BAP37 - Gastric pathology Flashcards

1
Q

4 parts of the stomach?

A
  1. Cardia
  2. Fundus
  3. Body
  4. Antrum
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2
Q

Where can mucus secreting glands be found in the stomach?

A

all 4 parts

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3
Q

Where are endocrine cells (G cells) located in the stomach? What do they secrete?

A

Antrum

Gastrin

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4
Q

Where are parietal cells located in the stomach? What do they secrete?

A

Body

HCl

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5
Q

Where are chief cells located in the stomach? What do they secrete?

A

Body

Pepsin

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6
Q

Acute gastritis means transient mucosal inflammation, which may lead to? (4 marks)

A

Erosion: breach in the epithelium of mucosa;
Ulcer: breach in the mucosa, with extension into submucosa or deeper

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7
Q

Name the possible etiologies of acute gastritis.

5

A
  1. NSAID, aspirin
  2. Metabolic: alcohol, chemical..
  3. Tramatuc: NG tube
  4. Severe stress, e.g. severe burns (Curling ulcer)
  5. CNS injury (Cushing ulcer)
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8
Q

Which of the following about acute gastritis is incorrect?
A. Curling ulcer occurs in proximal duodenum
B. Curling ulcer is associated with severe burns and trauma
C. Cushing ulcer occurs in stomach, duodenum and esophagus
D. Cushing ulcer is associated with stimulation of vagal nerve that causes an increase in acid secretion
E. It is always symptomatic

A

E

Can be asymptomatic.
Symptoms:
- epigastric pain
- bleeding: hematemesis, melena, massive blood loss

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9
Q

What are the 2 types of chronic gastritis? Which type is more common?

A
  1. H.pylori-associated (>80%)

2. Autoimmune (10%)

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10
Q

What disease is H.pylori chronic gastritis associated with?

A

Gastric and duodenal ulcer

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11
Q

What disease is autoimmune chronic gastritis associated with?

A

Pernicious anemia

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12
Q

H.pylori chronic infection is located at which part of the stomach?

A

Antrum

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13
Q

Autoimmune infection in chronic gastritis is located at which part of the stomach?

A

Body

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14
Q

Pathogenesis: features of H.pylori chronic gastritis?

4

A
  • Flagella: motility
  • Urease: generate ammonia to neutralise gastric acid
  • Adhesins: enhance adherence to foveolar cells (mucous cells)
  • Toxins (CagA): carcinogenesis
  • Overwhelm mucosal defences&raquo_space;> pangastritis
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15
Q

Pathogenesis of autoimmune chronic gastriris?

A
  1. Antibodies attack parietal cells > loss of H+/K+ ATPase
  2. no ATPase > achlorhydria > hypergastrinemia to produce more acid by G cell
  3. Lack IF, thus absorption of vitamin B12 reduced in ileum

> > Megaloblastic anemia (pernicious anemia)

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16
Q

Which of the following is correct?

A. HP chronic gastritis may cause gastric adenoCA
B. Autoimmune chronic gastritis may cause gastric adenoCA
C. Lymphoma is a complication of HP chronic gastritis
D. Peptic ulcer is a complication of HP chronic gastritis

A

All of the above

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17
Q

In histology of HP caused chronic gastritis, HP is concentrated in the mucous layer, __________ and ___________can be seen due to the acute and chronic inflammation.
Glandular atrophy can also be seen.

A

acute: neutrophils
chronic: lymphocytes

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18
Q

In autoimmune chronic gastritis, we can see ___________ hyperplasia.
Lymphocyte infiltration can be seen due to the chronic inflammation. Diffuse _______ atrophy too.

A

Endocrine G cell;

glandular

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19
Q

In both autoimmune and HP caused chronic gastritis, describe how it becomes adenoCA.

A

Intestinal metaplasia > Glandular dysplasia > Adenocarcinoma

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20
Q

What are the most common risk factors for peptic ulcer diseases (PUD)? (2)

A
  1. NSAID use
  2. HP infection

Pathogenesis: imbalances of mucosal defences and damaging forces > chronic gastritis > PUD

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21
Q

If the PUD is caused by HP infection, where is the MC location for the ulcer to be?

A

D1 of duodenum, then the antrum

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22
Q

PUD is common at lower esophagus if the patient has _______.

A

GERD

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23
Q

Which of the following about the clinical manifestation of PUD is incorrect?

A. Epigastric burning
B. Tend to occur 1-3 hours after meal
C. Pain is worse in the morning
D. Pain from duodenal ulcer is relieved by alkali or food

A

C

worse at night!

24
Q

Which of the following are complications of PUD?

A. Stenosis due to scarring
B. IDA
C. Perforation

A

All of the above

B: due to bleeding

25
Q

Describe the gross morphology of a peptic ulcer. (3)

A
  1. Solitary, round to oval ulcers
  2. with sharply punched-out, slightly elevated around the edges
  3. fibrosis causes puckering of surrounding mucosal folds (congestion, edematous)
26
Q

What are the 4 layers of ulcer?

A
  1. Necrotic debris
  2. Acute inflammation
  3. Granulation tissue
  4. Fibrosis

(NIGS)

27
Q

Are duodenal ulcers or gastric ulcers more common?

A

Duodenal ulcers (75%)

28
Q

Difference in location in duodenal vs gastric ulcer.

A

Duodenal: D1
Gastric: lesser curvature

29
Q

Risk of malignancy in duodenal vs gastric ulcer?

A

Duodenal: no, therefore no need for biopsy

Gastric: small risk , need for biopsy

30
Q

Duodenal vs gastric ulcer: which of their epigastric pain is exacerbated by food?

A

Gastric ulcer

Duodenal: relieved by food
happens few hours after eating when the acid goes down, food as buffer

31
Q

Complications of gastric ulcer include bleeding from the __________ artery and perforation.

A

left gastric

32
Q

Complications of duodenal ulcer include:

A. Bleeding from GDA
B. Perforation
C. Gastric outlet obstruction
D. pancreatitis
E. Posterior ulcer
A

All of the above

33
Q

Gastric polyps are mostly non-neoplastic/ neoplasitic?

A

Non-neoplastic >90%

34
Q

What are the 2 types of Non-neoplastic gastric polyps?

A
  1. Hyperplastic/inflammatory polyps in chronic inflammation

2. Fundic gland polyps, related to use of PPI

35
Q

For neoplastic gastric polyps, what can it become?

A

Adenocarcinoma

36
Q

State the 4 origins of malignant neoplasms in the stomach and state what type of neoplasm they will give rise to respectively.

A
  1. Epithelium: Carcinoma (85-90%)
  2. Lymph node: Lymphoma (5-10%)
  3. Stroma: Mesenchymal tumor (GI stromal tumor GIST)
  4. G cells (endocrine cells): Carcinoid tumor
37
Q

Where is the MC sites of gastric adenocarcinoma?

A

Lesser curvature and antrum&raquo_space;> cardia

38
Q
Which of the following are risk factors for gastric neoplasms?
A. Smoking 
B. HP infection
C. EBV infection
D. Nitrosamine diet
E.  Smoked food
F. Pernicious anemia
G. Lynch syndrome
A

All of the above

39
Q

What is type 4 linitis plastica (Borrmann classfication) in gastric neoplasms?

A

diffuse infiltration due to desmoplastic reaction that stiffens the gastric wall

40
Q

In Lauren classification, what are the 3 types of gastric neoplasms?

A
  1. Intestinal type (MC)
  2. Diffuse type
  3. Mixed type
41
Q

Which of the following about intestinal type of gastric neoplasms is incorrect?

A. No family history association
B. Mostly due to environmental factors and gastric disease
C. Histology shows discohesive picture with gland formation
D. 10-15% with HER2 amplification
E. Prognosis is better than diffuse type

A

C.

Histology shows cohesive, with gland formation and mucin!

42
Q

In diffuse type of gastric neoplasm, it is associated with Hereditary diffuse gastric cancer syndrome: with __________ mutation, in which cell junctions are defective, causing diffusion.

A

E-cadherin

43
Q

What can be seen in histology of diffuse type of gastric neoplasm?

A
  1. Discohesive mucinous cells > 2. signet ring cell
  2. Linitis plastica
  3. Poorly differentiated
44
Q

Which of the following can be the clinical findings of malignant neoplasms of the stomach?

A. Cachexia
B. Epigastric pain
C. Vomiting
D. Melena 
E. Metastasis
A

All of the above, but not necessary

45
Q

Give examples of metastasis from gastric neoplasm.

A
  1. Left supraclavicular node (Virchow)
  2. Umbilicus (Sister Mary Joseph nodule)
  3. Ovaries (Krukenberg tumor)
46
Q

Prognosis of gastric malignant neoplasm depends on _____________?
Early: limited to?
Advanced: infiltrated into?

A

TNM staging
• Early: limited to mucosa/submucosa
• Advanced (poor survival): infiltrated into muscularis propria

47
Q

What is the MC extra-nodal lymphoma?

A

Gastric lymphoma

48
Q

Gastric lymphoma is mostly non-Hodgkin B cell lymphoma, associated with ________ infection.

A

HP/EBV

*HP eradication thus treats 70% of the case

49
Q

How can gastric lymphoma be classified?

A

o Low grade B-cell lymphoma: MALToma, related to HP

o High grade B-cell lymphoma: transformed to diffuse large B-cell lymphoma (DLBCL)

50
Q

For GI stromal tumor, what are the MC site in the GI system?

A

Stomach > SB > LB

51
Q

_________ cells can be observed in GIST patients.

A

Spindle

52
Q

__________originates from interstitial cells of Cajal (ICC) in muscularis propria.

A

GIST

53
Q

GOF mutation of ________ or related PDGFRA (95%) causes GIST. Thus, what can be used to treat it?

A

c-KIT;

c-KIT Tyrosine kinase inhibitor (Imatinib) for unresectable/metastatic tumor

54
Q

Carcinoid tumor is the tumor of endocrine cells (G cells).

What are the 3 types of carcinoid tumors?

A

Type I: A/w autoimmune chronic atrophic gastritis (A-CAG)

Type II: A/w Multiple endocrine neoplasia type 1 (MEN-1) and Zollinger-Ellison syndrome

Type III: Sporadic

55
Q

Carcinoid tumors have organoid pattern in histology, as well as immunoreactivity to _______________ like synaptophysin and chromoganin.

A

neuroendocrine markers