Alimentary Pathology Flashcards
What is gastric oesophageal reflux disease?
Reflux of gastric acid/bile/pepsins from stomach into oesophagus –> mucosa exposure to these things –> cell loss and inflammation (can lead to erosive oesophagitis.
How do you investigate GORD?
Clinical diagnosis based on symptoms. Only do endoscopy if alarm features (wt loss, vomiting, dysphagia). Oesophageal pH and manometry may be useful.
What can cause GORD?
Increased transient relaxations of LOS, hypotensive LOS, delayed gastric emptying, decreased oesophageal acid clearance, decreased tissue resistance due to bile/acid, hiatus hernia.
What are the risk factors for GORD?
Pregnancy, obesity, drugs lowering LOS pressure, smoking, alcoholism and hypomotility.
What symptoms are associated with GORD?
Heartburn, cough, water brash, sleep disturbance (worse if lying flat).
What complications can arise as a result of GORD?
Malignant/benign stricture formation (due to fibrotic healing), thickening of squamous epithelium lining, ulceration, impaired oesophageal motility, oesophageal obstruction, Barrett’s oesophagus.
How do you manage GORD?
Lifestyle changes
Antacids (Maalox, contains Ag and Ml which neutralise gastric acid)
Alginates (Gaviscon, forms viscous gel over stomach)
Mucosal protectors (bismuth sucralfate, misoprostol)
H2RA (Rantidine)
PPIs (omeprazole, lanzoprazole - IRREVERSIBLY block proton pumps)
Pro-kinetic agents (e.g. metaclopramide, domperidone (dopamine antagonists - parasympathetic control of smooth muscle/sphincter tone via ACH domperidone - increase gut motility and gastric emptying).
Fundoplication (full/partial wrap) or laparoscopic hiatus hernia repair
What are the complications associated with hiatus hernia repair?
Dysphagia, difficulty belching/vomiting, gas, bloating, excess flatulence, diarrhoea.
What is a major SE of pro kinetic agents?
Can cause long QT syndromes.
How is oesophageal pH measured and what is manometry?
A thin, pressure sensitive tube passed down nose into oesophagus. Sensory probes at level of LOS and UOS - to measure muscle contractions as patient swallows liquid. pH sensors measure acid reflux. Patient records a symptom diary to correlate with the findings.
What areoesophageal pH and manometry used to measure?
Dysphagia, suspected motility disorders, spinster tonicity, relaxation of sphincters, oesophageal motility, heartburn and reflux.
How do you investigate dysphagia?
Oesophagi-Gastric duodenoscopy (OGC) and upper GI endoscopy (UGIE), barium swallow (exclude pharyngeal pouch/post-cricoid web in high dysphagia before endoscopy), oesophageal pH and manometry.
What is presbyoesophagus?
Age related degenerating motor function of oesophagus.
What can cause dysphagia?
Benign/malignant strictures, extrinsic compression, motility disorders (presbyoesophagus, achalasia), eosinophilic oesophagitis.
What are the two types of hiatus hernia?
- Sliding - fundus of stomach moves through hiatus, depends on patient position and whether eating.
- Paraoesophageal - GO position normal, but part of stomach protrudes into chest.
What symptoms are associated with hiatus hernia?
Heartburn, chest pain and other GORD symptoms. Many asymptomatic.
What risk factors are associated with hiatus hernia?
Obesity, ageing.
What is Barrett’s oesophagus?
Type of metaplasia (whereby squamous epithelium transforms into glandular epithelium due to long term exposure to oesophageal reflux).
What are the complications of Barrett’s oesophagus?
Predisposes to formation of adenocarcinoma (metaplasia –> dysplasia –> carcinoma).
How is Barrett’s oesophagus treated?
Endoscopic mucosal resection (removal of nodular areas via banding and ligation), then radiofrequency ablation to allow squamous tissue to grow back through, oesophagectomy in very rare cases may be needed.
What complications are associated with oesophageal cancer?
Obstruction (–> malnutrition), ulceration (tumour uses up blood supply so normal tissue necroses), BV erosion (–> anaemia/blood loss), spread (direct, lymphatic, blood or distant mets (liver, brain, lung, bone).
What signs/symptoms are associated with oesophageal cancer?
Progressive dysphagia, anorexia, wt loss, odynophagia, chest pain, heart burn, cough, pneumonia, trachea-oesophageal fistula, vocal cord paralysis, haematemesis.
Why is spread of oesophageal cancer common?
No peritoneal liming so invasion into adjacent structures more easy. Rich lymphatic supply in lamina propria leads to more lymph node involvement.
What are the two types of oesophageal cancer and where on the oesophagus do they tend to arise?
Adenocarcinoma - distal third (from Barrett’s)
Squamous - middle/proximal third. Preceded by dysplasia and carcinoma in situ.
What sort of tumours to squamous cell carcinomas often form?
From squamous tissue, often large exophytic tumours.
What are the risk factors for developing squamous cell carcinoma?
Smoking, alcohol, dietary carcinogens (?vit deficiencies), low socio-economic status.
What conditions are associated with squamous cell carcinoma?
Achalasia, caustic strictures, Plummer-Vinson syndrome.
How do you investigate oesophageal cancer?
Endoscopy, biopsy (at leas 8), OCG???, staging (CT, endoscopic US, PET, bone scan, laparotomy).
What risk factors are associated with adenocarcinoma of oesophagus?
Barrett’s metaplasia, abdominal obesity, male, middle aged, Caucasian.
How is adenocarcinoma of oesophagus treated?
Curative - oesophagectomy +/- adjuvant (after)/neoadjuvant (after) chemotherapy. Req nutritional support, long post-op recovery (10mnths).
Combined chemo and radiotherapy may improve long-term survival in advanced dx.
If mets - palliative care (dysphagia can be helped by endoscopic stunting, laser, APC, PEG, chemo, brachytherapy).
What are the different oesophagectomy techniques?
Ivor Lewis, trans-hiatal or left thoracic-adbominal.
What conduits can be used for oesophagectomy?
Stomach, colon.
What patients are offered curative therapy in oesophageal adenocarcinoma?
Localised dx, no com orbs, <70 usually.
What is APC?
Argon plasma coagulation - endoscopic procedure used to control bleeding from lesions in GIT and something to debulk tumours.
What is brachytherapy?
Radiotherapy, where a sealed radiation source is placed inside or next to the area requiring treatment.
What can oesophageal hypomotility lead to?
Failure of LOS mechanism.
What risk factors are associated with oesophageal hypomotility?
Connective tissue disease, e.g. scleraderma, diabetes, neuropathy.
What symptoms are associated oesophageal hypomotility?
Heartburn and reflux symptoms.
What is achalasia?
Degeneration of myenteric plexus ganglion cells in distal oesophagus and LOS (failure to relax normally during swallowing, leads to functional obstruction).
What investigations can you do for suspected achalasia and what results will confirm achalasia?
Xray - rat tail appearance at distal end and proximal dilation of oesophagus.
Manometry - high pressure in LOS at rest and failure of LOS to relax after swallowing, absence of useful peristaltic contractions in lower oesophagus (LAST TWO FEATURES REQUIRED FOR DIAGNOSIS).
What is the aetiology of achalasia?
Suspected inflammatory aetiology as histology shows lots of lymphocytes.
What symptoms are associated with achalasia?
Progressive dysphagia for solids, liquids, weight loss, chest pain, regurgitation, chest infections (aspiration risk).
What complications are associated with achalasia?
Aspiration pneumonia, lung disease, increased risk of squamous cell oesophageal carcinoma.
How is achalasia treated?
Nitrates, CCBs, endoscopically delivered botulinum toxin (few months relief in those unable to have definitive Rx), pneumatic balloon dilatation (lasts longer but symptoms tend to recur), myotomy (muscles of lower cardia cut allowing contents to pass into stomach).
What is gastritis?
Inflammation of the gastric mucosa (appears v red on endoscopy).
How do you investigate gastritis?
Endoscopy and biopsy to reach histological diagnosis if necessary.
What symptoms are associated with gastritis?
Dyspepsia, burning stomach pain, nausea and vomiting.
How is gastritis generally treated?
Antacids, H2RAs, PPIs.
What are the three different types of gastritis?
Type A - autoimmune
Type B - bacterial
Type C - chemical
B being the most common.
What is type A gastritis?
Organ-specific autoimmune disease. Antibodies are created against the parietal cells and intrinsic factor leading to atrophy and loss of specialised acid secreting gastric epithelium –> reduced acid secretion and loss of intrinsic factor.
What risk factors are associated with type A gastritis?
H. pylori exposure, NSAIDs, alcohol, aspirin, stress, acute illness. Associated with other autoimmune diseases.
What is type B gastritis?
H. pylori found in gastric mucous producing acute and chronic inflammatory response –> increased acid production as bacterial produces urease which catalyses urea –> ammonia, which the stomach tries to counteract.
How do you treat type B gastritis?
Antibx.
What cause type C gastritis?
Drugs (e.g. NSAIDs), alcohol and bile reflux.
Where can peptic ulceration affect?
Lower oesophagus, body, antrum of stomach, 1st and 2nd part of duodenum.
Are duodenal ulcers more common than gastric ulcers?
Yes.
How must you investigate a suspected peptic ulceration?
Endoscopy to identify those at risk of a bleed.
What can cause peptic ulceration?
Imbalance between acid secretion and mucous barrier.
May be associated with H. pylori (remember urease produced catalyses: urea –> ammonia + CO2, ammonia buffers acid and stomach tries to counteract).
NSAID use (trigger prostaglandin production which leads to reduced mucus and bicarbonate excretion).
Rarely due to other conditions, e.g. Zollinger-Ellison syndrome (gastrin-secreting pancreatic tumour - causes recurrent, poor healing ulcers), hyperparathyroidism, Crohn’s disease and stress.
What are the risk factors for developing a peptic ulcer?
Smoking, alcohol excess, ulcer may sit over carcinoma.
What are the signs of peptic ulcers?
Maelena, haematemesis, Fe deficient anaemia.
What symptoms are associated with peptic ulcers?
Burning/gnawing pain in stomach, indigestion, heartburn, nausea, haematemesis.
What complications are associated with peptic ulcers?
Bleeding (acute = haemorrhage, chronic = anaemia), perforation (peritonitis - medical emergency req. surgery), healing by fibrosis (–> strictures), gastric outlet obstruction (oedema/stricture near pylorus).
How do you manage peptic ulcers?
PPIs, endoscopic injection of adrenaline (1:10, 000), thermal contact (gold standard), mechanical (clip) haemospray. Combination therapy most effective (adrenaline + thermal or clips). If bleeding uncontrollably - endoscopic angiography with embolisation/laparotomy.
What are the differences in symptoms between a gastric and duodenal ulcer?
If gastric ulcer - pain not relieved by eating, haematemesis and pain occurs 1-2h after eating.
If duodenal ulcer - pain relieved by eating, melon and pain 3-4h after eating.
What BMI is considered overweight?
25-29.9
What BMI is considered obesity I?
30-34.9
What BMI is considered obesity II?
35-39.9
What BMI is considered obesity III?
40+
What are the complications of obesity?
Shorter life-expectancy, increased risk of: strokes, cataracts, coronary heart disease, diabetes, dislipidaemia, hypertension, severe pancreatitis, cancer, phlebitis, gout, skin problems, osteoarthritis, gynaecological abnormalities, gallbladder disease, NAFLD, pulmonary disease and idiopathic intracranial hypertension…
How can be surgically managed?
Bariatric surgery:
- Restrictive Surgery (decrease stomach size –> increased satiety with smaller portions, e.g. laparoscopic ajustable gastric banding, laparasopic sleeve gastrectomy
- Malabsorptive Surgery
(bypassing bowel, causing malabsorption of nutrients e.g. laparoscopic gastric bypass). - Combination surgery
(e. g. Roux-en-Y gastric bypass (gold standard)).
How is BMI calculated?
Weight (kg)/Height (m) squared
What are the complications of bariatric surgery?
Anastomatic leak, CVT/PE, infection, malnutrition, vit/mineral deficiency, hair loss, excess skin.
What are the advantages and disadvantages of laparoscopic adjustable gastric banding?
Adv: relatively minor surgery, reversible/adjustable. lower op complication rate and mortality.
Disadv: requires implanted medical device, easier to cheat, risk of prolapse and slippage. 15% require revision surgery.
What is the mechanism of laparoscopic adjustable gastric banding?
Hollow silicone band placed around stomach near upper end, creating pouch and narrow passage into remainder of stomach. Band inflated with isotonic fluids (can be tighter or looser).
What are the advantages and disadvantages of laparoscopic gastric bypass?
Adv: quick, dramatic weight loss, pedigree, causes dumping syndrome.
Disadv: surgery more complex, requires revision, and life-long supplements.
What is the mechanism of laparoscopic gastric bypass?
Small pouch is created to restrict food intake, a Y shaped section of small intestine is attached to the pouch to allow for food to bypass to the lower stomach, duodenum and first portion of the jejunum.
What are the advantages and disadvantages of laparoscopic sleeve gastrectomy?
Adv: good medium term outcomes, no dumping syndrome, no small bowel manipulation or foreign body.
Disadv: more invasive surgery, long staple line, short pedigree.
What is laparoscopic sleeve gastrectomy?
Removal of most of the stomach with the remainder resembling a banana. Stomach becomes fuller quicker and leads to decreased appetite.
Why is bariatric surgery useful?
Can decrease risk of death, cancer and MI related deaths.
What is pernicious anaemia?
Autoimmune condition whereby the body produces antibodies against the parietal cells producing intrinsic factor in the stomach.
How can pernicious anaemia be investigated?
Bloods.
What symptoms are associated with pernicious anaemia?
Liver has 3y store of B12 so present 3y after antibodies start attacking.
Fatigue, lethargy, breathlessness, feeling faint, headaches, pale skin, palpitations, tinnitus, appetite, weight loss, mouth ulcers, pins and needles, disturbed vision, irritability, depression…
How is vit B12 treated?
B12 injections 3monthly.
What is gastric outlet obstruction?
Aka. pyloric obstruction. Any disease impending gastric emptying.
How do you investigate gastric outlet obstruction?
UGIE (prolonged fast/aspiration of gastric contents), FBC.
What can cause gastric outlet obstruction?
Strictures, ulcers, tumours etc.
What are the signs of gastric outlet obstruction?
Gastric splash (lots of material in stomach that can’t go anywhere), metabolic alkalosis, FBC shows low Cl, Na, K, renal impairment.
What are the symptoms of gastric outlet obstruction?
If obstruction at pylorus, no bile in vomit. Vomiting fermented foodstuffs, abdominal distension, early satiety, wt loss, dehydration (loss of chlorine and hydrogen ions in vomit).
What are the two types of peritonitis?
Generalised
- represents failure of localisation, occurs when contamination too rapid/can’t produce inflammatory response (e.g. immuncomp/taken a lot of bacteria in). Consider role of adjuvants, e.g. faecal matter.
Localised
Why do penetrating injuries increase the chance of generalised peritonitis?
A vacuum is created to suck material in.
In investigation what are you wanting to find out if patient presents with peritonitis?
Where tract as perforated to consider what bacteria has leaked out to help to choose antibx.
What are the different routes of infection in peritonitis?
Perforation of GI/biliary tract, female genital tract, penetration of abdominal wall, haematogenous spread (more common in paeds/oncology), trauma.