Thrombotic Disorders — MCQs

10 questions

Etiology of disordered coagulation in antiphospholipid syndrome is

Deep vein thrombosis post-operatively is diagnosed by:

Disseminated intravascular coagulation (DIC) differs from thrombotic thrombocytopenic purpura. In this reference, DIC is most likely characterized by:

Hypercoagulability due to a defective factor V gene is called:

Warfarin-induced skin necrosis is more common in patients with

Which of the following is the MOST SIGNIFICANT modifiable predisposing factor for arterial thrombosis?

Factor V mutation most commonly initially presents as:-

Patient with clinical signs of DVT had tachycardia and history of bladder cancer. According to modified Well's scoring, the probability of pulmonary embolism would be :

Which of the following is the most common myeloproliferative disorder?

Q10

All of the following are seen in polycythemia rubra vera except :

Thrombotic Disorders Indian Medical PG Practice Questions and MCQs

Question 1: Etiology of disordered coagulation in antiphospholipid syndrome is

A. Hyper coagulation (Correct Answer)
B. Slow blood flow
C. Thrombocytosis
D. Vitamin K malabsorption

Explanation: ***Hyper coagulation*** - Antiphospholipid Syndrome (APS) is characterized by the presence of **antiphospholipid antibodies** that promote a **prothrombotic state**, leading to both arterial and venous clotting. [1] - These antibodies interfere with regulatory proteins of coagulation (e.g., **protein C, protein S**) and interact with phospholipids on cell surfaces, causing increased platelet activation and endothelial dysfunction. *Slow blood flow* - While **venous stasis** can contribute to thrombosis, it is not the primary etiological factor for disordered coagulation in APS itself. - Slow blood flow is a component of **Virchow's triad**, which also includes endothelial injury and hypercoagulability, with the latter being the core issue in APS. [2] *Thrombocytosis* - **Thrombocytosis** (an abnormally high platelet count) can increase the risk of thrombosis, but it is not the direct or primary cause of disordered coagulation in APS. - APS specificially involves **antibody-mediated hypercoagulability**, not just an increased number of platelets. *Vitamin K malabsorption* - **Vitamin K malabsorption** can lead to a *deficiency* in vitamin K-dependent clotting factors, typically resulting in a **bleeding tendency** rather than hypercoagulation. - This condition is associated with **hypocoagulability**, which is the opposite of the disordered coagulation seen in APS.

Question 2: Deep vein thrombosis post-operatively is diagnosed by:

A. Clinically
B. Ascending venography
C. USG (Correct Answer)
D. X-ray

Explanation: ***USG*** - **Duplex ultrasonography** is the preferred and most common imaging modality for diagnosing deep vein thrombosis (DVT) due to its non-invasive nature, accessibility, and high accuracy. - It visualizes the **vein lumen** and assesses **compressibility**, a key diagnostic feature for DVT. *Clinically* - Clinical diagnosis of DVT is unreliable, as symptoms like **leg swelling, pain, and tenderness** are non-specific and can be caused by other conditions. - While clinical suspicion can warrant further investigation, it is **insufficient for definitive diagnosis**. *Ascending venography* - **Ascending venography** was once considered the gold standard but is now rarely used due to its invasive nature, use of ionizing radiation, and potential complications. - It involves injecting **radiocontrast dye** into a foot vein and taking X-rays, making it less practical for routine use compared to ultrasound. *X-ray* - **X-rays do not directly visualize veins** or blood clots and are therefore not useful for diagnosing DVT. - They may be used to rule out other causes of leg pain or swelling, such as **bone fractures** or **arthritis**, but offer no diagnostic value for DVT itself.

Question 3: Disseminated intravascular coagulation (DIC) differs from thrombotic thrombocytopenic purpura. In this reference, DIC is most likely characterized by:

A. Elevated reticulocyte count
B. Low levels of coagulation factors (Correct Answer)
C. Severe thrombocytopenia
D. Presence of schistocytes in the blood smear

Explanation: ***Decreased coagulation factor levels*** - DIC is characterized by an activation of the coagulation cascade, leading to increased consumption of **coagulation factors** and resulting in low levels [1]. - This process causes a paradoxical increased risk of bleeding despite a **consumption coagulopathy** scenario [1]. *Significant thrombocytopenia* - While thrombocytopenia can occur in DIC, it is not as pronounced as in **thrombotic thrombocytopenic purpura** (TTP), which features **severe thrombocytopenia** as its hallmark [2]. - DIC typically presents with **variable platelet counts**, often fluctuating based on the underlying cause. *A brisk reticulocytosis* - Reticulocytosis is common in hemolytic processes, but it is not a defining characteristic of DIC, which primarily involves dysfunction in the **coagulation cascade** rather than increased red blood cell production. - In contrast, TTP may show reticulocytosis due to hemolysis, but this does not apply directly to DIC. *Significant numbers of schistocytes* - Schistocytes are seen in microangiopathic hemolytic anemias, but **quantity and significance** vary; they may not be prominently present in DIC cases compared to TTP, which is distinguished by more pronounced schistocytes [2]. - DIC primarily leads to a **consumption coagulopathy**, whereas schistocytes more specifically indicate **mechanical hemolysis** [2].

Question 4: Hypercoagulability due to a defective factor V gene is called:

A. Lisbon mutation
B. Antiphospholipid syndrome
C. Inducible thrombocytopenia syndrome
D. Leiden mutation (Correct Answer)

Explanation: ***Leiden mutation*** - The **Leiden mutation** refers specifically to a mutation in the **factor V gene** that leads to a hypercoagulable state, particularly increasing the risk of venous thromboembolism [1]. - It causes resistance to **activated protein C**, which normally regulates blood clotting, thus contributing to sustained clot formation [1]. *Lisbon mutation* - The **Lisbon mutation** is not a recognized term in the context of coagulation disorders or factor V. - There is no clinical relevance tied to clotting abnormalities related specifically to this mutation in the scientific literature. *Antiphospholipid syndrome* - Antiphospholipid syndrome is an autoimmune disorder characterized by **thrombosis** and pregnancy complications, but not specifically linked to the **factor V gene**. - It involves antibodies against phospholipids, which is unrelated to the genetic mutations affecting factor V. *Inducible thrombocytopenia syndrome* - This syndrome primarily involves **low platelet counts** induced by certain medications or conditions, not a defect in **factor V**. - It does not relate to hypercoagulability but rather to bleeding risks due to the **decreased platelet count**. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, pp. 133-134.

Question 5: 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 6: Which of the following is the MOST SIGNIFICANT modifiable predisposing factor for arterial thrombosis?

A. Antiphospholipid syndrome
B. Hyperlipidemia
C. Cigarette smoking (Correct Answer)
D. Homocystinuria

Explanation: ***Cigarette smoking*** - **Cigarette smoking** is a major modifiable risk factor for **atherosclerosis** and arterial thrombosis, primarily by promoting endothelial dysfunction, inflammation, and hypercoagulability. [1] - It damages the **endothelium**, leading to plaque formation and increasing the risk of **thrombotic events** such as myocardial infarction and stroke. [1] *Antiphospholipid syndrome* - This is an **autoimmune disorder** causing recurrent arterial and venous thromboses, but it is not a modifiable lifestyle factor. - While it dramatically increases thrombosis risk, therapeutic management focuses on anticoagulation rather than lifestyle modification. *Hyperlipidemia* - **Hyperlipidemia**, particularly elevated LDL cholesterol, is a significant risk factor for **atherosclerosis**, which can lead to thrombosis. [1] - However, while modifiable through diet and medication, its immediate thrombotic impact is often mediated through chronic plaque formation, whereas smoking has more direct prothrombotic effects on endothelium and platelet function. *Homocystinuria* - This is a rare, inherited **metabolic disorder** causing elevated homocysteine levels, leading to severe premature atherosclerosis and **thrombotic disease**. - It is a genetic condition and therefore not a modifiable risk factor in the same way as lifestyle choices.

Question 7: Factor V mutation most commonly initially presents as:-

A. Thrombosis
B. Disseminated Intravascular Coagulation (DIC)
C. Pulmonary Embolism
D. Deep Vein Thrombosis (DVT) (Correct Answer)

Explanation: ***Deep Vein Thrombosis (DVT)*** - Factor V Leiden mutation is a common inherited **thrombophilia**, significantly increasing the risk of **venous thromboembolism (VTE)**. - While VTE encompasses DVT and pulmonary embolism, **DVT is the most frequent initial presentation** because it is the primary thrombotic event leading to other complications [2]. *Thrombosis* - This is a general term for the formation of a **blood clot** that obstructs blood flow. - While Factor V Leiden causes thrombosis, **DVT is a specific and common type** of thrombosis that typically presents first [1]. *Disseminated Intravascular Coagulation (DIC)* - DIC is a complex, life-threatening condition characterized by widespread activation of coagulation leading to both **thrombosis and hemorrhage**. - It is typically triggered by severe underlying conditions like sepsis or trauma, and is **not a primary presentation of Factor V Leiden mutation**. *Pulmonary Embolism (PE)* - PE occurs when a **blood clot travels to the lungs**, often originating from a DVT. - While Factor V Leiden increases PE risk, **DVT is usually the antecedent event** and thus the more common initial clinical presentation [1].

Question 8: Patient with clinical signs of DVT had tachycardia and history of bladder cancer. According to modified Well's scoring, the probability of pulmonary embolism would be :

A. Low
B. High
C. Intermediate (Correct Answer)
D. Intermediate

Explanation: **Intermediate** - Clinical signs of **DVT (3 points)**, **tachycardia (heart rate > 100 bpm, 1.5 points)**, and a history of **cancer (1 point)** sum up to 5.5 points, which falls within the range for an intermediate probability (2-6 points) on the modified Well's score for PE. - The modified Well's criteria assigns specific points for risk factors and clinical findings, guiding the diagnostic approach for pulmonary embolism [1]. *Low* - A low probability for PE according to the modified Well's score is indicated by a total score of **less than 2 points** [1]. - The patient's presentation accumulates significantly more points than this threshold due to multiple contributing factors. *High* - A high probability for PE according to the modified Well's score is indicated by a total score of **greater than 6 points** [1]. - The patient's score of 5.5 points does not meet this threshold, placing them in the intermediate category.

Question 9: Which of the following is the most common myeloproliferative disorder?

A. Essential Thrombocythemia (Correct Answer)
B. Polycythemia rubra vera
C. CML
D. Myelofibrosis

Explanation: ***Essential Thrombocythemia*** - **Essential thrombocythemia (ET)** is the **most common myeloproliferative neoplasm**, with an incidence of approximately 1.5-2.4 per 100,000 per year. - It is characterized by **persistent thrombocytosis** (platelet count >450,000/μL) and megakaryocytic proliferation [1]. - Commonly associated with **JAK2 V617F mutation** (~55-60%), **CALR mutations** (~25-30%), and **MPL mutations** (~3-5%) [2]. *Polycythemia rubra vera* - **Polycythemia vera (PV)** is the **second most common** classic MPN, with an incidence of approximately 0.8-2.3 per 100,000 per year. - Characterized by increased red blood cell mass, often with leukocytosis and thrombocytosis [1]. - Strongly associated with **JAK2 V617F mutation** (present in >95% of cases) [2][3]. *CML* - **Chronic myeloid leukemia (CML)** has similar incidence to PV (approximately 1-2 per 100,000 per year). - Defined by the presence of the **Philadelphia chromosome (BCR-ABL1 fusion gene)** [2]. - Treated distinctly with tyrosine kinase inhibitors (TKIs). *Myelofibrosis* - **Primary myelofibrosis (PMF)** is the **least common** of the classic MPNs, with an incidence of approximately 0.3-1.5 per 100,000 per year. - Characterized by bone marrow fibrosis, extramedullary hematopoiesis, and splenomegaly [3]. - Associated with **JAK2, CALR, or MPL mutations** [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, pp. 627-628. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, p. 624. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 614-615.

Question 10: All of the following are seen in polycythemia rubra vera except :

A. Increased platelets
B. Increased Vit B12 binding capacity (>9000 micromols/dL)
C. Leucocytosis
D. Decreased LAP Score (Correct Answer)

Explanation: ***Decreased LAP Score*** - **LAP (Leukocyte Alkaline Phosphatase) score** is typically **increased or normal** in polycythemia vera. - A decreased LAP score is characteristic of **chronic myeloid leukemia (CML)**, which must be differentiated from polycythemia vera [2]. *Increased platelets* - **Thrombocytosis** (increased platelets) is a common feature of **polycythemia vera**, often contributing to vascular complications [1], [2]. - The unregulated proliferation of all myeloid cell lines, including megakaryocytes, leads to this increase [1], [3]. *Increased Vit B12 binding capacity (>9000 micromols/dL)* - Polycythemia vera often leads to **increased vitamin B12 levels** and **binding capacity** due to increased production of **transcobalamin I** by proliferating granulocytes. - While not a direct diagnostic criterion, it is a frequent finding supportive of the diagnosis. *Leucocytosis* - **Leukocytosis** (increased white blood cell count), particularly granulocytosis, is a common feature of polycythemia vera [1], [2]. - It results from the **clonal proliferation** of myeloid stem cells, leading to an overproduction of all myeloid lineage cells [1]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 614-615. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, pp. 626-627. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, pp. 627-628.

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