Introduction of GI and Hepatobiliary system

1. GI AND
HEPATOBILIARY
SYSTEM
DR. ROSHAN KHATIWADA

2. Learning Objectives:
 Gastritis
 Peptic Ulcer Disease
 Intestinal TB
 Appendicitis
 Carcinoma of stomach
 Carcinoma of colon
 Hepatitis
 Cirrhosis of Liver
 Cholecystitis
 Cholelithiasis

3. Clinical Anatomy and Physiology:

7. GASTRITIS:
A. ACUTE GASTRITIS: Acidic damage to the stomach mucosa
Pathophysiology: Due to imbalance between mucosal defenses and acidic environment.
Defenses include mucin layer produced by foveolar cells, bicarbonate secretion by surface epithelium, and
normal blood supply (provides nutrients and picks up leaked acid).

9. C. Risk factors:
i. Severe burn (Curling ulcer) — Hypovolemia leads to decreased blood supply.
ii. NSAIDs (decreased PGE)
iii. Heavy alcohol consumption
iv. Chemotherapy
v. Increased intracranial pressure (Cushing ulcer)—Increased stimulation of vagus nerve leads to increased acid
production.
vi. Shock—Multiple (stress) ulcers may be seen in ICU patients.

10.  Morphology: Acid damage results in superficial inflammation, erosion (loss of
superficial epithelium), or ulcer (loss of mucosal layer).

11. B. CHRONIC GASTRITIS: Chronic Inflammation of stomach mucosa
 Divided into two types based on underlying etiology:
1.Chronic Autoimmune gastritis and
2.Chronic H pylori gastritis

12. 1. Chronic autoimmune gastritis: It is due to autoimmune
destruction of gastric parietal cells, which are located in
stomach body and fundus.
Pathogenesis: It is associated with antibodies against
parietal cells and/or intrinsic factor; useful for diagnosis,
pathogenesis is mediated by T cells (type IV
hypersensitivity).

13. Clinical features:
i. Atrophy of mucosa with intestinal metaplasia
ii. Achlorhydria with increased gastrin levels and antral G-cell hyperplasia
iii. Megaloblastic (pernicious) anemia due to lack of intrinsic factor
iv. Increased risk tor gastric adenocarcinoma (intestinal type)

14. 2. Chronic Helicobacter pylori gastritis:
It is due to H pylori-induced acute and chronic
inflammation; most common form of gastritis (90%).
Etio-pathogenesis: H pylori ureases and proteases
along with inflammation weaken mucosal defenses;
antrum is the most common site.

15. Clinical Features:
i. Epigastric abdominal pain;
ii. Increased risk for ulceration (peptic ulcer
disease),
iii. Gastric adenocarcinoma (intestinal type)
iv. MALT lymphoma

16. Treatment : Involves triple therapy.
i. Resolves gastritis/ulcer and reverses intestinal metaplasia
ii. Negative urea breath test and lack of stool antigen confirm eradication of H pylori

18. Questions:
1. List the risk factors of acute gastritis. What are the clinical features of acute
Gastritis?
2. Explain about pathophysiology of acute gastritis.
3. Differentiate between chronic autoimmune and H.Pylori induced gastritis.

19. PEPTIC ULCER DISEASE:
 Peptic ulcer disease (PUD) refers to chronic mucosal ulceration affecting the
duodenum or stomach.
 Nearly all peptic ulcers are associated with H. pylori infection, NSAIDs, or
cigarette smoking.
 The most common form of peptic ulcer disease (PUD) occurs within the gastric
antrum or duodenum as a result of chronic, H. pylori induced antral gastritis,
which is associated with increased gastric acid secretion, and decreased
duodenal bicarbonate secretion.

20. Etiology:

21. Clinical Features:
Duodenal Ulcer:
i. Epigastric pain that improves with meals
ii. Diagnostic endoscopic biopsy shows ulcer
with hypertrophy of Brunner glands.
iii. May rupture leading to bleeding from the
gastroduodenal artery (anterior ulcer) or
acute pancreatitis (posterior ulcer)
Gastric Ulcer:
i. Presents with epigastric pain that worsens with
meals
ii. Ulcer is usually located on the lesser curvature
of the antrum.
iii. Rupture carries risk of bleeding from left
gastric artery

22. Morphology:
 Peptic ulcers occur most common in the proximal
duodenum while Gastric peptic ulcers are predominantly
located along the lesser curvature.
 Peptic ulcers are solitary in more than 80% of patients
peptic ulcer is a round to oval, sharply punched-out
defect.
 The mucosal margin may overhang the base slightly,
particularly on the upstream side, but is usually level with
the surrounding mucosa. In contrast, heaped-up
margins are more characteristic of cancers.
 Malignant transformation of peptic ulcers occurs
rarely.

23. Differential diagnosis of ulcers includes
carcinoma:
 Duodenal ulcers are almost never
(duodenal carcinoma is extremely rare).
 Gastric ulcers can be caused by gastric
carcinoma (intestinal subtype).
i. Benign peptic ulcers are usually small (< 3
cm), sharply demarcated ("punched-out"), and
surrounded by radiating folds of mucosa.
ii. Malignant ulcers are large and irregular with
heaped up margins.
iii. Biopsy is required for definitive diagnosis

24. Complication of PUD:

25. Questions:
1.List the risk factors of Peptic Ulcer disease. Mention about complications of it.
2.Explain about pathophysiology of Peptic ulcer and mention about morphology of
duodenal and gastric ulcer.
3.Differentiate between gastric and duodenal ulcer.

26. GASTRIC CARCINOMA:
 Malignant proliferation of surface epithelial cells (adenocarcinoma).
 Adenocarcinoma is the most common malignancy of the stomach, comprising more than 90% of
all gastric cancers.
 Most gastric adenocarcinomas involve the gastric antrum, the lesser curvature is involved more
often than the greater curvature.
 Sub classified into
1. Intestinal
2. Diffuse type

27. 1.Intestinal type:
 Intestinal type (more common) presents as a large, irregular ulcer with heaped
up margins; most commonly involves the lesser curvature of the antrum (similar
to gastric ulcer).
 Risk factors include intestinal metaplasia (e.g. due to H pylori and autoimmune
gastritis), nitrosamines in smoked foods (Japan) and blood type A.

28. Morphology:
 Gastric tumors with an intestinal morphology,
which tend to form bulky tumors, are composed of
glandular structures while cancers with a diffuse
infiltrative growth pattern are more often
composed of signet-ring cells.
 Microscopically, Intestinal-type adenocarcinoma
composed of columnar, gland-forming cells
infiltrating through desmoplastic stroma.

29. 2. Diffuse type:
 Diffuse type is characterized by signet ring cells that diffusely infiltrate the
gastric wall; desmoplasia results in thickening of stomach wall (linitis plastica).
 Not associated with H pylori, intestinal metaplasia, or nitrosamines

30. Etio-pathogenesis:
Risk Factors:
i. Familial—10%. Napolean and many members of his family died of carcinoma stomach. Familial gastric
cancer in associated with mutation of e-cadherin gene (90% risk). It causes hereditary diffuse gastric cancer.
ii. Inactivation of p53, over expression of growth factors, bcl-2
iii. Gene mutations are other genetic causes: HNPCC, Li-Fraumen syndrome.
iv. Gastric mucosa of people with blood group ‘A’ is more susceptible for carcinogens—diffuse type (due to
different mucopolysaccharide secretion)
v. Gastric polyps, adenomatous polyp > 2 cm.
vi. Pernicious anaemia—high-risk 6 times.
vii. Gastric remnant—15 years after gastrectomy and GJ

31. Precursors Lesion:
i. Chronic atrophic gastritis: It is the most common precursor lesion
ii. Adenomatous gastric polyps.
iii. Intestinal metaplasia
iv. Menetrier’s disease
v. Benign gastric ulcer

32. Morphology:
 These infiltrative tumors often evoke a desmoplastic
reaction that stiffens the gastric wall.
 When there are large areas of infiltration, diffuse rugal
flattening and a rigid, thickened wall may impart a leather
bottle appearance termed linitis plastica.
 Signet-ring cells can be recognized by their large
cytoplasmic mucin vacuoles and peripherally displaced,
crescent-shaped nuclei.

33. Clinical Features:
 Gastric carcinoma presents late with weight loss, abdominal pain, anemia and early satiety; rarely
presents as acanthosis nigricans or Leser-Trelat sign.
 Spread to lymph nodes can involve the left supraclavicular node (Virchow node).
 Distant metastasis most commonly involves liver; other sites include:
i. Periumbilical region (Sister Mary Joseph nodule); seen with intestinal type
ii. Bilateral ovaries (Krukenberg tumor); seen with diffuse type
iii. left axillary lymph node (Irish node)

34. Questions:
1.Write about etiology and pathogenesis of Gastric carcinoma.
2.Differentiate between intestinal and diffuse type of gastric carcinoma.
3.List the clinical features of gastric carcinoma.

35. Intestinal Tuberculosis:
 It is common in Nepal and developing countries.
 It is the 6th most common type of extrapulmonary tuberculosis.
 Its incidence is high in HIV infected patients.
 Types of Intestinal TB:
1. Ileocaecal region
i. Ulcerative—60%.
ii. Hyperplastic.
iii. Ulcero-hyperplastic.
2. Ileal region, commonly:
i. Stricture type

36. Modes of Spread of Intestinal Tuberculosis:
 By ingestion
---Ingestion of food contaminated with tubercle bacilli causing primary intestinal
tuberculosis.
 Ingestion of sputum containing tuberculous bacteria from primary pulmonary focus
causing secondary intestinal tuberculosis.
 Haematogenous spread from tuberculosis of lungs.
 From neck lymph nodes (tuberculous cervical lymphadenitis=5-10%) through
lymphatics.
 From fallopian tubes by retrograde spread to involve peritoneum (10%).

37. A. Ileocaecal TB:
Most common site of abdominal tuberculosis due to
presence of Peyer’s patches; and stasis of luminal
contents favoured by ileocaecal valve.

38. 1. Ulcerative—most common 60%
 Circumferential transverse often multiple ‘girdle’ ulcers—with skip lesions.
 It is common in old, malnourished people.
 Long-standing ulcers cause fibrosis and later stricture formation.
 Stricture (Napkin ring stricture) is common in ileal part.
 Often related intestinal nodes are also involved with caseation, abscess (cold)
formation.
 Bowel adhesions are common.

39. 2. Hyperplastic : Fibroblast reaction causing thickening of bowel wall and lymph
node enlargement, leading to nodular mass (tumour-like) formation.
 It is common in caecal part. It causes extensive chronic inflammation, fibrosis,
bowel adhesions, nodal enlargement, often presents with mass in the right iliac
fossa.
 It is commonly primary intestinal tuberculosis.
3. Ulcerohyperplastic—30%

40. Clinical Features:
 Abdominal pain is the most common symptom (90%).
 Anaemia, loss of weight and appetite
 Diarrhoea
 Fever
 Mass in right iliac fossa, (35%) which is hard, nodular, nonmobile, nontender with impaired
resonance, which may mimic carcinoma caecum.
 Subacute obstruction can occur.
 Ileocaecal tuberculosis can be associated with adenocarcinoma of caecum, or large bowel
lymphoma or HIV.
 Often ileocaecal TB can cause intestinal obstruction (20%).

41. Question:
1.List the type of intestinal TB.
2. What are the risk factors of Intestinal TB.
3.Mention about the morphology of Intestinal TB.

42. Acute Appendicitis:
 Acute inflammation of the appendix, can be due to obstruction by fecolith or
lymphoid hyperplasia (in children).
 Most common cause of acute abdomen.

43. Pathophysiology of acute appendicitis:
 Related to obstruction of the appendix by lymphoid hyperplasia (children) or a
fecolith (adults)→ Proximal obstruction of appendiceal lumen produces closed-
loop obstruction → Increased intraluminal pressure →stimulation of visceral
afferent nerve fibers at T8-T10 → Initial diffuse periumbilical pain →
Inflammation extends to serosa and irritates parietal peritoneum.

44. Clinical Features:
 Typically, early acute appendicitis produces
periumbilical pain that ultimately localizes to the
right lower quadrant, followed by nausea, vomiting,
low-grade fever, and a mildly elevated peripheral
white cell count.
 A classic physical finding is the McBurney sign,
deep tenderness located two thirds of the distance
from the umbilicus to the right anterior superior iliac
spine (McBurney point).

45. 1. What are risk factors and pathogenesis of acute appendicitis.
2. List the different clinical features of acute appendicitis.

46. Carcinoma Colon:
 Carcinoma arising from colonic or rectal mucosa; 3rd most common site of
cancer and 3rd most common cause of cancer-related death
 Peak incidence is 60-70 years of age.
 25% have a family history
 Iron deficiency anemia in males (especially > 50 years old) and postmenopausal
females raises suspicion.
 Risk Factors: Adenomatous and serrated polyps, familial cancer syndromes, IBD,
tobacco use, diet of processed meat with low fiber

47. Clinical Features:
 Rectosigmoid > ascending > descending colon
 Right side (cecal, ascending) associated with occult bleeding; left side
(rectosigmoid) associated with hematochezia and obstruction (narrower lumen).
 Ascending—exophytic mass, iron deficiency anemia, weight loss.
 Descending—infiltrating mass, partial obstruction, colicky pain, hematochezia.
 Can present with S bovis (gallolyticus) bacteremia/endocarditis or as an episode
diverticulitis

48.  Diagnosis:
i. Colonscopy
ii. “Apple core” lesion seen on barium enema x-ray.
iii. CEA tumor marker: good for monitoring
should not be used for screening

49.  Screening:
a. Low risk: Screen at age 50 with colonoscopy; alternatives
include flexible sigmoidoscopy, fecal occult blood testing
(FOBT), fecal immunochemical testing (FIT), FIT-fecal DNA,
colonography
b. Patients with a first-degree relative who has colon
screen at age 40 with colonoscopy, or 10 years prior to the
relative's presentation
c. Patients with IBD: distinct screening protocol

50. Hepatobiliary System

51. Hepatitis: Viral Hepatitis
 Inflammation of liver parenchyma, usually due to hepatitis virus; other causes
include EBV and CMV.
 Hepatitis virus causes acute hepatitis, which may progress to chronic hepatitis.

52. 1. Acute hepatitis: Presents as jaundice (mixed CB
and UCB) with dark urine (due to CB), fever, malaise,
nausea, and elevated liver enzymes (ALT > AST).
i. Inflammation involves lobules of the liver and portal
tracts and is characterized by apoptosis of
hepatocytes.
ii. Some cases may be asymptomatic with elevated
liver enzymes.
iii. Symptoms last < 6 months,

53. 2. Chronic hepatitis: Is characterized by symptoms
that last > 6 months.
i. Inflammation predominantly involves portal tract.
ii. Risk of progression to cirrhosis

56. 1.List the different etiology of Hepatitis.
2.List the causes of Viral hepatitis.
3.List the hepatitis viruses causing Hepatitis.
4.Mention about morphology of acute hepatitis.
5.Differentiate between acute and chronic hepatitis.

57. Cirrhosis:
 End-stage liver damage characterized by
disruption of the normal hepatic parenchyma
by bands of fibrosis and regenerative nodules
of hepatocytes.
 Fibrosis is mediated by TGF from stellate cells
which lie beneath the endothelial cells that line
the sinusoids.

58. Etiology:

59. Clinical Features:
1. Portal hypertension leads to
i. Ascites (fluid in the peritoneal cavity)
ii. Congestive splenomegaly/hypersplenism
iii. Portosystemic shunts (esophageal varices, hemorrhoids, and caput medusae)
iv. Hepatorenal syndrome (rapidly developing renal failure secondary to
cirrhosis)

60. 2. Decreased detoxification results in
i. Mental status changes, asterixis, and eventual coma (due to T serum ammonia);
metabolic, hence reversible
ii. Gynecomastia, spider angiomata. and palmar erythema due to hyperestrinism
iii. Jaundice

61. 3. Decreased protein synthesis leads to
i. Hypoalbuminemia with edema
ii. Coagulopathy due to decreased synthesis of clotting factors; degree of deficiency is
followed by PT.

63. Questions:
1.List the causes of cirrhosis of liver.
2.List the different clinic features of Cirrhosis of liver.
3.Explain about morphological changes in cirrhosis of liver.

64. Cholecystitis:
A. ACUTE CHOLECYSTITIS:
 Acute inflammation of the gallbladder wall
 Calculous cholecystitis—most common type; due
to gallstone impaction in the cystic duct resulting
in inflammation and gallbladder wall thickening;
can produce dilatation with pressure ischemia,
bacterial overgrowth (E coli), and inflammation
 Acalculous cholecystitis—due to gallbladder stasis,
hypoperfusion, or infection (CMV); seen in critically
ill patients.

65.  Clinical features: Presents with right upper quadrant pain, often radiating to right
scapula, fever, inspiratory arrest on RUQ palpation due to pain(Murphy sign).
Increased WBC count, nausea, vomiting, and increased serum alkaline
phosphatase (from duct damage)
 Risk of rupture if left untreated

66. B. CHRONIC CHOLECYSTITIS:
 Chronic inflammation of the gallbladder
 Due to chemical irritation from longstanding
cholelithiasis, with or without superimposed bouts
of acute cholecystitis
 Characterized by herniation of gallbladder mucosa
into the muscular wall (Rokitansky-Aschoff
sinus).

67. Clinical features:
 Presents with vague right upper quadrant pain,
especially after eating.
 Porcelain gallbladder is a late complication
i. Shrunken, hard gallbladder due to chronic inflammation,
fibrosis, and dystrophic calcification
ii. Increased risk for carcinoma
 Treatment is cholecystectomy, especially if porcelain
gallbladder is present,

68. Questions:
1.Explain the pathogenesis of acute cholecystitis.
2.List the clinical features of acute cholecystitis.
3.Differentiate between acute and chronic cholecystitis.

69. Cholelithiasis:
 Solid, round stones in the gallbladder
Pathogenesis:
 Due to precipitation of cholesterol (cholesterol stones) or bilirubin (bilirubin
stones) in bile
---Arises with
(I) supersaturation of cholesterol or bilirubin,
(II) decreased phospholipids (e.g., lecithin) or bile acids (normally increase
solubility),
(III) stasis

70. Types of Gall Bladder Stones:
1. Cholesterol stones (yellow) are the most common type (90%), especially in the West
(Fig. 1L2A),
i. Usually radiolucent (10% are radiopaque due to associated calcium)
Risk factors: include age (40s), estrogen (female gender, obesity, multiple
pregnancies and oral contraceptives), difibrate, Native American ethnicity, Crohn
disease, and cirrhosis.

72. 2. Bilirubin stones (pigmented) are composed of bilirubin.
--Usually radiopaque
 Risk factors include extravascular hemolysis (increased bilirubin in bile) and
biliary tract infection (e.g. E coli, Ascaris lumbricoides, and Clonorchis sinensis).
i. Ascitris lumbricoides is a common roundworm that infects 25% of the world's
population, especially in areas with poor sanitation (fecal-oral transmission); infects
the biliary tract, increasing the risk for gallstones
ii. Clonorchis sinensis is endemic in China, Korea, and Vietnam (Chinese liver fluke);
infects the biliary tract, increasing the risk for gallstones, cholangitis, and
cholangiocarcinoma.

73. Clinical features:
 Gallstones are usually asymptomatic; complications include biliary colic, acute and
chronic cholecystitis, ascending cholangitis, gallstone ileus, and gallbladder
cancer.

74. Questions:
1.Explain about pathogenesis of gall bladder stone .
2.List the types of gall bladder stones.
3.List the clinical feature of gall bladder.
4.List the complications of gall bladder stones.