BiM MSK

Question 1

1. What is scoliosis
2. What plane is this most common in
3. What is the cause of congenital scoliosis (what happens, when does it happen)
4. What is fibular hemimelia

Answer 1

1. Abnormal curvature of the spine
2. Coronal plane
3. Vertebrae fail to separate/form properly, during 4-6 weeks IUL
4. Congenital absence of fibula

Question 2

1. What is DDH and what causes it
2. What is the main complication of DDH
3. What is physical arrest
4. What is the most common cause of physical arrest
5. What causes a herniated disc
6. List 4 consequences of skeletal failure

Answer 2

1. Developmental dysplasia of the hip. Acetabulum doesn’t form properly
2. Failure in formation of femoral heads
3. Complete/partial early closure of growth plate
4. Trauma
5. Repeated micro traumas. Nucleus purposes (inner part of disc) bursts through worn annulus fibrosis (outer part of disc), causing pain
6. Pain, muscle weakness, loss of function, loss of mobility/independence, time off work/earning

Question 3

1. Where does haematopoiesis occur
2. Give 4 functions of the skeleton
3. What is the name of the way humans walk

Answer 3

1. Red bone marrow, mainly in non-long bones
2. Mechanical structure, metabolic storage/homeostasis, soft organ protection, hearing, breathing, locomotion
3. Bipedalism

Question 4

1. What are the names and functions of the 3 types of bone cell
2. What are osteoprogenitor (osteogenic cells) and where are they found
3. Briefly describe the process of how osteoprogenitor cells differentiate into osteoblasts
4. What other cells can osteoprogenitor cells differentiate into

Answer 4

1. Osteoblasts - produce bone matrix
   Osteocytes - maintain bone
   Osteoclasts - resorb bone
2. Mesenchymal stem cells. Present in bone marrow endosperm and periosteum. Precursors to more specialised bone cells
3. Minimal strain is present in local environment. Signalled by RunX2 and osterix, which is released by osteocytes that sense movement via mechanotransduction
4. Adipocytes, myocytes, chondrocytes, osteoblasts

Question 5

1. What are 2 functions of osteoblasts
2. Give a brief overview of bone production regulation
3. Describe the RANK/OPG axis
4. What are the 3 fates OBs have

Answer 5

1. Bone production (of non-mineralised matrix), osteoclast regulation
2. PTH stimulates production of type I collagen and ALP. ALP dephosphorylates organic molecules, initiating matrix calcification laying down. Vitamin d receptor stimulated to produce matrix. ALP and matrix proteins
3. Via RANK/OPG axis
   OBs release RANKL in response to PTH. RANKL binds to RANK, stimulating osteoclast precursors to differentiate into OCs, stimulating bone resorption.
   When OBs are stimulated to secrete osteoprotegrin (OPG - a decoy receptor), this binds to free RANKL preferentially over RANK, inhibiting the differentiation and activation of OCs, inhibiting bone resorption
4. Become osteocytes, apoptosis, differentiate into lining cells

Question 6

1. What is the function of an osteocyte
2. What is osteocytic osteolysis
3. What is mechanotransduction
4. How do osteocytes communicate with neighbouring cells
5. What is osteocyte signalling (what does it do)
6. Briefly describe the effects of osteocyte signalling

Answer 6

1. Maintain bone and cellular matrix, regulate Ca and PO4 concentration
2. When osteocytes rapidly release Ca in response to increasing PTH levels
3. Fluid squeezed out from tissue under compressive load and flows to an area of lower compression. Osteocytes sense this and signal over long distances via cellular processes
4. Via canaliculi
5. Regulation of bone remodelling in response to local mechanical or systemic signals
6. Sclerostin production increases OC formation and, as well as increased expression of RANKL leads to decreased bone formation
   Sclerostin production is inhibited by PTH and mechanical loading leads to increased bone formation

Question 7

1. What is the structure of an osteoclast
2. What do osteoclasts do
3. Briefly describe how osteoclast signalling occurs
4. What is the name of the small pits formed when bone resorption occurs
5. What is the function of the ruffled border

Answer 7

1. Multinucleated giant cell
2. Resorb bone (organic matrix and inorganic hydroxyapatite)
3. OCs have calcitonin receptors. RANKL binding causes osteoclast progenitor cells to fuse together, becoming multinucleated. They migrate to site of bone resorption, attach to the surface and activate. Once activated, one side of the cell seals to the bone surface (sealing zone) and the cell polarises to have different membrane domains (secretory zone at other side of cell releases breakdown products into interstitial fluid). Bone resorption occurs, forming small pits
4. Howship’s lacunae
5. Increases surface area of cell, aids secretion and absorption of enzymes and breakdown products (resorbs breakdown products from Howship’s lacunae, transporting them across cell for excretion via secretory domain)

Question 8

1. What are the components of the axial skeleton
2. What is the appendicular skeleton
3. Name 2 flat bones
4. Name 2 short bones
5. Where are sesamoid bones found, what do they do and name 2
6. Name 1 irregular bone
7. What is the % composition of bone
8. What is the most prominent component of bone

Answer 8

1. Bones of the head, spine, ribcage, vertebral column
2. Shoulder girdle, pelvis, upper limbs, lower limbs
3. Bones of skull, sternum
4. Carpal bones, tarsal bones
5. Exist in substance of tendons. Act to improve power in attached muscle. Patella, metatarso-phalangeal joint
6. Spinal vertebrae
7. 40% organic osteoid (collagen, proteoglycans, MMPs), 60% inorganic (hydroxyapatite)
8. Type I collagen (90% organic component)

Question 9

1. What are the 3 regions of a long bone
2. What type of tissue is periosteum
3. What is the function of periosteum
4. Name 4 long bones

Answer 9

1. Epiphysis - end of long bone (articular surface), metaphysis, diaphysis
2. Dense irregular CT
3. Blood supply to bone, provides fibroblasts and progenitor cells, aids in circumferential growth and fracture healing
4. Humerus, radius, ulna, femur, tibia, fibula, metacarpals, metatarsals, phalanges

Question 10

1. What is the structure of the Haversian system
2. In what type of bone is the Haversian system found
3. What is the difference in structure of cancellous bone compared to cortical bone
4. What is the relative turnover rate of cancellous and cortical bone
5. What is Wolff’s law
6. What is the benefit of a trabecular pattern of cancellous bone

Answer 10

1. Osteons (2-3mm bone cylinders, run parallel to long axis)
   Vascular canals (Haversian’s - parallel and Volkman’s - perpendicular)
   Neuromuscular network
   Interstitial lamellae
2. Cortical bone
3. Cancellous - less rigid, more elastic
4. Cancellous - high turnover
   Cortical - slow turnover
5. Bone will adapt to load under which it is placed - bone under increased load will remodel to become stronger over time, but only in response to the specific type of loading it is under
6. Strength without weight - fibres organised along lines of maximum mechanical stress, allowing transmission of loads

Question 11

1. Briefly describe the process of intramembranous ossification
2. Briefly describe the process of endochondral ossification
3. Name 2 bones that grow via intramembranous ossification
4. Name 2 bones that grown via endochondral ossification
5. Give the different types of macroscopic bone and their functions
6. What are the 2 types of microscopic bone and how do they arise/what are their features

Answer 11

1. Occurs during foetal development. Mesenchymal stem cells proliferate into fibrous tissue and differentiate into OBs which cluster together (ossification centre). OBs produce osteoid, which is then calcified by hydroxyapatite. OBs trapped in the matrix become osteocytes. Stem cells surrounding ossification centre continue to differentiate to maintain supply of OBs. Bone matures, creating trabecular matrix around BVs. Periosteum forms and traps more OBs in cellular layer (osteocytes) and BVs condense into red marrow
2. Mesenchymal stem cells differentiate into chondrocytes and form cartilaginous scaffold/precursor. Perichondrium forms on surface and becomes periosteum, forming periosteal collar (thin layer of bone) on surface of diaphyseal cartilage. More cartilage matrix is produced and chondrocytes at centre enlarge, calcify matrix and die and surrounding cartilage disintegrates. BVs invade space left, carrying osteogenic (osteoprogenitor) cells. Primary ossification centre forms in middle of cartilage scaffold, replacing cartilage with bone. New cartilage continues to form at end of bones, increasing length and secondary ossification centres are formed in epiphysis
3. Flat bones of the skull, clavicles, flat bones of the face, pelvis
4. Long bones of axial and appendicular skeletons, including the ribs, vertebrae, and limbs
5. Cortical - provides rigidity (resists bending/torsion)
   Cancellous - spongy trabecular bone, supports articular surface, resists impact and transfer weight evenly through bone
6. Woven - random/irregular/haphazard collage fibres, immature, rapid production (foetus/fracture)
   Lamellar - made by remodelling woven bone, collagen fibres in parallel/lamellae, organised, stress-oriented, strong

Question 12

1. What is the physis
2. What tissue is the physis
3. When does the physis fuse
4. How does the physis grow (name the process)
5. What are 3 arteries that provide vascular supply to the physis

Answer 12

1. Site of longitudinal growth - growth plate
2. Hyaline cartilage
3. 16M, 14F
4. Endochondral ossification
5. Perichondral artery (main), epiphyseal and metaphysical arteries

Question 13

1. Name the function/roles of the following microscopic physeal zones:
   a) Resting zone
   b) Proliferative zone
   c) Hypertrophic zone
   d) Metaphysical bone (2 components)
2. Achondroplasia/gigantism are defects of which zone (and what happens to the cells)
3. What gene is defective in Achondroplasia
4. What causes gigantism
5. What is acromegaly/when does it occur
6. What bones are affected in acromegaly
7. What zone is considered a ‘weak point’ and is the site of SUFE and SH fractures

Answer 13

1. a) Resting zone - sparsely packed chondrocytes, stores lipids, glycogen and proteoglycans. Resting/no activity
   b) Proliferative zone - cells transition from resting zone and stack in columns during bone formation. Increased cell multiplication. Produce cartilaginous ECM
   c) Hypertrophic zone - increase in cell size. 3 stages/sub-zones - maturation zone (double in size), degeneration zone (five-fold increase), provisional calcification zone (apoptosis, cells release Ca into matrix)
   d) Metaphyseal bone - primary (woven bone formed - haematogenous infiltration) and secondary (woven bone remodels to lamellar bone) spongiosa
2. Proliferative zone - increased inhibition of chondrocyte proliferation
3. FGFR 3 gene
4. Excess of growth hormone, typically due to pituitary adenoma
5. Gigantism after physeal closure
6. Hands, feet, forehead, jaw, nose
7. Hypertrophic zone

Question 14

1. Give the average time when the following key milestones occur
   a) Head control
   b) Sit
   c) Stand
   d) Walk
2. Name 2 types of angular skeletal deformity variants
3. Name 2 management options for angular skeletal deformities

Answer 14

1. a) 1-3 months
   b) 6-9 months
   c) 9-12 months
   d) 12-20 months
2. Bowlegs (genu varum), knock-knees (genu valgum)
3. Observe, osteotomy, eight plate (restrict growth in some areas, encourage growth in others)

Question 15

1. Name 4 conditions that can cause a limp in a child
2. Briefly describe a normal gait in children, including when it typically matures

Answer 15

1. DDH, transient synovitis, SUFE, perthes, tumours, septic arthritis, neuromuscular
2. Short stride length, fast cadence, low velocity, widened base of support. Matures around 7 years old

Question 16

1. What is transient synovitis
2. Give 3 features
3. Give 3 investigations
4. What age does transient synovitis typically affect
5. What is it often associated with

Answer 16

1. Non-specific, short-term inflammatory synovitis with synovial effusion of hip joint
2. Pain in hip/knee/thigh, synovial fluid effusion, hip held in flexion, lateral rotation and abduction
3. FBC, ESR, CRP, XRs (AP and frog leg lateral), US, MRI, bone scans
4. 3-6 years old
5. Viral infection

Question 17

1. What 2 tests are used for DDH examination
2. Give 2 features of DDH
3. Give 2 investigations
4. How is DDH treated
5. What age group does DDH typically affect

Answer 17

1. Barlow and Ortolani tests
2. Skin crease asymmetry, leg length discrepancy, reduced abduction
3. AP XR, USS
4. Stirrups with halter
5. 0-3 years old

Question 18

1. What is Perthes disease
2. What age group does Perthes typically affect
3. What social factor is associated with Perthes
4. Give 2 investigations
5. Give 2 treatment options

Answer 18

1. Osteonecrosis of femoral epiphysis
2. 4-8 years old
3. Low SES
4. Pelvic XR, MRI
5. Physio/rehab (prevent stiffness, contain femoral head in acetabulum), surgery

Question 19

1. What is SUFE
2. What age group does SUFE typically affect
3. Is SUFE more likely to be unilateral or bilateral
4. Give 2 RFs for SUFE
5. Give 3 features/exam findings in SUFE
6. Give 2 XR investigations
7. Give 2 management options

Answer 19

1. Slipped Upper Femoral Epiphysis - fracture in the growth plate of the thigh bone that causes the head of the bone to slip out of place
2. 13-16 years old
3. Unilateral (58%)
4. Obese, tall and slender, rapid growth
5. Pain in groin/thigh/knee, limp, antalgic gait, externally rotated and adducted limb, reduced RoM
6. AP and frog leg XR
7. Surgery (ORIF bilateral) or conservative Mx

Question 20

1. What is an antalgic gait
2. Give 3 red flags in a limping child that warrant further investigation/referral
3. What are 4 risk factors for NAI
4. What are 6 signs of NAI
5. Name 2 conditions that may often be mistaken for NAI

Answer 20

1. Abnormal walking pattern developed to avoid pain - shortened stance phase relative to swing phase (causes a limp)
2. Neonate with painful paralysed limb, asymmetry of spine/limb, school-aged child with limp, adolescent with knee pain, back pain, signs of NAI
3. First born, unplanned, premature, disabilities, single parent, unemployed, low SES, Hx of abuse, substance misuse, stepchildren
4. Human bite, burns (cigarette), fingertip bruising, multiple bruises at various stages of healing, peri-oral injuries, frenum injuries, multiple fractures at various stages of healing, child withdrawn, abnormal adult/child interaction, metaphyseal corner fracture, rib fracture, femoral fracture
5. Osteogenesis imperfecta, copper deficiency, prematurity

Question 21

1. Give 3 features of paediatric bones that are favourable in trauma
2. What is the Salter-Harris fracture classification
3. Give 2 common paeds fractures
4. What are the 3 types of supracondylar elbow fracture
5. What are the 2 main options in paeds fracture management

Answer 21

1. More elastic/plastic (less rigid), thicker periosteum, greater remodelling potential
2. SALTR
   I - straight (across physis). Favourable
   II - fracture line exits above physis (metaphyseal wedge attached to epiphysis)
   III - lower (fracture below physis). Intra-articular
   IV - through (physis). Intra-articular
   V - ruined (crush injury to physis)
3. Forearm, wrist, femur, elbow
4. I - undisplaced. II - angulated with intact posterior cortex (partially displaced). III - completely displaced.
5. Conservative (cast/traction) or surgery (reduction and fixation)

Question 22

1. Define gait
2. Describe the gait cycle during walking
3. What are 5 key differences in gait cycle during walking and running
4. What marks the transition between a fast walking gait and running gait

Answer 22

1. Locomotion of body via movements of limbs, resulting in forward propulsion
2. Time between first heel strike and next heel strike of same foot
   Stance phase - first heel strike until toe lifts off (limb in contact with ground)
   Swing phase - time when limb not in contact with ground (swinging from behind to in front). Ends with next heel strike.
   Two periods of dual support, one period of single support for each leg
3. Higher velocity, shorter cycle time, increased stride length, no dual support periods (float phase - neither foot in contact with ground), increased movement in leg joints, greater upper body movement, greater physiological requirements
4. Float phase (as well as lack of dual support)

Question 23

1. What is tendonoitis
2. What causes tendonitis
3. Give 3 features
4. Give 1 examination sign indicating tendonitis
5. Give 2 principles of treatment

Answer 23

1. Inflammation ± degeneration of tendon
2. Repeated supra physiological loading/repetitive strain injury
3. Pain, swelling, difficulty performing related action
4. Pain/weakened resisted movement
5. Rest, correct training errors

Question 24

1. What is a stress fracture
2. What causes a stress fracture
3. How do you manage a stress fracture
4. What is a potential consequence/sequelae of instability
5. How do you manage instability
6. What is the difference between a sprain and a strain injury

Answer 24

1. Microfractures in bone
2. Bone loaded with force above normal but below load which would cause outright fracture, also causing inflammation in surrounding periosteum and soft tissues
3. Rest and future prevention
4. Acute dislocation or subluxation
5. Physiotherapy
6. Sprain - injuries to ligaments (when stretching ligaments past elastic limit)
   Strain - injuries to muscle fibres or tendons (pulled muscles)

Question 25

1. What is the difference between the epiphysis and the apophysis
2. What is found in the apophysis
3. What causes acute avulsion of apophysis
4. How do you manage an acute apophyseal avulsion
5. What are 3 types of chronic apophysitis and what bones/areas are affected
6. How do you manage chronic apophysitis

Answer 25

1. Epiphysis - contributes to a joint
   Apophysis - site of tendon or ligament attachment
2. Secondary ossification centre
3. Sudden, forceful contraction
4. Rest, physio/stretching, rarely surgery
5. Osgood-Schaltter’s - tibial tuberosity
   Sinding-Larsen-Johansson - inferior pole of patella
   Sever’s disease - calcaneous
6. Rest, NSAIDs, stretching, activity modification

Question 26

1. What is the most common reason for a shoulder dislocation
2. What 3 types of shoulder dislocations occur
3. What is a key part of examination in shoulder dislocations
4. What are the 3 shoulder joints
5. Name 4 muscles involved in shoulder stability
6. Name 3 rotator cuff muscles and what do they do
7. What is a Hill-Sachs lesion
8. What is a Bankart lesion
9. How do you treat an acute shoulder dislocation

Answer 26

1. Contact sports
2. Anterior, posterior, luxatio erecta (inferior)
3. Axillary nerve sensation
4. Sternoclavicular, acromioclavicular, glenuhumeral joints
5. Deltoid, pec major, pec minor, biceps brachii
6. Subscapularis - internal rotation
   Supraspinatus - adduction
   Infraspinatus and teres minor - external rotation
7. Compressive fracture to posterolateral humeral head
8. Humeral head fractures edge of glenoid rim/rips through anterior labrum
9. Reduction, restriction, rehabilitation

Question 27

1. What are the colloquial names for the 2 types of elbow epicondylitis
2. What is the most accurate Ix for elbow epicondylitis
3. How do you manage elbow epicondylitis
4. Where is pain felt in medial epicondylitis
5. What causes medial epicondylitis
6. What nerve can be affected in medial epicondylitis
7. Where is pain felt in lateral epicondylitis
8. What causes lateral epicondylitis
9. What nerve can be affected in lateral epicondylitis

Answer 27

1. Lateral - tennis elbow
   Medial - Golfer’s elbow
2. Dynamic US
3. Rest, ice, passive stretching, bracing, NSAIDs. Surgery not common, but can be used (debridement, release)
4. On resisted wrist flexion/pronation (1cm distal/anterior to medial epicondyle)
5. Overuse of flexor-pronator mass, repetitive wrist flexion/forearm pronation
6. Ulnar nerve (neuritis)
7. Over ECRB, on resisted wrist/finger extension or passive wrist flexion in pronation
8. Overuse of common extensors (usually ECRB), repetitive wrist extension
9. Posterior interosseous nerve (compression)

Question 28

1. What type of cartilage is the knee meniscus made from
2. What is the function of the knee meniscus
3. What are the differences between the medial and lateral menisci
4. What meniscus is more prone to injury and why
5. When does swelling typically occur in knee meniscal tear injuries
6. What are 2 common examination findings in knee meniscal tear injuries
7. What are 2 specific tests used when examining meniscal tear injuries
8. What Ix are used in meniscal tears
9. What are the management options for meniscal tear injuries

Answer 28

1. Fibrocartilage
2. Transmit forces across knee, increase knee stability
3. Medial - semi-circular, less mobile
   Lateral - circular, more mobile
4. Medial - less mobile, attached to MCL
5. Delayed/intermittent - >30mins
6. Localised joint line tenderness, effusion (sweep/patellar tap)
7. McMurray’s, Apley’s compression test
8. Plain XRs, MRI
9. Conservative - NSAIDs, physio
   Surgery - typically arthroscopic (partial/total meniscectomy, transplant, repair)

Question 29

1. Where do the cruciate ligaments sit
2. Are they intra or extra capsular
3. Where does the ACL originate
4. Where does the ACL insert
5. What is the function of ACL
6. Where does the PCL originate
7. Where does the PCL insert
8. What is the function of PCL
9. Are collateral ligaments intra or extra capsular
10. Where does the MCL originate
11. Where does the MCL insert
12. What is the function of MCL
13. Where does LCL originate
14. Where does LCL insert
15. What is the function of LCL

Answer 29

1. Between medial and lateral femoral condyles
2. Intra-capsular
3. Lateral condyle
4. Anterior tibial plateau and tibial spines
5. Resists anterior translation of tibia on femur - prevents tibia from sliding forward of the femur and limiting rotational movements
6. Medial femoral condyle
7. Posterior aspect of proximal tibia
8. Resists posterior translation of tibia on femur - prevent the tibia from moving too far back on the femur when the knee flexed
9. Extra capsular
10. Medial femoral epicondyle
11. Proximal tibia
12. Resists valgus forces (force that moves knee away from midline)
13. Lateral femoral epicondyle
14. Fibular head
15. Resists varus forces (forces that move knee towards midline)

Question 30

1. What is the most likely cause of an ACL injury
2. What are 2 features of an ACL injury
3. What is the name of 2 tests/signs used to determine an ACL injury
4. What is the most likely cause of a PCL injury
5. What are 2 features of an PCL injury
6. What do PCL injuries often occur with

Answer 30

1. twisting injury
2. Immediate swelling, anterior knee pain, inability to play on, haemarthrosis
3. Lachman’s test, anterior drawer
4. Direct blow/hyperflexion or extension
5. Immediate swelling, posterior knee pain, posterior sag, posterior drawer, haemarthrosis
6. Posterolateral corner injury

Question 31

1. What is the most likely cause of a MCL injury
2. What are 2 features/signs of a MCL injury
3. What is the most likely cause of a LCL injury
4. What do LCL injuries often occur alongside
5. What are 2 features/signs of a LCL injury

Answer 31

1. Valgus stress/direct blow to lateral knee
2. Late swelling, valgus instability, medial knee pain, valgus ‘opening’
3. Varus stress or direct blow to medial knee
4. Posterolateral corner injury
5. Late swelling, varus instability, instability in full extension, varus ‘opening’ lateral knee pain

Question 32

1. What are 2 ligament injury investigations
2. What are 3 methods for preventing ligamentous injuries
3. How do you manage ruptured knee ligaments

Answer 32

1. Plan XRs, MRI
2. Plyometrics, neuromuscular training, hamstring strength, knee bracing
3. Conservative - cryotherapy, passive extension, surrounding muscle strength, exercises, NSAIDs
   Surgery - arthroscopic, grafting, when unstable/failed conservative management, full rupture

Question 33

1. What is tibial stress syndrome
2. What are 2 features of it
3. How is it managed
4. What is exertion compartment syndrome
5. What are 2 features of it
6. Who is it common in
7. How is it managed

Answer 33

1. Shin splints
2. Diffuse pain over mid-tibia that improves with running, tight achilles, pain on resisted plantar flexion (ankle)
3. NSAIDs, rest, physio, surgery (rare)
4. Reversible muscle ischaemia in lower leg compartments
5. Burning/aching pain over lower leg, related to exercise, relieved by rest, paraesthesia in first dorsal web space of foot (deep perineal nerve)
6. Runners and soldiers
7. Activity modification or surgery

Question 34

1. Define fracture
2. Define dislocation
3. Define subluxation
4. Define comminution
5. Define intra-articular
6. Define fracture dislocation
7. Define open fracture
8. What are the 3 general causes of fractures
9. What is the general epidemiological distribution of fractures
10. How can you describe a fracture

Answer 34

1. Disruption in bone continuity
2. Complete loss of continuity between two bones forming a joint
3. Partial loss of continuity of two bones forming a joint
4. Fracture into multiple fragments
5. Fracture extends into joint
6. Dislocated joint with associated fracture
7. Direct communication between fracture and external environment
8. Injury mechanism exceeds maximum force bone can withstand (normal bone, abnormal force)
   Co-morbidity that increases risk of fracture after injury (abnormal bone, normal force)
   Co-morbidity that increases risk of injury (normal bone, abnormal force)
9. Bimodal - first peak in younger males, second peak in older females
10. Complete/incomplete, simple (transverse, oblique, spiral)/complex/comminuted/compression, articular involvement, displaced/undisplaced, proximal/midshaft/distal

Question 35

1. Outline how primary healing occurs
2. What is required for primary healing to occur
3. What is primary healing also known as
4. What happens in the central resorption cavity
5. What is the reversal zone
6. What is the closing zone
7. Outline how secondary healing occurs
8. What is required for secondary healing to occur
9. What cells dominate in fracture healing in relation to movement/no movement
10. What happens when there is too much movement/strain in a fracture

Answer 35

1. OBs and OCs organised in units called cutting cones. Function is not to heal fractures, but ongoing bone turnover.
   BVs in centre of cutting cone bring progenitor cells in from circulation to replace OBs and OCs. Cutting cone moves through bone, with OCs resorbing bone in front and OBs forming new organised lamellar bone behind in osteons.
2. Absolute stability
3. Haversian remodelling
4. Where products of bone resorption are secreted by active OCs and progenitor cells can migrate and differentiate freely
5. OBs form behind osteoclastic activity and lay down lamellar bone
6. Where progressive layers of new bone have been laid down resulting in concentric circles
7. Inflammation - haematoma and inflammatory cells, OBs and fibroblasts proliferate, granulation tissue forms around bone edges.
   Repair - primary soft callus (cartilage) followed by endochondral ossification (forming disorganised woven bone)
   Remodelling - woven bone replaced by lamellar bone (cutting cones)
8. Relative stability
9. More movement/strain –> chondroblasts
   Less/no movement/strain –> osteoblasts
10. Non-union (no osteoblasts)

Question 36

1. What are 4 fracture healing complications
2. List 3 patient-related factors affecting healing
3. List 3 fracture-related factors affecting healing
4. List 3 treatment related factors affecting healing

Answer 36

1. Malunion (healing in suboptimal position)
   Delayed union (longer healing)
   Non-union (fragments remain separate)
   Infection
2. Smoking, alcohol, malnutrition, diabetes, vascular insufficiency, NSAIDs
3. Energy transfer of injury, associated soft tissue injury, fracture pattern/morphology, blood supply
4. Adequate stability, adequate fixation, soft tissue dissection, infection, patient compliance

Question 37

1. What are 3 aims of fracture care
2. What are the basic principles of fracture management
3. What are 3 features of a stable fracture
4. List 3 methods of conservative management of fractures
5. What are 2 advantages of surgery vs conservative management
6. What are 3 absolute indications for surgery
7. What are 2 relative indications for surgery

Answer 37

1. Prevent pain, preserve function, avoid complications
2. Resuscitate, reduce, restrict, rehabilitate
3. Remain in place under minimal physiological load, bone ends well aligned, minimal comminution, good soft tissue support
4. Closed reduction, plaster cast, KUO, functional brace
5. Less immobilisation, earlier rehab and pain control, possibility of anatomical reduction and fixation
6. Displaced intra-articular fracture, open fracture, pathological fracture, polytrauma to stabilise long bones
7. Failed conservative management, high risk of complications, morbidity of conservative management

Question 38

1. What are the principles of ATLS
2. What is a tension pneumothorax
3. Give 3 signs of a tension pneumothorax
4. How is a tension pneumothorax managed
5. How is an open pneumothorax managed
6. What is a flail chest
7. What is the definition of a massive haemothorax
8. What is the classification of haemorrhage shock
9. What are the life-threatening diagnoses featured in ATOM FC

Answer 38

1. A(c-spine)BCDE
2. Internal ‘one-way’ valve
3. Decreased air entry on affected side, hyper-resonant (increased percussion note), engorged neck veins, reduced lung expansion, trachea deviation to opposite side
4. High-flow oxygen, needle decompression (fifth intercostal space), definitive chest drain
5. Three-sided dressing, high flow O2, definitive chest drain
6. Separation of segment of thoracic cage, 2+ ribs fractured in 2 or more places, paradoxical movement of a segment
7. > 1500ml blood in pleural cavity
8. Class I - BP normal, <15% blood loss, HR <100
   Class II - BP normal, 15-30% blood loss, HR 100-120
   Class III - hypotensive, 30-40% blood loss, HR 120-140
   Class IV - hypotensive, >40% blood loss, HR >140
9. Airway obstruction, tension pneumothorax, open pneumothorax, massive harm-thorax, flail chest, cardiac tamponade

Question 39

1. What are the 4 most common limb-threatening injuries
2. Describe the Gustilo-Anderson classification of open fractures
3. Describe immediate ED management of an open fracture
4. How would you surgically manage an open fracture
5. What are 3 signs of an arterial/vascular injury in a lower limb fracture
6. How do you manage an arterial injury in a lower limb fracture
7. Define neuropraxia, axonotmesis and neurotmesis
8. How do you manage a nerve injury
9. What are 3 signs of compartment syndrome
10. How is compartment syndrome managed

Answer 39

1. Open fractures, arterial injuries, nerve injuries, compartment syndrome
2. Class I - <1cm, minimal soft tissue injury, no NV injury
   Class II - 1-10cm, moderate soft tissue injury, moderate comminution
   Class IIIA - >10cm, highly comminuted/segmental, extensive contamination. Requires local flap
   Class IIIB - as class IIIA but requires free flap (tissue loss)
   Class IIIC - as class III with arterial injury requiring repair. Often partial amputations/mangled extremities
3. Resuscitate, reduce, restrict, rehab
   IV ABx - 1.5g cefuroxime TDS (or gent if highly contaminated), anti-tetanus, splint/cast, sterile saline-soaked dressing to open wound
4. Debride, skeletal stabilisation.
   Secondary surgery - tissue inspection, wound closure
5. Cold foot, pale/dusky foot, pain, can’t find pulse
6. Resus, realign and splint leg, vascular/plastics referral
7. Neuropraxia - ischaemia from contusion/traction. Structure intact. Removal of cause leads to recover
   Axonotmesis - myelin sheath disruption, distal axon dies. Schwann cells and endoneurium intact. Nerve recovers down ‘pipe’ but myelin scarred and may not fully recover
   Neurotmesis - complete nerve division. No myelin sheath ‘guide’ for regeneration. Irreversible without surgical repair (rare with surgical repair)
8. Surgery or KUO, physio/rehab
9. Pain disproportionate to injury (excruciating pain), pain on passive stretching, paraesthesia, normal distal pulse, tight muscles in calf
10. Remove cast/anything constricting leg. Emergency fasciotomy

Question 40

1. What are 3 functions of calcium
2. What is the normal total plasma concentration (TPC) of calcium (serum calcium)
3. Where in the intestines is calcium absorbed
4. What regulates calcium absorption in the intestines
5. What regulates calcium excretion/reabsorption in the kidneys
6. Where do osteoclasts release calcium into when they resorb bone

Answer 40

1. Structural (inorganic bone), ion channels, protein binding, cell signalling
2. 2.2-2.6mmol/l
3. Brush border of interstitial epithelial cells
4. Calcitriol
5. Calcitonin and PTH (minor effect)
6. ECF

Question 41

1. Where is PTH secreted from within the parathyroid gland
2. When is PTH secreted
3. Where does PTH act
4. Where is calcitonin secreted from within the thyroid gland
5. When is calcitonin secreted
6. Where does calcitonin act

Answer 41

1. Chief cells
2. In response to low serum Ca (hypocalcaemia)
3. Kidneys, intestines and osteoblasts
4. Parafollicular cells
5. In response to high serum Ca (hypercalcaemia)
6. Bones (osteoclasts), kidneys, and central nervous system

Question 42

1. What is the key role of vitamin D
2. How is vitamin D obtained
3. What is the name of the inactive form of vitamin D3
4. Describe the process of vitamin D activation, including the alternative name of active vitamin D
5. What are the 3 main actions of vitamin D
6. How does oestrogen affect bone turnover/density

Answer 42

1. Regulate calcium metabolism/homeostasis
2. Via absorption of lipid soluble vitamin D (intestines) and by UVB generation (skin)
3. Cholecalciferol
4. 2 hydroxylation reactions
   First: vit D3 + 25 hydroxylase –> 25 hydroxyvitamin D (occurs in liver)
   Second: 25 hydroxyvitamin D + 1a hydroxylase –> 1,25-dihydroxyvitamin D/calcitriol (occurs in kidneys)
5. Increase GI absorption of calcium
   Increase renal reabsorption of calcium
   Stimulate OBs to release RANKL, stimulating OC activity, increasing serum calcium
6. Inhibits RANKL release from OBs, reducing OC activity and bone resorption (increasing/maintaining bone density)

Question 43

1. Describe the homeostatic response to hypercalcaemia
2. Describe the homeostatic response to hypocalcaemia

Answer 43

1. High serum Ca detected by thyroid
   Calcitonin released
   Renal reabsorption reduced (increased Ca excretion)
   Osteoclast activity inhibited (direct binding to surface receptors)
   Serum Ca levels reduce, returning to homeostasis
2. Low serum Ca detected by parathyroid
   PTH released
   Osteoblasts stimulated, which causes increase in IL and MCSF release, RANKL release and OPG inhibition, stimulating osteoclast activation
   Increase in bone resorption, releasing Ca into serum from bone
   Vitamin D activation stimulated, to further stimulate RANKL release and increase Ca uptake
   Serum Ca level rises, returning to homeostasis

Question 44

1. Name and briefly describe the stages of bone remodelling
2. What factors regulate bone remodelling
3. What is the role of osteocalcin
4. What is the role of osteopontin

Answer 44

1. Quiescence - resting state/period of inactivity. OBs inactive, OCs maintain matrix
   Activation - either local or systemic stimulus, causing RANKL and MCSF release, recruiting, differentiating and activating OCs
   Resorption - activated OCs migrate to target site, attach to bone and polarise (ruffled border and secretory domain). Dissolve inorganic material (release HCl from ruffled border and form resorption pits/Howship’s lacunae) and organic matrix (protease). Degredation products are removed
   Reversal - OCs apoptose/deactivate, signalling OBs. Osteoprogenitor cells migrate to resorption put and differentiate and activate. OBs activated and begin laying down new bone
   Formation - OBs lay down organic osteoid, fill in resorption pit, control mineralisation and become osteocytes
   Mineralisation - deposition of hydroxyapatite crystals
2. Local - mechanical stress, microdamage
   Systemic - PTH, vit D, endocrine hormones
3. Promote remineralisation
4. Inhibit mineral binding/crystal growth

Question 45

1. What is Paget’s disease
2. What are 2 types of Paget’s disease
3. Give 3 features of Paget’s disease
4. Briefly outline the pathophysiology of Paget’s disease
5. Name 2 Ix for Paget’s and the typical findings/results
6. How is Paget’s managed
7. What is one complication of Paget’s disease

Answer 45

1. Abnormal localised bone remodelling
2. Monostotic, polyostotic
3. Enlarged skull, nerve compression, bowing of long bones, bone pain, fractures, hypercementosis of teeth
4. OCs are increased in number, size and sensitivity. 3 phases - lytic (intense resorption), mixed (resorption and compensation), sclerotic (OB formation)
5. XRs - cotton wool appearance
   Bone scan - identify high metabolic activity
   Bloods - raised ALP
   Bone biopsy - OCs greater in size, number. Disorganised woven bone and fibrous vascular tissue
6. Bisphosphonates, calcitonin
7. Paget’s sarcoma - typically osteosarcoma (malignancy arising from mesenchymal cells)

Question 46

1. What is osteopetrosis
2. What is the pathophysiology of osteopetrosis
3. What are 2 features of osteopetrosis

Answer 46

1. Defective osteoclastic resorption (brittle bones)
2. Cannot resorb bone (cannot acidify Howship’s lacunae). Bone formed normally but not remodelled
3. Obliterated medullary canal, fracture risk, repeated fractures, brittle bones

Question 47

1. What causes HPT
2. What are the different types of HPT and what causes them
3. What are 2 effects of HPT
4. What are the Sx of HPT
5. What are common HPT Ix
6. How is HPT managed

Answer 47

1. Increase in circulating levels of PTH, due to excess producing by PT glands
2. Primary - intrinsic abnormality of PT glands, pathological increase in PTH production
   Secondary - hypertrophic PT gland(s) secondary to chronic low Ca or high phosphate
   Tertiary - prolonged PTH exposure causing PT gland dysregulation
3. Increase in bone resorption, increase in renal hydroxylation of vitamin D (activation)
4. Bones - bone pain, osteoporosis, arthritis
   Stones - kidney stones
   Abdominal groans - loss of appetite, GI ulcers, acute pancreatitis
   Thrones - diarrhoea, increased thirst, urination
   Psychic moans - fatigue, depression, forgetfulness, anxiety, confusion
5. Ca, PO4, PTH bloods
6. Parathyroidectomy, treat underlying cause (vitamin D therapy)

Question 48

1. Is rickets/osteomalacia a quantitative or qualitative bone disorder
2. What is the difference between rickets and osteomalacia
3. What causes them
4. Give 3 features/signs
5. How are they managed

Answer 48

1. Mineralisation defect - qualitative, due to inadequate Ca and PO4
2. Rickets - pre-physeal closure
   Osteomalacia - after physical closure
3. Lack of vitamin D in diet, lack of sunlight exposure, malabsorption, alcoholism, tumour
4. Bone and muscle pain, brittle bones, muscle hypotonia and weakness, flattening of skull, enlarged costal cartilage, kyphosis, enamel defects, delayed eruption, irritability
5. Vitamin D/calcium therapy, surgery

Question 49

1. What is osteoporosis
2. Is osteoporosis a qualitative or quantitative disorder
3. Give 3 common osteoporotic fractures
4. Give 3 signs/features
5. Give 4 osteoporosis risk factors
6. Give 2 Ix
7. Give 3 management options

Answer 49

1. Systemic skeletal disease, with low bone mass and deterioration of bony tissue, causing increase in fragility and fracture susceptibility
2. Quantitative
3. Wrist, spine, hip
4. Back pain, thoracic kyphosis, loss of height, fractures
5. Oestrogen deficiency, steroid use, prolonged inactivity, HPT, Cushing’s, age, FH, menopause, age
6. FRAX (fracture risk assessment tool), bone scan, bloods
7. Bisphosphonates, HRT, denosumab, vitamin D, calcium, calcitonin

Question 50

1. What are insufficiency fractures and what causes them
2. What are fatigue fractures and what causes them
3. What causes a fragility fracture
4. What is a common insufficiency spinal fracture
5. Give 2 consequences of this spinal fracture
6. What is a common insufficiency arm fracture
7. How is this fracture treated
8. Describe 2 different types of wrist fracture
9. What determines how a wrist fracture is managed and give the management options for each

Answer 50

1. Type of stress fracture, caused by cumulative result of repeated normal loading of abnormal bone
2. Cumulative result of repeated abnormal loading of normal bone
3. Application of force which would not normally fracture normal bone
4. Vertebral wedge compression fracture, affecting vertebral bodies throughout thoracolumbar spine
5. Height loss, reduced pulmonary volume, protruding abdomen, distension, constipation
6. Proximal humerus
7. Sling (collar and cuff)
8. Volar - wrist displaces and angulates volarly (surface where palm is)
   Dorsal - wrist displaces and angulates distally (surface where back of hand is)
9. Displacement
   Minimally displaced, extra-articular - accept, cast
   Displaced but can be reduced - dorsal (posterior) or simple intra-articular - unacceptable, but likely stable when reduced - MUA/cast, ORIF if slips
   Unacceptable/unstable if reduced - ORIF (comminuted, solar displacement, intra-articular step)

Question 51

1. What is the likelihood of hip fracture recovery
2. How are intra-capsular undisplaced hip fractures managed
3. How are intra-capsular displaced hip fractures managed
4. How are extra-capsular inter-trochanteric hip fractures managed
5. How are sub-trochanteric fractures managed

Answer 51

1. 1/3 return to function
   1/3 lose independence
   1/3 die within a year
2. In situ fixation (cannulated hip screw)
3. Arthroplasty (joint replacement)
4. Sliding hip screw
5. Intramedullary nail

Question 52

1. What type of cells form cartilage
2. What type of fibres are found in cartilage
3. What makes up cartilage ground substance
4. Name 3 types of cartilage, the microscopic cellular arrangement and an example of where each is found

Answer 52

1. Chondrocytes
2. Type II collagen, elastin
3. Hyaluronic acid, chondroitin sulphate, keratan sulphate, water
4. Hyaline - spherical condrocytes, collage only fibre. Costal, ends of long bones (joints)
   Elastic - elastic and collagen fibres. Epiglottis, larynx, outer ear
   Fibro - rows of thick collagen fibres alternating with rows of chondrocytes in matrix. Knee menisci, intervertebral discs

Question 53

1. What is the cellular arrangement and function of the following cartilage zones:
   a) superficial zone
   b) middle zone
   c) deep zone
2. What is the tidemark
3. What is a key feature of the tidemark, in relation to lacerations
4. What type of cartilage is formed as a healing response in a laceration involving cartilage damage
5. Describe the different changes in cartilage between ageing and OA for:
   a) water content
   b) modulus/stiffness
   c) chondrocytes
   c) proteoglycans
   e) collagen

Answer 53

1. a) Collagen fibres parallel to joint surface. Tensile strength
   b) Collagen fibres oblique to joint surface. Bridge zones
   c) Collagen fibres perpendicular to joint surface. Compressive strength
2. Junction between soft calcified articular cartilage and subchondral bone (hard calcified cartilage)
3. Crossing tidemark - involves subchondral bone and blood supply, allows vascular ingrowth (better healing)
4. Fibrocartilage
5. a) Ageing - decreases, OA - increases
   b) Ageing - more stiff, OA - less stiff
   c) Ageing - fewer, larger, OA - cells cluster
   d) Ageing - smaller, OA - unbound from hyaluronate
   e) Ageing - increased crosslinking/brittleness, OA - disorganised

Question 54

1. Give 4 features of an acute hot swollen joint
2. Define cellulitis
3. What groups of bacteria are most commonly associated with cellulitis
4. Define abscess
5. Define septic arthritis
6. Define prosthetic joint infection

Answer 54

1. Pain, erythema, swelling, discharge, heat, loss of function, blistering
2. Infection of skin and subcutaneous fat
3. Staph or strep
4. Closed collection of pus, containing bacteria and dead/dying WBCs
5. Infection within a joint
6. Infection (septic arthritis) relating to joint replacement

Question 55

1. Define acute monoarthritis
2. What are the differentials to consider when faced with an acute monoarthritis
3. What should an acute monoarthritis be treated as until proven otherwise
4. What do the bacterial toxins do to cartilage
5. What are the common pathogens involved in septic arthritis
6. How is septic arthritis managed

Answer 55

1. Inflammation of single joint. Acute (<2/52)
2. GRASP - gout, reactive arthritis, autoimmune/arthritis, septic arthritis, pseudogout
3. Septic arthritis
4. Cause rapid death and destruction of chondrocytes and joint
5. S. aureus, strep, H. influenzae (infants)
6. Aspirate joint, empirical ABx, washout, specific ABx, monitor

Question 56

1. What are 2 features of gout
2. What is the difference between gout and pseudogout
3. Give 3 gout RFs
4. How is gout managed

Answer 56

1. Acute monoarthritis of great toe (podagra), gouty top (firm nodules under skin)
2. Gout - monosodium urate crystals
   Psuedogout - calcium pyrophosphates dihydrate
3. Age, male, CKD, OA, alcohol, sugary drinks, obesity
4. Acute - rest, NSAIDs (± PPI)
   Chronic - lifestyle modification, urate lowering drugs (allopurinol)

Question 57

1. What is reactive arthritis
2. What are the features of Reiter’s syndrome
3. How is reactive arthritis managed
4. What is the definition of autoimmune/arthritis
5. What is polymyalgia rheumatica
6. Give 2 Sx of polymyalgia rheumatica
7. What is a serious complication that can occur
8. How is PR it managed

Answer 57

1. Aseptic arthritis, occurs 2-6/52 following bacterial infection elsewhere
2. Polyarthropathy (arthritis), conjunctivitis, urethritis
3. NSAIDs, physio, steroid injection
4. Acute flare of chronic condition (arthropathy)
5. Autoimmune attack of joint synovium
6. Pain, inflammation, widespread ache, flu-like Sx
7. GCA/temporal arteritis
8. NSAIDs, physio, steroids

Question 58

1. Define seronegative spondyloarthropathies
2. What are 2 immunopathologic Ix findings common in seronegative spondyloarthropathies
3. Name 3 seronegative spondyloarthropathies and briefly define them
4. What are 3 features of AS
5. How is AS managed

Answer 58

1. Group of MSK conditions with common clinical features and immunopathologic mechanisms
2. -ve/low RF, +ve HLAB27
3. Reactive arthritis - aseptic arthritis, occurs 2-6/52 following bacterial infection elsewhere
   Psoriatic arthritis - arthritis of hands, usually affecting finger DIPJs
   Enteropathic arthritis - associated with IBD
   Undifferentiated spondyloarthritis
4. Spinal ankylosis, uveitis, sacroilitis (lumbosacral pain), enthesitis (pain/inflammation at tendon/ligament insertion)
5. NSAIDs, biologics, DMARDs, physio, exercise

Question 59

1. Define RA
2. Give 6 typical RA presenting features
3. Give 2 usual RA blood Ix results and 2 XR features
4. List 3 risk factors/aetiological agents for RA
5. Briefly describe the pathophysiological process of RA
6. What is pannus

Answer 59

1. Chronic systemic autoimmune disease, with cell-mediated immune response against soft tissues and bone
2. Symmetrical, peripheral, morning joint stiffness, erosive and deforming, swan-neck deformity, z-deformity, ulnar finger deviation, bursitis, subcutaneous nodules
3. +ve RF, +ve anti-CCP. XR - joint space narrowing, gull-wing joint appearance, joint anklyosis, subchondral erosions
4. Genetics (HLA subtype), smoking, oestrogen, periodontitis (P. gingivalis), infections
5. Citrullination - arginine converted into citrulline, becomes immunogenic (antigen - not recognised by body - immune response)
   immune response - T-cell mediated. Antigen processed by B-cells, presented to T-cells. T-cells activate B-cells, releasing cytokines and autoantibody production
   T-cells release TNFs and interferons, causing increase in inflammation and synovial hypertrophy and transition into pannus, as well as OC activation (causing erosions)
6. Grossly thickened (inflamed) synovium that erodes and infiltrates bone and causes joint swelling

Question 60

1. What are the 4 stages of RA
2. What causes a swan-neck deformity
3. What causes a z-deformity of thumb
4. Give 2 red flags for RA
5. How is RA managed

Answer 60

1. Susceptibility, pre-clinical, early, established
2. PIPJ hyperextension, DIPJ flexion
3. IPJ hyperextension, MCPJ flexion
4. Atlanto-axial instability, pericarditis, monoarticular flare, scleritis
5. Methotrexate - Sx control, delay progression
   Other cDMARDs or bDMARDs (rituximab), monitor drug safety/side effects
   Sx control - exercise, physio, NSAIDs

Question 61

1. What is OA
2. How can OA be classified
3. Give 4 OA Sx
4. Give 4 typical XR features of OA
5. List 5 OA RFs
6. Briefly outline OA pathophysiology
7. How is OA managed

Answer 61

1. Heterogenous group of disorders with similar pathological and radiological features demonstrating ‘joint failure’. Articular cartilage degeneration, remodelling of subchondral bone, osteophyte formation
2. Primary (localised, generalised) or secondary (due to trauma, inflammation, metabolic, developmental, etc.)
3. Pain (worse when using joint), stiffness (worse after immobility), restricted movement, tenderness, bony swelling, crepitus, soft tissue swelling, loss of movement
4. Loss of joint space, osteophytes, subarticular sclerosis, subchondral cysts
5. Muscle strength, inactivity, age, sex, genetics, ethnicity, joint injury, leg length discrepancy, joint alignment, occupation, obesity, diet, bone metabolism
6. Cartilage damaged/bone changes/microfracture due to insufficiently protected impulsive loading, increases cartilage stress, enzymatic destruction of cartilage, bone remodelling, joint degeneration
7. Education, self-management, weight loss, muscle strengthening, physio, analgesics, IA steroids, surgery (TJR, osteotomy)

Question 62

Describe the differences between RA and OA in terms of:
1. Distribution
2. Swelling
3. Stiffness
4. Systemic involvement

5. Describe the analgesic pain ladder

Answer 62

1. RA - MCPJs, PIPJs, carpal bones, wrists. Spares DIPJs. Polyarticular, symmetrical
   OA - spine, DIPJs, knees, hips. Monoarticular, asymmetrical
2. RA - soft tissue, boggy
   OA - bony, osteophytes
3. RA - prominent, longer lasting (>30mins), worse in mornings
   OA - mild in morning, worse after immobility, short lasting (<30mins)
4. RA - systemic inflammation, erosions
   OA - nil
5. Pain ladder developed by WHO. Non-opioids –> weak opioids –> strong opioids. Oral admin, regular intervals, according to patient-described pain intensity, start at lowest dose and duration, administer consistently