Disorders of the Musculoskeletal System BONE CELLS 1.
Osteoblasts a. Major bone-forming cell b. Becomes osteocytes
Osteoclasts c. Cells which break down bone Osteocytes a. Trapped
osteoblasts; maintain the bone matrix Osteoclasts a. Cells which
break down bone b. Macrophage lineage Osteogenic cells a.
Undifferentiated cells that turn into osteoblasts b. Active during
normal growth c. Activated in adult with healing of
fractures/injuries
2. 3.
4.
Osteoblasts Responsible for shape and structure of the bone o
Secrete collagen o Produce osteocalcin & synthesize osteoid o
Cause calcium salts & phosphorus from blood to precipitate to
bone matrix (mineralization of bone) o Signal osteoclast activity
(through RANKL) Respond to parathyroid hormone Secrete Type I
collagen for mineralization of bone Alkaline phosphatase is
contained in osteoblasts & secreted during osteoblastic
activity Osteoblasts also have estrogen receptors o Estrogens can
increase osteoblastic activity & collagen & bone matrix
production Osteocytes Transformed osteoblast that are surrounded in
osteoid as it hardens from deposited minerals Synthesize matrix
molecules for bone calcification Osteocytes maintain bones o Play a
role in controlling extracellular concentration of calcium &
phosphate o Directly stimulated by calcitonin & inhibited by
Parathyroid hormone (PTH) Osteoclasts Secrete bone-reabsorbing
enzymes, which digest bone matrix o Phagocytic! Like macrophages o
Contain lysosomes filled with hydrolytic enzymes Calcitonin signals
osteoclast to dis-engage o Sparing loss of calcium from bone
Osteoclasts also have estrogen receptors o Estrogens can inhibit
their recruitment & decreases osteoclastic activity
BONE MATRIX 1. 2. 3. Collagen fibers a. Make up bulk of bone
matrix Proteoglycans a. Strengthen bone and assist bone calcium
deposition Glycoproteins a. Sialoprotein, osteocalcin, bone
albumin, alpha-glycoprotein b. Control collagen interactions that
lead to fibril formation Bone mineralization a. Calcium and
phosphate
4.
BONE TISSUE Compact (cortical) bone o 85% of the skeleton o
Haversian system Haversian canal, lamellae, lacunae, osteocyte, and
canaliculi Spongy (cancellous) bone o Lack haversian systems o
Trabeculae Periosteum
LONG BONES 1. 2. 3. 4. 5. Diaphysis Metaphysis Epiphysis a.
Epiphyseal plate Medullary cavity Endosteum
BONE RESORPTION CYCLE Human body is constantly removing old bone
& replacing it with new bone o Called "bone turnover To perform
bone turnover, your bone needs o Minerals (calcium and phosphorus)
o Bone protein matrix o Osteoclasts o Osteoblasts
REGULATION OF BONE RESORPTION 1. Parathyroid Hormone (PTH) a.
Increase recruitment & activity of osteoblasts and osteoclasts
b. Promotes release of calcium from bone c. If PTH secretion is too
high, there is an acceleration of the bone turnover Calcitonin a.
Secreted by Para-follicular cells of thyroid gland. b. Inhibits
release of calcium from bone
2.
*PTH & Calcitonin have opposite effects on Calcium levels 3.
Vitamin D a. Vitamin D tends to increase recruitment of osteoclasts
b. Plays a part in mineralization of bone matrix. c. Lack of
Vitamin D results in osteomalacia (impaired mineralization) d. Too
much Vitamin D entails bone loss Estrogen a. Increases osteoblast
activity/decreases osteoclast activity
4.
COMPACT VS CANCELLOUS BONE Compact Bone o More dense o Exterior
portion of bone Cancellous Tissue o Spongy tissue o Interior
portion of bone, more vascular
Which heals faster? Cancellous Tissue LIGAMENTS & TENDONS
Tendons o Muscle to bone Ligaments o Bone to bone
STRAINS Tearing or overstretching of muscle or tendons
Overstretching or tears of ligament structures DISLOCATIONS-look at
picture ROTATOR CUFF INJURIES Rotator cuff made up of 4 muscles
& their tendons These combine to form a "cuff" over head of
humerus Rotator cuff helps to lift & rotate arm & stabilize
ball of shoulder within joint
FRACTURES Break in continuity of bone Pathologic o Break at site
of preexisting abnormality Usually osteoporosis, cancer, Pagets
disease, infection, metabolic bone disorders Injurious/trauma-
trauma to bone Stress fractures (repeated strain) o Fatigue-
abnormal stress or torque applied to bone with normal ability to
deform & recover New activities: jogging, dancing, skating o
Insufficiency or fragility- bones without normal ability to deform
& recover from normal weight-bearing activity By force that
wouldnt normally produce fracture Arthritis, rickets, Pagets
disease
1.
Linear a. Runs parallel to axis of bone 2. Oblique a. Occurs at
oblique angle to shaft of bone 3. Spiral a. Encircles bone b.
Twisting injury c. Torque injury d. Unstable and may move after
reduction 4. Transverse (closed) a. Straight across bone b. Usually
simple to reduce 5. Comminuted a. Bone broken into >2 pieces b.
Probably needs surgery 6. Greenstick a. Torus or buckle fracture b.
Cortex buckles but does not break c. Typically in children d.
Incomplete fracture e. May be parallel to bone 7. Bowing a.
Longitudinal force applied to bone b. Common in children c.
Involves tibia/fibula or radius/ulna i. One bone in pair breaks and
forces bows other bone 8. Open Fracture a. Open to environment b.
Increased risk for infection c. Increased bleeding 9. Compression
a. Usually in vertebrae b. Can be due to osteoporosis 10. Impacted
a. Fragments wedged together
HEALING OF FRACTURES Direct or primary healing o Similar to
intramembraneous bone formation when adjacent bones cortices
contact one another o Most often with surgical fixation o No callus
formation Indirect or secondary healing o Similar to endochondral
bone formation o Involves formation of callus & remodeling of
solid bone 1. 2. Inflammatory phase a. Hematoma formation
Reparative Phase a. Cell proliferation/callus formation b.
Ossification Remodeling
3.
Inflammatory Phase: HEMATOMA FORMATION 48 - 72 hours
(Inflammatory Phase) o Torn vessels in bone & soft tissues
forms hematoma o Fibroblast arrives at the site of injury Initiates
healing process Fibrin meshwork forms Granulation tissue begins to
form Reparative Phase: CELL PROLIFERATION & CALLUS FORMATION nd
th 2 - 6 week of healing (Reparative Phase) o Osteoblast &
chondrobalst differentiate (periosteum) o Proteins produced by
osteoblasts & chondroblasts begin to consolidate into what is
known as cartilogenous soft callus o Ossification Begins Bone
begins to calcify Mature bone replaces soft callus (Bony Callus)
Fracture completely bridged, ends firmly united May remove cast at
this point Remodeling Phase Resorption of excess bony callus by
osteoclasts Directed by weight bearing Occurs after healing process
HEALING TIMES 1. 2. 3. Children a. 4-6 weeks Adolescents a. 6-8
weeks Adults a. 10-18 weeks
FACTORS INFLUENCING BONE HEALING Systemic Factors o Age o
Nutrition o Systemic Disease o Hormones Local Factors o Type of
bone o Degree of trauma o Vascular injury o Degree of
immobilization o Intraarticular fractures o Separation of bone ends
o Infection/ local pathology
COMPLICATIONS OF FRACTURES 1. 2. Infection Osteomyelitis a.
Usually caused by Staphylococcus Aureus b. May be due to: Direct
contamination (surgical or injury) Hematogenic source Chronic Acute
infection recurs Compartment Syndrome a. Increased pressure in
limited anatomic space b. Compromises circulation Result from
increase pressure in the tissue compartment Compromises circulation
Nerve impingement c. The 5 Ps: Pain Pallor Paresthesias Pulses
Paralysis d. May require fasciotomy Osteonecrosis a. Death of a
segment of bone b. Not uncommon (r/t ischemia) c.
Thrombosis/emboli, vascular compression, vessel injury d.
Causes/Risk factors: Long term treatments with steroids Excessive
alcohol use Sickle cell disease, radiation therapy, DM, gout,
atherosclerosis Dislocation or fractures around a joint
3.
4.
5.
Fat Emboli Syndrome a. Usually after fracture of long bones or
pelvis Fat released by bone marrow or adipose tissue at fracture
site Results in fat emboli in lungs (PE) b. Manifestations:
Tachypnea Dyspnea Use of accessory muscles Wheezing Inspiratory
stridor Petechial rash-neck, upper chest, shoulder, axillary and
buccal membranes HA Drowsiness Irritability Memory loss Confusion
Rapid pulse Apprehension Fever
BENIGN NEOPLASMS OF THE BONE 1. 2. 3. 4. Osteoma a. small bony
tumor on surface of long bone Chondroma a. Hyaline cartilage tumor
(hands or feet) Osteochondroma a. Most common, grows only during
skeletal growth, made of bone & cartilage Giant cell
tumor/osteoclastoma a. Aggressive/metastatic; knee/wrist/shoulder
metaphyseal regions
METASTATIC NEOPLASMS 1. Osteosarcoma- children & elderly a.
Most common malignant bone-forming tumor b. Formation of immature
bone by malignant osteoblasts; aggressive & undifferentiated
Ewings Sarcoma- common bone tumor in childhood a. Young males,
highly malignant; immature bone marrow cells become malignant (does
not make bone) b. Femur, pelvis, humerus; metastasizes fast
Chondrosarcoma- middle-aged & older adults (men) a. Common
primary malignant tumor of cartilage
2.
3.
CARPAL TUNNEL SYNDROME swelling in compartment in wrist that
contains wrist & finger muscles, nerves, & blood supply
Swelling puts pressure on nerve that travels in this compartment or
"tunnel Pressure on median nerve causes numbness, weakness, &
pain in wrist & hand
METABOLIC BONE DISEASES Osteopenia (fewer bone cells) Condition
in all metabolic bone diseases Osteomalacia (adults)/Rickets
(children) Inadequate & delayed mineralization in bone
Softening of bones Vitamin D, Calcium or Phosphorus deficiency
Paget Disease Excess osteoclast activity Excessive & abnormal
bone remodeling Repaired bone becomes vascular fibrous tissue
Osteoporosis Loss of bone mass/matrix Increased risk of fractures
> Caucasian > Darker skinned individuals Increased bone
resorption relative to bone formation 1.5 million fractures per
year r/t osteoporosis S/Sx pain & bone deformity (kyphosis),
height Post-menopausal higher risk WHY? o Estrogen deficiency &
other age-related causes o Glucocortocoids Pathogenesis &
Severity of Osteoporosis o Loss of cancellous or trabecular bone
(spongy) & compact bone can become more porous o Increased bone
resorption relative to bone formation o Osteoclast precursors are
stimulated by cytokines o Cytokines are held at bay by estrogen o
Decrease in estrogen increases osteoclast production &
stimulates cytokine activity (IL, TNF, TGF-, prostagladin, RANKL) o
Severity r/t peak bone mass correlated with skin pigment, exercise,
good nutrition Adequate Vitamin D & Calcium intake
OPG/RANKL/RANK System Risk Factors of Osteoporosis o Female o
Advanced Age o Small bone structure o Low body weight o
Postmenopausal o Genetic predisposition o Sedentary lifestyle o
Skin pigment - Caucasian > Darker skinned o Nutrition Calcium
& Vit D deficiency
JOINTS Joint classifications based on structure Fibrous Joins
bone to bone o Suture, syndesmosis, gomphosis Cartilaginous
Symphysis & synchondrosis Synovial Uniaxial, biaxial, or
multiaxial Joint capsule, synovial membrane, joint cavity, synovial
fluid, articular cartilage
OSTEOARTHRITIS- Degenerative Joint Disease Common disorder of
synovial joints o Disease of use & abuse increases with age
Loss & damage of articular cartilage, osteophytosis,
subchondral bone changes, mild synovitis, & thickening of joint
capsule Secondary to injury/inflammation, cytokine release o Exact
etiology unknown- involves genetic alterations & metabolic
disorders Proteases produced potentially destructive to joint
tissues with loss of proteoglycans Articular cartilage broken down
& lost with narrowing of joint space & possible bone spurs
o Bone rubs against bone which causes further damage (erosion) Risk
Factors of Osteoarthritis o Genetic predisposition o Obesity o
Athletes o Aged o > 3:2
ANKYLOSING SPONDYLITIS Chronic autoimmune inflammatory
arthropathy Rheumatic disease causing stiffening & fusion of
spine & sacroiliac joints o Can cause inflammation of eyes,
lungs, & heart valves Excessive bone formation at enthesis o
Fibrosis, ossification, & joint fusion Genetic marker- HLA-B27
misfolds
RHEUMATOID ARTHRITIS Proliferative synovitis r/t chronic
systemic autoimmune inflammatory disease Joint swelling ,
tenderness, destruction of synovial joint spreading to articular
cartilage, fibrous joint capsule, & surrounding ligaments &
tendons o Leads to disability & premature death > 3:1
Genetic predisposition but exact etiology unknown Affects ~1% of
population; increases with age RF (rheumatoid factor) present in
80% of RA patients; ACPA more sensitive o RF + IgG = inflammatory
response o Autoantibody which reacts with IgG
RA Pathogenesis o T-cell mediated response T cells express RANKL
promoting osteoclast formation & boney erosion o Cartilage
damage due to Activated neutrophils & other cells in synovial
fluid degrade surface of articular cartilage Inflammatory cytokines
induce enzymatic breakdown cartilage & bone T cells interact
with synovial fibroblasts converting synovium into pannus
Destruction of articular cartilage & bone erosion Pannus limits
movement of joint Swan neck deformity Boutonnires thumb Ulnar
deviation Evaluation o Four or more of the following: Morning joint
stiffness lasting at least 1 hour Arthritis of three or more joint
areas Arthritis of hand joints Symmetric arthritis Rheumatoid
nodules Abnormal amounts of serum rheumatoid factor Radiographic
changes
GOUT Syndrome caused by incomplete purine metabolism Uric acid
is end product of purine synthesis Increased uric acid
(hyperurecemia) o Overproduction of purines o Decreased salvage of
free purines o Increased cell turnover (augmented breakdown of
purines)- excessive production of uric acid o Decreased urinary
secretion of uric acid (90% cases) Overload of uric acid in the
body Uric acid is end product of purine synthesis Increased uric
acid: o Overproduction of purines o Increased cell turnover
(augmented breakdown of purines) o Decreased urinary secretion of
uric acid Uric acid crystallizes & deposits in connective
tissues o Form tophi- small white nodules Crystallization in
synovial fluid causes acute, painful inflammation or gouty
arthritis o Synovial fluid poor solvent for uric acid Precipitate
in joints especially great toe (podagra) causing joint damage &
pain Uric acid crystals tend to precipitate at lower temperatures
Trauma promotes precipitation
FIBROMYLAGIA Widespread musculoskeletal pain or aches
accompanied by fatigue, sleep, memory & mood issues (depression
& anxiety) Believe fibromyalgia amplifies painful sensations by
affecting way brain processes pain signals Symptoms begin after
physical trauma, surgery, infection or significant psychological
stress, or with no precipitating event Affects women more than men
& runs in families May also have headaches, TMJ, IBS, SLE No
cure but may be able to control symptoms o Medications, exercise,
relaxation, stress-reduction NEUROLOGICAL DISORDERS FUNCTIONS OF
THE NERVOUS SYSTEM Communication & coordination o Sensory input
Gathering information To monitor changes occurring inside &
outside the body (changes = stimuli) o Integration Process &
interpret sensory input & decide if action is needed o Motor
output Response to integrated stimuli Response activates muscles or
glands
STRUCTURAL CLASSIFICATION OF NERVOUS SYSTEM Central Nervous
System (CNS) o Brain & spinal cord o Protected by skull &
vertebrae Peripheral Nervous System o Nerves outside brain &
spinal cord o Input-output system for relaying information to CNS
Cells:neurons & supporting cells
NERVOUS TISSUE: NEURONS Nerve cells o Specialized cells that
transmit messages o Major regions of neurons Cell body nucleus
& metabolic center of cell Processes fibers that extend from
cell body Dendrites - carry impulses towards cell Axon - carry
impulses away from cell Neurons Most found in CNS o Gray matter
cell bodies & unmylenated fibers o Nuclei clusters of cell
bodies within white matter of CNS Ganglia collections of cell
bodies outside CNS Sensory (afferent) neurons o Carry impulses from
sensory receptors Motor (efferent) neurons o Carry impulses from
CNS
FUNCTIONAL CLASSIFICATION OF NEURONS Interneurons (association
neurons) o Found in neural pathways in CNS o Connect sensory &
motor neurons
HOW NEURONS FUNCTION Irritability ability to respond to stimuli
Conductivity ability to transmit an impulse Plasma membrane is
polarized at rest Depolarization a stimulus depolarizes neurons
membrane & initiates action potential o Deploarized membrane
allows sodium (Na+) to flow inside membrane o Potassium ions rush
out of neuron after Na ions rush in, which repolarizes membrane
Sodium-potassium pump restores original configuration
AXON & NERVE IMPULSES Action potential end in axonal
terminals Axonal terminals contain vesicles with neurotransmitters
Axonal terminals are separated from the next neuron by a gap o
Synaptic cleft gap between adjacent neurons Neurotransmitter
Post-synaptic receptors SYNAPTIC TRANSMISSION Neurotransmitters o
CNS o PNS Serotonin Dopamine Norepinephrine Epinephrine
Acetylcholine GABA Glutamate Glycine
NERVE TISSUE: Support Cells (Neuroglia or Glia) Astroglia o
Links neurons & blood vessels & forms barrier between
capillaries & neurons o Maintains Blood Brain Barrier o
Controls chemical environment of brain (CNS) Oligodendroglia o
Forms myelin in the CNS Microglia o Phagocytic cells Ependymal
cells o Lining of neural tube
PNS SUPPORTING CELLS Satellite Cells o Layer of cells separating
ganglia from other tissues o Satellite cells secrete a basement
membrane that protects cell body from diffusion of large molecules
Schwann Cells o Wraps around axon to form myelin sheath like a
jelly roll o Nodes of Ranvier Gaps in myelin sheath along axon
Increases saltatory conduction NEUROGLIA VS NEURONS Neuroglia
divide Most brain tumors are gliomas & involve neuroglia cells,
not neurons o Consider role of cell division in cancer! Support
neurons Maintain Blood-Brain Barrier Produce myelin sheath
(NEURONS) Neurons do not divide Afferent sensory Efferent motor
Sent signals/impulses via: o Presynaptic neuron o Release
neurotransmitter o Postsynaptic receptors Blood Brain Barrier
protect neurons Myelin sheath important for speed of transmission
DISORDERS OF BRAIN FUNCTION MECHANISMS OF BRAIN INJURY Brain
protected from external forces by: o Skull o Meninges o
Cerebrospinal fluid (CSF) Autoregulation Metabolic stability
required by its electrically active cells maintained by: o
Blood-brain barrier o Mechanisms that ensure its blood supply
Primary Injury o Global cerebral ischemia occurs commonly in
patients who have a variety of clinical conditions: Brain injury
Cerebrovascular Accident (CVA) or Stroke Ischemic Hemorrhagic
Seizures Indirect hypoxic: Cardiac arrest Shock Asphyxia
Pathways of Secondary Injury: o Glutamate efflux into
extracellular compartment Results in increases in intracellular
Calcium o Inflammation influx of cytoxins & edema Mechanisms of
Brain Injury Pathways of Secondary Injury o Role of Inflammation
Cerebral ischemia leads to inflammation Migration of peripheral
leukocytes into brain & activation of microglia Release of
cytokines (interleukin [IL]-1, tumor necrosis factor a [TNF-a])
Breakdown of the blood-brain barrier (BBB) Culminates in edema
formation Pathways of Injury: o Cerebral Edema Vasogenic Edema
Integrity of blood-brain barrier disrupted allowing fluid to escape
into interstitial spaces that surrounds brain cells Cytotoxic Edema
Swelling of brain cells due to an increase in fluid in the
intracellular space Results in increase in intracranial
pressure
INCREASED ICP Prolonged pressure >15mmHg Common pathway or
end-point of brain injury Normal 5 to 15 mm Hg Caused by increase
in intracranial content o Brain tissue o Blood o CSF Brain tissue
volume o Cerebral edema o Brain tumor CSF o Hydrocephalus Blood
volume increase / vasodilation in the brain o Acidosis o
Hypercapnia o Cerebral bleeding
HYDROCEPHALUS Enlargement of CSF compartment with increase in
CSF in cerebral ventricles, subarachnoid space, or both Congenital-
ventricular enlargement before birth Noncommunicating within
ventricular system (obstructive) o More common in children
Communicating o Defective reabsorption of CSF from subarachnoid
space More common in adults Acute after head injury Causes IICP
MONRO-KELLIE HYPOTHESIS Any increase in one requires
compensatory decrease in another CSF is the first to compensate Can
be displaced from the ventricles into spinal subarachnoid space Can
undergo increased absorption or decreased production Blood volume
diminishes Contained in low-pressure venous system as a means of
displacing blood volume Can lead to decreased cerebral perfusion
MANIFESTATIONS OF ICP- Look at powerpoint CUSHINGS TRIAD Occurs as
a result of Cushing reflex When Mean Arterial Pressure is less than
ICP Hypothalamus increases sympathetic stimulation
Vasoconstriction, increased contractility & cardiac output
Increased BP: detected by baroreceptors in carotid arteries
Triggers parasympathetic & induces bradycardia Bradypnea Result
of increased pressure on brainstem due to swelling, or from
brainstem herniation
COMPLICATIONS OF INCREASED ICP Herniation- displacement of brain
tissue
TRAUMATIC BRAIN INJURY A traumatic insult to brain possibly
producing physical, intellectual, emotional, social, &
vocational changes Causes: Transportation accidents Falls
Sports-related event Violence
CATEGORIES OF TBI Open (penetrating, missile) trauma Injury
breaks dura & exposes cranial contents to environment Causes
primarily focal injuries Specific grossly visible brain lesion in
precise location Closed (blunt, nonmissile) trauma Head strikes
hard surface or rapidly moving object strikes head Dura remains
intact & brain tissues not exposed to environment Focal (local)
Injury Contusions-blood leaking from damaged vessel Hematomas
Diffuse (general) brain injuries Diffuse axonal injury
Concussion
FOCAL BRAIN INJURY Contusion Observable brain lesion Force of
impact typically produces bleeding & contusions from small
tears in blood vessels Coup injury Injury directly below point of
impact Contrecoup Injury on pole opposite site of impact
HEMATOMAS Epidural Between dura & skull Subdural Between
dura & arachnoid layers Intracerebral Parenchymal
SUBDURAL HEMATOMAS Acute Rapid & high mortality rate
Subacute Less rapid with some improvement Chronic Symptoms occur
weeks after injury Common in older patients Severing of bridging
veins
DIFFUSE BRAIN INJURY Diffuse axonal injury (DAI) Shaking,
inertial effect Acceleration/deceleration Axonal damage Shearing,
tearing, or stretching of nerve fibers Severity corresponds to
amount of shearing force applied to brain & brain stem
Categories: Mild concussion Classical concussion Mild, moderate,
& severe diffuse axonal injuries (DAI) Mild Concussion
Temporary axonal disturbance causing attention and memory deficits
but no loss of consciousness I: confusion, disorientation, &
momentary amnesia II: momentary confusion & retrograde amnesia
III: confusion with retrograde & anterograde amnesia Classic
Cerebral Concussion Grade IV Disconnection of cerebral systems from
brain stem & reticular activating system Physiologic &
neurologic dysfunction without substantial anatomic disruption
Loss of consciousness (