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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 metaplasticcolumnar epithelium

Recurrent exposure of acid rich contents on the lower end (following GERD)

Greater risk for Ca esophagus Adenocarcinoma

Barrett esophagus

Barrett Esophasgus withulcerating 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%

50%

30%

20%

STARTS ASIN-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:: CardiaFundusBodyAntrumPylorus

Cells:: Mucous secreting cellsParietal 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 defenceNormal

Duodenal ulcer

Gastric ulcer

Excess Acid & pepsin secretion

Reduced mucosal protection

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 lossIt is one of the major cause of massive

hematemesis in alcoholics

CHRONIC GASTRITISPresence 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 SyndromeSystemic 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

Morphology:

50 - 60%

25%

40%

12%

INCIDENCE OF GASTRICCARCINOMA AT DIFFERENTSITES

Cardia

Lesser curvature

Greater curvature

Pylorus & antrum

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 invasionEarly 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 CrohnsDisease

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

Stricture

Crohns disease

Cobblestoned mucosa

Crohns disease

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

Proximal

Distal

Ulcerative Colitis

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 planuslesions

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:

Toxic nitrogen products gut bacteria.EncephalopathyMusty odor (mercaptans by gut bacteria)Foetar hepaticus

Esophageal varices. (hemorrhoids)Hematemesis

Coag. factor synthesisBleeding

Portal hypert, low alb, hyper aldosteroneAscitis

Bile obstruction Bile salt in blood.Pruritis

Bile obstruction.Steatorrhoea

Low albumin low oncotic pressure.OedemaBiliary obstructionPale stools

Conjugated hyperbil (vs. acholuric)Dark urine

Impaired conjugation or obstruction.Jaundice

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, Regeneratingparenchymal nodules.

Etiology of Cirrhosis

Alcoholic liver disease 60-70% Viral hepatitis 10% Biliary disease 5-10% Primary hemochromatosis 5% Cryptogenic cirrhosis 10-15% Wilsons, 1AT def rare

CirrhosisClinical

Features

Ascitis in Cirrhosis

Gynaecomastia in cirrhosis

Complications:

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

Hepatocellular carcinoma.

BRAIN

LIVER

Toxic N2 metabolitesFrom Intestines

Porta systemicshunts

Pathogenesis of Hepatic Encephalopathy

HEPATITIS VIRUSES:

Hepatitis A virus, Hepatitis B virus, Hepatitis C virus, Hepatitis D virus, Hepatitis E virus, Hepatitis G 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. Acute hepatitis,2. Nonprogressive chronic hepatitis,3. Progressive chronic hepatitis,4. Fulminant hepatitis,5. Asymptomatic carrier state,6. Backdrop for hepatitis D virus,7. Hepatocellular carcinoma;

Hepatitis BTRANSMISSION: 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;

Weeks after Exposure

Symptoms

HBeAg anti-HBe

Total anti-HBc

IgM anti-HBc

anti-HBsHBsAg

0 4 8 12 16 20 24 28 32 36 52 100

Tit

erAcute Hepatitis B Virus Infection with Recovery

Typical Serologic Course

Hepatitis B

IgM anti-HBc

Total anti-HBcHBsAg

Acute(6 months)

HBeAg

Chronic(Years)

anti-HBe

0 4 8 12 16 20 24 28 32 36 52

Weeks after Exposure

Tit

e r

Progression to Chronic Hepatitis B Virus InfectionTypical Serologic Course

+---Immunization++--Prior Infection

-+-+Chronic Hepatitis

--++Acute Hepatitis

--+-Window Period

IgG HBsAgAnti HBs

IgG HBcIgM HBcHBsAgHBeAgHBV DNA

HBeAg = High viral Proliferation; Anti HBe = Low proliferation

Acuteinfection

Subclinicaldisease

AcuteHepatitis

HealthyCarrier

PersistentInfection

ChronicHepatitis

RECOVERY

FULMINANTHEPATITIS

RECOVERY

CIRRHOSIS

HEPATOCELLULARCARCINOMA

DEATH

DEATH

60 - 65%

20-25%

5 - 10%

4%

100%

99%

< 1%

67 - 90%

10-33%20- 50%

10%HEPATITIS BINFECTIONOUTCOMES

Hepatitis C virus:

Distribution -- Worldwide, Transmission:

* Blood transfusions ( 90 = 95%)* Inoculations,* Sexual both hetero and homo,* Vertical transmission,

A IC NU FT EE C

TION

RESOLUTION

CHRONICHEPATITIS

FULMINANTHEPATITIS

STABLEDISEASE

CIRRHOSIS

HEPATOCELLULARCARCINOMA

STABLECIRRHOSIS

DEATH

15%

85%

Rare

80%

20%

50%

50%

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%

HCV RNA

Symptoms +/-

Time after Exposure

Tit

er

Anti-HCV

ALT

Normal

0 1 2 3 4 5 6 1 2 3 4YearsMonths

Hepatitis C