PUD cause patho symptom and RX

2. M Salman ijaz,Sumera Rehman,
Anam Khadim,Sehar shabir,
Zahida Parveen

3. At the end of this presentation the participents will be
able to:
 Define peptic ulcer.
 Identify epidemiology of peptic ulcer.
 Describe classification of peptic ulcer.
 List causes of peptic ulcer.
 Explain the pathophysiology of peptic ulcer.
 Recognize the typical clinical presetation and risk factors
for PUD.
 Integrate diagnostic test.
 Describe Treatment and Management of PUD.

4.  Peptic ulcers are produced by an imbalance between the
gastro-duodenal mucosal defense mechanisms and
damaging forces of gastric acid and pepsin.
 Imbalance between aggressive & protective
factors.Aggressive factor include gastric acid and
protective factor include mucosal barrier and bicarbonate
secretion.

7. ₪ Stomach (called gastric ulcer)
₪ Duodenum (called duodenal ulcer)
₪ Oesophagus (called Oesophageal ulcer)
₪ Types of peptic ulcers:
₪ Type I: Ulcer along the lesser curve of stomach
₪ Type II: Two ulcers present - one gastric, one duodenal
₪ Type III: Prepyloric ulcer
₪ Type IV: Proximal gastroesophageal ulcer
₪ Type V: Anywhere

9.  Duodenal sites are 4x as common as gastric sites
 Most common in middle age peak 30-50 years
 Male to female ratio—4:1
 More common in patients with blood group O
 Associated with increased serum pepsinogen
 H. pylori infection common up to 95%
 Smoking is twice as common

10.  common in late middle age incidence increases with age.
 Male to female ratio—2:1
 Use of NSAIDs - associated with a three- to four-fold
increase in risk of gastric ulcer .
 Less related to H. pylori than duodenal ulcers – about
80%.
 10 - 20% of patients with a gastric ulcer have a
concomitant duodenal ulcer .

11. CAUSES

12.  Helicobacter pylori, a bacteria that is frequently found in the
stomach
 Nonsteroidal anti-inflammatory drugs (NSAIDS) such as
ibuprofen.
 In addition, smoking and certain other genetic and
environmental factors (such as medications) may influence the
course of peptic ulcer disease.
 Psychological stress and dietary factors were once thought to
be the cause of ulcers, although these factors are no longer
thought have a major role.

13. Helicobacter pylori infection

14.  H. pylori is a helix-shaped.
 Gram-negative, slow-growing organism.
 About 3 micrometers long with a diameter of about
0.5 micrometers.
 Has 4–6 flagella.
 It produces oxidase, catalase, and urease

15. The bacterium persists in the stomach for decades in most
people. Most individuals infected by H. pylori will never
experience clinical symptoms despite having chronic
gastritis. Approximately 10-20% of those colonized by H.
pylori will ultimately develop gastric and duodenal ulcers.
H. pylori infection is also associated with a 1-2% lifetime
risk of stomach cancer.

16. NSAIDs inhibit production of an enzyme (cyclooxygenase)
that produces prostaglandins. These hormone-like substances
help protect stomach lining from chemical and physical
injury. Without this protection, stomach acid can erode the
lining, causing bleeding and ulcers.
Cont….

17. stretch
receptors
Medulla
oblongata
endocrine
cells
gastrin
Circulatory
system
stomach
secretes gastric juice

18.  Develop only in presence of acid environment
 Excess of gastric acid not necessary for ulcer
development
 Person with a gastric ulcer has normal to less than normal
gastric acidity compared with person with a duodenal
ulcer
 Pepsinogen is activated to pepsin in presence of HCl and
a pH of 2 to 3
 Secretion of HCl by parietal cells has a pH of 0.8
 pH reaches 2 to 3 after mixing with stomach contents

19.  Surface mucosa of stomach is renewed about every 3
days
 Mucosa can continually repair itself except in extreme
instances
 Mucosal barrier prevents back diffusion of acid from
gastric lumen through mucosal layers to underlying tissue
 Mucosal barrier can be impaired and back diffusion can
occur

20.  HCl freely enters mucosa when barrier is broken
Injury to tissue occurs
Result: cellular destruction and
inflammation
 Histamine is released
Vasodilation, ↑ capillary permeability
Further secretion of acid and pepsin

21.  Effects of smoking on PUD

Increased rate of gastric emptying
Diminished pancreatic bicarbonate secretion
Decreased duodenal pH
Reduced mucosal blood flow
Inhibition of mucosal prostaglandins

22. NICOTINE
parasympathetic nerve
activity in
gastrointestinal tract
increase
stimulation to
the enterochromaffin-like cells
and G cells
increases the
amount
of histamine and
gastrin secreted

23. Gastrinomas (Zollinger Ellison syndrome), rare
gastrin-secreting tumors, also cause multiple and
difficult to heal ulcers.
 Excessive alcohol consumption Alcohol can irritate and
erode the mucous lining of stomach and increases the
amount of stomach acid that's produced. It's uncertain,
however, whether this alone can progress into an ulcer or
if it just aggravates the symptoms of an existing ulcer.

24. Caffeine
Beverages and foods that contain caffeine can stimulate
acid secretion in the stomach. This can aggravate an
existing ulcer, but the stimulation of stomach acid can't be
attributed solely to caffeine.

25.  HELICOBACTER PYLORI
 Non Steroidal Anti-inflammatory Drugs
 Steroid therapy
 Smoking
 Excess alcohol intake
 Genetic factors
 Zollinger Ellison syndrome – rare syndrome caused by
gastrin-secreting tumour
 Blood group O
 Hyperparathyroidism

26. SYMPTOMS
Burning pain bloating
Nausea water brash
Unexplained weight loss hematemesis (vomiting of blood)
Appetite changes Melina
vomiting Blood in the stools
low blood cell count (anemia)
Stomach pain wakes you up at night
frequent burping or hiccupping An early sense of fullness with eating

27.  Perforation & Penetration—into pancreas, liver and
retroperitoneal space
 Peritonitis
 Bowel obstruction, Gastric outflow obstruction, &
Pyloric stenosis
 Bleeding--occurs in 25% to 33% of cases and accounts
for 25% of ulcer deaths.
 Gastric CA

29. Noninvasive
Urea Breath Test (UBT) Blood test
Invasive
Biopsy Urease TestHistology

30. Culture
Stool antigen test
Upper gastrointestinal (upper GI) X-
ray
Other tests
Endoscopy

31. GOALS OF TREATMENT
 lowering the amount of acid that stomach makes,
neutralizing the acid
 protecting the injured area so it can heal
 It's also very important to stop smoking and drinking alcohol
Prevent complications (bleeding, perforation, penetration,
obstruction)
Minimize recurrences
Reduce financial costs

32.  Medications: Triple therapy for 14 days is considered
the treatment of choice.
◦ Proton Pump Inhibitor + clarithromycin and
amoxicillin
 Omeprazole (Prilosec): 20 mg PO bid for 14 d or
Lansoprazole (Prevacid): 30 mg PO bid for 14 d
or
Rabeprazole (Aciphex): 20 mg PO bid for 14 d or
Esomeprazole (Nexium): 40 mg PO qd for 14 d
plus
Clarithromycin (Biaxin): 500 mg PO bid for 14
and
Amoxicillin (Amoxil): 1 g PO bid for 14 d
 Can substitute Flagyl 500 mg PO bid for 14 d if
allergic to PCN
◦ In the setting of an active ulcer, continue qd proton
pump inhibitor therapy for additional 2 weeks.

33.  Medications—treat with Proton Pump Inhibitors or H2
receptor antagonists to assist ulcer healing
◦ H2: Tagament, Pepcid, Axid, or Zantac for up to 8
weeks
◦ PPI: Prilosec, Prevacid, Nexium, Protonix, or Aciphex
for 4-8 weeks.

34. Surgery
Vagotomy Antrectomy Pyloroplasty
Tying off an
artery
Acupuncture Chiropractic Homeopathy Herbs
Other modes
Of treatment

35.  Avoid NSAIDs.
 Restrict beverages and food containing caffeine,
encourage dietary modifications.
 Vitals and hemodynamic monitoring.
 Stress reduction and relaxation techniques.
 Prevent from complication e.g. perforation and
hypovolimic shock.
 Left lateral position to prevent aspiration in case of
vomiting.
 Regularly spaced meals and avoid over eating.
 Life style modifications.

36. Don't smoke Limit or avoid alcohol
Avoid nonsteroidal
anti-inflammatory
drugs (NSAIDs)
Fruits and
Vegetables
Less
Coffee and
Carbonated
Beverages
Use of Olive Oil zz
Exercise
Stress Relief

37.  A peptic ulcer is a break in superficial epithelial cells
penetrating down to muscularis mucosa
 Duodenal > gastric ulcers
 Can be asymptomatic
 H pylori is a predominant risk factor
 H pylori diagnosed by c urea breath test, stool antigen or
if validated serology.
 Complications of PUD can lead to acute emergency of
upper GI bleed