Purba Java: Pathophysiology

<table cellpadding="0" cellspacing="0" class="tr-caption-container" style="float: left;"><tbody><tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEi_xdjo6qkzdAWhjftkOfM_X9EBlzlWvK6MLy-XuzgRE1lPk6Wa-cQSeOlTZUA4qog6l6a7EOLtu0I8YhtVjF-8kmQfiBlUEJQ1o3eJuW6j-rjUAyiZS32sOTZmi-GtwL-j3wY0A2lqBp-o/s1280/Pathophysiology+of+Malaria.jpg" imageanchor="1" style="clear: left; margin-bottom: 1em; margin-left: auto; margin-right: auto;"><img alt="Pathophysiology of Malaria" border="0" data-original-height="720" data-original-width="1280" height="180" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEi_xdjo6qkzdAWhjftkOfM_X9EBlzlWvK6MLy-XuzgRE1lPk6Wa-cQSeOlTZUA4qog6l6a7EOLtu0I8YhtVjF-8kmQfiBlUEJQ1o3eJuW6j-rjUAyiZS32sOTZmi-GtwL-j3wY0A2lqBp-o/w320-h180/Pathophysiology+of+Malaria.jpg" title="Pathophysiology of Malaria" width="320" /></a></td></tr><tr><td class="tr-caption" style="text-align: center;">Malaria</td></tr></tbody></table>Plasmodium parasites that reproduce by separating the body can multiply in the human liver system very quickly into thousands in just a few minutes after this parasite is injected by a feeding female Anopheles mosquito.There are two stages of development of malaria, namely the exoerthrocitic stage and the erythrocitic stage. The exoeryhrocitic stage is the stage where infection occurs in the human liver system caused by the plasmodium parasite, while the erythrocitic stage is the stage of infection in red blood cells (erythrocytes).After entering through the blood and reaching the human liver system, this parasite will multiply rapidly which then exits and infects red blood cells, which is the process that causes fever in malaria sufferers. Furthermore, the plasmodium parasite will continue to multiply in red blood cells which then come out to infect other red blood cells that are still healthy, this is what causes symptoms of fever or fluctuating fever in malaria sufferers.Although the human spleen system can actually destroy red blood cells infected by parasites, the Plasmodium falciparum parasite can make red blood cells stick to small blood vessels by releasing adhesive proteins, so that infected red blood cells cannot enter the spleen system to be destroyed. With this ability, Plasmodium falciparum often becomes an acute malaria disease, due to the ability to attach infected red blood cells to the walls of small blood vessels simultaneously so that it can block blood circulation to the brain which often results in a coma in malaria sufferers.In contrast, some plasmodium vivax or ovale parasites do not have a lethal tendency like Plasmdium falciparum, but have the ability to produce hypnosoites that remain active for months or even years. So that people with malaria caused by Plasmodium often experience new malaria relapses and relapses for several months or even years after being infected for the first time and is very difficult to eradicate completely from the infected human body.The pathophysiology of malaria is not known with certainty. The pathophysiology of malaria is multifactorial and may be related to the following:1. Erythrocyte destruction.The destruction of erythrocytes is not only by rupture of erythrocytes containing parasites, but also by phagocytosis of erythrocytes containing parasites and those that do not contain parasites, causing anemia and tissue anoxia. With severe intravascular hemolysis, hemoglobinuria (blackwater fever) may occur and may result in renal failure.2. Endotoxin-macrophage mediators.During schizogony, erythrocytes containing parasites trigger endotoxin-sensitive macrophages to release various mediators that play a role in changes in the pathophysiology of malaria. Endotoxin is not present in the malaria parasite, probably from the gastrointestinal tract. The malaria parasite itself can release tumor necrosis factor (TNF). TNF is a monokine, found in the blood of animals and humans infected with the malaria parasite. TNF and other related cytokines cause fever, hypoglycemia and adult respiratory distress syndrome (ARDS) with sequestration of neutrophil cells in the pulmonary vasculature. TNF can also destroy Plasmodium falciparum in vitro and can increase the attachment of parasitized erythrocytes to the capillary endothelium. Serum TNF concentrations in children with acute falciparum malaria are directly related to mortality, hypoglycemia, hyperparasitemia and disease severity.3. Sequestration of infected erythrocytes.Erythrocytes infected with Plasmodium falciparum at an advanced stage can form knobs on their surface. These protrusions contain malaria antigens and react with malaria antibodies and are related to the affinity of erythrocytes containing Plasmodium falciparum to the endothelium of blood capillaries in the internal organs, so that schizogony takes place in the internal circulation, not in the peripheral circulation. Infected erythrocytes adhere to the endothelium of the blood capillaries and form a clot (sludge) that blocks the capillaries in the internal organs.Proteins and fluids seep through the leaky capillary membrane (become permeable) and cause tissue anoxia and edema. Sufficiently widespread tissue anoxia can cause death. Histidine-rich protein P. falciparum was found in the protrusions, there were at least four kinds of protein for the cytoplasm of erythrocytes infected with Plasmodium P. falciparum. <a class="titlex" href="https://purba-java-indo.blogspot.com/2014/11/malaria-5-nursing-diagnosis.html" style="color: #0e0e0e; display: inline !important; font-family: "Open Sans", serif, sans-serif; font-size: 18px; font-stretch: normal; font-variant-east-asian: normal; font-variant-numeric: normal; font-weight: bold; line-height: 1.4em; margin: 0px; max-height: 200px; overflow: visible; text-decoration-line: none;">Malaria - 5 Nursing Diagnosis</a><a class="titlex" href="https://purba-java-indo.blogspot.com/2017/01/12-type-of-mosquito-that-may-be-around.html" style="background-color: white; color: #0e0e0e; display: inline !important; font-family: "Open Sans", serif, sans-serif; font-size: 18px; font-stretch: normal; font-variant-east-asian: normal; font-variant-numeric: normal; font-weight: bold; line-height: 1.4em; margin: 0px; max-height: 200px; overflow: visible; text-decoration-line: none;">12 Types of Mosquito That May be Around You</a><div><a class="titlex" href="https://purba-java-indo.blogspot.com/2021/09/pathophysiology-of-urticaria.html" style="color: #0e0e0e; display: inline !important; font-family: "Open Sans", serif, sans-serif; font-size: 18px; font-stretch: normal; font-variant-east-asian: normal; font-variant-numeric: normal; line-height: 1.4em; margin: 0px; max-height: 200px; overflow: visible; text-decoration-line: none;">Pathophysiology of Urticaria</a></div>

Pathophysiology of Malaria

Malaria Plasmodium parasites that reproduce by separating the body can multiply in the human liver system very quickly into thousands in jus...

<table cellpadding="0" cellspacing="0" class="tr-caption-container" style="float: left;"><tbody><tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgQPnmw2AXLdhABw8iOIeFO-XpON3AW8Ahw1waLmCj6EFu2Oa5RH6gdlf_BWWGc5SI3dcpFiDnlzkqDEFjZ28aNlkWlNrg8U0Gn4evDpIKpg6sqe_LZISX0do43J_4k2nQZrYz7dYPxlVY8/s800/Pathophysiology+of+Urticaria.jpg" imageanchor="1" style="clear: left; margin-bottom: 1em; margin-left: auto; margin-right: auto;"><img alt="Pathophysiology of Urticaria" border="0" data-original-height="543" data-original-width="800" height="217" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEgQPnmw2AXLdhABw8iOIeFO-XpON3AW8Ahw1waLmCj6EFu2Oa5RH6gdlf_BWWGc5SI3dcpFiDnlzkqDEFjZ28aNlkWlNrg8U0Gn4evDpIKpg6sqe_LZISX0do43J_4k2nQZrYz7dYPxlVY8/w320-h217/Pathophysiology+of+Urticaria.jpg" title="Pathophysiology of Urticaria" width="320" /></a></td></tr><tr><td class="tr-caption" style="text-align: center;">Urticaria</td></tr></tbody></table>Urticaria is common and results from mast cell degranulation (type 1 immunologic reaction) in response to antigens, with the release of histamine and other vasoactive mediators, leading to erythema and edema. Of these patients, 70% had idiopathic urticaria (where the antigen is unknown), the remainder had other forms of urticaria. Urticaria, if severe, can also affect the subcutaneous tissue and cause angioedema (swelling of the hands, lips, around the eyes, and although rare, it is important to pay attention to the tongue or larynx). (Davey, 2005)The process of acute urticaria begins with the binding of antigens to interconnected IgE receptors and then attachment to mast cells or basophils. Furthermore, activation of mast cells and basophils will mediate the release of various inflammatory mediators. Mast cells produce histamine, tryptase, chyme, and cytokines. These substances increase the degranulation ability of mast cells and stimulate increased ELAM and VCAM activity, which triggers migration of lymphocytes and granulocytes to the site of urticarial lesions (Anonymous, 2007).This event triggers an increase in vascular permeability and causes localized edema known as wheal. The patient feels itching and swelling in the dermal layer of the skin. Acute urticaria can occur systemically if the allergen is absorbed deeper into the skin and reaches the circulation. This condition occurs in contact urticaria, for example urticaria that occurs due to wearing latex gloves, where the latex is absorbed by the skin and enters the bloodstream, causing systemic urticaria.Acute urticaria can also occur on stimulation of mast cells in the absence of IgE binding to allergens. For example, on exposure to radiocontrast media, where during the radiological process, there will be a change in osmolality in the environment which causes mast cells to degranulate (Anonymous, 2007).Immunological and non-immunologic factors are able to stimulate mast cells or basophils to release these mediators. In the non-immunologic, cyclic AMP (adenosine mono phosphate) may play an important role in mediator release. Several chemicals such as amines and amide derivatives, drugs such as morphine, codeine, polymyxin, and some antibiotics play a role in this condition.Cholinergic substances such as acetylcholine, released by cutaneous cholinergic nerves whose mechanism is not yet known, can directly influence mast cells to release mediators. Physical factors such as heat, cold, blunt trauma, X-rays, and massage can directly stimulate mast cells. Some conditions such as fever, heat, emotion, and alcohol can stimulate the capillaries directly, resulting in vasodilation and increased permeability (Djuanda, 2008).Immunological factors play a more important role in acute urticaria than chronic, usually IgE binds to the surface of mast cells and/or basophil cells due to the presence of Fc receptors. This situation is clearly seen in type I reactions (anaphylaxis), such as drug and food allergies.Complement also plays a role, classically or alternatively activation of complement causes the release of anaphylatoxins (C3a, C5a) which can stimulate mast cells and basophils, for example seen as a result of venom or bacterial toxins. Complement binding also occurs in urticaria due to cytotoxic reactions and immune complexes in this condition are also released anaphylatoxins. Urticaria due to contact occurs using insect ingredients, cosmetic ingredients, and cephalosporins. <a href="https://purba-java-indo.blogspot.com/2014/11/pathophysiology-of-tinnitus.html" itemprop="url" style="background-color: white; color: #141414; display: inline !important; font-family: "Open Sans", serif, sans-serif; font-size: 18.6px; font-weight: 600; text-decoration-line: none;">Pathophysiology of Tinnitus</a>

Pathophysiology of Urticaria

Urticaria Urticaria is common and results from mast cell degranulation (type 1 immunologic reaction) in response to antigens, with the relea...