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

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

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)
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.
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
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
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
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
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
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

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
15. Dr.dr. I Gusti Ayu Sri Mahendra

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
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
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
15. Dr. dr. I Gusti Ayu Sri Mahendra

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

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 Sp.A Pediatri 08123920750 2nd floor:
1 B1
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
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
2017 12.00-12.30 Break
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
2017 12.00-12.30 Break
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
5 09.00-10.00 Clinical Pathology aspect of Alimentry and Dr. Wiradewi

Hepatobiliary System
10.00-10.30 Independent Learning
Thu 10.30-12.00 Small Group Discussion Room Facilitators
30 12.00-12.30 Break
Mar 12.30-14.00 Student project
2017 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
12.00-12.30 Break
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
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)
Apr 10.30-12.00 Small Group Discussion Room Facilitators
2017 12.00-12.30 Break
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
12.00-12.30 Break
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)
2017 12.00-12.30 Break
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
Mon 10.00-11.30 Break and Free Training dr. Mariadi
Oct dr. Somayana
2016 I.A. Alit
BCS 3
Tue 10.00-11.30 Break and Free Training dr. Mariadi
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
Apr dr. Somayana
2017 I.A. Alit
BCS 5
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)
Apr 12.00-12.30 Break
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
Apr 12.00-12.30 Break
Prof. Wibawa
19 Lecture 14:

08.00-08.30 Liver Disorder 2 (Fatty liver, amoebic liver 402 Dr. Somayana
abscess)
08.30-09.00 Gall Bladder, Bile Duct, and Pancreas Dr. Mariadi
Wed Disorders (acute cholecystitis)
2017 12.00-12.30 Break
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

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
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
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
15.00-16.00 Plenary Session 402 dr. Sugiritama, dr.
Adiarta
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
15.00-16.00 Plenary Session 402 dr. Surudarma,
dr. Wardana,
dr. Mayun
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
15.00-16.00 Plenary Session 402 dr. Adiarta, Dr.
Wihandani, Prof
Aman
Lecture 5:
10.00-10.30 Etiopathologenesis and Morphologic 402 dr.Iin Indrayani
Features of Alimentary Disorders

10.30-11.00 Etiopathologenesis and Morphologic Dr. Mahendra D

Features of Hepatobiliary Disorders
11.00-12.00 Clinical Pathology aspect of Alimentry and Dr. Wiradewi
5 Hepatobiliary System
Thu 12.00-12.30 Break
Mar 13.30-15.00 Small Group Disscussion Room Facilitators
2017 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.
31 12.00-13.30 Break and student project
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
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
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)
2017 11.30-13.30 Break and Student project
13.30-15.00 Small group Discussion Room Facilitators
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)
dr. Agus Sueta

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)
15.00-16.00 Plenary Session 402 dr. Mulyawan
BCS 1
13 Apr 11.30-14.00 Group Training Session dr. Agus Sueta
2017 dr. Somayana
I.A. Alit
BCS 2
Mon 10.00-11.30 Break and Free Training dr. Mariadi
Oct dr. Somayana
2016 I.A. Alit
BCS 3
Tue 10.00-11.30 Break and Free Training dr. Mariadi
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
2017 dr. Somayana
I.A. Alit
BCS 5
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)
21 Apr
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
Tue
25 Apr 11.30-13.30 Break and Student project
2017 13.30-15.00 Small group Discussion Room Facilitators
Prof. Wibawa

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
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

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.

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

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
ASSESSMENT METHOD

Final Assessment will be carried out on the 22 nd 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  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.

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,

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

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.

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.

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.

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

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

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

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.

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

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.
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
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,
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
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 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 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
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.

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
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)

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

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,

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 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.
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
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

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
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!
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
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?
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
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.
Fri, 24 Mar 2017

RATIONAL DRUG USE IN ALIMENTARY
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
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 )
Acute and Chronic Gastritis.
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
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!
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!
Thu, 30 Mar 2017

CLINICAL PATHOLOGY ASPECT OF ALIMENTARY
AND HEPATOBILLIARY SYSTEM
(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
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
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 SYSTEM

Fri, 31 Mar 2017
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?
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:
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:
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
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?
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.
4. Explain indication of esophagoscopy.
5. Describe and discuss management of achalasia.
Self-Assessment 3
1. Describe and discus etiology of atresia esophagus.
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
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?
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
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
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.
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
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.
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
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
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
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 :
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

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,
Hospital Visit Attendance Form

Date:
Group:
No NIM Name Sign
Chief Resident,
(.............................................)
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 & disorder - Andro & aging Pharmaceutic
(3 weeks) (2 weeks) & clinical - Geriatri al medicine &
Basic Infection 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 )

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

Încărcat de

Informații document

Titlu original

Drepturi de autor

Formate disponibile

Partajați acest document

Partajați sau inserați document

Opțiuni de partajare

Vi se pare util acest document?

Este necorespunzător acest conținut?

Drepturi de autor:

Formate disponibile

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

Încărcat de

Drepturi de autor:

Formate disponibile

Study Guide Alimentary & Hepatobiliary Systems & Disorders

Table of contents ……..………….……………………………………………………………. 1

Udayana University Faculty of Medicine, DME, 2017 1

Udayana University Faculty of Medicine, DME, 2017 2

a. Diagnose and manage independently enteritis case

Udayana University Faculty of Medicine, DME, 2017 3

1. Functional structure of alimentary and hepatobiliary system

STANDAR KOMPETENSI DOKTER INDONESIA

Udayana University Faculty of Medicine, DME, 2017 4

No Daftar Penyakit Tingkat Kemampuan

Udayana University Faculty of Medicine, DME, 2017 5

32 Fistula umbilikal, omphalocoele-gastroschisis 2

Udayana University Faculty of Medicine, DME, 2017 6

73 Intususepsi atau invaginasi 3B

Udayana University Faculty of Medicine, DME, 2017 7

Udayana University Faculty of Medicine, DME, 2017 8

NO NAME DEPT PHONE

11 dr. Ketut Suanda, Sp.THT-KL ENT 081337788377

15. Dr.dr. I Gusti Ayu Sri Mahendra

Udayana University Faculty of Medicine, DME, 2017 9

NO NAME DEPT PHONE

11 dr.Ketut Suanda, Sp.THT-KL ENT 081337788377

15. Dr. dr. I Gusti Ayu Sri Mahendra

Udayana University Faculty of Medicine, DME, 2017 10

English Class (Class B)

Udayana University Faculty of Medicine, DME, 2017 11

English Class (Class B)

08.00-09.00 Introduction to The Block Alimentary and 402 Prof. Wibawa

Udayana University Faculty of Medicine, DME, 2017 12

Udayana University Faculty of Medicine, DME, 2017 13

dr. Agus Sueta

Udayana University Faculty of Medicine, DME, 2017 14

Udayana University Faculty of Medicine, DME, 2017 15

09.00-10.00 Introduction to The Block Alimentary and 402 Prof. Wibawa

Udayana University Faculty of Medicine, DME, 2017 16

10.30-11.00 Etiopathologenesis and Morphologic Dr. Mahendra D

Udayana University Faculty of Medicine, DME, 2017 17

Udayana University Faculty of Medicine, DME, 2017 18

Udayana University Faculty of Medicine, DME, 2017 19

STUDENT PROJECT TIME TABLE

Regular Class (room 1)

English Class (room 2)

Udayana University Faculty of Medicine, DME, 2017 20

BCS TIME TABLE

Day Topic 1 Topic 2 Topic 3 Topic 4 Topic 5

1. Topic 1. Examination of Mouth and Tonsil : dr Suanda

Udayana University Faculty of Medicine, DME, 2017 21

HOSPITAL VISIT TIME TABLE

PIC : dr. I Ketut Mariadi, Sp.PD

Day Date Group

Udayana University Faculty of Medicine, DME, 2017 22

Udayana University Faculty of Medicine, DME, 2017 23

MACROSCOPIC STRUCTURE OF UPPER ALIMENTARY SYSTEM

MICROSCOPIC STRUCTURE OF UPPER ALIMENTARY TRACT

Udayana University Faculty of Medicine, DME, 2017 24

MACROSCOPIC AND MICROSCOPIC

MACROSCOPIC STRUCTURE OF LIVER, GALLBLADDER, AND PANCREAS

Udayana University Faculty of Medicine, DME, 2017 25

MICROSCOPIC STRUCTURE OF LIVER AND GALL BLADDER

Udayana University Faculty of Medicine, DME, 2017 26

FUNCTIONAL STRUCTURE OF UPPER ALIMENTARY SYSTEM

FUNCTIONAL STRUCTURE OF LOWER ALIMENTARY SYSTEM

FUNCTION OF HEPATOBILIARY SYSTEM AND IT’S CLINICAL IMPLICATION