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Mechanisms of abnormal skeletal muscle contractions
issues often related to ATP and electrolytes or problems with neurotransmitters.
Common problems with musculoskeletal disorders
weakness
fatigue
cramps
direct injury
Weakness (loss of strength) due to:
disuse (atrophy) muscle cells shrink, loss of noncontractile protein
Systemic wasting disorders. the muscle tissue is replaced by abnormal tissue.
Fatigue
the loss of power or force in the muscle
Intracellular acidosis (lactic acid)
Lack of energy production (disorders with rapid energy depletion)
Disruption in calcium flux
Cramps
involuntary muscle spasms due to dehydration or electrolyte depletion. The muscle remain in contractile state because of improper depolarization.
Direct injury are either:
Hematoma or muscle tears
Hematoma
bleeding into muscle tissue
Muscle tears
Myoglobin released in urine - filtered out by the kidneys
Myoglobinuria (rhabdomyolysis) - myoglobin in the urine, rhabdomyolysis is a life-threatening complication of muscle trauma.
Increased creatine phosphokinase (CPK) - damage to heat, muscle, brain
Risk for renal failure - especially with rhabdomyolysis, myoglobin can damage the kidney cells and kidney’s can’t clear waste like they should.
Pathological Muscle Disorders
Muscular dystrophies
Inflammatory myopathies
Cancer of muscle
Muscular Dystrophies
genetically transmitted through recessive gene on the X chromosome, produces
progressive muscle wasting. deterioration of skeletal muscle
Muscular dystrophies classifications
Rapidly progressing: Duchenne’s muscular dystrophy (onset at 5 years of age, most common form seen)
b. Slower progressing: Becker’s, limb-girdle
Pathophysiology of Muscular dystrophies
b. Defect in gene that produces dystrophin
c. Muscles cells die → phagocytosis (process to remove dead cells)
d. Replaced with fatty tissue (enters the muscle fibers and weakens the muscle)
e. Respiratory and cardiac failure (these muscles affected)
Dystrophin
protein thought to affect muscle contraction
CM of Muscular Dystrophies
Difficulties with early motor development (they could have normal development at birth but can be delay in walking)
Gower's maneuver - use the hands and arms to get up and walk because of the decrease in muscle strength in the hips and thighs. they walk up the body from sitting.
b. Progression - falls and wheelchair use
inflammatory Myopathies
Polymyositis
dermatomyositis
Fibromyalgia
Polymyositis
Inflammation of muscle groups
a. Autoimmune or viral - self-reactive B and T cells attack the muscle
b. Patchy muscle necrosis - neck, limbs, chronic inflammation results
c. May involve the joints - painful swelling
d. Progression of weakness - cardiac and respritory involvement
Dermatomyositis
the autoimmune response following infection causing muscle weakness
a. Rash and puffiness of the eyes and face
b. Sluffing of skin, calcification - manifests nodules in bony areas
Fibromyalgia
a. Chronic musculoskeletal pain with no evidence of arthritis
b. Stiffness, fatigue - tender areas, elevated by stress
c. Inappropriate levels of neurotransmitters (being investigated)
Decreased ATP and creatine phosphate levels in areas of tenderness - neck, hip, shoulders, low back
cancer of the muscle
Rhabdomyosarcoma - head, neck, abdomen, extremities. soft tissue mass
Disorders of the bones and joints
Fractures and associated injuries
bone disease
Alterations in joints
Fractures and Associated injuries (5)
classifications of fractures
dislocation
signs and symptoms of fractures
fracture healing
soft tissue traumas
Classifications of fractures
break in the continuity of a bone
Simple
2. Compound
3. Complete
4. Comminuted
5. Depressed
6. Compression
simple and compund
simple - no break in the skin, no separation of bone
compound - through the skin, bone protrudes
Comeplete
through entire bone with separation, could be simple or compound
Comminuted
three or more fragments of the bone
depressed
bone drawn inward
compression
one of more bones in the spine weaken or crumble, could be due to osteoporosis or loss of bone mass
Dislocation
involves the separation and displacement of the bone from the joint
Signs and symptoms of fractures
inflammatory process initiated at the cite
Swelling, bruising, soft tissue injury
2. Loss of function - depends on the cite
3. Deformity - ambulation
4. Pain - at the cite, increase with touch or movement
fracture healing
formation of new bone (osteoblasts - cells that help form the new bone cells) through sequential process - remodeling
immobilization problems
blood supply
infection (osteomyelitis)
Immobilization problems
movement occurs can compromise new development of bone
blood supply
need good blood supply, can’t if swelling is bad
Infection (osteomyelitis) - of the bone
a. Bloodstream or extension of infection - from another part of the body
b. Direct surgical or traumatic introduction - if fracture is open or trauma occurs where organisms can enter
Organism adheres to bone → inflammatory response
Exudate forms - collects along the bone
c. Nonunion (infection, movement) - bone fails to fuse and heal
d. Compartment Syndrome:
compartment syndrome
muscle and nerve damage due to excessive swelling. you need a fasciotomy to cut the facia and relieve the pressure
Enclosed area: pressure builds within the compartment - in the facia compartment
Fascia permits no outward enlargement - edema expands the enclosed area
Compression of blood vessels and nerves leads to necrosis and gangrene if no
intervention. decrease in oxygen to the tissues
Soft tissue traumas
tendon/ligament damage
visceral damage
sprains
strains
Tendon/ligament damage
a. Avulsion: pulling apart of piece of bone attached to tendon (separation usually)
b. Tendon laceration: Loss of ability to flex or extend - hands, knees, feet (Achilles tendon rupture)
c. Physical tear in ligament - torn ACL (most common)
d. Healing tendon or ligament - gradual process (several weeks)
Visceral damage
with fractures, when bone punctures other areas
organs - lungs, liver, spleen are common) ribs can puncture
Sprains
Ligaments or joint capsule. Damage caused by an abnormal movement of the joint
Stains
stretching or partial tear in muscle or muscle-tendon unit. A sudden abnormal stretch of a contracting muscle.
Bone diseases (5)
Osteoporosis
Osteomalacia
Paget Diseases (osteitis deformans)
Bone cancer
Disorders of bone growth
Osteoporosis
decrease in bone density and strength due to a reduction in bone matrix and mineralization. Usually in weight bearing bones
Reduction in bone matrix and mineralization
a. Numerous risk factors - age, smoking, loss of activity
b. Osteopenia - early decrease in bone density not quite osteoporosis
c. Bone loss exceeds bone formation leading to thinning of the cortex - minimal force/stress can develop a fracture (sometimes its not the fall but the bone broke first and then they fell.
Classification
Type 1 - develops with early post metapodial estrogen deficiency
Type 2 - calcium deficiency
CM of weakening bone
a. Fracture - (most common) hips, head of femur, distal radius
b. Loss of height - with a decrease in the density of the vertebrae
c. Kyphosis (dowager hump) - arch of upper back
Osteonecrosis
Eventual death of bone cells can result in rough not smooth.
Osteomalacia and etiology
Softening of bone (adult form of rickets)
Etiology:
1. calcium, vitamin D or phosphate deficiency - dietary intake or kidney disease
2. Medications, lack of sunlight - can decrease activation of VD synthesis.
Patho of Osteomalacia
a. Inadequate mineralization → weakening of bone
Cm of Osteomalacia
Pain, fractures, bowing of legs
Paget Disease (osteitis deformans) and etiology
next most common after osteoporosis of bone diseases
Etiology: genetic and environmental influences; greater incidence in men - can be triggered by a viral infection
Patho of Paget Disease
a. Excessive bone resorption - rapid destruction of bone
b. Disorganized bone repair with newly formed bone of poor quality - newly form bone is deposited chaotically
Mosaic like pattern - grow outward
c. Adjacent bone marrow replaced by loose connective tissue and blood vessel
CM of Paget Disease
Skeletal expansion and distortion - skull, jaw, long bones of leg
b. Headache, dizziness - if skull involved
c. Kyphosis - due to vertebral weakening
d. Bowing of leg bones
e. Increased risk for osteogenic sarcomas - occurs with extensive disease
Bone cancer (5)
Benign
malignant
pathophysiology
Hypercalcemia possible
Osteosarcoma
Benign
common in children and teens
a. Fibrous origin: common in growing bones
b. Cartilaginous origin: chondromas or osteochondromas - cancer starts in cartilage and moves to bones
Malignant: Primary or secondary
Primary: starts in the bones
Secondary: cancer originates elsewhere and metastasizes to the bone
usually seen in children and teens.
a. Rapid growth - beyond bone tissue
b. Symptoms: pain, unexplained swelling, feeling of warmth
Patho of bone cancer
a. increased production of abnormal bone, cartilage, or surrounding tissue
b. Malignant = destructive to adjacent normal cells - metastasizes to the lungs commonly
c. Weakens bone - because of loss of bone tissue
Hypercalcemia possible
Hormones secreted by tumor increase reabsorption of Calcium or increased parathyroid related peptides - more calcium pulled into the blood
Osteosarcoma
: circular ball-like mass in bone tissue - most common type of bone cancer
Disorders of bone growth (2)
Scoliosis
Osteogenesis Imperfects
scoliosis
lateral - curvature of the spine
Osteogenesis Imperfecta
a (brittle bone disease): genetic mutation
a. Disorder of synthesis of collagen - collagen are a major component of bones
b. Prone to fractures, osteoporosis, deformed limbs - they often need frequent operations
Alterations in joints (6)
Osteoarthritis (Degenerative joint disease: DJD)
Rheumatoid arthritis: Systemic autoimmune disease
Ankylosing Spondylitis
bursitis
Osteochondrosis
Gout: metabolic disorder
Osteoarthritis (Degenerative joint disease: DJD
progressive breakdown of cartilage (most prevalent joint disease)
Osteoarthritis (Degenerative joint disease: DJD) Patho
: depletion of matrix in articular cartilage - surface flakes off
Collagen fibers exposed - cartilage becomes thin and cracks develop
b. Synovial fluid enters the cracks: formation of cysts
c. Synovial capsule decreases in size → exposing bone (bone on bone)
CM of Osteoarthritis (Degenerative joint disease: DJD)
due to enlargement of joints
a. Pain, stiffness - particularly in weight bearing joints
b. Difficulty with movement - limp, limited range of motion
Rheumatoid arthritis
Systemic autoimmune disease - starts with joints
IgG/rheumatoid factor (RF) interaction (auto antibody)
2. Activation of a T-cell mediated response to an immunologic trigger (infection)
3. Inflammation in joints → thickening and destruction of cartilage
4. Synovial membrane thickens → pannus development → scar tissue (abnormal tissue growth in joints space)
CM of Rheumatoid arthritis
Systemic: fever, weakness, weight loss, stiffness
b. Joint pain, tenderness (part. in AM) - pressure with swelling
c. Warmth, bogginess - mushy texture in joint
d. Loss of mobility - progressive limitation
e. Rheumatoid nodules in skin, heart, lungs, and spleen
Ankylosing Spondylitis
autoimmune
Inflammation of skeletal joints (low back)
2. Stiffening and fusion of spine and sacroiliac joints - chronic inflammation leads to low back pain and stupped posture
Bursitis
1. Inflammation of a bursa - painful swelling of the sack that cushions and lubricates the joints
Excess fluid
Pressure on sensory nerve endings
2. Trauma, infection, rheumatoid arthritis
3. Knee, elbow, feet (overuse)
Osteochondroses
series of childhood disorders with a decrease of blood supplies to the
1. Joints Legg-Calve-Perthes Disease: affects femoral head - and blood supply to there, bone dies and stops growing
2. Osgood-Schlatter Disease - tibular and patellar tendonitis and inflammation, usually seen with athletic. peer adolescent age
Gout:
metabolic disorder - affects joints and causes pain
Increased levels of uric acid - causing inflammation
2. Uric acid crystals may precipitate into joint - and connective tissue