Cm Ii: Gastritis And Peptic Ulcer Disease

Front 1

Describe peptic ulcer disease.

Back 1

ulceration in lining of duodenum and stomach

Front 2

How does peptic ulcer disease arise?

Back 2

due to imbalance between mucosal protective factors and various damaging mechanisms

Front 3

Describe gastritis.

Back 3

self-limited inflammation of gastric mucosa

Front 4

If you have a patient with epigastric pain, N/V with variable blood in vomitus, what could you suspect?

Back 4

acute gastritis

Front 5

What are causes of acute gastritis?

Back 5

Aspirin and NSAIDs, alcohol, acid and alkali ingestion; stress, shock-related mucosal ischemia, sepsis

Front 6

How do gastric erosions develop?

Back 6

due to direct effects of toxic substancesor breakdown of mucosa

Front 7

What can cause gastric erosions?

Back 7

alcohol (via oversecretion of HCl); aspirin and NSAIDs; shock

Front 8

What are terms for gastric stress ulcers?

Back 8

cushing (brain injury) and curling (burns) ulcers

Front 9

What is a chronic inflammation of mucosa?

Back 9

non-erosive gastritis

Front 10

What are some causes of non-erosive gastritis?

Back 10

immunologic mechanisms, infection, prolonged ingestion of drugs, alcohol, cigarette smoking

Front 11

What is the difference between Chronic Type A gastritis and Chronic Type B gastritis?

Back 11

Type A is autoimmune and has increased risk of gastric adenocarcinoma; Type B is caused by H. pylori with infiltration of neutrophils in glands/lamina propria

Front 12

The late stages of Chronic Type A and Type B gastritis are a/w?

Back 12

atrophy of gastric glands, intestinal metaplasia, lymphocytic follicles in the mucosa

Front 13

If a patient has diffuse distribution of lesions in the fundus with reduced gastric secretion, low serum B12, increased gastrin, what could you suspect?

Back 13

Chronic Type A Gastritis

Front 14

If a patient has focal distribution of lesions in the pyloric antrum with normal gastric secretion, normal serum B12, normal gastrin and antibodies to H. pylori, what could you suspect?

Back 14

Chronic Type B Gastritis

Front 15

Which is more common Chronic Type A or Type B Gastritis?

Back 15

Chronic Type B Gastritis

Front 16

What does H. pylori secrete that can cause peptic ulcers?

Back 16

urease, protease, phospholipase

Front 17

In peptic ulcer caused by infection what can contribute to healing of the ulcers?

Back 17

eradication of H. pylori

Front 18

How predominant is H. pylori in duodenal ulcers? in gastric ulcers?

Back 18

90%; 65%

Front 19

What are the various causes of PUD?

Back 19

infection, neuro-endocrine, local mucosal factors

Front 20

How do NSAIDs contribute to peptic ulcers?

Back 20

reduce prostaglandins and damage mucosal barrier

Front 21

Where are peptic ulcers generally located?

Back 21

duodenum and stomach

Front 22

What is the most common type of peptic ulcer?

Back 22

duodenal and most are SOLITARY

Front 23

What is likely happening if there are multiple ulcers, or in unusual locations or not responding to usual treatment?

Back 23

gastrin-secreting tumor (zollinger-ellison syndrome)

Front 24

How can you differentiate between an ulcer and adenocarcinoma?

Back 24

smooth edges = ulcer

Front 25

What is the most common complication of peptic ulcer?

Back 25

hemorrhage

Front 26

Beyond hemorrhage, what are other complications of peptic ulcers?

Back 26

performation; stenosis and obstruction; penetration into pancreas and elevated serum amylase

Front 27

Histologic examination of peptic ulcer reveals....

Back 27

superficial zone of necrosis; acute inflammatory exudates full of NEUTROPHILS; granulation tissue rich in blood vessels; scarring at the bottom

Front 28

Where are gastric ulcers most commonly located?

Back 28

antrum

Front 29

A patient presents with hunger-like pain at the epigastrum that fluctuates in intensity throughout day/night with pain-free periods; pain occurs 2-4 hours after meal and patient finds relief with use of antacids or eating, what could you suspect?

Back 29

duodenal peptic ulcer

Front 30

If the patient's pain occurred sooner than 2-4 hours after meal and was not relieved by eating or antacids reliably, what could you suspect?

Back 30

gastric peptic ulcer

Front 31

If patient has a pyloric obstruction, what S/S would be present?

Back 31

N/V

Front 32

If patient has a perforation, what S/S would be present?

Back 32

rigid abdomen/rebound tenderness

Front 33

If patient has bleeding ulcer, what S/S would be present?

Back 33

hematemesis or melena

Front 34

If patient has acute or chronic blood loss, what S/S would be present?

Back 34

pallor, hypotension, tachycardia

Front 35

What tests should be done to work up a peptic ulcer?

Back 35

CBCs, LFTs, amylase, lipase, gastrin, fecal occult blood

Front 36

What is done in testing for H. pylori?

Back 36

endoscopy biopsy, urea breath test, stool antigen, specific antibody testing, serologic testing for antibodies

Front 37

What is essential in diagnosing GASTRIC ulcers?

Back 37

endoscopy

Front 38

What is the GOLDEN STANDARD for diagnosing esophagitis, gastritis, duodenitis?

Back 38

endoscopic biopsy for H. pylori

Front 39

What is a less expensive, less invasive method of diagnosis?

Back 39

UGI with DOUBLE contrast

Front 40

What is the treatment for peptic ulcers?

Back 40

eradication of H. pylori, lifestyle changes; H2RAs, PPIs, misprostol; vagotomy, subtotal gastrectomy; D/C ASA or NSAIDs, avoid tobacco, alcohol, caffeine; OTC antacids

Front 41

How long should drugs be taken for H. pylori?

Back 41

10 days to two weeks

Front 42

What drugs are indicated for H. pylori?

Back 42

antibiotics (metronidazole, TCN, clarithromycin, amoxicillian); H2RAs, PPIs; bismuth subsalicylate, misoprostol

Front 43

What is the most common malignant tumor of the stomach?

Back 43

adenocarcinoma

Front 44

What is the third most common GI cancer in the US?

Back 44

gastric cancer

Front 45

What are the risk factors for gastric cancers?

Back 45

high consumption of smoked fish containing nitrosamines; food spoilage; lower social classes; tobacco smoking

Front 46

What predisposes a patient to gastric cancer?

Back 46

H. pylori infection; chronic atrophic gastritis with intestinal metaplasia; postgastrectomy states; gastric adeomatous polyps

Front 47

What is the appearance of flat mucosal lesions?

Back 47

often not detectable

Front 48

What is the appearance of exophytic tumors?

Back 48

plypoid or fungating (cauliflower-like)

Front 49

What is the appearance of ulcerating tumors?

Back 49

irregular margins, crater-like

Front 50

What is the appearance of diffusely infiltrating tumors?

Back 50

give leather appearance (linitis plastic)

Front 51

Where are gastric cancers most likely to occur?

Back 51

pylorus and pyloric antrum

Front 52

Where does metatasis generally occur in gastric cancer?

Back 52

local lymph nodes; virchow node; liver and lungs

Front 53

What is the most common site of extra nodal malignant lymphoma?

Back 53

gastric lymphoma

Front 54

When is a GI stromal tumor considered malignant?

Back 54

> 6 cm; necrosis, hemorrhage, high mitotic rate