Disorders of Stomach + Duodenum Flashcards
The most common complication of peptic ulcer disease
- Bleeding
- Perforation
- Penetration
- Obstruction
Which ulcers do not require or require endoscopic followup
- Duodenal ulcers DO NOT require endoscopic followup
- Gastric ulcers DO require endoscopic followup
What is H pylori associated with?
Associations
• peptic ulcer disease (95% of duodenal ulcers, 75% of gastric ulcers)
• gastric cancer
• B cell lymphoma of MALT tissue (eradication of H pylori results causes regression in 80% of patients)
• atrophic gastritis
How is MALT lymphoma treated?
Eradication of h pylori causes regression in 80% of patients
What are the clinical features of gastric vs duodenal ulcers
Gastric Ulcers
- Pain increases shortly after eating = weight loss
- Less common nocturnal pain
Duodenal Ulcers
- Pain is relieved with food intake = weight gain
- Pain increases 2-5 hours after eating
- Nocturnal pain more common
In term of peptic ulcer perforation, which ulcers are more likely to perforate or bleed?
- Prepyloric gastric ulcers are the most common cause of perforation.
- POSTERIOR ulcers are more likely to BLEED (think at the back so near the vessels)
- ANTERIOR ulcers are more likely to PERFORATE
Features of atrophic gastritis
- The two forms of atrophic gastritis are H. pylori-associated and autoimmune.
- H. pylori-associated atrophic gastritis typically resolves with H. pylori eradication. Autoimmune atrophic
gastritis, however, has no cure.
Clinical Manifestations
- Pernicious anemia
- Iron deficiency anemia
- Hypergastrinemia, which result from the long-term effects of the associated parietal cell loss and subsequent development
of achlorhydria (stomach does not produce HCL).
- Hypergastrinemia is associated with an increased risk for the development of gastric carcinoid and adenocarcinoma; however, the risk is low enough that no
endoscopic surveillance program is endorsed
NSAID induced peptic ulcer disease
- Selective cyclooxygenase-2 (COX-2) inhibitors preferentially inhibit the COX-2 isoenzyme, which primarily modulates pain and inflammation, and minimally inhibit the COX-1 isoenzyme, which promotes generation of the gastric mucosal protective barrier, decreases gastric acid secretion, and helps to maintain good mucosaI blood flow.
- The risk of gastroduodenal ulcers and ulcer complications is significantly lower in
patients taking COX-2 inhibitors compared with nonselective NSAIDs. However, in high-risk individuals, such as those with previous PUD, a COX-2 inhibitor alone is no better than a nonselective NSAID coadministered with a PPI in preventing ulcer
complications.
NSAIDs
Non selective COX-1, Cox2 inhibitors: ibuprofen, diclofenac, indomethacin, naproxen, asprin
Selective COX-2 inhibitor: meloxicam, celecoxib
- COX1: generation of the gastric mucosal protective barrier, decreases gastric acid secretion, helps to maintain good mucosal blood flow
- COX2: modulates pain and inflammation
- COX1 inhibition: inhibition of TXA2 synthesis in platelets –> inhibit platelet aggregation (antithrombotic effect)
- COX2 inhibition: analgesic and anti-inflammatory effects
What is the diagnostic test for gastroparesis?
Diagnostic testing for gastroparesis consists of an initial assessment with upper endoscopy to exclude mechanical obstruction, followed by a gastric emptying study
Treatment for gastroparesis
- Metoclopramide (prokinetic)
SE: dystonia, parkinsonism type movements, tardive dyskinesia
Others: erythromycin, low dose tricyclic antidepressants
What size polyp would a polypectomy be recommended?
> 5mm
Gastric carcinoid tumours
- Where are they derived from?
- What are the 3 subtypes
- What are the clinical features
- Derived from enterochromaffin cells of the gastric mucosa
(1) Type I accounts for 80% and is associated with autoimmune atrophic gastritis and hypergastrinemia.
(2) Type II is associated with multiple endocrine neoplasia
type 1 and Zollinger-Ellison syndrome.
- Endoscopic polypectomy
is curative for type I and II NETs that are smaller than
1 cm. T
(3) Type III lesions account for 15% of gastric NETs; they
are gastrin independent and have the poorest prognosis.
- Gastric NETs secrete 5-hydroxytryptophan rather than serotonin; therefore, classic carcinoid syndrome is rare, while wheezing, lacrimation, swelling, flushing, and carcinoid heart and valvular disease may be seen owing to high systemic amine concentrations.
What are the clinical features of carcinoid syndrome
Investigations
Treatment
CLINICAL FEATURES
- Diarrhoea and abdominal cramps
- Cutaneous flushing
- Bronchospasm
- R valvular stenosis
- Dyspnoea, wheezing
- Palpitations
- Weight loss despite normal appetite
- Valvular heart disease - predominantly affects TRICUSPID valves
- Above symptoms occur due to release of SEROTONIN
- Histamine and adrenocorticotrophic can also be synthesised
- In a patient presenting with secretory diarrhea, episodic flushing, wheezing, and cardiac valvular abnormalities, consider a carcinoid tumor.
INVESTIGATIONS
- Elevated 5-hydroxyindoleacetic acid (5-HIAA) in 24 hour urine collection or in plasma
TREATMENT
Somatostatin Analogues
• Short Acting: Octreotide
• Long Acting: Lanreotide
Features of VIPoma
- Pancreatic neuroendocrine tumour
- Leads to WDHA syndrome - triad of watery diarrhoea, hypokalaemia, achlorhydria (low HCl)
Features of DUMPING SYNDROME
- Caused by the destruction or bypass of the pyloric sphincter where the stomach empties its contents too quickly into the duodenum.
- Pathophysiology: . Although the precise mechanism of dumping is incompletely understood, the syndrome is frequently attributed to the rapid emptying of hyperosmolar chyme (particularly carbohydrates) into the small bowel. The osmotic gradient is believed to draw fluid into the intestine, and this may release one or more vasoactive hormones, such as serotonin and vasoactive intestinal polypeptide
Clinical Presentation:
- EARLY DUMPING occurs 15-30mins post meal. GIT: abdominal discomfort, nausea, diarrhoea, bloating.
Vasomotor: flushing, palpitations, tachycardia, sweating, hypotension and rarely syncope
Occurs as a result of release of vasoactive hormones like SEROTONIN
- LATE DUMPING: same symptoms as above but occurs less commonly and symptoms occurs HOURS after eating. This phenomenon is not strictly due to alterations of osmotic gradients across the gastrointestinal (GI) tract but rather is thought to result from HYPOGLYCAEMIA following a postprandial insulin peak
Diagnosis is made clinically, gastric emptying studies/glucose challenge can help support diagnosis - present with gastrointestinal discomfort, including nausea, vomiting, cramps, and diarrhoea, as well as vasomotor symptoms such as diaphoresis, palpitations, and flushing 15 to 30 minutes after a meal.
Tx Dietary + Lifestyle modification: - High in fibre and rich in protein, eaten slowly and chewed well - Eliminate rapidly absorbable carbs - Le down for 30 mins post meals
Pharm
- Acarbose: for late dumping
- Short acting somatostatin analogue eg: octreotide
Complications post-gastrectomy
- cholelithiasis
- nephrolithiasis (due to increased urine oxalate
excretion) - dumping syndrome.
- anastomotic stricture.
- anastomotic ulceration
- small-bowel obstruction from internal hernias
- gastrogastric fistula.
Nutritional complications post gastrectomy
- Thiamine (vitamin B1)
- Pyridoxine (vitamin B6)
- Folate
- Cobalamin (vitamin B1)
- Vitamins C, A, D, E, and K
- Iron; zinc; selenium; magnesium; and
copper. - Acceleration in loss of bone mineral density
Features of zollinger ellison syndrome
- Zollinger–Ellison syndrome (Z-E syndrome) is a disease in which tumors cause the stomach to produce too much acid, resulting in peptic ulcers. Symptoms include abdominal pain and diarrhea.
- The syndrome is caused by a gastrinoma, a neuroendocrine tumor that secretes a hormone called gastrin. Too much gastrin in the blood (hypergastrinemia) results in the overproduction of gastric acid by parietal cells in the stomach. Gastrinomas most commonly arise in the duodenum, pancreas or stomach.
- In 75% of cases Zollinger-Ellison syndrome occurs sporadically, while in 25% of cases it occurs as part of an autosomal dominant syndrome called multiple endocrine neoplasia type 1 (MEN 1)
- Fasting gastrin levels > 1000 with low pH is high correlated with diagnosis of ZE
- If < 1000 and diagnosis is suspected, then SECRETIN STIMULATION TESTING (rise >200 15 mins after dosing is considered positive) or CALCIUM STIMULATION TESTING (where >395 is considered positive)
- Gastrin receptors bind cholecystokinin
- Gastrin promotes GASTRIC MUCOSAL GROWTH AND GASTRIC MUCOSAL HYPERTROPHY
- Gastrin synthesised in G cells (antrum of stomach)
Conditions associated with:
- High acid production
- Poor acid clearance
which can lead to GORD/ulcer
High acid production: zollinger ellison syndroe
Poor acid clearance: scleroderma/connective tissue disease, gastroparesis
What are RF for peptic ulcer disease
Common RF
- H pylori
- NSAIDs, COX2 inhibitors, aspirin
Environmental
- Smoking
- Stress
Rare Causes:
- Chemo
- Crohn’s disease
- Gastrinoma (Zollinger Ellison syndrome)
Comorbid Conditions
- COPD
- Organ transplantation
- ESRF, cirrhosis
What is the normal gastric feedback mechanism?
- Acidic pH increase somatostatin secretion from the gastric D Cells
- Somatostatin exerts a PARACRINE inhibition of gastrin release from G cells and therefore inhibits gastric acid production
