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25 Cards in this Set
- Front
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Bone Composition (adult bone).
Describe the two components |
-Organic component of the matrix:
-Osteoid: an organic chemical |
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Describe the organic component
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-Organic component of the matrix:
-1/3 of extracellular matrix is comprised of organic materials -Typically the cells: osteocytes (cell) osteoblasts(forms), osteoclasts (destroys) -made of collagen and proteoglycans (like inside of the basement membrane in renal) -Osteoid: an organic chemical -What this structural element does is adds flexibility to bone -allows bone to twist a little d/t geometric arrangement here -does NOT add strength to the bone |
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Describe the inorganic component
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-Inorganic component of the matrix:
-2/3 of extracellular matrix -made of hydroxyapatites (mineral salts of calcium and phosphate) -gives bone its hardness |
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Describe the three steps in BONE FORMATION AND DEVELOPMENT
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1)Bones develop from fibrous membranes and cartilage (essentially these by 6 weeks)
2)Bone growth through early adulthood: a) Longitudinal growth: grow bone longer (genetic) b) Appositional growth: increase or decrease size of the end of a long bone (physiologic). Could be due to amt of weight placed on bone. Appositional decrease/loss can occur when you try to lose weight. 3) Remodeling and repair =Within a week, you recycle 5-7% OF BONE MASS every week; ie. There is calcium entering and leaving bone on a daily basis(= 0.5 G CALCIUM enters and leaves bones daily) deposition and resorption see below. -----bone deposition and resorption occur at periosteal and endosteal surfaces you will get the above via osteoclasts and osteoblasts at above surfaces |
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Describe BONE DEPOSITION
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1)DEPOSITION- bone formation via osteoblasts; *need proteins,
*Vit. C for collagen (in the osteoid; gives flexibility. If you don’t produce collagen, the bones are non flexible=susceptible to fx), *Vit. A as a cofactor, and *Ca and phosphate mineral salts (to give strength) |
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Describe BONE RESORPTION
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Resorption: bone destruction/bone degrading via osteoclasts
-the organic matrix is destroyed (dissolved from lysosomal enzymes) -have to degrade the hardened mineral salts via metabolic acids: - converts Ca salts to soluble form Ca -can have some phagocytosis of byproducts *Must have balance of deposition and resorption -If rate of resorption exceeds rate of depositionbone becomes brittle -anything that alters the rate of activation or activity of osteoclast or osteoblast ultimately alters the way a bone is |
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describe Ca balance (hormonal control of the Ca level in your blood)
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If high blood calcium, you would want to form bone to remove Ca from the blood:
Thyroid (parafollicular cells) release calcitonin (hormone that is secreted) osteoblasts activated stimulate bone formation/deposition of the Ca in bone If have low Ca in blood, you would want to destroy bone to get Ca into blood stream: Parathyroid glands release parathyroid hormone (PTH) activates osteoclasts (cells to destroy bone) stimulate bone resorption (destroys the matrix; releases those mineral salts so that calcium will enter the blood) |
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describe Ca balance (hormonal control of the Ca level in your blood) again
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3)Ca balance
----Thyroid (paraollicular cells) release calcitonin-bone deposition (osteoblasts) ----parathyroid glands release parathyroid hormone, osteoclasts on diagrahm have a bunch of ca, not good, it is reactive. You get calcitonin, which stimulates calcium salt deposition have decrease in ca levels, stimulates thyroid gland, stim pth, osteoclasts bone matrix and release ca++ into blood (((know right here the thyroid/parathyroid gland Estrogen mediates pth-causes an inhibition of pth, so you do not have increased osteoclasts. If you are post menopausal, =no estrogen=increased pth=increased osteoclasts which degrade bone matrix and release ca into blood. Making bone more suceptable to fracture. |
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List 5 Bone disorders
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1)Fracture: complete or partial
2)Osteoporosis: resorption outpaces deposition 3)Osteomalacia: bones are not mineralized adequately/not hardened 4)Paget’s Disease: excessive and abnormal deposition and resorption (a lot & fast) 5)“0steomyelitis: inflammation of bone and bone marrow (inflammatory condition) |
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describe fracture
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Multiple kinds, broken a bone, recede it so you can get bone deposition, want osteoblasts to deposit stuff into it, want the collagen there
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describe B) OSTEOPOROSIS
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Osteoporosis: resorption outpaces deposition (increased osteoclast activity)
-makes bones porous and light weight (the weight that should have been provided by mineral salts has been degraded) Estrogen mediates PTH activity. (REM: PTH activates osteoclasts.) Without estrogen, PTH goes unregulated. Note: post menopausal women don’t produce estrogenosteoclasts unrulybones brittle & susceptible to fx. Main reason for estrogen replacement therapy (but there are potential complications of ERT including breast CA) |
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describe osteomalacia
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Osteomalacia: bones are not mineralized adequately/not hardened-weak and soft
-called Ricketts in children (In adults is called osteomalacia) -Ca insufficiency and Vitamin D deficiency (esp in Ricketts) |
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describe paget's disease
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Paget’s Disease: excessive and abnormal deposition and resorption (a lot & fast)
“Pagetic bone” (high ratio of spongy to compact bone) -bones are soft and weak -have poor mineralization -seen after 40 years of age -caused by virus (most common), tumors, vascular disorders (inadequate blood flow) reversable |
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Describe osteomyelitis
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inflammation of bone and bone marrow (inflammatory condition)
-caused by pus forming bacteria |
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what are the characteristics of Muscular Dystrophy?
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•Characterized as a “Metabolic defect” type of disorder.
•Muscle ultimately will degenerate necrosis; •Because of the metabolic defect remaining, the muscle cells are replaced by fat/connective tissue cells. Group of muscles that was supposed to contract cannot. |
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How is MD diagnosed?
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•Diagnosed by:
oEMG (electromyography) oBiopsy (check for/see degenerating muscle) oCreatine phosphokinase: (Kinase phosphyrlase) This should be inside cells; degraded muscles release this enzyme into the blood stream. |
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List the four types of Muscular Dystrophy
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1)Duchenne’s (20 year)
2)Laundouzy 3)Myotonic 4)LimbGirdle |
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Describe Duchenne's:
inheritance onset area progress |
Duchenne’s
X-linked on x chromosome onset= 2-3 yrs old, death at 20 area=Hip, leg affected 1st Progress=Rapid |
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Describe Laundouzy MD
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Laundouzy
inheritance: Autosomal Dominant Onset: Before 20 AREA: Shoulder/face Progression: Slow-moderate |
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Describe Myotonic MD:
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INHERITANCE:Autosomal Dominant (19th chromosome)ONSET: birth – 50 yrs
AREA: face/hands PROGRESS: slow |
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Describe Limb Girdle MD:
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NHERITANCE:Autosomal Recessive
ONSET:any age AREA:shoulder/pelvis PROGRESS: variable |
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there are 3 degrees of muscle strain, Describe 1st degree.
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1)1st degree (bench press manouvar)
manifestations-overstretched muscle so cant have cross bridges formed due to loss of actin/myosin overlap, muscle painful Treatment---24 -48 hours of ice b/c ice slows metabolism causing it to slowly begin to go back to the way it was supposed to be (heat would kick up the metabolism causing it to do work) |
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there are 3 degrees of muscle strain, Describe 2nd degree
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2) 2) 2nd degree muscle strain (have strain and bruising involved)
manifestations-overall whole muscle intact with tearing of muscle fibers treatment-above plus drugs antiinflamatory, alter ice and heat due to inflammatory response (hot-get more blood flow in order to repair the tear, you need to get the stuff there to heal it. ) |
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there are 3 degrees of muscle strain, Describe 3rd degree
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3) 3rd degree muscle strain (due to trauma of some kind)
-manifestations=tearing, rupture, bleeding -treatment=surgery, immobilize-to decrease metabolism. |
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what is uses of hot and cold for strain?
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Cold= decreases the metabolism of the strained muscle; reduce metabolic pathways of muscle; reduce need for O2, etc.
Heat = brings blood flow to site for the “torn” fibers—these need to heal with the flow |