Universitatea Titu Maiorescu Bucuresti

GASTROENTEROLOGY
LECTURE I

Prof Univ Dr Ion C. intoiu

1

Student Objectives
Explain

the main functions of the gastrointestinal system. Identify the main organs and accessory organs. Explain the role of the liver and gallbladder in digestion.

Student Objectives
Identify combining forms,

suffixes, and prefixes related to the GI system. Discuss pathology related to the GI system. Identify diagnostic, symptomatic, and therapeutic terms related to the GI system. Identify abbreviations and pharmacology related to the GI system.

BASIS IN GASTROENTERELOGY

Digestion
Phases

Ingestion Movement Digestion Absorption Further digestion

Digestive System Organization

Gastrointestinal

(Gl) tract (Alimentary

canal)
Tube within a tube Direct link/path between organs Structures
Mouth Oral Cavity Pharynx Esophagus Stomach Duedenum Jejenum Ileum Cecum Ascending colon Transverse colon,Descendent colon,rectum

Anatomy of the Mouth and Throat

Normal Esophagus

Anatomy of the Stomach

10

The Duodenum and Related Organs

11

Small Intestine
Control Requires

pancreatic enzymes & bile to complete digestion

12

The Digestive System

13

Digestive System Organization

Descending colon Sigmoid colon Rectum Anus

Accessory structures
Not in tube path Organs
Teeth Tongue Salivary glands Liver Gall bladder Pancreas
14

Esophagus
Usually

collapsed (closed) 3 constrictions

Aortic arch Left primary bronchus Diaphragm
Surrounded

by

SNS plexus Blood vessels

Functions

Secrete mucous Transport food

15

ESOPHAGUS
Receives food from pharynx and propels it to stomach Cardiac sphincter (lower esophageal sphincter) controls passage of food from esophagus into the stomach
Relaxes = food enters stomach Contracts = stomach contents prevented from reentering the esophagus

Anatomy
Diameter

of normal esophagus is about 2.5 cm. Three areas of narrowing:

Cricopharyngeus muscle is narrowest portion of adult GI tract, 14 mm. Esophagus crossed by left mainstem bronchus. Esophagogastric junction.
Normal

swallowing can occur with lumen of 12-13 mm.

. Drawing illustrates the AJCC divisions (left) and clinical divisions (right) of the esophagus.

Kim T J et al. Radiographics 2009;29:403-421

2009 by Radiological Society of North America

Peristalsis and Segmentation

19

Stomach
Usually

J shaped Left side, anterior to the spleen Mucous membrane

G cells make gastrin Goblet cells make mucous Gastric pit Oxyntic gland Parietal cells Make HCl Chief cells Zymogenic cells
Pepsin Gastric lipase

20

Digestive System Structures

Stomach

Fundus
Upper rounded portion

Body
Central part

Digestive System Structures

Stomach

Pylorus
Lower tubular part (also called the gastric antrum) Pyloric sphincter regulates passage of food from stomach into the duodenum

Folds in mucous membranes of stomach = Rugae

Digestive System Structures

Stomach

Gastric juices breakdown food in stomach Muscular action of stomach causes churning of food
Mixes food with the secretions Chyme = liquidlike mixture of partially digested food and digestive secretions

Anatomy of the Stomach

24

Stomach

3 muscle layers
Oblique Circular Longitudinal

Regions
Cardiac sphincter Fundus Antrum (pylorus) Pyloric sphincter

Vascular Inner surface thrown into folds Rugae

Contains enzymes that work best at pH 1-2
25

Stomach

Functions
Mix food Reservoir Start digestion of
Protein Nucleic acids Fats

Absorbs
Alcohol Water Lipophilic acid B 12

Activates some enzymes Destroy some bacteria Makes intrinsic factor B 12 absorption Destroys some bacteria
26

The Duodenum and Related Organs

27

Small Intestine
Control Requires

pancreatic enzymes & bile to complete digestion

28

Small Intestine

Secretes digestive enzymes

Peptidases
Amino Di Tri-

Sucrases Maltase Lactase Saccharidases

Di Tri-

Lipase Nucleases

29

Small Intestine

Extends from pyloric sphincter ileocecal valve Regions

Duodenum Jejenum Ileum

Movements
Segmentation Peristalsis

30

Small Intestine
Histology

Intestinal glands Intestinal enzymes Duodenal glands Alkaline mucous Paneth cells Lysozyme Microvilli Lacteals Plica circularis Smooth muscle Lymphatic tissue GALT Vascular
31

Small Intestine

Absorbs
80% ingested water Electrolytes Vitamins Minerals Carbonates
Active/facilitated transport Monosaccharides

Lipids
Monoglycerides Fatty acids Micelles Chylomicrons

Proteins
Di-/tripeptides Amino acids

32

Structure of the Villi in the Small Intestine

33

Large Intestine
Functions

Mechanical digestion
Haustral churning Peristalsis Reflexes
Gastroileal Gastrocolic

Absorbs More water Vitamins

B K

Concentrate/eliminate wastes

Chemical digestion Bacterial digestion

Ferment carbohydrates Protein/amino acid breakdown
34

Large Intestine
Extends
Regions

from ileocecal valve to anus

Cecum Appendix Colon

Ascending Transverse Descending

Rectum Anal canal

35

Anatomy of the Large Intestine

36

Large Intestine
Histology

No villi No permanent circular folds Smooth muscle

Taeniae coli Haustra

Epiploic appendages Otherwise like rest of Gl tract

37

Feces Formation and Defecation

Chyme dehydrated to form feces Feces composition

Water Inorganic salts Epithelial cells Bacteria Byproducts of digestion

Control

Parasympathetic Voluntary

Defecation
Peristalsis pushes feces into rectum Rectal walls stretch
38

Liver
Location

R. Hypochondrium Epigastric region

4

Lobes

Left Quadrate Caudate Right

Each

lobe has lobules Contains hepatocytes Surround sinusoids Feed into central vein
39

Liver

Functions
Makes bile
Detergent emulsifies fats Release promoted by:
Vagus n. CCK Secretin

Contains
Water Bile salts Bile pigments Electrolytes Cholesterol Lecithin
40

Liver
Detoxifies/removes
Drugs Alcohol

Stores
Gycolgen Vitamins (A, D, E, K) Fe and other minerals Cholesterol

Activates vitamin D Fetal RBC production Phagocytosis Metabolizes absorbed food molecules
Carbohydrates Proteins Lipids

41

Liver
Dual

blood supply

Hepatic portal vein

Direct input from small intestine

Hepatic artery/vein
Direct links to heart

42

The Duodenum and Related Organs

43

The Organs and Positions in the Abdominal Cavity

44

Structures of the Alimentary Canal

45

COMMON SIGNS and SYMPTOMS

Common Signs and Symptoms

Achlorhydria

Abnormal condition characterized by the absence of hydrochloric acid in the gastric juice
Anorexia

Lack or loss of appetite, resulting in the inability to eat

Common Signs and Symptoms

Aphagia

Condition characterized by the loss of the ability to swallow as a result of organic or psychologic causes
Ascites

Abnormal accumulation of fluid within the peritoneal cavity

Fluid contains large amounts of protein and electrolytes

Common Signs and Symptoms

Borborygmus

An audible abdominal sound produced by hyperactive intestinal peristalsis

Borborygmi are rumbling, gurgling, and tinkling noises heard when listening with a stethoscope

Common Signs and Symptoms

Constipation

Difficulty in passing stools, or an incomplete or infrequent passage of hard stools

Diarrhea

Frequent passage of loose, watery stools

Common Signs and Symptoms

Dyspepsia

Vague feeling of epigastric discomfort after eating Involves an uncomfortable feeling of fullness, heartburn, bloating, and nausea
Dysphagia

Difficulty in swallowing, commonly associated with obstructive or motor disorders of the esophagus

 Emaciation

Common Signs and Symptoms

Excessive leanness caused by disease or lack of nutrition

Emesis

Material expelled from the stomach during vomiting Vomitus

Common Signs and Symptoms

Eructation

Act of bringing up air from the stomach with a characteristic sound through the mouth Belching
Flatus;

Flatulence

Air or gas in the intestine that is passed through the rectum

Common Signs and Symptoms

Gastroesophageal

Reflux

Backflow of contents of stomach into esophagus Often result of incompetence of the lower esophageal sphincter

Icterus
A yellowish discoloration of the skin, mucous membranes, and sclera of the eyes, caused by greater than normal amounts of bilirubin in the blood Also called jaundice

 Melena

Common Signs and Symptoms

An abnormal, black, tarry stool containing digested blood

Nausea

Unpleasant sensation often leading to the urge to vomit

Pruritus

ani

A common chronic condition of itching of the skin around the anus

Common Signs and Symptoms

Steatorrhea

Greater than normal amounts of fat in the feces

Characterized by frothy, foul-smelling fecal matter that floats

Vomit

To expel the contents of the stomach through the esophagus and out of the mouth

Diagnostic, Symptomatic, Therapeutic Terms

Aerophagia
anorexia appendicitis ascites borborygmus

bulimia

Diagnostic, Symptomatic, Therapeutic Terms

cachexia
cholelithiasis cleft

palate Crohns disease cirrhosis colic

Diagnostic, Symptomatic, Therapeutic Terms

deglutition
dysentery dysphagia eructation fecalith

flatus
gastroesophageal reflux

disease

Diagnostic, Symptomatic, Therapeutic Terms

Halitosis
hematemesis irritable

bowel syndrome leukoplakia malabsorption syndrome melena obstipation

Diagnostic, Symptomatic, Therapeutic Terms

Peristalsis
pyloric

stenosis regurgitation steatorrhea visceroptosis

 Stomach
Glands:

Parietal cells found in fundus and body Secrete HCl & intrinsic factor Chief cells are more at fundus and body Secrete pepsinogen I & II

Congenital

Anomalies 1. Diaphragmatic Hernia:

A defect in the diaphragm away from the hiatal orifice (not hiatal hernia) Portions of stomach & small intestine herniates Results in respiratory impairment & pulmonary hypoplasia

COMMON DIAGNOSTIC METHODS

Teeth
Maxillary

arch (upper) Mandibular arch (lower)

anterior teeth for biting and tearing posterior teeth for chewing and grinding

dent/i

- teeth decidu/o - shedding Primary - 20 teeth Permanent - 32 teeth

ENDOSCOPY

ENDOSCOPY
Endoscopy, is the examination of internal body cavities using a specialized medical instrument called an endoscope. Physicians use endoscopy to diagnose, monitor, and surgically treat various medical problems.

An endoscope is a slender, flexible tube equipped with lenses and a light source. Illumination is done by the help of a number of optical fibres. Reflected light rays are collected by CCD( Charge coupled device) and electrical signals are produced, which are fed to the video monitor to get image. Thorough one channel of endoscope water and air is conducted to wash and dry the surgical site.

ENDOSCOPY

The endoscope also has a channel through which surgeons can manipulate tiny instruments, such as forceps, surgical scissors, and suction devices. A variety of instruments can be fitted to the endoscope for different purposes. A surgeon introduces the endoscope into the body either through a body opening, such as the mouth or the anus, or through a small incision in the skin.

ENDOSCOPY

The endoscope gives visual evidence of the problem, such as ulceration or inflammation It can be used to collect a sample of tissue; remove problematic tissue, such as polyps It is used to take photograph of the hollow internal organs

ENDOSCOPY

Depending on the body part, each type of endoscopy has its own special term, such as
laparoscopy (abdomen, uterus, fallopian tube), laryngoscopy (vocal cords), bronchoscopy (lungs), colonoscopy (colon), arthroscopy (joint) and Gastroscopy (Stomach).

EUS ESOPHAGIAL US
1

EUS - Characteristics
Layer
Size Echogenicity Vascularity

of origin

EUS Layer of Origin

Mary Lee Krinsky, DO and Kenneth Binmoeller, MD

Layer Mucosa Muscularis Mucosa Lesion GIST Lipoma Fibroma Carcinoid Granular Cell Tumor Pancreatic Rest Duplication Cyst Rare Rare Rare Common Rare

Submucosa Muscularis Propria Most common Always Always Most common Most common Common Always Rare Rare

EUS - Echogenicity
Anechoic

- black (water, clear fluid, cysts, vessels, gallbladder) Hypoechoic - lamina propria, muscularis propria, leiomyoma, GIST, mucin-filled cyst Hyperechoic - superficial mucosa, submucosa, serosa, lipoma Isoechoic - between Hypo and Hyper

EUS - Summary
AGA

GUIDELINES Endoscopy alone not reliable for detecting the etiology of a subepithelial mass Transabdominal US, CT, and MRI are reliable for extra- but not intralumenal lesions EUS is the most accurate imaging test for detecting layer of origin Symptomatic masses should undergo endoscopic or surgical resection Hypoechoic lesions in the 3rd and 4th layer are most prone to misclassification

ESOPHAGIAL PATHOLOGY

Hiatal Hernia

Rolling or Paraesophageal hernia

Esophagus: Normal Lower Esophageal and Squamocolumnar Junction Mucosae

Esophagus: Normal Squamous Epithelium

Esophagitis (Inflammation and Reactive Epithelial Changes of the Esophageal Mucosa) Has Many Causes

Esophagus: G-E Reflux Changes in Epithelium and Vascular Papillae

Esophagus: G-E Reflux Defenses Against Refluxinduced Injury

Esophagus: G-E Reflux - Symptoms and Endoscopic Findings in Reflux are NOT Predictive of Biopsy Findings

Esophagus: G-E Reflux Heightened Epithelial Turnover in G-E Reflux is Shown by Increased Epithelial Tritiated Thymidine Labeling

Esophagus: G-E Reflux - Reflux-induced Epithelial Change Is a Consequence Of Increased Cell Turnover

Acute (Neutrophilic) Inflammation and Erosion In Severe Reflux Esophagitis

Severe Epithelial Reactive Changes with Eosinophils (EOS) in Gastroesophageal Reflux

Sequelae Of Prolonged G-E Reflux

Esophagus: G-E Reflux Reflux-induced Epithelial Change Is a Consequence Of Increased Cell Turnover

Barretts Esophagus: Development And Anatomic Relationships

Endoscopic Landmarks In The GEJ Region: Normal Versus Barretts (Columnarlined) Esophagus With Location Of Lower Esophageal Sphincter (LES)

Requirements For Diagnosis Of Barretts Esophagus

Barretts Esophagus: Gross Appearance

Be Suspected And Confirmed By Biopsy When The Squamo-columnar Junction Is Displaced Or Highly Irregular

Barretts Mucosa (BM) With Submucosal Esophageal Gland (SMEG) Below Muscularis Mucosae (MM)

Barretts Mucosa: Distinctive (Specialized) Type

Agents Used to Treat Hyperacidity and Gastroesophageal Reflux Disease

Secretory Functions of the Stomach Lining

Parietal

cells secrete hydrochloric (HCl)

acid Chief cells secrete pepsinogen Mucoid cells secrete mucus

24 - 104

Stomach Hyperchlorhydria
Produced from:

Eating high-fat meals Increased alcohol intake Emotional turmoil

Copyright 2007

24 - 105

Goal of Antacid Therapy

Neutralize

the acid Inhibit pepsin activity Increase resistance of the stomach lining Increase tone of the lower esophageal sphincter

24 - 106

Antacids
Three Forms 1. Aluminum 2. Magnesium 3. Calcium Mechanism of action

Neutralization of gastric acidity Low doses promote gastric mucosal defensive mechanisms
24 - 107

Systemic Antacids
Useful

in short-term therapy Rapid onset Prolonged use causes an overload on the kidneys
Example: sodium bicarbonate

24 - 108

Nonsystemic Antacids
Remain

in gastrointestinal tract; useful in long-term therapy Most of the dose remains in the gastrointestinal tract Will not alter acid-base system
Examples: calcium carbohydrate (Tums, Rolaids), aluminum carbonate (Basaljel), magaldrate (Riopan), etc.
24 - 109

Side Effects and Adverse Effects

Magnesium: diarrhea
Aluminum:

constipation Calcium: constipation

24 - 110

Antacid Interactions
Binding

of other drugs to the antacid causes reduced availability of the other drugs to the client. Chemical inactivation Increases stomach and urine pH (alkaline), which decreases the absorption and excretion of certain drugs

24 - 111

Histamine (H2) Receptor Antagonists

Examples

Cimetadine (Tagamet) Famotidine (Pepcid) Nizatidine (Axid) Ranitidine (Zantac)

24 - 112

Proton Pump Inhibitors

Omeprazole

(Prilosec)

Blocks the final step of acid production in the stomach

Indicated for

clients with:

Gastroesophageal reflux disease (GERD) Gastric hypersecretory condition

Interactions

Causes warfarin (an anticoagulant) action to be increased

Copyright 2007 Thomson Delmar 24 - 113

Helicobacter Pylori
An

organism associated with the development of peptic ulcer disease Treatment

Metronidazole (Flagyl), an antimicrobial agent, along with bismuth subsalicylate (PeptoBismol) and tetracycline (antimicrobial) for 4 weeks to eradicate Helicobacter pylori

Copyright 2007 Thomson Delmar

24 - 114

Metoclopramide (Reglan)
A

drug that stimulates the motility of the upper GI tract without stimulating the production of gastric, biliary, or pancreatic solutions Action
Increases peristalsis in the duodenum and jejunum Decreases gastroesophageal reflux

Copyright 2007 Thomson Delmar

24 - 115

(continues)

(continued)

Metoclopramide (Reglan)
Adverse

effects

Produces extrapyramidal (Parkinson-like symptoms) effects Central nervous system depression Gastrointestinal upset

Copyright 2007 Thomson Delmar

24 - 116

CANCER OF THE ESOPHAGUS

Predisposing Factors for SCCA Esophagus

Tobacco Alcohol Diet Chronic Age Race Gender

esophagitis Role of HPV?

Other Risk Factors

Previous

head and neck or lung cancer (annual rate 3-7%). Plummer-Vinson syndrome (Iron deficiency). Esophageal diverticulae. Lye strictures: long latent period. Radiation injury (therapeutic, atomic bomb). Non-tropical sprue.

Presenting Symptoms
Retrosternal

discomfort or indigestion. Friction or burning when swallowing food. Dysphagia, odynophagia Weight loss. Hoarseness, cough Regurgitation, vomiting Hematemesis or melena (uncommon)

Adenocarcinoma of the Esophagus

Obesity Reflux

disease and Barrett's esophagus.

Diet
Smoking Scleroderma

Achalasia
Cancer

arises in 1-10% of patients symptomatic for an average 15-25 years. Usually squamous cell carcinoma of middle third of esophagus. Presents at younger age than usual.

Poor Prognosis
Coughing
Hiccups

after swallowing

Indicates tracheoesophageal fistula is present. Indicates involvement of diaphragm

Barrett's Esophagus
Dysplastic

changes in distal esophagus and gastroesophageal junction. 30-40 fold increase in adenocarcinoma of the esophagus. 10-15% of Barretts patients will develop adenocarcinoma. Risk of cancer is about 0.5% per year.

Malignant Transformation in Barrett's

Long-standing gastroesophageal reflux.

Field

cancerization effect. Medical therapy does not reverse progression to malignancy. With ablation, new epithelium may grow over dysplastic clones.

Adenocarcinoma of the Esophagus

6-8

times higher in men than in women. 3-4 times higher in whites than in blacks. White men represent 82% of cases.

Gut 50:368-372, 2002

Poor Prognosis
Significant dysphagia

Occurs after 50-75% of the esophageal lumen is occluded. Extensive involvement of esophagus and surrounding structures in 90% of cases.
Persistent

substernal pain unrelated to swallowing

May indicate mediastinal disease.

Adenocarcinoma of the GE Junction

Adenocarcinoma of the distal esophagus

Cancer of the cardia

II III

Subcardial cancer

Adenocarcinoma of GE Junction
Type

1: Associated with reflux leading to intestinal metaplasia (Barretts). Types 2 and 3: Associated with infection with Helicobacter pylori.

I II III

Squamous cell carcinoma

Adenocarcinoma of the distal esophagus

Cancer of the cardia Subcardial cancer Non-cardia cancer

Illustration

shows cancers of mid and distal esophagus and lymphatic drainage.

Iyer R B et al. AJR 2003;181:785-793

2003 by American Roentgen Ray Society

Endoscopic Surveillance of Barretts Esophagus

With

high-grade dysplasia, 19-26% develop invasive cancer within 2 to 7.5 years. American College of Gastroenterology:
No dysplasia x 2 years: q 2 years Low-grade dysplasia: q 6 mo. x 2, then q year High-grade dysplasia: surgery, ablation or EGD q 3 mo.
Am J Gastroenterol 1998; 93:1028-1032

Diagnosis of Esophageal Ca.

In

the United States, most patients present with advanced stage disease. At least have 75% have locoregional extension or distant metastases that prevent surgical cure.

Cancer of the Esophagus

15 Cricopharyngeu s

25
Carina

38 40

Hiatus
Histologic GE junction

Staging: Primary Tumor (T)

T1

Tumor invades lamina propria or submucosa T2 Tumor invades muscularis propria T3 Tumor invades adventitia T4 Tumor invades adjacent structures

Percent Lymph Node Metastases According to Tumor Stage

pT pT1 mucosa submucosa pT2 pT3 pT4 SCCA Adenoca. Gastric Esophagus GE Junction Carcinoma 0 23 64 71 82 1 19 77 83 96 4 14 66 86 90

Surg Clin N Am 2000; 80: 659-82

Staging
Endoscopy Endoscopic ultrasound CT

scans Mediastinoscopy or Laparoscopy (PET Scan)

CT Scans
5

mm thickness is upper limit of normal esophagus. T1-2 disease between 5-15 mm. T3 disease >15 mm with irregular outer mass. T4 disease: invasion of adjacent structures.
Contacts aorta >90 degrees. Indents or displaces the trachea.
CT

underestimates stage in > 40%.

Therapy: Cancer of the Esophagus

Complete

resection is the goal. If complete resection not possible, no role for palliative resection.
No survival benefit. Palliation of dysphagia with stents or combined chemoradiotherapy.

Preoperative Surgical Staging

Mediastinoscopy: difficulty in

sampling AP window, left paraaortic nodes. Thoracoscopy: accurate in detecting node metastases in 93%. Laparoscopy: accurate in detecting node metastases in 94%.
Can identify small volume lymph node or visceral disease.

Contraindications to Surgery
Extent of

tumor

Mediastinal or lymph node invasion Distant metastases/celiac node involvement

Medical

factors

FEV1 < 1.5 liter Weight loss of >20% Cardiac disease

Surgical Approaches for Esophageal Cancer

Ivor-Lewis Esophagectomy

3 Field Esophagectomy
Transhiatal Esophagectomy

Five Year Survival in Resected Patients

Tumor

confined to esophagus: 50% Involvement of adjacent tissues: 15% Involvement of regional nodes: 10% Overall survival: 20-25%

Attempts to Improve Outcome

Preoperative Chemotherapy

9 Phase III randomized trials. Major response in 17 to 66% of patients. One trial showed 4 month improvement in median survival. Preoperative Radiation Therapy No improvement in survival.
Surg Clin N Am 82:729-746, 2002

Attempts to Improve Outcome

Postoperative

Radiation Therapy Improved locoregional control. No improvement in survival. Indicated for positive surgical margins. Postoperative Chemotherapy No improvement in survival.

Attempts to Improve Outcome

Preoperative

Chemotherapy and Radiotherapy Pathologic complete responses in 20-30%. Improves prognosis for patients with objective tumor remission and complete resection. Increases morbidity and mortality in others. Lower locoregional recurrence.

Comparison of Treatment Modalities: Median Survivals

Surgery:

16.5 months
Radiotherapy and

Chemotherapy

14.5 months
Surgery,

Radiotherapy, Chemotherapy

16-18.6 months

Chemotherapy and Radiation Without Operation

Major

antitumor responses in 40-80% of patients. Median survival 8-22 months. 2 year survival 10-41%. Chemotherapy and radiation together better than radiation alone.
12.5 vs 8.9 month median survival

Palliative Modalities
(Surgical bypass)
Snare

Stents:

cautery Sclerotherapy Laser therapy Photodynamic therapy Chemotherapy

for dysphagia and tracheoesophageal fistula Radiation (external beam or brachytherapy)

Metal stent

56-year-old man after resection of esophageal cancer.

Iyer R B et al. AJR 2003;181:785-793

2003 by American Roentgen Ray Society

Stents

Universitatea Titu Maiorescu Bucuresti

GASTROENTEROLOGY
LECTURE II

Prof Univ Dr Ion C. intoiu

156

ESOPHAGIAL BENIGN LESIONS

Overview
Benign

Lesions

Benign Lesions

Lymphangioma Hemangioma Fibrovascular Polyps Granular Cell Tumors Adenomas Papillomas Esophageal Duplication Cysts Lipomas, Leiomyomas, Desmoid Tumors, Schwannomas

Lymphangioma

Malformation of sequestered lymphatic tissue <15 reported cases, children <2 years old Translucent, yellowish, compressible mass, <5mm Dilated endothelial spaces with cavities lined by flat endothelial cells containing eosinophilic material Solid on EUS, in submucosa, confirmed with tunneled biopsies

Resection for 4-5cm by band-assisted mucosectomy and endoscopic submucosal dissection or C02 laser

Hemangioma
Prevalence
Mostly

0.04%

cavernous, come capillary

Nodular,

soft, bluish-red, and typically blanch when pressed with biopsy forceps (ddx - Kaposi's sarcoma)

Usually

asymptomatic but can p/w bleeding and/or dysphagia Surgical or endoscopic resection

Fibrovascular Polyps

Fibromas, fibrolipomas, myomas, and lipomas Mix of fibrous, vascular, and adipose tissue covered by squamous epithelium Upper third of the esophagus, attach directly to the inferior aspect of the cricopharyngeus 75% M, 50-60s y/o Arise from a nodular thickening of redundant mucosal fold that elongate as the result of propulsive forces during repeated swallowing Asx but large lesions can prolapse into the larynx asphyxiation, dysphagia, cough, n/v, ulceration/bleeding Endoscopic or surgical rsxn if large feeding vessel present or base inaccessible

Granular Cell Tumors

10% GI, 65% esophagus 1% benign esophageal tumors, 10% multifocal 60% M, avg 45 y/o 1/3 dysphagia, mostly asx Sessile, yellowish-white, firm, rubbery Polygonal with eosinophilic granules, resemble Schwann cells, + S100 Malignancy increases when large or rapid growth (~4%) Endoscopic mucosal resection if 4 cm, surveillance endoscopy 1-2yrs if smaller

Adenomas

Associated with GERD/Barretts, distal esophagus and GE-junction Up to 1.5cm, sometimes multiple Inflammatory fibroid polyps include hamartomas, inflammatory pseudopolyps, and eosinophilic granulomas More common in stomach, small bowel, and colon than the esophagus Benign, reactive inflammatory lesions with connective tissue stroma and diffuse eosinophilic infiltrate Usually asx but can cause hemorrhage or dysphagia Resect only when symptomatic

Papillomas

Fingerlike projections, lined by squamous cells, connective tissue core Incidence 0.01-0.45% 50s, M>F, mostly solitary Chronic inflammation/GERD (70% in distal 1/3) vs HPV (546% in study) HPV detected in esophageal SCC with papillomas Small, whitish-pink, wart-like exophytic projections (ddx verrucous squamous cell carcinoma, granulation tissue, papillary leukoplakia) Association with tylosis, acanthosis nigricans, Goltz syndrome

Usually asymptomatic, if large may cause dysphagia Endoscopic resection, recurrence infrequent

Esophageal Duplication Cysts

Congenital anomalies most common in proximal small intestine but also in esophagus, stomach and colon 1/8000 live births, 80% dx <2 y/o 3 major characteristics: Within the esophageal wall Covered by two muscle layers Contain squamous epithelium 1/3 contain heterotopic gastric mucosa and/or Peyers patches 80% do not communicate with the esophageal lumen Most common on R lateral esophagus due to the dextrorotation of the stomach Dysphagia (70%), epigastric pain (20%), retrosternal pain (10%), hematemesis, and respiratory sx cough/stridor/wheezing Resection if symptomatic, malignancy rare

Diverticulosis
Diverticulitis
obstipation diverticulectomy

Pathology - Hernias
Diaphragmatic
Hiatal,

Gastroesophageal Inguinal Umbilical

Liver Cirrhosis
K. Dionne Posey, MD, MPH Internal Medicine & Pediatrics December 9, 2004

Introduction
The

two most common causes in the United States are alcoholic liver disease and hepatitis C, which together account for almost one-half of those undergoing transplantation

Introduction
12th leading cause of death in the united

states in 2002 On average about 27,000 deaths per year Patients with cirrhosis are susceptible to a variety of complications and their life expectancy is markedly reduced

Exactly How Much Do You Drink?

Estimated

that the development of cirrhosis requires, on average, the ingestion of 80 grams of ethanol daily for 10 to 20 years This corresponds to approximately one liter of wine, eight standard sized beers, or one half pint of hard liquor each day

Pathophysiology

Irreversible chronic injury of the hepatic parenchyma Extensive fibrosis - distortion of the hepatic architecture Formation of regenerative nodules

Clinical Manifestations
Spider angiomas Palmar erythema Nail changes

Muehrcke's nails

Terrys nails

Gynecomastia Testicular atrophy

Clinical Manifestations

Muehrcke's nails

Terrys nails

Clinical Manifestations
Fetor

hepaticus Jaundice Asterixis Pigment gallstones Parotid gland enlargement

Cruveilhier-

Baumgarten murmur Hepatomegaly Splenomegaly Caput medusa

Laboratory Studies
most

common measured laboratory test classified as LFTs include

the enzyme tests (principally the serum aminotransferases, alkaline phosphatase, and gamma glutamyl transpeptidase), the serum bilirubin tests of synthetic function (principally the serum albumin concentration and prothrombin time)

Radiologic Modalities
Can

occasionally suggest the presence of cirrhosis, they are not adequately sensitive or specific for use as a primary diagnostic modality Major utility of radiography in the evaluation of the cirrhotic patient is in its ability to detect complications of cirrhosis

Diagnosis

Liver biopsy
Obtained by either a percutaneous, transjugular, laparoscopic, or radiographicallyguided fine-needle approach Sensitivity of a liver biopsy for cirrhosis is in the range of 80 to 100 percent depending upon the method used, and the size and number of specimens obtained

Diagnosis
not necessary if the clinical, laboratory, and radiologic data strongly suggest the presence of cirrhosis liver biopsy can reveal the underlying cause of cirrhosis

Histopathology

Histopathology

Histopathology

Histopathology

Morphologic Classification
Micronodular cirrhosis Nodules less than 3 mm in diameter Believed to be caused by alcohol, hemochromatosis, cholestatic causes of cirrhosis, and hepatic venous outflow obstruction

Morphologic Classification
Macronodular

cirrhosis
Nodules larger than 3 mm Believed to be secondary to chronic viral hepatitis

Morphologic Classification

Relatively nonspecific with regard to etiology The morphologic appearance of the liver may change as the liver disease progresses
micronodular cirrhosis usually progresses to macronodular cirrhosis

Serological markers available today are more specific than morphological appearance of the liver for determining the etiology of cirrhosis Accurate assessment of liver morphology may only be achieved at surgery, laparoscopy, or autopsy

Evaluation of Cirrhosis

Complications
Ascites
Spontaneous Bacterial Hepatorenal

Peritonitis

syndrome Variceal hemorrhage Hepatopulmonary syndrome

Complications
Other

Pulmonary syndromes

Hepatic hydrothorax Portopulmonary HTN

Hepatic

Encephalopathy Hepatocellular carcinoma

Ascites
Accumulation of

fluid within the peritoneal

cavity Most common complication of cirrhosis Two-year survival of patients with ascites is approximately 50 percent

Ascites

Assessment of ascites
Grading
Grade 1 mild; Detectable only by US Grade 2 moderate; Moderate symmetrical distension of the abdomen Grade 3 large or gross asites with marked abdominal distension

Older system -subjective

1+ minimal, barely detectable 2+ moderate 3+ massive, not tense 4+massive and tense

Ascites
Imaging studies

for confirmation of ascites

Ultrasound is probably the most cost-effective modality

Ascites

Who gets a belly tap?

What do I want to order ?

Ascites
Treatment aimed

at the underlying cause of the hepatic disease and at the ascitic fluid itself Dietary sodium restriction
Limiting sodium intake to 88 meq (2000 mg) per day

Ascites
The

most successful therapeutic regimen is the combination of single morning oral doses of Spironolactone and Furosemide, beginning with 100 mg and 40 mg Two major concerns with diuretic therapy for cirrhotic ascites:
Overly rapid removal of fluid Progressive electrolyte imbalance

Spontaneous Bacterial Peritonitis

Infection

of ascitic fluid Almost always seen in the setting of endstage liver disease The diagnosis is established by
A positive ascitic fluid bacterial culture Elevated ascitic fluid absolute polymorphonuclear leukocyte (PMN) count ( >250 cells/mm3)

Spontaneous Bacterial Peritonitis

Clinical

manifestations:

Fever Abdominal pain Abdominal tenderness Altered mental status

Hepatorenal syndrome
acute

renal failure coupled with advanced hepatic disease (due to cirrhosis or less often metastatic tumor or
severe alcoholic hepatitis)

characterized

by:

Oliguria benign urine sediment very low rate of sodium excretion progressive rise in the plasma creatinine concentration

Hepatorenal Syndrome
Reduction

in GFR often clinically masked Prognosis is poor unless hepatic function improves Nephrotoxic agents and overdiuresis can precipitate HRS

Variceal hemorrhage
Occurs

in 25 to 40 percent of patients with cirrhosis Prophylactic measures Screening EGD recommended for all cirrhotic patients

Hepatopulmonary syndrome
Hepatopulmonary

syndrome

Liver disease Increased alveolar-arterial gradient while breathing room air Evidence for intrapulmonary vascular abnormalities, referred to as intrapulmonary vascular dilatations (IPVDs)

Hepatic Hydrothorax
Pleural

effusion in a patient with cirrhosis and no evidence of underlying cardiopulmonary disease Movement of ascitic fluid into the pleural space through defects in the diaphragm, and is usually right-sided Diagnosis -pleural fluid analysis
reveals a transudative fluid serum to fluid albumin gradient greater than 1.1

Hepatic hydrothorax
Confirmatory study:

Scintigraphic studies demonstrate tracer in the chest cavity after injection into the peritoneal cavity
Treatment

options:

diuretic therapy periodic thoracentesis TIPS

Portopulmonary HTN
Refers

to the presence of pulmonary hypertension in the coexistent portal hypertension Prevalence in cirrhotic patients is approximately 2 percent Diagnosis:
Suggested by echocardiography Confirmed by right heart catheterization

Hepatic Encephalopathy
Spectrum

of potentially reversible neuropsychiatric abnormalities seen in patients with liver dysfunction

Diurnal sleep pattern pertubation Asterixis Hyperactive deep tendon reflexes Transient decerebrate posturing

Hepatic Encephalopathy

Hepatic Encephalopathy
Monitoring for

events likely to precipitate

HE [i.E.- variceal bleeding, infection (such as

SBP), the administration of sedatives, hypokalemia, and hyponatremia]
Reduction

of ammoniagenic substrates

Lactulose / lactitol Dietary restriction of protein Zinc and melatonin

Hepatocellular Carcinoma
Patients

with cirrhosis have a markedly increased risk of developing hepatocellular carcinoma Incidence in well compensated cirrhosis is approximately 3 percent per year

Hepatocellular Carcinoma
Symptoms

are largely due to mass effect from the

tumor
Pain, early satiety, obstructive jaundice, and a palpable mass
Serum

AFP greater than 500 micrograms/l in a patient with cirrhosis are virtually diagnostic Median survival following diagnosis is approximately 6 to 20 months

Prognostic Tools
MELD

(model for end-stage liver disease)

Identify patients whose predicted survival postprocedure would be three months or less

MELD = 3.8[serum bilirubin (mg/dL)] + 11.2[INR] + 9.6[serum creatinine (mg/dL)] + 6.4

Prognostic Tools
Child-Turcotte-Pugh (CTP)

score

initially designed to stratify the risk of portacaval shunt surgery in cirrhotic patients based upon five parameters: serum bilirubin, serum albumin, prothrombin time, ascites and encephalopathy good predictor of outcome in patients with complications of portal hypertension

Prognostic Tools
APACHE

III (acute physiology and chronic health evaluation system)

Designed to predict an individual's risk of dying in the hospital

Treatment Options

The major goals of treating the cirrhotic patient include:

Slowing or reversing the progression of liver disease Preventing superimposed insults to the liver Preventing and treating the complications Determining the appropriateness and optimal timing for liver transplantation

Liver Transplantation
Liver

transplantation is the definitive treatment for patients with decompensated cirrhosis Depends upon the severity of disease, quality of life and the absence of contraindications

Liver Transplantation
Minimal

criteria for listing cirrhotic patients on the liver transplantation list include
A child-Pugh score 7 Less than 90 percent chance of surviving one year without a transplant An episode of gastrointestinal hemorrhage related to portal hypertension An episode of spontaneous bacterial peritonitis

Vaccinations
Hepatitis

A and B Pneumococcal vaccine Influenza vaccination

Surveillance
Screening recommendations:

serum AFP determinations and ultrasonography every six months

Avoidance of Superimposed Insults

Avoidance of:
Alcohol Acetaminophen Herbal medications

References

Up to Date Harrisons New England Journal

http://www.openclinical.org/aisp_apache.html Nail abnormalities: clues to systemic disease, American Family Physician, March 15, 2004 Robert Fawcett