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UNIVERSITY OF FLORIDA

DEPARTMENT OF SURGERY

AMERICAN BOARD OF SURGERY
IN-SERVICE TRAINING EXAM
(ABSITE)

BASIC SCIENCE 101

By

MATTHEW J. DELANO

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A BASIC SCIENCE REVIEW OF THE CORE TOPICS IN
GENERAL SURGERY FOR THE AMERICAN BOARD
OF SURGERY IN-SERVICE TRAINING EXAM

© 2008 MATTHEW J. DELANO

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"WEAKNESS OF ATTITUDE BECOMES WEAKNESS OF CHARACTER"

Albert Einstein

“CHANCE FAVORS THE PREPARED MIND"

Louis Pasteur

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ACKNOWLEDGMENTS

RICHARD E. DEAN, M.D.
JOHN ARMSTRONG, M.D.
GEORGE SAROSI, M.D.
KEVIN BEHRNS, M.D.
MICHAEL E. MAHLIA, M.D.
WILLIAM CANCE, M.D.
LYLE L. MOLDAWER, Ph.D.

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TABLE OF CONTENTS

Page

ACKNOWLEDGMENTS ...............................................................................................................4

CHAPTER

1 COURSE DESCRIPTION AND SYLLABUS: BASIC SCIENCE 101 ..................................7 

2 AMERICAN BOARD OF SURGERY IN-SERVICE TRAINING EXAM (ABSITE) ........10

3 BODY AS A WHOLE: SESSION 1

4 BODY AS A WHOLE: SESSION 2

5 BODY AS A WHOLE: SESSION 3

6 GASTROINTESTINAL SYSTEM: SESSION 4

7 GASTROINTESTINAL SYSTEM: SESSION 5 ...................................................................13 

Colon/Rectum .........................................................................................................................13 
Preferred Energy Source Colonocyte ..............................................................................13 
Hereditary Nonpolyposis Colorectal Cancer (HNPCC) Lynch Syndrome .....................14 
Colon Bacteria .................................................................................................................15 
Site of Colon Absorptive Activity ...................................................................................16 
Spleen .....................................................................................................................................17 
Diagnosis/Treatment for Immune Thrombocytopenic Purpura (ITP) .............................17 
Rationale for Splenectomy for ITP..................................................................................18 
Overwhelming Post Splenectomy Infection (OPSI)........................................................19 
Site of Extramedullary Hematopoiesis in Myelofibrosis ................................................20 
Pancreas ..................................................................................................................................21 
Arterial Supply to the Head of the Pancreas ...................................................................21 
Pancreatic Enzymes – Characteristics of Secretion.........................................................22 
Physiology of Secretin Release .......................................................................................23 
Activation of Pancreatic Proenzymes ..............................................................................24 
Electrolytes in Pancreatic Exocrine Secretion with Stimulation .....................................25 
Characteristics of Pancreatic Divisum.............................................................................26 
Results of Acinar Cell Injury in Acute Pancreatitis ........................................................27 
Biliary/Liver ...........................................................................................................................28 
Bile Salt Metabolism .......................................................................................................28 
Hormonal Stimulation of Hepatic Bile Flow...................................................................29 
Characteristics of Lithogenic Bile ...................................................................................30 
Composition of Primary Common Bile Duct Stones ......................................................31 
Biochemistry of Hepatic Lipid Degradation ...................................................................32 
Differential Diagnosis of Jaundice with Non-Dilated Ducts ...........................................33 

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..........40  Location of Anomalous Hepatic Arteries ............................................................................................37  Venous Tributaries of the Portal System ........................................................................................48  Bile Acid Synthesis ........................50  Biliary Tract Bacteria ...........................46  Anatomy of Common Bile Duct...............................45  Findings Associated with the Hepatorenal Syndrome.............................42  Prognostic Test of Liver Function Reserve ............................................................................................................................................................56  Basis for Chemoemboliztion of Hepatic Metastases .........................................................................................................51  Preoperative Measure of Portal Venous Pressure ..................44  Etiology of a Sudden Increase in End Tidal CO2 After Evacuating CO2 in a Laparoscopic Cholecystectomy Procedure ................55  Pathophysiology of Ascites in Alcohol Cirrhosis ...........................................39  Principles Associated with Chemo Embolization of Liver Metastases .......................................................................................................Diagnostic Test for Symptomatic Gall Bladder Disease Without Stones – Biliary Dyskinesia ..........................................34  Segmental Anatomy of the Liver .........................38  Susceptibility to Hepatoma (Hepatocellular Carcinoma) ...................................................................52  Best Test of Hepatic Biosynthesis ...................................................58  6 .............................49  Characteristics of Chylomicrons ...............................................................................................................................................................................36  Hepatic Acute Phase Response .............................................................................................................................................................................................................................................................................................................................35  Best Test of Hepatic Biosynthesis .......................................................................................57  Etiology of Liver Failure/Diagnosis of Ligation of Hepatic Artery (Unintended Hepatic Artery Ligation at Operation) ............................................47  Characteristics Hepatocytes............................41  Anatomy of Aberrant Right Hepatic Artery .......................................54  Hepatocellular Cancer in Chronic Hepatitis B (Complications Hepatitis B) ..............................................................................................................53  Abnormal Liver Function Test in Metastatic Colon Cancer ........43  Preoperative Treatment of Obstructive Jaundice ....

January 4. Armstrong. Take an on-line learning styles inventory at: http://www. 4.edu/learningstyles/ilsweb.D. ABSITE Score 3. Understand and comprehend the five fundamental areas of surgery related basic science knowledge that the ABSITE test. 4. Kevin Behrns’s Residence Sun. Improve individual ABSITE scores by 10-20%.PGY-7+) Review Session Time/Location: Dates: Sun. 2008 Dr. January 25. M.armstrong@surgery. 2.edu 7 . Audience All categorical and preliminary surgical residents (PGY-1 .edu office: 273-5675. 2009 Dr. 2009 Dr.D. Take pre-course test and post-course test. Understand the historical significance and current purpose of the ABSITE. 2.ncsu.D.D. Basic Science 101 will focus on building and reinforcing the fundamentals of surgical basic science knowledge which will serve as a foundation for further clinical and operative knowledge growth and ABSITE success. Ph. M.edu cell: 352-514-9451 John H. Review ABSITE appropriate surgery related basic science for each group session. george. December 14.ufl. Kevin Behrns’s Residence Behrns Residence: Assessment: 1. Attend each review session. pager: 413-5666.ufl. Individual accountability: Pre-course test score. CHAPTER 1 COURSE DESCRIPTION AND SYLLABUS: BASIC SCIENCE 101 Goals: 1. Kevin Behrns’s Residence Sun. Course Directors: Matthew J. Team accountability: Jeopardy Champion Expectations: 1. delanmj@surgery. Kevin Behrns’s Residence Sun. January 18. Kevin Behrns’s Residence Sun. 2008 Dr.C. 2009 Dr. 5. john... Promote personal lifelong habits of scientific surgical learning and self education. Be prepared to answer basic science questions during each session.sarosi@surgery..engr.. Kevin Behrns’s Residence Sun. December 21.. 3. take the ABSITE. 2008 Dr.ufl. 3. Kevin Behrns’s Residence Sun. Delano. cell: 786-255-4820 George Sarosi. F.S. December 7. Course attendance and participation 2. M. January 11.html.A. Post-course test score. 2009 Dr.

2009 CARDIOVASCULAR AND PULMONARY Chapter 8 January 25. 8 . The course material has been concentrated. These are not my topics of interest rather the topics that appear yearly on the ABSITE. No Exceptions. ENDOCRINE. 2009 GASTROINTESTINAL TRACT Chapter 6 January 11. Use these to test your knowledge and guide your studies.ncsu. HEAD AND NECK. HEMATIC AND LYMPHATIC SYSTEMS AND BREAST How to use the course materials: Before arriving at the first session you should take the on-line learning styles inventory at: http://www. 2008 BODY AS A WHOLE Chapter 3 December 14. Dean. 2009 GU. The course is broken down by basic science knowledge category as tested by the ABSITE. 2008 BODY AS A WHOLE Chapter 4 December 21.engr. which will provide feedback for you regarding your personal learning style. 2009 GASTROINTESTINAL TRACT Chapter 7 January 18. Each individual is expected to have covered the relevant information prior to each review session just as each individual is expected to review the pertinent details of a general surgery case prior to entering the operating room. This will enable you to better understand how you learn and prepare your own focused study plan.edu/learningstyles/ilsweb. Each chapter contains relevant basic science questions with answers at the end that frequently appear on the ABSITE in some form from year to year. by Richard E. Each review session will concentrate on the information and topics as related in the chapters as listed above from the aforementioned compiled source. SKIN.Course Schedule: Review Session Date: Topics to be covered: Course materials: December 7. NERVOUS. Chapter 9 MUSCULOSKELETAL. 2008 BODY AS A WHOLE Chapter 5 January 4. Please bring the results of your online learning inventory to the first review session so that we can review them and accommodate all your learner styles. and distilled from the past ten years worth of Michigan State Integrated ABSITE Reviews.html. fermented.

Matthew Warrick.D.D.D. 3rd Ed. 17th Ed. Kenneth L.D. Michael Hong.D. flail.D.D. M.D.D. M. Makesha Miggins. Nicole Croley. Trevan Fischer. M.D. M. Darrell Hunt. rather you will be asked questions directly from the course content presented here and your answers will immediately impact you. Peter Salerno. B. Nicole Kissane. Bo Neichoy.M. D.D. Craig Wengler. Peter Fiester. Jason Wilson. At the review sessions the information presented in this text will not be covered in a didactic nauseating fashion allowing you to irresponsibly coast. M. Reference Material: The Physiologic Basis of Surgery. M.. and more importantly your team members. M. Jeopardy Teams: Team Dragstedt: Team Woodward: Team Copeland Robert Browning. ISBN 0-7216-0409-9 9 .D. Robert Winfield. by Courney M. M. M. Chad Stasik. M. M. Alyson Waterman. M. M.D.D. Mark Wilson.D. Dean Yamaguchi. 2004. Claire Griffin. The team that answers the most questions correct over the seven review sessions will be the intellectual winner and will also receive a substantial prize to be decided. M. hide. M. D. M.D. Townsend Jr. 2002.D.D. Skeeter Salcedo. M.D. Elsevier Saunders. R.D.D.D. M. Brady McDonald.. Mark Evers. Mattox.D. M. Lippincott Wiliams & Wilkins.D.D. M. M.D. Lindsey Goldstein.D. Matthew Hughes. M. Robert Timmerman.D. Georgios Rossidis. M. Patrick O’Leary. M. Josef Braun. Ph.O. M. M.D. M. Damian Dyer. Tad Kim. M. flake and slide away from excellence. M. Omeni Osian.D. M. Sabiston Textbook of Surgery: The Biloigical Basis of Modern Surgical Practice. M. Constance Lee. Khayree Butler. ISBN 0-7817-3839-3. Lori Filichia. Ramy Nasr. M.D. M. Alice Coker. M.D. sleep.D. Angel Caban.D. Alex Cuenca.D. Gregory Gerber.D. M.D. Stancie Rhodes.B. M. by J. Elizabeth Warner.D.D.D. M. M.D.D. M.D. Trajan Cuellar. M. Vincent Mortellaro. Adrienne Buckman. Daniel Beauchamp. M. M. Luke Gutwein.

Residents are strongly encouraged to keep copies of their score report for their records. Examination Content Since 2006 the ABS offers the ABSITE as a junior level (PG-1 and -2) and senior level (PG-3 to -5) examination. 60% of the examination focuses on basic science. CHAPTER 2 AMERICAN BOARD OF SURGERY IN-SERVICE TRAINING EXAM (ABSITE) Introduction The American Board of Surgery offers annually to surgery residency programs the In-Training Examination (ABSITE). The relative emphasis on clinical content categories in the two examinations is shown in the following tables. multiple-choice examination designed to measure the progress attained by residents in their knowledge of basic science and the management of clinical problems related to general surgery. such as PGY level. The ABS will not discuss examination results with residents. Both the junior. The ABS will not provide residents with a score report or "transcript. 20% of the exam focuses on basic science and 80% on clinical management. The ABSITE is furnished to program directors as an evaluation instrument to assess residents' progress. Junior ABSITE Senior ABSITE % (# questions) % (# questions) Basic Science 60% (135) 20% (45) Clinical Medicine 40% (90) 80%(180) Total 100%(225) 100%(225) 10 . name. including a resident's individual score report. The ABS also will not regenerate any report as a result of miscoding of information. In the senior-level exam. a written. examinees are given five hours to take the exam. etc." Residents who request this information will be directed to contact their general surgery residency program.and senior-level versions consist of 225 multiple-choice questions. It is not available to individual residents and is not required as part of the certification process. The ABS provides program directors with various reports. The results are released only to program directors. Junior and Senior ABSITE basic science and clinical medicine breakdown. Any inquiries regarding the ABSITE must come directly from the program. as the ABS does not retain this information. Reporting of Results ABSITE results are made available to program directors in early March. For the junior-level exam. your program director can help with the interpretation of the results. Table 1. If you have questions once you have received your individual score report. while 40% centers on the management of clinical surgical problems.

80% 16.absurgery. Knowledge Category Junior ABSITE Senior ABSITE # questions # questions BODY AS A WHOLE Basic Science 90 10 Clinical Medicine 60 45 GASTROINTESTINAL TRACT Basic Science 15 10 Clinical Medicine 9 45 CARDIOVASCULAR AND PULMONARY SYSTEMS Basic Science 11 8 Clinical Medicine 6 30 GU. AND LYMPHATIC 7. HEMATOLOGIC.70% NERVOUS SYSTEMS ENDOCRINE. HEAD AND NECK. MUSCULOSKELETAL. Knowledge categories comprising the Junior and Senior ABSITE Knowledge Category Junior ABSITE Senior ABSITE % of Test % of Test BODY AS A WHOLE 66.80% 16.org/ 11 .Table 2. AND BREAST Clinical Medicine 6 30 Adapted from the American Board of Surgery: http://home.70% GU. SKIN. HEAD AND NECK.7 SYSTEMS .80% 16. AND BREAST Table 3. SKIN. Basic Science 11 8 AND NERVOUS SYSTEMS Clinical Medicine 6 30 ENDOCRINE. MUSCULOSKELETAL. AND LYMPHATIC Basic Science 11 8 SYSTEMS .60% 25% GASTROINTESTINAL TRACT 10% 25% CARDIOVASCULAR AND PULMONARY SYSTEMS 7. HEMATOLOGIC. AND 7. Junior and Senior ABSITE basic science and clinical medicine breakdown by knowledge category.

MUSCULOSKELETAL. HEMATIC.Table 4. SKIN. NERVOUS. HEAD AND NECK. LYMPHATIC. BREAST Basic Science 14 Clinical Management 7 As you can see the Junior ABSITE is over 60% basic science while the Senior ABSITE is predominantly clinical medicine. 12 . BODY AS A WHOLE: NUMBER OF QUESTIONS Basic Science 47 Clinical Management 57 GASTROINTESTINAL: Basic Science 29 Clinical Management 9 CARDIOVASCULAR AND RESPIRATORY: Basic Science 25 Clinical Management 7 GU. Breakdown of the 2007 Junior ABSITE. SYSTEMS: Basic Science 11 Clinical Management 7 ENDOCRINE.

“In vivo measurement of colonic butyrate metabolism in patients with quiescent ulcerative colitis. CHAPTER 7 GASTROINTESTINAL TRACT: SESSION 5 Colon/Rectum Preferred Energy Source Colonocyte Short-chain fatty acids (SCFAs) are produced in the colon by fermentation of dietary fiber by colonic bacteria.” Gastroenterology 83:424-9 Ahmad MS. “Utilization of nutrients by isolated epithelial cells of rate colon.” Gut 46:493-9 Simpson EJ. and butyrate. Substrates are metabolized by the colonic mucosa in the order of butyrate>glucose>ketone bodies>glutamine. et al. propionate. “Butyrate and glucose metabolism by colonocytes in experimental colitis in mice. Roedinger WE. Butyrate is the major source of fuel for the colonic epithelial cells. A lack of butyrate has been shown to result in colonic inflammation as seen in diversion colitis. The major SCFAs produced are acetate.” Gut 46:73-7 13 . It has been hypothesized that impaired metabolism of butyrate may be present in the colonocytes of patients with ulcerative colitis (UC). Use of SCFA enemas in the treatment of UC patients has been promising in early studies. et al. Butyrate enemas have been used satisfactorily as a treatment for this.

As the abnormal cells continue to divide. Familial predisposition for other primary cancers in addition to the predisposition for colon cancer. multiple colon cancers. This group is at greater risk for recurrence. CA is poorly differentiated or vascular/lymphatic invasion is present. MSH6. one of whom is a first degree relative of the other two. Colorectal CA must involve at least two generations. Variations in the MLH1. at least one CA case must occur before 50 years of age. Familial predisposition to colorectal cancer with right-sided predominance. Adenomas and carcinomas occur at an early age (adenomas in 20’s and 30’s—carcinomas 40-45 years of age) and are often proximal in location and multiple. site is often female reproductive organs. HNPCC Criteria: Females must have at least three relatives with colorectal CA. MSH2. 2nd Edition 14 . All of these genes are involved in the repair of mistakes made when DNA is copied (DNA replication) in preparation for cell division. Greenfield. Scientific Principles & Practice. particularly endometrial carcinoma. Diagnosis: Screening sigmoidoscopy every 3-5 years with yearly fecal occult blood tests beginning at age 50. stomach and urinary tract. the accumulated mistakes can lead to uncontrolled cell growth and possibly cancer. Lynch Syndrome I is an autosomal dominant. right-sided colon cancer. Predominantly early onset proximal colon carcinoma associated with other extracolonic adenocarcinomas. and long survival. Lynch Syndrome II Main Features: The same as Lynch Syndrome I with increased risk for cancer of the female genital tract (endometrial. Although mutations in these genes predispose individuals to cancer. Surgery. Treatment: Colonoscopy with polypectomy (to clear entire colon from possible synchronous adenomas). Main Features: No associated polyposis. ovarian). Colonoscopy: Every 3 years in patients w/out evidence of high-grade dysplasia or CA. Surgery: If < 2mm clear margins on polypectomy. and PMS2 genes increase the risk of developing Lynch syndrome. not all people who carry these mutations develop cancerous tumors. Predominantly early-onset proximal colon carcinomas. site-specific colon cancer. Mutations in any of these genes prevent the proper repair of DNA replication mistakes.Hereditary Nonpolyposis Colorectal Cancer (HNPCC) Lynch Syndrome HNPCC is an autosomal dominant familial colorectal cancer arising in discrete adenomas but polyposis does not occur.

Relative Frequency of Bacterial Species in Fecal Flora Rank Percent Organism(s) 1 12 Bacteroides vulgatus 2 7 Fusobacterium prausnitzii 3 6. A perforated appendix contains about 106 to 107 bacteria per gram of content. The most common components of fecal flora are listed below. p 62 15 . Sigmoid colon contains 1010 to 1011 bacteria per gram of content.5 Bacteroides thetaiotaomicron 7 3.5 Bifidobacterium adolescentis 4 6 Eubacterium aerofaciens 5 6 Peptostreptococcus productus II 6 4.06 Escherichia coli. Klebsiella pneumonia and 37 other bacterial species Simmons & Steed. fragilis 59-75 0. ovatus 29 0. p 190 O’Leary.6 Eubacterium eligens 8 3.3 Peptostreptococcus productus I 9 3.7 B.2 Eubacterium biforme 10 2. One should note that there are no pathogenic species among the most common 25 organisms. aerofaciens III 11 2.Colon Bacteria As opposed to disease-causing bacteria in the small intestine.3 Bacteroides distasonis 28 0. in which adherence is an important property. the long transit time in the colon makes adherence a much less important attribute.6 B. Anaerobes are favored 1000:1 versus aerobes in the colon.5 E. The bacterial density increases as one moves down the colon.13 Streptococcus faecalis 76-113 0.

p 1272 16 . The majority of water absorption occurs in the ascending colon. Schwartz. 7th Edition. The colon absorbs greater than 90% of the water and electrolytes presented to it.Site of Colon Absorptive Activity The major absorptive function of the colon is final regulation of water and electrolyte balance in the intestine. Principles of Surgery.

Any manifestations suggestive of intracranial bleeding demand emergency splenectomy.000 or less and at times approach zero. 6th Edition O’Leary. Acute ITP has an excellent prognosis in children under the age of sixteen. Platelet counts are generally reduced to 50. the results by splenectomy are significantly more impressive than are the results from steroids. 2nd Edition Sabiston. and if thrombocytopenia recurs. the platelet count rises to over 100. The spleen is the source of these factors. greater omentum. A Technetium scan may be useful in identifying the accessory spleen. splenectomy is performed. The term ITP should be reserved for a hemorrhagic disorder characterized by a subnormal platelet count in the presence of bone marrow containing normal or increased megakaryocytes and in the absence of any systemic disease or history of ingestion of drugs capable of inducing thrombocytopenia. Approximately 80% of these will recover completely without specific therapy. In most series. and gastrosplenic and gastrocolic ligaments. If the patient does respond. Principles of Surgery. Occasionally. Approximately 80% of the patients treated with splenectomy respond permanently and require no further steroid therapy. Female patients outnumber males at a ratio of 3:1. splenectomy is carried out. Platelets should be available for the procedure but should only be administered in patients who continue bleeding following removal of the spleen. In one series.000/mm3 in 7 days. Common sites are the splenic hilus. adjacent to the splenic vessels and tail of the pancreas. The generally accepted protocol for managing patients with diagnosed ITP includes an initial 6- week to 2-month period of steroid therapy. the steroid therapy is tapered off. Textbook of Surgery. Spleen Diagnosis/Treatment for Immune Thrombocytopenic Purpura (ITP) Idiopathic thrombocytopenic purpura (immune thrombocytopenic purpura ITP)) is an acquired disorder caused by the destruction of platelets exposed to circulating IgG antiplatelet factors. Physiologic Basis of Surgery. p 1196 17 . Schwartz. the disease recurs and patients achieve permanent cure following removal of an accessory spleen. If the patient does not respond. Approximately 20% of patients have an accessory spleen. 15th Edition. It is also the major site for sequestering sensitized platelets. 5 of 6 patients with ITP and life-threatening intracranial bleeding were saved by splenectomy. In most patients.

p 1193-95 18 . The thrombocytopenia is caused by a circulating anti-platelet factor that causes platelet destruction by the reticuloendothelial system. the anti platelet factor is an immune globulin (IgG) antibody directed toward a platelet associated antigen. Platelet destruction in ITP requires sufficient quantities of antigen (platelets). and splenic cells from patients with chronic ITP produce 5-6 times more IgG in culture than control splenic cells. are improved after splenectomy even if their platelet counts were not significantly increased by corticosteroid therapy. In most patients. The stagnant blood flow allows sensitized platelets to be readily removed by phagocytic cells. The spleen is the most active site of platelet destruction. Treatment: Considering the immune mechanisms involved. because 30% of the total circulating platelet mass is within the spleen at all times and serves as an exchangeable platelet pool. antibody and phagocytic cells in an environment that provides time for antibody binding and subsequent platelet phagocytosis.Rationale for Splenectomy for ITP Immune thrombocytopenic purpura. however. Most patients with ITP are improved with administration of this drug. Sabiston. 15th ed. The spleen is an important site of antibody production. formerly called idiopathic thrombocytopenic purpura. initial treatment normally consists of corticosteroid therapy (1 mg per kg per day). but requires several days for beneficial platelet increase to occur. Most patients. Intravenous gamma globulin is also useful. The spleen is ideally suited for this function.. is a syndrome characterized by a persistently low platelet count.

Sabiston. The infection progresses rapidly to hypotension. The mortality is 50-70% in fully developed cases in spite of appropriate antibiotics. coma. malaise. 1162 19 . OPSI has a prodromal phase with fever. DIC. pp 1146. OPSI is greater when splenectomy is completed for malignant or hematologic diseases and is a high risk for children less than 4 years of age. streptococcus.Overwhelming Post Splenectomy Infection (OPSI) Asplenic patients are at risk for developing OPSI. and death. pneumonia is the most frequently involved organism (50-90% of cases). respiratory distress. and other pneumonia species. 16th Edition. High-risk asplenic patients should be reimmunized within 3-6 years. pneumonia species and H. Asplenics have defective activation of complement. influenza. myalgia. S. OPSI continues as a risk and may be greater after 2 years and approaches 50% after 5 years. is impaired following splenectomy. neisseria meningitis. The opsonization of encapsulated bacteria. Others include haemophilus influenza. chills. and other nonspecific symptoms. the most common fatal complication of splenectomy. Immunization should precede splenectomy by 2 weeks if possible or soon after surgery when preimmunization is not possible. subnormal levels of IgM and a suppressed peripheral immunoglobin response. Prophylaxis for OPSI includes immunization for S. The infection is due to encapsulated bacteria. Textbook of Surgery. which involves immunoglobulin and complement.

or Agnogenic Myeloid Metaplasia (AMM). 35% have massive splenomegaly. is believed to be a response to a clonal proliferation of hematopoietic stem cells. Splenomegaly related symptoms are best treated with splenectomy. Extra-medullary hematopoiesis is manifest by splenomegaly and hepatomegaly in two thirds. Schwartz. Nucleated red blood cells and immature myeloid elements in blood are present in 96% of the cases. 8th Edition. Marrow failure often ensues. p 1304 20 .Site of Extramedullary Hematopoiesis in Myelofibrosis Myelofibrosis. Principles of Surgery.

430 21 . Pancreas Arterial Supply to the Head of the Pancreas The blood supply to the head of the pancreas is largely from the anterior and posterior pancreaticoduodenal arcades. The anterior superior and posterior superior pancreaticoduodenal arteries arise from the gastroduodenal artery. Anatomy for Surgeons. Vol. 2nd Edition. pp 418. The superior mesenteric artery gives rise to the inferior anterior and posterior pancreaticoduodenal arteries to complete the two arcades. 2. Hollinshead. a branch of the hepatic artery. These vessels provide the blood supply to the head of the pancreas and duodenum.

lipase breaks fats into glycerol and fatty acids.3mL per minute. phospholipase A2 • Amylolytic – amylase Lipase and amylase are secreted in their active forms. The end product is a clear. ribonuclease. Pancreatic enzymes are • Proteolytic – trypsin. Cholecystokinin (CCK) and vagal stimulation (acetylcholine) are the principal stimulants for the secretion of pancreatic enzymes. with neurohumoral stimulation the bicarbonate component increases in concentration while the chloride concentration falls. The proteolytic enzymes and phospholipase A2 are secreted as inactive “zymogens. 2nd Edition. and amylase converts starch to disaccharides and dextrans. phospholipase A2 catalyzes the conversion of biliary lecithin to lysolecithin. At basal secretory rates of . Secretin is the principal stimulant of pancreatic water and electrolytes secretion. deoxyribonuclease.2 to . In the intestine. carboxypeptidase. chymotrypsin.” Activation of trypsinogen to trypsin occurs when the zymogen is exposed to the duodenal enzyme enterokinase. elastase • Lipolytic – lipase. pp 452-5 22 . the proteolytic enzymes digest proteins into peptides. colipase. Water and electrolytes originate from the central acinar and intercalated duct cells. Physiologic Basis of Surgery. Trypsin then converts the other zymogens to their active forms.Pancreatic Enzymes – Characteristics of Secretion The digestive enzymes are synthesized and stored in the pancreatic acinar cells and are released in response to cholecystokinin and vagal stimulation. concentrations of chloride and bicarbonate ions are equivalent to plasma. isotonic solution with a pH of 8. However.

and gastrointestinal motility. inhibit gastrin release. p 807 Schwartz. It acts to stimulate release of water and bicarbonate from pancreatic ductal cells.5) or by contact with bile or perhaps fat. Greenfield. gastric acid secretion.Physiology of Secretin Release Secretin is a 27 amino acid helical peptide that is found in the S cells of the duodenum and jejunum. 1997. 1999. Its unique ability to release gastrin from gastrinomas allows parenteral secretion to be used as a diagnostic test in those patients suspected of having Zollinger-Ellison syndrome. The bicarbonate neutralizes gastric acid. It is a true hormone and is released by acidification of the duodenum (pH below 4. 2nd Edition. Secretin also acts to stimulate the flow of bile. 7th Edition. p 1228 23 .

pp 866-67 24 . Chymotrypsinogen is a 246-amino acid polypeptide converted to the active form. by acid. such as carboxypeptidases A and B. hydrolyze nucleic acids into mononucleotides. 2nd Edition. or by the active trypsin itself. and phospolipase. elastase. which converts trypsinogen to trypsin. carboxypeptidase. Other proteolytic enzymes. accelerating coagulation of the blood. enzyme activation is prevented by antiproteolytic enzyme secreted by the acinar cells. They are activated primarily by a duodenal enzyme. which protects the pancreatic tissue from autodigestion. The nucleolytic enzymes ribonuclease and deoxyribonuclease. This enzyme inactivates trypsin by direct binding.Activation of Pancreatic Proenzymes Pancreatic proteolytic enzymes are essential for protein digestion. in turn. are enzymes that further digest proteins that have been digested by trypsin and chymotrypsin. Trypsin. enterokinase. indirectly by enterokinase. These enzymes are secreted as proenzymes and require activation for proteolytic activity. by trypsin or. Within the pancreas.0 to 9. activates chymotrypsin. chymotrypsin.0. Trypsinogen can also be activated by a fall in pH below 7. Trypsinogen is a 229-amino acid polypeptide that hydrolyzes proteins and also acts as thrombokinase.0. The optimal activity of chymotrypsin and trypsin occurs at a pH of 8. but the change is accelerated by enterokinase. The enzyme hydrolyzes proteins in a mechanism similar to that of trypsin but cleaves the proteins at a different site. The proenzymes of trypsin and chymotrypsin are trysinogen and chymotrypsinogen. Greenfield. Trypsinogen can convert spontaneously to trypsin.

7th Edition.0-8. the bicarbonate concentration rises to approximately 140mm/L and the chloride concentration falls. With minimal stimulus to secrete. 1470 Physiologic Basis of Surgery.3) liquid containing more than 20 digestive enzymes. During the maximal pancreatic exocrine stimulus (secretin) the bicarbonate rich fluid is flushed through the pancreatic ducts. Schwartz. With maximal stimulus. 50mm/L). bicarbonate is passively reabsorbed and replaced with chloride when there is minimal stimulus. reducing opportunities for electrolyte equilibriation with plasma.Electrolytes in Pancreatic Exocrine Secretion with Stimulation The pancreas secretes 1 to 2 liters per day of a clear.g. watery. As the bicarbonate rich secretion passes through the larger pancreatic ducts toward the duodenum. pp 452-453 25 . The concentration of the principle anions (bicarbonate and chloride) varies. Principles of Surgery. alkaline (ph 8. which are always found in concentrations similar to plasma. The secretion of bicarbonate at high levels requires active transport and originates from the centroacinar and intercalated duct cells. 110mm/L). p.g. the chloride concentration is high (e. The cation of this juice is sodium and potassium. and that of bicarbonate low (e. 2nd Edition.

Characteristics of Pancreatic Divisum The pancreas appears at about the fifth or sixth week of gestation and is composed of a ventral and dorsal appendage. this occurs in about 70% of individuals. pp 257-59 O’Leary. In the other 30%. Both ducts (when present) empty into the second part of the duodenum. It is felt by many authors that pancreatitis can result from relative outflow obstruction as the minor papilla is not able to adequately accommodate such a large volume. and the remainder of the head. the proximal aspect of the dorsal duct (Santorini) regresses after anastomosis with the ventral duct (of Wirsung). In this case the “main” pancreatic duct empties through the minor papilla. the ventral duct is related to the common bile duct and the dorsal duct empties more proximally into the duodenum. In 4 – 10% of individuals there is failure of fusion of the dorsal and ventral ducts: this is termed pancreatic divisum. Drainage of the dorsal and ventral aspects of the pancreas remains separate and the majority of pancreatic exocrine secretion exits via the accessory duct. pp 63-65 26 . Schwartz. Patency of the dorsal duct beyond the site of fusion forms the accessory duct of Santorini. pp 1402. tail. 1408 Simmons/Steed. Only pancreatic drainage from the uncinate process drains through the ampulla of Vater. Fusion of dorsal and ventral ductal elements produces the major duct of Wirsung. At about seven weeks the anlage fuse secondary to asymmetric gut rotation. Principles of Surgery. Both appendage possess ducts. The ventral anlage forms the uncinate process and a portion of the head. The dorsal component forms the body. 6th Ed.

to form an autophagic cytoplasmic vacuole (zymogen lakes). In acute pancreatitis. The zymogen granules fuse with the lysosomes. carboxypeptidase. where they are converted enzymatically into active forms by enterokinase at the brush border. proteolytic enzymes. Collectively. these findings suggest that the outcome of acinar cell injury involves the intracellular activation of endogenous proteases leading to further injury and local extracellular discharge of acinar cell contents. These zymogen/lysosome vacuoles discharged through the basal lateral cell membrane where the proenzymes are activated resulting in extension of the inflammatory process and proteolysis of adjacent acinar cells. Greenfield. along with amylase and lipase. and elastase. These pro enzymes are packaged into a cytoplasmic zymogen granule. These vacuoles preferentially move to the basal lateral aspect of the acinar cell rather than the luminal apex. Textbook of Surgery. and phospholipases) in an inactive zymogen form. 16th Edition. Enzyme synthesis has been estimated at 107 enzyme molecules per acinar cell per minute. chymotrypsin. are liberated from the acinar cell by extravasation into the surrounding tissues where the enzymes are activated causing an intense inflammatory reaction. the zymogen granule is evacuated into the pancreatic duct lumen. The precursors are transported with water and bicarbonate into the duodenum. Through a process of exocytosis. The increasing activation of the proteolytic enzymes results in acute pancreatitis.Results of Acinar Cell Injury in Acute Pancreatitis The acinar cells of the pancreas contain zymogen granules that are responsible for the exocrine enzyme secretion. Sabiston. this normal orderly secretory sequence is disrupted. In acute pancreatitis. pp 874-875 27 . pp 1114-17 Results of Acinar Cell Injury with Acute Pancreatitis (Pathogenesis of Acute Pancreatitis) The pancreatic acinar cell synthesizes a number of proteases (trypsin. 2nd Edition.

0. Biliary/Liver Bile Salt Metabolism Bile salt synthesis requires high-energy expenditure.5gm of bile acid is lost each day in the stool and is replaced by the synthesis of bile acids from cholesterol in the canicular ducts of the liver. pp 428-429 Sabiston.2 to 0. 16th Edition. Physiologic Basis of Surgery. which allows for rapid diffusion into enterocytes of the terminal ileum. which are conjugated with glycine and taurine in the bile. Conjugation creates a more neutral charged molecule. 2nd Edition. The body therefore reduces this energy cost by recycling the bile salt pool (of 2-5gms) 6 to 15 times per day depending on dietary habits. The bile salts combine with a protein in the enterocyte and enter the portal circulation where they are extracted by the liver with great efficiency (80% in a single pass). pp 1008-1009 28 . Textbook of Surgery. The major bile acids are cholic and chenodeoxy cholic.

Secretin will stimulate canicular bile flow in bile stasis or in cystic fibrosis. Sabiston. 16th Edition. The bile acid pool is 2 – 5gms and the bile acids recirculate 6 – 15 times per day.Hormonal Stimulation of Hepatic Bile Flow Bile flow is dependent on bile acid/salt output and the term “bile acid-dependent flow” has been applied.5gms of bile acids are lost in stool daily and replaced by de Novo synthesis. Only 0. Textbook of Surgery. 1008 29 .2 – 0. Cholangiocytes contain receptors for epidermal growth factor Secretin and Somatostatin.

“Black” stones are created in individuals with hemolytic disorders where the bile becomes supersaturated with unconjugated bilirubin and then precipitates as the calcium salt. or glycoproteins. stasis. Nucleation is an unclear event that may be precipitated by calcium.Characteristics of Lithogenic Bile In the United States. Once nucleation has occurred. 30% of cholesterol is carried in micelles and the remaining 70% is carried in vesicles in a lipid bilayer arrangement. and stone growth. Maintenance of cholesterol in solution is dependent on presence of sufficient amounts of bile salts and phospholipids. The formation of cholesterol stones is dependent on 3 factors: Cholesterol saturation. further precipitation is enhanced by the stones themselves. pp 1447 30 . cholesterol stones account for 70% of gallstones and pigmented stones account for the remaining 30%. Schwartz. 7th Edition. Pigmented stones are thought to be induced by infection creating “brown” stones and are primarily found in Asia. Alterations which result in a relative increase in cholesterol predispose to stone formation. The stability of these vesicles is thought to be the key determinant in saturation and stone formation. mucous. abnormal gallbladder wall absorption. nucleation. or may be due to a lack of antinucleation substances.

Treatment must include identification of the abnormality leading to biliary stasis. Textbook of Surgery. p 1089 31 . The composition of primary bile duct stones is a result in stasis. which are soft and crumble easily with manipulation. which allows bacterial glucuronidases to deconjugate bilirubin diglucuronide and the precipation of bilirubin as a calcium salt. 16th Edition. These stones are usually brown pigment type. Primary common duct stones are associated with biliary stasis and infection.Composition of Primary Common Bile Duct Stones Primary bile duct calculi form within the biliary tract whereas calculi forming within the gallbladder are called secondary calculi. Sabiston.

which may be oxidized by tissues such as muscle and kidney or by the brain during starvation. p 228 32 . two carbons are cleaved from a fatty acyl CoA and released as acetyl CoA.Biochemistry of Hepatic Lipid Degradation Fatty acids. In liver. ATP is obtained when the products of β-oxidation are oxidized further. 1990. Biochemistry. The process of β-oxidation occurs in mitochondria. that is. This series of steps is repeated until the fatty acid is completely converted to acetyl CoA. In a series of four steps that produces FADH2 and NADH. which are the major source of energy in the human. during fasting and during starvation. Fatty acids in the blood are derived from triglycerides of the blood lipoproteins or from those of adipose stores. Marks. Fatty acid oxidation by tissues increases whenever the concentration of fatty acids in the blood increases. acetyl CoA is converted to ketone bodies. are oxidized by β-oxidation.

i. neonatal jaundice 4. and androgens 4. hepatitis or cirrhosis 3. acquired disorders such as hepatocellular disease.e. hemolysis of RBCs 2. i. drug-induced cholestasis. hepatitis or cirrhosis B.e. oral contraceptives. i.Differential Diagnosis of Jaundice with Non-Dilated Ducts The etiology of jaundice can be divided on the basis of bile conjugation: A. hereditary defects. alcoholic liver disease 5. 14th Edition. transferase deficiencies.e. TPN. p 253 33 . or hepatocellular disease. Jaundice with conjugated bile and with non-dilated ducts is found in: 1. i.e. i. hereditary disorders. Jaundice with high concentrations of unconjugated bile is found with: 1. sepsis Harrison’s Principles of Internal Medicine. Gilbert’s Syndrome 3.e. i. drug inhibition (Chloramphenicol).e. Dubin-Johnson Syndrome 2.

p 1087 34 . Cholecystokinin (CCK) is administered IV after the gall bladder is filled with 99TC-labeled radionuclide. the gall bladder ejection fraction is calculated.Diagnostic Test for Symptomatic Gall Bladder Disease Without Stones – Biliary Dyskinesia A subgroup of patients presenting with typical biliary colic do not have evidence of gallstones. 16th Edition. A cholecystectomy in these patients brings relief of symptoms in 85 – 94%. Textbook of Surgery. and the complete workup excludes any other pathology. Twenty minutes later. The Cholecystokinin-Tc-HIDA Scan will be useful in confirming the diagnosis of biliary dyskinsea. An ejection fraction less than 35% at 20 minutes is considered abnormal. Sabiston.

. 2nd Ed. The segmental anatomy of the liver defined by Couinaud (The French system) is based on hepatic vein drainage and segmental branching of the portal vein. The right lobe consists of segments 5 through 8. Segment I Caudate Lobe Segment II & III Lateral Left Lobe Anterior & Posterior Segment IV Medial Left Lobe Segment V & VI Right Lobe. Physiologic Basis of Surgery. hepatic artery and biliary ducts as they enter the hepatic parenchyma. Inferior Anterior & Posterior Segment VII & VIII Right Lobe. 25th Ed. in turn. Segmental liver anatomy.Segmental Anatomy of the Liver The segmental anatomy of the liver is determined by the sequential branching of the portal vein. Superior Anterior & Posterior Figure 14. This bifurcation divides the liver into right and left lobes which.. the left lobe of segments 2 through 4. pg 1048 35 . Depicted is segmental liver anatomy as originally described by Couinaud. O’Leary. hepatic artery and biliary tree. and the left lateral segment of segments 2 and 3. are in line with the fossa for the inferior vena cava (IVC) posteriorly and the gallbladder fossa anteriorly. pp 441-3 Sabiston.

thus a positive anabolic state can be determined by a rise in the serum transferrin levels. lipoproteins. Acute phase proteins produced by the liver in response to a systemic inflammatory state initiate a sudden transient rise in C reactive protein compliment and coagulation proteins. lipid metabolism which generates triglycerides from fatty acids. Sabiston. At least 17 of the major human proteins are synthesized and secreted by the liver. Of these factors. these synthetic functions are difficult to monitor. the reprocessing of biliary salts through the enterohepatic circulation. Albumin synthesis is decreased. Other proteins that are markers of hepatic biosynthesis include the coagulation proteins. 7 has the shortest half-live of 5 to 7 hours and because it is a Vitamin K dependent protein.Best Test of Hepatic Biosynthesis The liver is responsible for many biologic functions including bile formation. and cholesterol are synthesized by the liver but difficult to monitor. The half-life of this protein is 4 to 5 days. and the breakdown and metabolism of hemoglobin to bilirubin. Other major metabolic functions of the liver have to do with carbohydrate. Transferrin is a protein commonly used to assess hepatic synthesis. ketones (acetoacetate). 15th Edition. This test is dependent upon adequate amounts of functional Factor 7. and protein metabolism. pp 1055-1060 36 . Protein synthesis is the most common measure used to determine hepatic synthesis. lipid. absence of Vitamin K or blockage of the γ-carboxylation by Coumadin can be assessed by monitoring the prothrombin. Likewise. Although the liver synthesizes hepatic glycogen after eating and is responsible for burning lactic acid to pyruvate which is subsequently converted back to glucose. Although albumin is the most abundant serum protein (it accounts for up to 15% of total hepatic synthesis) the half-life of albumin (45 days) limits its ability to determine active hepatic synthesis of protein.

(See Table) The role of these proteins is to promote host defense against tissue damage and infection (e. to promote clotting mechanisms and wound healing. transport Fibrinogen Coagulation Hemopexin Hemoglobin binding. ceruloplasmin. and other globulins) while albumin synthesis is decreased. The amino acids are cleared by the hepatocytes through energy-dependent transport systems and are used as energy sources and for protein synthesis. bacterial or viral or parasitic infection or neoplastic growth). pp 411-412 37 . monocytes. This acute phase response is primarily mediated by hormone. fibrinogen. and paracrine messengers (tumor necrosis factor-α. and immune complexes and facilitate their clearance by phagocytic cells). and interferon) produced by activated macrophages.Hepatic Acute Phase Response During any inflammatory process (chemical or physical. autocrine. interleukin -1. C3 and C-reactive protein opsonize bacteria. tissue injury. and endothelial cells and hormones such as cortisol. cytokine transport Cysteine proteinase inhibitor Antiproteinase α1 – Acid glycoprotein Transport. Surgical Critical Care. the liver produces the acute-phase proteins (C3. to function as radical scavengers. to provide transport shuttles for nutrients and metabolites. such as muscle. The amino acids used for protein synthesis are either dietary or the products of degradation of endogenous proteins from other body compartments. parasites. fibroblasts. interleukin -6. 1996. such as drugs Some Increase in Production Haptoglobin Hemoglobin binding. particularly iron α1 – Proteinase inhibitor Antiproteinase Decrease in Production Albumin Transport Transferrin Transport Weigelt and Lewis. particularly iron Ceruloplasmin Oxygen radical scavenger. Liver protein synthesis is also sensitive to exogenous amino acids and can be enhanced by their administration.g. Functions of Acute-Phase Proteins during the Inflammatory Response Acute-Phase Protein Response Major Increase in Production Leukocyte Migration Complement C-reactive protein Opsonization α2 – Macroglobulin Antiproteinase. or from hepatocytes themselves when inadequate nutrients are present. and to enhance biotransformation reactions. foreign particles.

Branches of the inferior mesenteric veins drain to the superior hemorrhoidal veins 4. 16th Edition. Umbilical and periumbilical veins are recanalized from the obliterated umbilical vein. 3.Venous Tributaries of the Portal System Numerous tributaries of the portal vein connect outside the liver with the systemic venous system. which forms the ligamentum teres of the liver. these rudimentary communicating systems develop into large collateral veins. With portal hypertension. p 1001 38 . Textbook of Surgery. These collateral systems are 1. Submucosal veins of the stomach and esophagus carry venous blood to the coronary vein and then to the azygous vein and SVC 2. Retroperitoneal veins drain via the adrenal and renal veins Sabiston.

Cirrhosis of the liver plays an important role in the development of HCC in any part of the world. Oral contraceptives. The role of Hepatitis C in the etiology of HCC is largely due to the development of cirrhosis. which is common in chronic Hepatitis C. 16th Edition. Other risk factors include Wilson’s disease. and the incidence of this tumor has doubled in the United States since the early 1980s. thorotrast. androgens. Alcoholic cirrhosis ingestion of aflatoxin and chronic Hepatitis C are well-documented risks for HCC. tyrosinemia. pp 1020-1 39 .Susceptibility to Hepatoma (Hepatocellular Carcinoma) Hepatocellular carcinoma (HCC) is the most prevalent malignant disease in the world. Hepatitis C also acts in synergy with Hepatitis B in the development of HCC. Sabiston. Hepatitis B is strongly associated with HCC. Textbook of Surgery. parasites. and glycogen storage disease. and vinyl chloride have been implicated as risk factors.

The challenge is to selectively identify and embolize the feeding artery. p 333 40 . Systemic chemotherapy or hepatic arterial chemotherapy is the most common intervention for patients with non-resectable hepatic metastases.Principles Associated with Chemo Embolization of Liver Metastases Most liver metastases are not amenable to surgical excision. Ablative techniques include cryoablation or radio frequency ablation. 7th Edition. 7th Edition. Hepatic artery embolization and chemo embolization have therapeutic advantages in that tumor metastases to the liver derive their metabolic survival from the hepatic artery and its branches. thereby eliminating widespread destruction of hepatic tissue. which might require extensive removal of normal liver. Ablative techniques are generally considered in patients who cannot undergo complete removal of their lesions because of anatomic location. p 353 Current Surgical Therapy. Schwartz. These procedures are conducted at laparotomy with ultrasound guidance.

Left Hepatic Artery – The left hepatic artery receives two or more main arteries in up to 35% of the cases. and may be closely related to the posterior lateral aspects of the common duct. these are accessory vessels. splenic artery. pp 348-352 41 . In the majority of these individuals. Anomalous Blood Supply to the Liver Common Hepatic Artery – Arises from the celiac trunk in 90% of the cases.Location of Anomalous Hepatic Arteries Anomalous arterial blood supply to the liver may be the source of hepatic failure in that these vessels are located in abnormal locations and may be inadvertently ligated. Most commonly the superior mesenteric artery is the origin of an anomalous blood supply. superior mesentery artery. Anomalous hepatic arteries are characterized by the following terms: Accessory – These vessels are additional blood supply to the liver segments and may be ligated without risk of liver injury. left gastric artery. or aorta. and even behind the portal vein. Hollingshead.” an “aberrant replacing” right hepatic artery might easily be ligated with resultant liver injury. Approximately 80% of aberrant right hepatic arteries are “replacing arteries. and arise from the branches of the celiac trunk. in performing a “Whipple procedure. Right Hepatic Artery – The right hepatic artery may arise from the superior mesenteric artery in as many as 26% of individuals. proper hepatic artery. The aberrant vessel commonly runs an anomalous course and passes behind the common duct. however. 2nd Edition. Replacement Arteries – These vessels are anomalous in origin and are the total arterial blood supply to the liver segments which they supply.” and thus are the sole arterial blood supply to the right lobe of the liver. or the aorta. Anatomy for Surgeons. Thus. the common hepatic artery may arise from the superior mesenteric artery.

Greenfield. right gastric. then a trifurcation into right. gastroduodenal. the common hepatic artery arises from the celiac trunk. In 8% there is an accessory left hepatic artery in addition to the more common left hepatic artery. In 11% of individuals the right hepatic artery arises from near the base of the superior mesenteric artery and travels through or posterior to the head of the pancreas. 2nd Edition 42 . supraduodenal.Anatomy of Aberrant Right Hepatic Artery The arterial supply to the liver is quite variable. As an example. middle and left hepatic arteries. then continues as the proper hepatic artery. Variations in arterial anatomy are important in hepatic. In 10% the left hepatic artery arises from the left gastric artery. biliary. This artery then branches: first the cystic artery. In 55% of individuals. pancreatic and gastric procedures in which this vasculature is at risk of damage or insufficiency. In 7% there is an accessory right hepatic artery. the right hepatic artery may lie anterior to the hepatic duct and be confused with the cystic artery during cholecystectomy. gives off three branches.

Other quantitative tests include galactose elimination. These tests are more specific quantitative tests than any of the routine tests of liver function. transaminases.e. 16th Edition. Albumin and transferring are useful clinical markers of synthetic function. Textbook of Surgery. They are the measure of liver excretion as these agents are removed from circulation by the liver. Quantitative assessments of liver reserve are Bromsulphalein and Indocyanine Green. lidocaine metabolic formation (MEGX test).Prognostic Test of Liver Function Reserve Routine liver function tests. i. pp 1010-12 43 . Sabiston. and prothrombin time or a ratio of Factor VIII to V. alkaline phosphatase are used to detect and monitor liver disease. bilirubin.

and thus reduces the operative risk.Preoperative Treatment of Obstructive Jaundice Obstructive jaundice causes many physiologic abnormalities. Placement of endoscopic stents or catheters via endoscopy or percutaneous transhepatic route is also used. Sabiston. coagulation disorders. impaired protein synthesis. However. which increase the risk of surgery. Endoscopic sphincterotomy and extraction of common duct stones is now commonly used as definitive treatment pre-op. and wound healing are but a few of the changes associated with obstructive jaundice. 16th Edition. Recent studies have identified higher risk of infectious complications and morbidity and mortality when preoperative biliary drainage is routinely used. Textbook of Surgery. p 1082 44 . Preoperative biliary drainage has been used to improve liver function prior to surgery. Altered cell mediated immunity. this therapy may be used successfully in selected patients with advanced malnutrition or biliary sepsis.

inexpensive. pp 313-14 45 . An increased ventilatory rate is usually sufficient to compensate for this elevated PCO2 in exhaled air.Etiology of a Sudden Increase in End Tidal CO2 After Evacuating CO2 in a Laparoscopic Cholecystectomy Procedure CO2 is the preferred agent for most laparoscopic procedures because it is readily available. Zucker. The combination of residual CO2 being absorbed within the peritoneal cavity. This rapid diffusion property of CO2 allows it to be readily absorbed across the peritoneum. Surgical Laparoscopy. CO2 embolism resulting from residual intra-peritoneal CO2 entering open (torn or lacerated) large veins must be considered. could lead to an elevated end tidal CO2 in the post cholecystectomy patient. readily absorbed. which may result in a rise in PCO2. which is readily eliminated through the lungs. extubation of the patient who may be sedated and have diminished respiratory drive. The high diffusion coefficient of CO2 may also lessen the severity of any gas emboli introduced into the vascular system. Its rapid clearance from the blood stream results in an extremely fast rate of excretion from the body. and will suppress combustion. The high diffusion coefficient results in rapid clearing from the pulmonary venous system.

Textbook of Surgery. Sabistion. Some patients progress to severe renal failure. 16th Edition. The mechanism of the hepatorenal syndrome is unclear. although it is likely that elevated bilirubin and bile acids make the kidney more susceptible to ischemia and hypoperfusion. while others respond to improved liver function. but persists despite volume expansion. The acute renal failure associated with jaundice and liver disease initially presents as prerenal. p 212 46 .Findings Associated with the Hepatorenal Syndrome Biliary disease and major biliary reconstruction are associated with a form of renal failure termed the hepatorenal syndrome.

Usually. This intrapancreatic portion usually joins the pancreatic duct (Wurshung). Principles of Surgery. pp 649-56 Netter. The common bile duct’s blood supply is composed of a rich arterial plexus derived primarily from the retroduodenal or posterior superior pancreaticoduodenal artery. pp 276-78 47 . The distal segment is in intimate contact with the duodenum. This structure surrounds the orifice. Surgical Anatomy. It lies within the hepatoduodenal ligament. the distal common bile duct lies within the pancreas. 6th Edition. to the right of the hepatic artery and anterior to the portal vein. p 1368 Anson and McVay. Schwartz. and empties into the duodenum at the papilla of Vater. Atlas of Human Anatomy Plates. Considerable variation is possible.Anatomy of Common Bile Duct The common bile duct is approximately 8-9 cm long and begins at the junction of the common hepatic duct and the cystic duct. and is composed of the muscular elements that make up the sphincter of Oddi. passing behind the second portion of the duodenum through a groove on the surface of the pancreas. 6th Edition.

This accounts for the rapid growth of the hepatic remnant after major liver resections. are equipped for glycolysis and lipogenesis. pp 247-8 48 . They also produce the majority of proteins and are responsible for protein metabolism. an area with decreased oxygen tension. The function of any individual hepatocyte depends upon the position of the cell within the lobule and the proximity of the cell to the blood supply. Hepatocytes replicate rapidly. Basic Science Review for Surgeons. Zone 1 hepatocytes lie in closest proximity to the periportal region and contain the highest concentration of enzymes involved in glycogenesis. Ureagenesis occurs in Zones 2 and 3. Cells in Zone 3. 1992. Hepatocytes can be divided into three zones.Characteristics Hepatocytes The hepatocytes perform the major metabolic and excretory functions of the liver. Simmons & Steed. They are arranged in cords or plates of one cell thickness and are surrounded by the sinusoids. and it is estimated that the entire cell mass of the liver could be replaced every 50 days. The enzymes responsible for gluconeogenesis are much more abundant in the periportal area.

which amplifies the bile salt deficiencies needed for fat absorption. thus leading to steatorrhea. The major bile acids are cholic and chenodeoxycholic acieds. Physiologic Basis of Surgery. which is released from endocrine cells in the duodenum in response to peptide. amino acids. The bile salt pool is approximately 2 grams and is recycled 5 to 6 times a day. and reabsorbed in the liver from portal blood. the amount of bile salts reaching the colon is increased with a result in diarrhea.Bile Acid Synthesis The enterohepatic circulation is a cyclic process in which bile salts are secreted into the intestine. which are synthesized in the liver from cholesterol. Reabsorption of the bile acids in the distal small bowel occurs by passive absorption and active absorption as a sodium dependent process. With ileal resection or dysfunction. The secondary bile acids. are formed by anaerobic bacteria in the intestine and are eventually involved in the entero-hepatic circulation. pp 428-29 49 . effectively absorbed in the ilium. and lipid. Secretion into the intestine is mediated by cholecystokinin. Furthermore. All bile acids secreted by the liver are conjugated with glycine or taurine. the liver is unable to compensate for the fecal losses of bile salts. 2nd Edition. deoxycholic and lithocholic acids.

2nd Edition. cholesterol esters. The intestinal mucosal cells synthesize Apolipoprotein A and B. excluded from the portal blood. are essential for fat absorption. chylomicrons cannot cross intercellular junctions of the intestinal capillaries and are. From the lacteals. and fat-soluble vitamins. therefore. O’Leary. A congenital disorder. chylomicrons pass via larger lymphatic channels. The apolipoproteins. pp 427-28 50 . and they are added before the chylomicrons enter the golgi apparatus. The outer layer consists of 80-90% phospholipid and specialized apolipoproteins. leads to triglyceride accumulation within the endoplasmic reticulum and leads to the inability to digest fat.Characteristics of Chylomicrons Chylomicrons consist of an inner core containing 90% triglycerides. draining from intestine to thoracic duct. Reformed triglycerides within the golgi apparatus of intestinal enterocytes are transported out of the cell across the basolateral membrane as chylomicrons. which enter the central lacteal of the villus. abetaliproproteinemia. while accounting for only 1% of the mass. Because of their size. eventually into the left subclavian vein. a lesser amount cholesterol.

Proteus species. coli. pp 1126-29 51 . Textbook of Surgery. and four or more in the remainder. Enterobacter species and anaerobic Streptococci. Sabiston. Streptococcus faecalis. A single organism is found in approximately 40% of cases. These organisms include both Gram-positive and Gram-negative aerobes and anaerobes. Patients suspected of having acute cholecystitis should receive empiric antibiotic coverage against those organisms found in the bile of approximately 80% of patients. Those present most frequently are E. two species in about 30%. positive cultures of bile or gallbladder wall are found in 50 to 75% of patients. Clostridium welchii.Biliary Tract Bacteria The role of bacteria in the pathogenesis of acute cholecystitis is not clear. three in 20%. 15th Edition. Klebsiella aerogenes.

Sabiston. 8th Edition. 16th Edition. If prehepatic portal hypertension is suspected.Preoperative Measure of Portal Venous Pressure The normal pressure in the portal vein is between 3 and 5mmHg. pp 1061-3 Schwartz. In patients with cirrhosis and possible portal hypotension. p 1141 52 . Principles of Surgery. a hepatic venous wedge pressure will reflect the portal pressure. Textbook of Surgery. direct measurement of the portal system is required by umbilical venous cannulation or percutaneous puncture of the spleen. Pressures above 5 to 8mmHg stimulate portosystemic collateralization.

absence of Vitamin K or blockage of the γ-carboxylation by Coumadin can be assessed by monitoring the prothrombin. Of these factors. these synthetic functions are difficult to monitor. At least 17 of the major human proteins are synthesized and secreted by the liver. lipid metabolism which generates triglycerides from fatty acids. lipoproteins. ketones (acetoacetate). and cholesterol are synthesized by the liver but difficult to monitor. lipid. The half-life of this protein is 4 to 5 days. Albumin synthesis is decreased. 15th Edition. the reprocessing of biliary salts through the enterohepatic circulation. Sabiston. Other major metabolic functions of the liver have to do with carbohydrate. Protein synthesis is the most common measure used to determine hepatic synthesis. Other proteins that are markers of hepatic biosynthesis include the coagulation proteins. Although the liver synthesizes hepatic glycogen after eating and is responsible for burning lactic acid to pyruvate which is subsequently converted back to glucose. This test is dependent upon adequate amounts of functional Factor 7. Acute phase proteins produced by the liver in response to a systemic inflammatory state initiate a sudden intransient rise in C reactive protein compliment and coagulation proteins. and the breakdown and metabolism of hemoglobin to bilirubin.Best Test of Hepatic Biosynthesis The liver is responsible for many biologic functions including bile formation. Although albumin is the most abundant serum protein (it accounts for up to 15% of total hepatic synthesis) the half-life of albumin (45 days) limits its ability to determine active hepatic synthesis of protein. and protein metabolism. Transferrin is a protein commonly used to assess hepatic synthesis. 7 has the shortest half-life of 5 to 7 hours and because it is a Vitamin K dependent protein. Likewise. pp 1055-1060 53 . thus a positive anabolic state can be determined by a rise in the serum transferrin levels.

The screening protocol for determining liver metastases in colon cancer recommends a single liver imaging study. However. it also has the highest false positive rate (about 50%). can also be useful in detecting metastatic colon cancer. Sabiston.Abnormal Liver Function Test in Metastatic Colon Cancer The Lactic Dehydrogenase Study is reported to have the highest sensitivity (85%) of all standard liver function tests for the presence of hepatic metastases. 16th Edition. However. an elevated CEA can occur with other malignancies and benign conditions. plus selected blood tests. 5´ –necleotidase and alanine transaminase. Textbook of Surgery. The CEA. pp 1029-30 54 . Other blood tests that can reflect the presence of metastases include GGT levels. a tumor marker.

the risk of developing hepatocellular carcinoma was increased by 1000 fold. Japanese studies have identified Hepatitis C virus in 51 % of patients with Hepatocellular carcinoma.Hepatocellular Cancer in Chronic Hepatitis B (Complications Hepatitis B) Evidence of a causal relationship between chronic Hepatitis B and the development of Hepatocellular carcinoma is compelling. 15th Edition. The risk of developing Hepatocellular carcinoma in Hepatitis B virus carriers is 10%. Studies from Africa and Asia suggest that Hepatitis B virus is present in 70 – 80% of individuals with Hepatocellular carcinoma. In a 5-year study of Hepatitis B antigen positive patients. Hepatitis B & C virus act as independent risk factors but may act synergistically. pg 1070 55 . The role of Hepatitis C virus in the development of Hepatocellular carcinoma is less clear. Sabiston.

hypoalbuminemia and portal obstruction. The increased hydrostatic pressure promotes transfer of intravascular fluid into the interstitial space which results in weeping of lymphatic fluid from the liver. and mesentery. Reduced Portal Blood Flow Reduced portal blood flow occurs due to fibronodular changes in the liver. certain factors are known which are responsible for the development of Ascites. Abnormal Liver Function Abnormal liver function causes hypoalbuminemia and reduced rates in the metabolism of circulating aldosterone leading to hyperaldosteronism. Abnormal Renal Function Shunting of renal blood flow to the medullary nephrons with decreased glomerular filtration leads to renin release and elevated aldosterone levels. however. Ascites Formation Ascites formation is thus the result of sodium and water retention. pp 986-987 56 .Pathophysiology of Ascites in Alcohol Cirrhosis A number of theories persist. Water and sodium retention occurs. Greenfield. hyperaldosteronism. bowel.

Thus. Cancer Surgery. no randomized. The arterial supply can be occluded by gelfoam particles. it remains an experimental procedure. prospective trials have been performed to test the survival advantage of this technique. stainless steel coils or starch microspheres. The chemotherapeutic agent can be bound to the occluding agent or administered separately. 1996. To date. the combination of embolization and chemotherapy should increase the local concentration and time of exposure of the drug to the malignancy while decreasing systemic exposure and toxicity. Only the steel coils permanently occlude while the others are temporary. Harvey JC. In theory. 106-107 57 . Beattie EJ. pp.Basis for Chemoemboliztion of Hepatic Metastases The term chemoembolization describes a variety of techniques used to embolize the arterial supply to a tumor and simultaneously infuse chemotherapeutic agents.

However. Anomalous blood supply to the liver is well known. however. the “proper hepatic artery. Approximately 80% of aberrant right hepatic arteries are “replacing arteries. save the small amounts occurring through variable small anastomoses from the phrenic arteries. Thus. Ligating the common hepatic artery near the celiac axis allows for collateral circulation to the proper hepatic artery through gastroduodenal vessels. Anomalous hepatic arteries are characterized by the following terms: Accessory – These vessels are additional blood supply to the liver segments and may be ligated without risk of liver injury. in performing a “Whipple procedure.” an “aberrant replacing” right hepatic artery might easily be ligated with resultant liver injury.Etiology of Liver Failure/Diagnosis of Ligation of Hepatic Artery (Unintended Hepatic Artery Ligation at Operation) Liver failure without evidence of sepsis occurring in the post operative period following a major resection of the pancreas. or aorta. ligation above this point. 2nd Edition.” and thus are the sole arterial blood supply to the right lobe of the liver. superior mesentery artery. should suggest ligation of the hepatic artery.e. ligation of the common hepatic artery between gastroduodenal and the right gastric arteries can allow collateral circulation to the proper hepatic arteries via the right gastric artery. The proper hepatic artery is an “end vessel” in which there is little collateral blood supply other than through portal venous circulation. Replacement Arteries – These vessels are anomalous in origin and are the total arterial blood supply to the liver segments which they supply. at operation these aberrant vessels may not be recognized and thus inadvertently ligated. Anatomy for Surgeons. Hollingshead. i. However. In the majority of these individuals. the common hepatic artery may arise from the superior mesenteric artery. The aberrant vessel commonly runs an anomalous course and passes behind the common duct. these are accessory vessels. Most commonly the superior mesenteric artery is the origin of an anomalous blood supply. and arise from the branches of the celiac trunk. Similarly. or extended gastrectomy for cancer. and even behind the portal vein. Anomalous arterial blood supply to the liver may be the source of hepatic failure in that these vessels are located in abnormal locations and may be inadvertently ligated. Right Hepatic Artery – The right hepatic artery may arise from the superior mesenteric artery in as many as 26% of individuals. and may be closely related to the posterior lateral aspects of the common duct. Anomalous Blood Supply to the Liver Common Hepatic Artery – Arises from the celiac trunk in 90% of the cases. Left Hepatic Artery – The left hepatic artery receives two or more main arteries in up to 35% of the cases. pp 348-352 58 . proper hepatic artery. or the aorta. splenic artery. left gastric artery. difficult common duct operation.” deprives the liver of all arterial blood.