Upper GI & Colorectal Flashcards
Anatomical & physiological factors predisposing to GORD
Anatomical: hiatus hernia
Physiological: raised intra-abdominal pressure
Large meals late at night
Smoking
High caffeinated drink intake
High fatty food intake
Drugs (anticholinergics, nitrates, tricyclics, calcium channel inhibitors)
Define the anatomical location of the oesophageal hiatus and what passes through it
Oval apeture in the right crus of the diaphragm at T10
Contents: oesophagus, vagal nerve trunks, oesophageal branches of left gastric vessels, lymphatics
Types of hiatus hernia
Sliding: gastroesophageal junction slides through the hiatus to lie above the diaphragm
30% adults >50, usually asymptomatic, may be associated reflux
Para-oesophageal/rolling: small part of the fundus rolls up through the hernia alongside the oesophagus, but the sphincter remains competent below the diaphragm
Occasionally severe pain, requiring surgical intervention for gastric volvulus/strangulation
Dyspepsia definition and types
Chronic upper abdominal pain/discomfort
Reflux-type: heartburn & regurgitation (GORD)
Ulcer type: epigastric pain
Dysmotility type: bloating and nausea
GORD symptoms
Dyspepsia: exacerbated by bending over/lying down, when drinking hot liquids or alcohol, relieved by antacids
Regurgitation of food/acid: passive (not vomiting), more common when bending/lying
Waterbrash: sudden filling of the mouth with dilute saliva
Odynophagia: painful swallowing
Atypical chest pain due to distal oesophageal muscle spasm
Nocturnal cough/wheeze (asthma-like)
Upper GI symptoms that would indicate need for an endoscopy
ALARMS 55 Anaemia: Fe deficient Loss of weight Anorexia Recent onset, progressive symptoms Melaena/haematemeis Swallowing difficulties >55yo
Upper GI investigations
Endoscopy
Barium swallow
24h luminal pH monitoring and manometry: measures competent of sphincter - diagnose GORD if normal endoscopy
GORD long-term complications
Oesophagitis/ulcers
Benign strictures
Barratt’s oesophagus / oesophageal carcinoma
Barratt’s oeosphagus pathophysiology
Affects 2% adults in the UK
Long-standing reflux: normal stratified squamous epithelium undergoes metaplasia –> glandular columnar epithelium
Continued inflammation: dysplasia & malignant change (adenocarcinoma of the lower 1/3 of the oesophagus)
Barratt’s oesophagus presentation & investigations
Symptom’s of GORD
Diagnosis: upper GI endoscopy + biopsy to confirm
Causes of dysphagia
Diseases of the mouth/tongue: tonsillitis
Neuromuscular disorders: myasthenia gravis, motor neurone disease, bulbar palsy
Oesophageal motility disorders: achalasia, scleroderma, DM
Extrinsic pressure: goitre, lymph nodes, enlarged left atrium
Intrinsic lesion: foreign body, benign/malignant stricture, pharyngeal pouch, oesophageal web (Plummer-Vinson syndrome)
Types of dysphagia, causes and investigations
Oropharyngeal dysphagia: dfficulty initiating swallowing +/- choking/aspiration
Neurological disease
Investigate with neurological examination, videofluoroscopic swallowing assessment
Oesophageal dysphagia: food ‘sticks’ after swallowing +/- regurgitation
Dysmotility, stricture (benign peptic/intrinsic oesophageal malignancy/extrinsic bronchial carcinoma), oesophagitis, candidiasis in asthmatics/immunosuppressed, pharyngeal pouch
Investigate with barium swallow, endoscopy (OGD) and biopsy
Typical achalasia presentation
Young, long non-progressive Hx, no loss of weight
Typical upper GI malignancy presentation
Short Hx of progressive dysphagia, severe weight loss, elderly
Plummer-Vinson syndrome presentation
Triad of: dysphagia, koilonycia, glossitis
Pre-malignant condition due to hyperkeratinisation of the oesophagus causing an oesophageal web
Symptoms suggestive of oesophageal malignancy
>60y Progressive dysphagia Weight loss & anorexia Retrosternal chest pain Coughing/aspiration Occasional lymphadenopathy
Adenocarcinoma of the oesophagus pathology
Most common oesophageal carcinoma
Arise from areas of metaplasia in the lower 1/3 (Barrett’s oesophagus)
Risk factors = GORD risk factors
Metastasise earlier than SCC via lymphatics: liver, lungs, bones
<10% 5y survival
Squamous cell carcinoma of the oesophagus pathology
Heavy smoking & drinking males
Present late: lumen compromised = dysphagia
Regional lymph spread: early & common
More responsive to radiotherapy
<10% 5y survival
Aetiology of peptic ulcer disease
Helicobacter Pylori infection (90% of duodenal, 70% of gastric)
NSAIDs (30%)
Zollinger-Ellison syndroms: non-insulin secreting islet cell tumour of pancreas secreting gastrin-like hormone –> excessive acid secretion
Smoking, coffee consumption, hepatic/renal failure
Peptic ulcer disease symptoms
Epigastric pain, related to food intake, relieved by antacids Duodenal ulcers: pain relieved by eating Gastric ulcers: pain worstened by eating Nausea Weight loss & anorexia Haematemesis/malaena
Peptic ulcer disease investigations
Urgent oesophago-gastro-duodenoscopy (OGD) if fit ALARMS55 criteria: biopsies (histology) & brushing (cytology)
If previous ulcer, assume H. Pylori infection + commence triple therapy
If not ALARMS55 + symptoms persist: H. Pylori investigation
13C Urea breath test: patient ingests 13C labelled urea –> H. Pylori urease enzyme metabolises to 13CO2 –> detected on breath
No antibiotics for 4w, no PPIs for 2w = false -ve
OR gastric biopsy added to urea solution + phenol red –> colour change with H. Pylori present
Differences between gastric and duodenal ulcers
Gastric: >55y, lesser curve of stomach, pain worse on eating, relieved by antacids
Duodenal: 4x more common than gastric, 90% <2cm from pylorus
Pain at night before meals, relieved by eating/drinking milk
Alcohol intake = risk factor
H. Pylori mechanism of association to peptic ulcers
Produces gastritis, mainly in gastric antrum, activation of inflammatory infiltrate
Increased acid secretion: increased gastrin, decreased somatostatin –> epithelial damage
Abnormal mucus production –> epithelial damage
Atrophic gastritis in body of stomach –> metaplasia (pre-malignant)
Causally associated with duodenal ulcers
Smoking mechanism of association to peptic ulcers
Impairs gastric mucosal healing
Nicotine increases acid secretion
NSAID mechanism of association to peptic ulcers
NSAIDs inhibit COX enzymes –> anti inflammatory as COX-2 isoform normally causes inflammatory prostaglandin synthesis
Adverse GI effects: inhibition of COX-1 in the stomach (responsible for production of prostaglandins that inhibit acid secretion and protect the mucosa)
Co-administration of PPIs or PG analogues (misoprostol) can diminish NSAID negative effects
Steroids = similar effect
Upper GI bleeding causes
Peptic ulceration (40%) Gastroduodenal erosions (15%) Oesophagitis (15%) Mallory-Weiss syndrome (15%): tears at gastroesophageal junction due to violent vomiting Varices (10%) Upper GI malignancy (1%)
Upper GI bleeding symptoms
Haematemesis
Malaena (>50ml): blood altered by bacteria = tarry
Haematochezia: unaltered PR blood
Abdominal pain
Signs of underlying cause/shock
Chronic: signs/symptoms of iron deficiency anaemia
Risk factors of gastric cancer
H. Pylori infection leading to metaplasia
High salt/nitrate (red meat) diet
Smoking
Genetic: blood group A/HPNCC (hereditary nonpolyposis colorectal cancer), Japanese heritage
Pernicious anaemia
Adenomatous polyps
Low socio-economic status
Gastric cancer symptoms & signs
Often non-specific Epigastric pain (as with ulcer) Nausea + vomiting (especially if tumour near the fundus) Dysphagia (if near fundus) Anorexia/weight loss Palpable epigastric mass (50%) Virchow's node Hepatomegaly, jaundice, ascites Ancanthosis nigricans (areas of dark, velvety discoloration in body folds and creases)
Gastric cancer investigations
OGD & multiple ulcer edge biopsy
Endoscopic USS and CT for staging
Staging laparoscopy: locally advanced tumours if no other mets detected
Gastric cancer pathology
50-70y, Japanese
Most adenocarcinomas in antrum
Appear as polypoids/ulcerating lesions with rolled edges
Intestinal metaplasia in surrounding tissue: H. Pylori
Leather bottle stomach/linitis plastica: submucosal infiltration of tumour –> fibrous reaction –> small, thickened, contracted stomach
Mets: local invasion of abdominal viscera, lymphatic (Virchow’s), liver (portal dissemination)
Transcoelomic spread: peritoneal seedings, bilateral ovarian ‘Krukenberg’ tumours
Rare: stromal tumours (leiomyomas/leiomyosarcomas) from interstitial cells of Cajal
Acute abdomen inflammatory pain
Constant pain, raised temp, raised BP, leucocytosis
Peritonitis: localised pain, worse with movement, coughing/inspiration
Guarding: reflex contraction of abdominal muscles on palpation
Rigidity: increased tone at rest
Acute abdomen obstructive pain
Colicky pain, agitated patient
May become constant with superimposed inflammation
Acute abdomen referred visceral pain
Generally midline
Fore-gut: oesophagus to D2 (second part of duodenum): referred to upper abdomen
Mid-gut: D2 to transverse colon: referred to middle abdomen
Hind-gut: referred to lower abdomen
Acute abdomen differentials
Abdominal viscera: acute appendicitis, Meckel’s diverticulitis, intestinal obstruction, perforated viscus, acute pancreatitis, acute cholecystitis/cholangitis, renal calculi, acute scrotum, IBS
Vascular: AAA, mesenteric thrombosis/embolus
Medical: GORD, referred pain from pneumonia, MI, UTI/pyelonephritis
Gynae: ruptured ectopic, torted/ruptured ovarian cysts, salpingitis
Other: non-specific mesenteric adenitis
Acute abdomen investigations
Bloods: FBC, U&Es, LFTs, CRP, amylase, ABG Pregnancy test Urinalysis Erect CXR/AXR USS/CT
Acute appendicitis pathology
1/6th population affected
Appendix obstructed by a faecolith/foreign body, or lymphoid enlargement in the wall
Can follow URTI
Bacteria proliferate in closed bowel loop –> necrosis & perforation due to raised intraluminal pressure
