Clinical Case Studies Week 2 (Rheumatoid/Osteo Arthritis, Gout, UC and CD)

Question 1

What is rheumatoid arthritis?

Answer 1

Rheumatoid arthritis is a chronic autoimmune disease characterised by persistent synovitis, systemic inflammation and the presence of autoantibodies. Persistent joint inflammation can lead to the development of bony erosions, cartilage and tendon degradation, and joint deformity.

Question 2

What decreases likelihood of developing RA?

Answer 2

A healthy lifestyle (eg avoiding smoking, maintaining ideal body weight, eating a healthy diet) decreases the likelihood of developing rheumatoid arthritis.

Question 3

What are some features that suggest RA?

Answer 3

family history of inflammatory arthritis

early morning stiffness lasting longer than 1 hour

swelling in five or more joints

symmetry of the areas affected

bilateral compression tenderness of the metatarsophalangeal joints

RF positivity

anti-CCP antibody test positivity

symptoms present for longer than 6 weeks

bony erosions evident on X-rays of the wrists, hands or feet (uncommon in early disease)

raised inflammatory markers, such as CRP or ESR, in the absence of infection

presence of rheumatoid nodules

Question 4

General management approach for RA?

Answer 4

Patients with rheumatoid arthritis require integrated, multidisciplinary care that is designed to manage the broad spectrum of patient needs in a timely manner.

• All patients should have an individualised management plan that is negotiated between the patient, their specialist and general practitioner, and other health professionals involved in their care (eg physiotherapist, occupational therapist, podiatrist, psychologist).
• The management plan should include support for self-management, including advice on managing symptom exacerbations until specialist review.

Question 5

The goal of rheumatoid arthritis management is to maximise long-term health-related quality of life by?

Answer 5

controlling symptoms

normalising physical function

enabling participation in social and work-related activities

preventing joint damage

minimising cardiovascular complications

Question 6

What are some potential complications of RA?

Answer 6

Atherosclerosis, osteoporosis, depression, vasculitis, peptic ulcer disease, lung disease, neuropathy

• Systemic inflammation is the main contributor to the increased risk of developing atherosclerosis in patients with rheumatoid arthritis

Question 7

optimising the patient’s immune status, including ensuring that recommended vaccinations are up to date, because both rheumatoid arthritis and its treatment can increase the risk of infection

true or false

Answer 7

true

Question 8

Most important aspect in managing RA?

Answer 8

• Inducing clincial remission as early as possible
• Maintaining clinical remission

Question 9

What is clinical remission defined as?

Answer 9

symptom relief

normalisation of inflammatory markers

the absence of joint swelling.

Question 10

What drugs reduce or eradicate synovitis and thus prevent joint damage

Answer 10

Disease-modifying antirheumatic drugs (DMARDs) –> start as soon as possbile

Question 11

Corticosteroids are often combined with csDMARDs during the induction stage of treatment, why?

Answer 11

To provide rapid symptom relief

Question 12

Most patients need to be maintained on treatment indefinitely because rheumatoid arthritis rarely goes into drug-free remission and may be more difficult to control if it recurs after stopping treatment. Even patients with well-controlled disease may have persisting symptoms

true or false

Answer 12

true

Question 13

How to measure inflammation druing RA drug therapy?

Answer 13

Inflammation is most reliably assessed by the number of swollen or tender joints as well as the inflammatory markers C-reactive protein (CRP) and/or erythrocyte sedimentation rate (ESR); neither measure should be used alone.

Patient-reported outcomes include pain, physical function, psychological health, sleep patterns, relationships, and participation in social and work-related activities.

> Joint damage is usually assessed throughout the disease course by plain X-rays and ultrasound. Magnetic resonance imaging (MRI) may occasionally be used by specialists.

> Rheumatoid factor (RF) and antibodies to cyclic citrullinated peptides (CCP) are not used to monitor disease activity.

Question 14

Conventional synthetic disease-modifying antirheumatic drugs, what are examples of them and what is 1st line and what is this combined with?

Answer 14

Methotrexate is the drug of choice for most patients, and should form the backbone of the regimen when combination therapy is required.

• It may be used in combination with other csDMARDs (leflunomide, sulfasalazine, hydroxychloroquine) for patients with active disease and significantly impaired function

Question 15

What to use if methotrexate contraindicated or not tolerated?

Answer 15

If methotrexate is contraindicated or not tolerated, leflunomide is often substituted

> Monotherapy with hydroxychloroquine or sulfasalazine may be used if the patient has low-grade inflammation, few affected joints and no indicators of poor prognosis.

Question 16

How long to see an effect with synthetic DMARDs?

Answer 16

When csDMARD therapy is started, disease activity is regularly monitored and therapy adjusted to achieve clinical remission. A response to csDMARDs should be apparent within 12 weeks

Question 17

Methotrexate dose?

Answer 17

methotrexate 10 mg orally, on one specified day once weekly, increasing up to 25 mg orally or subcutaneously, on one specified day once weekly

PLUS

Folic acid 5 to 10 mg orally, per week (preferably not on the day methotrexate is taken).

Question 18

When disease control has been achieved and maintained with csDMARD therapy, the csDMARD dose may be reduced to the lowest dose that maintains disease control. Dose reductions should only occur in consultation with the treating specialist, and usually take place after corticosteroid therapy has been completely tapered.

True or False

Answer 18

True

Question 19

Corticosteroids have anti-inflammatory and disease-modifying effects in rheumatoid arthritis. Because of their rapid onset of action, corticosteroids are often used by specialists to achieve rapid symptom control at presentation, or during an exacerbation of disease, while awaiting a response to conventional synthetic disease-modifying antirheumatic drug (csDMARD) therapy (which can often take between 6 and 12 weeks).

Which types of corticosteroid are used?

Answer 19

If IM therapy indicated: methylprednisolone acetate 120 mg intramuscularly, as a single dose.

If Oral therapy indicated: prednis(ol)one 5 to 15 mg orally, daily.

Question 20

What limits the use of corticosteroids?

Answer 20

Although corticosteroids are effective, significant adverse effects limit their use. When disease remission is achieved, the dose of corticosteroid should be slowly tapered until the corticosteroid can be stopped.

Question 21

When are intrarticular corticosteroid injections effective?

Answer 21

small number of accessible joints are involved, and can minimise the use of systemic corticosteroids

Question 22

When are biological and targeted synthetic DMARDs used?

Answer 22

used by specialists for the treatment of rheumatoid arthritis if remission is not achieved, or significant disease activity persists, after trialling conventional synthetic disease-modifying antirheumatic drugs (csDMARDs).

• They are usually used in combination with csDMARD therapy. Several bDMARDs, with different mechanisms of action, are available.
• At the time of writing, tofacitinib is the only tsDMARD indicated for rheumatoid arthritis.

Question 23

Patients taking bDMARDs or tofacitinib are at increased risk of infections. Clinicians must always be alert to the possibility of infection (including opportunistic infection), particularly because the usual symptoms and signs (eg fever) are often absent.

Answer 23

True or False

Question 24

Examples of bDMARDs?

Answer 24

If response to initial drug choice is inadequate, an alternative first-line bDMARD may be used.

Question 25

What to do pateints with persistent inflammatory pain?

Answer 25

Consider referring patients with persisting inflammatory joint pain to their specialist for adjustment of the DMARD regimen

Question 26

If a patient with well-controlled disease (ie in clinical remission) experiences ongoing pain, it is likely to be noninflammatory in nature. How to manage this?

Answer 26

Combine nonpharmacological and pharmacological strategies, tailored to the individual patient Nonpharmacological strategies for residual noninflammatory joint pain include: rest and pacing activities, thermotherapy, splints/orthoses, exercise therapy, cognitive behavioural therapy (CBT), transcutaneous electrical nerve stimulation (TENS), psychotherapy, and relaxation, mindfulness and meditation When analgesia is indicated, the primary goals of management are to improve function and reduce disability, not just reduce the intensity of pain. Before escalating analgesia, consider and address biopsychosocial and environmental factors that may be contributing to the patient's experience of pain * use NSAID orally, but consider risks * fish oil at least 2.7 g (omega-3) orally, daily --\> mild anti-inflammatory effect in rheumatoid arthritis * Fish oil may take up to 3 months for maximal effectiveness, so it may be necessary to co-prescribe fish oil with an NSAID initially

Question 27

Opioid use in RA?

Answer 27

Opioids have a very limited role in the management of pain associated with rheumatoid arthritis because of modest, if any, benefits and a significant risk of harms. Opioids may be considered for patients with severe pain that is not adequately relieved by other analgesics (eg paracetamol plus an NSAID) and is interfering with their ability to function \> If opioids are used, they should be prescribed on a short-term trial basis, as part of an overall pain management strategy, with clear goals and regular review of treatment response and adverse effects

Question 28

How to manage fatigue in RA?

Answer 28

There are no pharmacological treatments for fatigue in rheumatoid arthritis. There is some evidence that physical activity (eg pool-based therapy, yoga, dynamic strength training, stationary cycling, low-impact aerobics, Tai Chi) and psychosocial interventions (eg cognitive behavioural therapy, mindfulness) have a small benefit, but the optimal treatment strategy is not yet established. \> Consider and manage potential contributors to fatigue, such as anaemia, hypothyroidism, drug adverse effects, depression, insomnia due to underlying pain, or loss of muscle mass

Question 29

Lifestlye management of RA?

Answer 29

* Land- and water-based aerobic exercises are beneficial for patients with rheumatoid arthritis at all stages of disease. Regular aerobic exercise improves physical function, helps maintain ideal body weight and also benefits psychological and cardiovascular health \> Patients may worry that rheumatoid arthritis disease activity is increased by exercise. Although some pain with exercise can be expected, patients should be reassured that the benefits of exercise significantly outweigh the risks. * The Mediterranean-style diet, characterised by a high consumption of fruit, vegetables, cereals and legumes, a little red meat but more fish, olive oil as the main source of fat, and a moderate intake of wine, appears to be the most universally accepted dietary intervention; it has the added benefit of weight control and reducing cardiovascular risk. * All patients with rheumatoid arthritis should be strongly advised to stop smoking. Not only is smoking linked to the development of rheumatoid arthritis, it is also linked to poor prognosis and is a predictor of poor response to therapy. Smoking also increases the risk of developing cardiovascular disease in a patient group already at increased risk

Question 30

Considerations before starting immunomodulatory therapy?

Answer 30

screen the patient for active infection check for history of tuberculosis infection and environmental exposure assess vaccination status assess the patient's serology and, as appropriate, consider vaccination, treatment or prophylaxis perform investigations to determine kidney, liver and bone marrow function, as well as chest X-ray. The results of these investigations may influence the choice of immunomodulatory drug and its dosing regimen, and provide a baseline measurement against which future results can be compared

Question 31

Consideraitons throughout immunomodulatory therapy?

Answer 31

ask about adherence to immunomodulatory therapy assess for adverse effects monitor kidney, liver and bone marrow function according to the schedule determined. This is not required for patients treated with corticosteroid or hydroxychloroquine monotherapy ensure that vaccinations remain up to date assess patients who present with fever, cough, systemic symptoms or unexplained illness for opportunistic infection, including tuberculosis or fungal infection continue to screen for and optimise the management of osteoporosis, residual pain and other common comorbidities (eg cardiovascular disease, diabetes, depression)

Question 32

for RA, There are some data to suggest that the following drugs may, with appropriate precautions, be safely used in pregnancy. What are these drugs?

Answer 32

azathioprine, ciclosporin, hydroxychloroquine, prednis(ol)one, sulfasalazine and tumour necrosis factor (TNF) inhibitors

Question 33

OA from now on...

Question 34

What is OA?

Answer 34

Osteoarthritis is a chronic musculoskeletal condition that affects the joints and peri-articular structures. The changes of osteoarthritis can affect the whole joint, including the cartilage, bone, synovial lining and synovial fluid \> increases with age Osteoarthritis can affect any joint; however, the most commonly affected joints are those of the hands (particularly the distal interphalangeal joints and the first carpometacarpal joints), the cervical spine, the lumbar spine, and the knees and hips.

Question 35

How to manage OA as a whole?

Answer 35

Osteoarthritis is best managed by an integrated chronic disease model of care that supports multidisciplinary involvement and is underpinned by a biopsychosocial approach. * Besides their general practitioner, based on the patient's needs, other members of the multidisciplinary team may include a physiotherapist, an exercise physiologist, a dietician, a psychologist, a nurse, an occupational therapist, a rheumatologist and/or an orthopaedic surgeon. * The general practitioner is usually the care coordinator.

Question 36

What are the goals of management?

Answer 36

enable pain coping and, where possible, reduce symptoms maintain and optimise physical function maintain and optimise ability to perform daily activities (eg participation in social, recreational and occupational activities) minimise associated disability maximise health-related quality of life.

Question 37

Other goals of management as holistic picture for OA?

Answer 37

* Educate and reassure the patient about the nature of the condition and provide support for self-management * Individualise the goals of management and the management plan through shared decision-making, taking into account the patient's affected joints, the stage and severity of their disease, their functional impairments, their risk factors for osteoarthritis, and their age, comorbidities and concomitant treatments. * Optimise the management of comorbidities, including other rheumatological diagnoses. * If the patient is overweight or obese, provide advice about weight loss and refer to services as required. * Provide advice about exercise and refer to services as required. * Provide advice about nonpharmacological intervention * If topical analgesia is needed, trial a topical NSAID or capsaicin. * If oral analgesia is needed, both paracetamol and oral NSAIDs have a role * Organise regular clinical review to monitor goals of management, and modify goals and the management plan as needed. If there are concerns about the patient's progress, consider specialist referral.

Question 38

What are some other interventions possible if the ones mentioned in the previous question dont work?

Answer 38

For patients with persisting functional impairment and pain * These include intra-articular corticosteroid injections, intra-articular hyaluronan injections and duloxetine * Options for end-stage disease include surgery and opioids. In all cases, patients should be encouraged to maintain lifestyle measures, such as exercise and weight loss.

Question 39

Strategies for self management?

Answer 39

Coping strategies for living with chronic pain Pacing physical activities (eg spreading physically hard jobs throughout the day with breaks in between to reduce sustained physical loading) lifestyle measures, such as exercise and weight loss use of physical aids strategies to minimise symptoms when performing activities of daily living (often referred to as joint protection techniques topical or oral analgesia for evoked pain monitoring pain levels using a pain management diary

Question 40

Lifestyle management of OA?

Answer 40

**Excercise** Exercise is important for all patients with osteoarthritis, irrespective of the affected joints or the stage or severity of the disease (including for patients awaiting surgery). Reported benefits of exercise include reduction in pain, and improvements in physical function and quality of life. Regular aerobic exercise has multiple well-recognised general health benefits that are relevant to patients with osteoarthritis. These include reduced risk of cardiovascular disease, weight loss, improved quality of life, improved mood and sleep patterns, and reduced risk of falling in older patients. Weight loss is particularly important because obesity is a modifiable risk factor for the development and progression of osteoarthritis. Appropriate exercise can be undertaken safely in a variety of settings (eg home, gym, group class or under clinical supervision). Referral to an appropriate health professional (eg physiotherapist, exercise physiologist) may be beneficial to initiate and reinforce an exercise program; this may include prescribing a personalised program of simple exercises (eg swimming, walking) that the patient can do unsupervised. Involving the patient's social supports (eg spouse) in the exercise program may also improve outcomes. **Weight loss** Obesity is a risk factor for both the development and progression of knee osteoarthritis. The majority of patients with knee osteoarthritis are overweight or obese. Of those patients undergoing joint replacement surgery for knee osteoarthritis, 60% are reported as obese. Obesity also appears to be a risk factor for hip, hand and spinal osteoarthritis; 40% of patients undergoing joint replacement surgery for hip osteoarthritis are reported as obese. There is strong evidence that weight loss is beneficial for knee osteoarthritis. Despite no good evidence that it helps hip or other forms of osteoarthritis, weight loss is still recommended because of the general health benefits.

Question 41

Physical treatment for OA?

Answer 41

In patients with knee or hip osteoarthritis, thermotherapy (application of heat or cold), or the use of a walking stick may reduce pain and enable physical activity Evidence suggests that acupuncture, transcutaneous electrical nerve stimulation (TENS), lateral heel wedge insoles, manual therapy, magnets and valgus braces are not effective in the management of osteoarthritis.

Question 42

Pyschological therapies of OA?

Answer 42

Patients with osteoarthritis who live with chronic pain, functional impairment and impaired quality of life are likely to experience a negative psychological impact. P sychological impairments may increase disability, affect adherence to self-management strategies and reinforce central sensitisation. Psychological therapies (eg cognitive behavioural therapy) may be useful to address psychological impairments and pain coping. Recent data also suggest a potential benefit from internet-delivered pain-coping programs.

Question 43

Topical nonsteroidal anti-inflammatory drugs (NSAIDs) and capsaicin can be considered when?

Answer 43

As an adjunct to other treatment strategies and as part of short-term self-management. \> because of minimal systemic absorption, topical NSAIDs are considerably safer than oral NSAIDs and limited evidence suggests they have similar efficacy to oral NSAIDs in patients with osteoarthritis a topical NSAID applied directly to the painful area, up to 4 times daily \> capsaicin 0.025% cream applied directly to the painful area, 3 to 4 times daily. --\> the main adverse effect is a transient burning at the site of application, which decreases over time

Question 44

Oral NSAIDs are more effective than paracetamol and can improve symptoms in most patients. However, oral NSAIDs also have a greater potential for harm, particularly in older people, who are the population most commonly affected by osteoarthritis. For patients at low risk of harms from NSAID use, a trial of an oral NSAID may be considered first line \> Avoid first-line use of oral NSAIDs in all other patients. True or false

Answer 44

True

Question 45

If response to paracetamol is inadequate, a judicious trial of NSAID use may be considered instead of, or in combination with, paracetamol. This decision should be based on an assessment of the benefit–harm profile for an NSAID in the individual patient. true or galse

Answer 45

true

Question 46

A single intra-articular corticosteroid injection may provide symptom relief lasting from 4 to 12 weeks in patients with?

Answer 46

knee OA \> intra-articular corticosteroid injection may be repeated at 3-monthly intervals if needed; evidence suggests that repeat injections are effective and do not alter disease progressio

Question 47

Whats the benefit of using a IA injection?

Answer 47

Because of their rapid onset of action, intra-articular corticosteroid injections may be useful if patients have to travel or participate in an important occasion; they may also enable participation in strengthening exercises

Question 48

Intra-articular corticosteroid injection provides greater short-term benefits in knee osteoarthritis than intra-articular \_\_\_\_\_\_\_\_, but pain relief from intra-articular hyaluronan injection may last slightly longer in patients who respond

Answer 48

hyaluronan injection \> pain relief from intra-articular hyaluronan injection may last slightly longer in patients who respond \> Intra-articular hyaluronan injection may be associated with temporary worsening of osteoarthritis symptoms, and the unit cost of intra-articular hyaluronan injection is much higher than the unit cost of intra-articular corticosteroid injection

Question 49

.... has been shown to reduce pain and improve physical function compared to placebo in patients with chronic pain due to knee osteoarthritis?

Answer 49

Duloxetine \> Duloxetine has also been shown to be an effective adjunct to oral NSAIDs. \> Duloxetine may be considered for patients with knee osteoarthritis who have persisting functional impairment and pain \> Duloxetine 30 mg orally, daily for 1 week, then increase to 60 mg daily. Maximum daily dose is 120 mg.

Question 50

When should opioids be used in OA?

Answer 50

Opioids may be considered for patients with severe persisting functional impairment due to pain \> Opioids are not recommended for osteoarthritis of the hand. \> Should be prescribed short term \> Studies up to 1 year in patients with knee or hip osteoarthritis indicate that tapentadol may have a more favourable safety profile than oxycodone

Question 51

Gout from this card onwards...

Question 52

What is gout?

Answer 52

* Gout is a chronic disease that involves the deposition of monosodium urate crystals in the body, in particular the joints, soft tissues and kidneys. The main symptoms of gout are joint pain and swelling, which may represent an initial or recurrent acute attack, chronic gouty arthritis, or an acute attack in a patient with underlying chronic gouty arthritis * The major manifestations of gout in the kidney are nephrolithiasis and chronic urate nephropathy; both of which can progress to chronic kidney disease.

Question 53

When does gout occur?

Answer 53

Gout occurs when the serum uric acid concentration is sufficiently elevated (usually greater than 0.42 mmol/L [7 mg/dL]), and the solubility coefficient of monosodium urate exceeded, long enough for crystals to form in tissues

Question 54

Risk factors for gout

Answer 54

Consumption of purine-rich foods (particularly meat and seafood), alcohol (particularly beer and spirits) and fructose-sweetened drinks can increase serum uric acid concentration and the risk of gout in susceptible individuals Comorbidities including hypertension, chronic kidney disease, dyslipidaemia, type 2 diabetes and obesity are risk factors for gout. A high concentration of endogenous insulin, as seen in patients with obesity, also inhibits the renal excretion of uric acid.

Question 55

Drugs that inhibit the renal excretion of uric acid can increase serum uric acid concentration and the risk of gout in susceptible individuals, wht are some of these drugs?

Answer 55

These drugs include thiazide diuretics (often taken as a combination product with an angiotensin converting enzyme inhibitor or angiotensin II receptor blocker), loop diuretics and ciclosporin. Diuretics are the most important cause of secondary gout in middle-aged and older people.

Question 56

What does an acute attack of gout constitute?

Answer 56

The first acute attack of gout is usually monoarticular, and often occurs in the big toe (the first metatarsophalangeal joint) or other part of the foot. The joint is usually very painful, red and swollen In women, the first attack may be polyarticular, typically in the hands and with gouty tophi. The presentation may be an acute inflammation in joints already affected by arthritis (eg the distal or proximal interphalangeal joints). Most patients who are not started on urate-lowering therapy will have a second acute attack of gout within 2 years.

Question 57

Characteristics of chronic gout?

Answer 57

If gout remains untreated with urate-lowering therapy, recurrent attacks may fail to resolve completely, slowly leading to a chronic crippling, destructive arthritis * Even in the absence of recognised recurrent attacks, urate crystals can deposit in the joints, soft tissues and kidneys, and can lead to joint damage and chronic kidney disease. * Gouty tophi are frequently seen in patients with chronic gout, and are usually present in the elbows (olecranon bursae), knees (prepatellar bursae) and peripheral joints (eg the toes and fingers).

Question 58

What is required for a diagnosis of gout?

Answer 58

Aspiration of an affected joint, bursa or tophus is required to confirm the diagnosis of gout.

Question 59

What does management of gout include?

Answer 59

providing rapid symptom relief for acute attacks prescribing lifelong urate-lowering therapy, using a treat-to-target approach, to prevent further acute attacks and to prevent and treat the complications of gout, such as tophi, chronic kidney disease and chronic destructive arthritis prescribing prophylaxis to prevent gout flares when starting or increasing urate-lowering therapy \> losartan and fenofibrate have modest uricosuric effects and, if clinically appropriate, may be preferable for the treatment of hypertension and dyslipidaemia respectively in a patient with gout \> low-dose aspirin can inhibit the excretion of uric acid and increase the risk of recurrent acute attacks of gout. However, given the substantial cardiovascular comorbidity associated with gout, low-dose aspirin should usually be continued with adjustment of urate-lowering therapy as necessary to achieve the target serum uric acid concentration

Question 60

Lifestyle advice for gout

Answer 60

explanation of the nature of the condition, the likelihood of recurrent acute attacks and long-term damage to the joints and kidneys if urate-lowering therapy is not started, and the need for adherence to lifelong urate-lowering therapy advice on maintaining a healthy lifestyle (eg maintaining ideal body weight, exercising regularly, stopping smoking); and limiting the intake of alcohol (especially beer and spirits), fructose-sweetened drinks and purine-rich foods. However, while there is strong evidence that lifestyle factors increase the risk of gout, there is a lack of evidence that correcting these factors improves outcomes in patients with gout

Question 61

How to manage acute gout?

Answer 61

Nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids (local injection or systemic use) and low-dose colchicine are all effective in treating acute gout. * NSAID indometacin has traditionally been used to treat acute attacks of gout because it is short-acting and the dose can be easily titrated according to symptomatic response; however, any NSAID may be used \> Naproxen appears to confer the least cardiovascular risk of all the NSAIDs, but has a higher risk of gastrointestinal adverse effects. \> Diclofenac has a lower risk of gastrointestinal adverse effects, but a higher cardiovascular risk; avoid diclofenac in patients who have an increased cardiovascular risk * Evidence suggests that systemic corticosteroids (oral or intramuscular) are as effective as NSAIDs in the treatment of acute gout, but systemic corticosteroids have a lower incidence of acute adverse effects than NSAIDs * Colchicine is effective in reducing pain and inflammation in acute gout, but has a high frequency of adverse effects (mainly gastrointestinal) that limit its usefulness. Paracetamol may be useful as an analgesic adjunct, but is not recommended as monotherapy. -- Local corticosteroid injection is appropriate if the acute attack involves one or two joints (or bursae) and joint (or bursal) infection has been excluded --\> once a definitive diagnosis of gout has been made, aspiration to exclude infection is not required before local corticosteroid injection for recurrent attacks unless infection is suspected --\> have to check for infection before using it first time by doing an aspiration.

Question 62

What to do after an acute attack of gout?

Answer 62

Once the acute attack has settled, implement the other aspects of gout management, including patient education and lifelong urate-lowering therapy. ## Footnote **If patients are already taking urate-lowering therapy, advise them not to stop or change therapy during an acute attack because sudden changes in serum uric acid concentration can prolong or worsen the attack.**

Question 63

Target concentration of serum uric acid concentrations?

Answer 63

The target serum uric acid concentration is less than 0.36 mmol/L (6 mg/dL) for patients with non-tophaceous gout, and less than 0.30 mmol/L (5 mg/dL) for patients with tophaceous gout (tophi)

Question 64

Urate lowering therapy precautions? How to mitigate this?

Answer 64

Starting or increasing urate-lowering therapy is associated with a high risk of gout flare Starting on a low dose of urate-lowering therapy minimises the risk of flares; the dose is then gradually increased until the target serum uric acid concentration is achieved. Flare prophylaxis is recommended for all patients starting or increasing urate-lowering therapy. Nonadherence to urate-lowering therapy also increases the risk of flare and is another common reason for treatment failure. Nonadherence to treatment is a particular problem in patients with gout because of the presence of relatively normal joint function between acute attacks initially, the complexity of the initial management regimen, and a natural reluctance of patients to take lifelong medication

Question 65

Starting urate-lowering therapy has traditionally been delayed until the acute attack has resolved; however, starting urate-lowering therapy concurrently with treatment for the acute attack may be appropriate, provided that treatment for the acute attack is adequate and the patient is well informed about the risk of flare. This may be best done under specialist guidance. True or false

Answer 65

True

Question 66

What is first line ULT? What to measure during concentration?

Answer 66

allopurinol should be used as first-line urate-lowering therapy * Measure serum uric acid concentration monthly during the dose titration phase. The target serum uric acid concentration is less than 0.36 mmol/L (6 mg/dL) or, if tophi are present, less than 0.30 mmol/L (5 mg/dL) * A substantial proportion of patients require allopurinol doses above 300 mg daily to achieve the target serum uric acid concentration; however, nonadherence should always be ruled out before increasing allopurinol to higher doses.

Question 67

Allopurinol renal impairment?

Answer 67

Renal impairment is not a contraindication to the use of allopurinol. The same (or lower) starting dose of allopurinol and the same (or slower) rate of up-titration to achieve the target serum uric acid concentration is recommended for patients with renal impairment, with close monitoring of renal function.

Question 68

Most common AE with allopurinol?

Answer 68

Skin rash is the most common adverse effect and may represent a maculopapular rash or allopurinol hypersensitivity syndrome * Allopurinol hypersensitivity syndrome is a rare, but potentially fatal, adverse effect comprising erythematous desquamating rash, fever, hepatitis, eosinophilia, and worsening renal function * Risk factors for allopurinol hypersensitivity syndrome include use of a high starting dose and rapid up-titration, renal impairment, older age, and the presence of human leucocyte antigen (HLA)-B\*5801 allele, which is more common in people of Asian ethnicity, especially the Han Chines * Advise patients to stop allopurinol immediately and seek medical advice if a skin rash develops *

Question 69

What to add onto allopurinol if not effective by itself?

Answer 69

If the target serum uric acid concentration cannot be achieved with allopurinol monotherapy (eg the dose of allopurinol required to achieve the target concentration is not tolerated), **probenecid** (a weak uricosuric) may be added to allopurinol * The efficacy of probenecid declines with declining renal function, but some efficacy is retained down to a glomerular filtration rate of 30 mL/minute. * Probenecid can increase the risk of urate nephrolithiasis and should be avoided in patients with known urate nephrolithiasis. * Once the patient is stable and the target serum uric acid concentration has been achieved, serum uric acid concentration can be checked annually to ensure the target concentration is maintained. Ongoing monitoring should also include renal function, liver biochemistry, and full blood count (in patients taking probenecid), as well as the frequency of gout attacks and, if applicable, tophi size.

Question 70

Second line ULT? What to monitor for both of these drugs

Answer 70

use febuxostat (xanthine oxidase inhibitor) or probenecid * Once the patient is stable and the target serum uric acid concentration has been achieved, serum uric acid concentration can be checked annually to ensure the target concentration is maintained. * Ongoing monitoring should also include renal function, liver biochemistry (in patients taking febuxostat), and full blood count (in patients taking probenecid), as well as the frequency of gout attacks and, if applicable, tophi size.

Question 71

When is febuxostat not appropriate?

Answer 71

Febuxostat is not recommended for patients with pre-existing major cardiovascular disease. Febuxostat should be used with caution in patients with hepatic impairment or moderate to severe renal impairment; seek specialist advice. Febuxostat is thought to behave similarly to allopurinol in reducing the metabolism of azathioprine and mercaptopurine, and increasing the risk of severe bone marrow toxicity.

Question 72

What is used for flare prophylaxis when starting or increasing urate lowering therapy? \> Starting or increasing urate-lowering therapy is associated with a high risk of gout flare, so flare prophylaxis is recommended

Answer 72

* Colchicine has the strongest evidence as a prophylactic drug for gout flares * Nonsteroidal anti-inflammatory drugs (NSAIDs) may be considered for patients in whom colchicine is contraindicated or ineffective * Oral corticosteroids are usually only used under specialist advice and are associated with long-term adverse effects \> If a patient has had multiple recurrent attacks of gout despite prophylaxis, combination therapy with colchicine plus either an NSAID or prednis(ol)one may be required \> Avoid concurrent use of NSAIDs and oral corticosteroids because of the significantly increased risk of gastrointestinal toxicity, and because NSAIDs are not likely to have additional benefit in patients taking oral corticosteroids.

Question 73

How long to use flare prophylaxis for?

Answer 73

The optimal duration of flare prophylaxis is unclear, but the frequency of flares, the duration of gout and the presence and size of tophi should be taken into account. Evidence supports the use of flare prophylaxis for at least 6 months, but the presence of tophi may warrant prolonged flare prophylaxis **In general, flare prophylaxis should be continued until the patient has no further attacks and the target serum uric acid concentration has been achieved. Typically, this takes at least 6 months, but may take longer in some individuals** * If the patient has a gout flare after prophylaxis has been stopped, restart prophylaxis and reassure patients that the urate-lowering therapy is working.

Question 74

UC after this...

Question 75

Immunomodulatory drugs are associated with an increased risk of infection and can cause significant adverse effects, what to do prior?

Answer 75

To minimise the risk of infection and adverse effects, screening and vaccination before starting an immunomodulatory drug are important, and ongoing monitoring during therapy is required \> immunomodulatory drugs commonly used in inflammatory bowel disease and associated with an increased risk of infection include corticosteroids, thiopurines (azathioprine, mercaptopurine), methotrexate, ciclosporin, tumour necrosis factor (TNF) inhibitors (eg adalimumab, infliximab) and anti-integrin antibodies (eg vedolizumab)

Question 76

What to monitor for azathioprine and mercaptopurine?

Answer 76

Assess baseline full blood count and liver biochemistry before starting azathioprine or mercaptopurine. Check full blood count every week for the first 4 weeks of therapy, then every 2 weeks for the next 4 weeks, again at 12 weeks, and every 3 months for the duration of therapy. Macrocytosis and lymphopenia are common effects of these drugs and do not require cessation of therapy. Assess liver biochemistry every 3 months. An annual skin check to detect early skin cancer is recommended.

Question 77

What to monitor for methotrexate?

Answer 77

Methotrexate commonly causes abnormal liver biochemistry, particularly in people with diabetes, obesity, impaired renal function, viral hepatitis or excessive alcohol intake Perform a full blood count and assess renal function and liver biochemistry monthly for the first 6 months, then every 1 to 2 months. In patients with a low risk of toxicity, consider increasing the interval between blood tests to 3 months

Question 78

What to monitor for Ciclosporin

Answer 78

In patients taking ciclosporin, assess full blood count, renal function, electrolyte concentrations, liver biochemistry, fasting lipids and blood pressure at baseline, and monitor as advised by the treating specialist. An annual skin check to detect early skin cancer is recommended.

Question 79

What is chrons disease?

Answer 79

Crohn disease (Crohn's disease) can affect any part of the gastrointestinal tract. Inflammation is often focal and transmural.

Question 80

What are the aims of drug therapy in chron disease?

Answer 80

Induce remission in active disease, maintain corticosteroid-free remission and prevent relapse, and achieve mucosal healing, where possible

Question 81

How is the treatment different to UC?

Answer 81

In contrast to ulcerative colitis, 5-aminosalicylates and rectal therapy have a limited role in Crohn disease.

Question 82

What is used for induction therapy for mild to moderate crohn disease?

Answer 82

Corticosteroids are the most effective drugs for treating active Crohn disease * prednis(ol)one 40 to 50 mg (child: 1 to 2 mg/kg up to 50 mg) orally, once daily in the morning until clinical response, then taper over 6 to 8 weeks to cease. Ileocaeal disease * budesonide controlled-ileal-release (adult and child 6 years or older) 9 mg orally, daily in the morning for 6 to 8 weeks, then taper over 2 to 4 weeks to cease

Question 83

Induction therapy for severe crohn disease? What to use if cannot use corticosteroid?

Answer 83

Initial therapy for severe Crohn disease is an intravenous corticosteroid. Suitable regimens include: * hydrocortisone 100 mg (child: 2 to 4 mg/kg up to 100 mg) intravenously, 6-hourly * methylprednisolone sodium succinate 100 mg (child: 1 mg/kg up to 50 mg) intravenously, daily. For patients who cannot tolerate or are refractory to corticosteroid induction therapy. * Azathioprine * Mercaptopurine * Methotrexate \> delayed onset of action give it around 3 months before they are deemed to have failed for patients who do not respond to at least 3 months of above therapy --\> use TNF inhibitor such as infliximab or adalimumab.

Question 84

What is used for maintenance therapy for crohn disease? \> Crohn disease is a relapsing and remitting condition; most patients need ongoing therapy to maintain remission.

Answer 84

Corticosteroids should not be used as maintenance therapy to prevent relapse of Crohn disease because they are no more effective than placebo and are associated with serious long-term adverse effects. **Azathioprine and mercaptopurine are effective for maintenance, and should be used for patients who have frequent relapses or are corticosteroid-dependent.**

Question 85

What to use if cant use azathioprine or mercaptopurine

Answer 85

Methotrexate * methotrexate 25 mg (child: 15 mg/m2) subcutaneously, intramuscularly or orally, on one specified day per week PLUS * folic acid 5 to 10 mg orally, per week (preferably not on the day methotrexate is taken). \> For luminal or fistulising Crohn disease that is refractory to the above therapy, tumour necrosis factor (TNF) inhibitors (eg infliximab, adalimumab) and vedolizumab are effective for maintaining remission if there was response to induction therapy with these drugs. **therapy is usually lifelong**

Question 86

What to use for perianal crohn disease?

Answer 86

metronidazole or ciprofloxacin \> Therapy may be needed for weeks to months. If metronidazole is used long term, monitor patients for evidence of peripheral neuropathy.

Question 87

How to reduce risk of reccurence of crohn disease after surgery?

Answer 87

To reduce the risk of recurrence, all patients should be counselled to stop smoking, and most patients will benefit from drug therapy. Patients without any of the above risk factors can be treated with a 5-aminosalicylate, or 3 months of metronidazole. For patients with one or more risk factors, add a thiopurine (azathioprine or mercaptopurine) and/or a TNF inhibitor (infliximab or adalimumab) if thiopurine intolerant. TNF inhibitors are the most effective postoperative prophylaxis. \> Patients at high risk of earlier postoperative recurrence are those who: * smoke * have perforating disease (abscesses or fistulas, or free perforation) * have had a prior resection.

Question 88

What is common in patients with crohn disease? What to do?

Answer 88

Malnutrition is common in patients with Crohn disease Diet has an important role in restoring and maintaining nutritional status * During an exacerbation of Crohn disease, short-term implementation of a diet low in insoluble fibre may help to control diarrhoea and pain related to food intake * Nutritional adequacy may be compromised, so encourage use of a multivitamin and mineral supplement, and monitor the patient’s weight * Correct micronutrient deficiencies with appropriate supplements (see Vitamin, mineral and trace element deficiencies). Micronutrients particularly at risk include iron, zinc, vitamin B12, calcium, magnesium, folic acid and vitamin D.

Question 89

Smoking and crohn disease?

Answer 89

There is strong evidence that relapse rates are lower in patients with Crohn disease who stop smoking, compared with patients who continue to smoke. Counsel patients accordingly, and provide appropriate support

Question 90

What to use for pregnancy in inflammatory bowel disease?

Answer 90

Active inflammatory bowel disease during pregnancy carries an increased risk of adverse outcomes for mother and fetus. This risk is greater than the risk of therapy, so active disease during pregnancy should be treated to control inflammation as quickly as possible. * The potential harm of corticosteroid use during pregnancy is much less than that of untreated disease * 5-aminosalicylates are generally considered safe for use in pregnancy, and their use is less hazardous than stopping therapy in patients whose disease has been difficult to control * Maintenance therapy with 5-aminosalicylates for ulcerative colitis should continue throughout pregnancy * Pregnant women taking sulfasalazine should take a high-dose folic acid supplement * Men taking sulfasalazine should be advised of the possibility of oligospermia and reduced sperm motility, which may affect fertility --\> effects reversed when drug is stopped. * The use of azathioprine or mercaptopurine during pregnancy is not associated with a discernible increased risk of congenital abnormalities * **Methotrexate is contraindicated in pregnancy and should be stopped 3 months before conception, if possible** * Adalimumab and infliximab are safe to use in pregnancy. However, their long-term effect on development of the fetal immune system is unknown.

Question 91

Bone health in IBD? How to treat prophylatically?

Answer 91

Inflammatory bowel disease is associated with an increased risk of osteopenia and osteoporosis; patients should be screened and monitored for these conditions * General preventive measures include regular weight-bearing exercise, adequate calcium intake (ie 1000 to 1300 mg elemental calcium daily), and stopping smoking and excessive alcohol consumption. * For patients starting systemic corticosteroid therapy, measure bone density, and give vitamin D and (if intake is inadequate) calcium supplements

Question 92

IDA in IBD?

Answer 92

Iron deficiency anaemia is the most common systemic complication of inflammatory bowel disease. Regularly assess patients for iron deficiency and treat deficiency if present * Oral iron therapy may worsen symptoms of inflammatory bowel disease, but can be used for mild anaemia in patients with clinically inactive disease who have previously tolerated oral therapy * **Parenteral iron therapy is generally preferred.** * After stopping iron therapy, iron deficiency recurs rapidly in patients with inflammatory bowel disease; frequent monitoring for recurrence is recommended

Question 93

UC from this card onwards...

Question 94

What are the areas affected in ulcerative colitis?

Answer 94

Large intestine (colon) and rectum Ulcerative colitis is a chronic inflammatory condition confined to the mucosal layer of the colon

Question 95

Aims of drug therapy in UC?

Answer 95

Induce remission in active disease, and then maintain corticosteroid-free remission and prevent relapse. The extent and severity of disease and the site(s) of affected colon determine which drugs and route of administration can be used.

Question 96

What to use if UC limited to the distal colon?

Answer 96

Effective treatment options include rectal and oral 5-aminosalicylates, rectal and oral corticosteroids, and other immunomodulatory drugs \> rectal 5-aminosalicylates are more effective than rectal corticosteroids for distal (left-sided) colitis, but are more expensive.

Question 97

What to use for initial therapy for active proctitis or distal colitis?

Answer 97

combination of rectal and oral 5-aminosalicylates; this is more effective than therapy by either route alone. Use: **mesalazine rectal preparation at induction dose** **PLUS** **5-aminosalicylate oral preparation at the standard acute (induction) dose**

Question 98

What to add to therapy if 5-aminosalicylates are ineffective?

Answer 98

* Budesonide rectally * Hydrocortisone rectally * Prednisolone rectally

Question 99

For patients who cannot tolerate rectal mesalazine, what to use?

Answer 99

Rectal corticosteroids may be the only rectal preparation \> Continue rectal therapy until symptoms have resolved, then taper over several weeks. If symptoms recur, restart rectal therapy (together with an oral 5-aminosalicylate) \> Rectal mesalazine may be considered as maintenance therapy for patients with repeated relapses

Question 100

What are examples of oral 5-aminosalicylates used in UC?

Answer 100

* Sulfasalazine * Mesalazine * Balsalazide * Olsalazine

Question 101

What to use for mild to moderate extensive ulcerative colitis?

Answer 101

Oral or parenteral corticosteoids in addition to 5-aminosalicylate preparations are the most effective treatment however use is limited by AE. For patients with mild extensive ulcerative colitis, an oral 5-aminosalicylate alone is often effective, but does not work as quickly as an oral corticosteroid * 5-aminosalicylate oral preparation at the standard acute (induction) dose \> For patients who do not respond to oral 5-aminosalicylate therapy alone or those with moderate disease, add an oral corticosteroid * Prednisolone 40 to 50mg then taper over 6 to 8 weeks to cease

Question 102

What to use for moderate to severe chronically active or frequently relapsing UC?

Answer 102

Some patients with ulcerative colitis do not respond to an oral 5-aminosalicylate and a corticosteroid --\> **add immunomodulatory drug or surgery** immunomodulatory drug: azathiprine, mercaptopurine, methotrexate, infliximab, vedolizumab **use** * azathioprine or mercaptopurine cannot tolerate aza or mercap --\> use * methotrexate 25 mg + folic acid 5-10mg orally per week not on the day methotrexate is taken **Immunomodulatory drugs are associated with significant adverse effects. Monitor carefully for complications, especially during the first 3 months of therapy** \> The onset of action of azathioprine, mercaptopurine and methotrexate may be delayed for several weeks or months. Azathioprine or mercaptopurine dosing can be optimised by measuring their metabolites

Question 103

What therapy to use for severe UC?

Answer 103

Fluid, electrolyte or blood replacement should be given when required, together with an intravenous corticosteroid. Suitable regimens include * hydrocortisone 100 mg (child: 2 to 4 mg/kg up to 100 mg) intravenously, 6-hourly * methylprednisolone sodium succinate 100 mg (child: 1 mg/kg up to 50 mg) intravenously, daily. \> Start a 5-aminosalicylate and either azathioprine or mercaptopurine; \> Avoid antidiarrhoeal drugs (including loperamide), anticholinergic drugs and opioids in severe ulcerative colitis

Question 104

What is used for maintenance therapy for UC?

Answer 104

Once remission achieved, rate of relapse reduced by 50% by using a 5-aminosalicylate with or without an immunomodulatory drug, use: * a 5-aminosalicylate oral preparation at the standard maintenance dose patients who responded to rectal mesalazine should continue it as maintenance therapy but at a reduced frequency, **For patients with severe initial disease or frequent relapses despite maintenance therapy with 5-aminosalicylates, prolonged remission may be achieved with an immunomodulatory drug --\> add** * azathioprine * mercaptopurine * methotrexate and folic acid for chronically active disease, refractory to above therapy * infliximab * vedolizumab

Question 105

Corticosteroids should not be used as maintenance therapy to prevent relapse of ulcerative colitis because they are no more effective than placebo and are associated with serious long-term adverse effects. true or false

Answer 105

yessir

Question 106

Therapy for ulcerative colitis is usually lifelong. De-escalation of therapy should only be considered in patients with stable disease in consultation with their gastroenterologist. true or false

Answer 106

true mabah

Question 107

Dietary measures in UC?

Answer 107

There is no evidence that the course of ulcerative colitis is modified by alterations in diet. A diet adequate in energy, protein and micronutrients is recommended, using normal foods and fluids, with the addition of oral nutritional supplements if required Restriction of dietary fibre is not routinely required. However, during an exacerbation, reducing intake of insoluble fibre may provide symptomatic relief of diarrhoea for some patients. Patients should avoid any foods that repeatedly exacerbate their symptoms.