Peptic ulcer disease & gastritis (GI) Flashcards

1
Q

Define PUD.

A

A break in the mucosal lining of the stomach or duodenum more than 5mm in diameter, with depth to the submucosa

Ulceration of areas of the GI tract due to exposure to gastric acid and pepsin

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2
Q

What name is given instead of PUD if the ulcer is smaller than 5mm/without obvious depth to the submucosa?

A

Erosions

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3
Q

Define gastritis.

A

Histological presence of gastric mucosal inflammation

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4
Q

Where do peptic ulcers occur?

A

Most commonly gastric and duodenal (duodenal more common)

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5
Q

What demographic do peptic ulcers happen to? (3)

A
  • M=F
  • duodenal ulcers: <30y
  • gastric ulcers: 50y
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6
Q

If untreated, what can gastritis progress to?

A

Peptic ulcer disease

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7
Q

Why do peptic ulcers arise?

A

Imbalance between:
1. factors promoting mucosal damage - gastric acid, pepsin, H. pylori infection, NSAID use
2. mechanisms promoting gastroduodenal defence - prostaglandins, mucus, HCO3-, mucosal blood flow, tight junctions, restitution

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8
Q

What is the difference in pathophysiology between duodenal and gastric ulcers?

A
  • duodenal - hypersecretion of gastric acid related to H. pylori infection
  • gastric - normal/low secretion of gastric acid
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9
Q

What are the most common causes of gastritis and PUD? (2)

A
  • H. pylori
  • NSAID use
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10
Q

How does NSAID use cause PUD?

A
  • direct damage: traps H+ ions
  • indirect damage: inhibition of COX-1
  • increase bleeding risk through antiplatelet actions
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11
Q

What are the rarer causes of PUD? (5)

A
  • gastric ischaemia
  • Zollinger-Ellison syndrome (gastrin-secreting NET)
  • medication (KCl, bisphosphonates)
  • sarcoidosis
  • TB
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12
Q

What are the types of gastritis? (4)

A
  • acute non-erosive gastritis (most commonly due to H. pylori)
    • chronic H. pylori infection in antrum predisposes to atrophic and autoimmune gastritis
  • acute erosive gastritis (commonly caused by chronic NSAID use, alcohol use) - decreased gastric mucosal blood flow with loss of mucosal protective barrier
  • autoimmune-mediated atrophic gastritis (antibodies to GPC)
  • phlegmonous gastritis
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13
Q

What are the clinical features of PUD? (8)

A
  • gnawing epigastric pain:
    • gastric ulcer - pain directly after meals (may lead to weight loss)
    • duodenal ulcer - pain couple hours after eating (pain may be relieved by eating –> weight gain) + radiates to BACK (due to penetration of ulcer into pancreas)
  • epigastric tenderness
  • ‘pointing sign’ - patients can indicate where pain is with one finger alone
  • nausea relieved by eating
  • vomiting after eating
  • early satiety - may indicate pyloric stenosis
  • GI bleeding –> anaemia
    • occult - stool haem test +ve
    • overt - haematemesis or melaena
  • diarrhoea (if ZES)
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14
Q

Describe the pain in a gastric ulcer.

A

Pain directly after meals (may lead to weight loss)

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15
Q

Describe the pain in a duodenal ulcer.

A

Pain a couple hours after eating/before meals/at night (pain may be relived by eating so may lead to weight gain)

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16
Q

Describe how a perforated ulcer may present.

A

Acutely unwell + haemodynamically unstable

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17
Q

What might you find on examination in PUD? (2)

A
  • hypotension or septic shock - from GI bleed or perforated ulcer
  • succussion splash - may be heard in pyloric stenosis, due to gastric outlet obstruction
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18
Q

What are the clinical features of gastritis? (4)

A
  • dyspepsia / epigastric discomfort
  • nausea / vomiting
  • loss of appetite (–> weight loss)
  • no red flags for cancer (GI bleeding, anaemia, early satiety, unexplained weight loss>10%, progressive dysphagia, odynophagia, persistent vomiting)
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19
Q

What features may indicate phlegmonous gastritis?

A

Severe vomiting, acute abdominal pain, fever

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20
Q

What might indicate autoimmune gastritis?

A

Co-existing autoimmune disease

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21
Q

What might you find on examination in gastritis?

A

Symptoms of vitamin B12 deficiency / pernicious anaemia –> autoimmune gastritis:

  • altered reflexes (upgoing plantar response) or sensory deficits
  • cognitive impairments
  • glossitis
  • anaemia symptoms
22
Q
A
23
Q

What are some risk factors for gastritis and PUD? (10)

A
  • H. pylori infection (90% in duodenal ulcers, 70% in gastric ulcers)
  • NSAIDs - high dose, long duration
  • alcohol
  • smoking
  • age
  • sertraline –> duodenal ulcers
  • personal/Fx
  • intensive care - mechanical vent/with coagulopathy/stress-induced GI bleeding
  • autoimmune disease –> autoimmune gastritis
  • immunocompromised
24
Q

What are the first-line investigations for PUD and gastritis? (4)

A
  • upper GI endoscopy - gold standard for PUD
  • H. pylori urea breath test
  • H. pylori faecal antigen test
  • FBC
25
Q

What is the gold standard investigation for PUD?

A

Upper GI endoscopy - may show ulcerations, can perform biopsies to detect cause (H. pylori)

26
Q

After doing upper GI endoscopy in PUD, who do we immediately refer?

A

Dyspepsia (indigestion) together with acute GI bleeding = same day referral to specialist

27
Q

What are the tests for H. pylori in gastritis and PUD? (2)

A
  • carbon-13 urea breath test:
    • no Abx in past 4 weeks
    • no PPI in past 2 weeks
  • stool antigen test
28
Q

What is important to remember before doing carbon-13 urea breath test for H. pylori? (2)

A
  • no Abx in past 4 weeks
  • no PPI in past 2 weeks
29
Q

What do we do if H. pylori +ve and symptoms do not improve on triple therapy?

A

Endoscopy is needed

30
Q

What might FBC show in gastritis/PUD?

A

Ordered if patient seems anaemic or has GI bleeding

Microcytic anaemia or high platelet count - may indicate malignancy

31
Q

What may erect CXR show in PUD? (2)

A
  • pneumoperitoneum (free air in abdomen) suggesting perforated duodenal ulcer
  • Dome sign - perforated gastric ulcer
32
Q

What would raised urea in PUD mean?

A

Upper GI bleed

33
Q

What might positive faecal occult blood show in PUD/gastritis?

A

GI bleed

34
Q

When do you refer a patient for upper GI endoscopy (PUD)?

A

Refer for upper GI endoscopy within 2 weeks if patient 55+ with weight loss and one of the following:

  • dyspepsia
  • reflux
  • upper abdominal pain

Repeat after 6-8 weeks if gastric ulcer to ensure healing and rule out malignancy

35
Q

What are some differential diagnoses for PUD/gastritis? (11)

A
  • oesophageal cancer (dysphagia, Fx, palpable mass)
  • stomach cancer - gastric lymphoma, gastric carcinoma
  • GORD (heartburn, worse when lying down)
  • gastroparesis (long-standing diabetes)
  • biliary colic
  • acute pancreatitis
  • functional dyspepsia (upper abdominal dysfunction commonly related to meals, diagnosis of exclusion)
  • Coeliac disease (malabsorption)
  • IBS
  • pleuritic pain
  • pericarditis
36
Q

What lifestyle advice do we give for gastritis/PUD?

A

Reduce smoking and alcohol intake

37
Q

What is the medical treatment for H. pylori +ve infection?

A

Triple therapy: PPI (omeprazole) + amoxicillin (or metronidazole if allergic) + clarithromycin

1 week course, taken 2x daily

38
Q

What is the medical treatment for H. pylori -ve (PUD)?

A
  • stop harmful drug causing ulcer e.g. NSAID
  • offer 4-8 weeks full dose PPI therapy (omeprazole 20mg) - H2 antagonist if no response
  • gastric ulcer - repeat endoscopy 6-8 weeks later to ensure ulcer healing and rule out malignancy
  • duodenal ulcer - repeat urea breath test for H. pylori 6-8 weeks later
39
Q

What is a side effect of PPIs on U&Es?

A

Hyponatraemia

40
Q

What is the treatment for active bleeding ulcer in PUD? (4)

A
  • fluids + possible blood transfusion
  • OGD
  • PPI IV infusion if endoscopic evidence/recent haemorrhage for 72h, then switch to oral
  • endoscopic clipping, thermal coagulation, fibrin or thrombin
41
Q

How do we follow up a gastric ulcer?

A

Repeat endoscopy 6-8 weeks later to ensure ulcer healing and rule out malignancy

42
Q

How do we follow up a duodenal ulcer?

A

Repeat urea breath test for H. pylori 6-8 weeks later

43
Q

How do we manage a patient at risk of stress gastritis?

A

H2 antagonist/PPI - famotidine/pantoprazole/esomeprazole

44
Q

How do we manage erosive gastritis? (3)

A
  • stop NASID
  • reduce/stop alcohol consumption
  • symptomatic therapy with PPI/H2 antagonist
45
Q

How do we manage autoimmune gastritis?

A

Cyanocobalamin (IM B12)

46
Q

How do we manage bile reflux gastritis? (3)

A
  • rabeprazole
  • sucralfate
  • surgery if persistent (Roux-en-y gastrectomy)
47
Q

How do we manage phlegmonous gastritis? (4)

A
  • admission
  • IV fluids
  • empirical broad spectrum Abx (ampicillin/sulbactam + ciprofloxacin)
  • gastrectomy - if deterioration despite optimal medical Rx, involvement of large portion of stomach or perforation
48
Q

What are some complications of gastritis? (6)

A
  • PUD (gastric/duodenal ulcer)
  • gastric carcinoma
  • gastric carcinoid
  • gastric MALT lymphoma
  • achlorhydria - due to H. pylori, longstanding gastritis and autoimmune gastritis
  • vitamin B12 deficiency - due to atrophic/autoimmune gastritis, chronic H. pylori etc
49
Q

What are some complications of PUD? (4)

A
  • penetration into adjacent organs - stomach, duodenum, pancreas –> standard ulcer treatment +/- surgery
  • gastric obstruction due to ulcer healing with scarring and oedema –> chronic pyloric stenosis
  • upper GI bleed (haematemesis, melaena, anaemia)
  • perforation (shock and peritonitis)
50
Q

Describe the prognosis of gastritis and PUD?

A

With PPI therapy, duodenal ulcers typically heal within 4 weeks and gastric ulcers within 8 weeks