CONTENTS
Table of contents……….………..………. 1 Curriculum………...………
2 Block Team………...
6 Facilitators………...………
8 Time Table Regular Class………
9
Time Table English Class………...……… 14
Student Project Time Table ……….…19
BCS Time table ……….20
Hospital Visit Time Table ………..21
Assessment method………..22
Learning Program……….. 23
Abstract……….…. 23
Learning Task and Self Assessment……….48
Standar Kompetensi Dokter Indonesia ………66
Curriculum Mapping………... 70 Reference ………..………… 71
Assessment Form ……….72
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:
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)
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:
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.
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
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
PLANNERS TEAM
NO NAME DEPT PHONE
1 Prof.Dr dr I Dewa Nyoman Wibawa
Sp.PD-KGEH (Head) Internal Medicine 0811398032
2 dr.Ni Nyoman Metriani Nesa, M.Sc, Sp.A Pediatry 081337072141 3 dr.N.Purwadi Sp.PD-KGEH Internal Medicine 0816298224
4 dr.G.A Suryadarma Sp.PD Internal Medicine 081558202728
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
8 dr.Made Agus Dwianthara Sueta,
Sp.B-KBD Surgery 081338648424
9. dr. Made Mulyawan, Sp.B Surgery 081241138971
10. drg. Mia Ayustina P Dentistry 08175053626
11 dr.Lely Rahayu, Sp.THT-KL ENT 08113809882
12 dr. Elysanti M, Sp.R Radiology 081805673099
13. Prof. dr. I G M Aman, Sp. FK Pharmacology 081338770650 14 dr. A. A Wiradewi Sp.PK Clinical Pathology 08155237937
15. Dr.dr. I Gusti Ayu Sri Mahendra
Dewi,Sp.PA (K) Pathology 081338736481
16. dr. L Pt Iin Indrayani M, Sp.PA(K) Pathology 08174761804
17. dr. I G N Mayun, Sp.HK Histology 08155715359
18. dr. Gde Somayana, SpPD Internal Medicine 0816579888 19. dr. Wayan Sugiritama, MKes Histology 08164732743
20. dr. Desak Made Wihandani, M. Kes Biochemistry 081338776244
21. dr. I Wayan Surudarma, M.Si Biochemistry 081338486589 22. dr. I Putu Adiartha Griadi, M.Fis Physiology 081999636899
23. Dra. I A Alit Widhiartini, Apt Pharmacology 08193600559
24. dr. Ketut Mariadi, Sp.PD Internal Medicine 08123853700
LECTURERS
NO NAME DEPT PHONE
1 Prof.Dr dr I Dewa Nyoman Wibawa
Sp.PD-KGEH (Head) Internal Medicine 0811398032
2 dr.Ni Nyoman Metriani Nesa, M.Sc, Sp.A Pediatry 081337072141
3 dr.N.Purwadi Sp.PD-KGEH Internal Medicine 0816298224
4 dr.G.A Suryadarma Sp.PD Internal Medicine 081558202728
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
8 dr.Made Agus Dwianthara Sueta,
Sp.B-KBD Surgery 081338648424
9. dr. Made Mulyawan, Sp.B Surgery 081241138971
10. drg. Mia Ayustina P Dentistry 08175053626
11 dr.Lely Rahayu, Sp.THT-KL ENT 08113809882
12 dr. Elysanti M, Sp.R Radiology 081805673099
13. Prof. dr. I G M Aman, Sp. FK Pharmacology 081338770650 14 dr. A. A Wiradewi Sp.PK Clinical Pathology 08155237937
15. Dr.dr. I Gusti Ayu Sri Mahendra
Dewi,Sp.PA (K) Pathology 081338736481
16. dr. L Pt Iin Indrayani M, Sp.PA(K) Pathology 08174761804
17. dr. I G N Mayun, Sp.HK Histology 08155715359
18. dr. Gde Somayana, SpPD Internal Medicine 0816579888 19. dr. Wayan Sugiritama, MKes Histology 08164732743 20. dr. Desak Made Wihandani, M. Kes Biochemistry 081338776244
21. dr. I Wayan Surudarma, M.Si Biochemistry 081338486589
22. dr. I Putu Adiartha Griadi, M.Fis Physiology 081999636899
23. Dra. I A Alit Widhiartini, Apt Pharmacology 08193600559 24. dr. Ketut Mariadi, Sp.PD Internal Medicine 08123853700
25. dr. Srie Laksminingsih, Sp.R Radiology 08164745561
FACILITATORS
Regular Class (Class A)No Name Group Departement Phone Venue
(3rd floor) 1 dr. I Wayan Gede Sutadarma
M.Gizi A1
Biochemistry 082144071268 3rd floor: R.3.09
2 dr. Gusti Ngurah Mayun Sp.HK A2 Histology 081237395050 3rd floor:R.3.10
3 dr. IGN Mahaalit Aribawa Sp.AnKAR B3 Anesthesiology 0811396811 3rd floor:R.3.11
4 dr.I B Ngurah, M.For AIFO A4 Pharmacology 08123687288 3rd floor:R.3.12
5 dr. Luh Ariwati A5 Parasitology 08123662311 3rd floor:R.3.13
6 Prof.dr. IDP Sutjana M.Erg A6 Physiology 08123924477 3rd floor:R.3.14
7 dr. Dewa Gede Mahiswara S Sp.Rad A7 Radiology 08123846307 3rd floor:R.3.15
8 Prof.Dr.dr. Ketut Tirtayasa, MS AIF.AIFO.Sp.Erg A8 Physiology 08123623422 3rd floor:R.3.16
9 dr.Ni Nengah Dwi Fatmawati Sp.MK PhD A9 Microbiology 087862200814 3rd floor:R.3.17
10 Prof.dr. Gusti Made Aman
Sp.FK A10
Pharmacology 081338770650 3rd floor: R.3.19
English Class (Class B)
No Name Group Departement Phone Venue
(3rd floor) 1 dr. IG P Suka Aryana,
Sp.PD-KGer-FINASIM B1
Interna 08164724600 3rd floor: R.3.09
2 Dr. dr .I Wayan Suranadi, Sp.AnKIC B2 Anesthesiology 08123847675 3rd floor:R.3.10
3 dr. I Wayan Surudarma, M.Si A3 Biochemistry 081338486589 3rd floor:R.3.11
4 dr. I Putu Budhiastra, Sp.M(K) B4 Opthalmology 085238238999 3rd floor:R.3.12
5 dr. Nyoman Suryawati, Sp.KK B5 Dermatology 0817447279 3rd floor:R.3.13
6 dr. I Gede Ngurah Harry Wijaya Surya Sp.OG B6 Obgyn 0811386935 3rd floor:R.3.14
7 dr. Lisna Astuti Sp.Rad(K) B7 Radiology 081337934497 3rd floor:R.3.15
8 Prof.Dr. dr I Nyoman Adiputra M.O.H PFK B8 Physiology 0811397971 3rd floor:R.3.16
9 dr.IB Putu Alit, Sp.F., DFM B9 Forensic 081916613459 3rd floor:R.3.17
TIME TABLE
Regular Class (Class A)Day/
Date Time Activity Venues Person-in-charge
1
Wed 21 Sept 2016 08.00-09.00 09.00-10.00 10.00-11.00 11.00-12.00 12.00-13.30 13.30-14.00 14.00-15.00Introduction to The Block Alimentary and Hepatobiliary System and Disorders Independent Learning and student project Lecture 1:
Macroscopic Structure of Upper and Lower Alimentary System
Independent Learning Small Group Disscussion Break Plenary Session 301 Room 301 Prof. Wibawa Dr. Wardana Facilitators Dr. Wardana
2
Thu 22 Sept 2016 08.00-08.30 08.30-09.00 09.00-10.30 10.30-12.00 12.00-14.00 14.00-15.00 Lecture 2:Microscopic Structure of Upper Alimentary System
Microscopic Structure of Lower Alimentary System
Independent Learning Small group Discussion Break and student project Plenary Session 301 Room 301 Dr. Sugiritama Dr. Sugiritama Facilitators Dr. Sugiritama Dr. Sugiritama
3
Fri 23 Sept 2016 08.00-08.30 08.30-09.00 09.00-10.30 10.30-12.00 12.00-14.00 14.00-15.00 Lecture 3:Macroscopic Structure of Hepatobiliary System
Microscopic Structure of Hepatobiliary System
Independent Learning Small group Discussion Break and student project Plenary Session 301 Room 301 Dr. Wardana Dr. Mayun Facilitators Dr. Wardana Dr. Mayun
4
Mon 26 Sept 2016 08.00-09.00 09.00-10.30 10.30-12.00 12.00-14.00 14.00-15.00 Lecture 4:Physiology aspect of Upper and Lower Alimentary System
Independent Learning Small Group Disscussion Break and Student Project Plenary Session
301
Room
301
Dr. Krisna D.
Facilitators
Dr. Krisna D.
5
Tue 27 Sept 2016 08.00-09.00 09.00-10.30 10.30-12.00 12.00-14.00 14.00-15.00 Lecture 5:Biochemistry aspect of Upper and Lower Alimentary System
6
Wed 28 Sept 2016 08.00-08.30 08.30-09.00 09.00-10.30 10.30-12.00 12.00-14.00 14.00-15.00 Lecture 6:Physiology aspect of Hepatobiliary System
Biochemistry aspect of Hepatobiliary System
Independent Learning Small group Discussion Break and student project Plenary Session 301 Room 301 Dr. Adiartha Dr. Wihandani Facilitators Dr. Adiartha Dr. Wihandani
7
Thu 29 Sept 2016 08.00-09.00 09.00-10.30 10.30-12.00 12.00-14.00 14.00-15.00 Lecture 7:Rational Drug Use in Alimentary and Hepatobiliary Disorders
Independent Learning Small group Discussion Break and student project Plenary Session 301 Room 301 Prof. Aman Facilitators Prof. Aman
8
Fri 30 Sept 2016 08.00-08.30 08.30-09.00 09.00-10.30 10.30-12.00 12.00-14.00 14.00-15.00 Lecture 8:Etiopathologenesis and Morphologic Features of Alimentary Disorders Etiopathologenesis and Morphologic Features of Hepatobiliary Disorders Independent Learning
Small group Discussion Break and student project Plenary Session
301
Room
301
Dr.Iin Indrayani
Dr. Mahendra D
Facilitators
Dr. Iin indrayani Dr. Mahendra D
9
Mon 3 Oct 2016 08.00-09.00 09.00-10.30 10.30-12.00 12.00-14.00 14.00-15.00 Lecture 9:Clinical Pathology aspect of Alimentry and Hepatobiliary System
Independent Learning Small group Discussion Break and student project Plenary Session 301 Room 301 Dr. Wiradewi Facilitators Dr. Wiradewi
10
Tue 4 Oct 2016 08.00-08.30 08.30-09.00 09.00-10.30 10.30-12.00 12.00-14.00 14.00-15.00 Lecture 10:Imaging Studies of Alimentary Disorders Imaging studies of Hepatobiliary system Independent Learning
Small group Discussion Break and student project Plenary Session
301
Room
301
Dr. Elysanti Dr. Srie L.
Facilitators
Dr. Elysanti Dr. Srie L.
11
Wed 5 Oct 2016 08.00-08.30 08.30-09.00 09.00-10.30 10.30-12.00 12.00-12.30 12.30-14.00 14.00-15.00 Lecture 11:Oral Cavity Disorders
- Mouth Disorders (Candidiasis, mouth ulcer, glositis, Angina Ludwig, Parotitis)
- Teeth and Periodontium Diseases (Caries, pulpitis, periodontitis) Independent Learning
Small group Discussion Break Student project Plenary Session 301 Room 301
dr. Agus Rudi A.
drg. Mia Ayustina P
Facilitators
12
Thu 6 Oct 2016 08.00-08.30 08.30-09.00 09.00-10.30 10.30-12.00 12.00-12.30 12.30-14.00 14.00-15.00 Lecture 12: Esophageal Disorders- Corrosive lession of esophagus - Reflux esophagitis
Independent Learning Small group Discussion Break Student project Plenary Session 301 Room 301
dr. I Wyn Sucipta Prof Wibawa
Facilitators
Dr. I Wyn Sucipta Prof Wibawa
13
Fri 7 Oct 2016 08.00-09.00 09.00-10.30 10.30-12.00 12.00-12.30 12.30-14.00 14.00-15.00 Lecture 13:Stomach and Duodenum Disorders 1 (Gastritis, gastric/duodenal ulcer, Gastrointestinal Bleeding, Demam tifoid) Independent Learning
Small group Discussion Break Student project Plenary Session 301 Room 301 Dr. Somayana Facilitators Dr. Somayana
14
Mon 10 Oct 2016 08.00-08.30 08.30-09.00 09.00-10.30 10.30-12.00 12.00-12.30 12.30-14.00 14.00-15.00 Lecture 14:Stomach and Duodenum Disorders 2 (Gastroenteritis)
Acute Abdomen (acute appendicitis, appendicular abscess, peritonitis, infeksi umbilicus)
Independent Learning Small group Discussion Break Student project Plenary Session 301 Room 301 Dr. Metriani
Dr. Agus Sueta
Facilitators
Dr. Metriani Dr. Agus Sueta
15
Tue 11 Oct 2016 08.00-09.00 09.00-10.30 10.30-12.00 12.00-12.30 12.30-14.00 14.00-15.00 Lecture 15:Abdominal wall disorders (Hernia); Colon and Anal Disorders 1 (Rectal and anal prolapse, proctitis, and haemorrhoids, abses peri/anal)
Independent Learning Small group Discussion Break Student project Plenary Session 301 Room 301 Dr. Mulyawan Facilitators Dr. Mulyawan
16
Wed 12 Oct 2016 08.00-10.00 10.00-11.30 11.30-14.00 BCS 1Lecture and Demonstration 1 Break and Free Training Group Training Session
Skill Lab Dr. Lely Rahayu dr. Mariadi dr. Mulyawan dr. Somayana dr. I.A. Alit
17
Thu 13 Oct 2016 08.00-10.00 10.00-11.30 11.30-14.00 BCS 2Lecture and Demonstration 2 Break and Free Training Group Training Session
18
Fri 14 Oct 2016 08.00-10.00 10.00-11.30 11.30-14.00 BCS 3Lecture and Demonstration 3 Break and Free Training Group Training Session
Skill Lab Dr. Lely Rahayu dr. Mariadi dr. Mulyawan dr. Somayana dr. I.A. Alit
19
Mon 17 Oct 2016 08.00-10.00 10.00-11.30 11.30-14.00 BCS 4Lecture and emonstration 4 Break and Free Training Group Training Session
Skill Lab Dr. Lely Rahayu dr. Mariadi dr. Mulyawan dr. Somayana dr. I.A. Alit
20
Tue 18 Oct 2016 08.00-10.00 10.00-11.30 11.30-14.00 BCS 5Lecture and Demonstration 5 Break and Free Training Group Training Session
Skill Lab Dr. Lely Rahayu dr. Mariadi dr. Mulyawan dr. Somayana dr. I.A. Alit
21
Wed 19 Oct 2016 08.00-09.00 09.00-10.30 10.30-12.00 12.00-12.30 12.30-14.00 14.00-15.00 Lecture 16:Colon and Anal Disorders 2 (IBS, Disentri, diverticulitis, and colitis)
Independent Learning Small group Discussion Break Student project Plenary Session 301 Room 301 Dr. Mariadi Facilitators Dr. Mariadi
22
Thu 20 Oct 2016 08.00-08.30 08.30-09.00 09.00-10.30 10.30-12.00 12.00-12.30 12.30-14.00 14.00-15.00 Lecture 17: Liver Disorder 1- Acute hepatitis - Chronic hepatitis B Independent Learning Small group Discussion Break Student project Plenary Session 301 Room 301 Dr. Metriani Prof. Wibawa Facilitators Dr. Metriani Prof. Wibawa
23
Fri 21 Oct 2016 08.00-08.30 08.30-09.00 09.00-10.30 10.30-12.00 12.00-12.30 12.30-14.00 14.00-15.00 Lecture 18:Liver Disorder 2 (Fatty liver, amoebic liver abscess)
Gall Bladder, Bile Duct, and Pancreas Disorders (acute cholecystitis)
Independent Learning Small group Discussion Break Student project Plenary Session 301 Room 301 Dr. Suryadarma Dr. Purwadi Facilitators Dr. Suryadarma Dr. Purwadi
24
Mon 24 Oct 2016 08.00-09.00 09.00-10.30 10.30-12.00 12.00-12.30 12.30-14.00 Lecture 19:Special Pediatric Cases (Intussuception) Independent Learning
14.00-15.00 Plenary Session 301 Dr. Metriani
25
Tue 25 Oct 201608.00-11.00 Student Project Presentation 301 Prof. Wibawa Prof Aman Dr. Elysanti Dr. Metriani Dr. Mayun Dr. Wardana Dr. Mulyawan Dr. Surudarma Dr. Iin Indrayani Dr. Wiradewi Dr. Sugiritama Dr. Mahendra Dewi Dr. Agus Sueta Dr. Wihandani Dr. Adiartha I A Alit Widhiartini Dr. Srie L. Dr. Lely Rahayu Dr. Purwadi Dr. Agus rudi Drg. Mia Ayustina Dr. Wyn Sucipta Dr. Suryadarma Dr. Mariadi Dr. Krisna D. Dr. Somayana
26
Preparation for Exam
27
Thu 27 Oct 2016
TIME TABLE
English Class (Class B)Day/
Date Time Activity Venues Person-in-charge
1
Wed 21 Sept 2016 09.00-10.00 10.00-11.00 11.00-12.00 12.00-13.00 13.30-15.00 14.30-15.00 15.00-16.00Introduction to The Block Alimentary and Hepatobiliary System and Disorders Independent Learning and student project Lecture 1:
Macroscopic Structure of Upper and Lower Alimentary System
Independent Learning Small Group Disscussion Break Plenary Session 301 Room 301 Prof. Wibawa Dr. Wardana Facilitators Dr. Wardana
2
Thu 22 Sept 2016 09.00-09.30 09.30-10.00 10.00-12.00 12.00-13.30 13.30-15.00 15.00-16.00 Lecture 2:Microscopic Structure of Upper Alimentary System
Microscopic Structure of Lower Alimentary System
Break and student project Independent Learning Small group Discussion Plenary Session 301 Room 301 Dr. Sugiritama Dr. Sugiritama Facilitators Dr. Sugiritama Dr. Sugiritama
3
Fri 23 Sept 2016 09.00-09.30 09.30-10.00 10.00-12.00 12.00-13.30 13.30-15.00 15.00-16.00 Lecture 3:Macroscopic Structure of Hepatobiliary System
Microscopic Structure of Hepatobiliary System
Break and student project Independent Learning Small group Discussion Plenary Session 301 Room 301 Dr. Wardana Dr. Mayun Facilitators Dr. Wardana Dr. Mayun
4
Mon 26 Sept 2016 09.00-10.00 10.00-12.00 12.00-13.30 13.30-15.00 15.00-16.00 Lecture 4:Physiology aspect of Upper and Lower Alimentary System
Independent Learning Break and Student Project Small Group Disscussion Plenary Session
301
Room
301
Dr. Krisna D.
Facilitators
Dr. Krisna D.
5
Tue 27 Sept 2016 09.00-10.00 10.00-12.00 12.00-13.30 13.30-15.00 15.00-16.00 Lecture 5:Biochemistry aspect of Upper and Lower Alimentary System
6
Wed 28 Sept 2016 09.00-09.30 09.30-10.00 10.00-12.00 12.00-13.30 13.30-15.00 15.00-16.00 Lecture 6:Physiology aspect of Hepatobiliary System
Biochemistry aspect of Hepatobiliary System
Independent Learning Break and student project Small group Discussion Plenary Session 301 Room 301 Dr. Adiartha Dr. Wihandani Facilitators Dr. Adiartha Dr. Wihandani
7
Thu 29 Sept 2016 09.00-10.00 10.00-12.00 12.00-13.30 13.30-15.00 15.00-16.00 Lecture 7:Rational Drug Use in Alimentary and Hepatobiliary Disorders
Independent Learning Break and student project Small group Discussion Plenary Session 301 Room 301 Prof. Aman Facilitators Prof. Aman
8
Fri 30 Sept 2016 09.00-09.30 09.30-10.00 10.00-12.00 12.00-13.30 13.30-15.00 15.00-16.00 Lecture 8:Etiopathologenesis and Morphologic Features of Alimentary Disorders Etiopathologenesis and Morphologic Features of Hepatobiliary Disorders Independent Learning
Break and student project Small group Discussion Plenary Session
301
Room
301
Dr.Iin Indrayani
Dr. Mahendra D
Facilitators
Dr. Iin indrayani Dr. Mahendra D
9
Mon 3 Oct 2016 09.00-10.00 10.00-12.00 12.00-13.30 13.30-15.00 15.00-16.00 Lecture 9:Clinical Pathology aspect of Alimentry and Hepatobiliary System
Independent Learning Break and student project Small group Discussion Plenary Session 301 Room 301 Dr. Wiradewi Facilitators Dr. Wiradewi
10
Tue 4 Oct 2016 09.00-09.30 09.30-10.00 10.00-12.00 12.00-13.30 13.30-15.00 15.00-16.00 Lecture 10:Imaging Studies of Alimentary Disorders Imaging studies of Hepatobiliary system Independent Learning
Break and student project Small group Discussion Plenary Session
301
Room
301
Dr. Elysanti Dr. Srie L.
Facilitators
Dr. Elysanti Dr. Srie L.
11
Wed 5 Oct 2016 09.00-09.30 09.30-10.00 Lecture 11:Oral Cavity Disorders
- Mouth Disorders (Candidiasis, mouth ulcer, glositis, Angina Ludwig, Parotitis)
- Teeth and Periodontium Diseases (Caries, pulpitis, periodontitis)
301 dr. Agus Rudi A.
10.00-11.30 11.30-13.30 13.30-15.00 15.00-16.00
Independent Learning Break and Student project Small group Discussion Plenary Session
Room
301
Facilitators
dr. Agus Rudi A. drg. Mia Ayustina P
12
Thu 6 Oct 2016 09.00-09.30 09.30-10.00 10.00-11.30 11.30-13.30 13.30-15.00 15.00-16.00 Lecture 12: Esophageal Disorders- Corrosive lession of esophagus - Reflux esophagitis
Independent Learning Break and Student project Small group Discussion Plenary Session
301
Room
301
dr. I Wyn Sucipta Prof Wibawa
Facilitators
Dr. I Wyn Sucipta Prof Wibawa
13
Fri 7 Oct 2016 09.00-10.00 10.00-11.30 11.30-13.30 13.30-15.00 15.00-16.00 Lecture 13:Stomach and Duodenum Disorders 1 (Gastritis, gastric/duodenal ulcer, Gastrointestinal Bleeding, Demam tifoid) Independent Learning
Break and Student project Small group Discussion
Plenary Session 301 Room 301 Dr. Somayana Facilitators Dr. Somayana
14
Mon 10 Oct 2016 09.00-09.30 09.30-10.00 10.00-11.30 11.30-13.30 13.30-15.00 15.00-16.00 Lecture 14:Stomach and Duodenum Disorders 2 (Gastroenteritis)
Acute Abdomen (acute appendicitis, appendicular abscess, peritonitis, infeksi umbilicus)
Independent Learning Break and Student project Small group Discussion
Plenary Session
301
Room
301
Dr. Metriani
Dr. Agus Sueta
Facilitators
Dr. Metriani Dr. Agus Sueta
15
Tue 11 Oct 2016 09.00-10.00 10.00-11.30 11.30-13.30 13.30-15.00 15.00-16.00 Lecture 15:Abdominal wall disorders (Hernia); Colon and Anal Disorders 1 (Rectal and anal prolapse, proctitis, and haemorrhoids, abses peri/anal)
Independent Learning Break and Student project Small group Discussion
Plenary Session 301 Room 301 Dr. Mulyawan Facilitators Dr. Mulyawan
16
Wed 12 Oct 2016 08.00-10.00 10.00-11.30 11.30-14.00 BCS 1Lecture and Demonstration 1 Break and Free Training Group Training Session
Skill Lab Dr. Lely Rahayu dr. Mariadi dr. Mulyawan dr. Somayana dr. I.A. Alit
Thu 13 Oct 2016 08.00-10.00 10.00-11.30 11.30-14.00
Lecture and Demonstration 2 Break and Free Training Group Training Session
Skill Lab Dr. Lely Rahayu dr. Mariadi dr. Mulyawan dr. Somayana dr. I.A. Alit
18
Fri 14 Oct 2016 08.00-10.00 10.00-11.30 11.30-14.00 BCS 3Lecture and Demonstration 3 Break and Free Training Group Training Session
Skill Lab Dr. Lely Rahayu dr. Mariadi dr. Mulyawan dr. Somayana dr. I.A. Alit
19
Mon 17 Oct 2016 08.00-10.00 10.00-11.30 11.30-14.00 BCS 4Lecture and emonstration 4 Break and Free Training Group Training Session
Skill Lab Dr. Lely Rahayu dr. Mariadi dr. Mulyawan dr. Somayana dr. I.A. Alit
20
Tue 18 Oct 2016 08.00-10.00 10.00-11.30 11.30-14.00 BCS 5Lecture and Demonstration 5 Break and Free Training Group Training Session
Skill Lab Dr. Lely Rahayu dr. Mariadi dr. Mulyawan dr. Somayana dr. I.A. Alit
21
Wed 19 Oct 2016 09.00-10.00 10.00-11.30 11.30-13.30 13.30-15.00 15.00-16.00 Lecture 16:Colon and Anal Disorders 2 (IBS, Disentri, diverticulitis, and colitis)
Independent Learning
Break and Student project Small group Discussion Plenary Session 301 Room 301 Dr. Mariadi Facilitators Dr. Mariadi
22
Thu 20 Oct 2016 09.00-09.30 09.30-10.00 10.00-11.30 11.30-13.30 13.30-15.00 15.00-16.00 Lecture 17: Liver Disorder 1- Acute hepatitis - Chronic hepatitis B Independent Learning
Break and Student project Small group Discussion
Plenary Session 301 Room 301 Dr. Metriani Prof. Wibawa Facilitators Dr. Metriani Prof. Wibawa
23
Fri 21 Oct 2015 09.00-09.30 09.30-10.00 10.00-11.30 11.30-13.30 13.30-15.00 15.00-16.00 Lecture 18:Liver Disorder 2 (Fatty liver, amoebic liver abscess)
Gall Bladder, Bile Duct, and Pancreas Disorders (acute cholecystitis)
Independent Learning
24
Mon24 Oct 2016
09.00-10.00 10.00-11.30 11.30-13.30 13.30-15.00 15.00-16.00
Lecture 19:
Special Pediatric Cases (Intussuception) Independent Learning
Break and Student project Small group Discussion Plenary Session
301
Room
301
Dr. Metriani
Facilitators
Dr. Metriani
25
Tue 25 Oct 201612.00-15.00
Lecture 20:
Student Project Presentation
301 Prof. Wibawa Prof Aman Dr. Elysanti Dr. Metriani Dr. Mayun Dr. Wardana Dr. Mulyawan Dr. Surudarma Dr. Iin Indrayani Dr. Wiradewi Dr. Sugiritama Dr. Mahendra Dewi Dr. Agus Sueta Dr. Wihandani Dr. Adiartha I A Alit Widhiartini Dr. Srie L. Dr. Lely Rahayu Dr. Purwadi Dr. Agus rudi Drg. Mia Ayustina Dr. Wyn Sucipta Dr. Suryadarma Dr. Mariadi Dr. Krisna D. Dr. Somayana
26
Preparation for Exam
27
Thu 27 Oct 2016
STUDENT PROJECT TIME TABLE
Regular Class (room 1)
Day Jam Group Topic
25 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
25 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
09.00-09.20 B5 Food poisoning
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
BCS TIME TABLE
Day Topic 1 Topic 2 Topic 3 Topic 4 Topic 5
16 A1-A4 A5-A8 A9-B2 B3-B6 B7-B10
17 B7-B10 A1-A4 A5-A8 A9-B2 B3-B6
18 B3-B6 B7-B10 A1-A4 A5-A8 A9-B2
19 A9-B2 B3-B6 B7-B10 A1-A4 A5-A8
20 A5-A8 A9-B2 B3-B6 B7-B10 A1-A4
Topic 1: Examination of Mouth and Tonsil Dr Lely Rahayu
Topic 2: Physical examination of abdomen Dr Ketut Mariadi
Topic 3: NGT insertion and ascites aspiration Dr Gde Somayana
Topic 4: Hernia Palpation, colok dubur, sacrum palpation, gloves inspection, Psoas Sign, Obturator Sign, Blumberg Test
Dr Mulyawan
Topic 5: Farmacy in Alimentary I A Alit Widhiartini
HOSPITAL VISIT TIME TABLE
PIC : dr. I Ketut Mariadi, Sp.PDActivity : Hospital visit
Venue : Angsoka room, RSUP Sanglah Time : 17.00-18.00 Wita
Day Date Group
2 Thu, 22 Sept 2016 A1
3 Fri, 23 Sept 2016 A2
4 Mon, 26 Sept 2016 A3
5 Tue, 27 Sept 2016 A4
6 Wed, 28 Sept 2016 A5
7 Thu, 29 Sept 2016 A6
8 Fri, 30 Sept 2016 A7
9 Mon, 3 Oct 2016 A8
10 Tue, 4 Oct 2016 A9
11 Wed, 5 Oct 2016 A10
12 Thu, 6 Oct 2016 A11
13 Fri, 7 Oct 2016 A12
14 Mon, 10 Oct 2016 B1
15 Tue, 11 Oct 2016 B2
16 Wed, 12 Oct 2016 B3
17 Thu, 13 Oct 2016 B4
18 Fri, 14 Oct 2016 B5
19 Mon, 17 Oct 2016 B6
20 Tue, 18 Oct 2016 B7
21 Wed, 19 Oct 2016 B8
22 Thu, 20 Oct 2016 B9
23 Fri, 21 Oct 2016 B10
24 Mon, 24 Oct 2016 B11
25 Tue, 25 Oct 2016 B12
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
Final Assessment will be carried out on the 27th day of the block period, Thu, 27 Oct 2016. The test will consist of 120 questions with 120 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.
Lecture 1, 2, 3
LEARNING PROGRAMS
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.
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.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.
Lecture 4, 5, 6
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)
Lecture 7:
RATIONAL DRUG USE IN ALIMENTARY DISORDERS
Drugs used in acid-peptic diseaseAcid-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
Lecture 8 & 9:
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.
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).
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.
Lecture 10
“desmoplastic response”). The appearance is usually that of a moderately to poorly 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.
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.
IMAGING STUDIES OF HEPATOBILIARY SYSTEM
Lecture 11
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
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 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.
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.
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.
Lecturer 12
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 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 bilater
