Basic Science Flashcards

1
Q

<b><div>RC 2018 - What is the function of BMP?</div><ol><li><div>Recruitment of mesenchymal stem cells</div></li><li><div>Differentiation of oseto progenitor to osteoblasts-like cells</div></li><li><div>Cell that survive implantation form bone</div></li><li><div>Promotes RANK to form bone</div></li></ol></b>

A

<b><div>B (maybe A)</div><div> </div><div>OKU 10</div><ul><li><div>Induces differentiation of mesenchymal stem cells to osteoprogenitor cells</div></li><li><div>Recruitment of mesenchymal stem cells</div></li><li><div>Stimulation of angiogenesis</div></li></ul></b>

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2
Q

RFs for Metal hypersensitivity? MCQ 2018

A

<b>female (not male): RR 4</b><div>piercings: 3.2</div><div>hand eczema: RR 3</div><div>smoking: RR 3</div>

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3
Q

MOA of BMP (MCQ 2018, SAQ 2010)

A

<div><b>Induces differentiation of mesenchymal stem cells to osteoprogenitor cells and osteoblasts (MCQ 2018)</b></div>

<div><div>Recruitment of mesenchymal stem cells</div> <div>Stimulation of angiogenesis</div></div>

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4
Q

peri-op mx of rheumatoid meds?

A

stop biologics 2 weeks before, start 2 weeks after (MCQ 2018)<div><br></br></div><div>continue MTX, plaquenil (hydroxy)</div>

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5
Q

HIV transmission?

A

0.3% HIV<div>3% Hep C</div><div>30% Hep B</div>

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6
Q

Complication with INFIX?

A

<b>LFCN palsy</b> - 0-30% (MCQ 2018)<div>HO 0-25%<br></br><div><br></br></div></div>

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7
Q

short vs long im nail for intertroch fracture?

A

short nail is cheaper<div><b>increased iatrogenic fractures in long (mcq 2018)</b></div><div>equal: torsional strength, risk of rotational abnormalities</div>

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8
Q

Properties of BG?

A

Osteogenic (OG): viable osteoblasts or stem cells (MSC) that can differentiate down bone forming lineage<div><br></br></div><div>Osteoconductive (OC): 3-D architecture (ie scaffold) that promotes bone formation</div><div><br></br></div><div>Osteoinductive (OI): BMPs to support cell proliferation or differentiation<br></br></div>

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9
Q

Dx criteria for RA?

A

“<img></img>”

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10
Q

Agents to decrease intra-op bleeding

A

“<div> <div> <div><img></img></div> </div></div>”

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11
Q

<div>RC 2014 - Name 6 modifiable risk factors for osteoporosis, excluding medications</div>

A

“<ul> <li>Sedentary Lifestyle</li> <li>Smoking</li> <li>Alcohol Intake</li> <li>Low body weight</li> <li>Diet low in calcium/vitamin D</li> <li>Diet low in protein</li></ul><div>RFs in general - SocHx, FHx, PMHx, Meds</div><div>Couple things together!</div><div><ul> <li>Smokers - COPD</li> <li>EtoH - liver dz</li> <li>Steroids - RA, MTX</li> <li>Low BMI - low protein intake - malabsorption syndromes</li></ul></div><div><img></img><br></br></div>”

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12
Q

<div>RC 2012 - All of the following regarding transient osteoporosis is true except:</div>

<ol> <li>Happens mostly in middle aged men</li> <li>Half of cases are in the upper extremity</li> <li>It is associated with no significant loss of range of motion</li> <li>It is self-limiting</li></ol>

A

B.<div><ul> <li>TO affects mostly young and <b><u>middle-aged men</u></b> and, rarely, women during the last 3 months of pregnancy or immediate postpartum period</li> <li><b><u>Typically involves only the lower extremities,</u></b> especially the hip joint and, less frequently, the knee, ankle and foot</li> <li>Pain worse with weight bearing and associated with limping, then gradual subsidence in 4-9 months</li> <li>Minimal restriction of ROM and pain at extremes</li> <li>Cause unknown</li> <li>Labs usually non-contributory, but differentiate from other pathologies</li> <li>Demineralization on radiographs (delayed 3-6 weeks from onset)</li> <li>TO is a self-limited disease</li></ul></div>

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13
Q

<div>RC 2014 - All of the following are true, EXCEPT?</div>

<ol> <li>Both rickets and osteomalacia are due to deficient mineralization of osteoid</li> <li>Osteoporosis in Caucasian females is defined as a bone mineral density T-score 1.5 below the mean</li> <li>Estrogen preserves bone mineral density by decreasing the frequency of bone remodeling cycles</li> <li>Vertebral compression fractures are twice as common as hip fractures</li></ol>

A

B.<div><ul> <li>Rickets = osteomalacia</li> <ul> <li>Adefect inmineralizationof osteoid matrix caused by inadequate calcium and phosphate</li> <ul> <li>prior to closure of physis known asrickets</li> <li>after physeal closure calledosteomalacia</li> </ul> </ul> <li>Osteoporosis t < -2.5</li></ul></div>

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14
Q

RC 2018 - What is the function of BMP? <ol> <li>Recruitment of mesenchymal stem cells</li> <li>Differentiation of oseto progenitor to osteoblasts-like cells</li> <li>Cell that survive implantation form bone</li> <li>Promotes RANK to form bone</li></ol>

A

“B.<div><br></br></div><div><img></img><br></br></div>”

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15
Q

<div><b>RC 2011 - What are two mechanisms of action of BMP?</b></div>

A

<div>o<b><i>OKU 10</i></b><b></b></div>

<div>·<b>Induces differentiation of mesenchymal stem cells to osteoprogenitor cells</b></div>

<div>·<b>Recruitment of mesenchymal stem cells</b></div>

<div>·<b>Stimulation of angiogenesis</b></div>

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16
Q

<div><b>RC 2015 - 65yo female with history of bisphosphonate use presents with proximal femur fracture. List 5 X-RAY findings associated with bisphosphonate therapy. </b></div>

A

<div><b><i>JAAOS - Atypical Femur Fractures</i></b><b></b></div>

<ul><li>Lateral cortical beaking</li> <li>Generalized increase in cortical thickness of femoral diaphysis</li> <li>Transverse tension side fracture line</li> <li>Minimal fracture comminution</li> <li>Bilateral incomplete diaphyseal fractures</li> <li>Delayed fracture healing</li></ul>

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17
Q

RC 2013 - Which drug do you have to stop before TKA for a rheumatoid patient <ol> <li>Hydroxychloroquine</li> <li>Glucosamine and Chondroitan </li> <li>Prednisone</li> <li>Methotrexate</li></ol>

A

“B.<div><ul> <li>the 5 g’s of herbal medicines to stop before surgery: Gingko balboa, garlic, glucosamine, guava, ginseng. They increase bleeding time (PTT)</li> <li>Hydroxycholorquine: This is Not an immunosuppressant and may confer benefits for anti-embolism post-op. Therefore, it should be continued peri-operatively.</li> <li>Prednisone: There is an increased risk of infection if the patient is using over 5mg per day, and this risk increases with increasing duration of therapy. You cannot stop it peri-operatively though because the patient will have their endogenous steroid production chronically suppressed from their prednisone treatment. They therefore cannot mount a stress response to produce their own corticosteroid. The European league against rheumatism has recommended stress dose of 100mg hydrocortisone intraop</li> <li>Methotrexate: This is continued perioperatively as recommended by an international task force. There is slight increase in post op infection risk, but the infection risk is higher with corticosteroids</li> <li>Anti-tnf agents such as infliximab should be stopped – they increase infection risk. Can be restarted 2 weeks after surgery.</li></ul></div>”

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18
Q

<div>RC 2012 - What is the mechanism of action of Botox?</div>

<ol> <li>Inhibits ACTH release from presynaptic vesicles</li> <li>Inhibits calcium release from sarcoplasmic reticulum</li> <li>Blocks ACTH post-synaptic receptor</li> <li>GABA agonist</li></ol>

A

A.<div><ul> <li>JAAOS 2003 - Botulinum Neurotoxin Type A</li> <ul> <li>The final effect of the toxin is a reduction in the release of acetylcholine at the nerve terminal (PRE-SYNAPTIC)</li> </ul> </ul> <div></div></div>

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19
Q

RC 2008 -<b>What is a side effect of bisphosphonates</b> <div><b>a. </b><b>femoral head necrosis</b></div> <div><b>b. </b><b>mandible osteonecrosis</b></div> <div><b>c. </b><b>osteopenia</b></div> <div><b>d. </b><b>Hypocalcemia</b></div>

A

B. madible avn really only an adult phenomenon<div><br></br></div><div> <div>o However transient hypocalcemia is seen when starting bisphosphonates, hence why they are used in acute hypercalcemia crisis</div></div>

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20
Q

<div>RC 2014 - Regarding bisphosphonate use in the pediatric population, all are true EXCEPT?</div>

<ol> <li>Osteonecrosis of jaw</li> <li>Flu-like symptoms</li> <li>Limb pain</li> <li>May have delayed healing of osteotomies performed in osteogenesis imperfecta patients</li></ol>

<div><div>RC 2013 - What is not a side effect of bisphosphonate treatment in kids</div> <ol> <li>Acute fever with administration</li> <li>Growth delay</li> <li>Prolonged effects on bone remodelling</li> <li>Immediate and transient hypocalcemia</li></ol></div>

A

RC 2014 - A.<div><br></br></div><div>RC 2013 - B</div><div><br></br></div><div><div>Side effects of Bisphosphonates</div> <div>1. Acute phase reaction: fevers, malaise, diarrhea, bone and muscle pain. Occur 1-3 days after administration.</div> <div>2. Transient Electrolyte abnormalities: hypocalcemia, hypophosphatemia, hypomagnesemia. These are mild and assymptomatic and resolve within a couple of days. Prevention can be done with Ca and Vit D supplementation</div> <div>3. Uveitis</div> <div>4. Thrombocytopenia</div> <div>5. Oral ulceration</div> <div>6. AVN of the jaw - only reported in adults, not in children (RC EXAM)</div> <div>7. Exacerbation of reactive airway disease (like asthma)</div> <div>8. Cross the placenta so may affect the fetus (not reported)</div> <div>9. Has NOT been shown to delay healing of fractures in kids, but may delay healing of osteotomies </div> <div>10. Suppressed bone turnover markers for up to 2 years after treatment.</div></div>

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21
Q

<div>RC 2016 - Mechanism of function of biologics in RA:</div>

<ol> <li>TNF agonist</li> <li>TNF antagonist</li> <li>IL-2 antagonist</li> <li>IL-2 agonist</li></ol>

A

“2.<div><br></br></div><div><div> <div> <div><img></img></div> </div></div></div>”

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22
Q

<div>RC 2016 - Fight bite. What antibiotic? </div>

<ol> <li>Keflex </li> <li>Amox-Clav </li> <li>TMP/SMX </li> <li>?</li></ol>

A

“b.<div><ul> <li>JAAOS 2015 - Human and Other Mammalian Bite Injuries of the Hand</li> <ul> <li>Common Bacteria Isolated from Infected Bite Wounds:</li> <ul> <li>Aerobic - Step, Staph, Eikenella, Haemophilus, Enterobacteriacae, Gernella, Neisseria</li> <li>Anaerobic - Prevotella, Fusobacterum, Eubacterium, Veillonella, Peptostreoptococcus</li> </ul> </ul> </ul> <div><img></img></div><div><br></br></div><div><br></br></div></div>”

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23
Q

<div>RC 2008 - Vancomycin. All are true EXCEPT</div>

<ol> <li>Cleared by glomerular filtration</li> <li>Red man syndrome can be prevented by slow administration</li> <li>Measuring peaks is more useful than measuring troughs in determining effective dosing</li> <li>Inhibits cell wall formation</li></ol>

A

<div>C.</div>

<ul> <li>See AAOS Review – Vancomycin acts by Bactericidal Inhibition of cell wall synthesis. Disrupts peptioglycan cross-linkageDOC for MRSA. Red man syndrome (5% to 13% of patients), side effects are nephrotoxicity/ototoxicity, neutropenia, thrombocytopenia.</li> <li>Vancomycin, JAAOS, 2005 - is nephrotoxic and ototoxic, monitor serum levels, inhitibs cell wall synthesis, poor GI absorption, better IV, glomerular filtration is the primary clearance, hepatic metabolism is minor, half life is 6 hours, adverse effects include infusion related erythema, pruritis, phlebitis and Red Man Syndrome (involves a pruritic, erythematous rash on the upper trunk, neck, and face associated with rapid vancomycin infusion causing histamine release), Vancomycin should be infused at a rate of 1,000 mg over 60 minutes, with larger doses taking proportionately longer to infuse, red man syndrome can be ameliorated with a slower rate of infusion and antihistamine premedication, trough serum concentrations of 5 to 10 μg/mL and peak serum concentrations of 20 to 40 μg/mL typically are desired, <b>in determining treatment outcome, evidence for monitoring trough concentrations is stronger than for monitoring peak concentrations</b></li></ul>

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24
Q

RC 2009 - In your hospital, among patients with a post-op wound infection, 35% of them have MRSA. What do you use for pre-op prophylaxis? <ol> <li>Cefazolin</li> <li>Vanco</li> <li>Clinda</li> <li>Gentamicin</li></ol>

A

“A.<div><ul> <li>2013 ASHP Clinical practice guidelines for anti-microbial prophylaxis in surgery</li> <ul> <li>"”Routine use of vancomycin prophylaxis is not recommended for any procedure. Vancomycin may be included in the regimen of choice when a cluster of MRSA cases have been detected at an institution. Vancomycin prophylaxis should be considered in patients with known MRSA colonization or at high risk for MRSA colonization in the absence of surveillance data””</li> <li><b>"”Although vancomycin is commonly used when the risk of MRSA is high, data suggest that vancomycin is less effective than cefazolin for preventing SSIs caused by MSSA.””</b></li> </ul></ul></div>”

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25
Q

<div>RC EXAM - 16 yr old with Gr II open tibia with zero tetanus vaccinations and an anaphylactic reaction to penicillin:</div>

<ul> <li>What antibiotic to use</li><ul><ul> </ul> </ul> <li>What Immunization</li><li>What surgical treatment to implement</li> </ul>

A

<ul><li>What antibiotic to use ?</li> <ul> <li>Clindamycin</li> <li>Piptazo also an option</li> <ul> <li>Redfern J (JOT 2016) Surgical site infections in patients with type 3 open fractures : comparing cefazolin plus genta vs piptaz</li> </ul> </ul> <li>What Immunization </li> </ul>

<div>Tetanus: give tetanus toxoid vaccine (Td 0.5mL) and tetanus immunoglobulin (TIG) - if you havent had the vaccine ever (or its been a while), you wont have circulating IGs to fight infection - so give it!</div>

<div><br></br></div>

<div> <div>Wound type</div> <div>Last tetanus immunization</div> <div></div> <div></div> <div></div> <div>Td < 10 yrs</div> <div>Td > 10 yrs</div> <div>No Td ever</div> <div>Clean</div> <div>No Td/ TIG</div> <div>Td only</div> <div>Td x 3</div> <div>Tetanus prone</div> <div>Td if > 5 yrs</div> <div>Td only</div> <div>Td + TIG</div> <div>Dirty/ neglected</div> <div>Td</div> <div>Td + TIG + Abx</div> <div>Td + TIG + Abx</div> </div>

<div></div>

<div>Tetanus Prone Wound:</div>

<ul> <li>More than 6 hours old</li> <li>Stellate</li> <li>Avulsion or abrasion configuration</li> <li>Depth more than 1 cm (ie Gustillo 2,3)</li> <li>Mechanism: missile, crush, burn, frostbite</li> <li>Signs of infected/devitalized tissue</li> <li>Grossly contaminated</li></ul>

<ul> <li>What surgical treatment to implement?</li> <ul> <li>Irrigation and debridement</li> <li>Early flap coverage if needed (shouldn’t need it II)</li> <li>Reamed IM nail</li> </ul></ul>

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26
Q

<div>RC 2014, 2011 - List 4 poor prognostic factors for septic arthritis.</div>

A

<ul> <li>Weston WC (Ann Rheum Dis 1999) Clinical features and outcome of septic arthritis in a single Uk Health District 1982-1991</li> <ul> <li>Risk Factors of Mortality:</li> <ul> <li>Confusion at presentation</li> <li>Age > 65</li> <li>Multiple joint sepsis</li> <li>Elbow involvement</li> </ul> <li>Risk Factors of Morbidity</li> <ul> <li>Age > 65</li> <li>DM</li> <li>Open surgical drainage</li> <li>Gram positive infection other than S aureus</li> </ul> </ul> <li>Gupta MN (Rheum 2001) Prospective 2 year study of 75 patients with adult-onset septic arthritis</li> <ul> <li>Poor prognosis/mortality</li> <ul> <li>Elevated WBC at presentation</li> <li>Development of abnormal renal function</li> </ul> </ul> <li>Shirtliff ME (Clin Microbiol Rev 2002) Acute Septic Arthritis</li> <ul> <li>Underlying joint disease (delay in diagnosis) </li> <li>Poly-articular involvement</li> </ul></ul>

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27
Q

<div>RC 2016, 2013 - A previously healthy kids presents with pain to mid tibia with a fever and elevated ESR. Consistent with osteomyelitis. Kid comes from an area with a high prevalence of MRSA. What antibiotic do you start?</div>

<ol> <li>Rifampin</li> <li>Cefazolin</li> <li>Clindamycin</li> <li>SMP-TMX</li></ol>

A

“C.<div><ol> <li>Stable MRSA infection: Clindamycin</li> <li>Serious/Invasive MRSA: Vancomycin</li> <li>Neonate: Vancomycin</li></ol></div><div>Apparently the 2013 Q had vanco as an option</div><div><br></br></div><div><img></img><br></br></div>”

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28
Q

<div>RC 2012 - C-diff, all true except?</div>

<ol> <li>Toxic megacolon can be a deadly complication </li> <li>Associated with toxins A & B </li> <li>Treatment of choice is oral Vanco or Flagyl </li> <li>Cannot caused by 1 dose of prophylactic abx</li></ol>

A

<b>D.</b><div><ul> <li>Enzyme immunoassay (EIA) testing for C. difficile toxin A and B is rapid but is less sensitive than the cell cytotoxin assay, and it is thus a suboptimal alternative approach for diagnosis (B-II). </li> <li>Metronidazole is the drug of choice for the initial episode of mild-to-moderate CDI. The dosage is 500 mg orally 3 times per day for 10–14 days. (A-I) </li> <li>Vancomycin is the drug of choice for an initial episode of severe CDI. The dosage is 125 mg orally 4 times per day for 10–14 days. (B-I) </li> <li>Receipt of antimicrobials increases the risk of CDI because it suppresses the normal bowel flora, thereby providing a “niche” for C. difficile to flourish. Both longer exposure to antimicrobials, as opposed to shorter exposure,47 and exposure to multiple antimicrobials, as opposed to exposure to a single agent, increase the risk for CDI.47 <b>Nonetheless, even very limited exposure, such as single-dose surgical antibiotic prophylaxis, increases a patient’s risk of both C. difficile colonization82 and symptomatic disease</b></li></ul></div>

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29
Q

<div>RC 2008 - Aquatic environments. All true except:</div>

<ol> <li>Vibrio is the most common bacteria in fresh and salt water</li> <li>Clostridium present</li> <li>Need antibiotic coverage for Aeromonas Hydrophilia</li> <li>Pseudomonas and Aeromonas Hemophilia are uncommon bacteria in salt water</li></ol>

A

A.<br></br><div><br></br></div><div><div>freshwater</div> <ul> <li>most common source of infections ® skin flora (Gram +ves)</li> <ul> <li>Staph aureus</li> <li>Strep pyogenes</li> </ul> <li>also have to cover Aeromanas hydrophilia (anaerobic gram –ve)</li> <ul> <li>Fluoroquinolone (cipro, levo)</li> <li>3rd or 4th generation cephalosporin (ceftazidime)</li> </ul> </ul> <div>· seawater</div> <ul> <li>Clostridium - need to cover with tetanus (booster vs. IG)</li> <li>Vibrio - fluoroquinolone (cipro, levo) or doxycycline + 3rd/4th generation cephalosporin (ceftazidime)</li></ul></div>

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30
Q

<div>RC 2016 - What is the mechanism of action of teraparitide?</div>

<ol> <li>Causes osteoclast apoptosis</li> <li>Causes increased osteoblast activity</li> <li>Increased RANK-L and decreased OPG, therefore increased osteoclasts and resorption</li> <li>Increased serum calcium by blocking renal excretion</li></ol>

A

B.JAAOS 2004 – Parathyroid Hormone Preferential stimulation of osteoblastic activity over osteoclastic activity<div><br></br></div>

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31
Q

<div>RC 2011 - 16 yo female with epilepsy, on Dilantin. Hx of osteomalacia. Why?</div>

<ol> <li>Failure of hydroxylation of 24-25 vitamin D</li> <li>Failure of hydroxylation of 25- vitamin D</li> <li>Failure of resorption calcium in kidney</li> <li>Gut irritation</li></ol>

A

“2.<div><ul> <li>Pack AM (CNS Drugs 2001) Adverse effects of antiepileptic drugs on bone structure</li> <ul> <li>Rat studies indicated phenytoin caused marked decrease in intestinal calcium transport</li> <li>Patients taking Dilantin have low levels of 25-vitamin D</li> </ul> </ul> <div>Vitamin D Physiology:</div> <div><img></img></div></div>”

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32
Q

<div>RC 2010 - What is true of the Osteoporosis Screening Index (OST) for men?</div>

<ol> <li>Age and weight</li> <li>BMI</li> <li>History of fragility fractures</li> <li>History of low energy fractures</li></ol>

A

<div>A</div>

<ul> <li>Alberta College of Fam Physicians</li> <ul> <li>Bottom-line: The Osteoporosis Self-Assessment Tool (OST) is simple, quick, and predicts osteoporosis as reliably as other more complicated instruments. It is a reasonable screening tool to identify those who would benefit from BMD testing.</li> <li>OST = weight (kg) - age</li> <ul> <li><10 -> perform DEXA</li> <li>>10 -> repeat OST q5 years</li> </ul> </ul></ul>

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33
Q

<div>RC 2008 - Which of the following is most likely to be associated with Type I osteoporosis:</div>

<ol> <li>Intertrochanteric fracture</li> <li>Femoral neck fracture</li> <li>Femoral shaft fracture</li> <li>Pubic ramus fracture</li></ol>

A

1.<div><br></br></div><div>type 1 typically Distal radius fracture and vertebral fracture.</div><div><br></br></div><div><div> <div></div> <div>Type I (Post menopausal)</div> <div>Type II (Senile)</div> <div>Age group</div> <div>Post menopausal (highest incidence in 50-70 years old)</div> <div>>70 years old</div> <div>Bone affected</div> <div>Almost exclusively trabecular</div> <div>Trabecular > cortical</div> <div>Bones fractured</div> <div>Distal radius and vertebral</div> <div>Hip and pelvis</div> <div>Effect on calcium</div> <div>Net negative change in calcium levels because of decreased intestinal absorption and increased urinary excretion of calcium.</div> <div>Poor calcium absorption</div> <div>Effect on Vit D</div> <div>Reduced circulating levels of total (but not free) 1,25 dihydroxyvitamin D.</div> <div></div> </div></div>

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34
Q

RC 2013 -All are true with regards to HIT, except: <div>a. Cannot be caused by LMWH</div> <div>b. Mild to Moderate thrombocytopenia in general</div> <div>c. Get arterial thrombosis</div>

A

<div>A.</div>

<div><br></br></div>

<div><div>· <i>DiGiovanni (FAI 2008) Current concepts review: Heparin-Induced Thrombocytopenia</i></div> <div> Clinically significant form of HIT occurs in 1-3% of patients receiving UFH and in only 0.3-0.8% of patients receiving LMWH</div> <div> Type 1:</div> <div>· Not immune mediated</div> <div>· Not thromboembolic or hemorrhagic</div> <div>· Mild, transient decrease in platelets 1-2 days after exposure…usually not below 100,000</div> <div> Type 2:</div> <div>· Systemic autoimmune response triggered by completes between heparin and platelet factor 4</div> <div>· At least 4 days after exposure</div> <div>· Life threatening</div> <div>· Increased rate of thrombotic events for up to 30 days</div> <div>· Precipitous drop in platelets greater than 50% from baseline</div></div>

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35
Q

RC EXAM -A patient is being chemoprophylaxed against DVT/PE after a TKA. You are worried about HIT. What is true? <div>1 – Because you used low molecular weight heparin, the patient is not at risk for thrombocytopenia. </div> <div> 2 – You need to start the HIT work up if platelets drop below 100,000.</div> <div> 3 – It can present 4 to 5 days after starting heparin</div>

A

“<div><b>Answer</b>: 3</div> <div></div> <div><b>Reference</b>:</div> <div>Can still get HIT in LMWH (1% patients)</div> <div>Start HIT workup if >50% drop in platelets</div><div>4T’s - thrombocytopenia, timing, thrombosis, alTernative</div> <div><img></img></div> <div>A score of 0–8 points is generated; if the score is 0-3, HIT is unlikely. A score of 4–5 indicates intermediate probability, while a score of 6–8 makes it highly likely. Those with a high score may need to be treated with an alternative drug while more sensitive and specific tests for HIT are performed, while those with a low score can safely continue receiving heparin as the likelihood that they have HIT is extremely low.</div><div><br></br></div><div>Treatment</div><div>-stop all sources of heparin (and warfarin)</div><div>-begin tx with DOAC or fondapiranaux</div><div>-only transfuse platelets if <50K or bleeding</div><div>-duration of anticoagulation depeds on whether pt had thrombotic event</div><div>-diagnosis: ELISA</div> <div></div>”

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36
Q

<div>RC 2010 - What is true about anabolic steroids?</div>

<ol> <li>Does not impact musculotendinous junction</li> <li>Decreased threshold to tendon rupture (Dal Stem)</li> <li>Effects are irreversible</li> <li>Increased strength of tendons</li></ol>

A

2.<div><ul> <li>Evans (AJSM 2004) Current Concepts Anabolic Steroids</li> <ul> <li>Tendon rupture is based on small number of case reports</li> <li>Induces reversible changes in tendon structure</li> <ul> <li>Stiffer, less elastic tendon</li> <li>Ultimate strength is unaffected</li> <li>Rapid increases in skeletal muscle are not matched in tendon structures (weak link in chain)</li> </ul> </ul></ul></div><div><br></br></div><div><div>Nineteen (22%) of the AAS users, but only 3 (6%) of the nonusers, reported at least 1 lifetime tendon rupture.</div></div><div><br></br></div>

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37
Q

<div>RC 2009 - Effect of T3 and T4 on bone</div>

<ol> <li>Increases bone resorption and deposition</li> <li>Decreases bone resorption and deposition</li> <li>Increases resorption, decreases deposition</li> <li>Increases deposition, decreases resorption</li></ol>

A

“A.<div><br></br></div><div><div>“High levels of T3 and T4 are associated with increased bone turnover. Bone cells are stimulated to both increase bone resorption and bone synthesis. The more profound effect of resorption results in demineralization of bone and therefore increases the risk of fractures and mineral abnormalities i.e hypercalcemia. Both osteoblastic and osteoclastic activities are upregulated, but the osteoclastic activity dominates, resulting in decreased BMD and an increased risk of fragility fractures.””</div> <div>Overt hyperthyroidism is associated with accelerated bone remodeling, reduced bone density, osteoporosis, and an increase in fracture rate.</div> <div>Thyroid hormone may affect bone calcium metabolism either by a direct action on osteoclasts or by acting on osteoblasts, which in turn mediate osteoclastic bone resorption</div></div>”

38
Q

RC 2012 - 4 ways a plate can function other than buttress

A

<ul> <li>Bridge plate</li> <li>Compression Plate</li> <li>Neutralization Plate</li> <li>Spring Plate</li> <li>Tension-band</li> <li>Rim Plate</li> <li>Locking/Fixed Angle Device</li></ul>

39
Q

RC 2015, 2012 - Definition of the area under the curve in a stress-strain curve: <ol> <li>Energy to yield point</li> <li>Energy to fatigue</li> <li>Energy to failure</li> <li>Stiffness</li></ol>

A

“C.<div><ul> <li>Toughness = amount of energy per volume a material can absorb before failure/fracture</li> </ul> <ul> <li><img></img></li></ul></div>”

40
Q

“<div>RC 2014, 2011 - Young’s modulus greatest to least:</div> <ol> <li>stainless steel, titanium, cortical bone, PMMA</li> <li>stainless steel, cobalt-chrome, PMMA, cortical bone</li> <li>stainless steel, titanium, PMMA, cortical bone</li></ol>”

A

“<div>A</div><ul> <li>Young’s modulus of elasticity measure of the stiffness (ability to resist deformation) of a material in the elastic zone </li> <li>Calculated by measuring the slope of the stress/strain curve in the elastic zone</li> <li>A higher modulus of elasticity indicates a stiffer martial</li> <li>Relative values of Young’s modulus of elasticity (numbers correspond to numbers on illustration to right)</li><li>first 4 - CAST Bone</li> </ul> <div>1. Ceramic (Al2O3)</div> <div>2. Alloy (Co-Cr-Mo)</div> <div>3. Stainless steel</div> <div>4. Titanium - closes to cortical bone</div> <div>5. Cortical bone</div> <div>6. Matrix polymers</div> <div>7. PMMA</div> <div>8. Polyethylene</div> <div>9. Cancellous bone</div> <div>10. Tendon / ligament</div> <div>11. Cartilage</div><div><br></br></div><div><img></img><br></br></div>”

41
Q

RC 2016 - What is an anisotropic substance? <ol> <li>Stainless steel</li> <li>Bone </li> <li>CoCr</li> <li>?</li></ol>

A

2.<div><ul> <li>Isotropic materials</li> <ul> <li>possess the same mechanical properties in all directions</li> <li>Example: golf ball</li> </ul> <li>Anisotropic materials</li> <ul> <li>possess different mechanical properties depending on the direction of the applied load</li> <li>Example: ligaments, bone</li> </ul> </ul> <ul> <li></li> <li>AAOS Comprehensive Review (p63)</li> <ul> <li>“Isotropic materials (for example, stainless steel, titanium alloys) have the same mechanical properties along all axes or in all directions within these materials”</li> <li>“In contrast to isotropic materials, anisotropic materials (bone, cartilage, muscle, ligaments, carbon-fiber composites) exhibit varying mechanical properties along different axes or in different directions within these materials under loading. This anisotropic behavior is a result of specifically oriented constituent parts of these materials, such as collage fibrils or crystals. “</li> <li>“Bone is anisotropic as a result of the orientation of its components”</li> </ul></ul></div>

42
Q

RC 2014 - What type of healing do you have with a statically locked femoral IM nail? <ol> <li>Absolute stability, primary healing</li> <li>Relative stability, secondary (callus) healing</li> <li>Absolute stability, secondary (callus) healing</li> <li>Relative stability, primary healing</li></ol>

A

B.

43
Q

<div>RC 2015 - The ability of a surface to resist plastic deformation is defined as:</div>

<ol> <li>Scratch resistance</li> <li>Surface tension</li> <li>Hardness</li> <li>Elasticity</li></ol>

A

C.<div><ul> <li>Wikipedia</li> <ul> <li>Hardnessis a measure of the resistance to localized plastic deformation induced by either mechanical indentation or abrasion</li> </ul> <li>Wisdom from Richard:</li> <ul> <li>Hardness is the resistance to plastic deformation (e.g., a local dent or scratch). Thus, it is a measure of plastic deformation, as is the tensile strength, so they are well correlated. Historically, it was measured on an empirically scale, determined by the ability of a material to scratch another, diamond being the hardest and talc the softer. Now we use standard tests, where a ball, or point is pressed into a material and the size of the dent is measured</li> </ul></ul></div>

44
Q

“RC 2018 -<b></b><b>Shown a stress-strain graph with 2 different curves. What it true of N compared to M? REPEAT</b> <div><b><img></img></b></div> <div>N= Steep elastic portion, then long plastic deformation, then fails earlier than M</div> <div>M= Less steep but longer elastic portion, short plastic portion, higher load to failure</div> <div>a) N has a lower elastic modulus</div> <div>b) N has more plastic deformation</div> <div>c) N has higher load to failure</div> <div></div> <div><br></br></div>”

A

“<div>Answer is B</div><div>Repeat</div><div>Plastic deformation (the further to the right they go the more plastic)</div><div>Elastic modulus (The point to which both stress and strain increase)</div><div>Strongest (highest strain)</div><div>Stiffest (steepest)</div><div><br></br></div><div><img></img><br></br></div><div><br></br></div><div><ul> <li>Stress</li> <ul> <li>Internal resistance of body to load </li> <li>Stress (Pa) = force (N)/area (m2)</li> <li>Note that Pressure is external resistance of body to load</li> </ul> </ul> <ul> <li>Strain</li> <ul> <li>Relative measure of deformation</li> <li>Strain = change in length/original length </li> </ul> </ul> <div><img></img></div> <ul> <li></li> <li>Young’s modulus of Elasticity</li> <ul> <li>Measure of stiffness</li> <li>E = Stress/Strain = slope in the elastic phase</li> <li>A material with a higher E can withstand greater forces than can material with a lower E</li> <li>Proportional increase with REVERSIBLE DEFORMATION</li> </ul> <li>Elastic limit (yield point) = proportional limit</li> <ul> <li>This is the transition point from elastic to plastic behavior. </li> <li>Beyond this point, the material’s structure is irreversibly changed. </li> <li>The elastic limit equals 0.2% strain in most metals. </li> </ul> <li>Plastic deformation </li> <ul> <li>Irreversible change after load is removed</li> <ul> <li>Occurs in the plastic range of the curve </li> <li>After the elastic limit, before the breaking point </li> </ul> <li>Ultimate strength<br></br>  Maximum strength (or stress) obtained by the material </li> <li>Breaking point<br></br>  Point at which the material fractures<br></br>  If deformation between the elastic limit and breaking point is large, the material is ductile.<br></br>  If this deformation is small, the material is brittle. </li> </ul> <li>Strain energy (toughness) </li> <ul> <li> Capacity of material (such as bone) to absorb energy </li> <li> Area under the stress-strain curve </li> <li> Total strain energy = recoverable strain energy (resil- <br></br> ience) + dissipated strain energy </li> <li> A measure of the toughness of material </li> <ul> <li> Ability to absorb energy before failure</li> </ul> </ul></ul></div>”

45
Q

<div><div>RC 2014, 2011 - Which of the following describes hydrodynamic lubrication?</div> <ol> <li>Water phase pushed out of cartilage </li> <li>Fluid between two surfaces with plastic deformation </li> <li>Decrease in friction between two opposing surfaces with a fluid boundary</li> <li>Fluid prevents two moving surfaces from contacting each other</li></ol></div>

A

D.<div><ul> <li>Elastohydrodynamic lubrication - elastic deformation of articular surfaces and thin films of joint lubricants separate surfaces</li> <ul> <li>Coefficient of friction a function of lubricant, not surfaces</li> </ul> <li>Boundary Lubrication - bearing surface is non-deformable, lubrication only partially separates surfaces</li> <li>Boosted (fluid entrapment) - lubricating fluid in pools, trapped by regions of surfaces that are in contact</li> <li>Hydrodynamic - fluid separates surfaces when one surface is sliding on the other</li> <li>Weeping - fluid shifts out of cartilage in response to load</li></ul></div>

46
Q

“RC 2015 - What decreases strain on the plate in plating a lateral tibial plateau fracture: <ol> <li>Medial purchase with the screws (Medial cortical contact)</li> <li>Larger screws</li> <li>Subchondral locking screws</li> <li>Decreased working length’</li></ol>”

A

“A<div><ul> <li>Lots of effort/stress by 2016 group….mainly around use of strain in the stem (likely word remember issues, as strain of the plate is inherent to its shape and materials and wouldn’t change)</li> <li>Logic:</li> <ul> <li>Larger screws increase level force placed through plate</li> <li>Subchondral locking screws –> locking screws move as a single unit and therefore transfer more force to the plate</li> <li>Decreased working length increases point stresses between closes screws</li> <li>Medial purchase reduces cantilever effect, therefore reducing force transfer</li> </ul></ul></div>”

47
Q

RC 2018, 2014 - Regarding tension band wiring, all are true EXCEPT? <ol> <li>The medial malleolus is an example of a dynamic tension band</li> <li>Tension band wire can neutralize tensile forces, and in fact can convert them in compression forces with joint flexion</li> <li>A plate on the tension side of bone can act as a tension band</li> <li>Using it on the tension side of a bone will lead to compression on the opposite cortex</li></ol>

A

“A.<div><div>If a tension band produces fairly constant force at the fracture site during motion, such as the medial malleolus, it is called a static tension band. Conversely, if the compression increases with motion, such as in the patella with knee flexion, the tension band is called dynamic””</div></div>”

48
Q

<ul> <li>RC 2012 - Regarding functional loads in stable joints, all are true except?</li> </ul>

<ol> <li>Small change in direction of functional loads will not result in sudden shift in the joint</li> <li>There is edge loading with normal ROM</li> <li>Joints have a smooth ROM </li> <li>Functional loads will not result in pain during normal ROM</li></ol>

A

B.

49
Q

<div>RC 2018 - What is the current recommended standard for the perioperative management of rheumatologic biologic/TNF-alpha antagonist medications?</div>

<div>a.Stop 2 weeks before surgery and restart immediately after surgery</div>

<div>b.Stop 2 weeks before surgery, and restart 2 weeks after surgery</div>

<div>c.Continue all preoperative medications</div>

<div>d.Stop 2 months before surgery, and restart 3 months after surgery</div>

A

B

50
Q

RC 2012 - All are ways to decrease HIV transmission in HIV patients except: <ol> <li>Use single gloves only when doing arthroscopy</li> <li>Doing instrument ties </li> <li>Wearing waterproof gowns</li> <li>Passing sharps in a bin</li></ol>

A

A

51
Q

RC 2013, 2011 - What are 3 advantaging of coning the xrays

A

“<ul> <li>Collimation reduces the size of the beam –> reduces scatter exposure to the surgeon</li> <li>Reduce radiation dose to the patient</li> <li>Better quality image</li> </ul> <div></div> <div><img></img></div>”

52
Q

<div>RC 2018, 2012 - Four changes in muscles with endurance training</div>

A

<ul> <li>AAOS Comprehensive Review 2</li> <ul> <li>Endurance Training:</li> <ul> <li>Changes in central and peripheral circulation (increased capillary density)</li> <li>Muscle metabolism</li> <li>Increased mitochondrial size, number and density</li> <li>Increase in Krebs enzymes</li> <li>Increased use of fatty acids over glycogen</li> <li>Oxidative capacity of all fibre types increased</li> <li>Increased percentage of type IIA fibres</li> </ul> </ul></ul>

53
Q

<div>RC 2012 - With depletion of ATP in hypoxia secondary to hypovolemia, which of the following represents the correct description for changes in the intracellular milieu? </div>

<ol> <li>Decreased sodium, increased potassium, decreased water</li> <li>Decreased sodium, decreased potassium, decreased water</li> <li>Increased sodium, decreased potassium, no change in water</li> <li>Increased sodium, decreased potassium, increased water</li></ol>

A

“<div>D</div><ul> <li>Increased Na/H20 (always follow eachother)</li> <li>Decrased K+</li><li><img></img><br></br></li> </ul> <ul> <li><img></img></li></ul>”

54
Q

<div>RC 2015, 2012 - What electrolyte abnormality is associated with hypovolemic shock resuscitated with normal saline?</div>

<ol> <li>Hyperchloremic metabolic alkalosis</li> <li>Hypochloremic metabolic acidosis</li> <li>Hyperchloremic metabolic acidosis</li> <li>Increased sodium bicarb</li></ol>

A

<div>C</div>

<ul> <li>2012, 2015</li> <li>Lira (Annals of Intensive Care 2014) Choices in fluid type and volume during resuscitation</li> <ul> <li>Normal saline use is associated with hyperchloremic metabolic acidosis and increased risk of AKI. The risk is decreased when balanced salt solutions are used.</li> </ul></ul>

55
Q

<div>RC 2013 - Which of the following is a reason NOT to put O2 on an old person in trauma</div>

<ul> <li>A. Chronic lung disease with increased PaCO2</li> <li>B. Chronic lung disease with decrease PaCO2</li> <li>C. Heart disease</li> <li>D. No reason to not put O2 on</li></ul>

A

“D. ““Supplemental oxygen should be placed on all elderly trauma patients. This practice provides the needed oxygen reserves if rapid sequence intubation is needed and contributes to cellular oxygenation”””

56
Q

RC 2014, 2009 - What causes muscular tears? <ol> <li>Eccentric contractures</li> <li>Concentric contractures</li> <li>Repetitive exertion to sub-injury levels</li> <li>Cannot remember the last option</li></ol>

A

A.<div><br></br></div><div>Forcible stretching of a muscle…most often during an eccentric contraction when the muscle is being lengthened as it contracts Generates higher forces than concentric<br></br></div>

57
Q

Intramembranous vs Enchondral bone formation?

A

<ul> <li>Intramembranous - occurs when mesenchymal stem cells (MSC) and osteoprogenitor cells form new bone directly i.e. Direct bone healing </li> <ul> <li>Primary bone healing (compression plating)</li> </ul> <li>Endochondral - occurs when cartilage is produced from differentiation of MSC into chondrocytes, which then undergo calcification --> transformed into bone</li> <ul> <li>Secondary bone healing - callus formation (IMN, casting)</li> </ul></ul>

58
Q

JAAOS Osteoimmunology

A

“<div> <div> <div> <ul> <li>Summary</li> <ul> <li>Early fracture stabilization decreases soft-tissue damage and improve the inflammatory response</li> <li>Factors that affect local inflammation</li> <ul> <li>Soft tissue injury</li> <li>Fracture hematoma</li> <li>Stability of # management</li> </ul> <li>Systemic factors that influence local response to injury</li> <ul> <li>Acute disease states: polytrauma, sepsis</li> <li>Chronic disease states: DM,endocrine/metabolic dz, inflammatory arthropathies</li> <li>Drugs: Anti-flamm</li> </ul> <li>Fracture union influenced by surrounding muscle and a clean wound bed</li> <ul> <li>95-100% success rate for flaps for open/mangled fractures if cleaned</li> <li>Skeletal muscle provides osteoprogenitor cells</li> <li>Muscle exposed to BMP show osteoblastic differentiation</li> <li>4 known muscle/bone factors likely involved in the inflammatory phase of fracture healing</li> <ul> <li>‘MIBO’</li> <li>Myostatin</li> <li>IGF-1</li> <li>BMP</li> <li>Osteonection</li> </ul> </ul> <li>Acute systemic inflammation, such as in patients with polytrauma, requires an interdisciplinary approach and interdisciplinary care to enhance the hemostasis of the inflammatory response</li> <li>Chronic systemica inflamm affects # healing</li> <ul> <li>RA</li> <li>DM, RFs:</li> <ul> <li>presence of peripheral neuropathy</li> <li>Surgery duration- every additional 10 minutes past a set time increases bone healing risk incrementally by 15%</li> <li>HbA1C>7%</li> </ul> </ul> <li>RFs for non-union in distal femur fractures (Rodriguez, 2014)</li> <ul> <li>Obesity</li> <li>Open #</li> <li>Infection</li> <li>Stainless Steel Plates</li> <li>No: smoking, DM, chronic steroids</li> </ul> <li>RFs for revision surgery for tibial non-union (Bhandari, 2003)</li> <ul> <li>Open #</li> <li>Transverse #</li> <li>Fracture gap</li> <li>No: smoking, DM, chronic steroids</li> </ul> <li>NSAIDs</li> <ul> <li>Indomethacin - only drug to truly delay fracture healing (Chen, 2013)</li> <li>Indomethacin seems to be worse for diaphyseal fractures</li> <ul> <li>Metaphysis has greater progenitor/stem cells</li> </ul> <li>Avoid in patients with risk of cerebral hemorrhage or soft-tissue bleeding</li> </ul> </ul> </ul> </div> </div></div>”

59
Q

“RC 2010 - 45 yr old male going for a TKA.<ol> <li>What level should their factor level (hemophilia) be pre-op ?</li> <li>How long should these levels be maintained post-op ?</li> <li>Bogus question - Exact wording ““How would this patient’s outcome compare with an unaffected person with Hemophilia”” ?</li></ol>”

A

<div>Manny’s list:</div>

<ul> <li>2 hrs preop infuse to attain 100% activity of normal</li> <li>intra-op continuous infusion of factor to maintain levels >60%</li> <li>immediate post-op continuous infusion to maintain >60% level until d/c</li> <li>2 weeks post op infusion of bolus doses to maintain levels 30-60%</li> <li>vigorous physio infused to a 30% level just before therapy</li></ul>

<ul> <li>in the absence of infection, durability of knee implants equivalent to other arthritic groups</li> <li>Equivalent rates of early infection, <b>higher rates of late infection (RC MCQ 2008)</b></li></ul>

60
Q

RC 2012 -Which of the following is false regarding proteoglycans? REPEAT <div>a. They consist of 30% of the articular cartilage by weight </div> <div>b. They are composed of a protein core </div> <div>c. They are hydrophobic </div> <div>d. They are sulfated</div>

A

<div>C. Hydrophilic --> draw in water</div>

<div><br></br></div>

<div>Articular cartilage is made up of cells and ECM (water, collagen II, proteoglycans)</div>

<div><br></br></div>

<div><ul><li>make up 10 to 15% of cartilage</li><li>function to providecompressive strength and <b><u>attract water</u></b></li><li>aggrecanis most responsible for hydrophilic behavior</li><li>produced by chondrocytes</li><li>proteoglycans composed of GAG subunits</li><ul><li>chondroitin sulfate</li><li>keratin sulfate</li></ul></ul></div>

61
Q

RC 2014, 2011 -<b></b>What cells produce hyaluronic acid for the synovial fluid? <div>a. Synoviocytes</div> <div>b. Chondrocytes near the tide mark</div> <div>c. Specialized synovial neutrophils</div> <div>d. Chondrocytes at the surface of the articular cartilage</div>

A

A.<div><div><br></br></div><div>Synovial Cells:</div> <div>· Type A - important in phagocytosis</div> <div>· Type B - fibroblast-like cells that produce synovial fluid</div> <div> </div> <div>Zones of cartilage (from joint space to bone):</div> <div>· Superficial: collagen oriented parallel to joint; <i>only zone where progenitor cells are found</i></div> <div>· Middle/intermediate: collagen oriented randomly</div> <div>· Deep: collagen oriented perpendicular to joint; highest concentration of proteoglycans (HYDROPHILIC)</div> <div>· Tidemark: transition from cartilage to subchondral zone (remnant of cartilage anlage)</div></div><div><br></br></div>

62
Q

RC 2011 - Which cell is not present in inflammatory phase of healing? <ol> <li>osteocytes</li> <li>osteoclasts</li> <li>PMNs</li> <li>Macrophages</li></ol>

A

A.<div><br></br></div><div><div>Osteocyte Apoptosis and Osteoclast Presence in Chicken Radii 0–4 Days Following Osteotomy – Calcified tissue international 2005 Clark</div></div>

63
Q

<div>RC 2011 - After fracture healing, when is blood flow greatest? (prob after fracture, during healing)</div>

<ol> <li>5-7 days</li> <li>2 weeks</li> <li>6 weeks</li> <li>4 weeks</li></ol>

A

B.<div><br></br></div><div><div>Blood flow initially decreases then rises within hours and peaks at week 2, returning to normal at 3-5 months</div></div>

64
Q

<div>RC 2014 - Type 2 collagen is the primary component of which structure</div>

<ol> <li>Annulus fibrosis</li> <li>Nucleus pulposis</li> <li>Vertebral body</li></ol>

A

B.<div><br></br></div><div>col 2 = H2O in middle ie nucleus</div><div><br></br></div><div><div>Nucleus pulposus cells generally synthesize only type-II collagen in alginate beads, whereas anulus fibrosus cells produce both type-I and type-II collagen</div></div>

65
Q

RC 2012 -With regards to proteoglycans, all of the following except <ol> <li>Proteoglycans are hydrophilic</li> <li>Proteoglycans are hydrophobic</li> <li>Proteoglycans are sulfated</li> <li>Proteoglycans are bound to a protein core</li></ol>

A

“B.<div><ul> <li>Proteoglycans can trap water in the ECM by their negative charge, regulating matrix hydration</li> <li>"”Proteoglycans are macromolecules of the cell surface or ECM in which one or more glucosaminoglycan chains are joined covalently to a membrane protein or a secreted protein””</li> <li>Most of the main GAG chains are sulfated, i.e. chondroitin sulfate, heparan sulfate</li> <li>"”The very hydrophilic clusters of carbohydrate alter the polarity and solubility of the proteins with which they are conjugated””</li></ul></div>”

66
Q

<div>RC 2014 - All of the following are true regarding somatosensory evoked potentials (SSEP), EXCEPT? Double check old question on previous exams for wording.</div>

<ol> <li>IV anesthetics interfere with SSEP more than inhalational</li> <li>Muscle relaxation will not interfere with SSEP & actually may be beneficial as it improves quality of readings</li> <li>SSEP may have to be volume averaged to decrease background noise</li> <li>SSEP may involve stimulation of posterior tibial nerve and recording transcranial cortical response</li></ol>

A

<div>ANSWER: A</div>

<ul> <li>AAOS Comprehensive Review 2</li> <ul> <li>Not a real-time test because information is averaged to extract background noise</li> <li>Cortical or subcortical responses to the repetitive stimulation of a mixed peripheral nerve</li> <li>Gives information on the posterior spinal column</li> <ul> <li>50% change in amplitude is cause for concern than changes in latency</li> </ul> <li>Can be changed by anesthetics, nitrous oxide, hypothermia, hypotension</li> </ul> <li>JAAOS - Spinal Monitoring</li> <ul> <li>Mention SSEP compromised by halogenated anesthetic agents and NO (inhalational)</li> </ul> <li><b>JAAOS - Neurologic Injury in the Surgical Treatment of Idiopathic Scoliosis</b></li> <ul> <li><b>To facilitate intubation, aesthesia is typically induced with IV propofol and a single dose of a non-depolarizing neuromuscular relaxant. This combination allows excellent sedation without interfering with neuromonitoring</b></li> <li><b>Inhalation agents may cause false reduction in recorded amplitude and increased latencies</b></li> </ul></ul>

67
Q

<div><b>RC 2018, 2012 - </b>What is associated with sickle cell anemia?</div>

<div>a. RBC’s can sickle at normal oxygen tension </div>

<div>b. Presentation of bone infarct is similar to osteomyelitis </div>

<div>c. Heterozygous individuals are symptomatic </div>

<div>d. No increased risk of infection</div>

<div></div>

<div><br></br></div>

A

“<div>ANSWER: B</div><div>· 2015</div><div>·<i>Almeida A (British Journal of Hematology 2005) Bone Involvement in Sickle Cell Disease</i></div><div> Osteomyelitis usually presents with pain, swelling and tenderness over the affected area. The most common sites are the femur, tibia or humerus. Most patients also have fever and elevated inflammatory markers (but the fever may be modest). These signs and symptoms are similar to those found in vaso occlusive crises, making the distinction between a painful crisis and osteomyelitis extremely difficult on clinical grounds.</div><div>·<i>Skaggs DL (JBJS 2001)</i></div><div> Differentiation between osteomyelitis and bone infarct is challenging</div><div>· JAAOS 2005 ““Total hip arthroplasties in sickle cell hemoglobinopathies””</div><div> Pyogenic infections occur secondary to splenic autoinfection. Makes you more susceptible to polysaccharide-encapsulated organisms. These can cause osteomyelitis</div>”

68
Q

<div>RC 2013 - The initial increase in strength when Sheehan and Furey were just little R2’s (resistance training) was due to:</div>

<ol> <li>Increased number of myofibrils</li> <li>Increased capillaries</li> <li>Recruitment of more motor unit</li> <li>Increase of oxidative capacity</li></ol>

A

C.<div><ul> <li>Increased muscle cross-sectional area</li> <ul> <li>Muscle hypertrophic rather than hyperplasia</li> </ul> <li>Increased motor unit recruitment or synchronization</li> <li>Adaptation of all fibre types</li></ul></div>

69
Q

<div>RC 2015 - What is an example of a closed chain exercise:</div>

<ol> <li>Hamstring curls</li> <li>Straight leg raise in a cast</li> <li>Eccentric contraction of biceps while holding a dumbbell</li> <li>Squatting 10lbs with feet on the ground</li></ol>

A

D<div><div>Closed Chain = feet fixed</div></div>

70
Q

RC 2015 - What is an example of a closed chain exercise: <ol> <li>Hamstring curls</li> <li>Straight leg raise in a cast</li> <li>Eccentric contraction of biceps while holding a dumbbell</li> <li>Squatting 10lbs with feet on the ground</li></ol>

A

D

71
Q

OI presentation in Adults?

A

<ul> <li>Fractures</li> <ul> <li>25% in adulthood</li> <li>High complications: 11% nonunion, 5% malunion, 5% implant loosening</li> <li>Normal healing time</li> </ul> <li>TKA</li> <ul> <li>IM alignment may be tough given previous deformity - use nav if needed</li> <li>Cement!</li> <li>May need constraint as 50% have lig laxity</li> </ul> <li>THA</li> <ul> <li>Protrusion in 50% - graft, cage, </li> <li>Cement</li> </ul> <li>Spine</li> <ul> <li>50% of fractures</li> <li>Bracing favoured</li> <li>Vertebroplasty contraindication</li> <ul> <li>Kyphoplasty ok</li> </ul> <li>Kyphoscoliosis </li> <ul> <li>>60o associated with >50 loss of vital capacity</li> <li>Standard fusion, but with post-op bracing</li> </ul> </ul> <ul> <li>Spondylolisthesis - dysplastic</li> <ul> <li>Non-op</li> </ul> </ul></ul>

72
Q

OI Medical manifestations and medical treatment?

A

<div>Non-Orthopedic Manifestations:</div>

<ul> <li>50% dentinogenesis --> dentist to avoid chronic infection</li> <li>50% hearing loss</li> <li>95% mitral valve +/- aortic valve insufficiency</li> <ul> <li>Enlargement of ventricles, pulmonary artery, aorta</li> </ul> <li>Basilar invagination:</li> <ul> <li>Age of onset adolescence or early adulthood</li> <li>HA, vertigo, nausea, CN dysfunction, myelopathy</li> <li>Treatment:</li> <ul> <li>Long posterior fusion (O-C5)</li> <li>Anterior odontoidectomy</li> </ul> </ul></ul>

<div><div>Medical Therapy:</div> <ul> <li>Second generation bisphosphonates:</li> <ul> <li>Alendronate, pamidronate</li> <ul> <li>Improvement in bone density, reduced fracture rates</li> <li>No evidence for improvement in bone pain, growth or QoL</li> <li>Slow progression of kyphoscoliosis</li> </ul> <li>No good evidence for milder forms </li> <li>High risk of complications due to long term use</li> <ul> <li>Osteonecrosis of jaw, atypical fractures, delayed union of spine surgery</li> </ul> </ul> <li>Teriparatide:</li> <ul> <li>Early evidence for improvement of BMD in type 1</li> <li>Promote fracture union and callus formation</li> <li>Consider use in atypical femur fracture due to bisphosphonate use</li> </ul> <li>Denosumab:</li> <ul> <li>Early evidence in kids for improved BMD, reduced rate of fracture, normalize dysmorphic vertebrae and improve mobility</li> </ul> <li>No effect:</li> <ul> <li>Calcitonin</li> <li>Anabolic steroids</li> <li>Supra-physiologic vitamin C or D</li> <li>Sodium Fluoride</li> <li>Magnesium</li> </ul></ul></div>

73
Q

Indications for measuring BMD?

A

“<img></img>”

74
Q

hormone (estrogen, testosterone) effect on bone?

A

<ul> <li>Estrogen</li> <ul> <li>Inhibits osteclasts</li> <li>After menopause E decreases</li> <ul> <li>Women 2x as likely to have fragility fracture in their life</li> </ul> </ul> <li>Testosterone stimulates osteoblasts</li></ul>

75
Q

“Cierny’s patient classification?”

A

<ul> <li>Class A: healthy</li> <li>Class B(Local): previous trauma, burns, scars, surgery to involved site</li> <li>Class B(Systemic): DM, immunocompromised, smoker, malnutrition, vascular disease</li> <li>Class C patients are either so compromised that the risks of treatment outweigh the benefits, or the symptoms of their infection are sufficiently limited that surgical treatment is not indicated.</li></ul>

76
Q

CRPS: Dx and Tx?

A

” <div> <div>-sensory: hyperalgesia</div><div>-motor: decreased ROM</div><div>-edema</div><div>-vasomotor: temp changes</div><div><br></br></div><div>-Treatment</div><div><ul><li>Nonoperative<a><img></img></a><ul><li>physical therapy and pharmacologic treatment<ul><li>indications<ul><li>first line of treatment</li></ul></li></ul></li><li>nerve stimulation<ul><li>indications<ul><li>symptoms present mainly in the distribution of one major peripheral nerve<br></br></li></ul></li></ul></li><li>nerve blockade<ul><li>indications<ul><li>failed initial nonoperative treatment</li></ul></li></ul></li><li>chemical sympathectomy<ul><li>indications<ul><li>acts as another option when physical therapy and less aggressive nonoperative management fails</li></ul></li></ul></li></ul></li><li>Operative<ul><li>surgical sympathectomy<a><img></img></a><ul><li>indications<ul><li>failed nonoperative management (including chemical sympathectomy)</li></ul></li></ul></li><li><strong>surgical decompression</strong><ul><li>indications<ul><li>CRPS type II with known nerve involvement (e.g. carpal tunnel release if median nerve involved)</li></ul></li><li>best success for CRPS is if you can find an associated nerve problem and treat it</li></ul></li></ul></li></ul></div><div><br></br></div> </div>”

77
Q

<div>RC 2009 - Woven bone has the following characteristics (need help for stems here)</div>

<ol> <li>Collagen is randomly oriented (or in disorder)</li> <li>Haversians</li> <li>Cement line interdigitation</li> <li>Canaliculi or something like that</li></ol>

A

“A.<div><ul> <li> <div> <ul> <ul> <li><u>Woven bone</u></li> </ul> <ul> <li>immature or pathologic bone that iswoven and random and isnot stress oriented</li> <li>compared to lamellar bone, woven bone has:</li> <ul> <li>more osteocytes per unit of volume</li> <li>higher rate of turnover</li> </ul> </ul> <ul> <li>weaker and more flexible than lamellar bone</li> </ul> </ul> <ul> <ul> <li><u>Lamellar bone</u></li> <ul> <li>secondary bone created by remodeling woven bone</li> <li>organized andstress oriented</li> </ul> </ul> <ul> <li>stronger and less flexible than woven bone</li> </ul> </ul> </div> </li> </ul> <div>Cortical</div> <ul> <li>80% of skeleton</li> <ul> <li>metabolism</li> <li>characterized byslow turnover rate andhigh Young’s modulus</li> <li>structure</li> <ul> <li>made of packedosteonsor Haversian systems</li> <ul> <li>osteons</li> <ul> <li>outer border defined by cement lines</li> </ul> <li>vascular canals</li> <ul> <li>contain arterioles, venules, capillaries, and nerves</li> <li>if oriented along long axis of bone:Haversian canals</li> <li>if oriented transversely to long axis of bone:Volkmann canals</li> </ul> <li>interstitial lamellae</li> <ul> <li>the region between osteons</li> </ul> </ul> </ul> </ul> </ul> <div>Cancellous bone(spongy or trabecular bone)</div> <ul> <li>metabolism</li> <li>lower Young’s modulus and more elastic</li> </ul> <ul> <li>high turnoverto remodel according to stress across the bone</li> </ul> <ul> <li>structure</li> <ul> <li>boney struts organized into a loose network</li> <li>each strut is approximately 200 micrometers in diameter</li> </ul> <li>30-90% of bone is porous and contains bone marrow</li> </ul> <ul> <li>increased porosity in osteoporosis</li></ul></div><div><br></br></div>”

78
Q

RC 2009 -<b></b><b>With the large c-arm. All of the following decrease radiation except:</b> <div><b>a. </b><b>Giving surgeon control</b></div> <div><b>b. </b><b>Inverting c-arm</b></div> <div><b>c. </b><b>Placing limb closer to x-ray generator</b></div> <div><b>d. </b><b>Something about collimation that was true</b></div>

A

C.<div><br></br></div><div><div>Potential decrease in radiation exposure can be accomplished by:</div> <div>· Reduced exposure time</div> <div>· Increased distance from beam</div> <div>· Increased shielding</div> <div>· Beam collimation/coning</div> <div>· Using lower dose</div> <div>· Inverting the C-arm</div> <div>· Surgeon control of C-arm</div><div><br></br></div><div><br></br></div></div>

79
Q

RC 2015 - Regarding MRI with gadolinium, which is true? <ol> <li>Can be fatal in patients with renal insufficiency</li> <li>Cannot distinguish between an abscess and a phlegmon</li> <li>Cannot differentiate between cyst and tumor</li> <li>Cannot differentiate between tumor and necrotic tissue</li> </ol> <div></div>

A

A.<div><div>Patients with kidney failure can get nephrogenic systemic fibrosis (NSF)</div></div><div><br></br></div>

80
Q

List from sup to inf the SERs?

A

“<div>piriformis</div><div>superior gamellus</div><div>obturator internus</div><div>inferior gamellus</div><div>quadratus femorus</div><div><br></br></div><div>note that obturator externus also does ER</div><img></img><br></br><div><img></img><br></br></div>”

81
Q

Important roots for nerves from Lumbosacral plexus?

A

Sciatic = L4-S3 - ant/post divisions<div>-Tibial nerve (L4-S3) -> medial and lateral plantar nerves</div><div>-Common peroneal</div><div><br></br></div><div>Femoral nerve = L2-L4</div><div>Obturator nerve = L2-L4</div><div><br></br></div><div>LFCN = L2-L3</div>

82
Q

Preganglionic Injury Findings?

A

“<ul> <li>Horner’s Syndrome</li> <li>Winged Scapula Medially</li> <ul> <li>Medial winging from long thoracic nerve (Serratus anterior) injury C5-C7</li> <li>If serratus and rhomboids working –> usually post-ganglionic</li> </ul> <li>Flail Arm on presentation</li> <li>Sensory deficits</li> <li>Absence of Tinel sign (tenderness to percussion) in the neck</li> <li>Normal histamine test (C8-T1 sympathetic ganglion)</li> <ul> <li>Post ganglionic injury has abnormal response</li> <ul> <li>With pre-ganglionic injury you will see redness, flare, and wheal</li> </ul> </ul> <li>Elevated hemi-diaphragm (phrenic nerve)</li> <li>Rhomboid Paralysis (dorsal scapular nerve)</li> <li>Supraspinatus/infraspinatus (suprascapular nerve)</li> <li>Latissimus dorsi (thoracodorsal)</li> <li>Severe pain in anesthesized limb –> root avulsion generally</li></ul>”

83
Q

Axillary artery anatomy?

A

“<div><img></img><br></br></div><div><img></img><br></br></div><div><br></br></div><img></img>”

84
Q

Bisphosphonate indications?

A

<ul> <li>Bisphosphonate treatment (or at least medical management of osteoporosis) recommended if:</li> <ul> <li>Hip or vertebral fractures and BMD T scores <2.5 OR</li> <li>If additional risk factors are present and T scores at the femoral head and spine are between 1.0 and 2.5 in post menopausal women and men >50 OR</li> <li>If patient has a 10 year hip fracture probability >3% or a fragility fracture risk >20% based on US-adapted WHO absolute fracture risk model</li> <li>SEE OSTEOPOROSIS SECTION UNDER TRAUMA PRINCIPLES</li> </ul></ul>

85
Q

Tx principles in AFF?

A

<ul> <li>Referral to endocrinologist</li> <li>Stop diphosphonates- contralateral fracture rate decreases from 41% to 19%.</li> <li>Check Vit D and Calcium levels</li> <li>Optimize nutritional status</li> <li>Consider treatment with recombinant parathyroid hormone- Teriparatide (forteo)</li> <li>Surgical stabilization with a cepholmedullary device</li></ul>

86
Q

Non-ortho manifestations of Ankylosing Spondylitis

A

<ul> <li>Head</li> <ul> <li>Uveitis</li> </ul> <li>Chest/Abdo</li> <ul> <li>Pulmonary fibrosis</li> <li>Conduction abnormalities - rbbb</li> <li>Aortic valve insufficiency</li> <ul> <li>Ascending aortic conditions (aortitis, stenosis, aortic regurg)</li> </ul> <li>Pulmonary fibrosis</li> <li>Renal amyloidosis</li> <li>IBD/colitis</li> </ul> </ul>

<ul> <li>Spine</li> <ul> <li>Spontaneous fusions</li> <li>Sacroiliitis</li> <li>Arachnoiditis</li> </ul> <li>GU</li> <ul> <li>Prostatitis</li> <li>Urethritis</li> </ul> <li>Others</li> <ul> <li>More susceptible to Klebsiella pneumonia synovitis</li> <li>HLA-B27</li> </ul> <li>Large joint arthritis</li> <ul> <li>33% hip involvement</li> </ul></ul>

87
Q

DCO indications

A

<div><ul><li>ISS >40 (without thoracic trauma)</li><li>ISS >20 with thoracic trauma</li><li>GCS of 8 or below</li><li>multiple injuries with severe pelvic/abdominal trauma and hemorrhagic shock</li><li>bilateral femoral fractures</li><li>pulmonary contusion noted on radiographs</li><li>hypothermia <35 degrees C</li><li>head injury with AIS of 3 or greater</li><li>IL-6 values above 500pg/dL</li></ul></div>

<div><br></br></div>

shock (BP < 90 mmHg, refractory to blood products, lactate > 2.5 mg/dL)<div><br></br></div><div>coagulopathy (platelet count < 90,000 mm3, fibrinogen < 1 g/L),</div><div><br></br></div><div>hypothermia (< 35°C)</div><div><br></br></div><div>significant chest, abdomen or pelvis injuries (pulmonary contusions, severe liver/spleen lacerations, pelvic ring disruption<br></br></div>

88
Q

DDH: associated pathologies?

A

“associated with ““packaging”” deformities which include<ul><li>congenital muscular torticollis(20%)</li><li>metatarsus adductus(10%)</li><li>congenital knee dislocation</li></ul>”

89
Q

JAAOS 2017 - RFs and tx for c. diff?

A

<ul> <li>Gram +ve anaerobic bacillus</li> <li>RFs: </li> <ul> <li>Host: age > 65, comorbidities, history of GI surgery</li> <li>Rx factors: Abx exposure, healthcare exposure, residency in long-term care facility, meds, tube feeding, surgery </li> <li>Ortho RFs: multiple comorbidities, Abx more than prophylaxis, Surgery > 24 hours after admission, increased LOS, revision surgery </li> </ul> <li>Patients usually tested if 3 or more loose stools in 24 hours </li> <li>Resistant to alcohol, need to wash hands with soap and water </li> <li>Abx: clindamycin, fluoroquinolones, vancomycin most common associated Abx</li> <li>Dx: toxogenic culture (GOLD)</li> <li>Rx: oral flagyl, oral vancomycin, IV flagyl+oral vanco in severe complicated cases</li></ul>

90
Q

What is not true regarding bisphosphonates?<div>A. Good oral bioavailability</div><div>B. Creates sclerotic lines below the physis</div><div>C. Causes growth arrest</div><div>D. Medication stays hidden in the bone for a long time after administration</div>

A

“Answer: C<div><br></br></div><div>Class of drugs that prevent bone mass loss by inhibiting osteoclast resorption. Prevent formation of osteoclast ruffled border microtubules, causing apoptosis.</div><div><br></br></div><div>Non-nitrogen containing (etidronate, clodronate) and nitrogen containing (alendronate, risedronate, pamidronate, zoledronate).</div><div><br></br></div><div>Renal excretion</div><div><br></br></div><div>Some are PO some are IV (A is true, = wrong)</div><div>Does cause sclerosis/sclerotic lines (B is true, = wrong)</div><div>Does not actually cause growth arrest, just harris lines<img></img>(C is WRONG = true)</div><div>High accumulation in bone (binding affinity to calcium) - D is true (= wrong)</div><div><br></br></div>”

91
Q

What is true regarding HIV-assiociated arthritis? (RC 2019)<div>A. Mimics degenerative OA</div><div>B. Symptoms progress rapidly over 3-6 months</div><div>C. Most commonly affected joints are the knees and elbows</div><div>D. Aspirate demonstrates a non-inflammatory reaction</div>

A

“Answer: D<div><ul><li><div>Radiological changes can occasionally mimic RA, with joint space narrowing, erosions and periarticular osteopenia. However, <span>some patients demonstrate new bone formation - a radiological finding unusual in RA.</span></div></li></ul><ul><li><div>HIV-associated arthritis tends to be <span>short lived</span> with its peak intensity occurring in <span>1 to 6 </span><span>weeks.</span></div></li></ul><ul><li><div>There is an inflammatory, but <span>sterile pattern on synovial fluid</span> analysis with WBC in the region of <span>50–2,600 cells/μL</span>, and <span>normal glucose</span>.</div></li><ul><li><div>ANA, RF and HLA-B27 are <span>negative.</span></div></li></ul></ul><ul><li><div>There remains considerable debate as to whether HIV infection is the cause of, or a coincidental finding in patients who are HIV positive and seronegative with an inflammatory arthritis.</div></li></ul><ul><li><div>Predominantly affects the knees and ankles.</div></li></ul></div>”