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A clinical study on the effect of Bhaskara lavana choornum in pandu Roga, K. SUNEETHA, Department of Kayachikitsa, PG unit Dr.BRKR Govt. Ayurvedic College, HYDERABAD

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Pandu kc016 hyd

  1. 1. My commitment increases my level of energy. My energy increases my level of action. Myaction increases my level of success. My success increases my level of commitment.Research in any field is the most important section of development. Ayurveda is inservice is for ages to the needy mankind to relieve their ailments and recording the factsfor the future generations. At present the Ayurveda research scholar, developing theAyurveda and understanding under the limelight of contemporary scientific backgrounds.The plagiarism is more and more now a day in the scientific community. This ishappening as the researches of the various institutions are not available for the commonresearcher. We wish to control this plagiarism by contributing the dissertations forscientific community. If you find any thesis is a copy of the previous publication, we takethis issue to the university authorities for proper action. The solution to prevent copy catsis … http://ayurvedaresearch.wordpress.com/ Dr. Shiva Rama Prasad Kethamakka technoayurveda@gmail.com,
  2. 2. ACKNOWLEDGEMENT I express my profound gratitude to my respected and honorable guideDr.V.VIJAYA BABU M.D. (Ayu.), Professor, P.G. Unit of Kaya Chikitsa., For hisexcellent guidance and co-operation conducting this research work successfully. I am highly indebted to my honoroble Dr. PRAKASH CHANDRA M.D. (Ayu.),Proffessor Head of the department of Kayachikitsa, for his valuable timelysuggestions, thought provoding leads ideas and support in Completing this thesiswork. I am very thankful to my co-guide Dr. RAMALINGESWARA RAO garu,Technical Assistant and Lecturer for their precious suggestions and help through outthe study. I convey my gratitude to the honorable Principal Dr. SADASIVA RAO, and Ex-Superintendent L. RADHA KRISHNA MURTHY and Present Superintendent V.L.N.SASTRY of Dr. B.R.K.R. Government Ayurvedic Hospital I am thankful to Dr. V.V.S. RAMA SASTRY, M.D.(Ayu.), Retired professor,and Dr.VASUDEVARAO garu retired professor, Dr. BASWANT garu RetiredProfessor, Dr. M.L. NAIDU garu for their valuable suggestions and encouragement. I am also thankful to teaching staff, Post graduate department of Kaya Chikitsaespecially Dr. VIJAYA LAKSHMI garu, Dr. NAGESWARA BABU garu, for theirprecious suggestions and help throughout the study.
  3. 3. I express highly thankful to my Parents Sri K. RAMAKRISHNAIAH & Smt.ARUNA whose love, support and encouragement for the initiating sources, whichdirected me towards progress and success in each and every step of my life. I express my special thanks to my Family members Mr. Vijay Kumar, Mr.GuruMurthy, Mr. Prabhakar, Mr. Sambasivam, Prasanth, Chinnamma, BhagyaLakshmi, Suneela, Sujatha, Seshanka, Surya Teja, AND Ganesh for the valuabesupport which made this work possible. I thank to my good neighbours Smt. Rajamani Garu, Mr. Srinivas & Neeraja,whose moral support has my spirit in difficult situations. It is pleasure to convey my thanks to my Co-PG Schoolars and friends especiallyDr. Jayalakshmi and her mother, Dr. Gnana Prasuna and her mother, Dr. V.K.M.Lavanya, Dr.Padmaja, Dr. Sireesha, Dr. Namrata, Dr. Usha Madhuri, Dr.Nageswara Rao, Dr. Ravi, Dr.Sivarama Krishna, Dr. Gayatri, Dr. Madhavi, Dr.Geetha, Dr. Kavitha and Dr. Sandhya for their constent support and helped methroughout this thesis work directly and indirectly. I special thanks to Dr. Yashoda MD (Ayu.) lecturer, in B.R.K.R. AyurvedicCollege for her valuable suggestions and encouragment. I sincerely thankful to Smt. Mamatha & Mr. Chakravarthy, VS GRAPHICShelps me in the computerized of the thesis. Hyderabad February 2008 (Dr. K. SUNEETHA )
  4. 4. CONTENTSPART – I PRELIMINARY PART 1. Intorcution 1 2. Historical Review of the diseasePART - II THE DISEASE - PANDU ROGA 1. Definition & Synonyms of the Disease 7 2. Classification 9 3. Sareera (Rachana & Kriya) 13 4. Nidana 40 5. Poorva Roopa 48 6. Roopa 51 7. Samprapti 64 8. Sadhya and Asadhya Lakshanas 67 9. Upadravas and Arishta Lakshanas 69PART - III CHIKITSA 1. Chikitsa krama 71 2. Pathyas and Apathyas 78PART-IV DRUG REVIEW 1. Criteria for selection of Drug 80 2. Description of individual drugs 82 3. Mode of preparation 99PART V CLINICAL STUDY 1. Materials and Methods 101 2. Observations 105 3. Results 112PART - VI 1. Discussion 121 2. Conclusion 125 3. Summary 127PART - VIISpecial case sheet for Pandu Roga130 2. Bibliography 134
  5. 5. INTRODUCTION Ayurveda is origin from vedas, mainly from Adharavana veda. According toAyurveda, definition of health includes both physical and mental well being andtreatment was mentioned for both Swastha in order to preserve health and Atura inorder to treat the disease. Chaaya and prabha are associated with skin and are based on the condition ofBhrajaka pitta. The discoloration like the colour of ketaki dooli, swetha, peeta, haritaetc., are the manifestations of pathological process caused not only by the etiologicalfactors of vitiated doshas but also by consumption of mrit in pandu roga. The pandu roga is one of the commenest alitments prevalent not only in Indiabut also world wide. The panduroga is included under the heading of"Varnopalakshita Roga" ie., Varna pradhanya disease. It is known since ancienttimes. The disease is referred as Vilohita, Harima, and Halima in vedas and susruthanamed it as Panaki, Laghavaka and Kumbhahwa. William D.Whitney an eminent authority of vedic literature compared vilomawith anaemia. It is the commonest disease irrespective of age, sex and religion. It isprevalent in women, pregnant in specific. As the prevalance of the disease is morecomparatively research studies are needed to evalutate proper eradication procedure,with the help of the system of medicine which has been existing since many centuriesi.e. Ayurveda. The iron deficiency is the commonest nutritional dificiency world overand its prevalence is highest in India.According to NFHS suffering with Anaemia. Female Children All over India 50% 70-72% Andhra Pradesh 52% 75%
  6. 6. Panduroga can be compared to a state of Anaemia in modern system ofmedicine, in which the haemoglobin concentration falls bellow the accepted normalrange due to the failure of haemoglobin synthesis and other conditions mentioned innidana and sareera. In particular where unhygienic, low socioeconomic and faultyfood habits are the contributing factors. It is even more common in pregnant women.Its prevalence in all the age groups and in both the sexes interested reserchers rightfrom ages. The Ayurvedic classics have mentioned a number of effective formulations fortreatment of pandu roga keeping in view of the above factors, the present studyentitled as "A clinical study on the effect of Bhaskara lavana choornum in panduroga" is carried out. The efficasy of this formulation in pandu roga can be justified by its indicationin Alpa rakta condition explained in the pages that follow. The preparation BhaskaraLavana churna is taken from Agnimanandya chikitsa Adhyaya of BhaishadjyaRatnavali. The drug fulfils the qualities of Bahu guna, Yogya, Sukha aswadana,Preenana, vyadhi nashana, avipathkara and gandha varna rasopeta. Thirty patients are randomly selected from those attending the out patientdepartment of post graduate unit of kayachikitsa, Dr. B.R.K.R. Govt. Ayurvediccollege / Hospital, Erragadda, Hyderabad. The drug Bhaskara lavana churna is triedon 30 patients and results are assessed periodically. The results are encouraging, which are discussed in length, in the chapter ofresults seperately, the entire work is devided into VII parts, covering all the aspects ofthe disease. Pandu roga and Drug Bhaskara Lavana Churnam.Part I consists of introduction and historic review of the disease. Part II consists ofvarious aspects of the disease such as definitions, synonyms, classification, sareeraRachana, Sareera kriya, Nidana, Samprapti and other aspects. Part III consists ofchikitsa krama of pandu roga in general. Part IV consists of various aspects of drugs indetail. Part V consists of clinical study, under which, materials and methods,observation and results are included. Part VI consists of discussion, conclusion andsummary. Part VII consists of special case sheets and Bibliography.
  7. 7. HISTORICAL REVIEW Ayuevedia is the most ancient system of medicine among the different systemsof medicine existing. Vedas are apourshayas. Vedas are the oldest knowledge books known to menaccording to Indian thought. So, it would be appreciable to explore the history rightfrom the period of Vedas to present period. On the scale of time, next to Veda arePuranas, Upanishads and Brahmanakas, Samhitas, Sangrahas, Nighantus andArvacheenakala Grandhas. Now, let us consider some of the points related toPanduroga mentioned in different texts/literature/knowledge available till date in astepwise manner under the following headings. 1. Veda Period 2. Purana Period 3. Samhita and Samgraha Period 4. Avracheena Period1. Vedic Period: In Vedas there are many references about the disease Pandu.Rigveda: Pandu roga has been mentioned under the name Harima. Suryanamaskarasand prescribed as its treatment in Rigveda.2. Yajurveda: In Yajurveda there is a reference about Pandu. A reference from thisveda quoted that there is some relation between yakrit, kloma and pitta in relation toPanduroga. Charaka and Susruta has elaborated this point in detail by stating that themoolasthana of raktavaha srotas lies with yakrit and pleeha and the predominant doshaassociated with Pandu is pitta.3. Atharvanaveda: This veda reiterated the same as above. There are references likeVilohita, Harima, Halima which can be taken as synonyms of Pandu. The significanceof sun rays is stressed in Atharvana veda for changing the colour in Pandu roga.Another reference from Atharvanaveda advocates godugdha as a remedy forPanduroga.
  8. 8. 4. Pouranika kala:Garuda Purana, valmiki Ramayana and Agni purana have alsomentioned about Pandu roga. In Garuda purana lohachoorna with takra anupaana isprescribed especially for Pandu patients, and Nidana, Lakshanas, Pathyaapathyavicharanas are also explained in detail. Mahabharata states that the Hastinapura king had suffered from Pandu rogawhose name itself is Pandu Raju. He acquired the disease as a curse from a saint. Thisexplains the karmasiddhanta of Panduroga. King Pandu acquired sterility due to PanduRoga as a complication and he even died of the disease.5. Samhita & Sangraha kala: This is the golden period of ayurveda, since most ofthe Ayurvedic Classics like Charakasamhita, Susruthasamhita, Bhelasamhita,Hareetasamhita, Kasyapasamhita took shape in this period. These samhitas are thebasis of Ayurveda that is being practiced throughout the world. Panduroga has beendescribed in detail along with treatment in all classics as stated below. Name of the book Sthana Chapter No. 1. Charaka Samhita Chikitsa 16th 2. Susruta Samhita Uttara 44th 3. Astanga Sangraha Nidana 13th 4. Astanga Sangraha Chikitsa 18th 5. Astanga Hridaya Nidana 13th 6. Astanga Hridaya Chikitsa 16th 7. Sarangadhara samhita Poorvakhanda 7th 8. Madhavanidana 8th 9. Bhavaprakasha Madhyamakhanda 8th 10. Vaidhya chintamani Pradhama samputa 4 th Even the works such as Chakradatta, vangasena, Yogaratnakara,Bhaishajyaratnavali, Basavarajeeyam, Madhavanidanam and Sarangadhara samhitaalso give a detailed description of Pandu roga.
  9. 9. We can find references of a number of medicinal plants that are proved to beuseful in Panduroga in Dhanvanthari, Kayyadeva and Astanga nighantus. The authorof Vidhyachintamani Srimad Indrakanta vallabha charyulu stated that Pandu is asenapathy (chief of army) for the disease Kshaya. With the advent of Rasakala, some mineral and metallic preparations replacedthe herbal drugs, after shodana and marana. Rasaratnasamucchaya, Rasapadhati andother literatures on Rasashastra have thousands of preparations which are prescribedfor the management of Pandu.5. Aravacheena Period: This is the starting period of modern system of medicine,William D. Whitney, who is a known authority on vedic literature compared vilohitamentioned in Vedas to anaemia. Hippocrates, the father of modern medicine in 460BC, described anaemia likesymptoms such as pallor and weakness. he attributed these symptoms to the chagnesof blood. Anaemia, in those days, was found predominately in virgins and was hencecalled demarbo virgina (the sickness of virgins) by Dr. Johanns Large in 1554 A.D.He described this is pallor of checks, breathlessness on exertion, increased pulsationof the temporal vessels and dysponea on climbing stairs or dancing. This illness waslater termed Chlorosis and clinical use of iron was first initiated in 17th century byThomas Sydenham. Dr. Grambiel andral succeeded in describing the changes of bloodmicorscopically in Anaemia during 1797-1876. Also the work of Thomas Addison, during the same period contributed to thediscovery of one of the type of anaemias - The Addisions Anemia. This is later ontermed as Perinicious Anemia, After the efforts of Dr. Wilks in 1855 and Dr.Biermers in 1872. Another type of anemia - Spleenic Anemia was described by Dr.Banti in 1882. Dr. Minot and Dr. Murphy in 1926, conducted a trial of diet consistingof liver and beef, which are rich in iron. this showed considerable improvement ofPerinicious Anemia. However, they could not provide enough explanation for thesame. This was bridged by the muchapplauded work of Dr. Castle.
  10. 10. G.R. Minot, W.P. Murphy and G.H. Whipple in 1934 shared Nobel Prize inPhysiology and Medicine for their work concerning the treatment of Anaemia withliver. In 460BC Hippocrates also explained the importance of consumption of liver incombating anaemia during pregnancy. The same was also recommended by Charakaand Susrutha in 500 B.C. Now-a-days, there are many clinical, pathological, and diagnostic technologiesavailable in regards to Anaemia. As per Modern system of medicine, anaemia is ofmany types. It is being treated on the whole by supplement of Iron and its source inthe form of daily nutrition or in medicines which would be seen in detail in the topicsthat follow, as and when in need. This disease is prevalent in most communities due tovarious causes and yet a lot has to be achieved. The above review clearly indicates that Pandu is blood related disease, itsrelation is to Raktavaha srotomoolas has long back been mentioned and Ayurvedicphysicians were aware of the disease and its management since vedic period. Thushistory of Pandu and its corelated disease. The Anaemia of Modern system ofmedicine has been briefly outlined.References: 1. Mc. Odonell and Keeth Vedic Index Vol II. 2. Whintney, W.D. Translation of Atharvana Veda, by Motilala Banarasidas, 1962. 3. Garuda Purana Chapter 184/29 4. A short history of Medicine II Edition by Singer and Underwood. 5. Pandu Roga by Pathak R.R. Published by C.A.R.I., 1987 6. Henry A.S. The Origin of the medical terms, Batlimore 1961. 7. Vedomme Ayurved. 8. Susruta Samhita Uttara sthana 44th chapter. 9. History of Indian Medicine by Dr. Rama Rao, P.V. Sharma and Others.
  11. 11. DEFINITION AND SYNONYMS Charaka classified rogas according to Ruja, Varna, Samuthana, Samsthanaand Stana. In this classification the disease pandu falls in the group of varna. In panduroga there is some significant change in the normal colour of the body.There are many definitions in Ayurvedic literature. One nirukti quated by vijayarakshit is “Pandutwenopo lakshito roga pandu roga” (madukosa) Which difenes that a person who acquires pandu varnatvam is a pandu roga. “Swetha peeta samayukta panduvarna prakirtitaha” (Amarakosa) The combination of white and yellow colours in equal proportion are calledpandu roga “Pandu shabdena swetatwa mabhideeyate: (Dalhana on S.Su.33/23) Dalhana, the commentary on susrutha samhita, started that pandu means whitecolour. “Pandutwam teshu chaditam yato ataha pandurityuktasa rogaha” (A.H.Chi. 13/13) Excessive colour of pandutwam is seen in panduroga “Sarveshu chiteshyapi pandu bhavo yato adhikaha khalu panduroga” (Su. Uttara 44/4)) Excessive pandu varnam is seen in pandu roga. “Panduhu swetavarna ketakidholi sannibha peetabhagarda varnabhedcha” (Shabdasthoma) Pandu has been compared with ketaki dhooli or ketaki pushpa colour i.e. thatcan be considered as combination of white and yellow colours. It can be concluded basing on the above that the disease has been regarded as anailment associated with colour of patient.
  12. 12. SYNONYMS OF PANDU ROGA The synonyms of pandu roga available from vedic literature are vilohita, harima,halima. Ref – Adharvana Veda 4-9-3-, 1-22-22) “Sa kamala panaki pandu roga kumbahwaya laghavakoalasakya vibhashyate lakshana masya kristam nibodha vakshyamyanu poorvashasthoth” (Su.Uttara 44) Susrutha used the terms Kamala, Panaki, Panduroga, Kumbahwayo,Laghavaka, Alasaka as synonyms of the disease.Definition: The word Anemia is derived from two words ‘an’ which means with orless and “emia” which means blood condition. Pandu (Anaemia) is a condition ofreduction in the haemoglobin concentration of the peripheral blood below the normallevel in relation to age and sex. These condition of white and yellow colors in equal proportions are calledpanduvarnam. Normal adult male – 16 gms/dl Normal adult female – 14 gms /dl Anaemia is also said to be present in adults if the "Hematocrit (packed RBC) isless than 41% in males and 37% in males. Anemia is also seen in patients in whom theRBC is less than the normal. Normal adult male RBC – 5,20,000/cumm. Normal adult female RBC – 4,700,000/cummReferences: l Charaka sutra sthanam 18/42 l Madhavanidanam l Amarakosha l Susrutha suthra stana 33/23 – Dalhana commentary uttara sthana – 44/4 l Astanga hridaya Chikitsa sthana – 13/3 l Sabdarnavam, l Shabda sthoma mahanidhi
  13. 13. CLASSIFICATION OF PANDU ROGA The pandu roga description available as old as from vedic literature. In vedicliterature there is no evidence of any classification regarding pandu roga. Onlysynonyms such as Harima, Halima, Vilohita are found on the literature. The detail description of pandu roga and is classification starts from Ayurvedicsamhitas only. The classification of pandu roga most of the acharyas accepted 5 types.Those are 1. Vataja (2) Pittaja (3) Kaphaja (4) Sannipathaja(5)Mrudbhakshanaja. But susrutha mentioned only 4 types. He excluded theMridbhakshanaja pandu and he explained for this as Mridbhakshanaja pandu mayinclude in vatadi doshaja pandu’s according to the rasa pradhanata of mrit1. In Haritha samhita “Rukshana” pandu is appears of mridbhakshanaja pandu. Theterm Rukshana may be used, because mridhbhakshanaja pandu mainly cause theRukshanatwa of the body2. Astanga sangrahas and many other texts followed the same order while susruthamentioned four types. Some commentators classified Pandu into eight types as follows: 1. Vataja 2. Pithaja 3. Kaphaja 4. Sannipataja 5. Mritbhakshanajanya 6. Sakhasrita kamala 7. Koshtasrita kamala 8. Haleemaka A Classification states that Mritbhaskhanajanya Pandu falls under sannipatajaPandu because of the following reasons. Intake of Kashaya rasa predominant Mrit leads to Vataja Pandu Intake of Kshara rasa predominant Mrit leads to Pittaja Pandu Intake of Madhura rasa predominant Mrit leads to Kaphaja Pandu Probably this may be the reason why Susruta included MritbhaskhanajanyaPandu under Sannipataja Pandu.
  14. 14. Classification of pandu according to different authors S.No Types Vata Pitta Kapha Tridosha Mritbhakshanaja 1 Charaka 5 + + + + + 2 Susrutha 4 + + + + - 3 Vagbhata-1 5 + + + + + 4 Vagbhata-2 5 + + + + + 5 Madhavakara 5 + + + + + 6 Sarangadhara 5 + + + + + 7 Bhavaprakasa 5 + + + + + 8 Haritha 5 + + + + Rukshana 9 Yogaratnakara 5 + + + + + 10 Basavarajeeyam 5 + + + +11 Vaidhya chintamani 5 + + + + + MODERN ASPECTClassification: Classification of anaemia is 2 types 1. Pathophysiologic classification 2. Morphological classification 1. Pathophysiology classification (Based on Etiology) 1. Anaemia due to blood loss: This has further two types Blood loss: 1. Acute haemorrhage 2. Chronic Haemorrhage 2. Anaemia due to impaired red cell formation: various causes may produce this anaemia. These causes are I. Deficiency of haematinic factors Ex: A) Iron deficiency
  15. 15. B) B12 deficiency C) Folate deficiency D) Protein deficiency II. Haemopoietic stem cell proliferation differentiation abnormality Ex: A) Aplastic B) Red cell aplasia III. Bone marrow failure due to systemic diseases A) Anaemia of infections B) Anaemia of renal diseases C) Anaemia of liver disease D) Disseminated malignancy E) Endo crinopathies IV. Bone marrow infiltration Ex: A) Leukaemia B) Lymphomas C) Myclosclerosis D) Multiple myeoloma V. Congenital anaemia Eg: A) Sideroblastic anaemia B) Congenital dyserythropoietic anaemiaIII. Increased destruction (Classification of Haemolytic anaemia) a) Haemolysis (Intransic) 1. Membrane – a) Heriditary spherocytosis b) Eleptocytosis 2. Haemoglobin a) Sickle cell b) Unstable haemoglobin 3. Glycolysis Pyruvati kinase etc 4. Oxidation G6 PD deficiency b) Haemolysis (Extrinsic) 1. Immune a) Auto immune b) Drug toxicity c) Lympho preliterative disease
  16. 16. 2. Morphological classification: Macrocytic anaemia: In this condition the size of RBC increases i.e. about 94.Normal is 78-94 as M.C.H. proportionately increased. Eg: Tropical nutritionalanaemia, megaloblastic anaemia of pregnancy, pernicious anaemia1. Normocytic anaemia: There is reduction in RBC with if all a slight increasingMCV, MCH remains normal throughout. Eg. Sudden loss of blood due to theantipartum, post partum haemorrhage2. Microcytic normocytic anaemia: There is reduction in red cell volume, Hbcontent with less MCH eg. Actute and chronic inflammatory disease3. Microcytic hypochromic anaemia: Reduction in RBC volume and Hb contentand reduced MCH4. Eg: Iron deficiency anaemia.References: 1. Susrutha samhita uttarastana 44th chapter 2. Haritha samhita truteeya stana 8 th chapter 3. Charaka samhita sutra 18th, chikitsa 16th chapter 4. Susrutha samhita uttarastana 44th chapter 5. Astanga hridaya nidana stanam 13th chapter 6. Astanga samgraha nidana sthana 13th chapter 7. Madhava nidana 8th chapter 8. Bhavapraksha medhyamakanda II volume 9. Sarangadhara samhita 10. Yogarathnakaram madhymakhandam Vol I pandu roga prakarana 11. Haritha samhita truteeya stana 8 th chapter 12. Basava rajeeyam panchama prakarana 13. Text book of pathology, by Byoid 14. Hand bood of human physiology 15. Medicine for students by Dr. Golwalla, 15th Edition 16. Davidson’s principles and practice of medicine – 15th Edition
  17. 17. SHAREERA RACHANA AND KRIYA “Dosha Dhatu Mala Moolam Hi Shareeram” Human body build up three doshas, seven dhatus and trimalas. Any diseaseoccurs the vitiation of dosha, doshyas from their normal functions.I. The Doshas involved in the samprapti of pandu roga are: 1. Vyanavata 2. Samanavata 3. Pachaka pitta 4. Rajakapitta 5. Bharajaka pitta 6. Kledaka kaphaII. The Dhatus are involved in Pandu Roga are: 1. Rasa 2. Rakta 3. Mamsa 4. Medas 5. Asthi 6. MajjaIII. Other factors: 1. Agni 2. Ojas 3. Yakrit 4. Pleeha, 5. Hridaya 6. Raktadharakala 7. Raktaasaya 8. Amasaya 8. Saraktamedas Since the anatomical and physiological aspect of the above mentioned factors isimportant in the study of the pandu roga. Abrief description of the above factors isneeded.
  18. 18. Doshas:1. Vata a. Yyanavata: Location: Hridaya – Seat of vyanavata (Vagbhata) Charaka and Susruta did not mentioned about the place of Vyanavata. Gunas: In general, it possesses all the gunas of vayu. They are ruksha, laghu, seeta,khara, sookshma, and chala. Karmas: i. Locomotion is entirely dependent on Vyana Vayu ii. Rasa Raktadi samvahana iii. Sweda & Asrik sravana. iv. Sareera Chestha: Prasarana, akunchana, vinnamana, unnamana andtiryaggamana v. Jrimba pravartana vi. Anna aswadana vii. Sroto vishodhana viii. Dhatu tarpana b. Samanavata: The Vayu that gives strength to Pachaka pitta is called samanavayu. Location: It resides near pachaka pitta. It courses between Amashaya andPakwashaya. It is also been said that it also occurs in Sweda, Rakta, and Ambu vahasrothas. Gunas: In general, it possess all the gunas of vayu. Karma: The important function of Samana Vayu is to strengthen Jataragni. Thusit helps in the digestion of food. After digestion, it divides ahara into saara and Kittabhaga. According to Vagbhata, samana vata does ahara graham (accepts food) intokoshta, anna grahana, Saara-Kitta vibhajana and it pushes the Kitta into Pureesha vahasrothas.
  19. 19. 2. Pitta a. Pachaka Pitta: We know that the entire body depends on the food weconsume and the way it is absorbed and assimilated into the body tissues. The type ofpitta that does the above said functions is dependent on Pachaka pitta. This pitta alsoregulates digestive capacity, Dhatu parinama and provides nutrition for the body. Thisis called as Pachakagni, Koshatagni, Antaragni, Kayagni, Jataragni or Agni,depending upon the context. It has also been said that vitiation of pachaka pitta leadsto disease. Location: Pachaka pitta is located in between Amashaya and Pakwashaya. Theregion between amashaya and pakwashaya is termed as Grahani and it containsPittadhara kala. In other words, Pittadhara kala or Grahani is seat of Pachaka Pitta. Gunas: Laghu, Vishra, Sara, Dravam, Sneha, Teekshna, Ushna, and Visada Rasas: Amla and Katu In Pachaka pitta, the tejo guna predominance is seen and because of it, thedravatwa guna in pachaka pitta is less when compared to other pittas. Karma: It has wide range of fuctions. The important functions among them areas follows: i. It digests the four types of food and liquids we consume. ii. It differentiates Saara bhaga and Kitta bhaga of the food after digesting it and absorbs into the body. iii. It is termed as ‘Jatara Agni’ many times, because it controls the action of other 12 types of agni in the body. iv. The other factors that are dependent on the action of Pachaka pitta are given below. A. Ojas B. Ayu. C. Deha pushti D. Bala E. Utsaha. F. Health in general G. Colour of skin It is also said that if Kayagni is healthy, then the person achieves longevity, else,he acquires diseases and if the Kayagni is totally destroyed, the person dies.
  20. 20. b. Ranjaka Pitta. The pitta that is transforms rasa dhatu into rakta dhatu is called Ranjaka pitta orRanjakagni pitta. “Amasayaasryayam Pittam ranjakam rasaranjanath” (A.H.S. 12-12) Location: According to Susruta - Yakrit and pleeha According to Vagbhata – Amashaya According ot Sarangadhara – Hridaya Gunas: Same as that of pachaka pitta Karma: Ranjaka pitta gives colour to the Rasa Dhatu when it is circulatedthrough Yakrit and Pleeha and transforms it into Rakta Dhatu. This act is evencontrolled by Rakta Dhatwagni. c. Bharajaka Pitta: The temperature of the body as well as the colour of the skin are dependent onBhrajaka pitta. “Twakstham bhrajakam bhrajana twachaha” (A.H.S. 12-14) Location: Skin is the site of Bhrajaka pitta. Avabhasini, which is the first layerof skin, lodges Bhrajaka pitta according to Dalhana. Gunas: Same as pachaka pitta. Karma: i. The main action of Bhrajaka pitta is to manintain temperature of the body. ii. In general, Bhrajaka pitta gives different colours to the body depending uponthe Mahaboota composition of the skin. According to Charaka Jala & Akasa Mahabhoota predominance leads Goura Varna Pridhvi Mahabhoota predominance leads Krishna Varna Pridhvi & Akasa Mahabhoota predominance leads Krishna Syama Varna According to Susruta: Jala & Akasa Mahabhoota predominance leads to Gowra Syama Varna iii. It reflects different characteristics of body in health and diseased states. iv. It absorbs the oils or medicines applied over the surface of the skin, in theform of Abhyanga, Parisheka, Avagahana and Lepana.
  21. 21. 3. KAPHA Kledakakapha Location: The site of kledaka kapha is Urdhwa Amashaya Gunas: In general, it possesses all the gunas of Kapha such as Shingdha, Seetha,Guru, Manda, Slakshna, Sandra, and Sthira. Karma: 1. Anna sanghata 2. Kledana The impirement of these functions are supposed to vitiate ahara which may resultinto Pandu.Dhatus The Dhatus that are involved in the pathogenesis of Pandu are Rasa, Rakta,Mamsa and Meda as per several authors. Rasa Dhatu: The involvement of rasadhatu is not directly related in thePathogenisis of Pandu roga samprapti. Pandu is included under rasa prodoshajadiseases. Location: Hridaya and Dasadhamanis. It circulates through out the body alongwith Rakta with the help of Vyanavatha. Pramana: 9 Anjalis Rasa: Madhura Varna: Swetha/Sukla Formation: It is formed from Saarabhaga of ahararasa after it has been subjectedto jatarapaka and Rasadhatwagnipaka. It stays in each dhatu for a period of 3015kalas. It circulates upwards like Agni, downwards like jala and transversely likeshabda. Karma: 1. Tarpana 2. Jeevana & Preenama 3. Vardhana 4. Dharana 5. Yapana 6. Uttaradhatu poshana
  22. 22. Rakta Dhatu: According to the Ayurvedic view, Rasadhatu contributes to the formation of therakta dhatu with the help of Ranjaka pitta. Therefore the Ranjakapitta plays anessential part in the formation of the Raktadhatu. “Tejo Rasanam sarvesrham manujanam yaduchyathe” Pittoshmanahasia Ragena Raso Raktatramrucchati The etiological factors of Raktadusti are similar to the Panduroga etiologicalfactors. The characteristic features of Pandu quite opposite to the characters ofShuddharaktapurusha. The Pandu roga is mentioned under Rakta kshaya lakshanas. “Yathu Yakritpleeho pittam Tasmin ranjakognirthi sangna Sa Rasasya Ragakruduktha ha” Location: Yakrit, Pleeha, Hridaya, Rakta vahadhamanis and Sarakta medas. Itcirculates in the entire body along with rasadhatu. Pancha bhoutika Sangatana of rakta: “Panchabouthikam twapare Jeevarakta maharacharyaha Visratha Dravatha Ragada spandanam Laghuta tatha Bhumyadenam guna hothe drushanthe chatra shonita Qualities of Rakta dhatu Bhuta Pradhanyatha 1. Visratha (Fleshy odour) Prodhweebhuta 2. Drava (Fluidity) Jalabhuta 3. Raga (movement) Agnibhuta 4. Spandhana (movement) Vayubhuta 5. Laghuta (lightness) Aakashabhuta Rasa: Madhura/Madhura lavana rasas. Varna of suddha rakta dhatu: “Tapaniyendra Gopabham padmalaktaka sannibham Gunjaphala savarnacha vishuddam vidhisonitham”
  23. 23. The pure blood looks lika a bright “Indragopa” Looks like Padma (Lotus flower) and Latuka (Laksha) Gunjaphala Savarnam – Brightly red like gunja seed. These colour indicative ofpure blood. Pramanas: Eight Anjalis. Gunas: Anushna, Seetha, Snigdha, Guru, Visra and Asamhata and Gunas ofPanchamahabhutas. Karma: Jeevana, Dharana, Bala, Varna, Sukhakara, Ayushkara, Pushtikara,Indriyaprasannatwa, mamsapushti and sparshagnanakara. Shuddha Raktasaara Purusha Lakshanas: A person whose karnamukha,jihwa, nasa, osthta, pani, paadatala nakha, lalata and mehana are having snigdha andrakta Varna is regarded as Shudda Raktasaarapurusha.Ojus: The involvement of ojus is specifically mentioned in Charaka Chikitsa 16thChapter. As the formation of all Dhatus is impaired in the disease Pandu, theformation of the essence of all Dhatus also impairs and ojokshaya lakshanas are seen. Location Hridayam, Sarva shareeram Types Para and Apara Pramana Para Ojus – Asta bindu Apara Ojus – Ardhanjali Rasa Madhura Varna Eshatpeeta varnam (or) Sarpivarnam.Karma Balakaram, Vyadhi kshamatwakaram, Tushtikaram, Pushtikaram, and it is associated with Ayu (life).
  24. 24. MODERN ASPECT The circulatory system is the transport system that supplies O2 and substancesabsorbed from the gastrointestinal tract to the tissues, returns CO2 to the lungs andother products of metabolism to the kidneys, functions in the regulation of bodytemperature, and distributes hormones and other agents that regulate cell function. The circulatory (or) vascular system is divided for descriptive purpose into twomain parts 1. The Lymphatic system 2. The Blood circulatory system The Disease pandu roga is similar to the disease Anaemia of modernmedicine. Anaemia is concerned with lower haemoglobin levels in the blood. It is acondition in which the oxygen carrying the capacity of the blood is reduced.The blood: Blood is described liquid as a connective tissue. It acts as communicationbetween the cells of different parts of the body and the external environment. Blood:constitutes 7% of the body weight. It is about 5-6 liters.Other Physical characters of blood: Viscocity – 4.5-5.5 (higher than water) Temperature – About 380C ( Slightly higher than normal body temperature PH-range – 7.35 to 7.45 Total blood volume – 72-10ml/kg body weight.Composition of the blood: Microscopically blood is composed of two parts.1. Blood plasma: Contains dissolved substances (55%), water, plasma proteinsclotting factors, inorganic salts, nutrient materials, hormones, enzymes, antibodies andgasses.
  25. 25. 2. Formed elements: Contains cell and cell fragments (45%) – Red blood cells orErythrocytes, white blood cells or leucocytes and platelets or thrombocytes presentless than 1% of the total blood volume.Formed elements: The element of the blood are: 1. Erythrocytes (Red blood cells) 2. Leucocytes (White blood cells) I. Granular leukocytes (Granulocytes) a. Neutrophils b. Eosinophils c. Basophils II. Agranular leukocytes (Agranulocytes) a. Moconcytes b. Lymphocytes (T cells, B cells and Natural killers) 3. Platelets (Thrombocytes) ERYTHROCYTES (The red blood cells) Erythrocytes: Of all the cells of the body RBCs are most abundant. The majorFunction of RBC also known as erythrocytes is to transport haemoglobin, which inturn carries oxygen from lungs to tissues. Haemoglobin is present in RBC in humans. RBC have other functions besides transport of hemoglobin. They contain largequantities of carbonic anhydrase, which catalyses the reactions between water andCO2, increasing the rate of this reversible reaction to as much as several thousandtimes. This makes it possible for water in blood to react with huge CO2 and therebytransport it to lungs from tissues in the form of BiCarbonate Ion (HCO3).
  26. 26. The Haemoglobin in the cells is an excellent Acid – Base buffer and isresponsible for most of buffering power of whole blood. Size and shape of RBC: Normal RBCs are bioconcave discs having a meandiabmeter of about 7.8  and a thickness of about 2.5 mm at the periphery and 1mm mof less in the center. The shape of RBCs can change remarkably as the cells passthrough capillaries. Concentration of RBCs in the blood: The average volume of the red bloodcells is 83 cubic micrometer In normal men - 5,200,000 (+/- 300,000) In normal women – 4,700,000 (+/- 300,000)Quantity of Hb in the cells: RBCs can accommodate 34 gms/dl of Hb in the cellfluid, when the heamatocrit ( the percentage of blood that is in the cells- normally 40to 45%) and the quantity of haemoglobin in each respective cells are normal. Thewhole blood contains an average of Haemoglobin in Men – 14-16 gms/dl Women 12-15 gms/dl Infants – 14-20 gms/dlEach gram of pure Hb is capable of combining with about 1.39 ml of oxygen.In normal man, Hb/dL of blood carries more than 21 ml of O2.In normal women, Hb/dl of blood carried more than 19ml of CO2.
  27. 27. PRODUCTION OF RBC AS PER AGE: l Yolk Sac: In early few weeks of embryonic life – primitive nucleated RBC are produced. l Liver spleen & Lymphnodes: During mid trimester of gestation – the liver is the main organ or production of RBC, although ressonable number of RBC are produced by spleen and lymph nodes. l Bone marrow: During the last months of gestation – RBC are produced exclusively from bone marrow. l Upto 5 years – Bone marrow of all the bones produces RBC. l After 20 years – Long bones stop prodcing RBC since fatty tissues occupy most of the cavity. Beyond this age RBCs are produced by marrow of membraneous bones such as verterbrae, sternum, ribs and ilia. Origin and development of Red Blood Cells: The first cell that can beidentified as belonging to the red blood cells series is the proerythroblast. Once theproerythroblast has been formed, It divides several more times, eventually formingmany mature red blood cells. The first generation cells are called Basophilicerythroblasts, which then develops into a Proerythroblast (Normoblast) erythroblast,the first cells in the sequence that begins to synthesize hemoglobin. The polychromatophilic erythroblast next develops into an acidophilic erythroblast, in whichhemoglobin synthesis is at a maximum. In the next stage, the acidophilic erythroblastejects is nucleus and becomes a reticulocyte. The reticulocyte in turn becomes anerythrocyte (or) mature red blood cell. Once the erythrocyte is formed, it leaves themarrow and enters the blood stream.Formation and destruction of red blood cells and recycling of hemoglobincomponents. Red blood cells live only about 120 days because of the wear and tear inflictedon their plasma membranes as they squeez through blood circulation worn-out redblood cells are removed from circulation and destroyed by fixed phagocytic
  28. 28. macrophages in the spleen and liver. The globin and heme protions ofhemoglobin are split apart. Globin is brokendown into amino acids, which can bereused to synthesize other proteins. Iron removed from the heme portion. Associateswith a plasma protein called transferring, which transports iron in the blood stream. Inmuscle fibers, liver cells, and macrophages of the spleen and liver, iron detaches fromtransferring and attachs to iron storage proteins called ferritin and hemosiderin.Upon release from a storage site or absortion from the gastrointestinal tract, ironattaches to transferring. It is then transported to bone marrow, where RBC precursorstake it up through receptor – mediated endocytosis. For use in production of newhemoglobin molecules. Erythropoiesis in red bone marrow results in the production ofred blood cells, which enters the circulation. At the same time, the non-iron protion of heme is converted to biliverdin,agreen pigment, and then into bilurubin, an orange pigment. Bilurubin enters theblood and is transported to liver with in the liver, bilirubin is secreted by liver cellsinto bile, which passed into the small intestine. Again which passed into the largeintestine, in large intestine bacteria convert bilurubin into urobilinogen. Someurobilinogen is obsorbed back into the blood, converted to urobilin, a yellow pigment,and excreted in urine. Most urbilinogen is eliminated in feces in the form of a brownpigment called stercobilin, which gives feces their characteristic colour.Erythropoietin: The principal factors that the stimulates red blood cell production isa circulating hormone called erythropoietin. Tissues oxygenation is a basic regulator of RBCs production. Any condition thatcauses the quantity of oxygen transported to the tissues to decrease ordinarly increasethe rate of RBCs production.Other factors controlling erythropoises: The red cells are constantly beingdestroyed and regenerated. Certain factors are necessary for the formation of redblood cells. They are:1. Diet: Proteins are very valuable supply of essential amino acids for the synthesis ofhemoglobin.
  29. 29. 2. Metals: Iron, Copper, Cobalt, Calcium and Manganese. Iron is essential for theformation of hemoglobin. Copper, Cobalt, Calcium and Manganese are indirectlyhelpful in the formation of RBCs.3. Bile satls: Presence of bile salts in the intestine is essential for the proper absorptionof these metals.4. Endocrine glands: Certain glands such as thyroid and adrenal glands are havingunknown role in the metabolism of RBC.s5. Vitamins: Vitamin C, B complex, and Folic acid are helpful in the formation ofRBCs.Erythropoietin and its formation: Erythropoietin is a hormone found in circulatingblood. It is a glycoprotein with molecular weight of 34,000. In the absence oferythropoietin, hypoxia has little or no effect in stimulating RBCs production. On theother hand, when Erythropoietin system is functional, hypoxia causes marked increasein Erythropoietin production, and this in turn enhances RBCs production until hypoxiais relieved.Role of kidneys in the formation of erythropoietin: In normal person, about 90% ofall erythropoietin is formed in the kidneys. Mainly, the liver forms the remainder. Therenal tubular epithelial cells secrete the erythropoietin because anemic blood is unableto deliver enough oxygen from peritubular capillaries to the highly oxygen –consuming tubular cells, thus stimulating erythropoietin production.Effect of erythropoietin on erythrogenesis: The important effect is to stimulate theproduction of proerythroblasts from hemopoietic stem cells in the bone marrow. Oncethe proerythroblasts are formed, the erythropoietin causes these cells also to pass morerapidly through the different erythroblastic stages than normal, further speeding up theproduction of new cells. The rapid production of cells continues as long as the personremain in low oxygen state or unitl enough RBCs are producted to carry adequateamounts of oxygen to the tissues.Formation of RBCs – Requirement of Vitamin B12 and Folic Acid: For the finalmaturation of RBCs, two vitamin – B12 and Folic acid are very imporntat. Both of
  30. 30. these are essential for the synthsis of DNA, because each in a different way is requiredfor the formation of Thymidine Triphosphate, an essential building block of DNA.Therefore, lack of either of these causes diminished DNA and consequently, failure ofnuclear formation and division. Therefore, it is said that Vit. B12 and folic aciddeficiency causes ‘maturation failure’ in the process of erythropoiesis.Folic Acid: The normal concentration range of folic acid in blood is 5-15 mg/ml. It isfound mainly in green vegetables, liver and whole grains. The reference nutrientintake is 50g/day. Following its uptake by the mucosal cells, folate undergoesreduction and methylation. Once, it arrives in the liver, the methyl derivative is takenup, undergoes demethylation and the tetrahydrofolate is converted into polyglutamylforms with 4,5 or 6 residues. The polyglutamyl forms contstitute a store of thevitamin. Prior to release from the store, and into the circulation, the compound isconverted to N-methyl-derivative, from which all but one of the glutamyl residues isremoved.Folate deficiency: The members of society most liable to folate deficicney arepregnant women and the elderly. It is now recognized as being good practice toadminister folate supplements as soon as pregnancy is confirmed and to continue untilterm. In the first trimester the supplementation in prophylactic, benefiting the foetus,because there is clear evidence that the occurance of neural tube defects such as Spinabifida and anencephaly is reduced by as much as two-thirds. Later in the pregnancythe supplementation is to prevent folate deficiency in the mother, which can easilyarise as foetal demands cause depletion of maternal foliate stores. Less commonly, folate defienciey may be seen in alcoholics, in those patientsbeing treated with anticonvulsants and in individuals with intestinal malabsorptionconditions.VITAMIN B12 : Normal daily requirement of Vitamin B12 is 1-2 g/day. It enters intofood chain only in food of animal origin. The acid conditions and the proteinhydrolysis that commences in the stomach jointly cause the release of Vitamin B12. Insaliva and also in gastric secretions are a group of mucins, termed R-Binders.
  31. 31. These glycoproteins bind vitamin B12 with high affinity in the acid environment of thestomach. In the more neutral surroundings of the duodenum the R-binders undergohydrolysis, thereby releasing their Vitamin B12 .Intrinsic factor: Maturation of the cell depends on a number of factors, especially thepresence of vitamin B12 and folic acid. These are present in sufficient quantity in anormal diet. Containing dairy products, meat and green vegetables. If the absorptionof vitamin B12 depends on a glycoprotein called intrinsic factor secreted by parietalcells in the gstric mucosa. Thus very little or none is absorbed in cases with perniciousanaemia and after gastrectomy as the intrinsic factor absent. In main it is produced bythe body of the stomach. It is glycoprotein.The essential property of the intrinsic factor is its ability to bind Vit B12 and to act asa carrier. The presence of hydrochloric acid probably facilities this binding in thestomach only the vitamin B12 part enter blood to be transported to red bone marrow.Process of absorption: 1. The intrinsic factor binds tightly with Vit.B12 and in this bond state, Vit. B12 is protected from digestion by the gastro intestinal enzymes. 2. Still in the bond state, the intrinsic factor binds to specific receptor sites on the brush border membranes of the mucosal cells in the ileum. 3. VitB12 is transported into the blood by the process of pinocytosis carrying the intrinsic factor and vitamin together through the membrane. This is a process that is dependent on Ca.2+. Lack of intrinsic factor, therefore causes loss of much of the vitamin, becauseof both digestive enzyme action in the gut and failure of its absorption. The transportof Vitamin B12 in the plasma occurs in association with two major bindingproteins:Transcobalamin I and Transcobalamin II.
  32. 32. IRON METABOLISM: Metal ion used most frequently in association of proteins often include iron intheir structures (sometimes copper, occasionally manganese). The use of iron as the metal in biological systems for this purpose seems, in part,to have arisen due to its great abundance in the environment. It has greater affinity foralready association with, and dissociation from its binding sites on protein i.e., itskinetic liability. The complexes formed, however, are thermodynamically stable. Themajor iron-bearing proteins in the body are not enzymes, however, but the dioxygen-binding and dioxygen-transport proteins myoglobin and hemoglobin.1. Sources: All animal food eg. Meat, liver, egg etc., excepting milk and butter.Vegetables, eg: peas, lentils, green leaves, fruit.2. Iron intake: In the normal population, requirements for iron replacement rangefrom 1.0 to 3.2 mg/day, and this must derive from, dietary srouces/Although iron iswidely distributed in foodstuffs, only a proportion, which may be 10% or less, isabsorbed from the diet. For this reason, the minimal amount needed to be ingesteddaily is set at 10 times the amount actually lost daily.3. Absorption and transport: Iron is absorbed mostly from the whole of the gastro-intestinal tract but a large amount is absorbed from the upper part of the smallintestine particularly the duodenum. Dietary iron is absorbed through the mucosalcells as Ferrous (Fe++) form. Iron in diet is mostly present as a ferric (Fe +++) statewhich is reduced to ferrous form during absorption. Vitamin C, glutathione and aminoacid – SH groups help in reduction of ferric to ferrous form. After entering themucosal cell as Ferrous form, the iron molecules are rapidly reconverted into ferricstate. A ferric iron as ferric – hyroxy phosphates combines with a protein, apoferritinwith a protein apoferritin of. The mucosal cells with the formation of iron-phosphorusprotein complex, ferritin, This ferritin is one of the storage forms of iron in the tissue.
  33. 33. 4. Absorption of iron depends upon the factors: The acidity of the gastric juicehelps absorption. The gastric HCL helps reduction from ferric form to ferrous. Partialgastrectomy often leads to iron deficiency anaemia. Calcium small amount decreasesthe formation of insoluble iron phosphates and thus helps absorption but large amountof Ca. inhibits iron assimilation. Vitamin – C increases the absorption of iron fromfoods, possibly reducing the ferric iron into the ferrous state.5. Time taken for absorption: The rate of absorption is determined by the ironrequiremen for Hb synthesis. In anaemic cases, after a single dose of iron, a rise ofserum iron takes place in 30 minutes, reaching its maximum in 3-5 hours and returnsto normal in about 12 hours. Maximum absorption is completed in 18 hours.6. Iron storage: iron is incorporated into the iron-storage protein Ferritin, inenterocytes, but the main stores of iron in the mammalian body are in the liver andspleen. In addition to storage as Ferritin, iron can also be found in a form calledHaemosiderin inside the liver.7. Iron balances: For an adult to stay healthy, the amount of iron lost each day muchbe replaced by an equivalent intake. Young rapidly growing children, on the otherhand, will require a positive iron balance. The factors that influence daily iron loss,daily iron intake and absorption from the gastrointestinal tract are to be mostlyconsidered.8. Iron excretion: Iron is unique among the trace elements in that there is noexcretory system for eliminating the metal from the body. This is generally lostthrough erythrocytes in bleeding. The routes for loss of iron may be classified aseither physiological or pathological.9. Physiological Iron Losses: The adult male and the non-menstruating female loseabout 1 mg iron per day. Of this total, 50-60% is accounted for by loss from thegastrointestinal tract, due either to biliary excretion or to the shedding of mucosalcells. The remainder is lost with hair, sloughing of skin or in the urine. Lossess duringmenstruation typically range, on average, from 1.4 to 3.2 mg Iron per day.
  34. 34. Losses associated with underlying pathology: A range of conditions give rise toblood loss, but is appropriate to discuss this under Nidana.10. Function of iron: (a) Formation of haemoglobin (b) Development of red cells (c)Oxygen carriage in blood (d) Related to tissue oxidation (e) Supplies O2 to themuscles (f) Relation with cell nucleus and oxidation in nerver cells.11. Deficiency signs: Iron deficiency causes secondary anaemia.Haemolysis: By the term haemolysis is meant the disrutption of red cells with theescape of haemoglobin from the corpascles to the plasma. Blood may be haemolysedin the different ways: 1. By adding fact solvents – Ex: Ether, chloroform, benzene etc 2. By causing osmotic disturbance 3. Disturbing the surface tension – addition bile salts 4. Physical methods – Alternate freezing and thawing of blood breakdown RBC 5. Mechanical – vigorous stirring and shaking 6. Addition of incompatible blood – Agglutinates the red cells. 7. Adding bacterial haemolysis 8. Adding snake venom (viper) 9. Drugs: like quinine, phenacetin, nitrates, chlorates etc.Leucocytes (The White blood cells) They are largest blood cells. They contain nuclei and some have granules in theircytoplasm. White blood corpuscles are an important variety of cells in the blood.These cells differ from the red cells in many respects. For instance. (1) They do not contain any haemoglobin (2) They are bigger in size (3) They are nucleated, living cells.
  35. 35. (4) They are actively amoeboid (5) They are much less in number (6) Their span of life is shorter. (7) Their origin is purely from extravascular tissue (8) Their functions are absolutely different from those of red cells. (9) There are several varieties of leucocytes, where as red cells are only one variety. Normal leucocytes count – 4000-11000/cumm.Classification and differential count of Leucocytes:The classification and differential count as generally accepted two major groups: 1. Granulocytes Polymorphonuclear leukocytes) Consequently this group includes three varieties: A) Neutrophil B) Eosinophil C) Basophil 2. Agranular leukocytes (A granulocytes) Two varieties A) Lymphocytes B) MonocytesAgain lymphocytes 3 types A) T – lymphocytes B) B- lymphocytes C) Natural killer cells(I) Granulocytes: These cells originate from stem cells (haemocytoblastas) in redbone marrow and go through several developmental stages befor entering blood, aprocess called granulopoiesis. They follow a common line of development throughmyeloblast before differentiating into the three types. Their names represent the
  36. 36. dyes they take up when stained in the laboratory. Eosinophils take up the red acid dye,basophiles take up the blue; and neutrophile are purple because they take up bothdyes.(A) Neutrophils: Neutrophil is about 10-12m in diameter. Most numerous in the adultblood, about 60-70%. The necleus is many-lobed; the number of lobes varies from 2to 7 or more. Neutrophils have limited life span of around 12-24 hours in the blood.Their main function is to protect against any foreign material that gains entry to thebody. Mainly microbes, and to remove waste material. They are attraced in largenumbers to any area of infection by chemical substances, released by damaged cells,called ‘Chemotaxins’. Neutrophils pass through the capillary walls in the infected areaby amoeboid movement. There after they ingest and kill the microbes by a processcalled “Phagocytoses”.(B) Eosinophils: Eosinophils is 10-12 m in diameter. Eosinophils are charecterised bytheir two-lobed. Nucleus they have significant proinflammatory and cytotoxic activityand play a role in the pathogenesis of various allergic, parasitic and neoplasticdisorders. The eosinophils are amoeboid but not phagocytic. Eosinophils is about 2-4%. The most common causes of eosinophilia in the world are allergic disorders suchas asthma, eczema and high fever. In developing contries parasitic infections arefrequently implicated. Other relatively common aetiologies are drug hypersensitivity,various skin disease and connective tissue disorders.(C) Basophils: Basophils is about 8-10m in diameter. The nucleus is kidney shaped.The cytoplasm contains a large numbers of round granules which take deep basophilicstain. Basophils are the least numerous of the blood leucocytes. Basophils secretehistamine which causes vaso dilatation and increases the permeability of capillarywalls. Basophils and their tissue equivalent, most cells, have receptors for the protionof I g E. They play a central role in immediate hypersensitivity reaction. Basophils
  37. 37. is usually associated disorders Eg. Chronic myeloid leukaemia. However it may bereactive to a range of systemic diseases including inflametory bowel disease andhypothyroidism. Basophil count about – 0.5-1%.(2) A granular leukocytes (Agranulocytes): The type of leukocyte with no granulesin their cytoplasm are monocytes and lymphocytes.(A) Monocytes: These are large mononuclear cells that originate in red bone marrow.Monocytes are 16-18mm in diameters. Monocytes developed from monoblasts. Somecirculate in the blood and are actively motile and phagocytic, while others migrate intothe tissues where they develop into macrophage.The macrophage system, some timecalled the lymphoreticular system, consisits of fixed pahgocytic cells which multiplyin situ. These cells are found in a wide variety of tissues. Eg. Histocytes in connective tissue, Microglia in the brain. Kuffer cells in liver sinusoids. Alveolar macrophages in the lungs. Sinus – living macrophages in the spleen, Lymphnodes & Thymus gland Mesangial cells in glomerulus of nephron in the kidney. Osteoclats in bone. Monocytopenia is less frequently noted but can be severe in patients receivingcortico steroid treatment. Monocytes count – 3.8%.Lymphocytes: Lymphocytes are developing from haemocytoblasts in red bonemarrow. Lymphocytes are associated with protection of the body against foreignmaterial. Lymphocytes are spread in the blood stream to lymphoid tissue else where inthe body where they are activated i.e. they become immunologically competent
  38. 38. which means they are able to respond to antigens (Foreign material). Lymphocytescount about 20-25%.The major types of lymphocytes are T-lymphocytes, B-lymphocytes and natural killercells. A. T. Lymphocytes: T.Lymphocytes, activated by thymosin in the thymus gland.They are sensitized when they encounter an antigen for the first time. Effector cellsact directly against antigens in conjuction with phagocytes. The main T-lymphocytesare cytotoxic and are responsible for long-term protection against some viruses,bacteria, fungi, cancer cells, pollenfrom flowers and platns, some large moleculedrugs Eg. Pencillin. They are also responsible for the rejection of transplanted organsT.Lymphocytes, which are responsible for cell mediated immunity. Other T-lymphocytes are helper T cells, which activate B cells, and suppresor T-cells, which inhibit B cell activity. T. Lymphocytes produce a number of chemicalsubstances (A) Lymphokines that attract macrophages to the site (B) Lymphotoxin that kills foreign cells eg-microbes (C) Interferons that prevent virus reproduction inside cells. B-Lymphocytes: B cells are derived from the stem cells of the bone marrow. B-lymphocytes are responsible for humoral immunity. B.Lymphocytes are activated byboth microbes and their toxins. B-Lymphocytes, which are responsible for humoralimmunity. These are five subclasses IgG, IgA. IgM, IgD and IgE. The antibodiespromote phagocytosis of foreign particles and neutralize toxins.Variations in normal count of white blood corpuscles: a) Muscular exercise (asphyxia) (b) Relation with after meal. (c) Injection of adrenaline
  39. 39. (d) Emotional stress (e) Relation with pregnancy and labour (f) Increased cellular destruction from injections & surgical operations (g) Asthma, high fever, skin disease (h) Starvation and administration of certain chemicals like benzene.Functions of white blood corpuscles: (a) Phagocytosis (b) Antibody formation (c) Formation of fibroblast (d) Manufacture of trephones (nutrition growth, and repair of tissues) (e) Secretion heparin (f) Antihistamin function(3) Thrombocytes (Platelets): They are very small non-nucleated discs derived from the cytoplasm ofmegakaryocytes in red bone marrow. The normal platelet count is between 2,50,000 to40,00,000/mm3 of blood. Platelets have a short life span. Normally, just 5-9 days.Aged and dead platelets are removed by fixed macrophages in the spleen and liver.Coagulation (Clotting): Normally, blood remains liquid as long as it stays with in itsvessels. If it is drawn from the body, however, it thickness and forms a gel. Eventuallythe gel separates from the liquid. The red-coloured liquid called serum. The gel iscalled clot. The process of gel formation it called clotting or coagulation. Clottinginvolves several substances known as clotting factors:
  40. 40. Clotting factor: S.No. Synonym Source Pathway I Fibrinogen Liver Common II Prothrombin Liver Common III Tissue factor (thrombo plastin) Damaged tissue & Activated platelets Extrinsic IV Calcium ions (Ca2+) Diet, bones, and platelets All V Proaccelerin, labile factor or Accelerator globalin (ACG) Liver and platelets Extrinsic & Intrinsic VII Serum prothrombin conversion Liver Extrinsic acceleralor stable factor or proconvertin VIII Antihemophilic factor (AHF) Platelet & Intrinsic Antihemophilic globulin (AHG) Endothelial IX Christamas factor, plasma Liver Intrinsic Thromboplastin component (PTC) Or antihemophilic factors B X Start factor, power factor, or Liver Extrinsic & Thrombokinase Intrinsic XI Plasma thromboplastin Liver Intrinsic antecedent (PTA) or antihe- mophilic factor C XII Hageman factor, glass factor, Liver Intrinsic Contact factor or antihemophiliac facrorXIII Firbin-stabilizing factor (fsf) Liver & Platelets Common There is no factor VI, prothrombinase (prothrombin activator) is a combination ofactivated factor 5 and 10.Haemostasis blood clotting is 3 basic stages Stage - I Stage – II Stage – III Stage-I : The formation of prothrombinase is initiated by either the extrinsic or theintrinsic pathways blood clotting.
  41. 41. Extrinsic path way: The extrinsic pathway of blood clotting has fewer steps than theintrinsic pathway and occurs rapidly, with in a matter of seconds if trama is severe.Damage to endothelim tissue protein called tissue factor (IF) also known asthromboplastin or coagulation factor III, leaks into the blood from cells out side(extrinsic to) blood vessels and initiates the formation of prothrombinase. IF ismixture with of lipoproteins and phospholipids released from the surfaces of damagedcell. It activates clotting factor VII, which next combines with factor X, thusactivating it. Once factor is activated, it combines with factor V in the presence ofcalcium ions (Ca2+) to form the active enzyme prothrombinase. This completes theextrinsic pathway.Intrinsic pathway: The intrinsic pathway of blood clotting is more complex than theextrinsic pathway. And it occurs more slowly, usually requiring several minutes. IFendothelial cells (cells in the blood vessel) become roughened or damaged, bloodcame in contact with collagen in the surrounding basal lamina, in addition, trama toendothelial cells causes damage to blood platelets, resulting in the release ofphospholipids by the platelets. Contact with collagen activates clotting factor XII. Inturn, factor XII activates XI which activates factor IX. Activated factor VII (Fromextrinsic pathway) also can activate factor IX. Activated factor IX joins with the factorVIII and Platelets phospholipids to activate factor X. Once factor X is activated itcombines with factor V to form the active enzyme prothrombinase.Stage2: Once prothrombinase is formed, the common pathway follows. In the secondstage of blood clotting, prothrombinase and Ca2+ catalyze the conversion ofprothrombin to thrombin.Stage3: In the third stage, thrombin, the presence of Ca2+, converts fibrinogen, whichis soluble to loose fibrin threads, which are insoluble. Thrombin also activates factorXIII (fibrin stabilizer factor), which strengthen and stabilized the fibrin threads into asturdy clot. - Bleeding time – 2.5 mints. - Prothrombin time – 11-16 sec - Clotting time – 6-7 mints.
  42. 42. Blood groups The surface of erythrocytes contain some glycoproteins and glycolipids that canact as antigens, are normal components of one person’s RBC plasma membrane thatcan trigger damaging antigen – antibody responses in other people. Based on thepresence or absence of various isoantigens. In there are four principal blood groups,designated O, A, B and AB. These blood groups deffer in the types of antigens thatare present on the erythrocytes. Persons with type A blood have a Aantigens. Thosewith type B, B antigens: Those with type AB, both A and B antigens: In addition, theplasma of group ‘O’ blood contains antibodies to A, B and AB. Group A plasmacontains antibodies to B antigens and group B plasma contains antibodies to Aantigens. Group AB plasma has no antibodies to O, A, or B antigens. In bloodtransfusions cross-matching is necessary to prevent agglutination of donor red cells byantibodies in the plasma of the recipient because plasma of groups A, B and AB hasno antibodies to group O erythrocytes, people with group ‘O’ blood are called‘Universal doners’. Conversely, persons with AB blood are called Universalrecipients, because their plasma has no antibodies to the antigens of the other threegroups.In addition to the ABO blood grouping, there are Rh (Rhesus factor) – positive andRH Negative groups. An RH-Negative person can develop antibodies to Rh positivered blood cells if that person is exposed to Rh. Positive blood. For example, duringpregnancy a mother who is Rh negative can make antibodies for Rh-possitive cells inthe fetus is Rh positive (inherited for Rh positive). Rh-positive red cells from the fetuscan enter the maternal blood stream at the time of plancental separation and induceRh-positive antibodies in the mother plasm. The Rh-positive antibodies from themother can also reach the foetus via the placenta, and agglutionate and haemolyzefoetal red cells. This condition is known as Erythroblastosis foetalis, a haemolylicdisease of the new born.
  43. 43. Functions of blood: 1. Transport of respiratory gases. It transports oxygen form the lungs to all cells and carbondioxid from cells to the lungs. 2. Transport of nutrition from the digestive organs. 3. It transports the waste products from the cells to the kidneys, lungs, and sweat glands. 4. Maintenance of water balance 5. Regulation of body PH and body temperature 6. It protects against toxins and foreign microbes. 7. It transport the enzymes and hormones to the cells 8. Regulation of blood pressure. 9. Maintenance of ion balance 10. It prevents the body fluids loss through clotting mechanism.References: 1. Charaka Samhita, Sareera Sthana, 7th Chapter 2. Charaka Samhita, Sutra Sthana, 24th and 28th Chapters. 3. Charaka samhita, Vimana Sthana, 5,7,8 Chpater 4. Susruta Samhita, Sareera Sthana, 1st Chpater 5. Susruta Samhita, Sutra Sthana, 14th, 21st, and 42nd chapters. 6. Astanga Hridaya, Sutra Sthana, 1st, 12th, 16th, 20th Chapters 7. Principles of Anatomy and Physiology by J. Tortora. 8. Textbook of Physiology by C.C. Chatterjee. 9. Applied Physiology by Samson Wrights. 10. Textbook of Medical Physiology by Guyton & Hall 11. Human Physiology by Chakrabarti, Ghosh and Sahana 12. Wills Biochemical Basis of Mecdicine. 13. Regional and Applied Human anatomy by Dr. B.D. Chaurasia.
  44. 44. NIDANA The word panchalakshana nidana indicates that there are five topics to discussunder this text. It helps a physician to come to exact diagnosis of the disease. They are I. NIDANA – The etiology II. POORVAROOPA- The prodromal symptoms signs. III. ROOPA – The signs ans symtpoms IV. UPASAYA & ANUPASAYA – The comforting and aggravating factors V. SAMPRAPTI - The pathogenesis.NIDANA (Etiology) Nidana is said to be disease producing factors and they are called as aeteologicalfactors in modern medicin. “Seti kartavyatako rogotpadaka Heturn nidanam” Means the factors, which plays an essential role in causing a disease vividhaahita ahara vihara which cause vyadhi by vitiating doshas and dhatus. Various factors are mentioned for the etiology of the disease. In the context ofPandu roga all factors responsible for aggravation of pitta are termed as specificnidanas. It can be stated that pitta prakopa nidanas cause the disease. The ahara andvihara which are responsible for the disease can be divided into following types. i. Ahara (Diet related factors) ii. Vihara (behavior related factors) iii. Manasika (psychological factors) iv. Nidanardhakara Rogas (other diseases leading to Pandu) and v. Acquired by papakarma (sinful act)
  45. 45. Ahara (Diet) related factors 1. Atikhara dravyas 2. Ati amala dravyas 3. Ati katu dravyas 4. Ati kashaya dravyas 5. Ati Ushana dravyas 6. Ati teekshana ahara 7. Vidagha dravyas 8. Asatmya dravyas 9. Nishpava 10. Masha 11. Pinyanaka 12. Tilataila 13. Mritbhakshanam (geophagia and pagophagia) In the above stated factors kshara, amla, katu, lavana dravyas directly aggravateto pitta. Especially, amlarasa does kapha vilayana, pitta vardhana, rakta dooshana andsydhilya (increased catabolism). Ati lavana rasa intake leads to Raktapitta,Amalapitta, Indralupta, vatarakata and other “pitta-rakta” related disorders.Viruddhahara leads to vitiation of “tridoshas”. Masha is ushna veerya and in turmincreases pitta, Tila is pittakara and ushna veerya. Ati teekshana ahara causes daha as it is of Agni boota predominance. Madhyadoes pitta vitiation.Vihara related factors: 1. Diwaswapna 2. Ati vyayama 3. Ati maidhuna
  46. 46. 4. Panchakarma vaishamya 5. Nidra nasha 6. Vega dharana 7. Rutu Vaishamya 8. Rakta mokshana vaishamya In the above mentioned factors ativyayama and ati mydhuna leads to increasedcatabolism, thus contributing to the cause of the disease. Panchakarma vaishamyavegavaroodha does vitiation especially to vata and thus cause disease pandu roga.Among all Panchakarma vyshamyas, Atiraktasravam during rakta mokshana is also acause for the occurence of the disease.Manasika factors: 1. Kama (desire) 2. Chinta (thinking) 3. Bhaya (fear) 4. Krodha (anger) 5. Shoka (sorrow) Kama, shoka and bhyaya vitiate vata, krodha vitiates pitta, and chinta vitiatesvata kapha and produce vataja, pittaja and kaphaja predominant Panduroga.Nidanardhakara factors: The disease which cause Pandu are grouped as 1. Rakta pradara 2. Raktapitta 3. Arshas 4. Krimiroga 5. Adhika raktasrava (due to abhighata) 6. Rakta arbuda 7. Rakta gulma
  47. 47. 8. Pleehodara 9. Katikatarunamarma vedha 10. Yakrit pleeha vedha 11. Rakta atipravartanam 12. Hridroga Apart from the above disease, all the conditions that end up in blood loss leads toPandu roga.Papakarma factors: (Sinful act) A person acquired Panduroga by sinful act according to the references fromVaidya chintamani i.e. one who steals things of Gods and Brahmanas, one who doesnot complete Agnistomadi karmas and one who kills a woman. Such persons acquirePandu with severe headache and with symptoms of kshaya. Such type of Pandu doesnot get cured within nine years. Thus the nidana of panu roga has been elaborately touched and discussedbecause it has been said that "Chikitsa is Nidana Parivarjanam"Nidana as mentioned in different classicsAhara (Diet) related factors: S.No. Description Charaka Susrutha Madhavakara Haritha Vagbhta 1 Kshara + - - + - 2 Lavana + + + + - 3 Katu - - - - + 4 Kashaya - - - + - 5 Atiteekshna - + + - - 6 Atiushna + - - - - 7 Virudha + - - - - 8 Vidagda + - - - - 9 Asatmya + - - - - 10 Nishpava + - - - - 11 Masha + - - - - 12 Pinyaka + - - - - 13 Tila taila + - - - - 14 Madya + - - - - 15 Mireya + + + + - 16 Amla + - - + - 17 Mrittika + + + + +
  48. 48. 2. Vihara factors: S.No. Description Charaka Susrutha Vagbhta Madhavakara Haritha 1 Diwaswapna + + + + + 2 Vyayama + - + + - 3 Maidhuna + + + - + 4 Panchakarma + - - - + vaishmya 5 Rutuvaishamya + - - - - 6 Vegavidhrana + - - - - 7 Nidranashnam - - - - + 8 Avyayama - - - - + 9 Shrama - - - - +3. Manasika factors S.No. Description Charaka Susrutha Vagbhata Madhavakara Haritha 1 Kama + - - - - 2 Chinta + - - - + 3 Bhaya + - - - - 4 Krodha + - - - - 5 Shoka + - - - - Charaka mentioned Pandu roga is the "Santharpanajanya Vyadhi". Though theintake of food may be more, the disease is aquired due to pitta Vardhaka ahara as wellas viharas. This imbalanced diet contains more fats, however deficiency of vitaminsand minerals leads to anaemia.
  49. 49. ETIOLOGICAL FACTORSAnaemia is caused due to various factors. They are grouped into following heading. 1. Idiopathic causes 2. Haemorrhagic anaemia 3. Dyshaemopoietic anaemia 4. Haemolytic 5. Aplastic or non-functioning Bone marrow1. Idiopathic: Causes may be due to the anorexia. Psychiatric, autoimmune disease.2. Haemmorhgic factors: Loss of blood due to trauma and various other causes. a. Acute: Acute and massive haemorrhage in antipartum haemorrhage, post partum haemorrhage, haematemesis, haemoptysis. b. Chronic: Small and recurrent bleeding tendency such as piles, bleeding gums, hookworms, etc, menorrhagia in females, chronic ulceration of gastro intestinal tract, GIT malignancy, long standing haematuria oesophagical varices.3. Dyshemopoietic (or) Due to defective blood formation: a. Due to nutritional deficiency (or) deficiency of extrinsic factors b. Failure of absorption of iron, proteins, B12 , folic acid and vitamin C. c. Lack of iron storage (due to liver damage large amount of iron & other necessary elements are not stored and leads to anaemia). d. Lack of releasing factors due to spleen enlargement. e. Defiiency of certain minerals like copper, cobalt, manganese and certain hormones like thyroxine, etc. f. Endocrind disorders eg. Myxodema, Addisons disease.
  50. 50. 4. Hemolytic anaemia:Normally RBCs are destroyed by Reticulo – endothelial cells, situated in liver, spleenand bone marrow. a. Due to abnormal formation of RBCs as in spherocytosis, thalassemia and sickle cell anaemia. b. Due to circulating haemolytic agential haemolytic anaemia and paroxysmal haemoglobinuria. c. Incompatibility of blood groups and Rh incompatibilities. d. Bacterial infections – septicemia e. Chemical agents – Aspheramine, coaltar, derivatives and poisoning. f. Snake venom and other poisionous bites cause anaemia due to haemolysis. g. Cytotoxic drugs such as phenyl hydrazine, hydrochlorosis and quinine also cause haemolysis.5. A plastic (Non-functioning) bone marrow: a. Lack of Utilization of haemopoetic factors by bone marrow is seen in primary Aplasia. b. Sometimes drugs such as chloromycetin, quinine, Benzol, Aspheramine and gold salts depress the bone marrow, causing secondary Hypoplasia. Radium salts, radioactive materials and X-rays also cause bone marrow.Warm – infestation:Parasites may cause disease Anaemia due to their presence in the lumen of theintestine, due to infiltration into the blood stream.Ex. Malarial Parasite may cause Anaemia due to Haemolysis (Distruction of Redcells). Nematodes like Ascaris, Enterobiasis (Pin warm), Tape warms and Hook warmsare caused to Anaemia in human being especially in children during the first decade oflife.
  51. 51. In effects individuals at all socio-economic level especially children crouded livingconditions predispose individuals to infection.The larwas are found in warm, damp soil and infect humans by penetrating the skin.They migrate to the lungs ascend thetrachea are swallowed and reside in the institine.The warms then mature and attach to the intestinal wall, when they suck blood, andshed eggs, caused by the Symptoms like Anorexia, Indigesation, Abdominal pain andFullness of abdomin, and Diarrhoea occurs. The major manifestation of infection issubsequent Anaemia.References: Charaka Samhita, Chikista Sthana 16/7-11 Susrutha Samhita, Uttara Sthana 44/1-3 Astanga Sangraha, Nidana Sthana 13/3-6 Astanga Hridaya, Nidana Sthana 13/1-3 Madhavanidana 8/2 Hareeta Samhita, Triteeya sthana 8/3-5. A text book of Human physiology by Dr. Sahana chakraborthy and Ghosh. A text book of Pathology by Boiyd Nelson Text Book of Paediatrics.
  52. 52. POORVA ROOPA According to susrutha, the sanchita and prakopita doshas are occumulated in aparticular stana it is termed as “Stana samshrayaavasta” a premonitory signs andsymptoms of manifestation of vyadhi. Those signs and symptoms which appearsearlier to the actual disease, as they are not clearly recongnisable and few in number.These are called poorvaroopas, This is very important stage, which is to be observedby the physician because it would be very easy to prevent the disease. “Poorva roopam pragutpathi lakshanam Vyadhi”- (Charaka Nidana – I Chapter) Poorvaroopam is a state where the prodromal signs and symptoms of a diseasestart to occur. In other words, it is described as the early stage of any disease. It is thatstate of the disease, where Dosha – Dooshya Sammoorchana occurs, i.e. there beginsan interaction between the doshas and the dooshyas. Poorva Roopa is of the following two types 1. Samanya poorva roopa 2. Visesha poorva roopa Samanya poorva roopa gives information about the disease, which occur in thefollowing days but not the detailed description of the predominant dosha. Viseshapoorva roopa gives most of the details of the occurring disease at an early stage.Samanya poorva roopa of Pandu are: 1. Twak sphotana 2. Shteevana 3. Gatrasaadana 4. Koota shodha 5. Avipaka 6. Hridaya spandana 7. Twak rushata 8. Swedabhava
  53. 53. 9. Sharama 10. Shareera pandutwa 11. Mrit bhakshanaapeksha 12. Alpagni 13. Shareera krishatwa 14. Angasaada 15. Aruchi 16. Vit., Mootra, PeetatwamPoorvaroopa – According to different acharyas :Sl Poorvaroopa Charaka Susrutha Vagbhata Hareeta1 Twaksphotana - + - -2 Shteevana - + - -3 Gatrasaada - + - -4 Kootashodha - + - -5 Avipaka - + - -6 Hridayaspandana + - - -7 Twakrushata + - - -8 Swedabhava + - - -9 Shrama + - - -10 Shareerapandutwa - - - +11 Aruchi - - + -12 Vit, mootrapeetatwam - + - -13 Mritbhakshanaapeksha - + - -14 Alpagni - - + -15 Angasaada - - + -16 Shareerakrishatwa - - + -
  54. 54. Though there is no detailed description of the vishesha poorva roopas by any ofthe classics, we can divide the above poorva roopas upon the doshic predominanceand can classify as follows: S.No. Vataja P.R. Pittaja P.R. Kaphaja P.R. Mritbhakshana P.R. 1 Twaksphotana Vit, mootra Shteevanam Mrit Bhakshana Peetatwa Shteevanam 2 Angasada Avipaka Alpagni - 3 Gatrasaada - Aruchi - 4 Twakrushata - Hridayaspandana - 5 Swedabhava - Kootashodha - 6 Sareera krishatwa - Sareera pandutwa - 7 Shrama - - POORVA ROOPA - MODERN ASPECT There are no definitive prodromal symtpoms mentioned as such in case ofAnemia. Especially, these depend upon oxygen carrying capacity of the blood. Theseverity of the signs and symptoms depend upon the degree of anemia, independent ofits type. Lassitude and Fatigue, though are seen in the early stages of the disease, theseare seen in many other disease. Pallor of skin, mucous membranes, palms andconjunctivae are seen after some period and these in addition to above may give abetter picture of this disease. The complete picture of the disease shall be discussedunder Roopa.References: Charaka Samhita Chikistasthana 16/12 Susrutha Samhita Uttara Sthana 44/5 Astanga Sangrata Nidanasthana 13/6 Astanga Hridaya Nidana Sthana 13/8 Hareeta Samhita, Trieeya sthana 8/6 Principles and Practice of Medicine by Davidson
  55. 55. ROOPA This is the stage of a disease where the signs and symptoms of the disease aretotally manifested, this termed as fifth kriya. Kaala of ‘vyaktibhava’. When thedisease starts to take its stage forth kriyakala namely in the Stanasamshrayaavasthaor Poorvaroopavasta and when it is not treated the doshas get accumulated andmanifestiation into the diseased state – “ROOPA”. “Tadeva vyaktatam yatam rupa mityabidiyate” The poorva roopa which has attained vyakthavastha known as roopam. Thesymtpems are mainly due to sroto dushti of the respective Srothases. The main srotasinvolved in pandu roga is Rasavaha srota drushi. Hence, almost all of Rasavaha sroto dushti lakshanas can be observed in pandusymptomatology. These are Aruchi, Ashraddha, Agnimandya, Hrillasa, Arasagnatha,Gouravam, Tandra, Angamarda, Pandutwam, Jwara, Klaibhyam, Sada, Krishnagataand phalitya. In general, the signs and symptoms of pandu roga are as follows: 1. Dhatu shaithilya 2., Alpa rakta 3. Ojoguna kshaya 4. Alpa medas 5. Sithil endriya 6. Hritdrava 7. Shoona akshi 8. Koota sadana 9. Kopana 10. Shteevana 11. Alpavak 12. Hataanala 13. Anna dwesha 14. Karna kshweda 15. Dourbalyata 16. Sisira dweshi 17. Shrama 18. Bhrama 19. Shoola 20. Jwara 21. Swasa 22. Gourava 23. Gatra peeda 24. Aruchi 25. Sheerna loma 26. Hata prabha 27. Nidradhikyata 28. Pindiko dwestta 29. Kati, Uru, Pada – ruk 30. Sannasakti 31. Sphurana 32. Nakha vakrata 33. Swetha akshi 34. Arosha naayasa
  56. 56. In addition to the above, kshayalakshanas of Rasa, Rakta, Medo, Mamsa, andOjus can also be observed in panduroga. The disease is classified into five types, according to the involvement of doshas. 1. Vataja pandu roga 2. Pittaja pandu roga 3. Kaphaja pandu roga 4. Sannipathaja pandu roga 5. Mritbakshanajanya pandu roga The lakshanas of all these varieties differ from each other, and they are stated inbelow.Lakshanas of vataja pandu roga:S.No. Symptoms/sign Cha Su Va Ma Bha Ha1 Aruna angata + - + + + -2 Aruna nakha - - + - - -3 Aruna netra - - + + + -4 Aruna sira - - + + - -5 Rkshna mala, mootra - - + + + -6 Ruksha netra - - + - - -7 Ruksha nakha - - + - - -8 Ruksha anga + + + + + -9 Krishna netra - + + + + -10 Aruna mala mootra - - + - + -11 Krishna nakha - + + - - -12 Vata vikara - + - + + -13 Anga marda + + - - - -14 Jwara + - + - - -15 Toda + - - - - -16 Kampa + - + + + +17 Parshwa shoola + - + + + -18 Shirah shoola + - + - - -19 Vitshoola + - + - - -
  57. 57. 20 Asya vairassya + - + - - -21 Shopha + - + - - -22 Anaha + - + + + -23 Balakshaya + - - - - -24 Bhrama - - - + + -25 Parushata - - - - - +26 Sirogurava - - - - - +27 Gadhavitakata - - - - - +28 Ruksha sira - - + + - -Lakshnas of pittaja pandu roga:S.No. Symptoms/sign Cha Su Va Ma Bha Ha1 Shareera peeta + + + + + +2 Shareera Harita + - + - - -3 Peeta mala, mootra + + + + + +4 Peeta netra - + + + + -5 Peetha nakhata - + + - - -6 Peetha sira - + + - - -7 Harita sira + - + + + +8 Jwara + - + + + +9 Daha + + + + + +10 Trishna + - + - - -11 Moorcha + - + - - -12 Sweda + - + - - -13 Annadwesha + - + - - -14 Katu kasyam + - + - - -15 Amlodgara + - + - - -16 Ushna, Amla anupasayata + - - - - -17 Vidaha + - - - - -18 Dourgandha + - + - - -19 Binnavarchasa + + + + - +20 Dourbalya + - - - - +21 Pitta vikara - - - - - -22 Tama + + + - - -23 Shopha - + - - - +
  58. 58. Lakshanas of kaphaja pandu rogaS.No. Symptoms/sign Cha Su Va Ma Bha Ha1 Swetha avabhasata + + + + + -2 Sukla akshi + + + + + -3 Shukla nakha - + + - - -4 Shukla, mala, mootra + + + + + -5 Shukla sira - + - - - -6 Gouravam + - + + + +7 Tandra + - + + + +8 Chardi + - - - - -9 Praseka + - + + + -10 Lomaharsha + - + - - -11 Angasadha + - - - - -12 Moorcha + - - - - -13 Bhrama, klama + - - - - -14 Swasa + - + - - -15 Kasa + - - - - +16 Alasyam + - - + + +17 Aruchi + - - - - -18 Vak, Swaragraha + - - - - -19 Katu kamata + - - - - -20 Ushna kamata + - - - - -21 Swayadu + - - + + +22 Madhurasyata + - - - - -23 Lavanakamata - - + - - -24 Swara kshaya - - + - - -25 Sleesma vikara - + - - - -26 Swedana - + - - - -

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