Orthopedic Pathology 4 Muscle pathologies

Question 0

Lacerations

Answer 0

Is a break or opening in the skin

Question 1

Reaction of Sckeletal muscles

Answer 1

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

Question 2

Scar

Answer 2

Is a collagen based tissue that develops as a result of the inflammatory process

Scares are weaker than the tissue it replaces

Question 3

Scar causes

Answer 3

Inflammatory responses from wound, burns, trauma, OA, artritides, prolonged immobilization, paralysis

Question 4

Scar types

Answer 4

Contracture
Adhesion
Scar tissue adhesion
Fibrotic adhesion
Irreversible contracture
Proud flesh
Hypertrophic scarring
Keloid

Question 5

Contracture type of scar

Answer 5

Contracture - is the shortening of CT supporting structures over or around a joint (muscles, tendons, joint capsule)

Question 6

Adhesion type of scar

Answer 6

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

Question 7

scar tissue adhesion

Answer 7

Occurs with an injury or an acute inflammatory process

Adhesions are contructures can form in a random pattern which can reduce ROM

Question 8

Fibrotic adhesions

Answer 8

Occur with ongoing chronic inflammation can cause moderate to severe restrictions in ROM
Difficult to eradicate

Question 9

Irreversible contracture

Answer 9

Occurs when fibrotic tissue or bone replaces muscle and CT

Permanent loss of ROM that can only be restored by surgical means

Question 10

Proud flesh

Answer 10

Term used to refer to the thick dermal granulation tissue that results from an abnormal healing process
Has a raised, red structure

Question 11

Hypertrophic scarring

Answer 11

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

Question 12

Keloid

Answer 12

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

Question 13

Myscular dystrophies

Answer 13

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

Question 14

Duchenn’s MD

Answer 14

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.

Question 15

Duchenne’s MD SS

Answer 15

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

Question 16

Beckers MD

Answer 16

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

Question 17

Etiology of Duchenne’s and Becker’s MD

Answer 17

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

Question 18

Diagnosis of Duchenne’s and Becker’s MD

Answer 18

History 
Exam
Blood text (muscle enzymes - creatine kinase)
EMG (muscle firing pattern)
Ultrasound (quality of muscle tissue)
Muscle biopsy (looking for dystrophin)
Genetic testing

Question 19

Duchenne’s and Becker’s MD treatment

Answer 19

Supportive 
physical therapy
speech therapy
Respiratory treatment
Dietary supervision
Surgery
Meds: corticosteroids to slow muscle degeneration

Question 20

Myotonic dystrophy

Answer 20

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

Question 21

Myotonic dystrophy SS

Answer 21

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

Question 22

Facioscapulohumeral MD

Answer 22

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

Question 23

Limb-girdle MD

Answer 23

Onset is early childhood to adulthood (3-20 years)
Initially effects the shoulders and hips (proximal limb distribution)
Moderate weakness
slow progression

Question 24

Congenital MD

Answer 24

not a shingle disorder but instead refers to muscular dystrophy evident at birth several rare forms of MD General muscle weakness Joint deformities

Question 25

Oculopharyngeal MD

Answer 25

Effects eyes and throat (initial sign is drooping eyelids) Onset- up to 40-60 years Slow progression

Question 26

Distal MD

Answer 26

Involves the muscles farthest away from the center of the body (hands, feet, forearms, lower legs) Slow progression Onset-40-60 years

Question 27

Emery-Dreifuss MD

Answer 27

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

Question 28

Inflammatory myopathies

Answer 28

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

Question 29

Inclusion Body Myositis

Answer 29

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

Question 30

Inclusion Body Myositis SS

Answer 30

``` first symptom falling or tripping may begin with weakness in the wrists and fingers difficult swallowing treatment supportive and symptomatic ```

Question 31

Polymyositis

Answer 31

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

Question 32

Polymyositis SS

Answer 32

``` 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 ```

Question 33

Poly Myositis Medical management

Answer 33

Diagnosis: blood test, biopsy, EMG Treatment: exercise, rest medication, speech therapy Prognosis: variable, remissions, relapse

Question 34

Dermatomyositis

Answer 34

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?

Question 35

Dermatomyositis SS

Answer 35

``` 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 ```

Question 36

Dermatomyositis

Answer 36

DX : MRI, presense of a rash, muscle testing, blood work Prognosis: good Treatment: medications, physical therapy, speech therapy

Question 37

Myasthenia gravis

Answer 37

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

Question 38

Myasthenia gravis Ethimology and pathogenesis

Answer 38

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

Question 39

Myasthenia gravis clinical manifestations

Answer 39

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

Question 40

Myasthenia gravis Diagnosis

Answer 40

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

Question 41

Myasthenia gravis treatment

Answer 41

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

Question 42

Necrotizing Fasciitis

Answer 42

Is a rare but very severe type of bacterial infection that can destroy the muscles, skin and underlying tissue, causes cell death

Question 43

Necrotizing fascilitis causes

Answer 43

Bacteria, most common Streptococcus pyogenes "flesh eating" | Enters body and releases harmful substances that kill tissue, interfere with blood flow and break down tissue

Question 44

Necrotizing fasciitis Symptons

Answer 44

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

Question 45

necrotizing fasciitis Dx and Tx

Answer 45

PE, blood tests, CT scan Treatment Broad-spectrum antibiotics Surgery

Question 46

Myofascial pain dysfunction

Answer 46

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

Question 47

Myofascial pain dysfunction etiology and risk factors

Answer 47

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

Question 48

Myofascial pain dysfunction clinical manifestation

Answer 48

``` Trigger points Reduced ROM Weakness Paresthesia Different sensation Diagnosis - palpation ```

Question 49

Myofascial pain dysfunction treatment

Answer 49

``` Injections of saline or anesthetic Ice/heat US/E stim/laser Manual pressure (ischemic) Vapocoolant spray Stretching/strengthening Supplement (vitamin B and C) ```