Fractures

Complete fracture

Bone is broken all the way through.

Incomplete fracture

Bone is damaged but still in one piece.

Closed or simple fracture (complete or incomplete)

Skin is intact.

Open or compound fracture (complete or incomplete)

Skin is broken.

Comminuted fracture

Bone breaks into more than two fragments.

Linear fracture

Fracture runs parallel to the long axis of the bone.

Oblique fracture

Fracture of the shaft of the bone is slanted.

Spiral fracture

Encircles the bone.

Transverse fracture

Occurs straight across the bone.

Greenstick fracture

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.

Fragility

Sequalae of osteoporosis.

Fatigue

Abnormal stress or torque applied to a bone with normal ability to deform and recover.

Insufficiency

Fragility fractures of osteoporosis and osteomalacia.

Transchondral

Fragmentation and separation of portion of articular cartilage that covers the end of a bone at the joint.

Patho and clinical manifestations of Fractures

Impaired function, unnatural alignment, swelling, muscle spasm, tenderness, pain, impaired sensation.

Evaluation and treatment of fractures

Closed manipulation, traction (skeletal or skin), open reduction, internal fixation, external fixation. Splints and casts.

Dislocation

Temporary displacement of bone from its joint.

Subluxation

Contact between the bones in the joint only partially lost.

Strain

Tear or injury to a tendon (fibrous connective tissue that attaches skeletal muscle to bone).

Sprain

Tear or injury to a ligament (fibrous connective tissue that connects bones).

Avulsion

Complete separation of a tendon or ligament from its bony attachment site.

Rhabdo

Release of intracellular potassium into circulation creating high K levels which might require dialysis to correct if extensive. Protein pigment myoglobin into extracellular space and bloodstream – causing cola colored urine.

Classic triad of complications Rhabdomyolysis

Muscle pain, weakness, and dark urine (from myoglobin). Tx with rapid IV hydration.

Osteoporosis

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

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.

Osteomyelitis

Is usually caused by a Staphylococcus aureus 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.

OA

Most common form of joint disease and is a disorder of synovial joints. Inflammatory (new evidence and cytokines) joint disease. No single patho. Loss of articular cartilage, sclerosis of underlying bone, and formation of bone spurs (osteophytes). Also called degenerative joint disease. Incidence increases with age. Leading cause of disability in middle aged and older populations.

Clinical manifestations of OA

Pain, stiffness, enlargement of the joint, tenderness, limited motion, and deformity. Joint swelling in the fingers:Heberden and Bouchard nodes.

RA

Symmetric joint swelling, joint deformities. Systemic manifestations of inflammation. Rheumatoid nodules in organs. Caplan syndrome. Painful, tender, stiff joints.

Ankylosing Spond

Chronic inflammatory joint disease of the spine or sacroiliac joints, causing stiffening and fusion of the 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.

Gout Clinical manifestations

Pain in the great toe (usually, but not always):Worse at night often in the metatarsophalangeal joint. 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.

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.

Polymyositis and dermatomyositis

Inflammation of connective tissue and muscle fibers. Polymyositis:Mediated by T cells. Dermatomyositis:Humorally mediated. Necrotizing myopathy. Inclusion body mitosis.

Myopathy

Is the term applied to a primary muscle disorder.

Bone formation begins in two phases at approximately

6 weeks’ gestation

Ossification occurs in two long bone centers

Diaphysis—long, central portion of bone Secondary center:Epiphysis—end portions of bone

Genu varum think arrogant cowboy(peaks by 30 months)

Bowleg. Occurring in all newborns as a result of intrauterine stress.

Genu valgum (peaks by 5–6 years)

Knock knees

If varum and valgum persist past their respective ages

Pathologic cause.

Rickets

Disorder causing mineralization failure, “soft” bones, and skeletal deformity.

Causes of Rickets

Insufficient vitamin D. Insensitivity to vitamin D. Renal wasting of vitamin D. Inability to absorb calcium or vitamin D in the gut.

Clinical manifestations of Rickets

Short stature. Bowing of the limbs with hypotonia and muscle weakness.

Tx of Rickets

Calcium, phosphorus, and vitamin D levels must be optimized before surgical intervention.

Osteochondrosis

Avascular diseases of the bone; insufficient blood supply to growing bones.

Osgood-Schlatter

Tendinitis of the anterior patellar tendon and osteochondrosis of the tubercle of the tibia.

Perthes disease

Blood supply to the femoral head is interrupted. Is a self-limiting disease. Ossification center first becomes necrotic, collapses, and then is gradually remodeled by live bone.

Clinical manifestations of Perthes Disease

Knee pain Spasm on inward rotation of the hip and a limitation of internal rotation flexion and abduction. Abnormal gait: Trendelenburg gait or abductor lurch

Duchenne Muscular Dystrophy

Most common muscular dystrophy. Poorly anchored fibers tear apart under the repeated stress of contraction; free calcium then enters the muscle cells, causing
cell death and fiber necrosis.

Duchenne MD Clinical Manifestations

Clinical manifestations appear by 3 or 4 years of age. Gait abnormalities. Progressive weakness in Muscles. Respiratory insufficiency. Cardiomyopathy. Scoliosis. Waddling gait. Gower sign: Climbing up the legs when rising. Cognitive dysfunction.