Introduction

Chronic heterogeneous disorder characterized by the abnormal metabolism of the fuels, particularly glucose, fat and proteins with a common feature of chronic hyperglycemia.

• Beta cells (B cells) of the Islets of Langerhans of the endocrine portion of pancreas secrete insulin, defective response or deficient synthesis causes Diabetes mellitus.

• Hallmarks of diabetes mellitus- three “polys”:

Polyuria– excessive urine production due to an inability of the kidneys to reabsorb water. 

Polydipsia– excessive thirst

Polyphagia– excessive eating.

If insulin is not present to aid the entry of glucose into body cells, most cells use fatty acids to produce ATP. Stores of Triglycerides in adipose tissue are catabolized to yield fatty acids and glycerol. The byproducts of fatty acid break down- organic acids called ketones or ketone bodies accumulate. Buildup of ketones causes blood pH to fall, a condition called Ketoacidosis. Unless treated quickly, ketoacidosis can cause death.

•  Breakdown of stored triglycerides also causes weight loss.
• Microangiopathy. – manifests as renal, retinal, nig heart and peripheral nerve disorders giving rise to diabetic retinopathy, nephropathy, many forms of diabetic cardiomyopathy.
• Lipds while treanspoting by the blood, lipid particles are deposited on the walls of the blood vessels, leading to atherosclerosis.

• Atherosclerosis leads to a multitude of cardiovascular problems including cerebrovascular insufficiency, ischemic heart disease and gangrene. (Macroangiopathy)

• Loss of vision is the complication due either to cataracts (Excessive glucose attaches to lens protein, causing cloudiness) or to damage to blood vessels of the retina.

• Kidney problems- damage to renal blood vessels.

 

Etiologic Classification of Diabetes Mellitus 

(As per American Diabetes Association, 2000). 

 I. Type 1 diabetes mellitus- earlier called Insulin-dependent, or juvenile- onset diabetes(IDDM)

II. Type 2 diabetes mellitus- earlier called non- insulin dependent, or maturity onset diabetes. (NIDDM)

III . Other specific types

1. Genetic defect of B-cell function
2. Genetic defect in insulin action
3. Diseases of exocrine pancreas
4. Endocrinopathies
5. Drug or chemical induced (steroids, B blockers etc)
6. Infections (e.g.Rubella)
7. Uncommon forms of immune-mediated(e.g. anti insulin receptor antibodies)
8. Other genetic syndromes (e.g. Down’s Syndrome, Turner’s syndrome etc) 

IV. Gestational diabetes mellitus.

Pathogenesis

Depending upon etiology of DM, Hyperglycemia may result from:

1. Reduced insulin secretion and defect in the release of insulin
2. Defect in the transport mechanism in the blood and deficiency in the number of and/ or affinity of receptors 
3. Decreased glucose use by the body 
4. Increased glucose production

• The basic phenomenon in type 1 DM is destruction of ẞ cell mass, usually leading to absolute insulin deficiency.
• The basic metabolic defect in type 2 DM is either a delayed insulin secretion relative to glucose load (impaired insulin secretion), or the peripheral tissues are unable to respond to insulin (insulin resistance). 

Pathological changes

1. Pancreas- B cells of the islets of Langerhans show reduction in number, degranulation and hyalinization.
2. Vascular- Microangiopathy affecting the basement membrane of small vessels ie, venules, capillaries and arterioles. Macroangiopathy- occlusive vascular disease in  medium sized arteries like coronary, cerebral and peripheral limb arteries.
3. Retinopathy-occurrence is related to the duration and not the severity of the disease. The early changes are venous dilatation and the appearance of small dot-like microaneurysms in the perimacular area.
4. Renal lesions- vascular changes include- arteriosclerosis of the renal artery, sclerosis of the arterioles and glomerulosclerosis (indicated by the presence of proteinuria)
5. peripheral nerves- systemic neuropathy is most characteristic. Segmental demyelination, Schwann cell injury and axonal damage are the basic pathological changes.

DIAGNOSIS OF DIABETES

1. Symptomatic cases- glucosuria and a random plasma glucose concentration above 200 mg/dl. 
2. If abnormal oral glucose tolerance test values are found but have normal fasting glucose level in the plasma- Chemical diabetes.
3. Urine testing– testing for the presence of glucose and ketones.
4. Oral Glucose tolerance test
5. Glycosylated haemoglobin (HbA1c)

 

COMPLICATIONS OF DIABETES

• Retinopathy, nephropathy and neuropathy are  relatively specific for diabetes and are characterised by pathologic endothelial changes, -no such as basement membrane thickening and increased vascular permeability.
• Retinopathy, nephropathy and neuropathy have been categorized as microvascular complications.
• The increased susceptibility to atherosclerosis and its ensuing complications are categorized as macrovascular complications.

1. ACUTE COMPLICATIONS
2. CHRONIC COMPLICATIONS/ LONG

ACUTE COMPLICATIONS

1. Metabolic derangements/complications

a) Diabetic ketoacidosis

b) Hyperosmolar nonketotic coma

c) Hypoglycemia and hypoglycemic coma

d) Lactic acidosis

2.Infections

a. Medical– skin infections, Respiratory tract infections, Urinary tract infections, Genital infections etc.

b. Surgical– boils, carbuncles, cellulitis, superficial end and deep abscesses, gangrene, foot infections etc.

3. Acute events occurring as a result of long- term complications

• Acute ischemic heart disease
• Renal failure
• Peripheral vascular occlusion 
• Loss of vision

Obstetric complications

a. Intrauterine fetal death

b. Hydramnios

c. Pre-eclamptic toxemia

d. Large baby (>4kg) giving rise to complications during delivery

e. Infections of the genital tract

f. Worsening of the diabetic state during pregnancy and postpartum

CHRONIC COMPLICATIONS/LONG TERM

1. Cardiovascular– early onset of atheroma, ischemic accidents, peripheral vascular occlusion, high incidence of hypertension.
2. Neurological– peripheral neuropathy, autonomic neuropathy, mononeuritis multiplex, occlusive vascular disease.
3. Excretory system– recurrent urinary infections, chronic diabetic pyelonephritis,glomerulosclerosis, end stage renal failure.
4. Ocular– cataract, retinopathy, iridocyclitis, KEY glaucoma, refractive changes induced by treatment (insulin presbyopia)

5. Respiratory– pulmonary TB
6. Alimentary– stomatitis, xerostomia, gingivitis, dental sepsis, hepatic enlargement, loosening of tooth, gastric dilation, nocturnal diarrhoea, paralytic ileus
7. Bones and joints– osteoporosis, osteoarthritis, neuropathic joints
8. Skin– chronic fungal infections skin, moniliasis of the mucous membrane of the genitalia and mouth, trophic ulcers of the feet 
9. Drug induced complications– hypoglycemia, drug allergy, toxicity to liver and bone marrow.

DM – Ayurvedic View-

DM comes under the umbrella of prameha which is one among Ashtamahagada. Prameha is a disorder of impaired agnivyapara at dhatu level. Prameha passes through distinct stages. When it manifests as santarppanaprameha, it is generally kapha dominant. Kaphajaprameha generally having Avarana as the key samprapti. Apatarppanaprameha is vata related, Vatajaprameha on the other hand is caused by dhatukshaya.

One of the unique features of prameha is the involvement of multiple dooshyas in its samprapti. Various dooshyas related with all the three doshas are involved in the different stages of prameha samprapti. Starting with soumya dhatus in the initial stage, passing rakta in the middle stage and through agneya dhatu ending with vata related dhatus and ojus, prameha is unique in its progression. Due to the multiple involvement Dooshyas, there is good number of upadravarogas associated with prameha. All pramehas will become vataja pramehas with definite signs of dhatukshaya and ojokshaya.

KEY POINTS OF DM

• Imbalance of Dhatwagnis
• Associated with Beejadushti
• Aggravated by Ahara – Viharas
• Results in Kleda Vridhi
• Presents with multi- level complications in different srotuses.

STEPS IN THE DM MANAGEMENT

1. Agni deepana
2. Amapachana and kleda shoshana
3. Srothoshodhana
4. Concerned dosha shamana
5. Prevention of further sthanasamsraya by koshtagathi of doshas
6. Ojokara

 

DM-TREATMENT PROTOCOL

❖ TREATMENT OF DM IN AYURVEDA IS NOT SIMPLY BASED ON GLUCOSE LEVEL IN BLOOD.

❖ PLEASE ASESS THE DOSHA DOMINATION OF INDIVIDUAL DM PATIENTS.

❖FIX THE DIAGNOSIS OF PRAMEHA AS KAPHAJA/PITHAJA/VATAJA

❖THEN WRITE MEDICINES BASED ON THEY KAPHA, PITHA OR VATA TYPES OF PRAMEHA.

 

DIABETIC RETINOPATHY

Diabetic retinopathy is an important cause of blindness. Other ocular complications of diabetes include glaucoma, Cataract and corneal disease.

DIABETIC RETINOPATHY – Ayurvedic Thoughts

1. Parathanthravyadhi 
2. Manifests in the later stages of kriyakala of Prameha
3. Specific dosha pattern in different stages
4. Sookshmasrothuses of Drishtimandala affected. its is INDRIYAPRADOSHAJA VYADHI

 

TREATMENT PROTOCOL OF DR

• Pramechahara chikitsa
• Rakthaprasadana Chikitsa
• Srothorodhahara Chikitsa
• Sophahara Chikitsa
• Vathanulomana Chikitsa

Role of panchakarma in DR

1. Virechana 
2. Seka
3. Anjana
4. Nasya
5. Tarpana

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