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GI II > Clinical Approach to the GI Patient: Dyspepsia/Pyrosis/ Heartburn/ Indigestion > Flashcards

Clinical Approach to the GI Patient: Dyspepsia/Pyrosis/ Heartburn/ Indigestion Flashcards

1
Q

what 3 things should you consider if a patient comes in with dyspepsia/ heartburn/ indigestion?

A

GERD, gastritis, or PUD

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2
Q

what is acute gastritis?

A

inflammatory changes in the gastric mucosa (imbalance between mucosal defenses and acidic environment)

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3
Q

what are the two categories of acute gastritis?

A

erosive (eg superficial erosions, deep erosions, hemorrhagic erosions) and non-erosive (generally caused by Helicobacter pylori: starts acute–> chronic)

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4
Q

how does acute gastritis present?

A

hitologic inflammation (neutrophil infiltration); may or may not have symptoms

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5
Q

what is the cause of acute gastritis?

A

alcohol, medications (NSAIDs/steroids), cocaine, ischemia (sepsis/shock), viral, bacterial, H. pylori, stress, radiation, allergy

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6
Q

if a patient with acute gastritis does have symptoms, what might they be?

A

abdominal pain (nondescript epigastric discomfort)- dyspepsia, nausea, vomiting, anorexia, belching, bloating

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7
Q

what might the physical exam be on a patient with acute gastritis?

A

likely normal; maybe epigastric pain

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8
Q

how do you make the diagnosis of acute gastritis?

A

EGD with biopsy and H. pylori testing

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9
Q

what is the treatment/management for acute gastritis?

A

endoscopy intervention for bleeding; PPI, sucralfate, H2 blockers; treat/avoid/stop underlying cause; avoid smoking and caffeine; treat H. pylori infection: eradication

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10
Q

what are the complications associated with acute gastritis?

A

bleeding and PUD

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11
Q

what is chronic gastritis and what are the two forms?

A

lymphocyte and plasma cell infiltration; Type A: auto immune; type B: bacterial H. pylori

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12
Q

where does type A chronic gastritis occur?

A

fundus of the stomach

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13
Q

how can type A chronic gastritis be characterized?

A

loss of rugal folds; common in the elderly; antibodies to parietal cells present in about 90% of cases; anti-intrinsic factor antibodies are present in 70% of cases

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14
Q

where does type B chronic gastritis occur?

A

antrum of the stomach

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15
Q

which type of chronic gastritis is the most common?

A

Type B

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16
Q

what is the common presentation/symptoms of someone with chronic gastritis?

A

often asymptomatic, could have abdominal pain (nondescript epigastric discomfort)- dyspepsia

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17
Q

what might the physical exam look like in a patient with chronic gastritis?

A

likely normal; epigastric pain, neuropathy (from vitamin B12 deficiency)- seen in both types; diarrhea/flushing (carcinoid symptoms)- seen in autoimmune type

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18
Q

how can you diagnose chronic gastritis in general?

A

with an EGD with biopsy

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19
Q

how can you diagnose type B chronic gastritis?

A

detection of H. pylori

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20
Q

what ways can you detect H. pylori?

A

fecal antigen test, urea breath test; IgA antibodies in serum; upper endoscopy with gastric biopsy for H. pylori

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21
Q

how can you diagnose type A chronic gastritis?

A

CBC, serum cobalamin (B12), intrinsic factor (IF) antibodies, parietal cell antibodies

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22
Q

what is the treatment for type b chronic gastritis?

A

eradication of H. pylori is recommended with PUD and Gastric MALT lymphoma

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23
Q

what is the treatment for type A chronic gastritis?

A

parenteral B12 (cyanocobalamin) supplementation; if dysplasia or small carcinoids are found, then this requires periodic endoscopic surveillance

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24
Q

what are the complications associated with both types of chronic gastritis?

A

B12 deficiency and an increased risk of gastric adenocarcinoma (autoimmune»H. pylori)

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25
Q

what are the complications associated with type A chronic gastritis?

A

Achlorhydria–> hypergastrinemia–> 5% can develop carcinoid tumors; pernicious anemia (gastritis)- megaloblastic (aka macrocytic)- B12 deficiency

26
Q

What are the complications associated with type B chronic gastritis?

A

MALT lymphoma (gastric B cell lymphomas)

27
Q

What are the microbiology characteristics associated with H. pylori?

A

gram negative, spiral (curved), microaerophilic, urease-producing rods (baccili) with flagella

28
Q

where do H. pylori mainly colonize?

A

the gastric antral mucosa

29
Q

what happens when H. pylori colonize the gastric antral mucosa?

A

90% of those colonized are asymptomatic and don’t need screening or treatment; 10% will develop ulcer disease/ gastritis

30
Q

what does H. pylori release that increases the risk of ulcer and gastric cancer?

A

Cag-A positive toxin

31
Q

what group of people is at risk for H. pylori infection?

A

immigrants from developing countries, poverty/low socioeconomic status, overcrowding, rural, limited education, increases with age

32
Q

how can you detect H. pylori?

A

fecal antigen test, urea breath test, IgA antibodies, upper endoscopy with gastric biopsy

33
Q

what are the complications associated with H. pylori infection?

A

gastritis–> can lead to atrophic gastritis and gastric cancer- adenocarcinoma- MALToma

34
Q

what is treatment for MALToma?

A

treating the H. pylori infection

35
Q

what is the treatment for H. pylori infection?

A

combination therapy: antibiotics and acid reducing medications (3-4 drugs) x 14 days

36
Q

What is important to note about post treatment of H. pylori infection?

A

you need to confirm successful eradication using either the urea breath test, fecal antigen test, or endoscopy with biopsy

37
Q

when should you check for successful eradication of H. pylori?

A

at least 4 weeks after completion of antibiotic treatment and 1-2 weeks after proton pump inhibitor treatment

38
Q

where do most of the gastric (peptic) ulcers occur?

A

in the lesser curvature of the antrum of the stomach

39
Q

what is the etiology of gastric (peptic) ulcers?

A

H. pylori (up to 75% of cases); smoking

40
Q

what are the risk factors for developing gastric ulcers?

A

glucocorticoids (corticosteroids) and chronic NSAID/salicylate use (15-30% if GUs)

41
Q

what might the history/ presentation be of someone with a gastric ulcer?

A

can be asymptomatic; dyspepsia- burning epigastric pain within 30 minutes of eating food, symptoms worse–> food aversion; nausea, anorexia–> weight loss, bloating, could have guarding or rigidity if complications

42
Q

how do you diagnose a gastric ulcer?

A

EGD with biopsy (diagnostic and therapeutic)- must do this to exclude malignancy in gastric ulcers; hemoglobin/hematocrit (anemia?); BUN/creatinine; x-ray/CT/MRI if suspect a complication; detection of h. pylori

43
Q

what is the treatment for gastric ulcers?

A

secondary prevention: exclude malignancy (follow endoscopically to healing: EGD with repeat biopsy of ulcer); acid suppression; eradicate H. pylori; stop smoking; discontinue NSAIDs; endoscopic intervention if there is active bleeding

44
Q

what are the complications associated with gastric ulcers?

A

perforation, bleeding, and obstruction (from edema)

45
Q

where do most duodenal (peptic) ulcers occur?

A

anterior wall of the proximal duodenum

46
Q

what is the cause of duodenal ulcers?

A

arise due to decreased mucosal protection and increased gastric acid secretion; up to 90-95% caused by H. pylori

47
Q

what are the risk factors for getting a duodenal ulcer?

A

glucocorticoids (corticosteroids), NSAIDs, Zollinger-Ellison syndrome (gastrinoma)

48
Q

what might the history/ presentation be of a person with a duodenal ulcer?

A

can be asymptomatic; dyspepsia- burning, gnawing epigastric pain occurring 1-3 hours after meals; often nocturnal (periods of fasting); relieved by food–> weight gain? (50% of patients report relief of pain with food or antacids and a recurrence of pain 2-4 hours later

49
Q

how do you diagnose a duodenal ulcer?

A

EGD with biopsy (diagnostic and therapeutic); nasogastric lavage can be considered; detection of h. pylori

50
Q

what if your nasogastric lavage is negative for blood?

A

this does not rule out a post pyloric duodenal ulcer

51
Q

what are the complications associated with a duodenal ulcer?

A

perforation, bleeding, obstruction (from edema)

52
Q

when can a perforated viscus occur?

A

can happen in PUD, can happen with any hollow organ that perforates (esophagus, stomach, intestine, uterus, bladder)

53
Q

how does someone with a perforated viscus present?

A

distressed

54
Q

what would be the findings of a person with a perforated viscus above the diaphragm? so aka the esophagus

A

a pneumomediastinum

55
Q

what would be the findings of a person with a perforated viscus below the diaphragm?

A

free air under the diaphragm, “acute” abdomen, rebound tenderness (pneumoperitoneum)

56
Q

what are the diagnostic tools used to diagnose a perforated viscus?

A

Free air under diaphragm or air in the mediastinum as seen on a CT or Plain X-ray

57
Q

what is the treatment for a perforated viscus?

A

NPO, IV antibiotics, preoperative labs, surgical consult; EMERGENT SURGERY

58
Q

what is the complication associated with a perforated viscus?

A

death

59
Q

what are the risk factors for developing gastric adenocarcinoma?

A

dietary factors: smoked fish and meats (dietary nitrosamines) and pickled vegetables; other: h. pylori, chronic gastritis, smoking tobacco, achlorhydria, menetrier’s disease, and gastric ulcer

60
Q

what might the history/ presentation be of someone with gastric adenocarcinoma?

A

malaise, anorexia–> weight loss, occult blood loss (iron deficiency anemia), dyspepsia; virchow’s node, sign of Leser-Trelat; sister mary joseph nodule

61
Q

what are the diagnostic tools used to diagnose gastric adenocarcinoma?

A

EGD with biopsy and abdominal CT/ other abdominal imaging for further staging

62
Q

what is the biopsy finding in a patient with gastric adenocarcinoma?

A

signet ring cells

GI II (20 decks)

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