PRAMEHA

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

3. PRAMEHA • प्रकर्षेण मेहति जनयति मूत्रं इति प्रमेहः ॥ • तत्र आविलप्रभूत मूत्र लक्षणः सर्व एव प्रमेहा ॥ सु. नि ६/५ • One of mahagada. • प्रत्यात्म लक्षण - प्रभूताविल मूत्रत

4. DOSHAS AND DHAATUS • All the three doshas are vitiated. • मांस–मेद–शुक्र–मज्जा–रस–रक्त are vitiated. • Other दूष्यास् are- ऒजस् - उदक - वसा – लसिका. The doshas chiefly concerned is kapha and among dhaatusमेद, उदक, मांस are principally involved. And रस–रक्त are moderately involved.

5. SROTAS • स्रोतस् involved in prameha are- उदकवह - मूत्रवह – मेदवह- स्वेदवहस्रोतस्

6. मेदवहस्रोतस् • मूल - वृक्क वपावहन • लक्षण- प्रमेह पूर्वरूप् (मुख,तालु,कण्ठ शोष, पिपास,आलस्य,मलसंचय,अंगसुप्ति,शरीर विस्रगंध,तन्द्र, निद्र ...

7. मूत्रवहस्रोतस्. • Moola- basti and vankshana. मूत्रवहस्रोतस् closely related to उदकवह- रसवह- स्वेदवह अन्नवहस्रोतस्. मूत्र is on of the मल of body. Which depends on अग्नि in अन्नवहस्रोतस् and धातुs. This स्रोतस् determine the quantity and quality of urine to be excreted out.

8. उदकवहस्रोतस् • उदकवहानां स्रोतसां तालु मूलं क्लोमा च ॥ च.वि ५ • उदक - अप् धातु • Acc to charaka.sarira 7/15- • अप् धातु is 10 anjali. • It does sariradhaarana.It forms part of pureesha, mutra, sweda, lasika etc. and dhatus like rasa, rakta, mamsa etc. • It helps in ahladana, kledana, bandhana , vishyandana.

9. स्वेदवहस्रोतस् • मूल - मेद and लोमकुप • लक्षण- अतिस्वेद, कण्डु, दौर्गंध्य

10. वृक्क • Acc to susruta एकोत वामपार्श्वस्थितः द्वितीय दक्षिण पार्श्व स्थितः । सु.नि • रक्त मेद प्रसादात् वृक्कौ । • मेदोवहे द्वे तयोर्मूलं कटि वृक्कौ च । • From above reference we can almost consider it as kidneys.

11. क्लोम • अ.हृ - कफाधिष्ठान • सु.नि- क्लोमो हि आमाशयस्त्वधः। क्लोमो हि शोणितजं क्लोमं कालखण्डादधस्तात् स्थितं दक्षिणपार्श्वस्थं तिलकं प्रसिध्दं ॥ • Udakavahasrotomoola. • Varuna is considered as creator of kloma. • Acc to srikantadatta - वृक्कादूर्ध्वं पिपासस्थानं । • 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 • अल्पमांसशोणितो आभ्यन्तरतः कट्या धनुर्वक्र एकद्वारो अधोमुखो बस्तिः ॥ अ.सं.शा ७/१९ • बस्ति देशः अयं नभिपृष्टकटिमुष्कगुदवङ्क्षणसेफसां मध्येऽलब्वाकृति सिरास्नयुपरिग्रहस्तनुत्वक्कौऽधोमुख एकद्वारश्च ॥ सु.नि ३/२० • Maana is 4 angula • A bag like structure that collect and store urine before excretion, it can be Urinary Bladder.

13. LAKSHANA • दन्तादीनां मलाठ्यत्वं • पाणि पाद दाह • जटिलीभाव केश • मधुरास्यत • करपाद सुप्ति • मुख तालु शोष • पिपास • आलस्य • विस्रंशरीर गन्ध • निद्र • तन्द्रं

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 MINOR CELLS

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 fibrillousprotien 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 • Non – enzymatic protienglycosylation • Polyol pathway mechanism

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

28. DIFFUSE NODULAR • Diabetic glomerulosclerosis

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

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 ayurvediclitrature 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.

35. THANK YOU