2015 Basic Science Flashcards by Olivier GK

Question 9
Increased levels of peroxisome proliferator-activated receptor gamma 2 (PPARy2) result in increased
1. bone.
2. adipose.
3. cartilage.
4. muscle.
5. tendon or ligament

adipose.

Regulates fatty acid and glucose metabolism.

PPAR-γ1 (found in nearly all tissues except muscle)

PPAR-γ2 (mostly found in adipose tissue and the intestine): Well established as a prime inducer of adipogenesis

RECOMMENDED READINGS
Lee FY, Drissi MH, Zuscik MJ, Chen D, Nizami S, Goto H. Molecular and cell biology in orthopaedics.
In: O’Keefe RJ, Jacobs JJ, Chu CR, Einhorn TA, eds. Orthopaedic Basic Science Foundations of Clinical
Practice. 4th ed. Rosemont, IL: American Academy of Orthopaedic Surgeons; 2013:3-42.
Takada I, Suzawa M, Matsumoto K, Kato S. Suppression of PPAR transactivation switches cell fate of
bone marrow stem cells from adipocytes into osteoblasts. Ann N Y Acad Sci. 2007 Nov;1116:182-95.
Epub 2007 Jul 26. Review. PubMed PMID: 17656564.

How well did you know this?

Not at all

Perfectly

Question 22
What is the mechanism of the anticoagulation effect of heparin?
1. Inhibition of Factor Xa
2. Activation of antithrombin (AT) III
3. Degradation of serine proteases
4. Interference with Factors Va and VIIIa
5. Blocking of vitamin K epoxide reductase (VKOR)

Activation of antithrombin (AT) III

RECOMMENDED READINGS
Pellegrini VD. Thrombolic disease and fat embolism syndrome. In: O’Keefe RJ, Jacobs JJ, Chu CR,
Einhorn TA. eds. Orthopaedic Basic Science: Foundations of Clinical Practice. 4th ed. Rosemont, IL;
American Academy of Orthopaedic Surgeons. 2013:117-133.
Roehrig S, Straub A, Pohlmann J, Lampe T, Pernerstorfer J, Schlemmer KH, Reinemer P, Perzborn E.
Discovery of the novel antithrombotic agent 5-chloro-N-({(5S)-2-oxo-3-[4-(3-oxomorpholin-4-yl)phenyl]-
1,3-oxazolidin-5-yl}methyl)thiophene-2-carboxamide (BAY 59-7939): an oral, direct factor Xa inhibitor. J
Med Chem.2005 Sep 22;48(19):5900-8. PubMed PMID: 16161994

How well did you know this?

Not at all

Perfectly

Question 24
What is the most likely cause of a pseudotumor in a well-positioned total hip arthroplasty?
1. Loosening of the cup at the bone interface
2. Fretting and corrosion reaction from the taper
3. Adhesive wear products from polyethylene
4. Backside wear of the polyethylene liner
5. Catastrophic polyethylene failure with metal-on-metal contact

Fretting and corrosion reaction from the taper

The first article reports two cases of metal on poly THA where they suggest there was insufficient locking of the head/neck junction and so the distal part of it had micromotion, then toggling of the implants which lead to metal debris and pseudotumor…

Key here is that pseudotumor = metal on metal. Based on that the only other answer possible would be 5. Answer 5 uses the word” catastrophic” poly failure with MoM contact (I’m assuming where the poly splits and the metal head contacts the metal cup..??) but that doesn’t sound like a “well-positioned THA” at all

RECOMMENDED READINGS
Cook RB, Bolland BJ, Wharton JA, Tilley S, Latham JM, Wood RJ. Pseudotumour formation due to
tribocorrosion at the taper interface of large diameter metal on polymer modular total hip replacements.
J Arthroplasty. 2013 Sep;28(8):1430-6. doi: 10.1016/j.arth.2013.02.009. Epub 2013 Mar 23. PubMed
PMID: 23528556.
Lieberman JR ed. AAOS Comprehensive Orthopaedic Review. Rosemont, IL; American Academy of
Orthopaedic Surgeons. 2009: 21.

How well did you know this?

Not at all

Perfectly

Question 36
Which gait pattern is most likely associated with knee osteoarthritis progression?
1. Abductor lurch
2. Ankle-flxed short stance
3. Increased adductor moment
4. Impulse loading after heel strike
5. Anterior cruciate ligament (ACL) protective gait

Increased adductor moment

Peak knee adduction moment (KAM) and peak knee flexion moment (KFM) during early stance were found to be related to medial joint OA. KAM for femoral-sided cartilage wear, and KFM on tibial-sided wear

RECOMMENDED READINGS
Li J, Hosseini A, Gadikota HR, Li G. Kinesiology of the knee joint. In: O’Keefe RJ, Jacobs JJ, Chu CR,
Einhorn TA, eds. Orthopaedic Basic Science Foundations of Clinical Practice. 4th ed. Rosemont, IL:
American Academy of Orthopaedic Surgeons; 2013:261-278.
Chehab EF, Favre J, Erhart-Hledik JC, Andriacchi TP. Baseline knee adduction and flxion moments
during walking are both associated with 5 year cartilage changes in patients with medial knee
osteoarthritis. Osteoarthritis Cartilage. 2014 Nov;22(11):1833-9. doi: 10.1016/j.joca.2014.08.009. Epub
2014 Aug 27. PubMed PMID: 25211281; PubMed Central PMCID: PMC4369510.

How well did you know this?

Not at all

Perfectly

Question 52
What is a major controlling molecule for tendon collagen fiber size?
1. Elastin
2. Fibrillin
3. Decorin
4. Biglycan
5. Fibronectin

PREFERRED RESPONSE: 3

RECOMMENDED READINGS
Reuther KE, Gray CF, Soslowsky LJ. Form and function of tendon and ligament. In: O’Keefe RJ, Jacobs
JJ, Chu CR, Einhorn TA. eds. Orthopaedic Basic Science: Foundations of Clinical Practice. 4th ed.
Rosemont, IL; American Academy of Orthopaedic Surgeons; 2013: 213-228.
Zhang G, Ezura Y, Chervoneva I, Robinson PS, Beason DP, Carine ET, Soslowsky LJ, Iozzo RV, Birk DE.
Decorin regulates assembly of collagen firils and acquisition of biomechanical properties during tendon
development. J Cell Biochem. 2006 Aug 15;98(6):1436-49. PubMed PMID: 16518859.

How well did you know this?

Not at all

Perfectly

Question 61
What is the principal cause of age-related increase in articular cartilage brittleness?
1. More rapid cleavage of collagen
2. Increase in advanced glycation end products
3. Increased association of type IX collagen with type II collagen
4. Loss of matrilin 3 association with collagen fibrils
5. Type II collagen replacement with type III collagen

PREFERRED RESPONSE: 2

One of the best studied aging-related matrix protein modification in cartilage is the formation of advanced glycation end-products (AGEs). AGEs are produced from the spontaneous nonenzymatic glycation of proteins that occurs when reducing sugars such as glucose, fructose or ribose, react with lysine or arginine residues. Because the articular cartilage has a relatively low turnover rate, it is particularly susceptible to AGE formation. Type II collagen, the most abundant matrix protein in cartilage, has a half-life that has been calculated to be over 100 years (not answer 1, 3 or 5). The accumulation of AGEs in cartilage has been suggested to play a role in the development of osteoarthritis

RECOMMENDED READINGS
Chubinskaya S, Malfait A-M, Wimmer MA. Form and function of articular cartilage. In: O’Keefe RJ,
Jacobs JJ, Chu CR, Einhorn TA. eds. Orthopaedic Basic Science: Foundations of Clinical Practice. 4th ed.
Rosemont, IL: American Academy of Orthopaedic Surgeons; 2013:183-197.
Shane Anderson A, Loeser RF. Why is osteoarthritis an age-related disease? Best Pract Res Clin
Rheumatol. 2010 Feb;24(1):15-26. doi: 10.1016/j.berh.2009.08.006. Review. PubMed PMID: 20129196.

How well did you know this?

Not at all

Perfectly

Question 67
The muscle energy source for a marathon athlete is predominantly
1. glycogen.
2. glycogen and fatty acids.
3. glycogen and lactic acids.
4. Adenosine triphosphate (ATP) and creatine phosphate.
5. ATP, creatine phosphate, and glycogen.

glycogen and fatty acids.

You don't have enough glycogen for a marathon. 
Type I (oxidation) = marathon runner = slow twitch
Type IIb (Creatine-P + ATP) = sprinter = fast twitch
Type IIa (lactic acid) = 800m runner = fast twitch

RECOMMENDED READINGS
Wright A, Gharaibeh B, Huard J. Form and function of skeletal muscle. In: O’Keefe RJ, Jacobs JJ, Chu
CR, Einhorn TA, eds. Orthopaedic Basic Science Foundations of Clinical Practice. 4th ed. Rosemont, IL:
American Academy of Orthopaedic Surgeons; 2013:229-237.
Garrett WE Jr, Best TM. Anatomy, physiology, mechanics of skeletal muscle. In: Buckwalter JA, Einhorn
TA, Simon SR, eds. Orthopaedic Basic Science: Biology and Biomechanics of the Musculoskeletal
System. Rosemont, IL: American Academy of Orthopaedic Surgeons; 2000:693-716.

How well did you know this?

Not at all

Perfectly

Question 72
Which molecule is most responsible for the hydration of the intervertebral disk?
1. Decorin
2. Versican
3. Aggrecan
4. Type I collagen
5. Type II collagen

Aggrecan

RECOMMENDED READINGS
Moss IL, An HS. Form and function of the intervertebral disk. In: O’Keefe RJ, Jacobs JJ, Chu CR,
Einhorn TA, eds. Orthopaedic Basic Science: Foundations of Clinical Practice. 4th ed. Rosemont, IL:
American Academy of Orthopaedic Surgeons; 2013:253-260.
Roughley PJ. Biology of intervertebral disc aging and degeneration: involvement of the extracellular
matrix. Spine (Phila Pa 1976). 2004 Dec 1;29(23):2691-9. Review. PubMed PMID: 15564918.

How well did you know this?

Not at all

Perfectly

Question 84
What is the mechanism of action for denosumab in the treatment of osteoporosis?
1. Blocking the parathyroid receptor
2. Blocking the carbonic anhydrase receptor
3. Attachment to osteoprotegerin (OPG)
4. Attachment to receptor activator of nuclear factor kappa beta (RANK)
5. Inhibition of RANK ligand (RANKL)

Inhibition of RANK ligand (RANKL)

OSTEOCLAST ACTIVATORS:
• RANKL: activates osteoclasts. (Tip: RANCLASTS) to stimulate bone resorption.
• PTH: binds to osteoblasts to stimulate production of RANKL
• IL-1: stimulates osteoclast differentiation
• Prostaglandin E2
• IL-6 and MIP-1A (myeloma)

OSTEOCLAST INHIBITORS:
• OPD (osteoprotegerin): decoy receptor used by osteoblasts that binds/sequesters RANKL (inhibits osteoclasts)
• Calcitonin: interacts with osteoclasts directly
• Estrogen: decreases RANKL
• TGF-B: increase in OPG
• IL-10: suppresses osteoclasts

RECOMMENDED READINGS
Bukata SV, Tyler WK. Metabolic bone disease. In: O’Keefe RJ, Jacobs JJ, Chu CR, Einhorn TA, eds.
Orthopaedic Basic Science: Foundations of Clinical Practice. 4th ed. Rosemont, IL: American Academy
of Orthopaedic Surgeons; 2013:353-364.
Yasuda H. RANKL, a necessary chance for clinical application to osteoporosis and cancer-related bone
diseases. World J Orthop. 2013 Oct 18;4(4):207-17. doi: 10.5312/wjo.v4.i4.207. Review. PubMed PMID:
24147256.
Capozzi A, Lello S, Pontecorvi A. The inhibition of RANK-ligand in the management of postmenopausal
osteoporosis and related fractures: the role of denosumab. Gynecol Endocrinol. 2014 Jun;30(6):403-8. doi:
10.3109/09513590.2014.892067. Epub 2014 Mar 5. PubMed PMID: 24592987.

How well did you know this?

Not at all

Perfectly

Question 87
What is the function of sclerostin in adult bone homeostasis?
1. Decreases bone formation by inhibiting osteoblastogenesis
2. Decreases bone formation by promoting osteoclastogenesis
3. Decreases bone formation by inhibiting osteocytes
4. Increases bone formation by promoting osteoblastogenesis
5. Increases bone formation by inhibiting osteoclastogenesis

Decreases bone formation by inhibiting osteoblastogenesis

3 x “decreases bone formation” vs. 2 “increases bone formation” = probably “decreases”

2x osteoclast, 2x osteoblast, 1x osteocytes = probably osteoclast or osteoblasts

So that leaves only options 1 and 2 as probably the right answer

Sclerostin inhibits the Wnt pathway = inhibits bone formation. Secreted by osteocytes.

RECOMMENDED READINGS
Suen PK, He YX, Chow DH, Huang L, Li C, Ke HZ, Ominsky MS, Qin L. Sclerostin monoclonal
antibody enhanced bone fracture healing in an open osteotomy model in rats. J Orthop Res. 2014
Aug;32(8):997-1005. doi: 10.1002/jor.22636. Epub 2014 Apr 30. PMID: 24782158.
Bukata SV, Tyler WK. Metabolic bone disease. In: O’Keefe RJ, Jacobs JJ, Chu CR, Einhorn TA, eds.
Orthopaedic Basic Science: Foundations of Clinical Practice. 4th ed. Rosemont, IL: American Academy
of Orthopaedic Surgeons; 2013:353-364.

How well did you know this?

Not at all

Perfectly

Question 100
After initial arthroplasty surgery, infection that occurs within how many days is considered a surgical-site
infection?
1. 30 days
2. 45 days
3. 60 days
4. 90 days
5. 365 days

365 days

Pure memorization for this one… No tips for you!

RECOMMENDED READINGS
Salava JK, Springer BD. Orthopaedic infections. In: Cannada LK, ed. Orthopaedic Knowledge Update 11.
Rosemont, IL: American Academy of Orthopaedic Surgeons; 2014:287-306.
Mangram AJ, Horan TC, Pearson ML, Silver LC, Jarvis WR. Guideline for Prevention of Surgical Site
Infection, 1999. Centers for Disease Control and Prevention (CDC) Hospital Infection Control Practices
Advisory Committee. Am J Infect Control. 1999 Apr;27(2):97-132; quiz 133-4; discussion 96. PubMed
PMID: 10196487.

How well did you know this?

Not at all

Perfectly

Question 106
A 5-year-old boy has progressive muscle weakness. Examination reveals pseudohypertrophy of the calf
and deltoid musculature and a positive Gower sign. How is this disorder most commonly inherited?
1. Non-Mendelian
2. Autosomal recessive
3. Autosomal dominant
4. X-linked dominant
5. X-linked recessive

X-linked recessive

Pseudohypertrophy of proximal muscles is a combination of : proximal muscle wasting (which makes the distal muscles look hypertrophied in comparison), and infiltration of muscles with connective tissue.

Gower’s sign: kid rises by walking hands up legs to compensate for gluteus maximus and quadriceps weakness (proximal muscle weakness)

These signs are stereotypically synonymous with Duchenne’s muscular dystrophy, but can also be present in Becker’s muscular dystrophy. Either way, both are x-linked recessive (easy to remember cause it mostly affects boys).

This is probably Duchenne though since average age of diagnosis = 2 yo, Becker’s = 8 yo

RECOMMENDED READINGS
Babis GC, Sakellariou VI. Muscle disorders. In: Cannada LK, ed. Orthopaedic Knowledge Update 11.
Rosemont, IL: American Academy of Orthopaedic Surgeons; 2014:237-252.
Shieh PB. Muscular dystrophies and other genetic myopathies. Neurol Clin. 2013 Nov;31(4):1009-29. doi:
10.1016/j.ncl.2013.04.004. Review. PubMed PMID: 24176421.

How well did you know this?

Not at all

Perfectly

Question 115
Which factor is most commonly used to stimulate cartilage regeneration in vitro?
1. Tumor necrosis factor (TNF)-alpha
2. Transforming growth factor (TGF)-beta
3. Platelet-derived growth factor (PDGF)
4. Fibroblast growth factor (FGF)
5. Insulin-like growth factor-1 (IGF-1)

Transforming growth factor (TGF)-beta

TGF-B superfamily includes: TGF-B1, BMP-2, BMP-7, CDMP-1 and CDMP2 (cartilage-derived morphogenetic protein). Some show promising results but deleterious effects to the articular environment.

I don’t really get this question since they seem to be all (except TNF-a) used in studies to stimulate cartilage regeneration according to the article cited.

RECOMMENDED READINGS
Klatt BA, Chen A, Tuan R. Arthritis and other cartilage disorders. In: Cannada LK, ed. Orthopaedic
Knowledge Update 11. Rosemont, IL: American Academy of Orthopaedic Surgeons; 2014:207-222.
Fortier LA, Barker JU, Strauss EJ, McCarrel TM, Cole BJ. The role of growth factors in cartilage repair.
Clin Orthop Relat Res. 2011 Oct;469(10):2706-15. doi: 10.1007/s11999-011-1857-3. Review. PubMed
PMID: 21403984; PubMed Central PMCID: PMC3171543.

How well did you know this?

Not at all

Perfectly

Question 118
Which immune cell type is involved in metal allergy associated with orthopaedic implants?
1. Mast cells
2. Dendritic cells
3. Natural killer cells
4. B lymphocytes
5. T lymphocytes

T lymphocytes

Better answer would be macrophages, but that’s not an option (Most delayed-type hypersensitivity participating cells are macrophages; only 5% of cells present are lymphocytes)

“The histologic and immunohistochemical appearance of the tissues is dominated by perivascular and diffuse infiltrates of T- and B-lymphocytes, including secondary lymphoid follicles that are morphologically suggestive of a hypersensitivity reaction”

T-cells are the initiators of the hypersensitivity by contact with the antigen. This recruits inflammatory cells…

RECOMMENDED READINGS
Jacobs JJ, Urban RM, Hallab NJ, Skipor AK, Fischer A, Wimmer MA. Metal-on-metal bearing surfaces. J
Am Acad Orthop Surg. 2009 Feb;17(2):69-76. PubMed PMID: 19202120.
O’Keefe RJ, Jacobs JJ, Chu CR, Einhorn TA, eds. Orthopaedic Basic Science: Foundations of Clinical
Practice. 4th ed. Rosemont, IL; American Academy of Orthopaedic Surgeons: 2013.

How well did you know this?

Not at all

Perfectly

Question 126
Which ion and ion channel are responsible for generation of a nerve action potential?
1. Sodium ion through a voltage-gated channel
2. Sodium ion through a transmitter-gated channel
3. Potassium ion through a voltage-gated channel
4. Potassium ion through a mechanically-gated channel
5. Chloride ion through a mechanically-gated channel

Sodium ion through a voltage-gated channel

Easy to remember.: Think of sodium + voltage because local anesthetics are sodium channel blockers and block sensory nerves, and neuropathic pain causes electric-shock-like pain (volt!).

Voltage-gated ion channels are a class of transmembrane proteins that form ion channels that are activated by changes in electrical membrane potential near the channel

Transmitter-gated channel open up when they attach to a ligand (Ex: acetylcholine)

Mechanically-gated channel: respond to mechanical cues (stretch or compress)

RECOMMENDED READINGS
O’Keefe RJ, Jacobs JJ, Chu CR, Einhorn TA, eds. Orthopaedic Basic Science: Foundations of Clinical
Practice. 4th ed. Rosemont, IL; American Academy of Orthopaedic Surgeons: 2013.
Lee DH, Claussen GC, Oh S. Clinical nerve conduction and needle electromyography studies. J Am Acad
Orthop Surg. 2004 Jul-Aug;12(4):276-87. Review. PubMed PMID: 15473679.
Catterall WA. Structure and function of voltage-gated sodium channels at atomic resolution. Exp Physiol.
2014 Jan;99(1):35-51. doi: 10.1113/expphysiol.2013.071969. Epub 2013 Oct 4. Review. PubMed PMID:
24097157; PubMed Central PMCID: PMC3885250

How well did you know this?

Not at all

Perfectly

Question 134
Figure 134 is the radiograph of a 50-year-old man.

AP pelvis: areas of increased/decreased bone density, hip osteoarthritis, loss of distinction between cortices and medullary cavity (remodeled cortices)

Laboratory tests were performed based on these
fidings, and results demonstrated an elevated alkaline phosphatase level. Which cell type is abnormally
altered in the underlying pathology of this disorder?
1. Osteoclasts
2. Osteoblasts
3. Osteocytes
4. Osteoprogenitor cells
5. Mesenchymal stem cells

Osteoclasts

Basically the key is recognizing Paget’s disease of the bone. Osteoclasts cause excessive bone resorption (lytic), which leads to osteoblasts laying down excessive new bone (blastic), or balanced (mixed) phases. These 3 phases can all be present simultaneously in the same bone.

Labs: elevated ALP, hydroxyproline (collagen breakdown), urinary N-telopeptide, alpha-C-telopeptide, deoxypyridinoline (probably not important as an orthopaedic surgeon). NORMAL calcium levels.

RECOMMENDED READINGS
Ralston SH, Langston AL, Reid IR. Pathogenesis and management of Paget’s disease of bone. Lancet.
2008 Jul 12;372(9633):155-63. doi: 10.1016/S0140-6736(08)61035-1. Review. PubMed PMID:
18620951.
Kaplan FS, Singer FR. Paget’s Disease of Bone: Pathophysiology, Diagnosis, and Management. J Am
Acad Orthop Surg. 1995 Nov;3(6):336-344. PubMed PMID: 10790672.

Question 142
A 46-year-old laborer has elbow pain for 1 year. The pain is located over the lateral aspect, and he denies
any trauma. Examination reveals pain to palpation just distal to the lateral epicondyle and pain with
resisted wrist extension with the elbow in extension. Where does the primary muscle involved in this
disorder insert?
1. Radial styloid
2. Base of the second metacarpal
3. Base of the third metacarpal
4. Base of the fourth metacarpal
5. Base of the fith metacarpal

Base of the third metacarpal

ECRB.

Article: anatomic study showing that ECRB tendon undersurface rubs against the lateral edge of the capitellum during elbow motion

RECOMMENDED READINGS
Brummel J, Baker CL 3rd, Hopkins R, Baker CL Jr. Epicondylitis: lateral. Sports Med Arthrosc. 2014
Sep;22(3):e1-6. doi: 10.1097/JSA.0000000000000024. Review. PubMed PMID: 25077751.
Bunata RE, Brown DS, Capelo R. Anatomic factors related to the cause of tennis elbow. J Bone Joint Surg
Am. 2007 Sep;89(9):1955-63. PubMed PMID: 17768192.

Question 148

Which physical examination fiding is consistent with the lesion seen on the MR images shown in Figures
148a and 148b?

MRI: L5-S1 disc herniation causing foraminal stenosis

Saddle anesthesia
Weak great toe extension
Decreased patellar tendon reflex
Decreased Achilles tendon reflex
Diminished sensation over the dorsum of the foot

Decreased Achilles tendon reflx

L5-S1 disc should affect S1 nerve root (unless it’s a far lateral disc)

Not large enough to look like cauda equina-causing.
EHL = L5 on ASIA scale (in reality, L4 > L5, and S1)
Patellar tendon reflex = L2-3-4 (quads)
Achilles tendon reflex = S1
This is in part true (medial aspect of foot), but not really “dorsum” of foot proper (L5). Superficial peroneal nerve (L4-S1) is a better “dorsum of foot” description

RECOMMENDED READINGS
O’Keefe RJ, Jacobs JJ, Chu CR, Einhorn TA, eds. Orthopaedic Basic Science: Foundations of Clinical
Practice. 4th ed. Rosemont, IL; American Academy of Orthopaedic Surgeons: 2013.
Hoppenfeld S, Thomas H. Physical Examination of the Spine and Extremities 1 st ed. East Norwalk, CT,
Appleton-Century Crofts, 1976.

Question 153
What happens to the size and cellularity of the nucleus pulposus proportional to the intervertebral disk
after birth?
1. Increase in size and cellularity
2. Increase in size and decrease in cellularity
3. Decrease in size and cellularity
4. Decrease in size and increase in cellularity
5. Size and cellularity remain constant

Decrease in size and cellularity

If you have ever seen a spine x-ray of an old person you can guess that “decrease in size” is correct. Even if you know nothing else, you have a 50% chance of answering this correctly if you know that.

Summarized from the article provided (actually pretty interesting):

Nucleus originates from notochord. In fetus and infant, nucleus has actively dividing notochordal cells, which produce proteoglycans/matrix products. In humans, by age 4 yo the notochordal cells disappear and are replaced by chondrocytic cells of unknown origin that continue to produce proteoglycans + also lots of collagen. Nucleus then becomes firmer and less hydrated, and becomes non-transparent. Cell density of adult nucleus is very low (0.5% cells per volume). This density of living cells decreases with age (?because disc is a large avascular tissue), to the point where hydration/proteoglycan concentration decreases. This allows clefts/fissures to form, and eventually the disc fails to do its mechanical duties.

RECOMMENDED READINGS
O’Keefe RJ, Jacobs JJ, Chu CR, Einhorn TA, eds. Orthopaedic Basic Science: Foundations of Clinical
Practice. 4th ed. Rosemont, IL; American Academy of Orthopaedic Surgeons: 2013.
Urban JPG, Roberts S, Ralphs JR. The Nucleus of the Intervertebral Disc from Development to
Degeneration. Amer Zool. 2000;40:53-61.
http://az.oxfordjournals.org/content/40/1/53

Question 155
What is the most common fiber type in the knee structure shown in the arthroscopic image in Figure 155?

“Image of an ACL”

Proteoglycans
Elastin
Sharpey fiers
Collagen type I
Collagen type II

Collagen type I

The ACL is a ligament.

Extracellular components consist of
o water
o Type I collagen (70% of dry weight)
o elastin: higher elastin content than tendons (makes sense)
o lipids
o proteoglycans
o epiligament coat: present in some ligaments, not all. analogous to epitenon of tendons

Cellular component  (for both ligaments and tendons)
o	Main cell type = fibroblast 
o	Low vascularity and cellularity
•	Ligaments vs. tendons

Composition of ligaments, compared to tendons have:

Lower % of collagen
Higher % of proteoglycans and water
Less organized collagen fibers
Rounder fibroblasts

RECOMMENDED READINGS
Duthon VB, Barea C, Abrassart S, Fasel JH, Fritschy D, Ménétrey J. Anatomy of the anterior cruciate
ligament. Knee Surg Sports Traumatol Arthrosc. 2006 Mar;14(3):204-13. Epub 2005 Oct 19. Review.
PubMed PMID: 16235056.
O’Keefe RJ, Jacobs JJ, Chu CR, Einhorn TA, eds. Orthopaedic Basic Science: Foundations of Clinical
Practice. 4th ed. Rosemont, IL; American Academy of Orthopaedic Surgeons: 2013.

Question 166
How does the World Health Organization (WHO) define osteopenia based on the dual-energy x-ray
absorptiometry test?
1. T-score between 0 and 1 standard deviation below the norm
2. T-score between 1 and 2.5 standard deviations below the norm
3. Z-score between 0 and 1 standard deviation below the norm
4. Z-score between 1 and 2.5 standard deviations below the norm
5. Bone mineral density below 2.5 standard deviations of the mean for a healthy 30-year-old

T-score between 1 and 2.5 standard deviations below the norm

Memorize for the OITE then quickly forget it… os-Two.5-open1a?

RECOMMENDED READINGS
Blake GM, Fogelman I. Role of dual-energy X-ray absorptiometry in the diagnosis and treatment of
osteoporosis. J Clin Densitom. 2007 Jan-Mar;10(1):102-10. Epub 2006 Dec 27. Review. PubMed PMID:
17289532.
Templeton K. Secondary osteoporosis. J Am Acad Orthop Surg. 2005 Nov;13(7):475-86. Review. PubMed
PMID: 16272272.

Question 170
Hemophilia A is a genetic disorder that is transmitted by which inheritance pattern?
1. Autosomal dominant
2. Autosomal recessive
3. X-linked recessive
4. X-linked dominant
5. Mitochondrial

X-linked recessive

If you wrote POS you will remember this ironed into your brain… Factor 8 (Hemophilia EIGHT) deficiency. More dudes affected than gals… So x-linked recessive.

RECOMMENDED READINGS
Vanderhave KL, Caird MS, Hake M, Hensinger RN, Urquhart AG, Silva S, Farley FA. Musculoskeletal
care of the hemophiliac patient. J Am Acad Orthop Surg. 2012 Sep;20(9):553-63. doi: 10.5435/
JAAOS-20-09-553. Review. PubMed PMID: 22941798.
Buckwalter JA, Einhorn TA, Simon SR, eds. Orthopaedic Basic Science: Biology and Biomechanics of the
Musculoskeletal System. 2nd ed. Rosemont, IL: American Academy of Orthopaedic Surgeons; 2000.

Question 176
Figures 176a through 176c are the MR images and biopsy specimen of a 42-year-old woman who has a
slow-growing mass in her right knee. Which translocation is associated with this condition?

MRI: Hypodense in T1, hyperdense in T2 infrapatellar lesion. Pathology slide: lots of undifferentiated spindly cells with large nuclei.

11:22
X:18
12:16
12:22
9:22

X:18

Synovial sarcoma:

Malignant lesion arising near (but not in) joints
Actually a misnomer cause the cells don’t come from a synovial origin
More males, and 15-40s (unlike the patient in the question)
90% will have X:18 translocation

MRI:
Typically dark in T1, bright in T2

Histology:

Spindle cells (fibrous type of cells): relatively small and uniform and found in sheets of malignant appearing cells with minimal cytoplasm and dark atypical nuclei
Epithelial cells: gland, nest, or cyst like cells

RECOMMENDED READINGS
Ladanyi M, Antonescu CR, Leung DH, Woodruf JM, Kawai A, Healey JH, Brennan MF, Bridge JA, Nef
JR, Barr FG, Goldsmith JD, Brooks JS, Goldblum JR, Ali SZ, Shipley J, Cooper CS, Fisher C, Skytting
B, Larsson O. Impact of SYT-SSX fusion type on the clinical behavior of synovial sarcoma: a multi
institutional retrospective study of 243 patients. Cancer Res. 2002 Jan 1;62(1):135-40. PubMed PMID:
11782370.
Kawai A, Woodruf J, Healey JH, Brennan MF, Antonescu CR, Ladanyi M. SYT-SSX gene fusion as a
determinant of morphology and prognosis in synovial sarcoma. N Engl J Med. 1998 Jan 15;338(3):153-
60. PubMed PMID: 9428816.
Chotel F, Unnithan A, Chandrasekar CR, Parot R, Jeys L, Grimer RJ. Variability in the presentation of
synovial sarcoma in children: a plea for greater awareness. J Bone Joint Surg Br. 2008 Aug;90(8):1090-6.
doi: 10.1302/0301-620X.90B8.19815. PubMed PMID: 18669969.

Question 186
The process of reading DNA information by RNA polymerase to make specific complementary mRNA is
known as
1. replication.
2. recombination.
3. translation.
4. translocation.
5. transcription.

transcription.

You should know this from grade 8 biology

RECOMMENDED READINGS
Zuscik MJ, Drissi MH, Chen D, Rosier RN. Molecular and cell biology in orthopaedics. In: Einhorn TA,
O’Keefe RJ, Buckwalter JA, eds. Orthopaedic Basic Science: Foundations of Clinical Practice, 3 rd ed.
Rosemont, IL: American Academy of Orthopaedic Surgeons; 2007:3-23.
Lieberman JR, ed. AAOS Comprehensive Orthopaedic Review. Rosemont, IL: American Academy of
Orthopaedic Surgeons; 2009:3-13.

Question 192 Achondroplasia is caused by a mutation in the gene encoding for fibroblast growth factor receptor 3 (FGFR3). This genetic mutation leads to 1. accumulation of the protein in the golgi. 2. gain of function of FGFR3 (turned on). 3. loss of function of FGFR3 (turned off. 4. increased production of the FGFR3 protein. 5. decreased production of the FGFR3 protein

2. gain of function of FGFR3 (turned on). Tip: think of a dwarf chanting "FURGAFURG, FURGAFURG, FURGAFURG (3x)" and you'll never forget it. FGFR3 mutation is a "activation" mutation. Leads to abnormal chondroid production by chondroblasts in the proliferative zone during enchondral bone formation at physes (quantitative, not qualitative defect). Only affects bones with physes (not head + skull) 80% sporadic mutation RECOMMENDED READINGS Morcuende JA, Alman BA. Skeletal dysplasias, connective tissue diseases, and other genetic disorders. In: Flynn JM, ed. Orthopaedic Knowledge Update 10. Rosemont, IL: American Academy of Orthopaedic Surgeons; 2011:797-810. Sponseller PD, Ain MC. The skeletal dysplasias. In: Morrissy RT, Weinstein SL, eds. Lovell and Winter’s Pediatric Orthopaedics. Philadelphia, PA: Lippincott Williams & Wilkins; 2006:205-250.

``` Question 198 Which factor promotes inflammation-related osteolysis around orthopaedic implants? 1. Interleukin-4 (IL-4) 2. IL-6 3. Osteoprotegerin 4. Interferon (IFN) gamma 5. Transforming growth factor beta ```

2. IL-6 Basically in the macrophage-activated macrophage activation/recruitment there are a bunch of osteolytic cytokines secreted. IL-6 is the only one from that list that is an option here: 1. TNF- alpha 2. TGF-beta 3. osteoclast activating factor 4. oxide radicals 5. hydrogen peroxide 6. acid phosphatase 7. interleukins (Il-1, IL-6) 8. prostaglandins Osteoclast activation and osteolysis: 1. increase of TNF- alpha increases RANK 2. increase of VEGF with UHMWPE enhances RANK and RANKL activation 3. RANKL mediated bone resorption 4. an increase in production of RANK and RANKL gene transcripts leads to osteolysis These two can be easily taken out since they don't cause bone resorption: Osteoprotegerin (OPG) (bone-protector-protein) = inhibits bone resorbtion TGF-B : inhibits bone resorption via OPG IFN and IL-4 have to do with lymphocyte immunologic functions that has nothing to do with osteolysis RECOMMENDED READINGS Yousef AA, Clohisy JC. The biological response to orthopaedic implants. In: Einhorn TA, O’Keefe RJ, Buckwalter, JA, eds. Orthopaedic Basic Science: Foundations of Clinical Practice. 3 rd ed. Rosemont, IL: American Academy of Orthopaedic Surgeons; 2007: 365-77. Talmo CT, Shanbhag AS, Rubash HE. Nonsurgical management of osteolysis: challenges and opportunities. Clin Orthop Relat Res. 2006 Dec;453:254-64. Review. PubMed PMID: 17016218.

``` Question 203 Materials that demonstrate stress-strain behaviors that are time dependent are 1. ductile. 2. brittle. 3. isotropic. 4. anisotropic. 5. viscoelastic. ```

5. viscoelastic. Recall the stress-strain curve. If the stress-strain behaviour is time-dependant, that means that the stress-strain curve changes with time. A good example of this is bone. This concept is why surgeons take little breaks when broaching the femur to "let the bone relax" under a constant strain (not sure if this actually does anything in that short period of time... but whatever) RECOMMENDED READINGS Lieberman JR, ed. AAOS Comprehensive Orthopaedic Review. Rosemont, IL: American Academy of Orthopaedic Surgeons; 2009:21-28. Lu L, Kaufman KR, Yaszemski MJ. Biomechanics. In: Einhorn TA, O’Keefe RJ, Buckwalter JA, eds. Orthopaedic Basic Science: Foundations of Clinical Practice, 3 rd ed. Rosemont, IL: American Academy of Orthopaedic Surgeons; 2007:49-64.

``` Question 207 The son of a man with Huntington disease is informed that he will likely develop a more severe form of the disease at a younger age than his father. This is an example of 1. anticipation. 2. DNA methylation. 3. histone deactylation. 4. loss of telomere length. 5. lyonization ```

1. anticipation. I had no idea this was a real genetics term, but it is. For Huntington's and more-importantly orthopaedically: myotonic dystrophy From wikipedia: In genetics, anticipation is a phenomenon whereby as a genetic disorder is passed on to the next generation, the symptoms of the genetic disorder become apparent at an earlier age with each generation. In most cases, an increase of severity of symptoms is also noted. Anticipation is common in trinucleotide repeat disorders, such as Huntington's disease and myotonic dystrophy, where a dynamic mutation in DNA occurs. RECOMMENDED READINGS Cook PC, Sanders JO. Genetic diseases in orthopaedics. In: O’Keefe RJ, Jacobs JJ, Chu CR, Einhorn TA, eds. Orthopaedic Basic Science: Foundations of Clinical Practice, 4th ed. Rosemont, IL: American Academy of Orthopaedic Surgeons; 2013: 43-53. Martorell L, Monckton DG, Sanchez A, Lopez De Munain A, Baiget M. Frequency and stability of the myotonic dystrophy type 1 premutation. Neurology. 2001 Feb 13;56(3):328-35. PubMed PMID: 11171897. Kamsteeg EJ, Kress W, Catalli C, Hertz JM, Witsch-Baumgartner M, Buckley MF, van Engelen BG, Schwartz M, Scheffr H. Best practice guidelines and recommendations on the molecular diagnosis of myotonic dystrophy types 1 and 2. Eur J Hum Genet. 2012 Dec;20(12):1203-8. doi: 10.1038/ ejhg.2012.108. Epub 2012 May 30. PubMed PMID: 22643181; PubMed Central PMCID: PMC3499739.

``` Question 227 An inactivating mutation in the receptor for 1,25 (OH)2 vitamin D3 is associated with which disorder? 1. Paget disease 2. Hypophosphatasia 3. Renal osteodystrophy 4. Familial hypophosphatemic rickets 5. Type II vitamin D-dependent rickets ```

5. Type II vitamin D-dependent rickets (hereditary resistance to Vitamin D) ``` Rickets = pre-closure of physis Osteomalacia = post-closure of physis ``` Fun fact: this has only been reported in 100 cases (total) - how great is it to learn such a useful topic? Basically in this disorder, you have end-organ resistance to vitamin D, so you get a high serum level of vitamin D (cause your body keeps pumping up the production). The treatment is actually giving them a big shitload of vitamin D and hope your cells respond to some of it (response depends on how your receptors respond). Oh, and also you give calcium to help replete the bones. RECOMMENDED READINGS Brinker MR. Basic Science: Bone. In: Miller MD, ed. Review of Orthopaedics. 3 rd ed. Philadelphia, PA: WB Saunders; 2000: 1-39. Liberman U, Marx S.Vitamin D-dependent rickets. In: Favus MK (ed). Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism, 5th ed. Washington, DC: The American Society for Bone and Mineral Research; 2003:311-316.

Question 237 A patient comes to you for a second opinion after undergoing surgery for a rotator cuf tear with another surgeon in your practice. Following your evaluation, you believe that surgeon error resulted in a poor outcome. What is your responsibility in reporting to the patient that this possible error may have contributed to the poor outcome? 1. You are lawfully required to disclose this information to the patient. 2. You are lawfully and ethically required to disclose this information to the patient. 3. You are ethically required to disclose this information to the patient. 4. You are ethically required to discuss this information with your partner. 5. No disclosures are required

3. You are ethically required to disclose this information to the patient This was a dumb question/answer From the JBJS article: "If he or she is compelled to believe the patient has been treated without regard to safety, then there is an ethical obligation to society to report the incident. In concert with an increasing public awareness of medical mistakes, the legislatures in several states have instituted voluntary or mandatory medical-error reporting systems. The American Medical Association has endorsed this effort, stating that, “Initial reports of incompetence should be made to the appropriate clinical authority who would be empowered to assess the potential impact on patient welfare and to facilitate remedial action.” "As the physician who is being relied upon for a second opinion, a consulting orthopaedic surgeon has an ethical responsibility to inform the patient of all relevant medical facts when those facts are requested, but he or she does not have a legal requirement to do so. Because he or she was not present during the original surgery, the consulting orthopaedic surgeon should express the inherent limitations of his or her knowledge but can still offer a meaningful opinion. Although it may be challenging to communicate, a frank discussion of the patient's condition is beneficial to all parties." RECOMMENDED READINGS Bhattacharyya T, Yeon H. "Doctor, was this surgery done wrong?" Ethical issues in providing second opinions. J Bone Joint Surg Am. 2005 Jan;87(1):223-5. PubMed PMID: 15634836. American Academy of Orthopaedic Surgeons. Second or Additional Medical Opinions in Orthopaedic Surgery. http://www.aaos.org/CustomTemplates/Content.aspx?id=22293. Accessed January 2016.

Question 255 A pregnant 28-year-old woman who is seen in the emergency department with a closed ankle fracture reports that she tripped and fell at home. The patient’s mother tells you that there is reason to suspect spousal abuse as a cause for the injury. The patient denies any domestic violence. What is your responsibility in reporting this possible abuse? 1. You should do nothing further because you have no proof of abuse. 2. You should investigate further by asking other family members if spousal abuse is suspected. 3. You are required to communicate this finding with the emergency department staff and social worker. 4. The patient should be encouraged to seek self-protection and consult with a social worker at the hospital. 5. To avoid disciplinary action, by law you must report this possible abuse to the authorities

4. The patient should be encouraged to seek self-protection and consult with a social worker at the hospital. Unlike child abuse you are not obligated to report it, but you should do the above. RECOMMENDED READINGS American Academy of Orthopaedic Surgeons: Child Abuse or Maltreatment, Elder Maltreatment, and Intimate Partner Violence (IPV): The Orthopaedic Surgeon’s Responsibilities in Domestic and Family Violence. Rosemont, IL: American Academy of Orthopaedic Surgeons. Available at http://www.aaos.org/ CustomTemplates/Content.aspx?id=22286&ssopc=1. Accessed January 2016. American Medical Association Council on Ethical and Judicial Affirs. Code of medical ethics: Opinion 2.02 – Physicians’ Obligation in Preventing, Identifying, and Treating Violence and Abuse. Available at http://www.ama-assn.org/ama/pub/physician-resources/medical-ethics/code-medical-ethics/opinion202. page?. Accessed January 2016.

Question 274 A thicker myelin sheath will affect nerve transmission by 1. decreasing the depolarization rate. 2. increasing the depolarization rate. 3. increasing the relative refractory period. 4. increasing the absolute refractory period. 5. increasing the speed of wave propagation

5. increasing the speed of wave propagation Myelin sheath functions to increased velocity of the nerve transmission. The thicker, the faster (unlike people) RECOMMENDED READINGS Jackson WM, Diao E. Peripheral nerves: form and function. In: O’Keefe RJ, Jacobs JJ, Chu CR, Einhorn TA. eds. Orthopaedic Basic Science: Foundations of Clinical Practice. 4th ed. Rosemont, IL: American Academy of Orthopaedic Surgeons; 2013;239-251. Peters A. The effcts of normal aging on myelin and nerve fiers: a review. J Neurocytol. 2002 Sep Nov;31(8-9):581-93. Review. PubMed PMID: 14501200.