Peptic Ulcer disease - B. Pharma 2nd Semester Pathophysiology notes pdf

Peptic Ulcer disease


Peptic Ulcer disease


       Risk factor





At the end of this lecture, student will be able to

       Define  peptic ulcer disease

       Explain the  etiology of peptic ulcer disease

       Describe the pathophysiology of peptic ulcer disease

Peptic Ulcer

       Breach in the mucosa of the alimentary tract, which extends through the muscularis mucosa into the submucosa or deeper

       Chronic  and most often solitary, lesions

       Any  portion of gastrointestinal tract exposed to the aggressive action of acid-peptic juices

       Erosion of GI mucosa resulting from  digestive action of HCl and pepsin

Duodenal vs gastric ulcers




More common

Less common


First part of duodenum – anterior wall

Lesser curvature of stomach


Acute or chronic




Benign or malignant

Peptic ulcer

     Imbalance between aggressive & protective factors

Aggressive factors

       Gastric acid

       Proteolytic enzyme

Protective factors

       Mucosal layer

       Bicarbonate secretion


Risk factors of peptic ulcers

       Helicobacter pylori

       Non Steroidal Anti-inflammatory Drugs

       Steroid therapy

       Smoking and Excess alcohol intake

       Genetic factors

       Zollinger Ellison syndrome – rare syndrome caused by gastrin-secreting tumour

       Blood group O   and Hyperparathyroidism

Pathophysiology of peptic ulcers

Gastric acid and pepsin

       Potential for producing mucosal damage is related to the secretion of gastric (hydrochloric) acid and pepsin

       Hydrochloric acid  - parietal cells - receptors for histamine, gastrin, and acetylcholine

       Increased acid secretion - duodenal ulcers -  HP infection

       Patients with ZES  have gastric acid hypersecretion resulting from a gastrin-producing tumor

       Patients with gastric ulcer - normal or reduced rates of acid secretion

Mucosal defense mechanisms

       Protect the gastroduodenal mucosa from noxious endogenous and exogenous substances

       Bicarbonate barrier protect the stomach from the acidic contents

       Epithelial cell restitution, growth, and regeneration

       Maintenance of mucosal integrity and repair is mediated by the production of endogenous prostaglandins         

H. pylori infection

Mechanisms include:

1)      Direct mucosal damage

2)      (b) Alterations in the host immune/inflammatory   response

3)      Hypergastrinemia leading to increased acid secretion        

       Virulence factors (vacuolating cytotoxin, cytotoxin-associated gene protein, and growth inhibitory factor)

       Elaborating bacterial enzymes (lipases, proteases, and urease), and adherence

       Lipases and proteases degrade gastric mucus

       Ammonia produced by urease - toxic to epithelial cells

       Bacterial adherence enhances uptake of toxins into gastric epithelial cells

NSAID Induced

       Direct or topical irritation of the gastric epithelium and 

       Systemic inhibition of endogenous mucosal prostaglandin synthesis

       Inhibit both COX-1 and COX-2 to varying degrees

       Neutrophil adherence may damage the vascular endothelium

       Lead to a reduction in mucosal blood flow

       Liberate oxygen-derived free radicals and proteases      

Symptoms of peptic ulcers

       Abdominal pain that is often epigastric  - burning -   vague discomfort, abdominal fullness, or cramping

        A typical nocturnal pain that awakens the patient from sleep

        Severity of ulcer pain varies from patient to patient

       May be seasonal, occurring more frequently in the spring or fall

       Episodes of discomfort usually occur in clusters lasting up to a few weeks followed by a pain-free period or remission lasting from weeks to years

       Heartburn, belching, and bloating often accompany the pain

        Nausea, vomiting, and anorexia

Complications of peptic ulcers

       Obstruction – pyloric stenosis and duodenal stenosis

       Hemorrhage – blood in stools; if chronic – leads to anemia


       Malignant transformation to carcinoma


       Ulcers are defined as a breach in the mucosa of the alimentary tract, which extends through the muscularis mucosa into the submucosa or deeper

       Etiological factors are helicobacter pylori infection, nonsteroidal anti-inflammatory drugs, critical illness, hypersecretion of gastric acid , viral infections ,vascular insufficiency

       HP infection alters host inflammatory response and damages epithelial cells directly by cell-mediated immune system whereas NSAID cause direct irritation to epithelium and decrease PGE2

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