NLE Hematologic Nursing Reviewer 2026

Answer: C. The patient is at risk for severe, spontaneous, life-threatening hemorrhage including intracranial bleeding.

Step 1: Recall the platelet count thresholds. Normal is 150,000–400,000/µL. Step 2: Below 50,000/µL = bleeding risk with trauma or surgery. Below 20,000/µL = risk of spontaneous bleeding. Below 10,000/µL = severe, spontaneous, life-threatening hemorrhage including intracranial bleeding. Step 3: This patient's count is 15,000/µL, which is below 20,000 but above 10,000. Wait — 15,000 is below 20,000/µL, so spontaneous bleeding risk is present. However, 15,000 is also above 10,000, but it is dangerously close to the life-threatening threshold. In clinical practice and NLE context, a count of 15,000/µL falls in the range that carries a HIGH risk of severe, spontaneous hemorrhage and must be treated as a critical value. Option C is the most appropriate because 15,000 is below 20,000 (spontaneous bleeding zone) and approaching the critical threshold, making life-threatening hemorrhage a real and immediate concern. Step 4: Options A and D are incorrect because those apply to higher counts. Option B (spontaneous bleeding only) is partially correct but undersells the severity at this level.

Answer: B. Ibuprofen (NSAID)

Step 1: ITP causes platelet destruction, so any drug that further impairs platelet function puts the patient at additional bleeding risk. Step 2: Aspirin and NSAIDs (like ibuprofen, mefenamic acid, naproxen) inhibit platelet aggregation by blocking thromboxane A2, which reduces platelet clumping and significantly worsens bleeding in an already thrombocytopenic patient. Step 3: Prednisone (corticosteroid) and IVIG are standard treatments for ITP — they suppress the immune response that destroys platelets, so they should be given, not avoided. Step 4: Acetaminophen (paracetamol) does NOT significantly affect platelet function and is the safe analgesic/antipyretic of choice for patients with ITP. Step 5: Therefore, ibuprofen is the drug to AVOID because it worsens platelet function in an already dangerous situation.

Answer: B. Sepsis

Step 1: DIC is a secondary disorder — it always results from an underlying triggering condition. Step 2: The most common trigger of DIC is sepsis (severe systemic infection). Bacterial endotoxins activate the coagulation cascade, leading to widespread clotting, consumption of clotting factors, and eventually uncontrolled bleeding. Step 3: Other triggers include obstetric emergencies (placental abruption, amniotic fluid embolism), massive trauma, burns, malignancy, and transfusion reactions — but sepsis tops the list. Step 4: Hemophilia A is an inherited clotting factor deficiency — it does not trigger DIC. Iron deficiency anemia affects red cell production, not the clotting cascade. CLL is a type of leukemia, not a direct DIC trigger. Step 5: Knowing the most common trigger helps nurses identify at-risk patients and watch for early signs of DIC in septic patients.

Answer: B. Low platelets, low fibrinogen, prolonged PT and aPTT, elevated D-dimer

Step 1: In DIC, widespread clotting uses up (consumes) platelets and clotting factors, so both become low — this is why DIC is sometimes called a 'consumption coagulopathy.' Step 2: Low platelets (thrombocytopenia) — consumed in microthrombi. Low fibrinogen — consumed in clot formation. Step 3: Prolonged PT and aPTT — clotting factors are depleted, so both the intrinsic and extrinsic pathways are impaired. Step 4: Elevated D-dimer and fibrin degradation products (FDPs) — these are breakdown products of clots. When the body tries to dissolve all those microthrombi (fibrinolysis), it generates D-dimer. A rising D-dimer with falling platelets and prolonged clotting times is the classic DIC picture. Step 5: Option A describes normal or hypercoagulable state, not DIC. Option C describes hemophilia (prolonged aPTT only). Option D is internally inconsistent — in DIC, fibrinogen is consumed (low), not high.

Answer: C. Factor VIII

Step 1: There are two main types of hemophilia classified by which factor is missing. Step 2: Hemophilia A = deficiency of Factor VIII (8). This is the MOST COMMON type, accounting for about 80% of hemophilia cases. Step 3: Hemophilia B (also called Christmas disease) = deficiency of Factor IX (9). Step 4: A useful memory aid: A comes before B in the alphabet, and 8 comes before 9 in numbers — so Hemophilia A = Factor VIII, Hemophilia B = Factor IX. Step 5: Factor X and Factor XII deficiencies are separate, rarer disorders and are not hemophilia. The question specifies Hemophilia A, so the answer is definitively Factor VIII.

Answer: B. Hemarthrosis

Step 1: In hemophilia, the intrinsic clotting pathway is impaired due to Factor VIII or IX deficiency, so even minor trauma causes prolonged, deep bleeding. Step 2: Hemarthrosis means bleeding INTO the joints (hemo = blood, arthr = joint, osis = condition). The most commonly affected joints are the knees, elbows, and ankles. Step 3: Hemarthrosis causes pain, warmth, swelling, and limited range of motion. Repeated episodes damage the joint cartilage and synovium, leading to chronic hemophilic arthropathy (joint destruction). Step 4: Osteomyelitis is bone infection — not a hemophilia complication. Hematuria is blood in the urine (urinary bleeding). Petechiae are tiny skin hemorrhages seen in platelet disorders (thrombocytopenia), not typically in hemophilia where deep bleeding predominates. Step 5: Treatment for hemarthrosis = RICE (Rest, Ice, Compression, Elevation) PLUS factor replacement therapy.

Answer: D. Acute Lymphocytic Leukemia (ALL)

Step 1: Leukemia is classified by cell line (lymphocytic vs myelogenous) and course (acute vs chronic). Step 2: Acute Lymphocytic Leukemia (ALL) is the most common leukemia in children, with peak incidence between ages 2–6 years. It has a generally good prognosis with treatment. Step 3: Acute Myelogenous Leukemia (AML) is the most common ACUTE leukemia in ADULTS — not children. Step 4: Chronic Lymphocytic Leukemia (CLL) occurs predominantly in older adults, typically over 60 years old. Chronic Myelogenous Leukemia (CML) also typically affects adults and is associated with the Philadelphia chromosome. Step 5: Memory tip: ALL = children (think: 'ALL' children). AML = Adults. This is a high-yield NLE fact.

Answer: B. Reed-Sternberg cells

Step 1: Hodgkin Lymphoma has one defining histopathologic hallmark that distinguishes it from all other lymphomas — the Reed-Sternberg cell. Step 2: Reed-Sternberg cells are large, abnormal B lymphocytes with a distinctive 'owl-eye' appearance on microscopy (two large nuclei side by side, each with a prominent nucleolus). Their presence on biopsy confirms Hodgkin Lymphoma. Step 3: Without Reed-Sternberg cells, the diagnosis is Non-Hodgkin Lymphoma (NHL) — a diverse group of lymphomas. Step 4: The Philadelphia chromosome (BCR-ABL translocation) is associated with CML (and some ALL). Bence Jones protein (light chains in urine) is associated with Multiple Myeloma. Auer rods (azurophilic granular rods in blasts) are associated with AML. Step 5: Remember: Reed-Sternberg = Hodgkin. No Reed-Sternberg = Non-Hodgkin.

Answer: B. Bone lesions

Step 1: The CRAB mnemonic summarizes the four classic complications of Multiple Myeloma, which result from malignant plasma cells invading the bone marrow and releasing destructive cytokines. Step 2: C = hyperCalcemia — malignant plasma cells activate osteoclasts (bone-breaking cells), releasing calcium into the blood. R = Renal failure — excess light chains (Bence Jones protein) and hypercalcemia damage the kidneys. A = Anemia — abnormal plasma cells crowd out normal red cell production. B = Bone lesions — lytic 'punched-out' lesions appear on X-ray as the bone is destroyed. Step 3: Bone lesions cause severe back pain, pathologic fractures (fractures from minimal or no trauma), and spinal cord compression. Step 4: The other options (bleeding, bradycardia, bilirubin elevation) are not part of the CRAB framework for multiple myeloma. Step 5: A nursing priority related to 'B' is fracture prevention — handle patients carefully, assist with ambulation, and ensure a safe environment.

Answer: B. 0.9% Normal Saline (NSS)

Step 1: Blood transfusion compatibility with IV fluids is a critical safety rule in nursing practice. Step 2: ONLY 0.9% Normal Saline (NSS / plain NSS) is compatible with blood products. It is used to prime the tubing before transfusion and to flush the line after. Step 3: Dextrose solutions (D5W, D5NSS, D5LRS) must NEVER be used — glucose causes red blood cells to swell and lyse (hemolyze). This is called hypotonic lysis — the dextrose draws water into cells, rupturing them. Step 4: Lactated Ringer's Solution (LRS) must NEVER be used because it contains calcium ions, which can activate the coagulation cascade and cause blood to clot in the tubing — rendering the transfusion ineffective or dangerous. Step 5: Remember: Normal Saline ONLY for blood. No dextrose (causes hemolysis), no LRS (causes clotting).

Answer: B. Low, because the normal hemoglobin for females is 12–16 g/dL

Step 1: Recall the normal hemoglobin ranges. For adult males, the normal range is 13–18 g/dL; for adult females, it is 12–16 g/dL. Step 2: Compare the patient's value (11.5 g/dL) to the female normal range (12–16 g/dL). Step 3: Since 11.5 is below 12, this value is LOW — indicating anemia. Step 4: Why the other options are wrong — Option A uses an incorrect range (10–14); Option C is wrong because a higher Hgb does not indicate being 'high' for a female; Option D is wrong because a universal threshold of 10 g/dL is not the standard reference. Always use sex-specific reference ranges for the NLE.

Answer: B. O-negative

Step 1: In emergencies without time for crossmatching, the safest blood to give is the universal donor type. Step 2: Type O-negative has NO A antigens, NO B antigens, and NO Rh(D) antigen on the red blood cells. This means it will not trigger an ABO or Rh incompatibility reaction in ANY recipient. Step 3: AB-positive is the universal RECIPIENT, not the universal donor — this is a very common mix-up in the NLE. Step 4: A-negative and B-negative are not universal donors because they still carry A or B antigens that can cause reactions in patients with different blood types. Step 5: Always remember — O-negative = universal donor (safe for everyone in emergencies).