Musculoskeletal Charts

Musculoskeletal Domain Overview
Condition Diagnose It Pathophysiology Pathology Clinical Course Genetics/Epi Treatment

The motor unit made up of: Lower motor neuron (Cell body + Axon) + NMJ + Skeletal muscle innervated by motor neuron
Peripheral nerve structure:
o Epineurium surrounds many fascicles
Fascicles: Contain Axons (Unmyelinated, Myelinated), Myelin made by Schwann Cells
Endoneurium = CT around axons
Surrounded by Perineurium
o Fiber diameter/number normally have a bimodal population in terms of diameter of fibers. This bimodal distribution
is disrupted in peripheral nerve disease
o Skeletal Muscle: Mm fibers are multinucleated syncytium nuclei are at periphery mostly. Reserve cells at
Muscle periphery regrow skeletal mm when damaged (less of this in cardiac mm)
physiology o Types of skeletal mm:
Review Type 1: Red, slow twitch, sustained action, high in oxidative enzymes, (aerobic), many mitochondria, abundant
(lecture) fat more lipid metabolism happens here
Type 2: White, fast twitch, sudden action, low in oxidative enzymes, (anaerobic), few mitochondria, little fat,
susceptible to disuse
Nerve innervating muscle fiber determines type
Characterization: ATPase stain:
Low pH Type 1 dark, Type 2 light
A little higher: can distinguish Type 2B from 2A (type 2B most vulnerable to disuse)
High pH Type 1 light, Type 2 dark
o Pathology: Atrophy, necrosis, regeneration, hypertrophy, denervation, fibrofatty replacement
Spinal SMA 1 Acute infantile (Wednig-Hoffman) floppy baby sx
Chromosome 5 (SMN gene in 98%). Contiguous NAIP gene associated w/severe
muscular SMA 2 Chronic infantile
phenotype
atrophy SMA 3 Kugelberg-welander
Short internodes, thinly myelinated axons
Seen with HMSN (Hereditary Motor Sensory Neuropathy =Charcot Marie
Segmental Axon intact, often begins Spinal roots involved
Tooth), CIDP(Chronic Inflammatory Demyelinating Polyneuropathy)
demyelination at nodes of Ranvier No denervation atrophy, possible disuse atrophy
Ex: Guillain-Barre, CIDP, HMSN (Charcot-Marie-Tooth)
Onion bulbs with chronic, repeated episodes of de/remyelination
Wallerian degeneration axonal degeneration distal to axotomy
Sprouting an attempt to establish connection with distal stump. If established, regrowth at 1-2 mm/day. Ex: Toxic diseases (organic solvents,
Axonal Destruction of axon plus
Traumatic neuroma mass lesion can form, can be painful. organophosphates, heavy metals,
degeneration myelin sheath
Neurogenic atrophy of skeletal mm if motor nerve vascular disease)
Chromatolysis (nissl substance pushed to periphery) in motor neuron cell body with axotomy
Chronic inflammation, segmental Ascending paralysis, slowed nerve Campylobacter jejuni is most
Guillain-Barre Polyradiculoneuropathy Immune-mediated, likely initiated by infection
demyelination conduction velocity common implicated organism
Chronic
Symmetrical proximal and distal Clinical presentation resembles Guillain Barre, but less acute/longer sx duration,
Inflammatory Lab = NCV and CSF changes like GBS (slow nn
Polyradiculoneuropathy weakness. Chronic inflammation, onion less frequent recovery,
Demyelinating conduction, cytoalbuminologic dissociation).
bulbs with repeated attacks. Relapses/remission in about .
Polyrad.
HMSN-1 Peripheral myelin protein 22 (PMP-22) mutations (usually 17p11.2 duplication) account for
Hypertrophic nerves, inverted
(Charcot- Polyradiculoneuropathy 90%. Function of protein is unknown. 20% have significant disability, 20% asx.
champagne bottle legs
Marie-Tooth): Others have HMSN1b or X-linked forms (connexin 32).
Diabetic Axonopathy, demyelination, or both. CSF protein Symmetrical distal polyneuropathy (stocking/glove), autonomic neuropathy (orthostasis, impotence, GI motility problems),
Polyradiculoneuropathy
Neuropathy often elevated. mono neuropathy or mononeuropathy multiplex (motor or sensory, LS plexus, femoral nerve have prominent atrophy).
o Altering ATP homeostasis Results in Phenotype Restructuring
5 basics things to know: o Changes in pattern of activity alter phenotype = mechanical + metabolic
o Muscles are controlled by nerves o Changes in metabolism with same activity alters phenotype
Skeletal mm cells are run by neurons: o Potential sites of action:
Motor unit = 1 neuron + many mm cells Direct modulation of genome expression by energy metabolism OR
1 to 1 AP transmission at neuron-muscle synapse (NMJ = endplate) Operates at physiologic level to alter common signal pathway
Skeletal mm APs: o Calcium homeostasis modulates function and phenotype and is sensitive to cellular energetic
Ionic basis: as in motor neuron depolarization due to fast voltage-gated Na+ status (ADP, ATP, etC)
channel, repolarization due to fast voltage-gated K+ and Cl- channel o Physiologic signals: Calcium cycling, Energy charge, REDOX, Mechanical strain
Conduction velocity along fiber very fast (~5 m/s large diameter) o Loading is important for homeostatic control of mass:
Relatively long spike duration and delayed repolarization due to t tubule system o mTOR involved in hypertrophy can modulate by lifting
Time course of AP, Ca, and force o Ubiquitin linked to atrophy
AP: 1-2 ms o Atrophy: Happens naturally (bedrest), antigravity, lack of use
o Loss of Ca and ATP Free Energy homeostasis results in disease pathology
Ca: peak 5-10 ms
o MM damage: Appears brighter in MR (up to 4 days later)
Force: peak 20-60 ms
o Satellite cells: Add mm mass in loading and injury
Ca transient normally big enough for full activation in a single twitch
Force rise time and peak twitch force depend on: Vmax (internal shortening to
stretch series elasticity) and Duration of Ca transient
Frog experiment:
Twitch: mechanical response to single AP
Tetanus: response to high frequency APs (twitch/tetanus force ratio ~0.2-0.25)
Skeletal Isometric no shortening allowed
Muscle Isotonic shortening with constant weight
Plasticity in Skeletal mm force is controlled by CNS, largely by variations in motor unit recruitment,
Health and motor unit firing rate NOT by varying cytoplasmic calcium. Skeletal mm cells should
Disease just do what they are told!
o Muscles are strong
Force*length = constant think physics mm have to be super strong to lift something!
Force-velocity curve: External work = force*distance; Power = work/time = force *
velocity
o Muscles are big and packed with proteins: Size: Diameter = 20-50 u; Length = up to 30 cm;
Multinuclear cells. Dont divide, but can grow with addition of satellite cells
o Not all muscles are the same in physiology and biochemistry the slower you get, the more
efficient you are in terms of ATP use
IIB: Fastest, use most ATP, Glycolytic metabolism, white color, fatiguable, large
IIA: Fast, high ATP use, mixed glycolytic/oxidative metabolism, red color, not bad in
fatiguing, medium size
I: slow, low ATP use, oxidative metabolism, red color, more endurance, small
Cardiac and Smooth: even slower, use even less ATP
o Exercise changes muscle phenotype (they have plasticity) endurance, strength, size
Studies of plasticity usually perturb mm workload/rate over protracted periods of time
Innervation determines fiber type
Sustained activity causes exercise capacity. mitochondria, changes in Ca handling,
and myosins, altered glucose transport/metabolism
loading causes in mm mass existing fibers and new fibers may develop (satellite
cells), Ca handling and metabolism altered
activity or loading causes mass myofiber dimensions
Inflammatory myopathy = lymphocytic infiltrates, fiber degeneration
Myopathies Neurogenic atrophy = fiber atrophy, fiber type grouping, grouped Can get trichinosis, bacterial infections of fascia/skeletal
and necrosis (pale pink), fiber regeneration bluish w/large vesicular
(Inflammatory) atrophy, absence of inflammation. mm (but not focusing on this for the domain)
nucleus, nucleolis
Women 40-60
Endomyseal T cells CD8 infiltrates
EMG = purely myopathy
Polymyositis lead to necrosis, followed by Myopathic weakness Risk of malignant
CPK = high (up to 50X)
regeneration neoplasms (esp lung
cancer)
Myopathic weakness
Rash/calcinosis is present
Women 40-60
EMG = purely myopathy Perivascular/perifascicular infiltrates,
Dermato-
CPK = high (up to 10- perifascicular atrophy CD4 and B- Risk of malignant
myositis
50X) cell mediated. neoplasms (esp lung
cancer)
Heliotrope eyelids
Rimmed vacuoles, amyloid-like

EMG = myopathy +/-
(nonbranching, + w/Congo red), Myopathic weakness, but
Inclusion body neurogenic component
filamentous inclusions (w/Amyloid sometimes distal weakness is
myositis CPK = high (not as high
beta, phosphorylated tao, ubiquitin, prominent
as PMS)
prion protein)
Disorders of the NMJ

Ptosis (most common initial
finding).
Autoab against Ach receptors (Type II

HS rxn) Ab inhibit/destroy receptors Men in 60s/70s
Tensilon (edrophonium
Women in 20s/30s
Myasthenia test) Inhibits AchE (d
Ab synthesized in thymus 85% have
Gravis Ach reverses mm
thymic hyperplasia w/germinal follicles Mm weakness improves d risk of developing
weakness)
w/rest thymoma (15%)
Fatigue without soreness or burning
Dysphagia for solids/lipids (in
striated mm of upper
esophagus)
Associated with
Lambert- Symptoms improve with
No reversal of sx with paraneoplastic
Eaton Auto ab to presynaptic Ca channels Proximal mm weakness muscle use!
AchE inhibitors alone diseases (small cell
Syndome
lung cancer)
Muscular Wide variation in fiber
excessive ENDOMYSIAL FIBROSIS fiber degeneration and regeneration,
Dystrophies diameter,
Lab: Serum CK 1st 10 Normal at birth, early
Type 1 AND 2 fibers involved milestones met
yrs, declines as muscle Varied fiber size (small and enlarged
degenerates fibers with fiber splitting); X-linked recessive
Walking often delayed, pt is Myostatin TGFB protein inhibits
internalized nuclei, Degeneration, clumsy/unable to keep up Xp21, but 1/3 are mm growth loss causes
Western blot necrosis/phagocytosis of mm fibers, new mutations
Duchenes - NO Dystrophin deficiency (normally with peers hyperplasia during development
mm fiber regeneration. Proliferation of and hypertrophy throughout life
dystrophin, Becker - anchors actin to membrane glycoprotein Most severe, most
endomyseal CT. Mm eventually Sx around 2-5 yrs: WONT fix the problem making
thinned bands. and attached to sarcoglycans I/M band common type
almost totally replaced by fat the mm stronger will make them rip
associated, possible role in maintaining (1:5,000)
ENDOMYSIAL FIBROSIS Weakness/wasting of pelvic apart faster. IGF-1 influences mm
myocyte membrane integrity
May also have pathological changes in muscles is 1st Child places mass too.
Duchennes w/contraction). Dystrophin deletions, Female carriers have
heart (HF, arrhthmias can develop) hands on knees to help stand,
Muscular point mutations w/frameshift. d serum CK
CENTRAL NUCLEI Gowers sign (tripod),
Dystrophy
Progressive degeneration of Type I/II
No CNS problems established, but
fibers causes infiltration of muscle tissue
cognitive component of disease
by fat (Pseudohypertrophy of calf)
Affects PROXIMAL mm and calves Waddling gait
Wheelchair by 12
Death by 20 from diaphragm

mm failure (pulmonary
infection, cardiac
decompensation, resp insuff)
Becker Dystrophin is defective (Normally
X-linked Xp21 (Other forms of MD AD or AR,
Muscular dystrophin transfers force of contraction Sx not as extreme as Duchennes
1:20,000 different presentations)
Dystrophy to CT)
d serum CK
Myotonia= sustained involuntary Facial weakness, myotonia
(worse w/maternal
contraction of a group of mm (especially AD most common
subsequent to voluntary contraction or inheritance), frontal balding,
adult muscular
irritation) cateracts, testicular atrophy,
dystrophy (TNT
Above = spontaneous cardiac involvement
Variation in fiber size repeat disorder)
mm discharge w/needle Myotonic dystrophy = defective splicing d internal nuclei (in chains) can have
insertion of muscle C1C1 channel mRNA caused Ring fiber: sub-sarcolemmal band of anticipation.
Myotonic by nuclear accumulation of CUG or cytoplasm, has myofibrils around
Dystrophy Can elicit myotonia by CCUG repeat RNA (most common longitudinally oriented fibrils.
percussing thenar human dystrophy) Sarcoplasmic mass may come out from
eminence ring (stain blue in H&E)
Dystrophila myotonia protein kinase
mRNA affected
Pt complains of difficulty
Selective atrophy of Type I fibers (early releasing grip,
on)
Physical exam: o Spinal stenosis:
Straight leg raising (80% Non-inflammatory rheumatoid pain Initial evaluation: look for red flags pseudoclodication pain
se, 40% sp), Contralateral o Cancer (age>50, previous cancer, in legs while walking
leg raising (90% sp, 25% Possible causes: herniated disc, disc wt loss, >1 month pain w/tx, no often relieved by leaning Assess non-spinal
se), one on its own not disease, spondylolisthesis, relief w/bed rest, fever) forward or sitting not causes for LBP
that great but put them spondylolysis, facet sx, spinal o Osteomyelitis (IV drugs, UTI, skin due to peripheral vascular rectal, UTI
together and they are instability, radiculopathy, fibromyalgia, infection, fever, immunocomp), disease. Dont donsider
Sciatica in 1st 3 months. Relief Questions to guide tx:
helpful. myofacial pain sx, somatic dysfunction, Low back- 60-90%
o Cauda equina syndrome with leaning forward What activities cant you do?
sacroiliac joint pain, CT disease, lifetime incidence,
(bladder/bowel, saddle anesthesia (shopping cart sign), What tx have you tried?
arachnoiditis, fractures, spinal stenosis, 5% annual incidence,
numb by butt, limb mm weakness). age>50 What do you do to stay in shape?
Sed rate and CBC - labs tumor, infection, osteoporosis, lumbar 5-25% incidence
What medications have you tried?
for suspected tumor strain, visceral/operant/central pain, lower back pain,
What want vs expect from tx?
Pagets, Scheurmanns, Job satisfaction, 40% get sciatica
Back Pain
X-rays: not psychogenic pain, malingering, short leg 50% recover in 1
(mechanical) NSAIDs, Tylenol, Benzodiazepams
recommended in 1st 4 sx, unlevel sacral base month, people get
(same as NSAIDs except drowsy),
weeks if no red flags recurrence
Boeing study: Psychological, Work
Not helpful: Steroids, Bed rest,
Reflexes:DTR/MSR/my satisfaction, and history of low back o Ankylosing spondylitis: Chronic (10% - get
Facet injections, epidurals without
otatic reflex pain were most predictive onset <50, not relieved in 80% of cost)
radiculopathy, opioids (and if used,
o 0=absent, supine position, morning only short-term)
o 1=trace, w/ Acute low back problems in adults: stiffness, pain>3 months
reinforcement, activity intolerance due to back related o Sciatica: if activity
o 2= lower of symptoms, over age 18, lasts < 3 mo. restrictions >1 month or
normal, Evidence - some care is inappropriate clear clinical;
o 3=upper of normal, disability despite tx. Spinal fusion not electrophyscompromise,
o 4=abnormally brisk, recommended, correlating imaging can
Note clonus separately refer to surgery.
Estrogen replacement tx helps
prevent post-menopausal loss.
X-ray: Not reliably detected porosity of skeleton from bone mass/density. Uncoupling of osteoblast 34 million at
Definition: skeletal disorder vs osteoclast activity. d thickness of cortical and trabecular bone.
until ~35% loss risk Prevention: exercise (wt bearing
characterized by compromised bone
(osteopenia) swimming doesnt help), Ca/Vit D
Bone Density Test: DXA scan strength predisposing a person to d Post-menopausal: tend to have vertebral fracture (lose height, lumbar 10 million intake, estrogen replacement,
fracture risk. lordosis, kyphoscoliosis) d risk of future fracture
(dual-energy absorp typically have biphosphonates (inhibit bone
check every 2 yrs), quant CT osteoporosis resorption), calcitonin (inhibits
(less commonly used) Peak bone mass: by 30, det by: Femoral neck/pelvis/spine fractures: cause pulmonary embolism, 1.5 million osteoclasts), recombinant PTH
hereditary (vit D receptor, pneumonia (~45,000 deaths/yr) new fractures (stimulates formation of bone in
( PtBMD YoungAdultMeanBMD)
collagen 1A1, estrogen receptor,
Tscore (1SDofYoungAdultMeanBMD ) ILGF-1), Localized (diffuse osteoporosis of limb) or systemic (metabolic bone
each year amounts > reabsorbed)
# of standard deviations from Physical activity, muscle disease). Generally asx until fragility well advanced Most common Eeduce sedating meds, tx dementia
mean compared to young adult. strength, diet, hormonal state
metab and vision problems
Normal = -1 or above Colles (distal radius) abnormality of
Osteopenia= -1 to -2.5 Bone loss: ~0.7% annually.
bone Adult <50 need 1,000 mg Ca and
Osteoporosis Osteoporosis: -2.5 or below Influences:
400-800 IU vit D daily
Severe Osteoporosis= -2.5 or Age (senile osteoporosis):
Primary Adult >50 need 1,200 mg Ca and
below with fragility fracture osteoblasts replicate less,
cause (most 800-1000 IU vit D daily
Use lowest to dx forearm, hip, proteins bound to ECM lose
common) =
femoral neck, spine biologic potency;
Fragility (insufficiency) fractures: fall from standing height or senile, post- Bone completely remodels in 18
Physical activity: mechanical
less/without trauma (33-50% of women, 15-33% of mens w/age). menopausal. months
Zscore ( PtBMD AgematchedBMD ) force needed to stimulate growth
(1SDofAgeMatchedMeanBMDing / cm 2 )
Genetic factors: Vit D receptor Typically hip, spine, wrist **Diagnostic even if normal mineral density**
low Z score (<-2.0) means pt >2 Women: 1/2
(~80% of peak mass variation);
SD below mean Risk: over 50 have
Nutritional state: Ca, vit D
Non modifiable: age, female, asian/Caucasian, previous fragility fracture, osteoporotic
Hormones: PTH, Estrogen
Serology: blood family hx of osteoporosis, small frame fracture (only
(causes Il-1/6, TNF more
Ca/PO4/alkaline phosphatase Modifiable: estrogen deficiency, body wt<127, Low Ca/Vit D intake, 25% men!)
osteoclast activity. Osteoblasts
level NOT diagnostic tend to cant keep up) Inadequate physical activity, excess alchohol, smoking, drugs
use in pt <50, kids (anticonvulsants, glucocorticoids, excess thyroid replacement)
Secondary
Long-term glucocorticoid tx: bone mass by bone resorp, bone formation on cortical/trabecular surfaces Space travel: bone stress (which is needed to stimulate remodeling)
Causes
Poor bone quality can result in stress fractures,
Prevention: educate parents, coaches of impact on athletes.
risk of other fractures
Discuss at pre-participation sports physical. Any visit for stress
Although most women w/ the triad dont fit
fracture, wt change, disordered eating, amenorrhea, bradycardia,
Age: Typical age of young athlete coincides with important criteria for anorexia or bulimia, they have
Early signs of arrhythmia, depression **any female athlete missing 3 consecutive
time of building bone greater risk of mortality than general
disordered eating periods or has intervals >35 days apart should be evaluated by
population
fatigue, anemia, physician
Diet: Eating disorder can result in low Ca and vit D and Prevalence unknown amenorrhea is more
electrolyte imbalance,
prevent reaching peak bone mass. May lead to common, but not normal in female athletes.
depression Tx: lifestyle changes, dietary changes (see dietician), get goal wt
irreplaceable bone loss Amenorrhea occurs in up to 66% of female
(above 127, gain 0.5-1 lb per week until goal), activity 10-20%
Female athlete athletes and 2-5% of general population.
Amenorrhea (rule out (dont have to stop), monitor wt every 2-3 months.
triad: Hormones: Low estrogen results in accelerated bone loss. Studies have reported disordered eating in 15-
other treatable causes)
Disordered Excessive training and stress from malnutrition can cause 62% of female college athletes (restricted food
Ultimate goal is to return normal menses through lifestyle changes,
eating, changes in hypothalamus (hypogonadotropic intake, vomiting, diet pill/laxative abuse)
DXA scanning: Lack of proper nutrition, revised training regimens, wt gain. Estrogen
amenorrhea, hypogonadism) leading to d estrogen levels. Low
evidence in use (young (estrogen-containing oral contraceptives or cyclic estrogen &
osteoporosis estrogen leads to amenorrhea, eventually bone loss Risk: frequent weigh-ins, punitive
female may not have progesterone). s BMD
(estrogen antiresorptive) consequences for wt gain, overly controlling
reached peak bone mass
o Amenorrhea: coach/parent, high risk sports (gymnastics,
yet). Z scores may be Ca 1200-1500 mg per day (for ages 11-24), Vit D 400-800 IU
o Primary: No spontaneous bleeding by age 16 figure skating, ballet, distance running,
helpful (compare to If severe disorder or depress, then psychological eval to consider
o Secondary: 6 month absence of menstrual bleeding swimming, diving)
average age, race, sex). SSRI
with prior hx of regular menses
Z score <2.0 (below
o Both can result from hypothalamic dysfunction Why? Performance improvement (runners),
expected for age) No drug approved for pre-menopausal females
from excessive exercise and eating disorders competitive thinness (gymnastics, figure
Biphosphonates can affect fetal bone development and have long
skating), weight categories (rowing, martial
biologic half life best avoided in females who may become
arts), revealing sports attire (swimming,
pregnant someday
volleyball, track and field)
Too little bone osteoporosis Type 1: acquired mutation AD inheritance
w/cortical thinning, attenuated lots of fractures early on (less
Pathological fractures at trabeculae, skeletal fragility into puberty), blue sclerae,
Defective synthesis of Type 1 collagen Type 2: lethal form,
birth hearing loss, dental fatal in utero/in
imperfections Exercise, pain medicine, physical
Osteogenesis neonatal period.
Blue sclera (reflection of therapy, wheelchairs, braces,
Imperfecta Incidence = 1:10,000
underlying choroidal surgery.
(Brittle bone
veins), deafness
disease)
May be confused with child abuse
NOT the same as Give biphosphonates to prevent

Disorganized bone Adult Vitamin D deficiency causes less
Histological: thickened matrix with osteoporosis, because bone loss
remodeling . intestinal absorption of Ca/PO4, PTH
normal trabeculae. osteoporosis is caused by
Osteomalacia, Contours not affected, will stimulate loss of Ca from bone to
production of osteoid, while Renal failure can lead to
rickets but bone is weak restore blood levels.
Eventually, difficult to differentiate osteomalacia is poor osteomalacia ( cant convert Vit D
(especially vertebral
from other osteopenias. formation of bone in to active form in kidneys to absorb
bodies, femoral necks). In kids, it leads to rickets.
remodeling. new Ca)
Osseous function: Bone composition: Mechanisms of bone formation:
Strength, cushioning, o Cells: o Cutting cones: to remodel bone.
mobility, endocrine, o Osteocytes: in lacunae, Reg bone Osteoclasts at front remove, Cytokines (IL1/4/6/11)
BMP (Bone Morphogenetic
Ca/Vit D dependent metab (response to stress/strain), Osteoblasts behind lay down new Platelet-derived resorption (IL1!) IL1/6 by
proteins):
Diaphyseal (cortical)=for o Canaliculi: canals, contain o Intramembranous (periosteal) growth factor: estrogen (assoc w/ post-
cell differentiation; BMP-3
stability osteocyte cell processes, formation: long bone grows in bone cell growth ( menopausal resorption?)
(osteogenin) mesenchymal
Metaphyseal preosteoblast-osteocyte width. Osteoblasts lay down Type 1 collagen
differentiation bone;
(cancellous) =cushioning connection (probably for response seams of osteoid. Doesnt involve synthesis by # of PG: osteoblastic formation,
endochondrial ossification
to mechanical, chemical factors) cartilage precursors. osteoblasts). PDGF- osteoclasts.
(BMP 2/7 in segmental
Types of bone: o Osteoblasts: from mesenchymal o Endochondral formation: long BB bone resorption
defects); Regulates ECM
o Lamellar bone: stem cells. Line surface of bone, bone grows in length osteoblasts by # of osteoclasts LT: osteoblast bone formation,
Bone production (BMP 1 cleaves
fibers in parallel produce osteoid. line a cartilage precursor. capacity of osteoclasts to form
physiology carboxy termini of
layers. Structure o Osteoclasts: Get rid of bone, Chondrocytes hypertrophy/calcify Insulin-like Growth resorption pits.
procollagens I-III)
(see picture below) from hematopoietic scs, ( O2). Vascular invasion of factor: IGF I
Trabeculae in multinucleated, in Howships cartilage ossification ( O2 production in liver Estrogen: fracture healing,
Fibroblast Growth Factors:
direction of stress lacunae. PTH stimulates triggers calcification) by GH. collagen & modulates release of IL-1 inhibitor
2 Forms: Acidic (FGF-1) &
o Woven bone (non- receptors on osteoblasts to matrix synthesis,
Basic (FGF-2)
lamellar) randomly activate osteoclastic resorption. Growth Factors: osteoblast Thyroid hormones: T3/T4
chondrocytes, osteoblasts,
oriented collagen. o Extracellular matrix: TGF (transforming growth factor): replication, bone osteoclastic bone resorption
callus formation,
Weaker. Usually o Organic (35): 90% type I precursors (osteoblasts, osteoclasts, collagen degradation.
FGF-2 angiogenesis
remodeled to collagen, also osteocalcin, chondrocytes); endochondral & Glucocorticoids: Ca absorption
lamellar. Seen at osteonectin, proteoglycans, intramembranous formation ; from gut (causes PTH more
sites of fracture glycosaminoglycans, lipids synthesis of cartilage proteoglycans, osteoclast bone resorption)
healing, attachment, (ground substance) type II collagen; collagen synthesis
pathology Inorganic (65): hydroxyapetite by osteoblasts.
CK form resorb
IL-1 + +++
TNFa + +++
TNFb + +++
TGFa -- +++
TGFb ++ ++
PDGF ++ ++
IGF-1 +++ 0
IGF-2 +++ 0
FGF +++ 0
Stability: Mature callus resorbs
Direct vs indirect healing Early: promotes revascularization, portions not physically
Direct: no motion at fracture site After 1st mo: loading promotes callus used changes until outline
(doesnt form callus). Cutting cone is formation, healing. of fractured bone is back,
Classification: formed, crosses fracture site. Inadequate stabilization: deformation medullary cavity is restored Most common
Complete vs incomplete Osteoblasts lay down lamellar bone at site, tissue bone (soft callus). *Wolffs law * bone is Immobilize, ensure proper
pathologic conditions
Closed (simple): skin behind the osteoclasts (form secondary Over stabilization: periosteal bone restructured in response to alignment, eliminate infections that
of bone
tissue intact osteon). Slow process ~18 months. formation (hard callus) stress and strain block healing
Compound: skin not Direct contact allows healing gap Problems: Bones cant bear
intact <00-500 microns filled w/woven bone, Stages of healing Displaced/comminuted Local anatomic factors that
weight until mature
Comminuted: bone larger ones filled with fibrous tissue = influence fracture healing:
First week: can have deformity (and callus forms after
splintered non-union slow splintered bone malnutrition (less
Inflammation: Hematoma fills 3rd week +
Displaced: ends of bone fracture gap, surrounds area. has to be resorbed 1st) activity/proliferation of
at not aligned Indirect: fractures not rigidly fixed. osteochondral cells, less callus
Fibrin mesh seals fracture site, Poor immobilization: Children/young
Pathologic: break in a Bridging periosteal (soft) callus and formation), smoking (inhibits
framework for growth. callus cant form adults can
bone already altered by medullary (hard) callus re-establish osteoblasts, vasoconstriction), DM
Platelets/inflam cells: PDGF, Nonunion w/motion anticipate perfect
Fractures disease structural continuity. Callus undergoes TGF-B, FGF activate (collagen defects and poor
along gap: central reconstitution.
(healing) Stress fracture: slowly endochondral ossification (4-6 weeks) construction)
osteoprogenitors stimulate callus has cystic
developing following osteoclast/blast (anti- degeneration, luminal Pediatric tend to
physical activity with Prerequisites to heal: inflammatory meds healing!) Electromagnetic field: in vitro
surface lined by fracture through
new repetitive loads (boot Blood supply: bone deformation produces
Soft tissue callus/procallus synovial-like cells hypertrophic zone.
camp) Nutrient a (intramedullary normal piezoelectric currents, stimulates
formed no structural rigidity to (pseudoarthrosis false
supply for cortex, enters long bone via bone healing (need negative charge
bear weight, anchors together joint) fix by removing Older tend to have
Harris lines (Pediatric nutrient foramen, forms medullary aa for bone to grow)
2nd/3rd week (if uncomplicated) soft tissues, stabilizing pathologic fracture
pts - look like growth down the bone),
ring on a tree happen Periosteal vessels (from periosteum, Osteoprogenitors deposit fracture site (osteoporosis, etc)
Physeal injuries heal in half the
in stress from temporary supply ~20% of cortex, but more when subperiosteal trabeculae of Infection: repair less, need
time it takes for nonphyseal
woven bone (perpendicular to (comminuted/open): mechanical
slowdown of normal injured medullary supply), fractures to heal in the same area.
cortical axis, in medullary cavity) have to eradicate before immobilization for
longitudinal growth). 6- Metaphyseal aa: in fracture, external
10 weeks after fracture. supply becomes more important than Endochondral ossification of union healing
internal supply cartilage line bony callus Low Ca/PO4, Vitamin
Early callus has excess fibrous Deficiencies, Systemic
tissue/cartilage/bone most infection, Diabetes,
volume at concave portion vascular insufficiency
Salter-Harris
Classifications
of Pediatric
Fractures
Type II most common! Buckle/Torus Fracture compression failure; usually at metaphyseal/epiphyseal junction. ** Greenstick fracture plastic deformation. Forearm, fibula common
Radiograph: bone Medullary infarct: Cancellous Medullary: chronically asx Other associated causes: Trauma,
density MRI is most bone/marrow affected, not cortex except for large ones in Infection, Dysbarism, radiation, CT
sensitive test All bone necrosis caused by (collateral blood flow). Gauchers, dysbarism, Causes 10% of disorders, pregnancy, Gauchers,
ISCHEMIA (microcirc disrupted) Subchondral infarct: hemoglobinopathies 500,000 joint Sickle cell/other anemias, alcohol,
Where? triangular/wedge-shaped tissue from replacements chronic pancreatitis, tumors,
Mech vasc interruption (fracture)
Femoral head (hip) subchondral bone plate to epiphysis Subchondral: Chronic pain annually! epiphyseal disorders
Avascular Corticosteroids
think fracture in (tip). Dead bone has empty lacunae (initially only with physical
necrosis Thrombosis/embolism (N bubbles)
elderly person, surrounded by adipocytes that rupture activity, then gets more Most cases Legg-Calve-Perthes is aseptic
sickle cell disease, Vessel injury (vasculitis, radiation) (FA bind Ca and form soaps) constant). Can collapse, idiopathic/after CS necrosis involving femoral head
long-term CS use intraosseous pressure Creeping substitution: osteoclasts cause severe secondary administration ossification in kids pain in
Scaphoid bone Venous HT resorb trabeculae, deposit new bone on osteoarthritis kneeling, limp is seen Mostly in
Digits (Dactylitis in non-resorbed trabeculae (doesnt help 3-10 yr old BOYS. Commonly
sickle cell) with subchondral infarct too slow) leads to secondary OA.
+ blood cultures, Pyogenic: Bacterial infection of a bone, Where (depends on where Antibiotics and surgical drainage
Have to biopsy/bone from hematogenous spread, extension blood supply is):
culture to id pathogen from another site, or direct implantation Neutrophils enzymatically destroy Before growth plates close: Complications: 5-25% wont resolve (can go
o 90% due to Staph Aureus bone (dead bone = sequestra) metaphysic/epiphysis pathologic fracture, chronic if dx delayed, extensive
(receptors for collagen) necrosis in 48 hrs. After growth plates close: secondary necrosis, short tx, poor debridement
o UG infection or IV drug user: E coli, more widespread amyloidosis, or immunocompromised)
Pseudomonas, Klebsiella Chronic disease: reactive bone endocarditis, sepsis,
o Neonates: Strep pyogenes, H flu formation in periosteum (involucrum) Brodie abscess: small, sarcoma
Osteomyelitis o Sickle cell: Salmonella paratyphi intraosseous involves
o But 50% cant find org! Kids: subperiosteal abscesses from cortex, walled off by reactive Metaphysis is most
o Pseudomonas often from puncture spread in Haversion canals bone common site (with
of foot through rubber footwear. hematogenous
Tuberculous form: hematogenous Draining tracts to skin surface Sclerosing osteomyelitis of spread)
spread from lung (goes to vertebra (danger of squamous cell carcinoma Garre in jaw, new bone
Clinical findings Potts disease, less often hip/knee) 1- developing at orifice of sinus tract) formation
Fever, bone pain, 3% get this. Multifocal in
elevated ESR immunocompromised.
Metaplastic bone present Lesion 3-6 cm across, well-delineated
Soft/glistening center; firm/gritty
Starts in musculature of periphery
proximal extremities
Early: cellular lesion with Depends on stage of
plum/long fibroblast-like cells
Radiograph: Soft tissue development:
(simulates nodular fasciitis)
fullness radiodensities Early Swollen/painful Athletic adolescents,
Morphologic zonation (within 3
Myositis at the periphery (3 wks) Metaplastic bone grows out in the Later Circumscribed, young adults Take it out! Usually solves the
weeks) merges with adjacent
ossificans filled in radiodensity muscle firm follows trauma in problem.
intermediate zone of osteoblasts,
woven bone deposited. Cancellous Even later painless, >50% of cases
Have to differentiate hard, well-demarcated
bone appearance on the outside.
from extraskeletal mass
Skeletal mm fibers/giant cells
osteosarcoma (in elderly,
often trapped in the margins.
cells are malignant,
tumor doesnt have Ossification of all: intertrabecular
zonation) spaces are filled with bone marrow
most frequent cause

of heel pain in
calcaneal apophysitis
children 8-13 yrs Self-limiting will disappear after
Severs (seen during periods bone growth finalized and growth
inflammation of the growth plate of the
of active bone plate closes (age 15-16)
calcaneus
growth), especially if
moderately obese
Boys 11-15 yrs of

age
Usually resolves with skeletal
Inflammation of proximal tibial maturity (when tibial tubercle fuses
apophysis at insertion of patellar tendon. to the remainder of the tibia)
Osgood- Stress on patellar tendon with repeat Ice after exercise, NSAIDs
Schlatter quadriceps contraction can cause
avulsion fractures and Syndig-Larson-Johansen syndrome
microtrauma/inflammation (causes lump involves the upper part of the
on knees) tendon, where it attaches to the
Radiograph not needed to patella!
diagnose, but confirm it
and rule out other causes Knobby appearing knees
of knee pain No effect on bone growth
Bone tumors
(basic epi and Location of tumor most Benign ones: - more common than Metastasis most common bone Malignant ones: - tend to be
characteristics key diagnostically malignant, younger people malignancy (mostly from breast CA) letal, in elderly
only)
Osteoma
Osteochondroma (exostosis) Males, Face,
Giant Cell: Male, <25, Mushroom capped Assoc w/Gardners polyposis
Osteoid osteoma
Female, 20-40
Enchondroma w/benign cartilage , Metaphysis Dont go malignant,
Male, 10-20 20-50
Cells look like osteoclasts (distal femur), Most common Big deal if compress something or
Cortex of proximal femur, Radiolucent focus Medullary, small tubular bones
Soap bubble, Spindle-shaped multi- benign, rare to go malig ugly.
(nidus) surrounded by sclerotic bone Hands/feet
nucleated cells
Multiple or solitary,
Epiphysis (distal femur/prox tibia)
Risk of chondrosarcoma Osteoblastoma
Male, 10-20
Osteoid osteoma in the vertebrae
Radiation bad malignant
transformation!
Chondrosarcoma
Male, 30-60
Pelvic bones, proximal femur
Mushroom shape
Ewings sarcoma Osteosarcoma

Male, <15 Male, 10-25
Pelvic girdle, Metaphysis of distal femur/proximal tibia
diaphysis/metaphysic of prox sunburst appearance (from calcified
femur/rib osteoid),
Small, round cell tumor Codmans triangle (tumor lifts periosteum),
Onion skin X-ray periosteal rxn. Metastasizes to lungs MOST COMMON
Possible fever/anemia PRIMARY BONE CA
Targets pelvis, skull (enlarged), femur

Cause unknown (virus - Risk of osteogenic sarcomas, risk of high-output HF
paramyxovirus?) (from AV connections in vascular bone) Elderly white men of Europe,
Or abnormal osteoclasts Australia, US, 5-11% of population
(hyperresponsive to vit D, RANKL) 1) Osteoclastic resorption of bone Generally asx affected in countries where it exists
(shaggy-appearing lytic lesions) Pain: most common problem, in the affected bone.
Overall, you gain bone mass, but its 2) Osteoblastic bone formation (d Microfractures/overgrowth (compressing nerve roots) Genetic link to 18q
Pagets Disease disordered in structure and structurally serum alkaline phosphatase, Normal Leontiasis ossea: craniofacial growth , difficult to
of the Bone unsound. Ca/PO4, thick/weak mosaic bone hold head erect -> platybasia (flattened skull base) Note: Parathyroid adenoma or
(Osteitis
formed) mixed w/osteoclast activity Bowing of femor/tibia causes secondary osteoarthritis hyperparathyroidism would be
Deformans)
3) Osteosclerotic phase (quiescent) Chalkstick-type fractures in long bones of lower different you get brown tumors,
extremities which are areas of d bone mass.
* Mosaic pattern of lamellar bone * Compression fractures of spine
Skin over pagetic bone is warm (hypervascularization) Suppress sx w/
Non-malignant: Giant cell reparative granulomas, giant calcitonin/biphosphates
Dx: Incidental cell tumor, extraosseous masses of hematopoiesis
radiographic NOT
usually in ribs, fibula, My hat size d!
small hand & feet bones
Rheumatologic Disorders
Lacrimal glands
(keratoconjunctivitis), Minor
Exocrinopathy problem in T-cell
salivary glands (sicca),
Shermers test: evaluate regulation, B cell expansion
Sjogrens Parotid gland (dry mouth,
for dry eyes (polyclonal), inflammation in
dental caries, parotidis),
EXOCRINE glands
Pancreas (achlorhydia,
abdominal pain)
General approach:
Lab: Slightly serum Most common
Hand involvement! disabling joint o Joint protection, stabilization,
alkaline phosphatase
Erosion/clefts seen in articular DIP enlargement disease! o Analgesia (NSAIDS, tramadol,
cartilage Heberdens nodes codeine),
Radiograph: asymmetric More in women,
Noninflammatory joint disease PIP enlargement universal after age 65 o Joint-specific (injections
loss of joint space,
Reactive bone formation at joint corticosteroids, hyaluronic acid
Eburnation (thickened cracking/narrowing of cartilage leads to Bouchards nodes
margins (osteophytes) causes analogues).
endplate resulting in reaction in underlying bone Secondary causes:
slightly alkaline phosphatase
osteophyte formation), Obesity, trauma
Focal arthritis = 90%. Loading/focal (valgus/varus stress Surgery not that great.
subchondral cysts,
Subchondral cysts
Osteoarthritis intraarticular loose bodies transarticular stress is main cause of of knee, meniscal or
hip/knee OA. ACL injury), In development: oral
Bone eventually rubs on bone immunomodulators, maybe anti-
*Cartilage* ochronosis
(producing dense, sclerotic bone) metaloproteases
Generalized osteoarthritis = 10% (alkaptonuria AR
(generally genetic association) disease w/deficient
NO joint ankylosis
homogentisic acid
Progressive degeneration of articular Oxidase,
Crepetis grinding in joints
cartilage targets wt bearing joints. accumulation of
Vertebral findings: homogentisic acid
Pain w/passive motion (secondary
Degenerative disease w/ which deposits in IV
synovitis)
compressive neuropathies discs urine will turn
black when oxidized)
Complications: Secondary Sjogrens; Swelling leading to pannus.

Synovial inflammatory disease: Periarticular osteopenia.
rheumatoid nodules, vasculitis,
proliferation, erosion into marginal bone Marginal erosion, joint space
entrapment neuropathy (carpal tunnel),
Lab: RF, pulmonary fibrosis, pleuro-pericarditis, narrowing, malalignment. Most develop
Cartilage: 70% water. Chondrocytes are
membranous glomerulonephritis. 3-4X structural damage
Rheumatoid 10% of tissue volume (manufactures,
Research: CCP ab for rr of lymphoma (also risk of lung early on (as early as
arthritis secretes, maintains matrix components
diagnostic? cancer maybe due to 4 months to 5 years
collagen, hyaluronic acid, proteoglycan).
immunosuppressive?), osteoporosis into disease) Education, OT, PT, NSAIDs,
*Synovitis*
Rice bodies floating (generalized inflammation causes IL-1 Prednisone, Synthetic DMARDs
Ag driving rheumatoid arthritis is
fibrogen in synovium related demineralization, and chronic HLA DR4 (Methotrexate, sulfasalazine,
unknown perhaps IgG Fc, CCP, Type
disease-related malnutrition), leflunomide, hydroxychloroquine),
II collagen. Initiating ag might differ
atherosclerosis (3 rr CV mortality due Biologic DMARDs tx (against
from perpetuating ags.
to acceleration!), ACD Usually doesnt affect DIPs TNF, IL-1, Tcell, Bcell, IL-6)
Now largely based on physician
preference
Joint morphology similar to Begins before age 16
adults targets and must be present
Usually rheumatoid Oligoarticular (<5 joints)
knee/wrist/elbows/ankles. for at least 6 weeks
nodules and rheumatoid Polyarticular (>=5 joints)
Genetic association w/HLA (DRB1), Warm, swollen, often to make diagnosis
factor absent. Systemic form more frequently
Juvenile RA infections, abnormal immunoregulation symmetrical involvement. 2:1 female (except
systemic than the adult form. Assoc w/
(CD4+ Tcells in joints) Complications pericarditis, 1:1 systemic)
Antinuclear ab high fever, rash, hepatosplenomegaly,
myocarditis, pulmonary ~40,000 in US
seropositivity common serositis.
fibrosis, glomerulonephritis, 1/3 -1/2 have active
uveitis, growth retardation disease after 10 yrs
Rheumatologic Disorders
4 Stages: Often men >30
1) Asx hyperuricemia Really important to tx early
(puberty in males, Assoc w/urate impairs quality of life, and a lot of
postmenopause in females) nephropathy, renal aspects of the disease due to
Lab: Hyperuricemia, Urates in joint fluid supersaturated, 2) Recurrent acute arthritis: stones, HT, CAD, duration/severity of hyperuricemia.
Lead poisoning
joint aspiration unknown event initiates release of Podagra: recurrent acute
(interstitial nephritis Hyperuricemia: not tx if asx
(arthrocentesis) Primary gout (90%): underexcretion of crystals into synovial fluid. Leukocyte arthritis in big toe 50%
confirmatory MSU chemotaxis, complement, LTB4, have as 1st manifestation interferes w/uric acid
uric acid in kidneys (lead poisoning,
excretion) Acute arthritis: NSAIDs,
crystals w/NEGATIVE alcoholism are secondary causes), Activation of Hageman factor Fever, pain, neutrophilic
biorefringence crystals colchicine, intra-articular
enzyme deficiencies are rare (HGPRT) leukocytosis
10% of US has corticosteroid injection, oral
Gout are YELLOW when MSU phagocytosed by hyperuricemia, but corticosteroids
parallel to slow ray, blue Secondary gout (10%): PMNs in synovial fluid
when no longer parallel. <0.5% develop gout
*Crystal* Overproduction of uric acid ( cell 3) Intercritical Gout
Recurrent arthritis or
turnover, chronic renal disease, 4) Chronic gout Risk of tophaceous gout:
diuretics). Estrogen s tubular excretion Tophi: deposits of MSU hyperuricemia o Allopurinol: inhibits Xanthine
of uric acid. in soft tissue around becoming gout: Oxidase to stop uric acid
joints. Granulomatous Age/duration, production
rxn w/multinucleated Genetic predisp o Febuxostat (hepatically
20% end up dying of renal failure giant cells destroy (multifactorial excreted, can be used in pts with
subadjacent bone (causes inheritance factors), renal failure)
erosive arthritis). White Alcohol use,
deposits on helix of ear Obesity, Drugs Want to bring uric acid level <6.
(thiazides), Lead
Lab: Calcium Frequently asx, but can

Hereditary form early
pyrophosphate crystals produce acute to chronic
Usually >age 50 development in life, get severe OA
phagocytosed by PMN arthritis that mimics other
Pseudogout Degenerative joint disease, usually (more w/ age) AD (ANKH mutation that
show + biorefringence things (RA, osteoarthritis)
(CPPD or involves knee. Crystals produce linear 30-60% of those >85 encodes transmembrane inorg
crystals BLUE when most commonly affects
chondro- deposits in articular cartilage elicit IL- have it pyrophosphate transport channel)
parallel to slow ray knees/wrists
calcinosis) 8 production (inflammatory rxn)
(white friable deposits,
Tx supportive (no known treatment
oval-blue staining, 50% have significant joint
to crystal formation)
geometric shapes) damage
Happens with IBD (Crohns, Initiated by
Immune-mediated manifestations, may Included Syndromes are PEAR:
ulcerative colitis) in addition environmental Need to tx underlying disease.
be triggered by T-cell response to Psoriatic arthritis
Spondylo- Seronegative (RF neg) to below. Generally due to factors (prior Exercise, adaptive footware.
unknown ags. Inflammatory Enteropathic arthritis
arthropathies: molecular mimicry infections/exposures) NSAIDs, Intra-articular steroids,
peripheral/axial arthritis w/inflammation Ankylosing Spondylitis
Sacroiliitis w/ or w/out DMARDs (Disease-modifying anti-
of tendinous attachment Reiters Syndrome
*Enteritis* peripheral arthritis Oligoarthritis (a few joints HLA-B27 link rheumatic drugs sulfalazine,
Undifferentiated (parts of all) also
causing arthritis usually methotrexate, anti-TNFa)
See below exists
knee/ankle) Male dominant
Similar histologically to RA (but less Sausage-shaped DIP joints (finger or
Radiology: Erosive joint severe, frequent remissions, joint toe Dactylitis 50%)
disease pencil in cup destruction happens less)
deformity Extensive nail pitting
Pt age 30-50
Joint sx have slow onset
Psoriatic 10% of psoriasis pts
(acute in 1/3 of pts)
arthritis have this
Sacroiliac/spinal involvement
(20-40%) - Sacroiliitis
Low back pain

Ankylosing Chronic inflammation of axial joints 1/3 have peripheral joint
Bilateral sacroiliitis
Spondylitis (especially sacroiliac, apophysial) involvement 20-30 yr old
w/morning stiffness
(rheumatoid Chronic synovitis w/ destruction of
spondylitis/Mar articular cartilage, bony ankylosis. Complications: spine Men 2-3X > women
Eventually involves
ie-Strumpell Inflammation of tendinoligamentous fracture, uveitis (blurry
vertebral column
disease) insertion sites (they ossify -> produce vision), aortitis (w/aortic 90% HLA-B27 +
(bamboo spine -> leads to
bony outgrowths) regurg), amyloidosis
forward curvature)
Radiology: Achilles
tendon periostitis is Cant see, cant pee, cant bend the Clinical Progression:
confirmatory sign. Noninfectious arthritis of appendicular knee Urethritis, Arthritis/Achilles Joint stiffness/low back Enthesitis (inflammation in
Really chronic - can
Reactive skeleton within 1 month of primary tendon periostitis, Noninfectious pain early on mostly cartilaginous transition between
have spine
Arthritis infection localized elsewhere in body. conjunctivitis but not all have all 3 ankles, knees, feet tendon and bone)
involvement
(Reiter Perhaps autoimmune reaction initiated (asymmetric pattern)
indistinguishable
syndrome, by prior infection. Extraarticular involvement: Synovitis of digital
from Ankylosing
enteritis- inflammatory balanitis, conjunctivitis, tendon sheath -> sausage
spondylitis
associated Follows infection: Chlamydia cardiac conduction abnormalities, finger/toe
arthritis) trachomatis (#1) or GI infection aortic regurg. Ossification of
(Shigella, Salmonella, Yersinia, tendoligamentous 80% HLA-B27 +
Campylobacter all have LPS) Waxing/waning arthritis, fasciitis, insertions -> calcaneal
tendinitis, lumbosacral back pain spurs/bony outgrowths
Sudden development of
Seeding during Bacteremia or neonates
Most common causes = H flu (<2 yrs), S acutely painful/hot/swollen Predisposed to it if
have spread from epiphyseal
aureus (older children/adults), joint with restricted range of immune deficiencies,
Suppurative osteomyelitis
gonococcus (late adolescence/young motion. illness, joint trauma,
arthritis
adulthood more in women), Systemic = fever, chronic arthritis, IV
Pasteurella multocida septic
Salmonella (sickle cell pts) leukocytosis, elevated sed drug abuse
arthritis/tendinitis due to cat bite.
rate
Mycobacterium tb hematogenous spread May or may not have systemic Insidious onset, gradual All ages, especially
TB arthritis
from visceral infection site symptoms. progressive pain. adults
Silver stain shows Borrelia burgdorferi skin infection Synoviocyte hyperplasia, fibrin Mostly in large
60-80% of untx pts
Lyme arthritis organisms near blood disseminates, suspected OspA cross deposition, mononuc cell infiltrates, joints/shoulders/elbows/ankle
get joint sx
vessels in 25%. reaction with proteins in joints onionskin thickening of aa walls s (attacks last weeks-months)
Observe characteristic
Question if this is Parvovirus B19, rubella, Hep C may 5ths disease: parvovirus direct
slapped cheek rash (not in
Viral arthritis involved in development be due to direct infection or autoimmune infection with secondary immune
adults, kids only). No tx
of RA reaction? reaction.
needed, spontaneously remits.
Some question if this
Symmetric pain, above and below the is causative or Relaxation techniques, improve
Pain all over waist. 11 of 18 tender points tender to secondary to chronic sleep disorder, stretching postural
Fibromyalgia Neck/shoulder/hips touch when examined by physician
Likely a thalamic problem of pain muscles, aerobic conditioning
especially a problem (occiput, low cervical, trapezius,
amplification. May be accompanied
*Amplification Pain impairs sleep supraspinatus, second rib, lateral
by depression, migraines, IBS NSAIDs, Tramadol, Tricyclic
Attachment* Migraine headaches epicondyle, gluteal, greater trochanter,
antidepressants, SSRI, Neuronitin,
Hyperemesis in pregancy knee) but no limit to where you will
Lyrica
feel pain
disease
Heterogeneous disease:
Sunscreens, Topical/oral steroids,
Malar butterfly rash,
Predisposed: hydroxychloroquine (reduce skin
mucosal ulceration, alopecia,
C1q/C2/C4 deficiencies, loss of 90% female, sensitivity), Azathiaprine,
SLE Serologic abnormalities (autoantibodies, inflammatory arthritis,
immune tolerance to nuclear autoags, childbearing age, mycophenolate, cyclophosphamide
compliment consumption, serositis (pleural effusion,
B-cell hyperactivity, T-cell EBV, exposure to
*Deposition antiphospholipid abs) pericarditis, ascites), Immune
dysregulation UV light, 8 Experimental: Anti-CTLA4, Anti
based cytopenias,
susceptible loci, CD20, Anti BlyS, Anti BAFF, B-
glomerulonephritis, cerebritis
cell tolerogan
(seizure/neuropsychiatric sx),
Ex:
Fever, Rash (skin o Wegeners granulomatosis,
o Temporal arteritis,
Systemic infarction), Inflammatory microscopic polyangiitis/Churg-
o Takayasus/Giant cell (large
Vasculitis arthritis, Mononeuritis Strauss syndrome (Small arteries)
arteries) Fever, Rash
multiplex, multiple o Cryoglobulinemia/cutaneous
o Classic polyarteritis
*Infarction* cortical infarctions, leukocytoclastic vasculitisHenoch-
nodosa/Kawasaki (medium
cellular casts Schonlein purpura (Arterioles)
arteries)
Labs: Anticentromere ab
Skin: atrophy, tissue
in 90%, Serum ANA + in No overall disease modifying drug
swelling starts in fingers and
70-90%, Anti- Sclerodactyly (tapered, claw-like) yet. Better agents needed for
extends proximally. Looks
topoisomerase ab + in bowel dysmotility
T-cell mediated release of cytokines like parchment. Extensive Respiratory:
15-40%
causes excessive production of dystrophic calcification in Interstitial
Renal crisis ACE inhibitors
collagen that primarily targets the skin, subcutaneous tissue. pulmonary fibrosis,
Crest Syndrome:
GI tract, lungs, kidneys Tightened facial features (d Pulmonary HT
Calcification, centromere Interstitial lung disease:
dermis, d epidermis),
ab Cyclophosphamide, Cellcept,
Scleroderma Small-vessel endothelial cell damage ulceration Renal: Vasculitis of
Raynauds phenomenon biologics (remicade, Rituxan)
produces blood vessel fibrosis and arterioles and
*Collagen* Telangiectasis ischemic injury GI: Dysphagia (Esophageal glomeruli
Pulmonary HT (short term
dysmotility no peristalsis in infarctions,
benefit): Coumadin, Bosantin,
Limited: only distal to elbows/knees lower 2/3 of esophagus Accelerated
Revatio, Ventavis, Remodulin,
Generalized: More serious, whole body because smooth muscle malignant HT
flolan
Morphea is a localized form of replaced by collagen). Small
scleroderma bowel has loss of villi Mostly women of
Digital ulcers: Ca channel
(malabsorption) and wide childbearing age
blockers, Viagra, Stellate ganglion
mouthed diverticuli (bacterial
block and palmar sympathectomy
overgrowth)
Esophageal dysmotility
fracture through the epiphyseal growth

plate of the proximal femur Males 12-15 yrs:
Klein's Line normally blacks,
Insidious onset of hip or thigh pin in situ with cannulated screws
disects part of the endocrinopathies,
SCFE (slipped pain, painful limp, d motion
femoral head, in SCFE thyroid
cap femoral (IR), do not reduce for fear of disruption
the line no longer disects
epiphysis) Signs: painless limp, knee of blood supply causing avascular
the head Girls 10-13 yrs
pain, d IR of hip necrosis
Bilateral in 25%
observation, brace (TLSO,

Cobb angle: standard complex lateral and rotational milwaukee), PT (electric muscle
Scoliosis
method for assessing the deformities of the spine stimulation), osteopathic,
curve quantitatively chiropractic, surgery
Screening by PE should begin at birth; a

PE shows inability to aBduct In childhood&
child who has not begun to walk The buttocks and perineum may be
the thighs to 90 degrees in adolescence, signs
by 18 mths should be suspected unusually broad and adductor folds
Congenital Hip flexion include a female
Sometimes not noticed until a limp or may be present on the medial aspects
Dislocation Ortolani jerk sign is contour to the
other abnormal gait is noticed when of the thighs.
pathogmonic for subluxation pelvis(both sexes
the child starts walking
have a male
Joint
Replacement
Support injured body part
Splint, cast duration depends on extent of injury

Encompass:
o Sprain (ligament injury)
Bony injury 4-6 weeks (older pt); 2-4 weeks (younger pt)
o Strain (other soft tissue injury)
Sprains, Other
History can often determine inciting event acute injury, changes o Contusion (bruise)
activity- Most common Soft tissue may put walking boot on pt for much longer
in training pattern or schedule o Fracture (hard tissues bone or
related musculoskeletal complaints (can take longer to heal)
cartilage)
disorders - in younger pts
Physical Exam can find soft tissue swelling, bruising/discoloration, o Stress reactions (ask body to do
Overuse and Medications: NSAIDs (relieve inflammation and pain),
ligament laxity, muscle defects something youre not capable of
injury: Analgesics (pt more comfortable, improve their
doing stress fracture, shin splints
functionality/mobility)
medial tibial stress syndrome)
Physical therapy the earlier pt up and moving, the faster
their recovery
NSAIDs: relieve underlying

inflammation, resulting in sx relief.
History: Usually insidious onset, no
Labs: Ex: Autoimmune Do not correct underlying problem
inciting incident (activity may make
Inflammatory ESR: non-specific elevation indicates an inflammatory process Exam: Inflammatory signs: and collagen
better or worse). But really, pt will
etiologies: ANA- Non-specific (high cross reactivity). Abnormal test must be soft tissue swelling, erythema, vascular arthritis, Immune modulators may provide
improve with exercise. Pt often report
correlated w/ elevated ESR inflammatory nodules Osteoarthritis longer sx control, more expensive
use of OTCs, alternative meds
Follow screens w/specific tests (like anti-dsDNA)
Physical therapy
Hereditary/ History: suggested by progressive Physical exam: Muscle

Depends on disease process. Physical therapy often an
other etiologies Lab: muscle biopsy, genetic testing muscle weakness. Positive family hx weakness (note symmetry,
important component.
suggests genetic transmission proximal vs distal
Antibiotics: Start w/broad spectrum, then change to more
specific antibiotic when culture returns. Bone infections
History: Insidious or acute onset; Exam: Local erythema, may require extended course.
Labs: CBC (nonspecific), C-reactive protein (non-specific), culture
Infectious fever/malaise common tender/fluctuant mass, bony
Radiologic eval: CT/MR may show soft tissue or bony infection.
etiologies tenderness, open weeping Surgery: Incision and drainage of abscess (have to no
Bone scan localizes at inflamed/remodeling bone. Tagged WBC scan
Cellulitis, soft tissue abscess, sore (osteomyelitis) good blood supply), Debridement of soft tissue infection,
localizes at site of infection.
osteomyelitis debridement of infected bone follow with course of
antibiotics
Primary Medical Areas of Concern:
Respiratory Screening
o CV, Respiratory, Illness/Fatigue, Neurological, GI, UG, Menstrual Irregularities, Eating Disorders,
o Asthma and exercise-induced asthma, pneumothorax, infectious process
Psychological
o Hx: wheezing, SOB, chest tightness, fatigue/feeling out of shape, chest pain, allergy
Annual Screening Exam: Ht, wt, BP, pulse, injury review/rehab review
o Exercise-induced asthma: flares with exercise, heightened environmental factors
Cardiac screening: Looking for prevention of sudden death ask about syncope, chest pain/palpitations
(allergies, smoke, cold weather, low humidity)
during or after exercise. Questions to ask: Sudden death in family member <50 yo, sudden family hx of heart
o Physical: lung auscultation, allergy sx, chronic sinusitis (hear after exercise, compare it
disease, syncope/lightheaded w/exercise, Dyspnea/easy fatigue w/exercise, palpitations/chest pain w/exercise,
to how they feel)
Previously detected murmur/elevated bp
o Tx: Allergy control, short-acting B-agonists (albuterol), Long-acting B-agonists
o Recent illness, medications/supplements, alcohol/substance abuse, direct blow vs non-contact, PPQRST,
(severent), anti-inflammatory agents (cromolyn), Steroid preps (advair)
Non-Operative other pertinent hx
o Pneumothorax: acute onset of chest pain w/dyspnea and tachycardia, Hx of a collision
Orthopedics o Physical exam: Vitals (essential Heart rate for rhythm and rate, pulses radial/carotid/femoral/
or this is spontaneous. Physical: Auscucltation (decreased breath, sounds on
Lecture dorsalis pedis, BP, resp rate, temp)
affected side), tachycardia, anxious, dyspnea, mediastinal shift
(Primary Care o Auscultation: S1/S2, murmurs, S3 can be normoal in young children and some athletes (question HF
o Infections: fever, malaise/fatigue, N/V, diarrhea, mm aches, lightheadedness, dizziness
Sports Med) if >40 yo), S4 (normal in athletes). Grade 3 murmurs or louder need greater work-up (esp if increase
o When to refer? Temp >101F, Chest pain/palpitations, dyspnea, head injury,
w/valsalva - cardiomyopathy or diastolic murmur-mitral stenosis, aortic regurg)
collapse/syncope, skin lesions, seizure hx, persistent weakness/paresthesias, severe
o Sudden Death: <35 yo due to hypertrophic cardiomyopathy, coronary a anomalies, arrhythmias, Long
allergies, loss of a paired organ, unexplained wt loss, menstrual changes
QT, Marfans, Prevalence 1:100,000 to 1:300,000 (School-aged), 1:15,000 (Joggers), 1:50,000
o Return to play is often gray: rest, fluids, sx control
(Marathoners)
Neurological
o Syncope: Vasovagal, cardiogenic, neurogenic
o Concussion (simple vs complex), have to do hx, PE to suggest that they need to stay
o Chest Pain/Palpitations: Arrythmias, Repiratory (asthma/bronchitis/pneumothorax), musculoskeletal,
from play longer. To return to play following concussion, want to ensure sx free at
psychogenic
rest, with minimal exertion, with light cardio/lifting, with gility drills/heard non-contact
o Marfans: Changes in aorta (can have rupture), lots of tall/lean athletes, sunken in chest, long fingers,
workout progress back to practice for tolerance
EKG, heart work-up really important in these pts.
Osteopathic treatments:
DO=Doctor of Osteopathic Medicine
o Muscle energy: direct technique pts activate mm opposite the area of restriction which causes
In other countries, osteopathy is often a form of complementary medicine emphasizing holistic
reciprocal inhibition and relaxation of the mm that are tight, can be used anywhere in body
approach to health care using manual medicine (bachelor degree equivalents these arent licensed
o Myofascial release: indirect soft tissue technique used to stretch and relax muscular and fascial
physicians)
restrictions, very gentle
Founder: Andrew Taylor Still MD (1917)
o Counterstrain indirect, focuses on identifying tender points. Places pt in position of ease
4 principles: 1) The body is a unit. 2) The body possesses self-regulatory mechanisms. 3) Structure
around the tender pt to reduce activity efferent nerves thereby decreasing pain. Goal is to hold
and function are reciprocally interrelated. 4) Rational therapy is based on understanding of 1 st 3
for 90 seconds and reduce pain by 70%, pt must be completely relaxed throughout tx
principles.
o Popping and Cracking high velocity low amplitude thrust. Mobilization with impulse. Direct
Key terms:
moves a dysfunctional segment through its restrictive barrier nd resets itself. To restore
o OPP: Osteopathic Principles and Practice
physiologic motion. Precise positioning and set-up is key. (Dont attempt this at home).
o OMT: Osteopathic Mnipulative Tx
Cautions: hypermobile joints, osteoporosis, acute fractures, radicular sx, contractures, pts
o OMM: Osteopathic Manipulative Medicine
w/rheumatoid arthritis. Risks: Permanent neurological damage, vertebral basilr thrombosis,
Uses of OMT: Infections, CHF, lymphedema, asthma/COPD exacerbations, chronic back/neck pain,
carotid a dissection, death or quadriplegia if disrupt transverse ligment of atlas
HA, Acute musculoskeletal injuries, post-operative ileus/constipation/diarrhea, arthritis (joint
o Lymphatic Pump: Maintains fluid balance purification and cleansing of tissues, defense
problems), Pregnancy issues, Newborn issues, Post CABG/CPR
against toxins/bacteriaviruses, nutrition, sympathetic nervous system constricts lymphatic
Somatic Dysfunction: An impairment or altered function among related components of the body,
vessels. OMT cn lymphatic fluid circulation. Lymphatic techniques include rib raising,
Osteopathic including skeletal, arthroidal, myofascial structures in addition to related vascular, lymphatic, and
thoracic inlet, doming diaphragm, pedal pump, liver/splenic pump, Galbraith technique. CI if
Medicine neural elements
Crcinoma, acute fracture in area of tx, abscess/localized infection, bacterial infection
Overview TART: Tissue texture changes (edema, warmth, redness, hypertrophy, atrophy, rigidity, bogginess,
w/temp>102
stringiness), Assymetry, Restriction, Tenderness
o Articulatory Techniques: Gentle, direct tx range of motion in restricted joint. Spencer
Barriers to motion:
technique of GH joint (OA, shoulder strain, frozen shoulder), rib raising (s chest wall motion,
o Anatomic (the limit of passive motion which if breached causes damage)
improves lymphatic return, normalizes sympathetic tone in pneumonia, COPD/asthma exac). CI
o Physiologic (the limit of active motion)
if acute fractures, acutely inflamed joints (caution in cervical area vertebral aa compression)
o Pathologic/Restrictive: functional limit within the anatomic motion which s the physiologic
o Craniosacral primary respiratory mechanism. Inherent motility of brain/spinal cord,
range
fluctuation of CSF, movement of intraspinal and intracranial membranes, articular mobility of
Acute Somatic Dysfunction: Vasocilation, Inflammation, Warm moist skin, d mm tone, edema,
cranial bones, involuntary mobility of the sacrum between the ilia. Firm attachments of dura to
bogginess, severe/cutting/sharp pain
foramen magnum, C2, C3, S2. Membranes that surround, support CNS are dura, arachnoid, and
Chronic Somatic Function: Cool pale skin, d mm tone, doughy tissue texture, stringiness, fibrotic
pia mater. There is a subtle, pulse-wave like motion of the brain/spinal cord. There are
changes, dull/achy/crawling/itching/burning/gnawing pain
measurable, inherent movements in these structures with respiration. Goals: balance motion
Reflexes: Viscerosomatic-viscerl input that is referred to a corresponding segmental somatic structure.
SBS, reduce venous congestion, enhance rate and amplitude of CRI, mobilize and correct
Somatovisceral-somatic stimuli produce responses in segmentally related visceral structures
membranous articular restrictions (contraindications intracranial hemorrhage or elevated ICP,
Direct techniques: Move tissues/joint into the barrier, or into the restriction uses force to create
skull trauma, seizures), Complications changes in HR/BP/RR, GI irritability, Tinnitis,
motion into and beyond the restrictive barrier
Dizziness, HA
Indirect techniques: Move tissue/joint to a position of ease, away from the barrier or restriction
Evidence-based medicine: Low back pain, carpal tunnel syndrome, otitis media, post-op pts, COPD
allows the bodys inherent neurologic or intrinsic forces to free up the restriction
excerbations
Non- Manual medicine (see DO lecture) Type Example Use
pharmologic Herbal/nutritional supplements Closed kinetic chin (both Leg press, squat Shoulder/knee rehab
Mnagement of o Early research lacking (lots of placebo effect, many preps lack purity). Most newer research reveals ends are attached)
Musculoskelet minimal utility Concentric (mm Flexor phase of biceps curl Increase mm mass and
al problems o Glucosamine/chondroitin: Building blocks of CT Glucosamine is an amino sugar, distributed in contracting in an equal strength
cartilate/other CT, Chondroitin is a complex carb, auds in water retention of cartilage. Both are fashion all the time)
normally made in the body. not sure how it works since these are both denatured in stomach acid. Core stability Abdominal crunch Relief of low back pain
Use in OA Eccentric (mm relaxes Extension phase of biceps Sport-specific
o DMSO (Dimethyl sulfoxide): industrial solvent. Can be used to aid in transport of other substances through the exercise) curl strengthening
into soft tissue has innate antioxidant and anti-inflammatory properties. Studies show pain relief in Isometric (mm doesnt Holding a wt Toning
OA. FEDA approved only for tx of interstitial cystitis. Know its working because you get a garlic taste shorten at all)
in your mouth. Isotonic Free-wt lifting conditioning
Acupuncture Open kinetic chain Quad extension Functional improvement in
o Balance of yin (cold/slow/passive) and yang (hot/excited/active). Health is a balance, disease is ADL
imbalance. Imbalance leads to blockage of qi (vital energy) along pathways (meridians). Acupuncture
points are connections between meridians.
Ultrasound:
o Uses: pain management interrupt transmission of painful impulses (decrease pain, increase o High frequency sound waves warm surrounding soft tissue
functionality), treat disease (by restoring balance to allow body to heal) o Uses tendon injuries, mm strain/spasm
o Current research: does it work, how? What are the complications local infections, puncture of
o Cautions with malignant tumors, bone, pacemakers, epiphyseal plates
organ/blood vessel. o Phonophoresis: use ultrasound to deliver meds to soft tissue (cs, NSAID, DMSO).
Physical Therapy modalities Minimal penetration of meds, possible systemic effects of meds
o Comprehensive tx plan therapeutic exercise, manual techniques, modalities. Important component of
o Iontophoresis: use electrical current to deliver meds to soft tissue use for CS,
tx for musculoskeletal problems. Adjunct tx for cardiac/pulmonary/developmental disorders acetic acid (in myositis ossificns). Avoid near metallic implants, wires, or staples
Therapeutic exercise: improves strength, mobility, function. Decreases pain/swelling, home-based (brief o Electrical stimulation: electrical stimulation generates muscle contraction use for
instruction in office, effective after ACL reconstruction), supervised (superior to home-based for low back injury
mm spasm or contusion. Electrical current alters sensory input (TENS
or OA, may involve home component) transcutaneous electrical nerve stimulation) use for neuropathic pain syndromes).
Avoid around pacemakers
Bracing and orthotics
o Low level laser tx: alters cellular oxidative metabolism. Uses: minor
musculoskeletal pain, OA, RA, carpal tunnel. Avoid in pregnant, malignancy
Plain X-ray: CT: Arthrography: put fluoroscopic
MR:. Ultrasound:
Bone scan: Indications: Osseous metastases, guidance or ultrasound guidance to
Strengths: Bony injury, Strengths: fracture detection, fractures (traumatic and stress) put contrast into a joint (gives you
Strengths: Best for Strengths: soft tissues
Availability, fast, inexpensive, fracture morphology, fracture better look at joint in question)
soft tissue, Bone (tendon, ligament, muscle,
if + imaging workup often healing, osseous fusion, Strengths: can help diagnose occult fracture
ok, multiplanar, no nerve), no radiation, dynamic,
done. Good for acute fracture, added specificity to MR, bone remodeling process takes up Strengths: powerful when
Evaluation of radiation cheaper than MR
arthritides, bone lesions multiplanar and 3D reformats. pyrophosphates and will be detectable in combined w/MRI/CT. Labrum
Injury
Less hardware artifacts areas of remodeling bone. Total body screen, (shoulder and hip TFC, SL, and LT
(different Limitations: Limitations: Operator
Limitations: Sensitivity, (multidetector), bone lesions. low cost (relative to MR), sensitive, ligaments wrist rotator cuff),
radiological Expensive, less dependent, bones (?) and deep
Cant see soft tissues, early Good for bony injury, some physiologic (perfusion, osteoblastic activity) chondralosteochondral lesions, post
tests, etc) available, weight tissues (if large pt size),
osseous pathology (stress utility for soft tissue. operative meniscus;
limitations, physician time, referring
injuries, mets/myeloma) Limitations: Lack of specificity (stress shoulder/hipwrist/elbow/ankle/knee
claustrophobia clinician consultation
Limitations: More expensive, reaction, fracture, arthritis, tumor, infection);
Contraindications
1st line screen high radiation exposure, soft elderly (>72 hrs). Expensive, less available Limitations: invasive, indirect
(implants, An excellent modality in
Definitive arthritis tissue, bone marrow (pyrophosphate degrades over time) information if not combined w/
pacemakers), time skilled hands
Indicative ex w/ACL pathology MRI or CT
Orthopedics Lectures:
Cervical
Depends on level involved
o C4-5 (C5 nr) = deltoid weakness,
not much numbness, shoulder pain
Tx: rest, cervical collar, traction/pt,
Causes nerve compression or irritation o C5-6 (C6 nr) = biceps, wrist Pain, numbness/tingling,
HNP: NSAIDs/Steroids, epidural
Commonly insidious, but can be from extension, NT along radial aspect weakness, limited motion, Age 30-50
Herniated disc injections or Surgery (discectomy,
trauma/injury o C6-7 (C7 nr) = triceps, finger ext, radicular
w/ or w/out fusion).
nt posterior to middle finger
o C7-T1 (C8 nr) = grip strength, NT
to little finger
Stenosis: anything that Arthritis: Insidious, accident/trauma,
Fracture: Traumatic (stable or Other: Stinger whole
causes narrowing of the disease process. See pain, restricted
DJD unstable), Flexion type = 45-75%, Cervical radiculopathy, hand/arm goes numb
canal or foramen motion, radicular sx, numbness/tingling,
(Degenerative extension type = 20-35%, Compression Brachial plexopathy can be due to hard hit on the
(arthritis, HNP, often times insidious onset, pt complains
Joint Disease) = 12% due to infection side tends to be a
dislocationsubluxation, they slept wrong, neck pain
temporary thing
infection)
Shoulder
Tx: conservative rest, NSAIDs,
acromial spur, clavicular spur, CA
subacromial injection, PT.
narrowing of the ligament thickening or calcification,
Causes rotator cuff irritation, tear; Then surgical subacromial
Impingement subacromial space (<7 hypertrophy of rotator cuff, loose body,
pain/weakness decompression arthroscopic or
mm by MRI) fracture (greater tuberosity), OS
open w/or w/out rotator cuff repair,
acromiale, secondary to instability.
correct instability
Hawkins test:
Test for subacromial Empty can test:
Neers test: The patient attempts to elevate the
impingement or rotator Drop arm test: raise arm as
Stabilize posterior shoulder, grab elbow arms against resistance while the
cuff tendonitis. Can high as possible, slowly lower
and forarm pronated passively move elbows are extended, the arms are
indicate pathology of to 90 degrees.
arm up. abducted and the thumbs are pointing
biceps brachii or rotator If rotator cuff tear or
Can indicate impingement of the rotator downward.
cuff. supraspinatous disfunction,
cuff tendons under the coracoacromial indicates tendinitis, tear of tendon,
Grasp elbow and wrist, their arm will drop to the side.
arch supraspinatous w/impingement.
Diagnose flex to 90 degrees. The patient may be able to
impingement Humerus passively lower the arm slowly to 90
internally rotated. degrees (because this is a
function mostly of the deltoid
muscle) but will be unable to
continue the maneuver as far
as the waist.
+ test if pain with motion.
Pain or weakness is +,
+ is with pain of motion.
Supraspinatus (helps deltoid abduct arm) suprascapular n (C5/6)

Infraspinatus (laterally rotates arm) - suprascapular n (C5/6)
Rotator cuff Teres minor (adducts and laterally rotates arm) axillary n (C5/6)
tear
Subscapularis (medially rotates and adducts arm)
subscapular/thoracodorsal nn
Glenohumeral joint from insidious,

traumatic, other often need to do injection to help
Arthritis
Acrohumeral joint from traumatic, pain/inflammation
osteolysis, insidious
Rarely in superior direction because
Frequently associated with axillary
rotator cuff would have to be torn first
nerve injury (wraps around humerus
and so would coracoacromial arch (95%
laterally around 1.5-2 inches inferior to
occur anterior and inferior where there is
acromion). Check sensory component
least ligamentous reinformcement it
Dislocation by checking pinprick sensation over
may look completely anterior because
lateral deltoid area
subscapularis pulls it medially, but it is
also inferior this is important to
Person will have arm down, be kind of
remember if you are setting it back into
holding it up to prevent movement
place)
Labral Around the glenoid, usually s stability Can put anchor in bone to help
Tear can lead to other problems
tear/Instability of ball in socket stabilize it.
Biceps Traumatic (throwers, car accident, tennis
tear/instability players)
Susceptible to injury because it is an

area of relatively poor vascularity.
catching sensation, pain with
Other parts of the labrum often heal
shoulder movements, most
SLAP tear more easily because the blood supply
often overhead activities such
delivers a healing capacity to the area
as throwing
of the tear.
Superior labrum tear anterior to posterior tend to fix laproscopically

Tenosynovitis inflammation in the tendon Can become calcified
Proximal humerus more common in
Fracture older pts,
clavicle, glenoid
pain, weakness, circulatory changes
Thoracic outlet compression of nerves/vasculature in the

syndrome neck
RSD (reflect
pain way out of proportion
sympathetic
with what you would expect
dystrophy
Elbow
Arthritis laborers traumatic or insidious
ulnar humeral, radial If large part broken, can fix
Instability fracture is monteggia,
head w/screws
Median n: Anterior interosseous nerve

Ulnar: Ulnar tunnel Snapping Ulnar
(largest branch, passes between 2 heads Radial n: Posterior interosseous n
syndrome (cubital tunnel, Nerve
of pronator teres impairs pinch (between 2 heads of supinator
Nerve between flexor carpi ulnaris (subluxation): 16%
ability) or Carpal tunnel syndrome (most functional involvement only) or Radial
Compression: mm heads d stretch of all individuals it
common thumb, index, middle finger tunnel syndrome
w/elbow flexion). moves
most discomfort at night)
Hand/Wrist
Treat by aspiration (50%
Tendon related (filled with synovial
Ganglion mostly in the wrist (90%) recurrence) or surgical excision (5-
fluid).
10% recurrence)
Tx: splint, NSAIDs, corticone,

TYPING DOESNT surgery (open or endoscopic).
Electrodiagnosis is the Numbness, weakness, atrophy CAUSE IT
Carpal tunnel
gold standard but sx of the hand (all fingers but Surgery found to be better than
syndrome
generally used the pinky) Insidious, sometimes splinting overall in a study
work-related Injection of steroids better than oral
steroids
Compression of median n at the wrist
Tenosynovitis (inflammation of the fluid

Pain, swelling, or sticking of
Trigger finger filled sheath synovium that Tx: cortisone, surgery to release.
the finger.
surrounds the tendon
finger, hand, wrist, distal

Fractures
radius
Instability (Scapho-lunate advanced due to either chronic untx scapohoid
SLAC Wrist collapse) fracture or scapholunate dissociation
Reflexes: Brachioradialis
Saturday
absent or d, triceps
Night Palsy Due to compression of radial nerve
usually normal
(hinted on test) Strength: weakness in wrist
extension, finger extension Sensory changes:
(primarily MCP joints); abnormal on dorsum
(hand over barstool wake up unable
triceps may be partially weak of hand
to move hand)
or normal.
Back (Lumbar)
Arthritis Degenerative or insidious.
Most common in lumbar spine
Fracture
osteoporosis
Knee
keeps knee from
subluxing
Positive anterior
drawer sign indicates
torn ACL Clipped from lateral side, causes
Anterior and
unhappy triad: MCL, Medial
Posterior refer to
meniscus, ACL
ACL where they are
attached on the
Abnormal passive abduction indicates
TIBIA
torn MCL
Patella usually subluxes laterally
Articular
OCD, Chrondromalacia, Fracture,
cartilage
Bone bruise
damage
cyst in the back of the knee.

Between gastrocnemius
Bakers cyst usually from meniscal tear medial head tendon and
semimembranous muscles. In
synovial sack of knee joint
Pigmented
villonodular thickened synovium
synovitis
Tendon
patellar tendon or quad tendon tx with surgery
ruptures:
Foot/Ankle
Arthritis (foot and ankle)
Fractures Foot, ankle
LisFrancs between 1st and 2nd metatarsal. 2nd

injury metatarsal extends into tarsal bones.
Wear tight shoes, whatever end up

Bunion getting this huge bump on the side of
your foot. Surgically removed.
Plantar
fasciitis: Inflamation of the plantar fascia
Diabetic
:
ulcers, RSD, :
Charcot foot
Other Musculoskeletal Disorders from Robbins (not on content list)
Ex: bone doesnt
Defect in nuclear proteins/transcription
develop, fusion of 2 LOCALIZED developmental anomalies HOXD-13 TF forms extra
factors
Dystotoses adjaent digits from problems in migration of digit between 3rd/4th digit, Uncommon
Craniorachischisis: Spinal
(syndactyly), develop mesenchyme cells, condensations form some syndactly
column/skull dont close
extra bones
Defect in Hormones/Signal
DIFFUSE problem due to mutations in
Dysplasias transduction
regulators of skeletal genesis
AD (point mutation
Shortened proximal
Achondro- FGFR3 constantly working to suppress on short arm of Chr
extremities with normal
plasia cartilage in physis 4)
trunk, enlarged head
Shortened limbs, relative
Thanatophoric macrocephaly, small Defect in extracellular structural Lethal (from respiratory
1/20,000 live births
dwarfism chest cavity, bell-shaped proteins insufficiency)
abdomen
Type 2/10/11
Collagen
Disease Early joint destruction Defects in folding/degradation of
(collagens in molecules
hyaline
cartilage
Lysosomal storage diseases ( enzymes
Pt short stature, chest Mesenchymal cells (*chondrocytes*)
Mucopolysacc to degrade dermatan sulfate, heparin
wall abnormal, most affected cause a lot of problems
haridoses sulfate, keratin sulfate)
malformed bones in hyaline cartilage
Defects in metabolic pathways
Infantile form AR, osteoclast bone resorption causes
lethal or causes major skeletal sclerosis.
Osteopetrosis Morphology: no medullary canal in
problems with d
(marble bone bones, long-bone ends are bulbous.
hematopoiesis (less Carbonic anhydrase II deficiency: Brittle bones (easily fracture) Bone marrow transplant can help
disease/Albers- Primary spongiosa persists. Woven
marrow space) Osteoclasts/renal tubule cells need it to
Schonberg) bone
Adult form: AD, benign, acidify the environment prevents
some anemia. digestion of bone.
Effect of PTH levels: Activates The whole body is affected
Hyper-
osteoblasts to release pro-osteoclast cortical bone affected >
parathyroidis PTH production
signals cancellous bone
m
Severe/untreated long-term PTH Brown tumor: mass of reactive tissue Observe cortical
usually diagnosed early from microfractures/secondary cutting cones with
X-ray pattern along radial hemorrhages/ingrowth of fibrous repair osteoclasts boring
Osteitis fibrosa aspect of middle Primary: autonomous hyperplasia or tissue Subperiosteal resorption => through (enlarge
cystica (von phalanges of tumor (adenoma) thinned cortices/lost lamina haversianvolkmann treat the hyperparathyroidism (sx
Recklinghause index/middle fingers Peritrabecular fibrosis dura around teeth canals) looks like will regress or disappear!)
n disease) Secondary: caused by prolonged railroad tracks
hypocalcemia state tend to have milder bone cell activity (dissecting osteitis)
skeletal abnormalities d bone density
(osteopenia)
Phosphate: failure to excrete phosphate secondary hyperparathyroidism

often a mixed pattern of disease
Calcium: failure to convert 25-(OH)D3 to 1,25 (OH)D3 (less Ca absorbed)
osteoclast resorption (looks like osteitis fibrosa cystica)
PTH: less 1,25 (OH)D3 to suppress parathyroid, less degradation/excretion of PTH
Delayed matrix mineralization (osteomalacia)
Metabolic acidosis: stimulates bone resorption, release of calcium hydroxyapatite
Renal Osteo- skeletal changes with Osteosclerosis
from matrix
dystrophy chronic renal disease Growth retardation
Aluminum deposition (dialysis solutions contain it): interferes with calcium
Osteoporosis
hydroxyapatite deposition osteomalacia results
-turnover osteodystrophy: bone resorption/formation (but more resorption occurs)
B-microglobulin in serum with long-term hemodialysis causes amyloid
-turnover/aplastic disease: little osteoclast/osteoblast activity, sometimes osteomalacia
deposition in bone!
Function: stimulates
intestinal absorption of
Ca/PO4, works with PTH
to mobilize Ca from
bone, stimulates PTH-
dependent reabsorption
of Ca in distal renal
tubules, likely helps
osteoclasts differentiate
from monocytes
Vitamin D
Ricketts: children have deranged bone growth, producing skeletal deformities

Overgrowth of epiphyseal cartilage from inadequate calcification, poor maturation of cartilage cells. Irregular cartilage project into marrow cavity, osteoid matrix is deposited on the weird cartilage.
Osteochondral junction enlarges, expands laterally.
Capillaries/fibroblasts overgrow in the area from microfractures/stresses on the crappy bone.
Skeleton gets deformed from loss of structural rigidity of developing bones
Clinical picture: Frontal bossing, Rachitic rosary, pigeon breast deformity, Harrisons groove (diaphragm pulls rib cage bottom in), lumbar lordosis, bowing of legs
Osteomalacia: Vitamin D deficiency causes less intestinal absorption of Ca/PO4, PTH will stimulate more loss of Ca from bone to restore blood levels. Adults have disorganized remodeling of bone.
Bone contours not affected, but bone is weak/vulnerable to fractures (especially vertebral bodies, femoral necks).
Histological: thickened matrix with normal trabeculae.
Eventually, difficult to differentiate from other osteopenias
Hypocalcemic tetany
Musculoskeletal Bugs
Bug Name Staining characteristics Clinical Features Epidemiology Virulence
Streptococcus sp G+ cocci in chains Osteomyelitis, Joint Infection Group B in 10-35% of all healthy adults Hyaluronic acid capsule
(Groups A/B): Facultative anaerobes (intestine, vagina, rectal) causes M protein
A=Strep pyo, Beta hemolytic (bacitracin sensitive) problems in NEONATES Streptolysin O, S
B=Strep Glucose fermenters
DNAses
agalactaciae Catalase neg, coagulase neg
Streptokinase A/B (lyses blood clots)
Hyaluronidase (degrades CT)
Exotoxins (super ags)
Staphlococcus G+, cocci in clusters Osteomyelitis 90% due to S. aureus! Transmission: Autoinnoculation (Normal Forms biofilms, Capsular polysaccharide
aureus Beta hemolytic, yellow colonies on blood agar flora in nasal mucosa/skin), Surgical (anti-phag/chemotactic), Slime layer
Ferments mannitol on MSA, Joint Infection (Bursitis) 80% is due to wounds, Lungs of CF pts, , Hands Protein A (Binds IgG Fc, prevents
salt tolerant staphylococcus. opsonization), MSCRAMM
Facultative anaerobe Risk: surgery/break in skin, tampons, SuperAg toxins (TSST-1)
Catalase +, Coagulase + ventilators, catheters, severe neutropenia, Hyaluronidase (hydrolyzes CT)
CF, IV drug use, Chronic granulomatous Penicillinase
disease Staphylokinase/fibrinolysin
Adhesin promoting collagen attachment
(osteomyelitis, septic arthritis)
Enterobacter sp G- rods Osteomyelitis, Joint Infection Link to contaminated parenteral fluid Most are resistant to 1st generation
Facultative anaerobe solutions cephalosporins, ampicillin. May be
Ferment lactose susceptible to 2nd/3rd generation
Normal GI tract flora (way less than E coli)
Haemophilus G- coccobacilli Osteomyelitis, Joint Infection Normal flora (20-80%, nasopharynx) Type B Polysaccharide Capsule (directly
influenzae Obligate parasite o Unimmunized children 6-18 months invades blood capillaries)
(faculatative anaerobic) Septic arthritis: joint pain, swelling, d mobility. most vulnerable - NEONATES IgA protease
Chocolate agar (requires o Most people acquire Ab by age 10, so Attachment pilli
factor X & V, CO2) infection rare in adults. Ampicillin resistance
Oxidase +
Neisseria G-, kidney-bean shaped diplococci (in PMNs) 1st Stage: Arthritis dermatitis syndrome: An STD (2nd most common) Pili with high ag variation (antiphagocytic,
gonorrheae No capsule, non-maltose fermenting Joint/tendon pain is most common in early More in males (females more frequently asx adhesive to mucosa)
Intracellular, aerobic infection. Migratory polyarthralgia, carriers) IgA Protease
Grows on Thayer-Martin especially of knees, elbows, more distal Highest rates in ages 15-30, unmarried, low LOS (creates sialic acid capsule)
Oxidase/catalase + joints, SE status Upregulates catalase in phagocytes
Tenosynovitis: flexor tendon sheaths (wrist), Receptors to scavenge FE from
Achilles tendon ("lovers' heels"). transferrin/lactoferrin
Dermatitis: maculopapular lesions, often
w/hemorrhagic component. 5-40 lesions,
peripherally located, painful before visible.
Fever common, but temp usually <39C.
2nd Stage: Septic Arthritis: skin lesions have
disappeared; blood culture results are nearly
always negative. Most commonly ends up in the
knee.
Musculoskeletal Drugs
Drug Name Mechanism of Action Effects: Whys it Used? Pharmokinetics Major Side Effects
Analgesic (non-opioid)
weak nonselective COX rapidly absorbed from GI, peak well tolerated by GI
analgesia, antipyretic equal to
inhibitor in presence of Tx mild pain & fever, fever from plasma conc in 30-60 min, overdose: liver tox w/ liver failure,
aspirin
Acetominophen peroxides virus metabolized in liver. Distributes to enhanced by chronic EtOH use
no antiinflammatory (if any,
inhibits COX3 (COX1b) in Mild arthritis - Analgesic peripheral tissue and CNS. Renal high chronic use associated with chronic
weak) or antithrombotic fx
brain. excretion. plasma life = 2-3hr renal failure
Inhibits uptake of NE and 5HT, Analgesic (non-opioid) Nausea, vomiting, dizziness, dry mouth,
Tramadol Use for mild to moderate pain
Weak Mu agonist Synthetic codeine analog, sedation, headache, seizures
Corticosteroids
Mech unclear, but T cells Anti-inflammatory, RA (immunosuppressive, anti- Hypercholesterolemia, cataracts,
(prednisone,
affected most immunosuppressive inflammatory) osteoporosis, HT w/prolonged use
methylprednisolone)
Ibuprofen Non-selective NSAID Gastric irritation, nausea, dyspepsia,
Pain & inflammation - trauma,
Propionic acid derivative analgesia bleeding, peptic ulcer disease. Acute
infection, autoimmune disorder, Take PO, Wide distribution. Liver
antipyretic renal failure in patients at special risk:
Naproxen neoplasms, joint degeneration -- metabolism, renal excretion
Reversible COX inhibition antiinflammatory volume depletion, preexisting renal dx,
RA, OA, AS
(COX1 and 2) CHF, hypotensive. Aspirin alt (children)
Non-selective NSAID Acetic Toxicity limits use in tx for gouty
Anti-inflammatory, analgesic,
Indomethacin acid derivative reversible COX Pain/inflammation arthritis, Ankylosing Spondylitis,
antipyretic
inhibitor osteoarthritis of hip
less GI tox compared to nonselective
antiinflammatory, analgesic
Selective NSAID - COX-2 COX inhibitors
antipyretic fx equivalent to Osteoarthritis, Rheumatoid Take PO, gut absorption.
Inhibitors. Sulfur group some renal tox, diarrhea, dyspepsia,
Celecoxib aspirin and ibuprofen arthritis. Analgesic not effective Liver metabolism (Cyt P450).
selectively binds COX-2, abdominal pain
no antithrombotic fx post surgery. Protective against Excreted in urine and feces
excludes COX-1 CV toxicity
colon carcinogenesis?
very expensive
Purine analog Gout
Hypersensitivity (rash) 3%
Reduces production of uric acid
Oral admin (completely absorbed) Acute gout attack (give w/colchicine &
by competitively inhibiting
drug of choice if hx of kidney Feces/urine excretion NSAIDs at beginning)
Xanthine Oxidase (the last 2
Allopurinol stones or if creatinine Nausea, Diarrhea
steps of uric acid biosynthesis)
clearance <50 mL/day 1 dose daily = ok (alloxanthine Affects metabolism of 6-mercaptopurine,
Xanthine and hypoxianthine are
metabolite has long life) azathioprine (need to reduce their doses
more soluble, less likely to
if given w/ Allopurinol)
precipitate in joints
Binds tubulin, depolymerizes it
Avoid if pt has creatining clearance <50
disrupts granulocyte
mL/min.
mobility Prophylaxis to reduce
Oral admin (rapid absorption by GI) Nausea, vomiting, abdominal pain,
occurrence of acute attacks,
Colchicines Gout Feces/urine excretion (unchanged) diarrhea
Blocks cell division (binds relieves pain give within 24-48
Myopathy, neutropenia, aplastic anemia,
mitotic spindles) hrs of attack onset
alopecia.
CI pregnancy, hepatic/renal/CV disease
Inhibits synthesis/release of LTs
Oral admin Drowsiness/confusion
Benzodiazepine Agonist at
Skeletal muscle relaxant, MS, Lipophilic, go through entire body Physical dependence
Diazepam GabaA receptor/Y-aminobutyric Enhances GABA effects
cerebral palsy Metabolized in liver Caution needed if liver disease,
acid target
Excreted in urine, crosses placenta glaucoma
Drowsiness, depression, HA
Unknown mech
Respiratory depression, d muscle
Cyclobenzaprine function
Appears to affect locus ceruleus
(Aka cyclone, mellow Blocks muscle spasms Skeletal muscle relaxant Oral admin Dry mouth
to inhibit NE uptake, appears to
yellow) Vision problems
inhibit alpha motor neurons in
High dose: Anticholinergic, ataxia
ventral horn of SC
CI w/ MAOIs
First Generation G+ cocci and G- rods IV/IM (poor oral absorption)
Beta lactam antibiotic work CI if penicillin allergy (likely to be
Cephalosporins Cross the placenta
like penicillin to disrupt cell Tx for osteomyelitis allergic to this too)
(Cephalexin, Resistant to penicillinase of Dont go into the CSF
membrane
cephalothin) staph, Active against PEKS: Urine elimination
Proteus, E coli, Klebsiella,
Staph
Cephazolin penetrates bone well
Diarrhea/nausea/vomiting
Neisseria
Inhibit replication of bacterial HA/dizziness
G- (enterobacteriaceae, Ingesting with antacids (Al, Mg, Zn,
DNA by interfering w/action of Phototoxicity, nephrotoxic
pseudomonas, H flu, Moraxella, Fe) can interfere w/absorption
Fluoroquinolones DNA gyrase and topoisomerase Cartilage erosion, can cause ruptured
Legionella, Chlamydia, Tx for osteomyelitis Distribute well to all tissues and body
(Loveofloxacin) Bactericidal tendons (fluoroquinolones hurt
Mycobacteria); fluids (bone )
attachments to your bones)
Some G+ (newer ones like Renal excretion
Levofloxacin = 3rd generation Can serum levels of warfarin, caffeine,
levofloxacin!)
cyclosporine
osteoclastic bone resorption:
o Inhibits osteoclastic proton
Biphosphonates Diarrhea, abdominal pain,
pump needed to dissolve
(etidronate, risedronate, Oral admin, without food musculoskeletal pain.
hydroxyapatite,
alendronate, (IV available)
o osteoclastic Preferred agent to prevent/treat Tx for osteoporosis, Pagets,
ibandronate, Bind hydroxyapatite in bone (cleared Some cause esophagitis/esophageal
formation/activation, postmenopausal osteoporosis bone metastases, hypercalcemia
pamidronate, over hrs to yrs) ulcers
o osteoclastic apoptosis,
tiludronate, zoledronic Renal excretion
o cholesterol biosynthetic
acid) Osteonecrosis of jaw
pathway needed for
osteoclast function
Intranasal admin
Reduces bone resorption but less But RELIEVES PAIN of Rhinitis
Calcitonin Tx for osteoporosis Parenteral form rarely used for
effective than biphosphonates osteopathic fracture Pagets pts have resistance (if long use)
osteoporosis
spinal bone density, s risk of
vertebral fracture. risk of osteosarcoma in rats
Recombinant segment of PTH
Teriparatide Should reserve for pt w/high Tx for osteoporosis Subcutaneous admin Safety/efficacy not evaluated beyond 24
Stimulates bone formation.
fracture risk or who cant months.
tolerate other txs
Rheumatoid arthritis -
Sufasalazine PABA analog to occupy early/mild RA in combo w/ Not absorbed orally or as suppository
Leukopenia
(a DMARD) dihydropteroate synthetase hydroxychloroquine and Onset takes 1-3 months
methotrexate
May inhibit phospholipase A2 Rheumatoid arthritis
and platelet aggregation, Doesnt slow joint damage when early/mild RA tx combo
Hydroxychloroquine
Membrane stabilization, effects used alone have to use in w/methotrexate & sulfasalazine Renal toxicity (?)
(a DMARD)
on immune system, combo
Antioxidant activity Also used for malaria
Doses needed for RA are much lower
than cancer use so side effects
Slows appearance of new
minimal, not like those assoc w/ cancer
Methotrexate Immunosuppressant (inhibits erosions in joints on radiographs Rheumatoid arthritis (or
Given 1X per week use.
(a DMARD) DHFR used to make folate) psoriatic)
Mucosal ulceration, nausea
Use alone or in combo
Cytopenias, cirrhosis, acute pneumonia-
like syndrome if chronic use
Immune modulator Chimeric Fever/chills/pruritus, urticaria
Cant use alone do combo Rheumatoid conditions,
IgGk monoclonal ab (human and Predisposed for infection
w/methotrexate (body will psoriasis (derm and arthritis),
Infliximab murine regions) IV admin, 9.5 day life Lymphoma?
develop anti infliximab ab if not ulcerative colitis, Ankylosing
*Binds human TNFa Leukemia, neutropenia,
in combo) Spondylitis, Crohns
(neutralizes it)* thrombocytopenia, pancytopenia
Robbins Notes:
Chapter 26 Bone/Joints/Soft Tissue Tumors: o Slow growing, stronger

Normal bone physiology: o 4 types: circumferential/concentric/interstitial (in cortex only) and
o Osteoprogenitor cells: undergo cell division, pluripotent, TF a1 stimulates them to make trabecular (makes up long bones)
osteoblasts Noncollagenous proteins from osteoblasts
o Osteoblasts: build bone. Cell receptors for PTH, Vit D, estrogen, growth factors, etc. Life Osteocalcin: unique to bone. Se/sp marker for osteoblast activity.
span = 3 months, then become osteocytes Cell adhesion proteins: osteopontin, fibronectin, thrombospondin
o Osteocytes: communicate via canaliculi. Can detect mechanical forces and induce certain Ca-binding proteins: Osteonectin, bone sialoprotein
signaling paths Mineralization proteins: Osteocalcin
o Osteoclast: bone resorption cells. From same cells that make monocytes/macrophages. Enzymes: Collagenase, alkaline phosphatase
Formation stimulated by IL 1/3/6/11, TNF, GM-CSF, M-CSF, Growth factors: IGF-1, TGF-B, PDGF
Rank RankL binding (blocked by osteoprotegerin OPG) Cytokines: Pg, Il-1/6, RANKL
Mature osteoclasts = form resorption pits (Howship lacunae) o Bone growth/development
As osteoclasts break down bone, the acidic environment releases growth factors to Long bones:
stimulate osteoblasts!
Homeobox genes: encodes TF for differentiation
Remodelling happens all the time (10% of skeleton replaced each yr)
Wk 8: Endochondral ossification starts, periosteal region is building cortex
Peak bone mass at 30s, then declines
(primary area of ostification)
o Bone proteins:
Chondrocytes remain at the physis (growth plate) regulated by Indian
Type 1 collagen: 90% of organic bone wt
hedgehog gene and PTHRH
Woven bone in fetal skeleton, growth plates.
Primary spongiosa: cartilage core, bone layer around it
o Quickly produced, resists forces from all directions equally.
o Presence in adult = pathological state (like rapid repair from a fracture, Clavicles, parts of the cranium:
around infection, makes up a tumor) Intramembranous formation osteoblasts only make the bone (bone deposited on
Lamellar bone pre-existing surface appositional growth)

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Musculoskeletal Domain Overview

Condition Diagnose It Pathophysiology Pathology Clinical Course Genetics/Epi Treatment

Rimmed vacuoles, amyloid-like

Disorders of the NMJ

Autoab against Ach receptors (Type II

Death by 20 from diaphragm

NOT the same as Give biphosphonates to prevent

most frequent cause

Boys 11-15 yrs of

Ewings sarcoma Osteosarcoma

Targets pelvis, skull (enlarged), femur

Complications: Secondary Sjogrens; Swelling leading to pannus.

Lab: Calcium Frequently asx, but can

Low back pain

fracture through the epiphyseal growth

observation, brace (TLSO,

Screening by PE should begin at birth; a

Splint, cast duration depends on extent of injury

NSAIDs: relieve underlying

Hereditary/ History: suggested by progressive Physical exam: Muscle

Supraspinatus (helps deltoid abduct arm) suprascapular n (C5/6)

Glenohumeral joint from insidious,

Susceptible to injury because it is an

Superior labrum tear anterior to posterior tend to fix laproscopically

pain, weakness, circulatory changes

Thoracic outlet compression of nerves/vasculature in the

Median n: Anterior interosseous nerve

Tx: splint, NSAIDs, corticone,

Compression of median n at the wrist

Tenosynovitis (inflammation of the fluid

finger, hand, wrist, distal

cyst in the back of the knee.

LisFrancs between 1st and 2nd metatarsal. 2nd

Wear tight shoes, whatever end up

Phosphate: failure to excrete phosphate secondary hyperparathyroidism

Ricketts: children have deranged bone growth, producing skeletal deformities

Chapter 26 Bone/Joints/Soft Tissue Tumors: o Slow growing, stronger

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