Lecture 7 Musculoskeletal & Rheumatological Flashcards
What does a ligament connect?
Connects bone to bone
explain the mechanism of injury to ligaments
1) injury = sprain
2) suddden overstretching, ROM, trauma
3) microfailing injury occurs before total failure
Grade 1 of ligament injury
Grade 1 = mild injury, stretching without instability
Tx: Rest, ice, compression, elevation, limit activities
Grade 2 of ligament injury
moderate, severe injury with a partial tear and instability
Tx: RICE, immobilize, pain management, promote recover/PT
Grade 3 of ligament injury
complete tear of ligament, significant swelling, bruising, pain, joint instability
Tx: surgical intervention, immobilization, pain management
What does a tendon connect
Bone to muscle
what type of injury is associated with tendon
Injury = Strain (think T for tendon)
Explain the pathophysiology of a strain
Injury occurs when stress surpasses the capability of the fibrous cords
Minor strain -> leads to complete tear/rupture
What is tendinitis
Inflammation of the tendon within sheath d/t injury/infection
S/Sx (all localized)
Aching at point of tendon attachment
Restricted joint motion
Pain with active ROM
Tx:
RICE, PT, corticosteroid injection
What is a joint capsule
Sac-like structure surrounding the synovial joint
Outer fibrous layer for structural support
Inner membrane for producing lubricating synovial fluid
Stabilizes the joint
Pathophysiology of a joint capsule injury
Fibrinous tissue builds up
Effusion can occur
ROM decreases (reduced capsular redundancy)
Prolonged immobilization -> capsule contraction (ex. Frozen shoulder)
Tx:
Injected corticosteroids to reduce the inflammation
Bone fractures (draw them out)
Displaced, non displaced, complete, incomplete, opne/compound
Types of fractures (draw them out)
transverse, spiral, longitudinal, oblique, conmminuted, impacted, stress, avulsion
Steps in the process of bone healing
1) hematoma formation
2) Fibrocartilaginous Callus Formation
3) Bony Callus Formation
4) Bone Remodeling
explain hematoma formation
Immune cells are stimulated to remove damaged tissue
Inflammatory response occurs over the course of 1-7 days
Vascular Endothelial Growth Factor (VEGF) released
Stimulates new blood vessel growth
Explain Fibrocartilaginous Callus Formation
Soft Callus Formation (Week 1-3)
Primarily composed of cartilage -> bridges any fracture gaps to stabilize bone
New blood vessels begin to grow into the area from VEGF
Mesenchymal stem cells differentiate to:
Fibroblasts
Chondroblasts (cartilage)
Osteoblast
explain Bony Callus Formation
Cartilage calcifies and is replaced by woven bone to create hard callus and stabilize the bone/restore strength
RANK-L
Protein that stimulates functionality of:
Chondroblasts
Chondroclasts
Osteoblasts
Osteoclasts
Cartilaginous callus reabsorbed, bone laid down
Proliferation of blood vessels
Calcification of callus and immature bone
Explain bone remodeling
Migration of osteoclasts/blasts
Balances resorption and formation
Replaces the callus with bone
what are the different types of complication in healing
delayed, fat emboli, DVT, osteomyelitis, compartment syndrome, osteonecrosis
What is delayed healing for 400
Dependent on amount of local damage done, secondary infection, systemic circulatory issues, nutritional issues
Medications (glucocorticoids suppress inflammation and healing)
Malunion
Bone fusion, improper alignment
Nonunion
Greater than 6 month delay in fusion
what is fat emboli for 600
Fat particles released from bone marrow
Especially pelvis and long bone fractures
24-72 hr after injury
S/Sx: similar to that of a pulmonary embolism/ other emboli
+ petechial rash (Check torso, axilla, conjunctiva), altered mental status
Dx:
CT PE, V/Q scan, CXR
what is DVT for 200
Formation 5+ days after injury (clot breaking off)
Increased risk d/t:
Multiple fractures, pelvic and long bone fractures, immobility, obesity, hx of clots, hypercoagulable disorders
Prevention
Early mobilization
VTE prophylaxis measures
what is osteomyelitis for 200
Infection of bone and local tissue through bacteremia or trauma/open wound in surrounding area
Indirect or direct introduction of foreign organism into bone
Usually from staph aureus
S/Sx:
Children
High fever, pain at site of bone involvement
Adults
More subclinical features
Fever, malaise, anorexia, night sweats, weight loss
what is compartment syndrome for 500
Accumulation of pressure in the soft tissue compartment
Decreases perfusion (by 30-40 mmHg) -> ischemic -> hypoxia and necrosis
Intrinsic or extrinsic causes (ex. Cast around limb)
S/Sx: 6 P’s
Pain (out of proportion to injury)
Paralysis
Paresthesia
Pallor
Poikilothermia (cool to touch)
Pulselessness
Tx:
Medical emergency!
Fasciotomy
Relief of pressure
what is osteonecrosis for 125
Result of unmanaged/ineffectively treated osteomyelitis
Necrotic bone can separate from healthy bone into dead segments called sequestra
Tx:
4-6 weeks antibiotic therapy
Debridement (abscesses)
Amputation
Involucrum formation blocks success of abx therapy
Encapsulates sequestra
Types of metabolic bone disease
osteoporosis, hyperparathyroidism, renal osteodystrophy, Paget’s disease
Osteoporosis pathophysiology
Rate of bone resorption exceeds bone formation
Osteoclasts breaking down bone mineral and calcium to release into bloodstream
Callus bone lost faster than cortical bone
Etiology
Hormonal/estrogen deficiency
Poor calcium
Disuse of bone (ex. Low amount of weight bearing exercise)
Osteoporosis Dx
Bone Mineral Density (BMD) Scan
DXA Scan
T-Score
< 2.5
Osteoporosis (increased likelihood of breakage)
Btw -1.0 and -2.5
Osteopenia (decrease in bone mineral density)
Osteoporosis s/s
Trabeculae (wavy matrix) decreased
Width and bone mass decreased
Fractures d/t fragility
Osteoporosis Tx
Calcium and Vitamin D supplements
Bisphosphonates
Slow bone resorption
PTH
Weight bearing activity to strengthen bone
Hyperparathyroidism
PTH -> stimulates Calcium release from bone
States of elevated PTH activity
Primary
Secondary
Ex. low blood calcium triggering release, dysregulation by pituitary, tumor secreting PTH, etc.
Renal Osteodystrophy
pathophysiology
Bone Disorder resulting from impaired kidney function (CKD)
Decreased renal function
Hyperphosphatemia
Decreased active Vitamin D
Hypocalcemia d/t decreased intestinal calcium absorption
Results in elevated PTH
-> Bone breakdown!
Renal Osteodystrophy. s/s
Bone pain and deformities + fractures
Muscle weakness
Impaired growth
Renal Osteodystrophy Tx
Phosphate binders
Vitamin D analogs
Dialysis or parathyroidectomy
Paget’ DIsease
Abnormal bone remodeling resulting in structurally disorganized bones
Excessive remodeling (built too fast)
Lowered structural integrity, hypertrophy
Etiology unknown
Viral or genetic components hypothesized
S/Sx:
Bone pain
Skeletal deformities
Fractures
Fatigue and anemia (d/t elevated serum calcium)
Bone tumor prefixes
Osteo = bone
Chondro = cartilage
Oma = tumor/swelling
Sarcoma = cancer forming in body soft tissue
Bone tumors s/s
Localized
Pathologic fracture
Pain/swelling/mass
Systemic
Fatigue, weight loss, fever
Lymphadenopathy
Osteosarcoma
Malignant
Bone forming
Pelvis and long bones of arm and legs
Chondrosarcoma
Cartilage forming
Occurring in cartilage of arm, leg, and pelvic bone
Malignant transformation of benign bone tumors
Ewing’s Sarcoma
Neither cartilage or bone forming
Medullary cavity of pelvis and long bones (femur, humerus, tibia, clavicle)
Osteochondroma
Benign
Cartilage forming
Occur in any bone formed by cartilage
Giant Cell Tumor
Tumors of Unknown Origin
Neither cartilage or bone forming
Derived from osteoclasts
Can spread to lungs (unpredictable)
S/Sx:
Pain and pathologic fracture in cancellous ends of arm and leg bones
Rheumatoid Arthritis (RA) pathophysiology
Autoimmune inflammatory disease
Targets synovial joints
Formation of pannus (inflamed granulation tissue)
Erodes the cartilage and bone
Rheumatoid Arthritis (RA) s/s
Bilateral symmetric polyarthritis
Red, warm, painful joints (smaller)
Diffuse musculoskeletal pain
Morning stiffness over 60 min
Boutonniere and swan neck deformities
d/t joint calcification and narrowing spaces
Rheumatoid Arthritis (RA) Tx
DMARDs (antirheum)
NSAIDs
Corticosteroids
Rheumatoid Arthritis (RA) Foss
For disease onset; in RA, pain typically develops quickly, over weeks or months.
With RA, morning stiffness lasts longer than 30 minutes, often an hour or more.
In RA, pain tends to be more constant and severe.
Osteoarthritis (OA) Pathophysiology
Breakdown of cartilage and underlying bone
Joint pain and stiffness
Mechanical etiologies
Osteoarthritis (OA) S/S
Morning stiffness ( about 30 min)
Heberden/Bouchard nodes
Bone spurs (osteophytes)
Pain worsens with activity, relieved by rest
Osteoarthritis (OA) Tx
NSAIDs to decrease pain and swelling
Joint injections
surgery
Osteoarthritis (OA) Foss
In OA, pain develops gradually over years and is associated with chronic overuse of the joint (this is what the slide is referring to as “usage-related”) . Within the disease processes, there are variations in pain and stiffness patterns.
In comparison with OA, morning stiffness typically improves within 30 minutes (with movement). Stiffness typically improves with use in OA, but once the activity is finished, it can reoccur and may be associated with an increase in pain.
For OA physical activity can both increase and decrease pain. Some activity types can make acutely pain worse, while over time regular exercise/ can usually help improve overall symptoms. (Acutely, pain can worsen with activity and improve with rest)In OA, one of the things that can contribute to variations in symptoms and increased pain and stiffness with any movement is the development of bone spurs. As the cartilage breaks down and the bone edges wear and boney cysts form. Osteophyte activity is stimulated due to joint damage leading to excessive boney growth. Typically you see this along the joint edges and in weight bearing joints. Bone spurs alter the pain/stiffness presentation as they can alter the mechanics of movement within the joint space.
Ankylosing Spondylitis pathophysiology
Multisystem inflammatory, autoimmune disease
Progressive stiffness and fusion of axial skeleton
Chronic inflammation leading to new bone formation -> resulting spinal fusion
From B-lymphocyte overactivity
Ankylosing Spondylitis s/s
Arthralgias
Synovitis
Butterfly rash (from systemic consequence)
Low back pain and stiffness, limited spinal mobility
Ankylosing Spondylitis tx
NSAIDs
Topical corticosteroids
Avoid sun exposure (trigger)
Immunosuppressive agents
Infectious arthritis pathophysiology
Can mimic other arthritis and gout
Etiology
Can result from tick bite in area
Usually from staph. aureus
Infectious arthritis s/s
Red, swollen, painful joint
Synovium is edematous and forming exudate from infection
Fever, chills
Systemic infection
Infectious arthritis tx
Antibiotic therapy
Joint drainage
Gout pathophysiology
Inflammatory arthritis caused by urate crystals depositing in joints/joint spaces
Hyperuricemia (necessary predisposing factor)
Gout attack
Acute attack
Sudden onset of severe pain, redness, swelling, warmth of joint (usually great toe)
Chronic gout
Tophi formation (in soft tissue)
Gout phase 1 asymptomic hyperuricemia
Asymptomatic hyperuricemia
Avoid purine rich foods and alcohol
Gout phase 2 Acute gouty arthritis
Confirm with synovial aspirate of urate crystals
gout phase 3 Intercritical gout
Ongoing process (crystals still found in synovial fluid)
gout phase 4 Chronic tophaceous gout
Urate crystal deposit (tophi); chronic inflammation
gout Tx
NSAIDs, steroids, colchicine (prophylactic or early tx)
die modification low on purines Avoid rich meats, alcohol, and sugary drinks to lower your risk of gout flare-ups! Dammit Bobby
Idiopathic Inflammatory Myopathies
Chronic muscle inflammation and weakness
Acquired, incurable
Systemic autoimmune disease
Polymyositis
Muscle weakness of neck (progress from proximal skeletal muscle)
S/Sx:
Dysphagia, dyspnea, dysphonia
Tx: corticosteroids, immunosuppressives
Dermatomyositis
Inflammatory myopathy characterized by muscle inflammation and skin rash
From immune mediated muscle damage
S/Sx:
Gottron’s papules (raised red/violet lesions)
Tx: IVIG, immunosuppressives, corticosteroids
Duchenne (dystrophies) pathophysiology
Progressive muscle degeneration from impaired dystrophin production
Lacking dystrophin leads to muscle fiber instability
Progressive muscle weakness
Duchenne (dystrophies) S/S
Difficulty with motor tasks
Gowers sign
Children using hands to climb up from floor d/t weakness
Progressive cardiomyopathy
Respiratory failure
Loss of ambulation by ~ age 12
Duchenne (dystrophies) Tx
Slow progression through supportive therapy and glucocorticoids
Diseases of Metabolism -general effects
Abnormal metabolism of carbs, fats, proteins
Enzyme deficiencies can lead to accumulation of toxic substrates or lack of essential biochemical products
S/Sx:
Neuro: developmental delay, seizure, neurodegeneration
Muscle weakness
Growth failure
Manage with diet and enzyme replacement therapies
Mitochondrial Diseases-general effects
Defective energy production from mitochondrial gene mutation
Oxidative stress and abnormal cell signaling
Multisystemic Sx
Neurological symptoms
Cardiomyopathy (dilated or hypertrophic)
Calcium Channel Disorders- general effects
Abnormal channel activity resulting in disrupted muscle contraction/neurotransmission
Muscle weakness and arrhythmia
Hypotonia
