Nursing Pharmacology – MIDTERMS REVIEWER #1

Introduction to the Immune Response and Inflammation

Body Defenses

1. First Line of Defense

a. Skin
 Physical barrier; normal bacterial flora helps destroy many disease-causing
pathogens.
b. Mucous Membranes
 Respiratory tract, gastrointestinal tract, genitourinary tract, perineal, and rectal
area.
 Secretes sticky mucus capable of trapping invaders and inactivating them.
 Cilia; tiny hair like processes that sweep any captured pathogen.
 GI Tract; mucous membrane serves as a) protective coating, preventing
erosion of GI cells, b) lubricates the GI tract to facilitate movement of the
food bolus and waste products, and c) acts as a thick barrier to prevent
pathogens from penetrating the GI tract.
 GU Tract; mucous membrane provides direct protection against injury and
trauma and traps any pathogen in the area.
c. Secretions
 Sebum, mucus enzymes that chemically inhibit the activity of pathogens.
d. Gastric Acid
 Acidity in the stomach destroys many pathogens that are either ingested or
swallowed.
e. Major Histocompatibility Complex (MHC)
 Genetic identification code is carried on chromosome.
 Produces several proteins called histocompatibility antigens, or human
leukocyte antigens.
 Histocompatibility Antigens; located on the cell membrane and allow the
body to recognize cells as being self-cells.
2. Second Line of Defense
 Inflammatory Response, Phagocytosis, NK Cells Lysis, Biologic Response Modifiers,
and Interferon Complement.
 Cellular Defenses; Stem cells in the bone marrow produces two types of WBC
(lymphocytes and myelocytes).
 Lymphocytes; Consists of T cells, B cells, and NK cells.
 Myelocytes; Neutrophils, basophils, eosinophils, and monocytes/macrophages.

a. Neutrophils
 Polymorphonuclear, capable of moving outside the blood stream (diapedesis)
and engulfing + digesting foreign materials (phagocytosis)
 Responds to bacterial infection (pyogenic infection), acute inflammation,
heart attack or burn.
b. Basophils
 Important for initiating and maintaining an immune or inflammatory response.
 Includes histamine, heparin, and other chemicals.
 Responds to chronic inflammation (rheumatoid arthritis, ulcerative colitis, and
inflammatory bowel disease), infections (chicken pox, tuberculosis),
myeloproliferative disorders (chronic myelogenous leukemia, essential
thrombocythemia, myelofibrosis) and severe allergies.
c. Eosinophils
 Found at the site of allergic reactions and may be responsible for removing the
protein and active components of the immune reaction from the site of an
allergic response.
 Responds to parasitic infection, allergic reaction, and cancer.
d. Monocytes/Macrophages
 Mature leukocytes capable of phagocytizing an antigen.
 Removes foreign material from the body, including pathogens, debris from
dead cells, and necrotic tissue from an injury site.
 Fixed in specific tissues such as the Kupffer cells in the liver, the cells in the
alveoli of the respiratory tract, and the microglia in the CNS, GI, circulatory,
and lymph tissues.
e. Lymphoid Tissues
 Lymph nodes, spleen, thymus gland, bone marrow, and lymphoid tissue
throughout the respiratory and GI tracts.
 Bone Marrow; differentiation of the cellular components of MPS.
 Thymus Gland; final differentiation of the T cells.
 Lymph Nodes and Tissues – store concentrated populations of myelocytes.
f. The Inflammatory Response

Kinin System

 Kallikrein; activated by the Hageman factor, found in the local tissues and
causes precursor substance kininogen to be converted to bradykinin and
other kinins.
 Bradykinin; causes local vasodilation, bringing more blood to the injured
area and allows WBC to escape into the tissues, and also stimulates nerve
endings to cause pain, alerting the body to the injury.
 Arachidonic Acid; released by bradykinin, releases substances called
autacoids.
 Autacoids; local hormones that cause an effect in the immediate area and
then are broken down.
 Prostaglandins; augment the inflammatory reactions and blocks it.
 Leukotrienes; cause vasodilation and increased capillary
permeability, and some block the reaction.
 Thromboxanes; cause local vasoconstriction and facilitates platelet
aggregation and blood coagulation.
 Histamine Release

 Histamine; causes vasodilations, it also alters capillary permeability,

making it easier for neutrophils and blood chemicals to leave the
bloodstream and enter the injured area. It stimulated pain perception.

Chemotaxis

 Property of leukotrienes which has the ability to attract neutrophils and to

stimulate them and other macrophages to be aggressive, leading to cell
injury and destruction.

Clinical Presentation

 Calor; heat caused by the increased blood flow in the area.

 Tumor; swelling caused by the fluid that leaks into the tissues.
 Rubor; redness caused by the increased blood flow in the area.
 Dolor; pain caused by the activation of pain fibers by histamine and the
kinin system.
 Function Laesa or Loss of Function
 Pyrogen; fever causing substance released by neutrophils.
 Leukotrienes; induces slow-wave sleep and causes myalgia and arthralgia.
3. Third Line of Defense
a. T Cells (Cell Mediated Immunity)
 Programmed in the thymus gland and provides cell-mediated immunity.

Cell Types

 Effector or Cytotoxic T Cells; aggressive against nonself cells, releasing

cytokine that can directly destroy a foreign cell or mark it for aggressive
destruction by phagocytes via inflammatory response.
 Helper T Cells; responds to the chemical indicators of immune activity and
stimulates other lymphocytes, including B Cells to be more aggressive and
responsive.
 Suppressor T Cells; responds to rising levels of chemical to suppress or slow
the reaction, allowing the body to conserve energy and the basic components
necessary for basic protection and to prevent cellular destruction from a
continued inflammatory reaction.
b. B Cells (Antibody Mediated Immunity)
 Found throughout the MPS in groups called clones.
 Programmed to identify specific proteins or antigens.
 Provides humoral immunity.
 Develops in the lymph nodes and spleen, and activates when it binds with a
specific antigen.
 Types of Antigen-Antibody Reactions

 Agglutination
 Precipitation
 Neutralization
 Lysis
 Opsonization
c. Complement Proteins
 Reacts in a cascade fashion to form a ring around the antigen-antibody
complex.
 Destroys the antigen by altering the membrane, allowing an osmotic inflow of
fluid that causes the cell to burst.
d. Antibody Formation
 Formation of antibodies takes several days.
 Once activated, the B cells form memory cells that will produce antibodies if
an antigen is encountered.

Types of Immunoglobulins

 IgM – first Ig being released when the body is exposed to an antigen.

 IgG – contains antibodies made by memory cells that circulate and enter
the tissue, most abundant Ig in the serum.
 IgA – found in tears, saliva, sweat, mucus, and bile, it is secreted by
plasma cells in the GI and respiratory tract and in epithelial cells. These
react with specific antigens encountered in exposed areas of the body.
 IgE – present in small amounts and is related to allergic responses and
activation of mast cells.
 IgD – role has not yet been determined.
e. Other Mediators
 Interferons; secreted by cells that have been invaded by viruses and possible
other stimuli. They prevent viral replications and also suppress malignant cell
replication and tumor growth.
 Interleukins; secreted by active leukocytes to influence other leukocytes. IL-1
stimulates T and B cells to initiate an immune response. IL-2 is released from
active T cells to stimulate the production of more T cells and to increase the
activity of B cells, cytotoxic cells, and NK cells. It causes fever, arthralgia,
myalgia, and slow-wave sleep inductions.
 Thymosin; thymus hormone that has been replicated, involved in the
maturation of T cells and cell mediated immunity.
 Tumor Necrosis Factor; cytokine that is released by macrophages that inhibits
tumor growth and can cause tumor regression.