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GI Fellowship > Stomach > Flashcards

Stomach Flashcards

1
Q

Which population has the higher risk of getting DM Gastroparesis? typ1 or 2?

A

type 1

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2
Q

What are the 5 main causes of gastroparesis?

A
  1. Diabetes
  2. Post-surgical
  3. Idiopathic
  4. Viral
  5. Meds
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3
Q

which type of gastroparesis resolves in 1 year in 80% of patients?

A

Viral gastroparesis

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4
Q

Which surgeries can lead to gastroparesis?

A
  1. Gastrojejunostomy
  2. Vagotomy for peptic ulcer disease
  3. Pancreaticoduodenectomy (whipple)
  4. Lap Fundoplication
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5
Q

Which meds can cause gastroparesis?

A
  1. GLP-1 agonist (Exenatide)
  2. Amylin agonist (Symlin)
  3. Opioids, tramadol, marijuana, TCA
  4. Dopamine agonists
  5. Anticholinergics
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6
Q

Which clinical syndrome is most associated with n/a, ab pain, early satiety, and bloating?

A

gastroparesis

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7
Q

How is gastroparesis diagnosed?

A

Scintigraphy gastric emptying study (of solids)

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8
Q

How does the gastroparesis scintigraphy emptying study work to dx gastroparesis?

A

Looks at the percentage of retained solids (low fat, egg white meal), at 4 hours.

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9
Q

What is the diagnostic criteria for gastroparesis for mild, mod, severe?

A

Mild: 11 to 20 % retained
Moderate: 21 to 35% retained
Severe: 36 to 50% retained
Very severe: More than 50% retained

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10
Q

What is an alternative to gastric emptying study with scintigraphy? (but not widely available)?

A

wireless motility capsule

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11
Q

what is the treatment for gastroparesis?

A
  1. Treat constipation (can make gastroparesis worse)
  2. Correct fluid/electrolyte imbalances
  3. Stop offending meds
  4. Small, low residue meals. In severe cases, consider liquid caloric supplementation
  5. Metoclopramide, Domperidone, Erythromycin, TCA
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12
Q

what is the mechanism of action of Metoclopramide?

A

central and peripheral dopamine antagonist and serotonin 5-HT3 antagonist with promotility and anti-emetic actions. FDA approved for gastroparesis for less than 12 weeks.

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13
Q

what is the black box warning for Metoclopramide?

A

Tardive dyskinesia , dystonia, seen after tx more than 3 months and with high doses

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14
Q

what general principles should be considered in pts taking Metoclopromide for gastroparesis?

A
  1. Use the minimum dose at 5mg
  2. stop tx if no response in 3 months
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15
Q

What are the medication treatment options for gastroparesis?

A
  1. Metoclopramide
  2. Domperidone
  3. Erythromycin
    6 Enteral feeding with nasoduodenal tube (preferred over TPN)
  4. Surgery
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16
Q

What is the benefit of using Domperidone for treatment of gastroparesis?

A

It doesnt cross the blood brain barrier, minimal neurological effects. However watch for QT (need baseline EKG)

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17
Q

Which medication acts as a motilin receptor agonist that stimulates antral contraction?

A

Erythromycin

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18
Q

what is the limit of time in which erythromycin can be used to treat gastroparesis and why?

A

2 weeks, after that treatment becomes less effective due to development of tachyphylaxis.

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19
Q

which method is preferred for nutrition in patients with gastroparesis and why? TPN vs Nasal duodenal tube?

A

Nasal duodenal tube is preferred, other options include venting gastrostomy, jejunostomy, or PEG-J placement

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20
Q

What is the benefit of gatsric electric stimlation in patients with gastroparesis?

A

It helps improved symptoms of nausea and vomiting but does not improve abdominal pain

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21
Q

How does G-Poem work for gastroparesis, and how effective is it?

A

Its basically endoscopic myotomy of the pylorus, it helps improves gastroparesis symptoms. success rate of 71%

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22
Q

WHICH CLINICAL syndrome is assoc with an idiopathic disorder characterized by recurrent, self limited episodes of nausea, and vomiting alternating with symptoms free intervals?

A

Cyclical vomiting syndrome

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23
Q

Which are the 3 required criteria for diagnosis of cyclical vomiting syndrome?

A

Must have:
1. Stereotypical EPISODES OF VOMITING with acute onset and duration less than 1 week
2. 3 or more episodes in the year prior, each more than 1 week apart
3. absence of vomiting between episodes

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24
Q

what other conditions are associated with cyclical vomiting syndrome?

A

MIGRAINES, then anxiety depression

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25
Q

which clinical condition is characterized by chronic excessive marijuana use, cycle episodes of nausea, vomiting, and abdominal pain., followed by relief with cessation of marijuana use?

A

Cannabinoid hyperemesis syndrome

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26
Q

patients with this condition tend to take frequent baths to relive their symptoms.

A

Cannabinoid hyperemesis syndrome

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27
Q

What is the management for patients wit Cannabinoid hyperemesis syndrome?

A
  1. Acute episode: hydration, antiemetics (ondansetron, promethazine, and can consider benzos
  2. Between episodes: Propranolol, amitriptyline, zonisamide, levetiracetam, stop weed
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28
Q

which clinical syndrome assoc with effortless regurgitation of undigested food within 10 to 15 min after eating (usually no retching, or nausea)?

A

Rumination syndrome

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29
Q

which demographic is typically affected by Rumination syndrome?

A

teenage, girls (associated with stress and anxiety)

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30
Q

what two diagnostic criteria must be present to diagnose rumination syndrome?

A
  1. Persistent or recurrent regurgitation of recently ingested food into the mouth with subsequent spitting or re-mastication and swallowing
  2. Regurgitation is not preceded by retching

Supportive: also if patient says the food taste good coming back up, means it likely does not have acid in it , and also if they have no nausea

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31
Q

How is Rumination syndrome treated?

A
  1. Behavioral therapy +/- biofeedback
    - This focuses on postprandial diaphragmatic breathing for 5 minutes before and after meals to compete with the urge to regurgitate
  2. Can also use Baclofen
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32
Q

Which clinical syndrome is associated with pain or discomfort in the central upper abdomen, early satiety, anorexia, belching, nausea. vomiting, bloating?

A

Dyspepsia

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33
Q

What are the main causes of dyspepsia

A
  1. PUD
  2. Gastritis
  3. Esophagitis
  4. Malignancy
  5. functional
  6. Medications
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34
Q

what are the most common medications that causes of dyspepsia?

A

NSAIDs, iron, narcotics, colchicine, acarbose

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35
Q

What are the criteria for diagnosis of functional dyspepsia?

A

Must have these 2 for the last 3 months with symptoms onset more than 6 months prior to diagnosis:

  1. At least one of the following symptoms: bothersome postprandial fullness, early satiety, epigastric pain or epigastric burning
  2. No evidence of structural disease that is likely to explain the symptoms (normal EGD)
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36
Q

WHAT ARE THE TWO SUBTYPES OF FUNCTIONAL DYSPEPSIA?

A
  1. Post prandial distress syndrome (postprandial fullness, early satiety)
  2. Epigastric pain syndrome (int epigastric pain not generalized or localized to other regions, not relieved by defecation, not related to gallbladder or Sphincter of oddi disease)
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37
Q

What is the recommended initial work up for patients with dyspepsia for those over age 60?

A
  1. Initial EGD
  2. If EGD normal, treat as functional dyspepsia- (treat with PPI, h pylori eradication, TCA, prokinetics, psychtherapy)
    (Avoid doing multiple EGD if the EGD and imaging is normal)
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38
Q

What is the recommended initial work up for patients with dyspepsia for those UNDER age 60?

A

EGD not recommended, regardless of the presence of alarming features. Alarming features increase the risk of malignancy, but the risk of malignancy in those with alarming features was low (1%)

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39
Q

which patients with dyspepsia would benefit from endoscopy?

A
  1. Progressive dysphagia
  2. Severe weight loss
  3. Abnormal imaging
  4. IDA
  5. Those with MULTIPLE alarming features
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40
Q

For patients younger than 60 with functional dyspepsia, what steps should be done for work up?

A
  1. Test and treat for h pylori
  2. If the pt does not respond, or tests negative, empiric treat with PPI daily for 4 weeks
  3. If no response, don’t increase it, there’s no role for BID in FD
  4. If treating for h pylori and with PPI don’t work, treat as functional with TCA, prokinetics or psychotherapy)
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41
Q

In patient having an EGD ONLY for dyspepsia, which areas should and should not be routinely biopsied?

A
  1. Dont routinely biopsy esophagus
  2. Do get biospies from stomach
  3. Dont routinely biopsy duodenum in the immunocompetent patients
  4. If immunocompromised, get biopsies from stomach and duodenum to rule ouf Graft vs host disease
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42
Q

what diet reccs are used for patients with functional dyspepsia?

A
  1. SMall meal sized
  2. Low fat diet
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43
Q

Which herbal medication is shown to be effective in functional dyspepsia?

A

STW-5 (Iberogast)

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44
Q

when are TCAs more effective in treating functional dyspepsia?

A

TCAs are better for functional abdominal paiN and IBS. A trial showed that Amitriptyline is better for functional dyspepsia

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45
Q

Even though not availible in the US, what is another treatment for dyspepsia that is a prokinetic agents that inhibits acetylcholinesterase ?

A

Acotiamide

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46
Q

What other medication options can be used for symptomatic treatment of dyspepsia that have been shown to be effective?

A
  1. Acotiamide
  2. Buspirone
  3. mirtazapine
  4. Acupuncture
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47
Q

what is the GI gram negative spiral shaped bacterium that lives in the gastric mucosal layer/

A

Helicobacter pylori

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48
Q

why is it important to eradicate the h pylori?

A

Eradicating h pylori decreases the risk of developing gastric cancer, which is a class 1 carcinogen

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49
Q

what are the ESTABLISHED main indications for h pylori testing?

A
  1. Active PUD
  2. History of H. Pylori with out treatment
  3. Low grade gastric MALT
  4. Following endoscopic resection of early gastric cancer
  5. Uninvestigated dyspepsia
  6. Long term NSAID users
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50
Q

In doing a urea breath test for h pylori, what must happens in regards to the PPI?

A

Stop PPI 2 weeks before and you have to fast for 1 hour prior to test

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51
Q

what happens to urea if if h pylori is present in the breath test?

A

Urea is converted by h pylori urease into tagged CO2. This co2 circulates in the blood, and is excreted through the lungs and detected in breath

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52
Q

Which tests are most sensitive for detecting h pylori?

A
  1. Biopsy, histology, urea breath test
  2. then stool antigen (False + with PPI, bismuth, and abx, and GI bleed)
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53
Q

between urea breath test and stool antigen, which test is more senaitive?

A

Breath

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54
Q

which test can be used to detect current or prior infection?

A

Serology IgG AB. If its negative in a pt with bleeding, repeat the test after bleeding resolves

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55
Q

How long after treatment should h pylori eradication be done?

A

4 weeks after completing therapy

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56
Q

What sites should be biopsied to test for h pylori in pts with normal mucosa?

A

Get biopsies from
1. Angularis
2. Antrum (greater curve
3 Body (greater curve
4 Antrum (lesser curve)
5 Body (lesser curve)

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57
Q

which h pylori test can not be used to confirm eradication?

A

sERUM ANTIBIODY TEST

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58
Q

What is the recommended first line treatment for h pylori?

A

Bismuth quadruple therapy for 14 days (rec over triple therapy)

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59
Q

in pts who need h pylori tx but say that have allergy to penicillin, what to do next?

A

send to allergy specialist to test of the allergy is significant

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60
Q

which clinical syndrome is associated with giant hypertrophic gastric folds?

A

Menetriers disease

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61
Q

what is the concern or risk of having GIANT hypertrophic folds (menetriers disease)?

A

Increased risk of gastric adenocarcinoma

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62
Q

which clinical syndrome is associated with giant hypertrophic gastric folds AND ab pain, n/v PLUS peripheral edema?

A

Menetriers dz

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63
Q

What is seen on endoscopy in patients with Menetriers disease?

A

EGD shows THICK gastric folds and increased mucous production

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64
Q

what parts of the stomach are usually affected by Menetriers disease?

A

Fundus and body

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65
Q

what type of endoscopic biopsies are REQUIRED for diagnosis of Menetriers disease?

A

Deep bxs, or snare resections of gastric mucosa, but supercial bxs wont cut it

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66
Q

What clinical syndrome is associated with histologic findings of preserved mucosal architecture, but has foveolar hyperplasia, tortuosity, dilation of the glands, forming a cork screw appearing and smooth muscle hyperplasia and decreased number of parietal glands?

A

Menetriers disease

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67
Q

what is the treatment for pts with Menetriers disease?

A
  1. Supportive
  2. octreotide
  3. In severe cases, gastric resection
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68
Q

what does the quadruple regimen for h pylori consist of?

A

(PBMT): PPI+ Bismuth +Metronidazole + Tetracycline x 14 days

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69
Q

what does the TRIPLE regimen for h pylori consist of?

A

PPI + Amoxicillin + Levofloxacin x14 days

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70
Q

which clinic syndrome has a fasting serum gastrin level greater than 200?

A

Hypergastrinemia

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71
Q

What is the difference between appropriate hypergastrinemia and inappropriate hypergastrinemia?

A
  1. appropriate hypergastrinemia is due to decreased gastric acid production (so it makes since to rev up the gastrin levels)
  2. inappropriate hypergastrinemia is seen with normal or increased acid production (so basically it had no reason to have high gastrin levels since the levels of gastric acid are already normal or high)
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72
Q

What are the 4 causes of appropriate hypergastrinemia

A
  1. Acid suppression (PPI, H2 blockers)
  2. Chronic metaplasia atrophic gastritis (autoimmune gastritis, pernicious anemia) then (h pylori pangastritis)
  3. chronic renal failure (maybe not clearing the gastrin levels)
  4. Vagotomy without antrectomy
73
Q

What are the 5 causes of inappropriate hypergastrinemia?

A
  1. Zollinger Ellison Syndrome
  2. Retained Antrum Syndrome
  3. Antral predominant Hpylori infection (G cell hyperplasia)
  4. Gastric outlet obstruction
  5. Small bowel resection
74
Q

which clinical syndrome is associated with inappropriate hypergastrinemia after billroth 2 surgery where a small segment of the antrum is retained in the duodenal stump?

A

Retained antrum syndrome

75
Q

What is the pathophysiology of Retained antrum syndrome and how does it causes elevated gastrin levels?

A

The retained gastric mucosa is only exposed to the alkaline duodenal contents. Without the negative feedback of an acidic environment it keeps secreting gastrin leading to recurrent peptic ulcers

76
Q

Gastrin levels greater than 1000 suggest which 2 clinical conditions?

A

ZES or chronic atrophic gastritis

77
Q

What clinical clues suggest a patient had ZES?

A
  1. Recurrent peptic ulcers in duodeneum
  2. severe heart burn
  3. MULTIPLE ULCERS
  4. Recurrent PUD, h pylori, or PUD with thick gastric folds
78
Q

What are the steps to diagnosing ZES?

A
  1. MEASURE FASTING SERUM GASTRIN. If normal, then no ZES
  2. If gastrin elevated more than 10 times ULN, think either ZES or atrophic gastritis
    . 3 Check gastric ph (if less than 2.5 thats ZES, if greater than 2.5 think atrophic gastritis)

2a. If gastrin elevated LESS than 10 times ULN, check gastric ph
3. If more than 2.5, think acid suppresion, atrophic gastritis, CKD, vagotomy
4. If less than ph 2.5, do a secretin stimulation test
5. If the secretin stim test, gastrin increases more than 120 its ZES, if it inclreases less than 120 or decreases, its either antral g hyperplasia, retained atnrum, or gastric outlet obstruction

79
Q

What is required for dx of ZES?

A

Elevated gastrin levels and low gastric pH (less then 2.5)

80
Q

In diagnosing ZES, what tests are needed if the gastrin level is >10 vs if the gastrin level is less than 10 times the upper limit?

A
  1. If gastrin >10 times upper limit (>1000), all you need is a gastric pH less than 2.5 to confirm diagnosis
  2. If gastrin levels less than 10 time upper limit normal, then you gotta get a gastric pH AND shown an abnormal secretin simulation test
81
Q

WHICH test differentiates ZES from other causes of hypergastrinemia?

A

secretin stimulation test

82
Q

what level of gastrin is considered to be a positive secretin test?

A

If the gastrin increases by at least 120 within 5 to 10 min

83
Q

Do patients who are taking a PPI have to stop before having the secretin test for ZES?

A

PPI can interfere with gastric Ph AND can elevate gastrin levels and affect secretin tests results . best to perform tests off of PPI

84
Q

In patients with a gastrinoma, what is the risk of stopping PPI?

A
  1. Exaggerated rebound gastric acid hypersecretion
  2. n/v/ab pain
    3 perforation
    .
85
Q

what other testing (besides secretin stim and gastric ph), can be used to dx ZES (not available widely)?

A

Basal acid output (greater than 150

86
Q

Which clinical syndrome is associated with patients features of ZES, who have normal gastric levels, but elevated cholecystokinin (CCK) due to a rare disorder?

A

Rare pancreatic neuroendocrine tumor secreting CCK

87
Q

after ZES is confirmed, what is the next step in management?

A

Search for the primary tumor using different imaging modalities (CT , MRI, EUS)

88
Q

Where do most gastrinomas arise?

A

Within the gastrinoma triangle: bound superiorly b ythe junction of the CBD and cystic duct, inferiorly by the junction of the 2nd/3rd duodenum, and medially by the head/neck of the pancreas.

89
Q

Prior to testing for ZES, how should PPIs be withdrawn?

A

Do an egd to document healed PUD and esophagitis
Wean PPI
Swich to high dose H2 blockers x 5 days
stop h2 blockers then give only antacids day before test

90
Q

Nearly 30 to 60% of pts with gastrinoma have what other condition?

A

MEN Type 1 (Test for pituitary gland tumors and hyperparathyroidism

91
Q

If a patient is found to have gastrinoma and hyperparathyroidism, what procedure should happen prior to gastrinoma resection surgery?

A

Parathyroidectomy

92
Q

Fundic gland polyps are associated with chronic use of which therapy?

A

Chronic PPI use

93
Q

What clinical condition is assoc with histologic findings of dilated fundic glands lined by normal gastric body type epithelium?

A

Fundic gland polyp

94
Q

How should fundic gland polyps be managed?

A

Always biopsy or resect gastric polyps to rule out adenomatous histology

95
Q

what screening should be done in patients with multiple and diffuse fundic gland polyps?

A

Screening colonoscopy

96
Q

Is routine surveillance for gastric polyps required?

A

No, them becoming malignant is rare (1%) in those larger than 1 cm

97
Q

How should fundic gland polyps >1cm be magaged?

A

Resection

98
Q

In what 3 conditions do we see multiple fundic gland polyps?

A
  1. Familial Adenomatous Polyposis
  2. MUTYH associated polyposis
  3. Gastric Adenocarcinoma and Proximal Polyposis of the Stomach (GAPPS)
99
Q

WHICH clinic condition is assoc with fundic gland polyps (with and without dysplasia) usually greater than 100 polyps,, that are RESTRICTED to the fundus and body of the somtach (ANTRUM IS SPARED)?

A

Gastric Adenocarcinoma and Proximal Polyposis of the Stomach (GAPPS)

100
Q

Does Gastric Adenocarcinoma and Proximal Polyposis of the Stomach (GAPPS) in crease the risk of stomach cancer or colon cancer?

A

Increased risk of gastric adenocarcinoma but not colon cancer

101
Q

why do gastric hyperplastic polyps develop? what usually causes them?

A

Chronic inflammation (h pylori, autoimmune gastritis)

102
Q

Where do MOST Gastric hyperplastic polyps developing?

A

Antrum

103
Q

which clinical condition is associated with histology showing dilated, elongated tortuous foveolar epithelium surrounded with an edematous reactive and inflammatory stroma?

A

Hyperplastic polyps (gastric)

104
Q

what size is the risk of malignant transformation in gastric hyperplastic polyps the greatest?

A

> 2cm

105
Q

All gastric adenomas require resection. For gastric adenomas that are resected, when should EGD surveillance occur?

A

1 year

106
Q

which clinic syndrome associated with replacement of normal gastric epithelium with intestinal type epithelium?, as a response to chronic injury?

A

Gastric Intestinal Metaplasia

107
Q

What is the difference between the two types of gastric intestinal metaplasia (Complete Intestinal Metaplasia vs Incomplete IM)?

A
  1. Complete IM, the crypts are organized, straight, goblet cells are round and well developed, and columnar cells have well developed brush border
  2. Incomplete IM: Crypts are distorted and branched, goblet cells vary in size, with some columnar cells present as immature intermediate call that contain mucous
108
Q

which phrase describes the phenomenon where the progression of pre-cancerous lesions to gastric adenocarcinoma through a series of steps? What are the steps?

A
  1. Correa precancerous cascade
  2. Normal gastric mucosa- Non atrophic gastritis (h pylori)- multifocal atrophic gastritis- gastric IM complete- gastric IM incomplete- low grade dysplasia- high grade dysplasia- adenocarcinoma
109
Q

what is the main cause and driver of progression in the Correa precancerous cascade? (the phenomenon where the progression of pre-cancerous lesions to gastric adenocarcinoma through a series of steps)

A

h pylori infection (esp CagA strain)

110
Q

in patients with atrophic gastritis and intestinal metaplasia what should be done to reduce the risk of adenocarcinoma?

A

test for and treat h pylori

111
Q

What additional testing should patients with pernicious have have any why?

A

Baseline endoscopy and biopsy of the proximal and distal gastric mucosa. As autoimmune gastritis can be associated with atrophic gastritis and IM.

112
Q

iN ENDOSCOPIC EVALUATION For intestinal metaplasia, what enhancement should be used during endoscopy?

A

Narrow band imaging in addition to standard white light

113
Q

iN ENDOSCOPIC EVALUATION For intestinal metaplasia, what should be done if an area is abnormal and found?

A

the area should be described and biopsied separately

114
Q

How many biopsies should be taken to detect and map the location of intestinal metasplaia?

A

at least 5, Two from antrum, one from incisura, 2 from body

115
Q

which biomarkers are associated with advanced atrophic gastritis ?

A

low pepsinogen 1 levels and/or low pepsinogen 1: pepsinogen 2 ratio. However dont use these to screen

116
Q

what evaluation should occur in pts with advanced atrophic gastritis ?

A

undergo endoscopy

117
Q

Which risk factors in risk of progression of intestinal metaplasia to dysplasia and gastric cancer

A
  1. 1st degree hx fam of gastric cancer
  2. Gastric bx with intestinal metaplasia of INCOMPLETE type
  3. multifocal IM in the gastric body AND antral (as opposed to unifocal just in one area)
  4. persistent h pylori infection
118
Q

How often should patients with intestinal metaplasia have screening?

A

3-5YEARS

119
Q

IF THERE IS FOCAL IM, with no other risk factors for progression, is endoscopic surveillance recommended?

A

No

120
Q

the sign of leser-trelat shows sudden onset of multiple seborrheic keratosis on the trunk, is concerning for what go condition?

A

GI cancer

121
Q

what are the 2 main histologic subtypes of of gastric adenocarcinoma?

A
  1. (intestinal) Well-differentiated
  2. (diffuse)- Poorly differentiated
122
Q

which histologic subtype of gastric adenocarcinoma is associated with older patients, lower SES, polypoid or fungating mass, distal stomach, assoc with atrophic gastritis, IM and dysplasia related to hpylori?

A

Intestinal type (well differentiated)

123
Q

which histologic subtype of gastric adenocarcinoma is associated with younger patients, higher SES, diffuse gastric thickening (linitis planica, proximal stomach, related to loss of E cadherin)?

A

(diffuse)- Poorly differentiated
(younger pts are poor)- SIGNET RING histology

124
Q

which 2 criteria (only one has to be met) are required for diagnosis of hereditary diffuse gastric cancer?

A
  1. Two or more documented cases of diffuse gastric cancer in 1st or 2nd relatives with at least one diagnosed before age 50
  2. Three or more cases of documented diffuse gastric cancer in the 1st or second degree relative no matter age
125
Q

which GI clinical condition is associated with the germline mutation in E-cadherin gene (CDH1) on chromosome 16 OR CTNNA1 on chromosome 5?

A

hereditary diffuse gastric cancer

126
Q

what treatment is recommended for patients with the E-cadherin gene (CDH1) MUTATION pertaining to hereditary diffuse gastric cancer?

A

Prophylactic total gastrectomy

127
Q

what surveillance is recommended for patients with the E-cadherin gene (CDH1) MUTATION who refuse Prophylactic total gastrectomy?

A

Annual EGD IN PTS LESS THAN 20 YEARS OLD

128
Q

What other cancer is associated with female patients with hereditary diffuse gastric cancer?

A

Increased risk of lobular breast cancer. Should have annual mammogram and MRI after 35

129
Q

what is the most common location for extra-nodal non-Hodgkin’s lymphoma?

A

GI tract (stomach)

130
Q

Which part of the GI tract is the most common location of GI lymphoma in the western world?

A

stomach

131
Q

This main histological feature (lymphoepithelial lesion) is associated with what GI condition?

A

gastric lymphoma

132
Q

which tissues does gastric lymphoma arise from?

A

MALT. Mucosa associated lymphoid tissue. (MALT)

133
Q

How is gastric lymphoma diagnosed?

A

EGD

134
Q

WHAT ARE THE 3 MAIN TYPES OF ENDOSCOPIC PATTERNS ASSOCIATED WITH GASTRIC LYMPHOMA?

A
  1. Exophytic type- polypoid mass
  2. Ulcerative types with ulcerations or multiple small erosions
  3. Hypertrophic type- with large gastric folds
135
Q

what are the 2 histologic subtypes of gastric lymphoma?

A
  1. MALToma (marginal b cell lymphoma)
  2. DLBCL (Diffuse Large B cell lymphoma)
136
Q

what is the different in the endoscopic appearance between the 2 histologic subtypes of gastric lymphoma (MALToma (marginal b cell lymphoma vs DLBCL (Diffuse Large B cell lymphoma)?

A
  1. MALToma (marginal b cell lymphoma) endoscopically appears ulcerative or hypertrophic
  2. DLBCL (Diffuse Large B cell lymphoma) appears nodular
137
Q

between the 2 histologic subtypes of gastric lymphoma (MALToma (marginal b cell lymphoma vs DLBCL (Diffuse Large B cell lymphoma), which is MORE and LESS likely to respond to treat for h pylori?

A

MALT is MORE a likely to respond to treat for h pylori

DLBCL is LESS likely to respond to treat for h pylori

138
Q

for those with MALT and evidence of stage 1 disease with + for h pylori, what is the treatment?

A

h pylori eradication, repeat EGD in 2 months with biopsies

139
Q

for patients with MALT, what is the recommended follow up for surveillance?

A

EHD q6 months for 2 years than annually

140
Q

compared to MALT, how are most patients with DLBCL treated?

A

Mostly with chemo +/- radiation since these pts dont really respond to h pylori tx

141
Q

What is the stepwise progression of stages, for h pylori t o become gastric cancer? and what’s the name of this process?

A

This stepwise progression has several discrete stages, which include normal mucosa, chronic non-atrophic gastritis, chronic atrophic gastritis, GIM, dysplasia, and cancer. through the Correa cascade,

142
Q

what is the optimal recommended optimal surveillance interval for gastrointestinal metaplasia?

A

Currently, data are insufficient to recom-
mend an optimal surveillance interval. Acknowledging that

some patients may have a higher risk of gastric can-
cer or put a higher value on a reduction in gastric

cancer mortality, it is reasonable to elect for surveil-
lance or repeat endoscopy within 1 year for risk

stratification based on shared decision-making with

patients.

143
Q

whats the difference between Extensive GIM and limited GIM ?

A

Extensive GIM involves both the antrum and corpus or corpus alone, versus limited GIM involving only the antrum or incisura.

144
Q

what does Complete GIM resemble on HE staining? what about incomplete GIM?

A

Complete GIM resembles small intestinal epithelium phenotype on hematoxylin and eosin (H&E) staining, and incomplete GIM resembles colonic epithelium phenotype on H&E staining.

145
Q

Which has the higher risk incident gastric cancer? Complete GIM or Incomplete GIM

A

among patients with GIM, incomplete
GIM IS associated with a 3.3-fold higher risk of incident gastric cancer compared with complete GIM during follow-up ranging from 3 to 12.8 years.

146
Q

In a pt not responding to PPI who is maxed out, taking the med correctly and still having sxs, what other reason is there for her not responding to PPI?

A

Another explanation for incomplete response to PPI may be metabolic, as PPIs undergo metabolism by the cytochrome P450 system via the isoenzymes CYP2C19 and CYP3A4 in the
liver and small intestine. The cytochrome P450 system has numerous polymorphisms, and variations in the CYP genes result in several different phenotypes, including ultrarapid, rapid, normal,
intermediate, or poor metabolizers of PPIs.

147
Q

Which proton pump inhibitor (PPI) has the
highest potency?

A

Rabeprazole

148
Q

WHAT is The risk most likely to be attributed to proton
pump inhibitor (PPI) use ?

A

eNTERIC INFECTION

149
Q

Menetrier disease is caused by increased signaling
in which of these pathways?

A

Epidermal growth factor receptor (EGFR)

150
Q

Which nsaid formulation is associated with the highest
risk of peptic ulcer disease complications?

A

Naproxen.

Diclofenac and meloxicam are selective COX-2 inhibitors and thus have a lower rate of gastrointestinal side effects than traditional
NSAIDs such as ibuprofen and naproxen.

151
Q

What is the primary mechanism by which nonsteroidal anti-inflammatory drugs (NSAIDs) increase the risk of peptic ulcer disease?

A

Decreased prostaglandin synthesis

152
Q

Which clinical syndrome is assoc with erosions or ulcerations at the
level of the diaphragmatic hiatus that are found within a hiatal hernia?

A

Cameron lesions are erosions or ulcerations at the
level of the diaphragmatic hiatus that are found
within a hiatal hernia. The presence
of Cameron lesions may also be a source of iron
deficiency identifiable on endoscopy and are more
common in the presence of a larger hiatal hernia
(ie, 5 cm in size or greater). As a result, these are
typically associated with mechanical trauma from
the hernia sac.

153
Q

Which of the following is the most sensitive test
to identify autoimmune atrophic gastritis as the
cause of vitamin B12 deficiency?

A

Anti-parietal cell antibody

154
Q

In immunocompetent patients without an identifiable lesion and in patients with dyspepsia, EGD biopsies should be taken from where? what is this protocol called?

A

AGA does recommend obtaining gastric biopsies to evaluate for Helicobacter pylori infection. Biopsies should be obtained according to the Sydney protocol, obtaining samples from the gastric body, antrum, and incisura. The Sydney protocol was shown to identify 100% of H pylori infections in one study. The AGA recommends against using separate jars as this is unnecessary and costly.

155
Q

in patients with peristent reflux symptoms on PPI, what other med can be used

A

Alginate. Buffering of, and potentially physically inhibiting, this layer with the use of alginates can reduce the symptoms of gastroesophageal reflux after meals.

156
Q

in a patient with history of a bilroth 2 surgery, what is a common reason for persistent ulcers

A

persistent ulcerations are likely due to retained antrum from a prior Billroth II operation. In this scenario, a portion of the antrum is inadvertently left behind after surgery and, when chronically bathed in alkaline fluid in the excluded portion, leads to unopposed gastrin hypersecretion and gastric acid production. A secretin stimulation test can differentiate between hypergastrinemia from gastrinoma or retained antrum.

157
Q

What feature increases the risk of dysplasia in
fundic gland polyps?

A

A. Antral gastritis.
Dysplasia is associated with presence of antral gastritis, familial adenomatous polyposis syndrome, and increasing size of the largest fundic gland polyp.

158
Q

Patients with low B12 level below the normal range and anti-intrinsic
factor antibodies are positive, have the highest risk of getting which cancer?

A

Noncardia gastric adenocarcinoma

159
Q

How is functional dyspepsia defined by the Rome 4 criteria?

A

the Rome IV criteria: the presence of 1 or more of the following symptoms: post-prandial fullness, early satiation, epigastric pain or epigastric burning, and no evidence of structural disease (including at upper endoscopy) to explain the symptoms.

160
Q

what is the first and second line treatment for functional dyspepsia?

A

Functional dyspepsia can be treated first with a trial of proton pump
inhibitors and, if ineffective, tricyclic antidepressants or prokinetic agents. Fundic relaxants (BUSPIRONE) may play a role in improvement in early satiation especially.

Buspirone is a serotonin 1A (5-HT1A) agonist
that has clinical efficacy for patients with anxiety
and has been shown to be superior to placebo in
alleviating symptoms of functional dyspepsia. The
symptoms most improved include postprandial
fullness, bloating, and early satiety, rather than

abdominal pain.

161
Q

Which increases the risk of developing a marginal ulcer? Long gastric pouch or short gastric pouch?

A

Long gastric pouch

A short gastric pouch is
associated with a reduced risk of marginal ulcer.

162
Q

In patients with a with a history of Roux-en-Y gastric bypass and abdominal pain, found to have marginal ulcer, what event likely led tio the ulcer?

A

Relative ischemia to the gastroenterostomy is a primary risk factor for the development of marginal ulcer in patients with a history of Roux-en-Y gastric bypass. This risk is increased in patients
who smoke, use nonsteroid antiinflammatory
drugs, or have diabetes.

163
Q

Inflammation of what cell type, leads to a gastric hyperplastic polyp?

A

hyperplastic polyp can result from inflammatory proliferation of mucous producing foveolar cells often in the setting of chronic bile exposure. This finding frequently is associated with mucosal atrophy but may be seen in the absence of autoimmune gastritis or Helicobacter pylori infection.

164
Q

what is the one independent risk factor for gastrointestinal bleeding in the context of critical illness?

A

Use of mechanical ventilation for more than 48 hours is an independent risk factor for gastrointestinal bleeding in the context of critical illness and warrants prophylaxis with proton pump

inhibitors.

165
Q

What is the risk of malignancy in a gastric neuroendocrine tumor.?

A

<5%

Gastric carcinoids arise in enterochromaffin-like (ECL) cells. Type 1 gastric carcinoid is the most common type of gastric carcinoid and is most commonly associated with chronic atrophic gastritis. They generally have the lowest metastatic risk at less than 5%.

166
Q

which clinical syndrome is assoc with acute symptoms of gastroesophageal reflux disease (GERD) after discontinuing PPIs abruptly?

A

Rebound hypergastrinemia.

This is usually temporary, and symptoms can be ameliorated with the use of on-demand acid suppression (such as histamine 2 receptor antagonists) or tapering of PPIs.

167
Q

which clincal syndrome is associated with diarrhea, esophagitis,
and duodenal ulcers, as well as elevated gastrin
level?

A

Zollinger-Ellison
syndrome (ZES) due to a gastrinoma.

168
Q

Which 3 substances stimulate gastric acid production? and which one suppresses gastric acid production?

A

Gastric acid is stimulated by 3 substances: gastrin,
histamine, and acetylcholine. Somatostatin acts as a feedback mechanism to suppress acid production, as does acid in the stomach itself.

169
Q

Which of the antacid therapies is most
likely to be associated with tachyphylaxis?

A

Famotidine

They are quite effec-
tive when used short-term, but compensation and

upregulation of the other associated pathways for
acid production and tachyphylaxis occurs with
prolonged use of histamine-receptor blockers.

170
Q

Symptoms of hypomagnesium include muscle cramps and weakness and ab pain. Which over-the-counter GERD medications is most likely
responsible for these current symptoms?

A

Omeprazole

The symptoms described in this presentation are
classic for hypomagnesemia, which is a rare but
potentially severe complication from proton pump

inhibitor use.

171
Q

How are PPIs linked to low vit B12?

A

Chronic proton pump inhibitor use has been
linked to B12 deficiency AND THE current
leading theory is that acid suppression reduces
the cleavage of cobalamin from dietary proteins
(as pepsin is not as readily activated outside of an
acidic milieu), reducing the ability of cobalamin
to bind in the stomach with intrinsic factor.

172
Q

In patients with brisk upper gastrointestinal bleeding before endoscopy, what other therapy besides PPI should be considered?

A

Intravenous erythromycin is reasonable to consider in patients with brisk upper gastrointestinal bleeding before endoscopy, with the hypothesis that this will speed gastric emptying and may al-
low better visualization and more optimal evaluation and therapy, with decreased need for repeat endoscopy thereafter.

173
Q

What would be the most sensitive test to evaluate
whether a patient still has active H pylori infection?

A

Urease breath test

Urease breath test and H pylori stool
antigen evaluation, when performed off proton
pump inhibitor therapy, are both believed to be
greater than 95% sensitive and would be the best
options for this situation.

174
Q

H pylori prevalence, has an inverse association
with what other GI condition?

A

Esophageal adenocarcinoma

It is not clear that there is a protective
effect per se, but there is an inverse association
that factors into treatment decisions in patients
with incidentally discovered asymptomatic H
pylori cases.

175
Q

In patients with systemic mastocytosis, what is the cause of excessive histamine production?

A

Acid hypersecretion can occur with systemic mastocytosis due to excessive histamine production. Histamine is the most important stimulator of acid secretion. It is released by enterochromaffin-
like cells and stimulates parietal cells to secrete acid.

176
Q

In a patient with an elevated serum gastric level in the context of a duodenal ulcer and diarrhea and suspected Zollinger-Ellison syndrome on PPI, what is the next step to evaluate for ZES? is

A

the serum gastrin level may related to ZES, but may also be elevated appropriately as a result of proton pump inhibitor (PPI)-induced acid suppression. The next step in evaluation would be to care-
fully stop the PPI (by tapering off) and repeat the gastrin measurement off PPI therapy to determine if it was a true elevation or simply spurious in the context of appropriate acid suppression.

177
Q

What are 3 three main risk factors for NSAID-induced GI bleeding?

A

Risk factors for NSAID-induced GI bleeding
include:
1. age greater than 65 years
2. prior history of peptic ulcer disease or GI hemorrhage,
3. concomitant anticoagulation drug use.

178
Q

Under what circumstances should aspsirin be continued or stopped (primary vs secondary prevention) in the setting of aspirin-associated bleeding ?

A

If aspirin is taken for primary prevention and
aspirin-associated bleeding occurs, antiplatelet
therapy should be discontinued unless the patient
is at high risk of cardiovascular complications. If
aspirin is taken for secondary prevention, then a
daily proton pump inhibitor should be added, and
aspirin should be continued if the benefits are believed to justify the potential risks.

179
Q
A

GI Fellowship (11 decks)

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