Anti infla#dg06gdg

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Pharmacognostical studies and anti inflammatory effect of kakamachi on albino rats – Gangoor, Department of Dravya Guna, Post Graduate Studies & Research Centre, D.G. MELMALAGI AYURVEDIC MEDICAL COLLEGE,GADAG

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Anti infla#dg06gdg

  1. 1. “PHARMACOGNOSTICAL STUDIES & ANTI-INFLAMMATORY EFFECT OF KAKAMACHI ON ALBINO RATS”. AN EXPERIMENTAL STUDY BY Dr. Shivakumar S. Gangoor. Dissertation submitted to the Rajiv Gandhi University of Health Sciences, Karnataka, Bangalore. In partial fulfillment of Regulations for award of degree of DOCTOR OF MEDICINE (AYURVEDA VACHASPATI) IN DRAVYAGUNA Under the guidance of Under the co-guidance of DR. G. V. MULAGUND. DR. KUBER. SANKH. M.D. (AYU) M.D. (AYU) PROFESSOR & H.O.D, LECTURER DEPARTMENT OF DEPARTMENT OFP. G. A. R. Center DRAVYAGUNA. P. G. A. R. Center DRAVYAGUNA. POST GRADUATE DEPARTMENT OF DRAVYAGUNA D.G MELMALAGI AYURVEDIC MEDICAL COLLEGE AND RESEARCH CENTER, GADAG - 582103. 2006
  2. 2. Rajiv Gandhi University of Health Sciences, Karnataka, Bangalore. DECLARATION BY THE CANDITATE I hereby declare that this dissertation / thesis entitled“PHARMACOGNOSTICAL STUDIES AND ANTI-INFLAMMATORYEFFECT OF KAKAMACHI”- By an Experimental Study is a bonafideand genuine research work carried out by me under the guidance of Dr. G. V.MULAGUND. MD (Ayu),Professor and H.O.D, Post Graduate Department ofDravyaguna, Shri D.G.M.A.M.C and Research center Gadag.Date: Signature of the CandidatePlace: (Dr.Shivakumar. S. Gangoor)
  3. 3. CERTIFICATE BY THE GUIDE This is to certify that the dissertation entitled “PHARMACOGNOSTICALSTUDIES AND ANTI-INFLAMMATORY EFFECT OF KAKAMACHI ONALBINO RATS ” – BY an Experimental Study is a bonafide research workdone by Dr. Shivakumar. S. Gangoor in partial fulfillment of the requirementfor the degree of Ayurveda Vachaspati in Drvyaguna. This work is applied, scientific and an original contribution in the field ofresearch in Ayurveda. I am fully satisfied with his original work and recommended the dissertation tobe put before the adjudication. Signature of the Guide Dr. G. V. MULAGUND. M.D (AYU) Professor and H.O.D Post Graduate Department of Dravyguna, D.G.M. Ayurvedic Medical College, Gadag.
  4. 4. ENDORSEMENT BY THE HOD, PRINCIPAL HEAD OF THE INSTITUTION This is to certify that the dissertation entitled “PHARMACOGNOSTICALSTUDIES AND ANTI-INFLAMMATORY EFFECT OF KAKAMACHI ONALBINO RATS ”- By an Experimental Study is a bonafide research work done byDr.Shivakumar S. Gangoor under the guidance of Dr. G. V.MULAGUND. MD(Ayu) Professor and H.O.D, Post Graduate Department of Dravyaguna, ShriD.G.M.A.M.C and research center Gadag and contributed good values to theAyurvedic research. We here with forward this dissertation for the evaluation and adjudication. Seal & Signature of the HOD Seal & Signature of thePrincipal Dr. G. V. Mulagund. Dr. G. B.Patil.
  5. 5. COPYRIGHT Declaration by the Candidate I here by declare that the Rajiv Gandhi University of Health Sciences,Karnataka shall have the rights to preserve, use and disseminate this dissertation /thesis in print or electronic format for academic / research purpose.Date: Signature of the CandidatePlace: Dr.Shivakumar S. Gangoor. © Rajiv Gandhi University of Health Sciences, Karnataka.
  6. 6. CERTIFICATE BY THE CO-GUIDE This is to certify that the dissertation entitled “PHARMACOGNOSTICALSTUDIES AND ANTI-INFLAMMATORY EFFECT OF KAKAMACHI ONALBINO RATS ” – BY an Experimental Study is a bonafide research workdone by Dr. Shivakumar. S. Gangoor in partial fulfillment of the requirement forthe degree of Ayurveda Vachaspati in Drvyaguna. This work is applied, scientific and an original contribution in the field of researchin Ayurveda. I am fully satisfied with his original work and recommended the dissertation to beput before the adjudication. Signature of the Co- Guide Dr. KUBER.SANKH. M.D (AYU) Lecturer, Post Graduate Department of Dravyguna, D.G.M. Ayurvedic Medical College, Gadag.
  7. 7. ABSTRACTBackground : Inflammation is fundamentally a protective response. These are exogenousand endogenous stimuli can cause cell injury. Due to cell injury there will bealterations in vascular caliber which leads to an increase in blood flow, changes inmicro vascular structure allow the plasma, proteins and leucocytes to leave thecirculation and get accumulated at the focus of injury leading to swelling. There aremultiple remedies available to reduce it with maximum side effects andcomplications. Inflammation is common pathological condition. It is livoited to any of the agegroup nor to any socio-economic class of society. It is having greater influence oftreatment factors and conditions. Since ancient times human societies have searched effective drugs of antiinflammatory actions. Kakamachi is also a best example for an anti-inflammatorydrug. The main objectives of the present protocol are1) Pharmacognostical Study: • Microscopic Evaluation • Standardization and validation • Extraction of phyto-chemical constituents. • TLC, UV and I R.2) Screening of fraction for anti-inflammatory activity.3) To evaluate the anti-inflammatory effect of Kakamachi on Carreginine induced albino rats in four different groups.
  8. 8. Method:For thoroughly completion of present protocol needs fallowing essentialities such asa) Source of data: present study i) Literary source of data ii) Experimental source of data It includes phyto-chemical investigations of the extraction. i.e. fractionationand characterization etc..b) Method of Collection of Data: In the present protocol the dried powder of Solanum nigrum extracted withalcohol soxhlet apparatus is fractionated and is characterized. Fractionated principletested for anti-inflammatory activity by Carreginine induced Rat paw oedema.a) Measurement by Carreginine induced inflammation in the hind paw of albino rats.b) Inflammation is measured before and after administration of Carreginine.c) The Carreginine 0.01 ml is injected to the dorsum of the foot.d) After one hour and three hours the readings were taken with the help of plethismograph.Observation; In pharmacognostical study, morphologically colour of the leaves is greenwith bitter taste. Shape is of ovate with characteristics acceptable odour and physicalevaluations of these respective entities are established. In phytochemical observationsof extractive and different preliminary phytochemical tests are Observed andIdentification by TLC are done and focused U V and I R spectroscopy observation onthe experimental studies are done on the basis of selection of Animal sample size,preparation of the test drug.
  9. 9. Interpretations and Conclusions: Different interoperations are done according to different points of view inconcern with the protocol and the study concern conclusions were drawn.Key words Kakamachi. Solanum nigrum. Pharmacognostical. Experimental. Anti-inflammatory.
  10. 10. ABBREVIATIONSA.H. Ashtanga HridayaA.P.I Ayurvedic Pharmacopoeia of IndiaA.S Astang sangrahaB.P Bhava PrakashnighantuC.S. Charaka SamhitaChi. ChikitsasthanaD.N Dhanvantari NighantuGroup C Control GroupGroup S Standard GroupGroup T Trial GroupK.N Kaideva NighantuM.N. Madanpala NighantuM.E.S. Maximal Electro-ShockR.N. Raj NighantuS.N Sodal nighantuS.S. Susharutha samhitaSh. N Shaligram NighantuSu. SutrasthanaT.L.C Thin Layer ChromatographyP.N. Priya NighantuTemp TemperatureD.W. Distilled water
  11. 11. ACKNOWLEDGEMENT I express my deep sense of gratitude to the Principal Dr. G. B. Patil andManagement Committee for giving me the opportunity to pursue my post graduationstudies in this institution. I am deeply inducted to my respected guide Dr. G. B. Mulgund M.D. (Ayu)Prof. & HOD Dept. of P.G. Studies in Dravya Guna for his inspiring paramountthoughts, zealous suggestions and guidance rendered for the successful completion ofthis research work. I also offer my deep felt gratitude to my co-guide Dr. Kuber Sankh M.D.(Ayu) for his invaluable support without which the study could not have materialized. I am thankful to associate guide Sri. B.S. Hunasi Lecturer Dept. ofPharmacognosy B.L.D.E. Pahrmacy College, Bijapur. and Botanist Sri. S.A. Kapalifor their timely guidance and help. The completion of this dissertation has a lot to dowith their constant support. I would like to express my profound gratitude to my department incharge Dr.G.S. Hiremath M.D. (Ayu), Dr. Shashidhar Nidagundi and Dr. Smt. Veena Kori fortheir guidance and inspiration given at various stages of my work. I express my sincere thanks to Sri. Nandakumar for his help in statisticalanalysis of results. I am highly indebted to Dr. A.I. Akki, Dr. S.V. Teggi, Dr. V. M. Sabarar, Dr.Wali, Dr. N.S. Shettar, Sri. Somashekahr T. for the able guidance and inspirationgiven at different stages of my work. I take this opportunity to thank the post graduate teaching staff of thisinstitution especially Dr. M.C. Patil, Dr. K.S.R. Prasad, Dr. Shivaramudu, Dr.
  12. 12. Shashidhar Dodamani and other lecturers of our college for their help and suggestionsduring my post graduation studies. I sincerely thank to my beloved classmates Dr. Jagadeesh H., Dr. AshokBingi, Dr. Shivakumar Sajjan, Dr. Savita G., Dr. Anand, Dr. C.B. Inamdar and allclassmates of other post graduation branches for their constant co-operation and help. I wish to convey my thanks to beloved librarian Sri. V.M. Mundinmani andS.B. Sureban for providing essential references in the study. I wish to convey my thanks to beloved friends Mr. S.M. Teggi, Mr. B.A.Tenginkai, Mr. M.H. Vaijapur, Mr. R.M. Vaijapur for their co-operation. I remember with respect my revered parents for their inspiration andencouragement. I sincerely thanks to Smt & Sri. S.B. Gangoor for their profound and neverending love. I am grateful to my sisters Smt. Vijaylaxmi and Smt. Saraswati for theiraffection. I am highly indebted to my mother-in-law and father-in-law Smt & Sri.K.S. Anneppanavar for their affection and love. This is incomplete without remembering my beloved wife Smt. Sunita whohelped in all respects to complete this valuable dissertation work and lastly sonNiranjan & lovely daughter Akshata for their affection. I express my gratitude to all those who helped me directly or indirectly incompleting this work.Date :Place : Dr. S. S. Gangoor
  13. 13. CONTENTSSl. No Particulars Page No i) Acknowledgement ii) Abbreviations iii) Abstract iv) List of Tables 1. Introduction 1-3 2. Objectives 4 3. Review of literature 5-54 Drug Review Disease Review 4. Methodology 55-70 Pharmacognostical study Phytochemical study Experimental study 5. Observations and Results 71-110 6. Discussion 111-119 7. Conclusion 120 8. Recommendation for further study 121 9. Summary 122-125 10. Bibliography 11. Annexure Photographs
  14. 14. INTRODUCTION INTRODUCTION Ayurveda is a primordial system of medicine. The quest of the man is to livehappily, health is the elemental factor for happiness. The task of the medicine is topreserve and restore the health by relieving the sufferings. Understanding themedicine is essential to reach these both the goals. Pain is universally understood as asign of diseases. It is the most common symptom that brings a patient to physiciansattention. The knowledge of this condition, to the modern medical science is just twocentury old. This is well known to Ayurveda since 5000 years. The modern line oftreatment that provides a range of analgesic, physiotherapy and surgery but not a finalanswer and there is a common problem of reoccurrence. An Ayurvedic approach ishelpful to improve the quality of life in-patient suffering from shotha. Ayurvedic management measures seem to be more satisfactory because oftheir simplicity, applicability, and easy availability and cost effectively. It is a seriousburning problem of the society. It is our contractual obligation to provide propermanagement to the patients who are suffering from it and make them get through theproblem. In the drug review, the different references from Samhitas, Vedas, in modernbooks have been mentioned with different synonyms, having different importantvaluable properties. The useful part of Kakamachi has panchanga having with doses, churna 3 to 6gms., kasaya 50 to 100 gms, patra swarasa 25 ml, phala churna 3 to 6 gms and usesof Solanum nigrum according to external application and amayika prayoga. The whole work comprises different sections. First section deals with theReview of literature under various sub headings wherein literatures available from 1
  15. 15. INTRODUCTIONdifferent references have been dealt. Material and Methods, Pharmacognostical study,Phytochemical and Experimental studies are made use in this work. Observations andResults, Discussions and Conclusion are given. It is hoped that the humble efforts in the form of this dissertation will help inunderstanding the effect of above mentioned measures as well as planning the futureresearch to find out the definite cure from Ayurvedic therapeutics. Inflammation is well known by all the human beings because each person ofthe world is certainly met with this condition at least once in their lifetime, whichaffects all the age groups and to both the sexes. It makes the human beings to feelfatigue, uneasiness, swelling, redness, and tenderness and disturb the day today life. Shotha is well known to mankind since the beginning, its references are foundin Vedas. Which are the older written documents of knowledge, mentioned thatinflammation is first disease to incarnate on the earth. In all Samhita’s, the shotha isexplained in detail. "Charaka" who is well known for his skills of chikitsa explained.It shows the redness, tenderness of the intolerable pain symptoms of shotha. Alsomany others like Brihathrayees, Laghutrayees and recent authors were resolvedsufficient literature to explain the Shotha (Inflammation). Inflammation is best defined in the teleogical terms, specifically it is a seriesof molecules and cellular responses acquired during evaluation, designed to eliminateforeign agents and promote repairs of damaged tissues. Unfortunately, these are notinfallible, pathogens have concurrently evolved inclusion to avoid elimination. Newpathogens occasionally emerge from the environment and under some circumstancesaberrant to inner inflammatory responses and damages the host. The complexity ofthe inner inflammatory system is a reflection of millions of years of mentalchallenges. It is becoming apparent that the system is not simple but rather a 2
  16. 16. INTRODUCTIONcompletely opposite of responses that were assembled approximately and whereelicited may synergize autogenic each other. The cursory of inflammations are multitudinous. Almost anything that injuresliving tissues there occurs the inflammation. By fast the most frequent causes ofinflammation is trauma, the minor injuries that escape our attention as well, andinfection by Bacteria, Viruses, Fungi as Parasites, to these must be added a host ofothers cause exogenous and endogenous. Such as eradication, poisoning, metallicdisorders and derangements of the immune system. The body reacts to almost anykind of injury by inflammation and other kinds of responses may follow butinflammation is the first and most constant response. In the present Phytochemical study of Solanum nigrum extraction, thepreliminary phytochemical tests were conducted and observed the presence orabsence of Proteins, Alkaloids, Saponnins, Tannins, Triterpenoids and Carbohydrateswith their characterizational findings, also with UV and IR methods and appropriatetechniques on identification by TLC method were done. During experimental study total 24 albino Rats were taken and subjected themin four groups (Group I to IV). Group I was standard while Group II was trial group with minimum dose andwhile group III was trial group with maximum dose and where as Group IV wasVehicle group. Here Carreginine was induced to all the 24 Albino rats by injecting inhind paw technique method. First inflammation on hind paw is observed andmeasured. After induction of Carreginine to all the groups, immediately theinflammation was observed and measured. 3
  17. 17. AIMS AND OBJECTIVES AIMS AND OBJECTIVES1. Pharmacognostical study- • Pharmacological Evaluation. • Microscopical Evaluation • Standardization and Validation • Extraction of Phyto chemical constituents • T.L.C, UV IR2. Screening of fraction for Anti-Inflammatory activity3. To evaluate the Anti-Inflammatory effect of Kakamachi on Carageenen induced albino rats in four different groups. 4
  18. 18. DRUG REVIEW DRUG REVIEWBOTANICAL NAME: Solanum nigrum. i. KULA : KANTHAKARI. II. GANAS Charkokta ganas : Tikta skanda.BOTANICAL CLASSIFICATION: Classification according to Bentham and Hooker. Table No : 1 Kingdom Plantae Division Spermatophyta Class Dicotyledonae Sub-class Gamopetalae Order Polemoniales Series Bicarpellatae Family Solanaceae Genus Solanum Species nigrum According to Engler and Prantl. Table No : 2 Kingdom Plantae Division Embryophyta siphonogamy Class Dicotyledon Sub-class Sympetalae Order Tubiflorae Family Solanaceae Genus Solanum Species nigrum 5
  19. 19. DRUG REVIEW According to Hutchinson Table No : 3 Phylum Angiospermae Sub-phylum Dicotyledones Division Herbaceae Order Solanales Family Solanaceae Genus Solanum Species nigrumDESCRIPTION OF FAMILY SOLANACEAE The family is spread over 90 genera and 2,000 species, Randle considered 85genera and 2,000 species, according to others the number of species included underthis is as much as 2,200. The genus Solanum alone has about 1,700 species. In Indiathe family is represented by approximately 21 genera and about 70 species.HABIT: Majority of the plants are annual herbs, some are shrubs, rarely soft woodtrees. Some of the plants are climbing or a few armed with spines. The genusSolanum with about 1,700 species shows diverse habits being herbs, shrubs, trees oreven creepers and woody climbers.VEGETATIVE CHARACTERISTICS: A branched taproot, the roots are thick and forked resembling human being inminiature, stem erect, climbing, spinous, tuberous, herbaceous, sometimes woody,branched, cylindrical, solid, sometimes hollow, hairy or glabrous. Leaves exstipulate, 6
  20. 20. DRUG REVIEWpetiolate, rarely sessile, usually alternate, sometimes opposite, simple entire,sometimes pinnately divided, spinous, variegated, reticulate and unicostate.FLORAL CHARACTERISTICS: Inflorescence usually cymose, extra axillary and leaf opposed cymes, helicoidcymes, axillary umbellate cymess, rarely helicoid, sometimes the flowers are solitaryor terminal in the main or lateral axis. Flowers bracteate or ebracteate, hypogynous,bisexual, actinomorphic, complete sometimes zygomorphic, usually pentamerous,variously coloured, large and showy in many species, sepals 5, fused 5, partite orlobed –lobes sometimes 4-6, corolla tubular or companulate urceolate when mature,ovate or imbricate, persistent, in Physalis calyx persistent and develops a bladder likehusk round the fruit, petals 5,fused,rotae, companulate, infundibular, lobed with 5 ormore lobes or bilabiate, ovate, sometimes imbricate, hairy on the outside variouslycoloured, covered with stellate hairs. Stamens 5,sometimes 4, free, alternate with thepetals, epipetalous, filaments usually of unequal length, rarely the stamens are 4 andare didinamous or only two, anthers two celled usually coming close together to forma cone round the pistil, dehiscing by terminal pores or longitudinal slits, connective,sometimes becoming tetra or tri to penta locular due to the formation of a false septa,placentation axile, ovules many in each locule placed on a swollen and obliqueplacenta. Fruit a berry, seeds small, numerous, smooth or pitted, endospermic,endosperm fleshy, embryo curved.FLORAL FORMULA+, K(5), C(5), A 5, G(2) 7
  21. 21. DRUG REVIEWFLORAL DIAGRAMFigure No 1.USEFUL PLANTS: S. tuberosum, S. xanthocarpum, S. melongena, S. nigrum.DESCRIPTION OF SOLANUM NIGRUMCOLLECTION: Kakamachi patra is collected in varsharutu.SYNONYMS TABLE NO : 4Bhavaprakash Nighantu Kakamachi,Dhwanksha, maachi, Kakahava, Vayasi.Nighantu Adarsha Kakashva, Vayasi.Dhanavantari Nighantu Kakhva, Vayasi, Katvi, Katuphala, Rasayanavara.Raja Nighantu Vayasi, Kakamaachi, katu.Kaideva Nighantu Kakasahava, kakamaachi, Kamata, Jaganephala, Sarvatikta, Bahuphala, Swadupakaphala, Kamachi, Kakini, Kushtaghni, Vayasi, Dhwanksha maachi, Gudaphala, Rasayanavara, Katu. 8
  22. 22. DRUG REVIEWVERNACULAR NAMESArabic : Ambussalap, Enabeddir.Assam : PichakatiBengal : Gurkamai, Kakmachi, Mako, Tulidun.Bombay : Ghati, Kamuni, Mako.English : Black Nightshade, Garden Nightshade, Hounds Berry, Morelle, Petty morel.Gujarat : Piludi.Hindi : Gurukamai, Kabaiya, Makoi.Latin : Solanum nigrum.Malayalam : Trong parachichit.Marathi : Ghati, Kakmachi, Kamoni, Laghukavali, Meko.Persian : RubahtareekPortuguese : Herva moura, Solano.Punjab : Kakmach, Kambei, Kwansaf, Mako, Riaungi.Sanskrit : Bahuphala, Bahutikta, Dhvankshamachi, Ghanaghana, Gucchaphala, Jaghenephala, Kaka, Kakamachi, Kakamata, Kakini, Katuphala, Kushtaghni, Rasayani, Sarvatikta, Sundari, Svadupaka, Tiktika, Vayasavha, Vayasi.Sindha : KanperumSinhalese : Kalukanweriya, Kalukungwareiya, Tibbatu.Tamil : ManattakkaliTelugu : Gajuchettu, Kachi, Kakamachi, Kamachi, Kanchipundu, Kasaka.Urdu : Makoya. 9
  23. 23. DRUG REVIEWTYPES:In Nighantu two types are mentioned. They are1. Shweta2. RaktaMORPHOLOGY OF SOLANUM NIGRUM Solanum nigrum is wild herb growing for most part of the year in wasteplaces, sometimes reaching a height of 90 cm. A variable annual, stem erect, glabrous or more less pubescent, muchdivaricately branched. Leaves numerous, 2.5-9 by 2.5 cm, Ovate-lanceolate, subacuteor acuminate, thin, entire sinuate toothed, tapering in to the petiole; petioles 2 cmlong. Flowers small, in extra axillary subumbellate 3-8 flowered cymes; peduncles 6-20 mm long, slender; pedicels 6-10 mm long, very slender. Calyx 3 mm long,glabrous or nearly so; lobes 5, oblong, obtuse, 1.25 mm long, not enlarged in fruit.Corolla 4-8 mm long, divided more than ½ way down into 5 oblong subacute lobes.Filaments short, flattened, hairy at the base ; anthers 2.5 mm long, yellow, oblong,obtuse, nothed at the apex. Ovary globose, glabrous; Style cylindric, hairy. Berry 6mm in diameter, globose, usually purplish black but sometimes red or yellow, smoothshining. Seeds discoid, 1.5 mm in diameter, minutely pitted, yellow. Calyx 5 sepals,gamosepalous, lobes oblong, acute, white, vivate or imbricate aestivation.Corolla- 5 petals, gamopetalous, rotate, lobes oblong, acute, white, twisted or ovateaestivation.Androecium- 5 stamens alternate to petals, polyandrous, epipetalous, filaments short,anthers oblong, connivent in a cone like structures, bicelled, introse, yellow, dehiscingby apical pores. 10
  24. 24. DRUG REVIEW Gynoecium- 2 carpals (bicarpellary), syncarpous, ovary obliquely placed in the flower, ovary superior, globose, bilocular, axile placentation, many shining ovules present on placenta, style simple hairy at the base, stigma one. DISTRIBUTION: Throughout India, Ceylon and all temperate and tropical regions of the world. PROPERTIES Table No : 5Name of Text Rasa Guna Viryo Vipaka Karma DoshaghnataRaja Nighantu Tika, Laghu Ushna Katu Vajeekara Rasayana Katu Shotha hara Tridosha haraDhanavantari Tikta Laghu Ushna Katu Swarya, Sarakam,Nighantu Kushtanashaka, Vajeekara Rasayana Tridosh haraKaideva Tikta Snigdha Ushna Katu HridyaNighantuNighantu Laghu Shukra vardhaka, Tridosha Swaraya, nashaka SarakaBhavaprakash Tikta, Snigdha, Ushna Katu Swaraya, ShukraNighantu Katu Ushna janana, Rasayana, Tridosha Netraya, Shotha hara nashaka KushtaghnaPriya Nighantu Tikta Ushna Katu Balya, Rasayana Shotha hara, Mutrala YakritrogaAdarsha Katu Ushna Katu Kushtaghna,Nighantu Tikta Shothaghna Rasayana Tridosha haraSusruta Samhita Katu Naatius Mushika visha Tikta hna nashaka, Tilla roga Sheeta nasahaka Tridosha haraCharaka Katu Naatius Kushtaghnam Tridosha haraSamhita Tikta hna Rasayanam Sheeta 11
  25. 25. DRUG REVIEWPARTS USED Pushpa, Phala, Panchaga, Beeja.MATRA (DOSE) : Table No : 6 1. Swarasa 10-20 ml 2. Phala Choorna 1-3 gm 3. Arka 20-50 mlTOXIC EFFECTS: Excessive intake of fruit of Solanum nigrum leads to chardi, Trishna,Udarashoola, Taraka Vispharana, Shirashool, Bhrama, Pralap, Akshepa, Sanyasa andat the severity may lead to Death.TREATMENT FOR TOXIC EFFECTS: Treatment is as similar to Dhatura visha chikitsa.USES OF SOLANUM NIGRUMExternal Uses : Shotha hara, Vrunashodhana, Vedana sthapana, Savarnikarana.Internal Uses :Digestive System: Deepana, Yakrut uttejaka, Pittasaraka and Rechaka.Circulatory System: Hridya, Rakta shodaka, Shothahara and reduces hypertension.Respiratory System : Kaphaghna, Hikkanigrahana and Shwasahara.Urinary System : Mootrala.Skin : Swedajanana and KushtaghnaFever : Jwaraghna. 12
  26. 26. DRUG REVIEWTHERAPEUTIC USES:1. Useful in diseases of the heart , eyes, piles, leucoderma, itch, worms in the ear, dysentary, hiccough, vomitting, asthama, bronchitis, fever, urinary discharges, improves the voice, favour conception and facilitate delivary and rat bite.2. The root bark is laxative and useful in the diseases of the ear, eye, and the nose. Good for ulcers on the neck, burning of the throat, inflammation of the liver, chronic fever, gripping and is harmful to the pregnant women.3. The Leaves have a bad odour and taste and used for headache and the diseases of the nose.4. The fruit is useful in thirst due to fever and inflammation.5. The seeds are laxative and are useful in giddiness, gonorrhea, thirst and inflammation.6. In Bengal the berrys are employed in fever, diarrhoea, eye diseases and hydrophobia.7. The juice in doses of six to eight ounces is given in the treatment of chronic enlargement of the liver and considered as valuable alternative. It acts as a hydrogogue catharic and diuretic.8. The syrup acts as an expectorant and diaphoretic, used as a cooling drink in fevers.9. In North-western province the juice is used in blood spitting, piles, dysentary etc.10. A decoction of the leaves in the dosage of drachm thrice daily in the treatment of dropsical affectin by the mooden sheriff. Its action is diuretic and laxative.11. The young shoots are given in the chronic skin diseases and psoriasis in the konkan region. 13
  27. 27. DRUG REVIEW12. The Chinese employ the juice of the leaves to alleviate the pain in inflammation of the kidneys , bladder and in virulent in gonorrhoea.13. The plant is given internally for cardialgia and externally in nephritic colic, corroding ulcer, suppurating chancre and in severe burnings and herpes.14. The decoction of the leaves is used as diuretic and depurative.15. The plant is used by Europians for convulsions. The herb is one of the native remedies for local application to anthrax pustules and a paste of the green berries is applied to ringworm. The Xosas use the plant for disinfecting anthrax infected meat.16. The Zulus administered as an enema to infants with abdominal upsets. The Sutos rub the burnt and powdered root in to the incisions on the back for relief of lumbgo.17. The fruit in combination with other drug is prescribed for snake bite and scorpion sting, but it is not an antidote to either snake venom or scorpion venom.18. The leaves are employed as poultice over rheumatic and gouty joints and as a remedy in skin diseases.19. Freshly prepared fluid extract from all the portions of the plant has been recommended in dropsy, in heart diseases, skin diseases, piles, gonorrhoea, inflammatory swellings and chronic cirrhosis of the liver and seen in doses of ½ to 2 drachms.20. A Syrup of the plant is useful as an cooling drink in fevers and promotes perspiration.21. Heated warm leaves are applied to the painful and swollen part of the testicles.22. Decoction of the berries and flowers are useful in cough. 14
  28. 28. DRUG REVIEWviii) CHEMICAL COMPOSITION The analysis of the leaves gave the following values in 100 gm of ediblematerial.Moisture- 82.1Protein- 5.9Fat- 1.0Minerals- 2.1Carbohydrates- 8.9Calcium- 410 mgPhosphorus- 70 mgIron- 20.5Leaf is a rich source of Riboflavin. The values for various vitamins present in the leafare (in 100 mg edible material)Riboflavin- 0.59Nicotanic acid- 0.92Vitamin C- 11 mgThe higher values for the vitamin C (20-40 mg) have been reported.The fruits contain-Glucose-15-20%Vitamin –CB-Carotene Green unripe fruits, however contain glycolalkaloids, consumption of thesame leads to toxic hazards to human beings as well as to the livestocks. Ripe fruitcontains very little alkaloids and can be consumed without ill effects. 15
  29. 29. DRUG REVIEW Seeds forming 9.5 percent of protein on dry weight basis. They yield agreenish yellow oil-21.5 % with the following physical and chemical constituents-Specific gravity-0.9198Acid value- 11.62Saponification value- 184.0Acet value- 25.7Iod value- 123.2Hehner value- 92.9R M value- 0.66Unsapon matter- 1.4 %The component fatty acids of the oil areLinolic- 46.63Oleic- 49.73Palmitic- 1.76Steraic- 1.88The unsaponifiable matter contains sitosterol. Immature green fruit of the plant contains four steroidal glycol alkaloids viz; • Solamargine • Solasonine • Solanigrine • Solanigrinine All these yeild Solasodine as the aglycone. It also contains a steroidal genin,tigogenin. (0.101 %) Solanigrine and (0.431 %) Solasonine are present in leavesrespectively. 16
  30. 30. DRUG REVIEWECONOMIC IMPORTANCE : Economically the Solanaceae family is fairly important. It comprises severalplants of food value, medicinal value, vegetable and ornamental values. In whichSolanum nigrum posses medicinal properties. The fruits are given in fevers, diarrhoea,eye diseases and hydrophobia. The juice of plant is given in chronic enlargements ofthe liver, in bleeding piles, dysentery. The fruits are edible and very much liked by thechildren. 17
  31. 31. DISEASE REVIEW REVIEW OF INFLAMMATION1. INTRODUCTION There are many features in the normal structure and physiologies of the body,which serve, protect it against injury. The continuity of skin and mucous surfacesprotects to a considerable extent against minor injuries. Normal or increased secretionfrom nose, eyes, urinary tract. Movements like that of eyelids or cilia of the trachealmucosa chemical constituents such as of gastric juice is other instances of naturaldefense mechanism against injury or bacterial invasion. Reflexes such as sneezing andcough are definite protective mechanisms, immune bodies present in the body fluids,which may be increased by the survival of natural disease and by the artificialprocesses, endow the organism with an important means of defense. Inflammation in addition to above means seems to be a better defensivereaction against an injury locally. It may be associated with general changes such asfires, leukocytosis and development of immune substances, but it itself operates onlyat the site of injury. The same exogenous and endogenous stimuli that causes cell injury also elicita complex reaction in vascularized connective tissues called inflammation. Reducedto its simplest terms, inflammation is a protective response intended to eliminate theinitial cause of cell injury as well as the necrotic cells and tissues resulting from theoriginal insult. Inflammation accomplishes its protective mission by dilating,destroying or otherwise neutralizing harmful agonists (e.g. microbes or toxins). It thussets into motion the events that eventually heal and reconstitute the sites of injury.Thus inflammation is also intimately interviews with repair processes wherebydamaged tissue is replaced by the regeneration of parenchymal cells, and loss byfilling of any residual defect fibrous scar tissues. 18
  32. 32. DISEASE REVIEW Although inflammation helps to clear infections and repairs, makes woundhealing possible, both inflammation and repairs have considerable potential to causeharm. Thus inflammatory responses are the basis of life threatening anaphylaticreactions to insect bites or drugs, as well as to cause certain diseases such asrheumatoid arthritis and athero-sclerosis, other harmful examples includeinflammation in the peritoneum leading to fibrous bands that cause intestinalobstruction or pericardial inflammation resulting in lenses encasing scar that impairscardiac function. The inflammatory response has many roles; these include circulating cells andplasma proteins, vascular wall cells and extra cellular matrix of the surroundingconnective tissue. The circulating cells include bone marrow derived polymorpho-nucleus. Leukocytes (neutrophils), eosinophils, basophils, lymphocytes, monocytesand platelets, the circulating proteins include clotting factors; kininogens andcomplement components, largely synthesized by the vascular wall cells include theendothelial cells in direct contact with the blood as well as the underlying smoothmuscle cells that are important to the vessels. The connective tissue cells includesentinels, macrophages and lymphocytes, in addition to the fibroblasts that synthesizethe extra cellular matrix and can proliferate to fill in a wound, the extra cellular matrix(ECM) consist of fibrous structural proteins (e.g. collagen and elastin), get formingproteglycous and adhesive glycoprotein (e.g. fibronectin) that are the cells – FCM=ECM-ECM connectors, as we see, these all interact to resolve local injury andrestore normal tissue function. Inflammation is divided into two basic patterns. Acute inflammation is ofrelatively short duration, lasting from a few minutes to a few days and is characterized 19
  33. 33. DISEASE REVIEWby fluid and plasma protein exudation, a predominantly neutrophilic leukocyteaccumulation. Chronic inflammation is of longer duration (day to years) and typicalby influx of lymphocytes and macrophages associated with vascular proliferation andscarring. However these basic forms of inflammation may have many factors andhistological appearances. The reaction of vascularized living tissue to local injury, invertebrates with novascular system, single celled organisms, and multicellular parasites have their ownresponses to local injury. These include phagocytosis of the injurious agents,endropment of the irritants by specialized cells haemocytes, which ingest it andneutralization of noxious stimuli by hypertrophy of the cell or one of its organelles.The inflammatory process in higher forms is the reaction of blood vessels leading tothe accumulation of fluid and blood cells. The inflammatory response is closely interwined with the process of repair, itserves to destroy, dilute the injurious agent, but sets into motion a complex series ofevents, heal and reconstitute the damaged tissue as far as possible.2. DEFINITION AND TERMINOLOGYDEFINITION: Inflammation is defined as the local response of living mammalian tissues toinjury due to any agent. It is a body defense reaction in order to eliminate or limit thespread of injurious agent as well as to remove the consequent necrosed cells andtissues.TERMINOLOGY: The majority of inflammatory serous are named by adding the suffix It is tothe anglicized form of the Greek hour of the tissue or organ involved. Thus we speakof dermatitis, gastritis, meningitis and so on. 20
  34. 34. DISEASE REVIEW The suffix It is derived from the Greek for belonging to the names ending in Itis do not imply the cause of the inflammation. For example, dermatitis may be due tothe infection or chemical injury, radiation or immunologic reaction and so on. All thename implies is inflammation of the skin. Inflammatory diseases have been known since ancient times and like others ofancient lineage, they sometimes bear strange names derived from the past Erysipelas aspreading Streptococcal infection of the subcutaneous tissue of the face was named bythe great Hippocrates 300 years before christ pneumonia is another old term still incommon use, these terms will be defined when we come to the diseases of the organsaffected. Inflammation is best defined in teleological terms, specifically it is a series ofmolecules and cellular responses acquired during evaluation designed to eliminateforeign agents and promote repair of damaged tissues. Unfortunately, these responsesare not infallible. Pathogens have concurrently evolved mechanism to avoidelimination; new pathogens occasionally emerge from the environment and undersome circumstances aberrant immuno inflammatory response damages the host. Thecomplexity of the immuno inflammatory system is a reflection of millions of years ofenvironmental challenges. It is becoming apparent that the system is not simple butrather a complex composite of responses that were assembled opportunitically andwhen elicited may synergize or antagonize each other.3. HISTORICAL BACKGROUND For centuries, humans have identified inflammation fire, undoubtedly, as aresult of the experience of reduces heat and pain associated its occurrence.Interestingly scientific investigation of inflammation has extended this analogy. Atthe microscopic level, inflammation is described as an accumulation of leukocytes 21
  35. 35. DISEASE REVIEWthat “spread” within tissues and then ultimately “burn out” and heal or lead“smoldering’ conditions. Similarly at the molecular level, leukocytes use an oxidativemechanism in essence a form of biologic fire that destroys micro-organisms anddamages tissues. Despite the essential truth of our intuitive sense of inflammation, theobjective under starting has come slowly. At least since the eighteenth century, inflammation has been considered asmanifestation of immunity, but the mechanisms governing inflammatory events haveremained enigmatic until recent decades. During the late nineteenth and much of thetwentieth centuries, important advances were made regard to manipulating gum oralimmunity as evidenced by the development of vaccines and the use of antiserum.These great advances tended to over shadow the role of phagocyte cells in resistanceto infection as promoted by the Zoologist Elie Metchnikoff like wisehistopathologists. Such as Rudolf Virechow and Julius Cohnheim speculated thatcellulus and vascular components of inflammation were critical elements, but theycould not ascertain full significance or relationship to humeral immunity. It is nowunderstood that inflammation is a dynamic interaction of humeral of cellularresponses. Recently studies of inflammation have focused on revealing the“molecules language” that dictates the observed events clearly. There is a complex eraof both humeral and cellular signals that determine the quality, intensity and durationof inflammation. The features of inflammation were described in an Egyptian paper around3000 BC. celsus, a Roman writer of the first century AD listed the four cardinal signsof inflammation, they were rubor (redness) tumor (swelling), calor (heat) and dolor(pain). These signs are more prominent in acute inflammation than in chronicinflammation. Later Virechow added the fifth sign of functiolaesa (loss of function). 22
  36. 36. DISEASE REVIEW Inflammation is not a disease but a non-specific response that has a salutoneffect on its host, this obvious fact was noticed by the Scottish surgeon John Hunter in1793. Julius Cohnheim (1839-1884) who provided one of the first and bestmicroscopic description of inflammation and observed inflamed blood vessels in thinand transparent membranes such as in the mesentery and tongue of frog. Noting theinitial vasolidation and changes in blood flow, the subsequent oedema caused byincreased vascular permeability and the characteristic leukocyte emigration. Elie Metchnikoff, a Russian biologist in 1882 discovered the process ofphagocytosis by observing the ingestion of rose thorns by amebocytes of starfishlarvae and of bacteria by mammalian leukocytes and concluded that the purpose ofinflammation was to bring phagocytic cells to the injured area to engulf invadingbacteria. Metchnikoff contradicted the prevailing theory, that the purpose ofinflammation (humoral theory of immunity) was to bring in factors from the serum toneutrilize the infectious agents. It became clear that both cells (phagocytes) and serumfactors (antibodies) were critical for defense against micro-organisms, thisstrengthened by the discovery of the antitoxins by Behring and Kitasato (1890) On the basis of simple experimental studies of inflammatory response on skin.Sir Thomas Lewis established the concept that chemical substances such as histaminelocally induced by injury, mediate the vascular changes of inflammation, thisfundamental concept underlies the important discoveries of chemical mediators ofinflammation and the use of anti-inflammatory agents.4. CAUSES OF INFLAMMATION1. The outstanding cause is injury by living agents; these can induce progressive inflammation due to two basic procones, early inflammatory response and 23
  37. 37. DISEASE REVIEW healing. These processes generally have protective role against injurious agents. Inflammation is distinct from infection, is being a protective response by the body and invasion into the body by harmful microbes and their ill effects by toxins. The causes may be due to physical agents i.e., heat, cold radiation, mechanical trauma.2. Chemical agents i.e., organic and inorganic poisons3. Infective agents like bacteria, viruses and their toxins4. Immunological agents like cell mediated and antigen antibody reactions. CAUSES OF INFLAMMATION CHART NO – 1 INJURIOUS AGENTS Living agents Non-living agents Physical agents Chemical agents I) Mechanical trauma I) Strong acids ii) Presence of foreign body ii) Strong alkalies iii) Under heat and cold iii) poisons iv) Pressure v) Ionising radiation5. SIGNS AND SYMPTOMS The Roman writer Celsus described four cardinal signs of inflammation as (a) Rubor (Redness): An acutely inflamed tissue appears red due to dilatation of small blood vessels within the damaged area. E.g., Skin affected by sunburn, cellulites by bacterial infection etc. 24
  38. 38. DISEASE REVIEW (b) Calor (Heat): Increase in temperature is seen only in peripheral parts of the body such as skin. It is due to increased blood flow (hyperaemia) through the region resulting in vascular dilatation and delivery of warm blood to the area. E.g., Systemic fever. (c) Tumor (Swelling): Swelling results from oedema, the accumulation of fluid in the extra vascular space as part of the fluid exudates and to a much lesser extent, from the physical mass of the inflammatory cells migrating into the area. (d) Dolor (Pain): Pain is the best-known feature of acute inflammation. It results partly from stretching and distortion of tissues due to inflammatory oedema and in particular from pus under pressure in an abscess cavity. Chemical mediators like bradykinin, prostglandins and serotonin are known to induce pain. (e) Loss of function (Functio laesa): Movement of an inflamed area is consciously and reflexly inhibited by pain, while severe swelling may physically immobilize the tissues.6. CLASSIFICATION OF INFLAMMATION CHART NO-2 CLASSIFICATION OF INFLAMMATIONAcute inflammation Sub Acute inflammation Chronic inflammationi) Catarrhal 1) Diffusedii) Fibrinous or Serofibrinous 2) Suppurativeiii) Suppurative or purulent 3) Granulomatousiv) Haemorrhagic 4) Fibrinoidv) Pseudo membranousvi) Allergic 25
  39. 39. DISEASE REVIEWI. ACUTE INFLAMMATION:a) CATARRHAL ACUTE INFLAMMATION: This is confined to mucous membrane, the mucous cells of the lining and ofthe mucous glands secrete large quantities of mucin, there is molecular desquamationof the surface lining, not so pronounced as to appear as ulceration. The discharge onthe surface or in the lumen consists of mucous plasma, leucocytes and desquamatedepithelial cells, it is mucoid in the early stages and becomes mucopurulent later.Acute catarrhal inflammation is mildest form of inflammation, but in some organs itcan progress to termination and can become chronic. E.g. Rhinitis of common cold,catarrhal bronchitis.b) FIBRINOUS OR SEROFIBRINOUS INFLAMMATION: This is seen in the serous membranes, the pericardium, pleura, peritoneum etc.It consists of plenty of fibrin in the exudates derived from the exudate plasma,irrespective of the nature of the irritant, they react in a stereotyped manner.Neutrophils and macrophages are seen in the fibrinous network.c) SUPPURATIVE OR PURULENT INFLAMMATION: This type is characterized by the formation of pus. In solid tissues and organssuppurative inflammation causes Abscesses, in contrast to the circumscribed affectionin abscess formation the process may become diffuse and spreading. Diffuse lesionsin the connective tissue are described as “Phlegmonous Inflammation or Cellulites”.d) ACUTE HAEMORRHAGIC INFLAMMATION: In certain cases, bacterial toxins produce intense injury to the capillary walland allow large number of Red Blood Corpuscles to escape, making the exudateshaemorrhagic. E.g. In Influenza Pneumonia, Acute Glomerulonephritis etc. 26
  40. 40. DISEASE REVIEWe) PSEUDO MEMBRANOUS INFLAMMATION: This form of inflammatory reaction is characterized by the formation of amembrane usually made up of precipitated fibrin, necrotic epithelium andinflammatory white cells. The reaction is encountered only on mucosal surfacescommonly in the Pharynx, Larynx, Respiratory passage etc. The membrane formationresults from an acute inflammation response to a powerful necrotizing toxin, outpouring of exudates traps the necrotic and cellular debris producing a dirty gray-white, rubbery membrane on the eroded surfaces. E.g. In Diphtheria.f) ALLERGIC INFLAMMATION: In this, Inflammation is primarily and exclusively by antigen-antibodyreactions. The injury in this is due to the occurrence of antigen-antibody union onwalls of the tissue cells, hypersensitivity has much greater significance. The vascularchanges are associated with a cellular exudates consisting of neutrophils, eosinophils,plasma cells and macrophages. Eosinophils may be spectacular components, tendencyto necrosis and tissue decay due to accelerated reaction and increase in the Phagocyticpower of the Leucocytes with increase of eosinophils are distinct features in allergicinflammation.2. CHRONIC INFLAMMATION The acute inflammatory response is unable to remove or neutralize aninjurious agent; the response is modified to chronic. It is not usual for a chronicresponse to last many months but years. As the inflammatory process continues, fluidexudates diminishes and cellular response assumes dominance, the chronic responseis dominated by a massive build up of cells in the affected tissue. These cells areprimarily macrophages and lymphocytes. In chronic inflammation the agent and thehost are just capable of resisting each other. The agents involved are of low inevitable 27
  41. 41. DISEASE REVIEWability. They are unable to penetrate deeply in to or spread throughout the body of thehost. Such agents may be bacteria, fungi, larger parasites. Foreign bodies which areinsoluble in body’s fluid can also elicit a chronic inflammatory response. Regardless of the specific nature of the inciting agent, its presence in the tissuepromotes a long term conflict with the phagocytic cells of the host; heavy infiltrationby the inflammatory cells progressively interferes with normal function. When theprocess continues over a month and years, the function detoriates as tissue isdestroyed, accumulating inflammatory cells replace functional tissues and scarringdevelops. This deterioration ultimately leads to somatic death.TYPES OF CHRONIC INFLAMMATIONSFollowing Four types are included in Chronic Inflammation: 1) Chronic Diffused Inflammation 2) Chronic Suppurative Inflammation 3) Chronic Granulomatous Inflammation and 4) Chronic Fibrinoid Inflammation.1) CHRONIC DIFFUSED INFLAMMATION: Exudates, which may be diffused or focal shows lymphocytes, plasma cellsand macrophages, under certain stimuli macrophages develop into epitheloid cells andmultinucleated giant cells. Fibroblasts are present, in older lesions fibrosisconspicuous. E.g. Chronic Ulcer.2) CHRONIC SUPPURATIVE INFLAMMATION: It is a non-specific inflammatory cell infilteration, in which infiltration bypolymorphs and abscess formation. E.g. Actinomycosis 28
  42. 42. DISEASE REVIEW3) CHRONIC GRANULOMATOUS INFLAMMATION: It is characterized by the formation of Granulomas, a tiny lesion composed ofepithelial cells and lymphoid cells at the periphery, also granulomas may have giantcells, necrosis and fibrosis. It is seen in specific infective granulomas as inTuberculosis, syphilis. Leprosy etc.4) CHRONIC FIBRINOID INFLAMMATION: It is a degenerative phenomenon like rheumatoid arthritis, reheumatic feveretc. DIFFERENCES BETWEEN ACUTE INFLAMMATION & CHRONIC INFLAMMATION Table No 7Acute inflammation Chronic Inflammation1.Duration: Usually for days or weeks 1. Duration: For months or Years2. Cardinal Signs: Present 2. Cardinal Signs: Doubtful or not perceptible3.Vascular Changes: Present 3.Vascular Changes: Not Marked4. Exudation of Plasma: Present 4. Exudation of Plasma: Doubtful or Absent5. Cellular Exudates: 5.Cellular Exudates:Neutrophils initially lates Macrophages and Histocytes Plasma cells lymphocytesFibroblasts Stage of repair Lymphocytes Fibroblasts are present Neutrophilsare few. absent or very less in numbers. 29
  43. 43. DISEASE REVIEW7. GENERAL MECHANISM OF INFLAMMATION The starting point of inflammation is the cell damage, living or inert, the cellswhich do not damage are not capable of producing inflammation. However once thedamage has occurred the reaction takes place inevitably and proceeds through adefinite series of events to its ultimate end, i.e. repair of damage and restoration offunction. CHART NO- 3GENERAL MECHANISM OF INFLAMMATION • Vascular phenomenon changes Vasodilation Active hyperemia Capillary dilation Static of blood Sludging of red cells in the capillaries Pavementation of leukocytes Exudation of fluid and out pouring of polymorphs • Cellular response Local Exudation Fluid of exudation Cells of the exudation General response Fever degeneration Leukocytosis • Repair of tissues 30
  44. 44. DISEASE REVIEW Degenerative Albuminous degeneration a. Repuls degeneration b. Healing cloudy swelling c. Regeneration Fatty degeneration a. Suppuration b. Abusers c. Boil d. Carbuncle e. Cellulites Proliferative Phagocytes a. Attachment b. Engulfment (i) Azophil (ii) Special groused c. Killing and degeneration (i) Oxygen dependent mechanism (ii) Oxygen independent mechanismCells included in the inflammatory exudates are : • Neutrophil • Eosinophils • Mast cells • Lymphocytes 31
  45. 45. DISEASE REVIEW • Plasma cells • MacrophagesMECHANISM OF INFLAMMATION -Management of inflammation and action of non-steroidal anti-inflammatory drugs(NSAID) Irrespective of the nature of causative factors or the type of inflammation, thetissue reaction in first few hours is stereotyped and similar. Its pathology can beunderstood in the fallowing steps. 1.Vascular phenomenon 2.Cellular phenomenon 3.Repair1.Vascular phenomenon:Following changes will occur in vascular phenomenon one by one i. Vasodilatation: Proceeded by transient vasoconstriction ii. Active hyperemia iii. Capillary dilatation iv. Stasis of Blood v. Sludging of red cells in the capillaries. vi. Pavementation of leukocytes. vii. Exudation of fluid and out pouring of polymorphs.There are number of cells present in the inflammatory exudates which performvarious functions. Those are a. Neutrophils b. Eosinophils 32
  46. 46. DISEASE REVIEW c. Mast cells d. Lymphocytes e. Plasma cells f. MacrophagesA brief description and the role is as follows.a) Neutrophils: Neutrophils or Polymorphs are the cells along with Basophils and Eosinophils are known as granulocytes, due to the presence of granules in the cytoplasm, contains substances like proteases,myloperoxidase and alkaline phosphates. Neutrophils are actively motile, get collected arround blood vessels and passes through the tissue by active amoeboid movements, there from the first line of defense in bacterial infections.b) Eosinophils: These are larger than the Neutrophils and constitute 2-4% of the total blood leucocytes. They appear only at the sites of inflammatory exudates of diseases of immunological origin. They remain in the circulation for a short peroid and rapidly attracted in the tiisues by the raised concentration of released histamine. Eosinophils are phagocytic in nature. These may share many structural and functional similarities with neutrophils, like their production in the bone marrow, locomotion, lobed nucleus and presence of granules in the cytoplasm. Granules of eosinophils are rich in myeloperoxidase than neutrophils and lack lysozyme. High level of steroid harmone (eosinopenia) leads to fall in number, and even disappear from the blood. These may be increased in certain conditions like Allergy, Parasitic infestations, skin diseases and certain malignant lymphomas.c) Mast cells: These cells contain coarse basophilic granules in the cytoplasm and a polymorphous nucleus, These granules are laden with heparin and 33
  47. 47. DISEASE REVIEW histamine. The functions of mast cells in normal Human being is not vivid. They are believed to produce the acid.d) Plasma cells: These are larger than the lymphocytes with more abundant cytoplasm and an eccentric nucleus. These cells are normally not seen in peripheral blood. They develop from lymphocytes and are rich in RNA and Gama-globulin in their cytoplasm. There is an inter relationship between Plasmocytosis and Hyperglobulinaemia. These cells are most active in antibody synthesis. The number will increase when prolonged infection with immunological responses. e.g. Syphilis, Rheumatoid Arthritis, Tuberculosis, Hypersensitivity states and multiple myeloma.e) Macrophages: These are large mono-nucleated cells play an important role in the stages of Acute and Chronic Inflammations. It is believed that many lymphocytes derived from the blood are converted in to microphages at the site of inflammation, by increase in cytoplasm and enlargement of the nucleus and are derived from Kuffer cells of the liver and histocytes. They form the scavenger cells of inflammation, combine to form giant cells and need phagocytic action. The giant cells are mainly of : i. Tumour Giant Cells a. Anaplastic Cancer Giant Cells b. Reed-Sternberg Giant Cells and c. Giant Cells of Tumour ii. Foreign Body Giant Cells.i. Tumour Giant Cells: It is of fallowing typesa. Anaplastic Cancer Giant Cells: 34
  48. 48. DISEASE REVIEW These are larger and have numerous nuclei which are hyper chromatic andvary in size. These giant cells are not derived from macrophages but are formed fromdividing nuclei of the neoplastic cells.b. Reed-Sternberg Giant Cells: These are malignant tumour giant cells , which are binucleate and are seen invarious histologic types of Hodgkins lymphomas.c. Giant Cells of Tumour: These cells are usually found in the bones, uniform distribution andosteoclastic giant cells spread in the stroma.ii. Foreign Body Giant Cells:- These contain numerous nuclei, which are uniform in size and shape andresemble the nuclei of macrophages, these nuclei are scattered throughout thecytoplasm, these are usually seen in the chronic infective granulomas.2.CELLULAR RESPONSE: Cellular response can be explained in to a) Local response and b) Generalresponse. The local response starts with the pavementing and emigration ofleukocytes before the cells of the damaged tissue release some chemicals that bringabout all the changes. The Vasodilation and increased permeability is due to thesubstances like "leukotoxin" and "histamines" are produced by the damaged tissuecells. These stimuli activate both Hematogenic and Histogenic cells, which carry outvarious functions like vascular phenomenon, pavementation and emigration ofleukocytes and various other cellular responses. 35
  49. 49. DISEASE REVIEW Following a local injury, there is a transient constriction in the vessels thatcause local Ischemia. This mommentary constriction is followed by an active phase ofhyperemia with dilation of vessels, this dilation chiefly occurs in arteries and venulesand at last in the capillary bed. The active hyperemia lasts for a few hours. Thecapillaries get changed and become prominent. The blood vessels keep on dilating and the active hyperemia is fallowed by thestagnation of blood, which is termed as stasis and the clotting takes place in thevessels. The blood supply to the tissue is lost and necrosis sets in the vasodilation thatfollows the transient vasoconstriction (due to neural reflex) It is recognized that asensory fibre has a vasodilator branch to an arteriole. When there is an injury, there isa reflex vasoconstriction and thus vasodilation sets in. The vasodilation occurs under the influence of chemical mediators also, it waspostulated by Lewis (1927) that "H" like substance cause vasodilation. FurtherMenklin postulated about "Leukotoxin". In addition, it increases the vascularpermeability and responsible for the emigration of leukocytes, the slowing of bloodflow in the vessels may be attributed to swelling of the endothelial lining of the bloodvessels, vasodilatation that decreases the pressure. Loss of blood fluid in interstitialspaces makes the blood viscous. There is sludging of red cells. The red cells becomesticky and adhere to one another in masses and to the walls of the vessels. In this slower blood stream, rearrangement of the corpuscles takes place, undernormal condition, the red and white cells flow intermingled in the central part of thevessels forming an axial stream, which is separated from the wall by a clear plasmaticzone free from cells. When there is some degree of injury, the leukocytes fall out ofthe axial stream and come to occupy the plasmatic zone adhere to the vessel wall andseem to drag themselves along with difficulty. In this way, the inner wall of the 36
  50. 50. DISEASE REVIEWcapillary becomes paved by a broken line of leukocytes without the admixture of asingle red blood cell. This arrangement is called pavementing of leukocytes. Normally the endothelial cells of the blood vessels and blood cells repel oneanother due to change in the electrical potential, where these carry negative chargeswith them, hence the repulsion. The endothelium becomes positvely charged and theleukocytes are the first of the cellular elements to be attracted to and adhere to thelining of the vessel. The endothelial cells also become enlarged, proliferated and thus assumeround shape. The inter-endothelial space widens and through these spaces leukocytesemigrate.A) EXUDATION: After dilation of blood vessels, the solid and fluid contents of plasma as wellas of the blood cells pass through the vessel walls and constitute within the tissues.Thus, the fluid is rich in protein contents and the cells constitute the exudates.B) FLUID OF THE EXUDATE: Normally the walls of the blood vessels are permeable to the fluid, some ionicsalts and the molecules with molecular weight less than 10,000 Daltons, large part ofthe fluid get reabsorbed and the remaining is carried by lymph channels. But during inflammation, this exudate fluid, which originates from plasmadiffers from it in several aspects. Its solid contents are almost double than the contentsof the lymph. Its specific gravity is 1.020. The main reason is that serum albumin andserum globulin is present in exudate. The fluid molecules come out of vessels due toincreased permeability of vessels. 37
  51. 51. DISEASE REVIEW Besides this protein, the exudate contains various extractions like Urea, fibrinforming elements, mucin ferments and immune bodies, oxidases, lipases and trysin.All type of immune bodies may be found including cytolysin, haemolysin,bacteriolysin, agglutinins, opsonins and complement fixing bodies. The formats andthe immune substances are distinctly higher in oedema than oedema produced due toother causes.FUNCTION OF FLUIDS OF EXUDATE :1. It dilutes the soluble poisons and irritates, thereby reduces their direct effect.2. It provides over runs of escape for the metabolites which are formed in excess.3. It maintains normal hydrogen concentration. The protolytic enzymes serve to complete the solution of the tissues whichhave been injured or killed, thus aid in their removal. Exudate is rich in fibrin formingproteins. The environment in which it is present favours fibrin formation, this servesas the limits of extent of the inflammatory process. The fibrin mesh in the lymphaticsserve as a filter and with solid materials especially bacteria, if it is not dissolving byprotolytic enzymes it provides a frame work on which connective tissue grows andhealing takes place.C) CELLS OF THE EXUDATES: After pavementing the leukocytes emigrate in extra vascular spaces, as theyemerge from the outer margin of endothelium, a new basement membrane formsbetween them and the endothelium disappears permitting release of the leukocytes into the extra vascular space without leaving any defect behind them, under theinfluence of various chemical mediators, this phenomenon is known as "Chemotaxis". 38
  52. 52. DISEASE REVIEWD) PHAGOCYTES: Phagocytes can be resolved in to three distinct ways 1. Attachment of the Particle to the surface of the phagocyte. 2. Engulfment. 3. Killing and degeneration of the ingested microbe or particle.1. Attachment of the Particle to the surface of the phagocyte: These cells are recognized and attracted to bacteria by chemotactic factorsreleased by bacterial products as well as by tissue proteins, in order to establish abond between bacteria and the cell membrane of phagocytic cells, the microorganisms get coated with opsonins which are naturally occurring factors in theserum. The main opsonin present in the serum IgG opsonin, is the Fe fragment ofimmunoglobulin G, antibody in the serum that coats the bacteria. C3b opsonin is thefragment of completement, which is generated by activation of completementpathway. Lactins are carbohydrate-bonding proteins in the plasma, which bind tobacterial cell wall. Receptors mediated attachment of opsonized bacteria has been therecognization step of Phagocytosis.2. Engulfment: Leukocytes are able to respond to opsonins for that they display leukocytebinding sites, once an opsonin coated particle is bound to the surface receptors of thephagocyte, the particle is readily engulfed. Binding of a particle to the phagocyticmembrane elicits the engulfment, the phagocytic membrane flows around the particleto enclose it in a cytoplasmic phagosome. Granular appearing lysosomes that contain 39
  53. 53. DISEASE REVIEWdestructive agents then merge with the phagosome membrane, thereby bringing theircontents in to contact with the particle. As lysosome merge with the phagosomes theirnumber within the phagocyte are reduced and the phagocyte is degenerated. If theparticle is too large to be easily engulfed i.e. a multicellular parasite. There may beregurgitation of the granule contents in to the tissue spaces. The leukocytes attemptingto engulf this large surface experiences frustrated phagocytosis and releases toxic anddegradative substances that damage the basement membrane and the surrounding cellsand the matrix. The neutrophil cytoplasm contains two types of granules Azusophil andSpecific granules. Lysosomes contain acid hydrolases, neutral proteases, cationicproteins, lysozyme.i) AZUSOPHIL: These lysosomes contain acid hydrolases, neutral proteases, cationic proteins,lysozyme.ii) SPECIFIC GRANULES: Which contain lysozyme and lectoferiin but no hydrolases or peroxides.Macrophages also contain azusophil granule. The process of degranulation pour in tothe phagosome powerful enzymes which kill the bacteria by different mechanisms.3. KILLING AND DEGENARATION: The micro-organisms after being killed by antibacterial substances aredegraded by hydrolytic enzymes, their mechanism fails to kill and degrade somebacteria.These are of mainly two types, Oxygen dependent and Oxygen Independent.1. Oxygen dependent: It is an important mechanism of microbicidal killing by the production ofreactive oxygen metabolites (O2 H2O2, OH, HOCL, HOL, HOBr) a phase of increased 40
  54. 54. DISEASE REVIEWoxygen consumption by activated phagocytic leukocytes in presence of NADPHoxidase.The NADPH oxidase which is present in the cell membrane of phagosomereduces oxygen to superoxide ion (O2). 2O2 NADPH 2O2 (superoxide anion) 2O2 + 2H─ H2O2 Suproxide is subsequently converted in to Hydrogen peroxide (H2O2) hasbactericidal properties, this bactericidal activity is carried out either enzymemyeloperoxidase present in the granules of neutrophils and monocytes or the enzymemyeloperoxidse acts on Hydrogen peroxide in the presence of halides (Chlorides,Iodide, Bromides) to form hypophalous acid (HOCl ). Which is more potentantibacterial agent than hydrogen peroxide. Reactive oxygen metabolites are useful in eliminating microbial organismsthat grow within phagocytes.2. Oxygen Independent: This mechanism involves the release of substances that damage bacterial cellwalls, disrupt bacterial replication and produce a low pH within the phagosomesresulting from accelerated glycolysis, Which may be directly toxic and may indirectlyaid the function of other enzymes.b) GENERAL RESPONSE: The general celleular respons may be Fever and Leukocytosis.i. Fever: Fever is one of the most prominent systemic manifestation, particularly ininflammation associated with spread of organisms into the blood stream. The patientmay have high fever charecterised by dramatic swings in the temparatur. The origin ofthe fever may be uncertain, although it may be caused by the release of bacterial 41
  55. 55. DISEASE REVIEWendotoxins. In addition interleukin – 1 (IL-), prevously described as endogeneouspyrogen released from the leukocytes is an important mediator of hyper pyrexia. Thismediator is taken up by lymphatics from the site of imflammation, which is circulatedin blood stream. It is believed that IL-1 initiates fever by inducing the synthesis ofPGE2 in the anterior hypothalamas and stimulating thermoregulatory centres.ii. Leukocytosis: Increase in the number of circulating white cell is another charecteristicsignificance of acute and chronic inflammation. When the inflammation is deep andthe local symptomatology is either not observes or impossible to demonstrate, thenleukocytosis is of assistance in determining the severity of the infection and thedegree of the resistance offered by the body. This requires not only an absolute count(i.e. the total number of white cells per mm) but also the relative number of each typeof leukocytes particularly the number of neutrophils. In making the differential count,the number of each kind of white cells in hundred is counted. • A high absolute count (T.L.C) with a high neutrophil percentage indicate severe infection and good body resisitance. • A high absolute count with a moderate neutrophil percentage indicates a moderate infection and good body resisitance. • A low absolute count with high neutrophil percentage indicates severe infection and weak resisitance of the body. • All inflammatory states do not evoke neutrophilic leukocytosis. Infectious mono nucleoses, whooping cough, mumps, rubella and undulent fever charecteristicaly produce lymphocytosis. 42
  56. 56. DISEASE REVIEW Allergic inflammatory reaction like hay fever, bronchial asthama and parasiticinfection typically elicit eosinophilia. Some infections may cause leukopenia instead,like infections caused by viruses, rickettsiae, protozoa and salmonelloses.C. TISSUE CHANGES OR REPAIR: There are two types of tissue changes a. Degenerative b. Proliferative.a. Degenerative: The two most common degenerations are 1. Albuminous degeneration or cloudy swelling 2. Fatty degeneration1. Albuminous degeneration or cloudy swelling: It is closely related to hydrophic or vascular degeneration. Being manifestationof a disturbance of protein metabolism, is called as Albuminous degeneration. It maybe caused by the bacterial toxins, chemical poison, malnutrition and otherdisturbances. The principle organs showing cloudy swelling are Kidneys, Liver and Heartmuscles. The organ affected is slightly enlarged owing to swelling of the cells ofwhich it is composed. It is pale as blood vessels being compressed by the swollencells. The cut surface has rather cloudy appearance and slightly opaque.2. Fatty degeneration: Fatty degeneration or Fatty metamorphosis is a true sickness of cells causedby some injurious influences. It is best seen in Liver, Kidney and Myocardium. Thefat metabolism is interferred with fat accumulations in the cell. In some cases there ismerely unmarking of fat already present. The causes of fatty degenerations are 43
  57. 57. DISEASE REVIEW • Poisons • Anoxia The organs look fatty. The liver and kidneys are pallor and softer than normal.The heart is soft and flabby. Ultimately the tissue becomes necrosed. If the irritant is intense, the effect is degenerative destruction. If it is mild, actsas stimulant and leads to proliferation. At the centre of the inflammatory area theaction of the irritant is severe, degeneration predominates at the periphery and theaction is mild. The tissue may be stimulated to proliferation. thus this part of theinflammation is known as repair or healing.i) SUPPURATION: If the dead tissue in an inflammed area undergoes softening and liquification isknown as the process of Suppuration, the fluid formed is called the Pus, by thismethod the dead material is removed from the body.There are three requisites forsuppuration. i. Necrosis ii. Presence of sufficient leukocytes iii. Digestion of the dead materials by protolytic fermentation. If any one of these are absent suppuration does not occurs.The digestiveenzymes are produced mainly by the leukocytes to a lesser extent by the necrosedtissue cells and the infecting bacteria. These are neutralized by anti enzymes presentin the serum. If there is less leukocytes or more serum liquification does not takeplace.ii. ABSCESS: It is an example of a localized suppuration. The inflammation is limited to thearea and as the irritant is pyogenic, pus is produced. The cells in the centre of the 44
  58. 58. DISEASE REVIEWinflammatory area are killed and liquified by protolytic enzymes. In this way a cavityis produced which contains pus. The wall of the abscess cavity consists of damagedbut still living tissues. Hence the spread of infection is limited, this limiting zone iscrowded with polymorph nucleus leukocytes and macrophages filled with debris. Puscells are continuously dicharged from this, thus the abscess is chronic or if theinfection is dying out, the macrophages will greatly outnumber the polymorphsfurther out, the tissue become more and more normal. If the infection is continuously active more and more material is added to theabscess, So that the pressure within the abscess increases. Thus it points in thedirection of less resistance. If the abscess enters the muscle sheath, it may extentalong a considerable distance.iii BOIL: It is an abscess of a Sebaceous gland or a hair follicle caused by theStaphylococcus aureus, which has penetrated the opening of the duct. There is amarked fibroblastic proliferation, which with intercellular formation of fibrin, causesthe characteristic indusation. The tension becomes high and causes pain. There maybe a very little liquification of the necrosed tissue, So that the centre of the boil iscomposed of a solid "Core" instead of Pus.iv. CARBUNCLE: It is the infection spread to the subcutaneous tissue where it causes a morediffused lesion which discharges on the surface by a series of openings. The pusbecomes inspected and the dead tissue is converted into a mass of fatty debris inwhich lime salts may be deposited. 45
  59. 59. DISEASE REVIEWv. CELLULITIS: When the suppuration spreads through the tissues, the condition is calledcellulitis. The fibrin that forms as a result of proliferation, inflammed part limit theinfection.3. REGENERATION: This implies to a complete renewal of the tissue as in liver. The process ofhealing if fundamentally the same in all the wounds. It consists of two parts. Removalof inflammatory material and necrotic debris, which may be more or little.Replacement or reconstruction of the original tissue to a greater degree as much aspossible. The repair involves the invasion and replacement of dying and dead tissue byimmature mesenchyma called Granulation tissue, which is a highly vascular tissue.On account of its cellularity a granulating surface has a remarkable power ofresistance against bacterial infection. The granulation tissue grows to maturity frombelow to up words. When the wound is aseptic the epithelium will grow in from theedges as a delicate blue pellicles, gradually it becomes thick and opaque. When the surface is covered by epithelium, the process of devascularizationbegins. The new vessels, being no more needed will gradually disappear. The scar thatis red becomes white and bloodless. 8. REVIEW OF ANTI-INFLAMMATION Drugs which can normally be used to almost every type of inflammatoryconditions are known as anti-inflammatory drugs These have two major groups. 1. Steroidal anti-inflammatory drugs in the form of gluco corticoids. 2. Non-Steroid anti-inflammatory drugs (NSAID)Mode of action of steroidal anti-inflammatory drugs 46
  60. 60. DISEASE REVIEW ACTH and Glucocorticoids prevent the clinical features of inflammation i.e.local heat, redness pain and swelling. Their action is based on reducing the increasedpermeability of capillaries and maintenance of the integrity of the cell membraneeven in the presence of toxins. Stabilization of lysosomes release from thegranulocytes by inhibiting phagocytosis. Also acts on fats phase of inflammation andinhibits capillary proliferation deposition of collagen cicatrisation. But fibrous tissueonce formed is not dissolve by corticosteroids. Hence the anti-inflammatory effect of steroidal therapy is non specific. Thesteroid inhibit the phospholipase enzyme which is essential to activate the cellmembrane. This activation release the arachidonic acid, which metabolises to produceinflammation. But once the chain is initiated it cannot be stopped by the steroidaltherapy, moreover in large doses, it may interface with wound healing.9. CLASSIFICATION OF ANTI-INFLAMMATION These are broadly classified into two groups. Narcotic Analgesics or opoidanalgesics and Non-narcotic analgesics or non opoid analgesic or NSAID, nonsteroidal anti-inflammatory drugs.1. NARCOTIC ANALGESICS: These agents are capable of relieving severe degree of pain but are moderatelyor strongly addicting. This group includes opoids which binds to the opoid receptors.These, further classified in to Natural opium alkaloids ( e.g. Morphin)., Semi-synthetic opiums (e.g. Diacetyle morphin or acetyle morphin) and Synthetic opoid(e.g. Pethedine).2. NON-NARCOTIC ANALGESICS OR NON OPOID ANALGESIC orNSAID: 47
  61. 61. DISEASE REVIEW In this the agents relieve mild to moderate degrees of pain and are consideredas non active. This group includes aspirin analgesic and other analgesics andantipyretic drugs and these have no affinity for the opoid receptors, but the site ofaction is only peripheral and further NSAID is divided in to Potent anti-inflammatoryand good analgesics, Potent anti-inflammatory and good analgesics, Moderate anti-inflammatory and moderate analgesics and Poor anti-inflammatory and goodanalgesics.A. POTENT ANTI-INFLAMMATORY AND GOOD ANALGESICS: i. Salcylates e.g. Aspirin 2. Oxy cum derivatives e.g. Paraoxicam.B. POTENT ANTI-INFLAMMATORY AND GOOD ANALGESICS: i. Pyrazolin derivatives e.g. Phenyl butazone. ii. In dol derivatives e.g. Indomethacin.3. MODERATE ANTI-INFLAMMATORY AND MODERATEANALGESICS: i. Propyonic acid derivatives e.g. Ibuprofen ii. Anthranlic derivatives e.g. Mefenamic acid. iii. Aryl acetic derivatives e.g. Diclofenac.4. POOR ANTI-INFLAMMATORY AND GOOD ANALGESICS: i. Para amono phenyl derivatives e.g. Paracetamol or acetaminoidene. ii. Pyrozolon derivatives e. g. Metamezole.10. MANAGEMENT OF INFLAMMATION AND ACTION OF NON- STEROIDAL ANTI INFLAMMATORY DRUGS (NSAID) 48
  62. 62. DISEASE REVIEW As stated earlier, the activation of cell membrane releases arachidonic acid, itis metabolized by cyclo-oxygenase pathway and produce prostaglandins (PGs).Theseinclude PGG2, PGH2, PGl2, PHE2 and PGE2 and cause vasodilatation and potentiateoedema. Some of these are supported to inhibit platelet aggregation. These further sensitize the chemical receptors of the afferent pain endings toother chemical mediators like bradykinin and histamine. Aspirin and asperin likeNSAID have been shown to inhibit release or synthesis of PG5 and thus producebeneficial anti-inflammatory condition where PGs are synthesized locally. It is unableto produce any analgesic effect where the sensory nerves are directly stimulated. Some of the NSAID produce anti-inflammatory effect indirectly,likeindomethacin. It inhibits phosphodiesterase and thus increases the intracellularconcentration of cyclic ATP, Cyclic ATP has been shown to stabilize membraneincluding lysosomal membrane in polymorphonuclear leukocytes. This prevent therelease of enzymes important in the inflammatory responses. Some drugs may inhibitthe activation of T-lymphocytes which release lymphokinase, which plays animportant role in mediating inflammation. 9. REVIEW ON SHOTA Nidana mean the causative factors which lead to the disease. nidanaparivarjana is the first line of treatment. According to different classics the nidanas ofshota can be classified as follows: 1. Ahara sambhandhi 2. Vihara sambhandhi 3. Anya.1. Ahara sambhandhi: Abhakta, Gunaheena Bhojana sevana by krisha and durbala person, kshara, Amla teekshana ushna, Guru padartha Adhika 49
  63. 63. DISEASE REVIEW sevana,Dadhi, Apakwa Bhojana, Mrittikia, Shaka, Viruddha Bhojana, Dushta Bhojana, Gara Visha.2. Vihara sambhandhi: Nishkriyata, Ashodhita,3. Anya: Marmopaghata, Vishama Prasooti,POORVAROOPA Daha, Engorged Veins, Anga gourava.ROOPA Roopas are those which are well manifested by which diseases are diagnosed.The samanya laxana of shota are as fallows-Sagourava • Anavashtitatwa • UshnataUtsedha Wherever there is utseda it is considered as shota.NIDANA • Siratanutwa • Saloma harsha • VivarnataBHEDA All the shothas are of single type but according to hetu vishesha they are againdivided in to different types. Charaka in his chikista sthana has mentioned seven types of shotha. They areas fallows:1. Vataja2. Pittaja3. Kaphaja 50
  64. 64. DISEASE REVIEW4. Dwandaja5. Sannipataja6. Abhigataja7. Vishaja. Where as Susruta has mentioned only five types of shotha, they are as follows:1. Vataja2. Pittaja3. Kaphaja4. Sannipataja5. Vishaja. Vagbhata in his Nidana sthana has mentioned Seven types of shotha1. Vataja2. Pittaja3. Kaphaja4. Dwandaja5. Sannipataja6. Abhigataja7. Vishaja. Where as in Madhava nidana we get again seven types of shotha1. Vataja2. Pittaja3. Kaphaja4. Dwandaja5. Sannipataja6. Abhigataja7. Vishaja. 51

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