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Pandu rn-005

  1. 1. A STUDY TO EVALUATE RELATIONBETWEEN HEMATOLOGICAL CHANGES AND MORBIDITY OF DOSHAS IN PANDU ROGA Dissertation submitted to the Kannur University, Kerala, in partial fulfillment of the regulations for the award of the degree of DOCTOR OF MEDICINE (Ayu) By Dr. MUKESH. E. B. A. M. S. Guide DR. M.S.SIVANANDAN, M.D. (Ayu) Professor (Rtd), Department of Roga Nidana Govt. Ayurveda College, Pariyaram, Kannur. Co-guide DR. R.SREEKUMAR, M. D. (Ayu) Professor and H.O.D, Department of Roga Nidana, Govt. Ayurveda College, Thiruvananthapuram. DEPARTMENT OF POSTGRADUATE STUDIES IN ROGANIDANA GOVERNMENT AYURVEDA COLLEGE, KANNUR, KERALA. 2006
  2. 2. DEPARTMENT OF POST GRADUATE STUDIES IN ROGANIDANA GOVERNMENT AYURVEDA COLLEGE, KANNUR – 670502 2006 CERTIFICATEThis is to certify that the dissertation entitled “A STUDY TO EVALUATERELATION BETWEEN HEMATOLOGICAL CHANGES AND MORBIDITY OFDOSHAS IN PANDU ROGA” is the record of the research work conducted byDr.MUKESH.E under our direct supervision and guidance. The candidate has put in sincere effort in both the conceptual andclinical studies. This title has not been awarded Degree, Diploma, Associateship,Fellowship or similar honours previously. We strongly recommend and forward the same for being submitted forevaluation to the adjudicators.Dr.R.Sreekumar MD (Ay), Dr.M.S.Sivanandan MD (Ay),Co - Guide and Professor, Guide and Professor (Rtd),Dept. of Roga Nidana, Dept. of Roga Nidana,Govt. Ayurveda College, Govt.Ayurveda College,Thiruvananthapuram. Pariyaram, Kannur.
  3. 3. DEPARTMENT OF POST GRADUATE STUDIES IN ROGANIDANA GOVERNMENT AYURVEDA COLLEGE, KANNUR – 670502 2006 CERTIFICATEThis is to certify that the dissertation entitled “A STUDY TO EVALUATERELATION BETWEEN HEMATOLOGICAL CHANGES AND MORBIDITY OFDOSHAS IN PANDU ROGA” is the record of the research work conducted byDr.MUKESH.E under the guidance of Dr.M.S.Sivanandan, Professor (Rtd),Department. Of Roganidana, Govt. Ayurveda College, Pariyaram andDr.R.Sreekumar, Professor and H.O.D, Department. Of Roganidana, Govt.Ayurveda College, Thiruvananthapuram. His findings are valuable and have contributed substantially to thepresent knowledge on the subject. This title has not been awarded Degree, Diploma, Associateship,Fellowship or similar honours previously. I strongly recommend and forward the same for being submitted forevaluation to the adjudicators. Place: Pariyaram Dr. John. K. George MD (Ay), Professor and Head of the Department, Date: Dept. of Roga Nidana, Govt. Ayurveda College, Pariyaram, Kannur.
  4. 4. AcknowledgementWith a bowed Head to the Almighty,With folded Hands to Revered TeachersAndA warm Heart to Good Friends………. This work is the result of the combined effort of a good number of people who include academicians, colleagues, and above all the patients who cooperated with us in all aspects. Moreover it is only because of Gods’ grace, the work could be accomplished as per my expectation. My deep sense of gratification is due for my parents who are the architects of my career. The culture, discipline and perseverance, which I could imbibe, are solely because of their painstaking nurture and strong moral support. Also I am indebted to my aunty Smt. Shanthakumari for her tireless support and care throughout my life. The inspiring force throughout this research work; was my guide Dr.M.S.SIVANANDAN, a person whose love and care became a source of light whenever I was in darkness, who provided necessary fuel for my innovative thoughts. I am deeply indebted for his guidance. My deep gratitude to Dr.R.SREEKUMAR, my co- guide whose guidance with accuracy and commitment towards research has helped me a lot from the very beginning to the end of this work.
  5. 5. I am thankful to DR.JOHN.K.GEORGE, H.O.D, Dept of ROGANIDANA, GAVC,KANNUR for his encouragement, timely suggestions, broadmindedness and affectiontowards me.I am very grateful to Dr.V.K.Ajithkumar, Reader and Dr.S.Gopakumar, Tutor, Deptof ROGANIDANA, GAVC, KANNUR for their timely help and suggestions.I am deeply indebted to Vivekananda Medical Mission hospital, Muttil, Wayanad,especially Dr. Anooj Singhal, for providing me cases of sickle cell anemia.I express my deep sense of gratitude to my teacher Dr. G. Srinivas Acharya,Professor, Dept. Of Kayachikitsa, S.D.M.College of Ayurveda, Udupi for hisguidance through out the work.I am here with soliciting gratitude to Dr.S.Jayadevan, Asst Professor, Dept ofCommunity medicine, ACME, Pariyaram for helping me in the statistical analysis.It is a privilege to convey regards to my teacher Dr. Niranjan Rao for his lovingadmonition and caring support in my difficult times.At this juncture, I would like to share my joy with my best friend Viswan, whoseeverlasting friendship is a boon for my life.I am deeply indebted to my close friends Kannan, Ananthan, Mathew, Mahesh, Giri,Gopi, Nirmal and Pramod for their rejoicing company and timely help.My special thanks to my Seniors Dr.Gopikrishna, Dr.Madhu.P.M andDr.K.S.Nandalal, for their advice and support.I am deeply obliged to Dr. Eby Abraham for helping me in recording the data.It remained pleasure to have worked with my colleagues, Dr.Ajith kumar, Dr.Surabhi,Dr.Sudarkodi, Dr.Anjali, Dr. Abhilash, Dr.Senthil, Dr.Sudhagopal, Dr.Surama and
  6. 6. juniors Dr.Yogesh, Dr.Arbind, Dr.Bindu, Dr.Pradip, Dr.Shambu and Dr.NandkumarsahniI wish to express my gratitude to the authorities of Govt.Ayurveda College, Kannur,for providing me all the requisite facilities to carry out this work.Also worth here mentioning is the affection and support my brothers have given methrough out my difficult days.At last I am thankful to all those who have helped me directly or indirectly during thisendeavor. I seek pardon and apology for errata, which still remains aversion.Pariyaram. Dr. Mukesh. E
  7. 7. CONTENTSList of TablesList of ChartsList of IllustrationsList of Abbreviations 1-3Introduction ………………………………………………………………..Chapter I – Historical Review……………………………………………. 4-7Chapter II– Conceptual Study II.1. Pandu roga ……………………………………………. 8-40 II.2. Anemia ………………………………………………….41-73 II.3. Laboratory investigations in anemia ………………… 74-85Chapter III- Clinical Study III.1.Patients and Methods………………………………… 86-92 III.2.Observations and analysis……………………………… 93-121Chapter IV- Discussion …………………………………………………… 122-134Chapter V- Summary and Conclusion …………………………………. 135-139References ………………………………………………………………. 140-146Bibliography ……………………………………………………………… 147-149Appendix-Case sheet
  8. 8. List of tables Page noTable No 1 Mithya aharas as Nidana 9Table No 2 Mithya viharas – Sareerika 12Table No 3 Nidana of Pandu Roga 14Table No 4 Classification of Pandu 24Table No 5 Poorva roopas of Pandu 28Table No 6 Samanya roopam 31Table No7 Vathaja pandu lakshanas 34Table No 8 Pithaja Pandu lakshanas 35Table No 9 Kaphaja pandu lakshanas 36Table No 10 Sannipathaja pandu lakshana 37Table No 11 Mirthbhakshanaja pandu laskhanas 37Table No 12 Upadrava of Pandu roga 38Table no 13 Causes of Acquired Hemolytic Anemia 68Table No 14 Classification of Hemoglobinopathies 69Table No 15 Normal Hb values 75Table No 16 Sex wise normal values of red cell indices 76Table No 17 Pathologic red cells in blood smears 85Table No 18 Assessment of vatha symptoms 89Table No 19 Assessment of pitha symptoms 90Table No 20 Assessment of kapha symptoms 90Table No 21 Distribution according to Age group 93Table No 22 Distribution according to sex 93Table No 23 Distribution according to marital status 94Table No 24 Distribution according to educational status 95Table No 25 Distribution according to socio economic status 96Table No 26 Distribution according to Religion 96Table No 27 Distribution according to Occupation 97Table No 28 Distribution according to Diet 97Table No 29 Distribution according to Addictions 97Table No 30 Distribution according to Bowel habit. 98
  9. 9. Table No 31 Distribution according to Pattern of sleep 98Table No 32 Distribution according to Menstrual history 98Table No 33 Distribution according to Saara 99Table No 34 Distribution according to Satmya 99Table No 35 Distribution according to Abhyavaharana sakthi 99Table No 36 Distribution according to Jaranasakthi 100Table No 37 Distribution according to Vyayamasakthi 100Table No 38 Distribution according to status of Agni 101Table No 39 Distribution according to preferred rasa - AMLA 101Table No 40 Distribution according to preferred rasa - LAVANA 101Table No 41 Distribution according to dietary habits – Virudha ahara 102Table No 42 Distribution according to dietary habits Matsya ahara 102Table No 43 Distribution according to dietary habits - Madyasevana 102Table No 44 Distribution according to dietary habits – Mrithbhakshana 103Table No 45 Distribution according to skin appearance 103Table No 46 Distribution according to presence of Icterus 104Table No 47 Distribution according to presence of pallor 104Table No 48 Distribution according to samanya lakshana - Karna kshweda 105Table No 49 Distribution according to samanya lakshana - Dourbalya 105Table No 50 Distribution according to samanya lakshana - Bhrama 105Table No 51 Distribution according to samanya lakshana - Anna dwesha 105Table No 52 Distribution according to samanya lakshana - Shrama 106Table No 53 Distribution according to samanya lakshana - Alasya 106Table No 54 Distribution according to samanya lakshana - Gourava 106Table No 55 Distribution according to samanya lakshana - Aruchi 106Table No 56 Distribution according to samanya lakshana - Nirutsaaha 107Table No 57 Distribution according to samanya lakshana - Nidralu 107Table No 58 Distribution according to samanya lakshana - Pindikodweshtana 107Table No 59 Distribution according to samanya lakshana - Oja kshaya 107Table No 60 Distribution according to samanya lakshana - Alpamedas 108Table No 61 Distribution according to samanya lakshana - Nissaratha 108Table No 62 Distribution according to samanya lakshana - Alpa rakthatha 108
  10. 10. Table No 63 Distribution according to samanya lakshana - Twachi pandutha 108Table No 64 Distribution according to lakshana – Peetha varnatha 109Table No 65 Distribution according to Samanya lakshana- Karshya 109Table No 66 Distribution according to Rasa vaha srothas involvement 109Table No 67 Distribution according to Rakta vaha srothas involvement 109Table No 68 Distribution according to Mamsa vaha srothas involvement 110Table No 69 Distribution according to Medovaha srothas involvement 110Table No 70 Distribution according to Dosha predominance 110Table No 71 showing Mean of the Hb % in both groups 113Table No 72 Distribution according to size of RBC 114Table No 73 Distribution according to Chromasia 114Table No 74 Distribution according to presence of Anisocytosis 115Table No 75 Distribution according to presence of Poikilocytosis 115
  11. 11. List of charts Page noChart No 1 Distribution according to sex 94Chart No 2 Distribution according to marital status 94Chart No 3 Distribution according to educational status 95Chart No 4 Distribution according to Religion 96Chart No 5 Distribution according to Bowel habit 98Chart No 6 Distribution according to Saara 99Chart No 7 Distribution according to Jaranasakthi 100Chart no 8 Distribution according to status of Agni 101Chart No 9 Distribution according to skin appearance 103Chart No 10 Distribution according to presence of Icterus 104Chart No 11 Distribution according to presence of pallor 104Chart No 12 Distribution according to Dosha predominance 111Chart No 13 Distribution according to Hb % 112Chart No 14 Distribution according to ESR in group 1 113Chart No 15 Distribution according to ESR in group 2. 114Chart No 16 Distribution according to Total RBC count in group 1. 115Chart No 17 Distribution according to Total RBC count in group 2. 116Chart No 18 Distribution according to Total leukocyte count in group 1 116Chart No 19 Distribution according to Total leukocyte count in group 2 117Chart No 20 Distribution according to PCV 117Chart No 21 Distribution according to MCV 118Chart No 22 Distribution according to MCH in group 1 119Chart No 23 Distribution according to MCHC in group 1 119 List of illustrationsIllustration no 1 Samprapthi of Pandu rogaIllustration no 2 Mrit Bhakshana janya PanduIllustration no 3 Initial evaluation of anemia
  12. 12. INTRODUCTION Ailment is the inseparable companion of life and with ailments springsimultaneously, the desire which soon turns into the effort to heal and it is thiseffort, whether primitive or advanced that has gone by the name of Medicinein every country.All the systems of medicine should act complementarily or supplement eachother for alleviating the miseries and giving solace to the suffering humanity.Ayurveda is one of the oldest systems of health care dealing with both thepreventive and curative aspects of life in a most comprehensive way andpresents a close similarity to the WHO’s concept of health propounded in themodern era.The tridosha theory forms the pivot on which the science of Ayurvedarevolves. It is the fundamental basis of Ayurvedic physiology, pathology andtreatment. It has held its values over a long period of time from externalinvasions and modifications.It is often criticized that Ayurvedic science is occult and subjective. But in factit has derived its principles by logical analysis and intellectual exercises. Eventhough technology and stress on direct perception have made the currentscience popular, in reality there is no difference in the ultimate goal of themodern science and the ancient one. Many a times it may be required toexplain Ayurvedic principles by comparing them to the facts of modernscience so that we can analyze and perceive it better in the present era.
  13. 13. In order to bring scientific substantiation to the principles of Ayurveda in themodern era and to contribute to its basic principles, the tridosha theory shouldbe supported with solid evidence. The presence of vatha, pitha and kapha ortheir functions in the body should be explicable according to modernparameters or it should be made into quantitative or qualitative data.The difficulty in attempting a perfectly intelligible translation of the tridosha liesin the fact that there is an inseparable blending, of the two entirely differentphenomena of organic life – of the physical with metaphysical and of thephysiological with the psychological.Based on these facts this study was planned to explore the possibilities ofvariation in the laboratory findings of a disease depending upon the doshapredominance. The aim is to derive a possible hypothesis regarding the roleof laboratory investigations in assessing the dosha predominance of a vyadhi.As it is impossible to conduct such a study generally, some specificity shouldbe attributed to it. Here the disease Pandu is selected because the disease iscommon in the society and there is definite delineation in the clinical findingsof Pandu caused by vatha, pitha and kapha. The classical references statethat Raktha dhathu is affected in the pathogenesis of Pandu roga along withrasa dhathu. Objective study of Raktha dhathu is possible by laboratoryparameters. The disease anemia is considered in this aspect as it has similarclinical presentation to that of Pandu roga. Pandu Roga and Anemia havebeen studied in parallel to facilitate a better understanding of the disease andthe laboratory investigations that are conducted in anemia are selected herefor the study.
  14. 14. This study highlights on both conceptual and clinical aspects related to thesediseases. The contents are divided into the following chapters: Ø Chapter I: Historical review. Highlights on the historical aspects of both Pandu roga and Anemia. Ø Chapter II : Conceptual study Deals with conceptual study of both Pandu roga and Anemia. It covers all the relevant matter pertaining to the diseases and Laboratory investigations in anemia. Ø Chapter III: Clinical study. Details of the clinical study of the disease and the investigations conducted. Ø Chapter IV: Discussion Discussion on both Pandu and Anemia, discussions on the clinical study and results have been described. Ø Chapter V: Summary and Conclusion Complete abstract of the dissertation and the conclusion are enumerated.
  15. 15. I. HISTORICAL REVIEW Truthful approach to the study of a disease lies in unraveling the originof the doctrine from the very beginning and tracing its development throughthe various schools of medical thoughts.Charaka has said – “the science of life has always been in existence andthere have always been people who understood it in their own way, it is onlywith reference to its first systematized comprehension or instruction that itmay be said to have a beginning”.1Ayurveda originated in India long back in pre-Vedic period. Rig-Veda andAtharva-veda (5000 years B.C.), the earliest documented ancient Indianknowledge have references on health and diseases.From this period onwards Ayurveda has evolved mainly in 4 periods – Vedickala, Samhita kala, Sangraha kala and the Adhunika kala.Vedic period [5000 B.C]:Ayurveda is regarded as upaveda of Rig-Veda (Kasyapa). Ayurveda is alsoconsidered as upanga or upaveda of Atharva veda because of its similarity.Classification of diseases into 3 vathaja, pithaja and kaphaja has been told inAtharva veda 2.In Rig-Veda and Atharva veda – diseases named Hariman and Harita areexplained. Sayana interprets Hariman as pallor and yellowishness of body3.Similar explanation is found in Rig-veda4.
  16. 16. The author of History of Medicine in India (Pg 20) states “ Hariman and Haritalook like synonyms but on careful examination the former appears to beJaundice while latter as pallor.Prof P.V.Sharma opines – “Initially it is Harita denoting pallor of skin (Pandu)developing further into Hariman (Kamala,Jaundice). In post Vedic texts thesame description about Pandu and kamala is observed. It is interesting tonote that they have retained the Vedic term Hariman in a slightly modifiedform as Halimaka and have described it as a type of kamala”.Rig-Veda prescribes its treatment with morning sun rays5.In Atharva veda6 red cow’s milk and the drug anjana has been said as Haritabheshaja7.Koushika sutra prescribes intake of cooked rice mixed with haridra andanointing the same over the body for this disease8.In Jaiminiya Brahmana there is reference regarding Hariman9.Samhita kala (1000 BC-500 AD):In this period, Ayurveda attained significant development in conceptual as wellas treatment principles. Pandu roga is elaborately dealt with in the Samhithasof this period with its effective treatment. 10Charaka , Susrutha11 and Vagbhata12, all have dealt with Pandu rogaextensively.Sangraha period (500-1700 AD):All the authors of this period including Dalhana13, Chakrapani 14 , Indu15, 16 17Vijayarakshitha , Srikanta datha , Madhavakara18, Sharangadhara19,
  17. 17. 20Bhavamisra , Yogaratnakara21, Arunadatha 22 , and Hemadri 23 have dealtwith Pandu in detail.Adhunika kala (1700 AD onwards):A complete book on Pandu roga has been written by Kaviraja Sri.Ramaraksha Patak. Rasa Tarangini by Sri. Sadananda Sharma andBhaishajya Ratnavali [B.R.Pandu] have also contributed in description ofPandu roga. History of AnemiaThe first recognized anemia was chlorosis, or "the green sickness," commonin girls until the early 1900s. Although the condition was recognized as earlyas the 1500s, the sickness itself was not understood until the 1800s. Frenchphysician Gabriel Andral is credited with introducing the term anemia around1829. Following are some of the landmarks in the field of research in anemia. ⇒ English physician Thomas Addison (1793-1860) gave the first complete description of the disease-"a remarkable form of general anemia"-in 1849. ⇒ American physician James B. Herrick (1861-1954) gave the first clear description of sickle-cell anemia in 1910 which is an inherited disorder. ⇒ Anemia of pregnancy, was first accurately described by German physician Hermann Nasse in 1836; ⇒ Chronic leukemia was described by Rudolf Virchow in 1845. ⇒ German bacteriologist Paul Ehrlich in 1888 differentiated Aplastic anemia.
  18. 18. ⇒ Fanconi’s anemia was named after Swiss pediatrician, Guido Fanconi, which is a form of aplastic anemia.⇒ Anemia of chronic infection was detailed by Adolf Edelmann, an Austrian physician, in 1925.⇒ Acute hemolytic anemia, characterized by rapid destruction of red blood cells, has been described by American pathologist Max Lederer in 1925.⇒ Thalassemia was reported by American physician Thomas B. Cooley (1871-1945) in 1927.
  19. 19. II.1.PANDU Naming of diseases in Ayurveda is based on several factors like ruja,varna, samuthana and other lakshanas. The disease Pandu is named basedon the varna or the color it imparts on the patient. Even though there are otherclinical features indicative of the disease, the prathyathma lakshana of Panduis Pandu varnata.II.1.1Nirukthi: ⇒ The word Pandu is derived from the root “Padi gatou”. ⇒ Pandu is a mixture of shweta and peeta Varna in equal proportions, which resembles the colour of pollen grains of Ketaki flower92. ⇒ In Shabdha kalpa Druma, it is stated that the Pandu Varna can be taken as combination of Shweta and Peeta. Thus it is very clear that the word Pandu is mainly the combination ofShweta and Peeta varna. All of the classics have reference about Panduroga. All the definitions carry nearly the same meaning. The differentdefinitions stated by different authors are as follows: 1. The disease in which Pandubhava is more is termed as Panduroga24. 2. The disease in which Pandutwa is more is called Panduroga25. 3. The disease is named after Pandu varna which is one among the Haritadi varnas explained is Panduroga27. 4. Vijayarakshita and Sharangadhara stated that the disease, which is named after Panduvarna, is called Panduroga26
  20. 20. II.1.2 NIDANA Various nidanas (causative factors) have been told for themanifestation of the disease Pandu in the Samhithas. Broadly they can beclassified into three different groups 1. Ahara. 2. Vihara. 3. Nidanarthakara rogas.1. Ahara:Both apatharpanakaraka as well as santharpanakaraka aharas are told in thenidana of Pandu roga.Table No 1 Mithya aharas as Nidana.Ksharatisevana Excess intake of alkaline foodAmaltisevana Excessive intake of sour foodLavanatisevana Excessive intake of salty foodAti ushna evana Excessive intake of hot foodVirudha ahara Incompatible foodAsatmyabhojana Intake of unwholesome dietNishpavatisevana Excess intake of dolicus speciesMashatisevana Excess intake of black gramPinyakatisevana Excessive intake of oil cakeTila athisevana Excessive intake of gingelyTaila athisevana Excessive intake of gingely oilMadya athisevana Excessive intake of alcoholMrit bhakshana Eating mud or soilAti teekshnapadartha Use of very pungent or spicy food.Etiologies like Asatmya bhojana, Atimadyapana, Kshara, Nishpava, Pinyakathat increase Vata and Pitta are told in the texts. These areapatarpanakaraka. This Apatharpana may be taken as, the inadequate dietaryintake which can cause Anaemia 130,131,132.
  21. 21. Asatmya bhojana – Leads to agnimandya leading to improper nutrition of thedhathus and also leads to dosha prakopa28.Atimadyapana - By the consumption of excessive madya the qualities likelaghu, ushna, teekshna, sukshma, amla, vyavayi, ashukari, ruksha, vikasi,vishada gets increased in the body, leading to dhathu kshaya and toPanduroga29.Ksharatiyoga – All the qualities of kshara like teekshnata, ushnatwa, lavana,tikta kashaya, katu rasas and katu vipaka leads to pitha prakopa and thusleads to Pandu roga30.Nishpava ati sevana – Excess intake of dolichos species can cause vathapitha prakopa and vidaha in the body leading to Pandu roga31.Pinyaka ati sevana – It is pitha vardhaka and gurupaki32.Ati theekshna ahara sevana – These cause pitha prakopa due to its similarqualities with pitha and also lead to dhatu kshaya finally resulting in Panduroga34.Mrit sevana - Intake of mrit (Mud) even though considered as a symptom ofanemia (pica) in modern view, has been told as one of the causative factors ofPandu in Ayurveda. By consumption of mrit (mud) the Tridoshas getsprovoked, the mrut of Kashaya rasa provokes Vatha dosha, that of Ushna(Kshareeya) rasa provokes Pitha dosha and Madhura rasa provokes Kaphadosha. The rusksha nature of mrit causes rukshata to the rasadi dhatus aswell as the ahara and causes srothorodha as it is difficult to be digested. Thenet effect is dhathukshaya and thus Pandu roga34.
  22. 22. Excess intake of Paya, Ikshu, Amla, Lavana, Masha, Asatmyabhojana causeAgnimandya and Ama, which can lead to decreased absorption from theGastro - intestinal tract and cause nutritional deficiency anemia. Even certaindiseases like Grahani can cause the same35.Amisha sevana – Excess intake of mamsa even though causes brimhana,some of the mamsas are ushna in guna leading to pitha prakopa36.Ikshu sevana – Excess intake of ikshu which is madhura, sheetha virya,sngidha and brimhana can lead to formation of ama, srothorodha andimproper nutrition of dhatus37.Paya sevana – Excess intake of milk can lead to agni mandya and Panduroga38.Tila taila – It is ushna and has katu rasa, excess intake of which can lead topitha vridhi39.Masha sevana – Excess intake of masha which is madhura and pitha kaphavardhaka can lead to agnimandya40.Amla – Amla rasa is pitha vardhaka and in excess quantities can lead todhatushoshana41.Lavana – Excess intake leads to pitha prakopa and causes pithaja andrakthaja vikara. Also it causes dhathu saithilya42. According to modern view also food plays a major role in causingPandu roga. Usually malnutrition, particularly the food deficient in folic acid,vitamin B12 and Iron were the causes of Anemia of different varieties43.
  23. 23. 2. Vihara:Table No 2 Mithya viharas – SareerikaDiva swapna Sleeping in day timeVyayamam Excess exerciseVyavayam Sexual congress in excessKarmavaishamyam Improper application of PanchakarmaVegadharana Suppression of natural urgesAthimaithuna, Vegadharana, Divaswapna especially during annavidaha kala,athivyayama44 and Ratrijagarana leads to Pandu roga.Atimaithuna – Excessive sexual indulgence leads to shula, karshya,swasa,Pandu, sukra kshaya and rajayakshma 45.Vegadharana – Suppression of natural urges, especially that of chardi leadsto Pandu roga46.Divaswapna – Sleeping during day time leads to kapha vridhi andsrothorodha47.Karmavaishamyam- Panchakarma pratikarma vaishamya like Sneha-vibhrama is also a nidana for Pandu roga48.Akala Sneha Prayoga49 - If Sneha is given in Sheetakala, Ratrikala to aSlaishmika person, he will suffer from complications like Pandu mainly due toAgnimandya.Atiyoga of Yapana Basti50 -Yapana basti mainly contains Brimhana oushadhiand is given for Yapana of vaya. Excessive administration will causeAgnimandya, Ama and various Rasa, Rakta vahasrothovikaras like Arsha,Jwara and Pandu.
  24. 24. Manasika viharas like kama, chinta, bhaya, soka in excess causes Panduroga. Krodha51, Bhaya and shoka52 produce pitha prakopa. Also all thesefactors may lead to reduced intake of food finally culminating in malnutrition.3. Nidanarthakara Rogas :Susrutha has told that Yakrit and Pleeha roga leads to Pandu roga becauseboth the organs were the sthana of Ranjaka pitta. Other disorders that maylead to Pandu roga are Raktatipravrutti53. Antarlohita54. Raktapittaupadrava55.Rakta Pradara56.Rakta Kshaya57. Rakta Srava58. PunaravartakaJwara59. Grahani60. Kaphaja Arshas 61.Pureeshaja Krimi62. Raktapitta63.Asrugdhara64.Kaphaja Yonivyapad66. Plihodara67. Yakrudalyudara68.Dushyodara69. Vyavaya Shosha70. Pittaja Pratishyaya71. Pittaja Kasa72.Antarmruta Shishu73. Revati Graha74. Shukra Kshaya75. BeejopaghathaKlaibya76. Pitta Dusta Stanya77. Paittika Prameha Upadrava78. Sharkarameha79.Kaphaja Shotha80. Raktaja Gulma81. Rasapradoshaja Vikara82.
  25. 25. Table No 3 Nidana of Pandu Roga:Sl Nidana C.S. S.S A.H M.N B.P DlNo1 Kshara sevana + - - - - -2 Amla sevana + + + + + +3 Lavana rasa sevana + + + + + +4 Atyushna bhojana + - - - - -5 Asatmya bhojana + - - - - -6 Virudha bhojana + - - - - -7 Matsya sevana - - - - - +8 Amisha sevena - - - - - +9 Ikshu sevana - - - - - +10 Pishta sevana - - - - - +11 Paya sevana - - - - - +12 Pinyaka ati sevana + - - - - -13 Mashati sevana + + - - - -14 Madya sevana - + - + + +15 Mrit bhakshana + + - + + +16 Teekshna ahara sevana - + + + + -17 Ati maithuna + - - - - -18 Vega vidharana + - - - - -19 Panchakarma vaishamya + - - - - -20 Ritu vaishamya + - - - - -21 Kama + - - - - -22 Krodha + - - - - -23 Chinta + - - - - -24 Bhaya + - - - - -25 Shoka + - - - - -26 Divaswapna + + - + + +27 Vyayama + + - + + +28 Bharaharana - - - - - +29 Nishpava sevana + - - - - -30 Tila taila sevana + + - - - +
  26. 26. II.1.3 SAMPRAPTHISamprapthi denotes the sequence of events that follows the nidana sevanaand ends up in manifestation of the disease including dosha dushyasammorchana. A detailed study of nidana, dosha, dushya, srothas, agni etcare part of understanding the sampratpthi in a better way. . Pandu can becaused by different etiology like Aharaja, Viharaja, Vaidyakrita,Nidanarthakara roga and even Sahaja factors. Charaka considers Pandu to be a rasa vaha srotho vikara andSusrutha says it as rakthavaha sroto vikara and both opines pitha dosha asthe major factor for the pathogenesis of Pandu. Due to the involvement ofrasa, raktha and ojas the main presenting symptoms are Panduta, indriya-bala- varnahani and nissaratha.Samprapthi of the disease Pandu can be studied under two headings - 1. Samanya 2. Vishesha 1) Samanya: It is the general pathogenesis in which the vitiated Doshas vitiate the Dushyas and Srothas. This is common to all types of Pandu. 2) Vishesha: It is the specific pathogenesis in which the disease is manifested according to the Samanya Samprapthi. However specific etiologies which can aggravate a specific Dosha, slightly modifies the general Samprapthi and produce a specific type of Pandu.
  27. 27. Samanya Samprapti: The study of Samprapthi ghatakas will help us to understand the pathogenesis in a better way. The Samprapthi ghatakas of Pandu are -1) Dosha93- Pitha pradhana tridosha2) Dooshya94- Rasa, Raktha, Medha3) Agni- mandagni4) Srothas- Rasa vaha srothas Rakthavaha srothas5) Udbhava sthana – Amashaya6) Sanchara sthana- Dashadhamanis and Sarvashareera7) Vyakta sthana – Sarva shareera8) Ashraya- Twak and Mamsa1) Dosha: Pandu is a disease caused by pitha pradhana tridosha prakopa93.Pitha: The predominantly involved Pitha are as follows-Pachaka Pitha: This is the first Pitha, which gets vitiated because of Nidanasevana and causes Agnimandya, Aruchi, Rasa pradosha and further canproduce Dhatu shaithilya.Ranjaka Pitha: Mulasthana of Ranjaka pitha is Yakrut, Pliha95andAmashaya96. Similarly, studies in contemporary science have also proved thatLiver and Stomach have a significant role in production and maturation ofRBC’s. In 1926, Minot and Murphy showed that liver was most effective in
  28. 28. treating Anemia in dogs. A factor in liver is essential for the maturation oferythrocytes and is demonstrated to be associated with non-protein fraction ofliver substance that is known as Anti Anemic or Haematinic principles. (Rickset. al. 1945). Ranjaka pitha gives Raga to the Raktha poshaka sara bhaga of Rasaand produces Raktha97. When this Ranjaka pitha is vitiated, it producesRaktha that is altered either quantitatively or qualitatively.Sadhaka pitha: This should be considered as the seat of sadhaka pitha ishridaya and the prakupitha doshas are taking hridaya as ashraya in Pandu.Vitiation of this Pitha cause Rasa dhathu agnimandya leading to Anutpadanaor Kshapana of Rakta poshaka sara bhaga. Sadhaka pitha vitiation producesthe psychological manifestations like krodha and Mrit-bhakshana in Pandu.Kapha:Pandu is told as one among the santharpana janya vyadhi98. Santharpanaleads to kapha prakopa in the body and Kaphaja vyadhi produces lakshanaslike Pandutwa and Panduta99. In spite of the Kapha being in its Prakrutha avastha, the decreasedVatha displaces it along with Pitha to all parts of the body causing Pandu100. Kapha in Twacha produces Shwetavabhasata. Kapha in Rakthaproduces Pandu101. Also avalambaka kapha should be considered in thiscontext as its seat being hridaya.Vatha: Vyana Vayu in Hridaya is responsible for the spread of the vitiatedPitha via the Dasha dhamanis to the whole body102. Also the dhathu kshayaor shaithilya that occurs in the Samprapthi leads to vatha prakopa in the body
  29. 29. and is responsible for some of the samanya lakshana of Pandu like karnakshweda etc.2) Dhatu:Rasa dhathu:Pandu is considered as a Rasa Pradoshaja Vikara129. Chakrapani commentsthat the aggravated Pitha causes Kshapana of the Raktha poshaka rasa andit’s Anutpadana. This in turn results in impaired preenana function of rasadhathu producing Dhathu shaithilya103. The symptoms indicating the rasainvolvement are Hritspandana104 (A.S.Su19/10), Hridrava105 and Shrama106.Raktha dhathu: In Samprapthi it is said that there is alparakthatha107. The doshas will 108vitiate Raktha dhathu (Raktham vidushya) and produce Panduta inTwacha.Chakrapani says Ojo guna kshaya means Raktha dhatu roopa oja kshaya, asRakta dhathu is similar to Ojus109. “Nayati Rudhira Shosham” is theexplanation given by Harita to denote Alpa rakthata110. Excess blood loss andArtava atipravruthi produces Pandu111. There will also be a desire towards 112.intake of blood The symptoms of raktha involvement are TwakRoukshya113, Twak Sphutana114, Bhrama115, Trushna116, Manda anala117 andPandutwam118.Mamsa dhathu:The term Mamsam Pradushya119 is used while explaining the samprapthi ofPandu. Again it is told that the vitiated doshas takes ashraya between twak
  30. 30. and mamsa leading to the discoloration. The symptoms of its involvement areGatra Toda120, Shrama121 and Gatra Roukshya122.Medo dhathu:Alpa meda123 is one of the main feature of Pandu roga which denotes theimpaired nutrition of the dhathus either due to mandagni or rasa and rakthadushti. The symptoms are Shrama124, Gatra Roukshya125and Mamsa KshayaLakshanas126.Ojas: Ojo Guna kshaya is the feature mentioned in the context of Pandu127. Inclassics Prakruta Kapha, Rasa, Raktha, Shukra, Sarva dhathu sara and Agniare also referred to as Ojas128. As per the pathology the general nutrition ofthe dhathus are affected in Pandu roga leading to the kshaya of sarva dhathusara i.e. the ojas.3) Agni: All three forms of agni viz jataragni, bhoothagni and dhathwagni areaffected in the pathogenesis of Pandu roga. Nidanas initially vitiates thejataragni and this inturn affects the other two forms as they are dependent onjataragni for their normal functions. As the nidanas are pitha kara in nature thedravatwa of pitha is increased leading to agnimandya. This leads to formationof ama rasa which then circulates all over the body leading to dhathu gourava.4) Srothas: Important Srothas affected in Pandu are Rasavaha andRakthavaha srothas. 1. Rasavaha srothas: Pandu is a Rasa pradoshaja vikara129. The involvement of rasavaha srothas can occur due to the specific nidana sevana or as the doshas takes hridaya as ashraya which is the moola of rasa vaha
  31. 31. srothas. The symptoms indicating its involvement are Hridrava130, Hridaya spandana131, Tama132, Aruchi132, Agninasha132, Jwara132, Angasada132, Pandutwa132, Shrama131 and Trushna131. 2. Rakthavaha srotas: Yakrit and Pliha are the Rakthvaha srothomula. Rasaranjana takes places in Yakrit and Pliha. The improper formation of Rasa dhathu leads to improper formation of Raktha133. Vitiation of pitha can directly lead to raktha dushti according to the ashrayashrayi bhava134.6) Udbhava sthana: Pandu is an Amashaya samutha vyadhi, after reaching toHridaya (Srotomula) the Doshas spreads throughout body.7) Sanchara Sthana: After taking hridaya as ashraya, the pitha pradhana doshas circulate allover the body through dasha dhamanis with the help of vyana vayu135.8) Ashraya: In Pandu, the Doshas take Ashraya135 between Twak and Mamsathereby causing vitiation of different Dhatus and producing different Varnas.Varna bheda in Pandu roga: An overview of the diverse discoloration of different body parts inPandu roga is useful in this context. According to classics Pitha dosha andRakta dhathu are responsible for Varna prasadana (Agni guna bhuyishta).
  32. 32. Pandu is a vyadhi that is named on the basis of discolouration of skinand this discolouration is elaborated in detail.Different discolourations of the body parts in Pandu are -Twak: • Varnakshaya135 • Varna nasha136 • Pandu137 • Haridra137 • Krushna Panduta138 • Arunangata138 • Shwetavabhasata139 • Pandura140Akshi: • Krushna140 • Peetata141 • Shuklata142 • Arunata143Mukha and Nakha: • Sweta144 • Peeta145 • Krushna146 • Aruna147Sira: • Sweta.148
  33. 33. • Peeta.149 • Krushna.150 • Aruna.151 Colour of the skin depends not only on Hb level in blood but also on the state of blood vessels, the amount of fluid in the subcutaneous tissue and the degree of skin pigmentation. Pallor of the palms particularly skin creases are more reliable than pallor elsewhere. Pallor of nail beds, mucous membrane of mouth and conjunctiva are more reliable than pallor of skin. Skin discolourations in anemia: • Dead white colour of skin- severe acute blood loss. • Pallor with ash tint of the skin- Acute Leukemia. • Lemon or Pale yellow-Advanced Pernicious Anemia. • Petechiae in Anemia-Thrombocytopenia. • Ecchymosis - Thrombocytopenia or disturbed coagulation.Vishesha samprapti: Even though Pandu is a disease caused mainly bypitha prakopa, predominance of either of other two doshas at one or otherstages of samprapthi leads to manifestation of the specific Pandu roga. 1) Vathaja Pandu- Etiological factors, which mainly increase vatha along with pithadi doshas, lead to the production of Pandu roga with vatha anubandha producing vathaja Pandu. 2) Pithaja Pandu- Etiological factors, which mainly increase pitha along with other doshas, leads to the production of pithaja Pandu.
  34. 34. 3) Kaphaja Pandu- Etiological factors, which mainly increase kapha along with pithadi dosha, leads to production of Pandu roga with kapha anubandha thus producing kaphaja Pandu. 4) Tridoshaja Pandu- Etiological factors, which mainly increase all the tridosha simultaneously, lead to production of tridoshaja Pandu. 5) Mrit bhakshanajanya Pandu67- Habitual indulgence in eating mrit aggravates one of the tridoshas. If the mrit is of kashaya rasa, then it aggravates vayu. If it is ushara, then pitha gets aggravated, if it is madhura kapha. Because of its ruksha, guna the mrit causes rukshata in the rasa then the undigested mrit produces avarodha of srotas and causes indriya bala hani, agnimandya and thus producing Pandu. Samprapti bheda of pandu 1) Sankhya samprapti: § 5 types of Pandu (Charaka and Vaghbata) § 4 types of Pandu (Sushruta) § 8 types of Pandu (Harita)Table No 4 Classification of PanduSl. C.S S.S A.H M.N H.SNo1. Vataja Vataja Vataja Vataja Vataja2. Pittaja Pittaja Pittaja Pittaja Pittaja3. Kaphaja Kaphaja Kaphaja Kaphaja Kaphaja4. Sannipataja Sannipataja Sannipataja Sannipataja Sannipata ja
  35. 35. 5. Mrut Mrutb Mrut Mrut bhakshanaja hakshanaja bhakshanaja bhakshanaja6. Kamala7. Kumba Kamala8. Haleemaka 2) Vidhi samprapti: The sequence in which the kupitha dosha leads to dosha dushya sammurchana and manifestation of vyadhi is vidhi samprapti (Illustration No.1). The swatantra Pandu is sadhya and paratantra Pandu is kashta sadhya. 3) Vikalpa samprapti: The amshamsha kalpana of the samprapti of Pandu is seperately dealt under the heading of samprapti ghatakas of Pandu. 4) Pradhanya samprapti: Pradhana dosha – pitha pradhana tridosha Swatantra Pandu is pradhana Nidanarthakara roga janita Pandu is apradhana Anubandhya Pandu is apradhana 5) Bala samprpati: The bala or strength of Pandu depends on the nidana and degree of manifestation of poorvaroopa and roopa. Pandu with Upadrava and Asadhya lakshanas are difficult to treat. 6) Kala samprapti:
  36. 36. It is the samprapti that confirms the role of a particular dosha in a disease i.e. the bala that produce the disease or increase its intensity with change in time like dina, ratri etc. or in accordance with the stage of digestion.Kulaja Pandu roga:Even though the reference about a kulaja Pandu roga is not available in ourclassics, many of the hereditary anemias presents as Pandu roga. A possibleexplanation of this should be formulated for better understanding of thedisease. A corresponding bheeja bhaga dushti may lead to the manifestationof the specific type of disease152. In case of Pandu dushti of the bheeja bhagaor bheeja bhaga avayava of rasa vaha and raktha vaha srothas may lead tomanifestation of Pandu. Raktha, hridaya, yakrith and pleeha are derived fromthe mathrija bhavas153 and all these avayavas are having role in themanifestation of Pandu roga. Hence any dushti of the matrija bhavas can leadto defects in the formation of these. In Mahabharata154, there is referenceabout Pandu who was the king of Hastinapura. The narration about how hegot this name gives a clue to this pathology. II.1.4 POORVAROOPA Poorva roopas or prodromal symptoms of a disease gives clues to thefuture manifestation of it, thus helps in arresting the disease process. Theseare produced during the stage of Sthana samshraya of vitiated doshas. Poorvaroopa may continue to exist in the actual state of disease asRoopa; some may disappear.1) Hridaya Spandana:
  37. 37. Pandu is a disease where rasa dhathu and raktha dhathu is affected. Hridaya being the moola of rasa vaha srothas will be exhibiting the features of rasa kshaya.2) Twak Roukshya or Twak Sphutana: Twak Roukshya or Twak Sphutana can be produced by rasa kshaya along with localization of vitiated vayu in twak.3) Swedabhavata: Sweda is mala of meda and in Pandu there is kshaya of medas.4) Shrama: This is also caused by rasaadi dhathu kshaya.5) Shteevana and Hrillasa: Due to Malaroopi kapha vriddhi produced by Rasa dhathwagnimandya, Shteevana and Hrillasa are seen in Pandu.6) Gatrasada: Rasa and ojokshaya leads to gatra sada.7) Mrit-bhakshana Iccha: it occurs due to the prabhava of the disease.8) Prekshana Kuta shotha: Increased Malaroopi kapha cause Srotorodha, thus causing Prekshana kuta shotha.9) Aruchi, Avipaka, Alpavahnita: Pitha prakopa leads to agnimandya producing Aruchi etc.10) Peetata of Vit and Mootra: These are due to pitha vridhi in the body.11) Rakthalochana:
  38. 38. Increased Pitha causes various discolorations like Rakthata, Peethataetc. of the body. 12) Shareera Pandutva: pandutwa is caused by the pitha vridhi along with predominance of kapha.Table No 5 Poorva roopas of Pandu.Sl Signs and C.S S.S A.H B.P M.N Sh.Sno symptoms1 Hridaya spandana Palpitation + - + - - -2 Roukshyam Dryness of skin + - + - -3 Swedabhava Anhidrosis + - + - - -4 Shama Fatigue + - + - - -5 Aruchi Anorexia - - + - - -6 Gatra sada General debility - + + + + -7 Alpavahnitha Impaired - - + - - - digestion8 Peetamootra Yellowish urine - + + + + -9 Twakspotana Cracking of skin - + - + + -10 Shteevana Spitting - + - + + - (Nausea?)11 Mritbhakshanecha Pica - + - + + -12 Akshikuta shotha Peri-orbital - + - + + - edema13 Peetha vit Yellow stool - + - + + -14 Avipaka Indigestion - + - + + -
  39. 39. II.1.5 ROOPA The term Roopa means signs and symptoms through which a diseaseis diagnosed or the clinical manifestations of the disease. Depending upontheir aid in identification and differential diagnosis of a disease, signs andsymptoms can be classified as follows: 1. Pratyatma Lakshana (cardinal signs & symptoms). 2. Samanya Lakshanas (general signs& symptoms) 3. Vishista Lakshanas (distinguishing features of doshanubandha)Pratyatma Lakshana:It is that lakshana by which the initial identification of a disease is done. The invariable feature, Panduvarna of twacha is considered as thePratyatma Lakshana of Panduroga. This is an abnormal colour imparted tothe skin due to Rasa and Rakta kshaya in the body. This colour is almost likethe pollens of Ketaki flower.Samanya Lakshanas84:These are the lakshanas that are found in the disease along with itspratyatma lakshana. Roopa may change from time to time according toprogression or regression of the disease. Some may newly appear and somemay disappear1) Karna Kshweda: Due to sithilendriyatha and increased Vatha, there will be abnormal sounds heard in the ears.2) Hataanala: Malfunctioning of agni will occur due to pitha prakopa.
  40. 40. 3) Dourbalya: Rasaadi dhathu kshaya leads to general debility in Panduroga.4) Karshya: Reduction of various Dhathus in body leads to affliction ofSamhanana leading to emaciation of Spik, Udara, Greeva and prominence ofDhamani jaala.5) Gatra peeda: Different types of pain in the different parts of the bodycaused by Vatha vriddhi due to dhathu kshaya.6) Pindikodweshtana: vatha prakopa and rasa kshaya leads to pain in thecalf region.7) Shoonakshi kuta shotha and shtivana: This is the continuation of signfrom Poorvaroopa stage. Kapha vriddhi producing Srothorodha producesShoonakshi kuta shotha8) Sheerna lomata: It is due to Asthi dhathu kshaya83.9) Hridrava: Involvement of Sadhaka pitha, Vyana vayu, Rakthavahasrothodushti and the localization of doshas in hridaya cause Hridrava.10) Swasa: Rasa kshaya leads to weakness in the hridaya which is alsomoola for the prana vaha srothas. This leads to swasa. In Samanya lakshanait refers to Arohana Ayasa (exertional dyspnea) i.e Kshudra Shwasa.11) Bhrama: Vatha-pitha-rajogunadhikya leading to various dhathu kshayalike Majja and Raktha producing Bhrama.12) Annadwesha: Charaka mentioned both Annadwesha and Aruchi inSamanya lakshana. Susrutha has mentioned this in Upadrava stage and iscaused due to Kapha vriddhi and Agnimandya.13) Gourava: Heavyness of body indicates Kapha and Amavriddhi.14) Jwara: Indicates Pitha prakopa.
  41. 41. 15) Harita Varna: Indicates Pitha vriddhi.16) Hata prabhatwa: Pitha prakopa, Oja kshaya cause Prabha hani.Table No 6 Samanya roopam.Sl Signs and C. S.S A.H B.P M.N Sh.Sno symptoms S1. Karnakshweda Tinnitus + - + - - -2. Hataanala Loss of appetite + - + - - -3. Dourbalya Weakness + - + - - -4. Sadana Malaise + - + - - -5. Annadwesha Aversion to food + - + - - -6. Shrama Exertion + - + - - -7. Bhrama Dizziness + - + - - -8. Gatrasoola Body aches + - + - - -9. Jwara Fever + - + - - -10. Gourava Heaviness of + - + - - - body11. Swasa Dyspnoea + - + - - -12. Aruchi Anorexia + - + - - -13 Gatra saada Feeling tired + - - - - -14. Gatra peeda Squeezing pain + - + - - - of body15. Gatronmathana Pounding pain + - - - - - of body16. Soonakshiluta Puffiness of eye + - + - - - lids17. Haritha varnatha Greenish colour + - - - - -18. Seerna lomatha Falling of hair + - + - - -19. Hatha prabha Loss of body + - - - - - luster20. Kopanathwa Short tempered + - + - - -
  42. 42. 21. Sisiradweshi Aversion to + - + - - - coldness22. Nidraluthwam Sleepiness + - - - - -23. Shteewana Spitting + - + - - -24. Alpa vaak Reduced talk + - + - - -25. Pindikodweshtana Cramps in calf + - - - - -26. Kati ruk Lumbar pain + - - - - -27. Uru ruk Pain in thighs + - - - - -28. Pada ruk Pain in feet + - - - - -29. Kati saada Lumbar + - - - - - flabbiness30 Uru saada Flabbiness in + - - - - - thighs31. Paada saada Flabbiness in + - - - - - feet32. Arohanaayaasa Dyspnoea on + - - - - - exertion33. Dhatu shaithilya Disruption of - - + - - - dhatus34. Ojogunakshaya Diminished ojas + - + - - -35. Alparakthatha Reduced qty of + - + - - - blood36. Alpa medaskatha Decreased + - + - - - medas37. Nissaratha Reduced sara + - + - - -38. Sithilendriya Impaired + - + - - - function of sense organs39. Hridravatha Discomfort in - - + - - - chest40. Sanna sakthita Reduced - - + - - - strength in lower limbs
  43. 43. Vishishta Lakshanas: These are the features that help to differentiate adisease according to its dosha predominance. These are produced bypredominance of the specific doshas in the disease process and are importantto plan the treatment and for prognosis of the disease.• Vathaja Pandu85: Vatha vriddhi produces various Vathaja manifestations in thepresentation of Pandu roga like Krushnata, Panduta and Arunangata of bodyparts, various types of Shoola. (See table no 7)• Pithaja Pandu86: Pitha vriddhi produces various Pithaja presentations like Peetabhata,Haritabhata, Jwara. (See table no 8)• Kaphaja Pandu87: Kapha vriddhi produces various Kaphaja manifestations likeShuklavarnata, Gourava and Shwayathu. (See table no 9)• Tridoshaja Pandu:Tridosha prakopa causes presentation of all the Tridoshaja lakshanas.Madhavakara has told sanipathaja pandu lakshanas. (See table no 10)• Mritbhakshanaja Pandu88: Mrit bhakshana causes Agnimandya, Roukshyata of body, Shotha,Dhathu dourbalya, Indriya-Teja-Bala-Oja-Virya kshaya and Krimi etc.Madhavakara has considered Mritbhakshana as vyadhi hetu. Susrutha has
  44. 44. considered this under Tridoshaja Pandu as Mritbhakshana produces Tridoshaprakopa. (See table no11).Table No7 Vathaja pandu lakshanasSl Signs and C.S S.S A.H B.P M.N Sh.Sno symptoms1. Krishna Blackish pallor + - - - - - pandutha2. Rukshangatha Dryness of body + - - - - -3. Arunangatha Reddish color of + - - - - - body4. Anga marda Crushing pain + - - - - -5. Ruja Pain in the body + - - - - -6. Anga toda Piercing pain + - + + + +7. Kampa Tremors + - + + + +8. Parswa ruja Pain in flanks + - + - - -9. Siro ruja Head ache + - + - - -10. Varcha sosha Scarce stools + - + - - -11. Asya vairasya Tastelessness + - + - - -12. Sopha Edema + - + - - +13. Anaha Flatulence + - + + + -14. Balakshaya Debility + - - - - -15. krishnekshana Blackish eye - + - + - -16. Krishna Blackish veins - + - - - - siravanadhata17. Krishna nakha Blackish nails - + + - - -18. Krishna anana Blackish face - + - - +19. Krishna vit Blackish stools - + + - - -20. Krishna Blackish urine - + + + + + mootratha21. Roosksha sira Dry veins - - + - - -22. Ruksha nakha Dry nails - - + - - -23. Rooksha vit Dry stools - - + - - -24. Rooskha mutra Rooksha urine - - + + + -25. Rooksha netra Dry eyes - - + + + -26. Aruna siratwa Red colored - - + - - - veins27. Aruna nakha Reddish nails - - + - - -28. Aruna vitkata Reddish stools - - + - - -29. Aruna mootra Reddish urine - - + + + +30. Aruna netrata Reddish eyes - - + + + -31. Gatra ruk Body ache - - + - - -32. Rooksha twak Dry skin - - - - + -33. Bhrama vertigo - - - - + +
  45. 45. 34. Krishna twak Blackish skin - - - - + +35. Aruna twak Reddish skin - - - - + +36. Twak sphotana Cracking of skin - - - + - -Table No 8 Pithaja Pandu lakshanas:Sl Signs and C.S S.S A.H B.P M.N Sh.Sno symptoms1. Gatra peethata Yellowish body + - + + - + color2. Harithabhata Greenish body + - + - - - color3. Jwara Fever + - + - - -4. Daha Burning + - + + + + sensation5. Trishna Thirst + - + + + +6. Murcha Syncope + - + - - -7. Peeta mootra Yellowish urine + + - + + +8 Peeta sakrith Yellowish stools + + + + + +9. Swedana Excess sweat + - + - - -10. Tama pravesa Black outs + - + - - -11. Seeta kamatha Desire for cold + - + - - - attires12. Anannabh- Anorexia + - - - - - inandana13. katukasyata Pungent taste in + - + - - - mouth14. ushnanupasaya Aggrevated by + - - - - - hot15. Amlanupasaya Aggrevated by + - - - - - amla16. Vidaaha Burning + - - - - - sensation17. Amlodgara Sour eructation + - + - - -18. Dourgandhya Unpleasant + - + - - - odour19. Bhinna varcha Loose bowels + - + + + +20. Dourbalya Debility + - - - - -21. Peetekshana Yellowish eyes - + + + + +22. Peeta sira Yellowish veins - + + - - -23. Peeta nakha Yellowish nails - + + + - -24. Peeta anana Yellowish face - + + - - -25. Anna vidagdata Abnormal + - - - - - fermentation of food26. Ati peeta vit Deep yellowish - - - + + - stools
  46. 46. Table No 9 Kaphaja pandu lakshanas :Sl Signs and C.S S.S A.H B.P M.N Sh.Sno symptoms1. Gourava Heaviness of + - - + + + body2. Tandra Lassitude + - + + + -3. Chardi Vomiting + - - - -4. Swethavabhasatha Whitish color + - - - - - of body5. Praseka Salivation + - - - + -6. Lomaharsha Horripilation + - + - - -7. Sada Loss of + - - - - - strength8. Murcha Syncope + - - - - -9. Bhrama Vertigo + - - - - -10. Klamam Exhaustion + - - - - -11. Swasa Dyspnoea + - - - - -12. Kasa Cough + - + - - -13. Alasya Laziness + - - + + -14. Aruchi Anorexia + - - - - -15. Vakgraha Difficulty to + - - - - - speak16. Swara graha Dysphonia + - - - - -17. Sukla moothra Whitish urine + + + + + +18. Suklaakshi Whitish eyes + + + + + +19. Sukla varcha Whitish stools + + + - + +20. Katukamata Desire for + - - - - - pungent taste21. Rooksha Desire for dry + - - - - - kaamatha attires22. Ushna kamata Desire for hot + - - - - - things23. Swayathu Oedema + - - + + -24. Madhurasyatha Sweet taste in + - - - - - mouth25. Sukla nakha Whitish nails - + + - - -26. Suklanana Whitish face - + - + + -27. Sukla sira Whitish veins - + + - - -28. Lavana vakthra Salty taste in - - + - - - mouth29. Swarakshaya Dysphonia - - + - - -30. Sukla twak Whitish skin - - - + + +31. Agni mandya Loss of - - - - - + appetite
  47. 47. Table No 10 Sannipathaja pandu lakshanaJwara - FeverArochaka - AnorexiaHrillasa - NauseaChardi - VomitingThrishna - Excessive thirstKlama - ExhaustionHatendriya - Dysfunction of sense organsIt is asadhya.Table No 11 Mrit bhakshanaja pandu laskhanas :Sl Signs and C.S S.S A.H B.P M.N Sh.Sno symptoms1 Balanasa Loss of strength + - - - + -2 Varna nasa Loss of + - - - + - complexion3 Agni nasa Impaired + - - - + - digestion4 Shunaskhikuta Puffiness of eyes + - - - + -5 Shunabhru Puffiness of eye + - - + + - brow6 Shuna nabhi Umbilical edema + - + + + -7 Shuna pada Pedal edema + - + + + -8 Shuna Genital edema + - + + + - mehana9 Krimi koshtata Intestinal worms + - - + + -10 Atisara Diarrhea + - - + + -11 Sasruk mala Blood mixed + - + + + - stools12 Sakapha mala Mucoid stools + - + + + -13 Bhinna vit Unformed stools - - + - - -14 Pureesha Worms in stools - - + - - - krimi15 Shuna anana Puffiness of face - - + - - -16 Indriya nasa Malfunction of + - - - + - sense organ17 Tandra Lassitude - - - + - -18 Alasya Laziness - - - + - -19 Sada Malaise - - - + - -20 aruchi Anorexia - - - + - -21 Soola Body pain - - - + - -
  48. 48. II.1.6 UPADRAVAThese are the disorders that manifest due to the same dosha dushti as themain disorder and occur in the later stages of the disease. If mild, theysubside by the treatment of the main disease and if severe they should betreated separately.Table No 12 Upadrava of Pandu roga 90:Sl. Vatha dosha Pitha dosha Kapha doshaNo.1. Hridaya peedanam Pipasa Aruchi2. Shwasa Jwara Agnisada3. Atisara Moorcha Shopha4. Kasa Abalatwa Chardi5. Shoola Daha Klama6. Swarabhedha Avipaka7. Swarasada8. Moorcha II.1.7 SADHYASADHYATA The signs, symptoms and other conditions indicating the incurability of Panduroga are as follows89: 1) When the disease is Chirotpanna. 2) When excessive Rukshata (Khaributa) has appeared in the patient. 3) When the patient is afflicted with Shotha due to the Kalaprakarsha of the disease. 4) When the Vit pravrutti is Alpa or Baddha.
  49. 49. 5) When the patient views everything as yellow. 6) Athisara with Harita and Sakapha mala pravruthi is present. 7) Deenatha. 8) Swetati-dagdanga. 9) When afflected with Chardi, Murccha, Trushna. 10) Pandu, Shwetavabhasa, due to Ati asruk kshaya. 11) Shotha in Antha (extremities) and emaciation of the trunk. 12) Shotha in trunk and wasting of Antha (extremities). 13) Shotha in Guda pradesha, Shepha and Mushka. 14) Tama pravesha. 15) Samgnyahani. 16) Jwara and Athisara. 17) Panduta of Danta-nakha-netra and Pandudarshi. 18) Mlanata, Indriya dourbalya, Tridoshaja Pandu rogi. 19) Complications of Pandu are difficult to treat and cannot be treated. II.1.8 Arishta lakshana The lakshanas that indicate the imminent death are called as Arishtalakshanas91 • Pandu varnata in excess. • Ati krushata. • Trushna. • Kupita ucchwasa. II.1.9 Treatment of Pandu roga Treatment advised for Pandu can be divided into two- 1. Shodhana 2. Shamana
  50. 50. Shodhana: - a) Snehana is done • This is done to produce dosha utklesha in case of shodhana. • To combat Alparakthata, Alpamedaska and Ojokshaya. b) Swedana Mridu swedana may be performed. c) Shodhana is done for Koshta Shuddhi. Both urdhwa and adho Shodhana in accordance with the condition ofrogi can be done depending on the bala of the patient. Shamana Oushadaand Pathya should follow Shodhana. In Mrit bhakshanajanya Pandu ChikitsaTeekshna Shodhana is done in order to remove the ingested Mruttika.Shamana: - In Shamana various single and compound preparations were told;which includes herbal, mineral and herbo-mineral preparations.
  51. 51. Illustration No 1 Samprapthi of Pandu roga Nidana sevana 1 1 Pitha pradhana Agni dushti Rasa vaha and tridosha parkopa rakthavaha srotho dushti Hridaya prapthi 2 Circulation through dasha dhamanis by vyana vayu 3 Rasa vaha and Raktha vaha srothas Dosha dushya Twak sammorchana mamsantharasraya 4 Dhathu shaithilya and dhathu gourava Alpa Raktha, alpa medas, nissara, shithilendria, oja kshaya Poorva rupa 5 Varna hani and samanya lakshanas 5 types of Pandu 1. Sanchaya 2. Prakopa 6 3. Prasara Upadrava, asadhya 4. Sthana samsraya lakshana and rishta 5. Vyaktha lakshana 6. Bheda
  52. 52. Illustration No 2 Mrit Bhakshana janya Pandu Mrit bhakshana Kashaya Vatha Ushara Pitha Madhura Kapha Avipakwatha Agni mandya of mrit and srotho rodha Dhathu shaithilya Indriya bala, ojo hani Respective dosha prakopaja Pandu
  53. 53. II.2 ANEMIAIntroductionAnemia signifies a decreased amount of hemoglobin in the blood. Anemia isdefined as a hemoglobin concentration in blood below the lower limit of thenormal range for the age and sex of the individual. In adults the lower extremeof the normal hemoglobin is taken as 13.0g/dl for males and 11.5g/dl forfemales. Anemia per se is not a diagnosis but sign of a disease.There is a decrease in the amount of oxygen reaching the tissues and thedifferent organs leading to the specific signs and symptoms. Hemoglobin ispresent in the red blood cell, i.e. about 95% of the dry weight of a red bloodcell is due to the hemoglobin content. Practically all the functions of the redblood cells are due to hemoglobin, which picks up, carry and disgorge oxygenas well as carbon dioxide.General signs and symptoms of anemia155:The presenting features of anemia are tiredness, easy fatigability, generalizedmuscular weakness, lethargy and headache. In older patients there may besymptoms of cardiac failure, angina pectoris, intermittent claudication,confusion and visual disturbances.Signs include pallor, hyper dynamic circulation, attacks of faintness, retinalhemorrhages, menstrual disturbances, mild proteinurea, anorexia andflatulence.
  54. 54. II.2.1 GENERAL CONSIDERATIONSErythropoiesis156A general overview of the hematopoiesis is necessary to understand anemiain detail. As early as the third week of gestation, blood cells are formed in theyolk sac outside the embryo. The liver and spleen take up hematopoiesis aftera few weeks. The bone marrow progressively takes over this function after the20th week. After birth hepatic and splenic hematopoiesis ceases and bonemarrow is the only site for blood formation. Normally in adults only the marrowin the axial skeleton, skull and end of long bones is active the rest remains ina dormant stage. In the adult 30% of hemopoiesis takes place in the pelvicbones. The bone marrow is a highly organized tissue supported by reticularcells and anchored in a spike like vascular structure. Functionally there aretwo components- 1. The micro environment- consists of the stromal cells, accessory cells and extra cellular matrix formed by them. The stromal cells include fibroblasts, macrophages, endothelial cells and adipocytes. The macrophages elaborate a wide range of cytokines, which influence growth of marrow cells either stimulatory or inhibitory. Function of the stroma is to provide a structural framework for the blood-forming cells and to produce cytokines. 2. The hematopoietic stem cells in various stages of proliferation and maturation- a rich network of blood vessels empties blood into sinuses. The hematopoietic cells lie in cords and islands between the vascular sinuses in a meshwork of reticular cells. Erythrocytes, myeloid cells and megakaryocytes develop outside the vascular compartment.
  55. 55. The pleuripotent stem cell differentiates first into the myeloid cell progenitor CFU-S (colony forming unit spleen). From this cell the progenitors of erythroid (BFU-E), myeloid and Monocyte cells (CFU- GM) and megakaryocytes (CFU-MK) arises. CFU-GM further differentiates into the precursor of macrophages (CFU-M) and granulocyte (CFU-G). Lymphoid cells arise in the bone marrow from the lymphocyte precursor.Erythrocyte formationThe most primitive committed erythropoietic precursor cells are callederythroid burst forming cells (BFU-E), since they give rise to multiple subcolonies when they are grown in vitro. As the primitive progenitor cellsreplicate and mature they become increasingly sensitive to erythropoietin andform erythroid colonies more rapidly (Erythrocyte colony forming units CFU-E). These develop into erythroblasts and erythrocytes. Erythropoietin is themain hormone which controls the proliferation and maturation of erythroidprecursors.Stages in the Development of ErythrocyteThere are different stages in the process of maturation of the erythrocytes.These are the proerythroblast, basophilic, polychromatophilic, andeosinophilic normoblasts, reticulocytes and mature erythrocytes. The nucleusof the normoblast degenerates and it is extruded to give rise to theretuclulocyte. In this cell, ribosomes, mitochondria and golgi apparatus persistfor a short time. These cytoplasmic organelles reveal a granular or strand likepattern when stained with vital stains like brilliant cresyl blue. These are called
  56. 56. reticulocytes. The remnants of the degenerating nucleus which are in theprocess of extrusion are demonstrable as Howell – Jolly bodies and Cabot’srings.The R.B.CThe mature erythrocyte is a non nucleated circular, biconcave disc mostsuited to perform the function of gaseous exchange. It has a diameter ofabout 7.5µm and thickness of 2µm. It contains hemoglobin and is the heaviestof all the formed elements. It is a highly specialized, metabolically active cellwhich obtains energy by utilizing glucose by anaerobic pathways. It isprovided with enzymes which are required for metabolism of glucose. Someof the important enzymes that take part in anaerobic glycolysis arehexokinase, glucose -6-phosphate isomerase, phosphofructokinase, andaldolase. Those taking part in oxidative glycolysis are glucose-6-phosphatedehydrogenase (G-6-PD), 6-Phospho gluconate dehydrogenase,transketolase and transaldolase. This pathway is connected with glutathionemetabolism through the enzymes glutathione reductase and glutathioneperoxidase.The red cell membrane is unique in that it maintains the biconcave shape ofthe red cell, it is capable of accommodating increase and decrease of volumeof the contents and it is deformable so as to pass through blood vessels ofsmaller caliber. The membrane consists of a bilayer of lipids and intervalproteins attached to an underlying protein skeleton.The protein skeleton consists of a two dimensional mesh of spectrin tetramersand oligomers, cross linked by protein 4.1 and actin. The protein skeleton is
  57. 57. attached to the membrane by the binding of spectrin to ankryn and of ankrynto another protein called band -3 which is an anion exchanger. Othermembrane proteins include pallidin. Abnormalities of these membraneproteins lead to early destruction of the erythrocytes.The protein skeleton helps to maintain the shape of the red cell. Thedeformability is grossly affected in defects of membrane of the erythrocyte asoccurs in spherocytosis and elliptocytosis and also when abnormalhemoglobins such as HbS induce polymerization under anoxic environment.Normal erythrocyte does not freely adhere to endothelium when in circulation.Under abnormal conditions the adhesive properties of the membrane alsochanges rendering them more adherent to endothelium.It has a major role in ion transport which is mediated by several membranechannels or pumps that can maintain the osmotic gradient within the cell.These functions which require can be modified by hormones, cyclicnucleotides, calcium and calmodulin.Anaerobic metabolism supplies 90% of the energy requirement and only 10%is supplied by the aerobic or pentose phosphate cycle. The mature red cell isincapable of protein synthesis as they have no nucleus or mitochondria.Energy is derived through the glycolytic Embden-Meyerhof pathway in whichglucose is metabolized with the production of lactate.The full complement of hemoglobin and enzymes present in erythrocytes ishanded down by the erythroblasts. Life of the red cells is 120 days. They aredestroyed in the reticulo endothelial system subsequently. The red cellnumber remains nearly constant in the range of 5-6millions per cmm (5-6 X1012/ liter) throughout life.
  58. 58. HemoglobinHemoglobin is a conjugated protein synthesized inside the immatureerythrocyte, consisting of the heme moiety (the red pigment) comprising ironand porphyrin and the protein moiety, globin. In adult hemoglobin (HbA) theglobin consists of two alpha chains each containing 141 amino acids and twobeta chains each with 146 amino acids. The fetal hemoglobin (HbF) consistsof two alpha chains and two gamma chains. After birth within 5-6 months thesynthesis of gamma chains stops and beta chains are formed in the requiredamounts. By the age of six months 98 – 99% of hemoglobin is made up ofHbA. The rate and amount of production of the alpha, beta and gamma chainsand their synthesis to form normal and abnormal hemoglobin are controlled byspecific genes. In normal persons the production of gamma chains fall rapidlyafter birth and give place to rapid increase in the production of beta chains.For the continuous production of red cells and synthesis of hemoglobinseveral nutrients are required. These are mainly iron, proteins, vitamin B12,folic acid, pyridoxine, vitamin C, nicotinic acid copper and cobalt.Figure showing RBC and Hemoglobin
  59. 59. Function of hemoglobinHemoglobin is responsible for transport of oxygen from lungs to tissues andremoval of carbon dioxide from tissues and delivery to lungs. Rise in H+ ionconcentration and CO2 levels in the environment reduce the oxygen bindingcapacity of hemoglobin. This is known as Bohr Effect. Increase in oxygenationof hemoglobin reduces its affinity to CO2. This is known as Haldane effect.Hematopoietic growth factorsThe expansion of the stem cell pool, maturation and expansion of precursorcells and their liberation into circulation are all under control of well definedhumoral influences. These include erythropoietin, granulocyte colonystimulating factor (G-CSF), macrophage colony stimulating factor, granulocytemacrophage colony stimulating factor (GM-CSF) and interleukin-3( alsoknown as multi colony stimulating factor).ErythropoietinDuring fetal life it is produced in the liver. In postnatal life, by far the mainsource is the kidneys; a small amount is also produced in the liver. The juxta-glomerular apparatus of renal cortex produces a substance callederythrogenin (renal erythropoietic factor REF). It acts on a plasma proteincalled erythropoietinogen and erythropoietinogen is converted intoerythropoietin. Its principal actions are on the developing erythroid precursorcells after the have become sensitive to erythropoietin. The erythroid
  60. 60. precursors are stimulated to proliferate and differentiate and this accelerateerythropoiesis.Erythropoietin production is tightly controlled to prevent inappropriate rise isred cell mass. Main stimulus for erythropoietin production is anoxia. Rise inred cell mass and viscosity of blood depress erythropoietin productionindependent of the tissue oxygenation status. The normal range of plasmaerythropoietin is 5-25u/L. Hematopoietic growth factors other thanerythropoietin are produced by fibroblasts, endothelial cells, monocytes andlymphocytes which are widely distributed.Granulocyte-macrophage colony stimulating factor (GM-CSF) acts on theprecursors of granulocytes, monocytes macrophages, erythrocytes and alsomegakaryocytes. II.2.2 CLASSIFICATION OF ANEMIAAnemia can be classified in different ways viz 1) Based on the morphology of red cell. 2) Based on the etiology or cause (functional).Functional classificationThe three major functional classes of anemia are: 1. Marrow production defects (hypo proliferation), 2. Red cell maturation defects (ineffective erythropoiesis), and 3. Decreased red cell survival (blood loss/hemolysis).This functional classification of anemia guides the selection of specific clinicaland laboratory studies designed to complete the differential diagnosis and toplan appropriate therapy. A hypo proliferative anemia is typically seen with a
  61. 61. low reticulocyte production index together with little or no change in red cellmorphology (a normocytic, normochromic anemia). Maturation disorderstypically have a slight to moderately elevated reticulocyte production indexthat is accompanied by either macrocytic or microcytic red cell indices.Increased red blood cell destruction secondary to hemolysis results in anincrease in the reticulocyte production index to at least three times normal,provided sufficient iron is available for hemoglobin synthesis. Hemorrhagicanemia does not typically result in production indices of more than 2.5 timesnormal because of the limitations placed on expansion of the erythroidmarrow by iron availability.Morphological classificationIt is based on MCV, MCH, MCHC and red cell morphology of red cell on ablood smear. a) Normochromic, normocytic anemia – • Anemia of acute blood loss • Anemia associated with leukemia. • Aplastic anemia. b) Hypochromic, microcytic anemia – • Iron deficiency anemia • Thalessemia c) Normochromic, macrocytic anemia – • Pernicious anemia • Anemia of folic acid and Vit B12 defeciency • Some cases of aplastic anemia d) Normochromic, microcytic anemia –
  62. 62. • Anemias of chronic infection.An alternative classification of anemia is based on the size of the red cell,which is most accurately indicated by the MCV. • A normal MCV suggests either acute blood loss or the anemia of chronic disease. • A low MCV suggests iron deficiency or thalessemia. • A high MCV suggests B12 or folate deficiency. II.2.3 HYPOPROLIFERATIVE ANEMIASAt least 75% of all cases of anemia are hypoproliferative in nature. Ahypoproliferative anemia reflects absolute or relative marrow failure in whichthe erythroid marrow has not proliferated appropriately for the degree ofanemia. A hypoproliferative anemia can result from marrow damage, irondeficiency, or inadequate erythropoietin stimulation but majority ofhypoproliferative anemias are due to mild to moderate iron deficiency orinflammation. If the red cell indices are normal, the anemia is almost certainlyhypoproliferative in nature. In general, hypoproliferative anemias arecharacterized by normocytic, normochromic red cells, although microcytic,hypochromic cells may be observed with mild iron deficiency or long-standingchronic inflammatory disease.The hypoproliferative category includes: • Iron deficiency anemia. • Anemia of acute and chronic inflammation (including many malignancies). • Anemia of renal disease.
  63. 63. • Hypometabolic states such as protein malnutrition. • Endocrine deficiencies. • Anemias from marrow damage e.g. aplastic anemia. The anemia of acute and chronic inflammation, like iron deficiency, is related in part to abnormal iron metabolism. The anemias associated with renal disease, inflammation, cancer, and hypometabolic states are characterized by an abnormal erythropoietin response to anemia. Iron Deficiency AnemiaIron deficiency anemia is the condition in which there is anemia and clearevidence of iron deficiency. It is the commonest cause of hypochromicmicrocytic anemia. In iron deficiency the amount of iron lost from the bodyexceeds the amount absorbed. The physiological demand for iron exceedsiron uptake.Causes of Iron DeficiencyConditions that increase demand for iron, increase iron loss, or decrease ironintake, absorption, or use can produce iron deficiency.Exogenous causes: here it is due to inadequate quantity of iron in food. Thequantity and absorbability of dietary iron varies with type of diet.Endogenous defects: absorption defects due to Achlorhydria, partialgastrectomy, celiac disease, sprue, idiopathic steatorrhea and defects in irontransport can lead to iron deficiency.Other causes:Hemorrhage – for every 10 ml of blood lost from the body there is loss ofabout 5mg of iron.