Drugs Affecting Blood and Blood Formation — MCQs

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

Question 341: Which of the following drugs inhibit platelet cyclooxygenase reversibly?

A. Alprostadil
B. Prednisolone
C. Aspirin
D. Ibuprofen (Correct Answer)

Explanation: ***Ibuprofen*** - Ibuprofen is a non-steroidal anti-inflammatory drug (**NSAID**) that **reversibly inhibits** both **COX-1** and **COX-2** enzymes. - Its inhibitory effect on platelet function is temporary and wears off as the drug is metabolized and cleared from the body. *Alprostadil* - **Alprostadil** is a synthetic **prostaglandin E1 (PGE1)** analogue; it does not inhibit cyclooxygenase. - It works by directly activating **prostaglandin receptors**, leading to vasodilation and inhibition of platelet aggregation. *Aspirin* - **Aspirin** *irreversibly inhibits* platelet cyclooxygenase (specifically **COX-1**) by **acetylation** of a serine residue. - This irreversible inhibition means that the effect on platelets lasts for their entire lifespan, requiring new platelets to be produced for normal function. *Prednisolone* - **Prednisolone** is a **corticosteroid** that works by inhibiting **phospholipase A2**, thereby preventing the release of arachidonic acid, the precursor for prostaglandins. - It does not directly inhibit cyclooxygenase enzymes, but rather acts upstream in the inflammatory pathway.

Question 342: All are antiplatelet drugs except:

A. Clopidogrel
B. Abciximab
C. Ticlopidine
D. Aprotinin (Correct Answer)

Explanation: ***Aprotinin*** - **Aprotinin** is a **serine protease inhibitor** used to reduce bleeding during complex surgeries, particularly cardiac surgery. - It works by inhibiting kallikrein and plasmin, thereby **preserving platelets** and **reducing fibrinolysis**, rather than inhibiting platelet aggregation. *Clopidogrel* - **Clopidogrel** is a **P2Y12 receptor inhibitor** that prevents platelet activation and aggregation. - It is commonly used in patients with **acute coronary syndrome** and for the prevention of thrombotic events. *Abciximab* - **Abciximab** is a **glycoprotein IIb/IIIa receptor antagonist** that blocks the final common pathway of platelet aggregation. - It is primarily used during **percutaneous coronary intervention (PCI)** to prevent ischemic complications. *Ticlopidine* - **Ticlopidine** is another **P2Y12 receptor inhibitor** that inhibits platelet aggregation similar to clopidogrel. - It is associated with a higher risk of **hematologic side effects** like neutropenia and thrombotic thrombocytopenic purpura (TTP) compared to clopidogrel.

Question 343: Which of the following is a non-peptide GP IIb/IIIa antagonist?

A. Tirofiban (Correct Answer)
B. Abciximab
C. Eptifibatide
D. Prasugrel

Explanation: **Tirofiban** is the correct answer as it is a **non-peptide GP IIb/IIIa antagonist**. ***Tirofiban*** - Tirofiban is a **non-peptide GP IIb/IIIa antagonist** (tyrosine derivative) that blocks the binding of **fibrinogen** to the receptor, thereby inhibiting platelet aggregation. - Its **small molecular weight** and **reversible binding** allow for rapid onset and offset of action. - Used in acute coronary syndromes and during percutaneous coronary interventions. *Abciximab* - Abciximab is the **Fab fragment** of a **monoclonal antibody** directed against the GPIIb/IIIa receptor, making it a **peptide-based** (antibody-based) antagonist. - It has high affinity for the receptor and a relatively **long duration of action** due to its antibody nature. *Eptifibatide* - Eptifibatide is a **cyclic heptapeptide** that mimics the RGD (arginine-glycine-aspartate) sequence found in fibrinogen, classifying it as a **peptide-based** antagonist. - It selectively binds to the **GPIIb/IIIa receptor**, preventing platelet aggregation. *Prasugrel* - Prasugrel is a **thienopyridine P2Y12 inhibitor**, which acts by irreversibly blocking the **ADP receptor** on platelets, preventing their activation and aggregation. - It is distinct from GP IIb/IIIa inhibitors as it targets a **different pathway of platelet activation** (not a GP IIb/IIIa antagonist at all).

Question 344: Which one of the following is used for the preservation of blood for transfusions?

A. Heparin
B. Citrate phosphate dextrose (Correct Answer)
C. Thrombin
D. EDTA

Explanation: ***Citrate phosphate dextrose*** - This anticoagulant solution is commonly used for blood preservation in blood banks because **citrate** chelates **calcium ions**, preventing coagulation. - The **phosphate** acts as a buffer to maintain pH, and **dextrose** provides energy for red blood cell metabolism during storage. - **CPD** allows blood storage for up to **21 days**, and when adenine is added (CPDA-1), storage can be extended to **35 days**. *Heparin* - **Heparin** is an anticoagulant that works by enhancing the activity of **antithrombin III**, but it is generally not used for long-term blood storage for transfusion due to its short half-life and potential to activate platelets upon prolonged contact. - While effective as an anticoagulant, heparin is not suitable for routine blood bank storage as it does not adequately support the viability of red blood cells over extended periods. *Thrombin* - **Thrombin** is a procoagulant enzyme involved in the final stages of the coagulation cascade, converting fibrinogen to fibrin, thus promoting clot formation. - Using thrombin would cause immediate blood clotting, making it entirely unsuitable for preserving blood for transfusion purposes. *EDTA* - **EDTA (Ethylenediaminetetraacetic acid)** is a chelating anticoagulant commonly used in **laboratory samples** for hematological testing (e.g., CBC). - However, it is **not used for blood transfusion** because it can cause morphological changes in cells and is toxic when transfused, making it unsuitable for therapeutic blood storage.

Question 345: Which of the following vitamins can be used in high doses to treat hypercholesterolemia?

A. Niacin (Correct Answer)
B. Vitamin B2
C. Vitamin B5
D. Vitamin B1

Explanation: ***Niacin*** - **Niacin** (Vitamin B3) in pharmacological doses effectively lowers **LDL cholesterol** and triglycerides while raising **HDL cholesterol**. - Its mechanism involves inhibiting **hepatic VLDL secretion** and decreasing the catabolism of **HDL**. *Vitamin B2* - **Vitamin B2** (riboflavin) is crucial for **cellular energy production** and acts as a cofactor in various enzyme reactions. - It does not have a significant role in **lipid metabolism** or in treating **hypercholesterolemia** at high doses. *Vitamin B5* - **Vitamin B5** (pantothenic acid) is a component of **coenzyme A**, essential for **fatty acid synthesis** and breakdown. - While involved in metabolism, it is not used therapeutically to manage **hypercholesterolemia**. *Vitamin B1* - **Vitamin B1** (thiamine) is vital for **carbohydrate metabolism** and **nerve function**. - There is no evidence supporting its use in treating **hypercholesterolemia**.

Question 346: A patient with hemophilia and rheumatoid arthritis may be prescribed which drug to relieve pain?

A. Acetaminophen (Correct Answer)
B. Acetylsalicylic acid
C. Phenylbutazone
D. Naproxen

Explanation: ***Acetaminophen*** - **Acetaminophen** is a preferred pain reliever for patients with hemophilia because it has **no antiplatelet effect** and thus does not increase the risk of bleeding. - It effectively manages mild to moderate pain associated with **rheumatoid arthritis** without impacting coagulation. *Acetylsalicylic acid* - **Acetylsalicylic acid** (aspirin) is an **NSAID** and a potent **antiplatelet agent**, which would significantly increase the risk of bleeding in a patient with hemophilia. - Its use is contraindicated in hemophilia due to the high risk of **hemorrhage**. *Phenylbutazone* - **Phenylbutazone** is an **NSAID** that is rarely used due to severe side effects such as **aplastic anemia** and **agranulocytosis**. - Like other NSAIDs, it inhibits platelet aggregation, posing a significant **bleeding risk** for hemophiliac patients. *Naproxen* - **Naproxen** is another **NSAID** that inhibits cyclooxygenase enzymes, which not only provides pain relief but also **impairs platelet function**. - Its use is contraindicated in hemophilia because it increases the risk of **gastrointestinal and other bleeding episodes**.

Question 347: Which of the following is most likely to be used in a young child with chronic renal insufficiency?

A. Desferrioxamine
B. Filgrastim (G-CSF)
C. Erythropoietin (EPO) (Correct Answer)
D. Cyanocobalamin (Vitamin B12)

Explanation: ***Erythropoietin (EPO)*** - **Chronic renal insufficiency** leads to decreased production of **erythropoietin** by the kidneys, resulting in **anemia**. - Administering exogenous **EPO** stimulates red blood cell production, correcting the anemia common in these patients. *Desferrioxamine* - This is a **chelating agent** used to treat **iron overload**, which can occur in patients receiving multiple blood transfusions or those with certain genetic disorders. - While some chronic renal patients may receive transfusions, **iron overload** is not the primary or most common issue addressed by this medication in the context of general renal insufficiency. *Filgrastim (G-CSF)* - **Granulocyte colony-stimulating factor (G-CSF)** is used to stimulate the production of **neutrophils**, typically in patients with **neutropenia** (low white blood cell count) due to chemotherapy or certain bone marrow disorders. - It does not directly address the primary hematological complications of chronic renal insufficiency, which is mainly **anemia**. *Cyanocobalamin (Vitamin B12)* - **Vitamin B12** is essential for red blood cell formation and neurological function; its deficiency can cause **megaloblastic anemia**. - While renal insufficiency can affect nutrient absorption, **B12 deficiency anemia** is not the most common or direct hematological complication of chronic kidney disease, which is primarily due to EPO deficiency.

Question 348: Fish oil is not used in the treatment of:

A. Type 2A Hyperlipoproteinemia (Correct Answer)
B. Type 2B Hyperlipoproteinemia
C. Type 5 Hyperlipoproteinemia
D. Type 3 Hyperlipoproteinemia

Explanation: ***Type 2A Hyperlipoproteinemia*** - **Fish oil** (omega-3 fatty acids) primarily lowers **triglyceride** levels. - In **Type 2A hyperlipoproteinemia**, the main lipid abnormality is elevated **LDL cholesterol**, with normal triglycerides, making fish oil less effective as a primary treatment. *Type 2B Hyperlipoproteinemia* - This condition involves elevated **LDL cholesterol** and moderately elevated **triglycerides**. - **Fish oil** can be beneficial in managing the elevated triglyceride component. *Type 5 Hyperlipoproteinemia* - Characterized by very high **triglyceride** levels and elevated **chylomicrons** and **VLDL**. - **Fish oil** is a key therapeutic agent for significantly reducing triglycerides in this severe form of hyperlipidemia. *Type 3 Hyperlipoproteinemia* - Also known as **familial dysbetalipoproteinemia**, this condition involves elevated **chylomicron remnants** and **VLDL remnants**. - **Fish oil** can help lower the triglyceride-rich lipoproteins seen in this disorder.

Question 349: What is the mechanism of action of Clopidogrel?

A. Inhibition of Thromboxane A2
B. Inhibition of GP IIb/IIIa receptors
C. No effect on platelet activation
D. Inhibition of ADP-mediated platelet activation (Correct Answer)

Explanation: ***Inhibition of ADP-mediated platelet activation*** - Clopidogrel is an **antiplatelet agent** that works by a direct antagonistic action at the **P2Y12 receptor** on the surface of platelets. - This binding prevents adenosine diphosphate (ADP) from binding to its receptor, thereby inhibiting the activation of the **GP IIb/IIIa receptor complex** and subsequent platelet aggregation. *Inhibition of Thromboxane A2* - This mechanism of action is characteristic of **aspirin**, which inhibits the enzyme **cyclooxygenase-1 (COX-1)**. - COX-1 inhibition leads to reduced production of **Thromboxane A2**, a potent platelet aggregator and vasoconstrictor. *Inhibition of GP IIb/IIIa receptors* - While Clopidogrel ultimately affects the activation of **GP IIb/IIIa receptors**, it does not directly inhibit them. - Drugs like **abciximab**, **eptifibatide**, and **tirofiban** are direct inhibitors of the GP IIb/IIIa receptors, preventing fibrinogen binding and platelet aggregation. *No effect on platelet activation* - This statement is incorrect as Clopidogrel is a well-established **antiplatelet drug**. - Its therapeutic effect is specifically to **reduce platelet activation** and aggregation, thus preventing thrombotic events.

Question 350: Folic acid deficiency is precipitated by:

A. Phenytoin
B. Trimethoprim
C. Cyclosporin
D. Methotrexate (Correct Answer)

Explanation: ***Methotrexate*** - **Methotrexate** is an **antimetabolite** that acts as a **folic acid analog**, competitively inhibiting **dihydrofolate reductase (DHFR)**, the enzyme responsible for converting dihydrofolate to tetrahydrofolate. - This inhibition blocks **DNA synthesis** and cell proliferation, leading to the therapeutic effects of methotrexate but also causing **severe folic acid deficiency** by preventing the formation of its active form. - **Most direct and potent** cause of drug-induced folate deficiency, requiring **leucovorin rescue** in high-dose therapy. *Phenytoin* - **Phenytoin** is an **antiepileptic drug** that **interferes with folate absorption** by inhibiting **intestinal conjugase enzyme** and affecting folate transport mechanisms. - Chronic use can lead to **clinically significant folate deficiency** and **megaloblastic anemia**, making it an important recognized cause. - However, compared to methotrexate, the mechanism is **indirect** (absorption interference) rather than direct enzyme inhibition, and the onset is more gradual. *Trimethoprim* - **Trimethoprim** also inhibits **dihydrofolate reductase**, but its affinity for **bacterial DHFR** is significantly higher (thousands of times) than for human DHFR. - While prolonged high-dose use can rarely cause **folate deficiency** in humans, it is much less common and clinically significant than with methotrexate or phenytoin. *Cyclosporin* - **Cyclosporin** is an **immunosuppressant** that primarily acts by inhibiting **calcineurin**, thereby preventing the activation of **T-lymphocytes**. - Its mechanism of action does not directly involve **folic acid metabolism**, and it is **not known** to cause folic acid deficiency.

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

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