Pop Quiz 2 Flashcards

1
Q

Factor I

A

(Fibrinogen) Plasma protein synthesized in the liver; converted to fibrin in the common pathway

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2
Q

Factor II

A

(Prothrombin) Plasma protein synthesized in the liver (requires vitamin K); converted to thrombin in the common pathway

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3
Q

Factor III

A

Thromboplastin (tissue factor) - Mixture of lipoproteins released from damaged tissue; required in the extrinsic pathway

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4
Q

Malaria

A

Caused by a protozoan introduced into blood by Anopheles mosquito; symptoms include chills and fever produced by toxins released when the protozoan causes red blood cells to rupture

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5
Q

Hemophilia

A

Genetic disorder in which clotting is abnormal or absent.

(each of the several types results from deficiency or dysfunction of a clotting factor; most often a sex-linked trait that occurs almost exclusively in males)

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6
Q

Von Williebrand Disease

A

Platelet plug formation and blood clotting are impaired due to low or dysfunctional von Willebrand factor.

(Treatment involves injections of von Willebrand factor or drugs that boost its levels, helping platelets stick to collagen and activate properly.)

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7
Q

Thrombocytopenia

A

Reduction in the number of platelets that leads to chronic bleeding through small vessels and capillaries;

(causes include genetics, autoimmune disease, infections, and decreased platelet production resulting from pernicious anemia, drug therapy, radiation therapy, or leukemias)

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8
Q

Anemia

A

deficiency of hemoglobin in the blood

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9
Q

Iron-deficiency anemia

A

Low iron leads to reduced hemoglobin production

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10
Q

Folate-deficiency anemia

A

Inadequate folate in the diet results in a reduction in cell division and therefore a reduced number of red blood cells

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11
Q

Pernicious anemia

A

Secondary folate-deficiency anemia caused by inadequate amounts of vitamin B12, which is important for folate synthesis

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12
Q

Hemorrhagic anemia

A

Results from blood loss due to trauma, ulcers, or excessive menstrual bleeding

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13
Q

Hemolytic Anemia

A

Occurs when red blood cells rupture or are destroyed at an excessive rate;

(causes include inherited defects, exposure to certain drugs or snake venom, response to artificial heart valves, autoimmune disease, and hemolytic disease of the newborn)

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14
Q

Aplastic Anemia

A

Caused by an inability of the red bone marrow to produce red blood cells,

(usually as a result of damage to stem cells after exposure to certain drugs, chemicals, or radiation)

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15
Q

Thalassemia

A

Autosomal recessive disease that results in insufficient production of globin part of hemoglobin

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16
Q

Steps for platelet Plug

A
  1. Platelet Adhesion: Platelets bind to exposed collagen at a damaged vessel, primarily through von Willebrand factor (vWF), which bridges collagen and platelets.
  2. Platelet Release Reaction: Activated platelets release ADP and thromboxanes, triggering a positive feedback loop that activates more platelets.
  3. Platelet Aggregation: Activated platelets express fibrinogen receptors, and fibrinogen bridges these receptors between platelets, forming a platelet plug.
17
Q

Extrinsic Pathway

A

Starts outside the blood: Triggered by damage to tissues.

Factor III (thromboplastin) Released: Damaged tissues release a protein called tissue factor (also known as factor III/Thromboplastin).

Activation of Factor X: With the help of calcium (Ca²⁺), tissue factor combines with factor VII to activate factor X.

18
Q

Intrinsic Pathway

A

Starts inside the blood: Triggered by damage to blood vessels.

Factor XII Activated: When blood vessel damage exposes collagen, factor XII is activated.

Chain Reaction: Factor XII activates factor XI, which then activates factor IX.

Activation of Factor X: Factor IX teams up with factor VIII, platelet phospholipids, and calcium (Ca²⁺) to activate factor X.

19
Q

Antithrombin

A

Produced by liver, slowly inactivates thrombin

20
Q

Prostacylin

A

Causes vasodilation and inhibits release of coagulating factors from platelets.

21
Q

Hemolytic Disease of the newborn

A

1. (Rh- negative woman) In the first pregnancy with an Rh-positive fetus, there’s usually no problem as there’s not enough time for the mother to make anti-Rh antibodies.

2. After exposure, the mother becomes sensitized and produces anti-Rh antibodies for future pregnancies.

3. In later pregnancies, these antibodies can harm an Rh-positive fetus if fetal blood mixes with the mother’s blood.

4. Anti-Rh antibodies can cross the placenta and destroy fetal red blood cells, causing hemolytic disease of the newborn (HDN).

22
Q

Common Pathway

A
  • Prothrombinase is formed from the intrinsic and/or extrinsic pathways, combining factor X, factor V, platelet phospholipids, and calcium (Ca²⁺).
  • Prothrombinase converts prothrombin into thrombin.
  • Thrombin converts fibrinogen to fibrin and activates factor XIII to stabilize the clot.
23
Q

Anticoagulants

A

prevent coagulation factors from initiating clot formation.