Rheumat SAQ Flashcards
M/50 delivery management 7th gouty attack in ankle, this time right ankle for 2 days
a) Treatment for the attack (2)
b) Indications for urate-lowering therapy (ULT)? (2).
c) MoA of probenecid and allopurinol? (2)
d) Goal urate level in ULT? (1)
e) How to initiate the urate lowering therapy to prevent further episodes of gouty attacks?
a) colchicine/NSAIDs/IA steroids (prednisolone 30-35mg daily for 5 days)
b) indicates in patients with hyperuricemia and >2 acute gouty attacks within 1 year and it can be started during acute attack. Patients wih 1 or more subcutaneous tophi; or radiographic damage (any modality) attributable to gout or urate renal calculi
c) xanthine oxidase inhibitor. Uricosurics inhibit reabsorption of uric acid in proximal convoluted tubule
d) < 360mg/L
e) allopurinol starting with lose dose 100mg daily; increase weekly to target dosage. Prophylaxis: add regular colchicine 0.5mg daily or bd, or NSAID.
Febuxostat (non purine selective xanthine oxidase inhibitor): alternative for patients with allopurinol SCAR/HLB5801 gene carrier
Lady previously diagnosed with SLE and newly dx proliferative lupus nephritis (presented with proteinuria) given prednisolone and MMF, started 10 days ago. Presents with vesicles with erythematous base on the L eye + forehead.
- Dx 2 ← this is 1 mark instead?
- Ix
- Tx
- How to adjust your medication to prevent this 2
- What discipline should review her + complication you’re worried about 2
- Long-term management to prevent this from occurring again and how it will affect lupus management 2
- Herpes zoster opthalmicus
- Vesicle fluid PCR c/st
- IV acyclovir for >7 days
- ??
- VZV opthalmitis consult eye, neuralgia (neuro)
- ??
A woman with PIPJ arthritis was diagnosed with rheumatoid arthritis. She was started on an oral DMARD that is taken weekly.
1. Marker for RA?
2. DMARD given weekly injection. Coadministered with another supplement to alleviate its AE. What drug is taken?
3. 2 side effects of this DMARD
4. This DMARD no use. Wants to start on biologics. What 2 infections to exclude before starting.
5. Name another 2 classes of biologics or small molecules drugs for RA and describe their MOA
- Anti CCP (cyclic citrullinated peptide)
- Methotrexate (given with folate, vit b9)
- Pulmonary fibrosis, hepatotoxic, teratogenic, nausea, vomiting
- TB, Hep B (HBsAg, Anti HBc (occult hep B))
- 1st line is anti TNFa (infliximab (binds to TNFa receptor), etarnecept (decoy TNFa receptor). Anti CD20 (rituximab): depletion of peripheral and synovial B cells. Costimlation blockade (abtacept): fused to extracellular domain of CTLA4 (blocks CD28-CD80/86 costimulatory activation of T cells).
Anti IL6R: tocilizumab.
Raynaud’s Phenomenon A woman with systemic sclerosis, admitted and IV drug was given for her Raynold Phenomenon
1. 2 drugs that are contraindicated for Raynaud
2. What is the parenteral drug
3. Mechanism of parenteral drug
4. 2 oral drugs that can be give nfor control
5. Referred to anesthesia department due to refractory disease, what intervention can be done to control?
- B blocker, bleomycin, ergots, all vasoconstrictors (adrenaline and alpha agonist) which reduces blood flow to peripherals
- Iloprost
- Prostaglandin analogue
- CCB, PDE5 inhibitor (sildenafil), endothelin receptor antagonsit (ambrisetan)
- Stellate ganglion block (test the response of sympathectomy which is a surgical consideration to cut the nerves causing vasoconstriction)
69/F, referred for suspected drug allergy, received diclofenac IM injection for OA at FM clinic, reaction after 15mins, presenting with rash, SOB and collapsed, BP65/40
1. What is the mechanism of action of Diclofenac?
2. What is this type of drug reaction?
3. What immediate medication to be given and route?
4. What blood test should be taken acutely after stabilisation?
Patient stabilised after treatment. Referred to immunology department, before provocative drug test done to confirm allergy to Diclofenac, in vivo and in vitro test is done.
5. What in vivo test should be done?
6. What in vitro test should be done?
- Non selective cox1 and cox 2 inhibitor
- Type 1 IgE mediated
- IM adrenaline
- Serum tryptase within 4 hours
- Skin prick test or intradermal test
- Radioallergosorbent IgE
a)
Creatinine/urea –> renal biopsy –> due to sudden decline of renal function
Low C3 –> antidsDNA to detect if there is MCTD with SLE involvement
b) Interstitial lung disease
c) CXR, HRCT and lung function test
d) Scleroderma renal crisis
Management of scleroderma renal crisis
SBP >180 or DBP >110: target DBP 100-100mg Hg within 24 hours –> IV nitrates, continue low dose iloprost
If BP not above than oral antihypertensives with 1st line: long acting ACEI (ramipril), short acting ACEI (captopril) only required if haemodynamically unstable. 2nd line: ARB (losartan).
Admit HDU
Seizures: IV phenytoin, brain imaging
Pulmonary edema: fluid and salt restriction, IV furosemide
Severe AKI: may need RRT
a) COX2 inhibitor which impedes production of prostaglandins which causes pain and swelling of inflammation
b) diarrhea, constipation, dyspepsia
c) Synovitis and tenosynovitis, synovial hypertrophy, bony erosion (better visualized with XR)
d) etanercept is a anti TNFa agent that acts as a decoy receptor where TNFa binds to it therefore less TNFa to induce inflammatory changes.
e) latent TB, demyelinating disease, heart failure
Psoriatic arthropathy. On methotrexate
a. What is the mechanism of action of methotrexate?
b. How often should methotrexate be taken?
c. List 3 side effects of methotrexate
d. List 3 types of psoriatic arthropathy
Despite the methotrexate, the patient still complains of finger joint pain and back pain.
e. Name 2 other drugs you can give to the patient
a. Inhibits bodies use of folate/antifolate
b. Weekly
c. Interstitial pneumonititis, hepatotoxicity, nephrotoxicity, teratogenicity, BM suppression
d. 5 types: asymmetrical inflammatory oligoarthritis, symmetrial polyarthritis, DIPJ arthritis, psoriatic spondylitis, arthritis mutilans (deforming erosive arthritis targeting fingers and toes)
e.
Other DMARDs: leflonamide
TNFa inhibitors (infliximab, etanercept)
Biologics: ustekinumab (anti IL12, IL23)
Billy Wong, a 21-year-old engineering student, has always enjoyed playing sports. However, since 3 months ago, he has noticed increased pain in his lower back following a game of basketball. His back is also stiff ooseltamivir
n first rise in the morning. He visited his family physician who suspected Billy may have some form of spondyloarthritis.
(a) Other than the features listed above, what other clinical manifestations may suggest Billy has inflammatory back pain? Name two.
(b) Billy’s doctor decided to arrange an x-ray of his pelvis and lumbar spine. Describe two possible x-ray appearances, appropriate to Billy’s presentation, which may suggest the diagnosis of spondyloarthritis.
(c) Billy’s doctor subsequently referred him to the Rheumatology Clinic for further evaluation of possible spondyloarthritis. Name two other investigations that the specialist may arrange.
a) back pain not improved wiht rest, pain at night with improvement upon getting up, good response to NSAID
b) widening of the SI joint space, irregular SI joine line, squaring of spinal vertebrae
c) CRP or ESR, MRI of spoine, HLA B27 tissue typing
a) CK, anti Jo1, anti Mi-2
b) polymyalgia rheumatica
c) high dose prednisolone
d) immunosuppression, hyperglycemia, hypoK
Mr. Wong, a 48-year-old bank manager, was diagnosed to have gout one year ago. He was treated with etoricoxib 120 mg per day on an as required basis.
(a) Name two long term side-effects of etoricoxib.
Although the initial response to etoricoxib was good, Mr. Wong had recurrent attacks of gout in the past one month. As a result, his family physician started him on allopurinol 300 mg per day and etori- coxib 90 mg per day. Two weeks after this treatment, Mr. Wong developed a generalised erythematous desquamating rash and was admitted through the emergency department.
(b) What is the current diagnosis?
(c) What pre-treatment blood test might have predicted the development of Mr. Wong’s cuta- neous disease?
(d) Highlight two treatment principles in the management of Mr. Wong’s cutaneous manifesta- tion.
(e) What alternative long term gout treatment would you recommend Mr. Wong after he has re- covered from his current illness? Name two.
(f) What should be noted regarding serum uric acid target level in his case?
a) increased CVS risk in high dose (MI, stroke), nephrotoxicity
b) SJS
c) HLA B5801 gene
d) without the medication (allopurinol), supportive tx (rehydration + antibiotics) to prevent complications
e) febuxostat, lifestyle modification
f) 0.36mmol/L
A 50-year-old woman with a diagnosis of rheumatoid arthritis is admitted for dry cough and progres- sive shortness of breath over two weeks. She has been treated with non- steroidal anti-inflammatory drug and hydroxychoroquine for her rheumatoid arthritis. Her polyarthritis had a flare up four weeks ago, for which she was given oral steroids (Prednisolone 20 mg daily for two weeks and then 10 mg daily till now), which improved her joint symptoms. CXR shows increased reticulonodular shadows and some ground glass haziness at the mid and lower lung fields on both sides. Physical examination shows oxygen saturation of 94% on room air, and crepitations in mid and lower lung fields posteriorly and at lateral aspects of lung base bilaterally.
(a) Name two major differential diagnosis for her respiratory symptoms, ranked in the order of likelihood, and for each diagnosis, describe two features in her which support that diagnosis.
(b) Name two investigations, and describe briefly the salient features that may be shown in each investigation that will be helpful for making a diagnosis of the lung condition.
a) pulmonary fibrosis secondary to RA: dry cough, bilateral ground glass haziness at mid and lower lung fields on CXR
Chest infection (e.g. pulmonary TB): immunosuppressed by long term steroids, progressive SOB over 2 weeks
b) CBC/D: leukocytosis more compatible with infection
HRCT for ILD features (GGO, honeycombing, tractional bronchiectasis)
Bronchoscopy with BAL x C/ST
A 36-year-old woman was diagnosed to have rheumatoid arthritis one year ago. She was treated with combination methotrexate and sulphasalazine for nine months but her arthritis remained active with multiple tender and swollen joints and raised C-reactive protein and erythrocyte sedimentation rate. Her rheumatologist decided to start her on infliximab, a monoclonal antibody against tumour necrosis
factor (TNF)-α, a pro-inflammatory cytokine.
(a) Name two contraindications for infliximab.
(b) Name two pre-treatment screening investigations.
(c) The patient’s response to infliximab was good in the first year. However, her arthritis gradually flared over the next six months despite regular use of this agent. What is the most likely mechanism?
a) heart failure, hypersensitivity to infliximab
b) IGRA/TST, CXR to screen for latent TB
HBsAg for chronic hep B
Antibody vs infliximab (should be used together with methotrexate)
a) DMARD due to high ESR, erosive arthritis, seropositive disease
b)
Methotrexate: air (lung toxicity), nausea (GI disturbance), child (teratogenic), hepatotoxicity, rash (photosensitivity), excreted renally
Sulphasalazine: skin rash, urine orange, loose bowel, pancreatitis, hepatotoxicity
Hydroxychloroquine: corneal deposits, bulls eye maculopathy, blue/back discoloration of skin
a) gonococcal septic arthritis (sexual history), acute gouty attack (alcoholism), trauma (alcoholic intoxication), reactive arthritis (a/w chlamydial infection)
b) cell count, gram stain, C/ST, polarizead microscopy x crystals. Blood culture, CBC/D
c) acute gouty attack
d) Immediate: NSAID, colchicine, oral steroid
Long term: low purine diet, stop drinking, consider urate lowering therapy if >2 attacks/y
a) syndrome syndrome associated type 4 RTA
b) VBG for HCO3- level. ANA, anti Ro/La associated with sicca syndrome, RFT for renal impairment, plasma aldosterone renin activity for alternative causes of hypoaldosteronism
