NATIONAL AND STATE NURSING EXAM- MCQ _MG_0089
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1. Intra vascular hemolysis can be seen in:
a. Falciparum malaria
b. Acute G6PD deficiency
c. Incompatible blood transfusion
d. All of these
Answer: d. All of these
Description:Intravascular hemolysis refers to the destruction of red blood cells (RBCs) within the blood vessels. In the conditions mentioned: a. Falciparum malaria: Plasmodium falciparum, the parasite that causes falciparum malaria, can invade and multiply within RBCs. As the parasite replicates, it ruptures the RBCs, leading to the release of hemoglobin into the bloodstream and subsequent intravascular hemolysis. b. Acute G6PD deficiency: Glucose-6-phosphate dehydrogenase (G6PD) deficiency is an inherited condition that affects the enzyme responsible for protecting RBCs against oxidative stress. When exposed to certain triggers (such as certain foods, medications, or infections), G6PD-deficient RBCs become susceptible to premature destruction, resulting in intravascular hemolysis. c. Incompatible blood transfusion: Incompatible blood transfusion refers to the transfusion of blood that is incompatible with the recipient's blood type. When incompatible blood is transfused, it can trigger an immune response, leading to the destruction of transfused RBCs. This immune-mediated destruction can occur within the blood vessels and result in intravascular hemolysis.
2. Extravascular hemolysis occurs in:
a. Thalassemia
b. Hereditary spherocytosis
c. Sickle cell disease
d. All of these
Answer: d. All of these
Description:Extravascular hemolysis can occur in multiple conditions, including thalassemia, hereditary spherocytosis, and sickle cell disease. Thalassemia is a genetic disorder characterized by decreased production of one or more of the globin chains that make up hemoglobin. It can lead to the destruction of red blood cells (hemolysis), which can occur both within and outside of blood vessels (extravascular hemolysis). Hereditary spherocytosis is a genetic condition in which red blood cells have a spherical shape instead of the normal biconcave shape. These abnormal-shaped red blood cells are more prone to destruction by the spleen, leading to extravascular hemolysis. Sickle cell disease is an inherited blood disorder characterized by abnormal hemoglobin that causes red blood cells to become stiff and sickle-shaped. The sickle-shaped cells can get trapped and destroyed in the spleen, resulting in extravascular hemolysis. Therefore, all of these conditions can lead to extravascular hemolysis.
3. Which among the following suggest problem hematological system?
a. Uremia
b. Polycythemia vera
c. Gout
d. Renal calculi
Answer: b. Polycythemia vera
Description:Polycythemia vera is a disorder of the hematological system characterized by the overproduction of red blood cells in the bone marrow. This leads to an increased number of red blood cells in the circulation, which can cause thickening of the blood and lead to various complications such as increased risk of blood clots, stroke, and heart attack. Uremia (a) refers to the buildup of waste products in the blood due to kidney dysfunction. It is not directly related to the hematological system. Gout (c) is a form of arthritis caused by the buildup of uric acid crystals in the joints. While it can cause inflammation and pain in the joints, it is not primarily a problem of the hematological system. Renal calculi (d), also known as kidney stones, are solid masses made up of crystals that form in the kidneys. They are not directly related to the hematological system, although certain medical conditions, such as hyperuricemia, can increase the risk of developing kidney stones.
4. Multiple myeloma occurs due to uncontrolled proliferation of:
a. B-lymphocyte
b. T-lymphocyte
c. Basophil
d. Plasma cell
Answer: d. Plasma cell
Description: Multiple myeloma is a type of cancer that occurs due to the uncontrolled proliferation of plasma cells, which are a type of white blood cell that produces antibodies. In multiple myeloma, these abnormal plasma cells accumulate in the bone marrow and interfere with the production of normal blood cells. This can lead to various complications, such as bone pain, anemia, weakened immune system, and kidney problems. Treatment options for multiple myeloma include chemotherapy, targeted therapy, immunotherapy, and stem cell transplantation.
5. Most common cause of traumatic splenic rupture is:
a. Blunt abdominal blows
b. Sharp injury to abdomen
c. Lymphoma
d. Rib fracture
Answer: a. Blunt abdominal blows
Description:The most common cause of traumatic splenic rupture is indeed blunt abdominal blows. This can occur due to various reasons such as motor vehicle accidents, falls, physical assaults, or any other direct impact to the abdomen. The spleen is a highly vascular organ located in the upper left abdomen, and its relatively fragile structure makes it susceptible to injury from blunt trauma. When a significant force is applied to the abdomen, the spleen can be compressed or lacerated, leading to splenic rupture. This condition can result in internal bleeding, which can be life-threatening and require immediate medical attention, including surgical intervention in some cases.
6. Most common cause of non-traumatic splenic rupture is:
a. Malaria
b. Cirrhosis
c. Thalassemia
d. ITP
Answer: a. Malaria
Description:The most common cause of non-traumatic splenic rupture is not malaria but actually infectious mononucleosis, also known as glandular fever or "mono." While malaria can sometimes lead to splenic rupture, it is not as common as infectious mononucleosis. Other causes of non-traumatic splenic rupture include certain blood disorders like idiopathic thrombocytopenic purpura (ITP), hematological malignancies, and certain infections like typhoid fever. Cirrhosis and thalassemia are not typically associated with non-traumatic splenic rupture.
7. Expected laboratory finding after splenectomy is:
a. Decreased WBC count
b. Increased hemoglobin
c. Decreased hemoglobin
d. Increased thrombocyte count
Answer: d. Increased thrombocyte count
Description:The expected laboratory finding after splenectomy is an increased thrombocyte count (platelet count). The spleen plays a role in removing aged or damaged blood cells, including platelets. When the spleen is removed (splenectomy), platelets are no longer sequestered or destroyed as efficiently, leading to an increase in their count in the bloodstream. Therefore, option d, "Increased thrombocyte count," is the correct answer.
8. Splenomegaly is evident in:
a. Malaria
b. Kala azar
c. Hemolytic anemia
d. All of these
Answer: d. All of these
Description:Splenomegaly, or enlargement of the spleen, can occur in various conditions, including malaria, kala azar (visceral leishmaniasis), and hemolytic anemia. Therefore, the correct answer is d) All of these.
9. Total no. of blood clotting factors are:
a. 12
b. 13
c. 14
d. 15
Answer: b. 13
Description:The total number of blood clotting factors is 13.
10. Which of the following is not a clotting factor?
a. Fibrinogen
b. Prothrombin
c. Calcium
d. Sodium
Answer: d. Sodium
Description:Sodium is not involved in clotting process.
11. Vitamin required for blood clotting is:
a. Vitamin - A
B. Vitamin – D
c. Vitamin – E
d. Vitamin – K
Answer: d. Vitamin – K
Description:That is correct. The vitamin required for blood clotting is Vitamin K. It plays a vital role in the clotting process by helping to activate proteins involved in the formation of blood clots. Without sufficient Vitamin K, blood clotting may be impaired, leading to an increased risk of bleeding.
12. Electrolyte required for blood clotting is
a. Na
b. K
c. Ca
d. P
Answer: c. Ca
Description:The correct electrolyte required for blood clotting is calcium (Ca). Calcium plays a crucial role in the coagulation cascade, a complex series of reactions that leads to the formation of a blood clot. It is necessary for the activation of various clotting factors and the formation of a stable fibrin clot. Other electrolytes such as sodium (Na), potassium (K), and phosphate (P) are important for various physiological processes but are not directly involved in blood clotting.
13. Antihemophilic factor – B is:
a. Factor 7
b. Factor 8
c. Factor 9
d. Factor 10
Answer: c. Factor 9
Description: Antihemophilic factor - B, also known as factor IX, is the answer (c). Factor IX is a clotting factor that plays a crucial role in the blood clotting process. It is deficient in individuals with hemophilia B, a genetic bleeding disorder. Treatment with factor IX concentrates, such as antihemophilic factor - B, is necessary to replace the missing or defective factor and control bleeding episodes in individuals with hemophilia B.
14. Antihemophilic factor –A is:
a. Factor 7
b. Factor 8
c. Factor 9
d. Factor 10
Answer: b. Factor 8
Description:Antihemophilic factor A is Factor 8. Antihemophilic factor A, also known as Factor VIII, is a blood clotting protein that is necessary for the normal clotting of blood. It is primarily used in the treatment of hemophilia A, a genetic disorder in which the body lacks or has low levels of Factor VIII, leading to impaired blood clotting.
15. Factor 9 is also known as:
a. Stuart prower factor
b. Hageman factor
c. Christmas factor
d. Thromboplastin
Answer: c. Christmas factor
Description:Factor 9 is actually known as the Christmas factor, which is named after the patient, Stephen Christmas, in whom the deficiency of this clotting factor was first identified. Therefore, the correct answer is option c.
16. Von Willebrand factor is secreted by:
a. Liver
b. Kidney
c. Vascular endothelium
d. Adrenals
Answer: c. Vascular endothelium
Description:Von Willebrand factor (vWF) is primarily secreted by the vascular endothelium, which is the inner lining of blood vessels. vWF is synthesized and released by the endothelial cells in response to various stimuli, including shear stress and certain hormones. It plays a crucial role in blood clotting by mediating platelet adhesion and stabilizing factor VIII in the blood. Although the liver also produces vWF, it is primarily responsible for the synthesis of other clotting factors, such as prothrombin and fibrinogen. The kidney and adrenals are not major sources of vWF secretion.
17. Coagulation factor VII is:
a. Thromboplastins
b. Accelerin
c. Proconvertin
d. Antihemophilic factor
Answer: c. Proconvertin
Description:Coagulation Factor VII is not any of the options mentioned. Coagulation Factor VII, also known as Stable Factor or Proconvertin, is a protein involved in the coagulation cascade. It is a vitamin K-dependent serine protease that plays a role in the initiation of blood clot formation.
18. Vitamin K dependent factor is:
a. Factor XII
b. Factor IV
c. Prothrombin
d. Factor V
Answer: c. Prothrombin
Description:Vitamin K is essential for the synthesis of various clotting factors in the blood. These clotting factors are known as vitamin K-dependent factors because their production requires the presence of vitamin K. One of the key vitamin K-dependent factors is prothrombin, also known as Factor II. Prothrombin is a precursor protein that plays a critical role in the blood clotting process. It is converted into thrombin, an enzyme that helps convert fibrinogen into fibrin, which forms the clot. Factor XII (a) is not a vitamin K-dependent factor. It is a clotting factor involved in the intrinsic pathway of coagulation. Factor IV (b) does not exist. The clotting factors are usually numbered, and there is no Factor IV. Factor V (d) is another vitamin K-dependent factor, also known as labile factor or proaccelerin. It works in conjunction with other clotting factors to activate prothrombin and facilitate the formation of thrombin.
19. All of the following clotting factors are vitamin K dependents; EXCEPT:
a. Factor II
b. Factor VII
c. Factor VIII
d. Protein IX
Answer: c. Factor VIII
Description:The key vitamin K-dependent proteins include: a. Coagulation proteins: Factors II (prothrombin) VII, IX and X b. Anticoagulation proteins: Proteins C, S and Z c. Others: Osteocalcin and matrix-Gia protein, and certain ribosomal proteins.
20. All of the following are platelet associated coagulation factors: EXCEPT:
a. Von Willebrand factor
b. Factor IX
c. Factor XI
d. Factor XIII
Answer: a. Von Willebrand factor
Description:Von Willebrand factor. Von Willebrand factor is not a platelet-associated coagulation factor. It is a glycoprotein that plays a role in platelet adhesion and the stabilization of factor VIII in the blood. Factors IX, XI, and XIII are indeed platelet-associated coagulation factors. Factor IX is involved in the intrinsic pathway of the coagulation cascade, while factors XI and XIII contribute to both the intrinsic and common pathways of coagulation.
21. Feature of factor XIII deficiency is:
a. Early solubilization of clot
b. Fibrinogen to fibrin conversion will not be there
c. Activation of platelet will be delayed
d. Small clot fragments
Answer: a. Early solubilization of clot
Description:Factor XIII deficiency is a rare inherited bleeding disorder characterized by a deficiency or dysfunction of factor XIII, also known as fibrin-stabilizing factor. Factor XIII plays a crucial role in the final step of the blood coagulation process, which involves the conversion of fibrinogen to fibrin. Fibrin is a fibrous protein that forms a mesh-like structure, providing stability to blood clots. In factor XIII deficiency, the impaired or absent factor XIII activity leads to inadequate fibrin stabilization, resulting in weak and unstable blood clots. Without proper fibrinogen to fibrin conversion and fibrin stabilization, the clot formed may be susceptible to premature dissolution or breakdown, leading to prolonged bleeding. Therefore, the correct feature of factor XIII deficiency is that fibrinogen to fibrin conversion will not occur properly, and this can contribute to the clinical manifestations of the disorder, such as delayed clot formation, excessive bleeding, and poor wound healing.
22. Hemophilia A is caused by lack of clotting factors:
a. VII
b. VIII
c. IX
d. X
Answer: b. VIII
Description:Hemophilia A is caused by a lack or deficiency of clotting factor VIII. Therefore, the correct answer is b. VIII. Hemophilia A is an inherited bleeding disorder characterized by the reduced or absent production of factor VIII, which plays a crucial role in the blood clotting process. Without sufficient factor VIII, individuals with hemophilia A may experience prolonged bleeding or spontaneous bleeding into joints, muscles, or other tissues.
23. Hemophilia B is caused by lack of clotting factors:
a. VII
b. VIII
c. IX
d. X
Answer: c. IX
Description:Hemophilia B, also known as Christmas disease, is caused by a deficiency or absence of clotting factor IX. The clotting factors play a crucial role in the coagulation cascade, which is the process that helps blood clot and prevents excessive bleeding. In individuals with hemophilia B, the reduced or missing clotting factor IX results in impaired blood clotting and a tendency to bleed easily.
24. Which of the following coagulation disorder is an autosomal dominant disease?
a. Hemophilia A
b. Hemophilia B
c. Von Willebrand disease
d. All of these
Answer: c. Von Willebrand disease
Description:Von Willebrand disease is an autosomal dominant disorder, which means that a person needs to inherit only one copy of the mutated gene from either parent to develop the condition. It is the most common inherited bleeding disorder, characterized by a deficiency or dysfunction of von Willebrand factor (VWF), a protein involved in blood clotting. Hemophilia A and Hemophilia B, on the other hand, are X-linked recessive disorders. Hemophilia A is caused by a deficiency of clotting factor VIII, and Hemophilia B is caused by a deficiency of clotting factor IX. These disorders are more commonly observed in males, as they inherit the mutated gene on the X chromosome from their carrier mothers.
25. Laboratory results of client with leukemia indicates elevated blood urea nitrogen (BUN) and uric acid levels. These laboratory result indicates:
a. Lymphadenopathy
b. Thrombocytopenia
c. Hepatic encephalopathy
d. Hypermetabolic state
Answer: d. Hypermetabolic state
Description:The hypermetabolic (increased rate of metabolism) state related to leukemia caused increased production of urea and uric acid (end products of metabolism). The end products get accumulated in the blood.
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