The author of this essay will be discussing a patient with type 2 Diabetes Mellitus and will also be discussing the nursing care that will be received by the patient following a hypoglycaemic attack.
The patient being described is a fictitious seventy year old lady called Mabel Gordon; she lives in a flat in a city centre with her husband Bert. Mabel has had type 2 diabetes for years which has been poorly controlled by medication and diet. Mabel’s diabetes has now progressively worsened; she has been commenced on a self-managed insulin therapy plan. She is cared for by the community nursing team and her GP; she attends the regular diabetic clinic. Mabel has no other medical conditions but is currently suffering a cold. On a trip to the chemists Mabel feels unwell, clammy, trembling and confused; the chemist calls Bert and the district nurse. On her arrival the district nurse treats Mabel for a hypoglycaemic attack, to which Mabel responds, but is concerned about Mabel’s high temperature, she arranges for Mabel to be admitted to hospital. Aetiology and Pathophysiology
Diabetes Mellitus has two principle classes, type 1 and type 2; approximately 90% of people with diabetes suffer from type 2, (Burden, 2003a). Type 1 diabetes is characterised by the destruction of the Beta cells. The Islets of Langerhans within the pancreas contain two types of cells, Alpha cells and Beta cells. Alpha cells secrete glucagons and Beta cells secrete insulin hormone. Patients with type 1 diabetes do not have this insulin production often due to the destruction of the Beta cells. Type 1 diabetes is therefore treated with insulin, (insulin was discovered in 1922 by Banting and Best). Type 1 diabetes is a catabolic disorder characterised by a lack of insulin, raised blood glucose levels and a breakdown of body fats and proteins. The lack of insulin in the body of type 1 patients means they are prone to the development of Ketoacidosis, (Porth, 2002).
Type 2 diabetes usually develops when the body no longer produces adequate insulin or when the body resists insulin action. This resistance to insulin stimulates further insulin secretion from the Beta cells to overcome the demand to maintain a normoglycemic state. Over time the response from the Beta cells declines due to exhaustion. Type 2 usually occurs in the over 40’s and is initially diet and exercise controlled, however, due to the decline in insulin production the patient may eventually need insulin therapy. The insulin resistance has been attributed to increased intra-abdominal fat; approximately 80% of type 2 sufferers are overweight. Obese people have an increased resistance to insulin action and an impaired suppression of glucose production, (Porth, 2002).
The signs and symptoms of diabetes appear more rapidly in type 1; type 2 may go undiagnosed for some time due to the slow onset, (Diabetes UK, 2000).
The most common signs and symptoms of diabetes are; glucosuria, polydipsia (excessive thirst), polyuria (passing excessive urine), infections, weight loss, muscle cramps, lethargy, visual disturbances and ketoacidosis may be present, (Burden, 2003a). Hypoglycaemic attack’s such as Mabel’s can occur in type 1 or 2 diabetes. Hypoglycaemia occurs when the blood glucose level falls below 3.5mmol/L however symptoms rarely appear until this level drops below 3mmol/L, the three main causes of hypoglycaemia are; excessive insulin, insufficient food and unusual exercise. Symptoms develop rapidly, usually taking 5-15 minutes, (Alexander, Fawcett and Runciman, 2002). Some of the signs and symptoms are sweating, confusion, headache, nausea, rapid pulse and trembling. These are described as being neuroglycopenic, characterised by an impaired cognitive function, unusual or aggressive behaviour, or they can be adrenergic involving the sympathetic and parasympathetic systems, (Burden, 2003b).
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