View
215
Download
0
Category
Preview:
Citation preview
8/13/2019 2013 Curs Lecture 1 Scurtat
1/227
GASTROENTEROLOGY
Universitatea Titu Maiorescu
Bucuresti
LECTURE I
Prof Univ Dr Ion C. intoiu
1
8/13/2019 2013 Curs Lecture 1 Scurtat
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.
8/13/2019 2013 Curs Lecture 1 Scurtat
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.
8/13/2019 2013 Curs Lecture 1 Scurtat
4/227
8/13/2019 2013 Curs Lecture 1 Scurtat
5/227
BASIS IN
GASTROENTERELOGY
8/13/2019 2013 Curs Lecture 1 Scurtat
6/227
6
Digestion
Phases
Ingestion
Movement
Digestion
Absorption
Further digestion
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
8/227
8
Anatomy of the Mouth and
Throat
8/13/2019 2013 Curs Lecture 1 Scurtat
9/227
NormalEsophagus
8/13/2019 2013 Curs Lecture 1 Scurtat
10/227
8/13/2019 2013 Curs Lecture 1 Scurtat
11/227
11
The Duodenum and Related
Organs
8/13/2019 2013 Curs Lecture 1 Scurtat
12/227
12
Small Intestine
Control
Requires pancreatic
enzymes & bile to
complete digestion
8/13/2019 2013 Curs Lecture 1 Scurtat
13/227
13
The Digestive System
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
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.
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
19/227
19
Peristalsis and Segmentation
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
21/227
StomachFundus
Upper rounded portion
BodyCentral part
Digestive System Structures
8/13/2019 2013 Curs Lecture 1 Scurtat
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
Digestive System Structures
8/13/2019 2013 Curs Lecture 1 Scurtat
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
Digestive System Structures
8/13/2019 2013 Curs Lecture 1 Scurtat
24/227
24
Anatomy of the Stomach
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
26/227
8/13/2019 2013 Curs Lecture 1 Scurtat
27/227
27
The Duodenum and Related
Organs
8/13/2019 2013 Curs Lecture 1 Scurtat
28/227
28
Small Intestine
Control
Requires pancreatic
enzymes & bile to
complete digestion
8/13/2019 2013 Curs Lecture 1 Scurtat
29/227
29
Small Intestine
Secretes digestiveenzymes
Peptidases
Amino-Di-
Tri-
Sucrases
Maltase
Lactase
Saccharidases
Di-
Tri-
Lipase
Nucleases
8/13/2019 2013 Curs Lecture 1 Scurtat
30/227
30
Small Intestine
Extends from pyloric
sphincterileocecalvalve
Regions Duodenum
Jejenum
Ileum
Movements
Segmentation
Peristalsis
8/13/2019 2013 Curs Lecture 1 Scurtat
31/227
31
Small Intestine
Histology
Intestinal glandsIntestinal enzymes
Duodenal glandsAlkaline mucous
Paneth cellsLysozyme
Microvilli
Lacteals
Plica circularis
Smooth muscle
Lymphatic tissueGALT
Vascular
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
33/227
33
Structure of the Villi in the Small Intestine
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
35/227
35
Large Intestine
Extends from ileocecal valve to anus
Regions
CecumAppendix Colon
Ascending
Transverse
Descending Rectum
Anal canal
8/13/2019 2013 Curs Lecture 1 Scurtat
36/227
36
Anatomy of the Large Intestine
8/13/2019 2013 Curs Lecture 1 Scurtat
37/227
37
Large Intestine
Histology
No villi
No permanent circular folds
Smooth muscle
Taeniae coli
HaustraEpiploic appendages
Otherwise like rest of Gl tract
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
39/227
39
Liver
Location
R. Hypochondrium
Epigastric region
4 Lobes
Left
Quadrate
Caudate
Right
Each lobe has lobulesContains hepatocytesSurround sinusoidsFeed into central vein
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
42/227
42
Liver
Dual blood supply
Hepatic portal vein
Direct input from small
intestineHepatic artery/vein
Direct links to heart
8/13/2019 2013 Curs Lecture 1 Scurtat
43/227
43
The Duodenum and Related
Organs
8/13/2019 2013 Curs Lecture 1 Scurtat
44/227
Structures of the Alimentary
8/13/2019 2013 Curs Lecture 1 Scurtat
45/227
45
Structures of the Alimentary
Canal
8/13/2019 2013 Curs Lecture 1 Scurtat
46/227
COMMON SIGNS and
SYMPTOMS
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
49/227
BorborygmusAn audible abdominal sound produced by
hyperactive intestinal peristalsis
Borborygmi are rumbling, gurgling, and tinklingnoises heard when listening with a stethoscope
Common Signs and Symptoms
8/13/2019 2013 Curs Lecture 1 Scurtat
50/227
ConstipationDifficulty in passing stools, or an incomplete or
infrequent passage of hard stools
DiarrheaFrequent passage of loose, watery stools
Common Signs and Symptoms
8/13/2019 2013 Curs Lecture 1 Scurtat
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
Common Signs and Symptoms
8/13/2019 2013 Curs Lecture 1 Scurtat
52/227
EmaciationExcessive leanness caused by disease or lack of
nutrition
Emesis
Material expelled from the stomach duringvomiting
Vomitus
Common Signs and Symptoms
8/13/2019 2013 Curs Lecture 1 Scurtat
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
Common Signs and Symptoms
8/13/2019 2013 Curs Lecture 1 Scurtat
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
Common Signs and Symptoms
8/13/2019 2013 Curs Lecture 1 Scurtat
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
Common Signs and Symptoms
8/13/2019 2013 Curs Lecture 1 Scurtat
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
Common Signs and Symptoms
8/13/2019 2013 Curs Lecture 1 Scurtat
57/227
Diagnostic, Symptomatic,
Therapeutic TermsAerophagia
anorexia
appendicitis
ascites
borborygmus
bulimia
8/13/2019 2013 Curs Lecture 1 Scurtat
58/227
8/13/2019 2013 Curs Lecture 1 Scurtat
59/227
Diagnostic, Symptomatic,
Therapeutic Termsdeglutition
dysentery
dysphagia
eructation
fecalith
flatus
gastroesophageal reflux disease
8/13/2019 2013 Curs Lecture 1 Scurtat
60/227
Diagnostic, Symptomatic,
Therapeutic TermsHalitosis
hematemesis
irritable bowel syndrome
leukoplakia
malabsorption syndrome
melena
obstipation
8/13/2019 2013 Curs Lecture 1 Scurtat
61/227
Diagnostic, Symptomatic,
Therapeutic TermsPeristalsis
pyloric stenosis
regurgitation
steatorrhea
visceroptosis
Stomach
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
63/227
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
65/227
ENDOSCOPY
8/13/2019 2013 Curs Lecture 1 Scurtat
66/227
ENDOSCOPY
Endoscopy, is theexamination of internal
body cavities using aspecialized medicalinstrument called anendoscope.
Physicians use endoscopy todiagnose, monitor, andsurgically treat variousmedical problems.
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
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).
8/13/2019 2013 Curs Lecture 1 Scurtat
71/227
8/13/2019 2013 Curs Lecture 1 Scurtat
72/227
EUS - Characteristics
Layer of origin
Size
Echogenicity
Vascularity
8/13/2019 2013 Curs Lecture 1 Scurtat
73/227
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
76/227
8/13/2019 2013 Curs Lecture 1 Scurtat
77/227
8/13/2019 2013 Curs Lecture 1 Scurtat
78/227
8/13/2019 2013 Curs Lecture 1 Scurtat
79/227
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
81/227
ESOPHAGIAL
PATHOLOGY
8/13/2019 2013 Curs Lecture 1 Scurtat
82/227
Hiatal Hernia
8/13/2019 2013 Curs Lecture 1 Scurtat
83/227
Rolling or
Para-
esophageal
hernia
Esophagus: Normal Lower
8/13/2019 2013 Curs Lecture 1 Scurtat
84/227
Esophagus: Normal Lower
Esophageal and Squamo-
columnar Junction Mucosae
E h N l
8/13/2019 2013 Curs Lecture 1 Scurtat
85/227
Esophagus: Normal
Squamous Epithelium
Esophagitis (Inflammation and Reactive
Epithelial Changes of the Esophageal Mucosa) Has
8/13/2019 2013 Curs Lecture 1 Scurtat
86/227
Epithelial Changes of the Esophageal Mucosa) Has
Many Causes
Esophagus: G-E Reflux -
8/13/2019 2013 Curs Lecture 1 Scurtat
87/227
p g
Changes in Epithelium and
Vascular Papillae
Esophagus: G-E Reflux -
8/13/2019 2013 Curs Lecture 1 Scurtat
88/227
p g
Defenses Against Reflux-
induced Injury
Esophagus: G-E Reflux - Symptoms and
8/13/2019 2013 Curs Lecture 1 Scurtat
89/227
p g y p
Endoscopic Findings in Reflux are NOT Predictive
of Biopsy Findings
Heightened Epithelial
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
91/227
Turnover
Acute (Neutrophilic)
8/13/2019 2013 Curs Lecture 1 Scurtat
92/227
( p )
Inflammation and Erosion In
Severe Reflux Esophagitis
Severe Epithelial Reactive Changes with
Eosinophils (EOS) in Gastroesophageal Reflux
8/13/2019 2013 Curs Lecture 1 Scurtat
93/227
Eosinophils (EOS) in Gastroesophageal Reflux
Sequelae Of Prolonged G E
8/13/2019 2013 Curs Lecture 1 Scurtat
94/227
Sequelae Of Prolonged G-E
Reflux
8/13/2019 2013 Curs Lecture 1 Scurtat
95/227
Barretts Esophagus:
8/13/2019 2013 Curs Lecture 1 Scurtat
96/227
p g
Development And Anatomic
Relationships
Endoscopic Landmarks In
8/13/2019 2013 Curs Lecture 1 Scurtat
97/227
The GEJ Region: Normal
Versus Barretts (Columnar-lined) Esophagus With
Location Of LowerEsophageal Sphincter (LES)
Requirements For
8/13/2019 2013 Curs Lecture 1 Scurtat
98/227
q
Diagnosis Of Barretts
Esophagus
Barretts Esophagus: Gross
8/13/2019 2013 Curs Lecture 1 Scurtat
99/227
Barrett s Esophagus: Gross
Appearance
Confirmed By Biopsy When
8/13/2019 2013 Curs Lecture 1 Scurtat
100/227
The Squamo-columnar
Junction Is Displaced OrHighly Irregular
arre s ucosaSubmucosal Esophageal
8/13/2019 2013 Curs Lecture 1 Scurtat
101/227
Submucosal Esophageal
Gland (SMEG) BelowMuscularis Mucosae (MM)
Barretts Mucosa:
8/13/2019 2013 Curs Lecture 1 Scurtat
102/227
Distinctive (Specialized)
Type
A
8/13/2019 2013 Curs Lecture 1 Scurtat
103/227
A
Agents Used to Treat
Hyperacidity and
Gastroesophageal Reflux
Disease
Secretory Functions of the
8/13/2019 2013 Curs Lecture 1 Scurtat
104/227
24 - 104
Stomach Lining
Parietal cells secrete hydrochloric (HCl)
acid
Chief cells secrete pepsinogenMucoid cells secrete mucus
8/13/2019 2013 Curs Lecture 1 Scurtat
105/227
Copyright 2007 24 - 105
Stomach Hyperchlorhydria
Produced from:
Eating high-fat meals
Increased alcohol intake
Emotional turmoil
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
108/227
24 - 108
Systemic Antacids
Useful in short-term therapy
Rapid onset
Prolonged use causes an overload on the
kidneys
Example: sodium bicarbonate
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
110/227
24 - 110
Side Effects and Adverse
EffectsMagnesium: diarrhea
Aluminum: constipation
Calcium: constipation
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
112/227
24 - 112
Antagonists
Examples
Cimetadine (Tagamet)
Famotidine (Pepcid)
Nizatidine (Axid)
Ranitidine (Zantac)
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
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)
8/13/2019 2013 Curs Lecture 1 Scurtat
116/227
Copyright 2007
Thomson Delmar
24 - 116
Metoclopramide (Reglan)
Adverse effects
Produces extrapyramidal (Parkinson-like
symptoms) effectsCentral nervous system depression
Gastrointestinal upset
8/13/2019 2013 Curs Lecture 1 Scurtat
117/227
CANCER OF THE
ESOPHAGUS
8/13/2019 2013 Curs Lecture 1 Scurtat
118/227
O i
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
121/227
Adenocarcinomaof the Esophagus
Obesity
Reflux disease and Barrett's esophagus.
Diet
Smoking
Scleroderma
A h l i
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
123/227
Coughing after swallowing
Indicates tracheoesophageal fistula is present.
HiccupsIndicates involvement of diaphragm
Poor Prognosis
B tt' E h
8/13/2019 2013 Curs Lecture 1 Scurtat
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.
8/13/2019 2013 Curs Lecture 1 Scurtat
125/227
Adenocarcinoma
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
127/227
Adenocarcinoma of the GE Junction
8/13/2019 2013 Curs Lecture 1 Scurtat
128/227
Adenocarcinoma of thedistal esophagus
Cancer of the cardia
Subcardial cancer
I
II
III
Adenocarcinoma of
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
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.
8/13/2019 2013 Curs Lecture 1 Scurtat
131/227
Iyer R B et al. AJR 2003;181:785-793
2003 by American Roentgen Ray Society
Endoscopic Surveillance
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
133/227
8/13/2019 2013 Curs Lecture 1 Scurtat
134/227
8/13/2019 2013 Curs Lecture 1 Scurtat
135/227
Cancer of the Esophagus
8/13/2019 2013 Curs Lecture 1 Scurtat
136/227
Cricopharyngeu
s
Carina
Hiatus
Histologic GE
junction
15
25
38
40
Staging: Primary Tumor (T)
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
139/227
Staging
Endoscopy
Endoscopic ultrasound
CT scansMediastinoscopy or Laparoscopy
(PET Scan)
CT Scans
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
144/227
Five Year Survival in
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
152/227
56-year-old man after resection of esophageal cancer.
8/13/2019 2013 Curs Lecture 1 Scurtat
153/227
Iyer R B et al. AJR 2003;181:785-793
2003 by American Roentgen Ray Society
Stents
8/13/2019 2013 Curs Lecture 1 Scurtat
154/227
Stents
Universitatea Titu Maiorescu
Bucuresti
8/13/2019 2013 Curs Lecture 1 Scurtat
155/227
GASTROENTEROLOGY
Bucuresti
LECTURE II
Prof Univ Dr Ion C. intoiu
156
8/13/2019 2013 Curs Lecture 1 Scurtat
156/227
ESOPHAGIAL BENIGN
LESIONS
Overview
8/13/2019 2013 Curs Lecture 1 Scurtat
157/227
Overview
Benign Lesions
Benign Lesions
8/13/2019 2013 Curs Lecture 1 Scurtat
158/227
Benign Lesions
Lymphangioma
Hemangioma
Fibrovascular Polyps Granular Cell Tumors
Adenomas
Papillomas
Esophageal Duplication Cysts Lipomas, Leiomyomas, Desmoid Tumors, Schwannomas
Lymphangioma
8/13/2019 2013 Curs Lecture 1 Scurtat
159/227
Lymphangioma
Malformation of sequestered lymphatic tissue
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
166/227
Diverticulitis
obstipation
diverticulectomy
8/13/2019 2013 Curs Lecture 1 Scurtat
167/227
8/13/2019 2013 Curs Lecture 1 Scurtat
168/227
Liver Cirrhosis
K. Dionne Posey, MD, MPH
Internal Medicine & Pediatrics
December 9, 2004
Introduction
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
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?
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
172/227
p y gy
Irreversible chronic injury of the hepatic
parenchyma
Extensive fibrosis - distortion of thehepatic architecture
Formation of regenerative nodules
Clinical Manifestations
8/13/2019 2013 Curs Lecture 1 Scurtat
173/227
Spider angiomas
Palmar erythema
Nail changesMuehrcke's nails
Terrys nails
GynecomastiaTesticular atrophy
8/13/2019 2013 Curs Lecture 1 Scurtat
174/227
Clinical Manifestations
8/13/2019 2013 Curs Lecture 1 Scurtat
175/227
Fetor hepaticus
Jaundice
Asterixis
Pigment gallstones
Parotid gland
enlargement
Cruveilhier-
Baumgarten murmur
Hepatomegaly
Splenomegaly
Caput medusa
8/13/2019 2013 Curs Lecture 1 Scurtat
176/227
8/13/2019 2013 Curs Lecture 1 Scurtat
177/227
Laboratory Studies
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
180/227
Diagnosis
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
182/227
Histopathology
8/13/2019 2013 Curs Lecture 1 Scurtat
183/227
Histopathology
8/13/2019 2013 Curs Lecture 1 Scurtat
184/227
Histopathology
8/13/2019 2013 Curs Lecture 1 Scurtat
185/227
8/13/2019 2013 Curs Lecture 1 Scurtat
186/227
Morphologic Classification
8/13/2019 2013 Curs Lecture 1 Scurtat
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
Morphologic Classification
8/13/2019 2013 Curs Lecture 1 Scurtat
188/227
Macronodular
cirrhosis
Nodules larger than 3mm
Believed to be
secondary to chronic
viral hepatitis
Morphologic Classification
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
190/227
Complications
8/13/2019 2013 Curs Lecture 1 Scurtat
191/227
Ascites
Spontaneous Bacterial Peritonitis
Hepatorenal syndromeVariceal hemorrhage
Hepatopulmonary syndrome
Complications
8/13/2019 2013 Curs Lecture 1 Scurtat
192/227
Other Pulmonary syndromes
Hepatic hydrothorax
Portopulmonary HTN
Hepatic Encephalopathy
Hepatocellular carcinoma
Ascites
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
195/227
Imaging studies for confirmation of ascites
Ultrasound is probably the most cost-effective
modality
8/13/2019 2013 Curs Lecture 1 Scurtat
196/227
Who gets a belly tap?
8/13/2019 2013 Curs Lecture 1 Scurtat
197/227
What do I want to order ?
8/13/2019 2013 Curs Lecture 1 Scurtat
198/227
Ascites
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
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=true8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
202/227
Clinical manifestations:
Fever
Abdominal pain
Abdominal tenderness
Altered mental status
Hepatorenal syndrome
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
204/227
Reduction in GFR often clinically masked
Prognosis is poor unless hepatic function
improves
Nephrotoxic agents and overdiuresis can
precipitate HRS
Variceal hemorrhage
8/13/2019 2013 Curs Lecture 1 Scurtat
205/227
Occurs in 25 to 40 percent of patients with
cirrhosis
Prophylactic measures
Screening EGD recommended for all
cirrhotic patients
Hepatopulmonary syndrome
8/13/2019 2013 Curs Lecture 1 Scurtat
206/227
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
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
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
Hepatic Encephalopathy
8/13/2019 2013 Curs Lecture 1 Scurtat
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
Hepatic Encephalopathy
8/13/2019 2013 Curs Lecture 1 Scurtat
211/227
Hepatic Encephalopathy
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
214/227
Prognostic Tools
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
217/227
Prognostic Tools
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
222/227
Hepatitis A and B
Pneumococcal vaccine
Influenza vaccination
Surveillance
8/13/2019 2013 Curs Lecture 1 Scurtat
223/227
Screening recommendations:
serum AFP determinations and ultrasonography
every six months
Avoidance of Superimposed
Insults
8/13/2019 2013 Curs Lecture 1 Scurtat
224/227
Avoidance of:
Alcohol
AcetaminophenHerbal medications
References
8/13/2019 2013 Curs Lecture 1 Scurtat
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
8/13/2019 2013 Curs Lecture 1 Scurtat
226/227
8/13/2019 2013 Curs Lecture 1 Scurtat
227/227
Recommended