Hematopoietic Growth Factors — MCQs
Drug inhibiting granulocyte migration is:-
Romiplostim mimics which of the following receptors?
What is an atypical side effect of montelukast?
Which of the following is a characteristic bone marrow finding in myelofibrosis?
Bleeding crisis in acute idiopathic thrombo-cytopenic purpura is managed by all except -
During the treatment of chronic myeloid leukemia, cytogenetic remission is least likely to occur with which one of the following treatment modalities?
What is the best treatment for anemia in patients with Chronic Renal Failure (CRF)?
Which of the following is the LEAST likely indication for intravenous iron administration?
What is the typical bone marrow finding in myelofibrosis?
A patient with a malignancy is undergoing chemotherapy. The platelet counts were reduced after the previous cycle of chemotherapy. Which of the following drugs can be used to treat this patient?
Hematopoietic Growth Factors Indian Medical PG Practice Questions and MCQs
Question 1: Drug inhibiting granulocyte migration is:-
- A. Montelukast
- B. Colchicine (Correct Answer)
- C. Cromoglycate
- D. Felbamate
Explanation: ***Colchicine*** - **Colchicine** inhibits **granulocyte migration** by binding to tubulin, thereby disrupting microtubule assembly and function [2]. - This action is crucial in its use for conditions like **gout**, where it reduces the inflammatory response by preventing neutrophil chemotaxis to crystal deposits [1], [2]. *Montelukast* - **Montelukast** is a **leukotriene receptor antagonist** that primarily reduces bronchoconstriction and inflammation. - While it affects inflammatory pathways, its direct action is not inhibiting granulocyte migration but rather blocking the effects of leukotrienes. *Cromoglycate* - **Cromoglycate** (e.g., cromolyn sodium) is a **mast cell stabilizer** that prevents the release of inflammatory mediators. - Its main mechanism involves preventing mast cell degranulation, not directly inhibiting granulocyte migration. *Felbamate* - **Felbamate** is an **antiepileptic drug** used in the treatment of seizures. - Its mechanism of action involves blocking NMDA receptors and modulating GABAergic transmission; it has no known role in inhibiting granulocyte migration.
Question 2: Romiplostim mimics which of the following receptors?
- A. IL 6
- B. IL 8
- C. PGE 1
- D. Thrombopoietin (Correct Answer)
Explanation: ***Thrombopoietin*** - **Romiplostim** is a **thrombopoietin receptor agonist**, meaning it binds to and activates the **thrombopoietin receptor** [1]. - This activation mimics the effect of endogenous thrombopoietin, stimulating the production of **platelets** in the bone marrow [2].*IL 6* - **Interleukin-6 (IL-6)** is a cytokine involved in inflammation, immune response, and hematopoiesis, but it is not the primary target of romiplostim. - While IL-6 can influence platelet production indirectly, romiplostim directly targets the thrombopoietin pathway.*IL 8* - **Interleukin-8 (IL-8)** is a chemokine primarily involved in neutrophil chemotaxis and inflammation. - It plays no direct role in the mechanism of action of romiplostim.*PGE 1* - **Prostaglandin E1 (PGE1)** is a lipid compound with various effects, including vasodilation and inhibition of platelet aggregation. - Romiplostim's mechanism of action is distinct from that of prostaglandins, as it specifically targets platelet production rather than platelet function or vascular tone.
Question 3: What is an atypical side effect of montelukast?
- A. Goodpasture syndrome
- B. Membranous glomerulonephritis
- C. Bronchial asthma
- D. Churg-Strauss syndrome (Correct Answer)
Explanation: ***Churg-Strauss syndrome*** - The apparent development of **Churg-Strauss syndrome** (eosinophilic granulomatosis with polyangiitis) has been reported in patients treated with montelukast, although it is believed to be related more to the unmasking of the disease rather than a direct drug effect. - This typically occurs when **corticosteroids** are tapered or withdrawn as montelukast takes over, revealing the underlying vasculitis. *Goodpasture syndrome* - **Goodpasture syndrome** is an autoimmune disease causing rapidly progressive glomerulonephritis and pulmonary hemorrhage, characterized by anti-glomerular basement membrane (GBM) antibodies. - There is no established association between montelukast use and the development of Goodpasture syndrome. *Membranous glomerulonephritis* - **Membranous glomerulonephritis** is a common cause of nephrotic syndrome, characterized by immune complex deposition on the glomerular basement membrane. - This condition is not typically linked to the use of montelukast. *Bronchial asthma* - **Bronchial asthma** is the condition montelukast is used to treat, acting as a leukotriene receptor antagonist to reduce inflammation and bronchoconstriction. - It is a primary indication for the drug, not a side effect.
Question 4: Which of the following is a characteristic bone marrow finding in myelofibrosis?
- A. Increased reticulin fibrosis (Correct Answer)
- B. Absence of fibroblasts
- C. Decreased megakaryocytes
- D. Hypocellular marrow from onset
Explanation: ***Leucoerythroblastosis*** - A hallmark finding in myelofibrosis is **leucoerythroblastosis**, characterized by the presence of immature white cells and nucleated red blood cells in the bloodstream [1][3]. - This reflects an **extramedullary hematopoiesis** due to the failure of normal marrow function and is commonly seen in myelofibrosis [1][2]. *Tear drop cells* - While **tear drop cells** (dacryocytes) can be associated with myelofibrosis, they are not exclusive findings and can appear in other conditions [1]. - They are indicative of **extramedullary hematopoiesis** but are not definitive for myelofibrosis specifically. *Leucocytopenia* - Myelofibrosis is associated with **neutrophilia** rather than leucocytopenia, which presents as low white blood cell counts. - The condition often leads to an increase in white blood cell counts due to reactive changes rather than a decrease. *All of the above* - This option is incorrect as it suggests that all previously mentioned findings are present in myelofibrosis. - Both **tear drop cells** and **leucocytopenia** are not definitive or accurate findings compared to **leucoerythroblastosis**. **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. 628-629. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 615-616. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 589-590.
Question 5: Bleeding crisis in acute idiopathic thrombo-cytopenic purpura is managed by all except -
- A. Intravenous immunoglobulin
- B. Prednisolone
- C. Eltrombopag (Correct Answer)
- D. RhIG
Explanation: ***Eltrombopag*** - **Eltrombopag** is a **thrombopoietin receptor agonist** used for chronic idiopathic thrombocytopenic purpura (ITP) to increase platelet production. - It is **not** used for the immediate management of an acute bleeding crisis, as its effects on platelet counts take several days to manifest. *Intravenous immunoglobulin* - **Intravenous immunoglobulin (IVIG)** works by blocking **Fc receptors** on macrophages, thereby reducing the destruction of antibody-coated platelets. - It is a **first-line treatment** for acute ITP, especially in cases with severe bleeding or very low platelet counts, providing a rapid increase in platelet count. *Prednisolone* - **Prednisolone**, a corticosteroid, is a **first-line treatment** for acute ITP, as it suppresses the immune system and reduces antibody production and platelet destruction. - It helps to quickly raise platelet counts and is effective in managing bleeding episodes, though its effects are not as immediate as IVIG. *RhIG* - **Rh immune globulin (RhIG)** is used in **Rh-positive** patients with ITP to cause a transient hemolytic anemia, which occupies splenic macrophages and reduces platelet destruction. - It `is an effective option` for acute ITP, particularly in patients who require a rapid increase in platelet count and are Rh-positive.
Question 6: During the treatment of chronic myeloid leukemia, cytogenetic remission is least likely to occur with which one of the following treatment modalities?
- A. imatinib mesylate
- B. Interferon-alpha
- C. Bone marrow transplantation
- D. Hydroxyurea (Correct Answer)
Explanation: ***Hydroxyurea*** - **Hydroxyurea** (hydroxycarbamide) is a cytoreductive agent that can control cell counts in **chronic myeloid leukemia (CML)** but it does not specifically target the **BCR-ABL fusion gene**. [1] - Its mechanism of action involves inhibiting **ribonucleotide reductase**, which prevents DNA synthesis and thus reduces cell proliferation, but it does not lead to **cytogenetic remission**. [1] *imatinib mesylate* - **Imatinib mesylate** is a **tyrosine kinase inhibitor (TKI)** that specifically targets the **BCR-ABL fusion protein**. [1] - It is highly effective in achieving **hematological and cytogenetic remission** in most CML patients. [1] *Interferon-alpha* - **Interferon-alpha** is an immunomodulatory agent that was formerly a standard treatment for **CML** before TKIs. [1] - It can induce **cytogenetic remissions** in a significant proportion of patients, though less frequently and with more side effects than TKIs. [1] *Bone marrow transplantation* - **Allogeneic hematopoietic stem cell transplantation (HSCT)**, or bone marrow transplantation, offers the only potential cure for CML. - It involves replacing the patient's diseased bone marrow with healthy donor cells, leading to sustained **cytogenetic and molecular remission** in a high percentage of patients. [1]
Question 7: What is the best treatment for anemia in patients with Chronic Renal Failure (CRF)?
- A. Oral Iron Therapy
- B. Erythropoietin Stimulating Agents (Correct Answer)
- C. Blood transfusion
- D. Androgenic Steroids
Explanation: ***Erythropoietin Stimulating Agents*** - **Erythropoietin Stimulating Agents (ESAs)** are the cornerstone of anemia treatment in CRF because the primary cause of anemia in these patients is inadequate production of **endogenous erythropoietin** by the damaged kidneys [1]. - ESAs stimulate the bone marrow to produce red blood cells, effectively reversing the anemia and improving symptoms like fatigue and exercise intolerance [1]. *Oral Iron Therapy* - While **iron deficiency** often coexists with **anemia of chronic disease** in CRF patients, oral iron alone is usually insufficient to correct the anemia; it only addresses the iron component. - Many CRF patients have **functional iron deficiency** due to chronic inflammation, which impairs iron utilization, making oral iron less effective even with adequate stores. *Blood transfusion* - **Blood transfusions** provide a rapid increase in hemoglobin but are not the preferred long-term treatment for anemia in CRF due to risks of **iron overload**, **alloreactions**, and potential sensitization, which can complicate future transplantation. - Transfusions are typically reserved for acute, severe anemia or specific circumstances where ESAs are ineffective or contraindicated. *Androgenic Steroids* - **Androgenic steroids** can stimulate erythropoiesis, but their use is limited due to significant side effects such as **hepatotoxicity**, **virilization**, and **cardiac complications**, making them a less favorable option compared to ESAs. - They are considered a secondary or tertiary option, often in patients unresponsive to primary treatments or when other options are exhausted.
Question 8: Which of the following is the LEAST likely indication for intravenous iron administration?
- A. Inability to Tolerate oral Iron
- B. Iron malabsorption
- C. Patients on Erythropoietin Therapy (Correct Answer)
- D. Intermittent Gastrointestinal blood loss
Explanation: ### Patients on Erythropoietin Therapy - While patients on **erythropoietin therapy** often require iron supplementation, **oral iron** is usually the first-line choice if tolerated. IV iron is primarily reserved for those who cannot absorb or tolerate oral iron, or have severe iron deficiency, not merely for being on erythropoietin [2]. - The need for iron in this setting is due to the increased demand for red blood cell production, but the route depends on other factors like significant deficiency or inability to use oral routes. *Iron malabsorption* - **Iron malabsorption** prevents adequate iron uptake from the GI tract, making oral iron ineffective [2]. - **Intravenous iron** bypasses the gastrointestinal system, ensuring effective delivery of iron to the body. *Inability to Tolerate oral Iron* - Patients who experience significant **gastrointestinal side effects** (nausea, constipation, diarrhea) from oral iron often cannot adhere to therapy. - **Intravenous iron** avoids these GI side effects, providing an alternative route for necessary iron supplementation. *Intermittent Gastrointestinal blood loss* - **Intermittent GI blood loss** can lead to chronic iron deficiency that is difficult to replete with oral iron alone due to ongoing losses [1, 3]. - **Intravenous iron** can rapidly replenish iron stores and compensate for continuous or significant blood loss more effectively than oral supplementation.
Question 9: What is the typical bone marrow finding in myelofibrosis?
- A. Megaloblastic cells
- B. Microcytic cells
- C. Thrombocytosis
- D. Dry tap (hypocellular) (Correct Answer)
Explanation: ***Dry tap (hypocellular)*** - In myelofibrosis, the bone marrow is often **hypocellular** due to fibrosis [1][2], leading to a **dry tap** during aspiration. - The presence of **reticulin** and collagen deposition replaces normal hematopoietic cells [2], resulting in ineffective hematopoiesis. *Thrombocytosis* - Myelofibrosis typically leads to **thrombocytopenia**, not thrombocytosis, due to ineffective megakaryopoiesis and splenic sequestration. - Though elevated platelets can occur, they are generally a **secondary response** to the disease and not a hallmark finding. *Megaloblastic cells* - Megaloblastic changes are associated with **vitamin B12** or **folate deficiencies**, which do not occur in myelofibrosis. - In myelofibrosis, the predominant issue is **marrow fibrosis** [1][2], which does not lead to megaloblastosis. *Microcytic cells* - Microcytic cells are commonly linked to **iron deficiency anemia**, not myelofibrosis. - Myelofibrosis typically results in **variable red cell morphology** [1], but microcytic anemia is not a primary characteristic. **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. 628-629. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 615-616.
Question 10: A patient with a malignancy is undergoing chemotherapy. The platelet counts were reduced after the previous cycle of chemotherapy. Which of the following drugs can be used to treat this patient?
- A. Oprelvekin (IL-11) - stimulates platelet production (Correct Answer)
- B. Filgrastim - stimulates white blood cell production
- C. Amifostine - protects against chemotherapy toxicity
- D. Erythropoietin - stimulates red blood cell production
Explanation: ***Oprelvekin (IL-11) - stimulates platelet production*** - **Oprelvekin** is a recombinant interleukin-11 (IL-11) that directly stimulates the proliferation and maturation of **megakaryocytes**, leading to increased platelet production. - It is specifically indicated for the prevention of **severe thrombocytopenia** and the reduction of the need for platelet transfusions following myelosuppressive chemotherapy. *Filgrastim - stimulates white blood cell production* - **Filgrastim** is a **granulocyte colony-stimulating factor (G-CSF)** that primarily acts on neutrophil precursors, promoting their proliferation and maturation. - It is used to prevent and treat **neutropenia** and reduce the incidence of febrile neutropenia, but it does not significantly affect platelet counts. *Amifostine - protects against chemotherapy toxicity* - **Amifostine** is a **cytoprotective agent** that reduces toxicities associated with chemotherapy and radiation by preferentially protecting non-malignant cells. - It does not directly stimulate blood cell production but rather acts as a **free radical scavenger** to mitigate damage from cytotoxic treatments. *Erythropoietin - stimulates red blood cell production* - **Erythropoietin** is a **hematopoietic growth factor** that specifically stimulates the production of **red blood cells** by promoting the proliferation and differentiation of erythroid progenitor cells. - It is used to treat **anemia**, particularly in patients with chronic kidney disease or those undergoing chemotherapy, but it has no role in managing thrombocytopenia.
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