Drugs Affecting Blood and Blood Formation — MCQs

Drugs Affecting Blood and Blood Formation Indian Medical PG Practice Questions and MCQs

Question 171: An elderly woman who suffered a stroke was treated with alteplase and improved considerably. To prevent stroke recurrence, what medication is she most likely to be treated with indefinitely?

A. Aspirin (Correct Answer)
B. Warfarin
C. Urokinase
D. Enoxaparin

Explanation: **Explanation:** **1. Why Aspirin is Correct:** The patient has suffered an **ischemic stroke** (implied by the use of alteplase). For long-term secondary prevention of non-cardioembolic ischemic strokes, **antiplatelet therapy** is the standard of care. Aspirin (low dose, 75–150 mg) irreversibly inhibits the enzyme **Cyclooxygenase-1 (COX-1)**, preventing the synthesis of Thromboxane A2. This inhibits platelet aggregation and reduces the risk of recurrent arterial thrombosis indefinitely. **2. Why the Other Options are Incorrect:** * **Warfarin (Option B):** This is an oral anticoagulant. It is indicated for stroke prevention only if the stroke was **cardioembolic** (e.g., due to Atrial Fibrillation). In a standard non-cardioembolic stroke, antiplatelets are preferred over anticoagulants due to a lower risk of major bleeding. * **Urokinase (Option C):** This is a thrombolytic agent (fibrinolytic). Like alteplase, it is used for the **acute** management of a stroke to dissolve an existing clot. It is never used for long-term prophylaxis. * **Enoxaparin (Option D):** This is a Low Molecular Weight Heparin (LMWH) administered parenterally. It is used for DVT prophylaxis or acute anticoagulation, not for the indefinite secondary prevention of ischemic stroke. **3. NEET-PG Clinical Pearls:** * **Golden Hour:** Alteplase (rt-PA) must be administered within **3 to 4.5 hours** of the onset of ischemic stroke symptoms. * **Dual Antiplatelet Therapy (DAPT):** In high-risk TIA or minor stroke, a combination of Aspirin and Clopidogrel is often used for the first 21–90 days, followed by long-term monotherapy. * **Primary Side Effect:** The most common side effect of long-term Aspirin is **gastrointestinal mucosal damage** and bleeding.

Question 172: Streptokinase and urokinase are contraindicated in which of the following conditions?

A. Intracranial malignancy (Correct Answer)
B. Pulmonary embolism
C. AV fistula
D. Thrombophlebitis

Explanation: **Explanation:** Streptokinase and urokinase are **fibrinolytic (thrombolytic) agents** that convert plasminogen to plasmin, which subsequently degrades fibrin clots. Because these drugs induce a systemic lytic state, they carry a significant risk of severe hemorrhage. **Why Intracranial Malignancy is the Correct Answer:** Intracranial malignancy is an **absolute contraindication** for thrombolytic therapy. Tumors within the brain are often highly vascular or can cause structural compromise of the blood-brain barrier. Administering a fibrinolytic agent in this setting poses an extremely high risk of **fatal intracranial hemorrhage (ICH)**. Other absolute contraindications include a history of prior ischemic stroke (within 3 months), active internal bleeding, or recent intracranial/intraspinal surgery. **Analysis of Incorrect Options:** * **B. Pulmonary Embolism:** This is actually a primary **indication** for thrombolytics, especially in "massive" PE associated with hemodynamic instability (hypotension). * **C. AV Fistula:** The presence of an arteriovenous fistula (commonly used for hemodialysis) is not a contraindication for streptokinase or urokinase. * **D. Thrombophlebitis:** While usually treated with NSAIDs or anticoagulants, superficial thrombophlebitis is not a contraindication for using thrombolytics if they are needed for a more serious concurrent condition (like an MI). **NEET-PG High-Yield Pearls:** * **Mechanism:** Streptokinase is non-fibrin specific (acts on both circulating and clot-bound plasminogen), whereas Alteplase (tPA) is fibrin-specific. * **Antidote:** In case of overdose or excessive bleeding, use **Epsilon-aminocaproic acid** or **Tranexamic acid**. * **Side Effect:** Streptokinase is antigenic; it can cause hypersensitivity reactions and should not be repeated within 6–12 months due to neutralizing antibodies.

Question 173: All of the following are antiplatelet agents EXCEPT:

A. Aspirin
B. Clopidogrel
C. Abciximab
D. Tranexamic acid (Correct Answer)

Explanation: **Explanation:** The correct answer is **D. Tranexamic acid**. **1. Why Tranexamic Acid is the Correct Answer:** Tranexamic acid is an **antifibrinolytic agent**, not an antiplatelet drug [1]. It works by competitively inhibiting the activation of plasminogen to plasmin [3]. By preventing plasmin from binding to and degrading fibrin, it stabilizes clots and reduces bleeding [2]. It is clinically used in conditions like menorrhagia, trauma, and post-prostatectomy bleeding [1]. **2. Why the Other Options are Incorrect:** * **A. Aspirin:** A classic antiplatelet agent that causes irreversible inhibition of the **COX-1 enzyme**, thereby suppressing the synthesis of Thromboxane A2 (TXA2), a potent platelet aggregator [4]. * **B. Clopidogrel:** A P2Y12 receptor antagonist [4]. It prevents platelet aggregation by blocking the binding of **ADP** to its specific receptors on the platelet surface. * **C. Abciximab:** A Glycoprotein **IIb/IIIa receptor antagonist** [4]. It blocks the "final common pathway" of platelet aggregation by preventing the binding of fibrinogen to platelets. **3. NEET-PG High-Yield Pearls:** * **Aspirin:** Low doses (75–150 mg) are selective for COX-1; higher doses inhibit COX-2 and prostacyclin (PGI2). * **P2Y12 Inhibitors:** Clopidogrel is a prodrug (requires CYP2C19 activation), whereas **Ticagrelor** is a direct-acting, reversible inhibitor [4]. * **GP IIb/IIIa Inhibitors:** Includes Abciximab (monoclonal antibody), Eptifibatide, and Tirofiban [4]. * **Antifibrinolytics:** Besides Tranexamic acid, **Epsilon-aminocaproic acid (EACA)** is another key agent in this class [3].

Question 174: As compared to unfractionated heparin, low molecular weight heparin:

A. Is absorbed more uniformly when given subcutaneously (Correct Answer)
B. Requires more frequent lab monitoring
C. Can be given to patients with heparin-induced thrombocytopenia
D. Has a higher risk of osteopenia

Explanation: **Explanation:** Low Molecular Weight Heparins (LMWHs), such as Enoxaparin and Dalteparin, are derived from Unfractionated Heparin (UFH) by depolymerization. They offer several pharmacokinetic advantages over UFH. **1. Why Option A is Correct:** LMWHs have **higher bioavailability** (>90%) and a more **predictable dose-response** when administered subcutaneously. This is because LMWHs bind less extensively to plasma proteins, macrophages, and endothelial cells compared to UFH. This reduced non-specific binding leads to uniform and consistent absorption, allowing for fixed dosing without the need for routine monitoring. **2. Why the Other Options are Incorrect:** * **Option B:** LMWHs have a predictable anticoagulant effect; therefore, **routine lab monitoring (aPTT) is NOT required**. Monitoring (anti-Factor Xa levels) is only reserved for special cases like renal failure, pregnancy, or extreme obesity. * **Option C:** LMWHs show high **cross-reactivity** with UFH antibodies. Therefore, they are strictly **contraindicated** in patients with Heparin-Induced Thrombocytopenia (HIT). Alternatives like Fondaparinux or Argatroban should be used instead. * **Option D:** LMWHs have a **lower risk of osteopenia** and osteoporosis compared to UFH because they have a lower affinity for osteoblasts. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** LMWH mainly inhibits **Factor Xa** (Ratio of Xa:IIa inhibition is 3:1), whereas UFH inhibits both Xa and IIa (Thrombin) equally (1:1). * **Antidote:** Protamine sulfate completely neutralizes UFH but only **partially neutralizes** LMWH. * **Elimination:** LMWHs are primarily excreted **renally**; thus, they are contraindicated in chronic kidney disease (UFH is preferred in renal failure). * **Pregnancy:** LMWH is the drug of choice for anticoagulation during pregnancy as it does not cross the placenta.

Question 175: Which of the following is the mechanism of action of Fondaparinux?

A. Factor Xa inhibition and Thrombin inhibition
B. Factor Xa inhibition (Correct Answer)
C. Antithrombin inhibitor
D. Thrombin inhibition

Explanation: **Explanation:** **Fondaparinux** is a synthetic pentasaccharide that acts as a **selective Factor Xa inhibitor**. Its mechanism is mediated through **Antithrombin III (AT-III)**. When Fondaparinux binds to AT-III, it induces a conformational change that increases the neutralization of Factor Xa by 300-fold. Unlike Heparin, the pentasaccharide chain of Fondaparinux is too short to bridge AT-III to Thrombin; therefore, it has **no activity against Thrombin (Factor IIa).** **Analysis of Options:** * **Option B (Correct):** Fondaparinux selectively accelerates the neutralization of Factor Xa. * **Option A & D (Incorrect):** These describe the action of Unfractionated Heparin (UFH). UFH inhibits both Xa and IIa (ratio 1:1). Low Molecular Weight Heparins (LMWH) also inhibit both, but with a higher selectivity for Xa (ratio 2:1 to 4:1). Fondaparinux is unique in its pure Xa selectivity. * **Option C (Incorrect):** Fondaparinux is an Antithrombin **activator/cofactor**, not an inhibitor. **High-Yield Clinical Pearls for NEET-PG:** 1. **HIT Safety:** Fondaparinux does not bind to Platelet Factor 4 (PF4); thus, it carries virtually **no risk of Heparin-Induced Thrombocytopenia (HIT)**. 2. **Pharmacokinetics:** It has a long half-life (~17 hours), allowing for once-daily subcutaneous dosing. 3. **Excretion:** It is primarily excreted unchanged by the kidneys; it is **contraindicated** in patients with severe renal impairment (CrCl <30 mL/min). 4. **Monitoring:** Unlike Warfarin (PT/INR) or UFH (aPTT), Fondaparinux does not require routine laboratory monitoring.

Question 176: Folate deficiency can occur due to which of the following medications?

A. Phenytoin
B. Phenobarbitone
C. Primidone
D. All of the above (Correct Answer)

Explanation: Explanation: Folate deficiency is a well-documented side effect of several long-term pharmacological therapies, particularly **Antiepileptic Drugs (AEDs)**. The correct answer is **D (All of the above)** because Phenytoin, Phenobarbitone, and Primidone all interfere with folate metabolism through similar mechanisms. **Mechanism of Action:** These drugs cause folate deficiency primarily by: 1. **Inhibition of intestinal conjugase:** This enzyme is required to break down dietary polyglutamates into monoglutamates for absorption. 2. **Induction of Hepatic Enzymes:** These drugs are potent inducers of the Cytochrome P450 system, which increases the demand for folate as a co-factor in microsomal hydroxylation reactions. 3. **Interference with cellular uptake:** They may also inhibit the transport of folate into tissues. **Analysis of Options:** * **Phenytoin:** The most common AED associated with megaloblastic anemia [2]. It significantly reduces serum folate levels in up to 50% of chronic users. * **Phenobarbitone & Primidone:** Both are barbiturate-class anticonvulsants (Primidone is metabolized into Phenobarbitone). They share the same enzyme-inducing properties that lead to accelerated folate depletion. **High-Yield Clinical Pearls for NEET-PG:** * **Megaloblastic Anemia:** While subclinical folate deficiency is common with these drugs, overt megaloblastic anemia occurs in <1% of patients [2]. * **The "Folate-Phenytoin Seesaw":** Supplementing folate in patients on Phenytoin can actually *lower* Phenytoin plasma levels (by increasing its metabolism), potentially precipitating seizures. * **Other Folate Antagonists (High Yield):** * **DHFR Inhibitors:** Methotrexate, Trimethoprim, Pyrimethamine [1]. * **Others:** Sulfasalazine (inhibits absorption), Oral Contraceptive Pills, and Triamterene. * **Teratogenicity:** Folate deficiency caused by these AEDs is a major contributor to **Neural Tube Defects (NTDs)**; hence, periconceptional folate supplementation (5mg/day) is mandatory for women on these medications.

Question 177: All of the following are target-specific oral anticoagulants except?

A. Betrixaban (Correct Answer)
B. Apixaban
C. Dabigatran
D. Rivaroxaban

Explanation: **Explanation:** The question asks to identify the drug that is **not** a target-specific oral anticoagulant (TSOAC), also known as Direct Oral Anticoagulants (DOACs). **Why Betrixaban is the correct answer (in the context of this specific question):** Actually, there is a technical nuance here. **Betrixaban, Apixaban, Dabigatran, and Rivaroxaban are ALL technically DOACs.** However, in many standard pharmacological classifications and older question banks used for NEET-PG, the "classic" DOACs frequently discussed are Dabigatran (Direct Thrombin Inhibitor), Rivaroxaban, and Apixaban (Factor Xa inhibitors). Betrixaban is the newest addition (FDA approved in 2017) and is often excluded from older lists. *Note: If this question appeared in a recent exam, it might be considered "controversial" as all four are target-specific. However, in a "select the exception" format, Betrixaban is often the intended answer if the examiner is using older reference material or focusing on drugs commonly used in standard clinical practice.* **Analysis of Options:** * **Dabigatran (Option C):** A direct thrombin (Factor IIa) inhibitor. It is the only oral DOAC that does not target Factor Xa. * **Rivaroxaban (Option D) & Apixaban (Option B):** These are direct Factor Xa inhibitors (indicated by the "-xa-" in their names). They are widely used for stroke prevention in atrial fibrillation and DVT prophylaxis. **High-Yield Clinical Pearls for NEET-PG:** 1. **Mechanism of Action:** Remember **"Xa"** in the name (Riva**xa**ban, Api**xa**ban, Edoxaban) means they inhibit **Factor Xa**. Dabigatran inhibits **Factor IIa** (Thrombin). 2. **Reversal Agents (Extremely High Yield):** * **Idarucizumab:** Specific reversal agent for **Dabigatran**. * **Andexanet Alfa:** Reversal agent for **Factor Xa inhibitors** (Rivaroxaban, Apixaban). 3. **Monitoring:** Unlike Warfarin (which requires PT/INR monitoring), DOACs have predictable pharmacokinetics and generally **do not require routine laboratory monitoring.** 4. **Renal Clearance:** Dabigatran is the most renally cleared DOAC; it must be used with caution in chronic kidney disease.

Question 178: Which of the following drugs is used for the treatment of sickle cell anemia?

A. Hydroxyurea (Correct Answer)
B. Cisplatin
C. Paclitaxel
D. Carboplatin

Explanation: **Explanation:** **Hydroxyurea** is the mainstay of pharmacological management for sickle cell anemia (SCA). Its primary mechanism of action involves the **inhibition of the enzyme ribonucleotide reductase**, but in the context of SCA, it works by **increasing the production of fetal hemoglobin (HbF)**. HbF interferes with the polymerization of hemoglobin S (HbS), thereby preventing the sickling of red blood cells, reducing vaso-occlusive crises, and decreasing the need for blood transfusions. Additionally, it has anti-inflammatory effects by lowering the white blood cell count and improving RBC hydration. **Analysis of Incorrect Options:** * **Cisplatin & Carboplatin (Options B & D):** These are platinum-based alkylating agents used as chemotherapy for solid tumors (e.g., lung, ovarian, and testicular cancers). They work by causing DNA cross-linking, leading to apoptosis, and have no role in treating hemoglobinopathies. * **Paclitaxel (Option C):** This is a taxane derivative that acts as a microtubule stabilizer. It is used in the treatment of breast, ovarian, and lung cancers but does not affect hemoglobin synthesis. **High-Yield Clinical Pearls for NEET-PG:** * **Dose-limiting toxicity:** The most common side effect of Hydroxyurea is **myelosuppression** (neutropenia and thrombocytopenia). * **Teratogenicity:** It is contraindicated in pregnancy (Category D). * **Other Indications:** Hydroxyurea is also used in chronic myeloid leukemia (CML) and polycythemia vera to reduce cell counts. * **Newer Drugs for SCA:** Keep an eye on **Voxelotor** (HbS polymerization inhibitor) and **Crizanlizumab** (P-selectin inhibitor), which are also FDA-approved for SCA.

Question 179: Which of the following iron preparations is used for parenteral iron therapy?

A. Iron dextran (Correct Answer)
B. Ferrous sulfate
C. Ferrous fumarate
D. Ferrous gluconate

Explanation: **Explanation:** **1. Why Iron Dextran is Correct:** Parenteral iron therapy is indicated when oral iron is not tolerated, ineffective (malabsorption), or when rapid replenishment of iron stores is required (e.g., chronic kidney disease or severe anemia in late pregnancy). **Iron dextran** is a complex of ferric hydroxide and dextran. It can be administered via deep intramuscular (IM) injection or slow intravenous (IV) infusion. It is a high-molecular-weight compound that allows for the delivery of large doses of iron in a single session (Total Dose Infusion). **2. Why the Other Options are Incorrect:** * **Ferrous sulfate, Ferrous fumarate, and Ferrous gluconate** are all **oral iron salts**. * These are the preferred first-line treatments for iron deficiency anemia due to their safety, low cost, and effectiveness. * Among these, Ferrous sulfate is the most commonly prescribed, while Ferrous fumarate contains the highest percentage of elemental iron (~33%). **3. High-Yield Clinical Pearls for NEET-PG:** * **Adverse Effects:** The most significant risk with Iron dextran is **anaphylaxis** (Type I hypersensitivity). A **test dose** is mandatory before the full therapeutic dose is administered. * **Z-track Technique:** When giving iron dextran intramuscularly, the Z-track technique must be used to prevent skin staining and local irritation. * **Newer Parenteral Agents:** Modern alternatives like **Iron Sucrose** and **Ferric Carboxymaltose** are often preferred over iron dextran because they carry a significantly lower risk of anaphylaxis and do not require a test dose. * **Calculation:** The dose of parenteral iron is calculated using the **Ganzoni Equation**: * *Iron deficit (mg) = Body weight (kg) × (Target Hb - Actual Hb) × 2.4 + Iron stores (500 mg).*

Question 180: Effect of Heparin is reversed by which of the following agents?

A. Vitamin K
B. Protamine (Correct Answer)
C. Hirudin
D. Tranexamic acid

Explanation: **Explanation:** **1. Why Protamine is the Correct Answer:** Protamine sulfate is the specific pharmacological antagonist for Heparin. [1] The mechanism is based on a **chemical neutralization** (acid-base reaction). Heparin is a highly acidic, negatively charged molecule, while Protamine is a strongly basic, positively charged protein (derived from salmon sperm). When administered intravenously, they combine to form a stable, inactive salt complex, thereby rapidly reversing the anticoagulant effect of Unfractionated Heparin (UFH). [1] **2. Analysis of Incorrect Options:** * **Vitamin K:** This is the specific antidote for **Warfarin** (Coumarin) toxicity. [2] It acts by promoting the hepatic synthesis of clotting factors II, VII, IX, and X, which takes several hours to manifest. [2] * **Hirudin:** This is a **Direct Thrombin Inhibitor (DTI)** derived from leech saliva. It is an anticoagulant itself, not an antidote. It is often used in patients with Heparin-Induced Thrombocytopenia (HIT). * **Tranexamic acid:** This is an **Antifibrinolytic** agent. It works by inhibiting the activation of plasminogen to plasmin. It is used to control bleeding in trauma or surgery but does not neutralize heparin. **3. High-Yield Clinical Pearls for NEET-PG:** * **Dosage:** 1 mg of Protamine neutralizes approximately 100 units of Heparin. [1] * **LMWH Reversal:** Protamine only **partially** reverses Low Molecular Weight Heparin (Enoxaparin) and has **no effect** on Fondaparinux. * **Adverse Effect:** Rapid injection of Protamine can cause "Protamine Reaction," characterized by hypotension, bradycardia, and anaphylaxis due to histamine release. [1] * **Monitoring:** The effect of Heparin is monitored by **aPTT** (activated Partial Thromboplastin Time).

Practice by Chapter

Hematopoietic Growth Factors

Practice Questions

Iron Preparations and Management of Iron Deficiency

Practice Questions

Vitamin B12 and Folic Acid

Practice Questions

Anticoagulants: Heparins and Direct Inhibitors

Practice Questions

Oral Anticoagulants

Practice Questions

Antiplatelet Drugs

Practice Questions

Thrombolytic Agents

Practice Questions

Hemostatic Drugs

Practice Questions

Plasma Expanders

Practice Questions

Blood Transfusion and Alternatives

Practice Questions

Want unlimited practice?

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

Start For Free