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PRAMEHA


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

• One of mahagada.

•               -
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.
SROTAS


•   involved in prameha are-
          -         –      -
•   -

•   -
.

• 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.
•

•        -
• 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.
•   -   and

•   -
•
• Acc to susruta



•
•
• From above reference we can almost consider
  it as kidneys.
•

•      -
•      -


• 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
• Basti

•

•



• Maana is 4 angula
• A bag like structure that collect and store urine
  before excretion, it can be Urinary Bladder.
LAKSHANA
•
•
•
•
•
•
•
•
•
•
•
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.
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.
PANCREAS
HISTOLOGY
ENDOCRINE PART
• 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
A- Alpha cell

B- Beta cell

D- Delta cell

F- PP cell
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.
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.
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
DIABETIC NEPHROPATHY
• Morphologically – 4 types of lesions
1. Diabetic glomerulosclerosis
2. Diabetic vascular lesion
3. Diabetic polynephritis
4. Tubular lesion
• 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
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
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
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.
Morphological changes in body due to prameha

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Morphological changes in body due to prameha

  • 1.
  • 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.
  • 14.
  • 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.
  • 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
  • 22.
  • 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
  • 27.
  • 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
  • 30.
  • 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
  • 32.
  • 33.
  • 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.