Transcript Review of Musculoskeletal System

Review of Skeletal
System
1
Skeletal System

Function:
– Protection
– Hematopoiesis
– Mineral homeostasis
 Calcium
 Phosphorus
 Carbonate
 Magnesium
2
Structure

Bone is a connective tissue:
– Matrix
 Collagen fibers for flexibility and
tensile strength
 Calcium for rigidity
 Hydroxyapatite Ca5(PO4)3OH
3

Cells:
– Osteoblast

Form organic components of matrix
– Osteocyte
– Osteoclasts
From monocytes
 Secrete citric and lactic acids
 Collagenases and other enzymes
 Stimulated by PTH
 Inhibited by Calcitonin

4
5
6
Types of Bone

Dense or Compact (85%)
– Osteon (Haversian System)
– Central (Haversian) canal
– Lamellae
– Lacunae with osteocytes
– Canaliculi

Spongy (cancellous) bone (15%)
– trabeculae
7
8
9
10
Periosteum


Outer layer is dense, irregular CT with
nerves and blood vessels
Inner layer
– Osteoblasts
– Anchored to bone by collagen fibers that
penetrate into bone
11
Joints

Degree of movement
– Synarthrosis – immovable joint
– Amphiarthrosis – slightly movable
joint
– Diarthrosis – freely movable joint
12

Synovial joints
– Joint capsule
 Fibrous CT
 Tendons and ligaments
 Nerves, blood and lymph vessels
– Synovial membrane
 Loose fibrous CT
 Many blood vessels – good repair
– Joint (synovial) Cavity
13
14


Synovial fluid
– Plasma filtrate
– Synovial cells and leukocytes
phagocytize debris and microbes
Articular cartilage
– Reduce friction
– Distribute force
15
Bone Pathophysiology

Inherited conditions:
– Osteogenesis imperfecta
 Inherited defect in collagen synthesis
 Osteopenia and brittle bones
 Often- defective tooth formation, blue
sclera, faulty hearing, other defects
 Inheritance can be dominant, recessive or
by new mutation
 Several degrees of severity ( I,II,III,IV)
 Biphosphate treatment can improve bone
mass in all types of the disorder
16
18

Achondroplasia
– Involves a defect in normal cartilage
development
– Epiphyseal plates close early in long bones;
individual has short arms and legs, but normal
spine and skull
– Dominant inheritance, but frequent new
mutations
– Other organs develop normally
– Individuals live a normal lifespan
19
Jyoti Amge, 15, just about 59.69
cm in height and 5.25 kg in weight,
is the world's smallest girl
recognized by the Indian Book of
Records.
Acquired disorders

Osteoporosis – “porous bone”
– Most common metabolic bone disease in North
America
– Can be attributed to genetics, diet or hormones
– Most osteoporosis is idiopathic osteoporosis
– Bone loss due to an identifiable cause is
secondary osteoporosis
– Bone tissue is mineralized normally, but over
time the structural integrity of bone is lost and
it becomes thinner and weaker, and more prone
to fractures.
23


Key features: bone fracture and the
associated pain.
WHO defines osteoporosis by bone
density:
– Normal bone > 833 mg/cm2
– Osteopenia 833 to 648 mg/cm2
– Osteoporosis < 648 mg/cm2


Can be generalized, involving major
portions of the axial skeleton
Can be regional, involving one segment of
the appendicular skeleton
24
25

Remodeling is constant
– Teen years more bone is laid down than
reabsorbed
– Peak bone mass or maximum density reached
at around 30 years of age
– After age 30, bone is reabsorbed faster than it
is laid down (loss of about 0.7% /year)
– In women, bone loss is most rapid in the first
years after menopause, but continues
throughout postmenopausal years
– Est. 55% of people over 50 have osteoporosis
or low bone mass.
27





Men also lose bone density, but start out
with more bone mass so takes longer.
By age 90 about 17% of males have had a
hip fracture, vs. 32 % of females
Vertebral fractures also occur → kyphosis
Most common in whites, but affects all
races.
African Americans have about half the
fracture rates of whites (higher peak bone
mass)
28
29
30
Risk factors









Family history
White race
Increased age
Female sex
Small stature
Fair or pale skin
Thin build
Early menopause (natural or surgical)
Late menarche
31
Risk factors cont.










Nulliparity
Obesity
Weight below a healthy range
Acidosis
Low dietary calcium and vitamin D
High caffeine intake
Sedentary life style
Smoker
Excessive alcohol consumption
Liver, kidney disease, rheumatoid arthritis, etc.
32




Often progresses silently for decades until
fracture occurs
Bones can fracture spontaneously
Most severe in spine, wrist and hips
Estrogens and androgens may be factors
in both sexes
– Testosterone is converted into estrogen in
peripheral tissues and decreases bone loss


Rapid bone loss is osteoclast mediated
Slow bone loss is osteoblast mediated
33
Clinical manifestations





Pain and bone deformity
Kyphosis caused by vertebral collapse
Fractures of long bones
Fatal complications include fat or
pulmonary embolism, pneumonia,
hemorrhage and shock
20 % die as a result of surgical
complications
34
Treatment








No known cure
Slow bone loss and promote bone
deposition
Calcium and vitamin D supplements
Nasal or subcutaneous calcitonin
Hormone replacement therapy
Biophosphates – inhibit osteoclasts
Dual x-ray absorptiometry for diagnosis
PREVENTION
35
Prevention






Intake of calcium, vitamin D, magnesium
and possibly boron
Regular, weight-bearing exercise
Avoid tobacco and glucocorticoids
No alcoholism
Hormone replacement?
Testosterone for men and possibly women
36
Rickets and Osteomalacia


Inadequate mineral deposition in
essentially normal organic matrix
Softened bone:
– Subject to malformation and distortion –pain
37
Rickets


Dietary vitamin D deficiency causes
inadequate mineralization of the
developing skeleton in infants and children
Rarely seen in Western nations
– Poverty
– Ignorance



Bones are soft and easily deformed
Tendency to fractures
Therapy: supply vitamin D and calcium
38
39
40
Osteomalacia




Rarely due to vitamin D deficiency
Usually GI malabsorption, renal defect or
chronic kidney or liver diseases.
Elderly often affected due to inadequate
diet or lack of outdoor activity
May accompany and complicate
osteoporosis.
42
Joint Disorders

Osteoarthritis
– Most common joint disease in North America
– Minimal inflammatory component
– Differentiated from inflammatory disease by:
Absence of synovial membrane inflammation
 Lack of systemic signs and symptoms
 Normal synovial fluid

– Much of the pain and loss of mobility associated
with aging.
44
Osteoarthritis







Incidence increases with age: 85% of people age
65 have some joint degeneration
Incidence similar, but women more severely
affected
Exceptional stress on joints: gymnasts, etc.
Biochemical defect in cartilage
Malformed joint, obesity and postural defects
Genetic component
Torn ACL or meniscectomy
45
Osteoarthritis



When associated with known risk factors it
is secondary Osteoarthritis
No risk factors – idiopathic Osteoarthritis
Pathological characteristics:
– Erosion of the articular cartilage
– Sclerosis of subchondral bone
– Formation of bone spurs or osteophytes
46
Osteoarthritis

Begins in articular cartilage
– Yellow-grey or brownish gray
– Thin, irregular, frayed
– Cracks or fissures develop (fibrillation)
– Fluid filled cysts may form
– Microfractures of subchondral bone
– Formation of fibrocartilage repair plugs
– Bone surface exposed
– Bone responds by becoming dense and hard
48
Osteoarthritis

Synovial membrane is indirectly affected
– Fragments of fibrocartilage cause
inflammation –pain
– Fibrous repair of joint capsule restricts motion
– Osteophytes form – pain and loss of motion
49
Osteoarthritis




Affects one or more weight-bearing joints
– Hand, wrist, lower cervical spine, lumbar spine
and sacroiliac, hip, knees, ankles, feet
Aches and stiffness
– Symptoms increase with activity; diminish with
rest
Usually no swelling or redness of adjacent tissues
Sometimes nocturnal pain – may be referred
50
Osteoarthritis
Primary signs and symptoms of joint disease
are:
pain, stiffness, enlargement or swelling,
tenderness, limited range of motion,
muscle wasting, partial dislocation, and
deformity, crepitus (cracking sound)
51
Osteoarthritis




Evaluation made through clinical
assessment and radiologic studies, CT
scan, arthroscopy and MRI
Treatment:
Glucosamine may decrease pain and slow
or stop progression – 1500 mg/day
Chondroitin sulfate – questionable
absorption
52
Osteoarthritis






Analgesics and antiinflammatory drugs (NSAIDs)
Injections of corticosteroids or sodium
hyaluronate (to improve lubrication)
Range of motion exercises
Reduce aggravating factors
– Weight loss
– Use of cane, crutches or walker
Surgical removal of bone spurs, and other
Replacement of joint
53
Rheumatoid Arthritis


Systemic disease with prominent
involvement of the joints
Inflammatory joint disease characterized
by:
– Inflammatory damage in the synovial
membrane or articular cartilage
– Systemic signs of inflammation: fever,
leukocytosis, malaise, anorexia,
hyperfibrinogenemia
54
Rheumatoid Arthritis





Systemic autoimmune disease that causes
chronic inflammation of connective tissue
Initially affects synovial membrane
Later articular cartilage, joint capsule,
ligaments and tendons, and bone
Affects small joints more like hands, wrists,
ankles, and feet, but shoulders, hips and
cervical spine may also be involved
Systemic effects on heart, kidney, lungs, skin
and other organs
55
Rheumatoid Arthritis









Mild to severe
Destroys and distorts joints
Reduces life expectancy
Remission and exacerbation
1 – 2% of adult population
Women : men = 3:1
Onset usually in 20’s or 30’s
Symptoms lessen during pregnancy
Seasonal variation
56
Rheumatoid Arthritis





Idiopathic disease
Immune-mediated destruction of joints
Rheumatoid factors (IgM and IgG) target
blood cells and synovial membranes
forming antigen-antibody complexes
Genetic predisposition
Possibly bacterial or viral infection
(Epstein-Barr)
57
Rheumatoid Arthritis







Chronic inflammation of synovial membrane
Cellular proliferation and damage to the
microcirculation
Synovial membrane becomes irregular
Swelling, stiffness and pain
Cartilage and bone destruction
Ankylosis or fusing of joint
Ligaments and tendons also affected
58
Rheumatoid Arthritis

Systemic effects:
– Generalized weakness and malaise
– Up to 35% develop granulomas called
rheumatoid nodules
– Systemic inflammation of blood vessels –
rheumatoid vasculitis
– Serous membranes may be affected
59
60
Rheumatoid Arthritis

Evaluation :
– history
– Physical examination
– X-ray
– Serologic tests for rheumatoid factor and
circulating antigen-antibody complexes, esp.
antibodies against cyclic citrullinated peptide
(CCP)

No cure
61
Rheumatoid Arthritis







Therapy:
Physical and emotional rest
Relieve pain and swelling and retain as
much joint function as possible
Resting the joint, or binding or splinting
Use of hot and cold packs
Diet high in calories and vitamins
Strengthening of associated muscles
62
Rheumatoid Arthritis

Drug therapy:
– NSAIDS
– Methotrexate
– Antimalarial drugs and immunosuppression

Surgical
– Synovectomy
– Correction of deformities
– Joint replacement
– Joint fusion
63
Review of Muscular
System
64
Muscle

Skeletal muscle
– > 600 muscles in body


Cardiac muscle
Smooth muscle
65
Muscle cell structure



Sarcolemma
motor end plate
transverse ( t- ) tubules
Sarcoplasm
Sarcoplasmic Reticulum – Stores Ca++
66
67
68

Proteins:
– Thick filaments – myosin
– Thin filaments – actin
 Troponin
 Tropomyosin
– Sliding Filament Model
69
70
71
72
73
Muscular Dystrophy






Group of rare diseases characterized by a
genetic etiology and progressive
degeneration of skeletal muscle.
X-linked recessive defect
Most common of the muscular dystrophies
1 in 3,500 live male births
Affects males
Gene located on the short arm of the X
chromosome.
74







30% of cases arise as a new mutation
Can be diagnosed immediately after birth
by high serum creatine kinase
Muscle weakness and delayed motor skills
can be detected early – obvious by age 5
Age 10 – require leg bracing
Age 12 – wheelchair
Age 15 completely bedridden
Death by 20 – 30 of cardiac arrest or
respiratory failure.
75

Fibrosis → contracture distorts skeletal
development
– Lordosis
– Scoliosis
– Compromised respiration

Respiratory insufficiency
– Respiratory infection

Cardiac muscle
– Dysrythmias
– Congestive heart failure

Mental sluggishness
76

Therapy
– Passive stretching, splints to prevent
deformities
– Sustain mobility
– Sustain respiratory function
– Possibly gene therapy
77
Myesthenia gravis




Autoimmune disease in which antibodies
(IgG) bind with acetylcholine receptors on
muscle cells. (T-lyphmocyte abnormalities)
Reduces the number of acetylcholine
receptors at the neuromuscular junction
Characterized by progressive muscle
weakness and fatigability
Also associated with other autoimmune
disorders, such as SLE, rheumatoid
arthritis, and thyrotoxicosis
78


In 10-25% of people with MG thymic
tumors are found
– More common in males than females
70 – 80 % have pathologic changes in the
thymus
79
Classification of myasthenia

Neonatal myasthenia
– Transitory condition in which 10-15 % of
infants born to mothers with MG show
symptoms of the disease



Congenital myasthenia
Juvenile myasthenia – onset about 10
years
Ocular myasthenia
– More common in males
– Weakness of eye muscles and eyelids, may
also include swallowing difficulties and slurred
speech
80

Generalized autoimmune myasthenia
– Involves proximal musculature throughout the
body, and has several courses:
 A course with periodic remissions
 Slowly progressive course
 Rapidly progressive course
 Fulminating course
81
Pathophysiology






Defect in the nerve impulse transmission at the
NMJ
Postsynaptic acetylcholine receptors are no longer
recognized as “self” and antibodies are produced
against them.
IgG blocks the binding of ACh
Eventually destroys the receptor
Causes diminished transmission of nerve impulse
across the NMJ and lack of muscle depolarization
Cause is unknown.
82
Clinical manifestations



Onset typically insidious
May first appear during pregnancy,
postpartum or with the administration of
certain anesthetic agents
Complaints are fatigue and progressive
muscle weakness
– Fatigue after exercise
– Recent history of recurrent upper respiratory
infections
83
Clinical manifestations

Muscles of the eyes, face, mouth, throat
and neck are usually affected first
– Levator and extraocular muscles affected most
-Diplopia, ptosis, and ocular palsies
– Muscles of facial expression, mastication,
swallowing and speech are the next most
involved
Facial droop, expressionless face; difficulties in
chewing and swallowing, drooling, episodes of
choking and aspiration
 Nasal, low volume, high-pitched monotonous speech
pattern

84

Less frequently involved are the muscles
of the neck, shoulder girdle and hip
flexors
– Fatigue requires periods of rest
– Weakness of arms and legs
– Difficulty maintaining head position
– Respiratory muscles of chest wall and
diaphragm become weak

In advanced stage all muscles are weak
85
Myasthenic crisis

Severe weakness causes quadriparesis or
quadriplegia, respiratory insufficiency and
extreme difficulty in swallowing
86
Cholinergic crisis







Anticholinesterase drug toxicity
Intestinal motility increases
Fasciculation
Bradycardia
Pupillary constriction
Increased salivation
Increased sweating
87
Evaluation





Improvement with edrophonium chloride
(Telison) for several minutes
EMG – amplitude of action potentials
declines
Antiacetylcholine receptor antibody titers
Antistriated muscle antibody titers
MRI to rule out thymoma
88
Progression




Varies
Appears first as a mild case that
spontaneously remits with a series of
relapses and symptom free intervals
Over time can progress leading to death
Ocular myasthenia has a good prognosis
89
Treatment






Anticholinesterase drugs
Steroids
Immunosuppressant drugs
Cyclophosphamide
Plasmapheresis during myasthenic crisis
Thymectomy is treatment of choice for
individuals with thymoma
90