OSTEOARTHRITIS/ AKA Degenerative Joint  Progressive wear and tear on cartilage

Disease/ Hypertrophic Arthritis leads to thinning of joint surface and

ulceration into the bone. The top layer
 a chronic non-systemic, slowly
of cartilage begins to breakdown and
progressing disorder that causes
wear away. This leads to a loss of joint
deterioration or degeneration of the
space within the joint, which allows the
articular cartilage. It affects weight
bones to grate upon each other.
bearing joints (hips and knees) as well
Therefore, there is no longer this
as joints of the distal interphalangeal
environment that allows for easy gliding
and proximal interphalangeal joints of
of bones during movement without
the fingers
friction. This leads to eroding of the
 It is the most common type of
bone and osteophyte formation.
arthritis that develops due to
Furthermore, pieces of cartilage and
the deterioration of the articular
bone can break off and float around in
cartilage. Remember articular cartilage
the joint space. All of this leads to
is hyaline cartilage.
extreme stiffness and pain.
 Leads to inflammation of the joint and
What is bone cartilage? 
increased blood flow and hyperthropy
 Bone cartilage is a rubbery, smooth
of subchondral bone
tissue found within the joint that
 When this happens, it leads to bone
covers the end of each bone.
break down because the bones within
 It acts as a protective mechanism for
the joint start to rub upon one another.
movement by providing this slick
This will cause changes inside and
surface for the bones to slide and glide
outside of the bone. (The inside of the
during movement. In addition, it
bone will start to experience abnormal
absorbs shock from movement.
hardening (sclerosis), and the outside
of the bone will form  osteophytes
Key Points about Osteoarthritis to Remember:
formation (bone spurs) altering the
 OA is also called degenerative joint
size and shape of the bone
disease and remember it is
the CARTILAGE NOT synovium.
Causes
 It happens and worsens overtime.
 It tends to most commonly occur in
PRIMARY OSTEOARTHRITIS 
the hands, knees, hips, and spine
 It is caused by the breakdown of cartilage,
(majorly the weight-bearing joints
a rubbery material that eases the friction
which experience a lot of stress) and
in your joints.
it does NOT affect other systems in the
 It can happen in any joint but usually
body and it’s unsymmetrical (a patient
affects your fingers, thumbs, spine, hips,
can have OA in both correlating joints
knees, or big toes.
or just one). Remember  RA is
symmetrical….it must be found in the
correlating joint.

Pathophysiology and Etiology

 Changes in articular cartilage occur first
(articular cartilage deterioration) then
soft tissue changes may occur
Secondary Osteoarthritis Causes and Risk
Factors
  Unknown
 Osteoarthritis is more common in older
people 50 above. The risk of OA increases
with age. Using your joints over and over
damages the cartilage, leading to pain
and swelling. Water builds up in the
cartilage, and its proteins break down. It
may start to flake or get tiny tears. In
severe cases, you can lose all the cartilage
between the bones of a joint so that they
rub together, making it harder and more
painful to use the joint.
 Sex. Women and men are affected
equally
 Obesity , which puts more stress on
your joints, especially your knees.
 Injury or surgery to the joint. Even if a
joint seems to heal the way it should,
it’s at higher risk for osteoarthritis later
on. Increased risk if patient has had
repeated joint injuries/ Previous
Trauma
 Genetics. Osteoarthritis sometimes
happens in multiple members of one
family, hinting that a gene change has
been handed down from parents to
children. Rarely, these cases are caused
Diagnostics Test
 No specific laboratory examination. No
conclusive test to diagnose OA. Must
evaluate patient’s signs and symptoms
and rule out other forms of arthritis
such as gout, rheumatoid arthritis.  and where they are found):
 X-ray may show: sclerosis of bones,
decreased joint space,
osteophytes/bone fragments in the
joint space, osteophytes (bone spur)
formation. may be helpful (remember a
x-ray ONLY shows bones, it doesn’t
show cartilage)
 Analysis of synovial fluid to
differentiates OA from RA
by problems in collagen, a tough protein
found in your connective tissue.
 Improper Body mechanics. Things that
change the way your body works, such
as an unusual way of walking or joints
that have a wider range of motion than
usual (called hypermobility), can put
more stress on them.
 Job or hobby that are strenous. Using a
joint to make the same motion over and
over again -- like squatting or lifting --
may be linked to osteoarthritis.
 Gout. Crystal deposits in the cartilage
can cause damage and osteoarthritis.
Uric acid crystals cause arthritis in gout,
while calcium pyrophosphate crystals
cause arthritis in pseudogout.
 Rheumatoid arthritis and other
inflammatory conditions of the joints,
which lead to joint damage and
cartilage breakdown.
 Diabetes and other hormone disorders,
which can cause inflammation that
leads to osteoarthritis.
 Menopause. Levels of estrogen, which
protects your bones and cartilage, fall
after menopause.
Signs and Symptoms of Osteoarthritis
“Osteo”
 Outgrowths that are bony, especially on
the hands due to bone spur formation
(*remember the names of the nodes
 Heberden’s Node (most
common): bony overgrowth at
the distal interphalangeal joint
 Bouchard’s Node: bony
overgrowth on the proximal
interphalangeal joint (middle
finger joint)
 Sunrise Stiffness (morning) LESS than 30
minutes (Remember RA is greater than
30 minutes)…pain will be the worst at
 the end of day from overuse than
compared to morning time
 Tenderness when touching the joint site
with bony overgrowths (joints will
be BONY and HARD), NOT warm or
boggy as with RA
 Experience grating (crepitus) of the
bones when moving/flexing joint from
bones rubbing together and joint pain
with activity which goes away with rest
 Only the joints: Asymmetrical/Uneven ,
limited to joints (joint site will be hard
and bony, NO warmth or boggy
synovitis with red inflammation) along
with limited mobility, not system
wide, (no fever, anemia, fatigue,
systemic inflammation…just the joints)
 Pain aggravated by use and relieved by
rest
 Decreased ROM
Nursing Assessment:
 Obtain history (previous Trauma,
Family history, job or harsh activity,
past disorders (DM, RA, Gout)
 Pain level and it’s characteristics,
including joints involved
 Evaluate ROM and strength
 Assess effect on ADL
Nursing Diagnosis
 Acute or Chronic pain related to joint
degeneration
 Impaired physical mobility related to
pain and limited joint motion
 Self care deficits related to pain and
limited joint movement
Planning
 To reduce pain
 To maintain physical mobility and
maximize joint movement to the extent
and to perform basic ADL related to self
care
Management
 There is no cure. It gets worse overtime
and damage can’t be reversed (cases
vary mild to severe).
 Managed with lifestyle changes
(exercise/losing weight), medication,
surgery (hip/knee joint replacement or
bone realignment “osteotomy’,
arthroscopic).
Nursing Interventions for Osteoarthritis:
 Pain assessment and ROM: patient’s
perception of the disease, effects of the
disease on the patient’s activities of
daily living, non-pharmalogical and
pharmacological approaches
Relieve Strain and prevent further trauma to
the joints
 Heat and cold compresses
 Use assistance devices such as cane and
walker to decrease weight bearing
stress
 Maintain good posture and body
mechanics
 Avoid excessive weight bearing and
continuous standing
 Importance of weight loss (BMI <25)
 Physical therapy and occupation
therapy including exercise, using
devices to maintain joint mobility and
muscle strength
Physical exercise
 is one of the most effective treatments
for OA….may help create more
lubrication to the cartilage allowing the
pain and stiffness to decrease,
strengthen muscles, help patient lose
weight, feel better mentally
 this is the last thing most patients want
to do but limiting activity and not
exercising leads to more pain, increased
joint damage, increased weight, and
decreased mental health.
Types of Exercise
Low impact: walking, water aerobics  Note: this is temporary relief of no
Strengthen training (lifting weights which helps more than a month or two.
strengthen muscles around the joint)
Range of motion exercises (ROM): improves the
mobility of the joint and decreases stiffness Opioids- if severe such as oxycodone, codeine,
hydrocodone
 AVOID: high impact exercise that will
increase the stress on weight bearing Hyaluronate (Hyalgan and Hylan G-F 20
joints, such as running/jogging, jump (Synvisc) Agents
rope, or any type of exercise where  Visco supplements, and are
both feet are off the ground. administered through intra articular
 Do NOT exercise painful, irritated joint injections into the knee
but let it rest  It relieve pain and most effective for
 Administer analgesics to promote people with mild to moderate Knee OA
comport or relieve pain  After injection, patient is instructed to
 Joint replacement avoid prolonged weight bearing
activities for 48 hours
 Contraindicated with joint infections
Medical Therapy and those with allergies to hyaluronate
PAIN RELIEF preparations, avian protein, bird
Non-narcotic analgesics feather and eggs
 topical creams, Tylenol
(acetaminophen) Glucosamine and chondroitin sulfate
NSAIDs  Are supplements and common
 (GI bleeding/ulcers)- to reduce pain alternative remedies that have
brought by inflammation potential cartilage re-building effects
 Aspirin, Diclopenac, Ibuprofen,  improve symptoms and function of the
Naproxen joints
COX-2 inhibitors
 Celecoxib (Celebrex) and Meloxicam Surgical Interventions
(Mobic)
 blocks the prostaglandin involved in Surgical Intervention is considered when the
inflammation, pain becomes intolerable to the patient and
 safe for the stomach who cannot take mobility is severely compromised
NSAIDS due to GU upset or risk of GI
bleeding. Arthroplasty
 Can be used in patients taking anti  A reconstructive surgery to repair or
coagulants because bleeding time and restore joint motion and function and
platelet aggregation are not affected by to relieve pain
these agents  Involves replacement of bony joint
 Monitor renal function it can cause structure by a prosthesis
renal impairment with long term use
Total Joint Replacement Arthroplasty
Corticosteroids  The replacement of both articular
 Intra-articular injections: …more surfaces with metal or plastic
effective than oral: components
 Reduces the inflammation of the  The most common type of joint
inflamed tendons and ligaments. replacement

Total Hip replacement
 Replacement of severe damage hip with
an artificial joint
 Consist of metal femoral component
topped by a spherical ball fitted into a
plastic acetabular socket
Total Knee Arthroplasty
 An implant procedure in which tibial,
femoral and patellar joint surfaces are
replaced because of destroyed knee
joint
Pre Operative Nursing Care
 Consent
 CP clearance (35 up)
 Anti embolism stockings to prevent
thrombophlebitis
 Skin preparation using antimicrobial
solution to reduce skin
microorganisms, a potential source of
infection
 Antibiotics as prescribed given
immediately pre operatively, intra op,
and post op to reduce incidence of
infection
Post Operative management
 Use appropriate positioning. To prevent
dislocation of prosthesis and facilitate
healing
After Hip Arthroplasty
 Positioned in Supine
 The affected extremity is in slight
abduction by either an abduction splint
or pillow or Buck’s extension traction to
prevent dislocation of prosthesis
 Avoid acute flexion of the hip. Patient
must NOT adduct or flex the operated
hip- may lead to subluxation or
dislocation of the hip. Signs of joint
dislocation: Shortened extremity,
increasing discomfort, inability to move
joints.
 Two nurses turn patient on unoperated
side while supporting operated hip
securely in an abducted position, the
entire length of the leg is supported by
pillows. Use pillows to keep the
abducted;
 Use overhead trapeze to assist with
position changes.
 Elevate the bed not more than 45
degrees. Placing patient in an upright
position put strain on the hip joint and
may cause dislocation.
 A fracture bedpan is used. Instruct to
flex the unoperated hip and knee and
pull up on the overhead trapeze to lift
buttocks onto pan.
After Knee Arthroplasty
 Immobilized the knee in extension with
firm compression dressings and an
adjustable soft extension splint or long
leg plaster cast.
 Elevate the affected leg using pillows
to control swelling
 Alternate, continuous passive motion
to facilitate joint healing and
restoration of joint ROM
Deterring Complication
 Use elastic hose and Sequential
Compression Device while patient in
bed. DC SCD if patient is ambulatory
Promoting Early Ambulation
 2 days after surgery, short periods of
standing may be ordered
 Transfer to the chair or ambulation
using walkers are encourage as
tolerated based on patient’s condition
and type of prosthesis
Promoting Mobility
After Hip Arthroplasty
 Use an abduction splint or pillows while
assisting patient to get out of bed.
 Keep the hip at maximum extension
 Instruct patient to pivot on unoperated
extremity
 When patient is ready to ambulate,
teach him or her to advance the walker
and then advance the operated
 extremity to the walker, permeating
weight bearing as prescribed.
 Teach him how to use walker, crutches
and canes
 Practice PT exercises to strengthened
muscles and prevent contractures
After Knee Arthroplasty
 Assist patient with transfer out of bed
into wheelchair
 No weight bearing is permitted util
prescribed
 Do passive ROM motion exercises as
prescribed
 This includes low-impact exercises
(walking, water aerobics, stationary
bike riding), strength training (lifting
weights), and range of motion
exercises.
 Avoid high-impact exercises such as
running, jogging, jump rope etc.
References:
1. “Osteoarthritis Fact Sheet |
Basics | Arthritis | CDC.” Cdc.gov.
N.p., 2017. Web. 29 Aug. 2017.
2. What Is Osteoarthritis?. U.S.
Department of Health and
Human Services Public Health
Service, 2014. Web. 29 Aug.
2017.
OSTEOPOROSIS
 Is a systemic skeletal disease
characterized by low bone mass leading
to bone fragility and an increase risk in
fracture
 It’s a disease process that thins the
bones to a point that the bones are not
strong enough to withstand everyday
stress and it breaks/fractures.
 Most common type of fracture seen in
patient with osteoporosis is
called Colles’ fracture. This is a fracture
of the lower part (distal) of the radius at
the wrist.
Pathophysiology
What is happening to the bones in
osteoporosis? 
 The inside of the bone (specifically the
spongy bone) becomes very porous and
the bone’s density decreases….making
it weak. Inside the spongy bone resides
cells called osteoblasts and osteoclasts.
Osteoclast CONSUME bone and
osteoblasts BUILD bone. Normally,
osteoblasts and osteoclasts work at the
same rate. However, in osteoporosis
the osteoclasts start to outwork the
osteoblasts.
 This disease suddenly sneaks up on a
patient (in most cases without signs and
symptoms). The patient is usually
surprised with a bone fracture.
 Osteoporosis most commonly affects
the wrists, hips, and spine.
Role of the bones
 Provides protection to our organs and
supports them
 Allows us to move with the
assistance of muscles, tendons, and
ligaments
 Gives our body its shape
 Inside of the bones (specifically the
bone marrow) there is an intricate
system maintaining out survival:
Functions
 It’s responsible for red blood cell,
platelet, and white blood cell
production (red marrow)
 Storage of these blood cells along with
storing our calcium and phosphorous
minerals for when we need them
 Preserving lipids for energy when
needed (yellow marrow)
Compact Bone vs. Spongy Bone
Compact Bone: is a strong, tight woven layer
than protects the inside of the bone and helps
maintain bone strength and resistance to stress
Spongy Bone: a matrix of pore-like components
(hence its name “spongy”),  such as proteins
and minerals (calcium and phosphate). In
osteoporosis this matrix starts to thin (it
becomes more porous…making the bone weak).
 Within the spongy bone
are OSTEOCLASTS (they consume
the bone matrix and remove
substances from the bone
(calcium) and puts it in the
bloodstream when we need it).
 OSTEOBLASTS build up the bone
matrix within the spongy bone by
taking substances (phosphate
and calcium) from the blood and
building up the bone.
 These cells are majorly
influenced by hormones (it is
important to understand how
these hormones work because
this will help you understand the
medication treatment which help
slow down osteoclast activity):
Hormones that play a role in Bone Health:
Parathyroid hormone (PTH):  When calcium
levels are low the parathyroid gland secretes
PTH (parathyroid hormone). This causes the
osteoclasts to break down the stores of calcium
in the bone so it can be placed in the
blood….hence increasing calcium levels. In
addition, PTH increases the small intestine
reabsorption of calcium, and decreases
the kidneys from excreting calcium.
 It is important to note that
parathyroid hormone
INDIRECTLY stimulates osteoclast
activity. It plays a role with
osteoblasts as well because PTH
actually binds to osteoblasts.. In
a sense the osteoblasts will
control/regulate the activity of
the osteoclasts under the
influence of PTH. Therefore, if
extra doses of PTH are given (as
with the medication treatment
drug Teriparatide “Forteo”) this
can actually improve bone health
by making the bone stronger and
more resistant to fractures.
Calcitonin:  When calcium levels are too high,
the thyroid gland creates calcitonin to decrease
the activity of the osteoclasts…..less break down
of bones, which will keep calcium levels normal.
Growth hormone: stimulates osteoblasts to
build up bones
Estrogen: controls the activity of osteoblasts
and osteoclasts by keep the bones strong and
prevent bone resorption by the osteoclasts.
Estrogen in a nutshell prevents the osteoclasts
from living too long.
 Why is this important to know?
Remember estrogen is secreted
by the ovaries. When a woman
enters menopause she will
produce less estrogen, which
places her at risk for
osteoporosis.
Testosterone: this is converted into estrogen to
keep bones stronger, as stated above. As men
age testosterone levels decrease and this puts
them at risk for osteoporosis.
It is important to note that during a person’s
mid 30’s most people reach peak bone mass.
The osteoclasts and osteoblasts are working at
the same rate. BUT after the mid 30’s the bones
are broken down faster than replaced….hence
why we see osteoporosis in older age.
Now let’s condense all the material above into a
mnemonic to help us remember the risk factors:
Risk Factors for Osteoporosis:
Remember: “CALCIUM”
 Calcium and vitamin D intake low
(osteoclasts break down the bones
more to keep calcium levels normal)
 Age 50 yo above (bones become
weaker as your age and bone mass
decreases after 30, lower testosterone
and estrogen levels)
 Lifestyle (cigarette smoking, alcoholic,
sedentary, immobile), Low activity
 Caucasian and Asian women (women
have less bone tissue than men)
 Inherited (genetics)/ History
 Underweight BMI <19 (thin or small
body frame..there is less bone mass and
the person loses it quicker…anorexia)
 Medications: Glucocorticoids…three
months or more - stimulates osteoclasts
and decreases osteoblast activity,
anticonvulsants:  phenobarbital,
carbamazepine (tegretol), phenytoin
(Dilantin), valproate (Depakote) (affect
the osteoclasts and osteoblast activity)
 Women are most commonly affected by
osteoporosis due to lower peak bone
mass and an accelerated bone loss in
the post menopausal period
 Osteoporosis is more common in Asian
women than in White women. The
fracture risk is lower for the Asian
Women
 Previous fracture
Note:
 Primary Osteoporosis reaches peak
bone mass, usually around the third
decade of life and lose bone density
gradually as one ages.
 Post Menopausal Osteoporosis -
Declining estrogen causes an increase is
osteoclastic activity and a resulting
imbalance between formation and
resorption
 Secondary Osteoporosis- cause by
diseases such as liver disease, RA, IBD,
lymphoma, thalassemia, acromegaly,
amyloidosis and leukemia.
Medications such as glucocorticoids.
Signs and Symptoms of Osteoporosis: “Frail”
 Fracture (hip, wrist, spine) caused by
normal regular activities
 Rounding of the upper back Dowager’s
Hump (spine deformity…stooped
posture) from spine fracture
 Asymptomatic until fracture
 Inches of height lost overtime since a
young adult (2-3 inches)…due to spinal
fracture or collapsing vertebracan be
painless
 Low back pain (T5-L5), neck or hip pain
(on palpation or with activity like
bending or increase stress put on the
bone)
Diagnostic Test
Bone density test (BMD bone mineral density
test): also called DXA or DEXA scan
 X-ray imaging taken to measure
calcium and other bone minerals
in the bones
 Patient Education: no calcium
supplements (TUMS, ROLAIDS,
other vitamins containing
calcium etc.) 24 hours before the
test
Nursing Interventions for Osteoporosis
 Assessing for risk factors: remember
the mnemonic CALCIUM
 Discussing with patient how to change
modifiable risk factors that can be
changed
 Assessing for possible signs and
symptoms FRAIL
 Education about tests: DEXA scan: no
calcium supplements 24 hours before
test
  Safety! Major concern…very simple fall
can lead to a fracture…Patient needs
the call light in reach at all times, room
need to be clutter free, assistive devices
(use correctly), non-slip sock, avoid
rugs, watch pets getting around feet,
using eyewear to see
 Good body mechanics, ROM exercise to
active exercise
Prevention
 Diet: Eating foods rich in calcium-
Yogurt, Sardines, Cheese, broccoli,
Collard greens, Tofu, Rhubarb, Milk,
salmon, tuna, cheese, egg yolks, beans,
cabbage, rice, sesame seeds
 Sufficient Vitamin D intake (helps body
absorb calcium)
 Weight-bearing exercise at least 30
minutes 5 days a week to helps increase
bone mass and total body calcium.
Lifting weights, hiking, tennis, ball room
dancing need stress of gravity on the
bones to build them up…low-impact
not as beneficial but good for
cardiovascular health
 A brisk walk is a relative term, since
“brisk” for some, is either slow or quite
speedy for others, depending on levels
of fitness. One measure to
quantify brisk walking is “steps per
minute,” and 100 steps per minute is
considered moderate intensity or brisk
walking.
 Smoking cessation and alcohol intake.
Smoking affects the body's ability to
absorb calcium, leading to
lower bone density and weaker bones.
affects the body's ability to absorb
calcium, leading to lower bone density
and weaker bones while
heavy alcohol use
decreases bone density and
weakens bones' mechanical properties.
Medications for Osteoporosis:
Calcium and Vitamin D supplements
Bisphosphonates
 slows bone break down
 Alendronate (Fosamax), Risedronate
(Actonel), Ibandronate (Bonvia),
Didronel (Etidronate). Actonel
(Residronate), Bonefos (Clodronate),
Aredia (Pamidronate),Skelid
(Tiludronate)
 It may cause GI upset and esophagus
problems: IMPORTANT!! Take
with full glass of water in morning
on empty stomach with NO other
medications and sit up for 30
minutes or more to prevent GI side
effects especially esophageal
irritation. (60 minutes with Bonvia)
 GI effects: gas, constipation, heartburn,
diarrhea, bloating, vomiting, stomach
pain
 After taking and don’t eat anything
for 1 hour..helps the body absorb
more of the medicine.
Calcitonin:
 made from salmon calcitonin, decreases
osteoclast activity. Remember
calcitonin is secreted by the thyroid
gland naturally.
 At risk for HYPOcalcemia
Hormone replacement therapy (HRT)
 used for short-term due to other
effects on the body: stroke, blood clots,
breast cancer
 raloxifene and Terparatide
 Raloxifene (Evista): selective estrogen
receptor modulator….monitor for deep
vein thrombosis
 Teriparatide (Forteo): severe cases of
osteoporosis…it provides extra
parathyroid hormone which stimulates
osteoblasts and make them live longer