Study Guide Alimentary & Hepatobiliary Systems & Disorders

STUDY GUIDE “Alimentary and Hepatobiliary System and Disorders” Semester IV

21 March – 2 May 2017

DEPARTMENT OF MEDICAL EDUCATION FACULTY OF MEDICINE UDAYANA UNIVERSITY DENPASAR 2017

Udayana University Faculty of Medicine, DME, 2017 1 Study Guide Alimentary & Hepatobiliary Systems & Disorders

CONTENTS

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Table of contents ……..………….……………………………………………………………. 1 Curriculum ……………………………………………………………………...……………… 2 SKDI …………………………………………………………………………………………….. 5 Block Team ….……………………………………………………………………...... 9 Facilitators …………………………………………………………...………………………… 11 Time Table English Class ….………………………………………………………………… 12 Time Table Reguler Class ..………………………………………...……………………… 16 Student Project ………..…………………………………………………………………….… 20 BCS ………..……………………………………………………………………………………. 21 Hospital Visit ………….……………………………………………………………………….. 22 Assessment method ………………………………………………………………………….. 23 Learning Program .…………………………………………………………………………….. 24 Abstract …..………………………………………………………………………………….…. 24 Learning Task and Self Assessment ……..…………………………………………………. 50 Reference ..…………………………………………………………………………..………… 72 Assessment Form .……………………………………………………………………………. 73 Curriculum Mapping .………………………………………………………………………….. 76

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CURRICULUM

Aims 1. Comprehend the biologic function of alimentary and hepatobiliary system to pathological process of alimentary and hepatobiliary system disorders. 2. Apply and interpret physical examination, laboratory, and imaging diagnosis of alimentary and hepatobiliary system disorders 3. Diagnose and manage patient with common alimentary and hepatobiliary system disorders 4. Diagnose and refer special patients with alimentary and hepatobiliary system disorders 5. Plan patient, family, and necessary community education about alimentary and hepatobiliary system disorders

Learning Outcomes 1. Describe the functional structure alimentary system and its general clinical implications 2. Describe the functional structure of hepatobilliary system and its general clinical implications 3. Comprehend the pathological basis underlying the symptoms and sign of alimentary and hepatobilliary disorders. 4. Recognize the potential uses of common diagnostic and therapeutic alimentary and hepatobilliary procedures 5. Manage oral cavity disorders: a. Diagnose and manage independently some mouth disorders such as Candidiasis, and mouth ulcers. b. Diagnose, give initial treatment and refer glossitis, caries, gingival disorders, periodintitis, pulpitis, toothache and infection c. Diagnose and refer some mouth disorders such as cleft lip and palate, micrognatia and macrognatia, and leukoplakia 6. Manage esophageal disorders: a. Diagnose, give initial treatment and refer corrosive lesion of esophagus and reflux esophagitis b. Diagnose and refer esophageal atresia, achalasia, esophageal varices and esophageal rupture 7. Manage abdominal wall disorders a. Diagnose, give initial treatment and refer umbilical hernia b. Diagnose and refer inguinal hernia, femoral hernia, ephigastric herhia, incisional hernia, diaphragmatic hernia, and hiatus hernia 8. Manage stomach and duodenum disorders: a. Diagnose and manage independently gastritis and gastroenteritis (refer if needed in pediatric cases, especially with dehydration)

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b. Diagnose, give initial treatment and refer gastric/duodenal ulcer and gastrointestinal bleeding. c. Diagnose and refer Zollinger-ellison syndrome, and Mallory-weis syndrome 9. Manage jejunum and ileum disorders: a. Diagnose and manage independently enteritis case b. Diagnose and refer intestinal atresia, Meckel’s diverticulum, umbilical fistula, omphalocoele-gastroschisis, and malrotation 10. Manage colon and anal disorders: a. Diagnose, give initial treatment and refer irritable bowel syndrome, necrotizing enterocolitis, diverticulitis, colitis, rectal and anal prolapse, proctitis, and haemorrhoids. b. Diagnose and refer (peri)anal abscess, fistula anal, and anal fissure 11. Manage acute abdomen cases: a. Diagnose, give initial treatment, and refer salphingitis (covered more details in The Genital System and Disorders Block), acute appendicitis, appendicular abscess, and ileus b. Diagnose and refer peritonitis, abscess in pouch of douglass, perforation, and mesenteric lymphadenitis. 12. Manage liver disorders: a. Diagnose and manage independently fatty liver, hepatitis A, uncomplicated hepatitis B, and Amoebic liver abscess. b. Diagnose, give initial treatment and refer active hepatitis C and cirrhosis hepatis c. Diagnose and refer liver failure. 13. Manage gall bladder, bile duct and pancreas disorders: a. Diagnose, give initial treatment and refer acute cholecystitis b. Diagnose and refer chole (docho) lithiasis, hydrops of gall bladder, empyema of gall bladder and pancreatitis. 14. Manage neoplasma of alimentary and hepatobiliary system a. Diagnose and refer neoplasma of Alimentary system, such as benign polyps, squamous cell carcinoma, adenocarcinoma, carcinoid tumor, lymphoma b. Diagnose and refer neoplasma of hepatobiliary system, such as liver cell adenoma, hepatocellular carcinoma, cholangiocarcinoma, and carcinoma of the pancreas 15. Manage special cases of alimentary in pediatric: a. Diagnose and manage independently worm infection (covered more details in The Infection and Infectious Diseases Block), peritonitis tuberculosis, and food allergy (covered more details in The Immune System and Disorders). b. Diagnose, give initial treatment and refer malabsorbtion and food intolerance cases. c. Diagnose and refer pyloric stenosis, intussussception, hirschsprung’s disease, chron’s disease, reye’s syndrome, ulcerative colitis and anal atresia. 16. Write rational and legal prescription for alimentary and hepatobiliary patients 17. Implement patient education in the prevention and early detection of common alimentary and hepatobilliary disorders.

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Curriculum contents 1. Functional structure of alimentary and hepatobiliary system 2. Pathological basis of alimentary and hepatobiliary disorders 3. Symptom and signs of alimentary and hepatobiliary system disorders a. cavity disorders b. esophageal disorders c. abdominal wall disorders d. stomach and duodenum disorders e. jejunum and ileum disorders f. colon and anal disorders g. acute abdomen h. liver disorders i. gall bladder, bile duct and pancreas disorders j. neoplasma of alimentary and hepatobiliary system k. special cases of alimentary in pediatric 4. Physical examination, laboratory investigation and imaging studies in alimentary and hepatobilliary disorders 5. Rational drug use in alimentary and hepatobiliary disorders 6. Management of alimentary and hepatobiliary disorders 7. Communication and basic principles in the prevention and early detection of alimentary and hepatobiliary disorders

Some contents of this Block are covered more details in the other blocks, such as: 1. Salphingitis is covered more details in The Genital System and Disorders Block 2. Worm infection is covered more details in The Infection and Infectious Disesases 3. Food allergy is covered more details in The Immune System and Disorders

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STANDAR KOMPETENSI DOKTER INDONESIA

Sistem Gastrointestinal, Hepatobilier, Pankreas

No Daftar Penyakit Tingkat Kemampuan

Mulut 1 Sumbing pada bibir dan palatum 2 2 Micrognatia and macrognatia 2 3 Kandidiasis mulut 4A 4 Ulkus mulut (aptosa , herpes) 4A 5 Glositis 3A 6 Leukoplakia 2 7 Angina Ludwig 3A 8 Parotitis 4A 9 Karies gigi 3A Esofagus 10 Atresia esofagus 2 11 Akalasia 2 12 Esofagitis refluks 3A 13 Lesi korosif pada esofagus 3B 14 Varises esofagus 2 15 Ruptur esofagus 1 Dinding, Rongga Abdomen dan Hernia Hernia (inguinalis, femoralis, skrotalis) reponibilis, 16 2 irreponibilis Hernia (inguinalis, femoralis, skrotalis) strangulata, 17 3B inkarserata 18 Hernia (diaframatika, hiatus) 2 19 Hernia umbilikalis 3A 20 Peritonitis 3B 21 Perforasi usus 2 22 Malrotasi traktus gastro-intestinal 2 23 Infeksi pada umbilikus 4A 24 Sindroma Reye 1 Lambung, Duodenum, Jejunum, Ileum 25 Gastritis 4A 26 Gastroenteritis (termasuk kolera, giardiasis) 4A 27 Refluks gastro-esofagus 4A

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28 Ulkus (gaster, duodenum) 3A 29 Stenosis pilorik 2 30 Atresia intestinal 2 31 Divertikulum Meckel 2 32 Fistula umbilikal, omphalocoele-gastroschisis 2 33 Apendisitis akut 3B 34 Abses apendiks 3B 35 Demam tifoid 4A 36 Perdarahan gastrointestinal 3B 37 Ileus 2 38 Malabsorbsi 3A 39 Intoleransi makanan 4A 40 Alergi makanan 4A 41 Keracunan makanan 4A 42 Botulisme 3B Infestasi Cacing dan lainnya 43 Penyakit cacing tambang 4A 44 Strongiloidiasis 4A 45 Askariasis 4A 46 Skistosomiasis 4A 47 Taeniasis 4A 48 Pes 1 Hepar 49 Hepatitis A 4A 50 Hepatitis B 3A 51 Hepatitis C 2 52 Abses hepar amoeba 3A 53 Perlemakan hepar 3A 54 Sirosis hepatis 2 55 Gagal hepar 2 56 Neoplasma hepar 2 Kandung Empedu, Saluran Empedu, dan Pankreas 57 Kolesistitis 3B 58 Kole(doko)litiasis 2 59 Empiema dan hidrops kandung empedu 2 60 Atresia biliaris 2 61 Pankreatitis 2 62 Karsinoma pankreas 2 Kolon 63 Divertikulosis/divertikulitis 3A 64 Kolitis 3A 65 Disentri basiler, amuba 4A 66 Penyakit Crohn 1 67 Kolitis ulseratif 1 68 Irritable Bowel Syndrome 3A

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69 Polip/adenoma 2 70 Karsinoma kolon 2 71 Penyakit Hirschsprung 2 72 Enterokolitis nekrotik 1 73 Intususepsi atau invaginasi 3B 74 Atresia anus 2 75 Proktitis 3A 76 Abses (peri)anal 3A 77 Hemoroid grade 1-2 4A 78 Hemoroid grade 3-4 3 79 Fistula 2 80 Fisura anus 2 81 Prolaps rektum, anus 3A Neoplasma Gatrointestinal 82 Limfoma 2 83 Gastrointestinal Stromal Tumor (GIST) 2

Sistem Gastrointestinal, Hepatobilier, Pankreas

Tingkat No Ketrampilan Tingkat Ketrampilan PEMERIKSAAN FISIK 1 Inspeksi bibir dan kavitas oral 4A 2 Inspeksi tonsil 4A 3 Penilaian pergerakan otot-otot hipoglosus 4A 4 Inspeksi abdomen 4A Inspeksi lipat paha/ inguinal pd saat tekanan abdomen 5 4A meningkat Palpasi (dinding perut, kolon, hepar, lien, aorta, rigiditas 6 4A dinding perut) 7 Palpasi hernia 4A 8 Pemeriksaan nyeri tekan dan nyeri lepas (Blumberg test) 4A 9 Pemeriksaan Psoas sign 4A 10 Pemeriksaan Obturator sign 4A 11 Perkusi (pekak hati dan area Traube) 4A 12 Pemeriksaan pekak beralih (shifting dullness) 4A 13 Pemeriksaan undulasi (fluid thrill) 4A 14 Pemeriksaan colok dubur (digital rectal examination) 4A 15 Palpasi sakrum 4A 16 Inspeksi sarung tangan paska colok dubur 4A

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17 Persiapan dan pemeriksaan tinja 4A PEMERIKSAAN DIAGNOSTIK 18 Pemasangan pipa nasogastrik (NGT) 4A 19 Endoskopi 2 20 Nasogastric suction 4A 21 Mengganti kantong pada kolostomi 4A 22 Enema 4A 23 Anal swab 4A 24 Identifikasi parasit 4A Pemeriksaan feses (termasuk darah samar, protozoa, parasit, 25 4A cacing) 26 Endoskopi lambung 2 27 Proktoskopi 2 28 Biopsi hepar 1 29 Pengambilan cairan asites 3

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PLANNERS TEAM

NO NAME DEPT PHONE Prof.Dr dr I Dewa Nyoman Wibawa 1 Internal Medicine 0811398032 Sp.PD-KGEH 2 dr. Ketut Mariadi, Sp.PD-KGEH Internal Medicine 08123853700 3 dr. Gde Somayana, SpPD Internal Medicine 0816579888 4 dr.Ni Nyoman Metriani Nesa, M.Sc, Sp.A Pediatry 081337072141 5 dr. Agus Rudi Asthuta,Sp.THT ENT 08123806637 6. dr. I Wayan Sucipta,Sp.THT ENT 08125318941 7 dr. Nyoman Gede Wardana, M.Biomed Anatomy 087860405625 dr.Made Agus Dwianthara Sueta, 8 Surgery 081338648424 Sp.B-KBD 9. dr. Made Mulyawan, Sp.B Surgery 081241138971 10. drg. Mia Ayustina P Dentistry 08175053626

11 dr. Ketut Suanda, Sp.THT-KL ENT 081337788377 12 dr. Elysanti M, Sp.R Radiology 081805673099 13. Prof. dr. I G M Aman, Sp. FK Pharmacology 081338770650 14 Dr. dr. A. A Wiradewi Sp.PK Clinical Pathology 08155237937 Dr.dr. I Gusti Ayu Sri Mahendra 15. Pathology 081338736481 Dewi,Sp.PA (K) 16. dr. L Pt Iin Indrayani M, Sp.PA(K) Pathology 08174761804 17. dr. I G N Mayun, Sp.HK Histology 08155715359 18. dr. Wayan Sugiritama, MKes Histology 08164732743 19. dr. Desak Made Wihandani, M. Kes Biochemistry 081338776244 20. dr. I Wayan Surudarma, M.Si Biochemistry 081338486589 21. dr. I Putu Adiartha Griadi, M.Fis Physiology 081999636899 22. Dra. I A Alit Widhiartini, Apt Pharmacology 08193600559 23. dr. Srie Laksminingsih, Sp.R Radiology 08164745561

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LECTURERS

NO NAME DEPT PHONE Prof.Dr dr I Dewa Nyoman Wibawa 1 Internal Medicine 0811398032 Sp.PD-KGEH 2 dr. Ketut Mariadi, Sp.PD-KGEH Internal Medicine 08123853700 3 dr. Gde Somayana, SpPD Internal Medicine 0816579888 dr. Ni Nyoman Metriani Nesa, M.Sc, 4 Pediatry 081337072141 Sp.A 5 dr. Agus Rudi Asthuta,Sp.THT ENT 08123806637 6. dr. I Wayan Sucipta,Sp.THT ENT 08125318941 7 dr. Nyoman Gede Wardana, M.Biomed Anatomy 087860405625 dr.Made Agus Dwianthara Sueta, 8 Surgery 081338648424 Sp.B-KBD 9. dr. Made Mulyawan, Sp.B Surgery 081241138971 10. drg. Mia Ayustina P Dentistry 08175053626

11 dr.Ketut Suanda, Sp.THT-KL ENT 081337788377 12 dr. Elysanti M, Sp.R Radiology 081805673099 13. Prof. dr. I G M Aman, Sp. FK Pharmacology 081338770650 14 Dr. dr. A. A Wiradewi Sp.PK Clinical Pathology 08155237937 Dr. dr. I Gusti Ayu Sri Mahendra 15. Pathology 081338736481 Dewi,Sp.PA (K) 16. dr. L Pt Iin Indrayani M, Sp.PA(K) Pathology 08174761804 17. dr. I G N Mayun, Sp.HK Histology 08155715359 18. dr. Wayan Sugiritama, MKes Histology 08164732743 19. Dr. dr. Desak Made Wihandani, M. Kes Biochemistry 081338776244 20. dr. I Wayan Surudarma, M.Si Biochemistry 081338486589 21. dr. I Putu Adiartha Griadi, M.Fis Physiology 081999636899 22. Dra. I A Alit Widhiartini, Apt Pharmacology 08193600559 23. dr. Srie Laksminingsih, Sp.R Radiology 08164745561

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FACILITATORS Regular Class (Class A) Venue No Name Group Departement Phone (2nd floor) Prof dr IDP Sutjana M.Erg Fisiologi 08123924477 2nd floor: 1 A1 R.2.01 dr Yuliana M.Biomed Anatomi 085792652363 2nd floor: 2 A2 R.2.02 dr I Wayan Surudarma M.Si Biokimia 081338486589 2nd floor: 3 A3 R.2.03 dr Made Agus Hendrayana Mikrobiologi 08123921590 2nd floor: 4 M.Ked A4 R.2.04 dr IGA Sri Darmayani Sp.OG DME 081338644411 2nd floor: 5 A5 R.2.05 Dr dr I Made Muliarta M.Kes Fisiologi 081338505350 2nd floor: 6 A6 R.2.06 dr IGN Sri Wiryawan M.Repro Histologi 082341768888 2nd floor: 7 A7 R.2.07 Prof dr GM Aman Sp.FK Farmakologi 081338770650 2nd floor: 8 A8 R.2.08 Prof Dr dr I Putu Adiatmika Fisiologi 08123811019 2nd floor: 9 M.Kes A9 R.2.21 dr I Nyoman Budi Hartawan Pediatri 081353027973 2nd floor: 10 A10 MSc Sp.A(K) R.2.22

English Class (Class B) Venue No Name Group Departement Phone (2nd floor) Dr dr IGA Putu Eka Pratiwi Pediatri 08123920750 2nd floor: 1 B1 Sp.A M.Sc R.2.01 dr I Wayan Sugiritama M.Kes Histologi 08164732743 2nd floor: 2 B2 R.2.02 Dr dr Ni Nyoman Sri Budayanti Mikrobiologi 08553711398 2nd floor: 3 SP.MK(K) B3 R.2.03 dr IG Kamasan Nyoman Arijana Histologi 085339644145 2nd floor: 4 M.Si Med B4 R.2.04 dr. I Gusti Ayu Harry DME 081805380277 2nd floor: 5 Sundariyati, S.Ked B5 R.2.05 dr IGA Artini M.Sc Farmakologi 08123650481 2nd floor: 6 B6 R.2.06 dr I Putu Bayu Mayura S.Ked Mikrobiologi 082236165801 2nd floor: 7 B7 R.2.07 dr Yukhi Kurniawan Sp.And Andrologi 08123473593 2nd floor: 8 B8 R.2.08 Dr dr BK Satriyasa M.Repro Farmakologi 087777790064 2nd floor: 9 B9 R.2.21 Prof Dr dr Ketut Tirtayasa MS Fisiologi 08123623422 2nd floor: 10 B10 AIF AIFO Sp.Erg R.2.22

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TIME TABLE English Class (Class B)

Day/ Time Activity Venues Person-in-charge Date

08.00-09.00 Introduction to The Block Alimentary and 402 Prof. Wibawa Hepatobiliary System and Disorders 1 Lecture 1 : Tues 09.00-10.00 Independent Learning 21 10.00-11.00 Macroscopic Structure of Upper and dr. Wardana Mar Lower Alimentary System 2017 11.00-12.00 Small Group Disscussion Room Facilitators 12.00-12.30 Break 12.30-14.00 Student Project 14.00-15.00 Plenary Session 402 dr. Wardana Lecture 2: 08.00-09.00 Microscopic Structure of Upper and 402 dr. Sugiritama Lower Alimentary System 2 09.00-10.00 Physiology aspect of Upper and Lower dr. Adiarta Wed Alimentary System 22 10.00-10.30 Independent Learning Mar 10.30-12.00 Small Group Discussion Room Facilitators 2017 12.00-12.30 Break 12.30-14.00 Student project 14.00-15.00 Plenary Session 402 dr. Sugiritama, dr. Adiarta Lecture 3: 08.00-09.00 Biochemistry aspect of Upper and Lower 402 dr. Surudarma Alimentary System 09.00-09.30 Macroscopic Structure of Hepatobiliary dr. Wardana System 3 09.30-10.00 Microscopic Structure of Hepatobiliary dr. Mayun Thu System 23 10.00-10.30 Independent Learning Mar 10.30-12.00 Small Group Discussion Room Facilitators 2017 12.00-12.30 Break 12.30-14.00 Student project 14.00-15.00 Plenary Session 402 dr. Surudarma, dr. Wardana, dr. Mayun Lecture 4: 08.00-08.30 Physiology aspect of Hepatobiliary 402 dr. Adiarta System 08.30-09.00 Biochemistry aspect of Hepatobiliary Dr. Wihandani System 4 09.00-10.00 Rational Drug Use in Alimentary and Prof. Aman Fri Hepatobiliary Disorders 24 10.00-10.30 Independent Learning Mar 10.30-12.00 Small Group Discussion Room Facilitators 2017 12.00-12.30 Break 12.30-14.00 Student project 14.00-15.00 Plenary Session 402 dr. Adiarta, Dr. Wihandani, Prof Aman Lecture 5: 08.00-08.30 Etiopathologenesis and Morphologic 402 dr.Iin Indrayani Features of Alimentary Disorders 08.30-09.00 Etiopathologenesis and Morphologic Dr. Mahendra D Features of Hepatobiliary Disorders

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5 09.00-10.00 Clinical Pathology aspect of Alimentry and Dr. Wiradewi Thu Hepatobiliary System 30 10.00-10.30 Independent Learning Mar 10.30-12.00 Small Group Discussion Room Facilitators 2017 12.00-12.30 Break 12.30-14.00 Student project 14.00-15.00 Plenary Session 402 dr. Iin Indrayani Dr. Mahendra D Dr. Wiradewi Lecture 6: 08.00-08.30 Imaging Studies of Alimentary Disorders 402 Dr. Elysanti 6 08.30-09.00 Imaging studies of Hepatobiliary system Dr. Srie L. Fri 09.00-10.30 Independent Learning 31 10.30-12.00 Small Group Discussion Room Facilitators Mar 12.00-14.00 Break and student project 2017 14.00-15.00 Plenary Session 402 Dr. Elysanti Dr. Srie L. Lecture 7: 08.00-08.30 Oral Cavity Disorders - Mouth Disorders (Candidiasis, 402 dr. Agus Rudi A. mouth ulcer, glositis, Angina Ludwig, Parotitis) 7 08.30-09.00 - Teeth and Periodontium Diseases drg. Mia Ayustina P Mon (Caries, pulpitis, periodontitis) 3 Apr 09.00-10.30 Independent Learning 2017 10.30-12.00 Small Group Discussion Room Facilitators 12.00-12.30 Break 12.30-14.00 Student project 14.00-15.00 Plenary Session 402 dr. Agus Rudi A. drg. Mia Ayustina P Lecture 8: Esophageal Disorders 08.00-08.30 - Corrosive lession of esophagus 402 dr. I Wyn Sucipta 08.30-09.00 - Reflux esophagitis Prof Wibawa 8 09.00-10.30 Independent Learning Fri 10.30-12.00 Small Group Discussion Room Facilitators 7 Apr 12.00-12.30 Break 2017 12.30-14.00 Student project 14.00-15.00 Plenary Session 402 dr. I Wyn Sucipta Prof Wibawa

Lecture 9: 08.00-09.00 Stomach and Duodenum Disorders 1 402 dr. Somayana 9 (Gastritis, gastric/duodenal ulcer, Mon Gastrointestinal Bleeding, Demam tifoid) 10 09.00-10.30 Independent Learning Apr 10.30-12.00 Small Group Discussion Room Facilitators 2017 12.00-12.30 Break 12.30-14.00 Student project 14.00-15.00 Plenary Session 402 dr. Somayana Lecture 10: 08.00-08.30 Stomach and Duodenum Disorders 2 402 dr. Metriani (Gastroenteritis, Intussuception) 10 08.30-09.00 Acute Abdomen (acute appendicitis, dr. Agus Sueta Tue appendicular abscess, peritonitis, infeksi 11 umbilicus) Apr 09.00-10.30 Independent Learning 2017 10.30-12.00 Small Group Discussion Room Facilitators 12.00-12.30 Break 12.30-14.00 Student project

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14.00-15.00 Plenary Session 402 dr. Metriani dr. Agus Sueta Lecture 11: 08.00-09.00 Abdominal wall disorders (Hernia); Colon 402 dr. Mulyawan and Anal Disorders 1 (Rectal and anal 11 prolapse, proctitis, and haemorrhoids, Wed abses peri/anal) 12 09.00-10.30 Independent Learning Apr 10.30-12.00 Small Group Discussion Room Facilitators 2017 12.00-12.30 Break 12.30-14.00 Student project 14.00-15.00 Plenary Session 402 dr. Mulyawan BCS 1 12 08.00-10.00 Lecture and Demonstration 1 Skill Lab dr. Suanda Thur 10.00-11.30 Break and Free Training dr. Mariadi 13 11.30-14.00 Group Training Session dr. Agus Sueta Apr dr. Somayana 2017 I.A. Alit BCS 2 13 08.00-10.00 Lecture and Demonstration 2 Skill Lab dr. Suanda Mon 10.00-11.30 Break and Free Training dr. Mariadi 17 11.30-14.00 Group Training Session dr. Agus Sueta Oct dr. Somayana 2016 I.A. Alit BCS 3 14 08.00-10.00 Lecture and Demonstration 3 Skill Lab dr. Suanda Tue 10.00-11.30 Break and Free Training dr. Mariadi 18 11.30-14.00 Group Training Session dr. Agus Sueta Apr dr. Somayana 2017 I.A. Alit BCS 4 15 08.00-10.00 Lecture and emonstration 4 Skill Lab dr. Suanda Wed 10.00-11.30 Break and Free Training dr. Mariadi 19 11.30-14.00 Group Training Session dr. Agus Sueta Apr dr. Somayana 2017 I.A. Alit BCS 5 16 08.00-10.00 Lecture and Demonstration 5 Skill Lab dr. Suanda Thur 10.00-11.30 Break and Free Training dr. Mariadi 20 11.30-14.00 Group Training Session dr. Agus Sueta Apr dr. Somayana 2017 I.A. Alit Lecture 12: 08.00-09.00 Colon and Anal Disorders 2 (IBS, Disentri, 402 dr. Mariadi 17 diverticulitis, and colitis) Fri 09.00-10.30 Independent Learning 21 10.30-12.00 Small Group Discussion Room Facilitators Apr 12.00-12.30 Break 2017 12.30-14.00 Student project 14.00-15.00 Plenary Session 402 dr. Mariadi Lecture 13: Liver Disorder 1 08.00-08.30 - Acute hepatitis 402 dr. Metriani 18 08.30-09.00 - Chronic hepatitis B Prof. Wibawa Tue 09.00-10.30 Independent Learning 25 10.30-12.00 Small Group Discussion Room Facilitators Apr 12.00-12.30 Break 2017 12.30-14.00 Student project 14.00-15.00 Plenary Session 402 dr. Metriani Prof. Wibawa

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Lecture 14: 08.00-08.30 Liver Disorder 2 (Fatty liver, amoebic liver 402 Dr. Somayana abscess) 19 08.30-09.00 Gall Bladder, Bile Duct, and Pancreas Dr. Mariadi Wed Disorders (acute cholecystitis) 26 09.00-10.30 Independent Learning Apr 10.30-12.00 Small Group Discussion Room Facilitators 2017 12.00-12.30 Break 12.30-14.00 Student project 14.00-15.00 Plenary Session 402 Dr. Somayana Dr. Mariadi 08.00-12.00 Student Project Presentation 402 Prof. Wibawa Prof Aman dr. Elysanti dr. Metriani dr. Mayun dr. Wardana dr. Mulyawan dr. Surudarma dr. Iin Indrayani 20 Dr. Wiradewi Thu dr. Sugiritama 27 Dr. Mahendra Dewi Apr dr. Agus Sueta 2017 Dr. Wihandani dr. Adiartha I A Alit Widhiartini dr. Srie L. dr. Agus rudi drg. Mia Ayustina dr. Wyn Sucipta dr. Mariadi dr. Somayana 21 Preparation for Exam 22 Tue 2 EXAMINATION May 2017

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TIME TABLE Reguler Class (Class A)

Day/ Time Activity Venues Person-in-charge Date

09.00-10.00 Introduction to The Block Alimentary and 402 Prof. Wibawa Hepatobiliary System and Disorders 1 10.00-11.00 Independent Learning Tues Lecture 1 : 21 11.00-12.00 Macroscopic Structure of Upper and Dr. Wardana Mar Lower Alimentary System 2017 12.00-12.30 Break 12.30-13.30 Student Project 13.30-15.00 Small Group Disscussion Room Facilitators 15.00-16.00 Plenary Session 402 Dr. Wardana 09.00-10.00 Independent Learning Lecture 2: 402 10.00-11.00 Microscopic Structure of Upper and dr. Sugiritama 2 Lower Alimentary System Wed 11.00-12.00 Physiology aspect of Upper and Lower dr. Adiarta 22 Alimentary System Mar 12.00-12.30 Break 2017 12.30-13.30 Student Project 13.30-15.00 Small Group Disscussion Room Facilitators 15.00-16.00 Plenary Session 402 dr. Sugiritama, dr. Adiarta 09.00-10.00 Independent Learning Lecture 3: 10.00-11.00 Biochemistry aspect of Upper and Lower 402 dr. Surudarma Alimentary System 11.00-11.30 Macroscopic Structure of Hepatobiliary dr. Wardana 3 System Thu 11.30-12.00 Microscopic Structure of Hepatobiliary dr. Mayun 23 System Mar 12.00-12.30 Break 2017 12.30-13.30 Student Project 13.30-15.00 Small Group Disscussion Room Facilitators 15.00-16.00 Plenary Session 402 dr. Surudarma, dr. Wardana, dr. Mayun 09.00-10.00 Independent Learning Lecture 4: 402 10.00-10.30 Physiology aspect of Hepatobiliary dr. Adiarta System 10.30-11.00 Biochemistry aspect of Hepatobiliary Dr. Wihandani 4 System Fri 11.00-12.00 Rational Drug Use in Alimentary and Prof. Aman 24 Hepatobiliary Disorders Mar 12.00-12.30 Break 2017 12.30-13.30 Student Project 13.30-15.00 Small Group Disscussion Room Facilitators 15.00-16.00 Plenary Session 402 dr. Adiarta, Dr. Wihandani, Prof Aman 09.00-10.00 Independent Learning Lecture 5: 10.00-10.30 Etiopathologenesis and Morphologic 402 dr.Iin Indrayani Features of Alimentary Disorders

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5 10.30-11.00 Etiopathologenesis and Morphologic Dr. Mahendra D Thu Features of Hepatobiliary Disorders 30 11.00-12.00 Clinical Pathology aspect of Alimentry and Dr. Wiradewi Mar Hepatobiliary System 2017 12.00-12.30 Break 12.30-13.30 Student Project 13.30-15.00 Small Group Disscussion Room Facilitators 15.00-16.00 Plenary Session 402 dr. Iin indrayani Dr. Mahendra D Dr. Wiradewi Lecture 6: 09.00-09.30 Imaging Studies of Alimentary Disorders 402 dr. Elysanti 6 09.30-10.00 Imaging studies of Hepatobiliary system dr. Srie L. Fri 10.00-12.00 Independent Learning 31 12.00-13.30 Break and student project Mar 13.30-15.00 Small Group Discussion Room Facilitators 2017 15.00-16.00 Plenary Session 402 dr. Elysanti dr. Srie L. Lecture 7: Oral Cavity Disorders 09.00-09.30 - Mouth Disorders (Candidiasis, 402 dr. Agus Rudi A. mouth ulcer, glositis, Angina Ludwig, Parotitis) 7 09.30-10.00 - Teeth and Periodontium Diseases drg. Mia Ayustina P Mon (Caries, pulpitis, periodontitis) 3 Apr 2017 10.00-11.30 Independent Learning 11.30-13.30 Break and Student project 13.30-15.00 Small Group Discussion Room Facilitators 15.00-16.00 Plenary Session 402 dr. Agus Rudi A. drg. Mia Ayustina P Lecture 8: Esophageal Disorders 09.00-09.30 - Corrosive lession of esophagus 402 dr. I Wyn Sucipta 8 09.30-10.00 - Reflux esophagitis Prof Wibawa Fri 10.00-11.30 Independent Learning 7 Apr 11.30-13.30 Break and Student project 2017 13.30-15.00 Small group Discussion Room Facilitators 15.00-16.00 Plenary Session 402 dr. I Wyn Sucipta Prof Wibawa Lecture 9: 09.00-10.00 Stomach and Duodenum Disorders 1 402 dr. Somayana 9 (Gastritis, gastric/duodenal ulcer, Mon Gastrointestinal Bleeding, Demam tifoid) 10 Apr 10.00-11.30 Independent Learning 2017 11.30-13.30 Break and Student project 13.30-15.00 Small group Discussion Room Facilitators 15.00-16.00 Plenary Session 402 dr. Somayana Lecture 10: 09.00-09.30 Stomach and Duodenum Disorders 2 402 dr. Metriani (Gastroenteritis,Intususepsi) 09.30-10.00 Acute Abdomen (acute appendicitis, dr. Agus Sueta 10 appendicular abscess, peritonitis, infeksi Tue umbilicus) 11 Apr 10.00-11.30 Independent Learning 2017 11.30-13.30 Break and Student project 13.30-15.00 Small group Discussion Room Facilitators 15.00-16.00 Plenary Session 402 dr. Metriani dr. Agus Sueta

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Lecture 11: 09.00-10.00 Abdominal wall disorders (Hernia); Colon 402 dr. Mulyawan and Anal Disorders 1 (Rectal and anal 11 prolapse, proctitis, and haemorrhoids, Wed abses peri/anal) 12 Apr 10.00-11.30 Independent Learning 2017 11.30-13.30 Break and Student project 13.30-15.00 Small group Discussion Room Facilitators 15.00-16.00 Plenary Session 402 dr. Mulyawan

BCS 1 12 08.00-10.00 Lecture and Demonstration 1 Skill Lab dr. Suanda Thur 10.00-11.30 Break and Free Training dr. Mariadi 13 Apr 11.30-14.00 Group Training Session dr. Agus Sueta 2017 dr. Somayana I.A. Alit BCS 2 13 08.00-10.00 Lecture and Demonstration 2 Skill Lab dr. Suanda Mon 10.00-11.30 Break and Free Training dr. Mariadi 17 11.30-14.00 Group Training Session dr. Agus Sueta Oct dr. Somayana 2016 I.A. Alit BCS 3 14 08.00-10.00 Lecture and Demonstration 3 Skill Lab dr. Suanda Tue 10.00-11.30 Break and Free Training dr. Mariadi 18 Apr 11.30-14.00 Group Training Session dr. Agus Sueta 2017 dr. Somayana I.A. Alit BCS 4 15 08.00-10.00 Lecture and emonstration 4 Skill Lab dr. Suanda Wed 10.00-11.30 Break and Free Training dr. Mariadi 19 Apr 11.30-14.00 Group Training Session dr. Agus Sueta 2017 dr. Somayana I.A. Alit BCS 5 16 08.00-10.00 Lecture and Demonstration 5 Skill Lab dr. Suanda Thur 10.00-11.30 Break and Free Training dr. Mariadi 20 Apr 11.30-14.00 Group Training Session dr. Agus Sueta 2017 dr. Somayana I.A. Alit Lecture 12: 09.00-10.00 Colon and Anal Disorders 2 (IBS, Disentri, 402 dr. Mariadi 17 diverticulitis, and colitis) Fri 10.00-11.30 Independent Learning 21 Apr 2017 11.30-13.30 Break and Student project 13.30-15.00 Small group Discussion Room Facilitators 15.00-16.00 Plenary Session 402 dr. Mariadi Lecture 13: Liver Disorder 1 09.00-09.30 - Acute hepatitis 402 dr. Metriani 09.30-10.00 - Chronic hepatitis B Prof. Wibawa 18 10.00-11.30 Independent Learning Tue 25 Apr 11.30-13.30 Break and Student project 2017 13.30-15.00 Small group Discussion Room Facilitators 15.00-16.00 Plenary Session 402 dr. Metriani Prof. Wibawa

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Lecture 14: 09.00-09.30 Liver Disorder 2 (Fatty liver, amoebic liver 402 dr. Somayana abscess) 09.30-10.00 Gall Bladder, Bile Duct, and Pancreas dr. Mariadi 19 Disorders (acute cholecystitis) Wed 10.00-11.30 Independent Learning 26 Apr 2017 11.30-13.30 Break and Student project 13.30-15.00 Small group Discussion Room Facilitators 15.00-16.00 Plenary Session 402 dr. Somayana dr. Mariadi 402 Prof. Wibawa 08.00-12.00 Student Project Presentation Prof Aman dr. Elysanti dr. Metriani dr. Mayun dr. Wardana dr. Mulyawan dr. Surudarma dr. Iin Indrayani 20 Dr. Wiradewi Thu dr. Sugiritama 27 Apr Dr. Mahendra Dewi 2017 dr. Agus Sueta Dr. Wihandani dr. Adiartha I A Alit Widhiartini dr. Srie L. dr. Agus rudi drg. Mia Ayustina dr. Wyn Sucipta dr. Mariadi dr. Somayana 21 Preparation for Exam

22 Tue EXAMINATION 2 May 2017

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STUDENT PROJECT TIME TABLE

Regular Class (room 1) Day Jam Group Topic 20 08.00-08.20 A2 Leukoplakia, Clift lift and Palate 08.20-08.40 A4 Atresia Esophagus, Achalasia 08.40-09.00 A6 Stenosis Pilorik, Syndroma Reye 09.00-09.20 A8 Food poisoning 09.20-09.40 A10 Fistula Umbilical, Ileus 09.40-10.00 A12 Perforasi Usus, Malrotasi 10.00-10.20 A1 Neoplasma of Alimentary System 10.20-10.40 A3 SirosisHepatis, Liver Failure 10.40-11.00 A5 Neoplasma of Hepatobiliary 11.00-11.20 A7 Pancreas Carcinoma 11.20-11.40 A9 Hirsprung’s Diseases, Chron’s Diseases 11.40-12.00 A11 Malabsorbsi

English Class (room 2) Day Jam Group Topic 20 08.00-08.20 B11 Leukoplakia, Clift lift and Palate 08.20-08.40 B9 Atresia Esophagus, Achalasia 08.40-09.00 B7 Stenosis Pilorik, Syndroma Reye B5 Food poisoning 09.00-09.20 09.20-09.40 B3 Fistula Umbilical, Ileus 09.40-10.00 B1 Perforasi Usus, Malrotasi 10.00-10.20 B12 Neoplasma of Alimentary System 10.20-10.40 B10 SirosisHepatis, Liver Failure 10.40-11.00 B8 Neoplasma of Hepatobiliary 11.00-11.20 B6 Pancreas Carcinoma 11.20-11.40 B4 Hirsprung’s Diseases, Chron’s Diseases 11.40-12.00 B2 Malabsorbsi

The lecturers are asked to become moderators and evaluator in the presentations of student project. Each grup are evaluated by 2 lecturers. Student project assessment form is attached in this study guide.

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BCS TIME TABLE

Day Topic 1 Topic 2 Topic 3 Topic 4 Topic 5 12 A1-A4 A5-A8 A9-B2 B3-B6 B7-B10 13 B7-B10 A1-A4 A5-A8 A9-B2 B3-B6 14 B3-B6 B7-B10 A1-A4 A5-A8 A9-B2 15 A9-B2 B3-B6 B7-B10 A1-A4 A5-A8 16 A5-A8 A9-B2 B3-B6 B7-B10 A1-A4

1. Topic 1. Examination of Mouth and Tonsil : dr Suanda 2. Topic 2. Physical examination of abdomen : dr Ketut Mariadi 3. Topic 3. NGT insertion and ascites aspiration : dr Gde Somayana 4. Topic 4. Hernia Palpation, colok dubur, sacrum palpation, gloves inspection, Psoas Sign, Obturator Sign, Blumberg Test : dr Agus Sueta 5. Topic 5. Farmacy in Alimentary : I A Alit Widhiartini

Training BCS assistants are the staff of Farmacy, and residen of surgery, internal medicine and ENT department, not the facilitator

BCS will be held from Thur, Apr 13th 2017 until Thur, Apr 20th 2017, in Skill Lab

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HOSPITAL VISIT TIME TABLE

PIC : dr. I Ketut Mariadi, Sp.PD Activity : Hospital visit Venue : Angsoka room, RSUP Sanglah Time : 17.00-18.00 Wita

Day Date Group 1 Tue, 21 Mar 2017 A1 2 Wed, 22 Mar 2017 A2 3 Thu, 23 Mar 2017 A3 4 Fri, 24 Mar 2017 A4 5 Thu, 30 Mar 2017 A5 6 Fri, 31 Mar 2017 A6 7 Mon, 3 Apr 2017 A7 8 Fri, 7 Apr 2017 A8 9 Mon, 10 Apr 2017 A9 10 Tue, 11 Apr 2017 A10 11 Wed, 12 Apr 2017 B1 12 Thu, 13 Apr 2017 B2 13 Mon, 17 Apr 2017 B3 14 Tue, 18 Apr 2017 B4 15 Wed, 19 Apr 2017 B5 16 Thu, 20 Apr 2017 B6 17 Fri, 21 Apr 2017 B7 18 Tue, 25 Apri 2017 B8 19 Wed, 26 Apr 2017 B9 20 Thu, 27 Apr 2017 B10

Students come to Angsoka room at sanglah hospital at 17.00. Group coordinator should report to Cief resident of internal medicine in Emergency Department. During the activity, students only act as observers. Students should using lab coat and sign the attendance form (attached in this study guide). Students are allowed to discuss the case with the cief resident. After the visit, each group have to make a report. If there is any problem please call the PIC

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ASSESSMENT METHOD

Final Assessment will be carried out on the 22nd day of the block period, Tue, May 2nd, 2017. The test will consist of 100 questions with 100 minutes provided for working. The student project topic will be included in the MCQ question (10-15% of the all MCQ Questions). The assessment will be held at the same time for both Regular Class and English Class. More detailed information or any changes that may be needed will be acknowledged at least two days before the assessment.

The passing score for this block is ³ 65. Final score will be sum up of student performance in small group discussion (5% of total score), student project (10% of total score), and score in final assessment (85% of total score). Clinical skill will be assessed in form of Objective structured clinical examination (OSCE) at the end of semester as part of Basic Clinical Skill Block’s examination.

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LEARNING PROGRAMS

Lecture 1,2,3

MACROSCOPIC STRUCTURE OF UPPER ALIMENTARY SYSTEM

The alimentary or digestive system consists of the organs and glands associated with the ingestion, mastication (chewing), deglutition (swallowing), digestion, and absorption of food and the elimination of feces (solid wastes) after the nutrients have been absorbed.The alimentary system includes organs of the alimentary canal (mouth, pharynx, esophagus, stomach, small and large intestine and accessory organs (teeth, tongue, salivary glands, liver, gallbladder, and pancreas). The mouth, pharynx, and esophagus: food enters the GI (gastro intestinal) tract via the mouth, which is continuous with the oropharynx posteriorly. The boundaries of the mouth are lips and cheeks, palate, and tongue. The tongue is mucosa-covered skeletal muscle. Its intrinsic muscles allow it to change shape; its extrinsic muscles allow it to change position. Saliva is produced by many small buccal glands and three pairs of major salivary glands-parotid, submandibular, and lingual-that secrete their product into the mouth via ducts. The 20 deciduous teeth begin to be shed at the age of 6 and are gradually replaced during childhood and adolescence by the 32 permanent teeth. Teeth function to masticate food. The C-shape stomach lies in the upper left quadrant of the abdomen. Its major regions are cardia, fundus, body, and pyloric region.

MICROSCOPIC STRUCTURE OF UPPER ALIMENTARY TRACT

The digestive system composed of the oral cavity, alimentary tract, and associated glands, function in the ingestion, mastication, deglutition, digestion, and absorption of food as well as elimination of its indigestible remnants. To perform these varied tasks, regions of the digestive system are modified and have specialized structures. The entire oral cavity is lined by a stratified squamous epithelium. The epithelial lining is divided into two types: (1) Masticatory epithelium, keratinised stratified squamous epithelium, covers the surfaces involved in the processing of food (tongue, gingivae and hard palate), and (2) Lining epithelium, non-keratinised stratified squamous epithelium, covers the remaining surfaces of the oral cavity. The tongue is a mass of striated muscle covered by a mucous membrane whose structure varies according to the region. The mucous membrane is smooth on the lower surface of tongue. The tongue’s dorsal surface is irregular covered anteriorly by great number papillae. The papillae consist of a connective tissue core covered with a stratified squamous epithelium. On the basis of their appearance four types of papillae can be distinguished : filiform, fungiform, circumvallate and foliate papillae Each tooth is composed of crown and roots, the crown is covered by enamel and the roots by cementum. The bulk of tooth is composed by dentin, which surrounds a space known as the pulp cavity. Tooth fixed firmly in its bony socket (alveolus) by periodontal ligament. The mucosa of oesophagus composed by a non-keratinised stratified squamous epithelium, a well-defined lamina propria and muscularis mucosae. Oesophageal glands are located in the submucosa produce a mucous secretion. The muscularis externa is somewhat unusual in that it contains striated muscle in its upper one third, a mixture of striated muscle and smooth muscle in its middle one-third and smooth muscle in its lower one-third. The adventitia consists only of a layer of loose connective tissue. The gastric mucosa consists of: (1) surface epithelium, that invaginates into the lamina propia forming gastric pits, (2) lamina propia is composed of loose connective tissue,

Udayana University Faculty of Medicine, DME, 2017 25 Study Guide Alimentary & Hepatobiliary Systems & Disorders filled with gastric glands which open into the bottom of each gastric pit, and (3) the muscularis mucosae. The fundal gastric glands are heavily branched tubular glands, subdivided into three region : (1) the isthmus, (2) the neck, and (3) the base. The glands is composed by six cells types: surface lining cells, parietal cells, stem cells, mucous neck cells, chief cells, and DNES cells. The gastric glands of the cardiac and pyloric region differs from that of the fundic region.

MACROSCOPIC AND MICROSCOPIC STRUCTURE OF LOWER ALIMENTARY TRACT

The small intestine is the longest portion of the alimentary tract, which 7 m in length. The small intestine has three regions: duodenum, jejunum, and ileum. Although these regions are similar histologically, their minor differences permit their identification. Throughout its length, the wall of small intestine is made up of the same four layers previously described for the stomach: (1) mucosa, (2) submucosa, (3) muscularis, (4) serosa. The luminal surface of small interstine is modified to increase its surface area. Three types of modifications have been noted: (1) plicae circulares (valves of Kerckring), (2) villi, (3) microvilli. The duodenum is the shortest segment of the small intestine, only 25 cm in length. It receives bile from the liver and digestive juices from the pancreas via the common bile duct and pancreatic duct, respectively. The duodenum differs from the jejunum and ileum in that its villi are broader, taller, and more numerous per unit area. It has fewer goblet cells, and there are Brunner’s glands in its submucosa. The villi of the jejunum are narrower, shorter, and sparser than those of the duodenum. The number of goblet cells per unit area is greater in the jejunum than in the duodenum. The villi of the ileum are the sparsest, shortest, and narrowest of the small intestine. The large intestine constitutes the terminal part of the alimentary system. It is divided into three main sections: cecum including the appendix, colon and rectum with the anal canal. The primary function of the large intestine is the reabsorption of water, inorganic salts and gases, through those processes the feces is formed and then excreted. The only secretion of any importance is mucus, which acts as a lubricant during the transport of the intestinal contents. The wall of large intestine is also divided into four layers as in the small intestine. Cecum and colon are similar histologically, they have no villi but its Crypts of Lieberkhun usually longer and straighter than small intestine. When its enter the rectum and anal, its become shorter and finally disappear in the distal half of anal canal. The histological appearance of appendix resembles the colon, except it is much smaller in diameter. Large intestine has specific structure, three flattened strands of outer longitudinal muscular layer, named taenia coli. In pectinate line region of anal the inner muscle layer is thickened to form internal sphincter.

MACROSCOPIC STRUCTURE OF LIVER, GALLBLADDER, AND PANCREAS

The liver is a lobed organ overlying the stomach. Its digestive role is to produce bile, which it secretes into the common hepatic duct. The gallbladder, a muscular sac that lies beneath the right liver lobe, stores and concentrates bile. The pancreas is retroperitoneal between the spleen and small intestine. Its exocrine product, pancreatic juice, is carried to the duodenum via the pancreatic duct. The subdivisions of the large intestine are the cecum (and appendix), colon (ascending, descending, and sigmoid portion, rectum, and anal canal. It opens to the body exterior at the anus. Liver and panceas secretion play important role in digestion process. Liver is synthesized and secreted bile and then store in the gall blader. Bile salt as one of the bile content is play important role in fat digestion as catalyst of pancreatic lipase. Pancreas secreted enzyme, amylase, lipase and proteolytic enzyme that digest carbohydrate, fat and

Udayana University Faculty of Medicine, DME, 2017 26 Study Guide Alimentary & Hepatobiliary Systems & Disorders protein in the intestine into smaller molecule and continued by eznzyme secreted bay enterocyter into monosaccharide and aminoacid. At the end of the study, medical student is expected to understand thefunction of bile salt and pancreatic enzyme and its regulatory

MICROSCOPIC STRUCTURE OF LIVER AND GALL BLADDER

The liver is the largest organ in the body,which completely enveloped by peritoneum, a simple squamous epithelium covering over the dense, irregular connective tissue capsule ( Glisson’ s capsule ) of the gland. The liver is composed of uniform parenchymal cells, the hepatocytes. The liver has both endocrine and exocrine function unlike pancreas. The superior aspect of the liver is convex, whereas the inferior region present a hillum-like identation the porta hepatis. The liver is subdivided into four lobes, right, left, quadrate and caudate lobes, in which each of lobe composed of three kind lobules (classical/hepatic, portal lobules and hepatic/portal acinus ). The three concepts of liver lobules based on blood flows, bile flows from periphery to the center of the lobule. The microscopic structure of the liver obviously seen that the hepatocytes arranged as a cells cord radialy to the central veins. Hepatocytes are polygonal cells that are closely packed together to form anastomosing plates of liver cells. The plasma membranes of hepotocytes are said have two domains, lateral and sinusoidal. The liver produces approximately 600 to 1200 ml of bile/day, which mostly water, contains bile salts ( bile acids ), bilirubin glucoronide ( bile pigment ), phospholipids, lecithin, cholesterol plasma electrolytes ( sodium and bicarbonate ) and IgA. It absorbs fat, eliminates approximately 80 % of cholesterol synthesized by the liver and excretes blood borne waste products such as bilirubin. In the lumen of the duodenum, bile salts emulsify fats and fasilate their digestion.

The gallbladder is, small, pear shaped organ situated on the inferior aspect of the liver. The bulk of the organ forms the body which is continuouswith cystic duct, is called the neck. It composed of four layers ; mucosa ( epithelium and lamina propria ), smooth muscle and serosa/ adventitia. The mucasa of empty gallbladder is highly folded to tall, paralel ridges. The lumen of gallbladder lined by simple columnar epithelium , whose cells are composed of two cell types : more common clear cells and infrequent brush cells. Histophysiology , the gallbladder stores, concentrate and releasesbile.Bile release is triggered by cholecystokinin and vagal stimulation.

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Lecture 2,4

FUNCTIONAL STRUCTURE OF UPPER ALIMENTARY SYSTEM

Food digestion is started in the mouth. Proper food digestion need both mechanical and enzymatic process. Mechanical process is support by teeth, tounge, chick and a group of skeletal muscle that open and closed the mouth during mastication. Enzymatic digestion is done by salivary enzyme, ptyalin, sedreted by salivary gland. the only enzyme in the saliva. Digested food than mix with saliva called bolus, readily to swallow. Complete swallowing process is started from mouth pass through stomach. The crusial point in swallowing process when bolus is pass through the pharynx. From pharynx bolur is move into the stomach by propulsive action of peristaltic. In stomach digestion is continued by mechanical and enzymatic process until the chime as the product of gastric digestion is emptied into the duodenum by pyloric pump mechanism. Complete digestion in duodenum need the participation of mechanical segmentl dan peristaltic movement) and enzymatic process secreted by pancreas, liver- gallblader and intestinal juice. The end product of digestion, then absorb epithelial cells of intestinal villi and transport into the liver through portal blood. or lymp vessels Both mechanical and enzymatic process are undercontrol by local reflex, hormonal and intramural and autonomic nervous system At the end of the study, medical student is expected to understand the phisiological process of both mechanical and enzymatic process and its regulatory.

FUNCTIONAL STRUCTURE OF LOWER ALIMENTARY SYSTEM AND IT’S CLINICAL IMPLICATION

The small intestine is the major digestive and absorptive organ. It extends from the pyloric sphincter to the ileocecal valve. Its three subdivisions are the duodenum, jejunum, and ileum. The bile duct and pancreatic duct join to form the hepatopancreatic ampulla and empty their secretions into the duodenum through the hepatopancreatic sphincter (of Oddi). The waste product of digestion is then pass through ileocarcal spincter into the colon. The process in colon is absorption of water and electrolit that the rest is drawn into the descend colon and everyday isthron out by defecation reflex At the end of the study, medical student is expected to understand the process digestion in the colon, defec ation process and its regulatory.

FUNCTION OF HEPATOBILIARY SYSTEM AND IT’S CLINICAL IMPLICATION (BILIRUBIN METABOLISM)

The Bilirubin as heme degradation product is transported to the liver where it reacts with a solubilizing sugar called glucoronic acid. This more soluble form of Bilirubin (conjugated) is excreted into the bile. The bile goes through the gall bladder into the intestines where the Bilirubin is changed into variety of pigments. The most important ones are stercobilin, which is excreted in the feces, and urobilinogen, which is reabsorbed back into the blod. The blood transports the urobilinogen back to the liver where it is either re- excreted into the bile or into the blood for transport to the kidneys. Urobilinogen is finally excreted as a normal component of the urine.

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Lecture 4

RATIONAL DRUG USE IN ALIMENTARY DISORDERS

Drugs used in acid-peptic disease Acid-peptic disorder includes hypersecretory, gastric ulcer, duodenal ulcer, and gastro esophageal reflux. Although the pathogenesis of peptic ulcer is not yet completely understood, it is clear that aggressive factors (HCl and pepsin) are dominant than defensive factor (gastroduodenal mucus, bicarbonate, microcirculation, prostaglandin and mucosal barrier. Helicobacter pylori has an important role in pathogenesis of acid-peptic disorder. Gastric HCl is secreted by parietal cell of the stomach, with it proton pump which influenced by K+ / H+ ATPase enzyme. Secretion of gastric HCl is stimulated by acetyl choline (M receptors), histamine (H2 receptor), and gastrin (G receptor). The aims of therapy in peptic ulcer includes relieve the pain, promote ulcer healing, decrease recurrent rate and eradicate Helicobacter Pylori, with reduce the acidity of the stomach or enhance defense mechanism of mucosal through cytoprotective agent or antimicrobial agent. Currently, drugs are available that may neutralize gastric acid (Antacid), reduce gastric acid secretion with anti-muscarinic (pirenzepine), H2 receptor antagonist (cimetidine, ranitidine, famotidine), Proton Pump Inhibitor (omeprazole, lansoprazole, rabeprazole), mucosal protective agents (sucralfate, colloidal bismuth, carbenoxolone, prostaglandins).

Drugs promoting gastrointestinal motility (prokinetic agents) Metoclopramid and cisapride: · Hasten esophageal clearance · Raise lower esophageal sphincter pressure · Accelerate gastric emptying · Shorten small bowel transit time

Antiemetic drugs Nausea and vomiting may happen in pregnancy, motion sickness, gastrointestinal obstruction, peptic ulcer, drug toxicity (cancer chemotherapy), myocardial infarction, renal failure and hepatitis. Antiemetic drugs include H1 antihistamine, phenothiazine, metoclopramide, ondansetron, marihuana, corticosteroids. Laxatives are used in constipation patients. These drugs are classified by 4 mechanism of action, such as irritants or stimulants, bulking agents, stool softeners, and lubricant. The most effective antidiarrheal drugs are diphenoxylate and loperamide. These are opioid derivative that have maximal antidiarrheal and minimal CNS effect. Adsorbents such as kaolin and pectin are also widely used. This drug able to adsorb compound from solution, presumably binding potential intestinal toxins. The principle drugs used in the treatment of chronic inflammatory bowel disease are Salicylate derivative, Corticosteroid and other immunosuppressive agents.

RATIONAL DRUGS USE IN HEPATOBILIARY DISORDERS

In pancreatic insufficiency, steatorrhea will occur because fat absorption is decrease. Two mayor type of preparation in use are Pancreatin and Pancrelipase. Cimetidine or Antacid enhances the effectiveness of these enzyme. The most side effect of the enzyme is uric acid renal stones.

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Lecture 5

ETIOPHATOGENESIS AND MORPHOLOGIC FEATURES OF ALIMENTARY DISORDERS

The alimentary tract is a hollow tube extending from the oral cavity to the anus, that consists of esophagus, stomach, small intestine, appendix, colon, rectum and anus. Each segment has unique complementary and highly integrated functions which together serve to regulate the intake, processing and absorbtion of the ingested nutrients the disposal of the waste product. The regional variations in structure and function are reflected in diseases of the alimentary tract which often affect one or another segment preferentially. When present within the esophagus, they were discovered shortly after birth, usually because they cause regurgitation during feeding. Another disorders or diseases in esophagus such as esophagitis, Barrett Esophagus, esophageal carcinoma. Diseases in stomach such as acute and chronic gastritis, gastric ulcer and tumors. Diseases in small and large intestine,such as developmental anomalies ( Hirschsprung Disease), vascular disorders (Ischemic Bowel Disease,Hemorrhoids), diarrheal diseases(Diarrhea and dysentery, Infectious Enterocolities, Malarbsorbtion Syndromes), Idiopathic Inflammatory Bowel Disease (Crohn Disease, Ulcerative Colitis),Colonic Diverticulosis, Bowel Obstruction, Benign and malignant tumors, Gastrointestinal lymphoma, Acute and Chronic Appendicitis. By learning the etiopathogenesis and morphologic changes also by using microbiology and immunology technology, pathology attempts to explain the ways and wherefores the signs and symptoms manifested in patients while providing a sound foundation for rational clinical care and therapy.

ETIOPHATOGENESIS AND MORPHOLOGIC FEATURES OF HEPATOBILIARY DISORDERS

LIVER The liver is vulnerable to a wide variety of metabolic, toxic, microbial, circulatory, and neoplastic insults. The liver has a relatively limited repertoire of cellular and tissue responses to injury, regardless of cause. The most common are : hepatocyte degeneration and intracellular accumulations, hepatocyte necrosis and apoptosis, inflammation, regeneration and fibrosis. Among inflammatory disorders, viral infection is by far the most frequent. Unless otherwise specified, the term viral hepatitis is applied for hepatic infections caused by a group of viruses known as hepatotropic virus (hepatitis viruses A, B, C, D, and E) that have a particular affinity for the liver (Table 18-4, page 844). Liver abscesses, a form of liver infection that is common in developing countries, deserve special mention. They are usually caused by echinococcal and amebic infections and less commonly, by other protozoal and helminthic organisms. In developed countries liver abscesses are uncommon; the incidence of amebic infections is low and is usually present in immigrants from endemic regions. Most such abscesses are pyogenic, representing a complication of a bacterial infection elsewhere. The organisms reach the liver by (1) the portal vein, (2) arterial supply, (3) ascending infection in the biliary tract (ascending cholangitis), (4) direct invasion of the liver from a nearby source, or (5) a penetrating injury. Morphologic features of liver abscess show solitary or multiple lesions, from millimeters to massive lesions (many centimeters) in diameter. Microscopic features consist of pyogenic abscess, occasionally fungi, parasites and bacteria can be identified. Excessive alcohol (ethanol) consumption is the leading cause of liver disease in most Western countries. In the United States, 50% of the population 18 years of age or

Udayana University Faculty of Medicine, DME, 2017 30 Study Guide Alimentary & Hepatobiliary Systems & Disorders older drink alcohol. A subset of these individuals suffer serious health consequences associated with alcoholism. Of greatest impact is alcoholic liver disease. There are three distinctive, albeit overlapping, forms of alcoholic liver disease: (1) hepatic steatosis (fatty liver disease), (2) alcoholic hepatitis, and (3) cirrhosis. Morphologic features of fatty liver show small (microvesicular) lipid droplets in hepatocytes, and become macrovesicular in chronic intake. Alcoholic hepatitis characterized by hepatocyte swelling and necrosis, present of Mallory bodies, infiltration of neutrophilic and fibrosis. Alcoholic cirrhosis characteristic by bridging fibrous septa, parenchymal nodules and disruption of the architecture of the entire liver. The most severe clinical consequence of liver disease is hepatic failure. The alterations that cause liver failure fall into three categories : acute liver failure, chronic liver disease and hepatic dysfunction without overt necrosis. Three particular complications associated with hepatic failure merit separate consideration, since they have grave implications : hepatic encephalopathy, hepatorenal syndrome, and hepatopulmonary syndrome. Malignant tumors occurring in the liver can be primary or metastatic. Most primary liver cancers arise from hepatocytes and are termed hepatocellular carcinoma (HCC). Much less common are carcinomas of bile duct origin, cholangiocarcinomas. The incidence of these two cancers is increasing in the United States. Four major etiologic factors associated with HCC have been established: chronic viral infection (HBV, HCV), chronic alcoholism, non-alcoholic steatohepatitis (NASH), and food contaminants (primarily aflatoxins). Other conditions include tyrosinemia, glycogen storage disease, hereditary hemochromatosis, non-alcoholic fatty liver disease, and α1-antitrypsin deficiency. Many factors, including genetic factors, age, gender, chemicals, hormones, and nutrition, interact in the development of HCC. HCC may appear grossly as unifocal, multifocal, and diffuse infiltrative. Histologically range from well differentiated lesions to poorly differentiated, globule of bile within cytoplasm of cell and in pseudocanaliculi, scant stroma, and acidophilic hyaline inclusion in cytoplasm. Cholangiocarcinoma mostly exhibit well- differentiated adenocarcinoma with abundant fibrous stroma (desmoplasia).

GALLBLADDER 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. There are two main types of gallstones. In the West, about 90% are cholesterol stones, containing more than 50% of crystalline cholesterol monohydrate. The rest are pigment stones composed predominantly of bilirubin calcium salts. When cholesterol concentrations exceed the solubilizing capacity of bile (supersaturation), cholesterol nucleate into solid cholesterol monohydrate crystals. Risk factors for gallstones : see table 18-9 (page 883). Inflammation of the gallbladder may be acute, chronic, or acute superimposed on chronic. It almost always occurs in association with gallstones. In acute cholecystitis the gallbladder is usually enlarged and tense, and it may assume a bright red or blotchy, violaceous to green-black discoloration, imparted by subserosal hemorrhages. The serosal covering is frequently layered by fibrin and, in severe cases, by a definite suppurative, coagulated exudate. In calculous cholecystitis, an obstructing stone is usually present in the neck of the gallbladder or the cystic duct. The gallbladder lumen may contain one or more stones and is filled with a cloudy or turbid bile that may contain large amounts of fibrin, pus, and hemorrhage. When the contained exudate is virtually pure pus, the condition is referred to as empyema of the gallbladder. The inflammatory reactions are not histologically distinctive and consist of the usual patterns of acute inflammation. The morphologic changes in chronic cholecystitis are extremely variable and sometimes minimal. The serosa is usually smooth and glistening but may be dulled by subserosal fibrosis. Dense fibrous adhesions may remain as sequelae of preexistent acute inflammation. On sectioning, the wall is variably thickened, and has an opaque gray-white appearance. In the uncomplicated

Udayana University Faculty of Medicine, DME, 2017 31 Study Guide Alimentary & Hepatobiliary Systems & Disorders case the lumen contains fairly clear, green-yellow, mucoid bile and usually stones. The mucosa itself is generally preserved. On histologic examination the degree of inflammation is variable. In the mildest cases, only scattered lymphocytes, plasma cells, and macrophages are found in the mucosa and in the subserosal fibrous tissue. In more advanced cases there is marked subepithelial and subserosal fibrosis, accompanied by mononuclear cell infiltration. Reactive proliferation of the mucosa and fusion of the mucosal folds may give rise to buried crypts of epithelium within the gallbladder wall. Outpouchings of the mucosal epithelium through the wall (Rokitansky-Aschoff sinuses) may be quite prominent. A major contributor to neonatal cholestasis is biliary atresia, representing one third of infants with neonatal cholestasis and occurring in approximately 1 : 12,000 live births. Biliary atresia is defined as a complete or partial obstruction of the lumen of the extrahepatic biliary tree within the first 3 months of life. It is characterized by progressive inflammation and fibrosis of intrahepatic or extrahepatic bile ducts. Biliary atresia is the single most frequent cause of death from liver disease in early childhood and accounts for 50% to 60% of children referred for liver transplantation, as a result of the rapidly progressing secondary biliary cirrhosis. The salient features of biliary atresia include inflammation and fibrosing stricture of the hepatic or common bile ducts, periductular inflammation of intrahepatic bile ducts, and progressive destruction of the intrahepatic biliary tree. On liver biopsy, florid features of extrahepatic biliary obstruction are evident in about two thirds of cases, that is, marked bile ductular proliferation, portal tract edema and fibrosis, and parenchymal cholestasis.

PANCREAS Pancreatitis is inflammation in the pancreas associated with injury to the exocrine parenchyma. The clinical manifestations range in severity from a mild, self-limited disease to a life-threatening acute inflammatory process, and the duration of the disease can range from a transient attack to a permanent loss of function. In acute pancreatitis the gland can return to normal if the underlying cause of the pancreatitis is removed. By contrast, chronic pancreatitis is defined by the irreversible loss of exocrine pancreatic parenchyma. The morphology of acute pancreatitis ranges from trivial inflammation and edema to severe extensive necrosis and hemorrhage. The basic alterations are (1) microvascular leakage causing edema, (2) necrosis of fat by lipolytic enzymes, (3) acute inflammation, (4) proteolytic destruction of pancreatic parenchyma, and (5) destruction of blood vessels and subsequent interstitial hemorrhage. Chronic pancreatitis is characterized by parenchymal fibrosis, reduced number and size of acini with relative sparing of the islets of Langerhans, and variable dilation of the pancreatic ducts. These changes are usually accompanied by a chronic inflammatory infiltrate around lobules and ducts. The interlobular and intralobular ducts are frequently dilated and contain protein plugs in their lumens. The ductal epithelium may be atrophied or hyperplastic or may show squamous metaplasia, and ductal concretions may be evident. Acinar loss is a constant feature. The remaining islets of Langerhans become embedded in the sclerotic tissue and may fuse and appear enlarged. Eventually, they too disappear. Grossly, the gland is hard, sometimes with extremely dilated ducts and visible calcified concretions. A broad spectrum of exocrine neoplasms can arise in the pancreas. They may be cystic or solid; some are benign, while others are among the most lethal of all malignancies. Approximately 60% of cancers of the pancreas arise in the head of the gland, 15% in the body, and 5% in the tail; in 20% the neoplasm diffusely involves the entire gland. Carcinomas of the pancreas are usually hard, stellate, gray-white, poorly defined masses. The vast majority of carcinomas are ductal adenocarcinomas that recapitulate to some degree normal ductal epithelium by forming glands and secreting mucin. Two features are characteristic of pancreatic cancer: It is highly invasive (even “early” invasive pancreatic cancers extensively invade peripancreatic tissues), and elicits an intense non-neoplastic host reaction composed of fibroblasts, lymphocytes, and extracellular matrix (called a “desmoplastic response”). The appearance is usually that of a moderately to poorly

Udayana University Faculty of Medicine, DME, 2017 32 Study Guide Alimentary & Hepatobiliary Systems & Disorders differentiated adenocarcinoma forming abortive tubular structures or cell clusters and showing an aggressive, deeply infiltrative growth pattern.

LIVER FUNCTION TEST

Liver function tests are useful in detecting, diagnosing, evaluating severity, monitoring therapy and assessing the prognosis of the liver disease and dysfunction. They are also useful in directing further diagnostic workup. The array of tests useful for these purposes include measurement in serum of total bilirubin, protein and albumin levels and the activity of enzymes such as the aminotransferases (AST and ALT), ALP, LDH and GGT. There is no one specific test for assessment of liver disease. However, the combination of a number of tests that assess different parameters of liver physiology obtained serially over time and interpreted within the clinical context may serve in establishing the diagnosis and prognosis and help in following the course of the hepatic dysfunction. The most useful laboratory tests in liver disease may be grouped into three categories. These are tests that reflect liver cell injury and necrosis, synthetic function of the liver and cholestasis from intra or extrahepatic biliary obstruction or infiltrative processes in the liver, or both.

Lecture 6

IMAGING OF ALIMENTARY SYSTEM

Upper GI tract includes pharynx, oesophagus, stomach and duodenum. Imaging examination for evaluating upper GI tract disorders are pharyngo-oesophagogram/ oesophagogram , upper GI study and abdominal CT scan. Every kind of imaging modality has its own indication. Lower GI tract includes ileum, jejunum, caecum, ascending colon, transverse colon, descending colon, sigmoid colon sigmoid and rectum. Imaging investigations in order to evaluate the lower GI tract are barium follow through, barium enema and abdominal CT scan for specific cases e.g tumor. For obstructive ileus, plain abdominal x-photo in several positions are needed to exclude perforation of the hollow organ. There are many imaging modalities for studying hepatobilier system and pancreas. Those could be non invasive, invasive, non-ionizing radiation or with ionizing radiation. Those include simple radiography, contrast study, ultrasound, radioisotope scanning, CT scan , MRI and angiography. When we are choosing for radiological examination, we better consider about indication, advantage and weakness of each imaging modality.

IMAGING STUDIES OF HEPATOBILIARY SYSTEM

There are many imaging modalities for studying hepatobilier system and pancreas. Those could be non invasive, invasive, non-ionizing radiation or with ionizing radiation. Those include simple radiography, contrast study, ultrasound, radioisotope scanning, CT scan , MRI and angiography. When we are choosing for radiological examination, we better consider about indication, advantage and weakness of each imaging modality.

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Lecture 7

ORAL CAVITY DISORDERS

GLOSSITIS Glossitis or inflamation of the tongue occurs in many form. It may be acute or chronic, superficial or deep and the disease maybe idiopathic or symptomatic. Moller’s glossitis, known as chronic superficial excoriation of the tongue or glossodynia exfoliata. Acute glossitis is condition characterized by an acute inflamation of the ephithelial cells of the tongue. Chronic glossitis may be caused by repeated acute attack of long continued irritation.

HERPPES SIMPLEX Primary herpes simplex (primary herpetic gingivostomatitis) usually occurs betwen one and five years of age and has been estimated to occur in less than 1 per cent of the population. The symptoms are the acute vesicular lesions last from 5 to 7 days and are accopanied by high fever, dehydration, malaise, nausea and even somnolence and convulsions. Initially the gingiva becomes swollen, with assosiated salivation, fetor oris, dysphagia and painful lymphadenopathy. Treatment consist largely supportive therapy, topical anestetics and enriched liquid diet. Secondary(recurrent) herpes simplex. The most common form of herpetic infection, secondary herpes simplex, possibly affect 25 to 50 per cent of adult population. The symptoms are burning, itching or tingling sensations in the region of the forming lesions. This consists of of groups of small clear vesicles than soon become transformed into pustules or crusted comfluent erotions located most often on the vermillion or mucocutaneus junction of the upper or lower lip. Treatment is largely ineffective. The immunosuppressed patient should be treated with oral or intravenous acyclovir.

RECURRENT APHTHOUS STOMATITIS Recurrent aphthous stomatitis is adisorder that affects abaut 20 per cent of the population. The disorder is of unknown etiology. The symptom is a burning sensation in the affected mucosa during the prodromal stage, the mucosa becomes focally erythematous and necrotic with formation of singel or multiple, round to oval ulcerations usually 2 to 10 mm n diameter. The ulcer is covered by a grayish whitefibrinous exudate and surrounded by a bright red halo. Treatment xylocaine ointment and tetracycline swish and swallow suspensions.

HERPES ZOSTER Herpes zoster is recurrent neutrophic manifestation of reactivated chickenpox virus. After an incubation period of 4 to 20 days, the disorder appears with a neuralgic prodromal phase.Withtin two to three days, grouped vesicles form in the area innervated by the involved nerve. On the oral mucosa, the lesions most diffuse. The unilocular zoster vesicle is especially short-lived. It rapidly changes into painful aphtha surounded by red halo. Treatment intravenous acyclovir or vidarabine.

CANDIDIASIS Candida albicans is universal and can be found in about 39 per cent of oral smears taken rountinely from patient. Oral candidiasis may be diffuse or localized as angular cheilosis, superficial monilial stomatitis, denture stomatitis and deep granulomatous candidiasis. In superficial monilial stomatitis, the clinical picture ranges from mild erythema with fine, whitish deposits to diffuse, imflamed white mouth. The lesions, resembling snow- white, curdled milk, can present as strips, plaques and diffuse pseudomembrane. In denture

Udayana University Faculty of Medicine, DME, 2017 34 Study Guide Alimentary & Hepatobiliary Systems & Disorders stomatitis, the patient complains of swelling, sensitivity and pain of the oral mucous membrane at the points of denture contact. Treament of oral candidiasis consists of improved oral hygiene and nutritional status, corection of the irritating factor, correction of the underlying disorder and the use oral nystatin suspension, ointment or tablets. Clotrimazole troches may also be used.

ANGINA LUDWIG’S This is a diffuse cellulitis of the floor of the mouth and neck, which may occur following extraction of an abscessed tooth. It has been obeserved associated with an acute parotitis. And it occasionally develos during or after an infectious fever. The usual organism found are streptococcus, staphylococcus, and pneumococcus: the presence of E.coli, gas bacillus and Vincent’s organisms has also been reported. The condition is characterized by a massive, brawny sewwling of the floor of the mouth, submaxillary and suprahyoid regions. The skin is edematous and reddened. Trismus is usually present and the tongue is swollen, tender and can be moved only with great difficulty and pain. Swallowing is painful and with very extensive edema, breathing becomes labored. The patient appears acutely ill and temperature is elevated. Immediate treatment is demanded. Multiple well-placed incisions to drain the various muscle and connective tissue planes are required. Tracheostomy may be indicated if breathing is difficult and should be done if extensive edema is a dominant feature. Cultures should be obtained and immediate antibiotic treatment instituted. These patients are best cared for in a semi-sitting position. Additional measures such as an oxygen tent, blood transfusions, and parenteral feeding may be indicated, depending on severity of the condition.

LEUKOPLAKIA Leukoplakia of the mucous membranes of the oral cavity is probably the most commonoral lesion. It is a white patch varying in thickness and in extent. Histologically, one sees a thickening of the squamous mucous membrane with hyperkeratinization on the surface. Inflammatory reaction in the subepithelial structures is commonly seen. Leukoplakia is considered to be caused by forms of chronic irritation such as tobacco, ill fitting dentures, and poor condtion of teeth. In many cases no visible form of chronic irritation can be found. Leukoplakia has been associated with avitaminosis. However, therapeutic doses of vitamin A nd B complex have failed to cure lekoplakia. The various causes of leukoplakia are still to be discovered. Leukoplakia not associated with syphilis is observed in about 40 per cent of the patients with cancer of the tongue. In cancer of the cheek it is reported in the literature to vary from 10 to 70 per cent. The malignant nature of leukoplakia is well demonstrated by the following case. M.K., age 77. First seen on July 19, 1946, at which time she had noted a white spot on left side of tongue of about one month duration. She denied smoking. Examination revealed a well developed, well nourished, elderly white female. She was edentulous but the appearance of the buccal and upper and lower alveolar ridge mucous membrane was normal. On the left lateral aspect of the tongue, adjacent to its junction with the mucous membranes of the floor of the mouth, was an area of leukoplakia 1 cm in diameter. There was no underlying induration nor any superficial ulceration. The Wassermann reaction was negative. Under conservative treatment of a nonirritating mouth wash, brewer’s yeast and leaving the dentures out of the mouth, the leukoplakia improved but never completely disappeared. She was observed periodically at interval of three months. On February 10, 1949, approximately two and a half years after her first visit, she was examined and although same leukoplakia was present, nothing unusual was noted. Two months later, April 14, the patient became alarmed because the area of leukoplakia had ulcerated and begun to increase in size. A biopsy which was immediately performed showed an invasive squamous cell carcinoma. A partial resection of the tongue was performed and the patient remain well until her dead from cardiovascular disease several years later.

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EPIDEMIC PAROTITIS (MUMPS) Epidemic parotitis is a swelling of a salivary glands, especially the parotids caused by a filterable virus which may be demonstrated in the blood stream and saliva of affected individuals. In the male the complication of orchitis may result in atrophy or destruction of the testes. Other complications such as oophoritis, mastitis and vulvitis are occasionally seen.

ACUTE SUPPURATIVE PAROTITIS This condition is characterized by a marked swelling of one parotid gland, high fever, tenderness and pain which is increased by mastication, followed later by redness of the skin and fluctuation. Thick greenish pus can be expressed from the duct. As the condition progresses all of the tissue of the face and oral cavity on the affected side become involved in a diffuse phlegmon. Spontaneous rupture may occur through the skin of the face, mucosa of the cheek and floor of the mouth. The phlegmon may extend to involve the tissues of the neck, not only unilaterally, but bilaterally. Facial paralysis, hemorrhage, septicemia and meningitis may occur. The mortality is reported to be as high as 45 per cent. Acute suppurative parotitis has been observed to occur (1) after severe infections in or about the mouth, (2) as complications of general infections, such as pyemia, scarlet fever , typhoid (3) following abdominal operations, and (4) following a history of chronic recurrent parotitis. The offending organism are usually staphylococci however streptococci have been reported. Treatment of this severe illness must be aggressive. Specific sensitivity to antibiotics should be determined immediately and antibiotics employed in therapeutic doses. Fluctuant areas should be widely incised to provided depended drainage. If this is not done fluctuant areas of skin will necrose and drain spontaneously. The gland is best drained by an incision parallel with and just anterior to the ear and a second one below the angle of the jaw in the upper neck. The position and extent of additional incisions will depend on the extent of infections. Drains should be kept in these incisions to prevent their closure and to permit irrigation of the abscessed areas with saline solution and antibiotics. Drainage within the oral cavity may be indicated and should be provided. Extensive edema along with a fulminating infection may encroach on the airway by pressure or laryngeal edema. Tracheotomy in such cases is imminent. Heat may be employed for local relief. Frequent oral irrigations with lukewarm water are indicated to cleanse the mouth. The blood picture should be studied at intervals and blood transfusions given as required. Parenteral feedings and analgesics are indicated.

CHRONIC SUPPURATIVE PAROTITIS Chronic suppurative parotitis is characterized by a recurrent swelling of the parotid and a discharge of thick pus or cloudy, flaky saliva from the duct. Not infrequently a very thick mucoid secretion may be obtained. As the secretion becomes inspissated, flakes of calcium or other detritus and sometimes casts of the duct can be expressed from the duct orifice. The swelling of the gland usually lasts from three to ten day and in some cases for even longer periods, the swelling may recur at intervals of weeks or months. The etiology is not always known. Sometimes this swellings occur spontaneously without any apparent reason. Quite frequently swelling of the gland occurs after eating. It is possible therefore that during mastication minute particle of food, mucoid debris or in the presence of oral infection small accumulation of pus are forced into the duct orifice, thereby producing an obstruction. This result in a retention of parotid secretion and the gland gradually becomes diffusely enlarged. It seems probable therefore that the bacteria trapped in such an obstructed duct are in a medium which promotes their multiplication while in a normal unobstructed duct they are continually washed out of the duct system. The roentgen findings in chronic recurrent parotitis are sometimes similar to those observed in acute inflammations. Stensen’s duct is generally dilated and may be observed presenting a pouting appearance. It may contain non opaque, inspissated collections which after

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Lipiodol injection present a beaded appearance on the roentgenograms. On the affected portions of the gland small spherical collections or droplets of Lipiodol, simulating the picture seen in the bronchiectasis are seen. Occasionally only portions of the gland may be involved, but more frequently the entire gland presents this roentgen appearance. In about 30 to 40 per cent of the cases the conditions is bilateral. Identical roentgen changes may be seen with duct calculi, intermittent duct obstruction by tumor and occasionally by stricture.

TEETH AND PERIODONTIUM DISEASES

Dental Caries is defined as an initial lesion (white spot) to deep cavities on the teeth which are cause by some multi factors that could establish the lesion or cavity. The severity of Dental Caries depends on the depth of the cavity and the symptoms that usually being complained by the patient. Gingivitis is defined as inflammation of the gingival while Periodontitis is defined as inflammation at the periodontal membrane, which are also caused by some multi factors that could establish the inflammation.

Lecture 8

ESOPHAGEAL DISORDERS

ACHALASIA Achalasia (cardio spasm) is the name of an esophageal condition characterized by failure of cardiac end of the esophagus to open and a dilatation of the esophagus proximal to this obstruction. This is apparently a disorder of the coordinated mechanism of deglutition. The exact cause is unknown. Etiology is always such a complex and controversial. Same investigators have reported the finding of peri esophageal fibrosis. Neurogenic changes in the vagus and over action of the sympathetic nerve as a cause of closure (aganglionair plexus of Auerbach). Dysphagia, epigastric pain and regurgitation are the characteristic symptoms. Diagnosis largely on a combination of patient complains and radiography. The x-ray esophagus with contrast Barium show obstruction of one-third distal esophagus with marked dilatation above, like mouse tail appearance. Management of achalasia are : dilatation with bougie through the esophagoscopy or operation if dilatation is no success.

ATRESIA ESOPHAGUS Congenital atresia of the esophagus with or without associated fistula intro the airway in the newborn can be remedied by prompt surgical treatment, provided the condition is diagnosed without delay. The symptoms are related to feeding, and any intake of fluid result in coughing, choking, and attacks of cyanosis. The symptoms disappears after feeding attempts are discontinued and the infants condition improves until subsequent liquid intake reproduces the respiratory distress. Roentgen film demonstrate air in the stomach and gastrointestinal tract when a connection exist between the air and food passages and an absence of air below the diaphragm when atresia of the esophagus is unaccompanied by fistula intro the tracheobronchial tree. The diagnosis is made by passing a small No.8 catheter down the esophagus until it stopped at the level of atresia. Confirmation can be obtained by the used of contrast media,

Udayana University Faculty of Medicine, DME, 2017 37 Study Guide Alimentary & Hepatobiliary Systems & Disorders preferably iodized oil. A certain amount of this material invariably enters the lung and if a barium mixture is used, severe pulmonary reaction develops. Prompt recognition of the characteristics symptoms will lead to the diagnosis so that surgical correction can be performed within the first 12 to 24 hours of life. It is necessary that the surgery be done early to prevent the pneumonitis occurring from aspiration. In a series of case from the Boston Children’s Hospital 75 per cent of those surviving operation were discharge after three weeks. Surgical treatment entails closure of the communication between the airway and the lower segment with direct anastomosis of the two esophageal segments if possible or closure of the fistula, exteriorization of the upper segment in the neck and anterior gastrostomy. Gastrostomy alone is not adequate.

CORROSIVE LESSIONS OF ESOPHAGUS Corrosive esophagitis is most commonly produced by ingestion of house hold cleaning agents, usually by children or in adult suicide attempts. The most destructive is sodium hydroxide, or lye which cause lysis of tissue and often deep penetration of the esophageal wall. Symptoms of the ingestion agent, is burn of the lips, mouth, tongue, palate and pharynx. Dysphagia due to burn and secondary infection develops. In the healing process of circumferential scar constricts the esophagus, producing an esophageal stenosis. The presence of esophageal lesions can be established only by esophagoscopy. Early diagnosis and treatment are essential to be avoided the stenosis. Systemic broad spectrum antibiotics are begun and continued thought therapy to control infection. Steroid therapy must be initiated in first 48 to 96 hours after the ingestion. When there is significant pain with swallowing, the patient is given no food by mouth, and a small polyethylene nasogastric tube is passed and left place until healing is complete. Follow up should include repeated esophagogram. In patients who develop strictures, dilatation may be accomplished using esophagoscope or mercury-filled rubber bougie.

GERD (GASTROESOPHAGEAL REFLUX DISEASE) Reflux-induced esophageal injury (reflux esophagitis) is recognized endoscopically by the presence of erosions and ulcerations in the squamous epithelium of the esophagus. When the reflux of gastric material into the esophagus causes symptoms, tissue damage, or both, the resulting condition is called gastroesophageal reflux disease (GERD). Term NERD (nonerosive reflux disease) was used for patient with symptom and negative on endoscopic finding. Heartburn and regurgitation are the symptoms most frequently associated with GERD. Heartburn, is an uncomfortable, hot or burning sensation located beneath the sternum. Reflux esophagitis can be complicated further by the development of esophageal strictures and columnar epithelial metaplasia (Barrett's esophagus). Diagnostic tests may be required for patients with atypical signs or symptoms or for patients with typical signs and symptoms that do not respond well to acid suppression. For patients who are found to have severe, ulcerative, reflux esophagitis, it may be appropriate to begin therapy immediately with potent acid suppression.

GASTRIC CANCER Diagnosis of gastric cancer should be suspected in patients over the age of ~ 50 years with epigastric symptoms of new onset, including early satiety, anorexia, nausea and vomiting, and especially when there are associated alarm symptoms of anemia, weight loss etc. However, by this stage the disease is likely to be advanced. Confirmatory diagnosis is usually made at endoscopies when biopsies and the intraluminal extent can be determined. Routine barium meal is of little value in diagnosis although the tumor will invariably be seen. Ultrasound may sometimes be helpful and abdominal CT scan can be used to determine the extent of disease and any metastasis spread. Gastric cancer may spread within the abdomen, for example to the ovaries (Krukenburg tumour).Staging of the tumor is usually

Udayana University Faculty of Medicine, DME, 2017 38 Study Guide Alimentary & Hepatobiliary Systems & Disorders undertaken to determine prognosis and progress of the cancer. The widely used TNM (Tumor, Node, Metastasis) system is usually used and can help decide on the best course of treatment. Staging determines characteristics of the tumor and the extent of spread to other parts of the body.Treatment of gastric cancer is usually surgical, although a palliative endoscopic procedure with tumour debulking may be considered in patients unfit for a definitive procedure. Surgical approaches involve partial, or sometimes total, gastrectomy depending on the location and extent of the tumour. The procedure may also involve removal of any lymph nodes involved in the malignancy. The more radical procedures will involve complex anastomosis to maintain continuity of the gut and esophago-jejunal anastomosis in the case of total gastrectomy. Careful long-term follow up of such patients is essential to maintain optimal nutritional status. Radiation therapy and chemotherapy may also be used depending on the extent and stage of the tumour. Current chemotherapeutic agents may include epirubicin, cisplatin, 5-fluorouracil while the newer generation of chemotherapeutic agents, such as gemcitabine, irinotecan and paclitaxel and the recent introduction of “biological” or immunological treatments or vaccines, which block growth signals, inhibit angiogenesis, stimulate the bodies own immune system etc., offer new hope for patients with a condition that has traditionally carried a very poor outlook. A healthy diet, rich in fruits and vegetables and low in salt, pickles, nitrates and nitrites is likely to carry a reduced risk of gastric cancer. It is not clear to what extent heredity is important although numerous reports of familial gastric cancer are documented. The common originating factor may still be infection with H. pylori in a household. The new information on genetics mentioned above will help clarify this. An important question that is not yet answered is whether widespread eradication of (or vaccination against) H. pylori infection will reduce or prevent gastric cancer. A large number of trials with differing endpoints is under way but it seems clear that treatment would need to be given relatively early in life before intestinal metaplasia and dysplasia have occurred for cancer to be prevented. Guidelines in Canada recommend that H. pylori infection be eradicated whenever detected.

Lecture 9

Stomach and Duodenum Disorders 1

Gastritis

Gastritis is defined as microscopic inflammation of the stomach and represents a histological, not a clinical entity, and the majority of persons with gastric inflammation are completely asymptomatic. A myriad of etiological agents can induce gastritis, but the most common cause is infection by Helicobacter pylori, a bacterium that resides in the mucus gel layer overlaying the gastric mucosa. Since that time, a strong link has been established between H. pylori and a diverse spectrum of gastroduodenal diseases, including gastric and duodenal ulceration, gastric adenocarcinoma, mucosa-associated lymphoid tumor (MALToma), and non-Hodgkin lymphoma of the stomach. H. pylori colonizes the stomach for years or decades, not days or weeks as is usually the case for bacterial pathogens, and this organism virtually always induces chronic gastritis; however,only a fraction of H. pylori-colonized individuals ever develop disease.

The most widely used method for classification of gastritis and reporting of non-neoplastic gastric biopsies in the research setting is the updated Sydney system, which classifies

Udayana University Faculty of Medicine, DME, 2017 39 Study Guide Alimentary & Hepatobiliary Systems & Disorders chronic gastritis based on topography, morphology, and etiology. More recently, a system of staging gastritis, the Operative Link for Gastritis Assessment (OLGA) has been proposed. The OLGA system incorporates the updated Sydney system biopsy mapping protocol but includes more detailed assessment of glandular atrophy, with the goal of providing increased information about gastric cancer risk.

A second group of conditions characterized by gastric mucosal aberrations with little or no inflammation were historically included in classifications of gastritis, but are now categorized as gastropathies

Peptic Ulcer Disease

Peptic ulcers are localized defects of the GI mucosa extending to at least the depth of the muscularis mucosa. Arteries are located deep to the muscularis so superficial lesions are less likely to result in complications. Through the endoscope, an ulcer is identified as a mucosal break with depth. The arbitrary criterion (used in most clinical trials) is that an ulcer has a diameter of 5 mm or larger, and lesions smaller than 5 mm are called erosions. The utility of this differentiation is debatable as they often reflect the same underlying disease. However, minor erosions can also be a normal finding and are much less likely than ulcers to cause symptoms, or lead to complications such as significant bleeding or perforation. Ulcers and erosions may be single or multiple.

Peptic ulcer disease most commonly affects the gastroduodenal mucosa and is divided into gastric ulcer (GU) and duodenal ulcer (DU), though can occur at more than one site. Mechanistically, DUs and pyloric and prepyloric GUs are distinct from other GUs. However, in practice there are only minor differences in their management. Ulcers may occur at other sites including the gastroesophageal junction, sites of GI anastamosis, and in ectopic gastric mucosa, most frequently within a Meckel's diverticulum or in esophageal inlet patches. Duodenal ulcers typically occur within the duodenal bulb. If ulceration is found more distally within the duodenum, etiologies other than H. pylori or NSAIDs should be suspected, such as gastrinoma. Gastric ulcers can occur anywhere in the stomach, but they are found most frequently in the transitional zone between antral and corporal mucosa, particularly on the lesser gastric curve.

Gastric ulcers

H. pylori is still the major cause of GUs worldwide, but in many developed countries has been overtaken by NSAIDs including low-aspirin as the primary cause. These GU patients usually have normal or reduced acid secretion. Ulcers occur in areas of heavy inflammation, transitional zones between different part of the stomach, or other areas of mucosal fragility. For example, they frequently occur in the transitional zone on the lesser gastric curve where oxyntic and antral mucosa meet, and in H. pylori-induced pangastritis this transitional zone is often heavily inflamed. They may also occur where atrophic mucosa from long-standing H. pylori infection abuts normal oxyntic mucosa. Some drug-induced ulcers or erosions occur in the dependent stomach where tablets cause local damage (pill ulcers). Recurrent GUs are often found at the same site as the original ulcer, reinforcing the important role of local mucosal defense in ulcer localization and pathogenesis.

Duodenal ulcers

Duodenal, pyloric and immediately prepyloric ulcers share a common pathogenesis and are generally classified together. The cause of the vast majority is H. pylori infection. DUs are usually associated with increased acid, most obviously in Zollinger-Ellison syndrome where DUs often extend distal to the duodenal bulb. However, H. pylori-induced DUs are also in part caused by increased acid, usually in association with elevated fasting serum gastrin

Udayana University Faculty of Medicine, DME, 2017 40 Study Guide Alimentary & Hepatobiliary Systems & Disorders levels. Patients have increased parietal cell mass, increased acid response to stimulation (for example by food), and prolonged acid secretion after a meal, due to a combination of increased production and reduced inhibition. Suppression of mucosal defense is also a factor in DU pathogenesis and bicarbonate secretion is reduced. As explained later, H. pylori inhabits areas of gastric metaplasia in the duodenum leading to local inflammation and damage. NSAIDs can cause DUs but much less commonly than they cause GUs.

Gastrointestinal Bleeding

Approximately 50% of admissions for GI bleeding are for upper GI (UGI) bleeding (from the esophagus, stomach, duodenum), 40% are for lower GI (LGI) bleeding (from the colon and anorectum), and 10% are for obscure (OGI) bleeding (source of bleeding as not been identified after esophagogastroduodenos-copy and colonoscopy have been performed). Hematemesis is defined as vomiting of blood, which indicates bleeding from the esophagus, stomach, or duodenum. Hematemesis includes vomiting of bright red blood, which suggests recent or ongoing bleeding, and dark material (coffee-ground emesis), which suggests recent bleeding. Melena is defined as black tarry stool and results from degradation of blood by digestive tract enzymes and intestinal bacteria. Melena can signify bleeding that originates from an UGI, small bowel, or proximal colonic source. Melena generally occurs when at least 50 mL of blood enters the GI tract (usually UGI tract), with passage of the characteristic stool several hours later. Hematochezia refers to bright red blood per rectum, and suggests either active UGI or small bowel bleeding or distal colonic or anorectal bleeding. Occult GI bleeding refers to subacute bleeding that is not clinically visible.

A. Upper GI bleeding

Upper gastrointestinal bleeding is broadly divided into two main patient groups, nonvariceal and variceal upper gastrointestinal bleeding. The initial assessment and aggressive resuscitation of patients who present with an episode of upper gastrointestinal bleeding are important before endoscopy and have been shown to reduce mortality.

Nonvariceal upper gastrointestinal bleeding

Peptic ulcer is the most common cause of nonvariceal upper gastrointestinal bleeding. These ulcers are mainly caused by Helicobacter pylori or by nonsteroidal anti inflammatory drugs. H. pylori can be found in the stomach in 95% of patients with a duodenal ulcer and in most patients with a gastric ulcer not associated with NSAID use. Daily NSAID usage causes an estimated 40-fold increase in gastric ulcer creation and an 8-fold increase in duodenal ulcer creation. As the peptic ulcer defect invades deeper into the gas-troduodenal mucosa, the arterial wall weakens and necrosis develops. This leads to the development of a pseudoaneurysm which can rupture and then bleeding may result. Duodenal ulcers are more common than gastric ulcers, but the incidence of bleeding is comparable for both. Bleeding vessels larger than 1.5 mm in diameter are associated with an increased mortality rate. There is evidence that therapy with high-dose proton pump inhibitors may decrease the rate of rebleeding after endoscopic therapy; this is thought to be due to its effect on increasing the gastric pH above 6, thereby stabilizing the clot.

Variceal hemorrhage

Patients who bleed from esophageal varices have a 70% risk of rebleeding and of these approximately 30% of further bleeding episodes are fatal. Mortality is high-est in the fi rst 24–48 hours after a bleeding episode and decreases slowly over the next 6 weeks. Again the pres-ence of comorbidities (i.e. renal, pulmonary, cardiovas-cular) predicts the highest

Udayana University Faculty of Medicine, DME, 2017 41 Study Guide Alimentary & Hepatobiliary Systems & Disorders mortality (20–65%).

Primary assessment

The amount of blood loss should be estimated. The patient's hemodynamic status should be determined. Clinical signs such as tachycardia > 100 beats/min (bpm), systolic blood pressure < 90 mmHg, cool extremities, syncope and other signs of shock such as ongoing hematemesis or hematochezia should alert the clinician to properly triage these patients to a high dependency setting. Patients who present with upper gastrointestinal bleeding associated with hemorrhagic shock have been shown to have a mortality of up to 30%.

B. Lower gastrointestinal or colonic bleeding

Lower gastrointestinal bleeding, as defined here, originates in the colon or anorectum. The annual incidence of colonic bleeding is approximately 20/100 000 population, with an increased risk in the elderly. The rate of hospitalization for colonic bleeding is lower than that for UGI bleeding. Patients usually present with painless hematochezia and a decrease in hematocrit value but without orthostasis. Diverticulosis is generally the most common cause of acute colonic bleeding, accounting for approximately 30% of cases, colonic polyps or cancer, colitis, and anorectal disorders each account for approximately 20% of cases. The overall mortality rate from colonic bleeding is 3.9%. Independent predictors of inhospital mortality are age above 70 years, intestinal ischemia, two or more comorbid illnesses, inpatient bleeding for an unrelated condition, coagulopathy, hypovolemia, need for red blood cell transfusions, and male gender. Colorectal polyps and hemorrhoids were associated with a lower mortality risk. In most cases, acute colonic bleeding will stop spontaneously, thereby allowing nonurgent evaluation in most cases. For patients with ongoing or recurrent hematochezia, urgent diag-nosis and treatment are required to control the bleeding. In a large patient series, 64% of patients with severe hematochezia required a therapeutic intervention to control continued bleed-ing or rebleeding. Among these patients, 39% underwent endoscopic treatment, 1% underwent angiographic emboliza-tion, and 24% underwent surgery.

Lecture 10

GASTROENTERITIS

Gastroenteritis is a Global health problem with high morbidity & mortality in developing countries. There are several etiology of gastroenteritis for instance: viruses, bacteria, and protozoa. Secretory diarrhea and osmotic diarrhea are two mechanism of watery diarrhea. There are three degree of dehydration in diarrhea wich are: 1. No sign of diarrhea dehydration, 2. Some dehydration and, 3. severe dehydration. Treatment of diarrhea divided into 3 plans depending on severity of dehydration. Indication of IV fluid in diarrhea patients in severe dehydration or with hypovolemia, unconscious, persistent vomiting, and prolonged oligouria or unuria. Antibiotics agent for diarrhea depending of etiologic causes like tetracycline or doxycycline, cotrimoxazole, chloramphenicol or metronidazole. Above of all prevention of diarrhea is the most modality we should do especially hand washing, using clean water for drink and safe behavior on feces disposing, breast milk for the first 4-6 of live, avoiding the use of infant feeding bottles, improving practices of preparation and storage of weaning foods and improving nutritional status.

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SPECIAL PEDIATRIC CASES (INTUSSUCEPTION)

Intussuception is the most common cause of intestinal obstruction between 3 months and 6 year of age. Intussuception occurs when a portion of alimentary tract is telescoped into an adjescent segment. The incidence varies from 1-4 per 1.000 live births. The cause of most Intussuception is unknown. It has been postulated that gastrointestinal infection or the introduction of new food proteins results in swollen peyer patches in the terminal ileum. In typical cases there is sudden onset, in a previously well child, of severe paroxysmal colicky pain that recurs at frequent intervals and is accompanied by straining efforts with legs and knees flexed and loud cries. On abdominal palpation usually reveals a sausage-shaped mass. During the colic cycles, the children may vomit or pass a bloody “current jelly” stool. Diagnosis is confirmed based on history, physical findings and radiologic examination (ultrasound and barium enema). Management of intussuception include supportive treatment and reduction of Intussuception. Untreated Intussuception in infants is almost fatal, the chance of recovery are directly related to the duration of Intussuception before reduction.

ACUTE ABDOMINAL PAIN

All of pathologic conditions in peritoneal cavity which need quick and accurate treatment is called as acute abdomen. These emergency conditions are caused by so many factors those principally could be grouping in 4 categories : passage disturbing of the gastrointestinal contents (ileus), injuries or trauma in the abdomen, infections or inflammations of the many organs in abdominal cavity and if there is bleeding process in the lumen of the gastrointestinal tract.

APPENDICITIS AND ITS COMPLICATIONS As classically conceptualized, acute appendicitis progreses inexorably, from obstruction to mucosal and then transmural inflamamation, necrosis, and then gangren with local in flammatory responses from the visceral and parietal peritoneum, to perforation with local abscess formation or speading peritonitis. Natural history and complications.

Local / mucosal appendicitis

Gangrenous appendicitis

Perforated appendicitis

Periappendicular mass Perappendicular abscess Peritonitis

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PERITONITIS Usually peritonitis is divided as primary peritonitis and secondary peritonitis. Primary peritonitis refers to an extra abdominal source of hematogenoucly transmitted bacterial infection such as spontaneus bacterial peritonitis (SBP), tuberculosis peritonitis, or peritonitis associated with chronic ambulatory peritoneal dialysis (CAPD) Secondary peritonitis refers to infections arising as a result of intraperitoneal processes such as hollow viscus perforation, biliary tract disease, bowel ischaemia, and pelvic inflammatory disease The primary treatment of secondary bacterial peritonitis is surgical of the anatomical pathology and peritoneal toilet. Empiric antibiotic therapy for established secondary bacterial peritonitis plays an important supplemental role

Lecture 11

HERNIA

Hernia may be generally defined as a protrusion of abdominal viscera Outside the abdominal cavity through a natural or acquired defect . This definition, however, does not include internal hernia in which abdominal viscera , usually the small bowel, enter performed intraperitoneal sacs Commonly found around the duodenum, cecum, and sigmoid colon.

ANORECTAL DISEASES

Patients suffering from anorectal disorder often complain of vague symptoms. A detailed description of these symptoms must therefore be obtained so that they may be associated whit a precise anatomic location to provide a basis for appropriate examinations and a reliable diagnosis. There are a total of eight principal symptoms due to anorectal disorder: 1. Rectal bleeding 2. Pruritus ani 3. Pain 4. Discharge 5. Incontinence 6. Diarrhea 7. Constipation 8. False need to defecate

COLORECTAL CANCER

Colorectal cancer is a cancer of colon and rectum. These usually occurs in elderly people. This carcinoma develop from adenoma (adenoma carcinoma sequence) and it need years until become carcinoma. Early cancer is asymptomatic and late cancer could manifest clinically as hematochesia or anemia or obstruction (Ilius)

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Lecture 12

IRRITABLE BOWEL SYNDROME (IBS)

Irritable bowel syndrome (IBS) is a functional bowel disorder characterized by abdominal pain or discomfort and altered bowel habits in the absence of detectable structural abnormalities. No clear diagnostic markers exist for IBS; thus the diagnosis of the disorder is based on clinical presentation. In 2006, the Rome II criteria for the diagnosis of IBS were revised (Table 17-1). IBS is one of the most common conditions encountered in clinical practice but one of the least well understood. Throughout the world, about 10–20% of adults and adolescents have symptoms consistent with IBS, and most studies show a female predominance. IBS symptoms tend to come and go over time and often overlap with other functional disorders such as fibromyalgia, headache, backache, and genitourinary symptoms. Severity of symptoms varies and can significantly impair quality of life, resulting in high health care costs. Advances in basic, mechanistic, and clinical investigations have improved our understanding of this disorder and its physiologic and psychosocial determinants. Altered gastrointestinal (GI) motility, visceral hyperalgesia, disturbance of brain-gut interaction, abnormal central processing, autonomic and hormonal events, genetic and environmental factors, and psychosocial disturbances are variably involved, depending on the individual. This progress may result in improved methods of treatment.

SHIGELLOSIS

The discovery of Shigella as the etiologic agent of dysentery—a clinical syndrome of fever, Intestinal cramps, and frequent passage of small, bloody, mucopurulent stools—is attributed to the Japanese microbiologist Kiyoshi Shiga, who isolated the Shiga bacillus (now known as Shigella dysenteriae type 1) from patients’ stoolsin 1897 during a large and devastating dysentery epidemic. Shigella cannot be distinguished from Escherichia coli by DNA hybridization and remains a separate species only on historical and clinical grounds.

CHRONIC DIARRHEA

Inflammatory bowel disease encompasses two distinct chronic, idiopathic inflammatory diseases of the gastrointestinal tract: Crohn's disease and ulcerative colitis. Although these two entities are frequently grouped together, it is important to appreciate the marked phenotypic differences between them, because these differences may have a profound impact on medical and surgical management. The incidence of Crohn's disease and ulcerative colitis in the United States is approximately 5 and 15 per 100,000 persons, respectively. There is evidence that the incidence of Crohn's disease has been increasing worldwide over the past several decades, although this rise appears to have plateaued over the past 10 years.

COLITIS

Colitis is an inflammation of the colon, also known as the large intestine. While there are many causes of colitis including infections, poor blood supply (ischemia), and autoimmune reactions, they share common symptoms of abdominal pain and diarrhea. Symptoms of colitis will depend upon the type of colitis a person has, but in general, colitis most often is associated with abdominal pain and diarrhea. Individuals with colitis may have

Udayana University Faculty of Medicine, DME, 2017 45 Study Guide Alimentary & Hepatobiliary Systems & Disorders mild, moderate or severe colitis. Types of colitis include microscopic colitis, C. diff colitis, infectious colitis, ischemic colitis, Crohn’s disease and ulcerative colitis (one type of inflammatory bowel disease), and chemical colitis.The diagnosis of colitis is made by patient history, physical examination, laboratory tests, colonoscopy, and imaging tests. Treatment for colitis depends on the specific type of colitis

DIVERTICULAR DISEASE

Among western populations, diverticulosis of the colon affects nearly one-half of individuals over age 60. Fortunately, only 20% of patients with diverticulosis develop symptomatic disease. However, in the United States, diverticular disease results in >200,000 hospitalizations annually, making it the fifth most costly gastrointestinal disorder. The mean hospital stay is 9.7 days, with an average cost of $42,000 per patient. The mean age at presentation of the disease is 59 years. Although the prevalence among females and males is similar, males tend to present at a younger age. Diverticulosis is rare in underdeveloped countries, where diets include more fiber and roughage. However, shortly following migration to the United States, immigrants will develop diverticular disease at the same rate as U.S. natives

Lecture 13

ACUTE HEPATITIS

Acute hepatitis is characterized by inflammation and necrosis of the liver. The underlying trigger for the inflammatory process may be toxic, autoimmune, infective (viruses, bacterial, protozoa and helminth), metabolic and others. The scope this paper will be acute viral hepatitis. Hepatitis A caused by hepatitis A virus (HAV). Hepatitis A virus most commonly give rise to asymptomatic infection, with less than 5 % of infected people having an identifiable illness .therefore its have a high prevalence in the worldwide. Transmission occurs by the fecal oral route, either by direct contact with an HAV-infected person or by ingestion of HAV- contaminated food or water. The onset of HAV infection usually is abrupt and accompanied by systemic complaints such as; fever, malaise and nausea. The symptoms of HAV are; right upper quadrant, pain, dark colored urine and jaundice. The diagnosis of HAV is established by serologic criteria. Hepatitis B caused by hepatitis B. HBV is 42 nm-diameter member of the Hepadnaviridae family. An estimated 6 million persons in the United State are infected, with approximately 300, new cases of HBV occurring each year with the highest incidence among adults age 20-39 yr. The most important risk factor for acquisition of HBV in children is perinatal exposure to an HBsAg positive mother. HBV is a noncytopathogenic virus that causes injury by immune-mediated processes. Many cases of HBV infection are asymptomatic, are evidenced by the high carriage rate of serum markers in persons who have no history of acute hepatitis. Several antigens and antibodies are used to confirm the diagnosis of acute infection Hepatitis C caused by hepatitis C. HCV is a single –stranded RNA virus, classified as a separate genus within the flaviviridae family. About 4 million people in the United Stated are estimated to be infected with HCV. Risk factor for HCV transmission blood transfusion, illegal drug use with exposure to blood or blood products, sexual transmission. HCV appears to cause injury primarily by cytopathic mechanisms, but immune-mediated injury also may occur. The clinical pattern of the acute infection is similar to that of he other hepatitis viruses. The clinically available assays for detection of HCV infection are based on detection of antibodies to HCV antigens or testing directly for viral RNA or DNA. The treatment of acute hepatitis is largely supportive and involves rest,

Udayana University Faculty of Medicine, DME, 2017 46 Study Guide Alimentary & Hepatobiliary Systems & Disorders hydration, and adequate dietary intake. Hospitalization is indicated for patient with severe vomiting and dehydration, a prolonged time, or evidence of early hepatic encephalopathy. The complications hepatitis A are included fulminant hepatitis, prolonged jaundice and relapse. Prevention of hepatitis A includes pre-exposure prophylaxis, post-exposure prophylaxis and personal hygiene. Mortality rate of Hepatitis A is 0-1 -0,4 %. Hepatitis B vaccine and hepatitis B immunoglobulin (HBIG) are available for prevention of HBV infection and mortality is more than 30 %. No vaccine is available to prevent HCV

CHRONIC HEPATITIS

The term chronic hepatitis means active, ongoing inflammation of the liver persisting for more than six months that is detectable by biochemical and histologic means. It does not imply an etiology. The biochemical hallmark of chronic hepatitis is an increased serum aminotransferase (AST and ALT) with minimal elevation of alkaline phosphatase. When the inflammation is severe and/or prolonged, hepatic dysfunction may become apparent with an increase in serum bilirubin and INR/prothrombin time, and a decrease in serum albumin. Typically, biochemical tests are used to identify and follow patients with chronic hepatitis, while liver biopsies serve to more precisely define the nature of the chronic hepatitis and provide useful information regarding the extent of damage and prognosis. Histologically, chronic hepatitis is characterized by infiltration of the portal tracts by inflammatory cells. These cells are predominantly mononuclear cells including lymphocytes, monocytes and plasma cells. Chronic hepatitis is designated as mild when the infiltrate is confined to the portal triad). It is designated as moderately severe chronic hepatitis.) when the infiltrate extends into the parenchyma (piecemeal necrosis) and when it extends to adjacent portal triads (bridging). The inflammatory process can also "bridge" from the portal tract to the central vein. Severe chronic hepatitis is associated with multilobular or confluent necrosis and is much more likely to progress to cirrhosis. The amount of fibrosis is staged separately. These newer terms, mild, moderate and severe chronic hepatitis, replace the older terminology including chronic persistent hepatitis and chronic active hepatitis, which are still frequently mentioned in older textbooks. By far, the commonest cause of chronic hepatitis is viral infections of the liver. Other causes include autoimmune hepatitis, drug-induced hepatitis, Wilson's disease, a1-antitrypsin deficiency and steatohepatitis.

ACUTE LIVER FAILURE

Acute liver failure is a complex multisystemic illness that evolves quickly after a catastrophic insult to the liver leading to the development of encephalopathy. The underlying aetiology and the pace of progression strongly influence the clinical course. The commonest causes are paracetamol, idiosyncratic drug reactions, hepatitis B, and seronegative hepatitis. Hepatic encephalopathy (HE) in acute liver injury signifies a serious prognosis. Brain edema and intracranial hypertension are major causes of death in this syndrome. Comparison of HE in acute liver failure (ALF) with that of cirrhosis allows recognition of important differences and similarities. A key role for ammonia in the pathogenesis of both HE and brain edema is now firmly supported by clinical and experimental data. Additional factors, such as infection, products of the necrotic liver, and synergistic toxins, may contribute to an altered mental state. A low plasma osmolarity, high temperature, and both high and low arterial pressure may affect brain water content. A combined derangement of cellular osmolarity coupled with cerebral hyperemia can explain the development of brain edema in ALF. Increasingly, study of the mechanisms responsible for brain swelling provides critical information for understanding the pathogenesis of HE. The pathogenic role of precipitating factors, well-recognized in the encephalopathy of

Udayana University Faculty of Medicine, DME, 2017 47 Study Guide Alimentary & Hepatobiliary Systems & Disorders cirrhosis, is often overlooked in ALF. Patients with acute liver failure may develop encephalopathy from the use of sedatives, as disturbances of sleep or agitation may be an early prodrome and are often medicated prior to arrival at a specialized center. Gastrointestinal hemorrhage, uremia, and electrolyte disturbances need to be ruled out. Infection, however, is the key precipitant to consider. It is necessary to outline the three main categories of liver failure. The first--Acute Liver Failure (ALF) is a rare condition and represents the most rapidly developing type being often known as fulminant hepatic failure, in which the patient without previous liver disease develops encephalopathy within 8 weeks of the onset of symptoms. The second--Acute-on-Chronic Liver Failure (A-CLF) is the common variety where manifestations of liver failure are precipitated in a patient with known chronic liver disease by acute events such as sepsis, bleeding varices or an alcoholic binge. The third--Chronic Liver Failure (CLF) is the clinical decompensation of end stage liver disease without precipitating event. Components of the clinical syndrome, namely jaundice, encephalopathy, systemic vasodilatation, hepatorenal syndrome and other manifestations of multiorgan failure are similar in all three types but with differences in severity and in their contribution to the overall clinical picture. The underlying pathophysiological disturbances are also likely to be similar, differing mainly in degree and to some extent affected by the nature of the liver disorder.

HEPATOCELLULAR CARCINOMA

The tumor is more commonly seen in males and usually arises from areas of long- standing liver injury with liver necrosis and repair, as in the cirrhotic liver. The risk of developing HCC is greatest in patients with chronic hepatitis B and C infections, hemochromatosis and cirrhosis from a1-antitrypsin deficiency. Hepatitis B can predispose to hepatoma in either a cirrhotic or noncirrhotic liver by the integration of the hepatitis B-DNA into portions of the human genome within the hepatocytes where growth-modifying genes are present. Recent studies suggest that in cases of HCC, HCV is substantially more common than HBV. HCC is not often seen in patients with alcoholic cirrhosis who continue to drink, unless the alcoholic has coexisting viral hepatitis. Hepatic co-carcinogens that appear to play a role in HCC include aflatoxin and vinyl chloride. The clinical recognition of HCC may be difficult, as the tumors often occur in patients with underlying cirrhosis, and the signs and symptoms may suggest progression of underlying liver disease. The more common presentations include deterioration of the known cirrhotic with rapid weight loss, an enlarging liver with a mass, abdominal pain or bloody ascites. A friction rub or bruit may be present over the liver. Patients may present with one of the many paraneoplastic syndromes, including erythrocytosis, hypercalcemia, dysproteinemia or hypoglycemia. Serum a-fetoprotein levels are greater than 500 µg/L in 70-80% of cases. Ultrasound and CT scan imaging are often used to identify the mass, but occasionally radionuclear scanning (using gallium) or x-ray angiography may help further define the nature of the mass lesion and provide important operative details. A biopsy of the mass or examination of the ascitic fluid for cytology may yield a conclusive diagnosis.

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Lecture 14

LIVER DISORDERS 2

Fatty Liver

Nonalcoholic fatty liver disease is characterized by fat accumulation in the liver in the absence of excessive alcohol consump-tion (less than 20 g/day) and exclusion of other secondary causes of hepatic steatosis. Primary NAFLD is closely associated with other features of metabolic syndrome, particularly insulin resistance (IR). Secondary causes of NAFLD can be related to nutrition (i.e., rapid weight loss, malnutrition), drug-induced toxicity (i.e., methotrexate, tamoxifen, chemo-therapies), metabolic conditions (i.e., lipodystrophy, abetaproteinemia), and other causes (i.e., bypass surgery, bacterial overgrowth, celiac disease, etc.).

Hepatic fat accumulation is the hallmark of NAFLD while steatohepatitis is the infiltration of the fatty liver with necroinflammatory cells and associated cellular injury. A two-hit model was proposed to help explain the progression to steatohepatitis. According to the model, the first hit is the accumulation of fat within hepatocytes and the second hit (genetic or environmental) results in hepatic inflammation, cellular injury, and fibrosis. The progression may not be linear and multiple concurrent processes contribute to the phenotype of steatohepatitis.

Liver Abscess

Abscesses within the parenchyma of the liver provide many challenges in diagnosis and management. Amebic and pyogenic liver abscesses share many clinical, laboratory, and imaging features, though they differ considerably with regards to epidemiology and management. The differences in epidemiology, associated conditions, treatment, and prognosis of amebic and pyogenic abscesses underscore the need for the physician to distinguish these entities. Effective management depends critically upon prompt and correct definition of the abscess type. Amebic abscess is the most common extraintestinal manifestation of infection by Entamoeba histolytica. Acquisition of amebic infection is via enteric transmission. The majority of amebic infections are asymptomatic. Symptoms of enteric infection can range from mild diarrhea to dysentery and severe abdomi-nal pain. Hepatic infection is established by invasion of the portal vein via the mesenteric circulation. Spread to the liver by portal vein invasion occurs infrequently, with population studies suggesting that the rates of amebic liver abscess are less than 1% the rates of symptomatic enteric amebiasis.

CHOLELITHIASIS (GALL STONE) AND CHOLECYSTITIS

Gallstones (cholelithiasis) are the most common cause of biliary tract disease in adults, afflicting 20-30 million persons in North America. Approximately one-fifth of men and one-third of women will eventually develop cholelithiasis. The recent advent of laparoscopic cholecystectomy has further increased the use of surgery. Such variance suggests overuse of our health-care system, particularly as few (20%) ever become symptomatic. Biliary colic pain ensues when an obstructing stone causes sudden distention of the gallbladder and/or the biliary tract. "Colic" is a poor term, as biliary pain typically does not increase and decrease spasmodically. Rather, abdominal pain onsets suddenly, quickly becomes severe, remains steady for 1 to 3 hours and then gradually disappears over 30 to 90 minutes, leaving a vague ache. Its duration may be less than an hour, but is not as brief as 15 to 30

Udayana University Faculty of Medicine, DME, 2017 49 Study Guide Alimentary & Hepatobiliary Systems & Disorders minutes. Although biliary-type pain can follow a fatty or spicy meal, such "fatty food intolerance" is not specific for biliary tract disease. Its location usually is the epigastrium or right upper quadrant.

ACUTE CHOLECYTITIS

The gallbladder becomes acutely inflamed. In most, a stone obstructs the cystic duct, resulting in a vicious cycle of increased secretion of fluid, causing distention, mucosal damage and the release of chemical mediators of the inflammatory process. Inflammatory damage results from agents such as lysolecithin, derived from the hydrolysis of lecithin by phospholipase, and prostaglandins whose synthesis increases. Any role that bile salts and regurgitated pancreatic enzymes may have is unclear. Bacterial infection is a late complication. Obstruction of the cystic duct results in the gallbladder becoming distended with bile, an inflammatory exudate or even pus. The gallbladder wall can go on to necrosis and perforation. If resolution occurs, the mucosal surface heals and the wall becomes scarred, but the gallbladder may not function (i.e., fill with contrast agent) on oral cholecystography

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LEARNING TASK

MACROSCOPIC STUCTURE OF ALIMENTARY 1 Tue, 21 Mar 2017 SYSTEM dr. I Nyoman Gede Wardana, M.Biomed

Vignette 1: A 6-year-old previously healthy boy presents with acute onset of fever of 39°C (102°F), severe throat pain that is exacerbated by swallowing, headache, and malaise. On examination his tonsils are symmetrically enlarged and red, with purulent exudate. He has multiple enlarged, painful anterior neck lymph nodes, but no other lymphadenopathy and no splenomegaly. He has no runny nose or cough, and no difficulty breathing. Learning Task: 1. Describe oral cavity and it boundary 2. Describe major salivary gland and mastication muscles

Vignette 2: A 35 years old woman complaining pain on her upper stomach with nausea and vomiting for 3 hours ago. The pain getting worse with after meal. Learning Task: 1. Describe structure of oesophagus and gaster 2. Describe blood supply for gaster

Vignette 3: A 28 year old male weight lifter comes to the emergency room because of a painful lump in their right scrotal area that began earlier in the morning. He is healthy with an unremarkable past medical history Learning Task: 1. Describe the abdominal wall 2. Describe adult anatomy of the inguinal canal

Vignette 4: A 17 year old male came to emergency room suffering fever from 2 hours ago and pain on his right lower belly. The pain gets worse as time goes on. He also suffer vomiting and loss of appetite Learning Task 1. Describe peritoneum, mesentery, ligament, and omental bursa 2. Describe small intestine and large intestine 3. Describe main blood supply for gastrointestinal tract

MICROSCOPIC STRUCTURE OF UPPER AND 2 Wed, 22 Mar 2017 LOWER ALIMENTARY SYSTEM dr. Wayan Sugiritama, M.Kes

Vignette A 40-year-old man comes to a doctor with complaints feels like a burning chest pain beginning behind the breastbone and moving upward to

the neck and throat. She feels like food is coming back into the mouth leaving an acid or bitter taste. The pain of heartburn can last as long as 2 hours and is often worse after eating, lying down or bending. The pains obtain relief by

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standing upright or by taking an antacid. The patient has body weight 90 kg and height of 160 cm and he is a heavy smoker. Learning tasks 1. Explain the structure of the esophagus and its role in the process of swallowing! 2. Does esophagus has a structure or mechanism that can protect against stomach acid? Explain! 3. What will happen to the structure of the esophageal mucosa if continuously exposed to stomach acid?

Vignette A 43-year-old advertising executive is brought to the emergency room with searing pain to the middle of the back and “coffee grounds” hematemesis. The present episode began shortly after eating a heavy lunch, which included two drinks. His history includes periodic attacks of heart burn, nausea, and pain in the epigastric region. These attacks are often relieved by antacid. He smokes two packs of cigarettes daily and admits to moderate social use of alcohol. After aspiration of the lesser sac, a 1-cm ulcer is seen on the superoposterior aspect of the pyloric antrum. The ulcer has eroded a small arterial branch, which is bleeding. Learning Task 1. Describe the histological structure of pyloric mucosa! 2. Mention and describe the structure of cell, which secretes the HCL (Hydrochloric acid) on stomach! 3. How are stomach cells protected from acid? 4. Mention and describe the structure of cell, which secretes alkaline mucus to protect the stomach mucosa from strong acid (HCL)!

Vignette A 17-year-old woman comes to a doctor with complaints of diarrhea and abdominal pain. Diarrhea suffered since 2 weeks, a frequency of 3 to 4 times a day with a soft consistency and contain mucus and blood. Patients feel weakness, decreased appetite and weight loss. The patient was a factory worker and always buy lunch at the street stalls. Learning Task 1. Describe the microscopic structure of small and large intestine! 2. Explain the structure of the intestine that play a role in the peristalsis! 3. Describe the structure of the small intestine that allows it to absorb nutrients!

Self-Assessment : 1. Describe the histological structure of lips! 2. Describe the histological structure of teeth and its associated structures! 3. Describe the histological structure of tongue! 4. Differentiate histological structure of lingual papillae! 5. Describe the histological structure of esophagus! 6. Describe the histological structure of stomach! 7. Describe the histological structure of gastric gland! 8. Differentiate the microscopic structure of cardia, fundus, and pylorus 9. Describe the histological structure of intestinal surface cells!

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10. What is the function of the intestinal villus! 11. Compare the microscopic structure of small intestine and colon! 12. Differentiate the microscopic structure duodenum, jejunum, and ileum! 13. Describe the Kripte Lieberkuhn! 14. Differentiate the microscopic structure of colon and rectum

UPPER AND LOWER ALIMEN PHYSIOLOGY Wed, 22 Mar 2017 dr. I Putu Adiartha Griadi, M.Fis

Vignette 1 A man of 30 years having lunch at food seller, while he has 3-5 spoon to eat suddenly his friend exciting him and the food regurgitate and thrown out of the mouth. Learning Task 1: 1. To have a proper digestion of food, the process consist of mechanical and enzymatic action. How both process is going on and regulated? 2. Explain the normal process of swallowing and factors that influence and facilitate swallowing? 3. Explain regurgitation reflex mechanism!

Vignette 2 It was at 12 noon, lunch time has arrived. Nina, a medical student, cannot eat

lunch because lecture is not over yet. She feel her saliva increasing and hear the stomach sound. All she can do only swallow. Learning Task 2: 1. Explain the stage of eating process! 2. Explain the mechanism of responses experienced by Nina!

Vignette 3 In the morning, we usually defecate we will spurt to locate the nearest toilet. If the toilet was full, you have to wait. Learning Task 3: 1. How can you control your defecation? 2. Defecation process is a reflex. Explain!

BIOCHEMISTRY ASPECT OF ALIMENTARY 3 Thu, 23 Mar 2017 SYSTEM dr. I Wayan Surudarma, M.Si

Vignette A Women comes to the emergency room with severe abdominal pain in the right upper quadrant as well as severe pain in her back. The pain began several hours after she consumed a meal of fried chicken and cheese-coated French fries. While surgery might be necessary in the future, conservative treatment was tried first. She was instructed to limit fried foods and high-fat dairy products. She was also given chenodeoxycholate to take orally. Question 1. Which organs of the body are part of the human digestive system? 2. What are the five human digestive secretions?

3. What is the approximate pH of saliva secretion? Is it an acidic or

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4. alkaline fluid? What are the main functions of saliva?

5. What digestive enzyme is contained in saliva? Which type of food does it digest and into which smaller molecules does it break down the food?

6. What is the pH inside the stomach? Why is it necessary to maintain that pH level? How is it maintained? What cells produce that pH?

7. Describe the process of production HCL in gaster.

8. What digestive enzyme acts within the stomach? Which type of food does it digest? What cells produce that enzyme?

9. Coming from the acidic pH of the stomach, what pH is present when chyme enters the duodenum? Why is it necessary to maintain that pH level in the small intestine? What organs are responsible for that pH level and how is it maintained?

10. How does pancreatic juice participate in the digestion of proteins? What enzymes are involved?

11. How does pancreatic juice proceed with the digestion of carbohydrates? What enzyme is involved?

12. In addition to pancreatic juice in the intestine, enteric juice containing digestive enzymes is also secreted. What are these enzymes and which type of molecule do each of these enzymes break down?

13. Why do protease-producing cells of the stomach and of the pancreas produce only the precursors to active proteolytic enzymes?

14. What are the digestive functions of the liver?

15. What substance produced in the liver is involved in digestion in the small intestine? What is the role of this substance in the digestive process?

16. What is the role of micelles in digestion of fat?

17. What is diagnosis of the case above?

18. Why was the patient instructed to limit fried foods and high-fat dairy products?

19. Why was she given chenodeoxycholate to take orally?

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MACROSCOPIC STUCTURE OF HEPATOBILIARY Thu, 23 Mar 2017 SYSTEM dr. I Nyoman Gede Wardana, M.Biomed

Vignette 1: A17-year-old patient was brought to the emergency room after suffering a traffic accident. Patient complains of pain in the right hypochondriac region and found any tenderness. Patients diagnosed with ruptured of the liver and soon will be perform segmentectomy Learning Task: 1. Describe surface of the liver 2. Differ between the portal hepatic with portal triad 3. Describe anatomical lobes and segmentation of the liver 4. Describe blood supply of the liver and portal vein

Vignette 2: A 42-year-old obese woman with seven children is brought to a local hospital by her daughter. Physical examination and her radiograph reveal that large gallstones have ulcerated through the posterior wall of the fundus of the gallbladder into the intestine. Learning Task: 1. Explain the flow of bile resulting from the liver drain into duodenum 2. Describe structure of gallbladder, cystic duct, and common bile duct

MICROSCOPIC STRUCTURE OF HEPATOBILIARY Thu, 23 Mar 2017 SYSTEM dr. I G N Mayun, Sp.HK

Learning Task 1. Describe the detail microscopic structure of liver and gall bladder! 2. How the pancreatic secretion is regulated by food (potatoes and meat) and beer? And explain the composition of pancreatic secretion induce by potatoes and meat (steak)! 3. How the gall bladder emptying is stimulated? 4. How many time bile salt cycling in each meal?

Self-assessment 1. Describe the microscopic structure of the liver 2. Describe the function of the liver both exocrine and endocrine functions 3. Describe the conceptualization of the liver lobules and how many lobules of the liver do you know 4. Describe the bile pathways after it produced by hepatocytes until it enter the duodenum. 5. Describe the microscopic structure and function of the gallbladder 6. Describe the histophysiology of the gallbladder

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PHYSIOLOGY AND BIOCHEMISTRY ASPECT OF HEPATOBILIARY SYSTEM 4 Fri, 24 Mar 2017 dr. I Putu Adiartha Griadi, M.Fis Dr. dr. Desak Made Wihandani, M.Kes

Vignette A man of 35 years old have dinner consist of potatoes and steak and a bottle of beer. In the intestinal the end product of potatoes and meat (steak) stimulate the pancreatic secretion and gall blader excretion. Learning Task

1. Please explain the bilirubin secretion mechanism 2. Describe how the liver processes bilirubin 3. Describe the biochemical cause of hyperbilirubinemia (jaundice) and its classification.

RATIONAL DRUG USE IN ALIMENTARY Fri, 24 Mar 2017 DISORDERS Prof. dr. I G. M. Aman, Sp.FK

Learning task 1. Name 7 different drug groups used in the treatment of peptic ulcer and describe their mechanism of action 2. Describe, why the Calcium Carbonate and Sodium Bicarbonate are less popular as antacid than the Magnesium Hydroxyde and Aluminum Hydroxyde 3. List the side effect of each antacid 4. List two drugs used as prokinetic and describe their differentiation, and what are the clinical effect of these prokinetic 5. List four groups of Antibiotic used in peptic ulcer, and describe the usefulness of antibiotics in the treatment of peptic ulcer 6. Name four drugs used in the prevention of vomiting and and list their side effect 7. List four groups of drug use as laxative and distinguish their mechanism

8. Identify 2 drugs commonly used as antidiarrheal agents 9. Identify the drugs used in the management of inflammatory bowel disease

Self-assessment 1. Identify the antacid drugs interaction 2. What are the clinical used of prokinetic drugs 3. Can you list the antiemetics that are value in preventing Cancer Chemotherapy induced vomiting 4. Identify the clinical use of Cimetidine, and list it side effects 5. Describe the kinetic of Omeprazole

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ETIOPATHOGENESIS AND MORPHOLOGIC FEATURES 5 Thu, 30 Mar 2017 OF ALIMENTARY DISORDERS dr. L Pt Iin Indrayani M, SpPA(K)

Vignett 1 An old man 50 years old came to hospital because of hematemesis and melena. He had history of long standing chronic hepatitis and sirosis. On esophagoscopy, the clinician found a macroscopic appearance of tortuous mucosal bulging and haemorrhage in the lower third of the esophagus. Learning Task 1. What is the most possible diagnosis of this esophageal lesion in this case? 2. Described the etiopathogenesis of this esophageal lesion. 3. Described the microscopic feature of this lesion.

Self-Assessment of Upper Alimentary Tract. 1. Describe the aetiology, pathogenesis and morphologic features of Esophageal Varices. 2. Describe the aetiology, pathogenesis and clinical features of the Esophagus Neoplasm ( Squamous Cell Ca and Adeno Ca ) 3. Describe the aetiology, pathogenesis and morphologic features of Acute and Chronic Gastritis. 4. Describe the aetiology, pathogenesis and morphologic features of Gastric ulceration (Peptic ulcer, and Acute Gastric ulceration)

Vignette 2 A 25 years old women come to the hospital with abdominal pain in the right lower quadrant, followed by nausea, vomiting, and fever. The peripheral white cell count was slightly increased. From the anamnesis, she told that the pain was begin at periumbilical area, then localized at right lower quadrant. Learning Task 1. What are the differential diagnosis of this case? 2. What is the possible diagnosis of this case? 3. Describe the etiopathogenesis and morphologic features (macroscopic and microscopic) of the diagnosis? 4. Where is the classic physical finding of the disease?

Self-Assessment of Lower Alimentary Tract 1. Describe the etiopathogenesis and morphologic features of Hirschsprung Disease / Congenital Megacolon . 2. Describe the etiopathogenesis, and morphologic features of Vascular disorders of Small and Large Intestine (Ischemic bowel Disease, Haemorrhoids) 3. Describe the etiopathogenesis and morphologic features of Idiopathic Inflammatory Bowel Disease.( Crohn Disease, Ulcerative Colitis) 4. Describe the etiopathogenesis and morphologic features of Colonic Diverticulosis, and Bowel Obstruction (Hernia, Adhesion, Intussusception, and Volvulus) 5. Describe the etiopathogenesis and morphologic features of Tumors of Small and Large Intestines ( Non-neoplastic Polyp, Adenomas, Familial Polyposis Syndromes, Colorectal adeno carcinoma, Small

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intestinal adeno carcinoma) 6. Describe the etiopathogenesis, and morphologic features of Acute Appendicitis

ETIOPATHOGENESIS AND MORPHOLOGIC Thu, 30 Mar 2017 FEATURES OF HEPATOBILIARY DISORDERS Dr.dr. I Gusti Ayu Sri Mahendra Dewi, Sp.PA(K)

1. Vignette : A 32 years old man came to a general hospital with fever and right upper quadrant pain and tender mass since 3 days ago. Abdomen USG showed hepatomegaly. Clinician suspect to hepatic inflammation. Liver biopsy was done in this patient. Learning Task : a. Mention the etiologic of hepatic inflammation! b. Describe the possibility source of infection in patient above! c. Describe the morphologic feature of the biopsy specimen in this patient!

2. Vignette : A 65 years old man came to a general hospital with pain and mass in the right upper abdomen that rapidly enlarged since a week ago. He also felt fever, fatigue, loss of appetite and body weight. The serum level of alpha- fetoprotein 1400 ng/mL. Biopsy from the liver was done and send for anatomical pathology examination. Learning Task : a. What are the differential diagnose of this patient? b. Describe the etiopathogenesis of disease in patient above! c. Describe the morphologic feature of the biopsy specimen in this patient!

Self-assessment

1. Describe five general responses of the liver to hepatic injury! 2. Describe the histopathological appearance of acute and chronic viral hepatitis! 3. Describe the macroscopic and microscopic features of liver abscess! 4. Describe the morphologic features of three forms of alcoholic liver disease! 5. Describe the morphologic feature of hepatocellular carcinoma!

3. Vignette : A 43 year old man came to a doctor with colic, pain radiating to the right shoulder, nausea and fever. Laboratory examination show increase blood conjugated bilirubin. Cholecystectomy was done in this patient. Learning Task : 1. What are the possibility diagnosis of this patient? 2. Mention the risk factor of this disease! 3. Describe the morphologic feature from the gallbladder specimen!

Self-assessment 1. Over 95 % of biliary tract disease is directly attributable to cholelithiasis (gallstones) or cholecystitis. Mention the risk factors for gallstones! 2. Describe the etiopathogenesis of the biliary atresia!

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4. Vignette : A 70 year old man came to a general hospital with pain in upper abdomen. From laboratory and clinical examination, the clinician diagnosed this patient as obstructive jaundice. CT scan show a nodule in the head of the pancreas, 2 cm in diameter. Incisional biopsy was done and send for anatomical pathology examination. Learning Task : 1. What are the possibility diagnosis of this patient? 2. Describe the morphologic feature of the biopsy specimen in this patient! 3. Describe the pathogenesis of pancreatic cancer!

Self-assessment 1. Describe the pathogenesis of acute pancreatitis! 2. Describe the morphologic features of acute and chronic pancreatitis!

CLINICAL PATHOLOGY ASPECT OF ALIMENTARY AND HEPATOBILLIARY SYSTEM Thu, 30 Mar 2017 (LIVER FUNCTION TEST) Dr. dr. AA Wiradewi, SpPK

1. Patient come to clinic with chief complain vomiting and abdominal pain. a. According to those symptoms, please mentioned some possible diseases b. Please mentioned any questions or other anamnesis needed to make the working and differential diagnosis c. Please mentioned any laboratory testing needed to support the diagnosis. 2. After conducting anamnesis and physical examination, if you suspect the patient suffering from gastrointestinal bleeding, : a. To support this diagnosis, what kind of examination that you will suggest to the patient? b. What kind of preanalytical factor that you will explain to the patient in order to get an accurate result of that examination? 3. Can we know whether there is a GI bleeding or other disease, and differentiate location of bleeding from the change of stool color? Please explain your answer. 4. Describe some laboratory examination/parameter that can be performed to determine the presence of H. pylori infection 5. Explain the advantages and disadvantages of the examination of tumor markers and mention some tumor markers in the alimentary and hepatobiliary system 6. A 62-year-old man presented to his primary care physician in June of 2009 with fatigue. He gave a history of two similar episodes of extreme fatigue in the past five years. During one of these episodes, elevated liver enzymes were found. He did not seek further attention at that time. An examination showed that he was otherwise healthy. He was not on medications, and he denied drinking. He had no known family history of liver disease. If you suspect that a patient suffering from hepatitis, what kind of laboratory examination/ parameter that can be performed to screen the hepatitis infection? 7. Describe how to interpret the results of liver function tests to make the

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differential diagnosis of icteric patient

Self-Assessment 1. In order to get an accurate result, please mention how to collect the stool specimens 2. There are two steps in stool analysis. Please mention it. 3. A change in stool color can provide information about pathologic conditions, organic dysfunction or intake of drugs. Please mention it. 4. What is the indication of occult blood test? 5. Mention some markers in hepatitis virus infection and explain its usefulness 6. Describe the four phases of chronic hepatitis

IMAGING STUDIES OF ALIMENTARY DISORDERS 6 Fri, 31 Mar 2017 Dr. dr. Elysanti M, SpRad

Learning task : 1. A 1,5-year old boy is came with his mother to emergency department with complaint of swallowing a coin What kind of imaging examination for this patient that can be useful to Evaluate the presence of the coin and its position?

2. A 27-year old man came with main complaint about abdominal pain at the right lower quadrant since these two days. The pain became worst, associated with fever, vomiting and worsen while he was walking. Physical examination showed pain while compression applied on the Mc Burney. Laboratory result showed leukocytosis. a. What is the diagnosis possibility? b. What kind of imaging examination do you choose to help establish the diagnosis? c. What kind of abnormality could revealed by the imaging examination above?

3. A 5-months age baby was brought to emergency ward with main

complaint about bloody defecation. Before admission, the baby was very uncomforted and often cried. One day before admission, the baby had eaten banana porridge. Before this, the baby only had breast feeding. From physical examination, abdomen seemed distended, with palpable mass at the right abdominal. a. What is the possible diagnosis? b. What kind of imaging examination that could be done to establish the diagnosis? c. What kind of abnormality that revealed by those imaging examination? d. If there were some complication happened (e.g. bowel perforation), what kind of imaging examination should be performed to establish the diagnosis of bowel perforation?

3. 5. A woman came to emergency department with severe abdominal pain since 2 days ago. During this 3 days she has not had defecation and during this day she also has not had any flatus. Physical examination revealed an abdominal distended, with increasing bowel

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sound (metallic sound). Question : a. What kind of imaging examinations that you will advise to this patient? b. What kind of condition that you need to evaluate from those initial imaging examinations above? c. If there any suspiciousness about abnormality in the small bowel, what kind of imaging examination you will advise? d. If there any suspiciousness about abnormality in the large bowel, what kind of imaging examination you will advise?

Self-Assessment : Are these statements right or wrong? 1. Barium follow through is used for evaluating anatomy of the phaynx- esopagus and functional abnormality of the swallowing process. 2. Suspiciousness about radiopaque foreign body in the oesophagus can be checked with barium and cotton. 3. Barium follow-through examination is contrast study to evaluate large bowel. 4. If plain abdomin x-photo (BOF) and lateral decubitus x-photos revealed free air in the abdominal cavity, the next imaging examination that should be done is Barium enema/ barium follow through, depend on the location of the abnormality. 5. If we suspect about obstructive ileus the small bowel, imaging examination that should be done is double contrast barium enema.

IMAGING STUDIES OF HEPATOBILLIARY Fri, 31 Mar 2017 SYSTEM dr. Srie Laksminingsih, SpRad

Vignette 1 Boy, 6 years old with enlargement of stomach, yellowish eyes and skin, pale faeces like “dempul”. On physical finding, abdomen was distended and enlargement of the liver. Learning task: 1. What is the diagnosis of this case?

2. What supporting diagnostic tool are suggested? What radiologic result will be found?

Vignette 2 Female 45 years old came with abdominal pain at right upper quadrant spreading to back, with nausea and vomiting. On physical finding, tenderness at right upper quadrant, enlargement of the liver and with hard, nodules surface, jaundice. Learning task: 1. What is probably the diagnosis?

2. What supporting diagnostic tool are suggested? What radiologic result will be found?

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Vignette 3 A men 50 years old, with enlargement of abdomen, nausea and vomiting. Decreasing body weight, jaundice, and have previous hepatitis B infection Learning task: 1. What is probably the diagnosis?

2. What supporting diagnostic tool are suggested to confirm the diagnosis?

3. What radiologic result will be found?

Vignette 4 A women 40 years old, with pain on all over of abdomen, and getting worse during last week, with fever, nausea and vomiting, and decreasing body weight. On physical finding, abdomen distended, hepatomegaly, temperature 38 C. Learning task: 1. What is probably the diagnosis?

2. What supporting diagnostic tool are suggested to confirm the diagnosis?

3. What radiologic result will be found?

ORAL CAVITY DISORDERS, TEETH AND PERIODONTIUM DISEASES 7 Mon, 3 Apr 2017 Drg. Mia Ayustina P dr. Agus Rudi A, SpTHT-KL

Vignette 1 1. A 20 year old female came to the puskesmas and she was complaining about the pain she had 2 days in a row, she couldn’t sleep and had to take an analgesic. From the clinical appearance, the doctor saw a cavity in the first upper molar, no swelling and the physical condition was good. Learning Task : According to the symptom : a. describe the diagnose of the first upper molar b. explaining the reason why you choose that diagnose c. Explain the gingival changing during pregnancy period and as a doctor what will you suggest to the pregnant patient

according that condition. 2. Draw structure of the anterior teeth and posterior teeth and what is the different between anterior and posterior teeth?

Vignette 2 Patient 45 years old male consults with complain pain and difficulty when swallowing, on the physical examination there are ulcer on the oral cavity and tongue. Learning Task 1. What is the other anamnesis should be added to this case? 2. If on physical examination there are multiple ulcer and fibrins exudates

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what is another physical finding can be found, what is the differential diagnosis to this case, what is the closest diagnosis, what is the treatment to this case? 3. If there are pseudo membrane what kind of physical examination should be done, what is the differential diagnosis to this case, what is the closest diagnosis and what is the treatment to this cases?

Vignette 3 Patient 50 years old male consults with complain pain and difficulty when swallowing, fever and the physical examination there are a massive, brawny swelling of the floor of the mouth, sub maxillary and suprahyoid regions Learning Task 1. What is the other anamnesis should be added to this case? 2. What is the differential diagnosis to this case, what is the closest diagnosis? 3. What is the other physical examination finding? 4. What is the treatment for this case?

SELF ASSESMENT GLOSSITIS 1. What are the systemic deceases with manifestation in the tongue? 2. What is the etiology of the Glossistis 3. What is the physical finding of the Moeller’s Glossitis, acute Glossitis and chronic Glossitis 4. How to treat those Glossitis disease? MOUTH ULCER 1. Explain the definition of recurrent apthous stomatitis! 2. Explain how to diagnosis recurrent apthous stomatitis! 3. How to treat the recurrent apthous stomatitis? 4. What are the different between apthous stomatitis and Sutton disease? 5. What are the physical examination finding on herpes disease? 6. How to treat herpes disease? CANDIDIASIS 1. Explain what is the definition of oral candidiasis? 2. What is the predisposition of oral Candidiasis? 3. How prevent oral Candidiasis? 4. What is the physical examination finding of oral Candidiasis? 5. How to treat oral Candidiasis? ANGINA LUDWIG’S 1. Explain what is the definition of Angina Ludwig’s? 2. What is the predisposition of Angina Ludwig’s? 3. What is the physical examination finding of Angina Ludwig’s? 4. How to treat Angina Ludwig’s? Leukoplakia 1. Explain the definition of leukoplakia! 2. Explain how to diagnosis leukoplakia! 3. How to treat the leukoplakia? 4. What are the physical examination finding on leukoplakia? Parotitis 1. Explain the definition parotitis! 2. Explain how to diagnosis parotitis! 3. What are the different between Epidemic parotitis, Acute suppurative parotitis And Chronic suppurative parotitis?

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4. What are the physical examination finding on parotitis? 5. How to treat parotitis?

ESOPHAGEAL DISORDERS 8 Fri, 7 Apr 2017 dr. I Wayan Sucipta, SpTHT-KL Prof. Dr. dr. IDN Wibawa, SpPD-KGEH

Vignette 1 Female, 19 years old was brought by her family to emergency Department General Hospital because vomiting and dysphagia, acutely without fever or cough. On that time, her mother was found a bottle of porstex in her daughter bed room. Learning Task 1. Find out the other symptoms to complete anamnesis. 2. Describe physical examination to support diagnosis. 3. Describe other examination to support diagnosis. 4. Explain management of this case.

Self-Assessment 1 1. Describe and discuss etiology of corrosive lesion of esophagus. 2. Explain pathogenesis of corrosive lesion of esophagus. 3. Describe clinical evaluation to support diagnosis. 4. Describe examination to support diagnosis. 5. Describe complications of corrosive lesion of esophagus. 6. Manage initial management or refer patient.

Self-Assessment 2 1. Describe pathogenesis of achalasia. 2. Describe clinical evaluation to support diagnosis. 3. Describe examination to support diagnosis. 4. Explain indication of esophagoscopy. 5. Describe and discuss management of achalasia.

Self-Assessment 3 1. Describe and discus etiology of atresia esophagus. 2. Describe clinical evaluation to support diagnosis. 3. Describe examination to support diagnosis. 4. Describe complications of atresia esophagus. 5. Manage initial management or refer patient.

Vignette 2 A women 40 y.o. obese, came to the Sanglah general hospital with complain burning sensation on the chest, pain sensation when take meal or beverage, experience the symptom of regurgitation wherein sour or bitter- tasting material appears in the mouth. Felt difficult to swallow and pain on the chest. This complains repeated since 6 weeks, menstruation still normal, cough and shortness of breath were denied. No history of heart disease. Learning task: 1. Discuss the possibility of differential diagnose that should we think in this case 2. What the diagnostic test should be done and how to interpretative it

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3. Explain the pathogenesis of reflux esophagitis 4. How to establish the diagnosis and the management of the patient above?

Self-Assessment: 1. Explain the definition of reflux esophagitis. 2. Explain the risk factor of reflux esophagitis. 3. Explain the pathogenesis of reflux esophagitis 4. Explain the clinical manifestation of reflux esophagitis (intra and extra esophageal) and it’s complications Explain the diagnostic criteria of reflux esophagitis and it’s management

STOMACH AND DUODENUM DISORDERS 1 9 Mon, 10 Apr 2017 dr. Gde Somayana, SpPD

Vignette 1

68-year old man present to the emergency department with coffee ground emesis, abdominal pain, weakness and nausea. He has had 3 episodes a coffee ground emesis over the past 2 hours. He has history of taking medicine for gouty arthritis since 2 weeks ago. Physical examination reveals blood pressure 90/60 mmHg, HR 120 x/mnt, haemoglobin 5 gr/dl and the both of extremities are cold.

Learning task 1. What is your working diagnosis? 2. What is the treatment of this patient? 3. What is your diagnostic plan?

Self assessment 1. The differentiation between gastritis and gastropathy 2. Explain the pathophysiology of NSAID related gastric injury 3. The risk factors of NSAID related gastric ulcer

Vignette 2

A-52-year old man come to your private clinic to consultation. He shows the result of upper endoscopy that reveal an ulcer at the bulbus duodenum.

Learning task 1. What are the causes of duodenal ulcer? 2. What is the treatment of this patient?

Self assessment 1. The pathophysiology of duodenal ulcer related H pylori 2. How to diagnose H pylori infection 3. The best non-invasive methods to confirm active Hp infection

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STOMACH AND DUODENUM DISORDERS 2 10 Tue, 11 Apr 2017 dr. Ni Nyoman Metriani N, SpA, M. Sc

Vignette A 9 months old baby girl were brought to the emergency department with complaints of watery stools, without blood nor mucous. Her mother also observed that the baby didn’t want to drink milk as usual. Learning Task 1. Mention the questions that should be asked to confirm the diagnosis as gastroenteritis (diarrhoea). 2. Mention the history that should be taken and physical examination that should be performed to confirm the ethology of the disease. 3. What is likely as the cause of the disease? Explain how it can cause diarrhoea. 4. Based on the data above, what kind of dehydration that the patient was suffered from? What other data (from history and physical examination) are needed to confirm the diagnosis of dehydration degree?

5. Explain the management of the patient. 6. The patient also had a smell of vinegar in her stool, and erythema skin around her perianal area. Due some reasons, she only got formula milk before got sick. What will you suggest regarding to this condition? Mention some complications that can be occurred? 7. Describe some complications of the disease?

Self-assessment 1. What are the aetiologies of gastroenteritis? 2. Explain how viruses, bacterial and protozoa cause diarrhea! 3. Explain how invasive bacterial and protozoa cause bloody diarrhoea. 4. Differentiate signs and symptoms of diarrhea patient with no dehydration, some signs of dehydration and severe dehydration! 5. Explain how to give fluids of each degree of dehydration! 6. Explain what the other management of diarrhea are.

SPECIAL PEDIATRIC CASES Tue, 11 Apr 2017 dr. Ni Nyoman Metriani N, SpA, M.Sc

Vignette A 4 months old baby boy was brought to the emergency department. The parent complained that the baby had vomited several times. At the beginning, the infant cried loudly, with flexed legs and knees, and followed by vomit. The parent noticed that their baby’s stool contained red blood and mucous. On physical examination, a sausage shape mass is palpable on a slight distended abdomen. The parent admitted, they tried to give a banana to the baby few days before. Learning tasks: 1. What other data that should be taken to confirm the diagnosis? 2. What are the differential diagnosis of this disease? 3. Describe the possible aetiology of Intussusception in the case 4. Describe signs and symptoms of intussusception 5. What are laboratory and radiologic examination to confirm the

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diagnosis 6. What are the management of the case

Self-assessment 1. Describe the aetiology of Intussusception 2. Describe the pathogenesis of Intussusception 3. Explain the supportive management of Intussusception. 4. Describe the complications of Intussusception.

ACUTE ABDOMEN Tue, 11 Apr 2017 dr. Made Agus Dwianthara Sueta, SpB-KBD

Learning task 1 1. Discuss about pathophysiology of the acute appendicitis. 2. Discuss about differential diagnosis of the acute appendicitis. 3. Discuss about pathophysiology of the periappendicular infiltrate. 4. Discuss about difficulties to make diagnosis of the acute appendicitis in childhood patients. 5. Discuss about acute appendicitis in pregnancy women.

Self Assesment 1. Describe about basic criteria to make diagnosis acute appendicitis. 2. Describe about: Ligath sign, Psoas sign, Obturator sign, Tenhorn sign, and Rebound phenomena. 3. How to manage the acute appendicitis patient? 4. How to manage the periappendicular cases? 5. How to manage the periappendicular abscess?

Learning task 2 1. Discuss about history taking of the patient with suspected peritonitis 2. Discuss about physical examination in evaluation of the patient with suspected peritonitis 3. Discuss about judicious use of laboratory test for the patient with suspected peritonitis 4. Discuss about available imaging studies in diagnostic evaluation of the patient with suspected peritonitis

Self Assesment 1. Describe about pathophysiology of the peritonitis 2. Describe about principle treatment of the secondary peritonitis 3. Describe about abscess in pouch of Douglass

ABDOMINAL WALL DISORDERS 11 Wed, 12 Apr 2017 dr. Made Mulyawan, SpB-KBD

Learning Task: 1. Discussion about the pathophysiology of the inguinal hernia.

2. Discussion about complication of hernia. 3. Discussion about management of hernia.

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Self-assessment: 1. What is the predisposing factor of hernia? 2. How to differentiate between direct hernia and indirect hernia? 3. What the definition of Reponible, Irreponible, Incarcerate, Strangulated Hernia?

COLON AND ANAL DISORDERS 1

Learning Task: 1. Discuss pathogenesis and etiology of hemorrhoids. 2. Discuss pathogenesis and etiology of anal fistula. 3. Discuss pathogenesis and etiology of anal fissure

Self-Assessment : 1. How to diagnosis and treatment of hemorrhoid? 2. How to diagnosis and treatment of anal fistula? 3. How to diagnosis and treatment of hemorrhoid? 4. How to diagnosis and treatment of anal fissure?

12 Thu, 13 Apr 2017 BCS 13 Mon, 17 Apr 2017 BCS 14 Tue, 18 Apr 2017 BCS 15 Wed, 19 Apr 2017 BCS 16 Thu, 20 Apr 2017 BCS

COLON AND ANAL DISORDERS (IBS, Dysentery, 17 Fri, 21 Apr 2017 Colitis, Diverticulosis/diverticulitis) dr. I Ketut Mariadi, SpPD-KGEH

Vignette 1 A 40-year-old man presented for the first time to your outpatient clinic. He had diarrea since 3 months. He had recurrent abdominal pain which improved with defecation.

Learning task 1. What other information you need to complete the anamnesis? 2. What is the differential diagnosis of this case? 3. What is the supportive diagnostic examination you need? 4. What is the treatment if this case confirms with IBS?

Self assessment 1. What is the definition of IBS? 2. Discuss “sign and symptom” of IBS in general 3. Explain the pathogenesis of IBS 4. Differentiate type of IBS 5. Explain the step to diagnose IBS 6. Discuss the supportive diagnostic examination for IBS 7. How to treat IBS

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Vignette 2 A man 65 years old came to emergency unit with abdominal pain and bloody diarrhea since 2 days. Faeces of patient mix with blood.

Learning task 1. Completed the anamnesis of this patient 2. What is the differential diagnosis of this patient? 3. What is the supporting test to confirm the diagnosis? 4. How to manage each of diagnosis

Self assessment 1. Describe sign and symptom of Colitis 2. Describe sign and symptom of diverticulitis 3. Describe sign and symptom of dysentri 4. How to diagnosis the dysentri, colitis, and diverticulitis 5. How to treat the dysentri, colitis, and diverticulitis?

LIVER DISORDER 18 Tue, 25 Apri 2017 dr. Ni Nyoman Metriani N, SpA, M.Sc Prof. Dr. dr. IDN Wibawa, SpPD-KGEH

Vignette 1 A 12 years old girl comes to the hospital with chief complaints of jaundice and fever. There was an outbreak in her school with the same complaints. She has 2 siblings: A 5 months old girl and 6 years old boy. Learning Task 1. What is the possible diagnosis of this patient? 2. Mention some differential diagnosis of this disease. 3. What are the laboratories examination needed to support that diagnosis? 4. What do you expect in her laboratories examination results? 5. How do you manage this patient? 6. How to prevent the transmission of the disease in her siblings and parents?

Self-Assessment: 1. What is mechanism jaundice in the hepatitis A viral infection? 2. What is the pathogenesis of hepatitis A infection? 3. What is the rote of transmission in hepatitis A infection? 4. What is diagnostic evaluation HVB and HVC? 5. How do you manage hepatitis B and C?

Vignette 2 Mr Ketut Toni, 22 years old, came to Sanglah Hospital with chief complaint: weakness, fatigue, and nauseated since 1 week ago. History of slight fever 2 week before admission. On physical examination patient look pale, icteric, liver enlarged, palpable 2 cm below costal cage, sharp and tender edge, and smooth surface. Spleen impalpable, ascites negative. Laboratory result: total bilirubin 12,3 mg%, direct bilirubin 9,6 mg%, ALT 598 IU/ml, AST 312 IU/ml; serologic marker for viral hepatitis: HBsAg negative, Anti-HBs positive, IgM anti HAV positive. Learning task 1. Describe the etio-pathogenesis of acute hepatitis. 2. Explain the transmission of viral hepatitis A,B, C, and E.

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3. Describe the diagnosis criteria of acute hepatitis! 4. Explain the medical management, complications, and prognosis of acute hepatitis.

Self-assessment 1. Taking and formulate a complete history of the case. 2. Perform and analysis physical examination. 3. Comprehend the clinical implication of pathogenesis of acute hepatitis. 4. Apply basic principle of clinical laboratory investigation on patient with acute hepatitis and interpret and analysis the results. 5. Differentiate clinically between several type of acute hepatitis (viral and non-viral). 6. Comprehend the epidemiological significance of acute hepatitis to assist management and prevention: patient education and family involvement. 7. Comprehend the medical management of acute hepatitis.

Vignette 3 Mr Made Rai, 38 years old, came to Sanglah Hospital with chief complain of right upper quadrant abdominal discomfort, fatigue, weakness since 13 months. History of acute hepatitis while he was on junior high school. On physical examination: sub icteric, liver enlarged 5 cm below costal cage. Laboratories data: total billirubin 1,55 mg%, albumin 3,2 mg %, globulin 4,4 gr%, Hb 11 gr%, ALT 248 IU/ml, AST 410 IU/ml, HBsAg positive, anti HCV negative. Learning task 1. Describe the etio-pathogenesis of chronic hepatitis. 2. Explain the clinical picture of chronic hepatitis 3. Describe the diagnosis criteria of chronic hepatitis! 4. Explain the medical management, complications, and prognosis of chronic hepatitis.

Self-assessment 1 1. Taking and formulate history, perform and analysis physical examination of patient with chronic hepatitis. 2. Comprehend the clinical implication of pathogenesis of chronic hepatitis. 3. Apply basic principle of clinical laboratory investigation on patient with chronic hepatitis. 4. Interpret and analysis the clinical laboratory results. 5. Differentiate clinically between several type of chronic hepatitis (viral and non-viral). 6. Prepare and refer the patients for special laboratory investigation and imaging. 7. Comprehend the epidemiological significance of chronic hepatitis to assist management and prevention: patient education and family involvement. 8. Diagnose clinically, provide management, prevent the progression to liver cirrhosis and refer, patient with chronic hepatitis if necessary

Self-Assessment 2 1. Definition and diagnosis criteria of acute liver failure 2. Most common etiology and risk factors

Udayana University Faculty of Medicine, DME, 2017 70 Study Guide Alimentary & Hepatobiliary Systems & Disorders

3. Renal manifestation, cerebral manifestation, coagulation disorder and other complication 4. Standard treatment, advance treatment and future treatment 5. criteria for referred

Self-assessment 3 1. Comprehend the ethio-pathogenesis and risk factors of hepatocellular carcinoma! 2. Describe the diagnostic criteria for hepatocellular carcinoma.!. 3. Differentiate clinically between benign and malignant tumors of the liver.. 4. Provide initial management, and or refer patient with hepatocellular carcinoma. 5. Comprehend the surgical options and non-surgical option in the management of hepatocellular carcinoma

LIVER DISORDERS 2 19 Wed, 26 Apr 2017 (FATTY LIVER, LIVER ABSCES) dr. Gde Somayana, SpPD

Vignette 1 A-45-year old woman is brought to your clinic by her husband because of the abnormal results of her abdominal USG. The results shows a fatty liver and slight hepatomegaly. Vital signs reveals blood pressure 150/80 mmHg, HR 82 x/mnt, temperature 36,7 degree Celsius, body weight 95 kg, height 160 cm. Physical examination is unremarkable.

Learning task 1. What is your working diagnosis ? 2. What is the risk factor of fatty liver in this patient? 3. What is your diagnostic plan?

Self assessment 1. The pathophysiology of fatty liver 2. The risk factor of NAFLD 3. The management of NAFLD

Vignette 2 A-25-year old man present to the ED of Sanglah hospital with fever and right upper quadrant pain. The patient was refferal from a district hospital because of a clinical response is not seen within 5 days of treatment. Vital signs reveal a temperature 38 degrees Celsius, HR 108 x/mnt, blood pressure 120/80 mmHg. On physical examination liver palpate 4 cm below the arcus costae and tenderness. The reminder of the examination is unremarkable. Laboratory findings leukocyte 18.000 /uL, haemoglobin 12 gr/dl, HbsAg and Anti-HCV was negative. Abdominal ultrasound shows a single abscess at right liver lobe with diameter 8 cm

Learning task 1. What is the treatment of this patient?

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2. What is the cause of liver abscess in this patient?

Self assessment 1. The pathophysiology of liver abscess 2. How to differentiate amoebic liver abscess with pyogenic liver abscess 3. The management of amoebic liver abscess

GALL BLADDER, BILE DUCT, AND PANCREAS DISORDERS Wed, 26 Apr 2017 (Acute Cholecystitis) Dr. I Ketut Mariadi, SpPD KGEH

Vignette A women 42 years old, came to emergency department with abdominal pain, the pain came suddenly and radiating to right scapula. The pain worsening when the patient takes a deep breath. The posture of patients was obese.

Learning task 1. What other information you need from the patien? 2. What is the specific physical examination you need to do to confirm the diagnosis? And how to do? 3. What is the differential diagnosis of the case? 4. What are the supporting examination you need to confirm the diagnosis? 5. How to manage the patient? 6. What is the complication if this case wasn’t treated well?

Self assessment 1. Describe the pathophysiology of Acute cholecystitis! 2. Describe sign and symptom of Acute cholecystitis and how to diagnose this condition! 3. Describe complications! 4. Describe the management of Acute cholecystitis

REFERENCES

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Moore KL, Agur AMR: Essential Clinical Anatomy, 3rd ed. Philadelphia, Lippincott Williams & Wilkins, 2007. ISBN 0-7817- 6274-X

Sadler TW: Langman’s Medical Embryology, 10th ed. Baltimore, Lippincott & Wilkins, 2006.ISBN 13:978-0-7817-9485-5

Fawcett DW, Jensh RP: Bloom & Fawcett’s Concise Histology, 2nd ed. London, Arnold, 2002.

Guyton AC, Hall JE: Textbook of Medical Physiology, 10th Ed. Philadelphia, W.B.Saunders Company, 2000.

Murray RK, Granner DK, Mayes PA, Rodwell VW: Harper’s Biochemistry, 25th Ed. Stamford, Appleton & Lange,2000. ISBN 0-8385-3684-0

Kumar V, Cotran RS, Robbins SL: Robbins Basic Pathology, 8 th ed. Philadelphia, Saunders, 2010.

Trevor AJ, Katzung BG, Masters SB: Katzung and Trevor’s Pharmacology, 6th Ed. New York, Lange Medical Books/Mc Graw-Hill, 2002. ISBN 0-8385-8147-1.

Adams GL., Boies LR, Hilger PA. Diseases of the lower air passages, esophagus and nediastinum : endoscopic considerations. In : Fundamentals of otolaryngology. 6th ed. Philadelphia, London : W.B. Saunders. Company ; 1989. p 471-480.

Jackson. C, Jackson CL. Diseases and abnormalities of the esophagus. In : Bronchoesophagology. 2th ed. Philadelphia and London : W.B. Sounders. Company ; 1964. p 263-317.

Sutton, D. Radiology and imaging for medical students. 7th ed,Churchill Livingstone.Chapter 7-9 (hal 117 – 169)

Longo DL, Faucy AS. Edts. HARRISON’S Gastroenterology and Hepatology. New York: McGraw-Hill. 2010

STUDENT PROJECT ASSESSMENT

Title :

Udayana University Faculty of Medicine, DME, 2017 73 Study Guide Alimentary & Hepatobiliary Systems & Disorders

Exam Date/Time :

Student Name : Student ID Number : Supervisor :

Assesment :

The final exam are approximately as follows:

No Item Assessment Range Score Score 1 Quality of material 0-55 2 Student’s presentation 0-15 performance 3 Critical thinking 0-15 4 Capability of information 0-15 searching Total 0-100

Final Result (Score): Criteria : A B C D E (please circling the criteria) Result range : A : 80-100 B : 70-79 C : 55-69 D : 45-54 E : 0-44

Evaluator,

(……………………………………..) NIP

Nb. Facilitator as supervisor and evaluator

Udayana University Faculty of Medicine, DME, 2017 74 Study Guide Alimentary & Hepatobiliary Systems & Disorders

Article Review Assessment Form Faculty of Medicine, Udayana University

______

Block : Musculoskeletal System and Connective Tissue Disorders Name : ______Student No. (NIM) : ______Facilitator : ______Title : ______

Time table of consultation

Point of discussion Week Date Tutor sign 1. Title 1 2. Refferences 2 3. Outline of paper 3 4. Content 4 5. Final discussion 5

Assessment A. Paper structure : 7 8 9 10 B. Content : 7 8 9 10 C. Discussion : 7 8 9 10

Total point : ( A + B + C ) : 3 = ______

Denpasar, ______

Facilitator,

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Hospital Visit Attendance Form

Date: Group: No NIM Name Sign

Chief Resident,

(...... )

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CURRICULUM MAP

Smstr Program or curriculum blocks 10 Senior Clerkship 9 Senior Clerkship 8 Senior Clerkship Health System- Community-based Evidence-based Elective Study IV Comprehensi 19 weeks 7 based Practice practice Medical Practice (evaluation) ve Clinic (3 weeks) (4 weeks) (2 weeks) Orientation BCS (1 weeks) Special topics : (3 weeks) (Clerkship) Health Ergonomy + medical & Health ethic Environment (4 weeks) (2 weeks) The Cardiovascular Medical Emergency The Urinary The Reproductive Elective 19 weeks 6 System and (2 weeks) System and System and Study III Disorders Disorders Disorders (3 weeks) (3 weeks) (4 weeks) (3 weeks) BCS (1 weeks) BCS (1 weeks) BCS (1 weeks) BCS (1 weeks) Neuroscience and The Respiratory The skin & Special Topic : Elective 18 weeks 5 neurological System and Disorders hearing system - Palliative med Study II disorders (4 weeks) & disorders - Complemnt & (2 weeks) (3 weeks) (3 weeks) Alternative Med. BCS (1 weeks) BCS (1 weeks) - Forensic BCS (1 weeks) (3 weeks) Musculoskeletal Alimentary The Endocrine Clinical Nutrition The Visual 19 weeks 4 system & & hepatobiliary System, and Disorders system & connective tissue systems & disorders Metabolism and (2 weeks) disorders disorders (3 Weeks) Disorders (2 weeks) (3 weeks) (4 weeks) BCS (1 weeks) BCS (1 weeks) BCS (1 weeks) BCS (1 weeks) BCS (1weeks) Basic microbiology Immune system & Hematologic Special Topic Basic 19 weeks 3 & parasitology disorders system & - Andro & aging Pharmaceutic (3 weeks) (2 weeks) disorder & - Geriatri al medicine & Basic Infection clinical oncology -Travel medicine drug etics & infectious (3 weeks) (4 weeks) diseases BCS (1 weeks) BCS (1 weeks) (1 weeks) (3 weeks) BCS (1 weeks) Medical Medical Behavior Change Elective Study I 19 weeks 2 communication Professionalism and disorders (2 weeks) (3 weeks) (2 weeks) + medical (3 weeks) Basic ethic (1 weeks) pharmacology Basic Anatomy (2 weeks) Pathology & Clinical BCS (1 weeks) pathology (3 weeks) BCS (1 weeks) BCS (1 weeks) Studium Generale The cell Growth & 19 weeks 1 and Humaniora as bioche- development (2 weeks) mical machinery (2 weeks) (2 weeks) Basic Anatomy Basic ( 4 weeks) Basic Histology Biochemistry Pratikum Anatomy (2 weeks) & Basic (2 weeks) (1 Weeks) Physiology BCS (1 weeks) (2 weeks) BCS (1 weeks)

Pendidikan Pancasila & Kewarganegaraan ( 3 weeks )

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