Orthopedic Pathology 4 Muscle pathologies Flashcards
Lacerations
Is a break or opening in the skin
Reaction of Sckeletal muscles
Disuse/Atrophy - after trauma, immobilization, poliomyelitis, myasthenia Gravis, Musclular dystrophy
Hypertrophy
Ischemic necrosis - Up to 6 ours without blood
Contractures - Polymyositis, Cerebral palsy (hypoxia @ birth), MD (muscluar dystrophies)
Regeneration
Scar
Is a collagen based tissue that develops as a result of the inflammatory process
Scares are weaker than the tissue it replaces
Scar causes
Inflammatory responses from wound, burns, trauma, OA, artritides, prolonged immobilization, paralysis
Scar types
Contracture Adhesion Scar tissue adhesion Fibrotic adhesion Irreversible contracture Proud flesh Hypertrophic scarring Keloid
Contracture type of scar
Contracture - is the shortening of CT supporting structures over or around a joint (muscles, tendons, joint capsule)
Adhesion type of scar
Adhesion - occurs when reduced motion of a joint allows cross-links to form among collagen fibers causing further reduced ROM. Most common when a tissue is left in a shortened position
scar tissue adhesion
Occurs with an injury or an acute inflammatory process
Adhesions are contructures can form in a random pattern which can reduce ROM
Fibrotic adhesions
Occur with ongoing chronic inflammation can cause moderate to severe restrictions in ROM
Difficult to eradicate
Irreversible contracture
Occurs when fibrotic tissue or bone replaces muscle and CT
Permanent loss of ROM that can only be restored by surgical means
Proud flesh
Term used to refer to the thick dermal granulation tissue that results from an abnormal healing process
Has a raised, red structure
Hypertrophic scarring
is an overgrowth of dermal tissue that remains within the boundaries of the wound.
Collagen fibers are randomly organized in nodular or whirl patterns
Associated with deep partial or full thickness burns skin grafts, sutures
Occurs commonly in the sternum, upper back, shoulder/deltoid, buttock dorsum of foot
Keloid
a dermal scar tissue that extends beyond the boundaries of the original wound in a tumor-like growth
Thought to contain increased amounts of collagen in a more random pattern than a hypertrophic scar
may continue to grow for years
Does not respond well to surgical excision
most common ear to waist, shoulder to elbow
most common in darker skinned people
Tx-steroids
Myscular dystrophies
more than 30 genetic diseases characterized b progressive weakness and degeneration of the striated muscles
- Duchenne’s MD
- Becker’s MD
- Myotonic dystrophy
- Facioscapulohumeral
- Limb-girdle
- Congenital
- Oculopharyngeal
- Distal
- Emery-dreifuss
Duchenn’s MD
Most common, 1/3300 males caused by dystrophin (anchor on cell membrane).
Most common and more severe than Becker’s
By school age in wheelchairs, skeletal muscle deformities, paralyzed by 12 years and may need respirator. Life expectancy is 20 years.
Duchenne’s MD SS
Initially affects the girdle (shoulder, hip) area Muscle weakness Lack of coordination spastic movements weight loss Contractures, loss of ROM, deformities - painful Mental retardation Respiratory muscle failure Frequent falls large calf muscles (pseudohypertrophy) Gowers sign Waddling gait Weak postural muscles
Beckers MD
Less common and less severe than Duchenne’s
1/20000 males
Due to faulty or decreased dystrophin
Begins in late childhood - 12-20 years old
Muscle weakness not significant until midlife
Can walk into teens/early adulthood
Symptoms same as Duchenne’s except later in life
Life span into 40’s 50’s
Etiology of Duchenne’s and Becker’s MD
Sex-linked recessive
Primarily affect males
Defect in the gene the codes for dystrophin - DMD
affects all muscle cells but effects are most apparent in skeletal muscle tissue
Diagnosis of Duchenne’s and Becker’s MD
History Exam Blood text (muscle enzymes - creatine kinase) EMG (muscle firing pattern) Ultrasound (quality of muscle tissue) Muscle biopsy (looking for dystrophin) Genetic testing
Duchenne’s and Becker’s MD treatment
Supportive physical therapy speech therapy Respiratory treatment Dietary supervision Surgery Meds: corticosteroids to slow muscle degeneration
Myotonic dystrophy
Aka Steinert's disease Inability to relax muscles Characterized by myotonia Autosomal dominant M=F Onset 10-30 years old Most common effects young adults Multisystem disease - variable presentation
Myotonic dystrophy SS
Muscles of entire body are affected (initially effects muscle of the eyelids, face distal limbs)
Particularly apparent in the distal limbs (fine movements difficult)
joint contractures
progressive weakening of muscle (due to always contracted, no relaxation period, no time for regeneration and repair)
Primarily head, neck face, voluntary muscles of arms and legs, distal muscles
Can also affect smooth muscles around uterus and intestines
can also include CV, endocrine, cataracts, mental retardation
Facioscapulohumeral MD
AKA Landouzy Dejerine disease
Initially effects the face and shoulder muscles
Onset (late teens early 20’s)
Autosomal dominant
Progression is slow
Characterized by slow progression and difficulty whistling closing the eyes and raising the arms (due to weakness of the scapular stabilizer muscles)
life expectancy is normal
Limb-girdle MD
Onset is early childhood to adulthood (3-20 years)
Initially effects the shoulders and hips (proximal limb distribution)
Moderate weakness
slow progression
Congenital MD
not a shingle disorder but instead refers to muscular dystrophy evident at birth
several rare forms of MD
General muscle weakness
Joint deformities
Oculopharyngeal MD
Effects eyes and throat (initial sign is drooping eyelids)
Onset- up to 40-60 years
Slow progression
Distal MD
Involves the muscles farthest away from the center of the body (hands, feet, forearms, lower legs)
Slow progression
Onset-40-60 years
Emery-Dreifuss MD
Begins in the muscles of the shoulders, upper arms (bicepts/tricepts common) and shins
Onset early teens
The heart is frequently Invovled, with atrial paralysis and conduction abnormalities
Progresses slow
Inflammatory myopathies
Inflammatory myopathies are a group of diseases that involve chronic muscle inflammation, accompanied by muscle weakness
The three main types of chronic, persistent, inflammatory myopathy are polymyositis, dermatomysitis and inclusion body myositis
Inclusion Body Myositis
one of a group of muscle disease know as the inflammatory myopathies
Idiopathic
Characterized by chronic, progressive muscle inflammation accompanied by muscle weakness
Onset is gradual and affects proximal and distal muscles
muscle weakness may be asymmetric
Affect individuals after age of 50
Prognosis : Poor
Inclusion Body Myositis SS
first symptom falling or tripping may begin with weakness in the wrists and fingers difficult swallowing treatment supportive and symptomatic
Polymyositis
Uncommon CT disease
Type of inflammatory myopathy
Characterized by muscle inflammation and weakness
Epidemology
most common in women (2:1)
Blacks > whites
Most common 30-50 years but can occur at any age
Idiopathic
Possibly autoimmune with viral or genetic component
Can be associated with other CT disorders, RA, SLE
Begins acutely or insidiously with muscle weakness, tenderness and discomfort
Polymyositis SS
Onset Gradual or rapid Symmetric weakness, tenderness and atrophy (proximal limb girdle muscles) Loss of muscle strength Muscle atrophy Fatigue General discomfort weight loss Difficulty getting out of chairs, climbing stairs, lifting above shoulders, swallowing (dysphagia), lifting head from pillow (1st sign), speech
Poly Myositis Medical management
Diagnosis: blood test, biopsy, EMG
Treatment: exercise, rest medication, speech therapy
Prognosis: variable, remissions, relapse
Dermatomyositis
Uncommon inflammatory disease marked by muscle weakness and a distinctive skin rash
Occurs at any age most common 40-60, 5-15 years old
Women >men
Idiopathic, Viral/bacterial autoimmue?
Dermatomyositis SS
Develop gradually, over weeks or months May have period of remission Idiopathic Violet colored or dusty red rash (most common on face, eyelids, and areas around nails, knucles, elbows, knees, chest and back) first sign. progressive systemic muscle weakness, in the muscles closest to the trunk weakness is symmetrical difficulty swallowing (dysphagia) Muscle pain or tenderness fatigue weight loss hardened deposits of calcium under the skin (calcinosis cutis) Lung problems
Dermatomyositis
DX : MRI, presense of a rash, muscle testing, blood work
Prognosis: good
Treatment: medications, physical therapy, speech therapy
Myasthenia gravis
motor end plate disorder
Characterized by weakness and rapid fatigue of any of the muscles under voluntary control
Women younger than 40
Men over 60 years
Myasthenia gravis Ethimology and pathogenesis
Autoimmune disorder
Immune system attacks Ach receptors
Auto-immune antibodies to Ach receptors Ach receptors are decreased or flattened
Associated with abnormal thymus (benign tumors), education of T-cell. It is not lethal disease
Myasthenia gravis clinical manifestations
Mild-severe
Muscle weakness - worsening with use
Eyes - ptosis (drooping), dipoplia (double vision) strabismus (lazy eye)
Altered speech, chewing, facial expressions
Altered ADL’s due to weakeness
Myasthenia gravis Diagnosis
history, clinical observation neurological exam, blood test
EMG
Edrophonium (tensilon) test - drug that blocks the effects of acetylcholinessterase
Ach stays in synaptic cleft
Allows for temporary muscle contraction
Myasthenia gravis treatment
Corticosteroids for immunosuppression
surgery to remove thymus
plasmaphoresis at life-sthreatening stages
-take blood out, clean out the ABs, then return blood to patient
-expensive, time consuming
AchE inhibitors
Prognosis - variable
Necrotizing Fasciitis
Is a rare but very severe type of bacterial infection that can destroy the muscles, skin and underlying tissue, causes cell death
Necrotizing fascilitis causes
Bacteria, most common Streptococcus pyogenes “flesh eating”
Enters body and releases harmful substances that kill tissue, interfere with blood flow and break down tissue
Necrotizing fasciitis Symptons
Small, reddish, painful spot or bump on the skin
- changes to very painful bronze or purple colored patch that grows rapidly
- center may be black and die
- skin may break open and ooze
- fever
- sweating, chills
- nausea, dizziness
- weakness
necrotizing fasciitis Dx and Tx
PE, blood tests, CT scan
Treatment
Broad-spectrum antibiotics
Surgery
Myofascial pain dysfunction
regional pain disorder characterized by trigger points
local condition of soft tissue structures
Related to dysfunctional end plate of skeletal muscle fibers
responds well to treatment
Myofascial pain dysfunction etiology and risk factors
Related to sudden overload of a muscle direct impact trauma, postural faults, psychological stress, chronic repetitive or sustained activity, structural abnormalities, overwork fatigue, chronic infection, visceral disease, arthritis, joint dysfunction, emotional stress
Myofascial pain dysfunction clinical manifestation
Trigger points Reduced ROM Weakness Paresthesia Different sensation Diagnosis - palpation
Myofascial pain dysfunction treatment
Injections of saline or anesthetic Ice/heat US/E stim/laser Manual pressure (ischemic) Vapocoolant spray Stretching/strengthening Supplement (vitamin B and C)
