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Aetiopathology of madhumeha
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Aetiopathology of madhumeha

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  • 1. AETIOPATHOLOGY OF MADHUMEHA I sivarama prq!94 I(ETHAMAKI4 When the pathology of Prameha is discussed in Madhava Nidana, Madhavakara, who followed a specific pattern has kept this (metabolic) disorder belore lfiedoroga (Obesity) and after the Ashmari (Urinary caliculi). The chapter of prameha consists of prameha pidika (boils). at the end as the complications of prameha. There are twenty pramehas explained, out of which 4 are vataia, 6 pittaja and 10 kaphajaBecause of Tulya dosha dooshyata normal and still the glucose levels are(Homologous etiologic factors of high (hyperglycemia). lt suggestsvitiation of doshas and dooshyas) clearly, in insulin dependent patients,kaphaja mehas are amenable to there are other causes other than thattreatment, where as vataja become of insulin. Madhumeha literally meansdifficult for the same reason. The madhuryata of mootra (r:enalmedoroga is said to be the glycosuria).nidanarthakara vyadhi for prameha SCAN:pidikaother than that of prameha. When we look in to the pathogenesisThus it is clgar, madhumeha - of meha vis a vis prameha it givesDiabetes mellitus, -is a disorder priority for medas (fat?) as dooshyapertained to the lipid metabolism. along. with mamsa (muscle) andToday when we observe the patients, shareera kleda (fluid contents"of themany of them are non-insulin body). The seat of accumulation ofdependent and very few are insulin fluid is vasti (bladder). ln the categorydependent. ln fact many of the of shareera kleda, the other dooshyaspatients those who are having (vitiated tissues) are rakta (blood),madhumeha, secrete more insulin sukra(semen), ambu (fluids), vasa(hyper insulinemia) than that ot (adipose tissue), lasika (lymph?), li
  • 2. Cover Etory majja (bone marrow), rasa (plasma) molecules for one.glncose molecule and ojas (essence of body tissues). and eicreted through, mootravahaWhen we are analyzing the srotas (kidney, ureter, :bladder) andpathogenesis, along witfr the dosha, ullirnately accumulates in vastithe sequencei of dooshya involvement (bladder), where re-absorptionis to be followed. mechanism fails (in Henleys loop)It is explained in medoroga, how and sweet urine or glycosuria isthe medagni gets the ama samjna witnessed ultimately in all mehas.and dustamedas is accumulated in Ama auto corrective mechanism :the body. For the accurnulation of ln the process of pathogenesis firstthe medas in the body jatharagni dowrbalyata is seen withmedovahasrotas avritatva the above said etiology. lnitially(encircling /covering), vata kaphavriddhi makes the Agni vitiationvitiation, jathara$ni vriddi and with its seeta and guru gunas. Thekapha medovardhaka nidana is agni dusthi leads to varieties ofnecessary. lt is a fact that, the obese Ajeerna according to the predominantpersons have the tendency of dosha associated. The Agnideveloping prameha or madhumeha. disturbances follow with,Arna, inln both prameha and medoroga pachakagni and spreads to Rasa, thekapha rnedodusti appears in the initial dhatu. lt further gets rooted inbody. the successive dhatui where firstEtiology: three make one set and rear three make another. ln between of theseThe etiology includes intake of two groups the Medas is notnavanna (newly harvested paddy) accessible for treatment. Here thewhich is rich of carbohydrates along Auto corrective mechanism:of thewith the gudavikriti (items made of body as protective mechanism actjaggery and sugar), Payamsi, dadhini (su.su.21l28) and makes the(diary products) which have lactose rectification of Ama in uttana dhatusand less" number of carbohydrate (Rasa, Rakta and Mamsa). This canchains and are easily metabolized, be under the neural or secretarygramyaanupa rasa (meat and flesh control, or ofeven both. But theof the water and land animals) are Medas is not going to be getrigh in proteins and lipids/tats, The corrected by auto rectification,food which is ingested getsassirnilated andulilized by jatharagni Ojas in pathogenesis :and this gets impaired to begiri with. ln the nidana of pranieha, the causeThus free glucose increases in the which increases sleshma, mootra. andblood which collects the seven water meda with a special reference to11,
  • 3. sleshma, which is abundantly watery Samprapti (Aetiopathology)(Bahudrava sleshma), is discussed. The description of pathogenesis inSpecificalty Madhumeha appears Susruta Nidana 614 stateswhen ojodusti.is seen a.nd because "Pravrittasyapaiipakwa" for whichthe sweetness in Ojas gets depleted Dalharra commenls as. Aparipakwaby vata and reachesthe vasti, whicli Ama". lt refers both Amadosha andis the cause of the cardinal symptom, Amadooshya. Further it is said assweet urine.: . Medascha Aparipakwam pertainingBrowse the symptoms : to the dooshya alone. There by Amatwa in dooshyas specificallyAmong the lakshanas mentioned in medas, isthe.meaning of "MedaschaMadhumeha the following are seen Aparipakwamn.as valuable for analysis.. Prabhootivila : mootrata Gayadasa explains it as "medascha aparinama mili asamyakparinatam", (polyuria) : Sweda vaha sroto in this the process of formation of avarodhata causes increased medas is not interrupted but impaired, urinary output with turbidig with the qualities of ama; " Ama+ Madhuratwa ln mootra : rasavadati snigdham" , snigdhatwa Glycosuria (explained later in will be in medas by virtue, but here it Samprapti)* Dantadinam mala sanchaya: will become pichhilatwa with atidravatwa. "Cha" usage indicates Becayge of ,Arra. depositions are not only medas but also other seen in mouth.. dooshyas in the pathogenesis as Pani pada daha: Abundance of explained by Charaka. And Gayadasa glucose ayailable in the blood is in his commentary said il is in not utilized by body tissue causes stanasamshritavasta, in which disturbance in the equillibrium of amalakshana in medas and other dhatus and doshas. lt gives rise to dooshyas are visualized. lmpaired pada pani daha (burning sensation jatharagni and dhatwagnis causes of feet and palm). the atidravatwa of the dogshyas of$ Chikkanata (stickiness): prameha. These draveebhootha (explained later in Samprapti) dhatus get dragged and excreted* Trishna (thirst - polydipsia): ln the through mootra vaha srotas. process of lypolysismore water is utilized. lt results in to activation " lt/ootrasya kledavahanam", there by of thirst center and Thirst. liquef ied waste/ non properlys Swadasyata : Sweetness is metabolized or Ama/ Amadooshyas experienced in the mouth due to dre excreted through mootravaha increase in the sugar level. srotas and its seat"is vasti, a place l3
  • 4. Caver Story Table - 1 Showing auto rectification of Agni giving rise increased Medas Mithya ahara and vihara Kaphaja Ahara Jatharagni dourbalya Ama in Jatharagni Ama in Rasa, Rakta, Non restricted Mamsa and Meda Medo ama / Aulo . rectilication Medoroga , Samanavata Nirama Dhatu and Agni Medo deposition Kindling Jatharagni Excessive Metabollsm 1 , Prabhoota mootrata 2. Avil mootrata 3. Madhura mootrata 4. Dantani mala sanchaya 5. Panipada daha 6. Chikkanata 7. Trishna 8. Abhishyanna deha
  • 5. Cover Story Table - 2 Sweet urine genesis - Polyglycosuria Kapha kara Ahara--> + Kapha Vatavriddhi Vi i MedovilayaRa Break down of the l-ligher level of molecules to.lower level molecules Table -3 lnterference of fat metabolism developing Diabetes mellitus Reaction inside outside of Mitochondria @1 in the presence of Carnitine (Lysine derivative) Helps iJcrossing Mitochondrial membrane Oxidised.f Iavoprotein stimulates in Mitochondria i Red,.rced f lavoprotein, Alpha, Beta unsaturated fatty acid CoA Carnitine deficiency Defective-.r ^ ..)l Garnnrne rncreaseY With the interaction of Hypoketonemia Liver and acelyl CoA Hypoglycemia Hyperketonemia gives rise beta Hyperglycemia hydroxy butyrate + Adversity or active productionof Acetone along with Beta oxidation of fatty acids .,----- Ketqne bodies will produce Hyperglycemia /OtneefeS (fatty aeid synthesis slops WIELLITUS/ when the chains in Aminoacids -----zare more then 16 Carbon atoms long)
  • 6. Cover Story for accumulalion of urine. Chakrapani kayagni amshas, which are on Cha.Ni.4/6comments as dravatwa responsible lor catabolic activity in the to kapha dosha. When kapha dosha tissues, are also diminished. The. is in abundant liquefied form thenonly dFiatus are subjected to increase. capable of generating the prameha, Here not only jatharagni vriddhi but.by mixing with the medas which is also kayagni amshas of medodhatufuriher liquefied and liquefy the ksheenata is expected. As a result ofmedas in association with ama blockage of medovaha srotas,lakshana. lmportance of drava ahara/ increased agni (jatharagni/pana in liquefying kapha and medas pachakagni) and decreased medoalong with lhe other dooshyas are to amshagnis cause the medoroga.be noticed. Kapha dosha is not Lastly, there is a similarity betweencapable of causing the prameha roga prarneha and medoroga in etiologywithout pitta or vata. The dooshyas with the factors capable ol causingare said to be medas, rakta, sukra, kapha vriddhi like madhura rasa,ambu (sareera kleda), vasa, lasika snigdha guna dravyas. The processmajja, rasa and ojas in chronological. of metabolism of fats in differentorder. stages gives rise either medoroga or prameha (santarpanothavikara).lnmedoroga rasa, rakta and Even in lakshanas of medoroga, wemamsagnis are normal, where asmedagni is Vitiated orfat metabolism see similarity with prameha lakshanas.is impaired: As medagni" is notcapable of assimilation of astayee Theflowcharts given will give cleartrnamsa, this agni is diverted. The insight about the discussed topics. The author is Reader in Kayachikitsa, Department of PG Sfudres, DGM Ayurvedic medical college, Gadag, Karnatalal6

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