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Stand up, be bold, be strong, Take the whole responsibility on your
shoulder, and know that you are the creator of your own destiny.
- - Swami Vivekananda.
CPC 4.2.5: Feeling dreadful…!
• Worsening abdominal pain. 12h, sudden, 9/10.• Cramping constant, severe, Nausea, vomiting, NSAID.• Blood in vomit, 8kg loss/3m, dark stool 2m.• Heart burn, NSAID use (backpain), stress, 10 cig/day, • Pale, sweaty, HR 125, faint pulse, BP 90/56 – shock*Differential Diagnosis: (acute compl.)• Perforated ulcer, Gastric Ca, Apendicitis, Dirverticulitis.• Acute Cholecystitis, Pancreatitis, Ruptured aneurysm. Investigations:• WBC 33.3, Hb 8.2, MCV 80, urea/creat, Lipase Nor.• USS – free fluid, X-Ray – free air shadow.
CASE STUDY: Mr E.K. 55-year-old Torres Strait Islander man. “I had a bit of a pain in my gut yesterday but today it is much worse and I feel really dreadful”.
Top differential diagnosis ?
1 2 3 4 5
0% 0% 0%
91%
9%
1. GORD with bleeding.
2. Bleeding PUD.
3. PUD + GORD
4. Perforated peptic ulcer.
5. Acute cholecystits+stones.
Most likely Aetiology?
1 2 3 4 5
27%
0%
64%
9%
0%
1. H.pylori
2. Obesity
3. Genetic
4. Smoking
5. NSAID use
Most likely Risk factor?
1 2 3 4 5
0% 0%
91%
9%
0%
1. Stress
2. GORD
3. Hiatus hernia
4. Smoking
5. NSAID use
Next step?
1 2 3 4 5
0% 0% 0%0%0%
1. Stop NSAID & counsel.
2. Surgical referral.
3. Stool occult blood test
4. Breath test for H.pylori
5. Stop soking & counsel.
Type of anemia ? Why?
1 2 3 4 5
0% 0% 0%0%0%
1. Acute Blood loss
2. Nutritional (B12+Iron)
3. Iron deficiency
4. Megaloblastic.
5. Hemolytic (NSAID)
PUD: KFP questions• Why name peptic ulcer? Common locations of ulcer?• What are the normal defense mechanisms in stomach ?• What are the causes & risk factors for peptic ulcer?• Briefly describe pathogenesis of peptic ulcer?• Briefly describe microbiology & diagnosis of H.pylori?• Why chronic, single, punched out, clean ? Multiple..?• Why radiating folds in benign not in malignant ulcer?• List Microscopic features?• List complications – short & Long term?• Briefly outline management?• Zollinger-Ellison syndrome?
CPC-2.4– KFP Questions:• Pathogenesis & pathology of Barrett’s oesophagus.• Which H. pylori-infected patients should be treated? • Does eradication of H. pylori infection benefit the patient
with peptic ulcer disease? Discuss.• What is the relationship between H. pylori infection and
gastric malignancy? • Pyloric stenosis: causes, presentation & pathology.• H. pylori induced other disorders ? • Carcinoma esophagus & Stomach
• Etiology, pathogenesis, Morphology & Complications.
Pathology CLI:• Major:
– Acute Abdomen – Overview differential diagnosis.• Appendicitis, Intestinal Obstruction, Self study.
– GORD, Barrett’s & oesophageal cancer.– Peptic ulcer disease & Gastric cancer.
• Minor:– Oesophagitis – Acute / Chronic.– Achalasia, Rings, Mallory Weiss, – Hiatus hernia, varices, plummer-Vinson sy. – Acute & Chronic gastritis.– Zollinger Ellison sy.– Pyloric stenosis,
"Each time you are honest and conduct yourself with honesty, a success force will drive you toward greater success.
Each time you lie, even with a little white lie, there are forces pushing you
toward failure."
- -Joseph Sugarman, Author and Marketing Specialist
Commitment to Excellence…
Pathology of Upper GI:
Oesophageal Disorders
Dr. Venaktesh M. ShashidharA/Prof. & Head of Pathology
School of Medicine
Introduction:
• Anatomy, Histology • Function – motility,
digestion, enzymes.• Common disorders.
– Oesophagitis.– GORD.– obstructions– Achalasia.– Barrett’s– PUD– Malignancy
Oesophagus
Stomach
Normal
Name the parts ?
?
?
?
?
?
?
?
?
Esophagus & Stomach Normal
Glandular – Gastric Normal Squamous Oesophagus
Dysphagia• Dysphagia: Difficulty in swallowing.
– Odynophagia: painful swallowing – inflam, ulcer, Carcinoma.
• Sites: – oropharyngeal, esophageal, esophagogastric, and
paraesophageal .
• Symptoms: – Solids – Mechanical Obstruction –
tumors/strictures.– Solids & Liquids – Motility disorders – Achalasia.– Liquids – Pharyngeal disorders.
• Causes:– Local, Systemic, central.– Mechanical, neural, functional.– ulcers, tears, webs, rings, tumors, strictures,
paralysis abnormal peristalsis. (stroke),
Esophageal Disorders:
• Reflux Oesophagitis.• Barrett’s• Stricture – Inflam.
• Mallory-Weiss.• Varices• Hernia• Zenker diverticulum• T-E Fistula.• Web – IDA – P-V Sy.
Herniations
Oesophagus motility Disorders:
Hernia: 30% incidence over 50years. (mostly asymptomatic)Achalasia: Lack of relaxation of lower sphincter.
95% 5%
Achalasia Hernia-Sliding Hernia-Rolling
Mallory-Weiss Tear (Syndrome)• Severe/forced vomiting.• Longitudinal mucosal
tear.• Chronic Alcoholics,• Over eating • Hiatal hernia in 75%.• Spontaneous healing.• Boerhaave syndrome –
with rupture (Pacific Islands)
Esophageal Varices:• Dilated veins – lower part.• Pathogenesis: Portal
hypertension (Cirrhosis) Porta-Systemic Shunts open varices of - lower esophageal veins, peri-umbellical, Rectal V
• Rupture massive bleeding.
Oesophagitis:• Acute: errosive, alcohol, infection.• Chronic: Acid reflux (GERD),
chemical, alcohol, smoking, candida, radiation, idiopathic (eosinophilic).
• Endoscopic view Microscopy: • Acute inflammation.• Eosinophils: Few (reflux) more in
Eosinophilic.
Candida
I know where I'm going and I know the truth, and I don't have to be
what you want me to be. I'm free to be what I want.
-- Muhammad Ali
Commitment to Excellence…
Pathology of GORD / GERD(Gastro O/esophageal Reflux Disease)
Dr. Venaktesh M. ShashidharA/Prof. & Head of Pathology
School of Medicine
GORD: Acid reflux disorders
• Gastric Acid pH-1 (million times more than blood…!)
• Oesophagus protected by Lower Sphincter.• Defective sphincter Reflux of acid Inflam.• Clinical Stages:
1. Functional Heartburn.
2. NERD – Non Erosive RD
3. MERD – Minimal change RD
4. GORD.
5. Barrett’s Oeophagus.
6. Adenocarcinoma
GORD: Clinical Classification
GORD
Heartburn
Oesophagitis24%
Barrett’s1%
Non-ErosiveReflex Disease (NERD)
(normal endoscopy)75%
Endoscopy24-hr pH Study
AET +veSI +ve
AET -veSI +ve
AET -veSI –ve
? MERD
AET: Acid Exposure IndexSI: Symptom Index.MERD: minimal change.. RD
Etiology: (LES)• Alcohol, Tobacco, • Obesity, • CNS depressants, • Pregnancy, • Hiatal hernia • Delayed gastric emptying • increased gastric volume
Not H.Pylori,
NSAID.
Pathogenesis & Stages:
A
B
C
D
Basal Hyperplasia
1. Acid reflux Symp.2. Inflammation3. Regeneration (basal).4. Metaplasia (Barretts)5. Mild Dysplasia6. High grade Dysplasia7. Adeno-Carcinoma
Adenocarcinoma
GERD: Pathogenesis.
Normal Hyperplasia Dysplasia Carcinoma
NormalSq. Ep.
MetaplasticCol. Ep.
InflammedSq. Ep.
Basal cell hyperplasia
Squamous Carcinoma - Adenocarcinoma.
• Less common• Upper end• Tobacco, diet, toxins.
• More common• Lower end• Reflux disease (Barretts)
Tumour
Normal
Tumour
Normal
Squam. Ca. - Adeno. Ca.
K. Pearl Glands
Pleomorphic, Hyperchromatic cells forming glands / keratin pearls(Infiltration, inflammation, hemorrhage, necrosis)
"Learn to enjoy every minute of your life. Be happy now. Don't wait for something outside of yourself to make you happy. Precious is the time you have, whether it's at work or leisure. Every minute should be enjoyed and savored."
Earl Nightingale1921-1989, Radio Announcer, Author and Speaker
Hakuna Matata….!
Commitment to Excellence…
Pathology of Gastric Disorders
Dr. Venkatesh M. ShashidharA/Prof. & Head of Pathology
School of Medicine JCU
Damage vs. Defense
Gastric defences:
• Acute Gastritis:– Drugs, toxins, alcohol, Ischemia.– Infections (H.pylori transient)
• Chronic Gastritis:– Autoimmune: Pernicious an.
(autoantibody)– Chem: NSAIDs, Bile reflux,
Alcohol.– Bacterial: Helicobacter pylori.
Gastritis:
Normal ↑
← Acute
Chronic ↓
Stomach: Acute stress ulcers:
Pathogenesis? PG…!
• Acute Stress Ulcers:• Curling Ulcers: Burns/trauma, prox. Duodenum.• Cushing’s ulcers: Intracranial lesions, deep, chance of perforation.
Complications:• Bleeding 20%• Perforation 5%• Obstruction 2%
Chronic Gastritis• Bacterial: Helicobacter pylori. (PUD) > 90% • Autoimmune:
– Atrophic, Pernicious anemia <10%. – Antibody to Parietal cell & intrinsic factor.
• Radiation, Bile reflux, etc. Rare• Systemic diseases – Crohn’s, amyloidosis
Normal – Chronic GastritisNot PUD
“I never thought of losing, but now that it' s happened, the only thing is to do it
right. That's my obligation to all the people who believe in me. We all have to
take defeats in life”
– Muhammad Ali, Champion Boxer
Commitment to Excellence…
Pathology of Peptic Ulcer Disease (PUD)
Dr. Venkatesh M. ShashidharA/Prof. & Head of Pathology
School of Medicine JCU
PUD: Overview• Helicobacter pylori infection*• Hyperacidity• Drugs - anti-inflammatory
(NSAIDs) & Corticostroids.• Cigarette smoking, Alcohol, • Rapid gastric emptying • Duodenal reflux.• Personality and stress• Genetic
Hurry, Worry, Curry
H.Pylori on the surface of gastric epithelial cells
Helicobacter pylori:• Common infection• 10% of men, 4% women develop PUD *• Positive in 70-100% of PUD patients.• 1st Part of duodenum > antrum > G-E junction.• H.pylori related disorders:
– Chronic gastritis – 90%– Peptic ulcer disease – 95-100%– Gastric carcinoma – 70%– Gastric lymphoma– Reflux Oesophagitis.– Non ulcer dyspepsia
H. Pylori Gastritis - Silver stain
Bacteria over epithelial cells
H. Pylori - PUD – Pathogenesis
• Gram negative, Spirochete.• Does not invade cells • Colonize Acidic Gastric mucosa only * • Protease Break down mucous expose
epithelium for digestion + urea.• Urease Breakdown urea ammonia
neutralise acid reflex Hyperacidity.• Chronic infl. Gastric Metaplasia Ulceration.• Complications: Bleeding, perforation, stenosis,
Carcinoma.
PUD - Diagnosis• Endoscopy – findings• Barium meal – contrast• Endoscopy, Biopsy/cytology, stains.• Culture – difficult – for research only.• HP fecal antigen test• Monoclonal antibody test on stool samples.
Specific (98%) and sensitive (94%). • C13 urea breath test – Radioactive – common.• H.pylori serology – IgG – new.
Peptic Ulcer Morphology:• Common in duodenum than stomach (4:1)• > 80% single ulcer• Round small, clean,• punched out, <2cm*.• Radiating folds.• Microscopy:
– Superficial necrotic layer.– Inflammatory cells zone.– Granulation tissue zone - B– Collagenous scar zone - C.
Note: Radiating mucosal folds from the ulcer.. Why?
Endoscopic Appearance
Gastric Ulcer
Rarely large / irregular / multiple ulcers
Gastric Peptic Ulcer
Gastric Peptic ulcer: Scar
Note: Radiating mucosal folds from the ulcer.. Why?
Double Benign, Chronic, Gastric Peptic Ulcer
Multiple peptic ulcer / severe peptic ulcer ? Etiology.
PUD Complications:• Chronic Bleeding – Anemia(IDA).• Acute Bleeding – Massive, shock, • Fibrosis, Stricture obstruction – pyloric stenosis.• Perforation – Peritonitis, pancreatitis.• Gastric carcinoma. (not duodenal ca)
Pancreas
Ulcer
Mucosa
Perforation Peritonitis
PUD - Perforation
Barry J Marshal, 2005 Nobel Prize….!
There were a lot of people who didn't believe what we said but they couldn't keep us quiet…!
A.A.Press.. 4 Oct 2005.
Barry J. Marshall & J. Robin Warren
was a trainee at that time…..!
Commitment to Excellence…
Gastric Carcinoma
Dr. Venkatesh M. ShashidharA/Prof. & Head of Pathology
School of Medicine JCU
Gastric Carcinoma:• Adeno Carcinoma (90%) Lymphoma (4%),
Carcinoid & Stromal tumors rare.• Adenocarcinoma Intestinal & Diffuse types.• Early (limited to mucosa) & Advanced stage.• Morphology: (Fungating & Diffuse infiltrative)
– Adenocarcinoma:• Intestinal type – fungating, Early diagnosis, better prognosis.• Diffuse type – diffuse infiltrating, late, poor prognosis.
– Gastric Lymphoma (MALT) – B cell, H.pylori.– Carcinoid tumor.– GastroIntestinal Stromal Tumor (GIST) *
sarcoma.
Gastric Adeno Carcinoma:
Intestinal Type• H.pylori Metaplasia• C. gastritis / atrophy• HER-2/NEU mutation• Well differentiated • No Signet ring cells.• Gland formation.• Better Prognosis
Diffuse Type• Idiopathic/familial.• No precursor lesion• E-Cadherin mutations• Poorly differentitated• Signet ring cells • No gland formation,• Poor Prognosis
Fungating Carconoma
Diffuse Ca - FibroticLinitis Plastica / Leather bottle stomach.
Malignant cells between fibrous stroma
Endoscopy
Gastric Carcinoma
Malignant
Normal Gland
Be content with what you have; rejoice in the way things are.
When you realize that there is nothing lacking,
the whole world belongs to you…!
--Lao Tzu
Points to Remember: PUD• Peptic ulcer – Gastric/duodenum - acid & Pepsin.• Etiology: H. pylori, Gram –ve, Spirochete does not invade
tissue. Protease & Urease • Mucosal damage – Inflammation – ulcer – cancer.• Perforation, stenosis, Ca (Not duodenal).• single, punched out, clean, radiating folds (not in ca). • Microscopy: spiral bacteria-silver stain, inflammation.• Ulcer : necrosis, inflammatory cells, granulation, fibrosis.• Treatment: antibiotics + Proton pump inhibitors.
“Only a man who knows what it is like to be defeated can reach down to the bottom of his soul and come up with the extra ounce of power it takes to win when the match is even.”
– Muhammad Ali, Champion Boxer
Case: 1• A 62-year-old female presented at the
clinic for evaluation of mild dry cough, affecting her sleep.
• Her medical history includes osteoporosis, HTN, mild memory loss, involuntary weight loss, has significant leg swelling. She takes 5 prescription medications for her medical conditions. She lives alone. She smokes about 1ppd and takes a glass of red wine to help sleep.
Case: 1Questions: • Does the patient have GERD? • List risk factors from the history for GERD?• Does the patient exhibit any symptoms of
GERD?• How should this patient be treated?• How should the patient be monitored? • What is NERD? how is it different?
Case 2• 72y white man at aged care nursing home,
chronic obstructive pulmonary disease, chronic alcohol abuse, chronic dementia, and multiple episodes of upper GI bleeding. He was admitted to the hospital with complaints of lightheadedness, syncope, and abdominal pain.
• Thin elderly man in no acute distress. BP 96/72, pulse 104, respiratory rate 24, and temperature 98.9°F. Hb 12.9%.
• The abdominal examination revealed mild epigastric pain on palpation. The rectal and prostate examinations were unremarkable;
• Black stool, tested positive for fecal blood.
Case 2
Questions: • Does the patient have GERD? • List risk factors from the history for
GERD?• Identify symptoms of GERD in this
patient?• How should this patient be treated?• How should the patient be monitored?
Barrett Oesophagus
A-B, Gross view of distal esophagus (top) and proximal stomach (bottom) showing (A) normal gastroesophageal junction and (B) the granular zone of Barrett esophagus (arrow). C, Endoscopic view showing red velvety gastrointestinal-type mucosa extending from the gastroesophageal orifice. Note paler squamous esophageal mucosa. (C, Courtesy of Dr. F. Farraye, Brigham and Women's Hospital, Boston, Massachusetts.)
Cancer
Norm Barrett
Barrett
Barretts Metaplasia:
Glandular E
p
Normal Sq. Ep
