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Anatomy

Musculoskeletal Sysytem Components:


Skeletal muscles, bones, joints, tendons, ligaments, 1.) Area of resting cells- uppermost near
bursae epiphysis; not active.
206 bones 2.) Zone of proliferation- active cells
Axial Skeleton (80) - growth of long bones begin.
-skull, vertebral column, thorax 3.) Area of hypertrophy- cells are swollen.
Appendicular skeleton (126) - metabolically inactive.
− extremities, shoulder, pelvis - epiphysial fracture separation in children.
Functions: 4.) Area of provisional calcification-
Framework Extracellular matrix hardens.
− Protection - arrest of bone calcification.
− Movement − deformity formation.
− Hematopoietic fxn.
− Storage of Ca and Phosphate Joints or Articulations
Bone Classification: − point where to bones meet.
• Long Bones (femur, radius, ulna, numerous) − Provides stability and mobility.
• Short Bones (carpals, tarsals, spongy) Joint classification
• Flat Bones (skull, cranium) 1.) Fibrous/ Synarthrodial- none movable.
• Irregular Bones (vertebrae) − Sutures- thin layer of fibrous tissue that
binds together interlocking flat bones.
Type of Mature Bone: e.g: skull bones in children
1.) Cancellous (spongy bone)
- interior
− Syndesmosis- consist of interrosseous
membrane/ ligament between the
- with trabeculae/ spicules
bones.
- lattice like network
e.g (in between) radius and ulna
- osteogenic cells- nagbubuild ng bone.
tibia and fibula
- filled with red and yellow marrow
*Red- hematopoietic function. − Gomphosis- conical projection is held
*Yellow marrow- fracture, emboli formation. there by a ligament .
e.g teeth held in maxilla/ mandible
* not movable
2.) Compact (cortical bone)- peripheral
2.) Cartiligenous/ Amphiarthroidal- minimal
- forms the outer shell
movement.
- densely packed calcified I.C matrix
- more rigid
Synchondoses- entire joint is covered by hyaline
- major component of tubullar bones.
cartillage.
Parts of a long bone:
e.g: costochondral joint (junction ng ribs, 9
cartilages- during breathing)
Epiphysis
Symphisis- joints have a fibrocartilage connection
between the bones and a thin layer of hyaline
cartilage covering the articular suface.
Diaphysis
e.g: symphisis pubis, intervertebral disk. (during
delivery)
Epiphysis 3.) Synovial/ Diarthrodal- allows free
movements of joints.
-consist of joint cavity and hyaline cartiage over
Nutrient Foramen: where nutrients are stored in the articular surface.
bone.
• Joint capsule- has rich nerve supply sensitive
Epiphysial Plate/ Growth Plate to pain, friction.
− region of longitudinal growth -sensitive to rate and direction of motion,
− disappears during skeletal maturity. compression, tension, vibration and pain.
-synovium
- joint swelling fluid increase here.
• Synovial Fluid- super filtrated plasma from History:
BV. Produced by synovial membrane. Medical Hx:
- fxn: lubricant, source of nourishment − identify infectious disease
− immunizations (OPV, Tetanus)
Characteristics of synovial fluid: − major illnesses/ hospitalization
a.) clear/ straw colored − medications
b.) non-clotting − lifestyle and daily activities
c.) 1- 8 ml Physical Exam:
d.) viscous − perform a head to toe assessment.
e.) WBC < 200 cells/ ml − Nurses need to inspect and palpate.
f.) synovial cells, phgocytes − Assess joint and muscle tone/ mov't
Types of freely movable joints:
− usually tape measure and protractor
− hinge- flexion and extension (goniometer- measures angle, ROM the
− pivotal- neck patient is able to do) are the only
− ball and socket- shoulders instruments.
− ellipsoidal- carpals Inspection:
− saddle joint − size, symmetry, swelling
− gliding joint- ankle, between tarsal joints − pigmentation, rashes. Scars
Tendons and ligaments − color, texture of the skin
- dense connective tissue structures − distribution of body hair
− connected to muscles and bones − assess pulses and arterial circulation. (Allen's
test)
a.) Tendon- muscle to bone. − CREPITUS- audible/ palpable because of
b.) Ligaments- bones to bone rubbing- grating sound ex. Fracture
c.) Bursae- closed sac formed by synovial membrane
− subcutaneous nodules
-contains synovial fluid
− gait, positive, muscular palpation, joint
palpation, ROM, muscle strength
*bursa- a small fluid-filled sac lined by synovial
membrane with an inner capillary layer of slimy
Diagnotic tests:
fluid (similar to that of an egg white). It provides a
cushion between bones and tendons and/or muscles
1.) Radiographs- most common lab
around a joint. This helps to reduce any friction
X-ray- handle area carefully
between the bones and allows free movement.
Bursae are filled with synovial fluid and are found − pain meds as ordered
around almost every major joint of the body; when − remove jewelry
they become inflamed, the condition is called − shield-pregnant may undergo but needs
bursitis. to wear shield
− lie still
d.)Cartilage- firm but flexible type of connective − inform patient that exposure to radiation
tissue (ear) is minimal and not dangerous.
-produced by chondrocytes. − Protect yourself wear apron/ shield.
- 65-80% weight 80% wt is H20 (no blood vessels) 2.) Arthrocentesis
Types: - needle is inserted into the joint and fluid is
a.) Elastic cartilage- ears withdrawn.
b.) Hyaline cartilage- most abundant and most Ex: swelling of joint –to lessen swelling
common.
− covers the load bearing portion. NR: - informed consent- invasive procedure
− Cartilage of fetal skeleton. - meds may be instilled into the joint to alleviate
− Adults: costal cartilages, respiratory tract, pain.
epiphysial plates − compress bandage
c.) Fibrocartilage- intermidiate between dense and − rest the joint 8-24 hours
hyaling cartilage − Notify MD- if ever joint swelling (infxn.)
e.g: intervertebral disk; symphisis pubis (pagka nagka impeksyon=osteomyelitis means may
staph aureus) 3.) Reinforce use of crutches for 5-7 days.
4.) Elevate extremity as often as possible for 2
3.) Arthrogram days.
- radiographic examination 5.) Ice compression
− 3 punctures 6.) Notify MD- fever, knee pain, edema > 3 days.
− use of contrast medium/ air
− series of x-rays is taken as the joint is moved 6.) Dual Energy Absorptiometry (DXA)
through the ROM - bone marrow density scan is a low dose x-ray w/c
NR: checks an area of the bone such as the hand and
1.) Ask patient to void. foot for signs of mineral loss and bone thinning.
2.) Tell patient that procedure is long.
3.) NPO 8 hours 7.) Bone Scan
4.) Informed consent - imaging study with the use of a contrast
5.) Allergy to iodine/ seafood- dye radioactive material- needs consent.
6.) Remain still unless when asked to reposition. -pretest: painless procedure, IV radio isotope is
7.) Minimize use of joint for 12 hours. used, pregnany is contra indicated.
8.) Joint will be edematous for 1-2 days- ice -Intra test- holds fluids for 4 hours before
pack procedure, isotope injection, 32 oz of H2O
9.) Pain meds have patient void after 1-3 hours scanning is
10.)Use of bandage for -4 days performed—to eliminate excess radioisotope.
11.) Crepitus may be felt for up to 2 days—notify Post test- increase Oral fluid intake to flush out
physician if more than 2 days. radioactive material, monitor injection site for
redness, swelling, tenderness.
4.) Bone Marrow Aspiration
− usually involves aspiration of marrow to BONE PHYSIOLOGY
diagnose disease like leukemia, aplastic Histology
anemia. Structural Elements of the Bone:
− Usual site is the sternum and iliac crest.-- 1.) Bone Cells- osteogenic cells (in periosteum,
rich supply of red marrow. endosteum, epiphyscalplate)
Early-tubular bone 2.) Bone Matrix
As we grow- iliac, sternum - ground substances (minerals—Ca & Phosphate)
- collagen-type 1 (most common)--skin, eyes, thin
NR: collagen, blue sclera
1.) Asceptic Technique - glycoprotein
2.) Pretest: consent • Collagen Fibers- 90-95%
Intratest: needle puncture may be painful - provides tensile strength for bone.
(infection) • Ground substance- hemogenous gelatinous
Post test: Maintain pressure dressing and WOF medium
bleeding. - proeoglycans, chondroin sulfate and hyaluronic
3.)Monitor signs for bleeding after. acid.
- Helps control deposition of Ca salts/ Ca
5.) Arthroscopy * Osteogenic Cells- differentiate into osteoblats.
-a direct visualization of joint cavity; invasive (found in: periosteum, endosteum, epiphysial plate)
- pretest: consent, explain procedure, NPO for at - active during normal growth—imp. in children.
least 8 hours prior to procedure—instruments are − activated during fracture healing
inserted to knee joint.
-Intra test: sedative, anesthesia, incision will be osteoBlast- Builds Bones
made. fnx:
-post test: maintain dressing, ambulation as soon as A- produce Alkaline phosphatase
awake, mild soreness of joint for 2 days, joint rest B- resp. for Bone matrix
for few days, ice application to relieve discomfort. C- resp. for Collagen Calcification
NR:
1.) Elastic wrap 2-4 days. *osteonic/ haversian canal-channel for exchange of
2.) Walks w/o wght bearing once sensation nutrients
returns but limit activity for 1-4 days. *frequent fracture- increase because it will be
released on the system. dihydroxycholecalciferol
• Ca as transport mediator for the transport.
OsteoCyte- Old,MatuRe bone cells -decrease renal Ca and Phosphate excretion
MONOCYTIC MACROPHAGIC LINEAGE -Increase Vit. D bone absorption
-maintains bone matrix -Decrease vitamin D- bone calcification, RICKETS
-release cut in the blood
-acts as chemical pathways SUMMARY:
* Lacuna- has EC fluid
* Canaliculi- conections to osteocytes
(all in haversian canal)

osteoClast- chewing cells- eat up bone- soft bone


− by producing citric and lactic acid
- collagenases
- comes from monocyte- macrophage lineage

Ca+ (9.4 mg/dL) Phosphate (4 mg/dL)


CAL SYAM FOUR PHATE

Importance of Ca: (main stimuli for PTH release)


1.) Contraction of muscles. (exchange of Na and
Ca= action potential for contraction)
2.) Blood clotting.
3.) Transmission of nerve impulses.

• HYPERCALCEMIA- would lead to CNS


depression
12 mg/ dL- depressive effects.
15 mg/ dL- marked depressive effects.
17 mg/ dL- parathyroid poisoning. (excessive
Ca will go to diff. Parts of the body)

• HYPOCALCEMIA- CNS excitation


-carpapedal spasm (twitching of the hand), tetany

Calcium in Plasma: 3 forms


1.) Protein-bound
2.) Non- ionized Ca
3.) Ionized Ca- most useful in body

1 L of milk- 1000 mg Ca+ Phosphate

Role of Vitamin D
-has hormonal effect
-potent effect in increasing Ca absorption in the
intestinal tract
-promotes phosphate absorption- by the intestine
• direct effect of 1, 25-
*HYPOPARATHYROID=HYPOALCEMIA

Calcitonin -peak bone mass-30 years-35 years


- hormone secreted by para follicular cells or C cells -after peak years=Ca stored in spongy bone
of the thyroid gland. leaves tissue that leads to decrease cancellous
− Opposite effect to that of PTH. (spongy)
− Increase in plasma Ca concentration—
calcitonin secretion
− Decrease concentration by: bone trabeculae decrease in # and width
1.) Decrease activity of osteoclast (shifts towards
bone deposition)
2.) Decrease bone formation or new osteoclasts marrow spaces are widened
− has weak effect
− PTH overrides the calcitonin effect
decrease cortical mass
− greater effect in children- vit. D deficiency

METABOLIC BONE DISEASES


bone mass further decreased
* Osteoporosis
* Osteomalacia
* Rickets
* Paget's Disease/ Osteitis Deformans − in men: rate of bone loss 0.&7% per years
− starts wih higher bone density
1.) Osteopenia − age 90: 17% of male has hip fracture (wt.
− common to all metabolic diseases. bearing areas)
− Low bone mineral density 32% of females has hip fracture
− term used to describe an apparent lack of − Role of TESTOSTERONE: has ANABOLIC EFECT
bone mass. TO BONE
- increase muscle mass=higher bone density
− Seen on x-ray studies
- converted to estrogen w/c prevents excessive
− risk for fracture
bone resorption.
− reduction in bone mass greater than
expected for age, sex or race
2.) Osteoporosis
− In ESTROGEN: decrease estrogen
− Imbalance between bone resorption and
bone formation
inc. cytokines
Reduction of bone mass production of osteoclast inc. osteoclast
differentiation (bone
Increase in bone fragility chewing)
Incidence: women> men loss of trabecular bone mass
− 1 in 3 women over 50 year
− 1 in 8 men over 50 year CLASSIFICATION OF OSTEOPOROSIS:
− affects all races, common in whites (kasi 1.) Type 1/ Postmenopausal Osteoporosis
malaki ang bone structure ng blacks) (more common type aka: SENILE
OSTEOPOROSIS)
Risk Factors: genetic 60-80% - no other underlying med. Condition
− life style—x exercise, diet - loss of trabecular bone
− hormonal & metabolic - predispose to fractures of the vertebrae and distal
− other illness: prob in PT gland radius and hips.
− Anthropometric(Age)- short stature 2.) Type 2 Osteoporosis
− Dietary- coffee, smoking, steroids - secondary osteoporosis
− Drugs - with underlying condition (hyperparathyroidism,
deficiency in diet)
premenopausal: 1000 mg Ca.
Postmenopausal: 1,500 mg Ca, Vit D
supplementation
BONE REMODELLING − Vit D
− Wt. bearing exercises- best is walking
osteoblast osteoclast − fall prevention prone to have fractures (hip
usually)
− mobility in hazard free env't
Bone Remodeling
− eliminate throw rugs in home
− use of body mechanics
− use of shower chair and hand rails when
- mechanical stress
bathing
- PTH & 1,25 dihydroxycalciferol
- calcitonin − use cane and walker as directed to decrease
- growth hormone work load on hips and knees
*cane on unaffected side
PATHOPHY: * move the cane at the same time as the
affected leg
Genetic Factor − use well- fitting, supportive shoes when
ambulating (no heels)
Physical PEAK BONE MASS Nutrition
Ability PHARMACOLOGIC MGT.:
1.) Anti-resorptive Agents (EBC)
Estrogen- mimic effect of estrogen in the bone
by reducing bone resorption.
- Selective estrogen receptor modulators. Given
Menopause Aging with PROGESTIN.
- S/E: leg cramps and hot flushes

Bi Phosphates- increase bone density and


OSTEOPOROSIS restores lost bone
- decrease incidence of fracture
ASSESSMENT: - ALEDRONATE (FOSAMAX)- 30 min rule
Subj: Weakness, pain H2O 30 MIN before food or other meds.
Obj: fracture, dec. in height, diff. Bending over, AVOID LYING DOWN for 30 min.
“DOWAGER HUMP”(prominence of cervial spinal - PAMIDRONATE- pain reliefs
vertebrae), obvious bone loss, dec. in height. - given IV (D5W/ NS)
- monitor tingling around mouth
DIAGNOSIS:
− P.E: non-specific Calcitonin- reduce bone resorption
− serial height measurement- ideal but not - slows decline in bone mass.
done - IV or intranasal
− no definite lab examination - give in the evening
- S.E: rhinitis
− x-ray- increase radiolucency, 25-30% bone
- hindi pwede mag breakfats pag nagtake nito
loss (to rule out fracture)
- Ca carbonate- 30-60 before meals
− Dual x-ray absorptiometry- Gold Standard,
2.5 SD below the young adut mean.
2.) Anabolic Agents- PTH, testosterone
MANAGEMENT:
* Prevention and Early detection
− Identify person in high risk group 3.) Osteomalacia (in adults) Rickets (in
− ABONE children)
* A- age 65 y/o and older CAUSE: Vit D deficiency
B- bulk- < 140 lbs. At menopause - inadequate intake of vit. D
ONE- never on estrogen for > 6 months. - malabsorption of vit. D.
− Adequate Nutrition
- inadequate exposure to sunlight DIAGNOSIS:
- intestinal absorption Laboratory
- inherited impairment of bone tubular reabsorption − BUN and Crea- for kidney function
of Phosphate. − Serum Ca- N or Low
- Hepatic or renal dse, malfunctio of PT gland − Serum Phosphate- inc. kasi narereabsorb
yung phosphate
− First 2 decades of life- skeleton undergoes − Alkaline phosphatase- inc. (in bone matrix)
continuous growth. − X-Ray- pseudofractures
- deposition> adsorption
- Looser's Zones- confirms the dx.
− At Puberty- growth plate stop dividing. - indicates reduced bone
- epiphysis & metaphysis fuse ossification.
− Bone Remodelling: - Pseudofractures (Milkman's Syndrome)
PHASE 1 (activation)
stimulus----bone cell precursor----osteoclast formation PATHO:
PHASE 2 (resorption)

osteoclast forms cutting cone“

bone resorption

formation of resorption cavity


PHASE 3 (formation)

lying down of new bone in layers (lamellae)

resorption cavity is reduced

narrow haversian canal

old haversian sys. Is destroyed

formation of new trabeculae (humihingi pa ng new scoop of


ice cream)

*OSTEIOD FORMATION- (new bone, affected during


rickets, sing lambot ng ice cream)

no mineral calcification and bone deposition

bone volume remains unchanged

replace bone consist of soft osteiod bone

Causes:

Inadequate dietary intake of vit. D (fat soluble)


Malabsorption of Vit. D
Inadequate exposure to unlight
Intestinal malabsorption
Intestinal impairment of renal tubular reabsorption
of phosphate.
Hepatic/ Renal Dse.
Malfunction of parathyroid gland.
bones, 24 urine collection—inc. In bone breakdown
− Increase serum Ca
− Increase in Alkaline Phosphatase
MANAGEMENT: − Anemia
− treat the cause
− diet MANAGEMENT:
− vit. D supplements 1.) Implement and Assess effectiveness of pain
− supplemental Ca relief measures
− adequate sun exposure a.) Heat therapy
− with tx, prognosis is good b.) Collaborate with PT or OT
− osteomalacia, bone deformities usually 2.) Encourage client to remain active
disappear 3.) Assess for s/sx of hypercalcemia—CNS
− Rikets, deformities usually persist. depression
4.) Instruct patient to increase OFI to 2-3 L/day
4.) Paget's Disease- osteitis deformans to enhance excretion of Ca.
-most common bone disease 5.) Instruct n safety to prevent pathologic
-slowly, progressive met. Bone disease fractures.
-accelerated patterns of bone remodelling 6.) Assist to adaption to hearing/ vision loss—
-incidence: male> female cranial nerve compressed.
DRUGS:
− > 40 y/o
- Etidronate
− CAUSE: unknown, no definite hereditary
- Calcitonin
pattern.
- Pilcamyin, Mithramy (Antibiotics)
− Theory: an early viral infection causes a -dec. Se Ca
dormant skeletal infection that erupts as - urinary hydroxyproline
Paget's disease. - dec. Se Alk Ph
− Other possible causes: - Pain Meds
* benign/ malignant bone tumors SURGERY: correct deformities, relieve neurologic
* Vit. D deficienccy during the bone developing yrs. impairment.
* Autoimmune disease
* estrogen deficiency
5.) Gouty Arthritis
accelerated bone remodelling---excessive resorption - MONOARTICULAR
- met. Disorder
- intermittent course
- increase in serum uric acid
AB bone formation - great toe—greatest affectation
− disorganized collagen fibers - good prognosis with tx.
− dec. glycoprotein - INCIDENCE: male> female
− trabeculate thickened andenlarged - 4th to 5th decade
- familial incidence

-assymptomatic for years TYPES:


-bone pain 1.) 1 gouty- idiopathic, inherited- metbolic
-cranial enlargement 2.) 2 gout- acqured
-pressure on the N
-skeletal deformities
-WADDLING GAIT- parang duck, pathologic fractures uric acid form

DIAGNOSIS:
X-Ray: increase bone expansion and density diet nucleotides
Bone Biopsy: Mosaic pattern Purine
Labs: xanthine oxidase
- Increase Hydroxyproiine (will tell the rate of bone Hypoxanthine
resorption, opposite ng alkaline phosphatase) in
Xanthine
Chronic topheous gout, repititive precipitation of
Uric Acid---excretion: intestine, kidneys urate crystals

uncrust articular surfaces


Uric Acid: Charac. Of monosodium urate crystals
1.) Precipitate at the periphery of the body. visible deposits in synovium
2.) Trauma promotes urate crystal precipitation.
3.) Changes in ion concentration and decrease in pH synoviumis characterized as: hyperplastic, fibrate,
enhances urate deposition thickened
N Level in MEN: 5.1 (+/-) 1 mg/ dL
WOMEN: 4.0 (+/-) 1 mg/ dL articular bone erosions

CLINICAL STAGES: tophi formations (nodules, non- tender)


1.) Asxmatic Gout- absence of sx., inc. UA 9-10
mg/dL large ulcerations of overlying skin
2.) Acute Gouty- sudden onset of painful swelling
and tenderness of great toe. 2 joint degeneration gouty neuropathy
- MONOARTICULAR (only 1 joint is affected)
- Fever (due to swelling) DX. TEST:
- Precipitated by trauma, alcohol, stress - Serum UA> 7.5 mg/dL
3.) Intercritical stage- no sx. For month to years - WBC and ESR- because there is increase cell
- repeat attack if not treated turnover
- permanent changes - 24 hour urine
4.) Chronic gout- urate continues to expand - synovial fluid analysis- (+) uric crystals or
- tophi monosodium urate crystals or Arthrocentesis- will be
-acute attack cloudy
- chalky discharge MANAGEMENT:
Risk Factors: age 1.) Diet: organ meat, wine, aged cheese—not
duration of hyperurecimia allowed, eat in moderation: mushroom, spinach,
genetic cauliflower, asparagus, poultry, beans, peas
heavy alcohol consumption - limit alcohol intake
obesity (r/t intake of excessive protein) 2.) Assist with reduction- gradual- to lyse cellular
content of body.
Asxmatic Hyperurecemia 3.) Instruct on strict CBR for 24 hours of acute
attack
Precipitation of MSU crystals in joint fluid 4.) Local application of heat and cold for pain.
5.) Provide bedstradle to relieve pressure from linen
urates in joint become super saturated at affected area.
6.) Administer meds as ordered
microtophi synovial lining and joint cartilages - instruct patient on med regmen
- instruct patient to increase OFI to 3L/ day
release of crystals - emphasize that prognosis is good with tx
compliance
Acute inflammatory response *not all patients wit gouty attack will experience
gouty neuropathy.
lysosomes free radicals MGT.:
G- up 3 L fluids/ day, Gulp no alcohol
increase inflammation O- organ meats not allowed
U- urine output increased to 2 l/ day
acute arthritis –pain, fever T- teach bed rest
COMPLICATIONS:
crystalization abates many crystals resolubilized 1.) Joint Deformity
2.) HPN
acute attacks remits—asxmatic intecritical pd. 3.) Kidney Involvement
MEDS: Acute attack erosion of articular cartillage
1.) NSAIDS
2.) Corticosteroid underlying bone is unprotected
3.) Aspirin
Uriosuric thickening and hardening of bone underneath
1.) Probenecid cartilages
2.) Sulfinpyrazone

6.) OSTEOARTHRITIS cartilage flakes invades synovium—synovial fluid


- POLYARTICULAR forced into defects—cyst formatio
- non- inflammatory
- chronic, slowly progressive
- disorder of movable joints irritation of synovial fluid
- “wear and tear” arthritis- kasi sa matatanda
nakikita fibrosis
- previously, “degenerative joint disease”
- incidence= male and female affectation up yo age limitation of/ in joint most/ joint stiffness
55, increase in female (because of menopause) after
this time. ASSESSMENT FINDINGS: S/SX
RISK FACTORS: 1.) Joint pain
1.) Increase Age 2.) Joint stiffness
2.) Obesity- increase weight 3.) Funx. Joint impairment limitation
3.) Repetitive use of joint with previous joint 4.) Joint involvement is assymetrical
damage 5.) Not systemic, no fever, no severe swelling
4.) Anatomical Deformity- clubfoot 6.) Atrophy of unused muscles
5.) Genetic susceptibility 7.) Usual joint are the wt. Bearing joints
6.) Occupational Overuse S/SX: Crepitus
-ex: nurse laging nakatayo − Heberden's Nodes (distal, before kuko)and
7.) Sport and recreational activity Bouchard's nodes (knuckles, interphalangeal
8.) Racial Differences joint)
TYPES: − Joint enlargement
1.) 1 or Idiopathic- most common − Altered gait
- aging, genetic DIAGNOSTIC FINDINGS:
- most common affected (joint: wt bearing joints) 1.) X-ray- narrowing of joint spaces
(knees) - loss of cartllage
2.) 2 OA- repetitive strain, sprain, joint - cyst like deposits
dislocation and fracture - osteophytes (spur) formations
-certain meds 2.) Blood tests will shw no evidence of systemic
ex: steroids-kasi maedecrease yung bone mass inflammation and are not useful
- traumatic arthritis GOAL OF MGT.:
1.) Relieve pain
Aging genetic—changes in chondrocyte fxn. (produce 2.) Maintain/ Improve mobility
cartilage, gives strenghth to bone N in type 2) 3.) Minimize disability
MEDICAL MGT.:
decrease amount of type 1 cartilage is laid down 1.) Wt reduction.
2.) Use of splinting devices to support joints.
change in collagen fiber, diameter and orientation 3.) OT and PT
4.) Pharmacologic mgt.
joint cartilage deteriorates - paracetamol, NSAIDS, topical analgesics (minimal
amount only), intra- articular, steroids to decrease
narrowing of joint spaces (nababawasan yung H2o inflammation.
content)
NR:
mechanical injury 1.) Provide relief of pain.
- Administer prescribed analgesics
- Application of heat modalities: Ice packs in acute
stage
- Plan daily activities when pain is less severe. stimulates inflammatory response
- pain meds before exercising
2.) Advise px to reduce wt
3.) Administer meds neutrophils and macrophages
4.) Position px to prevent flexion deformity
- use of foot boards, splint, wedges and pillows
5.) splints not used for prolonged pds. Phagocytise the immune complexes

Specific care for Arthritic Joints:


Hand- hot soaks releases lysosomal enzymes (destroys joint
- parafin dips cartilages)
Lumbar and Sacral spine- firm matress
- bed board destructive changes in joint cartilage
Use of cervical collar- check for constriction
-watch for skin redness continued presence of immune complexes
Hip
- moist heat packs
-assist with ROM synovial membrane hypertrophies and thickens
- strengthening exercises
-heck proper fit crutches, canes, braces
Knee- assist with ROM blood supply to area occluded
-elastic support braces

7.) Rheumatoid Arthritis


- POLYARTICULAR SYMMETRICAL cellular necrosis
- chronic, progressive, systemic, autoimmune with
inflammation
- INCIDENCE: Females> Males vascular granulation tissue formation
Middle age group (35-45)
Genetic link
STAGES OF RA: pannus
1. Localized Inflammation
- thickening of tissue
-edema and congestion extend into joint capsules and subchondral bone
2. Pannus formation (granuloma tissue)-
layer of inflammatory granulation
tissue- connective tissues only bone destruction
3. Fibrous Ankylosis- fibrous tissue is
invaded with tough fibrous tissue
that is converted to scar tissue. inflammatory process extends to tendons and
4. Bony Ankylosis- fibrous tissue calcify ligaments
and change into osseous tissue

bone destruction
genetic predisposition + Immunologic trigger
(rheumatoid factor)
inflammatory process extends to tendons and
ligaments

CD4 helper T-cells

Fibrous adhesions
formation of immune complexes
MEDICAL MGT:
joint immobility 1.) Aspirin and NSAIDS- main stay tx. To reduce
inflammation.
DIAGNOSTIS CRITERIA: 2.) Chemotherapy with Methofrexane, anti-
S welling/ effusion: 3/ more joints malarial, gold therapy and steroid.
S ymmetric 3.) For advanced cases: arthroplassty (repair of
W rist- MCP, PIP- proximal interpharengeal joint joints), synovectomy (removal of affected
A AM stiffness synovium)
N odules (Rheumaoid Nodules) 4.) Nutritional Therapy
GOLD THERAPY (obsolete)
P ostive Rheumatoid Factor -IM oral prep
E rosion/ decalcification on x-ray - takes several months (3-6) before effect can
*should be present at least 6 months be seen
-can damage the kidney and cause bone marrow
Joint Deformities: depression
S wan neck- PIP-DIP 5.) may not work for all individuals
U lnar drift- medial (papasok) NSG. MGT.:
B outonniere deformity- flexion of PIP and 1.) Relieves pain and discomfort
hyperextension of DIP (boto boto) - use splints to immobilize the affected
extremity during acute stage of the disease and
Rheumatoid Nodules: non-tender subutaneous inflammation to reduce deformity. (cold packs
nodule. and heat packs) Administer meds
− olecranom bursae, fore arm, over the areas. 2.) Decrease px fatigue.
- schedule activity when pain is less severe.
DIAGNOSTIC TESTS: - provide adequate rests.
1.) X-ray- minimal changes early stage 3.) Promote restorative sleep.
- narrowing or joint spaces 4.) Increase patient's mobility
- bone erosion - advise proper posture and body mechanics
- bone deformities evident bilaterally. - support joint in fnx. Position
- advise active ROM
ASSESSMENT: - avoid direct and over the joint
1.) Pain 5.) Provide diet therapy
2.) Joint swelling ad stiffness- symmetrical, - patient experience anorexia, nausea and wt.
bilateral Loss
3.) Warmth, erythema and lack of fnx. - regular diet with calorie restriction because
4.) Fever, wt loss, anemia, fatigue steroids may increase appetite
5.) Palpation of join reveals spongy tissue - supplements of vit, iron and protein
6.) Hesitancy in joint mov't 6.) Increase mobility and prevent deformity
ASSESSMENT FINDING: - lie flat on a firm mattress
* Joint involvement is symmetrical and bilateral. - lie prone several times to prevent hip flexion
* Characteristically beginning in the hands, wrist contracture
and feet. - use one pillow under the head because of risk
* Joint stiffness occurs early in the morning, of dorsal kyphosis.
lasts more than 30 minutes, not relieved by - no pillow under joint because this promotes
mov't, diminishes as the day progresses. flexion/ contraction
DIAGNOSTICS:
1.) Xray- shows bony erosion NSG. DX:
2.) Blood studies- (+) rheumatoid factor and ESR • Chronic Pain
and CRP and Anti-nuclear antibody (may • Disturbed Body Image
inflammation C reactive protein) • Activity Intolerance
3.) Arthrocentesis- shows synovial fluid that is • Self Care Deficit
cloudy, milky, dark yellow containing numerous • Powerlessness
WBC and inflammatory CHON. (kasi diba yung
neutrophils saka macrophages ineengulf yung
immune complex)
no pain
− uneven knees

RA OA

− onset is early − Onset is late


− chronic systemic disease − degenerative disease
− involves the synovium − Involves the cartilages
− involves joints are symmetrical, fingers, − involved joints are unilateral- wt bearing,
cervical spine knee, hips, spine
− malaise, fever. Anemia − no other s/sx systemic
− joint tenderness, swelling, warmth and − crepitus, stiffness in the morning
redness − dec. after activity
− sub nodules − rest the joints, avoids over activity, wt.
-rest the joint, cold and heat modalities, ASA, Reduction, cold and warm modalities, ASA
NSAIDS
− uncorrected: “duck waddle”, limp
SKELETAL DISORDERS IN CHILDREN: Other Assessment findings:
1.) DDH (Developmental Dysplasia or the Hip) 1.) Limitation of hip abduction
- formerly: congenital dislocation of the hip 2.) Asymmetric # of thigh skin folds (at the
- truly congenital back)
- description of an array of hip problems to 3.) Shortening of extremity.
describe shallow acetabulum, hip dislocation or 4.) Audible hip clicks.
sublaxation
- Incidence: First born (60%) Barlow Test- provocative test (suspicion only)
- females > males − dislocate an unstable hip
- < 3 y/o 1.) Stabilize pelvis with 1 hand.
- breech presentation 2.) Flex and adduct hip applying a posterior force.
CAUSE: unclear 3.) After release of posterior or force, hip relocates
1. Large neonates and twins spontaneously.
2.) Maternal Relaxation- hormone release when
pregnant=relaxes structure of pelvic muscle— Ortolani Test- reduce the recently dislocated hip
relaxation of joint ligaments in the fetus. − 1-2 mo. Of age *pag > 2 mo. Wala nang
3.) Breech presentation (30-50%) fibrous tissue
- rarely dislocated but “dislocatable”
− thigh flexed, abducted
− femoral head lifted anteriorly in acetabulum
extreme hip flexion limitation of hip motor
− reduction is felt as a “clunk”
stretching of already lax capsule and ligament
Galeazzi Sign- uneven knee levels when supine
hip dislocation infant's feet are placed together on the
examining table with the hips and knees flexed.

FORMS: Trendelenburg signs- child stand on his wt. On the


1.) Unstable Dysplasia- hip is positioned side of dislocation and lifts his other knee.
hormonally but can be dislocated by − the pelvis in the N side drops
manipulation. − child on his wt. On the N side, lifts his other
2.) Subluxation/ Incomplete Dysplasia knees
- femoral head rides on the edge of the − pelvis remains horizontal
acetabulum
3.) Complete dislocation- femoral head totally Imaging- to show location of the femur head and
outside. shallow acetabulum xrays, hip ultrasound- initially
kasi wala pang full development of hip.
ASSESSMENT: P.E
− newborn: no gross deformity MANAGEMENT:
• Birth - open in genital area allows normal urine bowel
- maintain hip in position of (flexion) and abduction elimination
-splint/ harness continuously for 3-6 mo, until hip is- maybe used to keep the hip joint of a child with
stable dev't hyperplasia.
− night splint. - made from fiber glass/ plaser
* 1-6 months - worn continuously 2-3 mos.
- with soft padding such as moleskin.
Pavlik Harness • 18 mo- 8 years
- harness has fabric straps and fasteners that fit - pelvis osteotomy/ femoral osteotomy
around baby's chest, shoulders and legs. - realign the pelvis
- harness holds the baby's legs in a spread position, deeper acetabulum
with the hips bent so that the thighs are around/
out to the sides. COMPLICATIONS:
- This keeps the head of the thigh bone (femur) in -avascular necrosis of the femoral head
the correct position in the hip socket for N dev't. - SOH tissue damage
- malformation / permanent disability
NR: - nerve injury/ arthritis
1.) Encourage N growth and dev't by allowing 2.) Leg- Calve- Perthes Dse
child to perform appropriate act. - coxa plana
2.) Reach parents to reapply harness - idiopathic osteionecrosis
3.) Explain rationale for maintaining abduction. - avascular necrosis
4.) Encourage parents to move child from one - osteochondritis deforman juvenelis
room to another- change of env't (stimulation) - incidence: males > females
5.) Encourage parents to touch and hold the - 2-12 y/o
child to express affection and reinforce security - 20% bilateral mean age of affectation:7 y/o
6.) Discuss modification in bathing, dressing and - cause: unknown
diapering with parents.
disturbance of irculation: decrease circulation
• sponge bath is recommended particularly in femoral head
• put undershirt under chest straps
• knee socks and leg pieces
• check skin area 2-3 times a day ischemia and necrosis of femoral head
• avoid use of lotion/ powder- irritation/
moisture
draw CHON impairment extend to epiphysis
• place diaper under strap
and aetabulum
• pad shoulder straps as needed
*road adjustment is not done by the parent MANIFESTATIONS:
*double diapering=hip extension 1.) Mild, intermittent pain anterior thigh
2.) Limp, painless limp
Bryant's Traction/ Divarication Traction 3.) Restriction in motion (activity intolerance)
− both extremities are held in traction 4.) Circulation/ proximal thigh atrophy (lumiliit
− 2-3 wks younger than 3y/o wt less than 35 kasi hindi nagagamit)
lbs (16 kg) 5.) Mild shortness of stature- blood supply to epi
gr plate
• Age 6-12 months
- hip spica cast X-ray
• Older than 18 months − cessation of CFE growth (caplial femoral
- surgical closed reduction epiphysis)
- immobilization with hip spica cast for 6-8 wks − subchondral fracture
− fragmentation
• Spica Cast − possibility of re- ossification
- hard covering over the waist, hips and legs that − healed/ residual stage
prevents mal of hips * local, self healing disorder
- bar bet. Legs strengthens cast tx goal- CONCEPT CONTAINMENT
1.) Non- Surgical containment a.) Congenital- idiopathic/ neurogenic
− 18 mo/ less 2.) -isolate abnormality
− abduction casts (nakabukaka yung patient) 3.) - single autosomal dominant gene
− scottish rite brace 4.) b.) Teratiologic- dissociated with
2.) Surgical containment neurovascular disorder
− Pelvic/ femoral osteotomy ex: myelodyplasia
− better outcome c.) Posistional- N foot that has been held in
deformed position while inside utero
− > 6 y/o
MANIFESTATIONS:
− done early before epiphysis becomes
a.) Variable rigidity of foot
necrotic
b.) mild calf atrophy
*expectant observation- < 6 y/o
calf and foot atrophy I older children
*intermittent sx tx
c.) Mild hypoplasia of the bones
-periodic bed rest / abduction stretching exercise.
ASSESSMENT:
*Definitive early tx:
1.) PE
1.) 6 years and older
2.) X-RAY- navicular bone (biggest bone most often
2.) Lateral portion of CE involved
affected.
3.) Loss of containment
NR:
MANAGEMENT:
1.) Teach parent's purpose, fnx, application and
1.) Non- operative
are of corrective device
-low success rate
2.) Importance of compliance
-serial casting after manipulation(until it returns to
3.) Continue to attend school
N. dennis brown every week change cast )
4.) Adaptation of school act may need to be
2.) )Operative
arranged with school personnel
-Soft tissue release
-naviaculectomy- removal bone metastasis
3.) GENU VALGUM and GENU VARUM
STAGES OF CORRECTION:
-N dev't of lower ext.
1.) Correct deformity
1.) Birth: greater bow legs
2.) Maintain correction until the foot regains N,
2.)18 mo: starts to straighten lower limb
muscle balance
3.) 3-4 y/o greater knock knees
3.) Observe foot closely for years.
4.) 7 y/o: straighten knock knees
4.) Sequential order
-causes* physiologic
-forefoot adduction
- N in utero positioning
-varus inversion
* thih posterior hip capsule
-plantar flexion
Bowlegs- 1st year of life spontaneous resolution with
N growth
NR:
2 years old- straight/ neutrally aligned ext.
1.) Stress to parents importance of prompt tx and
orthopedic supervision
Knock knees- physiologic
2.)Teach parents cast cae
− metabollic disorder (Vit D deficieny) 3. Emphasize need for long ter,m orthopedic
− N- 3-5 y/o: physiologic angular variation cae
− 5- 8 yo: n knee alignment 4.) Explain to older child that sx can iimprove club
GEN MGT: foot wit hgood n.
1.) Assess age of onset compared to N dev't but can not totally correct it
2.) Progression of deformity
3.) Assess diet 4.) PES PLANUS- flat feet
4.) aa\ssess for hx of trauma -neonates and toddlers
5.) X-ray – laxity in the bone ligaments complexes of the feet
TALIPES EQUINOVARIUS and far in
- 2 In 1,000 births the area of the medial longitudinal ligament
-male>female (2:1) -CAUSES: 1.) Tendo achilles contracture
-75% cases congenital 2.) Tarsal coalitions
-clubfoot
CLASSIFICATION: Neuromucular abnormality
Familial trait
-asxmatix in child
- no fxn limitations
-Radiologi eval.
-not indicated of asxymatic in child Fracture- a break in the continuity of the bone and
- no fxn. limitations is defined according to its type and extent
-Radiologic level. • severe mech .stress to bone—bone fracture
- not indicated if asyxmatic flat feet • direct blows
-dx. is not possible until after 6 y/ • Indirect blows-extreme muscle contraction,
TX: Conservative sudden twisting crushing force.
-indicated for N shoe wear TYPES
- medical logitudinal arc support 1.) Complete- involves a break across the entire
- sx: sub talar joint insert cross-section
5.) OTEOGENESIS IMPERFECTA 2.) Incomplete- the break occurs only through a
-brittle bone part of the bone/ cross section
-Type 3 more severe, multiple fracture, scoliosis -greenstick fracture
CAUSES: Genetic 3.) Closed- fracture does not cause break in skin
-chromosome 17 and & ___ 4.) Open- involves break in skin (compound fracture)
mutation in genes that det. The structure of
collagen * compression- bones crush a 3rd bone between them
(vertebrae)
Variation in assembly and maintenance of bone and * pathologic- occurs through areas of bone that have
connective tissue weakend (spontaneous break)
* stress/ fatigue- increase in activity
Pathologic fracture Impaired healing * greenstick- common in children one side bent one
side broken
TYPES:
-frequent fractures with poor healing • comminuted-involves prod w several bone
short stature fragments
- obvious deformities • simple- involves break into two part or more
- thin skin (proximal/ distal)
- bluish sclera
• Spiral fracture- child abuse
- Abtoth and enael devt.
ASSESSMENT:
- middle ear deafness
1.) Pain-continuous spasm hematoma formation,
-increase in serum alkaline phosphatase level
tissue anoxia
skin culture- de. Quality fibroblast-
2.) Loss of fnx.- abn. movt and pain
echocardiography – floppy valves
3.) Crepitus- grating sensation/ sound produced
INTENTIONAL INJURY-misdiagnosed
4.) Deformity- displacement, rotation of
-multiple fractures a various stages of dev't
fragments
posterior rib fracture
5.) Shortening
scapula, vertebrae clavicle
6.) Swelling and discoloration
*spiral fracture—abused
bilaterally slap marks/ mark bruising
P- ain
Intervention:
I- s swelling
-prevention of fractures
L- oss of fxn
-internal fixation stabilizaton and prevent
L- ength is decreased
deformities
A- different color
recent studiws : use of Biphosponates
Y- yes crepitus
(pamidronates)
− improve bone mass in all types of disorder DX. TEST:
− Scoliosis- lateral curvature of spine -x-ray- basic dx test
Emergency Situation:
1.) Immobilize- any suspected fracture
2.) Support extremity above and below when
moving the affected part from the vehicle
3.) Suggested temporary splints- hard board, 5.) sling—distribute weight evenly
stick, rolled sheets 1st 2 hours
4.) Apply sling if forearm fracture is suspected Restoration Ice
of the suspected fracture arm may be Compression
bandaged to chest. Embolism
5.) Open fracture- managed with clean sterile
gauze (to prevent contamination) Firm matress
6.) Do not attempt to reduce fracture. Foot drop (prevent)
ROM for unaffected extremities
MEDICAL MGT: Alignment
1.) Reduction of fracture either open/ closed, Complaications (evaluate)
immobilization and restoration of fxn. Trapez
2.) Pain meds and muscle relaxation, antibiotics, Urinary retention
pain medications Respiratory complications
3.) care for cast Evaluate for circulatory impairment
For open- administer antibiotics, tetany prophylaxis,
serial wound debridement. Admin drugs- corticosteoroids
-elevate extremity to prevent edema dopamine and morphine
-care f traction/ cast MGT: 1.) Immobilization of fracture
2.) Support to fractures bone during turning and
COMPLICATIONS: positioning
Early: shock 3.) 3adequate hydratin and electrolyte balance
fat emobolism 4.) minimal fracture manipulation
compartment syndrome • Early Complication: compartment syndrome-
infxn complication that develops when tissue
DVT perfusion in muscles is less req'd for tissue
Late viability
delayed union s/sx: Pain- deep throbbbing and unrelieved by
avascular necrosis opiods- reduction of the size of muscle
delayed reaction to fixation devices compartment by tight cast
*Fat embolism- in fractures of long bones paresthesia- burning/ tingling sensation
-fat globules may move into blood stream because numbness
the marrow is greater than capillary motor weakness
-fat globules occlude the small BV of lungs, brain, pulselessness, impaired cap. Refill, cyanotic skin
kidneys and another organs NR: a.) Assess frequently the neurovascular status
2.) Elevate extremity above level of heart.
s/sx 3.) Assist in cast removal and fasciotomy
1.) Sudden dyspnea and respi distress Factors affecting healing:
2.) tachydis Malignancy
3.) chest pain Amount of bone loss
4.) crackles, wheezes,cough Type of bone injured
5.) Peripheral rashes on chest, axilla and hard Infection
palate Nature of injury
Pulmo embolism- encourage early ambulation- x in Death
fat embolism Immobilization
MGT:
1.) Support resp fxn. sTrains- excessive stretching of a muscle tendon.
2.) 2.) Respis failure is common- O2 in high TENDON
concentration Mgt:
3.) - possible intubation and ventilation 1.) Immobilize affected parts
CARE OF CLIENT WITH CAST 2.) Apply cold pads initially, then heat packs
1.) Frequent neurovascular assessment 3.) Limit joint mov't
2.) Do not put any object 4.) NSAIDS and muscle relaxants
3.) keep dry
4.) Use blow drys Sprain- excessive stretching of LIGAMENTS.
Mgt.: Pre op care:
1.) Sama with strains -routine pre op care
2.) Compression bandage o relieve edema. remind px that he should lie on his back after
3.) Assist cast application operation
monitor for worsening sx
use anti embolic stocking
SPINAL CORD INJURY encourage ROM exercises
Herniated disk- all part of nucleous pulposus coordinate with pt
herniated/ forces through weakened/ torn outer fluids to prevent renal stones
ring (annulus pulposus) Incentive spirometry
− common in men maintain on bed restoration
− 90 % lumosacral herniation (L4 & L5) HOME ARE:
s/sx: back pain − avoid sitting for prolonged pd of time
3 steps/ stages: − avoid turning, bending at the walls
− 1.) Protrusion- nucleus polposus presse on − sleep on back
annullus fibrosus − proper wt. To prevent lordosis
2.) Extrusion- bulging of nuleus polposus AMPUTTION
3.) Sequestration- annulus fibrosus gives away as theNursing Intervention
disks coe bursts Post op care:
− Causes: trauma, strain, joint degeneration. 1.) Elevate stump for the first 2 hours to
ASSESEMENT: minimize edema and promote venous return.
1.) Severe low back pain radiate to feet, 2.) Assess skin for bleeding and hematoma.
buttocks or legs. 3.) Wrap the extremity with elastic bandage
2.) Motor and sensory loss in the area supplied HOME CARE:
by the compressed nerves cyatic nerve Use mirror to check stump
affectation Prostherer: used all day (from walking to sleeping)
3.) D: 1.) Straighten leg raising tst- (+) leg pain collaborate with PT and OT
2.) Le segue's tst- 90 knee and thigh (-) DTK
3.) X-ray
4.) CI
5.) MRI
Nsg. Implementation:
1.) Provide CBR (complete bed rest) for several days
2.) Heat application over the area to lessen pain
and muscle spasm
3.) Provide exercise on bed (w/ approval)
4.) Assist in pelvic traction application
6.) Provides drugs-aspirin, diazepam, muscle
relaxants

Laminectomy- removal of spinal lamina to stabilize


the vetebral joints and emoval of the protrding disk
-usally accompanied by insertion of metal plates
(harington rods)

Post op care
1.) Maintain on bed restoration
2.) Important: log rolling technique to turn
3.) Never lie on prone
4.) Hemova drainae system: check tubing for
kinks, record amt., report colorless moisture
in dressing
5.) Provide straight backed chair for limited
sitting only.