Diabetes is a metabolism disorder that affects insulin production, impaired insulin sensitivity, or both. The two most common kinds of diabetes are type 1 and type 2.

Normal insulin metabolism

Insulin is a endogeneous hormone produced by the beta cells in the pancreas. It regulates cellular uptake of glucose into fat, skeletal muscle and liver cells. Normally, insulin is continually released from the pancreas in small amounts, this is known as a basal rate. Increased release of insulin (bolus) from beta cells occurs in response to an increase in blood glucose levels after food is ingested. The ideal blood glucose levels are between 4-8mmom/L.

 

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Glucagon

Insulin is not the only hormone that is utilized in the regulation of blood glucose. Glucagon, produced from the alpha cells in the pancreas, counteracts the effects of glucose and is referred to a counter-regulator hormone. When blood glucose levels fall too low, glucagon is released from the pancreas and converts glycogen (stored glucose) in the liver and skeletal muscle cells back into glucose that is released into the blood stream. Insulin and glucose are the two main hormones involved in the feedback systems that maintains glucose homeostasis.

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Regulation of blood glucose

Insulin is known as an anabolic or storage hormone. Insulin an other regulatory hormones provide a sustained release of glucose into the bloodstream during periods of fasting or consuming food.

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An abnormal production of either of these hormones or impaired impaired insulin sensitivity can lead to the development of diabetes.

 

Type 1 diabetes

Type 1 diabetes is a chronic disease that usually develops before the age of 18. Type 1 diabetes accounts for 10-20% of all diabetes. Individuals with type 1 diabetes were commonly referred to as insulin dependent diabetics.

Type 1 diabetes develops as a result of an autoimmune process which progressively destroys pancreatic beta cells. The autoantibodies that are responsible for the destruction of islet cells are can be present for years before the condition is identified. Beta cell function decreases by 80-90% before symptoms of hyperglycaemia occurs. Once the pancreas is unable to produce insulin, individuals will have a rapid onset of symptoms.

Symptoms

  • weight loss
  • polyphagia (excessive hunger)
  • polydipsia (excessive thirst)
  • polyuria (frequent urination)
  • fatigue

 

Treatment requires the administration of exogenous insulin injections to regulate blood glucose levels to prevent the development of life threatening diabetic ketoacidosis.

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Type II diabetes

Type II diabetes is the most prevalent type of diabetes. It accounts for 80-90% of diagnosed diabetes. Type II diabetes is mainly a lifestyle disorder which can be attributed to obesity, sedentary lifestyle and unhealthy food intake. The majority of those diagnosed with type II diabetes are overweight.In New Zealand, diabetes is more prevalent among Maori. Maori are three times more likely to have diabetes than non-Maori.

 

Pathophysiology

In type II diabetes the pancreas can continue to produce insulin, although it is often insufficient for the bodies needs or cells are unable to utilize it effectively. There are three major abnormalities that have been identified in the development of type II diabetes: insulin resistance, impaired insulin production, and impaired glucose production.

Insulin resistance

This is where body tissues are unresponsive to the action of insulin. The insulin receptors located on skeletal muscle, fat, and liver cells are either insufficient in number or unresponsive to insulin. Without cells responding to insulin, glucose is unable to enter the cells, resulting in hyperglycaemia.

Impaired insulin production

Due to the cellular resistance to insulin, the beta cells in the liver produce higher amounts of insulin. This overproduction of insulin causes the cells to fatigue. This decreases the ability of the pancreas to continue producing adequate amounts of  insulin. The decrease in insulin coupled with decreased cellular sensitivity results in hyperglycaemia as glucose is unable to be removed from the blood stream and enter the cells.

Inappropriate glucose production

The glycogen stored in the liver undergoes inappropriate glycogenolysis (breakdown of glycogen to glucose). Dysfunction of this regulation system results in the liver regulating glucose levels that do not correspond with the bodies requirements. This often correlates to an increasing fasting blood glucose level.

 

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Symptoms 

  • recurrent infections
  • fatigue
  • prolonged wound healing
  • polyuria, polydipsia, polyphagia

 

Gestational diabetes

This type of diabetes develops during pregnancy. A pregnant woman needs two to three times the normal amount of insulin due to the growth demands of the developing foetus Additionally, during pregnancy the placenta releases hormones which can interfere with the function of insulin. This type of diabetes is usually temporary and resolves within 6 weeks postpartum. Despite this, a woman whom has had gestational diabetes is 50-60% more likely to go onto develop type II diabetes later in life. Gestational diabetes can cause complications during the pregnancy for both the mother and foetus.

Complications:

  • increased risk of UTI
  • increased risk for needing a caesarean sectio
  • high birth weight
  • prolonged new born jaundice
  • infant respiratory distress syndrome

 

 

References

Diabetes New Zealand. (2016). Gestational diabetes. Retrieved from http://www.diabetes.org.nz/about_diabetes/gestational_diabetes

Hoy, A., & Walding, M. (2015). Obesity and diabetes mellitus. In J. Craft & C. Gordon (Eds.), Understanding pathophysiology (2nd ed., pp. 1028–1060). Sydney, Australia: Mosby Elsevier.

Robbins, N., Shaw, C., Lewis, S., & Whitbread, C. (2008). Nursing management: Diabetes mellitus. In D. Brown & H. Edwards (Eds.), Lewis’s medical-surgical nursing: Assessment and management of clinical problems (2nd ed., pp. 1348–1382). Sydney, Australia: Mosby Elsevier.

 

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