Drugs Affecting Blood and Blood Formation Practice Questions

Q: Ravulizumab is a new drug approved for the treatment of which condition?

Paroxysmal nocturnal hemoglobinuria. **Explanation:** **Ravulizumab** is a long-acting monoclonal antibody that inhibits the **complement protein C5**. It is a second-generation terminal complement inhibitor, developed as an improvement over Eculizumab. 1. **Why Option A is correct:** **Paroxysmal Nocturnal Hemoglobinuria (PNH)** is characterized by a deficiency of CD55 and CD59 on red blood cells, making them susceptible to complement-mediated hemolysis. Ravulizumab binds to C5, preventing its cleavage into C5a and C5b, thereby blocking the formation of the Membrane Attack Complex (MAC). Its primary advantage over Eculizumab is its **extended half-life**, allowing for maintenance dosing every 8 weeks instead of every 2 weeks. 2. **Why the other options are incorrect:** * **Option B (Sickle cell anemia):** Managed with Hydroxyurea, L-glutamine, or Crizanlizumab (a P-selectin inhibitor). * **Option C (Acute hepatic porphyria):** Treated with **Givosiran**, an siRNA that targets aminolevulinic acid synthase 1 (ALAS1). * **Option D (Meningococcal infections):** This is actually a **contraindication/risk**. Because Ravulizumab inhibits terminal complement, patients are at a 1,000-fold increased risk of life-threatening *Neisseria meningitidis* infections. Vaccination is mandatory before starting therapy. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Humanized monoclonal antibody against C5. * **Indications:** PNH and Atypical Hemolytic Uremic Syndrome (aHUS). * **Key Difference:** Ravulizumab has a "recycling" mechanism (pH-dependent binding) that gives it a much longer duration of action than Eculizumab. * **Black Box Warning:** Meningococcal infection; patients must receive the meningococcal vaccine at least 2 weeks before the first dose.

Q: Aspirin is used for secondary prevention of ischemic heart disease because it:

Inhibits TXA2 synthesis by platelets. **Explanation:** Aspirin (Acetylsalicylic acid) is a mainstay in the secondary prevention of ischemic heart disease due to its role as an antiplatelet agent. **1. Why Option A is Correct:** Aspirin works by **irreversibly inhibiting the enzyme Cyclooxygenase-1 (COX-1)** via acetylation. In platelets, COX-1 is responsible for the synthesis of **Thromboxane A2 (TXA2)**, a potent vasoconstrictor and mediator of platelet aggregation. Since platelets are anuclear and cannot synthesize new enzymes, the inhibition lasts for the entire lifespan of the platelet (approx. 7–10 days). Reducing TXA2 levels prevents thrombus formation over atherosclerotic plaques, thereby reducing the risk of myocardial infarction. **2. Why Other Options are Incorrect:** * **Option B:** While aspirin can inhibit **Prostacyclin (PGI2)** synthesis in vascular endothelial cells, PGI2 is a vasodilator and anti-aggregatory agent. At low doses (75–150 mg), aspirin is "platelet-selective" because endothelial cells can regenerate COX enzymes, whereas platelets cannot. Inhibiting PGI2 is actually an unwanted effect. * **Option C & D:** Aspirin does not have a direct inhibitory effect on **Endothelium-Derived Relaxing Factor (EDRF/Nitric Oxide)** or **Endothelins**. These are regulated by different pathways (e.g., NO synthase and Endothelin-converting enzyme). **High-Yield Clinical Pearls for NEET-PG:** * **Low-dose Aspirin (75–150 mg/day):** Preferred for cardioprotection to achieve selective TXA2 inhibition while sparing PGI2. * **Irreversible Action:** Aspirin is the only NSAID that binds irreversibly to COX. * **Primary vs. Secondary Prevention:** Aspirin is strongly indicated for *secondary* prevention (post-MI/Stroke). Its use in *primary* prevention is now limited due to the increased risk of major GI bleeding. * **Aspirin Resistance:** Can be seen in patients with high platelet turnover or genetic polymorphisms.

Q: Warfarin skin necrosis is caused by which of the following?

Protein C or Protein S deficiency. **Explanation:** **Warfarin-induced skin necrosis (WISN)** is a rare but severe complication occurring typically 3–10 days after starting warfarin therapy. **Why Option A is correct:** Warfarin inhibits Vitamin K-dependent clotting factors (II, VII, IX, X) and natural anticoagulants (**Protein C and Protein S**). Protein C has a significantly shorter half-life (approx. 6 hours) compared to procoagulant factors like Factor X or II. Consequently, during the initial phase of warfarin therapy, Protein C levels drop rapidly while procoagulant factors remain active. This creates a transient **paradoxical hypercoagulable state**, leading to microvascular thrombosis, skin infarction, and necrosis. Patients with a pre-existing (hereditary) deficiency of Protein C or S are at the highest risk. **Why other options are incorrect:** * **B. APLAS:** While APLAS causes thrombosis, it is an autoimmune condition involving antibodies against phospholipids, not the specific mechanism triggered by warfarin initiation. * **C. Vitamin K deficiency:** Warfarin induces a functional Vitamin K deficiency, but the *necrosis* specifically results from the imbalance between anticoagulant and procoagulant factors, not the deficiency itself. * **D. Fibrinogen deficiency:** This leads to bleeding tendencies (hypocoagulability), rather than the microvascular thrombosis seen in WISN. **Clinical Pearls for NEET-PG:** * **Classic Presentation:** Painful, erythematous plaques progressing to hemorrhagic bullae and eschar, typically in areas with high subcutaneous fat (breasts, thighs, buttocks). * **Prevention:** Always "bridge" warfarin with a rapid-acting anticoagulant like **Heparin** to cover the initial hypercoagulable window. * **Treatment:** Immediate discontinuation of warfarin, administration of Vitamin K, and providing Protein C concentrates or Fresh Frozen Plasma (FFP).

Q: All are true about Romiplostim except?

It is recombinant erythropoietin.. ### Explanation **Romiplostim** is a novel **thrombopoietin (TPO) receptor agonist**, often referred to as a "peptibody." It is used primarily to treat chronic immune thrombocytopenic purpura (ITP). **1. Why Option A is the Correct Answer (The "Except" statement):** Romiplostim is **not** recombinant erythropoietin. Recombinant erythropoietin (e.g., Epoetin alfa) stimulates red blood cell production. Romiplostim, instead, mimics the action of endogenous thrombopoietin by binding to the TPO receptor (Mpl), which stimulates megakaryopoiesis and increases **platelet count**. **2. Analysis of Other Options:** * **Option B (Protein component):** Romiplostim is a fusion protein consisting of a bioactive peptide sequence linked to an IgG1 Fc domain. This structure allows it to activate the TPO receptor without sharing sequence homology with native TPO, reducing the risk of neutralizing antibodies. * **Option C (Variable half-life):** The pharmacokinetics of Romiplostim are non-linear. Its half-life is inversely proportional to the serum concentration and varies based on the individual’s platelet count (target-mediated drug disposition). * **Option D (Subcutaneous administration):** It is administered once weekly via **subcutaneous injection**, making it convenient for chronic management of ITP. **Clinical Pearls for NEET-PG:** * **Mechanism:** It is a TPO-mimetic "peptibody." * **Indication:** Chronic ITP in patients who have had an insufficient response to corticosteroids, immunoglobulins, or splenectomy. * **Comparison:** Unlike **Eltrombopag** (which is an oral, small-molecule non-peptide TPO agonist), Romiplostim must be injected. * **Side Effects:** Headache is common; risk of bone marrow reticulin deposition and rebound thrombocytopenia upon discontinuation.

Q: A 60-year-old male with angina presents with severe chest pain unresponsive to sublingual nitroglycerin. An ECG shows ST segment elevation in the anterolateral leads, and thrombolytic therapy is initiated. If streptokinase is given to this patient, it may produce thrombolysis after binding to which of the following proteins?

Plasminogen. ### Explanation **Mechanism of Action (Why Option C is Correct):** Streptokinase is a first-generation thrombolytic agent derived from *beta-hemolytic streptococci*. Unlike tissue plasminogen activator (tPA), streptokinase is **not fibrin-specific**. It works by forming a stable **1:1 stoichiometric complex with plasminogen**. This streptokinase-plasminogen complex undergoes a conformational change that exposes an active site, which then enzymatically converts free circulating plasminogen into **plasmin**. Plasmin subsequently degrades fibrin clots, as well as fibrinogen and other clotting factors (factors V and VII). **Analysis of Incorrect Options:** * **A. Antithrombin III:** This is a natural anticoagulant that inhibits thrombin and Factor Xa. It is the site of action for **Heparin**, not thrombolytics. * **B. Fibrin:** While newer agents like Alteplase, Reteplase, and Tenecteplase are "fibrin-selective" (binding preferentially to plasminogen already bound to fibrin), **Streptokinase does not bind directly to fibrin**. It acts systemically on all circulating plasminogen. * **D. Protein C:** This is a vitamin K-dependent natural anticoagulant that inactivates Factors Va and VIIIa. It is not involved in the mechanism of streptokinase. **High-Yield NEET-PG Pearls:** * **Antigenicity:** Because it is a bacterial protein, streptokinase is antigenic. It can cause **hypersensitivity reactions** (anaphylaxis) and should not be repeated in the same patient within 6–12 months due to neutralizing antibodies. * **Side Effects:** The most common side effect is bleeding. Unlike tPA, streptokinase can also cause significant **hypotension**. * **Comparison:** Tenecteplase is currently the preferred thrombolytic in STEMI due to its high fibrin specificity, long half-life (bolus dose), and lower bleeding risk compared to streptokinase.

Q: Which of the following is NOT an ADP inhibitor?

Tirofiban. **Explanation:** The question asks to identify the drug that does not belong to the **ADP (P2Y12) receptor antagonist** class. **1. Why Tirofiban is the correct answer:** Tirofiban is a **Glycoprotein (GP) IIb/IIIa inhibitor**, not an ADP inhibitor. It works by blocking the final common pathway of platelet aggregation—the binding of fibrinogen to the GP IIb/IIIa receptors on the platelet surface [1], [2]. It is administered intravenously, primarily in the management of Acute Coronary Syndrome (ACS) and during Percutaneous Coronary Intervention (PCI). **2. Analysis of incorrect options (ADP Inhibitors):** * **Ticlopidine:** A first-generation thienopyridine ADP inhibitor. It is rarely used now due to side effects like severe neutropenia and TTP [1]. * **Clopidogrel:** A second-generation thienopyridine. It is a prodrug activated by CYP2C19 [3]. It irreversibly inhibits the P2Y12 receptor. * **Prasugrel:** A third-generation thienopyridine. It is more potent and has a faster onset than clopidogrel [3] but carries a higher risk of bleeding. **High-Yield Clinical Pearls for NEET-PG:** * **Classification of Antiplatelets:** * **COX Inhibitors:** Aspirin. * **ADP (P2Y12) Blockers:** Clopidogrel, Prasugrel, Ticlopidine (Irreversible); **Ticagrelor, Cangrelor** (Reversible) [3]. * **GP IIb/IIIa Inhibitors:** Abciximab, Eptifibatide, Tirofiban. * **PDE Inhibitors:** Dipyridamole, Cilostazol. * **Ticagrelor** is unique because it is a direct-acting (not a prodrug) and reversible P2Y12 inhibitor [3]. * **Cilostazol** is the drug of choice for intermittent claudication (Peripheral Vascular Disease).

Q: Which of the following classes of drugs is generally precluded from administration via the intramuscular route?

Anticoagulants. The correct answer is **Anticoagulants**. **Why Anticoagulants are precluded from IM administration:** The primary reason for avoiding the intramuscular (IM) route for anticoagulants (such as Heparin or Warfarin) is the high risk of **hematoma formation**. Skeletal muscle is highly vascular; when a needle punctures these vessels in a patient with impaired coagulation, it leads to significant local bleeding. This can result in large, painful hematomas, potential nerve compression, and erratic drug absorption. Therefore, Heparin is administered intravenously (IV) or subcutaneously (SC) [1], [2], but never IM. **Analysis of Incorrect Options:** * **Anti-hypertensives:** Many can be given IM in emergencies (e.g., Hydralazine or Labetalol), though IV is preferred for rapid titration. * **Anti-diabetics:** While Insulin is typically SC, certain preparations can be given IM if necessary, and Glucagon (used for hypoglycemia) is frequently administered via the IM route. * **Anti-fibrinolytics:** Drugs like Tranexamic acid are primarily given IV or Orally. While IM is not the standard route, they do not carry the specific risk of causing uncontrollable bleeding/hematoma at the injection site. **High-Yield Clinical Pearls for NEET-PG:** * **Heparin vs. Warfarin:** Heparin is the anticoagulant of choice in pregnancy (does not cross the placenta), while Warfarin is teratogenic [3]. * **Monitoring:** Monitor Heparin with **aPTT** (Intrinsic pathway) and Warfarin with **PT/INR** (Extrinsic pathway). * **Antidotes:** The antidote for Heparin is **Protamine Sulfate** [1]; for Warfarin, it is **Vitamin K** (slow) or **Fresh Frozen Plasma** (rapid) [3]. * **Absorption:** Subcutaneous administration of Heparin is preferred over IM because the smaller needle and slower absorption profile reduce the risk of massive tissue hemorrhage.

Question 1

A 59-year-old woman with type II diabetes mellitus and a BMI of 30 experiences an episode of chest pain with exercise. Angiography reveals proximal coronary arterial narrowing with up to 70% stenosis. Which of the following pharmacologic agents ingested in low doses daily is most appropriate for reducing her risk for myocardial infarction?

Accepted Answer

Aspirin

Answer

Acetaminophen

Answer

Ibuprofen

Answer

Paclitaxel

Question 2

Ravulizumab is a new drug approved for the treatment of which condition?

Accepted Answer

Paroxysmal nocturnal hemoglobinuria

Answer

Sickle cell anemia

Answer

Acute hepatic porphyria

Answer

Meningococcal infections

Question 3

Aspirin is used for secondary prevention of ischemic heart disease because it:

Accepted Answer

Inhibits TXA2 synthesis by platelets

Answer

Inhibits prostacyclin synthesis

Answer

Inhibits the release of EDRF

Answer

Inhibits the synthesis of endothelins

Question 4

All of the following are true about oral iron therapy in anemia except:

Accepted Answer

It takes a minimum of 2 weeks for reticulocyte count to increase

Answer

May worsen inflammatory bowel disease

Answer

Generally, 3-6 months of therapy is required to replenish iron stores

Answer

Gastrointestinal side-effects often limit its dose

Question 5

Warfarin skin necrosis is caused by which of the following?

Accepted Answer

Protein C or Protein S deficiency

Answer

Antiphospholipid antibody syndrome (APLAS)

Answer

Vitamin K deficiency

Answer

Fibrinogen deficiency

Question 6

All are true about Romiplostim except?

Accepted Answer

It is recombinant erythropoietin.

Answer

It has a protein component in its structure.

Answer

Its half-life is variable.

Answer

It is given subcutaneously.

Question 7

Relative to filgrastim (G-CSF), what is a characteristic of sargramostim (GM-CSF)?

Accepted Answer

Stimulates production of a wider variety of hematopoietic stem cells

Answer

Has greater oral bioavailability

Answer

Is more likely to cause thrombocytopenia

Answer

Is more likely to elicit an allergic reaction

Question 8

A 60-year-old male with angina presents with severe chest pain unresponsive to sublingual nitroglycerin. An ECG shows ST segment elevation in the anterolateral leads, and thrombolytic therapy is initiated. If streptokinase is given to this patient, it may produce thrombolysis after binding to which of the following proteins?

Accepted Answer

Plasminogen

Answer

Antithrombin III

Answer

Fibrin

Answer

Protein C

Question 9

Which of the following is NOT an ADP inhibitor?

Accepted Answer

Tirofiban

Answer

Ticlopidine

Answer

Clopidogrel

Answer

Prasugrel

Question 10

Which of the following classes of drugs is generally precluded from administration via the intramuscular route?

Accepted Answer

Anticoagulants

Answer

Anti-hypertensives

Answer

Anti-diabetics

Answer

Anti-fibrinolytics

Drugs Affecting Blood and Blood Formation — MCQs

Drugs Affecting Blood and Blood Formation — MCQs

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