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GI Week 2 > Gastric Path Nelson > Flashcards

Gastric Path Nelson Flashcards

1
Q

Describe the normal damaging forces on gastric mucosa

A

Gastric Acidity

Peptic Enzymes

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2
Q

Describe the defensive forces of the gastric mucosa

A
  • Surface mucus secretion
  • Bicarb secreted in mucus
  • Mucosal Blood flow
  • Apical surface membrane transport
  • Epithelial regenerative capacity
  • Elaboration of prostaglandins
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3
Q

Main general mechanisms of mucosal injury

A 
-H. pylori infection
NSAIDS
Aspirin
Cigarettes
Alcohol
Gastric Hyperacidity
Duodenal-gastric reflux
Leads to:
Ischemia
Shock
Delayed gastric emptying
Host factors
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4
Q

What are the layers of an ulcer?

A

Necrosis
Inflammation
Granulation Tissue
Fibrotic scar (only present in chronic lesions)

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5
Q

What are some causes of acute gastritis?

A
  • Acute infection H. pylori
  • First time, large dose NSAIDS
  • Alcohol
  • Acute stress ulcers from shock trauma, sepsis, uremia, burns, etc.
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6
Q

Most common pathologic finding in H. pylori gastritis

A

Active chronic gastritis beginning in Antrum and progressing to fundus

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7
Q

Complications of H. pylori infection

A

MALT lymphoma

Gastric adenocarcinoma

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8
Q

How does one acquire H helmanni gastritis?

A

Reservoir in cats, dogs, pigs, and non human primates

Dogs licking your face????? WHAT????

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9
Q

Which H. pylori diagnostic test indicate active infection?

A
  • double check this one
  • Stool antigen
  • Urea breath test
  • Rapid urease test on fresh tissue biopsy
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10
Q

Pathogenesis of autoimmune gastritis

A

CD4+ T-cell mediated destruction of parietal cells (and chief cells).

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11
Q

Key findings and complications of autoimmune gastritis

A
  • decreased gastric acid secretion
  • Compensatory hypergastrinemia, hyperplasia of G cells and ECL cells
  • B12 deficiency (loss of intrinsic factor)
  • Reduced pepsinogen
  • Mucosal damage and atrophy
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12
Q

Common causes of chronic reactive gastrophy

A 
-chemical mucosal injury
NSAIDS
Aspirin
Bile reflux
Alcohol
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13
Q

Two common causes of peptic ulcer disease

A
  • H. pylori infection

- Chronic use of NSAIDS

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14
Q

Three complications of peptic ulcer disease

A
  • Bleeding
  • Perforation
  • Obstruction (especially when the ulcer is located in the pyloric channel)
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15
Q

Key features of eosinophilic gastritis

A

Eosinophil rich inflammation in the absence of a known cause for eosinophilia

Rare

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16
Q

Key features of granulomatous gastritis

A

Graulomatous inflammation

Usually secondary to underlying disorder: Crohn’s, Sarcoid, mycobacterial or fungal infections

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17
Q

Key features of lymphocytic gastritis, which T-cells?

A

Gastritis with lymphocytic inflammation = CD8+ T cells

18
Q

Menetrier’s Disease

A

Rare

Excessive secretion of transforming growth factor alpha (TGF-alpha)

Results in diffuse hyperplasia of the foveolar epithelium

19
Q

Zollinger-Ellison Syndrome

A

Caused by gastrin secreting tumors

Elevated gastrin results in increased parietal cells = increased gastric acid production

20
Q

Hyperplastic Polyp

A

Most common

Exaggerated mucosal response to tissue injury/inflammation

Associated with chronic gastritis

21
Q

Cystic fundic gland polyp

A

Most associate with PPIs secondary to increased gastric secretion in response to decreased gastric acid

22
Q

Gastric Adenoma

A

Neoplastic polyp morphologically similar to other adenomas found in GI tract

23
Q

Inflammatory fibroid polyp

A
  • mesenchymal polypoid proliferation
  • mixture of stromal spindles cells, blood vessels, inflammatory cells
  • common in middle aged females
24
Q

Clinical presentation and treatment of congenital hypertrophic pyloric stenosis

A

Stenosis due to hyperplasia of pyloric muscularis propria

more common in males

presents 3rd ish week of life: regurgitation and projectile vomiting

Surgical myotomy is curative

25
Q

Risk factors for gastric adenocarcinoma

A
  • Chronic gastritis
  • Dietary carcinogens
  • Menetrier’s Disease
  • Diets w/out antioxidants
  • Familial Adenomatosis Polyposis
26
Q

Two morphological patters of gastric adenocarcinoma

A

Intestinal type = invasive mass or ulcer, glandular differentiation

Diffuse type= thickening of gastric wall, signet-ring cells

27
Q

Most common location of GIST tumor

A

Stomach

28
Q

What types of cells do GIST tumors differentiate to?

A

interstitial cells of Cajal, specialized cells involved in gut peristalsis

29
Q

What is the key genetic defect of GIST tumor?

A

oncogenic, gain-of-function mutations of the gene encoding receptor tyrosine kinase KIT.

30
Q

What is the rational for the use of Gleever in GIST?

A

Gleever = tyrosine kinase inhibitor

To treat GIST (gain of function mutations for tyrosine kinase KIT)

31
Q

Most common risk factor for gastric MALT lymphoma

A

H. pylori infection

32
Q

First line therapy for gastric MALT lymphoma

A

Eradication of H. pylori infection with antibiotics

33
Q

Pathogenesis of carcinoid syndrome?

A

?

34
Q

Diagnostic test for carcinoid syndrome

A

?

35
Q

Define peritonitis, common causes?

A

Defined as inflammation of the thin, mesothelial covered layer of tissue that lines the abdominal cavity (peritoneum)

Many causes: perforation of viscus, diverticulitis, leakage of bile contents causing irritation, foreign material, localized hemorrhage

36
Q

Define ascites

A

Accumulation of excess fluid in peritoneal cavity

37
Q

Most common cause of ascites?

A

portal hypertension associated with cirrhosis

38
Q

Most significant complication of ascites?

A

spontaneous bacterial peritonitis

39
Q

Rational for laboratory test on ascitic fluid?

A

cell count- determine if infection
Gram stain/culture - duh
Albumin/total protein- determine if exudate or tansudate
Fluid cytology if malignancy is suspected

40
Q

Which two metastatic tumors are most common cause of malignant ascites?

A

?

41
Q

Define idiopathic retroperitoneal fibrosis

A

A dense fibrosing process that can result in renal failure due to ureteral obstruction

GI Week 2 (11 decks)

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