Unit 3 - Chapter 45 Alterations of musculoskeletal fx

Question 1

Direction of fracture line

Answer 1

1) linear - break parallel to long side of bone
2) oblique - break has curved or sloped pattern
3) spiral - one part of bone has been twisted at break point
4) transverse - broken piece of bone is at right angle to long bone’s axis (right across - separating

Question 2

Incomplete fractures that occur in children

Answer 2

1) greenstick - incomplete fracture (side) d/t bone is bent; occurs most often in children
2) torus - common with falling, as wrist absorbs most of impact and compresses the bony cortex on one side and remains intact on other side (bulging effect around incomplete fracture)
3) bowing (incomplete fracture of tubular longs bones in forearm [radius and ulna] // heal with remodeling

Question 3

fatigue fracture

Answer 3

• occurs in normal bone
• d/t abnormal stress

Question 4

normal weightbearing

Answer 4

can cause insufficiency fracture in abnormal bone

Question 5

Dislocation

Answer 5

• loss of contact between the surfaces of two bones
• subluxation is partial loss of contact between two bones
• as bone separates from joint it may cause:
  1) damage adjacent nerves
  2) damaged blood vessels, ligaments, tendons, and muscle

Question 6

Strains and sprains

Answer 6

• tendon tears (strains) - muscle to bone
• ligament tears (sprains) - bone to bone
• avulsion – complete separation of tendon or ligament from its attachment

Question 7

Epicondylopathy

Answer 7

• degeneration of tendon where it attaches to bone

Question 8

Bursitis

Answer 8

• inflammation of bursae (small sac line with synovial membrane and filled with synovial fluid); can be inflammatory, septic, or hemorrhagic

Question 9

Muscle strain

Answer 9

• mild - severe
• can lose muscle fx

Question 10

Rhabdomyolysis

Answer 10

• life-threatening complication of severe muscle trauma l/t leakage of muscle cell content into circulation (CK, myoglobin, and various electrolytes)
• may l/t myoglobinuria, presence of myoglobin in urine and associated with acute renal failure / end organ complications
• most common etiologies
  1) mechanical trauma or muscle ischemia (crush injury, electric shock, seizure, compartment syndrome)
  2) drugs and toxins (statins, antibiotics, anxiolytics, antipsychotics, cocaine, amphetamines, alcohol)
  3) infection (influenza a/b, coxasackievirus, staphylococcus aureus)
• sx:
  1) muscle weakness
  2) myalgias (muscle ache and pain - include ligaments, tendons, and fascia (soft tissues that connect muscles, bones, and organs)
  3) reddish-brown urine

diagnosis: hx + lab CK (creatine kinase of typically 5 times the upper limit

tx: IV fluids + other

Question 11

compartment syndrome

Answer 11

1) tissue edema that occurs after injury
2) if edema develops within a closed fascial compartment, typically in anterior or posterior compartment of legs [there is little expansion] => interstitial (compartment) pressure increases
3) if comparment pressure exceeds normal capillary pressure approximately 8 mm Hg, cellular perfusion slows and may stop (can disappear even if pulse is present)
4) tissue ischemia worsens edema in cycle
5) muscles necrose => can l/t rhabdomyolysis, infections, and hyperkalemia
6) loss of limb + death

note – hypotension or arterial insufficiency can compromise tissue perfusion with even mildly elevated compartment pressures can cause or worsen compartment syndrome
* contractures may develop after necrotic tissue heals

causes
* fractures, crush injuries (contusion), perfusion injury after vascualr injury or repair
* others: snakebites, burns, exertion, casts, tight bandages
* prolonged pressure on muscle during coma => rhabdomyolysis

sx
* worsening pain followed by:
* paresthesias, paralysis, pallor, pulselessness
* may feel tense when palpated for compartment and passive stretching can change pain severity
* pain more than expected of severity of apparent injury (consider compartment syndrome)

diagnosis
* >30 mm Hg or within 30 mm Hg of diastolic pressure w/ pressure monitor

tx
* fasciotomy (cutting open inflexible tissue to relieve the pressure) // debride any unviable tissue
* monitor potassium levels
* treat rhabdomyolysis
* cut off constricting structure (cast)
* correct hypotension, analgesia (inability to feel pain), supplemental o2
* amputation may be indicated

Question 12

Osteoporosis

Answer 12

• bone tissue normal mineralization
• density or mass of bone reduced d/t bone remodeling cycle being disrupted
• progresses silently for decades until fractures occur
• alteration in OPG/RANKL/RANK system

1) PTH stimulate osteoblast to express RANKL ligand on its surfrace which then stimluate osteoclast precursor to become active [has RANK receptors] // PTH inhibits OPG expression from osteoblast
2) OPG is competitor of RANKL and thus blocks it from activating osteoclast

Question 13

Postmenopausal osteoporosis

Answer 13

• middle aged / OA women
• increased osteoclast activity d/t
  1) changes in osteoprotegerin (regulate osteoclasts)
  2) degreased IGF levels (insulin-like growth hormone)
  3) inadequate dietary calcium intake and lack of vitamin D
  4) decreased Mg+ (low mg l/t release of PTH and low mg means bone density is low [60% of bone is mg])
  5) lack of exercise
  6) lower estrogen (promotes osteoblasts - formation of new bone)
  7) family hx

Question 14

Glucocorticoids

*

Answer 14

increase RANKL expression and inhibit OPG production by osteoblasts => lower bone density

Question 15

Osteomalacia

Answer 15

• metabolic bone disease
• inadequate bone mineralization

Question 16

Paget disease

Answer 16

• excessive and abnormal bone remodeling
• Spradic paget disease involves overexpression of RANKL
• l/t new born that is abnormally shpaed, weak, and brittle

Question 17

Osteomyelitis

Answer 17

• bone infection
• bacterial origin (s. aureua e.g)
• enter bone from outside (exogenous osteomyelitis or from infection sites within body (hematogenous osteomyelitis)

Question 18

Bone tumors

Answer 18

• bone, cartilage, fibrious tissue, or vascular marrow cells
• each cell produces a specific ground substance
• osteogenic (bone cell)
• chondrogenic (cartilage cell)
• collagenic (fibrious tissue cell)
• myelogenic (vascular marrow cell)

maliganant bone tumors
* large, aggressive [destroy surrounding bone]
* invade surrounding tissue
* initiate independent growth outside of origin

benign bone
* less destructive
* limit growth to anatomic confines of bone
* well-demarcated border

Question 19

Noninflammatory joint disease

Answer 19

differs from inflammatory joint disease that it does not have
* synovial membrane inflammation (under joint capsule, lining of joint cavity)
* systemic signs and sx

Question 20

Osteoarthritis

Answer 20

• inflammatory joint disease
• degeneration and loss of articular cartilage, sclerosis (hardening) of underlying bone, and formation of bone spurs (osteophytes) or overgrowth

Question 21

rheumatoid arthritis

Answer 21

• inflammatory joint disease, systemic disease that affects heart, lungs, kidneys, and skin, joints
• destruction of synovial membrane (under joint capsule), arcitular cartilage (line outside of bone ends), joint capsule (under tendon, muscle, bursa), and surrounding ligaments and tendons
• immune resposne and have transformed antibodies (rheumatoid factors) — attack healthy cells and tissues
• OPG/RANKL/RANK involved
• rheumatoid nodules (firm lumps that form under skin up t o 20% of RA patients)

Question 22

ankylosing spondylitis (bechterew’s disease)

Answer 22

• chronic inflammatory joint disease
• stiffening and fusion of spine and sacroiliac joints (pelvis/lower spine connection)
• d/t synovitis (synovium or synovial membrane becomes inflamed) and bone marrow inflammation
• (enthesis, connective tissue between tendon or ligament and bone) => alteration in sacrolilace joints [all together]

Question 23

Gout

Answer 23

• metabolic d/o d/t high uric acid levels in blood and body fluids
• uric acid crystallizes in connective tissue of joint; initiating inflammatory destruction of joint

Question 24

Contracture

Answer 24

permanenet muscle shortening d/t msucle spastiticity (increased stiffness) seen in CNS injury or severe muscle weakness

Question 25

Stress induced muscle tension

Answer 25

* caused by increased activity in reticular activating (RAS) system [arousal, sleep-wake, fight-flight; projects to nuclei of thalmi then to cerebral cortex] * increased activity in gamma loop [between spinal cord and muscles, quickly regulating level of tension in our muscles] * **progressive relaxation training and biofeedback** can reduce muscle tension

Question 26

Fibromyalgia

Answer 26

* chronic musculoskeletal syndrome * diffuse pain and tender points (include fatigue and trouble sleeping) * muscle is the end organ responsible for pain and fatigue of the disease * **comorbidities, such as irritable bowel syndrome, mood d/o, chronic fatigue, suggest a role for neuroendocrine and stress-response alterations**

Question 27

Chronic fatigue syndrome

Answer 27

* debilitating, complex d/o w/ profound fatigue not relievable by bed rest * hypothetical cause - CNS alterations, immunologic disruptions, and chronic proinflammatory cytokine

Question 28

How to decrease atrophy to some degree in immobilized persons

Answer 28

* isometric contractions (e.g shoulder retractions) require no movement; only steady hold * passive lengthening exercises (doorway stretch; supine single leg stretch)

Question 29

Myotonia

Answer 29

* caused by hyperexcitable membranes * **relaxation of muscle is impaired** * tx w/ drugs that decrease fiber excitability (Na+ channel blockers: procainamide, phenytoin, and mexiletine // tricyclic antidepressant drugs such as clomipramine or imipramine)

Question 30

Periodic paralysis

Answer 30

* unresponsive muscle membrane * also include changes in serum potassium level * d/t changes in muscle membrane + sarcoplasmic reticulum

Question 31

Metabolic muscle diseases

Answer 31

caused by: 1) endocrine disorders (adrenal, pituitary, thyroid..) 2) glycogen storage disease (a rare metabolic disorder where the body is not able to properly store or break down glycogen, a form of sugar or glucose. GSD affects the liver, muscles and other areas of the body, depending on the specific type.) 3) abnormal lipid function **muscles** depend on complex system of carbohydrates and fats converted by enzymes to make energy for muscle cells

Question 32

Viral, bacterial and parasitic infections of muscles

Answer 32

* produce characterisitic clinical and pathologic changes associated w/ "inflammation" * treatable and self-limiting

Question 33

Polymyositis, including dermatomyositis

Answer 33

* generalized muscle inflammation l/t muscle weakness * dertmatomyositis (polymyositis accompanied with skin rash) * include inflammation of connective tissue + muscle fibers and muscle fiber necrosis * d/t cell-mediated and humoral immune factors * immunosuppressive agests prove effective (steroid or corticosteroid, or azathioprine and methotrexate)

Question 34

Myopathies

Answer 34

* primary d/o w/ weakness and atrophy * Most common toxic myopathy caused by alcohol abuse Direct effects include: 1) alcohol-producing necrosis of muscle fibers 2) nutritional deficiency * abstinence and improved nutrition **Toxic effects of many drugs** 1) include local trauma to muscle fibers from direct needle injection 2) secondary infection 3) nonphysiologic changes in acidity and akalinity in the fibers

Question 35

Sarcomas of muscle tissues

Answer 35

* rare * Rhabdomyosarcoma - uniformly poor prognosis d/t aggressive invasion and early, widespread dissemination (tx'd w/ surgery, radiation, and chemo)