PEPTIC ULCER DISEASE


DEFINITION
Breach in the lining of the stomach or first part of the gut, with indigestion, bleeding and occasionally rupture, caused by an imbalance of factors that attack and defend the gut wall.

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INCIDENCE

Incidence

~10% incidence, 2% prevalence (US)
Decreasing (halved in 25 yrs).

Geography

GU in areas of social deprivation.
DU worldwide.

Age

20-50 yrs DU (10x more than GU)
40-60 = GU peak.

Sex
F>M GU.
M>F DU.

Risk Factors
H. Pylori, smoking and NSAIDs are the big 3
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AETIOLOGY
Pathogenesis

Normal Physiology

Acid is released from parietal cells in response to histamine, gastrin and vagal stimulation.
Pepsin is released from chief cells due to cholinergic stimuli, also gastrin.
Bicarbonate released from epithelium all the time, forming a gradient across the mucous layer against attacking acid.
Mucous layer protects against pepsin and acid diffusion, and bugs.

Normal Balance

Balance between attacking and defending factors is disturbed (see biological behaviour).

Attacking factors

"No acid, no ulcer"
Digestive enzymes (pepsin, HCl, bile salts).
Microorganisms - H. pylori colonizes and weakens mucosa.
Increased motility (in DU, as acid being dumped into the duodenum).
Stasis/ bile reflux in GU.

Defending Factors
.
Mucus, bicarbonate.
Turnover of epithelium.
Normal motility.

Aetiology

Acid secretion generally higher in PUD patients, but only 1/6 have secretions higher than normal range.

Increasing Attack
Deranged acid secretion (increased Parietal cells, increased response to secretory stimuli, increased gastrin release.
Increased serum pepsinogen I levels.
HSV 1.
Gastrinoma (Zollinger-Ellison Syndrome).
- rare; 1-2% of patients with duodenal ulcer.
Increasing ICP (Cushing Ulcers).
Hyperparathyroidism (DU) - hypercalcaemia increases gastrin production).
Systemic acidosis (decreases pH of mucosal cells).
ETOH.
Corticosteroids.
 - common to see lymphoma or transplant pts with ulcers.
Chronic renal failure/ Renal Dialysis (hypercalcaemia -> DU).
COPD (DU).
Alcoholic cirrhosis (DU).
Stress ulcers
- ventilation and coagulopathy; common to use prophylactic agents.
Burns (Curling Ulcers - DU).
Shock.
Intracranial injury/ surgery (Cushing Ulcers).
Probably, gastroduodenal dysmotility.

Decreasing Defense
H. Pylori (90% DUs and GUs).
- and if not treated, 80% will recur.
NSAIDs (break mucosal barrier; e.g. less bicarb under mucus)
Blood Group O --> increased bleeding.
Blood group non-secretion.
Mucous deficiency, bicarbonate Deficiency.
Defective cellular regeneration.
Abnormal microcirculation.
Prostaglandin deficiency.
Smoking.
Social deprivation.
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BIOLOGICAL BEHAVIOUR

Pathophysiology
Ulcers form when the balance between defensive and attacking factors is upset.
Tends to be increased attack factors in DU, and decreased defence factors in GU.
One of the factors above happens, either damaging the mucosa, or failing to protect it.
This leads to destruction of the mucosa.
-> non-specific acute inflammation.
-> granulation tissue.
-> chronic inflammatory cell infiltrate and endarteritis at the base of the ulcer.
Healing by fibrosis -> scarring.
Can cause problems if in the pylorus --> outflow obstruction (inflammation, scarring)

Natural History
Can sit quietly, but the majority will present with pain.
This can be episodic over many years, usually flaring up in periods of psychological stress.

Complications
Can lead to haemorrhage, anaemia, obstruction, or penetration into the pancreas.
- see upper gi bleeding
Can also perforate.
GU's can be malignant.
Chronic inflammation can cause stricture and gastric outflow obstruction.

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MANIFESTATIONS

Pain (most common), bleeding, perforation, obstruction.

SYMPTOMS

Local
GU
Gnawing/ burning/ aching pain, relieved by alkalis or food, vomiting.
- pain tends to occur 30m after eating.
- can go to back.
May get belching or reflux-type symptoms.
Can get night-time pains (increased gastric acid secretion during late night and early morning (circadian).
DU
Pain as above.
- often starts an hour or more after breakfast, relieved by lunch, recurs in afternoon, same in evening.
- may wake patient during night.
May involve pancreas posteriorly --> constant back pain.

Systemic
Weight loss
Anaemia if dripping

Complications
Bleed - malaena or haematemesis
Perforation
Gastric outflow obstruction
- suspect if vomiting, esp if old food/ copious/ persistent.
Gastric cancer

SIGNS

Observe
Pallor if bleeding, signs of shock.

Palpate
Epigastric tenderness (often the only sign; commonly absent).
Features of complications if relevant.

Auscultate
Succussion splash if pyloric stenosis.
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INVESTIGATIONS

Investigate those with good history / exam.

Haem

FBC (microcytic anaemia).

Biochem
Serum gastrin and pepsin
- 50-100 is N, >200 is high.
- gastrin may rise in hypo (atrophic gastritis; pernicious anaemia) or hyper-secretion (ZE, HyperPTH) states

Gastric acid analysis
- basal acid output measured, followed by stimulation by histamine or pentagastrin (maximal acid output).
--> increases from ~1.5-2.5 (3-5.5 in DU) to 20-30 (30-40 in DU)

Microbio

H. pylori.

Imaging

Barium swallow - "duodenal deformities and ulcer niche".
Less used now.
Showed the classic meniscus sign.

Scoping

Gastroscopy.
Sorry! Picture not possible for you.
All need this for confirmed diagnosis.
DU: 95% are within 2cm of the pylorus
GU: 95% on LC and 60% within 6 cm of pylorus.
And to exclude malignancy.
- cancer usually has flat edges cf overhanging edges if benign.
- cancer more common if >2 cm.
- if hard to distinguish, better prognosis if Ca --> 50-75% cure chance.
Biopsy should be taken at the same time for H pylori.
- Ideally 7+ bx (10=good) and brush biopsy.
- False +ve rare, false -ve in 5-10%.
Remember 10% of gastric ulcers are malignant
- particularly in older pts not on NSAIDs with new ulcers
- take 7 biopsies at least from around the lesion.

Classification of Gastric Ulcers
Type I: Most common; usually <2cm between boundary between parietal and pyloric mucosa; always in latter.
- antral gastritis accompanies. Usually H. pylori.
Type II: prepyloric, often associated with DU.  Low risk of Ca.
Type III: In antrum, associated with NSAIDs.

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MANAGEMENT

Principles
:
- heal the ulcer
- cure the disease

Medical
Stop smoking, NSAIDs, stress, foods that provoke it.
Most can be treated conservatively
Antacids for dyspepsia.
Evaluate indications for steroids so they can be discontinued.
Triple Therapy for H. pylori.
- eliminates in 90% at 6 weeks.
Continue proton Pump Inhibitors in GU (omeprazole, lansoprazole).
Repeat scope at 4-16 weeks (e.g. 6) in GU to assess healing.
Can stop PPIs after 2 months if underlying causes treated, with low risk of recurrence.

Other
Lesser used treatments.
- H2-antagonists (cimetidine, ranitidine).
- Sucralfate = a cytoprotective agent; used in active duodenal ulceration
Prostaglandins (misoprostol).

Surgical
Indications are obstruction, bleeding and perforation.
These days, intractability is rare, and only in complex non-compliant patients is vagotomy considered
Most of the literature is out of date, from the pre-modern-treatment era.
- most did well back then, these days, those referred are selectively the most difficult patients around.

Vagotomy
Now rather historical.
Now rarely indicated because recalcitrant cases are uncommon:

Truncal vagotomy
- 1-2cm resected as each trunk enters abdomen.
- accompanied by a drainage procedure to maintain gastric emptying, i.e. pyloroplasty
Small but real (10%) risk of dumping, diarrhoea and gastroparesis; don't use.

Proximal gastric ('parietal cell') vagotomy
- Spares the main nerves of Laterjet, takes the other branches (proximal 2/3 of stomach), close to stomach
- Dumping and diarrhoea far less frequent.
--> procedure of choice for recalcitrant ulceration
--> except in prepyloric ulcer

Highly selective vagotomy.

Grading System
Type I = lesser curve of body
Type II = combined gastric and duodenal
Type III = pre-pyloric
Type IV = juxto-oesophageal
Type V = drug-related

iamge

Distal Gastrectomy
Type I
Resect lower 50% of stomach
Can either anastomose to:
- duodenum (Billroth I); preferred
- or jejunum loop (Billroth II); acceptable if Billroth I not tension-free
--> either bring jejunal loop up anterior to the transverse colon (simpler), or posteriorly through a hole in the transverse mesocolon.

Antrectomy
Type II or III (hypersecretors).
Vagotomy now reserved for rare cases (e.g complicated ulcers in noncompliant pts)

Subtotal Gastrectomy
Historical.
Resect 2/3 - 3/4 of stomach.
Billroth II generally done.

High Ulcers
Type IV ulcers are challenging. 
Pouchet procedure is 1 option
- distal gastrectomy along lesser curve; vertical extension to include the ulcer, then Billroth I or II anastomosis.
Csendes procedure.
- when 2cm or less from GOJ
- most of stomach resected up to GOJ, excision and coverage of the hole with anastomosis to a Roux-limb.

image

Giant Gastric Ulcers
3cm+
Mostly along lesser curvature.
- malignant in 30%
Early surgical treatment and work up for cancer.
CT workup and en-bloc resection if an occult or obvious malignancy is present.

Complications of Surgery

Early
Duodenal stump leakage, gastric retention, haemorrhage in post-operative period.

Late

Recurrence
(10% vagotomy / pyloroplasty); 2-3% after vagotomy, antrectomy and subtotal gastrectomy.
- a deeply eroding ulcer could cause a colic fistula
--> severe diarrhoea, malnutrition, and weight loss.
--> diagnosed by barium enema reliably, and upper GI series unreliably.
--> resect, move to partial gastrectomy, restore colonic continuity.

Dumping Syndrome
- noted in most; problematic in only 1-2% of patients after months
- two types of symptoms
--> Cardiovascular & gastrointestinal
--> after eating, palpitations, sweating, weakness, dyspnea, flushing, cramps, vomiting, diarrhoea, rarely syncope.
- treat by diet therapy to reduce jejunal osmolality.  Low in carbs, high in fat and protein, may need to avoid milk. Dry meals, fluids between meals, ?somatostatin.

Alkaline Gastritis
- reflux of duodenal juice into stomach; invariable, usually innocuous, but sometimes causes marked gastritis.
- see a minor degree of gastritis in most Billroth II patients anyway; endoscopy fairly non-specific
- indication for operation is persistent severe pain
--> Roux-en-Y gastrojejunostomy with a 40 cm efferent jejunal limb.

Anaemia
Iron deficiency develops in 30% of partial gastrectomy patients in 5 years.
- ensure no recurrence (marginal ulcer) or tumor before diagnosing
Vit B12 anaemia may also occur

Post-vagotomy Diarrhoea
5-10%, 1% severely troubled.
Usually episodic, usually well treated with constipating agents.

Gastroparesis
Prokinetics may help

Emergencies
See perforation.
And bleeding.
And obstruction
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Refs

Updated from Doherty
And Cameron