PRESENTING BY
DIVYANGNA B. PATEL
B.A.M.S
2nd PG SCHOLAR,DEPT. OF KAYA CHIKITSA
GOVT. AKHANDANAND AYURVED COLLEGE, AHMEDABAD.
GUIDED BY
DR. SURENDRA A. SONI
M.D, PhD
PROF. & HEAD, PG DEPT. OF KAYA CHIKITSA
GOVT. AKHANDANAND AYURVED COLLEGE, AHMEDABAD, GUJARAT, INDIA.
INDEX TOPIC NAME:
1.INTRODUCTION 12.EPITHELIAL DYSPLASIA
2.DEFINATION 13.NEOPLASIA
3.PREVALANCE 14.MANAGEMENT
4.CAUSATIVE FACTOR 15.AYURVEDIC CONCEPT
5.SIGN AND SYMTOMS 16.AYURVEDIC PHYSIOLOGICAL
ASPECT
6.PATHOPHYSIOLOGY 17.ASSOSIATED DISEASE ACCORDING
TO AYURVEDA
7.DIAGNOSIS 18. INVOLVEMENT OF RASADI SAPTA
DHATU IN AMLAPITTA
8.EARLY DIAGNOSIS 19.UNDERSTANDING THE PROGRESS
OF AMLAPITTA AS BASED ON
SHADVIDHA KRIYA KALA.
9.METAPLASIA 20.SAMPRAPTI GHATAK
10.HYPERPLASIA 21.CHIKITSA SUTRA
11.DYSPLASIA 22.PATHYA-APATHYA, CONCLUSION
A CONDITION IS NAMED AFTER
SURGEON “NORMAN BARRETT”.
 THIS CONDITON IS GENERALLY
DISCRIBED BY “PHILIP
RAWLANDALLISON” IN 1946.
IT IS ALSO CALLED AS BARRETT‘S
OESOPHAGUS AND “COLUMNAR
EPHITHELIUM LINED LOWER
OESOPHAGUS”(CELLO).
INTRODUCTION:
DEFINATION:
 DAMAGE (DYSPLASIA) TO THE LOWER
PORTION OF THE OESOPHAGUS THAT
CONNECTS THE MOUTH AND
STOMACH.
 IT IS THE RESULT OF REPEATED
EXPOSURE OF STOMACH ACID AND
ALSO RESULT OF “GERD” (GASTRO
ESOPHAGEAL REFLUX DIESASE).
SYNONYMS: ALLISON-JOHNSTONE
ANOMALY.
ONLY 10% -15% CHANCE IN GERD WILL
DEVELOPE “BARRETT SYNDROME”.
BARRETT SYNDROME IS A SERIOUS
COMPLICATION OF GERD.
IT INCREASE THE RISK OF DEVELOPING
OESOPHAGEAL ADENOCARCINOMA WHICH IS
SEVERE POTENTIALLY FATAL CANCER OF
ESOPHAGUS.
IF BARRETT OESOPHAGUS TURN INTO CANCER IT
WILL TAKES SEVERAL YEARS.
IN “LOW RISK” CASES BARRETT OESOPHAGUS
TISSUE WILL TAKE 2 TO 8 WEEKS FOR HEAL.
PREVELANCE:
CAUSATIVE FACTORS:
LONG STANDING “GERD”.
NO MORE HARDWORK.
OBESITY (FAT AROUND ABDOMEN
MAY INCREASE
POSSIBILITY)
SPICY FOOD, IRREGULAR FOOD
HABITS.
EXCESSIVE SMOKING.
INDIGESTION
SIGN AND SYMPTOMS:
HEMATEMESIS: DUE TO GASTRIC
REFLUX.
WEIGHT LOSS: INDIGESTION
DYSPHAGIA: DUE TO GERD,
INFLAMMATION IN OESOPHAGUS.
HEART BURN: DUE TO GASRIC REFLUX.
PAIN IN STOMACH WHERE
OESOPHAGUS MEETS
STOMACH
 IT MAY BE INCREASE THE RISK OF
CENTRAL OBESITY.
PATHOPHYSIOLOGY:
 IT’S CHRONIC INFLAMMATION.
 IN THIS DISEASE STOMACH ACID, BILE, SMALL INTESTINE,
PANCREATIC CONTENTS DAMAGE THE CELL OF LOWER
OESOPHAGUS.
 WHEN CHRONIC OR LONG TERM REFLUX OF STOMACH
CONTAIN UP INTO OESOPHAGUS DAMAGE THE NORMAL INNER
LINING OF OESOPHAGUS.THIS PROCESS TAKES MANY YEARS.
 CELLULAR & DNA DAMAGE ALTERS THE DIFFERENTION
POTENTIAL OF PROLIFERATING EPITHELIAL CELLS.
 REASERCHERS ARE UNABLE TO PREDICT WHY HEART BURN
DEVELOPE IN BARRETT’S OESOPHAGUS.
 SOMETIMES SOME PEOPLE HAVE NO SYMTOMS OF HEART
BURN IN BARRETT’S OESOPHAGUS.
 IT’S PRINCIPLE OF CHRONIC INFLAMMATION IN “GERD”.
ESOPHAGEAL CANCER PROGRESSION:
DIAGNOSIS:
 ENDOSCOPY (ESOPHAGOGASTRODEODENOSCOPY) IN WHICH FIBRE
OPTIC INSERTED IN MOUTH AND EXAMINE THE OESOPHAGUS,
STOMACH, DEODENUM.
 BIOSCOPY
 BOTH MACROSCOPIC AND MICROSCOPIC EXAMINATION.
 COLUMNER EPITHALIAL CELL REPLACE THE NORMAL SQUAMOUS
EPITHALIAL CELL(METAPLASIA).
 THEY INCREASE THE RISK OF ADENOCARCINOMA.
 THE CELL OF BARRETT SYNDROME ARE CLASSIFIED IN 4 TYPES:
(1) NON DYSPLASTIC-CANCER CELL PRESENT, NO ABILITY
TO SPREAD.
(2)LOW GRADE DYSPLASIA-VERY EARLY FORM OF PRE CANCER
OF OESOPHAGUS. CELL LOOKS LIKE ABNORMAL CELL BUT NO
TO SPREAD.
(3)HIGH GRADE DYSPLASIA-PRE CANCEROUS CHANGE IN
OESOPHAGEAL CELL. LOOKS LIKE INTESTINAL CELL. ABNORMAL
CELL.
(4)FRANK CARCINOMA- SEVERE DYSPLASIA.
 IN WESTERN COUNTRIES THEY
OESOPHAGECTOMY AS FIRST LINE OF TREAMENT
FOR “HGD”(HIGH GRADE DYSPLASIA) AND
ADENOCARCINOMA BUT HAS LOW SUCCESS
RATE.
 ENDOSCOPIC TREATMENT IS SUGGESE IF
PATIENT IS UNFIT FOR SURGERY.
 ENDOSCOPY IS MORE EFFECTIVE AND LESS
EXPANSIVE THAN SURGICAL TREATMENT.
 AFTER ALL IT’S ALL DEPENT UPON DOCTOR
AND RATE OF SEVEARITY.
DIAGNOSIS:
EARLY DIAGNOSIS ? :
 IN THIS CONDITION 30 TO 50 FOLDS INCREASE THE
RISK OF ADENOCARCINOMA.
 SURVIVAL RATE OF OESOPHAGEAL CANCER IS ONLY
9%.
 70% PEOPLE DON’T PRESENT UNTIL THE DISEASE IS
STAGE III OR HIGHER.
 B.O. IS IMPORTANT FACTOR FOR OESOPHAGEAL
CANCER. STAGE OF CANCER SURVIVAL RATE
I 80%
II 30%
III 18%
IV 4%
METAPLASIA:
 IT IS THE TRANSFORMATION OF ONE
DIFFERENTIATED CELL TYPE TO ANOTHER
DIFFERENTIATED CELL TYPE.
 IF ORIGINAL CELL ARE NOT ROBUST ENOUGH
TO WITHSTAND THEIR ENVIRONMENT,SO THEY
WILL TRANSFORM INTO ANOTHER TYPE BETTER
SUITED TO THEIR ENVIRONMENT.
 IT IS EARLY PHASE OF CARCINOGENESIS,
SPECIFICALLY THOSE WHO HAS SUSPECTIBILITY
OF CANCER.
HYPERPLASIA:
 THE ENLARGEMENT OF AN ORGAN OR TISSUE
CAUSED BY AN INCREASE IN THE
REPRODUCTION RATE OF IT’S CELLS.
 MICROSCOPICALLY CELLS RESEMBLE NORMAL
BUT INCREASED IN NUMBERS.
 SOMETIMES IT IS CONFUSED WITH BENING
NEOPLASIA OR BINIGN TUMOR.
DYSPLASIA:
 THE PRESENCE OF CELLS OF AN ABNORMAL TYPE
WITHIN A TISSUE,WHICH MAY SIGNIFY A STAGE
PRECEDING THE DEVELOPEMENT OF CANCER.
 IT IS AN ABNORMAN DEVELOPEMENT OR
EPITHELIAL ANOMALY OF GROWTH AND
DIFFERENTIATION.
EPITHELIAL DYSPLASIA:
 AFTER DIAGNOSIS OF BARRETT’S SYNDROME IT MAY BE RISK TO
PROGRESSION TO CANCER DEVELOPEMENT OF EPITHELIAL
DYSPHAGIA.
 IT’S SUM OF VARIABLE DISTURBANCE OF EPITHALIAL
PROLIFARATION AND DIFEERNTIATION AS MICROSCOPIC LEVEL.
 SQAMOUS CELL WHICH IS FOUND ON TOP LAYER OF
OESOPHAGUS WHICH LOOK LIKE FISH SCALE WHEN VIEWED IN
MICROSCOPE.AND GOBLET CELLS NORMALLY LINED INTESTINE
NOT OESOPHAGUS .
 WHEN GOBLET CELL TAKE PLACE IN OESOPHAGUS IT’S CALLED
INTESTINAL METAPLASIA.WHEN INTESTINAL METAPLASIA
REPLACES SQAMOUS MUCOSA IN OESOPHAGUS IT WILL CALLED
BARRETT OESOPHAGUS.
NEOPLASIA:
IT IS A TYPE OF ABNORMAL AND EXCEESIVE
GROWTH OF TISSUE.WHICH IS
UNCOORDINATED WITH NORMAL
SURROUNDING TISSUE AND GROWING
ABNORMALLY,EVEN IF ORIGINAL TRIGGER IS
REMOVED.
THIS ABNORMAL GROWTH USUALLY FORMS A
MASS.
MANAGEMENT:
 HIGH GRADE DYSPLASIA: SURGICAL REMOVAL OF
OESOPHAGUS.
 ENDOSCOPIC RESECTION OR REDIOFREQUENCY ABLATION.
 LASER TREATMENT IN SEVERE DYSPLASIA.
 MALIGNENANCY :SURGERY,RADIATION
THERAPY(CHEMOTHERAPY).
 ENDOSCOPIC RESECTION KNOWN AS “NISSEN
FUNDOPLICATION” CAN REDUCE THE REFLUX OF ACID FROM
STOMACH IN TO OESOPHAGUS. REMOVAL OF MUCOSA AND
SUBMUCOSA LEAVING MUSCULARIS PROPIA EXPOSED AND
MAKE CONFIRM THAT CANCEROUS TISSUE HAS MARGINS
WITHIN THE RESECTED LESION.
 THIS SURGERY IS USEFULL IN “LOW RISK” (CANCER TISSUE
LIMITED IN MUCOSAL LAYER. “ HIGHER RISK” PATIENT GIVEN
POOR RESULT.
 ON OTHER SIDE “NSAIDS” DRUGS ALSO USED IN PREVENTION.
AYURVEDIC CONCEPT:
AYURVEDIC CORRELATE:
 AMLAPITTA
 UDAVARTA
 ANNA DRAVA SHOOLA
 PAITIKA CHARDI
 VATIKA CHARDI
 AMASHAYA VATA
 UDHVAGA RAKTA PITTA
AYURVEDIC PHYSIOLOGICAL
ASPECT:
ANNA NALIKA (LOWER
PORTION) FIBROSIS
PITTA PRAKOPA AHAR
VIHAR SEVAN
(SLESHMA HANI)
PITTA URDHVA GATI
VAIGUNYA VAYU
kapha
pitta
(Madhur
avstha paka)
(Amla
avtha paka)
(katu avstha
paka)
Due to some Interruption in
Mechanisum of Avstapaka
Vat vaigunya
vayu
ASSOSIATED DISEASE ACCORDING
TO AYURVEDA:
RAS,RAKTA,
MANSA
DHATUGATAVA -
(1) RAS
(2) RAKTA
(3) MANSA
(4)MEDA
(5)ASTHI
(6)MAJJA
(7)SUKRA
FIBROTIC
CHANGES IN 3
DHATU. RAS,
RAKTA, MANSA
DUSTI IN
MUCOSA LAYER
7 DHATU INVOLVEMENT OF RASADI SAPTA DHATU IN AMLAPITTA
(MADHAV NIDAN- UTTARARDHA 51/4,5,6,8,9,10,11,12, KASHYAP SAMHITA
16/13,14,15,16,17)
RAS ARUCHI,AVIPAKA,UTKLESH,AMLODGAR,GAURAV,NINDRA,
KANDU, (HARIT,PITTA,NILA,KRISHNA, RAKTA UDAKA
VAMAN), KAPHA NISHTHIVAN, ALASYA, PRASEK, MUKH
MADHURYA, TRISHNA, HRUDPIDA.
RAKTA (HRUDA,KUKSHI,KANTHA DAHA), HASTA PADA DAHA,
SHIRASHAITHILYA.
MANSA GATRA SADA, MANSA UDAK VAMAN, DHAMNI SHAITHILYA.
MEDA SANDHI SHUNYATA
ASTHI HARDNESS OF MUSCULAR TISSUE OF OESOPHAGUS,DANTA NAKH
BHEDAN.
MAJJA SHIR SHOOLA, VIBHRAM, TAMAH DARSHAN,ASTHI SHUNYATA.
SHUKRA AMLAPITTA DHATUGATTVA(IRREVERSIBLE), ARBUDA
 DHATUGATTVA OF AMLAPITTA-DHATUDUSTI OF
3 DHATU IN ANNA NALIKA .
BARRETT’S ESOPHAGUS IS A SPECIFIC ADVANCE
CONDITION OF AMLAPITTA PRESENTATION OF
AMLAPITTA PRESENTATION WITH PROGRESSIVE
DHATUGATTVA CAN COMPARE WITH MORE NEAR
TO VATADHIK AMLAPITTA, URDHVAG AMLAPITTA.
कम्पप्रलापमूच्छॉचिममचिममगात्रावसादशूलानि।
तमसो दशॅिववभ्रमववमोहहषॉण्यनिलकोपात ्।।9।।
MADHAV NIDAN UTTARDHA-51.
SHADVIDHA KRIYA KALA DISCRIPTION IS
EXCELLENT APPROCH TO UNDERSTAND ANY G.I.T.
DISORDER PROPERLY .
(1) SANCHAY
(2) PRAKOPA
(3) PRASAR
(4) STHAN SAMSHRAYA
(5) VYKTA
(6) BHEDA. 6 STAGES ARE FOR SHADVIDHA KRIYA
KALA.
 CHARAKOKTA AMASHAYA IS MAIN SITE FOR
COUGH AND PITTA DOSHA, ANY
DISTURBANCE/IMBALANCE IN AMASHAYA MAY
INITIATE THE SHADVIDHA KRIYA KALA PATTERN
ACCUMULATION /VITIATION/PROGRESS OF
VATADI DOSHAS AS PER SHADVIDHA KRIYAKAL
PATTERN.HENCE BEING A MAIN ASHAY THAT
ACCEPTS THE FOOD INGESTED IS VERY
IMPORTANT. THIS IS THE REASON THAT SHAD
VIDHA KRIYAKALA HAS GREAT IMPORTANCE IN
UNDERSTANDING/ANALYSE ALL DISEASE
SPECIALLY G.I.T. DISEASE.
SHADVIDHA KRIYA
KALA
UNDERSTANDING THE PROGRESS OF AMLAPITTA AS
BASED ON SHADVIDHA KRIYA KALA. (SHUSHRUT
SAMHITA SUTRA STHAN 21/18,27,32,33,34)
SANCHAY PARIDAHA, OSHA –CHOSHA, AROCHAK, AVIPAKA,
ANGSADA
PRAKOPA KOSHTHA TODA, PARIDAHA, SARVATODAHA, AMLIKA,
ANNA DWESHA, HRADAYOTKLEDA.
PRASAR ATOP, ANGASADA, AVIPAKA, AROCHAKA, VAMAN,
KOSHTH TODA, SANCHARAN.
STHAN SANSHRAYA KUSHTHA, VISARPA
VYAKTA FULLY BLOWN SIGN AND SYMTOMS OF THE DISEASE
AS PER DOSHAJ DOMINANCE.
BHEDA PROGRESS OF THE DISEASE IN RASADI SAPTA DHATU
AS DISPLAYED IN TABLE NO 1.
 DOSHA: PITTA PRADHAN.
 PACHAK PITTA,
SAMAN VAYU (VRUDDHA OR AVRUTT)
 KLEDAK KAPHA KSHAYA
 DUSHYA:RASA,RAKTA,MANSA,MEDA.
 STROTAS:RAS VAHA STROTASA
RAKTA VAHA STROTASA
MANSA VAHA STROTASA
MEDA VAHA STROTASA
ANNAVAHA STROTASA.
 ADHISTHAN: AMASHAYA, ANNA NALIKA.
 STROTO DUSHTI: VIMARG GAMANA,SANG.
 SADHYA-ASADHYATA: KRUCCHA SADHYA.
 SAM NIRAM: NIRAM
 AGNI:MANDA,VISHAM
SAMPRAPTI GHATAK:
CHIKITSA SUTRA :
(1) NIDANA PARIVARJANA
(2) ANULOMAN, DIPAN, PACHAN, SNEHAN.
(3)SANSHODHANA CHIKITSA: VIRECHANA (STRANSAN)
BASTI
(4) SHAMANA CHIKITSA :SUTA SHEKHAR RAS
AVIPATTI KAR CHURNA
VASA GHREET
KAMDUDHA RASA,
TIKTA GHRUT YOGA,
TRIVRUT, TRIFALA,
MULETHI, SHATAVARI
CHURNA etc.
 VIRECHAN KARMA:
STRANSAN VIRECHAN WITH TRIFALA, TRAYMANA,
KATUKI, ROHINI, TRIVRUT.
 BASTI: NIRUH BASTI: DASHMOOLA ,RASNADI
PUNARNAVADI KWATHA.
ANUVASAN BASTI: DASHMOOL TAILA,
CHANDANBALA LAXADI TAILA.
 RASAYAN DRUG:YATIMADHU, AMLAKI
RASAYAN,GILOY
 ANULOMAN: TRIPHALA GHREETA, KUSHMANDA
GHREETA AND PREPARATIONS.
 AGNIDIPAN AND AAMPACHAN: MUNG DAAL ,
MATAR DAL LIGHT KHICHDI WITH GHREETA.
BARRETT’S OESOPHAGUS -SYMPTOMATIC MANAGEMENT
HEART BURN (HRIDA
PARIDAHA)
SUTSHEKHAR RAS 2-0-2
VASA AVLEHA 1 TSF BD.
PATOL CHUNA, NIMBA CHURNA- 3GM.
KAMDUDHA RAS-25O TO 300 MG BD.
PRAVAL PANCHAMRUTA RAS-250 MG BD.
HEMATEMESIS (RAKTA
VAMAN)
SWARNA SUTSHEKHAR RAS 125 MG BD
MUKTA PRAVAL PANCHAMRUTA RAS-250-300
MG
BOL BADDHA RAS 1-2 TAB BD.
WEIGHT LOSS (KARSHYA) KUSHMANDA RAS
SHATAVARI GHRITA- 3 TSF BD.
PANCHTIKTA KSHEERA PAKA- 1 CUP
ASWAGANDHA SIDDHA KSHEERA PAKA -1
CUP
MASOOR DAL, MATAR DAL
DYSPHAGIA (NIGIRAN
KATHINYA)
DADIMAVLEHA -2 TSF BD
UDARAMRUTA YOGA- 2 TSF
ABHAYARIST-3TSF BD.
USHIRASAV- 3 TSF BD.
BARRETT’S OESOPHAGUS - SYMPTOMATIC MANAGEMENT
PAIN IN STOMACH TRIPHALA CHURNA,AVIPATTIKAR
CHURNA-3 GM TDS,SHANKH BHASMA-
250 MG BD,PRAVAL PANCHAMRUTA RAS
-250 MG BD,KAMDHUDHA RAS-250 MG
BD, YAV KSHAR-125-500 MG BD.
THIS ALL DOSE MAY CHANGE AS PER
SEVIRITY OF DISEASE.
PATHYA-APATHYA:
PATHYA: LAJA, YAVA, MUDAGA, MADHU, NIMBA
PATOLA, DUGDHA, PATOLA, KARANJ
SHATAVARI, KUSHMANDA , GOGRITA, GODUGDHA,
MASUR DAL etc.
APATHYA: GURU, VISHTAMBHI, VIDAHI AHARA,
SHITALA PEYA, VEGA VIDHARANA,
MADHYA, TIKSHNA DRAVYA.
CONCLUSION:
 BARRETT’S OESOPHAGUS IS AN ADVANCE CHRONIC
CONDITION OF AMLAPITTA DISEASE WHERE PROGRESS OF
THE DISEASE REACHES MANSA DHATU CROSSING THE RAS
AND RAKTA DHATU AS PER THE PRINCIPLE OF
DHATUGATTVA PATTERN MENTION BY ACHARYA CHARAK.
REFLUXED PITTA FROM ADHO AMASHAY TO URDHVA
AMASHAY MAINLY CAUSES THE DAMAGE AT CARDIAC
ORIFIC OF STOMACH. MANAGEMENT IS SO SIMPLE THAT IT
CAN BE CHECKED VERY EASILY WITH ANULOMAN,
DIPAN/PACHAN(TIKTA RAS), SNEHAN, BHRIHAN ETC.
 SUCH ALL VARIOUS G.I.T. CLINICAL PRESENTATION ARE
MAINLY BASED ON DOMINANCE OF VAYU/ INDIVIDUAL
DOSHA/ INVOLVEMENT OF EITHER RASADI DHATU ETC.
THE PATHOGENESIS OF ALL ABOVE CLINICAL
PRESENTATION MAINLY TAKES PLACE IN MAHASTROTAS
HENCE DIAGNOSIS IS USUALLY CONFIRED ON THE BASIS
OF DOMINANCE SIGN AND SYMPTOMS OF DOSHA, DHATU,
MALA.
Jeerna amlapitta

Jeerna amlapitta

  • 1.
    PRESENTING BY DIVYANGNA B.PATEL B.A.M.S 2nd PG SCHOLAR,DEPT. OF KAYA CHIKITSA GOVT. AKHANDANAND AYURVED COLLEGE, AHMEDABAD. GUIDED BY DR. SURENDRA A. SONI M.D, PhD PROF. & HEAD, PG DEPT. OF KAYA CHIKITSA GOVT. AKHANDANAND AYURVED COLLEGE, AHMEDABAD, GUJARAT, INDIA.
  • 2.
    INDEX TOPIC NAME: 1.INTRODUCTION12.EPITHELIAL DYSPLASIA 2.DEFINATION 13.NEOPLASIA 3.PREVALANCE 14.MANAGEMENT 4.CAUSATIVE FACTOR 15.AYURVEDIC CONCEPT 5.SIGN AND SYMTOMS 16.AYURVEDIC PHYSIOLOGICAL ASPECT 6.PATHOPHYSIOLOGY 17.ASSOSIATED DISEASE ACCORDING TO AYURVEDA 7.DIAGNOSIS 18. INVOLVEMENT OF RASADI SAPTA DHATU IN AMLAPITTA 8.EARLY DIAGNOSIS 19.UNDERSTANDING THE PROGRESS OF AMLAPITTA AS BASED ON SHADVIDHA KRIYA KALA. 9.METAPLASIA 20.SAMPRAPTI GHATAK 10.HYPERPLASIA 21.CHIKITSA SUTRA 11.DYSPLASIA 22.PATHYA-APATHYA, CONCLUSION
  • 3.
    A CONDITION ISNAMED AFTER SURGEON “NORMAN BARRETT”.  THIS CONDITON IS GENERALLY DISCRIBED BY “PHILIP RAWLANDALLISON” IN 1946. IT IS ALSO CALLED AS BARRETT‘S OESOPHAGUS AND “COLUMNAR EPHITHELIUM LINED LOWER OESOPHAGUS”(CELLO). INTRODUCTION:
  • 4.
    DEFINATION:  DAMAGE (DYSPLASIA)TO THE LOWER PORTION OF THE OESOPHAGUS THAT CONNECTS THE MOUTH AND STOMACH.  IT IS THE RESULT OF REPEATED EXPOSURE OF STOMACH ACID AND ALSO RESULT OF “GERD” (GASTRO ESOPHAGEAL REFLUX DIESASE). SYNONYMS: ALLISON-JOHNSTONE ANOMALY.
  • 5.
    ONLY 10% -15%CHANCE IN GERD WILL DEVELOPE “BARRETT SYNDROME”. BARRETT SYNDROME IS A SERIOUS COMPLICATION OF GERD. IT INCREASE THE RISK OF DEVELOPING OESOPHAGEAL ADENOCARCINOMA WHICH IS SEVERE POTENTIALLY FATAL CANCER OF ESOPHAGUS. IF BARRETT OESOPHAGUS TURN INTO CANCER IT WILL TAKES SEVERAL YEARS. IN “LOW RISK” CASES BARRETT OESOPHAGUS TISSUE WILL TAKE 2 TO 8 WEEKS FOR HEAL. PREVELANCE:
  • 6.
    CAUSATIVE FACTORS: LONG STANDING“GERD”. NO MORE HARDWORK. OBESITY (FAT AROUND ABDOMEN MAY INCREASE POSSIBILITY) SPICY FOOD, IRREGULAR FOOD HABITS. EXCESSIVE SMOKING. INDIGESTION
  • 7.
    SIGN AND SYMPTOMS: HEMATEMESIS:DUE TO GASTRIC REFLUX. WEIGHT LOSS: INDIGESTION DYSPHAGIA: DUE TO GERD, INFLAMMATION IN OESOPHAGUS. HEART BURN: DUE TO GASRIC REFLUX. PAIN IN STOMACH WHERE OESOPHAGUS MEETS STOMACH  IT MAY BE INCREASE THE RISK OF CENTRAL OBESITY.
  • 9.
    PATHOPHYSIOLOGY:  IT’S CHRONICINFLAMMATION.  IN THIS DISEASE STOMACH ACID, BILE, SMALL INTESTINE, PANCREATIC CONTENTS DAMAGE THE CELL OF LOWER OESOPHAGUS.  WHEN CHRONIC OR LONG TERM REFLUX OF STOMACH CONTAIN UP INTO OESOPHAGUS DAMAGE THE NORMAL INNER LINING OF OESOPHAGUS.THIS PROCESS TAKES MANY YEARS.  CELLULAR & DNA DAMAGE ALTERS THE DIFFERENTION POTENTIAL OF PROLIFERATING EPITHELIAL CELLS.  REASERCHERS ARE UNABLE TO PREDICT WHY HEART BURN DEVELOPE IN BARRETT’S OESOPHAGUS.  SOMETIMES SOME PEOPLE HAVE NO SYMTOMS OF HEART BURN IN BARRETT’S OESOPHAGUS.  IT’S PRINCIPLE OF CHRONIC INFLAMMATION IN “GERD”.
  • 12.
  • 13.
    DIAGNOSIS:  ENDOSCOPY (ESOPHAGOGASTRODEODENOSCOPY)IN WHICH FIBRE OPTIC INSERTED IN MOUTH AND EXAMINE THE OESOPHAGUS, STOMACH, DEODENUM.  BIOSCOPY  BOTH MACROSCOPIC AND MICROSCOPIC EXAMINATION.  COLUMNER EPITHALIAL CELL REPLACE THE NORMAL SQUAMOUS EPITHALIAL CELL(METAPLASIA).  THEY INCREASE THE RISK OF ADENOCARCINOMA.  THE CELL OF BARRETT SYNDROME ARE CLASSIFIED IN 4 TYPES: (1) NON DYSPLASTIC-CANCER CELL PRESENT, NO ABILITY TO SPREAD. (2)LOW GRADE DYSPLASIA-VERY EARLY FORM OF PRE CANCER OF OESOPHAGUS. CELL LOOKS LIKE ABNORMAL CELL BUT NO TO SPREAD. (3)HIGH GRADE DYSPLASIA-PRE CANCEROUS CHANGE IN OESOPHAGEAL CELL. LOOKS LIKE INTESTINAL CELL. ABNORMAL CELL. (4)FRANK CARCINOMA- SEVERE DYSPLASIA.
  • 14.
     IN WESTERNCOUNTRIES THEY OESOPHAGECTOMY AS FIRST LINE OF TREAMENT FOR “HGD”(HIGH GRADE DYSPLASIA) AND ADENOCARCINOMA BUT HAS LOW SUCCESS RATE.  ENDOSCOPIC TREATMENT IS SUGGESE IF PATIENT IS UNFIT FOR SURGERY.  ENDOSCOPY IS MORE EFFECTIVE AND LESS EXPANSIVE THAN SURGICAL TREATMENT.  AFTER ALL IT’S ALL DEPENT UPON DOCTOR AND RATE OF SEVEARITY. DIAGNOSIS:
  • 16.
    EARLY DIAGNOSIS ?:  IN THIS CONDITION 30 TO 50 FOLDS INCREASE THE RISK OF ADENOCARCINOMA.  SURVIVAL RATE OF OESOPHAGEAL CANCER IS ONLY 9%.  70% PEOPLE DON’T PRESENT UNTIL THE DISEASE IS STAGE III OR HIGHER.  B.O. IS IMPORTANT FACTOR FOR OESOPHAGEAL CANCER. STAGE OF CANCER SURVIVAL RATE I 80% II 30% III 18% IV 4%
  • 17.
    METAPLASIA:  IT ISTHE TRANSFORMATION OF ONE DIFFERENTIATED CELL TYPE TO ANOTHER DIFFERENTIATED CELL TYPE.  IF ORIGINAL CELL ARE NOT ROBUST ENOUGH TO WITHSTAND THEIR ENVIRONMENT,SO THEY WILL TRANSFORM INTO ANOTHER TYPE BETTER SUITED TO THEIR ENVIRONMENT.  IT IS EARLY PHASE OF CARCINOGENESIS, SPECIFICALLY THOSE WHO HAS SUSPECTIBILITY OF CANCER.
  • 18.
    HYPERPLASIA:  THE ENLARGEMENTOF AN ORGAN OR TISSUE CAUSED BY AN INCREASE IN THE REPRODUCTION RATE OF IT’S CELLS.  MICROSCOPICALLY CELLS RESEMBLE NORMAL BUT INCREASED IN NUMBERS.  SOMETIMES IT IS CONFUSED WITH BENING NEOPLASIA OR BINIGN TUMOR.
  • 19.
    DYSPLASIA:  THE PRESENCEOF CELLS OF AN ABNORMAL TYPE WITHIN A TISSUE,WHICH MAY SIGNIFY A STAGE PRECEDING THE DEVELOPEMENT OF CANCER.  IT IS AN ABNORMAN DEVELOPEMENT OR EPITHELIAL ANOMALY OF GROWTH AND DIFFERENTIATION.
  • 20.
    EPITHELIAL DYSPLASIA:  AFTERDIAGNOSIS OF BARRETT’S SYNDROME IT MAY BE RISK TO PROGRESSION TO CANCER DEVELOPEMENT OF EPITHELIAL DYSPHAGIA.  IT’S SUM OF VARIABLE DISTURBANCE OF EPITHALIAL PROLIFARATION AND DIFEERNTIATION AS MICROSCOPIC LEVEL.  SQAMOUS CELL WHICH IS FOUND ON TOP LAYER OF OESOPHAGUS WHICH LOOK LIKE FISH SCALE WHEN VIEWED IN MICROSCOPE.AND GOBLET CELLS NORMALLY LINED INTESTINE NOT OESOPHAGUS .  WHEN GOBLET CELL TAKE PLACE IN OESOPHAGUS IT’S CALLED INTESTINAL METAPLASIA.WHEN INTESTINAL METAPLASIA REPLACES SQAMOUS MUCOSA IN OESOPHAGUS IT WILL CALLED BARRETT OESOPHAGUS.
  • 21.
    NEOPLASIA: IT IS ATYPE OF ABNORMAL AND EXCEESIVE GROWTH OF TISSUE.WHICH IS UNCOORDINATED WITH NORMAL SURROUNDING TISSUE AND GROWING ABNORMALLY,EVEN IF ORIGINAL TRIGGER IS REMOVED. THIS ABNORMAL GROWTH USUALLY FORMS A MASS.
  • 22.
    MANAGEMENT:  HIGH GRADEDYSPLASIA: SURGICAL REMOVAL OF OESOPHAGUS.  ENDOSCOPIC RESECTION OR REDIOFREQUENCY ABLATION.  LASER TREATMENT IN SEVERE DYSPLASIA.  MALIGNENANCY :SURGERY,RADIATION THERAPY(CHEMOTHERAPY).  ENDOSCOPIC RESECTION KNOWN AS “NISSEN FUNDOPLICATION” CAN REDUCE THE REFLUX OF ACID FROM STOMACH IN TO OESOPHAGUS. REMOVAL OF MUCOSA AND SUBMUCOSA LEAVING MUSCULARIS PROPIA EXPOSED AND MAKE CONFIRM THAT CANCEROUS TISSUE HAS MARGINS WITHIN THE RESECTED LESION.  THIS SURGERY IS USEFULL IN “LOW RISK” (CANCER TISSUE LIMITED IN MUCOSAL LAYER. “ HIGHER RISK” PATIENT GIVEN POOR RESULT.  ON OTHER SIDE “NSAIDS” DRUGS ALSO USED IN PREVENTION.
  • 23.
    AYURVEDIC CONCEPT: AYURVEDIC CORRELATE: AMLAPITTA  UDAVARTA  ANNA DRAVA SHOOLA  PAITIKA CHARDI  VATIKA CHARDI  AMASHAYA VATA  UDHVAGA RAKTA PITTA
  • 24.
    AYURVEDIC PHYSIOLOGICAL ASPECT: ANNA NALIKA(LOWER PORTION) FIBROSIS PITTA PRAKOPA AHAR VIHAR SEVAN (SLESHMA HANI) PITTA URDHVA GATI VAIGUNYA VAYU kapha pitta (Madhur avstha paka) (Amla avtha paka) (katu avstha paka) Due to some Interruption in Mechanisum of Avstapaka Vat vaigunya vayu
  • 25.
    ASSOSIATED DISEASE ACCORDING TOAYURVEDA: RAS,RAKTA, MANSA DHATUGATAVA - (1) RAS (2) RAKTA (3) MANSA (4)MEDA (5)ASTHI (6)MAJJA (7)SUKRA FIBROTIC CHANGES IN 3 DHATU. RAS, RAKTA, MANSA DUSTI IN MUCOSA LAYER
  • 26.
    7 DHATU INVOLVEMENTOF RASADI SAPTA DHATU IN AMLAPITTA (MADHAV NIDAN- UTTARARDHA 51/4,5,6,8,9,10,11,12, KASHYAP SAMHITA 16/13,14,15,16,17) RAS ARUCHI,AVIPAKA,UTKLESH,AMLODGAR,GAURAV,NINDRA, KANDU, (HARIT,PITTA,NILA,KRISHNA, RAKTA UDAKA VAMAN), KAPHA NISHTHIVAN, ALASYA, PRASEK, MUKH MADHURYA, TRISHNA, HRUDPIDA. RAKTA (HRUDA,KUKSHI,KANTHA DAHA), HASTA PADA DAHA, SHIRASHAITHILYA. MANSA GATRA SADA, MANSA UDAK VAMAN, DHAMNI SHAITHILYA. MEDA SANDHI SHUNYATA ASTHI HARDNESS OF MUSCULAR TISSUE OF OESOPHAGUS,DANTA NAKH BHEDAN. MAJJA SHIR SHOOLA, VIBHRAM, TAMAH DARSHAN,ASTHI SHUNYATA. SHUKRA AMLAPITTA DHATUGATTVA(IRREVERSIBLE), ARBUDA
  • 27.
     DHATUGATTVA OFAMLAPITTA-DHATUDUSTI OF 3 DHATU IN ANNA NALIKA . BARRETT’S ESOPHAGUS IS A SPECIFIC ADVANCE CONDITION OF AMLAPITTA PRESENTATION OF AMLAPITTA PRESENTATION WITH PROGRESSIVE DHATUGATTVA CAN COMPARE WITH MORE NEAR TO VATADHIK AMLAPITTA, URDHVAG AMLAPITTA. कम्पप्रलापमूच्छॉचिममचिममगात्रावसादशूलानि। तमसो दशॅिववभ्रमववमोहहषॉण्यनिलकोपात ्।।9।। MADHAV NIDAN UTTARDHA-51.
  • 28.
    SHADVIDHA KRIYA KALADISCRIPTION IS EXCELLENT APPROCH TO UNDERSTAND ANY G.I.T. DISORDER PROPERLY . (1) SANCHAY (2) PRAKOPA (3) PRASAR (4) STHAN SAMSHRAYA (5) VYKTA (6) BHEDA. 6 STAGES ARE FOR SHADVIDHA KRIYA KALA.
  • 29.
     CHARAKOKTA AMASHAYAIS MAIN SITE FOR COUGH AND PITTA DOSHA, ANY DISTURBANCE/IMBALANCE IN AMASHAYA MAY INITIATE THE SHADVIDHA KRIYA KALA PATTERN ACCUMULATION /VITIATION/PROGRESS OF VATADI DOSHAS AS PER SHADVIDHA KRIYAKAL PATTERN.HENCE BEING A MAIN ASHAY THAT ACCEPTS THE FOOD INGESTED IS VERY IMPORTANT. THIS IS THE REASON THAT SHAD VIDHA KRIYAKALA HAS GREAT IMPORTANCE IN UNDERSTANDING/ANALYSE ALL DISEASE SPECIALLY G.I.T. DISEASE.
  • 30.
    SHADVIDHA KRIYA KALA UNDERSTANDING THEPROGRESS OF AMLAPITTA AS BASED ON SHADVIDHA KRIYA KALA. (SHUSHRUT SAMHITA SUTRA STHAN 21/18,27,32,33,34) SANCHAY PARIDAHA, OSHA –CHOSHA, AROCHAK, AVIPAKA, ANGSADA PRAKOPA KOSHTHA TODA, PARIDAHA, SARVATODAHA, AMLIKA, ANNA DWESHA, HRADAYOTKLEDA. PRASAR ATOP, ANGASADA, AVIPAKA, AROCHAKA, VAMAN, KOSHTH TODA, SANCHARAN. STHAN SANSHRAYA KUSHTHA, VISARPA VYAKTA FULLY BLOWN SIGN AND SYMTOMS OF THE DISEASE AS PER DOSHAJ DOMINANCE. BHEDA PROGRESS OF THE DISEASE IN RASADI SAPTA DHATU AS DISPLAYED IN TABLE NO 1.
  • 31.
     DOSHA: PITTAPRADHAN.  PACHAK PITTA, SAMAN VAYU (VRUDDHA OR AVRUTT)  KLEDAK KAPHA KSHAYA  DUSHYA:RASA,RAKTA,MANSA,MEDA.  STROTAS:RAS VAHA STROTASA RAKTA VAHA STROTASA MANSA VAHA STROTASA MEDA VAHA STROTASA ANNAVAHA STROTASA.  ADHISTHAN: AMASHAYA, ANNA NALIKA.  STROTO DUSHTI: VIMARG GAMANA,SANG.  SADHYA-ASADHYATA: KRUCCHA SADHYA.  SAM NIRAM: NIRAM  AGNI:MANDA,VISHAM SAMPRAPTI GHATAK:
  • 32.
    CHIKITSA SUTRA : (1)NIDANA PARIVARJANA (2) ANULOMAN, DIPAN, PACHAN, SNEHAN. (3)SANSHODHANA CHIKITSA: VIRECHANA (STRANSAN) BASTI (4) SHAMANA CHIKITSA :SUTA SHEKHAR RAS AVIPATTI KAR CHURNA VASA GHREET KAMDUDHA RASA, TIKTA GHRUT YOGA, TRIVRUT, TRIFALA, MULETHI, SHATAVARI CHURNA etc.
  • 33.
     VIRECHAN KARMA: STRANSANVIRECHAN WITH TRIFALA, TRAYMANA, KATUKI, ROHINI, TRIVRUT.  BASTI: NIRUH BASTI: DASHMOOLA ,RASNADI PUNARNAVADI KWATHA. ANUVASAN BASTI: DASHMOOL TAILA, CHANDANBALA LAXADI TAILA.  RASAYAN DRUG:YATIMADHU, AMLAKI RASAYAN,GILOY  ANULOMAN: TRIPHALA GHREETA, KUSHMANDA GHREETA AND PREPARATIONS.  AGNIDIPAN AND AAMPACHAN: MUNG DAAL , MATAR DAL LIGHT KHICHDI WITH GHREETA.
  • 34.
    BARRETT’S OESOPHAGUS -SYMPTOMATICMANAGEMENT HEART BURN (HRIDA PARIDAHA) SUTSHEKHAR RAS 2-0-2 VASA AVLEHA 1 TSF BD. PATOL CHUNA, NIMBA CHURNA- 3GM. KAMDUDHA RAS-25O TO 300 MG BD. PRAVAL PANCHAMRUTA RAS-250 MG BD. HEMATEMESIS (RAKTA VAMAN) SWARNA SUTSHEKHAR RAS 125 MG BD MUKTA PRAVAL PANCHAMRUTA RAS-250-300 MG BOL BADDHA RAS 1-2 TAB BD. WEIGHT LOSS (KARSHYA) KUSHMANDA RAS SHATAVARI GHRITA- 3 TSF BD. PANCHTIKTA KSHEERA PAKA- 1 CUP ASWAGANDHA SIDDHA KSHEERA PAKA -1 CUP MASOOR DAL, MATAR DAL DYSPHAGIA (NIGIRAN KATHINYA) DADIMAVLEHA -2 TSF BD UDARAMRUTA YOGA- 2 TSF ABHAYARIST-3TSF BD. USHIRASAV- 3 TSF BD.
  • 35.
    BARRETT’S OESOPHAGUS -SYMPTOMATIC MANAGEMENT PAIN IN STOMACH TRIPHALA CHURNA,AVIPATTIKAR CHURNA-3 GM TDS,SHANKH BHASMA- 250 MG BD,PRAVAL PANCHAMRUTA RAS -250 MG BD,KAMDHUDHA RAS-250 MG BD, YAV KSHAR-125-500 MG BD. THIS ALL DOSE MAY CHANGE AS PER SEVIRITY OF DISEASE.
  • 36.
    PATHYA-APATHYA: PATHYA: LAJA, YAVA,MUDAGA, MADHU, NIMBA PATOLA, DUGDHA, PATOLA, KARANJ SHATAVARI, KUSHMANDA , GOGRITA, GODUGDHA, MASUR DAL etc. APATHYA: GURU, VISHTAMBHI, VIDAHI AHARA, SHITALA PEYA, VEGA VIDHARANA, MADHYA, TIKSHNA DRAVYA.
  • 37.
    CONCLUSION:  BARRETT’S OESOPHAGUSIS AN ADVANCE CHRONIC CONDITION OF AMLAPITTA DISEASE WHERE PROGRESS OF THE DISEASE REACHES MANSA DHATU CROSSING THE RAS AND RAKTA DHATU AS PER THE PRINCIPLE OF DHATUGATTVA PATTERN MENTION BY ACHARYA CHARAK. REFLUXED PITTA FROM ADHO AMASHAY TO URDHVA AMASHAY MAINLY CAUSES THE DAMAGE AT CARDIAC ORIFIC OF STOMACH. MANAGEMENT IS SO SIMPLE THAT IT CAN BE CHECKED VERY EASILY WITH ANULOMAN, DIPAN/PACHAN(TIKTA RAS), SNEHAN, BHRIHAN ETC.  SUCH ALL VARIOUS G.I.T. CLINICAL PRESENTATION ARE MAINLY BASED ON DOMINANCE OF VAYU/ INDIVIDUAL DOSHA/ INVOLVEMENT OF EITHER RASADI DHATU ETC. THE PATHOGENESIS OF ALL ABOVE CLINICAL PRESENTATION MAINLY TAKES PLACE IN MAHASTROTAS HENCE DIAGNOSIS IS USUALLY CONFIRED ON THE BASIS OF DOMINANCE SIGN AND SYMPTOMS OF DOSHA, DHATU, MALA.