Flashcards in Gastroenterology - Diseases of the stomach and duodenum Deck (47):
What is congenital pyloric stenosis?
Progressive hypertrophy of the circular muscles of the pyloric sphincter. NOT present at birth but occurs over the ensuing 3-5 weeks. A deficiency of NO precipitates the disease.
Probable genetic basis, occurs in males>females. Affected fathers or mothers increases risk for child with CPS.
What are the clinical findings of congenital pyloric stenosis?
Projectile vomiting occurs, fluid is not bile stained.
Hypertrophied pylorus is palpated in the epigastrium (called an "olive").
What is gastroparesis?
Decreased stomach motility. Caused by either autonomic neuropathy or (e.g. DM) or previous vagotomy.
Clinical features include early satiety and bloating and vomiting of undigested food a few hours after eating.
Treatment is with frequent feeding of small meals and metoclopramide.
What causes acute haemorrhagic gastritis?
This is a result of erosions, which are breaches in the epithelium of the mucosa.
- Burns (called Curling ulcers), CNS injury (called Cushing ulcers)
- Anisakis (worm associated with eating raw fish)
What are the clinical features of acute haemorrhagic gastritis?
Often asymptomatic and self limiting, but can cause dyspepsia, anorexia, nausea, vomiting, haematemesis or melaena. In persistent cases, endoscopy is necessary to exclude peptic ulcer or cancer. Treatment involves avoiding the cause; symp- tomatic therapy with antacids, and acid suppression using PPIs or antiemetics may also be necessary.
What are the two types of chronic atrophic gastritis?
Type A - involves the body and fundus
- most often due to pernicious anaemia (autoimmune destruction of gastric parietal cells leading to loss of intrinsic factor)
Type B - involves the antrum and pylorus
- most commonly due to H.pylori infection
What is H.pylori?
H.pylori is a gram negative urease producing rod shaped bacterium found predominantly in the gastric antrum and in areas of gastric metaplasia in the duodenum. It is closely associated with chronic type B gastritis, peptic ulcer disease, (gastric and duodenal), gastric cancer and gastric B cell lymphoma. However, most patients with infection are asymptomatic.
What is the epidemiology of H.pylori infection?
Infection is acquired in childhood and persists for life until treated. Infection is associated with lower SES and is commoner in developing countries. Transmission is mostly via the oral-oral or faecal-oral route.
What is the pathology of H.pylori infection?
Produces urease, proteases and cytotoxins. Urease converts amino groups in proteins to ammonia. Secretion products produce gastritis and PUD.
H.pylori infection produces gastritis mainly in the gastric antrum. In some cases gastritis can involve the body of the stomach, leading to atrophic gastritis and in some individuals intestinal metaplasia, which is a premalignant condition.
How is H.pylori infection diagnosed?
This is by non invasive or invasive (antral biopsy for patients undergoing endoscopy).
Non invasive testing includes:
- 13C urea breath test
- Stool antigen
Invasive tests include:
- Rapid urease (CLO) test
What is the 13C urea breath test?
This is a non invasive test to diagnose H.pylori infection.
A patient consumes a drink containing carbon isotope 13 enriched in urea. Urea is broken down by ureases produces by H.pylori. After 30 minutes patients exhale into a glass tube. Mass spectrometry calculates the amount of 13C. This test has a high false negative rate if performed within 4 weeks of antibiotic or PPI treatment.
What is the rapid ureas test?
This is an invasive test t diagnose H.pylori infection. Biopsy sample is mixed with urea and pH indicator. There is a colour change if H.pylori urease activity. It is useful for diagnosing patients who are already undergoing endoscopy.
Which patients require H.pylori eradication?
All patients with peptic ulcer disease, atrophic gastritis, gastric B cell lymphoma, after gastric cancer resection and in patients with dyspepsia (test and treat strategy). It is also indicated for individuals who have a first degree relative with gastric cancer. Recurrence is rare after successful eradication.
How is H.pylori eradicated?
PPI based triple therapy for 7 days is the preferred option.
E.g. Omeprazole + metronidazole + clarithromycin, or
Omeprazole + amoxicillin + clarithromycin
What is Menetrier's disease?
The stomach has giant rugal folds due to hyperplasia of mucus secreting cells. It causes hyperproteinaemia (protein losing enteropathy) alongside atrophy of parietal cells causing achlorydia. This increases the risk of adenocarcinoma.
What is peptic ulcer disease?
A peptic ulcer is an ulcer (breakdown) of the mucosa in or adjacent to an acid bearing area. Most occur in the stomach and proximal duodenum.
What type of ulcer is most common?
Duodenal ulcers are nearly 3 times more common that gastric ulcers and occur in 15% of the population at any given time. They are more common in the elderly and in men.
Chronic gastric ulcers are usually single and most are situated on the lesser curve of the antrum. Gastric and duodenal ulcers co-exist in 10% of cases, and are multiple in 15%.
What is the aetiology of peptic ulcer disease?
H.pylori and NSAIDs are the most common causes of PUs. Co-administration of NSAIDs and steroids further increases the risk of an ulcer.
The role of H.pylori in duodenal ulcers (where it is most commonly associated) is better understood than gastric ulcers. H.pylori causes antral gastritis with depletion of somatostatin. The subsequent hypergastrinaemia stimulates parietal acid production, but usually without clinical consequences. In a few patients, especially smokers, this process is exaggerated leading to duodenal ulceration. In gastric ulcers H.pylori probably acts by reducing gastric mucosal resistance to acid and pepsin.
Aspirin and NSAIDs cause ulcers, at least in part, by reduced production of prostaglandins (through inhibition of cyclooxygenase-1) which provide mucosal protection in the upper gastroin- testinal tract. Less common causes of PUs are hyperparathyroidism, Zollinger–Ellison syndrome, vascular insufficiency, sarcoidosis and Crohn’s disease.
What are the clinical features of PUD?
Burning epigastric pain is the most common presenting complaint, typically relieved by antacids with a variable relationship to food. DU pain often occurs when the patient is hungry and classically occurs at night. Other symptoms such as nausea, heartburn and flatulence, may occur. GU pain is exacerbated by eating.
How is PUD investigated?
Patients less than 55 with ulcer type symptoms should undergo non invasive testing for H.pylori infection. OGD is not usually necessary. In patients who undergo endoscopy and are found to have GU, multiple biopsies from the centre and edge of the ulcer are taken because it is often impossible to distinguish by naked eye a benign from a malignant ulcer. A barium meal is useful if gastric outlet obstruction is suspected.
How is PUD managed?
Management depends on whether the ulcer is H.pylori associated or not.
H.pylori associated ulcers require eradication therapy which results in ulcer healing and prevents recurrence. There is usually no need to continue antisecretory treatment unless the ulcer is complicated by haemorrhage or perforation. Eradication is confirmed by either a urea breath test or faecal antigen testing in patients who remain symptomatic or who have had an ulcer complication.
H.pylori negative ulcers are usually associated with aspirin or NSAID ingestion. Treatment is with PPI's and stopping aspirin/ NSAIDs if possible. After ulcer healing, NSAIDs can only be continued with PPI prophylaxis or NSAID therapy is switched to a selective COX2 inhibitor. Follow up endoscopy plus biopsy is performed for all GUs to demonstrate healing and exclude malignancy.
When is surgery indicated for PUD?
Surgery is now rarely used for PUD but is reserved for the treatment of complications (e.g. perforation, persisting haemorrhage, gastric outflow obstruction or persisting or recurrent ulcer after medical treatment). Non-healing gastric ulcer is treated by partial gastrectomy, in which the ulcer and the ulcer-bearing area of the stomach are resected to exclude an underlying cancer. In the emergency situation, biopsies are taken, and then ‘under-running’ the ulcer for bleeding or ‘oversewing’ (patch repair) for perforation is sufficient.
What are the consequences of gastric surgery for PUD?
1) Dumping - rapid gastric emptying leads to distension of the proximal duodenum as the hypertonic contents draw fluid into the lumen. Causes flushing, tachycardia, hypotension, sweating and diarrhoea after eating
2) Bile reflux gastropathy - duodenogastric bile reflux leads to chronic gastropathy
3) Diarrhoea and maldigestion
4) Weight loss - reduced intake due to small gastric remnant
5) Anaemia - Fe deficiency most common many years after subtotal gastrectomy
6) Metabolic bone disease - e.g. osteoporosis and osteomalacia as a consequence of calcium and vitamin D malabsorption
7) Gastric cancer - highest in H.pylori, hypochlorydia, smoking and duodenogastric reflux of bile
What are the complications of a peptic ulcer?
Perforation - uncommon. DUs perforate more commonly than GUs, usually into the peritoneal cavity. Treatment is surgical closure of the perforation and drainage of the abdomen. H.pylori should subsequently be eradicated. Conservative treatment with IV fluids and antibiotics may be indicated in elderly patients.
Gastric outlet obstruction - ulcer disease causing obstruction is now rare and carcinoma is the commonest cause. Outflow obstruction occurs because of surrounding oedema and scarring following healing. Copious projectile vomiting is the main symptom and a succussion splash may be detectable clinically. Metabolic alkalosis may develop due to loss of acid. Surgery is rarely required. Nasogastric suction and large volumes of IV isotonic saline with potassium
What do investigations show in gastric outlet obstruction?
Low serum chloride and potassium
Raised bicarbonate and urea - dehydration results in enhanced renal absorption of Na+ in exchange for H+ and paradoxical aciduria
Nasogastric aspiration of at least 200ml after an overnight fast suggests the diagnosis
How should dyspepsia be managed?
Significant gastrointestinal pathology is uncommon in most young people with dyspepsia. Plus the close association of H.pylori with peptic ulcer disease and non invasive methods of detection means that endoscopy is unnecessary in most patients.
Dyspepsia that is predominantly heartburn should be managed as GORD.
Dyspepsia that is predominantly epigastric pain:
- with alarm symptoms or >55 ---> OGD + CLO
- all other non urgent patients ---> review medications for lifestyle factors, assess H.pylori status by non invasive method
----> positive ----> eradicate H.pylori
----> negative ----> symptomatic treatment: antacids, PPI
What patients are classed as non urgent referrals for a 2 week wait for suspected gastric cancer?
Patients with haematemesis
Patients aged >= 55 years who've got:
- treatment-resistant dyspepsia or
- upper abdominal pain with low haemoglobin levels or
- raised platelet count with any of the following: nausea, vomiting, weight loss, reflux, dyspepsia, upper abdominal pain
- nausea or vomiting with any of the following: weight loss, reflux, dyspepsia, upper abdominal pain
What is Zollinger-Ellison syndrome? What is the pathophysiology?
This rare disorder is characterised by a triad of severe peptic ulceration, gastric acid hypersecretion and a non beta cell islet tumour of the pancreas ("gastrinoma"). It is most common between the ages of 30 and 50 years. The gastrinoma secretes large amounts of gastrin, which stimulates and increases the parietal cell mass. The high acid output activates pancreatic lipase and precipitates bile acids. Diarrhoea and steatorrhoea result.
Where is the tumour commonly located in Zollinger-Ellison syndrome?
Around 90% of tumours occur in the proximal duodenal wall or the pancreatic head. Half are multiple and over half are malignant but slow growing. Multiple endocrine neoplasia type I is present in 20-60% of cases.
What is the clinical presentation of Zollinger-Ellison syndrome?
Suspicious symptoms for ZE syndrome are:
- multiple peptic ulcers
- ulcers resistant to therapy
- ulcer distal to first portion of the duodenum
- PUD plus diarrhoea
- family history of parathyroid or pituitary tumours (MEN type I syndrome)
- PUD without H.pylori or history of NSAIDs
How is Zollinger-Ellison syndrome investigated?
Serum gastrin levels >1000 pg/mL (best screen)
Secretin stimulation test (provocative test) shows a serum gastrin >200 pg/mL
Radiolabelled octreotide is used to localise the tumour
Treatment is with chemotherapy and PPIs.
What is meant by the term gastropathy?
Gastropathy is the term used when there is injury to the gastric mucosa associated with epithelial damage and regeneration. There is little or no accompanying inflammation.
What is gastritis?
Gastritis is inflammation of the gastric mucosa. The distinction between gastropathy and gastritis often causes confusion, since gastritis is often used to describe endoscopic or radiological characteristics of the gastric mucosa rather than specific histological findings.
What is the most common cause of gastropathy?
The commonest cause of gastropathy is mucosal damage associated with the use of aspirin or other NSAIDs. These drugs deplete mucosal prostaglandins by inhibiting the cyclo-oxygenase pathway which leads to mucosal damage. Other causes include infections - e.g. CMV and HSV - and alcohol in high concentrations.
Gastric erosions can also be seen after severe stress (stress ulcer), burns (Curling's ulcer) and in renal and liver disease.
What are the clinical features of gastropathy?
Symptoms include indigestion, vomiting, and haemorrhage, although these correlate poorly with endoscopic and pathological findings. Erosions (superficial breaks in the mucosa <3mm) and subepithelial haemorrhage are most commonly seen at endoscopy. Treatment is with a PPI with removal of the offending cause if possible. prophylaxis is given to prevent future damage in patients who continue to take aspirin or NSAIDs.
What is the most common cause of gastritis?
The most common cause of gastritis is H.pylori infection. Other causes include autoimmune gastritis (the cause of pernicious anaemia associated with antibodies to gastric epithelial cells and intrinsic factor), viruses and duodenal gastric reflux. Gastritis is a HISTOLOGICAL diagnosis and is usually discovered incidentally when a gastric mucosal biopsy is taken for histology at endoscopy. It is classified as either acute or chronic.
Acute gastritis is associated with neutrophilic infiltration, while chronic inflammation is characterised by mononuclear cells, chiefly lymphocytes, plasma cells and macrophages.
What are the clinical features of gastritis?
Gastritis is usually asymptomatic.
At endoscopy the mucosa may appear normal or reddened.
No specific treatment is required although eradication treatment for H.pylori is often given.
What is the epidemiology of gastric cancer?
Gastric cancer is the 4th most common cancer world-wide and the second leading cause of cancer related mortality. Incidence increases with age and is more common in men. The frequency varies geographically, being more common in Japan and Chile and relatively less common in the USA.
Although the incidence overall is decreasing worldwide, proximal gastric cancers are increasing in frequency in the west.
What is the aetiology of gastric carcinoma?
This is unknown. H.pylori infection is implicated causing chronic gastritis which in some individuals leads to atrophic gastritis and pre malignant intestinal metaplasia. Other risk factors are lifestyle (tobacco smoking, diets low in fruits and vegetables or high in salted, smoked or preserved food), pernicious anaemia, family history of gastric cancer, and after partial gastrectomy.
What is the pathology of gastric carcinoma?
Tumours most commonly occur in the antrum and are almost always adenocarcinomas. They are localised ulcerated lesions with rolled edges (intestinal type 1) or diffuse with extensive submucosal spread, giving the picture of linitis plastica.
What are the key features of diffuse type of gastric carcinoma?
Incidence has remained unchanged.
NOT associated with H.pylori infection.
Diffuse infiltration of malignant cells within the wall of the stomach
- linitis plastica
- stomach does NOT have peristalsis
- signet ring cells infiltrate the stomach wall
- produces Krukenberg tumours of the ovaries (signet ring cells spread haematogenously to both ovaries)
What are the clinical features of gastric carcinoma?
Pain similar to peptic ulceration is the most common symptom. With more advanced disease, nausea, anorexia and weight loss are common. Tumours near the pylorus cause outflow obstruction and vomiting and dysphagia occurs with lesions in the cardia.
Almost 50% have a palpable epigastric mass and a lymph node is sometimes felt in the supraclavicular fossa (Virchow's node). Metastases in the peritoneum and liver cause ascites and hepatomegaly.
Skin manifestations of malignancy such as dermatomyositis and acanthosis nigricans are occasionally associated. Metastases to the umbilicus producing the Sister Mary Joseph nodule is rare but can occur.
How should gastric cancer be investigated?
Gastroscopy (OGD) and biopsy is the initial investigation of choice. CT, EUS and laparoscopy are then used to stage the tumour in a similar manner to oesophageal cancer.
How is gastric cancer managed?
Surgery is the most effective form of treatment if the tumour is operable. Adjuvant chemoradiotherapy is given for more advanced tumours. Palliative chemotherapy is sometimes used for unresectable lesions.
What is the prognosis of gastric cancer?
The overall survival is poor (10% 5 year survival). Five year survival after "curative" surgery is 50%. In Japan there is active endoscopic screening programme and earlier diagnosis and an aggressive surgical approach have resulted in 5 year survival rates of around 90%.
What are GISTS?
These are the most common type of stromal or mesenchymal tumour of the GIT, and occur most commonly in the stomach and proximal duodenum. They were previously considered to be benign but on prolonged follow up, most have malignant potential. They are usually asymptomatic and discovered incidentally when an upper gastrointestinal endoscopy is performed for dyspepsia. They can ulcerate and bleed. Treatment is surgical or with imatinib for advanced disease.