Gastritis. Ulcer. Nud. Zes. Ibd

Front 1

55. A 58–year–old man to the office for evaluation of epigastric discomfort for the last several weeks.he's otherwise asymptomatic with no weight loss. This tool is heme–negative. What is the next best step in management?
a. Upper endoscopy
b. serology for H. pylori
c. urea breath testing for H. pylori
d. PPI, amoxicillin, and clarithromycin for two weeks.
e. Ranitidine empirically.

Back 1

Answer: A – upper endoscopy should be performed in any patient above the age of 45 with persistent symptoms of epigastric discomfort.
That is, essentially, to exclude the possibility of gastric cancer.
There is no way to be certain, without endoscopy, who has gastric cancer

Front 2

56. Non–ulcer dyspepsia?

Back 2

This is the most common cause of epigastric discomfort.
You can conclude that a person has non–ulcer dyspepsia. Only after endoscopy has excluded ulcer disease, gastric cancer, and gastritis: this is a diagnosis of exclusion.

Front 3

57. Treatment of non–ulcer dyspepsia?

Back 3

a. H2 blockers
b. liquid antacids
c. PPIs

Front 4

Can gastritis be associated with H. pylori?

Back 4

Yes (most common etiology). If it is present, treat with a PPI and 2 antibiotics.

Front 5

Causes of Type A Gastitis.

Back 5

Atrophy of the gastric mucosa caused by:

1. Autoimmune processes, such as vitamin B12 deficiency.

2. Diminished gastric acid production and achlorhydria. All patients with achlorhydria will have markedly elevated gastrin levels because acid inhibits gastrin release from G cells.

Front 6

Causes of Type B Gastitis.

Back 6

1. Helicobacter

2. NSAIDs
3. head trauma
4. Burns
5. intubation
6. Crohn's disease
7. Zollinger Ellison syndrome.

It is also associated with increased gastric acid production.

Front 7

Atrophic gastritis is caused by....?

Back 7

a. Pernicious anemia.
b. It is associated with vitamin B12 deficiency.
This type of gastritis will not improve with treatment for H. pylori.

Front 8

What most patients with gastritis present with?

Back 8

Asymptomatic bleeding.

Front 9

Most accurate diagnostic test for gastritis?

Back 9

a. Endoscopy with biopsy.
b. If this is done, no further testing is necessary for helicobacter.

Front 10

How vitamin B12 deficiency and pernicious anemia are initially diagnosed?

Back 10

Vitamin B12 deficiency and pernicious anemia are initially diagnosed with a low vitamin B12 level and an increased methylmalonic acid level.

Front 11

How the diagnosis of pernicious anemia is confirmed?

Back 11

Presence of antiparietal cell antibodies and anti-intrinsic factor antibodies.

Front 12

Serology testing for gastritis: sensitivity and specificity?

Back 12

a. Very sensitive but nonspecific.
b. If the serology is negative, this excludes helicobacter.
c. A positive test cannot distinguish between new and previous infection.
d. Breath testing and stool antigen testing: these are not the standard or routinely used. They can however distinguish between new and old disease.

Front 13

Treatment of gastritis?

Back 13

a. PPI and
b. clarithromycin and amoxicillin.
c. Only treat helicobacter if it's associated with gastritis or ulcer disease.

Front 14

Treatment for H. pylori fails, next step?

Back 14

a. Repeat treatment with two new antibiotics and a PPI.
b. Try metronidazole and tetracycline instead of clarithromycin amoxicillin.

Front 15

If repeat treatment fails?

Back 15

And evaluate for Zollinger–Ellison syndrome (Gastrinoma).

Front 16

How to treat H. pylori for nonulcer dyspepsia?

Back 16

Note: there is no proven benefit to treating H. pylori for nonulcer dyspepsia.

Front 17

What abnormality leads to metaplasia of the gastric mucosa as well as possible dysplasia and then to gastric cancer?

Back 17

MALT (mucosal-associated lymphoid tissue).

Front 18

Can tobacco smoking, alcohol, and the use of steroids by themselves to cause ulcer disease?

Back 18

Tobacco smoking, alcohol, and the use of steroids by themselves do not cause ulcer disease.
Tobacco and alcohol use can delay healing and are associated with the development of gastritis, but they do not cause ulcers

Front 19

58. what are the most common causes of peptic ulcer disease after H. pylori?

Back 19

1. NSAIDs (most common)
2. head trauma
3. Burns
4. intubation
5. Crohn's disease
6. Zollinger Ellison syndrome.

Front 20

59. In what percentage of patients with gastric ulcers does gastric cancer develop?

Back 20

4%

Front 21

The 3 stimulants to the production of acid from the gastric parietal cells.

Back 21

1. Gastrin - produced by G cells in the stomach, and its release is stimulated by distention of the stomach.

2. Histamine - released by enterochromaffin-like cells present in the same glandular elements of the stomach that have the parietal and chief cells.

3. Acetylcholine - released by Vagal stimulation

Front 22

How to distinguish duodenal ulcer and gastric ulcer by symptoms alone.

Back 22

There is no way to distinguish duodenal ulcer and gastric ulcer by symptoms alone. The alteration of pain with food is only suggestive, not definitive.
Food more often makes gastric ulcer pain worse and duodenal ulcer pain better.
However, for if the patient is above 45 and has epigastric pain, you must scope to exclude gastric cancer.

Front 23

Best diagnostic test for Ulcer disease?

Back 23

Endoscopy.

Front 24

Healthy patient <45 years old with persistent dyspepsia. Next step?

Back 24

1. "test-and-treat" approach (urea breath test).

2. empirical therapy with PPI.

Front 25

Patient >45 years old or those with alarm symptoms (weight loss, anemia, heme-positive stools, or dysphagia). Next step?

Back 25

endoscopy (Risk for cancer)

Front 26

69. stress ulcer prophylaxis?

Back 26

Routine prophylactic use of a PPI or H2 blocker or sucralfate should only be used if one of the following is present:
1. head trauma
2. intubation and mechanical ventilation
3. Burns
4. coagulopathy and steroid using combination
NSAID or steroid use alone is not an indication for routine stress ulcer prophylaxis.

Front 27

70. A 52–year–old man has epigastric discomfort. He is seropositive for H. pylori.upper endoscopy reveals no gastritis and no ulcer disease. Biopsy of the stomach shows helicobacter. What should you do for? Deactivating your new 362. Your new phone
a. Breath testing
b. PPI alone as symptomatic therapy.
c. Repeat endoscopy after six weeks of PPIs.
d. PPI, amoxicillin, and clarithromycin.

Back 27

B: PPI alone as symptomatic therapy.
You do not need to treat H. pylori, unless there is gastritis or ulcer disease.
This patient is epigastric pain and H. pylori, but no ulcer or gastritis.
This is non–ulcer dyspepsia.
Treated symptomatically with a PPI.
Enormous numbers of people are colonized H. pylori; you do not need to eradicate it from the worlds without evidence of disease.
H. pylori is not the cause of non–ulcer dyspepsia.

Front 28

71. A man is found to have ulcer disease. There are three ulcers in the distal esophagus 1–2 cm in size. The ulcers persist despite treatment for helicobacter. What should you do next?
a. Switch antibiotics
b. breath testing
c. gastrin level and gastric acids output.
d. CT scan of the abdomen
e. ERCP

Back 28

Answer: C – gastrin level in gastric acid output testing should be done when there is possibility of zollinger–Ellison syndrome.
ERCP will only show the ducts of the pancreas and gallbladder; it will not reveal gastrinoma.

Front 29

When should you test the gastrin level and gastric acid output?

Back 29

a. Large ulcer (> 1 cm)
b. multiple ulcers
c. distal location near the ligament of Treitz
d. recurrent or persistent despite helicobacter to treatment

Front 30

How is Zollinger–Ellison syndrome (ZES) or gastrinoma diagnosed?

Back 30

ZES is diagnosed through a finding of elevated gastrin level and elevated gastric acid output.

Front 31

What is the most accurate test of ZES?

Back 31

secretin stimulation test

Front 32

79. What is the normal effect of infusing secreting intravenously?

Back 32

a. Normal people decreased gastrin levels and acid output.
b. Patients with ZES show no change or increase in gastrin levels and no decrease in acid levels.

Front 33

74. If the gastrin level and acid output are both elevated, what should you do next?

Back 33

Localize the gastrinoma.

Front 34

75. What are the most accurate test to localize the gastrinoma?

Back 34

1. Endoscopic ultrasound (most sensitive)
2. nuclear somatostatin scan

Front 35

76. Benefit of endoscopic ultrasound for the ZES?

Back 35

An endoscopic ultrasound is like a transesophageal echocardiogram. It is much more sensitive than a surface ultrasound.

Front 36

77. Benefit of nuclear somatostatin scan for ZES?

Back 36

The nuclear somatostatin scan is very sensitive, because patients with ZES have an enormous increase in the number of somatostatin receptors.

Front 37

80. Treatment of ZES local disease?

Back 37

Surgical resection

Front 38

81. treatment of ZES metastatic disease?

Back 38

Lifelong PPIs.

Front 39

How is gastrin level in pt. on H2 blocker or PPI?

Back 39

Note: remember, everyone on an H2 blocker or PPI has an elevated gastrin level.

Front 40

83. Characteristics to most ulcers have?

Back 40

a. Single
b. < 1 cm
c. proximal near the pylorus
d. easily resolved with treatment

Front 41

84. what is the clue to the presence of a parathyroid problem with ZES and thus MEN syndrome?

Back 41

Hypercalcemia

Front 42

85. presentation of IBD (both Crohn's disease and ulcerative colitis)?

Back 42

1. Fever
2. Abdominal pain.
3. Diarrhea.
4. Blood in the stool.
5. Weight loss
b. UC most often presents with abdominal pain and bloody diarrhea.

Front 43

86. Six extra intestinal manifestations of IBD?

Back 43

1. Joint pain
2. Eye findings (iritis, uveitis, episcleritis)
3. skin findings (Pyoderma gangrenosum, erythema nodosum.
4. Sclerosing cholangitis

Front 44

87. what features are more common to Crohn's disease?

Back 44

1. Masses
2. skip lesion
3. involvement of the upper G.I. Tract
4. perianal disease
5. transmural granulomas
6. fistulae
7. hypocalcemia from fat malabsorption
8. obstruction
9. calcium oxalate kidney stones
10. cholesterol gallstones
11. vitamin B12 malabsorption from terminal ileum involvement.

12. Prothrombin time may be prolonged also because of malabsorption of vit K.

Front 45

Does Sclerosing cholangitis correlate to IBD activity?

Back 45

NO

Front 46

88. Diagnostic testing for both CD and UC?

Back 46

a. Endoscopy is diagnostic for both
b. barium studies are also diagnostic in both
c. when the diagnosis is not clear from endoscopy or barium studies, blood tests are helpful.

Front 47

89. ASCA (anti–Saccharomyces cerevisae) and ANCA (anti–neutrophil cytoplasmic anybody) in Crohn's disease?

Back 47

a. ASCA: positive
b. ANCA: negative

Front 48

90. ulcerative colitis ASCA and ANCA?

Back 48

a. ASCA: negative
b. ANCA: positive.

Front 49

91. Initial therapy for both CD and UC?

Back 49

Mesalamine derivatives:

Pentasa, Rowasa, Asacol.

Front 50

Pentasa usage?

Back 50

Pentasa is a form of mesalamine released in both the upper and lower bowel; hence, it is used in CD.

Front 51

Rowasa usage?

Back 51

Rowasa is used exclusively for rectal disease.

Front 52

Asacol usage?

Back 52

Asacol is a form of mesalamine released in the large bowel, and it is most useful for UC.

Front 53

92. Why is sulfasalazine, not the best initial therapy for either CD or you see?

Back 53

Because of the following adverse effects:
1. rash
2. hemolytic anemia
3. interstitial nephritis.

Front 54

93. 6 Other medical options for the treatment of IBD?

Back 54

a. Steroids: budesonide
b. azathioprine and 6–mercaptopurine.
c. Infliximab
d. metronidazole and ciprofloxacin
e. surgery

Front 55

Tx. of acute exacerbations of IBD.

Back 55

high-dose steroids (budesonide)

Front 56

94. utility of budesonide (steroid) in the treatment of IBD?

Back 56

a. Can be used to control ACUTE EXACERBATIONS of IBD.
b. It has extensive first pass effect in the liver and, therefore, has limited systemic adverse effects.

Front 57

95. Utility of azathioprine and 6–mercaptopurine in IBD?

Back 57

a. Used in severe disease who have recurrent symptoms when the steroids are stopped.
b. Azathioprine and 6MP are used to wean a patient off steroids..

Front 58

Most common SE of azathioprine and 6–mercaptopurine in IBD?

Back 58

drug-induced pancreatitis

Front 59

96. MOA of infliximab

Back 59

MOA of infliximab

Front 60

97. Utility of infliximab in IBD?

Back 60

a. TNF inhibitor that is most useful in controlling CD that is associated with fistula formation
b. TNF is what maintains a granuloma in place.
c. Administer a PPD and give isoniazid, if the PPD is positive prior to the use of infliximab.
d. Remember to screen for tuberculosis; infliximab can reactivate TB by releasing dormant TB from granulomas.

Front 61

98. Utility of metronidazole and ciprofloxacin in CD?

Back 61

These antibiotics are used for perianal involvement in Crohn's disease.

Front 62

99. Utility of surgery for IBD (UC vs CD)?

Back 62

a. Can be curative in UC by removing the colon.
b. Reoccur in CD. Occasionally, you must do surgery and CD, despite the risk of recurrence, if there is a stricture and obstruction.