NUR 0012 Lecture 15 Anatomy and Physiology 1 Lecture: Jake DechantOutline of Last Lecture I. Ch. 6 continuedA. Hydroxyapatite B. Intramembranous ossificationC. Endochondral ossificationD. Bone growthE. Bone remodeling and calcium homeostasisOutline of Current Lecture I. Ch. 6 wrap upA. Other hormones and growth factors impact boneB. NutritionC. Mechanical remodelingD. Bone repairE. Bone pathologiesF. Fracture typesCurrent LectureI. Ch. 6 wrap upA. Other hormones and growth factors also impact bone1. Growth hormone (GH)a. Hyposecretion: dwarfismThese notes represent a detailed interpretation of the professor’s lecture. GradeBuddy is best used as a supplement to your own notes, not as a substitute.b. Hypersecretion: gigantism or acromegaly in adulthood2. Thyroid hormone (TH): maintains metabolic rate3. Sex hormones (testosterone, estrogen, progesterone): initially spark bone growth during puberty, but also cause epiphyseal plates to ossifyB. Nutrition: vitamin D and C can affect bone growth and development1. Rickets: lack of vitamin D in children2. Osteomalacia (adult rickets): insufficient vitamin D in adults3. Scurvy: vitamin C is essential for synthesis of collagenC. Mechanical remodeling1. Wolff’s Law: bone remodels in response to mechanical stress2. Compact bone will thicken where there is the most stress3. Spongy bone will develop stress linesD. Bone repair: requires good blood flow1. Hematoma forms: blood vessels and surrounding periosteum are damaged forming a hematoma2. Fibrocartilage callus forms: blood vessels and uncommitted cells invade fracture site forming a clota. Phagocytes clean up damaged tissuesb. Fibroblasts and osteoblasts restructure bonec. Fibrocartilage callus forms to splint the bone3. Bony callus forms: new bony trabeculae begin to form inside fibrocartilage callusa. Gradually entire callus is converted to spongy bone4. Bone remodeling occurs: begins during bony callus formation and continues for several monthsa. Excess bone is removed and the fracture site is remodeled to original formE. Bone pathologies1. Hormone induced: pituitary dwarfism/gigantism, acromegaly2. Achondroplastic dwarfism: normal trunk but small limbs3. Osteogenesis imperfecta: insufficient collagen synthesis and brittle, sometimes curved bones4. Bacterial infections: osteomyelitis can infect bone marrow5. Tumors can be malignant or benign6. Decalcification/bone loss: osteomalacia (adult rickets) leads to softening of bones and osteoporosis leads to porous boneF. Fracture types1. Comminuted: bone fragments into 3+ pieces, common in aged more brittle bones2. Compression: bone is crushed, common in porous (osteoporotic) bones3. Spiral: common sports fracture, ragged break occurs when excessive twisting forces are applied4. Epiphyseal: epiphysis separates from diaphysis along epiphyseal plate, tends to occur where cartilage cells are dying and calcification of matrix is occurring5. Depressed: broken bone portion is pressed inward, typical skull fracture6. Greenstick: bone breaks incompletely, only one side of shaft breaks the other side bends, common in children whose bones have relatively more organic matrix and are more flexible than those of adults7. Others: open vs. closed and displaced vs.
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