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Musculoskele Musculoskele tal System tal System

Muscoloskeletal Patho Lecture Final

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Page 1: Muscoloskeletal Patho Lecture Final

MusculoskeletMusculoskeletal Systemal System

Page 2: Muscoloskeletal Patho Lecture Final

MusculoskeletMusculoskeletal Systemal System

A & P ReviewA & P Review

Page 3: Muscoloskeletal Patho Lecture Final

MusclesMuscles

SkeletalSkeletal– VoluntaryVoluntary

SmoothSmooth– Involuntary, internal organsInvoluntary, internal organs

CardiacCardiac– InvoluntaryInvoluntary

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Skeletal MusclesSkeletal Muscles

600 skeletal muscles 600 skeletal muscles

Organized by type of movement:Organized by type of movement:– Flexor: flexing of jointsFlexor: flexing of joints– Extensor: extension of jointExtensor: extension of joint

Page 5: Muscoloskeletal Patho Lecture Final

Skeletal MusclesSkeletal Muscles Muscle FibersMuscle Fibers

– Extend length of muscleExtend length of muscle– Perimysium: binds fibers into fasciculusPerimysium: binds fibers into fasciculus– Epimysium binds fasciculusEpimysium binds fasciculus– Epimysium becomes tendon coming off Epimysium becomes tendon coming off

musclemuscle

Page 6: Muscoloskeletal Patho Lecture Final

The BonesThe Bones

206 bones206 bones Classified by Shape and LocationClassified by Shape and Location

– Long: Humerus, radius, FemurLong: Humerus, radius, Femur– Short: Wrist, ankeShort: Wrist, anke– Flat: Scapula, ribs, skullFlat: Scapula, ribs, skull– Irregular: vertebra and mandibleIrregular: vertebra and mandible– Sesamoid: patellaSesamoid: patella

Page 7: Muscoloskeletal Patho Lecture Final

Skeletal StructuresSkeletal Structures

Epiphysis = endEpiphysis = end Metaphysis = Metaphysis =

widening before widening before the end of the the end of the bonebone

Page 8: Muscoloskeletal Patho Lecture Final

Skeletal StructuresSkeletal Structures

Diaphysis = shaftDiaphysis = shaft– Contains bone Contains bone

marrowmarrowº Red marrow: makes Red marrow: makes

blood cellsblood cellsº Yellow marrow: Yellow marrow:

contains fatcontains fat

Page 9: Muscoloskeletal Patho Lecture Final

Skeletal StructuresSkeletal Structures

PerisosteumPerisosteum– Outer lining Outer lining – Thick, fibrous Thick, fibrous

connective tissueconnective tissue EndosteumEndosteum

– Inner liningInner lining– Contain Osteoblast Contain Osteoblast

producing cellsproducing cells

Page 10: Muscoloskeletal Patho Lecture Final

Bone Tissue CompositionBone Tissue Composition

CellsCells Extracellular MatrixExtracellular Matrix

– Ground substanceGround substance– Protein fibersProtein fibers

Characteristics of the tissue Characteristics of the tissue depend on the extracellular matrixdepend on the extracellular matrix

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Bone CellsBone Cells

OsteoblastsOsteoblasts– lay down the extracellular matrixlay down the extracellular matrix– Results in new bone formationResults in new bone formation

OsteoclastsOsteoclasts– break down the extracellular matrixbreak down the extracellular matrix– Tear down old or excess bone structureTear down old or excess bone structure– ResorptionResorption

Break down of bone to release calcium back into systemic circulationBreak down of bone to release calcium back into systemic circulation

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Bone RemodelingBone Remodeling Osteoblasts and Osteoclasts are formed when Osteoblasts and Osteoclasts are formed when

they are needed to remodel bonethey are needed to remodel bone Osteoclasts remove damaged areas of boneOsteoclasts remove damaged areas of bone Osteoblasts come after them and replace the Osteoblasts come after them and replace the

extracellular matrixextracellular matrix

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Extracellular MatrixExtracellular Matrix Ground substance contains crystals of Ground substance contains crystals of

calcium saltscalcium salts These make the bone rigidThese make the bone rigid They block oxygen and food diffusion, so They block oxygen and food diffusion, so

bone must contain blood vesselsbone must contain blood vessels Types of bone are distinguished by the Types of bone are distinguished by the

pattern the crystals are laid down in:pattern the crystals are laid down in:– Compact bone: laid down in layers like an onionCompact bone: laid down in layers like an onion– Cancellous bone: a lattice of tiny struts of bone, Cancellous bone: a lattice of tiny struts of bone,

like a spongelike a sponge

Page 14: Muscoloskeletal Patho Lecture Final

Bone Tissue CompositionBone Tissue Composition

Outer LayerOuter Layer– Compact bone Compact bone

with Haversian with Haversian CanalsCanals

– Canals contain Canals contain arteriolesarterioles

– Found in Found in DiaphysesDiaphyses

Page 15: Muscoloskeletal Patho Lecture Final

Bone Tissue CompositionBone Tissue Composition

Inner LayerInner Layer– Cancellous Cancellous

(spongy) bone(spongy) bone– Interface to Interface to

form a form a latticeworklatticework

– Red marrow Red marrow fills in spaces fills in spaces of latticework of latticework (trabeculae)(trabeculae)

Page 16: Muscoloskeletal Patho Lecture Final

Cartilage Tissue CompositionCartilage Tissue Composition

Ground substance is a gel Ground substance is a gel containing 65%–80% watercontaining 65%–80% water

Oxygen and food can diffuse Oxygen and food can diffuse through this gelthrough this gel

Therefore, the tissue does not need Therefore, the tissue does not need blood vesselsblood vessels

Page 17: Muscoloskeletal Patho Lecture Final

Cartilage Tissue CompositionCartilage Tissue Composition

Different types of cartilage are Different types of cartilage are distinguished by how many protein distinguished by how many protein fibers are in the extracellular matrixfibers are in the extracellular matrix– Hyaline cartilage: very few fibersHyaline cartilage: very few fibers

Shock cushion – trachea, bronchi, nasal septumShock cushion – trachea, bronchi, nasal septum

– Fibrocartilage: some elastin fibersFibrocartilage: some elastin fibers Provides cushioning – Intervertebral disksProvides cushioning – Intervertebral disks

– Elastic cartilage: many elastin fibersElastic cartilage: many elastin fibers Provides support – auditory canal, epiglottisProvides support – auditory canal, epiglottis

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Tendons and LigamentsTendons and Ligaments

Extracellular matrix is filled with collagen fibersExtracellular matrix is filled with collagen fibers Strong and not elasticStrong and not elastic Tendons connect muscles to boneTendons connect muscles to bone Ligaments connect bones to one anotherLigaments connect bones to one another

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JointsJoints

Union of two or more bonesUnion of two or more bones

Synarthroses: little to no mobilitySynarthroses: little to no mobility– Skull suturesSkull sutures

Amphidiarthrosis: slight movementAmphidiarthrosis: slight movement– VertebraeVertebrae

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Diarthroses JointsDiarthroses Joints

Diarthroses: Diarthroses: highly mobile highly mobile and free movingand free moving– Joint capsule Joint capsule

connects the connects the two bonestwo bones

– sheet of fibrous sheet of fibrous connective connective tissue enclosing tissue enclosing a synovial joint. a synovial joint.

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Diarthroses JointsDiarthroses Joints

Diarthroses:Diarthroses:– Synovial Synovial

membrane membrane lines joint lines joint capsulecapsule

– Synovial fluid Synovial fluid in the joint in the joint capsule capsule lubricates lubricates jointjoint

Page 22: Muscoloskeletal Patho Lecture Final

Diarthroses JointsDiarthroses Joints

Diarthroses: Diarthroses: – Menisci are protective smooth cartilage Menisci are protective smooth cartilage

plates between the two bonesplates between the two bones– Act as shock absorberAct as shock absorber

Page 23: Muscoloskeletal Patho Lecture Final

Diarthroses JointsDiarthroses Joints

Diarthroses:Diarthroses:– Bursae are small synovial sacs Bursae are small synovial sacs

cushioning tendonscushioning tendons

Page 24: Muscoloskeletal Patho Lecture Final

Time to Think!!!!!!!!!!! Time to Think!!!!!!!!!!!

Which of the following is an example of Which of the following is an example of a synarthrodial joint?a synarthrodial joint?

a.a. ElbowElbow

b.b. WristWrist

c.c. Sutures of the skullSutures of the skull

d.d. Hip/coxalHip/coxal

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Answer Answer

c.c.Sutures of the skullSutures of the skull

RationaleRationale:: Synarthrodial joints have limited Synarthrodial joints have limited movement. The sutures of the skull do movement. The sutures of the skull do not move. All of the other joints are freely not move. All of the other joints are freely movable (diarthrodial) joints.movable (diarthrodial) joints.

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PTH is PTH is released released when blood when blood calcium calcium levels levels decreasedecrease

Parathyroid HormoneParathyroid Hormone

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Sustained PTH Sustained PTH raises blood raises blood calcium levels calcium levels three ways:three ways:º From boneFrom boneº From kidneysFrom kidneysº From From

intestinesintestines

Parathyroid HormoneParathyroid Hormone

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Vitamin DVitamin D Vitamin D is needed to absorb Vitamin D is needed to absorb

dietary calciumdietary calcium Created in skin cells under the Created in skin cells under the

influence of sunlightinfluence of sunlight Absorbed from the diet as a fat-Absorbed from the diet as a fat-

soluble vitaminsoluble vitamin

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CalcitoninCalcitonin

Released by thyroid when blood calcium is Released by thyroid when blood calcium is too hightoo high

Inhibits the release of calcium from boneInhibits the release of calcium from bone Reduces osteoclast activityReduces osteoclast activity Inhibits vitamin D activation in the kidneyInhibits vitamin D activation in the kidney Inhibits calcium reabsorption by the kidneyInhibits calcium reabsorption by the kidney

Page 30: Muscoloskeletal Patho Lecture Final

Time to Think!!!!Time to Think!!!!

As a result of hypocalcemia:As a result of hypocalcemia:

a. PTH is releaseda. PTH is released

b. Calcitonin is releasedb. Calcitonin is released

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Answer Answer

a. PTH is releaseda. PTH is released– released by the parathyroid gland when released by the parathyroid gland when

serum calcium levels are low. serum calcium levels are low. – PTH increases calcium levels by acting PTH increases calcium levels by acting

on:on: bone (bone cells release more calcium)bone (bone cells release more calcium) kidneys (more calcium is reabsorbed)kidneys (more calcium is reabsorbed) intestines (more calcium is reabsorbed). intestines (more calcium is reabsorbed).

Page 32: Muscoloskeletal Patho Lecture Final

Time to Think Again!!!!Time to Think Again!!!!

Two men have bone problems:Two men have bone problems:

– Man #1 developed a lung tumor that Man #1 developed a lung tumor that secreted constant high levels of secreted constant high levels of parathyroid hormone; he became very parathyroid hormone; he became very weak and developed weak bonesweak and developed weak bones

– Man #2 suffered complete kidney Man #2 suffered complete kidney failure; he also developed weak bones failure; he also developed weak bones

Page 33: Muscoloskeletal Patho Lecture Final

Time to Think Again!!!!Time to Think Again!!!!

Questions:Questions:Why did these men both develop Why did these men both develop

weak bones? weak bones?

Which of them is more likely to Which of them is more likely to have increased blood calcium have increased blood calcium levels?levels?

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Answers…Answers…

Why did these men Why did these men both develop weak both develop weak bones? bones? – Man #1 Man #1 – PTH released by the PTH released by the

parathyroid gland parathyroid gland when serum calcium when serum calcium levels are low. levels are low.

– PTH increases calcium PTH increases calcium levels by acting on:levels by acting on: bone (bone cells bone (bone cells

release more calcium)release more calcium)

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Answers…Answers… Why did these men Why did these men

both develop weak both develop weak bones? bones? – Man #2 Man #2 – In end-stage kidney In end-stage kidney

disease, the activation disease, the activation of vitamin D is of vitamin D is nonexistent. nonexistent.

– Vitamin D increases Vitamin D increases intestinal absorption of intestinal absorption of calcium, and it calcium, and it functions in the functions in the regulation of bone regulation of bone formation and formation and mineralization. mineralization.

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Answers…Answers… Which of them is more Which of them is more

likely to have increased likely to have increased blood calcium levels?blood calcium levels?

Man #1Man #1– PTH increases calcium PTH increases calcium

levels by acting on:levels by acting on:– bone (bone cells release bone (bone cells release

more calciummore calcium

Man #2Man #2– Vitamin D Vitamin D increases increases

intestinal absorption intestinal absorption of calciumof calcium, and it , and it functions in the regulation functions in the regulation of bone formation and of bone formation and mineralization.mineralization.

Page 37: Muscoloskeletal Patho Lecture Final

Musculoskeletal Musculoskeletal DisordersDisorders

Sprains and FracturesSprains and FracturesOsteomyelitisOsteomyelitisBone CancerBone CancerOsteoporosisOsteoporosis

Osteoarthritis Osteoarthritis GoutGout

Page 38: Muscoloskeletal Patho Lecture Final

Sprains and StrainsSprains and Strains SprainSprain

– Tear in a Tear in a ligament ligament – Ligaments connect Ligaments connect

bones to one anotherbones to one another Easily torn when Easily torn when

excessive force excessive force exerted on a jointexerted on a joint

Diagnosis: X-ray to Diagnosis: X-ray to rule out fracture and rule out fracture and to note extent of to note extent of damagedamage

Page 39: Muscoloskeletal Patho Lecture Final

Sprains and StrainsSprains and Strains StrainStrain

– Tear in a Tear in a tendontendon– Tendons connect muscles to Tendons connect muscles to

bonebone Easily torn when excessive Easily torn when excessive

force exerted on a jointforce exerted on a joint

Diagnosis: X-ray to rule out Diagnosis: X-ray to rule out fracture and to note extent of fracture and to note extent of damagedamage

Page 40: Muscoloskeletal Patho Lecture Final

Sprains and StrainsSprains and Strains

AvulsionAvulsion– Ligaments or Ligaments or

tendons tendons completely completely separated separated

– Painful (duh!), Painful (duh!), tenderness, tenderness, discoloration (due discoloration (due to hematoma to hematoma formation)formation)

Page 41: Muscoloskeletal Patho Lecture Final

Sprains and Strains Sprains and Strains RecoveryRecovery

Tear Tear → → inflammation inflammation Collagen fibers form to create links Collagen fibers form to create links

with existing tissuewith existing tissue Eventually healing mass bound Eventually healing mass bound

together with fibrous tissuetogether with fibrous tissue Healing up to 6 weeksHealing up to 6 weeks Severe damage requires surgerySevere damage requires surgery

Page 42: Muscoloskeletal Patho Lecture Final

What is a fracture?What is a fracture?

A fracture is a partial or complete break in the bone. A fracture is a partial or complete break in the bone. When a fracture occurs, it is classified as either open or When a fracture occurs, it is classified as either open or closed: closed:

Open fractureOpen fracture (Also called compound fracture)- the (Also called compound fracture)- the bone exist and is visible through the skin, or a deep bone exist and is visible through the skin, or a deep wound that exposes the bone through the skin. wound that exposes the bone through the skin.

Closed fractureClosed fracture (Also called simple fracture)-the bone (Also called simple fracture)-the bone is broken but the skin is intact. is broken but the skin is intact.

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GreenstickGreenstick – incomplete fracture. – incomplete fracture.

The broken bone is notThe broken bone is not complete complete

separated separated

TransverseTransverse- The break is in a - The break is in a

straight line across the bone.straight line across the bone.

SpiralSpiral –– the break spirals around the the break spirals around the

Bone common in a twisting injury. Bone common in a twisting injury.

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ObliqueOblique -- Diagonal break Diagonal break across the bone across the bone

ComminutedComminuted – the break is in three – the break is in three or more pieces or more pieces

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FracturesFractures

TransverseTransverseOblique Oblique Spiral Spiral ComminuteComminute

ddSegmental Segmental ButterflyButterfly ImpactedImpacted

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Bone Bone HealingHealing

Hematoma forms and Hematoma forms and fibrin network fills itfibrin network fills it

Cells grow along fibrin Cells grow along fibrin meshwork to form meshwork to form new tissuenew tissue

Calcium salts Calcium salts deposited in new deposited in new tissuetissue

New tissue remodeled New tissue remodeled into normal shapeinto normal shape

Page 48: Muscoloskeletal Patho Lecture Final

Extracellular Matrix of BoneExtracellular Matrix of Bone

Ground substance contains crystals Ground substance contains crystals of calcium saltsof calcium salts

These make the bone rigidThese make the bone rigid

Page 49: Muscoloskeletal Patho Lecture Final

OsteomyelitisOsteomyelitis OsteomyelitisOsteomyelitis= an infection of bone= an infection of bone

Can either be acute or chronicCan either be acute or chronic

Bacteria are the usual infectious Bacteria are the usual infectious agents.agents.– 1. primary infection of the bloodstream 1. primary infection of the bloodstream – 2. A wound or injury that permits 2. A wound or injury that permits

bacteria to directly reach the bone.bacteria to directly reach the bone.

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OsteomyelitisOsteomyelitis If not treatedIf not treated

– The infection and inflammation block blood vessels. The infection and inflammation block blood vessels.

– Lack of oxygen & nutrients cause the bone tissue to die, Lack of oxygen & nutrients cause the bone tissue to die, which leads to chronic osteomyelitis. which leads to chronic osteomyelitis.

– Other possible complications include blood poisoning and Other possible complications include blood poisoning and bone abscesses.bone abscesses.

– Treatment options include intravenous and oral antibiotics, Treatment options include intravenous and oral antibiotics, and surgical draining and cleaning of the affected bone and surgical draining and cleaning of the affected bone tissue.tissue.

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Causes of OsteomyelitisCauses of Osteomyelitis An An open injury to the boneopen injury to the bone, such as an open fracture with the , such as an open fracture with the

bone ends piercing the skin. bone ends piercing the skin. An An infectioninfection from elsewhere in the body that has spread to the from elsewhere in the body that has spread to the

bone through the blood. bone through the blood. A A minor traumaminor trauma, which can lead to a blood clot around the , which can lead to a blood clot around the

bone and then a secondary infection from seeding of bacteria. bone and then a secondary infection from seeding of bacteria. Bacteria in the bloodstreamBacteria in the bloodstream, which is deposited in a focal , which is deposited in a focal

(localized) area of the bone. This bacterial site in the bone then (localized) area of the bone. This bacterial site in the bone then grows, resulting in destruction of the bone. However, new bone grows, resulting in destruction of the bone. However, new bone often forms around the site. often forms around the site.

A A chronic open wound or soft tissue infectionchronic open wound or soft tissue infection can eventually can eventually extend down to the bone surface, leading to a secondary bone extend down to the bone surface, leading to a secondary bone infection. infection.

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Pathophysiology of Pathophysiology of OsteomyelitisOsteomyelitis

Usually bacterial in Usually bacterial in nature: most nature: most commonly commonly Staphylococcus Staphylococcus aureusaureus

Bone inflammation Bone inflammation is marked by is marked by edema, increased edema, increased vascularity & vascularity & leukocyte activity.leukocyte activity.

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Pathophysiology of Pathophysiology of OsteomyelitisOsteomyelitis

Infection develops Infection develops in bone, which may in bone, which may interfere with interfere with vascular supply to vascular supply to bone.bone.

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Pathophysiology of Pathophysiology of OsteomyelitisOsteomyelitis

Eventually necrosis Eventually necrosis occursoccurs

Because of blocked Because of blocked blood supply, blood supply, difficult for difficult for antibiotics to reach antibiotics to reach the bacteria within the bacteria within the bonethe bone

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Symptoms of Symptoms of OsteomyelitisOsteomyelitis

Localized bone pain Localized bone pain and/or tenderness in and/or tenderness in the infected areathe infected area

Reduced movement of Reduced movement of the affected body part the affected body part

The overlying skin may The overlying skin may be red, hot and be red, hot and swollen – inflammatory swollen – inflammatory responseresponse

The overlying skin may The overlying skin may contain pus/purulent contain pus/purulent drainage drainage

Spasms of associated Spasms of associated muscles muscles

Page 56: Muscoloskeletal Patho Lecture Final

Risk Factors for Risk Factors for OsteomyelitisOsteomyelitis

Long term skin infections. Long term skin infections. Risk factors for poor blood circulation, Risk factors for poor blood circulation,

which include high blood pressure, which include high blood pressure, cigarette smoking, high blood cholesterol cigarette smoking, high blood cholesterol and diabetes. and diabetes.

Prosthetic joints. Prosthetic joints. Hemodialysis Hemodialysis Weakened immune systems Weakened immune systems Intravenous drug abusers Intravenous drug abusers The elderly The elderly

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Neoplastic Disorders: Bone Neoplastic Disorders: Bone TumorsTumors

Tumors may be Tumors may be malignant or benignmalignant or benign– Benign tumors Benign tumors

grow slowly and do not grow slowly and do not invade surrounding invade surrounding tissues, tend to be less tissues, tend to be less destructive to normal destructive to normal bone.bone.

– Malignant tumors Malignant tumors grow rapidly and grow rapidly and

metastasize, tends to metastasize, tends to cause more bone cause more bone destruction, invasion of destruction, invasion of the surrounding tissues the surrounding tissues & metastasis& metastasis

Page 58: Muscoloskeletal Patho Lecture Final

Neoplastic Disorders: Bone Neoplastic Disorders: Bone TumorsTumors

Tumors can be Tumors can be primary (rare) or primary (rare) or metastatic lesionsmetastatic lesions – originating from primary originating from primary

tumors of prostate, tumors of prostate, breast, kidney, thyroid, breast, kidney, thyroid, lunglung

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Neoplastic Disorders: Bone Neoplastic Disorders: Bone TumorsTumors PathophysiologyPathophysiology

Cause unknownCause unknown– but connection exists but connection exists

between bone activity and between bone activity and development of primary development of primary bone tumorsbone tumors

Primary tumors cause Primary tumors cause osteolysisosteolysis– bone breakdown, which bone breakdown, which

weakens bone and leads to weakens bone and leads to bone fracturesbone fractures

Malignant boneMalignant bone – tumors invade and destroy tumors invade and destroy

adjacent bone tissueadjacent bone tissue

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OsteoporosisOsteoporosis Debilitating disease in which bones become Debilitating disease in which bones become

fragile and are more likely to breakfragile and are more likely to break Disorder characterized byDisorder characterized by

– (1)loss of bone mass (1)loss of bone mass – (2) increased bone fragility (2) increased bone fragility – (3) increased risk for fractures(3) increased risk for fractures

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OsteoporosisOsteoporosis Significant health threat for Americans: Significant health threat for Americans:

– estimated 28 million personsestimated 28 million persons– more common in aging womenmore common in aging women– half of women over 50 experience osteoporosis half of women over 50 experience osteoporosis

related fracture in lifetime (hip, wrist, vertebrae) related fracture in lifetime (hip, wrist, vertebrae) especially R/T fallsespecially R/T falls

Page 62: Muscoloskeletal Patho Lecture Final

Risk Factors for Risk Factors for OsteoporosisOsteoporosis

Gender- women are more likely to develop than men due to thinner, lighter bones & the decrease in estrogen production that occurs during menopause.

Age- the longer you live, the greater the likelihood of developing.

Family history-is due part to heredity. Ethnicity-Caucasian & Asian women are at

highest risk; African-American & Hispanic women at lower but significant risk.

Body size- low body weight (< 127 lbs.) & a small-boned frame place at increased risk.

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Risk Factors for Risk Factors for OsteoporosisOsteoporosis Calcium deficiency

– insufficient calcium in diet results in body removing calcium from bones; diets high in protein lead to acidosis, and high in diet soda are high in phosphate

Menopause– decreasing estrogen levels: estrogen replacement therapy

can reverse bone changes but may increase risk for other diseases

Cigarette smoking– decreased blood supply to bones

Excessive alcohol intake– toxic effect on osteoblastic activity; high alcohol intake

frequently associated with nutritional deficiencies Sedentary life style

– weight-bearing exercise such as walking positively influences bone metabolism

Use of specific medications– aluminum-containing antacids, corticosteroids,

anticonvulsants, prolonged heparin therapy, antiretroviral

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Osteoporosis - Osteoporosis - PathologyPathology

Diameter of bone increases, thinning outer Diameter of bone increases, thinning outer supportive cortexsupportive cortex

Trabeculae (spongy tissue) lost and outer Trabeculae (spongy tissue) lost and outer cortex thinscortex thins

Minimal stress leads to fractureMinimal stress leads to fracture

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Bone Tissue CompositionBone Tissue Composition

Outer LayerOuter Layer– Compact bone Compact bone

with Haversian with Haversian CanalsCanals

– Canals contain Canals contain arteriolesarterioles

– Found in Found in DiaphysesDiaphyses

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Bone Tissue CompositionBone Tissue Composition

Inner LayerInner Layer– Cancellous Cancellous

(spongy) bone(spongy) bone– Interface to Interface to

form a form a latticeworklatticework

– Red marrow Red marrow fills in spaces fills in spaces of latticework of latticework (trabeculae)(trabeculae)

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Osteoporosis - Osteoporosis - PathologyPathology

Trabeculae (spongy Trabeculae (spongy tissue) lost and outer tissue) lost and outer cortex thinscortex thins

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Osteoporosis - Osteoporosis - PathologyPathology

ManifestationsManifestations ““Silent Disease”Silent Disease”

– bone loss occurs without symptomsbone loss occurs without symptoms

Loss of heightLoss of height Progressive curvature of spine Progressive curvature of spine Low back painLow back pain Fractures of forearm, spine or hipFractures of forearm, spine or hip

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Osteoporosis - Osteoporosis - PathologyPathology

Dowager’s HumpDowager’s Hump– Cervical Lordosis Cervical Lordosis – with Kyphosiswith Kyphosis

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A normal spine at 40 years, and the A normal spine at 40 years, and the osteoporotic changes at ages 60 and 70 yearsosteoporotic changes at ages 60 and 70 years

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Osteoporosis - Osteoporosis - PreventionPrevention

PreventionPrevention By age 20, the average woman has acquired 98% of her By age 20, the average woman has acquired 98% of her

skeletal mass.skeletal mass. Building strong bones during childhood & adolescence can Building strong bones during childhood & adolescence can

be the best defense against developing osteoporosisbe the best defense against developing osteoporosis– Balanced diet rich in Calcium & Vitamin D.Balanced diet rich in Calcium & Vitamin D.

– Weight-bearing exercisesWeight-bearing exercises

– A healthy lifestyle with no smoking & limited alcohol intake.A healthy lifestyle with no smoking & limited alcohol intake.

– Bone density testing & medication when appropriate. Bone density testing & medication when appropriate.

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OsteoarthritisOsteoarthritis

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OsteoarthritisOsteoarthritis

Osteoarthritis is an idiopathic diseaseOsteoarthritis is an idiopathic disease Low-grade inflammation results in Low-grade inflammation results in

pain in the jointspain in the joints Caused by abnormal wearing of the Caused by abnormal wearing of the

cartilage Destruction or decrease of Destruction or decrease of

synovial fluid that lubricates those that lubricates those joints. joints.

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Factors ResponsibleFactors Responsible

AgeingAgeing GeneticsGenetics HormonesHormones MechanicsMechanics

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Pathologic lesionsPathologic lesions

Primary lesion appears to occur in Primary lesion appears to occur in cartilagecartilage

Leads to inflammation in synoviumLeads to inflammation in synovium Changes in subchondral bone, Changes in subchondral bone,

ligaments, capsule, synovial ligaments, capsule, synovial membrane and periarticular musclesmembrane and periarticular muscles

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OsteoarthritisOsteoarthritis

Commonly affects:Commonly affects:– hipships– feetfeet– spine spine – hips hips – knees (water on the knee)knees (water on the knee)– fingersfingers– toestoes

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Normal CartilageNormal Cartilage Avascular, alymphatic and aneural tissueAvascular, alymphatic and aneural tissue Smooth and resilientSmooth and resilient Extracellular matrix is a highly hydrated gel Extracellular matrix is a highly hydrated gel

containing 65%–80% watercontaining 65%–80% waterFunction of cartilage is critically Function of cartilage is critically

dependent on composition of ECMdependent on composition of ECM Allows shearing and compressive forces to Allows shearing and compressive forces to

be dissipated uniformly across the jointbe dissipated uniformly across the joint

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Primary OsteoarthritisPrimary Osteoarthritis

With age, water content of With age, water content of the cartilage decreases the cartilage decreases due to a reduced due to a reduced proteoglycan content in proteoglycan content in the ECM.the ECM.

Proteoglycan responsible Proteoglycan responsible for directing movement of for directing movement of water and solutes through water and solutes through the ECM.the ECM.

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Primary OsteoarthritisPrimary Osteoarthritis

Collagen fibers of the Collagen fibers of the cartilage can become cartilage can become susceptible to degradation susceptible to degradation – Thinning of cartilageThinning of cartilage

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Primary OsteoarthritisPrimary Osteoarthritis

Breakdown products Breakdown products from the cartilage are from the cartilage are released into the released into the synovial spacesynovial space– Leads to inflammatory Leads to inflammatory

responseresponse

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Primary OsteoarthritisPrimary Osteoarthritis

Damaged joint Damaged joint cartilage tries to cartilage tries to heal itselfheal itself– Creating Creating

osteophytes or spursosteophytes or spurs– Cartilage becomes Cartilage becomes

weak, rough, erodedweak, rough, eroded– No longer protects No longer protects

the surface of the the surface of the bonebone

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Heberden's NodesHeberden's Nodes

Distal interphalangeal jointsDistal interphalangeal joints

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Bouchard's nodesBouchard's nodes

Proximal interphalangeal joints Proximal interphalangeal joints

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Primary OsteoarthritisPrimary Osteoarthritis

Symptoms of Symptoms of Osteoarthritis are Osteoarthritis are caused by:caused by:– inflammatory inflammatory

responseresponse– osteophytes or spursosteophytes or spurs– weak, rough, eroded weak, rough, eroded

cartilagecartilage

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Secondary OsteoartritisSecondary Osteoartritis

Caused by other factors:Caused by other factors:– Pathophysiology is the samePathophysiology is the same– Sport injuries:Sport injuries:

Injuries resulting in broken ligaments can lead to Injuries resulting in broken ligaments can lead to instability of the joint and over time to wear on the instability of the joint and over time to wear on the cartilage and eventually osteoarthritis cartilage and eventually osteoarthritis

– ObesityObesity added weight on the joints, especially the knees added weight on the joints, especially the knees

– GoutGout uric acid crystals cause the cartilage to degenerate at crystals cause the cartilage to degenerate at

a faster pace a faster pace

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Rheumatoid ArthritisRheumatoid Arthritis

Presence of rheumatoid factors Presence of rheumatoid factors (RA or RF test)(RA or RF test)– Antibodies (IgG and IgM) against Antibodies (IgG and IgM) against

antibodiesantibodies Joint fluid presents with Joint fluid presents with

inflammatory exudateinflammatory exudate

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Rheumatoid ArthritisRheumatoid Arthritis

PathogenesisPathogenesis– CD4 T helper cells and other cells CD4 T helper cells and other cells

in the synovial fluid become in the synovial fluid become activated and release cytokinesactivated and release cytokines

– Recruitment and retention of Recruitment and retention of inflammatory cells in the joint inflammatory cells in the joint sublining regionsublining region

– Cycle of altered cytokine and signal Cycle of altered cytokine and signal transduction pathwaystransduction pathways

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Rheumatoid ArthritisRheumatoid Arthritis

Evaluation Evaluation – Four or more of the following:Four or more of the following:

Morning joint stiffness lasting at least 1 hourMorning joint stiffness lasting at least 1 hour Arthritis of three or more joint areasArthritis of three or more joint areas Arthritis of the hand jointsArthritis of the hand joints Symmetric arthritisSymmetric arthritis Rheumatoid nodules Rheumatoid nodules Abnormal amounts of serum rheumatoid Abnormal amounts of serum rheumatoid

factorfactor Radiographic changesRadiographic changes

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Rheumatoid ArthritisRheumatoid Arthritis

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Rheumatoid ArthritisRheumatoid Arthritis

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Rheumatoid ArthritisRheumatoid Arthritis

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Ankylosing SpondylitisAnkylosing Spondylitis

Inflammatory joint disease of the Inflammatory joint disease of the spine or sacroiliac joints causing spine or sacroiliac joints causing stiffening and fusion of the jointsstiffening and fusion of the joints

Systemic, immune inflammatory Systemic, immune inflammatory diseasedisease

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GoutGout

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Definition of GoutDefinition of Gout Gout is a heterogeneous disorder that Gout is a heterogeneous disorder that

results in the deposition of uric acid salts results in the deposition of uric acid salts and crystals in and around joints and soft and crystals in and around joints and soft tissues or crystallization of uric acid in the tissues or crystallization of uric acid in the urinary tract. urinary tract.

Uric acid is the normal end product of the Uric acid is the normal end product of the degradation of purine compounds. degradation of purine compounds. – Major route of disposal is renal excretion Major route of disposal is renal excretion – Humans lack the enzyme uricase to break Humans lack the enzyme uricase to break

down uric acid into more soluble form.down uric acid into more soluble form.

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GoutGout

Affects less than 0.5% of the populationAffects less than 0.5% of the population Due to familial disposition, incidence Due to familial disposition, incidence

may be as high as 80% in families may be as high as 80% in families affected by disorder.affected by disorder.

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EpidemiologyEpidemiology Incidence has increased significantly over the Incidence has increased significantly over the

past few decades.past few decades. Affects about 2.1million worldwideAffects about 2.1million worldwide Peak incidence occurs in the fifth decade, but can Peak incidence occurs in the fifth decade, but can

occur at any ageoccur at any age Gout is 5X more common in males than pre-Gout is 5X more common in males than pre-

menopausal females; incidence in women menopausal females; incidence in women increases after menopause. increases after menopause.

After age 60, the incidence in women approaches After age 60, the incidence in women approaches the rate in men.the rate in men.

People of South Pacific origin have an increased People of South Pacific origin have an increased incidence.incidence.

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What is Gout?What is Gout?

Inflammation occurs 2° deposits of Inflammation occurs 2° deposits of uric acid crystals in jointuric acid crystals in joint

Body produces too much uric acid Body produces too much uric acid (Overproduction)(Overproduction)– OrOr

Body excretes too little uric acid Body excretes too little uric acid (Underexcretion)(Underexcretion)

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Classification of Classification of HyperuricemiaHyperuricemia

Uric acid underexcretion in the Uric acid underexcretion in the KidneyKidney– Accounts for >90% of hyperuricemiaAccounts for >90% of hyperuricemia– Diminished tubular secretory rateDiminished tubular secretory rate– increased tubular reabsorptionincreased tubular reabsorption– diminished uric acid filtrationdiminished uric acid filtration

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Classification of Classification of HyperuricemiaHyperuricemia

Uric acid overproductionUric acid overproduction– Accounts for 10% of hyperuricemiaAccounts for 10% of hyperuricemia– Defined as 800mg of uric acid excretedDefined as 800mg of uric acid excreted– Acquired disorders Acquired disorders

Excessive cell turnover rates such as: Excessive cell turnover rates such as: myleoproliferative disordersmyleoproliferative disorders

Paget’s diseasePaget’s disease hemolytic anemiashemolytic anemias

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What is Uric Acid?What is Uric Acid?

Uric acid is a waste product formed Uric acid is a waste product formed from the breakdown of purinesfrom the breakdown of purines

High levels of purines are found in High levels of purines are found in organ meats (liver, brains, kidney), organ meats (liver, brains, kidney), anchovies, herring, mackerel. anchovies, herring, mackerel. – Alcohol and some drugs may affect purine Alcohol and some drugs may affect purine

excretion.excretion.

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Pathogenesis of Gouty Pathogenesis of Gouty InflammationInflammation

Urate crystals stimulate the release of Urate crystals stimulate the release of numerous inflammatory mediators in numerous inflammatory mediators in synovial cells synovial cells

The influx of neutrophils leads to The influx of neutrophils leads to development of acute crystal induced development of acute crystal induced synovitissynovitis

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Diarthroses JointsDiarthroses Joints

Diarthroses:Diarthroses:– Synovial Synovial

membrane membrane lines joint lines joint capsulecapsule

– Synovial fluid Synovial fluid in the joint in the joint capsule capsule lubricates lubricates jointjoint

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Stage 1 Stage 1 Asymptomatic Asymptomatic HyperuricemiaHyperuricemia

Uric acid levels elevated to 9-Uric acid levels elevated to 9-10 range (normals ~ 3 – 6)10 range (normals ~ 3 – 6)

No symptomsNo symptoms Client may not progress to Client may not progress to

symptomatic diseasesymptomatic disease

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Stage 2Stage 2Acute Gouty ArthritisAcute Gouty Arthritis

Sudden onset, acute pain, redness, swellingSudden onset, acute pain, redness, swelling Usually hits the big toe, may affect another Usually hits the big toe, may affect another

jointjoint Fever, chillsFever, chills ““Attack” lasts hours to weeksAttack” lasts hours to weeks 60% have recurrent attack in 1 yr 60% have recurrent attack in 1 yr

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Stage 3Stage 3Chronic Tophaceous Chronic Tophaceous

GoutGout Hyperuricemia Hyperuricemia untreateduntreated

Tophi (urate crystals Tophi (urate crystals deposits) develop in deposits) develop in cartilage, synovial cartilage, synovial membranes, tendons, membranes, tendons, soft tissuessoft tissues

Pain, ulceration, Pain, ulceration, nerve damagenerve damage

Uric acid crystals—Uric acid crystals—>kidney stones>kidney stones

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Stage 3Stage 3Chronic Tophaceous GoutChronic Tophaceous Gout

Chronic gouty inflammation Chronic gouty inflammation associated with cytokine driven associated with cytokine driven synovial proliferation, cartilage loss synovial proliferation, cartilage loss and bone erosionand bone erosion

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Treatment of Gout AttackTreatment of Gout Attack

Dietary ManagementDietary Management– Drink 3-4 quarts of fluids dailyDrink 3-4 quarts of fluids daily– Avoid alcohol (especially BEER… NOOO!!!!)Avoid alcohol (especially BEER… NOOO!!!!)– Low purine dietLow purine diet

– Avoid meats, seafood, yeast, beans, peas, lentils, Avoid meats, seafood, yeast, beans, peas, lentils, oatmeal, spinach, asparagus, cauliflower, mushroomsoatmeal, spinach, asparagus, cauliflower, mushrooms