Patho MSK

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Formation of bone through ossification or osteogenesis. Primary job is to lay down new bone.

Osteoblasts

Osteoid

Non-mineralized bone matrix

Osteoblast produce collagen and non-collagen proteins that make

Osteoid

Osteoblast and Osteocytes control

Osteoclast differentiation and bone resorption

Osteocytes

Mature, abandoned bone cells that become trapped by a space in the hardened bone matrix (Lacunae) involved in bone maintenance.

Canaliculi

Bone canals

Osteoclasts

Responsible for bone resorption and remodeling

Communicating cells that signal to osteoblasts and osteoclasts when and where to form new bone

Osteocytes

Osteocytes communicate to other Osteocytes through

Canaliculi

Osteoblast are derived from

Multipotent mesenchymal stromal cell (MSC)

Osteoclasts are derived from

Hematopoietic stem cell (HSC)

Myoblast is derived from

MSC

Derived from MSC and can differentiate into Chondrocytes

Osteochondral progenitor

Organic bone matrix

Collagen and Proteoglycans (35% of bone)

Inorganic Bone Matrix

Hydroxapatite (65% of bone) known as mineral of bone

Steps of Bone Remodeling

1. Quiescent 2. Activation 3. Resorption 4. Formation 5. Mineralization

Bone Matrix Flexible Strength

Organic: Collagen and Proteoglycans

Osteogenesis Imperfecta

Genetic disease affecting collagen production

Bone Martix Weight-Bearing Strength

Inorganic: Hydroxapatite

Bone outer surface. Double layer connecting tissue.

Periosteum

Lines bone cavities

Endosteum

Bone Shaft. Compact Bone.

Diaphysis

Compact Bone

85% of Skeleton

Spongy Bone

15% of Skeleton

End of Bone. Cancellous bone (spongy bone)

Epiphysis

Growth Plate

Epiphyseal Plate

Difference between young and adult bone

Young bone has Red Marrow only and Epiphyseal plates

Necessary for Ca absorption in intestines. Insufficiency causes Rickets and Osteomalacia (soft bones)

Vit D

Necessary for collagen synthesis by Osteoblasts. Deficiency causes Scurvy.

Vit C

Growth hormone from anterior pituitary regulates bone growth

Parathyroid Hormone

Hormone required for growth of all tissues

Thyroid hormone

Sex hormones involved in bone growth

Estrogen and Testosterone

Strong association with HLA-B27 antigen. HLA-B7 in blacks.

Spondylitis

Autoimmune associated with HLA-B27 gene. Inflammation of fibrocartilage and erosion. Repair and scar tissues. Calcification leading to joint fusion.

Spondylitis

Early symptoms: low back pain (early 20s), progressive leads to stiffness, pain, restricted motion. Loss of lumbar curvature (lordosis) and increased concavity of upper spine (kyphosis). Can also affect the eyes, aorta, tendons, and lungs.

Spondylitis

Idiopathic, Genetic, biochemical and biomechanical stress

Osteoarthritis

Local area of loss of cartilage, pro-inflammatory cytokines, joint thickness, Hallmark sign osteophytes (bone spurs), synovitis (inflammation)

Osteoarthritis

Pain worse with activity, stiffness diminished with activity, joint swelling, tenderness, limited mobility, deformity

Osteoarthritis

Multifactorial with strong genetic predisposition (HLA-DR4)

Rheumatoid Arthritis

Primary site synovial membrane, Ab formed against joint (RA factor). Type IV Hypersensitivity (T-cell mediated), Cytokines (TNF-a)—> cartilage/bone destruction, granulation tissue (pannus)

Rheumatoid Arthritis

Gradual onset affecting joints starting in wrists and fingers, symmetrical joint involvement, morning stiffness (>30mins), joint deformities, subcutaneous nodules. Labs: RF and ANA.

Rheumatoid Arthritis

Risks: Aging, low estrogen and testosterone, low Vit D, sedentary lifestyle. excess caffeine, phosphorus, alcohol, nicotine. glucocorticoids. low BMI. Family Hx. Endocrine disorders.

Osteoporosis

Manifestations: bone aches, weakness and deformities, fractures.

Osteoporosis

Low estrogen—>decreased OPG—>increased RANKL—> class formation and decrease class apoptosis and estrogen needed for extracellular kinases (ERKs) to decrease apoptosis blasts and increase apoptosis clasts not balanced

Osteoporosis

More likely to manifest with muscular dystrophy and cerebral palsy. Clinically significant curvature > 25-30 deg and >45-50 deg severe

Scoliosis

Caused my gene mutations affecting muscle protein such as dystrophin. Muscle fiber dropout; muscle cell apoptosis or necrosis; inflammatory cytokines; regeneration; fibrosis formation; fatty infiltration and replacement. Muscles loose function.

Pathophysiology of Muscular Dystrophy

Mutation in dystrophin (anchor protein for skeletal muscle cells)

Duchenne MD

Poorly anchored muscle fiber torn easily due yo muscle contraction. Ca overload. Cell death, fiber necrosis and apoptosis. Inflammatory cytokines released, increased central nuclei, fibrosis, fiber splitting, regeneration, fatty infiltration

Duchenne MD

First: muscle weakness that begins with hips, pelvis, and legs. Difficulty standing, walking, or sitting. Unsteady gait. Walking on toes or balls of feet. Affecting heart, lungs, and diaphragm.

Etiology: Aging, physically inactive, unhealthy diet

Sarcopenia

Nutritional, hormonal, metabolic immunological factors affect muscle, reduce muscle mass and strength

Sarcopenia

Muscle weakness, decreaed mobility, increased falling/loss of independence

Sarcopenia

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