msk Flashcards
what does the msk system consist of
bones, joints, ligaments, muscles, tendons, and connective tissues that support and bind tissues and organs together
ligaments vs tendons
Ligaments bind bones together at joints
ligaments = Connective tissue that attaches bone to bone at a joint; stabilizes joint and prevents movement beyond intended range of motion
Tendons attach muscles to bones
tendons = Connective tissue that attaches muscle to bone; tendon acts on bone when the muscle contracts to cause movement
skeletal bone provides
form, support, protection, stability, and movement to the body
Shape to the body
Physical support
Protection of organs
Stores minerals – calcium; and lipids
Responsible for blood cell formation
Muscle attachment sites – to facilitate movement
muscles
keep skeleton upright and facilitate body’s physical movement
attach to the bones of the skeletal system
- each muscle is a discrete organ composed of skeletal muscle tissue, blood vessels, tendons, nerves
- muscle tissue found in the heart, digestives organs, blood vessels
- ~ 700 muscles that account for half person’s body weight
how many bones in human body
206
-bones are formed from osseous tissue-provides structure and function to the body
nerves
- control the contraction of skeletal muscles
- interpret sensory information
- coordinate the activities of the body’s organ systems
osseous tissue composed of
composed of calcified connective tissue
Ground substance and 90-95% collagen fibers (ossein) create the bone matrix
Calcium and phosphorus stored in matrix adding strength and density
Osteocytes are contained in the matrix
cartilage
semi-rigid connective tissue deposited in areas where the bones need to move such as ribcage and joints
Soft connective tissue found between joints; shock absorber to reduce friction
structure of bone
Periosteum
Outermost layer of bone; protective sheath; thin tough membrane of fibrous tissue; provides support for tendons
Completely covers all bones except at joints where there is a layer of cartilage
Two layers: inner cellular osteogenic layer that forms new bone tissues and outer fibrous connective tissue layer for blood and nerve supply to bone
Osteogenic layer decreases in older bones
compact bone
under periosteum
hard outer layers of the bone; no spaces between lamellae
cancellous/spongy bone
under compact bone
lighter, softer, weaker, more porous but with greater surface area; spaces between lamellae; more vascular; “honeycomb appearance”
medulla
hollow cavity containing marrow within cancellous bone
bone development
Cartilage is the major component of skeleton when very young –provides greater flexibility and resiliency
Cartilage becomes harder with deposition of calcium phosphate in it
Some cartilage cells break loose and channels develop in the shaft of the bones
Blood vessels enter these channels and carry other connective tissue cells – some develop into osteoblasts and osteoclasts
Osteoblasts enter cartilage and form the layers of bone
Osteoclasts tear down old and excessive bone structures, allowing osteoblasts to rebuild with new bone – continuous process which slows down with age
osteoblasts
bone forming cells which secrete collage and substances to form the ground substance of bone
osteocytes
most common cell in mature bone
Responsible for bone growth and density
osteoclasts
cells that reabsorb bone tissue
lamellae
circular layers of bone matrix around the Haversian canal (osteon – functional unit of compact bone)
trabeculae
functional unit of cancellous bone; contain osteocytes but no osteons; receive nutrition from marrow tissue
bone marrow
Fills inner core of bones - the medullary cavity
Soft, gelatinous tissue – myeloid tissue
Red bone marrow for hematopoiesis OR yellow bone marrow filled with adipose tissue (or both)
red marrow
Primarily in central bones of adults – skull, vertebrae, sternum, ribs, pelvis, and upper thirds of long bones (humerus and femur)
In all bones until age seven – when need is high for new blood formation
yellow marrow
Primarily a storehouse for fats
Can be converted to red marrow under certain conditions (severe blood loss, fever)
Fill the cavities of other bones without red marrow
types of bone
endochondral and intramembranous long short flat sesamoid irregular
endochondral and intramembranous bones
Endochondral/intra-cartilaginous - ossification from centers arising in cartilage
Intramembranous – direct formation of bone on the mesenchyme (embryonic connective tissue) for formation of flat bones
ossification: formation of bone
Conversion of connective tissues into bone
Initiated at centers of ossification – points at which bone formation is started by osteoblasts through laying down of lamellae
Centers of ossification – primary or secondary
primary center of ossification
present before birth
first to start process of ossification
secondary center of ossification
usually appears after birth
process of ossification starts here after it has been started at the primary center
endochondral ossification
Embryonic mesenchymal cells develop into cartilaginous models which become ossified and form bone
Cartilage is gradually replaced by bone radiating out from the primary ossification center in the diaphysis to the epiphysis (secondary ossification center)
Cartilage remains at epiphysis as articular cartilage for joint movement
and as epiphyseal cartilage plate for bone
lengthening at junction with diaphysis
intramembranous ossification
Mesenchyme differentiates into osteoblasts which deposit osteoid (unmineralized matrix)
Then osteoblasts deposit calcium phosphate into the osteoid, and the osteoid is converted into a bony matrix called bony spicules
The osteoblasts transform into osteocytes
The spicules coalesce into layers (lamellae) which form around the blood vessels and develop into osteons (Haversian canal system); osteoblasts lay down lamellae at the surface of the developing bone forming compact bone
Mesenchyme differentiates into bone marrow
bone growth and remodeling
lengthening
growth in thickness
healing bone fractures
bone remodeling (bone metabolism)
bone lengthening
At diaphyseal-epiphysial junction where the epiphysial cartilages plate cells multiply, move towards diaphysis/shaft of bone, and become replaced by osteocytes
Is completed by puberty; growth in bone length stops [bone growth stops between ages of 18 and 30 years]
bone growth in thickness
Osteoblasts (bone forming cells) in periosteum (diaphysis/shaft) multiply continuously and form osteocytes, increasing the thickness of the bone
healing bone fractures
Cartilage laid down at edges of fracture
Endochondral process of bone replacing cartilage
bone remodeling (bone metabolism)
Purpose is to regulate calcium homeostasis, repair micro-damage to bones from everyday stress, and to shape the skeleton during growth
Lifelong, regulated process
Mature (old/defective) bone tissue is removed from the skeleton (bone resorption by osteoclasts) and new bone tissue is formed (ossification or new bone formation by osteoblasts)
types of muscles
voluntary involuntary striated skeletal smooth cardiac
voluntary muscles
muscle that can be consciously controlled
involuntary muscles
muscle that is controlled by the autonomic nervous system (not consciously controlled)
striated muscles
muscle tissue that has a striped appearance due to its fiber composition
skeletal muscle
voluntary and striated
attach to bones and control conscious movement
smooth muscle
involuntary and non-striated
in the hollow organs
cardiac muscle
involuntary and striated
only in heart and specialized to pump blood
each skeletal muscle is an organ
Composed of skeletal muscle fibers, blood vessels, nerve fibers, connective tissue
Enclosed by connective tissue – the epimysium
within each skeletal muscle
Bundles of muscle fibers/cells - fascicles
Enclosed by connective tissue – perimysium
Each muscle fiber/cell enclosed by connective tissue - endomysium
within each muscle fiber/cell
Multiple nuclei to produce large amounts of proteins and enzymes
Proteins organized into myofibrils
Hundreds to thousands of myofibrils within one muscle fiber/cell
Sarcoplasmic reticulum – store, release and retrieve calcium ions
within each myofibril
Thousands of sarcomeres
Sarcomeres – smallest functional unit of muscle fiber/cell
Each sarcomere - contains organized arrangement of contractile, regulatory and structural proteins
synovial fluid
synovia
lubricates the cartilage and reduces friction between the articular cartilages of the joints during movement
shock absorber by becoming more viscous under pressure to protect the joint from shocks
ATP required for
muscle contraction and relaxation:
ATP is stored in resting muscles
calcium required to
contract muscle fibers:
Calcium flows out to allow muscles to relax and lengthen again
nervous system signals
muscle fiber stimulating myosin filaments and pulling actin filaments closer together, shortening the sarcomeres within the fiber and causing it to contract
neuronal development in first trimester
– rapid brain growth with differentiation into cerebrum, cerebellum, brain stem and spinal cord; brain susceptible to injury
neuronal development in second trimester
neuronal development and differentiation [mature and specialize] leading to detectable reflex movements in fetus by 15th week of gestation; majority of neurons formed by end of second trimester
neuronal development in third trimester
formation of synapses between neurons and nervous system; myelination begins late in trimester and continues into adolescence
age related changes on bones and joints
decreased bone mass and minerals decreased calcium reabsorption shortening of vertebrae thinning of intervertebral disks deterioration of cartilage
age related changes on muscles
muscles fibres atrophy decreased muscle mass and strength decreased ROM shrinking/hardening of tendons muscles cramps more common
musculoskeletal disorders
Musculoskeletal disorders (MSDs) include injury or disorder of the muscles, tendons, ligaments, joints, nerves, blood vessels or related soft tissue including sprain, strain and inflammation
typical work related MSDs
tendonitis, hand-arm vibration syndrome, and back strains and sprains.
risk factors for msk disorders
Autoimmune disorder Calcium deficiency Falls Infection Metabolic disorders Neoplastic disorders Obesity Postmenopausal states Trauma and injury
msk system nursing assessment symptom analysis
location, quality, timing, severity, intensity of presented symptoms, and precipitating, alleviating, and associating factors
msk system nursing assessment functional assessment
Range of joint motion, muscle strength and tone, self-care deficits
msk system nursing assessment medical/family/personal/social history
Recent injury, arthritis, co-morbidities
Bone cancer, osteoporosis, arthritis/autoimmune
Dietary intake, exercise habits, sports, work hazards/potential for injury/repetitive motions
common msk assessment tests
phalen’s
bulge
mcmurray
blood tests specific to msk system
alkaline phosphate calcium phosphorous rheumatoid factor uric acid human leukocyte antigen creatine kinase
msk alkaline phosphate test
to identify bone diseases increased in bone cancer paget's disease healing fractures RA osteoporosis
msk calcium test
to monitor calcium levels and detect calcium imbalances
decreased with lack of calcium and vitamin d intake and with malabsorption form the GI tract
increased in bone cancer and multiple fractures
msk phosphorous test
to assess phosphorus levels
increased with bone tumors and phosphate healing fractures
msk rheumatoid factor test
to diagnose RA
also increased in lupus and scleroderma
msk uric acid test
to diagnose and monitor the treatment of gout
msk human leukocyte antigen test
to diagnose diseases such as juvenile RA and ankylosing spondylitis
msk creatine kinase test
to diagnose muscle trauma or disease
increased in muscular dystrophy and traumatic injuries
diagnostic evaluation of msk system
Radiographic examinations:
X-rays
CT scans
MRI
Bone scans
Bone density examination
Evaluate bone mineral density and evaluate the degree of osteoporosis
Arthrocentesis
Withdraw fluid from a joint by needle aspiration
Arthroscopy
Fiber-optic endoscope to examine the joint interior, to diagnose diseases, and to perform surgery
effects on immobilized client
Physiological Muscular Skeletal and skeletal Metabolic Decreased metabolic rate Negative nitrogen balance Hypercalcemia Cardiovascular Orthostatic hypotension Increased work of the heart Thrombus formation
psychological effects on immobilized client
Diminished environmental stimuli (isolation and boredom)
Altered perception of self and environment
Increased feelings of frustration, helplessness, anxiety
Depression, anger, aggressive behavior
osteoporosis
Metabolic disease characterized by bone demineralization, with loss of calcium and phosphorus salts leading to fragile bones and subsequent risk for fractures.
Occurs from imbalance between new bone formation and old bone resorption
Occurs most commonly in the wrists, hip, and vertebral column (thoracic and lumbar).
Affects 1 in 4 Canadian women and 1 in 8 Canadian men over 50
Fractures from osteoporosis are more common than heart attack, stroke, and breast cancer combined.
osteoporosis risk factors
Smoking Early menopause, pregnancy Excessive use of alcohol Family history of osteoporosis/osteoporotic fracture Female gender Increasing age Obesity, Cushing syndrome Insufficient intake of calcium, vitamin C & D, magnesium, phosphorus High caffeine intake, anorexia, malabsorption conditions Sedentary lifestyle White or Asian Medications Propensity to fall Small stature, thin build
osteoporosis patho
decreased mass (density of bone) and structural deterioration of bone tissue
Cortical bone becomes more porous and thinner
Trabecular bone structural integrity impaired; more porous/less dense framework
Hormones most commonly associated with osteoporosis are growth hormone, thyroid hormone, parathyroid hormone, cortisol
osteoporosis clinical manifestations
Classic dowager’s hump or kyphosis of the dorsal spine
Loss of height, often 2-3 inches
Back pain, often radiating around the trunk
Pathologic fractures: often occurring in the distal end of the radius and the upper third of the femur
Compression fracture of spine: assess ability to void and defecate
Fatal complications include fat or pulmonary embolism, pneumonia, hemorrhage, and shock.
osteoarthritis
Degradation and loss of articular cartilage, sclerosis of bone underneath cartilage, and formation of bone spurs [osteophytes]
Degenerative joint disease
Affects the weight-bearing synovial joints and synovial joints that receive the greatest stress, such as hips, knees, lower vertebral column, and hands.
osteoarthritis risk factors
People can inherit an increased risk of developing osteoarthritis, not the condition itself. This predisposition can be passed through generations in families, but the inheritance pattern is unknown.
Increased age (> 50)
Joint trauma, long-term mechanical stress
Endocrine disorders (hyperparathyroidism)
Drugs (steroids, indomethacin)
Obesity
Smoking
Rheumatoid arthritis
Congenital or acquired skeletal deformities
osteoarthritis patho
Altered joint function and damage
Degradation and eventual loss of articular cartilage
Excessive friction [bone against bone] combined with risk factors
Variable degrees of mild synovitis and thickening of the joint capsule
Degraded articular cartilage released into synovial cavity initiates synovial inflammation
primary (idiopathic) osteoarthritis
Most common, of unknown etiology
Localized OA [to one or 2 joints]: affects the hands, feet, knee, hip, and spine
Generalized OA [GOA/polyarticular/multi-joint OA]: involvement of 3 or more joint sites
secondary osteoarthritis
occurs after injury Post-traumatic or mechanical Post-inflammatory or post-infection Heritable skeletal disorders Endocrine disorder Atypical joint trauma due to loss of proprioceptive senses Avascular necrosis Congenital malformations
osteoarthritis diagnostic evaluation
X-ray studies of affected joints Joint space narrowing Subchondral sclerosis Subchondral cysts Osteophytes Hyaluronic acid Lubricating substance in cartilage and joint synovial fluid May be a useful marker indicating the presence and severity of OA
clinical manifestations of osteoarthritis
Appear in the 5th or 6th decade of life Pain Stiffness Enlargement of the joint Crepitus Tenderness Limited motion Deformities Weight loss Fever Heberden and Bouchard nodes
scoliosis
Most common spinal deformity
Abnormal sideways curvature of the spine – lateral curvature and rotation.
nonstructural vs structural scoliosis
Nonstructural – results from a temporary cause other than the spine itself (i.e. posture); involves only side-to-side curvature; Functional scoliosis
Structural – involves spinal rotation and side-to-side curvature; most common
adult degenerative scoliosis
Two categories: Degenerative Scoliosis and De novo (new) Scoliosis
Degenerative scoliosis occurs in an adult with a history of scoliosis
De novo scoliosis first appears in adulthood
Common condition that occurs later in life as the joints in the spine degenerate – “wear and tear” of spine due to age
Typically diagnosed after age of 50
scoliosis diagnostic evaluation
Adam’s Forward Bend Test: initial screening test
Standing radiographs to determine degree of curvature
Cobb angle: Measure scoliosis curve
Curve < 10 ° considered a postural variation
Curve < 20 ° is mild; if nonprogressive - no treatment required
Curve > 25 ° significant
Curve > 45-50° severe
Risser scale: Evaluate skeletal maturity on the radiographs
Tanner Scale: Assess maturity to predict curve progression
scoliosis clinical manifestations
Shoulders are uneven – one or both shoulder blades may stick out
Head is not centered directly above the pelvis
One or both hips are raised or unusually high
Rib cages are at different heights
Waist is uneven
The appearance or texture of the skin overlying the spine changes (dimples, hairy patches, color abnormalities)
The entire body leans to one side
muscular dystrophy types
duchenne MD becker MD psudohypertrophic MD limb-girdle MD facioscapulohumeral (landouzy-dejerine) MD
duchenne MD
DMD
Most severe and common of the muscular dystrophies of childhood:
Dystrophin protein is missing or found in very small amounts
Dystrophin protein is needed for muscles to function properly
X-linked recessive inheritance
Generally affects males
Female carriers – mild or no symptoms
Incidence: 1 in 3,600 male births
Early onset – usually between 3 and 5 years of age
Survival – early 30’s
DMD diagnostic evaluation
Mutations to the dystrophin gene Confirmation by electromyelography (EMG) Muscle biopsy Serum enzyme measurement Serum creatinine kinase levels are extremely high in the first 2 years of life, before the onset of clinical weakness.
DMD clinical manifestations
Slow motor development
Progressive weakness
Muscle wasting
Pseudohypertrophy:
Calf muscle hypertrophy in most patients
Muscular enlargement caused by deposits of fat and fibrous tissue
Sitting and standing are delayed
The child is clumsy, falls frequently, and has difficulty climbing stairs
As muscle weakness progresses respiratory weakness breathing difficulties (susceptible to respiratory tract infections)
Death from respiratory or cardiac failure:
Usually in late teens or 20’s
Some degree of learning disability—cognition and behaviour
Becker’s MD
X-linked recessive
Primarily affects males
Females as carriers
mutation in dystrophin gene – results in abnormal version of dystrophin
Symptoms are similar to Duchenne but onset is later in childhood and progression is slower
Initial signs:
Muscle weakness presents between 5 – 15 years of age
Cardiomyopathy can be first sign in some cases
Incidence: 1 in 30,000 live births for the Becker type
Death due to heart or respiratory complications in 4th decade
pseudohypertrophic MD
Muscular enlargement caused by deposits of fat and fibrous tissue
Gradual deterioration of muscles
limb-girdle MD
Autosomal dominant or recessive disease of later childhood, adolescence, or early adulthood
Atrophy/wasting and weakness of voluntary muscle of hip and shoulder areas
Varied progression depending on subtype
facioscapulohumeral MD
Inherited as an autosomal dominant disorder of early adolescence
Initially affects skeletal muscles of face, scapula, and upper arms
Progression is slow and the lifespan is usually unaffected
cerebral palsy
Defined as a group of permanent disorders of the development of movement and postures, causing activity limitations attributed to nonprogressive disturbances that occurred in the developing fetal or infant brain.
Characterized by abnormal muscle tone and coordination
Most common permanent physical disability in childhood
Global Incidence: 1.5 to > 4 per 1,000 live births
~ 40% of children with CP will also have epilepsy
cerebral palsy risk factors
Prenatal brain abnormalities: 80% of cases are caused by unknown prenatal factors Intrauterine exposure to intrauterine infection Intrauterine growth restriction 12% of infants born prior to 36 weeks Result of shaken baby syndrome Additional Factors: Bacterial meningitis Motor vehicle accidents Increased risk for CP is found in mother > 40 or < 20 years of age Mothers or fathers of African American ethnicity Premature Multiple births Low birth weight Blood type incompatibility Neonatal sepsis
types of cerebral palsy
spastic
dyskinetic (athetoid)
ataxic
mixed
spastic CP
Cerebral cortex or pyramidal tract injury
75% of cases
dyskinetic CP
Extrapyramidal, basal ganglia injury (may be associated with kernicterus)
10-15% of cases
ataxic CP
Cerebellar (extrapyramidal) injury
5-10% of cases
mixed CP
Injury to multiple areas (5-10% of cases)
cerebral palsy diagnostic evaluation
usually based on clinical findings (Achievement of Developmental Milestones Meeting standards for height and weight Reflexes Focus and Hearing Posture and movements) Ultrasonography Fetal and neonatal abnormalities of the brain Neuroimaging (CT, MRI) Metabolic and genetic testing Neuromotor tests Evaluate the presence of normal movement patterns and absence of primitive reflexes and abnormal tone Delays in key areas of motor function, such as: Holding his/her head up Rolling over Visual alertness Sitting Crawling Walking Picking up small objects
possible motor clinical signs of cerebral palsy
Lack of muscle coordination
Shaky, spastic movements
Muscles may become extremely stiff or extremely loose
Difficulty in controlling certain body movements
Inability to grasp small objects
Using the arms to pull themselves around while the legs drag behind (most prominent after 6 months of age and into the toddler years)
Slow, writhing movements
Excessive drooling due to the inability to control facial muscles
Favoring one side of the body over the other side
Poor head control and clenched fists after age 3 months
Stiff or rigid limbs
Arching back and pushing away
Floppy tone
Unable to sit without support at 8 months
Seizures, sensory impairment
After 6 months, persistent tongue thrusting
common developmental delays with cerebral palsy
Failure to sit alone without assistance by six months of age
Failure to roll over without assistance by four months of age
Failure to walk by age two
Failure to smile by six weeks of age
Failure to climb stairs by three years of age
Failure to stand on one foot (for a few seconds) by three years of age
possible behavioural clinical signs with cerebral palsy
Excessive irritability No smiling by age 3 months Excessive sleeping Lack of interest in surroundings Feeding difficulties 30-50% of CP patients have some level of cognitive impairment
spina bifida patho
Congenital neural tube defect
Incomplete closure of vertebrae of neural tube
3 types of spina bifida
Spina Bifida Occulta
Meningocele
Myelomeningocele
spina bifida predisposing factors
Folic Acid deficiency Genetic factors: family history, previous birth of child with spina bifida Additional factors: Maternal obesity Maternal diabetes mellitus Low maternal vitamin B12 Maternal hyperthermia
new born assessment of spina bifida occulta
Usually no signs or symptoms
May have visible indications – abnormal tuft of hair or small dimple/birthmark or lipoma usually midline lumbosacral
new born assessment of meningocele
CSF-filled sac; no central nervous tissue
No neurological defects
new born assessment of myelomeningocele
Severe form—diagnosed prenatally or at birth
Spinal canal remains open along several vertebrae in the lower or middle back.
Both the membranes and the spinal cord or nerves protrude at birth, forming a sac, which may or not be covered by skin.
spina bifida diagnostic evaluation
Clinical manifestations Examination of the meningeal sac Evaluate the brain and spinal cord: MRI Ultrasound CT Myelography Prenatal screening via ultrasound scan of the uterus Prenatal maternal concentration testing for α-fetoprotein (elevated
chronic challenges of living with spina bifida
Myelomeningocele – infant surgery Hydrocephalus -- infant shunt surgery; ongoing as child grows Tethered Spinal Cord Mobility and Physical Activity Using the Bathroom Skin Care Latex (Natural Rubber) Allergy Health Checks Other concerns –quality of life; mental health; lifestyle; learning; relationships
adults living with spina bifida
Have unique and specific medical and social needs
Pain issues: shoulders, back, neuropathic
Neurogenic bowel and bladder common – lead to kidney failure, dialysis
Hypertension
Lifelong management of hydrocephalus
Tethered cord syndrome – scoliosis, gait changes, spasticity
Cognitive impairment
