PUD Flashcards
Ulcera gastrica
- peggiora con il cibo! ( questo meccanismo è alla base della perdita di peso)
- sanguinano più facilmente rispetto alle ulcere duodenali
- la loro perforazione è più grave rispetto a quella duodenale (anteriormente)
- il vomito è un elemento caratteristico
Ulcera duodenale
- peggiora a digiuno
- peggiora di notte o al mattino
- peggiora 3 ore dopo i pasti
- ha una tendenza alla perforazione maggiore rispetto a quella gastrica, ma meno grave
- sanguina meno facilmente di quella gastrica, ma essendo in numero prevalente è la prima causa di Upper GI bleeding
- younger age of onset!💥
General findings
Peptic ulcer disease (PUD) refers to the presence of one or more ulcerative lesions in the stomach or lining of the duodenum. Possible etiologies include infection with the bacterium Helicobacter pylori (most common), prolonged use of nonsteroidal anti-inflammatory medicines (possibly in combination with glucocorticoids), conditions associated with an overproduction of stomach acid (hypersecretory states), and stress. Epigastric pain is a typical symptom of PUD, however, some patients may remain asymptomatic. Diagnosis occurs via direct visualization of the ulcer on esophagogastroduodenoscopy (EGD) and H. pylori detection (via biopsy or non-invasive testing). The first-line treatment for most peptic ulcers involves H. pylori eradication via triple therapy (a course of two different antibiotics in combination with a proton-pump inhibitor) and the withdrawal of offending agents. Antisecretory drugs (e.g., proton-pump inhibitors, or PPIs), which reduce stomach acid production, are continued for 4–8 weeks after eradication therapy and may be considered for maintenance therapy if symptoms recur. Surgical intervention may be necessary in rare cases, especially if complications such as perforation or massive bleeding occur. Stomach cancer is an important differential diagnosis and must be ruled out if risk factors are present.
Epidemiology
- Duodenal ulcers are 3 times more common than gastric ulcers.
- Duodenal ulcers occur on average 10–20 years earlier than gastric ulcers.
Etiology
Alcohol prolongs ulcer healing time, but does not induce ulcer formation!🧨
Risk factors
Chronic gastritis caused by H. pylori, a curved, flagellated gram-negative rod
Duodenal ulcers: up to 90% are due to H. pylori infection
Gastric ulcers: up to 80% are due to H. pylori infection
Chronic gastritis of other etiology
Long-term use of NSAIDs (e.g., patients with rheumatoid arthritis, SLE, etc.):
Risk for gastroduodenal ulcers increases 5-fold.
NSAID use seems to have a stronger association with gastric ulcers than with duodenal ulcers.
Long-term use of NSAIDs plus glucocorticoids: Risk increases 10 to 15-fold!
SSRIs
Smoking
Chronic alcohol consumption
Patients with blood type O have a higher risk for duodenal ulcers.
Age > 65 years
Stress (see “Subtypes and variants” below)
Rare risk factors:
Zollinger-Ellison syndrome (can result in duodenal ulcer)
Hyperparathyroidism
Classification
- Gastric ulcer: an ulcerative lesion in the stomach lining; typically manifests along the lesser curvature and the gastric antrum
- Duodenal ulcer: an ulcerative lesion located in the duodenum, typically in the first part (i.e., the duodenal bulb)
- Erosive gastritis: acute mucosal inflammation of the stomach that does not extend beyond the muscularis mucosae (Erosions are more superficial than ulcers. Ulcers involve damage to the gastric mucosa extending beyond the muscularis mucosa layer into the submucosa.)
An atypical location is suspicious for carcinoma or ZES!
Gastric secretions
- Helicobacter pylori gastritis (gastrite B, con normoipogastrinemia, invece la gastrite autoimmune A si caratterizza per ipergastrinemia): increased acid secretion, decreased protective factors/mucus production
- NSAIDs inhibit COX-1 and COX-2 → decrease in PGE2 (normally decreases gastric acid secretion and increases HCO3- and mucus secretion) → gastric mucosa erosions
✔Parietal cells
Secrete hydrochloric acid (HCl) and intrinsic factor🧨
Stimulated by acetylcholine, histamine, and gastrin
Inhibited by prostaglandins and somatostatin NB
✔Mucosal cells
Secrete protective mucus
Stimulated by acetylcholine, prostaglandins, and secretin
✔Chief cells
Secrete pepsinogen🧨
Stimulated by acetylcholine, gastrin, secretin, and vasoactive intestinal polypeptide (VIP)
Clinica
Gastric ulcers: in elderly, vomiting is a typical sign! Are found in the antrum and lesser curvature, with normal to diminuited acid secretion. Weight loss (il dolore aumenta con l’introito di cibo)
Duodenal ulcers: nocturn pain, at fasting (2,3 ore dopo i pasti). Pain increases 2–5 hours after eating
Pain on an empty stomach (hunger pain) that is relieved with food intake → weight gain
Increased parietal cell mass and acid secretion.
Dyspepsia: postprandial heaviness, early satiety, and gnawing, aching or burning epigastric pain
Pain relief with antacids
Potential signs of internal bleeding (anemia, hematemesis, melena)
∼ 70% of patients with PUD are asymptomatic
Stool sample positive for occult blood (see gastrointestinal bleeding)💥
Taking NSAIDs can often mask PUD symptoms until complications such as hemorrhage and perforation occur!
Stress ulcer
Decreased blood flow!
Acute damage to the gastric mucosa, resulting from increased levels of endogenous glucocorticoids and decreased blood flow to the stomach.
Causes: polytrauma, major surgery, SIRS, kidney failure, etc.
Types
1.Curling ulcer: severe burns → decreased plasma volume → decreased gastric blood flow → hypoxic tissue injury of stomach surface epithelium → weakening of the normal mucosal barrier
2.Cushing ulcer: In patients with brain injury, increased vagal stimulation leads to increased production of stomach acid via acetylcholine release!
Dieulafoy’s lesion
Sanguinamento submucosale
Description: In this rare disease, minor mucosal trauma can lead to major bleeding. It is caused by an abnormal submucosal artery.
Location: proximal stomach
Clinical presentation: signs of acute upper GI bleeding
Treatment: endoscopic hemostasis (injection therapy, hemoclips, etc.), excision of the susceptible mucosa
Diagnostic approach
≤ 55 years of age without alarm features: Urea breath test for H. pylori (or stool antigen)
> 55 years of age or presence of ≥ 1 alarm features: EGD with biopsies and rapid urease testing for H. pylori
✔If negative for H. pylori infection and NSAID intake; trial therapy unsuccessful
- Measure serum gastrin level at baseline and after secretin stimulation test: high levels in gastrinoma (Zollinger-Ellison syndrome)
- Measure serum calcium and parathyroid hormone: high levels in primary hyperparathyroidism
- Testing for Helicobacter pylori (EGDS plus bioptic samples)
Esophagogastroduodenoscopy (EGD)
Most accurate test
✔Patients > 60 years of age or presence of ≥ 1 alarm features, which include:
Certain symptoms: progressive dysphagia, painful swallowing (odynophagia), and/or persistent vomiting
Signs of active GI bleeding (e.g., melena, unexplained iron-deficiency anemia)
Signs of malignancy (e.g., unintended weight loss, lymphadenopathy, palpable mass)
Family history of upper GI malignancy in a first-degree relative
Jaundice
✔Biopsy samples from:
Edge and base of the ulcer (essential to rule out malignancy) .
Stomach lining distant from the ulcer (Helicobacter pylori testing for detection of underlying type B gastritis)
✔If active bleeding, EGD can be performed for diagnosis and subsequent hemostasis treatment (electrocautery) in the same session.
General management of dyspepsia
- H. pylori positive → eradication therapy (with antibiotics and a PPI) and supportive treatment → continue PPIs for 4–8 weeks → follow-up
- H. pylori negative → medical acid suppression (with a PPI) and supportive treatment for 4–8 weeks → follow-up
✔Medical treatment
Helicobacter pylori eradication therapy (with antibiotics)
Acid suppression: PPIs (most effective), H2 blockers, antacids (mainly used for symptom relief)
Mucosal protection: misoprostol , sucralfate (both substances are rarely used in PUD)
✔Supportive treatment
- Discontinue NSAIDs
- Restrict alcohol use/smoking/emotional stress
- Avoid eating before bedtime
✔Surgical treatment
With the advent of potent acid suppression in the form of PPIs, surgical intervention is rarely needed.
Indications
- Refractory syndromes despite appropriate medical treatment
- If cancer is suspected
- Complications that cannot be treated endoscopically (see “Complications” below)
-Partial gastrectomy (Billroth)
Billroth I: distal gastrectomy with end-to-end or side-to-end gastroduodenostomy
Billroth II: resection of the distal ⅔ of the stomach with a blind-ending duodenal stump and end-to-side gastro-jejunostomy. The Billroth I and II methods without a Brown’s anastomosis often lead to bile reflux into the stomach. This may result in type C gastritis in the region of the anastomosis. The chronic inflammation causes atrophic changes and increases the risk of cancer (anastomosis carcinoma).
-Vagotomy
Complications
La perforazione gastrica è comunemente anteriore!
Le ulcere duodenali invece sono soprattutto anteriori
✔Bleeding (see gastrointestinal bleeding)
Most common complication of PUD
Located posterior more commonly than anterior
Perforated gastric ulcers of the lesser curvature may cause hemorrhage of the left gastric artery.
!Duodenal ulcers of the posterior wall are more likely to cause massive bleeding because of their proximity to the gastroduodenal artery.
✔Gastric/duodenal perforation (see also secondary peritonitis and gastrointestinal perforation)
Second most common complication of PUD
Located anterior more commonly than posterior
Duodenal ulcers of the anterior wall are more likely to perforate into the abdominal cavity (ma è più grave una perforazione gastrica), causing pneumoperitoneum (free air below the diaphragm) and irritation of phrenic nerve (e.g., shoulder pain).
✔Subhepatic abscess
Etiology: may result from a perforated duodenal or gastric ulcer
Clinical presentation: fever and vomiting
Diagnosis: subhepatic gas on abdominal x-ray👓
Management
Treat underlying cause
IV antibiotics, percutaneous drainage!
✔Fistula formation
Clinical presentation
Increased severity of pain, which is no longer relieved by eating; radiation of pain to the back
Weight loss, diarrhea
✔Malignant transformation
Gastric ulcers: high malignant potential (progression to cancer in 5–10% of cases) → malignancy should be ruled out with biopsy [21]
Duodenal ulcers: usually benign → routine biopsy is not required
Gastric outlet obstruction
Definition: mechanical obstruction of the pyloric channel or duodenum
-Etiology
1.Malignancy (most common) 💥
2.PUD
Acute PUD → inflammation and edema
Chronic PUD → scarring and fibrosis
-Gastric volvulus
Less common causes that cause strictures in the pyloric channel: Crohn disease, history of ingestion of a caustic substance, chronic pancreatitis
Clinical presentation Postprandial, nonbilious vomiting Succussion splash Early satiety Progressive gastric dilation Weight loss
Diagnosis
Barium swallow
Upper endoscopy (confirmatory test): identification of the gastric pathology
Laboratory tests: hypokalemic hypochloremic 👓metabolic alkalosis
Saline load test
Management
Symptomatic: nasogastric suction, electrolyte and fluid replacement, and parental nutrition
Definitive: surgery or endoscopic dilation
