Pathophys ch. 9 & 10 test 2

• 1.Redness (rubor)
• 2.Swelling (tumor)
• 3.Heat (calor)
• 4.Pain (dolor)
• 5.Loss of function (function laesa)

i.Increased vascular permeability—mast cells release chemicals such as histamine, prostaglandins, & leukotrienes, which cause vasodilatation, and increased vascular permeability.

• ii.Emigration (diapedesis) of leukocytes from the bloodstream into tissues—neutrophils (and other WBCs) roll and stick to the sides of blood vessels, a process called margination or pavementing.
• a.selectins—are receptors that aid neutrophil pavementing
• b.integrins—aid neutrophil movement through the capillary walls (diapedesis).
• c.chemotaxis—is the process by which leukocytes are attracted to inflamed tissue.

iii.Phagocytosis—if a microbe is small enough to be internalized, the phagosome is fused by a lysosome and digested. Larger particles are attacked by extracellular secretion of digestive enzymes.

• i.Transport leukocytes & antibodies
• ii.Dilute toxins & other irritants
• iii.Transport nutrients necessary for tissue repair.

• i.B cells provide “humoral immunity” because they secrete antibody into body fluids or “humors.”
• ii.T cells provide “cell-mediated immunity” because they recognize antigens presented on the surface of cells.

i. T-cells recognize foreign antigens through specialized TCT's (which can recognize only a single epitope)

ii. T-cells that might react to self-antigens are eliminated in the thymus.

• iii.Once T cells’ own TCRs are stimulated, they react in 2 different ways:
• a.T helper (CD4) cells—the CD4 protein binds to a MHC protein, while the TCR binds to its corresponding antigen. Does remembering that we have 4 fingers on a “helping hand” help you remember the “CD4” term?
• b. Cytotoxic (CD8) cells—Cytotoxic T cells require T helper cells before they can be fully effective—cytokines alone are not adequate. How about this for a mnemonic?—8-year-olds can be toxic…

memory cells, and effector cells.

An antigenic determinant, is the part of a macromolecule that is recognized by the immune system, specifically by antibodies

• B-cell function, which have B-cell receptors (BCRs), which are specific for a single epitope.
• Some B-cells can respond to nonprotein antigen (like bacterial sugars and lipids). This is important, because T-cells can only respond to protein antigens!

1.memory B cells (which function a lot like memory T cells), and

• 2.plasma cells—which are antibody production factories.
• a. They are basically grown-up B cells that have left home and found a full-time job.

• i. IgG—most common (75-80% of circulating antibody),
• predominates in the secondary (anamnestic) immune response.
• *Monomer (1 y)

• ii. IgM—10% of circulating antibody
• a.works best to activate complement (only one molecule of IgM is needed to activate complement, while 2 of IgG is needed)
• b.predominant antibody in the primary immune response
• c. (this is the predominant antibody made when our immune system is exposed to a particular antigen for the first time.)
• d.pentamer. (5 “Y”s)

• iii.IgA—found in secretions onto mucus membranes.
• a.Dimer. (There are 2 legs on an “A”)

• iv.IgD—found on B-cell membranes. Functions not well understood.
• a.Monomer.

• v.IgE—found on basophils & mast cells; important in allergies;
• a.monomer

• 1.precipitation—pulling antigens out of solution (blood stream)
• 2.agglutination—sticking groups of antigens together.
• 3.neutralization—just by binding, can make some bacterial toxins ineffective.
• 4.opsonization—enhance the function of phagocytic cells.
• 5.complement activation—particularly IgM & IgG are good at this

transfer of pre-formed antibody against a particular antigen from an immune person to a non-immune person.

(passive immunity) injection of specific “immune globulins. Examples: rabies immune globulin, hepatitis B immune globulin, West Nile Virus immune globulin, etc.

• i.occurs by antigen exposure and immune response of the person’s own immune system. Can be either:
• a.immunization—deliberate administration of vaccines or
• b.active infection—actually get infected by an organism.

A measure taken for the prevention of a disease or condition.

• a.Autoimmunity—the immune system recognizing ones own antigens as foreign and mounting an immune response against them: the loss of self-tolerance.
• b.Hypersensitivity—an excessive or inappropriately triggered immune response. Four varieties exist: I-III involve antibody; IV only T cells.

1.strongly genetic;

2.immediate hypersensitivity reaction because signs/symptoms of allergic reaction occurs immediately after contact with an allergen.

• 3.Mast cells are the principal effector cells, with cross-linking of IgE receptors on mast cell membranes the stimulus for degranulation and release of chemical mediators, including histamine which causes reactions like:
• a.Increased vascular permeability
• b.Vasodilatation (with flushing)
• c.Urticaria
• d.Smooth muscle constriction
• e.Pruritis
• f.Increased gut permeability

4.Treatment ranges from: nothing (mild cases), antihistamines, epinephrine, steroids, allergic desensitization, allergen avoidance, mast cell stabilization, etc.

1.antibody binding to tissue-specific antigens, which then causes complement activation

• 2.Examples of Type II reaction mechanisms include:
• a.Transfusion reactions—you should understand ABO blood typing system and the basics of this reaction, which is complement mediated.
• b.Hemolytic disease of the newborn—direct phagocytosis by effector cell (like macrophages) of antibody-coated fetal erythrocytes.
• c.Myasthenia gravis—antibodies against acetylcholine receptors at the motor end-plate causes complement to attack the receptor.

1.Not tissue specific: the damage is done when complexes of antigen/antibody are deposited in tissues, then complement is activated & neutrophils & mast cells go into action.

2.The different between II & III is that in type III reactions, the antigen/antibody complexes precipitate out of the bloodstream into whatever tissue is nearby, or oppositely electrically charged

• 3.Examples:
• a.Immune complex glomerulonephritis—usually occurs after streptococcal bacterial infections, with immune complexes deposited in the glomerular basement membrane.
• b.Systemic lupus erythematosus (SLE)—characterized by autoantibodies against nuclear antigens. ANY organ system can be involved.

1.Tissue damage caused by delayed reaction to an antigen.

2. Antibody not involved;

3.principal mediators are lymphokines—produced by lymphocytes;

4.principal effector cells are mast cells (only early in the reaction), lymphocytes & macrophages (not neutrophils).

• 5.Examples:
• a.Contact hypersensitivity—an epidermal reaction to a hapten, which is processed by Langerhans cells. Antigens include such things as nickel, clothing, plant oils (poison ivy/oak), ointments, etc.
• b.Tuberculin-type reaction—a dermal reaction to injected tuberculosis antigen. Used to diagnose previous TB exposure.
• c.Granulomatous hypersensitivity—indigestible antigen engulfed by macrophages, which then form epitheliod cells +/or multinucleated giant cells.

A small molecule that can elicit an immune response only when attached to a large carrier such as a protein

• i.Primary immune deficiencies—not attributable to another cause;
• ii.Secondary immune deficiencies—consequence of other disease processes or treatments.

• 1.B-cell & T-cell combined disorders:
• a.severe combined immunodeficiency disorders—the most severe form is reticular dysgenesis: failure of ALL leukocytes to form.
• b.Wiskott-Aldrich Syndrome—X-linked; IgM low; IgA/IgE high, IgG variable.

• 2.T-cell disorders:
• a.DiGeorge syndrome or thymic hypoplasia—total or partial loss of thymus function. Total loss fatal.
• b.Chronic mucocutaneous candidiasis—autosomal recessive; selective deficiency of cell-mediated immunity against Candida albicans (“yeast”). The correct cytokine necessary to combat this organism is missing.

• 3.B-cell disorders:
• a.IgA deficiency—affects 1 in 400 people; can be either autosomal recessive or dominant. They tend to have lots of respiratory, GI, and genitourinary tract infections, a higher incidence of vascular & collagen autoimmune diseases. Usually doesn’t shorten life, and many cases not diagnosed.
• b.Bruton X-linked agammaglobulinemia (congenital hypogammaglobulinemia—lack of normal bursal-equivalent tissue (where B cells mature).
• c.It was the first immunodeficiency disorder identified—1952.

• i.Stress—burns, trauma, pregnancy, infancy,
• ii.surgery,
• iii.nutritional deficiencies (both malnutrition and overnutrition!),
• iv.cancer chemotherapy drugs,
• v.viruses,
• vi.post-splenectomy patients reduces serum IgM and the antibody response to encapsulated bacteria.
• vii.Advanced age
• viii.And lots of others…