Hematopathology — MCQs

A 60-year-old man is referred because of splenomegaly and generalized lymphadenopathy. The total white blood cell count is markedly elevated, and the differential count reveals a preponderance of mature appearing lymphocytes. Bone marrow examination reveals a diffuse infiltration with similar-appearing lymphocytes. Which of the following statements best characterizes this disorder?

Q270Easy

What is the typical lifespan of transfused platelets?

Hematopathology Indian Medical PG Practice Questions and MCQs

Question 261: Which type of mutation leads to sickle cell anemia?

A. Crossover mutation
B. Frameshift mutation
C. Deletion mutation
D. Point mutation (Correct Answer)

Explanation: ### Explanation **Correct Option: D. Point Mutation** Sickle cell anemia is a classic example of a **missense point mutation** [3]. It occurs due to a single nucleotide substitution in the **$\beta$-globin gene** located on **chromosome 11**. Specifically, there is a substitution of Adenine (A) by Thymine (T) at the 6th codon (**GAG $\rightarrow$ GTG**). This genetic change results in the replacement of the amino acid **Glutamic acid** (polar/hydrophilic) with **Valine** (non-polar/hydrophobic) at the 6th position of the $\beta$-globin chain [2]. This single change causes the hemoglobin (HbS) to polymerize under deoxygenated conditions, leading to the characteristic "sickling" of red blood cells [1]. **Why Incorrect Options are Wrong:** * **A. Crossover mutation:** This involves the exchange of genetic material between homologous chromosomes during meiosis. While it increases genetic diversity, it is not the mechanism behind sickle cell anemia. * **B. Frameshift mutation:** This occurs when nucleotides are inserted or deleted in numbers not divisible by three, altering the entire reading frame (e.g., Tay-Sachs disease). In sickle cell, the reading frame remains intact. * **C. Deletion mutation:** This involves the loss of one or more nucleotides. Deletions in the globin genes typically lead to **Thalassemias** (e.g., $\alpha$-thalassemia), where there is a quantitative deficiency of globin chains rather than a structural abnormality [4]. **High-Yield Clinical Pearls for NEET-PG:** * **Inheritance:** Autosomal Recessive [1]. * **Protective Effect:** Heterozygotes (Sickle cell trait) show resistance against *Plasmodium falciparum* malaria. * **Diagnosis:** **Hb Electrophoresis** is the gold standard (HbS moves slower than HbA toward the anode). * **Peripheral Smear:** Sickle cells and **Howell-Jolly bodies** (indicating functional asplenia). * **Metabisulfite Test:** Induces sickling in both trait and disease. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 652-654. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 598-599. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, pp. 50-51. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 147-148.

Question 262: Bart's hydrops fetalis is lethal because:

A. Hb Bart's cannot bind oxygen
B. The excess a-globin forms insoluble precipitates
C. Hb Bart's cannot release oxygen to fetal tissues (Correct Answer)
D. Microcytic red cells become trapped in the placenta

Explanation: **Explanation:** **1. Why Option C is correct:** Bart’s hydrops fetalis is the most severe form of **$\alpha$-thalassemia**, occurring when all four $\alpha$-globin genes are deleted ($--/--$) [1]. In the absence of $\alpha$-chains, the excess $\gamma$-globin chains (fetal) form tetramers ($\gamma_4$), known as **Hb Bart's**. The fundamental physiological defect is that Hb Bart's has an **extremely high affinity for oxygen** (the oxygen dissociation curve shifts severely to the left) [1]. While it can bind oxygen in the lungs/placenta, it **refuses to release it** to the peripheral fetal tissues. This results in severe intrauterine tissue hypoxia, high-output heart failure, massive edema (hydrops), and fetal death in utero or shortly after birth [2]. **2. Why other options are incorrect:** * **Option A:** Hb Bart's *can* bind oxygen; in fact, it binds it too tightly. * **Option B:** In $\alpha$-thalassemia, it is the **$\beta$-globin** (in adults) or **$\gamma$-globin** (in neonates) that is in excess, not $\alpha$-globin. Insoluble $\alpha$-globin precipitates are characteristic of $\beta$-thalassemia [3]. * **Option D:** While the cells are microcytic, the lethality is due to hypoxia and heart failure, not mechanical trapping in the placenta. **3. High-Yield Clinical Pearls for NEET-PG:** * **HbH Disease:** Deletion of 3 $\alpha$-genes ($--/-\alpha$). Excess $\beta$-chains form tetramers ($\beta_4$), called **HbH** [1]. * **Golf Ball Appearance:** HbH precipitates can be visualized using supravital stains (Brilliant Cresyl Blue) as multiple small inclusions. * **Electrophoresis:** On alkaline electrophoresis, Hb Bart's is the fastest-moving hemoglobin (moves furthest toward the anode). * **Management:** Intrauterine blood transfusions can occasionally save the fetus, but they will remain transfusion-dependent for life. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 649-650. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 470-472. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, p. 648.

Question 263: Aplastic anemia results from which of the following?

A. Cytotoxic drugs
B. Whole body irradiation
C. HIV infection
D. All of the above (Correct Answer)

Explanation: **Explanation:** Aplastic anemia is a bone marrow failure syndrome characterized by **pancytopenia** (anemia, neutropenia, and thrombocytopenia) and a **hypocellular bone marrow** where hematopoietic tissue is replaced by fat [3]. The underlying pathophysiology involves the destruction of multipotent hematopoietic stem cells due to direct injury or immune-mediated T-cell suppression [1], [2]. **Analysis of Options:** * **Cytotoxic Drugs (Option A):** This is the most common cause of secondary aplastic anemia. Drugs like alkylating agents (e.g., busulfan) and antimetabolites cause dose-dependent marrow suppression. Other drugs, like Chloramphenicol, can cause idiosyncratic (dose-independent) aplastic anemia [1]. * **Whole Body Irradiation (Option B):** Ionizing radiation causes direct DNA damage to hematopoietic stem cells [1]. While localized radiation affects specific areas, whole-body exposure leads to acute marrow failure. * **HIV Infection (Option C):** Viral infections are known triggers [1]. While Hepatitis (Non-A, Non-B, Non-C) is the most common viral cause, HIV can cause pancytopenia through direct infection of marrow stromal cells or by inducing an inhibitory cytokine environment. Since all three factors are established etiologies, **Option D (All of the above)** is the correct answer. **High-Yield Clinical Pearls for NEET-PG:** * **Gold Standard Diagnosis:** Bone marrow biopsy showing "dry tap" and **>90% fat cells** (hypocellularity) [3]. * **Morphology:** RBCs are typically **normocytic normochromic**, and there is a characteristically low reticulocyte count [3]. * **Fanconi Anemia:** The most common *inherited* cause of aplastic anemia (autosomal recessive, associated with DNA repair defects and thumb anomalies) [1]. * **Treatment of Choice:** Bone marrow transplantation (especially in young patients) or immunosuppressive therapy (Antithymocyte globulin + Cyclosporine) [2]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 595-596. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, p. 662. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 662-663.

Question 264: Which of the following is NOT a part of the triad associated with Hegglin anomaly?

A. Thrombocytopenia
B. Giant platelets
C. Albinism (Correct Answer)
D. Inclusion bodies in leukocytes

Explanation: **Explanation:** **May-Hegglin Anomaly (MHA)** is a rare, autosomal dominant inherited macrothrombocytopenia caused by a mutation in the **MYH9 gene**, which encodes the non-muscle myosin heavy chain IIA. **Why Albinism is the Correct Answer:** Albinism is **not** a feature of May-Hegglin Anomaly. It is, however, a hallmark of **Chediak-Higashi Syndrome**, which also features leukocyte inclusions. In Chediak-Higashi, the inclusions are giant peroxidase-positive lysosomal granules, whereas in May-Hegglin, they are RNA-containing cytoplasmic inclusions. **Analysis of Incorrect Options (The Triad of May-Hegglin):** The classic triad of May-Hegglin Anomaly consists of: * **Thrombocytopenia (Option A):** Most patients have a reduced platelet count, though they are often asymptomatic or have only mild bleeding tendencies. * **Giant Platelets (Option B):** Large, poorly granulated "megaplatelets" are seen on the peripheral smear. * **Inclusion Bodies in Leukocytes (Option D):** These are known as **Döhle-like bodies**. They are blue-gray, spindle-shaped cytoplasmic inclusions found in neutrophils, eosinophils, and monocytes. Unlike true Döhle bodies (seen in infections), these are present in all granulocytes and persist throughout the patient's life. **High-Yield Clinical Pearls for NEET-PG:** * **Gene Mutation:** MYH9 (located on chromosome 22q). * **Differentiating Feature:** Unlike Chediak-Higashi, May-Hegglin does **not** involve increased susceptibility to infections or albinism. * **Diagnosis:** Peripheral blood smear is the primary tool; inclusions are composed of precipitated myosin heavy chains and ribosomes. * **Associated Syndromes:** Other MYH9-related disorders include Sebastian, Fechtner, and Epstein syndromes, which may include additional features like sensorineural deafness or nephritis.

Question 265: Beta-2 microglobulin levels are typically elevated in which condition?

A. Multiple myeloma (Correct Answer)
B. Systemic lupus erythematosus
C. Immunocompromised patient
D. None of the above

Explanation: **Explanation:** **Beta-2 microglobulin (β2M)** is a low-molecular-weight protein that forms the light chain component of the **MHC Class I molecule**, found on the surface of all nucleated cells. **Why Multiple Myeloma is correct:** In Multiple Myeloma, there is a malignant proliferation of plasma cells [1]. Since these cells express MHC Class I molecules, a high turnover or high mass of tumor cells leads to increased shedding of β2M into the serum. In clinical practice, serum β2M is the **most important prognostic marker** for Multiple Myeloma. It is a key component of the **International Staging System (ISS)**; higher levels correlate with a higher tumor burden and renal impairment, indicating a poorer prognosis [2]. **Why other options are incorrect:** * **Systemic Lupus Erythematosus (SLE):** While β2M can be elevated in various inflammatory and autoimmune conditions due to lymphocyte activation, it is not a specific or primary diagnostic/prognostic marker for SLE in the context of standard medical examinations [1]. * **Immunocompromised patients:** Immunodeficiency itself does not characteristically elevate β2M unless there is an associated lymphoproliferative disorder or specific viral infection (like HIV) [1]. **High-Yield Clinical Pearls for NEET-PG:** * **ISS Staging for Myeloma:** * Stage I: β2M < 3.5 mg/L and Albumin ≥ 3.5 g/dL. * Stage III: β2M ≥ 5.5 mg/L. * **Renal Link:** β2M is filtered by the glomerulus but reabsorbed by proximal tubules. Therefore, levels also rise in **renal failure**, which is a common complication of myeloma (Myeloma kidney) [1, 5]. * **Dialysis-associated Amyloidosis:** Chronic elevation of β2M in dialysis patients can lead to its deposition as amyloid fibrils (Aβ2M amyloid) in osteoarticular structures. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, pp. 607-609. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 616-619.

Question 266: In sickle cell trait, how many hemoglobin bands are typically found?

A. 2 (Correct Answer)
B. 1
C. 4
D. 5

Explanation: In **Sickle Cell Trait (HbAS)**, the individual is a heterozygote, meaning they possess one normal adult hemoglobin gene ($\beta$) and one mutated sickle gene ($\beta^s$) [3]. Consequently, their red blood cells contain two distinct types of hemoglobin: **HbA** (normal adult hemoglobin) and **HbS** (sickle hemoglobin). [1] ### Why Option A is Correct: On alkaline hemoglobin electrophoresis (the standard screening method), these two types of hemoglobin migrate at different rates due to their electrical charges. This results in **two distinct bands**: 1. **HbA Band:** Usually comprises 55–60% of the total hemoglobin. 2. **HbS Band:** Usually comprises 35–45% of the total hemoglobin [2]. ### Why Other Options are Incorrect: * **Option B (1 band):** Found in normal individuals (HbAA) or those with homozygous Sickle Cell Disease (HbSS), where only one primary type of hemoglobin is present [1]. * **Option C & D (4 or 5 bands):** These are seen in complex compound heterozygous states (e.g., HbSC disease combined with other variants) or when multiple minor hemoglobins (like HbF or HbA2) are significantly elevated and visualized alongside variants, but they are not characteristic of simple Sickle Cell Trait. ### NEET-PG High-Yield Pearls: * **Electrophoresis Pattern:** On alkaline electrophoresis (pH 8.6), the order of migration from cathode (-) to anode (+) is **C → S → F → A** (Mnemonic: **C**ats **S**leep **F**ast **A**sleep). * **HbS Mutation:** Glutamic acid is replaced by **Valine** at the 6th position of the $\beta$-globin chain [1]. * **Clinical Significance:** Individuals with Sickle Cell Trait are usually asymptomatic and do not show "sickling" on a peripheral smear unless subjected to extreme hypoxia (e.g., unpressurized aircraft or high altitudes) [1]. * **Protective Effect:** Sickle cell trait provides a selective survival advantage against *Plasmodium falciparum* malaria. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 598-599. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 643-644. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 53-54.

Question 267: Decreased LAP score is found in:

A. Leukaemoid reaction
B. Myelofibrosis
C. Pernicious anemia (Correct Answer)
D. Polycythemia

Explanation: The **Leukocyte Alkaline Phosphatase (LAP) score** (also known as the Neutrophil Alkaline Phosphatase or NAP score) measures the enzyme activity within the secondary granules of mature neutrophils. It is a classic diagnostic tool used to differentiate between reactive leukocytosis and neoplastic processes. ### **Explanation of the Correct Answer** **C. Pernicious Anemia:** In megaloblastic anemias like Pernicious Anemia (Vitamin B12 deficiency), there is a defect in DNA synthesis leading to "ineffective hematopoiesis." [1] The neutrophils produced are often hypersegmented and biochemically abnormal, resulting in a **decreased LAP score**. Other conditions with low LAP scores include Chronic Myeloid Leukemia (CML), Paroxysmal Nocturnal Hemoglobinuria (PNH), and Hypophosphatasia. ### **Explanation of Incorrect Options** * **A. Leukemoid Reaction:** This is an exaggerated white blood cell response to infection or inflammation. The mature neutrophils are "stressed" and highly active, leading to a significantly **increased LAP score**. This is the primary way to distinguish it from CML. * **B. Myelofibrosis:** As a myeloproliferative neoplasm (MPN), primary myelofibrosis typically presents with a **normal or increased LAP score**, unlike CML. [2] * **C. Polycythemia Vera:** This is another MPN characterized by the overproduction of red cells. It is classically associated with an **increased LAP score**. ### **High-Yield Clinical Pearls for NEET-PG** * **LAP Score Range:** The normal range is typically **40–100**. * **Low LAP Score (Mnemonic: "PCH"):** **P**NH, **C**ML, **H**ypophosphatasia/Hereditary Sideroblastic Anemia (also Pernicious Anemia). * **High LAP Score:** Leukemoid reaction, Pregnancy (3rd trimester), Polycythemia Vera, and Down Syndrome. * **CML vs. Leukemoid Reaction:** This is the most common exam scenario. **CML = Low LAP; Leukemoid Reaction = High LAP.** **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 592-593. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, pp. 628-629.

Question 268: Schistocytes are seen in which of the following conditions?

A. Hemolytic Uremic Syndrome (HUS)
B. Thrombotic Thrombocytopenic Purpura (TTP)
C. Disseminated Intravascular Coagulation (DIC)
D. All of the above (Correct Answer)

Explanation: The presence of **Schistocytes** (fragmented red blood cells) is the hallmark of **Microangiopathic Hemolytic Anemia (MAHA)** [1], [2]. The underlying mechanism involves the formation of microthrombi (fibrin or platelet strands) within small blood vessels. As red blood cells circulate through these narrowed lumens, they are mechanically sheared by the meshwork of thrombi, resulting in fragmented cells shaped like helmets or triangles [2]. * **Hemolytic Uremic Syndrome (HUS):** Characterized by the triad of microangiopathic hemolytic anemia, thrombocytopenia, and acute renal failure [2]. Microthrombi predominantly affect the renal vasculature, leading to schistocyte formation. * **Thrombotic Thrombocytopenic Purpura (TTP):** Caused by a deficiency of ADAMTS13, leading to large vWF multimers and extensive platelet thrombi [3]. This mechanical obstruction causes significant RBC fragmentation. * **Disseminated Intravascular Coagulation (DIC):** Involves widespread activation of the coagulation cascade, creating fibrin strands across small vessels throughout the body, which slice passing RBCs [4]. Since all three conditions involve the mechanical destruction of RBCs within the microvasculature, schistocytes are a common finding in all of them. **High-Yield Clinical Pearls for NEET-PG:** * **Morphology:** Schistocytes are also known as "helmet cells" or "fragmentocytes." * **Lab Diagnosis:** A peripheral smear showing >1% schistocytes is highly suggestive of MAHA. * **Differential Diagnosis:** Other conditions showing schistocytes include prosthetic heart valves (mechanical hemolysis), severe burns, and malignant hypertension. * **Key Distinction:** In DIC, both PT and aPTT are prolonged (consumptive coagulopathy), whereas in TTP/HUS, PT and aPTT are typically normal [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 667-668. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 540-541. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 947-948. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 625-626.

Question 269: A 60-year-old man is referred because of splenomegaly and generalized lymphadenopathy. The total white blood cell count is markedly elevated, and the differential count reveals a preponderance of mature appearing lymphocytes. Bone marrow examination reveals a diffuse infiltration with similar-appearing lymphocytes. Which of the following statements best characterizes this disorder?

A. A progressive increase in the number of myeloblasts and promyelocytes is indicative of acceleration of the disease process.
B. Bacterial infections are common early in the disease due to hypogammaglobulinemia. (Correct Answer)
C. Mean survival is less than 1 year after diagnosis.
D. Myelofibrosis is a common complication.

Explanation: ### Explanation The clinical presentation of a 60-year-old male with splenomegaly, generalized lymphadenopathy, and a high count of mature-appearing lymphocytes is classic for **Chronic Lymphocytic Leukemia (CLL)**. [2] #### 1. Why Option B is Correct In CLL, the neoplastic B-cells are functionally incompetent. They fail to differentiate into plasma cells, leading to **hypogammaglobulinemia** (low levels of IgG, IgA, and IgM). This immune deficiency, often present early in the disease, makes patients highly susceptible to recurrent **bacterial infections** (e.g., *S. pneumoniae*, *S. aureus*), which are a leading cause of morbidity and mortality. #### 2. Why Other Options are Incorrect * **Option A:** An increase in myeloblasts and promyelocytes characterizes the "blast crisis" of Chronic Myeloid Leukemia (CML), not CLL. CLL may transform into a high-grade lymphoma (Richter’s Transformation), but not into an acute myeloid process. * **Option C:** CLL is typically an indolent, slow-growing malignancy. The mean survival is generally **5 to 10 years** or more, depending on the Rai or Binet stage [2]; it is certainly not less than 1 year. * **Option D:** While bone marrow involvement is diffuse, **myelofibrosis** (replacement of marrow by collagen) is a hallmark of Primary Myelofibrosis or late-stage CML, not a standard complication of CLL. #### 3. NEET-PG High-Yield Pearls * **Smudge Cells:** Characteristically seen on peripheral smears due to the fragility of CLL lymphocytes. [1] * **Immunophenotype:** CLL cells are unique because they co-express **CD5** (a T-cell marker) and B-cell markers (**CD19, CD20, CD23**). [1] * **Richter Transformation:** In ~5% of cases, CLL transforms into **Diffuse Large B-cell Lymphoma (DLBCL)**, signaled by sudden clinical worsening. * **Autoimmunity:** Patients may develop Autoimmune Hemolytic Anemia (AIHA) or thrombocytopenia despite having low overall gamma globulins. [1] **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, p. 602. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 612-613.

Question 270: What is the typical lifespan of transfused platelets?

A. <24 hours
B. 1-3 days
C. 3-5 days (Correct Answer)
D. 7-14 days

Explanation: **Explanation:** The correct answer is **3-5 days (Option C)**. **1. Understanding the Concept:** In a healthy individual, the physiological lifespan of endogenous platelets is approximately **7–10 days**. However, transfused platelets have a significantly shorter survival time. This reduction is due to the "storage lesion"—biochemical and structural changes that occur during collection, processing, and storage at room temperature (20–24°C). Once infused, these platelets are cleared more rapidly by the recipient's reticuloendothelial system. In a stable patient without complications, the expected survival of transfused platelets is typically **3 to 5 days**. **2. Analysis of Incorrect Options:** * **Option A (<24 hours):** This is seen in pathological states of increased consumption or destruction, such as Disseminated Intravascular Coagulation (DIC), ITP, or high-grade fever/sepsis, but it is not the "typical" lifespan. * **Option B (1-3 days):** While survival can be this short in moderately ill patients, 3-5 days is the standard textbook duration for a stable recipient. * **Option D (7-14 days):** This reflects the lifespan of natural, endogenous platelets in a healthy person, not transfused ones. **3. NEET-PG High-Yield Pearls:** * **Storage:** Platelets are stored at **20–24°C (Room Temperature)** with continuous agitation to prevent aggregation and maintain pH. * **Shelf Life:** Due to the risk of bacterial contamination at room temperature, the maximum storage life is only **5 days**. * **Dose Response:** One unit of Random Donor Platelets (RDP) typically increases the platelet count by **5,000–10,000/µL**, whereas one unit of Single Donor Platelets (SDP) increases it by **30,000–60,000/µL**. * **Refractoriness:** If the 1-hour post-transfusion increment is less than expected on two occasions, it suggests platelet refractoriness (often due to HLA alloimmunization).

Practice by Chapter

Anemias: Classification and Approach

Practice Questions

Hemolytic Anemias

Practice Questions

Myeloproliferative Neoplasms

Practice Questions

Myelodysplastic Syndromes

Practice Questions

Acute Leukemias

Practice Questions

Chronic Leukemias

Practice Questions

Lymphomas and Lymphoid Neoplasms

Practice Questions

Plasma Cell Disorders

Practice Questions

Bleeding Disorders

Practice Questions

Thrombotic Disorders

Practice Questions

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free