells and absent in this (it is present in reduced amounts in Becker type) -dystrophin mediates anchorage of the actin cytoskeleton of skeletal muscle fibers to the basement membrane through a membrane glycoproteins complex -the complete lack of dystrophin in severe type means that poorly anchored fibers tear themselves apart under the repeated stress of contraction -free calcium then enters the muscle cells, causing cell death and fiber necrosis. -over time, as muscles degenerate, there is increased endomysial connective tissue and fat, loss of strations, and concomitant hyaline, granular, and fatty degeneration of fibers -disorganization of tendinous insertions is associated with fat accumulation in these areas -although fibers regenerate in the younger child, regeneration is not able to keep up with muscle cell death. *clinical manifestations: Usually identified in children at approximately 3 years of age when the parents first notice slow motor development with progressive weakness and muscle wasting. Sitting, standing, and walking are delayed and the child is clumsy, falls frequently, and has difficulty climbing stairs. Muscular weakness begins in the pelvic girdle causing a waddling gate. Hypertrophy of the calf muscles is apparent in 80% of cases. The method of rising from the floor by climbing up the legs (gower sign) is characteristic and caused by weakness of the lumbar and gluteal muscles. The foot assumes equinovarus position and the child tends to walk on the toes because of weakness of the anterior tibial and peroneal muscles. the foot assumes an equinovarus position and the child tends to walk on the toes because of weakness of the anterior tibial and peroneal muscles. within 3 to 5 years muscles of the shoulder girdle become involved. Contractures and wasting of the muscles contribute to muscular atrophy and deformity of the skeleton. duchenne muscular dystrophy has serious complications although these are decreased by treatment with oral corticosteroids at diagnosis. The recent addition of oral corticosteroids early in the disease has dramatically improved outcome. children are able to walk an additional 2 to 5 years and life expectancy has increased. Complications such as compromise pulmonary function and kyphoscoliosis (humped upper spine) combined scoliosis are delayed. Full-scale IQ is 85 which is significantly lower than the average IQ of 100 although studies suggest this decrease may be caused by specific learning disabilities rather than a true decreased intelligence. As the condition develops constipation and incontinence of urine and stool may develop possibly because of smooth muscle involvement. Although the life expectancy of boys with duchenne continues to increase, death usually occurs from respiratory tract infection and a compromise respiratory system, with the majority of living into their middle 20s. Some individuals who have chosen ventilatory support live a decade or more longer.

developmental dysplasia of the hip- patho/clinical manifestations p.1594/1595

-the hip can be described as subluxation (partial contact only), dislocated (no contact between femoral head and acetabulum), and acetabulum dysplasia (the femoral head is located properly but the acetabulum is shallow) -the subluxation hip maintains contact with the acetabulum but is not well seated within the hip joint -the acetabulum is often dysplasia (or shallow) although the femur is often normal -the dislocatable hip is sometimes located but can be dislocated easily -the dislocated hip has no contact between the femoral head and the acetabulum -some degree of acetabular dysplasia is present in almost all cases -typically the acetabulum is shallow or sloping rather than cup shaped. -by approx 10 weeks of gestation, the femur, acetabulum and hip joint capsule are well developed -it appears that the most dysplasias occur within the second and third trimesters and are often the result of positioning factors -experimentally, this can be produced in lab animals by placing the developing hip in adduction and extension, replications the breech position -there is however, a genetic component that is poorly understood -some cases are teratologic or caused by a systemic syndrome, such as arthrogryposis or spina bifida in which muscle contracture or imbalance leads to this. -if left untreated in the growing child, secondary changes occur -if this hip remains subluxation or dislocated, the acetabulum becomes increasingly shallow and the soft tissues shorten around the proximal femur -subluxation leads to early osteoarthritis, and it is now estimated that at least 60% of all OA of this hip is regulated to this -if the hip is dislocated, the bone acetabulum fills with soft tissue and a false acetabulum forms where the femoral head contacts the iliac crest -an apparent limb length inequity and hip muscle weakness occurs, leading to a waddling gate -back pain and hip pain develop in adulthood -adult reconstruction of a dislocated hip even with an artificial hip is very difficult. *clinical manifestations: Vary with the severity of the condition and the age of the child- signs and symptoms that should be noted include the following: -Asymmetry of gluteal or thigh folds -Limb length discrepancy (galeazzi) -Limitation of hip abduction -positive barlow maneuver (hip reduced, but dislocatable) -positive ortolani sign (hip dislocated but reducible) -positive trendelenberg wattle gait (waddling) -pain (very late) The child also should be examined for other anomalies such as torticollis or metatarsus adductus which can be associated with DDH.

osteogenesis imperfecta (brittle bone disease)- patho/clinical manifestations p.1597/1598

-the major errors lie in the synthesis of collagen a triple helix with two matching alpha chains and one beta chain -collagen is present in bone, cartilage, eye tissue, skin and the vascular system -the severity of the phenotype and the related anomalies of the eye, dentition or vascular system are all dependent on the severity of the genetic anomaly and the part of the triple helix that is affected. -a number of metabolic abnormalities are associated with this -some individuals have increased serum thyroxine levels, suggesting hyperthyroidism -this is consistent with the findings of increased sweating, a resting tachycardia, and tachypnea -studies of leukocyte metabolism suggest an uncoupling of oxidative phosphorylation -reports of alterations of platelet function with defects in adhesion and clot retraction also exists. *clinical manifestations: The classic clinical manifestations of OI are osteoporosis and increased rate of fractures, possible bony deformation, triangular facies, possible vascular weakness (aortic aneurysm), possible blue sclerae and poured dentition. The sillence classification designated types one through four on the basis of severity. The most severe types two and three are comparable to osteogenesis imperfecta congenita. These two types are characterized by autosomal recessive inheritance and early-onset of manifestations. Both can cause stillbirth or severe neonatal deformity and a short life expectancy. Less severe are types I and IV which are comparable to osteogenesis imperfecta tarda. Type I is slightly more common than types II and III and type IV is quite rare. Types I and IV are inherited as autosomal dominant traits and vary in age of onset from birth to adulthood. Type IV especially when the sclerae are white is the least deforming type and is often confused with nonaccidental trauma (child abuse).

Anaphylactic shock

-the outcome of a widespread hypersensitivity to an allergen that triggers anaphylaxis --the inflammatory response is triggered, and a massive vasodilation with fluid shift into the interstitum follows -the relative hypovolemic leads to impaired cellular metabolism -a state of shock caused by a severe allergic reaction that lowers blood pressure and results in urticaria, breathing difficulties and possibly death

osteomyelitis- patho/clinical manifestations p.1559/1560

-the patho features of bone infection are similar to those in any other body tissue -first, the invading pathogen provokes an intense inflammatory response -inflammation in bone is characterized by vascular engorgment, edema, leukocyte activity, small blood vessel thrombosis, and abscess formation -once inflammation is initiated, the small terminal vessels thrombose and exudate seals the bone's canaliculi -inflammatory exudate extends into the metaphysics and the marrow cavity and through small metaphysical openings into the cortex -in children, exudate that reaches the outer surface of the cortex forms abscesses that lift the periosteum off underlying bone -lifting of the periosteum disrupts blood vessels that enter bone through the periosteum, which deprives underlying bone of its blood supply; this leads to necrosis and death of the area of bone infected, producing sequestrum, an area of devitalized bone -lifting of the periosteum also stimulates an intense osteoblastic response -osteoblasts lay down new bone that can partial lay or completely surround the infected bone -this layer of new bone surrounding the infected bone is called an involucrum -openings in the involucrum allow the exudate to escape into surrounding soft tissue and ultimately through the skin by way of sinus tracts -involucrum in adults is rare because the periosteum is firmly attached to the cortex and resists displacement -infection disrupts and weakens the cortex, which predisposes the bone to pathologic fractures. *clinical manifestations: Vary with the age of the individual, site of involvement, initiating event, infecting organism, and whether the infection is acute, subacute, or chronic. Acute osteomyelitis causes an abrupt onset of inflammation. if an acute infection is not completely eliminated the disease may become subacute or chronic. In subacute osteomyelitis signs and symptoms are usually vague and the chronic stage infection is indolent or silent between exacerbations. The microorganisms persist in small abscesses or fragments of necrotic bone and produce occasional flareups of acute osteomyelitis. The progression from acute to subacute osteomyelitis may be the result of inadequate or inappropriate therapy or the development of drug-resistant microorganisms. In the adult hematogenous osteomyelitis has an insidious onset. The symptoms are usually vague and include fever, malaise, anorexia, and weight-loss. Recent infection (urinary, respiratory, skin) or instrumentation (catheterization, cystoscopy, myelography, diskography) usually precedes onset of symptoms. back pain is the primary symptom in vertebral osteomyelitis. Pain may be intermittent or constant, aggravated by motion, and throbbing at rest. It may radiate in a reticular distribution and is commonly accompanied by spinal tenderness and rigidity. Hip contracture can occur in the presence of soft tissue inflammation as a result of irritation of the psoas muscle. Signs and symptoms of sacroiliac osteomyelitis are generally severe and include local pain, tenderness, and a limp. The pain may radiate to the buttock or the abdomen. Single or multiple abscesses (Brodie abscesses) characterized subacute or chronic osteomyelitis. abscesses are painless circumscribed lesions 1 to 4cm in diameter are usually in the ends of the long bones and surrounded by dense, ossified bone matrix. The abscesses are thought to develop when the infectious microorganism has become less virulent or the individuals immune system is resisting the infection somewhat successfully. In exogenous osteomyelitis signs and symptoms of soft tissue infection predominate. Inflammatory exudate in the soft tissues disrupts muscles and supporting structures and forms abscesses.Low-grade fever, lymphadenopathy, local pain, and swelling usually occur within days of contamination by a puncture wound. Osteomyelitis in the hand causes exquisite tenderness over the course of tendon sheaths.The fingers are usually in a semi-flexed position and extension usually causes severe pain. Palmer swelling or symmetric swelling of the fingers may be present.

osteoarthritis- patho/clinical manifestations p.1565/1566/1567/1568

-the primary defect is loss of articulate cartilage -early in the dz, the articulate cartilage loses its glistening appearance, becoming yellow-gray or brownish gray -as the dz progresses, surface areas of the articulate cartilage flake off and deeper layers develop longitudinal fissures (fibrillation) -the cartilage becomes thin and may be absent over some areas, leaving the underlying bone (subchondral bone) unprotected -consequently, the unprotected subchondral bone becomes sclerotic (dense and hard) -cysts sometimes develop within the subchondral bone and communicate with the longitudinal fissures in the cartilage -pressure builds in the cysts until the cystic contents are forced into the synovial cavity, breaking through the articulate cartilage on the way -as the articulate cartilage erodes, cartilage-coated osteophytes may grow outward from the underlying bone and alter the bone contours and joint anatomy -these spur-like bony projections enlarge until small pieces, called joint mice, break off into the synovial cavity -if osteophytes fragments irritate the synovial membrane, synovitis and joint effusion result -the joint capsule also becomes thickened and at times adheres to the deformed underlying bone, which may contribute to the limitation of movement. -articulate cartilage is lost through a cascade of cytokines and anabolic growth factor pathways -enzymatic processes, particularly those involving matrix metalloproetinases, break down the macromolecules of proteoglycans, glycosaminoglycans and collagen into large, diffusible fragments -the fragments are then taken up by the cartilage cells (chondrocytes) and digested by the cell's own lysosomal enzymes -the loss of proteoglycans from articular cartilage is a hallmark of this process. *clinical manifestation: Manifestations of OA typically appear during the fifth or sixth decade of life, although asymptomatic articular surface changes are common after age 40. Pain and stiffness in one or more joints usually weight-bearing or load bearing joints are the first symptoms of the disease. Use related joint pain relieved by rest is a key feature. Examination usually shows general involvement of peripheral and central joints. peripheral joints most often involved are in the hands, wrist, knees and feet. Central joints most often affected are in the lower cervical spine, lumbosacral spine, shoulders, and hips. Pain and stiffness are the predominant symptoms of OA. others include swelling, tenderness, or enlargement/deformity of joints. Symptoms are usually aggravated by weight bearing or use of the joint and relieved by resting the joint. Sometimes pain is referred to another part of the body for example osteoarthritis of the lumbar sacral spine may mimic sciatica causing severe pain in the back of the thigh along the course of the sciatic nerve. OA in the lower cervical spine may cause brachial neuralgia (pain in the arm) aggravated by movement of the neck. Osteoarthritic conditions in the hip causes pain that may be referred to the lower thigh and knee area. The actual mechanisms of joint pain are complex and poorly understood but several explanations are possible. Subchondral bone changes, weight-bearing stress, and inflammatory mediators may be sources of joint pain in OA. Nonetheless there is little correlation between radiologic appearance of OA and an affected persons pain level. articular distention and stretching of the fibrous joint capsule, which has an abundant nerve supply, may also contribute to pain. In addition inflammation of the joint capsule causes fibrous shrinking so that movement of the joint in any direction causes painful stretching. The origin of joint stiffness is unknown joint stiffness is generally defined as difficulty in initiating joint movement, immobility, or a loss of range of motion. The extent of cartilage degeneration also limits range of motion to some degree. The stiffness usually occurs as joint movement begins and dissipates within 30 minutes. Enlargement and bulging of joint contour, commonly described as swelling, may be caused by bone enlargement or the proliferation of osteophytes around the margins of the joint. These types of typical joint swelling in the fingers are termed herberden and bouchard nodes. Swelling also occurs if the inflammatory exudate or blood enters the joint cavity thereby increasing the volume of synovial fluid. This condition termed joint effusion is caused by: 1)the presence of osteophyte fragments in the synovial cavity 2)drainage of cysts from diseased subchondral bone 3)acute trauma to joint structures resulting in hemorrhage and inflammatory exudation into the synovial cavity Abnormal knee alignment (either varus or valgus of more than 5°) has been shown to increase progression of OA. gait abnormalities may ensue attributable to need malalignment.

Multiple Organ Dysfunction Syndrome (MODS)

-the progressive dysfunction of two or more organ systems resulting from a systemic inflammatory response after a severe illness or injury -the inflammatory response can be triggered by sepsis, necrotic tissue, trauma, burns, ARDS, acute pancreatitis, major surgery, circulatory shock, DIC, acute renal failure, blood transfusion, heat stroke, liver failure, mesenteric ischemia, propofol infusion syndrome, persistent inflammatory foci, and other severe injuries -primary is the immediate local or mild systemic response to the triggering event or illness -it primes the inflammatory system -secondary is the uncontrollable, excessive systemic inflammatory response that develops after a latent period and result in organ dysfunction -people at greatest risk for developing this are older adults, those with significant tissue injury or pre existing disease, and those in whom resuscitation from the intitiating illness or injury has been delayed or inadequate -a leading cause of mortality in surgical intensive care units -mortality for individuals with this increases progressively from 54% with two failing organ systems to 100% with five failing organ systems -involves the stress response; release of complement; coagulation and kinin proteins; changes in the vascular endothelium; and numerous inflammatory processes mediated by substances released by activated neutrophils and macrophages -the accumulation of activated neutrophils in organs is thought to play a key role in the pathogenesis of this, as well as macrophages -the consequences of the release of inflammatory mediators are vasodilation, increased vasopermeability and selective vasoconstriction resulting in maldistribution of blood flow; hyper metabolism; myocardial depression; and hypoxia injury to cells -Primary MODS is associated with maldistribution of blood flow, hypermetabolism, myocardial depression, and supply-dependent oxygen consumption. The progressive organ dysfunction of secondary MODS is the result of an excessive inflammatory reaction. -cellular hypoxia and acidosis impair cellular metabolism, leading to organ dysfunction -clinical manifestations of the development of this are general during the first 24 hours: low grade fever, tachycardia, tachypnea, dyspnea, and altered mental status -over the next several days, beginning with the lungs, individual organ systems show signs of failure -bc there is no specific therapy, early detection is extremely important so that supportive measures can be initiated a sap -at present the therapeutic mgmt consists of prevention or removal of triggering mechanisms and support of individual organs -recent scientific knowledge about inflammatory mediators has led to many promising future therapies -progressive disease often involving the ultimate failure of two or more organ systems after a severe illness or injury -disease process is initiated and perpetuated by uncontrolled systemic inflammatory and stress responses and is characterized by a hypermetabolic and hyper dynamic state that persists as organ dysfunction develops

Enzymes and OA p.1566 (left column)

-this destruction of articular cartilage begins in the matrix, with destruction of proteoglycans and collagen fibers -these, particularly stromelysin and matrix metalloproteinases (collagenase) affect proteoglycans by interfering with assembly of the proteoglycans subunit or the proteoglycans aggregate; levels of these are markedly elevated -changes in the conformation of proteoglycans disrupt the pumping action that regulates movement of water and synovial fluid into and out of the cartilage -without the regulatory action of the proteoglycans pump, cartilage absorbs too much fluid and becomes less able to withstand the stresses of weight bearing -also with aging, the proteoglycans content is decreased and the water content in cartilage can be increased by as much as 8%, affecting the strength of the cartilage -people with this, even those with fairly extensive cartilage destruction, have elevated levels of proteoglycans or fragments of proteoglycans in their synovial fluid, perhaps indicative of a more pronounced reparative phase -inflammatory cytokines, such as IL-1 and TNF, play a major role in cartilage degradation in part through induction of nitric oxide synthase and nitric oxide increased generation -cytokines release and activate proteolytic and collagenous tic enzymes, causing an imbalance of cell responses to growth factor activity.

Peak bone mass p.1550

-throughout a lifetime, old bone is removed (resorption) and new bone is added (formation) to the skeleton -during childhood and teenage years, new bone is added faster than old bone is removed -bones become larger, heavier and denser -bone formation continues at a pace faster than respiration until this, or maximum bone density and strength, is reached, around age 30, after which bones resorption slowly exceeds bone formation -in women, bone loss begins before menopause, and is most rapid in the first years after menopause but persists throughout the postmenopausal years -more common in women

Tendinopathy and bursitis- clinical manifestations p.1545/1546/1547

-trauma and repetitive stress can cause painful degradation of collagen fibers (tendinosis), inflammation of tendons (tendinitis) , or inflammation of bursal sacs. *clinical manifestations: Tendinopathy may be asymptomatic but generally there is localized pain that worsens with active more than passive motion. With symptomatic tendinopathy the pain is localized over the involved tendon and movement in the affected joint is limited. In bursitis, onset of pain may be gradual or sudden but movement of the joint itself is normal. Shoulder bursitis impairs arm abduction because of pain and swelling of the bursa. Bursitis in the knee produces pain when climbing stairs and crossing the leg is painful in bursitis of the hip. Lying on the side of an inflamed trochanteric bursa is also very painful. Signs of infectious bursitis may include the presence of puncture site, prior corticosteroid injection, severe inflammation, or an adjacent source of infection. **Table 44-3 common sites of bursitis p.1549

fractures- patho/clinical manifestations p.1541/1542/1543

-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 area) stimulates an intense inflammatory response characterized by vasodilation, exudation of plasma and leukocytes, and infiltration by inflammatory leukocytes and mast cells -cytokines, including TGF-b, PDGF, prostaglandins, and other factors that promote healing are released -within 48 hours after injury, vascular tissue invades the area from surrounding soft tissue and the marrow cavity, and blood flow to the entire bone is increased -bone-forming cells in the periosteum, endometrium, and marrow are activated to produce subperiosteal procallus along the outer surface of the shaft and over the broken ends of the bone -healing generally occurs in three overlapping phases -the initial inflammatory phase of healing lasts 3-4 days -Bone tissue destruction triggers an inflammatory response -Hematoma formation -during the next few days, the repair phase begins and capillary in growth, together with mononuclear cells and fibroblasts, begins the transformation of a hematoma into granulation tissue -Lasts several days -osteoblasts within the procallus synthesize collagen and matrix, which becomes mineralized to form callus -as the repair process continues, remodeling occurs, during which unnecessary callus is resorbed and trabeculae are formed along lines of stress; at the end of this stage, bone can withstand normal stresses -the last phase, remodeling, lasts for months to years -except for the liver, bone in unique among all body tissues in that after this it will heal with normal, not scar, tissue. *clinical manifestations: Vary according to the type of fracture site of the fracture and associated soft tissue injury. In general the signs and symptoms of fracture include impaired function, unnatural alignment, deformity, swelling, muscle spasm, tenderness, pain, and impaired sensation.The position of the bone segments is determined by the pull of attached muscles, gravity, and the direction and magnitude of the force that caused the fracture. One or both segments may be rotated inward or outward on the bones long axis (rotation), may be misaligned at an angle (angulation), slide over the other segment (over riding), or be out of normal position (displaced). The immediate pain of the fracture is severe and usually caused by trauma. subsequent pain may be produced by muscle spasm, overriding of the fracture segments, or damage to the adjacent soft tissues. Numbness is common and is caused by swelling, pinching, or severing of the nerve trauma, or by bone fragments. Pathologic fractures can cause angular deformity, painless swelling, or generalized bone pain. Stress fractures are painful not because of pain but because of accelerated remodeling. The pain occurs during activity and is usually relieved by rest. Stress fractures also cause local tenderness and soft tissue swelling. Transchondral fractures may be entirely asymptomatic or painful during movement. Range of motion in the joint is limited and movement may evoke audible clicking sounds (crepitus).

compensated shock

-when the systolic blood pressure is adequate for age, but there are signs of inadequate tissue perfusion the child is in this -although the systolic BP may be normal, the diastolic or mean blood pressure is typically low

sprains and strains of tendons and ligaments- patho/clinical manifestations p.1545

-when torn, an extensive cascade of inflammatory processes begins -an inflammatory exudate develops between the torn ends -later granulation tissue containing macrophages, fibroblasts, and capillary buds grows inward from the surrounding soft tissue and cartilage to begin the repair process -within 3-4 days after the injury, collagen formation begins -at first, collagen formation is random and disorganized -as the collagen fibers interweave and connect with pre-existing fibers, they become organized parallel to the lines of stress -eventually vascular fibrous tissue fuses the new and surrounding tissues into a single mass -as reorganization takes place, the healing this separates from the surrounding soft tissue -usually a healing this lacks sufficient strength to withstand strong pull for 4-5 weeks after the injury -if strong muscle pull doesn't occur during this time, these ends May separate again, which causes these to heal in a lengthened shape with an excessive amount of scar tissue that renders this functionless -scar remodeling may take months to years before it is complete. *clinical manifestations: Tendon and ligament injuries are painful and are usually accompanied by soft tissue swelling, changes in tendon or ligament contour, and dislocation or subluxation of bones. The pain is generally sharp and localized and tenderness persists over the distribution of the tendon or ligament. Painful joint swelling usually can be seen in finger and elbow sprains. Flexion deformities of the fingers and thumb occur in injuries to the extensor tendons. Crepitus may accompany tendon injury in the wrist. Pain in the elbow may be accentuated by flexion, supination, and extension of the elbow or by extension of the wrist. Lifting small objects requires extension of the wrist and therefore aggravates the pain. Tendon injuries in the upper arm causes weakness when the individual tries to flex the forearm. Pain is often the key symptom of shoulder injuries. It may be referred to the deltoid muscle or extend down the arm and is aggravated by attempts to actively raise the arms. Depending on the ligament or tendon involved, tendon and ligament injuries in the knee may produce pronounced immobility, absence of lateral movement, instability when walking downstairs, flexion deformity, crepitus, or an upward or downward shift of the patella.

Risk factors for OA p.1565

1) trauma, particularly sprains, strains, joint dislocations, and fractures 2) long-term mechanical stress associated with athletics, ballet dancing, or repetitive physical tasks worsened by obesity 3) the presence of inflammation in joint structures, during which inflammatory cells release enzymes capable of digesting cartilage cells 4) Joint instability caused by damage to supporting structures, such as the joint capsule, ligaments, or tendons 5) Neurological disorders (diabetic neuropathy, Charcot neuropathic joint) in which pain and proprioceptive reflexes are diminished or lost, increasing the tendency for abnormal movement, positioning or weightbearing 6) Congenital or acquired skeletal deformities 7) Hematologic or endocrine disorders, such as hemophilia, which causes chronic bleeding into the joints, or hyperparathyroidism, which causes bone to lose calcium 8) Drugs (colchicine, indomethacin, steroids) that stimulate the activity of collagen-digesting enzymes in the synovial membrane 9) obesity -all of these factors alter articulate cartilage in some way and accelerate the rate of cartilage loss

summary review- children p.1724-1725 1. shock and multiple organ dysfunction syndrome 2. burns

1. -Shock in children is present when there is signs of poor systemic perfusion regardless of blood pressure. -Hypovolemic shock is the common Type of shock in children and it most frequently results from dehydration or trauma. Hypovolemic shock also may result from expansion of the vascular space producing inadequate intravascular volume relative to the vascular space. -Hypotension is a sign of severe pre-terminal decompensated shock referred to as hypotensive shock. -Clinical manifestations of hypovolemic shock include inadequate systemic perfusion associated with intravascular fluid loss. Adrenergic compensatory mechanisms can produce tachycardia, redistribution of blood flow, peripheral vasoconstriction, cool extremities, delayed capillary refill, and oliguria. -Neurogenic shock is caused by loss of vasomotor tone after severe injury to the spinal cord. -Clinical manifestations of neurogenic shock include warm skin, hypotension with a low diastolic blood pressure, and poor systemic perfusion. Tachycardia does not present. -Cardiogenic shock with decreased cardiac output is observed most commonly after cardiovascular surgery or with inflammatory diseases of the heart such as cardiomyopathy and myocarditis. It is also found in children with obstructive congenital heart disease and those with drug toxicity or severe electrolyte or acid-base imbalance. -Clinical manifestations of cardiogenic shock include inadequate systemic perfusion despite adequate intravascular volume. Cardiac output is typically low. adrenergic compensatory mechanisms including peripheral vasoconstriction and decreased urine volume are similar to those found in hypovolemic shock. -Once septic shock is present- immediate treatment is urgently needed therapy in the first hour. includes aggressive fluid resuscitation typically 60 to 80 mL per kilogram administered in the first hour of therapy and approximately 200 to 240 mg per kilogram in the first eight hours of therapy. If the child does not respond to volume administration alone, vasoactive support must be initiated within the first hour of treatment. Antibiotics also must be administered within the first hour. Goals of therapy are to rapidly normalize the heart rate and blood pressure for age and to normalize capillary refill to less than two seconds. The child shock index (heart rate/systolic blood pressure) should fall during the first hour of management if therapy is effective. fluid and vasoactive therapy should support high cardiac output and oxygen delivery maintaining the SV02 at approximately 70%. -Sepsis is a systematic response to infection. it is present once manifestations of SIRS are observed. SIRS is present when the child demonstrates two or more of the following as an acute change from baseline values: Altered temperature, altered heart rate, altered respiratory rate, and alteration in the WBC count. The newborn often develops hypothermia rather than a fever as a sign of infection and may develop bradycardia instead of tachycardia. -Severe sepsis is present when there is evidence of SIRS and signs of organ dysfunction, hypoperfusion, and hypotension. -The development of septic shock is heralded when the child with severe sepsis develops signs of cardiovascular dysfunction. The child may become hypotensive despite adequate fluid resuscitation or require vasopressors to maintain blood pressure. -Reperfusion and inflammatory injury stimulate free oxygen radicals that can damage cell membranes, denature proteins, and disrupt chromosomes. This process likely effects endothelial cells and the microvasculature causing MODS. -Lactic acidosis rise and serum lactate may be the most sensitive indicator of inadequate systemic perfusion in children. Effective shock therapy should eliminate lactic acidosis. -The general goals of treatment for shock- maximization of oxygen delivery and minimization of oxygen demand. This requires support of airway oxygenation and ventilation. Supportive cardiovascular function requires support of appropriate heart rate and rhythm, adequate intravascular volume, good myocardial function, and appropriate vascular resistance and distribution of blood flow. The child should be kept warm but fever must be treated promptly. -The signs of shock should lessen or disappear if management of shock is effective. the warmth of the child's extremities, briskness of capillary refill, quality of peripheral pulses, level of consciousness and responsiveness, urine volume, oxygenation, ventilation, and acid-base status should improve throughout shock therapy. 2. -Burns in children are often the result of inadequate supervision, curiosity, inability to escape the burning agent, or intentional abuse. -Scold injuries are commonly seen in young children and results from exposure to hot water, grease, or other hot liquids whereas flame burns are more prevalent among older children. -The child's skin is thinner and thus more susceptible to injury than adults skin. the kitchen and bathroom are common sites of burn injury. -Approximately 10% of all forms of child abuse cases in the United States results from burn injury. -Flame burns involving flammable liquids most notable. gasoline are more common in older children. risk taking behaviors in young males can lead to electrical burns. children may be exposed to chemical injury by swallowing caustic agents at home. -Use of the standard rule of nines results in an inaccurate calculation of the percentage of TBSA. in children, a modified rule of nines deducts 1% from the head and adds .5% to each leg for each year of life after two years of age. -Major burn trauma involves all body systems and the consequences of injury includes shock, infection, hypermetabolism, organ failure, and functional limitations. These effects can be magnified in the pediatric population as a result of physiologic immaturity and age-related variation in treatment modalities. -Infection, trauma, or applying ice to the burn area may convert a partial thickness injury to a full thickness one, especially in young children who have thinner, more delicate skin. -Marked reduction and cardiac output occurs immediately after injury and is accompanied by an initial increase in systemic vascular resistance. The inefficient and labile peripheral circulation of the infant complicates management of the burn shock phase of treatment. Constriction of the chest and impairment of respiratory excursion may occur in the very young child because of the increased viability of the rib cage. Younger children are also more susceptible to increased intra-abdominal pressure. -The leading cause of death in children after burn injury, as in adults, is inhalation injury. -Children require fluid resuscitation for smaller burns than does the adult population as a result of limited physiologic reserves. Colloid replacement may be required in the very young child who failed to respond to fluid replacement. - children younger than two years lack the ability to concentrate urine because of the immaturity of the renal system and are therefore at increased risk for dehydration. Because children have a relatively larger body surface area in relation to weight than adults, they require proportionately increased fluid during burn shock resuscitation to compensate for evaporative water losses. - some children exhibit immunosuppression for a prolonged period after wound closure. -A biphasic pattern of physiologic responses is evident in the burn injured child. The initial ebb phase occurs during the immediate post burn. And continues for 3 to 5 days. This phase is characterized by reduced oxygen consumption, impaired circulation, and cellular shock. After this phase and the restoration of volumes, the metabolic response shifts to a catabolic or flow phase. This phase is characterized by hypermetabolism with an increased oxygen consumption and elevation of catecholamines, glucocorticoids, and glucagon. -Glycogen stores are limited in children making it hard for them to meet increased energy demands of the burn. This prolonged metabolic dysfunction may lead to loss of lean body mass and increased morbidity. -Although age was not found to be a predictor of hypertrophic scarring, children have greater skin tension and an accelerated collagen synthesis. -Children require specialized management to ensure optimal functional and cosmetic results. Long-term scar and contracture management is necessary because of changes in body composition as the child grows and matures.

summary review p.1694-1695 1. shock 2. multiple organ dysfunction syndrome 3. burns

1. -shock occurs when the cardiovascular system fails to perfuse tissues, cells, and organs adequately, causing a widespread impairment of cellular metabolism and tissue function. it is a downward physiologic spiral that in not reversed, can lead to MODs. -types of shock our cardiogenic, hypovolemic, neurogenic and vasogenic, anaphylactic, and septic. -The final common pathway in all types of shock is impaired cellular metabolism and cells switch from aerobic to anaerobic metabolism. Energy stores drop and cellular mechanisms relative to membrane permeability action potentials and lysozyme release fail. -Anaerobic metabolism results in activation of the inflammatory response, decreased circulatory volume, and decreasing pH. -Impaired cellular metabolism results in cellular inability to use glucose because of impaired glucose delivery or impaired glucose intake resulting in a shift of glycogenolysis, gluconeogenesis, and lipolysis for fuel generation. - glycogenolysis is affected for up to 10 hours. gluconeogenesis results in the use of proteins necessary for structure, function, repair, and replication that leads to more impaired cellular metabolism. lipolysis is ineffective because of a lack of transport serum proteins. - gluconeogenesis contributes to lactic acid, uric acid, and ammonia build up interstitial edema, and impairment of the immune system, as well as general muscle weakness leading to decreased respiratory function and cardiac output. -Cardiogenic shock results from persistent hypotension and tissue hypoperfusion caused by cardiac dysfunction in the presence of adequate intravascular volume and left ventricular filling pressure. -Hypovolemic shock is caused by loss of whole blood plasma or interstitial fluid in large amounts. The use of compensatory mechanisms maybe vigorous but tissue perfusion ultimately decreases and result in impaired cellular metabolism. -Neurogenic (vasogenic) shock results from massive vasodilation that results from an imbalance between parasympathetic and sympathetic stimulation of vascular smooth muscle. It causes a relative hypovolemia even though cardiac output maybe high, and results in impaired cellular metabolism. -Anaphylactic shock is the outcome of a widespread hypersensitivity to an allergen that triggers anaphylaxis. the inflammatory response is triggered and a massive vasodilation with fluid shifts into the interstitium follows. The relative hypovolemia leads to impaired cellular metabolism. -Septic shock begins with a impaired cellular metabolism caused by uncontrolled septicemia. The infecting agent triggers the inflammatory and immune responses. It is part of a continuum known as SIRS. Mortality for septic shock is very high. 2. -MODS is the progressive dysfunction of two or more organ systems resulting from a systemic inflammatory response after a severe illness or injury. The inflammatory response can be triggered by sepsis, necrotic tissue, trauma, burns, ARDS, acute pancreatitis, major surgery, circulatory shock, DIC, acute renal failure, blood transfusion, heat stroke, liver failure, mesenteric ischemia, propofol infusion syndrome, persistent inflammatory foci, and other severe injuries. -Primary MODS is the immediate local or mild systemic response to the triggering event or illness. It times the inflammatory system. -Secondary MODS is the uncontrollable excessive systemic inflammatory response that develops after a latent period and results in organ dysfunction. -people at greatest risk for developing MODS are older adults, those with significant tissue injury or preexisting disease, and those in whom resuscitation from the initiating illness or injury has been delayed or inadequate. -MODS is the leading cause of mortality in surgical intensive care units ICU. mortality for individuals with MODS increases from 54% with two failing organs to 100% with five failing organ systems. -Multiple organ dysfunction involves the stress response release of complement, coagulation, and kinin proteins, changes in the vascular endothelium, and numerous inflammatory processes mediated by substances released by activated neutrophils and macrophages. -The consequences of the release of inflammatory mediators in MODS and vasodilation, increased vasopermeability, and selective vasoconstriction resulting in maldistribution of blood flow, hypermetabolism, myocardial depression, and hypoxic injury to cells. Cellular hypoxia and acidosis impair cellular metabolism leading to organ dysfunction. -Clinical manifestations of the development of MODS are general during the first 24 hours- Low grade fever, tachycardia, tachypnea, dyspnea, and altered mental status. -Because there is no specific therapy for MODS early detection is extremely important so that supportive measures can be initiated as soon as possible. -At present the therapeutic management of MO DS consists of prevention or removal of triggering mechanisms and support of individual organs. Recent scientific knowledge about inflammatory mediators has led to many promising future therapies for MODS. 3. -Burns are classified according to depth and extent of injury. -First degree burns involve the superficial skin without loss of protective function. -Second degree burns are superficial (blister formation) or superficial involving partial skin thickness with a waxy white appearance and no involvement of dermal appendages. -Third degree burns involve full skin thickness and often underlying tissues. they are painless and can be life threatening as a result of hypovolemic shock and metabolic and immunologic responses. -The TBSA burned is estimated using either the rule of nines or the Lund and Browder chart. -Hypovolemia associated with burn shock is caused by increased capillary permeability with massive fluid losses from blood volume. -Altered cell membrane permeability and loss of electrolyte homeostasis contribute to burn shock. -Cardiac contractility is decreased during the first 24 hours with shunting of blood away from the liver, kidney, and gut. -Fluid resuscitation such as with lactated ringers solution involves infusion of fluid at a rate faster than the loss of circulating volume. -The most reliable criterion for adequate resuscitation of burn shock his urine output. -Capillary seal is the term used to indicate the end of burn shock. -Transmembrane potentials are altered in cells not directly damaged by heat, with the impairment of the sodium-potassium pump and loss of magnesium and phosphate. -Distress of a major burn activates the sympathetic nervous system with release of catecholamines, cortisol, glucagon, and insulin. -Burn injury produces a hypermetabolic state that persists until wound closure and is related to a higher thermal regulatory setpoint. -The local inflammatory response at the burn site releases cytokines, oxygen free radicals, chemotactic factors and eicosanides, which lead to a systemic inflammatory response and contributes to hypermetabolism. -Posttraumatic hypermetabolic response is associated with increased visceral heat production. -Alterations in clotting factors produce a hypercoagulable state following major burns. -The immune response following a burn is immediate, prolonged, and severe. -Numerous alterations in inflammatory cytokines are evident in the immediate burn period, affecting cellular immunity, antibody production, and attraction of neutrophils, and contributing to the vasodilation and increased capillary permeability associate with burn shock. -white blood cells are altered and there is decreased opsonization and phagocytosis contributing to the development of sepsis. -Changes in intestinal wall integrity lead to translocation of bacteria, endotoxemia, and septic shock. -Loss of intact skin with a major burn results in significant evaporative water loss contributing to hypovolemia. -Treatment of major burns involves meticulous wound management, adequate fluids and nutrition, early surgical excision and grafting, modulation of the hyper metabolic state, and pain management.

Comminuted fracture p.1541

A bone breaks in more than two fragments -multiple bone fragments

Avulsion p.1545

A complete separation of a tendon or ligament from its bony attachment site -result of abnormal stress on the ligament or tendon and is commonly seen in young athletes, esp sprinters, hurdles and runners

Avulsion fracture- Table 44-1 p.1542

A fragment of bone connected to a ligament or tendon breaks off from the main bone

RANKL p.1553

A member of the TNF family, is expresses by osteoblasts and their immature precursors and is necessary for osteoclast development -activates the receptor RANK, which is expressed on osteoclasts and their precursors and suppresses apoptosis, which leads to activation and prolongation of osteoclast survival -the effects of this are blocked by OPG, a glycoproteins that acts as a decoy receptor for this that prevents it from binding and activating RANK -cytokines and hormones regulate the balance between this and OPG -alterations of the this/RANK/OPG system can lead to the dysregulation and pathologic condition including osteoporosis, immune-mediated bone diseases, malignant bone disorders and inherited skeletal diseases -increased bone resportion results from enhanced development of osteoclasts and decreased osteoclast apoptosis -estrogen stimulates OPG secretion and down regulates this; drugs known as selective estrogen modifiers, also stimulate OPG production -in estrogen deficiency, the exact role of OPG is less clear. -postmenopausal women express higher levels of this on bone marrow stromal cells, T cells, and B cells than premenopausal women -this expression is increased when estrogen levels are decreased, leading to increased formation of osteoclasts while reducing osteoclast apoptosis -other factors such as sclerostin, a glycoproteins secreted by osteocytes are powerful inhibitors of osteoblast formation by binding to low density lipoprotein receptor-related protein 5 and prevent binding with frizzled protein and Wnt signaling, important factors in osteoblast and bone formation.

Ligament p.1545

Band of fibrous connective tissue that connects bones where they meet at a joint

Age-related bone loss p.1553

Beings in the 3rd to 4th de cause -cause remains unclear, but it is known that decreased serum growth hormone and IGF levels along with increased binding of RANKL and decreased OPG affect osteoblast and osteoblast formation -loss of trabecular bone in men proceeds in a linear fashion, with thinning of trabecular loss rather than complete loss as noted in women -men have approx 30% more bone mass than women, which would be a factor in their later involvement with osteoporosis -androgens promotes osteoprotegerin production, thus inhibiting the osteoclast if effect of RANKL -reduction in physical activity in older persons also may be a major factor in the degree of bone loss bc preservation of bone mass depends on skeletal stress (mechanical) though muscle contraction and weightbearing

Fatigue fractures p.1541

Caused by abnormal stress or torque applied to a bone with normal ability to deform and recover (joggers, dancers, military recruits) and are a type of stress fracture

Pathologic fracture p.1541

Break at the site of a pre existing abnormality (such as a tumor), usually by force that would not fracture a normal bone -any disease process that weakens a bone (esp the cortex) predisposes the bone to this, commonly associated with tumors, osteoporosis, infections, and metabolic bone disorders -occurs at a point in the bone weakened by disease

Hypovolemic shock

Caused by loss of whole blood, plasma, or interstitial fluid in large amounts -the use of compensatory mechanisms may be vigorous, but tissue perfusion ultimately decreases and results in impaired cellular metabolism -hemorrhage, burns, diaphoresis, diabetes mellitus, diabetes inspidus, emesis or dieresis -loss of whole blood or plasma causes this directly -loss of interstitial fluid causes an indirect "relative" this by promoting diffusion of plasma from the intravascular to the extra vascular space -beings to develop when intravascular volume has decreased by about 15% -offset initially by compensatory mechanisms -heart rate and SVR increase as a result of catecholamines release by the adrenals -this boosts cardiac output and tissue perfusion pressures -complelled by a decrease in capillary hydrostatic pressures, interstitial fluid moves into the vascular compartment -the liver and spleen add the blood volume by disgorging stored RBCs and plasma -in the kidneys, renin stimulates aldosterone release and the retention of sodium (and water), whereas ADH from the posterior pituitary gland increases water retention -as shock worsens, ADH in plasma decreases -results in compensatory vasoconstriction and increase SVR and after load in order to improve BP and perfusion to core organs of the body -the compensatory mechanisms are finite -if the initial fluid or blood loss is great or if loss continues, compensation fails, resulting in decreased tissue perfusion -nutrient delivery to the cells is impaired and cellular metabolism fails -mortality from traumatic hemorrhage shock ranges from 10-31%

Cold shock

Characterized by peripheral vasoconstriction, cold skin with prolonged capillary refill and decreased peripheral pulses -often associated with low cardiac output; these characteristics are present in almost half of children who present with septic shock -cardiac output may be low, normal or high regardless of skin temperature, perfusion and pulses; these characteristics alone will not identify the cardiovascular support required -when inadequate systemic perfusion persists, the child likely needs more aggressive fluid administration and titration of vasoactive drug therapy

Extracapsular fracture- Table 44-1 p.1542

Close to the joint but remains outside the joint capsule

Subluxation p.1544

Contact between the bones in the joint only partially lost -Associated with fractures, muscle imbalance, rheumatoid arthritis, other joint instability

Osteoclast differentiation pathway p.1553 (left column 3rd para)

Directed by a series of processes that include proliferation, differentiation, fusion, and activation, -these processes are controlled by hormones, cytokines, and paracrine stromal-cell microenvironment interactions -the intracellular communication in bone and the key molecular regulators are necessary for bone homeostasis -certain transcription factors, known as Forkhead box, help protect against the effects of OS by preventing excess accumulation of ROS and regulating certain genes that affect DNA repair and cell life span -FoxOs help remove damaged and abnormal cells by inducing apoptosis -interleukins, (1, 4, 6, 7, 11, 17), TNFa, transforming growth factor beta, prostaglandin E2, and hormones interact to control osteoclasts -normal bone hemeostasis is dependent on the balance between the cytokines receptor activator of nuclear factor kB ligand (RANKL) , it's receptor RANK and its decoy receptor osteoprotegerin; understanding this has led to a tremendously increased knowledge of osteoclast biology and pathogenesis of bone loss

Delayed Union p.1543

Does not occur until approximately 8 to 9 months after a fracture.

Spiral fracturep.1541

Encircles the bone

Intracapsular fracture- Table 44-1 p.1542

Extends into or is within the joint capsule

Tendon p.1545

Fibrous connective tissue that attached skeletal muscle to bone

Impacted fracture- Table 44-1 p.1542

Fragments are pushed into each other

Medial epicondylopathy p.1546

Golfer's elbow -degenerative process of the pronation there's, flexor carpi radialis, and palmaris longus tendons at the medial humeral condylar

Secondary septic arthritis p.1602

In cases in which the infection in the metaphysis occurs near the joint, the accumulating pus (bacteria, white blood cells, fluid) creates increasing pressure that may cause a rupture into the joint cavity -if rupture into the joint occurs, the pus causes inflammation and a condition called this -studies show that up to 40% of children will have adjacent joint involvement with osteomyelitis -the most common joint to be affected is the knee -osteomyelitis is most commonly caused by bacteria that reach the metaphysis through the bloodstream but may occur though secondary inoculation of microorganisms caused by trauma or contagious spread of infection from cellulitis in adjacent soft tissue

Tendinopathy p.1545

Included tendinitis, tendinosis, and paratendinitis -studies have shown that vascular in growth in this (neovascularization) is accompanied with nerve in growth, facilitating pain transmission in Achilles and patellar types -other causes include crystal deposits, postural. Misalignment, and hypermobility in a joint

Sprains and strains of tendons and ligaments p.1545

Injuries can accompany fractures and dislocations -support the bones and joints and either faciliates or limit motion -can be torn, ruptured, or completely separated from bone at their points of attachment -classified as first degree (least severe), second degree, and third degree (most severe)

Malunion p.1543

Is healing of the bone in a nonanatomic position.

Sprains p.1545

Ligament tears or injury -ligament tears and ruptures can occur at any joint but are most common in the wrist, ankle, elbow, and knee joints

Causative microorganisms of osteomyelitis in children p.1602 box 45-2

Newborns - s. Aureus, Group B strep, gram negative enteric rods Infants - S. Aureus, H. Influenzae Older Children - S. Aureus, Pseudomonas, Salmonella, N. Gonorrhoeae Adolescents and Adults - Psuedomonas, mycobacterium tuberculosis

Transverse fracture p.1541

Occurs straight across the bone -perpendicular to long axis of bone

Displaced fracture- Table 44-1 p.1542

One, both or all fragments out of normal alignment

Greenstick fracture p.1541

Perforated one cortex and splinters the spongy bone and is relatively unstable -name is derived from the damage sustained by a young tree branch when it's bent sharply -outer surface is disrupted, but the inner surface remains intact -typically occur in the metaphysics or diaphysis of the tibia, radius, and ulna -break on one cortex of bone with splintering of inner bone surface -common in children and older adults

Linear fracture p.1541

Runs parallel to the long axis of the bone

Oblique fracture p.1541

Slanted fracture of the shaft of a bone -at angle to long axis of bone

Secondary osteoporosis p.1552 (right column 3rd para)

Sometimes develops temporarily in individuals receiving large doses of heparin, because heparin promotes bone resorption by decreasing collagen synthesis or by increasing collagen breakdown -this caused by heparin therapy usually resolve when the therapy ceases -tx with other medications may lead to the development of this such as the use of glucocorticoid tx for RA -other meds increasing the risk of this include lithium, methotrexate, anticonvulsants, cyclophosphamide and cyclosporine

Dislocation p. 1544

Temporary displacement of bone from its joint

Lateral epicondylopathy p.1546

Tennis elbow -result of tissue degeneration or irritation of the extensor Carpi radialis brevis tendon at its origin

Complete fracture p.1541

The bone is broken all of the way through

Incomplete fracture p.1541

The bone is damaged but still in one piece -tend to occur in the more flexible, growing bones of children -three main types are greenstick, buckle or torus, and bowing

Paratenonitis with tendinosis- Table 44-1 p.1542

This associated with intratendinous degeneration -degenerative changes with mucoid degeneration with or without fibrous and scattered inflammatory cells in the paratenon alveolar tissue

osgood-Schlatter disease- patho/clinical manifestations p.1605/1606

The severity of the lesion varies from mild tendinitis to a complete separation of the anterior extension of the tibial epiphysis, which is the part of the epiphysis that contributes to growth of the tibial tubercle -the underlying pathologic alterations also vary -the mildest form causes ischemic (a saccular) necrosis in the region of the bone tibial tubercle, with hypertrophic cartilage formation during the stages of repair -in more severe cases the abnormality involves a true epiphyseal separation of the tibial tubercle. *clinical manifestations: The child experiences pain and swelling in the region of the patellar tendon and tibial tubercle, which becomes prominent and is tender to direct pressure. The pain is most severe after physical activity that involves vigorous quadriceps contraction or direct local trauma to the tibial tubercle area. Often the child experiences sudden acute discomfort referral to the affected region. Sudden onset of pain can represent a pathologic fracture through an area of ischemic necrosis.

Bowing fracture p.1541

Usually occur when a longitudinal force is applied to bone -common in children and usually involves the paired radius-ulna or fibula-tibia -a complete diaphyseal fracture occurs in one of the bones of the pair, which disperses the stress sufficiently to prevent a complete fracture of the second bone, which bows -resists correction (reduction) because the force necessary to reduce it must be equal to the force that bowed it -tx is difficult by the bowed bone intereferes with reduction of the fractured bone -bending of the bone

Compression fracture- Table 44-1 p.1542

Wedged or squeezed together on one side of the bone