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Evaluation of the efficacy of AMRUTADI YOGA IN GALAGANDA (GOITER) By Renjith. P. Gopinath, Department of Kayachikitsa, Post graduate studies and research center D.G. MELMALAGI AYURVEDIC MEDICAL COLLEGE, Gadag - 582 103

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Galaganda kc027 gdg

  1. 1. Evaluation of the efficacy ofAMRUTADI YOGA IN GALAGANDA (GOITER) By Renjith. P. Gopinath Dissertation submitted to the Rajiv Gandhi University of Health Sciences, Karnataka, Bangalore In partial fulfillment of the degree of Ayurveda Vachaspati M.D. In Kayachikitsa Under the Guidance of Dr. V. Varada Charyulu M.D. (Ayu) (Osm) Dr. Shiva Rama Prasad Kethamakka M.D. (Ayu) (Osm) M.A. (Jyotish), [Ph.D (Jyotish)] Department of Kayachikitsa Post Graduate Studies & Research CenterD.G. MELMALAGI AYURVEDIC MEDICAL COLLEGE, GADAG 2002-2005
  2. 2. J.S.V.V. SAMSTHE’S D.G.M.AYURVEDIC MEDICAL COLLEGE POST GRADUATE STUDIES AND RESEARCH CENTER GADAG, 582 103 Endorsement by the H.O.D, Principal/ head of the institution This is to certify that the dissertation entitled “Evaluation of the efficacy ofAMRUTADI YOGA IN GALAGANDA (GOITER)” is a bonafide research work done by“Renjith. P. Gopinath” under the guidance of Dr. V. VARADA CHARYULU, M.D.(Ayu) (Osm), Professor & HOD and Dr. SHIVA RAMA PRASAD KETHAMAKKA,M.D. (Ayu) (Osm) M.A. (Jyotish), [Ph.D (Jyotish)], Reader in Kayachikitsa, DGMAMC,PGS&RC, Gadag, in partial fulfillment of the requirement for the post graduation degree of“Ayurveda Vachaspati M.D. (Kayachikitsa)” Under Rajeev Gandhi University of HealthSciences, Bangalore, Karnataka.. (Dr. V. Varada charyulu) (Dr. G. B. Patil) Professor & HOD Principal, Dept. of Kayachikitsa DGM Ayurvedic Medical College, PGS&RC Gadag Date: Date: Place: Gadag Place: Gadag
  3. 3. D.G.M.AYURVEDIC MEDICAL COLLEGE POST GRADUATE STUDIES AND RESEARCH CENTER GADAG, 582 103 This is to certify that the dissertation entitled “Evaluation of the efficacy ofAMRUTADI YOGA IN GALAGANDA (GOITER)” is a bonafide research work done by“Renjith. P. Gopinath” in partial fulfillment of the requirement for the post graduationdegree of “Ayurveda Vachaspati M.D. (Kayachikitsa)” Under Rajeev Gandhi University ofHealth Sciences, Bangalore, Karnataka.Dr. SHIVA RAMA PRASAD Dr. V. VARADA CHARYULUKETHAMAKKA M.D. (Ayu) (Osm)M.D. (Ayu) (Osm) M.A. (Jyotish), [Ph.D (Jyotish)] GuideCo- Guide Professor & HODREADER IN KAYACHIKITSA Dept. of KayachikitsaDGMAMC, PGS&RC, Gadag PGS&RCDate: Date:Place: Gadag Place: Gadag
  4. 4. Declaration by the candidate I here by declare that this dissertation / thesis entitled “Evaluation of the efficacy ofAMRUTADI YOGA IN GALAGANDA (GOITER)” is a bonafide and genuine researchwork carried out by me under the guidance of Dr.V.Varada Charyulu M.D. (Ayu) (Osm) andDr. SHIVA RAMA PRASAD KETHAMAKKA, M.D. (Ayu) (Osm) M.A. (Jyotish), [Ph.D(Jyotish)], Reader in Kayachikitsa, DGMAMC, PGS&RC, Gadag.DatePlace (Renjith. P. Gopinath)
  5. 5. Copy right Declaration by the candidate I here by declare that the Rajiv Gandhi University of Health Sciences, Karnataka shallhave the rights to preserve, use and disseminate this dissertation/ thesis in print or electronicformat for the academic / research purpose.DatePlace (Renjith. P. Gopinath)© Rajiv Gandhi University of Health Sciences, Karnataka
  6. 6. Abstract Evaluation of the efficacy of Amrutadi yoga in Galaganda (goiter) By - Renjith. P. Gopinath The thyroid disorders are characterized by physical and mental interference. Wecan correlate goiter and some tumor pathology of thyroid to ‘Galaganda’ where thyroidfunctions may or many not are affected. Susruta defines Galaganda as a swelling (mass in the neck region), by thevitiation of Vata, Kapha and medo Dhatu where in Charaka named only Kaphacirculates in and around neck is the cause. Mental factors like chinta, sokha, krodha,bhaya, etc vitiate Vata Dosha. Goitrogens - suppress thyroid function and can inducehypothyroidism and goiter. Iodine restriction will cause the thyroid to increase in size (goiter) in an effort tofilter more blood to get more iodine. Once copper is replenished and copper metabolismis working properly, the body will tolerate iodine without increasing thyroid hormoneproduction. Lack of thyroid hormone can cause constipation. Thyroid hormonesincreases the rapidity of cerebration but also often dissociates this conversely, lack ofthyroid hormone decreases this function. Anemia is pre-condition for the production of thyroid disease. Greatly increasedthyroid hormones almost always decrease the body weight, and greatly decreasedhormone almost always increases the body weight. This study is a prospective clinical study of Amrutadi thailam in Galaganda. 17patients were selected for the study in one group. The goiter is present in both types ofthyroid disorders such as hypo thyroidism and hyperthyroidism. After the assessment of both subjective and objective parameters the results are,hypothyroidism patients were responded to the treatment, the euthyroid patients weremaintained with the treatment and the hyper thyroid patients were not responded to thetreatment. The observations are - thyroid disease is common in the middle-aged womenwith family history. It plays a vital role in the change of the character, and mental stateof the patients. In hypothyroidism patients the body weight will be increased and inhyperthyroidism patients, it will be reduced. The group Hyperthyroidism differssignificantly from Group Hypothyroidism and Group Euthyroidism. GroupHypothyroidism is Significant.
  7. 7. Acknowledgement At first my sincere thanks to the subjects who cooperated at my dissertation, without of them it would have been not a success. I express my deep gratitude to my guide Dr. V. Varadacharyulu M.D.(Ayu),Professor & H.O.D., for his advice and encouragement of every step of this work. I express my obligation to my co-guide Dr Kethamakka Shiva Rama Prasad,M.D.(Ayu) M.A,Ph. D (Jyotish), Reader in Kayachikitsa, for his time to time help andcritical suggestion associated with expert guidance at the completion of this dissertation. I express my obligation to beloved principal Dr. G. B. Patil, Principal for hisencouragement as well as providing all necessary facilities for this research work. I express my profound sense of gratitude to various departments H.O.D.s, teachersand colleagues of sister concern departments along with the ministerial and sub staff of theD.G.M. Ayurvedic Medical College, Gadag. I express my sincere thanks to Dr. Shashidar. H. Doddamani, Dr. R. V. Shettar, Dr.Kuber Sankh, Dr. P. Shivaramudu, Dr. Dilipkumar, Dr. V.M.Sajjan, Dr. U.V.Purad, Dr.Santhosh Belavadi and Dr Pawadshettar. I express my sincere thanks to Mr. Nandakumarfor his help in statistical analysis of results. I express my deepest gratitude to my beloved parents, Dr.P.S.Gopi, andDr.M.K.Indira, to my relatives and well wishers Rejitha.P.G, Dr.M.K.Unnikrishnan,Dr.M.K.Sathy, Dr.M.K.Baby, Mr. Babuprasad, M.Sc (IT) and Dr.M.Balakrishna Pillai fortheir inspiration. With respect and affection, I acknowledge my ever-remembering late Grand fatherShri M.P. Kunjan Vaidyan who inspired me all the timePlace:Date: Renjith. P. Gopinath
  8. 8. Table of contents Evaluation of the efficacy of Amrutadi yoga in Galaganda (goiter) Heading Page numberChapter -1 Introduction 1 to 4Chapter –2 Objectives 5 to 7Chapter –3 Review of literature 8 to 53Chapter –4 Methodology 54 to 79Chapter –5 Results 80 to 112Chapter –6 Discussion and Conclusion 113 to 134 Summary 135 to 139 Bibliographic References i to vi Annex – Case sheet 1 to 5
  9. 9. Tables Tables - Amrutadi yoga in Galaganda (goiter) Page1 Lakshana of Vataja Galaganda 312 Lakshana of Kaphaja Galaganda 323 Lakshana of Medoja Galaganda 334 Showing clinical features of Hyperthyroidism 355 Showing clinical features of Hypothyroidism 366 Differential diagnosis of Galagraha and Apachi 507 Differential features of Galaganda, Galavidradhi, Kanthashaluka and 51 Mamsatana.8 General survey of the thyroid patients for Hyper or Hypo thyroidism 629 Distribution of patients by age 8010 Distribution of patients by sex 8211 Distribution of patients by religion 8412 Distribution of patients by occupation 8513 Distribution of patients by economical status 8714 Distribution of patients by mode of onset 8815 Distribution of patients by intake of Goitrogens 9016 Distribution of patients by family history 9117 Distribution of patients by Agni 9218 Distribution of patients by sleep 9419 Distribution of patients by psychological features 9520 Distribution of patients by habits 9721 Distribution of patients by menstrual cycle 9822 Distribution of patients by built and nutrition 10023 Distribution of patients by Aharaja and Viharaja Nidana 101
  10. 10. Tables – continued : Amrutadi yoga in Galaganda (goiter) Page24 Distribution of patients by with systems involved 10325 Distribution of patients by chief complaints 10526 Subjective parameters enumerated (a) 10627 Subjective parameters enumerated (b) 10628 Showing the statistical analysis of the chief complaints 10729 Showing the statistical analysis of the lab investigations 10730 Anova – Table for the parameter T3 10831 Anova – Table for the T4 parameter 10832 Table show which pair of group is significant 10833 Anova- Table for parameter T.S.H. 10934 To show which pair of group is significant 10935 Showing the result of Amrutadi taila capsules in Galaganda 11236 Hyperthyroidism - Discussion on General and local symptoms 11937 Hyperthyroidism Systemic evaluation - Cardiovascular symptoms 11938 Hyperthyroidism Systemic evaluation - CNS symptoms 12039 Hyperthyroidism Systemic evaluation - Gasto-intestinal symptoms 12040 Hyperthyroidism Systemic evaluation - Dermatological symptoms 12141 Hypothyroidism -General features of hypothyroidism 12142 Hypothyroidism Systemic evaluation - Cardiovascular symptoms 12243 Hypothyroidism Systemic evaluation - CNS symptoms 122
  11. 11. Graphs Graphs - Amrutadi yoga in Galaganda (goiter) Page1 Showing Patients by age distribution 812 Showing Patients by gender distribution 833 Showing Patients by religion distribution 854 Showing Patients by occupation distribution 865 Showing Patients by economical status distribution 886 Showing Patients by mode of onset distribution 897 Showing Patients by intake of Goitrogens distribution 908 Showing Patients by family history distribution 929 Showing Patients by Agni distribution 9310 Showing Patients by sleep distribution 9511 Showing Patients by psychological features distribution 9612 Showing Patients by habits distribution 9813 Showing Patients by menstrual cycle distribution 9914 Showing Patients by built and nutrition distribution 10115 Showing Patients by Aharaja and Viharaja Nidana distribution 10216 Showing Patients by with systems involved 10417 Depicting the results of Amrutadi yoga on Galaganda 112 Figures Figures – Amrutadi yoga in Galaganda (goiter) Page1 Location and anatomy of the Thyroid gland 202 Functions of the thyroid follicles 233 Auto regulation of the thyroid hormone 254 Schematic representation of the Galaganda Samprapti 405 Contents of Amrutadi taila (Photograph) 66
  12. 12. INTRODUCTION Ayurveda, the science of life is the holistic alternative system of medicine. Theorigin of this science is already evident in Atharvanaveda. Eventually Ayurveda wasoriginated into its own compact system of health and considered as a branch ofAtharvanaveda. The main aims of this science are to maintain one’s health and to protect thehuman beings from various diseases, which are acquired. Among many things man aspires to attain in life, a healthy body and healthy mindare the first to be sought for. The aim of all medical system should be a healthy body andhealthy mind. Ayurveda is one such system that prevailed from many years. Health isdefined as the condition in which the sharirika and the manasika bhavas exist in a state ofequilibrated normalcy. Ayurveda mentions comfort (sukha) as health (arogyam) with synonyms of Arogyaand Swasthya. The Ayurvedic concept of evolution of a disease is remarkably wide.According to Ayurveda Vyadhi i.e. disease has been defined as the state in which both bodyand mind are subjected for pain and agony respectively. At the present millenium has shown us numerous disorders and we know that thechanges in atmosphere and the living conditions or habits are among the causes. This resultsin serious multi systemic metabolic disorders like diabetes, thyroid problems, hepaticdisorders etc., Ayurveda is the best way to handle them safe and naturally. The thyroid disorders are characterized by physical and mental interference.Previously it was thought that these groups of disorders are of sporadic in nature in some 1
  13. 13. parts of India. For e.g. Goitre is common among people of the Himalayas due to the iodinedeficiency. As medical aids reached to the feet of common man and communication isdeveloped in association with that of luxuries and changed dietetics this disorder prevailedall over the globe and especially a developing country, India. An increasing number ofpatients of Goitre and many more Thyroidectomies, either partial or complete are evidentialfor the above discussion. Ayurveda is a golden mean between pure sciences and philosophical sciences.Therefore it becomes interesting to know how Ayurveda looks to a problem, which appearsto be untouched in Ayurveda. Endocrine disorders and concept of hormone are suchproblems noted here. In Ayurveda there is not an exact term for thyroid gland. Therefore it is not possibleto get an explanation of physiology and pathology of thyroid gland from our ancient books.Some of the later Ayurvedic scholar tried to name the thyroid gland, but they could notcompare many thyroid disorders with any of the ancient descriptions. We can correlate goitre and some tumor pathology of thyroid to ‘Galaganda’ wherethyroid functions may or may not is affected. But hypothyroidism and hyper thyroidismhave the symptoms related to many portions of the body. It is very difficult to correlate thesetwo entities with any of the nomenclated diseases of Ayurveda. Further hypothyroidism andhyperthyroidism are not single disease entities and many conditions are included under eachheading. It is therefore, better not to restrict thyroid dysfunction to any one of the diseases.Similarly, there are not mere localized disorders. In such a situation, an Ayurvedist need notbe specific to it but can treat the disease by knowing the condition of Dosha, Dhatu andAgni components of pathogenesis etc. and their interrelation with the disease condition. 2
  14. 14. The competition among the medical systems is increasing day by day. Thecontemporary systems use the most advanced techniques in assessing the disease and in theaspect of treatment and research studies. So, it is our duty to conduct proper research andinvent new methods and medicines, which serves to the mankind.The need for study In this fast forward life, the life style of man has changed. He is very much busy withthe day today schedules to acquire more earnings. This more desire have made the man todeviate from following the swastha vrutta, thereby becoming a victim of diseases. So in theyoung adult age itself man, has become victim of severe degenerative diseases likeSandhivata, Manyasthamba etc., and other multi systemic metabolic disorders like endocrinediseases, diabetes, etc., Among such diseases Galaganda (goiter) is a common onenowadays. The gradual increase and prevalence of Galaganda draws attention over thedeviation of lifestyle and balanced diet in the modern society. Mass in the neck, pain in the neck etc characterizes the disease 1, and it is a seriousmetabolic disorder, as it affects almost all systems of the body. It is most common nowadaysin every part of the world. Which is considered as a serious metabolic disorder that makes astrong impact on one’s daily life. Contemporary medical science are able to pacify thedisease through anti thyroid drugs, radio active iodine and if needed through the surgicaltreatment as the final with its own limitations. In Ayurveda we can offer safe and effective management for Galaganda. So toovercome this problem at young age without producing any complication, the research inthis area is essential. Ayurveda the ancient system of medicine has suggested good old 3
  15. 15. techniques and recipes to pacify the swelling (mass in neck) and other symptom withoutcausing any complication. Since this area is prevalent in goiter, I have taken the present study as ‘Evaluation ofAmrutadi thailam in Galaganda with positive thoughts. Still more research works areessential to establish the same by using research techniques and by statistical methods.Role of Ayurveda in this area and recent advances In the contemporary system of medicine the treatment given to thyroid disorders areanti-thyroid drugs, radio active iodine and surgery which has its own disadvantages and sideeffects. The drug-induced goitre is an evident example of it2. Ayurveda the traditional Indian system of medicine, describes a reliable andeffective management of diseases with due consideration to protect the normal health also. Ayurvedic approach to the disease ‘Galaganda’ is to reduce the Ganda (mass in theneck), toda (pain around the neck), kandu (itching around the neck), difficulty in breathingetc., and to strengthen the Dhatus and pacifying the Vata and Kapha Dosha which hasspecial importance in the management. The recent studies carried out in the past are: - 1. Effect of kanchanara (Valvina variegata and Balvina purpura) in Galaganda by Sijoria K in 1977 at BHU, Varanasi. 2. Use of indigenous drugs in Galaganda by Pandit R K in 1987 at BHU, Varanasi3. 3. Galagandarog par jalakumbhiprayog by Manekar H B in 1991 at Shri Ayurved Mahavidyalay, Nagpur4. 4
  16. 16. OBJECTIVES OF THE STUDY The aims of the study are - 1. Evaluate the anti Goitrogenic effect of Amrutadi thailam in Galaganda. 2. Evaluate the effect of Amrutadi thailam on T3, T4 and TSH in Galaganda. 3. To evaluate the efficacy of Amrutadi thailam Pratimarsha Nasya in Galaganda Amrutadi thailam mentioned in Yogaratnakaram is a wonderful combination, whichreduces the swelling pain rashes, which restores the voice, as it is Kantyam, alleviates Vata,Kapha and Medas. So, this combination is most suitable in the treatment of Galaganda. The present work by Amrutadi thailam is focussed exclusively in Galaganda (goiter).In this study the most modern techniques are adopted in terms of diagnosis, investigationsassessment and medicine preparation. All together this study gives a scientific approach inthe management of Galaganda. 5
  17. 17. 1. To evaluate the anti Goitrogenic effect of Amrutadi thailam in Galaganda. The condition is said to be affecting the neck region as a swelling mentioned byvarious authors in Ayurveda is termed as Galaganda and its management through variousmethods, one out of them is Amrutadi thailam, which is included in the present study. The specificity of the anti-Galaganda properties is studied as the anti Goitrogeniceffect. The anti Goitrogenic effect of Amrutadi thailam in Galaganda can be evaluated byunderstanding the cumulative effect of the said yoga. The Amrutadi thailam comprises of the 9 herbs, which are of Kapha, Vata and Medohara in nature, which may reduce the mass and there by regulate the effect of concern organpathology i.e. Galaganda viz., goiter. This can be understood that by the study of baseline data to the final data differencesafter the drug administration to the affected patients those who are included by the presetparameters of exclusion and inclusion criteria. As there is an elaborate discussion made under the drug review of individual drugs, acumulate effect is drawn out of as Shothahara – anti tumor property, Kantyam – regulatoryeffect of neck pathology and Rakta shodhaka – blood purification. These said properties areeffective over Dosha predominance and Dushya – Dhatus to regulate to normalcy byfragmenting the underneath pathologies.2. To evaluate the effect of Amrutadi thailam on T3, T4 and TSH in Galaganda. T3, T4 and TSH are the objective parameters to ascertain the functional capacities ofthe thyroid. The present study under takes the said lab investigations to evaluate the efficacyof Amrutadi thailam in thyroid problem of either Hypothyroidism or hyperthyroidism. This 6
  18. 18. data with precise information regarding the functional capacities to estimate the prognosisand the medical management to the said Galaganda with reference to that of Goitrogenic andthyroid pathologies are anticipated. Thus the present study intends to have the study of Amrutadi thailam with referenceto the T3, T4 and TSH assay.3) To evaluate the efficacy of Amrutadi thailam Pratimarsha Nasya in Galaganda Nasya karma a therapeutic procedure of intranasal drug administration, is one of thewell-known Panchakarma. According to the disease of medicine. It is divided as marshanasya and Pratimarsha nasya. Pratimarsha Nasya is a daily 2-3 drops in each nostril, withoutany poorva karma and pathyas. The finest specification of this therapy is made in theAyurvedic books, as acting on the body parts above the neck, that is the parts lying up oninside the skill. The ancient authors of Samhita proclaim that the drugs administered inNasya shall enter the head. In the Galaganda, a disease developed above to the clavicle is evaluated with theAmrutadi taila Pratimarsha Nasya, which has the rechana property and with the Ushna,teekshana Gunas alleviates the Kapha Dosha. 7
  19. 19. LITERARY REVIEW There are vast areas in India with iodine deficiency disorders (IDD). Besides the subHimalayan region, other flood- prone regions and reverine areas, deltas and costal regionsare now recognized to have iodine deficiency, i.e. the iodine content of water is <1ppm.There are an estimated 150 million people in India who are considered to be at risk of iodinedeficiency, and of these 54 million have goiter. Earlier the only recognized effect of iodinedeficiency on health was goiter; however, there is now a better understanding of theperspective of IDD. IDD now includes the following 5 : - 1. Goitre at all ages 2. Endemic cretinism with associated mental retardation, deaf- mutism, spatic diplegia and lesser degree of neurological deficit. 3. Impaired mental function in children and adults. 4. Increased rates of abortion, stillbirth and perinatal and infant mortality. 6Etymology of Galaganda The word Galaganda comprises of two parts - gala and ganda. Gala - is a word of masculine gender and it is derived by the union of ‘Gal’ dhatu and ‘Ap’ pratyaya or by the union of ‘Gru’ dhatu and ‘Vyap’ pratyaya. It means the pathway of food, i.e., kantha. Ganda - is a word of masculine gender. It is derived either by the union of ‘Gadi’ dhatu and ‘Ach’ pratyaya or ‘Gata’ and ‘Njantadda’ sutra. As per Medini Kosha, it means pidaka or budbuda and as per Ramanathateeka on Amarakosha, it means sphotaka or granthi. 8
  20. 20. In a nutshell, Galaganda relays the meaning, the sphotaka or ganda in the ganda. Therelative term from the contemporary medical science is goiter. Goitre 7- The term goitre is derived from the French word ‘ goiter’; which is originally derived from the Latin word ‘gutter’- means ‘throat’. We use the term ‘goiter’ to denote the enlargement of thyroid gland irrespective of its cause. The pocket oxford dictionary speaks the meanings of Goitre as – Goitre n. (Brit. goitre) morbid enlargement of the thyroid gland. [Latin guttur throat] 8, Goitre n. (US goiter) morbid enlargement of the thyroid gland. [Latin guttur throat] The thyroid gland first discovered by Mr. Wharton in the 19th century, weighsaround 20gms in adults. The thyroid (from GK, thyroid meaning a shield, because it shieldsthe trachea9.Definitions In almost all Ayurvedic treatises Galaganda is described elaborately. Susruta defines it as a swelling (mass in the neck region), by the vitiation of Vata,Kapha and medo dhatu10. But Dalhana and Gayadasa, in their commentaries mention it as aswelling in the neck (Nibadhaswayathu) 11. Charaka mentioned that when a vitiated Kapha Dosha circulates around the neck, itwill cause swelling slowly is termed as Galaganda12. Madhava Nidana explanation is more authentic as it states that Galaganda is aswelling attached to the neck which hangs down like a scrotum13. He also quotes thedefinition of Bhoja here as “Mahantam shopham alpam va hanu manya galashraye” 14 i.e. A 9
  21. 21. swelling resembling and hanging like a scrotum in the Hanu, Manya, and Gala is called asGalaganda. From the contemporary medical science, Goitre is defined as a benign, non-toxicenlargement of the thyroid gland usually secondary to some form or other of the iodinedeficiencies. The disease is characterized by swollen throat, hoarseness of voice, slight pain,in the neck region, difficulty to swallow, etc 15.Historical review:- The Vedas are the old and prime documented source of knowledge. There is noreference regarding the disease Galaganda in the Vedic literatures. Ayurveda, a medicalscience deals with almost all diseases, mentions elaborately about Galaganda as one amongthose disease, which were explained in concern with Kaphaja Vyadhis. There was a period were the science developed and flourished much and considered asthe golden period of Ayurveda. Almost all Acharyas had mentioned Galaganda in theirrespective treatises. Among Brihatrayees, Susruta mentioned Galaganda elaborately. Likewise the otherAcharyas also followed the same descriptions in separate chapters except Charaka. AcharyaCharaka has mentioned about Galaganda in Trishopheeyam adhyaya of sutra sthana 16. In Susruta Nidana, mentions about the Galaganda Samprapti are very clear. It statesthat, the Vata, Kapha and Medo Dhatu will got vitiated by its etiological factors and producethe Ganda (mass in the neck); which have the symptoms of the three respectively. Susrutadescribes the Lakshana, Bheda, and Sadyaasadhyata in Nidana sthana and the detail Chikitsaat its Chikitsa sthana 18th chapter 17-18. 10
  22. 22. In Charaka Samhita, mentions of Galaganda are from Trishopheeyam chapter of sutrasthana describing it as a ‘Shopham’ – swelling occurring in the neck due to vitiated Kapha.Here the vitiated Kapha will stay around the neck region and produce swelling, which iscalled as Galaganda 19. In Astanga Hrudaya and Astanga Sangraha, Vagbhatas mentioned Galaganda Nidana,Bhedas, Lakshanas in the Mukha roga vijnaneeyam adhyayam of the Uttara sthana andChikitsa in Mukha roga pradheeshedam adhyaya 20. In Madhava Nidana, Madhavakara quoted the same as that of Susruta and mentions theNidana, Lakshana, Bhedas, and Sadyasadyata of Galaganda in detail 21. 22 23 24 The other treatises, such as Yogaratnakara , Bhavaprakasha , Chakradutta , 25Vangasena , etc also mentions about Galaganda. They elaborately described about theLakshanas, Bhedas, Samprapti, and Chikitsa in their respective works. In the contemporary system of medicine, the disease Galaganda can be correlated with‘Goiter’. Goitre is a common disease in the modern society as there is a gradual increase inthe deviation of lifestyles and balanced diet. It is mainly common in area where the Iodinecontent of water is less than 1PPM 26.Epidemiology:- The thyroid disorders and goitre are common in the females, in the certain ages, inspecific part of the world. So the epidemiological evidences of these diseases are very muchimportant in detecting the cause and is useful to decide the treatment and in the preventionof those diseases also 27. 11
  23. 23. Age:- The age of the patient is a Very important consideration. Simple goitre is commonlyseen in girls approaching puberty and in pregnant women because in puberty and inpregnancy, the requirement of hormone is augmented. Both multi-nodular and solitary nodular goitres as well as colloid goitres are found inwomen of 20s and 30s. The primary toxic goitre is usually present in young ones, where inHashimoto’s disease the victims are middle-aged women.Sex:- Majorities of the thyroid disorders are seen in females. All types of simple goitres arefar more common in the female than in male. Thyro-toxicosis is 8times common in femalesthan in males. Even thyroid carcinomas are more often seen in females in the ratio 3:1. The prevalence of hyperthyroidism is about 20/1000 females; males are affected 5times less frequently. The female to male ratio 28 of hypothyroidism is 6:1.Geographical distribution Except endemic goitres due to iodine deficiency, no other thyroid disorders liesamong peculiar geographical distribution. Certain areas are particularly known to have low iodine and food. These areas are,Rocky Mountains, e.g.-Himalayas, the Vindyas, the Satpudha ranges, which form the goitrebelts in India. Such goitres are common in Southern India than in Northern India. Endemic goitres are common in low land areas where the soil lacks iodides or thewater supply comes from far away mountain ranges. Calcium is also Goitrogenic and areasproducing chalks and limestones are also Goitrogenic areas. 12
  24. 24. Nidana According to the treatment point of view, the knowledge of hetu is important so as toenable the physician to advice the patient to avoid the practice of Nidana, as it is mentioned“Nidana Parivarchanam Eva Chikitsa” 29. Madhava Nidana has clearly mentioned that Nidana of all the disease is due to thevitiation of Mala 30. Galaganda is a Kaphaja nanamatja Vyadhi 31and it is mentioned by all treatises. But 32the etiological factors are not directly mentioned in the classical texts. Charaka hasmentioned Galaganda as a lump situated in the neck where the swelling generated slowly, ora Sopham – edematous; especially with the Kapha and Vata Dosha predominance. SusrutaSamhita states, as like Charaka and adds to it that the Galaganda does not occur due to Pitta(Dalhana). When we review the lakshanas of the Vata, Kapha, and Medoja Galaganda, thesymptoms are similar that of Vataja and Kaphaja sopham. The different etiological factors from various texts are referred as under with rationalheadings such as – Ahara Nidana, Vihara Nidana etc.,1.Aharaja Nidana 33-34 It can be divided into Vata prokapa, Kapha prakaopa and Medoprakopakaranas.Consumption of Aharas having Vatika and Kaphaja predominance causes vitiationof Kapha, Vata in the body. The intake of tikta, katu, kashaya rasa , rookshannam, alpamatara bhojanam etcvitiate then Vata Dosha . The intake of madhura,amla,Lavana,snigdha, guru,abhishyanda,seeta, types of foods will vitiate Kapha Dosha . 13
  25. 25. The method and time of taking the food is also important. As abhojana,heenabhojana,suskhabhojana vitiates the Vata Dosha . The virudha bhojana, atibhojana,vitiates the Kapha Dosha .2.Viharaja nidanam 35-36 Vegadharanam, Vegotheeranam, Nisajagaranam, Atyuchabhashanam,Shodanadiatiyogam, Bhayam, Dukham, Chinta, Sramam, Upavasam, etc will vitiate VataDosha. Aasyasukham, Swapnasukham, Ajeeranam, Divaswapnam, brhmanatiyogam,Shodanadi ayogam, Avyayamam, etc will vitiate the Kapha Dosha. These two factors (the aharaja and viharaja factors) will vitiate the Vata and KaphaDosha. These are all the etiological factors of Vataja and Kaphaja sopham also.3.Manasika karanas 37 Mental factors like chinta, sokha, krodha, bhaya, etc vitiate Vata Dosha. Directionof sense organs is one of the functions of Manas and Vata is said to be the controller andconductor of mind. Therefore, by above factors Vata prakaopa occurs in the indreeyaayatanaand produce psychic as well as the somatic disorders; as there is a pivot role for mind inproducing the thyroid disorders also by unbalancing the production of thyroid hormones.4. Medovaha Sroto dhushti The increased Vata and Kapha Dosha in the neck will vitiate the medo Dhatu by itsprakopa karanas respectively. Causes of vitiation of Medovaha Srotas 38 i. Avyayama( lack of exercises) ii. Divaswapna (sleep during the day time) iii. Excessive intake of fatty foods iv. Excessive intake of wines. 14
  26. 26. According to modern science The deficiency of iodine content in the food is the main cause for goitre.Goitrogens 39 Goitrogens are foods, which suppress thyroid function. In normal, Goitrogens caninduce hypothyroidism and goiter. In hypos, Goitrogens can further depress thyroidalfunction and stimulate the growth of the thyroid (goiter). In hyperthyroid, Goitrogens may help suppress thyroidal function until normalthyroidal functioning can be restored. However, this may not be a good strategy. Goitrogenswork by interfering with the thyroidal uptake of iodine. While many hyper secretaries tolimit thyroid output by iodine restriction, this strategy can backfire. Iodine restriction willcause the thyroid to increase in size (goitre) in an effort to filter more blood to get moreiodine. When iodine is then re-introduced to the diet or accidentally ingested, the now largerthyroid gland has the capacity for greater thyroid hormone production. The iodine restriction is not a good long-term method for controlling thyroidhormone production. Therefore the consumption of Goitrogens is not a good strategy. It isbetter to increase copper metabolism by supplementation of copper and the assistingnutrients. Once copper is replenished and copper metabolism is working properly, the bodywill tolerate iodine without increasing thyroid hormone production The gotrogens can be divided into two varieties:- 1. Goitrogens in the form of food items 2. Goitrogens in the form of drugs 15
  27. 27. 1) Goitrogens in the form of food items 40 The vegetables of the Brassica family, sea-weeds, oats, calcium rich foods, etc, areGoitrogens in nature. Many Goitrogens are generally members of the brassica family. These include: Broccoli, Cauliflower, Brussell Sprouts, Cabbage, Mustard, Kale,Turnips, Rape seed (Canola Oil), Other goitrogens include - Soy, Pine nuts, Millet, Peanuts Brassica family vegetablesnot only inhibits thyroid production, but they also inhibit cancer growth. We know thatsulfur, copper, and iron, work closely together and that excessive sulfur can deplete copperand/or iron. The excessive kale consumption will cause anemia. Generally anemia is theresult of low iron and/or copper. Because copper and iron are so important for thyroid function, it is not advisable toeat plants of the brassica family. The primary pre-condition for the production of thyroiddisease is the onset of anaemia. Brassica vegetables, with their high sulphur content, may befoods, which induce anaemia and consequently thyroid disease.2) Goitrogens in the form of drugs:- 41 Thiocyanates, Anti thyroid drugs, lithium, iodides, p- amino salicylic acid, etc arealso Goitrogenic. Iodides in large quantities are also Goitrogenic as they inhibit the organicbinding of iodine to give rise to ‘iodide goitre’.Hereditary Factors The goitre may be seen in families as well. The inborn error in the metabolism isgenerally inherited as an autosomal recessive gene. There is enzyme deficiency in thethyroid gland. This may impair iodine accumulation, oxidation or coupling of iodotyrosine.This leads to formation of decreased level of thyroid hormones, which will increase TSH, 16
  28. 28. and simple goitre is formed. Hyperthyroidism is often seen in several members of the samefamily 42.Endemic Goitre 43 In certain places there is low iodine content in the water and food. So the inhabitantsdo not get minimum requirement of iodine. This leads to reduced levels of thyroid hormonesand hence the goiter. These areas are Himalayas, Alps, Mountain areas, etc. In low landareas around the lakes, the soil lacks iodide. Calcium is available plenty in chalks andlimestones are Goitrogenic and places where they are available there the goiters arecommon.Physiological Causes In certain cases when there are high metabolic demands diffuse hyperplastic goitermay be seen. Such conditions are puberty, pregnancy, etc. In these conditions there is moredemand of the thyroid hormones than normal and if the thyroid gland falls to rise to theoccasion, TSH will be secreted more and leads to goiter 44.Causes of Hypothyroidism 45-46 § Congenital developmental defect § Interference with thyroid hormone synthesis § Iodine deficiency § Primary idiopathic § Radioactive iodine, Surgery § Post radiation § Bio-synthetic defects § Drug induced (Lithium, iodides, p-aminosalicylic acid etc) § Chronic thyroiditis § Hashimotos thyroiditis 17
  29. 29. Causes of Hyperthyroidism 47-48 § Graves disease, 76%, which is idiopathic § Multinodular goiter § Thyroiditis § Iodide-induced § Autonomously functioning thyroid nodule § Ingestion of exogenous thyroid hormoneAnatomy 49-50 and physiology The thyroid is an endocrine gland, situated in the lower part of the front and sides ofneck. It regulates the B.M.R, stimulates somatic and psychic growth and plays an importantrole in calcium metabolism. The gland consists of right and left lobes that are joined to each other by the isthmus.A third pyramidal, lobe may project up wards from the isthmus (or from one of the lobes).Some times a fibrous or fibromuscular band (levator of the thyroid gland) descends from thebody of the hyoid bone to the isthmus or to the pyramidal lobe. Accessory thyroid gland issometimes found as small-detached masses of thyroid tissue in the vicinity of the lobes orabove the isthmus.Situation and extent The gland lies against vertebrae C-5, 6 and 7 and T1 clasping the upper part oftrachea. Each lobe extends from the middle of the thyroid cartilage to the fourth or fifthtracheal ring. The isthmus extends from the second to the third tracheal ring. 18
  30. 30. Dimensions and weight Each lobe measures about 5cm +1.2cm. On an average the gland weights about 25g.However it is larger in females than in males and further increases in size duringmenstruation and pregnancy.Capsules of thyroid The true capsule is the perepheral condensation of the connective tissue of the gland.The false capsule is derived from the pre tracheal layer of the deep cervical fasica a densecapillary plexuses is present deep to the true capsule. To avoid hemorrhage during operationthe thyroid is removed along with the true capsule.Arterial supply Superior thyroid arteries supply the thyroid gland, which is the first anterior branchof external carotid artery. Inferior thyroid artery is a branch of the thyro-cervical trunk,which arises from sub-clavian artery.Venous drainage Lymph from the upper part of the gland reaches the upper deep cervical lymph nodesthrough pre-laryngeal nodes. Lymph from lower part drains into lower deep cervical nodes.Nerve supply Nerves are derived mainly from the middle cervical ganglian and partly also from thesuperior and exterior cervical ganglia. There are vaso constrictorsStructure and function The thyroid gland is made up of two types of secretary cells. Follicular cells liningthe follicles of the gland secrete tri-iodothyronin and tetera iodothyronin (thyroxin) whichstimulate the B.M.R and somatic and psychic growth. Para follicular cells lie in between the 19
  31. 31. follicles they secrete thyro-calcitonin which promotes deposition of calcium salts in skeletaland other tissues and tends to produce hypo-calcium.Applied anatomy Any enlargement of the thyroid gland is called a goiter. Removal of the thyroid maybe needed in hyperthyroidism (thyrotoxicosis). Hypothyroidism causes cretinism in childrenand Myxodema in adults. Benign tumors of gland may displace and even compressneighbouring structure pressure symptoms and nerve involvement is common in carcinomaof the gland. Figure - 1 Location and anatomy of the Thyroid gland 20
  32. 32. Thyroid follicles and thyroid hormones 51 The thyroid gland contains large numbers of thyroid follicles. Individual follicles arespheres lined by a simple cuboidal epilhelium. The follicle cells surround a follicle cavity.This cavity holds a viscous colloid, a fluid containing large quantities of suspended protein.A network of capillaries surrounds each follicle delivering nutrients and regulatoryhormones to the glandular cells and accepting their secretary products and metabolic wastes. Follicular cells synthesis a globular protein called thyroglobulin and secretes into thecolloid of the thyroid follicles. Each thyroglobulin molecule contains the amino acidtyrosine, the building block of thyroid hormones. The formation of thyroid hormonesinvolves three basic steps. 1. Iodide ions are absorbed from the diet at the digestive tract and delivered to the thyroid gland by the circulation. Carrier proteins in the basal membrane of the follicle cells transport iodide ions (I-) into the cytoplasm. The follicle cells normally maintain intracellular concentration of iodide that is many times higher than those in extra cellular fluid. 2. The iodide ions diffuse to the apical surface of each follicle cells, where they converted into an activated form of iodide (I+) by an enzyme called thyroid peroxidase. This reaction sequence also attaches either one or two of these iodide ions to the tyrosine molecules of thyroglobulin. 3. Tyrosine molecules to which iodide ions have been attached are paired forming molecules of thyroid hormones that remain incorporated into thyroglobulin. The pairing process is probably performed by thyroid 21
  33. 33. peroxidase. The hormone thyroxin also known as tetraidothyroxine or simply T4, which contains four iodide ions. Eventually, each molecule of thyroglobulin contains four to eight molecules of T3, T4 hormones or both. The major factor controlling the rate of thyroid hormones release is the concentrationof TSH in circulating blood. TSH stimulates iodide transport into the follicle cells andstimulates the production of thyroglobulin and thyroid hormones. Under the influence ofTSH the following steps occur. 1. Follicle cells remove thyroglobulin from the follicles through endocytosis. 2. Lysosomal enzymes then break the protein down and the amino acids and thyroid hormones enter the cytoplasm. The amino acids are recycled and used to synthesise thyroglobulin. 3. The released molecules of T3 and T4 diffuse across the basement membrane and enter circulation. Thyroxine (T4) accounts for roughly 90% of all thyroid secretions, and tri-iodothyronine (T3) is secreted in comparatively small amounts. 4. Roughly 75% of the T4 and 70% of the T3 molecules entering the circulation become attached to transport proteins called thyroid – binding globulin (TBGs). Most of the rest of the T4 and T3 in the circulation is attached to transthyretin, also known as thyroid binding prealbumin (TBPA) or to albumin, one of the plasma proteins. 22
  34. 34. Figure –2 Functions of the thyroid folliclesControl of the thyroid secretion 52 There are three major ways of controlling the thyroid secretion anterior pituitary - 1. the hypothalamus 2. auto regulation besides, some other factors like 3. sympathetic stimulation 4. exposure to cold are also importantTSH of the anterior pituitary TSH is secreted by the specialized cells, called thyrotrophs of the anterior pituitary. 23
  35. 35. 1. T.S.H stimulates almost all the major steps of thyroxin biosynthesis as well as the release of thyroid hormones. Hence more T.S.H = more secretion of thyroid. 2. In addition, it causes increased vascularity and cellular growth of the thyroid gland. T.S.H is controlled by ‘ negative feed back ‘ mechanism exerted by T4 and T3. Thecirculating T4 is converted into T3 at the level of the anterior pituitary and thus both T4 andT3 are active. Therefore when circulating T4 is in high concentration, the pituitarythyrotrophs is inhibited so that T.S.H secretion is depressed resulting in correction of excessT4 in blood. Reverse occurs when T4 concentration of blood is low. Hence more T4 = lowT.S.H. T.S.H is the single most important regulator of the thyroid secretion.Hypothalamus From the Hypothalamus, TRH is secreted. TRH acts on pituitary thyrotrophs andstimulates them to secrete TSH. Hence more TRH = more TSH. Probably T4 and T3 do notoperate at the level of the hypothalamus for the negative feed back mechanism. Anotherhormone called somateostatin inhibits the TSH secretion. It is released from thehypothalamus (somateostatin also secreted by the islets of Langerhans and stomach).Auto regulation of thyroid If there is deficiency of food iodine, the iodine trapping mechanism of the follicularcells become super efficient. If there is excess of the food iodine, the iodine trappingmechanism is less efficient and organifaction of the extra amount of iodine does not occur.Mechanism of auto regulation may be as follows - Less iodine makes thyroid gland moresensitive to TSH and viseversa. 24
  36. 36. Figure – 3 Auto regulation of the thyroid hormoneMechanism of action of thyroid hormones 53 The thyroid hormones act somewhat like steroid hormones. The free T4 enters thetarget cells (all most all tissues are target cells of T4, specially not able are the neurons,heart, liver, skeletal muscles, adipose tissue, mammary gland) converted into T3 HR(hormonerecepter) complex is formed within the nucleus HR attachment with DNA occursmore m RNA production synthesis of more proteins are biological action. 25
  37. 37. Iodine and thyroid hormones 54 Iodine in the diet is absorbed at the digestive tract as I-. The follicle cells in thethyroid gland absorb 120 to 150 of I- each day, the minimum dietary amount needed tomaintain normal thyroid function. The iodide ions are actively transported into the thyroidfollicle cells, so the concentration of iodine inside thyroid follicle cells is generally above 30times higher than that in the plasma. If plasma iodine levels rise, so do levels inside thefollicle cells. The thyroid follicle contains most of the iodide reserve in the body. The activetransport mechanisms for iodide is stimulate by TSH and the increased movement of iodideinto the cytoplasm accelerates the formation of thyroid hormones. A typical diet in developed countries provides approximately 500 g of iodide perday, roughly three times the minimum daily requirements. Much of the excess is due to theaddition of iodine to the table salt sold in the grocery stores as iodized salt. Thus iodidedeficiency is seldom responsible for limiting the thyroid hormone production (this is not thecase in other developing countries). Excess iodine is filtered out of the blood at the kidneys,and each day the liver into the bile excretes a small amount of iodine. The losses in the bile,which continue even if the diet contains less than the minimum iodine requirements cangradually deplete the iodide reserves in the thyroid. Thyroid hormone production maydecline, regardless of the circulating levels of TSH. Thus various thyroid disorders manifestsgradually. 26
  38. 38. Effect of thyroid hormone on growth 55 Thyroid hormone has both general and specific effects on growth. For instance, it haslong been known that thyroid hormone is essential for the metamorphic changes of thetadpole into frog. In human, the effect of thyroid hormone on growth is manifest mainly in growingchildren. In those who are hypo thyroid, the rate of growth is greatly retarded. In those whoare hyper thyroid, excessive skeletal growth often occurs, causing the child to becomeconsiderably taller at an earlier age. However, the bones also mature more rapidly and theepiphyses close at an early age, so that the direction of growth and the eventual height of theadult may actually be shortened. An important effect of thyroid hormone is to promote growth and development ofbrain during fetal life and first few years of post natal life.Effect of thyroid hormones on specific bodily mechanism 561. Stimulation of carbohydrate metabolism - the thyroid hormone stimulates almost all aspects of carbohydrate metabolism, including rapid uptake of glucose by the cells enhanced glycosis, enhanced gluconeogenesis, increased rate of absorption from the gastro intestinal tract even increased insulin secretion etc.., all these effects probably result from the over all increase in cellular metabolic enzymes caused by thyroid hormone.2. Stimulation of fat metabolism - all aspects of fat metabolism is also enhanced under the influence of thyroid hormone. In particular lipids are mobilized rapidly from the fat tissue. Which decreases fat stores of the body to a greater extent. 27
  39. 39. 3. Effect on plasma and liver fats - increased thyroid hormone decreases the concentrationof cholesterol, phospolipids and triglycerides in the plasma, even though it increases the freefatty acids. Conversely, decreased thyroid secretion greatly increases the plasmaconcentrations of cholesterol, phospholipids and triglycerides and almost always causesexcessive deposition of fat in the liver as well.Increased requirement for vitamins As thyroid hormones increases the quantities of many bodily enzymes and becausevitamins are essential part of some of enzymes and co-enzymes thyroid hormones causesincreased need for vitamins. Therefore a relative vitamin deficiency can occur when excessthyroid hormone is secreted.Increased BMR As thyroid hormone increases metabolism in almost all cells of the body, excessivequantities of the hormone can occasionally increased the BMR to 60 to 100% above normal.Conversely when no thyroid hormone is produced the BMR falls almost to one – halfnormal.Effect on body weight Greatly increased thyroid hormones almost always decrease the body weight, andgreatly decreased hormone almost always increases the body weight.Effect of thyroid hormone on Cardio vascular system Increased metabolism in the tissues causes more rapid utilization of oxygen. Thiseffect causes vasodilatation in most of the body tissues, thus increasing blood flow. As aconsequence of the increased blood flow, cardiac output also increases, some times rising to 28
  40. 40. 60% or more, when excessive thyroid hormone is present and falling to only 50% of normalin very severe hypothyroidism.Increased gastro-intestinal motility Thyroid hormone increases both the rates of secretion of digestive juices and themotility of the gastro intestinal tract. Diarrhea often results in hyper thyroidism. Lack ofthyroid hormone can cause constipation.Excitatory effect on the central nervous system Thyroid hormones increases the rapidity of cerebration but also often dissociates,conversely, lack of thyroid hormone decreases this function. The hyper thyroid individual islikely to have extreme nervousness and many psycho neurotic tendencies, such as anxiety,extreme worry paranoia.Effect on the functions of the muscles Slight increase in thyroid hormone usually makes the muscles react with vigour, butwhen the quantity of hormone becomes excessive, the muscles become weakened because ofexcessive protein catabolism. Conversely, lock of thyroid hormone causes the muscle tobecome sluggish and they relax slowly after a contraction.Effect on sleep Because of the exhausting effect of thyroid hormone on the musculature and on theCNS the hyperthyroid subject often has a feeling of constant tiredness, but because of theexcitable effects of thyroid hormone on the synapses, it is difficult to sleep. Converselyextreme somnolence is characteristic of hypothyroidism, with sleep some times lasting 12 to14 hours a day. 29
  41. 41. Effect of thyroid hormone on sexual function In men lack of thyroid hormone is likely to cause loss of libido, impotence, excess ofhormone. In women the same causes menorrhogia and polymenorrhea, in other women itmay cause irregular periods and even amenorrhea.Poorvarupa Poorvarupa are the prodromal symptoms of the forthcoming disease, which do notclarify the Samprapti of the disease. These symptoms will be few and not clear 57. According to Madhava Nidana, Poorvarupa are the symptoms which are producedduring the process of sthana samsraya by vitiated Doshas, when Samprapti has not beencompleted and disease has not been manifested 58. But prodromal symptoms of Galaganda are not mentioned in any of the classicaltexts. From the recorded data of the patients we can say the purvarupa in general. Thevitiated Kapha, Vata, and medas will show some lakshnas such as mild swelling of the neck,pain the neck, heaviness of the body, hoarseness of voice etc.Lakshana of Galaganda in detail All the authors except Charaka have mentioned the types of Galaganda. It is of threetypes as Vataja Galaganda, Kaphaja Galaganda and Medoja Galaganda. The Lakshanamentioned by various Acharyas are enlisted in the table. Description of Vataja, Kaphaja, andMedoja Galaganda are as follows: -1) Vataja Galaganda 59 The lakshanas of Vataja Galaganda are toda (pain in the neck region), krishna sira avannadha (blackish veins in the neck), krishna aruna ganda (blackish or reddish mass), meda anvitham (coupled with medas), snigdata (unctuous to touch), 30
  42. 42. arucha (without pain), parushyata (roughness of the mass), chiravridhi ganda (mass manifests slowly), apaka (no paka),aruchi (tastelessness) and talu gala prashosha (dryness and weakness of throat and palate). Table - 1 Lakshana of Vataja Galaganda 60-61-62-63SN Lakshana Susruta Vagbhata Yoga Bhavaprakas Ratnakara ha1 Toda + + + +2 Krishnasiravanadha + - + +3 Krishna-aruna ganda + + + +4 Medan avita ganda + - - -5 Snigdhatara + - - -6 Aruja + - - -7 Parushyayukta + - + +8 Chiravrudhi ganda + - + +9 Apaka + - + -10 Yadrucha paka + _ + +11 Talugala prasosha + + + +12 Aasyavairasya + + + +13 Krishnarajiman + - -2) Kaphaja Galaganda 64 The lakshanas of Kaphaja Galaganda are sthira ganda (compact mass in the neck),savarnavat (same as body color), alpa ruk (little pain), ugra kandu (more itching), seetha(cold to touch), mahan ganda (large mass), chirabhivridhi (manifests slowly), paka (paka 31
  43. 43. present), madhuraasyata (sweetnes in the mouth), talu gala pralepa (coating in the palate andthroat) and kandu (itching). Table -2 Lakshana of Kaphaja Galaganda 65-66-67-68 SN Lakshana Susruta Vagbhata Yoga Bhavapraka Ratnakara sha 1 Sthira ganda + + + + 2 Savarnavat + + + + 3 Alparuk + - + + 4 Ugra kandu + + + + 5 Seetha sparsha + + + + 6 Mahan ganda + - + + 7 Chira abhivrudhi + - + + 8 Chira paka + - + + 9 Madhura asyata + + + + 10 Talu gala pralepa + + + + 11 Guru - - + +3) Medoja Galaganda 69 The lakshanas of Medoja Galaganda are snigda (unctuous to touch), mrudu (soft),panduvarna (yellowish), durganda (bad smell), avedana (no pain), pralambhate (hanging),dehanurupa kshaya, vridhi (when body grows, mass grows and vice versa), snigdaasyata(unctuous in the mouth), aspashtasabdavat (irregular voice), swasa (difficulty in breathing)and swara sada(hoarseness of voice). 32
  44. 44. Vagbhata had stated that apart from these Medoja Galaganda might present someLakshanas of Kaphaja gala ganda also 70. The lakshanas explained by various texts are summarized in the tables. Table -3 Lakshana of Medoja Galaganda 71-72-73-74 Sl.No Lakshana Susruta Vagbhata Yoga Bhavapraka Ratnakara sha 1 Snigdha + - + + 2 Mrudu + - - + 3 Pandura + - + + 4 Anishtagandha + - + + 5 Neeruk + - - - 6 Atikandu + - + + 7 Alabuvat pralambana + - + + 8 Dehanuroopa + + + + kshayavrudhiyukta 9 Snigdha asyata + - + + 10 Anusabdakara + - + + 11 Swasa - + - - 12 Svarasada - + - - 13 Guru - - + - 14 Alparuk - - + + 33
  45. 45. Clinical features according to contemporary science1) Hyperthyroidism 75 Hyperthyroidism or thyrotoxicosis refers to a state wherein there is an excess ofcirculating thyroid hormones, T3 or T4. Thyrotoxicosis is designated primary when thegland is diffusely enlarged and there are signs of hyper metabolic state, eye signs may ormay not be present. Thyrotoxicosis is designated secondary when the patient had previouslyabnormal gland, i.e. nodular goitre (single or multiple), and now assumes hyper functionalstatus.Clinical manifestation of Hyperthyroidism: 76 Clinical features could be broadly stated as follows:-• Evidence of Hyper kinesis• Objective evidence of hyper metabolic state(weight loss, catabolic state)• Presence of Goitre with or without Opthalmopathy The American Thyroid Association has classified the eye signs of Graves disease asfollows 77:- Class Definition 0 No signs and symptoms 1 Only signs, no symptoms (signs limited to upper lid retraction, stare, lid lag) 2 Soft tissue involvement (symptoms and signs) 3 Proptosis more than 20mm (measured by Hertel Exophthalmo meter) 4 Extra –ocular muscle involvement 5 Corneal involvement 34
  46. 46. Table –4 showing clinical features of Hyperthyroidism 78-79-80Symptoms SignsGeneralDemour of anxiety, generalized Restlessness, inability to keep still,weakness, heat intolerance2, weight loss, excessive sweating,skin tanning, apathy3, thirst, and hair thinning and straighteningfatigue2Cardiovascular systemPalpitation2, irregular beats, shortness Tachycardia, increased pulse pressure,of breath, angina, dyspnoea on ectopic beats, atrial fibrillation3, sick sinusexertion2, syndrome, cardiac failure3exacerbation of asthmaCentral nervous system Fine tremors, hyperreflexia, proximal muscleHyperactivity, nervousness, emotional weakness, periodic paralysis*, ill sustained clonuslability2Gastro-intestinal systemDiarrhoea (non-infective), weight lossdespite normal or increased appetite2, Rapid bowel transit time2, steatorrhea*anorexia3, vomitingReproductive systemOligomenorrhea or aminorrhea,impotence, spontaneous abortion, loss Gynacomastia*of libidoThyroidEnlargement in anterior part, neck Diffuse or nodular goitre, bruit1, thrillpressure symptomsDermatological systemIncreased sweating2, pigmentation, Vitiligo1, digital clubbing1, pretibial myxoedema1alopecia, pruritisOphthalmic SystemStare, gritty sensation1, increased Lid retraction, lid lag1, chemosis1,lacrimal secretion1, diplopoia1, infiltrative ophthalmopathy, oculardiminished visual activity1 muscle paresis, exposure keratitis * - Less frequent 1 – Features of Graves disease only 2 – Most common symptoms/signs of Hyperthyroidism irrespective of cause 3 - Features found particularly in elderly patients 35
  47. 47. 2) Hypothyroidism Clinical manifestation due to lack of thyroid hormone is designated as hypothyroidism. The presentation varies depending on 81: - a) the age of the patient, b) the cause of the disorder, primary or secondary, and c) Pre-existing health status. In utero, a lack of thyroid hormone results in irreversible brain damage to the foetus. In children, there can be a reduction in growth and an arrest of pubertal development. Clinical features of Hypothyroidism Table –5 Showing clinical features of Hypothyroidism 82-83-84 Symptoms Signs General features Tiredness, cold intolerance, somnolence Weight gain, goiter, peri-orbital puffiness, hoarseness; monotonous, coarse speech psychomotor retardation, hypothermia, Mucous membrane infiltration of laryngeal muscles Dermatological system Dry flaky skin and hair, hair loss, purplish Non-pitting oedema, carotenaemia, lips and malar flush erythema ab igne (Granny’s tartan), alopacia, vitiligo Cardiovascular system Shortness of breath, angina, congestive Bradicardia, ischeamic heart disease, cardiac failure* pericardial and pleural effusion, hypertension Central nervous system Muscle aches and pains, stiffness, Delayed retraction of tendon reflexes, * deafness, psychosis, slowing of motor myotonia , carpel tunnel syndrome, functions slowing of cerebartion Gastro intestinal system Constipation Ileus*, ascites* Reproductive system Irregular menstruation (usually High FSH/LH, hyper prolactinaemia, menorrhagia), infertility, galactorrhoea* impotence* 36
  48. 48. Heamatological Pallor, none- responsive anaemia, bleeding Dimorphic anemia, pernicious anemia, tendency, iron deficiency (pre- menopausal megaloblastic anemia, co-agulation defects women) * - Rare, but well-recognized featuresGalaganda Samprapti The etiological factors contributing to disease and the vitiation of Doshas attack thebody every now and then. Some factors can be avoided by taking precautions, but factorslike kala, deha etc are mostly inevitable. If the body’s resistance, Vyadhikshamatwa is highand dhatus, srotases and Agni are functioning well, the body fights against the etiologicalfactors. But if the etiological factors are stronger than the resistance power of the body, theyvitiate the Dosha and Dosha dooahya samoorchana takes place and the process of diseasestarts. The pathological changes taking place in the body day to day Nidana sevana till thecomplete manifestation of disease is termed as Samprapti. The knowledge of Samprapti is very much essential from the Chikitsa point of viewas it helps in understanding the pathogenesis of a disease. Susruta has mentioned the vitiation of Vata, Kapha, and Medo dhatu by theetiological factors of the same; will manifests in the neck region and make a ‘Ganda’(massin the neck).it exhibits the symptoms of three respectively 85. But while describing the commentary Dalhana and Gayadasa are of the opinion thatGalaganda is a swelling in the neck, ”Nibadha swayathu” 86. Charaka has mentioned Galaganda as a swelling in the neck by the vitiation ofKapha Dosha .He describes that, the Kapha Dosha vitiated by the etiological factors willmanifests in the frontal part of the neck and produce a swelling slowly 87. 37
  49. 49. Vagbhata mentions the Samprapti in another way. The Vata, Kapha, and Medas gotvitiated by the etiological factors will produce the Galaganda in the outside part of the neck.It hangs like a scrotum without pain if left untreated 88. Madhavakara mentions the Galaganda in the Samprapti as ‘Nibadha swayathu’.I.e., a swelling attached to the neck which hangs down like a scrotum, which may be large orsmall in size. The swelling is slowly produced by the Vata, Kapha, and Medas, which isvitiated by the etiological factors89.1. Sankhya Samprapti of Galaganda There are three varieties of Galaganda are mentioned in all the classics exceptCharaka. They are Vataja galaganda, Kaphaja galaganda, and Medoja galaganda.2. Vikalpa Samprapti of Galaganda In Galaganda the Doshas involved are Kapha and Vata. The aggravating factors ofthem are Seeta, Snigda, guru, manda etc3. Pradhanya Samprapti of Galaganda The Samprapti caused by a major of independent Dosha is called as pradhanyasamprapti, and that which is caused by a minor or dependant Dosha is called as apradhanaSamprapti. Also it can be understood as the Samprapti of swatantara vyadhi is called aspradhanya Samprapti.4. Bala Samprapti of Galaganda The strength of a disease is depending upon the Nidana, purvarupa, and rupa andmanifest disease in total. Here almost all patients had the symptoms manifested completely.So the bala is more. 38
  50. 50. 5. Kala samprapti It is the Samprapti which confirms the role of a particular Dosha in a disease, whichcan increase the same with the change in time- like the day, night, season, with stages ofdigestion etc. Here the main Dosha is Kapha and there is involvement of Vata in it. At the same timethere is the involvement of Agni; i.e. is the derangement of Agni bala is present. Soaccording to the condition it may vary. No specific time, season, and stages of digestion areprovoking this disease.Samprapti Ghatakas Dosha : Kapha, Vata Dushya : Medas, Rakta, Rasam Srotas : Medovaha, Raktavaha, Rasavaha Agni : Jataragni, Dhatwagni Ama : Jataragnimandya, dhatwagnimandya Rogamarga : Bahya Roga marga Udbhavastanam : Amashaya Vyaktasthanam : Gala pradasha 39
  51. 51. Figure -4 Schematic representation of the Galaganda SampraptiVata Medoprakopa prakopaKarana KaranaKaphaprakopaKarana Vitiates Kapha Vitiates Vata Vitiates Medas Vitiation of Sanchita Vata Medodhatwagni and Kapha Sanchita Medas Gala (Kanta) Stanasamshraya Manifestation of Lakshana corresponding to the Stana, Dosha and Vyadhi Galaganda 40
  52. 52. Sadhyasadyata The physician who knows the difference between curable and incurable diseases andbegins the treatment in time with a through knowledge of the case succeeds in his effortswithout fail. So the physician, who knows the avasthas of the disease, can plan the treatment 90and can reject the cases, which are incurable . The sadyasadyata of Galaganda ismentioned in Susruta Samhita and are enlisted here 91- 1. Kruchra Swasa - severe difficulty in breathing 2. Softness of the body parts 3. Aruchi – tastelessness 4. Ksheena gatrata – emaciated body and 5. Bhinna swara – broken voiceUpadrava (complications) Upadrava is produced after the formation of main disease and it is dependent on themain disease. Upadrava can be major or minor. It is a secondary disease or complication,produced by the same Dosha it responsible for the formation of main disease 92. Susruta alsoopines that upadrava is a super added disease for which the basic causes, i.e. the Dosharesponsible is the same as in the main disease 93. The upadravas of Shopham are swasa, daha, balakshaya, jwara, chardi, aruchi, hikka,atisaram, kasa.The upadravas of Galaganda are not mentioned in any Samhitas 94. As per the modern science concerned some complication are described. Thecomplications of the hypothyroidism and the hyperthyroidism are 95- 41
  53. 53. a) Thyroid crisis The hyperthyroid patients, the complications can be termed as hyperthyroid crisis. Themost prominent signs are fever, agitation, confusion, tachycardia or atrial fibrillation and inolder patients cardiac failure. It is a medical emergency and despite early recognition andtreatment, the mortality rate is 10%.The crisis is precipitated by the following 96:- a. Stress as resulting from acute infection, trauma or emotional upheaval b. Surgical handling of thyroid without prior achievement of Eumetabolic state c. Metabolic upset, uncontrolled diabetes, electrolyte imbalance or parturition d. Sudden interruption of anti thyroid drug treatmentb) Hypo thyroid complication 97i) Myxodema coma Patient with extreme degree of hypothermia, when subjected to stressful situation,can assume a grave clinical state which if not reverted with timely treatment may endfatally. Extreme cold weather, use of narcotics, phenothiazines or anasthetic agents,infections or situations that can cause hypertension, may be the precipitating events formyxodema coma. Cardinal features of myxedema coma are Hypothermia, Altered consciousness andHypo ventilation.Pathology of goitre according to contemporary medicine 98 Hypothalomo-pituatiry disorders can be responsible for inducing under active oroveractive thyroid states. The thyroid disorders can be divided into three: - 42
  54. 54. 1. Diseases of thyroid itself 2. hypothalamo – pituitary diseases 3. Thyroid hormone resistance syndrome Basically it can be divided into:- 1. Hyperthyroidism 2. Hypothyroidism In both of the (Hyper and Hypo) the goitre is present as the main clinical feature.Pathology of goitre 99 The thyroid gland is diffusely enlarged and smooth. It may be nodular. There arecertain stages through which this type of goitre gradually passes through. In the first stagedue to TSH stimulation the lobules are composed of active follicles. This is called” stage ofdiffuse hyperplasia “. When TSH stimulation ceases by ingestion of iodine the secondstages appears. This is the stage of involution forming large follicles filled with colloid. Ifthis condition continues i.e., in the third stage the gland enlarges to an enormous extent thatis known as colloid goitre. Sometime due to fluctuating TSH levels a mixed pattern developswith areas of active lobules and areas of inactive lobules.Pathology of Hyperthyroidism 100 In “graves disease” the thyroid is uniformly enlarged and the surface ischaracteristically smooth, though slight modularity may be detected. Microscopically thethyroid is hyperplastic and the epithelia which line the acni are high columnar instead offlattened cuboidal type which is found in normal thyroid gland. They’re only minimalamount of colloid in the acini and many of them are even empty and others containvacuolated colloid. The nuclei of the thyroid cells exhibit mitoses. Papillary projections of 43
  55. 55. the hyperplstic epithelium into the acini are common. Lastly there is vascularity andlymphoid tissue around the acini. The clinical manifestation of the hyperthyroidism include changes referable to thehyper-metabolic state, included by excess of thyroid hormones as well as those related toover activity the sympathetic nervous system. Excessive levels of thyroid hormones result in an increase in Basal Metabolic Rate.Cardiac manifestations are the earliest and most consistent feature. Those patients withHyperthyroidism can have an increased cardiac output owing to - a) increased cardiac contractivity b) Increased peripheral oxygen requirement. In older patients’ atrial fibrillation occur frequently, but the actual cause is notknown. Pathological changes often call attention to hyperthyroidism- lid lag, staring gazeand wide appearances of the eye are due to sympathetic over stimulation of levator palpebresuperioris. In the neuromuscular system- increased activity of sympathetic nervous systemproduces- Tremor, Hyper activity, Emotional disturbances, Anxiety, Muscle weakens, etc. The skin of the patient tends to be warm, moist and flushed because of increasedblood flow and peripheral vaso-dilatation to increase heat loss. Increased sweating is due tohigher levels of calorigens. In the G.I.T system increased gut motility are due to increased sympathetic activitycause Increased thyroid hormone in the skeletal system, which stimulate the bone resorption,makes ultimately Increased porosity and reduced volume of bone i.e. osteoporosis. 44
  56. 56. Pathogenesis of Graves disease 101 “Graves disease” is caused by an autoimmune reaction against the thyroid.Antibodies react with the receptor for the thyroid- stimulating hormone and other antigenson the surface of the thyrocytes. Some of the antibodies stimulate the thyrocytes, causinghyperplasia. Some block the action of the thyroid-stimulating hormone some do not affectthe function of the thyrocytes. The first stimulatory antibody the blood of patients with “Graves disease” is calledthe long acting thyroid stimulator because it causes a long continued release of iodinatedcompounds from the thyroid in the animals. It or similar stimulatory antibodies aredemonstrable in the plasma of almost all patients with “Graves disease” and are the principlecause of hyperplasia. Antibodies against thyroglobulin or against the microsomes the thyrocytes arevpresent in 95% of the patients, usually in higher titer than in the patients with a non-toxicgoitre or carcinoma of thyroid, though not in the higher titer usually in Hashimotosthyroiditis. Hashimotos disease is unduly frequent in the families of patients with Graves diseaseis incidence of “Graves disease” is increased in the families of patients with Hashimotosdisease. Relatives of patients with “Graves disease” often have in their blood the antibodiesof Hashimotos disease. Occasionally a patient with Hashimotos disease develops “Graves disease”, or apatient with Graves disease ends with Hashimotos disease. Genetic factors are important inthe pathogenis of “Graves disease” in some patients, abnormal immuno-globulins of Gravesdisease are present in the plasma of close relatives in 60% of the patients. The frequency of 45
  57. 57. the antigens HLA-DR3 and HLA-B8 is increased in caucascians with “Graves disease”.HLA-BW 36 is unduly common in Japanese, HLA- BW 46 in Chinese. Probably the autoimmune response in Graves disease is initiated by a mechanismsimilar that in Hashimotos disease. HLA- DR antigens are present on the thyrocytes in thepatients with Graves disease, as they are in Hashimotos disease. Some think they are carriedby a viral infection and initiate the auto immune reaction against the thyroid. Some thinkthat the primary fault is in the suppressor T- cells and that the expression of the HLE-DRantigens is caused by the autoimmune reaction. The pathogens of the opthalmopathy in“Graves disease” are unknown. It is not due to the excess of thyroid hormones and is notcaused by the thyroid stimulating hormone. The cause of dermoapthy found in “Gravesdisease” is unknown.Non toxic goitre Pathogenisis 102 Iodine deficiency is the most common cause of both endemic and sporadic forms ofnon-toxic goitre. In all regions in which nontoxic goitre is endemic, the diet is deficient iniodine. In some patients toxic agents called Goitrogens are important in the causation of thegoitre. In some, an enzyme deficiency causes the enlargement of thyroid. In some patientswith sporadic goitre, the cause of the disease is unknown. If the intake of iodine is low, itsconcentration the plasma and its excretion by the kidneys fall. The thyroid gland is unable totake up enough iodine to maintain normal function and becomes hyperplastic. Thehyperplasia may be caused by increased secretion of the thyroid stimulating hormonescaused by a fall in the concentration of thyroid hormones in the plasma, but more probablyiodine deficiency causes the thyroid to respond exclusively to a normal concentration of theTSH. 46
  58. 58. Goitrogens cause non-toxic goitre or enhance the effect of iodine deficiency. In someHimalayan villages, a Goitrogens in the drinking water causes an agent produced by Esch.Coli non-toxic goitre, most probably an agent produced by Esch. Coli. Cabbage and relatedvegetables contain Goitrogens related to thiourea. Thiocyanates, perchlorate, paraamino salicylic acud, and other drugs inhibit themetabolism of the thyroid gland and cause goitre if given fir a long period. Fluoride andother halogens displace iodine and contribute to the causation of non-toxic goitre. Evenexcess of iodine can cause non-toxic goitre. The enzyme deficiency sometimes cause non-toxic goitre in children. Minoranomalies of this sort may explain some sporadic goitre. Sometimes sporadic goitres are offamilial, suggesting the possibility of a genetic defect. Antibodies against thyroid antigensare often present in the patients with a non-toxic goitre.Pathogenesis of hypothyroidism 103 Hypothyroidism can be again divided into Cretinism, Myxedema, HashimotosThyroditis, Sub-acute lymphocytic Thyroditis.Cretinism Cretinin refers to Hypothyroidism developing in infancy or early childhood. Theseverity of the mental impairment in cretinism appears to be directly influenced by the thimeat which thyroid deficiency occurs in utero. Normally, the maternal hormones, including T3,T4 cross the placenta and are critical to fetal brain development. If there is maternalthyroidal thyroid deficiency before the development of fetal thyroid gland, mentalretardation is severe. 47
  59. 59. Pathogenisis of Hashimotos thyroiditis 104 The disease is caused primarily by a defect of T- cells. One model fir this disorderproposes that T-cells from patients with this disorder recognized processed thyroid antigensin association with specific types of major Hist Compatibility Complex (MHC) antigens.Diminished suppresser T-cells may also play a role in the emergence of thyroid specifichelper T-cells. These activated T- cells have two roles in the disease. a. They interact with B cells and stimulate the secretion of a variety of anti thyroid antibodies, which may activate antibody- dependent cyto-toxicity mechanisms. b. The helper T- cells may induce the formation of CD8+ cells, which can be cyto-toxic to thyroid cells. B-lymphocytes from thyroid tissue of patients with Hashimotos thyroditis are activated and secrete a number of auto- antibodies detected against thyroid antigens. i. Thyroglobulin and thyroid peroxidase ii. TSH receptor iii. Iodine transporter Many thyroid auto-antibodies can fix compliments. As a result, complement-dependant, antibody mediated cytotoxicity may contribute to destruction pf thyroid tissue inpatients with Hashimotos thyroiditis.Investigations 1051) Serum Thyroxine (T4 ) Thyroxine is transported in the plasma mainly in the bound form with ThyroxinBinding Globulin (TBG), and by Thyroxin Binding Pre- albumin. Only a small amount 48
  60. 60. circulates in the blood in the free form. Measurement is more difficult and can be measuredby competitive Protein binding or Radio immuno assay method. The normal range variesfrom 58 to 140 µmol/L.2) SerumT3 The estimation is very difficult and is only possible by radio immuno assay method.This test is more effective in the sense that some cases of hyperthyroidism are due toexcessive production of T3 without any association of Serum T4. The normal range variesfrom 1.22 to 2.22 µmol/L.3) Serum TSH It is also measured by immuno assay method. The normal level is 0.3 to 4.0 µu/L It israised in primary hypothyroidism and almost undetectable in hyperthyroidism. This test is ofmore help in the diagnosis of hypothyroidism rather than hyperthyroidism. It also of value tomeasure TSH level is following radio-iodine therapy and sub total thyroidectomy.4) Thyroids scan. Scanning with tracer dose determines the functioning and not functioning (Hot orCold) of either full or part of the thyroid gland. A solitary nodule is palpated. Scanning ishelpful in the following way -1. In case of suspected retro sternal goiter2. Ectopic thyroid tissue A single non-functioning thyroid nodule is an indication of surgery. The other testsare BMR, Serum cholesterol, ECG, etc. these are of little value in the diagnosis, but todetermine the complications, ECG etc can be used. 49