45040396 Musculoskeletal System

7/28/2019 45040396 Musculoskeletal System

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MUSCULOSKELETAL SYSTEM

Functions of the Musculoskeletal System:

- Frameworkfor the attachment of muscles, tendons, and ligaments- Protects and maintains soft tissues in proper position- Provides stabilityfor the body and maintains the bodys shape- Storage reservoirfor calcium- Formation of blood cells in the hematopoietic connective tissue in central cavity of bones

Components of the Musculoskeletal System: muscles, bones, cartilage, joints, bursae, tendons, ligaments

1. Musclesa. Skeletal muscle voluntary, striatedb. Smooth muscle involuntaryc. Cardiac muscle involuntary, striated

2. Bones- 30% organic material (bone cells, blood vessels, nerves) and 70% salt deposits (calcium, phosphate)- Classified as long, short, flat, or irregular- 2 types of mature bones:

o Cancellous (spongy) bone Found in interior of bones, composed of trabeculae Considerable tensile strength and weight-bearing properties Not penetrated by blood vessels; nourished by diffusion through canaliculi

o Compact (cortical) boney Densely packed, calcified intercellular matrixy Found along the lines of stress on long bones and forms a protective shell on othersy Distribution of blood in the cortex occurs through the haversian and Volkmann canals

- Bone marrow cells involved in blood cell formation (red marrow) and fat cells (yellow marrow)- Bone cells:

o Osteoprogenitor cellsy Undifferentiated cells that differentiate into osteoblasts after stimulation by growth

factors

o Osteoblastsy Bone-building cells that synthesize and secrete the organic matrix of boney Participate in the calcification of the organic matrixy Express cell surface receptors that bind to hormones (PTH, vitamin D, estrogen),

cytokines, and growth factors

o Osteocytesy Mature bone cells that function in the maintenance of bone matrixy Play an active role in releasing calcium into blood

o Osteoclastsy Cytokines (IL, TNF, CSFs) and growth factors crucial to osteoclast differentiationy Phagocytic cells responsible for the resorption of bone matrixy Releases calcium and phosphate from boney Increased by PTH, reduced by calcitonin & estrogen

3. Cartilage 3 typesa. Elastic cartilage allows flexibilityb. Hyaline cartilage at ends of bones; provides support against shockc. Fibrocartilage intermediate between dense connective tissue & hyaline cartilage

4. Joints 2 typesa) Diarthrodial joint

o Freely movable, although movements differo Fibrous joint capsule surrounds and supports the joint where ends of the bones meet


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o Joint capsule consists of an outer fibrous layer and an inner membrane (synovium) Synovium secretes synovial fluid which lubricates the joint Normal synovial fluid is clear or pale yellow, does not clot Well-developed vascular supply to the synovium

o Bony surfaces of joints are covered by articular cartilage Nourished by the diffusion of substances in the synovial fluid Regeneration of cartilage is slow

o Bursae prevent friction on a tendon Sacs formed by synovial membranes Occur in areas where pressure is exerted b/c bones are physically close together or

where a tendon runs over a bone

Bursitis inflammation of bursaeo Ex: hands, hip, knee, shoulder, elbow

b) Synarthrodial jointo Bones held together by connective tissue, cartilage, ligaments, etc.o Lack a joint cavity; immobileo Ex: skull bones, ribs, intervertebral disks

5. Tendons- Bundles of collagen fibers that attach the muscles to the bones; relatively inextensible- Transmit force generated by the contracting muscle to the bone and move the bone- Tendonitis inflammation of the tendon

6. Ligaments- Strong fibrous connections between bones- Allow and limit joint movement- Exposure to excess stress causes tearing, which is extremely painful and accompanied by swelling

Bone Formation and Metabolism

- Exercise & weight-bearing stimulates osteoblast activity- Diet Calcium deficiency during adolescence will result in bones less dense than optimum later in life.Most of the

calcium present in bones in an individuals lifetime is deposited before age 20.

- Hormonal Controlo Estrogen, testosterone, and growth hormone

y Enhance osteoblast activity & bone growtho Parathyroid Hormone (PTH)

y Prevents serum calcium levels from falling below normal physiologic concentrationsy Prevents serum phosphate level from rising above normal physiologic concentrationsy Regulated by negative feedback of increased serum calcium levelsy Functions:

y Initiate calcium & phosphate release from boney Conservation/reabsorption of calcium by the kidneysy Urinary excretion of phosphate

y Ensures that increased release of phosphate from bone during mobilization of calciumdoes not produce an elevation in serum phosphate levels

y Increases in calcium and phosphate levels crystallization in soft tissuesy Enhanced intestinal absorption of calcium through activation of vitamin D

o Calcitoniny Lowers blood calcium levelsy Inhibits the release of calcium from boney Major stimulus for calcitonin synthesis & release is an increase in serum calcium levelsy Functions:

y Causes calcium to be sequestered in bone cellsy Inhibits osteoclast activity


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y Reduces the renal tubular reabsorption of calcium & phosphateo Vitamin D

y Must be converted to physiologically active compoundsy Sources: intestinal absorption and skin productiony Increases intestinal absorption of calcium and promotes the actions ofPTHy Stimulated by PTH & prolactin, inhibited by calcitonin

Bone Remodeling

- Osteoblasts and osteoclasts act in coordination and are considered the functional unit of bone, as the basicmulcicellularunit.

- Processes of boen formation/resorption are tightly coupled, and their balance determines skeletal mass.- Once skeletal growth has attained its adult size after bone modeling, the breakdown/renewal of bone

responsible for skeletal maintenance is called bone remodeling.

- Mature bone is made up of osteons or units of concentric lamellae and the haversian canal they surround.- Length of one bone remodeling cycle is approximately 4 months.- Ideally, the replaced bone should equal the resorbed bone.- Control of bone metabolism and remodeling:

o RANKL expressed by osteoblasts & their precursors; necessary for osteoclast differentiation & functiono RANK receptor for RANKL; expressed on osteoclasts & their precursorso O

steoprotegerin (OPG

) inhibitor receptor forR

ANK

L; protects against bone losso RANKL + RANK osteoclast differentiation & proliferationo RANKL + OPG blocks the action ofRANKLo Dysregulation ofRANKL/RANK/OPG pathway plays a prominent role in pathogenesis of bone diseases

(i.e. osteoporosis, RA).

o Estrogen stimulate OPG production.o Glucocorticoid exposure, which can cause steroid osteoporosis, enhancesRANKL expression and

suppressionOPG levels.

- Bone remodeling cycle:o Bone Resorption

Osteoclasts remove organic (protein matrix) and inorganic (mineral) components Creats a tunnel-like space in the osteon Soluble factors released during resorption aid in recruitment of osteoblasts to the site

o Bone Formation Osteoblasts begin to deposit the organic matrix (osteoid) on the wall of the osteon canal. PTH has minimal or no direct effect on osteoclasts. Once the osteoblast receives appropriate signal, it releases RANKL

- Metabolic bone disorders have their origin in the bone remodeling process.


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DISORDERS OF THE MUSCULOSKELETAL SYSTEM

Joint Injuries

- Strainso Trauma to a muscle or tendon caused by mechanical overloadingo Usually occurring when it is stretched beyond normal limitso May involve tissue tears or ruptureso Inflammation occurs with injuryo Manifestations: pain, stiffness, swelling

- Sprainso Trauma to a joint, usually related to a ligament injury from abnormal or excessive movemento Leads to inflammation, swelling, and paino Manifestations: pain, rapid swelling, heat, disability, discoloration, limitation of function

- Healingo Accomplished by fibroblasts from the inner tendon sheath or from the loose connective tissue that

surrounds the tendon

o Capillaries supply the fibroblasts with materials needed to produce large amounts of collagen- Treatment

o Elevation of part followed by local application of coldo Compression helps reduce swelling and provides supporto Immobilization

Hip Fractures

- The hip is a ball and socket joint in which the femoral head articulates in the acetabulum- Major public health problem particularly in the elderly- Results in hospitalization, disability, and loss of independence- Incidence increases with age, higher in women than men, higher in white women than nonwhite women- Risk factors: excessive consumption of alcohol & caffeine, physical inactivity, low body weight, tall stature, use

of psychotropic drugs, residence in an institution, visual impairment, dementia, osteoporosis

- Most result from falls- Generally a fracture of the proximal femur- Location of a hip fracture is important in terms of blood flow to the femoral head, which receives its blood

supply from vessels that course proximally up the femoral neck

- Diagnosis: clinical findings, standard radiographs- Goal of treatment: return to preinjury level of function asap

Fractures

- Discontinuity of bone- Most common type of bone lesion- Occurs when more stress is placed on the bone than it is able to absorb- 3 categories: sudden injury, stress/fatigue fractures, pathologic fractures- Classification:

o Location proximal, midshaft, distalo Type

Communication with the external environmenty Compound (open) Fracture

o Bone fragments have broken through the skino Complicated by infection, osteomyelitis, delayed union, or nonunion

y Closed fracture Degree of break in continuity of bone

y Greenstick Fracture


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o Partial break in bone continuityo Seen in children

Character of the fracture piecesy Comminuted Fracture more than 2 piecesy Compression fracture in the vertebral body; involves 2 bones crushed togethery Impacted fracture fracture fragments are wedged together

o Direction/pattern of the fracture liney Transverse Fractures

o Caused by simple angular forceso Not likely to become displaced or lose its position after restoration to normal

anatomic position (reduction)

y Spiral Fractures & Oblique Fractureso Results from a twisting motion or torqueo Often unstable and may change position after reduction

- Effects of bone fracture:o Bone cells die when a bone breakso Bleeding occurs around the site and into the soft tissues surrounding the boneo Inflammatory reaction follows the break WBCs & mast cells accumulate increased blood flow to are

phagocytes and removal of dead cell debris begin fibrin clot (fracture hematoma) forms at the break

fibrin clot reabsorbed

o Osteoblastic activity immediately stimulates immature new bone (callus) formed new bone cells areslowly remodeled to form true bone

o Healing takes several weeks to monthso Healing can be delayed or impaired if the fracture hematoma or callus is disrupted before true bone is

formed, or if the new bone cells are disrupted during calcification and hardening

- Manifestations:o Pain, tenderness, swelling, loss of function, deformity of affected part, abnormal mobilityo 3 types of deformities in long bones: angulation, shortening, rotationo Temporary loss of nerve function area numb, muscles flaccid

- Complications: loss of skeletal continuity, injury from bone fragments, pressure from swelling and hemorrhage,involvement of nerve fibers, development of fat emboli

- Diagnosis: history, physical manifestations, x-ray, soft tissue injury- Treatment:

o Goals: reduction of fracture, immobilization, preservation & restoration of the function of injured parto Reduction and internal fixationo Immobilization (splints, casts, traction) and external fixation

Tractiony Achieves immobility, maintains alignment of the bone ends and reductiony A pulling force applied to an extremity while a counterforce pulls in the opp. directiony Goals:

o Correct and maintain the skeletal alignment of bones/jointso Reduce pressure on a joint surfaceo Correct/lessen/prevent deformities (i.e. contractures, dislocations)o Decrease muscle spasmo Immobilize the fracture site to promote healing

y Types:o Manual pull exerted by the handso Skin pulling force applied to skin and soft tissueo Skeletal

Pulling force applied directly to bone Use of pins, wires, tongs Can be used for long periods w/ large amounts of weight Used for fractures of femur, humerus, cervical spine


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o Limb-lengthening systemso Exercises, active ROM

Osteopenia

- Definition: Reduction in bone mass greater than expected for age, race, or sex- Causes:

o Decrease in bone formationo Inadequate bone mineralizationo Excessive bone deossification

Osteoporosis

Disease summary #79.

Ankylosing Spondylitis

- Chronic, systemic inflammatory disease of the joints of the axial skeleton manifested by pain and progressivestiffening of the spine.

- More common in men than in women- Description:

o Produces an inflammatory erosion of the sites where tendons and ligaments attach to boneo Begins with bilateral involvement of the sacroiliac joints smaller joints of posterior spineo Results in ultimate destruction of these joints with ankylosis or posterior fusion of the spineo Vertebrae take on a squared appearance and bone bridges fuse vertebral bodies togethero Progressive spinal changes usually follow an ascending patterno Large synovial joints (hips, knees, shoulders) may be involved occasionallyo Small peripheral joints not usually affected

- Etiology:o Genetic (90% of patients possessHLA-B27 antigen) and environmental factorso (Auto)Immune response

- Manifestations:o Usually begin in late adolescence or early adulthoodo Periods of exacerbations & remissions commono Persistent or intermittent low back paino Lumbosacral pina, discomfort in the buttocks and hp areaso Prolonged stiffness after periods of resto Walking or exercise may be needed to provide comforto Loss of motion in the spinal columno Lumbar lordosis loss of lumbar lordosis kyphosis of thoracic spine & extension of necko Acute anterior uveitiso Abnormal weight bearing degeneration/destruction of hipso Peripheral arthritiso Weight loss, fever, fatigueo Osteoporosiso Fusion of costovertebral joints reduced lung volume

- D

iagnosis: history,PE

, x-ray, elevatedE

SR

- Treatment:o Proper posture and positioningo Sleeping on a firm mattresso Muscle-strengthening exerciseso Heat applications or shower/batho Swimming

o Maintaining ideal body weighto NSAIDs to reduce inflammation, relieve

pain, and reduce muscle spasm

o DMARDso Anti-TNF-alpha therapies

Gout

- Crystal-induced arthropathy caused by monosodium urate deposition- Gout syndrome:


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o Acute gouty arthritis crystal deposition in jointso Tophi accumulation of crystalline deposits in articular surfaces, bones, soft tissue, cartilageo Gouty nephropathy / renal impairmento Uric acid kidney stones

- Primary gout used to designate cases in which the cause of the disorder is unknown or an inborn error inmetabolism and is characterized by hyperuricemia and gout.

- Secondary gout may result from treatment for lymphoma/leukemia or from chronic renal disease- Pathogenesis:

o Elevation of serum uric acid levelso Uric acid is the end product of purine metabolismo Causes:

Overproduction of purines Decreased salvage of free purine bases Augmented breakdown of nucleic acids as a result of cell turnover Decreased urinary excretion of uric acid

o Monosodium urate crystals precipitation in the joint inflammatory responseo Crystal deposition usually occurs in peripheral areas of the body where the temperatures are

cooloer

o Crystals are also chemotactic to leukocytes and activate complemento Inflammation causes destruction of the cartilage and subchondral boneo Repeated attacks of acute arthritis chronic arthritis formation of tophi

Most commonly in the synovium, olecranon bursa, Achilles tendon, subchondral bone,extensor surface of the forearm

Tophi doesnt appear until 10+ years after the first gout attack- Manifestations:

o Often begins at night and may be precipitated by excessive exercise, medications, foods, alcohol,dieting

o Onset of pain abrupt, redness and swelling observedo Attack may last for days or week

- Diagnosis: monosodium urate crystals in the synovial fluid or tissue sections, serum uric acid levels- Treatment:

o Goal: termination & prevention of acute attacks, correction of hyperuicemia, consequent inhibitionof further precipiation of sodium urate already in the tissues

o NSAIDs to reduce joint inflammationo Colchicine, corticosteroidso Treatment of hyperuricemia is lifelong (allopurinol, uricosuric drugs)

RHEUMATOID ARTHRITIS(RA)

Definition:

- chronic, systemic, noninfectious, progressive, inflammatory disease- primarily affects the connective tissue of the body, especially synovial membranes of multiple joints-

inflammation invades cartilage and surrounding tissue- characterized by synotivis (infection of synovium) and joint destruction- autoimmune disease, immune system recognizes native tissue as foreign and targets them for destruction- can also affect a wide variety of extra-articular tissue- affects mostly older women- one of the most debilitating of all forms in arthritis- shortened life span if untreated- many serious complications caused by drug therapy

Causes & Risk Factors:

- genetic


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- environment- hormonal factors (estrogen, pregnancy)- multifactorial disease- HLA-DR4, HLA-DR1 within MHC complexes on T-cells- Antigens from microbes or viruses are suspected of being factors

Cell Interactions that drive RA process:

- CD4 T cells responsible for initiating and sustaining RA- T cells inappropriately recognize auto-antigens (HLA-DR) on APCs activating ofT-Cell- Stimulating release of cytokines macrophages- T cells stimulate B cells B cells release rheumatoid factors immune complexes, more proinflammatory

cytokines that activate macrophages

- Pro-inflammatory cytokines: IL-1, TNF-alpha degrade cartilage & bone matrix- Remember: cytokines are both pro-inflammatory & anti-inflammatory, thus their homeostasis is no longer

balanced

- IL -1:o Activates monocytes (serum) and macrophages (tissue) inflammationo Induce fibroblast proliferation overgrowth of synovial tissueo Activates chondrocytes destructive proteolytic enzymes that break down cartilageo Stimulates osteoclasts (and prevents osteoblasts) bone resorption

- Major cell types: T cells, macrophages, fibroblasts, plasma cells, endothelium,DCs, neutrophils- Autoimmune and inflammatory responses both happening at the same time

IL-1B and TNF-alpha: pro-inflammatory cytokines in the rheumatoid joint

- increased concentrations of IL-1 and TNF act to stimulate production of each other o degrade cartilage matrixo increase osteoclastso increase adhesion molecules in endothelium

neutrophils migration y synovial fibroblasts release IL-8, prostaglandins, IL-6 (acute chronic infl)

- NSAIDs are trying to stop pro-inflammatory cytokines, pannus formation, bone destruction- COX-2 inhibitors (COX-2),NSAIDs (prostaglandin)- Both cytokines both upregulate COX-2, PGE, NO, IL-6 (activate innate immune system)- Both increase expression of adhesion molecules & cytokines & collagenases (chrondrocytes)- IL-1: TNF, osteoclasts, angiogenic factors- TNF: IL-1, programmed cell death

Clinical Manifestations:

- Chronic swelling and thickening in symmetric peripheral joints- ROM limited- Feet worse than hands- Rheumatoid nodules (usually located over bony prominences)- N

onarticular muscular structures- Systemic disease- Skin is thin and shiny- Insidious: malaise, stiffness, joint pain, swollen/warm/tender joints- Low grade fever, loss of appetite, fatigue, weight loss- Dryness of eye, mouth, mucus membranes (more advanced)

Diagnosis:

- Splenomagaly, adenopathy- Serum abnormalities

o Antibodies to cyclic citrullinated peptide (95%) definitive


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CCP is 50% sensitive in early part of diseaseo 25% ANA positiveo IgG and IgM and ESR higho Mild to moderate anemiao WBC normal or slightly elevated, leucopeniao Platelet counts are elevated

- X-rayso Earliest changes in wrist and feeto Narrowing of joint spaces & erosion- Knee joint fluid examinationo Exceeds 3.5ml in volumeo Translucent to opaque in clarity and yellow to opalescent in coloro High neutrophils and high macrophages flareo Glucose level that is less than the patients serum glucose concentration

- Morning stiffness, swelling, nodules, RF, x-raysNon-Pharmalogical Treatment:

- education- systemic rest- joint rest- exercise- heat & cold- assistive devices

- splints- weight loss- apheresis- dietary modifications- PT

Pharmacologic Treatment:

- Be aggressive in management esp. in early stages (2 year window)- NSAIDS

o COX-2 inhibitorso PPI, H2 blockers

- MTX (methytrexate?) not used by itself- TNF-alpha inhibitors very expensive- Hydroxychloroquine sulfate anti-malarial

agent b/c of anti-inflammatory activity; visual

loss is a complication

- Corticosteroids phase them out- Abatacept- Rituximab- Sulfasalazine & monocylcline- Leflunomide- Anakinra- Combination therapies- Surgery when not having results

There is a lot of complications with this disease. Joint deformities and systemic problems.Most common cause of death

is infection, GI disease, respiratory, or renal failure.Many are attributed to complications of therapy.

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45040396 Musculoskeletal System