Hematology Practice Questions

Q: A 23-year-old man presents with prolonged nosebleeds. He has always noted easy bruising and ongoing bleeding after minor cuts. There is no prior history of surgery or dental procedures. His hemoglobin is 14.5 g/dL, platelets are 200,000/mL, and PT/PTT are normal. Further testing reveals that the bleeding time is elevated; the Factor VIII level is reduced, as is the ristocetin cofactor assay. What is the most likely diagnosis for this patient with a bleeding disorder?

von Willebrand's disease. ### Explanation **Correct Answer: A. von Willebrand's disease (vWD)** The patient presents with a classic **mucocutaneous bleeding pattern** (epistaxis, easy bruising, prolonged bleeding from minor cuts) [1]. The key to the diagnosis lies in the laboratory profile: 1. **Normal Platelet Count:** Rules out thrombocytopenia. 2. **Elevated Bleeding Time:** Indicates a defect in primary hemostasis (platelet adhesion) [2]. 3. **Reduced Ristocetin Cofactor Assay:** This is the most specific test for vWD; it measures the ability of von Willebrand Factor (vWF) to agglutinate platelets [1]. 4. **Reduced Factor VIII:** vWF acts as a carrier protein for Factor VIII, protecting it from degradation [1]. Therefore, a deficiency in vWF often leads to a secondary decrease in Factor VIII. **Why Incorrect Options are Wrong:** * **B & C (Hemophilia A & B):** These are disorders of secondary hemostasis (clotting factors). They typically present with deep-tissue bleeding (hemarthrosis, muscle hematomas) rather than mucosal bleeding [1]. In Hemophilia, the Bleeding Time is **normal**, but the **aPTT is prolonged**. * **D (TTP):** TTP is characterized by the pentad of microangiopathic hemolytic anemia, **thrombocytopenia** (which is absent here), neurological symptoms, fever, and renal failure. **High-Yield Clinical Pearls for NEET-PG:** * **Inheritance:** vWD is the most common inherited bleeding disorder (usually Autosomal Dominant). * **vWF Functions:** 1) Platelet-to-subendothelial adhesion (via GpIb receptor); 2) Carrier for Factor VIII [1]. * **Lab Findings:** Normal PT, Normal/Prolonged aPTT (depending on Factor VIII levels), and prolonged Bleeding Time/PFA-100. * **Treatment:** **Desmopressin (DDAVP)** is the drug of choice for Type 1 vWD as it releases stored vWF from Weibel-Palade bodies in endothelial cells [1].

Q: If a blood transfusion reaction develops due to incompatibility, what is the first immediate action to be taken?

Stop the transfusion. ### Explanation **1. Why "Stop the Transfusion" is Correct:** The most critical step in managing any suspected transfusion reaction—whether it is a simple febrile reaction or a life-threatening acute hemolytic reaction—is to **immediately stop the transfusion** [1]. This prevents further exposure to the offending antigen or antibody, limiting the severity of the immune response. Following this, the IV line must be maintained with normal saline using a new administration set to ensure vascular access for emergency medications [1]. **2. Analysis of Incorrect Options:** * **B & C (Hydrocortisone and Chlorpheniramine):** These are secondary treatments. Antihistamines (Chlorpheniramine) are used for allergic reactions (Urticaria), and steroids (Hydrocortisone) are used for severe allergic or febrile reactions. However, they should never be administered before stopping the offending agent. * **D (Furosemide):** This is indicated in cases of Transfusion-Associated Circulatory Overload (TACO) to reduce fluid volume or to maintain renal blood flow in hemolytic reactions. It is a supportive measure, not the primary immediate action. **3. NEET-PG High-Yield Clinical Pearls:** * **Acute Hemolytic Transfusion Reaction (AHTR):** Most commonly due to **ABO incompatibility** (clerical error). Classic triad: Fever, chills, and flank pain [1]. * **First Step:** Stop transfusion $\rightarrow$ Check vitals $\rightarrow$ Maintain IV access with NS $\rightarrow$ Notify blood bank [1]. * **Investigation:** Perform a **Direct Antiglobulin Test (DAT/Coombs test)** on the post-transfusion sample and check for hemoglobinuria [1]. * **Febrile Non-Hemolytic Reaction (FNHRT):** The most common reaction overall; caused by cytokines released from donor leukocytes. Prevented by **leukoreduction** [1].

Q: All are true regarding Thrombotic Thrombocytopenia Purpura (TTP), except?

Normal complement levels. Thrombotic Thrombocytopenic Purpura (TTP) is a life-threatening hematologic emergency caused by a deficiency of the metalloproteinase ADAMTS13. This enzyme is responsible for cleaving large von Willebrand factor (vWF) multimers; its absence leads to ultra-large multimers that cause spontaneous platelet aggregation and microthrombi formation. **Why Option A is the correct answer:** In TTP, the primary pathology is a **non-immune** platelet consumption [2]. Unlike conditions like Systemic Lupus Erythematosus (SLE) or certain types of Glomerulonephritis, TTP does **not** involve the activation or consumption of the complement system. Therefore, **complement levels (C3, C4) remain normal**. This is a crucial diagnostic differentiator from other systemic microangiopathies. **Analysis of other options:** * **B. Microangiopathic Hemolytic Anemia (MAHA):** This is a hallmark of TTP [1]. As RBCs pass through small vessels partially occluded by platelet thrombi, they are mechanically shredded, leading to the presence of **schistocytes** on a peripheral smear [1]. * **C. Thrombocytopenia:** Extensive formation of microthrombi consumes platelets, leading to severe consumption-based thrombocytopenia [2]. * **D. Thrombosis:** The core pathophysiology involves widespread hyaline microthrombi in small vessels, which leads to end-organ ischemia (notably in the brain and kidneys) [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 symptoms [1]. * **Coagulation Profile:** PT, aPTT, and Fibrinogen levels are typically **normal** in TTP (unlike DIC). * **Treatment of Choice:** Immediate **Plasmapheresis (Plasma Exchange)** to remove autoantibodies and replenish ADAMTS13.

Q: A 40-year-old woman with chronic lymphocytic leukemia (CLL) presents with rapidly increasing swellings in her neck and axilla over the past few months, accompanied by fever and weight loss. Which of the following is the most likely complication?

Richter transformation. ### Explanation **Correct Option: A. Richter Transformation** Richter transformation (RT) refers to the sudden clinicopathological transformation of Chronic Lymphocytic Leukemia (CLL) or Small Lymphocytic Lymphoma (SLL) into a more aggressive form of high-grade non-Hodgkin lymphoma, most commonly **Diffuse Large B-Cell Lymphoma (DLBCL)** (approx. 90%) [1] or rarely Hodgkin Lymphoma. The clinical hallmark of RT is the **"B-symptoms" triad**: rapid enlargement of lymph nodes (lymphadenopathy), drenching night sweats, fever, and significant weight loss [2]. Laboratory findings often show a sudden rise in Serum LDH levels [1]. This transformation occurs in about 2–10% of CLL patients and carries a poor prognosis. **Why Incorrect Options are Wrong:** * **B. Progression of CLL:** While CLL is a progressive disease, it typically follows an indolent course [1]. Rapid, localized lymph node enlargement with systemic B-symptoms is more characteristic of a high-grade transformation than the natural slow progression of CLL. * **C. Development of secondary infections:** CLL patients are prone to infections due to hypogammaglobulinemia [1]; however, infections usually present with acute inflammatory signs (cough, dysuria, etc.) rather than rapidly growing, painless lymphadenopathy. * **D. Immunodeficiency-associated hemolytic anemia:** While Autoimmune Hemolytic Anemia (AIHA) is a known complication of CLL, it presents with jaundice, pallor, and fatigue, not rapidly enlarging lymph nodes [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Most common transformation:** DLBCL (90%). * **Best Initial Test:** LDH (elevated) and PET-CT (to identify the most metabolically active node). * **Gold Standard Diagnosis:** Excisional Lymph Node Biopsy [2]. * **Prognosis:** Generally poor, with a median survival of less than 1 year. * **Key Trigger:** Often associated with mutations in *TP53* or *NOTCH1*.

Q: A patient presents with fever and altered consciousness. Investigations reveal anemia with fragmented red blood cells, a platelet count of 20,000/mm³, serum creatinine of 3.0 mg/dL, and normal prothrombin time (PT) and activated partial thromboplastin time (aPTT). Which of the following is the most appropriate treatment for this patient?

Plasma exchange therapy. ### Explanation The clinical presentation describes the classic **pentad of Thrombotic Thrombocytopenic Purpura (TTP)**: 1. **Microangiopathic Hemolytic Anemia (MAHA):** Fragmented RBCs (schistocytes) [2]. 2. **Thrombocytopenia:** Low platelet count (20,000/mm³) [3]. 3. **Neurological symptoms:** Altered consciousness. 4. **Renal dysfunction:** Elevated creatinine (3.0 mg/dL) [2]. 5. **Fever.** The hallmark of TTP is a deficiency of the **ADAMTS13** enzyme, leading to ultra-large von Willebrand factor (vWF) multimers that cause spontaneous platelet aggregation and microthrombi. **Why Plasma Exchange (PEX) is correct:** PEX is the **treatment of choice** and a medical emergency. It works by removing the autoantibodies against ADAMTS13 and replacing the deficient enzyme. It should be initiated immediately upon suspicion to prevent irreversible organ damage and death. **Why other options are incorrect:** * **B & C (Corticosteroids/IVIG):** While steroids are often used as an adjunct to PEX, they are not the primary treatment. IVIG is the treatment for Immune Thrombocytopenic Purpura (ITP), which lacks MAHA and renal failure [3]. * **D (Heparin):** Anticoagulation is ineffective and contraindicated as it increases the risk of bleeding in the setting of severe thrombocytopenia. **High-Yield Clinical Pearls for NEET-PG:** * **Coagulation Profile:** In TTP/HUS, PT and aPTT are **normal** (unlike DIC, where they are prolonged) [1]. * **HUS vs. TTP:** Hemolytic Uremic Syndrome (HUS) presents similarly but is more common in children, usually follows bloody diarrhea (EHEC O157:H7), and features **predominant renal failure** with fewer neurological symptoms [2]. * **Contraindication:** **Platelet transfusion** is generally contraindicated in TTP as it may "fuel the fire" by promoting further microthrombi formation.

Q: What is the recommended hemoglobin level in male patients with polycythemia rubra vera to avoid thrombotic episodes?

14 g/dL. In Polycythemia Vera (PV), the primary goal of management is to reduce the risk of arterial and venous thrombosis, which are the leading causes of morbidity and mortality [1]. The cornerstone of therapy is therapeutic phlebotomy. **1. Why 14 g/dL is correct:** The risk of thrombotic episodes in PV is directly correlated with blood viscosity, which rises exponentially once the hematocrit (Hct) exceeds 45%. Clinical guidelines (based on the landmark CYTO-PV trial) recommend maintaining a **hematocrit <45%** in men. Since the hemoglobin (Hb) level is roughly one-third of the hematocrit value, a Hct of 45% corresponds to an **Hb of 15 g/dL**. To ensure a safety margin and keep the Hct strictly below 45%, the target Hb is maintained at **14 g/dL**. (Note: In females, the target Hct is <42%, corresponding to an Hb of ~12-13 g/dL). **2. Why incorrect options are wrong:** * **12 g/dL (Option B):** While this is a safe level, it is the target for females rather than males. Aiming for 12 g/dL in males may lead to unnecessary phlebotomies and symptomatic iron deficiency. * **10 g/dL and 8 g/dL (Options C & D):** These levels are unnecessarily low. Maintaining such levels would induce severe iron deficiency anemia and related symptoms (pica, glossitis, fatigue) without providing additional protection against thrombosis compared to the 14 g/dL target. **High-Yield Clinical Pearls for NEET-PG:** * **Mutation:** >95% of PV patients have the **JAK2 V617F** mutation [1]. * **Diagnostic Hallmark:** Low serum Erythropoietin (EPO) levels (unlike secondary polycythemia). * **Symptom:** **Aquagenic pruritus** (itching after a warm bath) is a classic board-exam clue [1]. * **Treatment:** Low-dose Aspirin is indicated for all patients unless contraindicated. Hydroxyurea is the first-line myelosuppressive agent for high-risk patients (age >60 or prior thrombosis).

Q: Microcytic hypochromic anaemia is seen in all of the following conditions except?

Malaria. Microcytic hypochromic anemia is characterized by a Mean Corpuscular Volume (MCV) < 80 fL and a Mean Corpuscular Hemoglobin Concentration (MCHC) < 32 g/dL [3]. This occurs due to defects in hemoglobin synthesis (either heme or globin). **Why Malaria is the correct answer:** Malaria typically causes a **Normocytic Normochromic anemia** [4]. The primary mechanism is the destruction of mature red blood cells (hemolysis) and splenic sequestration, rather than a defect in hemoglobin production [3, 5]. While chronic or severe malaria can occasionally lead to dyserythropoiesis, it is not a classic cause of microcytosis [4]. **Analysis of incorrect options:** * **Iron Deficiency Anemia (IDA):** The most common cause of microcytic hypochromic anemia worldwide [1, 4]. Lack of iron leads to decreased heme synthesis. * **Beta Thalassemia:** A quantitative defect in globin chain synthesis. It presents with significant microcytosis (often very low MCV) and a characteristic "target cell" appearance on peripheral smear. * **Lead Poisoning:** Lead inhibits enzymes in the heme synthesis pathway (ferrochelatase and ALA dehydratase), resulting in microcytic anemia with characteristic **basophilic stippling**. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for Microcytic Anemia (TAILS):** **T**halassemia, **A**nemia of chronic disease (some cases), **I**ron deficiency, **L**ead poisoning, **S**ideroblastic anemia [1]. * **Mentzer Index:** (MCV/RBC count). If ** 13**, it suggests Iron Deficiency Anemia. * **RDW (Red Cell Distribution Width):** Usually increased in IDA (anisocytosis) but normal in uncomplicated Thalassemia trait.

Question 1

A 23-year-old man presents with prolonged nosebleeds. He has always noted easy bruising and ongoing bleeding after minor cuts. There is no prior history of surgery or dental procedures. His hemoglobin is 14.5 g/dL, platelets are 200,000/mL, and PT/PTT are normal. Further testing reveals that the bleeding time is elevated; the Factor VIII level is reduced, as is the ristocetin cofactor assay. What is the most likely diagnosis for this patient with a bleeding disorder?

Accepted Answer

von Willebrand's disease

Answer

hemophilia A

Answer

hemophilia B

Answer

thrombotic thrombocytopenic purpura (TTP)

Question 2

Which action by a nursing assistant when caring for a patient who is pancytopenic indicates a need for the nurse to intervene?

Accepted Answer

The nursing assistant assists the patient to use dental floss after eating.

Answer

The nursing assistant makes an oral rinse using 1 teaspoon of salt in a liter of water.

Answer

The nursing assistant adds baking soda to the patient’s saline oral rinses.

Answer

The nursing assistant puts fluoride toothpaste on the patient’s toothbrush.

Question 3

If a blood transfusion reaction develops due to incompatibility, what is the first immediate action to be taken?

Accepted Answer

Stop the transfusion

Answer

Administer hydrocortisone injection

Answer

Administer chlorpheniramine maleate injection

Answer

Administer furosemide injection

Question 4

A patient has Hb 6 gm%, folic acid 82 ng/ml, vitamin B12 60 pg/ml, serum iron 180 
g/dL, and MCV of 104 fL. What is the most likely diagnosis?

Accepted Answer

Vitamin B12 deficiency

Answer

Iron deficiency anaemia

Answer

Folic acid deficiency

Answer

Pyridoxine deficiency

Question 5

All are true regarding Thrombotic Thrombocytopenia Purpura (TTP), except?

Accepted Answer

Normal complement levels

Answer

Microangiopathic hemolytic anemia

Answer

Thrombocytopenia

Answer

Thrombosis

Question 6

Which of the following is not associated with multiple myeloma?

Accepted Answer

Carpopedal spasm

Answer

Bone pain

Answer

Metastatic calcification

Answer

Punched out lesion in the skull

Question 7

A 40-year-old woman with chronic lymphocytic leukemia (CLL) presents with rapidly increasing swellings in her neck and axilla over the past few months, accompanied by fever and weight loss. Which of the following is the most likely complication?

Accepted Answer

Richter transformation

Answer

Progression of CLL

Answer

Development of secondary infections

Answer

Immunodeficiency-associated hemolytic anemia

Question 8

A patient presents with fever and altered consciousness. Investigations reveal anemia with fragmented red blood cells, a platelet count of 20,000/mm³, serum creatinine of 3.0 mg/dL, and normal prothrombin time (PT) and activated partial thromboplastin time (aPTT). Which of the following is the most appropriate treatment for this patient?

Accepted Answer

Plasma exchange therapy

Answer

Corticosteroids and intravenous immunoglobulin

Answer

Immunoglobulins

Answer

Anticoagulation with heparin

Question 9

What is the recommended hemoglobin level in male patients with polycythemia rubra vera to avoid thrombotic episodes?

Accepted Answer

14 g/dL

Answer

12 g/dL

Answer

10 g/dL

Answer

8 g/dL

Question 10

Microcytic hypochromic anaemia is seen in all of the following conditions except?

Accepted Answer

Malaria

Answer

Beta thalassemia

Answer

Iron deficiency

Answer

Lead poisoning

Hematology — MCQs

Hematology — MCQs

On this page

Practice by Chapter

Want unlimited practice?