Morphological changes in body due to prameha

918 views

Published on

Published in: Education
0 Comments
1 Like
Statistics
Notes
  • Be the first to comment

No Downloads
Views
Total views
918
On SlideShare
0
From Embeds
0
Number of Embeds
1
Actions
Shares
0
Downloads
40
Comments
0
Likes
1
Embeds 0
No embeds

No notes for slide

Morphological changes in body due to prameha

  1. 1. PRAMEHA By Dr Akhil.H.S Dept of SHAREERA RACHANA ALVAS AYURVEDIC COLLEGE.
  2. 2. PRAMEHA••• One of mahagada.• -
  3. 3. 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.
  4. 4. SROTAS• involved in prameha are- - – -
  5. 5. • -• -
  6. 6. .• Moola- basti and vankshana. closely related to - - . is on of the of body. Which depends on in and s. Thisdetermine the quantity and quality of urine to be excreted out.
  7. 7. •• -• 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.
  8. 8. • - and• -
  9. 9. •• Acc to susruta••• From above reference we can almost consider it as kidneys.
  10. 10. •• -• -• 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
  11. 11. • Basti••• Maana is 4 angula• A bag like structure that collect and store urine before excretion, it can be Urinary Bladder.
  12. 12. LAKSHANA•••••••••••
  13. 13. 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.
  14. 14. 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.
  15. 15. PANCREAS
  16. 16. HISTOLOGY
  17. 17. ENDOCRINE PART
  18. 18. • 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
  19. 19. A- Alpha cellB- Beta cellD- Delta cellF- PP cell
  20. 20. 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.
  21. 21. 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.
  22. 22. MECHANISM OF COMPLICATION• The process of development of complications in D.M is explained by 2 mechanisms1. Non – enzymatic protien glycosylation2. Polyol pathway mechanism
  23. 23. DIABETIC NEPHROPATHY• Morphologically – 4 types of lesions1. Diabetic glomerulosclerosis2. Diabetic vascular lesion3. Diabetic polynephritis4. Tubular lesion
  24. 24. • Diabetic glomerulosclerosisDIFFUSE 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
  25. 25. 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
  26. 26. DIABETIC RETINOPATHYBACKGROUND 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
  27. 27. 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.

×