Nursing practice questions with comprehensive rationales
NurseDive Free Nursing Practice Question
Platelets are cell fragments that are released by what type of cell?
A. Megakaryocytes
Megakaryocytes: Megakaryocytes are large bone marrow cells whose cytoplasmic fragments become platelets (thrombocytes).
B. Macrophages
Macrophages: Phagocytic cells derived from monocytes; they do not produce platelets.
C. Monoblasts
Monoblasts: Immature precursors that develop into monocytes/macrophages, not platelets.
D. Reticulocytes
Reticulocytes: Immature red blood cells (RBC precursors) released from bone marrow—not a source of platelets.
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Full Explanation
A. Megakaryocytes: Megakaryocytes are large bone marrow cells whose cytoplasmic fragments become platelets (thrombocytes).
B. Macrophages: Phagocytic cells derived from monocytes; they do not produce platelets.
C. Monoblasts: Immature precursors that develop into monocytes/macrophages, not platelets.
D. Reticulocytes: Immature red blood cells (RBC precursors) released from bone marrow—not a source of platelets.
Similar Questions
Describe the role of plasmin.
A. Converts fibrinogen to fibrin, allowing the formation of a clot
Converts fibrinogen to fibrin: that reaction is carried out by thrombin, not plasmin.
B. Breaks down fibrin, dissolving the clot
Breaks down fibrin, dissolving the clot: plasmin is the primary enzyme of fibrinolysis, cleaving fibrin to dissolve formed clots.
C. Triggers the extrinsic clotting mechanism, leading to clot formation
Triggers the extrinsic clotting mechanism, leading to clot formation: the extrinsic pathway is initiated by tissue factor (factor III) interacting with factor VII, not plasmin.
D. Inactivates thrombin, slowing clot formation
Inactivates thrombin, slowing clot formation: plasmin’s main role is fibrin breakdown; thrombin is primarily regulated by antithrombin, thrombomodulin–protein C systems. (Plasmin can degrade some clotting proteins but it is not described as the main inactivator of thrombin.)
Full Explanation
A. Converts fibrinogen to fibrin: that reaction is carried out by thrombin, not plasmin.
B. Breaks down fibrin, dissolving the clot: plasmin is the primary enzyme of fibrinolysis, cleaving fibrin to dissolve formed clots.
C. Triggers the extrinsic clotting mechanism, leading to clot formation: the extrinsic pathway is initiated by tissue factor (factor III) interacting with factor VII, not plasmin.
D. Inactivates thrombin, slowing clot formation: plasmin’s main role is fibrin breakdown; thrombin is primarily regulated by antithrombin, thrombomodulin–protein C systems. (Plasmin can degrade some clotting proteins but it is not described as the main inactivator of thrombin.)
Jose has no A and no B antigens on his red blood cells. Jose's blood type is:
A. Туре В
Type B: Type B RBCs express B antigen, so “no A and no B” would not be type B.
B. Type A
Type A: Type A RBCs express A antigen, so not correct here.
C. Type O
Type O: Type O RBCs lack both A and B antigens (so they are “no A, no B”).
D. Туре АВ
Type AB: Type AB RBCs express both A and B antigens, opposite of “no A and no B.”
Full Explanation
A. Type B: Type B RBCs express B antigen, so “no A and no B” would not be type B.
B. Type A: Type A RBCs express A antigen, so not correct here.
C. Type O: Type O RBCs lack both A and B antigens (so they are “no A, no B”).
D. Type AB: Type AB RBCs express both A and B antigens, opposite of “no A and no B.”
The hormone
Full Explanation
A. Colony-stimulating factor; negative: colony-stimulating factors (CSFs) chiefly stimulate white blood cell production, not RBCs. The feedback characterization here is not applicable to erythropoiesis.
B. Erythropoietin; positive: erythropoietin (EPO) does stimulate RBC production, but the regulatory loop is negative feedback. So labeling it “positive” is wrong.
C. Erythropoietin; negative: EPO is the hormone that stimulates RBC production and it is regulated by a negative feedback mechanism based on tissue oxygenation.
D. Colony-stimulating factor; positive: CSFs affect leukocyte lines, and erythropoiesis is not regulated by a positive-CSF loop.