#03: Blood II Continued

Question 1

Blood types are important for clinical transfusions.

Answer 1

○ If a person is transfused with blood of an incompatible type, anti-bodies in the plasma bind to surface antigens of the transfused erythrocytes, and clumps of erythrocytes bind together in a process called agglutination.
§ Clumped RBCs can block blood vessels and prevent normal circulation of blood. Eventually some or all of the clumped cells may rupture in hemolysis. The release of RBC components into blood often causes further reactions and may damage organs.

Question 2

Rh

Answer 2

• There’s another common surface antigen on RBC membranes that’s part of the Rh blood type. It is determined by presence or absence of the Rh surface antigen.
○ Antibodies of the Rh factor appear in the blood ONLY when an Rh- person is exposed to an Rh+ blood.

Question 3

Hemolytic Disease

Answer 3

Rh antibodies are only really concerning in pregnant women who are Rh- and have an Rh+ fetus. An Rh incompatibility may result during pregnancy if the mother has been previously exposed to Rh+ blood (like from a previous fetus). Because the Rh antibody can cross the placenta, unlike other antibodies, the mother’s AB for Rh may cross the placenta and destroy the fetal RBCs, resulting in severe illness or death of fetus.

Treatment is done by giving women special immunoglobulins that prevents her from developing the Rh antibodies during pregnancy.

Question 4

Antibodies In Donor Blood?

Answer 4

• Antibodies are only produced when you need them. So donor blood will not have enough of them to make sizable impact on recipient.

Question 5

Antigen H

Answer 5

• Both A and B antigens come from a percursor called Antigen H.
○ Bombay Blood is where someone is a carrier of incomplete H deficiency (H/h). When two carriers mate, their h/h child is unable to produce any ABO blood group antigens and so despite inheriting the A or B antigen from a parent, the child’s RBC’s lack the A or B antigen as in blood type O.

Question 6

Leukopenia

Answer 6

• Leukopenia is a serious disorder where there’s a reduced number of leukocytes. May result from viral or bacterial infection, certain types of leukemia, or toxins that damage the bone marrow.

Question 7

Leukocytosis

Answer 7

• Leukocytosis results from an elevated WBC count and is often indicative of infection, inflammatory reaction, or extreme physiologic stress.

Question 8

Diapedesis

Answer 8

• WBCs leave blood by binding to capillary wall (margination) and squeeze between endothelial cells (emigration). Whole process is called diapedesis.

Question 9

Leukocyte Motion

Answer 9

• Leukocytes demonstrate amoeboid motion, or the ability to move like an amoeba by extending irregular cytoplasmic projections.

Question 10

Leukocytes Use Chemotaxis

Answer 10

• Leukocytes move to sites of infection by chemotaxis, the movement of cells in response to specific chemicals.

Question 11

Granulocytes vs. Agranulocytes

Answer 11

• Granulocytes have granular cytoplasms, while agranulocytes do not.

Question 12

List of Granulocytes

Answer 12

Neutrophils, Eosinophils, Basophils

Question 13

Neutrophils

Answer 13

○ Neutrophils are the most abundant (50-70%), first line of defense. They’re phagocytic, attract other phagocytes to area. Short life span, form pus at wound.

Question 14

Eonsinophils

Answer 14

○ Eosinophils are lowly abundant (2-4%). Phagocytic, remove larger particles/pathogens by exocytosis of chemicals, and regulate inflammation.

Question 15

Basophils

Answer 15

○ Basophils have abundancy of <1%. NOT phagocytic. They migrate to the site of injury and release histamine and heparin.
§ Histamine dilates blood vessels.
§ Heparin prevents blood clots.

Question 16

List of Agranulocytes

Answer 16

Monocytes & Lymphocytes

Question 17

Monocytes

Answer 17

○ Monocytes have 2-8% abundancey. Largest in size. They become macrophages, migrate to site of injury and attract other phagocytes & fibroblasts.

Question 18

Lymphocytes

Answer 18

○ Lymphocyte (20-30%) have 3 subtypes. T Cells (specific immunity), B cell (release antibodies) and NK cell (surveillance).

Question 19

Nonspecific Defense WBCs

Answer 19

• Nonspecific Defense (Innate Immune System): Neutrophil, Eosinophil, Monocyte, Basophil

Question 20

Specific Defense WBCs

Answer 20

• Specific Defense (Acquired Immune System): Lymphocytes

Question 21

Leukemia

Answer 21

• Leukemia is a cancer causing abnormal development and proliferation of WBCs, in both bone marrow and in the circulating blood.
○ Lymphocytic Leukemia is increased numbers of malignant lymphocytes and/or lymphocytic precursors (lymphoblasts). Often involves lymph nodes and spleen.
○ Monocytic Leukemia is increased number of malignant and immature monocytic cells.

Question 22

Platelets

Answer 22

• Platelets are irregular, membrane-enclosed cellular fragments that are about 2 micrometers in diameter. Sometimes called thrombocytes, tho they don’t have a nucleus.
○ Severe trauma to a blood vessel causes the blood to coagulate, or clot. They lead to production of a web of fibrin that traps RBCs and platelets to halt blood flow.

Question 23

Hemostasis

Answer 23

• Hemostasis is serious of processes that stop bleeding. Triggered by damage or destruction of endothelial cells lining blood vessels.

Three stages are vascular spasm, platelet plug formation, and coagulation.

Question 24

Vascular Spasm

Answer 24

1. Vascular Spasm is a temporary response. Blood vessel smooth muscle contracts. This vasoconstriction decreases blood vessel’s diameter. It can close small blood vessels to prevent flow of blood. Slows blood loss until a clot can form. This phase is triggered by chemicals released from damaged cells or RBCs, and by nervous system reflexes.
   i. At site of damage, platelets stick and release thromboxanes, which are derived from prostaglandins, and endothelial cells release endothelien. Both chemicals stimulate this phase.

Question 25

Platelet Plug Formation

Answer 25

2. Platelet Plug Formation now occurs. Platelets accumulate at injury. They’re exposed to collagen filaments that provide site of platelet attachment, to which they bind.
   i. Platelets adhere to exposed collagen. Whether it be through a protein, von Willebrand factor, or directly.
   ii. Platelets bound to collagen release chemicals into local environment (ADP, thromboxanes, and others). They stimulate adhesion of platelets to each other and damaged areas, and in a positive feedback manner, release more platelets.
   iii. After activation, platelets express surface receptors that bind to fibrinogen, a plasma protein. The protein forms a bridge between the surface receptors of different platelets, creating a plug.
   iv. Activated platelets produce phospholipids (platelet factor III) and coagulation factor V, which aid in formation of clots.

Question 26

Coagulation

Answer 26

3. Coagulation is closure of the damaged blood vessel. Results in formation of clot (made up of fibrin fibers, platelets, blood cells, and fluid). Requires number of factors, phospholipids, fibrinogen, platelets, and other proteins. Made of three steps but main point is conversion of fibrinogen to fibrin.

Question 27

Pro Clotting Factors

Answer 27

○ Pro Clotting Factors: low serotoni, ADP, TxA2, PDGF, clotting factors

Question 28

Limiting Clotting Factors

Answer 28

○ Limiting Clotting Factors: PGI2(Prostacyclin), Anti-ADP enzymes, high serotonin, physical isolation of plug by clot formation.