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Chapter 37 - Alterations of MS Function

Terms in this set (41)

Fracture
a fracture is a break in the continuity of a bone.

Classify it by ALOT
Complete/incomplete : closed or open.
Comminuted
Linear
Oblique
Spiral
Transverse
Greenstick
Toruus
Bowing
Pathologic
Stress
Highest incidence of fractures is 15 - 25
and than in > 65 y/o
The fractures in young ppl ; accidents like long bones, hands, feet.
The fractures in older ppl ; result of osteoporosis ; hip, upper femur and verterbrae
Complete Fractures are when the bone is broken in
2 pieces.
Incomplete fractures are when those that are damaged are
still in one place.
Open fracture is when the bone breaks
through the skin (compound fracture)
Closed fracture is when
it does not break the skin ; simple fracture.
Pathologic fracture are a break at the site of a preexisiting abnormality, usually a force that wouldn't fracture a normal bone ;
any disease process that weakens a bone predisposes the bone to a pathologic fracture (tumors, osteoporosis, infection & metabolic bone disorders.)
Stress fractures occur in normal and abnormal bone that is
subjected to REPEATED strain, such as occurs during athletics. The stress on the bone is CUMULATIVE and eventually causes a fracture.
Review SLIDE 3
It's the picture of the FRACTURES. ( KNOW THEM)
Bone fractures
broken bone causes damage to the surrounding tissue, periosteum, & BV in the cortex and marrow ; Hematoma formation.

*surrounding tissue comment ;
so if there is bone tissue ADJACENT to the fracture, it dies.....(This DEAD tissue is the one that STARTS that IR (down below) but it's like vasodilation, exudation of plasma, leukocytes, and infiltration by inflammatory leukocytes, and mast cells)

{Bone tissue destruction triggers an IR.}

And than we have bone- forming cells, and they are activated and produce a PROCALLUS along the outer layer of the shaft. (DOWN BELLOW ; PROCALLUS FORMATION)
Now the bone is remodeled into new bone, YAY.
The BONE AND LIVER are the only body tissue that can FORM NEW TISSUE when it heals and not scar tissue.
(wow, I DIDNT KNOW THAT)

Procallus formation.
Clinical Manifestations - Bone Fractures

Treatment:
often numbness up to 20 minutes following injury.
[ That numbness is SECONDARY to nerve injury @ the site. So like when that numbness dissipates, or is gone lol, the pain of the fracture can be SEVERE]

Other cm: unnatural alignment, swelling, muscle spasm, tenderness, pain, impaired sensation, and possible muscle spasms.

We treat it by closed manipulation, traction and open reduction, also by internal and external fixation.
Bone Fractures :
Improper Reduction or Immobilization
(nonunion, delayed union, and malunion)

Dislocation (ex of subluxation)
Temporary displacement of 2 bones.
Loss of contact bw articular cartilage.

Subluxation
Contact bw articular surfaces is only partially lost.
So nonunion is FAILURE of the bone ends to grow together.
Delayed union os the bone doesn't grow back until about 8-9 months after the fracture.
Malunion is when the healing of the bone in an incorrect anatomic position.

Disolcations (which are subxluations duh)
usually caused by trauma.
<20 y/o, associated w fractures.
The joints usually affected are shoulder, elbow, wrist, finger, hip and knee.
(FRACTURES, MUSCLE IMBALANCE, RHEUMATOID ARTHRITIS, JOINT INSTABILITY)

cm: pain, swelling, limitation of motion, joint deformity, and we treat all of these cm by reduction and immobilization for 2-6 weeks and to exercise to maintain normal range of motion in the joint.
Healing is usually complete within months to sometimes years.
Strain is a tear or injury to a
tendon.

(fibrous CT that attaches skeletal muscle to bone)
Sprain is a tear or injury to a
ligament.

(bands of fibrous CT that connects bones where they meet in a joint)
Alvusion is a complete separation of a tendon or ligament from WHERE?
It's bony attachment site.
Cm/ Treatments for Sprain/ Strains:
CM: Pain, soft tissue swelling, decreased joint mobility, weakness of the affected joints.

Treatment : acronym is PRICE (from the first 48-72 hours)
Protection
Rest
Ice
Compression
Elevate
Tenditis
inflammation of a tendon
Bursitis
inflammation of a bursa....
skin over bone, skin over muscle, and muscle tendon over bone.

(cause by repeated trauma ; septic bursitis is caused by a wound infection)
Epicondylitis
inflammation of a tendon where it attaches to a bone.
Tennis elbow ; aka lateral epicondylitis
Golfers elbow ; medial epicondylitis
Review SLIDE 43 -
it shows tendinopathy and bursitis (like the pictures of it)
Muscle Strain
is the sudden, FORCED motion causing the muscle to become stretched beyond it's normal capacity.

(LOCAL muscle damage, they can also involve the tendons)
Osteoporosis
It's porous bones, they are poorly mineralized bones.
Our bone density : 833 mg/cm2
Osteopenic bone: 833 to 648 mg/cm2
Osteoporosis bone: < 648 mg/cm2
Causes of Osteoporosis:
Decreased levels of estrogen & testosterone
Decreased activity level
Excess intake of caffeine, phosphorus, alcohol, nicotine.
Inadequate levels of vitamins D & C, or Mg**

(bone density is secondary to bone CALCIUM being absorbed into the bloodstream than is deposited in the bone)

We look at it by reduced bone mass/density and an imbalance of bone reabsorption & formation.
(Bone histology is usually normal but it lacks structural integrity)

CM: pain later in the disease process
easy to fracture
loss of veterbral collapse causes kyphosis(hunch back) which causes diminished height.

Treatment: Goal is to slow the rate of calcium & bone loss.
regulate moderate weight bearing exercise ( the mechanical stress of exercise stimulates bone formation)
Oral calcium supplements.
Medications that inhibit bone reabsorption.
Osteomyelitis
it's the most often caused by a staphylococcal infection.
(most common cause is open wound ; exogenous)
(blood-borne infection ; endogenous)
Osteomyelitis - CM & Treatment
CM: acute, and chronic inflammation
fever, pain, necrotic bone.

Treatment: very difficult to treat ; use antibiotic, debridement, surgery, hyperbaric oxygen therapy.
Review SLIDE 19 -
Shows the stages of OSTEOMYELITIS
Read slide 21
it's inflammatory vs noninflammatory joint disease
Osteoarthritis is the degeneration and loss of articular cartilage, sclerosis of bone underneath cartilage, and formation of bone spurs ; osteophytes.
also referred to as degenerative joint disease.
incidence increases w age.

PRIMARY DISEASE ; it's idiopathic
Risk factors - Osteoarthtits
increased age ; older ppl.
joint trauma, long term mechanical stress.
endocrine disorders ; hyperparathyroidism
drugs
obesity
CM: Pain, stifness, enlargement of the joint, tenderness, limited motion and deformity

Characteristics : local areas of damage and loss of articular cartilage, new bone formation of joint margins, subchondral bone changes, variable degrees of mild synovitis and thickening of the joint capsule.
Rheumatoid Arthritis
it's a chronic inflammatory autoimmune joint disease.
SYSTEMIC AUTOIMMUNE damage to CT, PRIMARILY in joints (synovial mem.)

(similar cm to osteoarthritis)
Cause : unknown, strong genetic predisposition.
With Rheumatoid Arthritis, there is a presence of rheumatoid factors (RA or RF test)
- antibodies (igg, and igm) against antibodies
(so like normal antibodies become antibodies and ATTACK the joint.)

So if we see our autoanitbodies like the igg, and igm in our serum it indicates Rheumatoid Arthritis.
we also see joint fluid w inflammatory exudate.
PATHO - Rheumatoid Arthritis
1. Neutrophils & other cells in the synovial fluid become activated.
2. Inflammatory Cytokines (tumor necrosis factor-alpha, interleukin-1 beta, interleukin-6, interleukin-7, etc induce enzymatic BREAKDOWN of cartilage and bone.)
3. T cells also interact w synovial fibroblasts through TNF, converting synovium into a thick, abnormal layer of granulation tissue ; pannus.

(THIS WHOLE PROCESS talks about our IMMUNE RESPONSE ATTACKING THE SYNOVIAL MEMBRANE AND THE JOINT.)
CM: RA
insidous onset, begins w systemic manifestationd of inflammation, fever, fatigue, weakness, anorexia, weight loss, and generalized aching and stiffness.

Over months/weeks, joints become painful, tender, stiff, warm, boggy and lose range of motion.
(see joint deformities)

Evaluation: LOOK AT SLIDE 32
main one RHEUMATOID NODULES.
These are a collection of inflammatory cells surround a central core of cellular debris.

RA tends to affects joints bilaterally.
GOUT is a metabolic disorder that disrupts the body's
control of uric acid production or excretion.

(You'll see high levels of uric acid in the BLOOD and other body fluids ; occurs when the uric acid concentration increases to high enough levels to crystalize)
So now we have these crystals deposit in CT throughout the body - GOUT
It's 50% of the initial attacks occur in the metartarosphalngeal joint of the great toe. ; heel, ankle, instep of the foot, knee, wrist, or elbow.

(When these crystals are in the SYNOVIAL JOINT, this inflammation is called GOUTY ARTHRITIS.)
Gout is related to WHAT
Purine(adenine & guanine) metabolism....

Patients can have accelerated purine syntheses, breakdown or poor uric acid secretion in the KIDNEYS
GOUT - These are the mechanisms where the crystals will be deposited, and also the RISK FACTORS:
Deposition: Lower body temp, decreased albumin or glycosaminoglycan levels, changes in ion concentration and PH, trauma.

Risk factors: male sex, increasing age, high intake of alcohol, red meat, and fructose, "used to be called a royalty disease, because back in the day they were wealthy enough to consume these foods", drugs.
Clinical Stages- GOUT
1) Asymptomatic hyperuricemia
2) Acute gouty arthritis
3) Tophaceous Gout

(go to page 1019 - NEED TO KNOW)
CM- GOUT
increase in serum urate concentrate ; hyperuricemia
recurrent attacks of monoarticular arthritis (inflammation of a single joint)
Depositions of monosodium urate monohydrate(toph) in and around the joints.
Renal disease involving glomerular, tubular, and interstitial tissues & BV)
Formation of renal stones.
CM: acute gouty attack
severe pain especially at night.
hot, red tender joint

(signs of a systemic inflammation)
-increased sedimentation rate, fever, leukocytosis
REVIEW SLIDE 23
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