Chapter 2: 1

Predominantly alterations in blood vessels to increase blood flow and edema, and the action of neutrophils.

Increased central venous pressure in congestive heart failure.

Within seconds.

Approximately 2 days.

They take on a more cuboidal shape.

They select for the formation of cells expressing immunoglobulin that can functionally bind antigen.

Congestion is a passive process due to decreased venous return, while hyperemia is an active physiological reaction.

Single, oval to kidney bean-shaped.

They contribute to pain (dolor) through neural stimulation and tissue effects.

Virally infected cells in the context of class I MHC antigens.

IL-5.

They undergo further activation and actively transmigrate between endothelial junctions into the interstitium.

Hemosiderin-containing macrophages.

Common lymphoid progenitor cells in the bone marrow.

To act as initial hemostatic effectors.

IgG, which accounts for 85% of the immunoglobulin in normal serum.

Vascular changes rather than inflammatory cell infiltration.

They act as antigen-presenting cells (APCs) and coordinate interactions between T and B cells.

They are directly involved in the killing of microorganisms.

1. Recognition, 2) Binding, 3) Engulfment.

Antigen binding to IgE or other stimuli like heat, cold, or mechanical stimulation.

Chemotactic factors direct the migration of inflammatory cells through the interstitial space to the site of inflammation.

The presence of specific antibodies for a particular pathogen.

To produce specific immunoglobulin molecules of high affinity that can react with exogenous antigens.

Platelet binding to surfaces and activated endothelial cells.

They interact with B cells and promote B cell maturation.

Hours.

A collection of neutrophils, macrophages, and necrotic debris that has undergone liquefaction.

They promote the binding of inflammatory cells to the endothelial surface and trigger their initial activation.

Neutrophils, often in association with eosinophils.

Megakaryocytes in the bone marrow.

They cause pain.

Myelomonocytic precursors in the bone marrow.

Less than 48 hours.

Secretion of interferon γ (IFN-γ) by T H 1 T cells.

It activates eosinophils.

Cytokines resulting in fever and other systemic symptoms.

Systemic edema and vasodilation, leading to anaphylactic shock.

Hemorrhage (bleeding) into tissue.

It transitions to a mixed acute and chronic inflammatory cell infiltrate.

Longer-lived mononuclear cells, such as macrophages and lymphocytes.

Lymphocytes, macrophages, and plasma cells.

Days to weeks.

It permits effective binding to Fc receptors on inflammatory cells, enhancing phagocytosis of microorganisms.

Various inflammatory mediators that cause vasodilation and increased vascular permeability.

Vascular dilatation.

Cytotoxic T cells.

The acute inflammatory response usually intensifies and may result in abscess formation.

It serves as a host defense against microorganisms and parasites, and is the first response to injuries.

They are put under pressure, disrupting their normal function and potentially causing cell death.

Acute inflammatory mediators.

Days to weeks.

Concentric nodules formed by histiocytes, often helpful in identifying the cause of inflammation.

IgA, which provides a barrier to some pathogens in the gastrointestinal tract.

Neutrophils, basophils, eosinophils, lymphocytes, monocytes, macrophages, and plasma cells.

Signal transduction mediated through the T-cell receptor complex (TCR).

They are necessary for antigen presentation to activate T cells.

Proteases and gelatinase, important for degrading basement membrane components.

Hypochlorite and superoxide free radicals.

PECAM (CD31) is a transmembrane protein that allows transmigration of inflammatory cells between endothelial cells into the interstitium.

It promotes blood flow to the injured area, increasing the potential number of inflammatory cells available.

Fibrosis and organ dysfunction.

Von Willebrand factor.

The presence of an inflammatory node containing compactly grouped mononuclear phagocytes.

Innate immunity and adaptive immunity.

The process by which inflammatory cells ingest microorganisms.

Increased vascular permeability and actions of inflammatory mediators.

They are important in responding to parasites and allergic reactions.

Accumulation may progress to abscess formation due to excess neutrophils.

Hours to days.

To detect tumors that may evade T cells by ceasing MHC expression.

Migration to lymph nodes or extranodal lymphoid organs.

Hyperemia, congestion, edema, and endothelial cell activation.

It provides the initial response to most insults and contains pathogens until adaptive immunity can respond.

They are prototypical cytotoxic T cells that induce apoptotic cell death.

IL-2 and IFN-γ.

Release of inflammatory mediators from injured endothelial cells.

They mediate transplant rejection in response to foreign histocompatibility antigens.

By releasing proteases that digest basement membrane material.

Inflammation is essential for initiating the tissue repair process.

Arachidonic acid-derived mediators, especially thromboxane.

Selectin and integrin proteins.

Secondary lymphoid follicles.

Adaptive immunity depends on specific antigen-recognition molecules.

Cytokines, including IL-1 and TNF-α.

Acid hydrolases, elastase, serine proteases, myeloperoxidase, and lysozyme.

IL-4 and IL-13.

They provide an early response before antigen-specific T cells are activated.

Serotonin and histamine.

Acute and chronic inflammation.

Cellular and molecular mechanisms of disease.

The persistence of viable bacteria in pyogenic bacterial infections.

They undergo apoptosis.

They secrete IFN-γ and other cytokines that convert macrophages to epithelioid histiocytes.

Evidence of prior infection.

CD8+ T cells.

They are the most important agents of response to pyogenic bacterial infections and initial responders to physical injury.

Rubor, calor, tumor, and dolor.

They are CD56-positive and express Fc receptors but do not express T-cell antigen receptors, CD8, or CD4.

It can cause generalized inflammation and infection, leading to empyema or peritonitis.

Prostaglandins and leukotrienes.

Fluid accumulation in tissues due to disrupted hydrostatic pressure.

They engulf cellular debris to facilitate tissue repair.

The generation of antigen-specific receptor molecules.

An active process where blood volume and flow are increased due to dilation of arterioles.

They are major effector cells involved in phagocytizing microorganisms and coordinating inflammatory processes.

They clear debris and damaged material to facilitate healing.

It activates macrophages and can convert them to epithelioid histiocytes.

Fluid oozing out of a tissue or its capillaries due to injury or inflammation.

48 hours in circulation, usually much less in inflamed tissues.

The cortex of the thymus.

It comprises cellular and humoral processes that respond independently of antigen-specific recognition molecules.

As T H 1 or T H 2 based on the types of cytokines they secrete.

Lymphocytes of intermediate size that are an important component of innate immunity.

Primary granules fuse with the phagosome.

By degranulating and releasing granule contents into the extracellular space.

Hydrolytic enzymes, inflammatory mediators, and oxygen-derived free radicals released from neutrophils.

The short tissue life span of neutrophils, usually measured in hours.