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Glucocorticoids indirectly inhibit lipoxygenase and cycloxygenase.

-They inhibit the number of circulating lymphocytes by redistributing them into

lymphoid tissue.-They increase the number of circulating neutrophils.

-Use glucocorticoids if NSAIDs arent working.

DMARD-Hydroxychloroquine or sulfasalazine for mild RA.

-Methotrexate for moderate to severe RA.

-Give TNF-a and methotrexate if still no response.-Methotrexate has poor response for large amounts of coffee intake.

-Methotrexate can cause liver cirrhosis.

-Methotrexate cannot be given in pregnancy or with liver, lung or kidney disease, or with

alcohol use.-Leflunomide inhibits the synthesis of pyrimidines, preventing lymphocytes from going

from G1 to S phase.

-Leflunomide is teratogenic.-Hydrochloroquine is safe, can be used in pregnancy, and occasionally causes

retinopathy.

-Sulfasalazine is converted to sulfapyridine (active metabolite) and 5-aminosalicylic acid

(anti-inflammatory).-TNF-alpha inhibitors cause serious infections and cannot be given to patients with TB.

Gout-Colchicine inhibits the production of crystal-induced chemotactic factor. It also binds to

tubulin, preventing leukocytes from migrating and phagocytosing.

-Uricosuric drugs are used in the treatment of tophaceous gout. They can only be used in

low uric acid excreters. They remove uric acid by competing with it in glomerulusreuptake.

-Uricosuric drugs also increase the retention of other drugs, like penicillin.

-Uricosuric drugs can cause kidney stones and can precipitate acute gouty attacks wheninitially started on treatment.

-Allopurinol is used in tophaceous gout. It competes with xanthine oxidase. Use

allopurinol when uric acid excretion is over 600 mg/day and with renal problems.

Liposarcomas tend to occur in the retroperitoneum. Lipomas tend to occur in subcutaneoustissue.

Osteoid osteomas are painful at night and respond to aspirin. Osteoblastomas do not respond to

aspirin. Osteosarcomas are cut and resected.

Drugs for Rheumatoid Arthritis

-

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Aspirin has anti-pyretic, anti-inflammatory, and analgesic effect. Acetaminophen only has anti-

inflammatory and anti-pyretic effect.

Aspirin Anti-inflammatory

1. Gastric irritation *No gastric complications

Not for ulcer patients *Choice analgesic for ulcer patients2. Inhibits platelet aggregation *No effect on platelet aggregationNot preferred for hemophiliacs *It is preferred.

Not used prior to surgery *Can be used

* Used in prevention of coronary diseases Not useful3. Displaces drugs from albumin *No displacement of drugs from albumin

Anticoagulants and anticonvulsants

4. Hypersensitivity reaction *No hypersensitivity reaction

(especially in asthmatics)5. Uricosuric effects *No uricosuric effects

Not given to gout patients

6. Children -- Reye's syndrome *No association with Reye's syndrome7. Analgesic and antipyretic activities Equal in potency

*8. Good anti-inflammatory activity No anti-inflammatory activity

Rheumatic Arthritis

Ankylosing Sponylitis

Reactive Arthritis

-GU and GI are precipitating causes

-Cant see, cant pee, cant climb a tree

Psoriatic Arthritis

-Sausage digits

-DIP

Osteoarthritis

-Onchronosis of the joints and the spine-Arthritis in unusual places, asymmetrical

Limited systemic scleroderma

Diffuse systemic sclerodermaSystemic sclerosis sine scleroderma

Morphoea

Linear scleroderma

Introduction to Musculoskeletal SystemMusculoskeletal disorders cause:

-Physical and social impact-Direct financial impact on treatment

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-Indirect financial impact on loss of work and productivity

Back pain accounts for half of all musculoskeletal impairments.

Musculoskeletal impairments cause a disproportionate amount of healthcare usage, including

much hospitalization (2

nd

to cardiac). The most common reason for a physician visit ismusculoskeletal-related.

Osteoporosis is related to age and affects women far more commonly than men. Hip fractures

and vertebral fractures are direct consequences of osteoporosis.-Hip fractures have a 25% mortality rate and 3 times as many women as men have hip

fractures.

Human Limb DevelopmentThe trilaminar disc of the embryo has an ectoderm layer, mesoderm, and endoderm. Muscle is

developed exclusively from the mesoderm. The mesoderm develops into three layers: the

somites, intermediate mesoderm (kidneys), and lateral plate mesoderm (serous membranes).-One somite is formed for every pair of spinal nerves. Each somite has a sclerotome

(forms vertebrae) and a dermomyotome (forms dermis and muscles of trunk and limbs).

Dermomyotomes are initially pluripotent. They receive differentiation signals and form

muscles of three regions: deep back, trunk, limbs+superficial back. Myoblasts also comefrom dermomyotomes.

-There are 8 dermatomyotomes for the upper limbs and 10 for the lower limbs.

-The 5 somites next to the upper limb bud (C5-T1) will contribute to the adult upperlimb. The same occurs with the six segments at L2-S2.

Initially, palms and soles of feet face each other. In this orientation, there is a medial and a lateral

compartment through the limb. Dermatomyotomes migrate into these compartments. Lateralcompartment dermomyotomes become extension muscles while medial compartment

dermomyotomes become flexion muscles.

-Ventral primary rami (C5-T1 or L2-S3) grow into developing limb buds before dividinginto anterior or posterior divisions. These correspond to embryonic anterior and posterior

divisions of nerves.

-Ventral primary rami innervate trunk muscles.-Multinucleated muscle fibers are formed from mononucleated myoblasts.

Undifferentiated myoblasts can also form a synctial cell called a myotube. These

myotubes eventually become myofibrils.

-The hand paddle undergoes apoptosis between the fingers and the absence of this stepleads to webbed fingers as an adult.

Upper limbs rotate laterally while lower limbs rotate medially. As such, upper limbs have

anterior compartments in the front while lower limbs have anterior compartments in the back.-The extension of C6-C8 somites of the upper limb bud explains the pattern seen in the

adult.

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Meromelia refers to part of a limb missing while amelia represents an entire limb missing.

Phocomelia shows a flipper-like appendage instead of a true limb. Duplication of digits

(polydactyly) or limbs (supernumerary limb) are also possible. Digits can fuse.-24 to 36 days of development is critical for limb development. Thalidomide is a famous

teratogen.

-Rotation occurs at about 6 to 7 weeks of development.

Skeletal Muscle Growth and FunctionThe individual unit of a muscle is the myofiber. Each muscle cell is surrounded by basal lamina.

Endomysium surrounds each myofiber, perimysium separates muscle fascicles, and epimysiumforms dense irregular connective tissue at the muscle periphery.

-Nuclei are located at the periphery of myofibers in order to receive signals more

efficiently.

-Myofiber length is constant but cell diameter fluctuates with use.-Each myofiber contains dozens of myofibrils. Each myofibril is surrounded by

sarcoplasmic reticulum and transverse tubules. Each myofibril is composed of hundreds

of sarcomeres. Mitochondria are located between myofibrils while other organelles are atthe periphery.

Myoblasts require fibroblast growth factor to differentiate.

-Red muscle fibers contain much myoglobin and mitochondria, making them fatigueresistant and slow twitch. These are postural muscles.

-White muscle fibers are for fast twitch but fatigue quickly. These are for rapid eye

movements and hand muscles.-There is much intermingling between fast twitch and slow twitch muscle fibers.

Alpha-motor neurons are located in the ventral horn of the spinal cord. A motor unit consists of

the alpha motor unit and the muscle fibers it innervates.-Acetylcholine released by the motor neuron depolarizes sarcolemma and T-tubules. This

causes a release of calcium and T-tubules invaginate deeply into muscles, allowing

calcium to be released and triggering a shortening of the sarcomere.-A triad consists of a T-tubule and 2 terminal cisternae of the sarcoplasmic reticulum.

Each sarcomere has two triads.

Muscle spindles and Golgi tendon organs provide feedback to the nervous system, allowing for

proprioception. Muscle spindles are composed of intrafusal fibers (extrafusal fibers are normal

muscle cells), which is a specialized type of muscle fiber composed of sensory and muscle cells.

-Nuclear bag fibers can be static or dynamic while nuclear chain fibers can only be static.Nuclear bag fibers are sensed by II nerve fibers while nuclear chain fibers are sensed by

Ia fibers.

-A stretched muscle activates the nerve sensory fibers with the rate of change of muscle

stretch being detected by Ia fibers.-Spindle sensory nerves synapse on alpha motor neurons, causing contractions of

extrafusal fibers.

-Muscle spindles allow for reflex contraction.-Golgi tendon organs prevent excessively heavy loads.

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Gamma motor neurons modulate tension on intrafusal fibers in order to adjust the sensitivity of

the muscle spindle. Stimulation of dynamic gamma motor neurons increases tension, therebyincreasing sensitivity of dynamic bag fibers. The stimulation of static gamma motor neurons

decreases the sensitivity of nuclear bag fibers.

Golgi tendon organs monitor the force of muscle contraction. They use Ib sensory nerve endingsand are located where muscle connects to bone. This provides negative feedback to alpha motor

neurons. This causes excessively heavy loads to be dropped, preventing the muscle from injury.

Bone Development and GrowthBone is calcified extracellular matrix. Organic components consist of type I collagen,

fibronectin, GAGs, proteoglycans, and several specialized proteins (the mixture is collectively

called osteoid). Calcification occurs from the deposition of hydroxyapatite crystals. Theextracellular matrix is maintained by osteoblasts, osteocytes, and osteoclasts.

-Bone undergoes appositional growth while cartilage undergoes both appositional and

interstitial growth.-Mesenchymal cells lead to osteoblasts, which cause bone formation.

-Osteoclasts break down bone and are responsible for resorption.

Cartilage forms isogenous groups. It is surrounded by perichondrium, which is involved incartilage repair. Chondrocytes become hypertrophied before dying and becoming calcified.

Cartilage has type II collagen and hyaluronic acid. Bone has type I collagen.

Bone formation

-Intramembranous bone formation occurs when bone is formed directly in mesenchymal

tissue. This applies to flat bones like the calveria, scapula, and sternum. Because of the

mesenchymal cells, these tissues are highly vascularized. Mesenchymal cells differentiateto form a primary ossification center.

-Osteoblasts secrete osteoid. Osteoblasts then become surrounded and

differentiate into osteocytes after becoming surrounded by bone matrix. They thenform lacunae.

-Endochondral bone formation is the process by which cartilage is replaced by bone. This

occurs in most bones including the long and short bones, vertebrae, pelvis, and base ofthe skull.

-This process involves osteogenic cells, which differentiate into osteoblasts.

These osteoblasts then form a bone collar around the diaphysis. The chondrocytes

in the center of the diaphysis undergo apoptosis, forming a cavity known as theprimary ossification center.

-Osteoblasts deposit osteoid, progressively replacing the original calcified

cartilage. Mineralization then forms a trabecular network and the formation of the

marrow cavity. The ends of the bones remain cartilaginous.-Secondary ossification centers form at the epiphyses after birth.

-Proliferation and hypertrophy of chondrocytes at the epiphyses allows for growth

at the end of bones. Deposition on the outer surface allows for the increase indiameter.

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-The epiphyseal plate is responsible for growth and remains present at the end of long

bones in children. In adults, it is replaced by an epiphyseal line. The layers are the zone

of resting, zone of cell proliferation, zone of cell maturation and hypertrophy, zone ofcalcification, and zone of ossification (bone deposited here).

Fracture hematomas occur when blood vessels are transected or torn in the periosteum, osteon, ormedullary cavity. Fractures cause cell death and inflammation with migration of neutrophils.Bone fragments are gradually resorbed over time.

Eventually, the broken periosteum resolves into granulation tissue. A hyaline cartilage calluseventually forms where the fracture occurred. The bone formed is immature woven bone that

eventually becomes remodeled into secondary bone.

The synovial cavity is lined by synovial membrane, which is a layer of squamous-to-cuboidalepithelial cells. Synovial cavities contain type A phagocytic cells and type B fibroblast-like cells.

The bones are lined with hyaline cartilage, termed articular cartilage.

Spicules eventually form trabecular bone. Secondary ossification occurs at the epihphysis.

Gross Structure and Function of Skeletal MuscleMuscles produce movement but are also important in moving lymph and venous blood.

When the muscle isnt contracting, the fascia serves as connective tissue to hold the muscle in

place.

Skeletal muscle has the following subunits:

-Myofilaments of actin and myosin

-Myofibrils, consisting of bundled myofilaments-Muscle fibers, consisting of myofibrils; all myofilaments within the muscle fiber

contract simultaneously because of the motor end plate

The number of muscle fibers in a muscle is fixed during embryonic development due to the

fusion of embryonic muscle cells. The length of a muscle can increase as actin-myosin segments

are added to the ends of myofilaments. The increase in diameter occurs through the addition ofmyofilaments after birth.

-Muscles are electrically silent at rest.

-The amount of time a muscle remains contracted depends on the individual muscle.

-Muscles contract by asynchronous recruitment until the number of motor units needed togenerate the required force are recruited.

Motor nerves typically enter muscle bundled with an artery and a vein. Each motor nerve carries

somatomotor, somatosensory, and symp/post components. A motor unit is a single neuron in themotor nerve. Muscles with multiple orientations may only show contraction of the part of the

muscle most suited for the particular movement.

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In terms of posture, very few bones or joints are specialized for stability. In the upper limbs,

ligaments and connective tissue are primarily responsible for maintaining posture.

-The presence of ligaments and connective tissue allows for muscles to be completelysilent at rest.

Contraction of a muscle involves actin and myosin filaments sliding past each other with theamount of force generated correlating with the amount of overlap. As such, a stretched musclegenerates very little force.

-Shortening contraction

-Isometric contraction occurs when a muscle remains the same length during contraction.Isotonic contraction occurs when the amount of force remains the same but muscle length

changes.

-Lengthening contraction occurs when a muscle lengthens but is also actively contracting

-The maximum amount of force is determined by the cross-section of the muscle becausethis correlates to how many myofilaments are available. The amount of movement a

muscle can make is proportional to the length of a muscle.

-Paralleled muscle fibers are adapted to movement-Pennate muscle fibers are adapted for force and are angled in order to have a

much larger cross-sectional area.

Some muscles connect to bone directly through their fascia (endomysium, perimysium,epimysium). Others connect through tendons. Tendons decrease overall movement of parallel

fibered muscles. However, tendons decrease the overall amount of force generated by pennate

muscles because tendons displace myofilaments.-Tendons take up a small amount of space, are 100-200 times stronger than muscle, and

have a low metabolic cost.

Muscles can be a prime mover, an antagonist, a fixator (stabilizes joint position), or a synergist(prevents unwanted movement).

-Synergists are used when making a fist in order to keep the wrist straight and prevent the

wrist from flexing.

Musculoskeletal Tumors of Mesenchymal OriginVimentin is an intermediate filament common to mesenchymal tissue. Desmin and actin arecommon to skeletal and smooth muscle. S-100 protein is found in sarcomas.

Benign mesenchymal tumors are more common than malignant. Children usually get sarcomas

but adults usually get carcinomas.-Sarcomas are more common in males.

Fatty tumors

-Lipomas are the benign tumors of adipocytes.-Liposarcomas present in the fifties and sixties.

Tumor-like lesions-Nodular fasciitis is a reactive lesion to trauma but is not actually a sarcoma.

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-Myositis ossificans is a reactive ossifying condition with granulation tissue.

-Desmoid tumors

Fibrous tumors

-Fibrosarcoma

-Fibrohistiocytoma

Physiology of Skeletal MuscleSkeletons used for posture or movement have tendonous attachments at both ends of the muscle.

Individual muscle cells are separated by sarcolemma, which is plasma membrane.

Red fibers are Type I fibers. They have much mitochondria and much heme-containing proteins

such as hemoglobin, myoglobin, and cytochromes. White fibers are type II fibers.

Myosin is attached to the M-line. The myosin head requires ATP for binding. Myosin type I

(found in type I fibers) hydrolyzes ATP slowly while myosin type II hydrolyzes ATP quickly.These types of myosin heads correspond with being found in type I or type II fibers. Thick

filaments are made up of bundles of myosin tails.

Thin filaments are made of actin, tropomyosin, and troponin. Troponin is composed of troponinC, troponin I, and troponin T. Troponin C binds to calcium. Actin forms a filamentous structure

between two F-actin polymers. Tropomyosin covers the grooves in the actin polymers and covers

seven actin monomers.-Troponin C binds to calcium. Troponin complex undergoes a conformational change,

causing the movement of tropomyosin. Tropomyosin no longer covers actin, allowing

myosin to bind.

Myosin and actin slide past each other and bind, allowing for the generation of force. Myosin

hydrolyzes ATP when it is bound to actin and calcium facilitates the binding of myosin to actin.

The release of ADP and Pi is the rate-limiting step of muscle contraction.-Calcium binds to troponin C. Troponin C then undergoes a conformational change,

which stops it from binding actin.

The motor end plate contains a high concentration of nicotinic acetylcholine receptors. The

binding of acetylcholine causes a depolarization along the sarcolemma, which causes the influx

of calcium and eventually muscle contraction.

-Calcium is located intracellularly in the sarcoplasmic reticulum.-The action potential is conducted along transverse tubules.

-Ca-ATPase pumps calcium back into the sarcoplasmic reticulum.

-A mutation in the ryanodine receptor causes calcium to leak out of the sarcoplasmic

reticulum. This causes a large utilization of ATP as the cell tries to pump calcium back inand causes malignant hyperthermia since some of the energy from ATP hydrolysis is

converted to heat.

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Duchennes muscular dystrophy shows an absence of dystrophin while Beckers muscular

dystrophy shows a mutated form of dystrophin. Both diseases show an abnormal excitation-

contraction coupling in skeletal muscle.

Tension is the force exerted by a contracting muscle while the load is the force exerted on the

muscle by the object. Tension must be greater than the load for the muscle to shorten. Inresponse to electrical stimulation, calcium is only released in an all-or-nothing response.

Skeletal Muscle Plasticity and Adaptations to ExerciseMuscles have different properties in terms of red or white, fast or slow twitch, Type I or Type II,metabolic characteristics, and myosin ATPase. Type I fibers are slow twitch while Type II fibers

are fast twitch. Type IIa fibers show a fast contraction but are adapted to quickly utilizing either

aerobic or anaerobic energy sources. They are known as fast oxidative-glycolytic fibers. Type IIb

fibers have the greatest anaerobic potential and are known as fast glycolytic fibers.-Half of fibers are type I, a quarter are type IIa, and a quarter are type IIb

-Endurance athletes and weightlifters show a switch from type IIb to type IIa fibers with

a proportional increase in mitochondria and a greater capacity to use the citric acid cycleand oxidative metabolism. The number of type I and type II fibers are fixed but the

proportion of myofilaments can be changed if one type of fiber is stimulated more than

the other.

-Aging shows a decrease in the amount of type II fibers, which accompanies a lack ofstrength.

-Strength training shows gains in function through neuromuscular adaptation at first.

Afterwards, muscle hypertrophy occurs and accounts for increases in strength gains.-Neuromuscular adaptation shows increased motor unit recruitment, increased

firing frequency of motor units, increased motor unit synchronization, increased

activation of synergist muscles, and increased inhibition of antagonist muscles.

-Myonuclei are important for providing proteins to a cell and are responsible forcontrolling a certain area of the myofiber. As such, larger muscles gain more myonuclei

so that the amount of myonuclei to cell area remains constant. Myonuclei are added

through satellite cells.-Strength training causes an increase of strength by increasing the cross-sectional area of

the muscle. Whether or not the proportion of type I to type II fibers changes is unknown.

-The amount of myofilaments increases but total mitochondrial volume remainsthe same. Thus, the ratio of mitochondria to muscle filaments actually decreases.

This increases the fibers anaerobic strength but reduces the fibers aerobic

capabilities.

-Capillary volume also remains the same.-Endurance training improves cardiovascular health by increasing the number of

mitochondria and capillary volume.

Delayed muscle onset soreness results from a combination of microscopic tears, fluid retention inthe surrounding tissue, muscle spasms, tearing of the muscles connective tissue harness, acute

inflammation, and cytotoxic damage from calcium influx. Eccentric muscle contraction (active

lengthening, such as running downhill) leads to greater muscle damage.-Progressive resistance training must be used by increasing resistance used to train.

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-Androgens are effective in increasing muscle mass by increasing protein synthesis and

decreasing degradation.

-Myostatin regulates muscle cell proliferation and is elevated in patients with musclewasting diseases.

Rheumatoid Arthritis and the SpondyloarthropathiesRheumatoid arthritis is a chronic, inflammatory systemic disease that largely targets synovialjoints. The disease typically presents symmetrically and affects the small joints of the hands and

feet (wrists and MCPs and PIPs but not DIPs), the wrists, knees, ankles, shoulders, hips, and

other synovial joints as well (cervical spine is commonly affected).-Joint pain typically presents as morning stiffness and fatigue. The duration of morning

stiffness is indicative of the progression of rheumatoid arthritis.

-Rheumatoid arthritis preferentially affects women. It affects joints but there are also

many extraarticular manifestations of the disease.-There is a peak in prevalence in the 20s and 30s and another peak in the 50s.

-HLA-DR4 (prevalent in whites) and HLA-DRB1 are genes associated with rheumatoid

arthritis.-Rheumatology is the study of joints. Rheumatism is fibromyalgia.

The pathogenesis of rheumatoid arthritis shows synovial inflammation and proliferation with

humoral and cellular immune responses that result in tissue damage. Specifically, activated B-cells and T-cells can be found in the synovium and this leads to the loss of hyaline cartilage as

well as bone erosion. The triggering antigen is unknown.

-Rheumatoid Factor is an antibody that targets the Fc region of IgG antibodies. It ispositive in most people with rheumatic arthritis and other autoimmune diseases such as

Sjogrens Syndrome, MCTD, and cryoglobulinemia.

-False positives for rheumatoid factor occur in arthralgias (viral infection, liver

disease, endocarditis) and has a low positive predictive value in these cases.-Detection of anti-citrullinated cyclic protein is specific to rheumatoid arthritis

and is found in the synovium.

-IL-1beta and tumor necrosis factor alpha are important cytokines.-Osteoclast differentiating factor causes macrophage differentiation into osteoclasts,

which leads to bone erosion.

-During pathology, synovial fluid increases in volume and in cell number withlymphocytes predominating early on. These lymphocytes form immune complexes with

IgG and IgM antibodies as well as complement activation (C5a attracts more leukocytes).

-Deposition into articular cartilage makes it difficult to clear immune complexes.

Articular cartilage is composed of collagen and matrix proteoglycans. Cartilage is degraded by

synovial and neutrophil collagenases and proteoglycans are degraded by proteases. Joint capsules

and tendons become degraded in a similar fashion.

Rheumatoid arthritis causes joint swelling from synovial thickening and increased synovial fluid

volume, increases temperature and erythema over inflamed joints, causes pain and stiffness

(particularly in the morning), and decreases the range of motion. The joint also contracts fromfibrosis.

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-The stereotypical presentation of rheumatic arthritis is joint pain in the wrists and

fingers, specifically in the joint capsule. Eventually, the disease can cause deformities in

the fingers.

Early rheumatoid arthritis is characterized by vague symptoms with variable aching and

inflammation and with little or no synovial swelling.

Tissue damage causes joint deformities, tendon ruptures, reduction in cartilage thickness, bone

erosion, and secondary osteoarthritis. Sometimes, joint fusion can occur.

-Osteopenia and osteoporosis are also symptoms of rheumatoid arthritis-Anemia of chronic disease results from rheumatoid arthritis.

-Muscle atrophy occurs from disuse as well as to rheumatoid myopathy.

-Rheumatoid nodules can form and signify a more severe disease.

-Circulating immune complexes can also be seen in the blood with some amount ofimmune complex deposition occurring in organs. This can result in vasculitis and

infarction.

-Peripheral nerve compression can result in neurologic involvement.-Sjogrens syndrome can also result.

-Type I rheumatoid arthritis is self-limited with one flare-up and no remission, type II is

intermediate, and type III is severe

Juvenile idiopathic arthritis occurs before the age of 18. There can be iridocyclitis (inflammation

of anterior chamber) but granulomas typically do not form.

-The stereotypical presentation can be polyarticular, oligoarticular, or monoarticular. Itcan also be systemic or acute febrile.

-Laboratory tests for erythrocyte sedimentation rate (anemic, low iron in red cells?).

Synovial fluid analysis for rheumatoid factor works in adults but not as often in children.

Anti-CCP is positive in adults as well. Radiographs allow for evaluation of damage fromrheumatoid arthritis.

-Eventually, joint contractures can occur along with muscle weakess, muscle loss, and

osteoporosis.

Medications can be NSAIDs and disease-modifying anti-rheumatic drugs, which reduce

inflammation and pain and prevent remission.-Drugs that target signaling for inflammation and tissue damage are also effective.

-Rehabilitation and orthopedic surgery can also be considered.

-Immunosuppressive drugs are also effective.

HLA-B27 arthritides differ from rheumatoid arthritis in that they show much spinal involvement,

are usually asymmetrical, affect men more often, and usually lack rheumatoid factor.

Seronegative arthritides are ankylosing spondylitis, reactive arthritis, psoriatic arthritis,enteropathic spondylitis, and juvenile spondyloarthropathy.

-Clinical manifestations show spinal features and peripheral arthritis (hips, shoulders)

instead of in the fingers, enthesopathy (tendon involvement), and extraarticular features.-There are genetic factors involved.

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-There is an association with HLA-B27, particularly ankylosing spondylitis (90%) and

reactive arthritis (80%).

-The stereotypical presentation is inflammatory back pain and peripheral arthritis.-Diagnosis is made through laboratory data on HLA-B27 and CRP, MRI or radiography,

and physical examination.

Ankylosing spondylitis is a chronic inflammatory systemic disease that targets the sacroiliacjoints and the cartilaginous and synovial joints of the spine.

-Patients are predominantly HLA-B27 positive.

-Ankylosing spondylitis typically occurs in young men (9:1).-Presentation shows low back pain and stiffness lasting over 3 months.

-Inflammation starts at the sacroiliac joints and move upwards. Eventually, ankylosis

(fusion) occurs at the paraspinal ligaments along with ossification. This leads to stiff

posture and stiff gait.-There is reduced chest expansion from intercostal involvement.

-Preipheral arthritis occurs in most patients over time.

-Fusion of the sacroiliac joints is also a common complaint.

Reactive arthritis shows asymmetric arthritis. It usually affects large joints like the hips and

knees. It is precipitated by genitourinary or gastrointestinal infections. It can result in repeated

attacks over many years.-Cant see, cant pee, cant climb a tree

Psoriatic arthritis commonly occurs with psoriasis. It can affect the DIP joints and can result innail pitting. It results in sausage digits and nail pitting.

Treatment of spondyloarthropathies involves treatment of symptoms, NSAIDs, DMARDS, and

TNF-alpha blockers.

Reconstructive surgery for rheumatoid arthritis is indicated when there is a loss of function or

unrelenting pain.

JIA with eye complications usually presents as pauciarticular. Oligoarticular JIA is associated

with antinuclear antibody but systemic JIA is associated with HLA-B27.

Osteoarthritis for the Medical StudentOsteoarthritis is the most common articular disease worldwide. Primary osteoarthritis affects the

small joints in the hands, the cervical and lumbar spine, hips and knees, and joints in the feet.Secondary osteoarthritis can affect any joint and can be caused from sports injuries. This can be

due to trauma, structural abnormalities, meniscectomy, congenital abnormalities, and infection.

Secondary osteoarthritis affects unusual joint locations and in younger patients.

-The cost of not treating rheumatoid arthritis is 30 times that of treating it.-Sepsis in the knee can lead to joint damage and so can plant thorns.

-Hypermobility syndromes get osteoarthritis and heart murmurs.

-Charcot joints result from degenerative neurological conditions.-Metabolic disorders like acromegaly, alkaptonuria, gout, and can cause osteoarthritis

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-Onchronosis causes a buildup in dark pigment in joints and the spine.

-Obesity causes osteoarthritis due to increased pressure on the knees.

-Secondary osteoarthritis can result from repeated hemorrhage from hemophilia,Marfans syndrome, and bleeding disorders.

-Osteoarthritis and osteoporosis have an inverse relationship.

-Osteoarthritis shows cartilage loss, subchondral thickening, and marginal osteophytes.-Osteoarthritis is managed with acetaminophen and NSAIDs.

Musculoskeletal Pharmacology

Drugs for rheumatoid arthritis target the following areas:-Anti-inflammatory drugs that treat symptoms and have a quick therapeutic response but

do not change or modify the disease process.

-Disease-modifying drugs that change the disease process.

NSAIDs block cyclo-oxygenase, which inhibits inflammation.

Glucocorticoids have anti-inflammatory and immunosuppressive actions. They havetranscriptional regulation in the nucleus and increase the expression of lipocortins, which blocks

phospholipase A2.

-UnlikeNSAIDs, glucocrticoids do not directly inhibit cyclooxygenase. Instead,

glucocorticoids affect transcriptional regulation.-Cortisol, cortisone, and prednisone are glucocorticoids.

-These are used for pain reliefand are used when NSAIDs are contraindicated (asthma).

-Since glucocorticoids suppress the immune system, they cause increased susceptibilityto infection.

-Fluid retention is caused sodium retention. Triamcinolone, dexamethasone, and

betamethasone do not have this property.

DMARDs commonly used are hydroxychloroquine, sulfasalazine

-Methotrexate acts as an anti-inflammatory and immunosuppressant. Methotrexate blocks

the production of adenosine.-Leflunomide has a high half-life and becomes an active M1 metabolite. It inhibits

dyhydroorotate dehydrogenase, which blocks pyrimidine synthesis. Leflunomide is

category X teratogenic.-Hydroxychloroquine inhibits DNA and RNA synthesis.

-Sulfasalazine is metabolized by bacteria and blocks TNF-alpha. It cannot be used by

patients with sulfa allergies. However, it also causes folate deficiency and can lead to

neural tube defects.-TNF-alpha inhibitors bind TNF-alpha and stop disease progression. It can be given with

methotrexate.

-Methotrexate and leflunomide have synergistic actions because they block purine and

pyrimidine synthesis, respectively.

Pathogenesis of Systemic Lupus ErythematosusSystemic lupus erythematous occurs when T-cells lose self-tolerance and display altered immunehomeostasis.

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-This can result if autoreactive T-cells escape destruction in the thymus (failure of clonal

deletion), if clonal anergy fails so that only one signal is required to activate the cell, if

there is decreased apoptosis, and if T-regs have impaired function in blocking T-cellproliferation or blocking antigen-presenting cells.

-Systemic lupus also results from the spontaneous activation of B-cells, particularly if

they express nuclearauto-antigens. The disease does not show abnormal cell-mediatedimmunity.-Interferon-alpha stimulates antigen-presenting cells.

Mutations in Foxp3 lead to the disease, IPEX, and Foxp3 is necessary for T-regs to functionappropriately.

Genetic factors involve HLA-D2 and low TNF-alpha and mutations in the FcR region. Genetic

factors typically cause T-cell defects such as hyper-responsiveness and resistance to toleranceinduction or B-cell abnormalities such as hyper-responsiveness and producing nuclear

autoantigens.

Environmental triggers can be infectious agents, sunlight (UV radiation), and drugs that activate

self-reactive T-cells by inhibiting DNA methylation.

Therapies include histone epitopes in order to desensitize antigen-presenting cells and generatingT-regs.

Systemic Lupus ErythematosusSystemic lupus erythematous is a rheumatoid disorder that affects primarily young women of

child-bearing age. Thebutterfly rash is pathognomonic.

Pathology includes inflammatory changes, blood vessel abnormalities, and immune complexdeposition in organs. Patients also become photosensitive.

-The most common presenting feature is joint and musculoskeletal involvement. The

pattern of joint involvement is very similar to that of rheumatoid arthritis and also resultsfrom inflammation of the synovial membrane. However, the inflammation is far less

intense such that joint deformity rarely occurs.

-SLE is less common in white people. African Americans, Hispanics, and Asians haveincreased rates.

-Anemia can result from auto-antibodies targeted against red blood cells.

-Leukopenia also results from the presence of auto-antibodies.

-Thrombocytopenia also results from the presence of auto-antibodies.-The presence of lupus anticoagulant is associated with hypercoagulability. This leads to

the condition known as antiphospholipid antibody syndrome.

-There can also be respiratory and cardiac involvement such that radiography shows an

increased heart shadow due to pericardial effusion.-Libman Sacks endocarditis occurs from vegetation on heart valves.

-Neuropsychiatric lupus shows involvement in both the peripheral nervous system and

central nervous system.

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-Renal disease is the major cause of morbidity and mortality from systemic lupus

erythematous. This results from the deposition of immunoglobulins and complement

factors in the glomeruli.-Antinuclear antibodies are positive but this test is not definitive for systemic lupus

erythematosus.

Discoid lupus erythematosus is localized and usually shows skin lesions at the ears, face, andscalp. There is typically no other organ involvement.

Antinuclear antibodies are the most characteristic serologic finding of systemic lupuserythematous.

-Antinuclear antibodies are not cytotoxic and fetuses of mothers of the disease do not

have health problems.

-Antinuclear antibodies deposit in the glomeruli. Circulating DNA becomes an antigenand forms immune complexes at the glomerulus. This can occur if defects in apoptosis

are present such that antigen-presenting cells pick up DNA and present them as antigens,

causing lymphocytes to produce anti-dsDNA antibodies.-Immune complexes that deposit in the glomeruli also activate the complement system

and cytotoxic factors then cause cell injury.

-Failing to clear immune complexes in the glomeruli only compounds the problem.

Neonatal lupus syndrome results when infants born to systemic lupus erythematous mothers

present with lupus symptoms (photosensitive skin rash, congenital heart block) a few weeks after

birth. However, the condition is benign and self-limited with the exception of heart block, whichwill persist.

-Heart block occurs because of maternal antibodies that cross the placenta and attack fetal

conduction tissues.

SclerodermaScleroderma is thickened hardened skin.

-Limited systemic sclerosis shows CREST: calcinosis, Raynauds, esophagealdysfunction (muscle paralysis, no peristalsis), sclerodactyly, telangtasia. There tends to

be distal limbs affected more than the hands and chest and pulmonary hypertension is

typical.-These are all cutaneous findings (plus esophagus).

-Diffuse systemic sclerosis shows early extra-cutaneous manifestations. The mouth

shows contracture. The skin shows edema, induration, then atrophy. Swelling occurs in

the entire finger rather than just a part of the finger as in rheumatic arthritis.-These are extra-cutaneous findings.

-Systemic sclerosis sine scleroderma shows no skin findings. Instead, there are

musculoskeletal, gastrointestinal (esophagus becomes impaired and prone to GERD,

stomach delays gastric emptying, small intestine shows atony, large intestine showsinfarction and pseudo-diverticula), pulmonary, cardiovascular, and renal symptoms.

Arthritis in joints is common along with tendon rubs and muscular atrophy.

-Watermelon stomach and pseudo-diverticula are common.-GI symptoms result because smooth muscle becomes replaced with collagen.

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-Pulmonary system shows interstitial fibrosis.

-Renal insufficiency leads to scleroderma renal crises. The vasculature of the

kidney undergoes fibrinoid necrosis, which is a vascular problem.-These changes show the replacement of smooth muscle with collagen.

Localized scleroderma-Morphoea shows plaque-like scleroderma and is most common.-Linear scleroderma is the most common type in children and shows longitudinal

lesions on limbs. It can cause joint contractures and muscle atrophy.

Scleroderma is caused by immunologic activity and vascular changes. There are an increased

number of activated fibrogenic fibroblasts.

Pharmacology of Muscle RelaxantsSpasticity shows flexor muscle spasms, an elevated tonic stretch reflex, muscle weakness, and

can result from cerebral palsy or stroke or multiple sclerosis. Spasticity results from upper motor

neuron lesions and shows hyperexcitability.

GABA and glycine agonists

-Diazepam and other benzodiazepines are GABA-A agonists. They are muscle relaxants

that also cause sedation.-Baclofen is a GABA-B agonist that acts presynaptically by opening potassium channels

and closing chloride channels.

-Progabide is a GABA-A and GABA-B agonist.-Gabapentin is an analogue of GABA that has no activity on GABA receptors although it

blocks calcium channels.

-Pregabalin is similar.

-Glycine is not a GABA agonist but it blocks spasticity in the dorsal root ganglion.

Other drugs

-Tizantidine is related to clonidine and it increases presynaptic and postsynapticinhibition. However, it also causes drowsiness, hypotension, and dry mouth.

-Riluzole is a glutamate release blocker that only treats ALS.

-Dantrolene blocks the release of calcium from the sarcoplasmic reticulum in skeletalmuscle but it spares cardiac muscle and smooth muscle. However, it also induces muscle

weakness and sedation. It is useful for treating malignant hyperthermia.

-Only peripherally acting one.

-Botulinum toxin blocks the release of acetylcholine.-Cyclobenzaprine produces a serotonergic block on the dorsal horn but also blocks 5HT2

receptors, leading to hallucination and sedation.

Inflammatory MyopathiesPolymyositis has an insidious onset with systemic symptoms. There is typically involvement of

the shoulder, pelvic girdle, and neck muscles. Occasionally, the pharyngeal muscles become

involved. Pulmonary involvement shows interstitial fibrosis but cardiac involvement is rare.

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-Biopsy shows muscle fibers in states of necrosis and regeneration. There are many

CD8+ cells and fibrous tissue will replace muscle fibers over time.

-Dermatomyositis does not show muscle fibers replaced with collagen. There are alsoCD4+ cells.

-Inclusion body myositis shows necrosis similar to poliomyositis. There are inclusion

bodies.-Polymyositis shows CD8+ cells while dermatomyositis shows CD4+ cells.

Diagnosis requires proximal muscle weakness, elevated muscle enzymes, myopathic EMG

changes, and muscle biopsy showing inflammation. Dermatomyositis will also show skin rash.

Inflammatory muscle diseases classically show increased insertional activity, fibrillations, and

sharp positive waves; spontaneous, bizarre high-frequency discharges; and polyphasic short

duration, low amplitude motor unit potentials.-MRI imaging is better than CT and ultrasound.

Dermatomyositis shows polymyositis findings as well as cutaneous changes. Amyopathicdermatomyositis is dermatomyositis without muscle findings.

-Histology shows mononuclear cell infiltrates and fiber atrophy.

Juvenile dermatomyositis shows dermatomyositis findings but also includes vasculitis,calcification, and lipodystrophy. Most cases resolve by adulthood with early treatment showing

better outcomes.

Antisynthetase syndromes show anti-Jo1 antibodies and inflammatory myositis with interstitial

lung disease, Raynauds, fever, and mechanics hands.

Inclusion body myositis occurs in people over 50 and shows asymmetric involvement with eitherproximal or distal muscles.

FibromyalgiaFibromyalgia causes fatigue (sleep disturbance, no stage 4 sleep disturbance) and diffuse,

chronic muscle pain. There is severe sleep disturbance, stiffness, headaches, irritable bowel and

bladder syndrome, and depression.-Diagnosis involves widespread pain for over 3 months and 11/18 points of pain.

-Sleep disturbance involves non-restorative sleep that leads to fatigue, cognitive

difficulties, and other stress-related symptoms.

-Sensory stimuli is often misinterpreted as pain. This may be due to increased levels ofexcitatory neurotransmitters such as glutamate and substance P. Additionally, tactile

allodynia may result from central sensitization beyond an area of injury.

-Fibromyalgia can occur as a result of other disorders such as post-Lyme disease

infection. In this case, treating fibromyalgia is actually more important than giving thepatient more antibiotics. Ehlers-Danlos syndrome and Lupus syndrome also result in

fibromyalgia.

-In older patients, polymyalgia rheumatica results in aching in proximal muscles but notspecific muscle weakness.

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-Medications can cause fibromyalgia.

-Being on call causes symptoms similar to fibromyalgia.

Fibromyalgia can be managed with regular exercise. Antidepressants are also effective because

they cause deeper sleep.

Crystal-Induced ArthropathiesCrystal-induced arthropathies occur from the deposition of crystalline substances in articular and

periarticular tissues. These crystals are typically monosodium urate, calcium pyrophosphate, and

apatite crystals.-Crystal inflammation stimulates the release of inflammatory mediators such as

arachadonic acid, IL-1, IL-6, IL-8, and TNF.

-Gout results from an altered metabolism of uric acid and shows deposition of

monosodium urate from supersaturated extracellular fluids.-Diagnosis of crystals involves a microscope to determine a characteristic birefringence.

-Monosodium urate crystals are yellow when parallel and have negative

birefringence.-Calcium pyrophosphate crystals are yellow when perpendicular and have

positive birefringence.

-Crystals can cause the release of inflammatory mediators from phagocytes and

synoviocytes through non-specific signal transduction pathways.-Gout shows an overproduction of purines (and uric acid as waste product) and faulty

renal excretion.

-Hyperuricemia may be present for many years before gout occurs.-Acute arthritis presents in clinical gout and presents with a sudden onset of severe pain

that lasts for days or weeks. The pain is precipitated by sodium urate crystals.

-The first MTP joint is typically affected first. This is thought to occur because of cooler

peripheral areas and because of walking.-Gout can also present with systemic symptoms such as fever and chills.

-Tophaceous gout results from 10 or more years of gout and there are no longer any pain-

free periods. Eventually, tophi may become deposited in unusual places such as brain andspinal cord.

-Gout is typically asymmetric and oligoarticular.

Gout is diagnosed by seeing crystals. Hyperuricemia may be present in patients without gout and

as such, it is not reliable as a diagnostic criterion. Additionally, elevated uric acid is typically

present in gout patients but not always.

-Synovial joint fluid in gout shows high WBCs and shows moderate inflammation.-Eventually, gout causes bone erosions from the joint surfaces and causes hypertrophic

areas as well. Additionally, dense soft tissue is present at the joints.

Treatment of acute attacks involves colchicines,NSAIDs, and corticosteroids. Chronic cases ofgout use uricosuric drugs and allopurinol and xanthrin oxidase inhibitors.

-Xanthrin oxidase inhibitors are used in urate overproducers, when tophi are already

present, nephorlithiasis (kidney stones), or if excessive turnover is present.

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Pseudogout manifests with crystals of calcium pyrophosphate deposits. This condition can

mimic gout, septic arthritis, or rheumatoid arthritis.

-There are typically acute attacks and the first attack is typically in the knee joint.However, all joints can become affected.

-A low grade fever is typical with acute attacks.

-Chronic attacks can present with osteoarthritis of the knees as well as rheumaticsymptoms in multiple joints.-This disease is also associated with many diseases, including hyperparathyroidism and

hemochromatosis.

-Chondrocalcinosis shows an accumulation of deposits on the hyaline cartilaginoussurfaces in the joints.

-Treatment of associated conditions does not remove crystals and there is currently no

way to remove crystals.

-Basic calcium phosphates cause Milwaukee shoulder and rotator cuff disease. Calcinosiscan occur in periarticular areas in patients with scleroderma.

-Diagnosis involves x-rays of soft tissue that reveals calcification because crystals cannot

be confirmed with a microscope (too small).

Pharmacology of GoutGout is caused by recurrent hyperuricemia and arthritis accompanied by severe pain. The

pathogenesis involved crystal-induced chemotactic factor LTB4. Drugs that relieve inflammationcan either treat acute attacks of gout (colchicines, NSAIDs) or long-term therapy management

of gout (uricosuric agents, decrease production of uric acid).

-Colchicine inhibits the production of crystal-induced chemotactic factor. It binds totubulin in order to prevent polymerization.

-NSAIDs blockleukotrienes (important in gout) and cyclooxygenases (important in

RA). Thus, the mechanisms of action by NSAIDs are different in RA and gout despite

being the same class of drugs.-Indomethacin

-Uricosuric agents are used in tophaceous gout (chronic form). They compete with the

organic acid transport carrier, preventing the active reabsorption of uric acid.-Allopurinol is used to treat tophaceous gout. It is a xanthine oxidase inhibitor

Overview of Musculoskeletal RadiologyAlways get two views of the same site.

X-rays are good in diagnosing fractures, bony lesions, dislocations, erosions, soft tissue edema,

and effusion. However, x-rays are not good at showing soft tissue. Additionally, x-rays causeionizing radiation so it is necessary to protect the patient and to avoid repeated examinations.

CTs shoot a thin fan beam of x-rays along a single plane of the patient. This gives significant

multiple plane visualization and minute details within slices (imaging hamate) that allows for 3Dreconstruction.

-Advantages include matrix mineralization.

-Disadvantages are adverse reactions to IV contrast agent and the dose of x-rays used,especially in children.

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-CT scans are useful for arthrograms and image guided injections.

MRI is excellent for soft-tissue imaging.-MRI is useful for imaging cartilage, ligaments, and soft tissue masses.

-T1 and anatomy.

-T2 and pathology.-PD is cartilage.-MRI cannot detect subtle calcifications but can detect avulsions and subtle calcific

tendonitis.

Ultrasound is useful for diagnosing tumoral calcinosis. This shows calcium sedimentation but

this diagnosis can also be made through x-ray.

Chronic osteomyelitis can be seen through imaging. So can chondrocalcinosis.

X-rays are the first modality used and is good for the differential diagnosis of osseous lesions. It

can image joint space narrowing and erosions but is not good with soft tissue.

CT can image matrix mineralization

Non-Narcotic AnalgesicsNon-narcotics act locally to block pain, reduce mild to moderate pain, and have no potential for

addiction or tolerance. Aspirin, profens, and acetaminophen are examples of non-narcotic

analgesics. In contrast, narcotic analgesics act in the CNS, control moderate to severe pain, andshow addiction and tolerance. Opioids are examples of narcotic analgesics.

-Aspirin has direct effects and is not a prodrug. Its pKa is 3.4, plasma pH is 7.4, and urine pH is

5.4. This means theres actually a gradient for the unionized form to get absorbed back into theplasma. Aspirin works against chronic postoperative pain or pain arising from inflammation

because it inhibits the production of prostaglandins. Aspirin irreversibly blocks cyclooxygenase,

unlike NSAIDs that reversibly block cyclooxygenase. Aspirin also elevates body temperaturebecause it inhibits the production of IL-1.

-Aspirin can uncouple oxidative phosphorylation, which means oxygen is consumed

more rapidly to compensate. This leads to hyperventilation, which can producerespiratory alkalosis and also causes the generation of lactic acid which can lead to

metabolic acidosis.

-These can both be treated by urine alkalization in order to prevent the unionized

form from returning to plasma.-Aspirin is correlated with Reyes syndrome

-Acetaminophen is the active metabolite of acetanilid and phenacetin. Acetaminophen is rapidly

absorbed. However, it has no anti-inflammatory activity because it only acts in the CNS.

Artificial Joint Replacements

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Surgical treatment for arthritis is considered when pain is unrelieved by medication, when

arthritis interrupts sleep, when arthritis hinders the ability to perform daily activities, and when it

reduces quality of life.-Surgery can mean osteotomy, debridement, arthrodesis, and arthroplasty

-Osteotomy is used for joint malalignment and is joint sparing. It may prevent the

need for joint replacement, though not indefinitely. Osteotomy is usuallyindicated for young and active patients. However, it requires some articularcartilage and should be limited to one compartment of the knee.

-Osteotomy of the hip can be used in acetabular dysplasia and for

congenital deformity of the proximal femur.-Osteotomy of the knee requires a stable knee.

-Osteotomy cuts and realigns bone, corrects joint realignment, and is joint

sparing.

-Debridement removes inflamed synovium and irregular articular surfaces.-Debridement is better if it addresses specific lesions.

-Arthrodesis is the fusion of joints and prevents pain by preventing motion. It is

commonly done on the hand, wrist, spine, foot, and ankle. However, it putsincreased stress on adjacent joints and requires the mobility of nearby joints to

compensate.

-Hip arthrodesis fuses in a slight flexion and is compensated by mobility

of the spine, knee, and opposite hip.-Knee arthrodesis is done for severe and uncontrollable septic arthritis.

The knee is fixed in a slight flexion and a slight valgus. It is rarely done.

-Arthrodesis eliminates motion at the joint.-Arthroplasty replaces the joint surface with something else. Total joint

arthroplasty can be done for pain relief, function, and motion but there is potential

for wear, loosening, and infection.

-Total joint replacement cannot be done with active infection.-It also cannot be done with morbid obesity, with progressive

neurological disease (like Parkinsons), and in people under 45

years of age.

Soft-tissue structures and unsatisfactory bone structures may not require orthopedic surgery.

Additionally, morbid obesity, neuropathic joints, progressive neurological diseases, IV drug use,non-compliance, non-ambulator, and young age are all contraindications.

Hip surface replacement uses a big head to reduce the risk of dislocation and uses metal/metal

articulation. It is also bone sparing on the femoral side. However, there is risk of femoral neckfracture in older women and avascular necrosis.

-Hip surface replacement has a lower risk of dislocation than total hip replacement

because it uses a larger head.

Complications of joint replacement involves infection and DVT.

Rehabilitation is more difficult with knee replacement than total hip replacement.

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Foot Physiology and MechanicsAnkle sprains are the most common injury to the ankle region which occurs with a simultaneous

plantar flexion and intorsion.-Physical exam reveals edema, tenderness, ecchymosis on lateral ligaments, medial

tenderness, and tenderness above ankle.

-Differential diagnosis includes fractures of talus, ankle, 5

th

metatarsal, calcaneus, orperoneal subluxation.-Radiographs are required to rule out fractures.

-Treatment of ankle sprain involves rest, ice, compression, and elevation.

Ankle fractures occur with external rotation of the supinated foot. Problems occur to both lateral

and medial sides of the ankles.

-Physical examination would reveal tenderness to the fracture site, deformity, swelling

pain, and neurovascular (?)-X-rays are required to rule out fracture of the medial or lateral fibular malleolus.

-Treatment involves closed reduction and a cast or splint.

-Follow-up at 1 and two weeks is required to ensure the ankle does not shift afterswelling subsides.

Hallux valgus is deviation of the big toe away from the midline. This can result from a bunion as

a prominent medial eminence.-Women get bunions far more often because they are associated with high-heeled,

narrow-toed shoes.

-A typical history of bunions will present with pain in close toed shoes but not in barefeet or normal shoes. Physical exam will show a prominent medial eminence that is

tender to palpation.

-There is also a splayed forefoot.

-Treatment for bunions involves wide shoes with low heels with a leather stretch overbunions.

-Surgery is considered based on the degree of deformity. All surgery for bunions involve

osteotomy.

Diabetes causes ulcers, neuropathy, and vasculopathy. Ulcers can occur secondary to excess

pressure. Significant peripheral neuropathy can result in numbness and tingling. Quantitativetesting is done with monofilament testing.

-Osteomyelitis (bone destruction) is common.

-Treatment involves debridement of the callus and nonviable tissue. After the ulcer heals,

custom orthotics are required for a lifetime with potential surgical revascularization.

Heel pain and plantar fasciitis occur and lead to disabling foot pain.

-Physical exam reveals point tenderness over the calcaneal tubercle and a tight calf

muscle.

Non-steriodal Anti-inflammatory Drugs

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NSAIDs block the action of cyclooxygenase, which inhibits the production of prostaglandins,

prostacyclins, and thromboxanes. At higher concentrations, NSAIDs can also block

lipoxygenases and thereby inhibit leukotrienes.-At high doses, NSAIDs also act on leukocyte membranes and prevent inflammatory

mediators.

Aspirin acts locally to block pain and reduces mild to moerate pain but does not cause addictionor tolerance. This is in contrast to opioid analgesics which act in the brain, control moderate to

severe pain, and lead to addiction and tolerance.

-The inhibition of COX-1 is responsible for antithrombotic effects because of the lack ofthromboxane.

-The inhibition of COX-2 is prothrombotic because it blocks prostacyclin (vasodilator) in

the endothelium.

-Aspirin is non-ionized in the stomach. Once it gets absorbed to the gastric mucosa, itbecomes ionized and gets trapped in the gastric mucosa. This causes local irritation and

induces tissue damage. Enteric-coated tablets are used in order to allow aspirin to reach

the intestines before dissolving.-Additionally, the inhibition of cyclooxygenases decreases the synthesis of

prostaglandins, which inhibits the secretion of mucus and bicarbonate.

-Lastly, cyclooxygenase prolongs GI bleeding.

-These effects are specific to COX-1 inhibitors and do not occur in COX-2 inhibitors.-Hypersensitivity occurs with COX-1 inhibition and in patients with asthma.

-In patients with congestive heart failure only, COX-2 inhibition leads to renal toxicity by

decreasing the glomerular filtration rate. This also promotes the retention of salt andwater, leading to severe edema.

-COX-2 inhibition delay follicular rupture, causing reversible infertility in eomrn.

-Rare side effects include hepatic toxicity, blood dyscracias, aplastic anemia, and

agranulocytosis.

Celecoxib and rofecoxib are selective cyclooxygenase 2 inhibitors. Because they do not affect

COX-1, they are just as effective as analgesics but they do not decrease gastric acid secretion.

NSAIDs cannot be given to children, to pregnant women (prevents closing of ductus arteriosus),

to those with hemophilia or hepatic damage, or to patients with peptic ulcers.

Non-Neoplastic Diseases of the Bone

Bone formation can occur through intramembranous ossification (flat bones) in which fibrous

tissue is replaced by bone or through endochondral ossification (long bones).-Osteoblasts are rich in alkaline phosphatase, which is also a marker of new bone

formation.

-Osteoclasts are involved in bone resorption.

-Osteocytes are osteoblasts that have become surrounded by bone matrix.-Extracellular substance is called osteoid and is primarily type I collagen. The major

mineral is calcium hydroxyapatite.

Bone disease results in pain, deformity, mass, fracture, and radiologic abnormality.

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-Congenital Diseases

-Osteogenesis imperfecta is a group of hereditary disorders that shows abnormal

type I collagen production. Type I shows survival into adulthood but type II islethal. Fractures occur early in life because of ill-formed bone but blue sclera, lax

ligaments, teeth, and deafness are also present.

-Achondroplasia is relatively common and is a mutation in fibroblast growthfactor 3. A defect in cartilage synthesis causes the failure of proliferation at theepiphysial plates, leading to short stature. However, membranous bones are

unaffected.

-Osteopetrosis (or Marble Bone) shows a defect in osteoclastic reabsorption thatleads to dense bone. Bones become brittle and marrow space is limited, leading to

pancytopenia (anemia, thrombocytopenia, susceptibility to infection) and nerve

compression.

-Marfan syndrome is a mutation in the fibrillin gene that leads to tall stature andlong fingers. Ectopia lentis and cardiovascular lesions are also common

complications.

-Infections of Bone-Acute pyogenic osteomyelitis occurs from trauma and shows fever and pain. It is

usually caused by S. aureus and results when organisms enter bone through the

bloodstream and spread through inoculation by trauma (or surgery).

-Sequestrum is bone necrosis as a result of acute inflammation. A reactivesleeve of new bone (involucrum) may develop beneath the periosteum as a

result.

-Radiology shows lytic and sclerotic features resulting from a combinationof necrosis and new bone formation.

-This responds to antibiotic therapy but not treating the disease leads to

chronic suppurative osteomyelitis. The chronic condition shows sinus

drainage to skin and secondary amyloidosis.-Tuberculosis of bone can occur with insidious onset and result in extensive bone

destruction that is difficult to control.

-Acid fast test (AFB test) is positive.-Immunocompromised patients are particularly at risk.

-The spine (Pott disease) and long bones are commonly affected.

-Radiographs show bone destruction.-Pathology shows subacute inflammation with granulomas and necrosis.

-Metabolic Diseases of Bone

-Osteoporosis results from a decrease in total bone mass. However, the ratio of

mineralized to unmineralized bone is normal. This causes a patient to becomesusceptible to fracture.

-Primary causes are due to aging and are idiopathic.

-Secondary causes arise from immobilization, endocrine disorders,

malnutrition, etc.-Osteomalacia (or Ricketts) is a structural abnormality caused by defective

mineralization of osteoid. However, osteoid is present in normal amounts.

-The lack of vitamin D leads to bone deformities.

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-Hyperparathyroidism results in increased osteoclastic activity that leads to

fracture and hemorrhage.

-Bone Diseases of Unknown Cause-Paget disease leads to bone thickening that leads to deformities such as

increasing skull size or bowing of long bones in legs. Radiologic findings show

enlarged affected bones.-There is a marked increase of alkaline phosphatase due to osteoblasticactivity.

-Paget disease goes through an enlargement phase, a lucency phase

(destructive phase), and then a mixed irregular sclerotic phase (patchy).-Thickened bone is Paget disease is actually very soft, which explains why

there is a propensity towards fracture and bowing.

-Because of bone growth, there is a risk of osteosarcoma.

-Fibrous dysplasia shows a progressive replacement of bone with a proliferationof benign fibrous tissue.

-Monostotic fibrous dysplasia affects one bone while polyostotic fibrous

dysplasia affects multiple bones.-On imaging, fibrous dysplasia shows well-demarcated lesions.

-Joint Diseases

-Pyogenic arthritis is most commonly caused by Staph aureus and Neisseria.

Infections typically travel through the bloodstream.-Tuberculous arthritis

-Lyme Disease

-Inflammatory arthritides-Rheumatoid arthritis shows a chronic, relapsing inflammatory disease that affects

multiple organ systems.

-Gout.

-Degenerative arthritis results from aging or from a congenitally abnormal joint.

Biomechanics of FracturesBone is living tissue that provides skeletal integrity and keeps muscles under tension while atrest. Bone also provides for calcium storage and is metabolically active, subject to turnover.

The ultimate strength of bone depends on bone density. Fractures occur when an applied forceexceeds ultimate strength. Metabolism, structure, and the way the force is applied all determine

the strength of bone.

-Metabolic factors like renal osteodystrophy (disruption in calcium or parathyroid

hormone), decreases in calcium, and the amount of matrix determine ultimate strength.-Osteoporosis occurs when the ratio of calcium to matrix is disrupted, when the

amount of matrix is below normal, when the amount of bone is decreased, and in

post-menopausal women.

-Physical properties like cross sectional diameter affect strength in that a small crosssectional diameter with thick walls is stronger.

-Age also affects bone in that bone quality decreases as bones lose wall thickness.

Additionally, homeostasis is altered with age in that the cortex becomes thinner.Diameter will increase to compensate.

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-The strength of bone can be determined through three point bending, torsional bending,

and stress-strain curves.

-Bones have less ultimate strength in tension than in compression.-An open fracture is more of an emergency than a closed fracture because the soft tissue

surrounding the bone becomes compromised.

Ligament failure and fractures can occur from the same force. A rapidly applied force will causea fracture while a slowly applied force will cause a ligament rupture. Deformities require surgery

because of the tension of muscles that will pull bone fragments out of place.

-Olecranon fractures are fractures of the elbow joint. The triceps pull up on the elbowjoint and cause a fragment of bone at the elbow.

-Galeazzi fractures are fractures of the distal radius. Fractures occur because of the

tension of the brachioradialis and the pronator quadratus.

-Femoral fractures occur as subtrochanteric fractures. Deformities are caused by theiliopsoas, quadriceps, hamstring muscles, and abductors.

Avascular necrosis can also result from fractures. This is particularly important when bloodsupply occurs in a retrograde fashion. This results in collapse of the bone, which manifests as

fracture.

-Femoral neck fractures interrupt blood supply from the retinacular arteries and cause a

loss of blood supply to the femoral head.-Talus fractures cause the talar body to lose blood supply (blood flows from head to

body).

Wolfs Law states that bone constantly remodels itself to resist forces. Stress fractures occur

when bone fails under fatigue.

-Primary bone healing shows a fracture that stabilizes very rigidly such that all motion at

the fracture site is eliminated.-Callous formation requires motion and axial motion is best.

-A non-union is an arrest in the healing process such that healing does not occur over

time. This leads to persistent fracture lines and sclerosis at the ends of bones.-Hypertrophic non-union occurs when bones show growth but do not undergo union.

There is a buildup of callus at both ends.

-Atrophic non-union occurs due to avascularity.-Fatigue failures of the bone can occur with a rapid change in activity, such as suddenly

going from a sedentary lifestyle to running a marathon. These are called stress fractures.

Factors affecting bone healing are metabolic factors such as nutrition, smoking, and NSAIDs.Blood supply from surrounding soft tissues also affects bone healing.

-Primary bone healing stabilizes fractures in a way that eliminates all motion at the

fracture site. Remodeling heals the bone across the fracture and does not involve

inflammation.-Callus formation forms new bone over the old bone and requires motion to work. It is a

form of fracture healing that will result in remodeling.

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Adult Respiratory Distress Syndrome shows an inability of lung to oxygenate blood and

pulmonary failure is treated by a ventilator. It is associated with trauma resulting in multiple

fractures. Fat emboli occur because of bone marrow. Pulmonary emboli results from DVT.

Compartment syndrome occurs when fluid gets trapped in a muscle compartment (fascia

provides an impermeable barrier). This results in the five Ps: pain, pressure, paralysis,pulselessness, pallor.

Fractures can also cause nerve injury. Vascular injuries can also occur because of fractures.

-Tibial fractures injure the femoral nerve.-Shoulder injury can injure the axillary nerve.

-Humerus can injure the radial nerve.

-The distal femur can damage the superficial femoral artery.

-Knee dislocations can injure the popliteal artery.

SPP: Low Back Pain

Excessive sitting and poor sitting posture contribute greatly to the prevalence of low back painand pain radiating to the leg (sciatica).

-Many problems occur from walking upright all the time.

-All other mammals do not have a lumbral curve like humans do.

Which contributes to back pain? All of these:

-Cigarette smoking

-Heavy lifting-Obesity

-Sedentary Lifestyle

-Sitting and slouching

Back muscles, connective tissue and ligaments, intervertebral discs, facet joints, and vertebrae

can cause back pain.

Which spinal area is subject to chronic forces and stress?

-L5-S1

Muscles tend to get smaller in obese patients, which predisposes them to back pain.

What causes the most pressure on the nucleosus pulposis?

-Lying-Sitting

-Sitting erect

-Sitting slumped

-Stooping forward in lifting This one

Mr. Jones has a disc herniation at L4-L5 that is compressing L5.

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A patient present with bilateral leg pain, lower extremity weakness, saddle anesthesia, and

difficulty holding urine. Which of these is correct?

-Spinal stenosis-Causa equina syndrome This one

-Spondylolysthesis

-Compression fracture

Case #1: Musculoskeletal strain

Case #2: Depression

Case #3: Metastatic cancer,

Clinical Applications of the SpineC5-biceps

C6-brachoradialis

C7-tricepsL4-patellar

S1-achilles

Spinal cord injury occurs most commonly from vehicle accidents.

Immobilization should include a rigid cervical collar and a firm spine board. Patients should be

log rolled.

Central Cord Syndrome

-Upper extremities show LMN signs

-Lower extremities show UMN signs-

Brown-Sequard Syndrome-Caused by penetrating injury

-Loss of contralateral pain and temperature with sparing of ipsilateral motor and light

touch and proprioception

Anterior Cord Syndrome

-Loss of motor and loss of pain/temperature

-Preservation of touch and proprioception

Posterior Cord Syndrome

-Loss of proprioception and light touch

-Sparing of motor, pain, and temperature-Foot Slapping Gait

Cauda Equina Syndrome-Results from loss of central spinal canal space, possibly from a space occupying lesion

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-Loss of L1-S5

-Saddle anesthesia, lower extremity pain, loss of bowel and bladder control.

-This is a surgical emergency

Cervical myelopathy is disease of the spinal cord that is caused by compression of the spinal

cord. It is characterized by clumsiness in the hand and gait imbalance. It is diagnosed with aconstellation of symptoms rather than on radiography and can be caused by a variety of factors.-There are positive Hoffmans signs, a positive Babinski test, and ankle clonus.

-Surgical intervention is required if progress stops but non-intervention is preferred. In

the case of surgery, the central canal would be widened.

Cervical radiculopathy is compression of the spinal nerve root.

-Symptoms follow specific dermatomes

-C5-shoulder, biceps reflex-C6-thumb, triceps reflex

-C7-middle finger, brachoradialis reflex

-C8-little finger, decrease in finger flexion-Cervical spondylolysis and disc herniation can cause cervical radiculopathy

-Spurlings test will reproduce the symptoms of pain because of compression

-Non-operative treatment is preferable but operations are indicated if symptoms do not

respond to other treatments or if weakness occurs.

Lumbrical radiculopathy shows dermatomal pain that radiates below the knee.

-There is often motor weakness, sensory changes, and loss of reflex-Straight leg-raising test (L5, S1) and femoral stretch test (L2, L3, or L4) will elicit pain,

useful in diagnosis

-L4 is required for patellar reflex

-S1 is required for achilles reflex

Lumbar spine stenosis results from a narrowing of the spinal canal.

-This can result from spondylolisthesis, facet osteophytes, disc herniations, synovialcysts, or hypertrophy of ligamentum flavum.

-There is a burning or tightness in the buttocks that occurs when walking.

-Old people who like to lean on carts do it in order to find relief.-Wide decompression and segmental fusion are potential operative therapies.

SPP: Shoulder Injury and Elbow InjuryThe axis of orientation of the glenoid fossa is pointed forwards in primates and cats. Humansare pointed laterally. This causes shoulders to be susceptible to injury.

What is most commonly broken from a fall on a bicycle?

-AC separation-Fracture of clavicle This one

-Fracture of humerus

-Rotator cuff tear-Shoulder dislocation

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Ten-foot fall backward onto arm and shoulder. What is the most likely injury?

-AC separation-Fracture of clavicle

-Fracture of humerus This one

-Rotator cuff injury-Shoulder dislocation

Fall while skiing and there is severe pain and cannot move shoulder. What is most likely injury?

-AC separation-Fracture of clavicle

-Fracture of humerus

-Rotator cuff injury

-Shoulder dislocation This one

Falls onto steps on the front of shoulder. What is the most likely injury?

-AC separation

This one, it heals on its own-Fracture of clavicle

-Fracture of humerus

-Rotator cuff tear

-Shoulder dislocation

Impingement Syndrome can be caused by shoulder instability (under 30 years old), chronic

rotator cuff and supraspinatus tendon (over 40), or tears of the supraspinatus tendon (over 60years old).

What sign is most suggestive of shoulder impingement syndrome?

-Tenderness to forceful palpation just inferior to acromion

The impingement test tests the supraspinatus, patient has arm laterally and is actively abducting.

Tennis elbow can result from lateral epicondylitis (tennis), medial epicondylitis (golf), other

ligamentous injury, trauma, arthritis, or neuropathy.

-In tennis elbow, the muscle most frequently involved is the extensor carpi radialis brevis

Orthopedic Soft Tissue Sports Medicine InjuriesSoft tissue injuries are typically sports-specific because of the nature of repetitive, stereotyped

motions involved in different sports.

Arthroscopy is a minimally invasive procedure with a low morbidity that has low cost and quick

recovery.

Rehabilitation focuses on recovery from injury, attaining full range of motion, and strengthening

(in that order).

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Disorders of the meniscus give mechanical problems. The meniscus has poor healing ability due

to a lack of blood supply. A damaged meniscus can be sewn back together. A torn meniscus is

very painful.-McMurrays test is used to diagnose a meniscal tear.

-The absence of an intact meniscus leads to long term arthritis.

-Menisci can be transplanted.

There are sensory neurons in ligaments that allow for sensory feedback.

-The ACL is the most commonly torn ligament. They tear from slower movements than

they do at faster movements. It is common to tear the ligaments in the absence of acontact injury.

-Damage to the ligament commonly causes a tear in the meniscus and articular cartilage

as well.

-Lachmanns test tests the movement of the knee in order to assess the integrity of theligaments.

-Grafts of the ligament involve filling a bone with collagen and allowing the bone to heal

and form a new ligament. The achilles tendon of cadavers is commonly used.-Bone-tendon-bone is used commonly.

-Rejection of grafts does not occur because collagen does not incite an

inflammatory response.

The inferior glenohumeral ligament holds the shoulder in place. Dislocation typically must occur

a number of times before surgery is considered.

Rotator cuff problems occur because of tendons, not ligaments.

-The vast majority of rotator cuff problems involve the supraspinatus.

-Adhesive capsulitis (frozen shoulder) results gradually over time and leads to loss of

movement.

SPP: Knee

Ligaments are responsible for protecting menisci. The meniscus distributes the load of weightacross the joint and removing the meniscus causes arthritis in 5-10 years. The articular cartilage

beneath the meniscus has no ability to repair itself.

-Valgus stress causes MCL injury-Varus stress causes LCL injury

-Direct blow to anterior knee causes a PCL injury. This usually is caused by a dashboard

injury in a car accident.

-An injury to a ligament like an ACL or MCL injury will prevent a person from walking.However, returning to the sport indicates a meniscus injury.

-The majority of ACL injuries are non-contact.

-A pivot shift and a Lachman test (anterior drawer test) are diagnostic of a torn ACL.

-In the absence of an ACL ligament, the meniscus will become a shock absorber. Assuch, repairing an ACL also protects the meniscus.

-A person with significant knee swelling will flex their knee because it provides the least

amount of pain.

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-MRI has the best resolution of soft tissue and is preferred when looking for meniscal

tears.

-An MCL tear will usually heal on its own.

Case: 35-year-old male was playing soccer when he injured his left knee.

-No contact-Could not return to the field

Bone and Joint Infections ISeptic arthritis can involve the joint space, which shows a high mortality and morbidity(disability). The knee and hip are most commonly involved but any joint can become infected.

Organisms typically invade from the bloodstream, spread from a contiguous site (abscess,

osteomyelitis), or inoculation.

-Infection typically involves a single joint.

Organisms that enter the joint space then adhere to articular cartilage (very little fluid movement,

hard to flush bacteria out). Neutrophils follow suit. Cartilage becomes damaged throughincreased intraarticular pressure, bacterial toxins, and the inflammatory process itself. Cartilage

destruction then leads to joint space narrowing.

-Staph aureus is the most common organism followed by Strep.

-Treatment involves debridement and antimicrobial treatment.-Mycobacterium and Borrelia Burgdorferi are less common bacteria involved in infection

of the joint (not on the east coast, Borrela Burgdorferi causes a chronic form of articular

infection).-Coccidioides immitus is a common fungal infection of the joint because of trophism but

Sporothrix schenckii is also common (gardening).

-Parvovirus, rubella, HIV, and HTLV can infect the joint as viral causes.

Treatment can involve debridement, arthroscopic surgery, or serial debridement. Antibiotic

treatment would involve a systemic antibiotic (cephalosporin+vanco) for 2-4 weeks. Local

antibiotics are

Osteomyelitis is infection of the bone. However, the pathophysiology and management are

different based on the specific joint infected.-Hematogenous spread is the most common form of spread while direct inoculation is

common in adults. Adjacent spread is also possible.

-Vertebral osteomyelitis can result from the spread from the GU tract or from IV drug

use.

In antimicrobial therapy, longer treatment is better because there is no known optimum time.

However, textbooks recommend 4-6 weeks.

-Osteomyelitis is never cured because the risk of recurrence is always present. As such,osteomyelitis can only be controlled due to factors involving the particular organism,

surgical skill at debridement, and specific risk factors involving the patient. The

exception is amputation, which actually has zero chance of remission but is typically notdone.

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Vertebral osteomyelitis involves vertebral bodies with subsequent destruction of the bone. It is

the most common of hematogenous spread of osteomyelitis in adults and typically spreads fromthe GU tract.

-Symptoms are non-specific back pain with low grade fevers and prolonged illness.

-Diagnosis is made based on radiographs showing erosion of vertebral bodies and anarrowing of disk space.-Confirmation is done by biopsy, which also allows for identification of the organism and

allows for the choice of therapy.

-The most common is Staph aureus but E. coli is also common. IV drug users get MRSA,P. aureginosa, and Serratia.

-Mycobacterium tuberculosis is called Potts Disease and it is the most common skeletal

target of M. tuberculosis. Therapy is required for 12 months.

-Unlike in long bone osteomyelitis, vertebral osteomyelitis does not require debridement(spine has good vascular supply, makes debridement unnecessary) but spine stabilization

is required to prevent vertebral compression.

The sacroiliac joint is usually infected only in IV drug users, patients with indwelling catheters,

and patients with endocarditis.

-Infection of the joint is typically caused by spread of osteomyelitis from adjacent bones.

-Patients present with fever and severe sacral and pelvic pain.-Diagnosis is made from MRI. Blood cultures are positive, which is not true of

osteomyelitis of other joints.

Brodies abscess is a chronic, localized abscess of the bone often seen in the distal tibia. Most

patients are under 25 years old.

-Brodies abscess can be confused with a neoplasm.

Sickle cell disease causes osteomyelitis, also with Staph aureus. They are also at particular risk

for Salmonella because its encapsulated. This is because of acute infarct of the bone.

Bone and Joint Infections IIDiagnosis of septic arthritis shows clinical symptoms that include fever and chills, painful joints,

swelling, erythema, limited motion, and joint effusion. Early septic arthritis shows soft tissueswelling but late septic arthritis shows joint narrowing (because of cartilage destruction)

-MRI is useful for determining bone involvement and soft tissue abscesses.

-Ultrasound is good for determining joint effusion.

-Laboratory diagnosis shows elevated C-reactive protein, elevated erythrocytesedimentation rate, elevated white blood cell count, and positive blood cultures.

-Synovial fluid analysis looks for increased WBCs and cultures are necessary to select

appropriate antibiotic therapy.

-Staph aureus is most common organism

Septic arthritis leads to cartilage destruction, pain and loss of function, degenerative arthritis,

avascular necrosis of the femoral head, subluxation and dislocation of the joint, and recurrentinfections.

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-Treatment involves antibiotic therapy, arthroscopic surgery, or needle aspiration (not the

hip).

Total joint replacements have complications with foreign body and biofilms that can adhere to

biomaterial surfaces. Biofilms make antibiotic therapy and antibody production ineffective and

allows the organism to exist in a subclinical state with the possibility of recurrent infection.-Treatment of infected replacement joints involves debridement and synovectomy ifcaught early enough, removal of implants and reimplantation if later. Antibiotic therapy

is required for at least 6 weeks.

Hematogenous spread to joints is the most common method of entry into joints by children and

IV drug users. Direct inoculation occurs from open fractures and during surgery. Spread from an

adjacent infection is also possible.

-Type I is medullary, hematogenous osteomyelitis-Type II is superficial, ulcer with exposed bone

-Type III is localized, cortex and medullary canal involvement

-Type IV diffus