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Dr. Barr MSP exam 1
Dr. Barr's NYCC MSP 1st exam
| Question | Answer |
|---|---|
| What are some s/s a patient may have if they suffer from a collagen synthesis disorder? | Ligament laxity (hypermobility) Fragile skin Aneurysms Bruising (vessel rigidity) Highly distensible skin Teeth issues Bone fragility |
| What determines the type of collagen that is formed? | Sequence of amino acids is genetically predetermined d/t mRNA transcription/translation in rough ER |
| How are the amino acid chains composed in collagen formation? | Repeating GLY-X-Y triplets |
| In collagen amino acid chain composition, what amino acids are commonly found in specific positions? | 1/3 of residues are glycine; proline most commonly found in X position; hydroxyproline most commonly found in Y position and hydroxylysine is another common AA in Y position. |
| What is needed to produce hydroxy- proline and lysine? | Enzymes, proline and lysine are hydroxylated. |
| What are the 3 enzymes that hydroxylate in collagen formation? | 1. Lysyl hydroxylase acts on lysine in X or Y position 2. Prolyl-4-hydroxylase acts on proline in Y position 3. Prolyl-3-hydroxylase acts on proline in the X position |
| What must be present for hydroxylation to occur? (4) | 1. A ferrous (+2) ion on enzyme 2. Molecular Oxygen 3. Ascorbic acid 4. Alpha ketogluterate |
| What occurs in the intracellular stage of collagen formation? | carboxylation occurs - glucose and galactose; 3 alpha chains twist together to form a super-helix, and connect w/ H-bonding to form procollagen; procollagen leaves fibroblast and enters extracellular space |
| What occurs in the extracellular stage of collagen formation what needs to be present? | Cleave off terminal extension from procollagen molecule which requires the enzyme: procollagen peptidase. |
| What do you call the forming collagen with the terminal extensions cleaved and how does it become mature? | Tropocollagen is immature since doesn't have tensile strength; further cross-linking w/ H-bonding is needed to form mature collagen |
| How do collagen molecules assemble themselves? | Quarter-staggered array |
| What are some pathologies associated with collagen synthesis? | Scurvy: hydroxylation step interrupted Ehlers-Danlos: problem w/ procollagen peptidase Marfan's and osteogenesis imperfecta |
| What are 5 functions of bone? | 1. protection 2. support 3. mechanical basis for movement 4. hematopoiesis 5. mineral storage |
| What does the bone matrix consist of and what do they do? | Type I collagen: provides tensile strength; resists pulling forces Solid particles: provides compressive strength; Calcium, Phosphate and other crystalline structures. |
| What are 3 important characteristics of bone? | 1. Bone is a rigid tissue that adapts to mechanical stresses (Wolff's) 2. Continuous deposition and removal of bone throughout life 3. 7 years to completely turn over skeletal bone in the body |
| In what 2 ways does mesenchymal condensation give rise to bone? | 1. Direct transition of mesenchyme to bone -> membranous bone (clavicles and parts of skull) 2. Majority of bones form in cartilage first then undergo ossification -> endochondral bone (long bones, needs O2) |
| What enzyme can be measured in the blood that shows increased osteoblastic activity? | Alkaline Phosphatase |
| What pathologies could show the presence of alkaline phosphatase in a blood test? | Fx, neoplasm, infection |
| What could cause disruption in a growth plate? | Fx, infection, CA of cartilage, metabolic problem, dwarfism, endocrine problem |
| What were the 2 methods used to prevent limb length discrepancies with poliomyelitis? | Removal of growth plate Put pressure on growth plate by stapling to epiphysis to metaphysis |
| How does membranous bone grow? | By process of accretion: adding bone to the surface and edges of the bone (i.e. closing of fontanels) |
| What occurs with formation and removal of bone? | Bone matrix secreted by osteoblasts that lie at the surface of existing matrix and deposit fresh layers of bone onto it; Appositional Bone Growth: osteocyte, osteoid (ECM), ossificaiton. |
| What are 3 requirements of healthy bone? | 1. Maintain an equilibrium of Calcium and other metabolites in blood and bone 2. Stress, pressure or load on the bone 3. Viable blood supply to oxygenate bone cells. |
| What has been shown to increase urinary calcium levels and why? | Prolonged bed rest; d/t lack of longitudinal pressure on bones; levels unaffected by heavy bicycle ergometer work |
| What is a fracture? | A break/discontinuity of bone. A break in the cortex can be applied to any anatomy with a cortex |
| What is the most common lesion in bone and the most common cause? | Fracture d/t trauma |
| What can predispose someone to fracture? | Anything that alters the structural integrity of the bone |
| Is a fracture as a pathology the same as a pathological fracture? | No, all fractures are pathologies but a pathological fracture is a fracture through diseased bone. |
| What is the difference b/w an open and closed fracture? | A closed fracture doesn't break the skin while an open one does. |
| What is an avulsion fracture? | Tearing away of bone fragment; pull from ligament, tendon or muscle |
| What is an occult fracture, what should be done and what are common bones affected? | A radiographically invisible fracture; re-radiograph in 7-10 days; scaphoid (FOOSH) and ribs |
| What is a bone bruise? | Hemorrhage, edema, trabecular microfracture (shearing of vasculature inside bone), not seen on radiographs but can be seen on MRI |
| What is fracture orientation based on? | Mechanism of injury |
| Describe transverse fractures. | They are uncommon and can be from a high velocity injury (falling from heights). They are often pathologic, usually Paget's "banana" fracture. |
| Describe oblique fractures. | They usually occur on shaft of tubular (long) bone and are 45 degrees to long axis and are very common in normal, healthy bone. |
| Describe spiral/torsion fractures. | They can be d/t torsion and axial compression, they are angulated with pointed ends. |
| What is a green stick fracture? | A type of incomplete fracture and are common in children. Shows seperation on convex side of force |
| What is a torus fracture? | Buckling fracture, resembles bump on radiograph. |
| What is a comminuted fracture? | 2 or more fragments have seperated, bone has been crushed or pulverized, can be called a "butterfly fragment" |
| What is a noncomminuted fracture? | Bone has one break and 2 fragments. |
| What is a compression fracture? | Usually d/t axial compression; used almost exclusively to describe vertebral fractures of this type. |
| What is the mechanism of injury in a clay shoveler's or coal miner's fracture? | Avulsion; occurs in the spine. |
| What is a fatigue fracture and where does it occur? | Stress fracture or march fracture; in healthy bone. d/t abnormal stress on normal bone, repetitive stress, gradual formation of microfracture. |
| What is an insufficiency fracture? | Stress fracture through diseased bone; a form of pathologic fracture. |
| What are the 3 phases of fracture repair? | 1. Inflammatory 2. Reparative 3. Remodeling |
| What are the first 4 things that occur in the inflammatory phase of fracture repair (1-2 days post fracture)? | 1. Rupture of blood vessels in both soft tissue and bone 2. Hematoma fills gaps, surrounds and seals off injury 3. Immediate tearing of periosteum 4. Necrosis of bone and soft tissue. |
| What occurs in the inflammatory phase of fracture repair 2-5 days post fracture? | 1. Fibrin mesh develops 2. Fibroblasts migrate into area and begin to form and lay down cartilage b/w bone ends 3. Necrosis and macrophage activity continues. |
| What occurs in the inflammatory phase of fracture repair 5-10 days post fracture? | 1. Soft tissue callus (procallus) is beginning to form 2. Macrophage activity is ongoing. |
| What occurs in the reparative phase of fracture repair? | Osteoclasts and mononuclear cells clean up, neovascularization occurs and fx may appear wider on x-ray; callus formation begins w/ significant osteoblastic activity |
| What occurs in the remodeling phase of fracture repair? | Starts once callus has sealed bone, bone adjusts its strength and shape (Wolff) Osteoclasts and -blasts are involved with increased activity relative to normal bone. |
| What is Clinical union regarding fracture? | Point when cast is removed, implies fracture is stable |
| What is malunion regarding fracture? | Fracture heals with residual deformity. |
| What is non-union with regards to fracture? | Fails to heal AFTER 6 months |
| What is delayed union regarding fracture? | Fails to heal UP TO 6 months |
| What is pseudoarthrosis regarding fracture? | Non-union fracture heals with pseudojoint |
| Where does alkaline phosphatase come from? | Secreted by osteoblasts when depositing bone. |
| When would you expect to see alkaline phosphatase increased in the blood? | Fx, neoplasia, growing children |
| What does an increased erythrocyte sedimentation rate (ESR) indicate? | Inflammatory process; will be increased in inflammatory stage of fracture repair; not limited to conditions of bone. |
| What % change can be detected in bone scans versus plain film? | bone scans can detect 2-4% change while films don't detect until 40-60% change has occurred; bone scans very sensitive but not specific |
| What 6 body functions depend on calcium? | 1. Enzymatic reactions 2. Hormone secretion; mediates hormone events 3. Neurotransmission 4. Muscle contraction 5. Blood clotting 6. Major cation in bone and teeth |
| How important is it to keep calcium w/in normal limits and what is the normal range in plasma? | VITAL to keep Ca in normal limits; 8.6-10.6 mg/dl: 50% available, 40% bound to something (albumin) 10% CaCO3 |
| How is calcium related to intake and how does the body maintain normal levels? | % intake absorbed is inversely related to intake; normal levels maintained by preventing overload w/ dietary surplus, w/ dietary deprivation, adaptive increase in absorption. |
| What 6 body functions depend on phosphate? | 1. All glycolytic compounds 2. ATP, ADP, AMP, creatine phosphate 3. Cofactors: NAD, NADPH 4. Lipids like phosphotidyl choline 5. Covalent modifier of enzymes 6. Major anion in bone |
| What is the normal range of phosphate in plasma and how is the balance maintained? | 2.5-4.5 mg/dl; amount absorbed in diet constant, adaptaive reg. at gut is minmal, urinary excretion is major mech. in phosphate balance. 90% conserved, 10% secreted in urine |
| What are the major regulators of plasma calcium, what hormone and how is it related to Ca levels? | Parathyroid glands; PTH (neg. feedback); secretion PTH inversely related to plasma Ca levels |
| How do levels of calcium affect the body? | Ionized Ca regulates PTH secretion w/in minutes; high Ca levels over time shut down PTH synth. and stores; low Ca levels over time cause gland hypertrophy |
| How does PTH moderate phosphate and calcium levels in the body? | Role of phosphate on PTH is indirect through mech.s that lower Ca levels; If inject phosphate, Ca level drops and PTH increases; PTH moderates hyperphosphatemia created w/ injection by increasing renal excretion. |
| Where does PTH act to raise Ca levels and decrease PO4? | Bone Gut Kidney |
| When PTH acts on organs what happens to Ca and PO4 levels? | Increases Ca influx in blood, increasing []; Plasma phosphate levels also rise but action of PTH on kidney causing efflux of phosphate in urine |
| Describe PTH action on bone, what cells are activated/deactivated? | Initially stimulates osteolysis by surface osteocytes putting free Ca into plasma; stimulates prod'n of osteoclasts and activates resorption of bone; all bone constituents liberated; PTH down regulates osteoblasts and inhibits collagen synth. (vit. D) |
| What happens when PTH takes action on the kidney? | Increase Ca reabsorption from distal tubule; MOST dramatic effect is inhibiting reabsorption of phosphate; stimulates synth. of vit D metabolite |
| What happens when PTH takes action on the gut? | Indirect: stimulates 1-25-OH2-D3 which directly increases active transport of Ca across lumen |
| Summarize the function of PTH. | Causes prompt increase of Ca and decrease of PO4 in plasma; Kidney dumps PO4 and conserves Ca initially; As plasma Ca levels rise, PTH levels accommodate, kidney filters more Ca, and urinary Ca levels rise to maintain homeostasis |
| What is the most common cause of hyperparathyroidism and what are the s/s of hypercalcemia? | single parathyroid adenoma; dulled mentation, lethargy, muscle weakness and hyporeflexia, anorexia and constipation (high Ca makes harder to open Ca channels for nt release; m. contraction not affected) |
| How does hyperparathyroidism affect the kidneys and what are sequela? | Excessive urinary Ca filtration = renal stones; persistent hypercalcemia = reduced renal function and irreversible renal failure; Peptic ulcers sequela |
| How does hyperparathyroidism affect bone? | Massive irregular resorption Weakening of bone Pain Fx (pathological) Deformities |
| How does hyperparathyroidism look radiologically? | Subperiosteal erosions/resorption Bone looks splotchy Deposition Ca in soft tissues |
| How does one distinguish hyperparathyroidism from other causes of hypercalcemia? | Elevated PTH levels Elevated plasma Ca levels Decreased plasma PO4 levels |
| Explain primary hyperparathyroidism. | common endocrine disorder - gland does not respond to rising Ca levels; 80-85% of time d/t single parathyroid adenoma; Pt.s found through blood analysis; symptoms mild if any |
| Explain secondary hyperparathyroidism. | Problem not in gland, asked to overfunction; PTH released but Ca levels not rising; glands become hyperplastic; Ca levels low-normal or low (below 8.6), PO4 levels low if kidney intact; Most frequent cause is chronic renal failure or malabsorption of Ca |
| What is the most common cause of hypoparathyroidism and what occurs? | Autoimmune idiopathic atrophy, rarely end organ resistance to PTH; Ca absorbed from gut diminished; Little vit D metabolite around; Decreased bone resorption |
| What are the clinical s/s of hypoparathyroidism? | Those of hypocalcemia: hyperactive reflexes, spontaneous m. contractions, convulsions and laryngeal spasm w/ airway obstruction |
| Describe plasma levels with hypoparathyroidism. | Low plasma Ca and elevated plasma PO4 levels essential to dx; Plasma PTH levels low in gland destruction (MC); Plasma PTH levels elevated when target tissue unresponsive. |
| How do you treat a pt with hypoparathyroidism? | supplement w/ 1-25-(OH)2-D3 supplement w/ calcium |
| What is calcitonin? | Hormone produced by parafollicular cells of the thyroid gland; PTH raises plasma Ca levels and calcitonin acts to lower plasma Ca |
| What are the actions of calcitonin? (3) | 1. Binds to membrane receptors, and cAMP levels increase 2. cAMP as second messenger initiates calcitonin action 3. Ca is sequestered into mitochondria which acts to lower cytosolic [Ca], lowering plasma [] by allowing more Ca into the cell |
| What are the effects of calcitonin? (4) | 1.Rapid fall in plasma Ca (magnitude of fall related to baseline rate of bone turnover) 2. Inhibit'n of osteolysis and bone resorption by bone cells 3. antagonist to PTH w/ respect to Ca 4. Same results as PTH on PO4 w/ diff. mechanism |
| What does vitamin D effect in gut, bone and where is the final active metabolite converted? | Increases Ca absorption from gut; important effect of bone deposition and resorption; Must be converted through series of reactions in liver and kidney |
| What are the 2 sources of vit. D and how are they different? | D3 - produced in skin via UV radiation D2 - Plant steroid ingested in diet; difference is D2 has more double bonds than D3 action in body identical |
| What does PTH's effect on the kidney do to vitamin D metabolite formation, what is made w/o PTH? | With PTH the 1,25-(OH)2-D3 metabolite is made -> bone resorption; w/o PTH the 24,25-(OH)2-D3 metabolite is formed does NOT -> bone resorption |
| What are the actions of the 1-25 (D) metabolite? | In kidney, binds w/ cell receptor and enters nucleus; stim.s protein synth. of product: CALBINDIN which helps Ca & PO4 absorption from gut; Stim. bone resorption, receptor found in bone cells; works synergistically w/ PTH at bone level to stim. breakdown |
| What are actions of Vitamin D? | Normal mineralization of bone is dependent on Vit D (not 1,25); Major storage site is muscle, profound m. weakness seen in deficiency; 25-OH may play role in m. metabolism and function |
| What is Vit D toxicity d/t, where is Ca absorption enhanced and where are increased Ca levels found? | d/t excessive administration or abnormal sensitivity to ordinary amounts of vit D; Absorption from gut and resorption from bone enhanced; See increased plasma and urinary levels of Ca. |
| Why do you see increased plasma and urinary levels of Ca in vit D toxicity? | PTH responds to raising levels of Ca, toxic amts of vit D facilitate PTH response, nothing to do w/ parathyroid glands. |
| What are the s/s of Vit D toxicity? | Same as hypercalcemia: dulled mentation, m. weakness and hyporeflexia, lethargy, anorexia and constipation |
| How do you differentiate b/w hyperparathyroidism and Vit D toxicity since have same clinical presentation? | Urinalysis |
| How is Vit D toxicity treated? | Block effects of Vit D by administering calcitonin or cortisol and wait for excess Vit D to clear. |
| What could Vit D deficiency be d/t? | Inadequate sun, dietary intake, decreased absorption, defective hydroxylation in liver or kidney |
| What does Vit D deficiency lead to? | Decreased GI absorption of Ca and PO4; Plasma Ca levels fall buffered by increased PTH secretion; PO4 lost in urine and Ca retained |
| What does the negative phosphate balance from Vit D deficiency cause? | W/ decrease in Ca levels together causes a decrease in the rate of bone mineralization, further aggravated by lack of Vit D needed for mineralizaiton and excessive osteoid accumulates. |
| What are the results, diagnostic profile and treatment of Vit D deficiency? | Rickets or Osteomalacia; slightly reduced plasma Ca, greatly reduced plasma PO4 and elevated levels of PTH; Replacement doses of Vit D and supplemental Ca. |
| What is osteomalacia? | Soft bone that has defective mineralization of osteoid in adults |
| What are s/s of osteomalacia? | Bone pain Muscle weakness Pseudo Fx (seam of demineralization looks radiolucent and body perceives as Fx -> Fx repair process but can't form procallus to callus; can't tell diff. on film. |
| What is Rickets? | Osteomalacia in a person w/ open growth plates; more severe consequences in a child w/ rickets than an adult w/ osteomalacia. |
| Where does Rickets lack control and what is seen radiographically? | Lack control over epiphyseal cartilage mineralization and over endplate growth; fuzzy growth plates, bowing bones, "paintbrush metaphysis" |
| What is osteoporosis? | Not one specific problem but an umbrella term for a group of conditions; A condition of bone mass, the bone is otherwise normal and healthy (ratio OK) |
| What factors aid in reaching peak bone mass? | Diet, genetics, lifestyle, gender, race, eating disorders, activity level, overall health (Rx) |
| What factors affect loss of bone? | Genetic factors play big role in addition to diet, lifestyle, gender, race, Rx (steroids, heparin, chemo), etc. |
| What is osteoporosis the most common cause of, what are the economic and human impacts of osteoporosis? | Pathological Fx; $20 billion/year; dramatically changes life, fear; hip Fx 50% mortality rate |
| What can be some clinical presentations of osteoporosis? | Vertebral body Fx, Height loss, Hip Fx, Colles' Fx, Loss of teeth |
| What are laboratory values of osteoporosis in terms of ESR, CA and PO4, Alkaline phosphatase? | ESR: not elevated Ca and PO4: normal Alkaline phosphatase: normal |
| What are some non-drug treatments of osteoporosis? | Exercise Diet Fall prevention |
| What are some prescriptions for osteoporosis? | Calcitonin Hormone replacement (high CA rates) Fosamax (Boniva is improvement; both downregulate osteoclasts) |
| What are the likelihoods of suffering osteoporotic Fx? | Women: 1 in 2 over 50 y/o Men: 1 in 4 over 50 y/o Juvenile osteoporosis: late teens early 20s, bone breaking Disuse osteoporosis |
| What is acromegaly? | Growth hormone abnormality in skeletally mature individuals; 3:1 million births, more common in females 3:2 |
| What are s/s of acromegaly? | Increase in soft tissues -> facial changes Small increase in skeleton Bigger ears and nose Thickened coursened jaw (lantern jaw) Frontal bone enlargement |
| What are treatments of acromegaly? | Removal of pituitary gland, radiation therapy, somatostatin therapy |
| What is gigantism? | Effect of excessive growth hormone on immature skeleton; symmetric and proportional overgrowth of all tissues. |
| What is Paget's disease and what is it also known as? | A thickening and disturbance of the architecture of bone; Remodeling problem, initially excessive resorption of bone then excessive remodeling of bone; AKA Osteitis Deformans. |
| What is the frequency of Paget's Disease and who commonly/uncommonly has it? | 5-11% of population over age 60, more common in males; found in western Europe, Australia, U.S.; Rare in come ethnic groups Scandinavians, Asians, Middle Eastern |
| How can Paget's be classified and where are common locations? | Monostotic or Polyostotic; pelvis, skull, spine, tibia, femur |
| What are the 3 stages of Paget's? | 1. Osteolytic 2. Mixed lytic and blastic 3. Sclerotic (burnout) |
| What are some clinical presentations of Paget's? (6) | 1. 95% asymptomatic 2. Enlarged hat size 3. Sabre Shin (ant. bowing) 4. Pathologic Fractures 5. Pagetic Steal (high vasculature present, dizziness w/ position change) 6. Heart failure d/t cardiomegaly |
| What is malignant degeneration in reference to Paget's? | Yochum's stage 4, very rare 1-2% polyostotic disease; Aberrant bone cells can be predisposed to osteosarcoma (more often) and chondrosarcoma |
| What are 4 hereditary diseases of bone? | 1. Achondroplasia 2. Marfan's Syndrome 3. Osteogenesis Imperfecta 4. Osteopetrosis |
| What is Achondroplasia? | No cartilage growth; most common form of dwarfism; 1/4,000 births; most common disorder of growth plates |
| How would someone with achondroplasia look and what are some changes visible on radiographs? | Small arms and legs w/ normal size torso; premature closure @ growth plates; O & I shrinks too w/ change in orientation of sacrum, almost parallel to floor; obturator foramen rotate to champagne glass deformity. |
| What is Marfan's Syndrome and what does it involve? | A connective tissue (type I collagen) disorder that involves the skeleton, lens of the eye, mitral valve prolapse, vascular system |
| How common is Marfan's and what is seen on radiographs? | 1/10K births; long slender extremities, arachnodactyly, hypermobility ("double jointed"), kyphoscoliosis d/t CT hypermobile everywhere; life expectancy altered d/t dissecting aneurysms |
| What is Osteogenesis Imperfecta? | AKA brittle bone disease; 4 types (I-IV); defect in type I collagen synthesis |
| What is the worst case scenario with osteogenesis imperfecta? | Type II - O. I. Congenita; Fatal condition; extremely brittle bones. |
| Describe a Type I Osteogenesis Imperfecta Tarda. | Abnormal skeletal fragility, decreased bone density, Fx.s, bowing deformities, eye sclera appears blue; hearing loss d/t bony deformities; dental imperfections. |
| What is Osteopetrosis and what are the two forms? | Marble bone disease or Albers - Schonberg disease; Mild - autosomal dominant, Lethal - autosomal recessive |
| How is osteopetrosis characterized and how would it appear on a radiograph? | Hypofuctioning of osteoclasts, too much bone, very brittle in nature; Radiopaque and wider, difficult to find medullary cavity and cortex. |
| Why would someone with osteopetrosis have a shortened lifespan and what would their PTH levels be? | Hematopoiesis decreased b/c medullary cavity small -> anemia, infection; PTH elevated body works harder to mobilize Ca, must get it from gut since osteoclasts not functioning. |
| What are 3 classifications of osteomyelitis? | 1. Acute: sudden onset or <6 months duration 2. Chronic: >6 months duration can go on for years 3. Subacute (Brodie's Abscess): Inflammation, pus, abscess in bone, Sx don't occur until pathological Fx occurs |
| What 3 ways can an infectious organism get into bone? | 1. Hematogenous (includes lymphatics) 2. Direct Extension 3. Implantation from foreign object |
| Describe Acute pyogenic osteomyelitis, who commonly affected, how spread and what organism causes? | A pus producing infection; usually bacterial in origin = S. aureus 80-90%/cases; hematogenous spread in metaphyseal area of bone (very active in children); can be very aggressive depending on virulence |
| Who is at high risk for Osteomyelitis? (7) | 1. Children 2. Diabetics 3. Elderly 4. Immunocompromised 5. IV drug abusers 6. Homeless 7. Post-surgical patients |
| What are s/s of acute pyogenic osteomyelitis? | Rapid, high fever; severe throbbing pain that worsens rapidly; pathologic Fx |
| Briefly describe the cellular events in bone infection. | Inflam cascade: vasodilation, PMNs, bacteria contacts bone cells which lyse and die, necrosis, WBCs in area continues to next cell and moves on, pus prod'n through cortex, bores thru periosteum, lifted w/ all pus/crud (OW!), reactive bone form'n... |
| What can occur d/t pyogenic osteomyelitis? | 10% go on to become chronic bone infections; pathologic Fx; Draining sinus; Squamous cell carcinoma and bone sarcomas are rare but d/t chronic irritations |
| What is Brodie's Abscess? | Subacute infection of bone, begins in children, osteolytic lesion gets walled off, sclerotic margin forms around walled off lesion, spontaneous sterilization, commonly in tibia prone to path. Fx |
| How common is TB in bone and how does it appear? | 1-3% of those w/ pulmonary TB can move into bone; general s/s of infection. |
| How does TB act in bone, what does it like and where is it most commonly found? | Extremely destructive and difficult to treat; likes areas of bone w/ high O2 content; spine: vertebral body; Gibbus deformity |
| TB in bone is AKA and what is it prone to? | Pott's disease; patho. Fx, neurologic involvement (spinal nn.), arthritis. |
| What are 2 types of syphilis? | Congenital and acquired |
| What does congenital syphilis do to bone? | Destroys epipyseal cartilage (wide growth plates); Reactive bone formation (thick cortex) both sides; May show changes 5th month in utero; Pseudo bowing also called sabre shin but d/t lifting of periosteum. |
| What does acquired syphilis do to bone? | Involves cortical bone and periosteum; Layering of bone on anterior tibia (Sabre shin); Lysis and collapse of nasal bones (infection can get to skull and destroy things); symptoms 2-5 years post. infection |
| What is Gumma? | Scattered radiolucencies; granulomatous mass of tissue can be scattered in bone w/ areas of osteolytic lesions (syphilis) |
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