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GI Week 2 > Gastric Pathology > Flashcards

Gastric Pathology Flashcards

1
Q

List the potential damaging forces acting on gastric mucosa.

A 
H pylori infection
NSAIDs
Aspirin
Cigarettes
Alcohol
Gastric hyperacidity
Duodenal-gatric reflux
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2
Q

List the protective forces acting on the gastric mucosa

A 
surface mucus
bicarbonate secretion
mucosal blood flow
apical surface membrane transport
epithelial regenerative capacity
elaboration of prostaglandins
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3
Q

What’s the main mechanism of gastric mucosal injury?

A

just an imbalance between the damaging and protective factors

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4
Q

What’s the difference between a mucosal erosion and a mucosal ulcer?

A

erosion is loss and necrrosis of the surface epithelium confined to the LAMINA PROPRIA

ulceration is necrotizing process extending beyond the mucosa into the SUBMUCOSA and MUSLCE

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5
Q

What are the main causes of ACUTE gastric ulceration?

A

Acute infection with H pylori
First time NSAID use
Ingestion of large quantities of alcohol

shock, trauma, sepsis, uremia, burns (Curling ulcer) and intracranial pressure (Cushing ulcer)

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6
Q

What are the three common causes of CHRONIC gastritis?

A

H pylori
autoimmune gastritis
chronic reactive gastropathy

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7
Q

Describe the most common pathologic finding in H pylori gastritis

A

active chronic gastritis in the antrum, progressing toward the fundus

chronic inflammation with lymphocytes and plasma cells

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8
Q

Describe the complications of H pylori gastritis

A

mucosal erosions and peptic ulcers

MALT lymphoma

Gastric adenocarcinoma

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9
Q

Describe how one typically acquires H helmannii gastritis.

A

spread through contact with people’s pets - cats, dogs, pigs and nonhuman primates are carriers

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10
Q

List which H pylori diagnostic tests indicate ACTIVE infection.

A 
Breath test (urease)
Stool test (antigen)
Biopsy stains

NOT the blood antibody test - that just shows exposure

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11
Q

Describe the pathogenesis of autoimmune gastritis

A

It’s due to autoimmune CD4+ T cell-mediated destruction of parietal cells

chief cells are also lost as collateral damage

NOTE: antibodies to parietal cells and intrinsic factor are produced as part of the autoimmune response, but are not pathogenic - can be used as a diagnostic test

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12
Q

Describe the key findings of autoimmune gastritis

A
  1. decreased gastric acid secretion
  2. compensatory hypergastrinemia and hyperplasia of antral gastrin-producing G cells
  3. vitamin B12 deficiency and associated symptoms
  4. reduced serum pepsinogen concentration (lost chiefs)
  5. inflammatory mucosal damage and atrophy of the mucosa in body and fundus
  6. intestinal metaplasia
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13
Q

Describe the complications of autoimmune gastritis.

A 
Megaloblastic anemia
atrophic glossitis
malabsorptive diarrhea
peripheral neuropathy
CNS cognitive alterations

also adenocarcinoma and carcinoid

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14
Q

List the common causes of chronic reactive gastropathy.

A

it’s basically reaction to anything bad in the stomach: chemical mucosal injury associated with NSAIDs, aspirin, bile reflux and alcohol ingestion

(get proveolar hyperplasia and mucin depletion)

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15
Q

What are the two most common causes of peptic ulcer disease?

A

H pylori
chronic NSAID use
worse with both

(others are Zollinger-Ellison, GERD, heterotopic gastri cmucosa in a Meckel’s diverticulum, smoking, corticosteroids)

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16
Q

What are the three main complications of peptic ulcer disease?

A

Bleeding - clinical hemorrhage or IDA

Perforation
Obstruction (particularly when located in pyloric channel)

plus any chronic gastritis can lead to gastric atrophy with intestinal metaplasia and gastric adenocarcinoma

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17
Q

Describe the key pathological finding of eosinophilic gastritis.

A

It’s eosinophil-rich inflammation int he abscence of a known cause for the eosinophilia

probably secondary to some type of food allergic reaction

patients may have peripheral blood eosinophilia and elevated IgE levels

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18
Q

Describe the key clinical features of eosinophilic gastritis.

A

Lesions may present with a mass, large ulcer or pyloric obstruction

usually presents with a gastroenteritis

typically includes involvement at multiple sites - esophagus, duodenum, stomach, etc.

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19
Q

Describe the pathologic features of granulomatous gastritis.

A

It’s gastritis with granulomatous inflammation

you’ll see granuloma formation in the mucosa of the stomach

usually secondary to an underlying disorder

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20
Q

What are the most common causes of granulomatous gastritis?

A

Crohn’s is the most common

sarcoidosis
mycobacterial, fungal and parasitic infections
foreign body reactions

21
Q

Describe the key pathologic features of lymphocytic gastritis?

A

Gastritis characterized by marked intraepithelial lymphocytic inflammation

with CD8+ T lymphocytes

22
Q

What are the key clinical features of lymphocytic gastritis?

A

40% of cases seen in patients with celiac disease - suggests an immune pathogenesis

also seen in other disorders like Menetrier’s, H pylori and lymphocytic/collagenous colitis

23
Q

Describe the pathogenic mechanism of Menetrier’s disease

A

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

results in marked diffuse hyperplasia of the foveolar epithelium of the body and fundus of the stomach

24
Q

What will Menetrier’s disease look like morphologically?

A

Huge rugae

25
Q

Describe the clinical features of Menetrier’s disease.

A

patients will have protein-dumping enteropathy and hypoproteinemia with diarrhea, weight loss and peripheral edema

NOTE -some cases are associated with infection (esp CMV in kids)

26
Q

Describe the pathogenic mechanism of Zollinger-Ellison syndrome.

A

there is a gastrin-secreting tumor - usually in the pancreas or small bowel

leads to elevated gastrin (diagnostic test!) and parietal cell hyperplasia and increased gastric acid production

also hyperplasia of mucus neck cells with mucus hyperproduction in response

27
Q

Describe the clinical presentation of Zolinger-Ellison.

A

patients often present with PUD or chronic diarrhea.

28
Q

Describe the key features of a hyperplastic polyp

A

Basically exaggerated mucosal response to tissue injury and inflammation - typically seen in association with chronic gastritis

75% of all gastric polyps are this type and most occur in the antrum

29
Q

Describe the key features of a cystic fundic gland polyp

A

Occur in the fundus

Involve cystic dilatation of the mucosa and gastric glands

Associated wiht use of PPIs! secondry to increased fastrin secreiton in response to decreased gastric acid.

also can be seen in familial adenomatous polyposis

30
Q

Describe the key features of a gastric adenoma

A

This is a neoplastic polyp that’s just an area of dysplasia that glomed together to form a polyp basically

incidence increases with age and more common in patients with FAP

Often occur in association with chronic gastritis and intestinal metaplasia - about 30% will have adenocarcinoma

31
Q

Describe the key features of an inflammatory fibroid polyp

A

It’s mesenchymal polypoid proliferation composed of a mixture of stomal spindle cells, small blood vessels and inflammatory cells

basically a reactive “pseudotumor” seen usually in middle-aged females

32
Q

Describe the clinical presentation of congenital hypertrophic pyloric stenosis.

A

Usuallly in males

patients present in 2nd or 3rd week of life with new-onset regurgitation and persistant profectile non-bilious vomiting

physical exam will reveal a firm abdominal mass like an olive

33
Q

What’s the treatment for congenital hypertorphic pyloric stenosis?

A

Surgical myotomy is curative

34
Q

Describe the risk factors for gastric adenocarcinoma.

A
  1. chronic gastritis: H pylori, autoimmune
  2. Dietary carcinogens like nitrosamines from smoked food (japan)
  3. Mnetrier’s disease
  4. Diet lacking in fruits/veggies (lack of antioxidants)
  5. familial adenomatosis polyposis
35
Q

What are the two morphologic patterns of gastric adenocarcinoma

A

intestinal and diffuse

36
Q

What’s the intestinal type like?

A

polypoid invasive mass or invasive ulcer. More localized than the diffuse type.

shows glandular differentiation

37
Q

What’s the diffuse type like?

A

diffuse involvement with thickening of the gastric wall, producing a rigidity and a leather-bottle appearance called linitis plastica

histologically will show signet-ring cells

38
Q

What is the most common location for a GIST tumor?

A

GI stomal tumors…

can arise anywhere in the GI tract, but the stomach is the most common site - 60%

39
Q

What type of cells do the GIST tumors differentiate to?

A

interstitial cells of Cajal

40
Q

What’s the key genetic defect for GIST tumors?

A

85% have an oncogenic gain-of-function mutation of the gene encoding a receptor tyrosine kinase called KIT

another 8% have a mutation in a related tyrosin kinase receptor called the platelet-derived growth factor receptor alpha

41
Q

What’s the rational for the use of Gleevec?

A

Gleevec is imatinib which is a tyrosine kinase inhibitor typically used in CML

but a tyrosine kinase inhibitor is a tyrosine kinase inhibitor

42
Q

What’s the most common risk factor for gastric MALT lymphoma?

A

chronic inflammation associated with H pylori infection

it activates transcription factors that promote B cell growth and survival. In some cases it’s due to a translocation, but H pylori just induces it naturally without the genetic mutation

43
Q

What’s the simple first line therapy for MALT lymphoma?

A

If there’s no mutation involved, you can get regression by just treating the H pylori! Works in 60-90% of cases !

44
Q

What are the key pathologic features of a carcinoid tumor?

A

They’re tumors of well-differentiated neuroendocrine cells

Most are relatively benign, but some can be malignant and invasive

45
Q

What’s the clinical presentation of carcinoid syndrome?

A

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

caused by bioactive substances secreted by the tumor - 5HT, histamine, bradykinine, etc.

most likely means there’s liver metastases since the liver usually metabolizes these substances. Most common initial location is midgut origin = jejunum, ileum, appendix, ascending colon

46
Q

What helpful diagnostic test can assist in diagnosi for carcinoid tumors?

A

24 hr urine 5-hydroxyindoecetic acid (5-HIAA) which is a metabolite of serotonin

47
Q

What’s another example of an active neuroendocrine tumor we already talked about?

A

a gastrinoma - Zollinger-Ellison syndrome

48
Q

What IH stain is used as a neuroendocrine marker for looking at neuroendocine tumors?

A

chromogranin

GI Week 2 (11 decks)

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