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Orthopedics Syllabus

Medical Specialization. The full Orthopedics syllabus: 8 chapters, 24 topics and 73 sub-topics, with 64 flashcards written against it.

8Chapters
24Topics
73Sub-topics
64Flashcards

Orthopedics syllabus — full chapter and topic list

Expand any chapter to see its topics and sub-topics. This is the whole examinable outline for Orthopedics, not a summary of it.

  1. Basic Science

    3 topics
    • Bone Biology
      • Bone Structure
      • Bone Cells
      • Bone Remodeling
      • Bone Healing
    • Cartilage Biology
      • Types of Cartilage
      • Cartilage Structure
      • Cartilage Repair
    • Muscle Physiology
      • Muscle Fiber Types
      • Muscle Contraction
      • Muscle Repair
  2. Trauma

    3 topics
    • Fracture Management
      • Fracture Types
      • Fracture Healing
      • Fracture Fixation Techniques
    • Soft Tissue Injuries
      • Ligament Injuries
      • Tendon Injuries
      • Muscle Injuries
    • Polytrauma
      • Initial Assessment
      • Damage Control Orthopedics
      • Definitive Care
  3. Pediatric Orthopedics

    3 topics
    • Developmental Dysplasia of the Hip
      • Diagnosis
      • Treatment Options
      • Prognosis
    • Pediatric Fractures
      • Growth Plate Injuries
      • Common Pediatric Fractures
      • Management Strategies
    • Congenital Limb Deficiencies
      • Types
      • Surgical Interventions
      • Rehabilitation
  4. Adult Reconstruction

    3 topics
    • Total Hip Arthroplasty
      • Indications
      • Surgical Techniques
      • Postoperative Management
    • Total Knee Arthroplasty
      • Indications
      • Surgical Techniques
      • Postoperative Management
    • Revision Arthroplasty
      • Indications
      • Challenges
      • Techniques
  5. Spine

    3 topics
    • Spinal Trauma
      • Classification
      • Management Principles
      • Surgical vs. Non-Surgical Treatment
    • Degenerative Spine Disorders
      • Lumbar Disc Herniation
      • Cervical Spondylosis
      • Spinal Stenosis
    • Spinal Deformities
      • Scoliosis
      • Kyphosis
      • Surgical Interventions
  6. Sports Medicine

    3 topics
    • Anterior Cruciate Ligament Injuries
      • Diagnosis
      • Surgical Techniques
      • Rehabilitation
    • Meniscal Injuries
      • Types
      • Management Options
      • Rehabilitation
    • Rotator Cuff Injuries
      • Diagnosis
      • Surgical Techniques
      • Rehabilitation
  7. Oncology

    3 topics
    • Bone Tumors
      • Benign Tumors
      • Malignant Tumors
      • Diagnostic Techniques
    • Soft Tissue Sarcomas
      • Types
      • Management Strategies
      • Prognosis
    • Metastatic Bone Disease
      • Common Primary Cancers
      • Management Options
      • Palliative Care
  8. Infections

    3 topics
    • Osteomyelitis
      • Acute Osteomyelitis
      • Chronic Osteomyelitis
      • Management Strategies
    • Septic Arthritis
      • Diagnosis
      • Treatment Options
      • Complications
    • Prosthetic Joint Infections
      • Risk Factors
      • Management Options
      • Prevention Strategies

Orthopedics flashcards

The complete Orthopedics deck: 64 questions with worked answers.

  1. What are the four main cell types in bone and their primary functions?

    Osteoblasts (bone formation, secrete osteoid), osteoclasts (bone resorption, multinucleated from monocyte/macrophage lineage), osteocytes (mature mechanosensor cells embedded in lacunae), and bone-lining cells (quiescent osteoblasts on surfaces).

  2. Distinguish woven bone from lamellar bone.

    Woven bone is immature, laid down rapidly with randomly oriented collagen, mechanically weak, and found in fetal bone/fracture callus. Lamellar bone is mature, organized in parallel collagen sheets (osteons/Haversian systems), and mechanically strong.

  3. What is the RANK/RANKL/OPG system's role in bone remodeling?

    RANKL (from osteoblasts) binds RANK on osteoclast precursors to stimulate osteoclast differentiation and resorption. Osteoprotegerin (OPG) is a decoy receptor that binds RANKL, inhibiting osteoclastogenesis. The RANKL:OPG ratio controls net resorption.

  4. Name the four zones of the epiphyseal growth plate from epiphysis to metaphysis.

    Reserve (resting) zone, proliferative zone, hypertrophic zone (further divided into maturation, degeneration, provisional calcification), and the zone of ossification. The hypertrophic zone is weakest and where most fractures/slips occur.

  5. What is the composition of bone matrix by weight (organic vs inorganic)?

    Approximately 65% inorganic mineral (hydroxyapatite, $\ce{Ca10(PO4)6(OH)2}$), 25% organic (~90% type I collagen plus non-collagenous proteins), and ~10% water.

  6. Compare intramembranous and endochondral ossification.

    Intramembranous ossification forms bone directly from mesenchyme without a cartilage model (flat bones of skull, clavicle). Endochondral ossification uses a hyaline cartilage template replaced by bone (long bones, most of skeleton).

  7. What are the three types of cartilage and a key location for each?

    Hyaline cartilage (articular surfaces, growth plate, costal cartilage), elastic cartilage (external ear, epiglottis), and fibrocartilage (menisci, intervertebral discs, pubic symphysis, tendon insertions).

  8. What are the four zones of articular (hyaline) cartilage from surface to bone?

    Superficial (tangential) zone with collagen parallel to surface, middle (transitional) zone, deep (radial) zone with collagen perpendicular to surface, and the calcified cartilage zone separated from the deep zone by the tidemark.

  9. What is the main proteoglycan of articular cartilage and how does it retain water?

    Aggrecan, which aggregates with hyaluronic acid via link protein. Its glycosaminoglycan side chains (chondroitin and keratan sulfate) carry fixed negative charges that attract cations and osmotically draw in water, giving cartilage its compressive stiffness.

  10. Why does articular cartilage have poor healing capacity?

    It is avascular, aneural, and alymphatic, receiving nutrition by diffusion from synovial fluid; chondrocytes have limited mitotic ability, so defects heal poorly (partial-thickness lesions barely heal; full-thickness lesions reaching bone fill with inferior fibrocartilage).

  11. State the sliding filament theory of muscle contraction in one sentence.

    Myosin heads bind actin and pull thin (actin) filaments toward the sarcomere center, shortening the sarcomere without changing the length of the filaments themselves, powered by ATP hydrolysis.

  12. What is the role of calcium and troponin/tropomyosin in skeletal muscle contraction?

    An action potential triggers $\ce{Ca^{2+}}$ release from the sarcoplasmic reticulum; $\ce{Ca^{2+}}$ binds troponin C, shifting tropomyosin off the actin binding sites, allowing myosin cross-bridge formation and contraction.

  13. Compare Type I and Type II skeletal muscle fibers.

    Type I (slow-twitch, oxidative): red, fatigue-resistant, high mitochondria/myoglobin, for endurance/posture. Type II (fast-twitch, glycolytic): white, rapid powerful contraction, fatigue quickly, for sprinting/power. Type IIa is intermediate (fast oxidative-glycolytic).

  14. What are the sequential stages of secondary (indirect) fracture healing?

    1) Hematoma/inflammation, 2) soft callus (fibrocartilage) formation, 3) hard callus (woven bone) formation via endochondral and intramembranous ossification, and 4) remodeling into lamellar bone. It requires micromotion and no rigid fixation.

  15. What distinguishes primary from secondary fracture healing?

    Primary (direct) healing occurs with absolute stability and anatomic reduction (e.g., rigid compression plating), through cutting cones with no visible callus. Secondary (indirect) healing occurs with relative stability/micromotion and proceeds via callus formation.

  16. State the components of the Gustilo-Anderson classification for open fractures.

    Type I: wound <1 cm, clean. Type II: wound 1–10 cm, moderate soft tissue damage. Type III: wound >10 cm or severe/high-energy — IIIA adequate soft tissue coverage, IIIB extensive periosteal stripping requiring flap coverage, IIIC associated arterial injury requiring repair.

  17. What are the classic 6 P's of acute compartment syndrome?

    Pain (out of proportion, worse on passive stretch — earliest sign), Paresthesia, Pallor, Paralysis, Pulselessness (late), and Poikilothermia (coldness). Diagnosis is clinical; the earliest and most reliable signs are pain on passive stretch and paresthesia.

  18. What compartment pressure threshold indicates fasciotomy in compartment syndrome?

    A delta pressure ($\Delta P$ = diastolic blood pressure − compartment pressure) of $\leq 30\ \text{mmHg}$, or an absolute compartment pressure $> 30\ \text{mmHg}$, supports the diagnosis and need for emergent fasciotomy.

  19. What does the Salter-Harris classification describe, and how is it graded?

    It classifies pediatric physeal (growth plate) fractures. Type I: through physis. Type II: through physis and metaphysis (most common). Type III: through physis and epiphysis (intra-articular). Type IV: through metaphysis, physis, and epiphysis. Type V: crush of physis. Mnemonic SALTR: Slipped, Above, Lower, Through, Rammed/cRush.

  20. What are the four Rs of fracture management principles?

    Reduction (restore alignment), Retention/Restriction (hold with cast/fixation), Rehabilitation (restore function), and often preceded by Resuscitation in polytrauma. Some cite reduce, hold, rehabilitate as the core sequence.

Show the other 44 Orthopedics flashcards
  1. Differentiate a sprain from a strain.

    A sprain is an injury to a ligament (bone-to-bone), graded I (stretch), II (partial tear), III (complete tear). A strain is an injury to a muscle or musculotendinous unit.

  2. How are ligament sprains graded and what is the clinical hallmark of each grade?

    Grade I: microscopic stretch, no laxity, mild pain. Grade II: partial tear, mild-moderate laxity with firm endpoint. Grade III: complete rupture, gross laxity with no endpoint. Function loss increases with grade.

  3. What is the initial management acronym for acute soft tissue injuries?

    RICE (Rest, Ice, Compression, Elevation), often expanded to PRICE (Protection added) or POLICE (Protection, Optimal Loading, Ice, Compression, Elevation) emphasizing early controlled loading over strict rest.

  4. What are the three phases of tendon healing?

    Inflammatory phase (days 0–7, cellular infiltration), proliferative/fibroblastic phase (weeks, type III collagen deposition), and remodeling/maturation phase (months, type III replaced by stronger organized type I collagen).

  5. Define polytrauma and the ISS threshold commonly used.

    Polytrauma is injury to multiple body regions/systems where at least one injury (or the combination) is life-threatening. It is commonly defined by an Injury Severity Score $\text{ISS} \geq 16$ (Berlin definition adds physiological derangement).

  6. How is the Injury Severity Score (ISS) calculated?

    The body is divided into 6 regions scored by the Abbreviated Injury Scale (AIS 0–6). The ISS is the sum of the squares of the three highest AIS scores from different regions: $\text{ISS} = A^{2} + B^{2} + C^{2}$, ranging 0–75. Any AIS of 6 automatically makes ISS = 75.

  7. Contrast 'Early Total Care' (ETC) with 'Damage Control Orthopedics' (DCO).

    ETC involves definitive fixation of major fractures within 24 hours in stable patients. DCO involves temporary stabilization (external fixation), hemorrhage/contamination control, and delayed definitive surgery in physiologically unstable ('borderline') polytrauma patients to avoid a second hit.

  8. List the ATLS primary survey sequence.

    ABCDE: Airway with cervical spine protection, Breathing/ventilation, Circulation with hemorrhage control, Disability (neurologic/GCS), and Exposure/Environment control (undress, prevent hypothermia).

  9. What is the 'lethal triad' (trauma triad of death)?

    Hypothermia, acidosis (metabolic), and coagulopathy — a self-perpetuating cycle in severe trauma that damage control resuscitation aims to interrupt.

  10. What are the key risk factors for Developmental Dysplasia of the Hip (DDH)?

    The '6 Fs' / classic factors: Female sex, Firstborn, Family history, Frank breech presentation, oligohydramnios, and left hip predominance. Mnemonic aids include 'the 4 Ps': positive family history, primiparity, podalic (breech) presentation, and packaging problems.

  11. Name the two provocative clinical tests for neonatal DDH and what they detect.

    Ortolani test (reduction — abduction with anterior lift, positive 'clunk' as dislocated hip relocates) and Barlow test (dislocation — adduction with posterior pressure, positive if reducible hip dislocates). Both are most reliable in the first weeks of life.

  12. What is the imaging modality of choice for DDH by age, and why the age cutoff?

    Ultrasound is used before ~4–6 months of age because the femoral head is largely cartilaginous. After ~4–6 months, when the ossific nucleus appears, plain radiographs (AP pelvis) become the modality of choice.

  13. What is the first-line treatment for DDH in an infant under 6 months?

    A Pavlik harness, which holds the hips in flexion and abduction to encourage concentric reduction. It is typically avoided/less effective after 6 months or in irreducible/teratologic dislocations.

  14. What is the significance of the greenstick and torus (buckle) fractures unique to children?

    Pediatric bone is more porous and has a thick periosteum. A torus/buckle fracture is a compression of one cortex; a greenstick fracture is an incomplete fracture where one cortex breaks and the other bends — both reflect the plasticity of immature bone.

  15. Why do pediatric fractures remodel and heal faster than adult fractures?

    Children have thick, metabolically active periosteum, open physes providing growth-driven remodeling potential, and greater osteogenic capacity. Remodeling is best for fractures near the physis, in the plane of joint motion, and in younger children with more growth remaining.

  16. What is a supracondylar humerus fracture and its key associated complication?

    A common pediatric elbow fracture (often extension-type from fall on outstretched hand). Key risks include neurovascular injury — the anterior interosseous nerve (median) is most commonly injured, and brachial artery injury can occur; malunion causes cubitus varus (gunstock deformity).

  17. What is amelia versus meromelia in congenital limb deficiency?

    Amelia is the complete absence of a limb. Meromelia is partial absence of a limb (e.g., hemimelia — absence of the distal half; phocomelia — hands/feet attached directly to the trunk with absent intermediate segments).

  18. Contrast fibular hemimelia and tibial hemimelia in terms of inheritance and stability.

    Fibular hemimelia is the most common long-bone deficiency, usually sporadic, causing limb shortening and foot deformity. Tibial hemimelia is rarer, often autosomal dominant/associated with syndromes, and produces an unstable knee since the tibia is the main weight-bearing bone.

  19. What are the main bearing surface options for Total Hip Arthroplasty and a key drawback of each?

    Metal-on-polyethylene (wear debris → osteolysis, improved with highly cross-linked PE), ceramic-on-ceramic (excellent wear but risk of squeaking/fracture), ceramic-on-polyethylene (low wear), and metal-on-metal (largely abandoned due to metallosis and adverse local tissue reactions/pseudotumors).

  20. What are the two main modes of THA fixation and how do they achieve stability?

    Cemented fixation uses polymethylmethacrylate (PMMA) as a grout for immediate stability. Cementless (press-fit) fixation relies on bone ingrowth/ongrowth into a porous-coated implant for biological fixation over time.

  21. What is the most common complication after primary THA and a key modifiable risk factor?

    Dislocation is among the most common early complications; risk is influenced by surgical approach (posterior approach historically higher unless capsule repaired), component malposition (outside the Lewinnek safe zone), and patient factors. The posterior approach classically restricts flexion/adduction/internal rotation.

  22. What is the target acetabular cup orientation ('Lewinnek safe zone') in THA?

    Approximately $40^{\circ} \pm 10^{\circ}$ of inclination (abduction) and $15^{\circ} \pm 10^{\circ}$ of anteversion, aiming to minimize dislocation and impingement (though the concept has limitations with spinopelvic mobility).

  23. What is the most common long-term reason for revision Total Knee Arthroplasty?

    Aseptic loosening is a leading cause of late revision, along with instability, polyethylene wear/osteolysis, and infection (the leading cause of early revision). Malalignment and stiffness also contribute.

  24. What are the alignment goals in Total Knee Arthroplasty (mechanical axis)?

    Traditional mechanical alignment aims to restore a neutral hip-knee-ankle axis ($0^{\circ} \pm 3^{\circ}$), with the femoral component perpendicular to the femoral mechanical axis and tibial component perpendicular to the tibial mechanical axis, balancing flexion and extension gaps.

  25. Differentiate cruciate-retaining (CR) from posterior-stabilized (PS) TKA designs.

    CR designs preserve the posterior cruciate ligament for femoral rollback. PS designs sacrifice the PCL and use a tibial post-and-cam mechanism to substitute for it, providing rollback and preventing posterior tibial subluxation.

  26. What is the gold-standard diagnosis of periprosthetic joint infection component (synovial fluid criteria)?

    Diagnosis uses major criteria (sinus tract communicating with prosthesis, or two positive periprosthetic cultures of the same organism) plus minor criteria including elevated serum CRP/ESR, elevated synovial WBC count, elevated synovial polymorphonuclear percentage, positive alpha-defensin, and elevated synovial CRP (MSIS/ICM criteria).

  27. What is the two-stage revision protocol for infected arthroplasty?

    Stage 1: remove implants, debride, and place an antibiotic-loaded cement spacer, followed by IV antibiotics (typically ~6 weeks). Stage 2: after infection clearance is confirmed, reimplant a definitive prosthesis. It remains the gold standard for chronic periprosthetic joint infection.

  28. What are the three columns of the spine (Denis classification) and their significance?

    Anterior column (anterior longitudinal ligament, anterior half of vertebral body/disc), middle column (posterior half of body/disc, posterior longitudinal ligament), and posterior column (pedicles, facets, posterior ligamentous complex). Involvement of $\geq 2$ columns generally indicates instability.

  29. What defines spinal shock versus neurogenic shock?

    Spinal shock is the transient loss of all reflexes/sensory-motor function below the injury level (resolution marked by return of the bulbocavernosus reflex). Neurogenic shock is hemodynamic — hypotension with bradycardia from loss of sympathetic tone in injuries above T6.

  30. What distinguishes a complete from an incomplete spinal cord injury (ASIA)?

    A complete injury (ASIA A) has no motor or sensory function preserved in the lowest sacral segments (S4–S5), including no sacral sparing. Incomplete injuries (ASIA B–D) have some preserved function below the neurologic level, including sacral sparing, and carry better prognosis.

  31. Compare central cord syndrome and anterior cord syndrome.

    Central cord syndrome (often hyperextension in older patients with cervical spondylosis): upper limb weakness > lower limb, variable sensory loss; best prognosis of incomplete injuries. Anterior cord syndrome (anterior spinal artery/flexion): loss of motor and pain/temperature below the lesion with preserved proprioception/vibration; worst prognosis.

  32. What are the pathological features distinguishing lumbar disc herniation from spinal stenosis symptoms?

    Disc herniation causes radicular pain (sciatica) from nerve root compression, worse with sitting/flexion and Valsalva, positive straight leg raise. Central lumbar stenosis causes neurogenic claudication — bilateral leg pain worse with standing/extension/walking, relieved by sitting/flexion ('shopping cart sign').

  33. What are the cardinal features of degenerative cervical/lumbar spondylosis on imaging?

    Disc space narrowing, osteophyte formation, facet joint hypertrophy/arthrosis, endplate sclerosis (Modic changes), and ligamentum flavum hypertrophy, which together can narrow the canal and foramina.

  34. Define scoliosis and the Cobb angle threshold for diagnosis.

    Scoliosis is a lateral curvature of the spine with rotation, defined as a Cobb angle $> 10^{\circ}$ in the coronal plane. The Cobb angle is measured between lines drawn along the endplates of the most tilted (end) vertebrae of the curve.

  35. What are the treatment thresholds for adolescent idiopathic scoliosis by Cobb angle?

    Curves $< 25^{\circ}$: observation. Curves $25^{\circ}$–$45^{\circ}$ in a skeletally immature patient: bracing (e.g., to prevent progression). Curves $> 45^{\circ}$–$50^{\circ}$: surgical correction (fusion) is generally considered.

  36. Differentiate scoliosis, kyphosis, and lordosis.

    Scoliosis is abnormal lateral (coronal) curvature with rotation. Kyphosis is excessive posterior convex (sagittal) curvature (e.g., thoracic hyperkyphosis, Scheuermann disease). Lordosis is excessive anterior concave (sagittal) curvature, typically lumbar (hyperlordosis).

  37. What is the classic mechanism of an ACL injury and the associated 'unhappy triad'?

    A non-contact pivoting injury — sudden deceleration with valgus and internal rotation (or hyperextension). The O'Donoghue 'unhappy/terrible triad' classically involves ACL tear, medial collateral ligament tear, and medial meniscus tear (though lateral meniscus involvement is now recognized as common).

  38. Name the primary clinical tests for ACL insufficiency and which is most sensitive/specific.

    Lachman test (30° flexion — most sensitive), anterior drawer test (90° flexion), and the pivot-shift test (most specific for functional instability, reproduces the giving-way). A soft/absent endpoint indicates ACL rupture.

  39. What is the primary blood supply pattern of the meniscus and its clinical relevance?

    Only the peripheral ~10–30% is vascular (the red-red and red-white zones) supplied by the perimeniscal capillary plexus; the inner white-white zone is avascular. Peripheral (red zone) tears can heal/be repaired, whereas central avascular tears usually require debridement.

  40. What clinical test and classic symptom suggest a meniscal tear?

    McMurray test (pain/click with knee flexion-extension under rotation), joint-line tenderness, and Apley grind test. Classic symptoms are mechanical locking, catching, and effusion following a twisting injury.

  41. What are the functions of the ACL and PCL respectively?

    The ACL is the primary restraint to anterior translation of the tibia on the femur (and secondary restraint to rotation). The PCL is the primary restraint to posterior translation of the tibia on the femur.

  42. Which rotator cuff muscle is most commonly torn and what is its innervation and action?

    The supraspinatus is most commonly torn. It is innervated by the suprascapular nerve and initiates the first ~15–30° of shoulder abduction (and depresses/stabilizes the humeral head in the glenoid).

  43. Name the four rotator cuff muscles (SITS) and their main actions.

    Supraspinatus (initiates abduction), Infraspinatus (external rotation), Teres minor (external rotation), and Subscapularis (internal rotation). Together they dynamically stabilize the glenohumeral joint by centering the humeral head.

  44. What are the key special tests for rotator cuff pathology?

    Jobe's empty can test (supraspinatus), external rotation lag/Patte test (infraspinatus/teres minor), lift-off and belly-press tests (subscapularis), and the Neer and Hawkins-Kennedy tests for subacromial impingement.

Orthopedics syllabus FAQ

What is in the Orthopedics syllabus?

The Orthopedics syllabus is split into 8 chapters: Basic Science, Trauma, Pediatric Orthopedics, Adult Reconstruction, Spine, Sports Medicine, Oncology and Infections. Together they contain 24 topics and 73 sub-topics.

How many chapters and topics are in the Orthopedics syllabus?

8 chapters and 24 topics, broken down further into 73 sub-topics. The largest chapter is Basic Science, with 3 topics.

Are there Orthopedics flashcards?

Yes — 64 question-and-answer flashcards, printed in full on this page and available in the Examius app with spaced repetition. The free plan covers one exam of your choice, including its flashcards; Examius Pro, a one-time purchase, unlocks every other exam and deck.