Mod 9 Musculoskeletal

Question 1

Closed fracture

Answer 1

Bone separates completely but does not break skin

Question 2

Incomplete fracture

Answer 2

Bone fragments sill partially joined

Question 3

Open (compound) fracture

Answer 3

Bone protrudes to outside of the body and skin surface is broken

Question 4

Compression fracture

Answer 4

Crushing of cancellous bone, usually from heavy object

Question 5

Transverse fracture

Answer 5

Bones are separated but close to each other

Question 6

Comminuted fracture

Answer 6

More than 1 fracture line and more than 2 bone fragments that may be shattered or crushed

Question 7

Spiral fracture

Answer 7

Twisting force to the thigh causing a fracture line that encircles the shaft

Question 8

Stress fracture

Answer 8

Failure of 1 cortisol surface of the bone caused by repetitive activity

Question 9

Avulsion fracture

Answer 9

Separation of a small fragment of bone at site of attachment of a ligament or tendon

Question 10

Impacted fracture

Answer 10

One part of the fracture is compressed into an adjacent part of the fracture

Question 11

Greenstick fracture

Answer 11

Incomplete break in bone that goes partially thru bone

Question 12

Bone healing stage 1:
Fracture & Inflam Phase

Answer 12

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

Question 13

Bone healing stage 2:
Granulation Tissue Formation

Answer 13

Fibroblasts are attracted to area of injury
Growth of vascular tissue
Nutrient & oxygen supply is significant
Lasts 2 WEEKS

Question 14

Bone healing stage 3:
Callus Formation

Answer 14

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

Question 15

Bone healing stage 4:
Lamellar Bone Deposition

Answer 15

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

Question 16

Bone healing stage 5:
Remodeling (FINAL PHASE)

Answer 16

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

Question 17

What type of renal injury does rhabdomyolysis cause?

Answer 17

Acute Renal Injury

Question 18

What is the relationship between orthopedics and DVTs?

Answer 18

Orthopedic surgery patients are particularly susceptible to DVT and PE bc venous stasis, vessel injury, and hypercoagulability of blood with venous pooling.

Question 19

Sprains & Strains

Answer 19

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.

Question 20

Muscle Contusions

Answer 20

Bruise results when muscle fiber and connective tissues are crushed. Torn blood vessels appear blue

Direct blow/impact like a fall

Question 21

Bone fractures

Answer 21

Made up of loading forces- tension, compression, bending, torsion, shear. When these forces exceed = fracture occurs (complete or incomplete disruption of bone)

Question 22

Soft tissue injury

Answer 22

contractile tissue and inert (muscle fxing) help differentiate exact site of injury
Extension of adjacent soft tissue infection: contiguous osteomyelitis.

Question 23

Osteoporosis

Answer 23

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

Question 24

Osteoarthritis

Answer 24

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

Question 25

What is a hallmark of OA?

Answer 25

Osteophyte formation is a hallmark of OA.

Question 26

RA

Answer 26

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

Question 27

Hallmark of RA?

Answer 27

Development of bone erosions due to activation of osteoclasts and invasive synovial pannus formation in the involved joints.

Question 28

OA vs RA

Answer 28

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

Question 29

Treatment for OA & RA?

Answer 29

RA- Methotrexate and monoclonal antibody agents OA- Acetaminophen, NSAIDs, Cox-2 inhibitors

Question 30

Triggers for gout

Answer 30

Rapid weight loss, alcohol, organ meats, binge drinking, dehydration

Question 31

Risks for hyperuricemia leading to gout

Answer 31

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)

Question 32

Stages of Lyme disease

Answer 32

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)

Question 33

How does Parkinson’s treatment lead to secondary gout?

Answer 33

Parkinson’s med like levodopa can cause secondary gout bc it increases uric acid in the blood

Question 34

Stages of osteomyelitis

Answer 34

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