Clinical Pharmacy II Flashcards
Muscoskeletal conditions
What are the risk factors of rheumatoid arthritis?
Gender (female higher risk)
Age (40-60) - can occur in children
Genetics - associated with HLA-DR4 allele
Cigarette smoking
How does rheumatoid arthritis arise?
Increase in number of inflammatory cells
Release cytokines -> proteolytic enzymes -> destruction of bone and cartilage
Clinical features of rheumatoid arthritis (symptoms and signs)
Joint pain and swelling - last more than 6 weeks -> symmetrical
Stiffness in the morning - more than 30 minutes
Fever
Weight loss
Fatigue and malaise
Depression
Presence of rheumatoid nodules
Raised CRP and ESR
Raised rheumatoid factor - not all patients
Deformity of bones
Why does the ESR reading increase in rheumatoid arthritis?
Inflammation -> produced proteins -> affect the repellant surface of RBC
RBC can stack easier -> faster rate of settlement -> higher ESR value
How is rheumatoid arthritis diagnosed?
No specific test
Suspected -> refer
Use some tests to speed up the diagnostic processes -> act like baseline measurement before treatment.
What are the tests that can be used as baseline measurement for the diagnosis and treatment monitoring of rheumatoid arthritis?
Full blood count - signs of anaemia
CRP and ESR level - inflammation
Urea and electrolytes - kidney function - risk from treatments
Liver function test - active RA can cause raised gamma-glutamic transferase and alkaline phosphatase
Rheumatoid factor level
Antinuclar Ig and anti-CCP Ig present - antibodies linked with RA
Imaging through MRI, ultrasoun - radiography of hand, feet and chest
What is anti-CCP IG and antinuclear Ig? How are they related to RA?
Antinuclear Ig - linked with connective tissue diseases
Anti-CCP Ig = anti-cyclic citrullinated peptide Ig - chronic inflammation produced Ig
What type of anaemia in rheumatoid disease?
Secondary anaemia
Number of immature RBC is normal or low
Morpholgy of bone marrow normal
What are the differences between anaemia of chronic disease and iron deficiency anaemia (IDA), in terms of blood measurement?
Both have low serum
Anaemia of chronic disease has normal or high serum ferritin (low in IDA)
Normal or low transferrin level (high in IDA)
Low total iron binding capcity (high in IDA)
Explain the trend of ferritin level, serum level and transferrin level in chronic disease anaemia.
Due to body response to inflammation
Increase IL-4 -> increase Hepcidin production from liver
Hepcidin - reduce Fe absorbed from gut -> low Fe serum
Body response -> reduce iron-transferring protein (transferrin) and increase iron-stored protein (ferritin)
What are the three management approach for RA?
Non-pharmacological treatment
Drug treatment
Surgical treatment
Can be combine or mono
What is the target of treating active RA in adults?
Treat-to-target therapy
Achieve target remission OR low disease activity if remission is impossible
Name the classes of drugs that need to be used for RA management
cDMARDs (conventional disease-modifying anti-rheumatic drugs)
biological DMARDs
NSAIDs, PPIs, glucocorticoids - symptom control
Describe the clinical management of active RA (first-line etc).
First-line: Monotherapy cDMARDs - ASAP, within 3 months of the onset of persistent symptoms - if toleratance, dose increase
Second-line: Combination of cDMARD - only start when dose escalation not work
Third-line: Biological DMARDs (with or without methotrexate) - only use if inadequate response to cDMARDs combo or if classed severe - withdraw if moderate resp not achieve within 6 months
Fourth-line: Rituximab + Methotrexate
Fifth-line: Sarilumab/Tocilizumab + Methotrexate
What is the consideration when switching cDMARDs?
Bridging therapy with glucocorticosteroids (short-term)
How is RA classed severe?
Das28 score above 5.1
What criteria is used to assess if the response to treatment is adequate?
EULAR criteria
Name cDMARDs used to manage RA in first and second-line
Methotrexate and sulfasalazine (most tolerated)
Gold (auranofin, sodium aurothionate)
Penicillamine
Hydroxychloroquine
Ciclosproins
Azathioprine
Monitoring requirements for cDMARDs
All require: FBCs, eGFRs, LFTs - some drugs require more:
Azathioprine - TPMT assay - level of metabolic enzyme
Ciclosporin - fasting lipids and BP - risk of hyperlipidaemia and HTN
Hydroxychloroquine - visual acuity - side effect of ocular toxicity
Methotrexate - chest X-ray - risk of pneumonitis
Why is FBC required to be monitored during RA treatment?
Most of the drugs cause myelosuppression - reduced blood cells production
Dose of methotrexate for RA.
7.5 - 22.5 mg once weekly
Dose of sulfasalazine for RA.
500 mg - 3 g daily
What to do if NSAIDs do not provide adequate symptom control?
Consider alternative NSAID
Review DMARD dose, consider change if no improvement
Consider short-term systemic steroid
How to manage the nausea and vomiting in patients taking methotrexate?
Folic acid
Add anti-emetic therapy
Change to parenteral MTX (if applicable)
How to manage disease flares when withdrawing systemic steroids?
Slower regimen
Consider reduce dose to lowest possible - only if withdrawal is impossible
How to manage the side-effects from long-term steroid treatment?
PPI, bisphosphonates and calcium + vitamin D preparations
Name examples of biological DMARDs used in third-line of RA management
Sarilumab
adalimumab
etanercept
infliximab
Which biological DMARDs are associated with stinging sensation at injection site?
adalimumab
etanercept
What is the solution for patients who cannot tolerate the stinging sensation of biological DMARDs administration?
Switch to infliximab
What is DAS28 score used for?
Used to consider the EULAR response of patients
Based on improvement in DAS28 score from baseline and DAS28 at endpoint
What aspects are taken into account of DAS28 score?
Number of joint tender
Number of joint swollen
ESR value
CRP value
Patient Global Health Input from HAQ
What is HAQ?
Health Assessment Questionaire
What are the risk factors of osteoarthritis?
Age
Obesity
Genetic components
Trauma and injuries
What causes the development of OA?
Imbalance between reparative and erosive processes in joint
Increase in proteolytic enzyme activity
Loss of cartilage around the joint
Bone outgrowths at joint margins -> harden -> deforming joint
What are the clinical features of OA?
Pain increases by activity, movement, loading of joints
Radiating pain
Stiffness in the morning - after rest - last less than 30 mins
Deformed joints
Who will not need clinical imaging investigation for the diagnosis of OA?
Older than 45 years old
Activity-related joint pain
No morning stiffness
Stiffness last less than 30 mins
No signs and symptoms of RA or gout
What are the core treatments for OA?
Therapeutic exercise
Weight management
Information and support
What information should the patients know about the therapeutic exercise for OA?
Might initially cause pain and discomfort
Long-term: reduce pain + improve functions
Besides the core treatment, name some adjunct treatments for OA patients.
Mannual therapy
Devices - walking aid
Pharmacological management - lowest effective dose for shortest time
What cases of OA that the patients can be considered for mannual therapy?
Hip and knee OA
What treatment that OA patients must NOT be offered by HCPs?
Acupuncture
Electrotherapy treatments
Routine insoles, braces, tapes, splints
What drugs should be recommended for OA patients?
Topical NSAID for knee OA
Consider topical NSAID for other OA-affected joints
If not work or unsuitable: oral NSAID + gastroprotective (PPIs)
Can consider intra-articular corticosteroid for short-term relief - only if other treatments are ineffective
What are the risk factors of gout?
Age
Dominant in males
Diet (red meat, seafood, alcoho)
Obesity
Genetic predispositions
Certain medications
Certain conditions
What are the medications that put patients at increased risk of gout?
thiazide and loop diuretics
ciclosporins
levodopa
What conditions are associated with increased risk of gout?
renal disease
diabetes
dyslipidaemia
hypertension
Causes of gout.
deposition of sodium urate crystals
precipitated from chronic hyperuricaemia
Why does gout normally attack the joints at extremities?
lower temperature -> easier to precipitate
Clinical features of gout.
No stiffness
Acute attack at big toe,
Painful, hot and red joint
Presence of tophi
Fever, elevated ESR
Prodromal symptoms before acute attack
What is tophi?
Bump of yellow uric crystals under the skin
Restrict the joint movement
What patients should be suspected with gout?
Rapid onset of severe pain + redness + swelling - MTP joints
If not MTP joints, consider
Tophi
What level of serum urate confirm the diagnosis of gout?
More than 360 micromol/l or 6 mg/dl
If less during a flare or strongly suspected, measure again at least 2 weeks later
What are the methods that can be used for diagnosis?
Present with symptoms
Confirm wih serum urate level
Joint aspiration + microscopy of synovial fluid
Imaging techniques (X-ray, ultrasound, CT)
How is acute gout flares managed?
1st-line: NSAID, colchicine, short-course of PO corticosteroids + PPIs (if needed)
2nd-line: intra-articular or IM corticosteroid
3rd-line: refer for an IL-1 inhibitor
Apply ice packs in addition to meds
What cases should the patients be referred toc rheumatology?
Diagnosis uncertain
CI treatment, not tolerated or ineffective
CKD stages 3b to 5
Had organ transplant