week 12 musculoskeletal function Flashcards
what is a fracture
-occurs when force applied exceeding tensile or compressive strength of bone
fracture incidence
- varies depending on bone involved, age, gender
- highest incidence of fractures occurs in young males age 15-24 and in adults 65 yrs and older
- rates of hip and wrist fractures tend to be higher in women
what is a complete fracture?
bone broken all the way through
what is an incomplete fracture
bone damaged but still in one piece
what is a closed or simple (complete or incomplete) fracture
-skin is intact
what is a open or compound (complete or incomplete)
-skin broken
what is a comminuted fracture
-bone breaks into more than two fragments
what is a linear fracture
-fracture runs parallel to long axis of bone
what is an oblique fracture
-fracture of shaft of bone is slanted
hidden fracture- we can’t see it
risk factors for fractures- paediatric population
-bone mineral content, bone size, bone accrual all lower low bone mineral density (BMD)
-genetic factors
-poor nutrition
inadequate intake of dietary calcium, milk avoidance, excessive consumption of carbonated beverages
-lack of weight-bearing physical activity
-obesity
-play and sport (exposure to trauma)
risk factors or fractures -older adults
- age
- gender
- osteoporosis (fragility fracture)
- smoking
- alcohol
- steroids
- diabetes
- previous fracture
what is the etiology of fractures?
are most commonly caused by falls, car accidents, and athletic injuries
pathophysiology of fractures
-When bone broken
disrupts periosteum and blood vessels in cortex, marrow, surrounding soft tissues
-Bleeding occurs from damaged ends of bone and from neighboring soft tissue
-Hematoma forms within medullary canal, between fractured ends of bone, and beneath periosteum
-Bone tissue immediately adjacent to fracture dies
-Necrotic tissue and any debris in fracture area stimulate intense inflammatory response
characterized by vasodilation, exudation of plasma and leukocytes, and infiltration by inflammatory leukocytes and mast cells
-Cytokines, including transforming growth factor-beta (TGF-_), platelet-derived growth factor (PDGF), prostaglandins, and other factors are released
promote healing
-Within 48 hours after injury
vascular tissue invades fracture area from surrounding soft tissue and marrow cavity
blood flow to entire bone is increased
-Osteoblasts and osteoclasts in periosteum, endosteum, and marrow are activated
produce subperiosteal procallus along outer surface of shaft and over broken ends of bone
true or false- after a fracture it will heal with normal tissue and no scar tissue?
true
inflammatory phase with healing in a fracture
- last 3-4 days
- bone tissue destruction triggers inflammatory response
- hematoma formation
repair phase with healing in a fracture
- last several days
- capillary ingrowth, monocular cells, and fibroblasts transform hematoma into granulation tissue
- osteoblast w/in pro callus synthesize collagen and matrix to form callus
remodelling phase in a fracture
- last months to years
- unnecessary callus
- is resorbed and trabecular formed
- at the end, bone can w/stand normal stress
- some people like diabetics never get to this stage =amputation or we put a rod in the bone to secure it for weight baring
what are the manifestations of fractures?
- vary according to type and site of fracture, soft tissue injury
- impaired function
- unnatural alignment
- swelling
- muscle spams
- tenderness
- impaired sensation (numbness)
- pain
- fractures usually caused by trauma
- immediate, often severe pain at site of injury occurs
- subsequent pain produced by muscle spasm, overriding of fracture segments, damage to adjacent soft tissues
what are the complications of fractures?
improper reduction or immobilization of fractured bone may result in nonunion, delayed union, or malunion
-Broken bone can damage surrounding tissue, periosteum, and blood vessels in cortex and marrow
-Dislocation and subluxation are most common in persons younger than 20 years
usually associated with fractures
what is nonunion?
failure of bone ends to grow together -this is our biggest fear- not as common in peds but common in diabetics
-gap between broken ends of bone fills with dense fibrous and fibrocartilaginous tissue instead of new bone
what is delayed union?
union that does not occur until approximately 8-9 months after a fracture
what is malunion?
healing of bone in nonanatomic position
age-related complications -paediatrics
-growth plates vulnerable to fracture
-can result in shorter or crooked limb
-we worry about this age group the most bc they are still growing
-growth plates- open space bone on top of bone-hard to see a fracture in this area
we treat peds clinically- we don’t need an x-ray bc this age group between 0-6 don’t know how to lie about pain
age-related complications- older adults
- increased morality, pain, disability, depression and loss of independence
- high risk of morbidity and mortality after osteoporotic fracture
treatment for fractures
- closed manipulation, traction (skeletal or skin), open reduction, internal fixation, external fixation
- Splints, casts
- treatment of delayed union and nonunion fractures
- use of various methods designed to stimulate new bone formation
what is osteoporosis?
-complex, multifactorial chronic disease than often progresses silently for decades until fractures occur
-low bone mineral density (BMD), impaired structural integrity of bone, decreased bone strength, risk of fracture
-those w/ lowest BMD are most at risk for fractures
-old bone reabsorbed faster than new bone being made
-bones loss density–> become thinner and more porous
-may continue until skeleton no longer strong enough to support itself
-bones fracture spontaneously or fracture from falls or bums that would have not previously have caused fracture
the bone is breaking down but it is not building more
statistics with osteoporosis
-at approx age 30
-bone resorption slowly exceeds bone formation
-osteoporosis is most common in women at a rate of 1 in 2 women
-bone loss beings before menopause
-most rapid in 1st years after menopause
-persist throughout postmenopausal years
-bc estrogen breaks down bone- after menopause –> inhibits osteoclast
-men are also at risk -1 in 4 men experience osteoporosis-related fractures
-adults older than 50 years
-prevalence in spine or femoral neck
3% to 10% in men
7% to 35% in women
what are the risk factors for osteoporosis?
- Post menopause
- Family hx of osteoporosis and age over 60 years
- Caucasian or Asian descent
- Testosterone deficiency
- Inadequate intake of vitamin D or calcium
- Tobacco use
- High alcohol or caffeine consumption
- Anorexia nervosa
- Physical inactivity
- Drugs that lower serum calcium levels
what is the etiology of osteoporosis? primary/idiopathic (most common)
-age-associated
aging skeleton and calcium deficiency
-postmenopausal
estrogen deficiency
etiology of osteoporosis- secondary osteoporosis
-endocrine diseases
hormone imbalances, diabetes, -hyperparathyroidism, hyperthyroidism
drugs
heparin, corticosteroids - glucocorticoids, phenytoin, -barbiturates, lithium
-other substances
tobacco
alcohol
Calcium Metabolism in Osteoporosis
- Osteoporosis develops when remodeling cycle—the process of bone resorption and bone formation—is disrupted
- Bone demineralization leads to decreased bone density (porous bones)
pathophysiology of osteoporosis
-Role of oxidative stress
when excess ROSs accumulate
oxidative stress occurs
results in loss of bone mass and bone strength
-Osteoclast differentiation pathway
directed by series of processes
proliferation, differentiation, fusion, activation
processes controlled by hormones, cytokines, and paracrine stromal-cell microenvironment interactions
-OPG/RANKL/RANK System
IL-1, IL-4, IL-6, IL-7, IL-11, IL-17, tumor necrosis factor-alpha (TNF-_), transforming growth factor-beta (TGF-_), prostaglandin E2, and hormones interact to control osteoclasts
normal bone homeostasis is dependent on balance between the cytokine receptor activator of RANKL, its receptor RANK, and its decoy receptor osteoprotegerin (OPG)
OPG/RANKL/RANK System
-RANKL
cytokine that activates receptor RANK, which is expressed on osteoclasts and their precursors
suppresses apoptosis, which leads to activation and prolongation of osteoclast survival
so…RANKL promotes antiapoptotic effects on osteoclasts → increases life span
-RANKL is blocked by OPG
OPG is a glycoprotein acting as an antagonist (decoy receptor) for RANKL
prevents RANKL from binding and activating RANK receptor on osteoclasts and their precursors
-Some examples
estrogen stimulates OPG secretion and down-regulates RANKL
RANKL expression increased when estrogen levels are decreased (menopause)
increased formation of osteoclasts while reducing osteoclast apoptosis
glucocorticoid induced osteoporosis
glucocorticoids increase RANKL expression and inhibit OPG production by osteoblasts
use of immunosuppressive drugs to reduce rejection of transplanted organs
alters OPG/RANKL/RANK system and can lead to post transplantation osteoporosis
OPG/RANKL/RANK System (pt 2)
Alterations of OPG/RANKL/RANK system can lead to osteoporosis
A: SKELETAL SYSTEM - promotes osteoclast differentiation and activation and cytoskeletal reorganization and survival that increase resorption and bone loss
B: IMMUNE SYSTEM - enhances bone loss that occurs in inflammatory bone diseases
C: VASCULAR SYSTEM - physiologic significance of the OPG/RANKL/RANK system in endothelial and smooth muscle cells being studied
what are the manifestations of osteoporosis?
-Depend on bones involved
-Fractures
-trabeculae of spongy bone become thin and sparse
-compact bone becomes porous
-fractures of long bones (femur, humerus), distal radius, ribs, vertebrae most common
-most serious are hip fractures
because of resultant chronic pain, disability, diminished quality of life, premature death
-Pain
with fragility fracture
- As bones lose volume, become brittle and weak, may collapse or become misshapen (bone deformity)
- vertebral collapse causes kyphosis (hunchback), reduced pulmonary function, diminished height
what are the complications of osteoporosis?
fatal complications of osteoporotic fractures include: fat or pulmonary embolism, hemorrhage, shock
aprox 20% of person w/ hip fracture die from surgical complications
Evaluation and Diagnostics for Osteoporosis
-Osteoporosis is asymptomatic unless fracture occurs
so, diagnosis often delayed
by time abnormalities detected by x-ray
25% to 30% of bone may be gone
Dual x-ray absorptiometry (DXA) estimates bone density
but, DXA does not provide info about bone strength or fracture risk
online tool called Fracture Risk Assessment (FRAX)
predicts 10-year probability of fracture
other evaluation procedures
-Computed Tomography (CT) scans
-serum calcium, phosphorus, alkaline phosphatase, protein electrophoresis
-body calcium levels also measured by neuron activation analysis
use of radioactive calcium-49, whose gamma activity can be measured with whole-body counter
prevention and treatment of osteoporosis
-Prevention of osteoporosis vital
But tx more common and focused on preventing fractures and maintaining optimal bone function
-Prevention
regular moderate weightbearing exercises
calcium intake sufficient to maintain normal calcium balance during adolescence
sufficient intake of magnesium
-Treatment
bisphosphonates
estrogen
diet
dietary requirements for osteoporosis
- Role of calcium intake to prevent and treat osteoporosis is controversial
- Diets higher in fruit and vegetable → higher BMD
-Other nutrients have positive impact on bone health
vitamin K2, docosahexaenoic acid or DHA (from purified fish oil)
magnesium
-required for normal calcium absorption as severe magnesium deficiency results in hypocalcemia
-helps prevent brittle bones
Bisphosphonates: Alendronate
MOA-Natural substance that inhibits bone resorption
improves osteoblast and osteocyte survival while suppressing osteoclast activity
-inhibits osteoclast acitivy
-shifts balance towards bone deposition
-Increases bone density thus reducing incidence of fractures by approx. 50%
highly effective in reducing vertebral and nonvertebral osteoporotic fractures
-most common drug class
Bisphosphonates: Alendronate -therapeutic effects
- decreases rate of bone resorption
- strengthens bone by slowing bone resorption
Bisphosphonates: Alendronate -Adverse effects
N/V, diarrhea, esophageal ulceration, acid reflux, esophageal perforation, esophageal cancer
osteonecrosis of jaw
risk of atypical femoral fractures
what is Osteoarthritis?
-Wear and tear of the cartilage of weight-bearing joints, including knees, hips, and spine and frequently used joints like the hands
-Degenerative, age-onset disease characterized by destruction of cartilage at articular joint surfaces
AKA degenerative joint disease
-Common age-related disorder of synovial joints
weight-bearing joints i.e. knee, vertebral column, hip
hands because they are frequently used
-Second most common cause of disability in Canada
affects between 3 to 4 million persons
what are the risk factors for OA?
- Age
- More common in women than men older than 50
-Drugs can stimulate collagen-digesting enzyme activity in synovial membrane
colchicine, indomethacin, steroids
-Abnormal knee alignment
varus or valgus disorders of knee more than 5 degrees assoc. with increased risk
Etiology of OA- primary- idiopathic
- most common type
- no known cause (but is associated with increasing age)
Etiology of OA- secondary
- trauma
- mechanical stress
- inflammation of joint structures
- neurological disorders
- certain drugs
- joint instability
- excessive weight
- decreased estrogen in menopausal women
- excessive growth hormone
- increased PTH
Is OA a Noninflammatory Joint Disease?
- Commonly classified as noninflammatory joint disease
- BUT…numerous cytokines, chemokines, prostaglandins, apoptotic molecules identified
-Low-grade inflammation, calcification of articular cartilage, interaction between transcription factors, cytokines, growth factors, matrix molecules, enzymes affect development and progression of OA
process of cartilaginous destruction begins long before osteoarthritic changes can be detected through use of MRI, arthroscopy, or x-ray
what is the Pathophysiology of OA
-Articular cartilage damaged/lost through cascade of cytokine, genetic/epigenetic, biochemical, growth factor pathways
-Proteoglycans, glycosaminoglycans, collagen fibres degraded by collagenase
loss of proteoglycans from articular cartilage is hallmark of osteoarthritic process
-Inflammatory cytokines (IL-1β, IL-6, and TNF-α), apoptotic molecules (COX-2, nitric oxide [NO], prostaglandin E2 [PGE2]), prostaglandins play major role in cartilage degradation
release and activate proteolytic and collagenolytic enzymes (chemokines & metalloproteinases)
-Articular cartilage loses glistening appearance, becomes yellow-gray or brownish gray
-Surface areas of articular cartilage flake off and deeper layers develop longitudinal fissures
fibrillations
-Cartilage becomes thin and may be absent
unprotected subchondral bone thickens (sclerotic bone)
-Changes lead to increased remodeling of articular cartilage and loss of smooth, frictionless joint
-Cysts can develop within subchondral bone and communicate with longitudinal fissures in cartilage
pressure builds in cysts until cystic contents forced into synovial cavity, breaking through articular cartilage
-As articular cartilage erodes, cartilage-coated osteophytes (bone spurs) grow outward from underlying bone and alter bone contours and joint anatomy
-Spurlike bony projections enlarge until small pieces (joint mice), break off into synovial cavity
joint mice can irritate synovial membrane → synovitis and joint effusion
-Joint capsule thickens and may adhere to deformed underlying bone
can contribute to limitation of movement
-Cartilage destruction initiates the IL-1β and TNF-α pathways of inflammation
-Affected joint becomes unstable and more susceptible to injury
partial joint dislocations and other deformities common in advanced disease
osteoarthritis causes- progressing stage
the cartilage to begin breaking down, first making it thinner and then creating cracks in its surface
what is a normal joint
heathy cartilage lubricated by synovial fluid, cushions the bones and allows them to move easily
what happens in advancing OA
- gaps in the cartilage can expand until they reach the bone itself
- pain starts
- synovial fluid leaks into cracks which can form in the bone’s surface when this replacement cartilage wears away. this causes further damage and in some cases can lead to cysts in the bone or other deformities
end stage OA
no cartilage present
-if not treated, damage can progress to the joint where the bones in the joint become seriously and permanently deformed
Genes in Pathophysiology of OA
- Effects of risk factors
- –>chondrocytes experience epigenetic events that occur in nucleus and microRNAs in cytoplasm
- Results in altered expression of transcription factors, cytokines, collagen, aggrecan, and matrix proteinases
- –>may disrupt fine balance of anabolic and catabolic activity and affect cartilage homeostasis
- –>articular cartilage degradation and development of OA
-MicroRNAs provide inhibitor effect on cartilage-degrading enzymes
-When deficits of microRNA exist
destruction of fibrils that give articular cartilage its tensile strength accelerates
exposes chondrocytes to continued mechanical stress and enzymatic attack
-
Genetic deficiencies of inhibitors of calcification may contribute to a proliferative calcification cascade of articular cartilage
what are the manifestations of OA
-Onset is gradual and typically appears later in life
-Tends to be non-symmetrical in presentation (meaning it starts on one knee first)
-Pain, tenderness, stiffness in one or more joints
1st manifestations
-Deep, aching, localized pain
aggravated by movement, relieved by rest
often accompanied by reports of progressive pain
nocturnal pain may be accompanied by paresthesias
-As disease advances
ROM of joint decreases
-Enlargement of joint from swelling
-Flexion contractures contribute to joint instability
what are the big 3 of OA?
- pain
- limited motion
- stiffness
=joint damage
OA is the leading cause of
disability in middle-age and older populations
evaluation and diagnostics for OA
Individual subjective reports Clinical assessment detailed history and physical examination Studies CT scan arthroscopy MRI X-rays
treatment of OA
-Determined by severity of pain and immobility
-Rest joint until inflammation subsides
-Low impact exercise, especially when large joints affected
—>nonimpact aerobic exercise
—>passive range-of-motion exercises
—>walking
-Physical therapy
-Cane, braces, walker
-Weight loss, if overweight
-Balanced diet
-Analgesic and antiinflammatory drugs
-Topical drugs (capsaicin cream and balms)
-Magnetic bracelets and acupuncture
-Intraarticular injection of viscosupplements
hyaluronic acid
-Surgery: Joint replacement
arthroscopic surgery no longer recommended as no better than exercise (Evidence Based!)
what are the dietary requirements for OA?
-Dietary recommendations include
–>increase intake of Omega-3 fatty acids
—> eat oily fish 2x per week
safe level of sun exposure
-eat rich vitamin D dietary sources or take vitamin D supplements
-increase vitamin K intake
–>eat green, leafy vegetables
pharmacotherapy- pain general principles
Pain: General principles
immediate goal
reduce pain to level that allows client to perform ADLs without pain or discomfort
anticipate adverse effects and manage as they appear
easier to maintain pain-free status than eliminate painful sensations
Pharmacotherapy- inflammation general principles
Inflammation: General principles
inflammation is symptom
ideal to treat underlying cause
inflammation is usually self-limiting
non-pharmacologic approaches are better than pharmacologic approaches
prevent or decrease intensity of inflammatory response
Non-Opioid Analgesic: Acetaminophen
Indications mild to moderate pain osteoarthritis of hip or knee fever Mechanisms of Action inhibits COX activity and inhibits synthesis of prostaglandins in CNS antipyretic action may be due to action at hypothalamus Desired effects reduces pain reduces fever Adverse effects (at recommended doses, adverse effects are uncommon) hepatotoxicity, acute liver failure renal failure
NSAID (selective inhibitor): Celecoxib
Indications for use
mild to moderate pain and inflammation assoc. with rheumatoid arthritis, OA, dysmenorrhea, dental procedures, headache
prophylaxis of adenomas or colorectal polyps
limited due to an increased risk of MI and stroke
Mechanisms of action
blocks COX-2 without inhibiting COX-1 _ analgesic, anti-inflammatory, and antipyretic effects
but prostacyclin may also be suppressed allowing platelet aggregation and blood vessels to constrict
Desired effects
reduction of pain, fever and inflammation
Adverse effects
may increase risk of serious and potentially fatal cardiovascular thrombotic events, MI, and stroke
GI adverse effects including bleeding, ulcer, and stomach or intestine perforation
chronic kidney disease (CKD) and hepatic impairment
NSAID (non-selective inhibitor):Ibuprofen
-Indications for use
relieve mild to moderate pain, fever, inflammation
management of pain in inflammatory conditions i.e. OA
-Mechanisms of action
block action of COX-1 and COX-2
reduces prostaglandin production
-Desired effects
reduction of pain, fever, inflammation
-Adverse effects nausea, heartburn, GI irritation & ulceration can decrease platelet function bleeding -Acute Kidney Injury (AKI) azotemia, increased BUN and creatinine
Proton Pump Inhibitors (PPIs): Pantoprazole
-Indications tx & prevent NSAID-induced ulcers take about 30 minutes before meals increases effectiveness -Mechanism of action inhibits action of H+/K+ pump on parietal cells reduces acid secretion -Desired effects achlorhydric: >90% gastric acid secretion is temporarily blocked -Adverse effects well tolerated with some exceptions action limited to effects on gastric acid secretion
