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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
what are the complications associated with type A chronic gastritis?
Achlorhydria--> hypergastrinemia--> 5% can develop carcinoid tumors; pernicious anemia (gastritis)- megaloblastic (aka macrocytic)- B12 deficiency
26
What are the complications associated with type B chronic gastritis?
MALT lymphoma (gastric B cell lymphomas)
27
What are the microbiology characteristics associated with H. pylori?
gram negative, spiral (curved), microaerophilic, urease-producing rods (baccili) with flagella
28
where do H. pylori mainly colonize?
the gastric antral mucosa
29
what happens when H. pylori colonize the gastric antral mucosa?
90% of those colonized are asymptomatic and don't need screening or treatment; 10% will develop ulcer disease/ gastritis
30
what does H. pylori release that increases the risk of ulcer and gastric cancer?
Cag-A positive toxin
31
what group of people is at risk for H. pylori infection?
immigrants from developing countries, poverty/low socioeconomic status, overcrowding, rural, limited education, increases with age
32
how can you detect H. pylori?
fecal antigen test, urea breath test, IgA antibodies, upper endoscopy with gastric biopsy
33
what are the complications associated with H. pylori infection?
gastritis--> can lead to atrophic gastritis and gastric cancer- adenocarcinoma- MALToma
34
what is treatment for MALToma?
treating the H. pylori infection
35
what is the treatment for H. pylori infection?
combination therapy: antibiotics and acid reducing medications (3-4 drugs) x 14 days
36
What is important to note about post treatment of H. pylori infection?
you need to confirm successful eradication using either the urea breath test, fecal antigen test, or endoscopy with biopsy
37
when should you check for successful eradication of H. pylori?
at least 4 weeks after completion of antibiotic treatment and 1-2 weeks after proton pump inhibitor treatment
38
where do most of the gastric (peptic) ulcers occur?
in the lesser curvature of the antrum of the stomach
39
what is the etiology of gastric (peptic) ulcers?
H. pylori (up to 75% of cases); smoking
40
what are the risk factors for developing gastric ulcers?
glucocorticoids (corticosteroids) and chronic NSAID/salicylate use (15-30% if GUs)
41
what might the history/ presentation be of someone with a gastric ulcer?
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
how do you diagnose a gastric ulcer?
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
what is the treatment for gastric ulcers?
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
what are the complications associated with gastric ulcers?
perforation, bleeding, and obstruction (from edema)
45
where do most duodenal (peptic) ulcers occur?
anterior wall of the proximal duodenum
46
what is the cause of duodenal ulcers?
arise due to decreased mucosal protection and increased gastric acid secretion; up to 90-95% caused by H. pylori
47
what are the risk factors for getting a duodenal ulcer?
glucocorticoids (corticosteroids), NSAIDs, Zollinger-Ellison syndrome (gastrinoma)
48
what might the history/ presentation be of a person with a duodenal ulcer?
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
how do you diagnose a duodenal ulcer?
EGD with biopsy (diagnostic and therapeutic); nasogastric lavage can be considered; detection of h. pylori
50
what if your nasogastric lavage is negative for blood?
this does not rule out a post pyloric duodenal ulcer
51
what are the complications associated with a duodenal ulcer?
perforation, bleeding, obstruction (from edema)
52
when can a perforated viscus occur?
can happen in PUD, can happen with any hollow organ that perforates (esophagus, stomach, intestine, uterus, bladder)
53
how does someone with a perforated viscus present?
distressed
54
what would be the findings of a person with a perforated viscus above the diaphragm? so aka the esophagus
a pneumomediastinum
55
what would be the findings of a person with a perforated viscus below the diaphragm?
free air under the diaphragm, "acute" abdomen, rebound tenderness (pneumoperitoneum)
56
what are the diagnostic tools used to diagnose a perforated viscus?
Free air under diaphragm or air in the mediastinum as seen on a CT or Plain X-ray
57
what is the treatment for a perforated viscus?
NPO, IV antibiotics, preoperative labs, surgical consult; EMERGENT SURGERY
58
what is the complication associated with a perforated viscus?
death
59
what are the risk factors for developing gastric adenocarcinoma?
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
what might the history/ presentation be of someone with gastric adenocarcinoma?
malaise, anorexia--> weight loss, occult blood loss (iron deficiency anemia), dyspepsia; virchow's node, sign of Leser-Trelat; sister mary joseph nodule
61
what are the diagnostic tools used to diagnose gastric adenocarcinoma?
EGD with biopsy and abdominal CT/ other abdominal imaging for further staging
62
what is the biopsy finding in a patient with gastric adenocarcinoma?
signet ring cells

GI II (20 decks)

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