musculoskeletal charts

8/12/2019 Musculoskeletal Charts

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Musculoskeletal DomainOverviewCondition Diagnose It Pathophysiology Pathology Clinical Course Genetics/Epi Treatment

Muscle

physiology

Review

(lecture)

The motor unit made up of: Lower motor neuron (Cell body + Axon) + NMJ + Skeletal muscle innervated by motor neuron

Peripheral nervestructure:o Epineuriumsurrounds many fascicles

Fascicles: Contain Axons (Unmyelinated, Myelinated), Myelin made by Schwann Cells

Endoneurium= CT around axons Surrounded by Perineurium

o Fiber diameter/numbernormally have a bimodal population in terms of diameter of fibers. This bimodal distributionis disrupted in peripheral nerve diseaseo Skeletal Muscle: Mm fibers are multinucleated syncytiumnuclei are at periphery mostly. Reserve cells at

periphery regrow skeletal mm when damaged (less of this in cardiac mm)

o Types of skeletal mm: Type 1: Red, slow twitch, sustained action, high in oxidative enzymes, (aerobic), many mitochondria, abundant

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 pHType 1 dark, Type 2 light

A little higher: can distinguish Type 2B from 2A (type 2B most vulnerable to disuse)

High pHType 1 light, Type 2 darko Pathology: Atrophy, necrosis, regeneration, hypertrophy, denervation, fibrofatty replacement

Spinal

muscular

atrophy

SMA 1Acute infantile (Wednig-Hoffman)floppy baby sx

SMA 2Chronic infantile

SMA 3Kugelberg-welander

Chromosome 5 (SMN gene in 98%). Contiguous NAIP gene associated w/severephenotype

Segmental

demyelination

Axon intact, often begins

at nodes of Ranvier

Short internodes, thinly myelinated axonsSpinal roots involved

No denervation atrophy, possible disuse atrophyOnion bulbswith chronic, repeated episodes of de/remyelination

Seen with HMSN (Hereditary Motor Sensory Neuropathy =Charcot MarieTooth), CIDP(Chronic Inflammatory Demyelinating Polyneuropathy)

Ex: Guillain-Barre, CIDP, HMSN (Charcot-Marie-Tooth)

Axonal

degeneration

Destruction of axon plusmyelin sheath

Wallerian degenerationaxonal degeneration distal to axotomy

Sproutingan attempt to establish connection with distal stump. If established, regrowth at 1-2 mm/day.Traumatic neuroma mass lesion can form, can be painful.Neurogenic atrophyof skeletal mm if motor nerve

Chromatolysis(nissl substance pushed to periphery) in motor neuron cell body with axotomy

Ex: Toxic diseases (organic solvents,organophosphates, heavy metals,vascular disease)

Guillain-Barre Polyradiculoneuropathy Immune-mediated, likely initiated by infectionChronic inflammation, segmental

demyelination

Ascending paralysis, slowed nerve

conduction velocity

Campylobacter jejuni is most

common implicated organismChronic

Inflammatory

Demyelinating

Polyrad.

PolyradiculoneuropathyLab = NCV and CSF changes like GBS (slow nn

conduction, cytoalbuminologic dissociation).

Symmetrical proximal and distalweakness. Chronic inflammation, onion

bulbs with repeated attacks.

Clinical presentation resembles Guillain Barre, but less acute/longer sx duration,less frequent recovery,

Relapses/remission in about .

HMSN-1

(Charcot-

Marie-Tooth):

Polyradiculoneuropathy

Peripheral myelin protein 22 (PMP-22) mutations (usually 17p11.2 duplication) account for

90%. Function of protein is unknown. 20% have significant disability, 20% asx.Others have HMSN1b or X-linked forms (connexin 32).

Hypertrophic nerves, inverted

champagne bottle legs

Diabetic

NeuropathyPolyradiculoneuropathy

Axonopathy, demyelination, or both. CSF protein

often elevated.

Symmetrical distal polyneuropathy (stocking/glove), autonomic neuropathy (orthostasis, impotence, GI motility problems),

mono neuropathy or mononeuropathy multiplex (motor or sensory, LS plexus, femoral nerve have prominent atrophy).


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Condition Diagnose It Pathophysiology Pathology Clinical Course Genetics/Epi Treatment

Skeletal

Muscle

Plasticity in

Health and

Disease

5 basics things to know:

o Muscles are controlled by nerves Skeletal mm cells are run by n eurons:

Motor unit = 1 neuron + many mm cells

1 to 1 AP transmission at neuron-muscle synapse (NMJ = endplate) Skeletal mm APs:

Ionic basis: as in motor neurondepolarization due to fast voltage-gated Na+channel, repolarization due to fast voltage-gated K+ and Cl- channel

Conduction velocity along fiber very fast (~5 m/s large diameter)

Relatively long spike duration and delayed repolarization due to t tubule system

Time course of AP, Ca, and force

AP: 1-2 ms

Ca: peak 5-10 ms

Force: peak 20-60 ms

Ca transient normally big enough for full activation in a single twitch

Force rise time and peak twitch force depend on: Vmax (internal shortening tostretch 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)

Isometricno shortening allowed

Isotonicshortening with constant weight Skeletal mm force is controlled by CNS, largely by variations in motor unit recruitment,

motor unit firing rate NOT by varying cytoplasmic calcium. Skeletal mm cells should

just do what they are told!o Muscles are strong

Force*length = constantthink physicsmm 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 biochemistrythe slower you get, the moreefficient 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 massexisting fibers and new fibers may develop (sa tellite

cells), Ca handling and metabolism altered activity or loading causes massmyofiber dimensions

o Altering ATP homeostasis Results in Phenotype Restructuringo Changes in pattern of activity alter phenotype = mechanical + metabolico Changes in metabolism with same activity alters phenotypeo Potential sites of action:

Direct modulation of genome expression by energy metabolism OR Operates at physiologic level to alter common signal pathway

o Calcium homeostasis modulates function and phenotype and is sensitive to cellular energeticstatus (ADP, ATP, etC)

o Physiologic signals: Calcium cycling, Energy charge, REDOX, Mechanical straino Loading is important for homeostatic control of mass:o mTORinvolved in hypertrophycan modulate by lifting

o Ubiquitinlinked to atrophyo Atrophy: Happens naturally (bedrest), antigravity, lack of use o Loss of Ca and ATP Free Energy homeostasis results in disease pathologyo MM damage: Appears brighter in MR (up to 4 days later)o Satellite cells: Add mm mass in loading and injury


3/27


Myopathies

(Inflammatory)Neurogenic atrophy= fiber atrophy, fiber type grouping, groupedatrophy, absence of inflammation.

Inflammatory myopathy= lymphocytic infiltrates, fiber degenerationand necrosis (pale pink), fiber regeneration bluish w/large vesicularnucleus, nucleolis

Can get trichinosis, bacterial infections of fascia/skeletalmm (but not focusing on this for the domain)

PolymyositisEMG = purely myopathy

CPK = high (up to 50X)

Endomyseal T cellsCD8 infiltrateslead to necrosis, followed by

regeneration

Myopathic weakness

Women 40-60

Risk of malignant

neoplasms (esp lung

cancer)

Dermato-

myositis

EMG = purely myopathy

CPK = high (up to 10-50X)

Perivascular/perifascicular infiltrates,

perifascicular atrophyCD4 and B-

cell mediated.

Myopathic weaknessRash/calcinosisis present

Heliotrope eyelids

Women 40-60

Risk of malignantneoplasms (esp lung

cancer)

Inclusion body

myositis

EMG = myopathy +/-

neurogenic componentCPK = high (not as highas PMS)

Rimmed vacuoles, amyloid-like(nonbranching, + w/Congo red),

filamentous inclusions (w/Amyloidbeta, phosphorylated tao, ubiquitin,prion protein)

Myopathic weakness, but

sometimes distal weakness isprominent

Disorders of the NMJ

Myasthenia

Gravis

Tensilon (edrophoniumtest)Inhibits AchE (dAch reverses mm

weakness)

Autoab against Ach receptors (Type II

HS rxn)Ab inhibit/destroy receptors

Ab synthesized in thymus85% have

thymic hyperplasia w/germinal follicles

Fatigue without soreness or burning

Ptosis (most common initialfinding).

Mm weakness improves

w/rest

Dysphagia for solids/lipids (in

striated mm of upperesophagus)

Men in 60s/70sWomen in 20s/30s

d risk of developingthymoma (15%)

Lambert-

Eaton

Syndome

No reversal of sx withAchE inhibitors alone

Auto ab to presynaptic Ca channels Proximal mm weaknessSymptoms improve withmuscle use!

Associated withparaneoplasticdiseases (small celllung cancer)


4/27


Muscular

Dystrophies

Wide variation in fiberdiameter,

excessive ENDOMYSIAL FIBROSIS fiber degeneration and regeneration,

Duchennes

Muscular

Dystrophy

Lab: Serum CK 1st10yrs, declines as muscle

degenerates

Western blotDuchenes - NOdystrophin, Becker -

thinned bands.

Dystrophin deficiency(normally

anchors actin to membrane glycoproteinand attached to sarcoglycansI/M band

associated, possible role in maintainingmyocyte membrane integrityw/contraction). Dystrophin deletions,

point mutations w/frameshift.

Progressive degeneration of Type I/II

fibers causes infiltration of muscle tissue

by fat (

Pseudohypertrophy of calf)Affects PROXIMAL mmand calves

Type 1 AND 2 fibers involvedVaried fiber size (small and enlarged

fibers with fiber splitting);internalized nuclei, Degeneration,

necrosis/phagocytosis of mm fibers,mm fiber regeneration. Proliferation ofendomyseal CT. Mm eventually

almost totally replaced by fatENDOMYSIAL FIBROSISMay also have pathological changes in

heart (HF, arrhthmias can develop)

CENTRAL NUCLEI

No CNS problems established, but

cognitive component of disease

Normal at birth, early

milestones met

Walking often delayed, pt is

clumsy/unable to keep up

with peers

Sx around 2-5 yrs:

Weakness/wasting of pelvicmuscles is 1stChild places

hands on knees to help stand,Gowers sign (tripod),

Waddling gaitWheelchair by 12

Death by 20 from diaphragmmm failure (pulmonary

infection, cardiacdecompensation, resp insuff)

X-linked recessive

Xp21, but 1/3 arenew mutations

Most severe, most

common type(1:5,000)

Female carriers haved serum CK

Myostatin TGFB protein inhibitsmm growthloss causes

hyperplasia during developmentand hypertrophy throughout lifeWONT fix the problem making

the mm stronger will make them ripapart faster. IGF-1 influences mmmass too.

Becker

Muscular

Dystrophy

Dystrophin is defective(Normallydystrophin transfers force of contraction

to CT)

Sx not as extreme as DuchennesX-linkedXp211:20,000

(Other forms of MD AD or AR,different presentations)

Myotonic

Dystrophy

d serum CK

Above = spontaneousmm discharge w/needleinsertion

Can elicit myotonia by

percussing thenar

eminence

Myotonia= sustained involuntarycontraction of a group of mm (especially

subsequent to voluntary contraction orirritation)

Myotonic dystrophy = defective splicingof muscle C1C1 channel mRNA caused

by nuclear accumulation of CUG orCCUG repeat RNA (most commonhuman dystrophy)

Dystrophila myotonia protein kinasemRNA affected

Selective atrophy of Type I fibers (ear lyon)

Variation in fiber sized internal nuclei (in chains)Ring fiber: sub-sarcolemmal band of

cytoplasm, has myofibrils aroundlongitudinally oriented fibrils.Sarcoplasmic mass may come out from

ring (stain blue in H&E)

Facial weakness, myotonia

(worse w/maternalinheritance), frontal balding,cateracts, testicular atrophy,

cardiac involvement

Pt complains of difficultyreleasing grip,

ADmost commonadult musculardystrophy (TNT

repeat disorder)

can haveanticipation.


5/27


Back Pain

(mechanical)

Physical exam:Straight leg raising (80%

se, 40% sp), Contralateralleg raising (90% sp, 25%se), one on its own not

that great but put them

together and they arehelpful.

Sed rate and CBC- labs

for suspected tumor

X-rays: notrecommended in 1st4weeks if no red flags

Reflexes:DTR/MSR/myotatic reflexo 0=absent,o 1=trace, w/

reinforcement,o 2= lower of

normal,o 3=upper of normal,o 4=abnormally brisk,

Note clonus separately

Non-inflammatory rheumatoid pain

Possible causes: herniated disc, discdisease, spondylolisthesis,

spondylolysis, facet sx, spinal

instability, radiculopathy, fibromyalgia,myofacial pain sx, somatic dysfunction,

sacroiliac joint pain, CT disease,arachnoiditis, fractures, spinal stenosis,

tumor, infection, osteoporosis, lumbar

strain, visceral/operant/central pain,Pagets, Scheurmanns, Job satisfaction,

psychogenic pain, malingering, short legsx, unlevel sacral base

Boeing study:Psychological, Work

satisfaction, and history of low backpain were most predictive

Acute low back problems in adults:activity intolerance due to back relatedsymptoms, over age 18, lasts < 3 mo.

Evidence - some care is inappropriatedisability despite tx. Spinal fusion not

recommended,

Initial evaluation: look for red flagso Cancer (age>50, previous cancer,

wt loss, >1 month pain w/tx, no

relief w/bed rest, fever)o Osteomyelitis(IV drugs, UTI, skin

infection, fever, immunocomp),Sciatica

o Cauda equina syndrome(bladder/bowel, saddle anesthesianumb by butt, limb mm weakness).

o Spinal stenosis:pseudoclodicationpainin legs while walkingoften relieved by leaning

forward or sittingnot

due to peripheral vasculardisease. Dont donsiderin 1st3 months. Relief

with leaning forward(shopping cart sign),age>50

o Ankylosing spondylitis:onset 3 monthso Sciatica: if activity

restrictions >1 month orclear clinical;

electrophyscompromise,correlating imaging can

refer to surgery.

Assess non-spinal

causes for LBPrectal, UTI

Low back- 60-90%lifetime incidence,

5% annual incidence,5-25% incidence

lower back pain,40% get sciatica50% recover in 1month, people get

recurrence

Chronic(10% - get80% of cost)

Questions to guide tx:What activities cant you do?

What tx have you tried?

What do you do to stay in shape?What medications have you tried?What want vs expect from tx?

NSAIDs, Tylenol, Benzodiazepams(same as NSAIDs except drowsy),

Not helpful: Steroids, Bed rest,

Facet injections, epidurals withoutradiculopathy, opioids (and if used,only short-term)


6/27


Osteoporosis

X-ray:Not reliably detecteduntil ~35% loss

Bone Density Test: DXA scan

(dual-energy absorp typicallycheck every 2 yrs), quant CT(less commonly used)

)1()(

DdultMeanBMSDofYoungAMeanBMDYoungAdultPtBMDTscore

# of standard deviations frommean compared to young adult.

Normal= -1 or aboveOsteopenia= -1 to -2.5Osteoporosis: -2.5 or below

Severe Osteoporosis= -2.5 or

below with fragility fractureUse lowest to dxforearm, hip,femoral neck, spine

)2/1(

)(

cmDingchedMeanBMSDofAgeMat

BMDAgematchedPtBMDZscore

low Z score (2

SD below mean

Serology: blood

Ca/PO4/alkaline phosphatase

level NOT diagnostic tend touse in pt


7/27


Osteogenesis

Imperfecta

(Brittle bone

disease)

Pathological fractures atbirth

Blue sclera (reflection ofunderlying choroidal

veins), deafness

Defective synthesis of Type 1 collagen

Too little boneosteoporosis

w/cortical thinning, attenuatedtrabeculae, skeletal fragility

Type 1:acquired mutation

lots of fractures early on (lessinto puberty), blue sclerae,hearing loss, dental

imperfections

AD inheritance

Type 2: lethal form,

fatal in utero/inneonatal period.

Incidence = 1:10,000

Exercise, pain medicine, physicaltherapy, wheelchairs, braces,surgery.

May be confused with child abuse

Osteomalacia,

rickets

Disorganized bone

remodeling .Contours not affected,

but bone is weak

(especially vertebralbodies, femoral necks).

Adult Vitamin D deficiency causes less

intestinal absorption of Ca/PO4, PTHwill stimulate loss of Ca from bone torestore blood levels.

In kids, it leads to rickets.

Histological: thickened matrix withnormal trabeculae.

Eventually, difficult to differentiatefrom other osteopenias.

NOT the same as

osteoporosis, becauseosteoporosis is caused by

production of osteoid, while

osteomalacia is poorformation of bone inremodeling.

Give biphosphonates to prevent

bone loss

Renal failurecan lead to

osteomalacia ( cant convert Vit Dto active form in kidneys to absorbnew Ca)

Bone

physiology

Osseous function:Strength, cushioning,

mobility, endocrine,

Ca/Vit D dependentDiaphyseal (cortical)=forstability

Metaphyseal(cancellous) =cushioning

Types of bone:

o Lamellar bone:fibers in parallellayers. Structure(see picture below)

Trabeculae indirection of stress

o Woven bone(non-lamellar)randomlyoriented collagen.

Weaker. Usuallyremodeled tolamellar. Seen at

sites of fracturehealing, attachment,

pathology

Bone composition:

o Cells:o Osteocytes:in lacunae, Reg bone

metab (response to stress/strain),o Canaliculi: canals, contain

osteocyte cell processes,

preosteoblast-osteocyteconnection (probably for responseto mechanical, chemical factors)

o Osteoblasts:from mesenchymalstem cells. Line surface of bone,

produce osteoid.o Osteoclasts: Get rid of bone,

from hematopoietic scs,

multinucleated, in Howshipslacunae. PTH stimulatesreceptors on osteoblasts to

activate osteoclastic resorption.o Extracellular matrix:

o Organic (35): 90% type Icollagen, also osteocalcin,osteonectin, proteoglycans,

glycosaminoglycans, lipids(ground substance)

Inorganic(65): hydroxyapetite

Mechanisms of bone formation:o Cutting cones:to remodel bone.

Osteoclasts at front remove,

Osteoblasts behind lay down newo Intramembranous (periosteal)

formation: long bone grows in

width. Osteoblasts lay downseams of osteoid. Doesntinvolvecartilage precursors.

o Endochondral formation:longbone grows in lengthosteoblasts

line a cartilage precursor.Chondrocytes hypertrophy/calcify(O2). Vascular invasion of

cartilage ossification (O2triggers calcification)

Growth Factors:TGF (transforming growth factor):precursors (osteoblasts, osteoclasts,chondrocytes); endochondral &intramembranous formation ;

synthesis of cartilage proteoglycans,type II collagen; collagen synthesis

by osteoblasts.

BMP (Bone Morphogenetic

proteins):cell differentiation; BMP-3(osteogenin) mesenchymal

differentiation bone; endochondrial ossification(BMP 2/7 in segmental

defects); Regulates ECMproduction (BMP 1 cleaves

carboxy termini ofprocollagens I-III)

Fibroblast Growth Factors:2 Forms: Acidic (FGF-1) &Basic (FGF-2)

chondrocytes, osteoblasts,

callus formation,FGF-2 angiogenesis

Platelet-derived

growth factor: bone cell growth (

Type 1 collagensynthesis by # ofosteoblasts). PDGF-BB bone resorption

by # of osteoclasts

Insulin-like Growth

factor: IGF I

production in liver by GH. collagen &matrix synthesis,

osteoblastreplication, bone

collagen degradation.

Cytokines (IL1/4/6/11)

resorption (IL1!) IL1/6 byestrogen (assoc w/ post-menopausal resorption?)

PG: osteoblastic formation, osteoclasts.

LT: osteoblast bone formation,

capacity of osteoclasts to formresorption pits.

Estrogen: fracture healing,modulates release of IL-1 inhibitor

Thyroid hormones: T3/T4 osteoclastic bone resorption

Glucocorticoids: Ca absorptionfrom gut (causes PTH more

osteoclast bone resorption)

CK form resorb

IL-1 + +++

TNFa + +++

TNFb + +++

TGFa -- +++

TGFb ++ ++

PDGF ++ ++

IGF-1 +++ 0

IGF-2 +++ 0FGF +++ 0


8/27


Fractures

(healing)

Classification:

Complete vs incomplete

Closed (simple): skin

tissue intactCompound: skin notintact

Comminuted: bonesplintered

Displaced:ends of boneat not alignedPathologic: break in a

bone already altered bydiseaseStress fracture: slowly

developing following

physical activity withnew repetitive loads (bootcamp)

Harris lines(Pediatricpts - look like growth

ring on a tree happenin stress from temporary

slowdown of normallongitudinal growth). 6 -10 weeks after fracture.

Direct vs indirect healingDirect:no motion at fracture site

(doesnt form callus). Cutting cone is

formed, crosses fracture site.Osteoblasts lay down lamellar bone

behind the osteoclasts (form secondary

osteon). Slow process ~18 months.Direct contact allows healing gap


9/27


Osteomyelitis

+ blood cultures,

Have to biopsy/boneculture to id pathogen

Clinical findings

Fever, bone pain,elevated ESR

Pyogenic: Bacterial infection of a bone,

from hematogenous spread, extensionfrom another site, or direct implantationo 90% due to Staph Aureus

(receptors for collagen)

o UG infection or IV drug user: E coli,Pseudomonas, Klebsiella

o Neonates: Strep pyogenes, H fluo Sickle cell: Salmonella paratyphio But 50% cant find org!o Pseudomonasoften from puncture

of foot through rubber footwear.Tuberculous form: hematogenous

spread from lung (goes to vertebraPotts disease, less often hip/knee)1-3% get this. Multifocal in

immunocompromised.

Neutrophils enzymatically destroybone (dead bone = sequestra)

necrosis in 48 hrs.

Chronic disease: reactive boneformation in periosteum (involucrum)

Kids: subperiosteal abscesses fromspread in Haversion canals

Draining tracts to skin surface

(danger of squamous cell carcinomadeveloping at orifice of sinus tract)

Where (depends on where

blood supply is):

Before growth plates close:metaphysic/epiphysis

After growth plates close:

more widespread

Brodie abscess: small,

intraosseousinvolvescortex, walled off by reactive

bone

Sclerosing osteomyelitis of

Garrein jaw, new boneformation

Complications:pathologic fracture,

secondary

amyloidosis,endocarditis, sepsis,sarcoma

Metaphysis is mostcommon site (with

hematogenousspread)

Antibiotics and surgical drainage

5-25% wont resolve (can go

chronic if dx delayed, extensivenecrosis, short tx, poor debridementor immunocompromised)

Myositis

ossificans

Metaplastic bone present

Starts in musculature ofproximal extremities

Radiograph: Soft tissue

fullness radiodensitiesat the periphery (3 wks) filled in radiodensity

Have to differentiatefrom extraskeletal

osteosarcoma (in elderly,cells are malignant,

tumor doesnt havezonation)

Lesion 3-6 cm across, well-delineated

Soft/glistening center; firm/grittyperiphery

Early: cellular lesion withplum/long fibroblast-like cells

(simulates nodular fasciitis)

Morphologic zonation (within 3weeks)merges with adjacentintermediate zone of osteoblasts,

woven bone deposited. Cancellousbone appearance on the outside.Skeletal mm fibers/giant cellsoften trapped in the margins.

Ossification of all: intertrabecularspaces are filled with bone marrow

Metaplastic bone grows out in themuscle

Depends on stage ofdevelopment:

EarlySwollen/painful

LaterCircumscribed,firm

Even laterpainless,hard, well-demarcatedmass

Athletic adolescents,young adultsfollows trauma in

>50% of cases

Take it out! Usually solves theproblem.

Severs

calcaneal apophysitis

inflammation of the growth plate of the

calcaneus

most frequent cause

of heel pain inchildren 8-13 yrs(seen during periods

of active bonegrowth), especially ifmoderately obese

Self-limitingwill disappear afterbone growth finalized and growth

plate closes (age 15-16)

Osgood-

Schlatter

Radiograph not needed todiagnose, but confirm it

and rule out other causesof knee pain

Inflammation of proximal tibialapophysis at insertion of patellar tendon.

Stress on patellar tendon with repeat

quadriceps contraction can causeavulsion fractures andmicrotrauma/inflammation (causes lump

on knees)

Knobby appearing knees

No effect on bone growth

Boys 11-15 yrs of

age

Usually resolves with skeletalmaturity (when tibial tubercle fusesto the remainder of the tibia)

Ice after exercise, NSAIDs

Syndig-Larson-Johansen syndromeinvolves the upper part of the

tendon, where it attaches to thepatella!


10/27


Bone tumors

(basic epi and

characteristics

only)

Location of tumor mostkey diagnostically

Benign ones: - more common thanmalignant, younger people

Metastasismost common bonemalignancy (mostly from breast CA)

Malignant ones: - tend to beletal, in elderly

Pagets Disease

of the Bone

(Osteitis

Deformans)

Dx: IncidentalradiographicNOTusually in ribs, fibula,

small hand & feet bones

Cause unknown (virus -paramyxovirus?)

Or abnormal osteoclasts(hyperresponsive to vit D, RANKL)

Overall, you gain bone mass, but itsdisordered in structure and structurally

unsound.

1) Osteoclastic resorption of bone(shaggy-appearing lytic lesions)2) Osteoblastic bone formation (d

serum alkaline phosphatase, Normal

Ca/PO4, thick/weak mosaic boneformed) mixed w/osteoclast activity

3) Osteosclerotic phase (quiescent)

* Mosaic pattern of lamellar bone *

Targets pelvis, skull (enlarged), femur

Risk of osteogenic sarcomas, risk of high-output HF

(from AV connections in vascular bone)

Generally asxPain: most common problem, in the affected bone.Microfractures/overgrowth (compressing nerve roots)

Leontiasis ossea: craniofacial growth , difficult to

hold head erect -> platybasia (flattened skull base)Bowing of femor/tibia causes secondary osteoarthritis

Chalkstick-type fractures in long bones of lower

extremitiesCompression fractures of spineSkin over pagetic bone is warm (hypervascularization)

Non-malignant: Giant cell reparative granulomas, giant

cell tumor, extraosseous masses of hematopoiesis

My hat size d!

Elderly white men of Europe,Australia, US, 5-11% of population

affected in countries where it exists

Genetic link to 18q

Note: Parathyroid adenoma orhyperparathyroidismwould be

different you get brown tumors,

which are areas of d bone mass.

Suppress sx w/

calcitonin/biphosphates

Giant Cell:Female, 20-40Cells look like osteoclasts

Soap bubble, Spindle-shaped multi-nucleated cellsEpiphysis (distal femur/prox tibia)

Osteoid osteomaMale, 10-20Cortex of proximal femur, Radiolucent focus

(nidus) surrounded by sclerotic bone

Enchondroma

20-50Medullary, small tubular bonesHands/feet

Multiple or solitary,Risk of chondrosarcoma

ChondrosarcomaMale, 30-60Pelvic bones, proximal femurMushroom shape

Osteochondroma (exostosis)Male,


11/27


Rheumatologic Disorders

SjogrensShermers test: evaluate

for dry eyes

Exocrinopathyproblem in T-cellregulation, B cell expansion

(polyclonal), inflammation inEXOCRINE glands

Lacrimal glands(keratoconjunctivitis), Minorsalivary glands (sicca),

Parotid gland (dry mouth,dental caries, parotidis),Pancreas (achlorhydia,

abdominal pain)

Osteoarthritis

*Cartilage*

Lab: Slightly serum

alkaline phosphatase

Radiograph: asymmetricloss of joint space,Eburnation (thickened

endplate resulting inosteophyte formation),subchondral cysts,

intraarticular loose bodies

Noninflammatory joint disease

cracking/narrowing of cartilage leads toreaction in underlying bone

Focal arthritis= 90%. Loading/focaltransarticular stress is main cause of

hip/knee OA.

Generalized osteoarthritis = 10%

(generally genetic association)

Progressive degeneration of articularcartilagetargets wt bearing joints.

Erosion/clefts seen in articular

cartilage

Reactive bone formation at joint

margins(osteophytes)causes

slightly alkaline phosphatase

Subchondral cysts

Bone eventually rubs on bone(producing dense, sclerotic bone)

NO joint ankylosis

Crepetisgrinding in joints

Pain w/passive motion (secondary

synovitis)

Hand involvement!

DIP enlargement

Heberdens nodes PIP enlargement

Bouchards nodes

Vertebral findings:

Degenerative disease w/compressive neuropathies

Most commondisabling joint

disease!

More in women,universal after age 65

Secondary causes:

Obesity, trauma(valgus/varus stressof knee, meniscal or

ACL injury),

ochronosis(alkaptonuriaAR

disease w/deficient

homogentisic acidOxidase,accumulation of

homogentisic acid

which deposits in IVdiscsurine will turn

black when oxidized)

General approach:o Joint protection, stabilization,o Analgesia(NSAIDS, tramadol,

codeine),o Joint-specific(injections

corticosteroids, hyaluronic acid

analogues).

Surgery not that great.

In development: oral

immunomodulators, maybe anti-metaloproteases

Rheumatoid

arthritis

*Synovitis*

Lab: RF,

Research: CCP ab fordiagnostic?

Rice bodiesfloatingfibrogen in synovium

Synovial inflammatory disease:proliferation, erosion into marginal bone

Cartilage: 70% water. Chondrocytes are10% of tissue volume (manufactures,

secretes, maintains matrix componentscollagen, hyaluronic acid, proteoglycan).

Ag driving rheumatoid arthritis isunknownperhaps IgG Fc, CCP, TypeII collagen. Initiating ag might differ

from perpetuating ags.

Complications: Secondary Sjogrens;

rheumatoid nodules, vasculitis,entrapment neuropathy (carpal tunnel),

pulmonary fibrosis, pleuro-pericarditis,

membranous glomerulonephritis. 3-4X

rr of lymphoma (also risk of lungcancermaybe due to

immunosuppressive?), osteoporosis

(generalized inflammation causes IL-1related demineralization, and chronic

disease-related malnutrition),atherosclerosis (3 rr CV mortality dueto acceleration!), ACD

Swelling leading to pannus.

Periarticular osteopenia.Marginal erosion, joint spacenarrowing, malalignment.

Usually doesnt affect DIPs

Most develop

structural damage

early on (as early as4 months to 5 years

into disease)

HLA DR4

Education, OT, PT, NSAIDs,

Prednisone, Synthetic DMARDs(Methotrexate, sulfasalazine,

leflunomide, hydroxychloroquine),Biologic DMARDs tx (againstTNF, IL-1, Tcell, Bcell, IL-6)

Now largely based on physicianpreference

Juvenile RA

Usually rheumatoid

nodules and rheumatoid

factor absent.

Antinuclear ab

seropositivity common

Genetic association w/HLA (DRB1),

infections, abnormal immunoregulation(CD4+ Tcells in joints)

Oligoarticular (=5 joints)

Systemic formmore frequentlysystemic than the adult form. Assoc w/high fever, rash, hepatosplenomegaly,

serositis.

Joint morphology similar toadultstargets

knee/wrist/elbows/ankles.Warm, swollen, often

symmetrical involvement.Complicationspericarditis,myocarditis, pulmonary

fibrosis, glomerulonephritis,uveitis, growth retardation

Begins before age 16and must be present

for at least 6 weeksto make diagnosis

2:1 female (except1:1 systemic)~40,000 in US

1/3 -1/2 have activedisease after 10 yrs


12/27


Rheumatologic Disorders

Gout

*Crystal*

Lab: Hyperuricemia,joint aspiration

(arthrocentesis)confirmatoryMSUcrystals w/NEGATIVE

biorefringencecrystals

are YELLOW whenparallel to slow ray, bluewhen no longer parallel.

Primary gout (90%):underexcretion of

uric acid in kidneys (lead poisoning,alcoholism are secondary causes),enzyme deficiencies are rare (HGPRT)

Secondary gout (10%):Overproduction of uric acid ( cell

turnover, chronic renal disease,

diuretics). Estrogen s tubular excretionof uric acid.

Urates in joint fluid supersaturated,unknown event initiates release ofcrystals into synovial fluid. Leukocyte

chemotaxis, complement, LTB4,Activation of Hageman factor

20% end up dying of renal failure

4 Stages:

1) Asx hyperuricemia(puberty in males,

postmenopause in females)

2) Recurrent acute arthritis:

Podagra: recurrent acutearthritis in big toe50%have as 1st manifestation

Fever, pain, neutrophilicleukocytosis

MSU phagocytosed byPMNs in synovial fluid

3) Intercritical Gout

4) Chronic gout

Tophi: deposits of MSUin soft tissue around

joints. Granulomatousrxn w/multinucleated

giant cellsdestroysubadjacent bone (causeserosive arthritis). White

deposits on helix of ear

Often men >30

Assoc w/urate

nephropathy, renalstones, HT, CAD,Lead poisoning

(interstitial nephritis

interferes w/uric acidexcretion)

10% of US hashyperuricemia, but85

have it

Hereditary formearly

development in life, get severe OAAD (ANKH mutation thatencodes transmembrane inorg

pyrophosphate transport channel)

Tx supportive (no known treatment

to crystal formation)


13/27


Spondylo-

arthropathies:

*Enteritis*

Seronegative (RF neg)

Sacroiliitis w/ or w/outperipheral arthritis

Immune-mediated manifestations, may

be triggered by T-cell response tounknown ags. Inflammatory

peripheral/axial arthritis w/inflammation

of tendinous attachment

See below

Included Syndromes are PEAR:

Psoriatic arthritisEnteropathic arthritisAnkylosing Spondylitis

Reiters Syndrome

Undifferentiated (parts of all) alsoexists

Happens with IBD (Crohns,

ulcerative colitis) in additionto below. Generally due tomolecular mimicry

Oligoarthritis(a few joints

causing arthritis usuallyknee/ankle)

Initiated by

environmentalfactors (priorinfections/exposures)

HLA-B27 link

Male dominant

Need to tx underlying disease.Exercise, adaptive footware.

NSAIDs, Intra-articular steroids,

DMARDs (Disease-modifying anti-rheumatic drugssulfalazine,

methotrexate, anti-TNFa)

Psoriatic

arthritis

Radiology: Erosive jointdiseasepencil in cupdeformity

Similar histologically to RA (but lesssevere, frequent remissions, jointdestruction happens less)

Sausage-shaped DIP joints (finger or

toeDactylitis50%)

Extensive nail pitting

Joint sx have slow onset

(acute in 1/3 of pts)

Sacroiliac/spinal involvement

(20-40%)- Sacroiliitis

Pt age 30-50

10% of psoriasis pts

have this

Ankylosing

Spondylitis

(rheumatoid

spondylitis/Marie-Strumpell

disease)

Low back pain

Bilateral sacroiliitisw/morning stiffness

Eventually involves

vertebral column(bamboo spine -> leads to

forward curvature)

Chronic inflammation of axial joints(especially sacroiliac, apophysial)Chronic synovitis w/ destruction of

articular cartilage, bony ankylosis.Inflammation of tendinoligamentous

insertion sites (they ossify -> producebony outgrowths)

1/3 have peripheral jointinvolvement

Complications: spinefracture, uveitis (blurry

vision), aortitis (w/aorticregurg), amyloidosis

20-30 yr old

Men2-3X > women

90% HLA-B27 +

Reactive

Arthritis

(Reitersyndrome,enteritis-

associatedarthritis)

Radiology: Achilles

tendon periostitis isconfirmatory sign. Noninfectious arthritis of appendicular

skeleton within 1 month of primary

infection localized elsewhere in body.

Perhaps autoimmune reaction initiatedby prior infection.

Follows infection: Chlamydiatrachomatis (#1) or GI infection(Shigella, Salmonella, Yersinia,

Campylobacterall have LPS)

Cant see, cant pee, cant bend the

kneeUrethritis, Arthritis/Achillestendon periostitis, Noninfectious

conjunctivitisbut not all have all 3

Extraarticular involvement:inflammatory balanitis, conjunctivitis,

cardiac conduction abnormalities,aortic regurg.

Waxing/waning arthritis, fasciitis,tendinitis, lumbosacral back pain

Clinical Progression:

Joint stiffness/low backpain early onmostly

ankles, knees, feet(asymmetric pattern)

Synovitis of digitaltendon sheath -> sausagefinger/toe

Ossification oftendoligamentous

insertions -> calcanealspurs/bony outgrowths

Really chronic - can

have spineinvolvement

indistinguishablefrom Ankylosingspondylitis

80% HLA-B27 +

Enthesitis(inflammation in

cartilaginous transition betweentendon and bone)

Suppurative

arthritis

Most common causes = H flu (


14/27


Fibromyalgia

*Amplification

Attachment*

Pain all over

Neck/shoulder/hips

especially a problemPain impairs sleepMigraine headaches

Hyperemesis in pregancy

Symmetric pain, above and below thewaist. 11 of 18 tender points tender to

touch when examined by physician

(occiput, low cervical, trapezius,supraspinatus, second rib, lateralepicondyle, gluteal, greater trochanter,

knee) but no limit to where you willfeel pain

Likely a thalamic problem of pain

amplification. May be accompaniedby depression, migraines, IBS

Some question if this

is causative orsecondary to chronic

disease

Relaxation techniques, improve

sleep disorder, stretching posturalmuscles, aerobic conditioning

NSAIDs, Tramadol, Tricyclicantidepressants, SSRI, Neuronitin,

Lyrica

SLE

*Deposition

Serologic abnormalities (autoantibodies,compliment consumption,

antiphospholipid abs)

C1q/C2/C4 deficiencies, loss ofimmune tolerance to nuclear autoags,

B-cell hyperactivity, T-celldysregulation

Heterogeneous disease:Malar butterfly rash,

mucosal ulceration, alopecia,inflammatory arthritis,serositis (pleural effusion,

pericarditis, ascites), Immunebased cytopenias,glomerulonephritis, cerebritis

(seizure/neuropsychiatric sx),

Predisposed:

90% female,childbearing age,

EBV, exposure toUV light, 8susceptible loci,

Sunscreens, Topical/oral steroids,

hydroxychloroquine (reduce skin

sensitivity), Azathiaprine,mycophenolate, cyclophosphamide

Experimental: Anti-CTLA4, AntiCD20, Anti BlyS, Anti BAFF, B-

cell tolerogan

Systemic

Vasculitis

*Infarction*

Fever, Rash (skininfarction), Inflammatoryarthritis, Mononeuritis

multiplex, multiplecortical infarctions,cellular casts

Ex:o Temporal arteritis,o Takayasus/Giant cell (large

arteries)o Classic polyarteritis

nodosa/Kawasaki (medium

arteries)

o Wegeners granulomatosis,microscopic polyangiitis/Churg-Strauss syndrome (Small arteries)

o Cryoglobulinemia/cutaneousleukocytoclastic vasculitisHenoch-Schonlein purpura (Arterioles)

Fever, Rash

Scleroderma

*Collagen*

Labs: Anticentromere abin 90%, Serum ANA + in

70-90%, Anti-topoisomerase ab+ in15-40%

Crest Syndrome:

Calcification, centromere

abRaynauds phenomenon

Esophageal dysmotility

Sclerodactyly (tapered, claw-like)

Telangiectasis

T-cell mediated release of cytokinescauses excessive production of

collagen that primarily targets the skin,GI tract, lungs, kidneys

Small-vessel endothelial cell damageproduces blood vessel fibrosis and

ischemic injury

Limited: only distal to elbows/knees

Generalized: More serious, whole body

Morphea is a localized form ofscleroderma

Skin: atrophy, tissue

swelling starts in fingers andextends proximally. Lookslike parchment. Extensivedystrophic calcificationin

subcutaneous tissue.Tightened facial features (d

dermis, d epidermis),

ulceration

GI: Dysphagia(Esophagealdysmotilityno peristalsis inlower 2/3 of esophagus

because smooth muscle

replaced by collagen). Smallbowel has loss of villi

(malabsorption) and widemouthed diverticuli (bacterialovergrowth)

Respiratory:Interstitial

pulmonary fibrosis,Pulmonary HT

Renal: Vasculitis ofarterioles and

glomeruliinfarctions,Accelerated

malignant HT

Mostly women of

childbearing age

No overall disease modifying drugyet. Better agents needed for

bowel dysmotility

Renal crisisACE inhibitors

Interstitial lung disease:Cyclophosphamide, Cellcept,

biologics (remicade, Rituxan)

Pulmonary HT (short termbenefit): Coumadin, Bosantin,

Revatio, Ventavis, Remodulin,flolan

Digital ulcers: Ca channelblockers, Viagra, Stellate ganglion

block and palmar sympathectomy

SCFE (slipped

cap femoral

epiphysis)

Klein's Linenormally

disects part of thefemoral head, in SCFE

the line no longer disects

the head

fracture through the epiphyseal growth

plate of the proximal femur

Insidious onset of hip or thigh

pain, painful limp, d motion(IR),Signs: painless limp, knee

pain, d IR of hip

Males 12-15 yrs:

blacks,

endocrinopathies,thyroid

Girls 10-13 yrs

Bilateral in 25%

pin in situ with cannulated screws

do not reduce for fear of disruptionof blood supply causing avascular

necrosis


15/27


Scoliosis Cobb angle:standard

method for assessing thecurve quantitatively

complex lateral and rotationaldeformities of the spine

observation, brace (TLSO,milwaukee), PT (electric musclestimulation), osteopathic,

chiropractic, surgery

Congenital HipDislocation

Screening by PE should begin at birth; a

child who has not begun to walk

by 18 mths should be suspectedSometimes not noticed until a limp or

other abnormal gait is noticed whenthe child starts walking

The buttocks and perineum may be

unusually broad and adductor foldsmay be present on the medial a spects

of the thighs.

PE shows inability to aBductthe thighs to 90 degrees in

flexionOrtolani jerk sign is

pathogmonic for subluxation

In childhood&adolescence, signs

include a femalecontour to thepelvis(both sexeshave a male

Joint

Replacement

Sprains, Other

activity-

related

disorders -Overuse and

injury:

Historycan often determine inciting event acute injury, changesin training pattern or schedule

Physical Examcan find soft tissue swelling, bruising/discoloration,ligament laxity, muscle defects

Encompass:o Sprain (ligament injury)o Strain (other soft tissue injury)o Contusion (bruise)o Fracture (hard tissuesbone or

cartilage)o Stress reactions (ask body to do

something yourenot capable of

doing stress fracture, shin splints

medial tibial stress syndrome)

Most common

musculoskeletal complaints

in younger pts

Support injured body part

Splint, castduration depends on extent of injury

Bony injury4-6 weeks (older pt); 2-4 weeks (younger pt)

Soft tissuemay put walking boot on pt for much longer

(can take longer to heal)

Medications: NSAIDs (relieve inflammation and pain),

Analgesics (pt more comfortable, improve theirfunctionality/mobility)

Physical therapythe earlier pt up and moving, the fastertheir recovery

Inflammatory

etiologies:

Labs:ESR: non-specificelevation indicates an inflammatory processANA- Non-specific (high cross reactivity). Abnormal test must be

correlated w/ elevated ESR

Follow screens w/specific tests (like anti-dsDNA)

History: Usually insidious onset, noinciting incident (activity may make

better or worse). But really, pt will

improve with exercise. Pt often reportuse of OTCs, alternative meds

Exam: Inflammatory signs:soft tissue swelling, erythema,

inflammatory nodules

Ex: Autoimmuneand collagenvascular arthritis,

Osteoarthritis

NSAIDs: relieve underlyinginflammation, resulting in sx relief.

Do not correct underlying problem

Immune modulatorsmay provide

longer sx control, more expensive

Physical therapy

Hereditary/

other etiologies Lab: muscle biopsy, genetic testing

History: suggested by progressive

muscle weakness. Positive family hxsuggests genetic transmission

Physical exam:Muscle

weakness (note symmetry,proximal vs distal

Depends on disease process. Physical therapy often an

important component.

Infectious

etiologies

Labs:CBC (nonspecific), C-reactive protein (non-specific), cultureRadiologic eval:CT/MR may show soft tissue or bony infection.Bone scan localizes at inflamed/remodeling bone. Tagged WBC scan

localizes at site of infection.

History:Insidious or acute onset;

fever/malaise common

Cellulitis, soft tissue abscess,

osteomyelitis

Exam:Local erythema,

tender/fluctuant mass, bonytenderness, open weepingsore (osteomyelitis)

Antibiotics:Start w/broad spectrum, then change to more

specific antibiotic when culture returns. Bone infectionsmay require extended course.

Surgery:Incision and drainage of abscess (have to n ogood blood supply), Debridement of soft tissue infection,

debridement of infected bonefollow with course ofantibiotics


16/27


Non-Operative

Orthopedics

Lecture(Primary Care

Sports Med)

Primary Medical Areas of Concern:

o CV, Respiratory, Illness/Fatigue, Neurological, GI, UG, Menstrual Irregularities, Eating Disorders,Psychological

Annual Screening Exam: Ht, wt, BP, pulse, injury review/rehab review

Cardiac screening: Looking for prevention of sudden deathask about syncope, chest pain/palpitations

during or after exercise. Questions to ask: Sudden death in family member 40 yo), S4 (normal in athletes). Grade 3 murmurs or louder need greater work-up (esp if increasew/valsalva - cardiomyopathy or diastolic murmur-mitral stenosis, aortic regurg)

o Sudden Death: 101F, Chest pain/palpitations, dyspnea, head injury,

collapse/syncope, skin lesions, seizure hx, persistent weakness/paresthesias, severe

allergies, loss of a paired organ, unexplained wt loss, menstrual changeso Return to play is often gray: rest, fluids, sx controlNeurologicalo Concussion (simple vs complex), have to do hx, PE to suggest that they need to stay

from play longer. To return to play following concussion, want to ensure sx free at

rest, with minimal exertion, with light cardio/lifting, with gility drills/heard non-contactworkoutprogress back to practice for tolerance

Osteopathic

Medicine

Overview

DO=Doctor of Osteopathic Medicine

In other countries, osteopathy is often a form of complementary medicine emphasizing holisticapproach to health care using manual medicine (bachelor degree equivalents these a rent licensed

physicians)Founder: Andrew Taylor Still MD (1917)4 principles:1) The body is a unit. 2) The body possesses self-regulatory mechanisms. 3) Structure

and function are reciprocally interrelated. 4) Rational therapy is based on understanding of 1st3

principles.Key terms:

o OPP: Osteopathic Principles and Practiceo OMT:Osteopathic Mnipulative Txo OMM:Osteopathic Manipulative MedicineUses of OMT:Infections, CHF, lymphedema, asthma/COPD exacerbations, chronic b ack/neck pain,

HA, Acute musculoskeletal injuries, post-operative ileus/constipation/diarrhea, arthritis (jointproblems), Pregnancy issues, Newborn issues, Post CABG/CPRSomatic Dysfunction: An impairment or altered function among related components of the body,including skeletal, arthroidal, myofascial structures in addition to related vascular, lymphatic, andneural elements

TART:Tissue texture changes (edema, warmth, redness, hypertrophy, atrophy, rigidity, bogginess,stringiness), Assymetry, Restriction, Tenderness

Barriers to motion:

o Anatomic (the limit of passive motion which if breached causes damage)o Physiologic (the limit of active motion)o Pathologic/Restrictive: functional limit within the anatomic motion which s the physiologic

range

Acute Somatic Dysfunction: Vasocilation, Inflammation, Warm moist skin, d mm tone, edema,bogginess, severe/cutting/sharp painChronic Somatic Function: Cool pale skin, d mm tone, doughy tissue texture, stringiness, fibroticchanges, dull/achy/crawling/itching/burning/gnawing pain

Reflexes: Viscerosomatic-viscerl input that is referred to a corresponding segmental somatic structure.

Somatovisceral-somatic stimuli produce responses in segmentally related visceral structuresDirect techniques: Move tissues/joint into the barrier, or into the restrictionuses force to create

motion into and beyond the restrictive barrier

Indirect techniques: Move tissue/joint to a position of ease, away from the barrier or restrictionallows the bodys inherent neurologic or intrinsic forces to free up the restriction

Osteopathic treatments:o Muscle energy: direct techniquepts activate mm opposite the area of restriction which causes

reciprocal inhibition and relaxation of the mm that are tight,can be used anywhere in body

o

Myofascial release: indirectsoft tissue technique used to stretch and relax muscular and fascialrestrictions, very gentleo Counterstrainindirect, focuses on identifying tender points. Places pt in position of ease

around the tender pt to reduce activity efferent nerves thereby decreasing pain. Goal is to holdfor 90 seconds and reduce pain by 70%, pt must be completely relaxed throughout tx

o Popping and Crackinghigh velocity low amplitude thrust. Mobilization with impulse. Directmoves a dysfunctional segment through its restrictive barrier nd resets itself. To restorephysiologic motion. Precise positioning and set-up is key. (Dont attempt this at home).

Cautions: hypermobile joints, osteoporosis, acute fractures, radicular sx, contractures, ptsw/rheumatoid arthritis. Risks: Permanent neurological damage, vertebral basilr thrombosis,carotid a dissection, death or quadriplegia if disrupt transverse ligment of atlas

o Lymphatic Pump: Maintains fluid balancepurification and cleansing of tissues, defenseagainst toxins/bacteriaviruses, nutrition, sympathetic nervous system constricts lymphaticvessels. OMT cn lymphatic fluid circulation. Lymphatic techniques include rib raising,thoracic inlet, doming diaphragm, pedal pump, liver/splenic pump, Galbraith technique. CI if

Crcinoma, acute fracture in area of tx, abscess/localized infection, bacterial infectionw/temp>102

o Articulatory Techniques: Gentle, direct tx range of motion in restricted joint. Spencertechnique of GH joint (OA, shoulder strain, frozen shoulder), rib raising (s chest wall motion,improves lymphatic return, normalizes sympathetic tone in pneumonia, COPD/asthma exac). CIif acute fractures, acutely inflamed joints (caution in cervical areavertebral aa compression)

o Craniosacralprimary respiratory mechanism. Inherent motility of brain/spinal cord,fluctuation of CSF, movement of intraspinal and intracranial membranes, articular mobility of

cranial bones, involuntary mobility of the sacrum between the ilia. Firm attachments of dura toforamen magnum, C2, C3, S2. Membranes that surround, support CNS are dura, arachnoid, and

pia mater. There is a subtle, pulse-wave like motion of the brain/spinal cord. There are

measurable, inherent movements in these structures with respiration. Goals: balance motionSBS, reduce venous congestion, enhance rate and amplitude of CRI, mobilize and correct

membranous articular restrictions (contraindicationsintracranial hemorrhage or elevated ICP,skull trauma, seizures), Complicationschanges in HR/BP/RR, GI irritability, Tinnitis,Dizziness, HA

Evidence-based medicine: Low back pain, carpal tunnel syndrome, otitis media, post-op pts, COPDexcerbations

Non- Manual medicine (see DO lecture) Type Example Use


17/27

pharmologic

Mnagement of

Musculoskelet

al problems

Herbal/nutritional supplementso Early research lacking (lots of placebo effect, many preps lack purity). Most newer research reveals

minimal utility

o Glucosamine/chondroitin:Building blocks of CTGlucosamine is an amino sugar, distributed incartilate/other CT, Chondroitin is a complex carb, auds in water retention of cartilage. Both arenormally made in the body. not sure how it works since these are both denatured in stomach acid.Use in OA

o DMSO (Dimethyl sulfoxide):industrial solvent. Can be used to aid in transport of other substancesinto soft tissuehas innate antioxidant and anti-inflammatory properties. Studies show pain relief in

OA. FEDA approved only for tx of interstitial cystitis. Know its working because you get a garlic tastein your mouth.

Acupunctureo Balance of yin (cold/slow/passive) and yang (hot/excited/active). Health is a balance, disease is

imbalance. Imbalance leads to blockage of qi (vital energy) along pathways (meridians). Acupuncturepoints are connections between meridians.

o Uses: pain managementinterrupt transmission of painful impulses (decrease pain, increasefunctionality), treat disease (by restoring balance to allow body to h eal)

o Current research: does it work, how? What are the complicationslocal infections, puncture oforgan/blood vessel.

Physical Therapy modalities

o Comprehensive tx plantherapeutic exercise, manual techniques, modalities. Important component oftx for musculoskeletal problems. Adjunct tx for cardiac/pulmonary/developmental disorders

Therapeutic exercise:improves strength, mobility, function. Decreases pain/swelling, home-based (briefinstruction in office, effective after ACL reconstruction), supervised (superior to home-based for low back injury

or OA, may involve home component)

Bracing and orthotics

Closed kinetic chin (bothends are attached)

Leg press, squat Shoulder/knee rehab

Concentric (mmcontracting in an equalfashion all the time)

Flexor phase of biceps curl Increase mm mass andstrength

Core stability Abdominal crunch Relief of low back pain

Eccentric (mm relaxesthrough the exercise)

Extension phase of bicepscurl

Sport-specificstrengthening

Isometric (mm doesnt

shorten at all)

Holding a wt Toning

Isotonic Free-wt lifting conditioning

Open kinetic chain Quad extension Functional improvement inADL

Ultrasound:o High frequency sound waves warm surrounding soft tissueo Usestendon injuries, mm strain/spasmo Cautions with malignant tumors, bone, pacemakers, epiphyseal plateso Phonophoresis: use ultrasound to deliver meds to soft tissue (c s, NSAID, DMSO).

Minimal penetration of meds, possible systemic effects of meds

o Iontophoresis:use electrical current to deliver meds to soft tissueuse for CS,acetic acid (in myositis ossificns). Avoid near metallic implants, wires, or staples

o Electrical stimulation: electrical stimulation generates muscle contractionuse formm spasm or contusion. Electrical current alters sensory input (TENStranscutaneous electrical nerve stimulation) use for neuropathic pain syndromes).

Avoid around pacemakerso Low level laser tx:alters cellular oxidative metabolism. Uses: minor

musculoskeletal pain, OA, RA, carpal tunnel. Avoid in pregnant, malignancy

Evaluation of

Injury

(different

radiological

tests, etc)

Plain X-ray:

Strengths: Bony injury,

Availability, fast, inexpensive,if + imaging workup oftendone. Good for acute fracture,

arthritides, bone lesions

Limitations: Sensitivity,Cant see soft tissues, early

osseous pathology (stressinjuries, mets/myeloma)

1stline screen

Definitivearthritis

Indicativeex w/ACL

CT:

Strengths: fracture detection,

fracture morphology, fracturehealing, osseous fusion,added specificity to MR,

multiplanar and 3D reformats.

Less hardware artifacts(multidetector), bone lesions.Good for bony injury, some

utility for soft tissue.

Limitations: More expensive,

high radiation exposure, softtissue, bone marrow

pathology

MR:.

Strengths: Best forsoft tissue, Boneok, multiplanar, no

radiation

Limitations:Expensive, lessavailable, weight

limitations,claustrophobiaContraindications

(implants,

pacemakers), time

Ultrasound:

Strengths: soft tissues(tendon, ligament, muscle,nerve), no radiation, dynamic,

cheaper than MR

Limitations: Operatordependent, bones (?) and deeptissues (if large pt size),

physician time, referringclinician consultation

An excellent modality in

skilled hands

Bone scan: Indications: Osseous metastases,fractures (traumatic and stress)

Strengths: can help diagnose occult fracturebone remodeling process takes up

pyrophosphates and will be detectable in

areas of remodeling bone. Total body screen,low cost (relative to MR), sensitive,

physiologic (perfusion, osteoblastic activity)

Limitations: Lack of specificity (stressreaction, fracture, arthritis, tumor, infection);

elderly (>72 hrs). Expensive, less available(pyrophosphate degrades over time)

Arthrography: put fluoroscopicguidance or ultrasound guidance to

put contrast into a joint (gives you

better look at joint in question)

Strengths: powerful when

combined w/MRI/CT. Labrum

(shoulder and hip TFC, SL, and LTligaments wrist rotator cuff),chondralosteochondral lesions, post

operative meniscus;shoulder/hipwrist/elbow/ankle/knee

Limitations: invasive, indirectinformation if not combined w/

MRI or CT


18/27


Orthopedics Lectures:

Cervical

HNP:

Herniated disc

Causes nerve compression or irritationCommonly insidious, but can be fromtrauma/injury

Depends on level involvedoC4-5 (C5 nr) = deltoid weakness,

not much numbness, shoulder pain

oC5-6 (C6 nr) = biceps, wristextension, NT along radial aspect

oC6-7 (C7 nr) = triceps, finger ext,nt posterior to middle finger

oC7-T1 (C8 nr) = grip strength, NT

to little finger

Pain, numbness/tingling,weakness, limited motion,radicular

Age 30-50

Tx: rest, cervical collar, traction/pt,

NSAIDs/Steroids, epiduralinjections or Surgery (discectomy,w/ or w/out fusion).

DJD

(Degenerative

Joint Disease)

Stenosis:anything thatcauses narrowing of thecanal or foramen

(arthritis, HNP,dislocationsubluxation,

infection)

Arthritis: Insidious, accident/trauma,disease process. See pain, restrictedmotion, radicular sx, numbness/tingling,

often times insidious onset, pt complainsthey slept wrong, neck pain

Fracture:Traumatic (stable orunstable), Flexion type = 45-75%,extension type = 20-35%, Compression

= 12%

Other:

Cervical radiculopathy,Brachial plexopathycan be

due to infection

Stingerwholehand/arm goes numbdue to hard hit on the

side tends to be a

temporary thing

Shoulder

Impingement

narrowing of thesubacromial space (


19/27


Dislocation

Rarely in superior direction becauserotator cuff would have to be torn firstand so would coracoacromial arch (95%

occur anterior and inferior where there is

least ligamentous reinformcement itmay look completely anterior becausesubscapularis pulls it medially, but it is

also inferior this is important toremember if you are setting it back into

place)

Frequently associated with axillarynerve injury (wraps around humerus

laterally around 1.5-2 inches inferior toacromion). Check sensory component

by checking pinprick sensation overlateral deltoid area

Person will have arm down, be kind ofholding it up to prevent movement

Labral

tear/Instability

Around the glenoid, usually s stability

of ball in socket Tear can lead to other problemsCan put anchor in bone to h elp

stabilize it.

Biceps

tear/instability

Traumatic (throwers, car accident, tennis

players)

SLAP tear

Superior labrum tear anterior to posterior

Susceptible to injury because it is an

area of relatively poor vascularity.Other parts of the labrum often h ealmore easily because the blood supply

delivers a healing capacity to the area

of the tear.

catching sensation, pain withshoulder movements, most

often overhead activities suchas throwing

tend to fix laproscopically

Tenosynovitis inflammation in the tendon Can become calcified

Fracture

Proximal humerusmore common inolder pts,clavicle, glenoid

Thoracic outlet

syndrome

compression of nerves/vasculature in theneck

pain, weakness, circulatory changes

RSD (reflectsympathetic

dystrophy

pain way out of proportion

with what you would expect

Elbow

Arthritis laborerstraumatic or insidious

Instabilityulnarhumeral, radialhead

fracture is monteggia,If large part broken, can fixw/screws

Nerve

Compression:

Median n: Anterior interosseous nerve

(largest branch, passes between 2 headsof pronator teresimpairs pinchability) or Carpal tunnel syndrome (most

common thumb, index,middle fingermost discomfort at night)

Radial n:Posterior interosseous n(between 2 heads of supinatorfunctional involvement only) or Radial

tunnel syndrome

Ulnar:Ulnar tunnel

syndrome (cubital tunnel,between flexor carpi ulnarismm headsd stretch

w/elbow flexion).

Snapping Ulnar

Nerve

(subluxation): 16%of all individuals it

moves


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Hand/Wrist

Ganglion mostly in the wrist (90%)Tendon related (filled with synovial

fluid).

Treat by aspiration (50%recurrence) or surgical excision (5-

10% recurrence)

Carpal tunnel

syndrome

Electrodiagnosis is the

gold standard butsx

generally used

Compression of median n at the wrist

Numbness, weakness, atrophy

of the hand (all fingers but

the pinky)

TYPING DOESNTCAUSE IT

Insidious, sometimeswork-related

Tx: splint, NSAIDs, corticone,surgery (open or endoscopic).

Surgery found to be better than

splinting overall in a studyInjection of steroids better than oral

steroids

Trigger finger

Tenosynovitis (inflammation of the fluidfilled sheathsynoviumthat

surrounds the tendon

Pain, swelling, or sticking of

the finger.Tx: cortisone, surgery to release.

Fractures finger, hand, wrist, distalradius

InstabilitySLAC Wrist

(Scapho-lunate advancedcollapse)

due to either chronic untx scapohoidfracture or scapholunate dissociation

Saturday

Night Palsy

(hinted on test)

Reflexes: Brachioradialis

absent or d, tricepsusually normal

Due to compression of radial nerve

(hand over barstool wake up unable

to move hand)

Strength: weakness in wrist

extension, finger extension(primarily MCP joints);triceps may be partially weak

or normal.

Sensory changes:abnormal on dorsum

of hand

Back (Lumbar)Arthritis Degenerative or insidious.

FractureMost common in lumbar spine

osteoporosis

Knee

ACL

keeps knee fromsubluxing

Positive anterior

drawer signindicatestorn ACL Clipped from lateral side, causes

unhappy triad:MCL, Medial

meniscus, ACL

Abnormal passive abduction indicates

torn MCL

Anterior and

Posterior refer towhere they areattached on the

TIBIA


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22/27

Other Musculoskeletal Disorders from Robbins (not on content list)


Dystotoses

Ex: bone doesntdevelop, fusion of 2adjaent digits

(syndactyly), developextra bones

LOCALIZED developmental anomaliesfrom problems in migration of

mesenchyme cells, condensations form

Defect in nuclear proteins/transcriptionfactorsCraniorachischisis: Spinal

column/skull dont close

HOXD-13 TF forms extradigit between 3rd/4thdigit,

some syndactly

Uncommon

DysplasiasDIFFUSE problem due to mutations inregulators of skeletal genesis

Defect in Hormones/Signal

transduction

Achondro-

plasia

Shortened proximalextremities with normal

trunk, enlarged head

FGFR3 constantly working to suppresscartilage in physis

AD (point mutation

on short arm of Chr4)

Thanatophoric

dwarfism

Shortened limbs, relativemacrocephaly, small

chest cavity, bell-shapedabdomen

Defect in extracellular structural

proteins

Lethal (from respiratory

insufficiency)1/20,000 live births

Type 2/10/11

Collagen

Disease

(collagens in

hyalinecartilage

Early joint destruction Defects in folding/degradation ofmolecules

Mucopolysacc

haridoses

Pt short stature, chestwall abnormal,

malformed bones

Lysosomal storage diseases ( enzymes

to degrade dermatan sulfate, heparinsulfate, keratin sulfate)

Defects in metabolic pathways

Mesenchymal cells (*chondrocytes*)most affectedcause a lot of problems

in hyaline cartilage

Osteopetrosis

(marble bonedisease/Albers-

Schonberg)

Infantile formAR,lethal or causes major

problems with d

hematopoiesis (less

marrow space)Adult form: AD, benign,some anemia.

osteoclast bone resorption causesskeletal sclerosis.

Carbonic anhydrase II deficiency:

Osteoclasts/renal tubule cells need it toacidify the environmentpreventsdigestion of bone.

Morphology: no medullary canal in

bones, long-bone ends are bulbous.Primary spongiosa persists. Woven

bone

Brittle bones (easily fracture) Bone marrow transplant can help

Hyper-

parathyroidis

m

PTH production

Effect of PTH levels: Activatesosteoblasts to release pro-osteoclastsignals

The whole body is affectedcortical bone affected >cancellous bone

Osteitis fibrosa

cystica (von

Recklinghause

n disease)

X-ray pattern along radialaspect of middle

phalanges of

index/middle fingers

Severe/untreated long-term PTH

usually diagnosed early

Primary: autonomous hyperplasia or

tumor (adenoma)

Secondary: caused by prolonged

hypocalcemia statetend to have milder

skeletal abnormalities

Brown tumor: mass of reactive tissue

from microfractures/secondaryhemorrhages/ingrowth of fibrous repairtissue

Peritrabecular fibrosis

bone cell activity

Subperiosteal resorption =>

thinned cortices/lost lamina

dura around teeth

Observe cortical

cutting cones withosteoclasts boringthrough (enlarge

haversianvolkmann

canals)looks likerailroad tracks(dissecting osteitis)

d bone density(osteopenia)

treat the hyperparathyroidism (sx

will regress or disappear!)

Renal Osteo-

dystrophy

skeletal changes withchronic renal disease

Phosphate: failure to excrete phosphate secondary hyperparathyroidismCalcium: failure to convert 25-(OH)D3 to 1,25 (OH)D3 (less Ca absorbed)PTH: less 1,25 (OH)D3 to suppress parathyroid, less degradation/excretion of PTH

Metabolic acidosis: stimulates bone resorption, release of calcium hydroxyapatitefrom matrixAluminum deposition (dialysis solutions contain it) : interferes with calcium

hydroxyapatite depositionosteomalacia results

B-microglobulin in serum with long-term hemodialysiscauses amyloiddeposition in bone!

often a mixed pattern of disease osteoclast resorption (looks like osteitis fibrosa cystica)Delayed matrix mineralization (osteomalacia)

OsteosclerosisGrowth retardationOsteoporosis

-turnover osteodystrophy: bone resorption/formation (but more resorption occurs)-turnover/aplastic disease: little osteoclast/osteoblast activity, sometimes osteomalacia


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Vitamin D

Function: stimulates

intestinal absorption ofCa/PO4, works with PTHto mobilize Ca from

bone, stimulates PTH-dependent reabsorptionof Ca in distal renal

tubules, likely helps

osteoclasts differentiatefrom monocytes

Ricketts: children have deranged bone growth, producing skeletal deformitiesOvergrowth 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 bonesClinical picture: Frontal bossing, Rachitic rosary, pigeon breast deformity, Harrisons groove (diaphragmpulls 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 b lood 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


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26/27

Proteus, E coli, Klebsiella,

StaphCephazolin penetrates bone well

Fluoroquinolones

(Loveofloxacin)

Inhibit replication of bacterial

DNA by interfering w/action ofDNA gyrase and topoisomerase

Bactericidal

Levofloxacin = 3rdgeneration

NeisseriaG- (enterobacteriaceae,

pseudomonas, H flu, Moraxella,

Legionella, Chlamydia,Mycobacteria);Some G+ (newer ones like

levofloxacin!)

Tx for osteomyelitis

Ingesting with antacids (Al, Mg, Zn,

Fe) can interfere w/absorption

Distribute well to all tissues and bodyfluids (bone )Renal excretion

Diarrhea/nausea/vomitingHA/dizziness

Phototoxicity, nephrotoxicCartilage erosion, can cause ruptured

tendons(fluoroquinolones hurt

attachments to your bones)Can serum levels of warfarin, caffeine,

cyclosporine

Biphosphonates(etidronate, risedronate,alendronate,

ibandronate,pamidronate,

tiludronate, zoledronicacid)

osteoclastic bone resorption:o Inhibits osteoclastic proton

pump needed to dissolvehydroxyapatite,

o osteoclasticformation/activation,

o osteoclastic apoptosis,o cholesterol biosynthetic

pathway needed for

osteoclast function

Preferred agent to prevent/treat

postmenopausal osteoporosis

Tx for osteoporosis, Pagets,

bone metastases, hypercalcemia

Oral admin, without food(IV available)

Bind hydroxyapatite in bone (clearedover hrs to yrs)

Renal excretion

Diarrhea, abdominal pain,musculoskeletal pain.

Some cause esophagitis/esophagealulcers

Osteonecrosis of jaw

CalcitoninReduces bone resorption but less

effective than biphosphonates

But RELIEVES PAIN of

osteopathic fractureTx for osteoporosis

Intranasal adminParenteral form rarely used for

osteoporosis

Rhinitis

Pagets pts have resistance (if long use)

TeriparatideRecombinant segment of PTHStimulates bone formation.

spinal bone density, s risk ofvertebral fracture.

Should reserve for pt w/highfracture risk or who cant

tolerate other txs

Tx for osteoporosis Subcutaneous admin

risk of osteosarcoma in rats

Safety/efficacy not evaluated beyond 24months.

Sufasalazine(a DMARD)

PABA analogto occupydihydropteroate synthetase

Rheumatoid arthritis -

early/mild RA in combo w/hydroxychloroquine and

methotrexate

Not absorbed orally or as suppositoryOnset takes 1-3 months

Leukopenia

Hydroxychloroquine

(a DMARD)

May inhibit phospholipase A2

and platelet aggregation,Membrane stabilization, effectson immune system,

Antioxidant activity

Doesnt slow joint damage whenused alone have to use incombo

Rheumatoid arthritisearly/mild RA txcombow/methotrexate & sulfasalazine

Also used for malaria

Renal toxicity (?)

Methotrexate

(a DMARD)Immunosuppressant (inhibits

DHFR used to make folate)

Slows appearance of new

erosions in joints on radiographs

Use alone or in combo

Rheumatoid arthritis (or

psoriatic)Given 1X per week

Doses needed for RA are much lowerthan cancer use so side effects

minimal, not like those assoc w/ canceruse.Mucosal ulceration, nausea

Cytopenias, cirrhosis, acute pneumonia-like syndrome if chronic use

Infliximab

Immune modulatorChimeric

IgGk monoclonal ab (human and

murine regions)*Binds human TNFa(neutralizes it)*

Cant use alone do combow/methotrexate (body will

develop anti infliximab ab if notin combo)

Rheumatoid conditions,

psoriasis (derm and arthritis),

ulcerative colitis, AnkylosingSpondylitis, Crohns

IV admin, 9.5 day life

Fever/chills/pruritus, urticaria

Predisposed for infection

Lymphoma?Leukemia, neutropenia,thrombocytopenia, pancytopenia


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Robbins Notes:

Chapter 26Bone/Joints/Soft Tissue Tumors:

Normal bone physiology:o Osteoprogenitor cells: undergo cell division, pluripotent, TF a1 stimulates them to make

osteoblasts

o Osteoblasts: build bone. Cell receptors for PTH, Vit D, estrogen, growth factors, etc. Lifespan = 3 months, then become osteocytes

o Osteocytes: communicate via canaliculi. Can detect mechanical forces and induce certainsignaling paths

o Osteoclast: bone resorption cells. From same cells that make monocytes/macrophages. Formation stimulated by IL 1/3/6/11, TNF, GM-CSF, M-CSF, RankRankL binding (blocked by osteoprotegerinOPG) Mature osteoclasts = form resorption pits (Howship lacunae) As osteoclasts break down bone, the acidic environment releases growth f actors to

stimulate osteoblasts!

Remodelling happens all the time (10% of skeleton replaced each yr) Peak bone mass at 30s, then declines

o Bone proteins: Type 1 collagen: 90% of organic bone wt

Woven bonein fetal skeleton, growth plates.o Quickly produced, resists forces from all directions equally.o Presence in adult = pathological state (like rapid repair from a fracture,

around infection, makes up a tumor)

Lamellar bone

o Slow growing, strongero 4 types: circumferential/concentric/interstitial (in cortex only) and

trabecular (makes up long bones) Noncollagenous proteins from osteoblasts

Osteocalcin: unique to bone. Se/sp marker for osteoblast activity.

Cell adhesion proteins: osteopontin, fibronectin, thrombospondin

Ca-binding proteins: Osteonectin, bone sialoprotein

Mineralization proteins: Osteocalcin Enzymes: Collagenase, alkaline phosphatase

Growth factors: IGF-1, TGF-B, PDGF

Cytokines: Pg, Il-1/6, RANKLo Bone growth/development

Long bones:

Homeobox genes: encodes TF for differentiation

Wk 8: Endochondral ossification starts, periosteal region is building cortex(primary area of ostification)

Chondrocytes remain at the physis (growth plate) regulated b y Indianhedgehog gene and PTHRH

Primary spongiosa: cartilage core, bone layer around it Clavicles, parts of the cranium:

Intramembranous formationosteoblasts only make the bone (bone deposited onpre-existing surfaceappositional growth)

musculoskeletal charts

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