stomach pathology Flashcards

1
Q

What is pyloric stenosis? presentation? treatment?

A

hypertrophy of the pyloric sphincter. more common in males. present about 2 wks after birth. projectile nonbilious vomiting, visible peristalsis, and an olive-like mass in the abdomen. treat by cutting away that muscle (myotomy).

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2
Q

acute gastritis: general schemata

A

burning of the stomach by acid: either from incr. acid production or decr. mucosal protection.

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3
Q

chronic gastritis: general schemata

A

either from H. pylori or autoimmune

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4
Q

acute gastritis: what are the normal protective forces for the stomach? risk factors?

A

imbalance btw environment and mucosal defenses.
defenses: epithelia (foveaolar cells) make mucus that protects the cells, and there is bicarb. normal blood supply is important- it takes away extra acid and keeps the epithelium alive.

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5
Q

Risk factors for acute gastritis, and why (big card- 6 reasons)

A
  1. severe burn can cause a curling ulcer (burns cause hypovolemia, which will reduce blood flow to the stomach)
  2. NSAIDs (prostaglandins are essential for creating protective border by decr. acid production and stimulating production of bicarb and mucusm and incr. blood flow
  3. EtOH: toxin damages the mucosa
  4. chemo: decreases regeneration of the cells
  5. increased intracranial pressure (VERY important). aka cushing ulcer: increased intracranial pressure = incr. vagal stimulation = increased acid production.
  6. shock (stress ulcers)
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6
Q

What are some consequences of acid damage in acute gastritis?

A
  1. superficial inflammation
  2. erosion/ loss of the epithelium
  3. ulcer (loss of the mucosal layer)
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7
Q

chronic autoimmune gastritis: where is the damage? what is damaged? what is the pathophysiology and consequence?

A

autoimmune destruction of the stomach muchos. causes destruction of the gastric parietal cells, which are located in the BODY and the FUNDUS.
T cell mediated process, which eventually causes antibodies in the blood

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8
Q

clinical features of chronic autoimmune gastritis. include location in the stomach.

A

atrophy of the mucosa with intestinal metaplasia

  1. achlorhydria (low acid production) with incr. gastrin levels and antral G-cell hyperplasia
  2. megaloblastic anemia d/t lack of intrinsic factor
  3. increased risk of gastric adenocarcinoma. (inflammatory cells cause of intestinal metaplasia in the stomach). On histo, you will see goblet cells in the stomach!
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9
Q

chronic H. pylori gastritis: causes, most common site of involvement.

A

H pylori induces acute and chronic inflammation becasue it makes ureases and proteases and inflammation. This process weakens mucosal defenses.
antrum is the most common site of involvement.

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10
Q

presentation of chronic H pylori gastritis

A

epigastric abdominal pain with an incr. risk of ulceration, gastric adenocarcinoma, and MALT lymphoma (germinal centers in the gastric wall and post-germinal center B cells- marginal zone. marginal zone only forms in chronic inflammation).

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11
Q

Treatment of H pylori; how do you know tx worked?

A

triple therapy. reduces the risk of gastritis/ulcer, reverses intestinal metaplasia. negative urea breath test and lack of stool antigen confirm eradication of H. pylori.

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12
Q

peptic ulcer disease

A

solitary mucosal ulcer involving either the proximal duodenum (90%) or distal stomach

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13
Q

duodenal vs. stomach ulcer: pain, causes, mechanism, risk of carcinoma, other factors

A

duodenal ulcer: pain decreases with meals (duodenum increases neutralizing substances whenever the patient has a meal). almost always caused by H. plyori, though zollinger-ellison syndrome (gastrinoma) is possible. usually benign. see hypertrophy of brunner glands on biopsy.
gastric ulcers:
pain worse with meals (stomach makes MORE acid in response to food)
causes: H. pylori in 70%, but also NSAIDs and bile reflux.
gastric ulcers can be caused by gastric carcinoma; often seen in older pts

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14
Q

What is a complication of duodenal ulcer?

A

1 and 2. bleeding from the gastroduodenal artery or acute pancreatitis.
remember, ulceration may be on anterior or posterior wall. anterior is more common, but if it happens on posterior wall, you can rupture the gastroduodenal artery or activate the pancreas.
3. perforation. may see free air under the diaphragm with pain referred to the shoulder.

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15
Q

gastric ulcer complications

A

ulcer usually located on the lesser curvature of the antrum. rupture carries a risk of bleeding from the left gastric artery.

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16
Q

characteristics of a benign vs. malignant ulcer

A

small, punched out ulcer with flat, normal surroundings.

malignant ulcer: larger, irregular, not punched out, lots of piling up of mucosa at the edge of the mucosa.

17
Q

What are the general characteristics of gastric carcinomas

A

malignant proliferation of surface epithelial cells (adenocarcinoma). may be intestinal type or diffuse type

18
Q

intestinal carcinoma: where is it, features, risk factors

A

large irregular ulcer with heaped up margins. most commonly involves lesser curvature of the antrum. risk factors include intestinal metaplasia (chronic autoimmune gastritis and H. pylori), nitrosamines in smoked foods, and blood type A
(sister mary joseph nodule in the periumbilical region)

19
Q

diffuse carcinoma: features,

A

signet ring cells that diffusely infiltrate the gastric wall. signet ring infiltration causes the stomach wall to react with white, fibrotic thickening, called desmoplasia (linitis plastica).
(krukenburg tumor to the bilateral ovaries)

20
Q

How does gastric carcinoma present?

A

weight loss, abdominal pain, anemia, early satiety. early satiety is for the diffuse type.
occasionally presents with acanthosis nigricans or Leser-trelat sign (dozesn of sebhorric keratosis that present all at the same time).

21
Q

Where will gastric cancer spread to?

A

left supraclavicular node (virchow node)- it drains the stomach.
distant mets usually involve the liver, though it may go to the periumbilical region (sister mary joseph nodule- seen with intestinal type). or, may be seen as bilateral mucinous ovary involvement- krukenberg tumor. seen with the diffuse type.

22
Q

menetrier disease

A

gastric hypertrophy with protein loss, parietal cell atrophy, and increased mucosus cells. precancerous. rugae of stomach are so hypertrophied that they look like brain gyri.