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Orthopedic Pathology > Orthopedic Pathology 4 Muscle pathologies > Flashcards

Orthopedic Pathology 4 Muscle pathologies Flashcards

0
Q

Lacerations

A

Is a break or opening in the skin

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1
Q

Reaction of Sckeletal muscles

A

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

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2
Q

Scar

A

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

Scares are weaker than the tissue it replaces

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3
Q

Scar causes

A

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

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4
Q

Scar types

A 
Contracture
Adhesion
Scar tissue adhesion
Fibrotic adhesion
Irreversible contracture
Proud flesh
Hypertrophic scarring
Keloid
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5
Q

Contracture type of scar

A

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

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6
Q

Adhesion type of scar

A

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

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7
Q

scar tissue adhesion

A

Occurs with an injury or an acute inflammatory process

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

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8
Q

Fibrotic adhesions

A

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

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9
Q

Irreversible contracture

A

Occurs when fibrotic tissue or bone replaces muscle and CT

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

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10
Q

Proud flesh

A

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

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11
Q

Hypertrophic scarring

A

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

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12
Q

Keloid

A

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

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13
Q

Myscular dystrophies

A

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
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14
Q

Duchenn’s MD

A

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.

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15
Q

Duchenne’s MD SS

A 
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
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16
Q

Beckers MD

A

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

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17
Q

Etiology of Duchenne’s and Becker’s MD

A

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

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18
Q

Diagnosis of Duchenne’s and Becker’s MD

A 
History 
Exam
Blood text (muscle enzymes - creatine kinase)
EMG (muscle firing pattern)
Ultrasound (quality of muscle tissue)
Muscle biopsy (looking for dystrophin)
Genetic testing
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19
Q

Duchenne’s and Becker’s MD treatment

A 
Supportive 
physical therapy
speech therapy
Respiratory treatment
Dietary supervision
Surgery
Meds: corticosteroids to slow muscle degeneration
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20
Q

Myotonic dystrophy

A 
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
21
Q

Myotonic dystrophy SS

A

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

22
Q

Facioscapulohumeral MD

A

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

23
Q

Limb-girdle MD

A

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

24
Q

Congenital MD

A

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

25
Q

Oculopharyngeal MD

A

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

26
Q

Distal MD

A

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

27
Q

Emery-Dreifuss MD

A

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

28
Q

Inflammatory myopathies

A

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

29
Q

Inclusion Body Myositis

A

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

30
Q

Inclusion Body Myositis SS

A 
first symptom
falling or tripping
may begin with weakness in the wrists and fingers
difficult swallowing
treatment supportive and symptomatic
31
Q

Polymyositis

A

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

32
Q

Polymyositis SS

A 
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
33
Q

Poly Myositis Medical management

A

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

34
Q

Dermatomyositis

A

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?

35
Q

Dermatomyositis SS

A 
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
36
Q

Dermatomyositis

A

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

37
Q

Myasthenia gravis

A

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

38
Q

Myasthenia gravis Ethimology and pathogenesis

A

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

39
Q

Myasthenia gravis clinical manifestations

A

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

40
Q

Myasthenia gravis Diagnosis

A

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

41
Q

Myasthenia gravis treatment

A

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

42
Q

Necrotizing Fasciitis

A

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

43
Q

Necrotizing fascilitis causes

A

Bacteria, most common Streptococcus pyogenes “flesh eating”

Enters body and releases harmful substances that kill tissue, interfere with blood flow and break down tissue

44
Q

Necrotizing fasciitis Symptons

A

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
45
Q

necrotizing fasciitis Dx and Tx

A

PE, blood tests, CT scan

Treatment
Broad-spectrum antibiotics
Surgery

46
Q

Myofascial pain dysfunction

A

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

47
Q

Myofascial pain dysfunction etiology and risk factors

A

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

48
Q

Myofascial pain dysfunction clinical manifestation

A 
Trigger points
Reduced ROM
Weakness
Paresthesia
Different sensation
Diagnosis - palpation
49
Q

Myofascial pain dysfunction treatment

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

Orthopedic Pathology (6 decks)

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