RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES,



Rajiv Gandhi University of Health Sciences,

Bangalore, Karnataka Proforma for registration of subjects for dissertation

|1. |NAME OF CANDIDATE AND ADDRESS |DR.ASHWINI.M.C. |

| |(IN BOLD LETTERS) |DR.B.R. AMBEDKAR MEDICAL COLLEGE, |

| | |K.G.HALLI |

| | |BANGALORE-560045 |

|2. |NAME OF INSTITUTION |DR.B.R.AMBEDKAR MEDICAL COLLEGE, |

| | |K.G.HALLI, |

| | |BANGALORE 560045 |

|3. |COURSE OF STUDY,SUBJECT AND DURATION |M.D. PATHOLOGY |

| | |3 YEARS |

|4. |DATE OF ADMISSION TO COURSE |31-5-2012 |

|5. |TITLE OF TOPIC |HISTOMORPHOLOGICAL STUDY OF DISEASES OF THE GALL BLADDER. |

|6. |BRIEF RESUME OF THE INTENDED WORK |6.1 NEED OF THE STUDY ANNEXURE I |

| | |6.2 REVIEW OF LITERATURE ANNEXURE II |

| | |6.3 AIMS AND OBJECTIVES ANNEXURE III |

|7. |MATERIALS & METHOD |7.1 SOURCE OF DATA ANNEXURE IV |

| | |7.2 METHOD OF COLLECTION ANNEXURE V |

| | |7.3 STAINING TECHNIQUES ANNEXURE VI |

|8. |ETHICAL COMMITTEE CLEARANCE |8 ANNEXURE VII |

|9. |BIBLIOGRAPHY |9 ANNEXURE VIII |

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| | |10. |

| | |SIGNATURE OF CANDIDATE |

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| | |11. |

| | |REMARKS OF GUIDE |

| | |SATISFACTORY |

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| | |12.1. |

| | |NAME AND DESIGNATION OF THE GUIDE |

| | |DR. B.N. SWARNA GOWRI |

| | |ASSOCIATE PROFESSOR |

| | |DEPARTMENT OF PATHOLOGY |

| | |DR.B.R AMBEDKAR MEDICAL COLLEGE, BANGALORE -560045 |

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| | |12.2. |

| | |SIGNATURE |

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| | |12.3. |

| | |HEAD OF DEPARTMENT |

| | |DR. MANJUNATHA Y.A |

| | |PROFESSOR AND HEAD OF DEPARTMENT |

| | |PATHOLOGY, |

| | |DR.B.R AMBEDKAR MEDICAL COLLEGE, BANGALORE-560045 |

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| | |12.4. |

| | |SIGNATURE |

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| | |12.5. |

| | |REMARKS AND SIGNATURE OF PRINCIPAL |

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ANNEXURE I

BRIEF RESUME OF THE INTENDED WORK.

6.1 NEED OF THE STUDY :-

Disorders of the biliary tract affect a significant portion of the world's population. Over 95% of biliary tract disease is attributable to cholelithiasis (gallstones). In the United States, gallstones affect 20 million people, and more than 700,000 cholecystectomies are performed annually at a cost of approximately $6 billion.

Gallstones are the commonest biliary pathology. Interest in the formation and clinical management of gall stone disease dates back to ancient times of the Egyptian civilization. The development and worldwide application of laproscopic cholecystectomy and the current changes in lifestyles of individuals pertaining to indulgement in unhealthy fat rich food, lack of exercise, obesity, sedentary lifestyles and various other factors have once again focused our attention to gall stones and diseases of the gall bladder. Awareness must be reinforced in this aspect.

Gallstones afflict 10% to 20% of adult populations in developed countries. The vast majority of gallstones (>80%) are “silent” and most individuals remain free of biliary pain or other complications for decades but these stones can also lead to various complications associated with cholecystitis and can cause significant morbidity and mortality . It is important to review and revise the factors, pathophysiology and histomorphological changes associated with disorders of the gall bladder in order to determine the incidence, prevalence, distribution, association with new risk factors and pathogenesis of the disease as well as the histomorphological features. This study is directed with these objectives.

ANNEXURE II

6.2 REVIEW OF LITERATURE:

While often underappreciated, the gall bladder maybe affected by a variety of pathological processes that have specific clinical correlates1. Inflammatory disease is by far the most common pathology of the gall bladder2. Usual stone associated cholecystitis has only mild inflammation but variants of cholecystitis may have abundant xanthoma cells, eosinophils or lymphocytes and plasma cells1.

CHOLELITHIASIS:-

Gall stone disease affects 10 to 15% of the western population with an annual incidence of 1 in 2003, and an overall prevalence of 3.2%4. Prevalence increases with age from 21 years to 80 years3. Indian studies have revealed a prevalence of 6.12% being more common in women (9.6%) than men (3.1%) with only 1 to 4% becoming symptomatic every year3.

Gallstones are hard, pebble like deposits varying in their composition with majority being cholesterol and remaining mixed and pigmented stones4. The gall bladder mucus plays a regulatory role in cholelithiasis as it promotes nucleation of stones5. Mucin, calcium and lipids act in concert to form gall stones5. Bile stasis is the prime factor for gall stone formation and major causative agent for stasis is gall bladder dyskinesia6. Stones form when there is an imbalance or change in the composition of bile4. Epithelium of the gall bladder is exposed to high concentrations of potentially harmful exogenous and endogenous compounds excreted into primary bile6.

Increased levels of estrogen may increase cholesterol levels in bile4. Post menopausal women on OCPs and women with increased number of pregnancies have increased risk of developing gall stones4. Fat, fertile female of forty is at risk of cholelithiasis7. In India 97% of the cases of cholelithiasis were found in non vegetarians the cause probably due to consumption of high protein and fat, obesity is also an important risk factor for gall stone formation4.

Light microscopic features include disrupted epithelium with discontinuous and irregular surface and vacuolated cytoplasm, the surface irregularity being due to interruption of the brush border showing a strong PAS positive reaction with abundance of mucus cells in the epithelium6. There is quantitative increase in the epithelial mucus production in the period before stone formation and PAS and alcian blue double stain help to evaluate the intraepithelial mucin content6.

Cholelithiasis produces diverse changes in the gall bladder mucosa namely acute inflammation, chronic inflammation, granulomatous inflammation, cholesterolosis and glandular hyperplasia6.

ACUTE AND CHRONIC CHOLECYSTITIS:-

Cholecystitis is defined as inflammation of the gall bladder that occurs mostly commonly because of an obstruction of the cystic duct from cholelithiasis7.

Acute cholecystits is acute inflammation of the gall bladder with gall stones being present in 90% of the cases8. Other causes include ischemia, chemicals entering biliary secretions, motility disorders associated with drugs, infestation with parasites and microorganisms, collagen diseases and allergic reactions9. Obstruction to the gall bladder drainage causes increase in intra luminal pressure, gall bladder distension and wall edema which may progress to venous and lymphatic obstruction, ischemia and necrosis8. Bile is sterile in early stages and infection is believed to be a secondary event mainly by E.coli, Klebsiella and Enterococcus and Salmonella typhi8.

Inflammation of the gall bladder without evidence of calculi or sludge is termed acute acalculous cholecystitis and it comprises 2 to 15% of all acute cholecystitis cases10. It is reported to be common in the 6th decade of life and is traditionally known to occur in critically ill patients, following cardiac or abdominovascular surgery, severe trauma, burns and in prolonged fasting and sepsis, complicated diabetes mellitus and auto immune diseases with hypertension being a comorbid condition10. Most patients have haemodynamic instability and associated atherosclerotic disease8. Post traumatic acute cholecystitis is an often unrecognized and potentially fatal complication seen in patients hospitalized for trauma11.

Chronic cholecystitis is more a morphological rather than a clinical entity and it is unclear as to the exact time frame of its evolution12. It maybe a sequel to repeated bouts of mild to severe cholecystitis but in many instances it develops in the apparent absence of antecedent attacks13.

Both acute and chronic cholecystitis gall bladder walls are thickened, acute one with mural edema and hypervascularity and the chronic one with fibrosis, coarse mucosal folds, muscular hyperplasia and Rokitansky-Aschoff sinuses12. In acute cholecystits the serosal covering is frequently layered by fibrin and in severe cases by definite suppurative, coagulated exudates13. When the contained exudate is virtually pus, the condition is termed empyema of the gall bladder13. Neither has infiltration of polymorphonucleocytes as a necessary significant finding as their presence denotes at least three days into injury12. Both acute and chronic cholecystitis may or may not have bacterial infection involved12. The degree of inflammatory reaction is quite variable in chronic cases ranging from scattered lymphocytes, plasma cells and macrophages to monocellular infiltrated fibrous tissue subepithelially and subserosally12. Acute exacerbation of a previously chronically injured gall bladder may have evidence of all changes12.

XANTHOGRANULOMATOUS CHOLECYSTITIS:-

It is an uncommon variant of chronic cholecystitis14, characterized by focal or diffuse destructive inflammation with varying proportion of fibrous tissue, acute on chronic inflammatory cells and accumulation of lipid laden macrophages15. Ulceration of gall bladder mucosa and rupture of Rokitansky-Aschoff sinuses with extravasation of bile is the initiating effect and intramural extravasation of bile and mucin causes histiocytes to phagocytose cholesterol and other lipids resulting in lesions of greyish yellow nodules or streaks in the gall bladder wall15. Xanthogranulomatous cholecystitis exists in a small but significant proportion of routine cholecystectomy specimens16. USG or CT scans do not have characteristic findings for xanthogranulomatous cholecystitis and the intra operative and post operative morbidity rates are high15.

EOSINOPHILIC CHOLECYSTITIS:-

This is a rare entity with cellular infiltrate comprising of 90% eosinophils17. When the infiltrate comprises 50 to 75% eosinophils along with other inflammatory cells it is termed lymphoeosinophilic infiltrate17. Etiology is obscure and is associated with rupture of hepatic hydatid cyst into bile ducts, Clonorchis sinensis and Ascariasis infection of the biliary tree and in association with systemic hyper eosiniophilic syndromes17.

In case of a chronically inflamed gall bladder, the epithelium maybe relatively normal or atrophic or show metaplastic changes18. Metaplasia of the antral and intestinal variety is frequently seen in gall bladder containing stones19.

The metaplasia can be of goblet cell ( intestinal ) or pyloric ( antral ) cell type, the former being accompanied by the appearance of Paneth cells and endocrine cells18. In contrast to the normal glands in the gall bladder neck, the cells of metaplastic glands contain non sulfated acid mucin and neutral mucin but little sulfated acid mucin18.

The features of pyloric gland metaplasia in the gall bladder epithelium were studied by histochemical staining for mucin and the immunoperoxidase method for pepsinogens (Pg) I and II 20. It was found that all the pyloric gland metaplastic cells contained class III mucin 20. Pyloric gland metaplasia was classified into complete and incomplete types20. The complete type of pyloric gland metaplasia contained neutral mucins and weak Pg I and strong Pg II activities like normal pyloric glands20. The incomplete type of pyloric gland metaplasia contained acid mucin and was further divided into 2 types, an incomplete type I which had Pg II but no Pg I activity and an incomplete type 2 which had no Pg I or II activity20.

There is high incidence of aberrant mucin expression in both intestinal metaplasia and carcinoma of the gall bladder supporting the assumption that intestinal metaplasia of the gall bladder may predispose to gall bladder21.

The frequency and severity of metaplasia is found to increase in with age and is commonly found in patients above 40 years of age19. It is widely accepted that metaplastic epithelium is more susceptible to malignant transformation than normal epithelium19.

CLINICAL FEATURES AND DIAGNOSIS :-

Acute cholecystitis mainly presents with pain in the right upper quadrant which is usually a constant severe pain and radiates to the back or tip of the right shoulder7. Chronic cholecystitis manifests with non specific symptoms like nausea, vague abdominal pain, belching and diarrhea7.

Ultrasound is the modality with maximum specificity and sensitivity for diagnosing symptomatic as well as asymptomatic gall bladder disease, reported accuracy is 90 to 98%22. Ultrasound has high availability, portability, low cost and is quick8. CT scan however has been mentioned as the first line in diagnosis work up of a patient with acute pain abdomen which may turn out to be symptomatic gall bladder disease22.

Uncomplicated cholecystitis has an excellent prognosis with a very low mortality rate but once complications like perforation, gangrene develop the prognosis become less favourable7. Patients with acalculous cholecystitis have a mortality ranging from 10 to 50% which far exceeds the expected 4% mortality observed in patients with calculous cholecystitis7. In patients who are critically ill with calculous cholecystitis and perforation of gangrene, mortality can be as high as 50 to 60%7.

Cholecystitis is a surgically managed disease most often treated by laproscopic cholecystectomy, this is necessary to avoid complications associated with the natural course of cholecystitis and its pathologic end points12.In all cases of cholecystectomy for gall stone disease, the gall bladder should be opened and examined in detail for macroscopic abnormalities, histopathology maybe selectively recommended for those specimens with visible macroscopic abnormalities3.

ANNEXURE III

6.3 OBJECTIVES OF THE STUDY:-

▪ To determine the risk factors associated with cholelithiasis and acute and chronic cholecystitis in patients for whom cholecystectomy has been carried out.

▪ To evaluate the percentage of cholelithiasis, acute & chronic cholecystitis, and cholesterolosis in cholecystectomy specimens.

▪ To study the histomorphological lesions associated with cholelithiasis, acute & chronic cholecystitis, and cholesterolosis in cholecystectomy specimens using H& E staining for studying the general histology, periodic acid-Schiff’s reaction (PAS) and Alcian blue for the demonstration of the intra-epithelial mucin content.

MATERIALS, METHODS AND DESIGN:-

ANNEXURE IV

7.1 SOURCE OF DATA:

• All cases of cholecystectomy form the material source.

• This is a prospective and retrospective study and will be carried out in the Department of Pathology at Dr. B.R. Ambedkar Medical College and Hospital, Bangalore .

INCLUSION CRITERIA:-

▪ Male and female patients of any age group.

▪ Patients with family history of cholecystitis.

EXCLUSION CRITERIA:-

• Autolysed Specimens.

SAMPLE VOLUME:-

Minimum of 100 cholecystectomy specimens collected from June 2012 to June 2014 from Dr. B.R.Ambedkar Medical College and Hospital are included.

METHOD:-

Appropriate statistical methods for evaluation will be utilized.

STUDY SAMPLE DESIGN:-

Prospective and retrospective study.

ANNEXURE V

7.2 METHOD OF COLLECTION :-

The specimens are collected in 10% formalin following scrutinizing the patient details and identity. The specimens of cholecystectomy are fixed in fresh formalin for 24 hours. Gross description of all the specimens is done. Sections are taken from the fundus, body and neck of the gall bladder, additional sections are taken from abnormal appearing mucosa.

This is followed by processing with routine histological techniques for paraffin embedding and sectioning at 4 micron thickness. The tissue sections are placed on a slide warmer for deparaffinisation and further deparaffinisation using xylene followed by Hematoxylin and Eosin and PAS and Alcian blue stain as enumerated below.

Morphological changes in all cases will be studied with special reference to degree of inflammatory reaction characterized by plasma cells, macrophages and lymphocytic infiltration in the mucosa and subserosal tissue, presence of Rokitansky- Aschoff sinuses and focal accumulation of cholesterol laden macrophages in the lamina propria and metaplastic glands containing non sulphated acid mucin and neutral mucin but little sulphated acid mucin.

ANNEXURE VI

7.3 STAINING TECHNIQUES :-

HEMATOXYLIN and EOSIN Procedure:-

1. Dewax sections, hydrate through graded alcohol to water.

2. Remove fixation pigments.

3. Stain in alum haematoxylin for 5 minutes.

4. Wash in running tap water until sections blue for 5 minutes or less.

5. Differentiate in 1%acid alcohol for 5-10 seconds.

6. Wash well in tap water until sections are again blue.

7. Blue by dipping in an alkaline solution (ammonia water) followed by a 5 min tap water wash.

8. Counter stain in 1% eosin Y for 30 seconds to 1 minute.

9. Dehydrate, clear and mount in DPX.

Results :-

Nucleus ( basophilic or blue.

Cytoplasm ( eosinophilic or pink.

P.A.S procedure :-

1. Bring sections to water.

2. Oxidize for 5 – 10 minutes in 1% aqueous periodic acid.

3. Wash in running water for 5 minutes and rinse in distilled water.

4. Treat with Schiff reagent for 10 – 30 minutes.

5. Wash for 10 minutes in running water.

6. Counter stain with haematoxylin.

7. Dehydrate, clear and mount in D.P.X or H.S.R.

Results :-

P.A.S positive substances ( bright red

Nuclei ( blue

Other tissue constituents ( yellow.

STANDARD ALCIAN BLUE METHOD procedure :-

(pH2.5) FOR ACID GROUPS :-

1. Bring sections to water

2. Stain in freshly filtered 1% Alcian blue 8 GX in 3% acetic acid (pH2.5) for 30 minutes.

3. Wash in water.

4. Dehydrate and mount.

5. Results:-

Acid polysaccharides ( deep blue

( nuclei may stain faint blue ).

(pH 1.0) FOR SULPHATE GROUPS :-

1. Bring sections to water.

2. Stain in 1% Alcian blue 8 GX in 0.1 N hydrochloric acid for 30 minutes. Rinse briefly in 0.1 N Hcl.

3. Blot dry with fine filter paper to prevent the staining which sometimes occurs after dilution with water in washing.

4. Dehydrate in alcohol, clear in xylol and mount.

Results :- Sulphated muco substances stain blue.

ANNEXURE VII

8. ETHICAL COMMITTEE CLEARANCE :-

Has ethical committee clearance been obtained for your study? ( Yes / No ) :- Yes.

ANNEXURE VII

9. BIBLIOGRAPHY :-

1. Hansel DE, Maitra A, Argani P. Pathology of the gall bladder a Concise Review. Current Diagnostic Pathology. 2004 Aug; 10 (4): 304-317.

2. Barcia JJ. Histological analysis of Chronic Inflammatory pattern in the gall bladder: Diagnostic Criteria for reporting Cholecystitis. J Ann diagnostic pathology. 2003 June; 7(3): 147-53.

3. Mittal R, Jesudason MR, Nayak S. Selective Histopathology in Cholecystectomy for gallstone disease. Indian J Gastroenterol. 2010 (Jan-Feb); 29(1):32-36.

4. ThamilSelvi R, Sinha P, Subramaniam PM, Konapu PG, Prabha CV. A Clinicopathological study of Cholecystitis with special reference to Analysis of Cholelithiasis. International Journal of Basic Medical Science. 2011 July; 2 (2).

5. Baidya R, Sigdel B, Baidya Nl. Histopathological Changes in gallbladder mucosa associated with Cholelithiasis. Journal of Pathology of Nepal. 2010; 2: 224-225.

6. Zaki M, Al-Refeidi A. Histological changes in the Human Gallbladder Epithelium associated with gallstones. Oman Medical Journal. 2009 Oct; 24( 4).

7. Abro AH, Haider IH, Ahmad S. Helicobacter pylori Infection in patients with Calcular Cholecystitis : A Hospital Based Study. Journal Ayub Med Coll Abbottabad. 2011; 23(1).

8. Yusoff IF, Barkun JS, Barkun AN. Diagnosis and Management of Cholecystitis and cholangitis. J Gastroenterol Clinic N Am. 32(2003) 1145-1168.

9. Kimura Y, Tahada T et al. Definitions, Pathophysiology and Epidemiology of Acute Cholangitis and Cholecystitis : Tokyo guidelines. J. Hepatobiliary Pancreatic Surgery. 2007; 14(1): 15-26.

10. Ganapathi IS, .Diddapur RK. Acute Acalculous Cholecystitis : Challenging the Myths. Journal of HepatoPancreatoBiliary Association (Oxford). 2007; 9(2): 131-134.

11. Ohada Y, Tanabe R, Mukaida M. Post Traumatic Acute Cholecystitis, Am J Forensic Medicine Pathology. 1987 June; 8(2): 164-8.

12. Christina A, Del Pin, Arthur KS, Honig C, Silverman EM. Laproscopic Cholecystectomy: Relationship of Pathology and Operative Time. Jour of the Society of Laproscopic surgeons. 2002 April-June; 6(2): 149-154.

13. Kumar, Abbas, Fausto, Aster. Robbins and Cotran Pathological Basis of Disease. 8th ed. Philadelphia: Saunders, 2009; 885-886.

14. Luo X, Yang T, Zhang B et al. Xanthogranulomatous Cholecystitis, misdiagnosed as gall bladder carcinoma, Retrospective Analysis of 10 cases. The Chinese-German Journal of Oncology.2007; 6(30): 215-219.

15. Karabulu Z, Besim H, Hamamci O, Korkmaz A. Xanthogranulomatous Cholecystitis :Retrospective Analysis of 12 cases. J Acta chir belg. 2003; 103: 297-299.

16. Dixit VK, .Prakash A, Gupta A, Pandey M, Gautam A, Kumar M, Shukla VK. Xanthogranulomatous cholecystitis. Digestive Diseases and Sciences (Impact Factor: 2:12) 1998; 43(5): 940-2.

17. Kumar S, Srivastava P, Chauhan N, Kishore S, Sachan PK Bhal DV. Eosinophilic Cholecystitis : A Case Report. The Internet Journal of Surgery : 1528-8242.

18. Rosai and Ackerman’s Surgical Pathology, Tenth edition, Volume one, Pgs 987 to 988.

19. Khanna R, Chansuria R, Kumar M, Shukla HS. Histological Changes in Gall Bladder due to stone disease. Indian Journal of Surgery. 2006; 68: 201 – 4.

20. Tatematsu M, Furihata C, Miki K, Ichinose M, Shirai T, Tatematsu K, Ito N. Complete and Incomplete Pyloric gland Metaplasia of human Gall Bladder. Pathology International. 1987 Jan; 37 (1): 39 – 46 .

21. De Boer WGRM, Ma J, Rees JW, Nayman J. (1981). Inappropriate Mucin production in Gall Bladder Metaplasia and Neoplasia-An Immunohistologicalstudy. Histopathology. 1981; 5: 295-303.

22. Verma A, Mohan S, Baija SS. Ultrasonographical Evaluation of Asymptomatic gall bladder disease : An Epidemiological study in North India. Journal of Clinical and Diagnostic Research. 2011 April ; 5 (2): 328-330.

PROFORMA

DR. B.R.AMBEDKAR MEDICAL COLLEGE AND HOSPITAL

|Name: Age: Sex: M/F |

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|Address: Case no: |

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|Brief personal history: |

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|Past family history: [ H/O DM / HTN / Hypercholesterolemia ] |

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|Family history: |

|[ H/O gall stones / cholecystectomy /obesity /Hypercholesterolemia]. |

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|Personal history: (Diet) |

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|In case of female patient: |

|Married Life: Obstetric score: OCP usage: |

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|Ultrasonography / CT findings : |

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|Indications for Cholecystectomy: |

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|Gross findings |

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|Histopathology: |

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|PAS STAIN: |

| Neurtal mucin Positive / Negative |

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| ALCIAN BLUE STAIN: |

| pH 2.5 Positive / Negative |

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| pH 1.0 Positive / Negative |

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DR.B.R.AMBEDKAR MEDICAL COLLEGE,

K.G.HALLI, BANGALORE 560045

DEPARTMENT OF PATHOLOGY

To,

The Ethical Committee,

DR.B.R. Ambedkar Medical College,

K.G. Halli,

Bangalore 560045

Subject: To obtain Ethical Clearance of subject for dissertation

Respected sir,

I, Dr.Ashwini.M.C postgraduate student in MD Pathology, enclose the Proforma for the dissertation subject titled “HISTOMORPHOLOGICAL STUDY OF DISEASES OF THE GALL BLADDER”. I kindly request you to register my topic of dissertation and do the needful.

Thanking you,

Yours faithfully,

Dr. Ashwini M.C.

DR.B.R.AMBEDKAR MEDICAL COLLEGE,

K.G.HALLI, BANGALORE 560045

DEPARTMENT OF PATHOLOGY

To,

The Principal,

DR.B.R. Ambedkar Medical College,

K.G. Halli,

Bangalore 560045

Subject: Proforma for registration of subject for dissertation.

Respected sir,

I, Dr.Ashwini.M.C postgraduate student in MD Pathology, enclose the Proforma of the subject for dissertation titled “HISTOMORPHOLOGICAL STUDY OF DISEASES OF THE GALL BLADDER”. I kindly request you to kindly forward it to Rajiv Gandhi University of Health Sciences, Bangalore and do the needful.

Thanking you,

Yours faithfully,

Dr. Ashwini M.C.

DR.B.R.AMBEDKAR MEDICAL COLLEGE,

K.G.HALLI, BANGALORE 560045

DEPARTMENT OF PATHOLOGY

To,

The Registrar,

Rajiv Gandhi University of Health Sciences,

Jayanagar 4th block,

Bangalore .

[Through proper channel]

Subject: Proforma for registration of subject for dissertation.

Respected Madam / Sir,

I, Dr. Ashwini. M.C. postgraduate student in MD Pathology enclose the Proforma of the subject for dissertation titled “HISTOMORPHOLOGICAL STUDY OF DISEASES OF THE GALL BLADDER.” I kindly request you to certify my topic of dissertation and do the needful.

Thanking you,

Yours faithfully,

Dr. Ashwini M.C.

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