Anatomy
Musculoskeletal Sysytem
Skeletal muscles, bones, joints, tendons, ligaments,
bursae
206 bones
Axial Skeleton (80)
-skull, vertebral column, thorax
Appendicular skeleton (126)
− extremities, shoulder, pelvis
Functions:
Framework
− Protection
− Movement
− Hematopoietic fxn.
− Storage of Ca and Phosphate
Bone Classification:
• Long Bones (femur, radius, ulna, numerous)
• Short Bones (carpals, tarsals, spongy)
• Flat Bones (skull, cranium)
• Irregular Bones (vertebrae)
Type of Mature Bone:
1.) Cancellous (spongy bone)
- interior
- with trabeculae/ spicules
- lattice like network
- osteogenic cells- nagbubuild ng bone.
- filled with red and yellow marrow
*Red- hematopoietic function.
*Yellow marrow- fracture, emboli formation.
2.) Compact (cortical bone)- peripheral
- forms the outer shell
- densely packed calcified I.C matrix
- more rigid
- major component of tubullar bones.
Parts of a long bone:
Epiphysis
Diaphysis
Epiphysis
Nutrient Foramen: where nutrients are stored in
bone.
Epiphysial Plate/ Growth Plate
− region of longitudinal growth
− disappears during skeletal maturity.
Components:
1.) Area of resting cells- uppermost near
epiphysis; not active.
2.) Zone of proliferation- active cells
- growth of long bones begin.
3.) Area of hypertrophy- cells are swollen.
- metabolically inactive.
- epiphysial fracture separation in children.
4.) Area of provisional calcification-
Extracellular matrix hardens.
- arrest of bone calcification.
− deformity formation.
Joints or Articulations
− point where to bones meet.
− Provides stability and mobility.
Joint classification
1.) Fibrous/ Synarthrodial- none movable.
− Sutures- thin layer of fibrous tissue that
binds together interlocking flat bones.
e.g: skull bones in children
− Syndesmosis- consist of interrosseous
membrane/ ligament between the
bones.
e.g (in between) radius and ulna
tibia and fibula
− Gomphosis- conical projection is held
there by a ligament .
e.g teeth held in maxilla/ mandible
* not movable
2.) Cartiligenous/ Amphiarthroidal- minimal
movement.
Synchondoses- entire joint is covered by hyaline
cartillage.
e.g: costochondral joint (junction ng ribs, 9
cartilages- during breathing)
Symphisis- joints have a fibrocartilage connection
between the bones and a thin layer of hyaline
cartilage covering the articular suface.
e.g: symphisis pubis, intervertebral disk. (during
delivery)
3.) Synovial/ Diarthrodal- allows free
movements of joints.
-consist of joint cavity and hyaline cartiage over
the articular surface.
• Joint capsule- has rich nerve supply sensitive
to pain, friction.
-sensitive to rate and direction of motion,
compression, tension, vibration and pain.
-synovium
 - joint swelling fluid increase here.
• Synovial Fluid- super filtrated plasma from
BV. Produced by synovial membrane.
- fxn: lubricant, source of nourishment
Characteristics of synovial fluid:
a.) clear/ straw colored
b.) non-clotting
c.) 1- 8 ml
d.) viscous
e.) WBC < 200 cells/ ml
f.) synovial cells, phgocytes
Types of freely movable joints:
− hinge- flexion and extension
− pivotal- neck
− ball and socket- shoulders
− ellipsoidal- carpals
− saddle joint
− gliding joint- ankle, between tarsal joints
Tendons and ligaments
- dense connective tissue structures
− connected to muscles and bones
a.) Tendon- muscle to bone.
b.) Ligaments- bones to bone
c.) Bursae- closed sac formed by synovial membrane
-contains synovial fluid
*bursa- a small fluid-filled sac lined by synovial
membrane with an inner capillary layer of slimy
fluid (similar to that of an egg white). It provides a
cushion between bones and tendons and/or muscles
around a joint. This helps to reduce any friction
between the bones and allows free movement.
Bursae are filled with synovial fluid and are found
around almost every major joint of the body; when
they become inflamed, the condition is called
bursitis.
d.)Cartilage- firm but flexible type of connective
tissue (ear)
-produced by chondrocytes.
- 65-80% weight 80% wt is H20 (no blood vessels)
Types:
a.) Elastic cartilage- ears
b.) Hyaline cartilage- most abundant and most
common.
− covers the load bearing portion.
− Cartilage of fetal skeleton.
− Adults: costal cartilages, respiratory tract, pain.
epiphysial plates
c.) Fibrocartilage- intermidiate between dense and
hyaling cartilage
e.g: intervertebral disk; symphisis pubis
History:
Medical Hx:
− identify infectious disease
− immunizations (OPV, Tetanus)
− major illnesses/ hospitalization
− medications
− lifestyle and daily activities
Physical Exam:
− perform a head to toe assessment.
− Nurses need to inspect and palpate.
− Assess joint and muscle tone/ mov't
− usually tape measure and protractor
(goniometer- measures angle, ROM the
patient is able to do) are the only
instruments.
Inspection:
− size, symmetry, swelling
− pigmentation, rashes. Scars
− color, texture of the skin
− distribution of body hair
− assess pulses and arterial circulation. (Allen's
test)
− CREPITUS- audible/ palpable because of
rubbing- grating sound ex. Fracture
− subcutaneous nodules
− gait, positive, muscular palpation, joint
palpation, ROM, muscle strength
Diagnotic tests:
1.) Radiographs- most common lab
X-ray- handle area carefully
− pain meds as ordered
− remove jewelry
− shield-pregnant may undergo but needs
to wear shield
− lie still
− inform patient that exposure to radiation
is minimal and not dangerous.
− Protect yourself wear apron/ shield.
2.) Arthrocentesis
- needle is inserted into the joint and fluid is
withdrawn.
Ex: swelling of joint –to lessen swelling
NR: - informed consent- invasive procedure
- meds may be instilled into the joint to alleviate
− compress bandage
− rest the joint 8-24 hours
− Notify MD- if ever joint swelling (infxn.)
(pagka nagka impeksyon=osteomyelitis means may
staph aureus)
3.) Arthrogram
- radiographic examination
− 3 punctures
− use of contrast medium/ air
− series of x-rays is taken as the joint is moved
through the ROM
NR:
1.) Ask patient to void.
2.) Tell patient that procedure is long.
3.) NPO 8 hours
4.) Informed consent
5.) Allergy to iodine/ seafood- dye
6.) Remain still unless when asked to reposition. -pretest: painless procedure, IV radio isotope is
7.) Minimize use of joint for 12 hours.
8.) Joint will be edematous for 1-2 days- ice
pack
9.) Pain meds
10.)Use of bandage for -4 days
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.
4.) Bone Marrow Aspiration
− usually involves aspiration of marrow to
diagnose disease like leukemia, aplastic
anemia.
− Usual site is the sternum and iliac crest.--
rich supply of red marrow.
Early-tubular bone
As we grow- iliac, sternum
NR:
1.) Asceptic Technique
2.) Pretest: consent
Intratest: needle puncture may be painful
(infection)
Post test: Maintain pressure dressing and WOF
bleeding.
3.)Monitor signs for bleeding after.
5.) Arthroscopy
-a direct visualization of joint cavity; invasive
- pretest: consent, explain procedure, NPO for at
least 8 hours prior to procedure—instruments are
inserted to knee joint.
-Intra test: sedative, anesthesia, incision will be
made.
-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.
2.) Walks w/o wght bearing once sensation
returns but limit activity for 1-4 days.
3.) Reinforce use of crutches for 5-7 days.
4.) Elevate extremity as often as possible for 2
days.
5.) Ice compression
6.) Notify MD- fever, knee pain, edema > 3 days.
6.) Dual Energy Absorptiometry (DXA)
- bone marrow density scan is a low dose x-ray w/c
checks an area of the bone such as the hand and
foot for signs of mineral loss and bone thinning.
7.) Bone Scan
- imaging study with the use of a contrast
radioactive material- needs consent.
used, pregnany is contra indicated.
-Intra test- holds fluids for 4 hours before
procedure, isotope injection, 32 oz of H2O
have patient void after 1-3 hours scanning is
performed—to eliminate excess radioisotope.
radioactive material, monitor injection site for
redness, swelling, tenderness.
BONE PHYSIOLOGY
Histology
Structural Elements of the Bone:
1.) Bone Cells- osteogenic cells (in periosteum,
endosteum, epiphyscalplate)
2.) Bone Matrix
- ground substances (minerals—Ca & Phosphate)
- collagen-type 1 (most common)--skin, eyes, thin
collagen, blue sclera
- glycoprotein
• Collagen Fibers- 90-95%
- provides tensile strength for bone.
• Ground substance- hemogenous gelatinous
medium
- proeoglycans, chondroin sulfate and hyaluronic
acid.
- Helps control deposition of Ca salts/ Ca
* Osteogenic Cells- differentiate into osteoblats.
(found in: periosteum, endosteum, epiphysial plate)
- active during normal growth—imp. in children.
− activated during fracture healing
osteoBlast- Builds Bones
fnx:
*osteonic/ haversian canal-channel for exchange of
nutrients
*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-

Calcitonin
- hormone secreted by para follicular cells or C cells
of the thyroid gland.
− Opposite effect to that of PTH.
− Increase in plasma Ca concentration—
calcitonin secretion
− Decrease concentration by:
1.) Decrease activity of osteoclast (shifts towards
bone deposition)
2.) Decrease bone formation or new osteoclasts
− has weak effect
− PTH overrides the calcitonin effect
− greater effect in children- vit. D deficiency
METABOLIC BONE DISEASES
* Osteoporosis
* Osteomalacia
* Rickets
* Paget's Disease/ Osteitis Deformans
1.) Osteopenia
− common to all metabolic diseases.
− Low bone mineral density
− term used to describe an apparent lack of
bone mass.
− Seen on x-ray studies
− risk for fracture
− reduction in bone mass greater than
expected for age, sex or race
2.) Osteoporosis
− Imbalance between bone resorption and
bone formation
Reduction of bone mass
Increase in bone fragility
Incidence: women> men
− 1 in 3 women over 50 year
− 1 in 8 men over 50 year
− affects all races, common in whites (kasi
malaki ang bone structure ng blacks)
Risk Factors: genetic 60-80%
− life style—x exercise, diet
− hormonal & metabolic
− other illness: prob in PT gland
− Anthropometric(Age)- short stature
− Dietary- coffee, smoking, steroids
− Drugs
*HYPOPARATHYROID=HYPOALCEMIA
-peak bone mass-30 years-35 years
-after peak years=Ca stored in spongy bone
leaves tissue that leads to decrease cancellous
(spongy)
bone trabeculae decrease in # and width
marrow spaces are widened
decrease cortical mass
bone mass further decreased
− in men: rate of bone loss 0.&7% per years
− starts wih higher bone density
− age 90: 17% of male has hip fracture (wt.
bearing areas)
32% of females has hip fracture
− Role of TESTOSTERONE: has ANABOLIC EFECT
TO BONE
- increase muscle mass=higher bone density
- converted to estrogen w/c prevents excessive
bone resorption.
− In ESTROGEN: decrease estrogen
inc. cytokines
production of osteoclast inc. osteoclast
differentiation (bone
chewing)
loss of trabecular bone mass
CLASSIFICATION OF OSTEOPOROSIS:
1.) Type 1/ Postmenopausal Osteoporosis
(more common type aka: SENILE
OSTEOPOROSIS)
- no other underlying med. Condition
- loss of trabecular bone
- predispose to fractures of the vertebrae and distal
radius and hips.
2.) Type 2 Osteoporosis
- secondary osteoporosis
- 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
ASSESSMENT:
Subj: Weakness, pain
Obj: fracture, dec. in height, diff. Bending over,
“DOWAGER HUMP”(prominence of cervial spinal
vertebrae), obvious bone loss, dec. in height.
DIAGNOSIS:
− P.E: non-specific
− serial height measurement- ideal but not
done
− no definite lab examination
− x-ray- increase radiolucency, 25-30% bone
loss (to rule out fracture)
− Dual x-ray absorptiometry- Gold Standard,
2.5 SD below the young adut mean.
MANAGEMENT:
* Prevention and Early detection
− Identify person in high risk group
− ABONE
* A- age 65 y/o and older
B- bulk- < 140 lbs. At menopause
ONE- never on estrogen for > 6 months.
− Adequate Nutrition
restores lost bone
- decrease incidence of fracture
- ALEDRONATE (FOSAMAX)- 30 min rule
H2O 30 MIN before food or other meds.
AVOID LYING DOWN for 30 min.
- PAMIDRONATE- pain reliefs
- given IV (D5W/ NS)
- monitor tingling around mouth
Calcitonin- reduce bone resorption
- slows decline in bone mass.
- IV or intranasal
- give in the evening
- S.E: rhinitis
- hindi pwede mag breakfats pag nagtake nito
- Ca carbonate- 30-60 before meals
2.) Anabolic Agents- PTH, testosterone
3.) Osteomalacia (in adults) Rickets (in
children)
CAUSE: Vit D deficiency
- inadequate intake of vit. D
- malabsorption of vit. D.
- 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
Uric Acid---excretion: intestine, kidneys
Uric Acid: Charac. Of monosodium urate crystals
1.) Precipitate at the periphery of the body.
2.) Trauma promotes urate crystal precipitation.
3.) Changes in ion concentration and decrease in pH synoviumis characterized as: hyperplastic, fibrate,
enhances urate deposition
N Level in MEN: 5.1 (+/-) 1 mg/ dL
WOMEN: 4.0 (+/-) 1 mg/ dL
CLINICAL STAGES:
1.) Asxmatic Gout- absence of sx., inc. UA 9-10
mg/dL
2.) Acute Gouty- sudden onset of painful swelling
and tenderness of great toe.
- MONOARTICULAR (only 1 joint is affected)
- Fever (due to swelling)
- Precipitated by trauma, alcohol, stress
3.) Intercritical stage- no sx. For month to years
- repeat attack if not treated
- permanent changes
4.) Chronic gout- urate continues to expand
- tophi
-acute attack
- chalky discharge
Risk Factors: age
duration of hyperurecimia
genetic
heavy alcohol consumption
obesity (r/t intake of excessive protein)
Asxmatic Hyperurecemia
Precipitation of MSU crystals in joint fluid
urates in joint become super saturated
microtophi synovial lining and joint cartilages
release of crystals
Acute inflammatory response
lysosomes free radicals
increase inflammation
acute arthritis –pain, fever
crystalization abates many crystals resolubilized
acute attacks remits—asxmatic intecritical pd.
Chronic topheous gout, repititive precipitation of
urate crystals
uncrust articular surfaces
visible deposits in synovium
thickened
articular bone erosions
tophi formations (nodules, non- tender)
large ulcerations of overlying skin
2 joint degeneration gouty neuropathy
DX. TEST:
- Serum UA> 7.5 mg/dL
- WBC and ESR- because there is increase cell
turnover
- 24 hour urine
- synovial fluid analysis- (+) uric crystals or
monosodium urate crystals or Arthrocentesis- will be
cloudy
MANAGEMENT:
1.) Diet: organ meat, wine, aged cheese—not
allowed, eat in moderation: mushroom, spinach,
cauliflower, asparagus, poultry, beans, peas
- limit alcohol intake
2.) Assist with reduction- gradual- to lyse cellular
content of body.
3.) Instruct on strict CBR for 24 hours of acute
attack
4.) Local application of heat and cold for pain.
5.) Provide bedstradle to relieve pressure from linen
at affected area.
6.) Administer meds as ordered
- instruct patient on med regmen
- instruct patient to increase OFI to 3L/ day
- emphasize that prognosis is good with tx
compliance
*not all patients wit gouty attack will experience
gouty neuropathy.
MGT.:
G- up 3 L fluids/ day, Gulp no alcohol
O- organ meats not allowed
U- urine output increased to 2 l/ day
T- teach bed rest
COMPLICATIONS:
1.) Joint Deformity
2.) HPN
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
- non- inflammatory
- chronic, slowly progressive
- disorder of movable joints
- “wear and tear” arthritis- kasi sa matatanda
nakikita
- previously, “degenerative joint disease”
- incidence= male and female affectation up yo age
55, increase in female (because of menopause) after
this time.
RISK FACTORS:
1.) Increase Age
2.) Obesity- increase weight
3.) Repetitive use of joint with previous joint
damage
4.) Anatomical Deformity- clubfoot
5.) Genetic susceptibility
6.) Occupational Overuse
-ex: nurse laging nakatayo
7.) Sport and recreational activity
8.) Racial Differences
TYPES:
1.) 1 or Idiopathic- most common
- aging, genetic
- most common affected (joint: wt bearing joints)
(knees)
2.) 2 OA- repetitive strain, sprain, joint
dislocation and fracture
-certain meds
ex: steroids-kasi maedecrease yung bone mass
- traumatic arthritis
Aging genetic—changes in chondrocyte fxn. (produce
cartilage, gives strenghth to bone N in type 2)
decrease amount of type 1 cartilage is laid down
change in collagen fiber, diameter and orientation
joint cartilage deteriorates
narrowing of joint spaces (nababawasan yung H2o inflammation.
content)
mechanical injury
forced into defects—cyst formatio
irritation of synovial fluid
fibrosis
limitation of/ in joint most/ joint stiffness
ASSESSMENT FINDINGS: S/SX
1.) Joint pain
2.) Joint stiffness
3.) Funx. Joint impairment limitation
4.) Joint involvement is assymetrical
5.) Not systemic, no fever, no severe swelling
6.) Atrophy of unused muscles
7.) Usual joint are the wt. Bearing joints
S/SX: Crepitus
− Heberden's Nodes (distal, before kuko)and
Bouchard's nodes (knuckles, interphalangeal
joint)
− Joint enlargement
− Altered gait
DIAGNOSTIC FINDINGS:
1.) X-ray- narrowing of joint spaces
- loss of cartllage
- cyst like deposits
- osteophytes (spur) formations
2.) Blood tests will shw no evidence of systemic
inflammation and are not useful
GOAL OF MGT.:
1.) Relieve pain
2.) Maintain/ Improve mobility
3.) Minimize disability
MEDICAL MGT.:
1.) Wt reduction.
2.) Use of splinting devices to support joints.
3.) OT and PT
4.) Pharmacologic mgt.
- paracetamol, NSAIDS, topical analgesics (minimal
amount only), intra- articular, steroids to decrease
NR:
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

joint immobility
DIAGNOSTIS CRITERIA:
S welling/ effusion: 3/ more joints
S ymmetric
W rist- MCP, PIP- proximal interpharengeal joint
A AM stiffness
N odules (Rheumaoid Nodules)
P ostive Rheumatoid Factor
E rosion/ decalcification on x-ray
*should be present at least 6 months
Joint Deformities:
S wan neck- PIP-DIP
U lnar drift- medial (papasok)
B outonniere deformity- flexion of PIP and
hyperextension of DIP (boto boto)
Rheumatoid Nodules: non-tender subutaneous
nodule.
− olecranom bursae, fore arm, over the areas.
DIAGNOSTIC TESTS:
1.) X-ray- minimal changes early stage
- narrowing or joint spaces
- bone erosion
- bone deformities evident bilaterally.
ASSESSMENT:
1.) Pain
2.) Joint swelling ad stiffness- symmetrical,
bilateral
3.) Warmth, erythema and lack of fnx.
4.) Fever, wt loss, anemia, fatigue
5.) Palpation of join reveals spongy tissue
6.) Hesitancy in joint mov't
ASSESSMENT FINDING:
* Joint involvement is symmetrical and bilateral.
* Characteristically beginning in the hands, wrist
and feet.
* Joint stiffness occurs early in the morning,
lasts more than 30 minutes, not relieved by
mov't, diminishes as the day progresses.
DIAGNOSTICS:
1.) Xray- shows bony erosion
2.) Blood studies- (+) rheumatoid factor and ESR
and CRP and Anti-nuclear antibody (may
inflammation C reactive protein)
3.) Arthrocentesis- shows synovial fluid that is
cloudy, milky, dark yellow containing numerous
WBC and inflammatory CHON. (kasi diba yung
neutrophils saka macrophages ineengulf yung
immune complex)
MEDICAL MGT:
1.) Aspirin and NSAIDS- main stay tx. To reduce
inflammation.
2.) Chemotherapy with Methofrexane, anti-
malarial, gold therapy and steroid.
3.) For advanced cases: arthroplassty (repair of
joints), synovectomy (removal of affected
synovium)
4.) Nutritional Therapy
GOLD THERAPY (obsolete)
-IM oral prep
- takes several months (3-6) before effect can
be seen
-can damage the kidney and cause bone marrow
depression
5.) may not work for all individuals
NSG. MGT.:
1.) Relieves pain and discomfort
- use splints to immobilize the affected
extremity during acute stage of the disease and
inflammation to reduce deformity. (cold packs
and heat packs) Administer meds
2.) Decrease px fatigue.
- schedule activity when pain is less severe.
- provide adequate rests.
3.) Promote restorative sleep.
4.) Increase patient's mobility
- advise proper posture and body mechanics
- support joint in fnx. Position
- advise active ROM
- avoid direct and over the joint
5.) Provide diet therapy
- patient experience anorexia, nausea and wt.
Loss
- regular diet with calorie restriction because
steroids may increase appetite
- supplements of vit, iron and protein
6.) Increase mobility and prevent deformity
- lie flat on a firm mattress
- lie prone several times to prevent hip flexion
contracture
- use one pillow under the head because of risk
of dorsal kyphosis.
- no pillow under joint because this promotes
flexion/ contraction
NSG. DX:
• Chronic Pain
• Disturbed Body Image
• Activity Intolerance
• Self Care Deficit
• Powerlessness

RA
− onset is early
− chronic systemic disease
− involves the synovium
− involves joints are symmetrical, fingers,
cervical spine
− malaise, fever. Anemia
− joint tenderness, swelling, warmth and
redness
− sub nodules
-rest the joint, cold and heat modalities, ASA,
NSAIDS
SKELETAL DISORDERS IN CHILDREN:
1.) DDH (Developmental Dysplasia or the Hip)
- formerly: congenital dislocation of the hip
- truly congenital
- description of an array of hip problems to
describe shallow acetabulum, hip dislocation or
sublaxation
- Incidence: First born (60%)
- females > males
- < 3 y/o
- breech presentation
CAUSE: unclear
1. Large neonates and twins
2.) Maternal Relaxation- hormone release when
pregnant=relaxes structure of pelvic muscle—
relaxation of joint ligaments in the fetus.
3.) Breech presentation (30-50%)
- rarely dislocated but “dislocatable”
extreme hip flexion limitation of hip motor
stretching of already lax capsule and ligament
hip dislocation
FORMS:
1.) Unstable Dysplasia- hip is positioned
hormonally but can be dislocated by
manipulation.
2.) Subluxation/ Incomplete Dysplasia
- femoral head rides on the edge of the
acetabulum
3.) Complete dislocation- femoral head totally
outside.
ASSESSMENT: P.E
− newborn: no gross deformity
no pain
− uneven knees
OA
− Onset is late
− degenerative disease
− Involves the cartilages
− involved joints are unilateral- wt bearing,
knee, hips, spine
− no other s/sx systemic
− crepitus, stiffness in the morning
− dec. after activity
− rest the joints, avoids over activity, wt.
Reduction, cold and warm modalities, ASA
− uncorrected: “duck waddle”, limp
Other Assessment findings:
1.) Limitation of hip abduction
2.) Asymmetric # of thigh skin folds (at the
back)
3.) Shortening of extremity.
4.) Audible hip clicks.
Barlow Test- provocative test (suspicion only)
− dislocate an unstable hip
1.) Stabilize pelvis with 1 hand.
2.) Flex and adduct hip applying a posterior force.
3.) After release of posterior or force, hip relocates
spontaneously.
Ortolani Test- reduce the recently dislocated hip
− 1-2 mo. Of age *pag > 2 mo. Wala nang
fibrous tissue
− thigh flexed, abducted
− femoral head lifted anteriorly in acetabulum
− reduction is felt as a “clunk”
Galeazzi Sign- uneven knee levels when supine
infant's feet are placed together on the
examining table with the hips and knees flexed.
Trendelenburg signs- child stand on his wt. On the
side of dislocation and lifts his other knee.
− the pelvis in the N side drops
− child on his wt. On the N side, lifts his other
knees
− pelvis remains horizontal
Imaging- to show location of the femur head and
shallow acetabulum xrays, hip ultrasound- initially
kasi wala pang full development of hip.
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.