Hematology & Oncology Flashcards

1
Q

Features of multiple endocrine neoplasia type 1?

A
  1. Pituitary adenomas
  2. Parathyroid adenomas
  3. Enteropancreatic tumors
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2
Q

Laboratory hallmarks of tumor lysis syndrome

A
  1. Hyperuricemia
  2. Hyperkalemia
  3. Hyperphosphatemia
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3
Q

Primary immune thrombocytopenia pathophysiology, presentation & management

A

(formerly known as idiopathic thrombocytopenia purpura)

  • Pathophysiology: anti-platelet Ab attack platelets –> peripheral platelet destruction
  • Presentation: petechiae, gingival bleeding, epistaxis, menorrhagia, GI bleed, ICH (in children, history of recent viral infection)
  • Management: supportive (children), corticosteroids & IVIG/anti-D immunoglobulin (adults); platelets (severe bleeding/extremely low platelet count) splenectomy (refractory cases), rituximab, thrombopoietin receptor agonist, immunosuppressants
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4
Q

Thrombotic thrombocytopenia purpura pathophysiology, presentation & management

A
  • Pathophysiology: severe ADAMTS13 deficiency 2/2 inhibitory auto-Abs
  • Presentation: fever, MAHA, thrombocytopenia, AMS & renal failure
  • Management: plasmapheresis
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5
Q

Tumor lysis syndrome pathophysiology, presentation & management

A
  • pathophysiology: death of numerous neoplastic cells releasing large quantities of intracellular content & uric acid (typically 1-5 days after chemotherapy) –> hyperuricemia, hyperkalemia, hyperphosphatemia & hypocalcemia
  • presentation: fatigue/lethargy, N/V, cloudy urine, muscle spasms & AMS
  • management: aggressive IV hydration (kidneys excrete uric acid, potassium & phosphate), allopurinol (prevents conversion of hypoxanthine to uric acid) or rasburicase (converts uric acid to inactive & soluble metabolite)
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6
Q

Acute myeloid leukemia epidemiology, pathophysiology, presentation & prognosis

A
  • epidemiology: most common leukemia in adults; 15-20% of childhood leukemias; median age of diagnosis 65 yr
  • pathophysiology: clonal proliferation of myeloid precursor cells –> reduction in production of other cells (RBC’s, platelets, mature granulocytes)
  • presentation: related to pancytopenia; pallor, fatigue, easy bruising, gingival bleeding, petechiae and infections; labs with normocytic normochromic anemia with Auer rods
  • prognosis: 5-year survival rate 25%
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7
Q

Acute lymphoblastic leukemia epidemiology, pathophysiology & presentation

A
  • epidemiology: most common cancer in children (age 3-7) with bimodal distribution (65 yo)
  • pathophysiology: proliferation of blast cells
  • presentation: bone pain, LAD, hepatosplenomegaly, CNS involvement
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8
Q

Chronic lymphocytic leukemia epidemiology, pathophysiology, presentation, management & prognosis

A
  • epidemiology: male predominance; median age of diagnosis 70 yr; most common leukemia in adults of Western countries
  • pathophysiology: monoclonal proliferation of incompetent mature B cells
  • presentation: asymptomatic at diagnosis; B symptoms, LAD (painless), splenomegaly, anemia & thrombocytopenia; peripheral smear with isolated lymphocytosis & smudge cells (fragile lymphocytes)
  • management: observation for early-stage or asymptomatic; purine analogs, antibodies, alkylating agents, IVIG (for hypogammaglobulinemia & frequent infection)
  • prognosis: virtually incurable; median survival 4-20 years
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9
Q

Chronic myeloid leukemia epidemiology, pathophysiology, presentation & management

A
  • epidemiology: least common leukemia
  • pathophysiology: Philadelphia chromosome –> neutrophilic leukocytosis
  • presentation: most asymptomatic; fatigue/weight loss, night sweats, LUQ pain, early satiety, bone pain, hepatosplenomegaly
  • management: allogenic hematopoietic stem cell transplant (only curative treatment), tyrosine kinase inhibitor, dasatinib, inferferon-alpha + cytarabine (greater toxicity)
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10
Q

Neutropenic fever diagnostic criteria

A

Fever (single oral temp >38.3 C OR >38.0 C for >1 hr) + neutropenia (ANC <500 OR <1,000 w/ predicted nadir of <500 in 48 hr)

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11
Q

Preferred AC for VTE in cancer patients

A

LMWH (cancer patients have variable responses to traditional vitamin K antagonist therapy)

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11
Q

Preferred AC for VTE in cancer patients

A

LMWH (cancer patients have variable responses to traditional vitamin K antagonist therapy)

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12
Q

Waldenstrom macroglobulinemia

A
  • plasma cell dyscrasia leading to abnormal synthesis of IgM paraproteins
  • most common cause of hyperviscosity syndrome
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12
Q

Waldenstrom macroglobulinemia

A
  • plasma cell dyscrasia leading to abnormal synthesis of IgM paraproteins
  • most common cause of hyperviscosity syndrome
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