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GI Week 2 - WLB > Stomach - Pathoma > Flashcards

Stomach - Pathoma Flashcards

1
Q

What is Gastroschisis?

A
  • Congenital malformation of abdominal wall
    • hole in abdominal wall
  • Leads to exposure of abdominal contents
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2
Q

What is an Omphalocele?

A
  • Persistent herniation of bowel into umbilical cord
    • contents are covered by peritoneum and amnion of umbilical cord
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3
Q

What is an Omphalocele due to?

A
  • Failure of herniated intestines to return to body cavity during development
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4
Q

What is pyloric stenosis?

A

Congenital hypertrophy of pyloric smooth muscle

(tightening of pyloric sphincter)

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5
Q

Is pyloric stenosis more common in males or females?

A

MALES

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6
Q

How does pyloric stenosis present clinically?

A
  • Not present at birth! => Takes time for stenosis to develop
    • present 2 weeks after birth with projectile nonbilious vomiting
    • peristalsis can be visible on abdomen
    • “olive-like” mass in abdomen
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7
Q

What is the treatment for pyloric stenosis?

A

Myotomy

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8
Q

What is acute gastritis?

A
  • Acidic damage to mucosa
    • “burning” of stomach by acid
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9
Q

What is acute gastritis due to?

A

Imbalance between mucosal defenses and acidic environment

  • Caused by either:
    • increased acid secretion
    • decreased protection by mucosa
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10
Q

What are the two types of Chronic Gastritis?

A
  1. Chronic Autoimmune Gastritis
  2. Chronic H. pylori Gastritis
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11
Q

What are the defenses normally present in the Mucosa of the stomach?

A
  • Epithelial lining (folveolar cells)
  • Mucus layer
  • Bicarbonate secretion
  • Normal blood supply providing nutrients and absorbing acid
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12
Q

What are the risk factors for Gastritis?

A
  • Severe burn (Curling ulcer)
    • hypovolemia, decreased blood flow, nutrient deficiency to mucosa
  • NSAIDs
    • prostaglandins decrease acid production, increase blood flow, activate mucus producing cells
  • Heavy alcohol consumption
  • Chemotherapy
    • knock out cells that are turning over => can’t regenerate cells in the stomach
  • Increased intracranial pressure (Cushing ulcer)
    • increased vagal stimulation => increased ACh => binds parietal cell receptor => increased acid production
  • Shock
    • severely decreased blood flow to stomach
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13
Q

Acid damage results in what three pathologic findings?

A
  • Superficial inflammation
  • Erosion
    • loss of epithelium
  • Ulcer
    • loss of mucosal layer
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14
Q

What happens in Chronic Autoimmune Gastritis? What is the damage associated with?

A
  • Autoimmune destruction of gastric parietal cells
    • in the body and fundus
    • T-cell mediated damage (Type IV HSR)
  • Associated with antibodies against parietal cells and/or intrinsic factor in the blood
    • useful for diagnosis
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15
Q

What clinical features are seen in Chronic Autoimmune Gastritis?

A
  • Atrophy of mucosa
  • Achlorhydria (low acid production) with increased Gastrin levels (loss of negative feedback) and antral G-cell hyperplasia
    • knocked out parietal cells
  • Megaloblastic (pernicious) anemia
    • due to lack of intrinsic factor
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16
Q

What is the most common cause of Vitamin B12 deficiency?

A

Chronic Gastritis

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17
Q

Because chronic inflammation induces intestinal metaplasia, patients with Chronic Gastritis are at increased risk for what?

A

Gastric Adenocarcinoma

18
Q

What is the most common form of gastritis?

A

Chronic H. pylori Gastritis

90%

(H.pylori-induced acute and chronic inflammation)

19
Q

What properties of H. pylori allows it to weaken mucosal defenses?

A
  • Proteases
  • Ureases
  • Inflammation
20
Q

What is the most common site of H.pylori infection in the stomach?

A

Antrum

21
Q

Patients with H.pylori-induced gastritis are at increased risk for what conditions?

A
  • Ulceration
  • Gastric adenocarcinoma
  • MALT lymphoma
    • generate germinal centers within gastric wall => develop post-germinal center B-cells => form marginal zone => Mucosa-Associated Lymphoid Tissue!
22
Q

What is the best way to resolve H.pylori gastritis/ulcers and reverse intestinal metaplasia?

A

Triple therapy treatment

23
Q

What diagnostic findings confirm eradication of H.pylori?

A
  • Negative urea breath test
  • Lack of stool antigen
24
Q

What is peptic ulcer disease?

A

Solitary mucosal ulcer involving proximal duodenum (90%) or distal stomach (10%).

25
Q

Duodenal ulcers are almost always due to what?

A

H.pylori

(rarely due to Zollinger-Ellison syndrome)

26
Q

How do patients with Peptic Ulcer Disease present clinically?

A
  • Epigastric pain that improves with meals
    • meal promotes => duodenum increases defenses and makes neutralizing substances
27
Q

What will diagnostic endoscopic biopsy show in Peptic Ulcer Disease?

A

Ulcer with hypertrophy of Brunner glands

28
Q

What is the major complication of a duodenal ulcer?

A
  • Rupture
    • can lead to:
      • bleeding from the gastroduodenal artery (posterior ulcers)
      • acute pancreatitis (posterior ulcers)
29
Q

What causes gastric ulcers in Peptic Ulcer Disease?

A
  • Usually H.pylori
  • NSAIDs
  • Bile reflux
30
Q

What clinical presentation distinguishes Gastric Ulcers from Duodenal Ulcers?

A

Gastric ulcers => pain WORSENS with meals

31
Q

Where are Gastric Ulcers usually located in the stomach?

A
  • Lesser curvature of the antrum
    • rupture carries risk of bleeding from left gastric artery
32
Q

What important disease should be included in the DDx of Ulcers?

A

CANCER

  • Duodenal ulcers are almost never malignant
  • Gastric ulcers can be caused by gastric carcinoma
33
Q

What is Gastric Carcinoma?

A

Malignant proliferation of gastric epithelial cells

(epithelial cells = columnar cells => adenocarcinoma)

34
Q

What defines the Intestinal Type Gastric Carcinomas?

A
  • Presents as large, irregular ulcer with heaped up margins
35
Q

Where are the Intestinal Type ulcers in gastic carcinoma usually found?

A

Most commonly involves lesser curvature of antrum

36
Q

What are the risk factors for Intestinal Type ulcers in gastic carcinoma?

A
  • Intestinal metaplasia
    • chronic gastritis
  • Nitrosamines in smoked food
  • Blood type A
37
Q

What defines the Diffuse Type gastric carcinoma?

A

Signet ring cells that diffusely infiltrate gastric wall

  • Signet ring cell = intracellular mucus pushing nucleus peripheral
  • Desmoplasia results in a thickening of stomach wall (linitis plastica)
    • Desmoplasia = fibrous tissue and blood vessels in response to tumor
38
Q

Unlike Intestinal Type, the Diffuse Type gastric carcinoma are not associated with what three things?

A
  • H. pylori
  • intestinal metaplasia
  • nitrosamines
39
Q

What is the clinical presentation of Gastric Carcinoma?

A
  • PRESENTS LATE!
  • Weight loss
  • Abdominal pain
  • Anemia
  • Early satiety
  • Rarely presents with acanthosis nigricans or Leser-Trelat sign
40
Q

Where does Gastric Carcinoma spread to?

A

Left supraclavicular node (Virchow node - drains the stomach)

41
Q

Distant metastasis of gastric cancer most commonly involves what organ?

A

The LIVER

  • Periumbilical type
    • Sister Mary Joseph nodule
    • seen with intestinal type
  • Bilateral ovaries
    • Krukenburg tumor
    • seen with diffuse type

GI Week 2 - WLB (11 decks)

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