Basic Science Flashcards
<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>
<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>
RFs for Metal hypersensitivity? MCQ 2018
<b>female (not male): RR 4</b><div>piercings: 3.2</div><div>hand eczema: RR 3</div><div>smoking: RR 3</div>
MOA of BMP (MCQ 2018, SAQ 2010)
<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>
peri-op mx of rheumatoid meds?
stop biologics 2 weeks before, start 2 weeks after (MCQ 2018)<div><br></br></div><div>continue MTX, plaquenil (hydroxy)</div>
HIV transmission?
0.3% HIV<div>3% Hep C</div><div>30% Hep B</div>
Complication with INFIX?
<b>LFCN palsy</b> - 0-30% (MCQ 2018)<div>HO 0-25%<br></br><div><br></br></div></div>
short vs long im nail for intertroch fracture?
short nail is cheaper<div><b>increased iatrogenic fractures in long (mcq 2018)</b></div><div>equal: torsional strength, risk of rotational abnormalities</div>
Properties of BG?
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>
Dx criteria for RA?
“<img></img>”
Agents to decrease intra-op bleeding
“<div> <div> <div><img></img></div> </div></div>”
<div>RC 2014 - Name 6 modifiable risk factors for osteoporosis, excluding medications</div>
“<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>”
<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>
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>
<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>
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>
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>
“B.<div><br></br></div><div><img></img><br></br></div>”
<div><b>RC 2011 - What are two mechanisms of action of BMP?</b></div>
<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>
<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>
<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>
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>
“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>”
<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.<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>
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>
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>
<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>
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>
<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>
“2.<div><br></br></div><div><div> <div> <div><img></img></div> </div></div></div>”
<div>RC 2016 - Fight bite. What antibiotic? </div>
<ol> <li>Keflex </li> <li>Amox-Clav </li> <li>TMP/SMX </li> <li>?</li></ol>
“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>”
<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>
<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>
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.<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>”
<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>
<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>
<div>RC 2014, 2011 - List 4 poor prognostic factors for septic arthritis.</div>
<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>
<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>
“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>”
<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>
<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>
<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.<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>
<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>
B.JAAOS 2004 – Parathyroid Hormone Preferential stimulation of osteoblastic activity over osteoclastic activity<div><br></br></div>
<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>
“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>”
<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>
<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>
<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>
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>
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>
<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>
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>
“<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>”
<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>
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>