Hematology Oncology
Showing 33 of 33 topics
A
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New pulmonary infiltrate plus fever and/or respiratory symptoms in sickle cell disease. Provide oxygen, antibiotics (cover atypicals), incentive spirometry, and bronchodilators; transfuse simple or exchange based on severity and Hb; involve hematology early.
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Identify the agent and last dose; provide targeted reversal and hemostatic support while controlling the bleeding source.
D
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Use Wells score to risk stratify; D-dimer to rule out in low-risk; confirm with compression ultrasound; start anticoagulation unless contraindicated; choose DOAC for most; treat 3 months minimum.
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DIC is a consumptive coagulopathy from systemic activation of coagulation (sepsis, malignancy, trauma, obstetric). Diagnose with clinical context and labs (↑PT/INR, ↑aPTT, ↓fibrinogen, ↑D‑dimer, thrombocytopenia). Treat cause; provide targeted blood products; consider heparin in chronic DIC.
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Consumptive coagulopathy from sepsis, trauma, or malignancy; treat underlying cause and support with products guided by bleeding and labs; consider heparin for thrombosis-predominant DIC.
F
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Defined as fever with ANC <500 (or expected). Start broad‑spectrum IV antibiotics within 60 minutes of presentation. Use MASCC/CISNE scores to triage for inpatient vs outpatient therapy; add antifungal coverage if persistent fever after 4–7 days or earlier if instability or imaging suggests fungal disease.
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Fever with ANC <500 (or expected to decline) after chemotherapy. Obtain cultures quickly and start an antipseudomonal β‑lactam within 60 minutes; add MRSA coverage only with specific indications. Use MASCC/CISNE for risk and consider outpatient oral therapy for low‑risk patients.
H
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Differentiate immune from non‑immune hemolysis using DAT and peripheral smear; treat underlying cause and initiate corticosteroids for warm AIHA; urgent support for severe hemolysis.
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Suspect HIT with platelet drop 5–10 days after heparin; use 4Ts score; stop all heparin and start non‑heparin anticoagulant while confirming diagnosis.
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Immune‑mediated thrombocytopenia with thrombosis risk 5–10 days after heparin exposure. Use 4Ts score for pretest probability, stop all heparin, send PF4 immunoassay with functional testing as needed, and start a non‑heparin anticoagulant while awaiting confirmatory testing.
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Classical HL: obtain PET‑CT, stage with Ann Arbor, document B symptoms, and plan ABVD‑based therapy with consideration of bulky disease and interim PET adaptation.
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Cancer‑related hypercalcemia requires isotonic fluids, short‑term calcitonin for rapid reduction, and anti‑resorptives (IV bisphosphonates or denosumab) for sustained control; add dialysis for severe/renal failure. Treat underlying malignancy and limit calcium/vitamin D.
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Treat symptomatic or severe hypercalcemia with aggressive IV saline, calcitonin for rapid effect, and IV bisphosphonate (zoledronic acid/pamidronate) or denosumab for sustained control; stop exacerbating drugs and treat the underlying malignancy.
I
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Diagnosis of exclusion; treat when platelets <30k or bleeding; first‑line corticosteroids or IVIG; second‑line TPO‑RA, rituximab, or splenectomy.
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Suspect iTTP with MAHA and thrombocytopenia; send ADAMTS13 urgently and begin plasma exchange plus high-dose steroids immediately; add caplacizumab when iTTP is likely to reduce time to platelet recovery and relapses.
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Many indolent NHLs (e.g., follicular) can be observed initially. Treat when GELF criteria or symptoms present; prefer anti‑CD20‑based regimens; monitor for transformation.
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Diagnose with ferritin and iron studies; identify bleeding sources; treat with oral or IV iron depending on severity/tolerance; replete stores and monitor response.
M
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Back pain with neurologic deficits in cancer patients requires urgent MRI, high dose steroids, and oncology and surgical consultation for decompression and radiotherapy.
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Oncologic emergency: back pain with neurologic deficits; give dexamethasone promptly, obtain urgent MRI, and coordinate radiation or surgery with oncology and neurosurgery.
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Back pain with neurologic deficits in cancer patients is an emergency. Give dexamethasone promptly, obtain MRI whole spine, and coordinate urgent surgical decompression and/or radiotherapy based on stability, radiosensitivity, and prognosis.
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Heterogeneous clonal disorders with cytopenias and risk of AML transformation. Diagnose with marrow morphology and cytogenetics/molecular profiling. Use IPSS‑R/IPSS‑M to stratify risk and guide therapy from supportive care to HMA or transplant.
N
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Oncologic emergency: start antipseudomonal antibiotics within 60 minutes; risk stratify (MASCC/CISNE); add MRSA coverage only for specific indications; consider antifungal if persistent fever after 4–7 days.
S
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New pulmonary infiltrate with fever and/or respiratory symptoms in sickle cell disease. Provide oxygen, incentive spirometry, pain control, antibiotics, and transfusion (simple vs exchange) based on severity; avoid fluid overload and treat concomitant VOC.
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Manage acute pain crises, prevent complications (ACS, stroke), and use disease‑modifying therapy (hydroxyurea, transfusions; selected newer agents). Vaccinate and provide comprehensive care.
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Rapid multimodal analgesia with opioids and NSAIDs when not contraindicated, aggressive hydration as needed, and vigilance for acute chest syndrome and infection.
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Obstruction of venous return from mediastinal mass or thrombosis causing facial and arm swelling, dyspnea, and venous distention; elevate head, give oxygen, obtain contrast CT, and coordinate urgent stent or tumor directed therapy.
T
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Restrictive transfusion is safe for many hospitalized adults; consider transfusion at hemoglobin around 7 g dL in stable noncardiac patients and higher thresholds in specific conditions.
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Oncologic emergency from rapid cell lysis causing hyperuricemia, hyperkalemia, hyperphosphatemia, and hypocalcemia. Prevent with risk stratification, vigorous hydration, and urate‑lowering therapy; manage electrolyte derangements promptly; dialyze if refractory.
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Oncologic emergency with hyperkalemia, hyperphosphatemia, hypocalcemia, and AKI; risk-stratify, hydrate aggressively, give allopurinol or rasburicase as indicated, and manage electrolytes.
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Identify high risk hematologic malignancies, start aggressive hydration, control uric acid with allopurinol or rasburicase, and manage electrolytes; dialyze when refractory.
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High‑grade hematologic malignancies carry TLS risk at chemo initiation. Stratify risk; give aggressive hydration, allopurinol for low‑moderate risk, or rasburicase for high‑risk or established hyperuricemia. Monitor electrolytes closely; treat hyperkalemia/hyperphosphatemia; consider early dialysis for AKI.
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TLS arises after cytotoxic therapy (or spontaneously) in high-burden hematologic malignancy. Prevent with aggressive isotonic fluids, strict monitoring of potassium, phosphate, calcium, uric acid, and renal function, and early uric acid–lowering therapy (rasburicase for high risk).
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Rapid tumor cell breakdown after cytotoxic therapy (or spontaneously) causing hyperuricemia, hyperkalemia, hyperphosphatemia, and hypocalcemia. Risk‑stratify, start aggressive hydration, give allopurinol for prevention or rasburicase for treatment, and monitor electrolytes/renal function closely; initiate dialysis when refractory.
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