MSK proper Flashcards
Q: What common cause of admission to casualty is facilitated by the Ottawa ankle rules?
A: Ankle fractures.
Q: According to the Ottawa ankle rules, when are x-rays necessary for ankle injuries?
A: If there is pain in the malleolar zone and any one of the following: inability to weight bear for 4 steps, tenderness over the distal tibia, or bone tenderness over the distal fibula.
unless neurovascular compromise - then do closed reduction then do xrays then manage
Q: What classification systems exist for describing ankle fractures?
A: Potts, Weber, and AO systems.
Q: What is the Weber classification related to?
A: The level of the fibular fracture.
Q: Describe a Type A fracture in the Weber classification.
A: Below the syndesmosis.
Q: Describe a Type B fracture in the Weber classification.
A: Starts at the level of the tibial plafond and may extend proximally to involve the syndesmosis.
Q: Describe a Type C fracture in the Weber classification.
A: Above the syndesmosis which may itself be damaged.
Q: What is a Maisonneuve fracture?
A: A spiral fibular fracture that leads to disruption of the syndesmosis with widening of the ankle joint, requiring surgery.
Q: What factors does the management of ankle fractures depend on?
A: Stability of the ankle joint and patient co-morbidities.
Q: Why should all ankle fractures be promptly reduced?
A: To remove pressure on the overlying skin and prevent subsequent necrosis.
Q: What is the typical management for young patients with unstable, high-velocity, or proximal ankle injuries?
A: Surgical repair, often using a compression plate.
Q: Why might elderly patients with potentially unstable ankle injuries fare better with conservative management?
A: Their thin bone does not hold metalwork well.
Q: When is an ankle x-ray required according to the Ottawa Rules?
A: If there is any pain in the malleolar zone and any one of the following findings: bony tenderness at the lateral malleolar zone, bony tenderness at the medial malleolar zone, or inability to walk four weight-bearing steps immediately after the injury and in the emergency department.
Q: What is an ankle sprain?
A: A stretching, partial, or complete tear of a ligament in the ankle.
Q: What is the difference between high and low ankle sprains?
A: High ankle sprains involve the syndesmosis, while low ankle sprains involve the lateral collateral ligaments.
Q: What is the most common mechanism of injury for low ankle sprains?
A: Inversion injury.
Q: Which ligament is most commonly affected in low ankle sprains?
A: The anterior talofibular ligament (ATFL).
Q: How are low ankle sprains classified?
A: Grade I (mild), Grade II (moderate), Grade III (severe).
Q: What are the characteristics of Grade I low ankle sprains?
A: Stretch or micro tear, minimal bruising and swelling, normal pain on weight-bearing.
Q: What are the characteristics of Grade II low ankle sprains?
A: Partial tear, moderate bruising and swelling, minimal pain on weight-bearing.
Q: What are the characteristics of Grade III low ankle sprains?
A: Complete tear, severe bruising and swelling, severe pain on weight-bearing.
Q: What is the investigation method for low ankle sprains?
A: Radiographs according to the Ottawa ankle rules, and MRI if there is persistent pain or to evaluate perineal tendons.
Q: What is the typical treatment for low ankle sprains?
A: Non-operative treatment with RICE (Rest, Ice, Compression, Elevation), possibly a removable orthosis, cast, and/or crutches. MRI and surgical intervention are rare but may be considered if symptoms fail to settle.
Q: What is the mechanism of injury for high ankle sprains?
A: External rotation of the foot causing the talus to push the fibula laterally.
Q: How are high ankle sprains typically diagnosed?
A: Radiographs showing widening of the tibiofibular joint (diastasis) or ankle mortise, and MRI if there is high suspicion of syndesmotic injury.
Q: What is the treatment for high ankle sprains if there is no diastasis?
A: Non-weight-bearing orthosis or cast until pain subsides.
Q: What treatment is needed if there is diastasis or failed non-operative management for high ankle sprains?
A: Operative fixation.
Q: What is avascular necrosis (AVN)?
A: The death of bone tissue secondary to loss of the blood supply, leading to bone destruction and loss of joint function.
Q: Which part of long bones is most commonly affected by avascular necrosis?
A: The epiphysis.
Q: What are common causes of avascular necrosis?
A: Long-term steroid use, chemotherapy, alcohol excess, and trauma.
Q: What are the early findings on a plain x-ray for avascular necrosis?
A: Osteopenia and microfractures may be seen, but x-rays may be normal initially.
Q: What sign on x-ray indicates collapse of the articular surface in avascular necrosis?
A: The crescent sign.
Q: What is the investigation of choice for avascular necrosis?
A: MRI, as it is more sensitive than radionuclide bone scanning.
Q: What may be necessary in the management of avascular necrosis?
A: Joint replacement.
Q: What is a Baker’s cyst?
A: A distension of the gastrocnemius-semimembranosus bursa, not a true cyst.
Q: What are the two types of Baker’s cysts?
A: Primary (no underlying pathology, typically in children) and secondary (associated with underlying conditions like osteoarthritis, typically in adults).
Q: Where do Baker’s cysts present?
A: As swellings in the popliteal fossa behind the knee.
Q: What are the symptoms if a Baker’s cyst ruptures?
A: Pain, redness, and swelling in the calf, similar to deep vein thrombosis. However, most ruptures are asymptomatic.
Q: Which tendon is most commonly ruptured in a biceps tendon injury?
A: The long tendon (90% of cases).
Q: What are common risk factors for biceps tendon rupture?
A: Heavy overhead activities, shoulder overuse or underlying shoulder injuries, smoking, and corticosteroid use (which weakens tendons).
Q: What symptoms are typically reported by patients with a biceps tendon rupture?
A: A sudden ‘pop’ or tear, followed by pain, bruising, and swelling.
Q: What weakness typically follows a biceps tendon rupture?
A: Weakness in the shoulder and elbow, often with difficulty in supination.
Q: What is the initial examination for suspected biceps tendon rupture?
A: Palpate the long head and distal biceps tendon and assess neurovascular function in the upper extremities.
Q: What does the biceps squeeze test assess?
A: If the biceps tendon is intact, squeezing the muscle will cause forearm supination.
Q: What is the first-line investigation for suspected biceps tendon rupture?
A: Musculoskeletal ultrasound performed by a skilled clinician.
Q: What is the investigation of choice for suspected distal biceps tendon rupture?
A: An urgent MRI, as diagnosis based on clinical signs alone is challenging and surgical intervention is usually required.
Q: What is the characteristic feature of Paget’s disease?
A: Focal bone resorption followed by excessive and chaotic bone deposition.
Q: Which bones are most commonly affected by Paget’s disease, in order?
A: Spine, skull, pelvis, and femur.
Q: What is the serum marker typically raised in Paget’s disease?
A: Serum alkaline phosphatase.
Q: What is seen on x-ray in Paget’s disease?
A: Abnormal thickened, sclerotic bone.
Q: What are the risks associated with Paget’s disease?
A: Risk of cardiac failure with >15% bony involvement and a small risk of sarcomatous change.
Q: What is the main treatment for Paget’s disease?
A: Bisphosphonates.
Q: What is the cause of osteoporosis?
A: Excessive bone resorption resulting in demineralised bone.
Q: What are the typical symptoms of osteoporosis?
A: It is usually asymptomatic, but there is an increased risk of pathological fractures.
Q: What serum markers are typically normal in osteoporosis?
A: Alkaline phosphatase and calcium.
Q: What are the main treatments for osteoporosis?
A: Bisphosphonates, calcium, and vitamin D.
Q: What characterizes secondary bone tumors?
A: Bone destruction and tumor infiltration.
Q: What scoring system is used to predict the risk of fracture in secondary bone tumors?
A: Mirel scoring.
Q: What serum markers may be elevated in secondary bone tumors?
A: Serum calcium and alkaline phosphatase.
Q: What are the main treatments for secondary bone tumors?
A: Radiotherapy, prophylactic fixation, and analgesia.
Q: What is a buckle (torus) fracture?
A: An incomplete fracture of the shaft of a long bone characterized by bulging of the cortex.
Q: In which age group are buckle fractures most commonly seen?
A: In children aged 5-10 years.
Q: How are buckle fractures typically managed?
A: They are usually self-limiting and do not require operative intervention, often managed with splinting and immobilization instead of a cast.
Q: Which bone is commonly affected by a buckle fracture in children?
A: The distal radius.
Q: What causes carpal tunnel syndrome?
A: Compression of the median nerve in the carpal tunnel.
Q: What are the common symptoms of carpal tunnel syndrome?
A: Pain/pins and needles in the thumb, index, and middle fingers, with symptoms sometimes ascending proximally. The patient may shake their hand to relieve symptoms, classically at night.
Q: What is a common sign of carpal tunnel syndrome on examination?
A: Weakness of thumb abduction (abductor pollicis brevis) and wasting of the thenar eminence (not hypothenar).
Q: What are the positive signs used in the examination of carpal tunnel syndrome?
A: Tinel’s sign (tapping causes paraesthesia) and Phalen’s sign (flexion of the wrist causes symptoms).
Q: What are some common causes of carpal tunnel syndrome?
A: Idiopathic, pregnancy, oedema (e.g., heart failure), lunate fracture, and rheumatoid arthritis.
Q: What is the recommended first-line treatment for mild to moderate carpal tunnel syndrome?
A: A 6-week trial of conservative treatments, including corticosteroid injections and wrist splints at night (especially useful for transient factors like pregnancy).
Q: What is the treatment for severe carpal tunnel syndrome or if symptoms persist despite conservative management?
A: Surgical decompression (flexor retinaculum division).
Q: What is cauda equina syndrome (CES)?
A: A rare but serious condition in which the lumbosacral nerve roots below the spinal cord are compressed, potentially leading to permanent nerve damage if untreated.
Q: What is the most common cause of cauda equina syndrome?
A: A central disc prolapse, typically occurring at L4/5 or L5/S1.
Q: What are some other causes of cauda equina syndrome?
A: Tumours (primary or metastatic), infection (e.g., abscess, discitis), trauma, and haematoma.
Q: What are some possible symptoms of cauda equina syndrome?
A: Low back pain, bilateral sciatica, reduced sensation/pins-and-needles in the perianal area, decreased anal tone, and urinary dysfunction (e.g., incontinence, reduced bladder awareness).
Q: What is a late sign of cauda equina syndrome that may indicate irreversible damage?
A: Urinary incontinence.
Q: What is a recommended practice in patients with new-onset back pain to help detect cauda equina syndrome?
A: Checking anal tone, although this has poor sensitivity and specificity for CES.
Q: What is the primary investigation for suspected cauda equina syndrome?
A: Urgent MRI.
Q: What is the management for cauda equina syndrome?
A: Surgical decompression.
Q: What is cervical spondylosis?
A: A degenerative condition affecting the cervical spine, particularly the intervertebral discs, vertebral bodies, and facet joints, often referred to as cervical osteoarthritis.
Q: What are common symptoms of cervical spondylosis?
A: Chronic neck pain, radiculopathy (radiating pain, paraesthesia, weakness), myelopathy (spinal cord compression), and occipital headaches.
Q: What is cervical spondylotic myelopathy?
A: A severe manifestation of cervical spondylosis caused by spinal cord compression, leading to symptoms like clumsiness, gait disturbance, limb weakness, and possibly bowel or bladder dysfunction.
Q: What examination findings are commonly associated with cervical spondylosis?
A: Reduced neck range of motion, tenderness over the cervical spine, and signs of radiculopathy or myelopathy (e.g., positive Spurling’s test, hyperreflexia, or gait instability).
Q: What imaging is used to diagnose cervical spondylosis?
A: X-rays (for disc space narrowing, osteophytes, facet joint arthropathy), MRI (gold standard for evaluating soft tissue structures), and electrophysiological studies (for differentiating radiculopathy).
Q: What is the first-line treatment for cervical spondylosis?
A: Nonsteroidal anti-inflammatory drugs (NSAIDs) for pain management.
Q: What is a Charcot joint?
A: A neuropathic joint that becomes disrupted and damaged due to a loss of sensation, most commonly seen in diabetics today.
Q: What are the common features of a Charcot joint?
A: Swelling, redness, warmth in the affected joint, and a less painful presentation than expected.
Q: What complications may arise as a Charcot joint progresses?
A: Joint instability, abnormal movements, increased risk of fractures and dislocations, significant deformities, and secondary complications like skin ulceration and infection.
Q: What is the typical mechanism of injury for a Colles’ fracture?
A: It classically follows a fall onto an outstretched hand (FOOSH).
Q: What is a Colles’ fracture?
A: A distal radius fracture with dorsal displacement of the fragments, often described as a dinner fork-type deformity.
Q: What are the three classical features of a Colles’ fracture?
A: 1) Transverse fracture of the radius, 2) 1 inch proximal to the radio-carpal joint, 3) Dorsal displacement and angulation.
Q: What deformity is associated with a Colles’ fracture?
A: The dinner fork deformity.
Q: What are the early complications of a Colles’ fracture?
A: Median nerve injury (acute carpal tunnel syndrome), compartment syndrome, vascular compromise, malunion, and rupture of the extensor pollicis longus tendon.
Q: What are the late complications of a Colles’ fracture?
A: Osteoarthritis and complex regional pain syndrome.
Q: What is compartment syndrome?
A: Compartment syndrome is a complication where raised pressure within a closed anatomical space compromises tissue perfusion, leading to necrosis.
Q: What are the typical features of compartment syndrome?
A: Pain (especially on movement), excessive use of breakthrough analgesia, parasthesiae, pallor, possible arterial pulsation, and paralysis of the muscle group.
Q: How is compartment syndrome diagnosed?
A: By measuring intracompartmental pressure; pressures over 20mmHg are abnormal, and pressures over 40mmHg are diagnostic.
Q: What is the treatment for compartment syndrome?
A: Prompt and extensive fasciotomy; if muscle groups are necrotic, they may require debridement or amputation.
Q: What potential complication can occur after fasciotomy for compartment syndrome?
A: Myoglobinuria, which may lead to renal failure, necessitating aggressive IV fluid therapy.
Q: How quickly can muscle groups die in compartment syndrome?
A: Muscle groups may die within 4-6 hours if untreated.
Q: What causes cubital tunnel syndrome?
A: Cubital tunnel syndrome is caused by compression of the ulnar nerve as it passes through the cubital tunnel.
Q: What are the clinical features of cubital tunnel syndrome?
A: Tingling and numbness in the 4th and 5th fingers, starting intermittently and becoming constant, weakness, muscle wasting, and pain that worsens with leaning on the affected elbow.
Q: What is a common history seen in cubital tunnel syndrome patients?
A: A history of osteoarthritis or prior trauma to the elbow area.
Q: What is the management for cubital tunnel syndrome?
A: Avoid aggravating activities, physiotherapy, steroid injections, and surgery in resistant cases.
Q: What is De Quervain’s tenosynovitis?
A: De Quervain’s tenosynovitis is an inflammation of the sheath containing the extensor pollicis brevis and abductor pollicis longus tendons.
Q: What are the clinical features of De Quervain’s tenosynovitis?
A: Pain on the radial side of the wrist, tenderness over the radial styloid process, and pain with abduction of the thumb against resistance.
Q: What is Finkelstein’s test, and how is it used to diagnose De Quervain’s tenosynovitis?
A: Finkelstein’s test involves pulling the patient’s thumb in ulnar deviation and longitudinal traction, causing pain over the radial styloid process and along the tendons of extensor pollicis brevis and abductor pollicis longus in De Quervain’s tenosynovitis.
Q: What is the management for De Quervain’s tenosynovitis?
A: Management includes analgesia, steroid injections, immobilisation with a thumb spica splint, and occasionally surgical treatment.
Q: What is discitis?
A: Discitis is an infection in the intervertebral disc space that can lead to complications like sepsis or an epidural abscess.
Q: What are the general clinical features of discitis?
A: Back pain, pyrexia, rigors, and sepsis.
Q: What neurological features may occur in discitis?
A: Changing lower limb neurology may occur if an epidural abscess develops.
Q: How is discitis diagnosed?
A: MRI is the most sensitive imaging modality, and a CT-guided biopsy may be required to identify the organism and guide treatment.
Q: What is Dupuytren’s contracture?
A: Dupuytren’s contracture is a condition where the fingers, especially the ring and little fingers, are affected by progressive contracture of the connective tissue in the palm.
Q: What are the risk factors for Dupuytren’s contracture?
A: It is more common in older males, and about 60-70% of cases have a positive family history. Specific causes include manual labor, phenytoin treatment, alcoholic liver disease, diabetes mellitus, and trauma to the hand.
Q: Which fingers are most commonly affected by Dupuytren’s contracture?
A: The ring finger and little finger are most commonly affected.
Q: When should surgical treatment be considered for Dupuytren’s contracture?
A: Surgical treatment should be considered when the metacarpophalangeal joints cannot be straightened, and the hand cannot be placed flat on a table.
Q: What are the features of lateral epicondylitis (tennis elbow)?
A: Lateral epicondylitis presents with pain and tenderness localized to the lateral epicondyle, worsened by resisted wrist extension with the elbow extended or forearm supination with the elbow extended. Episodes typically last 6 months to 2 years, with acute pain for 6-12 weeks.
Q: What are the features of medial epicondylitis (golfer’s elbow)?
A: Medial epicondylitis presents with pain and tenderness localized to the medial epicondyle, aggravated by wrist flexion and pronation. Symptoms may be accompanied by numbness or tingling in the 4th and 5th fingers due to ulnar nerve involvement.
Q: What is radial tunnel syndrome and its features?
A: Radial tunnel syndrome is caused by compression of the posterior interosseous branch of the radial nerve, often due to overuse. Symptoms are similar to lateral epicondylitis, but the pain is typically around 4-5 cm distal to the lateral epicondyle and worsens with elbow extension and forearm pronation.
Q: What are the features of cubital tunnel syndrome?
A: Cubital tunnel syndrome is due to compression of the ulnar nerve. Early symptoms include intermittent tingling in the 4th and 5th fingers, worsening when the elbow is resting on a firm surface or flexed for extended periods. Later, there is numbness in the 4th and 5th fingers with associated weakness.
Q: What is olecranon bursitis and its features?
A: Olecranon bursitis presents as swelling over the posterior aspect of the elbow, with associated pain, warmth, and erythema. It typically affects middle-aged male patients.
Q: What is a Smith’s fracture and how is it caused?
A: Smith’s fracture (reverse Colles’ fracture) involves volar angulation of the distal radius fragment, resulting in a “garden spade deformity.” It is caused by falling backwards onto the palm of an outstretched hand or falling with wrists flexed.
Q: What is a Bennett’s fracture and how is it caused?
A: Bennett’s fracture is an intra-articular fracture of the first carpometacarpal joint, typically caused by impact on the flexed metacarpal, such as in fist fights. X-rays show a triangular fragment at the ulnar base of the metacarpal.
Q: What is a Monteggia’s fracture?
A: Monteggia’s fracture involves a dislocation of the proximal radioulnar joint in association with an ulna fracture, typically caused by a fall on an outstretched hand with forced pronation. Prompt diagnosis is crucial to avoid disability.
Q: What is a Galeazzi fracture?
A: Galeazzi fracture involves a radial shaft fracture with associated dislocation of the distal radioulnar joint, usually caused by a direct blow.
Q: What is a Pott’s fracture?
A: Pott’s fracture is a bimalleolar ankle fracture caused by forced foot eversion.
Q: What is a Barton’s fracture?
A: Barton’s fracture is a distal radius fracture (Colles’ or Smith’s) with associated radiocarpal dislocation, typically caused by a fall onto an extended and pronated wrist.
Q: What are the respiratory features of fat embolism?
A: Respiratory features include early persistent tachycardia, tachypnoea, dyspnoea, hypoxia, and pyrexia, typically developing 72 hours following injury.
Q: What are the dermatological features of fat embolism?
A: Dermatological features include a red/brown impalpable petechial rash, seen in 25-50% of cases, along with subconjunctival and oral haemorrhage/petechiae.
Q: What are the CNS features of fat embolism?
A: CNS features include confusion, agitation, retinal haemorrhages, and intra-arterial fat globules observed on fundoscopy.
Q: How is fat embolism diagnosed?
A: Diagnosis may be challenging as imaging can be normal. Fat emboli tend to lodge distally, so CTPA may not show vascular occlusion, but a ground glass appearance may be seen at the periphery.
Q: What is the treatment for fat embolism?
A: Treatment includes prompt fixation of long bone fractures, DVT prophylaxis, and general supportive care. There is some debate regarding the benefit versus risk of medullary reaming in femoral shaft or tibial fractures.
Q: What are the three main causes of fractures?
A: Fractures may arise from trauma (excessive forces applied to bone), stress-related injury (repetitive low-velocity injury), or pathological causes (abnormal bone that fractures under minimal trauma).
Q: What are the different types of fractures and their descriptions?
Oblique fracture: Fracture lies obliquely to the long axis of the bone.
Comminuted fracture: More than two fragments.
Segmental fracture: More than one fracture along a bone.
Transverse fracture: Perpendicular to the long axis of the bone.
Spiral fracture: Severe oblique fracture with rotation along the long axis of the bone.
Q: What are the Gustilo and Anderson classifications for open fractures?
Grade 1: Low-energy wound <1 cm.
Grade 2: Wound >1 cm with moderate soft tissue damage.
Grade 3: High-energy wound >1 cm with extensive soft tissue damage.
3A: Adequate soft tissue coverage.
3B: Inadequate soft tissue coverage.
3C: Associated arterial injury.
Q: What are key points in the management of fractures?
Immobilise the fracture including the proximal and distal joints.
Carefully monitor and document neurovascular status.
Manage infection with tetanus prophylaxis and IV broad-spectrum antibiotics for open injuries.
Thoroughly debride open fractures and avoid internal fixation devices or use with caution.
Open fractures should be debrided and lavaged within 6 hours of injury.
Q: What is a ganglion and where is it most commonly seen?
A: A ganglion is a cyst arising from a joint or tendon sheath, most commonly seen on the dorsal aspect of the wrist. It is three times more common in women.
Q: What are the features of a ganglion?
A: A ganglion is a firm, well-circumscribed mass that transilluminates.
Q: How is a ganglion managed?
A: Ganglions often disappear spontaneously after several months. Surgical excision is indicated for cysts associated with severe symptoms or neurovascular manifestations.
Q: What is greater trochanteric pain syndrome also known as?
A: Greater trochanteric pain syndrome is also referred to as trochanteric bursitis.
Q: What are the features of greater trochanteric pain syndrome?
A: Features include pain over the lateral side of the hip/thigh and tenderness on palpation of the greater trochanter.
Q: What are Osler’s nodes?
A: Osler’s nodes are painful, red, raised lesions found on the hands and feet due to the deposition of immune complexes.
Q: What are Bouchard’s nodes?
A: Bouchard’s nodes are hard, bony outgrowths or gelatinous cysts on the proximal interphalangeal joints, a sign of osteoarthritis, caused by calcific spurs of articular cartilage.
Q: What are Heberden’s nodes?
A: Heberden’s nodes are bony outgrowths that develop in middle age, typically after chronic swelling or inflammation of the affected joints, often causing deformity of the fingertip.
Q: What types of hip dislocation exist, and how are they characterized?
Posterior dislocation (90% of cases): The affected leg is shortened, adducted, and internally rotated.
Anterior dislocation: The affected leg is abducted and externally rotated, with no leg shortening.
Central dislocation.
Q: What is the management approach for hip dislocation?
A: The management includes the ABCDE approach, analgesia, and reduction under general anaesthetic within 4 hours to reduce the risk of avascular necrosis. Long-term management includes physiotherapy.
Q: What are the complications of hip dislocation?
A: Complications include sciatic or femoral nerve injury, avascular necrosis, osteoarthritis (more common in older patients), and recurrent dislocation due to ligament damage.
Q: What is the prognosis for hip dislocation, and when is it most favorable?
A: The prognosis is best when the hip is reduced within 12 hours post-injury and when there is less damage to the joint. Healing typically takes 2 to 3 months.
Q: What are the classic signs of a hip fracture?
A: The classic signs of a hip fracture are pain, a shortened and externally rotated leg. Patients with non-displaced or incomplete fractures may still be able to weight bear.
Q: How are hip fractures classified by location?
Intracapsular (subcapital): From the edge of the femoral head to the insertion of the capsule of the hip joint.
Extracapsular: Can be trochanteric or subtrochanteric (lesser trochanter is the dividing line).
Q: What are the types of intracapsular fractures according to the Garden classification system?
Type I: Stable fracture with impaction in valgus.
Type II: Complete fracture but undisplaced.
Type III: Displaced fracture with rotation and angulation, still has bony contact.
Type IV: Complete bony disruption.
Blood supply disruption is most common in Types III and IV.
Q: What is the management of an undisplaced intracapsular hip fracture?
A: Management includes internal fixation or hemiarthroplasty if the patient is unfit for surgery.
Q: What is the management of a displaced intracapsular hip fracture?
A: NICE recommends replacement arthroplasty (total hip replacement or hemiarthroplasty) for all patients with displaced intracapsular hip fractures. Total hip replacement is favored over hemiarthroplasty if the patient is able to walk independently, is cognitively intact, and is medically fit for the procedure.
Q: What is the management of extracapsular hip fractures?
Stable intertrochanteric fractures: Managed with a dynamic hip screw.
Reverse oblique, transverse, or subtrochanteric fractures: Managed with an intramedullary device.
Q: What condition is often picked up during newborn examination and is associated with positive Barlow’s and Ortolani’s tests?
A: Developmental dysplasia of the hip.
Q: What is the typical age group for transient synovitis (irritable hip)?
A: 2-10 years.
Q: What is the most common cause of hip pain in children?
A: Transient synovitis (irritable hip), which is associated with viral infections.
Q: What is Perthes disease and what age group does it primarily affect?
A: Perthes disease is a degenerative condition affecting the hip joints of children, typically between the ages of 4-8 years, caused by avascular necrosis of the femoral head.
Q: What are the features of Perthes disease?
A: Hip pain developing progressively over a few weeks, limp, stiffness, reduced range of hip movement, and changes seen on X-ray, such as widening of joint space and later decreased femoral head size or flattening.
Q: What age group is typically affected by slipped upper femoral epiphysis (SUFE), and which children are at higher risk?
A: SUFE typically affects children aged 10-15 years, especially obese children and boys.
Q: What are the key features of slipped upper femoral epiphysis (SUFE)?
A: Knee or distal thigh pain, loss of internal rotation of the leg in flexion, and displacement of the femoral head epiphysis postero-inferiorly. A bilateral slip occurs in 20% of cases.
Q: What is juvenile idiopathic arthritis (JIA) and how is it classified?
A: JIA is arthritis occurring in children under 16 years old that lasts for more than three months. Pauciarticular JIA refers to cases with 4 or fewer joints affected, accounting for around 60% of JIA cases.
Salmon pink Rash
Q: What are the features of pauciarticular juvenile idiopathic arthritis (JIA)?
A: Joint pain and swelling, usually in medium-sized joints like the knees, ankles, or elbows, limp, and potentially positive ANA associated with anterior uveitis.
Q: What is septic arthritis and how does it present?
A: Septic arthritis is characterized by acute hip pain associated with systemic upset, such as pyrexia, and inability or severe limitation of the affected joint.
Q: What is an iliopsoas abscess?
A: An iliopsoas abscess is a collection of pus in the iliopsoas compartment (iliopsoas and iliacus muscles).
Q: What are the primary causes of iliopsoas abscess?
A: Primary iliopsoas abscess is due to haematogenous spread of bacteria, with Staphylococcus aureus being the most common pathogen.
Q: What are the secondary causes of iliopsoas abscess?
A: Secondary causes include Crohn’s disease (most common), diverticulitis, colorectal cancer, UTI, GU cancers, vertebral osteomyelitis, femoral catheter, lithotripsy, endocarditis, and intravenous drug use.
Q: What are the clinical features of iliopsoas abscess?
A: Fever, back/flank pain, limp, and weight loss.
Q: What is the clinical examination finding for iliopsoas abscess?
A: The patient is in the supine position with the knee flexed and hip mildly externally rotated. Specific tests include asking the patient to lift the thigh against your hand (causing pain) and hyperextending the affected hip (which causes pain).
Q: What is the investigation of choice for iliopsoas abscess?
A: CT abdomen is the investigation of choice.
Q: What is the initial management of iliopsoas abscess?
A: Initial management includes antibiotics and percutaneous drainage, which is successful in about 90% of cases.
Q: When is surgery indicated in the management of iliopsoas abscess?
A: Surgery is indicated if percutaneous drainage fails or if there is another intra-abdominal pathology that requires surgery.
Q: What is the unhappy triad in knee injuries?
A: The unhappy triad consists of damage to the anterior cruciate ligament (ACL), medial collateral ligament (MCL), and meniscus (classically the medial meniscus, but recent evidence shows the lateral meniscus is more commonly injured).
Q: What is the typical cause of damage to the anterior cruciate ligament (ACL)?
A: ACL damage may result from twisting injuries.
Q: Which tests may be positive for ACL damage?
A: The anterior drawer test and Lachman test may be positive if the ACL is damaged.
Q: What type of injury causes damage to the posterior cruciate ligament (PCL)?
A: PCL damage may occur following dashboard injuries.
Q: What is a common cause of damage to the medial collateral ligament (MCL)?
A: MCL damage is commonly caused by skiing and following valgus stress.
Q: What is a typical sign of damage to the MCL?
A: Damage to the MCL typically causes abnormal passive abduction of the knee.
Q: What causes damage to the menisci?
A: Meniscal damage often results from twisting injuries.
Q: What are common symptoms of meniscal damage?
A: Locking and giving way are common symptoms of meniscal damage.
Q: What are the common presentations of a ruptured ACL?
A: A ruptured ACL often presents with a loud crack, pain, and rapid joint swelling (haemoarthrosis).
Q: How is a ruptured ACL managed?
A: A ruptured ACL is managed with intense physiotherapy or surgery.
Q: Who is most commonly affected by chondromalacia patellae?
A: Chondromalacia patellae commonly affects teenage girls, typically following an injury to the knee (e.g., patellar dislocation).
Q: What is a common history in patients with chondromalacia patellae?
A: Patients often report pain on going downstairs or at rest, along with tenderness and quadriceps wasting.
Q: What is the typical cause of patellar dislocation?
A: Patellar dislocation most commonly occurs through direct trauma or severe contraction of the quadriceps with the knee stretched in valgus and external rotation.
Q: What is the mechanism of tibial plateau fractures?
A: Tibial plateau fractures occur when the knee is forced into valgus or varus, but the knee fractures before the ligaments rupture.
Q: What are the typical features of an ACL injury?
A: Features include knee swelling, instability, and the feeling that the knee will give way.
Q: What is the anterior drawer test used for?
A: The anterior drawer test is used to assess the integrity of the ACL by evaluating anterior motion of the tibia in comparison to the femur.
Q: What does an intact ACL prevent during the anterior drawer test?
A: An intact ACL prevents forward translational movement of the tibia.
Q: What is the Lachman’s test?
A: The Lachman’s test is a variant of the anterior drawer test, performed with the knee at 20-30 degrees, to evaluate anterior translation of the tibia in relation to the femur.
Q: Why is the Lachman’s test considered more reliable than the anterior drawer test?
A: The Lachman’s test is considered more reliable because it is less dependent on patient relaxation and is more sensitive in detecting ACL injuries.
Q: What is a common feature of knee pain caused by a meniscal tear?
A: Pain is often worse on straightening the knee.
Q: What symptom may occur with a meniscal tear that affects knee stability?
A: The knee may “give way” due to instability caused by the tear.
Q: What can displaced meniscal tears cause in terms of knee movement?
A: Displaced meniscal tears may cause knee locking.
Q: Where is tenderness typically found in a meniscal tear?
A: Tenderness is usually along the joint line.
Q: What is Thessaly’s test used to assess?
A: Thessaly’s test is used to assess for a meniscal tear.
Q: How is Thessaly’s test performed?
A: The patient is weight-bearing at 20 degrees of knee flexion and supported by the examiner. The test is positive if there is pain on twisting the knee.
Q: What are common characteristics of osteoarthritis of the knee in older adults?
A: Typically occurs in patients over 50 years, often overweight. Pain may be severe, with intermittent swelling, crepitus, and limited movement.
Q: What is infrapatellar bursitis (Clergyman’s knee) associated with?
A: Infrapatellar bursitis is associated with kneeling.
Q: What is prepatellar bursitis (Housemaid’s knee) associated with?
A: Prepatellar bursitis is associated with more upright kneeling.
Q: What is Leriche syndrome and how is it treated?
A: Leriche syndrome is a form of atheromatous disease involving the iliac vessels, leading to compromised blood flow to the pelvic viscera. It typically presents with buttock claudication and impotence. Diagnosis includes angiography, and iliac occlusions are treated with endovascular angioplasty and stent insertion.
Q: What are the red flags for lower back pain?
Age < 20 years or > 50 years
History of previous malignancy
Night pain
History of trauma
Systemically unwell (e.g., weight loss, fever)
thoracic pain
Q: What are common causes of lower back pain that require specific treatment?
Facet joint pain
Spinal stenosis
Ankylosing spondylitis
Peripheral arterial disease
Q: What are the clinical features of facet joint pain in lower back pain?
Pain may be acute or chronic
Pain is worse in the morning and on standing
Pain is aggravated by back extension
Tenderness over the facet joints on examination
Q: What are the key features of spinal stenosis?
Gradual onset of pain
Unilateral or bilateral leg pain, numbness, and weakness, which worsens with walking and is relieved by sitting down or leaning forward
MRI is required for diagnosis
Q: What are the symptoms of ankylosing spondylitis in lower back pain?
Typically occurs in young men
Morning stiffness that improves with activity
Peripheral arthritis in 25% of cases (more common in females)
Q: How does peripheral arterial disease manifest in patients with lower back pain?
Pain on walking, relieved by rest
Absent or weak foot pulses
History of smoking or vascular diseases
Q: What is the recommended first-line treatment for non-specific lower back pain according to NICE guidelines?
NSAIDs are the first-line treatment for back pain
Paracetamol monotherapy is not effective
Q: When should MRI be used in non-specific lower back pain?
MRI should only be offered if it is likely to change management or if malignancy, infection, fracture, cauda equina syndrome, or ankylosing spondylitis is suspected
Q: What are the typical features of a prolapsed lumbar disc?
Leg pain is usually worse than back pain
Pain often worsens when sitting
Associated with neurological deficits and clear dermatomal leg pain
Q: What are the features of L3 nerve root compression in prolapsed disc?
Sensory loss over the anterior thigh
Weak hip flexion, knee extension, and hip adduction
Reduced knee reflex
Positive femoral stretch test
Q: What are the features of L4 nerve root compression in prolapsed disc?
Sensory loss on the anterior aspect of the knee and medial malleolus
Weak knee extension and hip adduction
Reduced knee reflex
Positive femoral stretch test
Q: What are the features of L5 nerve root compression in prolapsed disc?
Sensory loss on the dorsum of the foot
Weakness in foot and big toe dorsiflexion
Reflexes are intact
Positive sciatic nerve stretch test
Q: What are the features of S1 nerve root compression in prolapsed disc?
Sensory loss on the posterolateral aspect of the leg and lateral aspect of the foot
Weakness in plantar flexion of the foot
Reduced ankle reflex
Positive sciatic nerve stretch test
Q: What is the management approach for a prolapsed lumbar disc?
Similar to musculoskeletal lower back pain: analgesia, physiotherapy, and exercises
First-line treatment: NSAIDs + proton pump inhibitors
If symptoms persist after 4-6 weeks, consider referral for MRI
Q: What are the motor functions and sensory distribution of the femoral nerve?
Motor: Knee extension, thigh flexion
Sensory: Anterior and medial aspect of the thigh and lower leg
Typical mechanisms of injury: Hip and pelvic fractures, stab/gunshot wounds
Q: What are the motor functions and sensory distribution of the obturator nerve?
Motor: Thigh adduction
Sensory: Medial thigh
Typical mechanism of injury: Anterior hip dislocation
Q: What are the motor functions and sensory distribution of the lateral cutaneous nerve of the thigh?
Motor: None
Sensory: Lateral and posterior surfaces of the thigh
Typical mechanism of injury: Compression of the nerve near the ASIS → meralgia paraesthetica (pain, tingling, numbness)
Q: What are the motor functions and sensory distribution of the tibial nerve?
Motor: Foot plantarflexion and inversion
Sensory: Sole of the foot
Typical mechanism of injury: Popliteal lacerations, posterior knee dislocation (rare injury due to nerve protection)
Q: What are the motor functions and sensory distribution of the common peroneal nerve?
Motor: Foot dorsiflexion and eversion, Extensor hallucis longus
Sensory: Dorsum of the foot and the lower lateral part of the leg
Typical mechanism of injury: Injury at the neck of the fibula, tightly applied lower limb plaster cast
Result: Foot drop
Q: What are the motor functions and sensory distribution of the superior gluteal nerve?
Motor: Hip abduction
Sensory: None
Typical mechanism of injury: Misplaced intramuscular injection, hip surgery, pelvic fracture, posterior hip dislocation
Result: Positive Trendelenburg sign
Q: What are the motor functions and sensory distribution of the inferior gluteal nerve?
Motor: Hip extension and lateral rotation
Sensory: None
Typical mechanism of injury: Generally injured with the sciatic nerve
Result: Difficulty rising from a seated position, inability to jump, and climb stairs
Q: What is lumbar spinal stenosis?
A: It is a condition where the central canal of the spine narrows due to tumor, disk prolapse, or degenerative changes, leading to compression of the nerve roots of the cauda equina.
Q: What are common symptoms of lumbar spinal stenosis?
A: Patients may present with a combination of back pain, neuropathic pain, and symptoms resembling claudication. Sitting is often better than standing, and walking uphill may be easier than walking downhill.
Q: What is a key feature that differentiates lumbar spinal stenosis from true claudication?
A: The positional nature of the pain. Patients with lumbar spinal stenosis often feel relief when sitting, and walking uphill may be easier than walking downhill.
Q: What are the pathological changes in lumbar spinal stenosis?
A: Degeneration of the intervertebral disk, hypertrophy of posterior facet joints, osteophyte formation, and thickening of the ligamentum flavum, leading to narrowing of the spinal canal and compression of nerve roots.
Q: How is lumbar spinal stenosis diagnosed?
A: MRI is the best modality for demonstrating canal narrowing. Historically, the bicycle test was used to differentiate it from true vascular claudication, as vascular claudicants could not complete the test.
Q: What is the main treatment for lumbar spinal stenosis?
A: Laminectomy, a surgical procedure to relieve pressure on the nerve roots.
Q: What is medial epicondylitis also known as?
A: Golfer’s elbow.
Q: What are the key features of medial epicondylitis?
A: Pain and tenderness localized to the medial epicondyle, aggravated by wrist flexion and pronation, and possible numbness/tingling in the 4th and 5th fingers due to ulnar nerve involvement.
Q: What activities or movements aggravate the pain in medial epicondylitis?
A: Wrist flexion and pronation.
Q: Which nerves may be involved in medial epicondylitis, causing additional symptoms?
A: The ulnar nerve, leading to numbness and tingling in the 4th and 5th fingers.
Q: What is meralgia paraesthetica?
A: Meralgia paraesthetica is an entrapment mononeuropathy of the lateral femoral cutaneous nerve (LFCN), causing paraesthesia or anaesthesia in the distribution of the nerve.
Q: What are the typical symptoms of meralgia paraesthetica?
A: Burning, tingling, coldness, shooting pain, numbness, or deep muscle ache in the upper lateral aspect of the thigh, aggravated by standing and relieved by sitting.
Q: How can meralgia paraesthetica be diagnosed?
A: Diagnosis can often be made with the pelvic compression test, which is highly sensitive. Local anaesthetic injection into the nerve and ultrasound-guided therapy are also effective.
Q: What is a metatarsal fracture?
A: A metatarsal fracture is a break in one or more of the metatarsal bones in the foot, often caused by direct trauma, crush injuries, or repeated mechanical stress.
Q: Which metatarsal is most commonly fractured?
A: The proximal 5th metatarsal is the most commonly fractured metatarsal and the most common site of midfoot fractures.
Q: What are the typical symptoms of a metatarsal fracture?
A: Symptoms include pain, bony tenderness, swelling, and an antalgic gait.
Q: What are Jones fractures, and how are they different from pseudo-Jones fractures?
A: Jones fractures are transverse fractures at the metaphyseal-diaphyseal junction of the 5th metatarsal, whereas pseudo-Jones fractures are avulsion fractures at the proximal tuberosity, often associated with lateral ankle sprains.
Q: What does Froment’s sign assess for?
A: Froment’s sign is used to assess for ulnar nerve palsy.
Q: How is Froment’s sign tested?
A: The patient holds a piece of paper between their thumb and index finger, and the object is pulled away. If there is ulnar nerve palsy, the patient will be unable to hold the paper and will flex the thumb at the interphalangeal joint due to compensation by the flexor pollicis longus.
Q: What does Phalen’s test assess for?
A: Phalen’s test is used to assess for carpal tunnel syndrome.
Q: How is Phalen’s test performed?
A: The wrist is held in maximum flexion. The test is positive if there is numbness in the median nerve distribution.
Q: What does Tinel’s sign assess for?
A: Tinel’s sign is used to assess for carpal tunnel syndrome.
Q: How is Tinel’s sign tested?
A: The median nerve is tapped at the wrist, and the test is positive if there is tingling or electric-like sensations over the distribution of the median nerve.
Q: How are open fractures graded?
A: Open fractures are graded using the Gustilo and Anderson system.
Q: What are the three grades of open fractures in the Gustilo and Anderson system?
Grade 1: Low energy wound <1cm
Grade 2: Wound >1cm with moderate soft tissue damage
Grade 3: High energy wound >1cm with extensive soft tissue damage
Q: What are the subgroups of Grade 3 open fractures in the Gustilo and Anderson system?
3A: Adequate soft tissue coverage
3B: Inadequate soft tissue coverage
3C: Associated arterial injury
Q: What system can help predict the need for primary amputation in Type IIIc injuries?
A: The Mangled Extremity Scoring System (MESS) can help predict the need for primary amputation in Type IIIc injuries.
Q: What is the initial management of open fractures?
A: Initial management should focus on careful patient examination, control of hemorrhage, assessment of associated injuries, and establishment of distal neurovascular status. The wound should be covered with a dressing, and antibiotics should be administered.
Q: What is the cornerstone of open fracture management?
A: Early debridement is the cornerstone of the management of open fractures, aimed at removing foreign material and devitalized tissue.
Q: How is the wound typically treated in open fractures?
A: The wound is typically left open after debridement, and the area is irrigated with around 6 liters of saline.
Q: How is the fracture stabilized in open fractures?
A: The fracture is stabilized with an external fixator in most cases.
Q: What causes osteoarthritis of the hand?
A: It results from the loss of cartilage at synovial joints and is often accompanied by the degeneration of underlying bone.
Q: What are some risk factors for osteoarthritis of the hand?
Previous trauma to a joint increases the risk.
Obesity.
Hypermobility of a joint increases the risk.
Occupations like cotton workers and farmers are more susceptible.
Osteoporosis reduces the risk.
Q: What are the common features of osteoarthritis of the hand?
Usually bilateral, with one joint affected at a time.
Commonly affects carpometacarpal joints (CMC) and distal interphalangeal joints (DIPJ).
Episodic joint pain, provoked by movement and relieved by rest.
Stiffness, worse after long periods of inactivity (e.g. morning stiffness).
Painless nodes:
Heberden’s nodes at the DIP joints.
Bouchard’s nodes at the PIP joints.
Squaring of the thumbs due to deformity of the carpometacarpal joint.
Q: How long does the stiffness last in osteoarthritis of the hand compared to rheumatoid arthritis?
A: Stiffness lasts only a few minutes in osteoarthritis of the hand, whereas in rheumatoid arthritis, stiffness lasts longer, especially in the morning.
Q: What is the functional impact of osteoarthritis of the hand?
A: Patients usually do not have functional problems. However, severe involvement of the DIPJs can lead to reduced grip strength and disuse atrophy.
Q: What is the primary diagnostic investigation for osteoarthritis of the hand?
A: X-ray is used to identify osteophytes and joint space narrowing. Signs may appear on X-ray before symptoms develop.
Q: What is osteoarthritis of the hip?
A: Osteoarthritis (OA) of the hip is the second most common presentation of OA after the knee and accounts for significant morbidity. Total hip replacement is a common operation for this condition.
Q: What are the risk factors for osteoarthritis of the hip?
Increasing age.
Female gender (twice as common in women).
Obesity.
Developmental dysplasia of the hip.
Q: What are the typical features of osteoarthritis of the hip?
Chronic history of groin ache following exercise, relieved by rest.
Red flag features suggesting an alternative cause include:
Rest pain.
Night pain.
Morning stiffness lasting more than 2 hours.
Q: How is the severity of osteoarthritis of the hip assessed?
A: The Oxford Hip Score is widely used to assess the severity of osteoarthritis of the hip.
Q: What investigations are recommended for osteoarthritis of the hip?
If features are typical, a clinical diagnosis can be made.
Plain x-rays are the first-line investigation if diagnosis is uncertain.
Q: What is the management of osteoarthritis of the hip?
Oral analgesia.
Intra-articular injections for short-term benefit.
Total hip replacement remains the definitive treatment.
Q: What are some complications of total hip replacement?
Perioperative complications:
Venous thromboembolism.
Intraoperative fracture.
Nerve injury.
Surgical site infection.
Leg length discrepancy.
Posterior dislocation:
Can occur during extremes of hip flexion, with acute pain, inability to weight bear, and internal rotation with shortening of the affected leg.
Aseptic loosening:
The most common reason for revision.
Prosthetic joint infection.
Q: What is joint replacement (arthroplasty) used for in osteoarthritis?
A: Joint replacement is the most effective treatment for osteoarthritis patients who experience significant pain and disability.
Q: What are the common surgical techniques for hip joint replacement?
Cemented hip replacement: A metal femoral component is cemented into the femoral shaft, with a cemented acetabular polyethylene cup.
Uncemented hip replacement: Becoming more popular, especially in younger, active patients. It is more expensive than cemented replacements.
Hip resurfacing: A metal cap is placed over the femoral head, often used in younger patients. It preserves the femoral neck for future surgery options
Q: What is involved in the post-operative recovery following joint replacement surgery?
Physiotherapy and home exercises are prescribed.
Walking sticks or crutches are typically used for up to 6 weeks after hip or knee replacement surgery.
Q: What advice is given to patients post-hip replacement to prevent dislocation?
Avoid flexing the hip more than 90 degrees.
Avoid low chairs.
Do not cross your legs.
Sleep on your back for the first 6 weeks.
Q: What are the complications of joint replacement surgery?
Wound and joint infection.
Thromboembolism: NICE recommends low-molecular weight heparin for 4 weeks following a hip replacement.
Dislocation.
Q: What is osteochondritis dissecans (OCD)?
A: OCD is a pathological process affecting the subchondral bone, often in the knee joint, with secondary effects on the joint cartilage, including pain, oedema, free bodies, and mechanical dysfunctions. It generally affects children and young adults.
Q: What are the typical symptoms of osteochondritis dissecans (OCD)?
Knee pain and swelling, typically after exercise.
Knee catching, locking, and/or giving way.
Severe symptoms are associated with the presence of loose bodies.
A painful ‘clunk’ when flexing or extending the knee, indicating involvement of the lateral femoral condyle.
Q: What signs are associated with osteochondritis dissecans (OCD)?
Joint effusion.
Tenderness on palpation of the articular cartilage of the medial femoral condyle, when the knee is flexed.
Wilson’s sign: Pain at around 30° flexion with internal rotation of the tibia, relieved by external rotation of the tibia.
Q: What investigations are used for diagnosing osteochondritis dissecans (OCD)?
X-ray (anteroposterior, lateral, and tunnel views) may show the subchondral crescent sign or loose bodies.
MRI is used to evaluate cartilage, visualize loose bodies, and assess the stability of the lesion.
Q: What is the management strategy for osteochondritis dissecans (OCD)?
A: Early diagnosis is important. Due to subtle early-stage signs, there should be a low threshold for imaging and/or seeking an orthopaedic opinion.
Q: What is osteomyelitis?
A: Osteomyelitis is an infection of the bone. It can be subclassified into haematogenous and non-haematogenous osteomyelitis.
Q: What is haematogenous osteomyelitis?
A: Haematogenous osteomyelitis results from bacteraemia, is usually monomicrobial, and is the most common form in children. Vertebral osteomyelitis is the most common form in adults. Risk factors include sickle cell anaemia, intravenous drug use, immunosuppression, and infective endocarditis.
Q: What is non-haematogenous osteomyelitis?
A: Non-haematogenous osteomyelitis results from the contiguous spread of infection from adjacent soft tissues or from direct trauma to the bone. It is often polymicrobial and is the most common form in adults. Risk factors include diabetic foot ulcers, pressure sores, diabetes mellitus, and peripheral arterial disease.
Q: What is the most common cause of osteomyelitis?
A: Staphylococcus aureus is the most common cause, except in patients with sickle cell anaemia, where Salmonella species predominate.
Q: What is the best imaging modality for osteomyelitis?
A: MRI is the imaging modality of choice, with a sensitivity of 90-100%.
Q: What is the typical management for osteomyelitis?
A: The typical treatment is flucloxacillin for 6 weeks. Clindamycin is used if the patient is penicillin-allergic.
Q: What guidelines does NICE recommend for assessing osteoporosis risk?
A: NICE guidelines recommend assessing all women aged ≥65 and all men aged ≥75. Younger patients should be assessed if they have risk factors such as a previous fragility fracture, use of glucocorticoids, history of falls, family history of hip fracture, or other secondary osteoporosis causes.
Q: What are some risk factors for osteoporosis?
A: Risk factors include previous fragility fracture, use of oral/systemic glucocorticoids, history of falls, family history of hip fracture, secondary causes such as hypogonadism, endocrine conditions (e.g., diabetes, hyperthyroidism), malabsorption conditions, rheumatoid arthritis, low BMI, smoking, and excessive alcohol intake.
Q: How should secondary causes of osteoporosis be managed?
A: Secondary causes should be excluded first, as underlying conditions may also require treatment, such as bone metastases, myeloma, and Paget’s disease.
Q: When should a DEXA scan be offered?
A: A DEXA scan should be offered for patients >50 with a fragility fracture, <40 with major risk factors, or before starting treatments that may impact bone density, such as sex hormone deprivation for breast/prostate cancer.
Q: What tools are recommended to assess fragility fracture risk?
A: NICE recommends using clinical prediction tools such as FRAX or QFracture to assess a patient’s 10-year risk of a fracture.
Q: What should be done if the 10-year fracture risk is ≥10%?
A: If the 10-year fracture risk is ≥10%, a DEXA scan should be arranged.
Q: How are FRAX results interpreted?
A: FRAX results give a colour-coded risk: green (low), orange (moderate), and red (high). Patients in the orange and red zones should have a DEXA scan if not already done to refine their 10-year risk.
Q: When should osteoporosis risk be reassessed?
A: Risk should be reassessed if the original risk was near the intervention threshold (after 2 years) or when there is a change in the patient’s risk factors.
Q: What is osteoporosis and how does it relate to fragility fractures?
A: Osteoporosis is a condition where bone mineral density decreases, increasing the likelihood of fragility fractures, which occur due to mechanical forces that would not usually cause a fracture.
Q: What is a common site of osteoporotic fractures according to NICE?
A: The spine (vertebra) is one of the most common sites for osteoporotic fractures.
Q: How common are osteoporotic vertebral fractures?
A: Osteoporotic vertebral fractures are common but difficult to quantify as not all patients present to clinicians, and fractures may not always be visible on X-ray.
Q: What are the main risk factors for osteoporotic vertebral fractures?
A: Major risk factors include advancing age, history of fragility fractures, prolonged glucocorticoid use, history of falls, family history of hip fracture, secondary osteoporosis causes (e.g., Cushing’s disease), low BMI, tobacco smoking, and excessive alcohol intake.
Q: How do osteoporotic vertebral fractures present?
A: They may be asymptomatic, cause acute back pain, breathing difficulties due to organ compression, and gastrointestinal issues. A history of fall or trauma is often absent.
Q: What signs are associated with osteoporotic vertebral fractures?
A: Signs include loss of height, kyphosis (spinal curvature), and localized tenderness over the spinous processes at the fracture site.
Q: What is the first-line investigation for osteoporotic vertebral fractures?
A: X-ray of the spine is the first investigation and may show wedging of the vertebra or old fractures.
Q: What other imaging investigations may be useful for osteoporotic vertebral fractures?
A: CT spine provides a detailed view of the bone structure, and MRI spine helps differentiate osteoporotic fractures from those caused by other pathologies, such as tumors.
Q: What is a complete fracture in paediatric fractures?
A: A complete fracture is where both sides of the bone cortex are breached.
Q: What is a toddler’s fracture?
A: A toddler’s fracture is an oblique tibial fracture in infants.
Q: What is a plastic deformity in paediatric fractures?
A: A plastic deformity occurs when stress on the bone results in deformity without cortical disruption.
Q: What is a greenstick fracture?
A: A greenstick fracture is a unilateral cortical breach only, often occurring in children.
Q: What is a buckle (torus) fracture?
A: A buckle (torus) fracture is an incomplete cortical disruption that results in a periosteal haematoma.
Q: What is the Salter-Harris classification used for?
A: The Salter-Harris system is used to classify growth plate fractures in children.
Q: What is a Type I Salter-Harris fracture?
A: A Type I Salter-Harris fracture involves a fracture through the physis only, often appearing normal on an X-ray.
Q: What is a Type II Salter-Harris fracture?
A: A Type II Salter-Harris fracture involves a fracture through the physis and metaphysis.
Q: What is a Type III Salter-Harris fracture?
A: A Type III Salter-Harris fracture involves a fracture through the physis and epiphysis, extending to include the joint.
Q: What is a Type IV Salter-Harris fracture?
A: A Type IV Salter-Harris fracture involves a fracture through the physis, metaphysis, and epiphysis
.Q: What is a Type V Salter-Harris fracture?
A: A Type V Salter-Harris fracture is a crush injury involving the physis and may appear normal on an X-ray.
Q: How should growth plate tenderness be treated?
A: Growth plate tenderness should be assumed to indicate an underlying fracture, even if the X-ray appears normal.
Q: Which Salter-Harris fracture types require surgery?
A: Types III, IV, and V fractures usually require surgery.
Q: What are pathological fractures?
A: Pathological fractures occur due to genetic conditions such as osteogenesis imperfecta or osteopetrosis.
Q: What is osteogenesis imperfecta?
A: Osteogenesis imperfecta is a genetic condition causing defective osteoid formation due to inadequate production of substances like osteoid, collagen, and dentine, leading to fragile bones.
Q: What is osteopetrosis?
A: Osteopetrosis is a condition where bones become harder and denser, typically seen in young adults, with radiological features of “marble bone” due to lack of differentiation between cortex and medulla.
Q: What are the two types of patella injuries?
A: Patella fractures can be caused by direct injury (from a blow or trauma) or indirect injury (from forceful quadriceps contraction against a blocked knee extension).
Q: What is a direct patella injury?
A: A direct patella injury typically occurs from a fall or dashboard injury causing an undisplaced crack or comminuted fracture, often without affecting the extensor mechanism.
Q: What is an indirect patella injury?
A: An indirect patella injury occurs when the quadriceps forcefully contracts against a blocked knee extension, often leading to a transverse patella fracture and possible extensor mechanism disruption.
Q: What are the clinical features of a patella fracture?
A: Clinical features include swelling, bruising, localized pain and tenderness around the knee, and a palpable gap in the patella. Extensor mechanism function is assessed by the patient’s ability to straight leg raise.
Q: What is the standard imaging for diagnosing patella fractures?
A: Plain X-rays with at least two views (AP and lateral) are typically sufficient for diagnosing patella fractures. Skyline views may be used if the diagnosis is unclear but can be uncomfortable to obtain.
Q: How are undisplaced patella fractures managed?
A: Undisplaced fractures, especially vertical fractures with an intact extensor mechanism, are managed non-operatively in a hinged knee brace for 6 weeks, with full weight-bearing allowed.
Q: When is operative management required for patella fractures?
A: Operative management is indicated for displaced fractures or those with extensor mechanism disruption. Treatment options include tension band wire, inter-fragmentary screws, or cerclage wires, followed by a hinged knee brace for 4-6 weeks.
Q: What is the most common cause of heel pain in adults?
A: Plantar fasciitis is the most common cause of heel pain in adults.
Q: Where is the pain usually located in plantar fasciitis?
A: The pain is usually worse around the medial calcaneal tuberosity.
Q: What are the management strategies for plantar fasciitis?
A: Management includes resting the feet, wearing shoes with good arch support and cushioned heels, and using insoles and heel pads.
Q: What are common risk factors for rib fractures?
A: Risk factors include polytrauma, osteoporosis, steroid use, chronic obstructive pulmonary disease, and cancer metastases (prostate cancer in men, breast cancer in women).
Q: What is the most common symptom of a rib fracture?
A: Severe, sharp chest wall pain, which worsens with deep breaths or coughing.
Q: What complications can arise from rib fractures?
A: Pneumothorax, lung injury, flail chest, and reduced oxygen saturation due to pain-induced reduced ventilation.
Q: What is flail chest?
A: Flail chest occurs with multiple rib fractures along three or more consecutive ribs, leading to paradoxical movement of the rib segment, which impairs lung ventilation and may cause serious lung injury.
Q: What are the best investigations for rib fractures?
A: A CT scan of the chest is the best diagnostic test, while chest X-rays may show fractures but are less informative for soft tissue injuries.
Q: How are most rib fractures managed?
A: Most are managed conservatively with good analgesia, and nerve blocks may be considered if pain is not controlled. Surgical fixation may be considered if fractures fail to heal after 12 weeks of conservative management.
Q: When should flail chest be urgently discussed with cardiothoracic surgery?
A: Flail chest segments should be urgently discussed with cardiothoracic surgery due to their potential to impair ventilation and cause significant lung trauma.
Q: What is a typical symptom of rotator cuff injury?
A: Shoulder pain, particularly worsening with abduction.
Q: What sign is indicative of rotator cuff injury?
A: Tenderness over the anterior acromion.
Q: What are sarcomas?
A: Sarcomas are a diverse group of malignant tumours originating from mesenchymal tissue, accounting for about 1% of adult cancers and 15% of paediatric cancers.
Q: How are sarcomas classified?
A: Sarcomas are classified into bone sarcomas (e.g., osteosarcoma, chondrosarcoma, Ewing’s sarcoma) and soft tissue sarcomas (e.g., liposarcoma, rhabdomyosarcoma, synovial sarcoma, fibrosarcoma, angiosarcoma, leiomyosarcoma).
Q: What are common symptoms of sarcomas?
A: Symptoms include pain, swelling or a palpable mass, impaired function, pathologic fractures (in bone sarcomas), and systemic symptoms like fatigue, weight loss, and fever.
Q: What are some imaging techniques used to diagnose sarcomas?
A: X-rays, CT scans, MRI, and PET scans are used to localize the tumour, assess its size, and evaluate metastatic spread.
Q: What is the role of biopsy in diagnosing sarcomas?
A: A biopsy (via FNA, core needle, or incisional biopsy) is used to obtain a tissue sample for histopathological analysis to confirm the diagnosis and grade the tumour.
Q: What is the primary treatment for most sarcomas?
A: Surgery, aimed at complete resection with negative margins to reduce local recurrence risk. Limb-sparing surgery may be performed, or amputation may be necessary for advanced tumours.
Q: How is radiation therapy used in sarcoma treatment?
A: Radiation therapy can be used preoperatively (neoadjuvant) to shrink the tumour or postoperatively (adjuvant) to minimize recurrence. Intraoperative radiation therapy (IORT) may also be used.
Q: What is a scaphoid fracture?
A: A scaphoid fracture is a wrist fracture, often caused by falling onto an outstretched hand (FOOSH), resulting in axial compression of the scaphoid with wrist hyperextension and radial deviation.
Q: What is the blood supply of the scaphoid, and why is it important?
A: The scaphoid’s blood supply comes primarily from the dorsal carpal branch of the radial artery, in a retrograde manner. Disruption of this blood flow, especially in proximal fractures, can lead to avascular necrosis.
Q: What are the clinical features of a scaphoid fracture?
A: Patients present with pain along the radial aspect of the wrist, at the base of the thumb, and loss of grip or pinch strength.
Q: What signs are indicative of a scaphoid fracture?
A: 1. Point of maximal tenderness over the anatomical snuffbox (sensitive but not specific)
2. Wrist joint effusion
3. Pain on telescoping of the thumb (longitudinal compression)
4. Tenderness of the scaphoid tubercle on the volar aspect
5. Pain on ulnar deviation of the wrist
Q: What investigations should be done for suspected scaphoid fractures?
A: Plain film radiographs (AP, lateral views), ‘scaphoid views’ (PA, oblique, Ziter view), and CT scans. MRI is the most definitive investigation for confirmation, especially when radiographs are inconclusive.
Q: What is the initial management of a suspected scaphoid fracture?
A: Immobilization with a Futuro splint or standard below-elbow backslab, referral to orthopaedics, and follow-up imaging 7-10 days later if radiographs are inconclusive.
Q: How are undisplaced scaphoid waist fractures managed?
A: Undisplaced scaphoid waist fractures are managed with a cast for 6-8 weeks, with union achieved in over 95% of cases.
If you cant see it on xray and there is suspicion, cast and repeat xray in 2 weeks
Q: How are displaced scaphoid waist fractures managed?
A: Displaced scaphoid waist fractures require surgical fixation.
Q: How are proximal scaphoid pole fractures managed?
A: Proximal scaphoid pole fractures require surgical fixation.
Q: What are the complications of scaphoid fractures?
A: Complications include non-union (leading to pain and early osteoarthritis) and avascular necrosis.
Q: What percentage of shoulder dislocations are anterior?
A: Over 95% of shoulder dislocations are anterior.
Q: What is adhesive capsulitis (frozen shoulder)?
A: Adhesive capsulitis, or frozen shoulder, is common in middle-aged individuals and diabetics, characterized by painful, stiff movement and limited range of motion in all directions, particularly loss of external rotation and abduction in about 50% of patients.
Q: What is supraspinatus tendonitis (subacromial impingement)?
A: Supraspinatus tendonitis, also known as subacromial impingement or painful arc, is a rotator cuff injury. It causes a painful arc of abduction between 60 and 120 degrees, with tenderness over the anterior acromion.
Q: What are the symptoms of a dorsal column lesion?
A: A dorsal column lesion causes loss of vibration and proprioception. Conditions associated include tabes dorsalis and subacute combined degeneration (SACD).
Q: What is the result of a spinothalamic tract lesion?
A: A spinothalamic tract lesion causes loss of pain sensation and temperature.
Q: What is the presentation of a central cord lesion?
A: A central cord lesion leads to flaccid paralysis of the upper limbs.
Q: What is the typical progression of osteomyelitis?
A: Osteomyelitis is typically progressive. It is associated with Staphylococcus aureus in intravenous drug users (IVDU), primarily affecting the cervical region, and fungal infections in immunocompromised patients. Tuberculosis (TB) commonly affects the thoracic region.
Q: What are the symptoms of spinal cord infarction?
A: Spinal cord infarction presents with dorsal column signs, including loss of proprioception and fine discrimination.
Q: What signs are associated with cord compression?
A: Cord compression leads to upper motor neuron (UMN) signs, which can be caused by malignancy, haematoma, or fracture.
Q: What is Brown-Séquard syndrome?
A: Brown-Séquard syndrome is caused by hemisection of the spinal cord, resulting in ipsilateral paralysis and loss of proprioception and fine discrimination, and contralateral loss of pain and temperature sensation.
Q: What are stress fractures and how do they present?
A: Stress fractures are small hairline fractures caused by repetitive activity and loading of normal bone. They are often not displaced, and surrounding soft tissue injury is uncommon. They may present late, with callus formation visible on radiographs. Early-stage injuries with severe pain may require immobilisation tailored to the site of injury.
Q: What is talipes equinovarus (club foot)?
A: Talipes equinovarus, or club foot, describes an inverted (inward turning) and plantar flexed foot.
Q: How is talipes equinovarus diagnosed?
A: Talipes equinovarus is usually diagnosed on the newborn exam and the deformity is not passively correctable; imaging is not normally needed.
Q: What conditions are associated with talipes equinovarus?
A: Conditions associated with talipes equinovarus include spina bifida, cerebral palsy, Edward’s syndrome (trisomy 18), oligohydramnios, and arthrogryposis.
Q: What is the primary cause of talipes equinovarus?
A: Most cases of talipes equinovarus are idiopathic.
Q: How is talipes equinovarus managed using the Ponseti method?
A: The Ponseti method consists of manipulation and progressive casting which starts soon after birth, usually correcting the deformity after 6-10 weeks. An Achilles tenotomy is required in around 85% of cases.
Q: What surgical intervention is often required in the Ponseti method, and how is it performed?
A: An Achilles tenotomy is required in around 85% of cases and can usually be done under local anaesthetic.
Q: What is trigger finger?
A: Trigger finger is a condition associated with abnormal flexion of the digits, caused by a disparity between the size of the tendon and the pulleys through which they pass.
Q: Which fingers are most commonly affected by trigger finger?
A: The thumb, middle, and ring fingers are more commonly affected.
Q: What are the initial features of trigger finger?
A: Initially, there is stiffness and snapping (‘trigger’) when extending a flexed digit, and a nodule may be felt at the base of the affected finger.
Q: How is trigger finger managed?
A: Steroid injection is successful in the majority of patients, and a finger splint may be applied afterwards. Surgery is reserved for patients who have not responded to steroid injections.
Q: What is the motor function of the musculocutaneous nerve (C5-C7)?
A: Elbow flexion (supplies biceps brachii) and supination.
Q: What is the sensory area supplied by the musculocutaneous nerve?
A: Lateral part of the forearm.
Q: What is a typical mechanism of injury for the musculocutaneous nerve?
A: Isolated injury is rare - usually injured as part of brachial plexus injury.
Q: What is the motor function of the axillary nerve (C5, C6)?
A: Shoulder abduction (deltoid muscle).
Q: What is the sensory area supplied by the axillary nerve?
A: Inferior region of the deltoid muscle.
Q: What is the motor function of the radial nerve (C5-C8)?
A: Extension (forearm, wrist, fingers, thumb).
Q: What is the sensory area supplied by the radial nerve?
A: Small area between the dorsal aspect of the 1st and 2nd metacarpals.
Q: What are the motor functions of the median nerve (C6, C8, T1)?
A: LOAF* muscles. Features depend on the site of the lesion: wrist - paralysis of thenar muscles, opponens pollicis; elbow - loss of pronation of forearm and weak wrist flexion.
Q: What is the sensory area supplied by the median nerve?
A: Palmar aspect of lateral 3½ fingers.
Q: What is the motor function of the ulnar nerve (C8, T1)?
A: Intrinsic hand muscles except LOAF* and wrist flexion.
Q: What is the sensory area supplied by the ulnar nerve?
A: Medial 1½ fingers.
Q: What is Erb-Duchenne palsy (‘waiter’s tip’)?
A: Due to damage of the upper trunk of the brachial plexus (C5, C6). May be secondary to shoulder dystocia during birth. The arm hangs by the side and is internally rotated, elbow extended.
Q: What is Klumpke injury?
A: Due to damage of the lower trunk of the brachial plexus (C8, T1). May be secondary to shoulder dystocia during birth or caused by a sudden upward jerk of the hand. Associated with Horner’s syndrome.
Q: What are anti-neutrophil cytoplasmic antibodies (ANCA) associated with?
A: Small-vessel vasculitides, including granulomatosis with polyangiitis, eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome), and microscopic polyangiitis.
Q: What is the first-line investigation approach for ANCA associated vasculitis?
A: Urinalysis for haematuria and proteinuria, blood tests (urea and creatinine, full blood count, CRP), ANCA testing, and chest x-ray.
Q: What is the target of cANCA?
A: Serine proteinase 3 (PR3).
Q: What is the target of pANCA?
A: Myeloperoxidase (MPO).
Q: Which conditions are associated with cANCA?
A: Granulomatosis with polyangiitis (90%).
Q: Which conditions are associated with pANCA?
A: Eosinophilic granulomatosis with polyangiitis (50%), microscopic polyangiitis (75%), ulcerative colitis (70%), primary sclerosing cholangitis (70%), anti-GBM disease (25%), and Crohn’s disease (20%).
Q: What is ankylosing spondylitis associated with?
A: HLA-B27.
Q: What is the typical presentation of ankylosing spondylitis?
A: A young man aged 20-30 years old presenting with lower back pain and stiffness of insidious onset.
Q: How does the stiffness in ankylosing spondylitis typically behave?
A: It is usually worse in the morning and improves with exercise.
Q: What might patients with ankylosing spondylitis experience at night?
A: Pain that improves on getting up.
Q: What is Schober’s test used for in ankylosing spondylitis?
A: To assess reduced forward flexion of the spine.
Q: What are the expected findings in Schober’s test for a healthy individual?
A: The distance between two lines (drawn 10 cm above and 5 cm below the back dimples) should increase by more than 5 cm when the patient bends forward.
Q: What are the clinical examination findings in ankylosing spondylitis?
A: Reduced lateral flexion, reduced forward flexion, and reduced chest expansion.
Q: What are some other features associated with ankylosing spondylitis? (Hint: ‘A’s)
A: Apical fibrosis, anterior uveitis, aortic regurgitation, Achilles tendonitis, AV node block, amyloidosis, and cauda equina syndrome.
Q: What inflammatory markers are typically raised in ankylosing spondylitis?
A: ESR and CRP.
Q: What is the most useful investigation in establishing the diagnosis of ankylosing spondylitis?
A: Plain x-ray of the sacroiliac joints.
Q: What are the early and later radiographic changes seen in ankylosing spondylitis?
A: Early: normal x-rays, later: sacroiliitis (subchondral erosions, sclerosis), squaring of lumbar vertebrae, ‘bamboo spine’, syndesmophytes.
Q: What is the next step if the x-ray is negative for sacroiliac joint involvement but suspicion for ankylosing spondylitis remains high?
A: Obtain an MRI to look for early inflammation involving sacroiliac joints (bone marrow oedema).
Q: What might spirometry show in ankylosing spondylitis and why?
A: A restrictive defect due to pulmonary fibrosis, kyphosis, and ankylosis of the costovertebral joints.
Q: What are the first-line treatments for ankylosing spondylitis?
A: Regular exercise, NSAIDs, and physiotherapy.
Q: What does the 2010 EULAR guideline suggest for patients with persistently high disease activity despite conventional treatments?
A: Anti-TNF therapy.
Q: What is antiphospholipid syndrome?
A: An acquired disorder characterized by a predisposition to both venous and arterial thromboses, recurrent fetal loss, and thrombocytopenia.
Q: What conditions is antiphospholipid syndrome most commonly associated with?
A: Systemic lupus erythematosus (SLE), where around 30% of patients with SLE have positive antiphospholipid antibodies.
Q: What are the main features of antiphospholipid syndrome?
A: Venous/arterial thrombosis, recurrent miscarriages, livedo reticularis, pre-eclampsia, and pulmonary hypertension.
Q: What antibodies are involved in the diagnosis of antiphospholipid syndrome?
A: Anticardiolipin antibodies, anti-beta2 glycoprotein I (anti-beta2GPI) antibodies, and lupus anticoagulant.
Q: What are common investigation findings in antiphospholipid syndrome?
A: Thrombocytopenia and prolonged APTT.
Q: What is the primary thromboprophylaxis management for antiphospholipid syndrome?
A: Low-dose aspirin.
Q: How is secondary thromboprophylaxis managed for initial venous thromboembolic events in antiphospholipid syndrome?
A: Lifelong warfarin with a target INR of 2-3.
Q: What is the management for recurrent venous thromboembolic events in antiphospholipid syndrome?
A: Lifelong warfarin; if events occurred while taking warfarin, consider adding low-dose aspirin and increase target INR to 3-4.
Q: How should arterial thrombosis be treated in antiphospholipid syndrome?
A: Lifelong warfarin with a target INR of 2-3.
Q: What causes antisynthetase syndrome?
A: It is caused by autoantibodies against aminoacyl-tRNA synthetase enzymes, with the most common autoantibody being anti-Jo-1.
Q: What is a hallmark clinical feature of antisynthetase syndrome?
A: Myositis, characterized by muscle weakness, especially in proximal muscles.
Q: What are common symptoms of myositis in antisynthetase syndrome?
A: Difficulty performing activities like climbing stairs or lifting objects, along with elevated muscle enzymes such as creatine kinase (CK).
Q: What is a common and serious manifestation of antisynthetase syndrome?
A: Interstitial Lung Disease (ILD), which can cause chronic dry cough, shortness of breath, and reduced exercise tolerance.
A: High-resolution CT scans are typically used for diagnosis.
A: High-resolution CT scans are typically used for diagnosis.
Q: What is a distinctive clinical sign of antisynthetase syndrome?
A: Mechanic’s hands, which are hyperkeratotic, thickened, and cracked skin on the sides of the fingers and palms.
Q: What other features may be present in antisynthetase syndrome besides myositis and ILD?
A: Arthritis, fever, fatigue, weight loss, and malaise.
Q: What is the management approach for antisynthetase syndrome?
A: Immunosuppressive therapy, including corticosteroids and other immunomodulatory drugs, to control inflammation and prevent progression. Additional treatments may be required for significant lung involvement, such as antifibrotic agents and supplemental oxygen.
Q: What is the active compound that azathioprine is metabolized into?
A: Mercaptopurine, a purine analogue that inhibits purine synthesis.
Q: Why might a thiopurine methyltransferase (TPMT) test be needed before using azathioprine?
A: To identify individuals prone to azathioprine toxicity.
Q: What are some adverse effects of azathioprine?
A: Bone marrow depression, nausea/vomiting, pancreatitis, and increased risk of non-melanoma skin cancer.
Q: What should be considered if infection or bleeding occurs in a patient taking azathioprine?
A: A full blood count.
Q: What significant drug interaction should be noted with azathioprine?
A: Interaction with allopurinol, requiring lower doses of azathioprine.
Q: What is the classic triad of symptoms in Behcet’s syndrome?
A: Oral ulcers, genital ulcers, and anterior uveitis.
Q: What genetic marker is associated with Behcet’s syndrome?
A: HLA B51.
Q: What are some features of Behcet’s syndrome apart from the classic triad?
A: Thrombophlebitis, deep vein thrombosis, arthritis, neurological involvement (e.g., aseptic meningitis), gastrointestinal symptoms (e.g., abdominal pain, diarrhea, colitis), and erythema nodosum.
Q: Is there a definitive test for Behcet’s syndrome?
A: No, the diagnosis is based on clinical findings.
Q: What is the mechanism of action of bisphosphonates?
A: Bisphosphonates inhibit osteoclasts by reducing recruitment and promoting apoptosis, decreasing bone demineralisation.
Q: What are the clinical uses of bisphosphonates?
A: Bisphosphonates are used in the prevention and treatment of osteoporosis, hypercalcaemia, Paget’s disease, and pain from bone metastases.
Q: What are the common adverse effects of bisphosphonates?
A: Oesophageal reactions (oesophagitis, oesophageal ulcers), osteonecrosis of the jaw, increased risk of atypical stress fractures (especially with alendronate), acute phase response (fever, myalgia, arthralgia), and hypocalcaemia.
Q: What should be corrected before starting bisphosphonate treatment?
A: Hypocalcaemia and vitamin D deficiency should be corrected before initiating bisphosphonates.
Q: What are the lab values in osteoporosis?
A: Calcium: Normal, Phosphate: Normal, ALP: Normal, PTH: Normal.
Q: What are the lab values in osteomalacia?
A: Calcium: Decreased, Phosphate: Decreased, ALP: Increased, PTH: Increased.
Q: What are the lab values in primary hyperparathyroidism (leading to osteitis fibrosa cystica)?
A: Calcium: Increased, Phosphate: Decreased, ALP: Increased, PTH: Increased.
Q: What are the lab values in chronic kidney disease (leading to secondary hyperparathyroidism)?
A: Calcium: Decreased, Phosphate: Increased, ALP: Increased, PTH: Increased.
Q: What are the lab values in Paget’s disease?
A: Calcium: Normal, Phosphate: Normal, ALP: Increased, PTH: Normal.
A: Calcium: Normal, Phosphate: Normal, ALP: Normal, PTH: Normal.
A: Calcium: Normal, Phosphate: Normal, ALP: Normal, PTH: Normal.
Q: What is an osteoma and its association?
A: Osteoma is a benign overgrowth of bone, typically occurring on the skull, and is associated with Gardner’s syndrome (a variant of familial adenomatous polyposis, FAP).
Q: What is osteochondroma (exostosis) and who is it most common in?
A: Osteochondroma is the most common benign bone tumor, typically occurring in males under 20 years old. It is a cartilage-capped bony projection on the external surface of a bone.
Q: What is a giant cell tumor and where does it occur?
A: Giant cell tumor is a tumor of multinucleated giant cells within a fibrous stroma, most commonly occurring in the epiphyses of long bones, with a peak incidence between 20-40 years. X-ray shows a “double bubble” or “soap bubble” appearance.
Q: What is osteosarcoma and its associations?
A: Osteosarcoma is the most common primary malignant bone tumor, seen mainly in children and adolescents. It occurs in the metaphyseal region of long bones. X-ray shows Codman triangle and “sunburst” pattern. Mutation of the Rb gene significantly increases the risk, and it is associated with retinoblastoma, Paget’s disease, and radiotherapy.
Q: What is Ewing’s sarcoma and its key features?
A: Ewing’s sarcoma is a small round blue cell tumor seen mainly in children and adolescents. It most frequently affects the pelvis and long bones, causing severe pain. X-ray shows an “onion skin” appearance. It is associated with t(11;22) translocation.
Q: What is chondrosarcoma and its common characteristics?
A: Chondrosarcoma is a malignant tumor of cartilage that commonly affects the axial skeleton, more common in middle age.
Q: What is dactylitis?
A: Dactylitis refers to the inflammation of a digit (finger or toe).
Q: What are the common causes of dactylitis?
A: Common causes of dactylitis include spondyloarthritis (e.g. Psoriatic arthritis, reactive arthritis), sickle-cell disease, and rare causes like tuberculosis, sarcoidosis, and syphilis.
Q: How is denosumab administered for osteoporosis treatment?
A: Denosumab is given as a subcutaneous injection of 60mg every 6 months for osteoporosis.
Q: What is denosumab?
A: Denosumab is a human monoclonal antibody used to treat osteoporosis by inhibiting RANKL, preventing the development of osteoclasts.
Q: What is the first-line treatment for osteoporosis, and how does denosumab fit in?
A: Oral bisphosphonates (e.g., alendronate) are first-line, and denosumab is considered if bisphosphonates are not tolerated or in cases with specific criteria met.
Q: What is dermatomyositis?
A: Dermatomyositis is an inflammatory disorder causing symmetrical, proximal muscle weakness and characteristic skin lesions. It may be idiopathic or associated with connective tissue disorders or underlying malignancy.
Q: What malignancies are commonly associated with dermatomyositis?
A: Dermatomyositis is associated with ovarian, breast, and lung cancer in 20-25% of cases, more commonly in older patients.
Q: What skin features are characteristic of dermatomyositis?
A: Characteristic skin features include a photosensitive macular rash over the back and shoulders, heliotrope rash in the periorbital region, Gottron’s papules on the extensor surfaces of fingers, and ‘mechanic’s hands’ with dry, scaly skin and cracks.
Q: What are Gottron’s papules in dermatomyositis?
A: Gottron’s papules are roughened red papules that appear over the extensor surfaces of the fingers in dermatomyositis.
Q: What is the significance of nail fold capillary dilatation in dermatomyositis?
A: Nail fold capillary dilatation is one of the skin manifestations observed in dermatomyositis.
Q: What are some systemic features of dermatomyositis?
A: Systemic features include proximal muscle weakness, Raynaud’s phenomenon, respiratory muscle weakness, interstitial lung disease, and dysphagia or dysphonia.
Q: What investigations are performed for dermatomyositis?
A: Investigations include ANA testing (positive in about 80% of cases) and testing for anti-synthetase antibodies (e.g., anti-Jo-1, anti-SRP, anti-Mi-2).
Q: What is discoid lupus erythematosus?
A: Discoid lupus erythematosus is a benign, autoimmune disorder commonly seen in younger females, characterized by erythematous, raised, sometimes scaly rashes. It very rarely progresses to systemic lupus erythematosus.
Q: What are the common features of discoid lupus erythematosus?
A: Features include an erythematous, raised rash, often photosensitive, primarily affecting the face, neck, ears, and scalp. Lesions heal with atrophy, scarring (which may cause scarring alopecia), and pigmentation.
Q: What is the treatment for discoid lupus erythematosus?
A: Treatment includes topical steroid creams as first-line, with oral antimalarials (e.g., hydroxychloroquine) as second-line. Patients should also avoid sun exposure.
Q: What is drug-induced lupus?
A: Drug-induced lupus is a condition where lupus-like symptoms occur due to medication use, but not all features of systemic lupus erythematosus (SLE) are present, particularly renal and nervous system involvement. It usually resolves once the drug is discontinued.
Q: What are the common features of drug-induced lupus?
A: Features include arthralgia, myalgia, skin involvement (e.g., malar rash), and pulmonary involvement (e.g., pleurisy). ANA is positive in 100% of cases, but dsDNA is negative. Anti-histone antibodies are found in 80-90% of cases, and anti-Ro, anti-Smith antibodies may be positive in around 5%.
Q: What are the most common causes of drug-induced lupus?
A: The most common causes include procainamide and hydralazine.
Q: What is Ehlers-Danlos syndrome?
A: Ehlers-Danlos syndrome is an autosomal dominant connective tissue disorder that primarily affects type III collagen, leading to increased tissue elasticity, joint hypermobility, and skin that is more elastic than normal.
Q: What are the key features of Ehlers-Danlos syndrome?
A: Features include elastic, fragile skin, joint hypermobility (leading to recurrent joint dislocations), easy bruising, and a range of cardiovascular and neurological complications.
Q: What are the complications of Ehlers-Danlos syndrome?
A: Complications include aortic regurgitation, mitral valve prolapse, aortic dissection, subarachnoid hemorrhage, and angioid retinal streaks.
Q: What is gout and how does it present?
A: Gout is a form of inflammatory arthritis characterized by episodes of pain, swelling, and erythema. Acute episodes typically develop rapidly and reach maximal intensity within 12 hours. Symptoms often resolve between flares.
Q: Which joint is most commonly affected during the first presentation of gout?
A: Around 70% of first presentations affect the 1st metatarsophalangeal (MTP) joint, historically called podagra. Other commonly affected joints include the ankle, wrist, and knee.
Q: What are the investigations used to diagnose gout?
A: Investigations include measuring uric acid levels and synovial fluid analysis. A uric acid level ≥ 360 µmol/L supports a diagnosis. Synovial fluid analysis shows needle-shaped, negatively birefringent monosodium urate crystals under polarised light.
Q: What are the radiological features of gout?
A: Radiological features include joint effusion, well-defined ‘punched-out’ erosions with sclerotic margins, relative preservation of joint space, eccentric erosions, and no periarticular osteopenia. Soft tissue tophi may also be seen.
Q: What is the cause of gout?
A: Gout is caused by microcrystal synovitis due to the deposition of monosodium urate monohydrate in the synovium, typically caused by chronic hyperuricaemia (uric acid > 450 µmol/l).
Q: What is the first-line treatment for acute gout management?
A: NSAIDs or colchicine are first-line treatments. NSAID doses should be maximized for 1-2 days after symptoms settle. Gastroprotection (e.g., proton pump inhibitors) may be indicated.
Q: What is the main side effect of colchicine?
A: The main side effect of colchicine is diarrhoea.
Q: When should oral steroids be considered in acute gout management?
A: Oral steroids (e.g., prednisolone 15mg/day) may be used if NSAIDs and colchicine are contraindicated.
Q: When is urate-lowering therapy (ULT) indicated in gout management?
A: ULT is recommended after the first attack if there are >= 2 attacks in 12 months, tophi, renal disease, uric acid renal stones, or if the patient is on cytotoxics or diuretics.
Q: When should urate-lowering therapy be started after an acute gout attack?
A: It is traditionally delayed until 2 weeks after an acute attack to avoid precipitating further attacks, but the British Society of Rheumatology now supports starting ULT once inflammation has settled.
Q: What is the first-line urate-lowering therapy for gout?
A: Allopurinol is first-line, typically started at 100 mg once daily with dose titration to achieve a serum uric acid level of < 360 µmol/L.
Q: What should be done when starting allopurinol in gout management?
A: Colchicine cover should be considered when starting allopurinol. NSAIDs can be used if colchicine cannot be tolerated, potentially for up to 6 months.
Q: What is Lesch-Nyhan syndrome, and how does it relate to gout?
A: Lesch-Nyhan syndrome is a genetic disorder caused by hypoxanthine-guanine phosphoribosyl transferase (HGPRTase) deficiency. It is X-linked recessive, affecting boys, and leads to gout, renal failure, neurological deficits, learning difficulties, and self-mutilation.
Q: What disease is associated with HLA-A3?
A: Haemochromatosis.
Q: What disease is associated with HLA-B51?
A: Behcet’s disease.
Q: What diseases are associated with HLA-B27?
A: HLA-B27 is associated with ankylosing spondylitis, reactive arthritis, acute anterior uveitis, and psoriatic arthritis.
Q: What disease is associated with HLA-DQ2/DQ8?
A: Coeliac disease.
Q: What diseases are associated with HLA-DR2?
A: HLA-DR2 is associated with narcolepsy and Goodpasture’s syndrome.
Q: What diseases are associated with HLA-DR3?
A: HLA-DR3 is associated with dermatitis herpetiformis, Sjogren’s syndrome, and primary biliary cirrhosis.
Q: What diseases are associated with HLA-DR4?
A: HLA-DR4 is associated with type 1 diabetes mellitus (especially DRB104:01 and DRB104:04) and rheumatoid arthritis.
Q: What is hydroxychloroquine used to treat?
A: Hydroxychloroquine is used in the management of rheumatoid arthritis and systemic/discoid lupus erythematosus.
Q: What is the main adverse effect of hydroxychloroquine?
A: The main adverse effect of hydroxychloroquine is bull’s eye retinopathy, which can lead to severe and permanent visual loss.
Q: What are the 4 types of hypersensitivity reactions in the Gell and Coombs classification?
A: The 4 types are Type I (Anaphylactic), Type II (Cell bound), Type III (Immune complex), and Type IV (Delayed hypersensitivity).
Q: What is the mechanism of Type I hypersensitivity?
A: In Type I hypersensitivity, an antigen reacts with IgE bound to mast cells.
Q: What are some examples of Type I hypersensitivity?
A: Examples include anaphylaxis, asthma, eczema, and hay fever.
Q: What is the mechanism of Type II hypersensitivity?
A: In Type II hypersensitivity, IgG or IgM binds to an antigen on the cell surface.
Q: What are some examples of Type II hypersensitivity?
A: Examples include autoimmune haemolytic anaemia, ITP, Goodpasture’s syndrome, pernicious anaemia, acute haemolytic transfusion reactions, rheumatic fever, and pemphigus vulgaris/bullous pemphigoid.
Q: What is the mechanism of Type III hypersensitivity?
A: In Type III hypersensitivity, free antigen and antibody (IgG, IgA) combine to form immune complexes.
Q: What are some examples of Type III hypersensitivity?
A: Examples include serum sickness, systemic lupus erythematosus, post-streptococcal glomerulonephritis, and extrinsic allergic alveolitis (acute phase).
Q: What is the mechanism of Type IV hypersensitivity?
A: Type IV hypersensitivity is T-cell mediated.
Q: What are some examples of Type IV hypersensitivity?
A: Examples include tuberculosis/tuberculin skin reaction, graft-versus-host disease, allergic contact dermatitis, scabies, extrinsic allergic alveolitis (chronic phase), multiple sclerosis, and Guillain-Barré syndrome.
Q: What is Langerhans cell histiocytosis (LCH)?
A: Langerhans cell histiocytosis is a rare disorder characterized by the proliferation of Langerhans cells, which are specialized dendritic cells that present antigens to T lymphocytes. It can affect multiple organs, including bones, skin, lungs, and the endocrine system.
Q: What are common features of Langerhans cell histiocytosis?
A: Common features include bone pain (typically in the skull or proximal femur), cutaneous nodules, pituitary involvement (leading to diabetes insipidus), pulmonary involvement (dyspnoea, cough, chest pain), recurrent otitis media/mastoiditis, and tennis racket-shaped Birbeck granules on electron microscopy.
Q: What is Marfan’s syndrome?
A: Marfan’s syndrome is an autosomal dominant connective tissue disorder caused by a defect in the FBN1 gene on chromosome 15, which codes for the protein fibrillin-1. It affects about 1 in 3,000 people.
Q: What are the common features of Marfan’s syndrome?
A: Common features include tall stature with arm span to height ratio > 1.05, high-arched palate, arachnodactyly, pectus excavatum, pes planus, scoliosis > 20 degrees, and cardiovascular, ocular, and skeletal manifestations.
Q: What cardiovascular problems are associated with Marfan’s syndrome?
A: Cardiovascular issues include dilation of the aortic sinuses (seen in 90% of patients), which can lead to aortic aneurysm, aortic dissection, and aortic regurgitation. Mitral valve prolapse is also present in 75% of cases.
Q: What is McArdle’s disease?
A: McArdle’s disease is an autosomal recessive type V glycogen storage disease caused by myophosphorylase deficiency, leading to decreased muscle glycogenolysis.
Q: What are the key features of McArdle’s disease?
A: Features include muscle pain and stiffness following exercise, muscle cramps, rhabdomyolysis, myoglobinuria, and low lactate levels during exercise.
Q: What are the main indications for methotrexate?
A: Methotrexate is used in the treatment of inflammatory arthritis (especially rheumatoid arthritis), psoriasis, and some chemotherapy regimens like acute lymphoblastic leukaemia.
Q: What are the common adverse effects of methotrexate?
A: Common adverse effects include mucositis, myelosuppression, pneumonitis, pulmonary fibrosis, and liver fibrosis.
Q: What monitoring is required when prescribing methotrexate?
A: Methotrexate requires regular monitoring of FBC, U&E, and LFTs. FBC, renal, and LFTs should be monitored weekly until therapy stabilizes, then every 2-3 months thereafter. Folate (5mg weekly) should be co-prescribed, taken more than 24 hours after the methotrexate dose.
Q: What are the drug interactions to be aware of when prescribing methotrexate?
A: Methotrexate should not be prescribed concurrently with trimethoprim or co-trimoxazole due to increased risk of marrow aplasia. High-dose aspirin can increase the risk of methotrexate toxicity by reducing excretion.
Q: What is the treatment for methotrexate toxicity?
A: The treatment of choice for methotrexate toxicity is folinic acid.
Q: What are the typical features of myopathies?
A: Myopathies typically present with symmetrical muscle weakness (proximal > distal), with common problems such as difficulty rising from a chair or getting out of a bath. Sensation and reflexes are usually normal, and fasciculations are absent.
Q: What are the common causes of myopathies?
Inflammatory: polymyositis
Inherited: Duchenne/Becker muscular dystrophy, myotonic dystrophy
Endocrine: Cushing’s syndrome, thyrotoxicosis
Alcohol-related myopathy
Q: Which joints are typically affected in osteoarthritis?
A: In osteoarthritis, the typical affected joints include large weight-bearing joints (hip, knee) and the carpometacarpal joint, along with DIP and PIP joints.
Q: Which joints are typically affected in rheumatoid arthritis?
A: In rheumatoid arthritis, the typical affected joints include MCP and PIP joints.
Q: What is the typical history in osteoarthritis?
A: Osteoarthritis typically presents with pain following use, improving with rest, unilateral symptoms, and no systemic upset.
Q: What is the typical history in rheumatoid arthritis?
A: Rheumatoid arthritis typically presents with morning stiffness, improving with use, bilateral symptoms, and systemic upset.
Q: What are the typical X-ray findings in osteoarthritis?
A: X-ray findings in osteoarthritis include loss of joint space, subchondral sclerosis, subchondral cysts, and osteophytes forming at joint margins.
Q: What are the typical X-ray findings in rheumatoid arthritis?
A: X-ray findings in rheumatoid arthritis include loss of joint space, juxta-articular osteoporosis, periarticular erosions, and subluxation.
Q: What are the first-line analgesics for osteoarthritis?
A: Topical NSAIDs are first-line analgesics, particularly beneficial for patients with OA of the knee or hand.
Q: What is the second-line treatment for osteoarthritis?
A: Oral NSAIDs are second-line treatment for osteoarthritis.
Q: What should be co-prescribed with oral NSAIDs?
A: A proton pump inhibitor should be co-prescribed with oral NSAIDs to protect the stomach.
Q: What can be tried if standard pharmacological treatments are ineffective in osteoarthritis?
A: Intra-articular steroid injections may be tried, but they provide only short-term relief (2-10 weeks).
Q: What should be considered if conservative methods fail for osteoarthritis?
A: If conservative methods fail, refer the patient for consideration of joint replacement.
Q: What does LOSS stand for in the context of osteoarthritis?
A: LOSS stands for Loss of joint space, Osteophytes, Subchondral sclerosis, and Subchondral cysts.
Q: What is the primary cause of Osteogenesis Imperfecta?
A: Osteogenesis Imperfecta is caused by an abnormality in type 1 collagen due to decreased synthesis of pro-alpha 1 or pro-alpha 2 collagen polypeptides.
What is the genetic inheritance pattern of osteogenesis imperfecta?
A: Osteogenesis Imperfecta is inherited in an autosomal dominant pattern.
Q: What are the common features of Osteogenesis Imperfecta?
A: Common features include fractures following minor trauma, blue sclera, deafness secondary to otosclerosis, and dental imperfections.
Q: What are the typical investigation results in Osteogenesis Imperfecta?
A: Adjusted calcium, phosphate, parathyroid hormone, and ALP levels are usually normal in Osteogenesis Imperfecta.
Q: What is Osteomalacia?
A: Osteomalacia describes softening of the bones secondary to low vitamin D levels, leading to decreased bone mineral content.
Q: What are the main causes of Osteomalacia?
A: Main causes include vitamin D deficiency, malabsorption, lack of sunlight, chronic kidney disease, drug-induced (e.g. anticonvulsants), inherited (e.g. hypophosphatemic rickets), liver disease (e.g. cirrhosis), and coeliac disease.
Q: What are common features of Osteomalacia?
A: Common features include bone pain, bone/muscle tenderness, fractures (especially femoral neck), and proximal myopathy (which may lead to a waddling gait).
Q: What are the typical investigations for Osteomalacia?
A: Investigations show low vitamin D levels, low calcium and phosphate (in about 30% of patients), and raised alkaline phosphatase (in 95-100% of patients). X-rays may show translucent bands (Looser’s zones or pseudofractures).
Q: What is the treatment for Osteomalacia?
A: Treatment includes vitamin D supplementation (often with a loading dose), and calcium supplementation if dietary calcium is inadequate.
Q: How should patients ≥ 75 years of age be managed after a fragility fracture?
A: Patients ≥ 75 years old who have had a fragility fracture are presumed to have underlying osteoporosis and should be started on first-line therapy (oral bisphosphonate) without the need for a DEXA scan.
Q: According to the 2014 NOGG guidelines, when should treatment be started for patients with a fragility fracture?
A: The 2014 NOGG guidelines suggest treatment should start in all women over 50 years old who have had a fragility fracture, although BMD measurement may sometimes be appropriate, particularly in younger postmenopausal women.
Q: How should patients < 75 years of age be managed after a fragility fracture?
A: For patients under 75 years old, a DEXA scan should be arranged. The results can be entered into a FRAX assessment (along with the history of fracture) to determine ongoing fracture risk.
Q: What are the major risk factors for osteoporosis used by risk assessment tools like FRAX?
History of glucocorticoid use
Rheumatoid arthritis
Alcohol excess
History of parental hip fracture
Low body mass index
Current smoking
Q: Which medications may worsen osteoporosis?
SSRIs
Antiepileptics
Proton pump inhibitors
Glitazones
Long-term heparin therapy
Aromatase inhibitors (e.g., anastrozole)
Q: What are the recommended investigations when diagnosing osteoporosis or after a fragility fracture?
History and physical examination
Blood cell count, sedimentation rate or C-reactive protein, serum calcium, albumin, creatinine, phosphate, alkaline phosphatase, and liver transaminases
Thyroid function tests
Bone densitometry (DXA)
Lateral radiographs of lumbar and thoracic spine/DXA-based vertebral imaging
Protein immunoelectrophoresis, urinary Bence-Jones proteins
25OHD, PTH, serum testosterone, SHBG, FSH, LH (in men), serum prolactin
24-hour urinary cortisol/dexamethasone suppression test
Endomysial and/or tissue transglutaminase antibodies (for coeliac disease)
Isotope bone scan, markers of bone turnover, urinary calcium excretion
Q: What minimum blood tests should be ordered for all patients diagnosed with osteoporosis or a fragility fracture?
Full blood count
Urea and electrolytes
Liver function tests
Bone profile
CRP
Thyroid function tests
Q: What does the T score in a DEXA scan represent?
A: The T score is based on the bone mass of a young reference population and indicates how much a person’s bone mass deviates from the average for a young, healthy person.
Q: What does a T score of -1.0 mean?
A: A T score of -1.0 means the bone mass is one standard deviation below that of the young reference population.
Q: What are the T score categories for interpreting DEXA scan results?
> -1.0 = Normal
-1.0 to -2.5 = Osteopaenia
< -2.5 = Osteoporosis
Q: What is the difference between the T score and the Z score in a DEXA scan?
A: The T score compares bone mass to a young reference population, while the Z score adjusts for age, gender, and ethnic factors.
Q: When should bone protection be started in patients likely to be on glucocorticoids for 3 months or longer?
A: Bone protection should be started immediately in patients who are likely to take glucocorticoids for at least 3 months, rather than waiting until 3 months have passed.
Q: What are the two groups for management of glucocorticoid-induced osteoporosis according to the 2002 Royal College of Physicians guidelines?
A: 1. Patients over 65 years or those who have had a fragility fracture should be offered bone protection.
2. Patients under 65 years should have a bone density scan to determine management.
Q: How is management determined in patients under 65 years with glucocorticoid-induced osteoporosis?
Greater than 0: Reassure
Between 0 and -1.5: Repeat bone density scan in 1-3 years
Less than -1.5: Offer bone protection
Q: What is the first-line treatment for glucocorticoid-induced osteoporosis?
A: The first-line treatment is alendronate. Patients should also be calcium and vitamin D replete.
Q: What is the first-line treatment for osteoporosis in patients at high risk of fragility fractures?
A: Oral bisphosphonates (e.g., alendronate, risedronate)
Q: How is osteoporosis managed in patients who are about to start glucocorticoid treatment?
A: If starting ≥7.5 mg/day prednisolone or equivalent for 3 months or more, start bone protective treatment immediately with oral bisphosphonates (e.g., alendronate, risedronate), without waiting for a DEXA scan.
Q: What is the management for a postmenopausal woman or a man aged ≥50 with a symptomatic osteoporotic vertebral fracture?
A: Start treatment immediately with oral bisphosphonates (e.g., alendronate, risedronate) along with general osteoporosis management.
Q: What are common side effects of bisphosphonates?
A: Gastrointestinal discomfort, oesophagitis, hypocalcaemia, and rare but serious risks like atypical femoral fractures and osteonecrosis of the jaw.
Q: What is Paget’s disease of the bone?
A: Paget’s disease is a disorder of increased, but uncontrolled, bone turnover, primarily affecting osteoclasts. It results in excessive osteoclastic resorption followed by increased osteoblastic activity.
Q: Which bones are most commonly affected by Paget’s disease?
A: The skull, spine/pelvis, and long bones of the lower extremities are most commonly affected.
Q: What are the clinical features of Paget’s disease?
A: Only 5% of patients are symptomatic. The typical presentation includes bone pain (e.g., pelvis, lumbar spine, femur) and an isolated raised alkaline phosphatase (ALP). Untreated features include bowing of the tibia and bossing of the skull.
Q: What are the common investigations for Paget’s disease?
Bloods: Raised alkaline phosphatase (ALP), normal calcium and phosphate (hypercalcaemia may occur with immobilisation)
X-rays: Osteolysis in early disease, mixed lytic/sclerotic lesions later, thickened skull vault
Bone scintigraphy: Increased uptake at sites of active bone lesions
Other markers of bone turnover include PINP, CTx, NTx, hydroxyproline.
Q: What is the first-line management for Paget’s disease?
A: Treatment is indicated for bone pain, skull or long bone deformity, fractures, and periarticular Paget’s disease. First-line treatments include bisphosphonates (oral risedronate or IV zoledronate), with calcitonin being used less frequently.
Q: What are the complications of Paget’s disease?
Deafness (due to cranial nerve entrapment)
Bone sarcoma (1% if affected for >10 years)
Fractures
Skull thickening
High-output cardiac failure
Q: What is polyarteritis nodosa (PAN)?
A: Polyarteritis nodosa (PAN) is a vasculitis that affects medium-sized arteries, causing necrotizing inflammation leading to aneurysm formation.
Q: What are the common features of polyarteritis nodosa?
Fever, malaise, arthralgia
Weight loss
Hypertension
Mononeuritis multiplex, sensorimotor polyneuropathy
Testicular pain
Livedo reticularis
Haematuria, renal failure
Q: What is the association between hepatitis B and polyarteritis nodosa?
A: Hepatitis B serology is positive in about 30% of patients with polyarteritis nodosa.
Q: What imaging findings are suggestive of polyarteritis nodosa?
A: Angiography may show beading and microaneurysms in the intrarenal and intrahepatic vessels. Similar changes may be seen in the arteries of the intestines, with a lack of normal arterial structures.
Q: What is polyarthritis?
A: Polyarthritis refers to the inflammation of five or more joints simultaneously, typically within the first six weeks of symptom onset.
Q: What are the common features of polyarthritis?
Patients with polyarthritis typically present with pain, swelling, and stiffness in multiple joints.
The joint involvement may be symmetrical (e.g., rheumatoid arthritis) or asymmetrical (e.g., psoriatic arthritis).
Systemic symptoms such as fever, weight loss, and fatigue may also be present, reflecting the underlying inflammatory process.
Q: What are the differential diagnoses for polyarthritis?
Inflammatory arthritis (e.g., rheumatoid arthritis, psoriatic arthritis, SLE)
Seronegative spondyloarthropathies
Infective causes (e.g., viral infections like EBV, HIV, hepatitis, mumps, rubella, tuberculosis, disseminated gonococcal infection)
Pseudogout
Henoch-Schonlein purpura
Sarcoidosis
Q: What is polymyalgia rheumatica (PMR)?
A: Polymyalgia rheumatica (PMR) is a relatively common condition seen in older people, characterized by muscle stiffness and raised inflammatory markers. The exact cause is unclear, and while it is closely related to temporal arteritis, it does not appear to be a vasculitic process.
Q: What are the typical features of polymyalgia rheumatica?
Age: Typically seen in patients > 60 years old
Onset: Usually rapid (< 1 month)
Symptoms:
Aching, morning stiffness in proximal limb muscles
Weakness is not a symptom of PMR
Mild polyarthralgia, lethargy, depression, low-grade fever, anorexia, night sweats
Q: What investigations are used for polymyalgia rheumatica?
Raised inflammatory markers, especially ESR > 40 mm/hr
Creatine kinase (CK) and EMG are typically normal
Q: How is polymyalgia rheumatica treated?
First-line treatment is prednisolone, typically starting at 15mg/od
Patients usually show a dramatic response to steroids.
Failure to respond should prompt consideration of an alternative diagnosis.
Q: What is polymyositis?
A: Polymyositis is an inflammatory disorder causing symmetrical, proximal muscle weakness, thought to be a T-cell mediated cytotoxic process directed against muscle fibers. It may be idiopathic or associated with connective tissue disorders and is associated with malignancy.
Q: What is dermatomyositis, and how does it relate to polymyositis?
A: Dermatomyositis is a variant of polymyositis where skin manifestations are prominent, such as a heliotrope rash (purple rash) on the cheeks and eyelids.
Q: What are the clinical features of polymyositis?
Proximal muscle weakness (often with tenderness)
Raynaud’s phenomenon
Respiratory muscle weakness
Interstitial lung disease (e.g. fibrosing alveolitis, organising pneumonia) seen in ~20% of patients, indicating a poor prognosis
Dysphagia and dysphonia
Q: What investigations are used to diagnose polymyositis?
Elevated creatine kinase
Other muscle enzymes (LDH, aldolase, AST, ALT) are elevated in 85-95% of patients
EMG
Muscle biopsy
Anti-synthetase antibodies, especially anti-Jo-1 antibodies, which are associated with lung involvement, Raynaud’s, and fever
Q: How is polymyositis managed?
High-dose corticosteroids tapered as symptoms improve
Azathioprine may be used as a steroid-sparing agent
Q: What is pseudogout?
A: Pseudogout is a form of microcrystal synovitis caused by the deposition of calcium pyrophosphate dihydrate crystals in the synovium. It is also known as acute calcium pyrophosphate crystal deposition disease.
Q: What are the typical clinical features of pseudogout?
Knee, wrist, and shoulder joints most commonly affected
Joint aspiration shows weakly-positively birefringent, rhomboid-shaped crystals
X-ray shows chondrocalcinosis, with linear calcifications of the meniscus and articular cartilage in the knee
Q: How is pseudogout managed?
Aspiration of joint fluid to exclude septic arthritis
NSAIDs or intra-articular, intra-muscular, or oral steroids as for gout
Q: What is psoriatic arthropathy?
A: Psoriatic arthropathy is an inflammatory arthritis associated with psoriasis and is classed as one of the seronegative spondyloarthropathies. It often precedes the development of skin lesions and correlates poorly with cutaneous psoriasis.
Q: What are the common patterns of psoriatic arthropathy?
Symmetric polyarthritis (30-40% of cases, similar to rheumatoid arthritis)
Asymmetrical oligoarthritis (typically affects hands and feet, 20-30% of cases)
Sacroiliitis
DIP joint disease (10%)
Arthritis mutilans (severe deformity of fingers/hands, ‘telescoping fingers’)
uveitis
SIDE (sacroiliitis, iritis, dactylitis, enthesitis)
Q: What are the additional signs of psoriatic arthropathy?
Psoriatic skin lesions
Periarticular disease:
Enthesitis (e.g. Achilles tendonitis, plantar fasciitis)
Tenosynovitis (typically of flexor tendons of the hands)
Dactylitis (diffuse swelling of fingers or toes)
Nail changes: pitting, onycholysis
Q: What is the typical X-ray appearance in psoriatic arthropathy?
Coexistence of erosive changes and new bone formation
Periostitis
‘Pencil-in-cup’ appearance
Q: How is psoriatic arthropathy managed?
Managed by a rheumatologist
Mild peripheral arthritis/axial disease: NSAIDs
Moderate/severe disease: Methotrexate, monoclonal antibodies like ustekinumab (IL-12, IL-23) and secukinumab (IL-17), apremilast (PDE4 inhibitor)
Psoriatic arthritis has a better prognosis than rheumatoid arthritis (RA).
Q: What are the secondary causes of Raynaud’s phenomenon?
Connective tissue disorders:
Scleroderma (most common)
Rheumatoid arthritis
Systemic lupus erythematosus (SLE)
Leukaemia
Type I cryoglobulinaemia, cold agglutinins
Vibrating tools use
Drugs: oral contraceptive pill, ergot
Cervical rib
Q: What are the factors suggesting an underlying connective tissue disease in Raynaud’s phenomenon?
Onset after 40 years
Unilateral symptoms
Rashes
Presence of autoantibodies
Features suggesting rheumatoid arthritis or SLE (e.g., arthritis, recurrent miscarriages)
Digital ulcers, calcinosis
Rarely: chilblains
Q: How is Raynaud’s phenomenon managed?
Referral to secondary care for suspected secondary Raynaud’s phenomenon
First-line treatment: Calcium channel blockers (e.g., nifedipine)
IV prostacyclin (epoprostenol) infusions may have lasting effects for weeks/months.
Q: What is Reactive arthritis?
A: Reactive arthritis is an arthritis that develops following an infection where the organism cannot be recovered from the joint. It is part of the HLA-B27 associated seronegative spondyloarthropathies.
Q: What is the mnemonic for Reactive arthritis symptoms?
“Can’t see, pee or climb a tree”:
See: Conjunctivitis
Pee: Urethritis
Climb a tree: Arthritis, typically affecting large joints (e.g., knees, ankles).
Q: How is Reactive arthritis managed?
Symptomatic treatment with analgesia, NSAIDs, and intra-articular steroids.
Sulfasalazine and methotrexate may be used for persistent disease.
Symptoms rarely last more than 12 months.
Q: What are the main features of Reactive arthritis?
Asymmetrical oligoarthritis (typically in the lower limbs)
Dactylitis
Symptoms of urethritis
Conjunctivitis (seen in 10-30% of patients)
Anterior uveitis
Circinate balanitis (painless vesicles on the coronal margin of the prepuce)
Keratoderma blenorrhagica (waxy yellow/brown papules on palms and soles)
Q: What is the time course of Reactive arthritis?
A: Reactive arthritis typically develops within 4 weeks of the initial infection. Symptoms generally last 4-6 months, with around 25% of patients having recurrent episodes and 10% developing chronic disease.
Q: What is Keratoderma blenorrhagica in Reactive arthritis?
A: Keratoderma blenorrhagica refers to waxy yellow/brown papules found on the palms and soles of patients with reactive arthritis.
Q: What are common respiratory complications of Rheumatoid arthritis (RA)?
Pulmonary fibrosis
Pleural effusion
Pulmonary nodules
Bronchiolitis obliterans
Methotrexate pneumonitis
Pleurisy
Q: What are the 2010 American College of Rheumatology criteria for diagnosing Rheumatoid arthritis (RA)?
Have at least 1 joint with definite clinical synovitis
Have synovitis not better explained by another disease
Q: What is the first-line antibody test for suspected rheumatoid arthritis (RA)?
A: Rheumatoid factor (RF) is recommended as the first-line antibody test for patients with suspected rheumatoid arthritis.
Q: What is anti-cyclic citrullinated peptide antibody (anti-CCP) and its role in rheumatoid arthritis (RA)?
A: Anti-CCP is an antibody that may be detectable up to 10 years before RA. It plays a key role in the diagnosis and allows early detection of patients suitable for aggressive anti-TNF therapy. It has a sensitivity of around 70% and a specificity of 90-95%.
Q: What does NICE recommend for patients with suspected rheumatoid arthritis who are rheumatoid factor negative?
A: NICE recommends testing for anti-cyclic citrullinated peptide antibody (anti-CCP) in rheumatoid factor negative patients.
Q: What x-rays are recommended for patients with suspected rheumatoid arthritis (RA)?
A: NICE recommends performing x-rays of the hands and feet for all patients with suspected rheumatoid arthritis.
Q: What is the recommended initial therapy for rheumatoid arthritis (RA)?
A: The initial therapy for RA includes DMARD monotherapy (disease-modifying antirheumatic drugs) +/- a short-course of bridging prednisolone.
Q: What is essential for monitoring when using methotrexate for rheumatoid arthritis (RA)?
A: Monitoring of FBC (full blood count) and LFTs (liver function tests) is essential due to the risk of myelosuppression and liver cirrhosis. Other side effects include pneumonitis.
Q: How does NICE recommend monitoring response to treatment in rheumatoid arthritis (RA)?
A: NICE recommends using a combination of CRP (C-reactive protein) and disease activity (using a composite score such as DAS28) to assess response to treatment.
Q: How are flares of rheumatoid arthritis (RA) typically managed?
A: Flares of RA are often managed with corticosteroids (oral or intramuscular).
Q: When is TNF-inhibitor therapy indicated in rheumatoid arthritis (RA)?
A: TNF-inhibitors are indicated for patients with inadequate response to at least two DMARDs, including methotrexate.
Q: What is rituximab and how is it used in rheumatoid arthritis (RA)?
A: Rituximab is an anti-CD20 monoclonal antibody that depletes B-cells. It is administered as two 1g intravenous infusions two weeks apart. Infusion reactions are common.
Q: What are the typical features of rheumatoid arthritis (RA)?
A: Rheumatoid arthritis typically presents with swollen, painful joints in the hands and feet, stiffness worse in the morning, and gradual worsening with larger joints becoming involved. The presentation usually develops insidiously over a few months.
Q: What does the ‘squeeze test’ indicate in rheumatoid arthritis (RA)?
A: A positive ‘squeeze test’ in rheumatoid arthritis (discomfort on squeezing across the metacarpal or metatarsal joints) indicates inflammation in the joints.
Q: What are swan neck and boutonniere deformities in rheumatoid arthritis?
A: Swan neck and boutonniere deformities are late features of rheumatoid arthritis and are unlikely to be present in a recently diagnosed patient.
Q: What are the poor prognostic features in rheumatoid arthritis?
A: Poor prognostic features in rheumatoid arthritis include rheumatoid factor positivity, anti-CCP antibodies, poor functional status at presentation, early erosions on X-ray (e.g. after < 2 years), extra-articular features (e.g. nodules), HLA DR4 positivity, and insidious onset.
Q: What are the early X-ray findings in rheumatoid arthritis?
A: Early X-ray findings in rheumatoid arthritis include loss of joint space, juxta-articular osteoporosis, soft-tissue swelling, periarticular erosions, and subluxation.
Q: What is the most common organism causing septic arthritis in adults?
Staph aureus
Q: What is the most common cause of septic arthritis in sexually active young adults?
A: The most common cause of septic arthritis in sexually active young adults is Neisseria gonorrhoeae (disseminated gonococcal infection).
Q: What is the most common location for septic arthritis in adults?
A: The most common location for septic arthritis in adults is the knee.
Q: What are the typical features of septic arthritis?
A: Typical features of septic arthritis include acute, swollen joint, restricted movement (80% of patients), warm to touch/fluctuant joint, and fever (present in the majority of patients).
Q: What is the most important investigation in septic arthritis?
A: Synovial fluid sampling is obligatory in septic arthritis and should be done prior to antibiotic administration if possible.
Q: What is the initial antibiotic treatment for septic arthritis?
A: Intravenous antibiotics covering Gram-positive cocci are indicated, such as flucloxacillin or clindamycin if penicillin allergic.
Q: How long is antibiotic treatment usually given for septic arthritis?
A: Antibiotic treatment for septic arthritis is typically given for 4-6 weeks, with a switch to oral antibiotics after 2 weeks.
Q: What are the management options for septic arthritis?
A: Management options for septic arthritis include intravenous antibiotics, needle aspiration to decompress the joint, and arthroscopic lavage if necessary.
Q: What common feature is shared by seronegative spondyloarthropathies?
A: Seronegative spondyloarthropathies are associated with HLA-B27 and are rheumatoid factor negative.
Q: What type of arthritis is commonly seen in seronegative spondyloarthropathies?
A: Seronegative spondyloarthropathies typically present with peripheral arthritis, which is usually asymmetrical.
Q: What is a characteristic feature of seronegative spondyloarthropathies affecting the spine?
A: A characteristic feature is sacroiliitis, which is inflammation of the sacroiliac joints.
Q: What are the types of spondyloarthropathies included under seronegative spondyloarthropathies?
A: The types of spondyloarthropathies include ankylosing spondylitis, psoriatic arthritis, reactive arthritis, and enteropathic arthritis (associated with IBD).
Q: What is Sjogren’s syndrome?
A: Sjogren’s syndrome is an autoimmune disorder affecting exocrine glands, resulting in dry mucosal surfaces. It can be primary or secondary to other autoimmune diseases like rheumatoid arthritis.
Q: What is the risk associated with Sjogren’s syndrome?
A: Sjogren’s syndrome is associated with a 40-60 fold increase in the risk of lymphoid malignancy.
Q: What are some common features of Sjogren’s syndrome?
A: Common features include dry eyes (keratoconjunctivitis sicca), dry mouth, vaginal dryness, arthralgia, Raynaud’s phenomenon, myalgia, sensory polyneuropathy, recurrent episodes of parotitis, and renal tubular acidosis.
Q: What are the key autoantibodies found in Sjogren’s syndrome?
A: Rheumatoid factor (RF) is positive in nearly 50% of patients, ANA in 70%, anti-Ro (SSA) in 70%, and anti-La (SSB) in 30% of patients with primary Sjogren’s syndrome.
Q: What is the treatment for Sjogren’s syndrome?
A: Treatment includes artificial saliva and tears, and pilocarpine may be used to stimulate saliva production.
Q: What are common features of Still’s disease in adults?
A: Common features include arthralgia, elevated serum ferritin, a salmon-pink maculopapular rash, pyrexia (rises late afternoon/evening), lymphadenopathy, and negative rheumatoid factor (RF) and anti-nuclear antibody (ANA).
Q: What is the pattern of fever seen in Still’s disease in adults?
A: Fever in Still’s disease typically rises in the late afternoon/early evening and is often associated with worsening joint symptoms and the rash.
Q: What is the first-line treatment for Still’s disease in adults?
A: NSAIDs are used first-line to manage fever, joint pain, and serositis. They should be trialled for at least a week before considering steroids.
Q: What type of drug is sulfasalazine and what conditions is it used to treat?
A: Sulfasalazine is a disease-modifying anti-rheumatic drug (DMARD) used in the management of inflammatory arthritis, especially rheumatoid arthritis, and inflammatory bowel disease.
Q: What are the cautions for using sulfasalazine?
A: Sulfasalazine should be used with caution in patients with G6PD deficiency and those with an allergy to aspirin or sulphonamides (due to cross-sensitivity).
Q: What are some adverse effects of sulfasalazine?
A: Adverse effects include oligospermia, Stevens-Johnson syndrome, pneumonitis / lung fibrosis, myelosuppression, Heinz body anaemia, megaloblastic anaemia, and staining of tears (which can stain contact lenses).
Q: What are the general features of Systemic Lupus Erythematosus (SLE)?
A: Fatigue, fever, mouth ulcers, and lymphadenopathy.
Q: What are the skin features of Systemic Lupus Erythematosus (SLE)?
A: Malar (butterfly) rash (spares nasolabial folds), discoid rash (scaly, erythematous, well-demarcated rash in sun-exposed areas), photosensitivity, Raynaud’s phenomenon, livedo reticularis, and non-scarring alopecia.
Q: What are the musculoskeletal features of Systemic Lupus Erythematosus (SLE)?
A: Arthralgia and non-erosive arthritis.
Q: What are the cardiovascular features of Systemic Lupus Erythematosus (SLE)?
A: Pericarditis (most common cardiac manifestation) and myocarditis.
Q: What are the respiratory features of Systemic Lupus Erythematosus (SLE)?
A: Pleurisy and fibrosing alveolitis.
Q: What are the renal features of Systemic Lupus Erythematosus (SLE)?
A: Proteinuria and glomerulonephritis (with diffuse proliferative glomerulonephritis being the most common type).
Q: What are the neuropsychiatric features of Systemic Lupus Erythematosus (SLE)?
A: Anxiety and depression, psychosis, and seizures.
Q: What is the antibody investigation result in Systemic Lupus Erythematosus (SLE)?
99% of patients are ANA positive, which is a useful rule-out test, but it has low specificity.
20% are rheumatoid factor positive.
Q: What is the significance of anti-dsDNA in Systemic Lupus Erythematosus (SLE)?
A: Anti-dsDNA is highly specific (>99%) for SLE but has lower sensitivity (70%).
Q: What is the significance of anti-Smith in Systemic Lupus Erythematosus (SLE)?
A: Anti-Smith is highly specific (>99%) but has low sensitivity (30%).
Q: What are other antibodies associated with Systemic Lupus Erythematosus (SLE)?
A: Anti-U1 RNP, SS-A (anti-Ro), and SS-B (anti-La).
Q: What are the monitoring investigations for Systemic Lupus Erythematosus (SLE)?
ESR is commonly used.
During active disease, CRP may be normal, and a raised CRP may indicate an underlying infection.
Complement levels (C3, C4) are low during active disease due to consumption by immune complexes.
Anti-dsDNA titres can be used for disease monitoring (but not present in all patients).
Q: What are the basic management strategies for Systemic Lupus Erythematosus (SLE)?
A: NSAIDs and sun-block are essential for basic management.
Q: What is the treatment of choice for Systemic Lupus Erythematosus (SLE)?
A: Hydroxychloroquine is the treatment of choice for SLE.
Q: What is the characteristic feature of Systemic Sclerosis?
A: Systemic sclerosis is characterized by hardened, sclerotic skin and other connective tissues.
Q: What is CREST syndrome in Systemic Sclerosis?
A: CREST syndrome is a subtype of limited cutaneous systemic sclerosis characterized by Calcinosis, Raynaud’s phenomenon, Esophageal dysmotility, Sclerodactyly, and Telangiectasia.
Q: What is the main feature of limited cutaneous systemic sclerosis?
A: In limited cutaneous systemic sclerosis, scleroderma predominantly affects the face and distal limbs, and it is associated with anti-centromere antibodies.
Q: What is the main feature of diffuse cutaneous systemic sclerosis?
A: In diffuse cutaneous systemic sclerosis, scleroderma predominantly affects the trunk and proximal limbs, and it is associated with anti-scl-70 antibodies.
Q: What are the key features of Temporal Arteritis?
A: Key features include headache (85%), jaw claudication (65%), vision problems (amaurosis fugax, vision loss), tender, palpable temporal artery, and features of Polymyalgia Rheumatica (PMR) in around 50% of patients.
Q: How is Temporal Arteritis diagnosed?
A: Diagnosis is supported by raised inflammatory markers (ESR > 50 mm/hr, CRP), temporal artery biopsy (showing skip lesions), and normal creatine kinase/EMG.
Q: What is the initial treatment for Temporal Arteritis?
A: High-dose glucocorticoids (e.g., prednisolone) should be given urgently as soon as Temporal Arteritis is suspected. If visual loss is evolving, IV methylprednisolone is usually given before starting oral steroids.
Q: Why is urgent ophthalmology review necessary in Temporal Arteritis?
A: Urgent ophthalmology review is necessary because visual damage can be irreversible if not treated promptly.
pneumonic for all nerve supplies
C1, 2 - Look at your shoe- Neck flexion/extension
C3 - A fallen tree - Neck lateral flexion
C4 - I’m not sure - Shoulder elevation
C5 - Arms out wide - Shoulder flexion, abduction, & lateral rotation
C6, 7, 8 - Close the gate - Shoulder extension, adduction & medial rotation
C5, 6 - Pick up sticks - Elbow flexion
C7, 8 - Lay them straight - Elbow extension
C5, 6 - Flick my wrists - Forearm supination
C7, 8 - The time is late - Forearm pronation
C6, 7 - Fly up to heaven - Wrist flexion & extension
C7 - Paper - Finger extension
C8 - Rock - Finger flexion (though some sources say C7, 8 does both finger extension and flexion)
T1 - Scissors - Finger abduction & adduction
(T1-12 - Supplies chest wall and abdominal muscles)
(L1 - Contributes to hip flexion & adduction)
Kicking a ball:
L2, 3 - Lift my knee - Hip flexion
L3, 4 - Kick the door - Knee extension (& knee-jerk reaction)
L4, 5 - Foot points to the sky - Ankle dorsiflexion
Bringing foot back to the floor:
L4, 5 - Extend my thigh - Hip extension
L5, S1, (S2) - Kick my bum (Run to poo) - Knee flexion
S1, 2 - Stand on my shoes - Ankle plantarflexion (& ankle jerk)
(Babinski plantar reflex/extensor response in UMN lesion is L5, S1, S2)
L2, 3, 4 - Modestly close the door - Hip adduction & internal/medial rotation
L4 - S2 - The opposite is true - Hip abduction & external/lateral rotation
[ SUPPLIES ]
C3, 4, 5 - Keeps the diaphragm alive â→ Innervates the diaphragm
S2, 3, 4 - Keeps s*** off the floor â→ Innervates bowel, bladder, sex organs, anal sphincter, pelvic muscles. (& anal wink reflex)
What is typical for pain in compartment syndrome
pain on passive stretch
positive simmonds sign
achilles rupture
Q: What is the most common cause of posterior heel pain?
A: Achilles tendon disorders.
Q: What are common features of Achilles tendinopathy (tendinitis)?
A: Gradual onset of posterior heel pain that worsens following activity, and morning pain and stiffness.
Q: What is the typical management for Achilles tendinopathy (tendinitis)?
A: Supportive management, including simple analgesia, reduction in precipitating activities, and calf muscle eccentric exercises (self-directed or physiotherapy-guided).
Q: What is the initial imaging modality of choice for suspected Achilles tendon rupture?
A: Ultrasound.
Q: What action should be taken following a suspected Achilles tendon rupture?
A: An acute referral to an orthopaedic specialist should be made.
which metatarsal most commonly gets stress fractures
2ns
pneumonic to distinguish between galeazzi and monteggia fracture
GRIMUS helps to remember which forearm bone is fractured and whether the distal (‘inferior’) or proximal (‘superior’) part of the bone is involved
* G: Galeazzi
- R: radius
- I: inferior
* M: Monteggia
- U: ulna
- S: superior
What does the straight leg raise test
sciatic nerve, L4-S1
management of scaphoid fracture
repeat xray 7-10 days later. MRI to check for avascular necrosis
if its an intracapsular fracture but they are old frail etc how do you treat
hemiarthroplasty rather than total hip replacement
What two fractures are most linked to compartment syndrome
supracondylar fractures and tibial shaft injuries
what relieves pain in spinal stenosis
sitting down and leaning forward
What should you do if theres ever neurovascular concern in a fracture (tingling etc)
Refer to surgeon
What are features of iliotibial band syndrome
tenderness 2-3cm above the lateral joint line
lateral knee pain
occurs in runners
What are features of subluxation of the radial head (pulled elbow)
most common upper limb injury in children under the age of 6
elbow pain and limited supination and extension of the elbow
How do you manage subluxation of the radial head
analgesia and passively supination of the elbow joint whilst the elbow is flexed to 90 degrees
For rib fractures, if analgesia doesnt work, what should you try
nerve blocks
What are features of flexor sheath tenosynovitis
- Surgical emergency
- Caused by human and animal bites (metacarpal strikes a tooth)
- Kanavel’s signs: fusiform swelling, tenderness over flexor sheath, semiflexed posture, pain on passive extension
- I.V antibiotics with elevation
- Mx Surgical debridement
Can lead to fibrosis and contractures which can be very disabling
What examination do you initially do for sarcomas
x ray
‘fracture of the proximal pole of a carpal bone’ management
scaphoid pole fracture - surgical fixation
How do scaphoid fractures present
Pain along the radial aspect of the wrist, at the base of the thumb
Loss of grip / pinch strength
Pain on longitudinal compression of the thumb
What are features of Subacromial impingement
painful arc syndrome
this is typically between 60 and 120 degrees. With rotator cuff tears the pain may be in the first 60 degrees
How do you manage webers A, B and C
Weber A: cast/boot and weight bear as tolerated
Weber B: cast/boot and weight bear as tolerated but if talar shift, ORIF
Weber C (unstable): ORIF
Follow-up in 6-8 weeks
Psoas sign for psoas abscess
discomfort upon hip extension
After starting alendronate for osteoporosis, what should you do in terms of fracture risk
reassess after 5 years
How should bisphosphonates be taken
Oral bisphosphonates should be swallowed with plenty of water while sitting or standing on an empty stomach at least 30 minutes before breakfast (or another oral medication); the patient should stand or sit upright for at least 30 minutes after taking
What is the link between osteoporosis and testosterone
Testosterone blood tests are important when suspecting osteoporosis in a man. Hypogonadism is a common cause of osteoporosis in men.
Malignancy + raised CK?
polymyositis
How do you differentiate between polymyositis and PMR
polymyositis has raised CK
What TB drug can lead to drug induced lupus
isoniazid
What examination should you do before starting TNF inhibitors
chest xray for TB as biologics can cause reactivation
What age group does temporal arteritis occur in
60+
How does joint aspirate in RA look like
high WBC count, predominantly PMNs. Appearance is typically yellow and cloudy with absence of crystals. ‘Sterile synovial fluid’
What is the first thing to do when suspecting dermatomyositis
urgent referral - link to malignancy
What is the most likely cause of STI resulting in reactive arthritis
chalmydia
What are features of Felty’s syndrome
RA + splenomegaly + low white cell count
Which TB drugs can increase uric acid levels
pyrazinamide and ethambutol
which antibody is most specific to drug induced lupus
anti histone
What is a common risk factor for pseudogout
haemochromatosis
Is CRP and ESR high in SLE
Only ESR, high CRP suggests infection
What type of antibiotics increase risk of tendon injuries
fluoroquinolones eg ciprofloxacin
facial rash, lymphadenopathy, dyspnoea and fatigue
sarcoidosis - lupus pernio (PURPLE rash)
purple facial rash
lupus pernio - sarcoidosis
additional screening done for dematomyositis
CT to check for malignancy
When can you weight bare after hip fracture surgery
immediately
Management for achilles tendonitis
rest, nsaids, physio
most common eye findings in temporal arteritis
anterior ischemic optic neuropathy - Fundoscopy typically shows a swollen pale disc and blurred margins
Where is the pain in avascular necrosis of hip
anterior groin
Management for Webers A,B and C fractures
Weber A -> 99% of times CAM boots as ankle is fine.
Weber B -> need radiograph (mortis view) to assess syndesmosis + mortis for ankle stability. It there is instability as ligaments are affect -> surgery. If not, then CAM boot.
Weber C -> 99% of times fracture will involve syndesmosis -> ankle instability -> required surgery (ORIF)
what should be prescribed with methotrexate
folic acid to prevent bone marrow suppression
What type of shoulder dislocation is linked to seizures and electric shock
posterior
What type of shoulder dislocation is linked to FOOSH
anterior
shoulder is locked in an internally rotated position
posterior dislocation
Difference between ulnar lesions at wrist vs at elbow
Ulnar injury at wrist : marked claw
Ulnar injury at elbow : less claw but get worse before getting better
What score do you use to assess hypermobility
Beighton Score
In gout, when should you start allopurinol
2-4 weeks after episode
What type of analgesia is used for people with hip fracture
Iliofascial nerve block
or spinal anaesthesia during surgery
how does meralgia paraesthetica present
numbness and pain over the lateral skin of the left/right thigh
What effect does SLE have on neutrophils
causes neutropaenia due to Autoimmune destruction of neutrophils
which artery is affected in avascular necrosis
medial circumflex femoral
Distal sensory loss, tingling + absent ankle jerks/extensor plantars + gait abnormalities/Romberg’s positive
subacute combined degeneration of the spinal cord
