The flashcards below were created by user
jessiekate22
on FreezingBlue Flashcards.
-
What is the function of a bone?
- - support, framework and protection
- - hematopesis (bone marrow)
- - involved in Ca metabolism and storage
-

-
What is the bone structure?
- - 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
-
What is bone remodelling?
- - 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)
-
How is bone remodelling controlled?
- - 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
-
What is local tissue signalling factors?
- - 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
-
How does bone grow?
- - 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.
-
What happens after bone fracture?
- 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

-
Which factors affect healing after bone fracture?
- Amount of damage
- Age
- Infection
- Systemic disease affecting circulation (eg diabetes)
- Mm spasm
-
What are possible complications of bone fractures?
- Ischemia
- compartment syndrome (compresion of nerve, blood vessels, and mm tissue> lack of O2> tissue death)
- Fat emboli
- Nerve damage
-
What os osteoporosis?
- - metabolic disorder, when bone resorbtion exceed bone formation.
- - causes decrease in bone matric and mineralization
-
What are the forms of osteoporosis?
- - primary- postmenapausal, senile, idiopathic
- - secondary-following other condition (eg crushing syndrome)
-
What are the risk factors of osteoporosis?
- Age- decrease osteoblastic activity
- decrease mobility- decrease mechanical stress stimulus
- Hormonal- hperparathyroidism, crushing syndrome, catabolic glucocoricoids
- nutrients- decrease calcium, vit D, protein, malabsorption sndromes
-
What are some of the clinical features of osteoporosis?
- - normal boney density 833mg/cm2- osteopenia 833-648, osteoporotic <648
- - back pain
- - kyphosis/ scoliosis- fractures- haunch
-
How do you manage osteoporosis?
- - increase Ca and Vit D intake
- - exercise
- - inhibitors of bone resorbtion
- - hormonal therapy
-
What are ricets and osteomalacia?
- both are metabolic bone disorders that are expressed as reduced bone mineralization
-
What is the main cause of rickets and osteomalacia?
- - dietary problems
- - malabsorption
- - lack of sun exposure
-
What is the process of ricket/ osteomalacia?
- - 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
-
-
-
What is the neural control of skeletal mm?
- - 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
-
What is the neuromm junction?
- - 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
 
-
What are the synaptic vessels at the nerve end terminal filled with?
Ach- acetilcholine
-
What activates ACh?
- cholinesterase
- this then allows pores to open and the AP to be transmitted
-
Phasic and tonic mm contractions
-
What are teh chemical agents that have effects on the transmission of messages for mm contraction?
-
What sensory receptros are present in the mm tendons?
- - golgi tendon organ- detects tension
- - mm spindle- detects changes in mm length

-
What is a reflex?
- - 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
-
Which areas of the brain control skeletal mms?
- - 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
-
High motor control- corticospinal (pyramidal) pathways
-
What tract controls mm contractions etc?
- corticospinal tract

-
What is mm dystrophy?
- a group genetic disorder that manifests as degneration of skeletal mm
-
What causes mm dystrophy?
- - mutations in dystrophin gene
- - dystrophin is a protein located in the membrane of mm fibres. Essential for maintaining cell shape and survival
-
What is the pathogenesis of mm dystrophy?
- - lack of dystropin
- - degeneration and necrosis of mm cells
- - mm cells replaced by fat and fibrous connective tissue
- - mm weak or cannot contract
-
-
What are the clinical signs of mm dystrophy?
- - mm weakness
- - tendon reflexes reduced
- - vertebral deformities
- - respiratory insufficience > lung infection
- - cardiac abnormality
- - mental retardation
Death usually before 20 due lung and heart failure
-
What is upper/ lower motor neurone dyndrome?
-
How are jts classified and what are the three types?
- - classified by the degree of movement
- - synarthroses- immovable (eg cranial sutures)
- - Amphiarthroses- slightly movable (eg ribs to sternum)
- - siarthroses (synovial)- freely movabble (shoulder)
-
What is the structure of a synovial jt?
- - 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

-
What are non-traumatic jt injuries?
- - overuse injuries such a tennis elbow
- - repetitive strain injuries (carpal tunnel syndrome)
-
What are traumatic jt injuries?
- - jt dislocation
- - injuries of tendons and ligaments
-
What is the pathogenesis of jt injuries?
trauma- inflammation- granulation tissue- collagen fibres- fibrous tissue
-
What are the classifications of tendon and ligament injuries?
- - strain- tear in a ligament
- - sprain- tear in a tendon
- - avulsion- detachment from a bone
-
What are the causes and signs and symptoms of lig and tendon injuries?
- traumna or excessie mm force
- pain, swelling, limited movements
- low blood to area- > 6w to heal
-
What is osteoarthritis?
- - degenerative jt disease
- - cause unknown- possibly genetic
-
What is the pathophysiology of osteoarthritis?
- - 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

-
What are the signs and symptoms of osteoarthritis
- - aching pain with Wb and movement
- - jt movement is limited
- - activites become limited due to pain
-
What will OA of the spine result in?
- scoliosis
- - asymmetric disk space as well as the larger osteophytes which develop in attempt to bear the weight of the body
-
What is rheumatoid arthritis?
- chronic systemic inflammatory disease that affects jts
-
What are the causes of RA?
- unknown- autoimmune mechanism is well established: formation of rheumatoid factor (RF)- an auto- antibody againt Ig G
-
What is the patho of RA?
- ?- 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
-
What are the pathologic changes in jt of RA?
- boney deformities- - ankylosis of jt
- - ulnar drift
-
What are the signs and symptoms of RA?
- 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
-
What are the systemic signs and symptoms of RA?
- - fatigue
- - mild fever
- - anorexia
- - generalised lymphadenopathy
-
What is juvenile RA?
- - different from adult form
- - more acute onset
- - large jts frequently afftected
-
What are teh three types of JRA?
- - 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)
-
What is infectious (septic) arthritis?
- infection of a jt that in turn causes arthritis
-
What are the causes of infectious septic 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
-
What is the pathogenesis of gout? (gouty arthritis?)
- - genetic factor (eg deficit of enzyme uricase) or poor renal excretion of urea
- - hyperurycemia
- - deposists of uric acid crystals in a jt
- - inflammation
-
What are some clinical feature of gouty arthritis?
- - 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
-
What is ankylosing spondylitis?
- - stiff, vertebra
- - cause is unknow (possibly autoimmune/ genetic)

-
What is the pathogenesis of ankylosing spondylitis
- - inflam of vertebral jts
- - fibrosis of jt, calcification and fusion of vertebra
- - lack of movement in the spine
-
What are the signs and symptoms of ankylosing spondylitis?
- - back pain and stiffness (initally lower back)
- - with progression- lack of movement of the spine
|
|