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NURS 350 patho musc
Pathophys - musculoskeletal
| Question | Answer |
|---|---|
| 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
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