January 10th, 2018
Essay on Type 2 diabetes mellitus
Type 2 diabetes mellitus T2DM presents a significant challenge to healthcare delivery due to its high prevalence in many countries and its significant contribution to morbidity and mortality. For instance, T2DM is estimated to account for up to 90% of all cases of diabetes globally, with the people having diabetes being estimated to be 346 million (World Health Organization – WHO, 2011). T2DM is argued to increase the risk of developing various conditions including heart disease, stroke, foot ulcers and blindness, and it is linked to about 3.4 million deaths globally, with such number of deaths estimated to double by 2030 (WHO, 2011).
Although initially referred to as adult onset diabetes, T2DM has subsequently been shown to also affect adolescents and children (Botero & Wolfsdorf, 2005). Accordingly, its designation as an adult-onset condition has been dropped. Similarly, T2DM former designation as non-insulin dependent diabetes mellitus (NIDDM), has subsequently been dropped with observations that T2DM is characterized by progressive impairment of insulin production, requiring exogenous insulin administration in chronic cases (Tibaldi, 2008; Strayer & Schub, 2011). This paper describes T2DM’s characteristics, epidemiology, effects on body systems, and treatment and management.
Characteristics and symptoms of T2DM
T2DM principally results from reduced sensitivity to insulin (insulin resistance) in muscle, liver and adipose tissue, accompanied by reduced secretion of insulin from β-pancreatic cells such that the insulin produced cannot overcome the resistance (Campbell, 2000; van Raalte & Diamant, 2011; Zinman, 2011). Overweight patients with T2DM are likely to have predominant insulin resistance whereas those who are not overweight are likely to have a predominant β-cell dysfunction (Campbell, 2000). In chronic cases of T2DM, insulin secretion is greatly curtailed requiring administration of exogenous insulin or insulin analogues to avert chronic hyperglycemia (Tibaldi, 2008; Campbell, 2000).
All types of diabetes mellitus are principally characterized by a high concentration of glucose in the blood (hyperglycemia), making the assessment of plasma glucose the basis for diabetes diagnosis (WHO and International Diabetes Federation – IDF, 2006). The diagnostic cut-off levels for the condition are determined by epidemiologic studies that highlight the blood glucose levels at which there is an increased prevalence of diabetic complications such as retinopathy (damage to the retina) and nephropathy – kidney damage (WHO & IDF, 2006; Strayer & Schub, 2011; WHO, 2011). Currently, such cut-offs are 126 mg/dl (7.0 mmol/L) for a fasting plasma glucose (FPG) evaluation and 200mg/dl (11.1 mmol/L) for a two-hour postprandial plasma glucose evaluation (American Diabetes Association – ADA, 2000; WHO & IDF, 2006; Strayer & Schub, 2011). The diagnosis is confirmed when such cut-offs are reached or surpassed in evaluations conducted on different days (Strayer & Schub, 2011) Additionally, a diagnosis of T2DM can be made where a casual reading of plasma glucose in symptomatic individuals indicates concentration equal to or higher than 200 mg/dl (Strayer & Schub, 2011).
Although symptoms of T2DM are less marked, they are similar to those of type 1 diabetes. These include polyuria (excessive urine excretion), polydipsia (excessive thirst), weight loss, constant hunger and fatigue (WHO, 2011). However, unlike type 1 diabetes mellitus (T1DM) where such symptoms occur early on condition development, most individuals with T2DM may remain asymptomatic for many years before the condition is diagnosed (Schub & Caple, 2011; WHO, 2011). Accordingly, relying on symptomatic manifestation as a diagnostic criterion for T2DM could lead to a late diagnosis, an aspect that impedes treatment approaches (American Diabetes Association, 2000). Apart from elevated blood glucose levels, T2DM may involve increased (>6.5%) glycosylated hemoglobin (HbA1c) levels and abnormal levels of glucose in urine (Strayer & Schub, 2011). Unlike in T1DM where there are islet cell autoantibodies in the early stages, in T2DM such autoantibodies are not present in early stages of T2DM (Strayer & Schub, 2011). Additionally, whereas in T1DM there are low c-peptide levels, the c-peptides are at normal or elevated levels in T2DM (Strayer & Schub, 2011). Go to part 2 here.