ciency then results in a failure of anabolic pro
cesses. Glucose cannot enter the ccils and ac
cumulates in the blood. The resulting hyper-
glycemia causes excess urination (polyuria)
then excess thirst (polydipsia) to compensate
the loss of water, followed by excess hunger
(polyphagia) because the cells are deficient
in fuel. In spite of polyphagia, there is cell
death and loss and so there is weight loss.
When fluid and food intake can no longer
keep up with the losses. dehydration and elec-
trolyte deficiency occurs. Fat breakdown re-
sults in free fatty acids (FFAs) being released
from fat cells. FFAs travel to the liver and
are changed into acetone, acetoacetic acid,
and betahydroxybuteric acid or ketone bod-
ies. The greater the formation of ketone bod-
ies, the greater the occurrence of acidosis.
The end result is ketoacidosis, resulting in
coma and death if untreated (further elucida-
tion to follow).
Treatment in ail persons with TIDM must
be with insulin-for life. Initial treatment
for diabetic ketoacidosis (DKA) is with in-
travenous CV) regular insulin as well as propriate fluids and electrolyte replacement.
Following DKA, there are a variety of insulin
regimen available and therapy should be tai-
lored to the needs of each individual and their
life needs and style.