Summary
NURS 2700 Cell, Immunity, Inflammation Summary
- Course
- - NURS 2700
- Institution
- Valdosta State University
This is a comprehensive and detailed summary on;Cell, Immunity, Inflammation. An Essential Study Resource !!
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2Inflammation
Inflammation is a reaction to: 1. infection, 2. injury (blunt/penetrating trauma) 3. physical or
chemical agents, 4. tissue necrosis, 5. immune reactions
-May be either acute or chronic inflammatory process
-Acute- short process, characterized by exudation of fluid and plasma proteins and leukocytes.
The Leukocytes that are primarily involved in inflammation are neutrophils.
-Chronic- may last for weeks, months or even years. Macrophages, lymphocytes, eosinophils
and mast cells predominate in chronic infection.
- Inflammation is the body’s defense mechanism to protect from infection and injury.
Inflammatory process attempts to localize and eliminate injurious agent and remove the
damage tissue to promote healing
- Inflammation is the reaction of vascularized tissues to cell injury or death. It is
characterized by the production and release of inflammatory mediators and movement
of fluid and leukocytes from the vasculature into the extravascular tissue.
- Inflammatory conditions are named by adding itis to the suffix of the organ or system.
Cells of inflammation
1. Endothelial cells line the blood vessels and are a key player in process. Separate intra
and extravascular fluids.
2. Platelets release inflammatory proteins that help to bind and kill bacteria and fungi.
Assist the WBCs.
3. Leukocytes- major component of defense. They are scavengers- engulf bacteria. These
are granulocytes, eosinophils (sign of chronic inflammation, parasites, allergic reaction
or cancer) and basophils (most prominate in allergic reactions. Release histamine which
results in increased blood flow, swelling and inflammation), Neutrophils (1st to arrive),
lymphocytes, and monocytes. Mast cells reside in mucosal surfaces such as lung, GI, and
dermis. /macrophages (seen in atherosclerosis. Have longer life and help to destroy the
agent.
4. Granulocytes and agranulocytes. Agranulocytes- monocytes/macrophages,
lymphocytes (T and B which are found in the lymph system. If increased in lymphocytes
then is usually viral.
Five cardinal signs of inflammation:
, 3
1. Tumor (swelling)
2. Rubor (redness due to increase in blood flow to area)
3. Calor (heat or warmth)
4. Dolor (pain
5. Functio lawsa (loss of function
6. Fever may occur and is usually a sign of systemic response.
Stages of Inflammation
Vascular stage: Vasodilation of vessels and leakage of proteins into extravascular space. Area
becomes congested causing erythemia (redness and warmth).
Cellular stage: 1. change in endothelial cells lining the vascular and increase in leukocytes into
area of injury 2. release in chemical mediators (mast and macrophages). 3. blood flow slows
and cytokines released to cause leuokocytes to slow and roll along the endothelial cell surface
and adhere. They transmigrate through the vessel wall and migrate to the tissue spaces. 4.
chemotaxis occurs and the leukocytes are directed to the site of problem. 5. Phagocytosis-
leukocytes engulf the microbes and kill them.
Cellular phase of acute inflammation involves delivery of leukocytes, mainly neutrophils, to the
site of injury to perform host defense. This delivery and activation may be divided into
1. Adhesion and margination (at the site of the precapillary venules the blood flow slows
and leukocytes flow closer to the cell wall.
2. Transmigration (leukocytes move from the vascular space into the extravascular tissue
3. Chemotazis (leukocytes migrate to the tissues by a chemical gradient)
Once the leukocytes arrive at the site of injury phagocytosis and cell killing begins. Neutrophils
recognizes the problem, traps it (adherence), engulfs it (cytoplasm moves around and encloses
it) and kills it.
Inflammatory Mediators
Mediators: chemicals derived from injured tissue cells or synthesized in the liver that are
responsible for the inflammatory event.
Plasma derived from the liver and cause 3 major cascades. See above, acute, coagulation
(clotting) and complement (vasodilation/vascular permeability, promotes leukocyte activation,
adherence and chemotaxis and augmenting phagocytosis.
Cell derived from cells at site.
Bradykinin – causes blood vessels to dilate
, 4
Fibrinolytic- break down of clots/thrombosis
Histamine- dilation of arterioles and increases the permeability of venules.
Serotonin- released within platelet granules
Lysosomal enzymes ROS-
Granuloma is an inflammation found in many diseases. It is a collection of immune cells known
as histiocytes(macrophages).[1] Granulomas form when the immune system attempts to wall off
substances it perceives as foreign but is unable to eliminate. Such substances include infectious
organisms including bacteria and fungi, as well as other materials such
as keratin and suture fragments.
Granulomatous- Distinctive form of chronic inflammation characterized by the walling off of
the agent epithelioid macrophages.
These are associated with foreign bodies such as splinters, sutures, silica and asbestos and with
microorganisms that cause tuberculosis, syphilis, sarcoidosis, deep fungal infections and
brucellosis.
Systemic inflammation: manifestations include fever, lethargy; increased erythrocyte
sedimentation rate (ESR), levels of C reactive protein (CRP), WBCs, enlargement of lymph
nodes that drain the affected area.
Severe bacterial infections (sepsis): large quantities of microorganisms in the blood result in
the production and release of inflammatory cytokines and development of systemic
inflammatory response syndrome.
Acute phase response- Liver increases the synthesis of fibrinogen, C reactive protein (CRP) and
serum amyloid A protein. This is stimulated by cytokines esp. TNF.
CRP increases with inflammation. It is a marker for MI and in Inflammation involving
atherosclerotic plaques in coronary arteries. This results in rise in fibrinogen and causes RBCs to
form stacks rapidly. Erythrocyte sedimentation (ESR) rate is elevated in inflammation. There is
an increase in WBCs.
White Blood Cell Response- Leukocytosis is a sign of inflammatory response esp. bacterial.
Increase in neutrophils
Fever Mechanisms
FEVER: is produced in response to pyrogens that act by prompting the release of prostaglandin
E or fever producing cytokines which resets the hypothalamic thermoregulatory center.
Pyrexia- (fever)- tends to cause feelings of weakness and fatigue.
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