Thrombotic Disorders Indian Medical PG Practice Questions and MCQs
Practice Indian Medical PG questions for Thrombotic Disorders. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Thrombotic Disorders Indian Medical PG 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
Thrombotic Disorders 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.
Thrombotic Disorders Indian Medical PG Question 2: Deep vein thrombosis post-operatively is diagnosed by:
- A. Clinically
- B. Ascending venography
- C. USG (Correct Answer)
- D. X-ray
Thrombotic Disorders 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.
Thrombotic Disorders Indian Medical PG 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
Thrombotic Disorders 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].
Thrombotic Disorders Indian Medical PG 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)
Thrombotic Disorders 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.
Thrombotic Disorders Indian Medical PG 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
Thrombotic Disorders 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.
Thrombotic Disorders Indian Medical PG 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
Thrombotic Disorders 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.
Thrombotic Disorders Indian Medical PG 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)
Thrombotic Disorders 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].
Thrombotic Disorders Indian Medical PG 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
Thrombotic Disorders 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.
Thrombotic Disorders Indian Medical PG 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
Thrombotic Disorders 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.
Thrombotic Disorders Indian Medical PG 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)
Thrombotic Disorders 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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