Upper GI Diseases Flashcards
Common upper GI pathology
Oral lesions.
GORD and PUD (dyspepsia).
Motility issues – achalasia, gastroparesis etc.
Upper GI bleed.
Cancer: oral, oesophageal, gastric, small bowel.
Exact division between upper and lower GI =
suspensory muscle of duodenum (attaches superior part of ascending duodenum to diaphragm)
Angular cheilitis
Candida infection.
Red swollen patches on corner of mouth.
Due to iron deficient anaemia.
Aphthous stomatitis
i.e. Canker sores (mouth ulcers).
Erythematous macules develop into ulcers, well demarcated with a reddish ‘halo’ surrounding ulcer, should go away within a week.
Common in anaemia or haematinic (vit. B12) deficiency.
Linked to IBD (crohns), coeliac etc..
Acute pseudomembranous candidiasis
Oral thrush
Oral cancer - causes
Alcohol and tobacco
HPV (16&18)
Candida
Low vitamin A, C and iron.
Oral cancer - common locations
High risk at soft sites (non-keratinizing squamous epithelium), ventral and lateral tongue, floor of mouth etc…
Rarely dorsal tongue and hard palate.
Oral cancer - warnings
Red/white lesions, lump, irregular shape, increasing size, etc…
Persistent sores, dysphonia, dysphagia, double vision, facial palsy…
Systemic symptoms of cancer.
Acute oesophagitis - causes
Rare.
Chemical ingestion.
Infection in immunocompromised (e.g. candidiasis, HSV, CMV)
Chronic oesophagitis - causes
Reflux oesophagitis. (GORD)
Rarer causes like Crohn’s.
Allergic oesophagitis - causes
Eosinophilic oesophagitis.
History of asthma/allergy or autoimmune disease.
Allergic oesophagitis presentation is similar to ——–
GORD
Allergic oesophagitis - investigation findings
pH probe negative for reflux.
Increased eosinophils in blood.
Failed course of PPIs.
Endoscopy: corrugated (feline) or spotty oesophagus.
Allergic oesophagitis - treatment
Removal of suspected allergen, steroids, cromoglycate etc.
endoscopic dilation sometimes necessary in severe cases with strictures/narrowing
Gastroesophageal reflux disease (GORD) - causes
Incompetent LOS. (e.g. hiatus hernia). Poor esophageal clearance. (abnormal motility). Barrier function/visceral sensitivity. Obesity/pregnancy. Stress.
GORD - symptoms
Heartburn. Reflux Waterbrash. Dysphagia, odynophagia. Weight loss. Chest pain. Hoarseness. Coughing.
GORD - investigations
PPI trial. Endoscopy. Barium swallow. Oesophageal manometry (tests sphincters) pH studies. Nuclear studies.
GORD - complications
Ulceration.
Stricture.
Barrets.
GORD - treatment
1) Lifestyle: smoking cessation, weight loss, avoid triggers (e.g. alcohol, spicy food), sit up in bed…
2) Antacids: PPIs, H2 Antagonists
3) Surgery: last resort - laparoscopic (Nissen fundoplication).
Barret’s oesophagus - mechanism of disease
Chronic acid reflux»_space; chronic inflammation of stratified squamous epithelium due to acid»_space; acid damages cells»_space; induces intestinal metaplasia»_space; change to simple columnar epithelium with interspersed goblet cells
(normally present in small intestine)
Barret’s - signs/symptoms
Chronic reflux. Dysphagia, odynophagia. Weight loss. Haematemesis. Retrosternal pain.
Barret’s - diagnosis
Endoscopy and biopsy.
Normal tissue = pale.
Abnormal tissue = red and velvety
Barret’s is a precursor to ———
adenocarcinoma of the oesophagus
Barret’s = PREMALIGNANT condition, can become dysplasia»_space; cancer
Barret’s – management
No dysplasia = surveillance
Low grade dysplasia = endoscopic radiofrequency ablation.
High grade dysplasia/cancer = oesophagectomy (for those unsuitable for surgery = ablation or endoscopic mucosal resection)
Oesophageal cancer - types
1) squamous cell carcinoma.
2) adenocarcinoma.
Oesophageal squamous cell carcinoma - causes
Smoking and alcohol. HPV (16,18) Vit. A and zinc deficiency. Tannic acid/strong tea. Oesophagitis. Genetic.
Oesophageal adenocarcinoma - causes
Commoner in white males.
Obesity.
Barret’s/GORD.
Commonest in lower 1/3 of oesophagus.
Oesophageal cancer - symptoms
Progressive dysphagia. Anaemia. Anorexia, weight loss. Malaise. Pain. Hoarse voice, cough. Haematemesis.
Oesophageal cancer - common sites of metastasis
Direct invasion - laryngeal nerves.
Lymphatic spread.
Haematogenous spread (liver, lung, bone, brain).
Oesophageal cancer – management
Nutritional support.
Open/minimally invasive oesophagectomy, alongside chemoradiotherapy. Lymph node dissection.
Palliative = managing obstructions/dysphagia, stents, RT, chemo (metastatic)
Gastritis - acute causes
Alcohol.
Irritant chemical injury.
Severe burns.
Shock/trauma.
Gastritis - chronic causes
Chemical (alcohol, NSAIDS, bile reflux).
Bacterial (h.pylori assoc.)
Autoimmune (pernicious anaemia).
Gastritis - other causes
do not fall under chronic or acute
Lymphocytic (assoc. h.pylori and coeliac).
Eosinophilic.
Granulomatous (infectious, non-infectious, idiopathic).
PUD (peptic ulcer disease)
Breach in GI mucosa due to a failure of defence against acid and pepsin attack.
Gastric or duodenal ulcer.
PUD - morphology
2-10 cm across.
Edges clear cut, punched out.
PUD - causes
** similar to gastritis H. pylori and NSAIDS most commonly. Gastric dysmotility. Outflow obstruction. Stress/alcohol/smoking etc..
PUD - complications
Pain predominant dyspepsia. Perforation. Penetration. Haemorrhage. Stenosis. Intractable pain.
Gastric ulcers vs duodenal ulcers
Gastric = weight loss, pain 1hr after meals, vomiting, eating increases pain Duodenal = most common, pain 3hrs after meals, food may decrease pain
How does H. Pylori lead to duodenal PUD?
Bacteria between epithelial cell surface and mucous barrier»_space; ammonia/proteases released by H. Pylori damage epithelium»_space; presence of bacteria excites acute inflammatory response (can progress to chronic)
Ulcers occur when protective mechanisms (e.g. mucous membrane) break down»_space; epithelium exposed to HCl/pepsin»_space; ammonia increases pH, G cells release gastrin to compensate»_space; excess acid production causes duodenal ulcer.
How do NSAIDS lead to PUD?
They decrease prostaglandin formation via COX inhibition (PGE2 and PGI2 normally increase pH via decreased acid secretion and increased mucous/bicarbonate secretion).
So NSAIDs increase acid production and decrease protection.
PUD - symptoms
Pain predominant dyspepsia. Often nocturnal. Aggravated or relieved by eating. Relapsing and remitting. Nausea/vomiting. Weight loss. Reflux.
PUD - investigations
1st line = carbon-13 urea breath test, faecal antigen test (FAT)
2nd line: re-test using urea breath test. serology (IgA antibodies)
Rarely, gastroscopy and biopsy.
Most common cause of upper GI bleeding =
peptic ulcer
Before conducting a urea breath test, ensure no —- has been taken in last 2 weeks, and no —– taken in last 4 weeks.
no PPI taken in last 2 weeks
no antibiotics in last 4 weeks
H Pylori eradication therapy
Triple therapy for 7 days:
1) PPI
2) Amoxicillin
3) Clarithromycin/metronidazole
(PPI + metronidazole + clarithromycin if penicillin allergic)
PUD - treatment
Full-dose PPI or H2RA therapy for 8 weeks.
- *H Pylori eradication when needed (re-test after 6-8 weeks)
- *If using NSAIDS, stop where possible.
PUD - complications
Anaemia.
Bleeding (chronic or acute - coffee grounds)
Perforation.
Gastric outlet/duodenal obstruction (fibrotic scar).
Cancer.
Dyspepsia = 2 syndromes =
1) Epigastric pain syndrome (bloating, epigastric pain/burning, reflux)
2) Post prandial distress syndrome (post-prandial fullness, early satiety, nausea/vomiting)
Dyspepsia – causes
Strongly associated with ——– (bacteria)
More common with use of ——— (drug group)
Overlaps with ———- (other GI conditions)
Strongly associated with H. pylori.
More common with use of NSAIDs.
Overlaps with GORD, PUD, IBS.
Dyspepsia – causes
25% organic = PUD, GORD, drugs (NSAIDs, COX-2 inhibitor), gastric cancer
75% functional = assoc. with functional gut disorders e.g. IBS (no evidence of structural disease)
ALARMS - symptoms
A – Anaemia. L – Loss of weight. A – Anorexia. R – Recent onset of progressive symptoms. M – Masses and Melena/Haematemesis. S – Swallowing difficulty.
OR
OVER 55
Anyone with dyspepsia/GORD that fits any of the ALARMS criteria receives ———–
Upper GI endoscopy
Management of dyspepsia
in the absence of ALARMS symptoms
1) Lifestyle measures (weight loss, trigger foods, smoking cessation, alcohol reduction, stress)
2) Assess medication
3) Medical treatment (1 month PPI, test for H Pylori - eradication if positive)
Gastric cancer - risk factors
Infections: H. pylori in up to 85% gastric cancers.
Smoking.
Diet: processed meats.
Obesity.
Gastric cancer histopathology:
90% are ———-
5% are ———-
90% are adenocarcinomas (intestinal or diffuse)
5% are lymphomas (MALT lymphomas, stomach lymphomas)
** carcinoid and stromal tumours may also occur.
Gastric cancer - symptoms
Dyspepsia
ALARMS or > 55 yrs
Gastric cancer - investigations
Endoscopy and biopsy.
CT scan.
Gastric cancer - treatment
Definitive treatment = surgery.
**For MALT lymphoma, treatment of underlying H Pylori infection results in remission in 80% of cases
Achalasia
Oesophageal motility disorder
Achalasia - pathogenesis
Failure of smooth muscle relaxation of LOS»_space; increased LOS tone»_space; lack of peristalsis due to degeneration of the myenteric plexus
(failure of distal inhibitory neurons – no known cause, can be cancer)
Achalasia - symptoms
Dysphagia – difficulty with both liquids and solids.
Regurgitation of undigested food.
Chest pain.
Weight loss.
Achalasia - investigations
Barium swallow study will show a BIRD BEAK APPEARANCE
X-ray may show dilated oesophagus.
Oesophageal manometry.
Endoscopy to rule out cancer.
Achalasia - management
CCB’s + nitrates relax the sphincter while waiting for more definitive surgery.
Young people get a Heller’s myotomy (cardiomyotomy)
Old people get balloon dilation.
Manometry
Test that evaluates the motility and muscle contractions of the oesophagus via catheter insertion
Gastroparesis
Delayed gastric emptying that IS NOT due to an obstruction
Gastroparesis - causes
Diabetes (diabetic autonomic neuropathy).
Chemotherapy induced neuropathy.
Smoking weed.
Gastroparesis - symptoms
Feeling of fullness. Bloating. Weight loss caused by ‘food fear’. Nausea/vomiting after meals (usually lunch and dinner). Abdo pain.
Gastroparesis - investigations
Gastric emptying studies.
Manometry
Gastroparesis - management
Nutritional support.
Metoclopramide.
Implantable gastric stimulation.
Vertical sleeve gastrectomy.
Haematemesis
blood in vomit
Melena
black, extremely foul smelling stool (old blood)
Acute upper GI haemorrhage - causes
Ruptured ulcers. Ruptured varices (19-40% bleed < 2 years). Mallory-Weiss tear. Oesophagitis and erosive duodenitis. Neoplasm. Other e.g. trauma.
Acute upper GI haemorrhage - assessment of severity
100 RULE
Systolic BP < 100
Pulse > 100
Hb < 100g/l
Also
Age > 60
Comorbid disease.
Postural BP drop.
Acute upper GI haemorrhage - management
Resuscitate (ABCDE).
Then facilitate prompt endoscopy»_space; find cause»_space; therapeutic manoeuvres»_space; assess risk of rebleed
Bleeding peptic ulcer - management
Endoscopy + adrenaline injection/heater probe thermo-coagulation/clips/haemospray. (NEW)
Omeprazole 80mg IV (acid suppression)
UNABLE TO STOP»_space; surgery
Why is omeprazole important in management of a bleeding peptic ulcer?
Acid suppression
acid and pepsin can cause clot dissolution
Acute variceal bleed - risk factors
Portal pressure > 12 Varices > 25% oesophageal lumen. Wale mark (red wale sign - suggesting recent haemorrhage) Degree of liver failure. Known history of cirrhosis. Chronic viral hepatitis.
Acute variceal bleed - treatment
1st line: Terlipressin
2nd line: SB balloon, EVL, scleropathy
3rd line: TIPSS
How does terlipressin treat an acute variceal bleed?
ADH analogue
causes vasoconstriction of splanchnic vessels»_space; reduces blood flow to portal vein»_space; reduces portal pressure
