Exam 4 Flashcards
Composition of muscle tissue
- Muscle cells, myocytes
- Connective tissue, containing blood and nerves, transmits muscular contraction forces
Sarcoplasm
Striated muscle Cytoplasm
Sarcolemma
Striated muscle plasma membrane
Sarcoplasmic reticulum
Striated muscle smooth ER
sarcomere
Structural unit of myofibril in striated muscle
Myofilaments
Actin and myosin filaments in striated muscle
Myofibrils
Elongated contractile thread in striated muscle
Myofiber/muscle fiber
Single muscle cell in striated muscle
Skeletal muscle
• arises by fusion of myoblasts and differentiation
Mesoderm—> Myoblast—> Large multi nucleated cells—> syncytium + Differentiation in the skeletal muscle fibers
Endomysium
Sheath of fine connective tissue that surrounds individual muscle fibers, Fine RT fibers and ground substance, tiny nerves and blood vessels run parallel to muscle fibers
Perimysium
Thick CT sheath that surrounds groups of muscle fibers (Fascicles/bundles). Continuous with tendon fibers, large nerves and blood vessels
Epimysium
Dense CT cells that surrounds collection of fascicles (entire muscle). Major nerves and blood vessels
General features of myofiber
• Single cell, myocyte
•  Striated, voluntary
• Well developed Sarcoplasmic reticulum
• Multi nucleated
• Nuclei at cell periphery
Myofibril
• multiple myofibrils per cell
• tiny contractile threads within Sarcoplasm
• Extend entire length of cell, filled with myofilaments (Actin and myosin)
• Responsible for appearance of cross striations
Myofibril bands
Dark bands: A band divided by H band
M line: divides H band
Light band: I band divided by Z line
Sarcomere: length between adjacent Z lines
Thin filaments
Actin, tropomyosin, troponin
Extend from Z line through A band to edge of H band
Thick filaments
Myosin
Extends length of a band, thin cross-bridges extending from each myosin filament towards neighboring actin filaments
M line
• Dense line at center of H band
• Contains Myomesin, C protein, and other proteins for special arrangement
• lattice arrangement maintained by interconnection of thick myosin filaments
Z line/ The matrix
• region where ends of actin filaments attach in adjacent sarcomeres
• Alpha actinin protein, Titin, Nebulin, etc
Sarcoplasm
• between myofibrils
• Beneath Sarcolemma
• Around nuclei
• Mitochondria appear in the same area
• Numerous invaginations along cell surface, forming the T tubules
Sarcoplasmic reticulum
Network of cisterns and membranous tubules running between and around myofibrils
• Forms collars at A-I Junctions in skeletal and Z lines of cardiac
• binds and releases calcium
Skeletal muscle triads
T tubule + 2 terminal cisternae or sarcoRetic 
• Facilitates transmission of electrical impulse from Sarcolemma to Interior depths of cells at A-I junctions
Actin- thin filaments
1.) G actin: Globular actin Polymerizes to form F actin
2.) F actin: two helically wound strands of polymerized G Actin 
Myosin
• four light chains and two heavy chains
• Heavy chain: light meromyosin and heavy meromyosin
Heavy meromyosin
• Rod-like portion lies parallel to backbone of filament
• globular head, ATPase activity and actin-binding sites
• Polarized, globular heads directed away from midpoint of myosin filament
Regulatory molecules
Tropomyosin and troponin complex: Runs in groove between actin molecules and mask the myosin binding site
Calcium: relocates the complex to expose the actin-myosin binding site
Contraction of skeletal muscle causes:
Z lines closer together, H band and I band become thinner, A band stays the same thickness always
Neuromuscular junction/motor end plate
• myelin sheath lost as nerve fiber approaches surface of muscle cell
• Axon branches near surface of muscle cell, occupy recesses in muscle surface, a.k.a. synaptic troughs or primary synaptic cleft
• subneural apparatus/modified SR
•  Synaptic vesicles
Myasthenia gravis
• characterized by weakness and easy fatigue of muscles, caused by auto immune response to the ACh receptor
• Administration of AChE inhibitors has both diagnostic and therapeutic values
Motor unit
Motor neuron and the muscle fibers innervated by it, one to one ratio is very fine control
 Muscle spindle
Specialized stretch receptor in all skeletal muscles. Signal transmitted via afferent nerve fibers (Motor neurons)
Golgi tendon organ
Spindle shaped bodies comprised of collagen and enclosed by a thin capsule. Afferent/sensory fibers (ONLY) penetrate between the collagen fibers 
Cardiac muscle
• Arises by differentiation of individual myoblasts, not by fusion of cells
• striated, involuntary, T tubule system, single nucleus per cell, Intercalated discs, glycogen storage
Intercalated discs
1.) dark cross bands on longitudinal sections
2.) Occur where a Z line should be, observed at ends of a sarcomere
3.) Mark spots of cell cell attachments ( Fascia adherens, desmosomes, gap junctions)
Cardiac muscle dyads
T tubule + a terminal portion of adjacent SR
+ intercalated discs
Atrial granules
Part of atrial cardiac muscle cells, contain atrial natriuretic peptide that lowers blood pressure by decreasing renal tubules ability to reabsorb sodium and water
Smooth muscle
• Arises by differentiation of individual myoblasts, not by fusion of cells (some arise by differentiation from ectoderm: pupil, sweat glands, mammary glands)
• No striations, no T tubules, involuntary
Functions of smooth muscle
1.) contractility
2.) Conductivity
3.) production of extra cellular products (collagen, elastin, GAGs, proteoglycans, growth factors)
Where is smooth muscle located?
Walls of hollow viscera, walls of blood vessels, larger ducts of compound glands, arrector pili muscles
Dense bodies 
Comparable to Z discs of skeletal and cardiac muscle, they serve as anchor sites for actin- myosin interactions as well as intermediate filaments
• located at Inner aspects of sarcolemma and throughout cytoplasm 
Caveolae 
• Pinocytotic like invaginations of sarcolemma
• Like T tubules
• Modulate calcium availability and contraction
Smooth muscle innervation
Sympathetic: norepinephrine
Parasympathetic: acetylcholine
Bone
• mineralize during development
• Vascular
• Innervated
• Grows appositionally
Cartilage
• mineralization leads to degeneration
• Avascular
• Aneural
• grows appositionally and interstitially
Appositional growth
Chondroblasts in perichondrium differentiate into chondrocytes, start producing matrix, and add to existing cartilage
Interstitial growth
Proliferation and hypertrophy of existing chondrocytes. Can create an isogenous group
Chondroblast cell morphology
• reside near perichondrium
• Dense irregular CT, contains capillaries
• Oval shape, round or elongated nucleus
• Well developed rER (Active secretory pathway)
Chondrocyte cell morphology
• resides in lacunae
• Cartilage matrix, avascular, aneural
• round cells, small round nucleus, well developed rER, large Golgi, vesicles, lipid droplets, rich in glycogen
Composition of cartilage matrix (hyaline)
- Intracellular water
- Collagens (type II, some 4/6)
- Proteoglycans
- Multiadhesive glycoproteins
- Cells
Hyaline cartilage
• most common, type two collagen
• Lacuna and isogenous groups of chondrocytes
• perichondrium: tense CT with fibroblasts
• Appositional and interstitial
• Precursor of bones that developed by endochondral ossification
Cartilage matrices
- Capsular matrix
- Territorial matrix
- Interterritorial matrix
Articular cartilage
Hyaline cartilage on the articular surface of bones
• Absence of perichondrium, breakdown occurs in osteoarthritis
Elastic cartilage
• located: pinna of ear, walls of external acoustic meatus, auditory tube, epiglottis
• contains elastic fibers, lacuna and isogenous groups, perichondrium
Fibrocartilage
• Located: intravertebral disc, symphysis pubis, meniscus of knee joint, triangular complex of wrist
• less amorphous ground substance, more fibrous type I collagen (Resistant compression and shearing forces
•• Chondrocytes placed singularly, in rows or an isogenous groups
• NO Perichondrium
Cartilage repair
Limited availability due to:
1.) Lack of vascular supply, immobility of chondrocytes, special constraints limit chondrocyte deliberation
2.) Hyaline cartilage replaced with bone in calcification
3.) perichondral wounding is repaired by pluripotent progenitor cells producing dense CT rather than cartilage
Wolffs law
Bone will adapt to the loads under which it is placed using adaptive changing ( More frequent heavy loads = thicker and stronger bones)
Bone remodeling
1.) resting stage
— Osteoclast recruitment and activation
2.) Bone resorption
— Osteoblast recruitment an activation, osteoclast removal
3.) transition
— Matrix synthesis
4.) Bone formation
Osteoblasts
• formed by growth factor activation: CBFA1 and RUNX2
• Synthesis of organic matrix, osteoid
• deposits in organic components, located on bone surfaces
• Epithelioid appearance, cuboidal to columnar, basophilic
Surface receptors for parathyroid hormone
Osteoblasts, they bind PTH and regulate secretion of RANKL and OPG that caused the fusion of osteoclast precursors. This modulate calcium in the serum vs bone
Osteocytes
• osteoblasts surrounded by matrix, reduced protein synthesis, maintains matrix, regulates calcium levels
• Reside in lacuna, and have canaliculi which are tunnels that help osteocytes connect
Osteoclasts
• large, multi nucleated cells responsible for bone resorption
• Derived from GMP, the same precursor as macrophages
• Mature cells are amitotic, and abundant in lysosomes
• ruffled membrane adjacent to bone surface
Alpha-v-beta-3 integrins
Binds bone to osteoclast
Howships lacuna
Resorption pit, a depression in the surface of the bone where an osteoclast resides
Cancellous bone
Spongy bone, spicules or trabeculae of bone united to form a network found in the interior of bone
Compact bone
Dense bone, found on the bone exterior
Diaphysis
• Bone shaft between epiphyseal plates, mostly compact bone
• Contain periosteum (outside lining) and Endosteum (lining marrow cavity)
• has marrow cavity, blood cells, reticular cells, fibers
Epiphysis
• distal ends of long bones, cap of articular cartilage
• Medullary cavity is spongy and contains a marrow cavity
Periosteum
• fibrous outer layer, protection
• Osteogenic inner layer
• Blood vessels and nerves present
• sharpeys fibers (layer of anchoring collagen)
Endosteum
Between bone marrow and bone matrix, layer of osteoblasts, osteoclasts, and a few osteogenic cells
Haversian system
• entire system fully formed is an osteon
• In the middle is a Haversian canal that contains a capillary/vessel in the tunnel
• concentric lamellae of bone (around 10) 
Volkmann canals
Vascular passage that runs radially (Perpendicular to Haversian canal to connect them)
Interstitial lamellae
Remnants of partially reabsorbed osteons, no vessels, found in between osteons
Intramembranous ossification
• Skull, mandible, maxilla, clavicle
• MSC condense and differentiate to osteoblasts that secrete matrix, remain connected by thin cytoplasmic processes
• Matrix begins to calcify and spicules/tuberculate are seen
• osteocytes maintain processes that become canaliculi 
Endochondral ossification
• hyaline cartilage precursor template Forms a general shape of the bone out of cartilage
• Differentiation occurs as chondrocytes die and osteoblasts take presence 
Five zones of endochondral ossification
1.) zone of reserved cartilage
2.) Zone of proliferation
3.) Zone of hypertrophy
4.) Zone of calcified cartilage
5.) Zone of resorption
Fracture repair
Bone necrosis and blood clot —> Soft callous formation, granulation tissue —> Hard to callous formed, fibrocartilage and spongy bone —> New compact bone following Haversian system
Synovial joint
Membrane is made out of:
fibroblasts — type B cells (Secrete synovial fluid, lubrication and nutrition)
macrophages — type A cells (Remove debris as joint pivots)
Contains lining cells, not an epithelium, made of fibroblasts and macrophages
Cross bridge cycle: Actin + myosin
1.) resting fiber, myosin head is not attached to the actin
2.) Myosin head binds to actin and forms cross bridge to Actin
3.) phosphate is released from myosin head, causing conformational change in myosin 
4.)  Power stroke causes filament to slide, ADP is released
5.) A new ATP binds to myosin head, allowing it to release from actin
6.) ATP is hydrolyzed and phosphate bonds to myosin, causing energized myosin head to return to its original orientation
Excitation-contraction coupling in skeletal muscles
1.) terminal synapse releases acetylcholine
2.) Nicotinic acetylcholine receptor on postsynaptic cell accepts acetylcholine
3.) skeletal muscle voltage gated sodium channel activates
4.) transverse tubules voltage gated calcium channels open
5.)  Sarcoplasmic reticulum calcium release channel opens (Majority of calcium comes from here)
Ca2+ -ATPase function
• On the sarcoplasmic reticulum,it uptakes calcium from cytoplasm, clearing it from the muscles, allowing relaxation
Stepwise function of muscle contraction
Somatic motor neuron—> ACh released—> Sarcolemma: binds to nicotinic ACh receptor, opens ligand gated channels, sodium diffusers in depolarizing membrane, action potential produced —> Transverse tubules: conducts action potential to open voltage gated calcium channels—> Sarcoplasmic reticulum: releases calcium from SR—> Myofibrils: have binding spots for calcium to troponin, stimulating contraction
 Inverse relationship of force-velocity
The greater the force (load opposing contraction), the smaller the Vmax
Isometric contraction
Muscle fibers do not change in length (Force load is equal to the muscles capabilities)
Concentric contraction
Muscle fibers shorten (Joint angle decreases)
Eccentric contraction
Muscle fibers lengthen (joint angle increases)
Titin filament
Resting elastic protein, contributes to the resting length of muscles (Tension and contractibility depends on the length of the muscle fibers)
Ideal length-tension length
2.0-2.25 microm
Energy consumption of muscles
• 70% of ATP is used by myosin ATPase for contraction
• 30% of ATP is used for calcium ATPase for relaxation and sodium potassium ATPase for the electrochemical gradient
— Comes from aerobic respiration of fatty acids, and muscle glycogen/blood glucose during exercise
Creatine phosphokinase or creatine kinase
Help facilitate the rapid transfer of phosphates to create ATP out of ADP ( Phosphocreatine—> creatine)
CPK/CK: Indicator of muscle damage
CK – MM: Increases in muscular dystrophy, skeletal
CK – MB: Increase in heart disease, cardiac
Maximal oxygen uptake (aerobic capacity, VO2 max)
The maximum rate of oxygen consumption by aerobic cellular respiration. It is determined primarily by a persons age, size, and sex
Lactate threshold
The percentage of maximal oxygen uptake at which a significant rise in blood lactate levels occurs. For average healthy people, a significant amount of blood lactate appears when exercise is performed at about 50 to 70% of VO2 max
Oxygen debt
When a person stops exercising the rate of oxygen uptake does not immediately return to pre-exercise levels, it occurs slowly in order to repay the excess post exercise oxygen consumption
Type I Muscle fibers/slow oxidative fibers (red)
• Sustain a contraction for a long time without fatigue (Postural muscles)
• high oxidative capacity for aerobic respiration
• rich in capillaries, mitochondria, aerobic respiration enzymes, and myoglobin
Myoglobin
Red pigment that improves the oxygen delivery to the slow-twitch fibers to help sustain contraction
Type IIA Muscle fibers/Fast oxidative fibers (red)
• Used for walking
• fast twitch fibers with high oxidative capacity, resistant to fatigue
Type IIX muscle fibers/fast glycolytic fibers (white)
• Used for explosive actions, exercise
• Powerful high tension contractions but fatigue quickly
• Large stores of glycogen and glycolytic enzymes which allow for anaerobic metabolism
• The fast twitch fibers have fewer capillaries, mitochondria, and myoglobin

Reasons for muscle fatigue
1.) increase concentration of PO4 From the breakdown of phosphocreatine
2.) Decreased ATP hinders the action of the Ca2+ pumps
3.) increased ADP in the cytoplasm decreases the velocity of muscle shortening
4.) Depletion of muscle glycogen decreases the release of calcium from the SR 
Central fatigue
Muscle fatigue caused by changes in the central nervous system, such as reduced activation of muscles by motor neurons
Effects of endurance training on skeletal muscles
No enlargement, instead increased size and number of mitochondria, improved ability to obtain ATP from oxidative phosphorylation, less lactic acid produced, improved efficiency in extracting oxygen from blood
Effects of resistance training on skeletal muscles
Muscle enlargement. Muscle hypertrophy associated with the increase in size of myofibrils and the increase in the number of myofibrils within the muscle fibers
Myostatin
Inhibits activation of muscle repair, ridding of this might lead to larger muscles
Upper motor neurons
Motor cortex:  planning, initiating and directing voluntary movement
Brain stem: postural control, locomotion, basic voluntary movement
Basal ganglia: getting proper initiation of movement
Cerebellum: sensory motor coordination
Lower motor neurons
Spinal cord and brain stem circuits: reflexes
Skeletal muscles: contraction
— Lower neurons directly innervate muscles
Alpha motor neurons
Efferent nerve fiber: Innervates extrafusal muscle fibers, with fast conduction
Stimulation of alpha motor neurons causes muscle shortening
Gamma motor neurons
Efferent nerve fiber: innervates intrafusal fibers, With slow connection
Stimulation of gamma motor neurons causes isometric contraction of spindles and enhances the stretch reflex
Disynaptic reflex of Golgi tendon organs
1.) tension on tendon activates sensory neuron
2.) Sensory neuron stimulates interneuron
3.) Interneuron inhibits motor neuron
4.) Tension on tendon is reduced
Reciprocal innervations of muscles
1.) muscle stretch activates spindle apparatus
2.) Agonist muscle contracts in stretch reflex
3.) Antagonist muscle relaxes
Double reciprocal innervation of muscles
Example: stepping on a nail
1.) Flexor contract and extensor relaxes to withdraw foot
2.) Simultaneously, extensor contracts and flexor relaxes and contra lateral leg to support the weight
Troponin tests
Cardiac-specific troponin T or troponin I released into the blood when myocardial cells die
— relies on antibodies, better than CK tests
Single-unit smooth muscle
Ex. Digestive tract
• one autonomic neuron, smooth muscle cells connected by gap junctions to continue electrical pulse transmission (only one cell innervated)
Multi-unit smooth muscle
Ex. Lens control
• multiple autonomic neurons
• smooth muscle cells not connected by gap junctions, each cell innervated separately
Developmental dysplasia of the hip (DDH)
• biggest risk factor is first born, breech presentation and Incorrect swaddling/ family history
• hip instability, subluxation/dislocation of the femoral head and or acetabular dysplasia in a developing hip joint
Ortolani diagnosis
DDH, reduction maneuver (Femoral head is out, and we put it back in)
Barlow’s diagnosis
DDH, dislocation maneuver (Femoral head is in the right position, we push it out) 
Frank dislocation
Complete hip dislocation, irreducible, arthrogryposis, myelodysplasia
Late diagnosis of DDH
• Limited abduction
• Galeazzi: apparent leg length discrepancy
• Unilateral leg folding
• Barlow/Ortolani: signs may not be present after 2 to 4 months of age
Obstacles to reduction
• tight muscles, adductors, iliopsoas
• intra-articular obstacles: Capsular construction/ileus OS tendon, ligamentum teres, labrum, TAL, pulvinar 
Treatment of DDH
• <6mo: Pavlik harness, successful 95% — Contraindicated in children with muscular imbalance
• >6mo: closed reduction, arthrogram, Spica casting, abduction orthosis following cast
• Open reduction if: failure closed reduction, persistent subluxation, soft tissue interposition, unstable reduction
DDH treatment for children older than two years old
• Open reduction
• femoral shortening
• Acetabular procedure (Cut acetabulum and bring rim down)
When to refer for DDH
1.) abnormal exam, ultrasound, or X-ray
2.) baby born in breech position, ultrasound around six weeks of age
Legg-calve-Perthes disease (LCPD)
• most common in boys, positive family history, Low birth weight, secondhand smoke
• Vascular insult of femoral epiphysis leads to osteonecrosis, AVN

Stages of legg-calve-Perthes disease
1.) initial: infarction produces a smaller, sclerotic epiphysis with medial joint space widening
2.) Fragmentation: presence of subchondral loosened line, femoral head appears to fragment or dissolve, patchy density and lucencies
3.) Re-ossification: ossific nucleus undergoes re-ossification with new bone appearing as necrotic bone is reserved
4.) Healing or remodeling: femoral head remodels until skeletal maturity
Clinical presentation of LCPD
• insidious limp, can be painful or painless, hip thigh or knee pain
• Limited abduction and internal rotation, synovitis, muscle spasm, thigh atrophy, leg length discrepancy
• Poor prognosis in children older than seven, percent of head involvement, protracted disease course
Treatment goals for LCPD
1.) Restore range of motion
2.) Containment of femoral head
3.) good outcome more than likely, 60% of patients require no surgical intervention
When to refer for LCPD
• School aged children with thigh, hip, knee pain
• decreased ROM, atrophy
• Abnormal imaging or labs 
Slipped capital femoral epiphysis, SCFE
• posterior and inferior displacement of the femoral head in relation to the femoral neck at the proximal femoral growth plate (Between epiphysis and metaphysis)
• risk factor: males, obesity, family history, endocrine/hormones 
Clinical presentation of SCFE
• Pain in thigh or knee
• limp: external rotated gait
• Limited internal rotation and flexion
• Obligatatory external rotation of hip with passive flexion
Treatment/ referral of SCFE
• In situ fixation, osteotomy for deformity, epiphysiodesis, prophylactic pinning of normal side
• Immediately refer any SCFE needs, strictly nonweightbearing
Increased femoral anteversion
• hip rotation, increased medial rotation compared to lateral
• 40° in infants, 10 to 60° average an older children
• Increases until age 10 and then normalizes, more common in girls
Internal tibial torsion
• thigh foot angle is 5 to 30° normally, Diagnosis of ITT is greater than 10° internal with in-toeing gate
• no treatment necessary, resolves on its own
• Osteotomy for severe persistent deformity an older children
When to refer for internal tibial torsion
1.) recent specific change in gate
2.) Functional problem
3.) Persistent problem and older children (older than six)
4.) Family wants referral
Genu Varum, Bow legged
• Bowing distributed between femur and tibia
• Early/agile walkers, family history common, bilateral
• Spontaneous correction and Serial photos are helpful
Blounts disease
• Osteochondrosis, deformity focused as proximal medial tibia causing metaphyseal Beaking
• Brace treatment in children less than three
• Valgus proximal tibia osteotomy in children between three and four years old
When to refer for bowing 
1.) height less than 5th percentile
2.) Positive family history
3.) asymmetry
4.) Progressive condition
5.) Localized Varus deformity
Genu valgum, knock knees 
• symmetric, apparent after two years, remodels to normal by age 7
• Patellar instability can be associated
• Treatment: hemiepiphysiodesis, stapling, eight points, osteotomy
When to refer for genu valgum
1.) less than 10th percentile for height
2.) Asymmetry
3.) Deformity increasing after age 7-8
4.) History of metabolic disease/skeletal dysplasia
Metatarsus adductus
• medial deviation of forefoot on hind foot
• likely caused by intrauterine positioning
• Hip dysplasia, bilateral in around 50%
Clinical features of metatarsus adductus
• forefoot Adductus
• Hindfoot neutral
• Medial crease
• forefoot slightly supinated
• Full dorsiflexion
• Supple versus rigid
When to refer for metatarsus adductus
1.) stiff foot
2.) No self correction at six months
3.) Shoe problems
4.) Hindfoot in valgus (skewfoof) or Equinus (Clubfoot)
Congenital talipes equinovarus — clubfoot
• most common MSK birth defect, isolated deformity and 80%, genetic
• forefoot adductus, hindfoot equinus, varus, cavus, shortening of foot, atrophy of calf 
Club foot treatment
1.) after birth: Ponsetti serial casts
2.) braces until four years old needed to prevent recurrence
3.) Percutaneous Achilles tenotomy
4.) Occasionally requires anterior tibial tendon transfer has an older child
Flexible flat feet (flexible pes planovalgus foot)
• often notice on child is standing, fat pad disrupts view of the arch however arch is the present when on tippy toes • Where are the causes problems in adults
Flat foot/ rigid flatfoot
• tight Achilles, may have pain
• Orthotics occasionally help with pain
• rigid: tarsal coalition, Congenital synostosis or failure of segmentation between two or more tarsal bones 
Types of rigid flat foot
• Calcaneonavicular
• talocalcaneal
• Talonavicular
• Calcaneocuboid
• Cubonavicular
Symptoms: lack of subtalar movement, frequent ankle sprains, tendon spasms
Treatment: orthotics, excision an interposition, fusion
Leg and arm postnatal growth
• 60% of growth of the legs from physis around knee
• 80% of growth of arm from proximal humerus and distal radial physis 
Physeal anatomy 
• reserve zone
• Zone of columns
• Hypertrophic zone
• Calcified cartilage zone
• primary spongiosa 
Treatment for physeal fractures
• simple immobilization
• Closed reduction
• Percutaneous fixation
• Internal fixation
• Displays fractures often need to be reduced
• Unstable fractures may need to fixation
• Salter three and four require anatomic reduction — intra-articular
Remodeling helps when:
1.) children with two or more years of predictive growth
2.) Fractures near the bone ends— distal
3.) Deformity in the plane of motion of the joint
4.) translation or bayonet position without shortening
Remodeling does not help:
1.) displaced intra-articular fractures
2.) Malrotated fractures
3.) Fractures with angulation out of the plane of motion
Proximal humerus fractures
• salter one common in neonates
• Metaphyseal fractures most common in 5 to 10 year olds
• Adolescence usually get Salter one or two, closed reduction and pinning
Supracondylar humerus fractures
Type one: nondisplaced
Type two: distal fragment extended
Type three: Marked displaced
Treatment: immobilization, closed reduction if displaced, open reduction if necessary
Complications of supracondylar fractures
•Neurapraxia, stretch nerve injury to anterior interosseous (Most common), radial, or ulnar (most common in flexion type)
•Vascular injury
• Malunion
Lateral condyle fracture of the humerus
Salter fracture of the distal humerus, localized soft tissue swelling, often delayed diagnosis
Treatment: non-displaced is closed, displaced greater than 2 mm is open reduction, displaced less than 3 mm is percutaneous pinning
Forearm fracture treatments
Nondisplaced: Long arm cast
Displaced: reduction and casting
Occasionally: internal fixation
Guidelines for acceptable reduction
- Age less than nine
- Complete displacement, 15° angulation in AP plane, 45° in lateral plane
- 10° of angulation
- Some bayonet if no shortening 
Distal radius fractures
• Metaphyseal and Salter fractures
• Occur from fall on outstretched hand, 20 to 40° dorsal/volar angulation in children less than 10 is okay
• Not OK: radioulnar angulation, large amounts of angulation and children older than 10 
Femur fractures
• High energy trauma
• Immediate spica cast, traction with delayed casting, flexible nailing, submuscular plating, rigid nailing, external fixation
Immediate spica cast for:
Femur fractures from low energy trauma, children under five, initial shortening less than 2 cm
Operative indications from femur fractures
Poly trauma, Head injury, open fracture, vascular injury, Pathologic fracture
Distal femoral physeal fractures
• valgus stress in adolescents — Watch for growth arrest
Proximal tibial physeal fracture
High incidence of vascular injury, popliteal injure artery, unstable
— Type I through type IV
Tibial eminence injury
• epiphyseal and articular fracture
Treatment:
Type I: Immobilization
Type II: reduction in extension
Type III: Open reduction, internal fixation with or without arthroscopy 
Patellar sleeve fracture
• unique to children, difficult to make diagnosis, cartilaginous portion on patella avulses Requiring open reduction
Tibia fractures
• more common in toddlers, proximal tibial metaphyseal fractures
Treatment: majority are closed reduction, long leg casting, weight-bearing cast when stable
Indication for open treatment of tibia fractures
Open fracture, unstable fracture pattern, compartment syndrome (older adolescent males), vascular injury
Ankle fractures
• often physeal
• Triplane fractures, tillaux fractures
• common in adolescence, may require reduction and fixation
• Triplane includes Salter two and three in different spots
Necrotizing fasciitis
Infection leading to the necrosis of subcutaneous tissue. Severe pain is common. Infection should be treated very seriously and aggressively through surgery and IV antibiotics and fluids
Acute infectious arthritis
Rapidly progressing join infection. Usually bacterial in origin
Osteomyelitis
Inflammation and destruction of bone caused by bacteria, mycobacteria, or fungi. Causes localized bone pain and tenderness. 80% of infections result from contagious spread or from open wounds
Myositis
Infection of the muscle that leads to muscle inflammation. Can be caused by many different micro organisms including viruses, bacteria, and helminths
Three ways bacteria initiate infection
1.) Breach the skin
2.) systemic disease
3.) Toxin mediated damage
Primary cause of necrotizing fasciitis
- Streptococcus pyogenes
- Can also be from staphylococcus aureus, or polymicrobial
- 50% of patients have experienced a recent minor trauma, surgery, or varicella infection
Description of Streptococcus pyogenes
Bacteria, gram-positive, Cocci, catalase negative, beta-hemolytic, bacitracin sensitive
Symptoms of necrotizing fasciitis
Septic appearing: high fever, high HR, AMS, low blood pressure, leukocytosis, positive cultures
— Rapid onset, painful, skin color changes
Erythrocyte sedimentation rate, ESR
Rate at which red blood cells precipitate in a period of one hour when anticoagulated blood is allowed to stand.
Normal: less than 20 mm/hr
Elevated in: anemia, endocarditis, kidney disease, osteomyelitis, pregnancy
C reactive protein, CRP
Produced in the liver and is present in circulation at low levels normally. Involved in the promotion of immune system through activation of the complement cascade. IL1, IL6
Normal: less than 1 mg/dL
Elevated in: bacterial infections, inflammation, acute rheumatic fever, acute rheumatoid arthritis, IBS
Necrotizing fasciitis differential
Air: gas gangrene, Compartmental syndrome
Bone destruction: osteomyelitis
Intramuscular abscess: deep muscle involved
Foreign body: would cause edema
Septic shock criteria
• SIRS
• Source of infection
• Organ dysfunction, Hypotension, hypoperfusion (severe sepsis)
• Severe sepsis despite adequate fluid resuscitation (Volume overload, continued low venous pressure)
Multiple organ dysfunction syndrome criteria
• septic shock criteria
• Evidence of two or more organs failing: elevated creatine kinase, elevated creatinine, elevated lactic acid, elevated AST/ALT
Treatment of necrotizing fasciitis with severe shock
1.) restoring tissue perfusion
2.) Antimicrobial therapy, vancomycin and clindamycin empirically
3.) Surgical debridement
Other sources of necrotizing fasciitis
Graham negative vibrio vulnificus— Associated with wound infections contaminated with Marine water containing this bacteria
Treatment: levofloxacin and doxycycline
Acute infectious arthritis
Rapid joint infection in synovial cavity or periarticular tissue causing pain, range of motion restriction, and positive synovial fluid and blood cultures
Organism: Staphylococcus aureus (everyone), neisseriera gonorrhea in sexually active young people
Treatment: IV antibiotics
Staphylococcus aureus description
Bacteria, gram-positive, cocci in clusters, Catalase positive, coagulase positive
Neisseria gonorrhea description
Bacteria, gram-negative, diplococci, oxidase positive, only glucose oxidizer
Causes of Osteomyelitis
• Staphylococcus aureus (Streptococcus pyogenes, strep. pneumonia), salmonella typhii (sickle cell), pasteurella multocida (cat/dog bite)
• more often in the legs in the arms
Salmonella, sickle cell, and osteomyelitis
- The combination of expanded marrow in sickle cell patients together with high oxygen demand and sluggish circulation means that bone is vulnerable to infarction
- Gut divided by station, incidence of invasion and bacteremia
3. Sickle cell pts have reduced bactericidal and opsonic activity against salmonella, capsular bacteria (abnormality in alternative complement) 
Myositis causes: muscle infections
- Clostridium perfringens
- Staphylococcus aureus
- Coxsackie A and B (B more common)
- Dengue fever
- Taenia solium (Helminth)
- Trichinella spiralis (Helminth)
Radiograph
• x-ray, differentiating tissue density and shape
• Radiopaque versus radiolucent
• history and physical or important to interpretation

Most common reasons to obtain radiographs
Traumatic: fractures (also dislocations and sprains)
Nontraumatic: arthritides (also tumors, lesions, infection, osteochondrosis) 
Fractures
A complete disruption in the continuity of a bone, radiolucent line on x-ray. Obtain two views, contralateral and children
Indirect signs of a fracture
1.) soft tissue swelling
2.) Obliteration or displacement of fat stripes
3.) Periosteal and endosteal reaction (callus formation)
4.) Buckling of the cortex
5.) Double cortical line
Displacement versus angulation
Displacement: translation, distal bone parts moves away from normal bone midline
Angulation:  Bones still have continuity, but angle
Radiology of arthritis
• x-rays are the most important radiologic imaging modality
• The radiographic diagnosis of arthritis is based on the morphology of an articular lesion and it’s distribution in the skeleton 
Radiographic features of arthritis
• periarticular osteoporosis, radiolucent
• Subchondral sclerosis, radiopaque
• soft tissue swelling/Subchondral cystlike lesions
• Subchondral erosion
• Narrowing of joint space/joint effusion
• Osteophyte formation
Osteoarthritis
• marginal osteophytes
• Cortical irregularity
• Subchondral sclerosis
• Subchondral cysts
• Joint space narrowing
Rheumatoid arthritis
• seen in more joints, widespread
• Periarticular osteoporosis
• Joint effusion
• Joint space narrowing
• Articular erosions/destruction
• Synovial cyst
• Deformities
Advantages and disadvantages of CT
Advantage: best evaluation of fracture and or dislocation patterns, relatively quick scanning and processing time
Disadvantage: limited contrast of tissue types compared to MR or US, Ionizing radiation, cost
Most common reasons for CT
1.) assess fracture: presence of it, fracture pattern, healing
2.) Assess integrity of joint fusion
3.) Preop planning for total joints 
Advantages and disadvantages of MRI
Advantage: multiplanar, soft tissue contrast, higher resolution of soft tissue, no ionizing radiation, contrast better tolerated
Disadvantage: discomfort/motion artifact, resolution of small structures, no metal, cost
Bone scan advantages and disadvantages
Advantage: widespread evaluation, Best evaluation of bone activity, not degraded by metal
Disadvantage: limited information, ionizing radiation, availability/cost
Ultrasound
Use of high frequency sound waves to image soft tissues and bony structures for the purpose of diagnosing pathology or guiding real time interventional procedures
Advantage: portability, cost, oversight, patient friendly
Disadvantage: limited field of view/penetration, and complete evaluation of bone and intra-articular structures, lack of competency
Woven bone
Immature bones, healing bones, rapid, weak, irregular, no consistent orientation. Primary/initial bone for healing
Lamellar bone
Mature bones, forms on or in existing matrix, slower forming, strong, regular, parallel fibrils form distinct Lamellae 
Sequence of bone fracture healing
1.) inflammation phase: Inflammatory mediators, vasodilation, edema, PMN lysis, Angiogenesis —> Fibroblast, osteoblast, chondrocytes
2.) Reparative phase: Soft callus —> hard callus, Recruitment of pluripotent mesenchymal cells to the side of the fracture. clinical union, radiographic union
3.) Remodeling phase: years, Replacement of woven bone by lamellae bone, resorption of unneeded callus 
Injury variables
1.) soft tissue damage, open versus closed
2.)  bone communition and displacement
3.) Location of bone injury
4.) Age

Fracture repair after internal plate fixation
Fracture gap closed by fixation, no formation of external callus. Lamellar bones form directly across fracture line, bypassing regular healing. This takes longer
Growth plate zones
- Proliferative zone
- Hypertrophic zone
- Metaphysis
Maturation occurs distal to proximal. Injury to the proliferative zone can cause bone deformity (Salter-Harris 3, 4 and 5 classification)
What do you need to maintain a healthy skeleton
• dietary intake of calcium, phosphorus, vitamin D
• Healthy gut, active kidney function, healthy liver
• Ability to exercise
• Healthy parathyroid gland
Four main systems of calcium phosphate homeostasis
1.) endocrine: Hormonal mediation via parathyroids
2.) GI: Absorption
3.) bones: turnover
4.) Renal system: filtration and absorption
99% of total body calcium stored as
Calcium hydroxyapatite in bones
Impact of acidity on calcium homeostasis
Increase in pH causes increased affinity of albumin to bind the calcium leading to hypocalcemia. Cramps, pain, paresthesia, spasms, Stimulation of PTH production
Hypercalcemia
Malignancy, vitamin D toxicity, thiazide diuretics, alkali syndrome, increase bone turnover
Hypocalcemia
Pseudohypoparathyroidism, Hypoalbuminemia, severe hypomagnesemia, renal osteodystrophy, calcium sequestration via pancreatitis, rhabdomyolysis, tumor lysis, acute renal failure
Phosphorus
Absorbed in the small intestine, or from bone release.
Increase in phosphate levels: bisphosphonates, vitamin D toxicity, hypoparathyroidism
Decreasing phosphate levels: renal disease, hyperparathyroidism, increase in insulin/glucose
Parathyroid
• regulated by serum calcium
• Increases serum calcium by bone resorption, Renal reabsorption, increases Renal production of Calcitriol
Thyroid
• stimulates growth hormone to increase bone growth
• Stimulates calcification in closure of cartilaginous growth plates
• Hyper thyroidism is associated with increased bone loss
• Calcitonin secretion
Calcitonin
• minor effect
• Secreted by parafollicular cells, as a response to high serum calcium
• Decreases resorptive activity of osteoclasts

Effect of PTH on calcium and phosphate metabolism
The net effect is:
1.) an increase in the plasma calcium concentration
2.) no change or a decrease in the plasma phosphate concentration
Estrogen and androgens in bones
Estrogen: affects terminally differentiated chondrocytes
Androgen: affects proliferating chondrocytes
Calcitriol
The most biologically active form of vitamin D, half life is 4 to 6 hours
1, 25-hydroxyvitamin D
Calcidiol
Major storage form of vitamin D and it generally is checked for lab testing. Half life is 2 to 3 weeks
25-hydroxyvitamin D
Enzymatic conversion of vitamin D to active form
Inhibited by: Increased phosphate, increased calcitriol, FGF23, PTH
Stimulated by: hypocalcemia (by PTH), hypophosphatemia 
Causes of vitamin D deficiency or resistance
1.) deficiency in intake or absorption
2.) Decreased skin synthesis
3.) Defective 25 hydroxylation
4.) Increase catabolism of vitamin D to inactive metabolites
5.) Loss of vitamin D binding protein
6.) Defective 1-alpha 25 hydroxylation
7.) Defective target organ response to calcitriol
Optimal level for healthy population of vitamin D
25 to 50 ng/mL
Vitamin D recommended supplementation
> 70: 800 IU
Average: 400 IU
Pregnancy: 600 IU
Looser zones
Seen on x-ray when bone is weak, insufficiency fractures. Usually right angles to bones, symmetrical, sclerotic irregular margins
Scene with: osteomalacia, Paget’s disease, fibrous dysplasia, hyperparathyroidism, OI, renal osteodystrophy
Osteoporosis
Bone thinning due to bone atrophy, imbalance in bone remodeling process resulting in increased fx risk. Reduction in bone mass but normal mineralization
Diagnosis: osteoporosis fracture, T score less than -2.5
Complication of inactivity after hip fractures
Bowel issues, skin ulcers, instability and second fractures 
Changes in age influence bone density by:
• Ability of kidneys to hydroxylate vitamin D to the active form
• post menopausal changes, diminished PTH, increased osteoclastic activity
• Decreased ability of osteoblasts to make matrix with age
Classic fractures of osteoporosis
- Hip fractures
- Colle’s fracture
- Vertebral compression fractures
Osteoporosis risk factors
• Low bone mass, inactivity
• Smoking
• Dietary issues
• Endocrine issues
• Estrogen issues
Bone density testing
Use dual energy x-ray absorptiometry (DXA)
Normal bone mass: -1.0 to -1.49
Low bone mass: -1.50 to -1.99
Low bone mass with high risk factors: -2.0 to -2.49
FRAX score
Screens for the tenure probability of a hip fracture or major osteoporotic fracture
First line treatment of osteoporosis
Bisphosphonates: inhibit osteoclast activity, reducing bone resorption and turnover
Primary hyperparathyroidism, PHPT
• bones, stones, abdominal moans, psychic groans
• Hypercalcemia due to hyperplasia or neoplastic enlargement of parathyroid glands
• elevated PTH: increase in osteoclastic activity
Secondary Hyperparathyroidism— Renal disease
Most commonly occurs because of decreased levels of 1,25-dihydroxyvitamin D, hyperphosphatemia, and hypocalcemia
Periosteal inflammation
Feathery bone, severe tuft changes in secondary HPT
Demineralization of the skull
Salt and pepper school/pepper Potts school: ground glass appearance, spotty the ossification
Osteomalacia
Decreased bone mineralization of newly formed osteoid at sides of bone turnover – wide Osteoid seams
Due to: hypocalcemia, hypophosphatemia, direct inhibition of the bone mineralization process, disorders of vitamin D metabolism (Rickets in kids)
Osteomalacia: causes and associations
• Poor diet, sun exposure, intestinal malabsorption, vitamin D deficiency, Celiac, gastric bypass
• Liver or renal disease, impaired hydroxylation of vitamin D
• Inborn errors in metabolism
• Genetic (OI) 
Clinical manifestation of Osteomalacia
• Bone pain
• muscle weakness, proximal
• fracture, looser zones
• Gait disturbance, waddling
• muscle cramps/spasms
• Severe hypocalcemia
Diagnosis of osteomalacia
• elevated alkaline phosphatase
• Elevated PTH
• Low calcium and phosphorus
• Decreased vitamin D
• Renal function/type to renal tubular acidosis
Avascular necrosis
Aseptic necrosis, osteonecrosis, atraumatic necrosis, ischemic necrosis. Bone infarct due to ischemia of varying and often poorly understood causations leading to progression of death of bone or marrow cells— Most common in femoral head
Diagnosis of Avascular necrosis
• alcohol use and steroids, 80%
• SLE
• Slow change over months to years: hyperemia —> demineralization —> Trabecular thinning —> Collapse
Associations of avascular necrosis
• fractures, legg-calve-Perthes disease
• gaucher’s disease
• Alcoholism, does linked
• SLE
• Sickle cell anemia
• caissons disease
• ALL
Gold standard and diagnosis imaging for avascular necrosis and osteomyelitis
MRI: high sensitivity, good visualization
Acute osteomyelitis
Inflammatory change from pathogenic bacteria, usually presents within two weeks of infection onset
Chronic osteomyelitis
Necrotic bone, usually present six weeks after onset of original infection
Involucrum
A thick sheath of new periosteal bone surrounding a sequestrum
Sequestrum
A piece of dead bone that has become separated from normal bone in the process of necrosis
Pott’s disease
A type of osteomyelitis resulting from tuberculosis
Paget’s disease
Deforming bone disease of middle aged to elderly adults. Focal disorder of bone metabolism seen in aging skeleton. Thick, cotton ball skull
— Prefers larger bones such as the skull, pelvis, tibia, femur, spine
Clinical features of paget’s
Asymptomatic typically, widening/bowing of long bones, distorted/widening pelvic bones, can mimic malignancy
— Genetic, viral, unknown causes
— Labs: elevated alkaline phosphatase, radiographic evidence, NORMAL calcium and phosphorus
Stages of Paget’s disease
- Lytic: osteoclasts with bone resorption
- Mixed: osteoclasts with osteoblasts
- Sclerotic: most characteristic radiologically: osteoblastic phase
- Quiescent: minimal osteoclast/osteoblast activity
Mosaic cement lines
Thick, abnormal mineralization along lamellar lines in paget’s
Osteogenesis imperfecta
Blue sclera, deformed teeth, brittle bones, Hearing loss
Congenital disorder of type one collagen resulting in insufficient/in adequate collagen for normal osteoid production, joint Laxcity, capillary fragility. Nine subtypes
Osteopetrosis
Marble bone disease, Albers Schonberger disease. Loss of osteoclastic bone resorption, preservation of normal osteoblastic bone formation leading to bones that are thick but brittle and fracture like chalk
Treat with bone marrow transplant, medications, surgery
Ligament
• STABILIZATION
•  special test: Lachman, anterior drawer, pivot shift (ACL) , milk jug (UCL of elbow), Ankle anterior drawer (ATFL)
Baseline radiographic imaging for ligament injury
X-ray
Ottawa rules: Ankle
• pain in malleolar zone
• bone tenderness at posterior edge or tip of lateral malleolus
• Bone tenderness at posterior edge or tip of medial malleolus
• Inability to bear weight both immediately and in emergency department
Ottawa rules: foot
• pain in mid foot zone
• Tenderness at base of fifth metatarsal
• Tenderness at navicular area
• Inability to bear weight both immediately and in emergency department
Tendon
• FUNCTION
• Tendon sheath, tendon, paratenon 
• transmits force of muscle contraction to bone to affect limb movement
Predisposed to tendon injury by:
Age related degeneration, muscle imbalance, weakness, inflexibility, glucocorticoids, inadequate blood supply
FLUORIDATED QUINOLONES 
Tendon injury special tests
1.) empty can: supraspinatus
2.) Thompson’s test: Achilles
3.) Hook test: distal biceps
Tendinopathy
• Degenerative, activity related pain, focal tendon tenderness, intratendionous imaging changes
• absence of inflammation/response
Tendon restoration: nonsurgical
TIME: 3-6 months
• Restoration: strengthening, eccentric movement, pro-inflammatory injections
• Pain relief: rest, activity modification, racing, ice, Acetamenophin, Peritendinous steroids
Tendon restoration: surgical
Complete ruptures/fulfilled take me to tears or susceptible to muscle retraction. Cannot be repaired with delay
Example: distal biceps, Achilles, flexor digitorum profundus
Fibrocartilage injury
• PAIN
• Loadbearing, shock absorption, joint stabilization.
• X-ray —> MRI 
Reasons for repair of fibrocartilage injuries
1.) vascular zone tears in young patients
2.) Unstable flaps, subluxates under condyle, tear > 1/2 meniscus length 
Muscle strain
• Half of all athletic injuries, occurs with powerful eccentric contraction
• most common: two joint muscles, quads, gastroc, hamstring
Hamstring strain
• eccentric contraction: water skiing, terminal swing phase
• Located at myotendonus Junction
• heals by scar formation, fibrosis, contractile tissue does not regenerate
• Relationship with sciatic nerve
Muscle strain prevention
Warm-up, conditioning, strength. Flexibility is less important
Muscle cramping causes
Dehydration, electrolyte disturbances, muscle fatigue, abnormal neuromuscular control
— Gastrocnemius is most common
Muscle contusions
Direct trauma causing damage and partial disruption of muscle fibers, intramuscular hematoma
Symptoms: tenderness, swelling, palpable hematoma, limits in strength/motion
Myositis ossifications
Complication of muscle contusion, Osteoblasts invade the hematoma and cost calcification or ossification at the injury site
— Seen in 20% of quadriceps hematomas
— can be prevented with NSAIDs, will stabilize after a few months
Compartment syndrome: acute
Caused by trauma direct to bone or soft tissue, elevated compartmental pressure compromises tissue perfusion
Solution: release fascia surgically
Compartment syndrome: chronic
Exertional compartment syndrome caused by muscle exertion, can see numbness in foot drop with exercise
— Resolves with rest, can do exercise stress testing, PT, activity modification
Acute articular cartilage injuries
Articular cartilage tear, osteochondral defect: bone loses blood supply
Chondromalacia
• repetitive stress on joint, muscle imbalance leading to uneven where causing pain
• Diagnosed with patellar compression test/palpation over joint
• X-ray/MRI/arthroscopy
• RICE, insects, PT
Bursitis
Can lead to crystalline arthropathy, inflammatory arthritis, infection.
Diagnosis: foggy, warm, erythematous, tender 
Treatment: protection, ice, NSAIDs, steroid injection, bursectomy
Fascia injuries
Most common: IT band and plantar fascia, comes from chronic overuse
Subacromial impingement
Causes: AC arthropathy, rotator cuff tendinopathy or tear, subacromial bursitis
Treatment: rest, ice, NSAIDs, PT, subacromial steroid injection, rotator cuff decompression/repair
The unhappy triad
Lateral direction of force on the knee leads to tear of ACL, MCL, and medial meniscus
Bucket handle meniscus tear
• Long longitudinal tear with displacement of the medial meniscus towards the cruciate ligament, flipped meniscus indicates an inversion of the parts within the knee joint
• Time sensitive. Lots of passive motion and inability to bear weight should raise suspicion. Limited opportunity for this meniscus repair
Femoral neck hip fracture
Circulation of femoral head is at risk, arthroplasty is the treatment of choice
Intertrochanter hip fracture
Good circulation, unstable, best treated with fracture stabilization surgery (pins)
ACL surgery
Requires a graft because it does not have good circulation, use arthroscopy
Knee replacement
Best predictor of post operative motion is pre-operative motion (ligament capacity)
Medical conditions can worsen outcome: smoking, diabetes, obesity
Ankle injuries
Achilles injury, fracture, dislocation, soft tissue injury
The most common malignancy involving the bone
Tumor metastasis, both lytic and blastic changes can be present.
Lung, breast, prostate are most common origin
Plasmacytoma
Hematologic malignancy INVOLVING bone– metastatic. Localized tumor of plasma cells, a solitary lesion in bone, sometimes extramedullary
Clinical feature: skeletal pain, fractures
Treatment: radiation, surgery, chemotherapy
Multiple myeloma
Relatively asymptomatic, older population affected, neoplastic, proliferation of small lymphoid cells leading to the production of monoclonal plasma cells proliferating in the bone marrow
Hypercalcemia, renal, insufficiency, anemia, bone pain
Fried egg appearance, with Clockface, chromatin plasma, morphology, cast nephropathy
Diagnostic criteria of multiple myeloma
Greater than or equal to 10% clonal plasma, cells, or biopsy proof
Plus: organ tissue impairment related to plasma cell disorder, or biomarker associated with and organ damage
Treatment of multiple myeloma
Chemotherapy, bisphosphonate, autologous, hemopoietic cell transplantation
Diaphysis primary bone lesion
•Round cell lesions, Ewing, sarcoma, myeloma
•Osteoid osteoma
•Fibrous dysplasia
Metaphysis primary bone lesions
•Osteosarcoma
•Simple bone cyst
•Osteochondroma
•Giant cell tumor
Metaphyseal fibrous defect: non-ossifying
Most common bone lesion, nonneoplastic, developmental defect in 1/3 of children, self resolves
metaphyseal cortical defect, fibrous cortical defect, bone scar. Well-demarcated, sclerotic border, asymptomatic. More worried when TIBIA involved
Fibrous dysplasia
Sporadic genetic disorder where portions of bone replaced by fibrous, connective, tissue and poorly formed trabecular bone. “ shepherd, crypt deformity: coxa varus angulation.”
Most common in the femur, tibia, ribs, skull, facial bones in younger people
Treatment: curettage, grafting, stabilization, bisphosphonates
Fibrosseous lesion: fibrous dysplasia
Lower extremity, mandible, sinonasal, pain associated with fractures, originates in cortex
Treatment: regress with the time, intervention to correct deformities
Osteoma
Benign outgrowth of membranous bone, para, nasal sinuses, skull, long bones. CT preferred.
— well-defined border, gardeners syndrome
— usually resolved spontaneously
Osteo blastoma
Destructive, larger than 2 cm, presents in young people, most common in the posterior column of the spine
Diagnoses: pain, CT or MRI
Treatment: curettage/grafting or excision, radiation
Osteochondroma
• 30% of benign tumors
• cartilage forming tumor
• painless mass, near a joint or axial skeleton, stop growing when epiphyseal plates close. Treatment is rarely needed.
Endochondroma
• stippled, calcification and preservation of cortex without Endosteal erosion
• cartilage forming tumor
• develop in medulla of long bones, long bones of the hand, humorous, femur
Treatment: curettage, graphing, rarely transforms into malignancy
Chondroblastoma
• very rare, cartilage, forming tumor
• well-defined, sclerotic border, may cross physis
Treatment: curettage, grafting
Condromyxoid fibroma
• very rare cartilage, forming tumor of the tubular long bones
• treatment: curettage and grafting, prognosis is good
Unicameral bone cyst
• lesion with cystic/vascular origin
• fluid filled cysts with a fibrous lining often presents as a pathological fracture
• fallen leaf sign, not recurrent
Treatment: spontaneously resolves in all patients, although fracture can occur before resolution
Aneurysmal bone cyst
• lesion with cystic/vascular origin, expansile, vascular lesions with blood filled channels, common and posterior spinal elements, femur, tibia
• treatment is curettage, graphing, chemical, cauterization, cryotherapy, denosumab
— they will expand until treated, locally, aggressive, and risk of reoccurrence
Giant cell tumor
• usually benign but can be malignant presents in twenties to forties
• association with Paget’s disease
• “soap bubble” CT
• BIOPSY PREFERRED
Treatment: surgery, medication, radiation therapy. Difficult to treat when sacral and spinal involvement.
Giant cell tumor, malignant transformation
Primary: high-grade sarcoma arising within a GCTB
Secondary: sarcoma arising at the site of previously treated GCTB. 20 to 50% of GCT be recur and 10% of those become malignant.
Benign tumors
Epiphysis: chondroblastoma, giant cell tumor
Metaphysis: Osteoblastoma, osteochondroma, non-ossifying, fibroma, osteoid osteoma, Condramyxoid fibroma, giant cell tumor
Diaphysis: enchondroma, fibrous dysplasia
Malignant tumors
Diaphysis: Ewings sarcoma, chondrosarcoma
metaphysis: osteosarcoma, juxtacortical osteosarcoma
Osteosarcoma
•Bimodal clusters: peaks in early adolescence and older adults
• symptoms of pain, fractures, cortical, breakthrough, abnormal, mineralization, poorly circumscribed
• “moth eaten” “ Sunburst” “ Codman’s triangle”
Treatment: chemo, surgery, more chemo
Chondrosarcoma
•Most common primary bone tumor of middle-aged and older adults, tend to grow very large and metastasized to the lung
• prefers larger, flat bone
• presents with swelling, pain, metrics mineralization
Treatment: surgical, excision, radiation, chemotherapy
Ewing sarcoma
• 10 to 15% of bone sarcomas
• family of tumors, genetic component
• most aggressive/lethal of all primary bone, tumors, second most common
• prefers diaphysis of long bones and flat bones
• soft tissue mass stuck to bone, cortical erosions, Sunburst, “onion skinning”
• primitive neural ectodermal, neoplasm tumors (PNET)
Treatment: 10 to 20% survival rate, surgery, radiation, chemo, high recurrence rate
The most common cause of disability and people under 45 years old
Lower back pain. Nine out of 10 people will have LBP at some point.
Sciatica
Pain in the distribution of the sciatic nerve
True radiculopathy
Nerve root pain from herniation of one or more lumbar intervertebral discs or compression due to stenosis
Increased risk for lower back pain
• height
• age
• genetic
• occupation
• smoking
• education/psychosocial factors
Facet joints
Allow movement between vertebrae, protect desk from sheer forces, excessive rotation
Intravertebral discs
• avascular
• receive nutrients from vertebral body end plates
• supplied by segmental arteries from aorta
• cells rely on glycolysis
• center of disks have colon low oxygen, low glucose, high lactic acid, low pH
a.k.a. discs do not heal well
Degenerative disc disease
Wear and tear degenerative changes through the spine related to age, genetic factors, activity, injury
Stages of disc herniation
1.) disc degeneration
2.) prolapse: impingement, bulge
3.) extrusion: nucleus, proposes breaks through the tirelike wall but remains within the disc
4.) sequestration or sequestered disc: nucleus, pulposus, breaks through the annulus fibrosis, and lies outside the disc of the spinal canal
Neurogenic claudication
Numbness, weakness of both legs which worsens the longer the patient stands or walks
Anatomical causes of LBP and radiculopathy
Lumbar degenerative disc disease, spondylosis, instability, herniated nucleus pulposus, spinal stenosis, spondylolisthesis, scoliosis
Non-skeletal causes of radiculopathy
Diabetes, infection, vascular problems, inflammation, malignancies
Yellow flags of LBP disability
Physical, individual, psychological
LBP red flags
Cancer history, unexplained weight loss, IV drug use, immunosuppression, infection, fever, bladder or bowel incontinence, urinary retention, weakness, neurological findings
Five categories of management options for LBP, and or radiculopathy
1.) modalities, PT, exercise
2.) medications
3.) injections
4.) bracing/orthotics
5.) integrative/alternative treatments
Acute low back pain care
Emphasize pain control, reduce inflammation and spasm
Avoid bed rest and resume normal activities ASAP
Medication’s for the acute phase
Anti-inflammatories, muscle relaxers, neuromodulating, opioids
Restorative phase
Directed toward normalizing range of motion, correcting biomechanical deficits, enhancing flexibility/strengthening torso and extremity muscles
Maintenance treatment phase
Directed toward sport/activity, specific training, and elimination of medication management
Surgical indications for lower back pain
• progressive, neuromotor deficits
• cauda equina syndrome
• cervical thoracic myelopathy
• intractible pain and functional limitation, failing to respond to nonoperative care
Salmonella typhii
Gram-negative, bacilli, lactose non-fermenter, oxidase negative, produces H2S, motile
Pasteurella multocida
Gram-negative, coccobacilli (pleomorphic), oxidase positive, catalase positive
Clostridium perfringens
Myositis: Gram-positive, bacilli, spore forming, obligate anaerobe, non-motile
Coxsackie A and B
Myositis: Heart concerns, virus, ssRNA positive, group 4, non-segmented, icosahedral nucleocapsid, non-enveloped, picornaviridae, enterovirus
Dengue fever
Myositis: Virus, ssRNA (+), group 4, non-segmented, icosahedral nucleocapsid, enveloped, flaviviridae
Taenia solium
Myositis, helminth, transmitted by ingestion, intestinal and tissue infection, (platyhelminthes) flatworm, (cestodes) tapeworm
Trichinella spiralis
Myositis, helminth, transmitted by ingestion, tissue, infection, nematodes (round worms)
Order of muscles layers
Myofilament -> myofibrils -> myofiber -> fascicle -> muscle
Neer and Hawkins tests
Neer: painful passive flexion of the arm
Hawkins: flex and internally rotate forearm
Both imply impingement syndrome, supraspinatus
Sulcus sign
General laxity: pull down on arm while a person is sitting/standing: divot/drawer appears above humerus
Lift off
Subscapularis: their hands behind their back, push against them to test strength
Cross body adduction
Acromioclavicular joint
Apprehension sign/ relocation test
Dislocation/subluxation: lay down, arm at 90 degrees, bend towards the floor near head, push on shoulder
Speeds test
Biceps tendon or labral pathology: supinate extended arms, push down on them
O’Brien test
Labral pathology: empty can test + adduction. Push on pt to try to adduct arms and also push down
Cranks test
Labral pathology: humerus + scapula, Raise arm out and to the side, push humerus into joint, forearm at 90 degrees, crank hand up and down
Anterior hip joint disease tests for osteoarthritis, neck fx, septic arthritis, fem-acetabular syndrome, AVN
- Log roll: internally rotate straight leg
- Compressions test at foot and knee: lift leg straight, tap on bottom of foot. Bend leg to 90 degrees, tap on knee toward hip
Lateral hip pain test: for greater trochanter bursitis, external snapping hip
- Palpation of greater trochanter
- external snapping hip: passive abduction and internal/external rotation: IT BAND OVER GR. TROCANTER
- Iliopsoas: flex, abduct, external rotation —> straighten
Posterior hip pain tests:
- Lumbar radiculopathy: straight leg raise against resistance
- FABER: Sacroiliac joint test, cross ankle over knee and push knee towards ground
- FADIR: femoral acetabular impingement, same as FABER but push knee across body
- Piriformis syndrome testing: yoga spinal twist, stretches piriformis
McMurray test
Knee: medial and lateral meniscus: medially/externally rotate leg and bend the knee
Valgus strain
MCL test: inward strain on knee
Varus strain test
LCL test: outward knee strain
Tinel test
Tibial nerve entrapment: tap on medial aspect of ankle
