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NUR 611 EXAM 2 REVIEW ALREADY A+ GRADED WITH EXPERT FEEDBACK|LATEST UPDATE |BRAND NEW!

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NUR 611 EXAM 2 REVIEW ALREADY A+ GRADED WITH EXPERT FEEDBACK|LATEST UPDATE |BRAND NEW!

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NUR 611 EXAM 2 REVIEW ALREADY A+ GRADED WITH EXPERT
EXAM 2 NUR 611 REVIEW
FEEDBACK|LATEST UPDATE |BRAND NEW!
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1. What is the 1. Innate immunity includes two lines of defense: natural barriers and inflamma-
purpose of tion. Natural barriers are physical, mechanical, and biochemical barriers at the
the inflammatory body's surface, and they have been in place since birth.
process? 2. If the surface barriers are breached, the second line of defense--inflammatory
response, is activated to protect the body from further injury, prevent infection,
and promote healing.
3. The inflammatory response is a rapid activation of biochemical and cellular
processes that is relatively nonspecific, with a similar response being initiated
against a wide variety of causes of tissue damage.

2. What are the Inflammation occurs in tissue that has a blood supply (vascularized) and results in
FOUR cardinal observable signs: redness, heat, swelling, and pain.
signs of inflam-
mation?

3. What is edema? Increased blood flow and capillary permeability result in plasma leakage from
vessels, causing swelling (edema) in the surrounding tissue.

4. Warmth and red- The increased blood flow and increasing concentration of red cells at the site of
ness in inflamma- inflammation cause locally increased warmth and redness. Leukocytes adhere to
tion vessel walls.

5. Pain in inflamma- At the same time, biochemical mediators (histamine, bradykinins, leukotrienes,
tion prostaglandins) stimulate endothelial cells that line capillaries and venules to
retract, creating spaces at junctions between cells.

6. Chemotactic fac- Biochemical substance that attracts leukocytes to the site of inflammation
tor

7. Phagocytosis The destruction of microorganisms and cellular debris.

Once a phagocytic cell enters the inflammatory site, the process of phagocytosis
involves four steps:


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1) opsonization--recognition of the target, and adherence of the phagocyte to it.
2) engulfment--ingestion or endocytosis, and formation of phagosome
3) fusion with lysosomal granules within the phagocyte (phagolysosome)
4) destruction of the target

8. Local inflamma- All the local manifestations of acute inflammation (ex, swelling, pain, heat, and
tion redness) result from vascular changes and the subsequent leakage of circulating
components into the tissue.

9. Systemic inflam- An early systemic response is FEVER, which is partially induced by specific cytokines,
mation for example, IL-1 released from neutrophils and macrophages. These fever-caus-
ing cytokines are endogenous pyrogens, differentiating them from pathogen-pro-
duced exogenous pyrogens.

Pyrogens act directly on the hypothalamus, the part of the brain that controls
the body thermostat. The release of endogenous pyrogens by inflammatory cells
occurs after phagocytosis, exposure to bacterial endotoxins, or exposure to anti-
gen-antibody complexes. Generating a febrile response can be beneficial because
the microorganisms that cause some conditions (syphilis) are susceptible to small
increases in body temperature.

10. Older adults and Older adult population is at risk for impaired inflammation and wound healing. In
inflammation some cases, impaired healing is not directly associated with aging in general but
can be linked to a history of chronic illness such as CV disease or DM.

Many older adults do not exhibit fever due to decreased immune responses.

11. Humoral Immu- Antibody circulates in the blood and binds to antigens on infectious agents. This
nity interaction can result in direct inactivation of the microorganism or activation of
a variety of inflammatory mediators (complement, phagocytes) that will destroy
the pathogen. Antibodies are primarily responsible for protecting against many
bacteria and viruses. This arm of the immune response is called humoral immunity.



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12. Cellular Immuni- T cells also undergo differentiation during an immune response and develop into
ty several subpopulations of cells that react directly with antigens on the surface of
infectious agents. Some develop into T cells that can stimulate the activities of other
leukocytes via cell-to-cell contact or through the secretion of cytokines. Others
develop into T-cytotoxic cells (Tc cells) that attack and kill targets directly. Targets
for Tc cells include cells infected by a variety of viruses and cells that have become
cancerous (need these to be functioning properly as one component to protect
against cancer). This arm of the immune response is termed cellular immunity.

13. Adaptive immu- Can be either active or passive, depending on whether the antibodies or T cells are
nity produced by the individual in response to antigen or are administered directly.

14. Active acquired remembers the pathogen and acts more rapidly on subsequent exposure" and
immunity (active is produced by an individual either after natural exposure to an antigen or after
immunity) immunization.

15. Passive acquired does not involve the host's immune response at all. Rather, passive immunity occurs
immunity (pas- when preformed antibodies or T lymphocytes are transferred from a donor to the
sive immunity) recipient (breast milk). This can occur naturally, as in the passage of maternal
antibodies across the placenta to the fetus, or artificially, as in a clinic using
immunotherapy for a specific disease (monoclonal antibody infusions).

16. Active Immunity Contracting and surviving an infectious disease is the most effective means of
(vaccines) developing lifelong immunity against a particular pathogen. In general, vaccine-in-
duced protection does not persist as long as infection-induced immunity. The pur-
pose of vaccination is to induce active immunologic protection before exposure to
the risks of debilitating or fatal infection. Even under optimized protocols, vaccines
are not completely protective. For every vaccine a small percentage of recipients do
not produce a protective immune response, referred to as primary vaccine failure.
Failure to induce an immune response: inactivated influenza vaccine may only
protect 30% to 40% of adults 65 or older. A recently approved, high-dose injectable

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