ANATOMY OF GASTROINTESTINAL TRACT MODULE Objectives The overall objective of this course is to provide an integrative understanding of the structure (gross and microscopic) and development of the gastrointestinal tract. We will employ multiple teaching modalities to solidify your knowledge in this area, and further hone your decision-making skills. We hope this is a valuable (and enjoyable) experience as you learn about the wonders of the GI tract. Module Phylosophy This is a graduate level module with the following assumptions: 1. Students learn best through actively participating in their own education where they can clarify their ideas and understanding of concepts and issues through discussion. 2. Medical students need opportunities for application of basic science into clinical context. 3. Students should work together to gain different perspectives on the material.
Course Materials Texts: Required Drake, Richard, Vogl, Wayne, Mitchell, Adam W. M. (2004). Gray's Anatomy for Students. Toy,Ross, Papasakelariou, (2012), Case File Anatomy Junqueira, Luiz C., Carneiro, J., Lange (2005), Basic Histology
Expectations of Students Be an active learner. This requires you to take an active role in your own learning and to share responsibility in the learning process with other students in the class. The components of active learning include the following: • Attendance. As a professional in the field, you should make a conscientious effort to attend each session and to be on time. History and experience show that students who attend classes regularly do much better work and earn better grades. Attendance in lectures and groups is strongly encouraged. • Adequate preparation for class. Do the assigned reading and make note of questions and areas of interest. • Active Participation. Participate actively in class discussion on the and during small group discussion , This will provide an opportunity to test your assumptions about professional practice, as well as expand the worldview of others in the class. • Study Groups. Research on learning indicates that students can better "make the material their own" through extensive discussion. Unfortunately, our short meeting time does not provide sufficient time for such in-depth discussion. Participation in a study group will significantly enhance your learning.
Kasus klinik 1 Dokter muda Ruben sedang belajar di stase Gastro Ilmu Penyakit Dalam RSSA. Hari itu kebetulan dia datang terlambat. Sayangnya, dia juga baru tahu jika tugas makalah yang sudah dikerjakannya semalaman ternyata tertinggal di rumahnya. Seniornya, Dokter Bogi, SpPD tampaknya tidak bisa memberikan toleransi. Akhirnya, dr. Bogi, SpPD menugaskan dokter muda Ruben mendampinginya melakukan pemeriksaan klinis terhadap pasien-pasiennya dan dia akan diberikan tugas terkait dengan kasus-kasus pasiennya tersebut. Kebetulan hari itu banyak pasien sudah menunggu di ruang poli. Dr. Bogi SpPD segera mempersilahkan pasiennya masuk. Pasien pertama masuk. Seorang eksekutif berusia 42 tahun mengeluh nyeri perut yang mulai sekitar 6 bulan sebelumnya, menetap sifatnya, terutama setelah makan, dan terletak pada bagian atas tengah perut, di sebelah superior terhadap umbilikus. Pasien tersebut juga menjelaskan adanya sedikit “panas ulu hati” yang terjadi selama setahun sebelumnya. Ia berada dalam kondisi stres terkait pekerjaan dan telah mengobati dirinya sendiri dengan antasida yang melebihi dosis, dan ada sedikit perbaikan. Ia mengatakan bahwa tinjanya telah berubah warna lebih dari 2 bulan sebelumnya dan kini sebentar-sebentar berwarna gelap dan kental seperti ter. Dokter menguji tinja penderita dan menemukan darah yang tak terlihat (darah samar). Dokter Bogi kemudian melakukan pemeriksaan klinis dan menuliskan sesuatu di lembar pemeriksaannya. Dokter muda Ruben mengamati lembar tersebut dan tampak olehnya Diagnosa yang ditulis oleh dokter Bogi, SpPD adalah tukak peptik. Oooo .... batin hati dokter muda Ruben. Setelah jam poli selesai, dokter Bogi, SpPD memberikan sebuah artikel sebagai berikut : Peptic ulcer is a term used to describe a group of ulcerative disorders that occur in areas of the upper gastrointestinal tract (e.g., gaster and duodenum) that are exposed to acid-pepsin secretions. A peptic ulcer can affect one or all layers of the gaster or duodenum. The ulcer may penetrate only the mucosal surface, or it may extend into the smooth muscle layers. Occasionally, an ulcer penetrates the outer wall of the gaster or duodenum. Spontaneous remissions and exacerbations are common. Healing of the muscularis layer involves replacement with scar tissue; although the mucosal layers that cover the scarred muscle layer regenerate, the regeneration often is less than perfect, which contributes to repeated episodes of ulceration. Causes of Peptic Ulcer There are two main causes of ulcers: (1) too little mucus production or (2) too much acid being produced in the gaster or delivered to the intestine. A variety of conditions may cause either or both of these disturbances. Decreased Mucus Production as a Cause of Ulcer Ulcers most commonly develop when the mucosal cells of the gut do not produce adequate mucus to protect against acid digestion. Causes of decreased mucus production can include anything that decreases blood flow to the gut, causing hypoxia of the mucosal layer and injury to or death of mucusproducing cells. This type of ulcer is called an ischemic ulcer. Decreased blood flow occurs with all types of shock. A particular type of ischemic ulcer that develops after a severe burn is called a Curling ulcer.
Decreased mucus production in the duodenum can also occur as a result of inhibition of mucusproducing glands, called Brunner glands, located there. Their activity is inhibited by sympathetic stimulation. Sympathetic stimulation is increased by chronic stress, thus making a connection between chronic stress and ulcer development. The main cause of decreased mucus production is related to infection with H. pyloribacteria. H. pyloricolonize the mucus-secreting cells of the gaster and duodenum, reducing their ability to produce mucus. The use of various drugs, especially nonsteroidal antiinflammatory drugs (NSAIDs) is also associated with an increased risk of ulcer development. Aspirin, especially, causes irritation of the mucosal wall, as do the other NSAIDs and glucocorticosteroids. These drugs contribute to ulcer development by inhibiting protective prostaglandins both systemically and in the gut wall. Gastric or intestinal bleeding can occur from NSAIDs, with little early warning. In contrast to peptic ulcer from other causes, NSAID-induced gastric injury often is without symptoms, and lifethreatening complications can occur without warning. Other drugs or foods associated with ulcer development include caffeine, alcohol, and nicotine. These drugs seem to injure the protective mucosal layer also. Excess Acid as a Cause of Ulcer Acid production in the gaster is necessary for activation of gaster digestive enzymes. Hydrochloric acid (HCl) is produced by the parietal cells in response to certain foods, drugs, hormones (including gastrin), histamine, and parasympathetic stimulation. Foods and drugs such as caffeine and alcohol stimulate the parietal cells to produce acid. Some individuals might be overreactive in their parietal response to these substances or other foods, or they may simply have a greater number of parietal cells than normal and therefore release excess acid. Aspirin is an acid, which may directly irritate or erode the lining of the gaster. Because gastrin stimulates the production of acid, anything that increases the secretion of gastrin can lead to excess acid production. The main example of this condition is called Zollinger–Ellison syndrome, a disease characterized by tumors of the gastrin-secreting endocrine cells. Other causes of excess acid include excessive vagal stimulation to the parietal cells that is seen after severe brain injury or trauma. Ulcers that develop under these circumstances are called Cushing ulcers. Excess vagal stimulation during psychological stress may also cause excess HCl production. Increased Delivery of Acid as a Cause of Duodenal Ulcer Too rapid movement of gaster contents into the duodenum can overwhelmthe protective mucus layer there. This occurs with irritation of the gaster by certain foods or microorganisms, as well as by excess gastrin secretion or abnormal distention. Rapid movement of gaster contents into the intestine also occurs in the condition called dumping syndrome. Dumping syndrome happens when the ability of the gaster to hold and slowly release chyme into the duodenum is compromised. One cause of dumping syndrome is surgical removal of a large part of the gaster. Dumping syndrome not only results in rapid delivery of acid to the intestine, but it can cause cardiovascular hypotension. Hypotension occurs because the delivery of multiple food particles to the intestine all at once results in a large amount of water moving from the circulation into the gut by osmosis.
The clinical manifestations of uncomplicated peptic ulcer focus on discomfort and pain. The pain, which is described as burning, gnawing, or cramp-like, usually is rhythmic and frequently occurs when the gaster is empty—between meals and at 1 or 2 o’clock in the morning. The pain usually is located over a small area near the midline in the epigastrium near the xiphoid and may radiate below the costal margins, into the back, or rarely, to the right shoulder. The pain is usually relieved by food or antacids. The complications of peptic ulcer include hemorrhage, obstruction, and perforation. Hemorrhage is caused by bleeding from granulation tissue or from erosion of an ulcer into an artery or vein. Obstruction is caused by edema, spasm, or contraction of scar tissue and interference with the free passage of gastric contents through the pylorus or adjacent areas. There is a feeling of epigastric fullness and heaviness after meals. With severe obstruction, there is vomiting of undigested food. Perforation occurs when an ulcer erodes through all the layers of the gaster or duodenum wall. Perforation develops in approximately 5% of persons with peptic ulcers, usually from ulcers on the anterior wall of the gaster or duodenum. Withperforation, gastrointestinal contents enter the peritoneum and cause peritonitis, or penetrate adjacent structures such as the pancreas. Radiation of the pain into the back, severe night distress, and inadequate pain relief with the eating of foods or taking of antacids in persons with a long history of peptic ulcer may signify perforation. MODUL TASK Berdasarkan artikel tersebut di atas, dokter muda Ruben diberikan tugas sebagai berikut : 1. Garis bawahi istilah2 yang terkait/menggambarkan struktur anatomi makros maupun mikros. 2. Deskripsikan struktur-struktur anatomi yang telah Anda identifikasi dalam narasi kasus di atas sesuai dengan lokasi atau topografinya di regio abdomen. Lengkapilah dengan deskripsi apapun yang terkait dengan Lengkapi istilah2 tersebut dengan keterangan yang relevan dalam sistem GIT! (bila terdapat duplikasi istilah, gunakan satu saja) ISTILAH
Lokasi/topografi
upper gastrointestinal tract
gaster duodenum layers of the duodenum
gaster
mucosal surface smooth muscle layers
or
DESKRIPSI
outer wall of the gaster or duodenum. outer wall of the gaster or duodenum scar tissue mucosal layers / mucosal wall peritoneum pancreas mucosal cells of the gut mucus mucus-producing cells mucus-producing glands / Brunner glands parietal cells pylorus anterior wall of the gaster or duodenum
3. Pada artikel di atas, disebutkan beberapa area berikut ini : small area near the midline in the epigastrium near the xiphoid1 and may radiate below the costal margins2, into the back3, or rarely, to the right shoulder4. Dengan menggunakan ilustrasi gambar di bawah ini, tandailah area-area yang tersebut di atas dengan jelas.
Bagaimana rasa nyeri tersebut dapat dijalarkan ke bagian tubuh yang jauh dari sumber nyeri? Jelaskan
4. Dalam narasi di artikel tersebut, terdapat fungsi-fungsi yang terkait dengan struktur anatomi tertentu. Sebutkan struktur yang dimaksud Fungsi
Struktur anatomi terkait
Keterangan mekanisme dasar
acid-pepsin secretions healing inhibition synthesis
of
prostaglandin
may radiate below the costal margins, into the back,
5. Apakah yang dimaksud adjacent structures dalam bacaan di atas?
Kasus Klinik 2 Dokter muda Luthfi sedang tegang menanti ujian dokter di Lab.IPD. Akan dapat pasien dengan diagnosa apa ya? Mudah-mudahan kasusnya cirrhosis, karena sebelumnya ia menyiapkan Morning Report kasus itu, jadi masih lumayan ingat. Kemudian, ia dipanggil ke poli penyakit dalam untuk memeriksa seorang pasien…Seorang pria berusia 38 tahun datang dengan keluhan perutnya terasa membesar dalam beberapa bulan ini. Ia memperhatikan juga kalau kulitnya bertambah kuning. Dokter muda Luthfi mulai bersemangat dengan kasus ini, ia bertanya apakah penderita pernah sakit hepatitis sebelumnya, pasien menyangkalnya. Tetapi pasien mengakui bahwa ia sering minum minuman beralkohol hampir setiap hari. Hmm…calon dokter kita ini semakin antusias,…ia mulai melakukan pemeriksaan fisik. Didapati telapak tangan pasien berwarna kemerahan, abdomennya membuncit , sedikit tegang , dan ada gelombang cairan saat diperkusi. Pada permukaan abdomen terutama region umbilicus terdapat pelebaran vascular yang mencolok. Dokter muda Luthfi, mulai menulis status pasiennya untuk dilaporkan kepada dosen pengujinya. Dan saat face to face dengan dr.Putra , SpPD, ia mulai bercerita tentang kisah hidupnya….eh pasiennya.
Diagnosa yang paling mungkin? Alcoholic cirrhosis with portal hypertension Organ apa saja yang mungkin terkena ? Liver and those drained by the portal venous system
CLINICAL CORRELATION This patient abuses alcohol and has manifestations of end-stage liver disease (cirrhosis). Cirrhosis results in severe fibrotic scarring of the liver, which decreases blood flow through the organ. Hypertension in the portal venous system is the result, with collateral venous flow, especially in organs having venous drainage by the portal and vena caval systems, such as the abdominal surface, and the esophagus. The spleen is frequently enlarged, and the ascites,fluid within the peritoneal cavity, is due to liver insufficiency. Death may ensue due to bleeding from esophageal varices or bacterial peritonitis of the ascitic fluid. Marked hepatic insufficiency is another complication.
PEMBELAJARAN ANATOMI HEPAR Learning Objective : 1. Dapat menjelaskan anatomi hepar dan vaskularisasinya yang unik. 2. Dapat memahami anatomi porto-caval anastomosis dan kepentingan klinisnya, yang ditunjukkan dengan menggambarnya. Modul Task : 1. Hepar adalah organ viscera terbesar, jelaskan struktur macrosnya, meliputi lobus-lobusnya, ligament dan perlekatan terhadap peritoneum, juga struktur penting lain pada hepar!
2. Hepar menerima dual blood supply. Apa maksudnya? Jelaskan!
3. Uraikan mengenai lobules-lobulus hepar, apakah ada keterkaitan dengan fungsi fisiologisnya?
4. Gambarlah secara skematik anatomi portocaval anastomoses dan korelasi klinisnya!
