HIP Final Exam Review – MSK 1

Question-and-answer flashcards covering pelvic apophyseal avulsions, FAIS, acetabular labral tears, GTPS, SCFE, LCPD, DDH, and RA.

What is the primary etiological factors for pelvic apophyseal fractures?

a. Young athletes due to increased intensive year round training and early specialisation in sport; b. Injuries due to forceful and violent eccentric muscle contraction; c. Activities involving running, kicking and jumping.

What are the pathophysiological findings for pelvic apophyseal fractures?

a. Secondary ossification center of the open apophysis is weaker than adjacent soft tissue, making avulsion fractures more common than muscle strains in young athletes. b. The injury mechanism involves cartilaginous growth plate that separates and retracts.

List 3 common signs and symptoms for pelvic apophyseal fractures?

a. Acute onset of pain in affected area with ‘pop’ sound b. Swelling in affected area c. Worsening with passive stretching but relived at rest.

What is the MOI for pelvic apophyseal fractures?

a. Sudden eccentric muscle contraction from sports like running (ASIS avulsion) and kicking (AIIS avulsion). b. This sudden force causes the unfused growth plate to separate and retract.

List 3 structures commonly affected in pelvic apophyseal avulsions?

a. Pelvic apophyses of the ischial tuberosity b. Pelvic apophyses of the ASIS c. Pelvic apophyses of the AIIS.

What should the clinician medically screen for when considering pelvic apophyseal avulsions?

Screen for overlapping symptoms, as patients with ischial tuberosity avulsions might misidentify their injury as hamstring sprain.

What is the difference between apophysitis and apophyseal avulsion?

a. Apophyseal avulsion is a traumatic injury where a fragment of the bone is pulled off at the site of the tendon attachment (apophysis). b. Apophysitis is an overuse injury due to repetitive stress or traction from attached tendons.

What is the difference between traction and pressure apophysitis?

a. Traction apophysitis occurs due to repetitive tensile forces from muscles being attached at the site of apophysis. b. Pressure apophysitis occurs due to repetitive compressive forces from weight bearing or joint loading.

Explain the primary etiological factors for FAIS (1.5 marks)

a. FAIS results from abnormal bone morphology at the femoral head-neck junction and/or acetabular rim, leading to abnormal contact during hip movement. b. Genetic factors may contribute to this hip pathology due to single polymorphisms (SNPs) such as HOX9 and DIO2 which are correlated to pincer lesions and specific proximal morphology.

Describe the pathophysiology of FAIS

a. Progressive damage to the acetabular labrum, chondrolabral junction and articular cartilage due to repetitive abnormal contact between the head-neck junction and acetabulum. This can lead to joint degeneration and early osteoarthritis (OA).

What is the difference between cam and pincer lesions relating to FAIS?

a. Cam deformity is the abnormal bony prominence at the junction of femoral head. b. Pincer lesion is an abnormal bony ‘hang’ of the anterolateral acetabular rim, resulting in over coverage of the femoral head.

How can early OA be suspected in a patient with FAIS?

The impingement can cause labral or cartilage injury, leading to development of OA.

List 3 common signs and symptoms of FAIS

a. Pain – in groin, lateral hip and thigh b. Clicking, catching, buckling c. Limited ROM.

Describe the MOI for FAIS

Repetitive abnormal and dynamic contact between femoral head-neck junction and acetabular rim causes shearing and compression stresses on labrum and cartilage, that occurs especially during hip flexion and internal rotation.

List 2 structures commonly affected with FAIS

a. Femoral head-neck junction and acetabular rim b. Acetabular labrum and cartilage.

List 3 conditions that can be medically screened when suspecting FAIS

a. Infection and tumour b. Hip dysplasia c. Osteonecrosis.

List 3 etiological factors of GTPS

a. Repetitive microtrauma and mechanical overload between the greater trochanter and IT band.

What are the 3 key pathophysiological findings of GTPS?

a. Abductor muscle tears b. Tendinosis and thickening of IT band c. Bursal inflammation.

List 3 common signs and symptoms of GTPS

a. Intermittent debilitating pain – lateral thigh and buttock b. Lateral hip tenderness c. Discomfort during hip rotation, abduction, adduction.

What is the MOI for GTPS?

Repetitive friction between greater trochanter and IT band due to running or stair climbing which lead to microtrauma of the gluteal tendons.

List 3 etiological factors of acetabular labral tears

a. Abnormal bony morphology b. Capsular laxity c. Traumatic event or repetitive microtrauma from pivoting or twisting.

Describe the pathophysiology of acetabular labral tears

Labral tears defunctions the labrum, meaning it affects joint congruity, load distribution, and stability. This defunction can lead to micro-instability, leading to ongoing articular damage and degeneration, contributing to OA.

List 3 signs and symptoms of acetabular labral tears

a. Pain in anterior hip or groin that worsens with hip flexion and pivoting b. Clicking or catching of the hip c. Stiffness or instability.

Describe the MOI for acetabular labral tears

a. Insidious onset. b. External rotation force in hyperextended position.

List 2 structures affected with acetabular labral tears

a. Acetabular labrum and cartilage b. Chondrolabral junction.

List 3 etiological factors of GTPS

a. Repetitive microtrauma and mechanical overload between the greater trochanter and IT band.

What are the 3 key pathophysiological findings of GTPS?

a. Abductor muscle tears b. Tendinosis and thickening of IT band c. Bursal inflammation.

List 3 common signs and symptoms of GTPS

a. Intermittent debilitating pain – lateral thigh and buttock b. Lateral hip tenderness c. Discomfort during hip rotation, abduction, adduction.

What is the MOI for GTPS?

Repetitive friction between greater trochanter and IT band due to running or stair climbing which lead to microtrauma of the gluteal tendons.

Explain the primary etiological factor of SCFE

SCFE occurs when the femoral epiphysis displaces due to high physiological axial load transmitted across a weak physis. Obesity increases the risk as it increases the mechanical weight. Endocrine and renal disorders can weaken the physis.

What are the pathophysiological findings of SCFE?

a. Displacement, typically posterior and inferior relative to femoral head and neck occurring at the hypertrophic zone of physis. b. The deformity exposes the metaphysis and neck edge to the anterolateral rim and labrum, causing impingement and articular damage.

What are 3 common signs and symptoms for SCFE?

a. Atraumatic hip, thigh, knee pain b. Limping or inability to bear weight c. Limited IR of involved hip.

What is the MOI for SCFE?

a. Shear forces acting on the physis, which is in a vertical position and has weakened perichondral support during adolescence. b. Progressive instability as presented by weeks of antecedent ache or limp.

List 3 structures affected with SCFE.

a. Capital femoral epiphysis b. Femoral epiphysis c. Anterior acetabular cartilage and labrum.

How can SCFE be medically screened?

a. Consider SCFE in pre-adolescents or adolescents with leg pain, even without trauma history. b. Screen for infectious etiologies such as septic arthritis c. Screen for endocrine or renal disorders.

What medical imaging technique is considered gold standard in SCFE?

Biplanar radiographic examination with supine AP and frog-leg lateral views.

What are the etiological factors for LCPD?

a. Idiopathic disease but its multifactorial disease b. Involves genetic, environmental and metabolic factors c. Trauma, steroid use, coagulopathy.

Explain the pathophysiology of LCPD.

a. Characterized by avascular necrosis of the femoral head b. Blood supply to femoral head is disrupted, leading to femoral head becoming sclerotic and flattened. c. Progression in disease results in deformities and loss of sphericity of femoral head.

List 3 common signs and symptoms for LCPD

a. Limping gait b. Restricted hip mobility – limited IR and abduction c. Isolated knee pain.

Explain the MOI for LCPD.

a. Deformities in the head occur when applied forces exceed its resistance capacity, as necrosis damages the mechanical properties of the bone and articular cartilage. b. The mechanism of avascularity involves formation of microthrombi that block blood flow to the femoral head.

What type of medical imaging is recommended for LCPD?

AP and frog leg X-rays but MRI is considered the best method as it can show abnormalities before radiograph and identify bone marrow changes.

Explain the etiology for DDH.

a. Multifactor etiology with abnormal hip development b. Genetic, environmental and mechanical factors.

What are the risk factors for DDH?

a. Female sex b. Breech position in last trimester c. Swaddling in adducted/extended position d. In utero restriction.

What are 4 pathophysiological findings that affect DDH?

a. Instability b. Acetabular dysplasia c. Subluxation d. Dislocation.

What are the common signs and symptoms for DDH?

a. Ortolani test positive b. Barlow maneuver – positive c. Limited hip abduction due to decrease in capsule laxity.

What is the MOI for DDH?

a. Ligamentous laxity from maternal hormones b. Physical limitations in uterus contribute to abnormal hip development c. Swaddling in certain positions can increase incidence.

What medical imaging is recommended for DDH?

a. US at 6 weeks b. X-ray preferred for dysplasia c. CT or MRI after closed reduction or spica casting.

What is the etiology for RA?

a. Systemic autoimmune disease caused by interaction between genes and environmental factors. b. Obesity may play a role or tobacco smoke.

What is the pathophysiology in the development of RA?

a. Chronic inflammatory arthritis that involves synovial joints, starting in the small peripheral joints and progressing to proximal joints. b. This inflammation leads to the destructions of the joint with loss of cartilage and bone erosions over time.

Explain the MOI for RA.

a. T cells interacting with B cells, activating antigen-specific B cells to produce rheumatoid factor (RF) and anti-citrullinated protein antibodies (ACPA). b. Autoantibodies – form immune complexes that propagate an intense inflammatory response through cytokine production, leading to joint damage.