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NARRATIVE PATHOPHYSIOLOGY: Cellulitis is a skin infection that extends into the deeper dermis and subcutaneous tissues and

causes deep, red erythema without sharp borders that spread widely through tissue spaces. The skin is erythematous, edematous, tender and sometimes nodular. The usual cause of infection includes Group A beta-hemolytic streptococci, staphylococcus aureus, haemaphilus influenzae type B. If cellulitis is untreated, gangrene, metastatic abscesses, and sepsis result, also associated with necrotizing fasciitis which is a more complicated type of skin infection, easily spreading across the fascial plane within the subcutaneous tissue. The patients precipitating factors include presence of skin cut/wound. The patients predisposing factors include diabetes mellitus type II. It started with the cut at the right foot of the patient which causes skin impairment. This open wound, with the influence of the patients condition Diabetes Mellitus Type II results to delayed wound healing. Due to insulin resistance, hyperglycemia occurs which results to increased blood viscosity. It leads to two different reactions; one is the decreased blood flow, resulting to decreased tissue perfusion and the other is that it results to an environment conducive to bacterial growth thereby causing infection. The open cut of the skin permitting entry of pathogens triggers a natural body response of activation of defensive cells; neutrophils, eusinophils, mast cells, etc. which in turn breaks down cellular components, resulting to inflammation causing cellulitis.

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The cellulitis and necrotizing fascilitis results to the same cascade of events which affects the patients medical condition. One reaction is that the increased leukocytes, macrophages, and tumor necrosis factor production, results to the release of the pyrogen, which in turn results to fever. Another reaction is that the increased capillary permeability permits the movement of plasma protein into tissues, increasing tissue oncotic pressure, resulting to edema. Then, the increased production of phagocytes results to the enlargement of the nearest lymph nodes to the affected body part, which is, in the case of the patient is inguinal lymphadenopathy. Due to the cell swelling during inflammation, the chromatin, which consists of DNA and proteins in a nucleus, is being digested resulting to disruption of the plasma membrane and organelle membranes. These further progresse to extensive DNA hydrolysis, then organelle breakdown, and finally, necrosis. The patient had signs and symptoms of asymmetrical wound area,

lymhadenopathy, edema, fever, acute swelling of affected extremity, visible reddish and with puss secretions wound site and wound that heals slowly. Her diagnostic examinations include increased Glycosylated Hemoglobin, CBC with increased WBC, neutrophil, hematocrit and wound culture testing. The patient then underwent treatment. The pharmacologic management includes treatment with Fluoroquinolones, Penicillin, Tetanus Toxiod, and Antibiotics. The medical management was wound debridement, wound incision and drainage, immobilization of the affected foot, and bed rest as rendered by the doctor. The nursing management includes the elevation of the affected extremity, wound care/ prevention of infection and provision of comfort for the patient, along with the other nursing
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responsibilities with the patient. The above mentioned management rendered resulted to good prognosis, leading to the discharge of the patient, with proper wound care and infection control measures instructed to her. It left untreated, it could have continued to necrotize as in chronic necrotizing fascitis, resulting to severe gangrene formation from death of tissue due to lack of blood perfusion and no sooner, the patient will have to undergo amputation, in order for the infection not to affect the other tissues of the body, the condition of the patient cloud have also gotten worse to the extent of having septicemia or infection of the blood, resulting to shock, leading to the death of the patient. In Diabetes Mellitus type II on the other hand, there is insulin resistance resulting to hyperglycemia. The precipitating factors present with the patient include high blood pressure, sedentary lifestyle, and her diet. Predisposing factors include her age, race, genetic predisposition, and history of gestational diabetes. A cascade of events follows this rise of blood glucose level. The One is that it decreases blood osmolality making the fluid shift from intracellular to extracellular resulting to cellular dehydration. In response of the body, the posterior surface of the hypothalamus signal this cellular dehydration to other parts of the brain, and thirst is experienced, we call it polydipsia. Another event that happens is when blood sugar exceeds renal threshold, glycosuria occurs resulting to osmotic dieresis wherein water is reabsorbed from the renal tubules causing increased urine output or polyuria. Because glucose cannot enter the cell, there is presence of cellular starvation increasing our sensation of hunger or polyphagia. Gluconeogenesis, a metabolic pathway that results in the generation of glucose from non-carbohydrate carbon substrates, is also activated in response to hyperglycemia.
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This leads to two different pathways, one is lipolysis wherein there is breakdown of lipids and involves the hydrolysis of triglycerides into free fatty acids and ketones. Ketone bodies are acidic in nature, and prolonged excess of ketone bodies can overwhelm normal compensatory mechanisms, leading to acidosis if blood pH falls below 7.35. As the body produces excess ketones, it is excreted together with the urine, a condition called ketonuria. The other by product, fatty acids, once accumulated, thickens the arterial walls leading to atherosclerosis. If not treated, it will result to diseases including cardiovascular accident/ stroke, myocardial infarction/heart attack and peripheral vascular disease/ peripheral arterial disease (a condition of the blood vessels that leads to narrowing and hardening of the arteries that supply the legs and feet), which eventually causes death. Other complications include neuropathy (loss of sensation, tingling/numbness, weakness), retinopathy (blindness) and nephropathy (end stage renal disease). The other pathway involves protein breakdown resulting to muscle wasting and poor wound healing. The metabolism of protein produces nitrogenous waste products ammonia, urea and uric acid, which are toxic to the brain characterized by variable consciousness, including lethargy, stupor, and coma; a tremor of the hands; personality change; memory loss; hyperreflexia; and hyperventilation. If these conditions be treated through pharmacological, medical and nursing management, it will lead to good prognosis, and the patient is discharged from hospital. Nevertheless, the patient continuous to monitor her blood glucose level, observe proper diet and regular exercises, combined with the treatment regimen (insulin and other maintenance drugs).
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