Comprehensive review (2) Flashcards

1
Q

Chronic, most often solitary lesions that occur in any portion of the GI tract exposed to the aggressive actions of acid/peptic juices, often <4 cm

A

Peptic ulcers

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2
Q

Histologic definition of peptic ulcer: a breach in the mucosa that penetrates the _______; may penetrate gastric wall

A

muscularis mucosa

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3
Q

more common location of peptic ulcers

A
  • Duodenum, first part
  • Stomach, usually antrum
  • Within Barrett mucosa
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4
Q

Most frequent complication of ulcers

A
Bleeding
• Most frequent complication
• Occurs in 15-20% of patients
• May be life-threatening
• Accounts for 25% of ulcer deaths
• May be first indication of an ulcer
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5
Q

Is perforation common in ulcers?

A

rare but accounts for 70% of ulcer

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6
Q

complication of ulcers located in pyloric channel

A

obstruction from edema or scarring

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7
Q

When do we see acute gastric ulceration?

A

stress, shock, burns, trauma, NSAIDS

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8
Q

Pathogenesis of acute gastric ulceration:

A

stimulation of vagal nuclei and secretion of acid, prostaglandin inhibition, decreased oxygenation,

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9
Q

Can manifest as ulcers or erosions

• Discrete lesions with no surrounding gastritis, no chronic scarring

A

Acute gastric ulceration

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10
Q

treatment for acute gastric ulceration

A

fix the cause

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11
Q

concretions formed in the alimentary canal

A

bezoar

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12
Q
• Acute gastritis
• Gastric varicies
• Mallory Weiss syndrome:
mucosal tear to due to severe retching
These can all lead to:
A

Gastric hemorrhage; can be asyptomtatic to life threatening

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13
Q

 Massive hyperplasia of surface mucous cells

A

Menetrier disease (type of hypertrophic gastropathy)

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14
Q

 Hyperplasia of parietal and chief cells

A

Hypertrophic-hypersecretory gastropathy

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15
Q

Gastric gland hyperplasia due to excessive gastrin secretion

A

 Setting of gastrinoma: Zollinger-Ellison syndrome (type of hypertrophic gastropathy)

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16
Q

Caused by gastrin-secreting

tumors, gastrinomas

A

ZE syndrome

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17
Q

What is in the gastrinoma triange?

A

 duodenal wall
 peripancreatic soft tissue
 pancreas

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18
Q

How do pts with ZE syndrome present?

A
  • Patients often present with duodenal ulcers, GERD, or chronic diarrhea
  • 90% of ZE patients have peptic ulcers
  • Proximal dudodenum or unusual locations (distal duodenum, jejunum)
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19
Q

effect of ZE syndrome on stomach

A

 doubling of oxyntic mucosal thickness

 fivefold increase in the number of parietal cells

20
Q

induces hyperplasia of mucous neck cells, mucin hyperproduction, and proliferation of endocrine
cells

A

Gastrin

21
Q

Tx of ZE syndrome

A

• TX includes blockade of acid hypersecretion
 proton pump inhibitors
 high-dose H 2 histamine receptor antagonists
 Peptic ulcers to heal and prevents gastric perforation
 Allows treatment to focus on the gastrinoma, which becomes the main determinant of long-term survival

22
Q

Gastrinoma: Grow slowly
• 60% to 90% are____
• 75% Gastrinoma is____ (40-50 yo)

A

malignant

sporadic

23
Q

solitary gastrinoma tumors can be:

A

surgically resected
represent 75% of gastrinoma
seen in 40-50 yo

24
Q

• 25% of gastrinomas are: Multiple endocrine neoplasia type I (MEN I) (20-30)
 Usually multiple tumors or metastatic disease and seen assoicated with what else?

A

 “PPP” Pituitary Andenoma (<40y/o)

25
Q

What may GAstrinomas respond to SST analogues

A

 Gastrinoma cells contain type 2 somatostatin receptors that bind somatostatin analogues (octreotide) with high affinity

26
Q

• All patients with gastrinoma have an

elevated

A

gastrin level

27
Q

Hypergastrinemia in the presence of

elevated acid production strongly suggests

A

gastrinoma

28
Q

how must we rule out MEN1 if we suspect gastrinomas?

A

measure serum Ca and parathyroid hormone

29
Q

Cells that stain with chromagranin are suggestive of:

A

hypergastrinemia( d/t increased gastrin secreation from chronic PPI use)

30
Q

nodule or mass projecting above the mucosa and uncommon in stomach

A

Polyps

31
Q

Majority of polyps are______(inflammatory
or hyperplastic), most frequently
associated with ______

A

non-neoplastic

chronic gastritis

32
Q

proliferative gastric mucosa with acute and chronic inflammatory infiltrates in lamina propria, often multiple

A

Hyperplastic polyps

33
Q

contains proliferative dysplastic epithelium, therefore potential for malignant transformation, usually single

A

Adenoma

34
Q

What do we do to polpys?

A

remove them

35
Q

majority of malignant gastric tumors are

A

Carcinomas(90-95%)… specifically adenocarcinomas

36
Q

Leading world-wide cause of cancer death

• 2 nd most common tumor in the world

A

Gastric carcinoma

***US has declined dramaticallY

37
Q

Which type of gastric carcinoma?
• Associated with defined risk factors
• Develops from precursor lesions
• 6 th decade, males>females

A

Intestinal

38
Q

Which type of gastric carcinoma?
• Relatively constant incidence with no
known precursor lesion
• 5 th decade, males=females

A

Diffuse

39
Q

Risks: environmental for Gastric Carcinoma

A

• Diet
 Nitrites (from nitrates in water, preserved food)
 Smoked & salted food, pickled vegetables
 Lack of fresh fruit & vegetables
• Cigarette smoking
• Low socioeconomic status
• Infection by H. pylori

40
Q

What cancer is H.pylori factor for?

A

intestinal type carcioma and MALToma

41
Q

Shit about H.pylori

A
  • H. pylori causes gastritis
  • Untreated gastritis is a risk factor for gastric cancer
  • Infection increases risk 5-6x
  • Prospective epidemiologic studies
  • Geographic and socioeconomic association
42
Q

People with chronic gastritsi have what risk factors?

A

– Hypochlorhydria (favors H. pylori colonization)
– Intestinal metaplasia: precursor lesion for CA
– Setting for development of gastric adenomas

43
Q

How are gastric adenomas correlated to risk for cancer in host?

A

• Gastric adenomas
– 40% harbor carcinoma at time of diagnosis
– 30% have adjacent carcinoma

44
Q

How is Barretts a risk for gastric carcinioma?

A

• Barrett esophagus

– Increased incidence of cancer at GEJ

45
Q

How do we determine prognosis of Gastric Carcinoma?

A

• Depth of invasion the most important
factor, then lymph node involvement,
metastasis; histology not as important

46
Q

Prognosis of Gastric Carcinoma if found early and its confined

A

 If early (confined to mucosa, submucosa), 5-year survival 90-95%
 good prognosis even with + local lymph nodes

47
Q

Prognosos if carcinoma found later?

A

Advanced (into muscularis propria): <15% fiveyear survival