Mod 9 Musculoskeletal Flashcards
Closed fracture
Bone separates completely but does not break skin
Incomplete fracture
Bone fragments sill partially joined
Open (compound) fracture
Bone protrudes to outside of the body and skin surface is broken
Compression fracture
Crushing of cancellous bone, usually from heavy object
Transverse fracture
Bones are separated but close to each other
Comminuted fracture
More than 1 fracture line and more than 2 bone fragments that may be shattered or crushed
Spiral fracture
Twisting force to the thigh causing a fracture line that encircles the shaft
Stress fracture
Failure of 1 cortisol surface of the bone caused by repetitive activity
Avulsion fracture
Separation of a small fragment of bone at site of attachment of a ligament or tendon
Impacted fracture
One part of the fracture is compressed into an adjacent part of the fracture
Greenstick fracture
Incomplete break in bone that goes partially thru bone
Bone healing stage 1:
Fracture & Inflam Phase
Inflam bleeding occurs
Hematoma develops
Inflam causes vascular permeability
WBC, macrophages, lymph all infiltrate bone area
48 HRS after injury and can last a week
Bone healing stage 2:
Granulation Tissue Formation
Fibroblasts are attracted to area of injury
Growth of vascular tissue
Nutrient & oxygen supply is significant
Lasts 2 WEEKS
Bone healing stage 3:
Callus Formation
Callus is formed – made up of osteoblasts & chondroblasts in granulation tissue
Synthesize extracellular woven bone & cartilage producing newly formed mineralized bone
6 WEEKS after post injury
Bone healing stage 4:
Lamellar Bone Deposition
Strengthening phase where ossification is beginning
Callus (mesh) of woven bone replaced by sheets (lamellae) of mineralized bone (stronger) than callus
Occurs weeks FOLLOWING CALLUS FORMATION, but length of time depends on injury
Bone healing stage 5:
Remodeling (FINAL PHASE)
Remodeling of the bone at the site of healing fracture by osteoclasts and osteoblasts
Formation is sculpted and refined by mechanical stresses imposed on the bone
Adequate strength occurs in 3-6 MONTHS
What type of renal injury does rhabdomyolysis cause?
Acute Renal Injury
What is the relationship between orthopedics and DVTs?
Orthopedic surgery patients are particularly susceptible to DVT and PE bc venous stasis, vessel injury, and hypercoagulability of blood with venous pooling.
Sprains & Strains
Sprain: overstretching of ligament with possible tear, in response to quick twist or pull of muscle. Most common around joints. Grade I is no tear, Grade II is partial tear, Grade III is complete tear of ligament and symptoms similar to bone fracture.
Strain: overstretching of tendons and muscle. Often in lower back or hamstring, resulting from overuse or improper use.
Muscle Contusions
Bruise results when muscle fiber and connective tissues are crushed. Torn blood vessels appear blue
Direct blow/impact like a fall
Bone fractures
Made up of loading forces- tension, compression, bending, torsion, shear. When these forces exceed = fracture occurs (complete or incomplete disruption of bone)
Soft tissue injury
contractile tissue and inert (muscle fxing) help differentiate exact site of injury
Extension of adjacent soft tissue infection: contiguous osteomyelitis.
Osteoporosis
Eti: bone demineralization that occurs with aging. Lack of calcium or vitamin D in the diet, immobility, age, gender, genetics, and certain medications can predispose patients to osteoporosis.
Patho: Reduction in bone density caused by imbalance between osteoclasts and osteoBlasts. Due to age osteoclasts outbalance osteoBlasts. Accelerated bone loss can occur in female athlete triad syndrome: a disorder in which a young woman exercises excessively, causing energy deficiency, amenorrhea, and osteoporosis
CM: silent disease because diagnosis is often not made until after the individual has already suffered an osteoporotic fracture. Weakening of vertebral bodies results in vertebral compression fractures.
Treatment: Bisphosphonates (antiresorptive) suppress osteoclast activity. Selective estrogen receptor modulators (SERMs) act like estrogen on bones. Denosumab, an injectable antiresorptive agent, can be used if other drugs prove ineffective or intolerable. Ca & vit D
Osteoarthritis
Risk Factors of OA: Aging, obesity, history of sports, trauma or overuse of joint, heavy occupational work
Eti: Stresses applied to the joints especially weight bearing joints (ankle, knee, hip)
Patho: Slowly progressive, degenerative, inflammatory disease. Excess pressure on a joint gradually wears away the cartilage surface, exposing the subchondral bone. Inflammation occurs as cytokines are released into the joint and degrade the cartilage. Excess fluid from proteoglycans causes swelling of the joint. At margin of cartilage loss, osteophytes can form (small bony growths that develop along joints).
Osteophyte formation is a hallmark of OA.
CM: complaints of deep, aching joint pain, occurring especially after exercise or weight-bearing. Symptoms may be relieved with rest. Other symptoms include joint pain during cold weather, stiffness when arising in the morning, crepitus of the joint during motion, joint swelling, altered gait, and limited ROM. The patient may report a burning sensation felt in the associated muscles and tendons or experience muscle spasm and contractions in the tendons with motion. Classic swelling called Heberden’s nodes and Bouchard’s nodes.
Treatment: Acetaminophen, NSAIDs, Cox-2 inhibitors
What is a hallmark of OA?
Osteophyte formation is a hallmark of OA.
RA
Patho: body’s immune system attacks its own synovial tissues, stimulating an inflammatory process that results in destruction of cartilage, bone, tendons, and ligaments.
Eti: Unknown, Genetic, environmental, hormonal, immunological, and infectious factors may play significant roles. Females are more commonly affected by RA
CM: symmetrical, tender, swollen joints, most commonly of the fingers, wrists, knees, hips, and feet, fatigue, fever, and general malaise. Patients commonly report painful, stiff joints lasting approximately 30 minutes to an hour in the morning or after a period of prolonged rest. chronic joint inflammation experienced by RA patients results in permanent damage of the surfaces of joints. The two classic rheumatoid deformities in the fingers are boutonnière deformity and swan neck deformity
Treatment: goals are to relieve pain, maintain mobility, and minimize disability. Methotrexate and monoclonal antibody agents
Hallmark of RA?
Development of bone erosions due to activation of osteoclasts and invasive synovial pannus formation in the involved joints.
OA vs RA
OA: degenerative disease
RA: autoimmune disease
OA:
Patho: Joint swelling and osteophyte formation
Caused by aging - older than 50 usually affected, both women and men
Joint pain only - Heberden’s and Bouchard’s nodes of fingers
Stiffness WORSE in the morning but rest decreases pain stiffness and better as day progresses
Movement of joint INCREASES pain
Can be asymmetrical or symmetrical small and LARGE joints (hip, knee, hand)
RA:
Patho: Joint swelling and deformity, intense inflammation with joint erosion
Fever, elevated WBC
Greater joint deformity
Symmetrical Hands only – Wan neck and boutonniere deformity of fingers
20-40 yrs old affected (women mainly)
Stiffness in morning but better with use of join = movement of joint DECREASES pain
Treatment for OA & RA?
RA- Methotrexate and monoclonal antibody agents
OA- Acetaminophen, NSAIDs, Cox-2 inhibitors
Triggers for gout
Rapid weight loss, alcohol, organ meats, binge drinking, dehydration
Risks for hyperuricemia leading to gout
thiazide and loop diuretic usage (for hypertension)
high alcohol consumption
males (estrogen is protective)
cancer chemotherapy - increased breakdown of cellular DNA leads to elevated uric acid levels
excessive purines in diet (red meat and seafood)
Stages of Lyme disease
early localized - 3-30 days after tick bite. Erythema migrans rash. Not painful or itchy. Sometimes flulike symptoms, enlarged lymph nodes in area draining the bite.
early disseminated - 3-12 weeks after tick bite. neck pain, intense headache, carditis, ocular changes
late disseminated - months to years after infection. Severe joint pain, swelling of large joints (often knees), subacute encephalopathy (confusion, difficulty with concentration)
How does Parkinson’s treatment lead to secondary gout?
Parkinson’s med like levodopa can cause secondary gout bc it increases uric acid in the blood
Stages of osteomyelitis
inflammation - vascular congestion, increased pressure in interior bone
Suppuration - infectious material within bones forces its way through Haversian system, forms abscess beneath bone surface
Sequestrum - increased pressure, vascular obstruction, thrombi compromise periosteal blood supply, causes bone necrosis in 7 days
Involucrum - new bone formation from stripped surface of periosteum
Resolution OR progression - with antibiotics and surgical treatment, osteomyelitis can resolve with no complications. Without resolution, can lead to gangrene
