Cardiovascular System (1B)

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Last updated 4:25 AM on 9/10/26
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49 Terms

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What is anemia and what can cause it?
Anemia is a deficiency of hemoglobin in the blood caused by either too few red blood cells or too little hemoglobin in the cells.
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What is hemorrhage blood loss anemia and what happens after rapid hemorrhage?
It occurs after rapid blood loss. The body replaces the fluid portion of plasma
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What are the characteristics of microcytic hypochromic anemia?
Red blood cells are much smaller than normal and contain too little hemoglobin.
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What is aplastic anemia and what can cause it?
Aplastic anemia is caused by a lack of functioning bone marrow. Possible causes include exposure to X-rays
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What is megaloblastic anemia and what causes it?
Megaloblastic anemia can result from loss of nutrients such as vitamin B12 or folic acid. This slows the reproduction of erythroblasts in the bone marrow
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What is hemolytic anemia and what are examples?
Hemolytic anemia results from abnormal breakdown of red blood cells
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What is polycythemia?
Polycythemia is an increase in the red blood cell count.
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What is secondary polycythemia and what happens to the RBC count?
Secondary polycythemia is associated with hypoxia. The red blood cell count commonly rises to about 6–7 million/mm³
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What is polycythemia vera (erythremia) and what causes it?
Polycythemia vera
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What are platelets and where do they come from?
Platelets are cytoplasmic fragments of megakaryocytes.
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What are the structural characteristics of platelets?
Platelets are flattened discs that appear spindle-shaped in a blood smear. They have an average diameter of 4 µm
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What is the lifespan of platelets and where are they removed?
Platelets have a lifespan of about 9–12 days and are then phagocytised in the spleen.
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What are the three major functions of platelets?
Platelets release chemicals important to clotting
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What is hemostasis?
Hemostasis is the process of halting blood loss. It is the arrest of bleeding from a broken blood vessel and the establishment of a framework for tissue repair.
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What are the three phases of hemostasis?
The three phases of hemostasis are the vascular phase
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What happens during the vascular phase of hemostasis?
When a blood vessel is cut
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What happens to endothelial cells during the vascular phase?
Endothelial cells contract and expose the basal lamina to blood. They release chemicals and hormones including ADP
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What is platelet adhesion?
Platelet adhesion is the process in which platelets stick to the endothelium
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What is platelet aggregation and what does it form?
Platelet aggregation occurs when platelets accumulate at the injury site and stick to one another
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What happens during platelet activation?
During platelet activation
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What are the major chemicals released by activated platelets and what are their functions?
ADP promotes platelet aggregation and secretion; thromboxane A2 and serotonin cause vascular spasms; clotting factors promote blood clotting; platelet-derived growth factors promote vessel repair; and calcium ions aid platelet aggregation and steps in the clotting process.
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What happens during the coagulation phase of hemostasis?
Blood clotting occurs through the conversion of fibrinogen to fibrin. Fibrin covers the platelet plug and traps blood cells
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What are the three pathways involved in coagulation?
The three pathways are the extrinsic pathway
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How does the extrinsic pathway begin and how does it activate Factor X?
The extrinsic pathway begins in the blood vessel wall. Damaged endothelial cells or peripheral tissues release tissue factor (Factor III). Tissue factor combines with Ca²⁺ and Factor VII to activate Factor X in the common pathway. It is a short and fast pathway.
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How does the intrinsic pathway activate Factor X?
Factor XII becomes activated when exposed to collagen fibres. Platelets release factors such as PF-3
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What happens in the common pathway after Factor X is activated?
Activated Factor X forms the enzyme prothrombinase. Prothrombinase converts prothrombin to thrombin
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What is the sequence of the common pathway?
Factor X activation → prothrombinase formation → prothrombin converted to thrombin → fibrinogen converted to fibrin.