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Pathology Block 1 Vocab (1,2,3,4,7,11,12)


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Aging (senile atrophy).
The aging process is associated with cell loss, typically seen in tissues containing permanent cells, particularly the brain and heart.
<embryology> A condition in which a part of the body (such as an organ or a tissue) does not completely develop or fails to develop at all.
The most common exogenous pigment is carbon or coal dust, which is a ubiquitous air pollutant of urban life. When inhaled, it is picked up by macrophages within the alveoli and is then transported through lymphatic channels to the regional lymph nodes in the tracheobronchial region. Accumulations of this pigment blacken the tissues of the lungs (anthracosis) and the involved lymph nodes. In coal miners, the aggregates of carbon dust may induce a fibroblastic reaction or even emphysema and thus cause a serious lung disease known as coal worker's pneumoconiosis
refers also to the absence of an organ but one owing to failure of development of the primordium.
occurs when a cell dies through activation of an internally controlled suicide program. It is designed to eliminate unwanted cells during embryogenesis and in various physiologic processes, such as involution of hormone-responsive tissues upon withdrawal of the hormone. It also occurs in certain pathologic conditions, when cells are damaged beyond repair, and especially if the damage affects the cell's nuclear DNA.
Shrinkage in the size of the cell by loss of cell substance is known as atrophy. It represents a form of adaptive response and may culminate in cell death. When a sufficient number of cells are involved, the entire tissue or organ diminishes in size, or becomes atrophic. Atrophy can be physiologic or pathologic.
refers to lysosomal digestion of the cell's own components. In this process, intracellular organelles and portions of cytosol are first sequestered from the cytoplasm in an autophagic vacuole formed from ribosome-free regions of the rough endoplasmic reticulum. The vacuole fuses with lysosomes or Golgi elements to form an autophagolysosome
The morphologic appearance of necrosis is the result of denaturation of intracellular proteins and enzymatic digestion of the cell. The enzymes are derived either from the lysosomes of the dead cells themselves, in which case the enzymatic digestion is referred to as autolysis, or from the lysosomes of immigrant leukocytes, during inflammatory reactions.
BAX binds to and antagonizes the apoptosis-inhibiting protein BCL-2; thus, BAX promotes cell death.
This pathway of apoptosis is the result of increased mitochondrial permeability and release of pro-apoptotic molecules into the cytoplasm, without a role for death receptors. Growth factors and other survival signals stimulate the production of anti-apoptotic members of the Bcl-2 family of proteins
The original red-blue color of hemoglobin is transformed to varying shades of green-blue, comprising the local formation of biliverdin (green bile), then bilirubin (red bile), and thereafter the iron moiety of hemoglobin is deposited as golden yellow hemosiderin
Caseous necrosis
Caseous necrosis, a distinctive form of coagulative necrosis, is encountered most often in foci of tuberculous infection . The term caseous is derived from the cheesy white gross appearance of the area of necrosis . On microscopic examination, the necrotic focus appears as amorphous granular debris seemingly composed of fragmented, coagulated cells and amorphous granular debris enclosed within a distinctive inflammatory border known as a granulomatous reaction. Unlike coagulative necrosis, the tissue architecture is completely obliterated.
present in peroxisomes, which decomposes H2 O2 (2 H2 O2 → O2 + 2 H2 O).
Coagulative necrosis
Necrosis that implies preservation of the basic outline of the coagulated cell for a span of at least some days. The affected tissues exhibit a firm texture. Presumably, the injury or the subsequent increasing intracellular acidosis denatures not only structural proteins but also enzymes and so blocks the proteolysis of the cell. The myocardial infarct is an excellent example in which acidophilic, coagulated, anucleate cells may persist for weeks. Ultimately, the necrotic myocardial cells are removed by fragmentation and phagocytosis of the cellular debris by scavenger leukocytes and by the action of proteolytic lysosomal enzymes brought in by the immigrant white cells.
The process of coagulative necrosis, with preservation of the general tissue architecture, is characteristic of hypoxic death of cells in all tissues except the brain.
dystrophic calcification
There are two forms of pathologic calcification. When the deposition occurs locally in dying tissues, it is known as dystrophic calcification; it occurs despite normal serum levels of calcium and in the absence of derangements in calcium metabolism.
<embryology> Abnormality of development, in pathology, alteration in size, shape and organisation of adult cells
Fat necrosis
a term that is well fixed in medical parlance but does not in reality denote a specific pattern of necrosis. Rather, it is descriptive of focal areas of fat destruction, typically occurring as a result of release of activated pancreatic lipases into the substance of the pancreas and the peritoneal cavity. This occurs in the calamitous abdominal emergency known as acute pancreatitis
gangrenous necrosis
Although gangrenous necrosis is not a distinctive pattern of cell death, the term is still commonly used in surgical clinical practice. It is usually applied to a limb, generally the lower leg, that has lost its blood supply and has undergone coagulation necrosis. When bacterial infection is superimposed, coagulative necrosis is modified by the liquefactive action of the bacteria and the attracted leukocytes (so-called wet gangrene).
Glutathione peroxidase protects against injury by catalyzing free radical breakdown (H2 O2 + 2 GSH → GSSG [glutathione homodimer] + 2 H2 O, or 2 OH + 2 GSH → GSSG + 2 H2 O). The intracellular ratio of oxidized glutathione (GSSG) to reduced glutathione (GSH) is a reflection of the oxidative state of the cell and is an important aspect of the cell's ability to detoxify reactive oxygen species
heat-shock proteins
Some chaperones are synthesized constitutively and affect normal intracellular protein trafficking, whereas others are induced by stress, such as heat (heat-shock proteins, e.g., hsp70, hsp90), and "rescue" shock-stressed proteins from misfolding. If the folding process is not successful, the chaperones facilitate degradation of the damaged protein. This degradative process often involves ubiquitin (also a heat-shock protein), which is added to the abnormal protein and marks it for degradation by the proteasome complex.
a yellowish brown granular pigment formed by breakdown of hemoglobin, found in phagocytes and in tissues especially in disturbances of iron metabolism (as in hemochromatosis, hemosiderosis, or some anemias), and composed essentially of colloidal ferric oxide
Whenever there are causes for systemic overload of iron, hemosiderin is deposited in many organs and tissues, a condition called hemosiderosis. It is seen with: (1) increased absorption of dietary iron, (2) impaired use of iron, (3) hemolytic anemias, and (4) transfusions because the transfused red cells constitute an exogenous load of iron.
the process of lysosomal digestion of materials ingested from the extracellular environment. Extracellular materials are taken up by cells through the general process of endocytosis. Uptake of particulate matter is known is phagocytosis; uptake of soluble smaller macromolecules is called pinocytosis. Extracellular materials are endocytosed into vacuoles (endosomes or phagosomes), which eventually fuse with lysosomes to form phagolysosomes, where the engulfed material is digested. Heterophagy is most common in the "professional" phagocytes, such as neutrophils and macrophages, although it may also occur in other cell types.
the Mallory body, or "alcoholic hyalin," is an eosinophilic intracytoplasmic inclusion in liver cells that is characteristic of alcoholic liver disease, although it can be present in other conditions. Such inclusions are composed predominantly of keratin intermediate filaments.
an increase in the number of cells
an increase in the sizes of individual cells
<embryology> The incomplete development or underdevelopment of an organ or tissue.
a deficiency of oxygen, which causes cell injury by reducing aerobic oxidative respiration. Hypoxia is an extremely important and common cause of cell injury and cell death. It should be distinguished from ischemia ,which is a loss of blood supply from impeded arterial flow or reduced venous drainage in a tissue
an area of ischemic necrosis caused by occlusion of either the arterial supply or the venous drainage in a particular tissue. Although venous thrombosis may cause infarction, it more often merely induces venous obstruction and congestion. Infarcts caused by venous thrombosis are more likely in organs with a single venous outflow channel, such as the testis and ovary
Ischemia-Reperfusion injury
Depending on the intensity and duration of the ischemic insult, variable numbers of cells may proceed to die after blood flow resumes, by necrosis as well as by apoptosis. The affected tissues often show neutrophilic infiltrates. This ischemia-reperfusion injury is a clinically important process in such conditions as myocardial infarction and stroke and may be amenable to therapeutic interventions.
The basophilia of the chromatin may fade (karyolysis), a change that presumably reflects DNase activity
characterized by nuclear shrinkage and increased basophilia. Here the DNA apparently condenses into a solid, shrunken basophilic mass
the pyknotic or partially pyknotic nucleus undergoes fragmentation
an insoluble pigment, also known as lipochrome and wear-and-tear or aging pigment. Its importance lies in its being the telltale sign of free radical injury and lipid peroxidation. It is seen in cells undergoing slow, regressive changes and is particularly prominent in the liver and heart of aging patients or patients with severe malnutrition and cancer cachexia
Liquefactive necrosis
characteristic of focal bacterial or, occasionally, fungal infections, because microbes stimulate the accumulation of inflammatory cells. hypoxic death of cells within the central nervous system often evokes liquefactive necrosis. Whatever the pathogenesis, liquefaction completely digests the dead cells. The end result is transformation of the tissue into a liquid viscous mass.
Primary lysosomes are membrane-bound intracellular organelles that contain a variety of hydrolytic enzymes, including acid phosphatase, glucuronidase, sulfatase, ribonu-clease, and collagenase
A reversible change in which one adult cell type (epithelial or mesenchymal) is replaced by another adult cell type. It may represent an adaptive substitution of cells that are sensitive to stress by cell types better able to withstand the adverse environment.
metastatic calcification
the deposition of calcium salts in otherwise normal tissues is known as metastatic calcification, and it almost always results from hypercalcemia secondary to some disturbance in calcium metabolism.
Necrosis refers to a spectrum of morphologic changes that follow cell death in living tissue, largely resulting from the progressive degradative action of enzymes on the lethally injured cell (cells placed immediately in fixative are dead but not necrotic). As commonly used, necrosis is the gross and histologic correlate of cell death occurring in the setting of irreversible exogenous injury. Necrotic cells are unable to maintain membrane integrity and their contents often leak out. This may elicit inflammation in the surrounding tissue.
Literally new growth, usually refers to abnormal new growth and thus means the same as tumour, which may be benign or malignant.
Unlike hyperplasia, neoplastic proliferation persists even in the absence of the original stimulus.
Accelerated aging syndrome in which most of the characteristic stages of human senescence are compressed into less than a decade. Defect probably in DNA repair.
Steatosis (Fatty Change)
The terms steatosis and fatty change describe abnormal accumulations of triglycerides within parenchymal cells. Fatty change is often seen in the liver because it is the major organ involved in fat metabolism, but it also occurs in heart muscle, and kidney. The cause of steatosis include toxins, protein malnutrition, diabetes mellitus, obesity, and anoxia. In industrialized nations, by far the most common cause of significant fatty change in the liver (fatty liver) is alcohol abuse.
Superoxide dismutase
found in many cell types and convert superoxide to H2 O2 (2 O2 - + 2 H → H2 O2 + O2 )
Accumulation of fat and connective tissue within the intima of arteries, often causing progressive narrowing of the lumen and decreased blood flow to tissues
Liver disease characterized pathologically by loss of normal microscopic lobular architecture with fibrosis and nodular regeneration
Cushing's syndrome
A constellation of clinical findings caused by excessive blood levels of glucocorticosteroid hormones
Disruption of normal neural supply, due to traumatic or degenerative damage to the peripheral nerve or central nervous system motor neurons.
Formerly known as dropsy or hydropsy. Swelling of any organ or tissue due to accumulation of excess lymph fluid, without an increase of the number of cells in the affected tissue. Edema can accumulate in almost any location in the body, but the most common sites are the feet and ankles
Areas of a cell or tissue that stain with eosin, a rose-colored dye. This dye usually stains the cytoplasm of a cell.
An iron-protein (apoferritin) complex. Chief form of intracellular iron storage present in many types of cells.
Fibrinoid necrosis
Conversion of necrotic tissue to an amorphous, fibrillar eosinophilic mass that resembles fibrin.
"Dry" gangrene
Tissue appears black grossly; not accompanied by bacterial infection.
"Wet" gangrene
Necrotic tissue secondarily invaded by bacteria, resulting in liquefactive necrosis.
Areas of a cell or tissue that stain with hematoxylin, a blue-purple crystalline stain. This stain usually stains the nucleus of a cell or leaked DNA
Regeneration refers to growth of cells and tissues to replace lost structures, such as the growth of an amputated limb in amphibians. In mammals, whole organs and complex tissues rarely regenerate after healing, and the term is usually applied to processes such as liver and kidney growth after, respectively, partial hepatectomy and unilateral nephrectomy. These processes consist of compensatory growth rather than true regeneration
A mobile organ twists obstructing its blood supply and/or drainage.
A serum glycoprotein that binds and transports iron (Fe).
a localized collection of neutrophils and necrotic debris (pus) in a cavity
Acute inflammation
immediate response to injury characterized by vasodilatation, increased capillary permeability, presence of an exudate and emigration of leukocytes (mostly neutrophils). Clinically: calor, rubor, turmor, dolor, and loss of function.
Acute phase protein
plasma proteins, mostly synthesized in the liver, whose synthesis increases several hundred-fold in response to inflammatory stimuli (e.g., cytokines such as IL6 and TNF). Best known: C-reactive protein (CRP), fibrinogen, and serum amyloid A (SAA). CRP and SAA bind to microbial cell walls, and may act as opsonins and fix complement. Also help clear necrotic cell nuclei and mobilize metabolic stores.
a crowded mass of independent but similar units; a cluster.
cells that respond to signaling substances produced by themselves
Polypeptide produced by action of Hageman factor and kallikrein; increases vascular permeability; also causes pain.
a complement cleavage product (“byproduct” of cell attack sequence); increases vascular permeability. Also called “anaphylatoxin” because C3a stimulate histamine release from mast cells.
remains attached to cells, activates the cell attack sequence of complement which leads to cell lysis; also the most important opsonin.
a complement cleavage product; increases vascular permeability and is a strong chemoattractant for neutrophils. Also called “anaphylatoxin” because C5a stimulates histamine release from mast cells.
Physical wasting with loss of weight and muscle mass caused by disease. Patients with advanced cancer, AIDS, and some other major chronic progressive diseases may appear cachectic. Cachexia is a wasting syndrome that causes weakness and a loss of weight, fat, and muscle. Anorexia (lack of apppetite) and cachexia often occur together. Cachexia can occur in people who are eating enough, but who cannot absorb the nutrients. Cachexia is not the same as starvation. A healthy person's body can adjust to starvation by slowing down its use of nutrients, but in cachectic patients, the body does not make this adjustment.
deep-seated pyogenic infection of the skin and subcutaneous tissues, usually arising in several contiguous hair follicles, with formation of connecting sinuses
inflammation of subcutaneous, loose connective tissue (formerly called cellular tissue)
Chediak-Higashi syndrome
hereditary defect that impairs the acute inflammatory response; is a defect in neutrophils; characterized by neutropenia, albinism, cranial and peripheral neuropathy, and a tendency to develop repeated infections. Is marked by the presence of abnormal white blood cells.
After extravasation, leukocytes emigrate in tissues toward the site of injury by a process called chemotaxis, defined most simply as locomotion oriented along a chemical gradient. All granulocytes, monocytes and, to a lesser extent, lymphocytes respond to chemotactic stimuli with varying rates of speed
Granulomatous inflammation
Granulomatous inflammation is a distinctive pattern of chronic inflammatory reaction characterized by focal accumulations of activated macrophages, which often develop an epithelial-like (epithelioid) appearance. It is encountered in a limited number of immunologically mediated, infectious and some noninfectious conditions. Tuberculosis is the prototype of the granulomatous diseases, but sarcoidosis, cat-scratch disease, lymphogranuloma inguinale, leprosy, brucellosis, syphilis, some mycotic infections, berylliosis, and reactions of irritant lipids are also included. Recognition of the granulomatous pattern in a biopsy specimen is important because of the limited number of possible conditions that cause it and the significance of the diagnoses associated with the lesions.
Chronic inflammation
inflammation of prolonged duration or slow progress marked histologically by an infiltration of mononuclear cells (lymphocytes, macrophages, and plasma cells), often with proliferation of fibroblasts and fibrosis.
An enzyme that is responsible for formation of important biological mediators called prostanoids (including prostaglandins, prostacyclin and thromboxane). Pharmacological inhibition of COX can provide relief from the symptoms of inflammation and pain; this is the method of action of well-known drugs such as aspirin and ibuprofen.
Chronic Granulomatous disease
Chronic granulomatous disease (CGD), an inherited disorder of phagocytic cells, results from an inability of phagocytes to undergo the respiratory burst necessary to kill certain types of bacteria and fungi. This leads to recurrent life-threatening bacterial and fungal infections.
a hormone-like mediator produced by inflammatory cells
an exudate or transudate that has passed into a part or tissue
passage of white blood cells through the endothelium and wall of small blood vessels.
secreting internally, most commonly into the systemic circulation; of or pertaining to such secretion.
focal, complete loss of epidermis
Erythema – redness due to capillary dilation
An inflammatory extravascular fluid that has a high protein concentration and cellular debris; sg above 1.020
containing amount of fibrin
Fibrinous inflammation
characterized with exudate rich in fibrin; usually found upon inflammation of serosal or mucosal surfaces
granulation tissue
so called because grossly, under the scab, it has a granular appearance; characterized by ingrowth of new blood vessels (angiogenesis) and scar tissue (myofibroblasts)
a specific form of chronic inflammatory response to antigens that cannot be eliminated during the acute inflammatory response; characterized histologically by collections of modified macrophages called “epithelioid cells” because they resemble epithelieal cells, usually surrounded by a rim of lymphocytes
Hageman factor
factor XII in clotting cascade
preformed inflammatory mediator; stored in mast cell and platelet granules, causes increased vascular permeability
intercellular adhesion molecule 1; is an endothelial / leukocyte adhesion molecule; belongs to immunoglobulin family of proteins; major role is adhesion, arrest, and transmigration of all leukocytes; binds integrins on leukocytes
the response of vascularized living tissue to injury
Most adhesion proteins, also called CAMs (cell adhesion molecules), can be classified into four main families: immunoglobulin family CAMs, cadherins, integrins, and selectins. The integrins have broader ligand specificity and are responsible for many events involving cell adhesion. Integrins bind both to matrix proteins such as fibronectin and laminin, mediating adhesiveness between cells and ECM, as well as to adhesive proteins in other cells, establishing cell-to-cell contacts
Interleukin 1 (IL-1)
produced by monocytes/macrophages, as well as many other cells; acts locally (chemotactic, stimulates macrophoages, stimulates T-cell IL-2 production, B-cell maturation) and systemically (induces fever, acute phase reactant proteins, and neutrophil release from bone marrow).
Kallikreins (tissue and plasma kallikrein) are serine proteases that liberate kinins (BK and KD) from the kininogens. Prekallikrein is the precursor of plasma kallikrein. It can only activate kinins after being activated itself by factor XII or other stimuli.
an exaggerated form of scar that protrudes upward from the skin. Characterized by the presence of dense connective tissue
Leukocyte adhesion
results from interaction between endothelial adhesion molecules and leukocyte receptors
Leukocyte adhesion deficiency
Leukocyte adhesion deficiency type I (LAD I) is a failure to express the CD18 (aMb2 and aLb2) integrin, which serves as the receptor for C3b on myeloid and lymphoid cells. Most patients with LAD I express no CD18 on lymphocytes, macrophages, and neutrophils
Leukocyte rolling
during inflammation there is increased permeability, which results in blood flow stasis allowing leukocytes to fall out of laminar flow and roll along endothelium
produced as a breakdown product of cell phospholipids by lipoxygenase pathway (production not inhibited by aspirin). In inflammation, most potent at increasing vascular permeability, but active relatively late; also chemotactic for neutrophils
An enzyme that plays a pivotal role in the synthesis of inflammatory mediators known as leukotrienes
Lipoxins are a recent addition to the family of bioactive products generated from AA. The principal actions of lipoxins are to inhibit leukocyte recruitment and the cellular components of inflammation. They inhibit neutrophil chemotaxis and adhesion to endothelium. There is an inverse relationship between the amount of lipoxin and leukotrienes formed, suggesting that the lipoxins may be endogenous negative regulators of leukotriene action and may thus play a role in the resolution of inflammation
accumulation of blood cells (neutrophils) along the endothelium
Nitric oxide (a.k.a. endothelium-derived relaxing factor)
produced by endothelial cells; stimulates relaxation of smooth muscle, thus playing a role in controlling vascular tone; inhibits platelet aggregation, contributing to endothelial thromboresistance
oncotic pressure
pressure resulting from or caused by edema or any swelling (oncosis)
a compound that attaches to a foreign cell, such as a bacterium, and makes it more susceptible to a phagocytic cell
Oxidative burst
The ultimate step in the elimination of infectious agents and necrotic cells is their killing and degradation within neutrophils and macrophages, which occur most efficiently after activation of the phagocytes.30 Microbial killing is accomplished largely by oxygen-dependent mechanisms. Phagocytosis stimulates a burst in oxygen consumption, glycogenolysis, increased glucose oxidation via the hexose-monophosphate shunt, and production of reactive oxygen intermediates (ROIs, also called reactive oxygen sepecies)
relating to a kind of hormone function in which the effects of the hormone are restricted to the local environment
In time, the endothelium can be virtually lined by white cells, an appearance called pavementing
PECAM-1 (platelet endothelial cell adhesion molecule 1)
also known as CD31, major role involves leukocyte transmigration through endothelium
a body formed by union of a phagosome or ingested particle with a lysosome having hydrolytic enzymes
the ingestion of particulate material (e.g., tissue debris, living or dead bacteria, other foreign cells) by phagocytic cells. Neutrophils and monocytes-macrohages are most important phagocytic cells
phagosome (secondary lysosome)
phagocytosis is characterized morphologically by internalization of the attached opsonized particle by pseduopodial extensions from the surface of the leukocyte, which enclose the foreign particle, forming an internalized vesicle, the phagosome The phagosomes then fuse with cytoplasmic lysosomes and form phagolysosomes.
-An inflammatory mass of the subcutaneous tissues that may progress to an abscess.
-Obsolete term for an acute suppurative inflammation of the subcutaneous connective tissue
the cellular process of actively engulfing liquid, a phenomenon in which minute incuppings or invaginations are formed in the surface of the cell membrane and close to form fluid-filled vesicles; it resembles phagocytosis
Platelet activating factor (PAF)
a phospholipid released from inflammatory cells of various types; activates release of enzymes from polymorphonuclear cell. Also causes platelet aggregation
produced as a breakdown product of cell phospholipids by cyclooxygenase pathway (product inhibited by aspirin). In inflammation, causes pain, increases vascular permeability, and causes vasodilation, but not as potent as leukotrienes; contributes to fever
proud flesh
results from excessive repair; excessive granulation tissue (exuberant granulation or proud flesh) can protrude above the surrounding skin and block reepithelialization. Excessive collagen accumulation forms a raised hypertrophic scar; progression beyond the original area of injury without subsequent regression in termed a keloid
containing, consisting of, or forming pus; pattern in inflammation is characterized by production of purulent exudates (pus) consisting of leukocytes and necrotic cells. An abscess refers to a localized collection of purulent inflammatory tissue accompanied by liquefactive necrosis (e.g., staphylococcal abscess)
A purulent inflammatory exudate rich in neutrophils and cell debris
producing pus
Residual Body (myelin figure)
-A rolled-up or scroll-like arrangement of a lipid bilayer within a cell, superficially resembling the myelin sheath of nerves; observed with the electron microscope in the cytoplasm or as inclusion in mitochondria and autophagic vacuoles where they may represent artifacts of lipid fixation.
-A cytoplasmic vacuole (lysosome) containing accumulated particulate products of metabolism
. In a perfect world, all inflammatory reactions, once they have succeeded in neutralizing and eliminating the injurious stimulus, should end with restoration of the site of acute inflammation to normal. This is called resolution and is the usual outcome when the injury is limited or short-lived or when there has been little tissue destruction and the damaged parenchymal cells can regenerate. Resolution involves neutralization or spontaneous decay of the chemical mediators, with subsequent return of normal vascular permeability, cessation of leukocytic infiltration, death (largely by apoptosis) of neutrophils, and finally removal of edema fluid and protein, leukocytes, foreign agents, and necrotic debris from the site
cell surface adhesion molecules playing important role in acute inflammation
induced by the cytokines interleukin-1 (IL-1) and tumor necrosis factor (TNF)
L-selectins – expressed on neutrophils and bind to endothelial mucin-like molecules such as GlyCam-1.
E- and P-selectins – expressed on endothelial cells and bind to oligosaccharides such as sialyl-Lewis X on the surface of leukocytes. P-selectins, stored in endothelial Weibel-Palade bodies and platelet granules, relocate to the plasma membrane after stimulation by mediators such as histamine and thrombin
denoting an exudate or a discharge composed of or containing serum and also blood
of exudate: virtually devoid of inflammatory cells or fibrin; resembles the appearance of serum
inflamed due to the formation of pus
Endogenous mediator / vasoactive amine similar to histamine;
Influences chemotaxis, vasomotor phenomena, vascular permeability, pain, and other aspects of the inflammatory process;
Derived from platelets
Liberated from platelets, along with histamine, during the release action
Serous inflammation
reflected by tissue fluid accumulation and indicates a modest increase in vascular permeability. In the peritoneal, pleural, and pericardial cavities, this is called an effusion, but it can occur elsewhere (e.g., skin burn blisters)
in inflammation: occurs when fluid loss causes concentration of red cells and increased blood viscosity, slowing the blood flow. With stasis, white cells (mostly neutrophils) accumulate along the endothelium (margination) and begin to emigrate through vessel walls
Substance P
powerful mediator of vascular permeability, transmits pain signals, regulates blood pressure, and stimulates immune and endocrine cell secretion. Local substance P release leads to plasma influx and amplification of an initial inflammatory stimulus
Suppurative inflammation
(suppurative – forming pus) synonymous with purulent: containing, consisting of, or forming pus; pattern in inflammation is characterized by production of purulent exudates (pus) consisting of leukocytes and necrotic cells. An abscess refers to a localized collection of purulent inflammatory tissue accompanied by liquefactive necrosis (e.g., staphylococcal abscess)
The protease thrombin provides the main link between the coagulation system and inflammation. Activation of the clotting system results in the activation of thrombin (factor IIa) from precursor prothrombin (factor II). Thrombin is the enzyme that cleaves circulating soluble fibrinogen to generate an insoluble fibrin clot and is the major coagulation protease. It binds to receptors that are called protease-activated receptors (PARs) because they bind multiple trypsin-like serine proteases in addition to thrombin. These receptors are seven-transmembrane G protein-coupled receptors that are expressed on platelets, endothelial and smooth muscle cells, and many other cell types. Engagement of the so-called type 1 receptor (PAR-1) by proteases, particularly thrombin, triggers several responses that induce inflammation. They include mobilization of P-selectin, production of chemokines, and expression of endothelial adhesion molecules for leukocyte integrins; induction of cyclooxygenase-2 and production of prostaglandins; production of PAF and nitric oxide; and changes in endothelial shape. As we have seen, these responses promote the recruitment of leukocytes and many other reactions of inflammation
Toll-like receptor (TLR)
plays part in leukocyte activation; surface molecule involved in leukocyte activation that mediates innate leukocyte responses to different classes of microbes, various cytokine receptors, and receptors for complement fragments and immunoglobulin that promote phagocytosis
Transforming growth factor-beta (TGF-B)
regulates integrin expression; is a growth inhibitor for many cell types and may aid in modulating the repair process; it is also a chemotactic factor for macrophages and fibroblasts
An extravascular fluid with low protein content and sg below 1.012; essentially an ultrafiltrate of blood plasma resulting from elevated fluid pressures or diminished osmotic forces in the plasma
Tumor necrosis factor-alpha (TNF-a)
Along with interleukin 1 are major cytokines mediating inflammation; they are produced primarily by activated macrophages. Most important actions in inflammation include effects on endothelium, leukocytes, and induction of the systemic acute-phase reactions.
TNF-alpha also regulates body mass by promoting lipid and protein mobilization and by suppressing appetite.
Sustained TNF production contributes to cachexia, a pathologic state characterized by weight loss and anorexia that accompanies some infections and neoplasias
a local tissue defect, or excavation involving the epithelial surface of an organ or tissue
lesion through the skin or a mucous membrane resulting from loss of tissue, usually with inflammation; can be caused by inadequate granulation tissue or collagen deposition and remodeling
Vasoactive amine
mediators in inflammation; they cause vasodilation and increased vascular permeability; histamine and serotonin are most notable
vascular cell adhesion molecule 1; is an endothelial / leukocyte adhesion molecule; belongs to immunoglobulin family of proteins; major role is adhesion of eosinophils, monocytes, and lymphocytes; binds integrins on leukocytes
the physiological process involving the growth of new blood vessels from pre-existing vessels
Autocrine signaling
Cells respond to the signaling molecules that they themselves secrete, thus establishing an autocrine loop. Several polypeptide growth factors and cytokines act in this manner. Autocrine growth regulation plays a role in liver regeneration, proliferation of antigen-stimulated lymphocytes, and the growth of some tumors. Tumors frequently overproduce growth factors and their receptors, thus stimulating their own proliferation through an autocrine loop
Basement membrane
produced by epithelial and mesenchymal cells and are closely associated with the cell surface. They consist of a network of amorphous nonfibrillar collagen (mostly type IV), laminin, heparan sulfate, proteoglycan, and other glycoproteins
Cell Adhesion Proteins
Most adhesion proteins, also called CAMs (cell adhesion molecules), can be classified into four main families: immunoglobulin family CAMs, cadherins, integrins, and selectins. These proteins are located in the cell membrane, where they function as receptors, or they are stored in the cytoplasm. As receptors, CAMs can bind to similar or different molecules in other cells, providing for interaction between the same cells (homotypic interaction) or different cell types (heterotypic interaction). Cadherins are generally involved in calcium-dependent homotypic interactions, while immunoglobulin family CAMs, because of the types of ligands they can bind, participate in both homotypic and heterotypic cell-to-cell interactions. The integrins have broader ligand specificity and are responsible for many events involving cell adhesion
Fibrillar collagens form a major portion of the connective tissue in repair sites and are important for the development of strength in healing wounds. Net collagen accumulation, however, depends not only on increased collagen synthesis but also on decreased degradation. Ultimately, the granulation tissue scaffolding is converted into a scar composed of spindle-shaped fibroblasts, dense collagen, fragments of elastic tissue, and other ECM components. Degradation of collagen and other ECM proteins is achieved by a family of matrix metalloproteinases (MMPs), which are dependent on zinc ions for their activity
The formation of new tissue in the process of wound healing
Contact inhibition
Cell-to-cell interactions mediated by cadherins and catenins play a major role in regulating cell motility, proliferation, and differentiation and account for the inhibition of cell proliferation that occurs when cultured normal cells contact each other ("contact inhibition").
Inadequate formation of granulation tissue or assembly of a scar can lead to two types of complications: wound dehiscence and ulceration. Dehiscence or rupture of a wound is most common after abdominal surgery and is due to increased abdominal pressure. This mechanical stress on the abdominal wound can be generated by vomiting, coughing, or ileus
Tissues such as blood vessels, skin, uterus, and lung require elasticity for their function. Although tensile strength is provided by the proteins of the collagen family, the ability of these tissues to recoil is provided by elastic fibers. These fibers can stretch to several times their length and then return to their original size after release of the tension. Morphologically, elastic fibers consist of a central core made of elastin, surrounded by a peripheral network of microfibrils. Substantial amounts of elastin are found in the walls of large blood vessels, such as the aorta, and in the uterus, skin, and ligaments
Endocrine signaling
Endocrine signaling: Hormones are synthesized by cells of endocrine organs and act on target cells distant from their site of synthesis, being usually carried by the blood. Growth factors may also circulate and act at distant sites, as is the case for HGF. Several cytokines, such as those associated with the systemic aspects of inflammation discussed in Chapter 2, also act as endocrine agents
Epidermal Growth Factor (EGF)
EGF is mitogenic for a variety of epithelial cells, hepatocytes, and fibroblasts. It is widely distributed in tissue secretions and fluids, such as sweat, saliva, urine, and intestinal contents. In healing wounds of the skin, EGF is produced by keratinocytes, macrophages, and other inflammatory cells that migrate into the area. EGF binds to a receptor (EGFR) with intrinsic tyrosine kinase activity
Transforming Growth Factor-α (TGF-α)
TGF-α was originally extracted from sarcoma virus-transformed cells and is involved in epithelial cell proliferation in embryos and adults and malignant transformation of normal cells to cancer. TGF-α has homology with EGF, binds to EGFR, and produces most of the biologic activities of EGF
Extracellular matrix
The ECM is secreted locally and assembles into a network in the spaces surrounding cells. It forms a significant proportion of the volume of any tissue. The ECM serves many functions. For example, matrix proteins sequester water that provides turgor to soft tissues and minerals that give rigidity to skeletal tissues. They also function as a reservoir for growth factors controlling cell proliferation. ECM is important for cell-to-cell interactions and provides a substratum for cells to adhere, migrate, and proliferate, directly modulating cell form and function. Synthesis and degradation of ECM accompanies morphogenesis, wound healing, and chronic fibrotic processes, as well as tumor invasion and metastasis. Three groups of macromolecules, which are often physically associated, constitute the ECM: (1) fibrous structural proteins, such as the collagens and elastins; (2) a diverse group of adhesive glycoproteins; and (3) proteoglycans and hyaluronic acid
Fibroblast Growth Factor (FGF)
This is a family of growth factors containing more than 10 members, of which acidic FGF (aFGF, or FGF-1) and basic FGF (bFGF, or FGF-2) are the best characterized. Released FGFs associate with heparan sulfate in the ECM, which can serve as a reservoir for storing inactive factors. FGFs are recognized by a family of cell-surface receptors that have intrinsic tyrosine kinase activity. A large number of functions are attributed to FGFs, including angiogenesis, wound repair, development of skeletal musckle and lung maturation, and hematopoiesis
the formation or development of excess fibrous connective tissue in an organ or tissue as a reparative or reactive process, as opposed to formation of fibrous tissue as a normal constituent of an organ or tissue
G0, G1, S, G2 stages of the cell cycle
The cell cycle consists of G1 (presynthetic), S (DNA synthesis), G2 (premitotic), and M (mitotic) phases. Quiescent cells are in a physiologic state called G0. Tissues may be composed primarily of quiescent cells in G0, but most mature tissues contain some combination of continuously dividing cells, terminally differentiated cells, stem cells, and quiescent cells that occasionally enter into the cell cycle.
Healing by first intention
The least complicated example of wound repair is the healing of a clean, uninfected surgical incision approximated by surgical sutures. Such healing is referred to as primary union or healing by first intention. The incision causes death of a limited number of epithelial and connective tissue cells as well as disruption of epithelial basement membrane continuity. The narrow incisional space immediately fills with clotted blood containing fibrin and blood cells; dehydration of the surface clot forms the well-known scab that covers the wound
Healing by second intention
When there is more extensive loss of cells and tissue, as in surface wounds that create large defects, the reparative process is more complicated. Regeneration of parenchymal cells cannot completely restore the original architecture, and hence abundant granulation tissue grows in from the margin to complete the repair. This form of healing is referred to as secondary union or healing by second intention. ⬢ Perhaps the feature that most clearly differentiates primary from secondary healing is the phenomenon of wound contraction, which occurs in large surface wounds
Hepatocyte Growth Factor (HGF)
Has mitogenic effects in most epithelial cells, including hepatocytes and cells of the biliary epithelium in the liver, and epithelial cells of the lungs, mammary gland, skin, and other tissues. Besides its mitogenic effects, HGF acts as a morphogen in embryonic development and promotes cell scattering and migration. This factor is produced by fibroblasts, endothelial cells, and liver nonparenchymal cells
Hyaluronic Acid
HA is a polysaccharide of the GAG family found in the ECM of many tissues. It is a huge molecule that consists of many repeats of a simple disaccharide stretched end-to-end. It binds a large amount of water, forming a viscous hydrated gel that gives connective tissue the ability to resist compression forces. HA helps provide resilience and lubrication to many types of connective tissue, notably for the cartilage in joints. HA is also found in the matrix of migrating and proliferating cells, where it inhibits cell-to-cell adhesion and facilitates cell motility. CD44, a surface glycoprotein expressed by leukocytes, binds HA. Through such binding, T cells may be retained in tissues and remain bound to endothelium at sites of inflammation
Insulin-like growth factors
polypeptides with high sequence similarity to insulin. IGFs are part of a complex system that cells use to communicate with their physiologic environment. This complex system (often referred to as the IGF "axis") consists of two cell-surface receptors (IGF1R and IGF2R), two ligands (IGF-I and IGF-II), a family of six high-affinity IGF binding proteins (IGFBP 1-6), as well as associated IGFBP degrading enzymes, referred to collectivly as proteases
A variety of naturally occuring polypeptides that are members of the family of cytokines which affect functions of specific cell types and are found in small quantities. They are secreted regulatory proteins produced by lymphocytes, monocytes and various other cell types and are released by cells in response to antigenic and non-antigenic stimuli. Interleukins are of the larger class of T-cell products, lymphokines which are now more frequently considered as cytokines. The interleukins, of which there are 12 identified to date, modulate inflammation and immunity by regulating growth, mobility and differentiation of lymphoid and other cells. Included among the cytokines are cachectin and lymphotoxin which are now known as tumor necrosis factor-alpha and tumor necrosis factor-beta, respectively. Interleukin-1 inhibitors are the first well-described proteins involved in the feedback regulation of interleukin activities
A family of glycoproteins derived from human cells which normally has a role in fighting viral infections by preventing virus multiplication in cells. They are secreted by vertebrate cells in response to a wide variety of inducers and confer resistance against many different viruses, inhibit proliferation of normal and malignant cells, impede multiplication of intracellular parasites, enhance macrophage and granulocyte phagocytosis, augment natural killer cell activity, and show several other immunomodulatory functions
Labile cells
In continuously dividing tissues (also called labile tissues) cells proliferate throughout life, replacing those that are destroyed. These tissues include surface epithelia, such as stratified squamous surfaces of the skin, oral cavity, vagina, and cervix; the lining mucosa of all the excretory ducts of the glands of the body (e.g., salivary glands, pancreas, biliary tract); the columnar epithelium of the gastrointestinal tract and uterus; the transitional epithelium of the urinary tract, and cells of the bone marrow and hematopoietic tissues. In most of these tissues, mature cells are derived from stem cells
Laminin is the most abundant glycoprotein in the basement membrane and has binding domains for both ECM and cell-surface receptors. In the BM, polymers of laminin and collagen type IV form tightly bound networks. Laminin can also mediate the attachment of cells to connective tissue substrates
Paracrine signaling
One cell type produces the ligand, which then acts on adjacent target cells that express the appropriate receptors. The responding cells are in close proximity to the ligand-producing cell and are generally of a different type. Paracrine stimulation is common in connective tissue repair of healing wounds, in which a factor produced by one cell type (e.g., a macrophage) has its growth effect on adjacent cells (e.g., a fibroblast).
Permanent cells
Nondividing (permanent) tissues contain cells that have left the cell cycle and cannot undergo mitotic division in postnatal life. To this group belong neurons and skeletal and cardiac muscle cells. If neurons in the central nervous system are destroyed, the tissue is generally replaced by the proliferation of the central nervous system supportive elements, the glial cells
Platelet derived growth factor (PDGF)
PDGF is a family of several closely related proteins, each consisting of two chains designated A and B. All three isoforms of PDGF (AA, AB, and BB) are secreted and are biologically active. PDGF is stored in platelet α granules and is released on platelet activation. It can also be produced by a variety of other cells, including activated macrophages, endothelial cells, smooth muscle cells, and many tumor cells. PDGF causes migration and proliferation of fibroblasts, smooth muscle cells, and monocytes
ECM scaffolds are essential for wound healing because they provide the framework for cell migration and maintain the correct cell polarity. In epithelial cells, the polarity meant is between apical and baso lateral regions, in moving cells, having a distinct front and rear
Proteoglycans and hyaluronic acid (HA, hyaluronan or hyaluronate) make up the third type of component in the ECM, besides the fibrous structural proteins and cell adhesion proteins. Proteoglycans consist of a core protein linked to one or more polysaccharides called glycosaminoglycans (GAGs). These are long repeating polymers of specific disaccharides in which one (or both) contains a sulfate residue
RGD motif
Several integrins bind to Arg-Gly-Asp (RGD) sequences in the fibronectin and vitronectin molecules
The goal of the repair process is to restore the tissue to its original state. The inflammatory reaction set in motion by the injury contains the damage, eliminates the damaging stimulus, removes injured tissue, and initiates the deposition of ECM components in the area of injury. Some tissues can be completely reconstituted after injury, such as the repair of bone after a fracture or the regeneration of the surface epithelium in a cutaneous wound. For tissues that are incapable of regeneration, repair is accomplished by connective tissue deposition, producing a scar. This term is most often used in connection to wound healing in the skin, but it is also used to describe the replacement of parenchymal cells by connective tissue, as in the heart after myocardial infarction. If damage persists, inflammation becomes chronic, and tissue damage and repair may occur concurrently. Connective tissue deposition in these conditions is usually referred to as fibrosis
Healing consists of variable proportions of two distinct processes-regeneration, and the laying down of fibrous tissue, or scar formation. Superficial wounds, such as a cutaneous wound that only damages the epithelium, can heal by epithelial regeneration. Incisional and excisional skin wounds that damage the dermis heal through the formation of a collagen scar
Stable Cells
Quiescent (or stable) tissues normally have a low level of replication; however, cells from these tissues can undergo rapid division in response to stimuli and are thus capable of reconstituting the tissue of origin. They are considered to be in the G0 stage of the cell cycle but can be stimulated to enter G1
A narrowing, especially of a tube or canal, due to scar tissue or tumour
Active TGF-β binds to two cell surface receptors (types I and II) with serine/threonine kinase activity and triggers the phosphorylation of cytoplasmic transcription factors called Smads. TGF-β has multiple and often opposing effects depending on the tissue and the type of injury. Agents that have multiple effects are called pleiotropic
Tumor Necrosis Factor (TNF)
A polypeptide hormone, produced by endotoxin-activated macrophages, which has the ability to modulate adipocyte metabolism, lyse tumor cells in vitro, and induce hemorrhagic necrosis of certain transplantable tumors in vivo
The cytokines TNF and IL-6 are implicated in the G0/G1 transition and the growth factors HGF and TGF-α are involved in cell-cycle progression after the cells reach G1.
Vascular Endothelial Growth Factor (VEGF)
VEGF is a potent inducer of blood vessel formation in early development (vasculogenesis) and has a central role in the growth of new blood vessels (angiogenesis) in adults. It promotes angiogenesis in tumors, chronic inflammation, and healing of wounds
passive process caused by decreased outflow of blood from area – hypoxia results
Deep vein thrombosis
Typically occurs in the deep veins. These thrombi are usually loosely attached and thus easily dislodged
an abnormal particle (like a thrombus) circulating in the blood
Heart failure
Inability of the heart to produce a high enough cardiac output to meet the body's needs. Right heart failure leads to edema and congestion in tissues drained by the vena cava (liver, spleen, & lower extremities). Left heart failure leads to edema and congestion in the lungs
Heart failure cells
macrophages in the lung during left heart failure that often carry large amounts of haemosiderin.
Active process – excess of blood in a body part (as from an increased flow of blood due to vasodilation) erythema results
Infarct or infarction
A localized area of ischemic necrosis resulting from obstruction of the arterial supply (or less commonly venous drainage). White (anemic) infarcts develop mostly in solid organs that do not have collateral circulation (spleen, heart, kidney) following an acute arterial occlusion. Red (hemorrhagic) infarcts develop in organs whose vasculature is in a pedicle, where venous compression can occur due to twisting (gonads, intestine), organs with a dual blood supply (lung), organs that contain great amount of loose tissue and previously congested organs that undergo ischemia of arterial origin. A brain infarct is a special case. The typical brain infarct is first an anemic infarct, that later undergoes liquefaction. When the occluded vessel reopens (re-perfusion), a hemorrhagic infarct ensues
Lines of Zahn
Laminations in a thrombus usually found in heart or aorta – not as likely in deep leg vein thrombosis
Mural thrombus
A non-occlusive thrombus, usually occurring in the heart or a large artery
Refers to ingrowth of endothelial cells, smooth muscle cells, & fibroblasts into the fibrin-rich thrombus to re-establish circulation – eventually to recanalize
Propagation of thrombus
increase in size of an already formed thrombus.
Reestablishment of a lumen, through organization, in a vessel previously obstructed by a thrombus
the lay term used to describe the sudden onset of signs and symptoms in a patient with a cerebral infarct
An intravascular blood clot that develops and attaches to the wall of an artery or vein. Arterial or myocardial thrombi are usually "white thrombi" because the rapid blood flow washes red cells away, leaving only platelets and fibrin. Venous thrombi are usually "red thrombi" because sluggish flow allows the thrombi to contain all normal blood constituents. Thrombus can be differentiated from postmortem clotted blood by the presence of fibrin/platelet/red blood cell laminations (lines of Zahn). Postmortem clotted blood contains a gelatin-like mass of red cells (currant jelly) overlaid by coagulated "chicken fat"-like plasma
A twisting of the intestine about the axis of its mesentery or around an abnormal fibrous band (often a postsurgical adhesion).
Adenosine diphosphate
Platelets adhere to exposed extracellular matrix (ECM) via von Willebrand factor (vWF) and are activated, undergoing a shape change and granule release; released adenosine diphosphate (ADP) and thromboxane A2 (TxA2) lead to further platelet aggregation to form the primary hemostatic plug
Air embolism
Embolism due to air bubbles entering the blood vessels after trauma, surgical procedures, or changes in atmospheric pressure
Reduced plasma osmotic pressure can result from excessive loss or reduced synthesis of albumin, the serum protein most responsible for maintaining colloid osmotic pressure. An important cause of albumin loss is the nephrotic syndrome, characterized by a leaky glomerular capillary wall and generalized edema. Reduced albumin synthesis occurs in the setting of diffuse liver pathology (e.g., cirrhosis) or as a consequence of protein malnutrition. In each case, reduced plasma osmotic pressure leads to a net movement of fluid into the interstitial tissues and a resultant plasma volume contraction. Predictably, with reduced intravascular volume, renal hypoperfusion with secondary aldosteronism follows. The retained salt and water cannot correct the plasma volume deficit because the primary defect of low serum proteins persists. As with congestive heart failure, edema precipitated by hypoproteinemia is exacerbated by secondary salt and fluid retention.
Anasarca is a severe and generalized edema with profound subcutaneous tissue swelling
Iinhibit the activity of thrombin and other serine proteases-factors IXa, Xa, XIa, and XIIa. Antithrombin III is activated by binding to heparin-like molecules on endothelial cells; hence the clinical usefulness of administering heparin to minimize thrombosis
Abnormal accumulation of serous fluid in the spaces between tissues and organs in the cavity of the abdomen. Also called hydroperitoneum
Cardiac cirrhosis
In severe, long-standing hepatic congestion (most commonly associated with heart failure), there may even be grossly evident hepatic fibrosis (cardiac cirrhosis
a change to a viscous, jellylike, or solid state; especially : a change from a liquid to a thickened curdlike state not by evaporation but by chemical reaction
Coagulation cascade
The coagulation cascade constitutes the third component of the hemostatic process and is a major contributor to thrombosis.
The coagulation cascade is essentially a series of enzymatic conversions, turning inactive proenzymes into activated enzymes and culminating in the formation of thrombin.Thrombin then converts the soluble plasma protein fibrinogen precursor into the insoluble fibrous protein fibrin.
Each reaction in the pathway results from the assembly of a complex composed of an enzyme (activated coagulation factor), a substrate (proenzyme form of coagulation factor), and a cofactor (reaction accelerator). These components are typically assembled on a phospholipid complex and held together by calcium ions. Thus, clotting tends to remain localized to sites where such assembly can occur (e.g., on the surface of activated platelets or endothelium).
Intrinsic pathway
Coagulation cascade initiated by the activation of Hageman factor (XII)
Extrinsic pathway
Coagulation cascade activated by tissue factor, a cellular lipoprotein exposed at sites of tissue injury
Congestive heart failure
Heart failure in which the heart is unable to maintain adequate circulation of blood in the tissues of the body or to pump out the venous blood returned to it by the venous circulation
Decompression sickness
a sometimes fatal disorder that is marked by neuralgic pains and paralysis, distress in breathing, and often collapse and that is caused by the release of gas bubbles (as of nitrogen) in tissue upon too rapid decrease in air pressure after a stay in a compressed atmosphere -- called also bends, caisson disease, decompression illness, decompression syndrome
Dense bodies
Gamma granules in platelets. They contain ADP, ionized calcium, histamine, serotonin, and epinephrine
Disseminated intravascular coagulation (DIC)
the sudden or insidious onset of widespread fibrin thrombi in the microcirculation – screws up kidneys, heart, brain, lungs
the escape of blood into the tissues from ruptured blood vessels marked by a livid black-and-blue or purple spot or area; also : the discoloration so caused -- > 1cm to 2 cm subcutaneous hematoma
Inflammatory edema
Because of increased vascular permeability, inflammatory edema is a protein-rich exudate, with a specific gravity usually over 1.02
Noninflammatory edema
Caused by increased hydrostatic pressure, reduced plasma osmotic pressure, lymphatic obstruction, and sodium retention
the sudden obstruction of a blood vessel by an embolus
Endothelial prostacyclin (PGI2)
Potent vasodilator – inhibits platelet aggregation – comes from endothelium – dukes it out with its nemesis TxA2 and wins in healthy status, but TxA2 dominates when injury is present which increases vasoconstriction and platelet aggregation
any of several polypeptides consisting of 21 amino acid residues that are produced in various cells and tissues, that play a role in regulating vasomotor activity, cell proliferation, and the production of hormones, and that have been implicated in the development of vascular disease
Endotoxin / lipopolysaccharide
a toxin of internal origin; specifically : a poisonous substance present in bacteria (as the causative agent of typhoid fever) but separable from the cell body only on its disintegration
Fat embolism
Fat from long bone marrow after a break, or occasionally tissue trauma becomes an embolus
a white insoluble fibrous protein formed from fibrinogen by the action of thrombin especially in the clotting of blood
Fibrin split products
Chemotactic agents from cleavage of fibrinogen – attracts neutrophils and monocytes – can also act as a weak anticoagulant after release from fibrin breakdown by plasmin (breaking up clot)
a plasma protein that is produced in the liver and is converted into fibrin during blood clot formation
Glycoprotein Ib (GpIb)
Platelet surface receptor – binds to vWF which in turn binds to exposed collagen at injury site. Deficiency causes Bernard-Soulier syndrome
a mass of usually clotted blood that forms in a tissue, organ, or body space as a result of a broken blood vessel
a copious discharge of blood from the blood vessels
1 : stoppage or sluggishness of blood flow
2 : the arrest of bleeding (as by a hemostatic agent)
Pale infarct
anemic – in harder organs (spleen, kidney, heart) blood can’t flow outside of infarct area – turns pale
Red infarct
hemmorhagic – softer tissue (gut, ovaries, lungs) blood is able to hemmorhage outside of infarct area
edema due to faulty lymphatic drainage
Nitric oxide
Similar to PGI2 – acts as vasodilator & inhibitor of platelet aggregation
Paradoxical embolism
Rarely an embolism may pass through an interatrial or interventricular defect and get into systemic circulation
a minute reddish or purplish spot containing blood that appears in skin or mucous membrane as a result of localized hemorrhage – 1-2mm diameter
venous thrombosis accompanied by little or no inflammation

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