TEST 4: Musculoskeletal Flashcards
Bone cells
(Lecture, p.1402)
Bone cells enable bone to grow repair itself, change shaped and synthesize new bone tissue and reabsorb old tissue
- Osteoblasts: responsible for bone formation through ossification and osteogenesis
Osteoid = no mineralized bone matrix
- Osteocytes= mature bone cells
-“bone in maintenance”
-Lacunae: spaces
-Canaliculi: canals - Osteoclasts: responsible for bone reabsorption and remodeling
Bone matrix
(Lecture, p.1405)
-Is made of the extracellular elements of bone tissue, specifically collagen fibers, structural proteins, carbohydrate- protein complexes, ground substance, and minerals
-Is 35% collagen and proteoglycan
-Like rebar, flexible strength
-If this is missing bone is brittle
-Is 65% mineralized bone (hydroxyapatite)
-The cement, weight bearing strength
-If missing bone is too flexible
Phases of Bone remodeling
(Lecture, p. 1407)
Quiescent (nothing is happening, restored bone)—> activation (phase 1, a stimulus activates cytokines to form osteoclasts)—> resorption (osteoblasts eating away old bone)—> formation (osteoblasts mature and help make new bone) —> mineralization (new matrix osteoblasts form is mineralized with calcium and phosphorus)
Factors that affect bone growth
(Lecture)
Nutrition:
-Vitamin D is needed for the absorption of calcium from the intestines (insufficiency results in the softening of bones)
-Ie rickets (children) osteomalacia (adults)
-Vitamin C is needed for collagen synthesis by osteoblasts (insufficiency results in scurvy)
Hormones:
-Growth hormone, thyroid hormone, estrogen, and testosterone
-Exercise and weight training
Factors that regulate bone remodeling
(Lecture, p. 1409)
-Is a balance between bone reabsorption (osteoclasts) with bone formation (osteoclasts)
-There must be a balance to maintain stable bone mass
The process can be altered by:
-Menopause related hormone changes
-Age related factors
-Changes in physical activity
-Drugs (steroids)
-Secondary diseases (renal)
3 types of Arthritis
(Lecture, p. 1452)
Spondylitis: inflammatory process that results in fibrosis, ossification
-The fusion of spine and and sacroiliac joints due to uncontrolled bone formation
-Genetic association with HLA
Osteoarthritis: loss, damage of weight bearing synovial joints
-Articular cartilage and joint capsule of central and peripheral joints
Rheumatoid arthritis: inflammatory, joint swelling and tenderness
-Synovial joint destruction
-Autoimmune
Ankylosing Spondylitis (AS)
(Lecture, p. 1459)
-Chronic inflammatory disease of the axial spine, arthritis of the spine!
-Risk factors: genetic (HLA-B27), more common in men than women, onset is 20-40 years old
-Manifestations: pain, stiffness in neck and lower back
-Patho: immune mediated inflammation
-Develop boney protuberances and erode the disc space—> Can result in fusion of vertebrae in spine
Osteoarthritis
(Lecture, p. 1452)
-Characterized by pathological changes in cartilage, bone, synovium, ligament, muscle, and periarticular fat.
-Most common form of age related joint disease involving synovial joints
-Chronic inflammation
-Risk factors: age, previous injury, obesity
-Manifestations: gradual pain aggravated by activity, stiffness lasting <30 mins after awakening or activity, occasional joint swelling
-Patho: synovial joint experiences local areas of damage to articular cartilage, new bone formation of joint margins, bone hypertrophy, bone thickening of the joint capsule
-Cartilage is worn down
Rheumatoid Arthritis
(Lecture, p. 1455)
-A chronic, systemic inflammatory autoimmune disease distinguished by joint swelling, tenderness, and destruction of synovial joints leading to disability.
-Risks: genetics, T cell abnormalities, autoantibody formation (IgG and IgM), more common in women, diagnosed between 35-50 years old
-Manifestations: symmetric joint swelling in hands/ wrists and large joints, pain unrelated to rest or use (improves over the course of the day)
-Patho: cytokine related inflammation (arginine—> citrulline) of synovial membranes —> articular cartilage, joint capsule, ligaments, and tendons—> thickening of articular membrane—> vascular changes (increased enzyme destruction)—> fibrin deposition
GEM— citrulline is considered an antibody and CAN be tested for to diagnose this
Osteoporosis
(Lecture, p. 1437)
-Characterized by low bone mineral density caused by altered bone microstructure that leads to an increased risk of fractures
-Risk: post menopausal, dietary changes that decrease calcium and vitamin D, decreased level of activity, low BMI, hormones (PTH, thyroid, cortisol, GH), medicines, alcohol, tobacco
-Post menopausal= decreased estrogen, increase ROS—> clasts—> blasts
-Manifestations: usually diagnosed with fractures, bone mass <648mg/cm2 measured with dual energy xray absorptiometry (DXA)
-Normal bone mass= 833 mg/cm2
How do we get osteoporosis?
(Lecture, p.1439)
we need a video on this, explained poorly
Bone destruction:
-RANKL (protein produced by osteoblasts): plays a role osteoclast formation, function, and survival
-RANK (receptor that RANKL will find) located on osteoclast precursors and mature osteoclasts
Bone protection:
-Osteoprotegerin (OPG): produced by osteoblasts, binds to and inhibits RANKL, protects against bone loss
Scoliosis
(Lecture, p.1484)
Is a rotational curvature of the spine
Classified as either—>
-Non structural: cause other than the actual spine (ie posture, leg length discrepancy, pain)
-Structural: associated with vertebral rotation
Can be: congenital, neuromuscular, trauma, bone and joint disorders, idiopathic (70%)
Patho: CNS abnormality involving balance (reticular system), curve increases most rapidly during period of growth
-Severity of curvature:
< 40 degrees = risk of progression is small
> 50 degrees = spine is biochemically unstable
> 80 degrees = decrease in pulmonary function
GEM— this is mainly a kid problem having to do with rapid growth spurts
Motor units for contraction
(Lecture, p.1414)
-Are comprised of multiple fibers innervated by a single motor neuron
Muscle patho
(Lecture)
Atrophy: a decrease in size or cell of tissue
-results from disuse, severing the nerve supplying the muscle
-Myofibrils will decrease in size (bones don’t atrophy but the density may decrease?
Strain: a trauma to muscle or tension when stretched beyond limit (may involved a tear/ rupture—> inflammation—> pain/ swelling)
Muscular dystrophy overview
(Lecture)
-Disease associated with progressive loss of muscle function
-Many types with distinct features
-Typically genetic in origin (mutation of muscle specific genes)
-Usually limited treatment options
Underlying patho of all dystrophies:
-Dystrophin anchors actin cytoskeleton to basement membrane of skeletal muscle fibers
-The absence of dystrophin results in poorly anchored fibers torn apart during muscle contraction—> calcium enters the cells—> cell death, fiber necrosis—> degeneration of muscles
