Coagulation Disorders — MCQs

10 questions

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

Bernard–Soulier syndrome is caused by a deficiency of which glycoprotein complex?

In a platelet poor plasma sample calcium and tissue thromboplastin are added. This is used to assess which of the following pathways?

Which of the following is not involved in local hemostasis?

Following injury to a blood vessel, immediate hemostasis is achieved by:

A35 yr old lady with Normal PT and increased aPTT. 2 year back, she was operated for cholecystectomy & did not have any bleeding episode. What is next investigation for clinical diagnosis -

What is a known complication of Parvovirus B19 infection?

Which of the following snakes is most commonly associated with hematologic abnormalities following envenomation?

Treatment of choice in severe dehydration is:

Q10

Which of the following conditions is primarily associated with stasis as a cause of thrombosis?

Coagulation Disorders Indian Medical PG Practice Questions and MCQs

Question 1: 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 2: Bernard–Soulier syndrome is caused by a deficiency of which glycoprotein complex?

A. TNF
B. von Willebrand factor (vWf)
C. Gp Ib-IX-V complex (Correct Answer)
D. Gp IIb/IIIa

Explanation: ***Gp 1b*** - Bernard–Soulier syndrome is primarily caused by a deficiency in **Gp1b**, which is crucial for platelet adhesion to the von Willebrand factor (vWF) [1]. - This results in **thrombocytopenia** and large platelets, which are characteristic features of the syndrome. *Gp 2b/3a* - Gp2b/3a is associated with **Glanzmann thrombasthenia**, not Bernard–Soulier syndrome [1]. - This receptor is essential for platelet aggregation and binds fibrinogen, contributing to a different bleeding disorder. *TNF* - Tumor Necrosis Factor (TNF) is a cytokine involved in systemic inflammation and does not directly relate to platelet function or deficiencies. - Deficiency of TNF is unrelated to bleeding disorders like Bernard–Soulier syndrome. *vWf* - von Willebrand factor (vWf) deficiency is associated with **von Willebrand disease**, which presents differently than Bernard–Soulier syndrome. - vWf is essential for the aggregation of platelets but is not the deficient factor in this syndrome. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 668-669.

Question 3: In a platelet poor plasma sample calcium and tissue thromboplastin are added. This is used to assess which of the following pathways?

A. Common
B. Intrinsic
C. Extrinsic (Correct Answer)
D. Fibrinolytic

Explanation: ***Extrinsic*** - The addition of **tissue thromboplastin** (containing tissue factor) and **calcium** to platelet-poor plasma directly activates the extrinsic pathway of coagulation. - This combination is used in the **prothrombin time (PT)** test, which specifically measures the integrity of the extrinsic and common pathways. *Common* - While the common pathway is utilized in this test, the direct activators of tissue thromboplastin and calcium specifically initiate the extrinsic pathway, which then feeds into the common pathway. - The PT test assesses the common pathway, but the initial trigger for the test setup outlined is the extrinsic arm. *Intrinsic* - The intrinsic pathway is initiated by factors present within the blood, such as contact with a negatively charged surface (e.g., glass), and is assessed by the **activated partial thromboplastin time (aPTT)**. - Tissue thromboplastin is not a component of the intrinsic pathway activation cascade. *Fibrinolytic* - The fibrinolytic pathway is responsible for the breakdown of clots and involves plasminogen activators and plasmin. - The addition of calcium and tissue thromboplastin is designed to initiate clot formation, not clot breakdown.

Question 4: Which of the following is not involved in local hemostasis?

A. Fibrinogen
B. Collagen
C. Calcium
D. Vitamin K (Correct Answer)

Explanation: ***Vitamin K*** - **Vitamin K** is crucial for the synthesis of **clotting factors (II, VII, IX, X, protein C, protein S)** in the liver, which are part of the **coagulation cascade** (secondary hemostasis). - Its role is systemic, affecting the production of factors involved in blood coagulation throughout the body, rather than directly participating in the *local* events at the site of injury. *Fibrinogen* - **Fibrinogen** is a soluble protein that is converted to **insoluble fibrin** by thrombin, forming the meshwork of the **blood clot** at the site of injury. - This conversion is a critical local event in strengthening the primary platelet plug during hemostasis. *Collagen* - Exposed **collagen** in the damaged vessel wall directly activates **platelets** (leading to their adhesion and aggregation) and also initiates the **intrinsic pathway** of the coagulation cascade. - It provides the initial signal and a crucial binding site for platelets, essential for forming the primary hemostatic plug. *Calcium* - **Calcium ions (Ca2+)** are essential cofactors for several steps in the **coagulation cascade**, including the activation of various clotting factors (e.g., factors X, IX, VIII, V, and prothrombin). - Its presence is required for the proper functioning of enzyme complexes that form on platelet surfaces, facilitating the generation of thrombin and fibrin at the local injury site.

Question 5: Following injury to a blood vessel, immediate hemostasis is achieved by:

A. Fibrin deposition
B. Vasoconstriction (Correct Answer)
C. Platelet adhesion
D. Thrombosis

Explanation: ***Vasoconstriction*** - Following blood vessel injury, **vasoconstriction** occurs immediately, reducing blood flow and minimizing blood loss. - It is a **reflex response** mediated by local factors and neural mechanisms aiming to maintain hemostasis. *Fibrin deposition* - **Fibrin deposition** occurs later in the hemostatic process, primarily during the **coagulation phase** after initial vascular responses. - It is not an immediate response; rather, it's part of the **clot stabilization** process, requiring activation of the clotting cascade. *Thrombosis* - Thrombosis refers to the formation of a **blood clot** within a vessel, which happens after initial hemostatic mechanisms are activated. - It is not the **immediate** response post-injury; there is a sequence of events that lead to thrombosis after vasoconstriction and platelet activation. *Platelet adhesion* - Although platelet adhesion is crucial in hemostasis, it occurs following **vasoconstriction** and is not an immediate response to vessel injury [1][2]. - This process is part of the **primary hemostasis** phase, which cannot occur efficiently without prior initial vasoconstriction. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 581-582. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, p. 128.

Question 6: A35 yr old lady with Normal PT and increased aPTT. 2 year back, she was operated for cholecystectomy & did not have any bleeding episode. What is next investigation for clinical diagnosis -

A. Platelet aggregation test
B. Anti viper venom assay
C. Ristocetin cofactor assay
D. Factor VIII assay (Correct Answer)

Explanation: ***Factor VIII assay*** - An isolated **increased aPTT** with a **normal PT** points to an abnormality in the **intrinsic pathway** of coagulation, which includes Factor VIII [1]. - The absence of bleeding episodes for a cholecystectomy suggests a **mild deficiency** or a defect that doesn't cause severe hemorrhage, making Factor VIII deficiency (Hemophilia A) a strong consideration [2]. *Platelet aggregation test* - This test evaluates **platelet function**, abnormalities of which typically present with mucocutaneous bleeding and a normal PT and aPTT. - The patient's presentation of an isolated prolonged aPTT does not primarily suggest a platelet function disorder. *Anti viper venom assay* - This test is primarily used to detect the presence of **lupus anticoagulant**, which can cause a prolonged aPTT but is often associated with thrombotic events, not bleeding. - While lupus anticoagulant can prolong aPTT without bleeding, a Factor VIII deficiency is a more common cause of an isolated prolonged aPTT that is compatible with no significant bleeding history. *Ristocetin cofactor assay* - This assay is used to evaluate **von Willebrand factor (vWF)** activity, which is involved in platelet adhesion and also stabilizes Factor VIII [3]. - While vWF deficiency can cause a prolonged aPTT, it typically presents with mucocutaneous bleeding, and the patient's history doesn't strongly suggest this [3].

Question 7: What is a known complication of Parvovirus B19 infection?

A. Erythema infectiosum
B. Arthritis
C. Aplastic anemia (Correct Answer)
D. All of the options

Explanation: Aplastic anemia - Parvovirus B19 has a tropism for erythroid progenitor cells in the bone marrow, specifically targeting and destroying them [1]. - This destruction can lead to a transient aplastic crisis, especially in individuals with pre-existing hemolytic conditions, causing a severe drop in red blood cell production [1]. Erythema infectiosum - This is the most common clinical manifestation of Parvovirus B19 infection, also known as fifth disease, characterized by a "slapped cheek" rash [1]. - While it is a symptom or disease caused by the virus, it is not considered a complication in the sense of a secondary, adverse outcome. Arthritis - Arthralgia and arthritis are common manifestations of Parvovirus B19 infection, particularly in adults, especially women [1]. - Similar to erythema infectiosum, it is a direct clinical manifestation rather than a "complication" representing a secondary, undesirable event. All of the options - While erythema infectiosum and arthritis are common clinical presentations of Parvovirus B19, they are direct disease manifestations. - Aplastic anemia stands out as a true complication, representing a secondary and potentially severe adverse outcome due to the virus's specific cellular tropism [1].

Question 8: Which of the following snakes is most commonly associated with hematologic abnormalities following envenomation?

A. Sea snake
B. Krait
C. Viper (Correct Answer)
D. Cobra

Explanation: ***Correct Answer: Viper*** - **Viper venom** contains **hemotoxic components** including **metalloproteinases** and **serine proteinases** that directly activate clotting factors - This leads to **consumptive coagulopathy** characterized by **thrombocytopenia**, **hypofibrinogenemia**, and prolonged coagulation times - Clinical manifestations include spontaneous **bleeding**, **ecchymoses**, **hemorrhage** at the bite site, and in severe cases, **disseminated intravascular coagulation (DIC)** - Viper envenomation is the **classic cause** of hematologic abnormalities among snake bites *Incorrect: Sea snake* - Sea snake venoms are primarily **neurotoxic** and **myotoxic**, causing paralysis and muscle damage - While they can cause **rhabdomyolysis** and subsequent **renal failure**, significant primary hematologic abnormalities are not their hallmark feature *Incorrect: Krait* - Krait venom is predominantly **neurotoxic**, leading to **flaccid paralysis** and **respiratory failure** - Does not typically cause the significant widespread **coagulopathies** seen with viper envenomation *Incorrect: Cobra* - Cobra venom primarily contains **neurotoxins** and **cytotoxins**, causing **paralysis**, **tissue necrosis**, and localized pain - While some cobras can cause minor local bleeding, they do not generally induce the severe and systemic **hematologic abnormalities** characteristic of viper bites

Question 9: Treatment of choice in severe dehydration is:

A. Plasma
B. Isolyte P
C. Ringer lactate
D. Normal saline (Correct Answer)

Explanation: ***Normal saline*** - **Normal saline (0.9% sodium chloride)** is an isotonic solution, making it the preferred initial intravenous fluid for rapidly correcting severe dehydration and restoring intravascular volume [1]. - Its **electrolyte composition** closely mimics the body's extracellular fluid, minimizing osmotic shifts and providing effective volume expansion [1]. *Plasma* - **Plasma** is primarily used for expanding blood volume in cases of **hemorrhage** or severe **protein deficiency**, not for simple dehydration. - It carries risks of allergic reactions and disease transmission, making it inappropriate for routine dehydration treatment. *Isolyte P* - **Isolyte P** is a hypotonic solution, typically used for maintenance fluid therapy in children, especially in situations where **sodium restriction** is desirable. - It is not suitable for rapid volume expansion in severe dehydration due to its low sodium content, which could worsen hypotonicity in an already depleted patient. *Ringer lactate* - **Ringer's lactate** is an isotonic crystalloid solution often used for fluid resuscitation, but it contains **lactate**, which is metabolized in the liver to bicarbonate. - While generally safe, in severe shock situations with impaired liver function or lactic acidosis, the metabolism of lactate can be compromised, potentially exacerbating acidosis. **Normal saline** avoids this concern as a first-line agent [2].

Question 10: Which of the following conditions is primarily associated with stasis as a cause of thrombosis?

A. Polycythemia
B. Dehydration
C. Sickle cell anemia
D. Venous stasis (Correct Answer)

Explanation: ***All of the above*** - Stasis can contribute to **thrombosis in various conditions**, including polycythemia, as it increases blood viscosity, and in sickle cell anemia due to impaired blood flow [2]. - **Venous circulation** is particularly affected by stasis, as it leads to venous thromboembolism, making it a critical factor in thrombosis [1]. *Polycythemia* - While **polycythemia** leads to increased blood viscosity, stasis itself isn't the primary mechanism for thrombosis in this condition. - Thrombosis in polycythemia is more due to *hyperviscosity* rather than stasis alone. *Venous circulation* - While stasis is indeed significant in **venous circulation**, it does not capture the full spectrum of thrombosis causes in the context of various conditions [1]. - Other factors such as **hypercoagulability** and **vascular injury** also contribute, making it not solely reliant on stasis [1]. *Sickle cell Anemia* - Thrombosis in sickle cell anemia occurs mainly due to **occlusion** from sickled cells, rather than stasis leading to thrombus formation [2]. - While stasis can occur, it is not the principal cause of thrombosis in this disease [2].

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