Download AAOS Comprehensive Orthopaedic Review by Jay R Lieberman MD PDF

By Jay R Lieberman MD

Designed to arrange orthopaedic citizens for the Orthopaedic In education examination (OITE), and the yankee Board of Orthopaedic surgical procedure (ABOS) Board Certification exam, this ebook is gifted in an easy-to-read define layout for speedy overview and prepared entry to big evidence. Dr. Lieberman and his editorial group of Board-certified orthopaedic surgeons constructed this thorough textual content in a concise define structure, supplying you with prepared entry to the $64000 evidence and a short bulleted overview of the techniques you want to know.AAOS accomplished Orthopaedic overview bargains sweeping insurance of the middle of orthopaedic wisdom that spans the spectrum of the orthopaedic specialties. collected in a single handy and accomplished textual content, you will discover the categorical info you must organize to your exam. geared up by means of uniqueness, all the 122 chapters is loaded with colour photos, illustrations, tables, and charts to aid the fabric and assist you maintain the knowledge

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Kinematics describes the motion of objects without regard to how that motion is brought about. 1. In general, kinematics is concerned with the geo- metric and time-dependent aspects of motion without considering the forces or moments responsible for the motion. 2. Kinematics principally involves the relationships among position, velocity, and acceleration. 3. Knowledge of joint kinematics helps in under- standing an articulation. As an example, this is important for the design of prosthetic implants to restore function and to understand joint wear, stability, and degeneration.

8 g/cm3. ii. 0 g/cm3. f. With aging, a progressive net loss of bone mass occurs beginning in the fifth decade and proceeding at a faster rate in women. This results in reduced bone strength, a reduced modulus of elasticity, and increased likelihood of fractures. g. Several radiographic studies have suggested that aging is associated with bone remodeling that affects force distribution. i. Subperiosteal apposition of bone occurs along with endosteal absorption in tubular bones, creating a cylinder of larger diameter.

3. The noncoding sequences contain promoter re- gions, regulatory elements, and enhancers. About half of the coding genes in human genomic DNA are solitary genes, and their sequences occur only once in the haploid genome. 4. Directionality—Single-strand nucleic acid is syn- AMERICAN ACADEMY OF ORTHOPAEDIC SURGEONS Chapter 1: Cellular and Molecular Biology, Immunology, and Genetics Table 3 Genetic Defects Associated with Metabolic Bone Diseases and Connective Tissue Disorders Genetic Disorder Genetic Mutation Functional Defect Characteristic Phenotypes X-linked hypophosphatemic rickets A cellular endopeptidase Vitamin D–resistant rickets Rickets, short stature, and impaired renal phosphate reabsorption and vitamin D metabolism Hypophosphatasia Alkaline phosphatase gene Generalized impairment of skeletal mineralization Rickets, bow leg, loss of teeth, short stature Familial osteolysis OPGL; RANKL Idiopathic multicentric osteolysis Typical facies with a slender nose, maxillary hypoplasia, and micrognathia; rheumatoid arthritis–like hand deformities Mucopolysaccharidosis α-L-iduronidase type I (MPS I) Deficiency of α-L-iduronidase (lysosomal enzymes for breaking glycosaminoglycans) Hunter syndrome; progressive cellular damage that affects the development of neurologic and musculoskeletal system (short stature and bone dysplasia) Mucopolysaccharidosis Iduronate sulfatase; type II (MPS II) X-linked recessive Deficiency of iduronate Hunter syndrome; mild to moderate features of sulfatase MPS Mucopolysaccharidosis Heparan N-sulfatase or type III (MPS III) N-acetylglucosamine 6-sulfatase Sanfilippo syndrome; severe neurologic syndrome Deficiency of heparan with mild progressive musculoskeletal syndrome N-sulfatase (IIIA); α-N-acetylglucosaminidase (IIIB); acetyl-coenzyme A:α-glucosaminide-Nacetyltransferase (IIIC); N-acetylglucosamine 6-sulfatase (IIID) Metabolic Bone Diseases 1: Basic Science Mucopolysaccharidosis Deficient enzymes Deficiency of lysosomal Morquio syndrome; bell-shaped chest, anomaly of type IV (MPS IV) N-acetylgalactosamine enzymes for breaking spine, shortened long bones, and dysplasia of the 6-sulfatase (type A) keratin sulfate hips, knees, ankles, and wrists or β-galactosidase Odontoid hypoplasia (type B) Connective Tissue Disorders Osteogenesis imperfecta Type I collagen Decreased amount and Common characteristics: fragile bone, low muscle poorer quality of tone, possible hearing loss, dentinogenesis imperfecta collagen than normal Type I: most common, mildest; blue sclera Type II: most severe, lethal after birth because of respiratory problem Type III: significantly shorter than normal, blue sclera Type IV: normal sclera Ehlers-Danlos syndrome Fibrillar collagen gene Laxity and weakness of connective tissue Lax joint, hyperextensible skin Marfan syndrome Fibrillin Abnormality of connective tissue Tall, scoliosis, myopia, lens dislocation, aortic aneurysm, mitral valve prolapse OPGL = osteoprotegerin ligand; RANKL = receptor activator for nuclear factor κB ligand.

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