Drugs Affecting Blood and Blood Formation — MCQs

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

Question 291: Which among the following is an iron chelator?

A. BAL
B. Desferrioxamine (Correct Answer)
C. EDTA
D. Penicillamine

Explanation: ***Desferrioxamine*** - **Desferrioxamine** is a specific iron chelator used to treat **acute iron poisoning** and chronic iron overload, such as in patients with **thalassemia** requiring frequent transfusions. - It works by binding to free iron in the bloodstream and promoting its **excretion via urine**. *BAL* - **BAL (dimercaprol)** is primarily used as a chelating agent for **heavy metal poisoning**, particularly **arsenic, mercury, and lead** [1], [2]. - While it can chelate some metals, its affinity and primary use are not for iron. *EDTA* - **EDTA (ethylenediaminetetraacetic acid)** is a chelator often used for **lead poisoning** [1], [2] and hypercalcemia. - It has a high affinity for various divalent and trivalent metal ions [2], but it is not the primary or most specific iron chelator. *Penicillamine* - **Penicillamine** is a chelating agent primarily used for the treatment of **copper overload** in **Wilson's disease**. - It is also used in the treatment of severe **rheumatoid arthritis** and **cystinuria**, but not typically for iron chelation.

Question 292: Which condition is most commonly associated with warfarin-induced skin necrosis?

A. Protein S deficiency
B. Protein C deficiency (Correct Answer)
C. Factor X deficiency
D. Factor VII deficiency
E. AT III deficiency

Explanation: ***Protein C deficiency***- **Warfarin** inhibits the synthesis of vitamin K-dependent clotting factors (II, VII, IX, X) and anticoagulant proteins (Protein C and Protein S) [1, 2].- In individuals with **Protein C deficiency**, warfarin initially reduces Protein C levels faster than the procoagulant factors, leading to a transient **hypercoagulable state** and microthrombi formation, causing skin necrosis [1, 2].*Protein S deficiency*- While **Protein S** is also a vitamin K-dependent anticoagulant and its deficiency can be associated with hypercoagulability, **Protein C deficiency** is the more common and significant predisposing factor for warfarin-induced skin necrosis.- Both Protein C and Protein S deficiencies increase the risk of thrombosis, but the rapid decline of Protein C activity upon warfarin initiation is particularly critical for this specific adverse event.*Factor X deficiency*- **Factor X deficiency** (Stuart-Prower factor) is a bleeding disorder, not a hypercoagulable state.- Individuals with Factor X deficiency would be prone to excessive bleeding, which is the opposite of the thrombotic process seen in warfarin-induced skin necrosis.*Factor VII deficiency*- **Factor VII deficiency** (proconvertin deficiency) is also a bleeding disorder, characterized by impaired extrinsic pathway coagulation.- It would lead to an increased risk of hemorrhage, not the thrombosis observed in warfarin-induced skin necrosis.

Question 293: Warfarin-induced skin necrosis is more common in patients with

A. Sickle cell anemia
B. Protein C deficiency (Correct Answer)
C. Antithrombin 3 deficiency
D. Factor V Leiden mutation

Explanation: ***Protein C deficiency*** - Warfarin treatment initially depletes protein C, a **natural anticoagulant**, faster than procoagulant factors, leading to a temporary **hypercoagulable state**. - In patients with pre-existing **protein C deficiency**, this imbalance is exaggerated, causing severe microthrombosis and subsequent skin necrosis. *Sickle cell anemia* - While sickle cell anemia is associated with thrombotic events, it does not directly predispose to **warfarin-induced skin necrosis**. - Its pathophysiology involves **hemoglobin S polymerization** and red blood cell sickling, leading to vaso-occlusion and chronic hemolysis. *Antithrombin 3 deficiency* - Antithrombin III deficiency increases the risk of **venous thromboembolism** but is not specifically linked to warfarin-induced skin necrosis. - Warfarin targets vitamin K-dependent clotting factors, and antithrombin III's role is independent of this pathway. *Factor V Leiden mutation* - Factor V Leiden mutation causes **resistance to activated protein C**, increasing the risk of venous thromboembolism. - While it involves protein C, the mechanism of warfarin-induced skin necrosis is due to the **initial pharmacological depletion of protein C concentrations**, not protein C resistance.

Question 294: Which is the drug of choice in Paget's disease?

A. Allopurinol
B. Calcitonin
C. Alendronate (Correct Answer)
D. Steroids

Explanation: ***Alendronate*** - **Bisphosphonates** like alendronate are the **first-line treatment** for Paget's disease due to their potent antiresorptive inhibitory effect on **osteoclasts**. - They reduce bone turnover, bone pain, and the risk of complications such as **fractures** and **bone deformities**. *Allopurinol* - This drug is used to treat **gout** by inhibiting **xanthine oxidase** and reducing uric acid production. - It has no role in the management of Paget's disease, which is a disorder of abnormal bone remodeling. *Calcitonin* - Historically, calcitonin was used for Paget's disease, but its effectiveness is **less than bisphosphonates** and it is associated with more side effects. - It is now generally reserved for patients who **cannot tolerate bisphosphonates** or have severe renal impairment. *Steroids* - **Corticosteroids** are potent anti-inflammatory and immunosuppressive agents. - They are primarily used in conditions like **autoimmune disorders** or severe inflammatory diseases, and are **not indicated** for the treatment of Paget's disease.

Question 295: 20 mEq (mmol) of potassium chloride in 500 ml of 5% dextrose solution is given intravenously to treat-

A. Hypokalemia (Correct Answer)
B. Hyperkalemia
C. Hypernatremia
D. Hyponatremia

Explanation: ***Hypokalemia*** - The administration of **potassium chloride (KCl)** is a direct method to **replenish potassium stores** in the body, effectively treating low serum potassium levels. - Adding KCl to an intravenous solution, such as **5% dextrose**, ensures systemic distribution to correct this electrolyte imbalance. *Hyperkalemia* - **Hyperkalemia** refers to dangerously high levels of potassium in the blood, so administering more potassium chloride would worsen this condition, not treat it. - Treatment for hyperkalemia typically involves measures to **shift potassium into cells** or **increase its excretion**, not supplementation. *Hypernatremia* - **Hypernatremia** is an elevated sodium level, usually caused by dehydration or excessive sodium intake. Giving potassium chloride would not directly address sodium balance. - Treatment primarily involves administering **hypotonic fluids** to dilute the excessive sodium. *Hyponatremia* - **Hyponatremia** is a low sodium level in the blood. While fluid management is crucial for hyponatremia, potassium chloride specifically targets potassium levels, not sodium. - For hyponatremia, treatment varies based on severity and acuity and often includes **sodium replacement** or fluid restriction.

Question 296: Arrange the following anticoagulant drugs in ascending order (shortest to longest) based on the pre-operative cessation time before surgery: 1) Clopidogrel 2) Ticlopidine 3) Low molecular weight heparin 4) Warfarin

A. 2>1>3>4
B. 4>3>2>1
C. 3>4>1>2 (Correct Answer)
D. 3>4>2>1

Explanation: ***3>4>1>2*** - The correct order, in ascending time from last dose to surgery, is **low molecular weight heparin (LMWH)** (12-24 hours), **warfarin** (5 days), **clopidogrel** (5-7 days), and **ticlopidine** (10-14 days). - This order reflects the varying half-lives and durations of action of these anticoagulants and antiplatelet agents. *2>1>3>4* - This order is incorrect as it places **ticlopidine** (longest withdrawal) before **clopidogrel** despite ticlopidine having a much longer recommended withdrawal period. - It also misplaces **LMWH** and **warfarin** in relation to the antiplatelet agents. *4>3>2>1* - This order incorrectly positions **warfarin** (5 days) as having the longest pre-surgical hold time, though it is shorter than ticlopidine and clopidogrel. - It also improperly orders the antiplatelets and **LMWH** with regard to their pre-operative cessation periods. *3>4>2>1* - This order incorrectly places **ticlopidine** after **clopidogrel**, when ticlopidine requires a significantly longer cessation period prior to surgery. - It correctly places **LMWH** and **warfarin** relative to each other, but the antiplatelet order is wrong.

Question 297: Haemaccel contains -

A. Calcium
B. Albumin
C. Degraded gelatin (Correct Answer)
D. Sodium

Explanation: ***Degraded gelatin (Polygeline)*** - **Haemaccel** is a plasma volume expander that primarily consists of **degraded gelatin polypeptides (polygeline)**. - These polypeptides help to increase the **colloid osmotic pressure** of the blood, drawing fluid into the intravascular space to restore circulating volume. - This is the **main active ingredient** responsible for its volume-expanding properties. *Calcium* - While Haemaccel formulation does contain **calcium chloride** as an electrolyte, it is **not the primary active component**. - Calcium is present to maintain electrolyte balance but does not contribute to the volume-expanding effect. - The key distinguishing feature is that degraded gelatin provides the colloid osmotic effect. *Albumin* - **Albumin** is a natural plasma protein and a common component of other colloid solutions, but it is **not present in Haemaccel**. - Albumin solutions are distinct colloid preparations (e.g., human albumin 5% or 20%) used for volume expansion. - Haemaccel uses synthetic gelatin polypeptides instead of natural albumin. *Sodium* - **Sodium chloride** is present in Haemaccel as an accompanying electrolyte for maintaining osmotic balance, but it is **not the main active component**. - The primary volume-expanding agent is degraded gelatin, not sodium. - Sodium provides isotonicity but not the colloid osmotic pressure needed for volume expansion.

Question 298: Warfarin induced skin necrosis is seen in?

A. Protein S deficiency
B. Antithrombin III deficiency
C. Hemophilia
D. Protein C deficiency (Correct Answer)

Explanation: ***Protein C deficiency*** - **Warfarin-induced skin necrosis** occurs due to an initial paradoxical hypercoagulable state caused by the rapid decline of **Protein C**, a natural anticoagulant. - Individuals with **pre-existing Protein C deficiency** are at a higher risk because their baseline levels of this protective anticoagulant are already low. *Protein S deficiency* - Similar to Protein C, **Protein S** is a vitamin K-dependent anticoagulant that works with Protein C. - While Protein S deficiency can also increase the risk of thrombosis, Protein C deficiency is the more direct and common cause of warfarin-induced skin necrosis due to its rapid decline. *Antithrombin III deficiency* - **Antithrombin III** is a crucial inhibitor of thrombin and other coagulation factors, and its deficiency leads to an increased risk of venous thromboses. - However, Antithrombin III deficiency does not directly explain the specific mechanism of warfarin-induced skin necrosis, which is primarily linked to the Protein C pathway. *Hemophilia* - **Hemophilia** is a genetic bleeding disorder characterized by a deficiency in clotting factors VIII or IX, leading to impaired blood clot formation. - It is a bleeding disorder, not a thrombotic disorder, and therefore does not predispose to warfarin-induced skin necrosis; in fact, warfarin would typically be contraindicated due to bleeding risk.

Question 299: Heparin interferes with which of the following results of ABG

A. pH
B. PO2
C. PCO2
D. All of the options (Correct Answer)

Explanation: ***Correct: All of the options*** Heparin interferes with **all three major parameters** of arterial blood gas (ABG) analysis when used in excess amounts: **pH - Acidic effect:** - Heparin is an acidic solution (pH approximately 5-7) - Excess heparin in the sample causes **falsely low pH** readings - The acidic nature of heparin directly lowers the pH of the blood sample **PO2 - Dilutional and metabolic effects:** - Heparin dilutes the blood sample, affecting oxygen concentration - Can cause **falsely decreased PO2** if excess liquid heparin is used [1] - Cellular metabolism in delayed samples can consume oxygen, further reducing PO2 - Effect is more pronounced if analysis is not performed promptly **PCO2 - Dilutional effect:** - Excess heparin causes **dilution** of the blood sample - Results in **falsely decreased PCO2** readings [1] - The dilutional effect is the primary mechanism affecting PCO2 measurement **Clinical Pearl:** To minimize interference, use the minimum amount of heparin necessary (just enough to coat the syringe), avoid liquid heparin when possible, and analyze samples promptly after collection.

Question 300: Which of the following is an inhibitor of platelet aggregation?

A. Thromboxane A2
B. Leukotriene A4
C. Prostacyclin (Correct Answer)
D. Prostaglandin H2

Explanation: ***Prostacyclin*** - **Prostacyclin (PGI2)** is a potent **vasodilator** and **inhibitor of platelet aggregation**, primarily produced by endothelial cells. - It counters the pro-aggregatory effects of **thromboxane A2**, maintaining blood vessel patency. *Thromboxane A2* - **Thromboxane A2 (TXA2)** is a potent **inducer of platelet aggregation** and a **vasoconstrictor**. - It is synthesized by activated platelets and promotes thrombus formation. *Leukotriene A4* - **Leukotriene A4 (LTA4)** is an intermediate in the synthesis of other **leukotrienes** (LTC4, LTD4, LTE4), which are involved in inflammation and bronchoconstriction. - It is not directly involved in the inhibition or activation of platelet aggregation. *Prostaglandin H2* - **Prostaglandin H2 (PGH2)** is an unstable intermediate in the synthesis of both **prostacyclin** and **thromboxane A2**. - Its effects are primarily dependent on the downstream enzymes present in specific cells (e.g., endothelial cells versus platelets).

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

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Oral Anticoagulants

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Antiplatelet Drugs

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Thrombolytic Agents

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Hemostatic Drugs

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Plasma Expanders

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Blood Transfusion and Alternatives

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