PATHOPHYSIOLOGY Narrative Form The pathophysiology of Dengue Fever begins at the act of the disease vectorAedes aegypti or Aedes albopticus, biting the human victim. Through this, Dengue virus carried by the vector enters the bloodstream and attaches to the specific antibody thereby forming an antigen-antibody complex. The antigen-presenting cells then act to phagocytise this complex and the viral antigens relay a presentation on the APC’s cell membrane. From this moment on, the immune system detects the antigen and mounts an immune response. Cytokines are released into the system and the inflammatory response is activated. This leads to a series of interconnected events that manifest the signs and symptoms seen in a dengue fever client. Take note that the target cells of the DV includes the platelets. At the onset of the inflammatory response, there is a notable increase in coagulation due to platelet activation. This leads to disseminated intravascular coagulation and consequently platelet aggregation. The over activity of platelet during this time in the infection leads to thrombocytopenia that is decreased platelet in the blood. Coagulation functions are then impeded causing the bleeding tendencies. Hypotension may resolve from this, which may further lead to shock and finally, death if not intervened properly. The remarkable chemotaxis in the inflammatory response triggers the release and systemic circulation of pyrogens by the neutrophils, paving the way for fever. Along side with the increased body temperature is the body’s mechanism to promote rest by inducing myalgia and althralgia (muscle and joint pain). Persistent hyperthermia may lead to dehydration due to insensible fluid loss which eventually leads to hypotension. The increase in vascular permeability results in a lot of complications. One of which is the plasma leakage, giving way to hypoproteinemia (decreased plasma proteins in the blood to the extent that even larger protein molecules

escape the blood vessel) and hemoconcentration caused by the diffusion of serum into the extravascular space. This impairment causes fluid from blood vessels to escape. body tissues are barred from proper oxygenation resulting to hypoxia. leading to pleural effusion diagnosed as pneumonia. Also. Chloride attracts water and thus diarrhea occurs. Dehydration consequently leads to hypotension. As a reaction to the inflammation. this leads to increased levels of cytokines in the intestinal tract which leads to intestinal inflammation. Increased vascular permeability also leads to increased gastric juices in the stomach which is manifested as epigastric pain. If this condition is prolonged. The increase in extravascular fluids leads to generalized fluid retention or edema as manifested by swelling or tumor. Following excessive fluid retention. . Moreover. capillaries found in the lungs are overly constricted proceeding hindrance to normal gas exchange. This can be confirmed by performing a tourniquet test. Another complication of vascular permeability is the rupture of the minute blood vessels leading to physical manifestations of rashes (petechiae). Diarrhea often leads to dehydration due to the fluids that are lost in the body. it can worsen to lung failure. with increased vascular permeability. the intestinal epithelial cells would then secrete chloride.

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