Patho

• - support, framework and protection
• - hematopesis (bone marrow)
• - involved in Ca metabolism and storage
• 

• - Bone matrix- haversian system are made up of collagen fibres and Ca phosphate salts, containing blood vessels
• - Bone Cells- osteoclasts (destroy old bone tissue), osteoblasts (create new bone matric), osteocytes (former osteoblasts- controlling/signalling function

• - bone reabsobed (osteoclasts)
• - new bone formation (osteoblasts)
• - bone may or may not change its density and thickness
• - purpose: repair micro damage; supply calcium to serum
• in adults- equilibrium; in
• in children- formation > resorbtion
• Aging- bone loss accentuated (resorbtion> formation)

• - mechanical stress (weight bearing or mm contraction); osteoblastic vs osteoclastic activity
• - hormones: lengthening via growth plate- growth hormone and sex hormone: parathyroid hormone or cortisol
• - RANK ligand
• - Osteoprotegerin

• - rank ligand- RANKL- a regulatory cytokine expressed by osteoblasts. It bins to RANK receptor on osteoclast and activates them. RANKL overproduction> degenerative bone disease
• -osteoprotegerin- OPG- a glycoprotein decoy receptor to which RANKL binds and thereby prevents RANKL binding to RANK
• - bone remodelling

• - chondrocytes (produce cartilage)
• - osteoblasts (produce bone matric and facilitate its mineralization
• - action of GH on bone is indirect, via IGF-1. By binding to its specific recptor, IGF- 1 causes mitogenic effects in chondrocytes (hypertrophy and proliferation), activated osteoblasts and inhibits of osteoclasts.

• 1. mechanical strain
• 2. breaking the bone and damage to blood vessels
• 3. bleeding
• 4. hematoma and inflammation

• Stages of bone healing:
• - hematoma
• - granulation
• - procallus
• - bony callus
• - remodlling
• 

• Amount of damage
• Age
• Infection
• Systemic disease affecting circulation (eg diabetes)
• Mm spasm

• Ischemia
• compartment syndrome (compresion of nerve, blood vessels, and mm tissue> lack of O2> tissue death)
• Fat emboli
• Nerve damage

• - metabolic disorder, when bone resorbtion exceed bone formation.
• - causes decrease in bone matric and mineralization

• - primary- postmenapausal, senile, idiopathic
• - secondary-following other condition (eg crushing syndrome)

• Age- decrease osteoblastic activity
• decrease mobility- decrease mechanical stress stimulus
• Hormonal- hperparathyroidism, crushing syndrome, catabolic glucocoricoids
• nutrients- decrease calcium, vit D, protein, malabsorption sndromes

• - normal boney density 833mg/cm2- osteopenia 833-648, osteoporotic <648
• - back pain
• - kyphosis/ scoliosis- fractures- haunch

• - increase Ca and Vit D intake
• - exercise
• - inhibitors of bone resorbtion
• - hormonal therapy

- both are metabolic bone disorders that are expressed as reduced bone mineralization

• - dietary problems
• - malabsorption
• - lack of sun exposure

• - deficit Ca/ phosphates/ vit D
• - lack of bone mineralisation
• - soft bones
• -deformations and low heigh in children
• - vit D is needed for absorbtion of Ca in the intestin
• NOTE- osteomalacia is the same disorder in adults- soft bones- compression fractures

• - thin filaments contain proteins- actin, tropomyosin, troponin- they are attached to the Z line
• - thick filaments- contain myosin
• 
• 

• - motor unit is the smallest functional unit for movements. It consists from a single alpha motorneuron, its axon plus all mm fibres inervated by this neuron
• - alpha motoneuron- in the ventral horn of the spinal cord- ventral root
• - Motorneuron pool is a group of neurons (a column) that innervate one mm

• - is a synapse between the motorneuron axon terminal and the mm fibre
• - arrival of electrical pulse (AP) along the motor neuron axon to the terminal causes release of neurotransmitters
• 
• 

Ach- acetilcholine

• cholinesterase
• this then allows pores to open and the AP to be transmitted

• - golgi tendon organ- detects tension
• - mm spindle- detects changes in mm length
• 

• - response to sensory stimuli without participation/ contribution of consciousness
• - knee (patellar) reflex:
• 1. Reflexes are elementary acts of behaviour
• 2. Stimulating of given input produces determined and predicted output
• 3. Performed without conscious control. Reflexes vs voluntary responses: in reflex, afferent input strictly determines output; no contribution of will

• - primary motor cortex (M1/Area 4)- precentral gyrus (aussie walter campbell)
• - - precentral gyrus is the motor cortex (wilder Penfield demo via small electrical currents being put into the cortex resulting in twitching around the body

• corticospinal tract
• 

- a group genetic disorder that manifests as degneration of skeletal mm

• - mutations in dystrophin gene
• - dystrophin is a protein located in the membrane of mm fibres. Essential for maintaining cell shape and survival

• - lack of dystropin
• - degeneration and necrosis of mm cells
• - mm cells replaced by fat and fibrous connective tissue
• - mm weak or cannot contract

• - mm weakness
• - tendon reflexes reduced
• - vertebral deformities
• - respiratory insufficience > lung infection
• - cardiac abnormality
• - mental retardation

Death usually before 20 due lung and heart failure

• - classified by the degree of movement
• - synarthroses- immovable (eg cranial sutures)
• - Amphiarthroses- slightly movable (eg ribs to sternum)
• - siarthroses (synovial)- freely movabble (shoulder)

• - articular cartilage- covering over ends of bones (very smooth, slippery surface)
• - Synovial membrane- produces synovial fluid (lubricant) which fills the space between ends of bone
• -articular capsule- consists of synovial membrane and a fibrous capsule
• - ligament- reinforce capsule, links bones, supports jt
• 

• - overuse injuries such a tennis elbow
• - repetitive strain injuries (carpal tunnel syndrome)

• - jt dislocation
• - injuries of tendons and ligaments

trauma- inflammation- granulation tissue- collagen fibres- fibrous tissue

• - strain- tear in a ligament
• - sprain- tear in a tendon
• - avulsion- detachment from a bone

- traumna or excessie mm force

- pain, swelling, limited movements

- low blood to area- > 6w to heal

• - degenerative jt disease
• - cause unknown- possibly genetic

• - articular cartilage is damaged
• - surface of cartilage becomes rough and worn
• - tissue damage causes release of enzymes, accelerating damage of cartilage
• - subchondral bone my be exposed
• - osteophystes (bone spurs) develop and may break off
• - jt cleft becomes narrower
• - secondary inflammation of surrounding tissue
• 

• - aching pain with Wb and movement
• - jt movement is limited
• - activites become limited due to pain

• scoliosis
• - asymmetric disk space as well as the larger osteophytes which develop in attempt to bear the weight of the body

- chronic systemic inflammatory disease that affects jts

- unknown- autoimmune mechanism is well established: formation of rheumatoid factor (RF)- an auto- antibody againt Ig G

• ?- activation of synovial macrophages and fibroblasts
• this results in the release of enzymes, acitvation and proliferation of chondrocyres and synovical cells, activation of osteoclasts
• activation of B lymphocytes (release of RF= deposition of immune complexes in jt

• All result in:
• -synovitis- marked unflam, cell proliferation
• - pannus formation- granulation tissue spreads
• - cartilage erosion- created an unstable jt
• - fibrosis-calcifies and obliterates jt space
• - anklyosis- jt fixation and deformity

• - boney deformities
• - ankylosis of jt
• - ulnar drift

• local:
• - affected jts extremely painful
• - stiffness of jt (especially in the morning)
• - redness and swelling of jts
• - jt involvement includes small jts and if often bilateral
• - jt movement impaired
• - eventually jt becomes fixed and dformed

• - fatigue
• - mild fever
• - anorexia
• - generalised lymphadenopathy

• - different from adult form
• - more acute onset
• - large jts frequently afftected

• - stills disease (systemic form)- fever, rash, lymphadoenopathy, hepatomegaly, in addition to jt involvemnt
• - second form of JRA causes polyarticular inflammtion
• - third form of JRA- four or fewer jts but causes uveitis (inflammation of iris, ciliary body and choroid of eye)

- infection of a jt that in turn causes arthritis

• - diret introduction of bacteria into jt eg trauma, non sterile injection or surgery
• - secondary infection due to bacteremia
• - gonococcus, staphylococcus, spirochete (lymes disease (tick bite)
• - usually dvelops in single jt
• - jt is red, swollen, painful and decreased movement

• - genetic factor (eg deficit of enzyme uricase) or poor renal excretion of urea
• - hyperurycemia
• - deposists of uric acid crystals in a jt
• - inflammation

• - intermittent course of disease
• - formation of tophus (nodule of precipitated urate crystal- in soft tissue causes local inflammtion, in jt bursae- extensor surface of forearm, pinnae of ear )
• - oftenaffects singe jt eg big toe

• - stiff, vertebra
• - cause is unknow (possibly autoimmune/ genetic)
• 

• - inflam of vertebral jts
• - fibrosis of jt, calcification and fusion of vertebra
• - lack of movement in the spine

• - back pain and stiffness (initally lower back)
• - with progression- lack of movement of the spine