Week three muscles

Mosby items and derived items © 2012 Mosby, Inc., an imprint of Elsevier Inc. 1
Alterations of Musculoskeletal
Function

Musculoskeletal Injuries
• Complete or incomplete
 Closed or open
• Comminuted
• Linear
• Oblique
• Spiral
• Transverse
• Greenstick
• Torus
• Bowing
• Pathologic
• Stress
 Fatigue and
insufficiency
 Transchondral
 Fractures
 A fracture is a break in the continuity of a bone
 Classifications:

Fractures

Bone Fractures
 A broken bone can cause damage to the
surrounding tissue, the periosteum, and
the blood vessels in the cortex and marrow
 Hematoma formation
 Bone tissue destruction triggers an
inflammatory response
 Procallus formation

Callus Formation

Callus Formation (cont’d)

Bone Fractures
 Manifestations:
 Often numbness up to 20 minutes following
injury
 Unnatural alignment, swelling, muscle spasm,
tenderness, pain, impaired sensation, and
possible muscle spasms
 Treatment:
 Closed manipulation, traction, and open
reduction
 Internal and external fixation

Bone Fractures (cont’d)
 Improper reduction or immobilization
 Nonunion, delayed union, and malunion
 Dislocation
 Temporary displacement of two bones
 Loss of contact between articular cartilage
 Subluxation
 Contact between articular surfaces is only
partially lost

Bone Fractures (cont’d)
 Dislocation and subluxation are associated
with fractures, muscle imbalance,
rheumatoid arthritis, or other forms of joint
instability

Support Structure Injuries
 Strain
 Tear or injury to a tendon
 Sprain
 Tear or injury to a ligament
 Avulsion
 Complete separation of a tendon or ligament
from its bony attachment site

Tendinopathy and Bursitis
 Tendinitis
 Inflammation of a tendon
 Tendinosis
 Painful degradation of collagen fibers
 Bursitis
 Inflammation of a bursa
• Skin over bone, skin over muscle, and muscle and
tendon over bone
 Caused by repeated trauma
 Septic bursitis is caused by a wound infection

Tendinopathy and Bursitis (cont’d)
 Epicondylitis
 Inflammation of a tendon where it attaches to a
bone
• Tennis elbow (lateral epicondylitis)
• Golfer’s elbow (medial epicondylitis)

Tendinopathy and Bursitis (cont’d)

Tendinitis and Epicondylitis

Muscle Strain
 Sudden, forced motion causing the muscle
to become stretched beyond its normal
capacity
 Local muscle damage
 Muscle strains can also involve the
tendons

Myositis Ossificans
 Complication of local muscle injury
 Inflammation of muscular tissue with
subsequent calcification and ossification of
the muscle
 Rider’s bone in equestrians
 Drill bone in infantry soldiers
 Thigh muscles in football players

Rhabdomyolysis
 Rhabdomyolysis (myoglobinuria) is a life-
threatening complication of severe muscle
trauma with muscle cell loss
 Crush syndrome
 Compartment syndromes
• Volkmann ischemic contracture
 Malignant hyperthermia

Osteoporosis
 Porous bone
 Poorly mineralized bone
 Bone density:
 Normal bone
• 833 mg/cm2
 Osteopenic bone
• 833 to 648 mg/cm2
 Osteoporosis
• <648 mg/cm2

Osteoporosis (cont’d)
 Potential causes:
 Decreased levels of estrogen and testosterone
 Decreased activity level
 Excess intake of caffeine, phosphorus, alcohol,
nicotine
 Inadequate levels of vitamins D and C, or Mg++

 Demonstrated by reduced bone
mass/density and an imbalance of bone
resorption and formation
 Bone histology is usually normal but it
lacks structural integrity

 Iatrogenic osteoporosis
 Regional osteoporosis
 Postmenopausal osteoporosis
 Glucocorticoid-induced osteoporosis
 Age-related bone loss

Osteomalacia
 Deficiency of vitamin D lowers the
absorption of calcium from the intestines
 Inadequate or delayed mineralization
 Bone formation progresses to osteoid
formation but calcification does not occur;
the result is soft bones
 Pain, bone fractures, vertebral collapse, bone
malformation

Paget Disease
 Also called osteitis deformans
 Excessive resorption of spongy bone and
accelerated formation of softened bone
 Disorganized, thickened, but soft bones
 Most often affects the axial skeleton

Paget Disease (cont’d)
 Thickened bones can cause abnormal
bone curvatures, brain compression,
impaired motor function, deafness, atrophy
of the optic nerve, etc.

Osteomyelitis
 Osteomyelitis is most often caused by a
staphylococcal infection
 Most common cause is open wound
(exogenous); also can be from a blood-
borne (endogenous) infection

Osteomyelitis (cont’d)
 Manifestations:
 Acute and chronic inflammation
 Fever
 Pain
 Necrotic bone
 Treatment:
 Very difficult to treat
 Antibiotics, debridement, surgery, hyperbaric
oxygen therapy

Inflammatory vs. Noninflammatory
Joint Disease
 Differentiated by:
 Absence of synovial membrane inflammation
 Lack of systemic signs and symptoms
 Normal synovial fluid analysis

Osteoarthritis
 Degeneration and loss of articular
cartilage, sclerosis of bone underneath
cartilage, and formation of bone spurs
(osteophytes)
 Also referred to as degenerative joint
disease
 Incidence increases with age
 Primary disease is idiopathic

Osteoarthritis (cont’d)
 Risk factors:
 Increased age
 Joint trauma, long-term mechanical stress
 Endocrine disorders (hyperparathyroidism)
 Drugs
 Obesity

 Characteristics:
 Local areas of damage and loss of articular
cartilage
 New bone formation of joint margins
 Subchondral bone changes
 Variable degrees of mild synovitis and
thickening of the joint capsule

 Manifestations:
 Pain (worsens with activity)
 Stiffness (diminishes with activity)
 Enlargement of the joint
 Tenderness
 Limited motion
 Deformity

Rheumatoid Arthritis
 Inflammatory autoimmune joint disease
 Systemic autoimmune damage to
connective tissue, primarily in the joints
(synovial membrane)
 Similar symptoms to osteoarthritis
 Cause unknown; multifactorial with strong
genetic predisposition

Rheumatoid Arthritis (cont’d)
 Presence of rheumatoid factors (RA or RF
test)
 Antibodies (IgG and IgM) against antibodies
 Joint fluid presents with inflammatory
exudate

 Pathogenesis
 Three Processes:
• Neutrophils and other cells in the synovial fluid
become activated
• Inflammatory cytokines (tumor necrosis factor-alpha
(TNF-α), interleukin-1 beta (IL-1β), interleukin-6 (IL-
6), interleukin-7 (IL-7), interleukin-21 (IL-21), induce
enzymatic breakdown of cartilage and bone
• T cells also interact with synovial fibroblasts through
TNF-α, converting synovium into a thick, abnormal
layer of granulation tissue (pannus)

Osteoarthritis
 Manifestations:
 Insidious onset
 Begins with general systemic manifestations of
inflammation, including fever, fatigue,
weakness, anorexia, weight loss, and
generalized aching and stiffness
 Over a period of weeks or months, the joints
become painful, tender, stiff, swollen, warm,
boggy, and lose range of motion
 Joint deformities

Rheumatoid Arthritis
 Evaluation
 Four or more of the following:
• Morning joint stiffness lasting at least 1 hour
• Arthritis of three or more joint areas
• Arthritis of the hand joints
• Symmetric arthritis
• Rheumatoid nodules
• Abnormal amounts of serum rheumatoid factor
• Radiographic changes

Ankylosing Spondylitis
 Inflammatory joint disease of the spine or
sacroiliac joints causing stiffening and
fusion of the joints
 Systemic, immune inflammatory disease
 Primary proposed site is the enthesis
 Site where ligaments, tendons, and the joint
capsule are inserted into bone

Ankylosing Spondylitis (cont’d)
 Cause unknown, but there is a strong
association with HLA-B27 antigen
 Begins with the inflammation of
fibrocartilage, particularly in the vertebrae
and sacroiliac joint
 Inflammatory cells infiltrate and erode
fibrocartilage
 As repair begins, the scar tissue ossifies
and calcifies; the joint eventually fuses

 Manifestations:
 Early symptoms:
• Low back pain that begins in early 20s and
progresses over time
• Stiffness
• Pain
• Restricted motion
 Loss of normal lumbar curvature (lordosis)
 Increased concavity of upper spine (kyphosis)

Gout
 Metabolic disorder that disrupts the body’s
control of uric acid production or excretion
 Gout manifests high levels of uric acid in
the blood and other body fluids
 Occurs when the uric acid concentration
increases to high enough levels to
crystallize

Gout (cont’d)
 Crystals deposit in connective tissues
throughout the body
 Sites:
• 50% of the initial attacks occur in the
metatarsophalangeal joint of the great toe
• Heel, ankle, instep of the foot, knee, wrist, or elbow
 When these crystals occur in the synovial
fluid, the inflammation is known as gouty
arthritis

Gout (cont’d)
 Gout is related to purine (adenine and
guanine) metabolism
 Affected patients can have accelerated
purine synthesis, breakdown, or poor uric
acid secretion in the kidneys

Gout (cont’d)
 Mechanisms for crystal deposition:”
 Lower body temperatures
 Decreased albumin or glycosaminoglycan
levels
 Changes in ion concentration and pH
 Trauma
 Risk factors:
 Male sex
 Increasing age
 High intake of alcohol, red meat, and fructose
 Drugs

Gout (cont’d)
 Clinical stages:
 Asymptomatic hyperuricemia
 Acute gouty arthritis
 Tophaceous gout

Gout (cont’d)
 Manifestations:
 An increase in serum urate concentration
(hyperuricemia)
 Recurrent attacks of monoarticular arthritis
(inflammation of a single joint)
 Deposits of monosodium urate monohydrate
(tophi) in and around the joints
 Renal disease involving glomerular, tubular,
and interstitial tissues and blood vessels
 Formation of renal stones

Gout (cont’d)
 Manifestations of acute gouty attack:
 Severe pain especially at night
 Hot, red, tender joint
 Signs of systemic inflammation:
• Increased sedimentation rate
• Fever
• Leukocytosis)

Gout (cont’d)

Disorders of Skeletal Muscle
 Contracture
 Muscle fiber shortening without an action
potential
 Caused by failure of the sarcoplasmic
reticulum (calcium pump) even with available
ATP
 Stress-induced muscle tension
 Neck stiffness, back pain, clenching teeth,
hand grip, and headache
 Associated with chronic anxiety

Disuse Atrophy
 Reduction in the normal size of muscle
cells as a result of prolonged inactivity
 Bed rest
 Trauma
 Casting
 Nerve damage
 Treatment
 Isometric movements
 Passive lengthening exercises

Fibromyalgia
 Chronic widespread diffuse joint pain,
fatigue, and tender points
 Vague symptoms:
 Increased sensitivity to touch
 Absence of inflammation
 Fatigue
 Sleep disturbances/non-restorative sleep

Fibromyalgia (cont’d)
 80% to 90% of individuals affected are
women, and the peak age is 30 to 50
years
 New research indicates a genetic
predisposition and environmental factors
play a role in development of symptoms

 Viewed as the result of central nervous
system dysfunction, where pain
transmission and interpretation are
amplified (central sensitization)
 Autoimmune disorders often coexist
 Studies of genetic factors have implicated
alterations in genes affecting serotonin,
catecholamines, and dopamine

 Manifestations:
 Prominent symptom of fibromyalgia is diffuse, chronic
(defined as being present more than 3 months) pain that
is burning or gnawing in nature
 Only reliable finding on examination is the presence of
multiple tender points; the pain often begins in one
location, especially the neck and shoulders, but then
becomes more generalized
 Profound fatigue
 Diagnosis
 Tenderness in eleven pairs of tender points along with a
history of diffuse pain

Muscle Membrane Abnormalities
 Myotonia
 Periodic paralysis:
 Hypokalemic
 Hyperkalemic

Diseases of Muscle Metabolism
 Endocrine disorders
 Hyperthyroidism
 Diseases of energy metabolism:
 McArdle disease
• Myophosphorylase deficiency
 Acid maltase deficiency
• Pompe disease
 Myoadenylate deaminase deficiency (MDD)
 Lipid deficiencies

Polymyositis and Dermatomyositis
 Collectively described by the term myositis
 Viral, bacterial, and parasitic myositis
 Staphylococcus aureus infections
 Trichinosis
• Trichinella infection
 Toxoplasmosis
 Polymyositis and dermatomyositis

Polymyositis and Dermatomyositis
(cont’d)

Toxic Myopathies/”Muscle
Damage”
 The most common cause of toxic
myopathy is alcohol abuse
 Acute attack of muscle weakness, pain, and
swelling
 Chronic weakness in a drinker of long duration
 Necrosis of individual muscle fibers
• Disturbance of energy turnover, gene dysregulation, and
initiation of apoptosis
 Other causes include lipid-lowering agents
(fibrates and statins), antimalarial drugs,
steroids, thiol derivatives, and narcotics

Toxic Myopathies/”Muscle
Damage” (cont’d)
 Manifestations:
 Acute muscle weakness
 Painless or severe pain if necrosis
 Most severe complication is
rhabdomyolysis (acute muscle fiber
necrosis with leakage of muscle protein
into the bloodstream) that leads to
myoglobinuria and acute renal failure

Bone Tumors
 May originate from bone cells, cartilage,
fibrous tissue, marrow, or vascular tissue
 Osteogenic
 Chondrogenic
 Collagenic
 Myelogenic

Bone Tumors (cont’d)
 Malignant bone tumors
 Increased nuclear/cytoplasmic ratio
 Irregular borders
 Excess chromatin
 A prominent nucleolus
 An increase in the mitotic rate

 Patterns of bone destruction:
 Geographic pattern
 Moth-eaten pattern
 Permeative pattern

 Osteosarcoma
 38% of bone tumors
 Predominant in adolescents and young adults;
occurs in seniors if they have a history of
radiation therapy
 Contain masses of osteoid
• Streamers: noncalcified bone matrix and callus
 Located in the metaphyses of long bones
• 50% occur around the knees

Osteosarcoma

Bone Tumors
 Chondrosarcoma
 Tumor of middle-aged and older adults
 Infiltrates trabeculae in spongy bone; frequent
in the metaphyses or diaphysis of long bones
 The tumor contains lobules of hyaline cartilage
that expand and enlarge the bone
 Causes erosion of the cortex and can expand
into the neighboring soft tissues

 Fibrosarcoma
 Firm, fibrous mass of collagen, malignant
fibroblasts, and osteoclast-like cells
 Usually affects metaphyses of the femur or
tibia
 Metastasis to the lungs is common

 Myelogenic tumors:
 Giant cell tumor
• Causes extensive bone resorption because of the
osteoclastic origin of the giant cells
• Located in the epiphyses of the femur, tibia, radius,
or humerus
• The tumor has a slow, relentless growth rate
 Myeloma

Muscle Tumors (cont’d)
 Rhabdomyosarcoma
 Malignant tumor of striated muscle
 Usually muscles of the tongue, neck, larynx,
nasal cavity, axilla, vulva, and heart
 Highly malignant with rapid metastasis
 Types:
• Pleomorphic
• Embryonal
• Alveolar

Muscular Dystrophy
 Group of inherited disorders that cause
degeneration of skeletal muscle fibers
 The muscular dystrophies cause
progressive, symmetric weakness and
wasting of skeletal muscle groups

Duchenne Muscular Dystrophy
 Most common of the muscular dystrophies
 X-linked recessive inheritance
 Deletion of a segment of DNA or a single gene
defect on the short arm of the X-chromosome
 Generally affects boys
 Duchenne muscular dystrophy gene
 Encodes for the dystrophin protein
 Dystrophin maintains the structural integrity of
the cytoskeleton

Duchenne Muscular
Dystrophy(Cont)
 Manifestations of the disorder begin to
appear by approximately 3 years of age:
 Slow motor development
 Progressive weakness
 Muscle wasting
 Sitting and standing are delayed
 The child is clumsy, falls frequently, and has
difficulty climbing stairs

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