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M2 GI > 7. Pathology of Gastric Diseases > Flashcards

7. Pathology of Gastric Diseases Flashcards

1
Q

Anatomy of the stomach: what are the various segments of the stomach? where is each located?

(Jullet don’t laugh at me!)

A

Cardia: area around LES

Fundus: comes after cardia; the first bulge

Body: after Fundus, the main part of the stomach

Antrum: the last part, just prior to the pylorus

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2
Q

Cardia: what kind of cells?

A

mucous cells

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3
Q

Fundus and body: what kinds of cells? what do they produce?

A

Parietal cells: produce acid (HCl)

Chief cells: produce pepsinogen

Mucosa of the fundus/body = oxyntic epithelium (acid-producing)

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4
Q

where is the incisura located? what section is distal to it?

A

the notch on the lesser curvature. distal to this is the Antrum

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5
Q

Antrum: what kinds of glands? what do they produce?

A

mucous glands (mucin)

G cells (gastrin)

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6
Q

Name the different areas of this stomach (E, C, F, P, D)

A

E = esophagus

C = cardia

F = fundus

P = pylorus/antrum

D = duodenum

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7
Q

What are rugae? what is teh pathology if they are flattened? what if they are hypertrophied?

A

the folds in the fundus/body. all the mucosa is in the rugae.

If flattened, atrophic gastritis

If hypertrophied, ZE syndrome

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8
Q

Name the 4 layers of the gastric wall in this pic.

A

Mucosa

submucosa

Muscularis propria

serosa (very thin at bottom)

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9
Q

There is gastric mucosa all over the stomach. what part of it is the same everywhere, and what part varies by region?

A

Foveolar Compartment (the superficial epithelium) is the same everywhere. (Kind of like the Fc region of antibodies)

The Glandular compartment varies by region:

Cardia: mucous-secreting epit.

Fundus/body: oxyntic/acid-producing epit.

Pylorus/antrum: mucous-secreting epit.

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10
Q

What is this an image of? What are the notable features?

A

Normal histo: foveolar compartment.

Note mucin-secreting cells w nuclei at bottom

“Gastric foveolar type epithelium”

He mentioned we should be able to recognize this ;)

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11
Q

What kind of mucosa is this? What is produced here?

A

Oxyntic mucosa of fundus and body.

Acid, pepsin produced here.

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12
Q

What is this a picture of? What are the pink cells producing? what are the blue cells producing?

A

Oxyntic glandular compartment.

Pink cells: granular cytoplasm, producing HCl

Blue cells: producing pepsin

This may be gastritis: not sure why.

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13
Q

Where in the stomach does this come from? what are the cells producing?

A

Antrum.

Mucin-producing mucosa

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14
Q

Where in the stomach is this taken from? What kinds of glands are these?

A

Antrum/pyloric area

These are typical of antral mucin-producing glands

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15
Q

What are the 5 components of the gastric mucosal protective barrier?

A
  • Mucus secretion
  • Bicarb secretion into mucus
  • Epithelial barrier (tight junctions)
  • Mucosal blood flow
  • Prostaglandin synthesis
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16
Q

Broadly, what are the categories of stomach pathologies?

A
  • Congenital lesions
  • Gastritis and ulcers
  • Neoplasms
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17
Q

Gastritis is divided into Acute and Chronic. Two types of Acute Gastritis, and two types of Chronic?

A

Acute: Hemorrhagic, Erosive

Chronic: H pylori, Autoimmune

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18
Q

Acute Gastritis: definition? morphology?

A

Acute mucosal injury usually of a transient nature which subsides if the inciting stimulus is removed. Morphologically characterized by mucosal injury and regenerative changes in the absence of significant inflammation in lamina propria.

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19
Q

Acute gastritis: common causes?

A

NSAIDs, EtOH

ingestion of acid or alkali

heavy smoking

severe hypotension/shock

severe stress (trauma, burns)

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20
Q

What’s this? What is notable?

A

Mucosa of acute gastritis.

note the multiple hemorrhages and several defects in the mucosa

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21
Q

Stress Ulcer: definition? What may be the cause?

A

Defined as the loss of tissue such that the defect extends into the submucosa.

Acute gastritis may progress to ulcer

May be due to trauma, burns, shock, sepsis

May result in life-threatening hemorrhage

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22
Q

What is this a picture of? What are the notable features?

A

Acute Erosive Gastritis

Note: at top, fibrin, neutrophils, damaged mucosa. Some of the epithelium has been destroyed by erosion

Underlying glands have reacted to stress and multiplied

Note especially: exudate, partial destruction of the mucosa

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23
Q

What is this picture? What is notable?

A

Chronic Gastritis.

Note PMN and plasma cell infiltrate in lamina propria (this is the main feature of chronic gastritis)

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24
Q

What is the diagnostic criterion for chronic gastritis?

A

increased chronic inflammatory cells in the lamina propria.

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25
Q

What is the cause of 90% of chronic gastritis?

Where does it start, how does it progress?

A

H Pylori!

Starts in the antrum, then invades the stomach upwards.

Bacterial colonization of the surface foveolar epithelium

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26
Q

What is this? what does it adhere to?

A

H pylori!

adheres superficially to foveolar epithelium

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27
Q

What is this?

A

H Pylori.

Stained with a specific stain.

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28
Q

What are some complications of chronic H Pylori gastritis?

A
  • Gastric Atrophy & Intestinal Metaplasia
  • Peptic Ulcer (Duodenal ulcers and 70% of Gastric Ulcers)
  • Gastric Dysplasia (Premalignant change)
  • Gastric Carcinoma
  • Gastric Lymphoma (MALT lymphoma)
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29
Q

What are these images of? This process is a complication of what?

A

Atrophy (left?) and intestinal metaplasia (right?). Mucosal change to a type like what we find in the intestines. Goblet cells are not normal for the stomach!

Both atrophy and intestinal metaplasia are complications of chronic gastritis

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30
Q

Salivary gland neoplasms: which glands are most likely to have malignant tumors?

A

Sublingual most likely (80% malig)

Submandibular (40%)

Parotid (30%)

Trend: the smaller the gland, greater the % malig

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31
Q

What is the most common type of BENIGN salivary gland tumor?

A

Pleomorphic Adenoma (50% of all tumors)

Warthin (5-10%)

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32
Q

What is the most common type of MALIGNANT salivary gland tumor?

A

Mucoepidermoid carcinoma (15% of all tumors)

Acinic cell carcinoma (5%)

Adenoid cystic carcinoma (5%)

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33
Q

What is this picture? what types of structures?

A

Salivary gland.

Can see acinar tissue and ductules.

serous glands are the pink/white granulated areas

mucinous glands have clear cells

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34
Q

which salivary gland has more serous glands, which has more mucinous glands?

A

Serous: partotid gland

Mucinous: sublingual gland

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35
Q

Pleomorphic Adenoma: benign or malig? what is risk? what is treatment?

What cells is it made of?

A

Benign tumor with definite risk of malignant transformation. Excise completely due to this risk.

Content: BIPHASIC tumor. Made of ductal/epithelial cells and myoepithelial cells.

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36
Q

Pleomorphic adenoma: more common in what glands? why does this make sense?

A

Most common in parotid. Makes sense because most parotid tumors are benign and this is a benign tumor.

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37
Q

what am I looking at?

A

Pleomorphic Adenoma (gross and histo)

R upper: tumor with some hemorrhage

L histo: epithelial component, duct structures. some scattered spindle-like cells, myoepithelial cells.

R histo: mesenchymal component.

38
Q

Warthin tumor: what gland is it most prevalent in? what are the risk factors?

What cell types is it made of?

A

Cystic tumor, almost always in the parotid. (Makes sense because this is a benign tumor and parotid tumors are primarily benign.)

Risk fx are being MALE and SMOKING

BIPHASIC: epithelial (very eosinophilic), lymphoid cell types

39
Q

what am I looking at? how can I tell?

A

warthin tumor (benign tumor of parotid gland)

Cystic. Cystic fluid looks like motor oil. Look for oncocytic cells and lymphoid cells on histo.

Black stuff is proteinaceous debris. (memory trick: connect black stuff with smoking, which is a risk factor !??)

40
Q

what kind of tumor, what are notable features?

A

Warthin Tumor.

Benign tumor of parotid.

Loook for epithelial cells, eosinophilic cells (very red), and note double membrane area, lots of mitochondria.

41
Q

Mucoepidermoid carcinoma: what cells is it made of? what is the difference between low grade and high grade?

A

2 components: mucus secreting cells and squamous cells. (the name of the tumor helps: muco-epidermoid)

LOW grade: mucous cells predominate. 90% 5yr survival.

HIGH grade: squamous cells predominate. 50% 5yr survival.

42
Q

another effing tumor. what is it this time?

A

Mucoepidermoid carcinoma.

43
Q

what is this? what is the circle around?

A

Mucoepidermoid carcinoma.

Circle is around mucus-secreting cells.

44
Q

What are these tissue types? What kind of tumor?

A

Left: squamous cells

Right: mucinous cells (stained with special stain)

Mucoepidermoid carcinoma.

45
Q

What kind of tumor? notable features?

A

Adenoid Cystic Carcinoma.

Note hyaline, basement membrane material, perineural invasion (left pic).

46
Q

Adenoid Cystic Carcinoma: prognosis, survival rate?

A

Initially good prognosis due to slow-growth, but high recurrence rate.

30% 10yr survival

47
Q

Esophageal anatomic pathology: what is atresia? what is a fistula?

A

atresia: esophagus is a tube that does not completely connect. (pic A)
fistula: a connection between the esoph and the trachea.

48
Q

Esophagus: what are some lesions that can be acquired?

A

Zenker’s diverticulum

Web

Stricture

Barrett’s Esophagus

Varices

Mallory-Weiss syndrome

49
Q

what is achalasia? What causes it?

A

condition associated with esophageal dysmotility. Inability to relax the LES.

Caused by damaged ganglion cells in the myenteric plexus. can be idiopathic or secondary to an insult (ie Trypanosoma cruzi infection - Chagas’ disease)

(Some of this was from Pathoma)

50
Q

Achalasia: clinical symptoms?

A

dysphagia for both solids and liquids

putrid breath

high LES pressure with esophageal manometry

‘Bird beak’ sign

Increased risk for exophageal squamous cell carcinoma

(all from pathoma)

51
Q

What are esophageal webs? what patients are most likely to get them?

A

Protrusion of the squamous epithelium of the upper esophagus.

Women over 40y are most likely.

52
Q

What is Plummer-Vinson symdrome?

A

Esophageal webs, iron deficiency anemia, glossitis, cheilosis, risk for carcinoma of the upper esoph.

53
Q

Esophageal Rings: what are they? “A” ring vs “B” ring? Clinical presentation?

A

Another form of mucosal overgrowth.

A ring: in lower esoph above the GE junction

B ring: (aka Schatzki’s) ring: at the GEJ

Present with episodic dysphagia

54
Q

What is this a picture of? Where anatomically does it occur? What clinical sx?

What can it progress to?

A

Mallory-Weiss Tear

Laceration at the GEJ

Presents with forceful vomiting

Can progress to Boerhaave syndrome

55
Q

What is Boerhaave Syndrome?

A

Esophageal rupture due to forceful vomiting.

Catastrophic event.

56
Q

What are these? What patients do they present in? What causes them?

A

Esophageal varices

Develop in 90% of cirrhotic patients.

Consequence of portal hypertension

57
Q

What is reflux esophagitis?

A

Reflux of acid damages esophagus, –> tissue change.

Characteristic on histo = eosinophil infiltration.

58
Q

What are the two main types of esophageal carcinoma? Which is more prevalent worldwide? in the US? Risk factors?

A

Squamous Cell Carcinoma: 90% of esop cancer worldwide. Due to alcohol, tobacco, fungus-derived carcinogens, nitrosamines

Adenoma carcinoma: 50% of esophageal cancer in US & incidence is rising. Majority arises in cases of Barrett esophagus

59
Q

What is this a pic of? how else can it present?

A

Esophageal squamous cell carcinoma - Ulcerative type (most common)

Can also present as circumferential constriction, or longitudinal ulceration.

60
Q

What are these pictures of? what is notable?

A

Esophageal squamous cell carcinoma.

Right pic is has cord-like structure, “infiltrative-looking”

61
Q

What are criteria for diagnosis of Barrett Esophagus? At what point is it more likely to develop into adenocarcinoma?

A

Endoscopic evidence of columnar epithelium in the distal esophagus

AND

Intestional metaplasia (ie goblet cells) on a mucosal biopsy from this segment.

A long segment (>3cm) of esophageal columnar epithelium is more likely to develop adenocarcinoma.

62
Q

What’s going on? what are the different types of tissue?

A

Barrett Esophagus.

Pale pink area is squamous cells

Darker area is columnar mucosa (stomach)

63
Q

What’s going on here? where are we anatomically?

A

Barrett Esophagus at the GE Junction.

Darker area is columnar mucosa, lighter pink is squamous.

64
Q

What’s this?

A

Barrett Esophagus. Note blurred GE junction with upward extension of the columnar mucosa (darker pink)

65
Q

What’s this (from the esophagus)? how can you tell?

A

Barrett Esophagus.

Presence of GOBLET cells defines the disease.

66
Q

Once you have diagnosed BE, what is important to screen for periodically?

A

Routine endoscopy to biopsy for dysplasia. Once dysplasia is found (even in normal-appearing mucosa) pt is at incr risk for progression to cancer (adenoma)

67
Q

What’s this? disease process? features?

A

Low grade dysplasia in BE. Note cells that are dark and stratified, not mature at the top (not every cell at the very edge meets with the basement membrane). Contrast with ‘normal’ BE cells.

68
Q

What’s going on? disease process?

Notable features?

A

High grade dysplasia in BE.

Nuclear:cytoplasmic ratio increased, cells are disorganized all the way to the top of the layer. No orderly arrangement. Glands are also disorganized (not back to back as normal)

69
Q

Bottom line for esophageal squamous cell carcinoma: benign or malig? more common where in world? more common where in the esophagus?

A

Malignant.

90% of esop cancer worldwide

More common in mid-esophagus.

70
Q

Bottom line for esophageal adenocarcinoma: benign or malig? more common where in world? more common where in the esophagus?

A

Malignant

50% of esop carcinoma in US

Most arise from barrett esophagus –> more common in LOWER THIRD of esop

71
Q

What’s this? notable features?

A

Benign Gastric Ulcer

Smooth base, non-elevated margins.

Rugae converce into ulcer/radiate from it.

72
Q

What is this? How is it defined as such?

A

Benign Gastric Ulcer.

Definition depends on the fact that it has eroded through the mucosa completely. (If mucosa was only halfway gone, would call it an erosion).

The distinction is important because the mucosa has only small capillaries: the major vessels are present in the submucosa. Therefore risk for hemorrhage is much higher for ulcer than for erosion.

73
Q

What’s this? how can you tell? What happens if it progresses?

A

Benign Gastric Ulcer. Can tell because it is within the muscularis propria (has gone through the mucosa).

If progresses ->can perforate the stomach wall. Stomach contents can get into the peritoneum, can be life-threatening.

74
Q

What is this? what is the likely cause?

A

Benign duodenal ulcer.

Likely cause is H Pylori

75
Q

What are the complications of gastric ulcers?

A
  • Bleeding (may be life threatening)
  • Perforation -> peritonitis
  • Gastric outflow obstruction (if ulcer is near antrum, if may heal and then fibrose, become stenotic, block outflow)
76
Q

autoimmune gastritis (AIG) is associated with what other condition?

What causes AIG?

What kinds of cells hypertrophy, and what is the risk?

A
  • Associated with pernicious anemia (B12-deficient)
  • Process = antibody-mediated destruction of parietal cells.
  • Gastric atrophy and intestinal metaplasia

Also endocrine cell hyperplasia (due to increased levels of gastrin, unsure why) –> risk of neuroendocrine tumors.

(there is low HCl production due to parietal cell destruction. The body increases gastrin release in attempt to increase HCl secretion (feedback) - hope this helps)

Long-term risk of adenocarcinoma 2-4%.

77
Q

What is this picture of?

A

Endocrine cell microcarcinoma in chronic AIG.

Note endocrine cells growing in ‘nests’ in between glands.

Look for endocrine cell hyperplasia. Here you can see intestinal metaplasia, goblet cells, some areas of oxycintic glands.

Some pyloric glands and lots of inflammation -> AIG

78
Q

What is a gastric polyp?

A

Proliferative lesion of the stomach - an outgrowth.

Can be benign or metaplastic.

79
Q

What is this a picture of? What diseases is it seen in?

A

Hyperplastic polyp.

Seen in AIG, H pylori gastritis

80
Q

What are the various types of gastric malignancies? What are the most prevalent?

A

Adenocarcinoma (90%)

Lymphoma (4%)

Neuroendocrine/Carcinoid Tumor (3%)

Gastrointestinal Stromal Tumor (2%)

81
Q

what are the two types of gastric (adeno)carcinoma?

A

Intestinal Type and Diffuse Type

82
Q

Describe the intestinal type of gastric (adeno)carcinoma. What forms can it take? What is the precursor? What does it form? M to F ratio? Incidence?

A

Exophytic, ulcerating, or infiltrative forms.

Dysplasia = precursor

Gland formation

M:F = 2:1

Decreasing incidence.

83
Q

Describe the diffuse type of gastric (adeno)carcinoma. What forms can it take? What is the precursor? What does it form? M to F ratio? Incidence?

A

Linitus Plastica (leather bottle appearance)

De Novo (no precursor)

M=F

Increasing incidence

Infiltrative growth pattern

Margins are hard to evaluate

84
Q

What is this a picture of? What are notable features?

A

Malignant gastric ulcer (carcinoma, intestinal type)

Features: irregular, necrotic base

Firm, raised margins

Rugae do not converge to center as with benign type

85
Q

What is this a picture of? what is notable?

A

Diffuse gastric cancer (carcinoma). Note leather bottle appearance. no discrete mass.

86
Q

What is this a picture of? Features?

A

Signet Ring cell carcinoma. Subcategory of Gastric Carcinoma (diffuse type)

Note large mucin-filled vacuoles with flattened peripheral nuclei.

More signet cells below.

87
Q

Gastric Adenocarcinoma: prognostic factors?

A

-Depth of invasion is most important variable

Early does NOT penetrate the muscularis propria; Advanced DOES penetrate the muscularis propria.

-Distant metastases are common in advanced stages (Virchow’s node, Krukenberg ovarian metastases)

88
Q

Gastric MALT lymphoma: what is the process that causes it?

A

H pylori infection stimulates T cells

T cells activate B cells

Initial B cell clone is T cell dependent: Lymphoma can be eradicated by antibiotics to clear H Pylori.

Later stages are T cell independent due to genetic changes (t11:18)

89
Q

What is this a picture of? What initially causes it?

A

Gastric MALT lymphoma.

Initially caused by H Pylori. Lymphocytes invade and destroy gastric glands.

90
Q

What is this? What stimulates it?

A

Gastric neuroendocrine tumor. Stimulated by gastrin. To confirm that the tumor is neuroendocrine, use an IHC stain as below.

M2 GI (41 decks)

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