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

Pathology Of Benign Gastric Disease Flashcards

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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
H.pylori chronic gastritis | Diagnosis:
▪ 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
26
Urea breath test
high CO2 indicates presence of H. pylori
27
< 10% of cases of chronic gastritis
Autoimmune gastritis
28
H. pylori most common in——-whereas Autoimmune gastritis
antrum Spares the antrum
29
Autoimmune gastritis Pathogenesis:
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
Autoimmune gastritis | due to destruction of parietal cells)
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
Autoimmune gastritis | due to loss of chief cells
Reduced serum pepsinogen I levels
32
Antral endocrine cell (G cells) hyperplasia → hypergastrinemia
33
Autoimmune gastritis Gross morphology:
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
Autoimmune gastritis | ➢ Histology:
▪ 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
Autoimmune gastritis ▪ Slow onset, Median age 60 yrs ▪ May be associated with other autoimmune diseases Other Clinical Features:
▪ 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
Autoimmune gastritis Diagnosis
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
Chemical gastritis aka
reactive gastritis, bile reflux gastritis or type C gastritis)
38
Chemical gastritis | Causes
-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
Chemical gastritis ommon denominator being repeated chemical injury Presentation
bilious vomiting or less severe dyspeptic symptoms, Repeated damage to mucosa may cause a gastric ulcer
40
``` Eosinophilic gastritis (rare) ➢ characterized by ```
oedema and increased eosinophils in absence of intestinal parasites (which also cause eosinophilia)
41
Eosinophilic gastritis association w/
history of atopy or | connective tissue disease (scleroderma, SLE)
42
Lymphocytic gastritis
presence of numerous lymphocytes within surface epithelium
43
Lymphocytic gastritis Seen in 45% of pts with——-), 10% with H. pylori infection, also patients with Crohn’s disease and allergies
gluten sensitive enteropathy (coeliac disease)
44
Granulomatous gastritis Histology
epithelioid cell granulomas
45
Granulomatous gastritis related to
``` infectious agents (TB, histoplasmosis, parasites), systemic granulomatous diseases (sarcoidosis, Crohn’s disease), presence of foreign bodies ```
46
Compilations of chronic gastritis:
PUD, mucosal atrophy, intestinal metaplasia and dysplasia
47
Peptic ulcers are
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
Peptic ulcers can occur in:
stomach (gastric ulcers) duodenum (duodenal ulcers)
49
stomach (gastric ulcers) commonly located in
lesser curvature of stomach near the | interface of the body and antrum
50
duodenum (duodenal ulcers) → commonly
within a few centimeters of the pyloric | valve,
51
duodenal ulcers
more common than stomach ulcers, duodenitis with Brunner cell hyperplasia and gastric mucin cell metaplasia
52
Ulcer sites: mostly at mucosal junctions
▪ antral-proximal duodenum (>95%) | ▪ other sites: Stomach, GE junction, Gastrojejunostomy site, Jejunum in ZE-syndrome
53
Peptic ulcer disease (PUD) | pathogenesis:
Imbalance between mucosal defenses and damagin forces → hyperacidity,
54
factors that cause hyperacidity:
H. pylori, parietal cell hyperplasia, excessive secretory responses, Insufficient inhibition of stimulatory mechanisms such as gastrin release e.g. Zollinger-Ellison syndrome
55
Risk of peptic ulcer
H. pylori, chronic NSAIDs use (decrease PGs), smoking (impairs BF), acidic drinks, stress, caffeine, corticosteroids (suppress PGs and impair healing)
56
▪ Age: ▪ Gender: ▪ Genetic:
-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
Acute vs chronic peptic ulcers:
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
Gross of peptic ulcer
Shape: Round to oval, Margins: Punched out, Edge: Overhanging, Floor: clean, Base: Firm Scarring -> puckering -> radiating mucosal folds (in spoke wheel pattern)
59
Microscopy
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
Symptoms of peptic ulcer
▪ Epigastric tenderness (Gastric: left of midline, Duodenal: mid to right of epigastrium) ▪ Sharp, burning, aching, gnawing pain ▪ Dyspepsia (indigestion), Nausea/vomiting, Belching
61
Gastric vs duodenal ulcers:
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
Diagnosis of peptic ulcer
▪ Esophagogastroduodenoscopy (EGD): ▪ Upper gastrointestinal series (UGI): ▪ Urea Breath Testing:
63
Urea Breath Testing: to
detect H. pylori
64
Esophagogastroduodenoscopy (EGD):
Endoscopic procedure → visualizes ulcer, take | tissue biopsy to R/O cancer and diagnose H. pylori
65
Upper gastrointestinal series (UGI):
Barium swallow → X-ray that visualizes structures of | the upper GI tract
66
Complications of peptic ulcers:
Hemorrhage Perforation Narrowing and obstruction (pyloric): Anemia
67
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
T
68
Mucosal atrophy and intestinal metaplasia | ➢ Associated w/
long-standing chronic gastritis & increases risk for gastric adenocarcinoma achlorhydria of gastric mucosal atrophy
69
achlorhydria permits
overgrowth of bacteria that produce carcinogenic nitrosamines
70
• Dysplasia
➢ 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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