Drugs Affecting Blood and Blood Formation Practice Questions

Q: Pegylated Filgrastim is used for the treatment of:

Neutropenia. **Filgrastim** is a recombinant **Granulocyte Colony-Stimulating Factor (G-CSF)** [1]. It acts by binding to specific receptors on myeloid progenitor cells in the bone marrow, stimulating the proliferation, differentiation, and activation of **neutrophils** [1]. **Pegylated Filgrastim (Pegfilgrastim)** is the long-acting version of Filgrastim, created by attaching a polyethylene glycol (PEG) molecule [2]. This modification decreases renal clearance and increases the half-life, allowing for once-per-chemotherapy-cycle dosing instead of daily injections [2]. It is primarily used to reduce the duration and incidence of febrile **neutropenia** in patients receiving myelosuppressive anticancer drugs [3]. **Why other options are incorrect:** * **Anaemia:** This is a deficiency of red blood cells (RBCs). It is treated with Erythropoiesis-Stimulating Agents (ESAs) like **Erythropoietin** or Darbepoetin. * **Thrombocytopenia:** This is a low platelet count. It is managed with Thrombopoietin (TPO) receptor agonists like **Romiplostim** or **Eltrombopag**, or IL-11 (Oprelvekin) [2]. * **Pancytopenia:** This refers to a deficiency of all three blood cell lines (RBCs, WBCs, and platelets). While Filgrastim may help the neutrophil component, it does not treat the underlying cause or the other cell deficiencies. **High-Yield NEET-PG Pearls:** * **Side Effect:** The most common side effect of Filgrastim/Pegfilgrastim is **medullary bone pain** (due to marrow expansion). * **Sargramostim:** This is a recombinant **GM-CSF** (Granulocyte-Macrophage CSF) which stimulates both neutrophils and macrophages [3]. * **Timing:** G-CSFs should not be administered within 24 hours before or after chemotherapy to avoid "killing" the rapidly dividing stimulated cells.

Q: Which of the following drugs inhibits plasminogen activation?

Tranexamic acid. **Explanation:** The question tests your understanding of the fibrinolytic system and its inhibitors. To prevent clot dissolution (fibrinolysis), a drug must inhibit the conversion of plasminogen to plasmin. **Correct Option: B. Tranexamic acid** Tranexamic acid is an **antifibrinolytic agent**. It works by competitively inhibiting the activation of plasminogen to plasmin. It binds to the lysine-binding sites on plasminogen molecules, preventing them from binding to fibrin. This stabilizes the clot and reduces bleeding. It is commonly used in menorrhagia, trauma, and post-extraction bleeding in hemophiliacs. **Incorrect Options:** * **A. Aspirin:** This is an antiplatelet drug. It irreversibly inhibits the **COX-1 enzyme**, reducing the synthesis of Thromboxane A2 (TXA2), thereby inhibiting platelet aggregation. It has no direct effect on plasminogen. * **C. Alteplase:** This is a recombinant **Tissue Plasminogen Activator (tPA)**. Instead of inhibiting activation, it directly *promotes* the conversion of plasminogen to plasmin. It is used as a "clot buster" in ischemic stroke and MI. * **D. Streptokinase:** This is a fibrinolytic agent derived from beta-hemolytic streptococci. It forms a complex with plasminogen to **activate** it into plasmin. Like Alteplase, it promotes fibrinolysis rather than inhibiting it. **High-Yield NEET-PG Pearls:** * **Epsilon-aminocaproic acid (EACA)** works via a similar mechanism to Tranexamic acid but is less potent. * **Aprotinin** is another antifibrinolytic that directly inhibits the enzyme plasmin (rather than just activation). * **Antidote for Fibrinolytics:** If a patient bleeds due to Streptokinase or Alteplase overdose, **Tranexamic acid** is the specific pharmacological antagonist.

Q: Warm antibody hemolytic anemia is seen in patients taking which of the following medications?

Methyldopa. **Explanation:** Drug-induced immune hemolytic anemia (DIIHA) occurs via different mechanisms. **Methyldopa** is the classic example of the **Autoimmune (True Autoantibody) Mechanism**. **1. Why Methyldopa is correct:** Methyldopa interferes with T-suppressor cell function, leading to the production of true autoantibodies (usually IgG) directed against the patient’s own Rh antigens on the RBC surface. This is termed **"Warm" antibody hemolytic anemia** because IgG binds optimally at 37°C. A key feature is that the Direct Antiglobulin Test (Coombs test) remains positive even in the absence of the drug, as the antibodies are directed against the RBC itself, not the drug. **2. Why other options are incorrect:** * **Penicillin (Hapten/Drug-Adsorption Mechanism):** Penicillin binds to the RBC membrane. Antibodies (IgG) are then formed against the penicillin-RBC complex. Hemolysis only occurs with high-dose intravenous penicillin. * **Quinine & Stibophen (Immune Complex/Bystander Mechanism):** These drugs form a complex with IgM antibodies in the plasma. This "drug-antibody" complex then sits loosely on the RBC, activates the complement system, and causes rapid intravascular hemolysis. This is often called the "innocent bystander" mechanism. **High-Yield Clinical Pearls for NEET-PG:** * **Methyldopa:** 15% of patients develop a positive Coombs test, but <1% develop actual hemolysis. * **Warm vs. Cold:** Warm antibodies are **IgG** (extravascular hemolysis in the spleen); Cold antibodies are **IgM** (intravascular hemolysis, seen in Mycoplasma or Mononucleosis). * **Other drugs causing Warm AIHA:** L-Dopa, Procainamide, and Cephalosporins (can act via multiple mechanisms).

Q: What agent is responsible for increasing factor VIII activity in hemophilia?

Deamino D Arginine vasopressin. **Explanation:** **Deamino D-Arginine Vasopressin (Desmopressin or DDAVP)** is a synthetic analogue of the antidiuretic hormone (ADH). It acts on **V2 receptors** located on vascular endothelial cells, triggering the release of stored **von Willebrand Factor (vWF)** and **Factor VIII** from Weibel-Palade bodies into the plasma. This transient increase (usually 3–5 fold) makes it the treatment of choice for patients with **Mild Hemophilia A** and **Type 1 von Willebrand Disease** before minor surgical procedures. **Analysis of Incorrect Options:** * **A & B (Epsilon Amino Caproic Acid & Tranexamic Acid):** These are **antifibrinolytics**. They work by inhibiting plasminogen activation, thereby preventing the breakdown of formed clots. While used as adjunctive therapy in hemophilia (especially for dental extractions), they do not increase the levels of Factor VIII. * **C (Avitene):** This is a **topical hemostatic agent** (microfibrillar collagen). It promotes platelet adhesion and activation at the site of application but has no systemic effect on clotting factor levels. **NEET-PG High-Yield Pearls:** * **Route:** DDAVP can be administered IV, SC, or via a high-concentration nasal spray (Stimate). * **Tachyphylaxis:** Repeated doses lead to a diminished response because endothelial stores of Factor VIII/vWF become exhausted. * **Contraindication:** It is generally avoided in **Type 2B vWF disease** as it can cause paradoxical thrombocytopenia. * **Side Effects:** Hyponatremia and water intoxication (due to its antidiuretic effect). It is also used in Central Diabetes Insipidus and Nocturnal Enuresis.

Q: Which of the following fibrinolytic agents is antigenic?

Streptokinase. **Explanation:** The correct answer is **Streptokinase**. **1. Why Streptokinase is the correct answer:** Streptokinase is a protein derived from **Group C Beta-hemolytic Streptococci**. Because it is a bacterial product and not a human enzyme, the human immune system recognizes it as a foreign antigen. This leads to the production of antistreptococcal antibodies. * **Clinical Significance:** These antibodies can cause hypersensitivity reactions (ranging from rashes to anaphylaxis) and can neutralize the drug, making it ineffective if administered again within 6 months to a year of the initial dose or a recent streptococcal infection. **2. Why the other options are incorrect:** * **Urokinase:** It is a human enzyme naturally synthesized by the kidneys and found in urine. Since it is of human origin, it is non-antigenic. * **Alteplase (rt-PA):** This is a recombinant form of human tissue-type plasminogen activator [1]. Being identical to endogenous human t-PA, it does not elicit an immune response. * **Tenecteplase:** This is a genetically engineered mutant of Alteplase with a longer half-life and higher fibrin specificity [1]. Despite the modifications, it remains non-antigenic. **3. High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Streptokinase is an **indirect** plasminogen activator; it forms a 1:1 complex with plasminogen to activate it. In contrast, Alteplase and Tenecteplase are **direct** activators [1]. * **Fibrin Specificity:** Streptokinase is **non-fibrin specific**, leading to a "systemic lytic state" and a higher risk of bleeding compared to the fibrin-specific agents (Tenecteplase > Reteplase > Alteplase) [1]. * **Side Effect:** Hypotension is a common side effect unique to Streptokinase infusion. * **Drug of Choice:** Tenecteplase is currently the preferred agent for STEMI due to its bolus dosing and high fibrin specificity [1].

Q: Macrocytic anemia is noted with all of the following drugs except?

Ciprofloxacin. **Explanation:** Macrocytic anemia (specifically megaloblastic anemia) occurs when DNA synthesis is impaired, usually due to a deficiency or interference with **Folic acid** or **Vitamin B12**. **1. Why Ciprofloxacin is the correct answer:** Ciprofloxacin is a fluoroquinolone that acts by inhibiting bacterial DNA gyrase and topoisomerase IV. Unlike the other options, it does **not** interfere with human folate metabolism or B12 absorption. Therefore, it does not cause macrocytic anemia. **2. Why the other options are incorrect:** * **Methotrexate:** A potent dihydrofolate reductase (DHFR) inhibitor. It prevents the conversion of dihydrofolate to tetrahydrofolate, directly halting DNA synthesis and leading to megaloblastic changes. * **Pyrimethamine:** Similar to methotrexate, it is a DHFR inhibitor (primarily used for toxoplasmosis/malaria). While it has a higher affinity for protozoal enzymes, high doses can inhibit human DHFR, causing macrocytic anemia. * **Phenytoin:** This antiepileptic drug causes macrocytic anemia by interfering with the intestinal absorption of dietary folate and increasing its catabolism. **High-Yield Clinical Pearls for NEET-PG:** * **Other drugs causing Macrocytic Anemia:** Trimethoprim (DHFR inhibitor), Zidovudine (AZT), 5-Fluorouracil, Hydroxyurea, and Metformin (decreases B12 absorption). * **Rescue Therapy:** Leucovorin (Folinic acid) is used to "rescue" bone marrow from methotrexate toxicity because it bypasses the inhibited DHFR enzyme. * **Phenytoin Side Effects:** Remember the mnemonic **HOT MALARIA** (Hirsutism, Osteomalacia, Teratogenicity, **Megaloblastic anemia**, Ataxia, Lymphadenopathy, Insulin inhibition, Rheumatoid-like arthritis, Adenopathy).

Question 1

All of the following statements about ticlopidine are true, EXCEPT:

Accepted Answer

It directly interacts with platelet membrane GpIIb/IIIa receptors.

Answer

It has a delayed onset of action.

Answer

It has a long duration of action.

Answer

It is used as an alternative to aspirin in patients with cerebrovascular disease.

Question 2

Pegylated Filgrastim is used for the treatment of:

Accepted Answer

Neutropenia

Answer

Anaemia

Answer

Thrombocytopenia

Answer

Pancytopenia

Question 3

Which of the following drugs inhibits plasminogen activation?

Accepted Answer

Tranexamic acid

Answer

Aspirin

Answer

Alteplase

Answer

Streptokinase

Question 4

Regarding streptokinase, which of the following statements is false?

Accepted Answer

Its complex with plasminogen is inhibited by alpha2-antiplasmin.

Answer

It is a protein produced by streptococci.

Answer

It may rarely produce anaphylaxis.

Answer

It is initially given as a loading dose.

Question 5

Warm antibody hemolytic anemia is seen in patients taking which of the following medications?

Accepted Answer

Methyldopa

Answer

Penicillin

Answer

Quinine

Answer

Stibophen

Question 6

What agent is responsible for increasing factor VIII activity in hemophilia?

Accepted Answer

Deamino D Arginine vasopressin

Answer

Epsilon amino caproic acid

Answer

Tranexamic acid

Answer

Avitene

Question 7

Which of the following statements regarding tissue plasminogen activator is true?

Accepted Answer

It is effective in lysing thrombi of myocardial infarction.

Answer

It is produced by recombinant DNA technology.

Answer

Induction of systemic lytic state is limited with its use.

Answer

It is a poor plasminogen activator in the absence of fibrin.

Question 8

Which of the following fibrinolytic agents is antigenic?

Accepted Answer

Streptokinase

Answer

Urokinase

Answer

Alteplase

Answer

Tenecteplase

Question 9

Aminocaproic acid would be recommended for a hemophilic child with which of the following conditions?

Accepted Answer

Epistaxis

Answer

Haematuria

Answer

Oral bleeding

Answer

Hemarthrosis

Question 10

Macrocytic anemia is noted with all of the following drugs except?

Accepted Answer

Ciprofloxacin

Answer

Phenytoin

Answer

Methotrexate

Answer

Pyrimethamine

Drugs Affecting Blood and Blood Formation — MCQs

Drugs Affecting Blood and Blood Formation — MCQs

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