Rheumatology & Haematology — MCQs
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A 56-year-old woman with established rheumatoid arthritis presents with sudden onset severe headache, fever, and neck stiffness. She has been taking methotrexate 20mg weekly and adalimumab fortnightly. Her temperature is 38.7°C, heart rate 105 bpm, blood pressure 128/82 mmHg. She is photophobic and has no focal neurological signs. CT head shows no abnormality. What is the most appropriate immediate management?
A 66-year-old woman presents with fatigue. Blood tests show: Hb 78 g/L, MCV 72 fL, ferritin 285 mcg/L, CRP 68 mg/L, ESR 85 mm/hr. She has a 3-month history of pain and stiffness in her shoulders and hips, worse in the morning. Creatine kinase is normal. What is the underlying mechanism of her anaemia?
A 58-year-old man presents with sudden onset pain and swelling of his left knee. He is currently being treated for acute myeloid leukaemia with chemotherapy and his WCC is 1.2 × 10⁹/L. He is pyrexial at 38.4°C. Joint aspiration yields turbid fluid with WCC 45,000 cells/μL (90% neutrophils). Gram stain is pending. Polarised light microscopy shows no crystals. What is the most appropriate initial antibiotic therapy?
What is the mechanism of action of tranexamic acid in the management of acute bleeding?
A 39-year-old woman with established rheumatoid arthritis on methotrexate 25mg weekly develops progressive shortness of breath over 6 weeks. Examination reveals fine inspiratory crackles at both lung bases. Oxygen saturation is 92% on room air. Chest X-ray shows bilateral reticular shadowing. High-resolution CT chest shows ground-glass opacification and interstitial changes. What is the most appropriate immediate management?
A 71-year-old man with a mechanical mitral valve replacement on warfarin (target INR 2.5-3.5) requires elective total knee replacement surgery. His INR has been stable. What is the most appropriate perioperative anticoagulation management?
A 44-year-old woman presents with a 4-week history of bilateral hand pain and morning stiffness lasting 90 minutes. Examination reveals synovitis of the MCP and PIP joints bilaterally. Blood tests show: CRP 35 mg/L, ESR 42 mm/hr, rheumatoid factor negative, anti-CCP antibody negative. X-rays of hands show soft tissue swelling only. What is the most appropriate classification of her condition?
A 52-year-old woman is diagnosed with iron deficiency anaemia. Upper GI endoscopy shows mild gastritis with no other abnormality. Colonoscopy is normal. She has regular menstrual periods. Coeliac serology (tissue transglutaminase antibody) is negative. She takes no regular medications. What is the most appropriate next investigation?
A 67-year-old man with psoriatic arthritis has failed treatment with methotrexate and leflunomide. He has extensive peripheral joint involvement affecting hands, wrists, and feet with significant functional impairment. He has a history of latent tuberculosis diagnosed 15 years ago for which he completed a full course of treatment. Chest X-ray is normal. What is the most appropriate next step before starting anti-TNF therapy?
A 29-year-old woman presents at 10 weeks gestation in her first pregnancy. She has a history of two previous unprovoked deep vein thromboses, the most recent being 18 months ago. She completed 6 months of anticoagulation with rivaroxaban after the last event. Thrombophilia screening performed 3 months after stopping anticoagulation showed heterozygous Factor V Leiden mutation. What is the most appropriate management?
Rheumatology & Haematology UK Medical PG Practice Questions and MCQs
Question 71: A 56-year-old woman with established rheumatoid arthritis presents with sudden onset severe headache, fever, and neck stiffness. She has been taking methotrexate 20mg weekly and adalimumab fortnightly. Her temperature is 38.7°C, heart rate 105 bpm, blood pressure 128/82 mmHg. She is photophobic and has no focal neurological signs. CT head shows no abnormality. What is the most appropriate immediate management?
- A. Perform lumbar puncture and administer broad-spectrum antibiotics immediately (Correct Answer)
- B. Perform lumbar puncture first, then start antibiotics if CSF analysis is abnormal
- C. Administer IV corticosteroids for possible CNS vasculitis
- D. Arrange urgent MRI brain to exclude abscess before lumbar puncture
- E. Start oral aciclovir and await lumbar puncture results
Explanation: ***Perform lumbar puncture and administer broad-spectrum antibiotics immediately*** - The patient presents with the classic triad of **meningitis** (fever, headache, neck stiffness, photophobia), and her immunosuppressed state due to **methotrexate** and **adalimumab** significantly increases the risk of serious infection, including bacterial meningitis. - Immediate **lumbar puncture** (after a normal CT head, which rules out contraindications like mass effect) followed by prompt administration of **broad-spectrum antibiotics** is crucial to improve outcomes and reduce mortality in suspected bacterial meningitis. *Perform lumbar puncture first, then start antibiotics if CSF analysis is abnormal* - Delaying the initiation of **antibiotics** until after **CSF analysis** results are available is a critical error in suspected bacterial meningitis, as treatment delay significantly increases mortality. - **Empirical broad-spectrum antibiotics** should be started as soon as possible after obtaining cultures (blood and CSF), or even before LP if there is a delay in performing it. *Administer IV corticosteroids for possible CNS vasculitis* - While **CNS vasculitis** is a consideration in rheumatoid arthritis, the acute onset of high fever and meningeal signs points strongly towards an **infectious process** (meningitis), which requires immediate antibiotic intervention. - **Corticosteroids** (like dexamethasone) are used as **adjunctive therapy** in specific cases of bacterial meningitis to reduce inflammation and neurological sequelae, but they are not the primary treatment and do not replace antibiotics. *Arrange urgent MRI brain to exclude abscess before lumbar puncture* - An **urgent CT head** has already been performed and shown no abnormalities, which is sufficient to proceed safely with a **lumbar puncture** in the absence of focal neurological signs or signs of raised intracranial pressure (e.g., papilledema). - Waiting for an **MRI brain** would cause an unacceptable and potentially fatal delay in the diagnosis and treatment of acute bacterial meningitis, where every hour counts. *Start oral aciclovir and await lumbar puncture results* - Although **viral meningitis/encephalitis** is a possibility, the patient's severe symptoms, high fever, and immunosuppressed state make **bacterial meningitis** a more immediate and life-threatening concern, demanding prompt empirical antibiotic therapy. - If **viral encephalitis** were suspected (e.g., HSV), **intravenous aciclovir** would be indicated, not oral, and it should never delay or replace the empirical treatment for bacterial meningitis when bacterial infection is a strong possibility.
Question 72: A 66-year-old woman presents with fatigue. Blood tests show: Hb 78 g/L, MCV 72 fL, ferritin 285 mcg/L, CRP 68 mg/L, ESR 85 mm/hr. She has a 3-month history of pain and stiffness in her shoulders and hips, worse in the morning. Creatine kinase is normal. What is the underlying mechanism of her anaemia?
- A. Chronic blood loss leading to iron depletion
- B. Hepcidin-mediated reduction in iron availability for erythropoiesis (Correct Answer)
- C. Autoimmune destruction of red blood cells
- D. Folate deficiency due to increased cellular turnover
- E. Direct bone marrow suppression by inflammatory cytokines
Explanation: ***Hepcidin-mediated reduction in iron availability for erythropoiesis*** - The patient's symptoms (pain and stiffness in shoulders and hips, worse in the morning) and high inflammatory markers (**CRP 68 mg/L**, **ESR 85 mm/hr**) are consistent with **polymyalgia rheumatica**, an inflammatory condition. - Inflammation leads to increased **hepcidin** production, which blocks **ferroportin**, thereby trapping iron within macrophages and hepatocytes and reducing its availability for erythropoiesis, causing **anaemia of chronic disease** (ACD) which can be microcytic. *Chronic blood loss leading to iron depletion* - **Iron deficiency anaemia** due to chronic blood loss would typically present with a **low ferritin** level, reflecting depleted iron stores. - This patient has a **high ferritin** (285 mcg/L), which is an acute-phase reactant and is elevated in inflammatory conditions, indicating iron sequestration rather than depletion. *Autoimmune destruction of red blood cells* - **Autoimmune haemolytic anaemia** usually presents with **normocytic** or **macrocytic anaemia** (due to reticulocytosis) and signs of haemolysis like elevated bilirubin or LDH. - The patient's anaemia is **microcytic** (MCV 72 fL) and there are no other indicators of haemolysis. *Folate deficiency due to increased cellular turnover* - **Folate deficiency** causes **macrocytic anaemia** (MCV > 100 fL) because of impaired DNA synthesis affecting erythroblast maturation. - The patient's anaemia is distinctly **microcytic** (MCV 72 fL), which contradicts a diagnosis of folate deficiency. *Direct bone marrow suppression by inflammatory cytokines* - While inflammatory cytokines can directly suppress erythropoiesis, this typically results in **normocytic anaemia**. - The **microcytic** nature of the anaemia in this context, combined with high ferritin and inflammatory markers, is primarily driven by restricted iron availability due to **hepcidin**.
Question 73: A 58-year-old man presents with sudden onset pain and swelling of his left knee. He is currently being treated for acute myeloid leukaemia with chemotherapy and his WCC is 1.2 × 10⁹/L. He is pyrexial at 38.4°C. Joint aspiration yields turbid fluid with WCC 45,000 cells/μL (90% neutrophils). Gram stain is pending. Polarised light microscopy shows no crystals. What is the most appropriate initial antibiotic therapy?
- A. IV flucloxacillin
- B. IV flucloxacillin and IV gentamicin
- C. IV vancomycin and IV gentamicin
- D. IV ceftriaxone
- E. IV piperacillin-tazobactam (Correct Answer)
Explanation: ***IV piperacillin-tazobactam*** - This patient presents with **septic arthritis** in the context of **neutropenic sepsis** (WCC 1.2 × 10⁹/L), requiring **broad-spectrum empirical coverage** for both Gram-positive and **Gram-negative organisms**, especially **Pseudomonas aeruginosa**. - **Piperacillin-tazobactam** is a potent **antipseudomonal beta-lactam** that provides comprehensive coverage, making it a first-line choice for **febrile neutropenia** and suspected sepsis in immunocompromised patients pending culture results. *IV flucloxacillin* - While it provides excellent coverage for **methicillin-sensitive Staphylococcus aureus**, a common cause of septic arthritis, it offers **no coverage for Gram-negative bacteria**. - In a **neutropenic patient** with sepsis, empirical therapy must cover **Gram-negative pathogens**, including *Pseudomonas*, to prevent rapid clinical deterioration. *IV flucloxacillin and IV gentamicin* - This combination adds **Gram-negative coverage** via **gentamicin**, but it's generally not the preferred first-line for **febrile neutropenia** over a single antipseudomonal beta-lactam. - **Gentamicin** is an **aminoglycoside** associated with potential **nephrotoxicity** and requires therapeutic drug monitoring, which is less ideal for initial empirical therapy compared to a broad-spectrum beta-lactam. *IV vancomycin and IV gentamicin* - This regimen covers **MRSA** (via vancomycin) and Gram-negative bacteria (via gentamicin), but **vancomycin** is typically reserved for suspected MRSA infections, which is not strongly indicated here. - Empiric coverage for **febrile neutropenia** usually prioritizes broad-spectrum Gram-negative coverage, including **Pseudomonas**, with an antipseudomonal beta-lactam, before adding vancomycin without specific risk factors for MRSA. *IV ceftriaxone* - **Ceftriaxone** is a third-generation cephalosporin effective against many Gram-positive and Gram-negative bacteria, but it **lacks activity against *Pseudomonas aeruginosa***. - In **neutropenic sepsis**, **Pseudomonas coverage** is critical due to its high virulence and prevalence in this patient population, making ceftriaxone insufficient as monotherapy.
Question 74: What is the mechanism of action of tranexamic acid in the management of acute bleeding?
- A. Activates Factor VII in the coagulation cascade
- B. Inhibits fibrinolysis by blocking plasminogen activation (Correct Answer)
- C. Promotes platelet aggregation at sites of vascular injury
- D. Increases synthesis of vitamin K-dependent clotting factors
- E. Enhances thrombin generation through Factor Xa activation
Explanation: ***Inhibits fibrinolysis by blocking plasminogen activation***- **Tranexamic acid** is a synthetic lysine analog that competitively inhibits the binding of **plasminogen** to fibrin.- By preventing plasminogen from converting into **plasmin**, it stabilizes the fibrin clot and reduces the breakdown of existing clots, thereby controlling **acute bleeding**.*Activates Factor VII in the coagulation cascade*- This describes the mechanism of action of **recombinant activated Factor VII (rFVIIa)**, which is used in specific bleeding disorders or massive hemorrhage.- Tranexamic acid primarily acts as an **antifibrinolytic** agent and does not directly activate coagulation factors like Factor VII.*Promotes platelet aggregation at sites of vascular injury*- **Platelet aggregation** is driven by factors such as ADP, thromboxane A2, and interaction with von Willebrand factor and collagen, facilitated by glycoprotein receptors.- Tranexamic acid has no direct effect on **platelet function** or their aggregation at injury sites; its role is purely in **fibrinolysis inhibition**.*Increases synthesis of vitamin K-dependent clotting factors*- The synthesis of **vitamin K-dependent clotting factors** (II, VII, IX, X, protein C, protein S) occurs in the liver and requires vitamin K.- Tranexamic acid is not involved in the **synthesis** of these factors; it affects the breakdown of fibrin, not its formation via factor production.*Enhances thrombin generation through Factor Xa activation*- **Thrombin generation** is a key step in the coagulation cascade, largely mediated by **Factor Xa** converting prothrombin to thrombin.- Tranexamic acid does not enhance **thrombin generation** or activate Factor Xa; instead, it prevents the enzymatic degradation of already formed fibrin clots.
Question 75: A 39-year-old woman with established rheumatoid arthritis on methotrexate 25mg weekly develops progressive shortness of breath over 6 weeks. Examination reveals fine inspiratory crackles at both lung bases. Oxygen saturation is 92% on room air. Chest X-ray shows bilateral reticular shadowing. High-resolution CT chest shows ground-glass opacification and interstitial changes. What is the most appropriate immediate management?
- A. Stop methotrexate, start high-dose prednisolone, refer urgently to respiratory team (Correct Answer)
- B. Continue methotrexate, add azathioprine as steroid-sparing agent
- C. Stop methotrexate, switch to hydroxychloroquine
- D. Continue methotrexate, add prophylactic co-trimoxazole for pneumocystis coverage
- E. Refer for urgent lung biopsy before making treatment changes
Explanation: ***Stop methotrexate, start high-dose prednisolone, refer urgently to respiratory team*** - The patient's presentation with progressive shortness of breath, hypoxia, fine inspiratory crackles, and HRCT findings of **ground-glass opacification** and **interstitial changes** in the context of **methotrexate** use strongly indicate **methotrexate-induced pneumonitis**, a severe hypersensitivity reaction. - Immediate management requires **stopping the offending agent** (methotrexate) and initiating **high-dose corticosteroids** (e.g., prednisolone) to rapidly suppress inflammation. Urgent referral to a respiratory team is crucial for specialized management of this potentially life-threatening condition. *Continue methotrexate, add azathioprine as steroid-sparing agent* - Continuing **methotrexate** is contraindicated as it is the most likely cause of the acute pulmonary toxicity; further administration could lead to irreversible lung damage or death. - **Azathioprine** is a slow-acting immunosuppressant and not an appropriate immediate treatment for acute, severe drug-induced pneumonitis. *Stop methotrexate, switch to hydroxychloroquine* - While stopping methotrexate is correct, **hydroxychloroquine** is a mild disease-modifying antirheumatic drug (DMARD) and has no role in the acute management of **interstitial lung disease** or drug-induced pneumonitis. - This approach critically omits **corticosteroid therapy**, which is essential for rapidly resolving the active inflammatory process in the lungs. *Continue methotrexate, add prophylactic co-trimoxazole for pneumocystis coverage* - Continuing **methotrexate** is dangerous when drug-induced **pulmonary toxicity** is suspected; the immediate priority is to remove the causative agent. - While **Pneumocystis jirovecii pneumonia (PJP)** is a differential, the clinical picture, imaging findings (ground-glass opacities), and history of methotrexate use are more consistent with drug-induced pneumonitis, demanding cessation and active treatment over prophylaxis alone. *Refer for urgent lung biopsy before making treatment changes* - An **urgent lung biopsy** is an invasive procedure that should not delay immediate, life-saving therapeutic interventions such as stopping the suspected drug and initiating **high-dose corticosteroids**. - The clinical and radiological findings provide sufficient evidence for a presumptive diagnosis of **methotrexate-induced pneumonitis**, warranting prompt treatment without delaying for definitive histological confirmation.
Question 76: A 71-year-old man with a mechanical mitral valve replacement on warfarin (target INR 2.5-3.5) requires elective total knee replacement surgery. His INR has been stable. What is the most appropriate perioperative anticoagulation management?
- A. Continue warfarin throughout, aiming for INR 2.0-2.5 on day of surgery
- B. Stop warfarin 5 days before surgery, start therapeutic LMWH, stop LMWH 24 hours pre-operatively (Correct Answer)
- C. Stop warfarin 5 days before surgery, start prophylactic LMWH, stop LMWH 12 hours pre-operatively
- D. Stop warfarin 3 days before surgery, no bridging anticoagulation required
- E. Stop warfarin 5 days before surgery, start IV unfractionated heparin infusion, stop 4 hours pre-operatively
Explanation: ***Stop warfarin 5 days before surgery, start therapeutic LMWH, stop LMWH 24 hours pre-operatively***- Patients with a **mechanical mitral valve** are at **high thromboembolic risk** and require **therapeutic bridging** anticoagulation when warfarin is interrupted.- Guidelines recommend stopping **warfarin 5 days prior** to allow the INR to normalize, with the last dose of **therapeutic LMWH** given **24 hours before** the procedure to balance clotting and bleeding risks.*Continue warfarin throughout, aiming for INR 2.0-2.5 on day of surgery*- For **high-bleeding risk** procedures like total knee replacement, an INR of 2.0-2.5 poses a significant risk of **major perioperative hemorrhage**.- Warfarin should typically be stopped to achieve an **INR <1.5** for major orthopedic surgery.*Stop warfarin 5 days before surgery, start prophylactic LMWH, stop LMWH 12 hours pre-operatively*- **Prophylactic dosing** of LMWH is insufficient to prevent **thrombosis** of a mechanical mitral valve, which requires full systemic anticoagulation.- A **12-hour gap** is generally too short for therapeutic-dose LMWH before major surgery, increasing the risk of **wound hematoma**.*Stop warfarin 3 days before surgery, no bridging anticoagulation required*- Stopping warfarin only **3 days before** is often inadequate for the INR to reach the safe target of **<1.5** for surgery.- Omitting bridging in a patient with a **mechanical mitral valve** is contraindicated due to the severe risk of **valve thrombosis and embolic stroke**.*Stop warfarin 5 days before surgery, start IV unfractionated heparin infusion, stop 4 hours pre-operatively*- While **IV unfractionated heparin (UFH)** is a valid bridging option, especially in **renal failure**, LMWH is generally preferred for elective cases due to ease of outpatient administration.- This option is less common than LMWH for elective surgery in stable patients and requires **hospital admission** several days prior to the procedure.
Question 77: A 44-year-old woman presents with a 4-week history of bilateral hand pain and morning stiffness lasting 90 minutes. Examination reveals synovitis of the MCP and PIP joints bilaterally. Blood tests show: CRP 35 mg/L, ESR 42 mm/hr, rheumatoid factor negative, anti-CCP antibody negative. X-rays of hands show soft tissue swelling only. What is the most appropriate classification of her condition?
- A. Definite rheumatoid arthritis requiring immediate DMARD therapy (Correct Answer)
- B. Seronegative inflammatory arthritis, monitor clinically
- C. Probable rheumatoid arthritis, start hydroxychloroquine
- D. Osteoarthritis with inflammatory component
- E. Viral arthropathy, manage conservatively
Explanation: ***Definite rheumatoid arthritis requiring immediate DMARD therapy*** - Under the **ACR/EULAR 2010 criteria**, the patient scores sufficiently for a diagnosis based on **symmetrical small joint involvement** (multiple MCP/PIP joints), elevated inflammatory markers (**ESR/CRP**), and clinical synovitis. - Early initiation of **DMARD therapy** (e.g., Methotrexate) is critical to prevent permanent **joint erosion** and improve long-term functional outcomes, even in **seronegative** cases.*Seronegative inflammatory arthritis, monitor clinically* - This approach risks missing the "**window of opportunity**" where early intervention can induce remission and prevent the progression of **radiographic damage**. - Approximately 15–20% of rheumatoid arthritis cases are **seronegative** (RF and anti-CCP negative), but they still require aggressive management similar to seropositive cases.*Probable rheumatoid arthritis, start hydroxychloroquine* - The clinical presentation (symmetrical small joint synovitis, prolonged morning stiffness, elevated inflammatory markers) meets the **ACR/EULAR 2010 criteria** for **definite RA**, not just probable. - **Hydroxychloroquine** is generally a milder DMARD, often insufficient as monotherapy for active RA with high inflammatory markers; stronger agents like **methotrexate** are typically preferred first-line for definite RA.*Osteoarthritis with inflammatory component* - Osteoarthritis typically involves the **DIP joints** and the first CMC joint, usually manifesting as stiffness lasting less than **30 minutes**. - This patient's **morning stiffness of 90 minutes**, symmetrical MCP/PIP involvement, and significantly elevated inflammatory markers are distinctive features of an **inflammatory synovitis** characteristic of RA, not degenerative disease.*Viral arthropathy, manage conservatively* - **Viral arthropathy** (e.g., Parvovirus B19) usually has a more acute onset, often resolves within **2 to 3 weeks**, and may be associated with other systemic symptoms like a rash. - Symptoms persisting for **4 weeks** with significantly raised inflammatory markers and prominent, symmetrical synovitis are more indicative of a chronic **autoimmune process** like RA, rather than a self-limiting viral infection.
Question 78: A 52-year-old woman is diagnosed with iron deficiency anaemia. Upper GI endoscopy shows mild gastritis with no other abnormality. Colonoscopy is normal. She has regular menstrual periods. Coeliac serology (tissue transglutaminase antibody) is negative. She takes no regular medications. What is the most appropriate next investigation?
- A. CT abdomen and pelvis
- B. Video capsule endoscopy
- C. Repeat upper GI endoscopy with duodenal biopsies (Correct Answer)
- D. Haemoglobin electrophoresis
- E. Reassure and treat with oral iron replacement only
Explanation: ***Repeat upper GI endoscopy with duodenal biopsies***- In a patient with **iron deficiency anaemia (IDA)** and negative coeliac serology, **duodenal biopsies** are crucial to exclude **seronegative coeliac disease** or other causes of malabsorption, which can be missed on visual inspection alone.- Current guidelines recommend obtaining duodenal biopsies during upper GI endoscopy for unexplained IDA, even if the mucosa appears normal, to detect subtle mucosal changes like **villous atrophy**.*CT abdomen and pelvis*- This imaging modality is primarily for evaluating **organ structures** and **masses**, and has a low sensitivity for detecting subtle mucosal abnormalities or inflammatory processes, which are key in IDA investigation.- It is generally not the initial investigation for **unexplained IDA** where mucosal pathology or bleeding from the GI tract is suspected after initial endoscopy.*Video capsule endoscopy*- This investigation is typically reserved for evaluating the **small bowel** for causes of obscure GI bleeding or malabsorption *after* both upper and lower endoscopies (including duodenal biopsies) have been unrevealing.- It should not precede a thorough endoscopic and histological assessment of the duodenum for conditions like **coeliac disease**, which can have focal or patchy involvement.*Haemoglobin electrophoresis*- This test is used to diagnose **haemoglobinopathies** (e.g., thalassemia, sickle cell disease) which cause microcytic anaemia due to abnormal haemoglobin production, not true **iron deficiency**.- Since the patient has a confirmed diagnosis of **iron deficiency anaemia**, investigating for structural haemoglobin variants is not indicated at this stage.*Reassure and treat with oral iron replacement only*- While the patient has regular menstrual periods, at 52 years old, **gastrointestinal blood loss** (even occult) or **malabsorption** must be thoroughly excluded as potential causes of IDA.- Failing to investigate the GI tract adequately in a patient with unexplained IDA can lead to missing significant underlying **pathology**, including malignancy.
Question 79: A 67-year-old man with psoriatic arthritis has failed treatment with methotrexate and leflunomide. He has extensive peripheral joint involvement affecting hands, wrists, and feet with significant functional impairment. He has a history of latent tuberculosis diagnosed 15 years ago for which he completed a full course of treatment. Chest X-ray is normal. What is the most appropriate next step before starting anti-TNF therapy?
- A. Proceed directly to anti-TNF therapy without further TB screening
- B. Perform interferon-gamma release assay (IGRA) only
- C. Perform tuberculin skin test (Mantoux test) only
- D. Perform IGRA and repeat chest X-ray, commence isoniazid prophylaxis if IGRA positive (Correct Answer)
- E. CT chest to exclude active tuberculosis
Explanation: ***Perform IGRA and repeat chest X-ray, commence isoniazid prophylaxis if IGRA positive*** - Screening for **latent tuberculosis (LTBI)** is mandatory before starting **TNF inhibitors** because these drugs significantly increase the risk of **TB reactivation**. - Even with a history of treated LTBI, a current assessment using **IGRA** and imaging ensures no recent reinfection or active disease is present before suppressing the immune system.*Proceed directly to anti-TNF therapy without further TB screening* - This is unsafe as the risk of **disseminated tuberculosis** or **miliary TB** is high in patients on anti-TNF therapy with undetected latent infection. - Professional guidelines require a fresh clinical and laboratory assessment of **TB status** immediately prior to the initiation of biologic therapy.*Perform interferon-gamma release assay (IGRA) only* - While IGRA is a crucial part of the screening process, it should be paired with a **clinical evaluation** and **radiological assessment** to rule out active disease. - A single test is insufficient to fully evaluate the risk; a **chest X-ray** is required to look for signs of old or active pulmonary tuberculosis.*Perform tuberculin skin test (Mantoux test) only* - The **Tuberculin Skin Test (TST)** can yield **false-positive** results in patients who have had a prior **BCG vaccination**. - **IGRA** is generally preferred over TST in older patients or those previously vaccinated, as it is more specific and not affected by the BCG status.*CT chest to exclude active tuberculosis* - A **CT chest** is not a routine screening tool and is reserved for cases where the **chest X-ray** is abnormal or clinical suspicion of active TB remains high. - Subjecting a patient to higher doses of **radiation** via CT is unnecessary if the patient is asymptomatic and the screening chest X-ray is normal.
Question 80: A 29-year-old woman presents at 10 weeks gestation in her first pregnancy. She has a history of two previous unprovoked deep vein thromboses, the most recent being 18 months ago. She completed 6 months of anticoagulation with rivaroxaban after the last event. Thrombophilia screening performed 3 months after stopping anticoagulation showed heterozygous Factor V Leiden mutation. What is the most appropriate management?
- A. Low-dose aspirin 75mg daily throughout pregnancy
- B. Prophylactic dose low molecular weight heparin antenatally and for 6 weeks postpartum
- C. Therapeutic dose low molecular weight heparin antenatally and for 6 weeks postpartum (Correct Answer)
- D. Warfarin throughout pregnancy with target INR 2-3
- E. Clinical surveillance only with compression stockings
Explanation: ***Therapeutic dose low molecular weight heparin antenatally and for 6 weeks postpartum*** - Patients with a history of **two or more previous unprovoked VTEs** are classified as high risk and require **therapeutic dose LMWH** throughout the pregnancy and the puerperium. - The addition of a **thrombophilia** (heterozygous Factor V Leiden) further increases the risk, necessitating full anticoagulation to prevent life-threatening recurrence. *Low-dose aspirin 75mg daily throughout pregnancy* - Aspirin is primarily used for the prevention of **pre-eclampsia** or in **antiphospholipid syndrome**; it is insufficient for preventing **venous thromboembolism**. - It does not provide the potent anticoagulant effect required for someone with a history of **recurrent unprovoked VTE**. *Prophylactic dose low molecular weight heparin antenatally and for 6 weeks postpartum* - While LMWH is the correct agent, a **prophylactic dose** is reserved for those with a single VTE or lower risk factors; it is insufficient for **recurrent unprovoked VTE** cases. - Guidelines specify that **recurrent unprovoked events** require higher intensity treatment (therapeutic or intermediate doses) due to the high risk of failure on standard prophylaxis. *Warfarin throughout pregnancy with target INR 2-3* - Warfarin is **teratogenic** and can cause **fetal warfarin syndrome** (including nasal hypoplasia and skeletal abnormalities) if used during the first trimester. - It also increases the risk of **fetal intracranial hemorrhage**; therefore, LMWH is the preferred anticoagulant as it does not cross the **placenta**. *Clinical surveillance only with compression stockings* - Surveillance alone is clinically dangerous for this patient given her history of **unprovoked VTE** and a confirmed **Factor V Leiden mutation**. - Compression stockings provide only mild risk reduction for **post-thrombotic syndrome** but are inadequate for the primary prevention of new clots in high-risk pregnancies.
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