Pathophysiology of Diabetes Mellitus

In Gestational Diabetes Mellitus just like the other types of Diabetes mellitus (type 1 and
2) the pancreas cannot produce adequate insulin to compensate or regulate body glucose level.
Because of insulin is low or insufficient the glucose cannot be used by the body. And glucose
provides energy for our daily activities, so with the absence of glucose as a source of energy, the
cells register the need for glucose, and the liver quickly converts stored glycogen to glucose
(Dolk,2012). But then again the inadequate amount of insulin in the regulation of glucose to
produce energy makes the conversion of glycogen into glucose an attributing factor to the
increase level of glucose in the blood which causes now hyperglycemia.
When the level of blood glucose reaches 150mg/100ml (normal level is 80 to 120mg/dl),
the kidney begin to excrete amount or quantities of glucose in the urine causing now glycosuria
or presence of glucose in the urine in attempt to lower the level. This causes large quantities of
fluid to be excreted with urine or what we called polyuria. The effect of this excessive urination
is dehydration wherein the blood serum becomes concentrated and the total volume of the blood
decreases. Decrease blood volume causes reduces blood flow causing now ineffective tissue
perfusion or cells do not received adequate oxygen forcing now the use of anaerobic metabolic
reaction but it contribute to the production of lactic acid. So to replace needed glucose, fat is
mobilized from fat stores to metabolize energy but the end product is acidic ketone bodies into
the bloodstream. As the process goes on, protein stores are tapped in a final attempt to find a
source of energy. Utilizing protein for energy this way reduces the supply of protein to the body
cells. As cells dies, they release K+ and Na-, which is loss from the body in the extensive
polyuria. These factors combined create an immediate severe metabolic acidosis. Long term
effects are vascular narrowing that leads to kidney, heart, and retinal dysfunction.

Pathophysiology of Gestational Diabetes Mellitus

Gestational Diabetes Mellitus is a condition where the bodys cells fail to respond to the
hormone insulin in the usual way. Several pregnancy hormones are thought to disrupt the usual
action of insulin as it binds to its receptor, most probably by interfering with cell signaling
pathways. And this is called insulin resistance.
Insulin is the primary hormone produced in the beta cells of the islets of Langerhans in
the pancreas. Insulin is key in the regulation of the bodys blood glucose level. Insulin stimulates
cells in the skeletal muscle and fat tissue to absorb glucose from the bloodstream. In the presence
of insulin resistance, this uptake of blood glucose is prevented and the blood sugar level remains
high. The body then compensates by producing more insulin to overcome the resistance and in
gestational diabetes, the insulin production can be up to 1.5 or 2 times that seen in a normal
pregnancy (A. Mandal, 2014).
The glucose present in the blood crosses the placenta via the GLUT1 carrier to reach the
fetus. If gestational diabetes is left untreated, the fetus is exposed to an excess of glucose, which
leads to an increase in the amount of insulin produced by the fetus. As insulin stimulates growth,
this means the baby then develops a larger body than is normal for their gestational age. Once the
baby is born, the exposure to excess glucose is removed. However, the newborn still has
increased insulin production, meaning they are susceptible to low blood glucose levels (S.
Robertson, 2014).