orthopedic pathology (joint pathologies) Flashcards
joint pathologies
..
types
degenerative
(Osteoarthritis)
inflammatory
(Reumatoid arthritis, Ankylosing spondylitis, Psoriatic arthritis)
metabolic
(Gout, pseudogout)
infectious
(Septic arthritis)
neurogenic
(Charcot’s arthropathy)
OA, aka
DJD
abut OA
Chronic, degenerative condition that affects joints, specifically articular cartilage and subchondral bone
what structure particularly affet
articular cartilage
subchondral bone
prealance increaes with
age
MOST COMMON JOINT DISORDER IS???
OA
primary vs seconary OA
Primary OA – idiopathic
Secondary OA – to joint trauma, infection, hemarthrosis, osteonecrosis, etc.
primary OA
MOST COMMON
via regualr wear/tear
caused by the breakdown of cartilage
secondary OA
caused by another disease, infection, injury, or deformity. Osteoarthritis starts with the breakdown of cartilage in the joint.
seconary via
joint trauma, infection, hemarthrosis, osteonecrosis, etc.
also eg
RA cause OA (?)
risk factors OA
joint immobilization
jint immobilziatson oa
Conclusions. Joint immobilization caused multiple OA-like lesions in both mice and humans. Joint immobilization induced progressive sensory innervation, synovitis, osteophyte formation, and cartilage loss in mice, which can be partially ameliorated by remobilization.
other isk fators
Altered biomechanics – developmental deformities; Genu valgum/varus
Immobilization
Trauma
Pathology
Genetics – familial forms of some hand OA
Gender – mc in women over age 50
Lifestyle- obesity (high correlation w/ knee OA and even hand OA)
Low vitamin D and Vitamin C intake are associated with increased risk of knee OA progression
which vitamin definicency, OA
Low vitamin D and Vitamin C intake
knee OA progression
OA define
can be defined as a gradual loss of articular cartilage, combined with thickening of the subchondral bone, bony outgrowths (osteophytes) at joint margins, and mild, chronic nonspecific synovial inflammation.
other features of oa
osteophytes (exostosis)
nonsepcific synovial infalmation
OA part of
aging
can you distinguish bw oa and aging
3 states identified
normal cartiage –> aginng cartilage –> OA cartilage
pathogeneiss OA
Phase 1: Edema and Microcracks
Edema of the extracellular matrix
Cartilage loses its smooth aspect and microcracks begin to appear
Cartilage softens and thins
Loss of joint space
There is a focal loss of chondrocytes
Unable to repair as normal
phase 2
Phase 2: Fissuring and Pitting
Microcracks deepen perpendicularly in the direction of tangential forces and along collagen fibers
Vertical clefts form in the cartilage above the subchondral bone
phase 3
Phase 3: Erosion
Fissures cause fragments of cartilage to detach off; causing:
Osteocartilaginous loose bodies
—> Synovial inflammation (often more focal than inflammation occurring due to rheumatoid synovitis)
—> Inflammation caused synovial hypertrophy and capsular thickening
Uncovering subchondral bone:
—> Sclerosing of subchondral bone
—> Subchondral cysts
—> Osteophyte formation
Dx oA
History
Physical exam
Lab tests
X-ray
Sx
Pain is the cardinal symptom of OA and is the major determinant of disability and functional impairment
Pain is not always present in patients with radiographic findings
Degree of radiographic findings does not always correlate with clinical symptoms
IMPORTANT NOTE: IS BAD OA ALWAYS WITH PAIN
no, very bad OA might not have proporitonal pain
and very mild OA might have a lot of pain
RADIOGRAPHIC FINDINGS NOT PROPORTIONAL WITH PAIN
mechanisms of pain?
multifactoral and may include:
Periostitis (bone remodeling)
Subchondral microfractures
Synovial inflammation
Periarticular muscle spasm
Bone ischemia
Elevated interosseus pressure
SSx OA
Monoarticular or polyarticular
Joint pain (usually relieved w/ rest)
Tenderness
Crepitus
Occasional effusion
Variable degrees of local inflammation
Bony enlargement
Stiffness (morning stiffness- less than 30min)
Decreased ROM
Deformities; misalignment
Muscle spasm/contractures
how long stiffness last OA
usually less than 30 mins
ROM OA
decrease
muscle spasms/conttractures OA
yes (bracing/protective spasms to avoid pain)
contractures due to prolonged limited ROM?
crepitus?
a grating sound or sensation produced by friction between bone and cartilage or the fractured parts of a bone.
common features/locaitons
hand
Heberden’s nodes at distal IP joint accompanied by lateral joint deviation
Bouchard’s nodes found at proximal IP joint
knee
Pain worsens with stair climbing, standing
Highly associated w/ obesity
spine
Vertebrae of L4, L5, C4-C7, upper T-spine
hip
Internal rotation and extension are reduced
note CPR:
mr/abd, f/e, er
treatment oa
Analgesics
Topical creams/gels
NSAIDs
Corticosteroids
other tx
Exercis:
Strengthening, low impact ROM exercise
Avoid stress on joints
Control weight
Warm-up/cool down
Ice
Pacing
note the dilemma
exercises that are good for osteoporosis cna be bad for OA
activiites that are good for OA, while not bad for osteoporosis, will not prevent it as well
either OA develops quicker, or osteoporosis
other tx OA, hydro surgery, complementary therapy (Vs allotherapy)
Hydrotherapy
Heat/cold (chronic)
Surgery
Clean up (arthroscopy) or replace joint
Complementary therapy
Acupuncture
Massage
Mobilization/manipulation
PT
chiro (?)
RA
A systemic inflammatory disease that predominantly manifests in the synovial membrane of diarthrodial joints
important feature of RA
hyperplasia of synovial fibroblasts
structural damage of cartilage, bone, and ligaments
where else?
extra articular manifestation
can effect a variety of organs and is a significant factor in morbidity and mortality of people w/ RA
Esp kidneys
etiolgoy
genetic + viral (?)
gender RA
Women > men (3:1)
age RA
ny age, prevalence incr. with age (25-50)
RA onset, remission
Onset gradual
Symptom free for months or years
Exacerbations and remissions
RA prognosis
Prognosis uncertain
Death can occur from extra-articular disease
RA and immune response
aberrant immune response in a genetically predisposed host that leads to chronic progressive synovial inflammation and destruction of joint archeticture
synovium and RA
Primary inflammatory lesion involves the synovium
Edema, fibrin exudation and hyperplasia of synovium
what type of exudate RA , where?
fibrin exudation and hyperplasia of synovium
other common feature/sx
Tenosynovitis is present in a majority of patients
extraarticualr menif
Extra-articular manifestations are common but individuals differ in the pattern of tissues involved
Ssx RA
Pain
Warm, red, swollen, tender joints
tiffness
Morning stiffness usually lasting more than 2 hours
Structural damage
Cartilage loss and erosion of periarticular bone (evident on xray)
how long morning stiffness
more than2 hours
where often begin RA
Often begins in hands and wrists
Usually symmetrical and uniform
most common site
PIP, MCP, wrists, knees, MTP, subtalar, C1, C2
(TV LIGAMENT OF C1-C2 articulation)
Han ddefomirtities
Swan neck – PIP hyperextended, DIP flexed
Boutonniere (buttonhole) – PIP flexed, DIP hyperextended
other ssx
tendon/muscle spasm (REFLEX MUSCLE GUARDING?)
Contracture (scar tissue, inflammation immune damage)
Subluxations and deformities may develop
Knee valgus
Baker’s cyst
d/t inflamed synovium
Neck pain
Unstable C1-C2 (important to rule out prior to mobilization/adjustments of upper cervical complex)
IMPORTANT CYST ASSOCIATED WITH RA
Baker’s cyst
d/t inflamed synovium
IMPORTANT LIGAMENT ASSOCIATED WITH RA NECK PAIN
TRANSVERSE LIGAMENT OF ATLAS
Unstable C1-C2 (important to rule out prior to mobilization/adjustments of upper cervical complex)
extra articular SSx
Rheumatic nodules
Develop in 50% of individuals
Form subcutaneously, in bursae and along tendon sheaths
Systemic symptoms include aching, stiffness, weight loss, fatigue
Ocular manifestaions
Dry eyes
Pericarditis
Pleurisy and laryngeal pain
Renal complications
Rare
Weight loss
Anemia
inflammation of SEROUS membranes
PERICARIDUM
pleura
Pleuritis (Pleurisy)
pericarditis
rheumatic nodules, devleop in what percentage of patients
Rheumatic nodules
Develop in 50% of individuals
Form subcutaneously, in bursae and along tendon sheaths
RA why dry eyes
Inflammation from RA causes abnormalities in the tear glands (lacrimal), significantly reducing fluid secretion
The symptoms associated with dry eyes are more common in the later part of the day, when tears from the tear gland (systemic) have dried up and evaporated.
RA why anemia
RA can be associated with different types of anemia, including anemia of chronic inflammation and iron deficiency anemia.
When you have an RA flare-up, the immune response causes inflammation in the joints and other tissues.
Chronic inflammation can lower the production of red blood cells in your bone marrow.
RA Dx
family history
Lab tests:
rheumatoid factor – present in 85% of people w/ RA
ESR & C-reactive protein
X-ray, imaging
C reactive protein test
C-reactive protein (CRP) is a protein made by the liver. The level of CRP increases when there’s inflammation in the body
ESR test (erythrocyte sedimentation rate)
What Is an ESR Test? An ESR test measures how far red blood cells settle to the bottle of a test tube in 1 hour.
Inflammation or infection can lead to extra proteins in the blood, which can make the red blood cells settle farther in a test tube. When this happens, the ESR is higher.
rheumatoid factor test
This test measures rheumatoid factors in a sample of your blood. High levels of rheumatoid factors may be a sign of rheumatoid arthritis
Tx RA
Corticosteroids to decrease inflammation and pain
Immunosuppressive drugs
NSAIDs
Surgery
Physiotherapy
RA prognosis
Difficult to establish d/t chronic nature of the disease, its variability and the difficulty in identifying milder forms
Spontaneous remission is possible
Approx 10% of cases
90% of joints affected are usually involved within the first few years of the disease
Patients with severe forms have a mortality rate approx 10 -15 years earlier than expected and d/t infections, pulmonary, renal, and gastrointestinal bleeding.
remission in what percentage
Spontaneous remission is possible
Approx 10% of cases
ankylosing spondylitis (AS)
etymology
ankylos meaning crooked, curved or rounded, spondylos meaning vertebra, and -itis meaning inflammation
AS affects
systemic disorder characterized by inflammation of the axial skeleton (SI joints, facets, IVDs) and large peripheral joints.
Seronegative spondyloarthropathy
MEDICINE
adjective: seronegative
giving a negative result in a test of blood serum, e.g. for the presence of a virus.
Spondyloarthropathies are a family of long-term (chronic) diseases of joints. These diseases occur in children (juvenile spondyloarthropathies) and adults. They include ankylosing spondylitis, reactive arthritis, psoriatic arthritis, and joint problems linked to inflammatory bowel disease (enteropathic arthritis).
Seronegative spondyloarthropathies
Seronegative spondyloarthropathies (SpA) are a family of rheumatologic disorders that classically include[1]: Ankylosing spondylitis (AS) Psoriatic arthritis (PsA) Inflammatory bowel disease (IBD) associated arthritis. Reactive arthritis (formerly Reiter syndrome; ReA)
ankylosis spondylitis
Ankylosis - immobility and fixation of a joint
Spondylitis - inflammation of the vertebrae
AS gender
Men > women (3:1)
Onset insidious
AS age
Typically occurs between ages 20 – 40
Average age is 26
remissions or no
Development variable
Exacerbations and remissions
Can lead to deformities
ettiology/cause
Idiopathic
genetic/ environmental
“Has genetic component (20% increased risk w/ 1st degree relative), but thought to be influenced by environmental factors”
HLA-B27 test
Human Leukocyte Antigen; subtype B27
The HLA-B27 test is primarily ordered to help strengthen or confirm a suspected diagnosis of ankylosing spondylitis (AS), reactive arthritis, juvenile rheumatoid arthritis (JRA), or sometimes anterior uveitis.
“Human leukocyte antigen B27 is a class I surface molecule encoded by the B locus in the major histocompatibility complex on chromosome 6 and presents antigenic peptides to T cells. “
ENTHESES ???????????????????????
Entheses are boney insertion sites of tendons and ligaments.
Enthesopathies are defined as the pathologies that affect the entheses.
ENTHESIS
“Enthesis” is rooted in the Ancient Greek word, “ἔνθεσις” or “énthesis,” meaning “putting in,” or “insertion.”
AS pathogneesis
Inflammation at the entheses is the central feature of AS (enthesitis)
(Entheses is the site where tendons and ligaments attach to bone.)
then what
Inflammation of ligaments results in fibrosis, bony erosions and eventually causes reactive bone growth and spurring
WHAT CAN HAPPEN EVENTUALLY
Eventual fusion of joint can occur
where usualyl begin ******
Usually begins in the lumbar spine and SI joints (sacroiliitis) and proceeds up the spine (over years)
AS and back pain
Insidious onset
Persistent for more than 3 months
Worse at night and w/ inactivity
Improved by activity
UNIQUE about AS (AS and ACTIVITY LEVELS)
Worse at night and w/ inactivity
Improved by activity
L spine stiffness in morning and time to improve
L-spine stiffness:
Typically AM
Takes more than 2 hours to get better
pain in posteiror thigh?
Pain in buttocks, low back, post. thigh
referral?)
what are some changes to spine posture?
thoracic hyperkyphosis
lumbar hypolordosis
Lumbar lordosis lost
Thoracic curve increases
Flexion contracture (hips)
AS and breathing problems
note fusion of vertebrae and surround joints/structures of costovertebral joints
Chest is fixed/flattened
Chest expansion limited
“Trouble breathing as the upper body curves forward and the chest wall stiffens. Severe ankylosing spondylitis can also cause scarring of the lungs (pulmonary fibrosis) and an increased risk of lung infection.”
decreased ROM of spine and pain
Pain diminishes over the years as fusion occurs
Muscle wasting
Fatigue
complications AS
Osteoporosis, fractures, stenosis, C1-C2 subluxation
SPINAL STENOSIS
Spinal stenosis happens when the space inside the backbone is too small. This can put pressure on the spinal cord and nerves that travel through the spine. Spinal stenosis occurs most often in the lower back and the neck.
“In severe cases, spinal stenosis may cause partial or complete leg paralysis that requires emergency medical treatment.”
AS c1-c2 subluxation
In ankylosing spondylitis, cervical spine can be involved and may progress to C1-C2 subluxation, also known as atlantoaxial subluxation, with a prevalence ranging from 13.8 to 21% in adults [5–8].
what percentage systemic manifestation
30% 1/3
which parts affected?
Uveitis, iritis, conjunctivitis
Inflammation of eyes
Pain, blurred vision, blindness
Large and small bowel disease
Cardiovascular involvement
is AS autoimmune?
Ankylosing spondylitis is an autoimmune disease.
Dx AS
History
Phiscal exam
Lab :
HLA B27 test
X-rays
Bamboo spine – vertebrae take on a fused appearance
Tx AS
Meds (anti-inflammatories)
Massage/Chiro/Physio
Sleep on hard mattress or cold floor (during inflammation)
Exercise, stretching
Breathing exercises
Surgery (severe cases)
AS breathing
Breathing exercises
AS where to sleep during flareup
Sleep on hard mattress or cold floor (during inflammation)
Psoriatic arthritis
Is an arthritis often associated with psoriasis of the skin
psoriasis
a skin disease marked by red, itchy, scaly patches.
psoriasis and arthritis
1 in 20 will develop arthritis with the skin condition
cause
idiopathic
psoriatic arthritis affects
Primarily affects distal joints of fingers and toes
When spine is affected (L/S and sacrum)
Stiffness, burning, pain
psoriatic arthritis Dx, Tx
same in men and women
Dx
Physical exam, joint swelling, skin sores
Tx
NSAIDS
Antirheumatic drugs
—> E.g. Methotrexate
Steroids
Surgery
RMT, PT, Hydro
polyarthritis define
the medical term for having arthritis that affects five or more of your joints at the same time
Gout (METABOLIC ARTHRITIS)
group of disorders in which crystals of monosodium urate (uric acid) are deposited in the tissues, accompanied by attacks of acute arthritis
where does uric acid go
Marked by an elevated level of serum uric acid and the deposition of urate crystals in the joints, soft tissue AND KIDNEYS
normal presence of uric acid
Uric acid is normally formed with the break down of purines (Adenine, Guanine)
Uric acids dissolves in the blood, passes through the kidneys and is then excreted
abnormal presence of uric acid
With too much production or with poor kidney function uric acid may precipitate out and accumulate in body tissues
Crystals frequently collect on articular cartilage
These trigger an inflammatory response resulting in local tissue necrosis and proliferation of fibrous tissue (scar tissue?)
tophi (tophus)
Tophi are ordered aggregates of monosodium urate (MSU) crystals that develop in long-lasting, neglected gout.
Most of them are subcutaneous and involve the feet, hands, knees, and elbows.
They are a feature of advanced gout and indicate a large crystal load.
1) primary hyperuricemia
Inherited disorder of uric acid metabolism
2) Secondary hyperuricemia
Occurs as a result of some other metabolic problem
Increased DNA turnover via Leukemia, lymphoma, chemotherapy
3) Idiopathic hyperuricemia
..
cause gout (metabolic arthritis)
Can be the result of urate overproduction or decreased urinary excretion of uric acid
note intracellular accumulation (?) uric acid underexretion, oversecretion, underutilization (?)
and gout (?)
..
risk factors
Diet rich in purines (adenine, guanine)
Nitrogen containing compounds found in foods
Purine-containing foods: red meats, organ meats, shellfish, sweet breads, dairy, beer
gender distribution, gout (Metabolic arthritis)
Male > female – 9:1
Usually 40-50 years
other risk factors, gout
Obesity
Excessive weight gain, especially with puberty
Moderate-heavy alcohol intake
Hypertension
Abnormal kidney function
Certain medications
more risk factors
Certain diseases - lymphoma, leukemia, hemoglobin disorders
—> Increased nuclear-protein turnover
Decreased thyroid function
Dehydration
Excessive dining
gout and kidney stones
Studies have shown that patients with gout are 60 percent more likely to develop kidney stones.
Kidney stones, also known as renal lithiasis, are similar to gout in that they are both related to a high concentration of uric acid in the blood.
most common where?
Most common - first MTP joint
Can also affect fingers, wrists, elbows, ankles, knees
onset of pain, and inflammation
Rapid onset pain, swelling, heat, redness, tenderness, +/- fever
tophi…
Nodular masses of uric acid depositing in soft tissues of body - tophi
is gout unilateral or bilateral
Tends to be unilateral
can be bilateral (..)
gout (metabolic arthritis) diagnosis
differential diagnosis (DDx)
—> RULE OUT OTHER POSSIBILITIES
E.g.
Septic (Infectious) Arthritis,
RA,
neoplasm (vs tophi)
important diagnostic tools
Monosodium urate crystals (tophi) are found within synovial fluid, connective tissue or articular cartilage
Serum uric acid levels are elevated
Gout treatment
To end acute attacks and prevent recurrent attacks (NSAIDS, Colchicine)
correct the hyperuricemia
Colchicine
a yellow compound present in the corms of colchicums, used to relieve pain in cases of gout.
Gout, Tx
Adequate fluid intake
Weight reduction
Dietary changes
Decrease alcohol (increases purine catabolism)
NSAIDS, corticosteroid injections, colchicine
Uric acid inhibitors (allopurinal)
infectious arthritis (SEPTIC ARTHRITIS)
Joint inflammation as a result of infection
Can be due to bacteria, fungus, virus
bacterial pathogens vs septic arthritis
Staphylococcus aureus - the most common cause in adults
(Staph Infection)
Haemophilus influenzae - the most common cause in children
Neisseria gonorrhoea - in sexually active young adults
other bacterial pathogens vs septic arthritis
Escherichia coli - in the elderly, IV drug users and the seriously ill
(E. coli)
M. tuberculosis - Cause septic spinal arthritis (Pott’s Disease)
Streptococcus
Gonococcus
how does infection get into joint for spetic arthritis
septicemia (blood poisoning)
blood poisoning, especially that caused by bacteria or their toxins.
the presence of microorganisms or their toxins in the blood, causing disease; septicemia.
how else does infection get into joints
Direct infection – needle users
Iatrogenic – medical treatment
Catheters
Trauma
Immunocompromised patients
Direct infection – needle users
Iatrogenic – medical treatment
Catheters
during medical treatment
insufficient protocols
pathogenesis, septic arthritis
Bacteria adheres to synovium:
Leads to scar tissue and synovium proliferation
Hydrolysis of proteoglycans and collagen (breaks down articular cartilage)
Cartilage and bone destruction occur:
Takes a very short time for joint death and direct pressure necrosis
infective arthritis clinical manifestations
Acute onset of joint pain, swelling, tenderness, loss of motion
Males and females (equal?)
Fever, chills
Pus
Skin lesions
Polyarthralgia
Joints primarily affected:
Shoulders, knee, hips (proximal joints)
Infective arthritis Dx
PE - pain, swelling, redness in joint
History - STI’s, IV drug use, IC state, surgery, trauma
Blood test - increased WBC count, high RBC sedimentation rate
—> ESR TEST
Fever
Aspirate and culture synovial fluid
X-ray
Aspirate and culture synovial fluid (Synovial Fluid Analysis)
Gram stain and bacterial culture: synovial fluid aspirate is analyzed for gram stain and both aerobic and anaerobic culture to determine the presence of infection; the presence of any organism indicates abnormal findings.
Infective arthritis Tx
Medical emergency
Antibiotics via IV
Drain infected joint to decrease pain
Rest
infective arthritis prognosis
Acute nongonococcal bacterial arthritis can destroy articular cartilage, permanently damaging the joint within hours or days
”
Although it’s rare, septic arthritis is a serious condition. It can cause permanent damage to your affected joint and other complications.
It can also cause death if it’s not treated. Be sure to see your healthcare provider or go to the nearest hospital immediately if you experience symptoms.
antibiotics
Septic arthritis often needs treatment right away with antibiotics. This can improve symptoms within 48 hours. Some infections caused by fungi need treatment with antifungal medicine. Viral infections are not treated with medicine.
Antibiotics often stop the infection in a few days, but in some cases, they must be given over several months. Infectious arthritis caused by a virus usually goes away on its own with no specific treatment and fungal infections are treated with antifungal medication. Joint Drainage.
Charcot disease
Aka Charcot’s arthropathy, neuropathic arthropathy
Progressive degeneration of the stress-bearing portion of a joint
Most commonly associated with diabetic neuropathy
Most commonly occurs in the foot
charcot
Involves bone destruction and absorption leading to deformity, dislocation, ulcerations, bone fragments and a unstable joint
Cause
Any condition that decreases peripheral sensation, proprioception and fine motor control
most common cause
DM neuropathy m/c
diabetic neuropathy
.
first theory of underyling mechanism
Neurotrauma: Loss of peripheral sensation and proprioception leads to repetitive microtrauma to the joint in question; this damage goes unnoticed by the neuropathic patient, and the resultant inflammatory resorption of traumatized bone renders that region weak and susceptible to further trauma. Indeed, it is a vicious cycle. In addition, poor fine motor control generates unnatural pressure on certain joints, leading to additional microtrauma.
second theory of underyling mechanism
Neurovascular: Neuropathic patients have dysregulated autonomic nervous system reflexes, and de-sensitized joints receive significantly greater blood flow. The resulting hyperemia leads to increased osteoclastic resorption of bone, and this, in concert with mechanical stress, leads to bony destruction.
both mechanisms?
In reality, both of these mechanisms probably play a role in the development of a Charcot joint.
charctor SSx
Swelling, warmth, redness,
subluxation/dislocation, deformity, fractures
Complications:
joint infections, hemarthrosis, septicemia
tx charcot
.
