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Clin Med III Unit I > 4 Peptic Ulcer Disease and Gastric Cancer > Flashcards

4 Peptic Ulcer Disease and Gastric Cancer Flashcards

1
Q

Defect in the gastric or duodenal mucosa that extends through the MUSCULARIS MUCOSA into the deeper layers of the wall

A

Peptic Ulcer

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2
Q

What are the main causes of PUD?

A
  1. Helicobacter pylori (H. pylori)
  2. NSAIDs
    (3. Non-NSAID, Non-H. pylori - very rare)
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3
Q

PUD is NOT caused by…

A 
Emotional stress
Alcohol
Spicy foods
Caffeine
Tobacco

Certain foods may cause dyspepsia, but do not cause ulcer disease

Alone, these factors do not cause ulcers, but they can make them worse and more difficult to heal

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4
Q

Most common cause of PUD worldwide

A

H. pylori

80% infected with H. pylori by age 50 in developing countries

PUD incidence 6-10x higher than non-infected

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5
Q

H. pylori infection can predispose you to…

A

Gastric CA

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6
Q

Why is H. pylori declining in developed countries?

A

Improved hygiene/decreased transmission

Correlates with decline in PUD

Increased rates of eradication

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7
Q

What does H. pylori look like?

A

Gram-negative rod with motile flagella

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8
Q

What does H. pylori use to attach to gastric mucosa?

A

Motile flagella

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9
Q

What is the route of transmission for H. pylori?

A

Oral-oral or fecal-oral to stomach

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10
Q

How does H. pylori disrupt protective properties of the stomach?

A

Decreases gastric mucus and mucosal bicarbonate secretion

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11
Q

Where do H. pylori attack?

A

Surface and foveolar epithelium

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12
Q

Even IV, SQ, IM NSAIDs can cause PUD because…

A

They cause decreased PGE2 synthesis

Prostaglandins:
• Block gastrin secretion
• Promotes epithelial cell production in stomach
• Stimulate mucus production

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13
Q

Factors than increase risk of PUD w/ use of NSAIDs

A

Prior hx of PUD/ulcer complications
Presence of H. pylori infection
Advanced age (>75)
Increased dose, time, and duration of use (10 days for a sprained ankle vs daily for arthritis)
Concomitant use of steroids, other NSAIDs, anticoagulants, low dose aspirin, SSRI, alendronate

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14
Q

70% of PUD patients present…

A

Asymptomatic

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15
Q

80% of symptomatic PUD patients present with….

A

Abdominal pain/discomfort

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16
Q

What is dyspepsia

A

“Burning abd pain”

Belching
Bloating
Distention

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17
Q

PUD Complications

A

Hematemesis
Melena
Fatigue
Dyspnea

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18
Q

Classic Sx of Gastric Ulcers

A

Mid-epigastric pain +/- RUQ

Pain worse AFTER meals (30 min-1 hr after meal)

Vomiting common

More likely to hemorrhage, and manifests as hematemesis

Weight loss/anorexia

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19
Q

Classic Sx of duodenal ulcers

A

Mid-epigastric pain +/- RUQ

Pain RELIEVED by meals (worse 2-3 hours after meal)

Vomiting uncommon

Less likely to hemorrhage, but if it occurs, manifests as melena

Weight gain (due to timing of the pain)

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20
Q

Alarm Sx for PUD

A 
Bleeding
Unexplained iron deficiency anemia
Early satiety
Unintentional weight loss
Progressive dysphagia/odynophagia
Acute onset of intense upper abdominal pain
Persistent vomiting
Family hx of upper GI cancer
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21
Q

Most common complication of PUD

A

BLEEDING**

Also:
Perforation
Penetration
Gastric Outlet Obstruction (rare)

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22
Q

Hemorrhage in PUD can present as…

A

Hematemesis, melena, or hematochezia (severe)

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23
Q

What to do if a PUD patient presents with bleeding

A

Stabilize with IV fluids or packed RBCs, start IV PPI, and perform EGD

EGD is diagnostic and allows for therapeutic interventions

Standard tx includes thermal coagulation, hemoclip placement, and injection therapy

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24
Q

Clinical presentation of perforation in PUD patients

A

Severe, diffuse abdominal pain*****
Tachycardia, weak pulse, N/V

May progress to “board-like abdominal rigidity”

25
Q

Dx and Tx of PUD perforation

A

Upright CXR and Abdominal X-rays, possibly CT to localize

Stabilize with IV fluids, NG tube, NG suction for gastric decompression, IV PPI, broad spectrum abx, and SURGERY

26
Q

What is contraindicated in cases of PUD perforation?

A

UGI with barium

27
Q

What is penetration in terms of PUD complications?

A

Penetration of the ulcer through the bowel wall w/o free perforation and leakage of luminal contents into the peritoneal cavity

28
Q

_____ is the most common adjacent structure affected by penetration in PUD

A

Pancreas

Might present with Sx of pancreatitis (pain w/o meal association, more intense pain, pain referral to back)

29
Q

Dx and Tx of PUD penetration is….

A

More difficult and not clear cut

30
Q

PUD complication caused by scarring/fibrosis or inflammation/edema in the pyloric channel

A

Gastric Outlet Obstruction

31
Q

Gastric Outlet Obstruction presents a lot like….

A

Gastric Cancer

Vomiting, early satiety, bloating, epigastric pain, weight loss, anorexia

32
Q

Dx and Tx of Gastric Outlet Obstruction

A

Imaging shows DILATED STOMACH

Stabilize with IV fluids, NG tube, gastric decompression, IV PPI

If failure with medical tx, consider EGD with endoscopic balloon dilation or surgery (rare)

33
Q

What is the succussion splash test?

A

For Dx of Gastric Outlet Obstruction

Succussion splash is elicited by placing the stethoscope over the upper abdomen and rocking the patient back and forth at the hips

Retained gastric material greater than 3 hours after meal will generate a splash sound and indicate the presence of a hollow viscus filled with both fluid and gas

34
Q

Best test to diagnose PUD

A

EGD*******

Can also do an Upper GI but EGD is best

35
Q

What are the different tests to Dx H. pylori?

A

UREA BREATH TEST
FECAL ANTIGEN TEST

Serology
Biopsy during EGD (most specific and sensitive*****)

36
Q

What is Urea Breath Testing?

A

Identifies H. pylori bacteria in the stomach (active infection)

Can be used to determine H. pylori Eradication

Patient drinks radioactively labeled urea, urease produced by H. pylori splits urea into CO2 and NH3, test measures labeled CO2 in breath

37
Q

What pt ed do you need before Urea Breath Testing and Fecal Antigen Testing?

A

D/c PPI 2 weeks prior and bismuth/abx 4 weeks prior to testing

38
Q

Test that identifies H. pylori antigen in feces (active infection)

A

Fecal antigen test

Can be used to determine H. pylori eradication

39
Q

Why is serology for H. pylori not used for routine testing?

A

High false positive and false negative rates

Identifies IgG antibodies - so any infection ever, not just current infection

40
Q

What are the main steps in Tx of PUD

A

Eradicate H. pylori if present and confirm eradication 4 weeks after completion of tx

If H. pylori absent or sx persist after eradication, 4-8 weeks of PPI

If sx persist, 8-12 weeks of TCA

If sx persist, 4 weeks of a prokinetic

If sx persist, PERFORM EGD if not done previously

41
Q

How do TCAs work again PUD?

A

Central effect on production of gastrin

42
Q

What is the mainstay of H. pylori tx in the US?

A 
Bismuth Quadruple Therapy x 14 days
• PPI BID
• Bismuth 524mg QID
• Tetracycline 500mg QID
• Metronidazole 250mg QID
43
Q

Syndrome in which gastrinomas (typically arising from the duodenum or pancreas) hypersecrete gastrin

A

Zollinger-Ellison Syndrome (ZES)

44
Q

What does gastrin do?

A

Stimulates the secretion of gastric acid by the parietal cells of the stomach and aids in gastric motility

45
Q

80% of ZES arise sporadically, but 20%…

A

As part of MEN1 (pituitary, pancreas, parathyroid)

Also, more common in men

46
Q

Clinical presentation of ZES

A

Recurrent PUD - often distal to duodenal bulb, or multiple gastric ulcers at the same time

Abdominal pain

Diarrhea, including STEATORRHEA (due to malabsorption)

47
Q

How is ZES diagnosed?

A

Fasting serum gastrin >1000pg/mL (10 times normal)

Gastric pH <2

Secretin stimulation test (baseline gastrin, give IV secretin and check gastrin 10 min later - if UP, (+) gastrinoma)

CT abdomen to localize tumor

48
Q

Treatment for ZES

A

PPIs

Or H2 blockers

But really PPIs

49
Q

Risk factors for Gastric Cancer

A

GASTRIC ULCERS**, adenomatous polyps, and intestinal metaplasia

Dietary (nitroso compounds, high-salt diet with few veggies)

Alcohol and tobacco use

Chronic H. pylori infection

50
Q

Early clinical presentation of gastric cancer

A

ASYMPTOMATIC

51
Q

Clinical presentation of gastric cancer (once symptomatic)

A 
Weight loss
Persistent abdominal pain
Early satiety
Nausea
Anorexia
Dysphagia
GASTRIC ULCER HISTORY (25%)****
Occult GI bleed
52
Q

Late clinical presentation of gastric cancer

A

Palpable stomach mass, succussion splash, paraneoplastic syndromes

53
Q

How is gastric cancer dx and staged?

A

EGD***** —> histology grading and differentiation of gastric versus esophageal cancer

2nd line: UGI

Staging = TNM (determine nodal involvement, distant lesions, invasion of vasculature, depth of tumor)

54
Q

90-95% of gastric cancers are….

A

Adenocarcinomas

55
Q

Early gastric cancer may appear on EGD as…

A

A subtle polyploid protrusion, a superficial plaque, mucosal discoloration, a depression, or an ulcer

TAKE A BIOPSY

56
Q

What are the signs of metastatic disease in patients with gastric cancer?

A

Virchow’s node*** (most common) - left supraclavicular lymph node

Sister Mary Joseph’s node (periumbilical nodule)

Left axillary node (Irish node)

57
Q

How is gastric cancer treated?

A

Early (very rare): endoscopic mucosal resection

More advanced cancer: total or partial gastrectomy if resection possible

For unresectable cancers: chemo vs chemoradiotherapy

58
Q

Bismuth quadruple therapy consists of _____, ______, ______, and _______ but in the US…

A

Bismuth, Metronidazole, Tetracycline, and a PPI

Given the limited info on abx resistance rates, we generally assume clarithromycin resistance rates are ≥15% unless local data indicates otherwise

Clin Med III Unit I (6 decks)

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