GI CONDITIONS
GASTRO-OESOPHAGEAL REFLUX DISEASE
PATHOPHYSIOLOGY: at the GOJ, the LOS relaxes to allow the food
to enter the stomach; after entry, sphincter contracts to prevent
reflux of stomach. If LOS relaxes inappropriately, stomach content
will wash back into the oesophagus. Persistent reflux-> local
inflammation -> oedema and erosion -> tissue damage
AETIOLOGY: Increased intra-abdominal pressure (pregnancy,
obesity), diabetes (damages vagus nerve-> delayed emptying),
smoking, genetic, hiatus hernia, scleroderma, Zollinger-Ellison
A 42-year-old woman has heartburn after meals syndrome, alcohol, fat-rich diet, caffeine, NSAIDs, CCB,
and a sour taste in her mouth. For the past 4-6 antidepressant
CLINICAL FEATURES: heartburn (retrosternal, after meals, worse
months she has had symptoms several times lying down or bending forward), regurgitation, indigestion, chest
per week. Symptoms are worse when she lies pain, dysphagia, odynophagia, cough, hoarseness, n&v. SEVERE:
iron def anaemia (blood loss from chronic inflammation), asthma,
down or bends over. Antacids help somewhat. dental erosion, laryngitis,
She has no dysphagia, vomiting, abdominal INVESTIGATIONS: clinical diagnosis, gastroscopy if patient has red
flags, 24-hour pH monitoring (gold standard, if endoscopy -ve), LA
pain, exertional symptoms, melena, or weight criteria to grade severity of oesophagitis, Demeester score >14.7 in
loss. Past medical history and family history are pH monitoring indicate GORD
RED FLAGS: weight loss, anaemia dysphagia, new onset dyspepsia
non-contributory. The patient drinks alcohol >55 years, symptoms refractory to treatment
occasionally and does not smoke. On physical MANAGEMENT: patient without red flags 4 week full dose PPI, If
symptoms return, start PPI at low dose for 1-2 months, after review,
examination, height is 1.63 m, weight 77.1 kg, step up if symptomatic and step down if controlled. Offer H2RA if
and blood pressure 140/88 mmHg. The inadequate response to PPI. Pt with GORD via endoscopy may be
remainder of the examination is unremarkable. increased to 8-week PPI course. Surgery if not responding to tx or pt
who don’t tolerate PPI (Nissen fundoplication). Lifestyle advice,
What is the likely diagnosis? head elevation, avoid eating within 2 hours of sleep, avoid RF drugs,
avoid hot drinks.
COMPLICATIONS: erosive oesophagitis, stricture, Barrett’s
DDX: achalasia, pericarditis, peptic ulcer, functional heartburn
OESOPHAGEAL CANCER
EPIDEMIOLOGY: SCC most common cause worldwide,
AC most common cause UK/ US
RISK FACTORS: smoking, alcohol, SCC (areca nuts,
previous partial gastrectomy, HPV 16&18, achalasia,
Plummer-Vinson syndrome, coeliac disease), AC
(Barret’s, chronic reflux, smoking, obesity, Zollinger-
Ellison
PATHOLOY: SCC (originates in squamous epithelium,
A 55-year-old man presents with severe usually upper 2/3 of oesophagus), AC (originate from
columnar glandular epithelium, usually near GOJ)
dysphagia to solids and worsening CLINICAL FEATURES: dysphagia (solids then liquids),
dysphagia to liquids. His social history is weight loss, fever, lethargy, haematemesis, melena,
significant for 40 pack-year cigarette retrosternal pain, aspiration, hoarseness, odynophagia,
heartburn, pain in chest/ back, vomiting,
smoking and a 6-pack of beer per day. He lymphadenopathy, cachexia, pallor, hepatomegaly.
has lost over 10% of his body weight and CANCER REFERRAL: 2WW (dysphagia, or >/=55 years
currently is nourished only by milkshake with weight loss and one of upper abdo pain, reflux,
dyspepsia)
supplements. He complains of some mild INVESTIGATIONS: diagnosis using upper GI endoscopy
odynophagia and is constantly coughing up with min 8 biopsies -> CT scan (chest, abdo, pelvis) -<
mucus secretions. What is the likely staging laparoscopy -> PET scan, bloods, HER-2 testing
STAGING: TNM staging
diagnosis? MANAGEMENT: operable disease, surgical resection
(Ivor-Lewis oesophagectomy)
, MANAGEMENT OF OESOPHAGEAL
CANCER
Operable disease is best managed by surgical
resection.
The most standard procedure is an Ivor- Lewis type
oesophagectomy. This procedure involves the
mobilisation of the stomach and division of the
oesophageal hiatus. The abdomen is closed and a
right sided thoracotomy performed. The stomach is
brought into the chest and the oesophagus mobilised
further. An intrathoracic oesophagogastric
anastomosis is constructed. Alternative surgical
strategies include a transhiatal resection (for distal
lesions), a left thoraco-abdominal resection (difficult
access due to thoracic aorta) and a total
oesophagectomy (McKeown) with a cervical
oesophagogastric anastomosis.
The biggest surgical challenge is that of anastomotic
leak, with an intrathoracic anastomosis this will result
in mediastinitis. With high mortality. The McKeown
technique has an intrinsically lower systemic insult in
the event of anastomotic leakage.
In addition to surgical resection many patients will be
treated with adjuvant chemotherapy.
PEPTIC ULCER DISEASE
EPIDEMIOLOGY: 40-50 years, more common in males.
95% DU associated with H. Pylori, 80% GU associated
with H. Pylori. DU more common in men
AETIOLOGY: H. pylori (starts in antrum, gram -ve,
release adherins and urease, virulence factors CagA and
VacA), NSAIDs (inhibits COX-1, reduce production of PG,
leads to less mucous and bicarbonate and disinhibition
A 40-year-old man presents to his primary care of HCl production), Zollinger-Ellison syndrome (hyper-
physician with a 2-month history of intermittent secreting gastrinoma, increase gastrin, increase HCl)
PATHOLOGY: punched out holes in mucosa, GU (usually
upper abdominal pain. He describes the pain as
in lesser curvature), DU (after pyloric sphincter)
a dull, gnawing ache. The pain sometimes CLINICAL FEAT: epigastric pain (DU relieved by foods,
wakes him at night, is relieved by food and GU exacerbated by eating), dyspepsia, heartburn, mild
drinking milk, and is helped partially by epigastric tenderness, acute presentations can be due to
famotidine. He had a similar but milder episode UGIB or perforation, gastric outlet obstruction can occur,
weight loss in GU, weight gain in DU
about 5 years ago, which was treated with INVESTIGATIONS: definitive diagnosis from endoscopy
omeprazole. Physical examination reveals a fit, but only small no require upper GI endoscopy, obs, H.
apparently healthy man in no distress. The only pylori testing, ECG, FBC, LFT,
abnormal finding is mild epigastric tenderness TREATMENT: avoid trigger foods (spicy foods, etc),
weight loss, stop smoking and reduce alcohol, H. pylori
on palpation of the abdomen. What is the likely
(no assoc with NSAID -> fist-line eradication, assoc with
diagnosis? NSAID -> 2 months full dose PPI then first-line
eradication), non-H.Pylori (4-8 weeks full dose PPI)
FIRST LINE ERADICATION: 7 day PPI, amox and
clarith, penicillin allergy (PPI, clarith, metro)
COMPLICATIONS: perforation, haemorrhage, GOO
A 77-year-old man presents to his general GASTRIC CANCER
practitioner with weight loss of 6.8 kg (15 lbs) TYPES: adenocarcinoma (columnar glandular
epithelium), lymphoma, carcinoid (G-cells,
and a 3-month history of dysphagia and neuroendocrine), leiomyosarcoma (smooth muscle cells)
abdominal pain. The only abnormal finding on EPIDEMIOLOGY: 4th mc malignancy around the world,
physical examination is stools positive for >75 years, more common in men
occult blood. He is referred for an upper RISK FACTORS: family hx, smoking, alcohol, obesity,
increased age, Intestinal adenocarcinoma (male, H.
endoscopy, which shows an exophytic,
, Pylori, type A, high salt and nitrate, autoimmune,
pernicious anaemia, achlorydia), Hereditary diffuse
cancer (CDH1 mutation)
ADENOCARCINOMA: intestinal (caused by H. Pylori ->
gastritis -> chronic gastritis and intestinal epithelial cell
mtp, well-differentiated), diffuse (undifferentiated,
mutations of CDH1 -> gastric linitis (leather bottle
appearance)
SYMPTOMS: initially (malaise, loss of appetite,
ulcerated mass in the cardia of the stomach. dyspepsia), progression (epigastric pain, n&v, weight
Biopsy reveals moderately differentiated loss constitutional sx), with ulcer (anaemia,
adenocarcinoma. What is the likely diagnosis? haematemesis, melaena)
SIGNS: pallor, cachexia, Virchow’s node, Mets
(hepatomegaly, SMJ nodule)
PARANEOPLASTIC SYNDROMES: Lesser-Trelat (seb
k), PAN, Trousseau syndrome (migratory thrombosis),
Acanthosis nigricans, dermatomyositis, erythema
gyratum repens, pseudo achalasia syndrome
INVESTIGATIONS: diagnosis using upper GI endoscopy
and 8 biopsies, FBC, iron studies, U&E, LFT, bone profile,
clotting, renal function, CT CAP, Abdo US, PET-CT
MANAGEMENT FOR GASTRIC CANCER
OPERABLE: surgery (resection), endoscopic
therapy (endoscopic mucosal resection,
endoscopic submucosal dissection),
systemic therapy (pre-op chemo)
Early stage operable: endoscopic or
surgical resection
Advances stage operable: resection if fit
enough, with chemo or chemoradiotherapy
NON-OPERABLE: systemic therapy (HER-2
-ve, standard chemo, HER-2 +ve,
trastuzumab),
A 51-year-old man with moderate obesity (body HIATUS HERNIA
mass index of 34 kg/m²) is seen in consultation EPIDEMIOLOGY: usually incidental finding, older age,
male, obesity
for heartburn and regurgitation. He has a CLASSIFICATION: type 1 (sliding, displacement of GOJ
diagnosis of gastro-oesophageal reflux disease above diaphragm), type II (para-oesophageal,
and has been treated with proton-pump dislocation of fundus, OGJ unchanged), type III (para-
inhibitors. His heartburn is less severe with the oesophageal, fundus and GOJ above the diaphragm),
medication, but he is still bothered by type IV (organ other than stomach in hernia sac)
AETIOLOGY: obesity and pregnancy, trauma, previous
regurgitation. His physical examination is gastro-oesophageal surgery, increasing age, congenital
unremarkable. A barium oesophagram and defects
upper endoscopy demonstrate displacement of PATHOPHYSIOLOGY: widening of oesophageal hiatus,
the GOJ above the diaphragm. The patient has increased laxity of phrenoesophageal membrane,
shortening of oesophagus that pulls stomach up
free reflux to the level of the cervical CLINICAL FEAT: small type I is usually asymptomatic,
, heartburn, regurg, dysphagia, epigastric pain, post-
prandial fullness, nausea, retching
INVESTIGATIONS: diagnosis made on imaging or upper
GI endoscopy, endoscopy (>2cm separation between z-
line and diaphragmatic impression), barium swallow, x-
ray (retrocardiac mass with or without air-fluid level), CT
MANAGEMENT: type I (do not require intervention),
oesophagus. symptomatic type I (PPI and surgery in selected
cases), para-oesophageal hernias (surgical
intervention)
COMPLICATIONS: rare in type I, in para-oesophageal
(gastric volvulus, strangulation, uncontrolled bleeding,
resp compromise, GOO, perforation)
BARRETT’S OESOPHAGUS
EPIDEMIOLOGY: more common in Caucasian males
PATHOPHYS: prolonged exposure to reflux -> GORD,
oesophagitis, erosions -> damage -> transformation or
normal squamous epithelium -> metaplastic columnar
A 55-year-old obese man presents with epithelial cells -> Barret’s -> precursor for
adenocarcinoma, common transformation zone is in
frequent heartburn. He describes a post-
lower oesophagus
prandial, retrosternal burning sensation RISK FACTORS: long-standing GORD, male, Caucasian,
following fatty and spicy meals. This symptom increasing age, obesity, smoking, FHx
also frequently wakes him from sleep, with CLINICAL FEAT: heartburn, regurg, chest discomfort,
occasional coughing and a sour taste in his dyspepsia, n&v, dysphagia (stricture or malignancy)
INVESTIGATIONS: endoscopic diagnosis and confirmed
throat. He has tried many non-prescription with biopsies, evidence of metaplastic columnar
antacids, which only relieve symptoms in the epithelium ≥1cm above the GOJ, biopsies should be
short term. He has suffered from this symptom taken to confirm diagnosis, Histology (saple using
for over 10 years. He denies dysphagia, Seatle protocol)
MANAGEMENT: PPI in all pt, non-dysplastic
odynophagia, or weight loss, but reports
(surveillance, anti-reflux surgery 2nd line), low-grade
frequent hoarseness in the mornings. His past dysplasia (radiofrequency ablation w/ or w/o
medical history is significant only for endoscopic mucosal resection or surveillance), high-
hypertension. His family history is grade dysplasia (radiofrequency ablation w/ or w/o
unremarkable. He did smoke cigarettes but endoscopic mucosal resection/ endoscopic submucosal
dissection)
stopped 5 years ago. What is the likely SCREENING: only in pt with chronic GORD and multiple
diagnosis? RF
A 5-week-old, full-term male infant presents PYLORIC STENOSIS
with progressive post-feeding emesis for EPIDEMIOLOGY: 1 in 500 live births, most cases
in infants 2-8 weeks
the past 2 weeks. Initially he was diagnosed AETIOLOGY: from hypertrophy and hyperplasia of
as having formula intolerance; formula type the pylorus -> mechanical obstruction to the
was changed several times without relief. outflow of gastric duodenum. Can also cause
Subsequently, he was thought to have hypertrophy of stomach muscles due to increased
gastro-oesophageal reflux. The parents demand for peristalsis. Obstruction of food -> non-
bilious projectile vomiting
continue to report non-bilious post-feeding RISK FACTORS: maternal smoking, bottle
emesis, which has become progressively feeding, family hx, macrolide abx, young boys,
forceful and projectile. What is the likely firstborn
diagnosis? PRESENTATION: non-bilious, projectile vomiting,
vomiting normally 30-60 mins after being fed,
examination (enlarged pylorus palpable in
epigastrium or RUQ as an “olive”), peristalsis may
be visible or palpable
Non-bilious vomit -> loss of stomach acid ->
dehydration and decreased HCl -> decreased CL
and retain Na+ and secrete K+ -> hypochloraemia
and hypokalemia -> decreased acidity (metabolic
alkalosis)
INVESTIGATIONS: abdominal USS, bloods
(hypochloraemia, hypokalaemia, metabolic
alkalosis)
