Platelet Disorders — MCQs

10 questions

Which of the following statements best describes the underlying mechanism of heparin-induced thrombocytopenia?

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

In shigella dysentery associated hemolytic uremic syndrome, the false statement is ?

A previously healthy child has sudden onset of red spots on body. There is a history of a preceding viral infection 1-4 weeks before the onset.

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

Thrombotic thrombocytopenic purpura is a syndrome characterized by which of the following?

A 35-year-old lady with normal PT and increased APTT. 2 years back, she was operated for cholecystectomy & did not have any bleeding episode. What is the next investigation for clinical diagnosis?

A 45-year-old lady presents with normal PT and increased aPTT. About 2 years ago, she underwent cholecystectomy and did not have any bleeding episode. What is the next investigation for clinical diagnosis?

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

Q10

The following is not true of platelet transfusion -

Platelet Disorders Indian Medical PG Practice Questions and MCQs

Question 1: Which of the following statements best describes the underlying mechanism of heparin-induced thrombocytopenia?

A. Low molecular weight heparin can also cause heparin-induced thrombocytopenia.
B. Vitamin K is not an antidote for heparin-induced thrombocytopenia.
C. Heparin-induced thrombocytopenia can occur after several days of heparin therapy.
D. Antibodies are formed against heparin-platelet factor 4 complexes. (Correct Answer)

Explanation: **_Antibodies are formed against platelet factor 4._** - The underlying mechanism of **heparin-induced thrombocytopenia (HIT)** involves the formation of antibodies against complexes of **heparin and platelet factor 4 (PF4)** [2]. - These antibodies bind to the **heparin-PF4 complexes** on the surface of platelets, leading to platelet activation, aggregation, and consumption, which results in thrombocytopenia and a prothrombotic state [2]. *Low molecular weight heparin can also cause heparin-induced thrombocytopenia.* - While **low molecular weight heparin (LMWH)** has a lower incidence of causing HIT compared to unfractionated heparin, it can still trigger the condition [1], [2]. - This is because LMWH, like unfractionated heparin, can form complexes with PF4, leading to the same immune response in susceptible individuals [2]. *Vitamin K is not an antidote for heparin-induced thrombocytopenia.* - **Vitamin K** is the antidote for warfarin overdose, which works by reversing its anticoagulant effects [3]. - It has no role as an antidote for HIT because HIT is an **immune-mediated reaction** involving platelet activation, not a direct anticoagulant effect that can be reversed by Vitamin K [2]. *Heparin-induced thrombocytopenia can occur after several days of heparin therapy.* - HIT typically manifests after **5 to 10 days of heparin exposure**, as it takes time for the immune system to produce antibodies against the heparin-PF4 complexes [2]. - However, in patients with prior exposure to heparin, HIT can occur much sooner, even within **24 hours**, due to pre-existing antibodies.

Question 2: 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 3: In shigella dysentery associated hemolytic uremic syndrome, the false statement is ?

A. Hepatic failure (Correct Answer)
B. Leucocytosis
C. Thrombotic angiopathy
D. Neurological abnormalities

Explanation: Detailed assessment of the complications of Hemolytic Uremic Syndrome (HUS) following Shigella infection shows that hepatic failure is not a characteristic component. ***Hepatic failure*** - **Hepatic failure** is not a typical hallmark or direct complication of **Shiga toxin-producing E. coli (STEC) HUS**, which primarily targets the kidneys. - The primary organs affected in **HUS** are the **kidneys (acute kidney injury)**, brain (neurological symptoms), and hematopoietic system (thrombocytopenia, microangiopathic hemolytic anemia) [2]. *Leucocytosis* - **Leucocytosis** (elevated white blood cell count) is a common finding in **Shigella dysentery**, reflecting the systemic inflammatory response to the infection. - It can be a predictive marker for the severity of **HUS** development in patients with **STEC** infection. *Thrombotic angiopathy* - **Thrombotic angiopathy** is the underlying pathological process in **HUS**, characterized by **microvascular thrombosis** and **endothelial damage** [1]. - These microthrombi lead to **thrombocytopenia**, **microangiopathic hemolytic anemia**, and **ischemic organ damage**, particularly in the kidneys [1], [2]. *Neurological abnormalities* - **Neurological abnormalities** such as seizures, altered mental status, and strokes can occur in a significant proportion of **HUS** patients. - These complications are due to **cerebral microthrombosis** and **endothelial damage** in the brain, affecting blood flow and neuronal function.

Question 4: A previously healthy child has sudden onset of red spots on body. There is a history of a preceding viral infection 1-4 weeks before the onset.

A. Dengue fever
B. Hemophilia A
C. Idiopathic thrombocytopenic purpura (Correct Answer)
D. Thrombotic thrombocytopenic purpura

Explanation: ***Idiopathic thrombocytopenic purpura (ITP)*** - This presentation, especially in a previously healthy child with a preceding viral infection 1-4 weeks prior, is highly characteristic of **acute ITP**, leading to **purpuric rash** (red spots). - The preceding viral infection often triggers an autoimmune response causing destruction of **platelets**, resulting in **thrombocytopenia**. *Dengue fever* - Dengue fever typically presents with **acute onset of fever**, **headache**, **myalgia**, and a rash that appears 3-4 days after fever onset, often with a shorter incubation period than 1-4 weeks. - While it can cause petechiae due to **thrombocytopenia**, the symptom constellation does not perfectly align with the scenario, particularly the sudden onset of spots without mention of fever or other acute symptoms. *Hemophilia A* - **Hemophilia A** is a **hereditary bleeding disorder** causing deficits in **Factor VIII**, leading to spontaneous bleeding into joints and muscles, and prolonged bleeding after trauma. - It does not present as sudden onset red spots (petechiae/purpura) following a viral infection but rather as larger **hematomas** or **hemarthroses**, and it's a chronic condition, not typically triggered by recent infection. *Thrombotic thrombocytopenic purpura (TTP)* - TTP is characterized by the **pentad of symptoms**: **fever**, **neurological symptoms**, **renal dysfunction**, **microangiopathic hemolytic anemia**, and **thrombocytopenia**. - While it involves thrombocytopenia and can cause purpura, the patient's presentation lacks the other severe systemic features typically associated with TTP, and it's less commonly triggered by a simple viral infection in children.

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: Thrombotic thrombocytopenic purpura is a syndrome characterized by which of the following?

A. Thrombocytopenia, anemia, neurological abnormalities, progressive renal failure and fever (Correct Answer)
B. Thrombocytopenia, anemia, neurological abnormalities, progressive hepatic failure and fever
C. Thrombocytopenia, normal anemia, neurological abnormalities, progressive renal failure and fever
D. Thrombocytopenia, anemia, no neurological abnormalities, progressive renal failure and fever

Explanation: ***Thrombocytopenia, anemia, neurological abnormalities, progressive renal failure and fever*** - Thrombotic thrombocytopenic purpura is characterized by **thrombocytopenia** and **microangiopathic hemolytic anemia**, along with neurological and renal complications [1][2]. - The presence of **fever** and other systemic symptoms is consistent with this **thrombotic microangiopathy** syndrome [1]. *Thrombocytosis, anemia, neurologic abnormalities, progressive renal failure and fever* - This option incorrectly lists **thrombocytosis** rather than **thrombocytopenia**, which is a hallmark of thrombotic thrombocytopenic purpura (TTP) [1]. - While it includes anemia, the absence of thrombocytopenia makes it inconsistent with TTP's classic presentation [2]. *Thrombocytopenia, anemia, neurologic abnormalities, progressive hepatic failure and fever* - Although it correctly states **thrombocytopenia** and **anemia**, it incorrectly identifies **progressive hepatic failure** instead of **renal failure**, which is a key feature of TTP [1]. - The presence of neurological abnormalities and fever does align with TTP; however, the hepatic failure aspect is misleading. *Thrombocytosis, anemia neurologic abnormalities, progressive renal failure and fever* - Again, this option incorrectly notes **thrombocytosis**, contradicting the characteristic finding of **thrombocytopenia** found in TTP [1]. - While other features align with TTP's clinical picture, the thrombocytosis excludes this option from being correct [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 947-948. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 667-668.

Question 7: A 35-year-old lady with normal PT and increased APTT. 2 years back, she was operated for cholecystectomy & did not have any bleeding episode. What is the next investigation for clinical diagnosis?

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

Explanation: ***Anti-viper venom assay*** - An **isolated prolonged APTT** with a normal PT and no bleeding history, especially in a young woman, strongly suggests **antiphospholipid syndrome (APS)**. [1] - The **dilute Russell's viper venom time (DRVVT)**, often referred to as anti-viper venom assay, is the most common screening test for **lupus anticoagulant**, a key feature of APS. *Factor VIII assay* - While **Factor VIII deficiency** (hemophilia A) causes isolated prolonged APTT, it typically presents with **significant bleeding** (e.g., during surgery) which is absent here. [1] - Furthermore, hemophilia A is an **X-linked recessive** disorder, making its occurrence in a woman less likely unless she is a carrier with extremely low factor levels or has inactivating antibodies. *Ristocetin Cofactor assay* - This assay is used to diagnose **von Willebrand disease (vWD)**, which can present with prolonged APTT. [2] - However, vWD usually causes **mucocutaneous bleeding** and would likely have manifested during a cholecystectomy, which did not occur in this patient. [2] *Platelet aggregation test* - This test evaluates **platelet function** and is used to diagnose disorders like **Glanzmann thrombasthenia** or **Bernard-Soulier syndrome**. - These disorders primarily cause **bleeding** and typically result in a **normal PT and APTT**, with abnormal bleeding time, which doesn't fit the patient's presentation.

Question 8: A 45-year-old lady presents with normal PT and increased aPTT. About 2 years ago, she underwent cholecystectomy and did not have any bleeding episode. What is the next investigation for clinical diagnosis?

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

Explanation: ***Dilute Russell viper venom assay*** - A normal PT and an increased aPTT, along with a history of no bleeding during surgery, are highly suggestive of **antiphospholipid syndrome** (APS). [1] - The dilute Russell viper venom time (DRVVT) is a specific and sensitive test for detecting **lupus anticoagulant**, a key feature of APS. [1] *Platelet aggregation test* - This test evaluates platelet function and is used for diagnosing primary **platelet disorders** like von Willebrand disease or Bernard-Soulier syndrome. - It would not be the primary next step for an isolated prolonged aPTT with no bleeding history, as this pattern points to a **coagulation factor issue** or an anticoagulant. [1] *Ristocetin cofactor assay* - This assay is primarily used to diagnose **von Willebrand disease** by measuring the activity of von Willebrand factor (vWF). [2] - While von Willebrand disease can cause a prolonged aPTT, the absence of bleeding during a major surgery (cholecystectomy) makes a severe vWD diagnosis less likely, and APS is a more probable cause in this context. [3] *Factor VIII assay* - A Factor VIII deficiency (Hemophilia A) can cause a prolonged aPTT, but severe deficiencies typically lead to **significant bleeding episodes**, especially after surgery. [3] - The lack of bleeding during cholecystectomy makes a clinically significant Factor VIII deficiency less likely, and it wouldn't explain the normal PT. [1]

Question 9: 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 10: The following is not true of platelet transfusion -

A. Used in DIC
B. Useful in ITP
C. Effective for 9-10 days (Correct Answer)
D. Effects decrease with repeated usage

Explanation: ***Effective for 9-10 days*** - Platelets have a normal lifespan of about 7-10 days in the circulation, but **transfused platelets** are effective for a much shorter duration, typically **3-4 days** at most. - This short post-transfusion lifespan is due to various factors including immediate consumption, destruction, and removal from the circulation. *Used in DIC* - Platelet transfusions are often indicated in **Disseminated Intravascular Coagulation (DIC)**, especially if there is significant bleeding and a platelet count below 50,000/microL [1]. - DIC involves widespread activation of the coagulation cascade, leading to the consumption of platelets and clotting factors, resulting in both **thrombosis** and **hemorrhage** [1]. *Useful in ITP* - Transfusions are generally **not useful in Immune Thrombocytopenic Purpura (ITP)**, except in severe, life-threatening hemorrhage. - In ITP, platelets are rapidly destroyed by **autoantibodies**, so transfused platelets would also be quickly destroyed, providing only a transient, minimal benefit. *Effects decrease with repeated usage* - With repeated transfusions, patients can develop **alloimmunization** to HLA antigens on donor platelets, leading to refractoriness. - This means subsequent transfusions may have a **diminished or no therapeutic effect**, as the immune system rapidly destroys the transfused platelets.

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free