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NURS 350 patho musc

Pathophys - musculoskeletal

4 bone cell types osteoblasts (mesenchymal origin)---osteoclasts (multinucleated, lysosomes, hydrolytic enzymes)---osteocytes (former blasts who are mature, now trappedin matrix it created)
bone is unique in that it doesn't form scar tissue when healing - forms new bone instead
which type of fracture is characterized by skin being broken open/compound fracture
what type of fracture broking in 2+ fragments comminuted fracture
what type of fracture runs parallel to long axis of bone linear
what type of fracture has damaged bone that is still in one piece incomplete fracture
Name 3 fractures in children greenstick (bends, perforates cortex, splinters spongy bone)---torus (cortex buckles, doesn't break)----bowing (involves pairs of bone radius/ulna, tibia/fibula where one has complete fracture and the other bends)
pathological fracture break at pre-existing abnormality by a force that wouldn't normally cause the bone to break
common causes of pathological fractures ***metastatic bone cancer---osteoporosis---infections---metabolic bone disorders
what is stress fracture fracture in bone that is repeatedly subjected to stress---atheletes/fatigue fracture---seen in bones without normal ability to deform and recover (insufficiency fracture)
Healing steps following bone breakages hematoma forms fibrous network---inflamm response/osetoblasts invade---granulation tissue (lengthen collagen, calcium deposition)---callus forms (osteoblasts/osteoclasts)---remodeling (xs callus resorbed, trabeular bone laid down)
What is end result of bone healing end result is new bone, not scar tissue, is formed
what is myoglobinuria----formerly known as rhabdomylosis life threataning complication of severe muscle trauma where excess myoglobin occurs in urine do to muscle damage
what are two forms of myoglobinuria compartment syndrome (local, less severe)----crush syndrome (most severe)
MOA of myoglobinuria muschle ischemia---edema---rising compartment pressure---tamponade/effusion ---muscle infarction/neural injury
causes of myoglobinuria viral infections---tetanus---heat stroke---strychnine poisoning---fractures---excessive exercise---status epilepticus---high voltage shock
recent cause of myoglobinuria complication of statin drugs used to lower cholesterol
complications of myoglobinuria renal failure---rigidity---tachy---dysrhyth---metab/respiratory acidosis---high body temp (43*C)
myoglobinuria can lead to these disease states cerebral edema, pulmonary edema, DIC=diseminated intravascular coagulation/bleeding----hypovolemic shock
osteoporosis definition reduced bone mass/density ----bone histologically/biochemically normal, but note enough of it to maintain skeletal integrity---spongy/trabelular bone exceeds loss of compact/cortical bone
what is most common metabolic disease/problem for older women osteoporosis - men get it too as they age
postmenopausal osteoporosis due to reduced estrogen---which activates RANKL cytokines who then ---bind RANK ---lack of apoptosis of clasts---increased resorption/bone loss
senile osteoporosis insufficient calcium intake/malabsorption---shrinking of blasts/clasts with decreased actions
risk factors for osteoporosis - vitamins and lifestyle deficits in Vit C and Vit D---caffeine, nicotine, ETOH
risk factors for osteoporosis - hormonal excessve TH---PTH---cortisol---GH
OPG function is a decoy receptor of RANKL. When it binds RANKL, it deactivates it's activity---decreases clasts activity---decreases bone resorption/loss
RANKL function is a cytokine, member of the TNF family, which is expressed by blasts/clast precursors---needed for clast development
MOA of RANKL activates RANK receptor on clasts---supress apoptosis---increase survival/activaton of clasts
what regulates the balance between RANKL and OPG cytokines and hormones
What does RANK do again? it is a receptor on clast - when bound by RANKL, clast is activated and its apoptosis is supressed
there is an inverse relationship between estrogen and RANKL. if estrogen at higher levels. . . Increased estrogen---RANKL expression decreased/OPG decoy production increased----decreased clast activity
estrogen and RANKL inverse relationship. if estrogen at lower levels lower estrogen ---increased RANKL/decreased OPG---clasts activated
take home message estrogen/RANKL increased estrogen/decreased RANKL/decreast clast activity -----decreased estrogen/increased RANKL/increased clast activity
what is osteomalacia inadequate/delayed mineralizaiton of bone. normal volume of bone that is soft osteioid instead of rigid bones----remodeling cycle is normal, but calcifaction/deposition doesn't occur
osteomalacia is to adults as Rickets is to children (normal bone size, soft/decalcified)
pathophys of osteomalacia lack of Vit D ---> dec Ca --> stimulates PTH ---> increased serum Ca BUT PHOSPATE LOST IN URINE
so, what specifically causes the lack of calcification in osteomalacia low PHOSPHATE levels prevent calcification
paget's disease - etiology unknown with this MOA INCREASED metabolic activity of bone --- excessive remodeling ---SOFT/ENLARGED bones
osteomyelitis ---infections bone disease difficult to treat ---inflamm cells can't penetrate channels---capilarries of bone sensitive to bacterial toxins ---bone cells limited capacity to replace bone DESTROYED BY INFECTION
most common joint disease osteoarthritis---degeneration and loss of periosteium/articular cartilage in synovial joints
forms of OA ***secondary, associated with known risk factors of joint stress, congenital, trauma-------------***idiopathic - associated with age-proteoglycans in cartilage decrease/genetic component
both forms of OA manifest as erosion of articular cartilage---sclerosis of underlying bone---formation of bone spurs
OA pathophys cartilage breaks/wears off---unprotected bone scelerotic---cysts develop in underlying bone and communicate with fissures in cartilage---cyst forms/ruptures/spills contents into cynovial cavity----cartilage coated bone cells grow outward/spurs
OA what happens when spurs break off they fall into synovial cavity---irritate synovial cavity---irritate synovial membrane
major class of classic inflammatory joint disease commonly called arthritis ---characterized by inflamm damage to sinovial membrane/articular cartilage. typical signs of inflamm
RA definition and SOA autoimmune - chronic inflammation of CT ---mostly joiunts, also lungs/heart/skin
progression of RA synovial mem affect---then inflam spreads to articular cartilage/fibrous joint capsule/surrounding ligaments/tendons---pain, joint deformity/loss of funciton
joints most affected in RA fingers/feet/wrist/ankles/knees----shoulders/hips/cervical spine possibly
does RA effect heart, lungs,kidney and skin yes, either primary to RA or secondary to tx
MOA RA unidentified antigen in genetically susceptible with aberrant immune response ---long term exposure creates auto-antibodies that attack host.
Can we test for RF (rheumatoid factors) yes, transformed antibodies can be identified in lab
RA - how does immune complex deposit trigger inflamm response cartilage is damaged by activation of CD4s---cytokines activate Bcells---inflamm cells recruited into lining region ---cycle of signal transduction/cytokine release---activated Bcells make more autoantibodies (RFs)---Tcells perpetuate inflamm---
is RANKL involved in RA yes, RANKL released with osteocyst (osteoclast?) activation
In RA, self-antigens are always there. Inflamm and immune complex formation can occur indefinitely . . .this leads to leads to thickening of synovial membrane---occlusion of microvasculature---hypoxia/metabolic acidosis---acidosis cause further enzyme release from synovial cells---erode articular cartilage/inflamm ligaments/tendons
in RA the inflamm ultimately causes causes hemorrhage---coagulation---fibrin deposition on synovial membrane and in synovial fluid
In RA, the final process that ultimately immobilies the joint fibrin develops into granulation tissue = pannus-----pannus formation leads to scar tissue, which immobilies joint
what is ankylosing spondylitis systemic immune inflamm disease characterized by stiffening and FUSION of spine & sacroiliac joints
in RA we get destruction of synovial joints. In ankylosing spondylitis, where is the SOA SOA is enthesis (insertion point) where ligaments/tendons/joint capsule are inserted into bone
what is end result of ankylosing spondylitis fibrosis-ossification and fusion of the joint
what is gout inflamm syndrome with high levels of uric acid in blood (hyeruricemia) AND in other body fluids INCLUDING SYNOVIAL FLUID
MOA of gout uric acid crystallizes, deposits in CT (or kidney stones)---crystals in synovial fluid---gouty arthritis
gout pathophysiology linked to purine metab/renal function----purine nucleotides (cAMP, ATP, cGMP, etc)break down --> overproduction of uric acid/salts-->salts filtered at glomerulus -->reabsorbed/excreted in renal tubules
gout - if uric acid salts not excreted then they form crystals which are deposited in synovial fluid/joint by unknown MOA
Created by: lorrelaws