Drugs Affecting Blood and Blood Formation — MCQs
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Gp2b3A inhibitors are all except?
What is the mechanism of action of dicumarol?
A patient on anti-cancer therapy developed an infection. Blood analysis revealed neutropenia. Which of the following drugs is likely to be effective in this patient?
In which condition erythropoietin will be useful for treatment?
Which of the following are correct regarding Blood substitutes ? 1. They are biomimetic. 2. They are extensively used in war injuries. 3. They are made of perfluorocarbon emulsions. 4. They are haemoglobin-based. Select the correct answer using the code given below :
Complications of heparin therapy in pregnancy include all except :
Which parenteral iron preparation does not cause anaphylaxis on intravenous administration?
A 62-year-old man, who is known to have recurrent thromboembolic strokes, presents to his physician for a routine follow-up visit. While assessing drug compliance, the physician realizes that the patient inadvertently doubled his dose of warfarin 1 month ago. When he is asked about any new complaints, the patient denies any symptoms, including bleeding. The physical examination does not show any signs of bleeding. Based on the patient’s lifestyle, the physician does not consider him to be at increased risk for bleeding. He then orders an international normalized ratio (INR) for this patient, which is 13.5. In addition to temporarily holding warfarin, which of the following drugs is indicated for this patient?
Which of the following drugs is a direct inhibitor of clotting factor Xa?
Which of the following is an oral direct thrombin inhibitor?
Drugs Affecting Blood and Blood Formation Indian Medical PG Practice Questions and MCQs
Question 281: Gp2b3A inhibitors are all except?
- A. Abciximab
- B. Eptifibatide
- C. Tirofiban
- D. Prasugrel (Correct Answer)
Explanation: **Explanation:** The Glycoprotein (GP) IIb/IIIa inhibitors are a class of antiplatelet drugs that block the "final common pathway" of platelet aggregation. They prevent the binding of fibrinogen and von Willebrand factor to the GP IIb/IIIa receptor on the platelet surface, thereby inhibiting cross-linking between platelets. **Why Prasugrel is the correct answer:** Prasugrel is **not** a GP IIb/IIIa inhibitor. It belongs to the **P2Y12 receptor antagonists** (Thienopyridines) class. It works by irreversibly inhibiting the ADP receptor on platelets, preventing the subsequent activation of the GP IIb/IIIa complex. Other drugs in this class include Clopidogrel and Ticlopidine. **Analysis of incorrect options:** * **Abciximab:** A chimeric monoclonal antibody that binds irreversibly to the GP IIb/IIIa receptor. It has the longest biological half-life among the three. * **Eptifibatide:** A synthetic cyclic peptide that acts as a reversible antagonist at the GP IIb/IIIa receptor. It is derived from rattlesnake venom. * **Tirofiban:** A non-peptide, small-molecule reversible antagonist of the GP IIb/IIIa receptor. **High-Yield NEET-PG Pearls:** * **Route of Administration:** All GP IIb/IIIa inhibitors (Abciximab, Eptifibatide, Tirofiban) are administered **intravenously**, whereas P2Y12 inhibitors like Prasugrel are administered **orally**. * **Clinical Use:** Primarily used in Acute Coronary Syndrome (ACS) and during Percutaneous Coronary Intervention (PCI). * **Side Effect:** The most significant side effect of GP IIb/IIIa inhibitors is bleeding and **thrombocytopenia**. * **Prasugrel Contraindication:** It is strictly contraindicated in patients with a prior history of **Stroke or TIA** due to a high risk of intracranial hemorrhage.
Question 282: What is the mechanism of action of dicumarol?
- A. Inhibitor of factor Xa
- B. Activates antithrombin III.
- C. Inhibits tissue plasminogen activator
- D. Inhibits vitamin K dependant Clotting factors (Correct Answer)
Explanation: Inhibits vitamin K dependant Clotting factors- Dicumarol, a classic anticoagulant, acts as a **vitamin K antagonist** (VKA), preventing the utilization of vitamin K [1].- It inhibits the enzyme **vitamin K epoxide reductase**, which is essential for the activation (**gamma-carboxylation**) of factors II (prothrombin), VII, IX, and X [4]. *Activates antithrombin III.*- This mechanism is characteristic of **unfractionated heparin** and **low molecular weight heparins** (LMWH).- Heparin binds to **antithrombin III** (ATIII), greatly accelerating its ability to neutralize activated clotting factors, particularly Thrombin (IIa) and Factor Xa [2]. *Inhibits tissue plasminogen activator*- Dicumarol affects the synthesis of clotting factors and has no direct influence on the **fibrinolytic system** (clot breakdown).- Inhibition of **tissue plasminogen activator** (tPA) or plasmin is the role of anti-fibrinolytic drugs like **tranexamic acid**. *Inhibitor of factor Xa*- This is the specific mechanism utilized by the direct oral anticoagulants (DOACs), such as **rivaroxaban** and **apixaban** (referred to as 'xabans') [3].- While dicumarol ultimately reduces active **Factor X** levels, it acts indirectly by preventing its synthesis/activation, not by directly binding to and inhibiting the already formed Factor Xa.
Question 283: A patient on anti-cancer therapy developed an infection. Blood analysis revealed neutropenia. Which of the following drugs is likely to be effective in this patient?
- A. Filgrastim (Correct Answer)
- B. Epoetin alfa
- C. Oprelvekin
- D. Romiplostim
Explanation: ***Filgrastim***- It is a recombinant form of **granulocyte colony-stimulating factor (G-CSF)**, which stimulates the proliferation and differentiation of neutrophil precursors in the bone marrow.- It is the standard treatment for **chemotherapy-induced neutropenia** (as seen in patients on anti-cancer therapy) to raise neutrophil counts and reduce infection risk.*Romiplostim*- This drug is a **thrombopoietin (TPO) receptor agonist** used to stimulate platelet production.- It is indicated for conditions like **immune thrombocytopenia** and would not be effective in stimulating neutrophil recovery in neutropenia.*Oprelvekin*- It is a recombinant form of **interleukin-11 (IL-11)**, indicated specifically for the prevention of severe **thrombocytopenia** following myelosuppressive chemotherapy.- While it has some broad hematopoietic effects, its primary clinical use is platelet restoration, making it ineffective for acute **neutropenia** in this context.*Epoetin alfa*- This drug is a recombinant form of **erythropoietin (EPO)**, primarily used to stimulate red blood cell production to treat **anemia**.- It specifically targets the erythroid lineage and has no clinical utility in increasing **neutrophil** counts.
Question 284: In which condition erythropoietin will be useful for treatment?
- A. Nutritional anemia
- B. Aplastic anemia
- C. Anemia in chronic kidney disease (Correct Answer)
- D. Anemia in myelodysplastic syndrome
Explanation: ***Anemia in chronic kidney disease*** - **Erythropoietin (EPO)** deficiency is the primary cause of anemia in chronic kidney disease (**CKD**), as the damaged kidneys cannot produce adequate amounts. - Recombinant human EPO (**rHuEPO**) is the standard treatment to stimulate **erythropoiesis** in the bone marrow, correcting the anemia and improving quality of life. ***Anemia in myelodysplastic syndrome*** - While erythropoiesis-stimulating agents (ESAs) like EPO are occasionally used in lower-risk myelodysplastic syndrome (**MDS**) patients, especially those who are transfusion-dependent, the response rates are variable and dependent on underlying cytogenetics and serum EPO levels. - The primary defect in MDS involves abnormal **hematopoietic stem cell function** (a primary bone marrow failure) rather than just EPO deficiency, making treatment difficult. ***Nutritional anemia*** - This category, including **iron deficiency anemia** and **megaloblastic anemia** (Vitamin B12 or folate deficiency), is primarily treated by supplementing the specific deficient nutrient. - Giving EPO would be ineffective unless the underlying nutritional deficit is corrected, as the bone marrow lacks the necessary building blocks for red blood cell production. ***Aplastic anemia*** - Aplastic anemia is a condition of **pancytopenia** caused by bone marrow failure due to the destruction or suppression of hematopoietic stem cells, often immune-mediated. - The primary treatment involves **immunosuppressive therapy** (e.g., antithymocyte globulin) or **hematopoietic stem cell transplantation**, as erythropoietin production is usually adequate, and the bone marrow is simply unable to respond.
Question 285: Which of the following are correct regarding Blood substitutes ? 1. They are biomimetic. 2. They are extensively used in war injuries. 3. They are made of perfluorocarbon emulsions. 4. They are haemoglobin-based. Select the correct answer using the code given below :
- A. 2, 3 and 4
- B. 1 and 3 only
- C. 1, 2 and 3
- D. 1, 3 and 4 (Correct Answer)
Explanation: ***1, 3 and 4*** - **Blood substitutes are biomimetic** - they are artificially engineered to mimic the oxygen-carrying capacity of natural red blood cells. - Blood substitutes fall into **two main categories**: perfluorocarbon (PFC) emulsions and hemoglobin-based oxygen carriers (HBOCs). Statement 3 and 4 correctly identify these two major types. - **PFC emulsions** can dissolve large amounts of oxygen and carbon dioxide, transporting gases to tissues through physical dissolution. - **Hemoglobin-based oxygen carriers** use modified hemoglobin (human, bovine, or recombinant) to bind and transport oxygen similar to natural red blood cells. *1, 2 and 3* - While statements 1 and 3 are correct, **statement 2 is incorrect**. - Blood substitutes are **NOT extensively used in war injuries** - most remain experimental or have very limited clinical approval. - Despite theoretical advantages (extended shelf life, no cross-matching needed), practical deployment has been minimal due to safety concerns and regulatory limitations. *2, 3 and 4* - This option incorrectly includes statement 2 about extensive use in war injuries, which is **factually inaccurate**. - Most blood substitutes have failed to gain widespread approval due to adverse effects including vasoconstriction, hypertension, and increased mortality in some trials. - It also incorrectly excludes statement 1 - the **biomimetic nature** is a fundamental defining characteristic of blood substitutes. *1 and 3 only* - While statements 1 and 3 are correct, this option is **incomplete**. - It fails to recognize that blood substitutes include **both perfluorocarbon-based AND hemoglobin-based** types - the two major categories in development. - Statement 4 about hemoglobin-based carriers is equally important and correct.
Question 286: Complications of heparin therapy in pregnancy include all except :
- A. Teratogenicity (Correct Answer)
- B. Thrombocytopaenia
- C. Osteoporosis
- D. Bleeding
Explanation: ***Teratogenicity*** - **Heparin** does not cross the placenta due to its large molecular weight, making it a safe anticoagulant choice during pregnancy regarding fetal malformations. - Therefore, it is **not associated with teratogenicity**, unlike some other anticoagulants like warfarin. *Thrombocytopaenia* - **Heparin-induced thrombocytopenia (HIT)** is a known complication, where antibodies against heparin-platelet factor 4 complexes lead to platelet activation and consumption. - While typically Type II HIT is more severe, a mild, transient drop in platelet count (Type I) can also occur. *Osteoporosis* - **Long-term heparin therapy**, particularly unfractionated heparin, is associated with an increased risk of bone demineralization and **osteoporosis** due to its direct effect on osteoblasts and osteoclasts. - This complication is less common with low molecular weight heparin (LMWH) but still a potential concern. *Bleeding* - As an anticoagulant, **heparin's primary mechanism of action** involves inhibiting coagulation factors, which inherently increases the risk of **bleeding**. - The risk of bleeding can range from minor ecchymoses to life-threatening hemorrhages depending on the dose and individual patient factors.
Question 287: Which parenteral iron preparation does not cause anaphylaxis on intravenous administration?
- A. Iron fumarate
- B. Iron sucrose (Correct Answer)
- C. Iron dextran
- D. Iron sorbitol
Explanation: ***Iron sucrose*** - **Iron sucrose** is a newer generation parenteral iron preparation with the **lowest risk of anaphylaxis** among IV iron formulations - This safety profile is primarily due to its **lack of dextran content**, which is responsible for the anaphylactic reactions seen with iron dextran - **Does not require a test dose** before administration, unlike iron dextran - Preferred for **intravenous administration** in patients requiring parenteral iron therapy [1] *Iron fumarate* - **Iron fumarate (ferrous fumarate)** is an **oral iron preparation only**, not a parenteral formulation - Since it is not administered intravenously, this option is **not applicable** to the question about parenteral IV iron preparations - As an oral preparation, it does not carry the risk of anaphylaxis associated with intravenous iron administration *Iron dextran* - **Iron dextran** is an older parenteral iron preparation with the **highest risk of anaphylactic reactions** due to the presence of dextran [2] - **Test dose is mandatory** before full administration due to significant hypersensitivity risk [2] - Can cause both **anaphylactoid reactions** (non-IgE mediated) and **true anaphylaxis** (IgE-mediated) [2] *Iron sorbitol* - **Iron sorbitol** is a parenteral iron preparation primarily used for **intramuscular administration**, not typically given intravenously - Can cause **allergic reactions** and has potential for **cardiovascular side effects** - Less commonly used today due to availability of safer alternatives like iron sucrose and ferric carboxymaltose [3]
Question 288: A 62-year-old man, who is known to have recurrent thromboembolic strokes, presents to his physician for a routine follow-up visit. While assessing drug compliance, the physician realizes that the patient inadvertently doubled his dose of warfarin 1 month ago. When he is asked about any new complaints, the patient denies any symptoms, including bleeding. The physical examination does not show any signs of bleeding. Based on the patient’s lifestyle, the physician does not consider him to be at increased risk for bleeding. He then orders an international normalized ratio (INR) for this patient, which is 13.5. In addition to temporarily holding warfarin, which of the following drugs is indicated for this patient?
- A. Phytonadione (Correct Answer)
- B. Fresh frozen plasma
- C. Protamine sulfate
- D. Recombinant factor VIIa
Explanation: ***Phytonadione*** - The patient has a highly elevated **INR (13.5)** due to an overdose of warfarin, a **vitamin K antagonist** [1, 2]. - **Phytonadione (vitamin K1)** - Is the most appropriate treatment to reverse warfarin's anticoagulant effects when there is a high INR but **no significant bleeding**, as it replenishes vitamin K-dependent clotting factors [1, 2]. *Fresh frozen plasma* - While it contains all clotting factors and can rapidly normalize INR, it is generally reserved for **life-threatening bleeding** or urgent invasive procedures when rapid reversal is critical. - Its use comes with risks such as **transfusion reactions** and **volume overload**, which are not justified in this asymptomatic patient. *Protamine sulfate* - This drug is used to reverse the anticoagulant effects of **heparin** and **low molecular weight heparins**, not warfarin. - It would have no effect on the highly elevated INR caused by warfarin. *Recombinant factor VIIa* - This agent is used to bypass deficiencies in the coagulation cascade and achieve rapid hemostasis. - It is typically reserved for **severe, refractory bleeding** that is unresponsive to conventional reversal agents, due to its **high cost** and potential for **thromboembolic complications**.
Question 289: Which of the following drugs is a direct inhibitor of clotting factor Xa?
- A. Argatroban
- B. Fondaparinux
- C. Apixaban (Correct Answer)
- D. Aspirin
Explanation: ***Apixaban*** - Apixaban is an **oral direct factor Xa inhibitor**, which means it directly binds to and inactivates factor Xa. - This inhibition prevents the conversion of **prothrombin to thrombin**, thereby disrupting the coagulation cascade. *Argatroban* - Argatroban is a **direct thrombin inhibitor** (DTI), meaning it selectively binds to and inhibits thrombin (factor IIa). - It is often used in cases of **heparin-induced thrombocytopenia (HIT)** due to its non-heparin-based mechanism of action. *Fondaparinux* - Fondaparinux is an **indirect factor Xa inhibitor** that binds to antithrombin, thereby enhancing antithrombin's ability to inactivate factor Xa. - It does not directly bind to factor Xa itself, but rather potentiates the action of a natural anticoagulant. *Aspirin* - Aspirin is an **antiplatelet agent** that inhibits cyclooxygenase (COX-1), thereby reducing the production of thromboxane A2. - This mechanism primarily inhibits **platelet aggregation** and adhesion, rather than directly inhibiting a clotting factor in the coagulation cascade.
Question 290: Which of the following is an oral direct thrombin inhibitor?
- A. Dabigatran (Correct Answer)
- B. Lepirudin
- C. Rivaroxaban
- D. Warfarin
Explanation: ***Dabigatran*** - **Dabigatran** is the correct answer because it is an **oral direct thrombin inhibitor (DTI)**, meaning it directly inhibits thrombin (factor IIa) to prevent clot formation. - It is one of the **novel oral anticoagulants (NOACs)**, used for conditions like atrial fibrillation and venous thromboembolism. *Lepirudin* - **Lepirudin** is a **direct thrombin inhibitor**, but it is administered **intravenously**, not orally. - It is typically used for **heparin-induced thrombocytopenia (HIT)** when heparin is contraindicated. *Rivaroxaban* - **Rivaroxaban** is an **oral anticoagulant**, but it is a **direct factor Xa inhibitor**, not a direct thrombin inhibitor. - This drug prevents the conversion of prothrombin to thrombin by inhibiting factor Xa. *Warfarin* - **Warfarin** is an **oral anticoagulant**, but it acts as a **vitamin K antagonist (VKA)**, inhibiting the synthesis of coagulation factors II, VII, IX, and X. - It does not directly inhibit thrombin, but rather reduces the production of thrombin precursors.
Practice by Chapter
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