Musculoskeletal radiology rewards pattern recognition across arthritis, bone tumours, trauma, and metabolic bone disease. These free MSK samples from the RadioQBank published set come with full explanations, exam pearls, and references so each attempt teaches, not just tests.
Question 1 · Tendons · easy
Which of the following best describes the 'magic angle effect' on MRI of tendons?
- a. Artificial T2 signal increase in tendons oriented at approximately 55° to the main magnetic field, seen on short TE sequences
- b. Low signal in tendons due to their dense fibrocartilaginous matrix
- c. Artifactual signal loss in tendons running perpendicular to the B0 field
- d. Gadolinium enhancement within tendon sheaths on MR arthrography
Answer: A. The magic angle effect is a well-known MRI artefact where tendons oriented at approximately 55° (magic angle) to the main magnetic field (B0) demonstrate artificially increased signal on short TE sequences (PD, T1W, GRE). This is because the dipole-dipole interactions between water protons become zero at 55°, prolonging T2* and increasing signal. It is most commonly seen in the supraspinatus (at the critical zone), curved portions of the Achilles, and other tendons that subtend this angle. Long TE (T2W) sequences resolve this artefact — genuine pathology persists on T2W while magic angle artefact disappears.
Exam pearl: Magic angle = 55° to B0 = T2 signal on SHORT TE sequences; disappears on long TE (T2W) — genuine pathology persists on T2W.
Radiographics 1996;16:1005; AIIMS-MAMC-PGI MSK Guide
Question 2 · Metabolic Bone Disease · easy
A 35-year-old woman presents with episodic bone pain, nephrolithiasis, and constipation. Serum calcium is elevated, PTH is elevated, and phosphate is low. X-rays show subperiosteal bone resorption, brown tumours in the pelvis, and generalised osteopenia. What is the diagnosis?
- a. Secondary hyperparathyroidism
- b. Primary hyperparathyroidism
- c. Osteomalacia
- d. Multiple myeloma
Answer: B. Primary hyperparathyroidism (PHPT) is caused by autonomous PTH secretion from a parathyroid adenoma (~85%), hyperplasia (~15%), or rarely carcinoma. The classic mnemonic is 'bones, stones, groans, and moans' (bone disease, nephrolithiasis, GI symptoms, neuropsychiatric). Elevated calcium + elevated PTH + low phosphate distinguishes it from secondary HPT (where Ca is low/normal). X-ray triad: subperiosteal bone resorption (radial aspect middle phalanges), brown tumours (giant cell-rich reactive lesions), and salt-and-pepper skull.
Exam pearl: High Ca + high PTH + low PO4 = primary HPT; subperiosteal resorption radial middle phalanx is pathognomonic.
Grainger & Allison 7th ed; Radiographics 2000;20(5):1,303–1,322
Question 3 · Arthritis · moderate
A 48-year-old man presents with right knee pain and swelling. Aspiration reveals cloudy fluid with crystals. Under polarised light microscopy, positively birefringent rhomboid crystals are seen. X-ray shows chondrocalcinosis. What secondary cause of CPPD should be investigated?
- a. Hyperuricaemia
- b. Haemochromatosis
- c. Hyperparathyroidism
- d. Both B and C
Answer: D. CPPD disease can be secondary to several metabolic conditions that increase inorganic pyrophosphate levels or impair its clearance. The most important secondary causes to screen for are: haemochromatosis (iron deposition impairs pyrophosphate clearance), hyperparathyroidism (elevated calcium/PTH promotes CPP crystal formation), hypomagnesaemia, hypophosphatasia, and Wilson's disease. Both haemochromatosis and hyperparathyroidism are classic exam triggers for CPPD investigation.
Exam pearl: CPPD secondary causes: Haemochromatosis, Hyperparathyroidism, Hypomagnesaemia, Hypophosphatasia — the '4H rule.'
Grainger & Allison 7th ed, Chapter 51; Rheumatology (Oxford) 2021
Question 4 · Bone Tumours · moderate
A 65-year-old man presents with multiple lytic bone lesions, renal insufficiency, hypercalcaemia, and a monoclonal spike on SPEP. Whole-body low-dose CT shows multiple well-defined 'punched-out' lytic lesions throughout the axial and appendicular skeleton without sclerotic borders. Which modality is currently recommended for staging and response assessment in this condition?
- a. Technetium-99m bone scan
- b. FDG PET/CT
- c. Whole-body low-dose CT alone
- d. Whole-body MRI (WBMRI)
Answer: D. Multiple myeloma predominantly causes osteolytic lesions through osteoclast activation without osteoblastic response. Technetium bone scans rely on osteoblastic uptake of the diphosphonate tracer, making them insensitive for myeloma (false negatives are common). Whole-body MRI (WBMRI) is the current gold standard for staging of myeloma per IMWG guidelines, as it detects diffuse marrow infiltration (before lytic lesions appear), focal lesions, and extramedullary disease. FDG PET/CT is the preferred alternative and is recommended by IMWG for post-treatment response assessment.
Exam pearl: Bone scan is FALSE NEGATIVE in myeloma (no osteoblastic response); WBMRI is gold standard for staging.
IMWG Guidelines 2023; Radiographics 2017;37(6):1817
Question 5 · Arthritis · hard
A 50-year-old man with AS is started on a TNF-alpha inhibitor. Six months later, he develops new spinal bone formation on X-ray. This finding in AS patients on anti-TNF therapy is called what?
- a. Paradoxical syndesmophyte formation
- b. Rebound ankylosis
- c. Treatment-induced osteitis
- d. Biosimilar arthropathy
Answer: A. Paradoxical syndesmophyte formation (also called 'radiographic progression despite anti-TNF therapy') has been observed in clinical trials. While anti-TNF therapy effectively suppresses inflammation, it does not fully arrest structural damage. New syndesmophyte formation can occur even during effective inflammatory suppression, possibly because TNF-alpha blockade decouples inflammation from osteoproliferation. This is an active area of research (OASIS, ASSERT, ATLAS trial data).
Exam pearl: Anti-TNF reduces inflammation in AS but may not stop syndesmophyte growth — structural monitoring is essential.
Ann Rheum Dis 2012 (OASIS trial); Radiographics 2015
Question 6 · Trauma · hard
A 45-year-old male is involved in a high-speed RTA. CT pelvis shows a Tile C1 pelvic ring injury. Which of the following structures, when disrupted, is most responsible for massive haemorrhage in vertical shear pelvic fractures?
- a. Internal iliac artery
- b. Presacral venous plexus
- c. Superior gluteal artery
- d. Obturator artery
Answer: B. In vertical shear pelvic fractures (Tile C), the majority of haemorrhage (approximately 85%) comes from disruption of the presacral and peripelvic VENOUS plexuses — not from arterial injury. The pelvic retroperitoneum acts as a tamponade, but Tile C injuries destroy this tamponade effect. Venous bleeding is harder to control by angioembolisation, which is why pelvic packing + external fixation is the primary haemorrhage control strategy in damage control scenarios. Arterial injury (superior gluteal, internal pudendal, obturator) accounts for only ~15% of haemorrhage but responds better to angioembolisation.
Exam pearl: Pelvic fracture haemorrhage: ~85% venous (presacral plexus) = pelvic packing; ~15% arterial = angioembolisation (superior gluteal artery most common).
AJR 2012;198(4):W332–W340; Radiographics 2014;34(3):753–777