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(J2) GI II Test 1 > Stomach > Flashcards

Stomach Flashcards

1
Q

What are acute gastritis and gastropathy?

A

Acute gastritis:

-inflammation of the gastric mucosa w/ inflammatory cells

Gastropathy:

-inflammation of the gastric mucosa w/o inflammatory cells

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2
Q

What are causes of acute gastritis?

A

-alcohol

-tobacco

  • medications (NSAIDs/steroids)
  • shock
  • radiation/chemo
  • infections (viral/H. pylori)
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3
Q

What are causes of gastropathy?

A

Chemical irritation:

  • NSAIDs
  • smoking
  • acohol

Systemic effects:

  • hypovolemia (burns)
  • parasympathetic stimulation (brain lesions)
  • DM
  • portal HTN
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4
Q

What are the main causes of chronic gastritis?

A
  • H. pylori infection (gastritis type B)
  • autoimmune gastritis (gastritis type A)
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5
Q

What is type B gastritis?

(cause and presentation)

A

Antral-type/H. pylori gastritis:

  • most common chronic gastristis (~90%)
  • caused by chronic H. pylori infection
  • predominantly in antrum of stomach
  • typically asymptomatic w/ normal exam
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6
Q

How is type B gastritis diagnosed and treated?

A

Diagnosis (testing for H. pylori)

  • fecal Ag test
  • urea breath test (more to confirm eradication)
  • endoscopy w/ biosy

Treatment (typically only w/ development of PUD or MALT lymphoma):

-eradication of H. pylori (double abx therapy with PPI)

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7
Q

How does type B gastritis appear on endoscopy?

A

-nodules between rugae

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8
Q

What complications are associated with type B gastritis?

A
  • gastric adenocarcinoma/intestinal metaplasia
  • MALT lymphoma​
  • PUD
  • B12 deficiency/pernicious anemia*
  • hypochlorhydria*

*less pronounced/common than in type A

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9
Q

How does acute gastritis due to H. pylori differ from chonic gastritis due to H. pylori?

A

acute typically will have increased acid production

chronic will typically have decreased acid produciton due to atrophy of gastric glands

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10
Q

What is type A gastritis?

(cause and presentation)

A

Fundus-type/autoimmune gastritis:

  • less common chronic gastristis (~10%)
  • caused by cell-mediated destruciton of parietal cells
  • anti-parietal cell Abs (>90%)
  • anti-intrinsic factor Abs (70%)
  • predominantly in fundus (near esophagus) of stomach
  • typically asymptomatic w/ normal exam but can present with symptoms of vitamin B12 deficiency (atrophic glossitis, megaloblastosis, and peripheral neruopathy)
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11
Q

How is type A gastritis diagnosed and treated?

A

Diagnosis (autoimmune/megaloblastic anemia detection)

  • test for anti-parietal cell Abs and anti-IF Abs
  • CBC (megaloblastic anemia)
  • low B12
  • elevated methylmalonic acid and homocysteine
  • endoscopy w/ biosy

Treatment:

-B12 supplementation

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12
Q

How does type A gastritis appear on endoscopy?

A

-mucosal atrophy (rugae absent)

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13
Q

What complications are associated with type A gastritis?

A
  • B12 deficiency/pernicious anemia*
  • achlorhydria* -> hypergastrinemia (lack of acid inhibition of G cells) -> carcinoid/neuroendocrine tumor (5%)
  • gastric adenocarcinoma/intestinal metaplasia

*more pronounced/common than in type B

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14
Q

What complications associated with chronic gastritis are unlikely in acute gastritis?

A

mucosal atrophy or intestinal metaplasia -> adenocarcinoma

gastric dysplasia (prolonged inflammatory damage/proliferative stimuli) -> carcinoma

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15
Q

How do NSAIDs and steroids cause gastropathy?

A

prostaglandins protection gastric mucosa by:

  • inhibiting acid secretion
  • stimulating mucous production
  • stimulating bicarbonate secretion

NSAIDs:

-inhibit COX-1/2 preventing prostaglandin formation

Steroids:

-inhibit phospholipases which produce arachadonic acid which is a precursor to prostaglandins

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16
Q

What is an upper GI bleed and how does it present?

Describe the symptoms and what causes them.

A

GI bleeding from a source proximal to the ligament of Treitz (esophagus, stomach, duodenum)

-4x more common than LGIB

Presentaiton:

  • hematemesis (either bright red blood or “coffee ground”)
  • melena (dark, tarry stool; as little as 50mL of blood)
  • hematochezia; mostly associated with LGIB but occurs with significant UGIB (bright red blood; >1000mL of blood)

frank blood (emesis or per recturm) -> likely more severe bleeing

coagulation and oxidation of heme by gastirc acid -> coffee ground ememsis

oxidation of heme by bacteria in intestine (slow process) -> melena

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17
Q

What are causes of upper GI bleeds?

A
  • PUD
  • esophageal varices
  • hemorrhagic gastropathy/gastrisits
  • Mallory-Weiss tear/Boerhaave syndrome
  • Dieulafoy lesion
  • GAVE syndrome
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18
Q

What is the difference between an erosion and an ulcer?

A

Depth:

  • erosion is to the lamina propria
  • ulcer is to the submucosa
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19
Q

What are peptic ulcers?

(where and why)

A

ulceration of the gastric mucosa from chronic gastritis

Duodenal ulcers:

  • 90% of PUD
  • almost entirely caused by H. pylori
  • rarely caused by Zollinger-Ellison syndrome

Gastric ulcers:
-10% of PUD, mostly lesser curvature

  • largely caused by H. pylori
  • also caused by NSAIDs, glucocorticoids, smoking, and alcohol

Can also occur anywhere in the GI tract that gastric ectopia occurs

20
Q

How do peptic ulcers present?

How does it differ for duodenal and gastric ulcers?

A
  • epigastric gnawing or “hunger-like” pain
  • pain is intermittent but occurs for weeks
  • signs of UGIB

duodenal ulcer pain acutely IMPROVES with meals but worsens >1 hour after

gastric ulcer pain acutely WORSENS with meals

21
Q

What do peptic ulcers looks like on endoscopy?

How do they appear different from malignant ulcers?

A

Ulcers:

-small (<3 cm), round, punched-out lesions

Malignant ulcers:

-large, irregular lesions

22
Q

How are peptic ulcers treated?

A
  • eradication of H. pylori (double abx therapy with PPI)
  • cessation of other irritating factors (ie. NSAIDs, smoking, alcohol consumption)
  • intervention for active bleeding
  • biospy of gastric ulcers to r/o carcinoma
23
Q

What are possible complications of peptic ulcers?

A
  • UGIB (gastroduodenal A. and L gastric A.)
  • perforation (mostly anterior) -> peritonitis and pneumoperitoneum

-perforation (when posterior) into liver or pancreas -> pancreatitis

  • progression to gastric carcinoma (intestinal type); almost exclusively in gastric ulcers
  • obstruction (when near pylorus)
24
Q

What are the different types/causes of stress ulcers?

A

Medical/surgical stress ulcer:

-present in those with severe illness/shock (common in ICU patients)

Curling ulcer:

  • severe burns (decreased plasma volume -> mucosal atrophy)
  • “burned with a curling iron”

Cushing’s ulcers:

-brain lesions -> overstimulation of vagus nerve -> excess acid

25
Q

What is GAVE syndrome?

(description and association)

A

Gastric antral vascular ectasia (watermelon stomach):

-superficial telangiectasias of the antrum -> watermelon appearance

Associated with:

  • systemic sclerosis
  • cirrhosis/portal HTN
26
Q

What is a complication of GAVE syndrome?

A

-UGIB (from telangiectasias)

27
Q

What are Dieulafoy lesions?

A

abnormal, large mucosal arteries

  • increased risk of bleeding
  • most common in stomach
  • cause of obscure GI bleeds; can occur without h/x of GI pathology
  • can be life-threatening; obscure nature requires awareness of this as a possibility
  • UGIB/IDA symptoms
28
Q

What is Zollinger-Ellison syndrome?

(associations)

A

Primary gastrinoma:

  • gastrin-secreting tumor
  • most commonly occurs in duodenum (45%) or pancreas (25%)
  • mostly likely to metastasize to the liver
  • 25% are associated with MEN 1 (pituitary neoplasm -> gastrinoma, hyperparathyroidism (elevated Ca2+)
29
Q

How does Zollinger-Ellison present?

A
  • PUD-like symptoms that don’t respond to treatment
  • diarrhea/steatorrhea (excess duodenal acid inactivates pacnreatic enzymes)
  • weight loss
30
Q

How is Zollinger-Ellison diagnosed/differentiated from other conditions?

A

EGD: large mucosal folds (hypertorphic gastropathy)

-elevated gastrin (fasting w/o acid supressing meds)

r/o secondary gastrinoma due to MEN 1 (pituitary tumor):

  • normal PTH
  • normal prolactin
  • normal LH/FSH
  • normal GH
31
Q

How is Zollinger-Ellison treated?

A
  • PPI
  • tumor reseciton (non-metastatic)
  • chemo (metastatic)
  • treat hyperparathyroidsism (if MENS 1 related)
32
Q

What is gastroparesis?

A

-delayed gastric emptying w/o an obstuctive cause (gastric dismotility)

33
Q

What are common causes of gastroparesis?

A
  • diabetes
  • post-viral neuropathy
  • upper GI surgery (vagal injury)
  • Ménétrier’s disease (due to hypertrophy)
  • opioids
  • anticholinergics
34
Q

What symptoms are associated with gastroparesis?

A
  • N/V
  • early satiety
35
Q

How is gastroparesis treated?

A

-metoclopramide

36
Q

What is Ménétrier’s disease?

(appearance)

A

gastropathy with massive cerebriform thickening of mucosal folds

  • most prominent in gastric body and fundus
  • foveolar hyperplasia (biopsy)
37
Q

What are complications of Ménétrier’s disease?

A

protein loss -> severe hypoproteinemia with anasarca (full body swelling)

-risk of progression to gastric adenocarcinoma

38
Q

What are causes of benign gastric tumors?

(ssociation and descripition)

A
  • inflammatory and hyperplastic polyps - H. pylori (cystically elongated foveolar gland)
  • fundic gland polyps - PPI use or FAP (cystically dilated w/ flattened chief/parietal cells)
  • gastric adenoma -FAP (intestinal metaplasia)
39
Q

What are types of malignant gastric tumors?

A
  • gastric adenocarcinoma (intestinal or diffuse)
  • MALT
  • carcinoid (neuroendocrine)
  • GIST (gastrointestinal stromal tumor)

uncommon compared to other malignant tumors

40
Q

What are the subtypes of gastric adenocarcinoma?

(compare: appearance and cause)

A

Intestinal type (50%):

  • bulky, exophytic lesion (mostly lesser curvature)
  • precursor lesions: gastric ulcers (H. pylori) and Ménétrier disease
  • more common in Japan/eastern Asia (smoked foods) and men
  • genetic: APC mutation -> FAP; β-catenin gain-of-function

Diffuse (40%):

  • diffuse thickening of stomach (linitis plastica)
  • no precursor lesion, no population preferenece
  • genetic; loss of E-cadherin (allows diffuse spread
  • signet ring cells (biopsy)
41
Q

What are the metastatic patterns of gastric adenocarcinoma?

What type, if any, is each associated with?

A

Virchow node: mass in left supraclaviucal fossa

Sister Mary Joesph nodule: mass in periumbilical region (intestinal type)

Krukenburg tumor: mass in bilateral ovaries (diffuse type)

  • liver
  • lung
42
Q

What are rare signs associated with gastric carcinoma?

A
  • Leser-Trélat sign (suddent onset of multiple seborrheic keratoses)
  • acanthosis nigricans
43
Q

What is gastric MALT lymphoma?

A

marginal zone B-cell lymphoma associated with chronic gastritis due to H. pylori

  • frequently resolves with eradication of H. pylori
  • lymphocytic infiltrate of the lamina propria
  • associated with t(11;18) translocation
44
Q

What are gastric carcinoid tumors?

A

well-differentiated neuroendocrine carcinomas

  • can occur throughout GI tract (jejunum/ileum most common)
  • in stomach present MEN-1 (histamine/somatostatin) or in duodenum as Zollinger-Ellison syndrome (gastrin)
45
Q

What are GISTs?

(cell type and association)

A

gastrointestinal stromal tumor; mesenchymal origin

  • derived from interstitial cells of Cajal
  • tyrosine kinase c-KIT mutations (imatinib)
  • 50% occur in stomach
  • most common abdominal mesenchymal tumor

(J2) GI II Test 1 (14 decks)

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