Hematology Practice Questions

Q: Which of the following is the least common presentation of multiple myeloma?

Hyperviscocity. **Explanation:** Multiple Myeloma (MM) is a neoplastic proliferation of plasma cells characterized by the "CRAB" features (Calcium elevation, Renal failure, Anemia, and Bone lesions). **Why Hyperviscosity is the correct answer:** While Multiple Myeloma involves the overproduction of monoclonal immunoglobulins (M-protein), **Hyperviscosity Syndrome** is relatively rare, occurring in only about **2–6%** of patients. It is much more characteristic of **Waldenström Macroglobulinemia**, where the large size of IgM pentamers significantly increases blood viscosity. In MM, hyperviscosity usually only occurs if the M-protein concentration is extremely high (typically IgA or IgG3 subtypes). **Analysis of Incorrect Options:** * **Anemia (Option A):** This is the most common hematological finding (present in ~73% of cases) due to bone marrow infiltration by plasma cells and cytokine-mediated suppression of erythropoiesis. * **Bone Pains (Option C):** This is the most common presenting symptom (~58-70%). Plasma cells produce Osteoclast Activating Factors (OAFs) like IL-6 and RANK-L, leading to lytic "punched-out" lesions and pathological fractures. * **Infection (Option D):** This is a leading cause of morbidity and mortality. Patients have functional hypogammaglobulinemia (decreased normal antibodies), making them highly susceptible to encapsulated organisms like *S. pneumoniae*. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause of death:** Infection (Sepsis) followed by Renal Failure. * **Radiology:** "Punched-out" lytic lesions; **Bone scans are often negative** because they detect osteoblastic activity, which is absent in MM. * **Blood Film:** **Rouleaux formation** (due to decreased zeta potential between RBCs by paraproteins). * **Urinalysis:** Bence-Jones proteins (free light chains) are detected by heat precipitation test, **not** by standard dipsticks.

Q: Which of the following conditions is typically associated with a normal platelet count?

Shaken baby syndrome. **Explanation:** The correct answer is **Shaken baby syndrome (B)**. This condition is characterized by the clinical triad of subdural hemorrhage, retinal hemorrhage, and encephalopathy. Unlike the other options, it is a mechanical injury caused by physical abuse (acceleration-deceleration forces), which does not inherently involve a consumption or sequestration of platelets. Therefore, the platelet count remains **normal**. **Analysis of Incorrect Options:** * **Disseminated Intravascular Coagulation (DIC):** This is a consumptive coagulopathy. Widespread activation of the coagulation cascade leads to the formation of microthrombi, which consumes platelets and clotting factors, resulting in **thrombocytopenia**. * **Microangiopathic Hemolytic Anemia (MAHA):** Conditions like TTP or HUS involve the formation of platelet-rich thrombi in small vessels. These thrombi mechanically shear RBCs (schistocytes) and consume platelets, leading to **thrombocytopenia**. * **Splenomegaly:** The spleen normally stores about one-third of the body's platelets. In splenomegaly (congestive or infiltrative), the spleen sequesters a significantly higher percentage of platelets, leading to **sequestration-induced thrombocytopenia**. **NEET-PG High-Yield Pearls:** * **Shaken Baby Syndrome:** Always look for the "triad" in forensic/pediatric questions. A normal coagulation profile and platelet count help rule out bleeding diathesis as a cause of the intracranial bleed. * **Pseudothrombocytopenia:** Always remember that EDTA-induced platelet clumping can cause a falsely low count on automated analyzers; check a peripheral smear. * **Isolated Thrombocytopenia:** In a patient with a low platelet count but otherwise normal CBC and no organomegaly, **ITP (Immune Thrombocytopenic Purpura)** is the most likely diagnosis.

Q: Thrombotic thrombocytopenic purpura involves which of the following phenomena, except?

High complement level. Thrombotic Thrombocytopenic Purpura (TTP) is a life-threatening hematological emergency caused by a deficiency of the metalloproteinase **ADAMTS13**. This deficiency leads to the persistence of ultra-large von Willebrand factor (vWF) multimers, which cause spontaneous platelet aggregation and microthrombi formation. **Why Option C is the correct answer:** TTP is primarily a disorder of platelet aggregation and is **not** mediated by the complement system. Therefore, complement levels (C3, C4) remain **normal**. In contrast, low complement levels are characteristic of conditions like Systemic Lupus Erythematosus (SLE) or certain types of glomerulonephritis. Note that *Atypical Hemolytic Uremic Syndrome (aHUS)* involves complement dysregulation, but classic TTP does not. **Analysis of incorrect options:** * **A. Microangiopathy:** TTP is a classic Microangiopathic Hemolytic Anemia (MAHA) [1]. The microthrombi in small vessels shear passing RBCs, leading to schistocyte formation. * **B. Neural dysfunction:** Fluctuating neurological symptoms (confusion, seizures, focal deficits) are a hallmark of the TTP pentad, caused by microthrombi in the cerebral vasculature. * **D. Intravascular hemolysis:** The mechanical destruction of RBCs by fibrin strands/microthrombi results in non-immune, intravascular hemolysis (elevated LDH, low haptoglobin, and indirect hyperbilirubinemia) [1]. **High-Yield Clinical Pearls for NEET-PG:** * **The Classic Pentad (FAT RN):** **F**ever, **A**nemia (MAHA), **T**hrombocytopenia, **R**enal failure, and **N**eurological deficits. * **Diagnosis:** Decreased ADAMTS13 activity (<10%). * **Peripheral Smear:** Presence of **Schistocytes** (helmet cells). * **Coagulation Profile:** PT, aPTT, and Fibrinogen are typically **normal** (distinguishes TTP from DIC). * **Treatment:** Emergency **Plasmapheresis (Plasma Exchange)** is the gold standard. Never delay treatment for ADAMTS13 results.

Q: With oral iron therapy, when can a rise in hemoglobin percentage be observed?

3 weeks. **Explanation:** The therapeutic response to oral iron therapy in patients with iron deficiency anemia (IDA) follows a predictable physiological timeline. While the bone marrow begins producing new red blood cells quickly, a measurable rise in hemoglobin (Hb) concentration takes time to manifest in the peripheral blood. 1. **Why 3 weeks is correct:** After starting oral iron, the **reticulocyte count** peaks within 7–10 days (the earliest sign of response). However, a significant and clinically observable **rise in hemoglobin** (typically 2 g/dL or more) generally takes about **3 weeks**. Complete normalization of hemoglobin levels usually occurs within 2 months of therapy. 2. **Analysis of Incorrect Options:** * **1 week (Option A):** At this stage, only the reticulocyte count increases. Hemoglobin levels have not yet risen significantly. * **4 weeks (Option B) & 6 weeks (Option D):** While hemoglobin continues to rise during these periods, the *initial* observable rise occurs earlier, at the 3-week mark. These options represent the progression toward normalization rather than the first point of measurable increase. **NEET-PG High-Yield Pearls:** * **Earliest sign of response:** Increase in Reticulocyte count (peaks at 7–10 days). * **Rate of Hb rise:** Approximately 0.1 g/dL per day or 0.5–1.0 g/dL per week. * **Duration of therapy:** Iron should be continued for **3–6 months** *after* hemoglobin normalizes to replenish depleted iron stores (measured by Serum Ferritin). * **Best Absorption:** Oral iron is best absorbed on an empty stomach; Vitamin C (Ascorbic acid) enhances absorption, while antacids, tea, and milk inhibit it.

Q: A 50-year-old man presented with an orbital mass. Systemic examination revealed anemia, and investigations revealed hypergammaglobulinemia. What condition should be investigated to explain these findings?

Multiple myeloma. **Explanation:** The clinical presentation of an **orbital mass** associated with **anemia** and **hypergammaglobulinemia** is a classic triad pointing toward **Multiple Myeloma (MM)**. **Why Multiple Myeloma is correct:** Multiple Myeloma is a neoplastic proliferation of plasma cells. These cells produce excessive monoclonal immunoglobulins (M-protein), leading to **hypergammaglobulinemia**. The infiltration of bone marrow by plasma cells causes **anemia** and "punched-out" lytic lesions. In the orbit, MM typically manifests as a rapidly progressing plasmacytoma, often involving the orbital bones (most commonly the frontal bone), resulting in proptosis and a palpable mass. **Why the other options are incorrect:** * **Squamous cell carcinoma:** While it can involve the orbit (usually via local spread from the eyelid or sinuses), it does not typically cause systemic hypergammaglobulinemia. * **Optic nerve glioma:** This is a benign tumor primarily seen in children (often associated with Neurofibromatosis type 1). It presents with axial proptosis and vision loss, not systemic hematological abnormalities. * **Malignant melanoma:** Uveal melanoma is the most common primary intraocular tumor in adults. While it can metastasize, it does not present with hypergammaglobulinemia. **High-Yield Clinical Pearls for NEET-PG:** * **Orbital Plasmacytoma:** May be the first sign of occult Multiple Myeloma. * **Ocular signs of MM:** Include "pars plana cysts" (highly characteristic), crystalline keratopathy, and hyperviscosity retinopathy (venous dilation and hemorrhages). * **Diagnostic Triad for MM:** Plasma cells in bone marrow >10%, lytic bone lesions, and M-protein in serum/urine. * **Bence-Jones proteins:** Light chains found in the urine of MM patients.

Q: A 60-year-old male presents with generalized bone pain. On examination, there is an elevated ESR of 100 mm/hr, serum globulin of 7 g/dL, lytic lesions in the skull, serum creatinine of 3.5 mg/dL, and serum calcium of 11 mg/dL. What is the most likely diagnosis?

Multiple myeloma. The clinical presentation is a classic case of **Multiple Myeloma (MM)**, a neoplastic proliferation of plasma cells [1]. The diagnosis is confirmed by the **CRAB** criteria (Calcium elevation, Renal insufficiency, Anemia, and Bone lesions), all of which are present here: * **Bone Pain & Lytic Lesions:** Plasma cells produce OAFs (Osteoclast Activating Factors), leading to "punched-out" lytic lesions (skull) and bone pain [1]. * **Renal Insufficiency:** Serum creatinine of 3.5 mg/dL indicates "Myeloma Kidney," caused by the precipitation of Bence-Jones proteins (light chains) in the tubules. * **Hyperglobulinemia & High ESR:** The monoclonal (M) protein spike leads to a reversal of the Albumin:Globulin ratio and causes "Rouleaux formation," which significantly elevates the ESR [1]. **Why other options are incorrect:** * **Waldenstrom’s Macroglobulinemia:** Characterized by IgM paraprotein and hyperviscosity [1]. Crucially, it **lacks** lytic bone lesions and hypercalcemia. * **Hyperparathyroidism:** While it causes hypercalcemia and bone resorption (osteitis fibrosa cystica), it does not explain the massive hyperglobulinemia (7 g/dL) or the extremely high ESR. * **Osteomalacia:** This involves defective mineralization of the bone matrix, typically presenting with **low** calcium and phosphate, not lytic lesions or renal failure. **NEET-PG High-Yield Pearls:** * **Most common initial symptom:** Bone pain (back/ribs). * **Best initial test:** Serum Protein Electrophoresis (shows M-spike) [1]. * **Gold standard:** Bone marrow biopsy (>10% clonal plasma cells) [1]. * **Note:** Bone scans are often negative in MM because they detect osteoblastic activity; **Skeletal Survey (X-ray)** or MRI is preferred to find lytic lesions [1].

Question 1

Which of the following is the least common presentation of multiple myeloma?

Accepted Answer

Hyperviscocity

Answer

Anemia

Answer

Bone pains

Answer

Infection

Question 2

All are benefits of repeated phlebotomy in hemochromatosis, EXCEPT:

Accepted Answer

Reversal of testicular atrophy

Answer

Improved control of diabetes

Answer

Decrease in skin pigmentation

Answer

Normalization of the liver enzymes

Question 3

Which of the following conditions is typically associated with a normal platelet count?

Accepted Answer

Shaken baby syndrome

Answer

Disseminated intravascular coagulation (DIC)

Answer

Microangiopathic hemolytic anemia

Answer

Splenomegaly

Question 4

Pancytopenia with hypocellular bone marrow is seen in which of the following conditions?

Accepted Answer

Fanconi's anemia

Answer

Paroxysmal nocturnal hemoglobinuria

Answer

Hairy cell leukemia

Answer

Myelopthisis

Question 5

Thrombotic thrombocytopenic purpura involves which of the following phenomena, except?

Accepted Answer

High complement level

Answer

Microangiopathy

Answer

Neural dysfunction

Answer

Intravascular hemolysis

Question 6

What is the treatment of choice for anti-CD120 antibody?

Accepted Answer

All low-grade non-Hodgkin's lymphomas

Answer

Relapsed B cell follicular lymphomas

Answer

Relapsed Hodgkin's disease

Answer

Chronic lymphatic leukemia

Question 7

With oral iron therapy, when can a rise in hemoglobin percentage be observed?

Accepted Answer

3 weeks

Answer

1 week

Answer

4 weeks

Answer

6 weeks

Question 8

Which of the following is NOT to be used in the treatment of thrombotic thrombocytopenic purpura (TTP)?

Accepted Answer

Platelet transfusion

Answer

Corticosteroids

Answer

Immunotherapy

Answer

Plasmapheresis

Question 9

A 50-year-old man presented with an orbital mass. Systemic examination revealed anemia, and investigations revealed hypergammaglobulinemia. What condition should be investigated to explain these findings?

Accepted Answer

Multiple myeloma

Answer

Squamous cell carcinoma

Answer

Optic nerve glioma

Answer

Malignant melanoma

Question 10

A 60-year-old male presents with generalized bone pain. On examination, there is an elevated ESR of 100 mm/hr, serum globulin of 7 g/dL, lytic lesions in the skull, serum creatinine of 3.5 mg/dL, and serum calcium of 11 mg/dL. What is the most likely diagnosis?

Accepted Answer

Multiple myeloma

Answer

Waldenstrom's macroglobulinemia

Answer

Hyperparathyroidism

Answer

Osteomalacia

Hematology — MCQs

Hematology — MCQs

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