Musc Flashcards

Question

What does myelo mean?

Answer 1

SC or BM related

Answer 2

An idiopathic pain syndrome characterised by >3months of widespread body pain, defined by pain in 11+/18 regions (tender point sites) with 4kg force, defined by american college rheumatology.

Answer 3

Other pain syndromes, female, rheumatoid disease, 20-60, FHx

Answer 4

Diffuse pain on palpation, chronic | Cog dec, sleep disturbance, fatigue unrelieved by rest, mood disturbance, numbness/tingling, stiffness, axial headaches

Answer 5

Clinically - 11+/18 Rule out hypothyroid, vit D def, B12 def, RHf, ID anaemia, SLE

Answer 6

Mono/oligo articular syndrome resulting from the deposition of urate crystals. Further causes renal glomerular, tubular and interstitial disease.

Answer 7

Foot-ankle-knee-finger-wrist-elbow

Answer 8

Male, BEER, MEAT, FISH, aspirin, pyrazinimide, diuretics, inc age, DM, adiposity

Answer 9

``` Acute onset pain + Tenderness Swelling and erythema Limited joint motion Stiffness - morning = inflammatory Tophi - crystal deposition in skin - elbows, Achilles heal, ear, feet, knees MONO/OLIGO ```

Answer 10

ASPIRATE ASPIRATE joint space (atheroscentesis) - INC WCC in aspirate - Negative birfringence testing (confirms gout vs pseudo) Uric acid levels serum - increased >416men, >360 F X-ray of affected joint - punched out periarticular lesions USS - erosions, tophi, double contour

Answer 11

PPP - PSUEDOGOUT - calcium PYROPHOSHATE, POSITIVE birefrigence, PALE X-ray calcification of tendons/joints

Answer 12

Inc age, >15% of over 65s | Gout, injury, HPTism (inc ca), haemochromatosis, FHx, hypomag/phos

Answer 13

Shoulders, MCP, wrist Effusion and fluctuance more common CAN GET A FEVER

Answer 14

Atheroscentesis - In general pseudo = tends to be bloodier - No WCC, +ve BIREFRINGENCE X-ray - calcification of tendons, joint edges, sub chondral cysts, joint degeneration Mg, ALP = N/L

Answer 15

A mono/oligoarthritis caused by pathogenic infection of a joint. Direct/haematogenous

Answer 16

Inc age, immunosuppression, DM, IVDU, prosthesis, breaks in skin, corticosteroid injection,

Answer 17

Erythematous, warm, swollen, limited motion, Fever Acute onset/short duration

Answer 18

``` Synovial fluid aspiration + culture + gram stain (empirical) Blood culture, WCC ESR CRP UP Plan radiograph - extent of disease MRI - if suspect osteomyelitis ```

Answer 19

A complex multifactoral disease characterised by low back pain w/w/o the features of radiculopathy confirmed disc disease

Answer 20

Old age, occupation, DM, smoking, abnormal pelvic morphology, changes in Sagittal alignment.

Answer 21

LOWER back pain, pain on motion, restriction of motion +/- radiculopathy signs - radicular leg pain - neuro symptoms if cauda equina compression/radicular - bladder/bowel/weakness/sensory loss STRAIGHT LEG SIGN = pain on straight leg raise = inflammatory /compromise nerve root.

Answer 22

CT myelography - narrowing foramina/compromise Lumbar X-ray/MRI - disc osteophytic changes, disc space narrowing, foraminal narrowing X-ray with exten/flex - abnormal movement Discography = pain on insertion of dye shows disease presence, allows visualisation of discs

Answer 23

Result of biological and mechanical factors that destabilise the normal process of degredation and synthesis of articular cartilage chondrocytes, Extra cellular matrix and subchondral bone. Entire joint affected - articular cartilage loss, sclerosis of bone and osteophyte formation.

Answer 24

Female, BMI inc, genetic (50%), abnormal anatomy, occupation

Answer 25

``` Oligo/Poly (can be mono) Stiffness in morning lasts <30mins Pain ease with rest Limited motion + pain on motion SPARE THE MCP (rh doesn't) Heberdens / bouchards Crepitus Usually weight baring joints. ``` Can have antalgic gait + effusions (rare)

Answer 26

X-ray - joint space narrowing, subchndral sclerosis and osteophytes CRP ESR WCC - N RF anti CCP - -ve MRI - show cartilage loss (better for soft tis)

Answer 27

Staphylococcus + Streptococcus

Answer 28

Staph aureus | Ecoli and group B strep also cause

Answer 29

Infection of the bone either haemategenously or contiguous

Answer 30

``` Limited motion Pain = non specific + vague Swelling, erythema Low grade fever - 1-3 months duration Urinary tract symptoms Malaise and fatigue ```

Answer 31

``` WCC ESR CRP - H Culture fluid aspirate/blood X-ray - areas of infection appear DARK, soft tissue swelling, periosteal thickening Can do MRI/CT Sinus tract culture (consider) ```

Answer 32

An inflammatory arthritis occurring after exposure to certain GU/GI infections. Commonly a triad of post infectious arthritis, non genococcal urethritis, conjunctivitis

Answer 33

Salmonella + campylobacter+shigella + yersinia -> diarrhoea | Chlamydia trachomatis

Answer 34

Male, B27, Preceding chalmidyal / GI infection

Answer 35

``` Peripheral arthritis = asymmetrical Usually involves lower limbs Often enthesitis - where tendons connect to bone Fever, fatigue and WL Non spec pain - exercise makes better ``` keratoderma blennorrhagium - pustular thickening on soles / hands Circulate balantidis - single painless lesion on shaft/glans Ant Uveitis + conjunctivitis Cardiac manifestations - Aortitis - AR -> HF

Answer 36

``` ESR CRP - H NO ELEVATED WCC ANA RF neg X-ray - enthesopathy / sacroiliitis Atheroscentesis - NEG WCC B27 - often pos NAAT for gonorrheoa/chalmidya ```

Answer 37

A chronic, systemic inflammatory disorder affecting 1% of the population. Most common arthritis seen by physicians. M:F 1:2

Answer 38

B27, PTPN22 | Weak = smoking

Answer 39

Stiffness in morning >1hr Limited motion Pain + swelling Active SYMMETRICAL arthritis Commonly affects small bones in hand/feet first NEVER DIPS, DOES HAVE MCPS Swann neck, boutonnière, rheum nodules (extensor surf) Pluritic pain, scleritis, uveitis, vasculitic lesions

Answer 40

Clinical + RF 60%, + antiCCP 70% X-ray - late stage - erosions. Begin at joint margins (where no cartil) Psoriatic arthritis = most similar - also small joints BUT less symmetrical and associated psoriasis

Answer 41

A chronic granulomatous disorder characterised by lymphocyte and macrophage infiltration to the lungs. Can affect virtually any organ. Lung + LNs affected in >90%. Inc in female and scandinavians/areas where TB/MM + b burgdorfi endemic.

Answer 42

20-40, female, non smoker, scandinavian, black=uveitis seen, european=erythemanod

Answer 43

Dyspnoea, DRY cough, wheezing, rhonchi, Lymphadenopathy, fatigue Erythema nod, uveitis, lupus pernio Low grade fever, hepatomegaly, seizures, HB

Answer 44

CXR - bilateral lymphadenopathy - hilar or paratracheal, predominantly apical bilateral infiltrates, pleural eff poss EBUS with aspiration - non caseating granulomas Skin biopsy - non caseating granulomas THINK ABOUT MACRO+LYMPH MIGRATION FBC - anaemia , leukopenia LFT - all raised SERUM ACE INC

Answer 45

The most common systemic a/i disorder, characterised by dry eyes and mouth a a consequence of lymphocytic invasion into the lacrimal and salivary glands. F:M 9:1 60% secondary

Answer 46

Female, 20s-30s, 50+ secondary to RhA, scleroderma and SLE HLA II

Answer 47

``` Dry eyes, dry mouth, fatigue Dry mouth causes - low saliva pool, burning mouth, increased infections Dry eyes - corneal ulceration Arthralgia/myalgia Large salivary glands Vasculitis ```

Answer 48

Anti60KD-RO and Anti-La antibodies Shwirmers test = <5mm paper wetted after 5 mins in eye Saliometry =

Answer 49

A granulomatous vasculitis characterised by the narrowing of large and medium sized vessels. Primarily affects the branches of the external carotid. Most common systemic vasculitis in adults

Answer 50

Female, 50+, atherosclerosis, smoking, infections

Answer 51

Headache (temporal/occipital), PMR symptoms (neck/shoulder stiffness) LOSS OF VISION (20%) - caution Jaw claudication Claudication in lower extremities if large vessel inclusive Absent temporal pulse, bruit if large vessel

Answer 52

ESR >50. CRP HH FBC - normochromic normocytic anaemia with inc plts LFTs - ASTALTALP raised TEMPORAL ARTERY BIOPSY - display granulomatous infiltration USS of TEMPORAL - show HALO sign - thickening of the wall/stenosis/occlusion

Answer 53

Plantar fasciitis is an acute or chronic pain in the inferior heel at the attachment of the medial band of the plantar fascia to the medial calcaneal tubercle. It has been described as a chronic inflammatory process and may be an overuse injury. Pain is worst when taking the first few steps out of bed in the morning and after periods of rest. Although an aggravating condition, pain is self-limiting and usually resolves between 6 to 18 months without treatment. Most commonly affects people between 40 and 60 years of age who are overweight or obese. Also occurs in 10% of runners. Diagnosis is usually based on a thorough history and physical examination. There is no laboratory test that can confirm or rule out the diagnosis. Plain film x-rays are of little benefit in typical cases, although they may be helpful in ruling out other pathology. Infracalcaneal spurring is found in only 39% to 50% of cases. Non-surgical treatment is the standard of care for acute heel pain, although 10% of cases are recalcitrant and unresponsive to non-surgical care in 12 months. In recalcitrant cases, surgery has been shown to be generally effective. Conservative treatment involves combination therapy (e.g., heel padding, shoe changes, low-Dye strapping, non-steroidal anti-inflammatory drugs, and stretching exercises).

Answer 54

Plantar fasciitis is the most common cause of infracalcaneal pain and accounts for 11% to 15% of all foot complaints that require professional treatment. It occurs in about 10% of people who run regularly peaks between the ages of 40 and 60 years.

Answer 55

The true aetiology of the condition is unknown. However, several predisposing factors have been suggested including equinus, pes planus, pes cavus, obesity, and prolonged standing on hard surfaces such as concrete. Most of these suggestions are based on case series and have not been shown to be directly associated.

Answer 56

STRONG Obesity Equinus - Gastrocnemius or gastroc-soleus equinus is an inability to reach 10 degrees of dorsiflexion at the ankle joint. This puts excessive strain on the plantar fascia during gait and predisposes to plantar fasciitis ``` WEAK Pes planus Pes cavus >40yo Hx prolonged standing Runners ```

Answer 57

Heel pain - stabbing Relief with rest Post static dyskinesia (pain) Pain worse walking bare foot No Hx of injury Improvement with NSAIDs Self limiting Unilateral Positive dorsiflexion-eversion test - Pain with dorsiflexion of the ankle joint and eversion of the subtalar joint. Windlass test - Pain with metatarsophalangeal joint extension. Negative Tinel's sign - Paraesthesia with percussion of the tibial nerve or its branches. Performed on every patient to rule out nerve entrapment, tarsal tunnel, and neuritis.

Answer 58

Clinical X ray if suspicion of a stress fracture or other cause of heel pain.

Answer 59

``` Rest + management of RFs NSAIDS Stretching Low dye taping Foot orthotics Night splint ``` Possible steroid injection Extra corporeal shockwave therapy Surgery - considered for patients who have persistent and severe symptoms, and who have failed 6 to 12 months of conservative care.

Answer 60

Controlled randomised studies typically compare combination therapies rather than relying on a single treatment to provide complete long-term resolution. Studies also vary in their means of measurement of a successful outcome, frequently relying more on patients' subjective reports than on a single objective measurement tool. Nonetheless, the outcome for individuals with acute plantar fasciitis has been studied and is usually favourable. Recurrence of plantar fasciitis is not the most common course. If pain does recur, treatment should be resumed at once.

Answer 61

plantar fasciitis

Answer 62

Bursitis is an acute or chronic inflammatory condition of a bursa. A bursa is a jelly-like sac that usually contains a small amount of synovial fluid. A bursa lies between a tendon and either bone or skin to act as a friction buffer and facilitate movement of adjacent structures. Over 150 bursae are located throughout the human body. Some are superficial and more vulnerable; others are deeper and better protected. In primary care, bursitis most commonly presents in the knee, subacromial (subdeltoid), trochanteric, retrocalcaneal, and olecranon bursae. The acute or chronic inflammation of a bursa. A bursa is a sac containing a small amount of synovial fluid that lies between a tendon and either skin or bone to act as a friction buffer. There are >150 bursae in the body and these can be deep (e.g., the subacromial bursa) or superficial (e.g., the olecranon bursa). In bursitis there is thickening and proliferation of the synovial lining, bursal adhesions, villus formation, tags, and deposition of chalky deposits. This may result from repetitive stress, infection, autoimmune disease, or trauma. Key diagnostic findings are localised pain and tenderness over a bursa and swelling if superficially sited. Treatment for non-septic bursitis involves modified physical activity, rest, and analgesia. Corticosteroid injections are reserved for those cases that do not respond to conservative management. Bursal excision is a last resort. The first-line treatment for septic bursitis is aspiration and antibiotic therapy. Surgical debridement and lavage may be required.

Answer 63

The epidemiology of bursitis is unclear, and reliable data for incidence, age, and sex predilection or geographical spread are not available. A retrospective cohort study published in 2005 found trochanteric pain (not restricted to trochanteric bursitis) to be a significant chronic disease affecting 1.8 in 1000 patients per year.

Answer 64

The aetiology of bursitis is unknown. The term bursitis suggests inflammation in one of several bursae in the body. This inflammation may be caused by a number of different processes: Repetitive injury or acute trauma: any repetitive pattern of movement that puts pressure on a bursa, such as compression of the subacromial bursa under the coracoacromial arch. An alteration in gait pattern caused by lower limb discrepancy or iliotibial band contracture may affect the stresses on the subtrochanteric bursa. Certain professions have been thought to be more at risk of certain types of bursitis due to repetitive action in their daily work; this led to the colloquial naming of 'clergyman's knee' and 'student's elbow' for infrapatellar and olecranon bursitis, respectively. Poorly fitting footwear can cause retrocalcaneal bursitis by exerting excessive pressure on the heel. Crystal deposition secondary to gout or pseudogout: crystal arthropathy can result in crystal deposition within the bursa and subsequent inflammation of the synovial lining, resulting in bursitis. Bursitis can also be the first presenting feature of a crystal arthropathy. Autoimmune disease: e.g., rheumatoid arthritis has been associated with bursitis. Infection, acute or chronic: may follow a penetrating injury from a foreign body. Osteoarthritis of the hip: has been implicated as a cause of trochanteric bursitis through osteophyte deposition, but this remains unproven.

Answer 65

``` WEAK Occupational (stress) RhA Gout/pseudo Penetrating injury Osteoarthritis of hip Infection in nearby joint Lower limb length discrepancy Iliotibial band contracture Lumbar spondylosis Valgus knee deformity Low-riding shoes Anatomical or functional ```

Answer 66

``` COMMON Pain at bursa site Tenderness to palpation Possible reduced range of motion RFs Low grade temp (septic bursitis) Swelling Erythema (septic B) Warmth (septic B) Painful arc - (subacromial bursitis) Lateral hip pain (trochanteric) Pseudoradiculopathy = trochanteric bursitis Impalpable patella (prepatellar bursitis) Palpable bump over heal (retrocalcaneal) ```

Answer 67

Clinical If infected -> aspirate

Answer 68

Non-septic Conservative management involves avoiding activities that worsen symptoms and resting the affected area. Ice can be used to reduce swelling in the first 24 hours by topical application every few hours. Many patients with trochanteric and infrapatellar bursitis find crutches or a walking stick useful. Gentle mobilisation exercise is important to maintain range of movement in a joint, particularly in the shoulder. Simple analgesia such as paracetamol or non-steroidal anti-inflammatory drugs (NSAIDs) can be given for pain relief. These agents can also be used in combination. 2. Corticosteroid injection 3. Surgery SEPTIC ABx + aspiration (MC+S) May need surgical debridement / lavage

Answer 69

Most patients respond well to conservative management and recover completely. Those who participate in sport or have an occupation entailing repetitive activity that is likely to have precipitated the bursitis will benefit from advice on modifying their activity and using protection to prevent recurrence.

Answer 70

Infection Tendon rupture secondary to steroid injection Septic arthritis

Answer 71

bursitis Presenting symptoms and signs vary according to the anatomical site of the affected bursa, but localised swelling and fluctuance are usually present. Male patients with inflammation of the iliopsoas or iliopectineal bursa can present with chronic back and hip pain that radiates into the scrotum and down the anterior aspect of the thigh and is refractory to both surgical and medical management

Answer 72

Epicondylitis of the elbow is a condition associated with repetitive forearm and elbow activities. Both lateral epicondylitis (commonly known as tennis elbow) and medial epicondylitis (commonly known as golfer's elbow) are characterised by elbow pain during or following elbow flexion and extension. A combination of poor mechanics, microtears in areas of hypoperfusion, and a delayed healing response contribute to the pathophysiology of the condition. Typically occurs during the 4th and 5th decades of life. Patients describe a history of activities contributing to overuse of the forearm muscles that originate at the elbow. People with lateral epicondylitis are tender approximately 1 cm distal and anterior to the lateral epicondyle. They report pain during resisted wrist and digit extension, and during passive wrist flexion with the elbow extended. People with medial epicondylitis have tenderness along the medial elbow, approximately 5 mm distal and anterior to the medial epicondyle. Pain is exacerbated with resisted forearm pronation and resisted wrist flexion. Most patients will have complete resolution of symptoms with arm rest and non-steroidal anti-inflammatory drug (NSAID) therapy. Patients with continued symptoms may require further treatment, including physiotherapy, injection therapy, or surgical debridement. The principal complication is continued pain. All other complications may arise from interventions attempting to alleviate the pain.

Answer 73

1.3% to 3% laterally, and 0.4% to 5% medially, in a population sample of people aged 30 to 64 years. Current epidemiological studies on epicondylitis have failed to demonstrate incidence rate differences between sexes or ethnic groups 4th and 5th decades of life are at a significantly increased risk

Answer 74

Repetitive motion of the elbow and forearm over prolonged periods of time prompts the development of both medial and lateral epicondylitis. Many recreational and occupational activities have been implicated. These include: ``` Tennis Fencing Golf Rowing Baseball (pitching) Hammering Typing Meat-cutting Plumbing Painting. ```

Answer 75

``` STRONG 40-60 Hx Repetitive activitys Poor mechanics during activites Inadequate physical conditioning Smoking ``` WEAK Improper equipment Obesity Symptoms occurring on same side as hand predominance

Answer 76

COMMON Elbow pain Worse with repetition Decreased grip strength (Lateral) Reproducible pain over the origin of the common extensor mass when the arm is placed in extension while the examiner maximally flexes the wrist. (Lateral ) Reproducible pain over the origin of the common extensor mass when the arm is extended and the patient is asked to resist an applied force at the wrist. increased pain with resisted forearm pronation or wrist flexion (medial epicondylitis) ``` Normal range of movement at elbow Normal sensation Tinels neg Weak wrist extension (lat) Swelling ```

Answer 77

initial presentation 1st line – rest + ice + NSAID + brace/strap No response at 6w Physio + lidocaine injection No response at 6-12m Surgery EC-shock wave therapy Other injection modalities, including autologous blood, platelet-rich plasma, hyaluronic acid, and botulinum toxin, have been proposed as treatments for recalcitrant lateral and medial epicondylitis.

Answer 78

The prognosis for both medial and lateral epicondylitis is excellent. The mainstay of treatment for both continues to be elbow and forearm rest, ice, oral non-steroidal anti-inflammatory drugs (NSAIDs), and orthotics. These therapeutic interventions resolve the majority of the patients' symptoms Recent reports indicate that about 90% of lateral epicondylitis patients will have normal elbow motion and be participating in athletic pursuits 10 years post-surgery.

Answer 79

Fat atrophy after corticosteroid Hypopigmentation after corticosteroid injection Scar formation post surgery Infection post surgery Grip strength weakness post surgery The ulnar nerve on the medial side of the elbow poses the greatest risk with medial epicondylitis surgery.

Answer 80

epicondylitis Lateral - tennis elbow Medial - golfers elbow If the presentation is not entirely typical, it is important to rule out cubital tunnel radiculopathy or other neurogenic pain.

Answer 81

epicondylitis Lateral - tennis elbow Medial - golfers elbow If the presentation is not entirely typical, it is important to rule out cubital tunnel radiculopathy or other neurogenic pain.

Answer 82

epicondylitis Lateral - tennis elbow Medial - golfers elbow If the presentation is not entirely typical, it is important to rule out cubital tunnel radiculopathy or other neurogenic pain.

Answer 83

Psoriatic arthritis is a chronic inflammatory joint disease associated with psoriasis. It is a seronegative inflammatory arthritis differentiated from rheumatoid arthritis (RA) by several clinical features. These include a frequent oligoarticular or monoarticular initial pattern of joint involvement, as well as distal interphalangeal joint (DIP) involvement. Dactylitis, a fusiform swelling of an entire digit, and sacroiliitis are manifestations not observed in RA. Over time, many patients will progress to a polyarticular pattern of joint involvement with erosive arthritis. Polyarticular psoriatic arthritis distinguished from rheumatoid arthritis by the presence of dactylitis and the absence of anticyclic citrullinated peptide antibodies. Non-steroidal anti-inflammatory drugs (NSAIDs) usually sufficient to treat limited disease. Patients with progressive peripheral arthritis (polyarthritis, joint erosions) or oligoarthritis refractory to NSAIDs and/or intra-articular corticosteroids require disease-modifying antirheumatic disease therapy (e.g., methotrexate) early in the disease course. Tumour necrosis factor (TNF)-alpha inhibitors may be considered as second-line therapy for most disease manifestations.

Answer 84

Psoriatic arthritis occurs equally in men and women, although earlier disease onset is observed in males. The incidence of psoriatic arthritis in women peaks in the 6th decade, mirroring an age-specific rise in the incidence of the skin disease in females. It is hypothesised that hormonal factors influence this sex difference.

Answer 85

The presence of distal interphalangeal (DIP) joint involvement and dactylitis uniquely distinguishes psoriatic arthritis from rheumatoid arthritis Psoriatic arthritis is a disease of the cellular immune system, with CD8+ T cells playing a primary role in both the skin and synovium. These cells have been demonstrated to be predominately activated, clonally expanded memory T cells. Compared with rheumatoid synovium, psoriatic synovium is characterised by hypervascularity and morphologically tortuous vessels. Angiogenic growth factors, including vascular endothelial growth factor (VEGF) and transforming growth factor (TGF) beta, are over-expressed in psoriatic tissue and not only contribute to the vascular changes but, together with tumour necrosis factor (TNF), contribute to the characteristic bone changes of psoriatic arthritis. HLA-C allele Cw0606

Answer 86

STRONG Psoriasis FHx WEAK Hx of joint or tendon trauma HIV

Answer 87

``` COMMON Hx psoriasis Joint pain + stiffness (inflammatory) Inflammatory joint pain is characterised by prolonged morning stiffness (>30 minutes), improvement with use, and recurrence with prolonged rest. Peripheral arthritis ``` Psoriatic arthritis frequently presents in a pattern of monoarticular or oligoarticular joint involvement. In patients with multiple joints involved, the pattern lacks the symmetry of rheumatoid arthritis. Dactylitis Scalp/nail problems - Patients may not know they have psoriasis. The disease may be misinterpreted as scalp dandruff, seborrhoea, or onychomycosis. UNCOMMON Spinal stiffness Reduction of cervical spine mobility

Answer 88

Plain Xray - erosion in the distal interphalangeal (DIP) joint and periarticular new-bone formation; osteolysis and pencil-in-cup deformity in advanced disease ESR - H CRP - H Anti-CCP - negative Lipid profile - Because of the increased risk of metabolic syndrome in psoriatic disease, patients should have the appropriate metabolic screening, including a lipid profile. Fasting BG - Because of the increased risk of metabolic syndrome in psoriatic disease, patients should have the appropriate metabolic screening, including fasting blood glucose Uric acid level - negative Synovial fluid aspiration and analysis - absence of monosodium urate crystals

Answer 89

Limited disease: NSAIDs, physio, corticosteroid injection Progressive disease: DMARDs - methotrexate: 7.5 to 25 mg orally/subcutaneously/intramuscularly once weekly on the same day each week OR ciclosporin: 2.5 to 4 mg/kg/day orally given in divided doses every 12 hours + NSAIDs, physio, corticosteroid injection Possible to use TNF-a inhibitor / mAB Ustekinumab - IL12/23 Secukinumab - IL17

Answer 90

CV disease Methotrexate hepatotoxicity Rx related malignancy

Answer 91

Early cohort studies of established psoriatic arthritis revealed that at least 20% of patients develop progressive and disabling arthritis. Up to 7% of patients with psoriatic arthritis may require joint surgery.

Answer 92

psoriatic arthritis Approximately 10% of patients may present with an arthritis compatible with psoriatic arthritis but without skin disease. Some of these patients have a family history of psoriasis or may develop skin disease at a later date. Presentation with axial psoriatic spondylitis without peripheral joint involvement is uncommon.

Answer 93

psoriatic arthritis Approximately 10% of patients may present with an arthritis compatible with psoriatic arthritis but without skin disease. Some of these patients have a family history of psoriasis or may develop skin disease at a later date. Presentation with axial psoriatic spondylitis without peripheral joint involvement is uncommon.

Answer 94

Rhabdomyolysis may result from any traumatic or medical injury to the sarcolemma (the myocyte cell membrane) of the skeletal muscle cells. The subsequent release of intracellular ions, myoglobin, creatine kinase (CK), and urates into the circulation results in electrolyte disturbances, acidaemia, disseminated intravascular coagulation, renal failure, and multi-organ failure. The measurement of serum CK levels at more than 5 times the upper limit of normal is used as diagnostic criterion. End result of any disease process that causes muscle cell (myocyte) lysis. May have an obvious presentation, such as traumatic 'crush' injury, or may be insidious, requiring a high clinical index of suspicion. Muscular pain or discomfort is common, but rhabdomyolysis can have no symptoms or physical signs. Diagnosis is confirmed by elevated serum creatine kinase level. Fluid hydration is the mainstay of therapy.

Answer 95

Rhabdomyolysis is the end result of any disease process that causes muscle cell (myocyte) lysis. Estimates of the incidence rate and prevalence of rhabdomyolysis are, therefore, not available. Statistical analyses detailing its diagnosis within each causal process are unavailable or difficult to delineate.

Answer 96

Rhabdomyolysis is a consequence of different disease entities that cause muscle fibre destruction. These processes may be classified as traumatic or medically induced. Trauma, including over-exertional states, results in direct muscle injury. There are various medical causes. Rare, inherited muscle enzyme defect disorders, as well as seizures, infections, metabolic abnormalities, hypoxic conditions, temperature-related entities, and certain immunological diseases, may result in rhabdomyolysis. ``` Cocaine, amphetamines, and phencyclidine may cause hyperdynamic muscular states. Narcotics and other central nervous system depressants (barbiturates, sedative-hypnotics) may cause tissue hypoperfusion and prolonged immobilisation and limb compression. Salicylate toxicity uncouples oxidative phosphorylation, which inhibits adenosine triphosphate (ATP) formation. Diuretics may lead to potassium depletion severe enough to result in rhabdomyolysis. Statin therapy for cholesterol control has a significant unwanted effect of rhabdomyolysis.[6][7] The mechanism is not clearly defined. Antipsychotic use is a risk factor for rhabdomyolysis. It has been reported in the presence or absence of neuroleptic malignant syndrome.[11][12] Certain antidepressants (venlafaxine, escitalopram, sertraline) when used in combination with other medications, including antiretrovirals (tenofovir) or antibiotics (daptomycin), or with alcohol, can have a synergistic effect on muscle breakdown and cause rhabdomyolysis. Dipeptidyl peptidase 4 (DPP-4) inhibitors (e.g., sitagliptin) can cause myopathy and rhabdomyolysis when used in association with statins. ```

Answer 97

Risk factors ``` STRONG trauma alcohol cocaine amfetamine phencyclidine narcotics diuretics statins salicylate toxicity toxins envenomation inflammatory disorders muscle hypoxia genetic disorders ``` ``` WEAK metabolic disorders infection increased body temperature antipsychotics ```

Answer 98

COMMON Recent crush injury Prolonged immobilisation Muscular pain ``` UNCOMMON Malaise Dark urine Swelling Muscular tenderness Diminshed peripheral pulse Prolonged CAP ```

Answer 99

CK - increased to at least 5 times normal Serum electrolytes - elevated potassium, magnesium, and phosphate; low calcium Renal function - elevated urea and creatinine Liver function - ALT and AST raised Myoglobin - increased levels in blood and/or urine MAY DEVELOP DIC: FBC - may be decreased haemoglobin and platelet count Coagulation studies - elevated prothrombin time, activated PTT, and INR Urine dip/microscopy - blood

Answer 100

Crush injury Hydration therapy Urine alkalinisation Diuretic therapy Anuric or unresponsive to hydration therapy - haemodialysis

Answer 101

Permanent damage from both traumatic and non-traumatic rhabdomyolysis is minimal. Complete recovery is the normal result following appropriate treatment.

Answer 102

``` Acute renal failure Electrolyte abnormalities Compartment syndrome DIC Multi-system failure ```

Answer 103

Rhabdo Unlike traumatic presentations, medical presentations of rhabdomyolysis are often subtle and must be suspected given the appropriate clinical setting. The patient may be without symptoms or may have vague complaints of increased fatigue or generalised malaise. Rather than complaining of muscular discomfort, the patient with drug use or an infection may present with dark-coloured urine or oedema of the limbs. In one general review, only 50% of patients complained of muscular symptoms, and physical findings of rhabdomyolysis were present in only 4% on admission.[1] Unless the diagnosis is suspected and specific laboratory evidence is obtained, rhabdomyolysis may not be diagnosed until complications ensue.

Answer 104

Rhabdo Unlike traumatic presentations, medical presentations of rhabdomyolysis are often subtle and must be suspected given the appropriate clinical setting. The patient may be without symptoms or may have vague complaints of increased fatigue or generalised malaise. Rather than complaining of muscular discomfort, the patient with drug use or an infection may present with dark-coloured urine or oedema of the limbs. In one general review, only 50% of patients complained of muscular symptoms, and physical findings of rhabdomyolysis were present in only 4% on admission.[1] Unless the diagnosis is suspected and specific laboratory evidence is obtained, rhabdomyolysis may not be diagnosed until complications ensue.

Answer 105

An inherited disease of progressive fibrous tissue contracture of the palmar fascia, Dupuytren's contracture is seen predominantly in men of northern European descent aged >40 years. Its inheritance pattern is believed to be autosomal dominant with variable penetrance. An inherited disease of progressive fibrous tissue contracture of the palmar fascia. Predominantly affects men of northern European descent aged >40 years old who smoke, drink alcohol, or have diabetes. Patients present with a small lump or multiple lumps with pits in the palm of the hand, progressing to contractures of the fingers. Intralesional corticosteroid injections have been shown to reduce the need for surgery. Surgical referral should be made when metacarpophalangeal joint contractures reach 30 degrees, or if any degree of proximal interphalangeal joint contracture is present. Percutaneous needle fasciotomy and collagenase injections are significant therapeutic alternatives to surgery.

Answer 106

The overall prevalence of the disease in the UK is about 4%, rising to about 20% in those aged >65 years. The incidence of Dupuytren's contracture increases with age.

Answer 107

Dupuytren's contracture is a progressive fibroproliferative disease that is believed to show autosomal dominant inheritance with variable penetrance. The higher prevalence of the disease in men is probably due to the fact that androgen receptors are expressed in Dupuytren nodules. Greater weekly alcohol intake is associated with an increased likelihood of Dupuytren's contracture. Diabetes mellitus has a strong association with Dupuytren's contracture.

Answer 108

``` STRONG Male sex >40yo FHx DM ``` ``` WEAK High alcohol intake Smoking Trauma Anticonvulsant ```

Answer 109

``` COMMON Difficulty with manual activities Palmar nodule Palmar skin changes Pretendinous cords MCP joint contracture PIP joint contracture ``` Positive Hueston table-top test Involves the patient attempting to lay the palm of the hand flat on a table surface. The result is positive if the patient is unable to flatten the hand on the table. Bilateral UNCOMMON Garrod's nodes Involvement of plantar surface of feet - Patients with Dupuytren's diathesis are more likely to have systemic fascial disease, including Ledderhose's disease, which affects the plantar surface of the feet. Involvement of penis - Patients with Dupuytren's diathesis are more likely to have systemic fascial disease, including Peyronie's disease in men, which affects the penis.

Answer 110

Clinical Possible to use US

Answer 111

Prevention: Corticosteroid injection: triamcinolone acetonide <30 degrees MCP joint contracture 1. Collagenase injection 1. Needle aponeurotomy 1. Corticosteroid injection 1. Percutaneous fasciotomy ``` >30 degrees SAME OR Open partial fasciectomy + preoperative ABx + Post-op splinting ```

Answer 112

Dupuytren's contracture is progressive, with 75% of patients developing features of more advanced stages of the disease. Men seem to progress more rapidly than women, and patients aged <50 years tend to progress more rapidly than older patients. Although most patients will progress in severity, about 10% will regress. Smoking and alcohol use increase the likelihood of progression to surgery.

Answer 113

Intraoperative neurovascular injury Post-op haematoma, infection, stiffness, Recurrence

Answer 114

Dupuytren's contracture

Answer 115

Ganglion cysts are smooth, soft, benign masses that are usually located on the wrist (dorsal or volar aspect) with one or more communicating stalks into the wrist joint or surrounding structures. They can be single or multi-loculated and are filled with viscous, sticky, mucinous fluid. Most common benign lesion of the hand/wrist. Typically, insidious onset with no predisposing conditions. Usually only a cosmetic problem but local pain and neurovascular compression may occur. Conservative management usually suffices if no neurovascular compromise. Aspiration of dorsal cysts can be therapeutic and diagnostic. Surgical excision has a higher rate of resolution but recurrence is possible. No reported malignant transformation.

Answer 116

Ganglions are the most common type of tumour located within the hand and wrist. Female to male ratio of 3:1 Second to fourth decades

Answer 117

There is no specific identifiable causative factor; however, there is much speculation regarding aetiology. Traumatic events may be recalled and linked to the ganglion in anywhere from 10% to 40% of patients. Scapholunate injury has also been hypothesised to lead to dorsal ganglia. Arthrographic studies have demonstrated radiopaque dye passing from the wrist joint into the ganglion cyst uni-directionally, leading to the theory that a small hole in the wrist capsule may cause a one-way valve allowing growth of the cyst. Ganglions may also represent benign tumours of synovial origin; however, there is no specific synovial lining noted on histological examination. Synovial fluid leaking into the surrounding tissue may lead to formation of a cyst wall enclosing cystic fluid. Mucoid degeneration of collagen in the surrounding tissue may lead to cyst formation.

Answer 118

``` WEAK Female 10-30 Trauma Scapholunate instability ```

Answer 119

``` COMMON Subcutaneous wrist mass Wrist pain Non-tender Increased mass after activity Transilluminating Unable to recall onset Cosmetically unpleasing ``` UNCOMMON Hand or finger coolness Parasthesia/weakness of fingers Reduced sensation in hand Dorsal ganglia may compress the superficial radial nerve causing reduced sensation on the dorsum of hand. Volar ganglia may compress the ulnar nerve causing reduced sensation of the small and ring fingers. Volar ganglia may also compress the median nerve mimicking carpal tunnel syndrome.

Answer 120

1. Observe Conservative treatment can lead to spontaneous resolution in up to 58% of adults and up to 93% of children over a 9- to 12-month period. Discomfort or aching, especially after activity, can usually be alleviated by NSAIDs. 2. Cyst aspiration + corticosteroid injection triamcinolone acetonide: 10 mg into affected area as a single dose and lidocaine: (1%) 1-2 mL into the affected area as a single dose Cysts that are recalcitrant to conservative management may be addressed surgically if they are painful or cosmetically unpleasing and the patient desires excision of the mass Patients with neurovascular compromise related to ganglia are typically treated with surgical resection. Completely devascularised fingers/hand are not typical presentations of ganglia, so surgical intervention can usually be performed in a non-emergent but timely manner.

Answer 121

With observation, up to 58% of cysts have been reported to resolve. Cyst puncture and aspiration If the original procedure is not successful, multiple treatments may be required. Puncture of dorsal ganglion cysts has been reported to have a 13% success rate with single aspiration. This can be increased to approximately 40% if the wrist is splinted for 3 weeks afterwards, and approximately 85% with up to 3 treatments. Recurrence rates of dorsal ganglia after open treatment range from 3% to 9% in the literature.

Answer 122

Rx related radial artery injury Rx related median nerve injury Fatty atrophy post corticosteroid injection Skin pigmentation post corticosteroid injection Rx related septic arthritis Wrist stiffness post immobilisation Surgical complications - scar, infection, neurovascular injury

Answer 123

ganglion cyst Ganglion cysts can also present on the volar aspect or occultly; however, this is less common than the dorsal variant. Presentation is usually due to cosmetic deformity; however, occasional pain, weakness, or paraesthesia may be present secondary to impingement on surrounding neurological structures, and coolness of the hand or fingers may be present secondary to radial nerve compression. Occult ganglions are usually undetectable by physical examination but may be a cause of vague wrist pain.

Answer 124

Tenosynovitis of the hand and wrist is a group of entities with a common pathology involving the extrinsic tendons of the hand and wrist and their corresponding retinacular sheaths. They usually start as tendon irritation manifesting as pain, and can progress into catching and locking when tendon gliding fails. Trigger digits and de Quervain's disease are the 2 most common forms of tenosynovitis tendinopathy. Diagnosis is usually clinical. If required, the single most useful and accurate investigation is a high-resolution ultrasound scan. Treatment may involve non-steroidal anti-inflammatory drugs (NSAIDs), splinting, corticosteroid/local anaesthetic injections, or surgery.

Answer 125

Tendinopathy is one of the most common reasons for a visit to a hand clinic. It is more common in women, with a peak incidence at about the sixth decade of life. Incidence is probably not related to repetitive tasks such as keyboard use The most common presentation is trigger finger, followed by de Quervain's disease (thumb extensor tendon tendonitis in the first dorsal compartment). Pregnant and postnatal women have increased incidence of de Quervain's disease at a younger age

Answer 126

The basic aetiology is a stenosing tenosynovitis as the tendon passes through its retinacular sheath. The retinacular sheath is a fibro-osseous canal that functions as a pulley system to reorientate the vector of pull of the tendon towards the hand and digits. Repetitive shear stress through the canal causes irritation to the tendon and its synovial lining (tenosynovium) with inflammation and hypertrophy, along with fibrosis of the retinacular sheath. Over time, the canal will narrow to a point that precludes smooth gliding of the tendon: stenosing tenosynivitis. It may involve any of the 21 extrinsic (9 flexor and 12 extensor) tendons of the hand and wrist.

Answer 127

``` STRONG 5th-6th decades Female Involvement of dominant hand Insulin-dependent diabetes Pregnancy and lactation ``` WEAK Degenerative joint disease or trauma

Answer 128

COMMON Location over and around a retinacular sheath Pain increased with motion Response to anaesthetic Pain may be present without motion, but it should increase with active and passive motion. Trigger finger presents with painful catching or popping of the flexor tendon, which occurs as the patient flexes and extends the digit. The digit may be locked in flexion. Passive manipulation into extension may release the locking. Prolonged neglect will result in flexion contracture of the finger. Trigger finger - A tender nodule may be palpable at the level of the metacarpal head in the palm de Quervain's disease presents with pain, tenderness, and swelling localised to the radial side of the wrist 1 to 2 cm proximal to the radial styloid. It is aggravated by thumb movement. Pain is exacerbated by ulnar deviation of the wrist when the thumb is clasped in the palm (Finkelstein test) Intersection syndrome presents as pain and swelling 4 cm proximal to the wrist joint. In severe cases, redness and palpable, and sometimes audible, crepitus are noted on examination. Pain is greatly increased by resisted wrist extension. Presenting features of extensor pollicis longus entrapment. Thumb interphalangeal joint motion causes pain at Lister's tubercle. Ulnar-sided wrist pain, increased with all motions of the wrist, is suggestive of extensor carpi ulnaris tenosynovitis. Pain with extension/ulnar deviation against resistance is suggestive. Suggestive of flexor carpi radialis tenosynovitis. Increased pain with resisted wrist flexion and radial deviation is pathognomonic. Localised swelling and a ganglion cyst may be present.

Answer 129

High res US scan - effusion, tendon sheath thickening, hyperaemia CONSIDER x-ray - Not indicated in most cases. Used to rule out other pathologies when suspected, such as fractures or dislocations, arthritis, calcific tendonitis, soft tissue masses.

Answer 130

Trigger finger: 1. NSAIDs 2. Flexor tendon sheath injection with corticosteroids Opinion varies as to the choice of corticosteroid compound and its preparation. Methylprednisolone, triamcinolone, and betamethasone are among the most commonly used 3. Surgery De Quervain's disease 1. NAIDS + splinting 2. First dorsal compartment injection +/- splinting 3. Surgery Extensor pollicis longus tenosynovitis 1. Surgery Although oral non-steroidal anti-inflammatory drugs (NSAIDs) can be offered for pain, surgical exploration should be planned as soon as possible (within days to weeks) to avoid attritional rupture of the tendon.

Answer 131

Trigger finger: Splinting alone can be effective in 55% to 66% of cases. Corticosteroid injections are successful in 48% to 93% of cases. de Quervain's disease Splinting alone is not highly effective. One or two corticosteroid injections are successful in 50% to 80% of cases. In one small prospective study, the combination of corticosteroid injection and splinting was more effective than injection alone. In pregnancy and lactation, non-operative treatment is highly effective; the condition tends to resolve after cessation of lactation. For resistant cases, open release is the definitive treatment. Endoscopic release has also been described.

Answer 132

``` Contracture Tendon rupture Surgery related injury to nerves Subluxation Neuritis (de Quervain's) ```

Answer 133

tenosynovitis of the hand and wrist [Trigger digits and de Quervain's disease] Stenosing tendinopathy can involve any extrinsic tendon of the hand or wrist. It usually presents with pain and swelling in the area where the tendon passes through its retinacular sheath. Early on the tendon shows full active motion. Later the tendon progresses into catching and ultimately locking, such as in trigger finger.

Answer 134

Systemic sclerosis (SSc), also known as scleroderma, is a multi-system, autoimmune disease, characterised by functional and structural abnormalities of small blood vessels, fibrosis of skin and internal organs, and production of auto-antibodies. A non-contagious, chronic, multi-system disease. Initial symptoms are non-specific and include fatigue, vague musculoskeletal complaints, diffuse swelling of hands, and Raynaud's phenomenon. Aetiology and pathogenesis are unknown. Disease course is variable, but the condition rarely subsides spontaneously. There are two main subtypes of systemic sclerosis (SSc): limited cutaneous SSc and diffuse cutaneous SSc. The limited cutaneous form tends to have less severe internal organ involvement and a better prognosis, but these subjects still need to be followed closely for possible complications. Clinical course is determined by extent of vascular and fibrosing complications. Vascular involvement includes Raynaud's phenomenon, ischaemic digital ulcers, hypertensive crisis, and pulmonary arterial hypertension. Fibrosis can involve lungs, heart, and GI tract. Treatment is targeted on disease processes that are potentially reversible (e.g., active inflammation or vasoconstriction) and aims to minimise functional impairment of the patient.

Answer 135

88 per million in England. Women are affected much more frequently than men, with a female-to-male ratio of about 5:1 Scleroderma is rare in childhood, is more common in young adults, and has a peak incidence in the 5th decade

Answer 136

Anti-topoisomerase I (anti-Scl 70) antibody is seen in about 20% of cases and is associated with an increased risk of interstitial lung disease and with diffuse skin involvement Anti-RNA polymerase III antibody (also about 20% of cases) is associated with renal crisis Anti-centromere antibodies (20% to 25% of cases) are associated with limited skin involvement and a better overall prognosis The remaining 40% have scleroderma but do not have an as-yet-identified scleroderma-specific auto-antibody. Also genetics + environmental

Answer 137

STRONG FHx +ve ANA WEAK Exposure to silica dust / solvents

Answer 138

``` COMMON Raynauld's Digital pits/ulcers Swelling of hands and feet Loss of function of hands Sclerodactylyl Heartburn, reflux + dysphagia Bloating Faecal incontinents Arthralgias+ myalgias Abnormal nail fold capillaroscopy Telangiectasias Subcutaenous calcinosis Dyspnoea Dry crackles at ling bases Fatigue Dry cough ``` ``` UNCOMMON Tendon friction rub Abrupt onset HTN WL Inflammatory arthritis Inflammatory myositis Synovitis Increased S2 Signs of anaemia ```

Answer 139

Positive ANA in more than 90% of patients FBC - may be normal; microcytic anaemia with chronic GI bleed; micro-angiopathic haemolytic anaemia with scleroderma renal crisis U+E - usually normal; elevated serum urea and creatinine with scleroderma renal crisis ESR - usually normal, occasionally elevated CRP - occasionally elevated, particularly in severe disease Urine microscopy - normal; mild proteinuria with few cells or casts occurs with scleroderma renal crisis PFTs - Important to evaluate for restrictive lung disease and for pulmonary hypertension. ECG - normal; may demonstrate cardiac involvement such as arrhythmias Echo - pulmonary hypertension: a rise in right ventricular systolic pressure (RVSP); pericardial effusion, or right ventricle (RV) or left ventricle (LV) diastolic dysfunction, may be present CXR - normal; evidence of interstitial lung disease demonstrated by bi-basilar interstitial infiltrates; cardiomegaly or signs of right heart failure may be present Barium swallow - diminished oesophageal peristalsis and gastroparesis; diminished muscle tone in the lower oesophagus, with reflux of barium; strictures

Answer 140

Renal crisis: ACEi Additional hypertensives May need dialysys Cardiac tamponade Pericardial window + prednisolone ``` Raynaulds Conservative (avoid cold + smoking) 1. CCB +/- aspirin or pentoxifyllline +/- Topical nitrates ``` General skin involvement: Emolients Oral antihistamine WITH THICKENING -> cyclophosphamide or methotrexate Rx GORD -> Mild symptoms include reflux due to oesophageal dysmotility. Lifestyle advice includes: not eating 2 to 3 hours before bedtime, avoiding caffeine and carbonated beverages, and elevating the head of the bed. Advice is given in addition to proton-pump inhibitors. Treatment is usually lifelong. IMMUNOSUPPRESSANTS for ILD, synovitis, myopathy

Answer 141

Those with limited cutaneous systemic sclerosis (SSc) have a better prognosis than those with the diffuse form of the disease. However, some patients with limited disease will go on to have significant visceral involvement, hence the need for vigilant monitoring. Treatment options often result in undesirable adverse effects. It can be challenging to find a balance between treatment effects and disease suppression. For this reason, treatment with immunosuppression is used under defined conditions. Considering diffuse SSc, most patients will have an initial progressive course of skin fibrosis, followed by stabilisation and then regression. Tendon friction rubs, which may be present in early stages of diffuse disease, are a poor prognostic indicator. Patients with tendon friction rubs should be evaluated for immunosuppressive therapy, such as methotrexate, if persistent and interfering with function (e.g., ankle friction rubs interfering with ambulation). Severe and life-threatening renal disease develops in 10% to 15% of scleroderma patients, usually, but not exclusively, in those with diffuse SSc. The risk for scleroderma renal crisis is greatest in the first 5 years of disease. Angiotensin-converting enzyme (ACE) inhibitors should be initiated early in patients with suspicion of renal crisis and/or for the treatment of essential HTN, to avoid irreversible kidney damage. Symptoms of heartburn should be treated early to avoid long-term complications, including strictures and Barrett's metaplasia. Interstitial lung disease (ILD) occurs in the first few years of disease onset and can be slowly progressive. Again, the risk is greater in diffuse rather than limited disease, but some individuals with limited skin disease can develop significant ILD. However, those with the anti-centromere antibody seldom develop progressive ILD, so it is worthwhile to keep the auto-antibody profile in mind when considering monitoring and treatment. Pulmonary artery hypertension can occur as a late manifestation and does include those with anti-centromere antibodies as well as other SSc-specific antibodies. Patients may present with subtle complaints, including fatigue and decreased exercise tolerance. Yearly PFTs (spirometry, lung volumes, and diffusion capacity measurement) and echocardiograms should be done for surveillance. Referral for lung transplantation should be made for lung involvement (ILD or pulmonary arterial hypertension) not amenable to treatment. Survival rates in SSc following lung transplantation are similar to those with idiopathic pulmonary fibrosis and pulmonary HTN (5-year survival 50% to 60%).[42] Survival Mean survival is about 12 years after diagnosis but there is a wide variation in survival reflecting the heterogeneity in disease severity.

Answer 142

skin ulcers (in addition to digital ulceration) hypothyroidism secondary skin infection osteomyelitis malabsorptive diarrhoea, steatorrhoea, and weight loss variable digital amputation sicca symptomatic hypotension associated with calcium-channel blocker pulmonary artery HTN oesophageal stricture Barrett's oesophagus aspiration pneumonia severe pan-GI dysmotility with inability to maintain nutrition cardiac arrhythmias hepatic fibrosis and cirrhosis associated with methotrexate therapy neutropenia associated with cyclophosphamide haemorrhagic cystitis and bladder cancer associated with cyclophosphamide hypersensitivity pneumonitis associated with methotrexate therapy infertility associated with cyclophosphamide therapy

Answer 143

systemic sclerosis (scleroderma) On rare occasions, patients can present with scleroderma renal crisis, consisting of accelerated hypertension, renal compromise, and micro-angiopathic haemolytic anaemia. Raynaud's phenomenon and sclerodactyly may be present but overlooked by the patient and therefore not previously brought to medical attention.

Answer 144

systemic sclerosis (scleroderma) On rare occasions, patients can present with scleroderma renal crisis, consisting of accelerated hypertension, renal compromise, and micro-angiopathic haemolytic anaemia. Raynaud's phenomenon and sclerodactyly may be present but overlooked by the patient and therefore not previously brought to medical attention.

Answer 145

Ankylosing spondylitis (AS) is a chronic progressive inflammatory arthropathy. Patients present with severe pain and spinal stiffness, which ultimately may lead to spinal fusion. These patients suffer extreme disability as a consequence. AS mainly affects the axial skeleton, although peripheral joints, entheses (tendon or ligament attachments to bone), and extra-articular sites such as the eye[2] and bowel[3] are frequently affected. Levels of disability are comparable with those who have rheumatoid arthritis. Classified as a seronegative spondyloarthropathy. The seronegative spondyloarthropathies (including psoriatic arthritis, enteropathic arthritis, and reactive arthritis) are a heterogenous group of conditions with overlapping clinical manifestations and association with the gene HLA-B27. Predominantly affects the sacroiliac joints and axial spine. Inflammatory back pain is the hallmark clinical feature. This is defined as back pain that is of insidious onset, is worse in the morning, and improves with exercise. A positive response to non-steroidal anti-inflammatory drugs (NSAIDs) is characteristic of most patients. Physiotherapy and NSAIDs are the cornerstone of treatment. In people whose symptoms are refractory to these approaches, tumour necrosis factor (TNF)-alpha inhibitors play a key role.

Answer 146

The mean AS prevalence per 10,000 people (from 36 eligible studies) has been estimated as 23.8 in Europe, 16.7 in Asia, 31.9 in North America, and 10.2 in Latin America. Juvenile-onset AS has greater peripheral joint involvement and has a worse clinical outcome. AS is commonly associated with psoriasis or inflammatory bowel disease (approximately 10% of AS patients). Subclinical bowel inflammation is detectable histologically in approximately 60% of cases. Decades ago, the prevalence ratio of AS in males to females was suggested to be approximately 10:1, and it is likely that this was due to marked under-recognition of the disease in women. More recent estimates suggest the amle:female ratio to be more in the region of 2.5:1, and this is reflected by similar diagnostic delays between the sexes in recent years.

Answer 147

There is a strong genetic component in the risk of developing AS, with heritability of 97%. Condition severity is also largely genetically determined, with heritability of disease activity, functional impairment, and radiographic disease extent estimated at 51%, 76%, and 62%. HLA-B27 is present in about 90% of patients who have AS, and approximately 6.5% of those with HLA-B27 develop the condition. Immunohistochemical studies have found T-cells and macrophages to be abundant in inflamed sacroiliac joints

Answer 148

STRONG HLAB27 ERAP / IL23R genes FHx WEAK Klebsiella pneumonia

Answer 149

``` COMMON Inflammatory back pain Iritis/uveitis Enthesitis Presentation in late teens/early 20s Male FHx Fatigue Sleep disturbance Loss of lumbar lordosis (positive schobers testing) Sacroiliac tenderness Dyspnoea (chostochondral joint involvement) Spinal kyphosis ``` UNCOMMON Association with psoriasis / IBD Sx

Answer 150

Pelvic XRAY - sacroiliitis MRI - usually not ordered but - has been instrumental in allowing clinicians to diagnose AS early. Possible to do HLAB27 but not necessary

Answer 151

CONSERVATIVE All patients with AS should participate in regular daily stretches. In addition, all patients are encouraged to attend regular group sessions, which ideally should include regular access to a hydrotherapy pool 1. NSAIDs - naproxen +/- codeine phosphate 15-60mg (4-6hrly) / paracetamol 2. Hydrocortisone injection 5-50mg 3. Sulfsalazine REFRACTORY 1. TNF-a - adalimumab, golimumab, etanercept 2. Secukinumab 3. IV bisphosphonates - pamidronate

Answer 152

In a population-based study, no difference was found in mortality of men with AS and the general male population. A prospective cohort study of patients with early axial spondyloarthritis showed that the presence of syndesmophytes (sign of radiographic damage) at baseline, elevated markers of systemic inflammation (CRP and ESR) time-averaged over 2 years, and cigarette smoking were all independently associated with spinal radiographic progression at 2 years.

Answer 153

``` Osteoporosis Cardiac involvement CF, IHD Hip involvement Iritis Pulmonary involvement Neurological involvement - watch out for caudal equine ```

Answer 154

ankylosing spondylitis Spondyloarthropathy is also seen in children although less commonly than in adults. It is classified under enthesitis (inflammation of the tendon or ligament attachments to bone)-related arthritis in the classification of juvenile idiopathic arthritis. There are significant differences in the pattern of onset and course of disease between children and adults. The usual mode of presentation is in the form of asymmetrical oligoarthritis in an adolescent. The joints involved are usually of the lower limbs, including the hips and tarsal joints. It is unusual to have spinal involvement early in the course of disease. Sacroiliitis can be the presenting symptom and may manifest as low back pain. Enthesitis can be the presenting feature or may be seen in association with arthritis. The common sites in children are the calcaneal insertion of the Achilles tendon and plantar fascia, plantar fascia attachments to the base of the fifth metatarsal and the heads of the metatarsals. Although early spinal involvement is uncommon, measurements of lumbosacral mobility using the Schober test are important in detecting it in children with enthesitis-related arthritis.[13] HLA-B27 is positive in about 90% of children with enthesitis-related arthritis. Acute anterior uveitis is also seen in 10% to 15% of these children, and is usually unilateral. In a significant number of adults with AS, the disease onset is seen in the juvenile period. There are data to show that juvenile-onset AS is associated with significant delay in diagnosis and worse functional outcomes compared with adult-onset AS.[14] Studies have also suggested differences in clinical presentation in women, which may explain the under-recognition of the disease in this group. Women tend to have more cervical and peripheral joint pain than men, and may also be more likely to have peripheral arthritis. However, radiographic severity is lower in females. In addition, women report higher degrees of functional impairment for given degrees of radiographically evident damage. These factors may contribute to misdiagnosis in female patients.[15]

Answer 155

Gout is a syndrome characterised by: hyperuricaemia and deposition of urate crystals causing attacks of acute inflammatory arthritis; tophi around the joints and possible joint destruction; renal glomerular, tubular and interstitial disease; and uric acid urolithiasis. The disease most commonly affects the first toe (podagra), foot, ankle, knee, fingers, wrist, and elbow; however, it can affect any joint. Acute onset of severe joint pain. Swelling, effusion, warmth, erythema, and/or tenderness of the involved joint(s). Arthrocentesis with synovial fluid analysis shows strongly negative birefringent needle-shaped crystals under polarised light. Non-steroidal anti-inflammatory drugs (NSAIDs), colchicine, or corticosteroids are used to treat acute disease. Allopurinol, febuxostat, probenecid, lesinurad, or sulfinpyrazone may be used as uric acid-lowering drugs when long-term prevention of crystal deposition is indicated. Complications include joint destruction, kidney disease, and urolithiasis.

Answer 156

The incidence increases with age. The annual incidence of gout in men increases from 1 per 1000 under 45 years of age, to 1.8 per 1000 at 55 to 64 years of age. Gout is more common in men and is rare in pre-menopausal women The prevalence in the western world is about 1%, with a male to female ratio of 7:1 to 9:1; in the UK and Germany the prevalence is 1.4%

Answer 157

There is a causal relationship between hyperuricaemia (high urate level) and gout. Urate is a metabolite of purines and the ionised form of uric acid (a weak acid at a physiological pH); hence, uric acid exists mostly as urate. Hyperuricaemia does not always lead to gout, but the incidence of gout increases with urate level. Risk factors for hyperuricaemia may eventually lead to gout and include dietary factors such as consumption of seafood, meat, and alcohol, especially beer Another source of purines and urate is endogenous production due to high cell turnover, such as from haematological cancer and chemotherapy. A small proportion of over-producers have a specific genetic enzymatic abnormality. Drugs such as diuretics can increase urate levels. Other risk factors for gout include obesity, insulin resistance, and hypertension. Humans and some other higher primates develop gout spontaneously. Humans no longer express the gene for the enzyme uricase, which degrades uric acid to the more soluble compound allantoin in animals. This, coupled with a high rate of renal re-absorption of urate, results in hyperuricaemia and gout.

Answer 158

``` COMMON SO severe pain Joint stiffness Foot joint distribution Few affected joints -Pattern is usually monoarticular or oligoarticular (<4 joints). Can be polyarticular, affecting multiple joints in the hands and feet, especially in older people. Swelling and effusion Tenderness Tophi Erythema + warmth FHx ```

Answer 159

Arthrocentisis + synovial fluid analysis -> NEGATIVE BIREFRINGANCE (needle shaped, in polarised light), WCC count >2.0 x 10^9/L CONSIDER Uric acid 2w after insult - >416 micromol/L (7 mg/dL) in men; >360 micromol/L (6 mg/dL) in women Xray - periarticular erosions (may have an overhanging edge or punched-out appearance) US - erosions, tophi, double contour line

Answer 160

ACUTE 1. NSAIDs 2. Colchicine 3. Corticosteroids ONGOING 1. Allopurinol + NSAIDs Possible to add uricosuric agent Lesinurad Febuxostat Refractory tophaceous gout - pegloticase

Answer 161

Gout attacks are painful and debilitating, but self-limiting. In patients untreated with uric acid-lowering drugs, the risk of recurrence after the first attack is 62%, 78%, and 84% during the first, second, and third year, respectively In untreated gout, about 2% of patients developed severe debilitating arthritis typically 20 years after the first attack. Gout and untreated hyperuricaemia may be associated with renal insufficiency.

Answer 162

Acute uric acid nephropathy | Nephrolithiasis

Answer 163

gout Gout may also present as acute bursitis, especially in the olecranon and prepatellar bursae. Chronic tophaceous gout may cause inflammatory destructive polyarthritis. This usually occurs in people with a long-standing history of attacks (mean 10 years) and with higher uric acid levels.

Answer 164

gout Gout may also present as acute bursitis, especially in the olecranon and prepatellar bursae. Chronic tophaceous gout may cause inflammatory destructive polyarthritis. This usually occurs in people with a long-standing history of attacks (mean 10 years) and with higher uric acid levels.

Answer 165

``` STRONG Older age Male Post menopausal Consumption of meat, seafood, alcohol Use of diuretics Use of ciclosporin/tacrolimus Use of pyrazinimide Use of aspirin High cell turnover ``` ``` WEAK Adiposity and insulin resistance HTN Renal insufficiency DM Hyperlipidaemia ```

Answer 166

``` STRONG Older age Male Post menopausal Consumption of meat, seafood, alcohol Use of diuretics Use of ciclosporin/tacrolimus Use of pyrazinimide Use of aspirin High cell turnover ``` ``` WEAK Adiposity and insulin resistance HTN Renal insufficiency DM Hyperlipidaemia ```

Answer 167

Calcium pyrophosphate deposition (CPPD) is associated with both acute and chronic arthritis. Acute CPP crystal arthritis is an acute inflammatory arthritis of one or more joints. Knees, wrists, shoulders, ankles, elbows, or hands can be affected. The chronic form of CPP arthritis mimics osteoarthritis or rheumatoid arthritis and is associated with variable degrees of inflammation CPPD typically occurs in older people but can occur in younger people with associated metabolic conditions, such as hyperparathyroidism and haemochromatosis. Calcium pyrophosphate arthritis is caused by deposition of calcium pyrophosphate (CPP) crystals. It can be difficult to diagnose as CPP crystals in synovial fluid can be small, sparse, and difficult to find. In patients <60 years of age, underlying metabolic conditions associated with calcium pyrophosphate deposition (CPPD), such as hyperparathyroidism or haemochromatosis, should be investigated. There is no definitive treatment for CPP arthritis but intra-articular corticosteroids can be effective for both acute and chronic forms.

Answer 168

The aetiology of CPPD is not known. The hallmark of the disease is the deposition of CPP crystals in the mid-zone of articular hyaline and fibro-cartilage. These crystals typically occur in the peri-cellular matrix around phenotypically altered articular chondrocytes. Factors that promote CPPD crystal formation include alterations in the structure and composition of the peri-cellular matrix and over-production of the pyrophosphate component of the CPPD crystal by chondrocytes

Answer 169

``` STRONG Advanced age Injury HPTism Haemochromatosis FHx of pseudogout Hypomagnesaemia Hypophosphatasia ``` WEAK Gout Other metabolic conditions

Answer 170

``` COMMON Painful + tender joints Osteoarthritis like involvement of joints Sudden worsening of osteoarthritis Red + swollen Joint effusion and fluctuance ``` UNCOMMON Fever + malaise

Answer 171

Athrocentesis + synovial fluid analysis - POSITIVE BIREFRINGEANCE - also often BLOODY FLUID Xray of joints - linear calcific deposits, calcified tendons, subchondral cysts Serum calcium - exclude HPTism PTH - high or inappropriately normal in HPTism Iron studies - check haemochromatosis Serum magnesium - Excludes hypomagnesaemia. Serum ALP - Excludes hypophosphatasia.

Answer 172

1. Corticosteroid injections if inaccessible - NSAIDs 2. Systemic corticosteroids Analgesia

Answer 173

Many patients with acute CPP arthritis can expect significant improvement in their symptoms over days and weeks. An unknown percentage, however, will have recurrent disease. Patients with chronic CPP arthritis often have chronic joint pain and loss of function despite treatment. Similar to osteoarthritis, if there is severe joint damage, little can be done to restore normal joint function and reduce pain.

Answer 174

Bleeding and bruising around the injection site are common and require no intervention. Infection from intra-articular corticosteroids is rare. If it occurs, antibiotics and joint drainage should be instituted. The rare cases of facial flushing after intra-articular corticosteroids can usually be treated supportively.

Answer 175

pseudogout Arthritis associated with CPP crystals is often called the great mimic and can have a wide variety of presentations.[1] Although the acute mono-articular arthritis resembling gout is perhaps the most commonly recognised form of CPP arthritis, it is not the most common form of the disease. The most common form of CPP arthritis presents as a chronic degenerative arthritis that resembles osteoarthritis and may occur with or without inflammatory episodes. CPP arthritis typically affects joints not commonly affected by osteoarthritis, such as the wrists or shoulders. In addition to its presentation as an acute mono-articular or oligo-articular arthritis, it can present with a polyarticular, symmetrical inflammatory arthritis similar to rheumatoid arthritis; or, less commonly, with the diffuse aching similar to that seen in polymyalgia rheumatica. CPPD is associated with an increased risk of vascular calcification, and low bone mineral density.[5][6] The neuropathic form is rare but is characterised by severe destructive arthritis with bone fragmentation and loose bodies.

Answer 176

pseudogout Arthritis associated with CPP crystals is often called the great mimic and can have a wide variety of presentations.[1] Although the acute mono-articular arthritis resembling gout is perhaps the most commonly recognised form of CPP arthritis, it is not the most common form of the disease. The most common form of CPP arthritis presents as a chronic degenerative arthritis that resembles osteoarthritis and may occur with or without inflammatory episodes. CPP arthritis typically affects joints not commonly affected by osteoarthritis, such as the wrists or shoulders. In addition to its presentation as an acute mono-articular or oligo-articular arthritis, it can present with a polyarticular, symmetrical inflammatory arthritis similar to rheumatoid arthritis; or, less commonly, with the diffuse aching similar to that seen in polymyalgia rheumatica. CPPD is associated with an increased risk of vascular calcification, and low bone mineral density.[5][6] The neuropathic form is rare but is characterised by severe destructive arthritis with bone fragmentation and loose bodies.

Answer 177

Fibromyalgia is a chronic pain syndrome diagnosed by the presence of widespread body pain (front and back, right and left, both sides of the diaphragm) for at least 3 months in addition to tenderness (digital palpation at an approximate force of 4 kg) of at least 11 out of 18 designated tender point sites as defined by the American College of Rheumatology 1990 classification criteria. Patients typically present with chronic, widespread body pain and almost always have accompanying comorbid symptoms such as fatigue, memory difficulties, and sleep and mood difficulties Physical examination is typically normal but there is often diffuse tenderness, which may be assessed by counting the number of tender points or by palpating several areas of the body. Many therapies have been shown to be beneficial. Non-pharmacological therapies include patient education, exercise, and cognitive behavioural approaches. Pharmacological therapies include tricyclics, gabapentinoids, and serotonin-norepinephrine (noradrenaline) reuptake inhibitors. Patients often fare better when several different types of treatment are used together. Even though practitioners may have a problem recognising fibromyalgia as a discrete disorder, they should understand the diagnostic and therapeutic importance of 'centralisation' of pain as exemplified by a typical fibromyalgia patient. When a patient with any chronic pain state develops evidence of centralisation of pain, it is likely that treatments that work well for acute pain or pain primarily due to nociceptive input (NSAIDs, opioids, anti-inflammatories, immunosuppressives, injections, surgical procedures) will be less effective.

Answer 178

Studies show the prevalence in the general population to be between 0.5% and 5% Age of onset is typically between 20 and 60 years, with an average age of 35 years. Prevalence increases with age and the risk also appears greater in women.

Answer 179

Fibromyalgia is well established as being one of many pain disorders that co-aggregate strongly in individuals and families, including irritable bowel syndrome, temporomandibular joint disorder, interstitial cystitis, vulvodynia, and tension headaches. Individuals will sometimes only have one of these 'idiopathic' pain syndromes over the course of their lifetime; but more often, people with one of these entities, and their family members, are likely to have several of these conditions

Answer 180

``` STRONG FHx fibromyalgia Rheum conditions Age 20-60 Female ``` WEAK Presence of associated conditions

Answer 181

``` COMMON Chronic pain Diffuse tenderness OE Fatigue unrelieved by rest Sleep disturbance Mood disturbance Cognitive dysfunction Headaches Numbness/tingling sensations Stiffness Fluid retention Sensitivity to sensory stimuli such as bright lights, odours, noises ```

Answer 182

Clinical diagnosis ``` ESR/CRP - normal TFT - exclude hypothyroidism RhF/CCP - exclude RA ANA - exclude SLE Vit D - likely to be normal ```

Answer 183

1. Amitriptyline, cyclobenzaprine 2. duloxetine, pregabalin, gabapentin Conservative - CBT, biofeedback techniques, education about chronic pain Exercise and relaxation eg yoga / t'ai chi Analgesics: Naproxen / tramadol Referral to a psychologist is appropriate at initial diagnosis. In addition, although most patients note a significant improvement with pharmacotherapy and non-pharmacological approaches such as education, exercise, and cognitive behavioural therapy, some patients (especially those with long-standing symptoms and functional consequences such as disability or compensation issues, those on high-dose opioids, those with significant psychiatric comorbidities, and those who have had multiple 'failed' surgical procedures) will not respond to these approaches and will need further interdisciplinary care.

Answer 184

Fibromyalgia is a chronic illness and the patient can expect exacerbations and remissions to vary over time. With good adherence to exercise, sleep, and behavioural therapy, most patients will improve over time. The goal of treatment is to decrease physical and mental symptoms and to increase functioning, not to cure. Treatment beyond behavioural therapy and exercise is often trial and error for individual patients.

Answer 185

fibromyalgia Chronic, widespread pain, which is ultimately diagnosed as fibromyalgia, often begins following a significant injury, trauma, illness, admission to hospital, or emotionally stressful period, but an inciting event is not always seen. Fibromyalgia often co-exists with other rheumatological conditions, such as rheumatoid arthritis, SLE, and osteoarthritis; importantly, the presence of these conditions does not exclude a concomitant diagnosis of fibromyalgia (i.e., fibromyalgia is not a diagnosis of exclusion). Patients with fibromyalgia often have co-existent depression and anxiety at a higher frequency than patients without the disease, but mental illness is not a pre-requisite for its diagnosis.

Answer 186

Giant cell arteritis (GCA) is a granulomatous vasculitis of large and medium-sized arteries. It primarily affects branches of the external carotid artery, and it is the most common form of systemic vasculitis in adults. GCA typically occurs in people 50 years of age or older and is more common in women. Symptoms of polymyalgia rheumatica are frequently present. The most common serious consequence of GCA is irreversible loss of vision due to optic nerve ischaemia. GCA is sometimes also referred to as temporal arteritis, cranial arteritis, or granulomatous arteritis. Giant cell arteritis (GCA) is a common form of vasculitis in people aged 50 years or older. The extracranial branches of the carotid artery are usually affected. Irreversible blindness is the most common serious consequence. Aortic aneurysms and large vessel stenoses may occur as a long-term complication. Temporal artery biopsy is the definitive test to establish diagnosis. Patients with jaw claudication, diplopia, and an abnormal temporal artery on examination are more likely to have a temporal artery biopsy that is positive for GCA. GCA is unlikely if levels of inflammatory markers are normal. Prednisolone is highly effective therapy. Treatment should not be delayed while awaiting biopsy. Tocilizumab is a novel biological with therapeutic and corticosteroid-sparing benefit in the treatment of GCA.

Answer 187

The condition typically occurs in people 50 years of age or older. Its incidence rises steadily after age 50 and is highest between 70 and 80 years. Women are affected 2 to 4 times as often as men.

Answer 188

The condition is probably triggered by an environmental cause in a genetically predisposed person. Several infectious agents have been implicated, but conclusive evidence is lacking. These agents include Mycoplasma pneumoniae, parvovirus B19, parainfluenza virus, Chlamydia pneumoniae, and the varicella-zoster virus. Genetic polymorphisms of the human leukocyte antigen (HLA) class II region, specifically HLA-DRB1*04 and DRB1*01 alleles, are associated with susceptibility to GCA.

Answer 189

STRONG Age >50 Female ``` WEAK Genetic factors Smoking Atherosclerosis ?Environmental infective factors ```

Answer 190

COMMON Headache - Usually located over the temporal or occipital areas. It may be accompanied by scalp tenderness. Polymyalgia rheumatic symptoms - Typically include aching and stiffness in the neck, shoulders, hips, and proximal extremities that worsen after a period of inactivity and with movement. Pain and swelling of the distal joints may occur. Extremity claudication Cranial artery tenderness ``` UNCOMMON Loss of vision Amaurosis fugal / diplopia Superficial temporal artery tenderness, thickening or nodularity Absent temporal artery pulse Pallor + oedema of optic disc ``` UNCOMMON Bruit on auscultation of carotid or supraclavicular or brachial arteries Asymmetric blood pressure

Answer 191

ESR - >50 CRP - elevated FBC - normochromic normocyctic anaemia LFTs - transaminases and alkaline phosphatase are often mildly elevated Temporal artery biopsy - granulomatous inflammation; in about 50% of cases, multinucleated giant cells are present; inflammatory infiltrate may be focal and segmental Temporal artery US - may show wall thickening (halo sign), stenosis or occlusion Consider aortic arch angiography

Answer 192

No visual or neurological Sx or Sx - prednisolone: 1 mg/kg/day orally for 4 weeks, maximum 80 mg daily; gradually taper dose over 6-12 months Visual signs PULSE THERAPY - methylprednisolone: 1 g intravenously once daily for 3 days Ongoing - Glucocorticoids have broad immunosuppressive and anti-inflammatory properties; the goal is to improve symptoms and prevent vision loss. +/- aspirin +/- osteoporosis prevention Calcium carbonate + vitamin D + bisphosphonates Relapsing / unresponsive to glucocorticoids: tocilizumab: 162 mg subcutaneously once weekly; a dose of 162 mg every 2 weeks may be prescribed based on clinical considerations

Answer 193

Lack of response to therapy should alert the physician to question the diagnosis; however, up to 50% of adequately treated patients experience unpredictable disease relapses and recurrence of symptoms. A treatment course of 1 to 2 years with glucocorticoids is often necessary, with some patients requiring low-dose prednisolone for several years. Glucocorticoid-related adverse effects are therefore common, occurring in over 60% of patients. Major consequences of this therapy include diabetes mellitus and osteoporotic fractures. Use of tocilizumab may allow for more accelerated glucocorticoid tapering, but the optimal duration of tocilizumab therapy remains unclear. The overall survival for patients with GCA is similar to that of the general population

Answer 194

Large vessel stenoses Aortic aneurysms Glucocorticoid related adverse effect Vision loss These may include managing glucocorticoid-induced diabetes, monitoring for and treating elevated blood pressure, and preventing glucocorticoid-induced bone loss with calcium, vitamin D, and bisphosphonates. If on >20mg pred -> need PCP prophylaxis

Answer 195

Giant Cell Arteritis / Temporal Arteritis When present, symptoms of jaw claudication and diplopia are powerful predictors of a positive temporal artery biopsy result. Neurological manifestations occur in about one third of patients and may include stroke, transient ischaemic attack, or neuropathy. Respiratory tract symptoms are uncommon but may include cough or sore throat. Rarely, dental pain, tongue pain, or infarction of the tongue may be present. An older person may present with a new headache. In addition, some patients who predominantly have polymyalgia rheumatica can have subtle evidence of GCA that could be missed. GCA can rarely present as an unexplained systemic illness or fever of unknown origin with elevated levels of inflammatory markers without headache, jaw claudication, shoulder or hip girdle stiffness, or visual disturbances. Patients with large-vessel stenoses (approximately 10% to 15% of patients) may present with claudication of (usually) upper extremities, asymmetric blood pressures, or decreased pulses. Rarely, involvement of lower extremity vessels results in leg claudication

Answer 196

Idiopathic inflammatory myopathies constitute a heterogeneous group of sub-acute, chronic, and, rarely, acute diseases of skeletal muscle that have in common the presence of moderate-to-severe proximal muscle weakness and inflammation on muscle biopsy. Based on distinct features, they are divided into 3 groups: polymyositis, dermatomyositis, and inclusion body myositis. Polymyositis and dermatomyositis seem to have an autoimmune pathogenesis, whereas inclusion body myositis seems to have an autoimmune and degenerative pathogenesis. Heterogeneous group of muscular disorders characterised by progressive muscle weakness. Presentation is sub-acute or chronic and rarely acute. May be associated with dysphagia, fatigue, difficulties with breathing, and skin lesions. Diagnosis is confirmed by elevated serum muscle-derived enzymes, typical electromyography (EMG) findings, and inflammation on muscle biopsy. Corticosteroids are first-line therapy. Intravenous immunoglobulin, methotrexate, and azathioprine are used as second-line therapy. Third-line therapies include cyclophosphamide, mycophenolate, ciclosporin, and tacrolimus.

Answer 197

Polymyositis is seen after the second decade of life and very rarely in childhood. Its incidence is higher in women Dermatomyositis affects both children and adults. About half of the UK hospital cases were in patients aged between 15 and 59. The condition also affects women more often than men.

Answer 198

Aetiology is unknown at present. However, several factors have been suggested. Infection: several viruses including coxsackievirus, influenza virus, retroviruses, cytomegalovirus, and Epstein-Barr virus (EBV) seem to be associated with these myopathies.[1][2][20][21][22][23] Other associated infectious agents include protozoa, cestodes, nematodes, and Borrelia species.[1] Genetic: specific human leukocyte antigen (HLA) subtypes are believed to confer increased risk of development of idiopathic inflammatory myopathies.[24] Environmental: UV radiation intensity has been shown to be the strongest contributor, out of 13 geoclimatic variables, to the relative proportion of dermatomyositis in a population.[25] Hydroxyurea has also been implicated in cases of dermatomyositis.[26] Immunological: various autoantibodies have been found in up to 20% of patients. Among them, the antisynthetases anti-Jo-1 antibodies have been associated with a high incidence of interstitial lung disease.[27]

Answer 199

``` STRONG Children and age >40 Increased UV exposure FHx Female / black - poly and dermato Male / white - inclusion body ``` ``` WEAK Lipid lowering agents HIV Viral infections D-penicillamine Vaccination ```

Answer 200

All forms result in difficulties with tasks requiring the use of proximal muscles (e.g., getting up from a chair, climbing steps, lifting objects, and combing hair). Having the patient stand from the sitting position (especially from a low foot stool) with the arms crossed is a good way to examine proximal leg muscle strength. Often a patient with a myopathy is unable to do this. Severe muscle weakness is usually associated with muscle atrophy. In inclusion body myositis, quadriceps and distal wrist and finger flexor atrophy is common Heliotrope rash (A blue-purple discoloration of the upper eyelids, with oedema) + gottrons papules (Erythema over the knuckles, accompanied by raised violaceous scalp eruption) = DERMATOMYOSITIS Falls, WL, SOB, fever, dysphagia, myalgia, arthralgia, palpitations, Erythematous rash in V shape - dermatomyositis Skin calcinosis MI increased Arrythmias increased Peripheral neuropathy

Answer 201

CK - VERY high in polymyositis, raised in dermatomyositis EMG - short duration, low amplitude, spontaneous activity Biopsy - mandatory for definitive diagnosis Aldolase - elevated LDH - elevated ALT - high Myoglobin - high ANA - +ve Anticytoplasmic antibodies against translational components (e.g., antisynthetase antibodies and anti-SRP antibodies) are usually associated with relatively severe muscle disease. Antibodies against Mi-2 and Mas antigens are usually associated with relatively mild muscle disease. Up to 79% of patients with dermatomyositis have Mi-2 antibodies

Answer 202

2x types IV corticosteroid +/- IVIG if acute life-threatening weakness Ongoing: 1. Oral corticosteroids Creatine 2. IVIG or methotrexate or azathioprine

Answer 203

Five- and 10-year survival rates of 95% and 84%, respectively, have been reported. Factors associated with poor survival include older age, malignancy, delayed initiation of corticosteroid therapy, pharyngeal dysphagia with aspiration pneumonia, interstitial lung disease (ILD), and myocardial involvement. Among the serum autoantibodies, anti-SRP is the worst prognostic marker; the antisynthetases are also associated with recurrent disease flares and lower survival. Conversely, 5-year survival rates among the subsets with antipolymyositis-Scl and anti-Mi-2 antibodies approach 95%

Answer 204

``` Corticosteroid SE: Myopathy, DM, osteoporosis Immunosuppression infections Cardiac disease Pulmonary disease Dysphagia Malgnancy - In up to 45% of patients with dermatomyositis, it has been associated with a malignancy. ```

Answer 205

idiopathic inflammatory myopathies (polymyositis, dermatomysotitis) Extramuscular manifestations may be predominant. Dysphagia is most prominent in dermatomyositis and inclusion body myositis. Cardiac involvement (e.g., heart failure, arrhythmias, and MI) is recognised as an important prognostic factor of death. Interstitial lung disease may precede muscular symptoms. Other pulmonary manifestations include drug-induced pneumonitis, pulmonary capillary angiitis, and pulmonary failure due to thoracic muscle weakness. Systemic features such as fever and weight loss occur especially with co-existent associated connective tissue disease. IIM may be associated with malignancy.[4][5][6][7][8][9] The highest risk is near the time of diagnosis and up to 3 years after the diagnosis of myositis and is equal in males and females. Patients with dermatomyositis have a higher risk of developing malignancy than patients with polymyositis.[4][6] There is 3 to 6 times increased risk of developing cancer in dermatomyositis, with 58% of neoplasms occurring after myositis diagnosis. The most frequent malignancies are ovarian cancer,[8][10] pancreatic cancer, and non-Hodgkin's lymphoma.[8] Patients with polymyositis have a 1.4 to 2 times increased risk of developing cancer compared with the general population. The most frequent malignancies observed with polymyositis are non-Hodgkin's lymphoma, lung cancer, and bladder cancer.[8]

Answer 206

idiopathic inflammatory myopathies (polymyositis, dermatomysotitis) Extramuscular manifestations may be predominant. Dysphagia is most prominent in dermatomyositis and inclusion body myositis. Cardiac involvement (e.g., heart failure, arrhythmias, and MI) is recognised as an important prognostic factor of death. Interstitial lung disease may precede muscular symptoms. Other pulmonary manifestations include drug-induced pneumonitis, pulmonary capillary angiitis, and pulmonary failure due to thoracic muscle weakness. Systemic features such as fever and weight loss occur especially with co-existent associated connective tissue disease. IIM may be associated with malignancy.[4][5][6][7][8][9] The highest risk is near the time of diagnosis and up to 3 years after the diagnosis of myositis and is equal in males and females. Patients with dermatomyositis have a higher risk of developing malignancy than patients with polymyositis.[4][6] There is 3 to 6 times increased risk of developing cancer in dermatomyositis, with 58% of neoplasms occurring after myositis diagnosis. The most frequent malignancies are ovarian cancer,[8][10] pancreatic cancer, and non-Hodgkin's lymphoma.[8] Patients with polymyositis have a 1.4 to 2 times increased risk of developing cancer compared with the general population. The most frequent malignancies observed with polymyositis are non-Hodgkin's lymphoma, lung cancer, and bladder cancer.[8]

Answer 207

Osteoarthritis (OA) is the result of mechanical and biological events that destabilise the normal process of degradation and synthesis of articular cartilage chondrocytes, extracellular matrix, and subchondral bone. It involves the entire joint, including the articular cartilage, subchondral bone, pericapsular muscles, capsule, and synovium. The condition leads to loss of cartilage, sclerosis and eburnation of the subchondral bone, osteophytes, and subchondral cysts. It is clinically characterised by joint pain, stiffness, and functional limitation. A degenerative joint disorder; prevalence increases with age. Most commonly affected joints are the knee, hip, hands, and lumbar and cervical spine. Presents with joint pain and stiffness that is typically worse with activity. Radiographs show loss of joint space, subchondral sclerosis, and osteophytes. Treatments are non-pharmacological and pharmacological. Joint replacement surgery is effective for controlling the pain of osteoarthritis in advanced disease.

Answer 208

OA is common in women and becomes more common with advancing age. OA increases with age from 27% in people younger than 60 years to 44% in those older than 70 years.

Answer 209

There is no single cause for OA, and the exact aetiology for OA is unknown. There are a host of biological and mechanical factors that culminate in the development of OA. Age, hereditary predisposition, female gender, and obesity are associated with increased risk of OA. Articular congenital deformities or trauma to the joint also enhance the risk of developing OA. In addition, high bone mineral density and low oestrogen status, such as in post-menopausal women, may be associated with higher risk of knee and hip OA. The above factors might lead to a joint environment that is susceptible to trauma and to external mechanical stressors that are exacerbated by certain physical activities. Local mechanical factors, such as periarticular muscle weakness, misalignment, and structural joint abnormality (e.g., meniscal tear), further facilitate the progression of the disease. The internal and external factors combined lead eventually to a failed joint.

Answer 210

``` STRONG Age >50 Female Obesity Genetic factors Physical/manual occupation Knee alignment ``` WEAK High bone mineral density

Answer 211

``` COMMON Pain Functional difficulties Knee, hip, hand or spine involvement Hand OA spares the MCP joints and involves the PIP and DIP joints, which helps to distinguish it from rheumatoid arthritis. Bony deformities Limited range of motion Malalignment Tenderness Crepitus ``` UNCOMMON Stiffness - Early morning stiffness is usually present for only a few minutes and, almost invariably, <30 minutes. This helps to differentiate OA from other inflammatory arthritis, including rheumatoid arthritis. Effusion - In OA these are usually small and lack other inflammatory signs such as warmth and redness. Antalgic gait - painful, reduced stance phase relative to swing phase.

Answer 212

Xray of affected joints - new bone formation (osteophytes), joint space narrowing, and subchondral sclerosis and cysts CRP - NORMAL ESR - NORMAL Anti-CCP / RhF - NEG

Answer 213

CONSERVATIVE Exercise programmes, education, physiotherapy and occupational therapy. Manual mobilisation, strengthening quadriceps tendon, knee bracing, correct footwear. 1. NSAIDs - diclofenac topical + Paracetamol + NSAIDs +/- gastroprotection Viscosupplementation with intra-articular hyaluronic acid derivatives is classified under instrumental therapy. - sodium hyaluronate: consult specialist for guidance on dose STEP up pain -> opioids SURGERY

Answer 214

OA is a chronic slowly progressive disease and is almost ubiquitous with advancing age. There is no cure, but a combination of different modalities of treatment can provide adequate pain control and preserve function and quality of life for many patients. Despite treatment, most patients usually continue to have some degree of pain and functional limitation affecting their desired activities and quality of life. Complications of medication, particularly NSAIDs, are also problematic. In patients who do not respond to medical and non-medical therapies, total joint replacement provides good long-term pain relief for most people.

Answer 215

``` Functional decline + inability to perform ADLs Spinal stenosis in cervical + lumbar OA NSAID GI bleed Effusion NSAID renal dysfunction Effusion ```

Answer 216

osteoarthritis

Answer 217

osteoarthritis

Answer 218

Polymyalgia rheumatica (PMR) is an inflammatory rheumatological syndrome that manifests as pain and morning stiffness involving the neck, shoulder girdle, and/or pelvic girdle in individuals older than age 50 years. Peripheral musculoskeletal involvement may also be present. PMR occurs either as an isolated condition or associated with giant cell arteritis. Patients describe difficulty rising from seated or prone positions, varying degrees of muscle tenderness, shoulder/hip bursitis, and/or oligoarthritis. More common in women. About 15% to 20% of patients with polymyalgia rheumatica (PMR) have giant cell arteritis (GCA); 40% to 60% of GCA patients have PMR. Diagnosis is made via history and with supportive laboratory tests indicating an elevated ESR or CRP. Rapid improvement often occurs within 24 to 72 hours with low-dose prednisolone.

Answer 219

Disease incidence increases with age, occurring in those older than 50 years and rarely in younger individuals. Incidence appears highest in those of northern European descent. PMR rarely occurs in individuals younger than 50 years of age. For those 50 and older, the US prevalence has been estimated at 6/1,000, and the US average annual age- and sex-adjusted incidence estimated at 52.5/100,000. The incidence is higher in females at 61.7/100,000, compared with 39.9/100,000 in males.

Answer 220

The exact cause of PMR is unknown. There have been conflicting observations regarding seasonal variation on the incidence of PMR. These observations have suggested a role of infectious agents such as adenovirus, respiratory syncytial virus, parainfluenza virus type I, parvovirus B19, Mycoplasma pneumoniae, and Chlamydia pneumoniae A potential hormonal role has been suggested by the observation of adrenal gland hypofunction in untreated patients. Inappropriately normal cortisol levels and low levels of dehydroepiandrosterone have been observed.

Answer 221

STRONG Age >50 GCA WEAK Feminine

Answer 222

The typical presentation is morning stiffness for >1 hour in the shoulder girdle in 70% to 95% of patients and/or pelvic girdle pain in 50% to 70% of patients. The typical presentation is inflammatory pain for >1 hour in the morning in the shoulder girdle in 70% to 95% of patients and/or pelvic girdle pain in 50% to 70% of patients. Response to a corticosteroid therapeutic trial is typically dramatic and rapid, usually occurring within 24 to 72 hours. ``` Generally acute onset Anorexia WL Malaise Depression Asthenia Oligoarticular arthritis ```

Answer 223

``` ESR - high CRP - high FBC - variable US - bursitis, joint effusions One systematic search of the literature regarding the use of imaging in PMR found that tenosynovitis of the long head of the biceps tendon, bilateral subacromial bursitis, and trochanteric bursitis were consistent findings in patients with PMR. ``` NOT SPECIFIC ENOUGH TO BE A TEST - IL-6 stimulates many acute phase proteins. Elevated IL-6 is characteristic in PMR.

Answer 224

1. corticosteroid prednisolone: 12.5 to 25 mg orally once daily initially, then taper to 10 mg once daily over 4-8 weeks, then taper by 1 mg/month thereafter Secondary options methylprednisolone: 120 mg intramuscularly every 3 weeks for 3 months then taper dose gradually, consult specialist for further guidance on dose + calcium, vit D + bisphosphonates +/- NSAID 2. Methotrexate 3. Some case reports of tocilizumab - anti IL6

Answer 225

The overall prognosis is good. Although response to treatment typically occurs within 24 to 72 hours, relapses or symptom exacerbations are common. Treatment also typically requires 2 to 3 years. Less commonly, there is a chronic relapsing course that may require a longer course of treatment. PMR may also be associated with giant cell arteritis (GCA) and, if present, the prognosis and treatment is directly related to GCA. Increased risk of relapse or prolonged therapy has shown association with female sex, high ESR (>40 mm/hour), and peripheral arthritis.

Answer 226

Relapsing PMR GCA ``` Corticosteroid SEs: Increased infection Osteoporosis HTN Prox myopathy Cataracts Glaucoma Skin thinning with increased bruising found with chronic use of corticosteroids. ``` ``` Methotrexate SEs: Myelosuppression Oral ulcers Hepatotoxicty ILD ``` Cardiovascular, cerebrovascular, and peripheral vascular event rates were higher in patients with PMR compared with those without from 6 months to 12 years of follow-up.

Answer 227

polymyalgia rheumatica Less common peripheral musculoskeletal manifestations include a monoarthritis or polyarthritis, pitting oedema of the hand, carpal tunnel syndrome, and tenosynovitis. A second presentation is the presence of the characteristic neck, shoulder girdle, and hip girdle symptoms associated with normal serum markers of systemic inflammation (i.e., ESR or CRP).

Answer 228

An inflammatory arthritis that occurs after exposure to certain gastrointestinal and genitourinary infections. The classical triad of post-infectious arthritis, non-gonococcal urethritis, and conjunctivitis is frequently described but found only in a minority of cases and not required for diagnosis. ReA belongs to the family of spondyloarthropathies, which share similar clinical, radiographic, and laboratory features that include spinal inflammation and an association with HLA-B27. They include psoriatic arthritis, ankylosing spondylitis, arthritis related to inflammatory bowel disease, and undifferentiated spondyloarthropathy. Patients may give a history of an antecedent genitourinary or dysenteric infection 1 to 4 weeks before the onset of arthritis. Presenting features include systemic symptoms such as fever, peripheral and axial arthritis, enthesitis (inflammation where tendons insert into bone), dactylitis (swelling of an entire finger or toe), conjunctivitis and iritis, and skin lesions including circinate balanitis and keratoderma blennorrhagicum. The peripheral arthritis in reactive arthritis (ReA) is usually an asymmetrical oligoarticular arthritis affecting the large joints of the lower limb, although monoarticular and polyarticular arthritis can also occur. There is no specific test for diagnosing ReA. Rather, a group of tests is used to confirm the suspicion in someone who has clinical symptoms suggestive of an inflammatory arthritis in the post-venereal or post-dysentery period. Treatment is aimed at symptomatic relief and preventing or halting further joint damage. Typical agents include non-steroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and disease-modifying antirheumatic drugs (DMARDs). Approximately 30% to 50% of patients will go on to develop some form of chronic ReA.

Answer 229

ReA occurs mainly in adults The prevalence is thought to be 30 to 40 cases per 100,000 adults, with an annual incidence of 4.6 per 100,000 for Chlamydia-induced arthritis and 5 per 100,000 for enterobacteria-induced arthritis The attack rate of ReA after a C trachomatis infection ranges from about 4% to 8% and that of post-dysentery ReA ranges from 1.5% to about 30%

Answer 230

The most commonly implicated bacterial species are Chlamydia, Salmonella, Campylobacter, Shigella, and Yersinia species, although ReA has been described after many other bacterial infections. They are gram-negative organisms with a lipopolysaccharide component within their cell wall, and the bacteria and bacterial components have been identified in synovial tissue

Answer 231

STRONG Male HLAB27 Hx chlamidya or GI

Answer 232

The arthritis is most commonly an asymmetrical oligoarthritis. However, polyarticular and monoarticular arthritis can occur. There is usually a predilection for the larger joints in the lower extremity. The inflammation often leads to painful, swollen, warm, red, and stiff joints, especially in the morning. Swelling of entire digits (fingers or toes), termed dactylitis, is a specific finding within the spondyloarthropathies arising from flexor tenosynovitis. Usually, patients are defined as having chronic reactive arthritis (ReA) when joint symptoms have been present for more than 6 months. Clinical symptoms typically begin within 1 to 4 weeks after the onset of infection. The latency in developing arthritis associated with post-chlamydial infections may be longer than that associated with post-dysenteric infections Spinal inflammation, especially of the sacroiliac joints and lumbosacral spine, is a common finding. Symptoms manifest as non-specific low back pain and/or buttock pain and stiffness, especially during times of inactivity. Symptoms are generally relieved by exercise, which distinguishes spinal inflammatory arthritis from mechanical causes of back pain. Thoracic and cervical spine involvement occurs with chronic ReA. Enthesitis - This is inflammation at sites where tendons insert into bones. Common sites include the Achilles' tendon and plantar fascia at the calcaneus, which manifest as heel pain. Patients may develop superficial painless oral ulcers along with urethritis and sterile dysuria. Inflammation of the bladder and prostate can lead to cystitis and prostatitis. Keratoderma blennorrhagicum is a skin disorder characterised by hyperkeratotic skin in about 12% of patients. It appears as a vesicular lesion that becomes plaque-like or pustular and is microscopically indistinguishable from pustular psoriasis. These lesions most often occur on the soles or palms, but have been described elsewhere. Ocular inflammation in the form of conjunctivitis can cause redness, tearing, and a sterile purulent discharge during the acute period. Anterior uveitis (iritis), associated with HLA-B27 positivity, causes symptoms of pain, redness, and photophobia. Iritis often becomes chronic. Inflammation of the aorta can lead to aortitis, which can cause aortic regurgitation, precipitating heart failure. Arrhythmias occur secondary to scarring of the conduction system by chronic inflammation.

Answer 233

ESR + CRP - H ANA + RF + CCP - ve Plain xray - sacroiliitis or enthesopathy To rule out crystal-induced arthritis such as gout. This same test could also be considered as a subsequent test with future flares.

Answer 234

NSAID corticosteroids DMARD - sulfasalazine if prolonged

Answer 235

Approximately 50% of patients can expect symptoms to resolve within the first 6 months However, 30% to 50% of patients will develop chronic reactive arthritis

Answer 236

Secondary osteoarthritis IRITIS / UVEITIS Keratoderma blenorhagicum

Answer 237

reactive arthritis

Answer 238

Conservative: wear wide shoes with a low heel and soft sole hold an ice pack (or a bag of frozen peas wrapped in a tea towel) to the bunion for up to 5 minutes at a time try bunion pads (soft pads you put in shoes to stop them rubbing on a bunion) – you can buy these from pharmacies take paracetamol or ibuprofen try to lose weight if you're overweigh Surgery do not wear high heels or tight, pointy shoes

Answer 239

``` Physiotherapy NSAIDs Muscle relaxants - diazepam or tizanidine Steroidal injections Cervical nerve root block Surgical nerve decompression ```

Answer 240

Axial neck pain with cervical spondylosis has no cure and is usually considered to deteriorate with age. Yet many patients with severe cervical spondylosis (on radiographic studies) have no axial neck pain; the presence of pain may not necessarily correlate with the degree or severity of radiographic spondylosis. Patients presenting with axial neck pain typically improve over time, although the pain may recur and may be severe. The patient may need lifelong pain management treatment if the pain is persistent and prolonged. Patients presenting primarily with axial neck pain rarely develop a more severe condition in the sense of the degenerative joint disease leading to either radiculopathy or myelopathy.

Answer 241

Progressive degeneration after surgical intervention leading to disease at adjacent levels Acute myelopathy or quadriplegia

Answer 242

cervical spondylosis A less common presentation is cervical spondylotic myelopathy. This presentation is more commonly loss of function in the upper limbs (i.e., loss of fine motor function in the hands) rather than the lower limbs (i.e., gait ataxia). This syndrome is epitomised by numb or clumsy hand symptoms where the patient has initial difficulty in fine motor function. This can progress to more diffuse weakness in the upper extremities. Most of these symptoms reflect upper motor neuron pathology directly attributable to pressure on the cervical spinal cord (between the C2 and C7 levels) with resulting hyper-reflexia (depending on the level in upper and lower extremities) and, rarely, direct sensory loss. Many patients also have axial neck pain because the compression on the spinal cord is due to severe degenerative changes in the cervical spine. Radicular arm pain is rarely present.

Answer 243

Spondylolysis (spon-dee-low-lye-sis) is defined as a defect or stress fracture in the pars interarticularis of the vertebral arch.[1] The vast majority of cases occur in the lower lumbar vertebrae (L5), but spondylolysis may also occur in the cervical vertebrae

Answer 244

Clinical Signs:[4][5] Pain on completion of the stork test (placed in hyperextension and rotation) Excessive lordotic posture Unilateral tenderness on palpation Visible on diagnostic imaging (Scottie dog fracture) Symptoms:[4][5] Unilateral low back pain Pain that radiates into the buttocks or legs Onset of pain can be acute or gradual Pain that can restrict daily activities Pain that worsens after strenuous activity Pain aggravated with lumbar hyperextension Difficulty in movement in spinalcord +ve one-legged hyperextension test - It involves having the patient stand upon one leg and then lean backwards. The test should produce pain on the same side of the spine as the leg that you are standing on. If it produces pain this indicates spondylolysis on that side. The test is then performed on the other side assessing for pain again. The test can be positive on one side, both sides or neither. RFs = sport

Answer 245

It involves having the patient stand upon one leg and then lean backwards. The test should produce pain on the same side of the spine as the leg that you are standing on. If it produces pain this indicates spondylolysis on that side. The test is then performed on the other side assessing for pain again. The test can be positive on one side, both sides or neither. Surgery = spinal fusion or laminectomy

Answer 246

Xray / CT /MRI

Answer 247

Xray / CT /MRI

Answer 248

Spondylolisthesis is the displacement of one spinal vertebra compared to another. While some medical dictionaries define spondylolisthesis specifically as the forward or anterior displacement of a vertebra over the vertebra inferior to it (or the sacrum). Spondylolisthesis is classified as one of the six major etiologies: degenerative, traumatic, dysplastic, isthmic, pathologic, or post-surgical, which are discussed in further detail below

Answer 249

A general stiffening of the back and a tightening of the hamstrings, with a resulting change in both posture and gait. A leaning-forward or semi-kyphotic posture may be seen, due to compensatory changes. A "waddle" may be seen in more advanced causes, due to compensatory pelvic rotation due to decreased lumbar spine rotation. A result of the change in gait is often a noticeable atrophy in the gluteal muscles due to lack of use. Generalized lower-back pain may also be seen, with intermittent shooting pain from the buttocks to the posterior thigh, and/or lower leg via the sciatic nerve. Other symptoms may include tingling and numbness. Coughing and sneezing can intensify the pain. An individual may also note a "slipping sensation" when moving into an upright position. Sitting and trying to stand up may be painful and difficult The most common finding is pain with lumbar extension.[17] The following physical involves specific assessment for spondylolisthesis. However, a general examination, most importantly neurological examination, must be done to rule out alternative causes for signs and symptoms. Neurological examination is often normal in patients with spondylolisthesis, but lumbosacral radiculopathy is commonly seen in patients with degenerate spondylolisthesis

Answer 250

Xray AP + lateral MRI CT scan

Answer 251

Low impact exercise Bracing possible NSAID Three indications for potential surgical treatment are as follows: persistent or recurrent back pain or neurologic pain with a persistent reduction of quality of life despite a reasonable trial of conservative (3month) management, new or worsening bladder or bowel symptoms, or a new or worsening neurological deficit.

Answer 252

Patellofemoral pain syndrome is defined as knee pain resulting from mechanical and biochemical changes to the patellofemoral joint. Patellofemoral pain syndrome is one of the most common disorders of the knee, accounting for 25% of knee injuries seen in a sports medicine clinic. The causes of patellofemoral problems are multifactorial, including abnormal patellofemoral joint mechanics, lower kinetic chain alterations, and overuse. Patients typically note the insidious onset of an ill-defined ache localised to the anterior knee behind the patella. There is no one physical examination or imaging test that is a standard for diagnosis. Treatment is focused on activity modification and correction of specific risk factors. Non-operative treatment is successful in the majority of cases.

Answer 253

Patellofemoral pain syndrome is one of the most common disorders of the knee, accounting for 25% of knee injuries seen in the sports medicine clinic It is most common in the second and third decade of life.

Answer 254

``` Abnormal patellofemoral joint mechanics Bony and structural abnormalities Tightness of soft tissue structures Decreased patellar mobility Quadriceps muscle weakness Altered lower-extremity alignment and/or motion Subtalar joint pronation Excessive hip internal rotation Hip abductors weakness Gait deviations Overuse Training errors. ```

Answer 255

``` ill-defined ache pain aggravated by compressive force Q angle pain on palpation of patellar retinaculum patellar tilt test mediolateral glide test patellar mobility test patellar apprehension test patellar maltracking test decreased muscle flexibility muscle weakness ```

Answer 256

Clinical | Xray/MRI

Answer 257

The treatment programme should focus on relative rest and activity modification (i.e., lower levels of activity, particularly of those exerting compressive force). During the acute phase, ice or other methods of cold application may be used for 10 to 15 minutes, 2 to 3 times daily, to further reduce symptoms. Heat is generally not recommended. NSAIDs Patellar bracing Physio

Answer 258

Most patients are successfully treated by conservative means, with few requiring surgical intervention. The current standard of care is conservative treatment including physiotherapy to address biomechanical issues, with quadriceps-based strengthening; iliotibial band, hamstring, and quadriceps stretching; and proximally focused hip stabilisation programmes, as well as orthotic intervention, taping, and bracing.[7] However, there is no one exercise modality that is clearly superior to others, and each patient with patellofemoral pain should be given an individualised programme based on their specific deficits.[95][96] A period of 4 to 6 weeks is usually adequate for resolution of symptoms. Successful long-term outcomes (67%-85%) have been reported with a comprehensive home exercise programme.[97][98]

Answer 259

Iliotibial band syndrome is the most common cause of lateral knee pain in runners. Runners predisposed to this injury are typically in a phase of over-training and often have underlying weakness of the hip abductor muscle. Male runners may exhibit kinematic faults such as increased hip internal rotation and knee varus, and weakness in the external rotator muscles of the hip. Female runners may exhibit increased hip adduction and knee internal rotation, and abnormal iliotibial band strain and strain rate. In the acute phase, treatment includes activity modification, ice, non-steroidal anti-inflammatory drugs, and corticosteroid injection in cases of severe pain or swelling. During the sub-acute phase, emphasis is on stretching of the iliotibial band and soft-tissue therapy for any myofascial restrictions. The recovery phase focuses on a series of exercises to improve hip abductor strength and integrated movement patterns. The final return to running phase is begun with an every-other-day programme, starting with easy sprints and avoidance of hill training with a gradual increase in frequency and intensity. Surgery can be considered in refractory cases.

Answer 260

Excessive friction of the distal iliotibial band (ITB) sliding over the lateral femoral epicondyle occurs as the knee flexes during deceleration into stance-phase running

Answer 261

NOBLES Physician applies pressure over the lateral femoral epicondyle while extending the knee from 90° of flexion.[8] Pain occurs when knee is flexed around 30°. OBERS Normal tightness is when the leg can be passively stretched to a position horizontal but not completely adducted to a table. Moderate tightness is when the leg can be passively adducted to horizontal at best. If the leg cannot be passively adducted to horizontal, this is maximal tightness THOMAS The patient sits on the end of an examining table, rolls back to a supine position, and holds both knees to the chest. The patient holds the knee on the asymptomatic side close to the chest, keeping the hips on the table, and avoiding excessive posterior tilt (lumbar lordosis flattened).[33] The examiner then slowly lowers the affected limb towards the floor.[8]The test is positive if the femur is above the horizontal of the table (psoas), knee extends (rectus femoris and psoas), and abduction of the femur deepens the iliotibial band (tensor fascia lata and iliotibial band).

Answer 262

``` NSAIDs Modify activity Corticosteroids Physio Elective surgery ```

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