2013 Curs Lecture 1 Scurtat

8/13/2019 2013 Curs Lecture 1 Scurtat

1/227

GASTROENTEROLOGY

Universitatea Titu Maiorescu

Bucuresti

LECTURE I

Prof Univ Dr Ion C. intoiu

1


2/227

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.


3/227

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.


4/227


5/227

BASIS IN

GASTROENTERELOGY


6/227

6

Digestion

Phases

Ingestion

Movement

Digestion

Absorption

Further digestion


7/227

7

Digestive System Organization

Gastrointestinal (Gl) tract (Alimentarycanal)

Tube within a tube

Direct link/path between organs

StructuresMouth

Oral Cavity

Pharynx

Esophagus

Stomach Duedenum

Jejenum

Ileum

Cecum

Ascending colon

Transverse colon,Descendent colon,rectum


8/227

8

Anatomy of the Mouth and

Throat


9/227

NormalEsophagus


10/227


11/227

11

The Duodenum and Related

Organs


12/227

12

Small Intestine

Control

Requires pancreatic

enzymes & bile to

complete digestion


13/227

13

The Digestive System


14/227

14

Digestive System Organization

Descending colon

Sigmoid colon

Rectum

Anus

Accessory structures

Not in tube path

Organs

Teeth

TongueSalivary glands

Liver

Gall bladder

Pancreas


15/227

15

Esophagus

Usually collapsed (closed)

3 constrictions

Aortic arch

Left primary bronchus

Diaphragm

Surrounded by

SNS plexus Blood vessels

Functions

Secrete mucous

Transport food


16/227

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 fromreentering the esophagus

ESOPHAGUS


17/227

Anatomy

Diameter of normal esophagus is about 2.5 cm.

Three areas of narrowing:

Cricopharyngeus muscle is narrowest portion of adultGI tract, 14 mm.

Esophagus crossed by left mainstem bronchus.

Esophagogastric junction.

Normal swallowing can occur with lumen of12-13 mm.


18/227

. 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


19/227

19

Peristalsis and Segmentation


20/227

20

Stomach

Usually J shaped

Left side, anterior to the spleen

Mucous membraneG cellsmake gastrin

Goblet cellsmake mucous

Gastric pitOxyntic glandParietal cellsMake HCl

Chief cellsZymogenic cellsPepsin

Gastric lipase


21/227

StomachFundus

Upper rounded portion

BodyCentral part

Digestive System Structures


22/227

StomachPylorus

Lower tubular part (also called the gastric antrum)

Pyloric sphincter regulates passage of food from stomachinto the duodenum

Folds in mucous membranes of stomach = Rugae



23/227

StomachGastric juices breakdown food in stomach

Muscular action of stomach causes churning of

foodMixes food with the secretions

Chyme = liquidlike mixture of partially digested foodand digestive secretions



24/227

24

Anatomy of the Stomach


25/227

25

Stomach

3 muscle layers Oblique

Circular

Longitudinal Regions

Cardiac sphincter

Fundus

Antrum (pylorus)

Pyloric sphincter

Vascular

Inner surface thrown intofoldsRugae

Contains enzymes that workbest at pH 1-2


26/227


27/227

27


Organs


28/227

28

Small Intestine

Control

Requires pancreatic

enzymes & bile to

complete digestion


29/227

29

Small Intestine

Secretes digestiveenzymes

Peptidases

Amino-Di-

Tri-

Sucrases

Maltase

Lactase

Saccharidases

Di-

Tri-

Lipase

Nucleases


30/227

30

Small Intestine

Extends from pyloric

sphincterileocecalvalve

Regions Duodenum

Jejenum

Ileum

Movements

Segmentation

Peristalsis


31/227

31

Small Intestine

Histology

Intestinal glandsIntestinal enzymes

Duodenal glandsAlkaline mucous

Paneth cellsLysozyme

Microvilli

Lacteals

Plica circularis

Smooth muscle

Lymphatic tissueGALT

Vascular


32/227

32

Small Intestine

Absorbs 80% ingested water

Electrolytes

Vitamins Minerals

Carbonates

Active/facilitated transport

Monosaccharides

ProteinsDi-/tripeptides

Amino acids

Lipids

Monoglycerides

Fatty acids

Micelles

Chylomicrons


33/227

33

Structure of the Villi in the Small Intestine


34/227

34

Large Intestine

Functions

Mechanical digestion

Haustral churning

Peristalsis

Reflexes

Gastroileal

Gastrocolic

Chemical digestion

Bacterial digestionFerment carbohydrates

Protein/amino acidbreakdown

Absorbs

More water

Vitamins

BK

Concentrate/eliminatewastes


35/227

35

Large Intestine

Extends from ileocecal valve to anus

Regions

CecumAppendix Colon

Ascending

Transverse

Descending Rectum

Anal canal


36/227

36

Anatomy of the Large Intestine


37/227

37

Large Intestine

Histology

No villi

No permanent circular folds

Smooth muscle

Taeniae coli

HaustraEpiploic appendages

Otherwise like rest of Gl tract


38/227

38

Feces Formation and

Defecation Chyme dehydrated to

form feces

Feces composition

Water Inorganic salts

Epithelial cells

Bacteria

Byproducts of digestion

Defecation Peristalsis pushes feces into

rectum

Rectal walls stretch

Control

Parasympathetic

Voluntary


39/227

39

Liver

Location

R. Hypochondrium

Epigastric region

4 Lobes

Left

Quadrate

Caudate

Right

Each lobe has lobulesContains hepatocytesSurround sinusoidsFeed into central vein


40/227

40

Liver

Functions Makes bile

Detergentemulsifies fats

Release promoted by: Vagus n.

CCK

Secretin

Contains Water

Bile salts Bile pigments

Electrolytes

Cholesterol

Lecithin


41/227

41

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


42/227

42

Liver

Dual blood supply

Hepatic portal vein

Direct input from small

intestineHepatic artery/vein

Direct links to heart


43/227

43


Organs


44/227

Structures of the Alimentary


45/227

45

Structures of the Alimentary

Canal


46/227

COMMON SIGNS and

SYMPTOMS


47/227

Common Signs and SymptomsAchlorhydriaAbnormal condition characterized by the absence

of hydrochloric acid in the gastric juice

AnorexiaLack or loss of appetite, resulting in the inability to

eat


48/227

Aphagia

Condition characterized by the loss of the

ability to swallow as a result of organic orpsychologic causes

Ascites

Abnormal accumulation of fluid within the

peritoneal cavity

Fluid contains large amounts of protein andelectrolytes

Common Signs and Symptoms


49/227

BorborygmusAn audible abdominal sound produced by

hyperactive intestinal peristalsis

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



50/227

ConstipationDifficulty in passing stools, or an incomplete or

infrequent passage of hard stools

DiarrheaFrequent passage of loose, watery stools



51/227

Dyspepsia

Vague feeling of epigastric discomfort after

eatingInvolves an uncomfortable feeling of fullness,

heartburn, bloating, and nausea

Dysphagia

Difficulty in swallowing, commonly associatedwith obstructive or motor disorders of theesophagus



52/227

EmaciationExcessive leanness caused by disease or lack of

nutrition

Emesis

Material expelled from the stomach duringvomiting

Vomitus



53/227

EructationAct of bringing up air from the stomach with a

characteristic sound through the mouth

BelchingFlatus; Flatulence

Air or gas in the intestine that is passed through therectum



54/227

Gastroesophageal Reflux Backflow of contents of stomach into esophagus

Often result of incompetence of the lower esophageal

sphincter

IcterusA 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



55/227

MelenaAn abnormal, black, tarry stool containing

digested blood

NauseaUnpleasant sensation often leading to the urge to

vomit

Pruritus ani

A common chronic condition of itching of the skin

around the anus



56/227

SteatorrheaGreater than normal amounts of fat in the feces

Characterized by frothy, foul-smelling fecal matter thatfloats

Vomit

To expel the contents of the stomach through the

esophagus and out of the mouth



57/227

Diagnostic, Symptomatic,

Therapeutic TermsAerophagia

anorexia

appendicitis

ascites

borborygmus

bulimia


58/227


59/227


Therapeutic Termsdeglutition

dysentery

dysphagia

eructation

fecalith

flatus

gastroesophageal reflux disease


60/227


Therapeutic TermsHalitosis

hematemesis

irritable bowel syndrome

leukoplakia

malabsorption syndrome

melena

obstipation


61/227


Therapeutic TermsPeristalsis

pyloric stenosis

regurgitation

steatorrhea

visceroptosis

Stomach


62/227

Glands:

Parietal cellsfound in fundus and body

Secrete HCl & intrinsic factor

Chief cellsare more at fundus and body

Secrete pepsinogen I & II

Congenital Anomalies

1. Diaphragmatic Hernia:

A defect in the diaphragm away from the hiatal orifice (nothiatal hernia)

Portions of stomach & small intestine herniates Results in respiratory impairment & pulmonary hypoplasia


63/227


64/227

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


65/227

ENDOSCOPY


66/227

ENDOSCOPY

Endoscopy, is theexamination of internal

body cavities using aspecialized medicalinstrument called anendoscope.

Physicians use endoscopy todiagnose, monitor, andsurgically treat variousmedical problems.


67/227

An endoscope is a slender,flexible tube equipped withlenses 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 thevideo monitor to get image.

Thorough one channel ofendoscope water and air isconducted to wash and dry thesurgical site.

A


68/227

The endoscope also has a channelthrough which surgeons canmanipulate tiny instruments, such as

forceps, surgical scissors, andsuction devices.

A variety of instruments can befitted to the endoscope for different

purposes.

A surgeon introduces the endoscopeinto the body either through a bodyopening, such as the mouth or theanus, or through a small incision inthe skin.

ENDOSCOPY


69/227

ENDOSCOPY The endoscope

gives visual

evidence of theproblem, such asulceration orinflammation

It can be used to

collect a sample oftissue; remove

problematic tissue,such as polyps

It is used to takephotograph of thehollow internalorgans


70/227

ENDOSCOPY

Depending on the body part, each type of endoscopy hasits own special term, such as

laparoscopy (abdomen, uterus, fallopian tube),laryngoscopy (vocal cords),

bronchoscopy (lungs),

colonoscopy (colon),

arthroscopy (joint) andGastroscopy (Stomach).


71/227


72/227

EUS - Characteristics

Layer of origin

Size

Echogenicity

Vascularity


73/227


74/227

Layer

Lesion

Mucosa Muscularis

Mucosa

Submucosa Muscularis

Propria

GIST Rare Mostcommon

Lipoma Always

Fibroma Always

Carcinoid Rare Rare Mostcommon

Rare

Granular

Cell Tumor

Rare Most

common

PancreaticRest

Common Common Rare

Duplication

Cyst

Always


75/227

EUS - Echogenicity

Anechoic - black (water, clear fluid, cysts,vessels, gallbladder)

Hypoechoic - lamina propria, muscularispropria, leiomyoma, GIST, mucin-filledcyst

Hyperechoic - superficial mucosa,

submucosa, serosa, lipoma

Isoechoic - between Hypo and Hyper


76/227


77/227


78/227


79/227


80/227

EUS - Summary

AGA GUIDELINESEndoscopy alone not reliable for detecting

the etiology of a subepithelial mass

Transabdominal US, CT, and MRI are

reliable for extra- but not intralumenallesions

EUS is the most accurate imaging test fordetecting layer of origin

Symptomatic masses should undergoendoscopic or surgical resection

Hypoechoic lesions in the 3rd and 4th layer aremost prone to misclassification


81/227

ESOPHAGIAL

PATHOLOGY


82/227

Hiatal Hernia


83/227

Rolling or

Para-

esophageal

hernia

Esophagus: Normal Lower


84/227

Esophagus: Normal Lower

Esophageal and Squamo-

columnar Junction Mucosae

E h N l


85/227

Esophagus: Normal

Squamous Epithelium

Esophagitis (Inflammation and Reactive

Epithelial Changes of the Esophageal Mucosa) Has


86/227

Epithelial Changes of the Esophageal Mucosa) Has

Many Causes

Esophagus: G-E Reflux -


87/227

p g

Changes in Epithelium and

Vascular Papillae

Esophagus: G-E Reflux -


88/227

p g

Defenses Against Reflux-

induced Injury

Esophagus: G-E Reflux - Symptoms and


89/227

p g y p

Endoscopic Findings in Reflux are NOT Predictive

of Biopsy Findings

Heightened Epithelial


90/227

Heightened Epithelial

Turnover in G-E Reflux is

Shown by Increased

Epithelial Tritiated

Thymidine Labeling

Esophagus: G-E Reflux - Reflux-induced EpithelialChange Is a Consequence Of Increased Cell


91/227

Turnover

Acute (Neutrophilic)


92/227

( p )

Inflammation and Erosion In

Severe Reflux Esophagitis

Severe Epithelial Reactive Changes with

Eosinophils (EOS) in Gastroesophageal Reflux


93/227

Eosinophils (EOS) in Gastroesophageal Reflux

Sequelae Of Prolonged G E


94/227

Sequelae Of Prolonged G-E

Reflux


95/227

Barretts Esophagus:


96/227

p g

Development And Anatomic

Relationships

Endoscopic Landmarks In


97/227

The GEJ Region: Normal

Versus Barretts (Columnar-lined) Esophagus With

Location Of LowerEsophageal Sphincter (LES)

Requirements For


98/227

q

Diagnosis Of Barretts

Esophagus

Barretts Esophagus: Gross


99/227

Barrett s Esophagus: Gross

Appearance

Confirmed By Biopsy When


100/227

The Squamo-columnar

Junction Is Displaced OrHighly Irregular

arre s ucosaSubmucosal Esophageal


101/227

Submucosal Esophageal

Gland (SMEG) BelowMuscularis Mucosae (MM)

Barretts Mucosa:


102/227

Distinctive (Specialized)

Type

A


103/227

A

Agents Used to Treat

Hyperacidity and

Gastroesophageal Reflux

Disease

Secretory Functions of the


104/227

24 - 104

Stomach Lining

Parietal cells secrete hydrochloric (HCl)

acid

Chief cells secrete pepsinogenMucoid cells secrete mucus


105/227

Copyright 2007 24 - 105

Stomach Hyperchlorhydria

Produced from:

Eating high-fat meals

Increased alcohol intake

Emotional turmoil


106/227

24 - 106

Goal of Antacid Therapy

Neutralize the acid

Inhibit pepsin activity

Increase resistance of the stomach lining

Increase tone of the lower esophageal

sphincter


107/227

24 - 107

Antacids

Three Forms1. Aluminum

2. Magnesium

3. Calcium Mechanism of action

Neutralization of gastric acidity

Low doses promote gastric mucosal defensivemechanisms


108/227

24 - 108

Systemic Antacids

Useful in short-term therapy

Rapid onset

Prolonged use causes an overload on the

kidneys

Example: sodium bicarbonate


109/227

24 - 109

Nonsystemic Antacids

Remain in gastrointestinal tract; useful in

long-term therapy

Most of the dose remains in thegastrointestinal tract

Will not alter acid-base system

Examples: calcium carbohydrate (Tums,Rolaids), aluminum carbonate (Basaljel),

magaldrate (Riopan), etc.

Side Effects and Adverse


110/227

24 - 110

Side Effects and Adverse

EffectsMagnesium: diarrhea

Aluminum: constipation

Calcium: constipation


111/227

24 - 111

Antacid Interactions

Binding of other drugs to the antacid causesreduced 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

Histamine (H2) Receptor


112/227

24 - 112

Antagonists

Examples

Cimetadine (Tagamet)

Famotidine (Pepcid)

Nizatidine (Axid)

Ranitidine (Zantac)


113/227

Copyright 2007

Thomson Delmar

24 - 113

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


114/227

Copyright 2007

Thomson Delmar

24 - 114

Helicobacter Pylori

An organism associated with the

development of peptic ulcer disease

TreatmentMetronidazole (Flagyl), an antimicrobial agent,

along with bismuth subsalicylate (Pepto-

Bismol) and tetracycline (antimicrobial) for 4

weeks to eradicateHelicobacter pylori


115/227

Copyright 2007

Thomson Delmar

24 - 115

Metoclopramide (Reglan)

A drug that stimulates the motility of the upperGI tract without stimulating the production of

gastric, biliary, or pancreatic solutions

ActionIncreases peristalsis in the duodenum and jejunum

Decreases gastroesophageal reflux

(continues)

(continued)


116/227

Copyright 2007

Thomson Delmar

24 - 116

Metoclopramide (Reglan)

Adverse effects

Produces extrapyramidal (Parkinson-like

symptoms) effectsCentral nervous system depression

Gastrointestinal upset


117/227

CANCER OF THE

ESOPHAGUS


118/227

O i


119/227

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.

P i S


120/227

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


121/227

Adenocarcinomaof the Esophagus

Obesity

Reflux disease and Barrett's esophagus.

Diet

Smoking

Scleroderma

A h l i


122/227

Achalasia

Cancer arises in 1-10% of patients

symptomatic for an average 15-25 years.

Usually squamous cell carcinoma of middlethird of esophagus.

Presents at younger age than usual.

P P i


123/227

Coughing after swallowing

Indicates tracheoesophageal fistula is present.

HiccupsIndicates involvement of diaphragm

Poor Prognosis

B tt' E h


124/227

Barrett's Esophagus

Dysplastic changes in distal esophagus and

gastroesophageal junction.

30-40 fold increase in adenocarcinoma ofthe esophagus.

10-15% of Barretts patients will develop

adenocarcinoma.Risk of cancer is about 0.5% per year.


125/227

Adenocarcinoma


126/227

de oc c oof 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


127/227

Adenocarcinoma of the GE Junction


128/227

Adenocarcinoma of thedistal esophagus

Cancer of the cardia

Subcardial cancer

I

II

III

Adenocarcinoma of


129/227

GE Junction

Type 1:

Associated with reflux leadingto intestinal metaplasia

(Barretts).Types 2 and 3:

Associated with infectionwith Helicobacter pylori.

I

II

III


130/227

Non-cardia cancer

Squamouscell carcinoma

Adenocarcinoma of thedistal esophagus

Cancer of the cardia

Subcardial cancer

Illustration shows cancers of mid and distal esophagus and lymphatic

drainage.


131/227

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

2003 by American Roentgen Ray Society

Endoscopic Surveillance


132/227

p

of Barretts Esophagus

With high-grade dysplasia, 19-26% developinvasive 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


133/227


134/227


135/227

Cancer of the Esophagus


136/227

Cricopharyngeu

s

Carina

Hiatus

Histologic GE

junction

15

25

38

40

Staging: Primary Tumor (T)


137/227

Staging: Primary Tumor (T)

T1 Tumor invades lamina propria or

submucosa

T2 Tumor invades muscularis propriaT3 Tumor invades adventitia

T4 Tumor invades adjacent structures

Percent Lymph Node Metastases


138/227

According to Tumor Stage

Surg Clin N Am 2000; 80: 659-82

SCCA Adenoca. Gastric

pT Esophagus GE Junction Carcinoma

pT1

mucosa 0 1 4submucosa 23 19 14

pT2 64 77 66

pT3 71 83 86pT4 82 96 90

Staging


139/227

Staging

Endoscopy

Endoscopic ultrasound

CT scansMediastinoscopy or Laparoscopy

(PET Scan)

CT Scans


140/227

5 mm thickness is upper limit of normalesophagus.

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


141/227

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


142/227

Preoperative Surgical Staging

Mediastinoscopy: difficulty in samplingAP 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 orvisceral disease.

Contraindications to Surgery


143/227

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


144/227

Five Year Survival in


145/227

Resected Patients

Tumor confined to esophagus: 50%

Involvement of adjacent tissues: 15%

Involvement of regional nodes: 10%

Overall survival: 20-25%

Att t t I O t


146/227

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.

Attempts to Improve Outcome

Surg Clin N Am 82:729-746, 2002

Attempts to


147/227

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


148/227

Preoperative Chemotherapy and RadiotherapyPathologic complete responses in 20-30%.

Improves prognosis for patients with

objective tumor remission and completeresection.

Increases morbidity and mortality in others.

Lower locoregional recurrence.

p p

Comparison of Treatmenti i i S i


149/227

Modalities: Median Survivals

Surgery:

16.5 months

Radiotherapy and Chemotherapy14.5 months

Surgery, Radiotherapy, Chemotherapy

16-18.6 months

Chemotherapy and RadiationWi h O i


150/227

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


151/227

Palliative Modalities

(Surgical bypass)

Snare cautery

SclerotherapyLaser therapy

Photodynamic

therapyChemotherapy

Stents: for

dysphagia and

tracheoesophageal

fistula

Radiation

(external beam or

brachytherapy)

Metal stent


152/227

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


153/227

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

2003 by American Roentgen Ray Society

Stents


154/227

Stents

Universitatea Titu Maiorescu

Bucuresti


155/227

GASTROENTEROLOGY

Bucuresti

LECTURE II

Prof Univ Dr Ion C. intoiu

156


156/227

ESOPHAGIAL BENIGN

LESIONS

Overview


157/227

Overview

Benign Lesions

Benign Lesions


158/227

Benign Lesions

Lymphangioma

Hemangioma

Fibrovascular Polyps Granular Cell Tumors

Adenomas

Papillomas

Esophageal Duplication Cysts Lipomas, Leiomyomas, Desmoid Tumors, Schwannomas

Lymphangioma


159/227

Lymphangioma

Malformation of sequestered lymphatic tissue


160/227

Hemangioma

Prevalence 0.04%

Mostly cavernous, come capillary

Nodular, soft, bluish-red, and typically blanchwhen pressed with biopsy forceps (ddx - Kaposi's

sarcoma)

Usually asymptomatic but can p/w bleeding and/or

dysphagia

Surgical or endoscopic resection

Fibrovascular Polyps


161/227

Fibrovascular Polyps

Fibromas, fibrolipomas, myomas, and lipomas

Mix of fibrous, vascular, and adipose tissue covered bysquamous 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 thatelongate as the result of propulsive forces during repeatedswallowing

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 orbase inaccessible

Granular Cell Tumors


162/227

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 Schwanncells, + S100

Malignancy increases when large or rapid growth (~4%) Endoscopic mucosal resection if 4 cm, surveillance

endoscopy 1-2yrs if smaller

Adenomas


163/227

de o s

Associated with GERD/Barretts, distal esophagus andGE-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


164/227

p

Fingerlike projections, lined by squamous cells, connectivetissue core

Incidence 0.01-0.45%

50s, M>F, mostly solitary

Chronic inflammation/GERD (70% in distal 1/3) vs HPV (5-46% 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


165/227

p g p y

Congenital anomalies most common in proximal small intestine butalso in esophagus, stomach and colon

1/8000 live births, 80% dx


166/227

Diverticulitis

obstipation

diverticulectomy


167/227


168/227

Liver Cirrhosis

K. Dionne Posey, MD, MPH

Internal Medicine & Pediatrics

December 9, 2004

Introduction


169/227

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


170/227

12th leading cause of death in the united

states in2002

On average about 27,000 deaths per yearPatients with cirrhosis are susceptible to

a variety of complications and their life

expectancy is markedly reduced

Exactly How Much Do You

Drink?


171/227

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


172/227

p y gy

Irreversible chronic injury of the hepatic

parenchyma

Extensive fibrosis - distortion of thehepatic architecture

Formation of regenerative nodules

Clinical Manifestations


173/227

Spider angiomas

Palmar erythema

Nail changesMuehrcke's nails

Terrys nails

GynecomastiaTesticular atrophy


174/227

Clinical Manifestations


175/227

Fetor hepaticus

Jaundice

Asterixis

Pigment gallstones

Parotid gland

enlargement

Cruveilhier-

Baumgarten murmur

Hepatomegaly

Splenomegaly

Caput medusa


176/227


177/227

Laboratory Studies


178/227

most common measured laboratory testclassified as LFTs include

the enzyme tests(principally the serum

aminotransferases, alkaline phosphatase, andgamma glutamyl transpeptidase), the serum

bilirubin

tests of synthetic function(principally the

serum albumin concentration and prothrombintime)

Radiologic Modalities


179/227

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


180/227

Diagnosis


181/227

not necessary if the clinical, laboratory, and

radiologic data strongly suggest the presence of

cirrhosis

liver biopsy can reveal the underlying cause ofcirrhosis

Histopathology


182/227

Histopathology


183/227

Histopathology


184/227

Histopathology


185/227


186/227

Morphologic Classification


187/227

Micronodular cirrhosisNodules less than 3 mm in diameter

Believed to be caused by alcohol,

hemochromatosis, cholestatic causes ofcirrhosis, and hepatic venous outflow

obstruction



188/227

Macronodular

cirrhosis

Nodules larger than 3mm

Believed to be

secondary to chronic

viral hepatitis



189/227

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


190/227

Complications


191/227

Ascites

Spontaneous Bacterial Peritonitis

Hepatorenal syndromeVariceal hemorrhage

Hepatopulmonary syndrome

Complications


192/227

Other Pulmonary syndromes

Hepatic hydrothorax

Portopulmonary HTN

Hepatic Encephalopathy

Hepatocellular carcinoma

Ascites


193/227

Accumulation of fluid within the peritoneal

cavity

Most common complication of cirrhosis

Two-year survival of patients with ascites is

approximately 50 percent

Ascites


194/227

Assessment of ascites

Grading

Grade 1mild; Detectable only by US

Grade 2moderate; Moderate symmetrical distension of the

abdomen

Grade 3large or gross asites with marked abdominaldistension

Older system -subjective

1+ minimal, barely detectable2+ moderate

3+ massive, not tense

4+massive and tense

Ascites


195/227

Imaging studies for confirmation of ascites

Ultrasound is probably the most cost-effective

modality


196/227

Who gets a belly tap?


197/227

What do I want to order ?


198/227

Ascites


199/227

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


200/227

The most successful therapeutic regimen isthe combination of single morning oraldoses of Spironolactoneand Furosemide,

beginning with 100 mg and 40 mgTwo major concerns with diuretic therapy

for cirrhotic ascites:

Overly rapid removal of fluidProgressive electrolyte imbalance

Spontaneous Bacterial

Peritonitis
http://www.utdol.com/application/topic.asp?file=drug_l_z/246562&drug=truehttp://www.utdol.com/application/topic.asp?file=drug_a_k/113157&drug=truehttp://www.utdol.com/application/topic.asp?file=drug_a_k/113157&drug=truehttp://www.utdol.com/application/topic.asp?file=drug_l_z/246562&drug=true


201/227

e to t s

Infection of ascitic fluid

Almost always seen in the setting of end-

stage 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


202/227

Clinical manifestations:

Fever

Abdominal pain

Abdominal tenderness

Altered mental status

Hepatorenal syndrome


203/227

acute renal failure coupled with advanced hepatic

disease (due to cirrhosis or less often metastatic tumor orsevere alcoholic hepatitis)

characterized by:Oliguria

benign urine sediment

very low rate of sodium excretion

progressive rise in the plasma creatinine concentration

Hepatorenal Syndrome


204/227

Reduction in GFR often clinically masked

Prognosis is poor unless hepatic function

improves

Nephrotoxic agents and overdiuresis can

precipitate HRS

Variceal hemorrhage


205/227

Occurs in 25 to 40 percent of patients with

cirrhosis

Prophylactic measures

Screening EGD recommended for all

cirrhotic patients



206/227


Liver disease

Increased alveolar-arterial gradient while

breathing room air

Evidence for intrapulmonary vascular

abnormalities, referred to as intrapulmonary

vascular dilatations (IPVDs)

Hepatic Hydrothorax


207/227

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 usuallyright-sided

Diagnosis -pleural fluid analysis

reveals a transudative fluid

serum to fluid albumin gradient greater than 1.1

Hepatic hydrothorax


208/227

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


209/227

Refers to the presence of pulmonaryhypertension in the coexistent portalhypertension

Prevalence in cirrhotic patients isapproximately 2 percent

Diagnosis:

Suggested by echocardiography

Confirmed by right heart catheterization



210/227

Spectrum of potentially reversible

neuropsychiatric abnormalities seen in

patients with liver dysfunction

Diurnal sleep pattern pertubation

Asterixis

Hyperactive deep tendon reflexes

Transient decerebrate posturing



211/227



212/227

Monitoring for events likely to precipitate

HE [i.E.- variceal bleeding, infection (such asSBP), the administration of sedatives,

hypokalemia, and hyponatremia]

Reduction of ammoniagenic substrates

Lactulose / lactitol

Dietary restriction of protein

Zinc and melatonin

Hepatocellular Carcinoma


213/227

Patients with cirrhosis have a markedly

increased risk of developing hepatocellular

carcinoma

Incidence in well compensated cirrhosis is

approximately 3 percent per year


214/227

Prognostic Tools


215/227

MELD (model for end-stage liver disease)

Identify patients whose predicted survival post-

procedure 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


216/227

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 withcomplications of portal hypertension


217/227

Prognostic Tools


218/227

APACHE III (acute physiology and chronic

health evaluation system)

Designed to predict an individual's risk of dying

in the hospital

Treatment Options


219/227

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 optimaltiming for liver transplantation

Liver Transplantation


220/227

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


221/227

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 hypertensionAn episode of spontaneous bacterial peritonitis

Vaccinations


222/227

Hepatitis A and B

Pneumococcal vaccine

Influenza vaccination

Surveillance


223/227

Screening recommendations:

serum AFP determinations and ultrasonography

every six months

Avoidance of Superimposed

Insults


224/227

Avoidance of:

Alcohol

AcetaminophenHerbal medications

References


225/227

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


226/227


227/227

Documents

2013 Curs Lecture 1 Scurtat