wk 2 nfk 202
TRANSCRIPT
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THEME CONVENOR MRS. L.MATAITINI.
YEAR 2 SEMESTER 2, 2011 08/08/11
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This week, we will introduce you to thedisorders of the musculoskeletal system.
Musculoskeletal system includes the bones,joints and muscles of the body togetherwith the associated structures such as theligaments and tendons. These disorders
affects person of all age groups and allwalks of life, causing pain and disability.
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At the end of this session the studentshould be able to:
Define the key terms
Discuss the different causes ofmusculoskeletal disorders.
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Explain the clinical manifestations of eachdisorders.
Discuss the pathophysiological problems ofeach musculoskeletal system.
Discuss the different types of therapeutic
procedures available for each disorders.
Discuss the different drugs available to treat
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Pathophysiological changes of themusculoskeletal.
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Musculoskeletal disorders divides up intothree according to the structures:
(i) Tissue(ii) Joints(iii) Bones
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Physical forces such as:
Blunt tissue trauma.
Disruptions of tendons and ligaments Fractures of the bony structures.
Other causes:
Motor vehicle accident
Motorcycle accident Falls
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rugby
athletes
other sports
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SOFT TISSUE INJURY.
Contusion
Hematoma
Laceration
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It is the injury to softtissue that results fromdirect trauma and is
usually caused bystriking a body part
against a hard object.
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CLINICAL MANIFESTATIONS
ecchymosis-due to hemorrhagediscoloration gradually changes tobrown and yellow as the blood isreabsorbed.
Hematoma- blood accumulates and exertspressure on nerve endings.
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CLINICAL MANIFESTATIONpain- increases with movement ,swelling ,
infection due to bacterial growth, split skindue to increase pressures and produce
drainage of the hematoma
TREATMENT:apply cold compress during the 1
st
24hrs ofinjury.
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After the 1st 24hrs, heat or coldcompression to be done intermittentlyfor 20mins at a time.
Laceration:Injury in which the skin is torn or itscontinuity is disrupted. The
seriousness of the lacerationdepends on the size and depth of thewound.
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Punctured wounds from nails or rustedmaterial provide the setting for growth of
anaerobic bacteria such as those that causetetanus and gas gangrene.
TREATMENT:Wound closure after cleaning the wound well
and apply sterile dressing antibiotics.
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Strains
Sprains
Dislocation
Knee injuries
Meniscus injuries.
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STRAINS:A strain is a stretching injury to a muscle or amusculotendinous(joint)unit caused by amechanical overloading.
.
CAUSE : unusual muscle contraction.
excessive forcible stretch . overweight or excessive exercises.
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Pain.
Stiffness.
Swelling.
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Lower back Cervical region of the spine
Elbow
Shoulder foot
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TREATMENT:
Bed rest. traction.
application of heat.
massage.
cold compression for the 1st 24hrsto educe pain and swelling of the
affected area.
exercises, correct posture and goodbody mechanics.
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SPRAINS:Involves the ligamentous structuressurrounding the joints, resemble astrain, but the pain and swellingsubsides slowly.CAUSE:
abnormal and excessive movement ofthe joint.
CLINICAL MANIFESTATIONS:pain.
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Rapid swelling.
Heat. Disability.
Discoloration
Limitation of function
DIAGNOSTIC TESTS: history of the injury.
x-ray.
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TREATMENT: Bed rest. elevation of the injured part cold compression.
adhesive straps or removablesplint cast applied on severe sprains.
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Displacement or separation of the bone endsof the joint with loss of articulation.
Usually follows a severe trauma that disrupts
the holding ligaments.
Most common sites are the shoulders andacromioclavicular joints.
Sublaxation is a partial dislocation in which
the bone ends in the joint are still in partialcontact with one another.
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Dislocations can be congenital, traumatic orpathologic.
Traumatic dislocations occur after falls,blows, or rotational injuries.
CAUSE: trauma .
motor vehicle accidents. fall.
sports.
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CLINICAL MANIFESTATIONS.pain.limitation of movementswellingdeformity
DIAGONISTIC TESTS.history.physical examination
x-ray.TREATMENT.Bed rest.manipulationsurgical repair.
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It is a common site of injury, particularly sport
related injuries in which the knee is subjectedto abnormal twisting and compression forces.These forces can result in injury to themeniscus, patella sublaxation and dislocation .
MENISCUS INJURY:Meniscus injury commonly occurs as the result
of rotational injury from a sudden or sharp
instrument or a direct blow to the knee, as inhockey, basketball or football.
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CLINICAL MANIFESTATIONS.pain .swelling
DIAGNOSTIC TEST:physical examinationx-ray.arthroscopy
TREATMENT:conservativerest
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A break in the continuity of the bone. A fractureoccurs when the stress placed on the bone isgreater than the bone can absorb.
TYPES OF FRACTURE:open fracture skin involveclosed fracture-skin not involvecomplete fracture-involves the entire
cross section of the bonepathologic fracture-through an area of
diseased bone.
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Greenstick-one side of the bone is broken
Transverse-straight across the bone. Oblique at an angle across the bone.
Spiral-twists around the shaft of the bone.
Comminuted-bone splinted into more than threefragments.
Depressed-fragments indriven.
Compression-bone collapses in on itself.
Avulsion fragment of bone pulled of byligament.
Impacted-fragment of bone wedged into otherbone fragment.
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COMPOUND FRACTURE
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Pain
Tenderness Swelling
Loss of function
Deformity of the affected side
Angulations Shortening of the bones
Rotation deformity
Crepitus or grating may be felt as the bonefragments rub each other.
Bleeding
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PICS SUPPLEMENT
PATTERNS OF FRACTURE CONT
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Hypovolemic shock due to bleeding.
Numbness of the affected area.
DIAGNOSTIC AND THERAPEUTIC.history
physical examination
x-ray examination
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Reduction-to align the bones Immobilization-prevents movement of the
bones
External fixation
COMPLICATIONS OF FRACTURES. fracture blisters
Compartment syndrome Muscle wasting Fat embolism
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Osteomylitis:
Acute and chronic infection of thebone.
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Direct extension or contamination of
the open fracture.Wide variety of microorganisms
introduced during injury, operativeprocedures or from the blood
stream.Usually bacteria in origin; isolated
organisms which include :staphylococcus aureusEscherichia coli
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Pseudomonas
Klebsiella Salmonella
Proteus
2.Hematogenous Infection-through thebloodstream.
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PATHOPHYSIOLOGY:1. Site inoculated.
2.Inflammatory and immunologic response;pus formationedema.vascular congestion.
3. Vascular occlusion leads to ;
ischemiabone necrosis.
4. Infections spread through the bone viaVolkmann's and haversian canals,
causing further vascular occlusions
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Ischemia allows necrotic bone to separatefrom the living bone, forming sequestra.
Sequestra enlarge, spreading toward andbreaching the cortex, forming a subperiosteal
abscess, further interfering with the vascular
supply.
Vascular supply may remain sufficient to
maintain life of bone tissue.
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New bone is created
Bone healing occurs.
Diminished vascular supply leads to deadbones and bones become inert.
Small pieces of bone may be completelydestroyed by granulation tissue.
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Large pieces of dead bone cannot be
destroyed . Central residual remains a sequestrum
composed of cancellous
New bone is laid down beneath the elevated
periosteum and tends to form an encasementaround the sequestrum.
Pockets of infection are walled off in whichorganisms can lie dormant long periods
Chronic sinuses may form that eventuallyreach the surface and drain
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Drainage continues until infection quietsonce more. Channels become plugged withgranulations and remain closed until thepressure of the pus builds up and causes
the sinuses to reopen or reach the surfacethrough new channels(chronicosteomyelitis)
Complete healing takes place only when allthe dead bone has destroyed, discharged orexcised
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COMPLICATIONS: Chronic osteomyelitis
Pathological fracture
Joint destruction
Skeletal deformities
Limb length discrepancies
Life threatening if untreated
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CLINICAL MANIFESTATIONS Localised pain
Swelling
Erythema
Fever
Malaise
Irritability.
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DIAGNOSTIC TESTS Blood culture Needle aspiration
Full blood count
X-ray.
TREATMENT: Intravenous antibiotics-4to 8weeks
Additional 4to8weeks oral antibiotics Surgical intervention(incision and drainage).
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Development dysplasia of the hip:congenital dislocation of the hip.
CAUSE: Unknown Hereditory-high risk with family history
Increased ligamentous laxity secondary tomaternal hormones.
Breach presentation First born
In-utero restrictions to fetal movement
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Joint Arthroplasty(Reconstruction or Replacement)
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Swaddling in the postnatal period, where thehips are in abduction and extension
PATHOPHYSIOLOGY: Acetabelum tends to be shallow and oblique Head of the femur tends to smaller than
normal.
Ossification centers are delayed in
appearance. Dysplasia-shallow acetabelum, roof slants
upward
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Sublaxation acetabular surface of thefemoral head is in contact with shallowdysplastic.
Dislocation-articular cartilage of completelydisplaced femoral head does not contactacetabular articular cartilage
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COMPLICATION:
Avascular necrosis of femoral head
Loss of range of movement. Leg length inequality.
Early osteoarthritis
Recurrent dislocation or unstable hip.
CLINICAL MANIFESTATIONS: Asymmetry of high or gluteal folds
Abnormal gait pattern Ortolanis sign and positive Barlows test.
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DIAGNOSTIC TEST: X-ray-cartilagenous femoral head is difficult
to visualise in the newborn
Ultrasound examination
Arthrogram- outline the cartilagenousportions of the acetabulum and femoral head
Physical examination
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TREATMENT: Splinting-Birth to 3months
Close reduction3months to 2years.
Surgical intervention -2yrs +
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Congenital anomaly characterised by a threepart deformity of the foot, consisting of theheel(varus), adduction and supination of theforefoot, and ankle equinus.
CAUSE: Unknown.
Suggested contributing factor;
.intrauterine position..primary arrest in fetaldevelopment.
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Familial tendency.
PATHOPHYSIOLOGY: Foot is planter flexed at the ankle and the
subtalar joints.
Hind foot is inverted.
Midfoot and hind forefoot are adducted and
inverted. Contractures of the soft tissues maintain the
malalignments.
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COMPLICATIONS: Deformity becomes fixed if untreated.
Disturbances in epiphyseal plates fromoveraggressive manipulations
Child bearing weight on lateral border of foot
Gait is awkward
Recurrent deformity
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CLINICAL MANIFESTATION:
Deformity is obvious at birth with varying degreerigidity and ability to correct position.
DIAGNOSTIC TEST: clinical presentation
Physical examination X-ray
TREATMENT: Manipulation-pop cast Corrective footwear Surgical intervention
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DEFINITION:Lateral curvature of the spine with vertebralbody rotation.
CAUSE: Unknown Classified into three groups.
Infants-presentation 3years
Juvenile -3to10years.Adolescents-10years
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Congenital scoliosis exact cause is unknown Neuromuscular scoliosis-child has a definite
neuromuscular condition that directlycontributes to the deformity.
PATHOPHYSIOLOGY: Vertebral column develops lateral curvature
Vertebral rotate to the convex side of the
curve Vertebral become wedged shape
Disk shape is altered
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Deformity progress, changes in the thoracic
cage worsened.
Changes in the thoracic cage, ribs andsternum lead to further characteristicsdeformities such as rib hump.
Neurological compromise-very rare.
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COMPLICATION: Untreated progressive scoliosis may lead to
significant deformity
Cardiopulmonary compromise
Shortened life expectancy
Increased back pain
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CLINICAL MANIFESTATIONS: Poor posture Uneven should height One hip appears more prominent Crooked neck Lump on the neck Rib hump Uneven waistline
Uneven breast size Visualization deformity Back pain
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DIAGNOSTIC TEST: X-ray of the spine upright position
Myelogram
Tomograms
C.T. Scan
TREATMENT: Medical management
Exercise therapy
Surgical intervention
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OSTEOPOROSIS: DEFINITION:
Condition in which the bone matrix is lost,thereby weakening the bones and makingthem susceptible to fractures.
PATHOPHYSIOLOGY: The rate of bone resorption increases over the
rate of bone formation, causing loss of bonemass .
Calcium and phosphate salts are lost-creatingbrittle bones.
Occurs most frequently in postmenopausalwomen.
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Age
Inactivity Chronic illness
Medications such as corticosteroids
Calcium and vitamin D deficiency
Family history
Smoking
Diet caffeine is a risk factor
Race white and Asians have higher risk
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CLINICAL MANIFESTATIONS.
Asymptomatic until later stages Fracture after minor trauma may be first
indications.
Vague complaints related to aging process.
Stiffness
Pain
Weakness
DIAGNOSTIC TEST: X-ray-shows changes only after30% to60% of
bone.
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Computed Tomography (CT Scan) Bone biopsy.
COMPLICATION
Fracture
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DEFINITION:
Degenerative joint disease is a chronic noninflammatory, slowly progressing disorderthat causes deterioration of articular cartilage
It affects weight- bearing joints( hips and
knees) as well as joints of the distalinterphalanges and of the fingers.
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PATHOPHYSIOLOGY:Changes in particular cartilage occurs first
Soft tissue changes may occur next.
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Progressive wear and tear on cartilage leads
to thinning of joint surface Ulceration into bone
Inflammation of the joint and increased bloodflow..
Hypertrophy of suprachondral bone .
New cartilage and bone formation at jointmargin results in osteophytosis altering the
size and shape of bone
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CAUSE:
unknown
Aging and obesity are contributing factors
Previous trauma may cause secondaryosteoarthritis
DIAGNOSTIC TESTS: Physical examination
X-ray of affected joints
Bone scan Analysis of synovial fluid differentiates
osteoarthritis and rheumatoid arthritis
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DEFINITION:Musculoskeletal neoplasm include primary
sarcoma, metastic bone disease, and benigntumors of the bone.
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PATHOPHYSIOLOGY Benign bone tissue
Osteoid osteoma Chondroma
Osteoclastoma
Malignant bone tumors Chondrosarcoma and osteosarcoma are
examples of primary malignant bonetumors
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Hematogenous spread to the lungs occurs Multiple myeloma is a malignant neoplasm
arising from the bone marrow .
METASTATIC BONE TUMORS;Metastic bone tumors are most
frequently associated with cancers ofthe breast, prostate and lung (primarymalignancy site) .
Bone metastasis most frequently occursin the vertebrae and results inpathological fracture.
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CLINICAL MANIFESTATIONS:
Pain in the involved bone-worst at night. Swelling and limitations of motion and joint
effusions
Physical findings-palpable, tender fixedboney mass. Increase in skin temperatureover the mass. Superficial veins dilated andprominent.
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DIAGNOSTIC TEST X-ray
CT Scan
Bone scan
bone biopsy
blood test-serum alkaline phosphate
chest x-ray and lung scan
arteriography-to assess soft tissue
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TREATMENT: Surgery
Chemotherapy
Radiotherapy
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QUESTION TIME? ? ?