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HCR 240 MODULE 4 QUESTIONS WITH CORRECT ANSWERS

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HCR 240 MODULE 4 QUESTIONS WITH CORRECT ANSWERS

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Interleukins
Interferons
TNF-α


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major inflammatory cytokines

,The vascular response is followed by a cellular response that begins with white blood
cells (leukocytes) attaching to adhesion molecules in vessel walls near the area of
injury. These leukocytes also release cytokines that increase vascular permeability of
the capillaries. When the cellular response is activated, the leukocytes roll down the
surface of the endothelial cells toward the openings in the vascular wall. They then
squeeze through these openings and migrate toward the area of injury. Additional
fluid, cells, and protein are also able to leak out.


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cellular response




is an example of a clinical disorder demonstrating a lack of control over the plasma
protein systems. It is characterized by a genetic defect in C1 esterase inhibitor,
resulting in hyperactivation of all three plasma protein systems. Symptoms include a
self-limiting edema of cutaneous and mucosal membranes in the hands, feet, face,
intestines, and airway. Severe abdominal pain, nausea, and vomiting may result from
intestinal wall edema. Airway edema can lead to death by asphyxiation.


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Hereditary angioedema




Acute inflammation is a response limited to the elimination of the initial threat. This
usually takes 8 to 10 days from onset to healing. If the acute response is not adequate
to eliminate the threat, then chronic inflammation may develop and last for weeks to
months. Each of the phases of inflammation involves different biochemical mediators
and cells that function synergistically. If the acute and chronic phases are successful
in leading to healing, the progression to the development of a granuloma is avoided.


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, Acute and Chronic Inflammation




The inflammatory response, with its removal of foreign invaders, is necessary for
wound healing. Further preparation of the injured tissue includes débridement by
fibrinolytic enzymes followed by reversal of the vasodilation and endothelial
permeability. Repair begins with the goals of filling, sealing, and shrinking the wound.
If the wound is small and the edges are clean and closely apposed, then very little
epithelialization and contraction are required. Wounds that heal under the condition
of minimal tissue loss are described as healing by primary intention. An example of a
wound that heals by primary intention is a surgical wound that is sutured with the
wound edges or margins in close approximation to each other.


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primary intention




Phagocytes squeeze between retracted endothelial cells and cross the basement
membrane into the tissues. Additional adhesion molecules help the phagocyte move
between the endothelial cells.


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Diapedesis




is activated when the vessel wall is damaged and Hageman factor (factor XII) in
plasma contacts negatively charged subendothelial substances.


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, contact activation (intrinsic) pathway




Epithelial cells produce an array of substances that help prevent pathogen invasion as
a part of innate immunity's first line of defense.


Mucus, perspiration, saliva, tears, and earwax can trap potential invaders and contain
substances such as lysozymes that can disable or kill pathogens.
Sebum (produced by sebaceous glands) contains antibacterial and antifungal fatty
acids that can kill bacteria and fungi. These substances create an acidic environment
that is unfavorable for growth of most bacteria.
Secreted by epithelial cells, antimicrobial peptides kill or inhibit growth of disease-
causing bacteria, fungi, and viruses. More than a thousand of these peptides have
been discovered. Well-known classes of antimicrobial peptides include the
cathelicidins, defensins, and collectins.


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3c. Biochemical Barriers: Epithelial Cell-Derived Chemicals




Dendritic cells provide a major link between the innate and acquired immune
response systems. Although dendritic cells are the primary cells of phagocytosis in
peripheral organs and skin, they do not completely degrade infectious molecules that
are internalized through phagocytosis. Rather, they migrate to lymphoid tissue such as
lymph nodes, where they generate an acquired immune response through presenting
parts of infectious molecules to T lymphocytes. T lymphocytes then initiate
development of a subset of helper T cells that coordinate the development of
functional B and T cells that protect against future infection by that infectious
organism.


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