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GI Internal Medicine PDF
GI Internal Medicine PDF
Course: Gastroenterology
Week: 1-5
Lect urer: Dra. Cham
Topic: Esophagus & Stomach
Source: L ecture
Stomach ..................................................... 6
Gastritis .........................................................6
Table of Contents
Acute Gastritis .......................................................... 6
Esophagus ...................................................1 Chronic Gastritis ....................................................... 6
2 Major functions ...................................................... 1 Upper GI Bleeding .............................................7
2 esophageal sphincters .............................................. 1 Peptic Ulcer Disease ................................................. 7
Esophageal Diseases .......................................... 1 Zollinger-Ellison Syndrome ....................................... 9
Symptoms ................................................................. 1 Gastric Adenocarcinoma .....................................9
Diagnostic Tests ........................................................ 1 Stomach Cancer Types .............................................. 9
Esophageal Motor Disorders ...................................... 2 GAC Major Environmental Risk Factors ................... 9
GERD ...................................................................... 3 High Risk Factors for GAC ....................................... 9
Barrett’s Esophagus ................................................... 3 GAC Precursors ........................................................ 9
Esophageal Carcinoma .............................................. 4 GAC Clinical Features .............................................. 9
Diverticula ................................................................ 4 GAC Dx ................................................................... 9
Webs and Rings ......................................................... 5 GAC Management.................................................... 9
Hiatal Hernia ............................................................ 5
Mallory-Weiss Syndrome........................................... 5
Foreign Body in Esophagus ....................................... 5
Caustic Ingestion ....................................................... 5
Esop hagus
2 Major functions 2 esophageal sphincters
• Transport of food from mouth to 1) Upper sphincter 2) Lower sphincter
stomach -‐ Elastic wall -‐ Intrinsic myogenic tone
• Prevent backflow of GI contents -‐ Tonic contraction o Pre-ganglionic vagus n.
o Cricopharyngeus m. o Post-ganglionic nerve
o Inf pharyngeal m.
ESOPHAGEAL DISEASES
Lecture 1 mra
Med3C Cham – Prelim Topics Gastro 3a
Bird’s Beak
Cork Screw
Lecture 2 mra
Med3C Cham – Prelim Topics Gastro 3a
LA Classification of Esophagitis
Grade Mucosal Breaks Description
A 1+ <5mm
B 1+ >5mm but not continuous btwn tops of 2 mucosal folds
C Continuous btwn tops of 2+ mucosal folds <75% of circumference
D Mucosal breaks involving >75% of circumference
Caustic Ingestion
Alkali – Lye, KOH CI Management:
• Liquefaction necrosis • Maintain on NPO
• Deep penetration – full thickness burn • TPN
• Critical ph • IV H2 Blocker or PPI
o 12.5 à ulceration • Antibiotics for serious infection
o 14 à stricture (Lye) • Surgery in extensive tissue necrosis, perforation,
Acid – HCl, Sulfuric, Sodium Bisulfate peritonitis and severe hemorrhage
• Coagulation necrosis
• Eschar – protective (limit deep tissue injury) CI Complications:
• Shallow burn esoph; worse if in antrum • Severe hemorrhage
• Esoph and gastric Va dev in scarred mucosa 10-15y after • Perforation
• Peritonitis
CI Diagnosis • Inferior Mediastinitis
1. Barium or soluble contrast studies - not accurate • Stricture – noted in 2-8 weeks after
a. After 1-2months extent of fibrosis and stricture o Tx: dilatation – after acute injury heals
2. Endoscopy o Surgery: for severe strictures
a. w/in 24h of digestion
b. Remove by suction remaining substance
3. Serial plain abdomen and chest XR = perforation
Lecture 5 mra
Med3C Cham – Prelim Topics Gastro 3a
Sto mach
GASTRITIS
• Inflammation of gastric mucosa o CMV, herpes, MTb, candida – in
• Diffuse or localized immunocompromised
• 2 types of gastritis
o Acute – usually self limited AG Clinical features
o Chronic – superficial lymphocytic infiltrates • “Dyspepsia” – any discomfort in the epigastrium
in the lamina propria o GI upset
§ Chronic type A o May feel nausea or Indigestion even leading
§ Chronic type B to vomiting
o Dysphagia
Acute Gastritis • Epigastric pain – burning; most common
Etiology of Acute Gastritis • GI bleeding – may be severe; hematemesis or melena
• Drugs – aspirin, NSAIDs
o Especially seen in the elderly AG Diagnosis
• Caustic substances ingestion • Endoscopy (EGD) w/ or w/o biopsy
o Strong alkali and acid o Test for H. pylori
o Suicide attempt
• Stress AG Treatment
o Related to severe illness 1) Medical: Antacids, PPI, H2A – neutralize the acidity
o ICU patients – Sepsis, CVA, elderly pts 2) Surgery
• Infections a. Rarely necessary
o H. pylori – most significant b. Unless there is severe bleeding
o Phlegmonous gastritis – bacterial invasion
of stomach wall esp Grp B strep; rare but
fatal
Images: Terms to describe types of injury, more than one term can be applied
Erosive gastritis Pan gastritis Radial gastritis
Chronic Gastritis
Etiology of chronic gastritis Helicobacter
pylori
• Gram (-), microacrophilic curved bacillus
• Prolongation use of alcohol, aspirin and NSAIDS
• Motile, flagella
• Radiation or thermal injury
• Predisposition to human gastric mucosa
• Immunologic factors
• 92% in active chronic gastritis (type B)
• Infections (H. pylori)
o 88 – 100% in DU
o 58 – 100% in GU
o 46 – 94% among gastric Ca
• Live beneath the mucus layer
• Ability to pro urease (normally found in stomach)
• (+) Bx for Hp – main choice for dx
o Usually in antrum – site for biopsy
o Best at the margins but if you suspect
diffuse chronic gastritis get additional
samples from greater and lesser curvature
• (+) Urea breath test (C13 and C14)
o If endoscopy is not available
Lecture 6 mra
Med3C Cham – Prelim Topics Gastro 3a
UPPER GI BLEEDING
Keep NGT
for (-) Active Remove
Clear several bleeding NGT Endoscopy
hours
Melena or Angiogram
Hematemesis NGT
Non-
Saline diagnostic
irrigiation
– Surgery
Bleeding
(+) bleeding stops EGD
rapidly,
clears
stomach Specific
Diagnostic Rx ?
• Hematemesis
• Melena Peptic Ulcer Disease
• Do NGT • Disorders/ulcers/problems of upper GIT
o Distinguish upper and lower GI bleeding o Upper GIT: Stomach, duodenum
o See if active bleeding or not o Duodenum most commonly involved
• Irrigation • Caused by acid and pepsin
o Cold saline solution but do not aspirate à • M>F; DU 3x > GU
adds pressure which can damage already o Males are more prone
injured mucosa à ~bleed to death • Relapse: DU is 80%, GU is 33% after 1yr
• Bleeding stops in 24h • Spectrum of illness, chronology
o Endoscopy and therapeutics 1. Undetectable mucosal injury
• Variceal bleeding 2. Erythema
o From varices in esophagus and stomach; 3. Erosions
discussed with liver 4. Frank ulcers
• Non-variceal bleeding – Peptic Ulcer disease
o Do injection therapy with 1:100000
epinephrine à vasoconstriction to stop
bleeding
Lecture 7 mra
Med3C Cham – Prelim Topics Gastro 3a
Types of PUD
Gastric
Ulcer
Duodenal
Ulcer
• Pain aggravated by food • Relieved by food and antacid
• Weight loss is common • Usually 3h after eating
• Awakens patient at night
st
• Peak in > 60 y/o • 3x common in 1 degree relatives
• Increased in bld grp O non-secretors
• Increased in HLA-B5 aging white males
• ↑Serum gastrin • N fasting gastrin level
• More commonly leads to malignancy • Higher incidence of severe bleeding (related to higher
• Giant ulcers may lead to Ca recurrence)
o Important to rule these out
PUD Pathogenesis
Aggressive
factors
(injurious
agents)
Protective
factors
(mucosal
defense)
• Endogenous – acid, pepsin, bile acids • Normal mucosa resist corrosive effect of acid and
• Exogenous – ethanol, aspirin, HP, NSAIDS, smoking, pepsin
steroids • Gastric mucosal barrier = gastric mucosa resist back
• Gastrin – most potent gastric acid stimulant diffusion of H++
o Normal in fasting; increased in post-prandial • Cytoproduction = endo PG is protective
(DU) • Mediators of mucosal protection
o Increased in fasting and PP state (GU) o Mucus
o ACID + PEPSIN à Tissue injury à PUD o Bicarbonate
o Hydrophobic layer of phospholipid
PUD Complications
• Hemorrhage – most common
• Perforation – more common in DU
o X-ray: air under diaphragm; pneumo-
peritoneum
• Gastric outlet obstruction
• Penetration – posteriorly to the pancreas; ↑amylase,
↑lipase
Lecture 8 mra
Med3C Cham – Prelim Topics Gastro 3a
Zollinger-Ellison Syndrome
• Non-islet beta cell tumopr à Gastrin ZES Dx
• Assoc w/ ↑gastric acid secretion + PUD • X-RAY – Large mucosal folds
• Malignant in 60% - slow-growing Ca • Angio + CT – Tumors highly vascular
• 1/3-2/3 - - pancreas (head) • RIA – increased serum gastrin level
• Other sites: stomach, duodenum, spleen and LN
• Assoc w/MEN-1 (Pancreas, pituitary, PTh tumors) ZES Tx
• Mistaken as carcinoid tumor • Surgery
• Medical – PPI, H2A
ZES S/Sx
• Ulcer/s
• LBM, Steatorrhea
• Vit B12 malabsoption
GASTRIC ADENOCARCINOMA
• M 2x > F High Risk Factors for GAC
• Usually bet 50-70 y/o • Family hx
• Unknown cause • Prior hx of Gastric carcinoma
• Most common type of gastric CA and GI • Chronic active gastritis
(except esophagus( (90%) • Intestinal metaplasia
• Seen in blood group A • Post-antrectomy (10-20 yrs post-Billroth II)
• Polyps (only adenomatous >2cm)
Stomach Cancer Types • Gastric dysplasia
85% adenocarcinomas, 15% lymphoma, GIST and leiomyoma • Menetrier’s dse
1. Diffuse Type GAC • GU (+) H. pylori – 10% à Ca
• No cellular cohesion • Males, elderly
• Infiltrates and
thickens abdominal GAC Precursors
wall • Pernicious anemia
o Linitis plastic • Atrophic gastritis – especially in elderly
– leather-like • Adenomatous polyps (<2cm)
thickening of • Achlorhydria
mucosa • Giant hypertrophic gastritis (Menetrier’s)
o Seen in • Post – gastrectomy (10-20 yrs post Billroth II)
severe • H. pylori infection
adenoca
o Poor prognisis
GAC Clinical Features
• Epigastric pains – 70%
2. Intestinal Type GAC • Early satiety – common with linitis plastic
• Characterized by • (+/-) N/V
glandular-like • Weight loss
tubular structures • Anemia
• Ulcerative, seen • Upper GI bleeding
in lesser
curvature GAC Dx
• UGIS X-ray - Mass, ulcer or thickened and non-
distensible “leather-bottle” stomach (linitis plastic)
3. Lymphoma • DoC: Endoscopy – with biopsy or brush
4. Gastrointestinal Stromal Tumors cytology
• Pink looking, smooth mucosa with pus • EUS – best to determine depth of invasion
5. Leiomyoma o There are 5 layers of gastric mucosa
• CEA – tumor marker
CT Scan
GAC Major Environmental Risk Factors •
• Hgb/Hct
• H. pylori
• Alk Phos
• Diet
o Salted & preserved foods (nitrates– tocino,
tapa) GAC Management
• Cigarette smoking • Surgery – procedure of choice
o 5 yr SR (EGC = 90%; AGC = 10%)
• Chemotherapy
o 5 FU, Mitomycin, Doxo,,,
Lecture 9 mra