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GI week 2 > gastric path > Flashcards

gastric path Flashcards

1
Q

What are the normal damaging forces of the gastric mucosa

A

acid, peptic enzymes

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2
Q

What are the some of the defense organisms of the gastric mucosa?

A

mucus, bicarb, epithelial regeneration, elaboration of prostiglandins, ect

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3
Q

What are the injury causing forces on the gastric mucosa?

A

H. pylori, NSAIDS. ASA, smoking, OH, hyperacidity, ULCER,

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4
Q

what kind of inflammation do you see if acute gastritis

A

acute NEUTROPHILS!

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5
Q

Whats the difference btwn mucosal erosion and musocsal ulcer?

A

Erosion is the loss and necorisis of surface epithelium just in the lamina propria, ulcer is beyond the mucosa- though the muscular wall

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6
Q

What are the 4 main causes of ACUTE gastric ulceration>

A
  1. Acute infection with Helicobacter organisms
  2. First time use of large doses of NSAIDs and aspirin (cyclooxygenase inhibition)
  3. Ingestion of large quantities of alcohol (direct toxic effect)
  4. Patients with shock, trauma, sepsis, uremia, severe burns, and intracranial disease can get acute stress ulcers (burns – Curling’s ulcers in duodenum; CNS injury – Cushing’s ulcers)
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7
Q

What is the the most common pathologic finding in H. pylori gastritis

A

active chronic gastritis that began in the antrum and goes into the fundus.

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8
Q

what are complications of h. pylori infections?

A

MALT-lymphoma and gastric adenocarcinoma.

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9
Q

how does one typically acquire H. helmannii gastritis.

A

organism has reservoirs in cats, dogs, pigs, and nonhuman primates-similar presentation to H. pylori

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10
Q

What are tests to see if you have an active H. pylori infection?

A

H&E stain on biopsy specimen obtained by endoscopy
diff-quick “blue stain”
immunohistochemical stains can also be used to assist in finding the organism on the biopsy.
Other diagnostic tests include H. pylori stool antigen, urea breath test, serology, and rapid urease test on fresh tissue biopsy.

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11
Q

what is th epathogensis of autoimmune gastritis

A

Due to autoimmune CD4+ T-cell mediated destruction of parietal cells; chief cells are also lost during destruction of the gastric glands (non-immune mechanism). Antibodies to intrinsic factor are also produced as part of the autoimmune response.

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12
Q

What are the key findings in autoimmune gastritis?

A

Atrophy, metaplasia, chronic inflammation in the fundus and body of stomach* but long list
Decreased gastric acid secretion (achlorhydria).
Compensatory hypergastrinemia and hyperplasia of antral gastrin-producing G cells, along with endocrine cell hyperplasia in the fundus and body of the stomach.
Vitamin B12 deficiency due to loss of secreted intrinsic factor (pernicous anemia with increased RBC MCV).
Reduced serum pepsinogen I concentration.
Inflammatory mucosal damage and atrophy of the gastric mucosa in the body and fundus with sparing of the antrum and cardia.

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13
Q

What is the clinical presentation years after autoimmune gastritis?

A

CNS changes due to B12 def, megaloblastic enemau, peripheral neuropathy,

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14
Q

What are the the common causes of chronic reactive gastropathy

A

Chemical mucosal injury associated with NSAIDs, aspirin, bile reflux and alcohol ingestion.

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15
Q

Whats the pattern seen in chronic reactive gastropathy?

A

foveolar hyperplasia*, muscin depleteion, vascular congesti`on and edema

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16
Q

Gastric antral vascular ectasia (GAVE) is like chronic reactive gastropathy, but has what interesting feature?

A

WATERMELON stomach*

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17
Q

What are the the two common causes of peptic ulcer disease

A

H. pylori chronic gastritis

chronic use of NSAID

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18
Q

what are 3 complications of peptic ulcer disease?

A

a. Bleeding (clinical hemorrhage as well as iron deficiency anemia).
b. Perforation
c. Obstruction, particularly when the ulcer is located in the pyloric channel, secondary to edema and fibrosis.
Clinically, patients present with epigastric burning or aching pain, (often occurring 1-3 hours after eating and relieved with food)*, GI bleed, iron deficiency anemia, or perforation.

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19
Q

What is Eosinophilic Gastritis? whats it possibly due to?

A

defined as eosinophil rich inflammation, in the absence of a known cause for eosinophilia, Most cases are thought secondary to some type of allergic reaction to a food allergen so yo u may see, Most cases are thought secondary to some type of allergic reaction to a food allergen , isolated site rare

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20
Q

What is Granulomatous Gastritis? What is it due to?

A

defined as gastritis with granulomatous inflammation; most cases are secondary to an underlying disorder, such as CROHNS8, sarcaoidiss, TB,

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21
Q

Granulomatous Gastritis is also in associated with what cancers?

A

gastric adenocarcinoma and gastric non-MALT lymphomas.

22
Q

lymphocytic gastritis is characterized by what? And usually seen in patients with what other condition?

A

intraepithelial lymphocytic inflammation (CD8+ T lymphocytes). celiac disease*, menetriers disease, h pylori

23
Q

What is menetriers disease caused by what? what do you see in the cells?

A

by excessive secretion of transforming growth factor alpha, see diffuse hyperplasia of the foveolar epithelium of the body and fundus of the stomach

24
Q

what are the patients symptoms with menetriers disease?

A

protein losing enteropathy and hypoproteinemia, with diarrhea, weight loss, and peripheral edema. Some cases of Menetrier’s disease are associated with an infection (e.g. CMV in children). ALSO at risk for gastric andeocaricoma

25
Q

What is Zollinger-Ellison Syndrome caused by?

A

Caused by gastrin secreting tumors (gastrinomas, a functioning type of neuroendocrine tumor), which are most commonly found in the pancreas and small bowel.

26
Q

What is the diagnostic test for ZES?

A

increased gastrin levels, this increases the number of parietal cells, and hyperplasia of the muscus cells, , and proliferation of endocrine cells in the stomach which can result in gastric carcinoid tumors.

27
Q

How do patients present with ZES?

A

PUD or chronic diarrhea

28
Q

Most gastrinomas are sporadic but the rest are associated with what?

A

MEN type 1

29
Q

what is hyperplastic polyp ASSOCAITED with? Where are they located?

A

chronic gastritis (H. pylori gastritis, chronic reactive gastropathy, autoimmune gastritis);and most occur in the gastric antrum, followed by the body

30
Q

cystic fundic gland polyp are asscoaited with what

A

proton pump inhibitors, secondary to increased gastrin secretion in response to decreased gastric acid. These polyps can also be seen in individuals with familial adenomatous polyposis (FAP). Cystic dialatesd glands with parietal, chief and foveolar cells

31
Q

gastric adenoma are asscoaited with what?

A

Neoplastic-gastric adenomas increases with age, with most occurring in patients age 50 years and older. Gastric adenomas are also increased in incidence in patients with FAP. “polypoid areas of dysplasia. “

32
Q

inflammatory fibroid polyp is what kind of polypod?

A

Mesenchymal polypoid proliferation composed of a mixture of stromal spindle cells, small blood vessels, and inflammatory cells, particularly eosinophils.

33
Q

Where do inflammatory fibroid polyp occur and who gets them?

A

Can occur anywhere in the GI tract but stomach and small intestine are the most common sites.
Usually occur in middle aged females, and are felt to represent a reactive “pseudotumor.”

34
Q

What is congenital hypertriphic pyloric stenosis due to? More common in who? What are the symptoms?

A

to hyperplasia of the pyloric muscularis propria.MALES,

35
Q

What are the symptoms of congenital hypertrophic pyloric stenosis? Cure?

A

Patients typically present in the second or third week of life with new-onset regurgitation and persistent, projectile, non-bilious vomiting. Physical examination may reveal a firm abdominal ovoid “olive” mass. Surgical myotomy is curative.

36
Q

What are the risk factors for gastric andemocarcioma?

A

Chronic gastritis, such as H. pylori* gastritis and autoimmune* gastritis (intestinal metaplasia-dysplasia-carcinoma sequence).
o Dietary carcinogens (nitrosamines, smoked foods).
o Menetrier’s disease.
o Diets lacking in fruits/vegetables (antioxidants).
o Patients with familial adenomatosis polyposis (FAP).

37
Q

Whats the most common maligancy of the stomach?

A

gastric adenocarcioma

38
Q

the intestional type of gastric carcinoma has what morphology?

A

can present as a polypoid invasive mass or invasive ulcer. Microscopically, tumor shows glandular differentiation.

39
Q

the diffuse type of gastric carcinoma has what morphology?

A

presents as diffuse involvement and thickening of the gastric wall (mucosa, submucosa, and muscularis propria). Microscopically, see signet-ring cells. Sometimes, this type of tumor can occur in younger adults. Diffuse involvement of the gastric wall can produce rigidity and a leather bottle appearance (linitis plastica)*.

40
Q

Where do most adenocarcinomas happen?

A

@ GE junction and atrum

41
Q

What kind of tumor is a GIST tumor?

A

cKIT- one hit mutation gain of function mutations coding for TYROSINE KINASE!, Another 8% platelet-derived growth factor receptor alpha (PDGFRA).

42
Q

Where is a GIST tumor located

A

stomach is the most common site (60% stomach) followed by jejunum, ileum, and duodenum, colorectal is the rarest

43
Q

What kind of cells are in the GIST tumors?

A

towards interstitial cells of Cajal, specialized cells involved in gut peristalsis.

44
Q

Why use gleevac in GIST tumors?

A

inhibits tyrosine kinase

45
Q

Whats the most comon gastric lymphoma? whats a major risk factor?

A

MALT- chronic inflammation H. PYLORI!

46
Q

Whats a simple way to prevent malt?

A

treat the H. pylori infection -eradication of H. pylori infection with antibiotics will cause regression of gastric MALT lymphoma in 60-90% of cases

47
Q

what are the signs of carcinoid syndrome>

A

cutaneous flushing, sweating, bronchospasm, colicky abdominal pain, diarrhea, and right sided valvular fibrosis.

48
Q

what is carcinoid syndrome due to

A

seratonin, histamine, and bradykinin .

49
Q

what does carcinoid syndrome indicate?

A

Most of the neuroendocrine tumors producing carcinoid syndrome are of midgut origin (jejunum and ileum, appendix, ascending colon). metastatic disease ,

50
Q

How do you diagnosis carcinoid syndrome?

A

24 hour urinary 5-hydroxyindoleacetic acid (5-HIAA), a metabolite of seratonin.

GI week 2 (8 decks)

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