1. PATH Pt 1: Bones, Joints, and Soft Tissue

Question 1

Bone matrix is the extracellular component of bone, osteoid (35%) is an organic compound, and 65% is mineral component, what type of collagen is seen with small amounts of glycosaminoglycans and other proteins?

Answer 1

Type I collagen in bone matrix

Question 2

Matrix protein is called osteopontin (aka osteoclacin) and is from osteoblasts and cause bone formation, mineralization and calcium homeostasis, the inorganic hardness of bone matrix is due to?

Answer 2

Hydroxyapatite (99% of bodys calcium and 85% of its phosphate)

Question 3

What type of bone (histological) is produced rapidly during fetal development and fracture repair, has haphazard arrangement of collagen- less structural integrity, and is abnormal in adults but not* specific for any bone disease?

Answer 3

Woven Bone

Question 4

What histological type of bone is slowly produced with parallel collagen fibers and is stronger bone?

Answer 4

Lamellar Bone

Question 5

Osteoblasts are on the surface of the matrix, and synthesize, transport and assemble the matrix, what type of cell is an *inactive osteoblast with decreased cytoplasm, *embedded in matrix, with canaliculi (tunnels that their processes use to network), they control calcium and phosphate leels, and use mechanotransduction to deteck mechanical forces and translate them into biological activity?

Answer 5

Ostecytes (less cytoplasm)

Question 6

What cells are multinucleated macrophages derived from circulating monocytes, they resorb bone, and form resorption pits which utilizes cell surface integrins to attach, creates sealed extracellular trench, secretes matrix metalloproteases (MMPs), which disolve inorganic and organic compounds of bone?

Answer 6

Osteoclasts (multinucleated)

Question 7

Endochondral ossification is responsible for the development of long bones has a cartilage mold = anlagen, and deposits new bone at the BOTTOM of growth plates aka longitudinal growth. What type of ossification is responsible for the development of *flat bones and facial bones, depositing new bone on *preexisting surface aka appositional growth?

Answer 7

Intramembranous Ossification (bone development and remodeling)

Question 8

The adult skeleton is constantly turning over, 10% of skeleton is replaced annually. BMU or bone multicellular unit has coupled osteoblast and osteoclast activity and are regulated by cell-cell interactions and cytokines. Peak bone mass is acheived WHEN?

Answer 8

In early adulthood after cessation of skeletal growth (fourth decade is characterized by resorption > formation = dec skeletal mass)

Question 9

Homeostasis and remodeling of bone is controlled via multiple signaling pathways. What is a receptor activator for NF-kB on osteoclast precursors which when stimulated by RANKL - ACTIVATES transcription factor NF-kB which is essential for generation and survival of osteoclasts* = breakdown of bone?

Answer 9

RANK (needs to be in presence of macrophage colony stimulating factor)

Question 10

RANKL (ligand) is expressed on osteoblasts and marrow stromal cells which also causes breakdown of bone. What is aka OPG, and is a ‘decoy’ receptor made by osteoblasts and several other types of cells that can bind RANKL and prevent interaction with RANK, allowing BUILDING of bone?

Answer 10

Osteoprotegrin

Question 11

What signaling pathway has proteins produced by osteoprogenitor cells that bind to LRP5 and LRP6 receptors on osteoblasts, triggering activation* of a pathway, producing OPG, this process is inhibited by sclerostin which is produced by osteocytes?

Answer 11

WNT/ B-Catenin

Question 12

Balance between net bone formation and resorption is modulated by RANK and WNT, building of bone is influenced by estrogen, testosterone and vit D, and breakdown of bone is influenced by PTH, glucocorticoids, and?

Answer 12

IL-1***

Question 13

M-CSF aka monocyte colony stimulating factor which binds M-CSF receptor on osteoclast precursors to stimulate tyrosine kinase cascade that is CRUCIAL for generation of osteoclasts. Breakdown of matrix by osteoclasts liberates and activates matrix proteins, growth factors, cytokines and enzymes, which are used to stimulate?

Answer 13

Osteoblasts (breakdown of bone to its elemental units stimulate renewal of bone)

Question 14

Developmental disorders of the bone if via inherited mutations occur in earliest stages of bone formation (neonates) while if has acquired mutation you will see it in adults. Dysostosis is problems in migration and condensation of mesenchyme and its differentiation into cartilage anlage. Dysostosis is d/t transcription factors such as homeobox genes, and can be isolated or part of a syndrome. Aplasia is absence of bone or entire digit, supernumerary digits are extra bones or digits and what is abnormal fusion of bones?

Answer 14

Syndactyly or Craniosynostosis

Question 15

Developmental disorders of bone have defects in nuclear proteins and transcription factors. Homeobox proteins are common*- causing abnormal differentiation in osteoblasts and chrondrocytes. Brachydactyly types D and E are associated with what mutation, causing short terminal phalanges of the thumb and big toe?

Answer 15

HOXD13* (homeobox)

Question 16

What is an AD disorder associated with mutation in RUNX2 causing patent fontanelles, delayed closure of cranial sutures, wormian bodies which are extra bones within cranial sutures, delayed eruption of secondary teeth, primitive clavicles and a short height?

Answer 16

Cleidocranial dysplasia (dustin from stranger things)

Question 17

What is the most common* skeletal dysplasia and a major cause of dwarfism due to an AD mutation in FGFR3 (which normally when activated inhibits endochondral-cartilage- growth, so a GOF causes suppressed growth), so retarded cartilage growth with short proximal extremities, NORMAL trunk length, enlarged head, bulging forehead, NO** change in longevity intelligence or reproductive status?

Answer 17

Achondroplasia

Question 18

What dysplasia is the MC lethal form of dwarfism, due to a GOF mutation in FGFR3 that differ from achondroplasia, assoc w diminished proliferation of chondrocytes and disorganization in the zone of proliferation, see micromelic shortening of limbs, frontal bossing, macrocephaly, small chest cavity (resp. insufficiency) and bell shaped abdomen- typically die at birth or soon after?

Answer 18

Thanatophoric Dysplasia

Question 19

Type 1 collagen diseases such as WHAT, are the MC inherited disorder of connective tissue, principally bones issues but also includes joints, eyes ears skin teeth (blue sclera, hearing loss, dental imperfections), AD mutation of COL1A1/1A2 = a1/a2 chains of type 1 collagen, and has 4 subtypes*, assoc with dec. synthesis of normal collagen = mild skeletal abnlity?

Answer 19

Osteogenesis Imperfecta

Question 20

Osteogenesis Imperfecta is associated with accordion-like shortening of the limbs due to numerous fractures in virtually all the bones.

Answer 20

MEOW

Question 21

What subtype of Osteogenesis Imperfecta, is the BEST prognosis, and MC, where collagen structure is normal but the amount is decreased, fractures occur before puberty and dec. with age, normal lifespan, with normal stature, have loose joints/laxity, sclera are blue/purple/gray tint*, triangular face, bone deformity is minimal, brittle teeth is possible, and hearing loss due to abnl bone formation- in the early 20s/30s?

Answer 21

Type I Osteogenesis Imperfecta (collagen type 1 disorder) *AD and NO LUNG or chest cavity issues

Question 22

What subtype of Osteogenesis Imperfecta is the most severe and fatal form, where collagen is improperly formed, lethal due to resp problems, see numerous fractures and severe bone deformity, small stature with underdeveloped lungs**?

Answer 22

Type II Osteogenesis Imperfecta - worst prognosis AR

Question 23

The following are seen both in child abuse AND Osteogenesis Imperfecta, including fractures in many stages of healing, rib fractures, spiral fractures, and fractures with no explanation of trauma- so before wrongly blaming parents for child abuse, what should be looked at to differentiate between OI and abuse?

Answer 23

BONE PATHOLOGY

Question 24

Treatment for Osteogenesis Imperfecta is surgical rodding of long bones, exercise, keep a healthy weight and good nutrition, dont* take steroids and of course, what should you not do?

Answer 24

DONT SMOKE

Question 25

What is aka Marble bone disease or albers-schonberg disease, due to a mutation in CLCN7* which encodes proton pumps on the surface of osteoclasts- leading to a def. of carbonic anhydrase 2 (CA2) which is required by osteoclast and renal tubular cells (causing renal tubular acidosis) to generate protons from carbon dioxide and water, impairing function of osteoclasts = reduced bone absorption and symmetrical sclerosis of bone?

Answer 25

Osteopetrosis- CA2=AR

Bone is not remodeled but WOVEN

Question 26

Osteopetrosis due to deficient osteoclast activity leads to the bone lacking a medullary cavity, see bulbous ends of long bones = erlenmyer flask, neural formaina are small which can compress nerves (II/VII/VIII), aka as stone like bone BUT it is actually brittle like?

Answer 26

Chalk (yikes)

diffuse sclerotic bones with poor formation of distal metaphyses

Question 27

There is a mild AD form of Osteopetrosis usually diagnosed in adolescence or adulthood with repeated fractures and mild cranial nerve deficits & anemia. What type is AR seen in children of mediterranean and arab race, have cranial N. deficits such as optic atrophy, deafness, and facial paralysis, assoc with postpartum mortality due to fractures, anemia and hydrocephaly?

Answer 27

Severe Infantile type of Osteopetrosis

Treat with HSC transplant

Question 28

What are lysosomal storage diseases caused by deficiency in enzymes that degrade dermatan/heparan/keratan sulfate, mostly acid hydrolase enzymes affected, mesenchymal cells (chondrocytes) degrade ECM mucopolysaccharides thus mucopolysaccharides accumulate* in the chondrocytes causing apoptotic death of cells and in the extracellular space as well causing structural defects in articular cartilage, present with short stature, chest wall abnls, and malformed bones?

Answer 28

mucopolysaccharidoses

Question 29

Osteopenia is decreased bone mass 1-2.5 SD below the mean, osteoporosis is osteopenia severe enough to increase risk of fracture in which the bone mass is at least 2.5 SD below mean, most common forms are senile and posmenopausal (primary), physical activity, muscle strength, diet, and hormonal state make important contributions to bone health, What signifies and is pathognomonic for Osteoporosis?

Answer 29

Atraumatic / vertebral compression fractures

Question 30

Once maximal skeletal mass is attained (young adulthood) small deficits in bone formation accrues with every resorption and formation cycle, normal age related bone loss is 0.7% per year. Age related changes such as senile Osteoporosis is a low turnover variant, there is decrease proliferative and biosynthetic potential, and decrease cellular response to GF, decrease physical acitivity is assoc with immobility, paralysis, astronauts in zero gravity, load mag influences bone density > # of load cycles, what type of exercise is best?

Answer 30

Resistance exercises

Question 31

Genetic factors are important factors in Osteoporosis such as LRP5 gene defect along with RANKL, OPG, RANK, HLA, and VitD receptor gene (uncommon causes). Calcium nutritional state is important esp in adolescent girls have insufficient calcium intake during period of rapid growth which might restrict their peak bone mass - what did she seem to focus on?

Answer 31

Anorexic Girls during HS/college leads to quikc decrease in bone health

Question 32

Postmenopausal Osteoporosis is hormonally influenced and asso with accelerated bone loss, 30-40yrs post menopause there is 35% cortical and 50% cancellous bone lost, mainly due to what, because its decrease increases both resorption and formation but MORE resorption =high* turnover rate, dec in this increases osteoclast recruitment and inc RANKL?

Answer 32

ESTROGEN

Tamoxifen = breast cancer tx = inc risk osteoporosis

Question 33

Osteoporosis is normal bone but decreased in quantity of trabecular bone. Postmenopausal has INC osteoclast activity, bones with increased surface area (vertebral bodies) with trabeculae that is perforated, thinned and lose interconnection which causes microfractures and vertebral collapse. What Osteoporosis is characterized by a thinned cortex due to subperiosteal and endosteal resorption- haversian system is widened?

Answer 33

Senile Osteoporosis

OP has CHARACTERISTIC loss of horizontal trabeculae and thickened vertebral trabecuale

Question 34

In advanced Osteoporosis, trabecular bone of the medulla and the cortical bone are markedly thinned, cortex also gets thinner but takes longer than trabecular bone. Higher chances of Osteoporosis if you are white with light hair and eyes, gaurunteed Osteoporosis if you dont eat enough calcium esp in teen years*, and if you eat too much what, which is associated with milk, cheese, beans, peas, buts, and SODA?

Answer 34

Too much phosphorus

*Smoking = bad

Question 35

Diagnosis of Osteoporosis is done via bone mineral density test (DEXA-scan) usually at 50 y/o because early signs may not show up on XRAY, there are no labs* needed for its diagnosis but most times are done to check for secondary causes such as renal or hepatic failure and?

Answer 35

Hyperthyroidism

Question 36

Osteoporosis clinically presents with thoracic and lumbar vertebral fractures, loss of height due to lumbar lordosis and kyphoscoliosis (leading to dowager’s hump), complications of fractures include PE and pneumonia, prevention via exercise, calcium and Vit D, treatment of OP inlcudes hormone therapy, denosumab (anti-RANKL), anti-sclerostin, and what which decreases osteoclast activity and induces apoptosis?

Answer 36

Bisphosphonates

Question 37

Acquire disorder Pagets disease which is aka what, is assoc with increase but disordered and structurally unsound bone mass, it is monostotic meaning involving single bone 15% of the time, otherwise 85% of pagets is polystotic, occuring in 70s, MC affects axial skeleton and femur, MC in whites in england, france, austria, germany, australia, and USA?

Answer 37

Paget Disease (Osteitis Deformans)

Rare in scandinavia, china, japan, africa

Question 38

Paget Disease (Osteitis Deformans) affects men more than women and its pathogenesis is both genetic and environmental, 50% is familial dz, 5-10% is sporadic with mutations in SQSTM1 which increases NFkB and osteoclast activity, commonly see ONLY inc. in alk phos and what on CT of the scalp which is thickened calvarium?

Answer 38

Cotton Wool

Question 39

Paget Disease (Osteitis Deformans) has a jig-saw like appearance with prominent cement lines = haphazard oriented units of lamellar bone, assoc with 3 phases including: 1) initial lytic phase with large osteoclasts with 100 nuclei*, 2) mixed phase: clasts and blasts, primarily osteoblastic 3) burned-out osteosclerotic stage with coarsely thicken trabeculae and cortices that are soft and porous, lacking structural stability, easy fracture, what is BAD and seen in less than 1%?

Answer 39

Sarcomatous transformation** (osteosarcoma* or fibrosarcoma)

Question 40

What is the HALLMARK of Paget Disease (Osteitis Deformans) which is present/seen in the sclerotic phase?

Answer 40

Mosaic pattern of woven and lamellar bone*

Question 41

Paget Disease (Osteitis Deformans) is worse on weight bearing bones- will see bowing of femurs and tibia, distoring the femur head causing secondary osteoarthritis, chalk stick like fractures of long bones of legs, compression fractures causing kyphosis, what of the bone warms the overlying skin**, assoc w increased blood flow causing high output heart failure?

Answer 41

Hypervascularity of Paget Bone* - unique

MCC of increase alk phos**

Question 42

Paget Disease (Osteitis Deformans) will have an increased serum alkaline phosphatase, NORMAL serum calcium and phosphorus*, sometimes see leontiasis ossea (lion face) = enlargement of craniofacial skeleton = cant hold head up, and platybasia = invagination of skull base due to weak bone and compression of posterior fosaa… paget is treated with what bisphosphonates and what to suppress the sx?

Answer 42

Calcitonin

inc thickness of bones/skull-not symmetrical

Question 43

Rickets and osteomalacia are both manifestations of Vit D deficiency or its abnormal metabolism, impairment of mineralization and resultant accumulation of unmineralized matrix, which is in children and intereferes with deposition of bone in the growth plate and which is in adults in which the bone formed during remodeling is undermineralized leading to fractures?

Answer 43

Osteomalacia = is in adults in which the bone formed during remodeling is undermineralized leading to fractures
Rickets = is in children and interferes with deposition of bone in the growth plate

Question 44

Other causes of rickets includes renal rickets, hypophosphatemia, malabsorption, and short gut syndrome. Rickets is associated with frontal bossing, squared off head, anterior protrusion of chest/pigeon chest, lumbar lordosis, bowed legs and what of the ribs?

Answer 44

Rachitic Rosary of the ribs (nodules)

Question 45

PTH increases RANKL on osteoblasts, causing osteoclast activation, so hyperPTH leads to significant skeletal changes related to unabated osteoclast activity, PTH leads to a net increase in?

Answer 45

Serum calcium

bone changes ARE reversible

Question 46

Hyperparathyroidism increases resorption of Ca by renal tubules, increases urinary excretion of phosphates, and increases synthesis of active VitD1, primary Hyperparathyroidism is autonomous and secondary is not as severe or prolonged and usually due to an underlying?

Answer 46

Renal Disease (leads to excessive osteoclast activation and bone resorption)

Question 47

Untreated primary Hyperparathyroidism leads to 3 things. 1) osteoporosis most severe in phalanges, vertebrae and proximal femur 2) dissecting osteitis- clasts tunnel into and dissect trabeculae = railroad tracks 3) what- which are microfractures that elicit influx of macrophages and ingrowth of reparative fibrous tissue creating a mass of reactive tissue, usually vascular, hemorrhagic, hemoiderin deposition w cystic degeneration?

Answer 47

Brown tumors

Question 48

Von Recklinghausen disease of bone is aka as what, which is increased bone cell activity, peritrabecular fibrosis and cystic brown tumors, is the hallmark of severe Hyperparathyroidism, which is now rare due to early treatment?

Answer 48

Generalized Osteitis Fibrosis Cystica**

Question 49

What are skeletal changes that occur in chronic renal disease, including those associatd with dialysis, manifest as osteopenia/osteoporosis, osteomalacia, and growth retardation, on histo can see high turnover, low turnover or asplastic disease, or a mixed pattern of disease with both?

Answer 49

Renal osteodystrophy

Question 50

Renal osteodystrophy causes skeletal abnls through 3 mechanisms.. 1) tubular dysfunction - renal tubular acidosis assoc w low pH dissolves hydroxyapatite = demineralization 2) generalized renal failure - chronic hyperphosphatemia/hypocalcemia 3) dec production of secreted factors - kidney converts VitD to active form (1-25OH2-VitD3) and secretees BMP7 and Klotho which induces osteoblast differentiation and proliferation….. Decreased VitD3 leads to hypocalcemia and contributes to secondary?

Answer 50

hyperparathyroidism

Question 51

Renal osteodystrophy is most serious in children because their bones are still growing, it slows growth and causes deformities, such as legs bend inward or outward = renal rickets, also associated with what?

Answer 51

Short Stature

Question 52

Match the following fractures with their definition…..
Simple
Compound
Pathologic
Greenstick
Stress
Displaced
Comminuted
-overlying skin intact
-bone communicates with skin surface
-ends of the bone at fracture site are not aligned
-slowly developing fracture that follows a period of incresed physical activity in which the bone is subjected to repetitive loads
-extending only partially through the bone, common in infants when bones are soft
-involving bone weakend by an underlying disease process such as a tumor

Answer 52

Simple -overlying skin intact
Compound -bone communicates with skin surface
Comminuted -ends of the bone at fracture site are not aligned
Stress -slowly developing fracture that follows a period of incresed physical activity in which the bone is subjected to repetitive loads
Greenstick -extending only partially through the bone, common in infants when bones are soft
Pathologic -involving bone weakend by an underlying disease process such as a tumor

Question 53

Healing of fractures: immediately post fx, rupture of blood vessels results in a hematoma which fills the fracture gap and surrounds the area of bone injury. What leads to fibrin mesh that seals the site and creates frame work for influx of inflam cells and ingrowth of fibroblasts and new capillaries?

Answer 53

Clotted Blood

Question 54

Degranulated platelets and mgirating inflam cells release PDGF, TGFB and FGF which activate osteoprogenitors in the periosteum, medullary cavity and surrounding soft tissues and stimulate osteoclastic and osteoblastic activity, at the END of the first week what can be seen?

Answer 54

soft tissue callus or procallus

Question 55

After 2 weeks post fracture, soft tissue callus is transformed into a BONY callus, activated osteoprogenitor cells deposit subperiosteal trabeculae of woven bone that are oriented perpendicular to cortical axis and in medullary cavity… Bony calluses reach maximum girth at the end of the 2/3rd week to help stabilize fracture site, newly formed cartilage undergoes what to form a network of bone with newly deposited trabeculae in medulla and beneath periosteum?

Answer 55

Endochondral ossification

Question 56

Early callus has excess fibrous tissue, cartilage and woven bone, as the callus matures and is subjected to weight bearing forces, portions not physically stressed are resorbed, callus is reduced in size and outline of fractured bone are reestablished as what, with healing complete with restoration of medullary cavity?

Answer 56

Lamellar bone

Question 57

What is aka as avascular necrosis in which infarction of the bone and marrow occurs, cortex is not typically affected due to collateral blood flow, most cases due to fractures or corticosteroid tx leading to vascular insuficiency through mechanical injury to blood vessels, thromboembolism, external pressure on vessels or venous occlusion, symptoms depending on location and extent of infraction?

Answer 57

Osteonecrosis (avascular necrosis)

commonly seen after joint replacements

Question 58

Osteonecrosis (avascular necrosis) has subchondral infarcts that cause pain and is initially associated only with activity, then becomes constant, they often collapse and may lead to severe secondary osteoarthritis. What type of infarcts are usually small and clinically silent, except occur with gaucher disease*, dysbarism (bends), and sickle cell anemia**?

Answer 58

Medullary Infarcts (Osteonecrosis (avascular necrosis))

Question 59

Medullary infarcts are geographic and involve trabecular bone and marrow, cortex is NOT affected because of collateral flow. Which infarcts produce triangle or wedge shaped infarcts within subchondral bone plate as its base, but overlying articular cartilage is viable and obtains nutrients from synovial fluid?

Answer 59

Subchondral Infarcts*

Question 60

Dead bone is empty lacunae surrounded by necrotic adipocytes that frequently rupture, released FAs bind calcium and form insoluble calcium soaps that persist for life, osteoclasts resorb necrotic trabecular, what are trabeculae that remain-act as scaffolding for deposition of new bone but collapse because it is too slow?

Answer 60

Creeping substitution

Question 61

Common conditions associated with Osteonecrosis (avascular necrosis) includes bisphosphonate therapy (JAWBONES), corticosteroid admin, and trauma such as a fracture. Grossly with subchondral infarcts, there is a space between articular cartilage and bone due to trabecular compression fractures and what type of pale yellow are of osteonecrosis is seen?

Answer 61

Wedge or Traingular shape necrosis (subchondral***)

Question 62

What is inflammation of the bone and marrow, virtually always following infection, may be a complication of systemic infection but frequently a primary solitary focus of disease, can be due to viruses, parasites, fungi, and bacteria but MOST caused by pyogenic bacteria and mycobacteria?

Answer 62

Osteomyelitis

Question 63

Pyogenic Osteomyelitis is always bacterial, and accesses bone via hematogenous spread (MC in healthy kids), extension from contiguous site or direct implantation. Adults get this from complications of open fractures, surgical procedures and diabetic* infections of the feet. What is the MC bacteria assoc with osteomyelitis, who expresses cell wall proteins that bind to bone matrix (collagen), facilitating adherence of the bacteria to bone?

Answer 63

Staph Areus (catalase and coagulase +)

Question 64

E. Coli, pseudomonas, and klebsiella are more often isolated in patients with UTIs or IV drug users (gram -), mixed bacterial MC seen in surgery or open fractures, H. influenzae and Grp B strep (neonatal), Salmonella Typhi in SICKLE cell patients, which bug is associated with increased susceptibilty if there is a C5/6/7/8/9 or MAC deficiency?

Answer 64

Neisseria*

gram negative diplococci

Question 65

Acute Osteomyelitis: bacteria proliferate and neutrophils present, necrosis of bone cells and marrow by 48 hours. For kids- periosteum is loosely attached causing sizable subperiosteal abscesses to form along bone surface- which may impair blood supply and cause necrosis, what is dead bone following subperiosteal abscess?

Answer 65

Sequestrum

Question 66

if there is rupture of periosteum due to abscess (kids) soft tissue abscess can form which can channel to becoming a draining sinus, sequestrum (dead bone) may crumble and release fragments through this sinus tract. In what age group can one see epiphyseal infection spreading through the articular surface or along capsular and tendoligamentous insertions into joints leading to septic or suppurative arthritis?

Answer 66

Infants** (rare in adults)

note: this can destroy articular cartilage causing permanent disability

Question 67

Chronic Osteomyelitis occurs after the first week, chronic inflam cells release cytokines that stimulate osteoclastic resorption, ingrowth of fibrous tissue and deposition of reactive bone at the periphery. Involucrum (usually next to dead bone/sequestrum) is newly deposited bone that forms a Shell of living tissue around the segment of devitalized bone. What are small interosseous abscesses frequently involved in the cortex and is walled of by reactive bone?

Answer 67

Brodie Abscess

Question 68

What Osteomyelitis is of the jaw, and associated with extensive new bone formation that obscures much of the underlying osseous structure?

Answer 68

Sclerosing Osteomyelitis of Garre

Question 69

Hematogenous/acute Osteomyelitis clinical course may cause malaise fever chills leukocytosis marked to intense throbbing pain over affected region. Subtle: fever in infants or pain in adults, Radiograph shows lytic focus of bone destruction surrounded by zone of sclerosis, bx and culture required to ID pathogen, abx/surgical drainage is usually?

Answer 69

Curative

Question 70

Chronic Osteomyelitis is 5-25% of acute, and see a delay in dx, extensive bone necrosis, seen with inadequate abx tx, or surgical debridement, or weakened host defense, usually punctuated by acute flare ups later, complications include pathologic fracture, secondary amyloidosis, endocarditis, sepsis, devel of SCC in draining sinus tracts and what in the infected bone?

Answer 70

SARCOMA

Question 71

What type of Osteomyelitis is usually blood borne, originating from a focus of active visceral disease during intial stages of primary infection, can be direct extension, bone infection may persist for years* before being detected, sx: localized pain, low grade fevers, chills and weight loss*, more resistant-destructive than pyogenic Osteomyelitis, and histo shows caseous necrosis and granulomas?

Answer 71

Mycobacterial Osteomyelitis

seen in immigrants/immunocompromised pts

check for pulmonary findings-duh

Question 72

Mycobacterial Osteomyelitis is associated with what in the spine (40% of the time), in which it breaks through the intervertebral discs to infect multiple vertebrae and soft tissues, permanent compression fractures leads to scoliosis or kyphosis and neurological deficits d/t SC and nerve compression, complications include tuberculous arthritis, sinus tract formation, psoas abscess and amyloidosis?

Answer 72

Tuberculous Spondylitis = POTTS Disease

acid fast stain

Question 73

Syphilis (T. pallidum and T. pertenue) can involve the bone. Congenital syphilis has bone lesions appearing at 5th month gestation such as saber shin= massive reactive periosteal bone deposition on medial and anterior surfaces of tibia. What occurs 2-5 years after infection, and associated with saddle nose, palate and skull and extremities (long tubular bones like tibia)?

Answer 73

Acquired Syphilis in Tertiary stage*