Regarding the anti-clotting mechanisms, all are true except: a) Plasmin lyses fibrin and fibrinogen into fibrinogen degradation products (FDP). b) Thromboxane A2 released from plat... Regarding the anti-clotting mechanisms, all are true except: a) Plasmin lyses fibrin and fibrinogen into fibrinogen degradation products (FDP). b) Thromboxane A2 released from platelets prevents platelet plug formation. c) The clotting factors are formed by the liver in an inactive form. d) Heparin and antithrombin III inhibit the activity of some clotting factors in the liver. Regarding normocytic normochromic anemia: a) It is caused by acute massive bleeding. b) Total Hb concentration is not affected. c) The amount of Hb in each RBC is reduced. d) The size of the single RBCs is reduced.
Understand the Problem
The question is addressing anti-clotting mechanisms and aspects of normocytic normochromic anemia. It asks for clarification on which statements regarding these topics are true or false.
Answer
Thromboxane A2 prevents platelet plug formation is incorrect.
The correct statements are: a) Plasmin lyses fibrin, c) Clotting factors are made in inactive form, and d) Heparin and antithrombin III inhibit clotting factors. The incorrect statement is: b) Thromboxane A2 released from platelets prevents platelet plug formation.
Answer for screen readers
The correct statements are: a) Plasmin lyses fibrin, c) Clotting factors are made in inactive form, and d) Heparin and antithrombin III inhibit clotting factors. The incorrect statement is: b) Thromboxane A2 released from platelets prevents platelet plug formation.
More Information
Thromboxane A2 actually promotes the formation of the platelet plug by promoting platelet aggregation. Normocytic normochromic anemia usually results from acute blood loss or chronic disease, affecting total Hb levels.
Tips
A common mistake is misunderstanding the role of Thromboxane A2; it promotes rather than inhibits platelet aggregation and plug formation.
Sources
- Physiology, Clotting Mechanism - StatPearls - NCBI Bookshelf - ncbi.nlm.nih.gov
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