1. Fractures
    • Disruption in the continuity of a bone
    • Occurs when more stress is placed on the bone than it is able to absorb
    • Three categories:
    • 1.Fx caused by sudden injury
    • 2.Fatigue stress fractures
    • 3.Pathologic stress fractures
  2. Manifestations of Fractures
    • Pain, tenderness at site of bone disruption, swelling, loss of function, deformity of the affected part, abnormal mobility
    • Nerve function at the fracture site may be temporarily lost: numbness; called local shock; good time to reduce fx
  3. Diagnosis/Treatment of Fractures
    • History and manifestations
    • X-ray
    • Treatment depends on location, any associated injuries, and whether fx is open or closed
    • Splint can be used for immobilization
  4. Complications of Fractures and Injuries
    • Compartment Syndrome
    • Fat Embolism Syndrome
  5. Compartment Syndrome
    • Increased pressure within a limited space (abdominal and limb compartments)
    • Compromises circulation and function of the tissues within the space
    • If pressure in the compartment is high, circulation is compromised, causing death of nerve and muscle cells
    • Permanent loss of function can occur
    • Causes can include tight dressings and casts, burns, and closure of fascial defects
    • Bleeding and edema from fx and bone surgery
    • Drug overdose or carbon monoxide poisoning when the extremity is compressed by the head or torso
    • Fasciotomy may be needed: the fascia is incised longitudinally and separated so the compartment can expand and blood flow can be reestablished
  6. Fat Embolism Syndrome
    • Presence of fat droplets in the vessels of the lung or other organs after a long bone fx or other major trauma
    • Fat emboli are released from the bone marrow or adipose tissue at the fx site into the venous system
  7. S/S of Fat Embolism Syndrome
    • respiratory failure
    • cerebral dysfunction often seizures)
    • skin/mucosal petechiae
  8. Bone Infections
    • Osteomyelitis: acute or chronic infection of the bone and marrow
    • Inspite of ABT, they are difficult to treat
    • Can be caused by viruses, bacteria, fungi, parasites
    • Microorganisms introduced during injury, during operations, or from blood-stream
  9. Most common cause of Bone Infections
    Staphylococcus aureus
  10. S/S of Bone Infections
    • Pain
    • Fever
    • Chills
    • Malaise
    • Local Tenderness and Loss of Movement
  11. Osteonecrosis
    • Aseptic destruction of a bone segment due to an interruption in blood flow rather than an infection
    • Bone necrosis results from ischemia; what causes the ischemia is varied: mechanical interruption such as occurs with fracture; thrombosis, embolism, vessel injury (radiation therapy)
  12. S/S of Osteonecrosis
    • Depend on site and extent
    • Usually pain that initially is with activity, but over time patient has pain at rest
  13. Treatment of Osteonecrosis
    • Depends on pathology: immobilization, NSAIDs, limitation of weight-bearing
    • Joint replacement
  14. Osteosarcoma
    • Aggressive, highly malignant bone tumor Most common malignant bone tumor
    • 75% of cases are in persons younger than 20
    • Cause is unknown
    • Aggressive tumors that grow in a circular, ball-like mass in the bone tissue
    • Early metastasis to the lung is common
  15. S/S of Osteosarcoma
    • Deep, localized pain with nighttime awakening
    • Swelling in the affected bone
    • Skin over the tumor may be warm, shiny, and stretched
    • ROM restricted
  16. Treatment of Osteosarcoma
    • Surgery with chemotherapy before and after surgery
    • Amputation may be needed
  17. Legg-Calve-Perthes Disease
    • Idiopathic osteonecrotic disease of the proximal femoral epiphysis
    • Affects kids, between 4-8 not exclusively
    • Boys more than girls
    • Cause unknown
    • Insidious in onset and child is otherwise healthy
  18. S/S of Legg-Calve-Perthes Disease
    • Pain in the groin, thigh, knee and difficulty in walking
    • Painless limp
    • Limited abduction and internal rotation
    • Flexion contracture of the affected hip
  19. Osgood-Schlatter Disease
    • Microfractures in the area where the patellar tendon inserts in to the tibial tubercle
    • Condition most frequent in boys between 10 and 15 years
    • Pain in the front of the knee associated with inflammation and thickening of the patellar tendon
    • Sudden or continued strain from the patellar tendon during periods of growth while associated with running, bicycle riding, or stair climbing
  20. Treatment of Osgood-Schlatter Disease
    Rest, restriction of activities and knee immobilizer
  21. Osteopenia
    • Reduction in BMD greater than expected for age, race or gender and happens because of a decrease in bone formation, inadequate bone mineralization, or excessive bone deossification
    • Is a term used to describe a lack of bone density on x-ray studies
    • Can involve a decrease in bone matrix due to an imbalance between bone formation and destruction, or a decrease in mineralization
  22. Causes of Osteopenia
    • Osteoporosis
    • Osteomalacia
    • Multiple myeloma
    • Endocrine problems such as hyperparathyroidism and hyperthyroidism
  23. Osteomalacia
    • General bone condition in which there is inadequate mineralization of bone
    • High incidence in the elderly because of diets deficient in calcium and vitamin D
    • May also occur in patients on long-term treatment with medications such as anticonvulsants that decrease the activation of vitamin D
  24. Causes of Osteomalacia
    • Insufficient calcium absorption form the intestine due to lack of dietary calcium or a deficiency of vitamin D
    • Pphosphate deficiency caused by increased renal losses or decreased intestinal absorption
  25. Manifestations of Osteomalacia
    • Bone pain, tenderness and fractures as the disease progresses
    • Predisposes patient to pathologic fractures especially those in the distal radius and proximal femur
    • Different from osteoporosis in that is does not significantly cause hip fractures
    • Accompanied by compensatory hyperparathyroidism caused by low serum calcium levels
  26. Treatment of Osteomalacia
    Determined by cause: if nutritional, restoring amounts of calcium and vitamin D to diet may be enough
  27. Rickets
    • Metabolic bone disorder characterized by a failure or delay in calcification of the cartilaginous growth plate in kids whose epiphyses have not yet fused
    • Nutritional rickets results from inadequate sunlight exposure, or inadequate intake of vitamin D, calcium or phosphate
  28. S/S of Rickets
    • Bones are deformed
    • Ossification at the epiphyseal plates is delayed and disordered; new bone is unmineralized
    • Skull is enlarged and soft
    • Fontanels are slow to close
    • Teeth are slow to develop
    • May have difficulty standing
  29. Paget Disease
    • Second most common bone disease after osteoporosis
    • “collage of matrix madness”
    • Areas of excessive osteoclast-mediated bone reabsorption preceding disorganized osteoblast-mediated bone repair
    • Men twice as likely as women to have
    • Probably genetic and environmental component
    • The poor quality of new bone that is formed accounts for bowing and fractures of the bones
  30. S/S of Paget Disease
    • Often asymptomatic and may be discovered incidentally on x-ray
    • Kyphosis caused by enlargement, weakening, and collapse of the vertebrae
    • Weight bearing causes bowing of the femur and tibia
    • Mild to moderate pain, aching in nature, persists thru the day and at rest and becomes worse at night
    • Tumors often develop in pagetic bones, especially sarcoma
  31. Diagnosis and Treatment of Paget Disease
    • Based on bone deformities and x-ray changes
    • Elevated levels of serum alkaline phosphatase
    • Bone scans
    • Pain can be reduced with NSAIDs
    • Bisphosphonates and calcitonin prevent spread of disease
    • Need adequate doses of calcium and vitamin D
  32. Systemic Autoimmune Rheumatic Disease
    • Chronic autoimmune systemic disease
    • Affects women 2.5 times more than men
    • Peak incidence is between 40 and 50 years of age
    • Cause is uncertain; thought to be genetic predisposition and the development of joint inflammation that is immunologically mediated
  33. Manifestations of Systemic Autoimmune Rheumatic Disease
    • Joint involvement is symmetric and polyarticular
    • c/o joint pain and stiffness that lasts for 30 minutes and often several hours Limitation of joint motion that occurs early in the disease is due to pain; later on it is due to fibrosis
    • Pain in the ball of foot upon arising
    • Pain with turning door knobs, opening jars, buttoning shirts due to swelling of the wrists and small joints of the hand
    • •May be fatigued, weak, anorexia, weight loss due to systemic inflammation
    • ESR and C-reactive protein (CRP)
    • Rheumatoid nodules: granulomatous lesions that may be tender or nontender, movable or nonmovable, small or large
    • Dryness of eyes, mouth, and other mucous membranes
  34. Diagnosis and Treatment of Systemic Autoimmune Rheumatic Disease
    • Findings on the history
    • Physical examLab tests criteria for RA developed by the American Rheumatism Association: at least 4 criteria must be present to make diagnosis of RA
    • Goals are to reduce pain, minimize stiffness and swelling, maintain mobility
    • Physical rest and therapeutic exercise
    • Proper posture, positioning, body mechanics, supports
    • NSAIDs and corticosteroids will help
  35. Systemic Lupus Erythematosus
    • Chronic inflammatory disease
    • Can affect almost any organ system, including the MS system
    • Primarily a disease of young women
    • Peak incidence between ages 15 and 40 years
    • More common in African-Americans, Hispanics, and Asians
    • Characterized by formation of autoantibodies and immune complexes (type III hypersensitivity)
  36. Manifestations of Systemic Lupus Erythematosus
    • -“great imitator” because it can affect many body systems, including the MS, skin, CV, lungs, kidneys, CNS, RBC’s and platelets
    • -Characterized by exacerbations and remissions
    • -Arthralgias and arthritis are among the most commonly occurring symptoms
    • -Skin lesions include a “butterfly” rash on the nose and cheeks
    • -Hair loss is common
    • -Sun sensitivity even with mild exposure
    • -Renal involvement in ½ to 2/3 of persons with SLE: glomerulonephritis may occur
    • -May have nephrotic syndrome with edema in the legs and abdomen and around the eyes
    • -Pulmonary involvement occurs in about 30% of patients and results primarily in pleural effusions or pleuritis
    • -Pericarditis is most common CV problems
    • -CNS: seizures can occur and are more frequent when renal problems exist
  37. Diagnosis and Treatment of Systemic Lupus Erythematosus
    • Complete history, physical exam, labwork
    • ANA most common test: 95% of patients have high ANA levels: not specific for SLE
    • Treatment focuses on symptoms of disease
    • Goal is to prevent loss of organ function and reducing exacerbations
  38. Systemic Sclerosis/Scleroderma
    • Autoimmune disease of connective tissues that causes fibrosis throughout the body
    • Women 4 times as frequently as men
    • Peak age: 35-50 year olds
    • Skin involvement is usually the first symptom: but involvement with other organs is what causes morbidity
  39. Manifestations of Limited Scleroderma
    • Dkin changes limited to the fingers, forearms, and face
    • May develop CREST syndrome:
    • C= calcinosis (calcium deposits in the subcutaneous tissue
    • R= Raynaud’s phenomenon
    • E= esophageal dysmotility
    • S= sclerodactyly Scleroderma of fingers
    • T= telangiectasia
  40. Manifestations of Diffuse Scleroderma
    • Severe, widespread, progressive skin involvement
    • Face is described as “stone facies”
    • Restricted movement of the mouth
    • Raynaud’s
    • Hair loss on involved skin
    • Telangiectasis on the face, chest, hands
    • Difficulty swallowing
  41. Treatment of Systemic Sclerosis/Scleroderma
    • Symptomatic and supportive
    • Category of ACE inhibitors in those with renal problems as decreased mortality with hypertensive renal disease
  42. Gout
    • Cause is unknown or an inborn error in metabolism and is characterized by hyperuricemia and gout
    • Primarily a disease of men
    • Pathogenesis: elevation of serum uric acid levels (uric acid is the end product of purine metabolism)
    • An attack occurs when monosodium urate crystals precipitate in the joint and initiate an inflammatory response
    • Large, hard nodules called tophi can result; they are found on the synovium, Achilles tendon, and forearm and may be mistaken for rheumatoid nodules
  43. Manifestations of Gout
    • Initial attack affects one joint, usually the first metatarsophalangeal joint
    • Onset of pain is abrupt
    • Redness and swelling
    • May be precipitated by exercising, alcohol, dieting, certain meds or foods
  44. Diagnosis and Treatment of Gout
    • Hyperuricemia is the hallmark of gout, but many people have hyperuricemia and never develop gout
    • Diagnosis can only be made when urate crystals are present in the synovial fluid or in tissue sections of tophi
    • Goal: prevent attacks of gouty arthritis and correcting hyperuricemia
    • Pharmacological management is aimed at reducing joint inflammation
    • NSAID’s good
    • Avoid purine-rich foods (liver, kidney, sardines, anchovies)
    • Meds such as Allopurinol and colchichine
Card Set
Dr. Tuck Exam 3