An arteriole is a small-diameter blood vessel in the microcirculation that extends and branches out from an artery and leads to capillaries. Arterioles are the primary site of vascular resistance; the greatest change in blood pressure and velocity of blood flow occurs at the transition of arterioles to capillaries. In a healthy vascular system the endothelium lines all blood-contacting surfaces, including arteries, veins, venules and heart chambers; this healthy condition is promoted by the ample production of nitric oxide by the endothelium, which requires a biochemical reaction regulated by a complex balance of polyphenols, various nitric oxide synthase enzymes and L-arginine. In addition there is direct electrical and chemical communication via gap junctions between the endothelial cells and the vascular smooth muscle. Blood pressure in the arteries supplying the body is a result of the work needed to pump the cardiac output through the vascular resistance termed total peripheral resistance by physicians and researchers.
An increase in the media to lumenal diameter ratio has been observed in hypertensive arterioles as the vascular wall thickens and/or lumenal diameter decreases. The up and down fluctuation of the arterial blood pressure is due to the pulsatile nature of the cardiac output and determined by the interaction of the stroke volume versus the volume and elasticity of the major arteries; the decreased velocity of flow in the capillaries increases the blood pressure, due to Bernoulli's principle. This induces gas and nutrients to move from the blood to the cells, due to the lower osmotic pressure outside the capillary; the opposite process occurs when the blood leaves the capillaries and enters the venules, where the blood pressure drops due to an increase in flow rate. Arterioles receive autonomic nervous system innervation and respond to various circulating hormones in order to regulate their diameter. Retinal vessels lack a functional sympathetic innervation. Further local responses to stretch, carbon dioxide, pH, oxygen influence arteriolar tone.
Norepinephrine and epinephrine are vasoconstrictive acting on alpha 1-adrenergic receptors. However, the arterioles of skeletal muscle, cardiac muscle, pulmonary circulation vasodilate in response to these hormones when they act on beta-adrenergic receptors. Stretch and high oxygen tension increase tone, carbon dioxide and low pH promote vasodilation. Pulmonary arterioles are a noteworthy exception. Brain arterioles are sensitive to pH with reduced pH promoting vasodilation. A number of hormones influence arteriole tone such as angiotensin II, bradykinin, atrial natruretic peptide, prostacyclin. Arteriole diameters decrease with exposure to air pollution. Any pathology which constricts blood flow, such as stenosis, will increase total peripheral resistance and lead to hypertension. Arteriolosclerosis is the term used for the hardening of arteriole walls; this can be due to decreased elastic production from fibrinogen, associated with ageing, or hypertension or pathological conditions such as atherosclerosis.
The muscular contraction of arterioles is targeted by drugs that lower blood pressure, for example the dihydropyridines, which block the calcium conductance in the muscular layer of the arterioles, causing relaxation. This decreases the resistance to flow into peripheral vascular beds, lowering overall systemic pressure. A "metarteriole" is an arteriole. Surface chemistry of microvasculature Venule
Streptococcus pyogenes is a species of Gram-positive bacterium in the genus Streptococcus. These bacteria are aerotolerant and an extracellular bacterium, made up of non-motile and non-sporing cocci, it is clinically important for humans. It is an infrequent, but pathogenic, part of the skin microbiota, it is the predominant species harboring the Lancefield group A antigen, is called group A streptococcus. However, both Streptococcus dysgalactiae and the Streptococcus anginosus group can possess group A antigen. Group A streptococci when grown on blood agar produces small zones of beta-hemolysis, a complete destruction of red blood cells, it is thus called group A streptococcus, can make colonies greater than 5 mm in size. Like other cocci, streptococci are round bacteria; the species name is derived from Greek words meaning'a chain' of berries and pus -forming, because streptococcal cells tend to link in chains of round cells and a number of infections caused by the bacterium, produce pus. The main criterion for differentiation between Staphylococcus spp. and Streptococcus spp. is the catalase test.
Staphylococci are catalase positive. S. pyogenes can be cultured on fresh blood agar plates. Under ideal conditions, it has an incubation period of 1 to 3 days. An estimated 700 million GAS. While the overall mortality rate for these infections is 0.1%, over 650,000 of the cases are severe and invasive, have a mortality rate of 25%. Early recognition and treatment are critical. S. pyogenes colonises the throat, genital mucosa and skin. Of healthy individuals, 1 % to 5 % have vaginal, or rectal carriage. In healthy children, such carriage rate varies from 2% to 17%. There are four methods for the transmission of this bacterium: inhalation of respiratory droplets, skin contact, contact with objects, surface, or dust, contaminated with bacteria or, less transmission through food; such bacteria can cause a variety of diseases such as streptococcal pharyngitis, rheumatic fever, rheumatic heart disease, scarlet fever. Although pharyngitis is viral in origin, about 15 to 30% of all pharyngitis cases in children are caused by GAS.
The number of pharyngitis cases is higher in children when compared with adults due to exposures in schools, as a consequence of lower host immunity. Such cases Streptococcal pharyngitis occurs more from December to April in seasonal countries due to changing climate, behavioural changes or predisposing viral infection. Disease cases are the lowest during autumn. MT1 clone is associated with invasive Streptococcus pyogenes infections among developed countries; the incidence and mortality of S. pyognes was high during the pre-penicillin era, but had started to fall prior to the widespread availability of penicillin. Therefore, environmental factors do play a role in the S. pyogenes infection. Incidence of S. pyogenes is 2 to 4 per 100,000 population in developed countries and 12 to 83 per 100,000 population in developing countries. S. pyogenes infection is more found in men than women, with highest rates in the elderly, followed by infants. In people with risk factors such as heart disease, malignancy, blunt trauma, surgical incision, virus respiratory infection, including influenza, S. pyogenes infection happens in 17 to 25% of all cases.
GAS secondary infection happens within one week of the diagnosis of influenza infection. In 14 to 16% of childhood S. pyogenes infections, there is a prior chickenpox infection. Such S. pyogenes infection in children manifests as severe soft tissue infection with onset 4 to 12 days from the chickenpox diagnosis. There is 40 to 60 times increase in risk of S. pyogenes infection within the first two weeks of chickenpox infection in children. However, 20 to 30% of S. pyogenes infection does occur in adults with no identifiable risk factors. The incidence is higher in children with no known risk factors; the rates of scarlet fever in UK was 4 in 100,000 population, however, in 2014, the rates had risen to 49 per 100,000 population. Rheumatic fever and rheumatic heart disease occurs at 2 to 3 weeks after the throat infection, more common among the impoverished people in developing countries. From 1967 to 1996, the global mean incidence of rheumatic fever and RHD was 19 per 100,000 with the highest incidence at 51 per 100,000.
Maternal S. pyogenes infection happens in late pregnancy. This represents 20 to 100 times increase in risk for S. pyogenes infections. Clinical manifestations are: pneumonia, septic arthritis, necrotizing fasciitis, genital tract sepsis. According to a study done by Queen Charlotte’s hospital in London during the 1930s, the vagina was not the common source of such infection. On the contrary, maternal throat infection and close contacts with carriers were the more common sites for maternal S. pyogenes infection. In 1928, Rebecca Lancefield published a method for serotyping S. pyogenes based on its cell-wall polysaccharide, a virulence factor displayed on its surface. In 1946, Lancefield described the serologic classification of S. pyogenes isolates based on their surface T-antigen. Four of the 20 T-antigens have been revealed to be pili, which are used
Foam cells are the fat-laden M2 macrophages that serve as the hallmark of early stage atherosclerotic lesion formation. As these plaques mature, they become more inflamed. Foam cell formation is triggered by a number of factors including the uncontrolled uptake of modified low density lipoproteins, the upregulation of cholesterol esterification and the impairment of mechanisms associated with cholesterol release. Foam cells are formed when circulating monocyte-derived cells are recruited to the atherosclerotic lesion site or fat deposits in the blood vessel walls. Recruitment is facilitated by the molecules P-selectin and E-selectin, intercellular adhesion molecule 1 and vascular cell adhesion molecule 1. Monocytes are able to penetrate the arterial wall as a result of impaired endothelial integrity which increases permeability. Once in the sub endothelium space, inflammation processes induce the differentiation of monocytes into mature macrophages. Macrophages are able to internalize modified lipoproteins like βVLDL, AcLDL and OxLDL through their binding to the scavenger receptors such as CD36 and SR-A on the macrophage surface.
These scavenger receptors act as "Pattern recognition receptors" on macrophages and are responsible for recognizing and binding to oxLDL, which in turn promotes the formation of foam cells through internalization of these lipoproteins. Coated-pit endocytosis and pinocytosis are responsible for lipoprotein internalization. Once internalized, scavenged lipoproteins are transported to endosomes or lysosomes for degradation, whereby the cholesteryl esters are hydrolyzed to unesterified free cholesterol by lysosomal acid lipase. Free cholesterol is transported to the endoplasmic reticulum where it is re-esterified by ACAT1 and subsequently stored as cytoplasmic liquid droplets; these droplets are responsible for the foamy appearance of the macrophage and thus the name of foam cells. At this point, foam cells can either be degraded though the de-esterification and secretion of cholesterol, or can further promote foam cell development and plaque formation – a process, dependent on the balance of free cholesterol and esterified cholesterol.
Low-density lipoprotein cholesterol and modified forms of LDL cholesterol such as oxidized, glycated, or acetylated LDL, is contained by a foam cell - a marker of atherosclerosis. The uptake of LDL-C alone does not cause foam cell formation. Modified LDL affects the intracellular trafficking and metabolism of native LDL, such that not all LDL need to be modified for foam cell formation when LDL levels are high. Foam cell degradation or more the breakdown of esterified cholesterols, is facilitated by a number of efflux receptors and pathways. Esterified cholesterol from cytoplasmic liquid droplets are once again hydrolyzed to free cholesterol by acid cholesterol esterase. Free cholesterol can be secreted from the macrophage by the efflux to ApoA1 and ApoE discs via the ABCA1 receptor; this pathway is used by modified or pathological lipoproteins like AcLDL, OxLDL and βVLDL. FC can be transported to a recycling compartment through the efflux to ApoA1 containing HDLs via aqueous diffusion or transport through the SR-B1 or ABCG1 receptors.
While this pathway can be used by modified lipoproteins, LDL derived cholesterol can only use this pathway to excrete FC. The differences in excretory pathways between types of lipoproteins is a result of the cholesterol being segregated into different areas; the maintenance of foam cells and the subsequent progression of plaque build-up is caused by the secretion of chemokines and cytokines from macrophages and foam cells. Foam cells secrete pro-inflammatory cytokines such as interleukins: IL-1, IL-6. Macrophages within the atherosclerotic legion area have a decreased ability to migrate, which further promotes plaque formation as they are able to secrete cytokines, reactive oxygen species and growth factors that stimulate modified lipoprotein uptake and vascular smooth muscle cell proliferation. VSMC can accumulate cholesteryl esters. To summarize, in chronic hyperlipidemia, lipoproteins aggregate within the intima of blood vessels and become oxidized by the action of oxygen free radicals generated either by macrophages or endothelial cells.
The macrophages engulf oxidized low-density lipoproteins by endocytosis via scavenger receptors, which are distinct from LDL receptors. The oxidized LDL accumulates in the macrophages and other phagocytes, which are known as foam cells. Foam cells form the fatty streaks of the plaques of atheroma in the tunica intima of arteries. Foam cells are not dangerous as such, but can become a problem when they accumulate at particular foci thus creating a necrotic centre of atherosclerosis. If the fibrous cap that prevents the necrotic centre from spilling into the lumen of a vessel ruptures, a thrombus can form which can lead to emboli occluding smaller vessels; the occlusion of small vessels results in ischemia, contributes to stroke and myocardial infarction, two of the leading causes of cardiovascular-related death. Foam cells are small in size and can only be detected by examining a fatty
A capillary is a small blood vessel from 5 to 10 micrometres in diameter, having a wall one endothelial cell thick. They are the smallest blood vessels in the body: they convey blood between the arterioles and venules; these microvessels are the site of exchange of many substances with the interstitial fluid surrounding them. Substances which exit include water and glucose. Lymph capillaries connect with larger lymph vessels to drain lymphatic fluid collected in the microcirculation. During early embryonic development new capillaries are formed through vasculogenesis, the process of blood vessel formation that occurs through a de novo production of endothelial cells which form vascular tubes; the term angiogenesis denotes the formation of new capillaries from pre-existing blood vessels and present endothelium which divides. Blood flows from the heart through arteries, which branch and narrow into arterioles, branch further into capillaries where nutrients and wastes are exchanged; the capillaries join and widen to become venules, which in turn widen and converge to become veins, which return blood back to the heart through the venae cavae.
Individual capillaries are part of the capillary bed, an interweaving network of capillaries supplying tissues and organs. The more metabolically active a tissue is, the more capillaries are required to supply nutrients and carry away waste products. There are two types of capillaries: true capillaries, which branch from arterioles and provide exchange between tissue and the capillary blood, metarterioles, found only in the mesenteric circulation, they are short vessels that directly connect the arterioles and venules at opposite ends of the beds. Metarterioles are found in the mesenteric microcirculation; the physiological mechanisms underlying precapillary resistance is no longer considered to be a result of precapillary sphincters outside of the mesentery organ. Lymphatic capillaries are larger in diameter than blood capillaries, have closed ends; this structure permits interstitial fluid to flow into them but not out. Lymph capillaries have a greater internal oncotic pressure than blood capillaries, due to the greater concentration of plasma proteins in the lymph.
There are three types of blood capillaries: Continuous capillaries are continuous in the sense that the endothelial cells provide an uninterrupted lining, they only allow smaller molecules, such as water and ions to pass through their intercellular clefts. Lipid-soluble molecules can passively diffuse through the endothelial cell membranes along concentration gradients. Continuous capillaries can be further divided into two subtypes: Those with numerous transport vesicles, which are found in skeletal muscles, fingers and skin; those with few vesicles, which are found in the central nervous system. These capillaries are a constituent of the blood–brain barrier. Fenestrated capillaries have pores in the endothelial cells that are spanned by a diaphragm of radially oriented fibrils and allow small molecules and limited amounts of protein to diffuse. In the renal glomerulus there are cells with no diaphragms, called podocyte foot processes or pedicels, which have slit pores with a function analogous to the diaphragm of the capillaries.
Both of these types of blood vessels have continuous basal laminae and are located in the endocrine glands, intestines and the glomeruli of the kidney. Sinusoid capillaries are a special type of open-pore capillary, that have larger openings in the endothelium; these types of blood vessels allow red and white blood cells and various serum proteins to pass, aided by a discontinuous basal lamina. These capillaries lack pinocytotic vesicles, therefore utilize gaps present in cell junctions to permit transfer between endothelial cells, hence across the membrane. Sinusoid blood vessels are located in the bone marrow, lymph nodes, adrenal glands; some sinusoids are distinctive in. They are called discontinuous sinusoidal capillaries, are present in the liver and spleen, where greater movement of cells and materials is necessary. A capillary wall is simple squamous epithelium; the capillary wall performs an important function by allowing nutrients and waste substances to pass across it. Molecules larger than 3 nm such as albumin and other large proteins pass through transcellular transport carried inside vesicles, a process which requires them to go through the cells that form the wall.
Molecules smaller than 3 nm such as water and gases cross the capillary wall through the space between cells in a process known as paracellular transport. These transport mechanisms allow bidirectional exchange of substances depending on osmotic gradients and can be further quantified by the Starling equation. Capillaries that form part of the blood–brain barrier however only allow for transcellular transport as tight junctions between endothelial cells seal the paracellular space. Capillary beds may control their blood flow via autoregulation; this allows an organ to maintain constant flow despite a change in central blood pressure. This is achieved by myogenic response, in the kidney by tubuloglomerular feedback; when blood pressure increases, arterioles are stretched and subsequently constrict to counteract the
Anatomical terms of location
Standard anatomical terms of location deal unambiguously with the anatomy of animals, including humans. All vertebrates have the same basic body plan – they are bilaterally symmetrical in early embryonic stages and bilaterally symmetrical in adulthood; that is, they have mirror-image left and right halves if divided down the middle. For these reasons, the basic directional terms can be considered to be those used in vertebrates. By extension, the same terms are used for many other organisms as well. While these terms are standardized within specific fields of biology, there are unavoidable, sometimes dramatic, differences between some disciplines. For example, differences in terminology remain a problem that, to some extent, still separates the terminology of human anatomy from that used in the study of various other zoological categories. Standardized anatomical and zoological terms of location have been developed based on Latin and Greek words, to enable all biological and medical scientists to delineate and communicate information about animal bodies and their component organs though the meaning of some of the terms is context-sensitive.
The vertebrates and Craniata share a substantial heritage and common structure, so many of the same terms are used for location. To avoid ambiguities this terminology is based on the anatomy of each animal in a standard way. For humans, one type of vertebrate, anatomical terms may differ from other forms of vertebrates. For one reason, this is because humans have a different neuraxis and, unlike animals that rest on four limbs, humans are considered when describing anatomy as being in the standard anatomical position, thus what is on "top" of a human is the head, whereas the "top" of a dog may be its back, the "top" of a flounder could refer to either its left or its right side. For invertebrates, standard application of locational terminology becomes difficult or debatable at best when the differences in morphology are so radical that common concepts are not homologous and do not refer to common concepts. For example, many species are not bilaterally symmetrical. In these species, terminology depends on their type of symmetry.
Because animals can change orientation with respect to their environment, because appendages like limbs and tentacles can change position with respect to the main body, positional descriptive terms need to refer to the animal as in its standard anatomical position. All descriptions are with respect to the organism in its standard anatomical position when the organism in question has appendages in another position; this helps avoid confusion in terminology. In humans, this refers to the body in a standing position with arms at the side and palms facing forward. While the universal vertebrate terminology used in veterinary medicine would work in human medicine, the human terms are thought to be too well established to be worth changing. Many anatomical terms can be combined, either to indicate a position in two axes or to indicate the direction of a movement relative to the body. For example, "anterolateral" indicates a position, both anterior and lateral to the body axis. In radiology, an X-ray image may be said to be "anteroposterior", indicating that the beam of X-rays pass from their source to patient's anterior body wall through the body to exit through posterior body wall.
There is no definite limit to the contexts in which terms may be modified to qualify each other in such combinations. The modifier term is truncated and an "o" or an "i" is added in prefixing it to the qualified term. For example, a view of an animal from an aspect at once dorsal and lateral might be called a "dorsolateral" view. Again, in describing the morphology of an organ or habitus of an animal such as many of the Platyhelminthes, one might speak of it as "dorsiventrally" flattened as opposed to bilaterally flattened animals such as ocean sunfish. Where desirable three or more terms may be agglutinated or concatenated, as in "anteriodorsolateral"; such terms sometimes used to be hyphenated. There is however little basis for any strict rule to interfere with choice of convenience in such usage. Three basic reference planes are used to describe location; the sagittal plane is a plane parallel to the sagittal suture. All other sagittal planes are parallel to it, it is known as a "longitudinal plane".
The plane is perpendicular to the ground. The median plane or midsagittal plane is in the midline of the body, divides the body into left and right portions; this passes through the head, spinal cord, and, in many animals, the tail. The term "median plane" can refer to the midsagittal plane of other structures, such as a digit; the frontal plane or coronal plane divides the body into ventral portions. For post-embryonic humans a coronal plane is vertical and a transverse plane is horizontal, but for embryos and quadrupeds a coronal plane is horizontal and a transverse plane is vertical. A longitudinal plane is any plane perpendicular to the transverse plane; the coronal plane and the sagittal plane are examples of longitudinal planes. A transverse plane known as a cross-section, divides the body into cranial and caudal portions. In human anatomy: A transverse plane is an X-Z plane, parallel to the ground, which s
The lymphatic system is part of the vascular system and an important part of the immune system, comprising a large network of lymphatic vessels that carry a clear fluid called lymph directionally towards the heart. The lymphatic system was first described in the seventeenth century independently by Olaus Rudbeck and Thomas Bartholin. Unlike the circulatory system, the lymphatic system is not a closed system; the human circulatory system processes an average of 20 litres of blood per day through capillary filtration, which removes plasma while leaving the blood cells. 17 litres of the filtered plasma is reabsorbed directly into the blood vessels, while the remaining three litres remain in the interstitial fluid. One of the main functions of the lymph system is to provide an accessory return route to the blood for the surplus three litres; the other main function is that of defense in the immune system. Lymph is similar to blood plasma: it contains lymphocytes, it contains waste products and cellular debris together with bacteria and proteins.
Associated organs composed of lymphoid tissue are the sites of lymphocyte production. Lymphocytes are concentrated in the lymph nodes; the spleen and the thymus are lymphoid organs of the immune system. The tonsils are lymphoid organs that are associated with the digestive system. Lymphoid tissues contain lymphocytes, contain other types of cells for support; the system includes all the structures dedicated to the circulation and production of lymphocytes, which includes the bone marrow, the lymphoid tissue associated with the digestive system. The blood does not come into direct contact with the parenchymal cells and tissues in the body, but constituents of the blood first exit the microvascular exchange blood vessels to become interstitial fluid, which comes into contact with the parenchymal cells of the body. Lymph is the fluid, formed when interstitial fluid enters the initial lymphatic vessels of the lymphatic system; the lymph is moved along the lymphatic vessel network by either intrinsic contractions of the lymphatic passages or by extrinsic compression of the lymphatic vessels via external tissue forces, or by lymph hearts in some animals.
The organization of lymph nodes and drainage follows the organization of the body into external and internal regions. The lymph vessels empty into the lymphatic ducts, which drain into one of the two subclavian veins, near their junction with the internal jugular veins; the lymphatic system consists of lymphatic organs, a conducting network of lymphatic vessels, the circulating lymph. The primary or central lymphoid organs generate lymphocytes from immature progenitor cells; the thymus and the bone marrow constitute the primary lymphoid organs involved in the production and early clonal selection of lymphocyte tissues. Bone marrow is responsible for both the creation of T cells and the production and maturation of B cells. From the bone marrow, B cells join the circulatory system and travel to secondary lymphoid organs in search of pathogens. T cells, on the other hand, travel from the bone marrow to the thymus. Mature T cells join B cells in search of pathogens; the other 95 % of T cells begin a process of a form of programmed cell death.
Secondary or peripheral lymphoid organs, which include lymph nodes and the spleen, maintain mature naive lymphocytes and initiate an adaptive immune response. The peripheral lymphoid organs are the sites of lymphocyte activation by antigens. Activation leads to clonal affinity maturation. Mature lymphocytes recirculate between the blood and the peripheral lymphoid organs until they encounter their specific antigen. Secondary lymphoid tissue provides the environment for the foreign or altered native molecules to interact with the lymphocytes, it is exemplified by the lymph nodes, the lymphoid follicles in tonsils, Peyer's patches, adenoids, etc. that are associated with the mucosa-associated lymphoid tissue. In the gastrointestinal wall the appendix has mucosa resembling that of the colon, but here it is infiltrated with lymphocytes. Tertiary lymphoid organs are abnormal lymph node–like structures that form in peripheral tissues at sites of chronic inflammation, such as chronic infection, transplanted organs undergoing graft rejection, some cancers, autoimmune and autoimmune-related diseases.
TLOs are regulated differently from the normal process whereby lymphoid tissues are formed during ontogeny, being dependent on cytokines and hematopoietic cells, but still drain interstitial fluid and transport lymphocytes in response to the same chemical messengers and gradients. TLOs contains far fewer lymphocytes, assumes an immune role only when challenged with antigens that result in inflammation, it achieves this by importing the lymphocytes from lymph. The thymus is a primary lymphoid organ and the site of maturation for T cells, the lymphocytes of the adaptive immune system; the thymus increases in size from birth in response to postnatal antigen stimulation to puberty and regresses thereafter. The loss or lack of the thymus results in severe immunodeficiency and subsequent high susceptibility to infection. In most species, the thymus consists of lobules divided by septa which are made up of epithelium and is therefore an epithelial organ. T cells mature from
Inflammation is part of the complex biological response of body tissues to harmful stimuli, such as pathogens, damaged cells, or irritants, is a protective response involving immune cells, blood vessels, molecular mediators. The function of inflammation is to eliminate the initial cause of cell injury, clear out necrotic cells and tissues damaged from the original insult and the inflammatory process, initiate tissue repair; the five classical signs of inflammation are heat, redness and loss of function. Inflammation is a generic response, therefore it is considered as a mechanism of innate immunity, as compared to adaptive immunity, specific for each pathogen. Too little inflammation could lead to progressive tissue destruction by the harmful stimulus and compromise the survival of the organism. In contrast, chronic inflammation may lead to a host of diseases, such as hay fever, atherosclerosis, rheumatoid arthritis, cancer. Inflammation is therefore closely regulated by the body. Inflammation can be classified as either chronic.
Acute inflammation is the initial response of the body to harmful stimuli and is achieved by the increased movement of plasma and leukocytes from the blood into the injured tissues. A series of biochemical events propagates and matures the inflammatory response, involving the local vascular system, the immune system, various cells within the injured tissue. Prolonged inflammation, known as chronic inflammation, leads to a progressive shift in the type of cells present at the site of inflammation, such as mononuclear cells, is characterized by simultaneous destruction and healing of the tissue from the inflammatory process. Inflammation is not a synonym for infection. Infection describes the interaction between the action of microbial invasion and the reaction of the body's inflammatory response—the two components are considered together when discussing an infection, the word is used to imply a microbial invasive cause for the observed inflammatory reaction. Inflammation on the other hand describes purely the body's immunovascular response, whatever the cause may be.
But because of how the two are correlated, words ending in the suffix -itis are sometimes informally described as referring to infection. For example, the word urethritis means only "urethral inflammation", but clinical health care providers discuss urethritis as a urethral infection because urethral microbial invasion is the most common cause of urethritis, it is useful to differentiate inflammation and infection because there are typical situations in pathology and medical diagnosis where inflammation is not driven by microbial invasion – for example, trauma and autoimmune diseases including type III hypersensitivity. Conversely, there is pathology where microbial invasion does not cause the classic inflammatory response – for example, parasitosis or eosinophilia. Acute inflammation is a short-term process appearing within a few minutes or hours and begins to cease upon the removal of the injurious stimulus, it involves a coordinated and systemic mobilization response locally of various immune and neurological mediators of acute inflammation.
In a normal healthy response, it becomes activated, clears the pathogen and begins a repair process and ceases. It is characterized by five cardinal signs:An acronym that may be used to remember the key symptoms is "PRISH", for pain, immobility and heat; the traditional names for signs of inflammation come from Latin: Dolor Calor Rubor Tumor Functio laesa The first four were described by Celsus, while loss of function was added by Galen. However, the addition of this fifth sign has been ascribed to Thomas Sydenham and Virchow. Redness and heat are due to increased blood flow at body core temperature to the inflamed site. Loss of function has multiple causes. Acute inflammation of the lung does not cause pain unless the inflammation involves the parietal pleura, which does have pain-sensitive nerve endings; the process of acute inflammation is initiated by resident immune cells present in the involved tissue resident macrophages, dendritic cells, Kupffer cells and mast cells. These cells possess surface receptors known as pattern recognition receptors, which recognize two subclasses of molecules: pathogen-associated molecular patterns and damage-associated molecular patterns.
PAMPs are compounds that are associated with various pathogens, but which are distinguishable from host molecules. DAMPs are compounds that are associated with host-related cell damage. At the onset of an infection, burn, or other injuries, these cells undergo activation and release inflammatory mediators responsible for the clinical signs of inflammation. Vasodilation and its resulting increased blood flow causes increased heat. Increased permeability of the blood vessels results in an exudation of plasma proteins and fluid into the tissue, which manifests itself as swelling; some of the released mediators such as bradykinin increase the sensitivity to pain. The mediator molecules alter the blood vessels to