ANATOMIC DISORDERS OF

ESOPHAGUS
Atresia, Fistula (tracheo-esophageal)
Diverticula
Stenosis
Hiatal hernia
Esophageal webs & Rings
Achalasia cardia
Lacerations (Mallory- Weiss syndrome)

Tracheo- Esophageal Fistula

Congenital connection B/w esophagus &
trachea
- Often associated with esophageal atresia
- Discovered soon after birth

Esophageal diverticulum

Weakness in the wall of the esophagus

Zenkers diverticulum
Traction diverticulum
Epiphrenic Diverticulum

Barium studies is the investigation of

choice

ESOPHAGEAL WEB

Ring like constriction of upper esophagus

Can be idiopathic web or associated with Plummer-Vinson
Syndrome
Middle-aged females
Plummer-Vinson Syndrome=Patterson-Kelly syndrome

Iron deficiency anemia

Stomatitis
Glossitis
Dysphagia
Spoon-shaped nails
Esophageal webs

Location

Cervical esophagus anteriorly at level of the cricopharyngeous (C5-C6)

Distal esophageal webs may arise from gastroesophageal reflux

Imaging Findings

Thin, transverse filling defects

Usually less than 3mm in thickness

ESOPHAGEAL WEB

REFLUX ESOPHAGITIS:
Reflux of gastric contents into lower
esophagus
CAUSES

CNS depressants, Alcohol

Hypothyroidism,
Pregnancy
Systemic sclerosing disorders,
Nasogastric tube
Hiatus hernia
Delayed Gastric emptying

Protracted exposure of esophagus to

gastric juices,
Acid - Peptic action
Inflammation and ulceration.

 Clinical features
* Dysphagia,
* Heartburn,

Complications:
* Bleeding,
* Stricture,
* Barrett esophagus formation
* Dental erosion

Normal Esophagus and stomach

BARRETTS ESOPHAGUS
Distal squamous epithelium of the
esophagus is replaced by metaplastic
columnar epithelium
Recurrent exposure of acid rich contents
on the lower end (following GERD)
Greater risk for Ca esophagus
Adenocarcinoma

Barrett esophagus

Barrett Esophasgus with

ulcerating adenocarcinoma

ACHALASIA CARDIA
Absence of Myentric plexus of Auerbach
within the submucosa of lower end of
esophagus
Progressive dilatation of proximal part of
normal esophagus segment
Diagnosis is by Barium swallow & (Barium
meal)

SQUAMOUS CELL CARCINOMA

Geographic Variability in incidence,
Age 50 yrs.,

M : F = 20 : 1,
Incidence - Variable
Lifestyle:

Alcohol consumption
Tobacco use
Preexistent Esophageal disorders
Longstanding Esophagitis
Achalasia
Plummer-Vinson syndrome

Morphology:
GROSS:
* Polypoid - 60%,
* Flat - - - - - 15%,
* Excavating - 25%

20%
50%

30%
STARTS AS
IN-SITU-CARCINOMA

Clinical Features of SCC Esophagus:

Insidious Onset,
Dysphagia - Gradual Obstruction,
Weight Loss & Debility,
Hemorrhage,

Sepsis,
Tracheo-esophasgeal Fistula
PROGNOSIS:

5 Yr. SURVIVAL: SUPERFICIAL - 75%

ADVANCED - 25%
[Local & distant spread common ]

Irregular, reddish, ulcerated mass mid-esophagus:

Squamous cell carcinoma

ADENOCARCINOMA of
Esophagus
Most common tumor in the distal end of
Esophagus
Secondary to long standing Barretts
Esophagus
Genetic predisposition: Point mutation in
p53 gene
Other risk factors like alcohol, Smoking
associated

Esophagus - Adenocarcinoma

Anatomy of the Stomach

NORMAL STOMACH

 Stomach::

Cardia
Fundus
Body
Antrum
Pylorus
Cells:: Mucous secreting cells
Parietal cells or Oxyntic cells (HCL, IF)
Chief cells or Peptic cells (Pepsinogen)
Endocrine cells-G cells

Stomach: Congenital disorders

Pyloric Stenosis
- Marked muscular hyperplasia
- Gastric outlet obstruction
M>F
Turners & Edwards syndrome
Regurgitation & Vomiting by 2nd week of
life, Visible Peristalsis, Abdominal mass

Gastric fundal mucosa, with short pits lined

by pale columnar mucus cells

ACUTE GASTRITIS
An important cause of GI bleeding
An acute mucosal inflammatory process
In severe cases bleeding & erosions

PATHOGENESIS
An imbalance between
aggressive factors ( acid & pepsin )
and
those that defend the

mucosa

Acid & pepsin

Mucosal defence

Excess Acid & pepsin secretion

Reduced mucosal protection

Normal

Duodenal
ulcer

Gastric
ulcer

ETIOLOGY

NSAID particularly Aspirin

Excessive alcohol consumption
Heavy smoking
Chemotherapy
Uremia
Systemic Infections (salmonella )
Severe stress
Ischemia & shock

Clinical features of Acute Gastritis

Asymptomatic
Epigastric pain , nausea & vomiting
Massive hematemesis , melena
&potentially fatal blood loss
It is one of the major cause of massive
hematemesis in alcoholics

CHRONIC GASTRITIS
Presence of chronic inflammatory
changes
Mucosal atrophy & epithelial Metaplasia
Dysplasia
CARCINOMA

PATHOGENESIS
Helicobacter pylori infection
Autoimmune

Toxic : alcohol & cigarette smoking

Drs. Barry Marshall and Robin Warren

H . pylori INFECTION
Chronic gastritis
Peptic ulcer disease
Gastric Carcinoma
Gastric Lymphoma

H . pylori
Gram - ve curved bacillus well adapted to
gastric environment.
Motility
Urease
Binding to gastric epithelial cells via
bacterial adhesin

Helicobacter Pylori

Silver stain

Giemsa stain

Peptic Ulcer Disease

Location: duodenum, stomach, ectopic
gastric mucosa
Imbalance between acid/pepsin and
mucosal defense mechanisms
H.pylori associations
Complications: bleeding, perforation,
stenosis

Location of Peptic Ulcer

Duodenum - 1st portion

Stomach - antrum
Gastro - Esophageal junction
Margins of gastro - jejunostomy
Duodenum/ stomach / jejunum in ZE
syndrome
Meckel s Diverticulum with ectopic
gastric mucosa

Duodenal ulcer Genetic considerations

Group - O
HLA - B5
Monozygotic twins
Genetically Determined Syndromes
ZE Syndrome
Systemic Mastocytosis

shallow gastric ulcerations known as

"stress ulcers"

Acute gastric ulcer

Gastric Ulcer

Complications
of gastric
ulcers (either
benign or
malignant)
include pain,
bleeding,
perforation,
and
obstruction.

GASTRIC ULCER

Duodenal Ulcer

Perforation:

Epidemiology of Gastric
Carcinoma
Higher in Japan, China compared to US,
UK
More common in lower socio-economic
groups
Male to Female ratio is 2: 1
Steady decline in incidence & mortality for
the past 6 decades

Risk factors:

Smoked fish & meat

Pickled vegetables
Nitrosamines
H. Pylori
Chronic atrophic gastritis
Blood type A
Smoking

25% Cardia

Morphology:
40% Lesser curvature
12%

50 - 60%

Greater curvature

Pylorus & antrum

INCIDENCE OF GASTRIC
CARCINOMA AT DIFFERENT
SITES

CLASSIFICATION
Gastric carcinoma classification is based on
- Depth of Invasion (Early & Advanced)
- Morphologic type (Exophytic, Flat,
excavated, Linitis plastica)
- Histologic type (Intestinal type, Diffuse
type)

 Depth of invasion
Early gastric carcinoma - lesion
confined to mucosa & submucosa
regardless of presence / absence of LN
Advanced gastric carcinoma - lesion
has extended below submucosa into
muscular wall

Early gastric carcinoma

Advanced gastric carcinoma

Morphologic types of
Carcinoma Stomach
Fungating
Ulcerating
Diffuse

Fungating Carcinoma Stomach

Clinical features
Insidious , asymptomatic until late in
course
Weight loss , abdominal pain .

anorexia , vomiting , altered bowel habits

dysphagia

anemic symptoms , hemorrhage

Spread
Penetrate wall & spread to regional &
distant LN
Virchow node
Local invasion into duodenum , pancreas
retroperitoneum
Metastasis to liver , lung , peritoneal
seedlings
Krukenberg tumor

Spread of Gastric Ca

Disorders of Intestine

Obstruction Hernia, volvulus etc.

Malabsorption
Infections Enterocolitis
Inflammatory bowel disorders
Neoplasms Polyps, Carcinoma

Intestinal Obstruction:

Paralytic ileus
Tumors
Volvulus
Intussusception
Hernia

Diverticular Disease
Outpouchings of colon, particularly in
rectosigmoid colon
Disease of Western civilization and has
risen since 1900
Most affected individuals asymptomatic
Only 20% of cases have clinical
manifestations

Incidence of Diverticulosis
Uncommon before age 40
Post-mortem reports suggest up to 50% of
over 60 years
Left-sided in industrialized countries
Right-sided in Japan
Due to low fiber diet resulting in
intraluminal hypertension

Diverticula

Diverticula

Inflammatory bowel disease

Crohns disease
Ulcerative colitis
Indeterminate colitis

Inflammatory Bowel Disease

Active inflammation

Cryptitis, crypt abscess formation

Erosions and ulcers

Chronic inflammation

Crypt distortion/atrophy
Surface villiform change
Basal plasmacytosis

Diagnosis of IBD

Clinical history
Physical exam
Endoscopic exam
Radiographic exam
Histologic exam
Serologies

Crohns Disease
Intermittent diarrhea, pain, fever
Epidemiological peaks in 20-30s, another
in 60-70s
Stress associated with flare-ups
Extraintestinal manifestations
Arthritis/joint pain
Erythema nodosum

Oral Manifestations of Crohns

Disease

Occurs in 8-9% of patients

Diffuse labial, gingival, or mucosal swelling
Cobblestoning of the buccal mucosa and
gingiva
Aphthous ulcers
Mucosal tags
Angular cheilitis
Oral granulomas may occur

Crohns Disease: gross

Creeping fat

Mesenteric fat wraps around the bowel

Skip lesions

Intervening normal mucosa between inflamed areas

when multiple segments of bowel involved

May involve ANY portion of the GI tract

Cobblestone mucosa

Area of spared mucosa with affected mucosa

Strictures, fistulas or sinus tracts

Crohns disease

Stricture

Crohns disease

Cobblestoned mucosa

Ulcerative Colitis
Epidemiological peak in 20-30s
Recurring attacks of bloody mucoid
diarrhea lasting several days
Lower abdominal pain relived by
defecation

Ulcerative Colitis
Extraintestinal manifestations

Arthritis/joint pain
hepatic involvement (Primary Sclerosing
Cholangitis)
Oral Aphthous ulcers

Ulcerative Colitis

Proximal

Distal

Colorectal adenocarcinoma
Older patients (>60)
Geographic differences (US highest) dietary and lifestyle
NSAIDS protective

Colorectal adenocarcinoma
Polypoid and exophytic (right-sided)
Present with anemia

Circumferential (left-sided)

Present with rectal bleeding, pain

Infiltrative type associated with ulcerative

colitis
Stage based on depth of invasion, most
important predictor

Colorectal adenocarcinoma

Adenocarcinoma of the colon

Anal canal
Adenocarcinoma (usually extension of
rectal)
Squamous cell carcinoma
HPV infection
Immunosuppressed (AIDS)

Basaloid pattern (poorly differentiated

squamous)

Appendix
No known function
Rich in lymphoid tissue
Atrophies during life

Acute Appendicitis
Any age group, but especially in children
False positive diagnosis (surgery when not
needed) in 20-25%
Outweighed by morbidity and mortality of
perforation

Acute Appendicitis
Classic presentation

Pain, first periumbilical then RLQ

Nausea and vomiting
Abdominal tenderness
Fever
Elevated WBC

Acute Appendicitis

Oral Manifestations in Liver

Diseases
Chronic liver disease impacts many systems of the body
Impaired hemostasis due to Vit K deficiency
Petechiae or excessive gingival bleeding with minor trauma in
Absence of inflammation

Advanced liver disease Jaundice, yellow pigment

deposition of bilirubin in the submucosa
Hepatitis C is the leading cause of chronic hepatitis and
cirrhosis
Hepatitis C infection is associated with oral lichen planus
lesions
Greater in Europe and Asia

LICHEN PLANUS

Liver Functions:
Metabolism Carbohydrate, Fat &
Protein
Secretory bile, Bile acids, salts &
pigments
Excretory Bilirubin, drugs, toxins
Synthesis Albumin, coagulation factors
Storage Vitamins, carbohydrates etc.
Detoxification toxins, ammonia, etc.

Disorders of Liver:
Acute Liver Disorder:

Viral, Drug, Gall stones, alcohol toxicity.

Chronic Liver Disease:

Chronic hepatitis, Cirrhosis, viral, alcohol, cong.

Autoimmune hepatitis. PBS.

Congenital Disorders:

Hemochromatosis, Wilsons, 1AT def,

Tumors:

Benign: Adenoma, angioma, Nodular hyperplasia

Malignant: Hepatocellular carcinoma,
Cholangiocarcinoma, Hepatoblastoma,
Angiosarcoma.
Cysts: Simple, Hydatid

Pathogenesis of clinical features:

Jaundice

Impaired conjugation or obstruction.

Dark urine

Conjugated hyperbil (vs. acholuric)

Pale stools

Biliary obstruction

Oedema

Low albumin low oncotic pressure.

Steatorrhoea

Bile obstruction.

Pruritis

Bile obstruction Bile salt in blood.

Ascitis

Portal hypert, low alb, hyper aldosterone

Bleeding

Coag. factor synthesis

Hematemesis

Esophageal varices. (hemorrhoids)

Encephalopathy

Toxic nitrogen products gut bacteria.

Foetar hepaticus Musty odor (mercaptans by gut bacteria)

Jaundice
Yellow discoloration of skin & sclera due to
excess serum bilirubin. >40umol/l,
(3mg/dl)
Conjugated & Unconjugated types
Obstructive & Non Obstructive (clinical)
Pre-Hepatic, Hepatic & Post Hepatic
types
Jaundice - Not necessarily liver disease *

Common Causes of Jaundice

Post Hepatic (Obstructive) Stone,
tumor

Conjugated/Direct Bil, High colored urine,

Pre Hepatic (Acholuric) - Hemolytic

Unconjugated/Indirect Bil, pale urine

Hepatocellular Viral, alcohol, toxins,

drugs
Liver damage - unconjugated
Swelling, canalicular obstruction Conjugated

Jaundice

Jaundice

Cirrhosis:
End stage complication of liver disease
Diffuse disorder of liver characterised by;
Complete loss of architecture, Replaced by
extensive fibrosis with, Regenerating
parenchymal nodules.

Etiology of Cirrhosis

Alcoholic liver disease

Viral hepatitis
Biliary disease
Primary hemochromatosis
Cryptogenic cirrhosis
Wilsons, 1AT def

60-70%
10%
5-10%
5%
10-15%
rare

Cirrhosis
Clinical
Features

Ascitis in Cirrhosis

Gynaecomastia in cirrhosis

Complications:
Congestive splenomegaly.
Bleeding varices.
Hepatocellular failure.
Hepatic encephalitis / hepatic coma.
Hepatocellular carcinoma.

Pathogenesis of Hepatic
Encephalopathy
BRAIN
Porta systemic
shunts
LIVER

Toxic N2 metabolites
From Intestines

HEPATITIS VIRUSES:

Hepatitis
Hepatitis
Hepatitis
Hepatitis
Hepatitis
Hepatitis

A
B
C
D
E
G

virus,
virus,
virus,
virus,
virus,
virus;

Hepatitis A

Benign, self-limited disease,

Clinically asymptomatic or mild,
Occurs throughout the world;
NO CHRONIC HEPATITIS OR
CARRIER STATE,

Hepatitis A
Spread: fecal-oral route,
Shed in stool 2 to 3 wks. Before to 1 wk. After
jaundice
Endemic:
* Affects commonly children,
* Substandard hygiene and sanitation,
* Waterborne,
25% of evident acute hepatitis,
Fatality rate: 0.1% ( Fulminant hepatitis);

HEPATITIS B

Can cause:
1.
2.
3.
4.
5.
6.
7.

Acute hepatitis,
Nonprogressive chronic hepatitis,
Progressive chronic hepatitis,
Fulminant hepatitis,
Asymptomatic carrier state,
Backdrop for hepatitis D virus,
Hepatocellular carcinoma;

Hepatitis B
TRANSMISSION:

Transfusion of blood and blood products,

Through Body fluids:
Semen, Saliva, Sweat, Tears, breast milk,
Pathologic effusions,
Dialysis,
Needle stick accidents,
Intravenous drug abuse,
Homosexual activity;

Neonatal infection > carrier for life;

Hepatitis B
Acute H epatitis B Virus Infection w ith Recovery
Typical Serologic Course
S ym ptom s

HB eAg

anti-HB e

Titer

Total anti-HBc

IgM anti-HBc
anti-HBs

HBsAg

12

16

20

24

28

32

36

W eeks after Exposure

52

100

Progression to Chronic Hepatitis B Virus Infection

Typical Serologic Course
Acute

Chronic

(6 months)

(Years)

HBeAg

anti-HBe

HBsAg

Titer

Total anti-HBc

IgM anti-HBc

12 16 20 24 28 32 36

52

Weeks after Exposure

HBsAg
HBeAg
HBV DNA

IgM HBc

IgG HBc

IgG HBsAg
Anti HBs

Window
Period

Acute
Hepatitis

Chronic
Hepatitis

Prior
Infection

Immunization

HBeAg = High viral Proliferation; Anti HBe = Low proliferation

Subclinical
disease
60 - 65%

Acute
infection

4%

Acute
20-25% Hepatitis
Healthy
Carrier
5 - 10%
Persistent
Infection
10-33%

100%
RECOVERY
99%
FULMINANT
< 1% HEPATITIS

DEATH

RECOVERY
67 - 90%
CIRRHOSIS
10%

HEPATITIS B Chronic20- 50%

HEPATOCELLULAR
INFECTION
Hepatitis
CARCINOMA
OUTCOMES

DEATH

Hepatitis C virus:
Distribution -- Worldwide,
Transmission:
* Blood transfusions ( 90 = 95%)
* Inoculations,
* Sexual both hetero and homo,
* Vertical transmission,

RESOLUTION
15%
A
C
U
T
E

STABLE
DISEASE

STABLE
CIRRHOSIS

I
80%
N
CHRONIC
50%
F
HEPATITIS
E 85%
20%
CIRRHOSIS
C
T
50% DEATH
I Rare
O
FULMINANT
HEPATOCELLULAR
N
HEPATITIS
CARCINOMA

OUTCOME OF HCV INFECTION

Seropositivity high in:

House contacts,
Homosexuals,
Hemodialysis patients,
Hemophiliacs,
I V drug abusers ( 50 to 90% )
Patients with unexplained cirrhosis >
> 50 % HCV Infection
High rate of progression to cirrhosis,
-- > 50%

Hepatitis C
Anti-HCV

Symptoms +/-

Titer

HCV RNA

ALT
Normal
0

Months

Time after Exposure

Years