Diseases of the Stomach and Duodenum Flashcards

1
Q

Common complaint with disorders of the stomach

A

Dyspepsia

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2
Q

inflammatory changes in the gastric mucosa

A

gastritis

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3
Q

Common causes for erosive and hemorrhagic gastritis conditions

A

stress, NSAIDs, and alcohol, portal hypertension

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4
Q

What are contributors for nonerosive, nonspecific gastritis?

A

H. pylori, pernicious anemia, eosinophilic gastritis

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5
Q

Symptoms include: anorexia, epigastric pain, N/V, and upper GI bleeding

A

erosive or hemorrhagic gastritis

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6
Q

What symptoms are associated with upper GI bleeding?

A

melena, coffee ground emesis, blood w/nasogastric suction

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7
Q

What is included in the work-up of an upper GI bleed?

A

CBC, serum Fe, upper endoscopy

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8
Q

How soon might stress gastritis occur in a critically ill patient?

A

within 72 hrs of admission

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9
Q

Treatment for GI bleeding secondary to stress induced gastritis

A

IV PPI bolus followed by continuous infusion

Sucralfate suspension given orally

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10
Q

What subtype of NSAIDs have a lower incidence of significant ulcer formation?

A

Cox-2 inhibitors

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11
Q

What should be ordered if a patient presents with dyspepsia and any of the following symptoms: severe pain, weight loss, vomiting, GI bleeding, anemia?

A

upper endoscopy-these are red flags

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12
Q

What is the treatment for a patient who presents with dyspepsia and no associated red flags?

A

discontinue NSAIDs, trial PPI 2-4wks. If no improvement, endoscopy referral

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13
Q

Due to excessive ETOH consumption. Symptoms include dyspepsia, nausea, emesis, minor hematemesis

A

Alcoholic Gastritis

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14
Q

Treatment for alcoholic gastrititis

A

H2 blockers or PPIs and sucralfate 2-4 weeks

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15
Q

Treatment for portal hypertensive gastropathy

A

propranolol or nadolol

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16
Q

Break in the gastric or duodenal mucosa >5mm in diameter and extend through muscularis mucosae. Can be caused by too much acid or pepsin

A

Peptic ulcer disease

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17
Q

Most common location for gastric ulcers

A

antrum

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18
Q

What is the difference between duodenal ulcers and gastric ulcers in terms of their age distribution at presentation?

A

duodenal ulcers more common btw 30-55yrs and gastric ulcers are more common btw 55-70 yrs

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19
Q

What are the two most common etiologies of peptic ulcers?

A

NSAIDs and chronic H.pylori infection

20
Q

Clinical presentation includes: dyspepsia, periodic pain in epigastric region relieved w/food or antacids, sometimes nocturnal pain

A

peptic ulcers

21
Q

Physial exam is often normal. Might be epigastric tenderness w/deep palpation. FOBT or FIT may be positive

A

peptic ulcers

22
Q

Test of choice for the work-up of peptic ulcers

A

upper endoscopy

23
Q

What type of imaging is needed if ulcer perforation is suspected?

A

abdominal CT

24
Q

What are the primary pharmacological medications for peptic ulcer disease?

A

PPIs and H2 blockers

25
Q

What are the second line agents to enhance mucosal defenses in peptic ulcer disease?

A

bismuth, misoprostol, and antacids

26
Q

How soon are 90% of duodenal and gastric ulcers healed after PPI therapy has been initiated?

A

duodenal ulcers in 4 weeks.

gastric ulcers in 8 weeks.

27
Q

How soon are 85-90% of duodenal ulcers and gastric ulcers healed after initiation of H2 blocker therapy?

A

duodenal ulcers at 6 weeks. gastric ulcers at 8 weeks

28
Q

Drug that should be avoided with H2 blockers

A

Cimetidine

29
Q

Causes 75-90% of duodenal ulcers. Associated with increased gastric acid secretion. fecal-oral spread. Increases risk of gastric cancer

A

h. pylori infection

30
Q

Combination therapy for H.pylori eradiaction

A

2-3 antibiotics + PPI or bismuth (“Triple or Quadruple Therapy”)

31
Q

Treatment after triple or quadruple therapy for ulcers

A
Small ulcer (<1 cm) no further treatment. Large or complicated ulcer 
continue PPI for up to 6 weeks
32
Q

When should a patient be retested for H.pylori?

A

> 4 weeks post antibiotic therapy and > 2 weeks post discontinuation of PPI

33
Q

Gastrin secreting gut neuroendocrine tumor. Causes hypergastrinemia from increase acid secretion

A

Zollinger-Ellison Syndrome (Gastrinoma)

34
Q

Where are most tumors located in Zollinger-Ellison Syndrome (Gastrinoma)?

A

duodenal wall (45%)

35
Q

Cinical presentation includes: dyspepsia, peptic ulcers, diarrhea/steatorrhea/weight loss if pancreas affected

A

Zollinger-Ellison Syndrome (Gastrinoma)

36
Q

What is the best imaging study to find tumors associated with Zollinger-Ellison Syndrome (Gastrinoma)?

A

SPECT: Somatostatin receptor scintigraphy (SRS)

37
Q

Delayed gastric emptying in the absence of a mechanical obstruction

A

gastroparesis

38
Q

Common causes of gastroparesis

A

1-idiopathic (~50%), post-op, DM

39
Q

Which type of DM patient is more likely to experience gastroparesis?

A

type 1

40
Q

What are two viruses that may cause gastroparesis?

A

norwalk and rotavirus

41
Q

Symptoms include: N/V, early satiety, bloating, upper abdominal pain

A

gastroparesis

42
Q

What are the dietary modifications to help treat gastroparesis?

A

small meals 4-5x, low fat, avoid insoluble fiber/ETOH/carbonation/tobacco

43
Q

Name the prokinetics used to treat gastroparesis

A

Metaclopramide and Macrolide antibiotics

44
Q

Prokinetic that is used as a liquid formulation 15 min prior to eating. serious drug interactions that can lead to irreversible tardive dyskinesia. 12 week prescription with 2 week holiday

A

Metoclopramide

45
Q

Prokinetic that induces gastric contraction and stimulates fundic contractility. Liquid formulation 40-250mg TID. Use no longer than 4 weeks

A

Erythromycin

46
Q

First line antiemetic for persistant N/V caused by gastroparesis

A

Diphenhydramine 12.5mg po q 6-8 hrs

47
Q

Surgical treatment for refractory cases of gastroparesis

A

Gastrostomy tube for decompression and jejunostomy for feeding