Bone is capable of altering its shape and density in response to mechanical demands.

Bone tissue may be dense and compact (cortical) or lighter and trabecular.

In long bones, the epiphyseal plate is the site of linear growth. Fracture through this plate may lead to limb length discrepancy after fracture healing in children. Increases in bone width are mediated by osteocytes in the periosteum.

Bone cells responsible for deposition are called osteoblasts (bone building cells); osteoclasts mediate bone resorption (bone-eating cells). Absence of bone stress because of immobility or altered weight bearing leads to demineralization of bone and increases risk of fracture.

Joint configuration dictates possible motions of a joint. Types of joint movement include flexion, extension, adduction, abduction, and rotation. Joints that allow these types of movement are called diarthroses (synovial joints). The ends of bone in a synovial joint are held together by a joint capsule composed of two layers of connective tissue.

The lateral and medial menisci in the knee serve as shock absorbers between the femur and tibia. The medial meniscus has strong attachments to the collateral ligaments, whereas the lateral meniscus has weak attachments to the lateral area of the joint capsule. Thus, because of its strong attachment, the medial meniscus is more likely to be torn than the lateral meniscus.

Intervertebral disks are pad-like structures that act as cushions between vertebrae. A strong annulus fibroses surrounds a gelatinous, high-water-content nucleus pulposus that can herniated and press on spinal nerves.

The joint capsule is composed of two layers of connective tissue: an outer fibrous membrane and an inner synovial membrane.

Synovial fluid provides nourishment and lubrication for cartilage. It becomes more viscous with slow movement and low temperatures and less viscous with fast joint movement and high temperatures.

Some bones are held together by joints that allow little or no movement. These joints are called synarthroses (non-synovial joints). Examples include sutures between skull bones, tooth-jawbone joints, and the symphysis pubis joint.

The ends of bones are covered with articular cartilage, which helps distribute mechanical loads placed on the joint and minimize friction and wear.

An important component of articular cartilage is collagen, which provides strength and tensile stiffness. A second component, proteoglycan, increases compression tolerance.

Articular cartilage is avascular and relies on synovial fluid for nutrition and waste removal.

Synovial fluid lubricates articular surfaces to reduce friction and minimize wear.

Articular cartilage has limited capacity for repair and regeneration. It is very difficult and time consuming to heal.

Interfacial joint wear occurs because of insufficient lubrication.

Fatigue joint wear occurs because of repetitive stress injuries.

Sudden imposition of excessive stress may also cause trauma to the joint matrix.

Ligaments and joint capsules connect bones to bones and provide stability to joints.

Tendons attach bones to muscles to allow movement.

Tendons and ligaments are composed of dense connective tissue formed by fibroblasts.

Collagen and elastin are the primary protein components in tendons and ligaments. Most tendons and ligaments have little elastin, which makes them strong but not very compliant. An exception is ligaments that connect adjacent vertebrae, which have more elastin than collagen.

Tendons are composed of many very fine fibers, each of which originates on endomysium.

Ligament and tendon strength is determined by the quantity and quality of collagen cross-links.

Maximal strength is achieved in young adulthood; pregnancy and aging reduce collagen strength.

Ligaments and tendons respond to increased functional demand by increasing strength. Disuse results in weakened structures.

A single muscle fiber is one elongated muscle cell packed with contractile proteins and cytoplasmic organelles.

Connective tissue encases each fasciculus (endomysium) and the muscle as a whole (perimysium). Tendons that attach muscle to bone are continuous with the perimysium.

The arrangement of fibers within a muscle may be parallel or oblique.

A parallel arrangement occurs in muscles having greater range of motion.

Oblique patterns occur in muscles with large force potential.

Skeletal muscle is striated because of an orderly arrangement of contractile proteins in muscle cells.

Myosin is the primary component of the thick filament. Thin filaments are composed mainly of actin, with smaller amounts of the regulatory proteins troponin and tropomyosin.

The fundamental unit of muscle contraction is the sarcomere.

A sarcomere extends from one Z line to the next and consists of interdigitating thick and thin filaments.

Muscle contraction occurs when myosin head regions bind to sites on the actin filament to form cross-bridges.

•  After binding, myosin tugs on the actin filament, which causes thick and thin filaments to overlap more.
•  Myosin then releases and proceeds to bind at another point farther along the actin filament. Each cross-bridge cycle requires one molecule of ATP.

For contraction to occur, the cytoplasm must have sufficient calcium ions.

•  In the absence of calcium, tropomyosin covers binding sites on the actin filament and prevents cross-bridge formation.
•  Another regulatory protein, troponin, controls the position of tropomyosin.
•  When calcium is bound to troponin, tropomyosin is moved to expose binding sites on actin, and cross-bridge formation ensues.

Calcium ions are stored in the sarcoplasmic reticulum and released into the cytoplasm when the muscle cell depolarizes during an action potential.

A group of skeletal muscle cells innervated by a single motor neuron is called a motor unit. All of the cells in the unit contract simultaneously when the motor neuron depolarizes.

An action potential in the α-motor neuron releases acetylcholine at the motor end-plate. Acetylcholine binds to receptors on the muscle cell membrane and triggers an action potential in the cell. To generate more force in the muscle, a greater number of motor units can be activated, a process termed recruitment.

Activation of a motor unit by a single action potential results in a brief twitch contraction.

A train of action potentials in the motor neuron results in a sustained contraction, in which calcium is released into the cytoplasm faster than it is removed.

Sustained contraction in response to repetitive stimulation is termed summation.

Muscle contraction does not always result in muscle shortening.

o Isometric contraction refers to contraction with no change in muscle length.

o Eccentric contraction occurs when the muscle lengthens while contracting (because of a high load).

o Muscle shortening with contraction is termed concentric.

o Isometric contraction generates greater tension than concentric contraction does; eccentric contraction may generate the highest tension.

The behavior of contracting muscle is governed by several mechanical principles:

o Length-tension relationship: Up to a point, a greater resting length of the muscle generates a greater force of contraction. Optimal actin-myosin overlap occurs at about the usual resting muscle length.

o Load-velocity relationship: The velocity of muscle shortening is inversely related to the applied load.

o Force-time relationship: A longer contraction is associated with a greater force of contraction.

Creatine phosphate is a storage form of energy that is quickly converted to ATP when cellular ATP levels fall.

Fatigue results when energy and nutrient supply are insufficient.

A higher rate of muscle oxygen consumption occurs during and for a period after muscle activity.

Lack of muscle use (disuse) leads to a reduction in muscle mass and slowing of oxidative enzyme activity.

Early activity after injury is associated with quicker recovery of tensile strength, less atrophy, and better circulation

discontinuity of the bone that occurs when more stress is placed on the bone than it is able to absorb.

Causes: May be direct (a blow) or indirect (massive muscle contraction)

1. open/compound- broken through the skin complications- infection, osteomyelitis, delayed union or nonunion

2. Comminuted has more than 2 pieces.

3. Closed- not broken through the skin.

4. Greenstick-  seen in children- partial break in bone continuity

5. Compression- occurs in vertebral body bones are crushed or squeezed together

6. Impacted- fragments are wedged together occurs in humerus

7. Transverse- simple angular forces

8. Spiral – twisting motion

• Pain

• Tenderness at the site of bone disruption

• Swelling

• Loss of function

• Deformity of the affected part 

• Abnormal mobility

• Bleeding from an open fracture

• Crepitus (grating of bones)

displacement or separation of the bone ends of a joint with loss of articulation usually follows a severe trauma.

Common sites: shoulder, acromioclavicular

• Congenital – hip and knee

• Traumatic- occur after falls, blows or rotational injuries

• Pathologic- occur with infection, paralysis, neuromuscular injuries, rheumatoid arthritis

Dislocation Manifestations:

• Pain

• Deformity

• Limited

movement

unusual muscle contraction and excessive forcible stretch

Common sites:

• lower back

• cervical region of spine

• elbow

• shoulder

• foot (weight bearing stresses- inadequate muscular and ligamentous support, overweight, or excessive exercise) 

Pain, swelling

Sprain Causes:

Sprain Injury sites:

• Ankle

• Knee

• Elbow

• Wrist

Sprain Manifestations:

• pain

• rapid swelling

• heat

• disability

• discoloration

• limitation of function

Osteoporosis

is the loss of mineralized bone mass causing increased porosity of the skeleton and susceptibility to fractures. There is an imbalance between bone resorption and formation, bone resorption exceeds bone formation. Osteoporosis develops due to aging, gender, genetic predisposition, activity level and nutritional status.

chronic systemic inflammatory disease with bilateral involvement of synovial or diarthrodial joints. The onset is insidious. The disease has periods of exacerbation and remission. The joints involve includes any diarthrodial joint (fingers, hands (proximal interphalangeal, metacarpophalangeal, distal interphalangeal), wrists, knees and feet and cervical spine. Joint involvement is symmetrical and polyarticular. The disease causes progressive joint destruction that leads to subluxation (dislocation resulting in misalignment) of the joint.

• fatigue

• anorexia

• weight loss

• aching

• stiffness and joint pain (last for 30 minutes to several hours)

• limitation of joint motion

• swelling and thickening of synovium (leads to stretching of the joint capsule and ligaments)

• deformity

• Rheumatoid nodules-tender or non, small or large, movable or non movable

• vasculitis (inflammation of small or medium sized arteries)

Systemic Lupus Erythematosus Manifestations:

• MS- Arthralgia/arthritis (early symptoms), flexion contractures, hyperextension of the interphalangeal joints, subluxation of the carpometacarpal joints(causes deformity/loss of function in hands)

• Skin- butterfly rash on the nose and cheeks, hair loss, mucous membrane    lesions

• Renal- glomerulonephritis, nephrotic syndrome, renal failure

• Pulmonary-pleural effusion, pleuritis,

• CV- pericarditis, myocarditis, ischemic heart disease, hypertension

• CNS-stoke/hemorrhage due to vasculitis, seizures, depression, decreased cognitive functioning, confusion, altered LOC

• Hematologic- hemolytic anemia, leukopenia, lymphopenia, thrombocytopenia, lymphadenopathy

• discoid lesions (head, scalp and neck)-red, swollen patches of skin

is an autoimmune disease of connective tissue characterized by excessive collagen deposition in the skin and internal organs (lungs, heart, kidneys, GI). The skin is thickened through fibrosis with an accompanying fixation of subdermal structures (sheaths/fascia covering tendons and muscles).

Two Types of Scleroderma: diffuse and Crest

- hardening (trunk and proximal extremities)- severe and progressive disease of the skin.

• stone facies- tightening of the facial skin with restricted motion of the mouth
• esophagus- hypomotility/difficulty swallowing
• pulmonary- dyspnea, respiratory failure
• kidney- renal insufficiency and malignant hypertension
• cardiac – pericarditis, heart block, myocardial fibrosis

-hardening of the skin (hands and face), calcinosis (calcium deposits in the subcutaneous tissues that erupt through the skin, raynaud phenomenon, esophageal dysmotility, sclerodactyly (localized scleroderma of the fingers) and telangiectasia

• Develops Raynaud (reversible vasospasms of the arteries supplying the fingers)
• C- calcium deposits in the skin
• R- raynauds phenomenon, spasm of blood vessels in response to cold or stress
• E- esophageal dysfunction, acid reflux and decrease in motility of esophagus
• S- sclerodactyly thickening and tightening of the skin on the fingers and hands
• T- telangiectasis, dilation of capillaries causing red marks on surface of skin

Ankylosing Spondylitis Manifestations:

• low back pain (persistent or intermittent) worse when resting

• prolonged stiffness (morning and after rest)

• loss of motion in spinal column

• loss of lumbar lordosis occurs as disease progresses, followed by kyphosis of thoracic spine and extension of the neck.

• peripheral arthritis

• weight loss

• fever

• fatigue

• osteoporosis

• reduced lung volume (fusion of costovertebral joints)

 also known as wear and tear arthritis, it is a degenerative joint disease that occurs from repetitive stress. It is a non inflammatory process. An initial injury causes release of enzymes from chondrocytes, resulting in collagen breakdown; collagen fatigue and microfractures occur with the stress of weight bearing. Structural breakdown of cartilage involves fissuring, pitting, and erosion; resulting structural changes include osteophyte spur formation, sclerosis of subchondral bone, and cyst formation. Osteophytes may break off into joints and form “loose bodies.” Progressive loss of articular cartilage and synovitis results from inflammation caused when cartilage attempts to repair itself. The articular cartilage has several roles: serves as a smooth weight bearing surface and transmits the load down to the bone, dissipating the mechanical stress.

It is the leading cause of disability and pain in the elderly. It can be an idiopathic disorder or secondary. Idiopathic is localized or generalized and secondary can be congenital or acquired defects, trauma, metabolic disorders, or inflammatory diseases. Predisposing conditions may include joint trauma, genetic predisposition, congenital disorders, lifestyle factors (stress to joints), primary diseases affecting joints (Paget disease, diabetes mellitus), joint sepsis, aging (wear and tear), hormonal status (postmenopausal women more frequently affected), and the immune response. It affects the hips, knees, lumbar and cervical vertebrae, proximal and distal joints of the hands, first carpometacarpal joint and first metatarsophalangeal joints of the feet. The onset can be sudden or insidious.

Osteoarthritis Manifestations:

• joint pain (aching) worsens with activity and relieved by rest

• stiffness

• limitation of motion

• joint instability

• deformity

• crepitus

• joint enlargement

• heberden nodes and Bouchard nodes are enlargements of the distal interphalangeal (DIP) joints and proximal interphalangeal (PIP) joints, respectively; they are commonly found. Heberden nodes are the most common deformity of the hands.

Gout Manifestations:

Pain is abrupt (begins at night)

Redness and swelling

may be acute or chronic.

It is caused by direct penetration or contamination of open fracture or wound (exogenous origin). It is introduced to the bone by a penetrating wound, open fracture or surgery.  The bacteria involved are Staphylococci and Streptococci.

Osteomyelitis Manifestations:

• fever

• increased pain at the operative site

• poor incisional healing with wound drainage

Can occur as seeding through the blood stream. It occurs in children and adults. In adults it occurs in people with debilitating conditions, chronic skin infections, urinary tract infections (UTI’s), IV drug user, and immunologically suppressed persons.

• chills

• fever

• malaise

• pain on movement of the affected extremity,

• loss of movement and local tenderness (redness and swelling)

is secondary to an open wound (bone or surrounding tissue). It results from delayed or inadequate treatment of acute hematogenous osteomyelitis or osteomyelitis caused by direct contamination of bone by exogenous organisms. It can persist for years.

It can occur in skin infections with people that have vascular insufficiency. It can develop with a skin lesion, and chronic or ischemic foot ulcers with diabetes. They will present with ingrown toenails, cellulitis, perforating foot ulcer which makes diagnosising difficult. It is diagnosed when bone is exposed in the ulcer bed or after debridement. Can be an acute, subacute or chronic condition. It is caused by viruses, parasites, fungi, and bacteria such as staphylococcus aureus, E. coli, Neisseria gonorrhoeae, haemophilus influenza, and salmonella.

Any type of Osteomyelitis is extremely difficult to treat. It can take up to 6 months of antibiotic treatment to eradicate the offending organism.

Chronic osteomyelitis

Manifestations:

• infected dead bone has separated from the living bone (sequestrum)

• Signs of infection are not present

is one of the important regulators of calcium and phosphate levels in the blood.   Secreted by the parathyroid gland, these are located on the thyroid itself.  PTH prevents serum calcium levels from falling below and the serum phosphate levels from rising above normal concentrations in the blood. 

Parathyroid hormone accomplishes its job by stimulating at least three processes:

Mobilization of calcium from bone: Although the mechanisms remain obscure, a well-documented effect of parathyroid hormone is to stimulate osteoclasts to reabsorb bone mineral, liberating calcium into blood.
Enhancing absorption of calcium from the small intestine: Facilitating calcium absorption from the small intestine would clearly serve to elevate blood levels of calcium. Parathyroid hormone stimulates this process, but indirectly by stimulating production of the active form of vitamin D in the kidney. Vitamin D induces synthesis of a calcium-binding protein in intestinal epithelial cells that facilitates efficient absorption of calcium into blood.

Suppression of calcium loss in urine: In addition to stimulating fluxes of calcium into blood from bone and intestine, parathyroid hormone puts a brake on excretion of calcium in urine, thus conserving calcium in blood. This effect is mediated by stimulating tubular reabsorption of calcium. Another effect of parathyroid hormone on the kidney is to stimulate loss of phosphate ions in urine.

        Secrete acid, which dissolves calcified material

     Secrete hydrolytic enzymes, which digest the collagen matrix

          Secrete collagen to form a surrounding matrix, which then becomes calcified

         Once osteoblasts become embedded they are called osteocytes, mature bone cells

Epiphysis – mostly composed of spongy bone, it is wide to provide stability for the joint. Muscles are also attached here. This end is also covered with articular cartilage that provides for a smooth surface for joint movement

Diaphysis - This is the main bone shaft. It provides structural support and is composed mostly of compact bone.

Metaphysis – Also composed of spongy bone. the wider proximal and distal ends of the shaft of the long bone, adjacent to the growth plate. This is adjacent to the growth plate in children, so you don’t want any fractures here because it will disrupt growth and lead to a short extremity and can cause functional problems.

Hyaline, Elastic and Fibrous

Rigid connective tissue found in synovial joints supporting soft tissues and provides articular surfaces for joints.

Hyaline- most common type has moderate amount of collagen fibers located in the trachea, bronchi, nose, epiphyseal plate and articular surfaces of bones.

Fibrous cartilage mostly consists of collagen and tough tissues that act as shock absorbers. Examples would be area between the vertebral disk, pelvic girdle, knees and shoulder.

Bone remodeling is a continous process which occurs throughout your life. Two types: structural remodeling and internal remodeling

25% is replaced each year

Major influences on equilibrium of bone tissue, mechanical stress, calcium and phosphate levels in the blood

hormones, local growth factors and cytokines

Trabecular bone is lattice like structured bone that contains the marrow. The interior also cancellous bone

Mechanical stress stimulates osteoblastic activity and formation of the organic matrix of bone

Calcium and phosphate levels – bone serves as a storage site for these and alterations in them will effect their deposition in bone

Hormones – PTH and Calcitonin – PTH promotes bone resorption and and calcitonin inhibits bone resorption

involves the deposition of new bone on the outer shaft of the bone, while bone is resorbed at the inner aspect of the shaft. It occurs during growth and results in bone having its shape

involves the replacement of trabecular bone and occurs throughout adulthood.

condition common to all metabolic bone diseases.

Chracterized by a reduction in bone mass; lack of bone seen on X-Ray.

occurs due to a decrease in bone formation, inadequate bone mineralization, or excessive bone de-ossification

Causes:

osteoporosis, osteomalacia, multiple myeloma, hyperparathyroidism, hyperthyroidism

Osteopenia ("too little" bone) is a descriptive term for a loss of bone density observed radiologically. Osteopenia may be local (as in disuse atrophy of an immobilized limb) or generalized. There are many causes of generalized osteopenia, among them: osteoporosis unrelated to other disease, endocrinopathies (hypercortisolism, hypogonadism, hyperparathyroidism, hyperthyroidism), deficiency states (rickets/osteomalacia, scurvy, malnutrition), neoplastic diseases ( multiple myeloma, metastatic carcinoma, leukemia), chronic diseases (malabsorption syndromes, chronic renal failure), drugs (glucocorticoids, heparin, alcohol), and hereditary diseases (osteogenesisimperfecta, homocystinuria).

increased porosity of bone due to loss of mass

most often associated with aging

positively correlates with amount of skin pigmentation

most often seen in postmenopausal women

Risk factos: poor nutrition, prolonged use of medications (antacids, steroids), excesive intake of diet soda high in phosphates, diet high in protein, smoking, alcohol, family history

Rare in children unless due to disease

prematurely appears in female athletes related to eating disorders and amenorrhea (female athlete triad)

Osteoporosis is often called the "silent disease" because bone loss occurs without symptoms. People may not know that they have osteoporosis until their bones become so weak that a sudden strain, bump, or fall causes a hip fracture or a vertebra to collapse. Collapsed vertebra may initially be felt or seen in the form of severe back pain, loss of height, or spinal deformities such as kyphosis, or severely stooped posture. 

Caucasians have least bone mass, and africanamericans have most

Corticosteroids have several adverse effects on bone metabolism.

Direct inhibition of osteoblast function

Direct enhancement of bone resorption

Inhibition of gastrointestinal calcium absorption

Increases in urine calcium loss

Inhibition of gonadal hormones

Risk factors you cannot change: 
    Gender - Your chances of developing osteoporosis are greater if you are a woman. Women have less bone tissue and lose bone more rapidly than men because of the changes involved in menopause.   Age - the older you are, the greater your risk of osteoporosis. Your bones become less dense and weaker as you age.   Body size - Small, thin-boned women are at greater risk.   Ethnicity - Caucasian and Asian women are at highest risk. African-American and Latino women have a lower but significant risk.   Family history - Susceptibility to fracture may be, in part, hereditary. People whose parents have a history of fractures also seem to have reduced bone mass and may be at risk for fractures. 

Risk factors you can change: 
    Sex hormones: abnormal absence of menstrual periods (amenorrhea), low estrogen level (menopause), and low testosterone level in men.   Anorexia.   A lifetime diet low in calcium and vitamin D.   Use of certain medications, such as glucocorticoids or some anticonvulsants.   An inactive lifestyle or extended bed rest.   Cigarette smoking.   Excessive use of alcohol. 

imbalance between bone and resorption and bone formation

decrease in number and activity of osteoblasts (bone builders)

increase in number as activity of osteoclasts (bone-resorbing)

during early menopause, there is rapid osteoclast mediated bone loss

postmenopausal, these changes can be reversed with estrogen therapy

Changes occur in the diaphysis and metaphysis of bone

diameter enlarges causing the outer cortex to become thinner

can occur to the point that minimal stress can result in fracture

2 types of processess:

type 1-early postmeopausal estrogen deficiency; predisposed to fractures of vertebrae and distal radius

type 2- caused by calcium deficiency; hip fractues more common

Peak bone mass is the maximum mass of bone achieved by an individual at skeletal maturity, typically between ages 25 and 35. After peak bone mass is attained, both men and women lose bone mass over the remainder of their lifetimes. Because of the subsequent bone loss, peak bone mass is an important factor in the development of osteoporosis [

pain r/t fractures

skeletal fractures

loss of height- wedging collapse of vertebrae

kyphosis- dowager's hump

usually no generalized bone tenderness

avascular necrosis of hip and compression fractures

Bone density assessment tests: dual-energy x-ray of spine and hip (DEXA), single or dual photon beams of the calcaneus

Serial heights

abone- used to determine if a screening is needed: "A" age (>65), "B" bulk (weight >140 at menopause), "one" never on estrogen

Also known as the DEXA scan

Following a comprehensive medical assessment, your doctor may recommend that you have your bone mass measured. Bone mineral density (BMD) tests measure bone density in the spine, wrist, and/or hip (the most common sites of fractures due to osteoporosis), while others measure bone in the heel or hand. These tests are painless, noninvasive, and safe. Bone density tests can: 
    Detect low bone density before a fracture occurs.  

Confirm a diagnosis of osteoporosis if you have already fractured.  

Predict your chances of fracturing in the future.  

Determine your rate of bone loss and/or monitor the effects of treatment if the test is conducted at intervals of a year or more. 

ABONE- a pneumonic to use to aid in determine whether or not a screen should be done.  .  . 

Systemic inflammatory disease

characterized by diffuse inflammatory vascular lesions and degenerative changes in connective tissue

affects 0.3% to 1.5% of population

women 2-3x greater than men

peak incidence:40-60 years of age

onset: 30-50 years of age

Rheumatoid arthritis is a chronic disease, mainly characterized by inflammation of the lining, or synovium, of the joints. It can lead to long-term joint damage, resulting in chronic pain, loss of function and disability.

Rheumatoid arthritis (RA) progresses in three stages. The first stage is the swelling of the synovial lining, causing pain, warmth, stiffness, redness and swelling around the joint. Second is the rapid division and growth of cells, or pannus, which causes the synovium to thicken. In the third stage, the inflamed cells release enzymes that may digest bone and cartilage, often causing the involved joint to lose its shape and alignment, more pain, and loss of movement.

What is inflammatory arthritis?This chronic disease results when, for unknown reasons, the immune system mistakenly attacks the tissue that lines and cushions the joints. As cartilage wears away, the knee often becomes stiff and swollen. A well-known example is rheumatoid arthritis.

In some types of arthritis, such as rheumatoid arthritis, the synovium becomes inflamed. This inflammation causes chemicals to be released that thicken the synovium and damage the cartilage and bone of the affected joint. This leads to inflammation of the synovium causing pain and swel

70-80% have the RA Factor

this is an antibody that reacts with a fragment of immunoglobulin G (IGG), an autologous (self-produced) antibody, to form immune complexes

this production can be stimulated by many things: viral, genetic predisposition

produced by lymphocytes in the inflammatory infiltrate of synovial fluid

other WBC's congregate

PML and macrophages phagocitize the immune complex and then release lysosomal enzymes that cause destructive changes in joint cartilage

sets in motion a chain of events that perpetuates the condition

synovial cells and subsynovial tissue proliferate

vasodilation= warmth and redness

increased capillary permeability causes swelling of the affected area

there is development of an extensive network of new blood vessels in the synovial membrane that contributes to the advancement of RA synovitis; called "Pannus"

extends from synovium to a bare area at junction between cartilage and subchondrial bone

pannus has destructive effect on adjacent cartilage and bone

this reduces joint motion, joint instability, muscle atrophy, stretching of ligaments

destructive changes are irreversible

Autoimmune diseases are illnesses which occur when the body tissues are mistakenly attacked by its own immune system. The immune system is a complex organization of cells and antibodies designed normally to "seek and destroy" invaders of the body, particularly infections. Patients with these diseases have antibodies in their blood which target their own body tissues, where they can be associated with inflammation. Because it can affect multiple other organs of the body, rheumatoid arthritis is referred to as a systemic illness and is sometimes called rheumatoid disease.

While rheumatoid arthritis is a chronic illness, meaning it can last for years, patients may experience long periods without symptoms. Typically, however, rheumatoid arthritis is a progressive illness that has the potential to cause joint destruction and functional disability.

Rheumatoid arthritis develops when the immune system's white blood cells attack healthy tissues, a process called an "autoimmune response." The most common target is the lining of a joint, called the synovium -- which comprises of synovial fluid and a synovial membrane, (however, damage can also occur in organs such as; the heart, lungs, and eyes). The synovium becomes inflamed during the assault, and the cartilage that cushions the joint starts to expand. While the cartilage grows abnormally, the bones, ligaments, and muscles in the joint slowly erode.  

Nobody knows why the body turns against itself; although it's possible an unknown virus may spur the white blood cells into action. Experts also think genetics may make some people more susceptible to the condition than others.

Though rheumatoid arthritis can strike at any age, it most commonly begins between the ages of 20 and 50 -- unlike osteoarthritis, which tends to afflict older people -- and it's three times more common in women than in men.

Synovial cells become hyperplasic

Swelling accompanies the inflammatory process

PML- polymorphonuclear lymphocytes

Pannus- destructive vascular granulation tissue

RA Manifestations:

fatigue, anorexia, weight loss, generalized aching and stiffness

may only involve a few joints for brief time or may be relentness

joint manifestations: symmetric

most affected: fingers, hands (swan neck and boutonniere deformity) knees, feet (bulge sign, bakers cyst) cervical spine

RA usually affects joints symmetrically (on both sides equally), may initially begin in a couple of joints only, and most frequently attacks the wrists, hands, elbows, shoulders, knees and ankles

Rheumatoid arthritis (RA) usually affects the same joint on both sides of the body.

It occurs most frequently in the:

fingers

wrists

elbows

shoulders

jaw

hips

knees

toes

fatigue, weakness, anorexia, weight loss, low grade fever.

elevated sed rate

anemia with low serum iron level

nodules (granulomatous lesions) around blood vessels at pressure points

vasculitis of small & medium arterioles with long history and high titers of RA factor: ischemia of nail and digital fold, ulcer of lower extremities, neuropathy, visceral organs

eye lesions: episcleritis, scleritis

hematologic abnormalities

pulmonary disease

cardiac complications

infection

felty's syndrome- leukopenia with or without splenomegaly

Anemia usually resistant to iron therapy.  .  Iron is unable to bind with RBC’s

Nodules may be large or small, tender or nontender, movable or nonmovable.  .  May be removed surgically, or may resolve on their own over time

Vaculaitis is uncommon

Scleritis may cause inflammation of the anterior and/or posterior segments of the eye and manifests as severe eye pain.

Episcleritis is an inflammatory condition of the connective tissue between the
conjunctiva and sclera known as the episclera.
Felty's syndrome: Atypical form of rheumatoid arthritis with fever, splenomegaly
and leukopenia and, in some cases, anaemia and thrombocytopenia.

The white part of the eye may appear red, swollen, and there may be a nodule present which is painful to touch. Scleritis can be associated with iritis, and in some cases with swelling under the retina leading to visual loss. Treatment is usually with oral medication, and eyedrop medication as needed. Treatment of the underlying medical problem may be necessary

Extra-articular involvement. Rheumatoid vasculitis with skin ulceration on the dorsum of the foot.

Joint heat, swelling, tenderness, warmth and reduced motion

positive RA factor (only positive in 1-5%)

cloudy synovial fluid with elevated WBC

criteria: am stiffness for one hour for at least 6 weeks; 3 or more joints of hands or fingers swollen for at least 6 weeks; x-ray changes; RA nodules

FATIGUE, ANOREXIA, WEIGHT LOSS, GENERALIZED ACHING & STIFFNESS

MAY ONLY INVOLVE A FEW JOINTS FOR BRIEF TIME OR MAY BE RELENTLESS

JOINT MANIFESTATIONS

SYMMETRIC

MOST AFFECTED

FINGERS, HANDS (SWAN NECK & BOUTONNIERE DEFORMITY)

KNEES, FEET (BULGE SIGN, BAKER’S CYST)

CERVICAL SPINE

Chronic inflammatory disease that can affect any organ system

major RA disease

females> males

500,000 ave the disease

> in non-white population

some familial tendencies are present

Systemic lupus erythematosus (also called SLE, or lupus) is an autoimmune disease of the body's connective tissues. Autoimmune means that the immune system attacks the tissues of the body. In lupus, the immune system primarily attacks parts of the cell nucleus.

Systemic Lupus Erythematosus:

Etiology and Pathogenesis

etiology is unknown

patho: formation of autoantibodies and immune complexes

hormonal: estrogen favors development- heightness helper T-cell and weakens suppressor T-cell

immunologic: the above could lead to the development of auto-antibodies

environmental: uv light, chemicals-hydralazine, procainamide, hair dye, foods, infectious agents

Process begins with activation of polyclonal b-cells

this causes exaggerated production of autoantibodies

autoantibodies combine with antigen to form immune complexes

the complexes are deposited in vascular and tissue surfaces

this triggers the inflammatory response causing local tissue injury; can also affect components of the blood, organs

Systemic Lupus Erythematosus:

Manifestations

acute or insidious

course is characterized by exacerbations and remissions

musculoskeletal: polyarthritis in 90% without articular destruction- involves more than one joint; deformities of ligament, tendons and joint capsule

skin: acular or "butterfly rash", hair loss, mucus membrane lesions during exacerbations, especially with exposure to sunlight

Renal: glomerulonephritis, nephritis, nephrotic syndrome, renal failure

Pulmonary: pleural effusion, pleuritis, pulmonary embolism

Cardiovascular: pericarditis, myocarditis, HTN, ischemic heart disease

CNS: stroke- hemorrhage, seizures, psychosis

Hematologic: hemolytic anemia, leukopenia, lymphopenia, thrombocytopenia

Other: discoid SLE- plaque-like lesions on scalp, face, neck

subacute cutaneous SLE- resembles psoriasis, on sun-exposed areas of face, chest, upper back and arms, mild systemic, low renal involvement

Systemic Lupus Erythematosus:

Diagnosis

complicated and difficult

history

physicla exam

blood work: immunoflorescence test for ANA (not very specific for Lupus because it an be elevated in healthy persons or be associated with other disorders; Anti-DNA antibody is more specific; CBC- anemia, leukopenia, thrombocytopenia

systemic

two types: generalized (diffuse) and limited (crest variant)

involves the lungs, esophagus, heart, duodenum, kidneys

fibrotic thickening of the skin with fixation to the subdermal structures

Manifestations: muscular atrophy, pain edema, calcification, arthrodesis

Crest Syndrome:

a variant of scleroderma

calcinosis

raynauds syndrome

esophageal dysmotility

sclerodactyly- fingers become waxy appearing, tight, and hard

telangiectasia- dilated superficial blood vessels

Systemic sclerosis is a clinically heterogeneous, systemic disorder which affects the connective tissue of the skin, internal organs and the walls of blood vessels. It is characterized by alterations of the microvasculature, disturbances of the immune system and by massive deposition of collagen and other matrix substances in the connective tissue.

Major criterion for diagnosis:

proximal diffuse (truncal) sclerosis (skin tightness, thickening, non-pitting induration)

Minor criteria:

sclerodactyly (only fingers and/or toes)

digital pitting scars or loss of substance of the digital finger pads (pulp loss)

bibasilar pulmonary fibrosis

chronic systemic inflammotory disease of the axial skeleton manifested by pain and progressive stiffening of the spine: sacroiliac joints, inter-vertebral disk spaces

small peripheral joints not involved

sites of ligament insertion into bone are eroded by inflammatory cells with formation of woven bone

causes fibrosis, calcification and ossification of joints

ankylosis- bone replaces ligament

usually affects men more than women

Ankylosing spondylitis (AS) causes inflammation of the joints of the spine. Spondylitis is the medical term for inflammation of the joints of the spine. Ankylosis is the medical term for the stiffening caused by the inflammation.

The axial skeleton forms the central axis of the body. It consists of the skull, the vertebral column, the ribs and the sternum or breastbone

Ankylosing spondylitis:

Etiology and pahtogenesis

HLA-B27 antigen: A hereditary marker: usually present in 90% of all patients with disease

immune response with presence of mononuclear cells

possibly due to an autoimmune response or increased susceptibility to infections or environmental agents

(Human Leukocyte Antigen) HLA- B27

The human leukocyte antigens (HLAs) are proteins present on the surface of all body cells that contain a nucleus, and are in especially high concentrations in white blood cells (leukocytes).

Ankylosing spondylitis:

Manifestations

low back pain: persistent or intermittent, worse when resting, especially in bed; lumbosacral pain; discomfort in buttocks and hip areas; radiate to thigh like sciatic pain; prolonged stiffness in the morning and after rest; mild activity or hot shower reduces pain

Loss of motion in the spinal column: kyphosis; constrict heart and lungs

Peripheral arthritis in hips and shoulders

Extraskeletal involvement: acute anterior uveitis

systemic symptoms: weight loss; fever; fatigue

osteoporosis

ocular inflammation encountered. It is a common cause of a painful red eye. Inflammation of the iris may appropriately be termed iritis, while inflammation of the iris and the ciliary body is called iridocyclitis. Iritis may be subdivided into 2 broad categories: granulomatous and nongranulomatous.

Ankylosing spondylitis:

diagnosis

H&P

X-Ray (rigid, bamboo-like spine, squared appearance of vertebrae)

assessment of mobility

chest expansion

Lab: elevated sed rate; mild normocytic, normochromic anemia

most prevelant form of arthritis

can lead to loss of mobility and cause chronic pain

can be: primary- localized or generalized; secondary- trauma, inflammation, metabolic

gener and age play a role

Virtually everyone over the age of 75 is affected in at least one joint.

Women are generally affected at a younger age than men.

Osteoarthritis:

Pathogenesis

articular damage cause physiologic imbalance between the stress applied to the joint tissue to withstand the stress

injury results in a chondrocyte response that causes degredation in the upper ayers pf the cartilagewhich cause release of interleukin-1

this cause release of proteolytic enzymes that damage the chondrocytes

progressive in nature

Articular cartilage injury that occurs in OA is thought to be related to the release of cytokines such as interleukin-1.   These chemical messengers stimulate production and release of enzymes that digest cartilage

Cracks start to develop and eventually these cracks reach the bone surface and continue to cause damage to cartilage and bone surfaces

Osteoarthritis:

manifestations

aching, non-localized pain

worsens with activity and relieved by rest

crepitus when joint is moved

joints: hips, knees, lumbar spine, cervical spine, distal joints in the hands, first metatarsals in feet

limit in motion and stability

joint enlargment

Osteoarthritis:

diagnosis

H&P

x-Ray studies: joint space narrowing; subchondral bone sclerosis; osteophytes

slight elevation of sed rate

normal synovial fluid

presence of monosodium urate or uric acid crystals in joint cavities

uric acid is a metabolite of purines, adenine and guanine

2/3 is excretes via kidneys, 1/3 in GI tract

reduced urate clearance

salicyclates and thiazide diuretics can interfere with excretion of uric acid

Gout results from a build-up in the body of too much uric acid, which forms crystals that deposit in joints and cause inflammation. Uric acid is a substance that normally forms when the body breaks down waste products called purines. Gout can be inherited or happen as a complication of another condition.

The first episode usually occurs between the ages of 40 and 50 in men and after menopause in women. Gout is a form of rheumatic disease caused by uric acid deposits in the joints. It can affect any joint -- the fingers, wrist, elbow, knee, ankle, or foot. The most commonly affected joint is the big toe.

Uric acid is a waste product in your blood that is removed by the kidneys and eliminated in urine. The body’s overproduction of uric acid or the kidney’s inability to eliminate it efficiently can cause an excessive build-up, known as hyperuricemia. Over time this excess uric acid can deposit in the joints where it forms into sharp, uric acid crystals that lead to pain and swelling in the affected joint. A gout attack occurs suddenly and may come and go in intensity over a period of several days.

Gout:

Etiology and Pathogenesis

primary: genetic defect in purine metabolism

secondary: disease conditions and medications

a rise in sreum urate level causes monosodium crystals precipitate in a joint and initiate an inflammatory response

polymorphonuclear leukocytes(pmls) respond and then die

This causes release of lysosomal enzymes that causes destruction of cartilage and subchondral bone

Gout:

Manifestations

affects first: metatarsophalangeal joint (big toe); also can affect instep, ankles, heel, knees, wrist, fingers, elbows

begins at night and may be precipitated by excessive exercise, foods, alcohol, dieting

abrupt with redness and swelling

may be months or years betwen attacks

extremely painful