GI 1 Flashcards
at what point does reflux of gastric contents into the oesophagus become GORD, instead of a normal occurrence?
when it begins to cause symptoms
what 3 problems might prolonged GORD cause?
oesophagitis, benign oesophageal strictures, Barrett’s oesophagus
give 3 causes of GORD
lower oesophageal sphicter hypotension, hiatus hernia, loss of oesophageal peristaltic function, abdominal obesity, gastric acid hypersecretion, slow gastric emptying
give 3 risk factors for GORD
overeating, smoking, alcohol, pregnancy, surgery in achalasia, drugs, systemic sclerosis
explain the pathophysiology of GORD
LOS tone reduced + frequent transient LOS relaxation.
increased mucosal sensitivity to gastric acid + reduced oesophageal clearance of acid.
describe the pain felt in GORD
burning pain, aggravated by lying flat/bending over and on drinking hot drinks/alcohol, after big meals - relieved by antacids.
give 2 features of GORD, apart from chest pain
belching, acid/bile regurgitation, increased saliva production, odynophage (painful swallowing)
give 2 extra-oesophageal features of GORD
nocturnal asthma, chronic cough, laryngitis (hoarseness, throat clearing), sinusitis
give 2 possible complications of GORD
oesophagitis, ulcers, benign stricture, iron-deficiency. Barrett’s oesophagus.
what is Barrett’s oesophagus? how does it put GORD patients at greater risk of oesophageal cancer?
distal oesophageal epithelium undergoes metaplasia from squamous to columnar.
metalplasia -> dyplasia -> neoplasia.
this pattern means those with low-grade Barrett’s oesophagus are more likely to progress to cancer.
give 3 differential diagnoses of GORD
oesophagitis due to corrosives, NSAIDs, herpes, Candida. duodenal/gastric ulcers or cancers. non-ulcer dyspepsia. sphincter of Oddi malfunction. cardiac disease.
give 3 red flag features of upper GI diseases. what would you do if a patient had these?
ALARM symptoms: Anaemia (iron-deficiency) Loss of weight. Anorexia. Recent onset/progressive symptoms. Malaena/haematemesis. Swallowing difficulty.
endoscopy to check for upper GI cancers.
describe the lifestyle changes you would advise a GORD patient to make
lose weight, avoid alcohol, hot drinks, citrus fruits, fizzy drinks, spicy foods etc.
smoking cessation.
raise bed head.
eat small regular meals, don’t eat close to bed time.
how might you manage GORD, beyond lifestyle changes?
antacids or alginates.
oesophagitis - PPIs (lansoprazole, omeprazole etc).
H2-receptor blockers (rantidine).
laprascopic surgery - increase LOS pressure.
how do alginates/antacids work?
usually given as compound preparations.
antacids buffer stomach acid.
alginates increase the viscosity of stomach contents.
they form a floating ‘raft’ separating gastric contents from the gastro-oesophageal junction.
how do PPIs work?
irreversibly inhibit gastric H+/K+-ATPase.
block luminal secretion of gastric acid.
by targeting this final stage of gastric acid production, they can suppress it almost completely - more effective than H2 receptor blockers.
how do H2 receptor antagonists work?
reduce gastric acid secretion. they block the H2 (histamine) receptors on the gastric parietal cell, preventing activation of the proton pump.
pump still stimulated by other pathways, so H2 receptor blockers are not as effective as PPIs.
what causes a Mallory-Weiss tear? how might it present
persistent vomiting/retching - causes haematemesis via an oesophageal mucosal tear.
what are Mallory-Weiss tears associated with?
alcoholism and eating disorders
what is a peptic ulcer? where do they usually occur?
an ulcer of the mucosa in/adjacent to an acid-bearing area.
stomach + proximal duodenum. - duodenum more common.
what two things cause most peptic ulcers?
H. pylori
NSAIDs/aspirin
list 3 risk factors for duodenal ulcers
- H pylori
- NSAIDs, steroids, SSRIs
increased gastric acid secretion.
increased gastric emptying (lowers duodenal pH).
blood group O.
smoking.
list 3 risk factors for gastric ulcers
H pylori, smoking, NSAIDs, reflux of duodenal contents, delayed gastric emptying
what are the differences between the epigastric pain of a gastric ulcer and of a duodenal ulcer?
gastric - worse with food, better when hungry.
duodenal - worse when hungry, better with food or milk.
give 2 features of peptic ulcer disease apart from epigastric pain
bloating, fullness after meals, heartburn, tender epigastrium.
what investigations would be carried out in peptic ulcer disease? what would you expect to see?
endoscopy - biopsy all ulcers to exclude malignancy.
C13-urea breath test for H pylori ± stool antigen test - immunoassay using monoclonal antibodies.
how would you treat an H pylori +ve peptic ulcer patient?
eradication regimens - omeprazole + metronidazole + clarithromycin.
how would you treat an H pylori -ve peptic ulcer patient?
stop aspirin/NSAIDs.
PPIs - lansoprazole (or rantidine - H2 blocker).
give 2 possible complications of peptic ulcer disease
perforation (surgical closure, drain abdo).
bleeding.
malignancy.
gastric outflow obstruction.
what group of patients is at highest risk of developing oesophageal varices? why?
cirrhosis patients - portal hypertension causes dilated collateral veins at site of portosystemic anastomoses
what is the complication risk with oesophageal varices?
that they will cause an acute haemorrhage - life-threatening.
the varices protrude into oesophageal lumen so are easily traumatised by passing food.
how would you manage a patient bleeding from oesophageal varices?
restore blood volume and correct clotting abnormalities - vit K.
endoscopic banding, sclerosing or cauterising.
vasocontrictors - terlipressin.
give 3 clinical features of achalasia
dysphagia for both solids and liquids.
regurgitation of food, esp at night.
chest pain due to oesophageal spasm.
weight loss.
what is achalasia?
oesophageal motility disorder - LOS fails to relax due to degeneration of the myenteric plexus.
explain the pathogenesis of achalasia
inflammation of myenteric plexus of the oesophagus with ganglion loss - causes loss of nitric oxide, so impaired relaxation of the LOS and oesophageal peristalsis
what might you find on barium swallow of a patient with achalasia?
lack of peristalsis and swan neck/beak deformity at lower oesophagus
what cosmetic drug might help a patient with achalasia?
botulinum toxin A (botox) - injected into LOS
what surgical treatments are available to treat achalasia?
endoscopic balloon dilation or Heller’s cardiomyotomy (surgical division of LOS)
what is the most common cause of gastritis?
H pylori
how do NSAIDs cause gastritis?
they inhibit the COX pathway - COX1 is involved in mucus production so there is a depletion of mucosal prostaglandins
explain the pathology of autoimmune gastritis
combination of atrophic gastritis and loss of parietal cells, which affects the fundus and body of the stomach. there are serum antibodies to gastric parietal cells, which can lead to pernicious anaemia.
what is gastritis?
inflammation of the gastric mucosa - histological diagnosis, usually an incidental finding on gastric mucosal biopsy
list 3 causes of gastritis
H pylori, NSAIDs, autoimmune, viruses, hiatus hernia, alcohol
how might gastritis present?
asymptomatic, or epigastric pain, vomiting, haematemesis
how would you treat gastritis?
ranitidine (H2 blocker) or PPI.
H pylori eradication if needed.
give 3 causes of malabsorption that are common in the UK
coeliac disease, chronic pancreatitis, crohn’s disease
give 3 rarer causes of malabsoprtion
decreased bile - primary biliary cirrhosis, ileal resection, biliary obstruction.
pancreatic insufficiency - pancreatic cancer, cystic fibrosis.
small bowel mucosa - Whipple’s disease, tropical sprue, small bowel resection.
infection - giardiasis, strongloidiasis.
what 3 signs would be seen on histology in coeliac disease?
crypt hyperplasia and villous atrophy + lymphocytic infiltration
what is coeliac disease?
gluten-sensitive enteropathy. T cell mediated autoimmune disease.
abnormal jejunal mucosa that improves when gluten is removed and relapses when gluten is reintroduced.
explain the pathogenesis of coeliac disease
HLA-DQ2/DQ8.
alpha gliadin passes through damaged epithelium of small intestine - deaminated by tissue transglutaminase.
interacts with APCs to activate T cells.
inflammation - leads to villous atrophy and crypt hyperplasia.
give 5 clinical features of coeliac disease
stinking, pale stools that are hard to flush (steatorrhoea).
diarrhoea, abdo pain, bloating, nausea/vomiting, aphthous ulcers, angular stomatitis, weight loss, fatigue, weakness, osteomalacia, failure to thrive.
list 3 differential diagnoses of coeliac disease
IBS, lactose/other food intolerances, IBDs, dermatitis herpetiformis, tropical sprue, bacterial overgrowth, intestinal resection, Whipple’s disease, radiation enteritis.
what 2 signs would you see on serology of a patient with coeliac disease?
low folate/iron, IgA anti-tissue transglutaminase antibodies, anti-enodmyseal antibodies (anti-EMA)
what is the gold standard investigation for coeliac disease?
small bowel biopsy by endoscopy
why would coeliac disease patients be advised to get regular vaccinations?
hyposplenism is common, making them more susceptible to infections
how would you manage coeliac disease?
life-long gluten free diet (must reintroduce gluten a couple of weeks before biopsies taken, but can be stopped initially as a way of identifying coeliac disease).
avoid - wheat, rye and barley.
gluten-free biscuits, flour, bread and pasta are prescribable.
give 2 possible complications of coeliac disease
anaemia, secondary lactose intolerance, increased risk of malignancy, osteoporosis
what is tropical sprue?
a progressive small intestinal disorder occurring in residents/visitors to endemic areas in tropics
describe the pathological features of tropical sprue
villous atrophy + malabsorption (esp. fat and vit B12)
how does tropical sprue present?
diarrhoea, steatorrhoea, megaloblastic anaemia
how would you treat tropical sprue?
tetracycline + folic acid and mineral supplements.
exclude coeliac disease and acute infective diarrhoea.
where in the GI tract might Crohn’s disease affect?
mouth to anus.
describe the lesions seen in Crohn’s disease
skip lesions - there are areas of unaffected bowel between areas of active disease.
there’s transmural inflammation (inflammation spanning full depth of wall) - causes ulceration of superficial mucosa, possibly granulomas
what would you see on endoscopy in Crohn’s disease?
cobblestone appearance - due to skip lesions of inflammation/ulceration and deep fissures.
give 3 symptoms of Crohn’s disease
diarrhoea/urgency.
abdo pain.
weight loss.
fever, malaise, anorexia.
give 3 signs of Crohn’s disease
aphthous ulcers (in mouth). abdo tenderness/mass. perianal abscess/fistulas/anal strictures.
extra-GI - clubbing, conjunctivitis, peripheral arthropathies, erythema nodosum, fatty liver, renal stones.
list 3 possible complications of Crohn’s disease
small bowel obstruction, toxic megacolon, abscess formation, fistulae, perforation, colon cancer, fatty liver, PSC, renal stones, osteomalacia, malnutrition, amyloidosis
list 3 differential diagnoses of Crohn’s
UC.
TB, carcinoid syndrome, amyloidosis, infective diarrhoea, bowel carcinoma, ischaemic colitis, diverticulitis, coeliac disease, IBS