Upper GI Flashcards
angular cheilitis
candida infection fungus red swollen patches on corner of mouth due to iron deficient anaemia self limiting
apthous stomatitis
canker sores
erythematous macules develop into ulcers
yellow fibrinous membrane can be scraped away
reddish halo
go awy in a week
anaemic or haematinic deficiency
IBD, coeliac
oral thrush
acute pseudomembranous candidiasis
common in severe asthma, due to oral steroid
lichen planus
wickham’s striae
oral cancer aetiology
alcohol and tobacco - synergistic
HPV - 16 and 18
candida
low vitamin A, C and iron
oral cancer location
high risk at soft sites non keratinizing squamous epithelium ventral and laterl tongue floor of mouth rarely dorsal tongue and hard palate
oral cancer warning signs
red and white lesions, lump or thickening irregular shape and increasing size persistent sores that do not heal numb feeling dysphonia, dysphagia facial palsy, double vision systemic symptoms of cancer
4 key questions for oral cancer
how long
painful
smoke/drink
colour
acute oesophagitis
rare
chemical ingestion
infection in immunocompromised
candidiasis, HSV, CMV
chronic oesophagitis
common
reflux oesophagitis GORD
rarer causes - Crohn’s
allergic oesophagitis
eosinophilic
history of atopic or autoimmune disease
similar presentation to GORD
allergic oesophagitis investigations
pH probe negative for reflux
increased eosinophils in blood
failed course of PPIs
endoscopy corrugated or spotty
allergic oesophagitis treatment
removal of antigen, steroids, cromoglycate
causes of GORD
incompetent LOS poor esophageal clearance barrier function/viscera; sensitivity obesity/pregnancy stress
GORD symptoms
heartburn reflux watebrash dysphagia odynophagia weight loss chest pain hoarsness coughing
GORD investigation
PPI trial endoscopy barium swallow oesophageal manometry ph studies nuclear studies
GORD complications
ulceration
stricture
Barrets
GORD treatment
lifestyle
antacids
PPIs, H2 antagonists
surgery - laparoscopic antireflux surgery - nissen fundoplication
Barrets cell change
stratified squamous epithelium to simple columnar epithelium with goblet cells
Barrets signs and symptoms
chronic reflux Dysphagia, odynophagia weight loss haematemesis retrosternal pain
Barrets diagnosis
endoscopy and biopsy
Barrets pre malignant condition
chronic reflux oesophagitis barrets metaplasia low grade dysplasia high grade dysplasia adenocarcinoma
Barrets management
no dysplasia - surveillance
low grade - endoscopic radiofrequency ablation
high grade/intramucosal cancer - oesophagectomy
endoscopic therapy
endoscopic radiofrequency abblation
endoscopic mucosal resection
oesophageal cancer squamous cells aetiology
smoking and alcohol HPV 16 and 18 Vita min A and zinc deficiency tannic acid oesophagitis genetic
oesophageal cancer adenocarcinoma aetiology
commoner in white males
obesity
Barrets/GORD
lower 1/3 of oesophagus
oesophageal cancer symptoms
progressive dysphagia anaemia anorexia, weight loss anaemia malaise pain hoarse voice, cough haematemesis
oesophageal cancer metastasis
direct invasion - laryngeal nerves
lymphatic spread
haematogenous spread - liver, lung, bone, brain
TNM staging
oesophageal cancer management
nutritional support
open or minimally invaive oesophagectomy
alongside neoadjuvant or adjuvant chemo
lymph node dissection
palliative
acute gastritis causes
alcohol
irritant chemical injury
severe burns
shock/trauma
chronic gastritis causes
chemical - alcohol, NSAIDs, bile reflux
bacterial - h.pylori
autoimmune - pernicious anaemia
causes of gastritis
lymphocytic - h.pylori and coeliac
eosinophilic
granulomatous
H.pylori
gram -ve flagellated bacilus often acquired in infancy consequences later in life direct contact, oral oral, faecal oral increased risk of duodenal ulcer, gastritis, gastric ulcer, carcinoma, lymphoma
peptic ulcer disease
breach in GI mucosa due to a failure of defense against acid and pepsin attack
gastric duodenal ulcer
2-10 cm across
edges clear cut, punched out
peptic ulcer disease microscopic
layer appearance
floor of necrotic fibropurulent debris
base of granulation tissue
deepest layer fibrotic scar tissue
causes of PUD
H.pylori
NSAIDs
gastric dysmotility
outflow obstruction
complications of PUD
pain predominant dyspepsia perforation penetration haemorrhage stenosis intractable pain
H.pylori and PUD
acute inflammatory response which can progress to chronic
ammonia and proteases released damage epithelium
H.pylori increased pH increases gastrin production
excess acid can cause duodenal ulcers to form
H.pylori ammonia production
2H2O +H - urease - ammonium bicarbonate
urease us an enzyme produced by H.pylori
NSAIDs and PUD
decrease prostaglandin formation via COX inhibition
PGE2 and PGI2 normally increase pH
NSAIDs increase acid production and decrease protection
PUD symptoms
pain predominant dyspepsia often nocturnal aggravated or relieved by eating relapsing and remitting nausea and vomiting weight loss reflux
PUD investigations
first line - carbon 13 urea breath test, faecal antigen test
second line - re-test urea breath test, serology IgA antibodies
rarely gastroscopy and biopsy
treatment of PUD
tested positive for H.pylori - triple therapy for 7 days:
PPI
amoxicillin
cllarithromycin/metrindazole
people using NSAIDs - stop NSAIDs, PPI or H2RA, and H.pylori eradication
negative for H.pylori and NSAIDs - PPI or H2RA
PUD complication
anaemia bleeding - haematemesis, melena perforation gastric outlet/duodenal obstruction cancer
PUD follow up
duodenal ulcer - only if ongoing symptoms
gastric ulcer - endoscopy at 6-8 weeks, ensure healing and no malignancy
dyspepsia
a collection of symptoms
epigastric pain syndrome - bloating, epigastric pain/ burning in stomach/ abdomen, felux
post prandial distress syndrome - post prandial fullness, early satiety, nausea and vomiting
dyspepsia causes
organic - PUD, GORD, NSAIDs, COX-2 inhibitor, gastric cancer
functional - no evidence of structural disease, associated with IBS
ALARMS symptoms
anaemia loss of weight anorexia recent onset of progressive symptoms masses and melena/haematemesis swallowing dificulty over 55 anyone with dyspepsia/GORD that fits any of this criteria receives upper GI endoscopy
management of dyspepsia
absence of ALARMS
lifestyle measures
assess medication
medical treatment - PPI, test for H.pylori
gastric cancer risk factors
infections - H.pylori
smoking
diet - processed meats
obesity
gastric cancer histopathology
90% adenocarcinoma - intestinal or diffuse
5% lymphomas - MALT lymphomas
cacinoid and stromal tumours may occur
gastric cancer symptoms
dyspepsia
ALARMS or >55 years
gastric cancer investigations
endoscopy and biopsy
CT scan
gastric cancer treatment
surgery is definitive treatment
chemo and radiotherapy
MALT lymphoma - treatment for H.pylori
Achalasia
oesophageal motility disorder
failure of smooth muscle relaxation of LOS - increased LOS tone, lack of peristalsis, due to degradation of the myenteric plexus
failure of distal inhibitory neurons
achalasia symptoms
dysphagia
regurgitation of undigested food
chest pain
weight loss
achalasia investigations
x-ray may show dilated oesophagus
barium swallow study will show a bird beak appearance
oesophageal manometry
endoscopy to rule out cancer
achalasia management
CCBs and nitrates
young - heller’s myotomy (cardiomyotomy)
old - balloon dilation
gastroparesis
delayed gastric emptying that is not due to an obstruction
can be caused by diabetes
chemotherapy induced neuropathy
can be caused by smoking weed
gastroparesis symptoms
feeling of fullness bloating weight loss caused by food fear nausea and vomiting after meals abdomen pain
gastroparesis investigations
gastric emptying studies
manometry
gastroparesis management
nutritional support
metoclopramide
implantable gastric stimulation
vertical sleeve gastrectomy
haematemesis
blood in vomit
melena
black, foul smelling stool
