Platelets and Hemostasis — MCQs
Activated protein C inhibits the clotting mechanism by inactivating which of the following clotting factors?
Hemophilia B is a deficiency of which factor?
Von Willebrand factor is secreted by which of the following?
The clot formed after the coagulation cascade is not stable unless extensive cross-linking occurs. This is done by:
Which of the following is not typically seen in Disseminated Intravascular Coagulation (DIC)?
NO acts on platelets through what mechanism?
All of the following are true about blood coagulation, except which of the following?
Cortisol increases all of the following components except:
A patient on aspirin for secondary prevention of cardiovascular disease is selected for an elective surgery with low-to-moderate bleeding risk. What should be done regarding aspirin management?
Cortisol increases all of the following components, EXCEPT:
Platelets and Hemostasis Indian Medical PG Practice Questions and MCQs
Question 1: Activated protein C inhibits the clotting mechanism by inactivating which of the following clotting factors?
- A. Factor Va and Factor VIIIa (Correct Answer)
- B. Factor III and Factor VIIIa
- C. Factor VIIIa and Factor IX
- D. Factor Va and Factor VII
Explanation: ***Factor Va and Factor VIIIa*** - **Activated protein C (APC)** functions as a natural anticoagulant by specifically inactivating the activated forms of **Factor V (Va)** and **Factor VIII (VIIIa)**. - By inactivating these cofactors, APC effectively downregulates the functioning of the **prothrombinase complex** and **tenase complex**, thereby slowing down thrombin generation and subsequent fibrin formation. *Factor III and Factor VIIIa* - **Factor III (tissue factor)** initiates the extrinsic coagulation pathway, but it is not directly inactivated by activated protein C. - While **Factor VIIIa** is a target of APC, the combination with Factor III makes this option incorrect. *Factor VIIIa and Factor IX* - **Factor VIIIa** is indeed inactivated by APC. - However, **Factor IX** (the inactive zymogen) and its activated form **Factor IXa** are not direct targets for inactivation by APC; Factor IXa remains active to participate in the tenase complex until its co-factor Factor VIIIa is inactivated. *Factor Va and Factor VII* - **Factor Va** is a known target for inactivation by APC. - **Factor VII** (the inactive zymogen) and its activated form **Factor VIIa** are not inactivated by APC; Factor VIIa plays a role in the initiation of coagulation by forming a complex with tissue factor.
Question 2: Hemophilia B is a deficiency of which factor?
- A. IX (Correct Answer)
- B. XII
- C. VIII
- D. X
Explanation: ***IX*** - Hemophilia B, also known as **Christmas disease**, is caused by a deficiency in **Factor IX** [1]. - This condition is an **X-linked recessive disorder** that impairs the blood's ability to form clots, leading to prolonged bleeding [1]. *XII* - Deficiency in **Factor XII** (Hageman factor) is usually **asymptomatic** and does not lead to a bleeding disorder. - Individuals with Factor XII deficiency often have a **prolonged aPTT** but no clinical bleeding. *VIII* - A deficiency in **Factor VIII** causes **Hemophilia A**, which is the more common form of hemophilia [1]. - Hemophilia A also presents with bleeding symptoms, but it is distinct from Hemophilia B due to the specific factor involved [1]. *X* - Deficiency in **Factor X** (Stuart-Prower factor) is a rare **autosomal recessive** bleeding disorder. - Factor X deficiency affects both the intrinsic and extrinsic coagulation pathways, leading to prolongation of both **PT and aPTT**.
Question 3: Von Willebrand factor is secreted by which of the following?
- A. Platelets
- B. Fibroblasts
- C. Macrophages
- D. Endothelial cells (Correct Answer)
Explanation: ***Endothelial cells*** - **Von Willebrand factor (vWF)** is primarily synthesized and secreted by **endothelial cells** lining blood vessels. - It is stored in **Weibel-Palade bodies** within endothelial cells and is released upon stimulation, playing a crucial role in **hemostasis**. *Platelets* - While **platelets** can bind to and carry vWF, they do not synthesize it. - Platelets have **vWF receptors** (e.g., glycoprotein Ib) that allow them to adhere to vWF at sites of vascular injury. *Fibroblast* - **Fibroblasts** are connective tissue cells that produce components of the extracellular matrix, such as collagen and elastin. - They are not involved in the synthesis or secretion of **vWF**. *Macrophages* - **Macrophages** are immune cells involved in phagocytosis and antigen presentation. - They do not produce **vWF**; their primary role is in immune surveillance and removal of cellular debris.
Question 4: The clot formed after the coagulation cascade is not stable unless extensive cross-linking occurs. This is done by:
- A. Plasmin
- B. Factor XIII (Correct Answer)
- C. Thrombin
- D. High molecular weight kininogen
Explanation: ***Factor XIII*** - **Factor XIIIa** (activated Factor XIII) is a **transglutaminase** that catalyzes the formation of **covalent bonds** between **fibrin monomers**, specifically between lysine and glutamine residues. - This cross-linking strengthens the **fibrin clot**, making it more resistant to mechanical stress and proteolytic degradation. *Plasmin* - **Plasmin** is an enzyme responsible for **fibrinolysis**, meaning it breaks down fibrin clots. - It acts to remodel and **dissolve clots**, not to stabilize them. *Thrombin* - **Thrombin** (Factor IIa) is a key enzyme in the coagulation cascade that converts **fibrinogen into fibrin monomers**. - While essential for clot formation, thrombin's primary role is to create the fibrin mesh, not to extensively cross-link it for stability. *High molecular weight kininogen* - **High molecular weight kininogen (HMWK)** is a cofactor in the **intrinsic coagulation pathway**, facilitating the activation of Factor XII and prekallikrein. - It is involved in initiating coagulation but does not directly participate in the cross-linking and stabilization of the fibrin clot.
Question 5: Which of the following is not typically seen in Disseminated Intravascular Coagulation (DIC)?
- A. Thrombocytopenia
- B. PT elevation
- C. Fibrinogen decreased
- D. Normal aPTT (Correct Answer)
Explanation: ***Normal APTT*** - In Disseminated Intravascular Coagulation (**DIC**), **APTT** is typically **prolonged** due to consumption of clotting factors [1]. - The presence of normal APTT indicates that coagulation pathways are not significantly affected, which is contrary to what is seen in DIC. *Fibrinogen decreased* - **Decreased fibrinogen levels** are common in DIC, reflecting its consumption during the coagulation process [1]. - This depletion is linked to the increased clotting and is a hallmark of DIC, making this statement false in the context of the question. *Thrombocytopenia* - **Thrombocytopenia** occurs in DIC as platelets are consumed during the formation of microclots [1]. - A significant drop in platelet count is a key feature of DIC, therefore this statement does not align with the "except" clause. *PT elevation* - Prothrombin Time (**PT**) is usually **elevated** in DIC due to the consumption of clotting factors [1]. - This reflects the ongoing activation of the coagulation cascade, supporting the exclusion in the question context. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 625-626.
Question 6: NO acts on platelets through what mechanism?
- A. Adenosine
- B. cGMP (Correct Answer)
- C. cAMP
- D. TXA2
Explanation: ***cGMP (inhibits platelet activation)*** - **Nitric oxide (NO)** diffuses into platelets and activates **guanylate cyclase**, leading to an increase in intracellular **cyclic guanosine monophosphate (cGMP)**. - Elevated **cGMP** levels then activate protein kinase G, which phosphorylates various proteins involved in platelet signaling, ultimately inhibiting **platelet activation**, adhesion, and aggregation. *cAMP (modulates platelet function through other pathways)* - While **cAMP** also plays a role in inhibiting platelet aggregation, it is primarily generated through the activation of **adenylyl cyclase** by agents like **prostacyclin (PGI2)**, not directly by NO. - NO's direct effect on platelets is mediated by **cGMP**, not **cAMP**. *Adenosine (vasodilator)* - **Adenosine** is a nucleoside known for its **vasodilatory** properties and can also influence platelet function, but it is not the primary mechanism by which NO acts on platelets. - **Adenosine** exerts its effects by activating specific **purinergic receptors** on the platelet surface, distinct from NO's intracellular signaling pathway. *TXA2 (a mediator of platelet aggregation and vasoconstriction)* - **Thromboxane A2 (TXA2)** is a potent **pro-aggregatory** and **vasoconstrictive** eicosanoid produced by platelets through the **cyclooxygenase pathway**. - NO's action on platelets is to *antagonize* the effects of **TXA2**, promoting **platelet inhibition** rather than mediating it.
Question 7: All of the following are true about blood coagulation, except which of the following?
- A. Factor X directly activates both intrinsic and extrinsic pathways. (Correct Answer)
- B. Calcium is required in several steps of coagulation.
- C. Extrinsic pathway is activated by tissue factor released from damaged tissues.
- D. Intrinsic pathway can be activated in vitro by contact with collagen.
Explanation: ***Extrinsic pathway is activated by contact with negatively charged surfaces*** - The **extrinsic pathway** is actually activated by tissue factor, not by contact with negatively charged surfaces [1]. - This statement is therefore **incorrect**, making it the exception among the other statements. *Factor X is part of both intrinsic and extrinsic pathways* - Factor X is indeed a key component involved in both the **intrinsic** and **extrinsic pathways** of coagulation, leading to the common pathway [1]. - The presence of Factor X is crucial for the conversion of prothrombin to thrombin in both pathways [2]. *Calcium is required in several steps of coagulation* - Calcium (**factor IV**) is essential for several reactions in the coagulation cascade, playing a pivotal role in both pathways [1]. - It acts as a cofactor that facilitates various enzyme-substrate interactions necessary for the coagulation process [2]. *Intrinsic pathway can be activated in vitro* - The **intrinsic pathway** can be activated in vitro using substances like kaolin or glass that promote contact activation [1]. - This means the statement is not an exception, as it's true regarding the properties of the intrinsic pathway. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, pp. 128-130. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 582-583.
Question 8: Cortisol increases all of the following components except:
- A. Monocytes
- B. RBCs
- C. Platelets
- D. Eosinophils (Correct Answer)
Explanation: ***Eosinophils*** - Cortisol causes **eosinopenia** (a decrease in eosinophils) by increasing their sequestration in tissues and promoting their apoptosis. - This effect is a classic indicator of stress and can be observed in conditions of elevated endogenous or exogenous cortisol. *Monocytes* - Cortisol typically causes a **mild monocytosis** (increase in circulating monocytes), although this effect can vary. - It impacts the trafficking and differentiation of monocytes, leading to their transient increase in the bloodstream. *RBCs* - Cortisol can lead to a slight **increase in red blood cell (RBC) count** or hemoglobin concentration. - This effect is partly due to hemoconcentration and partly by promoting erythropoiesis. *Platelets* - Cortisol generally causes a **thrombocytosis** (increase in platelet count). - This effect is thought to be mediated by various factors, including cytokine interactions and direct effects on megakaryopoiesis.
Question 9: A patient on aspirin for secondary prevention of cardiovascular disease is selected for an elective surgery with low-to-moderate bleeding risk. What should be done regarding aspirin management?
- A. Stop aspirin for 7 days
- B. Infusion of fresh frozen plasma
- C. Infusion of platelet concentrate
- D. Go ahead with surgery maintaining adequate hemostasis (Correct Answer)
Explanation: ***Go ahead with surgery maintaining adequate hemostasis*** - For patients on **aspirin for secondary prevention** undergoing **low-to-moderate bleeding risk elective surgery**, current guidelines (ACC/AHA, ESC) recommend **continuing aspirin** perioperatively. - The risk of **major adverse cardiovascular events** (MI, stroke, cardiovascular death) from stopping aspirin outweighs the increased bleeding risk in most surgical procedures. - **Adequate hemostasis** can typically be achieved with careful surgical technique, and aspirin-related bleeding is usually manageable. - Examples of low-moderate risk surgeries: most general surgical procedures, orthopedic procedures, dental procedures, cataract surgery. *Stop aspirin for 7 days* - Stopping aspirin **7-10 days** before surgery is recommended only for **high-bleeding-risk procedures** where bleeding would be catastrophic (intracranial neurosurgery, spinal canal surgery, posterior chamber eye surgery, transurethral prostate resection). - This allows time for **platelet function recovery** (platelet lifespan is 7-10 days), as aspirin irreversibly inhibits platelet cyclooxygenase. - However, for **low-to-moderate risk surgeries**, stopping aspirin increases thrombotic risk without sufficient bleeding risk reduction benefit. *Infusion of fresh frozen plasma* - **Fresh frozen plasma (FFP)** contains clotting factors but **no functional platelets**, so it cannot reverse aspirin's antiplatelet effect. - Aspirin inhibits **platelet function**, not coagulation factors, making FFP ineffective for this indication. - FFP is used for **coagulation factor deficiencies**, warfarin reversal, or massive transfusion protocols—not for aspirin-induced platelet dysfunction. *Infusion of platelet concentrate* - **Platelet transfusion** is not routinely recommended prophylactically for aspirin-treated patients undergoing surgery. - It may be considered for **active severe bleeding** during surgery when aspirin is contributing, or in emergency high-risk procedures when aspirin cannot be stopped in advance. - Routine prophylactic platelet transfusion has **transfusion-related risks** (infection, allergic reactions, TRALI) that outweigh benefits in elective surgery.
Question 10: Cortisol increases all of the following components, EXCEPT:
- A. Platelets
- B. Monocytes
- C. RBCs
- D. Eosinophils (Correct Answer)
Explanation: ***Eosinophils*** - **Cortisol** is a powerful **anti-inflammatory** and immunosuppressive hormone that causes a decrease in circulating eosinophils. This is a classic finding in states of **hypercortisolism** (e.g., Cushing's syndrome) or stress. - The suppressive effect on eosinophils is due to their increased apoptotic rate and decreased release from the bone marrow under glucocorticoid influence. *Platelets* - **Cortisol** can indirectly increase platelets, particularly during chronic stress or inflammation, although this effect is not as direct or immediate as other blood components. - Increased cortisol levels are associated with a **thrombophilic state**, which can include elevated platelet counts. *Monocytes* - **Cortisol** generally causes a transient increase in circulating monocytes. - This effect is part of the early immune response induced by glucocorticoids, mobilizing monocytes from the marginated pool. *RBC's* - **Cortisol** stimulates **erythropoiesis**, leading to an increase in red blood cell (RBC) production. - This is partly mediated by increased production of **erythropoietin** and direct effects on bone marrow progenitor cells.
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