PEPTIC ULCER DISEASE- EPIGASTRIC PAIN
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• Dear Viewers,
• Greetings from “Surgical Educator”
• Today I have uploaded a video on Peptic Ulcer Disease- a didactic lecture.
• It is one of the common surgical problems you see in surgical wards.
• I have discussed the various causes for Epigastric pain, epidemiology, etiopathogenesis, clinical features, investigations, complications and treatment of Peptic Ulcer Disease.
• I have also included a mind map and a treatment algorithm for Peptic Ulcer Disease.
• I hope the video will be very useful and you will enjoy it.
• You can watch all my surgical teaching videos in the following link:
• youtube.com/c/surgicaleducator
• Thank you for watching the video.
4. PEPTIC ULCER DISEASE
Applied Anatomy
Celiac Axis:
Left Gastric
Common Hepatic
Splenic
-Rt Gastric from
Hepatic artery proper
-Rt Gastroepiploic
from Gastroduodenal
-Short Gastric from
Splenic artery
5. PEPTIC ULCER DISEASE
Applied Physiology
Chief cells
Pepsinogen
Parietal cells
Hydrochloric acid
and intrinsic factor
G cells Gastrin
D cells Somatostatin
Intrinsic factor is
needed for the
absorption of Vit B12
Autoimmune
destruction of
parietal cells causes
deficient B12
Pernicious Anemia
1. Gastrin from G cells
2. Acetylcholine from vagus
nerve
3. Histamine from paracrine
release via mast cells
8. PEPTIC ULCER DISEASE
EPIDEMIOLOGY
A peptic ulcer is a break in the epithelial
surface of the stomach or duodenum caused
by the action of gastric secretions (acid and
pepsin) and infection with Helicobacter
pylori.
Mucosal infection with Helicobacter pylori is
a major cause for PUD
Patients with duodenal ulcers have an
increased capacity for gastric acid secretion
relative to normal people.
Hemorrhage is the leading cause of death
associated with peptic ulcer.
Each year, approximately 300,000 t o 500,000
new cases of PUD occur.
Three to four million patients are self-
medicating for symptoms of PUD
30,000 surgeries are performed annually for
PUD .
The incidence and prevalence of PUD varies
based upon the presence of Helicobacter pylori
(H. pylori). Higher rates are found in countries
where H. pylori infection is higher
DUs occur two decades earlier than GUs,
particularly in males .
10. PEPTIC ULCER DISEASE
Clinical Features
Symptoms of Gastric ulcers
Male : female 3:1, peak incidence 50+
years.
Epigastric pain induced by eating.
Aversion to food because of pain
Nausea or vomiting.
Hemetemesis and Melenemesis
common
Weight loss.
Dyspepsia: Bloating and early satiety
Heartburn, which is a burning
sensation in the chest
Anemia from chronic blood loss.
11. PEPTIC ULCER DISEASE
Clinical Features
Symptoms of Duodenal ulcers and Type 2 Gastric
ulcers
Male : female 1:1, peak incidence 25–50 years.
Epigastric pain during fasting (hunger pain),
relieved by food/antacids, often nocturnal, typically
exhibits periodicity (i.e. recurs at regular intervals).
Nausea or vomiting.
Weight gain.
Dyspepsia: Bloating and early satiety
Boring back pain if ulcer is penetrating posteriorly
Haematemesis from ulcer penetrating
gastroduodenal artery posteriorly.
Peritonitis if perforation occurs with anterior DU.
Vomiting if gastric outlet obstruction (pyloric
stenosis) occurs (note succussion splash and watch
for hypokalaemic, hypochloraemic alkalosis).
15. PUD- INVESTIGATIONS
H.Pylori TestingNON-INVASIVE INVASIVE
H. pylori is a helical gram-
negative rod with flagella
that resides beneath the
mucous layer of stomach
& duodenum
Production of the enzyme
urease allows H. pylori to
survive in the acidic
environment of the
stomach.
16. PUD- INVESTIGATIONS
Contrast Radiology
Upper gastrointestinal radiology is not used
as much as in previous years, as endoscopy
is a more sensitive investigation
Computed tomography (CT) imaging with
oral contrast has also replaced contrast
radiology where anatomical information is
sought, eg large hiatus hernias of the
rolling type
17. PUD- COMPLICATIONS
Four major complications of peptic
ulcer disease (PUD)
- Bleeding,
-Perforation,
-Penetration,
-Obstruction.
18. PUD- TREATMENT
PPls are the gold
standard with80 to-90%
healing at 8 weeks (e.g.
omeprazole,
lansoprazole).
H2 antagonists have a
high recurrence rate
eg.Cimetidine, Ranitidine
PPIs need acidic
environment to get
activated. So, shouldn’t
combine with antacids
and H-2 blockers
Acid neutralizing & inhibitory drugs
19. PUD- TREATMENT
Cyto-Protective Drug H.Pylori Eradication
H.Pylori should be eradicated in all patients with
documented PUD
No single drug is effective in eradication
Combination of drugs should be given for 14 days
Triple therapy: H. pylori eradication (Rx:amoxicillin
500 mg,and clarithromycin 500 mg) and PPI (20 mg
omeprazole or 30 mg lansoprazole b.d.) for 7–14
days. Metronidazole may replace amoxicillin in
penicillin-allergic patients.
Quadruple therapy: bismuth, metronidazole,
tetracycline and PPI for 7–14 days.
The test of choice for documenting eradication is
Urea breath test
20. PUD- TREATMENT
- SURGERY
Elective for intractable GU: Billroth I gastrectomy.
Normal vagal innervation of stomach
21. PUD- TREATMENT
- SURGERY
Elective for intractable DU: Highly selective vagotomy
Selective Vagotomy
Truncal Vagotomy
23. PUD- TREATMENT
- SURGERY
Gastric & duodenal ulcer perforation
For DU Perforation- Graham’s
omentopexy+Peritoneal toileting For GU Perforation- Graham’s omentopexy
+ Biopsy of the ulcer
+ Peritoneal toileting