Patho 2009 - Unit 3

Front 1

Compare and contrast humoral and cellular immunity.
Pg. 213

Back 1

Humoral (B cell mediated)
A. Initiation of the immune response
B. Plasma cell production of memory cells and immunglobulins (antibodies)
C. The different classes of antibodies, their structure(heavy and light chains, Fab and Fc portions and their functions), size, and function
D. The Complement System
1. A number (of three different sources, I have three different numbers ranging from 8 to 18) of proteins and their components (which are designated numbers and letters by the "C".
2. Requires an antibody/antigen (usually IgG is the antibody) complex to begin the classic pathway cascade.
3. The following are important for you to know and are well explained in your book:
a. The actions of the complement system (how does the system aid in immunity?) For example, opsonization, chemotasix, etc.
b. The complement protein that begins the alternative pathway
c. What stimulates the alternative pathway
d. The role of complement in the inflammatory process
E. The secretory immune system
1. Location of antibodies in the secretory immune system
2. The principle secretory antibody in this system. What other antibodies are present in secretion?
3. The primary role of the secretory antibody?
4. The differences between the body immune system and the secretory immune system.
Cellular Immunity
A. The five types of T cells and their functions
B. The way T cells proliferate and mature
C. The importance of the Cluster of Differentiation - CD. They are produced by the T cell during maturation in the Thymus and inserted into the plasma membrane of the T cell. These antigens participate in the immune response.
D. The effects of mature T cells binding with an antigen and the difference between T cell proliferation in the Thymus versus T cell proliferation when bound to an antigen
E. The main effects of cell-mediated immune response
F. Natural Killer cells NK
G. Cellular interactions in the immune response - This is an important concept for you to understand. Remember that very few antigens bind with B cells without the help of T cells. We go back to another unit where we know that cells are social and they talk with one another. There is this transmission system in the body between cells. Most of the time, all the cells involved in immunity are needed to get the job done. In most cases, the antigen is first met by the macrophage that processes the antigen and presents it to a T cell. This is usually a T helper (Th) cell that than presents the antigen to a B cell or T cytotoxic cell (Tc). The B cell and the Tc cell than begin to differentiate and proliferate.
H. Cytokines - The "hormones of the immune response".
1. Functions
2. Interleukins
3. Interferon
4. Tumor Necrosis Factor
5. Colony Stimulation Factor
6. Transforming Growth Factor

Front 2

Discuss the different types of antibodies with a focus on origin, function, and specificity.
Pg. 238

Back 2

Direct or indirect antibodies, antibodies of the systemic immune system, cytotoxic T cells, natural killer cells. Look this one up, way too complicated to write down. Getting patho for dummies!!

Front 3

Discuss the significance of HLA in defending the body.
Pg. 218

Back 3

A. An area on the short arm of chromosome 6
B. Contains coding for three classes of HLA's
C. HLA's are found on all nucleated body cells (remember erythrocytes are not nucleated).
D. These are genetically determined, so even though they are antigens, the body sees them as "self" so they do not normally trigger the immune response. The distinguishing of "self" is their main function during the immune response. There is also part of the MHC that controls the quality and quantity of the immune response.
E. The different classes of antigens are found on different types of cells. For example, Class I antigens are found on the surface of almost all nucleated cells but Class II antigens are found on specific cells such as B lymphocytes, macrophages, and some epithelial cells.
F. Named Human Leukocyte Antigen because they were first seen on white cells.

Front 4

Define primary and secondary immune responses.
Pg. 214

Back 4

Primary immune response is time interval between the first and second exposure to an antigen, during which antibodies against the antigen are produced.
Secondary immune response – the rapid, strong response by T and B cells to a second or subsequent appearance of an immunogen. This occurs because of the availability of T and B lymphocyte memory cells.

Front 5

Discuss the inflammatory response.
Pg. 175

Back 5

Our bodies second line of defense against invading microorganisms, is nonspecific, rapidly initiated, and has no memory cells.

Front 6

State the local and systemic manifestations of inflammation.
Pg. 198

Back 6

Local – are the result of the vascular changes associated with the inflammatory process, including vasodilation and increased capillary permeability. The symptoms include redness, heat, swelling, and pain. The vascular changes are to dilute toxins, carry plasma proteins and leukocytes to the injury site, and carry bacterial toxins and debris away from the site.
Systemic – three primary systemic effects of inflammation are fever, leukocytosis, and increase in levels of circulating plasma proteins. Acute phase reactants are proteins produced by the liver during acute inflammation and include fibrinogen, c reactive protein, haptoglobin, amyloid a antitrypsin, and ceruloplasminl.

Front 7

Describe the role of the mast cell in the activation of the immune response. Include the effects of histamine, serotonin, the leukotrienes, and prostaglandins.
Pg. 187

Back 7

Mast cell – of the connective tissue that produces substances that cause activation of the inflammatory response, vasoconstriction, and muscle contraction
Histamine – vasoactive amine that causes temporary, rapid constriction of the large vessel walls and dilation of the postcapillary venules, both of which result in increased blood flow into the microcirculation. Increased vascular permeability resulting from retraction of endothelial cells lining the capillaries.
Serotonin -
Leukotrienes – a mediator of the prolonged inflammatory response that acts to contract smooth muscle, increase vascular permeability, and attract neutrophils.
Prostaglandins – a mast cell derived substance that increases vascular permeability, muscle contraction and neutrophil chemotaxis, as well as induces pain, and potentially inhibits some aspects of inflammation.

Front 8

Discuss the role of the different cell types involved in inflammation

Back 8

Too much to list!

Front 9

Discuss the inflammatory response. Pg 179

Back 9

the inflammatory response, our body’s second line of defense against invading microorganisms, is rapidly initiated and has no memory cells.
Vascular response-observable characteristic-redness, heat, swelling, and pain 1) blood vessel dilation 2) increased vascular permeability and leakage of fluid out of the vessel3) wbc adherence to the inner walls of vessels and their migration through vessel walls to the site of injury.
Three plasma protein systems provide a biochemical barrier against invading pathogens in the circulation. These include the complement system, the clotting system, and the kinin system.
The plasma protein systems work together with each other as well as with antimicrobial peptides and the cellular component of the innate immune system to prevent microbial infection
The complement proteins can be activated in three pathways: the classical pathway, the alternative pathway, and the lectin pathway.
Activation of the complement pathways results in opsonization, activation of anaphylaxotins, cell lysis, and leukocyte chemotaxis.
The clotting cascade prevents spread of microorganisms, contains microorganisms and foreign bodies at site of greatest inflammatory cell activity and provides a framework for repair and healing.
The kinin system proteins promote vasodilatation and increased capillary permeability and induce pain.
Plasmin and Hageman factor (factor XII) interact to activate the clotting cascade, the complement system, and the kinin proteins.
The plasma proteins are finely regulated to prevent injury host tissue to guarantee activation when needed; some of the inhibitors in the plasma protein systems include carboxypeptidase, histaminases, kinases, and C₁ esterase inhibitor.

Front 10

State the local and systemic manifestations of inflammation. 198-199

Back 10

Local manifestations of inflammation are the result of the vascular changes associated with the inflammatory process, including vasodilatation and increased capillary permeability. The symptoms include redness, heat, swelling and pain. The function of vascular changes are to dilute toxins, carry plasma proteins and leukocytes to the injury sire and carry bacterial toxins and debris away from the site.
Systemic manifestation of acute inflammation. The three primary systemic effects of inflammation are fever, leukocytosis, and increase in levels of circulating plasma proteins. Acute phase reactants are proteins produced by the liver during acute inflammation and include fibrinogen, C-reactive protein, haptoglobin, amyloid A, α₁-antitrypsin, and ceruloplasmin

Front 11

Describe the role of the mast cell in the activation of the immune response. Include the effects of histamine, serotonin, the leukotrienes, and prostaglandins. Pg 187

Back 11

Many different types of cells are involved in the inflammatory process including mast cells, neutrophils, monocytes, and macrophages, eosinophils, natural killer (nk) cells, platelets, and nonleukocytic cells

The cells of the innate immune system secrete many biochemical mediators that are responsible for the vascular changes associated with inflammation and for modulating the localization and activities of other inflammatory cells, the mediators include histamine, chemo tactic factors, leukotrienes, prostataglandins, and platelet-activating factor.

The inflammatory response is initiated upon tissue injury or when pathogen-associated molecular patterns (PAMPS) are recognized by pattern recognition receptors (PRRs) in cells of the innate immune system.

The PRR’s include toll-like receptors (TLRs) complement, scavenger, glycan, and mannose receptors.

TLRs recognize PAMPs’ complement receptors recognize complement fragments; and scavenger receptors promote phagocytosis.

Front 12

Discuss the role of the different cell types involved in inflammation 184-196

Back 12

Most cells are central cells if inflammation and release histamine, chemotactic factors, cyctokines, leukotriense, prostoglandins, growth factors, and other mediators.

H1 histamine receptors promote inflammation, and H@ histamine receptors inhibit the inflammatory response.

Phagocytosis the destruction of microorganisms and cellular debris
The stages of phagocytosis include recognition and adherence, engulfment, lysosomal fusion and destruction.

Phagocyctic killing can oxygen –dependent with the production of reactive oxygen intermidiates or oxygen-independent with lysosomal enzymes.

Neutorphils are the predominant phagocyte of early inflammation. They are attracted to the inflammatory site by chemotoxins.

Monocytes and macrophages arrive at the inflammatory site later than neutrophils and remain longer to clean up debris and promote wound healing.

Eosonophils help control mast mast cell vascular mediators and defend against parasite infection.

Natural killer cells recognize and eliminate viruses, cancer cells and other abnormal cells

Platelets interact with the coagulation cascade to stop bleeding and release a number of mediators that promote and control inflammation

Front 13

Identify the cytokines that take part in the inflammatory response. Include their origin and their role. 196

Back 13

Cytokines are soluble factors that regulate the inflammatory response and include interleukins, interferons and tumor necrosis factor.

Interleukins (IL) are biochemical messengers primarily produced by macrophages and lymphocytes and significantly help regulate the inflammatory response.

Interferons (INFs) provide protection from viral infections in uninfected cells.
Tumor necrosis factor is primarily produced by macrophages and promotes inflammation with both local and systemic effects.

Chemokines are synthesized by a number of different cells and induce leukocytes chemotaxis and are classified as either CC or CXC, depending on their amino acid arrangement, cc chemokines generally affect neutrophils.

Front 14

Describe the steps in wound healing. Pg 201-205

Back 14

Resolution (regeneration) is the return of tissue to nearly normal structure and function. Repair is healing by scar tissue formation.
Inflammatory lesions proceed to resolution, meaning that original tissue structure and function have been restored, if little tissues has been lost or injured tissue is capable of regeneration. This is called healing by primary intention.
Inflammatory lesions that involve extensive damage or tissues incapable of regeneration heal by the process of repair that results in the formation of a scar. This is called healing by secondary intention.
Resolution and repair occur in two separate phases, the reconstructive phase in which the wound begins to heal and the maturation phase in which the healed would is remolded.

Front 15

Discuss the types of dysfunctional wound healing. Pg 204-206

Back 15

Dysfunctional wound healing may occur if any the involved processes occurs abnormally. This can include abnormalities in the inflammatory response itself, insufficient or excessive repair, or if a wound is re-infected. Abnormalities may result from a predisposing disease, such as DM or from an acquired condition such as hypoxemia. Numerous drugs and nutrients can affect wound healing as well.
Dysfunction during inflammatory response- healing may be prolonged if bleeding during acute inflammation.