Contoh Percakapan Perawat Dengan Pasien Tentang Diabetes

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  1. Contoh Percakapan Perawat Dengan Pasien Tentang Diabetes 2
  2. Diabetes Mellitus
  3. Introduction Of Diabetes Mellitus

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The cause ofboth type 1 and type 2 diabetes remains unknown, although genetic factors mayplay a role. Diabetes mellitus results from insulin deficiency or resistance.Insulin transports glucose into the cell for use as energy and storage asglycogen. It also stimulates protein synthesis and freefatty acid storage. Insulin deficiency or resistance compromises thebody tissues’ access to essential nutrients for fuel and storage.

The resultinghyperglycemia can damage many of the body’s organs and tissues. Insulin also inhibitsthe breakdown of stored glucose, protein, and fat. Duringfasting periods (between meals and overnight), the pancreascontinuously releases a small amount of insulin (basal insulin);another pancreatic hormone called glucagon (secreted by the alpha cells of theislets of Langerhans) is released when blood glucose levels decrease andstimulate the liver to release stored glucose. The insulin and the glucagontogether maintain a constant level of glucose in the blood by stimulating therelease of glucose from the liver. Initially, the liver produces glucosethrough the breakdown of glycogen (glycogenolysis). After 8 to 12hours without food, the liver forms glucose from the breakdown ofnoncarbohydrate substances, including amino acids (gluconeogenesis).

This form of diabetesis immune-mediated in over 90% of cases and idiopathic in less than 10%. Therate of pancreatic B cell destruction is quite variable, being rapid in someindividuals and slow in others. Type 1 diabetes is usually associated withketosis in its untreated state. It occurs at any age but most commonly arisesin children and young adults with a peak incidence before school ageand again at around puberty. It is a catabolic disorder in which circulatinginsulin is virtually absent, plasma glucagon is elevated, and the pancreatic Bcells fail to respond to all insulinogenic stimuli. Exogenous insulin istherefore required to reverse the catabolic state, prevent ketosis, reduce thehyperglucagonemia, and reduce blood glucose.

Contoh Percakapan Perawat Dengan Pasien Tentang Diabetes 2

Most patientswith type 1 diabetes mellitus have circulating antibodies to isletcells (ICA), insulin (IAA), glutamic acid decarboxylase (GAD65), andtyrosine phosphatases (IA-2 and IA2-) at the time the diagnosis is made. Theseantibodies facilitate screening for an autoimmune cause of diabetes,particularly screening siblings of affected children, as well as adults withatypical features of type 2 Diabetes). Antibody levels decline with increasingduration of disease.

Diabetes Mellitus

Also, low levels of anti-insulin antibodies develop inalmost all patients once they are treated with insulin. The two main problemsrelated to insulin in type 2 diabetes are insulin resistance and impairedinsulin secretion. Insulin resistance refers to a decreased tissue sensitivityto insulin. Normally, insulin binds to special receptors on cell surfaces andinitiates a series of reactions involved in glucose metabolism. In type 2diabetes, these intracellular reactions are diminished, thus rendering insulinless effective at stimulating glucose uptake by the tissues and at regulatingglucose release by the liver. Clinical manifestationsof all types of diabetes include the “three Ps”: polyuria, polydipsia, andpolyphagia.

Introduction Of Diabetes Mellitus

Polyuria (increased urination) and polydipsia (increased thirst)occur as a result of the excess loss of fluid associated with osmotic diuresis.The patient also experiences polyphagia (increased appetite) resulting from thecatabolic state induced by insulin deficiency and the breakdown of proteins andfats. Other symptoms include fatigue and weakness, sudden vision changes,tingling or numbness in hands or feet, dry skin, skin lesions or wounds thatare slow to heal, and recurrent infections. The onset of type 1 Diabetes mayalso be associated with sudden weight loss or nausea, vomiting, or abdominalpains, if DKA has developed.

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