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Acid Secretion (figure a, phases of Acid Secretion):
- Direct (vagal stimulation)
- Indirect (outside stimulus, food, gastric distension)
- passage of food into duodenum stimulates hormonal release (inhibits acid secretion).

Stomach Anatomy and Function:
- stomach serves as a food reservoir
- facilitates chemical and mechanical digestion.

- The stomach has 3 muscle layers (see figures):
- Outer longitudinal
- Inner oblique
- Middle Cicular

- Parietal cells secrete HCL and chief cells secrete pepsionen

- Antral mucosal cells release PGs that stimulate mucus and bicarbonate secretions --> vasodilate cells and are involved in inflammation (inhibit platelet activity, can facilitate uterine contraction, mucus)
- NSAIDs block PGs by inhibiting COX enzymes, which facilitate fever, pain, and attract immune cells.
- In short: help inflammation (therefore NSAIDs block both the protective and inflammatory functions of PGs).

- Stomach stretches in size when food is consumed.

-Chief cells release gastrin --> stimulate acid production.
- Mucosal parietal cells: protect epithelium from various outer and inner substances.

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Parietal cells (blue) results in secretion of acid through H+/K+ATPase. Histamine directly activates acid secretion through a cascade that includes a G-inhibitor, which inhibits the acid secretion cascade when bound to PGs. Acid secretion is further stimulated by Gastrin and Ach.

There is direct vagus innervation, which explains why high levels of stress can stimulate acid secretion and promote ulcer formation as a result of stressful/traumatic event.

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Why does the stomach have a thicker mucous layer than the duodenum?

Where are prostaglandins secreted and what do they stimulate?

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Aetiologies (**merge with other sections)

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Aetiologies (**merge with other sections)

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What are different causes of gastric and duodenal disorders?

Effect of H. Pylori infection?

Effect of NSAIDs?

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Complications of Ulcers?

Bleeding

Perforation, gastric outlet obstruction?

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Symptoms?

Difference in duodenal and gastric ulcer when eating?

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- Epidemiology:
90% prevalence in developping countries.
20-50% in developped countries. Infection usually occurs during childhood (foecal-oral or oral-oral). Infection is often associated with Gastric carcinomas and gastric inflammation.

- Pathogenesis:
No fully understood. Bacterium very adapted to highly acidic environmnet. Induces damage to the gastric epithelium. H. pylori creates urease and employs it to survive in the gastric environment. Pathogenesis highly dependent in Genetic Predispositions of host.

H pylori synthesizes urease that produces ammonia which neutralizes pH and allows the bacterium to live viably in the acidic environment of stomach.

- Diagnosis (Invasive Vs. Non-invasive):

Non-invasive: serological tests (IgG), Urea breath test (ingestion of urea drink, and concentration is measured after breaths as well as [CO2], method is unreliable if PPIs or antibiotics have been used before the test), stool antigen test.

Ivasive: endoscopy, biopsy (presence of urea, ammonia, histology, culture --> antobiotic sensitivity).

- Treatment & Eradication Therapy

Usually combination of 2 antibiotics paired with a PPI. This is highly practical and efficient in eliminating the bacterium from the stomach environment.

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Breaks in superficial epithelium of stomach/duodenum (10% in adults) that can penetrate into mucosa. Increase in inflammatory cells. Peptic ulcers are more common in higher ages, and are highly variable according to region/geography.

- Epidemiology (**remaining edit)

- Clinical Features
Burning epigastric pain, patients experience weight loss, nausea, emesis. Can also result in posterior pain dependent on location of ulcer.

Patients under 55 y/o --> eradication therapy if (+) for H pylori w/o further investigations. Older patients may require more investigations to eliminate risk of cancer.

Gastric ulcers are more painful when eating, but duodenal ulcers get better after a meal (not a good diagnostic tool, better to assume general ulcer and confirm it with with an endoscopy).

- Complications of Peptic Ulcers:

Hemorrhage

Bleeding due to ulcers eroding into blood vessels underneath (can become a problem when they portrude on a medium/large vein/artery).

If the patient has a non-evident ulcer, it can result in development of chronic anaemia.

Perforation

Ulcers go through layers of disgestive tract and form a 'hole'. More common in gastric ulcers.

Gastric Outlet Obstruction

Namely caused when an active ulcer has an acting oedema. When ulcer scars and results in fibrotic tissue, forming an obstruction of the gastric outlet.

Surgical Treatments

surgical only performed with severe complications that require invasive/acute treatment.

More employed in the past.

The role of associated diseases (gastric adenocarcinoma & gastric B cell lymphoma)

NSAIDS, H. Pylori and ulcers

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4th most common cancer wordwide. Associated with Barret's oeasphagus, arises from previously modified cells. Strong link to H. pylori and has certain lifestyle and genetic risk factors.

Type 1: intestinal, well formed glandular structure. Polypoid or ulcerating lesions. Metaplasia.

Type 2: Diffuse. Undifferentiated tumour from rest of parenchyma, worse prognosis than type 1.

- Epidemiology & Pathogenesis (link to H. pylori)
High prevalence in japan due to high sodium in diet and 'smoky' foods.

- Screening

- Pathology

- Clinical features and symptoms
Half the cases asymptomatic. Anorexia, weight loss, anaemia, gastric pain (**remaining).

- Diagnosis
Gastroscopy (and subsequent biopsy) and numerous imaging techniques. CT, transabdominal ultrasound, endoscopy, PET scan.

- Staging/Investigation
Staging employed to categorize tumours and predict survival and prognosis.

- Treatment
Early, non-ulcerated lesions can be removed successfully. Surgery is most succesful form of treatment, and can be paired with chemoradiation. Palliative care common due to high mortality.

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GI Stromal tumours mesenchymal tumours associated with mutation in protooncogene KIT, increases expression of Tyrosine Kinase (**remaining edit).

Usually asymptomatic.

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PGL are 90% caused by H pylori. R

Results in epigastric pain and ulcers. Associated with muscosa of lymphatic tissues.

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GPs are usually found in 1% of endoscopies by chance, rarely symptomatic.

Histological analysis through biopsy can suggest whether removal is necessary or not

Hyperplastic polyps (most common), adenomatous, cystic gland polyps, inflammatory polyps (eosinophil infiltrated).

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Disease involves duodenum.

Inflammation of mucosa of small bowel, characterized by autoimmune inflammation due to intolerance to gluten.

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(**remaining edit: summarize figure in short text).

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Either no symptoms or non-specific ones:
- fatigue
- diarrhoea
- long-term induced osteoporosis (possible in young patients whose bone structure is of weak quality).

Toddlers can have failure to thrive due to destruction of villi. Despite intake of normal nutrition babies can display sign of malnutrition.

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Often misdiagnosed (patients diagnosed at late age).

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Blood analysis (anaemia)
Serology (Igs)
(**remaining edits)
--> osteoporotic patients (vit D, B12, Calcium)

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Important to stop the intake of gluten to limit the inflammation of the intestinal lining.
- Fe
- Vit D.
- supplements that might provide non-diet absorbed nutrients.

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- Oesophageal cancer
- T-cell lymphoma
- Refractor Coeliac disease.
- Additional complications if pateint unresponsive to gluten free diet.
- Clusters of itchy rashes at joints (knees, elbows)

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Physiological effects of PGs

What is their relationship to NSAIDs?