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GI Pathology > Stomach > Flashcards

Stomach Flashcards

1
Q

Pyloric stenosis

A

Congenital hypertrophy of pyloric smooth muscle

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2
Q

Classic presentation

A

2 weeks after birth (takes time to develop)

  1. Projectile nonbilious vomiting (b/c bile enters duodenum and contents haven’t met the duodenum)
  2. Visible (can see!) peristalsis
  3. Olive-like/ovoid mass in abdomen (thigh pyloric sphincter)
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3
Q

Acquired pyloric stenosis

A

Comes from antral gastritis or peptic ulcers near pylorus

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4
Q

Normal body/fundic/corpus mucosa

A

Very thick
Shallow pits (foveolae)
Highly cellular glands w/prominent pink cytoplasm (from parietal cells which secrete gastric acid) in upper layers and more purplish cytoplasm in lower layers (from chief cells which secrete pepsinogen, gastric lipase, chymosin, purple b/c of lots of rER)

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5
Q

Normal antral mucosa

A

Still thick
Deep pits (foveolae)
Cellular glands now produce mostly mucus (so stain more pale)
Minimum LP (not very cellular)

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6
Q

Acute gastritis

A

Acidic damage to stomach mucosa

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7
Q

Pathophys of acute gastritis

A

Due to imbalance b/w mucosal defenses and acidic environment

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8
Q

Defenses of gastric mucosa (4)

A
  1. Mucin layer (produced by foveolar cells) –> elderly produce less so have increased susceptibility
  2. Bicarbonate secretion by surface epithelium
  3. Normal blood supply (provides nutrients and picks up leaked acid
  4. Epithelial regenerative capacity
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9
Q

Risk factors for Acute Gastritis (6)

A
  1. Severe burn (Curling ulcer) –> hypovolemia leads to decreased blood supply to mucosa
  2. NSAIDS (decreased PGE2) –> decreased bicarb
  3. Heavy alcohol consumption and smoking –> direct cellular injury
  4. Chemotherapy –> mitotic inhibitors –> decrease epi regeneration
  5. Increased intracranial pressure (Cushing ulcer) –> increased stimulation of CN10 –> increased ACh –> increased acid production
  6. Shock –> multiple stress ulcers (ICU pts) –> can also be due to sepsis or severe trauma –> hypoxia and decreased BF b/c of stress-induced splanchnic vasoconstriction
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10
Q

What does PGE2 do as protection of gastric mucosa?

A
  1. Increased bicarb secretion
  2. Decreases acid secretion
  3. Increases mucin synthesis
  4. Increases vascular perfusion
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11
Q

How often is gastric mucosa regenerated?

A

Entire mucosal layer is replaced every 2-6 days

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12
Q

How does acid damage appear morphologically? (3 possibilities)

A
  1. Superficial inflammation (normally there are NO inflammatory cells in gastric mucosa)
  2. Erosion (loss of superficial epi)
  3. Ulcer (loss of mucosal layer)
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13
Q

Sx of acute gastritis?

A

ASx or epigastric pain w/ N/V

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14
Q

Morphology of acute gastric ulcer

A

Shallow, rounded, small
Rugae normal
Base = brown/black b/c acid digestion of extravasated blood
No scarring or thickening of BV seen in chronic gastritis
Marked expansion of lamina propria by mononuclear inflammatory cells

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15
Q

2 causes of chronic gastritis

A

Helicobacter pylori gastritis (90%) and autoimmune gastritis (10%)

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16
Q

Autoimmune gastritis - Cause

A

Autoimmune destruction of gastric parietal cells (located in stomach body/corpus and fundus)

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17
Q

Autoimmune gastritis associated w/

A

Antibodies to parietal cells and/or intrinsic factor (IF) –> useful for Dx, NOT cause of damage, consequence of damage

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18
Q

Pathogenesis of autoimmune gastritis

A

Type 4 hypersensitivity –> T cell mediated to parietal cells

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19
Q

Clinical features of autoimmune gastritis (6)

A
  1. Atrophy of mucosa w/ intestinal metaplasia
  2. Achlorhydria (due to defective gastric acid secretion) w/ increased gastrin levels (body’s compensation for decreased acid secretion) and antral G-cell hyperplasia
  3. Megaloblastic (pernicious anemia) due to lack of IF (b/c parietal cells make IF, no parietal cells = no IF –> disables terminal ileal vit B12 absorption. IF binds B12 in intestine)
  4. Increased risk for gastric adenocarcinoma (intestinal type)
  5. Decreased serum pepsinogen I from chief cell destruction (b/c gastric gland destroyed during attack on parietal cells)
  6. Associated w/other autoimmune diseases (e.g. DM and Graves disease)
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20
Q

Tx for autoimmune gastritis

A

Immunosuppression so that glands are not destroyed and so stem cells can regenerate mucosa

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21
Q

Morphology for autoimmune gastritis

A 
Loss of rugae 
Atrophic mucosa in body and fundus 
Intestinal metaplasia (goblet cells + NCCE) 
Located in body of stomach 
Increased lymphocytes and macrophages
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22
Q

Chronic H. pylori gastritis - Cause

A

H. pylori-induced acute and chronic inflammation

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23
Q

Most common type of gastritis

A

H. pylori gastritis

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24
Q

Pathophys behind H. pylori gastritis

A

H. pylori ureases (NH4 inhibit gastric bicarb transporters) and proteases + inflammation weaken mucosal defenses

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25
Q

Most common site for H. pylori gastritis

A

Antrum

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26
Q

Sx of H. pylori gastritis

A

Epigastric abdominal pain

Increased risk for ulceration (PUD), gastric adenocarcinoma (intestinal type), and MALT lymphoma (gastric)

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27
Q

Tx for H. pylori gastritis

A

Triple therapy (PPI and antibiotics, PPI to allow ulcer/gastritis to heal and intestinal metaplasia to reverse and antibiotics to kill off H. pylori)

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28
Q

How to confirm eradication of H. pylori?

A

Negative urea breath test and lack of stool antigen

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29
Q

4 Features of H. pylori

A
  1. Flagella allow motility in viscous mucus
  2. Urease –> NH4 –> increase gastric pH –> inhibit bicarb and increase acid production
  3. Adhesins –> to stick to foveolar cells
  4. Toxins –> can lead to ulcer/cancer (uncertain mxn)
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30
Q

Morphology of H. pylori gastritis

A

Neutrophils in gland epi

Giemsa stain for organisms (locked in mucin layer at surface of epi, have spiral/helical shape)

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31
Q

Reminder –> pernicious anemia (B12 def) –> MOST COMMON CAUSE IS CHRONIC AUTOIMMUNE GASTRITIS

A

Atrophic glossitis (smooth, beefy red tongue)
Epithelial megaloblastosis
Malabsorptive diarrhea
Peripheral neuropathy (numbness/paresthesias)
Spinal cord lesions (loss of vibration and position sense, sensory ataxia w/ + Romberg sign, limb weakness, spasticity, extensor plantar responses)
Irreversible cerebral dysfunction (mild personality changes to memory loss to psychosis)

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32
Q

PUD - location of ulcer

A

Solitary mucosal ulcer involving proximal duodenum (90%) or distal stomach (10%)

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33
Q

Duodenal ulcer - cause

A

H. pylori (most common, >95%)

Zollinger-Ellison Syndrome (ZES; rare)

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34
Q

Presentation of duodenal ulcer

A

Epigastric pain that improves w/meals (b/c duodenum prepares itself to receive acidic food bolus from stomach by secreting acid-neutralizing substances)

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35
Q

Endoscopy biopsy of duodenal ulcer

A

Hypertrophy of Brunner glands (only found in duodenum of small intestine, secrete bicarbonate-rich mucus to protect against acidic chyme from stomach; also secrete urogastrone –> inhibits parietal and chief cells of the stomach from secreting acid and their digestive enzymes)

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36
Q

Complication of duodenal ulcer

A

Rupture –> bleeding from gastroduodenal artery (posterior ulcer) or acute pancreatitis (posterior ulcer)

37
Q

Gastric ulcer - cause

A

H. pylori (75%)

Other causes = NSAIDS and bile reflux

38
Q

Presentation of gastric ulcer

A

Epigastric pain that worsens w/meals (b/c meal –> increased gastric acid secretion –> increased mucosal inflammation)

39
Q

Location of gastric ulcer

A

Lesser curvature of antrum

40
Q

Complication of gastric ulcer

A

Risk of bleeding from L gastric artery (b/c it runs along the lesser curvature of stomach)

41
Q

DDx of ulcers includes…

A

Carcinoma

42
Q

Are duodenal ulcers malignant?

A

Extremely rarely

43
Q

Gastric ulcers can be caused by…

A

Gastric carcinoma (intestinal subtype)

44
Q

Appearance of benign peptic ulcers

A

Small, sharply demarcated (“punched out”), surrounded by radiating folds of mucosa

45
Q

Appearance of malignant peptic ulcers

A

Large, irregular, heaped up margins

46
Q

How to tell for sure b/w benign and malignant peptic ulcers?

A

Biopsy

47
Q

Ultimate cause of PUD?

A

Imbalance b/w mucosal defenses and acid production

48
Q

Microscopic appearance to ulcer

A

Superficially (luminal side) –> layer of mucus, cellular debris, inflammatory cells (esp. neutrophils)
Next –> layer of granulation tissue (capillaries, fibroblasts, variable inflammation)
Deepest –> fibrous tissue + variable inflammation

49
Q

In general PUD complications

A

Perforation, Bleeding, Obstruction (esp. in duodenum b/c of fibrosis deformation and narrowing of lumen)

50
Q

Gastric Adenocarcinoma

A

Malignant proliferation of surface epithelial cells

51
Q

2 types of Gastric Adenocarcinoma

A

Intestinal and diffuse types

52
Q

Which subtype is more common?

A

Intestinal

53
Q

How does the intestinal type of gastric adenocarcinoma present?

A

Large, irregular ulcer with heaped up
margins
Tumors typically grow as a single recognizable mass, whether it be exophytic, flat, or ulcerated
Precursor lesion = chronic gastritis

54
Q

Where is most common location of intestinal subtype of gastric adenocarcinoma?

A

Lesser curvature of the antrum (similar to gastric ulcer)

55
Q

Risk factors for intestinal subtype of gastric adenocarcinoma?

A 
Intestinal metaplasia (e.g., due to H pylori and autoimmune gastritis)
Nitrosamines in smoked foods (Japan)
Blood type A
56
Q

Morphology of diffuse subtype of gastric adenocarcinoma

A

Signet ring cells that diffusely infiltrate the gastric
wall
Desmoplasia (reactive stromal response) results in thickening of stomach wall (w/diffuse rugal flattening –> leather bottle appearance = linitis plastica)
Do not form recognizable glands and do not typically produce a discrete mass
No precursor lesion

57
Q

Does the diffuse subtype of gastric adenocarcinoma have similar risk factors to intestinal subtype?

A

NO!

NOT associated w/H. pylori, intestinal metaplasia, or nitrosamines

58
Q

How are signet ring cells formed in diffuse subtype gastric adenocarcinoma?

A

Tumor cells produce abundant cytoplasmic mucus, which expands the cell and pushes the nucleus to the side, resulting in a signet ring appearance

59
Q

Presentation of gastric carcinoma

A

Late with weight loss, abdominal pain, anemia, and early satiety
This last sign is classic for diffuse type b/c thickening of stomach wall prevents full stomach distension so pts get full faster
Rarely presents as acanthosis nigricans (thickening and darkening of axillary region) or Leser-Trelat sign (explosive onset of multiple seborrheic keratoses; aka many pigmented skin lesions)

60
Q

Spread to lymph nodes in gastric carcinoma involves which LN?

A

Left supraclavicular node (Virchow node)

61
Q

What sites are involved in metastatic gastric carcinoma?

A

Most commonly = liver
Other sites =
1. periumbilical region (Sister Mary Joseph nodule –> seen with intestinal type)
2. Bilateral ovaries (Krukenberg tumor –> seen with diffuse type)

62
Q

Are peptic ulcers pre-malignant?

A

NO

“Cancers often ulcerate, but ulcers never cancerate”

63
Q

2 Types of hypertrophic gastropathy

A

Menetrier dx and Zollinger-Ellison Syndrome (ZES)

64
Q

Features of Menetrier Dx (7)

A
  1. Diffuse hyperplasia of foveolar epi of body and fundus
  2. Hypoproteinemia due to protein-losing enteropathy (decreased albumin)
  3. Wt loss
  4. Diarrhea
  5. Peripheral edema
  6. Rare
  7. Children (self-limiting, after resp. infxn); adults (increased risk of gastric adenocarcinoma)
65
Q

Morphology of Menetrier Dx

A

Irregular enlargement of gastric rugae in body and fundus
Hyperplasia of foveolar mucus cells
Corkscrew glands

66
Q

Tx for Menetrier Dx

A

Supportive w/ IV albumin and parenteral nutritional supplementation

67
Q

Cause of ZES?

A

Gastrin-secreting tumors (gastrinomas)

68
Q

Features of ZES?

A

Slow growing
Malignant
Sporadic (75%)
Found most often in small intestine and pancreas

69
Q

Morphology of ZES

A

Thickening of mucosal layer b/c of increased parietal cells

Increased mucin production b/c hyperplasia of mucus neck cells

70
Q

Tx of ZES

A

Blockade of acid hypersecretion (PPIs, H2R blockers)

71
Q

What does prognosis of ZES depend on?

A

Gastrinoma

72
Q

Types of Gastric Polyps (3)

A
  1. Inflammatory/Hyperplastic (75%)
  2. Fundic gland (15%)
  3. Gastric adenoma (10%)
73
Q

Features of inflammatory/hyperplastic gastric polyp?

A

50-60 y.o.
Chronic gastritis (reactive hyperplasia)
Risk of dysplasia increases w/size
Multiple, ovoid, smooth

74
Q

Features of fundic gland gastric polyp?

A

50 y.o.
»F
Sporadic or FAP (familial adenomatous polyposis)
Increased incidence b/c of PPI tx (due to increased gastrin secretion due to decreased gastric acid –> glandular hyperplasia)
Sx = Asx or N/V w/epigastric pain
Morphology = no inflammation, smooth surface

75
Q

Features of gastric adenoma (gastric polyp)?

A 
50-60 y.o. 
>>> M
Incidence increases w/age 
FAP + background of chronic gastritis w/atrophy and intestinal metaplasia 
Increased risk of adenocarcinoma w/size 
Located in antrum of stomach
76
Q

Gastric lymphoma (MALTomas) - Most common cause

A

Chronic H. pylori infection

77
Q

Gastric lymphoma (MALTomas) - morphology

A

Dense lymphocytic infiltrate in LP
Dx lymphoepithelial lesions
Reactive-appearing B-cell follicles

78
Q

Gastric lymphoma (MALTomas) - Sx

A

Dyspepsia and epigastric pain
Less common = Hematemesis, melena, and constitutional symptoms such as weight loss
Difficult to distinguish b/w gastric MALTomas and H. pylori gastritis

79
Q

Carcinoid (carcinoma-like) tumor

A

Well-differentiated neuroendocrine carcinomas

80
Q

Carcinoid tumor associated w/

A

Endocrine cell hyperplasia, chronic atrophic gastritis, and Zollinger-Ellison syndrome

81
Q

Carcinoid tumor - Morphology

A

Yellow or tan in color and are very firm due to intense desmoplastic reaction –> kinking of the bowel and obstruction
Salt and pepper appearance –> microscopically

82
Q

Carcinoid tumor - Clinical features

A

Peaks in 6th decade
Sx determined by the hormones produced (e.g. Gastrin –> Zollinger-Ellison syndrome; ileal tumors –> carcinoid syndrome = cutaneous flushing, sweating, bronchospasm, colicky abdominal pain, diarrhea, and right-sided cardiac valvular fibrosis)

83
Q

Carcinoid tumor - Most important prognostic determination

A

Location of tumor –> foregut (stomach + duodenum; rarely metastasize, cured by resection); midgut (jejunum and ileum) = multiple and aggressive; hindgut (appendix and colorectum) = incidental; appendix ones = benign; rectal = produce polypeptide hormones and if Sx, then abdominal pain and weight loss

84
Q

Most common mesenchymal tumor of abdomen?

A

Gastrointestinal stromal tumor (GIST)

85
Q

Clinical features of GIST

A

> in M
Peak age = 60
Sx = mass effects, ulceration –> blood loss and anemia (50%)

86
Q

Pathogenesis of GIST

A

Majority caused by oncogenic, gain-of-function mutations of the gene encoding the tyrosine kinase c-KIT (CD117), which is the receptor for stem cell factor

87
Q

Morphology of GIST

A

Can be large, solitary, well-circumscribed fleshy mass w/ulcerated mucosa
Metastases = multiple serosal nodules throughout the peritoneal cavity or 1 or > nodules in the liver; spread outside of the abdomen is uncommon
Spindle cell type and/or epithelioid type
Best dx marker = c-KIT

88
Q

Tx of GIST

A

Complete surgical resection

89
Q

Prognosis

A

Based on tumor size (recurrence = 10 cm common) mitotic index, and location

GI Pathology (5 decks)

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