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N5315 Advanced Pathophysiology Inflammation, Altered Immunity and Infection Core Concepts Objectives with Advanced Organizers $15.99   Add to cart

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N5315 Advanced Pathophysiology Inflammation, Altered Immunity and Infection Core Concepts Objectives with Advanced Organizers

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N5315 Advanced Pathophysiology Inflammation, Altered Immunity and Infection Core Concepts Objectives with Advanced Organizers

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  • June 9, 2022
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  • 2021/2022
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N5315 Advanced Pathophysiology
Inflammation, Altered Immunity and Infection
Core Concepts Objectives with Advanced Organizers
Immune System
1. Examine the structure and function of the immune system.
a. Describe how the normal function of T-lymphocyte and B-lymphocyte cells
differ.

Each individual T & B cell have the ability to recognize almost any foreign
antigen found in the environment. Each individual T or B cell, however,
specifically only recognizes only one particular antigen, but the sum of the
population of lymphocyte specificities may represent millions of foreign antigens.
The process is called generation of clonal diversity and occurs in specialized
(primary) lymphoid organs- the thymus for T-cells and bone marrow for B-cells,
where they mature and commit to either becoming a B or T cell and then are
released to the organs as immature cells ready to react with antigens. They remain
dormant until antigens initiate the second phase response, clonal selection. To
initiate an effective response the antigen must be processed and presented because
they cannot react directly with the cell and need to be shown in a very specific
manner. This is done by the APC’s. 3 groups of cells must cooperate to illicit an
immune response. The APC interact with subpopulations of T-cells that facilitate
immune response (T-helper), and immunocompetent T & B cells, resulting in
activation of B cells into active antibody producing cells (plasma cells) and T
cells into effector cells, such as T-cytotoxic cells.

b. Differentiate between function of humoral and cell mediated immunity and
describe the implications for practice.

 Humoral immunity is that immunity conferred by the B-Cells. It provides
immunity against some viral infections, toxin induced diseases and
diseases caused by pneumococci, meningococci, or Haemophilus.
 B-cells mature into plasma cells that then produce antibodies (5 classes
of antibodies - glycoproteins: IgG, IgE, IgM, IgA, IgD)

 Cell-Mediated immunity is that Immunity conferred by T-Cells. Immunity
is active against cells infected with intracellular bacteria or viruses. It
defends against fungal infections, parasitic infections, tumors, and is
responsible for organ transplantation rejection.


c. Describe the difference between active acquired immunity and passive acquired
immunity and the implications for health promotion.
 Acquired Immunity is the state of immunity that is obtained after exposure
to an antigen. It improves with repeat exposure and it is specific. Active

, acquired immunity is produced by the host after exposure to an antigen or
an immunization. This is the basis of vaccinations.

 Passive acquired immunity is that immunity acquired via the transfer of
antibodies, or T-cells to the recipient. Natural Passive immunity occurs via
mother to fetus. Antibodies cross the placenta or in the breast milk.
Artificial Passive Immunity occurs when antibodies are given to a
recipient to provide immunity. This is used to treat rabies, tetanus,
hepatitis, snake bites. It is a good way to fight infection, has immediate
protection but the immunity only lasts as long as the antibodies,
approximately 2 weeks.

d. Evaluate the purpose of the terms and describe the importance to clinical practice.
 Antigen – is a molecule that can react with antibodies or antigen receptors on
B & T cells. Most but not all antigens are immunogens. An antigen that is an
immunogen will induce an immune response resulting in the production of
antibodies or functional t cells.
Criteria: being foreign to the host, being appropriate in size, having an
adequate chemical complexity, being present in sufficient quantity.

 Self-antigen – is an antigen that fulfill this criteria (antigen) except
foreignness does not normally elicit an immune response. Thus, most
individuals are tolerant to their own antigens. The immune system has an
exquisite ability to distinguish self (self-antigens) from non-self (foreign
antigens).

 Allergens – antigens that induce an allergic response. {In general, large
molecules (>10000 Daltons) such as proteins, polysaccharides, and nucleic
acids. LMW molecules such as amino acids, fatty acids and the purine and
pyrimidine bases tend to be unable to induce response. Many small molecules
can function as haptens: antigens that are too small to be immunogens by
themselves but become immunogenic in combination with larger molecules
that function as carriers for the hapten. Such as PCN and poison ivy (haptens)
but they initiate and allergic response only after binding to larger molecular
weight proteins in the allergic individuals blood or skin.}

, 2. Evaluate the role and function of the cells of the immune system.
a. Evaluate the structure and function of the antibodies produced by the B-
lymphocyte cells and describe the implications for clinical practice.

The overall functions of antibodies include the neutralization of bacterial toxins,
they coat the bacteria to enhance phagocytosis and the formation of antigen
antibody complex activates the complement cascade. B-cells mature into plasma
cells that then produce antibodies There are 5 classes of antibodies
(glycoproteins):

Type of B-Lymphocyte Function Implications for Clinical Practice
Cells
IgA IgA is the main immune
globulin in secretions and
mucous membranes. It
prevents the attachment of
microorganisms to the
mucous membranes.
IgM IgM is the main immune A high level of IgM antibodies
globulin produced early in indicates a recent infection.
the primary immune
response.
IgG IgG is the most prominent Levels rise in response to
immune globulin. It binds subsequent exposure to an
with viruses, bacteria and antigen. It is the only immune
toxins. It activates globulin that crosses the placenta.
complement and binds to
macrophages. It is the
primary antibody in the
secondary immune response.
IgE IgE binds to mast cells, It is involved in parasitic
eosinophils and basophils. infections and hypersensitivities
reactions.

b. Evaluate the function of the following T-Lymphocyte cells.
Type of T-lymphocyte Cells Function

T-cytotoxic cells Direct killing of foreign and/or abnormal cells.
pg. 255 Responsible for the cell-mediated destruction of
such targets of tumor cells or cells infected with
viruses. To perform this function, they adhere to
the target cell through presentation (MHC 1
molecules). Tc cells can recognize antigens on
any cell surface that has become
infected/cancerous. After attachment killing can

, occur by at least 2 mechanisms that induce
apoptosis: though actions of perforin and
granzymes or direct receptor interactions.
NK Killer cells Recognition and elimination of cells infected
Pg. 213 with viruses, although they are also somewhat
effective of other abnormal host cells. NK cells
seem to be more efficient when they encounter
an infected cell within the circulatory system
opposed to those in the tissues. NK cells have
additional inhibitory and activating receptors
allowing it to differentiate between infected,
tumor and normal cells. If it binds to a target
cell the it produces cytokines and toxic
molecules that can kill the target cell.
T-Regulatory cells One form of peripheral tolerance of the self-
Pg. 257 antigen, a subpopulation of CD4+ T cells. Treg
cells are activated by antigen presentation
(MHC class II) and differentiation under the
control of specific cytokines. The role of the
Treg cell is to control and limit the immune
response to protect the host’s own tissues
against autoimmune reaction.
T-Helper cells Helps the antigen driven maturation of both B
Pg. 245 & T cell. They perform this task by facilitating
and magnifying the interaction between APC’s
and the immunocompetent lymphocytes. This
extremely important role involves three
important steps: 1) the Th cell directly interacts
with the APC through a variety of antigen-
specific and antigen-independent receptors, 2)
the Th cell undergoes a differentiation process
during which a variety of cytokine genes are
activated and 3) depending on the pattern of
cytokines expressed, the mature Th cell
interacts with either immunocompetent B or T
cells to enhance their response to antigen, which
results in differentiation into either plasma cells
or effector T cells, such as T-cytotoxic cells.
The Th cells are critical to most immune
responses, and a variety of Th cell defects can
lead to severely diminished immune responses.

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