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GI 4th Year > Pathology Of Benign Gastric Disease > Flashcards

Pathology Of Benign Gastric Disease Flashcards

1
Q

Congenital gastric disease

A

Pyloric stenosis

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2
Q

Pyloric stenosis

A

Idiopathic hypertrophy of circular pyloric muscle → outflow obstruction

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3
Q

Pyloric stenosis

Affect

A

M: F =
4 – 5:1

Familial /genetic basis

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4
Q

Pyloric stenosis

Symptoms

A

Projectile vomiting 2-3 weeks after birth

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5
Q

Pyloric stenosis

Treatment

A

surgical incision of hypertrophic muscle

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6
Q

Gastropathy

A

Epithelial cell damage and regeneration with minimal or no inflammation

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7
Q

Gastritis

A

inflammation associated with gastric mucosal injury

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8
Q

Gastropathy + gastritis

Symptoms

A

▪ asymptomatic or epigastric pain, nausea, and vomiting
▪ In severe cases: mucosal erosion, ulceration, hemorrhage, hematemesis, melena, or
massive blood loss

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9
Q

Gastropathy

Causes

A
  • chemical (reactive) : alcohol, bile reflex, NSAIDs….
  • vascular : portal hypertensive(congestive) gastropathy, gastric antral vascular ectasia
  • ischemic gastropathy : cocaine, hypovolemia, sepsis,burns, trauma,..
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10
Q

Gastritis

Causes

A
  • Infectious: h pylori…….
  • autoimmune
  • granulomatous disease: crohns, sarcoidosis
  • other; ..
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11
Q

Gastropathy + gastritis

Pathogenesis

A

Imbalance
between defensive and
damaging forces

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12
Q

Chronic gastritis

Causes

A

▪ Helicobacter pylori – most common
▪ NSAIDs, Chemical-Bile reflux, radiation
▪ Autoimmune gastritis
▪ Lymphocytic
▪ eosinophilic – food allergy
▪ granulomatous – Crohn’s disease, sarcoidosis

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13
Q

H. pylori

Shape

A

Spiral-shaped or curved Gram-negative bacilli

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14
Q

H. pylori

associated with ———-status and
———-, acquired in———, prevalence rises with age

A

low socioeconomic

poor hygiene

childhood

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15
Q

H. pylori

Routes of infection:

A

Oral,
Fecal-oral,
Environmental spread

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16
Q

H. pylori

Present in

A

90% chronic antral gastritis,

100% in duodenal ulcer

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17
Q

H. pylori

Virulence due to:

A

▪ Flagella

▪ Urease

▪ Adhesins

▪ Toxins(encoded by cytotoxin-associated gene A (CagA) )

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18
Q

Chronic gastritis caused by h
h.pylori
Two types?

A
  • Antral predominant gastritis

- Body predominant/pan-gastritis:

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19
Q

Antral predominant gastritis ( most common)

A

increased acid production resulting in

duodenal ulceration in 10–15%

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20
Q

Body predominant/pan-gastritis:

A

decreased acid secretion and gastric ulceration

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21
Q

Body predominant/pan-gastritis: decreased acid secretion and gastric ulceration (due to

A

reduction in parietal cell mass → low acid secretion → hypergastrinemia → intestinal
metaplasia → 3-6 fold increased risk of gastric adenocarcinoma)

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22
Q

——biopsies are preferred for evaluation of H. pylori gastritis ,
Why?

A

antral

H. pylori shows tropism for gastric foveolar epithelium (in antrum)

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23
Q

H.pylori chronic gastritis
Histology

▪ The organism is concentrated in

▪ Mucosa is

▪ Inflammatory cells:

▪ Lymphoid

A

-superficial mucus overlying epithelial cells (mostly
in antrum)

  • erythematous, Thickened (initial stages) → Atrophic (later stages)
  • intraepithelial neutrophils +subepithelial plasma cells

-Lymphoid aggregates with germinal centers – May progress to (MALT) lymphoma – type
of NHL

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24
Q

H.pylori chronic gastritis

Clinical features:

A

Nausea, Upper abdominal discomfort, Vomiting

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25
Q

H.pylori chronic gastritis

Diagnosis:

A

▪ Serologic tests for anti-H. pylori antibodies
▪ Fecal bacterial detection
▪ Urea breath test
▪ Biopsy Rapid urease test, Culture (stains: H&E, giemsa, silver stain,
immunohistochemical stain which stains organism brown), PCR

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26
Q

Urea breath test

A

high CO2 indicates presence of H. pylori

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27
Q

< 10% of cases of chronic gastritis

A

Autoimmune gastritis

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28
Q

H. pylori most common in——-whereas Autoimmune gastritis

A

antrum

Spares the antrum

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29
Q

Autoimmune gastritis

Pathogenesis:

A

Autoantibodies against parietal cell (specifically H+,K+ -ATPase) → Loss of parietal
and chief cells → Deficient acid secretion stimulates gastrin release → hypergastrinemia and hyperplasia of antral G cells → if prolonged can develop NET (neuroendocrine tumor)

30
Q

Autoimmune gastritis

due to destruction of parietal cells)

A

Antibodies to parietal cells and intrinsic factor

-Vitamin B12 deficiency leading to pernicious anemia and neurologic changes (due to loss
of intrinsic factor)

-Achlorhydria ( absence of Hcl)

31
Q

Autoimmune gastritis

due to loss of chief cells

A

Reduced serum pepsinogen I levels

32
Q

Antral endocrine cell (G cells) hyperplasia → hypergastrinemia

A
33
Q

Autoimmune gastritis

Gross morphology:

A

Diffuse atrophy of gastric mucosa resulting in loss of HCl secretion
(hypochlorhydria) → acid producing mucosa in body and fundus markedly thinned,
and
rugal folds are lost

34
Q

Autoimmune gastritis

➢ Histology:

A

▪ Infiltrated by lymphocytes, plasma cells, Inflammation extends deep into mucosa
▪ Loss of parietal and chief cells
▪ Fibrosis of the lamina propria
▪ Intestinal metaplasia (goblet cells) in body mucosa
▪ Antral endocrine cell (foveolar cells / G cells) hyperplasia → carcinoid (NET) tumors

35
Q

Autoimmune gastritis

▪ Slow onset, Median age 60 yrs ▪ May be associated with other autoimmune diseases
Other
Clinical Features:

A

▪ Atrophic glossitis (beefy red tongue)
▪ Peripheral neuropathy → paresthesia and numbness ▪ Spinal cord lesions → loss of vibration and position sense
▪ Cerebral manifestations → personality changes and memory loss to psychosis

36
Q

Autoimmune gastritis

Diagnosis

A

antibodies to intrinsic factor or parietal cells,
elevated fasting serum gastrin level,
staining with anti-chromogranin antibodies can show endocrine cell hyperplasia →endocrine
cells stain brown

37
Q

Chemical gastritis aka

A

reactive gastritis,
bile reflux gastritis or
type C gastritis)

38
Q

Chemical gastritis

Causes

A

-reflux of alkaline duodenal contents after partial distal gastrectomy,
-secondary motility
disturbances in patients with gallstones and after cholecystectomy,
-long-term use of NSAIDs, corticosteroids or chemoradiotherapy

39
Q

Chemical gastritis

ommon denominator being repeated chemical injury

Presentation

A

bilious vomiting or less severe dyspeptic symptoms, Repeated damage to mucosa
may cause a gastric ulcer

40
Q 
Eosinophilic gastritis (rare)
➢  characterized by
A

oedema and increased eosinophils in absence of intestinal parasites (which
also cause eosinophilia)

41
Q

Eosinophilic gastritis association w/

A

history of atopy or

connective tissue disease (scleroderma, SLE)

42
Q

Lymphocytic gastritis

A

presence of numerous lymphocytes within surface epithelium

43
Q

Lymphocytic gastritis Seen in 45% of pts with——-), 10% with H. pylori
infection, also patients with Crohn’s disease and allergies

A

gluten sensitive enteropathy (coeliac disease)

44
Q

Granulomatous gastritis Histology

A

epithelioid cell granulomas

45
Q

Granulomatous gastritis related to

A 
infectious agents (TB, histoplasmosis, parasites), systemic granulomatous diseases
(sarcoidosis, Crohn’s disease), presence of foreign bodies
46
Q

Compilations of chronic gastritis:

A

PUD,
mucosal atrophy,
intestinal metaplasia and dysplasia

47
Q

Peptic ulcers are

A

solitary lesion that can occur in any part of the GIT which is exposed to acid-peptic juices [Acid & Pepsin are required for peptic ulceration]

48
Q

Peptic ulcers can occur in:

A

stomach (gastric ulcers)

duodenum (duodenal ulcers)

49
Q

stomach (gastric ulcers) commonly located in

A

lesser curvature of stomach near the

interface of the body and antrum

50
Q

duodenum (duodenal ulcers) → commonly

A

within a few centimeters of the pyloric

valve,

51
Q

duodenal ulcers

A

more common than stomach ulcers, duodenitis with Brunner cell hyperplasia and
gastric mucin cell metaplasia

52
Q

Ulcer sites: mostly at mucosal junctions

A

▪ antral-proximal duodenum (>95%)

▪ other sites: Stomach, GE junction, Gastrojejunostomy site, Jejunum in ZE-syndrome

53
Q

Peptic ulcer disease (PUD)

pathogenesis:

A

Imbalance between mucosal defenses and damagin forces → hyperacidity,

54
Q

factors that cause hyperacidity:

A

H. pylori,
parietal cell hyperplasia,
excessive secretory responses,
Insufficient inhibition of stimulatory mechanisms such as gastrin release e.g. Zollinger-Ellison syndrome

55
Q

Risk of peptic ulcer

A

H. pylori, chronic NSAIDs use (decrease PGs), smoking (impairs BF),
acidic drinks, stress, caffeine, corticosteroids (suppress PGs and impair healing)

56
Q

▪ Age:
▪ Gender:
▪ Genetic:

A

-Duodenal 30-50, Gastric over 60
-Duodenal → increasing in older women
-family history, blood groups (blood group O are at increased risk of peptic
ulcers due to enhanced binding of H. pylori to their epithelial cells)

57
Q

Acute vs chronic peptic ulcers:

A

Acute: acute gastritis, mucosal ischemia, extreme hyperacidity e.g. Zollinger-Ellison
Syndrome

Chronic: occurs where acid and pepsin first come in contact with susceptible mucosa
e.g. antral and proximal duodenum, associated with HP or chemical gastritis

58
Q

Gross of peptic ulcer

A

Shape: Round to oval, Margins: Punched out, Edge: Overhanging, Floor: clean, Base:
Firm
Scarring -> puckering -> radiating mucosal folds (in spoke wheel pattern)

59
Q

Microscopy

A

4 zones
▪ Zone of exudation (thin layer of fibrinoid necrosis)
▪ Zone of inflammatory cell infiltration
▪ Zone of granulation tissue
▪ Zone of scarring (only in chronic lesions)

60
Q

Symptoms of peptic ulcer

A

▪ Epigastric tenderness (Gastric: left of midline, Duodenal: mid to right of epigastrium)
▪ Sharp, burning, aching, gnawing pain
▪ Dyspepsia (indigestion), Nausea/vomiting, Belching

61
Q

Gastric vs duodenal ulcers:

A

Gastric: Pain occurs 1-2 hours after meals & usually does not wake patient &
accentuated by ingestion of food, has risk for malignancy, ulcer is deep and penetrating

Duodenal: Pain occurs 2-4 hours after meals & wakes up patient & relieved by food,
very little risk for malignancy

62
Q

Diagnosis of peptic ulcer

A

▪ Esophagogastroduodenoscopy (EGD):

▪ Upper gastrointestinal series (UGI):

▪ Urea Breath Testing:

63
Q

Urea Breath Testing: to

A

detect H. pylori

64
Q

Esophagogastroduodenoscopy (EGD):

A

Endoscopic procedure → visualizes ulcer, take

tissue biopsy to R/O cancer and diagnose H. pylori

65
Q

Upper gastrointestinal series (UGI):

A

Barium swallow → X-ray that visualizes structures of

the upper GI tract

66
Q

Complications of peptic ulcers:

A

Hemorrhage

Perforation

Narrowing and obstruction (pyloric):

Anemia

67
Q

Hemorrhage: if ulcer erodes into muscles of stomach or duodenal wall and damages
underlying BVs → Coffee ground vomitus or bloody tarry stools
▪ Perforation: if an ulcer erodes even further through the entire wall and reaches
peritoneum → Bacteria and partially digested fool spill into peritoneum (usually sterile)
→ peritonitis
▪ Narrowing and obstruction (pyloric): Swelling and scarring (especially in duodenal
ulcers near pyloric sphincter) → obstruction of food leaving stomach → repeated
vomiting and crampy abdominal pain
▪ Anemia: due to hemorrhage and blood loss → iron deficiency anemia

A

T

68
Q

Mucosal atrophy and intestinal metaplasia

➢ Associated w/

A

long-standing chronic gastritis & increases risk for gastric adenocarcinoma

achlorhydria of gastric mucosal atrophy

69
Q

achlorhydria permits

A

overgrowth of bacteria that produce carcinogenic nitrosamines

70
Q

• Dysplasia

A

➢ Chronic gastritis over time → accumulation of genetic alterations that result in adenocarcinoma ➢ Preinvasive lesion: variations in epithelial size, shape, coarse chromatin, hyperchromasia

GI 4th Year (11 decks)

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