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steps in acute inflammation
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Inflammation
Inflammation is the bodies normal response to injured tissues, although it can sometimes lead to further tissue damage. It was first described around 30 BC by Celsius, as tumour (swelling), rubor (redness), calor (heat) and dolour (pain); although excess secretion and loss of function are now commonly added. Inflammation is a response which has evolved to try and put things right in a damaged tissue, for example the pain and loss of function allow the tissue to heal easier whilst the heat and redness are caused by an increased blood flow to the tissue. (1) Inflammation occurs to control infection or injury, to eliminate pathogens, and to initiate healing and tissue repair. (2)
An inflammatory pathology is usually indicated by the suffix '-itis', such as in bronchitis, dermatitis, orchitis and enteritis, and can be either acute or chronic. (1) It is a non-specific defence and so the response of the body to a cut, burn, radiation, bacteria or virus are all very similar. There are three basic stages to inflammation:
1) Vasodilation and increased permeability of blood vessels,
2) Phagocyte emigration, and
3) Tissue repair (3)
Unfortunately, sometimes inflammation can be the cause of, or increase the symptom severity of a disease, such as in:
Tuberculosis, leprosy and syphilis, which are persistent infections with low virulence micro-organisms Silicosis, atherosclerosis and radiation, prolonged exposure to potentially toxic agents.
Rheumatoid arthritis and Hashimoto's thyroiditis, autoimmune diseases (4)
Body
Acute inflammation occurs rapidly, within a few hours after the injury or infection occurs to which the inflammation is acting. Initially venules and arterioles dilate, causing hyperaemia. This then decreases and the vessels increase their permeability, allowing blood plasma and platelets into the tissue as serous exudate. this causes an oedema (excess fluid in the tissue). Fibrinogen in the exudate is converted to fibrin, which deposits itself to help to localise tissue damage and control bleeding. (2) Within an hour of the inflammation starting neutrophils, and then hours later monocytes, arrive on the scene. They leave the bloodstream by emigration (also known as diapedesis), dependent on chemotaxis; they are attracted by microbes, kinins, complement and other neutrophils. These neutrophils attempt to destroy the foreign bodies by phagocytosis. Any remaining dead phagocytes or damaged tissue after a few days becomes purulent exudate, or pus. This may be broken down in the body or may reach the surface of the body, but if it cannot be an abscess may be formed.
The immunologic events that are happening at the local level during Carlton's acute inflammatory response would be:
Also, cytokines are used as they can destroy the infection, however there is a problem with this diagnosis as excessive production can cause tissue and organ damage. The pathological physiological outcomes of sepsis is that there is a multi-organ dysfunction that includes the heart, brain, kidneys and the lungs. Acute respiratory distress syndrome (ARDS) is a condition where there is a low oxygen level in the blood, this mostly affects the lungs, people who have sepsis will be affected by ARDS as their breathing rate will decrease. Another reason for multi-organ dysfunction is that there is a lack of blood being given to the organs, this causes low blood pressure or as it’s called hypotension, this mostly affects diabetic people which leads them to having sepsis.
Lupus is inflammatory disease caused when the immune system attacks its own tissues and organs, and this inflammation affects many different body parts such as the joints, skin, kidneys, blood cells, brain, heart and lungs. Second is the Celiac disease and it is an autoimmune reaction from eating gluten, and it may lead to damage in the small intestine because this disease attacks the villi, the projections that line the small intestine for protection. The last example is Rheumatoid Arthritis, an inflammatory disorder in which affects many joints, mainly in hands and feet, and then causing your joints to painfully swell and possibly cause bone erosion.
inflammatory infiltrates, add fuel to the fire so to say. Lymphocytes infiltrate the spinal and
Researchers think that this immune system response may be triggered by bacteria or viruses, material in the intestinal contents, or a defective signal from the body’s own cells, called an autoimmune response. Inflammation results in pain, heat, redness, and swelling of the tissue. Chronic inflammation can harm the function of tissues and organs (U.S. News, 2009). Crohn’s disease also appears to affect certain ethnic groups more than others. American Jews of European descent are four to five times more likely to de... ...
Two of the most significant bloodborne pathogens are HBV (Hepatitis B Virus) and HIV (Human Immunodeficiency Virus). Some of the other bloodborne pathogens include Hepatitis C, Hepatitis D, and Syphilis. These are less significant and not as life threatening as the two listed above.
The job of the immune system is to keep “foreign” invaders out of the body, or if one gets in, to seek it out and kill it. These foreign invaders are called pathogens, which are tiny organisms that can cause an infection in the body. Pathogens can be bacteria, parasites, and fungi (http://www.niaid.nih.gov/topics/immuneSystem/pages/whatisimmunesystem.aspx).
The main diseases that showed the most virulence during the time were cholera, yellow fever and consumption now known as tuberculosis. The 9th census mortality data showed that 1 out 7 deaths from disease were caused by tuberculosis and 1 out of 24 disease deaths were resulting from cholera. . Until the 1870s...
... and quickly grow. Secondly, invasins help the bacteria spread in the host’s tissues. An invasion is a protein that acts locally to damage host cells to facilitate the growth and spread of the pathogen. More simply, Staphylococcus aureus and Streptococcus pyogens have a small army of invasins that basically attack the host very quickly and spread the bacteria out far – into the blood and organs. Another virulence factor of both Staphylococcus aureus and Streptococcus pyogens is their cellular secretions. The secretions include antigens, enzymes, and toxins that assist with various functions needed to feed the bacteria and fend off the host’s immune defences.
Pathogens are a type of microorganism that spreads viral and bacterial diseases. These diseases when present in human blood and body fluids are known as blood borne pathogens, and can spread from one person to another. (Worcester polytechnic institute) The most serious types of blood borne diseases are the hepatitis B virus (HBV) and hepatitis C virus (HCV), which can cause liver damage; and HIV (human immunodeficiency virus), which is responsible for causing AIDS (acquired immune deficiency syndrome). The blood borne pathogens can be spread when the blood or body fluids (semen, vaginal fluid, breast milk, and amniotic fluid) of an infected individual comes into contact with mucous membranes or an open sore or cut on the skin of another person. Mucus membranes are located in the eyes, nose, mouth, and other areas as well. ("Bloodborne pathogens: MedlinePlus Medical Encyclopedia") Two of the most common ways that pathogens are transmitted is through the exchange of fluids during sexual intercourse or by sharing infected IV needles. (Worcester polytechnic institute)
Sepsis is defined as an exaggerated, overwhelming and uncontrolled systemic inflammatory response to an initially localised infection or tissue injury, which may lead to severe sepsis and septic shock if left untreated (Daniels, 2009; Robson & Daniels, 2013; Dellinger et al, 2013; Perman, Goyal & Gaieski, 2012; Vanzant & Schmelzer, 2011). Septic shock can be classified by acute circulatory failure as a result of massive vasodilation, increased capillary permeability and decreased vascular resistance in the body, causing refractory hypotension despite adequate fluid resuscitation. This leads to irreversible tissue ischaemia, end organ failure and ultimately, death (McClelland & Moxon, 2014; Sagy, Al-Qaqaa & Kim, 2013, Dellinger et al, 2013).
The inflammatory response is a nonspecific response to cellular injury and bacterial invasion. Inflammation is the primary defense in early gingivitis. Biofilm can initiate an inflammatory response if it is left undisturbed for as little as seventy two hours. Redness and swelling are two of the cardinal signs of inflammation and can be observed clinically in gingivitis. Histamine is released by mast cells and responsible for the redness and swelling of tissues. Histamine causes both an increase in vascularity and permeability of blood vessels at the site of injury. Swelling may occur in response to the accumulation of fluid at a specific site. The inflammatory response includes cellular components of the immune system polymorphonuclear leukocytes and macrophages. Polymorphonuclear leukocytes are crucial to the cellular immune response. Polyporphonuclear leukocytes are the first cells that arrive at an inflammatory site. Polymorphonuclear leukocytes arrive at the site via chemotaxis, and begin to phagocytize bacteria. As the disease continues and the inflammatory reaction is not strong enough to subside the bacterial infection the immune response is further
Tuberculosis is transmitted by inhalation of aerosols containing the tubercle bacilli. The required inoculum size for infection is usually high, but easily occurs with exposure to a patient who is currently infected. The products of dried aerosols, droplet nuclei, are particularly infectious because they remain in the air for an extended time, and upon inhalation easily move to the alveoli. The severe damage related to infection is caused by the reaction of the host. The tuberculosis infection has two phases, primary and secondary.
Immediately after wounding, the first phase of hemostatsis sets in motion with vascular constriction which restricts the blood flow in the blood vessels followed by the platelets plug formation which creates a temporary blockage of blood flow and then coagulation takes place with fibrin clot formation. The clot and surrounding tissue release pro-inflammatory growth factors and cytokines such as transforming growth factor (TGF)-13, platelet-derived growth factor (PDGF), fibroblast growth factor (FGF) and epidermal growth factor (EGF).
The white blood cells destroy any unfamiliar pathogens in the bloodstream and can cause inflammation. Therefore, the inflammation causes a surplus of white blood cells to clot the wound for healing.