HISTORY OF DIABETES
Diabetes is one of the oldest of disease known. It was described in ancient Indian writings and in words of Charaka and Susruta as ‘sweet urine’, or ‘honey urine’.
Term diabetes which is derived from Greek word meaning ‘to run through a siphon’, was used by Aretaeus (1st century AD). Suffix mellitus, which is derived from Greek word meaning ‘sweet’, was added centuries later to distinguish it from diabetes insipidus.
It was described in Egyptian papyrus, dated 1500 BC, that ants were attracted to urin of diabetes because of high glucose content. Distinction was also made between two types of diabetes
- First from was noted in children and young adults who were thin. These persons essentially ‘wasted away’ and had dismal future, with death occurring in 1 to 2 years.
- Another from was noted in older, overweight individuals who typically lived for many years.
Claude Bernard demonstrated hyperglycaemia as characteristic feature of diabetes in 1850. Langerhans described islet cells in 1869. Banting and best discovered insulin in 1921.
Multifactorial clinical syndrome of glucose metabolism due to absolute or relative deficiency of insulin secreted by beta cells of pancreas or its diminished biologic effectiveness resulting in impaired carbohydrate tolerance and persistent hyperglycaemia with or without glycosuria, and characterized by polyuria, polyuria, polyphagia and weight loss.
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ETIOLOGY OF DIABETES
Primary Diabetes Mellitus
Type 1 or insulin Dependent Diabetes Mellitus (IDDM):
- Juvenile onset.
- Exact cause is not known.
- Probably autoimmune disorder
- Resulting in destruction of pancreatic islet cells by anti-islet cell antibodies.
- Association with HLA-DR3 and HLA-DR4.
Type 2 or non-insulin Dependent Diabetes Mellitus (NIDDM):
– Exact cause is not known.
– Predisposing cause
- Familial predisposition.
- Maturity onset diabetes of young (MODY).
- Especially in precipitating latent form of disease.
Secondary Diabetes Mellitus
– Impair glucose tolerance and increase insulinresistance
– Common Conditions include
- cushing s syndrome
– Reduction in beta call mass
– 80% of islet mass must be destroyed for clinical hyperglycaemia to occur
– Pancreatic destuction due to excessive iron accumulation
– Known as bronze diabetes due to dark skin pigmentation resulting from iron accumulation.
Pregnancy (gestational diabetes mellitus)
– State of glucose intolerance occurring in late second trimester.
– As growing foeto-placental unit increases in size
- Human placental lactogen (HPL) and human placental growth hormone (HPGH) are secreted in large amounts.
- Increase insulin resistance.
– In susceptible individuals.
- Gestational diabetes will result.
– Risk factors include: Obesity, Family history of NIDDM, Advanced maternal age.
– Usually resolves after delivery.
– Iatrogenic: Steroids, Contraceptives, Thiazide diuretics.
CLASSIFICATION OF DIABETES MELLITUS
Potential (pre-clinical) diabetes mellitus
GTT is normal, but increased susceptibility to diabetes in any time of life for following causes
– Both parents are diabetic
– one parent is diabetic and other is having family history of diabetes
– history of given birth to abnormally large baby (> 4.5 kg)
– Identical diabetic twin
– Latnt (sub-clinical) diabetes mellitus Abnormal glucose tolerance during
– steroid or thiazide therapy
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Clinical diabetes mellitus
– preclinical (potential diabetic)
– Secondary stage
– Early secondary stage Diabetic GTT but Asymptomatic
– Late secondary stage
– Symptomatic full blown/s/s
– Tertiary stage
– with complications
PATHOLOGY OF DIABETES MELLITUS
Pathogenesis is complex and is still not clear
– Factors possibly responsible for development of diabetes mellittus include
– Deficiency of insulin
– Presence of insulin antagonists
– Excessive neoglucogenesis
– Islet cell antibodies (ICA) result in
– Inflammation and destruction of islet cells
– With persevation of exocrine cells
About 70% of new onest IDDM have positive ICA at time of diagnosis.
– Levels may be detected several years before clinical diabetes results.
– Eventually,antibody levels diminish in most patients.
Sequence of events include
– Reduction of islet cell mass
- 90 % over period of years.
– Decreased insulin secretion diagnosis of diabetes.
– Brief partial recovery of insulin secretion
– Deu to substantial insulin reserve,brief state of remission occurs after treatmant.
– Symptoms and glucose levels normalise.
– Phase is short lived (typically several month).
– Absent insulin secretion
– Absolute dependence on exogenous insulin.
– Aggressive treatment with insulin is recommended,as it tends to preserve insulin reserve.
– Death without exogenous insulin.
State of insulin resistance
Insulin receptors lose their sensitivity to insulin
Sequence of events include
– Insulin levels are elevated early in disorder
– In time, impaired glucose tolerance occurs
– Followed by overt hyperglycaemia
– Develoment of diabetes mellitus
– Diagnosis of diabetes but asymptomatic
– Appearance of clinical symptoms and signs
– Eventual diminished insulin secretion after many years(beta cell burnot)
– Glucose toxicity
– Phenomenon in which hyperglycaemia impairs insulin secrtion
– This results in low insu;in leves
– Restoretion of normoglycaemia may improve insulin secretion
– Mechanism of insulin resistance
– Most common reason for insulin resistance is obesity
– This results in reversible decrease in receptors and receptor binding
– Similar defects are produced in susceptible persons with:
– Excess growth hormone (Acromegaly)
– Excess of glcocorticoids (Cushing,s syndrome)
– Two uncommon forms of insulin resistance occur
– Type A insulin resistance:
Seen in young women with
– Type B insulin resistance
– Occurs in older women
– They have insulin recetor antibody that decreases insulin activity
– They often have
– High titres of other autoantibodies
– Evidence of other systemic autoimmune disease
– Absence of androgenic features Occasionallu fasting glucose is often high in those with NIDDM
– Related to increased hepatic gluconeogenesis at night
– Increased GH secretion at night (dawn phenom enon)
– Increases insulin resistance
– Contributes to fasting hyperglycaemia
– Maturity onset Diabetes of young (MODY)
– Atypical form of NIDDM
– Occurs in teenagers or young adults
– Inherited as autosomal dominant
– MODY Patients lack
– HLA-DR3/DR4 association
– Patient hes first degree relatives with ketosis resistant diabetes developed at young age
– Most patients are not obese
– can be controlled on oral agents
– Deficiency of insulin leads to
– Decreased anabolism
– Increased catabolism
– Hyperglycaemia develops slowly over many months or even years
– As sugar is not burnt
– Fat is mobilised from adipose tissues
– Large quantities of free fatty acids circulate in blood
– Incompletely metabolised carbohydrates also accumulate in blood (Ketoacidosis)
– Due to deficient insulin, blood sugar level steadily rises
– Glycosuria results when
– Blood sugar crosses renal threshold level i.e capacity of renal tubules to reabsorb glucose from glomerular filtrate
– Renal threshold level (180 mg%) however varies with age and pergnancy
– Glucose increases osmolarity of glomerular fil trate
– It also takes back obligatory volume of water during elimination
– This result in profuse diuresis even upto 10 15litres per day associated with
– Due to continuous loss of sugar in urine
– Neoglucogensis from protein is stimulated resulting in
– Wasting of muscles
– Increased urinary loss of nitrogen
– Increased frequcncy of urination
– Amount of urine may be 10- 15 litres in 24 hours
– This is due to excessive sugar in urine which acts as diuretic
– Excessiv thirst
– Patient may consume several litres of water in 24 hours
– With deyness of mouth throat
– Excessive hunger
– Always feels hungry
– May have craving for carbohydrate food sweets sugaar
– This symptom is due to non utilisation of sugar for energy expenditure
– Inspite of good appetite there is
– Lack of energy
– Weight loss
– There may be rapid emaciation due to
– Tissue starvation
– Mobilisation of fat from fat depot
– Bowel movement may occur after every 2-3 days
– Stools become hard
– Intense itching
– usually in anus or exteral genitalia
– This due to
– Irritant action of sugar on tissues
– superimposed fungal or bacterial infection
– other features
– Burning in feet
– Impotency in males
– Tendency to infections
– Delayed wound healing
– Brittle diabetes mellitus
– Macrovascular diseases
– Coronary artery disease
– Cerebrovascular disease
– Peripheral vascular disease
– Microvascular diseases
– Diabetic retinopathy
– Diabetic nephropathy
– Somatic neuropathy
– Autonomic neuropathy
– Other complications
– Diabetic foot
– Pre-senile cataract
– Diabetic ketoacidosis
– Variety of sikin lesions
– syndrome x
– Complications of gestational diabetes Maternal risks if untreated
– pre-eclamptic toxaemia
– Increase in caesarian section rate Foetal risks if untreated
– Foetal growth disturbance
– Increase in perinatal morbiddity and mortality
HOMEOPATHIC MEDICINE FOR DIABETES
Constitutional/ Symptomatic drugs
– Abroma augsta
– Arsenicum album
– Cephalandra indica
– Conium maculatum
– Gymnema sylvestre
– Lactic acid
– Natrum muriaticum
– Natrum sulphuricum
– Nux vomica
– Syzygium jambolanum
– Uranium nitricum
– Carcinosin .
– sulphur .
– syphilinum .
– thuja occidentalis .
– Cardiouascular Complications .
– Arsenicum album .
– bothrops .
– crataegus .
– lachesis .
– phosphorus .
– vanadium .
– Phosphorus .
– Vanadium .
– Osmium .
– Naphthalin .
– Arsenicum .
– phosphosrus .
– Uranium .
– Urea .
– Cuprum arsenicum .
– Neuropathy .
– phosphosrus .
– thallium .
– Curare .
– Vanadium .
– diabetic foot
– Arsenicum album .
– kali bichromicum .
– Lachesis .
– Insulin .
– Phosphorus .
– Thallium .
– Insulin .
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