muscoskelital

Muscle shortening occurs during

contraction but can be seen also during pathologic and physiologic contracture.

legge-calve-perthes is characterized by

epiphyseal necrosis or degeneration of the head of the femur followed by regeneration or recalcification

The nonprotein muscle constituents provide an

energy source for contraction and regulate protein synthesis, enzyme systems, and membrane stabilization.

Hematoma formation provides the

fibrin framework for formation and organization of granulation tissue.

Cartilaginous joints are connected by

fibrocartilage or hyaline cartilage.

Speed of contraction is affected by several factors:

muscle fiber type, temperature, stretch, and weight of the load.

Clubfoot can be

positional, idiopathic, or teratologic.

3. Bone tissue is continuously being

resorbed and synthesized by bone-remodeling units of osteoclasts and osteoblasts.

The most common type of childhood soft tissue tumor is

rhabdomyosarcoma.

8. Actin and myosin filaments form cross-bridges that cause the

sarcomere to shorten, a process now known as the cross-bridge theory of muscle contraction.

11. The outer layer of the periosteum contains blood vessels and nerves that penetrate the inner structures of the bone by way of which structure? a. Volkmann canals c. Sharpey canals b. Canaliculi d. Trabeculae

ANS: A All bones are covered with a double-layered connective tissue called the periosteum. The outer layer of the periosteum contains blood vessels and nerves, some of which penetrate to the inner structures of the bone only through channels called Volkmann canals (see Figure 43-4). PTS: 1 REF: Page 1517

2. Which type of fracture usually occurs in an individual who engages in a new activity that is strenuous and repetitive? a. Stress c. Insufficiency b. Greenstick d. Pathologic

ANS: A Only a stress fracture occurs in normal or abnormal bone that is subjected to repeated stress, such as repetitive and strenuous activities that occur during athletics. PTS: 1 REF: Page 1541

Noninflammatory joint disease is differentiated by

Absence of synovial membrane inflammation Lack of systemic signs and symptoms Normal synovial fluid Arthropathies: Diseases of the joints

Cytokines -

Bone Remodeling

Malunion

Is healing of the bone in a nonanatomic position.

Epicondylitis

Is inflammation of a tendon where it attaches to a bone.

Clinical manifestations support structure trauma

Is painful and usually accompanied by soft-tissue swelling and changes in tendon or ligament contour.

Other benign bone tumors include

simple bone cysts, aneurysmal bone cysts, osteoid osteoma, and fibrous dysplasia.

Callus formation

(2-6 weeks)

17. Most childhood osteosarcoma tumors occur between the ages of

10 and 18 years. 18.

6. Muscle fibers reach their maximal size in females at

10 years of age and at 14 years of age in males.

Osteosarcoma

38% of bone tumors

Joints provide

stability and mobility to the skeleton.

8. Bone injuries are repaired in

stages.

Osteoporosis

<648 mg/cm2

17. The hyaline cartilage joints between the ribs and sternum are examples of which type of joint? a. Synchondrosis c. Gomphosis b. Symphysis d. Syndesmosis

ANS: A A synchondrosis is the only type of joint in which hyaline cartilage, rather than fibrocartilage, connects the two bones. The joints between the ribs and the sternum are synchondroses and are not examples of any of the other types. PTS: 1 REF: Page 1520

33. What term is used to identify an interlacing bundle of dense, white fibrous tissue that is richly supplied with nerves, blood vessels, and lymphatic vessels? a. Procallus c. Hematoma b. Joint capsule d. Elastin fibers

ANS: B The joint capsule is made up of parallel, interlacing bundles of dense, white fibrous tissue. It is richly supplied with nerves, blood vessels, and lymphatic vessels. None of the other options are associated with this structure. PTS: 1 REF: Page 1522

Clinical manifestations sequestra and involucrum

Acute and chronic inflammation, fever, pain, necrotic bone

Treatment osteomalacia

Adjust serum calcium and phosphorus levels to normal. Suppress secondary hyperthyroidism. Chelate bone aluminum, if needed. Administer calcium carbonate to decrease hyperphosphatemia. Administer dietary supplements of vitamin D. Use renal dialysis. Renal transplantation for renal osteodystrophy.

Treatment pagets

Bisphosphonates and calcitonin

Pathologic

Break occurs at the site of a preexisting abnormality.

muscle strain

Causes local muscle damage.

Treatment of fracture

Closed manipulation, traction (skeletal or skin), open reduction, internal fixation, external fixation Improper reduction or immobilization[ Nonunion Is the failure of the bone ends to grow together.

Myositis Ossificans Also called heterotopic ossification

Complication of local muscle injury

Within the synovial joint capsule is a small fluid-filled space. The fluid in the space nourishes

the articular cartilage that covers the ends of the bones meeting in the synovial joint.

5. The appendicular skeleton (extremities) grows faster during childhood than does

the axial skeleton.

Subluxation

Contact between the bones in the joint only partially lost

Torus

Cortex buckles but does not break.

Treatment giant cell tumor

Cryosurgery and resection with adjuvant polymethylmethacrylate (PMMA) for bone grafts.

A person has rhabdomyolysis. Which typical clinical manifestation will the nurse find upon assessment?

Dark urine Scar-tissue calcification "Tennis elbow" "Rider's bone"

OPG - (osteoprotegerin)

Decoy receptor for RANKL

Osteopenic bone:

Decreased bone mass 833 to 648 mg/cm2

Potential causes 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

Improper reduction or immobilization Treatment:

Designed to stimulate new bone formation Implantable or external electric current devices, electromagnetic field generations, and low-density ultrasound Stem cell and gene therapy

Evaluation

Dual x-ray absorptiometry (DXA)

Spiral

Encircles the bone.

The primary defect in osteoarthritis is:

Enlargement and softening of bones Development of pannus Loss of articular cartilage Permeative pattern of bone destruction

Treatment osteoporsis

Estrogen Bisphosphonates, denosumab, teriparatide, parathyroid hormone (PTH) 1-84

Joint effusion:

Exudate or blood entering the joint

Stress

Fatigue and insufficiency

Systemic signs of inflammation inflammatory joint disease clinical manifestations

Fever, leukocytosis, malaise, anorexia, and hyperfibrinogenemia Infectious or noninfectious

Reparative phase bone healing

Fibrocartilage formation (3 days - 2 weeks): pro-callus layer: collagen

Joint swelling in the fingers:

Heberden and Bouchard nodes

Inflammatory response bone healing

Hematoma formation (1-3 days)

compartment syndrome treatment

Immediate fasciotomy and débridement

Musculoskeletal Disorders Part 1- Bone Development, Fracture & Complications Dr. Hunter Osteoblasts & osteoclasts http://www.youtube.com/watch?v=78RBpWSOl08 Please watch: 2.11 min. movie explaining bone formation Regulation of osteoclast activity http://www.youtube.com/watch?v=GpMV197xZXc 2.5 min movie- please watch- explains text. Cytokines -Bone Remodeling RANKL - (receptor activator of nuclear factor kB ligand) Formation and activation of osteoclasts Increase bone resorption OPG - (osteoprotegerin) Decoy receptor for RANKL Prevents RANKL from triggering bone resorption Bone remodeling Osteoblasts and osteoclasts in bone remodeling ( iliac crest) Bone balance and remodeling Musculoskeletal Injuries Trauma Is the leading cause of death of people, ages 1 to 44 years, of all races and at all socioeconomic levels. Fracture Is a break in the continuity of a bone. Occurs when force is applied that exceeds the tensile or compressive strength of the bone. Musculoskeletal Injuries (cont'd) Fracture classifications Complete: Bone is broken all the way through. Incomplete: Bone is damaged but still in one piece. Closed or simple (complete or incomplete): Skin is intact. Open or compound (complete or incomplete): Skin is broken. Comminuted Bone breaks into more than two fragments. Linear Fracture runs parallel to the long axis of the bone. Oblique Fracture of the shaft of the bone is slanted. Musculoskeletal Injuries (cont'd) Fracture classifications (cont'd) Spiral Encircles the bone. Transverse Occurs straight across the bone. Greenstick Perforates one cortex and splinters the spongy bone. Torus Cortex buckles but does not break. Bowing Longitudinal force is applied to a bone. Pathologic Break occurs at the site of a preexisting abnormality. Stress Fatigue and insufficiency Transchondral Fractures Bone Fractures 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. Pathophysiology Inflammatory response Hematoma formation (1-3 days) Reparative phase Fibrocartilage formation (3 days - 2 weeks): pro-callus layer: collagen Callus formation (2-6 weeks) Ossification Remodeling continues until repair complete (6 weeks - 1 year: may be considered delayed union if this long) Bone Fractures Fracture healing Bone Fractures Callus formation Bone Fractures (cont'd) Clinical manifestations Unnatural alignment, swelling, muscle spasm, tenderness, pain, impaired sensation Treatment Closed manipulation, traction (skeletal or skin), open reduction, internal fixation, external fixation Splints and casts Bone Fractures (cont'd) External fixation Bone Fractures Improper reduction or immobilization Nonunion 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. Delayed union Does not occur until approximately 8 to 9 months after a fracture. Malunion Is healing of the bone in a nonanatomic position. Improper reduction or immobilization Bone Fractures Treatment: Designed to stimulate new bone formation Implantable or external electric current devices, electromagnetic field generations, and low-density ultrasound Stem cell and gene therapy Bone graft or synthetic materials (calcium phosphate cement): To fill large defects Dislocation and Subluxation Dislocation Temporary displacement of bone from its joint Subluxation Contact between the bones in the joint only partially lost Associated with fractures, muscle imbalance, rheumatoid arthritis, other joint instability Clinical manifestations Pain, swelling, limitation of motion, joint deformity Treatment Reduction and immobilization for 2 to 6 weeks Exercises Support Structure Trauma Support Structure Trauma (cont'd) Pathophysiology Inflammatory exudate develops between the torn ends. Granulation tissue grows inward, and then collagen formation begins 3 to 4 days after injury. Vascular fibrous tissue fuses the new and surrounding tissues into a single mass. Healing tendon or ligament lacks sufficient strength to withstand a strong pull for 4 to 5 weeks after the injury. Support Structure Trauma (cont'd) Clinical manifestations Is painful and usually accompanied by soft-tissue swelling and changes in tendon or ligament contour. Treatment Splinting, early motion, and rehabilitation Suturing: To treat a complete rupture If suturing is not possible: Tendon or ligament grafting Prolonged rehabilitation exercises Fat embolism Tendinopathy and Bursitis Tendinitis Inflammation of a tendon Tendinosis Painful degradation of collagen fibers Bursitis Inflammation of a bursa Are sacs lined with synovial membrane and filled with synovial fluid; sacs (bursa) are located among the tendons, muscles, and bony prominences. Is caused by repeated trauma. Septic bursitis: Is caused by a wound infection. Tendinopathy and Bursitis (cont'd) Epicondylitis Is inflammation of a tendon where it attaches to a bone. Tennis elbow: Lateral epicondylitis Golfer's elbow: Medial epicondylitis Treatment for tendinopathy and bursitis Systemic analgesics, ice or heat applications, or local injection of an anesthetic and a corticosteroid to reduce inflammation Bursitis: Aspiration to drain excess fluid Physical therapy Muscle Strain Is a sudden, forced motion, causing the muscle to become stretched beyond its normal capacity. Causes local muscle damage. Can also involve the tendons. Regardless of the cause of trauma, muscle cells can usually regenerate. May take up to 6 weeks. Myositis Ossificans Also called heterotopic ossification Complication of local muscle injury Inflammation of muscular tissue with subsequent calcification and ossification of the muscle "Rider's bone" in equestrians "Drill bone" in infantry soldiers Thigh muscles in football players Rhabdomyolysis Life-threatening complication of severe muscle trauma with muscle cell loss Crush syndrome versus crush injuries Compartment syndromes Rapid breakdown of muscle that causes the release of intracellular contents Protein pigment myoglobin into extracellular space and bloodstream Rhabdomyolysis (cont'd) Classic triad Muscle pain, weakness, and dark urine (from myoglobin) Treatment Rapid intravenous hydration: To maintain adequate kidney flow Hyperkalemia: May require temporary hemodialysis Rhabdomyolysis (cont'd) Question 1 A person has rhabdomyolysis. Which typical clinical manifestation will the nurse find upon assessment? Dark urine Scar-tissue calcification "Tennis elbow" "Rider's bone" Compartment Syndrome Complication of fractures Blood flow to affected area is compromised because of increased venous pressure, leading to decreased arterial inflow, ischemia, and edema. Clinical manifestations Pain: Out of proportion to the injury Paresthesia, pallor, pulselessness, and paralysis (late sign) Compartment Syndrome (cont'd) Evaluation Rising compartment pressure can be directly measured by inserting a wick catheter, needle, or slit catheter into the muscle. Treatment Immediate fasciotomy and débridement Emergency treatment may be required to save an affected limb. Musculoskeletal Disorders Part 2, Metabolic bone Disease & Tumors Dr. Hunter Osteoporosis Porous bone 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/cm2 Osteoporosis (cont'd) Osteoporosis (cont'd) Potential causes 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 Osteoporosis OPG/RANKL/RANK system Osteoporosis (cont'd) Reduced bone mass or density and an imbalance of bone resorption and formation Bone histologic anatomy: Usually normal but lacks structural integrity Evaluation Dual x-ray absorptiometry (DXA) Osteoporosis (cont'd) Normal bone versus osteoporotic bone Epidemiology of Osteoporosis 44 million Americans 80% women; are males at risk? Primary Postmenopausal ( estrogen, RANKL, T & B cells Decreased testosterone Secondary Steroids( RANKL & OPG), Cushing's, hyperthyroidism, immobilization, CKD, anticonvulsants; Vitamin D3 deficiency Osteoporosis (cont'd) Types of osteoporosis Perimenopausal Iatrogenic Regional Postmenopausal Glucocorticoid-induced Age-related bone loss Clinical manifestations Pain, bone deformity, fractures, kyphosis (hunchback), and diminished height Osteoporosis (cont'd) Prevention Regular moderate weight-bearing exercises Calcium intake sufficient to maintain normal calcium balance during adolescence Sufficient intake of magnesium Treatment Estrogen Bisphosphonates, denosumab, teriparatide, parathyroid hormone (PTH) 1-84 Osteomalacia Deficiency of vitamin D lowers the absorption of calcium from the intestines. Mineralization is inadequate or delayed. Bone formation progresses to osteoid formation, but calcification does not occur; result is soft bones. Clinical manifestations: Pain, bone fractures, vertebral collapse, bone malformation, waddling gait Osteomalacia (cont'd) Treatment Adjust serum calcium and phosphorus levels to normal. Suppress secondary hyperthyroidism. Chelate bone aluminum, if needed. Administer calcium carbonate to decrease hyperphosphatemia. Administer dietary supplements of vitamin D. Use renal dialysis. Renal transplantation for renal osteodystrophy. Paget Disease Also called osteitis deformans State of increased metabolic activity in bone Is abnormal, and bone resorption and formation are excessive. Enlarges and softens the affected bones. Most often affects the axial skeleton. Clinical manifestations Brain compression, impaired motor function, deafness, atrophy of the optic nerve Treatment Bisphosphonates and calcitonin Osteomyelitis 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 Osteomyelitis (cont'd) Sequestration and involucrum Osteomyelitis (cont'd) Clinical manifestations Acute and chronic inflammation, fever, pain, necrotic bone Treatment Antibiotics, débridement, surgery, hyperbaric oxygen therapy Osteomyelitis (cont'd) Question 2 Which information is correct regarding the pathophysiologic process of osteomyelitis? Osteomyelitis produces: Bone density less than 648 mg/cm2 Stimulation of osteoclasts Formation of fistula Sequestrum Bone Tumors May originate from bone cells, cartilage, fibrous tissue, marrow, or vascular tissue Osteogenic, chondrogenic, collagenic, and myelogenic Malignant bone tumors Increased nuclear-cytoplasmic ratio, irregular borders, excess chromatin, prominent nucleolus, increase in the mitotic rate Bone Tumors Derivation of bone tumors Bone Tumors (cont'd) Patterns of bone destruction Geographic Well-defined margins of lytic bone with normal bone Moth-eaten Areas of partially destroyed bone adjacent to completely lytic areas Permeative Abnormal lytic bone imperceptibly merges with surrounding normal bone Bone Tumors (cont'd) Osteosarcoma 38% of bone tumors Predominant in adolescents and young adults; occurs in seniors with a history of radiation therapy Contain masses of osteoids: Bone-forming tumors Streamers: Noncalcified bone matrix and callus Location: In the metaphyses of the long bones 50% occur around the knees Clinical manifestations Pain and swelling Treatment Systemic chemotherapy and surgery Osteosarcoma Chondrosarcoma Produces cartilage or chondroid. Is a tumor of middle-aged and older adults. Infiltrates trabeculae in spongy bone; is frequently in the metaphyses or diaphysis of long bones. Contains lobules of hyaline cartilage that expand and enlarge the bone with no ossification. Causes erosion of the cortex and can expand into the neighboring soft tissues. Clinical manifestations: Pain and swelling Treatment: Wide surgical excision Chondrosarcoma Fibrosarcoma Are firm, fibrous masses of collagen, malignant fibroblasts, and osteoclast-like cells. Usually affects the metaphyses of the femur or tibia. Metastasis to the lungs is common. Clinical manifestations: Pain, swelling, local tenderness, palpable mass, and limitation of motion; pathologic fracture Treatment: Radical surgery and amputation Giant cell tumor Causes extensive bone resorption as a result of the osteoclastic origin. Is located in the epiphyses of femur, tibia, radius, or humerus. Has slow and relentless growth rate; metastasis is rare. Clinical manifestations: Pain, local swelling, and limitation of movement. Treatment: Cryosurgery and resection with adjuvant polymethylmethacrylate (PMMA) for bone grafts. Giant cell tumor Musculoskeletal Disorders Part 3 Joint Disease Dr. Hunter Inflammatory versus Noninflammatory Joint Disease Noninflammatory joint disease is differentiated by Absence of synovial membrane inflammation Lack of systemic signs and symptoms Normal synovial fluid Arthropathies: Diseases of the joints Osteoarthritis Common age-related disorder of synovial joints Non-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 Osteoarthritis Local areas of damage and loss of articular cartilage, new bone formation of joint margins, and thickening of joint capsule Clinical manifestations Pain, stiffness, enlargement of the joint, tenderness, limited motion, and deformity Joint swelling in the fingers: Heberden and Bouchard nodes Joint effusion: Exudate or blood entering the joint Degenerative joint disease Osteoarthritis Treatment Rest of involved joint until inflammation subsides Aerobic exercise and range-of-motion exercise Cane, crutches, or walker Weight loss, if obese Analgesic and antiinflammatory drug Magnetic bracelets and acupuncture Intraarticular injection of high-molecular-weight viscosupplements, particularly hyaluronic acid Surgery: Joint replacement Osteoarthritis Examples Osteoarthritis (cont'd) Question 3 The primary defect in osteoarthritis is: Enlargement and softening of bones Development of pannus Loss of articular cartilage Permeative pattern of bone destruction Classic Inflammatory Joint Disease 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 Rheumatoid Arthritis Rheumatoid arthritis (RA): Inflammatory joint disease Systemic autoimmune destruction to synovial membrane and joints Presence of rheumatoid factors (RFs): RA or RF test Antibodies (immunoglobulin G

IgG

Location:

In the metaphyses of the long bones 50% occur around the knees

Glucocorticoids osteoporosis

Increase RANKL expression and inhibit OPG production by osteoblasts, leading to lower bone density

Formation and activation of osteoclasts

Increase bone resorption

Tennis elbow:

Lateral epicondylitis

Bowing

Longitudinal force is applied to a bone.

Bone Tumors

May originate from bone cells, cartilage, fibrous tissue, marrow, or vascular tissue Osteogenic, chondrogenic, collagenic, and myelogenic

regeneration of muscle cells length of time

May take up to 6 weeks.

Golfer's elbow:

Medial epicondylitis

Classic triad in compartment syndrome

Muscle pain, weakness, and dark urine (from myoglobin)

Streamers:

Noncalcified bone matrix and callus

OPG, a protein, binds to a protein called

OPG ligand.

Clinical manifestations bone cancers

Pain and swelling

Clinical manifestations osteoporosis

Pain, bone deformity, fractures, kyphosis (hunchback), and diminished height

Clinical manifestations osteomalacia

Pain, bone fractures, vertebral collapse, bone malformation, waddling gait

Clinical manifestations giant cell tumor

Pain, local swelling, and limitation of movement.

Greenstick

Perforates one cortex and splinters the spongy bone.

Chondrosarcoma

Produces cartilage or chondroid.

This attachment serves as a decoy receptor for

RANKL and blocks osteoclast activity, thus decreasing bone resorption.

Treatment fibrosarcoma

Radical surgery and amputation

Evaluation compartment syndrome

Rising compartment pressure can be directly measured by inserting a wick catheter, needle, or slit catheter into the muscle.

Open or compound (complete or incomplete):

Skin is broken.

Closed or simple (complete or incomplete):

Skin is intact.

Treatment support structure trauma

Splinting, early motion, and rehabilitation

Paget Disease Also called osteitis deformans

State of increased metabolic activity in bone Is abnormal, and bone resorption and formation are excessive. Enlarges and softens the affected bones. Most often affects the axial skeleton.

Bone graft or synthetic materials (calcium phosphate cement):

To fill large defects

Suturing: support structure trauma

To treat a complete rupture

Bone histologic anatomy:

Usually normal but lacks structural integrity

Treatment:chrondrosarcoma

Wide surgical excision

ATP and phosphocreatine can be generated

aerobically or anaerobically.

Emergency treatment in compartment syndrome may be required to save

an affected limb.

Clinical manifestations of rhabdomyosarcoma depend on the

anatomic location; superficial tumors exhibit a painless palpable mass, whereas deep-seated tumors cause functional impairment.

2. Procedures used to evaluate joint function include

arthrography, arthroscopy, MRI, and synovial fluid analysis.

7. There are 206 bones in the body, divided into the

axial skeleton and the appendicular skeleton.

Smaller canals, called

canaliculi, interconnect the osteocyte-containing spaces.

Granulation tissue provides a

cartilage model for the formation and crystallization of bone matrix.

. The primary treatment for Ewing sarcoma is a combination of

chemotherapy, radiation, and surgery.

3. Articular cartilage is a highly organized system of

collagen fibers and proteoglycans.

1. Muscle bulk and strength slowly

decline with aging, although not to a pathologic degree.

6. Rickets is a condition caused by

deficiencies in vitamin D, calcium, and usually phosphorus that is characterized by the failure of bones to become mineralized (ossified) and results in skeletal deformity.

Rhabdomyosarcoma originates from

embryonal rhabdomyoblasts that normally differentiate into mature striated muscle.

5. Muscle contraction includes

excitation, coupling, contraction, and relaxation.

Thigh muscles in

football players

Granulation tissue grows

inward, and then collagen formation begins 3 to 4 days after injury.

2. Developmental dysplasia of the hip (DDH)

is an abnormality in the development of the femoral head, acetabulum, or both. It is a serious and disabling condition in children if not diagnosed and treated early, preferably in infancy

When a motor unit responds to a single nerve stimulus,

it develops a phasic contraction.

7. Scoliosis is a

lateral curvature of the spinal column that can be caused by congenital malformations of the spine, neuromuscular disease, trauma, extraspinal contractures, bone infections, metabolic bone disorders, joint disease, and tumors.

Phosphocreatine concentration is an extremely sensitive indicator of

muscle fiber activity.

tauma Vascular fibrous tissue fuses the

new and surrounding tissues into a single mass.

2. Evidence of soft tissue injury, corner fractures, and fractures at different stages of healing is extremely helpful in making a diagnosis of

nonaccidental trauma.

4. All social strata are at risk for

nonaccidental trauma.

14. The two most common forms of benign bone tumors include n

onossifying fibroma and osteochondroma.

1. Skeletal muscle is the largest

organ in the body and is made up of millions of individual fibers.

Healing occurs in

phases.

Bones are classified by

shape as long, short, flat, or irregular.

Healing tendon or ligament lacks

sufficient strength to withstand a strong pull for 4 to 5 weeks after the injury.

The balance between RANKL and OPG determines

the quality of bone.

muscle strain Can also involve

the tendons.

. 3. Clubfoot (equinovarus) is a common deformity in which the foot is

twisted out of its normal shape or position.

1. A joint is the site of attachment of

two or more bones.

There are two types of muscle fibers,

type I and type II, determined by motor nerve innervation.

Joints also can be classified by the

type of connecting tissue holding them together.

1. Nonaccidental trauma must be considered with any

long bone injury in a preambulatory child.

The bone remodeling cycle takes

longer to complete, and the rate of mineralization slows.

myoobrils and myofilaments which interact to form cross-bridges during

muscle contraction.

3. Serum creatine kinase concentration is useful in detecting

muscle damage

Bone is unique: After a fracture it will heal with

normal tissue, not scar tissue.

1. What type of fracture occurs at a site of a preexisting bone abnormality and is a result of a force that would not normally cause a fracture? a. Idiopathic c. Pathologic b. Incomplete d. Greenstick

ANS: C Only a pathologic fracture is a break at the site of a preexisting abnormality, usually by force that would not fracture a normal bone. PTS: 1 REF: Page 1541

9. Skeletal muscle requires a constant supply of

ATP and phosphocreatine to fuel muscle contraction and for growth and repair.

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.

Delayed union

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

Fibrous joints are connected

by dense fibrous tissue, ligaments, or membranes.

3. Muscle fibers contain bundles of

myofibrils arranged in parallel along the longitudinal axis and include the muscle membrane, myofibrils, sarcotubular system, aqueous sarcoplasm, and mitochondria.

Bacteria are usually introduced by direct extension from a

nearby infection, through the bloodstream, or by trauma.

Comminuted

Bone breaks into more than two fragments.

6. Muscle strength is graded by the

"all or nothing" phenomenon and recruitment.

The central nervous system smoothly grades the force generated by

"recruiting" additional motor units and varying the discharge frequency of each active motor unit.

Remodeling continues until repair complete

(6 weeks - 1 year: may be considered delayed union if this long)

1. Skeletal growth and development consists of two phases:

(a) delivery of bone cell precursors to sites of bone formation and (b) the aggregation of these cells at primary centers of ossification where they mature to secrete osteoid

3. Peak bone mass is achieved by the middle to late

20s.

Epidemiology of Osteoporosis

44 million Americans

Bone density Normal bone

833 mg/cm2

16. Which type of joint holds teeth in the maxilla or mandible? a. Amphiarthrosis c. Synarthrosis b. Diarthrosis d. Gomphosis

ANS: D A gomphosis is a special type of fibrous joint in which a conical projection fits into a complementary socket and is held in place by a ligament. Gomphosis is the only term used to identify the joint that holds teeth in the maxilla or mandible. PTS: 1 REF: Page 1520

Treatment sequestra

Antibiotics, débridement, surgery, hyperbaric oxygen therapy

Fibrosarcoma

Are firm, fibrous masses of collagen, malignant fibroblasts, and osteoclast-like cells. Usually affects the metaphyses of the femur or tibia. Metastasis to the lungs is common.

Bursitis tx

Aspiration to drain excess fluid Physical therapy

Complication of fractures compartment syndromes

Blood flow to affected area is compromised because of increased venous pressure, leading to decreased arterial inflow, ischemia, and edema.

Incomplete:

Bone is damaged but still in one piece.

Contain masses of osteoids:

Bone-forming tumors

Clinical manifestations pagets

Brain compression, impaired motor function, deafness, atrophy of the optic nerve

Osteoarthritis

Common age-related disorder of synovial joints Non-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

Osteomalacia

Deficiency of vitamin D lowers the absorption of calcium from the intestines. Mineralization is inadequate or delayed. Bone formation progresses to osteoid formation, but calcification does not occur; result is soft bones.

Malignant bone tumors

Increased nuclear-cytoplasmic ratio, irregular borders, excess chromatin, prominent nucleolus, increase in the mitotic rate

Postmenopausal osteoporosis

Increased osteoclast activity, changes in OPG, insulin-like growth factor (IGF), and family history

Bursitis

Inflammation of a bursa Are sacs lined with synovial membrane and filled with synovial fluid; sacs (bursa) are located among the tendons, muscles, and bony prominences. Is caused by repeated trauma.

Myositis Ossifican

Inflammation of muscular tissue with subsequent calcification and ossification of the muscle

Classic Inflammatory Joint Disease Commonly called arthritis

Inflammatory damage or destruction in the synovial membrane or articular cartilage

Pathophysiology trauma

Inflammatory exudate develops between the torn ends.

Rhabdomyolysis

Life-threatening complication of severe muscle trauma with muscle cell loss

Septic bursitis:

Is caused by a wound infection.

Osteoarthritis

Local areas of damage and loss of articular cartilage, new bone formation of joint margins, and thickening of joint capsule

Transverse

Occurs straight across the bone.

Clinical manifestations osteoarthritis

Pain, stiffness, enlargement of the joint, tenderness, limited motion, and deformity

Clinical manifestations sublixation

Pain, swelling, limitation of motion, joint deformity

Clinical manifestations fibrosarcoma

Pain, swelling, local tenderness, palpable mass, and limitation of motion; pathologic fracture

Tendinosis

Painful degradation of collagen fibers

Derivation of bone tumors

Patterns of bone destruction Geographic Well-defined margins of lytic bone with normal bone Moth-eaten Areas of partially destroyed bone adjacent to completely lytic areas Permeative Abnormal lytic bone imperceptibly merges with surrounding normal bone

Types of osteoporosis

Perimenopausal Iatrogenic Regional Postmenopausal Glucocorticoid-induced Age-related bone loss

Involucrum:

Periosteal new bone

Osteoporosis

Porous bone Poorly mineralized bone Primary versus secondary

80% women; are males at risk? Primary causes osteoporis

Postmenopausal ( estrogen, RANKL, T & B cells Decreased testosterone

osteosrcoma age

Predominant in adolescents and young adults; occurs in seniors with a history of radiation therapy

OPG

Prevents RANKL from triggering bone resorption

Compartment syndromes

Rapid breakdown of muscle that causes the release of intracellular contents Protein pigment myoglobin into extracellular space and bloodstream

Treatment compartment syndroms

Rapid intravenous hydration: To maintain adequate kidney flow Hyperkalemia: May require temporary hemodialysis

Treatment sublixation

Reduction and immobilization for 2 to 6 weeks Exercises

Prevention osteoporosis

Regular moderate weight-bearing exercises Calcium intake sufficient to maintain normal calcium balance during adolescence Sufficient intake of magnesium

Osteoarthritis Treatment

Rest of involved joint until inflammation subsides Aerobic exercise and range-of-motion exercise Cane, crutches, or walker Weight loss, if obese Analgesic and antiinflammatory drug Magnetic bracelets and acupuncture Intraarticular injection of high-molecular-weight viscosupplements, particularly hyaluronic acid Surgery: Joint replacement

Sequestra:

Sections of dead bone from periosteal separation

Secondary cause osteoporois

Steroids( RANKL & OPG), Cushing's, hyperthyroidism, immobilization, CKD, anticonvulsants; Vitamin D3 deficiency

Treatment for tendinopathy and bursitis

Systemic analgesics, ice or heat applications, or local injection of an anesthetic and a corticosteroid to reduce inflammation

Treatment bone cancer

Systemic chemotherapy and surgery

6. BMPs are part of the

TGF-β superfamily and are involved in multiple crucial functions in the skeletal system.

Dislocation

Temporary displacement of bone from its joint

Clinical manifestations of fracture

Unnatural alignment, swelling, muscle spasm, tenderness, pain, impaired sensation

4. Congenital muscle disorders (myopathies) include

absence of muscles, hypoplasia, hyperplasia, and faulty intrinsic development.

4. Myofibrils and myofilaments contain the major muscle proteins

actin and myosin,

10. Several factors determine how force is transmitted from the

actin-myosin cross-bridges on individual muscle fibers to accomplish whole-muscle contraction.

The fibers firmly anchor the c

artilage to the bone, and the proteoglycans control the loss of fluid from the cartilage.

4. Joints help move

bones and muscle.

. 12. Osgood-Schlatter disease is characterized by inflammation or partial separation of the tibial tubercle caused by

chronic irritation, usually as a result of overuse of the quadriceps muscles. The condition is seen primarily in muscular, athletic adolescent males.

5. Osteogenesis imperfecta (brittle bone disease) is a genetic disorder of

collagen that affects primarily bones and results in fractures of many bones.

Rhabdomyosarcoma is treated with a

combination of surgery, radiation, and chemotherapy.

5. Bones in the body are made up of

compact bone tissue and spongy bone tissue.

"Rider's bone" in

equestrians

Synovial joints are connected by a

fibrous joint capsule.

Compact bone is

highly organized into haversian systems that consist of concentric layers of crystallized matrix surrounding a central canal that contains blood vessels and nerves.

"Drill bone" in

infantry soldiers

7. The two types of muscle contraction are

isometric and isotonic.

5. The healthcare provider is

legally responsible to report suspected nonaccidental trauma.

16. Osteosarcoma, the most common

malignant childhood bone tumor, originates in boneproducing mesenchymal cells and is most often located in the distal end of the femur or proximal end of the tibia.

Large joints are

most commonly affected

The fundamental concept of muscle function is the

motor unit, defined as all muscle fibers innervated by a single motor nerve.

. Electromyography is used to assess the

muscle membrane's capacity to function.

Remodeling restores the

original shape and size to the injured bone.

1. Procedures used to evaluate bone function include analysis

of gait, evaluation of urinary bone resorption markers, measurement of serum calcium and phosphorus levels and serum bone-specific alkaline phosphatase (BAP) level, x-ray films, angiography, bone scanning, and MRI.

Regardless of the cause of trauma, muscle cells can usually

regenerate.

The primary treatments for osteosarcoma are

surgery and chemotherapy

2. Joints are classified as

synarthroses, amphiarthroses, or diarthroses, depending on the degree of movement they allow.

1. The most common congenital defect of the upper extremities is

syndactyly (webbing of the fingers).

2. Whole muscles vary in size

(2 to 60 cm in length) and shape (fusiform and pennate). Each skeletal muscle is encased in a three-part connective tissue framework.

. 2. Ossification takes place in two centers in long bones:

(a) the primary center, or the diaphysis (the long, central portion of the bone); and (b) the secondary center, or the epiphysis (the end portions of the bone).

RANKL -

(receptor activator of nuclear factor kB ligand)

Cytokines

-Bone Remodeling

19. Ewing sarcoma is more common in males and is diagnosed most often between the ages of

5 and 15 years.

4. By 1 year of age

50% of the total growth of the spine has occurred, and most children have achieved 50% of their adult height by 2 years of age.

Rheumatoid arthritis (RA)

: Inflammatory joint disease Systemic autoimmune destruction to synovial membrane and joints Presence of rheumatoid factors (RFs): RA or RF test Antibodies (immunoglobulin G

Clinical manifestations chrondrosarcoma

: Pain and swelling

If suturing is not possible support structure trauma

: Tendon or ligament grafting Prolonged rehabilitation exercises

31. Which statement is false about aging and the musculoskeletal system? a. Haversian system erodes, the canals nearest the marrow cavity widened, and the endosteal cortex converts to spongy bone. b. The remodeling cycle increases because of a decreased ability of the basic multicellular units to resorb and deposit bone. c. Cartilaginous rigidity increases because of decreasing water content and decreasing concentrations of glycosaminoglycans. d. Muscle ribonucleic acid (RNA) synthesis declines, although the regenerative function of muscle tissue is reportedly normal in older adults.

ANS: A Aging does not typically have an effect on the haversian system as described. The remaining options are accurate statements regarding the effects of aging. PTS: 1 REF: Page 1536

23. Which statement is false about muscles? a. Muscle comprises 50% of an adult's body weight and 40% of a child's body weight. b. Muscle is 75% water, 20% protein, and 5% organic and inorganic compounds. c. Muscle contains 32% of all protein stores for energy and metabolism. d. Muscles are encased in fascia.

ANS: A Muscle constitutes 40% of an adult's body weight and 50% of a child's body weight. The other options are true statements regarding muscles. PTS: 1 REF: Pages 1526-1527

29. In which type of contraction does the muscle maintain a constant tension as it moves? a. Isotonic c. Hypertonic b. Isometric d. Hypotonic

ANS: A Only during an isotonic contraction does the muscle maintain a constant tension as it moves. PTS: 1 REF: Page 1535

20. Which statement does not present accurate information concerning synovial fluid? a. Synovial fluid contains protein polysaccharides to repair the synovial membrane after injury. b. It lubricates the joint surfaces. c. Synovial fluid nourishes the pad of the articular cartilage. d. It contains leukocytes to phagocytize joint debris and microorganisms.

ANS: A Synovial fluid lubricates the joint surfaces, nourishes the pad of the articular cartilage that covers the ends of the bones, and contains free-floating synovial cells and various leukocytes that phagocytose joint debris and microorganisms. The other options provide accurate information about synovial fluid. PTS: 1 REF: Page 1522

6. Which glucoprotein is believed to inhibit calcium phosphate precipitation and play a part in bone resorption by recruiting osteoclasts? a. Osteocalcin c. Laminin b. Osteonectin d. Osteopontin

ANS: A The roles of osteocalcin may be to inhibit calcium phosphate precipitation and play a part in bone resorption by recruiting osteoclasts. This statement is not true of any other option. PTS: 1 REF: Page 1516

34. In adults, hematopoiesis takes place in which bone marrow cavities? (Select all that apply.) a. Skull b. Shoulders c. Sternum d. Long bones e. Pelvis

ANS: A, B, C, E The marrow cavities within certain bones serve as sites of blood cell formation. In adults, blood cells exclusively originate in the marrow cavities of only the skull, vertebrae, ribs, sternum, shoulders, and pelvis. PTS: 1 REF: Page 1510

35. Which statements are true regarding osteocytes? (Select all that apply.) a. An osteocyte is a transformed osteoblast. b. An osteocyte obtains nutrients from capillaries in the canaliculi. c. The functioning of an osteocyte is well understood. d. Osteocytes signal osteoclasts and osteoblasts to form new bone. e. An osteocyte helps maintain levels of calcium and phosphorus in blood plasma.

ANS: A, B, D, E An osteocyte is a transformed osteoblast. Osteocytes communicate with each other and help concentrate nutrients in the matrix. They obtain nutrients from capillaries in the canaliculi, which contain nutrient-rich fluids and also help synthesize and replace needed elements of the matrix by signaling osteoclasts and osteoblasts to resorb and form new bone. Through exchanges among these cells, hormone catalysts, minerals, and optimal levels of calcium, phosphorus, and other minerals are maintained in blood plasma. PTS: 1 REF: Pages 1514-1515

36. Which minerals are stored in bones? (Select all that apply.) a. Carbonate b. Phosphate c. Selenium d. Magnesium e. Calcium

ANS: A, B, D, E Bones have a crucial role in mineral homeostasis and in storing and releasing minerals (e.g., calcium, phosphate, carbonate, magnesium) that are essential for the proper working of many delicate cellular mechanisms. Selenium is not stored in the bones. PTS: 1 REF: Page 1510

37. Which factors influence the rate of protein synthesis of skeletal muscles? (Select all that apply.) a. Insulin b. Cortisol c. Parathyroid hormone d. Growth hormone e. Amino acid substrates

ANS: A, E The rate of protein synthesis is related to insulin levels amino acid substrates and to overall nutritional status. PTS: 1 REF: Page 1533

10. Which part of an injured joint becomes insensitive to pain and regenerates slowly and minimally? a. Synovium c. Bursa b. Articular cartilage d. Tendon

ANS: B Articular cartilage has no blood vessels, lymph vessels, or nerves. Therefore it is insensitive to pain and regenerates slowly and minimally after injury. These statements are not true of the other options. PTS: 1 REF: Page 1525

21. What anchors articular cartilage to the underlying bone? a. Sharpey fibers c. Glycoproteins b. Collagen fibers d. Elastin fibers

ANS: B Collagen fibers are important components of the cartilage matrix because they anchor the cartilage securely to underlying bone. This statement is not true of the other options. PTS: 1 REF: Pages 1524-1525

3. Which term is used to identify the temporary displacement of two bones causing the bone surfaces to partially lose contact? a. Dislocation c. Malunion b. Subluxation d. Nonunion

ANS: B Dislocation is the temporary displacement of a bone from its normal position in a joint. If the contact between the two surfaces is only partially lost, then the injury is referred to as a subluxation. This selection is the only option that

14. The stage of healing in the bone that involves procallus formation entails which process? a. Formation of a hematoma that allows the development of a fibrin network b. Production of granulation tissue by fibroblasts, capillary buds, and osteoblasts c. Development of a primitive bone matrix termed woven bone d. Remodeling of the periosteal and endosteal bone surfaces

ANS: B Fibroblasts, capillary buds, and osteoblasts move into the wound to produce granulation tissue called a procallus. None of the other options are associated with this process. PTS: 1 REF: Page 1520

30. Which term is used to identify a functional muscle contraction in which the muscle contracts but the limb does not move? a. Isotonic c. Eccentric b. Isometric d. Concentric

ANS: B Only during an isometric contraction (static or holding contraction) does the muscle maintain a constant length as tension is increased. Isometric contraction occurs, for example, when the arm or leg is pushed against an immovable object. The muscle contracts, but the limb does not move. PTS: 1 REF: Page 1535

4. Which bone cells are large and multinucleated and contain lysosomes filled with hydrolytic enzymes? a. Osteoblasts c. Osteocytes b. Osteoclasts d. Fibrocytes

ANS: B Osteoclasts are the major resorptive cells of bone. They are large multinucleated cells with a short life span and contain lysosomes (digestive vacuoles) filled with hydrolytic enzymes. This selection is the only option that is described in this manner. PTS: 1 REF: Page 1515

3. Which cells function to maintain bone matrix? a. Osteoclasts c. Osteoblasts b. Osteocytes d. Osteophytes

ANS: B Osteocytes help synthesize and replace needed elements of the matrix by signaling osteoclasts and osteoblasts to resorb and form new bone. This selection is the only option that performs that function. PTS: 1 REF: Pages 1514-1515

19. What is the function of the synovial membrane's type A cells within the intima? a. To release mast cells, initiating the inflammatory process after joint injury b. To ingest and remove bacteria and debris by phagocytosis in the joint cavity c. To secrete hyaluronate, a binding agent that gives synovial fluid its viscous quality d. To store fat cells and glycogen, providing adenosine triphosphate for joint activity

ANS: B The intima contains two types of synovial cells: A and B. Type A synovial cells ingest and remove bacteria and particles of debris by phagocytosis in the joint cavity. None of the remaining options accurately describes the function of the synovial membrane's type A cells. PTS: 1 REF: Page 1522

18. The joint that contains a synovial membrane that lines the inner joint capsule is an example of which type of joint? a. Amphiarthrosis c. Synarthrosis b. Diarthrosis d. Biarthrosis

ANS: B The joint that contains a synovial membrane that lines the inner joint capsule is a diarthrosis. A synovial joint consists of the following parts: (1) fibrous joint capsule (articular capsule), (2) synovial membrane that lines the inner surface of the joint capsule, (3) joint cavity (synovial cavity or space formed by the capsule), (4) synovial fluid, which fills the joint cavity and lubricates the joint surface, and (5) articular cartilage, which covers and pads the articulating bony surfaces. PTS: 1 REF: Page 1522

8. How is the work function of a muscle usually calculated? a. Muscle type c. Foot pounds b. Calculating force distance d. Kilograms

ANS: B The ultimate function of muscle is to accomplish work. Although expressed in such measures as foot-pounds or kilogram-meters, work refers to the amount of energy liberated or the amount of force exerted over a distance (work force distance). Muscle type is not relevant. PTS: 1 REF: Page 1533

24. Which characteristic is true of type II (white fast-motor) muscle fibers? a. Slow contraction speed c. Profuse capillary supply b. Fast conduction velocities d. Oxidative metabolism

ANS: B Type II fibers, also called white fast-motor fibers, are innervated by relatively large type II alpha motor neurons with fast conduction velocities. This selection is the only correct option provided. PTS: 1 REF: Page 1529

13. After puberty, the epiphyseal plate calcifies, and the epiphysis merges with the __________. a. Epiphyseal line c. Metaphysis b. Epiphyseal plate d. Articular cartilage

ANS: C After puberty, the epiphyseal plate calcifies and the epiphysis merges only with the metaphysis. PTS: 1 REF: Page 1518

12. What is the function of Sharpey fibers? a. To anchor the outer layer of the periosteum to the inner layer b. To contain blood vessels and nerves on the outer layer of the periosteum c. To help attach tendons and ligaments to the periosteum d. To attach muscles to the periosteum

ANS: C Collagenous fibers (Sharpey fibers) that penetrate the bone anchor the inner layer of the periosteum to the bone. Sharpey fibers help hold or attach tendons and ligaments, not muscle, but to the periosteum of bones. PTS: 1 REF: Page 1517

28. Which type of ion directly controls the contraction of muscles? a. Sodium c. Calcium b. Potassium d. Magnesium

ANS: C Contraction begins as the calcium ions combine with troponin, a reaction that overcomes the inhibitory function of the troponin-tropomyosin system. This selection is the only option that has such a direct association with muscle contraction. PTS: 1 REF: Page 1533

26. Which statement describes a neuroregulin? a. Chemical mediator that initiates signals from the anterior horn cell of the spinal card to the axon of motor nerve branches of groups of muscle fibers b. Neurotransmitter that provides a means of reporting changes in length, tension, velocity, and tone in muscles c. Proteoglycan secreted by neurons, which increases acetylcholine receptors d. Mechanoreceptor that lies parallel to muscle fibers and responds to muscle stretching

ANS: C Motor and sensory neurons secrete a proteoglycan called neuroregulin that increases acetylcholine receptors and helps in the formation of muscle spindle fibers. This selection is the only option that accurately describes a neuroregulin. PTS: 1 REF: Pages 1528-1529

5. Which bone cell secretes hydrochloric acid to help dissolve bone minerals and collagenase, thus aiding in the digestion of collagen? a. Osteocytes c. Osteoclasts b. Osteoblasts d. Osteophytes

ANS: C Only osteoclasts bind to the bone surface of cell attachment proteins called integrins. They bring about resorption of bone by secreting hydrochloric acid and cathepsin K (a protease enzyme) that help dissolve bone minerals and collagenase, which aids in digesting collagen, along with the action of cytokines. PTS: 1 REF: Page 1515

22. What controls the movement of synovial fluid through cartilage? a. Cartiloregulins c. Proteoglycans b. Hyaluronate d. Chondroitin

ANS: C Only proteoglycans give articular cartilage its stiff quality and regulate the movement of synovial fluid through the cartilage. PTS: 1 REF: Page 1525

32. Which component is found in synovial fluid? a. Protein polysaccharides c. Leukocytes b. Water d. Chondrocytes

ANS: C Synovial fluid lubricates the joint surfaces, nourishes the pad of the articular cartilage that covers the ends of the bones, and contains only free-floating synovial cells and various leukocytes that phagocytose joint debris and microorganisms. None of the remaining options are found in synovial fluid. PTS: 1 REF: Page 1522

2. What happens to the original bone during the second phase of bone remodeling? a. The original bone is replaced. c. The original bone is resorbed. b. It hardens. d. It is synthesized.

ANS: C The distribution of these apoptotic osteocytes provides osteoclasts with information about where to begin resorbing damaged bone. In the second phase of remodeling (resorption), the osteoclasts form a cutting cone that gradually resorbs bone, leaving behind an elongated cavity termed a resorption cavity. This selection is the only option that accurately describes what happens when bone is resorbed. PTS: 1 REF: Pages 1519-1520

15. Which term describes a freely movable joint? a. Synarthrosis c. Biarthrosis b. Amphiarthrosis d. Diarthrosis

ANS: D Based on movement, a joint is classified as a synarthrosis (immovable joint), an amphiarthrosis (slightly movable joint), or a diarthrosis (freely movable joint). Biarthrosis is not a term used to describe a freely movable joint. PTS: 1 REF: Page 1520

27. Which four-step process correctly describes muscle contraction? a. Coupling, contraction, relaxation, excitation b. Contraction, relaxation, excitation, coupling c. Relaxation, excitation, coupling, contraction d. Excitation, coupling, contraction, relaxation

ANS: D Muscle contraction is a four-step process: excitation, coupling, contraction, and relaxation. PTS: 1 REF: Page 1533

OPG - (osteoprotegerin) Decoy receptor for RANKL Prevents RANKL from triggering bone resorption Bone remodeling Osteoblasts and osteoclasts in bone remodeling ( iliac crest) Bone balance and remodeling Musculoskeletal Injuries Trauma Is the leading cause of death of people, ages 1 to 44 years, of all races and at all socioeconomic levels. Fracture Is a break in the continuity of a bone. Occurs when force is applied that exceeds the tensile or compressive strength of the bone. Musculoskeletal Injuries (cont'd) Fracture classifications Complete: Bone is broken all the way through. Incomplete: Bone is damaged but still in one piece. Closed or simple (complete or incomplete): Skin is intact. Open or compound (complete or incomplete): Skin is broken. Comminuted Bone breaks into more than two fragments. Linear Fracture runs parallel to the long axis of the bone. Oblique Fracture of the shaft of the bone is slanted. Musculoskeletal Injuries (cont'd) Fracture classifications (cont'd) Spiral Encircles the bone. Transverse Occurs straight across the bone. Greenstick Perforates one cortex and splinters the spongy bone. Torus Cortex buckles but does not break. Bowing Longitudinal force is applied to a bone. Pathologic Break occurs at the site of a preexisting abnormality. Stress Fatigue and insufficiency Transchondral Fractures Bone Fractures 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. Pathophysiology Inflammatory response Hematoma formation (1-3 days) Reparative phase Fibrocartilage formation (3 days - 2 weeks): pro-callus layer: collagen Callus formation (2-6 weeks) Ossification Remodeling continues until repair complete (6 weeks - 1 year: may be considered delayed union if this long) Bone Fractures Fracture healing Bone Fractures Callus formation Bone Fractures (cont'd) Clinical manifestations Unnatural alignment, swelling, muscle spasm, tenderness, pain, impaired sensation Treatment Closed manipulation, traction (skeletal or skin), open reduction, internal fixation, external fixation Splints and casts Bone Fractures (cont'd) External fixation Bone Fractures Improper reduction or immobilization Nonunion 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. Delayed union Does not occur until approximately 8 to 9 months after a fracture. Malunion Is healing of the bone in a nonanatomic position. Improper reduction or immobilization Bone Fractures Treatment: Designed to stimulate new bone formation Implantable or external electric current devices, electromagnetic field generations, and low-density ultrasound Stem cell and gene therapy Bone graft or synthetic materials (calcium phosphate cement): To fill large defects Dislocation and Subluxation Dislocation Temporary displacement of bone from its joint Subluxation Contact between the bones in the joint only partially lost Associated with fractures, muscle imbalance, rheumatoid arthritis, other joint instability Clinical manifestations Pain, swelling, limitation of motion, joint deformity Treatment Reduction and immobilization for 2 to 6 weeks Exercises Support Structure Trauma Support Structure Trauma (cont'd) Pathophysiology Inflammatory exudate develops between the torn ends. Granulation tissue grows inward, and then collagen formation begins 3 to 4 days after injury. Vascular fibrous tissue fuses the new and surrounding tissues into a single mass. Healing tendon or ligament lacks sufficient strength to withstand a strong pull for 4 to 5 weeks after the injury. Support Structure Trauma (cont'd) Clinical manifestations Is painful and usually accompanied by soft-tissue swelling and changes in tendon or ligament contour. Treatment Splinting, early motion, and rehabilitation Suturing: To treat a complete rupture If suturing is not possible: Tendon or ligament grafting Prolonged rehabilitation exercises Fat embolism Tendinopathy and Bursitis Tendinitis Inflammation of a tendon Tendinosis Painful degradation of collagen fibers Bursitis Inflammation of a bursa Are sacs lined with synovial membrane and filled with synovial fluid; sacs (bursa) are located among the tendons, muscles, and bony prominences. Is caused by repeated trauma. Septic bursitis: Is caused by a wound infection. Tendinopathy and Bursitis (cont'd) Epicondylitis Is inflammation of a tendon where it attaches to a bone. Tennis elbow: Lateral epicondylitis Golfer's elbow: Medial epicondylitis Treatment for tendinopathy and bursitis Systemic analgesics, ice or heat applications, or local injection of an anesthetic and a corticosteroid to reduce inflammation Bursitis: Aspiration to drain excess fluid Physical therapy Muscle Strain Is a sudden, forced motion, causing the muscle to become stretched beyond its normal capacity. Causes local muscle damage. Can also involve the tendons. Regardless of the cause of trauma, muscle cells can usually regenerate. May take up to 6 weeks. Myositis Ossificans Also called heterotopic ossification Complication of local muscle injury Inflammation of muscular tissue with subsequent calcification and ossification of the muscle "Rider's bone" in equestrians "Drill bone" in infantry soldiers Thigh muscles in football players Rhabdomyolysis Life-threatening complication of severe muscle trauma with muscle cell loss Crush syndrome versus crush injuries Compartment syndromes Rapid breakdown of muscle that causes the release of intracellular contents Protein pigment myoglobin into extracellular space and bloodstream Rhabdomyolysis (cont'd) Classic triad Muscle pain, weakness, and dark urine (from myoglobin) Treatment Rapid intravenous hydration: To maintain adequate kidney flow Hyperkalemia: May require temporary hemodialysis Rhabdomyolysis (cont'd) Question 1 A person has rhabdomyolysis. Which typical clinical manifestation will the nurse find upon assessment? Dark urine Scar-tissue calcification "Tennis elbow" "Rider's bone" Compartment Syndrome Complication of fractures Blood flow to affected area is compromised because of increased venous pressure, leading to decreased arterial inflow, ischemia, and edema. Clinical manifestations Pain: Out of proportion to the injury Paresthesia, pallor, pulselessness, and paralysis (late sign) Compartment Syndrome (cont'd) Evaluation Rising compartment pressure can be directly measured by inserting a wick catheter, needle, or slit catheter into the muscle. Treatment Immediate fasciotomy and débridement Emergency treatment may be required to save an affected limb. Musculoskeletal Disorders Part 2, Metabolic bone Disease & Tumors Dr. Hunter Osteoporosis Porous bone 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/cm2 Osteoporosis (cont'd) Osteoporosis (cont'd) Potential causes 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 Osteoporosis OPG/RANKL/RANK system Osteoporosis (cont'd) Reduced bone mass or density and an imbalance of bone resorption and formation Bone histologic anatomy: Usually normal but lacks structural integrity Evaluation Dual x-ray absorptiometry (DXA) Osteoporosis (cont'd) Normal bone versus osteoporotic bone Epidemiology of Osteoporosis 44 million Americans 80% women; are males at risk? Primary Postmenopausal ( estrogen, RANKL, T & B cells Decreased testosterone Secondary Steroids( RANKL & OPG), Cushing's, hyperthyroidism, immobilization, CKD, anticonvulsants; Vitamin D3 deficiency Osteoporosis (cont'd) Types of osteoporosis Perimenopausal Iatrogenic Regional Postmenopausal Glucocorticoid-induced Age-related bone loss Clinical manifestations Pain, bone deformity, fractures, kyphosis (hunchback), and diminished height Osteoporosis (cont'd) Prevention Regular moderate weight-bearing exercises Calcium intake sufficient to maintain normal calcium balance during adolescence Sufficient intake of magnesium Treatment Estrogen Bisphosphonates, denosumab, teriparatide, parathyroid hormone (PTH) 1-84 Osteomalacia Deficiency of vitamin D lowers the absorption of calcium from the intestines. Mineralization is inadequate or delayed. Bone formation progresses to osteoid formation, but calcification does not occur; result is soft bones. Clinical manifestations: Pain, bone fractures, vertebral collapse, bone malformation, waddling gait Osteomalacia (cont'd) Treatment Adjust serum calcium and phosphorus levels to normal. Suppress secondary hyperthyroidism. Chelate bone aluminum, if needed. Administer calcium carbonate to decrease hyperphosphatemia. Administer dietary supplements of vitamin D. Use renal dialysis. Renal transplantation for renal osteodystrophy. Paget Disease Also called osteitis deformans State of increased metabolic activity in bone Is abnormal, and bone resorption and formation are excessive. Enlarges and softens the affected bones. Most often affects the axial skeleton. Clinical manifestations Brain compression, impaired motor function, deafness, atrophy of the optic nerve Treatment Bisphosphonates and calcitonin Osteomyelitis 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 Osteomyelitis (cont'd) Sequestration and involucrum Osteomyelitis (cont'd) Clinical manifestations Acute and chronic inflammation, fever, pain, necrotic bone Treatment Antibiotics, débridement, surgery, hyperbaric oxygen therapy Osteomyelitis (cont'd) Question 2 Which information is correct regarding the pathophysiologic process of osteomyelitis? Osteomyelitis produces: Bone density less than 648 mg/cm2 Stimulation of osteoclasts Formation of fistula Sequestrum Bone Tumors May originate from bone cells, cartilage, fibrous tissue, marrow, or vascular tissue Osteogenic, chondrogenic, collagenic, and myelogenic Malignant bone tumors Increased nuclear-cytoplasmic ratio, irregular borders, excess chromatin, prominent nucleolus, increase in the mitotic rate Bone Tumors Derivation of bone tumors Bone Tumors (cont'd) Patterns of bone destruction Geographic Well-defined margins of lytic bone with normal bone Moth-eaten Areas of partially destroyed bone adjacent to completely lytic areas Permeative Abnormal lytic bone imperceptibly merges with surrounding normal bone Bone Tumors (cont'd) Osteosarcoma 38% of bone tumors Predominant in adolescents and young adults; occurs in seniors with a history of radiation therapy Contain masses of osteoids: Bone-forming tumors Streamers: Noncalcified bone matrix and callus Location: In the metaphyses of the long bones 50% occur around the knees Clinical manifestations Pain and swelling Treatment Systemic chemotherapy and surgery Osteosarcoma Chondrosarcoma Produces cartilage or chondroid. Is a tumor of middle-aged and older adults. Infiltrates trabeculae in spongy bone; is frequently in the metaphyses or diaphysis of long bones. Contains lobules of hyaline cartilage that expand and enlarge the bone with no ossification. Causes erosion of the cortex and can expand into the neighboring soft tissues. Clinical manifestations: Pain and swelling Treatment: Wide surgical excision Chondrosarcoma Fibrosarcoma Are firm, fibrous masses of collagen, malignant fibroblasts, and osteoclast-like cells. Usually affects the metaphyses of the femur or tibia. Metastasis to the lungs is common. Clinical manifestations: Pain, swelling, local tenderness, palpable mass, and limitation of motion; pathologic fracture Treatment: Radical surgery and amputation Giant cell tumor Causes extensive bone resorption as a result of the osteoclastic origin. Is located in the epiphyses of femur, tibia, radius, or humerus. Has slow and relentless growth rate; metastasis is rare. Clinical manifestations: Pain, local swelling, and limitation of movement. Treatment: Cryosurgery and resection with adjuvant polymethylmethacrylate (PMMA) for bone grafts. Giant cell tumor Musculoskeletal Disorders Part 3 Joint Disease Dr. Hunter Inflammatory versus Noninflammatory Joint Disease Noninflammatory joint disease is differentiated by Absence of synovial membrane inflammation Lack of systemic signs and symptoms Normal synovial fluid Arthropathies: Diseases of the joints Osteoarthritis Common age-related disorder of synovial joints Non-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 Osteoarthritis Local areas of damage and loss of articular cartilage, new bone formation of joint margins, and thickening of joint capsule Clinical manifestations Pain, stiffness, enlargement of the joint, tenderness, limited motion, and deformity Joint swelling in the fingers: Heberden and Bouchard nodes Joint effusion: Exudate or blood entering the joint Degenerative joint disease Osteoarthritis Treatment Rest of involved joint until inflammation subsides Aerobic exercise and range-of-motion exercise Cane, crutches, or walker Weight loss, if obese Analgesic and antiinflammatory drug Magnetic bracelets and acupuncture Intraarticular injection of high-molecular-weight viscosupplements, particularly hyaluronic acid Surgery: Joint replacement Osteoarthritis Examples Osteoarthritis (cont'd) Question 3 The primary defect in osteoarthritis is: Enlargement and softening of bones Development of pannus Loss of articular cartilage Permeative pattern of bone destruction Classic Inflammatory Joint Disease 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 Rheumatoid Arthritis Rheumatoid arthritis (RA): Inflammatory joint disease Systemic autoimmune destruction to synovial membrane and joints Presence of rheumatoid factors (RFs): RA or RF test Antibodies (immunoglobulin G 48 IgG and IgM) against antibodies Joint fluid with inflammatory exudate Rheumatoid Arthritis Pathophysiology Rheumatoid Arthritis Joint pathophysiology Rheumatoid Arthritis Clinical manifestations Symmetric joint swelling, joint deformities Rheumatoid nodules in organs Caplan syndrome Autoantibodies RF Significantly more specific serum marker, anticitrullinated protein antibody (ACPA) Present for years to decades before synovial or radiographic changes become apparent Rheumatoid Arthritis Evaluation (four or more of the following) Morning joint stiffness lasting at least 1 hour Arthritis of three or more joint areas Arthritis of the hand joints Symmetric arthritis Rheumatoid nodules Abnormal amounts of serum RF Anti-CCP (cyclic citrullinated peptide) Radiographic changes Rheumatoid Arthritis Treatment Education Nonsteroidal antiinflammatory drugs (NSAIDs), glucocorticoids, intraarticular steroid injections Disease modification agents: methotrexate Physical and occupational therapy with therapeutic exercise and use of assistive devices Surgery: Synovectomy or joint replacement Rheumatoid Arthritis Treatment Disease-modifying antirheumatic drugs (DMARDs) such as methotrexate (MTX, first line), azathioprine, sulfasalazine, hydroxychloroquine, leflunomide, and cyclosporine Biological DMARDs (bDMARDs): Medications affect specific processes in the development of RA: Tumor necrosis factor inhibitors anti-TNF - use only after other fail to control- very expensive and dangerous Monoclonal antibodies Ankylosing Spondylitis Chronic inflammatory joint disease of the spine or sacroiliac joints, causing stiffening and fusion of the joints Uncontrolled bone formation Enthesis: Primary proposed site Where ligaments, tendons, and joint capsule are inserted into bone Unknown cause but strong association with human leukocyte antigen B27 (HLA-B27) Ankylosing Spondylitis Begins with inflammation of the fibrocartilage, particularly in the vertebrae and sacroiliac joint. Inflammatory cells infiltrate and erode the fibrocartilage. As repair begins, scar tissue ossifies and calcifies; the joint eventually fuses. Clinical manifestations Low back pain, stiffness, pain, and restricted motion, "bamboo" spine Loss of normal lumbar curvature Ankylosing Spondylitis Typical posture Ankylosing Spondylitis Treatment Physical therapy: Maintenance of skeletal mobility and prevention of natural progression of contractures Support groups NSAIDs, analgesic medications Corticosteroid injections to locally inflamed joints Gout 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 of uric acid crystals Gout Uric acid synthesis and elimination Gout 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 Gout 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. Gout Acute gouty arthritis Gout Clinical manifestations Pain in the great toe (usually, but not always): Worse at night Increase in serum urate concentration: Hyperuricemia Recurrent attacks of monoarticular arthritis: Inflammation of a single joint Deposits of monosodium urate monohydrate (tophi) in and around the joints Renal disease, involving glomerular, tubular, and interstitial tissues and blood vessels Formation of renal stones Gout Treatment NSAIDs and xanthine oxidase inhibitors: Allopurinol and febuxostat Acute attacks: Colchicine and NSAIDs Hydrocortisone: May be injected into the joint Ice: For inflammation of the joint Avoidance of weight-bearing movements on involved joint until acute attack subsides Weight reduction Avoidance of alcohol Consumption of low-fat dairy products, cherries, soybeans, and vegetable sources of protein Gout (cont'd) Question 4 A person has gout. Which typical clinical manifestation will the nurse find upon assessment? Crepitus Polyarticular arthritis Tophi Decreased uric acid Musculoskeletal Disorders Part 4 Muscle Disorders Dr. Hunter Disorders of Skeletal Muscle Physiologic Contracture Muscle fiber shortening without an action potential Cause: Failure of the sarcoplasmic reticulum (calcium pump) even with available ATP Usually temporary Pathologic Contracture Muscle shortening caused by muscle spasm or weakness Plentiful ATP and occurs despite a normal action potential Permanent Disorders of Skeletal Muscle (cont'd) Stress-induced muscle tension Abnormally increased muscle tension Clinical manifestations Neck stiffness, back pain, and headache Association with chronic anxiety Treatment Progressive relaxation training, yoga, meditation, and biofeedback Fibromyalgia Chronic widespread joint and muscle pain, fatigue, and tender points Central nervous system (CNS) dysfunction Amplified pain transmission and interpretation: Central sensitization Vague symptoms Increased sensitivity to touch, absence of inflammation, fatigue, sleep disturbances Possible factors Flu-like viral illness, chronic fatigue syndrome, human immunodeficiency viral (HIV) infection, Lyme disease, medications, physical or emotional trauma Potential Triggers Significant emotional distress Sleep disturbance or disorder Difficult life situation or life trauma Limited coping skills Treatment: Exercise & Cognitive Behavioral Therapy Fibromyalgia Clinical manifestations Diffuse, chronic pain Nine pairs (18) of tender points Must have tenderness in 11 of these tender points Treatment Medications that improve sleep and vitamin D supplementation: May be helpful Pregabalin Combination of modalities, including education, medication, exercise, and cognitive-behavioral therapy Fibromyalgia Tender points Chronic Fatigue Syndrome Also known as myalgic encephalomyelitis Debilitating and complex disorder Profound fatigue, neurologic energy production, and immune impairments Possible causes CNS dysregulation, cardiovascular and immune system abnormalities, chronic proinflammatory cytokines, dysfunction of cellular energy metabolism, dysfunction of ion transport Chronic Fatigue Syndrome (cont'd) Clinical manifestations Unrestful sleep Debilitating fatigue made worse by physical or mental exercise (postexertional fatigue), muscle pain, noninflammatory joint pain, headaches, flu-like symptoms, and memory or concentration problems Treatment Consideration of psychosocial factors, and symptomatic and supportive care Acupuncture, massage, and therapeutic touch Disuse Atrophy Normal size of muscle cells are reduced as a result of prolonged inactivity. Bed rest, trauma, casting, or nerve damage Oxidative stress causes decreased protein synthesis and increased proteolysis. Prevention and treatment Isometric movements and passive lengthening exercises Muscle Membrane Abnormalities Myotonia Delayed muscle relaxation after voluntary contractions Cause: Lack of chloride Treatment: Medication to reduce muscle fiber excitability Muscle Membrane Abnormalities Periodic paralysis Autosomal dominant inherited mutations of the skeletal muscle channels; muscle cannot contract Hypokalemic periodic paralysis Alterations in potassium ion channels regulated by T3 Treatment: Potassium-sparing diuretics; high-salt diet Long-term treatment: Acetazolamide, dichlorphenamide, and a low-salt diet Hyperkalemic periodic paralysis Genetic mutation of sodium channels Treatment: Small carbohydrate-rich meals, light exercise, and intravenous calcium gluconate Endocrine Disorders Endocrine disorders affect musculoskeletal system Thyrotoxicosis: Proximal weakness, paresis of the extraocular muscles (exophthalmic ophthalmoplegia) Hypothyroidism: Decrease in muscle mass and strength, with weak, flabby skeletal muscles and sluggish movements Familial hypomagnesemia: Autosomal recessive disease, affecting the renal system and causing hypomagnesemia and secondary hypocalcemia Tetany and convulsions Diseases of Energy Metabolism Muscle needs carbohydrates (glycogen) and lipids (free fatty acids) for energy Stored glycogen or lipids cannot be used because of a lack of an enzyme Cramps, fatigue, and exercise intolerance result. Examples McArdle disease: Myophosphorylase deficiency Acid maltase deficiency or Pompe disease: Glycogen Myoadenylate deaminase deficiency Lipid deficiencies Inflammatory Muscle Diseases: Myositis Viral, bacterial, and parasitic myositis Tuberculosis and sarcoidosis: Granulomas found in muscle Trichinellosis: Muscle stiffness Treatment: Corticosteroids and antiparasitic agents Viral infections: Acute myositis Muscle pain, tenderness, signs of inflammation, and creatine kinase (CK) elevation Polymyositis, Dermatomyositis, and Inclusion Body Myositis Autoimmune diseases target skeletal muscle. Is characterized by symmetric proximal muscle (pelvic and shoulder girdle) weakness and myalgia that develops over weeks to months. Polymyositis and dermatomyositis Inflammation of connective tissue and muscle fibers Polymyositis: Generalized muscle inflammation; mediated by T cells Dermatomyositis: Polymyositis, accompanied with skin rash; humorally mediated Polymyositis, Dermatomyositis, and Inclusion Body Myositis Inclusion body myositis Degenerative changes of muscle Accumulation of multiple proteins within muscle fibers Evidence of endoplasmic reticular stress with misfolding of proteins Weakness of the wrist and finger flexors, as well as asymmetric atrophy and quadriceps weakness Polymyositis, Dermatomyositis, and Inclusion Body Myositis Treatment Immunosuppressive drugs Corticosteroids initially High-dose intravenous immunoglobulin Azathioprine and methotrexate Creatine supplements Physical therapy Polymyositis, Dermatomyositis, and Inclusion Body Myositis Pathophysiology Polymyositis, Dermatomyositis, and Inclusion Body Myositis Question 5 Which information is correct regarding polymyositis? Is mediated humorally. Is mediated by T cells. Involves cutaneous manifestations. Involves muscle degeneration Myopathy Is the term applied to a primary muscle disorder. Affects muscle strength, tone, and bulk. Is associated with weakness—usually significant weakness and atrophy. Injections of drugs can affect muscle fibers Local trauma to the muscle fibers from direct effects of the needle Toxic Myopathy Alcohol abuse: Most common cause Benign cramps and pain, resolving in a matter of hours to severe weakness Significantly increased CK, associated with myoglobinuria and renal failure Necrosis of individual muscle fibers Disturbance of energy cell turnover, gene dysregulation, and initiation of apoptosis Treatment Abstinence of alcohol Improved nutrition Muscle Tumors Rhabdomyoma Rare benign tumor of striated muscle Rhabdomyosarcoma Malignant tumor of striated muscle Highly malignant with rapid metastasis Types Pleomorphic: Spindle cell- older Embryonal: Tadpole or tennis racquet- young children Alveolar: Lattice-like Treatment Surgical excision, radiation therapy, and systemic chemotherapy Musculoskeletal System in Neonates & Children Lori Rubarth, PhD, APRN, NNP-BC Creighton University NNP Program Embryology The skeletal system & muscular system develop from mesoderm and neural crest cells. Cells lateral to the notochord & neural tube thickens to form 2 columns of paraxial mesoderm 3rd Week of Fetal Life - 2 columns become segmented into blocks = somites Embryology Each somite differentiates into 2 parts; Sclerotome vertebrae & ribs Dermomyotome MYOTOME myoblasts muscle DERMATOME dermis skin Embryology Cellular differentiation of skeletal muscles Somitomeres Somites Sclerotomes Somitomeres Hensen's node and primitive streak regress caudally, they leave the notochord and the induced neural plate Lateral to the neural plate, paraxial mesoderm present as closely packed mesenchymal cells, from within this packing are somitomeres New pairs of somitomeres are formed along Hensen's node as it regresses Somitomeres (cont) Once 20 pairs of somitomeres are formed, masses of paraxial mesoderm or somites are formed. They begin at about the 7th pair of somitomeres Somites are more brick shaped, day 20 of conception Somites Formed through the transformation of cells, with a mesenchymal morphology, to a sphere of epithelial cells within the paraxial mesoderm The first 7 pairs of somitomeres remain as such, lacking the same characteristics of the somites. The 8th pair of somitomeres are "sacrificed" to become the 1st pair of somites Somites (cont) Approximately every few hours, another pair of somitomeres, caudal to the last, becomes transformed into another somite pair. And a new somitomere pair is positioned at the caudal end of the paraxial mesoderm near Henson's node Once Hensen's node has regressed completely, no more somitomeres are formed Somites (cont) Somites continue formation until the last of the somitomeres are obliterated Somites appear bilaterally as pairs at the same time and form earliest at the cranial end (rostral, brain) of the neural groove and add sequentially at the caudal end. Sclerotomes Formed as a result of the notochord and ventral wall of the neural tube serve as an inductive stimulus on the somite on the ventral medial wall (sclerotome) The result of the inductive influence is a burst of mitosis, loss of cellular adhesion, and transformation of epithelial cells in that region to a mesenchymal morphology: "secondary mesenchyme" Sclerotomes (cont) These cells migrate or are displaced medially from the somite and produce chondroitin sulfate proteoglycans and other cells of a cartilage matrix Sclerotomes These cells will then give rise to the vertebrae and ribs The remainder of the epithelial somite is the dermomyotome (muscles & skin) The dorsomedial border form the myotome which gives rise to the musculature of the body The remainder of the somite is the dermatome, which gives rise to the dermis of the skin Bone Formation Bone formation begins in two phases at about the 8th week of gestation Delivery of bone cell precursors to sites of bone formation Aggregation of the bone cell precursors at primary centers of ossification Where they mature & begin to secrete osteoid Bone Formation Intramembranous formation On or within the mesenchyme Endochondral formation - dev from cartilage Cartilage anlage by 6 weeks gestation Perichondrium = dense connective tissue Cells develop into osteoblasts Periosteal collar formed around cartilage model Secondary centers of ossification Limb Development Day 33 - hand, forearm, arm & shoulder Day 37 - carpal region & digital plate; thigh, leg and foot distinct Day 38 - Finger rays (digital rays) visible Apoptotic cell death between digits Day 44 - Toe rays visible Day 47 - ventral flexion of upper arm Day 52 - upper limbs bent at elbow & feet approaching midline Day 56 - all legs & arms are well-defined Terminology Osteoblast = cells derived from mesenchymal stem cells produce type I collagen responsive to parathyroid hormone produce osteocalcin when stimulated by 1,25 Di-OH vitamin D Active on outer surface of bones Form a single layer of cells Bring about formation of new bone by synthesis of osteoid (non-mineralized bone matrix) Terminology Osteocyte = a transformed osteoblast that is trapped or surrounded in osteoid as it hardens from minerals that enter during calcification (within a lacuna) modifies and maintains bone matrix Osteoclast = the major resorptive cells of bone Large, multinucleated cells Short life span Contain lysosomes filled with hydrolytic enzymes Dissolves bone minerals & digests collagen Bone Formation Bones Long bones Diaphysis (middle) Metaphysis (neck) Epiphysis (broad ends) Epiphyseal plate = growth plate Epiphyseal line Medullary cavity Endosteum (layer of connective tissue lining the surface of the marrow cavity) Long Bone Bone Remodeling Bone-remodeling units Repairs microscopic injuries and maintains bone integrity Bone Reformation fast in NB - slow in older adults Phases Activation of the remodeling cycle Reabsorption Formation of new bone Pediatric Bone Growth Until adult stature is achieved, bone growth occurs at the epiphyseal plate through endochondral ossification Cartilage is replaced with bone Factors affecting bone growth Growth hormone Nutrition General health Many growth factors and regulators / maternal hormone "relaxin" Joints Joint classifications based on movement Synarthrosis Amphiarthrosis Diarthrosis Joints Joint classifications based on structure Fibrous Suture, syndesmosis, gomphosis Cartilaginous Symphysis and synchondrosis Synovial Joint capsule, synovial membrane, joint cavity, synovial fluid, articular cartilage Muscle Development Between birth and maturity, muscle nuclei in the body increase 14 times in boys and 10 times in girls The composition and size of muscles vary with age Muscle Fibers Myoblasts Myofibrils Skeletal muscle Voluntary Striated Sarcomeres Motor unit Lower motor neurons Innervation ratios Sensory receptors Myofibrils Muscle Contraction Activation Muscle fiber action potential - Actin/Myosin Coupling Contraction Cross-bridge theory Relaxation Cardiac = Ca++ movement within cell ATP http://www.youtube.com/watch?v=mWPmUqRZYls&NR=1 http://www.youtube.com/watch?v=InIha7bCTjM&feature=related Musculoskeletal Pathophysiology of Neonatal & Pediatric Defects Skeletal Development In the newborn, the entire spine is concave anteriorly (kyphosed) In the first 3 months of life, the cervical spine begins to arch (lordotic) Curve of the lumbar spine develops with sitting Compared to an adult, a newborn has a large head, long spine, and short extremities Skeletal Development Genu recurvatum Knee joint hyperextended (cong. dislocation) Early treatment prevents deformity Genu varum (peaks by 2½ years) Bowleg Normal in young child Genu valgum (5-6 years) Knock-knee Bone Fractures Most common = Clavicular Dislocation Temporary displacement of two bones Loss of contact between articular cartilage Subluxation Contact between articular surfaces is only partially lost Dislocation and subluxation are associated with fractures, muscle imbalance, rheumatoid arthritis, or other forms of joint instability Congenital Defects Syndactyly Webbing of the fingers Fusion of the soft tissues of the fingers True syndactyly also includes fusion of the bones and nails Vestigial tabs - Polydactyly Extra digit Polydactyly & Syndactyly Congenital Defects Developmental Dysplasia of the Hip (DDH) Abnormality of the proximal femur, acetabulum, or both Risk factors Female sex, metatarsus adductus, torticollis, oligohydramnios, first pregnancy, and breech presentation The hip can present as subluxated, dislocatable, or dislocated Anatomy of the HIP Congenital Defects Developmental Dysplasia of the Hip (DDH) Manifestations Asymmetry of gluteal or thigh folds Limb length discrepancy Galeazzi Sign = knee lower Limitation of hip abduction Positive Ortolani sign Positive Barlow test "Waddling" gait Pain = LATE SIGN!! Developmental Dysplasia of the Hip DDH Diagnosis DDH Diagnosis DDH - Treatment Triple Diapers Pavlik Harness Casting - "Hip Spica" Traction Congenital Defects Deformities of the foot Metatarsus adductus "toes go towards midline" Equinovarus deformity Talipes Equinovarus (Clubfoot) Pes planus (Flatfoot) IU positioning vs. deformity Congenital Torticollis "Wry neck" from Intramuscular hematoma - mass felt in neck at 1-4 weeks of age. Position in-utero Shortened sternocleidomastoid muscle Congenital vertebral fusion (Klippel-Feil) Fusion of 2 of the 7 cerebral vertebrae Restricted mobility of the neck Osteogenesis Imperfecta "Brittle bone disease" Defect in collagen production Bone and vessel collagen Sillence classification - mild to lethal 8-10 Types now - Type I mildest & most common autosomal dominant autosomal recessive Results in osteoporosis, fractures, bowed and deformed limbs, short stature, spine curvature, and bluish sclera Can be evident before birth (in utero fractures) Types II and III (most severe - congenital) Osteogenesis Imperfecta Rickets Disorder causing mineralization failure, "soft" bones, and skeletal deformity Causes Insufficient vitamin D Insensitivity to vitamin D Renal wasting of vitamin D Inability to absorb calcium or vitamin D in the gut Rickets Normal vs. Rickets of Prematurity Scoliosis Scoliosis is a rotational curvature of the spine Nonstructural The curvature is from a cause other than the spine Structural Spine curvature associated with vertebral rotation Skeletal abnormalities, neuromuscular disease, trauma extraspinal contractures, bone infections of the vertebrae, metabolic bone disorders, joint disease, and tumors Important to screen in adolescents Osteomyelitis Infection of the bone Males > Females 3yrs-12 yrs most prevalent Staph aureus is usual causative agent in young children (~80%) MRSA ~ 30% Bacteria enter through blood supply. Abscess ---- periosteum Cerebral Palsy A static disorder of muscle tone and balance caused by an ischemic insult to the brain Perinatal disorder Disease patterns Hemiplegia, diplegia, quadriplegia Muscular Dystrophies Group of disorders that cause degeneration of skeletal muscle fibers The muscular dystrophies cause progressive, symmetric weakness and wasting of skeletal muscle groups Duchenne Muscular Dystrophy Most common of the muscular dystrophies X-linked recessive inheritance Deletion of a segment of DNA or a single gene defect on the short arm of the X-chromosome Duchenne muscular dystrophy gene Encodes for the dystrophin protein Dystrophin mediates the anchorage of the actin cytoskeleton of the skeletal muscle fiber to the basement membrane Duchenne Muscular Dystrophy Manifestations of the disorder begin to appear by approximately 3 years of age Slow motor development Progressive weakness Muscle wasting Sitting and standing are delayed The child is clumsy, falls frequently, and has difficulty climbing stairs Disorders of the Gastrointestinal Tract 1. Most alterations of digestive function in children are caused by congenital anomalies of the intestinal tract; disorders of digestion, absorption, or nutrition; or liver disease. 2. Cleft lip and cleft palate may occur separately or together, and both defects are associated with multiple gene-environmental interactions and deficiency of B vitamins. The fissure may affect the uvula, soft palate, hard palate, nostril, and maxillary alveolar ridge. 3. Nonsyndromic (isolated) CLP is the most common malformation with an incomplete separation between nasal and oral cavities without any associated anomaly. 4. Esophageal atresia, a condition in which the esophagus ends in a blind pouch, may occur with or without tracheoesophageal fistula, a connection between the esophagus and the trachea. As the infant swallows oral secretions or ingests milk, the pouch fills, causing either drooling or aspiration into the lungs. 5. Infantile hypertrophic pyloric stenosis, an obstruction of the pyloric outlet caused by hypertrophy and hyperplasia of circular muscles in the pyloric sphincter, is more common in male infants and may require surgical correction. 6. Intestinal malrotation occurs with failure of the colon to rotate during fetal development, and an obstructing band or volvulus (twisting of the bowel on itself) may partly or completely occlude the gastrointestinal tract and its blood vessels. 7. Meckel diverticulum is an outpouching of all layers of the small intestine caused by failure of the fibrous band that connects the small intestine to the umbilicus. 8. Hirschsprung disease (aganglionic megacolon) is caused by an absence of enteric ganglia and malformation of the parasympathetic nervous system in a segment of the colon, resulting in inadequate colon motility and functional obstruction. 9. Idiopathic intestinal pseudo-obstruction is repetitive episodes or continuous symptoms of intestinal obstruction without an obstructing lesion and may be associated with atrophy of enteric nerves and/or muscles. 10. DIOS, formerly called meconium ileus equivalent, can occur when intestinal contents become abnormally thick and obstruct the intestinal lumen. CF, pancreatic enzyme deficiency, and dehydration are common causes. 11. Duodenal, jejunal, and ileal obstructions can be caused by meconium ileus, atresia, peritoneal bands, or acquired obstructive disorders. 12. Malformations of the anus and rectum range from mild congenital stenosis of the anus to complex deformities, all of which are classified as imperforate anus. 13. Meconium aspiration syndrome is a type of newborn respiratory distress caused by fetal inspiration of meconium-contaminated amniotic fluid associated with fetal hypoxic distress and in utero gasping respirations. 14. Meconium ileus is a condition in the newborn in which intestinal secretions and amniotic waste products produce a thick tarry plug that obstructs the intestine, usually from lack of Chapter Summary Review Copyright © 2019, Elsevier Inc. All rights reserved. 43-2 fetal digestive enzymes. From 10% to 15% of neonates with CF have meconium ileus as neonates. 15. GERD is caused by the relaxation or incompetence of the lower esophageal sphincter. Infants are susceptible to reflux because the sphincter is not fully mature, their diet consists of liquids, and they are seldom in an upright position. 16. Eosinophilic esophagitis involves an eosinophilic inflammation of the esophagus with dysphagia and vomiting that can be associated with asthma and eczema. 17. The most common cause of acquired intestinal obstruction in infants is intussusception, a condition in which one portion of the bowel telescopes or invaginates into another. It occurs most commonly in the area of the ileocecal junction. 18. CF is an inherited disease caused by a dysfunction of the CF transmembrane regulator (CFTR) protein with a pathophysiologic triad that includes pancreatic enzyme deficiency (which causes maldigestion), overproduction of mucus in the respiratory tract, and abnormally elevated sodium and chloride concentrations in sweat. 19. Celiac disease is an immune-mediated lifelong disease with a genetic predisposition characterized by the loss of mature villous epithelium in the presence of a gluten-containing diet. It results in malabsorption and growth failure. Nonceliac gluten sensitivity is wheat allergy without the autoantibodies associated with celiac disease. 20. Severe acute malnutrition is a group of disorders resulting from a severe dietary deficiency of proteins (kwashiorkor), carbohydrates, or both (marasmus). Starvation causes stunted mental and physical development. Kwashiorkor occurs most often in toddlers who have stopped breast-feeding and subsist on a high-carbohydrate diet. 21. Failure to thrive or growth faltering is inadequate physical growth of a child associated with multifactorial conditions that include biologic, psychosocial, and environmental contributions resulting in delayed growth and malnutrition. 22. Necrotizing enterocolitis is a disorder in neonates, particularly low birth weight or premature infants, thought to result from stress and anoxia of an immature bowel wall and immature intestinal innate immunity. Bacteria invade the mucosa and can cause colitis, necrosis, intestinal perforation, sepsis, and death. 23. Acute diarrhea in infants and children is often caused by infection from contaminated food and/or water and can rapidly cause dehydration and electrolyte imbalances because fluid reserves are relatively small. The most common cause of acute diarrhea in children is bacterial or viral enterocolitis. 24. Chronic diarrhea (diarrhea persisting longer than 4 weeks) can be caused by a wide variety of underlying conditions and often leads to growth failure and delayed development. 25. Lactose malabsorption and intolerance causes diarrhea when failure to produce lactase results in osmotic diarrhea with ingestion of lactose-containing dairy products. Disorders of the Liver 1. Physiologic jaundice of the newborn is caused by mild hyperbilirubinemia that subsides in 1 to 2 weeks. Pathologic jaundice is caused by severe hyperbilirubinemia and can cause brain damage (kernicterus). Chapter Summary Review Copyright © 2019, Elsevier Inc. All rights reserved. 43-3 2. Biliary atresia is a congenital malformation of the bile ducts that obstructs bile flow. Atresia causes jaundice, biliary cirrhosis, portal hypertension, and liver failure. Biliary atresia is the most common reason for liver transplantation in children. 3. Acute hepatitis has the same clinical course in children and adults but children have milder cases of the disease. Hepatitis A is the most common form of childhood hepatitis and is spread by contact with contaminated stool and poor handwashing. 4. Young children more readily develop chronic HBV or HCV hepatitis because of their immature immune system. HBV and HCV can be acquired by maternal vertical transmission in newborns or by parenteral (i.e., use of shared needles) transmission in older children. 5. Cirrhosis is fibrotic scarring of the liver and is rare in children but can develop from most forms of chronic liver disease. 6. Portal hypertension in children usually is caused by extrahepatic obstruction. Thrombosis of the portal vein is the most common cause of portal hypertension in children and splenomegaly is the most common sign. 7. The three most common metabolic disorders that cause liver damage in children are galactosemia, fructosemia, and Wilson disease. All are rare, are inherited as genetic traits, and permit the accumulation of toxins in the liver. 8. Wilson disease causes defective copper uptake and metabolism. Copper that is not excreted accumulates in the liver, brain, kidney, and corneal cells. Damage from accumulated copper is gradual; the disease is usually not diagnosed before age 4 or 5 years. Chapter 43: Structure and Function of the Musculoskeletal System 1. Which bone cells produce osteocalcin when stimulated by 1,25-dihydroxyvitamin D and synthesize osteoid? a. Osteoclasts c. Fibrocytes b. Osteocytes d. Osteoblasts

ANS: D Osteoblasts are cells derived from mesenchymal stem cells and produce several substances, including osteocalcin, transforming growth factor-beta (TGF-) (a growth inhibitor for many cells), macrophage colony-stimulating factor, receptor activator of nuclear factor kappa-B ligand, osteoprotegerin (OPG), and bone matrix when stimulated by 1,25-dihydroxyvitamin D. This statement is not true of the other options. PTS: 1 REF: Page 1514

7. Which glucoprotein is thought to transport essential elements such as hormones, ions, and other metabolites to and from the bone cells? a. Osteocalcin c. Laminin b. Osteonectin d. Bone albumin

ANS: D Researchers believe bone albumin transports essential elements such as hormones, ions, and other metabolites to and from the bone cells and maintain the osmotic pressure of bone fluid (fluid surrounding mineral crystals and osteoblasts). This statement is not true of any other option. PTS: 1 REF: Page 1516

9. What is the basic structural unit in compact bone? a. Small channels called canaliculi c. Tiny spaces within the lacunae b. Osteocytes within the lacunae d. Haversian system

ANS: D The basic structural unit in compact bone is the haversian system (see Figure 43-4). This selection is the only option that accurately identifies the basic structure of compact bone. PTS: 1 REF: Page 1517

25. As the innervation ratio of a particular organ increases, what other property also increases? a. Control c. Coordination b. Movement d. Endurance

ANS: D The greater the innervation ratio of a particular organ, the greater is its endurance. Low-innervation ratios promote control and coordination, whereas high ratios promote strength and endurance. An increase in the innervations ratio does not result in an increase in movement. PTS: 1 REF: Page 1528

Which information is correct regarding the pathophysiologic process of osteomyelitis? Osteomyelitis produces:

Bone density less than 648 mg/cm2 Stimulation of osteoclasts Formation of fistula Sequestrum

Bone remodeling Osteoblasts and osteoclasts in bone remodeling ( iliac crest) Bone balance and remodeling Musculoskeletal Injuries Trauma Is the leading cause of death of people, ages 1 to 44 years, of all races and at all socioeconomic levels. Fracture Is a break in the continuity of a bone. Occurs when force is applied that exceeds the tensile or compressive strength of the bone. Fracture classifications Complete:

Bone is broken all the way through.

Transchondral

Broken bone can damage the surrounding tissue, periosteum, and blood vessels in the cortex and marrow.

Giant cell tumor

Causes extensive bone resorption as a result of the osteoclastic origin. Is located in the epiphyses of femur, tibia, radius, or humerus. Has slow and relentless growth rate; metastasis is rare.

Pain is the usual presenting symptom for either

osteosarcoma or Ewing sarcoma.

Oblique

Fracture of the shaft of the bone is slanted.

Linear

Fracture runs parallel to the long axis of the bone.

Muscle Strain

Is a sudden, forced motion, causing the muscle to become stretched beyond its normal capacity.

chondrosarcoma

Is a tumor of middle-aged and older adults. Infiltrates trabeculae in spongy bone; is frequently in the metaphyses or diaphysis of long bones. Contains lobules of hyaline cartilage that expand and enlarge the bone with no ossification. Causes erosion of the cortex and can expand into the neighboring soft tissues.

Osteomyelitis

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

Clinical manifestations compartment syndrome

Pain: Out of proportion to the injury Paresthesia, pallor, pulselessness, and paralysis (late sign)

8. Osteomyelitis is a local or generalized

bacterial infection of bone and bone marrow.

The crystallized matrix in spongy bone is arranged in

bars or plates.

Long bones have a

broad end (epiphysis), broad neck (metaphysis), and narrow midportion (diaphysis) that contains the medullary cavity.

Genetic evaluation is useful in

detecting, diagnosing, and developing specific treatment for certain inheritable muscle diseases such as muscular dystrophy.

Loss of satellite cells appears to play a major role in the

development of sarcopenia.

subluxation Associated with

fractures, muscle imbalance, rheumatoid arthritis, other joint instability

2. Bone formation begins during embryonic development with the differentiation of mesenchymal cells into either chondrocytes or preosteoblasts. Bone minerals then either crystallize on a cartilage

framework or become bone-forming cells without cartilage.

13. The muscular dystrophies are a group of

genetically transmitted diseases characterized by progressive atrophy of symmetrical groups of skeletal muscles without evidence of involvement or degeneration of neural tissue. There is an insidious loss of strength in all forms of the disorder with increasing disability and deformity.

Ewing sarcoma originates from cells within the bone marrow space and is located most often

in the midshaft of long bones, in ribs, or in flat bones.

2. Exercise in older adults improves

muscle strength, helps increase bone mineral density, and improves balance, coordination, lean body mass, and mobility.

. 10. Avascular diseases of the bone are collectively referred to as

osteochondroses and are caused by an insufficient blood supply to growing bones.

11. Legg-Calvé-Perthes disease is one of the most common

osteochondroses.

4. RANKL induces

osteoclast activation and bone resorption.

Spaces containing

osteocytes are dispersed between the bars or plates and interconnected by canaliculi.

Septic arthritis (bacteria within the joint) may be associated with

osteomyelitis and is a surgical emergency.

15. The two main types of malignant childhood bone tumors are

osteosarcoma and Ewing sarcoma.

. Juvenile idiopathic arthritis is an inflammatory joint disorder characterized by

pain and swelling.

When nonaccidental trauma is suspected, a child must be evaluated

radiographically for other fractures, head trauma, and retinal hemorrhage.

3. Age-related loss in skeletal muscle is referred to as

sarcopenia.

Dispersed throughout the concentric layers of crystallized matrix are

small spaces containing osteocytes.

1. Bones provide support and protection for the body's

tissues and organs and are important sources of minerals and blood cells.