CH 2 - Acute Inflammation Flashcards
Thick, yellow fluid draining from a breast fissure is
a purulent exudate.
Purulent exudates and effusions are associated with
pathologic conditions such as pyogenic bacterial infections, in which the predominant cell type is the segmented neutrophil (polymorphonuclear leukocyte).
Mast cells are
granulated cells that contain receptors for IgE on their cell surface. They are additional cellular sources of vasoactive mediators, particularly in response to allergens.
B lymphocytes and plasma cells are
mediators of chronic inflammation and provide antigen-specific immunity to infectious diseases.
Complement proteins
act upon one another in a cascade, generating biologically active fragments (e.g., C5a, C3b) or complexes (e.g., C567).
Products of complement activation cause
local edema by increasing the permeability of blood vessels. They also promote chemotaxis of leukocytes and lyse cells (membrane attack complex) and act as opsonins by coating bacteria.
Kinins
are formed following tissue trauma and mediate pain transmission.
The most potent chemotactic factors for leukocytes at the site of injury are
(1) complement proteins (e.g., C5a); (2) bacterial and mitochondrial products, particularly low molecular weight N-formylated peptides; (3) products of arachidonic acid metabolism (especially LTB4); and (4) chemokines (e.g., interleukin-1 and interferon g
Plasmin is
a fibrinolytic enzyme generated by activated Hageman factor (clotting factor XII).
Histamine is
one of the primary mediators of increased vascular permeability.
During acute inflammation, neutrophils (PMNs) adhere to
the vascular endothelium.
What happens to PMNs after they adhere to the vascular endothelium?
They flatten and migrate from the vasculature, through the endothelial cell layer, and into the surrounding tissue.
About 24 hours after the onset of infarction, PMNs are observed to do what?
infiltrate necrotic tissue at the periphery of the infarct.
What is the of the PMNs in acute inflammation?
function is to clear debris and begin the process of wound healing.
Lymphocytes and plasma cells are
mediators of chronic inflammation and provide antigen specific immunity to infectious diseases.
Fibroblasts and macrophages regulate what?
scar tissue formation at the site of infarction.
Forces that regulate the balance of vascular and tissue fluids include
(1) hydrostatic pressure, (2) oncotic pressure, (3) osmotic pressure, and (4) lymph flow.
Inflammatory edema
1) an increase in the permeability of the endothelial cell barrier results in local edema. 2) Vasodilation of arterioles exacerbates fluid leakage 3) vasoconstriction of postcapillary venules increases the hydrostatic pressure in the capillary bed potenti
Vasodilation of venules
decreases capillary hydrostatic pressure and inhibits the movement of fluid into the extravascular spaces.
Acute inflammations’ effect on plasma oncotic pressure
it is not associated with changes in plasma oncotic pressure
Hageman factor
(clotting factor XII) provides a key source of vasoactive mediators.
Activation of Hageman
plasma protein at the site of tissue injury stimulates (1) conversion of plasminogen to plasmin, which induces fibrinolysis; (2) conversion of prekallikrein to kallikrein, which generates vasoactive peptides of low molecular weight referred to as kinins;
Septicemia (bacteremia) denotes
the clinical condition in which bacteria are found in the circulation. It can be suspected clinically, but the final diagnosis is made by culturing the organisms from the blood.
In patients with endotoxic shock
lipopolysaccharide released from Gram-negative bacteria stimulates monocytes/macrophages to secrete large quantities of TNF alpha.
LPS causes
direct cytotoxic damage to capillary endothelial cells.
Suppurative inflammation
describes a condition in which a purulent exudates is accompanied by significant liquefactive necrosis. It is the equivalent of pus.
Chronic inflammation
is nonsuppurative.
Fibrinoid necrosis is observed in areas of
necrotizing vasculitis.
Granulomatous inflammation is seen in patients with
tuberculosis.
Reactive gliosis is
a normal response of the brain to injury and infection but is not visible on the cut surface of the brain at autopsy.
A transudate denotes
edema fluid with low protein content
An exudate denotes
edema fluid with high protein content.
A purulent exudate or effusion contains
a prominent cellular component (PMNs).
A serous exudate or effusion is characterized
by the absence of a prominent cellular response and has a yellow, strawlike color.
Fibrinous exudates does not contain
leukocytes.
Serosanguineous exudate contains
RBCs and has a red tinge.
Eosinophils are particularly evident during
allergic-type reactions and parasitic infestations.
Infections with Trichinella are accompanied by
eosinophilia, and skeletal muscle is typically infiltrated by eosinophils.
Patients with muscular dystrophy show
elevated serum levels of creatine kinase, but eosinophils are not seen on muscle biopsy.
Bacterial infections are associated with
neutrophilia, and affected tissues are infiltrated with PMNs.
Viral infections are associated with
lymphocytosis, and affected tissues are infiltrated with B and T lymphocytes.
Polymyositis,
an autoimmune disease, does not feature eosinophils.
The importance of oxygen dependent mechanisms in the bacterial killing by phagocytic cells is exemplified in
chronic granulomatous disease of childhood.
Children with CGD
suffer from a hereditary deficiency of NADPH oxidase, resulting in a failure to produce superoxide anion and hydrogen peroxide during phagocytosis.
Persons with CGD are susceptible to
recurrent bacterial infections.
Patients deficient in myeloperoxidase cannot produce
hypochlorous acid (HOCl)
Patients deficient in myeloperoxidase experience
an increased susceptibility to infections with the fungal pathogen Candida.
Catalase
converts hydrogen peroxide to water and molecular oxygen.
Deficiency of C1 inhibitor
with excessive cleavage of C4 and C2 by C1s, is associated with the syndrome of hereditary angioedema.
Hereditary angioedema is characterized by
episodic, painless, nonpitting edema of soft tissues.
Hereditary angioedema is the result of
chronic complement activation, with the generation of a vasoactive peptide from C2
Hereditary angioedema may be life threatening because of
the occurrence of laryngeal edema.
Chronic granulomatous disease
is due to a hereditary deficiency of NADPH oxidase.
Myeloperoxidase deficiency
increases susceptibility to infections with Candida.
Selective IgA deficiency and Wiskott-Aldrich syndrome are
congenital immunodeficiency disorders associated with defects in lymphocyte function.
Eosinophils are recruited in
parasitic infestations and would be expected to predominate in the portal tracts of the liver in patients with schistosomiasis.
Eosinophils contain
leukotrienes and platelet-activating factor, as well as acid phosphatase and eosinophil major basic protein.
Plasma cells
are differentiated B lymphocytes that secrete large amounts of monospecific immunoglobulin.
Inflammation has historically been referred to as either acute or chronic, depending on
the persistence of the injury, clinical symptoms, and the nature of the inflammatory response.
The cellular components of chronic inflammation are
lymphocytes, antibody producing plasma cells and macrophages.
The chronic inflammatory response is often
prolonged and may be associated with aberrant repair (i.e., fibrosis).
Neutrophils are featured in
acute inflammation and menstruation
patient with viral myocarditis will show an accumulation of
lymphocytes in the affected heart muscle.
Naïve lymphocytes encounter
antigen-presenting cells (macrophages and dendritic cells) in the secondary lymphoid organs.
Naïve lymphocytets with APCs in the secondary lymphoid organs
In response to this cell-cell interaction, they become activated, circulate in the vascular system, and are recruited to peripheral tissues (e.g., heart).
Binding of vasoactive mediators to specific receptors on endothelial cells results in
contraction and gap formation leading to the leakage of intravascular fluid into the extravascular space.
Direct injury to endothelial cells also leads to
leakage of intravascular fluid.
A fibrinous exudate contains
large amounts of fibrin as a result of activation of the coagulation system.
When a fibrinous exudate occurs on a serosal surface, such as the pleura or pericardium, it is referred to as
fibrinous pleuritis or fibrinous pericarditis.
Release of exogenous pyrogens by bacteria, viruses, or injured cells stimulates
the production of endogenous pyrogens such as IL-1 alpha, IL-1 beta, and TNF-alpha.
IL-1 is
a 15-kDa protein that stimulates prostaglandin synthesis in the hypothalamic thermoregulatory centers, thereby altering the “thermostat” that controls body temperature.
Inhibitors of cyclooxygenase
(e.g., aspirin) block the fever response by inhibiting PGE2 synthesis in the hypothalamus. Chills, rigor (profound chills with shivering and piloerection), and sweats (to allow heat dissipation) are symptoms associated with fever.
Many inflammatory cells are able to
recognize, internalize, and digest foreign materials, microorganisms, and cellular debris. This process is termed phagocytosis, and the effector cells are known as phagocytes.
Phagocytosis of most biologic agents is enhanced by
their coating with specific plasma components (opsonins), particularly immunoglobulins or the C3b fragment of complement.
The primary role of neutrophils in inflammation is
host defense and débridement of damaged tissue.
However, when the neutrophilic response is extensive or unregulated, the chemical mediators of inflammation may
prolong tissue damage. Thus, the same neutrophil-derived lysosomal enzymes that are beneficial when active intracellularly can be harmful when released to the extracellular environment.
Proteolytic enzymes that are released by phagocytic cells during inflammation are regulated by
a family of protease inhibitors, including alpha 1-antitrypsin and alpha 2-macroglobulin.
These plasma-derived proteins alpha 1-antitrypsin and alpha 2-macroglobulin do what?
inhibit plasmin-activated fibrinolysis and activation of the complement system and help protect against nonspecific tissue injury during acute inflammation.
Lysozyme is
a glycosidase that degrades the peptidoglycans of Gram positive bacterial cell walls.
Myeloperoxidase is contained within
neutrophil granules.
Selectins are
sugar-binding glycoproteins that mediate the initial adhesion of leukocytes to endothelial cells at sites of inflammation.
