Diabetes Introduction:
Diabetes (also called "diabetes mellitus"
or DM for short ) is a common medical problem. It occurs
when there is a deficit of insulin in the supply and demand system created by
the interplay of blood sugar and insulin or when there is overproduction of insulin,
but a lack of insulin receptors. Either way not enough sugar gets into the cells,
which is at the center of the pathophysiology of DM. Blood sugar (medical term:
glucose) can come from food or from broken down glycogen (the storage form of
glucose). Glycogen can be broken down in the liver or the muscles and the resulting
increased blood glucose value is called "hyperglycemia". This
doctor language term simply means "too much sugar in the blood". The
function of the pancreas is threefold: Most of the pancreatic cells are producing
digestive enzymes, which are collected through a duct system and then sent via
the pancreatic duct into bowel called the duodenum. The second and third function
is through the endocrine gland of the pancreas, which consists of a multitude
of cell clumps distributed throughout the pancreas called the Langerhans islets.
In these islands of hormone producing cells two hormones are produced, called
glucagon and insulin. They are balancing each others in action: glucagon increases
glucose by releasing glucose from the glycogen of the liver. Glucagon is produced
by the alpha cells of the Langerhans islets. The beta cells of the Langerhans
islets produce insulin, which lowers blood sugar and in some clinical conditions,
where too much of it is around, hypoglycemia would result. This term simply means
"too little sugar in the blood". Hypoglycemia is a very dramatic condition
as the person passes out, often in a coma. There can be life threatening
seizures with very low blood sugars. The effect of a hypoglycemic attack is fast
and the patient recovers fairly quickly from it, if he/she gets glucose by intravenous
injection. On the other hand the hyperglycemia associated with diabetes can be
hidden for many months and years and often only, when there is a diabetic coma
developing, is this suddenly brought to the attention of the medical profession.
By that time there can already be severe irreversible damage in the body. It can
take months and often it is too late to change the outlook for the person severely
affected with diabetes. Below I will emphasize how vitally important it is to
intervene at the earliest possible stage through preventative steps and early
effective therapy. Type 1 diabetes is associated with some autoimmune diseases
such as Hashimoto's thyroiditis, idiopathic Addison's disease and Graves' disease.
In type 1 diabetes mellitus the pancreas is running out of insulin. In type 2
diabetes mellitus there is too much insulin circulating in the blood("hyperinsulinism"),
but because of ineffective or deficient receptors the blood sugar, which is elevated,
will not enter into the cells. The same mechanism of hyperinsulinemia is present
in the diabetes of pregnancy (gestational diabetes). Pathophysiology
and classification: There are three main categories of DM as follows,
type 1diabetes, type 2 diabetes and gestational diabetes. The 4th category is
diabetes insipidus, which is due to an entirely different cause. See links
to more details through the above table. A simpler
review of diabetes with emphasis
on the effect diabetes has on your life.
Diabetes
insipidus (or "DI")
Introduction: This
disease was termed "diabetes" long before all of the hormones that play
a role were known. Like with diabetes mellitus the clinical presentation consists
of a lot of fluid intake and urination, but there are different reasons for his.
There are two types of diabetes insipidus (DI), central DI and nephrogenic DI.
The central DI can be due to a host of causes
such as a basal skull fracture, tumors or inborn or acquired abnormalities that
cause a disruption of vasopressin (= anti-diuretic hormone) production in the
hypothalamus, a central part of the brain. The nerve cells that produce vasopressin
in the hypothalamus have long tentacles that reach into the back part of the pituitary
gland (posterior lobe). There the vasopressin is stored until the body needs it.
When the blood gets too thick from water that was lost through the kidney, the
osmolality (a measure of soluble substances) in the blood goes above a critical
value, which triggers release of vasopressin into the blood stream. This in turn
will be registered in specialized kidney cells near the filtering mechanism where
special receptors will now signal that water needs to be reabsorbed at a faster
rate. Normally this is a very efficient mechanism, which regulates itself automatically.
However, with central DI there is no vasopressin that arrives at the level of
the kidney. With nephrogenic DI there are too
few or no receptors in the kidney that could respond to the normally produced
vasopressin. Both of these conditions lead to polydipsia (too
much drinking of fluids) and polyuria (too much urinating). However,
as we will see later central DI will respond to vasopressin by normalizing polydipsia
and polyuria, whereas with nephrogenic DI vasopressin will not change these symptoms.
There is one other condition, called compulsive water drinking
(or psychogenic water drinking), where the person has emotional
problems and keeps on drinking large quantities of water. A water deprivation
test can be utilized to distinguish this from the other conditions. Here is more
information on central and nephrogenic DI.
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