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Gastroenterology > PUD and Gastritis > Flashcards

PUD and Gastritis Flashcards

1
Q

This is defined as a disruption of the mucosal integrity of intestinal lining resulting in a local defect due to inflammation.

A

Ulcer

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2
Q

This is a condition where there is a disruption of the mucosal integrity due to the caustic effects of acid and pepsin.

A

Peptic Ulcer

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3
Q

Who is more likely to get PUD (Peptic Ulcer Dz), men or women?

A

Men&raquo_space; Women (2:1)

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4
Q

When is the typical onset for PUD?

A
  1. Duodenal ulcers = 20-50 yo

2. Gastric ulcer prevalence 40+ yo

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5
Q

Pathophysiology of PUD

A

Gastric epithelium under constant assault by HCl, pepsin/pepsinogen, bile salts, medications, and/or bacteria

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6
Q

What are the components of the body that are involved in providing the gastroduodenal mucosal defense and repair?

A
  1. CCK - Cholecystokinin
  2. CRF - Corticotropin Releasing Factor
  3. EGF - Epidermal Growth Factor
  4. HCl - Hydrochloride
  5. IGF - Insulin-like Growth Factor
  6. TGF - Transforming Growth Factor
  7. TRF - Thyrotropin Releasing Factor
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7
Q

What the hell is pepsin?

A

Proteolytic enzyme that is come from pepsinogen which is secreted by gastric mucosa. Pepsinogen is converted to pepsin by acidic pH. Therefore the secretion mimics acid scretion.

Pepsinogen release is stimulated by gastrin, histamine, and ACh

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8
Q

What the hell is HCl?

A
  • Released from parietal cells in the gastric body.
  • It activates the H+ transport via H+, K+ ATPase (aka the Proton Pump)
  • Provides optimal pH for pepsin
  • Stimulates pancreativ HCO3- secretion
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9
Q

What factors can cause PUD to occur?

A
  1. H. pylori infection
  2. NSAID use
  3. Gastric Acid Hypersecretion
  4. EtOH (inc. susceptibility to H. pylori)
  5. Smoking (alters gastric motility; increased oxygen free radicals)
  6. Ischemia
  7. Stress (sepsis, shock, mechanical ventilation)
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10
Q

When performing an endoscopy, you would most likely from gastric ulcers in which part of the stomach?

A

Body or Antrum NOT the Fundus

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11
Q

If the gastric ulcer is caused by H. pylori, where would you expect to find it?

A

Antrum

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12
Q

True/False: NSAID-related GUs are accompanied by chronic active gastritis.

A

False!! They are not accompanied by chronic active gastritis. BUT they may be accompanied by chemical gastropathy.

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13
Q

Where do the majority of duodenal ulcers occur?

A

95+% are in the first portion of the duodenum and typically well demarcated around 1 cm (but can be 3-6 cm)

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14
Q

True/False: Malignant duodenal ulcers are extremely common.

A

No ma’am! They are extremely rare.

You are the weakest link, goodbye.

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15
Q

This type of peptic ulcer usually consists of a zone of eosinophilic necrosis with surrounding fibrosis at the base.

A

Duodenal Ulcers

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16
Q

How does PUD present?

A

Epigastric (RUQ, LUQ) aching pain (gnawing hunger pain)

DU – increases by fasting and 1-3 hr after eating or at night. Improved when eating or on antiacids.

GU - Pain is precipitated by eating with occ. N/V

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17
Q

True/False: 70% of people with epigastric aching, gnawing pain have PUD.

A

False, 70% with this pain do NOT have PUD. Just make sure it’s in your differential.

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18
Q

True/False: 40% of patients with PUD are no pain.

A

True

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19
Q

True/False: Vital signs will be normal in a pt with PUD.

A

True, unless it’s a bleeding ulcer, then the vital signs might be different.

20
Q

An abdominal physical exam for a patient with PUD would show?

A
  • Normal bowel sounds
  • High pitched w/ obstructive ulceration
  • Possible succession splash if retained gastric content
  • Epigastric Tenderness
21
Q

For a patient presenting with PUD signs/symptoms, what else will be in your DDx?

A
  1. Non-ulcerative Dyspepsia (acid-peptic symptoms without ulceration)
  2. IBS
  3. Gastroparesis
  4. GERD
  5. Pancreatitis
  6. Biliary Tract Dz
  7. Gastric Carcinoma
  8. Mesenteric Ischemia
  9. Abdominal Aortic Aneurysm
22
Q

Complications of PUD

A
  1. GI Bleeding can lead to hematemesis, melena, or hematochezia if large-volume bleed. ~15% of PUD patients get this
  2. Penetration to pancreas, liver, fistulas
  3. Perforations of the abdominal cavity (peritonitis). Common with NSAIDs in the elderly. ~6-7% PUD pts get this.
  4. Obstruction: Gastric Outlet – Duodenal
23
Q

How do you evaluate PUD?

A
  1. Endoscopy: 90+% sensitivity
  2. Upper GI series 60-90% sensitivity
  3. H. pylori testing (endoscopic bx, serologic antibody, stool antigen testing)
  4. Empiric trial of acid suppression for 2-4 weeks and H. pylori testing?
24
Q

This is a medical condition characterized by a large tortuous arteriole in the stomach wall that erodes and bleeds. It can cause gastric hemorrhage but is relatively uncommon.

A

Dieulafoy’s Lesion

25
Q

Ulcers in the hiatal sac of patients with hiatal hernia. They are usually asymptomatic and uncommon.

A

Cameron Ulcers/Lesions

26
Q

This is a gram negative S-shaped rod with muliple flagella that resides primarily in the antrum of the stomach when it is infectious. It generally does not invade epithelial cells, but it does release urease that alkalinizes the environment.

A

H. pylori

27
Q

This is a known carcinogen associated with gastric cancer (adenocarcinoma, MALToma) and Chronic atrophic gastritis.

A

H. Pylori

28
Q

Although only 15% of patients with H. pylori infections develop PUD, H. pylori is associated with _____ of Duodenal ulcers and ______ of Gastric ulcers.

A

90%; 70-90%

29
Q

How do you test for H. pylori?

A
  1. H. pylori Ab serology (will show previous or current infection)
  2. Histologically on biopsy
  3. Stool antigen test (sensitive/specificity 90+%
  4. Urea breath test
  5. Retest 4-6 weeks after Rx to check for eradication.
30
Q

NSAID-Induced PUD Factoids

A
  • 20k deaths/year due to complications of this
  • 4x greater risk of developing GU
  • 1.7-3.2x risk of DU
  • 40% of this presents asymptomatically.
31
Q

How do NSAIDs cause PUD?

A

NSAIDs inhibit prostaglandin secretion and therefore decreases the mucus secretion in the gut and interferes with cell turnover. It also diminished the bicard secretion and mucosal blood flow leading to a direct topical injury as a result of intracellular trapping in ionized form.

32
Q

How do you treat PUD?

A
  1. Discontinue NSAIDs
  2. Treat H. pylori if present
  3. Acid Suppression!!!
  4. Re-endoscope gastric ulcers to assess healing and rule out malignancy ***DUs don’t need this
  5. Quit smoking/drinking
  6. Sx rarely needed
33
Q

What Acid Suppressing Drugs are there?

A
  1. Antacids (mylanta, maalox, tums, gaviscon)
  2. H2 receptor antagonists (cimetidine, ranitidine, famotidine, nizatidine)
  3. PPI (omeprazole, lansoprazole, rabeprazole, pantoprazole, esomeprazole)
34
Q

What Mucosal Protective Agents are there?

A
  1. Sucralfate

2. Prostaglandin Analogue (Misoprostol)

35
Q

How do you treat a H. pylori Infection?

A
  1. PPI BID, Amoxacillin 1g BID and Clarithromycin 500 mg BID (14 day treatment) —80-95% efficacy
    OR
  2. Omeprazole 20 mg BID and Bismuth 2 tabs QD and Tetracycline 500 mg QD and Metronidazole 500 mg TID (14 days treatment) – 90-95% efficacy
36
Q

This is a condition where gastric acid hypersecretion results in severe PUD. Due to a gastrin releasing tumor usually in the pancreas or duodenum. Assc with PUD, Diarrhea, and GERd

A

Zollinger-Ellison Syndrome

37
Q

_____% of patients with PUD have Zollinger-Ellison Syndrome

A

0.1-1%

38
Q

True/False: Males are more likely to get Zollinger-Ellison Syndrome that females.

A

True! Most commonly between 30-50 yo

39
Q

How do you diagnose Zollinger-Ellison Syndrome?

A
  1. Check fasting gastrin level (150-200+ is indicative if they are not on a PPI, hypo or achlorhydria)
  2. If elevated, confirm inc. acid output by checking Basal Acid Output of gastric pH test
  3. Can perform secretin stimulation test. (Inc in gastrin of 200+ within 15 mins has 90+% sens/spec for ZES.
  4. Tumor localization (CT/US/MRI)
40
Q

This is defined as inflammation of gastric mucosa classfied by timing (acute/chronic), histologically (atrophic vs. nonatrophic), and anatomic distribution (antral vs. body predominant)

A

Gastritis, yo.

41
Q

What are the two types of Chronic Gastritis?

A

Type A and B

42
Q

This type of chronic gastritis is more common and generally associated with H. pylori. It is predominantly antral and can expand to involve the entire stomach?

A

Type B - Nonatrophic Chronic Gastritis

43
Q

This type of Chronic Gastritis can be autoimmune or multifocal. It is definitely less common and can be assc. with pernicious anemia. It primarily involves the fundus and the body of the stomach but not the antrum. It can also be associated with H. pylori, but not usually.

A

Type A - Atrophic Chronic Gastritis

44
Q

65 y/o man presents with gnawing mid-epigastric abdominal pain. No fevers or chills, no nausea or vomiting. Pain is particularly worse when he hasn’t eaten. Has lost about 2-3 lbs because of the abd pain. No change in bowel function. Never had EGD or colonoscopy.
Hx of HTN, CAD
Meds - antihypertensives, baby ASA, statin
PE - relatively nl exam, only significant for some mild mid-epigastric tenderness, stool heme (+)
Endoscopy: solitary ulcer; bx shows granulation tissue and necrotic debris
H. pylori is negative
Treated with PPI for 8 weeks
Instruct patient to hold ASA

What do we do now!?

A
  1. Repeat EGD and the ulcer remains unhealed

2. Biopsy shows adenocarcinoma

45
Q

True/False: NSAIDs and H. pylori cause 90+% of PUD

A

True

46
Q

True False: Only 25% of H. pylori infected patients develop PUD

A

False, 5-15%

47
Q

Note:

A

Gastric neoplasm in gastric ulcers in pts 50+ yrs

Gastroenterology (12 decks)

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