Musculoskeletal Disorders (MODULE 9) Flashcards
Name the two “main” types of arthritis
• Osteoarthritis (OA)
• Rheumatoid Arthritis (RA)
What is osteoarthritis (OA)?
Most common form of arthritis affecting synovial joints
• Common in the knees, hips, hands, cervical and thoracic spine
• Becomes symptomatic in 40/50s and is nearly
universal by age 80
***Chronic, progressive arthropathy
What are the clinical manifestations of OA?
What are the OA classifications?
• Progressive changes to cartilage
and bone within joint • Loss of cartilage and joint space • Hypertrophic changes to bone
(osteophyte formation)
Classified as:
* Primary Osteoarthritis
• Idiopathic (do not know why it occurred)
* Secondary Osteoarthritis
• Caused by a known cause
• Trauma, diseases, infections
Signs and symptoms of OA include
• Locking and instability
movement
• Osteophytes (bone spurs)
• Inflammation symptoms
• Pain, swelling, redness, heat
• Pain, discomfort, and tenderness
• On activity, alleviated with rest
• Stiffness
• Especially after lack of motion, inactivity
• Decreased ROM and flexibility
• Swelling
• Crepitus and crunching sounds with
What are the chondrocytes role in OA?
Synthesize ECM components
Chondrocytes are in a continuous process of making new cartilage (ECM)
and degrading old cartilage components
Collagen fibers overview:
Hard, insoluble, and fibrous protein • Most abundant protein • Produced by fibroblasts and other cells such as chondrocytes
• Vitamin C is the essential cofactor for the two enzymes required for collagen synthesis
• Support structures and anchor cells to each other
• Type I Collagen Fibers
• Most prevalent in the body
• Found in skin, tendon, ligaments, artery walls, scar and bone tissue
• Provides structural support with tensile strength
• Type II Collagen Fibers
• Most prevalent in cartilage, especially hyaline
• Provide tensile strength
health and function of cartilage depends upon?
Chondrocytes maintain the balance of cartilage breakdown and synthesis
• Cartilage Breakdown vs Cartilage Production
OA is progressive loss of articular cartilage that leads to bones rubbing on each other (friction) which leads to inflammation which leads to tissue damage and PAIN
Pathophysiology of OA involves?
SOMETHING (risk factors) causes damage to the articular cartilage
• Trigger of articular damage is often unknown
• Can be initiated by trauma, age, or even medications (risk factors)
*Exact mechanism is not 100% understood
—> Macrophages in the synovial joint become activated and secrete CYTOKINES
Cytokines Lead To:
• 1. Recruitment of more leukocytes
• 2. Stimulate osteoblast activity
• 3. Stimulate other cells - Chondrocytes and synovial cells to secrete Matrix metalloproteinases (MMPs)
What is MMPs? What do they do?
At the same time MMPs are doing their thing…. What is taking place?
Matrix Metalloproteinases
- Enzymes that breakdown the matrix within the cartilage
Chondrocytes are trying to
repair the damaged cartilage
• Switch to becoming more cartilage destructive than synthesis
Chondrocytes start making less of the proteoglycans and switch to making
type I collagen fibers (should be Type II)
• Totally weird
• Type I collagen fibers and the proteoglycans don’t mix as well as type II collagen fibers • Cartilage LOSES ELASTICITY and becomes further damaged!
How does the chronic portion of OA work pathophysiologically?
Chondrocytes eventually (over years) ”burn out” and undergo apoptosis. —> Causes cartilage to become softer, weaker, and loss elasticity- oh no! • The articular cartilage starts to break down and fractures occur in the
cartilage
**Called FIBRILLATION- cracking of the cartilage
• Fibrillation can lead to pieces of the cartilage breaking off
**Called joint mice (eww!)
• Cells in the synovial membrane try to remove the joint mice, it triggers
further inflammation and release of more cytokines
—> Synovitis
• Eventually the cartilage complete erodes away, exposing the bone
• As the exposed bone grinds against each other leads to subchondral
ossification and osteophyte formation
—>Cytokines stimulate osteoblast
• When bone is rubbing on bone- it leads to BONE EBURNATION
—> Subchondral bone is converted to an ivory-like (marbled) surface at the site of friction
—> Called subchondral sclerosis
—>Over time, irreversible destruction of bone, cartilage, ligaments
• Loss of cartilage and joint space
Seronegative vs Seropositive Arthritis
Detection of auto antibodies within the blood • Can still have disease autoimmune diseases with or without a
positive detection of autoantibodies • If have a positive detection- it typically means disease progression
will be more severe
The main distinction between seronegative and seropositive arthritis is the presence or absence of certain antibodies in the blood, which helps differentiate between different types of arthritis. Seronegative arthritis includes conditions like ankylosing spondylitis and psoriatic arthritis, while seropositive arthritis is most commonly associated with rheumatoid arthritis
Bone hypertrophy
Osteophyte formation - growth of the bone at the lateral edges
Bone eburnation and Subchondral sclerosis
• Exposed bone appears polished
• Exposed bone regions undergo bone thickening
How many stages of OA?
OA and ADLs:
4
Inability to complete activities of daily life
—Decreased movement and ability to exercise
• Increases risk for diabetes, weight gain, CVD • Increased risk for falls and fractures
—People with osteoarthritis experience as much as 30 percent more falls and
have a 20 percent greater risk of facture than those without OA (Arthritis Foundation)
• Mental health
—Depression can occur due to lack of movement and ADL
35
What are the treatments for OA?
Analgesics -
- over the counters (acetaminophen; can cause liver damage) NSAIDS (GI disturbances/stomach ulcers
- Prescription
- Corticosteroids
Non-Drug Treatments
- Exercise - weight loss 0 assistant dives - chiropractic care and PT therapies - Tens unit
Surgical replacement - Common for Hip and Knee
The role of MMPs in osteoarthritis is that directly kill chondrocytes.
• A. True
• B. False
F
Chondrocytes and synovial cells to secrete Matrix metalloproteinases (MMPs).. These enzymes play a crucial role in the brakdown and remodeling of th extra cellular matrix (ECM)
Enzymes that breakdown the matrix within the cartilage
• At the same time MMPs are doing their thing…..Chondrocytes are trying to
repair the damaged cartilage
All of the options are true regarding bone eburnation, except?
• A. Is a result of joint mice
• B. Occurs when there is bone on bone contact
• C. It involves the subchondral bone
• D. Also referred to as subchondral sclerosis
A
All of the options are true regarding osteoarthritis, except?
• A. Fibrillation is the cracking of the elastic cartilage
• B. MMPs lead to the further destruction of the cartilage’s matrix
• C. Chondrocytes can die to being overworked and stimulated
• D. Joint mice can lead to increased release of cytokines and MMPs
A
Break down and fractures in articular cartilage; fibrillation can lead to pieces of the cartilage braking off = called joint mice
What is joint mice?
Fibrillation can lead to pieces of the cartilage breaking off
Joint mice can lead to increased release of cytokines and MMPs
Cells in the synovial membrane try to remove the joint mice, it triggers
further inflammation and release of more cytokines
• Synovitis
What are the two seropositive autoantibodies and what do they do?
Rheumatoid Factor (RF)
• Autoantibody found within autoimmune conditions
• Target healthy cells in joints, glands, and other tissues of the body
• Not specific to rheumatoid arthritis
Anticyclic Citrullinated Peptide (anti-CCP)
• Autoantibodies that are directed towards proteins that are citrullinated
—>Arginine amino acid residues are converted to citrulline
• Target healthy cells in joints
• Used to help diagnose RA
RA is what and is initiated by what hypersensitivity reaction?
RA is chronic inflammation of synovial joints that is mediated by an autoimmune reaction
Type III hypersensitivity reaction
T or F
RA can lead to total joint destruction leading to fusion of bones
T
Loss of ROM and disfigurement occurs
T or F
In RA the heart and lungs can eventually be damaged
T
Damage to other organs can be involved including the heart and lungs
Chronic inflammation leads to 4 changes in the synovium. What are these?
• Synovial hyperplasia
• Pannus formation
• Erosion of cartilage and bone
• Joint deformities
Synovial cells proliferate in response to chronic inflammation
• Leads to the development of a pannus
Pannus Formation will?
• Damage cartilage
• Erode bone
• Cause secretion of MMPs which further destroys cartilage
• Causes irreversible damage, leading to joint deformities and functional impairment
*Synovial fibroblasts proliferate in response to chronic inflammation; this proliferation leads to the formation of pannus, an abnormal, thickened, and inflamed tissue, mass; pannus invades cartilage and bone, causing cartilage destruction, bone erosion, and joint deformations; pannus is a hallmark of RA and contributes significantly to the progressive joint damage and disability characteristics of the disease.
What is the key goal of pannus formation associated inflammation? (RA)
The control of pannus formation and its associated inflammation is a key goal in the treatment of rheumatoid arthritis.
As the disease progresses- joint space is replaced with fibrous
connective tissue that eventually leads to bone fusion
• Fibrous ankylosis ——> Bony ankylosis
Inflammatory cells and chemical mediators eventually leave the synovial joint and affect other joints and organs too
These include?
Brain, skin, lungs, heart, vessels, liver
T or F
RA is unilateral
FALSE
Always bilateral
Small joints of phalanges in the hands, wrist, and feet affected first
What are the RA deformations?
• Ulnar Deviation
• Boutonniere Deformity
—>Extensor tendon ruptures
• Swan Neck Deformity
—>Flexor tendon ruptures
What is the diagnosis and treatment for RA?
Diagnosis - Physical examination; imaging; Blood work (Rheumatoid factor (RF) antibodies; Anti-cyclic citrullinated peptide (CCP) antibodies; Erythrocyte sedimentation rate; C-reactive protein (CRP))
Treatment - No cure; medications (NSAIDs, Corticosteroids, Biological agents, Disease-modifying anti-rheumatic drugs); Physical and occupational therapy; surgery.
What is Juvenile Idiopathic Arthritis (JIA)?
• AKA Juvenile Rheumatoid Arthritis • Basically, RA in juveniles
• JIA affects one or more joints for at least 6 weeks in a child age 16
or younger
—> Affects bone development
• Children grow out of it (not chronic)
• Nearly half of children fully recover from joint damage
• Multiple types of JIA
T or F
There is a cure for JIA
F
No cure
Can medicate with NSAIDs, corticosteroids, biological agents, disease-modifying antirheumatic drugs, physical and occupational therapy
What are the signs and symptoms of JIA?
Similar to OA and RA
Slow Growth
Diagnosis of JIA involves?
Imaging, blood work (Rheumatoid factor antibodies (RF factor); Anti-cyclic citrullinated peptide antibodies (CCP); Erythrocyte sedimentation rate (ESR or sed rate); C-reactive protein (CRP))
All of the options are true regarding a pannus formation, except?
• A. It is due to the thickening and hardening of the articular cartilage and synovial
membrane
• B. Can lead to increased destruction of bone and cartilage
• C. Increases the release of MMPs
• D. Leads to bony ankylosis
A
What option is TRUE regarding RA?
• A. Most RA patients are seronegative
• B. It is because of a type 4 hypersensitivity reaction
• C. The pannus formation is an abnormal hardening of articular cartilage
• D. It is bilateral in its clinical presentation
D
RA only affects the joints.
• A. True
• B. False
F
What is Lyme disease? Overview:
If untreated Lyme infection can lead to an array of symptoms including inflammation of joints and…?
Lyme disease is the most common vector-borne disease in the US
—>Caused by the bacterium Borrelia burgdorferi
• Transferred by deer tick bite
• Commonly unilateral
• Commonly larger joints- knee
• Causes severe joint pain and swelling
• Headaches and Fevers!!!
• Body aches
• Extreme fatigue • Skin Rash
If not treated, damage could become permanent
T or F
Lyme disease is unilateral
T
Diagnosis for Lyme disease and treatment involves?
Diagnosis
• Checking for antibodies • ELISA (enzyme-linked immunosorbent assay) test • Western blot test
Treatment
• Antibiotics: ~1 month • Sometimes repeated doses
Gouty Arthritis (Gout) overview:
Arthritis of a joint caused by urate crystals being deposited into a joint
• Commonly only affects 1 joint at time
• First metatarsal joint of big toe
Signs/Symptoms
Of Gouty Arthritis
• Can have flare-ups (gout flares) that last days to weeks • When no symptoms- remission • Repeated and chronic episodes of flare ups can lead to gouty arthritis • Sudden, intense, burning/fire feeling joint pain
• Even a bed sheet on it is painful • Redness and swelling of joint
What is hyperuricemia is and what arthritis does it associate with?
Hyperuricemia
• High levels of uric acid in the blood
• Uric acid is not very soluble in fluid
• Forms sharp monosodium urate crystals
Hyperuricemia Causes: 1. Increased Dietary Intake of Purines
a. Red meat, organ meats,
seafood, HFCS
2. Decreased Uric Acid Excretion
a. Dehydration: Decreased water
and increased alcohol
Gouty arthritis
What is uric acid? What condition does it associated with?
Uric acid is a by product of purine degradation
within the kidneys
• Attracts WBCs and cytokines to induce inflammation
and is then able to be excreted from the body via urine
• These urate crystals get deposited in joints and within the kidneys
Associated with gout toe
Diagnosis and treatment of Gouty Arthritis
Diagnosis
• Joint fluid extraction • Blood test of uric acid
• Ultrasound
Treatment
• NSAIDs, corticosteroids
• Medications that block uric acid production and improve excretion
• Dietary changes
What is psoriatic arthritis?
Psoriasis is an autoimmune skin disorder that causes proliferation
of skin in random areas on the body
• Red/purple/white, itchy, patchy scales on the skin
• Due to autoimmune condition- psoriatic arthritis can occur
T or F
Some individuals who have psoriases can develop psoriatic arthritis
T
What are the signs and sympomts of psoriatic arthritis?
Joint pain and inflammation
(bilateral or unilateral) • Swollen fingers and toes • Foot pain at Achilles tendon
T or F
Psoriatic arthritis is commonly a seronegative arthritis, and has a cure
F
Commonly a seronegtive arthritis BUT has NO cure
What is reactive arthritis?
Used to be called: Reiter’s syndrome (NBCE loves this) • Joint pain and swelling triggered by an infection in another part of
the body
• Usually targets the knees, ankles and feet • Can also affect the eyes and urinary system
• Mainly bacterial infection (foodborne and sexually) • Campylobacter, Chlamydia, Clostridioides difficile, Escherichia coli,
Salmonella, Shigella, Yersinia • Most often the intestines, genitals or urinary tract
Which arthritis is treated with antibiotics?
• A. Gouty arthritis
• B. Psoriatic arthritis
• C. Lyme disease arthritis
• D. Osteoarthritis
• E. Reactive arthritis
C, E
All of the options are true regarding gouty arthritis, except?
• A. Gout can have flare ups and remission
• B. It caused by high levels of antibody-antigen complexes deposited in the joint
• C. Causes an intense amount of pain
• D. Commonly affects the big toe
B
All of the following options are true regarding Lyme disease, except?
• A. It is caused by a bacterial infection
• B. Headaches and fevers are common symptoms
• C. Joint arthritis is bilateral
• D. Fatigue is a common symptom
C
Disc components review
• Nucleus Pulposus
Gel like structure; 75% water
Accounts for much strength and flexibility of spine
• Annulus Fibrosis
Concentric rings of collagen fibers
Effective resistance of multidirectional movements
• Vertebral Endplate
Located superior and inferior portions of IVD
Allows diffusion and is main source of nutrition
• Disc degeneration, mechanical compression, poor posture abnormal
rotational stress, spinal stenosis, spondylolisthesis, pregnancy
Degenerative Disc Disease (DDD) overview
• Is not necessarily a disease but a condition where the intervertebral
discs undergo degenerative changes and causes pain
• Anatomical changes • Loss of function
• As you age, your discs are going to ”wear out”
-Some faster than others
-But not everyone has pain associated with it
• Common Causes
-Disc injury
- Disc becoming dehydrated
-Disc tears from daily activities and physical activities
Symptoms, treatment of DDD
Symptoms - pain increases with bending, twisting, lifting
Numbness/tingling in extremities
Transient pain
Treatment- Chirpractic care, NSAIDs/Corticosteriods, icing, lifestyle changes
Poor outcomes - Damage that is done is done, must correct postural imbalances
What is slipped capital femoral epiphysis? What does this ential?
Common hip condition in adolescents
• Growth plate present • Growth plate fractures and causes a slippage of the neck of femur
from the epiphysis (capital)
• Technically the femoral neck is displaced anterolaterally and superiorly
slippage is severe- can tear the epiphyseal blood vessels
• Causes avascular necrosis of femoral head • Causes of slippage is unknown but risk factors:
• Obesity
• Trauma
• Family history
Signs/symptoms of slipped capital femoral epiphysis
Diagnosis/treatment
Mild case - pain increases the groin; worsen with activities and may lead to limp
Severe case - walking is greatly affected; leg length inequality; externally rotated leg
Diagnosis - x-ray; MRI
Treatment - Surgery
Osteochondrosis overview: Pathophysiology:
Cause is unknown but believed to involve?
Osteochondrosis is a group of disorders that affect the growth plates of bones in
children and adolescents, leading to disturbances in bone growth and development
• Caused by the loss of blood supply to bone tissue, leading to necrosis and potential collapse of the
affected bone structures • Results in severe joint pain and dysfunction
Pathophysiology:
• Loss of blood flow to the epiphysis
• Causes bone necrosis
• Re-establishment of blood flow
• Leads to removal of necrotic bone tissue and little recalcification
Cause is unknown but believed to involve:
• Rapid Growth Phases
• Physical Activity
• Nutritional and Hormonal Factors
What are the three classifications of osteochonrodsis?
- Spinal (Physeal)
• Affects the growth plates (physes) specifically
• Scheuermann’s Kyphosis - Articular Osteochondrosis
• Affects the joints
• Legg-Calvé-Perthes disease, Köhler’s disease, Freiberg’s infraction - Non-Articular Osteochondrosis
• Affects sites other than the joint spaces- typically where tendons and ligaments
attach to bones • Osgood-Schlatter’s disease, Sever’s disease
Scheuermann’s Kyphosis overview
Scheuermann’s Disease
• Juvenile osteochondrosis of the spine affecting the thoracic vertebrae
— Leads to increased kyphosis of the thoracic spine
• Caused by osteochondrosis of growth plates within the thoracic spine
— Causes disruption of normal growth and ossification at the vertebral growth plates
— Wedge shaped vertebrae
— Anterior portion grows slower than posterior
*Results in an increase kyphotic curve of thoracic spine
• Stooped posture
• Patients cannot consciously correct their posture
• About 25% will develop scoliosis
Signs/Symptoms/treament of scheuermann’s kyphosis
S/S - Pain in the neck/back; postural imbalances; hyperhypoosis (hunchback); hyperlordosis; Schmorl’s nodes; muscle spasms; decreased lung capacity; tight hamstrings
Treatment - monitoring/exercise; chiropractic; PT; bracing; surgery if severe
What option is TRUE?
• A. Scheuermann’s disease is associated with a hyperkyphosis curve in the
thoracic spine
• B. Degenerative disc disease is reversible
• C. Slipped capital femoral epiphysis commonly occurs in adults
• D. Schmorl’s nodes are associated with degenerative disc disease
A
Slipped capital femoral epiphysis could lead to avascular necrosis.
• A. True
• B. False
A
Degenerative disc disease can lead to neuropathies.
• A. True
• B. False
A
All of the following options are true regarding osteochondrosis,
except?
• A. Osgood-Schlatter’s disease pertains to the tibial tuberosity
• B. It is due to increase activity of osteoclasts
• C. Scheuermann’s disease creates wedged vertebrae
• D. Can disrupt endochondral ossification
B
Spondylo terminology
Spondyl/o
vertebrae; spine
Spondylitis
-itis: inflammation
Spondylosis
destruction
-osis: condition of
Spondylolisthesis
-listhesis: slipping or falling
Spondylopathy
-pathy: condition of
Spondylolysis
-lysis: separation, breakdown,
What is spondylogysis?
Condition where there is a break in the pars interarticularis of the
vertebral arch
• Spondylolysis
—Fracture can be unilateral or bilateral • Spondylolysis
• Commonly occurs at L5
— Can also occur at L4 and rarely in the cervical spine
• Etiology
— Unknown but associated with activities (sports) that have forceful blows to the
spine or repetitive force/stress and hyperextension
• Stress factures in this region are common for adolescents
• Affects 3-7% of population
Signs/symptoms/diagnosis/treament/concerns of spondylolysis
Signs/Symptoms
• Asymptomatic
• Low back pain that increases on activity
Diagnosis
• X-ray (oblique view)
• Scotty dog
• Scotty dog
• Scotty dog
• MRI
Treatment
• Monitor
• Bracing
• Strengthening exercises
• Activity restrictions • Surgery
• Do you adjust a spondylolysis? No
Concerns
• Can lead to a spondylolisthesis
What is spondylolisthesis?
The cousin to spondylolysis
* Displacement or slippage of one vertebrae compared to another
• Commonly it is L5 slipping off the sacral base
• Slippage can technically occur in any direction but is most commonly
anterior (forward) displacement
—Will focus on anterolisthesis
- Important to note- you can have a spondylolisthesis WITHOUT a
spondylolysis
Types of spondylolisthesis
• 1. Congenital spondylolisthesis
• 2. Isthmic spondylolisthesis
• Due to spondylolysis
• 3. Degenerative spondylolisthesis
• Most common type
• Due to aging
• 4. Traumatic spondylolisthesis
• 5. Pathological spondylolisthesis
• 6. Post-surgical spondylolisthesis
Signs/Symptoms of Spondyloisthesis
• Asymptomatic • Tenderness/pain over the area • Pain on hyperextension of lower back • Intermittent sciatica symptoms • Increased intrathecal pressure may cause momentary increase of pain • Possible gait changes due to pain and muscle changes
• Tight hamstrings
• 4-6% of population has this condition • If diagnosed 50+ yoa; then degenerative spondylolisthesis • If diagnosed <40 yoa; then isthmic spondylolisthesis
What does DISH stand for? What does this entail?
Diffuse Idiopathic Skeletal Hyperostosis (DISH)
• Skeletal condition characterized by the calcification and
ossification of ligaments, tendons, and soft tissues
—Hyperostosis: excessive growth or thickening of bone
—Primarily affects the spine (thoracic)
• DISH occurs when there is calcification of the ligaments, tendons,
and soft tissue surrounding the thoracic spine
—Leads to the formation of syndesmophytes that can bridge adjacent
vertebrae giving the spine a distinctive “flowing” appearance on X-ray images
—Posterior and anterior longitudinal ligament can be affected
—Primarily the anterior longitudinal ligament
What’s the difference between marginal syndesmophytes and non-marginal syndesmophytes?
• Marginal Syndesmophytes
— Ligament ossification that develop along the edges of the vertebrae
• Non-Marginal Syndesmophytes
— Ligament ossification that develops beyond the edges of the vertebral margin
Clinical manifestation of DISH
Clinical Manifestations
• Flowing candle wax appearance on X-
ray • Non-marginal syndesmophytes
** Four contiguous vertebrae
• Disc height preserved
• No SI joint involvement
• No presence of osteopenia
Etiology, S/S, Diagnosis, and Treament of DISH
*Slide 124
Etiology
Diagnosis
• There is no known cause to the
pathophysiology of DISH • High majority of causes develop
after the age of 50 years of age
Signs/Symptoms
Treatment
impingement
• Commonly are asymptomatic • Back pain • Decreased ROM • Stiffness with flexion/extension • Dysphagia
• Imaging • Ossification along the anterolateral aspect of
at least 4 contiguous vertebrae • Disc height preserved
124
• No cure or treatment to stop calcification • Manage the symptoms
• Stretching/Strengthening
• Heat
• Analgesics • Surgery if there is nerve/structure
What is Ankylosing Spondylitis?
Ankyl/o = Bent, crooked, stiff, fused, fixed, closed
• Chronic inflammation due to an autoimmune response
—Classified as a seronegative spondyloarthropathy
—No autoantibody has been found
• Chronic inflammation of the intervertebral joints, facet
joints, and SI joints
• More commonly diagnosed in individuals under 40
• Males primarily
T or F
Ankylosing Spondylitis is an autoimmune response
T
What is the pathophysiology of Ankylosing spondylitis?
Most individuals have gene HLA-B27 that impacts the self-tolerance of self
antigens
• About 5% of population with HLA-B27 gene will develop ankylosing spondylitis
• About 90% of individuals who have ankylosis spondylitis have HLA-B27 gene
• Immune system ”attacks” intervertebral discs, facet joints, and SI joints
• Causes massive inflammation and joint damage
• Joint damage is then replaced with fibrous fibers (fibrin) by fibroblasts
126
• Limits ROM • Eventually, this fibrous fiber undergoes ossification
• Syndesmophyte formation
• Drastic loss of ROM
Clinical Manifestations of Ankylosing spondylitis
CM - Bamboo spine; squaring of vertebrae; marginal syndesmophytes; Romani’s lesions; bilateral SI joint erosion/sacrolilitis; osteopenia
S/S - Relasping and remitting pain and stiffness in the back and hips; decrease ROM; hyperkyphosis
Complications - Eye
• Develop eye inflammation and lead to vision problems
• Compression fractures
• Can have osteopenia develop
• Heart valve
• Aortic valve complications
Treatment for Ankylosing spondylitis
Treatment
• Goal is to relieve pain and impede/delay complications and
deformities • Medications for pain and trying to reduce autoimmune function • Stretching and strengthening exercises
What is Pagett’s disease of bone?
• Dysregulated bone tissue homeostasis and remodeling
• Excessive bone reabsorption followed up excessive and
disorganized bone formation
— Leads to abnormal structural changes, deformities, and weakened bone
structure
• Commonly affects the skull, lumbar spine, pelvis, femur
• Etiology
• Exact cause is unknown
• Can be triggered by a viral infection
• Genetic influence
What are the phases of Pagett’s disease?
• 1. Lytic (osteoclast) Phase
• Osteoclasts demineralize bone (bone reabsorption)
• 20x more than usual
• 2. Mixed (lytic and blastic) Phase
• Due to increased and continued osteoclast activity, osteoblasts are recruited
to the area
• 3. Sclerotic (osteoblastic) Phase
• Bone formation exceeds bone resorption • Bone is structurally disorganized and weakened
Stats associated with Pagett’s disease
** on slide 131
What is osteogenesis imperfecta?
**S/S and treatment on slide 133
AKA: Brittle Bone Disease
• Group of genetic disorders that affect primarily affect the bones
causing osteoporosis and fragile bones
• Affects bone density and quality of bone tissue
• Genetic mutation that leads to improper collagen fiber formation
• Type I collagen fiber • Many different types that can affect other areas of the body
• Eyes, nervous system, gastrointestinal
All of the options are true regarding DISH, except?
• A. Syndesmophyte formation
• B. SI joint involvement
• C. A flowing wax appearance of vertebrae on X-ray
• D. It is a result of calcification of ligaments, tendons, and soft tissue
B
Spondylolysis is when the vertebral body is slipping off the vertebrae below it.
• A. True
• B. False
B
All of the statements are true, except?
• A. Ankylosing spondylitis leads to a bamboo spine on X-ray
• B. Paget’s disease of bone is due to mutations of type 1 collagen fibers
• C. A sign/symptom of osteogenesis imperfecta is blue sclera
• D. Spondylolisthesis could lead to serious spinal complications
B
Bone fractures: Fractures can occur due to trauma or pathological processes that
make the bone weaker
• Various characteristics, features, complications, treatments
depending on the type of fracture; what are the types?
• Closed/Simple Fracture
—Overlying skin is intact
• Open/Compound Fracture
—Bone breaks through the surface of the skin surface
• Displaced Fracture
—Bone breaks into two or more pieces and moves out of alignment
• Non-Displaced Fracture
—Bone breaks but does not move out of alignment
Classifications of bone fractures
(Do not need to know for exam; just board exam)
• Avulsion Fracture
—When a fragment of bone is separated from the main mass
• Buckled Fracture
—Also referred to as impacted fracture
—Ends are driven into each other; commonly seen in arm fractures in children
• Comminuted Fracture
—The bone breaks into several piecesr
• Compression or Wedge Fracture
—Usually involves the bones in the back (vertebrae)
• Greenstick Fracture
—An incomplete fracture in which the bone is bent; occurs most often in children
• Linear Fracture
—The break is parallel to the bone’s long axis
• Oblique Fracture
— The break has a curved or sloped pattern
• Pathologic Fracture
—Caused by a disease that weakens the bones
• Spiral Fracture
— One part of the bone has been twisted at the break point
• Stress Fracture
— Hairline crack
• Transverse Fracture
—The broken piece of bone is at a right angle to the bone’s axis
What is osteomyelitis?
Bone infection - Infection of bone tissue (bone/bone marrow) from a bacteria or fungus
Develops from different routes to get into the blood:
• Bloodstream (Hematogenous spread)
—Lung infection, urinary tract infection
• Direct invasion
—Open fracture, surgery
• Contiguous Spread
—Foot ulcer or cellulitis spreading to bone
S/S of osteomyelitis
Fever
• Inflammation in bone that is infected
• Pain, swelling, redness, heat
• Fatigue
• Weight loss
• Pathology
• Most common pathogen: Staphylococcus aureus
(NBCE loves this)
Acute Osteomyelitis
• Bacteria reach the bone and initiates the immune response
• Bone marrow can swell and can compress blood vessels
• Avascular regions can develop causing necrosis of bone
• Commonly, immune system resolves the issue fully with assistance
of antibiotics
• Osteoblasts/clasts repair the damage over a few weeks
Chronic Osteomyelitis
Can last months to years
• Affected bone can become necrotic within healthy bone tissue
—Abscess formation
—Sequestrum: dead bone tissue; completely separated from surrounding bone
—Involucrum: new bone tissue produced around the infection
(NBCE loves these)
—Cloaca: gap in the cortex of a bone affected by chronic osteomyelitis that allows the drainage of pus or other material from the bone into the adjacent tissues
• Can lead to infections of soft tissue over bone
—Causing possible drainage externally
Abscess can spread superficial and cause separation of periosteum
from bone
—Subperiosteal abscess
• Vertebral osteomyelitis is a rare form of osteomyelitis
—Persistent back pain and tenderness when touched
***Diagnosis and treatment for osteomyelitis on slide #13
What is avascular necrosis?
Can be a result from osteomyelitis
Osteonecrosis, Aseptic Necrosis
• Localized necrosis (death) of bone tissue due to decreased or loss of blood
flow
Can Be Categorized As:
1. Traumatic
— Most common cause
— From a displaced fracture or dislocation (hip fracture/dislocation)
- Nontraumatic
—Disease/condition that blocks vessels
—Corticosteroids
—Chronic, excessive alcohol use
• Spontaneous osteonecrosis of the knee
***S/S Avascular Necrosis on slide #15
This term is associated with the formation of new bone produced around
infected bone?
• A. Subperiosteal abscess
• B. Avascular necrosis
• C. Sequestrum
• D. Involucrum
D
All of the following are mechanisms for development of osteomyelitis, except?
• A. Hematogenous spread
• B. Direct invasion
• C. Contiguous spread
• D. Overuse of antibiotics
D
•Avascular necrosis can occur from a fractured bone.
T or F
T
What are rickets and osteomalacia?
Etiology? S/S? Diagnosis? Treatment?
• Softening and weakening of bones mainly due to a long-term deficiency of vitamin D
• Commonly called rickets in children and osteomalacia in adults
Etiology
• Lack of vitamin D due to decreased production (sunlight) and/or decreased intake
• Certain medications
Signs/Symptoms
• Dull, ache, pain in bones
• Bowing of the bones
• Diagnosis
• Examination and imaging
• Blood test- Vitamin D
• Treatment
• Vitamin D supplementation
Vitamin D Reveiw (Overview) *for general knowledge
• Vitamin D2 (Ergocalciferol)
• Derived from plant sources
• Cheaper to produce- commonly found in supplements
• Physiologically inactive form of Vitamin D
• Vitamin D3 (Cholecalciferol)
• Derived animal sources
• Derived from sun exposure and skin
• Physiologically inactive form of Vitamin D
• Vitamin D2 (Ergocalciferol) and Vitamin D 3 (Cholecalciferol) must
ultimately be converted into active form of Vitamin D: Calcitriol
• Undergo two hydroxylation reactions in the body for activation
Osteoporosis overview
• Literally means condition of porous bones
• Bone tissue is very dynamic- Bone Remodeling
—Spongy bone is replaced every 3-4 years
—Compact bone is replaced every ~10 years
• Bone remodeling dependent upon serum calcium levels
—PTH, Calcitonin, and Vitamin D
Peak Bone Mass overview for men and women
• Amount of bony tissue present at the end of the skeletal maturation
• Important indicator of osteoporosis risk later in life
• Genetics, diet, exercise, and lifestyle factors will influence peak bone mass
• After achieving peak, bone mass plateaus for about 10 years
—Bone formation approximately equals bone resorption
• Then bone loss occurs at a rate of about 0.3 to 0.5% per year
• Menopause accelerates bone lose in women to 3 to 5% per year for about 5 to 7 years and then the rate of loss decelerates
• Peak Bone Mass
• Males: ~ 25- 30 years of age • Females: ~18-30 years of age (about 95% of a young woman’s peak bone mass is present by age 20)
Osteoporosis: DEXA Scan
What is this type of scan?
DEXA: Dual-energy x-ray absorptiometry
—Uses small amounts of ionizing radiation to measure bone mineral density
—Commonly examines the lumbar spine and pelvis
—Specialized X-ray
• Results are given in the form of a T score:
• T score of -1.0 or higher
—Considered normal bone density
• T score between -1.0 and -2.5
—Low bone density (osteopenia) and may be at risk for developing osteoporosis
• T score of -2.5 or less
—Osteoporosis
Osteoporosis vs Osteopenia
Both relate to loss of bone mineral density, but osteoporosis is more
severe
Pathology is associated with not achieving a high peak bone mass
density and then not maintaining activities/lifestyles to keep lower
activity of osteoclasts afterwards
• Both pertain to the same factors that increase risk for bone mass loss
What main factors increase done mass loss
Decrease physical activity (stress)
- sedentary lifestyle
Decreased calcium intake
-Foods high in calcium
- Low levels of vitamin D
- Imbalance with calcium homeostatsis
Smoking
-Alcohol intake
Medications (glucocorticoids, proton pump inhibitors)
Disease
Low estrogen levels
- menopause and post menopause
Low testosterone levels
***S/S, diagnosis of osteoporosis and Osteopenia on slide 82
Classification (osteoporosis)
Primary Osteoporosis
- 95% in women and 80% in men
- No exact identifiable cause
Secondary Osteoporosis
- Due to a specific medial condition or situation (parathyroid, kidney dysfunction)
***Clinical manifestations/ treatment of osteoporosis and osteopenia slide 84-85
All of the options are associated with accelerated bone mass loss, except?
• A. Low testosterone levels
• B. Smoking
• C. Glucocorticoids
• D. Proton pump inhibitor
• E. Antibiotics
E
All of the options are true regarding osteoporosis and osteopenia, except?
• A. Peak bone mass occurs around 20-30 years of age
• B. DEXA scans assist with detecting micro-fractures
• C. Can be asymptomatic
• D. Femoral neck fractures can lead to increased morbidity and mortality
B
What is Rhabdomyosarcoma
Rare cancer that forms in skeletal muscle or even smooth muscle
• Epidemiology
• About 400 to 500 new cases of rhabdomyosarcoma (RMS) occur each year
—Most often diagnosed in children and teens, with more than half of them in
children younger than 10 years old
—About 3% of all childhood cancers are RMS
• Etiology
—Cause is unknown and few risk factors are known
in the United States
** Rhabdomyosarcoma S/S, Diagnosis, treatment on slide 143
Rhabd/o =
Rod shape
Rhabdomyolysis: Overview
Commonly called: Rhabdo Rhabd/o = rod shape
• Breakdown of damaged muscle (skeletal)
• Causes release of muscle fiber components into blood
• Damages the kidneys • Characterized by muscle necrosis and the release of intracellular
muscle constituents into the circulation
• Myoglobin and creatine kinase (CK) released into the blood
• Myoglobin that is released into the blood is metabolized into components that
are harmful to the kidneys
• Can occur anytime muscle is damaged or killed
• Can be fetal
** S/S, etiology, diagnosis, treatment of rhabdomyolysis on slide 145
What is compartment syndrome? What are the clinical manifestations (5 P’s) and treatment
• Painful condition resulting from a build-up of pressure in a group
of muscles
—Commonly happens in lower legs
• Leading theory: Swelling of the muscles during exercise affecting
the blood supply to a whole group of muscles
• Can Occur From:
• Muscle damage (rhabdo) • Regular repetitive exercise
Clinical Manifestations (5 P’s)
• Pain • Pallor • Paresthesia (numbness and pins/needles feeling) • Pulselessness • Paralysis
Treatment
• Acute- medical emergency • Chronic- limit aggravating activities • Both may need surgery
All of the following options are true regarding rhabdomyolysis,
except?
• A. Can be caused by extreme physical exertion
• B. Red/brown urine is a possible symptom
• C. Can lead to kidney damage due to the release of actin
• D. Focused on skeletal muscle damage and release of intracellular
components
C
condition is associated with increased spinal kyphosis within teenagers?
A. Spondylolysis.
B. Scheuermann?s disease.
C. Slipped capital femoral epiphysis.
D. Paget?s disease.
B
What statement is TRUE?
A. Diffuse idiopathic skeletal hyperostosis presents with SI joint inflammation.
B. Osteomyelitis commonly occurs in children and older adults.
C. Osteophytes more frequently occur with rheumatoid arthritis compared to osteoarthritis.
D. abscess is associated with avascular necrosis.
B
All of the following are variables/factors that lead to increased bone mass loss, except?
A. Increased weight bearing exercises.
B.Decreased dietary intake of calcium.
C.Low estrogen and testosterone levels.
D. Smoking.
A
All the options are true regarding degenerative disc disease, except?
A. It can be diagnosed through an X-ray.
B. Only occurs in the lumber spine.
C. Neurological symptoms can occur.
D. Pain increases while standing or sitting
B
What statement is true regarding slipped capital femoral epiphysis?
A. Caused by accelerated growth.
B. It occurs primarily in adults.
C., Avascular necrosis can occur of the femoral head.
C
All of the options are true regarding osteoporosis, except?
A. Glucocorticoids can lead to decreased bone mass.
B. Low testosterone levels can lead to decreased bone mass.
C. Peak bone mass occurs around 20-30 years of age.
D. Bone eburnation is a common radiograph sign with osteoporosis
D
What is the most common bacterial infection for osteomyelitis?
A. Staphylococcus aureus.
B. Campylobacter jejuni.
C. Escherichia coli.
D. Streptococcus agalactiae.
A
Which arthritic condition would present with bilateral clinical presentation?
A. Gouty arthritis.
B. Lyme disease arthritis.
C. Osteoarthritis.
D. Rheumatoid arthritis.
E. Ankylosing spondylitis.
F. Psoriatic arthritis
D
All of the options are true regarding rheumatoid arthritis (RA), except?
A. Autoantibodies start the process of joint inflammation and destruction.
B. It commonly affects joints bilaterally.
C. Pannus formation is an extension of the synovial membrane.
D. Most RA patients are seronegative.
D
All of the following statements are true regarding rhabdomyolysis, except?
A. Red-brown urine is a symptom.
B. Caused by the excessive breakdown of both skeletal and smooth muscle.
C. Release of myoglobin into the blood leads to symptomology.
D. Can lead to kidney damage.
B
What condition will present with a bamboo spine, Romanus lesions, and SI joint inflammation on radiographic images?
A. Diffuse idiopathic skeletal hyperostosis.
B. Ankylosing spondylitis.
C. Osteoporosis.
D. Spondylolisthesis.
B
What is an accurate clinical finding that assists with differentiating ankylosing spondylitis and diffuse idiopathic skeletal hyperostosis (DISH)?
A. DISH will create syndesmophytes and ankylosing spondylitis does not.
B. Ankylosing spondylitis will affect the sacroiliac joints and DISH will not.
C. Auto antibodies will be present with DISH and not ankylosing spondylitis.
D. DISH tends to affect younger individuals (20-40 YOA)
B
What option is accurate regarding osteoporosis?
A. Peak bone mass for males occurs in their 40?s.
B. Osteoporotic compression factors only occur in the cervical spine.
C. Femoral neck fractures are a dangerous possible complication of osteoporosis.
D. Trabeculae of spongy bone is only affected, not cortical bone.
C
This condition only occurs in children and can lead to avascular necrosis.
A. Juvenile rheumatoid arthritis.
B. Diffuse idiopathic skeletal hyperostosis.
C. Ankylosing spondylitis.
D. Slipped capital femoral epiphysis.
E. Ostegenesis imperfecta
D
Subchondral sclerosis is an identifiable radiographic characteristic of what condition?
Correct answer:
A. Osteoarthritis.
B. Lyme disease arthritis.
C. Psoriatic arthritis.
D. Diffuse idiopathic skeletal hyperostosis.
A
Explain the mechanism of OA related to collagen fibers
chondroctes start making less of the proeoglycans and switch to making type I collagen fibers = OA mechanism
Type I collagen fibers and the proteoglycans don’t mix as well as type II collagen fibers • Cartilage LOSES ELASTICITY and becomes further damaged!
