Peptic Ulcer Flashcards
Definition
chronic relapsing disease characterised by
a violation of the integrity of its mucosa with the formation of a
scar
Causes/risk factors
Helicobacter pylori
•NSAID (Nonsteroidal anti-inflammatory
drugs)
•Genetic/hereditary factor
Smoking
Age over 65
Certain medical conditions like Zollinger-Ellison syndrome (gastric tumors) liver cirrhosis kidney disease
Diet
Alcohol
Stress
Aggressive factors
EXOGENEOUS
• H. pylori
• NSAIDs
ENDOGENEOUS
• H+ ions
• Pepsin
• Bile acid
Protective factors
Gastric mucus - 0,1-0,5 mm soluble
vs. gel phase – mucin (MUC1, MUC2,
MUC5AC, and MUC6 produced by
collumnar epithelium – gel thickness
prostaglandins (PG E2) COX I inhibitors
Bicarbonate (HCO3 -) secretion –
columnar epithelium in stomach,
pancreatic juice to duodenum –
enters the soluble and gel mucus,
buffers H+ ions
Mucosal (epithelial) barrier –
mechanical support against H+
Blood supply into mucose – removal
of H+ ions – supply with HCO3
Classification of the peptic ulcer
III. By numbers:
1. Single
2. Multiple
IV. By sizes (in PUD)):
1. Small ulcers up to 0,5cm
2. Middle ulcers – 0,6 -1,9cm in the stomach & 0,6-1,2cm in
the duodenum
3. Large ulcers – 2,0-3,’0cm in the stomach & 1,3-1,9cm in
the duodenum
4. Giant ulcers over to 3cm in the stomach & over 2cm in duodenum
VI. By the presence of complications:
1. Hemorrhage (bleeding)
2. Perforation
3. Penetration
4. Perigastritis, periduodenitis
5. Pyloric stenosis
6. Malignization
Modified Johnson Classification of peptic ulcers
Type I: Ulcer along the lesser curve of stomach
Type II: Two ulcers present - one gastric, one duodenal/prepyloric
Type III: Prepyloric ulcer
Type IV: Proximal gastroesophageal ulcer
Type V: Anywhere (associated with chronic NSAID use
Mechanism, of action
Imbalance between aggressive and defensive factors
Clinical Presentation of PUD
Typical Symptoms:
• Epigastric pain(• Gnawing or burning
• Occurs 1-2/2-5 hours after meal, hunger pain (
• Relieved by food or antacids
• Might occur at night
• Might radiate to back (consider penetration)
• Nausea
• Fullness
• Bloating
• Early satiety
• Nocturnal pain
Dyspepsia, including belching, bloating, distention, fatty food intolerance
Complicated PUD:
• Vomiting, which might be related to partial or complete gastric outlet
obstruction
• Hematemesis or melena resulting from gastrointestinal bleeding
Alarm Symptoms:
• Anemia
• Hematemesis
• Melena
• Heme-positive stool
• Bloody vomiting
• Anorexia or weight loss
• Persisting upper abdominal
pain
radiating to the back
• Severe, spreading, upper
abdominal pain
Clinical comparison of Gastric ulcer and Duodenal ulcer
Clinical comparison of Gastric ulcer and Duodenal ulcer
Gastric Ulcer
• O c c u r in t h e s t o m a c h
• Epigastric pain 1-2 hours after eating
C a n c a u s e hematemesis (vomiting blood)or m e l e n a(dark tart stool )
• Heartburn, chest discomfort and early
satiety are commonly seen
Can cause gastric carcinoma (mostly in the
elderly)
Duodenal ulcer
Occur in the duodenum
• Epigastric pain 2-5 hours after eating
• Can cause melena or hematochezia
• Heartburn, chest discomfort are less
common but may be seen
• Pain may awaken patient during the night
Physical examination:
Inspection: pale, weight loss, coating of tongue …
• Palpation: left or epigastric tenderness, pain radiation,
Vasilenko’s sign
• Percusion: Mendel’s sign
Physical examination (in complicated PUD):
• Guaiac-positive stool resulting from occult blood loss
• Melena resulting from acute or subacute gastrointestinal
bleeding
• Succussion splash resulting from partial or complete gastric
outlet obstructio
Diagnostics
Detection of H. pylori
Endoscopic or invasive tests
1. Rapid urease test
2. Histopathology
3. Culture
Nonendoscopic tests
1. H. pylori antibody detection in blood
2. stool antigen test
Endoscopy
• Detection of ulcer— fiberoptic endoscopy, double-contrast
barium X-ray
• Diagnose H. pylori infection — urease test, serological test,
biopsy, etc.
• Detection of mucosa abnormalities — endoscopy, double-
contrast barium X-ray
• Study of motor function — endoscopy, X-ray
• Examination of secretory function ????
• Diagnosis of complications — CBC…..US
Treatment
- Etiological treatment
• eradication of H. pylori (eg. tetracycline, clarithromycin, amoxicillin or
metronidazole)
• cessation of NSAIDs?,
• psychotherapy, regimen, special diet… - Decrease gastric secretion
Antisecretory drugs
• H2 blockers (cimetidine, ranitidine, famotidine, and nizatidine)
• Proton pump inhibitors (омеprazole, lansoprozole and others),
Antacids - Enhance mucosal defense (trophic effects on the ulcerated mucosa):
• Sucralfate - Normalize motor function
• Prokinetics: Metoclopramide, Domperidone, Itopride hydrochloride, Cisaprid
Medications
The medications that inhibit acid secretion act either on the
three receptors on the parietal cell or on the acid pump:
They include
• H2-receptor antagonists (cimetidine and ranitidine),
• muscarinic-receptor antagonists (pirenzepine,
propantheline),
• gastrin-receptor antagonists (proglumide) and
• H+/K+-ATPase inhibitors (omeprazole
Proton pump inhibitors bind to and inhibit the H+/K+-
adenosine triphosphatase (ATPase) pump of the parietal cell,
resulting in a marked decrease in acid secretion.
• Proton pump inhibitors have some direct antibacterial effect,
and their antisecretory properties aid in ulcer healing:
Omeprazole (Prilosec)
Lansoprazole (Prevacid)
Esomeprazole (Nexium)
Rabeprazole (Aciphex
H2-receptor blockers – H2-receptor antagonists selectively
block H2-receptors on parietal cells, resulting in diminished
acid secretion and ulcer healing:
Cimetidine (Tagamet)
Ranitidine (Zantac)
Famotidine (Pepcid)
Nizatidine (Axid
Eradication therapy
First-line eradication therapy: one of the following two-week
triple therapy regimens is used
• A ‘PAC’ regimen (a PPI (Proton pump inhibitor) plus
Amoxicillin 1 g and Clarithromycin 500 mg, all given twice a
day)
• Or (for people with penicillin hypersensitivity) a ‘PCM’
regimen (a PPI plus Clarithromycin 250 mg and plus
Metronidazole 400 mg, all given twice a day)
• Note: an alternative antibiotic should be used in the
eradication regimen, if a course of clarithromycin or
metronidazole has previously been given (for any
indication).
Triple therapy
The BEST among all the Triple therapy regimens is
• Omeprazole/Lansoprazole • Clarithromycin • Amoxycillin - 20/30 mg BD
- 500 mg BID
- 1 gm BD
Given for 14 days followed by P.P.I. for 4-6 weeks
Eradication therapy
Second-line eradication therapy: if first-line eradication therapy fails,
PRODIGY recommends that one of the following one-week eradication
regimens is used.
• Quadruple therapy (a PPI twice a day, bismuth 120 mg four times a
day, metronidazole 400 mg three times a day, and oxytetracycline
500 mg four times a day)
• If quadruple therapy is not tolerated, consider using a triple-therapy
regimen that contains antibiotics that have not been used before.
• Second-line eradication therapy should use different antibiotics to first-
line therapy. The HPA Helicobacter Working Group recommends that two
antibiotics are chosen from the following options: amoxicillin,
clarithromycin, metronidazole, or oxytetracycline.
• Other antibiotics can be considered, but advice should be sought from
the Helicobacter Reference Laboratory
Complications of Peptic Ulcer Disease
Acute
• perforation
• hemorrhage, which can be massive
Chronic
• Pyloric stenosis
• Deformity (scarring) in the
duodenal bulb
• penetration
• perivisceritis (perigastritis,
periduodenatis, ..
Causes of acute upper GI bleeding
Causes of acute upper GI bleeding
• Peptic Ulcer Disease or secondary ulcer
• esophageal varices secondary to portal hypertension
• Erosive gastritis
• Oesophagitis
• Mallory Weiss tear
• Ulcer «in Hiatus Hernia»
• Cancer of the esophagus, stomach
• Hemophilia
• Aorta-intestine fistula
• Other
Clinical picture of ulcer bleeding and treatment
Clinical picture of ulcer bleeding
Hemorrhage is the most common complication of peptic
ulcer disease
Risk factors are present.
Frequently without pain and predisposing factors!
• hematemesis or coffee ground vomiting
• passage of bloody or black tarry stools (hematochezia
and melena, respectively)
• weakness, orthostasis, syncope, thirst, and sweating
caused by blood loss (from hypovolemia to haemorrage
shock)
Definitions
• Haematemesis is vomiting fresh red blood
• Coffee ground vomiting is vomiting of altered black blood
• Melaena is the passage of black tarry stool
Additional examination
Main tasks:
• Esteblish the site of upper GI bleeding - continuous gastric
aspiration via a nasogastric tube may be used in a vomiting
patient and helps monitor continuing or recurrent
hemorrhage. Lavage through a large tube may help cleanse
the stomach of clots, especially before diagnostic
endoscopy.
• Determine of volume loss: pulse rate, BP, and CBA (platelet
count!, Hct)
• Esteblish degree of coagulopathy: prothrombin time, partial
thromboplastin time with repeated monitoring of Hb and
Hct.
• Assess the state of the internal environment: CBC,
electrolytes, etc.
Assessment and restoration of blood
loss
• Most GI bleeding stops spontaneously (e.g. in about 80% of
patients without portal hypertension).
• Major blood loss is manifested by pulse > 110 beats/min,
systolic BP < 100 mm Hg, orthostatic drop in systolic BP of
>= 16 mm, oliguria, cold clammy extremities, and often,
mental status changes resulting from decreased cerebral
perfusion (confusion, disorientation, somnolence, loss of
consciousness, coma).
Assessment and restoration of blood
loss
• Transfusions usual complicating vascular disease is
present, if severe comorbid conditions or critical illness is
present, or if the patient is elderly
• Most transfusion physicians now recommend only blood
component therapy
• After adequate blood volume is restored, the patient must be
observed closely for evidence of further bleeding (eg,
increased pulse; decreased BP; vomiting of fresh blood;
recurrence of loose, tarry stools)
Specific therapy (1)
• Depends on the bleeding site.
• Emergency operation is occasionally required to control
acute bleeding or rebleeding, although endoscopic
coagulation (with bipolar electrocoagulation, injection
sclerosis, heater probes, or laser), available in most
hospitals, is usually successful in that it stops the bleeding
at least temporarily
Specific therapy (2)
• It is particularly important to consider early operative
control of gastric bleeding in the elderly to minimize
mortality rates.
• At the time of the diagnostic endoscopy, treatment of
active ulcer bleeding or of nonbleeding visible vessels in
ulcers is indicated with endoscopic coagulation
