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USMLE Hematology Question Bank

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Hematology is the study of blood and the disorders related to it. Human blood consists of blood cells and plasma.

USMLE Hematology Question Bank

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1. What carcinoma is associated with infectious mononucleosis? 2. What lymphomas is it associated with?

1. Coagulopathy caused by endothelial injury that causes thrombosis and fibrinolysis. 2. -Thrombi in organs -Mucosal surface bleeding -Thrombocytopenia -Prolonged PT/PTT -Decreased fibrinogen -Increased products of fibrinolysis 3. Schistocytes aka helmet cells1. Nasopharyngeal carcinoma 2. Burkitts lypmoma, Hodgkin lyphoma1. -Fever -Acute renal failure -Neurologic symptoms -Thrombocytopenia -Microangiopathic hemolytic anemia1. Glanzmann thrombasthenia; and autosomal recessive disorder. 2. Binds fibrinogin and allows platelet aggregation.

2. What condition is associated with a deficiency of platelet GP2b/3a? 2. What does GP 2b/3a do?

1. Coagulopathy caused by endothelial injury that causes thrombosis and fibrinolysis. 2. -Thrombi in organs -Mucosal surface bleeding -Thrombocytopenia -Prolonged PT/PTT -Decreased fibrinogen -Increased products of fibrinolysis 3. Schistocytes aka helmet cells1. -Fever -Acute renal failure -Neurologic symptoms -Thrombocytopenia -Microangiopathic hemolytic anemia1. Glanzmann thrombasthenia; and autosomal recessive disorder. 2. Binds fibrinogin and allows platelet aggregation.1. Nasopharyngeal carcinoma 2. Burkitts lypmoma, Hodgkin lyphoma

3. What is DIC? 2. Clinical features of DIC? 3. What is seen on blood smear?

1. Coagulopathy caused by endothelial injury that causes thrombosis and fibrinolysis. 2. -Thrombi in organs -Mucosal surface bleeding -Thrombocytopenia -Prolonged PT/PTT -Decreased fibrinogen -Increased products of fibrinolysis 3. Schistocytes aka helmet cells1. Nasopharyngeal carcinoma 2. Burkitts lypmoma, Hodgkin lyphoma1. Glanzmann thrombasthenia; and autosomal recessive disorder. 2. Binds fibrinogin and allows platelet aggregation.1. -Fever -Acute renal failure -Neurologic symptoms -Thrombocytopenia -Microangiopathic hemolytic anemia

4. What are the clinical features associated with thrombotic thromboctyopenic purpura?

1. -Fever -Acute renal failure -Neurologic symptoms -Thrombocytopenia -Microangiopathic hemolytic anemia1. Coagulopathy caused by endothelial injury that causes thrombosis and fibrinolysis. 2. -Thrombi in organs -Mucosal surface bleeding -Thrombocytopenia -Prolonged PT/PTT -Decreased fibrinogen -Increased products of fibrinolysis 3. Schistocytes aka helmet cells1. Glanzmann thrombasthenia; and autosomal recessive disorder. 2. Binds fibrinogin and allows platelet aggregation.1. Nasopharyngeal carcinoma 2. Burkitts lypmoma, Hodgkin lyphoma

5. In hemolytic uremic syndrome what happens to the following. Do they increase or decrease? 1. BUN 2. D-Dimer 3. Haptoglobin 4. LDH 5. Reticulocyte percentage

1. Glanzmann thrombasthenia; and autosomal recessive disorder. 2. Binds fibrinogin and allows platelet aggregation.1. Coagulopathy caused by endothelial injury that causes thrombosis and fibrinolysis. 2. -Thrombi in organs -Mucosal surface bleeding -Thrombocytopenia -Prolonged PT/PTT -Decreased fibrinogen -Increased products of fibrinolysis 3. Schistocytes aka helmet cells1. BUN: Is elevated HUS causes renal failure and creatinine is elevated too. 2. D-Dimer: Is normal, HUS is not a thromboembolic disease like DIC. 3. Haptoglobin: Is decreased because it is bindin to the free hemoglobin from the hemolysis. 4. LDH: Is an enzyme found in cells so as RBC are lysing it is released into blood so this would be increased.' 5. In anemia bone marrow trys to make more RBC. SO Reticulocyte percentage will be increased.1. Nasopharyngeal carcinoma 2. Burkitts lypmoma, Hodgkin lyphoma

6. Hemophilia A 1. What is the deficiency? 2. What is its mode of inheritance? 3. What effect is there on PT and aPTT? 4. What is treatment?

1. Nasopharyngeal carcinoma 2. Burkitts lypmoma, Hodgkin lyphoma1. Glanzmann thrombasthenia; and autosomal recessive disorder. 2. Binds fibrinogin and allows platelet aggregation.1. Low factor 8 2. X-linked recessive 3. PT is prolonged but aPTT is normal 4. Concentrated factor 8 replacement1. Coagulopathy caused by endothelial injury that causes thrombosis and fibrinolysis. 2. -Thrombi in organs -Mucosal surface bleeding -Thrombocytopenia -Prolonged PT/PTT -Decreased fibrinogen -Increased products of fibrinolysis 3. Schistocytes aka helmet cells

7. What is most common malignancy in children? 2. Which type is seen more in young children and which type is seen more in teen males? 3. What is seen on smear? 4. What do the malignant cells stain strongly with and what are they usually positive for? 5. What CDs are they usually positive for?

1. Nasopharyngeal carcinoma 2. Burkitts lypmoma, Hodgkin lyphoma1. Glanzmann thrombasthenia; and autosomal recessive disorder. 2. Binds fibrinogin and allows platelet aggregation.1. Coagulopathy caused by endothelial injury that causes thrombosis and fibrinolysis. 2. -Thrombi in organs -Mucosal surface bleeding -Thrombocytopenia -Prolonged PT/PTT -Decreased fibrinogen -Increased products of fibrinolysis 3. Schistocytes aka helmet cells1. Acute lymphoblastic leukemia. 2. B-ALL = young T-ALL = teens. 3. Large immature cells 4. Stain strongly for PAS and positive for TdT. 5. B-ALL = CD 10 + and CD 19 +

8. A child who has a mutated defective enzyme responsible for catalyzing the last step in glycolysis has what condition? 2. What does this condition cause an accumulation of? 3. What does this accumulation cause?

1. Coagulopathy caused by endothelial injury that causes thrombosis and fibrinolysis. 2. -Thrombi in organs -Mucosal surface bleeding -Thrombocytopenia -Prolonged PT/PTT -Decreased fibrinogen -Increased products of fibrinolysis 3. Schistocytes aka helmet cells1. Nasopharyngeal carcinoma 2. Burkitts lypmoma, Hodgkin lyphoma1. Pyruvate kinase deficiency 2. 2-3 biphosphoglycerate 3. Decrease affinity of oxygen in RBC.1. Glanzmann thrombasthenia; and autosomal recessive disorder. 2. Binds fibrinogin and allows platelet aggregation.

9. What is considered profound thrombocytopenia?

10. What is HbA? 2. When is this the predominant Hb in human body? 3. Electrophoresis that shows low or absent HbA and elevated HbF and HbA2 is indicative of what? 4. What is made prior to six months? Why do children with this condition take that long to present?

1. Coagulopathy caused by endothelial injury that causes thrombosis and fibrinolysis. 2. -Thrombi in organs -Mucosal surface bleeding -Thrombocytopenia -Prolonged PT/PTT -Decreased fibrinogen -Increased products of fibrinolysis 3. Schistocytes aka helmet cells1. Glanzmann thrombasthenia; and autosomal recessive disorder. 2. Binds fibrinogin and allows platelet aggregation.1. Nasopharyngeal carcinoma 2. Burkitts lypmoma, Hodgkin lyphoma1. HbA = hb that has two alpha and two beta globulins. 2. After 6 months of age. 3. Beta thalassemia 4. HbF which is Hb made of two alpha globulins and two lambda globulins. After six months stop making lambda and replace with beta globulin but their beta globulin is defective.

11. An adult with an infarcted spleen who develops bacteremia should be suspected of having what condition?

Sickle cell anemia.1. Coagulopathy caused by endothelial injury that causes thrombosis and fibrinolysis. 2. -Thrombi in organs -Mucosal surface bleeding -Thrombocytopenia -Prolonged PT/PTT -Decreased fibrinogen -Increased products of fibrinolysis 3. Schistocytes aka helmet cells1. Nasopharyngeal carcinoma 2. Burkitts lypmoma, Hodgkin lyphoma1. Glanzmann thrombasthenia; and autosomal recessive disorder. 2. Binds fibrinogin and allows platelet aggregation.

12. What is Taenia solium?

1. Nasopharyngeal carcinoma 2. Burkitts lypmoma, Hodgkin lyphoma1. Glanzmann thrombasthenia; and autosomal recessive disorder. 2. Binds fibrinogin and allows platelet aggregation.1. Coagulopathy caused by endothelial injury that causes thrombosis and fibrinolysis. 2. -Thrombi in organs -Mucosal surface bleeding -Thrombocytopenia -Prolonged PT/PTT -Decreased fibrinogen -Increased products of fibrinolysis 3. Schistocytes aka helmet cells1. Pork tapeworm

13. Clinical features presenting with renal cell carcinoma? 2. What condition is associated with bilateral RCC? 3. What are characteristics of this condition?

1. Nasopharyngeal carcinoma 2. Burkitts lypmoma, Hodgkin lyphoma1. Coagulopathy caused by endothelial injury that causes thrombosis and fibrinolysis. 2. -Thrombi in organs -Mucosal surface bleeding -Thrombocytopenia -Prolonged PT/PTT -Decreased fibrinogen -Increased products of fibrinolysis 3. Schistocytes aka helmet cells'1. Flank pain, hematuria, fever, polycythemia. 2. Von Hippel Lindau syndrome 3. Remember ''HARP'' Hemangioblastoms (retina,brain,spinal cord) Angiomatosis: (proliferatin capillaries) RCC bilateral Pheochromocytoma'1. Glanzmann thrombasthenia; and autosomal recessive disorder. 2. Binds fibrinogin and allows platelet aggregation.

14. Why are women on OCP at increased risk of VTE? 2. What other condition is associated with increased VTE risk for same reason as OCP?

1. Nasopharyngeal carcinoma 2. Burkitts lypmoma, Hodgkin lyphoma1. Coagulopathy caused by endothelial injury that causes thrombosis and fibrinolysis. 2. -Thrombi in organs -Mucosal surface bleeding -Thrombocytopenia -Prolonged PT/PTT -Decreased fibrinogen -Increased products of fibrinolysis 3. Schistocytes aka helmet cells1. OCP causes activated protein C resistance so there protein c (a natural anticoagulant) is less effective. 2. Factor V leiden.1. Glanzmann thrombasthenia; and autosomal recessive disorder. 2. Binds fibrinogin and allows platelet aggregation.

15. What are the signs of lead poisoning in a child? 2. What does lead impair regarding heme synthesis? 3. What does treatment involve?

1. Glanzmann thrombasthenia; and autosomal recessive disorder. 2. Binds fibrinogin and allows platelet aggregation.1. Anorexia, apathy, aggressiveness, abdo pain, poor coordingation, constipation/diarrhea. A,B,C,D,E A: Anorexia, Anemia B: Basophillic stippling, Burtonian line C: Constipation, Collic D: Drop (foot/wrist) E: Encephalopathy F: Foul breath/Foul taste in mouth 2. Impairs aminolevulinate dehydratase and ferrochelatase = microcytic, hypochromic anemia with basophilic stippling. 3. Chelation therapy with dimercaprol (BAL) amd ethylenediaminetetraacetic acid (EDTA).1. Coagulopathy caused by endothelial injury that causes thrombosis and fibrinolysis. 2. -Thrombi in organs -Mucosal surface bleeding -Thrombocytopenia -Prolonged PT/PTT -Decreased fibrinogen -Increased products of fibrinolysis 3. Schistocytes aka helmet cells1. Nasopharyngeal carcinoma 2. Burkitts lypmoma, Hodgkin lyphoma

16. A neonate with an enlarged spleen and chronic hemolysis is most likely to have what condition?

1. Nasopharyngeal carcinoma 2. Burkitts lypmoma, Hodgkin lyphomaPyruvate kinase deficiency.1. Coagulopathy caused by endothelial injury that causes thrombosis and fibrinolysis. 2. -Thrombi in organs -Mucosal surface bleeding -Thrombocytopenia -Prolonged PT/PTT -Decreased fibrinogen -Increased products of fibrinolysis 3. Schistocytes aka helmet cells1. Glanzmann thrombasthenia; and autosomal recessive disorder. 2. Binds fibrinogin and allows platelet aggregation.

17. What complication right after post partum can cause DIC? 2. What will you see on peripheral blood smear?

18. 27 yo women has: -easy bruising -bleeding gums when brushing teeth -hematoma that occurs easily with a passage of cather - Her platelets are normal -Prothrombin time is normal -activated partial thromboplastin time is prolonged 1. What condition is she likely to have with this clinical picture? 2. What is the function of the product that is deficient?

1. Coagulopathy caused by endothelial injury that causes thrombosis and fibrinolysis. 2. -Thrombi in organs -Mucosal surface bleeding -Thrombocytopenia -Prolonged PT/PTT -Decreased fibrinogen -Increased products of fibrinolysis 3. Schistocytes aka helmet cells1. Von willibrand disease 2. VWF binds to exposed collegen and cofactor of CF 8 so prevents CF 8 premature degradation. That is why VWF deficiency = prolonged aPTT because CF 8 is also a little low.1. Glanzmann thrombasthenia; and autosomal recessive disorder. 2. Binds fibrinogin and allows platelet aggregation.1. Nasopharyngeal carcinoma 2. Burkitts lypmoma, Hodgkin lyphoma

19. What is Glucose 6 phosphate dehydrogenase deficiency? 2. What can occur with this condition? 3. What are some triggers?

1. X-linked disease that affecst pentose phosphate pathway. And production of antioxidants to offset affect of ROS. 2. Episodic hemolysis 3. Infection, drugs (primaquine, sulfamethoxazole, fava beans)1. Nasopharyngeal carcinoma 2. Burkitts lypmoma, Hodgkin lyphoma1. Glanzmann thrombasthenia; and autosomal recessive disorder. 2. Binds fibrinogin and allows platelet aggregation.1. Coagulopathy caused by endothelial injury that causes thrombosis and fibrinolysis. 2. -Thrombi in organs -Mucosal surface bleeding -Thrombocytopenia -Prolonged PT/PTT -Decreased fibrinogen -Increased products of fibrinolysis 3. Schistocytes aka helmet cells

20. What inheritance is VWF disease? 2. What are features of VWF (in women)? 3. Briefly what is the pathophys of VWF disease? 4. What drug can be given that will improve menorrhagia and other symptoms? How does it work?

1. Autosomal dominant 2. Mucosal bleeding, anemia, menorrhagia 3. Not enough VWF = less platelet adhesion to subendothelial collagen and less CF 8 = increase in bleeding time and aPTT. 4. Desmopressin: Directly stimulates vWF and factor 8 from endothelial cells.1. Glanzmann thrombasthenia; and autosomal recessive disorder. 2. Binds fibrinogin and allows platelet aggregation.1. Coagulopathy caused by endothelial injury that causes thrombosis and fibrinolysis. 2. -Thrombi in organs -Mucosal surface bleeding -Thrombocytopenia -Prolonged PT/PTT -Decreased fibrinogen -Increased products of fibrinolysis 3. Schistocytes aka helmet cells1. Nasopharyngeal carcinoma 2. Burkitts lypmoma, Hodgkin lyphoma

21. Autoantibodies to erythrocyte membrane proteins is the cause of what disease?

22. What sort of infections are people without spleens have increased susceptibility to? 2. Which is most common? 3. What sort of organism is this?

1. Glanzmann thrombasthenia; and autosomal recessive disorder. 2. Binds fibrinogin and allows platelet aggregation.1. Nasopharyngeal carcinoma 2. Burkitts lypmoma, Hodgkin lyphoma1. Coagulopathy caused by endothelial injury that causes thrombosis and fibrinolysis. 2. -Thrombi in organs -Mucosal surface bleeding -Thrombocytopenia -Prolonged PT/PTT -Decreased fibrinogen -Increased products of fibrinolysis 3. Schistocytes aka helmet cells1. Encapsulated organisms 2. Streptococcus pneumoniae 3. Gram +, Catalase -, alpha hemolytic diplococcus

23. What is used to treat von willibrand disease?

1. Nasopharyngeal carcinoma 2. Burkitts lypmoma, Hodgkin lyphomaDesmopressin; causes release of vWF from Weibel-Palade bodies1. Coagulopathy caused by endothelial injury that causes thrombosis and fibrinolysis. 2. -Thrombi in organs -Mucosal surface bleeding -Thrombocytopenia -Prolonged PT/PTT -Decreased fibrinogen -Increased products of fibrinolysis 3. Schistocytes aka helmet cells1. Glanzmann thrombasthenia; and autosomal recessive disorder. 2. Binds fibrinogin and allows platelet aggregation.

24. 35 yo male: -Painful palpable masses in groin -Multiple enlarged abscessed lymph nodes draining through skin through indolent sinuses. 1. What is likely diagnosis? 2. What is the causative organism?

25. What is the cause of the sickle shape in sickle cell anemia? 2. What causes the cells to sickle? 3. How are these sickles removed? What is this called?

1. Coagulopathy caused by endothelial injury that causes thrombosis and fibrinolysis. 2. -Thrombi in organs -Mucosal surface bleeding -Thrombocytopenia -Prolonged PT/PTT -Decreased fibrinogen -Increased products of fibrinolysis 3. Schistocytes aka helmet cells1. Point mutation in the hemoglobin Beta globin chain. It is a valine substitution of glutamic acid. 2. Low O2 tension = HbS polymerizes and causes sickling. 3. Removed by spleen = extravascular hemolysis.1. Glanzmann thrombasthenia; and autosomal recessive disorder. 2. Binds fibrinogin and allows platelet aggregation.1. Nasopharyngeal carcinoma 2. Burkitts lypmoma, Hodgkin lyphoma

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❤ If you liked Fatskills, consider supporting us by checking out The Life Manuals You Never Got.

About | Explore | User Guide | Topics | Subjects | Doubt Solver | Career Aptitude Test | Answers | Free Tools | What Should We Know? Privacy | Terms |

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All trademarks, logos and brand names are the property of their respective owners. All company, product and service names used in this website are for identification purposes only. Use of these names, trademarks and brands does not imply endorsement.

About | Explore | User Guide | Topics | Subjects | Doubt Solver | Career Aptitude Test | Answers | Free Tools | What Should We Know?
Privacy | Terms |

Without work one finishes nothing. - Ralph Waldo Emerson
© 2026 Fatskills.com