Prameha described in Ayurveda is comparable to diabetes mellitus. Both conditions are characterized by excess sugar in the urine. In prameha, the doshas of vata, pitta, and kapha are vitiated, especially kapha dosha. The dhatus of mutra, meda, and lasika are principally involved. The srotas or channels involved include those of the basti, mutra, and udakavaha. Complications of prameha/diabetes include damage to tissues and organs over the long term due to high blood sugar levels. Early diagnosis and treatment can help prevent complications.

2. PRAMEHA
By
Dr Akhil.H.S
Dept of SHAREERA RACHANA
ALVAS AYURVEDIC COLLEGE.

3. PRAMEHA
•
•
• One of mahagada.
• -

4. DOSHAS AND DHAATUS
• All the three doshas are vitiated.
• – – – – – are vitiated.
• Other are-
- - – .
The doshas chiefly concerned is kapha and
among dhaatus , , are principally
involved. And – are moderately
involved.

5. SROTAS
• involved in prameha are-
- – -

6. • -
• -

7. .
• Moola- basti and vankshana.
closely related to - -
.
is on of the of body. Which depends on
in and s. This
determine the quantity and quality of urine to
be excreted out.

8. •
• -
• Acc to charaka.sarira 7/15-
• is 10 anjali.
• It does sarira dhaarana.It forms part of
pureesha, mutra, sweda, lasika etc. and
dhatus like rasa, rakta, mamsa etc.
• It helps in ahladana, kledana, bandhana ,
vishyandana.

9. • - and
• -

10. •
• Acc to susruta
•
•
• From above reference we can almost consider
it as kidneys.

11. •
• -
• -
• Udaka vaha sroto moola.
• Varuna is considered as creator of kloma.
• Acc to srikantadatta -
• As a koshtanga it should come in thoracic/abdominal
cavity.
• An organ Rt and Below liver is pancreas
• Above kidney- Supra renal glands

12. • Basti
•
•
• Maana is 4 angula
• A bag like structure that collect and store urine
before excretion, it can be Urinary Bladder.

13. LAKSHANA
•
•
•
•
•
•
•
•
•
•
•

15. DIABETES MELLITUS
•
• What is DIABETES MELLITUS?
• Acc to W.H.O –
• It is heterogeneous metabolic disorder
characterized by common feature of chronic
hyperglycemia with disturbance of carbohydrate,
fat, and protein metabolism.
• Depending on the etiology, hyperglycaemia may
result from
• a) reduced insulin secreation.
• b) Decreased glucose use by the body.
• c) increased glucose production.

16. INSULIN
• It’s a peptide hormone (a protien ) secreted by
beta cells of islets of langerhans.
• It helps to transport glucose into the target
cells of the body. And reduces the increased
glucose level of blood.

17. PANCREAS

18. HISTOLOGY

19. ENDOCRINE PART

20. • MAJOR CELLS
Beta cells 70% of islet cells INSULIN
Alpha cells 20% GLUCAGONE
Delta cells 5-10 % SOMATOSTATIN
Pancreatic 1-2 % PANCREATIC
Polypeptide cells POLYPEPTIDE
MINOR CELLS
D1 cells Vaso active Intestinal peptide
Entero chromaffin cells SEROTONIN

21. A- Alpha cell
B- Beta cell
D- Delta cell
F- PP cell

23. SOME MORPHOLOGICAL FEATURES IN
PANCREATIC ISLETS
• Insulitis –
Type 1 – In early stagethere is lymphatic infiltration of t-cells,
macrophages etc
Type2 – Little fibrillous protien deposit.
• Islet cell mass destruction –
Type 1 – As DM become chronic there will be progressive Depletion
of beta cells, eventually result in total loss of pancreatic B-cell
Type 2 –Mildly effected.
• Amyloidosis.
Type 1 –are absent.
Type 2 - Amyloid deposit around capillaries of islet. Causing
compression and atrophy of islet tissue.
Degranulation of B-cells.

24. FEATURES IN DM
• TYPE 1- Absence of insulin due to destruction
of beta cell.
• TYPE 2- Insulin secreation is normal
• a) Insulin resistance.
b) failure of beta cells.

25. MECHANISM OF COMPLICATION
• The process of development of complications
in D.M is explained by 2 mechanisms
1. Non – enzymatic protien glycosylation
2. Polyol pathway mechanism

26. DIABETIC NEPHROPATHY
• Morphologically – 4 types of lesions
1. Diabetic glomerulosclerosis
2. Diabetic vascular lesion
3. Diabetic polynephritis
4. Tubular lesion

28. • Diabetic glomerulosclerosis
DIFFUSE NODULAR
• Thickening of vessels • 1 or More .
• Increase matrix • Ovoid/spear
• Prolyferation of • Surrounded by
matrix capillaries
• Renal ischemia
• Tubular atropy
• Interstitial fibrosis
• Small contracted
kidney

29. DIABETIC NEUROPATHY • Effects all nervous
system.(peripheral
neuropathy is more
clear)
• Basic pathological
changes – . . .
• Glucose deposit in micro
capillaries.
• Demyelination
Schwann cell injury
Axonal damage

31. DIABETIC RETINOPATHY
BACKGROUND RETINOPATHY PROLIFERATIVE RETINOPATHY
• Basement membrane • After long term
thickness increase. • Neovascularisation of retina
• Degeneration of pericytes at optic disc.
and loss of endothelial cells • Friability of newly formed
• Capillary micro-anurism B.V cause easy bleeding-
• Waxy exudate accumilation haemorrhage of vitrous
near micro anurism. • Also proliferation of fibrous
(hyperlipidemia) tissue around B.V
• Dot and Blot – Retina • Contraction of fibro –
• Soft Cotton-wool spot vascular tissue = Retinal
detachment

34. DISCUSSION
• Prameha can not only be compared to D.M, but electrolyte
imbalance etc are also related to prameha.
• The syndrome of D.M is largely covered under prameha.
• Apathyanimitta prameha, sthula prameha in ayurvedic
litrature has similarities with D.M. Madhumeha can almost
be Diabetes Mellitus.
• But to understand remaining 19 types of prameha we need
wide discussion and proper reasoning.
• In general destruction of B-cell mass and obesity are most
important cause of diabetes.
• So approach in treating DM should be to control diet and
good life style.
• Early diagnose and treatment can prevent complications
due to prameha.