Diabetes mellitus is a clinical syndrome known since 1500 B.C. Sushruta had also described this condition in 400-500 B.C. It is characterized by hyperglycemia due to relative or absolute deficiency of insulin Lack of Insulin whether absolute or relative affects the metabolism of carbohydrate protein fat water and electrolytes.
HISTORY:-
1500 BC – Diabetes was first discovered in ancient Egypt.
1000 BC – Condition like diabetes was described by Sushruta.
150 AD – A Greek philosopher named it ‘DIABETES’ meaning ‘SIPHON’ also differentiated between Diabetes mellitus and Diabetes incipidus.
1000 – Greek physician used to prescribe exercise preferably on horse back to relieve urination.
1859 – Paul Langarhans described islet cells in pancreas.
1889 – J. Von Mering and O. Minoski discovered that removing pancreas cause diabetes in dogs.
1922 – Insulin was discovered.
1950 – Genetically engineered human insulin was prepared.
1993 – An important study proves that controlling of blood sugar level can minimize the risk of development of various complications of Diabetes.
2000 onwards – Research continues.
INTRODUCTION:-
Diabetes mellitus is a clinical syndrome known since 1500 B.C. Sushruta had also described this condition in 400-500 B.C. It is characterized by hyperglycemia due to relative or absolute deficiency of insulin Lack of Insulin whether absolute or relative affects the metabolism of carbohydrate protein fat water and electrolytes.
Syndrome is known for its complications both acute and chronic. All organs like brain, heart, kidney, eyes, blood vessels and peripheral nerves are affected.
Primary diabetes mellitus is divided into INSULIN DEPENDENT DIABETES MELLITUS (now known as Type 1) & NON INSULIN DEPENDENT DIABETES MELLITUS (now known as Type 2). In IDDM or insulin secreting cells of pancreas largely disappears from pancreas, so that plasma immuno-reactive insulin is either very low or undetectable whereas in NIDDM there is only moderate reduction in total mass of islet cells of pancreas with a measurable, though when related to blood glucose level, reduce concentration of insulin plasma.
EPIDEMIOLOGY-
Diabetes is world wide in distribution and incidence of both types (IDDM & NIDDM) is rising. However the prevalence of both varies considerably in different parts of world, About 50% of cases of NIDDM remain undetected.
* Globally 7th leading cause of death.
* 4th leading cause of death in U.S.
* More than 150 million people are affected globally.
* Prevalence 7% in U.S., 3-4% in Europe and 3-5% in India.
* About 50% cases remain undetected.
CLASSIFICATION
* Primary- (Type 1 and Type 2).
* Gestational-
* Other specific types –
* Due to pancreatic diseases.
* Due to excessive production of hormone antagonistic to insulin.
* Due to medication.
* Association with genetic syndromes.
AETIOLOGY:-
Although the precise etiology is unknown in both main types of diabetes mellitus, however both the pattern of inheritance and environmental factors differ in IDDM & NIDDM.
IDDM:-
GENETICS :- Heredity is supposed to be playing an important role in incidences of IDDM. Inheritance is polygenic. It has been estimated that about 50% of inheritance is contributed by the HLA II genes, which determine immune responsiveness.
ENVIRONMENTAL FACTORS:-
* Viruses – The evidence the vital infections might cause some form of human IDDM is derived from epidemiological studies.
* Diet – There are circumstantial evidence supporting the proposition that diet may at least in certain circumstances influence the development of human IDDM.
Wheat and milk protein have been shown to have the strongest diabetogenic effect and are evidently capable of triggering the string of events which results ultimately in destruction of pancreatic islets, insulin secreting cells.
Recent studies have shown that the introduction of cows milk before the age of 2-3 months is associated with the presence of antibodies to bovine serum albumin and an increased risk of developing IDDM.
IMMUNOLOGICAL FACTORS:- There are enough evidence to support the fact that IDDM is a slow auto immune disease. Detailed family studies have produced evidence that contrary to clinical impression destruction of insulin secreting cells in the pancreas is a slow process occurring over many years. Hyper glycaemia accompanied by the classical symptoms of diabetes occur only when 90% of insulin secreting cells are already destroyed.
NIDDM:-
GENETICS:- Study of mono zygotic twins have shown that genetic factors are more important in the development of NIDDM then IDDM, but there is little information what is inherited.
Due of the most characteristic features of NIDDM is that it is commonly associated with several other disorders like obesity, hypertension and hyper lipidaemia.
ENVIRONMENTAL FACTORS:-
* Life style – Epidemiological studies of NIDDM provide evidence that over eating especially when combined with obesity and under activity is associated with the development of NIDDM.
* Age – Over 70% of diabetes occur after the age of 40. So NIDDM is principally a disease of the middle aged and elderly.
* Pregnancy – Hyper glycaemia occurring first time during pregnancy is known as gestational diabetes. Repeated pregnancies may increase the likelihood of developing permanent diabetes particularly in obese woman. 80% of women gestational diabetes ultimately develop permanent clinical diabetes requiring treatment.
Problem appears to be closely related with-
* Urbanization.
* Westernization.
* Mechanization.
PATHOPHYSIOLOGY:- Whatever the etiology in all cases the hyper glycaemia of diabetes develop because of on absolute (IDDM) or deficiency of insulin which leads to
* Increased catabolism
* Decreased anabolism
CLINICAL FEATURES:
IDDM:- Patients with IDDM usually show physical signs attributable to diabetes. The most striking features are those of salt and water depletion i.e.
– Loose dry skin.
– Furred tongue.
– Cracked lips.
– Tachycardia.
– Hypertension.
– Reduced intra-ocular pressure.
– Breathing may be deep or signing due to acidosis.
– Breath is usually fetid & sickly sweet smell of acetone.
– Mental apathy, confusion, or coma may also be present.
NIDDM:- Physical signs is NIDDM depends on mode of presentation.
Due to infections
a) Pruritus vulvae
b) Balanitis
Due to diabetic retinopathy
a) Dimness of vision.
b) Cataract.
c) Loss of vision.
Due to diabetic neuropathy
a) Loss of tendon reflexes at ankles
b) Impaired perceptions of vibration sensation distally in legs
Signs of atherosclerosis
a) Hypertension
b) Diminished or impalpable pulses in feet.
c) Bruits over carotid or femoral arteries.
d) Gangrene of feet.