Self-test 1-1

1. Increase in blood flow in the injured part.
2. Starling s law deals with the relationship between hydrostatic pressure and osmotic pressure in the movement of fluid in and out of arterioles, capillaries, and venules.
3. Vasodilatation and increased vascular permeability. These result in increased intravascular hydrostatic pressure, reduced intravascular osmotic pressure, and increased osmotic pressure in the extravascular space.
4. Severity of the injury.
5. Increased blood flow in arterioles, capillaries, and venules.
6. Increases blood flow in capillary bed by allowing more blood to enter capillaries and opening inactive capillaries.
7. Loss of fluid from the bloodstream resulting in an increase in the concentration of RBCs.
8. Increased vascular permeability leading to loss of fluid from vessels and hemoconcentration. Leukocyte margination contributes by increasing resistance to blood flow.
9. Postcapillary venules.
10. Contraction of endothelial cells.
11. Albumin, fibrinogen, immunoglobulins, and other high molecular weight proteins.

Self-test 1-2

1. Vasodilatation, vascular stasis, and increased vascular permeability.
2. 1. Vasodilatation.
   2. Intracellular gaps between endothelial cells.
   3. Increased hydrostatic pressure in vessels.
   4. Destruction of endothelial cells can also increase permeability (providing the basement membrane remains intact, otherwise there would be hemorrhage).
3. The severity of the injury determines the extent to which chemical mediators that control the vascular response are produced or released.
4. Fluid, plasma proteins, or cells leave the vessels and enter the tissues.
5. An abnormal amount of fluid in the tissue spaces.
6. Serous exudate is fluid that is low in protein, whereas a fibrinous exudate is rich in protein, particularly fibrinogen.
7. Biphasic means that there is an immediate increase in vascular permeability followed first by a decrease and later by another increase.
8. Exudation is an inflammatory process involving increased vascular permeability. Transudation is a noninflammatory condition that results from one or more of the following: (a) increased intravascular hydrostatic pressure, (b) decreased osmotic pressure in vessels, (c) increased osmotic pressure in extravascular compartment.
9. They perform an important function by removing leukocytes, cellular debris, plasma proteins, and fibrin.
10. Fluid can be drained by blood vessels, particularly the venules.

Self-test 2-1

1. Histamine.
2. Refer to list on page 32.
3. When activated, it gives rise to prekallikrein activator (PKA).
4. By coming into contact with collagen or basement membrane in the walls of damaged blood vessels.
5. Histamine’s action is of short duration—probably only a few minutes.
6. Kinin system, fibrinolytic system, complement system.
7. 1. Release of proteases such as trypsin and pepsin from injured cells.
   2. Activation of Hageman factor.
   3. Passage of prekallikrein into tissues.
   4. Activation of plasminogen during blood clotting.
8. Vasodilatation: increases vascular permeability.
9. Formation of kinins. Formation of vasoactive peptides from fibrin and fibrinogen.
10. Histamine.
11. Kallikrein cleaves kininogen to produce bradykinin. It can also activate Hageman factor.

Self-test 2-2

1. Histamine, kinins, fibrin split products, prostaglandins, leukotrienes, and complement components C3a and C5a.
2. Arachidonic acid.
3. When it binds specifically to antigen the structure of the antibody molecule is altered. This provides a binding site for C1q.
4. Cleavage of C2 results in formation of a kinin-like molecule. In addition, the anaphylatoxins C3a and C5a are vasoactive agents.
5. Lipoxygenase pathway.
6. Leukotrienes C₄, D₄, and E₄. SRS-A produces bronchospasm, vasodilatation, increased vascular permeability, and it stimulates mucus secretion.
7. C3.
8. Cleavage of C3 yields C3a and C3b. C3b can bind to B yielding C3b,B. C3b,B can stimulate further formation of C3a and C3b, and so on. This is an important amplification mechanism.
9. Convertase.
10. It induces vascular smooth muscle relaxation.
11. Axon reflex (antidromic stimulation).

Self-test 3-1

1. Phagocytes (neutrophils and macrophages).
2. Postcapillary venules.
3. Cells must marginate.
4. Interaction between specific adhesion molecules present on the surfaces of leukocytes and endothelial cells.
5. 1. Stimulate direction of migration.
   2. Combine with receptor sites on cell membrane of leukocyte.
   3. Water soluble, diffusible.
   4. Usually polypeptides or small proteins.
   5. Come from a number of sources, endogenous and exogenous.
6. C5a.
7. Rearrangement of cytoskeletal microtubules and microfilaments.
8. Substances that enhance phagocytosis by helping leukocytes to adhere to cells to be ingested.
9. C3a—anaphylatoxin C3b—opsonization C5a—anaphylatoxin, chemotaxin C8 and C9—cell lysis.

Self-test 3-2

1. Complement component C3b and opsonizing antibodies.
2. Phagocytic vacuole.
3. Microbes are killed by antibacterial agents (if possible), and the remains are digested by lysosomal enzymes.
4. The granules fuse with the phagocytic vacuole and release their contents into the vacuole.
5. There is a sharp increase in oxygen consumption with formation of reduced forms of oxygen (oxygen-derived free radicals).
6. By converting oxygen to free radicals that are bactericidal.
7. NADPH oxidase.
8. Lactic acid, hydrogen peroxide, hydroxyl radical, and hypochlorous acid.
9. Lysosomal enzymes, cytolytic proteinases, cationic proteins, lysozyme, lactoferrin, and myeloperoxidase.
10. By damaging host tissue (free radicals, proteolytic enzymes).
11. By enzymes such as superoxide dismutase and catalase; antioxidants like vitamin E and glutathione.

Self-test 3-3