1. 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.

2. 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”.

3. 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.

4. 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

5. 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

6. 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.

7. 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)

8. 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?

9. 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.

10. 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,

11. "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

12. Commitment to Excellence…
Pathology of Upper GI:
Oesophageal Disorders
Dr. Venaktesh M. Shashidhar
A/Prof. & Head of Pathology
School of Medicine

13. Introduction:
• Anatomy, Histology
• Function – motility,
digestion, enzymes.
• Common disorders.
– Oesophagitis.
– GORD.
– obstructions
– Achalasia.
– Barrett’s
– PUD
– Malignancy
Oesophagus
Stomach
Normal
Name the parts ?
?
?
?
?
?
?
?
?

14. Esophagus & Stomach Normal
Glandular – Gastric  Normal  Squamous Oesophagus

15. 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),

16. Esophageal Disorders:
• Reflux Oesophagitis.
• Barrett’s
• Stricture – Inflam.
• Mallory-Weiss.
• Varices
• Hernia
• Zenker diverticulum
• T-E Fistula.
• Web – IDA – P-V Sy.
Herniations

17. Oesophagus motility Disorders:
Hernia: 30% incidence over 50years. (mostly asymptomatic)
Achalasia: Lack of relaxation of lower sphincter.
95% 5%
Achalasia Hernia-Sliding Hernia-Rolling

18. 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)

19. 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.

20. 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

21. 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

22. Commitment to Excellence…
Pathology of GORD / GERD
(Gastro O/esophageal Reflux Disease)
Dr. Venaktesh M. Shashidhar
A/Prof. & Head of Pathology
School of Medicine

23. 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

24. GORD: Clinical Classification
GORD
Heartburn
Oesophagitis
24%
Barrett’s
1%
Non-Erosive
Reflex Disease (NERD)
(normal endoscopy)
75%
Endoscopy24-hr pH Study
AET +ve
SI +ve
AET -ve
SI +ve
AET -ve
SI –ve
? MERD
AET: Acid Exposure Index
SI: Symptom Index.
MERD: minimal change.. RD
Etiology: (LES)
• Alcohol, Tobacco,
• Obesity,
• CNS depressants,
• Pregnancy,
• Hiatal hernia
• Delayed gastric emptying
• increased gastric volume

25. Pathogenesis & Stages:
A
B
C
D
Basal
Hyperplasia
1. Acid reflux Symp.
2. Inflammation
3. Regeneration (basal).
4. Metaplasia (Barretts)
5. Mild Dysplasia
6. High grade Dysplasia
7. Adeno-Carcinoma
Adenocarcinoma

26. GERD: Pathogenesis.
Normal  Hyperplasia  Dysplasia  Carcinoma
Normal
Sq. Ep.
Metaplastic
Col. Ep.
Inflammed
Sq. Ep.
Basal cell hyperplasia

27. Squamous Carcinoma - Adenocarcinoma.
• Less common
• Upper end
• Tobacco, diet, toxins.
• More common
• Lower end
• Reflux disease (Barretts)
Tumour
Normal
Tumour
Normal

28. Squam. Ca. - Adeno. Ca.
K. Pearl Glands
Pleomorphic, Hyperchromatic cells forming glands / keratin pearls
(Infiltration, inflammation, hemorrhage, necrosis)

29. "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 Nightingale
1921-1989, Radio Announcer, Author and Speaker
Hakuna Matata….!

30. Commitment to Excellence…
Pathology of
Gastric Disorders
Dr. Venkatesh M. Shashidhar
A/Prof. & Head of Pathology
School of Medicine JCU

31. Damage vs. Defense
Gastric defences:

32. • 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 ↓

33. 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%

34. 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

35. Normal – Chronic Gastritis
Not PUD

36. “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

37. Commitment to Excellence…
Pathology of
Peptic Ulcer Disease (PUD)
Dr. Venkatesh M. Shashidhar
A/Prof. & Head of Pathology
School of Medicine JCU

38. 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

39. 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

40. H. Pylori Gastritis - Silver stain
Bacteria over
epithelial cells

41. 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.

42. 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.

43. 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?

44. Endoscopic Appearance

45. Gastric Ulcer
Rarely large / irregular / multiple ulcers

46. Gastric Peptic Ulcer

47. Gastric Peptic ulcer: Scar
Note: Radiating mucosal folds from the ulcer.. Why?

48. Double Benign, Chronic, Gastric Peptic Ulcer
Multiple peptic ulcer / severe peptic ulcer ? Etiology.

49. PUD Complications:
• Chronic Bleeding – Anemia(IDA).
• Acute Bleeding – Massive, shock,
• Fibrosis, Stricture obstruction – pyloric stenosis.
• Perforation – Peritonitis, pancreatitis.
• Gastric carcinoma. (not duodenal ca)
Pancreas

50. Perforation Peritonitis

51. PUD - Perforation

52. 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…..!

53. Commitment to Excellence…
Gastric Carcinoma
Dr. Venkatesh M. Shashidhar
A/Prof. & Head of Pathology
School of Medicine JCU

54. 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.

55. 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

56. Fungating Carconoma

57. Diffuse Ca - Fibrotic
Linitis Plastica / Leather bottle stomach.
Malignant cells between fibrous stroma 
Endoscopy

58. Gastric Carcinoma
Malignant
Normal Gland

59. 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

60. 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.

61. “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

62. 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.

63. Case: 1
Questions:
• 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?

64. 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.

65. 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?

66. 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.)
Norm
Barrett
Barrett

67. Barretts Metaplasia: