Gi_Stomach: Inflammatory Disease Of The Stomach And Duodenum

Front 1

a medical condition characterized by indigestion with chronic or recurrent pain in the upper abdomen, upper abdominal fullness and feeling full earlier than expected with eating

Back 1

DYSPEPSIA

Front 2

This is often accompanied by bloating, belching, nausea, or heartburn.

Back 2

DYSPEPSIA

Front 3

What are possible ETIOLOGIES of DYSPEPSIA?

Back 3

1. gastro-duodenal ulcer
2. GERD
3. gastritis
4. functional (non-ulcer) dyspepsia (60%)
5. gastric cancer
6. occasionally medication

Front 4

What MEDICATIONS could possibly cause DYSPEPSIA?

Back 4

1. calcium antagonists
2. nitrates
3. theophylline
4. bisphosphonates
5. corticosteroids
6. NSAIDs

Front 5

inflammation of gastric mucosa

Back 5

GASTRITIS

Front 6

What are the CATEGORIES of GASTRITIS?

Back 6

1. erosive and hemorrhagic gastritis
2. nonerosive, nonspecific (histologic) gastritis
3. specific types of gastritis (distinctive histologic and endoscopic features that are diagnostic of d/o)

Front 7

What are the most common CAUSES of EROSIVE GASTRITIS?

Back 7

1. drugs
2. alcohol
3. stress due to severe medical or surgical illness
4. portal hypertension ("portal gastropathy")
--not so common:
5. caustic ingestion
6. radiation

Front 8

A pt with this condition is usually asymptomatic; however, those with symptoms experience:
1. anorexia
2. epigastric pain (dyspepsia)
3. nausea
4. vomiting
5. upper gastrointestinal bleed (not a significant bleed, but this sx is the most common clinical manifestation)

Back 8

EROSIVE GASTRITIS

Front 9

T/F. Dyspepsia develops in >25% of pts on chronic NSAID use.

Back 9

FALSE; <25%

Front 10

What is the initial treatment of NSAID GASTRITIS?

Back 10

1. discontinue agent or reduce NSAID to lowest effective dose
2. give PPI
3. administer with meals

Front 11

If the INITIAL TREATMENT of NSAID GASTRITIS fails, and s/he experiences persistent sxs, what should you do?

Back 11

an endoscopy; if no ulcerations, pt can be tx'd symptomatically with:
1. H2 blocker
2. sucralfate
3. proton pump inhibitor

Front 12

This accounts for 20% of upper GI bleeds in chronic alcoholics.

Back 12

ALCOHOLIC GASTRITIS

Front 13

How would you treat ALCOHOLIC GASTRITIS?

Back 13

1. H2 blocker
2. sucralfate
3. PPI prescribed for 2-4 weeks
4. discontinue alcohol use

Front 14

Mucosal erosion and subepithelial hemorrhage develop within 72 hours of patients becoming critically ill with this condition.

Back 14

STRESS GASTRITIS

Front 15

What are MAJOR RISK FACTORS of STRESS GASTRITIS?

Back 15

1. mechanical ventilation
2. coagulopathy
3. trauma
4. burns
5. hypotension
6. burns
7. hypotension
8. sepsis
9. CNS injury
10. hepatic or renal failure
11. multiorgan failure

Front 16

How would you PROPHYLACTICALLY treat pts with risk factors of STRESS GASTRITIS?

Back 16

1. enteral nutrition reduces the risk of stress-related bleeding
2. H2 blocker of sucrlfate

Front 17

What are the MAIN CAUSES of NONEROSIVE, NONSPECIFIC GASTRITIS?

Back 17

1. Helicobacter pylori infection
2. pernicious anemia
3. lymphocytic gastritis

Front 18

--a spiral, gram-negative bacillus with unipolar flagella
--found in >50% of adults over 60 years of age in U.S.
--transmission is person to person (via gasto-oral--> exposure to vomit)

Back 18

Helicobacter pylori

Front 19

A pts has a biopsy of an inflamed gastric tissue, which reveals the presence of Polymorphonuclear lymphocytes. What should be a part of your differential?

Back 19

Helicobacter pylori gastritis

Front 20

This condition it associated with:
1. peptic ulcer disease (PUD)
2. gastric adenocarcinoma
3. low-grade B cell gastric lymphoma (MALT) by 2 to 6 fold

Back 20

HELICOBACTER PYLORI GASTRITIS

Front 21

MALT

Back 21

mucosa associated lymphoid tissue

Front 22

Testing for HELICOBACTER PYLORI is indicated for who?

Back 22

1. pts with active or past hx or PUD
2. gastric MALToma
3. pts with family hx of gastric carcinoma (esp if Asian descent)
4. uncomplicated dyspepsia (no "alarm" sxs") in pts <45 yo, not requiring endoscopy

Front 23

What types of TESTS could you use to to diagnose HELICOBACTER PYLORI?

Back 23

1. serologic tests (ELISA)
2. fecal antigen test
3. urea breath or blood test
4. endoscopy biopsy

Front 24

How would you generally TREAT HELICOBACTER PYLORI?

Back 24

PPI + 2 antibiotics

Front 25

Characteristics of this condition include:
1. autoimmune d/o
2. achlorhydria
3. fundus severe gland atrophy and intestinal metaplasia
4. parietal cell antibodies present in 90% of pts (destruction causes loss of intrinsic factor secretion)
5. vitamin B12 malabsorption

Back 25

PERNICIOUS ANEMIA GASTRITIS

Front 26

Associated with this condition:
1. development of small, multicentric carcinoid tumors in 5% of pts
2. adenocarcinoma increased 3 fold, prevalence is 1-3%
3. endoscopy and biopsy is indicated in pts at the time of dx!

Back 26

PERNICIOUS ANEMIA GASTRITIS

Front 27

This is used to evaluate d/o's associated with malabsorption of vitamin B12
--pts are given oral dose of radioactive B12, then an IM dose of nonradioactive B12
--urine is collected for 24 hrs and analyzed for radioactive B12
(IM B12 flushes the radioactive B12 into the urine; failure of radioactive B12 to appear indicates impaired absorption of the vitamin)
--during repeat testing, intrinsic factor is administered orally along with radioactive B12, then the IM dose of B12
--if radioactive B12 now appears in the urine, it indicates the pt has a lack of intrinsic factor
--if radioactive B12 still does not appear in the urine, there is another pathologic process

Back 27

SCHILLING TEST

Front 28

A break in the gastric or duodenal mucosa, usually >5mm in diameter

Back 28

PEPTIC ULCER DISEASE (PUD)

Front 29

______ ulcers are more common than ______ uclers.

Back 29

duodenal > stomach

Front 30

PEPTIC ULCER DISEASE is more common in pts taking ____ and those with _____ infection.

Back 30

--NSAIDS
--H. pylori

Front 31

Increased risk of PEPTIC ULCER DISEASE is associated with what?

Back 31

SMOKING (not alcohol, dietary factors, or emotions/stress)

Front 32

What are the main CAUSES of PEPTIC ULCER DISEASE?

Back 32

1. Helicobacter pylori
2. NSAIDs/ASA
3. Acid hypersecretory states (i.e., Zollinger-Ellison Syndrome)
--25% of ulcers are idiopathic

Front 33

These are typically located in the antrum of the stomach, and a biopsy for helicobacter pylori is indicated.

Back 33

GASTRIC ULCER

Front 34

If you suspect a pt over 40 yo has a GASTRIC ULCER, even if s/he has known NSAID/ASA use, what should you do? Why?

Back 34

bxs to r/o gastric cancer

Front 35

This usually develops in the PYLORIC CHANNEL when more acid is secreted than can be neutralized. It is always benign and the pt does not need a biopsy (except in the setting of CROHN'S DZ)

Back 35

DUODENAL ULCERS (a gastric bx for H. pylori should be done, though)

Front 36

Clinical presentation of this condition includes:
1. epigastric pain (dyspepsia)--hallmark sign
2. vomiting
3. anorexia
4. weight loss

Back 36

PEPTIC ULCER DISEASE

Front 37

Pts with these usually report relief of pain WITH FOOD or ANTACIDS; recurrence of pain 2-4 hours AFTER.

Back 37

DUODENAL ULCERS

Front 38

Pts with these usually report LESS PAIN with FASTING, and onset of pain usually occurs shortly AFTER EATING (5-15 min)

Back 38

GASTRIC ULCERS

Front 39

Is the below symptom better or worse with GASTRIC or DUODENAL ULCERS?
1. nocturnal pain that awakens pt
2. vomiting
3. anorexia

Back 39

1. duodenal > gastric
2. gastric > duodenal
3. gastric > duodenal

Front 40

What could help you diagnose PEPTIC ULCER DISEASE?

Back 40

1. upper GI series
2. endoscopy ("Gold Standard")
3. lab
a. fasting gastrin level if Zollinger-Ellison Syndrome is suspected)
b. H. pylori test

Front 41

How would you treat PEPTIC ULCER DISEASE?

Back 41

--risk factor intervention
1. treat H. pylori
2. avoid asprin, NSAIDs (if possible)
3. cigarette smoking cessation

Front 42

What are the ACID-ANTISECRETORY AGENTS for the treatment of PEPTIC ULCER DISEASE?

Back 42

1. Proton-pump inhibitors (preferred agent)
2. H2 blockers (2nd line therapy)

Front 43

This ACID-ANTISECRETORY AGENT
1. has a duration of action of >24hrs,
2. inhibits over 90% of acid secretion,
3. is administered 30 min before a meal once a day,
4. is used for at least 8 weeks for gastric ulcers or at least 4 weeks for duodenal ulcers

Back 43

PPI

Front 44

This ACID-ANTISECRETORY AGENT
1. blocks nocturnal acid secretion,
2. is less effective at inhibiting meal-stimulated acid-secretion,
3. and is taken for 6-8 weeks

Back 44

H2 BLOCKERS

Front 45

Besides the main acid-antisecretory agents, what are other possible drug treatments for PUD?

Back 45

--cytoprotective drugs
a. sucralfate
b. misoprostol

Front 46

What are possible COMPLICATIONS associated with PUD?

Back 46

1. obstruction of the lumen by scarring or edema
2. hemorrhage form erosion of ulcer into artery
3. perforation form penetration of ulcer through all layers of gastroduodenal wall and into peritoneum (severe, sudden abdominal pain, lie still with rigid abdomen, pale, hypotensive, appear very ill; CXR = free air under the diaphragm; surgical emergency)
4. penetration when ulcer extends full thickness and into adjacent organs

Front 47

another word for GASTRINOMA

Back 47

ZOLLINGER-ELLISON SYNDROME

Front 48

What are some KEY POINTS of ZOLLINGER-ELLISON SYNDROME?

Back 48

1. PUD may be severe or atypical
2. gastric acid hypersecretion
3. hypergastrinemia
4. diarrhea common; relieved by nasogastric suction
5. most cases sporadic; 25% with multiple endocrine neoplasia type 1 (MEN 1)
6. gastrin-secreting neuroendocrine tumor (gastrinoma--2/3 = malignant)
7. PUD is usually in the duodenal bulb or more distal

Front 49

Clinical presentation of this condition includes:
1. upper abdominal pain, mimicking sxs of PUD
2. heartburn
3. nausea/vomiting
4. upper GI bleed due to ulcers
5. diarrhea
6. steatorrhea
7. weight loss
(the last 3 usually due to acid hypersecretion that inactivates pancreatic enzymes)

Back 49

ZOLLINGER-ELLISON SYNDROME

Front 50

How would you diagnose ZOLLINGER-ELLISON SYNDROME?

Back 50

1. elevated serum gastrin (>1000 pg/mL)
2. gastric analysis
a. pH < 2.0
b. gastric secretory study = acid hypersecretion
3. EGD: hypertrophic folds and duodenal ulcers can be seen
4. somatostatin receptor scintigraphy (SRS) --if not available, then CT
5. endoscopic ultrasound

Front 51

How would you treat ZOLLINGER-ELLISON SYNDROME?

Back 51

1. surgical removal of the tumor
2. control acid secretion with HD PPI