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GI > Stomach > Flashcards

Stomach Flashcards

1
Q

definition of dyspepsia

A

epigastric fullness, belching, bloating, discomfort, and heartburn

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2
Q

Alarm signs for dyspepsia

A

but if onset is recent and the patient is > 40 years, it is organic until proven otherwise.

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3
Q

Organic causes of dyspepsia

A 
PUD,
gastritis, 
GERD, 
biliary colic, 
gastroparesis, 
pancreatitis, 
and cancer
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4
Q

Non-ulcer dyspepsia

A

recurrent upper abdominal pain with a normal EGD

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5
Q

gastropathy

A

subepithelial hemorrhage

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6
Q

common causes of gastropathy

A

NSAIDs, alcohol, severe physiologic stress

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7
Q

stress-related mucosal damage (SRMD) risk factors

A 
ICU
severe physiologic stress, such as that induced by major surgery or bums
severe CNS injuries
being on a ventilator
having a coagulopathy
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8
Q

How to decrease the incidence of erosive gastritis?

A 
H2 receptor antagonists, 
antacids, 
PPls, 
sucralfate, 
and even early feedings
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9
Q

the most effective treatment for SRMD

A

Continuous infusion of an H2 receptor antagonist

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10
Q

Chronic gastritis classification (different ways)

A
  1. Histologically

2. by location

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11
Q

Histological classification of chronic gastritis

A 
lymphocyte and plasma cell infiltrate
•superficial gastritis (early)
•atrophic gastritis (mid)
•gastric atrophy (Iate}-also called metaplastic atrophic gastritis.
mid & late=chronic gastritis
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12
Q

“By location” classification of chronic gastritis

A

Type A

Type B

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13
Q

Type A chronic gastritis

A 
It affects the proximal stomach (fundus&body)
Autoimmune.
Atrophic. 
pernicious Anemia, 
Achlorhydria
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14
Q

universal feature of atrophic gastritis

A

Metaplasia is a universal feature of atrophic gastritis, and it appears before and is associated with. both pernicious anemia and gastric cancer

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15
Q

the incidence of gastric cancer in patients with atrophic gastritis

A

the incidence of gastric cancer is so low with atrophic gastritis that if there is no cancer or dysplasia on initial endoscopic exam, periodic endoscopic exams are not warranted

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16
Q

the most common form of chronic gastritis (80%)

A

Type B

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17
Q

Type B chronic gastritis

A

Helicobacter pylori infection is the cause

chronic distal/antral gastritis

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18
Q

should all the patients with H.pylori be treated?

A

only the symptomatic ones are treated

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19
Q

Is H. pylori responsible for dyspeptic symptoms in the absence of ulcers’?

A

This is complicated, and most controlled studies
show no benefit of H. pylori eradication over placebo in the H. pylori-infected, non-ulcer dyspeptic patient. However, if a patient presents with dyspeptic symptoms and does not have
warning signs, it is reasonable to look for H. pylori
and treat if positive.

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20
Q

So when do you look for H. pylori?

A
  1. Any prior history of PUD, complicated or uncomplicated
  2. Current findings on EGD of ulcer disease, erosive gastritis, or duodenitis
  3. Dyspeptic symptoms in the non-evaluated patient if the strategy is “test and treat;”
  4. Family history of gastric cancer.
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21
Q

The gold standard for H. pylori testing

A

histologic examination of biopsied antral mucosa

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22
Q

Urease tests(invasive test) good for?

A

good for checking for active disease and response to therapy

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23
Q

Urease tests are less sensitive if the patient….

A

Urease tests are less sensitive if the patient is on a drug that may blunt the effect of H. pylori infection, such as PPls and antibiotics-so these should be Stopped for 2 weeks before testing

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24
Q

first choice for checking effectiveness of treatment

A

Urea breath tests (UBT),

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25
Q

non invasive test that is a good method for primary diagnosis of H.pylori

A

Stool antigen tests

26
Q

A test in a dyspeptic patient that rules out H. pylori as the cause

A

Serologic tests (ELlSA- lgG)

27
Q

Which type of H. pylori tests is not good for checking effectiveness of treatment?

A

Serologic tests (ELlSA- lgG)

28
Q

Risk factors for conventional NSAID-induced PUD

A 
First 3 months of use, 
high doses, 
elderly patient, 
history of ulcer disease, 
cardiac disease, 
concurrent steroids, 
serious illness, 
and concurrent ASA(such as for cardioprotection).
29
Q

the leading cause of bleeding ulcers in the U.S.

A

NSAIDs

30
Q

If a perforated ulcer is suspected

A

do the upright x-ray first! EGD and UGI are contraindicated.

31
Q

If 1st course of therapy (PPl and 2 antibiotics) fails to eradicate H. pylori.

A

some recommend PPI + amoxicillin + levofloxacin.

32
Q

drug of choice for PUD in renal patients

A

Sucralfate is often the drug or choice in renal patients because it also binds PO4.

33
Q

smoking in PUD

A

it increases risk of recurrence and perforation in ulcers not associated with H. pylori or untreated H. pylori ulcers.

34
Q

Indications for surgery in PUD

A
  • UGI bleed—active bleed unable to stop via endoscopic therapy.Surgery is required in only 5% of UGI bleeds.
  • Gastric outlet obstruction— initial treatment is balloon dilation. Surgery required in -25%.
  • Perforation—laparascopic repair may be possible.
  • Recurrent/refractory ulcers (rare).
  • Zollinger-Ellison syndrome (ZES).
35
Q

Treatment of Gastric ulcers not associated with H. pylori

A

are treated for 3 months because these heal more slowly than duodenal ulcers. PPls and misoprostol (a synthetic prostaglandin) are superior to H2 blockers and sucralfate in the prevention of NSAID induced ulcers.

36
Q

Risk factors indicating a severe bleed and/or a high risk of further rebleed include:(PUD)

A
  • hemodynamic instability
  • recurrent red-colored hernatemesis or hematochezia
  • lack of clearing of gastric lavage effluent
37
Q

when we should consider angiographic therapy in bleeding ulcers?

A

only if the patient is not a candidate for surgery

38
Q

what drug in bleeding ulcer?

A

Several studies have shown aggressive inhibition of acid when an oral PPI is given bid. Oral PPI bid or intravenous PPI reduces the risk of reblccding, Most patients with a bleeding ulcer should have prompt IV treatment

39
Q

The most common presentation of ZES

A

diarrhea

40
Q

where are the most common locations of Gastrinomas?

A

Gastrinomas most frequently occur in the duodenum (-50%) or pancreas (-25%), and less frequently in the stomach, lymph nodes, and spleen.

41
Q

ZES is associated with what group of disease?

A

MEN type 1

42
Q

What is the usual cause of carcinoid?

A

Gastric carcinoids can be caused by long standing hypergastrinemic states-especially pernicious anemia

43
Q

When to consider ZES?

A
  • recurrent ulcers and no other risk factors,
  • recurrent complicated ulcers,
  • post-bulbar duodenal ulcers,
  • ulcers and chronic diarrhea (or severe esophagitis and chronic diarrhea)
44
Q

How to evaluate ZES?

A

To evaluate ZES, first order a serum gastrin while patient is off PPI therapy. If the gastrin level is elevated in a patient with gastric acid, present workup usually requires abdominal CT, endoscopic ultrasound, and somatostatin receptor imaging.

45
Q

Treatment of ZES

A

All patients with newly diagnosed ZES without evidence of metastatic disease warrant surgical exploration. 1/3 will be cured by resection of the primary tumor. Even with metastatic disease, treat ZES aggressively with resection of the primary tumor because the mass effect of the tumor tissue can eventually cause problems. A PPI is now the drug of choice for medical treatment of ZES,although the doseis higher than usual.

46
Q

conditions associated with an elevated gastrin level

A 
ZES
pernicious anemia, 
vitiligo, 
chronic gastritis, 
renal failure, 
hyperthyroidism, 
and achlorhydria induced by PPI use
47
Q

Gastric carcinoids are rare (0.5% of gastric tumors) and usually seen with (Types)

A

a chronic hypergastrinernic state. such as that seen ln:
• autoimmune gastritis/pernicious anemia (type I)
• ZES. when it occurs as part of multiple endocrine neoplasia-MEN-I (type 2)
Least often, it is spontaneous (type 3)

48
Q

carcinoid is associated with which dermatologic disease?

A

vitiligo

49
Q

Does PPI cause carcinoids?

A

The PPI omeprazole has not been shown to cause carcinoids in humans

50
Q

carcinoids characteristics

A

It is unusual for gastric carcinoids to metastasize or be symptomatic. They are slow growing and almost never cause carcinoid syndrome.

51
Q

4 significant malignancies of the stomach

A

I) curcinoids

2) adenocarcinoma
3) lymphoma
4) GIST (gastrointestinal stromal tumors,e.g., leiomyosarcoma)

52
Q

the Most common malignancy of stomach

A

adenocarcinoma (most common-95%!)

53
Q

2 distinct forms of gastric adenocarcinoma

A

a proximal diffuse type

and a distal intestinal type

54
Q

The risk factors and associations with gastric cancer include:

A

I) Chronic H. pylori (independent of ulcer disease) 2) Metaplastic (chronic) atrophic gastritis

3) Menetrier disease
4) Adenomatous gastric polyps

55
Q

It appears that distal gastric cancer is most strongly associated with

A

environmental factors, especially:
•a diet low in fruits and vegetables and high in dried, smoked, and salted foods, and
•foods rich in nitrates (animal studies).

56
Q

How to dianose and treat MALT?

A

some patients may develop MALT. This is diagnosed by EGD and biopsy. When the H.pylori infection treated, the MALT may resolve.Close endoscopic follow-up is necessary

57
Q

Does either alcohol consumption or gastric ulcer cause gastric cancer?

A

Neither alcohol consumption nor gastric ulcers has been proven to cause gastric cancer-as previously alleged even though gastric cancer appears as an ulcer.

58
Q

Diagnosis of gastric cancer

A

Often an ulcer is picked up on barium contrast study (double contrast is better). If it appears benign, it can be treated. Endoscopy and biopsy are necessary only if it does not heal. Endoscopy with multiple biopsies is the diagnostic procedure of choice. Tumor markers, such as carcinoembryonic antigen (CEA) and alpha fetoprotein (AFP), are of no use as early markers for gastric cancer.

59
Q

How to stage gastric cancer?

A

CT scan and endoscopic ultrasound

60
Q

Treatment of Gastric cancer

A

Treatment consists of surgical removal of the cancer and adjacent lymph nodes. Adjuvant combination chemotherapy prolongs survival.Adjuvant radiotherapy is investigational.

61
Q

Gastroparesis Dx and Rx

A

Diagnose suspected delayed gastric emptying with a radioisotope-labeled solid meal. Treat with metocloprarnide, Erythromycin stimulates gastric motility but is not useful as a long-term therapy

62
Q

If achlorhydria is present, how to use ketoconazole?

A

Oral ketoconazole requires gastric acidity to be effective, If achlorhydria is present, give either ketoconazole with acid or oral fluconazole, which is similar but not affected by low gastric acid. Note: 50% of AIDS patients have decreased stomach acid and arc especially prone to ketoconazole failure

GI (17 decks)

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